SNBTS Research Strategy - Scottish National Blood Transfusion ...

SNBTS Research, Development & 

Innovation 

Strategy 2012-2017 

SNBTS_RDI_Strategy_2012-17_10 July2012 final.doc Page 1 of 74

Contents 

Page Number 

Introduction 3 

Workforce 4 

Financial Summary 5 

 

 

 

 

Publications & 

Grants Summary 

Tissue and Cellular 

Therapies Theme 

Group ~ Summary 

Microbiology & 

Components Theme 

Group ~ Summary 

Clinical Transfusion 

Theme Group ~ 

Summary 

Figure 1: Proposed Staff 

Structure October 2012 

References 9 

o Appendix 1 RDI Workforce Plan 2012- 

10 

2017 

o Appendix 2 Tissue and Cellular 

Therapies Theme Group 

Plan 

11 

o Appendix 3 


Components Theme Group 

Plan 

o Appendix 4 Clinical Transfusion 

34 

Theme Group Plan 

o Appendix 5 Publications & Grants 42 

o Appendix 6 Healthcare Quality Impact 

Assessment Template 

72 

5 

6 

7 

7 

8 

23 


Introduction 

Current SNBTS Strategy was laid out in the SNBTS Strategic Development Plan 2009- 

2014, approved by NSS Board in March 2009 1 . In 2011 a Strategy Refresh was initiated in 

order to adapt the organisation to the changing external environment including the 

Healthcare Quality Strategy 2010 2 , the global recession and consequent public sector fiscal 

retrenchment and our ageing Scottish demography. Internal drivers include retirement of a 

large cohort of senior and experienced staff, the requirement to find efficiency savings and 

the need to refocus research effort to ensure maximum quality, impact and relevance. 

The SNBTS Strategy Refresh 3 provides the framework for this 5 year Research, 

Development and Innovation plan which supports the strategic objectives in addressing the 

critical issues facing the organisation, particularly those around continuing threats to blood, 

tissue and cell safety from new and emergent infections, ensuring the continuing quality and 

effectiveness of clinical products and services and managing changes in demand for 

existing and new products due to ageing demography. The Penrose Inquiry 4 has 

highlighted the role of SNBTS research, development an innovation in addressing the 

challenges to the blood and plasma product supply posed by HIV and HCV in the 1970s 

and 1980s. Whilst the nature of the threats to supply, safety and quality evolve with the 

times, our fundamental responsibility to manage them in a timely and effective manner is a 

constant. Moreover, SNBTS has a broader responsibility in helping NHS Scotland to 

manage the forthcoming rise in chronic degenerative conditions and to support the Scottish 

Government’s Healthcare Quality 2 and Life Sciences ambitions 5,6 . 

In order for SNBTS to continue to deliver high quality / impact research in support of its 

strategic objectives, it will focus on three research themed areas. Each will be aligned to 

one of the 3 SNBTS Operational Directorates, but will also interface both with the main 

research intensive Scottish Universities in Edinburgh, Glasgow, Aberdeen and Dundee and 

with partner organisations such as the National CJD Surveillance Unit and the Roslin 

Institute, in order to leverage a range of resources and capabilities which the organisation 

itself does not necessarily possess. SNBTS currently has in place formal agreements with 

the Universities of Aberdeen, Edinburgh and Glasgow to participate in collaborative 

research work in the field of transfusion medicine. Additionally, The Scottish Centre for 

Regenerative Medicine (SCRM) GMP cell therapy manufacturing facility is now complete 

and it is proposed that SNBTS will co-manage this with Roslin Cells for a period of 5 years. 

This will involve input from within SNBTS Tissues and Cells, Quality and RDI and this will 

not only facilitate NSS SNBTS’ central role in the development of cell therapy to direct 

clinical value to patient health but will also support the Scottish Government Life Sciences 

strategy in regenerative clinical and translational medicine. 

SNBTS will continue to work in partnership with other research-active divisions of NSS and 

the wider NHS Scotland, as well as with other UK and International Blood Services in order 

to ensure clinical relevance and efficient use of resources. Regular, quarterly joint meetings 

with research staff from Health Protection Scotland have been initiated to investigate areas 

of mutual interest, while senior staff from SNBTS, HPS and ISD are actively involved in the 

formulation of a Research Strategy for NSS. 


The proposed three new Theme Groups are: 

Tissue and Cellular Therapies 

The support of established cell and tissue therapies such as haematopoietic stem cell 

transplantation as well as the implementation of new cell based therapies such as 

pancreatic islet transplantation are both of importance. 

The development of a new generation of cellular therapies is a strategic objective for 

both the Scottish 5 and UK 7 Governments as evidenced for example by the building of 

the Scottish Centre for Regenerative Medicine in Edinburgh 8 and the recent 

announcement of funding for a Cellular Therapy Catapult Centre respectively 9 . 

Microbiology & Components 

The quality, safety and sufficiency of the blood supply is clearly the core responsibility of 

SNBTS. Research and development in this field is essential to ensure the organisation 

is prepared for the potential introduction of a vCJD screening assay on blood donation; 

enable rapid response to new and emergent infections and to evaluate the effectiveness 

and clinical safety of pathogen reduction and removal technologies. 


Immunological matching of blood, tissue and cells and solid organs for transplantation is 

key to ensuring survival of the transfused/transplanted human tissue and to manage 

potential adverse impacts on recipients. Research and development in this area is 

essential to maintain and improve the efficacy and safety of blood transfusion for 

patients in Scotland while also leading to the development and application of new 

diagnostic and therapeutic approaches. 

In addition there is increasing evidence to suggest that excessive transfusion particularly 

with aged blood can have a detrimental impact on patients. Further evaluation of this risk 

through both clinical and laboratory studies is essential. 

Workforce 

The strategic leadership of the Research, Development & Innovation Directorate will be 

performed by a Head of RDI, working with the Medical Director and with the support of the 

newly identified Theme Leaders to develop and implement the strategies required to 

achieve these organisational goals. The post of Head of RDI has been identified in the 

Workforce Plan as a key to this delivery and approval to fill this position has been granted. 

The recruitment process is underway and it is hoped the position will be filled before the end 

of 2012. Operational leadership will be performed by the Theme Leaders and Senior 

Research Scientists within each group and many of these senior staff have already been 

identified and are in post or will be appointed from within the existing establishment. 

Analysis of the probable R&D staffing complement over the next 5 years, taking into 

account likely retirals, options for succession by existing more junior staff, identification of 

critical posts and potential revenue savings has been carried out. This has considered 

restructuring of the staffing in each themed area, taking account of existing skills-mix and 

identified where gaps in the required skills and numbers are apparent. This has revealed a 

likely overall reduction in R&D staff numbers from 52 (2011-12) to approximately 32 (2012- 

13) and a recurring annual revenue saving of around 20%. This reduction and saving takes 

into account replacement or review of 8 posts considered to be critical for business 


continuity and/or staff succession. The expected staff structure in October 2012 is shown in 

Figure 1 below and the summarised Workforce Plan (2012-17) is shown in Appendix 1. 

Financial Summary 

In addition to the salaries, staff related costs and goods & services budgets proposed in 

each of the three Theme Group sections of this report, there are costs involved in the 

overall management and administration of the RDI Directorate. These costs are identified 

below in the financial summary. 

Research Development & Innovation Directorate Financial Summary 2012-13 

Salaries Staff Related Goods & Services Total 

Costs 

RDI Central £187,726 £16,410 £96,086 £300,222 

Tissue & Cellular Therapies £540,086 £15,157 £67,232 £622,475 

Microbiology & Components £462,737 £23,409 £107,743 £593,889 

Clinical Transfusion £367,635 £16,019 £48,059 £431,713 

TOTAL £1,558,184 £70,995 £319,120 £1,948,299 

Publications & Grants 2008-2012 

Year 

Journal 

Publications 

Books & Book 

Chapters 

Posters 

& 

Abstracts 

New 

Grants 

Total Grant Income for 

Year 

(£ x 10 6 ) 

2008/09 85 7 17 5.1 

2009/10 66 8 55 16 7.2 

2010/11 63 4 62 8 5.1 

2011/12 46 2 36 13 5.9 

Full details of publications and grants can be found in Appendix 5. 


Fig 1: RDI Proposed Staff Structure Oct 2012 

Medical Director 

Prof Marc Turner 

Head of RDI 

TBA 

Central RDI Staff 

Research Administrator: 

Isabel Ward 

Librarian: June MacLeod 


Theme Group 

Lead: Prof Mark 

Vickers 

Tissue & Cellular 

Therapies Theme 

Group 

Lead: Dr Jo Mountford 


Components Theme 

Group 

Lead: Dr Juraj Petrik 

Product Testing Unit 

Pentlands Science Park 

Lead: Dr Davor Fatori 

Staff salaries derived 

from SNBTS 

Staff salaries not 

SNBTS-derived 

Aberdeen ATMU 

Dr Sylvia Armstrong-Fisher 

Dr Mike Moss 

Ms Sadie Henderson 

Ms Anne Taylor (PA) 

Glasgow SNBTS 

Dr David Colligan 

Dr Dick Drake 

Dr Anne Mackie 

Mr Paul Hopkinson 

Edinburgh NSL 

Dr Anne Leaver 

University of Glasgow 

Dr Lamin Marenah 

Dr Niove Jordanides 

Dr Emmanuel Olivier 

Prof T Holyoake 

Ms Elaine Allan 

University of Edinburgh 

Dr L Forrester 

Dr P de Sousa 

Dr Ronnie Gallagher 

Ms Kay Samuel 

Edinburgh NSL 

Components 

Dr Ian Downing 

Dr Shirley MacDonald 

Ms Loraine McMillan 

Mr Alex Morrison 

Ms Sandie Young 

(Secretary) 

Edinburgh NSL 

Microbiology 

Mr Sandy Cleland 

Ms Pamela Gilhooly 

Dr Stuart Imlach 

Dr Osmany-Larralde-Diaz 

Ms Karen McGowan 

Ms Kristen Mulligan 

Dr Katrina Thom 

Clinical Services Tissues & Cells Supply Chain 

Clinical Services 

Lead: Dr Rachel Green 

Product Services Dept 

Lead: Ms Jane Pelly 

Microbiology Reference 

Unit 

Lead: Dr Lisa Jarvis 

Better Blood Transfusion 

Group 

Lead: Mrs Sandra Gray 

vCJD Group 

Lead: Dr Mike Jones 

Other Research 

Active Groups 


Tissue and Cellular Therapies Theme Group 

Over the next 5 years the Cell Therapy group will build on established expertise and 

collaborations to concentrate our research and development studies on three blood/bone 

marrow derived cell populations: blood cells (including red blood cells, macrophages), 

vascular endothelial cells and mesenchymal stem cells. There is increasing evidence that 

these cell populations can be used to treat a number of serious health issues that are 

particularly prevalent in the Scottish population and represent significant unmet clinical 

need. These include cardiovascular disease, liver failure and diabetes mellitus and the 

continuing requirement for a secure supply of blood components for transfusion. 

Primary Aim: To support the development of Cellular Therapeutics and Regenerative 

Medicine in alignment with the Scottish Government’s Life Sciences and Healthcare Quality 

strategies. 

Scope 

We will make use of cells derived from adult sources (peripheral blood, bone marrow, cord 

blood) and from pluripotent stem cells (human embryonic SC or induced pluripotent SC); 

our studies will span from clarifying the applied biology of these cells to understand their 

differentiation and functionality, through GMP-compliant production and regulatory approval 

to clinical trialing for safety and efficacy. We will work closely with the SNBTS Tissues & 

Cells and Quality Directorates to ensure our research provides developmental support for 

existing SNBTS products and delivers a new generation of cell therapies. We will 

collaborate with the Scottish Centre for Regeneratve Medicine and international Blood 

Services in developing our work in this field. 

Impact 

Most importantly the enhanced understanding of these cell populations and the capacity to 

harness their potential should lead directly to new clinical treatments for major degenerative 

diseases, an alternative supply of blood for transfusion and should have significant impact 

on the health of the Scottish population in the longer-term. Successful development of 

these projects and their translation into clinical practice will also result in high impact 

publications, leading to further external peer-reviewed funding and the generation of 

valuable know-how, technological advances and intellectual property that may be exploited 

commercially. 

Full details of the proposed programme of work for this Theme group can be found in 

Appendix 2. 

Microbiology & Components Theme Group 

Using rigorous research, development and validation techniques we expect to safeguard 

our preparedness for new and emerging blood borne pathogens. High quality surveillance, 

epidemiological and molecular data will significantly facilitate this goal. At the same time it 

is an imperative to continue to improve the safety of blood and tissue products for 

vulnerable patient groups, such as immunocompromised individuals including 

Haematopoietic Stem Cell and Solid Organ transplant recipients. This group of patients 

frequently suffer from complications caused by common pathogens immunologically 

controlled in the healthy population. 


Continued work is required on the quality and safety of the current generation of blood and 

tissue products. 

Primary Aim: To maintain a high level of microbiological safety of blood and tissue 

products and where possible, to improve it through the development and application of new 

screening technologies combined with pathogen reduction/removal measures. At the same 

time our aim is to continuously improve the quality and safety of blood components leading 

to improved clinical outcomes for patients. We will work on achieving these targets in 

partnership with and in support of the Donor and Manufacturing Directorates. 

Scope 

We consider a rational combination of novel multiplexing diagnostic techniques with 

pathogen reduction technologies the most logical way forward for the future, since no single 

approach is able to achieve complete microbiological blood safety on its own. 

Quality and safety of blood components is of critical importance for patients’ clinical 

outcomes. By focusing our research on reducing the causes of storage lesion and 

participating in international studies comparing and standardising our tests and procedures 

we aim at improvements in component quality, safety and logistics of their production and 

distribution. 

We will continue to collaborate with Health Protection Scotland, UK and European Blood 

services in pursuit of these aims. 

Impact 

Achieving these goals by studying and applying new approaches and technologies, will 

facilitate further improvement in blood safety and quality for benefit of patients in Scotland 

and beyond, and maintain SNBTS’s prominent place in the forefront of Transfusion 

Medicine. 


Appendix 3. 

Clinical Transfusion Theme Group 

Over the next five years, this group will concentrate on assessing the demand and 

effectiveness of blood transfusion and its potential adverse effects through epidemiological, 

clinical and laboratory studies. This reflects the SNBTS strategic objective to manage 

demand and also recent evidence implicating red cell transfusion as a cause of increased 

patient morbidity and mortality. Work will continue on the immunological matching of blood, 

tissues, cell and organs and in the development of diagnostic and therapeutic 

immunohaematological approaches for diseases of the blood, some of which will continue 

to be progressed into the commercial sector. 

Primary Aim: To improve the efficacy and safety of blood transfusion and tissue, cell and 

organ transplantation for patients in Scotland while continuing development and 

commercialisation of diagnostic and therapeutic approaches for diseases of the blood. 

Scope 

We will analyse the ways in which blood products are used in Scotland, paying particular 

attention to differences between hospitals without readily apparent explanations, as well as 


oth initiate and take part in trials to assess the optimum trigger points to give transfusions. 

The possibility that red cell transfusions can act as harmful inducers of inflammation or 

thrombosis will be investigated in both clinical trials and the laboratory. We will continue to 

provide development and support for molecular diagnostic services as well as progress 

previously developed peptide based diagnostic platforms and vaccines into the commercial 

sector. 

Impact 

These studies will help to optimise clinical decisions concerning blood transfusion and also 

help to optimise the duration and conditions of blood storage, so increasing the safety of cell 

products provided by SNBTS. Improved immunological matching will increase the 

availability, quality and safety of organ and cellular transplants. Income generation from the 

development of new diagnostic and therapeutic materials may also result. 


Appendix 4. 

References 

1. SNBTS Strategic Development Plan. ‘Meeting the Transfusion Needs of Patients in 

Scotland: SNBTS Strategy 2009 – 2014. March 2009. 

2. NHS Scotland Quality Strategy – putting people at the heart of our NHS. May 2010. 

3. SNBTS Strategy Refresh April 2012- March 2017. 

4. The Penrose Inquiry, Preliminary Report. September 2010. 

5. Scottish Life Sciences Strategy 2011: Creating Wealth, Promoting Health. 

6. Health and Wealth in Scotland: A Statement of Intent for Innovation in Health. June 

2012. 

7. Department of Business Innovation and Skills. Strategy for UK Life Sciences. 

December 2011. 

8. http://www.lifesciencesscotland.com 

9. Cell Therapy Technology and Innovation Centre ‘Call For Expressions of Interest’, 

Technology Strategy Board, May 2011 


RDI Workforce Plan 2012-2017 Appendix 1 

AfC Band 2012/13 2013/14 2014/15 2015/16 2016/17 Comments 

RDI Central 9 1 1 1 1 1 Head Of RDI, advertised June 2012. Appointment 

expected in last quarter of 2012. 

8B 0.5 0.5 0 0 0 Remainder of 1 wte transferred to Clinical Transfusion 

5 1 1 1 1 1 

Sub-Total RDI Central 2.5 2.5 2.0 2.0 2.0 

Cell Therapy 8D 0.25 0 0 0 0 Retiral July 2012 

8C 0.5 0 0 0 0 Retiral Oct 2012 

8B 2.35 2.1 2.1 2.1 2.1 IDTransfer to M&C July; 0.7 DC, AM, RD 

8A 3.25 3 3 3 3 SM Transfer to M&C July 

7 2 2 2 2 2 KS, EA 

4 0.7 0.7 0.7 0.7 0.7 PH 0.7 wte 

Non-AfC 1.95 2.2 2.2 2.2 2.2 JM, EO & TH (0.2) 

(University) 

Sub-Total Cell Therapy 11 10 10 10 10 

Microbiology & Components 8C 1 1 1 1 1 JP 

8B 0.75 1 1 1 1 ID 

8A 0.75 1 1 1 1 SM 

7 5 5 5 5 5 AC,AM,SI,OL-D,KM(0.5)&KT(0.5) 

6 2 2 2 2 2 KM,LM 

4 2 2 2 2 2 PG, SY 

Sub-Total Micro & Components 11.5 12 12 12 12 

Clinical Transfusion 8B 3.4 3.4 3.9 3.9 2.9 RD,DC, & AM (0.3); HAL 0.5-1.0 wte; 

SSAF & MM 1.0 wte 

5 0.5 0.5 0.5 0.5 0.5 SH 

4 1.3 1.3 1.3 1.3 1.3 AT & PH (0.3) 

Non-AfC 1 1 1 1 1 LC 

(University) 

Sub-Total Clin Transfusion 6.2 6.2 6.7 6.7 6.7 

TOTAL 31.2 30.7 30.7 30.7 30.7 


Tissue and Cellular Therapies Appendix 2 

Over the next 5 years the Cell Therapy group will build on established expertise and 

collaborations to concentrate our research and development studies on three blood/bone 

marrow derived cell populations: blood cells (including red blood cells, macrophages), 

vascular endothelial cells and mesenchymal stem cells. There is increasing evidence that 

these cell populations can be used to treat a number of serious health issues that are 

particularly prevalent in the Scottish population and present significant unmet clinical need. 

These include cardiovascular disease, liver failure and diabetes mellitus and the continuing 

requirement for a secure supply of red blood cells for transfusion. 

Primary Aim: To support the development of Cellular Therapeutics and Regenerative 

Medicine in alignment with the Scottish Government’s Life Sciences strategy. 

Scope 

We will make use of cells derived from adult sources (peripheral blood, bone marrow, cord 

blood) and from pluripotent stem cells (human embryonic SC or induced pluripotent SC); 

our studies will span from clarifying the applied biology of these cells to understand their 

differentiation and functionality, through GMP-compliant production and regulatory approval 

to clinical trialing for safety and efficacy. We will work closely with the SNBTS Tissues & 

Cells and Quality Directorates to ensure our research provides developmental support for 

existing SNBTS products and delivers a new generation of cell therapies. 

Impact 

Most importantly the enhanced understanding of these cell populations and the capacity to 

harness their potential will lead directly to new clinical treatments for major diseases, an 

alternative supply of blood for transfusion and will have significant impact on the health of 

the Scottish population. Successful development of these projects and their translation into 

clinical practice will also result in high impact publications, leading to further funding and the 

generation of valuable know-how, technological advances and intellectual property that may 

be exploited commercially. 

Expected Achievements [Outputs]: 

Project 1. To have performed first in man studies of pluripotent stem cell-derived red cells 

Project 2. Identified optimal cell source for the regeneration of vascular endothelium in 

ischemic limb disease and initiated clinical trial. 

Project 3. To perform a clinical trial of MSC as adjunct therapy to islet transplant. 

Project 4. Completion of initial clinical trials for of limbal stem cell therapy and the delivery 

of cytotoxic T-cell and CD133+ and/or monocyte cell therapies 

Benefits to SNBTS and NHS Scotland [Outcomes]: 

1. A cultured source of red cells that would help to manage problems of sufficiency, 

immune compatibility and transfusion transmitted infection as well as the potentially the 

adverse effects of iron loading in multi-transfused patients and from aged red cells 

2. A reliable GMP source of mesenchymal cells that could be used as immunomodulatory 

therapy for major diseases such as MS and diabetes, and haematopoietic or solid organ 

transplantation. 

3. Development of novel therapies for cardiovascular disease which represent the 

predominant cause of morbidity and mortality in Scotland 

4. Increased yield and survival of pancreatic islet isolates that will allow more patients to 

be transplanted and to gain longer duration of beneficial effect, helping to better manage the 

problem of type 1 diabetes 


5. The translation of research findings to GMP compliance will allow the delivery of novel 

allogeneic cell therapies such as limbal stem cells and cytotoxic T-cells to clinical practice 

demonstrating SNBTS’s world-leading expertise in Cell Therapy development. 

6. The early identification of intellectual property and know-how that can be protected and 

exploited to generate income from new therapeutic materials, processes and diagnostic 

assays 

Project 1. Blood Cells 

Blood Transfusion has become a mainstay of modern medical practice. However problems persist 

both nationally and internationally in maintaining adequacy of supply, managing the risk of 

transmission of infectious agents and ensuring immune compatibility between donor and recipient. 

Resources to be allocated in year 1: 6.65 FTE + associated G&S/SRC = £421,420 

Grant funded by Wellcome Trust, SFC and SE 

Additional applications in progress 

a. Generation of GMP-grade red blood cells from pluripotent stem cells (to include application for 

regulatory approval for trials of PSC derived RBCs and derivation of a stable haematopoietic or 

erythroid progenitor population that can be used for industrial scale RBC production) 

Pluripotent stem cells (PSCs) have unique properties in that they can be maintained indefinitely in 

culture in an undifferentiated state and yet retain the ability to form all the cells and tissues within the 

body. They therefore offer a potentially limitless source from which to generate red cells for use in 

clinical transfusion. We will continue to develop methods for the production of these in vitro RBCs 

and perform initial in vivo safety testing and ex vivo functional assays. This work also involves the 

generation of haematopoietic stem cells (HSC) as an intermediate stage to RBCs. These HSC may 

closely resemble HSC isolated from cord blood and bone marrow and could therefore, be extremely 

valuable as a model to examine the maintanence and expansion of normal HSC and how they may 

be used more effectively for transplantation. We will specifically assess the capacity of hESCderived 

HSC to repopulated haematopoiesis in mice (With Dr Lesley Forrester & Prof Alexander 

Medvinsky; CRM, U of Ed) and investigate the effect of hypoxia on their expansion and definitive 

characteristics (Prof Tessa Holyoake & Dr Kamil Kranc, U of Glasgow). 

b. Production of induced pluripotent stem cells from adult haematopoietic cells 

The successful use of pluripotent cell lines for cell therapy will be dependent on immunological 

compatibility between the pluripotent cell line and the patient. Furthermore, the ethical concerns 

surrounding the use of embryonic stem cells in medical applications may limit the global uptake of 

such a product. A real alternative to hESC has been developed over the last 5 years, such that it is 

now possible to generate induced pluripotent stem cells (iPSC) that may be suitable for clinical use. 

We will make fully and partially reprogrammed iPSC lines at research grade in the first instance from 

donor tissue of defined blood group status. In the longer term we will work with Roslin Cells and the 

SCRM to generate GMP-grade, clinical iPSC lines. The first of these will be a type ORhD- “Universal 

Donor” line for RBC generation. 

c. Generation of monocytes from pluripotent stem cells 

In addition to RBC, pluripotent SC can be specifically differentiated into other blood lineages 

including monocytes, neutrophils and platelets. Monocytes have been tested as potential vectors for 

the local production of anti-inflammatory molecules that can ameliorate acute renal inflammation and 

offer a new therapeutic option for renal injury. The use of unmanipulated monocytes has also been 

proposed for liver disease (See Project 4e below). We will isolate monocytes from peripheral blood, 

and also generate large numbers of monocytes from PSC as a potential source of homogenous 

GMP-grade cells that would provide an “off the shelf” cell therapy solution for use in acutely ill 

patients. 

Project 2. Endothelial Cells 


Ischaemic disease, often the result of diabetes or atherosclerosis, occurs when a patient’s blood 

vessels become blocked, interrupting the flow of blood to tissues and organs. Current therapies 

include drug therapy, bypass and angioplasty but are clearly sub-optimal since this remains a major 

burden to the NHS. Peripheral vascular or arterial disease has an age-adjusted prevalence of 20 

percent for the general population above age 70 and contributes significantly to the cost of treating 

CVD was estimated to cost the NHS £14.3 billion in 2006, with 20% of NHS expenditure 

representing direct costs of treating CVD (British Heart Foundation, 2008). Hence effective new 

treatments for ischaemic disease would offer therapeutic options to patients who are currently bare 

a high burden of morbidity and premature mortality and could make a large impact in a disease that 

carries a large cost to the NHS and the wider Scottish society. 

a. Generation of endothelial cells from pluripotent stem cells 

b. Isolation and expansion of endothelial progenitors from adult sources 

c. Generation GMP-grade endothelial cells from pluripotent stem cells 

The projects above will investigate the generation of vascular endothelial cells from various human 

SC sources (2a &b) with the dual aims of generating direct cell therapies (2c) but also elucidating 

mechanisms underlying this condition and identifying opportunities to develop pharmacological drug 

interventions to safely and locally induce angiogenesis in ischaemic tissues 


Addition funding from BHF, application made to MRC 

Project 3. Mesenchymal Cells 

Mesenchymal stromal cells (MSC) have been extensively studies for their capacity to regenerate 

skeletal tissue including bone and cartilage, however, this focus has recently shifted with the 

realisation that they have profound immunoregulatory capacities. These capacities are so 

remarkable that MSC can prevent mixed lymphocyte reactions in vitro and, in pre-clinical models, 

MSC can support the transplantation of allogeneic tissues. Thus, this new role for MSC as a 

powerful mediator of recipient immune responses is now the focus of considerable interest. The 

clinical utility of pluripotent stem cell-derived therapies has been questioned because of their 

allogeneic origin and their potential to induce immune responses and rejection in the recipient. 

However, immune conditioning of a recipient with MSC derived from the PSC source or even from a 

third party allogeneic donor, may greatly facilitate the transplantation of SC-derived tissue without 

rejection or immune suppressive therapy. This concept is currently being tested in Phase I/II trials to 

mitigate GvHD after HSC transplants. Additionally, there is growing recognition that many chronic 

diseases are the result of dysregulated inflammatory or immune responses, these include diabetes, 

multiple sclerosis, atherosclerosis, some forms of acute lung injury and liver disease. MSCs may 

also have the potential to re-set or regulate the immune response in these settings and could 

represent an important new treatment option for these intractable diseases. However, we will also 

continue our collaborations with academic colleagues who wish to use MSC for their established 

capacity to regenerate bone and cartilage. MSC can be isolated from various tissues including cord 

blood, we will work with the Scottish Cord Blood Bank to make use of units that have been collected 

under their quality systems but are not suitable for storage and transplantation. 

a. GMP-grade tissue collection and MSC isolation/expansion (CMT Gp) 

MSC are routinely isolated from bone marrow, cord blood or adipose tissue. We will make the 

appropriate applications to the SNBTS Committee for the Governance of Samples and also to the 

appropriate Local Ethics Committee to collect cord blood (rejected donations from the CB Bank), 

apheresis cones, adipose tissue from liposuction and waste platelet units for platelet lysate. We will 

establish GMP-compatible protocols in research laboratories and SNBTS “clean rooms” before 

transferring these to SCRM for conversion to full GMP compliant SOPs. 

b. Generation of MSC from pluripotent stem cells, characterisation and comparison of MSC from 

different sources, their capacity to modulate immune function and potential for co-transplantation 

We have the capacity and resource to generate these cells from many different sources at both 

research and GMP-grade. However, we need to look more thoroughly at the efficacy of these cells 


in in vitro and in vivo assays. This work will require additional external funding and close 

collaboration with colleagues such as Prof S Forbes and Dr L Forrester who are already using these 

damage models. It will also be essential to work with the SNBTS Clinical Histocompatability & 

Immunogenetics group (H&I; Prof Phil Dyer) to assess the HLA-type of all tissues and cells. 

c. Development of MSC for co-transplantation with pancreatic tissue 

SNBTS in collaboration with National Service Division (NSD) has successfully introduced an Islet 

transplantation programme and has undertaken numerous transplantation, which have shown 

excellent results in the outcome for the insulin dependant diabetic recipients (n=10 in 2011), these 

patients have successfully recovered their glycaemic awareness and some have become insulin 

independent. However, the effects of the transplant can be transient and further transplantation is 

needed. It is well established in animal models that co-transplantation of islet cells with 

mesenchymal stem cells (MSCs) improves function and survival of transplanted islets. Accordingly, 

it is anticipated that either co-culture prior to transplantation or MSC infusion post-islet 

transplantation would lead to improved outcomes in islet recipients. Also, animal models have 

shown that the addition of MSCs to the transplantation process would provide clinical benefit with 

lower yields of islets, allowing good clinical outcomes with yields would be considered unsuitable for 

transplant and thereby increasing availability of this therapy. The GMP-compliant protocols for 

autologous and allogeneic MSCs developed and tested in Project 2a-c above, could be used to 

generate MSC as ATMPs for transplantation with an initial application for use as co-administration 

with islets. In addition to the established adult and hESC sources it has also been reported that 

MSC can be derived from the exocrine and connective tissue waste that remains after the islets 

have been isolated from a cadaveric pancreas for transplant. We will isolate MSC from this 

alternative source and investigate their use as an adjunct therapy matched to the islet graft. 

This work would be undertaken with Tissues & Cells Directorate, initially using SNBTS resources but 

with applications for external funding to be made as soon as possible. 


Addition input from T&C and H&I directorates 

Additional grant funding to be sought 

Project 4. Clinical Development (lead by Tissue & Cells Directorate and Product Services 

group with R&D support from Cell Therapy group) 

The majority of these projects (4b-e) are currently in translation to GMP/clinical practice and do not 

require immediate input from R&D staff at this time, input of scientific staff may be needed to in 

future to response to specific issues in development and support will be provided by CT R&D as 

required 

a. Pancreatic islets – support to TCD to enhance survival of isolated cells, develop storage 

protocols, identify markers on the active cell population within a graft. 

SNBTS Tissues & Cells, in conjunction with NHS Lothian have established a GMP compliant 

pancreatic islet cell isolation service for the treatment of Type I diabetic patients presenting with 

severe disease. The first transplant took place in early 2011 and to date there have been 16 

transplants in patients throughout Scotland and North-East England, with all patients demonstrating 

restoration of glycaemic awareness, reduced number of hypoglycaemic events, reduced insulin 

requirements and in some cases insulin independence. In the year 2011-12, 10 of the UK’s 19 

transplants were performed in Scotland. SNBTS Tissues and Cells are also able to provide a source 

of human pancreatic islet cells for research and development. We intend to use this material to 

improve the current procedure by developing quantification assays, cryopreservation and transport 

conditions and by correlating outcome with graft quality. 

Improving Islet Quality Assurance via Retrospective Analysis 

In collaboration with the University of Newcastle, SNBTS Tissues and Cells are currently involved in 

the retrospective analysis of clinical islet cell samples for quality control purposes. It is recognised 

internationally that the current mechanisms employed in the release of islets for transplant remain 


limited, subjective and usually devoid of any functional analysis. Current methodology is restricted 

to the quantification of islet cell equivalents, purity and viability. SNBTS Tissues and Cells intend to 

collect tissue and supernatant samples from clinical isolations, which are then fixed or frozen for 

retrospective testing at centres throughout the UK with expertise in 3D viability analysis of beta-cells, 

gene and protein expression analysis and functional in vitro assays. This data will allow correlation 

of islet quality with clinical outcomes in transplanted patients and will ultimately aid the development 

of a standardised series of assays to be employed in the UK prior to clinical release of islets, thus 

ensuring patients are only transplanted with preparations meeting evidence-based stringent criteria 

that are consistent with good clinical outcomes. 

In addition, SNBTS Tissues and Cells plan to validate a transport box designed to control 

temperature and optimum physical conditions. Currently, transport of islets in the UK is highly 

variable with islet quality often deteriorating following extended periods in transit. Validation of such 

a device will ensure consistency throughout the UK and be integral to the development of an organ 

allocation service whereby organs are sent to the nearest centre for islet isolation, storage and 

subsequent transport to the recipient centre, ensuring reduced organ ischaemia, and accordingly 

improved isolation outcomes, and ultimately leading to increased numbers of transplants and more 

economical use of whole pancreata. 

Cryopreservation of Pancreatic Islet Cells 

The shortage of donor pancreata and the inability to consistently isolate large number of viable islets 

(average worldwide ~50%) suggests a role for the long-term storage of islets. Cryopreservation 

would allow indefinite storage of islet cells, leading to specific HLA matching to recipients and permit 

strict quality control through the ability to test all preparations for virological markers (inclusive of 

NAT) and microbial contamination. Although cryopreserved islets are unlikely to induce insulin 

independence in recipients per se, these preparations would be invaluable in ‘topping-up’ recipients 

via 2 nd or 3 rd transplants to sustain long-term function. 

Islet cryopreservation is not currently used clinically in the UK because of the lack of GMP-compliant 

cryopreservation equipment and storage facilities in the other UK laboratories. SNBTS Tissues and 

Cells have considerable experience and equipment required for controlled rate cryopreservation and 

considerable storage facilities required to perform GMP-translation of established protocols. 


Addition input from T&C directorate 

Additional grant funding to be sought in FY2012 

b. Limbal Stem Cell Study 

Stem cells residing in the limbal region of the eye are responsible for renewing the corneal 

epithelium. Limbal stem cell deficiency (LSCD) results in ocular surface disease (OSD) 

characterised by reduced vision or blindness, ocular irritation and visual glare. Current treatment for 

OSD included standard corneal transplantation and limbal tissue grafting. Both treatments have 

limitations with respect to tissue availability and success rates. Ex vivo expansion of limbal stem 

cells is therefore an alternative process for providing sufficient cells for corneal epithelium repair 

from small pieces of donor tissue. 

SNBTS is therefore involved in a study to establish a GMP process for the ex vivo expansion of 

limbal stem cells, from cadaveric donor tissue, on human amniotic membrane. A pilot clinical trial is 

being performed using this product, in collaboration with NHS Lothian, and NHS Greater Glasgow 

and Clyde, and will compare the outcome in 10 patients treated with the product, with 10 patients 

receiving an amniotic membrane control product. This is the first prospective trial to make this 

comparison and will provide information on whether transplantation of the ex vivo expanded corneal 

limbal stem cells product is feasible, efficient and safe; whether this procedure lead to improvements 

in vision and quality of the ocular surface; and how immunosuppression and ex vivo limbal stem cell 

transplantation compare with immunosuppression and amniotic membrane alone. 


SNBTS’s involvement in this study makes us a key player in this pilot study in that we have 

developed and established a suitable GMP grade product, which, following evaluation of the results 

of the pilot study, could lead to establishment of this product for a wider number of patients suffering 

from OSD. In addition, the manufacturing facility has been licensed by the MHRA as the clinical 

product is considered an Investigational Medicinal Product (IMP). This manufacturing licence 

(MA(IMP)) not only allows the facility to manufacture the LSC product, but other products considered 

as IMP’s. This together with the MHRA license to conduct the clinical trial has established SNBTS 

as one of the first centres in UK to be manufacturing an Advanced Therapy Medicinal Product for 

clinical use. 

During 2012, SNBTS will also process ES derived retinal (RPE) cells for a clinical trial examining 

safety and efficacy in six patients with congenital retinal disease in collaboration with the US 

company Advanced Cell Technology (ACT). 

c. Cytotoxic T-cell therapy 

Epstein-Barr virus (EBV) is a common persistent infection controlled by cytotoxic T cells in healthy 

people, but can cause post transplant lymphoproliferative disease (PTLD), which is often fatal. 

Previously a bank of 100 cytotoxic T cell lines (CTL) has been grown from healthy blood donors and 

used to treat PTLD. A phase II clinical trial used these allogeneic EBV-specific showed a 52 per cent 

response rate at six months in PTLD patients unresponsive to all other conventional therapies. This 

treatment is now ready for transfer to the clinic. However, the CTL lines developed for the initial 

proof of principle trial were grown under good laboratory practice, but these conditions did not 

comply with the subsequent 2004 EU Directive on Tissues and Cells and requirements for HTA or 

MHRA licensure. An award from the Wellcome Trust Technology Transfer Committee has funded 

the creation of a new EBV specific T cell bank at SNBTS Aberdeen, a specials license has now 

been granted by the MHRA for the supply of these donor - derived EBV - directed cytotoxic 

lymphocytes. It is planned to increase the size of the bank from the current five to twenty by the end 

of 2013. The bank will then be maintained at a replacement level. If demand for the cells justifies 

further expansion, the range of HLA types available will be extended using donors from Europe and 

America. It is also planned to extend the utility of these cells in trials of Epstein-Barr virus 

associated lymphomas beyond that of the post-transplant setting. This work is undertaken by the 

Clinical Directorate under Prof Mark Vickers in Aberdeen with R&D support available from CT as 

required. 

d. CD133+ cells for the treatment of liver disease 

Liver disease is a rapidly rising cause of morbidity and mortality in the western world. Liver 

transplantation is currently the only curative treatment available for end stage liver disease and there 

is a rising demand for transplantation, which has not been matched by an increased supply of donor 

organs. In addition, transplantation requires lifelong immunosuppression with associated side effects 

including renal failure, cardiovascular complications and increased risk of malignancy. Several 

studies have therefore investigated the effects of stem cell therapy in liver disease in humans. 

However all have been small, non-randomised, and have made no attempt to formally evaluate the 

effect on either liver disease severity or stage of fibrosis, nor have sought to identify the mechanism 

by which adult stem cells exert their effect. 

SNBTS is therefore in collaboration with the University of Edinburgh to participate in a two centred, 

phase II, randomised controlled trial in liver disease. The study aims not only to evaluate two 

different mechanisms of cell therapy against standard conservative management but also to 

examine the efficacy and safety of bone marrow stem cell therapy in patients with compensated 

cirrhosis, and to demonstrate improvement in liver function and reduction in liver fibrosis in patients 

receiving these therapies compared with those receiving standard conservative management. 

This trial is the first randomised control trial for liver stem cell therapy, therefore SNBTS’s 

involvement will make a contribution to this field and establish a GMP system for preparation and 

cryopreservation of CD133+ selected G-CSF mobilised stem cells. Depending on the outcome of 

the trial, this process has the potential to be used in future for a wider number of patients suffering 

from liver cirrhosis. 


e. Monocyte/macrophage cells for liver disease 

This study is in collaboration with the University of Edinburgh and also aims to look at treatment of 

patients suffering from liver disease, but using treatment with autologous macrophages, as there is 

evidence from mouse models that macrophage therapy improves fibrosis, regeneration and liver 

function. This project is currently at the research phase with the translation to GMP planned for 

2012-13, with associated process validation conducted by SNBTS Cellular Therapy staff within the 

GMP Translational Facility of the SCRM and a clinical trial is planned for 2013. Given SNBTS’s 

experience in licensing of an ATMP product for use in the corneal stem cell clinical trial, we have the 

necessary experience and skills to progress this study to clinical trial and as such determine the 

outcome of this novel regenerative medicine study in humans. 

HEALTHCARE QUALITY IMPACT ASSESSMENT (Appendix 6) 

(Estimated amount of impact on patient/population: small +;medium ++ ;high +++) 

STUDY SAFE EFFECTIVE EFFICIENT EQUITABLE 

1a In vitro RBCs +++ +++ ++ ++ 

1b iPSC from blood +++ ++ ++ ++ 

1c In vitro monocytes/macrophages ++ ++ + + 

2a-c In vitro generated endothelial cells ++ +++ +++ +++ 

3a GMP compliant MSC collection +++ +++ +++ ++ 

3b In vitro generation of MSC from ++ +++ +++ ++ 

optimal source 

3c MSC from pancreatic tissue +++ +++ +++ ++ 

4a Pancreatic islet optimisation +++ +++ +++ +++ 

4b Limbal Stem cell Study ++ +++ ++ + 

4c Cytotoxic T-cell therapy ++ +++ + ++ 

4d CD133+ cells for liver disease ++ +++ + + 

4e Monocytes/macrophages for liver 

disease 

++ ++ + ++ 

None of these projects is expected to impact on timeliness or person centeredness. 

Total resources allocated FY 2012-13 

Project Staff Cost G&S SRC TOTAL 

1. Blood cells £362,934 £49,219 £9,267 £421,420 

2. Endothelial cells £43,680 £6,082 £1,277 £51,039 

3. Mesenchymal stem cells £106,905 £9,571 £3,632 £120,108 

4. Pancreatic islets and 

£26,567 £2,360 £981 £29,908 

clinical support 

TOTAL £540,086 £67,232 £15,157 £622,475 

5 yr Project Objectives 

Project 1. To have performed first in man studies of pluripotent stem cell-derived red cells 

Project 2. Identified optimal cell source for the regeneration of vascular endothelium in ischemic 

limb disease and initiated clinical trial. 

Project 3. To perform a clinical trial of MSC as adjunct therapy to islet transplant. 


Project 4. Completion of initial clinical trials for of limbal stem cell therapy and the delivery of 

cytotoxic T-cell and CD133+ and/or monocyte cell therapies to clinical practice 

Project Milestones (TBC = To be completed by) 

Project Objective Yr 1 

04/12-03/13 

1 

Initiate FIM Complete initial 

PSC RBC studies of WT grant 

pluripotent stem 

cell derived 

RBCs 

Yr 2 

04/13-03/14 

Initial detailed 

discussions 

with 

EMA/MHRA 

Milestones 

Yr 3 

04/14-03/15 

Detailed 

discussions 

with 

EMA/MHRA to 

finalise 

requirements 

for application 

Yr 4 

04/15-03/16 

Plan FIM safety 

trial in healthy 

volunteers and 

phase I in 

thalassaemia 

patients 

Yr 5 

04/16-03/17 

Initiate FIM trial 

in healthy 

volunteers 

TBC Dec 12 

Apply for short 

term extension 

of WT grant to 

Apr 13 

TBC Mar 14 

TBC Mar 15 

TBC Sept 15 

Compile 

regulatory 

application and 

discuss with 

EMA/MHRA 

TBC Mar 17 

Finalise 

regulatory 

application 

TBC July 12 

Apply for 2nd 

phase WT STA 

award to run 

4/13-3/17 

Initiate scale-up 

studies 

incorporating 

new partners if 

necessary 

TBC Mar 16 

TBC Mar 17 

TBC Dec 12 

Continue basic 

science studies 

to enhance 

enucleation & 

maturation 

Rolling 

Continue basic 

science studies 

to enhance 

enucleation & 

maturation 

Finalise 

protocol for 

production of 

enucleated 

erythrocytes 

In vitro & in vivo 

testing of 

enucleated 

RBCs 

Rolling 

Produce 1011 

nucleated 

erythroid cells 

under GMP at 

Roslin Cells 

Rolling 

GMP 

conversion of 

protocols 

TBC Mar 15 

TBC Mar 16 

Finalise GMP 

grade protocol 

for production 

of enucleated 

erythrocytes 

Produce 1013 

GMP grade 

enucleated 

erythrocytes 

1 

PSC HSC 

Mar 2017 

Identify the 

repopulating 

capacity of PSC 

derived HSC 

TBC Mar 13 

Generate first 

reprogrammed 

cell lines from 

PB MNCs 

TBC Mar 13 

Application for 

funding to LLR 

Rolling 

Convert 

research 

protocol for 

reprogramming 

to GMP 

TBC Mar 14 

Application to 

MRC Regen 

Med Platform 

for Blood 

Program 

Produce GMP 

grade 

reprogrammed 

cells 

(with Roslin 

Cells) 

TBC Mar 15 

TBC Sept 15 

Differentiate 

RBC from GMP 

reprogrammed 

cells 

TBC Mar 16 

TBC Jul 16 

Generate first 

reprogrammed 

cell lines from 

PB MNCs 

TBC Mar 13 

Mar 2016 

TBC Mar 13 

Identification of 

sub-populations 

of PSC derived 

HSC/HPC over 

timecourse 

TBC Mar 14 

Complete in 

vitro 

assessment of 

HSC/HPC on 

stroma 

Transfer 

findings to other 

blood projects 

where 

applicable 


TBC Mar 13 TBC Mar 14 Rolling 

Initiate in vivo 

transplant 

assays 

In vivo 

transplant 

assays 

Complete long 

term in vivo 

repopulation 

assays 

Assessment and 

publication of 

the effect of 

hypoxia on the 

expansion and 

maintenance of 

HSC from PSC 

and adult 

sources 

Mar 2015 

Transfer of staff 

to project 

TBC Oct 12 

Complete staff 

training in 

specific 

techniques 

TBC Mar 14 

Complete 

optimisation of 

haemopoietic 

assays under 

normoxia and 

various hypoxic 

conditions 

TBC Apr 13 

In vitro assays) 

for epansion of 

HSCs/HPCs 

under hypoxic 

conditions 

Rolling 

In vivo assays 

of HSCs/HPCs 

expanded 

under hypoxic 

conditions 

TBC Mar 15 

Complete 

titration of PHD 

inhibitors in 

HSCs/HPCs. 

Initial 

characterisation 

of HSC/HPC 

functions 

following PHD 

inhibition 

TBC Mar 16 

TBC Mar 13 

TBC Mar 14 

TBC Mar 15 

Generation of 

HIF and Cited2 

knockdown 

HSCs and 

generation of 

RNA for RNA 

sequencing 

TBC Mar 15 

Assess 

progress and 

re-plan 

accordingly 

1 PSC 

Monocyte 

Identify whether 

the generation of 

monocytes from 

pluripotent stem 

cells is a viable 

clinical option 

Differentiation 

of monocytes 

from hESC 

Assess protocol 

for GMP 

translation 

TBC Mar 15 

Close out if not 

clinically 

applicable 

Mar 2014 

TBC Mar 13 


specific 

monocytes & 

macrophage 

sub groups that 

can be 

generated from 

hESC 

TBC Mar 14 

Apply for further 

funding 

TBC Mar 15 

Close out if 

funding not 

sucessful 

2 Endoth 

Cells 

Identify optimal 

cell source for 

the regeneration 

TBC Mar 13 

Optimisation of 

research SOP 

to produce 

TBC Mar 14 

TBC May 15 

Complete in 

vivo testing of 

hESC derived 

Secure further 

funding or close 

out 


of vascular 

endothelium in 

ischemic limb 

disease and 

initiated clinical 

trial 

endothelial cells 

from hESC 

endothelial cells 

Mar 2017 

TBC Mar 13 

Application to 

BHF MBH 

Initiative for a 

Centre for 

Vascular 

regeneration. 

TBC Mar 15 TBC Dec 15 

Finalise 

protocol for 

GMP isolation 

and expansion 

of pericytes 

from adipose 

tissue (SCRM) 

Grant 

application to 

fund 

collaboration 

with Roslin 

Cells 

EPSRC-CASE 

PhD 

studentship to 

start (11/12) 

TBC Apr 13 

Conversion of 

research SOPs 

to GMP 

TBC Mar 15 

GMP 

production of 

10 9 endothelial 

cells from hESC 

Secure further 

funding or close 

out 

3 MSC Initiate clinical 

trial of GMP 

MSCs for 

immunomodulati 

on 

Sept 2015 

TBC Jul 12 

Establish ethics 

and SOPs for 

tissue collection 

at GMP, 

including 

platelet lysate, 

peripheral 

blood/buffy 

coats, cord 

blood 

TBC Mar 13 

Finalise 

research grade 

SOP for 

isolation and 

expansion of 

adult MSC 

TBC Mar 14 

Apply for 

external funding 

Initial 

discussion with 

EMA/MHRA 

TBC Mar 14 

Translation 

research SOP 

to GMP 

TBC Mar 15 

TBC Dec 15 

TBC Mar 13 

TBC Sept 13 

Routine 

isolation and 

expansion of 

MSC from adult 

sources at GMP 

(SCRM) 10 8 

cells per 

sample 

TBC Dec 13 

Define potency 

assays 

TBC Jan 14 

Regulatory 


EMA/MHRA 

Initiate trial 


3 

PSC MSC 

GMP production 

of PSC derived 

MSC 

Full 

phenotypical 


of MSC from 

hESC 

compared to 

adult 

TBC Mar 14 TBC Sep 14 

Complete Establish GMP 

comparison of SOPs for 

cytokine profile production of 

of ESC-MSC hESC-MSC 

and adult MSC 

TBC Mar 13 

TBC Mar 14 

Establish 

appropriate in 

vivo models 

with 

collaborators at 

UofG and CRM 

Edinb 

TBC Mar 15 

Apply for 


3/4 

Pancreas 

MSC 

Mar 2015 

Initiate clinical 

trial of MSC as 

adjunct therapy 

to islet 

transplant for 

regulatory 

approval 

Isolate MSC 

from exocrine 

pancreatic 

tissue 

TBC Mar 13 

TBC Mar 14 

Apply for 


TBC Apr 13 

Complete 


of MSC from 

pancreas and 

comparision to 

hESC-MSC and 

adult MSC in 

MLR, cytokines 

assays 

TBC Mar 15 

In vitro and in 

vivo pre-clinical 

testing 

Compile 

regulatory 

application 

EMA/MHRA 

for 


4 

Clinical 

Devt 

Cornea 

4 

Clinical 

Devt 

Retina 

4 

Clinical 

Devt 

Mar 2016 

Complete initial 

clinical trial of 

limbal stem cell 

therapy 

Mar 2015 

Complete 

clinical trial of 

RPE cells for 

Stargadt’s 

disease, with 

ACT 

Mar 2016 

Clinical delivery 

of cytotoxic T- 

cell therapy 

Initiate 

trial 

clinical 

TBC Mar 13 

Expansion of 

cell bank to 25 

deposits 

TBC Mar 14 

Plan expansion 

of trial beyond 

post-transplant 

(PTLPD) setting 

TBC Mar 15 

Complete 

recruitment 

TBC Mar 15 

Complete 

recruitment 

TBC Mar 15 


TBC Mar 16 

Complete 

recruitment 

CTL 

4 

Clinical 

Devt 

Pancreas 

Mar 2017 

Delivery of an 

improved 

pancreatic islet 

graft therapy 

TBC Mar 13 


viability and cell 

marker 


studies of 

pancreatic islets 

with T&C group 

TBC Mar 13 

TBC Jun13 

Apply for 


TBC Dec 13 

TBC Mar 15 

TBC Dec 16 


Complete 

retrospective 

analysis of graft 


vs clinical 

outcome 

Direction 

dependent 

Yr1-2 

on 

4 

Clinical 

Devt 

CD133 

4 

Clinical 

Devt 

Monocyte 

Mar 2017 


clinical trials for 

CD133+ cell 

therapy for liver 

disease 

Mar 2017 


clinical trials for 

monocyte cell 

therapy for liver 

disease 

Mar 2017 

Initiate trial in 

Edinburgh 

TBC Mar 13 

Application for 

trial approval 

and funding 

TBC Mar 13 

TBC Mar 14 

Initiate trial in 

Edinburgh 

TBC Mar 13 

Complete 

recruitment 

TBC Mar 16 

Complete 

recruitment 

TBC Mar 16 


Microbiology & Components Appendix 3 

Theme Group: 

Microbiology and Components (MC) R&D 

Our mission is to maintain high level of microbiological safety of blood and tissue supply, 

and where possible, to improve it through the development and application of new 

diagnostic technologies, combined with pathogen reduction/removal measures. At the 

same time our aim is to continuously improve the quality and safety of blood components 

leading to improved clinical outcomes for patients. We work on achieving these targets in 

partnership with and in support of the Supply Chain. 

Summary of Support Proposed: 

Salary: £462,737 13 staff (12FTE) 

SRC: £23,409 

G&S: £107,743 


1. Evaluation of the availability of commercial or in-house assays for emerging blood borne 

pathogens. 

2. Evaluation of the proportion of common viruses harmful to immunocompromised 

recipients, originating in blood and blood products 

3. Determination of the hepatitis E virus seroprevalence and RNA frequency in Scottish 

blood donors and its threat to blood supply 

4. Identification of synthetic polymer ligands for difficult-to-inactivate viruses, for their 

potential removal 

5. Evaluation of the suitability of new diagnostic platforms for blood testing and safety 

margin increase 

6. Evaluation of the effects of new platelet and red cell additive solutions on storage and 

quality of blood components 

7. Investigation of beneficiary effect of a kinase –inhibitor on platelet storage lesion 

8. Determination of key platelet activation pathways through a comparison of the activation 

by natural and synthetic activators 

9. Input into validations (with Supply Chain) for new microbiology assays and components 

safety and quality improvements 

10. Validation of vCJD confirmatory assay 

11. Determination of Borrelia burgdorferi seroprevalence in Scottish blood donors 


1. Improvements of microbiological safety of blood supply through up-to-date diagnostics 

2. Improvements of microbiological safety of Scottish blood supply through new pathogen 

reduction/removal materials and techniques 

3. Safety and quality improvements in storage and provision of blood components 

4. Building on a successful income generation through IP and technology sale (eg 

microarray blood grouping), by developing new diagnostics and pathogen reduction 

materials and techniques 


Proposed projects: 

MC1: Epidemiology, pathogenesis and diagnostics of blood borne pathogens 

1a: Impact of new and emerging pathogens on Scottish Blood and Tissue Supply 

Indigeneous cases of West Nile virus, Chikungunya, Dengue, Usutu and Chagas disease 

have all been described in some European countries and epidemiologists do not rule out 

the possibility of certain mosquito-borne pathogens reaching north European countries. But 

even substantial spread to traditional southern tourist destinations (Spain, France, Italy and 

Portugal) may have potentially highly damaging effect on UK blood supply. We have to 

have at our disposal reliable validated assays - commercial or developed in-house - suitable 

to deal with the potential spread of these infections. Together with MRU we are evaluating 

in house and commercial WNV assays to be selected as a confirmatory assay after 

introduction of WNV screening in Scotland in 2013. Assay development for other abovementioned 

targets will depend on SACTTI risk assessments for UK and availability of 

commercial assays. Hepatitis E is a zoonosis in developed countries and we are assessing 

the threat to Scottish blood supply in project 1bII (below). 

Within NSS, we are looking for ways to complement SNBTS laboratory research with 

surveillance techniques used by Health Protection Scotland (HPS) for epidemiological 

studies. Since we face similar problems with other UK blood services, we aim at 

coordination of our approaches with NHS BT, Welsh and Irish BT. 

1b: Impact of common viruses potentially transmitted through blood components on 

immunosuppressed recipients. 

1bI) Epidemiology and impact of human papillomaviruses, polyomaviruses, herperviruses 6, 

7, 8 and parvovirus B19 on immunosuppressed individuals 

CSO grant application was not funded. A large part of this application has now been 

incorporated into the NIHR/MRC EME program application coordinated in Cambridge 

(submitted June 2012), using new card PCR diagnostics. Another part will be used in an 

FP7 application also coordinated in Cambridge (1st stage of the application process 

October 2012). 

Immunosuppression commonly leads to reactivation and increased susceptibility to 

infection. Majority of viral replication are represented by reactivated viruses, in a proportion 

a superinfection or primary infection would originate from transplanted organ/tissue and 

transfused blood products. This proportion is currently unknown in many cases, but needs 

to be established as a part of duty of care, so that any measures necessary to 

reduce/eliminate these transmissions can be developed and implemented. 

1bII) Epidemiology and identification of potential transmission routes of autochthonous 

Hepatitis E virus (HEV) in Scotland and clinical relevance of HEV in chronic liver disease. 

ETM 32 is a collaboration between Glasgow Caledonian University, SNBTS, Norwich 

University Hospital Glasgow Royal Infirmary, Edinburgh Royal Infirmary Royal Cornwall 

Hospital Truro and Health Protection Scotland. 

This is CSO-funded project (ETM 32). 

Unlike HepE in endemic regions, HepE acquired in developed countries appears to be 

caused by genotype 3 (genotype 4 in China and Japan). Data also suggests that 

subclinical and/or unrecognised HepE infection is common and there is evidence to suggest 

that zoonotic transmission between swine (possibly shellfish) and humans may be 

responsible. 


Transmission of HEV to humans by eating infected meat has been demonstrated. In 

addition, HEV transmission via blood components has been reported. Chronic HEV 

infection was reported in immunosuppressed individuals. 

In order to assess the risk posed by HEV infection and facilitate suitable preventive 

measures, further epidemiological investigations are essential. Studies to date have been 

conducted in England (~10 - 13 % seroprevalence) with an absence of corresponding data 

for Scotland. So far we have carried out ELISA antibody prevalence study on majority of 

planned samples. Prevalence in Scottish donors determined to date is substantially lower 

than in England (~4.8 % vs 10-13%), closer to figures determined for New Zealand. PCR 

study to detect any active infection in blood donors, using plasma minipools is ongoing. 

1c: Effect of mutants on routine assays 

A separate issue is how efficient the routine current assays are in detection of viral 

variants/mutants. Some missed samples by certain HIV PCR assays have been highlighted 

recently, and similar situation have been described for hepatitis B surface antigen (HBsAg) 

assays. We have investigated this problem by cloning, sequencing and expression of the 

HBsAg from identified achived donations and found a new mutant in the process. We plan 

to expand on these studies in collaboration with NMRU, pending external funding. It is 

important to establish the molecular background behind the detectability of mutants by 

various assays. We have been in touch with Abbott where they have an established 

research program for characterisation of mutants. 

MC2: New diagnostic and pathogen reduction technologies for safer blood provision 

The safety of transfused blood and blood products in relation to blood borne pathogens is 

achieved through a combination of measures: donor selection, testing of donated blood and 

use of pathogen reduction/inactivation technologies (PRT). 

PRT represents a viable alternative to bacterial testing, viable replacement for gamma 

irradiation to avoid GVHD; it is generally efficient for enveloped viruses; could potentially 

reduce unknown pathogens and pathogen levels during window period (even if not 

eliminated completely). PRT however suffers from a lower efficiency of 

reduction/inactivation for some non-enveloped viruses, bacterial spores and does not 

inactivate protein-only infectious agents such as vCJD. It introduces extra steps during 

processing; any PRT leads to certain loss of blood component efficacy. 

In the situation where testing cannot guarantee 100 % detection and PRT cannot guarantee 

100 % inactivation, the most logical approach would be a rational combination of screening 

and PRT. Even if PRT could improve to a level it could guarantee a safe blood supply, it 

needs to be complemented by the efficient multiplexing testing platform acting as a Quality 

assurance tool. Microarrays, new nucleic acid amplification technologies and next 

generation sequencing (NGS) can provide such multiplexing platforms. 

As a rule, these technologies are being developed for much wider applications than blood 

testing, which is a niche market. It means that the task of monitoring and evaluating these 

new technologies for their suitability and potential adoption as next generation blood testing 

platforms depends on blood services’ R&D units. 

MC2a: Synthetic polymer ligands for removal of difficult-to inactivate non-enveloped 

viruses. 

Seed funding (12 months) was awarded by the Foundation Alliance Biosecure (France). 


We are planning to apply for an extension of this study and/or a joint application with 

Professor Mark Bradley, School of Chemistry, University of Edinburgh for Proof of Concept 

funding (or similar) for this project and MC3b(also exploiting synthetic polymer libraries) 

Based on current performance of PRT, in order to improve blood safety we still need 

alternative and/or complementary approaches. One of them could be a removal of difficultto-inactivate 

non-enveloped viruses using specific reagents. Such approach is being 

evaluated for prions (prion filters) which due to their chemical nature cannot be inactivated 

by current PRT which is based on nucleic acid inactivation. Synthetic polymers are more 

suitable for large scale application than more expensive, more difficult to prepare and more 

labile antibody-based reagents. Availability of a virus removal option would further improve 

blood safety. 

MC2b: Novel diagnostic approaches and technologies: microarrays, biochips, 

nucleic acid amplification technologies (NAT) and next generation sequencing (NGS) 

2-year collaborative project on the development of viral microarray for mandatory targets 

was supported until November 2011 by Alba Bioscience. 

For 2012 we have been invited to join the application for FP7 European funding, lead by the 

University of Lyon and Etablissement Francais du Sang (EFS) Montpellier. 

As mentioned above microarrays, new nucleic acid amplification technologies and next 

generation sequencing (NGS) can provide multiplexing platforms. Monitoring, development 

and evaluation of novel diagnostic technologies which are suitable or can be adopted for the 

highly specialised and regulated field of blood testing is important for future blood bank 

operations and improved safety of blood supply. Future development will determine if 

diagnostics or PRT will be dominant in blood safety. Nevertheless, any scenario will 

depend on a rational combination of best components of the two approaches. In diagnostics 

it means the development and selection of a cost-efficient and reliable multiplexing platform. 

Since the commercial launch of the massively parallel pyrosequencing platform, the last 5 

years have been dominated by the relentless progress of high throughput genomic analysis, 

termed next generation sequencing (Metzker, 2005). What really positioned NGS to be 

considered for diagnostic applications was continuous reduction in the cost of runs, 

contributed to also by the NHGRI’s Revolutionary Genome Sequencing Technologies 

program, aimed at the sequencing of a human genome for $1000 or less. 

In transfusion medicine, targeted sequencing could identify a variety of relevant blood-borne 

viruses, bacteria and parasites, present in individual samples, including transplant recipients 

with potentially a number of replicating pathogens due to the immunosuppression. 

Application of NGS to genotyping of complex blood group systems is already being 

addressed (Stabentheiner et al, 2011). It can also be expected that NGS analysis of newly 

produced cell lines and differentiated cells resulting from stem cell technology will become a 

requirement. The availability of lower throughput, more economical benchtop NGS 

instrument makes their use realistic and future SNBTS R&D would undoubtedly be 

accelerated by the system availability. Joint capital bid of Microbiology and Components 

theme group with Tissue and Cellular Therapy theme group (Dr. J. Mountford) is proposed. 

A lease for the technology evaluation (but not for stem cell-derived lines quality control) 

would be a less favourable option which could be pursued if capital funding was 

unsuccessful. 


MC3: Improvements in quality and safety of blood components 

The main purpose of studies included in this project is included in the title. We are trying 

continuously to find ways to reduce the storage lesion, while positively effecting the storage 

period, and to increase the microbiological safety of components. Some of the studies are 

initiated by BEST-collaborative, some performed in collaboration with manufacturers 

(egPAS5). 

3a: Effect of preparation, storage conditions, pathogen reduction on quality of blood 

components and their metabolic state. 

Rationale and impact 

All three studies (A-C) in this project relate to the quality of platelets investigating various 

aspects of storage lesion and mechanisms of platelet activation, which are not completely 

understood. They also relate to a safety aspect, especially PAS 5 study on replacing 99% 

of plasma with new platelet additive solution and reducing potential for vCJD transmission 

and allergic transfusion reactions. These studies usually produce pilot data for any potential 

subsequent validation studies (see MC4: Validations). Some of these studies are initiated 

by BEST-collaborative group (SNBTS is a member of the group) allowing for participation 

and standardisation of various methods. Studies in this project will be updated/initiated 

accordingly. 

3aI) Platelet additive solution (PAS) 5 (Collaboration with and reagent support from 

Fenwall) 

Study of >99% plasma replacement in apheresis platelet donations with PAS5, a new 

platelet additive solution, in order to reduce the risk of vCJD transmission and to prevent 

allergic transfusion reactions. 

Platelets for transfusion are collected in 100% donor plasma. This plasma can cause 

transfusion reactions in some patients. It has also been shown that secondary transmission 

of vCJD prions can occur by transfusion of blood components including plasma. In addition, 

some pathogen inactivation technologies seem to work better in PAS. Therefore, being 

able to remove almost 100% of the plasma would be beneficial. Two different apheresis 

machines, Amicus and Trima, will be tested and, therefore, 20 units in total will be required. 

A range of tests looking at platelet morphology, metabolism, activation, lysis and reflection 

of in vitro function will be performed. Testing will be carried out until day 7, evaluating the 

potential for shelf life extension. 

3aII) p38 MAPK inhibitor 

During storage, platelets undergo various biochemical and structural changes collectively 

known as the platelet storage lesion. Based on new data on platelet metabolism and 

pathways, we intend to determine if use of specific inhibitory molecules could reduce the 

platelet storage lesion. 

It has been demonstrated recently that p38 MAPK plays a role in regulation of some of 

these processes. p38 MAPK inhibitor resulted in less activation and less glycocalicin 

production, but DMSO used as a solvent appears to counteract any benefits. We have 

decided to extend the initial studies using alternative solvent(s) for inhibitor (SB203580) and 

include soluble P-selectin measurement in order to determine if low levels of CD62P (Pselectin) 

are due to low activation or to cleavage. 


3aIII) Platelet activation: molecular analysis (Collaboration with the School of Chemistry 

UoE) 

Mechanisms of platelet activation are not fully understood. Using a comparative model of 

natural and synthetic polymer platelet activators which we identified earlier (Hansen et al, 

2011, Biomaterials, 32, 7034), we aim to analyse, at a molecular level, if natural and 

synthetic activators activate the same or different pathways. We intend to use the obtained 

data to identify specific metabolic steps and/or inhibitors which could be targeted to reduce 

the storage lesion. 

3b: Use of synthetic polymer ligands for separation and evaluation of fresh and aged 

blood. 

Rationale and impact 

There is a longstanding debate on potential negative effect of aged blood on clinical 

outcomes. There are numerous papers in support and those opposing this concept. We do 

not have many reliable markers for aging erythrocytes and the subpopulations are usually 

separated by centrifugation, based on changing erythrocyte shape/size/density. An 

alternative can be provided by separation of populations of different age using specific 

synthetic polymer ligands. This would facilitate studies leading to clarification of this issue, 

extremely important for clinical practice. 

There is a direct link to the Clinical Transfusion new grant-funded project investigating how 

transfused red cells might cause immune activation and dysfunction. Any new set of 

markers and/or separation method could be helpful within BloodPharma project on in vitro 

erythrocyte production using stem cell technology (Cell Therapy). 

Technically, this project will use synthetic polymer libraries prepared by the School of 

Chemistry, UoE, similarly to project MC2a searching for ligands for specific virus removal. 

MC4: Validation studies for Components and Microbiology: Interface between 

Supply Chain and R&D 

Rationale and Impact: 

It has been recognised that there is a need for a Validation laboratory, representing a link 

between R&D and Supply chain for various validation studies and which is crucial for a 

successful transition of methods and procedures from the laboratory to routine use. 

4a: Overnight (O/N) hold 

This validation may impact substantailly on the delivery of blood and blood components 

from manufacturing (P&T) sites to clinical banks, improving the logistics of the process. 

Summary: 

Maco Pharma B & T bags. 

Short hold = Whole blood held O/N and processed 14 – 16h post donation. 

Long hold = Whole blood held O/N and processed 22 – 24h post donation. 

- 20 short hold units and 20 long hold units will be tested on day 35; 

- 20 short hold and 20 long hold units, irradiated on day 14, will be tested on days 15 and 

28. 

4b: Platelet Pathogen Reduction (lead by Supply Chain) 

Pathogen reduction technologies are in use in over 80 centres in more than 15 countries. 

The most frequently quoted reasons for introduction were problems with bacterial testing, 

replacement of gamma irradiation, inactivation of emerging pathogens and extension of 


platelet shelf life to 7 days (see also MC2). In Scotland 7 day platelets would help to reduce 

the wastage significantly, especially in more remote northern regions. 

The validation protocol will be prepared in co-operation with the Supply Chain and selected 

provider of PRT, a health economic evaluation will also be carried out and a pilot study will 

be run. 

4c: Additive solutions (candidate solutions : PAS5, SOLX) 

PAS5 is currently a subject of initial evaluation study (see MC3a). The preliminary data is 

encouraging. If the final study outcome is equally positive PAS5 will be proposed for a 

validation study. 

SOLX: At the most recent BEST-collaborative meeting, a promising data was presented on 

the extension of erythrocyte storage after various periods of initial rt hold. We plan to do an 

initial small scale study if it can be agreed with the manufacturer. SOLX validation would be 

a logical extension of 4a: Overnight hold. 

MC 5: Non-Viral Pathogens 

A) Development of PMCA as a variant CJD confirmatory assay. 

Detection of the abnormal form of the prion protein (PrP Sc ): WO 2011/138578. 

PMCA (Protein Misfolding Cyclic Amplification) 

4 th round product CDI (Conformation Dependent Immunoassay) 

Sensitivity: 10 -8 dilution of brain homogenate and 10 -5 of spleen homogenate in 

plasma 

Evaluation: 

1) 250 normal UK donor samples. One PRNP-129MM (No45) repeat-reactive. 

Positive, negative controls and No45 products inoculated tg650 mice + and 45 

spleen accumulation, some clinical disease (completed April 2012). 

2) 400 normal US plasma samples. Spiked with brain and spleen homogenates 

(NIBSC), 20 weeks to complete. Request for clinical samples depending on 

satisfactory evaluation data. 

Alliance BioSecure project: 

1) Select the best assay (most efficient plasma pre-treatment method and PMCA 

substrate; most sensitive PrP Sc detection method). 

Pre-treatment: NaCl precipitation ~ magnetic beads capture ~ streptomycin 

precipitation. 

Detection: CDI > Western blotting. 

Ongoing evaluation and validation. 

2) PrP Sc amplification = amplification of infectivity? 

Products of spiked samples inoculated into tg650 mice ~ 2 years to complete. 

B) Lyme borreliosis 

Lyme borreliosis (Lyme Disease) is caused by the spirochete Borrelia burgdorferi 

transmitted in Scotland by the Ixodes ricinus tick. Increased incidence was described in 

recent years, with Highlands being a hot spot, although the prevalence in the Scottish 

population is generally unknown. 

NMRU and National Lyme Borreliosis testing Laboratory (Inverness): 706 donor samples 

tested, 5.7 %. Study currently being extended to samples from east of Scotland (~700), as 

an increased incidence was indicated in Tayside. 



Project Safe Effecti- Efficient Equitable Comment 

ve 

1a +++ +++ ++ ++ It is not known if WNV, Dengue, Chikungunya, Usutu viruses, 

Trypanosoma parasite can get established in the UK, or on a larger 

scale in Europe tourist destinations. Preparedness for such eventuality 

in a form of having risk assessments and evaluated working assays is 

necessary, since the impact on the UK blood supply could be 

significant. 

1b-I +++ ++ ++ ++ A proportion of human papillomaviruses, polyomaviruses, herpes v. 

6,7,8 or parvovirus B19 which originate in blood or blood products and 

may harm immunosuppressed recipients is judged minor in 

comparison with activation (except B19), but not known. Preventative 

measures, if practicable should improve the post-transplant outcomes 

and decrease/eliminate blood services’ liability. 

1b-II +++ ++ + ++ Determining the Scottish prevalence figures for HEV should indicate if 

any form of (partial) screening may be necessary. HEV is known to 

cause a chronic infection in immunosuppressed. 

1c ++ + + ++ Mutants represent a danger for any screening assay. HBsAg is the 

most common assay for HBV and some interference of the assay 

caused by mutants and vaccination is known. Improvements by 

inclusion of additional monoclonal antibodies could be beneficial. 

2a +++ ++ ++ ++ Non-enveloped viruses pose problem for pathogen reduction 

technologies (PRT). It may be easier to remove, rather than inactivate 

them. Synthetic polymers are good candidate materials for this 

purpose. Partnering with commercial partner is envisaged. 

2b +++ +++ + ++ Combination of new diagnostic technologies with PRT seems most 

feasible for future improvements of blood safety. Niche market 

applications such as blood screening have to be addressed largely by 

blood establishments as they are usually too small for exclusive 

commercial development. Microarrays, new nucleic acid testing 

methods and next generation sequencing are intertwined in much 

improved future diagnostics. Joint development with commercial 

partner can bring IP, income generation. 

3a-I-III ++ +++ +++ ++ Materials (PAS5) and techniques (inhibition of activation, targeting new 

molecules involved in activation) for reduction of platelet storage lesion 

and extension of shelf life are an important part of improving the blood 

component quality, benefiting the patients. 

3b ++ ++ + + All important question of the effects of fresh and aged blood has not 

been resolved yet and new approaches facilitating clarification are 

important. Use of synthetic polymers for separation and/or assaying 

fresh and aged subpopulations complements other R&D projects in 

addressing this problem. 

4a-c +++ ++ +++ ++ Successful validations are important precondition of translation of R&D 

into practice and require input from both, R&D and Supply chain. O/n 

hold may impact substantailly on delivery of blood and blood 

components from manufacturing (P&T) sites to clinical banks, 

improving the logistics of the process. PRT is expected to contribute 

substantially to blood safety. Better additive solutions would impact on 

the quality and shelf life of blood components. 

5a ++ +++ +++ + Good confirmatory vCJD assay is essential for a potential introduction 

of the screening assay, to avoid excessive blood wastage. 

5b ++ ++ + ++ Prevalence estimation for Borrelia burgdorferi will serve as a guide for 

potential future measures. 

Project Milestones 

(TBC = To be completed by) 

Project 

1 

Epidemiology 

pathogenesis 

& diagnostics 

of blood 

borne 

pathogens 

Objective 

Evaluate available 

commercial or inhouse 

assays for 

emerging blood 

borne pathogens in 

response to SACTTI 

Yr 1 

04/12- 

03/13 

Compare 

candidate 

confirmatory 

PCR assays 

for West 

Nile virus 

Yr 2 

04/13- 

03/14 

Complete 

evaluation 

of 

confirmatory 

PCR assay 

for West 

Milestones 

Yr 3 

04/14- 

03/15 

Yr 4 

04/15-03/16 

Yr 5 

04/16-03/17 

Develop/evaluate assays in response to SACTTI 

prioritisation (Dengue, Chikungunya, Usutu, 

Chagas) 


priorities 

Mar 2017 

Evaluation of the 

proportion of 

patients acquiring 

common viruses 

harmful to 

immunocompromis 

ed recipients 

originating from 

blood products 

Mar 2017 

Determination of 

hepatitis E virus 

seroprevalence and 

RNA frequency in 

Scottish blood 

donors and its 

threat to blood 

supply 

TBC Dec 

12 

Submit new 

applications 

for funding 

TBC 

June12; 

Oct 12 

Complete 

experimenta 

l part of the 

project to 

determine 

HEVantibody 

& 

RNA 

prevalence 

in Scottish 

blood 

donors 

Nile virus 

TBC May 

13 Rolling - TBC Mar 2017 

Carry out systematic Determine the proportion 

collaborative study of transfusion-transmitted (rather than 

effects on transplant reactivated) viruses for relevant 

recipients. Determine combinations of virus – transplant 

which viruses are relevant recipient 

for particular transplant 

recipient groups. 

Determine prevalences in 

blood donors. 

TBC Mar 2017 

TBC Mar 2015 

Produce 

final report 

and submit 

publication. 

Submit 

funding 

application 

Carry out chronic hepatitis 

study in parallel with 

immunosuppressed study 

(above) 

2 

New 

diagnostic & 

pathogenreduction 

technologies 

March 2015 


synthetic polymer 

ligands for difficultto-inactivate 

viruses, for their 

potential removal 

TBC Nov 

12 

Produce 

final report 

and submit 

an 

application 

for 

extended 

funding 

TBC Jun 13 

Identify 

potential 

commercial 

partners 

Rolling Mar 2015 

Participation in development of 

virus removal filtration/capture 

material/device 

Feb 2016 

Evaluation of the 

suitability of new 

diagnostic 

platforms for blood 

testing and safetymargin 

increase 

TBC Jan 13 

Prepare and 

submit 

business 

case for 

funding to 

evaluate 

next 

generation 

sequencing 

for safety 

and QC 

testing 

TBC Jul 13 

Pilot study 

on 

diagnostics 

of bloodborne 

pathogens. 

Rolling 

Pilot study on use of the 

technology to QC stem cell 

derived lines/ products 

(with JM – Tissue & Cellular 

Therapies) 

Comparison with 

approved testing 

methods and 

cost-efficiency 

evaluation 

3 

Improvement 

s in quality & 

safety of 

blood 

components 

To identify the best 

available platelet 

and red cell additive 

solutions and 

supplements for 

optimal quality of 

blood components 

Mar 2017 

TBC Dec 

12 

Publish 

results of 

PAS 5 study 

TBC Nov 

12 

TBC Mar 14 

Evaluate 

feasibility of 

PAS 5 

validation in 

conjunction 

with 

pathogen 

reduction 

Rolling 

Carry out 

SOLX 

evaluation 

Rolling 

TBD – further studies on additive 

solutions 


Identification of an 

improved storage 

protocol to prevent 

activation of 

platelets 

Identify best 

solvent for 

the inhibitor, 

not 

interfering 

with platelet 

activation 

TBC Mar 14 TBC Mar 15 Rolling 

Investigatio N/A 

n of 

beneficiary 

effect of a 

MAPK 

kinase – 

inhibitor on 

platelet 

storage 

lesion 

Dec 2014 

Determination of 

key platelet 

activation pathways 

using natural and 

synthetic activators 

TBC Mar 13 

Submit 

paper 

analysing 

miRNA 

profiles. 

Submit 

grant 

application. 

TBC Dec 

14 

Correlate 

miRNA data 

with gene 

expression 

studies 

Select the 

key 

activation 

molecules 

Investigate 

potential 


storage lesion 

4 

Validation 

studies for 

Components 

& 

Microbiology 

Feb 2016 

Validation of 

overnight hold & 

pathogen reduction 

technologies in 

collaboration with 

Supply Chain 

TBC Mar 13 

TBC Mar 14 TBC Mar 15 

Perform required tests for 

validation 

TBC Feb 16 

5 

Non-Viral 

Microbiology 

research 

March 2014 

Validation of vCJD 

confirmatory 

assay 

Mar 2014 

Development of an 

assay to detect 

active Borrelia 

burgdorferi 

infection 

Complete 

optimisation 

of PMCA 

and initial 

evaluation 

with NIBSC 

blinded 

spiked 

plasma 

panel 

TBC Mar 13 

Design 

primers and 

probes and 

optimise 

PCR assay 

March 2014 

Complete 

validation 

of PMCA 

test 

for vCJD 

TBC Mar 14 

Carry out 

pilot study 

Report on 

assay 

suitability; 

SACTTI risk 

assessment 

and SABTO 

position 

statement 

June 2014 

Mar 13 

TBC Mar 14 

TBC June 

14 



Project Staff Cost G&S SRC TOTAL 

MC1 Epidemiology, 

£138,563 £23,650 £5,710 £167,923 

pathogenesis & diagnostics 

of blood borne pathogens 

MC2 New diagnostic & 

£147,544 £39,205 £5,910 £192,659 

pathogen-reduction 

technologies 

MC3 Improvements in 

£106,936 £36,310 £7,640 £150,886 

quality & safety of blood 

components 

MC4 Validation studies for £69,694 £8,578 £4,149 £73,886 

Components & 

Microbiology 

MC5 Non-Viral 

Microbiology research 

NMRU 

(NMRU) 

TOTAL £462,737 £107,743 £23,409 £593,889 


Clinical Transfusion Appendix 4 

Over the next five years, the theme will concentrate most of its resource on evaluating and 

minimising adverse effects of blood transfusion in light of the accumulating evidence that 

excessive transfusion especially of aged cells causes excess morbidity and mortality in 

patients. This may be a ‘silent epidemic’ in which case we ought to be investigating it and 

carrying out mitigating actions where possible. There are also a number of diagnostic and 

therapeutic development projects which we wish to transition to the commercial sector. 

The underlying strategy will be to link pre-existing expertise into specific subject areas 

where it is judged we can become internationally competitive. 


1. To determine whether red cell transfusion can increase mortality in sick patients. 

2. To understand whether and how uptake of transfused blood by macrophages may 

induce inappropriate activation of the immune system. 

3. To determine whether and how red cell transfusion may induce inappropriate 

activation of coagulation. 

4. To investigate determinants of red cell alloantibody formation. 

5. To provide support for molecular diagnostic services. 

6. To commercialise array-based diagnostics (‘mimotopes’). 

7. To commercialise peptide based therapies, directed initially against RhD. 

8. To test immunological properties of erythrocytes produced from Bloodpharma. 

9. To monitor HLA sensitisation after cell therapies provided by SNBTS. 

10. To develop human monoclonal antibodies against red cell antigens. 

11. To test new therapeutic antibodies using placental transport models. 

12. To measure haematopoietic stem cell kinetics after transplanation. 


1. To optimise clinical decisions concerning the appropriateness of blood transfusion. 

2. To optimise the duration and conditions of blood storage. 

3. To improve the safety of cell products provided by SNBTS. 

4. To generate income from new diagnostic and therapeutic materials. 

1. To determine whether red cell transfusion increases mortality in sick patients. 

This project will comprise support for three clinical trials: 

A. The REstrictive and LIberal transfusion strategies in intEnsiVE care (RELIEVE) study. 

B. The Age of Blood Evaluation (ABLE) study. 

C. The Transfusion in Gastrointestinal Bleeding (TRIGGER study). 

The background to these trials is that blood transfusion has been previously assumed to be 

clinically beneficial to anaemic patients in most clinical situations, but has not been 

subjected to rigorous, modern testing in the same way that drugs or other clinical 

interventions have been. Some studies have suggested that liberal transfusion regimens 

are associated with higher morbidity and mortality rates then conservative ones in some 

patient groups and that aged red cell concentrates may be associated with higher rate of 

adverse outcomes than younger red cell concentrates. It is important to establish therefore 


oth whether these initial findings are correct and the potential mechanisms thereof in order 

to guide further policy. 

More specifically: 

A. The RELIEVE study will test whether transfusion triggers of 70 vs 90g/L are associated 

with better / worse outcomes in patients requiring ventilation in intensive care. Current 

pilot data indicate that a more liberal transfusion strategy is associated with a higher 

mortality. It is therefore critical to determine whether this effect is true. 

B. The ABLE study addresses whether ‘older’ blood increases mortality. Blood is currently 

stored for up to 35 days before it is considered out of date, a figure determined mainly 

from in vitro studies. Several recent studies have suggested that recipients of blood that 

has been stored for longer periods have a higher mortality than those receiving younger 

blood. It is important to note that these studies had design faults and other, apparently 

similar, studies have not confirmed the effects. If the effects are confirmed, this would 

suggest that red cell transfusion, as currently practiced, may be contributing to excess 

morbidity / mortality in some patient groups. It is therefore important that this effect is 

investigated in a large, prospective, randomised trial. We feel it is important that 

Scotland takes part in the international ABLE study. 

C. The TRIGGER study will address what threshold should be used for red cell 

transfusions in acute upper gastrointestinal bleeding (AUGIB), one of the leading 

indications for transfusions. This is a UK based multi-centre cluster randomised 

controlled trial with Edinburgh as one of the six centres. 

Resources to be allocated: 

It is proposed that co-ordination of these three trials will be performed by SNBTS Product 

Services Department. 

For these three trials, the first milestone will be recruitment of first Scottish patients and this 

is scheduled for April 2013. 


2. To understand whether and how uptake of transfused blood by macrophages 

may induce inappropriate activation of the immune system. 

The recent evidence implicating older stored red cells as contributors to mortality highlights 

the surprising lack of knowledge we have about how red cells are marked for destruction in 

vivo and the immunological implications of the different modes of death. It has long been 

known that up to 25% of red cells from older bags of blood are removed from circulation 

within one hour of being transfused, by splenic and hepatic macrophages. Data from 

animals indicate that those cells cause inappropriate activation of the immune system and 

subsequent death. It is therefore proposed to determine which of several proposed 

mechanisms mark red cells that have come to the end of their lives and the responses of 

macrophages that take up these effete red cells. 

This work will proceed with the support of a Wellcome Trust funded programme grant. The 

SNBTS contribution will comprise several strands: 

(A) Optimise an in vitro macrophage uptake assay. 

(B) Assess the responses of macrophages that have taken up red cells using a 

transcriptomic approach. 

(C) Link with the Blood Pharma erythroid differentiation system to knock down specific 

red cell proteins, notably CD47, to test their functional effects on red cell uptake. We 

will also test whether the erythrocytes resulting from the Blood Pharma project are 

taken up by macrophages in a similar fashion to normally derived red cells. 


Strand A: One non-tenured post-doctoral scientist (LC) for 5 years. 

Strand B: One tenured post-doctoral scientist (MM) for 5 years. 

Strand C: 30% of Glasgow team for 2 years (DC, AM, DD) 

3. To determine whether and how red cell transfusion may induce inappropriate 

activation of coagulation. 

A further way in which red cells may cause harm is to stimulate inappropriate coagulation. 

Our approach here will be firstly, to titrate red cells into a coagulation system that allows for 

their introduction (thromboelastography (TEG)) and measure thrombin production. 

Secondly, we will assay the presence of prothrombin surface markers using flow cytometry. 


£5,000 for consumables in Dundee (TEG) 

£5,000 for consumables in Edinburgh (FACS) 

0.5wte for salary in Edinburgh (SM/ID) 


4. To determine whether HLA type determines propensity to red cell alloantibody 

formation. 

The formation of alloantibodies against blood remains a significant clinical problem, which 

complicates and may delay the provision of appropriately matched cells. A study will be 

undertaken to examine the relationship between HLA alleles and RBC alloantibody 

formation in the West of Scotland patient population. 

Resources to be allocated: 5% of AM’s time for 2 years, to collect samples. Consumables 

funding will depend on successful grant application and if this is not obtained, project will be 

abandoned. 

5. To provide support for molecular diagnostic services. 

Specialised red cell, platelet and granulocyte genotyping services, including prenatal 

diagnosis, benefit from the input of senior R&D staff. The support encompasses both 

troubleshooting and the development of new diagnostic tests (prenatal diagnosis of anti- 

HPA mediated diseases, diagnosis of PNH). 

Resources to be allocated: 0.2 FTE for 5 years (SAF) 

6. To commercialise array-based diagnostics (‘mimotopes’). 

The project has been taken beyond “proof of concept” to proof of potential utility and is well 

positioned to be taken on by a commercial entity to further develop (in combination with an 

existing platform) to a marketable product / system. 

For this reason all SNBTS developments are on hold. However, the Principal Investigator 

Mike Moss remains available to support, to a limited degree, a third party development 

endeavour and this input will be critical in progressing this project into a commercial arena. 

Resources to be allocated: 0.1 FTE for 2 years (MM). 

7. To commercialise peptide based therapies, directed initially against RhD. 

No further laboratory work is currently planned on this project. However, input of scientific 

staff will be critical to progress this project into a commercial arena. 

Resources to be allocated: 0.1 FTE for 2 years (LC) 

8. To test immunological properties of erythrocytes produced from Bloodpharma. 

The red cells to be produced from the Blood Pharma project will need to be rigorously 

tested for equivalence to their normal counterparts, before studies in humans. We will 

utilise the assays developed as part of project 2 to test the surface properties and 

immunological effects of these red cells. 

Resources to be allocated: 0 in years 1 & 2, contribution in year 3 dependent on 

BloodPharma project progress. 

9. To monitor HLA sensitisation after cell therapies provided by SNBTS. 

This project will support two treatments arising from the Cellular Therapy programme (islet 

cell transplantation and Epstein-Barr virus cytotoxic lymphocytes (EBV-CTLs)) by 


establishing whether the presence of anti-HLA antibodies in recipients correlates with 

clinical outcome. Also, it is proposed to identify donors homozygote for common HLA 

haplotypes in a Scottish population, for subsequent development of iPS cells. Cross refer to 

relevant CT projects. 


Year 1: £10,500 for HLA typing 

Years 2-4: £11,200 per annum for anti-HLA antibody detection. 

DN: you’ve identified the money for this within budget? 

10. To develop human monoclonal antibodies against red cell antigens. 

A monoclonal antibody against HbH would be useful for prenatal diagnosis of 

thalassaemias in ethnic minority populations. 


Year 1: £5,000 consumables + 0.2FTE of AM time in Glasgow. 

KPI: If no suitable antibody has been isolated in the first year, the project will be abandoned. 

11. To test new therapeutic antibodies using placental transport models. 

SNBTS has been involved in testing the properties of three antibodies that have the 

potential to be useful in the treatment of haemolytic disease of the newborn and neonatal 

alloimmune thrombocytopenia. 


No specific resource is planned to support these antibodies, 0.1FTE of SAF’s time for 2 

years. 

12. To measure haematopoietic stem cell kinetics after transplanation 

By measuring the presence of mutant red cells, the behaviour of stem cells collected and 

transplanated by SNBTS can be deduced. 


0.1FTE of MM’s and SH’s time for 5 years. 

HEALTHCARE QUALITY IMPACT ASSESSMENT (Appendix 6) 


STUDY SAFE EFFECTIVE EFFICIENT EQUITABLE 

ABLE +++ ++ ++ 

1 RELIEVE +++ ++ ++ 

TRIGGER +++ ++ ++ 

2 Red cell signalling +++ + ++ 

Macrophage response 

3 Red cells and ++ + 

coagulation 

4 Red cell alloantibodies ++ + 

5 Molecular diagnostic + +++ + 

support 

6 Mimotopes + +++ ++ 

7 Peptide therapies for 

+++ + 

HDN 


8 Blood Pharma testing + +++ 

9 Cellular therapies HLA ++ ++ 

testing 

10 Anti-HbH development ++ ++ ++ 

11 Placental transport of 

+++ 

antibodies 

12 To measure 

haematopoietic stem cell 

kinetics posttransplanation 

+ + + 

None of these projects is expected to impact on timeliness person centeredness 

Project Milestones 

(TBC = To be completed by) 

Project 

1 

Determine 

whether red 

cell 

transfusion 

increases 

mortality in 

sick patients 

Objective 

Participate in ABLE 

study (multi-centre 

trial comparing 

outcomes of 

transfusing fresh vs 

standard RBC in 

ICU) 

Yr 1 

04/12- 

03/13 

Yr 2 

04/13-03/14 

Start patient recruitment to study 

Milestones 

Yr 3 

04/14- 

03/15 

Yr 4 

04/15-03/16 

Complete patient 

recruitment and 

analyse data 

Yr 5 

04/16-03/17 

Dec 2015 

Carry out RELIEVE 

study (comparing 

restrictive vs liberal 

transfusion in 

intensive care) 

Apr 13 and ongoing 

Publish Initiate 

internal RELIEVE 

feasibility study multicentre 

and plan larger study and 

scale trial complete 

recruitment of 

25 patients at 

6 centres by 

April 2013 

TBC Dec 15 

Continue patient recruitment to study 

Participate in 

TRIGGER study 

(comparing 

restrictive vs liberal 

transfusion in GI 

bleeding) 

TBC Dec 12 

Start patient 

recruitment 

TBC Apr 13 

Initiate scaleup 

studies 

incorporating 

new partners 

if necessary 

Rolling 

2 

Red cell 

signalling 

macrophage 

response 

Mar 2016 

Investigate the 

effect of transfused 

blood on the 

immune system 

(5yr study) 

Oct 12 

Complete 

recruitment of 

volunteers/pati 

ents and 

complete 

protocol 

design. Isolate 

macrophages 

that have 

taken up red 

cells for 

Rolling 

Continue investigation on effects of aged RBC uptake on human 

phagocytic cells 

Investigate how accumulation of ‘storage lesions’ in blood for 

transfusion alters the immune effects of RBC clearance 

Determine the role of CD47 in RBC senescence 


transcriptomic 

analysis by 

Mar 2017 

Perform 

comprehensive 

glycomic analysis 

of red cells stored 

for transfusion 

Aug 12. Rolling - TBC Mar 17 

Establish panel 

of linkage 

specific 

glycosyl 

binding 

molecules. 

Establish mass 

spectroscopic 

analysis 

techniques in 

partnership 

with UCL 

Test stored 

blood for 

glysosylation 

patterns using 

reagents & 

techniques 

established 

from 2012/13 

3 

Red cells and 

coagulation 

4 

Red cell 

alloantibodies 

Assess 

immunological 

consequences of 

red cell uptake by 

splenic/hepatic 

macrophages 

Investigate how red 

cell transfusion 

may induce 

inappropriate 

activation of 

coagulation 

March 2014 

Determine if HLA 

type determines 

propensity to red 

cell alloantibody 

formation 

Mar 13 

Establish 

assay for take 

up of red cells 

by 

macrophages 

Mar 13 

Plan 

experiments to 

determine 

effects of red 

cells on 

clotting by 

thromboelasto 

graphy and 

assess 

expression of 

coagulation 

markers on red 

cells by flow 

cytometry 

TBC Mar 13 

Submit ethics 

and apply for 

grant funding 

Mar 14 

Perform transcriptomic analyses 

of macrophage responses to 

transfused cells 

Mar 15 

Initiate 

experimental 

work 

Rolling 

Collect patient 

samples and 

carry out study 

Complete 

experimental 

work and 

submit for 

publication 

TBC Mar 14 

Submit for 

publication 

Submit for 

publication 

Mar 16 

5 

Molecular 

diagnostic 

support 

March 2014 

Implement noninvasive 

prenatal 

diagnosis (NIPD) 

for Rh status in 

pregnancy 

(screening) 

TBC Mar 13 

Complete 

implementation 

trial for NIPD 

TBC Mar 14 

TBC Mar 15 

6 

Mimotopes 

7 

Peptide 

therapies 

HDN 

for 

Dec 2013 

Commercialise 

array-based 

diagnostics 

(‘mimitopes’) 

Commercialise 

peptide based 

therapies, directed 

TBC Mar 13 

Continue to negotiate with prospective commercial 

partners. No further experimental work planned 

unless funded by potentially interested commercial 

partner 

Rolling 

Continue to negotiate with prospective commercial 

partners. No further experimental work planned 

unless funded by potentially interested commercial 

partner 


8 

Blood Pharma 

testing 

9 

Cellular 

therapies HLA 

testing 

against RhD or 

GPIIb/IIIa 

Test immunological 

properties of 

erythrocytes 

produced from 

BloodPharma 

March 2017 

Monitor HLA 

sensitisation after 

cell therapies 

provided by 

SNBTS 

Rolling 

Test red cells from BloodPharma 

project in macrophage uptake assay 

Precise timing dependent on 

progress of BloodPharma 

project 

Collect and analyse samples when required. Timing depends on progress of 

various cellular therapy projects. 

10 

Anti-HbH 

development 

Dec 2016 

Generate a murine 

monoclonal 

antibody against 

HbH 

Rolling 

Perform 

mouse 

immunisation, 

fusion, 

screening, 

cloning and 

characterisatio 

n of antibodies 

Project 

terminates 

11 

Placental 

transport of 

antibodies 

March 2013 

Obtain external 

funding for testing 

new therapeutic 

antibodies using 

placental transport 

models 

TBC Mar 13 

Continued experimental 

work dependent on specific 

externally-funded projects 

12 

Measure 

haematopoieti 

c stem cell 

kinetics posttransplanation 

May 2014 

Measure 

haematopoietic 

stem cell kinetics 

after transplanation 

Rolling 

Collect and freeze samples 

Analyse 

samples-may 

need external 

funding 


Theme Project No Staff Cost G&S SRC TOTAL 

1 Non-RDI Staff 

2 £184,507 £5,488 £13,744 £203,729 

3 £61,048 £6,567 £67,615 

Improve Efficacy & 

Safety of Blood 

Transfusion for Patients 

in Scotland 

Development of 

Diagnostic and 

Therapeutic 

Approaches for 

Diseases of Blood 

4 £5,235 £693 £1,566 £7,494 

5 £44,515 £3,190 £9,457 £57,162 

6 £10,168 £1,109 £2,882 £14,159 

7 £8,177 £694 £1,567 £10,438 

8 

9 £23,951 £1,942 £5,512 £31,405 

10 £9,698 £693 £1,000 £11,391 

11 £10,168 £1,110 £2,882 £14,160 

12 £10,168 £1,110 £2,882 £14,160 

TOTAL £367,635 £16,019 £48,059 £431,713 


Publications & Grants 2008-2012 Appendix 5 

2008-2009 

Aldhous, M. C., Prescott, R. J., Roberts, S., Samuel, K., Waterfall, M., and Satsangi, J. Does nicotine 

influence cytokine profile and subsequent cell cycling/apoptotic responses in inflammatory bowel disease? 

Inflamm Bowel Dis. 2008: 14: 1469-1482. 

Appleford NE, Wilson K, Houston F, Bruce LJ, Morrison A, Bishop M, Chalmers K, Miele G, Massey E, Prowse 

C, Manson J, Will RG, Clinton M, MacGregor I, Anstee DJ. alpha-Hemoglobin stabilizing protein is not a 

suitable marker for a screening test for variant Creutzfeldt-Jakob disease. Transfusion. 2008; 48: 1616-26. 

Balabanov S, Gontarewicz A, Ziegler P, Hartmann U, Kammer W, Copland M, Brassat U, Priemer M, Hauber 

I, Wilhelm T, Schwarz G, Kanz L, Bokemeyer C, Hauber J, Holyoake TL, Nordheim A, Brummendorf TH. 

Hypusination of eukaryotic initiation factor 5A (EIF05A): a novel therapeutic target in BCR-ABL-positive 

leukemias identified by a proteomics approach. Blood 2007, 109: 1701-1711. 

Bateman AP, McArdle F, Walsh TS. Time course of anemia during six months follow up following intensive 

care discharge and factors associated with impaired recovery of erythropoiesis. Crit Care Med. 2009 

Jun;37(6):1906-12 

Beattie LM, Harrison E “SAGM blood for neonatal large volume transfusion.” Transfusion Alternatives in 

Transfusion Medicine 2008; 10: pp 34-36 

Bessos H, Matviyenko M, Brown P, Husebekk A, Killie MP, Segatchian J, Santoso S, Urbaniak SJ What’s 

happening – probing of HPA-1a antigen-antibody interaction by surface plasmon resonance technology. 

Transfusion and Apheresis Science (2008), 39; 179-182 

Bessos H, Matviyenko M, Killie MK, Husebekk A, Urbaniak S. Direct comparison between ELISA and MAIPA 

in the measurement of anti-HPA-1a (in IU/ml and AU/ml) in Neonatal Alloimmune Thrombocytopenia. 

Transfusion and Apheresis Science (2008), 39, 221-227 

Bessos H, Killie MK, Seghatchian J, Skogen B, Urbaniak SJ. What's Happening - The Relationship of Anti- 

HPA-1a Amount to Severity of Neonatal Alloimmune Thrombocytopenia - Where Does it Stand? Transfus 

Apher Sci. 2009; 40: 75-8 

Brazma D, Grace C, Howard J, Melo JV, Holyoake T, Apperley JF, Nacheva EP. Genomic Profile of CML: 

Imbalances Associated with Disease Progression. Genes, Chromosomes and Cancer, 2007: 46(11) 1039-59. 

Brunskill SJ, Prowse C, Garrioch M, Gill R, Hebert P, Thompson J, Hyde C, Stanworth S, Roberts D. Blood 

substitutes for avoiding allogeneic blood transfusion (Protocol)The Cochrane Library 2008, Issue 1, pp1-6. 

Burgess STG, Kenyon F, O’Looney N, Ross AJ, Chong Kwan M, Beattie J, Petrik J, Ghazal P, Campbell C: A 

multiplexed protein microarray for the simultaneous serodiagnosis of HIV/HCV infection and typing of whole 

blood. Analytical Chemistry 2008; 382:9-15. 

Cardigan R, Prowse CV, Williamson LM. Processing of Components: leucodpeletion and pathogen reduction. 

Chapter 19 in “Transfusion Microbiology”, editors Barbara JAJ, Regan FAM, Contreras MC; publishers 

Cambridge University Press. 2008. pp239-258. 

Copland M, Hamilton A, Holyoake TL. Conventional Western blotting techniques will not reliably quantify p210 

BCR-ABL. Blood, (letter) 2007: 109 (3): 1336. 

Copland M, Pellicano F, Richmond L, Allan EK, Hamilton A, Lee FY, Weinmann R, and Holyoake TL. (2008) 

BMS-214662 potently induces apoptosis of chronic myeloid leukemia stem and progenitor cells and 

synergizes with tyrosine kinase inhibitors. Blood, 2008; 111(5):2843-53. 

Coste J, Prowse C, Eglin D, Fang C. A Report on Transmissible Spongiform Encephalopathies and 

Transfusion Safety. Vox Sanguinis 2009; 96: 284-291. 

Davidson F, Yirrell D, Lycett C, Petrik J, Dow BC. HIV subtypes detected in Scottish blood donors. Vox 

Sanguinis 2009 ;96:160-2 

Duncan C, Roddie H. Dendritic cell vaccines in Acute Leukemia. Best Practice & Research Clinical 

Haematology 2008 21(3) 521-41 


Ferguson E, Prowse C, Townsend E, Spence A, Hilten JA, Lowe K. Acceptability of blood and blood 

substitutes. J Intern Med. 2008; 263: 244-55. 

Fisher SA, Tremelling M, Anderson CA, Gwilliam R, Bumpstead S, Prescott NJ, Nimmo ER, Massey D, 

Berzuini C, Johnson C, Barrett JC, Cummings FR, Drummond H, Lees CW, Onnie CM, Hanson CE, Blaszczyk 

K, Inouye M, Ewels P, Ravindrarajah R, Keniry A, Hunt S, Carter M, Watkins N, Ouwehand W, Lewis CM, 

Cardon L; Wellcome Trust Case Control Consortium, Lobo A, Forbes A, Sanderson J, Jewell DP, Mansfield 

JC, Deloukas P, Mathew CG, Parkes M, Satsangi J. Genetic determinants of ulcerative colitis include the 

ECM1 locus and five loci implicated in Crohn's disease. Nat Genet. 2008 ; 40: 710-2. 

Fletcher, J., Cui, W., Samuel, K., Black, J. R., Hannoun, Z., Currie, I. S., Terrace, J. D., Payne, C., Filippi, C., 

Newsome, P., Forbes, S. J., Ross, J. A., Iredale, J. P., and Hay, D. C. The inhibitory role of stromal cell 

mesenchyme on human embryonic stem cell hepatocyte differentiation is overcome by Wnt3a treatment. 

Cloning Stem Cells 2008: 10: 331-339. 

Graham SM, Vass JK, Holyoake TL, Graham GJ. Transcriptional analysis of quiescent and proliferating 

CD34+ human haemopoietic cells from normal and CML sources. Stem Cells, 2007: 25:3111-20. 

Gray A, Hart M, Dalrymple K, Davies T. Promoting safe transfusion practice: right blood, right patient, right 

time. Br J Nurs. 2008 Jul 10-23;17(13):812, 814-7. 

Griffiths SD, Burthem J, Unwin RD, Holyoake TL, Melo JV, Lucas GS, Whetton AD. The use of isobaric tage 

peptide labelling (iTRAQ) and mass spectrometry to examine rare, primitive hematopoietic cells from patients 

with chronic myeloid leukemia. Molecular Biotechnology, 2007: 36(2): 81-9. 

Harkness M, Clark V. The use of cell salvage during obstetric procedures: an audit of Scotland's maternity 

units.Scott Med J. 2008;53:24-7 

Harkness M, Freer Y, Prescott RJ, Warner P. Implementation of NICE recommendation for a policy of routine 

antenatal anti-D prophylaxis: a survey of UK maternity units. Transfus Med. 2008;18:292-5 

Harkness M, Palmer JB, Watson D, Walsh TS. A questionnaire-based survey of perioperative blood 

conservation practice for revision hip arthroplasty in Scotland. Transfus Med. 2008 Oct;18(5):296-301 

Haque T, Wilkie GM, Jones MM, Higgins CD, Urquhart G, Wingate P, Burns D, McAulay K, Turner M, Bellamy 

C, Amlot PL, Kelly D, MacGilchrist A, Ghandi MK, Swerdlow AJ, Crawford DH. Allogeneic cytotoxic T cell 

therapy for EBV-positive post transplant lymphoproliferative disease: results of phase II multicentre clinical 

trial. Blood 2007; 110: 1123-31. 

Halsey C, Fisher C, Strathdee G, Gibson B, Holyoake T, Vyas P, Graham G. GATA1 mutational analysis in 

chronic myeloid leukaemia. British Journal of Haematology, 2007: 137: 375-6. 

Hay DC, Fletcher J, Payne C, Terrace JD, Gallagher RCJ, Snoeys J, Black JR, Wojtacha D, Hannoun Z, 

Pryde A, Filippi C, Currie IS, Forbes SJ, Ross JA, Newsome PN, Iredale JP. Highly efficient differentiation of 

hESCs to functional hepatic endoderm requires ActivinA and Wnt3a signalling. Proceedings of the National 

Academy of Sciences of the USA 2008 105, 12301-12306. 

Heaney NB, Holyoake TL. Therapetuic targets in chronic myeloid leukaemia. Hematological Oncology, 2007: 

25: 66-75. 

Heaney NB, Copland M, Stewart K, Godden J, Parker AN, McQuaker IG, Smith GM, Crawley C, Shepherd P, 

and Holyoake TL. (2008) Complete molecular responses are achieved after reduced intensity stem cell 

transplantation and donor lymphocyte infusion in chronic myeloid leukemia. Blood, 2008; 111(10) 5252-5. 

Holyoake TL, Heaney NB. Novel treatment strategies for chronic myeloid leukaemia. Clinical Review. Hospital 

Pharmacy Europe. 2007: 19-20. 

Hornsey VS, McColl K, Drummond O, MacGregor IR, Prowse CV. Platelet storage in Fresenius/NPBI 

polyolefin and BTHC-PVC bags: a direct comparison. Transfus Med. 2008; 18: 223-227. 

Hornsey VS, McMillan L, Morrison A, Drummond O, MacGregor IR, Prowse CV. Freezing of buffy coatderived, 

leukoreduced platelet concentrates in 6 percent dimethyl sulfoxide. Transfusion. 2008; 48: 2508-2514 

Hornsey VS, Drummond O, McMillan L, Morrison A, Morrison L, MacGregor IR, Prowse CV. Cold storage of 

pooled, buffy-coat-derived, leucoreduced platelets in plasma. Vox Sang. 2008; 95: 26-32 


Jarvis L, Becker J, Tender A, Cleland A, Queiros L, Aquiar A, Azevedo J, Aprili G, Bressan F, Torres P, Nieto 

S, Ursitti A, Montoro J, Vila E, Ramada C, Saldanha J. Evaluation of the Roche cobas s 201 system and 

cobas TaqScreen multiplex test for blood screening: a European multicenter study. Transfusion, 2008; 

48(9):1853-61. 

Jones M, Peden AH, Prowse CV, Groner A, Manson JC, Turner ML, Ironside JW, MacGregor IR, Head MW. 

In vitro amplification and detection of variant Creutzfeldt-Jakob disease PrP Sc . Journal of Pathology 2007; 213: 

21-26. 

Jones M, Peden AH, Yull H, Bishop MT, Prowse CV, Turner ML, Ironside JW, Head MW, MacGregor IR. 

Human platelets as a substrate source for the in vitro amplification of the abnormal prion protein (PrP Sc ) 

associated with variant Creutzfeldt-Jakob disease. Transfusion. 2009: 49: 376-384. 

Jones M, Wight D, McLoughlin V, Norrby K, Ironside JW, Connolly JG, Farquhar CF, MacGregor IR, Head 

MW. An Antibody to the Aggregated Synthetic Prion Protein Peptide (PrP106-126) Selectively Recognizes 

Disease-Associated Prion Protein (PrP(Sc)) from Human Brain Specimens. Brain Pathol. 2009; 19: 293-302 

Jones M, Peden A, Wight D, Prowse C, MacGregor I, Manson J, Turner M, Ironside JW, Head MW. Effects of 

sporadic Creutzfeldt-Jakob disease prion protein type and PRNP codon 129 genotype in an in vitro prion 

protein conversion assay. NeuroReport 2008; 19: 1783-1786. 

Jones M, Peden AH, Wight D, Prowse C, MacGregor I, Manson J, Turner M, Ironside JW, Head MW. Effects 

of human PrPSc type and PRNP genotype in an in-vitro conversion assay. Neuroreport. 2008;19:1783-1786 

Kilpatrick, D.C. Lectin-glycoconjugate interactions in health and disease. Biochemical Society Transactions 

2008; 36: 1453-1456 

Kilpatrick DC. Stem Cell Transplantation and MBL Replacement Therapy. Current Stem Cell Research and 

Therapy 2008; 3: 85-87 

Kilpatrick DC. Mannan-binding lectin and stem cell transplantation. In: Hematopoietic Stem Cell 

Transplantation Advances (Karl B. Neumann, ed), 2008, pp 1-6. 

Konig H, Holtz M, Modi H, Manley P, Holyoake TL, Forman SJ and Bhatia R. Enhanced BCR-ABL kinase 

inhibition does not result in increased inhibition of downstream signaling pathways or increased growth 

suppression in CML progenitors. Leukaemia 2008; 22(4): 748-55. 

Konig H, Holyoake TL, Bhatia R. Effective and selective inhibition of chronic myeloid leukemia primitive 

hematopoietic progenitors by the dual Src-Abl kinase inhibitor SKI-606. Blood, 2008; 111(4): 2329-38. 

Larson RA, Druker BJ, Guilhot F, O'Brien SG, Riviere GJ, Krahnke T, Gathmann I, Wang Y, International 

Randomized Interferon vs STI571 Study Group. Imatinib pharmacokinetics and its correlation with response 

and safety in chronic-phase chronic myeloid leukemia: a subanalysis of the IRIS study. Blood, 2008; 111(8) 

4022-8. 

Loos RJ, Lindgren CM, Li S, Wheeler E, Zhao JH, Prokopenko I, Inouye M, Freathy RM, Attwood AP, 

Beckmann JS, Berndt SI; Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, Jacobs KB, 

Chanock SJ, Hayes RB, Bergmann S, Bennett AJ, Bingham SA, Bochud M, Brown M, Cauchi S, Connell JM, 

Cooper C, Smith GD, Day I, Dina C, De S, Dermitzakis ET, Doney AS, Elliott KS, Elliott P, Evans DM, Sadaf 

Farooqi I, Froguel P, Ghori J, Groves CJ, Gwilliam R, Hadley D, Hall AS, Hattersley AT, Hebebrand J, Heid 

IM; KORA, Lamina C, Gieger C, Illig T, Meitinger T, Wichmann HE, Herrera B, Hinney A, Hunt SE, Jarvelin 

MR, Johnson T, Jolley JD, Karpe F, Keniry A, Khaw KT, Luben RN, Mangino M, Marchini J, McArdle WL, 

McGinnis R, Meyre D, Munroe PB, Morris AD, Ness AR, Neville MJ, Nica AC, Ong KK, O'Rahilly S, Owen KR, 

Palmer CN, Papadakis K, Potter S, Pouta A, Qi L; Nurses' Health Study, Randall JC, Rayner NW, Ring SM, 

Sandhu MS, Scherag A, Sims MA, Song K, Soranzo N, Speliotes EK; Diabetes Genetics Initiative, Syddall HE, 

Teichmann SA, Timpson NJ, Tobias JH, Uda M; SardiNIA Study, Vogel CI, Wallace C, Waterworth DM, 

Weedon MN; Wellcome Trust Case Control Consortium, Willer CJ; FUSION, Wraight, Yuan X, Zeggini E, 

Hirschhorn JN, Strachan DP, Ouwehand WH, Caulfield MJ, Samani NJ, Frayling TM, Vollenweider P, Waeber 

G, Mooser V, Deloukas P, McCarthy MI, Wareham NJ, Barroso I, Jacobs KB, Chanock SJ, Hayes RB, Lamina 

C, Gieger C, Illig T, Meitinger T, Wichmann HE, Kraft P, Hankinson SE, Hunter DJ, Hu FB, Lyon HN, Voight 

BF, Ridderstrale M, Groop L, Scheet P, Sanna S, Abecasis GR, Albai G, Nagaraja R, Schlessinger D, Jackson 

AU, Tuomilehto J, Collins FS, Boehnke M, Mohlke KL. Common variants near MC4R are associated with fat 

mass, weight and risk of obesity. Nat Genet. 2008; 40: 768-75. 


MacDonald, S.L., Downing, I., Turner, M.L. & Kilpatrick, D.C. Is mannan-binding lectin (MBL) detectable on 

monocytes and monocyte-derived immature dendritic cells? Biochemical Society Transactions 2008; 36: 1497- 

1500 

McLintock LA, Cook G, Holyoake TL, Jones BL, Kinsey SE, Jackson GH. High loading dose AmBisome ® is 

efficacioius and well tolerated in the management of invasive fungal infection in haematology patients. 

Haematologica/The Hematology Journal. 2007: 92(04): 572-3. 

Mahmood, A., Gosling, P., Barclay, R., Kilvington, F., and Vohra, R. (2008). Splanchnic Microcirculation 

Protection by Hydroxyethyl Starches During Abdominal Aortic Aneurysm Surgery. Eur J Vasc Endovasc Surg. 

2009 ;37: 319-25. 

Mountford JC. Human embryonic stem cells: Origins, characteristics and potential for regenerative therapy. 

Transfus Med. 2008;18: 1-12. 

O’Looney N, Burgess STG, Chong Kwan M, Ross AJ, Robb JS, Forster T, Beattie JS, Ghazal P, Petrik J, 

Campbell C. Evaluation of a protein microarray method for immuno-typing erythrocytes in whole blood. Journal 

of Immunoassays & Immunochemistry, 2008; 29:197-209. 

Peden A, Head MW, Jones M, MacGregor I, Turner ML, Ironside J. Advances in the development of a 

screening test for vCJD. Expert Opinion on Medical Diagnostics 2008: 2: 207-219. 

Petrik J. Microbiological blood testing and new technologies. In “Transfusion Microbiology” (JAJ Barbara, MC 

Contreras and FAM Regan eds.) Cambridge University Press, 2008; 227-237. 

Prowse CV and Roberts D J. "Blood substitutes". Chapter 35 of "Practical Transfusion Medicine, Third 

edition" 2009 (editors Murphy MF , Pamphilon DH) pp390-399. 

Prowse CV. Pathogen inactivation of blood components. Transfusion Alternatives in Transfusion Medicine 

2008, 10, Issue 3, 139 -146 (& chapter II-E of planned NATA book). 

Prowse C. Pathogen Inactivated Plasma. Transfusion Medicine Reviews 2009; 23:124-33. 

Prowse C: Credit Accumulation and Transfer (CAT) & MSc Courses in Transfusion & Transplantation. BBTS 

Bloodlines Spring 2008 

Prowse C. Blood Substitutes: Where are we now? Blood Matters (autumn 2008) 26: 21-24. 

Reesink HW, Engelfriet CP, Hyland CA, Coghlan P, Tait B, Wsolak M, Keller AJ, Henn G, Mayr WR, Thomas 

I, Osselaer JC, Lambermont M, Beaten M, Wendel S, Qiu Y, Georgsen J, Krusius T, Mäki T, Andreu G, Morel 

P, Lefrère JJ, Rebulla P, Giovanelli S, Butti B, Lecchi L, Mozzi F, van Hilten JA, Zwaginga JJ, Flanagan P, 

Flesland Ø, Brojer E, Letowska M, Akerblom O, Norda R, Prowse C, Dow B, Jarvis L, Davidson F, Kleinman 

S, Bianco C, Stramer SL, Dodd RY, Busch MP. Biobanks of blood from donors and recipients of blood 

products. Vox Sang. 2008 ; 94: 242-60. 

Rocchi MS, Anderson MJ, Eaton SL, Hamilton S, Finlayson J, Steele P, Barclay GR, Chianni F. Three colour 

flow cytometric detection of PrP in ovine leucocytes. Vet Immunol Immunopathol 2007; 116: 172-181. 

Shepherd P, Dhanapala C, Maguire C, White J, Drummond M, Holyoake T, Johnson PRE. Successful use of 

national cancer registry data to monitor the effective use of Imatinib for treating CML. Scott Med J. 2008;53:8- 

12 

Slight RD, Buell R, Nzewi OC, McClelland DB, Mankad PS. A comparison of activated coagulation time-based 

techniques for anticoagulation during cardiac surgery with cardiopulmonary bypass. J Cardiothorac Vasc 

Anesth. 2008 Feb;22(1):47-52 

Slight RD, O'Donohoe P, Fung AK, Alonzi C, McClelland DB, Mankad PS. Rationalizing blood transfusion in 

cardiac surgery: the impact of a red cell volume-based guideline on blood usage and clinical outcome. Vox 

Sang. 200;95:205-10 

Slight RD, Lux D, Nzewi OC, McClelland DB, Mankad PS. Oxygen delivery and hemoglobin concentration in 

cardiac surgery: when do we have enough? Artif Organs. 2008 Dec;32(12):949-55 

Slight RD, Alston RP, McClelland DB, Mankad PS. What factors should we consider in deciding when to 

transfuse patients undergoing elective cardiac surgery? Transfus Med Rev. 2009 Jan;23(1):42-54 


Slight RD, Nzewi O, McClelland DB, Mankad PS. Red cell transfusion in elective cardiac surgery patients: 

where do we go from here?Br J Anaesth. 2009 Mar;102(3):294-296 

Slight RD, Ferguson R, Stirling D, McClelland DB, Mankad PS. Experience with sodium fluorescein flow 

cytometry in the determination of red cell volume Int J Lab Hematol. 2009 Apr;31(2):233-5 

Spence A, Townsend E, Prowse C, Palmer P, Fleming P, Joost A. Van Hilten, Ferguson E. A Multi-Level 

Analysis of the Stability of the Information Source-Trust Association for Blood Transfusion. Transfusion 2009: 

Apr 20. [Epub ahead of print] 

Swierzko AS, Atkinson APM, Cedzynski M, MacDonald SL, Szala A, Domzalska-Popadiuk I, Bokowska-Klos 

M, Jopek A, Szczapa J, Matsushita M, Szemraj J, Turner ML, Kilpatrick DC. Two factors of the lectin pathway 

of complement, L-ficolin and mannan-binding lectin, and their associations with prematurity, low birthweight 

and infections in a large cohort of Polish neonates. Mol Immunol. 2009;46:551-8 

Swierzko AS, Szala A, Cedzynski M, Domzalska-Popadiuk I, Borkowska-Klos M, Jopek A, Szczapa J, 

Szemraj J, Atkinson APM, MacDonalD SL, Turner ML, Kilpatrick DC. Mannan-binding lectin genotypes and 

genotype-phenotype relationships in a large cohort of Polish neonates. Hum Immunol. 2009;70:68-72 

Swierzko AS, Cedzynski M, Domzalska-Popadiuk I, MacDonald SL, Borkowska-Klos M, Atkinson AP, Szala A, 

Jopek A, Jensenius JC, Kawakami M, Szczapa J, Matsushita M, Szemraj J, Turner ML, Kilpatrick DC. 

Mannan-binding lectin-associated serine protease-2 (MASP-2) in a large cohort of neonates and its clinical 

associations Mol Immunol. 2009;46:1696-701 

Thomson RC, Petrik J, Nash AA, Dutia BM: Expansion and activation of NK cell populations in a 

gammaherpesvirus infection. Scandinavian J Immunology 2008; 67:489-95. 

Turner Ml. Transmission of vCJD by blood and tissues: managing the risk. The Biomedical Scientist 2007; 

Sept: 737-8. 

Turner ML, Hewitt P, Bruce M, Ironside JI. Prion Diseases. In: Barbara JAJ, Regan FAM, Contreras MC (eds). 

Transfusion Microbiology. 2 nd Edition. Cambridge University Press April 2008. 141-151. 

Turner ML. Transfusion Reactions. Chapter 75. In: Strachan MWJ, Sharma SK, Hunter JAA (eds). Davidson’s 

International Clinical Cases in Medicine. Churchill Livingstone, Elsevier. Edinburgh 2008. 

Turner ML. Variant CJD. In: Practical Transfusion Medicine. 3rd Edition Murphy MF, Pamphilion DH (eds). 

2008. Oxford: Blackwell Science. 

Turner ML. Prion Diseases. In: Rossi’s Principles of Transfusion Medicine 4th Edition, Simon TL, Snyder EL, 

Solheim BG, Stowell CP, Strauss RG, Petrides M (eds). Blackwell Publishing. Publisher: Wiley-Blackwell, 

ISBN:1405175885, 1112 pages, 2009). 

Turner ML, Ludlam CA. An Update on the Assessment and Management of the Risk of Transmission of 

variant Creutzfeldt-Jakob Disease by Blood and Plasma Products. Br J Haematol. 2009;144:14-23. 

Walsh TS "Perioperative blood component therapy and haemostasis" In: The Year in Anaesthesia and Critical 

Care. Eds. Hunter, Cook, Priebe, Struys. Clinical Publishing. Oxford 2008 (chapter) 

Ward FJ, Hall AM, Cairns LS, Leggat As, Urbaniak SJ, Vickers MA, Barker RN 

Clonal regulatory T cells specific for a red blood cell autoantigen in human autoimmune haemolytic anemia. 

Blood (2008) 111; 680-687 

Urbaniak SJ [editorial] Noninvasive approaches to the management of RhD haemolytic disease of the fetus 

and newborn. Transfusion (2008) 48; 2-5 


Urbaniak, SJ. Why RHD is so immunogenic – and therefore important – and how we develop immune 

responses to blood cells. Blood Matters (2008), Issue 26, pp16-17 

SNBTS Active Grants 2008-09 

Wellcome Trust 

Turner ML, Crawford D, Haque T, Vickers MA, Forsythe J. Establishment of a bank 

of EBV specific cytotoxic T cells for clinical treatment of post-transplant lymphoproliferative 

disease. £431,069. April 2009 – Sept 2011. 

Turner ML, Mountford J, Forrester L, De Sousa P, Anstee D, Courtney A, Murphy 

W. Proof of principle: human embryonic stem cell derived red cell concentrates for 

clinical transfusion. £2,745,549 April 2009 – March 2012 (BloodPharma) 

Scottish Funding Council. 

Wilmut I, Turner M, Illius A, Savill J. Strategic Development Grant for Centre of 

Regenerative Medicine. £2,030,000 (August 2006 to July 2010) 

UK Stem Cell Foundation 

Noble B. Autologous stem cell based therapies in musculoskeletal regenerative 

medicine. UK Stem Cell Foundation / Medical Research Council/ Scottish 

Enterprise / Chief Scientist’s Office £1,400,000 May 2008 – May 2010. 

Dhillon B, Ramesh K, Turner ML. Ex vivo expanded corneal limbal stem cell 

transplantation: from laboratory to clinical application. UK Stem Cell Foundation, 

Scottish Enterprise and Chief Scientists Office. £307,820. Jan 2009 – Dec 2011 

Translational Medicine Research Collaboration 

Newby DE, Burdess A, Richards J, Lang N, Roddie H, McKillop G, Wardlaw J, 

Turner M, Hart S, Barclay R, Chalmers R, Simpson J, Dhaliwal K, Marshall I, 

Bastin M. Magnetic resonance imaging of human atherosclerosis. Translational 

Medicine Research Collaboration £566,995. June 2007 – August 2009 

Sir Jules Thorn Charitable Trust 

Forbes SJ, Iredale J, Hayes P, Kluth D, Turner ML, Bellamy C, Marshall I. Stem 

cell therapy for liver cirrhosis. £999,565. Oct 2007 – Sept 2012 

Medical Research Council 

Holyoake TL, Brunton V. Koschmieder S. Is Bcr-Abl expression relevant for the 

survival of cancer stem cells in chronic myeloid leukaemia? £680,000. (June 2007 

– May 2010) 

European Union 

SJ Urbaniak, SS Armstrong-Fisher, M Moss. Special non-invasive advances in 

fetal and neonatal evaluation network (SAFE). £113,195 (current share of 12 

million euro) SAFE Fellow & PhD student. EU (Network of Excellence) (2004-2009) 

Franklin IM, Hart M, Arthur E, McClelland DBL, Pirie E The EU optimal blood use 

project. 890,285 Euros €500,000 (56.16% EC funded) (3 years 2007-2010) 

Leukaemia Research Fund 

Holyoake TL. Brunton V, Koschmider S. Is Bcr-Abl expression relevant for the 

survival of cancer stem cells in chronic myeloid leukaemia? £28,221. (3 years 

January 2007 – December 2009) 

Holyoake TL, Bartholomew C, Strathdee G, Melo J. EVII isoform expression and 

knockdown in CML. Leukaemia Research Fund. £45,000. April 2008 – March 

2011. 

Biotechnology and Biological Sciences Research Council 

De Sousa P, Turner ML, Pells S. A novel characterisation and separation 


technique for pluripotent human embryonic and haematopoietic stem cells. BBSRC 

£131,765. Jan 2009 – Dec 2012. 

British Heart Foundation 

Barclay GR, Hadoke P, Mills N, Newby DE, Turner ML. Preclinical in vivo 

evaluation of potential sources of human endothelial progenitor cells for autograft 

cellular therapy of ischaemia. £239,930 (3 years July 2006 to June 2009). 

Mills NL, Newby DE, Barclay GR, de Belder MA, Robinson SD. Endothelial 

progenitor cells in acute vascular injury and repair. £242,685 (August 2007-July 

2010) 

Mountford J. Generation of cardiomyocytes from mesenchymal stem cells derived 

from adult human sternal bone marrow. (as Principal Investigator for Clinical 

Research Fellow funding) £149,478 (3 years from January 2005-December 2008) 

Chief Scientist Office. 

De Sousa P, Head MW, Turner ML, Manson J. Proof of principle validation of a 

human embryo cell based screen for susceptibility to infectious prion transmission. 

£125,438. (August 2007 – December 2008). 

Head MW, Peden A, Prowse C, Manson J, Bishop M, Ironside J. The use of 

human recombinant prion protein as a substrate in an improved in vitro 

amplificationbased blood test for Creutzfeldt-Jakob disease infectivity £193,512 

over 2 years to December 2010 (£90,000pa) 

Holyoake T, Copland MC. Consumables £24,000. (3 years June 2006 - May 

2009). 

De Sousa P, Head M, Turner M, Manson J. Proof of principle demonstration of 

human embryo stem cell based detection of prions.£127,707 (18 months to June 

2009). 

Walsh T, Forbes J, Langston A, McClelland DBL, Pelly J, Ramsay P, Watson D, 

Prowse C. 

A feasibility randomized trial comparing REstrictive and LIberal blood transfusion 

strategies in patients requiring six or more days in intEnsiVE care (RELIEVE study) 

£182,577 over 18 months to October 2010 (£100,000pa) 

Armstrong-Fischer SS, Urbaniak SJ. Non-Invasive Prenatal Fetal D typing (follow 

up on optimasation assay timing) £62, 259 over 12 months from June 2009 

Department of Health 

Houston F, Prowse C, Turner M, MacGregor I, Hornsey V, Hunter N, Foster J, 

Groschup M. The effect of leucodepletion on transmission of BSE by transfusion of 

sheep blood components. £3,424,382 (6 years to December 2010.) 

Extensionto 2011 and possible increase under negotiation by Jean Manson 

Navigant Inc. 

Prowse C et al. Validation of riboflavin treated fresh frozen plasma. £52,310 . (1 

year to July 2008) 

UK Blood Services Forum 

Prowse C, Turner M, Jones M, Head M: “ vCJD confirmatory assay developments” 

£179,563 over 3 years from 1 st April 2008-2011 (£60,000pa) 

SNBTS component of Prion filter trial (PRISM) 

National Services Scotland (Scottish National Blood Transfusion Service) 

Prowse C, Turner M, Jones M, Head M: for infrastructure and routine support of 

vCJD assay development CVP £65,000 capital and £80,648 pa salary and 

consumables over 3 years until 31st March 2011 

Polish State Committee for Scientific Research 


Swierzko AS, Szczapa J, Cedzynski M, Szemraj J, Domzalska-Popadiuk, I, Klink 

M, Kilpatrick D.C. Lectin pathway of complement in defence against infection in 

newborns. £21,000 ( 3 years May 2005-May 2008). 

Cedzynski M, Atkinson APM, Swierzko AS, Szemraj J, MacDonald SL, Kilpatrick 

DC, Buczylko K, Zeman K. Investigation of the role of insufficiency of L-ficolin and 

other components of the lectin pathway of complement activation in recurrent 

respiratory infections in children with allergies. £26,000 (3 years April 2006- April 

2009). 

Iranian Government 

SJ Urbaniak, RN Barker, M Moss Gholamreza Sarab 2004-2008 

PhD studentship – HPA-1a GP IIIa peptide binding and processing. 

External overall funding = £93,900 . SNBTS contribution for 2008 – £5000 

consumables. 

SJ Urbaniak, SS Armstrong-Fisher. Ali Varzi 2004-2008 

PhD Studentship – identification of fetal DNA genetic markers in maternal plasma. 

£91,400. SNBTS contribution for 2008 – £5000 consumables. 

Saudi Arabian Government 

M Moss, S Urbaniak (Abdulla Meshi) 

Characterisation of the human humoral immune response to RhD derived synthetic 

peptides. 

£89,745 2008-2011 

DiaMed AG 

RH Fraser. Development of novel monoclonal blood grouping reagents (Research 

Assistant salary funding). 200,000 SFr £88,000 (Rolling grant from years 2004- 

2008) 

NHS Grampian University Hospitals Division (GUHT) Endowments. 

SJ Urbaniak. Research Technician. (Sadie Henderson) 2007-2009 

£36,000. 

Nestech Partnership 

SJ Urbaniak, L Cairns, RN Barker, E Rattray. Peptide immunotherapy to suppress 

antibodies to red blood cells. £203,875. (3 years from 2005-2008) 

NHS National Services Scotland - Service Redesign Bid 

SJ Urbaniak, SS Armstrong-Fisher. 

Service Redesign Committee– pilot study of non-invasive RhD genotyping on 

maternal plasma. £56,480. 2006-2009. 

NHS Blood and Tissues (England) 

SS Armstrong-Fisher, SJ Urbaniak. Placental transfer of recombinant antibodies. 

£5000. SNBTS contribution for 2008 - £4000 2006-2008 

University of Bristol 

SS Armstrong-Fisher, SJ Urbaniak. Fetal DNA genetic markers in maternal 

plasma. (Funding support of PhD Studentship) £15,000 (in year 2007-2008) 

University of Bristol 

Scottish Enterprise Proof of Concept 

M Moss, S Urbaniak. Blood group mimotopes. £248,945. (3 years 2008-2010) 

Glasgow Royal Infirmary Endowments 

Holyoake TL and Allan E. Targeting quiescent CML stem cell by combining G-CSF 

and 

imatinib mesylate £9,700 (6 years to January 2011) 

Holyoake T, Mysinna S. Is survival of primitive, quiescent stem cells from patients 

with chronic myeloid leukaemia Bcr-Abl dependent or not? 


£31,000. January 2008 – November 2008 

Alba BioScience 

Juraj Petrik Microarray diagnostics for blood borne viruses 

2009:£ ~ 56,000. 2010:£ ~ 58,000 

2009-2010 

Allan EK, Hamilton A, Hatziieremia S, Zhou P, Jorgensen HG, Vigneri P, Holyoake TL. Nuclear 

entrapment of BCR-ABL by combining imatinib mesylate with leptomycin B does not eliminate CD34+ 

chronic myeloid leukaemia cells. Leukemia. 2009; 23: 1006-8 

Anani Sarab G, Moss M, Barker RN, Urbaniak SJ. Naturally processed peptides spanning the HPA-1a 

polymorphism are efficiently generated and displayed from platelet glycoprotein by HLA-DRB3*0101 - 

positive antigen-presenting cells. Blood. 2009;114:1954-7. 

Ban M, Goris A, Lorentzen AR, Baker A, Mihalova T, Ingram G, Booth DR, Heard RN, Stewart GJ, 

Bogaert E, Dubois B, Harbo HF, Celius EG, Spurkland A, Strange R, Hawkins C, Robertson NP, 

Dudbridge F, Wason J, De Jager PL, Hafler D, Rioux JD, Ivinson AJ, McCauley JL, Pericak-Vance M, 

Oksenberg JR, Hauser SL, Sexton D, Haines J, Sawcer S; Wellcome Trust Case-Control Consortium 

(WTCCC), Compston A. Replication analysis identifies TYK2 as a multiple sclerosis susceptibility factor. 

Eur J Hum Genet. 2009; 17: 1309-13. 

Bellodi C, Lidonnici MR, Hamilton A, Helgason GV, Soliera AR, Ronchetti M, Galavotti S, Young KW, 

Selmi T, Yacobi R, Van Etten RA, Donato N, Hunter A, Dinsdale D, Tirrò E, Vigneri P, Nicotera P, Dyer 

MJ, Holyoake T, Salomoni P, Calabretta B. Targeting autophagy potentiates tyrosine kinase inhibitorinduced 

cell death in Philadelphia chromosome-positive cells, including primary CML stem cells. J Clin 

Invest. 2009 May;119(5):1109-23. 

Bessos H, Killie MK, Seghatchian J, Skogen B, Urbaniak SJ. The relationship of anti-HPA-1a amount to 

severity of neonatal alloimmune thrombocytopenia - Where does it stand? Transfus Apher Sci. 

2009;40:75-8. 

Biggin K, Warner P, Prescott R, McClelland B. A review of methods used in comprehensive, descriptive 

studies that relate red blood cell transfusion to clinical data. Transfusion. 2010; 50: 711-718. 

British Committee for Standards in Haematology (Harris AM (BCSH Lead), Atterbury CLJ, Chaffe B, 

Elliott C, Hawkins T, Hennem SJ, Howell C, Jones J, Murray S, New HV, Norfolk D, Pirie L (British 

Transplantation Society Lead), Russell J, Taylor C. Guideline on the Administration of Blood 

Components. London: British Society for Haematology. BCSH web site. 2009; December: 1-60. 

Cedzynski M, Atkinson APM, Swierzko AS, MacDonald SL, Szala A, Zeman K, Buczylko K, Bak- 

Romaniszyn L, Wiszniewska M, Matsushita M, Szemraj J, Banasik M, Turner ML, Kilpatrick DC. L-Ficolin 

(Ficolin-2) insufficiency is associated with combined allergic and infectious respiratory disease in 

children. Molecular Immunology 2009; 47: 415-419. 

Chapman CE, Stainsby D, Jones H, Love E, Massey E, Win N, Navarrete C, Lucas G, Soni N, Morgan 

C, Choo L, Cohen H, Williamson LM; on behalf of the Serious Hazards of Transfusion Steering Group 

(McClelland DBL et al). Ten years of hemovigilance reports of transfusion-related acute lung injury in the 

United Kingdom and the impact of preferential use of male donor plasma. Transfusion. 2009; 49: 440- 

452. 

Clark P, Wu O, Greer IA, Lowe GDO. Venous thrombosis prevention – more that just guidelines. British 

Journal of Haematology. 2010; 149: 50-54 

Coste J, Prowse C, Eglin R, Fang C. Subgroup on TSE. A report on transmissible spongiform 

encephalopathies and transfusion safety. Vox Sang. 2009: 96: 284-291. 

Crawford J, Turner M. Stem cell therapies: hype or reality? J R Coll Physicians Edinb 2008; 38: 221-3 

Davies A, Jordanides NE, Giannoudis A, Lucas CM, Hatziieremia S, Harris RJ, Jørgensen HG, Holyoake 


TL, Pirmohamed M, Clark RE, Mountford JC. Nilotinib concentration in cell lines and primary CD34(+) 

chronic myeloid leukemia cells is not mediated by active uptake or efflux by major drug transporters. 

Leukemia. 2009; 23: 1999-2006. 

Davidson F, Yirrell, D, Lycett C, Patrik J, Dow BC. HIV subtypes detected in Scottish blood donors. Vox 

Sang. 2009; 96: 160-162. 

Davison KL, Dow B, Barbara JA, Hewitt PE, Eglin R. The introduction of anti-HTLV testing of blood 

donations and the risk of transfusion-transmitted HTLV, UK: 2002-2006. Transfus Med. 2009;19:24-34 

Dehghan A, Yang Q, Peters A, Basu S, Bis JC, Rudnicka AR, Kavousi M, Chen MH, Baumert J, Lowe 

GD, McKnight B, Tang W, de Maat M, Larson MG, Eyhermendy S, McCardle WL, Lumley T, Pankow JS, 

Hofman A. Massaro JM, Rivadeneira F, Kolz M, Taylor KD, van Dujin CM, Kathiresan S, Illig T, 

Aulchenko YS, Volcik KA, Johnson AD, Uitterlinden AG, Tofler GH, Gieger C, Wellcome Trust Case 

Control Consortium, Psaty BM, Couper DJ, Boerwinkle E, Koenig W, O’Donnell CJ, Witteman JC, 

Strachan DP, Smith NL, Folsom AR. Association of novel genetic Loci with circulating fibrinogen levels: 

a genome-wide association study in 6 population-based cohorts. Circ Cardiovasc Genet. 2009; 2(2): 

125-133 

Drummond MW, Heaney N, Kaeda J, Nicolini FE, Clark RE, Wilson G, Shepherd P, Tighe J, McLintock 

L, Hughes T, Holyoake TL.A pilot study of continuous imatinib vs pulsed imatinib with or without G-CSF 

in CML patients who have achieved a complete cytogenetic response. Leukemia. 2009; 23:1199-201. 

Ferguson E, Spence A, Townsend E, Prowse C, Palmer J, Fleming P, Van Hilten JA (RASPH Research 

Group) What type of information is trusted by whom? A multi-level analysis of the stability of the 

information source-trust association for blood transfusion. Transfusion. 2009; Apr 20. [Epub ahead of 

print] 

Fielding AK, Rowe JM, Richards SM, Buck G, Moorman AV, Durrant IJ, Marks DI, McMillan AK, Litzow 

MR, Lazarus HM, Foroni L, Dewald G, Franklin IM, Luger SM, Paietta E, Wiernik PH, Tallman MS, 

Goldstone AH. Prospective outcome data on 267 unselected adult patients with Philadelphia 

chromosome-positive acute lymphoblastic leukemia confirms superiority of allogeneic transplantation 

over chemotherapy in the pre-imatinib era: results from the International ALL Trial MRC 

UKALLXII/ECOG2993. Blood. 2009 ;113:4489-96. 

Foo J, Drummond MW, Clarkson B, Holyoake T, Michor F. Eradication of chronic myeloid leukemia stem 

cells: a novel mathematical model predicts no therapeutic benefit of adding G-CSF to imatinib. PLoS 

Comput Biol. 2009 Sep;5(9):e1000503. Epub 2009 Sep 11. 

Fotaki V, Larralde O, Zeng S, McLaughlin D, Nichols J, Price DJ, Theil T, Mason JO. Loss of Wnt8b has 

no overt effect on hippocampus development but leads to altered Wnt gene expression levels in 

dorsomedial telencephalon. Development Dynamics. 2010; 239: 284-296. 

Goldman JM, Green AR, Holyoake T, Jamieson C, Mesa R, Mughal T, Pellicano F, Perrotti D, Skoda R, 

Vannucchi AM.Chronic myeloproliferative diseases with and without the Ph chromosome: some 

unresolved issues. Leukemia. 2009; 23: 1708-15. 

Hamilton A, Alhashimi F, Myssina S, Jorgensen HG, Holyoake TL.Optimization of methods for the 

detection of BCR-ABL activity in Philadelphia-positive cells. Exp Hematol. 2009; 37: 395-401. 

Harrison SJ, Franklin IM, Campbell JD. Enumeration of blood dendritic cells in patients with multiple 

myeloma at presentation and through therapy. Leuk Lymphoma. 2008; 49: 2272-83. 

Hatziieremia S, Jordanides NE, Holyoake TL, Mountford JC, Jørgensen HG. Inhibition of MDR1 does not 

sensitize primitive chronic myeloid leukemia CD34+ cells to imatinib. Exp Hematol. 2009;37:692-700. 

Hochhaus A, O'Brien SG, Guilhot F, Druker BJ, Branford S, Foroni L, Goldman JM, Müller MC, Radich 

JP, Rudoltz M, Mone M, Gathmann I, Hughes TP, Larson RA; IRIS Investigators. Six-year follow-up of 

patients receiving imatinib for the first-line treatment of chronic myeloid leukemia. Leukemia. 2009; 23: 

1054-61. 

Holotnakova T, Tylkova L, Takacova M, Kopacek J, Petrik J, Pastorekova S, Pastorek J. Role of the HBx 

oncoprotein in carbonic anhydrase 9 induction. J Med Virol 2009; 82:32-40 


Hornsey VS, Drummond O, Morrison A, McMillan L, MacGregor IR, Prowse CV. Pathogen reduction of 

fresh plasma using riboflavin and ultraviolet light: effects on plasma coagulation proteins. Transfusion. 

2009; 49: 2167-2172. 

Jones M, Peden AH, Yull H, Wight D, Bishop MT, Prowse CV, Turner ML, Ironside JW, MacGregor IR, 

Head MW. Human platelets as a substrate source for the in vitro amplification of the abnormal prion 

protein (PrP) associated with variant Creutzfeldt-Jakob disease. Transfusion. 2009; 49: 376-84 

Jones M, Wight D, Barron R, Jeffrey M, Manson J, Prowse C, Ironside JW, Head MW. Molecular model 

of prion transmission to humans. Emerging Infectious Diseases. 2009; 15: 2013-2016. 

Jones M, Wight d, Barron R, Jeffrey M, Prowse C, Ironside JW, Head MW. Modeling the Molecular 

component of Prion Transmission to Humans. In preparation for Nature Medicine 2009 . 

Jones M, Wight D, McLoughlin V, Norrby K, Ironside JW, Connolly JG, Farquhar CF, MacGregor IR, 

Head MW. An antibody to the aggregated synthetic prion protein peptide (PrP 106-126) selectively 

recognizes disease-associated prion protein (PrP) from human brain specimens. Brain Pathol. 2009; 

19: 293-302. 

Jones M, McLoughlin V, Connolly JG, Farquhar CF, MacGregor IR, Head MW. Production and 

characterization of a panel of monoclonal antibodies against native human cellular prion protein. 

Hybridoma (Larchmt). 2009; 28: 13-20. 

Joseph BG, Hendry C, Walsh TS. Red blood cell use outside the operating theater: a prospective 

observational study with modeling of potential blood conservation during severe blood shortages. 

Transfusion. 2009; 49: 2060-2069. 

Kilpatrick DC, Chalmers JD, MacDonald SL, Murray MP, Mohammed A, Hart SP, Matsushita M, Hill AT. 

Stable bronchiectasis is associated with low serum L-ficolin concentrations. Clinical Respiratory Journal 

2009, 3, 29-33 

Mahmood A, Gosling P, Barclay R, Kilvington F, Vohra R. Splanchnic microcirculation protection by 

hydrozyethyl starches during abdominal aortic aneurysm surgery. Eur. J. Vasc. Endovasc. Surg. 2009; 

37: 319-325. 

Milojkovic D, Nicholson E, Apperley JF, Holyoake TL, Shepherd P, Drummond MW, Szydlo R, Bua M, 

Foroni L, Reid A, Khorashad JS, de Lavallade H, Rezvani K, Paliompeis C, Goldman JM, Marin D. Early 

prediction of success or failure using second generation tyrosine kinase inhibitors for chronic myeloid 

leukemia. Haematologica. 2009 Oct 14. [Epub ahead of print] 

Mills NL, Tura O, Padfield GJ, Millar C, Lang NN, Stirling D, Ludlam C, Turner ML, Barclay GR, Newby 

DE. Dissociation of phenotypic and functional endothelial progenitor cells in patients undergoing 

percutaneous coronary intervention. Heart. 2009; 95: 2003-2008. 

Mountford J, Olivier E, Turner M. Prospects for the manufacture of red cells for transfusion. British 

Journal of Haematology. 2010; 149: 22-34. 

Myssina S, Helgason GV, Serrels A, Jørgensen HG, Bhatia R, Modi H, Baird JW, Mountford JC, 

Hamilton A, Schemionek M, Koschmieder S, Brunton VG, Holyoake TL. Combined BCR-ABL inhibition 

with lentiviral-delivered shRNA and dasatinib augments induction of apoptosis in Philadelphia-positive 

cells. Exp Hematol. 2009; 37: 206-14. 

Nicholson E, Holyoake T. The chronic myeloid leukaemia stem cell. Clin. Lymphoma Myeloma. 2009; 

9: Suppl. 4: S376-81 Review. 

Orozco G, Hinks A, Eyre S, Ke X, Gibbons LJ, Bowes J, Flynn E, Martin P, Wellcome Trust Case Control 

Consortium, YEAR consortium, Wilson AG, Bax DE, Morgan AW, Emery P, Steer S, Hocking L, Reid 

DM, Wordsworth P, Harrison P, Thomson W, Barton A, Worthington J. Combined effects of three 

independent SNPs greatly increase the risk estimate for RA at 6q23. Hum Mol Genet. 2009; 18: 2693- 

2699. 

Pellicano F, Copland M, Jorgensen HG, Mountford J, Leber B, Holyoake TL. BMS-214662 induces 


mitochondrial apoptosis in chronic myeloid leukemia (CML) stem/progenitor cells, including CD34+38- 

cells, through activation of protein kinase Cbeta. Blood. 2009;114:4186-96 

Pellicano F, Cilloni D, Helgason GV, Messa F, Panuzzo C, Arruga F, Bracco E, Allan E, Huntly BJ, 

Holyoake TL, Saglio G. FOXO transcription factor activity is partially retained in quiescent CML stem 

cells and induced by tyrosine kinase inhibitors in CML progenitor cells. Blood. 2009 Dec 1. [Epub ahead 

of print] 

Petrik J. Microarray blood testing: Pros & cons. Biologicals. 2010; 38: 2-8. 

Pirie, L. Green, J. (2009) A framework to support Nurses and Midwives making the clinical decision and 

providing the written instruction for blood component transfusion. 

http://www.transfusionguidelines.org.uk/Index.aspx?Publication=BBT&Section=22&pageid=1298 

Prowse C. Properties of pathogen-inactivated plasma components. Transfus. Med. Rev. 2009; 23: 

124-133. 

Reesink HW, Panzer S, McQuilten ZK, Wood EM, Marks DC, Wendel S, Trigo F, Biagini S, Olyntho S, 

Devine DV, Mumford I, Cazenave JP, Rasonglès P, Garraud O, Richard P, Schooneman F, Vezon G, Al 

Radwan R, Brand A, Hervig T, Castro E, Lozano M, Navarro L, Puig L, Almazán C, Maclennan S, 

Cardigan R, Franklin IM, Prowse C. Pathogen inactivation of platelet concentrates. Vox Sang. 2010 Mar 

10. [Epub ahead of print] 

Reikvam H, Prowse C, Roddie H, Heddle NM, Hervig T (for the BEST collaborative). A pilot study of the 

possibility and the feasibility of haemoglobin dosing with red blood cells transfusion. Vox Sanguinis. 

2010; Mar 10 [Epub ahead of print] 

Robb AO, Mills NL, Smith IB, Short A, Tura-Ceide O, Barclay GR, Blomberg A, Critchley HO, Newby DE, 

Denison FC. Influence of menstrual cycle on circulating endotheilial progenitor cells. Hum. Reprod. 

2009; 24: 619-625. 

Schemionek M, Elling C, Steidl U, Bäumer N, Hamilton A, Spieker T, Göthert JR, Stehling M, Wagers A, 

Huettner CS, Tenen DG, Tickenbrock1 L, Berde WE, Hubert Serve H, Holyoake TL, Müller-Tidow C, 

Koschmieder S. BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells 

Blood 2010; 115: 3185-3195. 

Slight RD, Alston RP, McClelland DB, Mankad PS. What factors should we consider in deciding when to 

transfuse patients undergoing elective cardiac surgery? Transfus Med Rev. 2009;23:42-54. 

Sullivan, G. J., Hay, D. C., Park, I. H., Fletcher, J., Hannoun, Z., Payne, C. M., Dalgetty, D., Black, J. R., 

Ross, J. A., Samuel, K., Wang, G., Daley, G. Q., Lee, J. H., Church, G. M., Forbes, S. J., Iredale, J. P., 

and Wilmut, I. Generation of functional human hepatic endoderm from human induced pluripotent stem 

cells. Hepatology 2009, (Epub ahead of print) 

Swierzko AS, Atkinson APM, Cedzynski M, MacDonald SL, Szala A, Domzalska-Popadiuk I, Bokowska- 

Klos M, Jopek A, Szczapa J, Matsushita M, Szemraj J, Turner ML, Kilpatrick DC. Two factors of the 

lectin pathway of complement, L-ficolin and mannan-binding lectin, and their associations with 

prematurity, low birthweight and infections in a large cohort of Polish neonates. Molecular Immunology 

2009; 46: 551-558. 

Swierzko, AS, Szala A, Cedzynski M, Domzalska-Popadiuk I, Borkowska-Klos M, Jopek A, Szczapa J, 

Szemraj J, Atkinson APM, MacDonald SL, Turner ML, Kilpatrick DC. Mannan-binding lectin genotypes 

and genotype-phenotype relationships in a large cohort of Polish neonates. Human Immunology 2009; 

70: 68-72. 

Swierzko AS, Cedzynski M, Domzalska-Popadiuk I, MacDonald SL, Borkowska-Klos M, Atkinson APM, 

Szala A, Jopek A, Jensenius J, Kawakami M, Sxcxapa J, Matsushita M, Szemraj J, Turner ML, Kilpatrick 

DC. Mannan-binding lectin associated serine protease-2 (MASP-2) in a large cohort of neonates and its 

clinical associations. Molecular Immunology 2009; 46: 1696-1701. 

Szabo SM, Levy AR, Davis C, Holyoake TL, Cortes J. A Multinational Study of Health State Preference 

Values Associated with Chronic Myelogenous Leukemia. Value Health. 2009 Jul 29. [Epub ahead of 

print] 


Taylor K, Rolfe M, Reynolds N, Kilanowski F, Pathania U, Clarke D, Yang D, Oppenheim J, Samual K, 

Howie S, Barran P, Macmillan D, Campopiano D, Dorin J. Defensin-related peptide 1 (Defr 1) is allelic to 

Defb8 and chemoattracts immature DC and CD4+T cells independently of CCR6. Eur. J. Immunol. 

2009; 39: 1353-1360. 

Terrace JD, Hay DC, Samuel K, Payne C, Anderson RA, Currie IS, Parks RW, Forbes SJ, Ross JA. 

Side population cells in developing human liver are primarily haematopoietic progenitor cells. Exp. Cell. 

Res. 2009; 315: 2141-2153. 

Turner ML. Prion diseases. In: Rossi’s Principles of Transfusion Medicine 4th Edition, Simon TL, Snydr 

EL, Solheim BG, Stowell CP, Strauss RG, Petrides M (eds). 2009 Blackwell Publishing 791-800. 

Urbaniak SJ. Alloimmunization to the platelet antigen human platelet antigen-1a and characterization of 

the helper T-cell responses in Fetomaternal Alloimmune thrombocytopenia. Vox Sang. 2009; 41) 

107-110. 

Urbaniak SJ. Recommendations of the ISBT working party on granulocytes immunobiology for 

leucocyte antibody screening in the investigation and prevention of antibody-mediated transfusionrelated 

acute lung injury ISBT working party on granulocytes immunobiology. Vox Sang. 2009; 96: (3) 

266-269. 

Vanhoutte VJ, McAulay KA, McCarrell E, Turner M, Crawford DH, Haque T. Cytolytic mechanisms and 

T-cell receptor Vbeta usage by ex vivo generated Epstein-Barr virus-specific cytotoxic T lymphocytes. 

Immunology. 2009; 127: 577-586. 

Walsh TS, MacIver CR. A clinical scenario-based survey of transfusion decisions for intensive care 

patients with delayed weaning from mechanical ventilation. Transfusion. 2009; 49: 2661-2667. 

Walsh TS, MacIver for The Scottish Critical Care Trials Group And Scottish National Blood Transfusion 

Service Clinical Effectiveness Group. A clinical scenario-based survey of transfusion decisions for 

intensive care patients with delayed weaning from mechanical ventilation. Transfusion. 2009 Aug 4. 

[Epub ahead of print] 

Franklin IM. Introduction: recent evolution of transfusion medicine. In: Practical Transfusion Medicine 

(3rd Edition). Murphy MF, Pamphilon DH (Eds). Oxford: Blackwell Publishing. 2009; Ch1: 1-4 

McClelland B, Walsh T. Good blood management: the effective and safe use of blood components. In: 

Practical Transfusion Medicine (3rd Edition). Murphy MF, Pamphilon DH (Eds). Oxford: Blackwell 

Publishing. 2009; Ch 25: 265-284. 

McQuaker IG, Franklin IM. Haemopoietic stem cell transplantation. In: Practical Transfusion Medicine 

(3rd Edition). Murphy MF, Pamphilon DH (Eds). Oxford: Blackwell Publishing. 2009; Ch 40: 443-452. 

Prowse CV and Roberts D J. Blood substitutes. In: Practical Transfusion Medicine (3rd Edition). Murphy 

MF, Pamphilon DH (Eds). Oxford: Blackwell Publishing. 2009; Ch 35: 390-399. 

Turner ML. Variant Creutzfeldt-Jakob disease. In: Practical Transfusion Medicine (3rd Edition). Murphy 

MF, Pamphilon DH (Eds). Oxford: Blackwell Publishing. 2009; Ch 15: 153-161. 

Turner ML. Prion Diseases. In: Rossi’s Principles of Transfusion Medicine 4th Edition, Simon TL, Snyder 

EL, Solheim BG, Stowell CP, Strauss RG, Petrides M (eds). 2009 Blackwell Publishing. 791-800. 

Aubuchon J, Prowse C. AABB monograph on Pathogen Inactivation – in preparation 2009 (Chapters 

and book editor) 

Dow BC, Franklin IM, Munro H, Gunson R. Syphilis nucleic acid testing: usefulness in syphilis 

confirmation? Transfusion. 2010; 50(3): 737-739. 

Franklin IM. Prevention of rhesus haemolytic disease of the fetus and newborn. Lancet. 2009;373:1082. 




Turner ML, Crawford 

D, Haque T, Vickers 

MA, Forsythe J. 

Turner ML, Mountford 

J, Forrester L, De 

Sousa P, Anstee D, 

Courtney A, Murphy 

W. 

Establishment of a bank of EBV 

specific cytotoxic T cells for clinical 

treatment of post-transplant 

lympho-proliferative disease. 

Proof of principle: human 

embryonic stem cell derived red 

cell concentrates for clinical 

transfusion. 

[‘Blood Pharma’] 

£ 431,069 

(. Jan 2010 – June 2012) 

£2,745,549 

(3 years: July 2009 – June 

2012) 

Scottish Funding Council 

Wilmut I, Turner M, 

Illius A, Savill J 

Strategic Development Grant for 

Centre of Regenerative Medicine 

2,030,000 

(4 years August 2006 to 

July 2010) 

UK Stem Cell Foundation/ Medical Research Council/Scottish Enterprise/Chief Scientist’s Office 

Noble B, Turner ML. Autologous stem cell based 

therapies in musculoskeletal 

regenerative medicine. 

£1,400,000 

(2 years May 2008 to May 

2010) 

CZB/4/6 

57 

Dhillon B, Ramaesh K, 

Turner ML. 

Ex vivo expanded corneal limbal 

stem cell transplantation: from 

laboratory to clinical application 

£307,820 

(3 years January 2009 to 

December 2011) 

Translational Medicine Research Collaboration 

Newby DE, Burdess 

A, Richards J, Lang N, 

Roddie H, McKillop G, 

Wardlaw J, Turner M, 

Hart S, Barclay R, 

Chalmers R, Simpson 

J, Dhaliwal K, Marshall 

I, Bastin M. 

Magnetic resonance imaging of 

human atherosclerosis. 

£566,995 

(2 years June 2007 to 

August 2009) 


Forbes SJ, Iredale J, 

Hayes P, Kluth D, 

Turner ML, Bellamy C, 

Marshall I. 

Stem cell therapy for liver cirrhosis £999,565 

(5 years October 2007 to 

September 2012) 


Holyoake TL, Brunton 

V. Koschmieder S. 

Holyoake T, 

Koschmieder S, 

Calabretta B, Salmoni 

P. 

Is Bcr-Abl expression relevant for 

the survival of cancer stem cells in 

chronic myeloid leukaemia? 

Is the introduction of autophagy by 

tyrosine kinase inhibitors a key 

survival mechanism for chromic 

myeloid leukaemia stem cells? 

£680,000 

(3 years June 2007 to May 

2010) 

£1,117,312. Proposed start 

date 1st January 2010 for 3 

years. 

European Union – Network of Excellence 

Urbaniak SJ, 

Armstrong-Fisher SS, 

Moss M. 

Special non-invasive Advances in 

Foetal and Neonatal Evaluation 

network (SAFE) on non-invasive 

foetal RhD genotyping and 

evaluation 

(SAFE Fellow & PhD studentship) 

£113,195 

Share of 12m Euros (over 5 

years 2004 to 2009 with 19 

core laboratories) 

2004 – 2009 


European Union – Public Health Executive Agency 

Franklin IM, Hart M, EU Optimal Blood Use Project 

Arthur E, McClelland 

DBL, Pirie E 

€890,285 Euros 

€500,000 (56.16% EC 

funded) 

(3 years 2007 – 2010) 


LRF 

Grant No 

06075 

Holyoake TL. Brunton 

V, Koschmider S 




£28,221 (3 years Oct 2007 - 

Sept 2010.) 

LRF 

Grant No 

08018 

Holyoake TL, 

Bartholomew C, 

Strathdee G, Melo J. 

EVII isoform expression and 

knockdown in CML. 

£45,000 

(3 years April 2008 to March 

2011) 

LRF 

Grant No 

08071 

Whetton T, 

Holyoake T. A 

phosphoproteomic investigation of 

key BCR-ABL mediated signally 

pathways in CML stem cells: where 

does tyrosine kinase inhibitor 

resistance lie?. 

£353,479 Jan 09 – Dec 2011 

Cancer Research United Kingdom. 

Holyoake T, Whetton 

T, Girolami M. 

Key survival pathways in chronic 

myeloid leukaemia (CML) stem 

cells and novel approaches to their 

eradication. Cancer Research 

United Kingdom. 

Biotechnology, Biophysical Scientific Research Council (BBSRC) 

De Sousa P, Turner 

ML, Pells S. 

A novel characterisation and 

separation technique for pluripotent 

human embryonic and 

haematopoietic stem cells. 

£1.1 million. Proposed start 

date 1st January 2010 2009 

for 5 years. Amount applied 

for £1,138,122. 

£131,765 




BHF 

Project 

Grant No 

PG/06/0 

51 

BHF 

Project 

Grant No 

PG/07/0 

17/2240 

5 

Barclay GR, Mills N, 

Newby D, Hadoke P, 

Turner ML. 

Mills NL, Newby DE, 

Barclay GR, de Belder 

MA, Robinson SD 

Preclinical in vivo evaluation of 

potential sources of human 

endothelial progenitor cells for 

autograft cellular therapy of 

ischaemia 

Endothelial progenitor cells in 

acute vascular injury and repair. 

£239,930 

(3 years July 2006 to June 

2009) 

- extended to end June 

2010 (i.e. 4 years total) 

because of 2 sets of 

maternity leave by O Tura). 

£242,685 

(3 years August 2007 to July 

2010) 


Manson J, Houston F, 

Prowse C, Turner M, 

MacGregor I, Hornsey 

V, Hunter N, 

Foster J, Groschup M. 

The effect of leucodepletion on 

transmission of BSE by transfusion 

of sheep blood components. 

£3,424,382 (6 years to 


Extension to 2012 agreed 

with DoH & Jean Manson 

Chief Scientist Office – Scottish Executive Health Department (CSO SEHD) 

Holyoake T, Copland 

MC 

Consumables 24,000. (3 years June 2006 

to May 2009. 

De Sousa P, Head .. Proof of principle validation of a £125,438. Aug 2007 – Dec 


MW, Turner ML, 

Manson J 

Head MW, Peden A, 

Prowse C, Manson J, 

Bishop M, Ironside J. 

Walsh T, Forbes J, 

Langston A, 

McClelland DBL, Pelly 

J, Ramsay P, Watson 

D, Prowse C. 

human embryo cell based screen 

for susceptibility to infectious prion 

transmission. 

The use of human recombinant 

prion protein as a substrate in an 

improved in vitro amplificationbased 

blood test for Creutzfeldt- 

Jakob disease infectivity 

A feasibility randomized trial 

comparing REstrictive and LIberal 

blood transfusion strategies in 

patients requiring six or more days 

in intEnsiVE care (RELIEVE study) 

2009. 

£193,512 over 2 years to 

December 2010 

(£90,000pa) 

£182,577 over 18 months to 

October 2010 

(£100,000pa) 

Grant No 

CAF/08/ 

09. 

Grant no 

CZB/4/6 

90. 

CZB/4/6 

57 

Irvine D, Holyoake T, 

Copland M. 

Holyoake T, Pellicano 

F. 

Armstrong-Fischer SS, 

Urbaniak SJ. 

CSO (submitted) 

Dr Juraj Petrik (coapplicant): 

Prof B Dhillon, Dr K 

Ramaesh, Prof M 

Turner 

Do self renewal pathways 

represent a potential therapeutic 

target in the treatment of Chronic 

Myeloid Leukaemia. Chief 

Scientist Office 

An investigation of the role of 

FOXO transcription factors in CML 

stem cell quiescence and as 

potential targets in CML stem cell 

eradication 

Non-Invasive Prenatal Fetal D 

typing (follow up on optimisation 

assay timing) 

Epidemiology and identification of 

potential transmission routes of 

autochthonous Hepatitis E virus 

(HEV) in Scotland and clinical 

relevance of HEV in chronic 

infection 




£189,257. Jan 2009 – Dec 

2011 

£223,375. April 2009 – 

march 2012 

£62, 259 over 12 months 

from June 2009 

Follow on bid submitted 

for ~ £170,000 

2-year grant: appr. 

£310,000. 

SNBTS (18 months): 

£60,000 

76,955 for 2 years 

contract under negotiation 

Foundation BioAlliance BioSecure 

Coste J, Jones M, 

Prowse C, Segarra C, 

head M, Laude H, 

Eglin R, Haik S, Flan 

B, 

Perret-Liaudet A, 

Clewley J. 



Jones M, Head M: 

To develop “Screening and 

confirmatory testing for 

vCJD” on blood samples 

vCJD confirmatory assay 

developments 

SNBTS component of Prion filter 

trial (PRISM) 



Jones M, Head M 

For infrastructure and routine 

support of vCJD assay 

development 

euro 252,000 over two years 

from October 2009 to 

September 2011 

(126,000 euro pa) 

£179,563 over 3 years from 

1 st April 2008-2011 

(£60,000pa) 

2 part time nurses and 

patient costs 

CVP £65,000 capital and 

£80,648 pa salary and 

consumables over 3 years 

until 31st March 2011. 

(£26,882 pa) 

SJ Urbaniak, SS 

Armstrong-Fisher. 

Service Redesign Committee– pilot 

study of non-invasive RhD 

genotyping on maternal plasma. 

£56,480. (2006-2009) 



Moss M, Urbaniak SJ. Blood group mimotopes 248,945 

(3 years 2008 to 2010) 

Moss M, Urbaniak SJ. Blood group mimotopes £90,015. 

(1 year 2009-2010) 

ITI Life Sciences 

Mountford J, Houslay 

MD, Milligan G, Baker 

AH. 

Stem Cells for Safer Medicine 

Mountford J, Baker 

AH. 

Stem Cell Technologies 

Programme renewal 

Optimisation and functional 

validation of directed differentiation 

of human embryonic stem cells to 

cardiomyocytes. 

£762,320 January 2009 – 

December 2009. 

£66,160. Aug 2009 – July 

2010. 


SJ Urbaniak, L Cairns, 

RN Barker, E Rattray. 

Peptide immunotherapy to 

suppress antibodies to red blood 

cells. 

£203,875. (2005-2010) 

Polish State Committee for Scientific Research 

Cedzynski M, Atkinson 

APM, Swierzko AS, 

Szemraj J, MacDonald 

SL, Kilpatrick DC, 

Buczylko K, Zeman K. 

Investigation of the role of 

insufficiency of L-Ficolin and other 

components of the lectin pathway 

of complement activation in 

recurrent respiratory infections in 

children with allergies 

£26,000 

(185,000 zl) 

(3 years April 2006 to April 

2009) 

Kay Kendall Leukaemia Fund 

Holyoake T, Salmoni 

P. 


Moss M, Urbaniak S 

(Abdulla Meshi) 

DiaMed AG (Division of Bio-Rad) 

R H Fraser 

UCB Celltech 

S Armstrong-Fisher, 

SJ Urbaniak 


Petrik, Juraj 

RH Fraser, CV 

Prowse 

Targeting autophagy as a tool to 

potentiate Imatinib-induced cell 

death in CML cells.. 

Characterisation of the human 

humoral immune response to RhD 

derived synthetic peptides. 

Development of novel monoclonal 

blood grouping reagents. 

Evaluation of UCB Molecule 

Certolizumab Pegol in the human 

placental transport in vitro model. 

Microarray diagnostics for blood 

borne viruses 

Development of Anti-Kell Murine 

Monoclonal Antibody 

£330,216. Proposed start 

date 1st October 2009 for 3 

years. 

£89,745 

2008-2011 

50,000 SFr per annum 

(£22,000) SNBTS 

contribution for 2009 - £4000 

Goods & Services (2004- 

2010) 

2009: £91,861. SNBTS 

contribution for 2009 – Nil 

[NB: SNBTS share of grant 

£28k] 

Follow on contract work 

agreed 

2009: £ ~ 56,000. 2010: £ 

~ 58,000 

2009: £20,628. 


Chemgenex 

Holyoake T. 

The role of omacetaxine in 

targeting cancer stem cells in CML. 

Edinburgh University (IKTF fund and CJD surveillance Unit) 

Jones M, Prowse C, 

Head M. 

Salary for technician to 

characterise anti-prion monoclonal 

antibodies : 

£12,000. June 2009 to May 

2010; 


December 2010 

GUHT Endowments 

SJ Urbaniak. Research Technician £36,000. (2008-2010) 


Holyoake TL and Allan 

E. 

Targeting quiescent CML stem cell 

by combining G-CSF and imatinib 

mesylate. 

TMERF (Transfusion Medicine Education and Research Fund) 

Douglas Watson/ Tim Support for statistical analysis on 

Walsh 

ISOC (plasma audit) 

9,700 

(6 years to January 2011) 

(2008/ 09) - £15,000 

2010-2011 

Andrews PD, Becroft M, Aspegren A, Gilmour J, James MJ, McRae S, Kime RA, Allcock RW, Abraham A, 

Jiang Z, Strehl R, Mountford JC, Milligan G, Houslay MD, Adams DR, Frearson JA. High content screening 

of feeder-free human embryonic stem cells to identify pro-survival small molecules. Biochem J. 2010; 432: 

21-33. 

Barr PJ, Donnelly M, Morris K, Parker M, Cardwell C, Baillie KEM. The epidemiology of red cell transfusion. 

Vox Sanguinis (2010) 99: 239-250 

Burton P, Adams DR, Abraham A, Allcock RW, Jiang Z, McCahill A, Gilmour J, McAbney J, Kane NM, Baillie 

GS, McKenzie FR, Baker AH, Houslay MD, Mountford JC, Milligan G. Identification and characterization of 

small-molecule ligands that maintain pluripotency of human embryonic stem cells. Biochem Soc Trans. 2010 

Aug; 38: (4):1058-61 

Burton P, A Adams DR, Abraham A, Allcock RW, Jiang Z, McCahill A, Gilmour J, McAbney J, Kaupisch A, 

Kane NM, Baillie GS, McKenzie FR, Baker AH, Milligan G, Houslay MD, Mountford JC. Erythro-9-(2- 

hydroxy-3-nonyl) Adenine (EHNA) blocks differentiation and maintains the expression of pluripotency 

markers in human embryonic stem cells. Biochem. J. Oct 2010 

Chalmers JD, Fleming GB, Hill AT, Kilpatrick DC. Impact of mannose-binding lectin insufficiency on the 

course of cystic fibrosis: A review and meta-analysis. Glycobiology 2011 Mar; 21: (3) 271-282. 

Clark P, Walker ID, Langhorne P, Crichton L, Thomson A, Greaves M, Whyte S, Greer IA. SPIN (Scottish 

Pregnancy Intervention) study: a multicenter, randomised controlled trial of low-molecular-weight heparin and 

low-dose aspirin in women with recurrent miscarriage. Blood. 2010; 115: (21): 4162-4167. 

Dehghan A, Yang Q, Peters A, Basu S, Bis JC, Rudnicka AR, Kavousi M, Chen MH, Baumert J, Lowe GD, 

McKnight B, Tang W, de Maat M, Larson MG, Eyhermendy S, McArdle WL, Lumley T, Pankow JS, Hofman 

A, Massaro JM, Rivadeneira F, Kolz M, Taylor KD, van Duijn CM, Kathiresan S, Illig T, Aulchenko YS, Volcik 

KA, Johnson AD, Uitterlinden AG, Tofler GH, Gieger C; Wellcome Trust Case Control Consortium, Psaty 

BM, Couper DJ, Boerwinkle E, Koenig W, O'Donnell CJ, Witteman JC, Strachan DP, Smith NL, Folsom AR. 

Wellcome Trust Case Control Consortium. Association of novel genetic Loci with circulating fibrinogen 

levels: a genome-wide association study in 6 population-based cohorts. Circ Cardiovasc Genet. 2009; 2: 

125-33. 

Devine DV, Reesink HW, Panzer S, Irving DO, Kormoczi GF, Mayr WR, Blais Y, Zhu Y, Qian Kk, Zhu Z, 

Greinacher A, Grazzini G, Pupella S, Catalano L, Vaglio S, Liumbruno GM, Smeenk JW, Josemans EAJ, 

Briet E, Letowska M, Lachert E, Antoniewicz-Papis J, Brojer E, Gulliksson H, Scott M, Williamson L, Prowse 

C, AuBuchon JP, Lopez JA, Hoffman P, Busch MP, Norris PJ, Tomasulo P, Dodd RY. Research and 

development. Vox Sanguinis 2010; 99: 382-401 


Dijkstra-Tiekstra MJ, van der Meer PF, Cardigan R, Devine D, Prowse C, Sandgren P, and de Wildt-Eggen 

J. Platelet concentrates from fresh or overnight-stored blood, an international study. Transfusion 2011; 

51: 38S-44S. 

Estes JD, Harris, LD, Klatt, NR, Tabb B, Pittaluga S, Paiaardini M, Barclay GR, Smedley J, Pung, R, Oliveira 

KM, Hirsch VM, Silvestri G, Douek DC, Miller CJ, Haase AT, Lifson J, and Brenchley JM. Damaged 

Intestinal Epithelial Integrity Linked to Microbial Translocation in Pathogenic Simian Immunodeficiency Virus 

Infections. PLoS Pathogens Aug. 2010 6: Issue 8 e1001052 

Fotaki V, Larralde O, Zeng S, McLoughlin D, Nichols J, Price DJ, Theil T, Manson JO. Loss of Wnt8b has no 

overt effect on hippocampus development but heads to altered Wnt gene expression levels in dorsomedial 

telencephalon. Dev Dyn 2010; 239: 284-296. 

Graham D. All water in this establishment has been passed by the management. Medical Device 

Decontamination. 2011; 15 (2) 14-18 

Grozeva D, Kirov G, Ivanov D, Jones IR, Jones L, Green EK, St Clair DM, Young AH, Ferrier N, Farmer AE, 

McGuffin P, Holmans PA, Owen MJ, O'Donovan MC, Craddock N; Wellcome Trust Case Control 

Consortium. Rare copy number variants: a point of rarity in genetic risk for bipolar disorder and 

schizophrenia. Arch Gen Psychiatry. 2010; 67: 318-27. 

Hay, D, Ross J, Gallagher R, Bagnaninchi P. Special Edition: The Complexities of Engineering Human 

Stem Cell-Derived Therapeutics. J. Biomed. & Biotech. Volume 2010 

Hornsey V, Casey C, McColl K, Young H, Drummond O, McMillan L, Morrison A, Prowse C. 

Characteristics of prion filtered red cells suspended in pathogen inactivated plasma (MB treated or solventdetergent 

treated) for neonatal exchange transfusion. Vox Sanguinis 2011; 101: 28-34 

Jarvis, L.M., Mulligan, K.E., Dunsford, T.H., McGowan, K., Petrik, J. Suitability of an automated nucleic acid 

extractor (easyMAG) for use with HCV and HIV-1 NAT assays. J. Virol. Methods 2010. In press. Available 

online 30/11/2010. 

Jones M, Peden AH, Head MMW, Ironside JW. The application of in vitro cell-free conversion systems to 

human prion diseases. Acta Neuropathol. 2010 

Kane NM, Meloni M, Spencer HL, Craig MA, Strehl R, Milligan G, Houslay MD, Mountford JC, Emanueli C, 

Baker AH. Derivation of endothelial cells from human embryonic stem cells by directed differentiation: 

analysis of microRNA and angiogenesis in vitro and in vivo. Arterioscler Thromb Vasc Biol. 2010; Jul; 30: 

(7):1389-97. Epub 2010 Apr 29 

Khanim FL, Hayden RE, Birtwistle J, Lodi A, Tiziani S, Davies NJ, Ride JP, Viant MR, Gunther UL, 

Mountford JC, Schrewe H, Green RM, Murray JA, Drayson MT, Bunce CM. Combined bezafibrate and 

medroxyprogesterone acetate: potential novel therapy for acute myeloid leukaemia. PLoS One. 2009 Dec 

7;4: (12):e8147 

Larralde-Diaz OG, Smith RWP, Malik P, Graham SV, Gray NK. Regulation of poly(A) binding protein during 

herpes simplex virus infection. Int. J. Infection. Dis 2010; 14: e470. 

Lozano M, Knutson M, Tardivel R, Cid J, Maymo R, Hof HM, Roddie HP, Pelly JP, Docherty AR, Sherman 

CD, Lin M, Propst M, Corash L, Prowse CV. A Multi-Centre Study of the Efficacy and Safety of Platelet 

Components prepared with Pathogen Inactivation (Intercept TM) stored for 6 or 7 days prior to Transfusion 

(TESSI) Brit. J. Haematol. 2011; 153: 393-401 

MacDonald SL, Downing I, Atkinson APM, Gallagher RCJ, Turner ML, Kilpatrick DC. Dendritic cells 

previously exposed to mannan-binding lectin (MBL) enhance cytokine production in allogeneic mononuclear 

cell cultures. Human Immunology 2010; 71: 1077-1083 

Morrison A, McMillan L, Hornsey VS, Prowse CV. Stored red-blood-cells inhibit platelet function under 

physiologic flow. Vox Sanguin. 2010 99: 362-368 

Mountford JC, Olivier E, Jordanides NE, de Sousa P, Turner ML. Red blood cells from pluripotent stem cells 

for use in transfusion. Regen Med. 2010 May; 5: (3): 411-423. 


Mountford J, Olivier E, Turner M. Prospects for the manufacture of red cells for transfusion. Br. J. 

Haematology, 2010; 149: (1) 22-34. 

Pellicano F, Copland M, Jorgensen HG, Mountford J, Leber B, Holyoake TL. BMS-214662 induces 

mitochondrial apoptosis in chronic myeloid leukemia (CML) stem/progenitor cells, including CD34+38- cells, 

through activation of protein kinase Cbeta. Blood. 2009 Nov 5:114(19):4186-96. 

Prowse CV, Murphy WG. Kills 99% of known germs. Transfusion. 2010; 50: 1636-1639. 

Prowse CV, Cuthbertson B, Turner M. Risk reduction strategies for variant Creutzfeldt-Jakob disease 

transmission by UK plasma products. Letters to the Editors - Haemophilia 2011; 17: p.703-720 

Reesink HW, Paner S, McQuilten K, Wood EM, Marks DC, Sendel S, Trigo F, Biagini S, Olyntho S, Devine 

DV, Mumford I, Cazenave JP, Rasongles P, Garraud O, Richard P, Schooneman F, Vezon G, Radwan RAl, 

Brand A, Hervig T, Castro E, Lozano M, Navarro L, Puig L, Almazan C, MacLennan S, Cardigan R, Franklin 

IM, Prowse CV. Pathogen inactivation of platelet concentrates. Vox Sanguinis 2010; 99: 85-95. 

Reikvam H, Prowse C, Roddie H, Heddle NM, Hervig T. A pilot study of the possibility and the feasibility of 

haemoglobin dosing with red blood cells transfusion. Vox Sanguinis. 2010; 99: 71-76. 

Reikvam H., van de Watering L., Prowse C., Devine D., Heddle NM., Hervig T. Evaluation of non-invasive 

methods for the estimation of haemoglobin content in red blood cell concentrates. Transf. Med. 2011; 21: 

145-149 

Salaun C, MacDonald AI, Larralde O, Howard L, Lochtie K, Burgess HM, Brook M, Malik P, Gray NK, 

Graham SV. Poly (A) Binding Protein 1 (PABP1) relocalisation to the nucleus during HSV-1 infection is 

ICP27-independent and does not inhibit virus replication. J. Virology 2010; 84: (17) 8539-8548 

Sarab GA, Moss M, Barker RN, Urbaniak SJ. Naturally processed peptides spanning the HPA-1a 

polymorphism are efficiently generated and displayed from platelet glycoprotein by HLA-DRB3*0101-positive 

antigen-presenting cells. Blood. 2009; 114: 1954-1957. 

Thom K, Cleland A, Salaskova M, Candotti D, Petrik J. Prevalence and genetic heterogeneity on SEN virus 

genotypes D and H in blood donors from Central and Western Europe and West Africa. Transfusion 

Medicine. 2010; 1365-3148. 

Tura O, Crawford J, Barclay GR, Samuel K, Hadoke PWF, Roddie H, Davies J, Turner ML. Granulocyte 

colony-stimulating factor (G-CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells 

for vascular regeneration therapy. J. Thrombosis & Haemostasis. 2010; 8: 1614-1623. 

Walsh, T.S., Stanworth S., Prescott, RJ., Lee RJ., Watson DM., Wyncoll D. Prevalence, management, and 

outcomes of critically ill patients with prothrombin time prolongation in United Kingdom Intensive care units. 

Critical Care Med. 2010; 38: (10) 1939-1946 

Watson DM., Stanworth SJ., Wyncoll D., McAuley D., Perkins GD., Young D., Biggin KJ., Walsh TS. A 

national clinical scenario-based survey of clinicians’ attitudes towards fresh frozen plasma transfusion for 

critically ill patients. Transf. Med. 2011; 21: 124-129. 

AuBuchon JP. And Prowse CV. Pathogen Inactivation: The Penultimate Paradigm Shift. AABB Press, 2010 

ISBN: 978-1-56395-309-5 

Prowse CV. United Kingdom: Imported US-Source Methylene-Blue- Treated Plasma (Chapter 10 in 

AuBuchon JP, Prowse CV. Pathogen Inactivation: The Penultimate Paradigm Shift. 2010; AABB publications 

Tomaskova, J., Labudova, M., Kopacek, J., Patorek, J., Petrik, J., Pastorekova, S. Lymphocytic 

choriomeningitis virus (Chapter 67). In “Molecular Detection of Human Viral Pathogens”. (D. Liu ed.), CRC 

Press, Taylor & Francis group (Boca Raton, London New York), 2011 735-747. 











W. 








transfusion. 


£ 431,069 

(. Jan 2010 – June 2012) 

£2,745,549 

(3 years: July 2009 – June 2012) 

Scottish Funding Council 

Wilmut I, Turner M, 

Illius A, Savill J 

Strategic Development Grant for 

Centre of Regenerative Medicine 

2,030,000 


2010) 

Scottish Funding Council Horizon Fund 

Cell Therapy Group 

Glasgow Univ, Heriot 

Watt Univ., Edinburgh 

Univ. Dundee Univ, 

SNBTS, Roslin Cells, 

SE. 

Industrial generation of RCs for 

transfusion “New Blood Project” 

£3.25 million. 

Aug. 2011 - 2016 


Noble B, Turner ML. Autologous stem cell based 

therapies in musculoskeletal 

regenerative medicine. 

£1,400,000 

(2 years May 2008 to May 2010) 

CZB/4/6 

57 


Turner ML. 




£116,064 over 2 years from 1 st 

April 2010 to31st March 2012. 

Project runs from Dec 2009 to 

31 st Jan 2014 





Marshall I. 





Holyoake TL, Brunton 

V. Koschmieder S. 

Holyoake T, 



P. 








£680,000 

(3 years June 2007 to May 2010) 

£1,117,312. Proposed start date 

1st January 2010 for 3 years. 

European Union – Public Health Executive Agency 

Franklin IM, Hart M, EU Optimal Blood Use Project 

Arthur E, McClelland 

DBL, Pirie E 

€890,285 Euros 

€500,000 (56.16% EC funded) 

(3 years 2007 – 2010) 


LRF Holyoake TL. Brunton Is Bcr-Abl expression relevant for £28,221 (3 years Oct 2007 - Sept 


Grant No 

06075 

V, Koschmider S the survival of cancer stem cells in 


2010.) 

LRF 

Grant No 

08018 

Holyoake TL, 

Bartholomew C, 

Strathdee G, Melo J. 

EVII isoform expression and 

knockdown in CML. 

£45,000 

(3 years April 2008 to March 

2011) 

LRF 

Grant No 

08071 

Whetton T, 

Holyoake T. A 
















ML, Pells S. 





£353,479 Jan 09 – Dec 2011 

£1.1 million. Proposed start date 


Amount applied for £1,138,122. 

£131,765 




BHF 

Project 

Grant No 

PG/06/0 

51 

BHF 

Project 

Grant No 

PG/07/0 

17/2240 

5 

Barclay GR, Mills N, 

Newby D, Hadoke P, 

Turner ML. 

Mills NL, Newby DE, 

Barclay GR, de Belder 

MA, Robinson SD 

Preclinical in vivo evaluation of 

potential sources of human 

endothelial progenitor cells for 

autograft cellular therapy of 

ischaemia 

Endothelial progenitor cells in 

acute vascular injury and repair. 

£239,930 

(3 years July 2006 to June 2009) 

- extended to end June 2010 

(i.e. 4 years total) because of 2 

sets of maternity leave by O 

Tura). 

£242,685 


2010) 





V, Hunter N, 






Head MW, Peden A, 

Prowse C, Manson J, 

Bishop M, Ironside J. 

Grant No 

CAF/08/ 

09. 

Walsh T, Forbes J, 

Langston A, 

McClelland DBL, Pelly 

J, Ramsay P, Watson 

D, Prowse C. 


Copland M. 

The use of human recombinant 

prion protein as a substrate in an 

improved in vitro amplificationbased 

blood test for Creutzfeldt- 

Jakob disease infectivity 

A feasibility randomized trial 

comparing REstrictive and LIberal 

blood transfusion strategies in 

patients requiring six or more days 

in intEnsiVE care (RELIEVE study) 






£3,424,382 (6 years to 


Extension to 2012 agreed with 

DoH & Jean Manson 

£193,512 over 2 years to 

December 2010 (£90,000pa) 


October 2010 

(£100,000pa) 

£189,257. Jan 2009 – Dec 2011 

Grant no Holyoake T, Pellicano An investigation of the role of £223,375. April 2009 – March 


CZB/4/6 

90. 

F. FOXO transcription factors in CML 



eradication 


Urbaniak SJ. 





assay timing) 






infection 

2012 

£62, 259 over 12 months from 

June 2009 

Follow on bid submitted for ~ 

£170,000 

2-year grant: appr. £310,000. 

SNBTS (18 months): £60,000 

CZB/4/6 

57 



Turner 







31 st Jan 2014 






B, 


Clewley J. 





from October 2009 to September 

2011 

(126,000 euro pa) 





developments 


trial (PRISM) 


April 2008-2011 (£60,000pa) 

2 part time nurses and patient 

costs 



Jones M, Head M 

For infrastructure and routine 

support of vCJD assay 

development 

CVP £65,000 capital and 

£80,648 pa salary and 

consumables over 3 years until 

31st March 2011. (£26,882 pa) 


Moss M, Urbaniak SJ. Blood group mimotopes 248,945 

(3 years 2008 to 2010) 

Moss M, Urbaniak SJ. Blood group mimotopes £90,015. 

(1 year 2009-2010) 

Stem Cells for Safer Medicine. 

Mountford J, Baker 

AH. 


SJ Urbaniak, L Cairns, 

RN Barker, E Rattray. 

Optimisation and functional 

validation of directed differentiation 

of human embryonic stem cells to 

cardiomyocytes. 

Peptide immunotherapy to 

suppress antibodies to red blood 

cells. 

£66,160. Aug 2009 – July 2010. 

£203,875. (2005-2010) 




P. 




DiaMed AG (Division of Bio-Rad) 

R H Fraser 

UCB Celltech 


SJ Urbaniak 


Petrik, Juraj 

Chemgenex 

Holyoake T. 



death in CML cells. 




Development of novel monoclonal 

blood grouping reagents. 





borne viruses 

The role of omacetaxine in 

targeting cancer stem cells in CML. 

£330,216. Proposed start date 

1st October 2009 for 3 years. 

£89,745 

2008-2011 

50,000 SFr per annum (£22,000) 

SNBTS contribution for 2009 - 

£4000 Goods & Services (2004- 

2010) 


contribution for 2009 – Nil [NB: 

SNBTS share of grant £28k] 

Follow on contract work 

agreed 

2009: £ ~ 56,000. 2010: £ ~ 

58,000 

£12,000. June 2009 to May 

2010; 

Edinburgh University (IKTF fund and CJD surveillance Unit) 

Jones M, Prowse C, 

Head M. 

Salary for technician to 

characterise anti-prion monoclonal 

antibodies : 


December 2010 

GUHT Endowments 

SJ Urbaniak. Research Technician £36,000. (2008-2010) 


Holyoake TL and Allan 

E. 

Targeting quiescent CML stem cell 

by combining G-CSF and imatinib 

mesylate. 

£9,700 (6 years to January 2011) 

2011-2012 

Allan EK, Holyoake TL, Craig AR, Jorgensen HB. Omacetaxine may have a role in chronic myeloid 

leukaemia eradication through down-regulation of Mcl-1 and induction of apoptosis in stem/progenitor cells. 

Leukemia 2011 Apr 5 In press. 

Balabanov S, Gontarewicz A, Keller G, Raddrizzani L, Braig M, Bosotti R, Moll J, Jost E, Barett C, Rohe I, 

Bokemeyer C, Holyoake TL, Brümmendorf TH. Abcg2 overexpression represents a novel mechanism for 

acquired resistance to the multi-kinase inhibitor Danusertib in BCR-ABL-positive cells in vitro. PLoS One. 

2011 Apr 26;6(4):e19164. PubMed PMID: 21541334; PubMed Central PMCID: PMC3082549. 

Baylis SA, heath AB, and the Collaborative Study Group* (including Jarvis L and Cleland A). World Health 

Organisation collaborative study to calibrate the 3 rd International Standard for Hepatitis C virus RNA nucleic 

acid amplification technology (NAT)-based assays. Vox sang. 2011; epub ahead of print. 


Bessos, H. Transfusion and Apheresis Science 2011: 45, 29 

Bessos, H. Fraser, R. Seghatchian, J. Scotblood 2010: Key presentations of the past, present, and future of 

transfusion medicine to mark Scottish national blood transfusion service (SNBTS) anniversaries. 

Transfusion and Apheresis Science 2011: 45: 213-221. 

Bessos, H., Fraser, R., Seghatchian, J. Scotblood 2011 features advances in translational medicine, 

haemophoietic progenitor cells and milestones of blood banking systems. Transfusion and Apheresis 

Science 2011: 445: 315-320. 

Chalmers JD, Fleming GB, Hill AT, Kilpatrick DC. Impact of mannose-binding lectin insufficiency on the 

course of cystic fibrosis: A review and meta-analysis. Glycobiology. 2011 Mar;21(3):271-82. Epub 2010 Nov 

2. Review. PubMed PMID: 21045008. 

Crowther M, Chan YLT, Garbett IK, Lim W, Vickers MA, and Crowther MA (2011) Evidence based focused 

review of the treatment of idiopathic warm IgG hemolytic anemia in adults. Blood 118:4036-40. 

Farrugia A, Prowse, C, Hornsey, V. Conditions for plasma processing. Letters to the Editor, Transfusion. 

2011: 51: p.1875-76 

Gallipoli P, Abraham SA, Holyoake TL. Hurdles toward a cure for CML: the CML stem cell. Hematol Oncol 

Clin North Am. 2011 Oct;25(5):951-66, v. Epub 2011 Oct 19. PubMed PMID: 22054728. 

Hall AM, Zamzani OM, Whibley N, Hampsey DP, Haggart AM, Vickers MA, Barker RN (2012) Production of 

the effector cytokine interleukin-17, rather than interferon- is more strongly associated with autoimmune 

haemolytic anemia. The Haematology Journal (in press) 

Hansen A, McMillan L, Morrison A, Petrik J, Bradley M. Polymers for the rapid and effective activation and 

aggregation of platelets. Biomaterials 2011; 32:7034-41. 

Hardie, I. Rooney, C. The increasing importance of intellectual property in transfusion medicine. Transfusion 

and Apheresis Science 2011: 45: 99-107. 

Hay DC, Ross JA, Gallagher R, Bagnaninchi P. The complexities of engineering human stem cell-derived 

therapeutics. J Biomed Biotechnol. 2010;2010:654964. Epub 2011 Mar 31. PubMed PMID: 21490704; 

PubMed Central PMCID: PMC3070168. 

Hornsey VS, Casey C, McColl K, Young H, Drummond O, McMillan L, Morrison A and Prowse CV (2011) 

Characteristics of prion-filtered red cells suspended in pathogen-inactivated plasma (MB treated or solventdetergent 

treated) for neonatal exchange transfusion. Vox Sang. 101, 28-34 

Ibrahim AR, Clark RE, Holyoake TL, Byrne J, Shepherd P, Apperley JF, 

Milojkovic D, Szydlo R, Goldman J, Marin D. Second-generation tyrosine kinase inhibitors improve the 

survival of patients with chronic myeloid leukemia in whom imatinib therapy has failed. Haematologica. 2011 

Dec;96(12):1779-82. Epub 2011 Aug 22. PubMed PMID: 21859733; PubMed Central PMCID: PMC3232259. 

Ivanovs, A, Rybtsov, S., Welch, l., Anderson, R.A., Turner, M.L., Medvinsky, A. Highly potent human 

hematopoietic stem cells first emerge in the intraembryonic aorta-gonad-mesonephros region. J. Exp.Med. 

2011: 208: No. 12; 2417-2427 

Jarvis LM, Mulligan K, Dunsford TH, McGowan K, Petrik J. Suitability of an automated nucleic acid extractor 

(easyMAG) for use with hepatitis C virus and human immunodeficiency virus type 1 nucleic acid amplification 

testing. J Virol Methods 2011; 171:364-8. 

Krejciova Z, Pells S, Cancellotti E, Freile P, Bishop M, Samuel K, Barclay RG, Ironside JW, Manson JC, 

Turner ML, De Sousa P, Head MW. Human embryonic stem cells rapidly take up and then clear exogenous 

human and animal prions in vitro. J. Pathol. 2011 Apr; 223 (5): 635-645. 

Larralde-Diaz OG, Smith RWP, Malik P, Graham SV, Gray NK. Regulation of poly(A) binding protein during 

herpes simplex virus infection. Int. J. Infection Dis. 2010; 14: e470. 

Lidonnici MR, Audia A, Soliera AR, Prisco M, Ferrari-Amorotti G, Waldron T, Donato N, Zhang Y, Martinez 

RV, Holyoake TL, Calabretta B. Expression of the transcriptional repressor Gfi-1 is regulated by 


C/EBP{alpha} and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABLexpressing 

cells. Cancer Res. 2010 Oct 15;70(20):7949-59. Epub 2010 Oct 5. PubMed PMID: 20924107; 


MacDonald SL, Downing I, Atkinson AP, Gallagher RC, Turner ML, Kilpatrick DC. Dendritic cells previously 

exposed to mannan-binding lectin enhance cytokine production in allogeneic mononuclear cell cultures. Hum 

Immunol. 2010 Nov;71(11):1077-83. Epub 2010 Aug 9. PubMed PMID: 20705112. 

Marenah L, Allan EK, Mountford JC, Holyoake TL, Jørgensen HG, Elliott MA. Investigation into omacetaxine 

solution stability for in vitro study. Biomed Chromatogr. 2011 Aug 9. doi: 10.1002/bmc.1686. [Epub ahead of 

print] PubMed PMID:21830228. 

Martineau HM, Cousens C, Imlach S, Dagleish MP, Griffiths DJ. Jaagsiekte sheep 

retrovirus infects multiple cell types in the ovine lung. J Virol. 2011 Apr;85(7):3341-55. Epub 2011 Jan 26. 

PubMed PMID: 21270155; PubMed Central PMCID:PMC3067841. 

McCutcheon S, Blanco A.R.A, Houston E.F, de Wolf, C, Tan, B.C, Smith, A, Groschup M.H, Hunter, N, 

Hornsey, V.S, MacGregor, I.R, Prowse, C.V, Turner, M. Manson, J.C. All clinically-relevant blood 

components transmit prion disease following a single blood transfusion: A sheep model of vCJD. PLoS 

One, 2011: 6: Issue 8, 1-11 e23169. 

Metcalfe P, Rigsby P, Tait E, Urbaniak SJ (2011) An international reference reagent for the detection of RHD 

and SRY DNA in plasma. Vox Sang Epub 2011 Oct 4. DOI:10.1111/j.1423-0410.2011.01543.x 

Milliken SVI, Wassall H, Lewis BJ, Logie J, Barker RN, Macdonald H, Vickers MA, Ormerod AD (2012) 

Effects of ultraviolet light on human serum 25-hydroxyvitamin D and systemic immune function. Journal of 

Allergy and Clinical Immunology, 129, 1554-61 

Mitchell SA, Jacobsohn D, Thormann Powers KE, Carpenter PA, Flowers ME, Cowen EW, Schubert M, 

Turner ML, Lee SJ, Martin P, Bishop MR, Baird K, Bolaños-Meade J, Boyd K, Fall-Dickson JM, Gerber LH, 

Guadagnini JP, Imanguli M, Krumlauf MC, Lawley L, Li L, Reeve BB, Clayton JA, Vogelsang GB, Pavletic 

SZ. A multicenter pilot evaluation of the National Institutes of Health chronic graft-versus-host disease 

(cGVHD) therapeutic response measures: feasibility, interraterreliability, and minimum detectable change. 

Biol Blood Marrow Transplant. 2011 Nov;17(11):1619-29. Epub 2011 Apr 12. PubMed PMID: 21536143; 


Mountford JC, Turner, M. In vitro production of red blood cells. Transfusion and Apheresis Science 2011: 

45: 85-89. 

Mukhopadhyay A, Helgason GV, Karvela M, Holyoake TL. Hydroxychloroquine for chronic myeloid leukemia: 

complete cure on the horizon? Expert Rev Hematol. 2011 Aug;4(4):369-71. PubMed PMID: 21801126. 

Helgason GV, Karvela M, Holyoake TL. Kill one bird with two stones: potential efficacy of BCR-ABL and 

autophagy inhibition in CML. Blood. 2011 Aug 25;118(8):2035-43. Epub 2011 Jun 21. Review. PubMed 

PMID: 21693757. 

Nightingale MJ, De Korte D, Chabanel, A, Hughes, W, Rowe, GP, Nicholson G. Eurobloodpack: a common 

European design for blood bag systems with integral Leucodepletion filters. Vox Sang. Online 18/04/2011 

doi: 10.1111/j.1423-0410.2011.01480. 

Olivier EN, Bouhassira EE. Differentiation of human embryonic stem cells into mesenchymal stem cells by 

the "raclure" method. Methods Mol Biol. 2011;690:183-93. PubMed PMID: 21042994 

Payne CM, Samuel K, Pryde A, King J, Brownstein D, Schrader J, Medine CN,Forbes SJ, Iredale JP, 

Newsome PN, Hay DC. Persistence of functional hepatocyte-like cells in immune-compromised mice. Liver 

Int. 2011 Feb;31(2):254-62. doi: 10.1111/j.1478-3231.2010.02414.x. Epub 2010 Dec 10. PubMed PMID: 

21143581. 

Pellicano F, Holyoake TL. Assembling defenses against therapy-resistant leukemic stem cells: Bcl6 joins the 

ranks. J Exp Med. 2011 Oct 24;208(11):2155-8. PubMed PMID: 22025499; PubMed Central PMCID: 

PMC3201197. 

Pellicano F, Simara P, Sinclair A, Helgason GV, Copland M, Grant S, Holyoake TL. The MEK inhibitor 

PD184352 enhances BMS-214662-induced apoptosis in CD34+ CML stem/progenitor cells. Leukemia. 2011 


Jul;25(7):1159-67. doi:10.1038/leu.2011.67. Epub 2011 Apr 12. PubMed PMID: 21483442 

Pellicano F, Sinclair A, Holyoake TL. In search of CML stem cells' deadly weakness. Curr Hematol Malig 

Rep. 2011 Jun;6(2):82-7. Review. PubMed PMID: 21373837. 

Petrik J. Microarrays for blood testing: pros and cons. Biologicals 2010; 38: 2-8. 

Petrik J, Coste J, Fournier-Wirth C. Advances in transfusion medicine in the first decade of the 21st century: 

Advances in miniaturized technologies. Transfus Apher Sci. 2011; 45:45-51. 

Prowse C, Cuthbertson, B, Turner, M. Risk reduction strategies for variant Creutzfeldt-Jakob disease 

transmission by UK plasma products. Haemophilia 2011: 17: 703-720 

Stephen J, Cairns LS, Pickford WJ, Vickers MA, Urbaniak SJ and Barker RN (2012) Identification, 

immunomodulatory activity and immunogenicity of the major helper T cell epitope on the K blood group 

antigen. Blood, 119, 5563-74 

Stuge, T.B. Skogen B, Ahlen, M.T., Husebekk, A., Urbaniak, S.J., Bessos, H. The cellular immunobiology 

associated with fetal and neonatal alloimmune thrombocytopenia. Transfusion and Apheresis Science. 

2011: 45: p.53-59. 

Thom K, Cleland A, Salakova M, Candotti D, Petrik J: Prevalence and genetic heterogeneity of SEN virus 

genotypes D and H in blood donors from Central and Western Europe and West Africa. Transfus Med 2011; 

21:42-50. 

Tomaskova J, Labudova M, Kopacek J, Pastorek J, Petrik J, Pastorekova S. Lymphocytic choriomeningitis 

virus. In: “Molecular detection of human viral pathogens” Chapter 67. CRC Press, Taylor & Francis group 

(Boca Ratan, London, new York), 2011 p. 735-747. 

Wagner S.J. Pathogen Inactivation: The Penultimate Paradigm Shift. Ed. AuBuchon JP, Prowse CV. 

Transfusion Medicine Reviews Vol. 25 No: 2 April 2011 p.162 

Walsh TS, Palmer J, Watson D, Biggin K, Seretny M, Davidson H, Harkness M, Hay A. Multicentre cohort 

study of red blood cell use for revision hip arthroplasty and factors associated with greater risk of allogeneic 

blood transfusion. Brit. J. Anaesthesia 2012; 108: (1) 63-71. 

Watkins NA, Dobra S, Bennett P, Cairns J, Turner ML. The Management of Blood Safety in the Presence of 

Uncertain Risk: A United Kingdom Perspective. Transfus Med Rev. 2011 Nov 28. [Epub ahead of print] 

PubMed PMID: 22126710. 

Yung S, Ledran M, Moreno-Gimeno I, Conesa A, Montaner D, Dopazo J, Dimmick I,Slater NJ, Marenah L, 

Real PJ, Paraskevopoulou I, Bisbal V, Burks D, Santibanez-Koref M, Moreno R, Mountford J, Menendez P, 

Armstrong L, Lako M. Large-scale transcriptional profiling and functional assays reveal important roles for 

Rho-GTPase signalling and SCL during haematopoietic differentiation of human embryonic stem cells. Hum 

Mol Genet. 2011 Dec 15;20(24):4932-46. Epub 2011 Sep 21. PubMed PMID: 21937587. 










W. 








transfusion. 


£ 431,069 

(Jan 2010 – June 2012) 

£2,745,549 

(3 years: July 2009 – June 2012) 


Vickers M, Barker R 

Erwig L 

Immune consequences of red cell 

aging, death and disposal 

£1,252,158 

(5 years Jan 2012-2017) 

Scottish Funding Council Horizon Fund 

Cell Therapy Group 

Glasgow Univ, Heriot 

Watt Univ., Edinburgh 

Univ. Dundee Univ, 

SNBTS, Roslin Cells, 

SE. 

Industrial generation of RCs for 

transfusion “New Blood Project” 

£3.25 million. 

Aug. 2011 - 2016 


CZB/4/6 

57 


Turner ML. 







31 st Jan 2014 





Marshall I. 





Holyoake T, 



P. 


LRF 

Grant No 

08071 

Whetton T, 

Holyoake T. A 










£1,117,312. Proposed start date 


£353,479 Jan 09 – Dec 2011 











ML, Pells S. 





£1.1 million. Proposed start date 


Amount applied for £1,138,122. 

£131,765 







V, Hunter N, 





£3,424,382 (6 years to 


Extension to 2012 agreed with 

DoH & Jean Manson 


Grant No 

CAF/08/ 

09. 


Copland M. 




£189,257. Jan 2009 – Dec 2011 


Grant no 

CZB/4/6 

90. 

Holyoake T, Pellicano 

F. 


Urbaniak SJ. 


Scobie L. et al 




An investigation of the role of 

FOXO transcription factors in CML 



eradication 



assay timing) 






infection 

£223,375. April 2009 – March 

2012 

£62,259 over 12 months from 

June 2009 

Follow on bid submitted for ~ 

£170,000 

2-year grant: appr. £310,000. 

SNBTS (18 months): £60,000 

Start October 2010 

CZB/4/6 

57 



Turner 







31 st Jan 2014 






B, 


Clewley J. 




Petrik J. SYNPOLYVIR 43,000 Euros 

2011-2012 


from October 2009 to September 

2011 

(126,000 euro pa) 





developments 


trial (PRISM) 


April 2008-2011 (£60,000pa) 

2 part time nurses and patient 

costs 


Moss M, Urbaniak SJ. Blood group mimotopes £248,945 

(3 years 2008 to 2011) 



P. 




UCB Celltech 


SJ Urbaniak 



death in CML cells. 







£330,216. Proposed start date 

1st October 2009 for 3 years. 

£89,745 

2008-2011 


contribution for 2009 – Nil [NB: 

SNBTS share of grant £28k] 

Follow on contract work agreed 



Petrik, Juraj 


borne viruses 

2009-10: £ ~ 56,000. 

2010-11: £ ~ 58,000 


HEALTHCARE QUALITY IMPACT ASSESSMENT FOR SERVICE REDESIGN TEMPLATE Appendix 6 

Which health 

impacts could 

the project 

achieve? 

(tick all that 

apply) 

Estimate amount 

of impact on 

patient/population 

small + 

medium ++ 

high +++; 

or quantify where 

possible 

How will the project achieve this 

health impacts? 

What is the 

evidence base for 

this? 

Is it possible to 

define the improved 

health outcome for 

the patient 

Are there key 

dependencies in 

achieving the 

health impact? 

What measures 

of health 

impact could 

be used? 

INDIRECT 

HEALTH 

IMPACTS 

Safer 

More 

effective 

More 

efficient 

More 

equitable 

More 

timely 

More 

person 

centred 


What 

health 

outcomes 

could the 

project 

achieve? 

How will the project achieve these 

health outcomes? 

What is the 

evidence base for 

this? 

Are there key dependencies in 

achieving the health outcome? 

What measures of 

health outcomes 

could be used? 

DIRECT 

HEALTH 

IMPACT 

(to be used for 

direct patient 

care) 


DESCRIPTIONS OF INDIRECT HEALTH IMPACTS - CONTRIBUTIONS TO THE QUALITY OF CARE 

Safe 

Effective 

Efficient 

Equitable 

Timely 

Person 

centred 

avoiding injuries to patients from care that is intended to help them; providing an appropriate, clean and safe 

environment; reducing harm from infectious and environmental hazards 

providing the most appropriate treatments, interventions, support and services 

avoiding waste, including waste of equipment, supplies, ideas and energy 

providing care that does not vary in quality because of personal characteristics such as gender, ethnicity, 

geographic location or socio-economic status 

reducing waits and sometimes harmful and distressing delays for both those who receive care and those who 

give care 

providing care that is responsive to individual preferences, needs and values and assuring that patient values 

guide all clinical/health related decisions

SNBTS Research Strategy - Scottish National Blood Transfusion ...

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