FM December 2020 digital P

in hematopoietic development via
retinoic acid-inducible gene (RIG-I)-like
receptors (RLRs) family. The RLR family
included three different members,
namely RIG-I, MDA5 and LGP2. In their
experiments, the team showed that the
absence of either Rig-I or melanoma
differentiation-associated protein 5
(Mda5) severely reduced the numbers
of HSCs in zebrafish embryos. On the
contrary, the absence of the third
family member, Lgp2, which negatively
modulated the immune response to
dsRNA, increased the numbers of
HSCs. Modulating the expression of the
signalling mediator, tumour necrosis
factor receptor (TNFR)-associated factor
6 (TRAF6) in RLR deficient embryos
restored HSPC numbers. The study
could open new ways to induce the
development of HSCs.
protein which is essential to initiate the
cell entry. The virus requires protease
in order to cleave parts of the spike
protein which could then dock onto
ACE2 receptors on the surface of the
host cell. In cell culture experiments with
various cell types, the protease inhibitor
aprotinin inhibited virus replication
by preventing SARS-CoV-2 entry into
host cells. Aprotinin displayed anti-
SARS-CoV-2 activity in different colon
epithelial cells, human lung cancer cell
line, and primary bronchial epithelial
cell air-liquid interface cultures and
against four virus isolates. The protease
inhibitor showed to inhibit the virus
replication at therapeutically achievable
concentrations. The team suggested that
the use of the approved aprotinin aerosol
in the market may have the potential
for the early local control of SARS-CoV-2
replication.
Source: Cells 2020, 9(11), 2377; 30 October
https://doi.org/10.3390/cells9112377
Source: Immunity VOLUME 53, ISSUE 5, P934-
951.E9, NOVEMBER 17, 2020 DOI: https://doi.
org/10.1016/j.immuni.2020.10.007
Aprotinin inhibits
SARS-CoV-2
replication
Denisa Bojkova et al
discovered that the
protease inhibitor aprotinin
could prevent SARS-CoV2
infection by inhibiting the
host cell enzyme from
cleaving the virus spike
Prediabetes can cause
significant macular thinning
JenniMaria Huru et al investigated
early vascular and neurally based
changes in the prediabetic and
diabetic retina. The team detected
significant thinning of the macula
and ganglion cell complex (GCL)
in the prediabetes group in a
population-based cohort study. Of
the 2005 participants from Finland,
310 had normal glucose metabolism,
1638 were prediabetic and 57 had
diabetes. The assessment
of the total thickness
of the macula
using Cirrus HD-OCT 4000 showed
that diameters of retinal arteries
decreased, whereas those of venules
increased in parallel with impaired
glucose metabolism. The study
results showed significant macular
thinning (−2.69 μm) especially in
the pericentral area among the
prediabetic group. Macular cube
average thickness (−0.10 mm3) and
macular cube volume also decreased
significantly as glucose metabolism
worsened. The researchers found
that central retinal arteriolar
equivalent (CRAE) decreased with an
increase in diabetes measures. The
study provides a new perspective
since it revealed that the early
and subtle changes caused by
prediabetes as macular thinning
had a significant average causal
mediation effect (ACME) on retinal
vessels, therefore supporting
the neurodegenerative theory of
diabetes-induced changes in the
retina.
Source: British Journal of Ophthalmology
07 October 2020 https://bjo.bmj.
com/content/early/2020/10/07/
bjophthalmol-2020-317414.full
December 2020 / FUTURE MEDICINE / 55