Vol 31, Part I - forums.sou.edu • Index page - Southern Oregon ...

ABSTRACTS – Contributed Posters
161 The Impact of Traffic and Heavy Vehicles on Air quality:
A Case Study in Portland, Oregon, ADILENE AMARO-
ZURITA (Department of Civil Engineering, Portland State
University, Engineering Building Suite 200,
1930 SW 4th
Ave. 
Portland, OR 97201; ceedept@cecs.pdx.edu).
Air quality in traffic corridors are affected by traffic
volumes and the types of vehicles used. Persons that use these
corridors as public transit users, pedestrians, and cyclists are
exposed to air pollutants that can adversely affect human
health such as particulate matter, carbon monoxide, and carbon
dioxide. This case study is looking at the impacts of congestion,
traffic volumes and weather variables on the levels of PM 2.5
,
PM 1
, PM 10
, and Ultrafine particles. Particulate matter is fine
particles that can be found in the air and smoke. Because of its
microscopic size, it can pass through the nose, throat, and deep
into the lungs and across the lungs into cardiovascular system
and aggravate heart and lung diseases. The objective of this
research is to try explain changes in level of PM 2.5
, PM 1
, PM 10
,
and Ultrafine particles as a function of traffic and weather
variables. Some of the equipment used for data collection was:
• The Wavetronix sensor, which is a radar unit, were used to
measure traffic volumes of cars and heavy vehicles at the
intersection.
• Dustrak Aerosol monitors were used to measure particulate
matter levels.
• A Young Ultrasonic Anemometer Model 81000 was used to
measure the wind speed and direction.
The data indicate that PM 2.5
levels can be highest during
peak traffic periods (e.g. 9/15/2011 data) fairly steady in
other days (e.g. 9/29/11). There seems to be a correlation
between PM 2.5,
PM 1
, and PM 10
levels, heavy vehicle traffic
and wind speed.
CELL and MOLECULAR BIOLOGY
162 Tetracycline-Inducible Overexpression of Human
Oncostatin M in Breast Cancer, DOLLIE LaJOIE* and
CHERYL L JORCYK (Department of Biological Sciences,
Boise State University, 1910 University Drive, Boise, ID
83725; dollielajoie@boisestate.edu, cjorcyk@boisestate.edu).
Oncostatin M (OSM) is a signaling factor that binds to its
receptors to induce various changes in breast cancer cell growth
and metastasis. We are creating stable human breast cancer cell
lines that will inducibly overexpress human OSM by lentiviral
transduction. Confirmation of tetracycline-inducible OSM
overexpression will be determined by ELISA. The cell lines will
be further characterized in vitro. In vivo, these cells will allow
us to evaluate the effects of OSM on breast cancer metastasis.
Research supported by Susan G. Komen for the Cure (KG100513),
American Cancer Society (RSG-09-276-01-CSM), INBRE (P20RR016454
& P20GM103408).
163 In Vitro Investigation of Cytokine-Induced
Osteoclastogenesis by Mammary Tumor Cells, ERIK
STOLL*, CELESTE BOLIN, and CHERYL JORCYK
(Department of Biological Sciences, Boise State University,
1910 University Drive, Boise, ID 83725).
Breast cancer metastasis to bone often results in a
pathological condition that can cause bone degradation and
pain. These metastases disrupt normal bone homeostasis,
which is regulated by bone forming osteoblasts and bone
resorbing osteoclasts. In particular, breast cancer metastases
promote the differentiation of preosteoclasts to mature
osteoclasts during the process of osteoclastogenesis.
Previous results from our lab have shown that an IL-6
family cytokine member can promote osteoclastogenesis in in
vitro models of breast cancer metastasis to bone. Specifically,
we have shown that the mechanism of this cytokine-induced
increased osteoclastogensis is through an increase in growth
factor secretion by mammary tumor cells. These in vitro
studies were performed with mouse mammary tumor cells in
co-culture with mouse preosteoclast cells. To investigate the
importance of tumor cell-secreted factors versus membrane
bound factors on the promotion of osteoclastogenesis, we
performed a transwell experiment in which mouse mammary
cells were separated from mouse preosteoclast cells by a 0.4
µm porous membrane. The mouse mammary cells were pretreated
with a neutralizing antibody for growth factors of
interest, and osteoclastogenesis was measured by tartrateresistant
acid phosphatase (TRAP) staining, a marker for
mature osteoclasts. Results from this study further our
investigation on the importance of direct cell-to-cell contact
in cytokine-induced osteoclastogenesis.
Funding: NASA - NNX10AN29A; INBRE - (NIH/NCERR) – NIH/NCRR
P20RR016454 and P20GM103408; Komen – KG100513; ACS – RSG-09-
276-01-CSM
164 The Effect of JMJD Inhibitors on Head and Neck
Cancer Cell Proliferation, MARIA VIDAL* 1 , NAILAH
WADE* 1 , DAVID BAE 2 , ERIC TANG 2 , CUN-YU WANG 2
( 1 Howard Hughes Medical Institute Pre-College Science
Education Program; 2 UCLA School of Dentistry, 10833
Le Conte Avenue, 63-007 CHS, Los Angeles, CA 90095;
mariavidal95@yahoo.com, nsolufemi@hotmail.com).
Jumonji domain (JMJD) proteins can demethylate lysine
or arginine residues on histones and have been found to play
an important role in development and cancer.Objective: To
examine how two JMJD2 inhibitors, A70 and SD70, affect
proliferation of two established squamous cell carcinoma
(SCC) cell lines SCC1 and SCC23. Methods: To determine
effects on proliferation, proliferation assay was performed
whereby SCC cell lines were grown on 6 well dishes with
or without inhibitors and cell number was counted daily
using a hemacytometer for four days. To analyze protein
expression, western blot analysis was performed on cells
from day four. To identify the progression of cell cycle
upon treatment, we performed cell cycle analysis of SCC
cell lines on day four. Results: Proliferation assay revealed
that both JMJD2 inhibitors A70 and SD70 drastically
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