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Research Scientists

Cavanaugh, Alice H. PhD; Google Scholar Profile
Research Scientist II
Weis Center for Research
100 North Academy Avenue
Danville, PA 17822
Phone: 570-271-6674
Fax: 570-271-6701
acavanaugh@geisinger.edu
Research Interests: The calcium sensing receptor (CaSR), a member of the G-protein coupled receptor family (GPCR) class C was originally cloned from bovine parathyroid in 1993. CaSR plays a key role in the maintenance of extracellular calcium homeostasis. This is achieved by the sensitivity of the CaSR to changes in extracellular calcium ion concentrations and then regulating the synthesis and release of parathyroid hormone. CaSR is mainly expressed in parathyroid cells as well as renal tubular epithelial cells, thyroid C cells, brain, pituitary, intestine, bone marrow, skin and the cardiovascular system. Like other GPCR family C members the CaSR has a seven transmembrane domain that is involved in G protein activation. The CaSR also has a venous flytrap domain which contains the calcium binding site. Upon synthesis in teh CaSR is trafficked from the endoplasmic reticulum to the Golgi apparatus shere it becomes glycosylated before its delivery to the plasma membrane. Our goal is to determine the length of time this process takes and also to determine conditions and factors that regulate the movement of the CaSR from the endoplasmic reticulum to the Golgi.

Chernousov, Michael A. PhD; Google Scholar Profile
Research Scientist II
Weis Center for Research
100 North Academy Avenue
Danville, PA 17822
Phone: 570-271-5361
Fax: 570-271-6701
mchernousov@geisinger.edu
Research Interests: The major cellular constituents of the mammalian peripheral nervous system are neurons (axons) and Schwann cells. During peripheral nerve development, Schwann cells proliferate and migrate out along newly formed axons, deposit basal lamina and collagen fibrils and, finally, myelinate and ensheathe nerve fibers. In adult animals, Schwann cells play an important role in nerve regeneration after injury, by undergoing the cell division to replace damaged Schwann cells and synthesizing a new basal lamina and myelin sheaths.

In vitro studies have shown that if Schwann cells are prevented from forming basal lamina then normal myelination and ensheathment of axons does not occur. Addition of exogenous basal lamina components restores the ability of Schwann cells to myelinate axons. These finding demonstrate that basal lamina assembly and interactions of Schwann cells with basal lamina components are critical steps in Schwann cells development.

My research interests focus on the molecular mechanisms through which Schwann cells interact with basal lamina material. In particular, we are trying to identify new molecule(s) that might be involved in this process. During this studies we purified a to bind in vitro to N- syndecan, a transmembrane heparin-binding protein, tentatively named p200, from conditioned medium of cultured Schwann cells. p200 was identified by its ability heparan sulfate proteoglycan expressed on the surface of neonatal Schwann cells.

Chu, Xin, PhD; Google Scholar Profile
Research Scientist I
Weis Center for Research
100 North Academy Avenue
Danville, PA 17822
Phone: 570-271-5563
Fax: 570-271-6701
xchu@geisinger.edu
Research Interests:The development of modern technologies in fields such as automation, molecular biology, genetics, biochemistry, bioinformatics, epidemiology, and computer science has made it possible to integrate large scale bio-banking, whole genome assay techniques, and clinic information database like electronic health record (EHR) to form a new platform for human genomic research and impact the future health care. To address this challenge, a clinic genomic core facility in Geisinger has been established since 2004. Up to today, over dozen research projects have been developed and supported in the core through the collaborations with clinicians and investigators in different departments. Significant progresses have also been made in a variety of studies including obesity and a related disease called non-alcoholic steatohepatitis (NASH), the two tasks I have focused on. Since obesity is a multifactorial condition with substantial evidence supporting a strong genetic component, thus, their identification may be important in guiding treatment. We performed genotyping on DNA samples from a total of 707 adult patients with a BMI at least 40 and undergoing open or laparoscopic Roux-en-Y gastric bypass operations for morbid obesity and shown that approximately 21% of patients were homozygous for the FTO obesity SNP variant, 13% were homozygous for the INSIG2 obesity SNP variant, and 3.4% were homozygous for both. Although mean BMIs in the groups homozygous for each of these genes were not significantly different from nonhomozygotes, FTO/INSIG2 double homozygotes and homozygote/heterozygote pairs had significantly higher BMIs than the other groups, an indication that increased BMI in morbid obesity is associated with a combination of FTO and INSIG2 SNPs.

Lin, Qiong, PhD; Google Scholar Profile
Research Scientist II
Weis Center for Research
100 North Academy Avenue
Danville, PA 17822
Phone: 570-214-9369
Fax: 570-271-6701
qlin1@geisinger.edu
Research Interests: The development of modern technologies in fields such as automation, molecular biology, genetics, biochemistry, bioinformatics, epidemiology, and computer science has made it possible to integrate large scale bio-banking, whole genome assay techniques, and clinic information database like electronic health record (EHR) to form a new platform for human genomic research and impact the future health care. To address this challenge, a clinic genomic core facility in Geisinger has been established since 2004. Up to today, over dozen research projects have been developed and supported in the core through the collaborations with clinicians and investigators in different departments. Significant progresses have also been made in a variety of studies including obesity and a related disease called non-alcoholic steatohepatitis (NASH), the two tasks I have focused on. Since obesity is a multifactorial condition with substantial evidence supporting a strong genetic component, thus, their identification may be important in guiding treatment. We performed genotyping on DNA samples from a total of 707 adult patients with a BMI at least 40 and undergoing open or laparoscopic Roux-en-Y gastric bypass operations for morbid obesity and shown that approximately 21% of patients were homozygous for the FTO obesity SNP variant, 13% were homozygous for the INSIG2 obesity SNP variant, and 3.4% were homozygous for both. Although mean BMIs in the groups homozygous for each of these genes were not significantly different from nonhomozygotes, FTO/INSIG2 double homozygotes and homozygote/heterozygote pairs had significantly higher BMIs than the other groups, an indication that increased BMI in morbid obesity is associated with a combination of FTO and INSIG2 SNPs.

Mirshahi, Uyenlinh, PhD; Google Scholar Profile
Research Scientist II
Weis Center for Research
100 North Academy Avenue
Danville, PA 17822
Phone: 570-214-7756
Fax: 570-271-6701
umirshahi1@geisinger.edu
Research Interests: The regulation and structure/function of potassium channels are the major focus of our work, as potassium channels are important in neuronal and cardiac cellular excitability. Downstream form G-protein coupled receptor (GPCR) stimulation, Kir3 channels are activated by the G bg that is released upon GTP-GDP exchange. Four Kir3 subunits are assembled in the endoplasmic reticulum (ER) to form a channel before they are expressed on the cell surface. How and when specific Ga, Gb, and Gg subunits are recruited during GPCR stimulation to induce K channel opening is of major interest. For example, does activation of adenosine (A1) receptor recruit a specific set of Ga, Gb, and Gg proteins that is different from those recruited for the activation of GABAB receptor?  In addition, we would like to understand whether the G proteins and K channels first interact at the intracellular level or at the cell surface, and does this interaction play a role in the stability and trafficking of Kir channels and the G proteins.

Ness-Myers, Jennifer, PhD; Google Scholar Profile
Weis Center for Research
100 North Academy Avenue
Danville, PA 17822
Phone: 570-271-5573
Fax: 570-271-6701
jkmyers@geisinger.edu
Research Interests: My research interests are focused on the molecular signaling pathways involved in glial cell development and injury response. The myelinating cells in the peripheral (Schwann cells) and central nervous system (oligodendrocytes) are essential to the proper function of the nervous system. During injury, the capacity of both Schwann cells and oligodendrocytes to proliferate and remyelinate axons can determine the level of recovery. In multiple sclerosis, the eventual loss of oligodendrocyte progenitors and the failure to remyelinate will result in permanent loss of function. In peripheral nerve regeneration, Schwann cells are uniquely able to dedifferentiate and proliferate, forming a pathway that enables axonal regrowth and recovery of signal transmission. Understanding the cell:cell and intracellular signaling pathways regulating glial cell injury response will lead to improved therapies for nervous system diseases.

Smelser, Diane T, PhD; PubMed Link
Research Associate
Weis Center for Research
100 North Academy Avenue
Danville, PA 17822
Phone: 570-214-5117
Fax: 570-214-5170
dtsmelser@geisinger.edu
Research Interests: Dr. Smelser's research interest is exploring the genetic component of complex diseases including obesity, type 2 diabetes, metabolic syndrome, and cancer. Her goal is collaboration with clinicians and other investigators to ascertain genes and risk factors that cause susceptibility to disease. She has been studying the epidemiological and genetic risk factors of abdominal aortic aneurysms, with the goal of creating a risk profile. Another study involves the association of obesity candidate genes with postmenopausal breast cancer. She is also interested in the association of candidate genes with childhood obesity. Ascertaining significant genetic and environmental interactions could identify populations at highest risk for developing the disease. These populations could then be targeted for early medical interventions and treatments that reduce the incidence and severity of disease.