Institution
Medical University of South Carolina
Education•Charleston, South Carolina, United States•
About: Medical University of South Carolina is a education organization based out in Charleston, South Carolina, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 23436 authors who have published 45440 publications receiving 1769397 citations. The organization is also known as: MUSC & Medical College of the State of South Carolina.
Topics: Population, Poison control, Medicine, Cancer, Stroke
Papers published on a yearly basis
Papers
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TL;DR: D dorsal hippocampus, basolateral amygdala, and dorsomedial prefrontal cortex play critical roles in contextual reinstatement of cocaine-seeking behavior and the involvement of the DH in explicit CS- and cocaine-induced reinstatement is investigated.
519 citations
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TL;DR: This review focuses on the salvage pathway in ceramide metabolism, its regulation, its experimental analysis, and emerging biological functions.
519 citations
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518 citations
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TL;DR: It is demonstrated that Ex-4 can protect neurons against metabolic and oxidative insults, and they provide preclinical support for the therapeutic potential for exendin-4 in the treatment of stroke and PD.
Abstract: Glucagon-like peptide-1 (GLP-1) is an endogenous insulinotropic peptide secreted from the gastrointestinal tract in response to food intake. It enhances pancreatic islet beta-cell proliferation and glucose-dependent insulin secretion, and lowers blood glucose and food intake in patients with type 2 diabetes mellitus (T2DM). A long-acting GLP-1 receptor (GLP-1R) agonist, exendin-4 (Ex-4), is the first of this new class of antihyperglycemia drugs approved to treat T2DM. GLP-1Rs are coupled to the cAMP second messenger pathway and, along with pancreatic cells, are expressed within the nervous system of rodents and humans, where receptor activation elicits neurotrophic actions. We detected GLP-1R mRNA expression in both cultured embryonic primary cerebral cortical and ventral mesencephalic (dopaminergic) neurons. These cells are vulnerable to hypoxia- and 6-hydroxydopamine-induced cell death, respectively. We found that GLP-1 and Ex-4 conferred protection in these cells, but not in cells from Glp1r knockout (-/-) mice. Administration of Ex-4 reduced brain damage and improved functional outcome in a transient middle cerebral artery occlusion stroke model. Ex-4 treatment also protected dopaminergic neurons against degeneration, preserved dopamine levels, and improved motor function in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease (PD). Our findings demonstrate that Ex-4 can protect neurons against metabolic and oxidative insults, and they provide preclinical support for the therapeutic potential for Ex-4 in the treatment of stroke and PD.
517 citations
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TL;DR: Evidence is provided that modulation of EpCAM expression can affect cell migration, invasion, and proliferation by enhancing E-cadherin-mediated cell-to-cell adhesion and that this hypothesis is a potential novel target for breast cancer gene therapy.
Abstract: EpCAM (epithelial cell adhesion molecule) is a cell surface molecule that is known to be highly expressed in colon and other epithelial carcinomas. EpCAM is involved in cell-to-cell adhesion and has been the target of antibody therapy in several clinical trials. To assess the value of EpCAM as a novel target for breast cancer gene therapy, we performed real-time reverse transcription-PCR to quantify the level of EpCAM mRNA expression in normal breast tissue and primary and metastatic breast cancers. We found that EpCAM is overexpressed 100- to 1000-fold in primary and metastatic breast cancer. Silencing EpCAM gene expression with EpCAM short interfering RNA (siRNA) resulted in a 35–80% decrease in the rate of cell proliferation in four different breast cancer cell lines. EpCAM siRNA treatment decreased cell migration by 91.8% and cell invasion by 96.4% in the breast cancer cell line MDA-MB-231 in vitro . EpCAM siRNA treatment was also associated with an increase in the detergent-insoluble protein fraction of E-cadherin, α-catenin, and β-catenin, consistent with the known biology of EpCAM as a regulator of cell adhesion. Our hypothesis is that modulation of EpCAM expression can affect cell migration, invasion, and proliferation by enhancing E-cadherin-mediated cell-to-cell adhesion. These data provide compelling evidence that EpCAM is a potential novel target for breast cancer gene therapy and offer insights into the mechanisms associated with EpCAM gene silencing.
516 citations
Authors
Showing all 23601 results
Name | H-index | Papers | Citations |
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Edward Giovannucci | 206 | 1671 | 179875 |
Ronald Klein | 194 | 1305 | 149140 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Yusuke Nakamura | 179 | 2076 | 160313 |
John J.V. McMurray | 178 | 1389 | 184502 |
Nora D. Volkow | 165 | 958 | 107463 |
L. Joseph Melton | 161 | 531 | 97861 |
Gregg C. Fonarow | 161 | 1676 | 126516 |
Michael Boehnke | 152 | 511 | 136681 |
Charles B. Nemeroff | 149 | 979 | 90426 |
Deepak L. Bhatt | 149 | 1973 | 114652 |
Clifford R. Jack | 140 | 965 | 94814 |
Scott D. Solomon | 137 | 1145 | 103041 |
Karl Swedberg | 136 | 706 | 111214 |
Charles J. Yeo | 136 | 672 | 76424 |