New York Medical College is a medical university based in Valhalla, New York, 13 Miles North of New York City. It specializes in health science, medical arts, public advocacy, and allied health profession training. Metropolitan Hospital Center is the University Hospital of New York Medical College, defining the border of the Upper East side neighborhood of Yorkville and East Harlem in Manhattan. It has been affiliated with New York Medical College since it was founded in 1875, representing the oldest partnership between a hospital and a private medical school in the United States. Metropolitan is part of the New York City Health and Hospitals Corporation , the largest municipal hospital and healthcare system in the countryThe Valhalla campus includes the main academic medical center Westchester Medical Center University Hospital, Maria Fareri Children's Hospital, the Heart Center, the Cancer Center, the Neuroscience Center, the Transplant Center, the Behavioral Health Center and the Westchester Institute for Human Development. The academic medical center provides structured interactions between physicians and NYMC students, unique research opportunities, and access to cutting edge resources for the medical college. In addition, a branch campus affiliated with St. Joseph's Healthcare System in Paterson, New Jersey, offers clinical rotations for third and fourth year students. On June 9th, 2014, St. Michaels in Newwark,NJ became the newest addition to the 28 hospital affiliates and partnerships at NYMC.The university specializes in research within the areas of cardiovascular disease, cancer, senescence, neuroscience, renal disease, stem cells, molecular modeling, epilepsy and infectious disease.Three schools comprise New York Medical College: the Graduate School of Basic Medical science, the School of Health science and Practice and the School of Medicine. Total enrollment is 1,660 students in addition to 800 residents and clinical fellows. NYMC employs 1,350 full-time faculty members and 1,450 part-time and voluntary faculty. The university has more than 12,000 alumni active in medical practice, healthcare administration, public health, teaching and research.New York Medical College joined the Touro College and University System in 2011. Wikipedia.
Lue N.F.,New York Medical College
Trends in Biochemical Sciences | Year: 2010
Telomeres, the nucleoprotein structures located at linear eukaryotic chromosomal termini, are essential for chromosome stability and are maintained by the special reverse transcriptase named telomerase. In the Saccharomycotina subphylum of budding yeast, telomere repeat sequences and binding factors, as well as telomerase components, are exceptionally diverse and distinct from those found in other eukaryotes. In this survey, I report a comparative analysis of the domain structures of telomere and telomerase-related factors made possible by the recent sequencing of multiple yeast genomes. This analysis revealed both conserved and variable aspects of telomere maintenance. Based on these findings, I propose a plausible series of evolutionary events in budding yeast to account for its exceptional telomere structural divergence. © 2009 Elsevier Ltd. All rights reserved.
Cesarman E.,New York Medical College
Annual Review of Pathology: Mechanisms of Disease | Year: 2014
Epstein-Barr virus (EBV) and Kaposi's sarcoma herpesvirus (KSHV), formally designated human herpesvirus 4 (HHV-4) and 8 (HHV-8), respectively, are viruses that can cause a variety of cancers in humans. EBV is found in non-Hodgkin and Hodgkin lymphomas, as well as in lymphoproliferative disorders, which occur more commonly but not exclusively in individuals with immunodeficiency. EBV also causes nonlymphoid malignancies such as nasopharyngeal carcinoma. KSHV causes primary effusion lymphomas, multicentric Castleman's disease, and Kaposi's sarcoma. The frequency of lymphoid malignancies related to infection by one of these two herpesviruses is greatly increased in individuals with immunodeficiency, whether primary or acquired, for example, as a consequence of HIV infection and AIDS or in the case of therapeutic immunosuppression for organ transplantation. Our current understanding indicates that EBV and KSHV contribute to lymphomagenesis by affecting genomic stability and by subverting the cellular molecular signaling machinery and metabolism to avoid immune surveillance and enhance tumor cell growth and survival. Understanding the viral associations in specific lymphoproliferative disorders and the molecular mechanisms of viral oncogenesis will lead to better prevention, diagnosis, and treatment strategies for these diseases. © 2014 by Annual Reviews. All rights reserved.
Lin P.C.,New York Medical College
Cancer research | Year: 2013
Androgen receptor signaling plays a critical role in prostate cancer pathogenesis. Yet, the regulation of androgen receptor signaling remains elusive. Even with stringent androgen deprivation therapy, androgen receptor signaling persists. Here, our data suggest that there is a complex interaction between the expression of the tumor suppressor miRNA, miR-31, and androgen receptor signaling. We examined primary and metastatic prostate cancer and found that miR-31 expression was reduced as a result of promoter hypermethylation, and importantly, the levels of miR-31 expression were inversely correlated with the aggressiveness of the disease. As the expression of androgen receptor and miR-31 was inversely correlated in the cell lines, our study further suggested that miR-31 and androgen receptor could mutually repress each other. Upregulation of miR-31 effectively suppressed androgen receptor expression through multiple mechanisms and inhibited prostate cancer growth in vivo. Notably, we found that miR-31 targeted androgen receptor directly at a site located in the coding region, which was commonly mutated in prostate cancer. In addition, miR-31 suppressed cell-cycle regulators including E2F1, E2F2, EXO1, FOXM1, and MCM2. Together, our findings suggest a novel androgen receptor regulatory mechanism mediated through miR-31 expression. The downregulation of miR-31 may disrupt cellular homeostasis and contribute to the evolution and progression of prostate cancer. We provide implications for epigenetic treatment and support clinical development of detecting miR-31 promoter methylation as a novel biomarker.
Kocherlakota P.,New York Medical College
Pediatrics | Year: 2014
Neonatal abstinence syndrome (NAS) is a result of the sudden discontinuation of fetal exposure to substances that were used or abused by the mother during pregnancy. Withdrawal from licit or illicit substances is becoming more common among neonates in both developed and developing countries. NAS continues to be an important clinical entity throughout much of the world. NAS leads to a constellation of signs and symptoms involving multiple systems. The pathophysiology of NAS is not completely understood. Urine or meconium confirmation may assist the diagnosis and management of NAS. The Finnegan scoring system is commonly used to assess the severity of NAS; scoring can be helpful for initiating, monitoring, and terminating treatment in neonates. Nonpharmacological care is the initial treatment option, and pharmacological treatment is required if an improvement is not observed after nonpharmacological measures or if the infant develops severe withdrawal. Morphine is the most commonly used drug in the treatment of NAS secondary to opioids. An algorithmic approach to the management of infants with NAS is suggested. Breastfeeding is not contraindicated in NAS, unless the mother is taking street drugs, is involved in polydrug abuse, or is infected with HIV. Future studies are required to assess the long-term effects of NAS on children after prenatal exposure. Copyright © 2014 by the American Academy of Pediatrics.
Nathan C.,New York Medical College
Science Translational Medicine | Year: 2012
If discovery of new antibiotics continues to falter while resistance to drugs in clinical use continues to spread, society's medicine chest will soon lack effective treatments for many infections. Heritable antibiotic resistance emerges in bacteria from nonheritable resistance, also called phenotypic tolerance. This widespread phenomenon is closely linked to nonproliferative states in ways that scientists are just beginning to understand. A deeper understanding of the mechanisms of phenotypic tolerance may reveal new drug targets in the infecting organisms. At the same time, researchers must investigate ways to target the host in order to influence hostpathogen relationships. Government must reform the regulatory process for approval of new antibiotics. The private sector, government, and academia must undertake multiple, organized, multidisciplinary, parallel efforts to improve the ways in which antibiotics are discovered, tested, approved, and conserved, or it will be difficult to sustain the modern practice of medicine.