Hawthorne, NY, United States

New York Medical College

www.nymc.edu
Hawthorne, NY, United States

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.

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Eoh H.,New York Medical College | Rhee K.Y.,New York Medical College
Proceedings of the National Academy of Sciences of the United States of America | Year: 2014

Few mutations attenuate Mycobacterium tuberculosis (Mtb) more profoundly than deletion of its isocitrate lyases (ICLs). However, the basis for this attenuation remains incompletely defined. Mtb's ICLs are catalytically bifunctional isocitrate and methylisocitrate lyases required for growth on even and odd chain fatty acids. Here, we report that Mtb's ICLs are essential for survival on both acetate and propionate because of its methylisocitrate lyase (MCL) activity. Lack of MCL activity converts Mtb's methylcitrate cycle into a "dead end" pathway that sequesters tricarboxylic acid (TCA) cycle intermediates into methylcitrate cycle intermediates, depletes gluconeogenic precursors, and results in defects of membrane potential and intrabacterial pH. Activation of an alternative vitamin B12-dependent pathway of propionate metabolism led to selective corrections of TCA cycle activity, membrane potential, and intrabacterial pH that specifically restored survival, but not growth, of ICL-deficient Mtb metabolizing acetate or propionate. These results thus resolve the biochemical basis of essentiality for Mtb's ICLs and survival on fatty acids.


Holthuis J.C.M.,University of Osnabrück | Holthuis J.C.M.,University Utrecht | Menon A.K.,New York Medical College
Nature | Year: 2014

The lipid composition of cellular organelles is tailored to suit their specialized tasks. A fundamental transition in the lipid landscape divides the secretory pathway in early and late membrane territories, allowing an adaptation from biogenic to barrier functions. Defending the contrasting features of these territories against erosion by vesicular traffic poses a major logistical problem. To this end, cells evolved a network of lipid composition sensors and pipelines along which lipids are moved by non-vesicular mechanisms. We review recent insights into the molecular basis of this regulatory network and consider examples in which malfunction of its components leads to system failure and disease. © 2014 Macmillan Publishers Limited. All rights reserved.


Iadecola C.,New York Medical College
Neuron | Year: 2013

Vascular cognitive impairment defines alterations in cognition, ranging from subtle deficits to full-blown dementia, attributable to cerebrovascular causes. Often coexisting with Alzheimer@s disease, mixed vascular and neurodegenerative dementia has emerged as the leading cause of age-related cognitive impairment. Central to the disease mechanism is the crucial role that cerebral blood vessels play in brain health, not only for the delivery of oxygen and nutrients, but also for the trophic signaling that inextricably links the well-being of neurons and glia to that of cerebrovascular cells. This review will examine how vascular damage disrupts these vital homeostatic interactions, focusing on the hemispheric white matter, a region at heightened risk for vascular damage, and on the interplay between vascular factors and Alzheimer@s disease. Finally, preventative and therapeutic prospects will be examined, highlighting the importance of midlife vascular risk factor control in the prevention of late-life dementia.


Eoh H.,New York Medical College | Rhee K.Y.,New York Medical College
Proceedings of the National Academy of Sciences of the United States of America | Year: 2013

Mycobacterium tuberculosis is a chronic, facultative intracellular pathogen that spends the majority of its decades-long life cycle in a non- or slowly replicating state. However, the bacterium remains poised to resume replicating so that it can transmit itself to a new host. Knowledge of the metabolic adaptations used to facilitate entry into and exit from nonreplicative states remains incomplete. Here, we apply 13C-based metabolomic profiling to characterize the activity of M. tuberculosis tricarboxylic acid cycle during adaptation to and recovery from hypoxia, a physiologically relevant condition associated with nonreplication. We show that, as M. tuberculosis adapts to hypoxia, it slows and remodels its tricarboxylic acid cycle to increase production of succinate, which is used to flexibly sustain membrane potential, ATP synthesis, and anaplerosis, in response to varying degrees of O2 limitation and the presence or absence of the alternate electron acceptor nitrate. This remodeling is mediated by the bifunctional enzyme isocitrate lyase acting in a noncanonical role distinct from fatty acid catab-olism. Isocitrate lyase-dependent production of succinate affords M. tuberculosis with a unique and bioenergetically efficient metabolic means of entry into and exit from hypoxia-induced quiescence.


Iadecola C.,New York Medical College | Anrather J.,New York Medical College
Nature Neuroscience | Year: 2011

Ischemic stroke remains a vexing public health problem. Although progress has been made in prevention and supportive care, efforts to protect the brain from ischemic cell death have failed. Thus, no new treatment has made it from bench to bedside since tissue plasminogen activator was introduced in 1996. The brain has a remarkable capacity for self-preservation, illustrated by the protective responses induced by ischemia, preconditioning and exercise. Here we describe the mechanisms underlying brain self-protection, with the goal of identifying features that could provide insight into stroke therapy. Unlike traditional therapeutic approaches based on counteracting selected pathways of the ischemic cascade, endogenous neuroprotection relies on coordinated neurovascular programs that support cerebral perfusion, mitigate the harmful effects of cerebral ischemia and promote tissue restoration. Learning how the brain triggers and implements these protective measures may advance our quest to treat stroke. © 2011 Nature America, Inc. All rights reserved.


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.


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.


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.


Holloman W.K.,New York Medical College
Nature Structural and Molecular Biology | Year: 2011

BRCA2 is the product of a breast cancer susceptibility gene in humans and the founding member of an emerging family of proteins present throughout the eukaryotic domain that serve in homologous recombination. The function of BRCA2 in recombination is to control RAD51, a protein that catalyzes homologous pairing and DNA strand exchange. By physically interacting with both RAD51 and single-stranded DNA, BRCA2 mediates delivery of RAD51 preferentially to sites of single-stranded DNA (ssDNA) exposed as a result of DNA damage or replication problems. Through its action, BRCA2 helps restore and maintain integrity of the genome. This review highlights recent studies on BRCA2 and its orthologs that have begun to illuminate the molecular mechanisms by which these proteins control homologous recombination. © 2011 Nature America, Inc. All rights reserved.


Ruan J.,New York Medical College
Blood | Year: 2013

Pericytes and vascular smooth muscle cells (VSMCs), which are recruited to developing blood vessels by platelet-derived growth factor BB, support endothelial cell survival and vascular stability. Here, we report that imatinib, a tyrosine kinase inhibitor of platelet-derived growth factor receptor β (PDGFRβ), impaired growth of lymphoma in both human xenograft and murine allograft models. Lymphoma cells themselves neither expressed PDGFRβ nor were growth inhibited by imatinib. Tumor growth inhibition was associated with decreased microvascular density and increased vascular leakage. In vivo, imatinib induced apoptosis of tumor-associated PDGFRβ(+) pericytes and loss of perivascular integrity. In vitro, imatinib inhibited PDGFRβ(+) VSMC proliferation and PDGF-BB signaling, whereas small interfering RNA knockdown of PDGFRβ in pericytes protected them against imatinib-mediated growth inhibition. Fluorescence-activated cell sorter analysis of tumor tissue revealed depletion of pericytes, endothelial cells, and their progenitors following imatinib treatment. Compared with imatinib, treatment with an anti-PDGFRβ monoclonal antibody partially inhibited lymphoma growth. Last, microarray analysis (Gene Expression Omnibus database accession number GSE30752) of PDGFRβ(+) VSMCs following imatinib treatment showed down-regulation of genes implicated in vascular cell proliferation, survival, and assembly, including those representing multiple pathways downstream of PDGFRβ. Taken together, these data indicate that PDGFRβ(+) pericytes may represent a novel, nonendothelial, antiangiogenic target for lymphoma therapy.

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