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Albany, NY, United States

The New York State Department of Health is the department of the New York state government responsible for public health. It is headed by the Health Commissioner, a position held January 24, 2011 through May 4, 2014 by Nirav R. Shah, M.D., M.P.H.. Since May 4, 2014, Howard A. Zucker, M.D., J.D. has been the acting commissioner. Wikipedia.

Wolpaw J.R.,New York State Department of Health
Neuroscientist | Year: 2010

The work of recent decades has shown that the nervous system changes continually throughout life. Activity-dependent central nervous system (CNS) plasticity has many different mechanisms and involves essentially every region, from the cortex to the spinal cord. This new knowledge radically changes the challenge of explaining learning and memory and greatly increases the relevance of the spinal cord. The challenge is now to explain how continual and ubiquitous plasticity accounts for the initial acquisition and subsequent stability of many different learned behaviors. The spinal cord has a key role because it is the final common pathway for all behavior and is a site of substantial plasticity. Furthermore, because it is simple, accessible, distant from the rest of the CNS, and directly connected to behavior, the spinal cord is uniquely suited for identifying sites and mechanisms of plasticity and for determining how they account for behavioral change. Experimental models based on spinal cord reflexes facilitate study of the gradual plasticity that makes possible most rapid learning phenomena. These models reveal principles and generate concepts that are likely to apply to learning and memory throughout the CNS. In addition, they offer new approaches to guiding activity-dependent plasticity so as to restore functions lost to injury or disease. © The Author(s) 2010. Source

Ansari S.A.,New York State Department of Health
Transcription | Year: 2012

The tail module subunits of Mediator complex are targets of activators both in yeast and metazoans. Here we discuss recent evidence from studies in yeast for tail module specificity for SAGA-dependent, TATA-containing genes including highly regulated stress response genes, and for independent recruitment and function of the tail module. Source

Hamza T.H.,New York State Department of Health
Nature genetics | Year: 2010

Parkinson's disease is a common disorder that leads to motor and cognitive disability. We performed a genome-wide association study of 2,000 individuals with Parkinson's disease (cases) and 1,986 unaffected controls from the NeuroGenetics Research Consortium (NGRC). We confirmed associations with SNCA and MAPT, replicated an association with GAK (using data from the NGRC and a previous study, P = 3.2 x 10(-9)) and detected a new association with the HLA region (using data from the NGRC only, P = 2.9 x 10(-8)), which replicated in two datasets (meta-analysis P = 1.9 x 10(-10)). The HLA association was uniform across all genetic and environmental risk strata and was strong in sporadic (P = 5.5 x 10(-10)) and late-onset (P = 2.4 x 10(-8)) disease. The association peak we found was at rs3129882, a noncoding variant in HLA-DRA. Two studies have previously suggested that rs3129882 influences expression of HLA-DR and HLA-DQ. The brains of individuals with Parkinson's disease show upregulation of DR antigens and the presence of DR-positive reactive microglia, and nonsteroidal anti-inflammatory drugs reduce Parkinson's disease risk. The genetic association with HLA supports the involvement of the immune system in Parkinson's disease and offers new targets for drug development. Source

Liao C.,New York State Department of Health
Environmental science & technology | Year: 2012

Bisphenol A has been reported to be a ubiquitous contaminant in indoor dust, and human exposure to this compound is well documented. Information on the occurrence of and human exposure to other bisphenol analogues is limited. In this study, eight bisphenol analogues, namely 2,2-bis(4-hydroxyphenyl)propane (BPA), 4,4'-(hexafluoroisopropylidene)diphenol (BPAF), 4,4'-(1-phenylethylidene)bisphenol (BPAP), 2,2-bis(4-hydroxyphenyl)butane (BPB), 4,4'-dihydroxydiphenylmethane (BPF), 4,4'-(1,4-phenylenediisopropylidene)bisphenol (BPP), 4,4'- sulfonyldiphenol (BPS), and 4,4'-cyclohexylidenebisphenol (BPZ), were determined in indoor dust samples (n = 156) collected from the United States (U.S.), China, Japan, and Korea. Samples were extracted by solid-liquid extraction, purified by automated solid phase extraction methods, and determined by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The total concentrations of bisphenols (∑BPs; sum of eight bisphenols) in dust were in the range of 0.026-111 μg/g (geometric mean: 2.29 μg/g). BPA, BPS, and BPF were the three major bisphenols, accounting for >98% of the total concentrations. Other bisphenol analogues were rare or not detected, with the exception of BPAF, which was found in 76% of the 41 samples collected in Korea (geometric mean: 0.0039 μg/g). The indoor dust samples from Korea contained the highest concentrations of both individual and total bisphenols. BPA concentrations in dust were compared among three microenvironments (house, office, and laboratory). The estimated median daily intake (EDI) of ∑BPs through dust ingestion in the U.S., China, Japan, and Korea was 12.6, 4.61, 15.8, and 18.6 ng/kg body weight (bw)/day, respectively, for toddlers and 1.72, 0.78, 2.65, and 3.13 ng/kg bw/day, respectively, for adults. This is the first report on the occurrence of bisphenols, other than BPA, in indoor dust. Source

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which is abundant in tobacco smoke, is a potent lung procarcinogen. The present study was aimed to prove that transgenic expression of human cytochrome P450 2A13 (CYP2A13), known to be selectively expressed in the respiratory tract and be the most efficient enzyme for NNK bioactivation in vitro, will enhance NNK bioactivation and NNK-induced tumorigenesis in the mouse lung. Kinetic parameters of NNK bioactivation in vitro and incidence of NNK-induced lung tumors in vivo were determined for wild-type, Cyp2a5-null and CYP2A13-humanized (CYP2A13-transgenic/Cyp2a5-null) mice. As expected, in both liver and lung microsomes, the loss of CYP2A5 resulted in significant increases in Michaelis constant (K m) values for the formation of 4-oxo-4-(3-pyridyl)-butanal, representing the reactive intermediate that can lead to the formation of O(6)-methylguanine (O(6)-mG) DNA adducts; however, the gain of CYP2A13 at a fraction of the level of mouse lung CYP2A5 led to recovery of the activity in the lung, but not in the liver. The levels of O(6)-mG, the DNA adduct highly correlated with lung tumorigenesis, were significantly higher in the lungs of CYP2A13-humanized mice than in Cyp2a5-null mice. Moreover, incidences of lung tumorigenesis were significantly greater in CYP2A13-humanized mice than in Cyp2a5-null mice, and the magnitude of the differences in incidence was greater at low (30mg/kg) than at high (200mg/kg) NNK doses. These results indicate that CYP2A13 is a low K m enzyme in catalyzing NNK bioactivation in vivo and support the notion that genetic polymorphisms of CYP2A13 can influence the risks of tobacco-induced lung tumorigenesis in humans. Source

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