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Search Results: 1 - 10 of 153088 matches for " Vanessa H. Routh "
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Glucose Sensing Neurons in the Ventromedial Hypothalamus
Vanessa H. Routh
Sensors , 2010, DOI: 10.3390/s101009002
Abstract: Neurons whose activity is regulated by glucose are found in a number of brain regions. Glucose-excited (GE) neurons increase while glucose-inhibited (GI) neurons decrease their action potential frequency as interstitial brain glucose levels increase. We hypothesize that these neurons evolved to sense and respond to severe energy deficit (e.g., fasting) that threatens the brains glucose supply. During modern times, they are also important for the restoration of blood glucose levels following insulin-induced hypoglycemia. Our data suggest that impaired glucose sensing by hypothalamic glucose sensing neurons may contribute to the syndrome known as hypoglycemia-associated autonomic failure in which the mechanisms which restore euglycemia following hypoglycemia become impaired. On the other hand, increased responses of glucose sensing neurons to glucose deficit may play a role in the development of Type 2 Diabetes Mellitus and obesity. This review will discuss the mechanisms by which glucose sensing neurons sense changes in interstitial glucose and explore the roles of these specialized glucose sensors in glucose and energy homeostasis.
Hypothalamic S-Nitrosylation Contributes to the Counter-Regulatory Response Impairment following Recurrent Hypoglycemia
Xavier Fioramonti, Adam Deak, Srinidhi Deshpande, Lionel Carneiro, Chunxue Zhou, Nazish Sayed, Branly Orban, Joshua R. Berlin, Luc Pénicaud, Corinne Leloup, Annie Beuve, Vanessa H. Routh
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068709
Abstract: Aims Hypoglycemia is a severe side effect of intensive insulin therapy. Recurrent hypoglycemia (RH) impairs the counter-regulatory response (CRR) which restores euglycemia. During hypoglycemia, ventromedial hypothalamus (VMH) production of nitric oxide (NO) and activation of its receptor soluble guanylyl cyclase (sGC) are critical for the CRR. Hypoglycemia also increases brain reactive oxygen species (ROS) production. NO production in the presence of ROS causes protein S-nitrosylation. S-nitrosylation of sGC impairs its function and induces desensitization to NO. We hypothesized that during hypoglycemia, the interaction between NO and ROS increases VMH sGC S-nitrosylation levels and impairs the CRR to subsequent episodes of hypoglycemia. VMH ROS production and S-nitrosylation were quantified following three consecutive daily episodes of insulin-hypoglycemia (RH model). The CRR was evaluated in rats in response to acute insulin-induced hypoglycemia or via hypoglycemic-hyperinsulinemic clamps. Pretreatment with the anti-oxidant N-acetyl-cysteine (NAC) was used to prevent increased VMH S-nitrosylation. Results Acute insulin-hypoglycemia increased VMH ROS levels by 49±6.3%. RH increased VMH sGC S-nitrosylation. Increasing VMH S-nitrosylation with intracerebroventricular injection of the nitrosylating agent S-nitroso-L-cysteine (CSNO) was associated with decreased glucagon secretion during hypoglycemic clamp. Finally, in RH rats pre-treated with NAC (0.5% in drinking water for 9 days) hypoglycemia-induced VMH ROS production was prevented and glucagon and epinephrine production was not blunted in response to subsequent insulin-hypoglycemia. Conclusion These data suggest that NAC may be clinically useful in preventing impaired CRR in patients undergoing intensive-insulin therapy.
Hypothalamic glucose sensing: making ends meet
Vanessa Routh,Zhenyu Sheng,Chunxue Zhou
Frontiers in Systems Neuroscience , 2014, DOI: 10.3389/fnsys.2014.00236
Abstract: The neuroendocrine system governs essential survival and homeostatic functions. For example, growth is needed for development. Thermoregulation maintains optimal core temperature in a changing environment. Reproduction ensures species survival. Stress and immune responses enable an organism to overcome external and internal threats. The circadian system regulates arousal and sleep such that vegetative and active functions do not overlap. All of these functions require a significant portion of the body’s energy. As the integrator of the neuroendocrine system, the hypothalamus carefully assesses the energy status of the body in order to appropriately partition resources to provide for each system without compromising the others. While doing so the hypothalamus must ensure that adequate glucose levels are preserved for brain function since glucose is the primary fuel of the brain. To this end, the hypothalamus contains specialized glucose sensing neurons which are scattered throughout the nuclei controlling distinct neuroendocrine functions. We hypothesize that these neurons play a key role in enabling the hypothalamus to partition energy to meet these peripheral survival needs without endangering the brain’s glucose supply. The goal of this review is to describe the varied mechanisms underlying glucose sensing in neurons within discrete hypothalamic nuclei. We will then evaluate the way in which peripheral energy status regulates glucose sensitivity. For example, during energy deficit such as fasting specific hypothalamic glucose sensing neurons become sensitized to decreased glucose. This increases the gain of the information relay when glucose availability is a greater concern for the brain. Finally, changes in glucose sensitivity under pathological conditions (e.g., recurrent insulin-hypoglycemia, diabetes) will be addressed. The overall goal of this review is to place glucose sensing neurons within the context of hypothalamic control of neuroendocrine function.
A Study on Integration of 802.11 WLAN and UMTS Networks
International Journal of Advanced Research in Electrical, Electronics and Instrumentation Engineering , 2013,
Abstract: Mobile computing for personal communication system (PCS) that offers mobile users anytime, anywhere, bi-directional reliable access to the Internet. Mobile IP as a network layer protocol provides solution to requirements of mobile computing. Due to terminal mobility and change of service area, efficient mobile IP support is an important issue in heterogeneous network in order to minimize packet loss and Hand off latency to the mobile users. In our project we have proposed a loosely coupled UMTS/WLAN integration architecture with mobile IP as a service continuity solution. We have used generic routing encapsulation as a tunneling protocol between these two dissimilar networks. After designing the architecture we created a simulation model using OPNET 14 as a simulation tool. Through simulation we have analyzed the performance of the proposed architecture.
The Hamiltonian Form of Topologically Massive Supergravity
Alasdair Routh
Physics , 2013, DOI: 10.1103/PhysRevD.88.024022
Abstract: We construct a "Chern-Simons-like" action for N=1 Topologically Massive Supergravity from the Chern-Simons actions of N=1 Supergravity and Conformal Supergravity. We convert this action into Hamiltonian form and use this to demonstrate that the theory propagates a single massive (2, 3/2) supermultiplet.
Random Descent by Jayanta Mahapatra
Nikunja Bihari Routh
Journal of Literature, Culture and Media Studies , 2009,
Conflicting Readings of R.K. Narayan's The Guide
Journal of Literature, Culture and Media Studies , 2009,
Graham Greene: The Serious Entertainer
N.B. Routh
Journal of Literature, Culture and Media Studies , 2009,
Time Operator in Quantum Mechanics  [PDF]
Adwit Kanti Routh
Open Access Library Journal (OALib Journal) , 2019, DOI: 10.4236/oalib.1105816
We can not only bring time operator in quantum mechanics (non-relativistic) but also determine its Eigen value, commutation relation of its square with energy and some of the properties of time operator like either it is Hermitian or not, either its expectation value is real or complex for a wave packet etc. Exactly these are what I have done.
Deregulation of Hepatic Insulin Sensitivity Induced by Central Lipid Infusion in Rats Is Mediated by Nitric Oxide
Nicolas Marsollier, Nadim Kassis, Karima Mezghenna, Maud Soty, Xavier Fioramonti, Amélie Lacombe, Aurélie Joly, Bruno Pillot, Carine Zitoun, José Vilar, Gilles Mithieux, René Gross, Anne-Dominique Lajoix, Vanessa Routh, Christophe Magnan, Céline Cruciani-Guglielmacci
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0006649
Abstract: Background Deregulation of hypothalamic fatty acid sensing lead to hepatic insulin-resistance which may partly contribute to further impairment of glucose homeostasis. Methodology We investigated here whether hypothalamic nitric oxide (NO) could mediate deleterious peripheral effect of central lipid overload. Thus we infused rats for 24 hours into carotid artery towards brain, either with heparinized triglyceride emulsion (Intralipid, IL) or heparinized saline (control rats). Principal Findings Lipids infusion led to hepatic insulin-resistance partly related to a decreased parasympathetic activity in the liver assessed by an increased acetylcholinesterase activity. Hypothalamic nitric oxide synthases (NOS) activities were significantly increased in IL rats, as the catalytically active neuronal NOS (nNOS) dimers compared to controls. This was related to a decrease in expression of protein inhibitor of nNOS (PIN). Effect of IL infusion on deregulated hepatic insulin-sensitivity was reversed by carotid injection of non selective NOS inhibitor NG-monomethyl-L-arginine (L-NMMA) and also by a selective inhibitor of the nNOS isoform, 7-Nitro-Indazole (7-Ni). In addition, NO donor injection (L-arginine and SNP) within carotid in control rats mimicked lipid effects onto impaired hepatic insulin sensitivity. In parallel we showed that cultured VMH neurons produce NO in response to fatty acid (oleic acid). Conclusions/Significance We conclude that cerebral fatty acid overload induces an enhancement of nNOS activity within hypothalamus which is, at least in part, responsible fatty acid increased hepatic glucose production.
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