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Search Results: 1 - 10 of 403752 matches for " Ann M Stowe "
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CCL2 upregulation triggers hypoxic preconditioning-induced protection from stroke
Ann M Stowe, Bradley K Wacker, Petra D Cravens, Jennifer L Perfater, Min K Li, Ruilong Hu, Angela B Freie, Olaf Stüve, Jeffrey M Gidday
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-33
Abstract: Adult male SW/ND4, CCL2-null, and wild-type mice were used in these studies. Cortical CCL2/CCR2 message, protein, and cell-type specific immunoreactivity were determined following HPC (4 h, 8% O2) or room air control (21% O2) from 6 h through 2 weeks following HPC. Circulating leukocyte subsets were determined by multi-parameter flow cytometry in na?ve mice and 12 h after HPC. CCL2-null and wild-type mice were exposed to HPC 2 days prior to tMCAo, with immunoneutralization of CCL2 during HPC achieved by a monoclonal CCL2 antibody.Cortical CCL2 mRNA and protein expression peaked at 12 h after HPC (both p < 0.01), predominantly in cortical neurons, and returned to baseline by 2 days. A delayed cerebral endothelial CCL2 message expression (p < 0.05) occurred 2 days after HPC. The levels of circulating monocytes (p < 0.0001), T lymphocytes (p < 0.0001), and granulocytes were decreased 12 h after HPC, and those of B lymphocytes were increased (p < 0.0001), but the magnitude of these respective changes did not differ between wild-type and CCL2-null mice. HPC did decrease the number of circulating CCR2+ monocytes (p < 0.0001) in a CCL2-dependent manner, but immunohistochemical analyses at this 12 h timepoint indicated that this leukocyte subpopulation did not move into the CNS. While HPC reduced infarct volumes by 27% (p < 0.01) in wild-type mice, CCL2-null mice subjected to tMCAo were not protected by HPC. Moreover, administration of a CCL2 immunoneutralizing antibody prior to HPC completely blocked (p < 0.0001 vs. HPC-treated mice) the development of ischemic tolerance.The early expression of CCL2 in neurons, the delayed expression of CCL2 in cerebral endothelial cells, and CCL2-mediated actions on circulating CCR2+ monocytes, appear to be required to establish ischemic tolerance to focal stroke in response to HPC, and thus represent a novel role for this chemokine in endogenous neurovascular protection.Preconditioning occurs when an organism, tissue, or cell is exposed
Memory Capacity of a Random Neural Network
Matt Stowe
Computer Science , 2012,
Abstract: This paper considers the problem of information capacity of a random neural network. The network is represented by matrices that are square and symmetrical. The matrices have a weight which determines the highest and lowest possible value found in the matrix. The examined matrices are randomly generated and analyzed by a computer program. We find the surprising result that the capacity of the network is a maximum for the binary random neural network and it does not change as the number of quantization levels associated with the weights increases.
The Response of Cerebral Cortex to Haemorrhagic Damage: Experimental Evidence from a Penetrating Injury Model
Sivaraman Purushothuman, Lauren Marotte, Sally Stowe, Daniel M. Johnstone, Jonathan Stone
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0059740
Abstract: Understanding the response of the brain to haemorrhagic damage is important in haemorrhagic stroke and increasingly in the understanding the cerebral degeneration and dementia that follow head trauma and head-impact sports. In addition, there is growing evidence that haemorrhage from small cerebral vessels is important in the pathogenesis of age-related dementia (Alzheimer’s disease). In a penetration injury model of rat cerebral cortex, we have examined the neuropathology induced by a needlestick injury, with emphasis on features prominent in the ageing and dementing human brain, particularly plaque-like depositions and the expression of related proteins. Needlestick lesions were made in neo- and hippocampal cortex in Sprague Dawley rats aged 3–5 months. Brains were examined after 1–30 d survival, for haemorrhage, for the expression of hyperphosphorylated tau, Aβ, amyloid precursor protein (APP), for gliosis and for neuronal death. Temporal cortex from humans diagnosed with Alzheimer’s disease was examined with the same techniques. Needlestick injury induced long-lasting changes–haem deposition, cell death, plaque-like deposits and glial invasion–along the needle track. Around the track, the lesion induced more transient changes, particularly upregulation of Aβ, APP and hyperphosporylated tau in neurons and astrocytes. Reactions were similar in hippocampus and neocortex, except that neuronal death was more widespread in the hippocampus. In summary, experimental haemorrhagic injury to rat cerebral cortex induced both permanent and transient changes. The more permanent changes reproduced features of human senile plaques, including the formation of extracellular deposits in which haem and Aβ-related proteins co-localised, neuronal loss and gliosis. The transient changes, observed in tissue around the direct lesion, included the upregulation of Aβ, APP and hyperphosphorylated tau, not associated with cell death. The findings support the possibility that haemorrhagic damage to the brain can lead to plaque-like pathology.
A Kleptoparasitic Cecidomyiid and Other Flies Associated With Spiders
John Sivinski,Mark Stowe
Psyche , 1980, DOI: 10.1155/1980/27685
Abstract:
Neural Network Capacity for Multilevel Inputs
Matt Stowe,Subhash Kak
Computer Science , 2013,
Abstract: This paper examines the memory capacity of generalized neural networks. Hopfield networks trained with a variety of learning techniques are investigated for their capacity both for binary and non-binary alphabets. It is shown that the capacity can be much increased when multilevel inputs are used. New learning strategies are proposed to increase Hopfield network capacity, and the scalability of these methods is also examined in respect to size of the network. The ability to recall entire patterns from stimulation of a single neuron is examined for the increased capacity networks.
What's new in tuberculosis vaccines?
Ginsberg,Ann M.;
Bulletin of the World Health Organization , 2002, DOI: 10.1590/S0042-96862002000600014
Abstract: over the past 10 years, tuberculosis (tb) vaccine development has resurged as an active area of investigation. the renewed interest has been stimulated by the recognition that, although bcg is delivered to approximately 90% of all neonates globally through the expanded programme on immunization, mycobacterium tuberculosis continues to cause over 8 million new cases of tb and over 2 million deaths annually. over one hundred tb vaccine candidates have been developed, using different approaches to inducing protective immunity. candidate vaccines are typically screened in small animal models of primary tb disease for their ability to protect against a virulent strain of m. tuberculosis. the most promising are now beginning to enter human safety trials, marking real progress in this field for the first time in 80 years.
Update on the management of symptoms in schizophrenia: focus on amisulpride
Ann M Mortimer
Neuropsychiatric Disease and Treatment , 2009, DOI: http://dx.doi.org/10.2147/NDT.S3949
Abstract: ate on the management of symptoms in schizophrenia: focus on amisulpride Review (5446) Total Article Views Authors: Ann M Mortimer Published Date May 2009 Volume 2009:5 Pages 267 - 277 DOI: http://dx.doi.org/10.2147/NDT.S3949 Ann M Mortimer Department of Psychiatry, Hertford Building, The University of Hull, Cottingham Road, Hull HU6 7RX, United Kingdom Abstract: Amisulpride is an atypical antipsychotic drug with a unique receptor pharmacology which is dose dependent. It is a standard treatment in dysthymia as well as in psychosis. Amisulpride is efficacious, effective and well tolerated in positive symptoms of schizophrenia: there is extensive evidence that it treats negative symptoms when given in low doses, although relative lack of EPS and an antidepressant effect may contribute. In first-episode patients amisulpride is an option, although there is little comparative work available. Amisulpride has the best evidence as an effective adjunct to clozapine treatment. Regarding intellectual function, amisulpride appears cognitive sparing but the clinical relevance of this remains obscure. There is evidence that amisulpride can improve social function but again there is little comparative work to demonstrate any particular advantages. Regarding the current conventional versus atypical antipsychotic controversy, amisulpride did better in switching studies and meta-analyses than in the single large pragmatic randomized trial reported to date. It is a versatile drug, and may offer advantages over other atypical antipsychotic drugs in the treatment of negative and depressive symptoms, and tolerability advantages such as the avoidance of weight gain. Essentially it rests with the treating clinician to employ a rational psychopharmacological approach towards the individual patient: there will be few circumstances in which amisulpride will not be a likely contender as a treatment choice.
How should physician interpret the new guidelines on breast self-exam?
Ann M. Stewart
University of Toronto Medical Journal , 2001, DOI: 10.5015/utmj.v79i1.938
Abstract:
The Value of Mammography in Screening for Breast Cancer
Ann M. Stewart
University of Toronto Medical Journal , 2001, DOI: 10.5015/utmj.v78i2.1023
Abstract:
Update on the management of symptoms in schizophrenia: focus on amisulpride
Ann M Mortimer
Neuropsychiatric Disease and Treatment , 2009,
Abstract: Ann M MortimerDepartment of Psychiatry, Hertford Building, The University of Hull, Cottingham Road, Hull HU6 7RX, United KingdomAbstract: Amisulpride is an atypical antipsychotic drug with a unique receptor pharmacology which is dose dependent. It is a standard treatment in dysthymia as well as in psychosis. Amisulpride is efficacious, effective and well tolerated in positive symptoms of schizophrenia: there is extensive evidence that it treats negative symptoms when given in low doses, although relative lack of EPS and an antidepressant effect may contribute. In first-episode patients amisulpride is an option, although there is little comparative work available. Amisulpride has the best evidence as an effective adjunct to clozapine treatment. Regarding intellectual function, amisulpride appears cognitive sparing but the clinical relevance of this remains obscure. There is evidence that amisulpride can improve social function but again there is little comparative work to demonstrate any particular advantages. Regarding the current conventional versus atypical antipsychotic controversy, amisulpride did better in switching studies and meta-analyses than in the single large pragmatic randomized trial reported to date. It is a versatile drug, and may offer advantages over other atypical antipsychotic drugs in the treatment of negative and depressive symptoms, and tolerability advantages such as the avoidance of weight gain. Essentially it rests with the treating clinician to employ a rational psychopharmacological approach towards the individual patient: there will be few circumstances in which amisulpride will not be a likely contender as a treatment choice.Keywords: amisulpride, negative symptoms, clozapine, depression
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