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Search Results: 1 - 10 of 325229 matches for " Matcheri S. Keshavan "
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MRI structural findings in schizophrenia
Gilbert Andrew R,Keshavan Matcheri S
Revista Brasileira de Psiquiatria , 2001,
Abstract:
Sleep spindle deficits in antipsychotic-na?ve early course schizophrenia and in non-psychotic first-degree relatives
Dara S. Manoach,Erin J. Wamsley,Debra M. Montrose,David Kupfer,Robert Stickgold,Matcheri S. Keshavan
Frontiers in Human Neuroscience , 2014, DOI: 10.3389/fnhum.2014.00762
Abstract: Introduction: Chronic medicated patients with schizophrenia have marked reductions in sleep spindle activity and a correlated deficit in sleep-dependent memory consolidation. Using archival data, we investigated whether antipsychotic-na?ve early course patients with schizophrenia and young non-psychotic first-degree relatives of patients with schizophrenia also show reduced sleep spindle activity and whether spindle activity correlates with cognitive function and symptoms. Method: Sleep spindles during Stage 2 sleep were compared in antipsychotic-na?ve adults newly diagnosed with psychosis, young non-psychotic first-degree relatives of schizophrenia patients and two samples of healthy controls matched to the patients and relatives. The relations of spindle parameters with cognitive measures and symptom ratings were examined. Results: Early course schizophrenia patients showed significantly reduced spindle activity relative to healthy controls and to early course patients with other psychotic disorders. Relatives of schizophrenia patients also showed reduced spindle activity compared with controls. Reduced spindle activity correlated with measures of executive function in early course patients, positive symptoms in schizophrenia and IQ estimates across groups. Conclusions: Like chronic medicated schizophrenia patients, antipsychotic-na?ve early course schizophrenia patients and young non-psychotic relatives of individuals with schizophrenia have reduced sleep spindle activity. These findings indicate that the spindle deficit is not an antipsychotic side-effect or a general feature of psychosis. Instead, the spindle deficit may predate the onset of schizophrenia, persist throughout its course and be an endophenotype that contributes to cognitive dysfunction.
Homeostatic Imbalance of Purine Catabolism in First-Episode Neuroleptic-Na?ve Patients with Schizophrenia
Jeffrey K. Yao,George G. Dougherty Jr.,Ravinder D. Reddy,Matcheri S. Keshavan,Debra M. Montrose,Wayne R. Matson,Joseph McEvoy,Rima Kaddurah-Daouk
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009508
Abstract: Purine catabolism may be an unappreciated, but important component of the homeostatic response of mitochondria to oxidant stress. Accumulating evidence suggests a pivotal role of oxidative stress in schizophrenia pathology.
Associations between Purine Metabolites and Clinical Symptoms in Schizophrenia
Jeffrey K. Yao, Ruth Condray, George G. Dougherty, Matcheri S. Keshavan, Debra M. Montrose, Wayne R. Matson, Joseph McEvoy, Rima Kaddurah-Daouk, Ravinder D. Reddy
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042165
Abstract: Background The antioxidant defense system, which is known to be dysregulated in schizophrenia, is closely linked to the dynamics of purine pathway. Thus, alterations in the homeostatic balance in the purine pathway may be involved in the pathophysiology of schizophrenia. Methodology/Principal Findings Breakdown products in purine pathway were measured using high-pressure liquid chromatography coupled with a coulometric multi-electrode array system for 25 first-episode neuroleptic-na?ve patients with schizophrenia at baseline and at 4-weeks following initiation of treatment with antipsychotic medication. Associations between these metabolites and clinical and neurological symptoms were examined at both time points. The ratio of uric acid and guanine measured at baseline predicted clinical improvement following four weeks of treatment with antipsychotic medication. Baseline levels of purine metabolites also predicted clinical and neurological symtpoms recorded at baseline; level of guanosine was associated with degree of clinical thought disturbance, and the ratio of xanthosine to guanosine at baseline predicted degree of impairment in the repetition and sequencing of actions. Conclusions/Significance Findings suggest an association between optimal levels of purine byproducts and dynamics in clinical symptoms and adjustment, as well as in the integrity of sensory and motor processing. Taken together, alterations in purine catabolism may have clinical relevance in schizophrenia pathology.
Lipidomics Reveals Early Metabolic Changes in Subjects with Schizophrenia: Effects of Atypical Antipsychotics
Joseph McEvoy, Rebecca A. Baillie, Hongjie Zhu, Peter Buckley, Matcheri S. Keshavan, Henry A. Nasrallah, George G. Dougherty, Jeffrey K. Yao, Rima Kaddurah-Daouk
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068717
Abstract: There is a critical need for mapping early metabolic changes in schizophrenia to capture failures in regulation of biochemical pathways and networks. This information could provide valuable insights about disease mechanisms, trajectory of disease progression, and diagnostic biomarkers. We used a lipidomics platform to measure individual lipid species in 20 drug-na?ve patients with a first episode of schizophrenia (FE group), 20 patients with chronic schizophrenia that had not adhered to prescribed medications (RE group), and 29 race-matched control subjects without schizophrenia. Lipid metabolic profiles were evaluated and compared between study groups and within groups before and after treatment with atypical antipsychotics, risperidone and aripiprazole. Finally, we mapped lipid profiles to n3 and n6 fatty acid synthesis pathways to elucidate which enzymes might be affected by disease and treatment. Compared to controls, the FE group showed significant down-regulation of several n3 polyunsaturated fatty acids (PUFAs), including 20:5n3, 22:5n3, and 22:6n3 within the phosphatidylcholine and phosphatidylethanolamine lipid classes. Differences between FE and controls were only observed in the n3 class PUFAs; no differences where noted in n6 class PUFAs. The RE group was not significantly different from controls, although some compositional differences within PUFAs were noted. Drug treatment was able to correct the aberrant PUFA levels noted in FE patients, but changes in re patients were not corrective. Treatment caused increases in both n3 and n6 class lipids. These results supported the hypothesis that phospholipid n3 fatty acid deficits are present early in the course of schizophrenia and tend not to persist throughout its course. These changes in lipid metabolism could indicate a metabolic vulnerability in patients with schizophrenia that occurs early in development of the disease.
Idiopathic Reactive Hypoglycemia: Mechanisms of Onset and Remission with High Protein Low Carbohydrate Diet  [PDF]
Keshavan Prakash, Mary Kabadi, Udaya M. Kabadi
Open Journal of Endocrine and Metabolic Diseases (OJEMD) , 2015, DOI: 10.4236/ojemd.2015.59015
Abstract: Objective: Idiopathic reactive hypoglycemia is defined as early postprandial hypoglycemia occurring on ingestion of high carbohydrate containing meal. Remission ensues with high protein low carbohydrate diet. This study assessed roles of insulin and glucagon in its onset and remission. Methods: Plasma glucose, insulin and glucagon were determined after an overnight fast and repeatedly until 180 minutes on ingestion of 3 meals; 100 g glucose; 100 g pure protein liquid and mixture of 50 g each at 14 days’ interval. Five adults with IRH and 6 age matched healthy volunteers participated. Results: In IRH, glucose ingestion induced prompt rise in glucose (5.1 ± 0.8 to10.5 ± 1.2 mM/L) followed later by hypoglycemia (2.6 ± 0.4 mM/L). Insulin rose from 7 ± 2 to 90 ± 18 mU/L. Glucagon rose initially (10% ± 2%) from elevated basal concentration (373 ± 57 mU/L) followed by later decline (-43% ± 12%). On protein ingestion, glucose declined followed by a restoration to basal level while both insulin and glucagon rose (28 ± 6 mU/L; 148% ± 38%, p < 0.01). However, insulin response was lower and glucagon rise was greater when compared to responses on glucose ingestion (p < 0.01). With mixed meal, glucose (8.2 ± 0.6 mM/L), insulin (65 ± 12 mU/L) and glucagon (48% ± 7%) responses were lesser than rises following glucose ingestion (p < 0.05) and hypoglycemia did not occur. Conclusion: In IRH, initial hyperglycemia on glucose ingestion may be exacerbated by paradoxical glucagon rise and hypoglycemia may be induced by increased insulin and declining glucagon responses. Resolution of hypoglycemia with high protein low carbohydrate diet may be attributed to blunting of insulin response and concurrent glucagon rise.
A Gradient Descent Algorithm on the Grassman Manifold for Matrix Completion
Raghunandan H. Keshavan,Sewoong Oh
Computer Science , 2009, DOI: 10.1016/j.trc.2012.12.007
Abstract: We consider the problem of reconstructing a low-rank matrix from a small subset of its entries. In this paper, we describe the implementation of an efficient algorithm called OptSpace, based on singular value decomposition followed by local manifold optimization, for solving the low-rank matrix completion problem. It has been shown that if the number of revealed entries is large enough, the output of singular value decomposition gives a good estimate for the original matrix, so that local optimization reconstructs the correct matrix with high probability. We present numerical results which show that this algorithm can reconstruct the low rank matrix exactly from a very small subset of its entries. We further study the robustness of the algorithm with respect to noise, and its performance on actual collaborative filtering datasets.
Regularization for Matrix Completion
Raghunandan H. Keshavan,Andrea Montanari
Statistics , 2010,
Abstract: We consider the problem of reconstructing a low rank matrix from noisy observations of a subset of its entries. This task has applications in statistical learning, computer vision, and signal processing. In these contexts, "noise" generically refers to any contribution to the data that is not captured by the low-rank model. In most applications, the noise level is large compared to the underlying signal and it is important to avoid overfitting. In order to tackle this problem, we define a regularized cost function well suited for spectral reconstruction methods. Within a random noise model, and in the large system limit, we prove that the resulting accuracy undergoes a phase transition depending on the noise level and on the fraction of observed entries. The cost function can be minimized using OPTSPACE (a manifold gradient descent algorithm). Numerical simulations show that this approach is competitive with state-of-the-art alternatives.
Matrix Completion from Noisy Entries
Raghunandan H. Keshavan,Andrea Montanari,Sewoong Oh
Computer Science , 2009,
Abstract: Given a matrix M of low-rank, we consider the problem of reconstructing it from noisy observations of a small, random subset of its entries. The problem arises in a variety of applications, from collaborative filtering (the `Netflix problem') to structure-from-motion and positioning. We study a low complexity algorithm introduced by Keshavan et al.(2009), based on a combination of spectral techniques and manifold optimization, that we call here OptSpace. We prove performance guarantees that are order-optimal in a number of circumstances.
Matrix Completion from a Few Entries
Raghunandan H. Keshavan,Andrea Montanari,Sewoong Oh
Computer Science , 2009,
Abstract: Let M be a random (alpha n) x n matrix of rank r<
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