Publications by authors named "Thaker G"

Purpose: Our purpose was to use real world data to assess trends in radiation therapy (RT) treatment fractionation and cost under the Oncology Care Model (OCM) through the first 8 performance periods (PPs).

Methods: We identified 17,157 episodes of care from 9898 patients treated at a statewide multispecialty health system through the first 8 6-month PPs (PP1-8: July 1, 2016, to June 30, 2020) of the OCM. Spending was stratified by 10 expenditure domains (eg, Part B/D drugs, radiation oncology [RO], etc), and 21 disease sites were extracted from claims data, from which an analysis of RO expenditures was performed on 2219 episodes from 2033 patients treated with RT.

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Purpose: The Radiation Oncology Alternative Payment Model (RO Model) will test prospective radiotherapy episode-based payments for 16 common disease sites. We created an automated analytics platform to calculate the impact of the RO Model vs historical fee-for-service episode reimbursements for brachytherapy treatments within five community oncology practices for prostate, uterine, and cervical cancer.

Methods And Materials: Claims data between January 1, 2017 and October 2, 2019 for prostate, uterine, and cervical cancer were analyzed as per the RO Model Final Rule methodology.

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Although smooth pursuit eye movement (SPEM) is a reliable endophenotype of schizophrenia, exact underlying cognitive and neural substrates remain unknown. A simple mechanistic model of SPEM assumes an efficient interaction in integrating sensory input from the medial temporal (MT)/medial superior temporal (MST) brain regions and subsequent motor response through the frontal eye field (FEF). Poor functional connectivity between these two regions could explain impaired motion perception and SPEM maintenance in schizophrenia.

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Bipolar and schizophrenia network for intermediate phenotypes is a network of investigator-driven laboratories focused on developing phenotypes, genotypes, and biomarkers for psychosis. Over the last 5 years, the consortium has accomplished a dense phenotyping protocol using probands with a lifetime history of psychosis, their relatives, and healthy controls. This has established a library of biomarker information on individuals with schizophrenia, schizoaffective disorder, and bipolar disorder with psychosis.

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Objectives: Bipolar I disorder is a disabling illness affecting 1% of people worldwide. Family and twin studies suggest that psychotic bipolar disorder (BDP) represents a homogeneous subgroup with an etiology distinct from non-psychotic bipolar disorder (BDNP) and partially shared with schizophrenia. Studies of auditory electrophysiology [e.

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Objective: Developing categorical diagnoses that have biological meaning within the clinical phenotype of psychosis (schizophrenia, schizoaffective disorder, and bipolar I disorder with psychosis) is as important for developing targeted treatments as for nosological goals. The Bipolar-Schizophrenia Network on Intermediate Phenotypes (B-SNIP) was formed to examine a broad array of intermediate phenotypes across psychotic disorders and to test the hypothesis that intermediate phenotype characteristics are homogeneous within phenomenologically derived DSM-IV diagnoses.

Method: The consortium recruited 933 stable probands with schizophrenia, schizoaffective disorder, or psychotic bipolar I disorder, 1,055 of their first-degree relatives, and 459 healthy comparison subjects for clinical characterization and dense phenotyping.

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Objective: Cognitive dysfunction is a core feature of schizophrenia, and persons at risk for schizophrenia may show subtle deficits in attention and working memory. In this study, we investigated the relationship between integrity of functional brain networks and performance in attention and working memory tasks as well as schizophrenia risk.

Methods: A total of 235 adults representing 3 levels of risk (102 outpatients with schizophrenia, 70 unaffected first-degree relatives of persons with schizophrenia, and 63 unrelated healthy controls [HCs]) completed resting-state functional magnetic resonance imaging and a battery of attention and working memory tasks (Brief Test of Attention, Hopkins Verbal Learning Test, and Brief Visuospatial Memory Test) on the same day.

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OBJECTIVE Both schizophrenia and bipolar disorder are hypothesized to involve disordered brain connectivity. Prior studies show low white matter integrity, measured with diffusion tensor imaging, for both disorders. The authors studied disease specificity and endophenotypic status of these abnormalities by examining patients and their unaffected relatives.

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Background: This study examined smooth pursuit eye movement (SPEM), prepulse inhibition (PPI), and auditory event-related potentials (ERP) to paired stimuli as putative endophenotypes of psychosis across the schizophrenia-bipolar disorder dimension.

Methods: Sixty-four schizophrenia probands (SZP), 40 psychotic bipolar I disorder probands (BDP), 31 relatives of SZP (SZR), 26 relatives of BDP (BDR), and 53 healthy controls (HC) were tested. Standard clinical characterization, SPEM, PPI, and ERP measures were administered.

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Background: Reduced amplitude of the P300 event-related potential in auditory oddball tasks may characterize schizophrenia (SZ) but is also reported in bipolar disorder. Similarity of auditory processing abnormalities between these diagnoses is uncertain, given the frequent combination of both psychotic and nonpsychotic patients in bipolar samples; abnormalities may be restricted to psychosis. In addition, typically only latency and amplitude of brain responses at selected sensors and singular time points are used to characterize neural responses.

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Background: Deficits in smooth pursuit eye movements are an established phenotype for schizophrenia (SZ) and are being investigated as a potential liability marker for bipolar disorder. Although the molecular determinants of this deficit are still unclear, research has verified deficits in predictive pursuit mechanisms in SZ. Because predictive pursuit might depend on the working memory system, we have hypothesized a relationship between the two in healthy control subjects (HC) and SZ and here examine whether it extends to psychotic bipolar disorder (BDP).

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Background: Schizophrenia and bipolar disorder share overlapping symptoms and genetic etiology. Functional brain dysconnectivity is seen in both disorders.

Methods: We compared 70 schizophrenia and 64 psychotic bipolar probands, their respective unaffected first-degree relatives (n = 70, and n = 52), and 118 healthy subjects, all group age-, gender-, and ethnicity-matched.

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This study sought to characterize the psychosis phenotype, contrasting cognitive features within traditional diagnosis and psychosis dimension in a family sample containing both schizophrenia and psychotic bipolar I disorder. Seventy-six probands with psychosis [44 probands with schizophrenia, 32 probands with psychotic bipolar I disorder] and 55 first-degree relatives [30 relatives of schizophrenia probands, 25 relatives of bipolar probands] were recruited. Standardized clinical and neuropsychological measures were administered.

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Individuals with schizophrenia (SZ) or bipolar disorder with psychosis (BPP) may share neurophysiological abnormalities as measured in auditory paired-stimuli paradigms with electroencephalography (EEG). Such investigations have been limited, however, by quantifying only event-related potential peaks and/or broad frequency bands at limited scalp locations without considering possible mediating factors (e.g.

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Background: There is increasing evidence for phenomenological, biological and genetic overlap between schizophrenia and bipolar disorder, bringing into question the traditional dichotomy between them. Neurobiological models linked to dimensional clinical data may provide a better foundation to represent diagnostic variation in neuropsychiatric disorders.

Method: To capture the interaction between psychosis and affective symptoms dimensionally, we devised a brief descriptive scale based on the type and relative proportions of psychotic and affective symptoms over the illness course.

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Objectives: We hypothesized that an oscillatory abnormality that is consistently observed across various testing paradigms may index an elementary neuronal abnormality marking schizophrenia risk.

Methods: Compared neural oscillations in resting EEG and sensory gating conditions in schizophrenia patients (n=128), their first-degree relatives (n=80), and controls (n=110) and calculated phenotypic and/or genetic correlation of the abnormal measure across these conditions.

Results: Using a uniform, single trial analytical approach, we identified two prominent oscillatory characteristics in schizophrenia: (1) augmented neural oscillatory power was pervasive in medicated schizophrenia patients in most frequencies, most prominent in the theta-alpha range (4-11 Hz) across the two paradigms (all p<0.

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Context: The administration of nicotine transiently improves many neurobiological and cognitive functions in schizophrenia and schizoaffective disorder. It is not yet clear which nicotinic acetylcholine receptor (nAChR) subtype or subtypes are responsible for these seemingly pervasive nicotinic effects in schizophrenia and schizoaffective disorder.

Objective: Because α4β2 is a key nAChR subtype for nicotinic actions, we investigated the effect of varenicline tartrate, a relatively specific α4β2 partial agonist and antagonist, on key biomarkers that are associated with schizophrenia and are previously shown to be responsive to nicotinic challenge in humans.

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Context: Kynurenic acid, a metabolite of the kynurenine pathway of tryptophan degradation, is an antagonist at N-methyl-d-aspartate and α7 nicotinic acetylcholine receptors and modulates glutamate, dopamine, and acetylcholine signaling. Cortical kynurenic acid concentrations are elevated in the brain and cerebrospinal fluid of schizophrenia patients. The proximal cause may be an impairment of kynurenine 3-monooxygenase (KMO), a rate-limiting enzyme at the branching point of the kynurenine pathway.

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Background: Emerging data indicate the neuromodulator adenosine may play a role in the therapeutics of schizophrenia. Adenosine A(2A) receptor stimulation exerts a functional antagonism at postsynaptic D(2) receptors. Data from animal models relevant to schizophrenia support a therapeutic effect of modulating adenosinergic transmission in the ventral striatum.

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Schizophrenia and nicotine addiction are both highly heritable phenotypes. Because individuals with schizophrenia have a higher rate of smoking than those in the general population, one could hypothesize that genes associated with smoking might be overrepresented in schizophrenia and thus help explain their increased smoking incidence. Although a number of genes have been proposed to explain the increased smoking risk in schizophrenia, none of them have been consistently linked to smoking and schizophrenia, and thus difficult to explain the increased smoking in schizophrenia.

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Whole-genome searches have identified nicotinic acetylcholine receptor alpha5-alpha3-beta4 subunit gene variants that are associated with smoking. How genes support this addictive and high-risk behavior through their expression in the brain remains poorly understood. Here we show that a key alpha5 gene variant Asp398Asn is associated with a dorsal anterior cingulate-ventral striatum/extended amygdala circuit, such that the "risk allele" decreases the intrinsic resting functional connectivity strength in this circuit.

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The present clinical trial was conducted to evaluate the efficacy of Shirodhara and Saraswatarishta as compared to hormone replacement therapy (HRT) in the management of menopausal syndrome, along with the assessment of Manasika Bhavas. The subjects were randomly divided into three groups. A total 48 patients were selected for the study, out of which 43 patients completed the study.

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Categorization of psychotic illnesses into schizophrenic and affective psychoses remains an ongoing controversy. Although Kraepelinian subtyping of psychosis was historically beneficial, modern genetic and neurophysiological studies do not support dichotomous conceptualization of psychosis. Evidence suggests that schizophrenia and bipolar disorder rather present a clinical continuum with partially overlapping symptom dimensions, neurophysiology, genetics and treatment responses.

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