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Markers of inhibitory neurotransmission are altered in the prefrontal cortex (PFC) of subjects with schizophrenia, and several lines of evidence suggest that these alterations may be most prominent in the subset of GABA-containing neurons that express the calcium-binding protein, parvalbumin (PV). To test this hypothesis, we evaluated the expression of(More)
The mediodorsal thalamic nucleus (MD) is the principal relay nucleus for the prefrontal cortex, a brain region thought to be dysfunctional in schizophrenia. Several, but not all, postmortem studies of the MD in schizophrenia have reported decreased volume and total neuronal number. However, it is not clear whether the findings are specific for schizophrenia(More)
Dysfunction of inhibitory neurons in the prefrontal cortex (PFC), represented by decreased expression of GABA-related genes such as the 67 kDa isoform of glutamate decarboxylase (GAD67) and parvalbumin (PV), appears to contribute to cognitive deficits in subjects with schizophrenia. We investigated the involvement of signaling mediated by brain-derived(More)
OBJECTIVE In a previous study the authors found that dendritic spine density was reduced on prefrontal pyramidal neurons in layer 3 of subjects with schizophrenia. From a neural circuitry perspective, understanding the pathophysiological significance of this finding requires knowledge of whether pyramidal neurons in other cortical layers are similarly(More)
BACKGROUND Subjects with schizophrenia have decreased gray matter volume of auditory cortex in structural imaging studies and exhibit deficits in auditory sensory processing that might reflect impairments of feedforward and/or feedback circuits within the auditory cortex. Recently, we reported that one component of these circuits, pyramidal cells in deep(More)
BACKGROUND Somal volumes of pyramidal cells are reduced within feedforward but not feedback circuits in areas 41 and 42 of the auditory cortex of subjects with schizophrenia. Because neuronal somal volume depends on both the number of axonal terminations onto and furnished by the neuron, we hypothesized that axon terminal densities are reduced in(More)
FMS-like tyrosine kinase 3 receptor (FLT3) internal tandem duplication (ITD) mutations result in constitutive activation of this receptor and have been shown to increase the risk of relapse in patients with acute myeloid leukemia (AML); however, substantial heterogeneity in clinical outcomes still exists within both the ITD mutated and unmutated AML(More)
Therapeutic resistance, i.e. failure to achieve complete remission (CR) despite not incurring treatment-related mortality (TRM), or relapse after achieving CR, is the principal cause of failure in acute myeloid leukemia (AML). Many clinical, cytogenetic, and molecular characteristics are strongly associated with resistance. 1 However, using areas under(More)
Single-cell network profiling (SCNP) data generated from multi-parametric flow cytometry analysis of bone marrow (BM) and peripheral blood (PB) samples collected from patients >55 years old with non-M3 AML were used to train and validate a diagnostic classifier (DXSCNP) for predicting response to standard induction chemotherapy (complete response [CR] or CR(More)
A novel mixture model is presented for repeated measurements in which correlation among repeated observations on the same subject is induced via correlated unobservable component indicators. The mixture components in our model are linear regressions, and the mixing proportions are logits with random effects. Inference is facilitated by sampling from the(More)
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