This paper presents a detailed case study of a 48-year-old male who underwent ascending aortic aneurysm repair with a bioprosthetic valve five years prior and subsequently developed septic embolic encephalitis, an infrequent yet critical complication following cardiac valve replacement. The patient exhibited an array of initial symptoms, including generalized weakness, fatigue, fevers, chills, diarrhea, and altered mentation. Microbiological analysis of blood cultures revealed the presence of , and echocardiogram examination demonstrated vegetation on the prosthetic valve.
View Article and Find Full Text PDFSerotonin 2A receptors (5-HTRs) mediate the hallucinogenic effects of psychedelic drugs and are a key target of the leading class of medications used to treat psychotic disorders. These findings suggest that dysfunction of 5-HTRs may contribute to the symptoms of schizophrenia, a mental illness characterized by perceptual and cognitive disturbances. Indeed, numerous studies have found that 5-HTRs are reduced in the brains of individuals with schizophrenia.
View Article and Find Full Text PDFFast spiking, parvalbumin (PV) expressing hippocampal interneurons are classified into basket, axo-axonic (chandelier), and bistratified cells. These cell classes play key roles in regulating local circuit operations and rhythmogenesis by releasing GABA in precise temporal patterns onto distinct domains of principal cells. In this study, we show that each of the three major PV cell classes further splits into functionally distinct sub-classes during fast network events in vivo.
View Article and Find Full Text PDFThe immediate-early gene early growth response 3 (Egr3) is associated with schizophrenia and expressed at reduced levels in postmortem patients' brains. We have previously reported that Egr3-deficient (Egr3(-/-)) mice display reduced sensitivity to the sedating effects of clozapine compared with wild-type (WT) littermates, paralleling the heightened tolerance of schizophrenia patients to antipsychotic side effects. In this study, we have used a pharmacological dissection approach to identify a neurotransmitter receptor defect in Egr3(-/-) mice that may mediate their resistance to the locomotor suppressive effects of clozapine.
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