Sanford Stout (playturkey6)

Background Cognitive dysfunction is one of the most disabling non-motor symptoms of Parkinson's disease (PD), though its pathological correlates still remain elusive. Hippocampal Lewy pathology has recently been correlated by compelling evidence from post-mortem and imaging studies. Animal models recapitulating cognitive impairment in PD are essential to better understand the underlying pathophysiology. To investigate the hippocampal involvement in cognitive dysfunction of PD, we generated an experimental model by inducing midbrain and hippocampal α-synuclein pathology simultaneously. Methods Rats were injected either with human α-synuclein or green fluorescent protein (GFP) expressing adeno-associated viral vectors (AAV), or saline bilaterally into substantia nigra (SN) and dentate gyrus (DG). A group of untreated animals were used as naïve controls. Cognitive and behavioral changes were evaluated with tests probing for spatial learning, short-term memory, anxiety and hedonistic behavior. Immunohistochemicals, suggesting preferential susceptibility of CA2 to produce α-synuclein induced pathology. Conclusion Bilateral α-synuclein overexpression in DG and SN reproduced partial motor and hippocampus related cognitive deficits. Using this model, we showed a predisposition of CA2 for pathological α-synuclein accumulation, which may provide further insights for future experimental and clinical studies.A 65-year-old man was hospitalized owing to fever (38.6 °C) and dry cough since 4 days. He visited Wuhan 8 days ago. At admission, nasopharyngeal swab samples were taken, and polymerase chain reaction analysis confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA positivity. On day 9, after admission, the chest computed tomography scan showed diffuse ground-glass shadows in the patient's bilateral lungs. On day 11, his respiratory symptoms worsened. Subsequently, type I respiratory failure was diagnosed, coinciding with kidney injury, and subsequently, type II respiratory failure occurred, coupled with multiorgan failure including the heart and liver. However, the patient's constitution worsened although SARS-CoV-2 tests were negative since day 13. He died on day 21. Lung biopsy showed areas of diffuse alveolar damage, characterized by extensive acute alveolitis with numerous intra-alveolar neutrophil, lymphocyte, and macrophage infiltrations. Microthrombi were seen in the dilated pulmonary capillaries. Immunohistochemistry staining for SARS-CoV-2 N protein was negative. Taken together, the patient died of multiorgan failure although the SARS-CoV-2 infection was cleared already, implicating that for disease worsening, no active SARS-CoV-2 infection is required.The relationship between circadian rhythms and mood disorders has been established, circadian dysregulations are believed to exacerbate the severity of mood disorders and vice versa. Although many studies on diurnal changes of clock genes in animal model of depression have been performed from the RNA level, only a few studies have been carried out from the protein level. In this study, we investigated the diurnal changes induced by chronic unpredictable stress (CUS) using various methods, including free-running wheel test, enzyme-linked immunosorbent assay (ELISA) and Western Blotting (WB). Besides, we examined the depression-like behaviors of rats by sucrose preference test (SPT) and forced swim test (FST). We found that CUS induced significant reductions in the quantity of free-running wheel activity and the amplitude of melatonin secretion rhythm. We also found that CUS induced rhythmic disruptions of clock proteins in hippocampus. Furthermore, we found that the amplitude of PER1 in CA1 was positively related to the severity of depression-like behaviors. These results suggest that stress results in both changes in circadian rhythms and in depression-like behaviors and that it is suggested that these changes are related.We aimed to examine reactions to g