Brain research
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Neonatal hypoxic-ischemic encephalopathy (HIE) always results in severe neurologic dysfunction, nevertheless effective treatments are limited and the underlying mechanism also remains unclear. In this study, we firstly established the neonatal HIE model in the postnatal day 7 SD rats, Zea-Longa score and TTC staining were employed to assess the neurological behavior and infarct volume of the brain after cerebral hypoxia-ischemia (HI). Afterwards, protein chip was adopted to detect the differential proteins in the right cortex, hippocampus and lung, ultimately, PDGF was noticed. ⋯ Moreover, the protein level of P-PI3K and P-AKT signaling pathways were largely decreased following PDGF-shRNA application in the cortical neurons. In conclusion, PDGF suppression aggravated neuronal dysfunction, and the underlying mechanism is associated with inhibiting the phosphorylation of P-PI3K and P-AKT. Together, PDGF regulating PI3K and AKT may be an important panel in HIE events and therefore may provide possible strategy for the treatment of HIE in future clinic trail.
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Irritable Bowel Syndrome (IBS) is a common functional gastrointestinal disorder which is characterized by altered bowel habits. A growing number of studies investigate the association between IBS and cognitive impairments. Current studies report conflicting results regarding cognitive impairment in IBS patients. We therefore conducted the first systematic review to examine the association between IBS and cognitive impairment and identify the types of cognitive domain involved. ⋯ There is evidence of attentional bias in individuals with IBS; the evidence on cognitive impairment was either inconclusive or insufficient in other cognitive domains. Further studies are needed to confirm prevalence rates and examine potential mechanisms.
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Distance organ dysfunction is the major cause of death in the patients with acute kidney injury (AKI). However, the neurobiological basis of AKI-induced brain disorders and their mediators are poorly understood. This study was aimed to find out the links between AKI and brain injury and also the underlying cellular and electrophysiological mechanisms of memory deficit following induction of AKI via different experimental models of renal ischemia with or without uremia and uremia without renal ischemia. ⋯ Apoptosis was stimulated in the hippocampus intensively by BIR but moderately by UIR and BNX. However, BIR and UIR were associated with profoundly disturbed BBB, increased CA1 neuronal excitability, impaired LTP induction and memory deficit. Therefore, AKI most likely through inflammatory mediators leads to hippocampal apoptosis and electrophysiological impairments, BBB disruption and memory loss, whereas uremia may contribute to necrotic neuronal death.