Brain research
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The employment of explosive weaponry in modern warfare exposes populations to shock wave-induced and impact-related brain injuries. Among the most common clinical complaints resulting from traumatic brain injury (TBI) are sleep-wake disturbances. The current study assessed the acute effects of mild concussive brain injury (CBI) and mild blast wave-induced brain injury (BTBI) on mouse behavior and orexin-A expression. ⋯ CBI treatment caused increased CD11b immunostaining. However, neither injury was accompanied by an alteration in the number of orexin-A hypothalamic neurons. Taken together, shock wave exposure and concussive injury transiently reduced mouse activities, but some differences between the two injuries were seen.
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Evidence from human and animal studies has shown that experiences of early attachment can influence brain development and structure. Adult attachment style develops from early attachment experiences. However, little is known about the relationship between gray matter volume and attachment style. ⋯ Further analysis revealed that attachment avoidance was negatively correlated with the volume of the right middle occipital gyrus in women, but the inverse correlation was found in men. These findings suggest that differences in adult attachment styles are correlated with structural brain differences in adulthood, and that sex-related differences in adult attachment styles are associated with intrinsic structural brain differences involved in visual processing. These findings may improve our understanding of the pathophysiology of attachment-related disorder.
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Cerebral ischemia/reperfusion injury (IRI) is a serious complication during the treatment of stroke patients with very few effective clinical treatment. Hydrogen (H2) can protect mitochondria function and have favorable therapeutic effects on cerebral IRI. Mitophagy plays an important role in eliminating damaged or dysfunctional mitochondria and maintaining mitochondria homeostasis. ⋯ The result revealed H2 and RAP could activate mitophagy while 3-MA inhibit mitophagy. In addition, the study found H2 and RAP could significantly induce the expression of PINK1 and Parkin in OGD/R neurons which was inhibited by 3-MA. Taken together, our findings demonstrated H2 had a neuroprotective effect on OGD/R damaged neurons by protecting mitochondrial function and the potential protection mechanism may closely related to enhancement of mitophagy mediated by PINK1/Parkin signaling pathway.
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Early brain injury (EBI) plays a pivotal role in the prognosis of patients with subarachnoid haemorrhage (SAH). Dexmedetomidine (DEX), a highly selective α2 receptor agonist, is reported to exert multiple protective effects in many neurological diseases. This study was designed to investigate whether DEX had neuroprotective functions in EBI after SAH, and to explore the possible mechanisms. ⋯ In addition, DEX alleviated cell apoptosis at 24 h after SAH. Notably, DEX could also suppress the activation of the TLR4/NF-κB pathway and the NLRP3 inflammasome. These findings suggested that treatment with DEX after SAH attenuated SAH-induced EBI, partially through the suppression of the TLR4/NF-κB pathway and the NLRP3 inflammasome.
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Pyroptosis is a highly specific type of inflammatory programmed cell death that different from necrosis or apoptosis. It is initiated by cellular detection of acute damage via recognizing pathogen-associated molecular patterns (PAMPs) by NOD-like receptors (NLRs) or AIM2-like receptor (AIM2). NLRs and AIM2 could trigger the formation of a multi-protein complex, known as inflammasome. ⋯ These effects contributed to improving the neurological outcome of CCI mice. In conclusion, NLRs and AIM2 inflammasome-mediated pyroptosis could aggravate BBB damage after TBI. Targeting and controlling pyroptosis in injured BBB would be a promising therapeutic strategy for TBI in the future.