Neuroscience
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This study explored surface brain morphometry in type 1 diabetes including focus on painful diabetic peripheral neuropathy (DPN). Brain MRI was obtained from 56 individuals with diabetes (18 without DPN, 19 with painless DPN, 19 with painful DPN) and 20 healthy controls. Cortical thickness, sulcus depth, and gyrification were analysed globally and regionally in each group and in the combined diabetes group. ⋯ Cortical thinning manifested across the brain cortex in diabetes, especially for painful DPN. Altered postcentral gyrus morphometry may be associated with neuropathic pain. Assessing cortical morphometry may be critical for comprehending central neuropathy and the manifestation of painful DPN in diabetes.
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Media multitasking has become pervasive in our daily lives, yet its impact on cognitive abilities remains contentious, with more evidence supporting adverse effects (scattered attention hypothesis) than benefits (trained attention hypothesis). Recent studies have increasingly focused on the training effects of behavioral training on anticipatory brain functions, which involve cognitive and motor preparation before stimulus onset, assessed using event-related potentials (ERPs). This study investigated whether media multitasking enhances anticipatory brain functions and how task difficulty influences this relationship. ⋯ Our results suggest that HMM can flexibly adjust resource allocation based on task demands to maintain their response speed advantage. These findings suggest that LMM may possess a relatively steady acceleration/brake system, whereas HMM exhibit a more adaptable system capable of responding flexibly to diverse situations. Overall, these results underscore the training effects of media multitasking on anticipatory brain functions, supporting the trained attention hypothesis.
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Myelination is the process by which oligodendrocytes ensheathe axons to form myelin sheaths. Myelination is a crucial aspect of brain development and is closely associated with central nervous system abnormalities. However, previous studies have found that advanced maternal age might affect the myelination of offspring, potentially through the pathway of disrupting DNA methylation levels in the offspring's hippocampus. ⋯ The demethylation level of oligodendrocyte progenitor cells was detected by immunofluorescence co-expression of OLIG2 and DNA hydroxylase ten-eleven translocation 1 (TET1), TET2, and TET3. Our study found that advanced maternal age could impair myelination in the hippocampus and corpus callosum of offspring. Ascorbic acid intervention may induce TET1 and TET2-mediated hydroxymethylation to ameliorate myelination disorders, promote myelination and maturation, and reverse the effects of advanced maternal age on offspring.
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The cerebrospinal fluid-contacting nucleus(CSF-contacting nucleus) is a pair of unique nuclei in the brain parenchyma which has long been demonstrated to play an important role in pain signal processing. However, the mechanisms by which the CSF-contacting nucleus intervenes in pain is unclear. The NRG1-ErbB4 signaling plays an important role in the nervous system and has been shown to be involved in the regulation of pain. ⋯ With immunofluorescence staining and Western blot, the NRG1-ErbB4 signaling in the CSF-contacting nucleus showed upregulated during the acute pain phase. And, activating NRG1-ErbB4 signaling in the CSF-contacting nucleus specifically by intracranial injection of drugs, the naïve mice displayed thermal hyperalgesia while inhibiting this signaling by intracranial injection could reverse the hyperalgesia caused by CSF-contacting nucleus activation, and execute an analgesic effect during the painful phase in mice. Our study suggested that the CSF-contacting nucleus plays a regulatory role in thermal pain in mice via NRG1-ErbB4 signaling.
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Microglia polarization plays a crucial role in inflammatory injury of brain following intracerebral hemorrhage (ICH). Heme oxygenase-1 (HO-1) has demonstrated protective properties against inflammation and promote hematoma clearance after ICH. The objective of this study was to explore impacts of HO-1 on microglia polarization and phagocytosis after ICH, along with the underlying mechanism. ⋯ Therefore, our data demonstrated that HO-1 alleviated nerve injury and induced M2 polarization and phagocytosis of microglia after ICH via inhibiting NF-κB signaling pathway, which could provide deepen the pathological understanding of ICH and provide potential intervention targets and drug candidate for ICH.