Aging Us
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There have been an increasing number of functional magnetic resonance imaging (fMRI) reports on brain abnormalities in mild traumatic brain injury (mTBI) at different phases. However, the neural bases and cognitive impairment after acute mTBI are unclear. This study aimed to identify brain functional hubs and connectivity abnormalities in acute mTBI patients and their correlations with deficits in cognitive performance. ⋯ Additionally, acute mTBI showed decreased inflows from the left MFG to bilateral middle temporal gyrus (MTG), left medial superior frontal gyrus (mSFG), and left anterior cingulate cortex (ACC). Correlation analyses revealed that changes in network centrality and causal connectivity were associated with deficits in cognitive performance in mTBI. Our findings may help to provide a new perspective for understanding the neuropathophysiological mechanism of acute cognitive impairment after mTBI.
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An anticorrelated relationship in the spontaneous fluctuations between the default mode network (DMN) and dorsal attention network (DAN) is a robust feature of intrinsic brain organization in healthy individuals. Prior studies have reported a decreased anticorrelation between the DMN and the DAN in Alzheimer's disease (AD) and mild cognitive impairment (MCI). However, it is unclear how this anticorrelation changes as MCI progresses to AD. ⋯ Resting-state functional connectivity analysis revealed that aMCI-s and aMCI-m groups demonstrated different magnitudes of increased anticorrelation between the DMN and DAN relative to the AD group. Furthermore, in aMCI-s, aMCI-m and AD participants, hypoconnectivity was found in specific regions within the DMN, including the precuneus and angular gyrus, and hyperconnectivity was found in areas outside the typical DMN networks, including the middle occipital gyrus, lingual gyrus and visual cortex, which indicated disease-related adaptations of brain networks. Our findings suggest that DMN-DAN anticorrelation may shed light on the understanding of the adaptations in brain function during the progression from MCI to AD and may serve as a potential biomarker to detect AD in the preclinical stage.
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As an important downstream factor in the Hippo pathway, yes-associated protein 1(YAP1) has been detected to be elevated in various cancers and demonstrated to play a role in tumor development. Therefore, we evaluated by a meta-analysis the prognostic value of YAP1 in cancer patients. ⋯ We searched for potential publications in several online databases and retrieved relevant data. Overall and subgroup analyses were performed. Begg's and Egger's tests were used to assess publication bias. Online dataset GEPIA was used to generate the survival curves and verify the prognostic role of YAP1 in patients with tumors.
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Old age is a known risk factor for mortality in acute respiratory distress syndrome (ARDS)/acute lung injury. Mesenchymal stem cells (MSCs) possess potent immunomodulatory properties, while aging MSCs have reduced capacity. Recent studies have demonstrated that MSC-derived extracellular vesicles (MSC-EVs) are able to mimic MSCs in alleviating acute lung injury. ⋯ In addition, the internalization of aging MSC-EVs by macrophages was significantly lower compared with that of young MSC-EVs. Furthermore, aging and young MSC-EVs differed in levels of several miRNAs relating macrophage polarization. In conclusion, aging and young MSC-EVs have differential effects in alleviating acute lung injury and macrophage polarization, which may be associated with internalization of EVs and their miRNA content.
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Long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of gastric cancer; however, their mechanisms of action remain largely unknown. The aim of this study was to identify lncRNAs involved in the tumorigenesis of gastric cancer and to investigate the signaling pathways they affect. Using microarray and RT-qPCR analyses, candidate lncRNAs were screened in paired gastric cancer tissues. ⋯ Using RNA pull-down and mass-spectrometry analyses we found and verified a direct and novel interaction between MIR4435-2HG and desmoplakin (DSP), the most abundant desmosomal protein. Overexpression and knockdown experiments revealed opposing roles for DSP and MIR4435-2HG, unmasking a cascade through which MIR4435-2HG binds to and inhibits DSP, leading to activation of WNT/β-catenin signaling and epithelial-mesenchymal transition in gastric cancer cells. We propose that the MIR4435-2HG/DSP/WNT axis serves as a critical effector of carcinogenesis and progression of gastric cancer, and could be exploited therapeutically to improve patients' outcomes.