AIM OF THE STUDY: The purpose of this study was to determine the in situ cytotoxicity effect P. macrocarpa fruit ethyl acetate fraction (PMEAF) and the underlying molecular mechanism of cell death.
MATERIALS AND METHODS: MDA-MB-231 cells were incubated with PMEAF for 24h. Cell cycle and viability were examined using flow cytometry analysis. Apoptosis was determined using the Annexin V assay and also by fluorescence microscopy. Apoptosis protein profiling was detected by RayBio® Human Apoptosis Array.
RESULTS: The AO/PI staining and flow cytometric analysis of MDA-MB-231 cells treated with PMEAF were showed apoptotic cell death. The cell cycle analysis by flow cytometry analysis revealed that the accumulation of PMEAF treated MDA-MB-231 cells in G0/G1 and G2/M-phase of the cell cycle. Moreover, the PMEAF exert cytotoxicity by increased the ROS production in MDA-MB-231 cells consistently stimulated the loss of mitochondrial membrane potential (∆Ψm) and induced apoptosis cell death by activation of numerous signalling proteins. The results from apoptosis protein profiling array evidenced that PMEAF stimulated the expression of 9 pro-apoptotic proteins (Bax, Bid, caspase 3, caspase 8, cytochrome c, p21, p27, p53 and SMAC) and suppressed the 4 anti-apoptotic proteins (Bcl-2, Bcl-w, XIAP and survivin) in MDA-MB-231 cells.
CONCLUSION: The results indicated that PMEAF treatment induced apoptosis in MDA-MB-231 cells through intrinsic mitochondrial related pathway with the participation of pro and anti-apoptotic proteins, caspases, G0/G1 and G2/M-phases cell cycle arrest by p53-mediated mechanism.
METHODS: A sample of 837 Chinese students in elementary and middle school was collected for this study. The Perceived Stress Scale, the Social Support Scale, the Emotional Intelligence Scale, and the Post-Stress Growth Scale were employed to examine them. The data were analyzed using SPSS 25.0 software.
RESULTS: The results indicate a significant negative association between perceived stress and post-stress growth. Among perceived stress and social support, the former acted as a mediator, while the latter as a moderator. This study sheds light on the post-stress growth of Chinese left-behind children. The findings validated a model of moderated mediation that shows the relationship between perceived stress, emotional intelligence, social support, and post-stress growth.
CONCLUSION: This study confirmed that social support is one of the most important factors among left-behind children, from perceived stress to post-stress growth. Furthermore, the study reveals that emotional intelligence can adjust the relationship between perceived stress and social support to post-stress growth. Therefore, for both family education and school education, the result provides a new direction.
METHODS: We performed a systematic review on all published analyses of LH versus OH for IIH. We identified studies published in 2000 to 2018 from Medline, PubMed, Embase, Google Scholar, and Cochrane databases. We included only studies that compared both surgical techniques on children aged 18 years or younger. Search terms were variations of "incarcerated inguinal hernia," "hernia repair," "laparoscopy," and "child." We categorized complications as major (testicular atrophy, ascending testis, recurrence, iatrogenic visceral injury) and minor (wound infection). Heterogeneity was assessed using I2; meta-analyses were performed using random- or fixed-effects models as appropriate. Weighted mean differences (WMDs) or odds ratios (ORs), with their corresponding 95% confidence intervals (CIs), were used for analysis of continuous and dichotomous variables, respectively. Significance level was at p-value less than 0.05.
RESULTS: Our initial search yielded 549 unique citations. Eight retrospective cohort (RC) studies (584 patients) were included in the final analysis (339 LH, 245 OH). Overall, major complications (eight RC; n = 584; OR = 0.38; 95% CI: 0.17-0.88; p = 0.02) were more common in OH. When each complication was assessed individually, there were no differences between groups. The length of hospital stay in the LH group was shorter than in the OH group (five RC; n = 418; WMD = - 1.39; 95% CI, -2.56 to -0.22; p = 0.02).
CONCLUSION: Laparoscopic repair for IIH is associated with less major complications and shorter hospital stay, but data are limited due to the absence of randomized controlled trials.
METHODS: In contrast, ViTs have demonstrated proficiency in capturing global signal patterns. In light of these observations, we propose a novel approach to enhance AD risk assessment. Our proposition involves a hybrid architecture, merging the strengths of CNNs and ViTs to compensate for their respective feature extraction limitations. Our proposed Dual-Branch Feature Fusion Network (DBN) leverages both CNN and ViT components to acquire texture features and global semantic information from EEG signals. These elements are pivotal in capturing dynamic electrical signal changes in the cerebral cortex. Additionally, we introduce Spatial Attention (SA) and Channel Attention (CA) blocks within the network architecture. These attention mechanisms bolster the model's capacity to discern abnormal EEG signal patterns from the amalgamated features. To make well-informed predictions, we employ a two-factor decision-making mechanism. Specifically, we conduct correlation analysis on predicted EEG signals from the same subject to establish consistency.
RESULTS: This is then combined with results from the Clinical Neuropsychological Scale (MMSE) assessment to comprehensively evaluate the subject's susceptibility to AD. Our experimental validation on the publicly available OpenNeuro database underscores the efficacy of our approach. Notably, our proposed method attains an impressive 80.23% classification accuracy in distinguishing between AD, Frontotemporal dementia (FTD), and Normal Control (NC) subjects.
DISCUSSION: This outcome outperforms prevailing state-of-the-art methodologies in EEG-based AD prediction. Furthermore, our methodology enables the visualization of salient regions within pathological images, providing invaluable insights for interpreting and analyzing AD predictions.
METHODS: Rat CIRI models were established via middle cerebral artery occlusion (MCAO). Primary nerve cells were isolated and cultured in fetal rat cerebral cortex in vitro, and oxygen-glucose deprivation/reperfusion (OGD/R) models of primary nerve cells were induced. After intervention with DN with different concentrations in MCAO rats and OGD/R nerve cells, 2,3,5-triphenyltetrazolium chloride staining was used to quantify cerebral infarction size in CIRI rats. Modified neurological severity score was utilized to assess neurological performance. Histopathologic staining and live/dead cell-viability staining was used to observe apoptosis. Levels of glutathione (GSH), superoxide dismutase (SOD), reactive oxygen species (ROS) and malondialdehyde (MDA) in tissues and cells were detected using commercial kits. DN level in serum and cerebrospinal fluid of MCAO rats were measured by liquid chromatography tandem mass spectrometry. In addition, expression levels of proteins like Kelch like ECH associated protein 1 (Keap1), nuclear factor erythroid 2-related factor 2 (Nfr2) and heme oxygenase 1 (HO-1) in the Nrf2/HO-1 pathway, and apoptosis-related proteins like Cleaved caspase-3, BCL-2-associated X protein (Bax) and B-cell lymphoma-2 (Bcl-2) were determined by Western blot and immunofluorescence.
RESULTS: DN can significantly enhance neurological function recovery by reducing cerebral infarction size and weakening neurocytes apoptosis in MCAO rats. It was further found that DN could improve oxidative stress (OS) injury of nerve cells by bringing down MDA and ROS levels and increasing SOD and GSH levels. Notably, DN exerts its pharmacological influences through entering blood-brain barrier. Mechanically, DN can reduce Keap1 expression while activate Nrf2 and HO-1 expression in neurocytes.
CONCLUSIONS: The protective effect of DN on neurocytes have been demonstrated in both in vitro and in vivo circumstances. It deserves to be developed as a potential neuroprotective agent through regulating the Nrf2/HO-1 signaling pathway to ameliorate neurocytes impairment caused by OS.