Abstract Background School bullying victimization is associated with increased risk of anxiety in children and adolescents. However, little is known about the role of resilience in this association. The purpose of this study was to investigate the possible mediation by resilience in this association in a large group of Chinese children and adolescents. Methods A population-based cross-sectional study adopting two-stage simple random cluster sampling was implemented in Yunnan province, southwestern China. A comprehensive questionnaire was used to collect information from the participants. Among all the participants, 4624 were included in the final analysis. Descriptive statistics were used to present general characteristics of the study participants. Univariate and multivariate logistic regression models were adopted to estimate crude and adjusted associations among bullying victimization, anxiety, and resilience. A path model was used to analyze the hypothesized mediation by resilience in the association between bullying victimization and anxiety. Results Analytical results of multivariate logistic regression models suggested that bullying victimization was significantly associated with anxiety in Chinese children and adolescents; compared with individuals who had not been bullied, victims of bullying were more likely to experience anxiety symptoms, with an adjusted odds ratio (OR) of 3.02 (95% CI 2.46–3.71). Path analysis revealed a prominent mediating effect of resilience in the association between bullying victimization and anxiety, accounting for 31.89% of the total association. Further analysis indicated that, among the five dimensions of resilience, emotional regulation, interpersonal assistance, and family support were significant mediators, accounting for 30.34%, 10.79%, and 8.35% of the total association. Conclusions Our major findings highlighted the promising role of resilience-based intervention measures in reducing the risk of anxiety associated with school bullying victimization in Chinese children and adolescents. 

/pdf/school-bullying-victimization-associated-anxiety-in-chinese-i9qmue0m.pdf

School bullying victimization-associated anxiety in Chinese children and adolescents: the mediation of resilience

During fibrosis, (myo)fibroblasts deposit large amounts of extracellular matrix proteins, thereby replacing healthy functional tissue. In liver fibrosis, this leads to the loss of hepatocyte function, portal hypertension, variceal bleeding, and increased susceptibility to infection. At an early stage, liver fibrosis is a dynamic and reversible process, however, from the cirrhotic stage, there is significant progression to hepatocellular carcinoma. Both liver-resident macrophages (Kupffer cells) and monocyte-derived macrophages are important drivers of fibrosis progression, but can also induce its regression once triggers of chronic inflammation are eliminated. In liver cancer, they are attracted to the tumor site to become tumor-associated macrophages (TAMs) polarized towards a M2- anti-inflammatory/tumor-promoting phenotype. Besides their role in thrombosis and hemostasis, platelets can also stimulate fibrosis and tumor development by secreting profibrogenic factors and regulating the innate immune response, e.g., by interacting with monocytes and macrophages. Here, we review recent literature on the role of macrophages and platelets and their interplay in liver fibrosis and hepatocellular carcinoma.

Macrophages and platelets in liver fibrosis and hepatocellular carcinoma

The present study retrospectively examined gender differences in bullying and suicidal behaviour (ideation, plan, and attempts) as well as associations between selected risk factors and suicidal behaviour among secondary school Filipino students.The study used a secondary data set from the GSHS developed by the World Health Organization, which was conducted in the Philippines in 2011. Participants included 5290 Filipino students (male N = 2279, female N = 2986). A two-tailed Chi-square of independence was used to test for gender differences and a multivariate logistic regression model explored statistical associations between risk factors and outcome variables.Chi-square results suggested that gender differences were statistically significant for being bullied χ2 (1, N = 2384) = 10.6, p = .001, experiencing suicidal ideation χ2 (1, N = 857) = 61.7, p = .000, making suicide plans χ2 (1, N = 590) = 10.2, p = .001, and suicide attempts χ2 (1, N = 674) = 8.4, p = .004, with females showing higher vulnerability to examined risk factors. The logistic regression model also suggested that adolescents claiming to have no close friends were three to four times more likely to attempt suicide. Other strong predictors of suicidal behaviours were loneliness and getting in trouble due to alcohol consumption.Bullying is an independent yet, not the strongest predictor associated with adolescents' suicidal behaviour in the present study. The strongest predictors of Filipino adolescents' suicidal behaviours in the 2011 cohort included having no close friends, loneliness, anxiety and getting in trouble due to alcohol use among both genders. Peer and mental health support programmes need to be made available and accessible for adolescents in the Philippines. Considering the increase in suicide rates in 2020/2021 among Filipino young adults due to the Coronavirus pandemic, it is suggested that preventing suicidal vulnerability in adolescence can hinder this occurrence later on in the lifetime. 

https://bmcpsychiatry.biomedcentral.com/counter/pdf/10.1186/s12888-022-04085-w

Bullying and other risk factors related to adolescent suicidal behaviours in the Philippines: a look into the 2011 GSHS Survey

Abstract Mitochondria are important for the activation of endothelial cells and the process of angiogenesis. NDUFS8 (NADH:ubiquinone oxidoreductase core subunit S8) is a protein that plays a critical role in the function of mitochondrial Complex I. We aimed to investigate the potential involvement of NDUFS8 in angiogenesis. In human umbilical vein endothelial cells (HUVECs) and other endothelial cell types, we employed viral shRNA to silence NDUFS8 or employed the CRISPR/Cas9 method to knockout (KO) it, resulting in impaired mitochondrial functions in the endothelial cells, causing reduction in mitochondrial oxygen consumption and Complex I activity, decreased ATP production, mitochondrial depolarization, increased oxidative stress and reactive oxygen species (ROS) production, and enhanced lipid oxidation. Significantly, NDUFS8 silencing or KO hindered cell proliferation, migration, and capillary tube formation in cultured endothelial cells. In addition, there was a moderate increase in apoptosis within NDUFS8-depleted endothelial cells. Conversely, ectopic overexpression of NDUFS8 demonstrated a pro-angiogenic impact, enhancing cell proliferation, migration, and capillary tube formation in HUVECs and other endothelial cells. NDUFS8 is pivotal for Akt-mTOR cascade activation in endothelial cells. Depleting NDUFS8 inhibited Akt-mTOR activation, reversible with exogenous ATP in HUVECs. Conversely, NDUFS8 overexpression boosted Akt-mTOR activation. Furthermore, the inhibitory effects of NDUFS8 knockdown on cell proliferation, migration, and capillary tube formation were rescued by Akt re-activation via a constitutively-active Akt1. In vivo experiments using an endothelial-specific NDUFS8 shRNA adeno-associated virus (AAV), administered via intravitreous injection, revealed that endothelial knockdown of NDUFS8 inhibited retinal angiogenesis. ATP reduction, oxidative stress, and enhanced lipid oxidation were detected in mouse retinal tissues with endothelial knockdown of NDUFS8. Lastly, we observed an increase in NDUFS8 expression in retinal proliferative membrane tissues obtained from human patients with proliferative diabetic retinopathy. Our findings underscore the essential role of the mitochondrial protein NDUFS8 in regulating endothelial cell activation and angiogenesis. 

The requirement of the mitochondrial protein NDUFS8 for angiogenesis

Proteolysis, an irreversible post-translational modification catalyzed by proteases, plays a crucial role in various biological processes. Exploring abnormally hydrolyzed proteins in pathological tissues is a valuable approach for elucidating the mechanisms underlying disease development. Herein, we have developed a cleavable 2-pyridinecarboxyaldehyde probe (2PCA-Probe) that enables efficient and in-depth N-terminomics detection, addressing limitations of previous methods. Furthermore, we unexpectedly discovered a new marker capable of identifying N-terminal chemical labeling with the 2PCA-Probe and elucidated the reaction mechanism. Using this probe, we identified 4686 N-terminal peptides in colorectal cancer and adjacent tissues, significantly expanding the depth of the N-terminome and revealing the potential role of abnormal protein hydrolysis in colorectal cancer development. 

Advancing In-Depth N-Terminomics Detection with a Cleavable 2-Pyridinecarboxyaldehyde Probe

School bullying associated suicidal risk in children and adolescents from Yunnan, China: the mediation of social support

NADH:ubiquinone oxidoreductase core subunit S8 (NDUFS8) is an essential core subunit and component of the iron-sulfur (FeS) fragment of mitochondrial complex I directly involved in the electron transfer process and energy metabolism. Pathogenic variants of the NDUFS8 are relevant to infantile-onset and severe diseases, including Leigh syndrome, cancer, and diabetes mellitus. With over 1000 nuclear genes potentially causing a mitochondrial disorder, the current diagnostic approach requires targeted molecular analysis, guided by a combination of clinical and biochemical features. Currently, there are only several studies on pathogenic variants of the NDUFS8 in Leigh syndrome, and a lack of literature on its precise mechanism in cancer and diabetes mellitus exists. Therefore, NDUFS8-related diseases should be extensively explored and precisely diagnosed at the molecular level with the application of next-generation sequencing technologies. A more distinct comprehension will be needed to shed light on NDUFS8 and its related diseases for further research. In this review, a comprehensive summary of the current knowledge about NDUFS8 structural function, its pathogenic mutations in Leigh syndrome, as well as its underlying roles in cancer and diabetes mellitus is provided, offering potential pathogenesis, progress, and therapeutic target of different diseases. We also put forward some problems and solutions for the following investigations.

/pdf/emerging-roles-of-ndufs8-located-in-mitochondrial-complex-i-30tkm4y9.pdf

Emerging Roles of NDUFS8 Located in Mitochondrial Complex I in Different Diseases

Abstract Background Nonalcoholic steatohepatitis (NASH) is an advanced form of chronic fatty liver disease, which is a driver of hepatocellular carcinoma. However, the roles of the C5aR1 in the NASH remain poorly understood. Here, we aimed to investigate the functions and mechanisms of the C5aR1 on hepatic inflammation and fibrosis in murine NASH model. Methods Mice were fed a normal chow diet with corn oil (ND + Oil), a Western diet with corn oil (WD + Oil) or a Western diet with carbon tetrachloride (WD + CCl 4 ) for 12 weeks. The effects of the C5a–C5aR1 axis on the progression of NASH were analyzed and the underlying mechanisms were explored. Results Complement factor C5a was elevated in NASH mice. C5 deficiency reduced hepatic lipid droplet accumulation in the NASH mice. The hepatic expression levels of TNFα, IL-1β and F4/80 were decreased in C5-deficient mice. C5 loss alleviated hepatic fibrosis and downregulated the expression levels of α-SMA and TGFβ1. C5aR1 deletion reduced inflammation and fibrosis in NASH mice. Transcriptional profiling of liver tissues and KEGG pathway analysis revealed that several pathways such as Toll-like receptor signaling, NFκB signaling, TNF signaling, and NOD-like receptor signaling pathway were enriched between C5aR1 deficiency and wild-type mice. Mechanistically, C5aR1 deletion decreased the expression of TLR4 and NLRP3, subsequently regulating macrophage polarization. Moreover, C5aR1 antagonist PMX-53 treatment mitigated the progression of NASH in mice. Conclusions Blockade of the C5a–C5aR1 axis reduces hepatic steatosis, inflammation, and fibrosis in NASH mice. Our data suggest that C5aR1 may be a potential target for drug development and therapeutic intervention of NASH. 

/pdf/blockade-of-c5ar1-alleviates-liver-inflammation-and-fibrosis-2u5tgdb7.pdf

Blockade of C5aR1 alleviates liver inflammation and fibrosis in a mouse model of NASH by regulating TLR4 signaling and macrophage polarization.

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School bullying associated suicidal risk in children and adolescents from Yunnan, China: the mediation of social support

Emerging Roles of NDUFS8 Located in Mitochondrial Complex I in Different Diseases

Blockade of C5aR1 alleviates liver inflammation and fibrosis in a mouse model of NASH by regulating TLR4 signaling and macrophage polarization.