Characteristics and risk factors for invasive fungal infection in hospitalized patients with acute-on-chronic hepatitis B liver failure: a retrospective cohort study from 2010 to 2023.

Background and aim: The global burden of invasive fungal infections (IFIs) is emerging in immunologic deficiency status from various disease. Patients with acute-on-chronic hepatitis B liver failure (ACHBLF) are prone to IFI and their conditions are commonly exacerbated by IFI. However, little is known about the characteristics and risk factors for IFI in hospitalized ACHBLF patients. Methods: A total of 243 hospitalized ACHBLF patients were retrospectively enrolled from January 2010 to July 2023. We performed restricted cubic spline analysis to determine the non-linear associations between independent variables and IFI. The risk factors for IFI were identified using logistic regression and the extreme gradient boosting (XGBoost) algorithm. The effect values of the risk factors were determined by the SHapley Additive exPlanations (SHAP) method. Results: There were 24 ACHBLF patients (9.84%) who developed IFI on average 17.5 (13.50, 23.00) days after admission. The serum creatinine level showed a non-linear association with the possibility of IFI. Multiple logistic regression revealed that length of hospitalization (OR = 1.05, 95% CI: 1.02-1.08, P = 0.002) and neutrophilic granulocyte percentage (OR = 1.04, 95% CI: 1.00-1.09, P = 0.042) were independent risk factors for IFI. The XGBoost algorithm showed that the use of antibiotics (SHAP value = 0.446), length of hospitalization (SHAP value = 0.406) and log (qHBV DNA) (SHAP value = 0.206) were the top three independent risk factors for IFI. Furthermore, interaction analysis revealed no multiplicative effects between the use of antibiotics and the use of glucocorticoids (P = 0.990). Conclusion: IFI is a rare complication that leads to high mortality in hospitalized ACHBLF patients, and a high neutrophilic granulocyte percentage and length of hospitalization are independent risk factors for the occurrence of IFI.

STING contributes to lipopolysaccharide-induced tubular cell inflammation and pyroptosis by activating endoplasmic reticulum stress in acute kidney injury.

Recently, innate immunity and inflammation were recognized as the key factors for acute kidney injury (AKI) caused by sepsis, which is closely related to high mortality. Stimulator of interferon genes (STING) has emerged as a critical component of innate immune and inflammatory responses. However, the role of STING in the pathogenesis of septic AKI remains unclear. This study demonstrated that the STING was significantly activated in tubular cells induced by lipopolysaccharide (LPS) in vivo and in vitro. Tubule-specific STING knockout attenuated LPS-induced renal dysfunction and pathological changes. Mechanistically, the STING pathway promotes NOD-like receptor protein 3 (NLRP3) activation. STING triggers endoplasmic reticulum (ER) stress to induce mitochondrial reactive oxygen species (mtROS) overproduction, enhancing thioredoxin-interacting protein activation and association with NLRP3. Eventually, the NLRP3 inflammasome leads to tubular cell inflammation and pyroptosis. This study revealed the STING-regulated network and further identified the STING/ER stress/mtROS/NLRP3 inflammasome axis as an emerging pathway contributing to tubular damage in LPS-induced AKI. Hence, targeting STING may be a promising therapeutic strategy for preventing septic AKI.

How marital events explain the suicide rate among Chinese.

AIMS: The aims for this study was to prove the impacts of marital events (marriage rate, divorce rate and marriage squeeze), economic development, and social development on the suicide rate among urban and rural Chinese and reveal the differences in these impacts between urban and rural areas and between genders. METHODS: An explanatory time-series analysis methodology was adopted to analyze the nation-wide data ranging from 1987-2017. RESULTS: Marriage rate was a protective factor against the suicide rate among urban and rural men, and rural women; however, divorce rate was a protective factor against the suicide rate only among rural women. For the four groups, the economic development level measured by per capita GDP is a protective factor, while social development measured by urbanization and rural-urban labor migration rates in rural areas plays different roles. CONCLUSIONS: Marriage and divorce rates were found to have different meanings for the four groups. This study offers a reference for designing relevant policies and projects to intervene in suicidal behaviors among different groups.

Health perceptions and attitudes on mobile health apps in China.

Since the COVID-19 pandemic, the use of mobile health apps has been increasing significantly. Many have started using mobile health apps to manage their health and well-being. People need to develop healthy habits that will increase their job productivity, life expectancy and improve their social relationships. This study tests the Health Belief Model with adults in China in influencing health motivation and in turn improving their health behavior. A mobile and online survey was developed, and 120 usable responses were collected. A structural equation modeling was used to test the relationships between perceived benefits, perceived susceptibility, perceived barriers, health motivation, and health behavior. We found perceived self-efficacy, perceived benefits, and perceived susceptibility predicts health motivation, and health motivation predicts health behavior. We did not find that perceived barrier is a predictor for health motivation. We conclude that to encourage behavioral change, it is important to enhance self-efficacy and address the benefits; in the meantime, educating people on susceptibility is also important.

A mutation in TBXT causes congenital vertebral malformations in humans and mice.

T-box transcription factor T (TBXT; T) is required for mesodermal formation and axial skeletal development. Although it has been extensively studied in various model organisms, human congenital vertebral malformations (CVMs) involving T are not well established. Here, we report a family with 15 CVM patients distributed across four generations. All affected individuals carry a heterozygous mutation, T c.596A>G (p.Q199R), which is not found in unaffected family members, indicating co-segregation of the genotype and phenotype. In vitro assays show that T p.Q199R increases the nucleocytoplasmic ratio and enhances its DNA-binding affinity, but reduces its transcriptional activity compared to the wild-type. To determine the pathogenicity of this mutation in vivo, we generated a Q199R knock-in mouse model that recapitulates the human CVM phenotype. The heterozygous Q199R mice show subtle kinked or shortened tails, while the homozygous mice exhibit tail filaments and severe vertebral deformities. Overall, we show that the Q199R mutation in T causes CVM in humans and mice, providing new evidence supporting the function of T in the genetic etiology of human CVM.

Volatility Parametrization of Low-Volatile Components of Ambient Organic Aerosols Based on Molecular Formulas.

Evaluating the volatility of organic compounds based solely on their molecular formulas would avoid tough demands in deriving molecular structures. Here, we deployed an iodide-adduct Long Time-of-Flight Chemical Ionization Mass Spectrometry (LToF-CIMS) combined with a Filter Inlet for Gases and AEROsols (FIGAERO) to investigate molecular formulas and thermograms of organic compounds on ambient particulate samples collected in the summer of 2021 in a suburban site of Shanghai and to estimate saturation vapor pressures of low- and semivolatile components of ambient organic aerosols. Then, a hierarchical cluster analysis and a subsequent classification of obtained clusters by similarity calculation were applied to the measured data set of molecular formulas and saturation vapor pressures of organic aerosols with at least a 2/3 appearance frequency, together with a similar data set collected at a rural site in the Beijing-Tianjin-Hebei region during the winter of 2018 (Ren et al., 2018), to classify all compounds into multiple groups. For each group of compounds, parametrizations between volatility and elemental composition were derived, and then relationships between each group of parameters and the mean O:C were established to achieve a volatility-molecular formula parametrization with the O:C as a key input. Statistical comparison of estimated volatilities of low-volatile organic compounds shows a much better performance of our parametrization than previous molecular formula-based ones.

PFKFB3 downregulation aggravates Angiotensin II-induced podocyte detachment.

Podocytes play a critical role in maintaining normal glomerular filtration, and podocyte loss from the glomerular basement membrane (GBM) initiates and worsens chronic kidney disease (CKD). However, the exact mechanism underlying podocyte loss remains unclear. Fructose-2,6-biphosphatase 3 (PFKFB3) is a bifunctional enzyme that plays crucial roles in glycolysis, cell proliferation, cell survival, and cell adhesion. This study aimed to determine the role of PFKFB3 in angiotensin II (Ang II) kidney damage. We found that mice infused with Ang II developed glomerular podocyte detachment and impaired renal function accompanied by decreased PFKFB3 expression in vivo and in vitro. Inhibition of PFKFB3 with the PFKFB3 inhibitor 3PO further aggravated podocyte loss induced by Ang II. In contrast, activating PFKFB3 with the PFKFB3 agonist meclizine alleviated the podocyte loss induced by Ang II. Mechanistically, PFKFB3 knockdown likely aggravate Ang II-induced podocyte loss by suppressing talin1 phosphorylation and integrin beta1 subunit (ITGB1) activity. Conversely, PFKFB3 overexpression protected against Ang II-induced podocyte loss. These findings suggest that Ang II leads to a decrease in podocyte adhesion by suppressing PFKFB3 expression, and indicates a potential therapeutic target for podocyte injury in CKD.

STING deletion alleviates podocyte injury through suppressing inflammation by targeting NLRP3 in diabetic kidney disease.

An increasing number of studies have shown that immune inflammatory response plays a vital role in diabetic kidney disease (DKD). Nod-like receptor protein 3 (NLRP3) inflammasome-dependent inflammatory response is a key mechanism in the initiation and development of DKD. The stimulator of interferon genes (STING) is an adaptor protein that can drive noninfectious inflammation and pyroptosis. However, the mechanism of STING regulating immune inflammation and the interaction with NLRP3-dependent pyroptosis in high glucose state still remains unclear. This study evaluated the potential role of STING in high glucose (HG)-induced podocyte inflammation response. STING expression was significantly increased in db/db mice, STZ-treated diabetic mice, and HG-treated podocytes. Podocyte-specific deletion of STING alleviated podocyte injury, renal dysfunction, and inflammation in STZ-induced diabetic mice. STING inhibitor (H151) administration ameliorated inflammation and improved renal function in db/db mice. STING deletion in podocytes attenuated the activation of the NLRP3 inflammasome and podocyte pyroptosis in STZ-induced diabetic mice. In vitro, modulated STING expression by STING siRNA alleviated pyroptosis and NLRP3 inflammasome activation in HG-treated podocytes. NLRP3 over-expression offset the beneficial effects of STING deletion. These results indicate that STING deletion suppresses podocyte inflammation response through suppressing NLRP3 inflammasome activation and provide evidence that STING may be a potential target for podocyte injury in DKD.

Ox-LDL aggravates contrast-induced injury of renal tubular epithelial cells.

Hypercholesterolemia can aggravate contrast-induced acute kidney injury, and the exacerbation of renal tubular epithelial cell (RTEC) injury is a major cause. However, the exact mechanisms remain obscure. Mitophagy, a type of autophagy, selectively eliminates damaged mitochondria and reduces mitochondrial oxidative stress, which is strongly implicated in cell homeostasis and acute kidney injury. Oxidized low-density lipoprotein (Ox-LDL) is accumulated in hypercholesterolemia and has a cytotoxic effect. This study aimed to determine whether and how ox-LDL exacerbates contrast-induced injury in RTECs and to further explore whether PINK1/Parkin-dependent mitophagy is involved in this process. Iohexol and ox-LDL were used alone or in combination to treat HK-2 cells. Rapamycin pretreatment was utilized to enhance mitophagy. Cell viability, apoptosis, mitochondrial membrane potential (MMP) and mitochondrial reactive oxygen species (mtROS) were detected by cell counting kit-8, TUNEL staining, JC-1 kit and MitoSOX fluorescence, respectively. The expression of mitophagy-related proteins (including PINK1, Parkin, and so on) and cleaved caspase-3 was confirmed by western blot. Colocalization of MitoTracker-labeled mitochondria and LysoTracker-labeled lysosomes was observed by fluorescence microscopy to evaluate mitophagy. The results of our study showed that ox-LDL aggravated MMP decline, mtROS release and apoptosis in iohexol-treated HK-2 cells, accompanied by a further increased autophagy level. Enhancement of PINK1/Parkin-dependent mitophagy by rapamycin alleviated apoptosis and mitochondrial injury in HK-2 cells in response to iohexol under ox-LDL condition. Therefore, our findings indicate that ox-LDL aggravates contrast-induced injury of RTECs by increasing mitochondrial damage and mitochondrial oxidative stress, which may be associated with the relative insufficiency of PINK1/Parkin-dependent mitophagy.

Exercise-induced endothelial Mecp2 lactylation suppresses atherosclerosis via the Ereg/MAPK signalling pathway.

BACKGROUND AND AIMS: Lactylation, a recently identified post-translational modification (PTM), plays a central role in the regulation of multiple physiological and pathological processes. Exercise is known to provide protection against cardiovascular disease. However, whether exercise-generated lactate changes lactylation and is involved in the exercise-induced attenuation of atherosclerotic cardiovascular disease (ASCVD) remains unclear. The purpose of this study was to investigate the effects and mechanisms of exercise-induced lactylation on ASCVD. METHODS AND RESULTS: Using the high-fat diet-induced apolipoprotein-deficient mouse model of ASCVD, we found that exercise training promoted Mecp2 lysine lactylation (Mecp2k271la); it also decreased the expression of vascular cell adhesion molecule 1 (Vcam-1), intercellular adhesion molecule 1 (Icam-1), monocyte chemoattractant protein 1 (Mcp-1), interleukin (IL)-1ß, IL-6, and increased the level of endothelial nitric oxide synthase (Enos) in the aortic tissue of mice. To explore the underlying mechanisms, mouse aortic endothelial cells (MAECs) were subjected to RNA-sequencing and CHIP-qPCR, which confirmed that Mecp2k271la repressed the expression of epiregulin (Ereg) by binding to its chromatin, demonstrating Ereg as a key downstream molecule for Mecp2k271la. Furthermore, Ereg altered the mitogen-activated protein kinase (MAPK) signalling pathway through regulating the phosphorylation level of epidermal growth factor receptor, thereby affecting the expression of Vcam-1, Icam-1, Mcp-1, IL-1ß, IL-6, and Enos in ECs, which in turn promoted the regression of atherosclerosis. In addition, increasing the level of Mecp2k271la by exogenous lactate administration in vivo also inhibits the expression of Ereg and the MAPK activity in ECs, resulting in repressed atherosclerotic progression. CONCLUSIONS: In summary, this study provides a mechanistic link between exercise and lactylation modification, offering new insight into the anti-atherosclerotic effects of exercise-induced PTM.

IL-22-producing CD3 + CD8- T cells increase in immune clearance stage of chronic HBV infection and correlate with the response of Peg-interferon treatment.

Interleukin (IL)-22 regulates host defense. This study investigated the predominant IL-22-producing cell subsets under HBV associated immune stages. We found circulating IL-22-producing CD3 + CD8- T cells were significantly increased in immune active (IA) stage than those in immunotolerant stage, inactive carrier and healthy controls (HCs). The plasma IL-22 level was higher in IA and HBeAg-negative CHB compared to HCs. Importantly, CD3 + CD8- T cells were identified as the predominant source of plasma IL-22 production. Up-regulated IL-22-producing CD3 + CD8- T cells obviously correlated with the grade of intrahepatic inflammation. The proportions of IL-22-producing CD3 + CD8- T cells were significantly down-regulated after 48 weeks of Peg-interferon treatment, and the differences were of great significance in patients with normalize ALT levels at 48 weeks, rather than those with elevated ALT levels. In conclusion, IL-22 might play a proinflammatory function in. chronic HBV infected patients with active inflammation and Peg-interferon treatment could attenuate the degree of liver inflammation through down-regulating IL-22-producing CD3 + CD8- T cells.

Effects of Caprylic Acid and Eicosapentaenoic Acid on Lipids, Inflammatory Levels, and the JAK2/STAT3 Pathway in ABCA1-Deficient Mice and ABCA1 Knock-Down RAW264.7 Cells.

Our previous studies have found that caprylic acid (C8:0) can improve blood lipids and reduce inflammation levels and may be related to the upregulation of the p-JAK2/p-STAT3 pathway by ABCA1. This study aims to investigate the effects of C8:0 and eicosapentaenoic acid (EPA) on lipids, inflammatory levels, and the JAK2/STAT3 pathway in ABCA1-deficient mice (ABCA1-/-) and ABCA1 knock-down (ABCA1-KD) RAW 264.7 cells. Twenty 6-week ABCA1-/- mice were randomly divided into four groups and fed a high-fat diet, or a diet of 2% C8:0, 2% palmitic acid (C16:0) or 2% EPA for 8 weeks, respectively. The RAW 264.7 cells were divided into the control or control + LPS group, and the ABCA1-KD RAW 264.7 cells were divided into ABCA1-KD with LPS (LPS group), ABCA1-KD with LPS + C8:0 (C8:0 group), and ABCA1-KD with LPS + EPA (EPA group). Serum lipid profiles and inflammatory levels were measured, and ABCA1 and JAK2/STAT3 mRNA and protein expressions were determined by RT-PCR and Western blot analyses, respectively. Our results showed that serum lipid and inflammatory levels increased in ABCA1-/- mice (p < 0.05). After the intervention of different fatty acids in ABCA1-/- mice, TG and TNF-α were significantly lower, while MCP-1 increased significantly in the C8:0 group (p < 0.05); however, LDL-C, TC, TNF-α, IL-6, and MCP-1 levels decreased significantly and IL-10 increased significantly in the EPA group (p < 0.05). In the aorta of ABCA1-/- mice, C8:0 significantly decreased p-STAT3 and p-JAK2 mRNA, while EPA significantly reduced TLR4 and NF-κBp65 mRNA. In the ABCA1-KD RAW 264.7 cells, TNF-α and MCP-1 were increased significantly and IL-10 and IL-1ß were significantly decreased in the C8:0 group (p < 0.05). The protein expressions of ABCA1 and p-JAK2 were significantly higher, and the NF-κBp65 was significantly lower in the C8:0 and EPA groups (p < 0.05). Meanwhile, compared to the C8:0 group, the NF-κBp65 protein expression was significantly lower in the EPA group (p < 0.05). Our study showed that EPA had better effects than C8:0 on inhibiting inflammation and improving blood lipids in the absence of ABCA1. C8:0 may be involved mainly in inhibiting inflammation through upregulation of the ABCA1 and p-JAK2/p-STAT3 pathways, while EPA may be involved mainly in inhibiting inflammation through the TLR4/NF-κBp65 signaling pathway. The upregulation of the ABCA1 expression pathway by functional nutrients may provide research targets for the prevention and treatment of atherosclerosis.

Zebrafish pigment cells develop directly from persistent highly multipotent progenitors.

Neural crest cells are highly multipotent stem cells, but it remains unclear how their fate restriction to specific fates occurs. The direct fate restriction model hypothesises that migrating cells maintain full multipotency, whilst progressive fate restriction envisages fully multipotent cells transitioning to partially-restricted intermediates before committing to individual fates. Using zebrafish pigment cell development as a model, we show applying NanoString hybridization single cell transcriptional profiling and RNAscope in situ hybridization that neural crest cells retain broad multipotency throughout migration and even in post-migratory cells in vivo, with no evidence for partially-restricted intermediates. We find that leukocyte tyrosine kinase early expression marks a multipotent stage, with signalling driving iridophore differentiation through repression of fate-specific transcription factors for other fates. We reconcile the direct and progressive fate restriction models by proposing that pigment cell development occurs directly, but dynamically, from a highly multipotent state, consistent with our recently-proposed Cyclical Fate Restriction model.

Family and social class differences in sports behavior motivation among college students: An empirical study based on the latent class model.

Objective: This article aims to explore the potential categories of college students' sports behavior motivation and the differences between different family social classes on potential categories. Participants: In total, 1,092 college students were investigated in this study. Methods: This article used the "College Students' Sports Behavior Motivation Questionnaire" to survey 1,092 college students using the whole group sampling method. The potential profile analysis method was applied to classify the types of college students' sports behavior motivation and further analyze the characteristics of different family social classes and sports behavior motivation. Results: College students' sports behavior motivation types can be divided into the following four categories: "low motivation type" (0.82%), "healthy appearance type" (11.45%), "healthy fun type" (37.36%), and "high motivation type" (50.37%). The higher the family's social class, the more the sports behavior motivation of college students tends to be healthy appearance, health, fun, and high motivation. The lower the family social class, the more motivational sports behavior of college students tends to be low motivation. The better the perception of health, the higher the probability that college students belong to the high-motivation type. The fewer chronic diseases that college students have are associated with a healthy appearance and high motivation. Conclusion: There is a certain relationship between the type of college students' sports behavior motivation and their family social class. Therefore, in school physical education, we should open all kinds of sports activities according to college students' sports behavior motivation needs and focus on college students with lower family social class in order to intervene precisely on their motivation for sports behaviors, improve participation, and promote the overall health of college students.

Finite-Time Stability of Nonlinear Impulsive Systems With Applications to Neural Networks.

This article studies the problem of finite-time stability (FTS) and finite-time contractive stability (FTCS) for nonlinear impulsive systems, where the possibility of time delay in impulses is fully considered. Some sufficient conditions for FTS/FTCS are constructed in the framework of Lyapunov function methods. A relationship between impulsive frequency and the time delay existing in impulses is established to reveal FTS/FTCS performance. As an application, we apply the theoretical results to finite-time state estimation of neural networks, including time-varying neural networks and switched neural networks. Finally, two illustrated examples are given to show the effectiveness and distinctiveness of the proposed delay-dependent impulsive schemes.

Sirt3 mitigates LPS-induced mitochondrial damage in renal tubular epithelial cells by deacetylating YME1L1.

Acute kidney injury (AKI) is often secondary to sepsis. Increasing evidence suggests that mitochondrial dysfunction contributes to the pathological process of AKI. In this study, we aimed to examine the regulatory roles of Sirt3 in Lipopolysaccharide (LPS)-induced mitochondrial damage in renal tubular epithelial cells (TECs). Sirt3 knockout mice were intraperitoneally injected with LPS, and cultured TECs were stimulated with LPS to evaluate the effects of Sirt3 on mitochondrial structure and function in TECs. Electron microscopy was used to assess mitochondrial morphology. Immunofluorescence staining was performed to detect protein expression and examine mitochondrial morphology. Western blotting was used to quantify protein expression. We observed that LPS increased apoptosis, induced disturbances in mitochondrial function and dynamics, and downregulated Sirt3 expression in a sepsis-induced AKI mouse model and human proximal tubular (HK-2) cells in vitro. Sirt3 deficiency further exacerbated LPS-induced renal pathological damage, apoptosis and disturbances in mitochondrial function and dynamics. On the contrary, Sirt3 overexpression in HK-2 cells alleviated these lesions. Functional studies revealed that Sirt3 overexpression alleviated LPS-induced mitochondrial damage and apoptosis in TECs by promoting OPA1-mediated mitochondrial fusion through the deacetylation of i-AAA protease (YME1L1), an upstream regulatory molecule of OPA1. Our study has identified Sirt3 as a vital factor that protects against LPS-induced mitochondrial damage and apoptosis in TECs via the YME1L1-OPA1 signaling pathway.

The impact of urban spatial environment on COVID-19: a case study in Beijing.

Epidemics are dangerous and difficult to prevent and control, especially in urban areas. Clarifying the correlation between the COVID-19 Outbreak Frequency and the urban spatial environment may help improve cities' ability to respond to such public health emergencies. In this study, we firstly analyzed the spatial distribution characteristics of COVID-19 Outbreak Frequency by correlating the geographic locations of COVID-19 epidemic-affected neighborhoods in the city of Beijing with the time point of onset. Secondly, we created a geographically weighted regression model combining the COVID-19 Outbreak Frequency with the external spatial environmental elements of the city. Thirdly, different grades of epidemic-affected neighborhoods in the study area were classified according to the clustering analysis results. Finally, the correlation between the COVID-19 Outbreak Frequency and the internal spatial environmental elements of different grades of neighborhoods was investigated using a binomial logistic regression model. The study yielded the following results. (i) Epidemic outbreak frequency was evidently correlated with the urban external spatial environment, among building density, volume ratio, density of commercial facilities, density of service facilities, and density of transportation facilities were positively correlated with COVID-19 Outbreak Frequency, while water and greenery coverage was negatively correlated with it. (ii) The correlation between COVID-19 Outbreak Frequency and the internal spatial environmental elements of neighborhoods of different grades differed. House price and the number of households were positively correlated with the COVID-19 Outbreak Frequency in low-end neighborhoods, while the number of households was positively correlated with the COVID-19 Outbreak Frequency in mid-end neighborhoods. In order to achieve spatial justice, society should strive to address the inequality phenomena of income gaps and residential differentiation, and promote fair distribution of spatial environments.

Risky or protective? Online social support's impact on NSSI amongst Chinese youth experiencing stressful life events.

BACKGROUND: This study was designed to investigate potential gender differences in the interrelations between different types of stressful life events and non-suicidal self injury (NSSI) among Chinese youth, as well as to test the direct and moderating impacts of online social support on Chinese students' NSSI engagement under the pressure of different types of stressful life events. METHODS: Based on the data of 2200 students from middle - highschools and universities in Northwestern China, gender difference (male/female binary) in stressful life events, online social support, NSSI and their correlations were analyzed in the study. RESULTS: Among different types of stressful life events, male students were reported to experience a significantly higher impact of punishment and interpersonal relationship than females. Female students only experienced significantly higher learning pressure than males; Gender difference was not indentified in NSSI among youth; Stressful life events related to punishment could significantly predict NSSI engagement among males. Stressful life events related to learning pressures, interpersonal relationships, and adaption were significantly correlated to NSSI engagement among females; Online social support didn't had a significant direct effect on youth's NSSI, although it did significantly moderate the relationship between specific types of stressful life events (i.e., loss, interpersonal relationships, adaption among males and all types among females) and their NSSI. CONCLUSION: The present study has provided evidence of specified types of stressful life events being risk factors in affecting youth's NSSI: For male students, the higher impacts of stressful life events related to punishment they experienced, the more likely they were about to engage in NSSI. For female students, stressful life events related to learning pressure, interpersonal relationships and adaption were all proved as significant predictors and risky factors of female youth's NSSI; Online social support did not impact on individual's NSSI engagement directly, but moderated it significantly as a protective factor.

A Micro-Level Explanation for Suicidal Ideation Based on Marriage-Squeeze and Social Support Among Rural Men in China.

Higher sex ratio at birth often leads to sex imbalance and a severe squeeze on the marriage market. Up to now, no systematic studies have examined the relationship between marriage squeeze and suicidal ideation among rural men in a context of sex imbalance. Using surveys conducted in Chaohu (Anhui Province) and Ankang (Shaanxi Province) in China, this study analyzed the impact of marriage squeeze and social support on suicidal ideation among rural men. The perceived marriage squeeze significantly and positively affected suicidal ideation and the perceived social support negatively affected suicidal ideation among married and unmarried rural men. Objective social support did not significantly affect suicidal ideation among married men; however, it negatively affected suicidal ideation among unmarried men. Marriage squeeze increased the incidence of suicidal ideation among rural men, but perceived social support acted as a protective factor against suicidal ideation. These findings support the main effect hypothesis of social support. Objective social support is a double-edged sword, which may increase suicidal ideation incidence among rural men. The article ends with the conclusions and limitations of this study.