Background: Non-suicidal self-injury (NSSI) and depression often co-occur among adolescents with more severe clinical symptoms. This study examined the network structures of NSSI and depressive symptoms in adolescents. Methods: Participants were recruited in the psychiatric outpatient clinics of three tertiary hospitals between April 10 and July 10, 2023. All participants been already found with self-injury behaviors in outpatient when enrolled. NSSI diagnostic criteria and Patient Health Questionnaire-9 (PHQ-9) were utilized to collect NSSI and depressive symptoms separately. We performed a network analysis to visualize the correlation between each symptom and to identify core and bridging symptoms in comorbidities. Results: A total of 248 patients were enrolled in the study, with a mean age of 15.48 (SD = 1.62). Based on the PHQ-9 scores and grades, our results showed that the incidence of depression in adolescents with non-suicidal self-injury behavior was relatively high (N=235, 94.76%), with the majority having severe depression. The network analysis revealed that nodes D-6 “feeling bad, failing or letting yourself or your family down”, D-1 “little interest or pleasure” and D-4 “feeling tired” were the most vital and most central symptoms. The most crucial bridging symptom is the node NSSI-8 “frequent thinking about self-injury”, which connects the NSSI to the depression comorbid network. Conclusion: This study offers a significant symptom-level conceptualization of the association between NSSI and depressive symptoms in a clinical sample of adolescents, which not only enhances our understanding of the comorbid but also identifies potential treatment targets to prevent and treat comorbidity between adolescent NSSI and depression.

This study explored the relationship between body temperature and adverse outcomes in patients with heat stroke to identify the optimal target body temperature within the first 24 h. This retrospective, multicentre study enrolled 143 patients admitted to the emergency department and diagnosed with heat stroke. The primary outcome was the in-hospital mortality rate, while secondary outcomes included the presence and number of damaged organs and neurological sequelae at discharge. A body temperature curve was built using a generalized additive mixed model, and the association between body temperatures and outcomes was established by logistic regression. The threshold and saturation effects were used to explore the targeted body temperature management. Cases were divided into the surviving and non-surviving groups. The cooling rate within the first 2 h was significantly higher in the survival group than the non-survival group (β: 0.47; 95% confidence interval [CI]: 0.09–0.84; P = 0.014), while the non-survival group exhibited a lower body temperature within 24 h (β: − 0.06; 95% CI: − 0.08 to − 0.03; P ≤ 0.001). Body temperature after 2 h (odds ratio [OR]: 2.27; 95% CI: 1.14–4.50; P = 0.019) and lowest temperature within 24 h (OR: 0.18; 95% CI: 0.06–0.55; P = 0.003) were significantly related to in-hospital mortality rate. When the body temperature at 0.5 h was 38.5–40.0 °C, the number of damaged organs was at its lowest. In patients with heat stroke, both hyperthermia and hypothermia were associated with adverse outcomes. Hence, an accurate body temperature management is required during the early stages of care.

Transient neuronal dysfunction may occur in most brain regions with heatstroke (HS). This study aimed to explore the prognostic significance of initial Glasgow Coma Scale (GCS) scores in HS. Retrospective data regarding HS were obtained from six hospitals. The primary outcome was neurological sequelae at discharge. Secondary outcomes included acute respiratory failure (ARF) and intensive care unit (ICU) admission. Logistic regression models and random forest imputation were used to assess the independent association between GCS score and outcomes. Interaction and stratified analyses of body temperature (BT) at 0.5 hours were also conducted. Receiver operating characteristic curves and decision curve analysis were used to estimate prognostic values. Of 206 patients, 44 (21.36%) had neurological sequelae at discharge. The mean ± standard deviation initial GCS score was 8.17 ± 4.05. After adjustment for confounders, GCS, as a continuous variable, was significantly related to neurological sequelae at discharge [odds ratio (OR): 0.65; 95% confidence interval (CI): 0.50–0.85; P = 0.002], ARF (OR: 0.76; 95% CI: 0.66–0.87; P = 0.001), and ICU admission (OR: 0.68; 95% CI: 0.53–0.87; P = 0.003). These relationships were consistent in the random forest imputation cohort. The OR between GCS and neurological sequelae at discharge was much lower (P = 0.048) in participants with BT at 0.5 hours ≤39°C than in those with BT at 0.5 hours >39°C. The GCS and National Early Warning Score (NEWS) had similar prognostic ability for all outcomes, whereas the net benefits were greater with the GCS compared with the NEWS. Initial GCS score was an independent prognostic factor for neurological sequelae at discharge in HS. Rapid cooling played a positive role in this relationship. Brain damage caused by heatstroke (HS) can be transient or result in irreversible injury. Early recognition of those at risk of death or developing neurological complications is very important for improving the outcomes of HS. Initial Glasgow Coma Scale (GCS) score was an independent prognostic factor for neurological sequelae at discharge, acute respiratory failure, and intensive care unit (ICU) admission in HS. Rapid cooling played a positive role in this relationship. The GCS upon emergency department admission can be a useful predictor of prognosis in patients with HS.

Background: Neuroinflammation is a frequent cause of brain damage after intracerebral hemorrhage (ICH). Gut microbiota are reported to regulate neuroinflammation. Berberine has been found to have anti-inflammatory actions, including in the central nervous system. However, it is not known whether berberine regulates neuroinflammation after ICH, nor is the relationship between the antineuroinflammatory actions of berberine and the gut microbiota after ICH understood. Methods: ICH was induced in male mice by collagenase injection. Immunofluorescent staining and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to detect microglia/macrophage phenotypes. Immunofluorescent staining, ELISA, and FITC-dextran were conducted to determine gut function. 16S rRNA sequencing of the fecal material was conducted to determine alterations in the gut microbiota. Antibiotic cocktail treatment and fecal microbiota transplantation (FMT) were used to deplete or restore the gut microbiota, respectively. Cylinder, forelimb placement and wire hanging tests were conducted to evaluate neurobehavioral function. Results: Berberine significantly reduced neuroinflammation and alleviated neurological dysfunction by preventing microglial/macrophage proinflammatory polarization in ICH mice. Berberine also enhanced the function of the intestinal barrier, as shown by reductions in the levels of lipopolysaccharide-binding protein. Neuroinflammation in ICH mice was markedly reduced after transplantation of microbiota from berberine-treated mice, similar to treatment with oral berberine. In addition, a reduction in the microbiota reversed the neuroprotective effect of berberine. Conclusions: Berberine is a potential treatment for ICH-induced neuroinflammation, and its effects are at least partially dependent on the gut microbiota.

Background: Sarcopenia is an age-related syndrome characterized by progressive loss of muscle mass and function. While it is considered a key predictor of adverse health outcomes, comprehensive evidence regarding its long-term impact on functional decline and mortality in community-dwelling older adults remains limited. Objective: To evaluate the longitudinal association between baseline sarcopenia and risks of functional decline and all-cause mortality among community-dwelling older adults, with subgroup analyses based on methods of sarcopenia assessment and domains of functional decline. Methods: We conducted a systematic review and meta-analysis following PRISMA 2020 and MOOSE guidelines. Seven databases were searched from inception to September 30 ^th , 2025. We included cohort studies of older adults aged 60 years and above, with sarcopenia defined by recognized criteria, and reporting effect estimates for functional decline or mortality with follow-up for 1 year or longer. A meta-analysis based on heterogeneity was conducted using either common or random-effects models. Results: A total of 39 studies involving 76151 participants were included. Sarcopenia was significantly associated with an increased risk of all-cause mortality (29 publications, OR = 1.79, 95%CI: 1.55~2.06) and functional decline (16 publications, OR = 1.90, 95%CI: 1.55~2.32). Subgroup analyses revealed consistent associations across different muscle mass assessment methods (DXA, BIA, and CT). Notably, sarcopenia was associated with both physical (OR = 1.91, 95%CI: 1.52~2.40) and cognitive/psychological functional decline (OR = 2.03, 95%CI: 1.35~3.05). Heterogeneity was moderate to high but did not substantially alter the results in sensitivity analyses. Conclusion: This meta-analysis confirms that sarcopenia significantly predicts long-term functional decline and mortality in community-dwelling older adults, with robust associations across multiple muscle mass measurement methods and functional domains. These findings highlight the importance of standardized sarcopenia screening and early intervention to mitigate long-term functional impairment and mortality risk in aging populations. Clinical trial registration: PROSPERO (ID CRD42024595362).