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Background Parental rearing is well documented as an important influencing factor of interpersonal sensitivity (IS). However, little research has focused on the extent by which various aspects of parental rearing in fluence IS. This study aimed to analyze the effects of parental rearing on IS, using quantile regression. We analyzed the extent of the influence of parental rearing on IS by quantile regression to provide definitive evidence on the family education of adolescents with IS problems. Methods The multiple cross-sectional studies were conducted among 3345 adolescents from Harbin, China, in 1999, 2006, 2009 and 2016. Furthermore, a multistage sampling method (stratified random cluster) was used to select participants. IS was assessed using a subscale of the Symptom Checklist-90-Revision. Perceived parental rearing was assessed using the Egna Minnen av. Barndoms Uppfostran. The ordinary least squares (OLS) linear regression was used to determine the average effect of parental rearing on IS. The quantile regression was conducted to examine the established associations and to further explain the association. Results Paternal emotional warmth was found to be associated with IS across the quantile, especially after the 0.6 quantiles; however, this association was not found for maternal emotional warmth. Paternal punishment was associated with IS at the 0.22–0.27 and 0.60 quantile; however, maternal punishment had no significant effect on IS. QR method found that paternal overinvolvement was associated with IS at the 0.48–0.65 quantiles, but paternal overprotection was associated with IS across the quantile; however, maternal overinvolvement and overprotection was positively correlated with IS at the 0.07–0.95 quantiles. The correlation between paternal rejection and IS was found at the 0.40–0.75 and > 0.90 quantiles; maternal rejection was associated with IS within the 0.05–0.92 quantiles. Conclusions Parental rearing practices predict different magnitudes of IS at varying levels. This study provides suggestions for parents to assess purposefully and systematically, intervene, and ameliorate adolescent IS problems. We also highlight the role of paternal rearing in children’s IS problems, providing new ideas for family education.

Background: Gliomas are the most malignant tumors of the nervous system. Even though their survival outcome is closely affected by immune-related genes (IRGs) in the tumor microenvironment (TME), the corresponding regulatory mechanism remains poorly characterized.Methods: Specific enhancer RNAs (eRNAs) can be found in tumors, where they control downstream genes. The present study aimed to identify eRNA-regulated IRGs, evaluate their influence on the TME, and use them to construct a novel prognostic model for gliomas.Results: Thirteen target genes (ADCYAP1R1, BMP2, BMPR1A, CD4, DDX17, ELN, FGF13, MAPT, PDIA2, PSMB8, PTPN6, SEMA6C, and SSTR5) were identified and integrated into a comprehensive risk signature, which distinguished two risk subclasses. Discrepancies between these subclasses were compared to explore potential mechanisms attributed to eRNA-regulated genes, including immune cell infiltration, clinicopathological features, survival outcomes, and chemotherapeutic drug sensitivity. Furthermore, the risk signature was used to construct a prognostic tool that was evaluated by calibration curve, clinical utility, Harrell’s concordance index (0.87; 95% CI: 0.84–0.90), and time-dependent receiver operator characteristic curves (AUCs: 0.93 and 0.89 at 3 and 5 years, respectively). The strong reliability and robustness of the established prognostic tool were validated in another independent cohort. Finally, potential subtypes were explored in patients with grade III tumors.Conclusion: Overall, eRNAs were associated with immune-related dysfunctions in the TME. Targeting of IRGs regulated by eRNAs could improve immunotherapeutic/therapeutic outcomes.

Background Large-dose melatonin treatment in animal experiments was hardly translated into humans, which may explain the dilemma that the protective effects against myocardial injury in animal have been challenged by clinical trials. Ultrasound-targeted microbubble destruction (UTMD) has been considered a promising drug and gene delivery system to the target tissue. We aim to investigate whether cardiac gene delivery of melatonin receptor mediated by UTMD technology optimizes the efficacy of clinically equivalent dose of melatonin in sepsis-induced cardiomyopathy. Methods Melatonin and cardiac melatonin receptors in patients and rat models with lipopolysaccharide (LPS)- or cecal ligation and puncture (CLP)-induced sepsis were assessed. Rats received UTMD-mediated cardiac delivery of RORα/cationic microbubbles (CMBs) at 1, 3 and 5 days before CLP surgery. Echocardiography, histopathology and oxylipin metabolomics were assessed at 16–20 h after inducing fatal sepsis. Results We observed that patients with sepsis have lower serum melatonin than healthy controls, which was observed in the blood and hearts of Sprague–Dawley rat models with LPS- or CLP-induced sepsis. Notably, a mild dose (2.5 mg/kg) of intravenous melatonin did not substantially improve septic cardiomyopathy. We found decreased nuclear receptors RORα, not melatonin receptors MT1/2, under lethal sepsis that may weaken the potential benefits of a mild dose of melatonin treatment. In vivo, repeated UTMD-mediated cardiac delivery of RORα/CMBs exhibited favorable biosafety, efficiency and specificity, significantly strengthening the effects of a safe dose of melatonin on heart dysfunction and myocardial injury in septic rats. The cardiac delivery of RORα by UTMD technology and melatonin treatment improved mitochondrial dysfunction and oxylipin profiles, although there was no significant influence on systemic inflammation. Conclusions These findings provide new insights to explain the suboptimal effect of melatonin use in clinic and potential solutions to overcome the challenges. UTMD technology may be a promisingly interdisciplinary pattern against sepsis-induced cardiomyopathy.