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The association between serum 25-hydroxyvitamin D [25(OH)D] and type 2 diabetes mellitus (T2DM) remains inconclusive. Moreover, whether inflammatory biomarkers are involved in this association has not been explored. This study aims to investigate serum 25(OH)D in relation to T2DM in a Chinese population and provide clues for the inflammatory mechanism whereby serum 25(OH)D deficiency increases T2DM risk. A cross-sectional study of 47,803 participants aged 18–96 years was performed in a health management center in 2017. Multivariate linear or logistic regression models and mediation analysis were used to examine the relationships between serum 25(OH)D, inflammatory biomarkers (white blood cell counts and mean platelet volume), and T2DM. Of the 47,803 participants included, 5.2% were diabetic and 51.4% were serum 25(OH)D deficient. The study revealed a significant inverse association between serum 25(OH)D and T2DM risk after adjustment for potential confounders (P for trend = 0.002); the multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) across serum 25(OH)D levels (sufficiency, insufficiency, and deficiency) were 1.00 (reference), 1.17 (1.03–1.33), and 1.25 (1.09–1.43), respectively. This study also showed a significant indirect effect of serum 25(OH)D on T2DM risk through total white blood cell count, neutrophil count, lymphocyte count, and monocyte count (P values < 0.05); the proportions mediated were 9.89%, 7.51%, 2.94%, and 2.82%, respectively. Serum 25(OH)D deficiency was independently associated with an elevated risk of T2DM in a Chinese adult population and low-grade systemic inflammation might be one of its biological mechanisms. [ABSTRACT FROM AUTHOR]

This longitudinal cross-lagged research attempts to examine the directions of relations between Internet addiction and both internalizing and externalizing problems, with attention to the potential moderating effects of peer relationships and gender. 897 Chinese junior middle school students (56.97% boys, M age = 12.73 years, SD = 0.42) completed self-reported Internet addiction, depressive symptoms, and peer-nominated aggressive behavior at two time points, one year apart, as well as self-reported friend support/conflict and positive/delinquent peers at baseline. Cross-lagged panel analyses revealed that adolescents' Internet addiction would elevate both depressive symptoms and aggressive behavior over time, rather than vice versa. Furthermore, friend conflict (rather than support) moderated these unidirectional relationships that when individuals perceived lower friend conflict, these links were no longer significant. Moreover, similar results were found for adolescents who possessed more positive peers or fewer delinquent peers. In addition, gender differences were found that addicted boys were more vulnerable to aggressive behavior, while addicted girls were more vulnerable to depressive symptoms. These findings suggest that establishing and maintaining good peer social networks would help adolescents keep away from the harmful impacts of Internet overuse on maladjustment. • Adolescents' Internet addiction would elevate both depressive symptoms and aggressive behavior over time, but not vice versa. • Peer relationships played salutary roles in the effects of Internet addiction on internalizing and externalizing problems. • Higher friend conflict would make addicted adolescents more vulnerable to internalizing and externalizing problems. • Affiliation with more positive peers or less delinquent peers protected addicted adolescents from aggressive behavior. • Due to overindulge in the Internet, boys were prone to aggression, whereas girls were prone to depression. [ABSTRACT FROM AUTHOR]

Family violence as an inducing factor of depressive symptoms has been confirmed in previous studies. However, the mechanisms underlying this association are not well understood, particularly in Chinese adolescents. Guided by the social-ecological diathesis-stress model, this three-wave longitudinal study aimed to examine the effects of an individual's cognitive vulnerabilities (rejection-sensitivity anxiety and negative cognitive error) and positive societal contexts (peer support) on the link between family violence and depressive symptoms in Chinese society. A total of 859 Chinese adolescents (44.35 % female; M age = 12.73, SD = 0.43 at baseline) completed self-reporting surveys that assessed variables associated with study and peer-nominated peer support. The results showed that family violence increased the incidence of depressive symptoms in adolescents after two years, resulting in rejection-sensitivity anxiety and negative cognitive error. Surprisingly, higher self-reported peer support, although not peer-nominated support, exacerbated rather than mitigated this indirect effect, supporting the reverse stress-buffering model and extending the healthy context paradox. Most of the measures were based on participants' self-reports. These results emphasize the importance of individual cognition and societal contexts in adolescents with traumatic experiences and provide empirical evidence for the intervention and clinical treatment of depressive symptoms. • The experience of family violence at baseline significantly predicted adolescent depressive symptoms two years later. • Family violence increased adolescent depressive symptoms 2 years later via cognitive vulnerabilities. • Higher self-reported peer support exacerbated this indirect effect between family violence and depressive symptoms. [ABSTRACT FROM AUTHOR]

• Heterozygous UGT1A1*28 and *6 or homozygous UGT1A1*28 results in Chinese Han with GS. • Single heterozygous UGT1A1*6 or UGT1A1*28 are major genotypes in the non-GS group. • Homozygous UGT1A1*28 is associated with the highest risks of hyperbilirubinemia. • The STB level of GS with the single homozygous UGT1A1*28 is remarkably high. • The distribution of UGT1A1*28, UGT1A1*6, and UGT1A1*7 is related to STB levels. Gilbert's syndrome (GS) is a mild condition characterized by periods of hyperbilirubinemia, which results in variations in the UDP-glucuronosyltransferase 1 (UGT1A1) gene. Variant genotypes of UGT1A1 vary in different populations in the world. The present study aimed to determine the genotype of the UGT1A1 promoter and exon that are related to the serum total bilirubin (STB) level in the Chinese Han population. A total of 120 individuals diagnosed with GS (GS group) and 120 healthy individuals (non-GS group) were enrolled. Routine blood, liver function tests, and antibodies associated with autoimmune liver diseases were assessed. Blood samples were collected for DNA purification. Sequencing of the UGT1A1 promoter and exons was conducted for post segment amplification by PCR. Compound heterozygous UGT1A1*28 and UGT1A1*6 (25/120, 20.83%), single homozygous UGT1A1*28 (24/120, 20.00%) and single heterozygous UGT1A1*6 (18/120, 15.00%) were the most frequent genotypes in the GS group. However, single heterozygous UGT1A1*6 (30/120, 25.00%) and single heterozygous UGT1A1*28 (19/120, 15.83%) were the most frequent genotypes in the non-GS group. Further, the frequencies of single homozygous UGT1A1*28, compound heterozygous UGT1A1*28 and UGT1A1*6, and compound heterozygous UGT1A1*28, UGT1A1*6 and UGT1A1*27 were significantly higher in the GS group than those in the non-GS group. The STB levels of GS patients with the homozygous UGT1A1*28 genotype were remarkably higher than those of patients with other genotypes. Homozygous UGT1A1*28 and heterozygous UGT1A1*6 variants were associated with the highest and lowest risks of hyperbilirubinemia, respectively. Our study revealed that compound heterozygous UGT1A1*28 and UGT1A1*6, or single homozygous UGT1A1*28 are major genotypes associated with GS in Chinese Han people. These findings might facilitate the precise genomic diagnosis of Gilbert's syndrome. [ABSTRACT FROM AUTHOR]