Temperament in infancy and behavioral and emotional problems at age 5.5: The EDEN mother-child cohort.

OBJECTIVE:Early temperamental characteristics may influence children's developmental pathways and predict future psychopathology. However, the environmental context may also shape or interact with infant temperament and indirectly contribute to increased vulnerability to adverse developmental outcomes. The aim of the present study is to explore the long-term contribution of temperamental traits at twelve months of age to the presence of emotional and behavioral problems later in childhood, and whether this association varies with the child's sex, parental separation, family socioeconomic status and maternal depression. METHOD:1184 mother-child pairs from the EDEN mother-child birth cohort study based in France (2003-2011), were followed from 24-28 weeks of pregnancy to the child's fifth birthday. Infant temperament at 12 months was assessed with the Emotionality Activity and Sociability (EAS) questionnaire and behavior at 5.5 years was assessed with the Strengths and Difficulties Questionnaire (SDQ). RESULTS:Emotional temperament in infancy predicts children's overall behavioral scores (β = 1.16, p<0.001), emotional difficulties (β = 0.30, p<0.001), conduct problems (β = 0.51, p<0.001) and symptoms of hyperactivity/inattention (β = 0.31, p = 0.01) at 5.5 years. Infants' active temperament predicts later conduct problems (β = 0.30, p = 0.02), while shyness predicts later emotional problems (β = 0.22, p = 0.04). The association between the child's temperament in infancy and later behavior did not vary with children's own or family characteristics. CONCLUSION:An emotional temperament in infancy is associated with higher levels of emotional and behavioral difficulties at the age of 5.5 years. Children who show high emotionality early on may require early prevention and intervention efforts to divert possible adverse developmental pathways

Child, mother and family characteristics of EDEN cohort study participants (n = 1903).

<p>Child, mother and family characteristics of EDEN cohort study participants (n = 1903).</p

Temperament at 12 months and children’s overall behavioral score at age 5.5 years in the EDEN cohort study- moderation analyses.

<p>Temperament at 12 months and children’s overall behavioral score at age 5.5 years in the EDEN cohort study- moderation analyses.</p

Temperament at 12 months and children’s behavioral scores at age 5.5 years in the EDEN cohort study stepwise linear regression models (n = 1184, 2003–2011 France, β, 95% CI, p-value).

<p>Temperament at 12 months and children’s behavioral scores at age 5.5 years in the EDEN cohort study stepwise linear regression models (n = 1184, 2003–2011 France, β, 95% CI, p-value).</p

Prevalence and risk factors of frailty among adults living with HIV aged 70 years or older

International audienceObjectives and design:Frailty is a phenotype associated with adverse health outcomes in older persons. It has been evaluated mainly in middle-aged persons with HIV (PWH). The French multicenter prospective ANRS EP66 SEPTAVIH study aimed to assess frailty prevalence and risk factors in PWH aged 70 years or older on antiretroviral treatment (ART) for at least 12 months.Methods:At baseline, Fried frailty phenotype criteria, sociodemographic data, medical/HIV history, functional status, comorbidities, including impaired cognitive function, depression, history of falls, and co-medications were collected. We measured the prevalence of frailty and compared the characteristics of frail versus prefrail and robust participants using univariate (Kruskal-Wallis tests for continuous variables and Chi2tests for categorical variables) and multivariate analyses.Results:Five hundred and ten PWH, mostly male (81.4%), were included with a median age of 73 years. The median HIV and ART durations were 22.7 years and 15.7 years, respectively. The prevalence of frailty was 13.5%, and of prefrailty 63.3%. In the multivariate analysis, increasing age [odds ratio (OR) 1.79 for each 5-year increment; 95% confidence interval (CI) 1.32-2.41], deprived socioeconomic status (OR 3.17; 95% CI 1.76-5.70), and multimorbidities (three or more) (OR 2.03; 95% CI 1.06-3.90) were associated with frailty.Conclusion:A low prevalence of frailty was reported (13.5%) in PWH aged 70 years or older, whereas two-thirds of them were prefrail. Age, low socioeconomic status, and multimorbidities, but no HIV-related factors, were associated with frailty, suggesting the need to target these factors to help promoting successful aging in this population

Quantitative Evaluation of Serum Proteins Uncovers a Protein Signature Related to Maturity-Onset Diabetes of the Young (MODY)

Maturity-onset diabetes of the young (MODY) is an inherited monogenic type of diabetes. Genetic mutations in MODY often cause nonsynonymous changes that directly lead to the functional distortion of proteins and the pathological consequences. Herein, we proposed that the inherited mutations found in a MODY family could cause a disturbance of protein abundance, specifically in serum. The serum samples were collected from a Uyghur MODY family through three generations, and the serum proteins after depletion treatment were examined by quantitative proteomics to characterize the MODY-related serum proteins followed by verification using target quantification of proteomics. A total of 32 serum proteins were preliminarily identified as the MODY-related. Further verification test toward the individual samples demonstrated the 12 candidates with the significantly different abundance in the MODY patients. A comparison of the 12 proteins among the sera of type 1 diabetes, type 2 diabetes, MODY, and healthy subjects was conducted and revealed a protein signature related with MODY composed of the serum proteins such as SERPINA7, APOC4, LPA, C6, and F5

Hepatic acetyl CoA links adipose tissue inflammation to hepatic insulin resistance and type 2 diabetes

Impaired insulin-mediated suppression of hepatic glucose production (HGP) plays a major role in the pathogenesis of type 2 diabetes (T2D), yet the molecular mechanism by which this occurs remains unknown. Using a novel in vivo metabolomics approach, we show that the major mechanism by which insulin suppresses HGP is through reductions in hepatic acetyl CoA by suppression of lipolysis in white adipose tissue (WAT) leading to reductions in pyruvate carboxylase flux. This mechanism was confirmed in mice and rats with genetic ablation of insulin signaling and mice lacking adipose triglyceride lipase. Insulin\u27s ability to suppress hepatic acetyl CoA, PC activity, and lipolysis was lost in high-fat-fed rats, a phenomenon reversible by IL-6 neutralization and inducible by IL-6 infusion. Taken together, these data identify WAT-derived hepatic acetyl CoA as the main regulator of HGP by insulin and link it to inflammation-induced hepatic insulin resistance associated with obesity and T2D