Background Hypertension in children and adolescents is on the rise worldwide, especially in China. The prevalence of hypertension is related to many factors, such as obesity. In the era of smart phones, it is important to study the negative health effects of mobile phones on blood pressure. The purpose of this study was to investigate the prevalence of hypertension and its association with smartphone addiction among junior school students in China. Methods A school-based cross-sectional study was conducted, including total 2639 junior school students (1218 boys and 1421 girls), aged 12–15 years old (13.18 ± 0.93 years), enrolled in the study by random cluster sampling. Height, weight, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured following standard protocols, and the body mass index (BMI) was calculated. Overweight/obesity and hypertension were defined according to sex- and age-specific Chinese children reference data. The Smartphone Addiction Scale short version (SAS-SV) and the Pittsburgh Sleep Quality Index (PSQI) were used to assess smartphone addiction and sleep quality among the students, respectively. Multivariate logistic regression models were used to seek associations between smartphone addiction and hypertension. Results The prevalence of hypertension and smartphone addiction among participants were 16.2% (13.1% for females and 18.9% for males) and 22.8% (22.3% for females and 23.2% for males), respectively. Obesity (OR = 4.028, 95% CI: 2.829–5.735), poor sleep quality (OR = 4.243, 95% CI: 2.429–7.411), smartphone addiction (OR = 2.205, 95% CI: 1.273–3.820) were significantly and independently associated with hypertension. Conclusions Among the junior school students surveyed in China, the prevalence of hypertension was high, which was related to obesity, poor sleep quality and smartphone addiction. These results suggested that smartphone addiction may be a new risk factor for high blood pressure in adolescents.

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BackgroundTrans-fatty acids (TFAs) occur in small amounts in nature but became widely produced by the food industry. The hazardous effects of different TFA subtypes to human health are controversial. We aimed to evaluate the association of plasma TFAs levels (elaidic acid, vaccenic acid, palmitelaidic acid, and linoelaidic acid) with mortality.MethodsUtilizing 1999–2000 Nutrition Examination Survey (NHANES) and linked mortality data, we performed a cohort study with 1456 participants and used Cox proportional hazards models and penalized smoothing spline plots to elucidate the relationships between TFAs and all-cause, cardiovascular diseases (CVD) and cancer mortality.ResultsDuring 16,034 person-years of follow-up, a total of 221 deaths occurred. In the multivariate model, including mutual adjustment for the 4 TFA subtypes, elaidic acid associated with higher all-cause mortality (hazard ratio (HR) = 2.00, 95% confidence interval (CI) = 1.18 to 3.40, fourth quartiles versus second quartiles) and CVD mortality (HR = 1.64, 95% CI = 1.07 to 2.50, per 10 units increase). Higher palmitelaidic acid levels were associated with increased cancer mortality (HR = 2.91, 95% CI = 1.09 to 7.81, fourth quartiles versus second quartiles). A J-shaped pattern was observed in the regression curve of elaidic acid and all-cause mortality, as well palmitelaidic acid and cancer mortality.ConclusionsPlasma elaidic acid levels are associated with higher risk of all-cause and CVD mortality, and palmitelaidic acid levels are associated with higher cancer mortality in later life. Further studies are needed to investigate current inconsistent results in this field and the possible underlying mechanisms.Electronic supplementary materialThe online version of this article (10.1186/s12944-017-0567-6) contains supplementary material, which is available to authorized users.

Prenatal caffeine exposure (PCE) can induce testicular developmental toxicity. Here, we aimed to explore the underlying mechanism of this process in reference to its intrauterine origin. Pregnant rats were intragastrically administrated caffeine (30 and 120 mg/kg/day) from gestational days 9 to 20. The results showed that the male fetuses exposed to high dose of caffeine (120 mg/kg/day) had a decreased bodyweight and inhibited testosterone synthetic function. Meanwhile, their serum corticosterone concentration was elevated and their testicular insulin-like growth factor 1 (Igf1) expression was decreased. Moreover, the histone 3 lysine 14 acetylation (H3K14ac) level in the Igf1 promoter region was reduced. Low-dose (30 mg/kg/day) caffeine exposure, however, increased steroidogenic enzymes expression in male fetuses. After birth, the serum corticosterone concentration gradually decreased in the PCE (120 mg/kg/day) offspring rats, whereas the expression and H3K14ac level of Igf1 gradually increased, with obvious catch-up growth and testicular development compensation. Intriguingly, when we subjected the offspring to 2 weeks of chronic stress to elevate the serum corticosterone concentration, the expression of Igf1 and testosterone synthesis were inhibited again in the PCE (120 mg/kg/day) group, accompanied by a decrease in the H3K14ac level in the Igf1 promoter region. In vitro, corticosterone (rather than caffeine) was proved to inhibit testosterone production in Leydig cells by altering the H3K14ac level and the expression of Igf1. These observations suggested that PCE-induced testicular developmental toxicity is related to the negative regulation of corticosterone on H3K14ac levels and the expression of Igf1.