There remains some uncertainty about the magnitude of the associations between elevated blood pressure (BP) in childhood or adolescence and cardiovascular morbidity and mortality in adulthood. We summarized evidence on the long-term impact of elevated BP in childhood or adolescence on cardiovascular morbidity and mortality in adulthood. PubMed and Embase databases were searched up to August 1, 2019, and retrieved studies were reviewed manually. Our systematic review included all eligible prospective cohort studies on the associations between BP status in childhood or adolescence and intermediate markers or hard outcomes of cardiovascular disease in adults, including high pulse wave velocity, high carotid intima-media thickness, left ventricular hypertrophy, and cardiovascular disease (fatal and nonfatal) and total mortality. A total of 19 articles were finally included, and 12 could be synthesized by meta-analysis. Elevated BP in childhood or adolescence was significantly associated, in adulthood, with high pulse wave velocity (3 articles, N=3725; pooled odds ratio [OR], 1.83 [95% CI, 1.39–2.40]); high carotid intima-media thickness (2 articles, N=4152; OR, 1.60 [95% CI, 1.29–2.00]); and left ventricular hypertrophy (2 articles, N=3019; OR, 1.40 [95% CI, 1.20–1.64]). Additionally, our systematic review also shows evidence of associations of elevated BP in youth with cardiovascular disease and mortality in adulthood. In conclusion, our systematic review and meta-analysis confirms that elevated BP in childhood or adolescence is associated with several intermediate markers and hard outcomes of cardiovascular disease in adulthood. These findings emphasize the importance for children and adolescents to have their BP within normal values.

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During plant embryogenesis, once the suspensor organ of the plant embryo has fulfilled its role, it is removed by programmed cell death (PCD). The pro-death cathepsin protease NtCP14 initiates this PCD, but is inhibited by the cystatin NtCYS until the suspensor function is fulfilled.

Long non-coding RNAs (lncRNAs) were playing critical roles in tumorigenesis. However, in prostate cancer, the roles and mechanisms of lncRNAs especially ANRIL were largely unknown. We investigated the effects of ANRIL on the proliferation and migration of prostate cancer cells using CCK-8 assay and Transwell migration assay. Real-time PCR and western blotting assays were used to analyze the levels of ANRIL, let-7a, TGF-β1, p-Smad2 and p-Smad7. Our results showed that ANRIL was significantly overexpressed in prostate cancer tissues compared with corresponding normal tissues. Knockdown of ANRIL significantly inhibited the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. Knockdown of ANRIL significantly decreased the levels of TGF-β1 and p-Smad2, and increased the level of p-Smad7 in prostate cancer LNCap cells. We further found that knockdown of ANRIL significantly enhanced the expression of let-7a, and rescue experiment found that let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. And let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the activity of TGF-β1/Smad signaling pathway in prostate cancer LNCap cells. Taken together, our findings indicated that overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-β1/Smad signaling pathway.