Leucocyte telomere length (LTL) has been reported to be linked to ageing, cancer and cardiovascular disease (cVD). this study aimed to explore the association between LtL and cVD risk in a nationally representative sample of U.S. adults. Complex associations, including nonlinearity and interaction, were also examined. A total of 7,378 subjects from the National Health and Nutrition Examination Survey (NHANES) 1999-2002 were collected. Telomere length was detected from DNA samples and expressed as the mean t/S ratio (telomere repeats per single-copy gene). We performed multiple logistic regression models and interactive analysis to explore the associations between LtL and cVD risk by adjusting for potential confounders. We also performed a sensitivity analysis to investigate the robustness of our results. Among all participants, LTL was associated with the risk of CVD (OR = 0.79, 95% CI: 0.63~0.98, P = 0.033) in a linear manner rather than in a nonlinear manner (P = 0.874). Interaction effects of LTL with both education (P = 0.017) and hypertension (P = 0.007) were observed. Furthermore, using subgroup analyses, protective effects of LTL on CVD risk were found in females and in individuals who were college graduates or above, had serum cotinine >10 ng/ml, did not have hypertension, or had normal white blood cell levels. LTL is linearly inversely associated with CVD risk in the general population of the United States. Telomeres are repetitive sequences of nucleotides at the ends of chromosomes that play a role in the maintenance of genic integrity. Telomeres are involved in many physiological processes 1 such as cell senescence 2 and endometrial regeneration 3. Leucocyte telomere length (LTL) is the longest at birth and decreases with age 4. Moreover, the shortening of LTL affects the progression of diseases, including ageing 5,6 , immune dysfunction 7 , post-traumatic stress disorder 8 , diabetes 9 , cardiovascular disease (CVD) 10 , and cancer 5,11. CVD refers to heart and blood vessel abnormalities and is one of the most common causes of noncommunicable disease mortality 12 , accounting for approximately 17.5 million deaths worldwide 13. The United States has the largest number of CVD patients in the world 14. Reportedly, approximately 1,500,000 U.S. adults are affected by CVD each year 15 , and millions of Americans have CVD risk factors 16. Peng et al. found that longer LTL was associated with cardiovascular health (CVH) indices (i.e., a surrogate measure of CVD risk) in American Indians 17. Similarly, Gebreab et al. explored the associations between LTL and CVH and observed similar results in the general U.S. population, especially in females and non-Hispanic whites 18. Another report showed an inverse association between LTL and coronary artery calcification in African Americans 19. A meta-analysis reported an inverse association between LTL and the risk of CVD 10. However, among the general U.S. population, the association between LTL and the risk of CVD remains unclear. In addition, people of different eth...
Background The purpose of this meta‐analysis is to assess the effects of exercise training on quality of life, specific biomarkers, exercise capacity, and vascular function in congenital heart disease ( CHD ) subjects after surgery. Methods and Results We searched the Cochrane Central Register of Controlled Trials, MEDLINE , and EMBASE from the date of the inception of the database through April 2019. Altogether, 1161 records were identified in the literature search. Studies evaluating outcomes before and after exercise training among postoperative patients with congenital heart disease were included. The assessed outcomes were exercise capacity, vascular function, serum NT ‐pro BNP (N‐terminal pro‐B‐type natriuretic peptide) levels and quality of life. We analyzed heterogeneity by using the I 2 statistic and evaluated the evidence quality according to the Grading of Recommendations Assessment, Development, and Evaluation ( GRADE ) guidelines. Nine randomized controlled trials were included. The evidence indicated that exercise interventions increased the one of the quality of life questionnaire score (mean difference=3.19 [95% CI , 0.23, 6.16]; P =0.03; I 2 =39%) from the score before the interventions. However, no alterations in exercise capacity, vascular function, NT‐proBNP or quality of life were observed after exercise training. The results of the subgroup analysis showed that NT‐proBNP levels were lower in the group with exercise training than in the group without exercise training over the same duration of follow‐up. The evidence quality was generally assessed to be low. Conclusions In conclusion, there is insufficient evidence to suggest that physical exercise improves long‐term follow‐up outcomes of congenital heart disease, although it has some minor effects on quality of life.
Objective: Patent ductus arteriosus (PDA) is a congenital heart defect with an unclear etiology that occurs commonly among newborns. Adequately understanding the molecular pathogenesis of PDA can contribute to improved treatment and prevention. Plasma proteins may provide evidence to explore the molecular mechanisms of abnormal cardiac development. Methods: Isobaric tags for relative and absolute quantitation (iTRAQ) proteomics technology was used to measure different plasma proteins in PDA patients (n = 4) and controls (n = 4). The candidate protein was validated by ELISA and Western blot (WB) assays in a larger sample. Validation of the location and expression of this protein was performed in mouse heart sections. Results: There were three downregulated proteins and eight upregulated proteins identified in the iTRAQ proteomics data. Among these, protein disulfide-isomerase A6 (PDIA6) was further analyzed for validation. The plasma PDIA6 concentrations (3.2 ± 0.7 ng/ml) in PDA patients were significantly lower than those in normal controls (5.8 ± 1.2 ng/ml). In addition, a WB assay also supported these results. PDIA6 was widely expressed in mouse heart outflow tract on embryonic day 14.5. Conclusion: Plasma proteomics profiles suggested novel candidate molecular markers for PDA. The findings may allow development of a new strategy to investigate the mechanism and etiology of PDA.
Objective: To determine the neurodevelopmental function in patients with congenital heart disease (CHD) after cardiac surgery and the influence of surgical repair versus transcatheter repair on neurodevelopment.Methods: We searched PUBMED, EMBASE and Cochrane Controlled Trials (Central) in September 2019 by using Medical Subject Headings. We extracted data using a customized data extraction sheet and employed standard methodological procedures as expected by Cochrane. We used a fixed-effect or random-effect model for meta-analysis. Results: We included a total of seven articles. The assessed neurodevelopment outcomes were the full intelligence quotient (full IQ), verbal intelligence quotient (verbal IQ) and performance intelligence quotient (performance IQ). The intelligence quotient was statistically significant after cardiac surgery compared with that of the normal control (full IQ: mean difference = -5.79 [95% CIs -10.14, -1.44], P = 0.009, I2=71%; verbal IQ: mean difference = -4.46 [95% CIs -7.99, -0.93], P = 0.01, I2=56%; performance IQ: mean difference = -7.13 [95% CIs -10.90, -3.35], P =0.0002, I2=64%). The neurodevelopment functions were no different after surgical repair versus transcatheter repair (full IQ: mean difference = 0.19 [95% CIs -4.10, 4.49], P = 0.93, I2=0%; verbal IQ: mean difference = 2.29 [95% CIs -1.60, 6.18], P = 0.25, I2=0%; performance IQ: mean difference = -2.49 [95% CIs -6.49, 1.52], P = 0.22, I2=0%).Conclusion: We found that patients with CHD undergoing cardiac surgery may exhibit a negative effect on neurodevelopment, and there may be no difference in the effects of the two different surgical methods on neurodevelopment.
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