Exposure to Chinese famine and the risk of hyperuricemia in later life: a population-based cross-sectional study

BackgroundLimited studies have investigated the relationship between famine exposure and the risk of hyperuricemia in later life. Consequently, the primary purpose of the current study was to examine the potential association between exposure to Chinese famine and hyperuricemia, as well as any gender disparities in this relationship.MethodThe data were obtained from the China PEACE (China Patient-Centered Evaluative Assessment of Cardiac Events) Million Persons Project in Rongchang. The study participants were enrolled into different cohorts based on their birthdates: the fetal-exposed cohort (born between 1959 and 1962), the childhood-exposed cohort (born between 1949 and 1958), the adolescence-exposed cohort (born between 1941 and 1948), and the non-exposed cohorts (born between 1963 and 1974). The potential association between famine exposure and hyperuricemia was assessed using binary logistic regression models.ResultsA total of 6,916 individuals were enrolled in the current study with an average age of 60.11 ± 9.22 years, out of which 3,544 were women. After adjusting for confounding factors, fetal (OR = 0.530, 95% CI: 0.411–0.0.683), childhood (OR = 0.642, 95% CI: 0.494–0.833) exposure to the Chinese famine for men was negatively associated with hyperuricemia. Conversely, exposure to the Chinese famine during fetal (OR = 2.144, 95% CI: 1.622–2.834), childhood (OR = 1.485, 95% CI: 1.105–1.997), and adolescence (OR = 1.967, 95% CI: 1.465–2.641) for women was positively associated with hyperuricemia. Furthermore, the impact of famine on hyperuricemia that has been observed in exposed women might be intensified by the presence of dyslipidemia, abdominal obesity, and overweight/obesity.ConclusionWomen exposed to the Chinese famine during fetal, childhood, and adolescence were positively associated with hyperuricemia, while men exhibited a negative association during fetal and childhood. Additionally, the effect of famine on hyperuricemia in exposed women appears to be intensified by the presence of dyslipidemia, abdominal obesity, and overweight/obesity

A whole-cell bioreporter assay for quantitative genotoxicity evaluation of environmental samples

Whole-cell bioreporters have emerged as promising tools for genotoxicity evaluation, due to their rapidity, cost-effectiveness, sensitivity and selectivity. In this study, a method for detecting genotoxicity in environmental samples was developed using the bioluminescent whole-cell bioreporter Escherichia coli recA::luxCDABE. To further test its performance in a real world scenario, the E. coli bioreporter was applied in two cases: i) soil samples collected from chromium(VI) contaminated sites; ii) crude oil contaminated seawater collected after the Jiaozhou Bay oil spill which occurred in 2013. The chromium(VI) contaminated soils were pretreated by water extraction, and directly exposed to the bioreporter in two phases: aqueous soil extraction (water phase) and soil supernatant (solid phase). The results indicated that both extractable and soil particle fixed chromium(VI) were bioavailable to the bioreporter, and the solid-phase contact bioreporter assay provided a more precise evaluation of soil genotoxicity. For crude oil contaminated seawater, the response of the bioreporter clearly illustrated the spatial and time change in genotoxicity surrounding the spill site, suggesting that the crude oil degradation process decreased the genotoxic risk to ecosystem. In addition, the performance of the bioreporter was simulated by a modified cross-regulation gene expression model, which quantitatively described the DNA damage response of the E. coli bioreporter. Accordingly, the bioluminescent response of the bioreporter was calculated as the mitomycin C equivalent, enabling quantitative comparison of genotoxicities between different environmental samples. This bioreporter assay provides a rapid and sensitive screening tool for direct genotoxicity assessment of environmental samples

Di(2-ethylhexyl) phthalate induces apoptosis through mitochondrial pathway in GC-2spd cells

Di(2-ethylhexyl) phthalate (DEHP), a plasticizer of synthetic polymers, is a well-known endocrine disrupting chemical (EDC) and reproductive toxicant. Addressing the unclear mechanism of DEHP-induced reproductive dysfunction, this study used GC-2spd cells to investigate the molecular mechanism involved in the DEHP-induced toxicity in the male reproductive system. The results indicated that the apoptotic cell death was significantly induced by DEHP exposure over 100 μM. Furthermore, DEHP treatment could induce oxidative stress in GC-2spd cells involving in the decrease of superoxide dismutase (SOD) activity (200 μM) and glutathione peroxidase (GSH-Px) activity (50 and 100 μM). In addition, DEHP induction also caused the elevated ratios of Bax/Bcl-2, release of cytochrome c and decomposition of procaspase-3 and procaspase-9 in GC-2spd cells. Taken together, our work provided the evidence that DEHP exposure might induce apoptosis of GC-2spd cells via mitochondria pathway mediated by oxidative stress. © 2016 Wiley Periodicals, Inc. Environ Toxicol, 2016

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council

The association between atherosclerotic renal artery stenosis and acute kidney injury in patients undergoing cardiac surgery.

BACKGROUND: Atherosclerotic renal artery stenosis (ARAS) and coronary artery disease (CAD) commonly co-exist. Some patients with unidentified ARAS may undergo cardiac surgery. While acute kidney injury (AKI) is a frequent and serious complication of cardiac surgery, we aim to evaluate the influence of ARAS on the occurrence of postoperative AKI in patients with normal or near-normal baseline renal function following cardiac surgery. METHODS: A total of 212 consecutive patients undergoing aortography after coronary angiography and cardiac surgery were retrospectively studied for their preoperative and intraoperative conditions. AKI was defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (≥26.4 µmol/l) or a percentage increase in creatinine of more than or equal to 50% (1.5-fold from baseline) after cardiac surgery. A propensity score-adjusted logistic regression models was used in estimating the effect of ARAS on the risk of postoperative AKI. RESULTS: ARAS (≥50%) was observed in 50 (23.6%) patients, and 83 (39.2%) developed AKI after cardiac surgery. A correlation existed between renal artery patency and preoperative-to-postoperative %ΔCr in patients with ARAS (r = 0.297, P<0.0001). The propensity score-adjusted regression model showed the occurrence of postoperative AKI in patients with ARAS was significantly higher than those without ARAS (OR 2.858, 95% CI 1.260-6.480, P = 0.011). CONCLUSION: ARAS is associated with postoperative AKI in patients with normal or near-normal baseline renal function after cardiac surgery

Association between Self-Reported Global Sleep Status and Prevalence of Hypertension in Chinese Adults: Data from the Kailuan Community

Background: Assessment of sleep only by sleep duration is not sufficient. This cross-sectional study aimed to investigate the potential association of self-reported global sleep status, which contained both qualitative and quantitative aspects, with hypertension prevalence in Chinese adults. Methods: A total of 5461 subjects (4076 of them were male) were enrolled in the current study and were divided into two groups with the age of 45 years as the cut-off value. Sleep status of all subjects was assessed using the standard Pittsburgh Sleep Quality Index (PSQI). Hypertension was defined as blood pressure ≥140/90 mmHg in the current study. Results: After adjusting for basic cardiovascular characteristics, the results of multivariate logistic regression indicated that sleep status, which was defined as the additive measurement of sleep duration and sleep quality, was associated with hypertension prevalence in males of both age groups (odds ratio (OR) = 1.11, 95% confidence interval (CI), 1.07–1.15, p &lt; 0.05; OR = 1.12, 95% CI, 1.08–1.15, p &lt; 0.05) and in females aged ≤45years (OR = 1.10, 95% CI, 1.02–1.18, p &lt; 0.05). As one component of PSQI, short sleep duration was associated with hypertension prevalence only in Chinese male subjects, but this association disappeared after the further adjustment of the other components of PSQI that measured the qualitative aspect of sleep. Conclusion: Association between sleep status and hypertension prevalence in Chinese adults varied by age and sex. Sleep should be measured qualitatively and quantitatively when investigating its association with hypertension

Response to Huang et al. Comments on Lu et al. Association between Self-Reported Global Sleep Status and Prevalence of Hypertension in Chinese Adults: Data from Kailuan Community. Int. J. Environ. Res. Public Health 2015, 12, 488–503

We thank Huang et al. [1] for their interest in reading our article and their time in writing their comments on our work [2]. Our response to their concerns are as follows:[...

The Effect of Home-Based Cardiac Rehabilitation on Functional Capacity, Behavior, and Risk Factors in Patients with Acute Coronary Syndrome in China

Aim: To investigate the effect of home-based cardiac rehabilitation on functional capacity, health behavior, and risk factors in patients with acute coronary syndrome in China. Methods: Eighty patients with acute coronary syndrome were enrolled in this prospective randomized controlled study. Patients in the cardiac rehabilitation group (n=52) received home-based cardiac rehabilitation with a heart manual and a home exercise video for 3 months and patients in the control group (n=28) received only routine secondary prevention. The 6-min walk distance, laboratory test results, healthy behavior (questionnaire), quality of life (12-item Short Form Health Survey), anxiety (7-item Generalized Anxiety Disorder Questionnaire), and depression (9-item Patient Health Questionnaire) were evaluated at the beginning and after treatment for 3 months. Results: Compared with baseline data, 52 patients who participated in cardiac rehabilitation had longer 6-min walk distance (515.26±113.74 m vs 0.445.30±97.92 m, P<0.0002), higher proportions of “always exercise” (78.26% vs. 28%, P<0.05), “always limit food with sugar” (65.22% vs 12%, P<0.05), “always eat fruits 200–400 g every day” (82.61% vs. 4%, P<0.05). and “always eat vegetables 300–500 g every day” (21.74% vs. 12%, P<0.06) after treatment for 3 months. The low-density lipoprotein cholesterol control rate (52.17% vs. 28%, P<0.05) and the systolic blood pressure control rate (100% vs. 68%, P<0.05) were also significantly increased after treatment for 3 months in the cardiac rehabilitation group. No significant increase was found in the control group after treatment for 3 months. No cardiac-event related to home exercise was reported in both groups. Conclusion: Home-based cardiac rehabilitation is a feasible and available cardiac rehabilitation mode in China

Preoperative Medication Use in Patients Undergoing Cardiac Surgery.

<p>ACE: angiotensin-converting enzyme; AKI: acute kidney injury.</p