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BackgroundHyperuricemia is associated with cardiovascular mortality, but the association of the age at hyperuricemia onset with cardiovascular disease (CVD) and mortality is still unclear.ObjectiveThe purpose of this study was to examine the associations of hyperuricemia onset age with CVD and all-cause mortality.MethodsA total of 82,219 participants free of hyperuricemia and CVD from 2006 to 2015 in the Kailuan study were included. The analysis cohort comprised 18,311 new-onset hyperuricemia patients and controls matched for age and sex from the general population. Adjusted associations were estimated using Cox models for CVD and all-cause mortality across a range of ages.ResultsThere were 1,021 incident cases of CVD (including 215 myocardial infarctions, 814 strokes) and 1459 deaths during an average of 5.2 years of follow-up. Patients with hyperuricemia onset at an age < 45 years had the highest hazard ratios (HRs) (1.78 (1.14–2.78) for CVD and 1.64 (1.04–2.61) for all-cause mortality relative to controls). The HRs of CVD and all-cause mortality were 1.32 (1.05–1.65) and 1.40 (1.08–1.81) for the 45–54 years age group, 1.23 (0.97–1.56) and 1.37 (1.11 to 1.72) for the 55–64 years age group, and 1.10 (0.88–1.39) and 0.88 (0.76–1.01) for the ≥ 65 years age group, respectively.ConclusionsThe age at hyperuricemia onset was identified as an important predictor of CVD and all-cause mortality risk, and the prediction was more powerful in those with a younger age of hyperuricemia onset.Graphic abstractEarly onset of hyperuricemia is associated with increased cardiovascular disease and mortality risk.

Obesity is associated with abnormal repolarization manifested by QT interval prolongation, and oxidative stress is an important link between obesity and arrhythmias. However, the underlying electrophysiological and molecular mechanisms remain unclear. The aim of this study is to evaluate the role of obesity in potassium current in ventricular myocytes and the potential mechanism of NADPH oxidase 2 (Nox2). We investigated the effect of Nox2 on cardiac repolarization without compromising its expression and function in other systems using mice with conditional cardiac-specific deletions of Nox2 (knockout [KO]). Wild-type, KO, and Flox littermate mice were randomized to either the control or high-fat diet (HFD) groups. Surface electrocardiograms were recorded to analyze repolarization in vivo. Whole-cell patch-clamp techniques were used to evaluate the electrophysiological phenotype of isolated myocytes in vitro. Western blotting was performed to assess protein expression levels. Compared with the control mice, the HFD group had a prolonged QTc. The consequences of an HFD were not attributed to delayed rectifier K + and inward-rectifier K + currents but were associated with reduced peak outward K V and fast transient outward K + currents. Downregulated expression of K V 4.2 and KChIP2, comprising functional I to channel pore-forming (α) and accessory (β) subunits, was detected in HFD mice. Nox2-KO reversed the effect of obesity on I peak and I to amplitude. Our data demonstrate that obesity mediates impaired cardiac repolarization in mice, manifested by QTc at the whole organism level and action potential duration at the cellular level, and correlated with Nox2. The electrophysiological and molecular aspects of this phenomenon were mediated by repolarizing outward K + currents.

Background Although obesity has been associated with risk of atrial fibrillation (AF), the associations of variability of obesity measures with AF risk are uncertain, and longitudinal studies among Chinese population are still lacking. We aimed to evaluate the impacts of obesity and variability of body mass index (BMI) and waist circumference (WC) on the risk of atrial fibrillation (AF) in a large Chinese cohort study. Methods A total of 44,135 participants of the Kailuan Study who were free of cancer and cardiovascular disease and underwent three consecutive surveys from 2006 to 2010 were followed for incident AF until 2020. Average BMI and WC over time and variability were calculated. Cox proportional hazards regression models were used to assess hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of obesity and variability in BMI and WC with AF risk. Results During a mean follow-up of 9.68 years, there were 410 cases of incident AF. In multivariable-adjusted models, compared with normal BMI/WC, individuals with general obesity and abdominal obesity had increased risk of AF, with corresponding HRs of 1.73 (95% CI: 1.31–2.30) and 1.38 (95% CI: 1.11–1.60), respectively. The short-term elevation in AF risk persisted for the obese even after adjustment for updated biologic intermediaries and weight. Variability in BMI and WC were not associated with the risk of AF. The restricted cubic spline models indicated significant linear relationships between levels of WC and BMI and risk of AF. Conclusions Elevated levels of BMI and WC were associated with an increased risk of AF, whereas variability in BMI and WC were not. Therefore, achieving optimal levels of BMI and WC could be valuable in AF prevention.

Elevated resting heart rate (RHR) and systolic blood pressure (SBP) are independent risk factors for all-cause mortality in hypertensive patients. However, the association of the visit-to-visit variation (VVV) in SBP and RHR with the risk of mortality in hypertensive patients remains unknown. The aim of this study was to investigate the effects of the VVVs in SBP and RHR on the risk of all-cause mortality. We enrolled 16,602 hypertensive patients from the Kailuan cohort study who underwent three health examinations from 2006 to 2010. The VVVs in SBP and RHR were defined by the coefficient of variation, standard deviation, variability independent of the mean, and average real variability. High variability was defined as the highest quartile of variability. Participants were classified numerically according to the number of high-variability parameters (e.g., a score of 2 indicated high variability in two parameters). Cox proportional hazards models were used to estimate hazard ratios for mortality. High VVVs in SBP and RHR were associated with an increased risk of all-cause mortality in hypertensive patients. In the multivariable-adjusted model comparing a score of 0 with a score of 2, the hazard ratios (95% confidence intervals (CIs)) for all-cause mortality were 1.38 (1.11-1.69), 1.52 (1.24-1.87), 1.32 (1.07-1.63), and 1.43 (1.16-1.75) using the coefficient of variation, standard deviation, variability independent of the mean, and average real variability, respectively. High VVVs in SBP and RHR constituted an independent risk factor for all-cause mortality in hypertensive patients. High VVVs in SBP and RHR additively increased the risk of all-cause mortality in hypertensive patients.

Salinity is one of the major abiotic stresses besides drought and cold stress. The application of plant growth regulators (PGRs) is an effective method to mitigate yield losses caused by salinity. However, we investigated the effects of exogenous regulatory substances (γ-aminobutyric acid (GABA), salicylic acid (SA), and brassinolide (BR) on the growth and development of “Kyoho” grapevine under salt stress. The results showed that exogenous regulators GABA, SA, and BR alleviated the inhibition of grape growth by saline stress and regulated the effects of salinity stress on grape fruit development and quality. All three regulators significantly increased fruit set, cross-sectional diameter, weight per unit, and anthocyanin content. In conclusion, this study provides a theoretical basis for grape production practices by using exogenous aminobutyric acid (GABA), salicylic acid (SA), and brassinolide (BR) to mitigate the hazards of salinity stress.

The clinical characteristics of patients with the comorbidities of hypertension and coronary artery disease (HT-CAD) and atrial fibrillation (AF) are largely unknown. This study aimed to investigate the prevalence of AF in patients with HT-CAD and clinical characteristics of patients with both HT-CAD and AF. This cross-sectional study was conducted in Chinese People's Liberation Army General Hospital in Beijing, China, and included 20,747 inpatients with HT-CAD with or without AF from August 2008 to July 2018. We examined the overall prevalence, clinical characteristics, comorbidity profiles, treatment patterns, and blood pressure (BP) control of patients with both HT-CAD and AF. Multivariate logistic regression was used to investigate the associations of cardiovascular risk factors with AF in patients with HT-CAD. The overall prevalence of AF in patients with HT-CAD was 4.87% (1011/20,747), and this increased with age; to be specific, the prevalence in women and men increased from 0.78% (2/255) and 1.02% (26/2561) at the age of <50 years to 8.73% (193/2210) and 10.28% (298/2900) at the age of ≥70 years, respectively. HT-CAD patients who had AF had a higher prevalence of cardiovascular-related comorbidities than those without AF. Multivariate logistic regression showed that age, gender (male), body mass index, heart failure, and chronic kidney disease were independently associated with the risk of AF in patients with HT-CAD. For those with both HT-CAD and AF, 73.49% (743/1011) had a CHA 2 DS 2 -VASc score of ≥4, and only about half of them had the BP controlled at <140/90 mmHg, which indicated a high risk of thromboembolism and stroke. The use of oral anticoagulation increased during the study period (10.00% [20/200] in 2008 to 2011 vs. 30.06% [159/529] in 2015 to 2018, P  < 0.01), but remained at a relatively low level. AF is highly prevalent among patients with HT-CAD. Patients with both HT-CAD and AF have a higher prevalence of cardiovascular-related comorbidities, lower BP control rate, and lower use of oral anticoagulation.

Background No study has concentrated on the association of LE8 with cancer risk and death. We aim to examine the association of LE8 with death and cancer. Methods A total of 94733 adults aged 51.42 ± 12.46 years and 77551 participants aged 54.09±12.06 years were enrolled in longitudinal and trajectory analysis respectively. Baseline LE8 was divided into three groups based on the American Heart Association criteria and three trajectory patterns by latent mixture models. We reviewed medical records and clinical examinations to confirm incident cancer during the period from 2006 to 2020. Death information was collected from provincial vital statistics offices. Cox models were used. Results 12807 all-cause deaths and 5060 cancers were documented during a 14-year follow-up. Relative to participants with high LE8 at baseline, participants with lower levels of LE8 have a significantly increased risk of mortality and incident cancer. All these risks have an increasing trend with LE8 level decreasing. Meanwhile, the trajectory analysis recorded 7483 all-cause deaths and 3037 incident cancers after approximately 10 years. The associations of LE8 with death and cancer were identical to the longitudinal study. In the subtype cancer analysis, LE8 has a strong effect on colorectal cancer risk. Moreover, the cut point is 56.67 in the association between LE8 and death, while the cut point altered to 64.79 in the association between LE8 and incident cancers. These associations were enhanced among younger adults. Conclusions There was a significant association of LE8 with death and cancer risk, especially for the young population.

(1) Background: Mineral nutrient deficiencies are a major constraint on grapevine growth and productivity, yet the clear identification of deficiency symptoms and their physiological impacts remains challenging. (2) Methods: In this study, ‘Thompson Seedless’ grapevines were grown hydroponically under the controlled omission of ten essential nutrients (N, P, K, Ca, Mg, Fe, Mn, B, Zn, Cu) to assess their impact on growth, leaf morphology, chlorophyll content, photosynthesis, respiration, and tissue nutrient concentrations. (3) Results: Deficiencies in N, P, K, Mn, and B caused distinct leaf symptoms: nitrogen (N) deficiency led to pale leaves with bluish-green veins, phosphorus (P) deficiency caused yellowing in apical leaves followed by interveinal chlorosis, and potassium (K) deficiency induced pale yellow discoloration, curling, and rotting of the leaves. Manganese (Mn) and boron (B) deficiencies showed symptoms such as irregular leaf shapes and brittle, glossy leaves, respectively. These deficiencies resulted in reduced dry matter accumulation, decreased shoot length, and lower chlorophyll content. In contrast, iron (Fe) and copper (Cu) deficiencies had minimal effects, closely resembling those of the control conditions with only slight growth suppression. Notably, N, B, and Mg deficiencies led to significant reductions in Cu, Mg, B, and N levels, particularly evident through distinct symptoms in newly formed leaves. (4) Conclusions: Deficiencies in N, P, K, Mg, and B significantly affect grapevine growth, physiological processes, and nutritional quality. These findings emphasize the importance of maintaining balanced mineral nutrition for optimal grapevine health and productivity.

Time in target range (TTR) and blood pressure variability (BPV) of systolic blood pressure (SBP) are independent risk factors for major adverse cardiovascular events (MACE) and all‐cause mortality in hypertensive patients. However, the association of the combination of low TTR and high BPV of SBP with the risk of MACE and all‐cause mortality is unclear. This study sought to investigate the combined effect of the TTR and BPV on the risk of MACE and all‐cause mortality in patients with hypertension. A total of 11 496 hypertensive patients from the Kailuan cohort study were included in our study. All participants were divided into four groups according to their TTR and BPV levels. Cox proportional hazards regression models were used to calculate the hazard ratios (HRs) and 95% confidence interval (CI) for incident MACE and all‐cause mortality. During a median follow‐up of 5.64 years, 839 MACEs (included 99 cases of myocardial infarction, 591 cases of stroke, and 191 cases of heart failure) and 621 deaths occurred. Compared with the high‐TTR and low‐BPV group, the HRs (95% CI) of MACE and all‐cause mortality were 1.309 (1.025–1.671) and 1.842 (1.373–2.473) for the high‐TTR and high‐BPV group, 1.692 (1.347–2.125) and 1.731 (1.298–2.309) for the low‐TTR & low‐BPV group, 2.132 (1.728–2.629) and 2.247 (1.722–2.932) for the low‐TTR & high‐BPV group. Our study suggests that the combination of low TTR and high BPV of SBP was associated with a higher risk of MACE and all‐cause mortality in patients with hypertension.

Obesity is associated with abnormal repolarization manifested by QT interval prolongation, and oxidative stress is an important link between obesity and arrhythmias. However, the underlying electrophysiological and molecular mechanisms remain unclear. The aim of this study is to evaluate the role of obesity in potassium current in ventricular myocytes and the potential mechanism of NADPH oxidase 2 (Nox2). We investigated the effect of Nox2 on cardiac repolarization without compromising its expression and function in other systems using mice with conditional cardiac-specific deletions of Nox2 (knockout [KO]). Wild-type, KO, and Flox littermate mice were randomized to either the control or high-fat diet (HFD) groups. Surface electrocardiograms were recorded to analyze repolarization in vivo. Whole-cell patch-clamp techniques were used to evaluate the electrophysiological phenotype of isolated myocytes in vitro. Western blotting was performed to assess protein expression levels. Compared with the control mice, the HFD group had a prolonged QTc. The consequences of an HFD were not attributed to delayed rectifier K.sup.+ and inward-rectifier K.sup.+ currents but were associated with reduced peak outward K.sub.V and fast transient outward K.sup.+ currents. Downregulated expression of K.sub.V 4.2 and KChIP2, comprising functional I.sub.to channel pore-forming ([alpha]) and accessory ([beta]) subunits, was detected in HFD mice. Nox2-KO reversed the effect of obesity on I.sub.peak and I.sub.to amplitude. Our data demonstrate that obesity mediates impaired cardiac repolarization in mice, manifested by QTc at the whole organism level and action potential duration at the cellular level, and correlated with Nox2. The electrophysiological and molecular aspects of this phenomenon were mediated by repolarizing outward K.sup.+ currents.