Explore the vast range of titles available.

Sodium intake shows a positive correlation with blood pressure, resulting in an increased risk for cardiovascular diseases (CVD). Salt reduction is a key step toward the WHO's goal of 25% reduction in mortality from non‐communicable diseases (NCDs) by 2025. This study aims to assess the current condition and temporal changes of the global CVD burden due to high sodium intake (HSI). We extracted data from the Global Burden of Disease (GBD) study 2019. The numbers and age‐standardized rates of mortality and disability‐adjusted life‐years (DALYs), stratified by location, sex, and socio‐demographic Index (SDI), were used to assess the high sodium intake attributable CVD burden from 1990 to 2019. The relationship between the DALYs rates and related factors was evaluated by stepwise multiple linear regression analysis. Globally, in 2019, the deaths and DALYs of HSI‐related CVD were 1.72 million and 40.54 million, respectively, increasing by 41.08% and 33.06% from 1990. Meanwhile, the corresponding mortality and DALYs rates dropped by 35.1% and 35.2%, respectively. The high‐middle and middle SDI quintiles bore almost two‐thirds of CVD burden caused by HSI. And the leading cause of HSI attributable CVD burden was ischemic heart disease. Universal health coverage (UHC) was associated with the DALYs rates after adjustment. From 1990 to 2019, the global CVD burden attributable to HSI has declined with spatiotemporal and sexual heterogeneity. However, it remains a major public health challenge because of the increasing absolute numbers. Improving UHC serves as an effective strategy to reduce the HSI‐related CVD burden.

Albuminuria is strongly associated with the development and progression of cardiovascular disease. We aimed to investigate the association between Life’s Essential 8 (LE8) and albuminuria. The cross-sectional study enrolled 8,648 adults and excluded individuals with incomplete LE8 index data, missing serum creatinine or albumin/creatinine ratio data, and a diagnosis of chronic kidney disease. Albuminuria was defined as urinary albumin to creatinine ratio (uACR) ≥ 30 mg/g. According to the recommendation of the American Heart Association (AHA), the LE8 score was categorized into three groups: high cardiovascular health (CVH), medium CVH, and low CVH. To evaluate the relationship between LE8 and albuminuria, logistic regression and restricted cubic spline models were employed. Of the 8,648 participants, 949 (11.0%) had albuminuria. After adjusting for potential confounding factors, compared with the low CVH group, the moderate CVH group (odds ratio: 0.552; 95% confidence interval: 0.388 to 0.786; P  = 0.001) and high CVH group (OR: 0.253; 95%CI: 0.173 to 0.372; P  < 0.001) showed a significant lower odds of albuminuria, and a significant linear negative association between LE8 scores and uACR levels was observed, as well as a non-linear connection between LE8 score and albuminuria. The prevalence of albuminuria was greater among female individuals across all CVH groups compared to their male counterparts. The LE8 scores exhibited a negative correlation with albuminuria levels. Adhering to optimal cardiovascular health is associated with better kidney health.

Background The triglyceride-glucose index (TyG index) has emerged as a reliable surrogate marker of insulin resistance associated with arterial stiffness. However, most studies were based on a cross-sectional design, and few studies have evaluated the longitudinal impact of the TyG index on arterial stiffness. This study aimed to investigate the associations of single time point measurement and the long-term trajectory of the TyG index with arterial stiffness in a Chinese cohort. Methods Data are derived from the Hanzhong Adolescent Hypertension Cohort study. A total of 2480 individuals who participated in the 2017 survey was included in the cross-sectional analysis. A sample of 180 individuals from the sub-cohort with follow-up data in 2005, 2013, and 2017 was enrolled in the longitudinal analysis. The TyG index was calculated as ln (fasting triglyceride [mg/dL] × fasting glucose [mg/dL]/2), and arterial stiffness was determined using brachial-ankle pulse wave velocity (baPWV). The latent class growth mixture modeling method was used to identify the TyG index trajectories from 2005 to 2017. Results In the cross-sectional analysis, the median age of the study population was 42.8 (39.8, 44.9) years, and 1351 (54.5%) were males. Each one-unit increment in TyG index was associated with a 37.1 cm/s increase (95% confidence interval [CI] 23.7–50.6 cm/s; P  < 0.001) in baPWV, and similar results were observed when the TyG index was in the form of quartiles. In the longitudinal analysis, we identified three distinct TyG index trajectories and found that the highest TyG index trajectory carried the greatest odds of increased arterial stiffness, with a fully adjusted odds ratio (OR) of 2.76 (95% CI 1.40, 7.54). Conclusions Elevated levels of baseline TyG index and higher long-term trajectory of TyG index were independently associated with increased arterial stiffness. Monitoring immediate levels and longitudinal trends of the TyG index may help with the prevention of arterial stiffness in the long run.

MicroRNAs (miRNAs) are small endogenous RNA molecules that play an essential role in various disease processes including elevated blood pressure (BP). Although the effects of dietary salt and potassium intake on BP regulation have been established, their co‐interaction with miRNAs are still unclear. The purpose of the current study was to explore the connection between miRNA gene polymorphisms and BP response to salt and potassium intake, and the relationship between miRNA gene polymorphisms and long‐term BP changes and hypertension development. A total of 333 participants underwent a chronic sodium‐potassium dietary intervention trial, which included a 3‐day normal diet, followed by a 7‐day low‐salt diet, then a 7‐day high‐salt diet, and finally a 7‐day high‐salt with potassium‐supplemented diet. This cohort was subsequently followed for up to 14 years. Single‐nucleotide polymorphisms (SNPs) rs115254818 in miR‐26b‐3p, rs11191676 and rs2292807 in miR‐1307‐5p, and rs4143957 in miR‐382‐5p were significantly correlated with systolic BP (SBP) and mean arterial pressure (MAP) responses to high‐salt intake, whereas rs11191676 and rs2292807 in miR‐1307‐5p exhibited significant associations with SBP response to potassium‐supplemented diet. Furthermore, SNPs rs2070960 in miR‐3620‐5p and rs12364149 in miR‐210‐3p demonstrated significant correlations with diastolic BP and MAP alterations at 14 years of follow‐up. Generalized linear mixed model analysis revealed a significant association between rs2070960 in miR‐3620‐5p and hypertension development over a 14‐year period. Our study indicates that miRNA gene polymorphisms are pivotal in the salt and potassium sensitivity of BP, as well as in the longitudinal BP progression and hypertension incidence. Trial Registration: ClinicalTrials.gov identifier: NCT02734472

BackgroundAlthough it is well established that obesity is a risk factor for chronic kidney disease, the impact of distinct long-term body mass index (BMI) developmental patterns on renal function in later life is poorly understood.MethodsThis study utilized data derived from the Hanzhong Adolescent Hypertension Cohort, a prospective cohort followed over 30 years. We used latent class growth mixture modeling method to identify the BMI trajectories of participants who had received BMI measurements at least three times from childhood (age: 6–15 years) to adulthood (age: 36–45 years). The modified Poisson regression model was used to identify potential associations between BMI trajectories and subclinical renal damage (SRD) in midlife.ResultsWithin a total of 2162 individuals, we identified four distinct long-term BMI trajectories: stable normal (54.72%), moderately increasing overweight (32.42%), resolving (10.27%), and progressively increasing obese (2.59%). By the latest follow-up in 2017, a total of 257 (13.1%) individuals were diagnosed with SRD. Compared with the stable normal group, the moderately increasing overweight group and the progressively increasing obese group exhibited significantly a higher urinary albumin-to-creatinine ratio and a higher odd of existing SRD in 2017 (risk ratio [RR], 1.70 [95% confidence interval (CI), 1.33–2.19] and 4.35 [95% CI, 3.00–6.30], respectively). However, individuals who resolved their elevated BMI in early life had a similar risk for SRD as those who had never been obese or overweight (RR, 1.17 [95% CI, 0.77–1.79]).ConclusionsChild-to-adult BMI trajectories that worsen or persist at high levels were associated with an increased risk for SRD in midlife. Maintaining a normal BMI or reversing an elevated BMI in early life may be beneficial to renal function over the long term.

Background The sensitive period during which the adult cardiovascular system is particularly vulnerable to body mass index (BMI) changes remains unclear. This study aimed to examine how rates of BMI change from childhood to adulthood influence the risk of subclinical cardiovascular outcomes in mid-adulthood. Methods This cohort study included 2446 participants from the Hanzhong Adolescent Hypertension Study who had at least two BMI measurements in childhood/adolescence (6–18 years) and at least two in adulthood (≥ 19 years). The BMI growth curve from ages 6 to 52 years was modeled using random-effects mixed models with restricted cubic splines. These models yielded age-specific estimates of BMI levels and rates of change, the latter of which were subsequently residual-adjusted for concurrent BMI levels. Multivariable logistic regression models were used to examine the associations of BMI levels and level-adjusted rates of change from 6 to 52 years with left ventricular hypertrophy (LVH) and arterial stiffness in mid-adulthood. Results BMI at each age from 10 to 52 years was associated with mid-adult LVH and arterial stiffness, and these associations became stronger with increasing age at BMI measurement. Additionally, age-level–adjusted rates of BMI change at most ages from childhood to adulthood were positively associated with a higher risk of both subclinical cardiovascular outcomes. However, the odds ratios (ORs) for both LVH and arterial stiffness per 1-SD increase in BMI change rate declined with increasing age. For LVH, the ORs decreased from 2.49 (95% confidence interval (CI): 2.01–3.08) at 6 years to 1.23 (1.01–1.50) at 34 years. Similarly, for arterial stiffness, the ORs decreased from 1.60 (95% CI: 1.41–1.81) at 6 years to 1.13 (1.01–1.27) at 42 years. Of note, from childhood to adolescence, age-level–adjusted rates of BMI change showed stronger associations with LVH and arterial stiffness than contemporaneously measured BMI levels. Conclusions Rapid rates of BMI increase, particularly during childhood/adolescence, are strongly associated with a higher risk of mid-adulthood subclinical cardiovascular outcomes. These findings highlight childhood/adolescence as sensitive periods for the influence of BMI on cardiovascular disease development, emphasizing the need for early prevention and intervention.

Codes on permutations and multi-permutations have been received much attention due to their potential applications in communications and storage systems. This paper proposes two constructions for balanced multi-permutation codes capable of correcting a single burst of deletions of length t and length up to t , respectively. For any target value of t , the first construction is based on the interleaving of t sub-codes on permutations, whereas the second one is based on the interleaving of t + 1 sub-codes on multi-permutations that are arranged in all possible orders using a stabilizer subgroup. The decoding methods are included in proofs and verified by examples. Numerical results show that both constructions can achieve higher code rates than existing ones while maintaining simple interleaving structures.

Background Polymerase delta-interacting protein 2 (Poldip2) is a novel regulator of vascular permeability that has been shown to be involved in aggravating blood–brain barrier (BBB) disruption following stroke; however, the underlying mechanisms are unknown. While endothelial tight junctions (TJ) are critical mediators of BBB permeability, the effect of Poldip2 on TJ function has not been elucidated yet. Here, we aim to define the mechanism by which Poldip2 mediates BBB disruption, specifically focusing on phosphorylation and stabilization of the TJ integral protein ZO-1. Methods and Results Cerebral ischemia was induced in endothelial-specific Poldip2 knockout mice and controls. Cerebral vascular permeability was assessed by Evans blue dye extravasation. Endothelial-specific Poldip2 deletion abolished Evans blue dye extravasation after ischemia induction. In vitro permeability assays demonstrated that Poldip2 knockdown suppressed TNF-α-induced endothelial cell (EC) permeability. Immunofluorescence staining showed that Poldip2 depletion prevented TNF-α-induced ZO-1 disruption at interendothelial junctions. Conversely, Poldip2 overexpression increased endothelial permeability, loss of ZO-1 localization at cell–cell junctions and enhanced reactive oxygen species (ROS) production. Treatment with the antioxidant N-acetyl cysteine (NAC) reduced Poldip2-induced ZO-1 disruption at inter interendothelial junctions. Immunoprecipitation studies demonstrated Poldip2 overexpression induced tyrosine phosphorylation of ZO-1, which was prevented by treatment with NAC or MitoTEMPO, a mitochondrial ROS scavenger. Conclusions These data reveal a novel mitochondrial ROS-driven mechanism by which Poldip2 induces ZO-1 tyrosine phosphorylation and promotes EC permeability following cerebral ischemia. Graphical Abstract

Sodium and potassium intake in hypertensive patients in China is not clear. The authors aimed to investigate the distribution of sodium and potassium intake in hypertensive patients in China, and to analyze the relationship between sodium and potassium intake and blood pressure. The study was performed in 130 hospitals from 23 provinces across China from 2016 to 2019. Finally, 9501 hypertensive patients average aged 54 years were included. 24 h urinary sodium and potassium excretion were measured. Distribution of urinary electrolytes were described according to age, gender and region. The association between urinary electrolytes and blood pressure was analyzed by multivariate linear regression. Hypertensive patients exhibited an average 24 h urinary sodium and potassium excretion of 156.7 ± 81.5 mmol/d and 39.2 ± 20.2 mmol/d (equivalent to sodium chloride of 9.2 g/d, potassium chloride of 2.9 g/d), sodium/potassium ratio (median) of 4.14 (2.92,5.73). Urinary electrolytes were lower in women than men (sodium: 171.1 vs 138.7, p < .05; potassium: 40.3 vs 37.7, p < .05), in the elderly than in the younger (sodium: 168.7 vs 139.9, p < .05; potassium: 39.5 vs. 37.5, p < .05). For every 1 unit of Na/K ratio increase, blood pressure increased by 0.46/0.24 mmHg. Blood pressure was 2.75/1.27 mmHg higher in quartile 4 than quartile 1 of Na/K. It remains high sodium and low potassium for hypertensive patients in China. Decreased sodium, Na/K ratio and increased potassium may help for blood pressure management.