BACKGROUND: Stroke is one of the leading causes of death among children, yet evidence on stroke incidence and prognosis in this population is largely neglected worldwide. The aim of this study was to estimate the latest burden of childhood stroke, as well as trends, risk factors, and inequalities from 1990 to 2019, at the global, regional, and national levels. METHODS: The Global Burden of Disease 2019 study was utilized to evaluate the prevalence, incidence, years lived with disability, years of life lost (YLLs), and average annual percentage changes in stroke among populations aged 0 to 19 years from 1990 to 2019. RESULTS: The global age–standardized incidence of stroke increased (average annual percentage change, 0.15% [95% uncertainty interval, 0.09%–0.21%]), while YLLs decreased substantially (average annual percentage change, −3.33% [95% uncertainty interval, −3.38% to −3.28%]) among children and adolescents between 1990 and 2019. Ischemic stroke accounted for 70% of incident cases, and intracerebral hemorrhage accounted for 63% of YLLs. Children under 5 years of age had the highest incidence of ischemic stroke, while adolescents aged 15 to 19 years had the highest incidence of hemorrhagic stroke. In 2019, low-income and middle-income countries were responsible for 84% of incident cases and 93% of YLLs due to childhood stroke. High-sociodemographic index countries had a reduction in YLLs due to stroke that was more than twice as fast as that of low-income and middle-income. CONCLUSIONS: Globally, the burden of childhood stroke continues to increase, especially among females, children aged <5 years, and low-sociodemographic index countries, such as sub-Saharan Africa. The burden of childhood stroke is likely undergoing a significant transition from being fatal to causing disability. Global public health policies and the deployment of health resources need to respond rapidly and actively to this shift.

Background: Hypertension is closely associated with excessive sodium intake, and low-sodium salt has been shown to lower blood pressure. However, whether low-sodium salt interacts with genetic variation related to salt sensitivity of blood pressure is unclear. Methods: A total of 259 hypertensive patients who completed the previous 3 years of a low-sodium salt vs. normal salt intervention were included in our study. Genetic risk scores (GRSs) of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were respectively built for each participant. A general linear regression model and a generalized mixed model were applied to identify the interaction effects between low-sodium salt intervention and ENaC genetic variation on SBP/DBP changes and trajectories over 3 years. Findings: during the 3-year intervention, both SBP and DBP levels showed a significant decline in the low-sodium salt intervention group than those in the normal salt intervention group over 3 years (P_{salt intervention group} = 0.001 for SBP and P_{salt intervention group} = 0.006 for DBP). Furthermore, a gene–diet interaction was found for the SBP change trajectory over 3 years (P_{SBP-GRS×salt intervention group} = 0.011); specifically, significant SBP reductions were found between salt intervention groups in the high SBP-GRS group (−18.77 vs. −9.58 mmHg, P_{salt intervention group} = 0.001), but not in the low SBP-GRS group (−15.71 vs. −14.62 mmHg, P_{salt intervention group} = 0.791). No interaction effect between low-sodium salt intervention and genetic variation of ENaC was found for changes in DBP. Conclusions: Higher ENaC genetic variation is associated with a greater reduction in SBP in response to a low-sodium salt intervention. Hypertensive patients with higher ENaC genetic variation may experience a greater benefit in SBP reductions by consuming low-sodium salt. (Trial registration: chiCTR-TRC-09000538, https://www.chictr.org.cn).

This study aimed to assess the effects of GH adjuvant therapy on the cumulative live birth rate in patients with poor embryo quality and to determine the characteristics of patients who are more responsive to GH. A retrospective cohort study was carried out in patients who have suffered from previous IVF failure due to poor embryonic development and underwent IVF with or without a 6-week pretreatment with GH in the subsequent cycle from January 2018 to December 2020. Clinical parameters including the cumulative live birth rate between the (−) GH and (+) GH groups were compared. Multivariate analysis was performed to ascertain associations between clinical parameters and cumulative live birth rate. Upon analysis of the clinical data from 236 IVF cycles, 84 patients received GH and 152 did not receive GH. In frozen embryo transfer cycles, compared with the (−) GH group, the implantation rate and live birth rate were significantly higher in the (+) GH group (p < 0.05). After adjusting for possible confounding factors, GH improved cumulative live birth per oocyte retrieval cycle by 1.96 folds (p = 0.032). Furthermore, when patients were subdivided based on age and BMI, a significant increase in the cumulative live birth rate was found in the (+) GH group of patients between 35 and 42 years old and BMI ≥ 24 kg/m², respectively (p < 0.05). GH may increase the live birth rate in women who experienced IVF failure because of poor embryonic development, particularly in obese patients and women with advanced age.

Background: As the global aging process continues to accelerate, heart failure (HF) has become an important cause of increased morbidity and mortality in elderly patients. Chronic atrial fibrillation (AF) is a major risk factor for HF. Patients with HF combined with AF are more difficult to treat and have a worse prognosis. The aim of this study was to explore the risk factors for 1-year mortality in patients with HF combined with AF and to develop a risk prediction assessment model. Methods: We recruited hospitalized patients with HF and AF who received standardized care in the Department of Cardiology at Shengjing Hospital of China Medical University from January 2013 to December 2018. The patients were randomly divided into modeling and internal validation groups using a random number generator at a 1:1 ratio. Multivariate Cox regression analysis was used to identify risk factors for all-cause mortality during a one-year follow-up period. Then, a nomogram was constructed based on the weights of each index and validated. Receiver operating characteristic curve, the area under the curve (AUC), decision curve, and calibration curve analyses for survival were used to evaluate the model’s predictive and clinical validities and calibration. Results: We included 3,406 patients who met the eligibility criteria; 1,703 cases each were included in the modeling and internal validation groups. Eight statistically significant predictors were identified: age, sex, New York Heart Association cardiac function class III or IV, a history of myocardial infarction, and the albumin, triglycerides, N-terminal pro-b-type natriuretic peptide, and blood urea nitrogen levels. The AUCs were 0.793 (95% confidence interval: 0.763–0.823) and 0.794 (95% confidence interval: 0.763–0.823) in the modeling and validation cohorts, respectively. Conclusions: We present a predictive model for all-cause mortality in patients with coexisting HF and AF comprising eight key factors. This model gives clinicians a simple assessment tool that may improve the clinical management of these patients.