Systemic chronic hypoxia is a feature of many diseases and may influence the communication between bone marrow (BM) and gut microbiota. Here we analyse patients with cyanotic congenital heart disease (CCHD) who are experiencing chronic hypoxia and characterize the association between bone marrow mesenchymal stem cells (BMSCs) and gut microbiome under systemic hypoxia. We observe premature senescence of BMSCs and abnormal d-galactose accumulation in patients with CCHD. The hypoxia that these patients experience results in an altered diversity of gut microbial communities, with a remarkable decrease in the number of Lactobacilli and a noticeable reduction in the amount of enzyme-degraded d-galactose. Replenishing chronic hypoxic rats with Lactobacillus reduced the accumulation of d-galactose and restored the deficient BMSCs. Together, our findings show that chronic hypoxia predisposes BMSCs to premature senescence, which may be due to gut dysbiosis and thus induced d-galactose accumulation.

Background Congenital heart disease (CHD) is the leading cause of morbidity and mortality from birth defects worldwide. We report an overview of trends in CHD mortality in 204 countries and territories over the past 30 years and associations with age, period, and birth cohort.Methods Cause-specific CHD mortality estimates were derived from the Global Burden of Disease 2019 study. We utilised an age-period-cohort model to estimate overall annual percentage changes in mortality (net drifts), annual percentage changes from 0 to 4 to 65−69 years (local drifts), period and cohort relative risks (period/cohort effects) between 1990 and 2019. This approach allows for the examination and differentiation of age, period, and cohort effects in the mortality trends, with the potential to identify disparities and treatment gaps in cardiac care.Findings CHD is the leading cause of deaths from non-communicable diseases (NCDs) in those under 20 years. Global CHD deaths in 2019 were 217,000 (95% uncertainty interval 177,000−262,000). There were 129 countries with at least 50 deaths. India, China, Pakistan, and Nigeria had the highest mortality, accounting for 39.7% of deaths globally. Between 1990 and 2019, the net drift of CHD mortality ranged from −2.41% per year (95% confidence interval [CI] −2.55, −2.67) in high Socio-demographic Index (SDI) countries to −0.62% per year (95% CI: −0.82, −0.42) in low-SDI countries. Globally, there was an emerging transition in the age distribution of deaths from paediatric to adult populations, except for an increasing trend of mortality in those aged 10−34 years in Mexico and Pakistan. During the past 30 years, favourable mortality reductions were generally found in most high-SDI countries like South Korea (net drift = −4.0% [95% CI −4.8 to −3.1] per year) and the United States (−2.3% [−2.5 to −2.0]), and also in many middle-SDI countries like Brazil (−2.7% [−3.1 to 2.4]) and South Africa (−2.5% [−3.2 to −1.8]). However, 52 of 129 countries had either increasing trends (net drifts ≥0.0%) or stagnated reductions (≥−0.5%) in mortality. The relative risk of mortality generally showed improving trends over time and in successively younger

Our study indicates that the accumulation of 4-hydroxy-2-nonenal plays an important role in lung ischemia-reperfusion injury. Alda-1 pretreatment can attenuate lung ischemia-reperfusion injury, possibly through the activation of aldehyde dehydrogenase-2, which in turn removes 4-hydroxy-2-nonenal in human pulmonary alveolar epithelial cells. Alda-1 pretreatment has clinical implications to protect lungs during cardiopulmonary bypass.

Background Socioeconomic status ( SES ) is associated with health‐related quality of life ( HRQOL ) for children with critical congenital heart disease; however, literature from newly industrialized countries is scarce. Methods and Results This cross‐sectional study included 2037 surviving patients operated on for critical congenital heart disease at a tertiary hospital in China between May 2012 and December 2015. All eligible patients were aged 2 to 12 years. HRQOL was measured by the Pediatric Quality of Life Inventory 4.0 generic and 3.0 cardiac modules. Family SES was assessed by a composite of household income in the past year and occupation and education level of each parent in the family. Mean scores of major domains in HRQOL were significantly lower in the low‐ SES group than in the medium‐ and high‐ SES groups (total generic scores: 71.2±7.9 versus 75.0±8.0 and 76.0±7.9, respectively [ P <0.001]; psychosocial functioning: 70.8±9.0 versus 74.4±8.4 and 75.3±8.4 [ P <0.001]; physical functioning: 71.6±10.4 versus 76.0±9.7 and 77.1±9.4 [ P <0.001]; heart symptoms: 71.9±11.6 versus 75.7±11.0 and 76.8±10.3 [ P <0.001]; cognitive problems: 65.4±11.1 versus 69.4±12.1 and 74.6±13.6 [ P <0.001]). After adjustment for other clinical and demographic variables in the multivariable linear regression model, family SES significantly affected all dimensions of HRQOL except for treatment barriers, treatment anxiety, physical appearance and communication. Conclusions Family SES is an important factor associated with HRQOL in patients with critical congenital heart disease. Further targeted interventions to improve HRQOL that consider the family and environmental issues confronted by those who are economically disadvantaged might help these patients have better outcomes.