Efficient pollutant degradation by peroxymonosulfate activated by a Co/Mn metal-organic framework.

In this work, a three-dimensional bimetallic metal-organic framework (BMOF), BUC-101 (Co/Mn-Hchhc, Hchhc = -1,2,3,4,5,6-cyclohexane-hexacarboxylic acid, BUC = Beijing University of Civil Engineering and Architecture) was synthesized by a one-pot solvothermal method and characterized in detail by single crystal X-ray diffraction (SCXRD), Fourier transform infrared spectroscopy (FTIR), X-ray photoelectron spectroscopy (XPS) and scanning electron microscopy (SEM) element mapping analysis. BUC-101 showed excellent catalytic peroxymonosulfate (PMS) activation performance to degrade rhodamine B (RhB) without energy input. In addition, BUC-101 can maintain good stability and recyclability during the PMS activation processes, in which 99.

Discovery of as a new gene underpinning congenital heart defects.

Objective: Aggregating evidence convincingly establishes the predominant genetic basis underlying congenital heart defects (CHD), though the heritable determinants contributing to CHD in the majority of cases remain elusive. In the current investigation, was selected as a prime candidate gene for human CHD mainly due to cardiovascular developmental abnormalities in -knockout animals. The objective of this retrospective study was to identify a new mutation responsible for CHD and characterize the functional effect of the identified CHD-causing mutation.

Somatic mutation contributes to tetralogy of Fallot.

Tetralogy of Fallot (TOF) is the most prevalent cyanotic congenital heart pathology and causes infant morbidity and mortality worldwide. GATA-binding protein 4 (GATA4) serves as a pivotal transcriptional factor for embryonic cardiogenesis and germline mutations are causally linked to TOF. However, the effects of somatic mutations on the pathogenesis of TOF remain to be ascertained.

Can China's vehicular emissions regulation reduce air pollution?-a quasi-natural experiment based on the latest National Vehicular Emissions Standard (stage-VI).

The existing evidence on the environmental effects of vehicular emissions regulation almost comes from developed countries, but the effectiveness of this policy tool in developing countries, especially in China, remains unclear. This study, for the first time, examined the mitigating effects of China's vehicular emissions regulation on air pollution at the prefecture level cities, by using the latest implementation of China's National Vehicular Emissions Standard VI (CHINA-VI) as a quasi-natural experimental process of policy shocks. To this end, monthly data from 2018 to 2020 was applied to construct a difference-in-differences (DID) model.

Discovery of (Cx45) as a New Gene Underlying Congenital Heart Disease and Arrhythmias.

As the most prevalent type of birth malformation, congenital heart disease (CHD) gives rise to substantial mortality and morbidity as well as a socioeconomic burden. Although aggregating investigations highlight the genetic basis for CHD, the genetic determinants underpinning CHD remain largely obscure. In this research, a Chinese family suffering from autosomal dominant CHD (atrial septal defect) and arrhythmias was enrolled.

Percentile curves of normal echocardiographic measurements values for left heart structures in 1570 Han Chinese preterm and term infants.

Objective: This study was designed to evaluate echocardiographic measurements in Han Chinese preterm and term infants and to build percentile curves of normal echocardiographic measurements values related to the weight.

Method: From December 2014 to December 2021, a total of 797 male infants and 773 female infants born in * were included in the study. The echocardiographic measurements of each subject were as follows: left ventricular internal diameter at end-diastole (LVIDd), left ventricular internal diameter at end-systole (LVIDs), left ventricular posterior wall thickness at end-diastole (LVPWd), left ventricular posterior wall thickness at end-systole (LVPWs), interventricular septal thickness at end-diastole (IVSd), interventricular septal thickness at end-systole (IVSs), ascending aorta diameter (AO), left atrium (LA) dimension, left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS) and left ventricular mass (LVM).

Short-term effects of air pollution on respiratory diseases among young children in Wuhan city, China.

Background: The high risks for childhood respiratory diseases are associated with exposure to ambient air pollution. However, there are few studies that have explored the association between air pollution exposure and respiratory diseases among young children (particularly aged 0-2 years) based on the entire population in a megalopolis.

Methods: Daily hospital admission records were obtained from 54 municipal hospitals in Wuhan city, China.

SMAD1 Loss-of-Function Variant Responsible for Congenital Heart Disease.

As the most common form of developmental malformation affecting the heart and endothoracic great vessels, congenital heart disease (CHD) confers substantial morbidity and mortality as well as socioeconomic burden on humans globally. Aggregating convincing evidence highlights the genetic origin of CHD, and damaging variations in over 100 genes have been implicated with CHD. Nevertheless, the genetic basis underpinning CHD remains largely elusive.

SOX17 Loss-of-Function Mutation Underlying Familial Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) refers to a rare, progressive disorder that is characterized by occlusive pulmonary vascular remodeling, resulting in increased pulmonary arterial pressure, right-sided heart failure, and eventual death. Emerging evidence from genetic investigations of pediatric-onset PAH highlights the strong genetic basis underpinning PAH, and deleterious variants in multiple genes have been found to cause PAH. Nevertheless, PAH is of substantial genetic heterogeneity, and the genetic defects underlying PAH in the overwhelming majority of cases remain elusive.

A New ISL1 Loss-of-Function Mutation Predisposes to Congenital Double Outlet Right Ventricle.

Occurring in about 1% of all live births, congenital heart defects (CHDs) represent the most frequent type of developmental abnormality and account for remarkably increased infant morbidity and mortality. Aggregating studies demonstrate that genetic components have a key role in the occurrence of CHDs. Nevertheless, due to pronounced genetic heterogeneity, the genetic causes of CHDs remain unclear in most patients.

Functional metabolomics discover pentose and glucuronate interconversion pathways as promising targets for Yang Huang syndrome treatment with Yinchenhao Tang.

Yinchenhao Tang (YCHT), a classic traditional Chinese medicine (TCM) formulae, plays an important role in the treatment of Yang Huang syndrome (YHS). With the emergence of new biomarkers of YHS uncovered metabonomics, the underlying functional mechanisms are still not clear. Functional metabolomics aims at converting biomarkers derived from metabonomics into disease mechanisms.

GATA6 loss-of-function mutation contributes to congenital bicuspid aortic valve.

Congenital bicuspid aortic valve (BAV), the most common form of birth defect in humans, is associated with substantial morbidity and mortality. Increasing evidence demonstrates that genetic risk factors play a key role in the pathogenesis of BAV. However, BAV is a genetically heterogeneous disease and the genetic determinants underpinning BAV in an overwhelming majority of patients remain unknown.

UPLC-G2Si-HDMS untargeted metabolomics for identification of metabolic targets of Yin-Chen-Hao-Tang used as a therapeutic agent of dampness-heat jaundice syndrome.

Yin-Chen-Hao-Tang (YCHT), the classic formulae of traditional Chinese medicine (TCM), is widely used to treat dampness-heat jaundice syndrome (DHJS) and various liver diseases. However, the therapeutic mechanism of YCHT is yet to have an integrated biological interpretation. In this work, we used metabolomics technology to reveal the adjustment of small molecule metabolites in body during the treatment of YCHT.

A Novel MEF2C Loss-of-Function Mutation Associated with Congenital Double Outlet Right Ventricle.

Congenital heart defect (CHD) represents the most prevalent birth defect, and accounts for substantial morbidity and mortality in humans. Aggregating evidence demonstrates the genetic basis for CHD. However, CHD is a heterogeneous disease, and the genetic determinants underlying CHD in most patients remain unknown.

Serum metabolomics strategy for understanding the therapeutic effects of Yin-Chen-Hao-Tang against Yanghuang syndrome.

Yin-Chen-Hao-Tang (YCHT), a classic Chinese herbal formula, is characterized by its strong therapeutic effects of liver regulation and relief of jaundice, especially Yanghuang syndrome (YHS). YHS is a type of jaundice with damp-heat pathogenesis, and it is considered a complicated Chinese medicine syndrome (CMS). The accurate mechanism for healing YHS has not yet been completely reported.

GATA4 Loss-of-Function Mutation and the Congenitally Bicuspid Aortic Valve.

Aggregating evidence suggests that genetic determinants play a pivotal role in the pathogenesis of the congenitally bicuspid aortic valve (BAV). BAV is of pronounced genetic heterogeneity, and the genetic components underlying BAV in an overwhelming majority of patients remain elusive. In the current study, the whole coding exons and adjacent introns, as well as 5' and 3' untranslated regions of the GATA4 gene, which codes for a zinc-finger transcription factor crucial for the normal development of the aortic valve, were screened by direct sequencing in 150 index patients with congenital BAV.

TBX1 loss-of-function mutation contributes to congenital conotruncal defects.

Conotruncal defects (CTDs) account for ~30% of all types of congenital heart disease and contribute to increased morbidity and mortality rates. Increasing evidence suggests that genetic risk factors are involved in the pathogenesis of CTDs. Mutations in a number of genes, including the gene that codes for a T-box transcription factor essential for normal cardiovascular development, may contribute to the development of CTD.

A novel NR2F2 loss-of-function mutation predisposes to congenital heart defect.

Congenital heart defect (CHD) is the most common type of birth defect in humans and a leading cause of infant morbidity and mortality. Previous studies have demonstrated that genetic defects play a pivotal role in the pathogenesis of CHD. However, the genetic basis of CHD remains poorly understood due to substantial genetic heterogeneity.

MEF2C loss-of-function mutation contributes to congenital heart defects.

Congenital heart disease (CHD) is the most common type of developmental abnormality in humans, and is a leading cause for substantially increased morbidity and mortality in affected individuals. Increasing studies demonstrates a pivotal role of genetic defects in the pathogenesis of CHD, and presently mutations in more than 60 genes have been associated with CHD. Nevertheless, CHD is of pronounced genetic heterogeneity, and the genetic basis underpinning CHD in a large proportion of patients remains unclear.

MESP1 loss‑of‑function mutation contributes to double outlet right ventricle.

Congenital heart disease (CHD) is the most common form of birth defect in humans, and remains a leading non‑infectious cause of infant mortality worldwide. An increasing number of studies have demonstrated that genetic defects serve a pivotal role in the pathogenesis of CHD, and mutations in >60 genes have been causally associated with CHD. CHD is a heterogeneous disease and the genetic basis of CHD in the majority of patients remains poorly understood.

HAND1 loss-of-function mutation contributes to congenital double outlet right ventricle.

Congenital heart defects (CHDs), a wide variety of developmental abnormalities in the structures of the heart and the great thoracic blood vessels, are the most common form of birth defect in humans worldwide. CHDs are accountable for substantial morbidity and are still the leading cause of birth defect‑related deaths. Recent studies have demonstrated the pivotal roles of genetic defects in the pathogenesis of CHDs, and a great number of genetic mutations have been associated with CHDs.

Prevalence and Spectrum of TBX5 Mutation in Patients with Lone Atrial Fibrillation.

Atrial fibrillation (AF), the most common type of cardiac rhythm disturbance encountered in clinical practice, is associated with substantially increased morbidity and mortality. Aggregating evidence demonstrates that abnormal cardiovascular development is involved in the pathogenesis of AF. A recent study has revealed that the TBX5 gene, which encodes a T-box transcription factor key to cardiovascular development, was associated with AF and atypical Holt-Oram syndrome.

A novel HAND2 loss-of-function mutation responsible for tetralogy of Fallot.

Congenital heart disease (CHD), the most common type of developmental abnormality, is associated with substantial morbidity and mortality in humans worldwide. The basic helix-loop-helix transcription factor, heart and neural crest derivatives expressed 2 (HAND2), has been demonstrated to be crucial for normal cardiovascular development in animal models. However, whether a genetically defective HAND2 contributes to congenital heart disease (CHD) in humans remains to be explored.