Predicting Hospital Readmissions in Patients Receiving Novel-Dose Sacubitril/Valsartan Therapy: A Competing-Risk, Causal Mediation Analysis.

Backgrounds: Our study aimed to identify and predict patients with heart failure (HF) taking novel-dose Sacubitril/Valsartan (S/V) at risk for all-cause readmission, as well as investigate the possible role of left ventricular reverse remodeling (LVRR). Methods and results: There were 464 patients recruited from December 2017 to September 2021 in our hospital with a median follow-up of 660 days (range, 17-1494). Competing risk analysis with Gray's Test showed statistically significant differences in all-cause readmission (p-value< .001) across the three different dose groups. Models 1 and 2 were developed based on the results of univariable competing risk analysis, least absolute shrinkage and selection operator approach, backward stepwise regression, and multivariable competing risk analysis. The internal verification (data-splitting method) indicated that Model 1 had better discrimination, calibration, and clinical utility. The corresponding nomogram showed that patients aged 75 years and above, or taking the lowest-dose S/V (≤50 mg twice a day), or diagnosed with ventricular tachycardia, or valvular heart disease, or chronic obstructive pulmonary disease, or diabetes mellitus were at the highest risk of all-cause readmission. In the causal mediation analysis, LVRR was considered as a critical mediator that negatively affected the difference of novel-dose S/V in readmission. Conclusions: A significant association was detected between novel-dose S/V and all-cause readmission in HF patients, in part negatively mediated by LVRR. The web-based nomogram could provide individual prediction of all-cause readmission in HF patients receiving novel-dose S/V. The effects of different novel-dose S/V are still needed to be explored further in the future.

Impact of coronary artery disease in patients with hypertrophic cardiomyopathy.

BACKGROUND: Atherosclerotic coronary artery disease (CAD) often occurs concurrently with hypertrophic cardiomyopathy (HCM). However, the influence of concomitant CAD has not been fully assessed in patients with HCM. METHODS: Invasive or computed tomography coronary angiography was performed in 461 patients with HCM at our hospital to determine the presence and severity of CAD from March 2010 to April 2022. The primary end points were all-cause, cardiovascular, and sudden cardiac deaths. The survival of HCM patients with severe CAD was compared with that of HCM patients without severe CAD. RESULTS: Of 461 patients with HCM, 235 had concomitant CAD. During the median (interquartile range) follow-up of 49 (31-80) months, 75 patients (16.3%) died. The 5-year survival estimates were 64.3%, 82.5%, and 86.0% for the severe, mild-to-moderate, and no-CAD groups, respectively (log-rank, p = 0.010). Regarding the absence of cardiovascular death, the 5-year survival estimates were 68.5% for patients with severe CAD, 86.4% for patients with mild-to-moderate CAD, and 90.2% for HCM patients with no CAD (log-rank, p = 0.001). In multivariate analyses, severe CAD was associated with all-cause and cardiovascular death after adjusting for age, left ventricular ejection fraction, hypertension, and atrial fibrillation. CONCLUSIONS: This study showed a worse prognosis among HCM patients with severe CAD than among HCM patients without severe CAD. Therefore, timely recognition of severe CAD in HCM patients and appropriate treatment are important.

Miz1 promotes KRAS-driven lung tumorigenesis by repressing the protocadherin Pcdh10.

Targeting KRAS-mutated non-small-cell lung cancer (NSCLC) remains clinically challenging. Here we show that loss of function of Miz1 inhibits lung tumorigenesis in a mouse model of oncogenic KRAS-driven lung cancer. In vitro, knockout or silencing of Miz1 decreases cell proliferation, clonogenicity, migration, invasion, or anchorage-independent growth in mutant (MT) KRAS murine or human NSCLC cells but has unremarkable impact on non-tumorigenic cells or wild-type (WT) KRAS human NSCLC cells. RNA-sequencing reveals Protocadherin-10 (Pcdh10) as the top upregulated gene by Miz1 knockout in MT KRAS murine lung tumor cells. Chromatin immunoprecipitation shows Miz1 binding on the Pcdh10 promoter in MT KRAS lung tumor cells but not non-tumorigenic cells. Importantly, silencing of Pcdh10 rescues cell proliferation and clonogenicity in Miz1 knockout/knockdown MT KRAS murine or human tumor cells, and rescues allograft tumor growth of Miz1 knockout tumor cells in vivo. Miz1 is upregulated in MT KRAS lung tumor tissues compared with adjacent non-involved tissues in mice. Consistent with this, Miz1 is upregulated while Pcdh10 is downregulated in human lung adenocarcinomas (LUAD) compared with normal tissues, and high Miz1 levels or low Pcdh10 levels are associated with poor survival in lung cancer patients. Furthermore, the Miz1 signature is associated with worse survival in MT but not WT KRAS LUAD, and Pcdh10 is downregulated in MT compared to WT KRAS LUAD. Taken together, our studies implicate the Miz1/Pcdh10 axis in oncogenic KRAS-driven lung tumorigenesis.

Hospitalized patients with isolated distal deep vein thrombosis: anticoagulation therapy or not?

BACKGROUND: Isolated distal deep vein thrombosis (IDDVT), a disease frequently detected in hospitalized patients, can progress to proximal deep vein thrombosis (PDVT) and pulmonary embolism (PE). Here, we evaluated the effects of anticoagulation in hospitalized IDDVT patients. METHODS: We conducted a retrospective study in our hospital and enrolled hospitalized IDDVT patients diagnosed by compression ultrasonography (CUS) from January to December 2020. Participants were divided into anticoagulation (AC) and non-anticoagulation (non-AC) groups. After propensity score matching (PSM), multivariate Cox regression analyses were performed to assess whether anticoagulation was associated with PDVT/PE, and all-cause mortality. RESULTS: A total of 426 IDDVT inpatients with CUS follow-up were screened from 1502 distal DVT patients and finally enrolled. The median age was 67 years with 51.4% males and 15.5% cancer patients. The median follow-up was 11.6 months. There were 288 and 138 patients treated with or without anticoagulants, respectively. Patients in the non-AC group had less body mass index and more comorbidities. Patients in the AC group were treated with rivaroxaban or dabigatran (52.1%), low molecular weight heparin (42.7%), and warfarin (5.2%). The PSM generated 111 pairs of well-matched IDDVT patients with or without anticoagulation. The Kaplan-Meier analysis demonstrated that neither the incidence of PDVT/PE (5.4% vs. 2.7%, log-rank p = 0.313) nor all-cause mortality (27.9% vs. 18.9%, log-rank p = 0.098) was significant different between groups. Anticoagulation was not associated with PDVT/PE and all-cause mortality in the multivariable Cox regression analyses using the matched cohorts. The main risk factors for all-cause mortality were age, malignancy history, BMI, sepsis, heart failure, and white blood cell (WBC) count. CONCLUSIONS: In hospitalized IDDVT patients, the thrombosis extension rate to PDVT/PE was low. Anticoagulation did not reduce the incidence of thrombosis extension of IDDVT and was not associated with all-cause mortality.

Maintenance of recovered dilated cardiomyopathy patients with half-dose neurohumoral blockades (MED-CHARM): A protocol for an open-label, pilot, randomized trial.

Dilated cardiomyopathy (DCM) has brought great damage to the patients' health and social economy. The number of patients with recovered dilated cardiomyopathy (recDCM) has increased over the years as treatment progresses. However, there is a lack of relevant evidence to support the clinical management of patients with recDCM, thereby, the recommendations in guidelines remains sparse. Accordingly, the exploration of recDCM is important to improve patient prognosis and reduce societal burden. This is an open-label, randomized controlled, prospective study that will compare the safety and efficacy of original dose and halved dose of neurohumoral blockades for patients with recDCM. Methods: An open-label, randomized controlled, prospective study will be conducted among eligible patients with recDCM. During the pilot study phase, we will recruit 50 patients. The primary endpoint is hospitalization for heart failure or heart failure relapse within 12 months. Secondary endpoint is major adverse cardiovascular events, including cardiovascular mortality, myocardial infarction, stroke, sustained atrial tachycardia, or ventricular tachycardia. The results will be analyzed using intention-to-treatment analysis. Discussion: The study will provide important evidence of whether it is safe and effective to halve the dosage of neurohumoral blockades in recDCM patients. Trial registration number: ChiCTR2100054051 (www.chictr.org.cn).

Iodine in household cooking salt no longer plays a crucial role in iodine status of residents in Tianjin, China.

PURPOSE: The contribution of household cooking salt to population iodine status is decreasing in China, the applicability of the coverage rate of iodized salt (IS), proportion of adequately iodized salt (AIS), and salt iodine concentration (SIC) of household cooking salt used for iodine status assessment of residents requires further investigation. METHODS: Through the IDD control project, 16,445 children and 4848 pregnant women were recruited from Tianjin, China and the relationship between the coverage rate of IS, proportion of AIS, SIC, and population iodine status was analyzed. Additionally, through the thyroid health survey project, 856 children with IS or noniodized salt were recruited. The effects of different household cooking salts on individual iodine status and thyroid health were analyzed. RESULTS: After adjusting for confounding factors, no relationship was found between the coverage rate of IS, proportion of AIS, SIC of household cooking salt, and iodine status of children and pregnant women (all P > 0.05). No differences in levels of thyroid function and structural indicators were found in children with different household cooking salts (all P > 0.05). Additionally, no relationship was found between noniodized salt exposure and goiter, overt hyperthyroidism, overt hypothyroidism, thyroid nodules, antibody single positivity, or subclinical hypothyroidism (all P > 0.05). CONCLUSION: Iodine in household cooking salt no longer plays a crucial role in iodine status in Tianjin, China. Other indicators must be identified as beneficial supplements for precise iodine status evaluation not only in Tianjin but also in other large cities in China.

Risk factors for incomplete thrombosis in false lumen in sub-acute type B aortic dissection post-TEVAR.

There is scarce information about the risk factors for incomplete false lumen thrombosis (FLT) among type B aortic dissection (AD) patients, particularly in the sub-acute phase following thoracic endovascular aortic repair (TEVAR). We enrolled consecutive sub-acute type B AD patients at Xinqiao Hospital (Chongqing, China) from May 2010 to December 2019. Patients with severe heart failure, cancer, and myocardial infarction were excluded. The postoperative computed tomography angiography (CTA) data were extracted from the most recent follow-up aortic CTA. Multivariate logistic regressions were applied to identify the association between FLT and clinical or imaging factors. Fifty-five subjects were enrolled in our study. Twelve participants showed complete FLT, and 2 of these died during the follow-up, while 8 patients died in incomplete FLT group. In the multivariate analysis, maximum abdominal aorta diameter (OR 1.20, 95% CI 1.016-1.417 p = 0.032) and the number of branches arising from the false lumen (FL) (OR 15.062, 95% 1.681-134.982 p = 0.015) were significantly associated with incomplete FLT. The C-statistics was 0.873 (95% CI 0.773-0.972) for the model. The FL diameter (p < 0.001) was significantly shorter following TEVAR, while the true lumen diameter (p < 0.001) and maximum abdominal aorta diameter (p = 0.011) were larger after the aortic repair. There were 21.8% of sub-acute type B AD patients presented complete FLT post-TEVAR. Maximum abdominal aorta diameter and the number of branches arising from the FL were independent risk factors for incomplete FLT. The true lumen diameter, maximum abdominal aorta diameter, and FL diameter changed notably following TEVAR.

Effects of air pollution and green spaces on impaired lung function in children: a case-control study.

The occurrences of impaired lung function during childhood could substantially influence the health states of the respiratory system in adults. So, the effects of air pollution and green spaces on impaired lung function in children were investigated in this study. The lung function of each student was tested every year from 2015 to 2017 and the method of case-control study was applied. 2087 students aged from 9 to 11 years old of primary schools in Tianjin were ultimately included in this study. The method of propensity score matching (PSM) was performed to minimize the confounding bias and the conditional logistic regression model was carried out to evaluate the effects of indoor and outdoor environmental risk factors on the occurrences of impaired lung function in children. For every interquartile range (IQR) increase in the mixture of six air pollutants at the lag1, lag2, and lag3 periods, the risks of getting impaired lung function were increased by 53.4%, 34.7%, and 16.9%, respectively. The protective effect of greenness at lag2 period (odds ratios (OR)) = 0.022 (95% confidence interval (CI): 0.008-0.035)) was stronger than that at lag1and lag3 periods, respectively. Separate and combined effects of most air pollutants at different lag periods exerted hazardous effects on the lung function of students. Exposure to greenness had protective effects on the lung health of children.

Health risks of PM2.5-bound polycyclic aromatic hydrocarbon (PAH) and heavy metals (PPAH&HM) during the replacement of central heating with urban natural gas in Tianjin, China.

To investigate the health effects of fine particulate matter (≤ 2.5 µm in aerodynamic diameter; PM2.5)-bound heavy metals and polycyclic aromatic hydrocarbons (PAHs) before and after the implementation of the Urban Natural Gas Heating Project (UNGHP), the lifetime cancer risks, hazard quotients (HQs) of heavy metals and PAHs were calculated. Seven kinds of heavy metals (Al, As, Cd, Cr, Mn, Ni and Se) and 12 kinds of PAHs including acenaphthylene (ANY), acenaphthene (ANA), fluoranthene (FLT), pyrene (PYR), chrysene (CHR), benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF), benzo[k]fluoranthene (BkF), benzo[a]pyrene (BaP), dibenz[a,h]anthracene (DBA), benzo[ghi]perylene (BPE) and indeno[1,2,3-cd]pyrene (IPY) were analyzed and used for the health risk assessments. It was found that HQ of Mn fell from 1.09 in the coal-burning period to 0.72 in the gas-burning period in the suburban area. And lifetime cancer risks of PAHs fell from 35.7 × 10-6 in the coal-burning period to 17.22 × 10-6 in the gas-burning period in the urban area. It could be concluded that, during the gas-burning period, downward trends were observed for the lifetime cancer risks and HQs of most kinds of heavy metals and PAHs in all regions of Tianjin compared to those during the coal-burning period. The UNGHP was effective, and we should also take other measures to control the pollution.

Moderating Role of TSHR and PTPN22 Gene Polymorphisms in Effects of Excessive Fluoride on Thyroid: a School-Based Cross-Sectional Study.

We aimed to investigate the relationship between the effects excessive of fluoride on thyroid health in children and the moderating role of thyroid stimulating hormone receptor (TSHR) or protein tyrosine phosphatase nonreceptor-22 (PTPN22) gene polymorphisms. Four hundred thirteen children (141 with dental fluorosis and 198 boys) were enrolled from both historical endemic and non-endemic areas of fluorosis in Tianjin, China. The fluoride exposure levels, thyroid health indicators, and TSHR (rs2268458) and PTPN22 (rs3765598) polymorphisms were examined. Multiple logistic models were applied to evaluate the relationship between dental fluorosis and thyroid abnormalities. Children over 9 year old with dental fluorosis have lower FT4 and TGAb levels and thyroid volume and higher TPOAb levels (all P < 0.05). In overall participants, children with dental fluorosis were more likely to have thyroid antibody single positive issues (adjusted P = 0.039) and less likely to have a goiter according to age or body surface area (age or BSA) (adjusted P = 0.003); In the TSHR (rs2268458) SNP = CC/CT or PTPN22 (rs3765598) SNP = CC subgroup, dental fluorosis may cause thyroid antibody single positive (adjusted P = 0.036; adjusted P = 0.002); in the TSHR (rs2268458) SNP = TT or PTPN22 (rs3765598) SNP = CC subgroup, dental fluorosis may protect children from goiter (age or BSA) (adjusted P = 0.018; adjusted P = 0.013). Excessive fluoride may induce thyroid antibody single positive and reduce goiter in children. Heterogeneity exists in the relationship between excessive fluoride and thyroid antibody single positive or goiter issues across children carrying different TSHR (rs2268458) or PTPN22 (rs3765598) genotypes.

miR-221-5p-Mediated Downregulation of JNK2 Aggravates Acute Lung Injury.

Sepsis and acute lung injury (ALI) are linked to mitochondrial dysfunction; however, the underlying mechanism remains elusive. We previously reported that c-Jun N-terminal protein kinase 2 (JNK2) promotes stress-induced mitophagy by targeting small mitochondrial alternative reading frame (smARF) for ubiquitin-mediated proteasomal degradation, thereby preventing mitochondrial dysfunction and restraining inflammasome activation. Here we report that loss of JNK2 exacerbates lung inflammation and injury during sepsis and ALI in mice. JNK2 is downregulated in mice with endotoxic shock or ALI, concomitantly correlated inversely with disease severity. Small RNA sequencing revealed that miR-221-5p, which contains seed sequence matching to JNK2 mRNA 3' untranslated region (3'UTR), is upregulated in response to lipopolysaccharide, with dynamically inverse correlation with JNK2 mRNA levels. miR-221-5p targets the 3'UTR of JNK2 mRNA leading to its downregulation. Accordingly, miR-221-5p exacerbates lung inflammation and injury during sepsis in mice by targeting JNK2. Importantly, in patients with pneumonia in medical intensive care unit, JNK2 mRNA levels in alveolar macrophages flow sorted from non-bronchoscopic broncholaveolar lavage (BAL) fluid were inversely correlated strongly and significantly with the percentage of neutrophils, neutrophil and white blood cell counts in BAL fluid. Our data suggest that miR-221-5p targets JNK2 and thereby aggravates lung inflammation and injury during sepsis.

Identification of the SARS-CoV-2 Entry Receptor ACE2 as a Direct Target for Transcriptional Repression by Miz1.

Multiple lines of evidence have demonstrated that cigarette smoke or Chronic Obstructive Pulmonary Disease upregulates angiotensin-converting enzyme 2, the cellular receptor for the entry of the severe acute respiratory syndrome coronavirus 2, which predisposes individuals to develop severe Coronavirus disease 2019. The reason for this observation is unknown. We recently reported that the loss of function of Miz1 in the lung epithelium in mice leads to a spontaneous COPD-like phenotype, associated with upregulation of angiotensin-converting enzyme 2. We also reported that cigarette smoke exposure downregulates Miz1 in lung epithelial cells and in mice, and Miz1 is also downregulated in the lungs of COPD patients. Here, we provide further evidence that Miz1 directly binds to and represses the promoter of angiotensin-converting enzyme 2 in mouse and human lung epithelial cells. Our data provide a potential molecular mechanism for the upregulation of angiotensin-converting enzyme 2 observed in smokers and COPD patients, with implication in severe Coronavirus disease 2019.

Fluoride exposure and children's intelligence: Gene-environment interaction based on SNP-set, gene and pathway analysis, using a case-control design based on a cross-sectional study.

BACKGROUND: Excessive fluoride exposure has been associated with intelligence loss, but little is known about gene-fluoride interactions on intelligence at SNP-set, gene and pathway level. OBJECTIVES: Here we conducted a population-based study in Chinese school-aged children to estimate the associations of fluoride from internal and external exposures with intelligence as well as to explore the gene-fluoride interactions on intelligence at SNP-set, gene and neurodevelopmental pathway level. METHODS: A total of 952 resident children aged 7 to 13 were included in the current study. The fluoride contents in drinking water, urine, hair and nail were measured using the ion-selective electrode method. LASSO Binomial regression was conducted to screen the intelligence-related SNP-set. The gene-fluoride interactions at gene and pathway levels were detected by the Adaptive Rank Truncated Product method. RESULTS: The probability of high intelligence was inversely correlated with fluoride contents in water, urine, hair and nail (all P < 0.001). The SNP-set based on rs3788319, rs1879417, rs57377675, rs11556505 and rs7187776 was related to high intelligence (P = 0.001) alone and by interaction with water, urinary and hair fluoride (P = 0.030, 0.040, 0.010), separately. In gene level, CLU and TOMM40 interacted with hair fluoride (both P = 0.017) on intelligence. In pathway level, Alzheimer disease pathway, metabolic pathway, signal transduction pathway, sphingolipid signaling pathway and PI3K-AKT signaling pathway interacted with fluoride on intelligence in men. CONCLUSIONS: Our study suggests that fluoride is inversely associated with intelligence. Moreover, the interactions of fluoride with mitochondrial function-related SNP-set, genes and pathways may also be involved in high intelligence loss.

Prognostic Significance of B-Type Natriuretic Peptide in Patients With Left Ventricular Thrombus.

Background and Aims: There is sparse information on the prognostic value of B-type natriuretic peptide (BNP) for the outcomes in patients with left ventricular thrombus (LVT). Methods: Patients diagnosed with LVT by transthoracic echocardiography between November 2009 to July 2020 at our institution were included. The endpoints were all-cause mortality and systemic embolism. Results: Ninety-two subjects were finally included in the study. The mean age of the cohort was 56.73 ± 14.12, and 80.4% of the patients were male. The median BNP (1st quartile-3rd quartile) was 437.5 (112.74-1317.5). The total all-cause mortality rate was 30.44% (28/92), and the 1-year, 2-year, and 3-year cumulative survival rates were 85.4, 75.5, and 66.5%, respectively. Systemic embolism was identified in 10 subjects. COX multivariate analysis showed that Log BNP (HR, 4.16; 95%CI, 1.81-9.56; P = 0.001) and BMI (HR, 0.86; 95%CI, 0.73-0.99; P = 0.048) were significantly associated with all-cause mortality. In addition, patients with BNP levels in the upper median (≥ 437.5 pg/ml) had significantly higher all-cause mortality rate compared to those with lower median BNP (<437.5 pg/ml; P = 0.004). The area under the receiver operating characteristic curve for BNP and all-cause mortality was 0.71. In the linear trend test, BNP quartiles were significantly related to all-cause mortality in all models, and the P-values for trend in models 1, 2, and 3 were 0.005, 0.006, and 0.048, respectively. Conclusion: BNP level is a prognostic factor for all-cause mortality in LVT patients, and elevated BNP is indicative of a higher risk of LVT.

Interactive effect between temperature and fine particulate matter on chronic disease hospital admissions in the urban area of Tianjin, China.

This study focuses on effects of fine particulate matter (PM2.5) on chronic disease under different levels of temperature. We obtained type 2 diabetes, cerebral stroke and coronary heart disease hospital admissions (HAs) from five hospitals in urban Tianjin as well as the concentrations of PM2.5, nitrogen dioxide (NO2) and sulphur dioxide (SO2). We used distributed lag nonlinear models to explore nonlinear and lag effects of PM2.5. In single-pollutant models, PM2.5 was positively associated with type 2 diabetes, cerebral stroke and coronary heart disease HAs, with strongest effects at lag1, lag0 and lag06, respectively. The corresponding relative risk rates (RR%) were 1.836%, 2.083% and 6.428%. In co-pollutant models, the correlation between PM2.5 and HAs on high-temperature days was generally stronger than that on low-temperature days. This study indicated that PM2.5 can increase HA rates for these chronic diseases, and effects of PM2.5 on high-temperature days were stronger than that on low-temperature days.

Fluoride exposure, dopamine relative gene polymorphism and intelligence: A cross-sectional study in China.

BACKGROUND: Excessive fluoride exposure is related to adverse health outcomes, but whether dopamine (DA) relative genes are involved in the health effect of low-moderate fluoride exposure on children's intelligence remain unclear. OBJECTIVES: We conducted a cross-sectional study to explore the role of DA relative genes in the health effect of low-moderate fluoride exposure in drinking water. METHODS: We recruited 567 resident children, aged 6-11 years old, randomly from endemic and non-endemic fluorosis areas in Tianjin, China. Spot urine samples were tested for urinary fluoride concentration, combined Raven`s test was used for intelligence quotient test. Fasting venous blood were collected to analyze ANKK1 Taq1A (rs1800497), COMT Val158Met (rs4680), DAT1 40 bp VNTR and MAOA uVNTR. Multivariable linear regression models were used to assess associations between fluoride exposure and IQ scores. We applied multiplicative and additive models to appraise single gene-environment interaction. Generalized multifactor dimensionality reduction (GMDR) was used to evaluate high-dimensional interactions of gene-gene and gene-environment. RESULTS: In adjusted model, fluoride exposure was inversely associated with IQ scores (ß = -5.957, 95% CI: -9.712, -2.202). The mean IQ scores of children with high-activity MAOA genotype was significantly lower than IQ scores of those with low-activity (P = 0.006) or female heterozygote (P = 0.016) genotype. We detected effect modification by four DA relative genes (ANKK1, COMT, DAT1 and MAOA) on the association between UF and IQ scores. We also found a high-dimensional gene-environment interaction among UF, ANKK1, COMT and MAOA on the effect of IQ (testing balanced accuracy = 0.5302, CV consistency: 10/10, P = 0.0107). CONCLUSIONS: Our study suggests DA relative genes may modify the association between fluoride and intelligence, and a potential interaction among fluoride exposure and DA relative genes on IQ.

Prognostic Value of Preoperative Hemoglobin Levels for Long-Term Outcomes of Acute Type B Aortic Dissection Post-thoracic Endovascular Aortic Repair.

Background and Aims: There is scant information available about the prognostic value of preoperative hemoglobin (Hb) levels on the long-term outcomes of acute type B aortic dissection (ABAD) following thoracic endovascular aortic repair (TEVAR). Methods: A retrospective analysis of consecutive patients from 2010 to 2018 regarding the relationship between Hb level and long-term outcomes was conducted. The primary endpoint was all-cause mortality. Major adverse cardiovascular events (MACEs) included all-cause death, recurrent ruptures, and secondary procedures. Results: In total, 391 subjects treated by TEVAR were enrolled, with a mean age of 57.1 ± 12.0 years; 79.5% of them were male. Cox multivariate analysis showed that the preoperative Hb level was independently associated with all-cause death [adjusted hazard ratio (HR) 0.797 (per 1 g/dl), 95% confidence interval (CI) 0.693-0.918, p = 0.002] and MACEs (adjusted HR 0.795, 95% CI 0.672-0.871, p = 0.000). The area under the receiver operating characteristic curve of Hb for all-cause death and MACEs were 0.617 (95% CI 0.548-0.687, p = 0.008) and 0.617 (95% CI 0.551-0.684, p = 0.005), respectively. In the linear trend test, Hb concentration was significantly related to all-cause mortality (p for trend = 0.001) and MACEs (p for trend = 0.000). Moreover, in Kaplan-Meier analysis, lower Hb levels (< 12 g/dl) were significantly different from higher Hb (≥12 g/dl) levels for both all-cause death (log-rank p = 0.001) and MACEs (log-rank p = 0.001). Similar results were found when assessing the prognostic value of red blood cell count and anemia. Conclusions: Preoperative Hb may serve as a prognostic marker for long-range adverse outcomes for ABAD patients post-TEVAR.

How the constituents of fine particulate matter and ozone affect the lung function of children in Tianjin, China.

As the pollution of fine particulate matter (≤ 2.5 µg/m3 in aerodynamic diameter; PM2.5) and ozone (O3) is becoming more and more serious in developing countries, we, hereby, investigated the effects of PM2.5, constituents of PM2.5 and O3 on the lung function of children in Tianjin, China. The lung functions of 198 pupils from nine primary schools in Tianjin were examined (repeated five times) during the months of October to December in 2016, 2017 and 2018, respectively. And the mixed-effect models were used to evaluate the effects of air pollutants. A 10 µg/m3 increase in PM2.5 and O3-8h might lead to reductions of forced vital capacity (FVC) in 1.03% (- 1.87 to - 0.19%) and 21.09% (- 25.54 to - 16.58%), respectively, while a 10 ng/m3 increment in ANY might account for the 166.44% (- 221.32 to - 112.31%) decreases in FVC. PM2.5 and O3-8h might be more harmful to the lung functions of female students and participants with PS exposure at home. And the main sources of pollution resulting in the decrease in pulmonary function might be traffic pollution and coal combustion.

Health benefits on cardiocerebrovascular disease of reducing exposure to ambient fine particulate matter in Tianjin, China.

With the development of the industrialization level in China, high concentrations of fine particulate matter (≤ 2.5 µg/m3 in aerodynamic diameter (PM2.5)) could have a great impact on the health of the population. Our study is to quantify the health benefits on cardiocerebrovascular disease of reducing exposure to PM2.5 in Tianjin, China. We obtained the data on cardiovascular disease (CVD), ischemic heart disease (IHD), and cerebrovascular disease (CD) mortalities to quantify the association between CVD, CD, and IHD mortalities and PM2.5 and calculate health and economic benefits when the annual average concentration of PM2.5 was reduced to National Ambient Air Quality Standard (NAAQS) and World Health Organization (WHO) guidelines by using our concentration response (C-R) functions. There were 435.22 (95% CI 253.86 to 616.57) all-cause, 130.22 (95% CI 66.34 to194.09) IHD, and 204.07 (95% CI 111.66 to 296.47) CD deaths attributed to PM2.5 and the economic benefits obtained by preventing all-cause, IHD, and CD mortalities were equivalent to be 2.79%, 0.83%, and 1.31% of Baodi's GDP in Tianjin in 2017, respectively. PM2.5 concentration was positive with all-cause, IHD, and CD mortalities in rural, suburban, and urban area of Tianjin, China. Meanwhile, the number of avoidable deaths and economic cost of reducing PM2.5 concentrations to NAAQS and WHO guidelines was highest in the rural area.

Stopping the supply of iodized salt alone is not enough to make iodine nutrition suitable for children in higher water iodine areas: A cross-sectional study in northern China.

BACKGROUND: For the sake of children's health, iodized salt supply has been stopped in many areas with excessive iodine in the drinking water, but children's iodine nutrition status and thyroid function after terminating the iodized salt supply is unknown. Objective We assessed the iodine nutrition, thyroid function and influencing factors for thyroid abnormalities in children from areas with different concentrations of water iodine; the supply of iodized salt has been stopped in high water iodine areas. This study aimed to evaluate whether the strategy of stopping the supplies of iodized salt alone is enough to avoid thyroid dysfunction in all areas with excess water iodine while still meeting the iodine nutrition needs of children. METHODS: A cross-sectional study was conducted in children from four areas with different drinking water iodine concentrations in Tianjin, China. The drinking water samplings and spot urine samples were collected to estimate the external and internal iodine exposure levels. The thyroid volume was measured, and blood samples were collected to assess thyroid function. Logistic regression analysis was used to analyze risk factors for thyroid abnormalities. A dietary survey was conducted to determine the sources of iodine nutrition among the areas with different iodine concentrations in the drinking water. RESULTS: In the area with a drinking water iodine concentration ≥300 µg/L, the median urinary iodine concentration (UIC) in children was 476.30 (332.20-639.30) µg/L, which was higher than that in other groups (all P < 0.05), and the prevalence of thyroid nodules and the thyroid goiter rate were higher than those in the <100 µg/L, 100-150 µg/L and 150-300 µg/L areas (all P < 0.01). Binary logistic regression analysis indicated that the risk of thyroid abnormalities was significantly increased in the UIC 200-299 µg/L group (OR: 4.534; 95% CI: 1.565, 13.135; bootstrapped 95% CI: 1.689, 21.206, P = 0.004) and in the UIC ≥ 300 µg/L group (OR: 6.962; 95% CI: 2.490, 19.460; bootstrapped 95% CI: 2.838, 32.570, P = 0.001) compared to the 100-199 µg/L group. The iodine contribution rates from water in areas with water iodine concentrations ≥300 µg/L are up to 63.04%. CONCLUSIONS: After termination of the iodized salt supply, the level of iodine nutrition of children in the area with drinking water iodine concentrations ≥300 µg/L is still excessive. The water source needs to be replaced in this area. In the area with a water iodine concentration of 150-300 µg/L, it is proposed that stopping the supply of iodized salt is sufficient to achieve the proper iodine nutrition status in children.