Background Takotsubo syndrome (TTS) is frequently misdiagnosed as acute coronary syndrome (ACS), yet a substantial proportion of patients present without typical ACS features—often leading to delayed recognition and suboptimal management. The prognostic implications of the non-ACS phenotype remain poorly characterized, particularly in Asian populations. Objectives This study aimed to investigate the treatment patterns and outcomes of non-ACS TTS. Methods Using data from the multicenter TAKOC (Takotsubo syndrome of Chinese patients) Registry (18 tertiary hospitals in China), we compared 421 TTS patients stratified by initial presentation: ACS-like (typical chest pain, ischemic electrocardiogram changes, and peak troponin >10-fold the upper limit of normal) versus non-ACS. Inverse probability of treatment weighting was applied to account for baseline imbalances. Results Non-ACS TTS (n = 257, 61.0%) was associated with male sex, physical triggers, dyspnea as primary symptom, lower left ventricular ejection fraction, and higher incidence of cardiogenic shock. Paradoxically, despite significantly lower troponin levels, these patients experienced markedly higher 30-day all-cause mortality (adjusted HR: 2.28; 95% CI: 1.18-4.41; P = 0.017) and long-term mortality (adjusted HR: 2.44; 95% CI: 1.32-4.51; P = 0.043). Patients in the non-ACS group required more intensive in-hospital support—including diuretics, vasoactive drugs, and mechanical circulatory support; however, they received fewer cardiovascular medications (antiplatelets, beta-blockers, and renin-angiotensin-aldosterone system inhibitors) that were independently associated with lower 30-day mortality. Conclusions Non-ACS presentation defines a high-risk TTS subtype characterized by atypical symptoms and disproportionately poor outcomes—despite less pronounced biomarker elevation. These findings underscore the critical need for heightened clinical suspicion and exploring effective treatment strategies for patients with TTS. (Registration number: ChiCTR2300075095).

Background: The role of sodium-glucose cotransporter-2 inhibitors in patients with acute myocardial infarction remains elusive.Aim: To evaluate the effect of early application of a sodium-glucose cotransporter-2 inhibitor on ventricular remodelling and prognosis in patients with anterior wall acute myocardial infarction.Methods: In this prospective study, 102 patients diagnosed with anterior wall acute myocardial infarction were enrolled and divided into intervention and control groups according to the use of dapagliflozin within 24 hours after admission. Demographic and clinical data, including age, sex, associated co-morbidities, number of lesions, length of hospital stay, N-terminal prohormone of brain natriuretic peptide, left ventricular ejection fraction, left ventricular end-systolic and end-diastolic diameters and drug-related adverse reactions, were collected and analysed between the two groups. All patients were followed up 1, 3 and 6 months after discharge.Results: At 6 months, left ventricular ejection fraction was higher (55.98 ± 7.17% vs 52.71 ± 7.78%; P = 0.03) and N-terminal prohormone of brain natriuretic peptide was lower (141.52 ± 83.18 vs 203.69 ± 152.13 pg/mL; P = 0.01) in the intervention group versus the control group. Left ventricular end-systolic diameter (35.68 ± 4.32 vs 38.00 ± 5.01 mm; P = 0.01) and left ventricular end-diastolic diameter (50.48 ± 4.90 vs 52.67 ± 4.91 mm; P = 0.03) were smaller in the intervention group versus the control group. Event-free survival rates were better in the intervention group than in the control group (90% vs 74.5%; P = 0.03). The cumulative incidence of drug-related adverse reactions was similar in the two groups (14% vs 4.0%; P = 0.15).Conclusions: Use of dapagliflozin within 24 hours after admission can improve cardiac function, inhibit ventricular remodelling, improve clinical prognosis and have high safety in patients with anterior wall acute myocardial infarction during 6-month follow-up.

Background: Rheumatic heart disease (RHD), which is caused mainly by Group A Streptococcus, leads to fibrotic damage to heart valves. Recently, endothelial‒mesenchymal transition (EndMT), in which activin plays an important role, has been shown to be an important factor in RHD valvular injury. However, the mechanism of activin activity and EndMT in RHD valvular injury is not clear. Methods: Our study was divided into two parts: in vivo and in vitro. We constructed a small interfering RNA (ACVR2A-siRNA) by silencing activin receptor type IIA (ACVR2A) and an adeno-associated virus (AAV-ACVR2A) containing a sequence that silenced ACVR2A. The EndMT cell model was established via human umbilical vein endothelial cells (HUVECs), and the RHD animal model was established via female Lewis rats. ACVR2A-siRNA and AAV-ACVR2A were used in the above experiments. Results: EndMT occurred in the valvular tissues of RHD rats, and activin and its associated intranuclear transcription factors were also activated during this process, with inflammatory infiltration and fibrotic damage also occurring in the valvular tissues. After inhibition of ACVR2A, EndMT in valvular tissues was also inhibited, and inflammatory infiltration and fibrosis were reduced. Endothelial cell experiments suggested that mesenchymal transition could be stimulated by activin and that inhibition of ACVR2A attenuated mesenchymal transition. Conclusions: Activin plays an important role in signal transduction during EndMT after activation, and inhibition of ACVR2A may attenuate RHD valvular damage by mediating EndMT. Targeting ACVR2A may be a therapeutic strategy to alleviate RHD valvular injury.

Accurate prediction of intensive care unit (ICU) survival remains challenging due to heterogeneous clinical data. This study shows that contextualized biomedical language processing markedly enhances ICU survival prediction. Multimodal models integrating structured laboratory data with unstructured text (chief complaints and International Classification of Diseases [ICD] entries) were trained and validated using MIMIC-IV, MIMIC-III, and eICU datasets. The BioBERT-enhanced convolutional neural network achieved area under the receiver operating characteristic curves (AUROCs) of 0.889 (strict cohort, n = 5,795) and 0.974 (lenient cohort, n = 58,615) during external validation. Excluding text features or replacing free-text ICD entries with coded formats reduced performance (AUROC from 0.983 to 0.946-0.947), highlighting the importance of contextual embeddings. As a secondary task, cerebrospinal fluid culture prediction achieved AUROC = 0.853. Overall, integrating contextualized biomedical language representations significantly improves multimodal learning and ICU survival prediction.

Previous findings have indicated the potential benefits of the Chinese traditional medicine Qiliqiangxin (QLQX) in heart failure. Here we performed a double-blind, randomized controlled trial to evaluate the efficacy and safety of QLQX in patients with heart failure and reduced ejection fraction (HFrEF). This multicenter trial, conducted in 133 hospitals in China, enrolled 3,110 patients with HFrEF with NT-proBNP levels of >= 450 pg ml(-1) and left ventricular ejection fraction of <= 40%. Participants were randomized to receive either QLQX capsules or placebo (four capsules three times daily) alongside standard heart failure therapy. The trial met its primary outcome, which was a composite of hospitalization for heart failure and cardiovascular death: over a median follow-up of 18.3 months, the primary outcome occurred in 389 patients (25.02%) in the QLQX group and 467 patients (30.03%) in the placebo group (hazard ratio (HR), 0.78; 95% confidence interval (CI), 0.68-0.90; P < 0.001). In an analysis of secondary outcomes, the QLQX group showed reductions in both hospitalization for heart failure (15.63% versus 19.16%; HR, 0.76; 95% CI, 0.64-0.90; P = 0.002) and cardiovascular death (13.31% versus 15.95%; HR, 0.83; 95% CI, 0.68-0.996; P = 0.045) compared to the placebo group. All-cause mortality did not differ significantly between the two groups (HR, 0.84; 95% CI, 0.70-1.01; P = 0.058) and adverse events were also comparable between the groups. The results of this trial indicate that QLQX may improve clinical outcomes in patients with HFrEF when added to conventional therapy.

Rheumatic heart disease (RHD) is an important and preventable cause of cardiovascular death and disability, but the lack of clarity about its exact mechanisms makes it more difficult to find alternative methods or prevention and treatment. We previously demonstrated that increased IL-17 expression plays a crucial role in the development of RHD-related valvular inflammatory injury. Macrophage autophagy/polarization may be a pro-survival strategy in the initiation and resolution of the inflammatory process. This study investigated the mechanism by which IL-17 regulates autophagy/polarization activation in macrophages. A RHD rat model was generated, and the effects of anti-IL-17 and 3-methyladenine (3-MA) were analyzed. The molecular mechanisms underlying IL-17-induced macrophage autophagy/polarization were investigated via in vitro experiments. In our established RHD rat model, the activation of the macrophage PINK1/Parkin autophagic pathway in valve tissue was accompanied by M1 macrophage infiltration, and anti-IL-17 treatment inhibited autophagy and reversed macrophage inflammatory infiltration, thereby attenuating endothelial-mesenchymal transition (EndMT) in the valve tissue. The efficacy of 3-MA treatment was similar to that of anti-IL-17 treatment. Furthermore, in THP-1 cells, the pharmacological promotion of autophagy by IL-17 induced M1-type polarization, whereas the inhibition of autophagy by 3-MA reversed this process. Mechanistically, silencing PINK1 in THP-1 blocked autophagic flux. Moreover, IL-17-induced M1-polarized macrophages promoted EndMT in HUVECs. This study revealed that IL-17 plays an important role in EndMT in RHD via the PINK1/Parkin autophagic pathway and macrophage polarization, providing a potential therapeutic target.

aDepartment of Ophthalmology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China bDepartment of Vascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China cDepartment of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi Province, China Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. Published online ■ ■ *Corresponding author. Address: Department of Ophthalmology, The Second Affiliated Hospital of Xi'an Jiaotong University, No. 157, West Five Road, Xi'an, Shaanxi, 710004, China. Tel: +86 29 87679449. E-mail address: [email protected] (Z. Liu). This is an open access article distributed under the Creative Commons Attribution-NoDerivatives License 4.0, which allows for redistribution, commercial and non-commercial, as long as it is passed along unchanged and in whole, with credit to the author. http://creativecommons.org/licenses/by-nd/4.0/

Purposes: This study aims to explore the sensitivity and efficacy of the TyG index in the screening of postmenopausal osteoporosis, and to provide an objective new method for the prevention and early screening of postmenopausal osteoporosis. Methods: This retrospective study selected 1032 subjects who completed bone mineral density examination in the Department of Nuclear Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine from January 2021 to December 2023 according to the inclusion and exclusion criteria. The baseline data include age, weight, height, BMI, lumbar spine T-value (LS T-value), total hip T-value (TH T-value), femoral neck T-value (FN T-value), fasting blood glucose (FBG), triglyceride (TG), the TyG index and OSTA. After grouping, the differences in postmenopausal osteoporosis were compared. The correlation of the TyG index and OSTA with baseline data was analyzed. The ROC curve results of the TyG index in the total population, 60-year-old stratification, FBG and TG stratification were analyzed, and the sensitivity and efficacy of the TyG index in the screening of postmenopausal osteoporosis were obtained. Results: In 1032 postmenopausal women, there were significant differences (P< 0.001) in age, weight, height, BMI, and T-values of three different sites, the TyG index and OSTA. The results of correlation analysis showed that the TyG index and OSTA were positively correlated with weight, BMI, and T-values of three different sites in 1032 postmenopausal women and after 60-year-old stratification (P<0.001). In the total population and after stratification by 60 years old, the TyG index was positively correlated with FBG and TG (P<0.001), but not correlated with age and height. Meanwhile, OSTA was negatively correlated with age (P<0.001) and positively correlated with height (P<0.001). OSTA was not correlated with FBG and TG in the total population and in postmenopausal women aged <60, but was positively correlated with TG in postmenopausal women aged≥60 (P<0.001). ROC curve analysis showed that the area under the curve of the TyG index and OSTA was close in postmenopausal women aged≥60 with abnormal FBG and/or TG. The cut-off value of the TyG index in postmenopausal women aged≥60 was higher than that in postmenopausal women aged<60, indicating that the risk of osteoporosis increased in postmenopausal women aged≥60 with increased TyG index. Conclusion: The TyG index has the potential to objectively screen osteoporosis in postmenopausal women aged≥60 and postmenopausal women aged≥60 with abnormal FBG and/or TG.

This study aims to evaluate the effects of Omaha System framework interventions on quality of life, emotional well-being, and sleep quality in 507 mid to late-stage lung cancer patients. Retrospectively, we compared data of 294 patients receiving conventional care (conventional group) with 213 patients undergoing Omaha System interventions (intervention group) from January 2019 to January 2023. Key indicators included quality of life (FACT-L), anxiety (SAS), depression (SDS), sleep quality (PSQI), hope (HHS), and dignity (PDI). Post-intervention, the intervention group showed a significant increase in FACT-L scores (P<0.001), indicating enhanced quality of life. There was a notable reduction in PSQI scores (P<0.001), suggesting improved sleep quality. Additionally, their anxiety and depression levels significantly decreased, as evidenced by lower SAS (P<0.001) and SDS scores (P<0.001). Logistic regression revealed that care nursing intervention scheme (P=0.007), age (P=0.008), marital status (P=0.002), per capita monthly household income (P=0.004), SAS after intervention (P=0.002), and PSQI after intervention (P=0.002) had a positive influence on quality of life. In conclusion, the Omaha System interventions markedly improved the quality of life, emotional state, and sleep in lung cancer patients.

OBJECTIVE:To explore the relationship between serum irisin levels and glucose and lipid metabolism among adolescents in Yinchuan City. METHODS:From 2017 to 2020, a conbination of convenient sampling and stratified cluster random sampling method were used to select 1219 adolescents aged 12 to 18 years old in Yinchuan City as research subjects. The height and weight were measured using the height and sitting height meter and the bioelectrical impedance analyzer. Blood indicators such as fasting plasma glucose(FPG), totalcholesterol(TC), triglyceride(TG), low-density lipoprotein cholesterol(LDL-C) and high-density lipoprotein cholesterol(HDL-C) were measured using fully automatic biochemical analyzer. Serum irisin levels were measured by enzyme-linked immunosorbent assay(ELISA). Binary logistic regression was used to analyze the correlation between irisin and abnormal glucose and lipid metabolism. RESULTS:The FPG, TC, HDL-C and LDL-C levels of subjects in the highest tertile of irisin levels were significantly lower than those of subjects in the lowest tertile of irisin levels(F values were 5.13, 3.15, 3.07 and 5.01, P&lt;0.05), and the differences were statistically significant(all P&lt;0.05). The serum irisin levels in the hyperglycemia group(t=2.87, P&lt;0.01), hypercholesterolemia group(t=2.36, P=0.02) and hyperLDL-Cemia group(t=2.34, P=0.02) were significantly lower than those in the normoglycemia group, normal TC group and normal LDL-C group. Meanwhile, the irisin level in the low HDL-Cemia group(t=-2.57, P=0.01) was significantly higher than that in the normal HDL-C group, and the differences were statistically significant(P&lt;0.05). Participants in the highest tertile of irisin had 0.51, 0.49 and 0.50 times the risk of hyperglycemia(OR=0.51, 95%CI 0.29-0.87), hypercholesterolemia(OR=0.49, 95%CI 0.27-0.89) and hyperLDL-cemia(OR=0.50, 95%CI 0.25-0.99) compared with those in the lowest tertile. CONCLUSION:Low levels of irisin are associated with the occurrence of hyperglycemia, hypercholesterolemia, and hyperLDL-Cemia in adolescents.

Background: Rheumatic heart disease (RHD) is caused by inflammatory cells mistakenly attacking the heart valve due to Group A Streptococcus (GAS) infection, but it is still unclear which cells or genes are involved in the process of inflammatory cells infiltrating the valve. Inflammatory infiltration into the target tissue requires an increase in the expression of phosphorylated vascular endothelial-cadherin (p-VE-cad), p-VE-cad can increase the endothelial permeability and promote the migration of inflammatory cells across the endothelium. P-VE-cad is potentially regulated by RAS-related C3 botulinum substrate 1 (RAC1), together with phosphorylated proline-rich tyrosine kinase 2 (p-PYK2). While RAC1/p-PYK2/p-VE-cad is triggered by the activation of vascular cell adhesion molecule-1 (VCAM-1). VCAM-1 is related to M1 macrophages adhering to the endothelium via very late antigen 4 (VLA4). Inflammatory infiltration into the valve is extremely important in the early pathogenesis of RHD. However, there is no relevant research on whether M1/VLA4/VCAM-1/RAC1/p-PYK2/p-VE-cad is involved in RHD; therefore, what we explored in this study was whether M1/VLA4/VCAM-1/RAC1/p-PYK2/p-VE-cad is involved. Methods: We established a rat model of RHD and a cell model of M1 macrophage and endothelial cell cocultivation. Subsequently, we measured the degree of inflammatory cell infiltration, the levels of IL-6/IL-17, the degree of fibrosis (COL3/1), and the expression levels of fibrosis markers (FSP1, COL1A1 and COL3A1) in the heart valves of RHD rats. Additionally, we detected the expression of M1/M2 macrophage biomarkers in rat model and cell model, as well as the expression of M1/VLA4/VCAM-1/RAC1/p-PYK2/p-VE-cad. We also tested the changes in endothelial permeability after coculturing M1 macrophages and endothelial cells. Results: Compared to those in the control group, the levels of inflammatory cell infiltration and fibrotic factors in the heart valves of RHD rats were significantly higher; the expression of M1 macrophage biomarkers (iNOS, CD86 and TNF-α) in RHD rats was significantly higher; and significantly higher than the expression of M2 macrophage biomarkers (Arg1 and TGF-β). And the expression levels of VLA4/VCAM-1 and RAC1/p-PYK2/p-VE-cad in the hearts of RHD rats were significantly higher. At the cellular level, after coculturing M1 macrophages with endothelial cells, the expression levels of VLA4/VCAM-1 and RAC1/p-PYK2/p-VE-cad were significantly higher, and the permeability of the endothelium was significantly greater due to cocultivation with M1 macrophages. Conclusions: All the results suggested that M1 macrophages and the VLA4/VCAM-1 pathway are potentially involved in the process of inflammatory infiltration in RHD.

Background: Rheumatic heart disease (RHD) is an autoimmune disease caused by recurrent infections of Group A streptococcus (GAS), ultimately leading to inflammation and the fibrosis of heart valves. Recent studies have highlighted the crucial role of C-C chemokine receptor type 2-positive (CCR2+) macrophages in autoimmune diseases and tissue fibrosis. However, the specific involvement of CCR2+ macrophages in RHD remains unclear. Methods: This study established an RHD rat model using inactivated GAS and complete Freund’s adjuvant, demonstrating a correlation between CCR2+ macrophages and fibrosis in the mitral valves of these rats. Results: Intraperitoneal injection of the CCR2 antagonist Rs-504393 significantly reduced macrophage infiltration, inflammation, and fibrosis in valve tissues of RHD rats compared to the solvent-treated group . Existing evidence suggests that C-C motif chemokine ligand 2 (CCL2) acts as the primary recruiting factor for CCR2+ cells. To validate this, human monocytic leukemia cells (THP-1) were cultured in vitro to assess the impact of recombinant CCL2 protein on macrophages. CCL2 exhibited pro-inflammatory effects similar to lipopolysaccharide (LPS), promoting M1 polarization in macrophages. Moreover, the combined effect of LPS and CCL2 was more potent than either alone. Knocking down CCR2 expression in THP-1 cells using small interfering RNA suppressed the pro-inflammatory response and M1 polarization induced by CCL2. Conclusions: The findings from this study indicate that CCR2+ macrophages are pivotal in the valvular remodeling process of RHD. Targeting the CCL2/CCR2 signaling pathway may therefore represent a promising therapeutic strategy to alleviate valve fibrosis in RHD.

Introduction: The relationship between sleep duration and metabolic syndrome (MetS) remains debatable. In the present study, we analysed the link between total sleep duration (including nighttime sleep and nap duration) and MetS as well as its components among the Chinese population. Material and methods: This was a cross-sectional study from a prospective population cohort including 8616 participants over 40 years in Guangxi, China, evaluated from April 2011 to January 2012. MetS was diagnosed using modified criteria from the National Cholesterol Education Program's Adult Treatment Panel III. Sleep information was obtained through a standard self-report-based questionnaire. The connection between sleep duration and MetS prevalence as well as its components was evaluated using a logistic regression model. Results: After adjusting for potential confoundings, the longer daily sleep duration (>= 10 hours) group was observed to have the higher odds of having MetS than the reference group with >= 7 and < 8 hours of sleep [odds ratio (OR): 1.25, 95% confidence interval (CI): 1.03-1.52, p = 0.023], as well as the highest odds of having elevated triglycerides (OR: 1.25, 95% CI: 1.03-1.52) and fasting blood glucose (OR: 1.21, 95% CI: 1.01-1.45). Further analysis demonstrated that sleeping > 9 hours per night was correlated to MetS in females (OR: 1.27, 95% CI: 1.02-1.58), while napping >= 90 minutes was correlated to MetS (OR: 1.44, 95% CI: 1.11-1.87) in males. Conclusion: Both longer nighttime sleep duration and longer naps may be associated with the development of MetS.

Background: Qiliqiangxin (QLQX) is a traditional Chinese medicine used to treat heart failure but its effects on the clinical outcomes in addition to current standard of care have not previously been assessed in a randomised controlled trial. We aimed to investigate the efficacy and safety of QLQX in patients with chronic heart failure.Methods: This randomised, double-blind, clinical trial was conducted at 133 hospitals from May 24, 2019, to May 24, 2021 in China, involving consecutive patients with chronic heart failure (with left ventricular ejection fraction ≤40% and NT-proBNP ≥ 450pg/ml). A total of 4064 patients were assessed for eligibility, and 3110 were enrolled and followed up for at least 12 months. Patients were randomised to QLQX 4 capsules thrice daily or matching placebo 4 capsules thrice daily, in addition to established heart failure therapy. The primary outcome was major adverse composite endpoint of cardiovascular (CV) death and/or hospitalisation for heart failure (HHF). This study is registered with Chinese Clinical Trial Registry, ChiCTR.org.cn (ChiCTR1900021929).Findings: Over a median of 18.3 months follow-up, a primary outcome event occurred in 389 of 1555 patients (25.02%) in the QLQX group and in 467 of 1555 patients (30.03%) in the placebo group (hazard ratio [HR], 0.78; 95% confidence interval [CI], 0.68 to 0.90; p<0.001). This effect was related to both lower risks of HHF and CV death in the QLQX group. HHF occurred in 243 patients (15.63%) in QLQX group and 298 patients (19.16%) in placebo group (HR, 0.76; 95% CI, 0.64 to 0.90; p=0.002). Death from cardiovascular causes occurred in 207 patients (13.31%) in the QLQX group and in 248 patients (15.95%) in the placebo group (HR, 0.83; 95% CI, 0.68 to 0.996; p=0.045); 221 patients (14.21%) and 262 patients (16.85%), respectively, died from any cause (HR, 0.84; 95% CI, 0.70 to 1.01; P=0.058). The frequency of adverse events did not differ between two treatment groups.Interpretation: In patients with heart failure and a reduced ejection fraction, QLQX reduced the incidence of death from cardiovascular causes or hospitalisation for heart failure compared with those who received placebo.Trial Registration: This study is registered with Chinese Clinical Trial Registry, ChiCTR.org.cn (ChiCTR1900021929).Funding: Supported by National Key Technologies R&D Program, Modernization of Traditional Chinese Medicine of Ministry of Science and Technology (China), Key Program of National Natural Science Foundation (China), General Program of National Natural Science Foundation (China), and Shijiazhuang Yiling Pharmaceutical Co., Ltd.Declaration of Interest: QUEST is funded by National Key Technologies R&D Program, Modernization of Traditional Chinese Medicine of Ministry of Science and Technology of the People's Republic of China (Project No. 2017YFC1700500 to Zhenhua Jia, 2017YFC1700505 to Xinli Li), the Key Program of National Natural Science Foundation of China (81730106 to Xinli Li), and General Program of National Natural Science Foundation of China (81970339 to Xinli Li, 82270394 to Haifeng Zhang, 82200425 to Rongrong Gao). Shijiazhuang Yiling Pharmaceutical Co., Ltd. (Shijazhuang, People’s Republic of China) provided part of the funding and the study drug for this research. Prof. Xinli Li and Zhenhua Jia are Associate Fellows at National Key Laboratory for Innovation and Transformation of Luobing Theory. Prof. Xinli Li and Haifeng Zhang are Associate Fellows at the Collaborative Innovation Center for Cardiovascular Disease Translational Medicine. All funding sources are not involved in the design of the study and collection, enrollment, statistical analysis, interpretation of data and in writing the manuscript. Prof. Xinli Li reports receiving grant support (all grant support listed paid to the First Affiliated Hospital with Nanjing Medical University) from Novartis and China Heart Failure Center, receiving lecture fees and consulting fees from AstraZeneca, Bayer, Novartis, Roche, and Yiling. Prof. Zhenhua Jia reports affiliated to Hebei Yiling Hospital, a non-profit medical institution, which is two completely independent legal entities with Shijiazhuang Yiling Pharmaceutical Co., LTD. Prof Zhenhua Jia is the spouse of Ms. Rui Wu, who holds shares and serves as a director of Shijiazhuang Yiling Pharmaceutical Co., LTD. He has fully disclosed these interests to the research committee and have developed an approved plan to manage any potential conflicts that may arise from such an arrangement and ensured the scientificity, objectivity, and authority of the research results. Prof. Haifeng Zhang reports receiving lecture fees from AstraZeneca, Bayer, Novartis, and Servier. Dr. Iokfai Cheang reports receiving lecture fees from Haoyishu and Novartis. Dr. Wenming Yao reports receiving lecture fees from Bayer, Novartis, Sanofi, and Yiling. Dr. Yanli Zhou reports receiving lecture fees from Novartis. Dr. Shengen Liao reports receiving lecture fees from Novartis. Dr. Jianhua Wu reports receiving lecture fees from AstraZeneca and Novartis. Dr. Chunxin Cha reports receiving lecture fees and consulting fees from AstraZeneca, Bayer, and Pfizer. Dr. Qian Ren reports receiving lecture fees and consulting fees from Bayer, Qilu pharmaceutical, and China Medical System. No other potential conflict of interest relevant to this article was reported.Ethical Approval: The protocol was reviewed and approved by the independent ethics committee of the First Affiliated Hospital of Nanjing Medical University (Approved No. of ethic committee: 2018-SR-275) and each participating study center.

BackgroundHeart Failure (HF) is the end-stage cardiovascular syndrome with poor prognosis. Proteomics holds great promise in the discovery of novel biomarkers and therapeutic targets for HF. The aim of this study is to investigate the causal effects of genetically predicted plasma proteome on HF using the Mendelian randomization (MR) approach.MethodsSummary-level data for the plasma proteome (3,301 healthy individuals) and HF (47,309 cases; 930,014 controls) were extracted from genome-wide association studies (GWASs) of European descent. MR associations were obtained using the inverse variance-weighted (IVW) method, sensitivity analyses, and multivariable MR analyses.ResultsUsing single-nucleotide polymorphisms as instrumental variables, 1-SD increase in MET level was associated with an approximately 10% decreased risk of HF (odds ratio [OR]: 0.92; 95% confidence interval [CI]: 0.89 to 0.95; p = 1.42 × 10−6), whereas increases in the levels of CD209 (OR: 1.04; 95% CI: 1.02–1.06; p = 6.67 × 10−6) and USP25 (OR: 1.06; 95% CI: 1.03–1.08; p = 7.83 × 10−6) were associated with an increased risk of HF. The causal associations were robust in sensitivity analyses, and no evidence of pleiotropy was observed.ConclusionThe study findings suggest that the hepatocyte growth factor/c-MET signaling pathway, dendritic cells-mediated immune processes, and ubiquitin-proteasome system pathway are involved in the pathogenesis of HF. Moreover, the identified proteins have potential to uncover novel therapies for cardiovascular diseases.

Objective:To explore the role of professional organ procurement nurses in organ donation and procurement efforts.Methods:The data of donors who underwent organ donation before and after setting up professional organ procurement nurses in the First Affiliated Hospital of Xi′an Jiaotong University were retrospectively analyzed. The 215 donors who underwent organ donation from September 1, 2021 to August 31, 2022 after setting up professional organ procurement nurses were used as the observation group, and the 203 donors who underwent organ donation from September 1, 2020 to August 31, 2021 before setting up professional organ procurement nurses were used as the control group. The donor sex, age, primary disease, and the organ procurement operation time, organ warm ischemia time and organ transport time were compared between the two groups.Results:There were no statistically differences in sex, age and primary disease between the two groups (all P>0.05). In the control group and the observation group, there were 176 and 185 donors underwent combined liver and kidney procurement, and the operation time was (36±4) and (32±4) min, respectively, and the difference was statistically significant (t=10.21, P<0.05). Among them, there were 124 and 82 Chinese Ⅱ and Chinese Ⅲ organ donations, respectively, and the organ warm ischemia time was (8.6±1.5) and (8.2±1.7) min, and the difference was statistically significant (t=1.99, P<0.05). In the control group and the observation group, 34 and 76 organs were transferred to the external transplantation center, and the organ transfer time was (6.0±0.8) and (5.1±1.0) h, respectively, and the difference was statistically significant (t=5.47, P<0.05).Conclusion:Professional organ procurement nurses play an active role in promoting organ donation and procurement, providing a solid foundation for the quantity and quality assurance of organ donation and transplantation, and providing a practical basis for organ donation specialization, organ procurement organization construction discipline, and transplantation discipline systematization.

Data regarding different metabolic phenotypes and bone markers including bone mineral content (BMC) and osteocalcin (OCN) among children and adolescents are very limited. Hence, the purpose of this investigation was to explore the relationship between different metabolic phenotypes and BMC or OCN among Chinese children and adolescents. This cross-sectional study included 1,328 children and adolescents aged between 12 and 18 years who were selected from four schools in Yinchuan city from 2018 to 2020 by stratified cluster random sampling. Subjects were divided into four groups according to BMI and metabolic status, as follows: metabolically healthy obesity (MHO), metabolically unhealthy obesity (MUO), metabolically unhealthy normal weight (MUNW), and metabolically healthy normal weight (MHNW). The MHNW, MUNW, MHO, and MUO phenotypes in boys were 48.4%, 30.5%, 6.7%, and 14.4%, respectively, and were 47.8%, 33.6%, 6.6%, and 12.1% in girls, respectively. The MHO and MUO phenotypes had higher BMC than the MHNW or MUNW phenotype (all p < 0.05), and the MUO phenotype with BMC was significantly higher than MHO group in boys (p < 0.05). We discovered a significant positive correlation between BMC and the MHO (OR = 8.82, 95% CI = 2.04-38.16), MUO phenotypes (OR = 13.53, 95% CI = 4.10-44.70), while no association was found between OCN and metabolic phenotypes in neither boys nor girls. Overweight/obese children and adolescents had higher BMC, and there existed sex differences in the effect of metabolic status on BMC among them. OCN was not supposed to be an index of bone health in this study.

The underlying mechanisms of the development of unhealthy metabolic phenotypes in obese children and adolescents remain unclear. We aimed to screen the metabolomes of individuals with the unhealthy obesity phenotype and identify the potential metabolic pathways that could regulate various metabolic profiles of obesity in Chinese adolescents. A total of 127 adolescents aged 11–18 years old from China were investigated using a cross-sectional study. The participants were classified as having metabolically healthy obesity (MHO) or metabolically unhealthy obesity (MUO) based on the presence/absence of metabolic abnormalities defined by metabolic syndrome (MetS) and body mass index (BMI). Serum-based metabolomic profiling using gas chromatography–mass spectrometry (GC–MS) was undertaken on 67 MHO and 60 MUO individuals. ROC analyses showed that palmitic acid, stearic acid, and phosphate could predict MUO, and that glycolic acid, alanine, 3-hydroxypropionic acid, and 2-hydroxypentanoic acid could predict MHO (all p < 0.05) from selected samples. Five metabolites predicted MUO, 12 metabolites predicted MHO in boys, and only two metabolites predicted MUO in girls. Moreover, several metabolic pathways may be relevant in distinguishing the MHO and MUO groups, including the fatty acid biosynthesis, fatty acid elongation in mitochondria, propanoate metabolism, glyoxylate and dicarboxylate metabolism, and fatty acid metabolism pathways. Similar results were observed for boys except for phenylalanine, tyrosine and tryptophan biosynthesis, which had a high impact [0.098]. The identified metabolites and pathways could be efficacious for investigating the underlying mechanisms of the development of different metabolic phenotypes in obese Chinese adolescents.

Objective The aim of the study was to explore the relationship between a body shape index（ABSI）,onicity index（CI）,three-dimensional body mass index（TMI）,and dyslipidemia in children and adolescents in Yinchuan. The results of the study were expected to provide a stronger basis for the prevention of dyslipidemia in children and adolescents. Methods A cluster sampling method was used to randomly select 1 175children and adolescents aged 12-18 years in Yinchuan City as the research objects. Questionnaire survey,physical examination,and blood lipid level measurement were carried out. The predictive ability of different fat indicators and dyslipidemia was studied by using receiver operating characteristic curve（ROC）. Results Normal body mass index（BMI）,waist-to-height ratio（WHt R）,ABSI,and CI were positively correlated with total cholesterol（TC）,triglyceride cholesterol（TG）,and Low-density lipoprotein cholesterol（LDL-C）in both males and females（P all＜0.001）. BMI,waist circumference（WC）,WHt R and CI were negatively correlated with high-density lipoprotein cholesterol（HDL-C）in males（P all＜0.001）. Roc was plotted with high TC,high TG,low HDL-C,and dyslipidemia as dependent variables. The area under the ROC curve（AUC）of WC and CI in males and females was larger than that of BMI and WHt R,the AUC area of male CI was the largest（0.77,0.79,0.71,0.64 respectively）,while the area under the ROC curve of ABSI and TMI was smaller.Conclusion WC and CI have a strong correlation with the level of blood lipids,and have a good effect in predicting high TC,high TG,low HDL-C,and abnormal blood lipids,and CI has a better effect in predicting the risk of high TC and high TG in males.