BACKGROUND:Although a few studies have found that healthy lifestyle is linked to a range of non-communicable chronic diseases (NCDs), its association with the onset, progression, and prognosis of multimorbidity of NCDs (MNCDs) has never been studied. METHOD:A total of 332 444 adults aged 39-73 years who were free of heart disease, stroke, diabetes, and cancer at baseline were selected. Then we used multi-state model to analyze the associations between healthy lifestyle and transition trajectory were analyzed with results expressed as hazard ratio (HR) and 95% confidence interval. RESULTS:A total of 62 994 participants developed first NCDs (FNCDs). After adjustment for potential confounders, healthy lifestyle was negatively associated with the transition trajectory from baseline to FNCD (HR = 0.38), from FNCDs to MNCDs (HR = 0.30), etc. Further, the transition trajectory from FNCDs to MNCDs became more pronounced among the offspring who aged ˂60 (HRFNCDs → MNCDs = 0.29), who never took medicine(HRFNCDs → MNCDs = 0.25). Besides, possessing all five healthy lifestyle factors could extend the life expectancy of MNCD participants. CONCLUSION:This study suggests that healthy lifestyle is associated with almost all transition phases of MNCDs development and decreases the mortality risk of MNCDs.

High-dimensional proteomics data present significant challenges in biomarker discovery due to technical noise, feature redundancy, and multicollinearity. Current feature selection methods, including filter, wrapper, and embedded approaches, struggle with stability, sparsity, and computational efficiency. To address these limitations, we propose Soft-Thresholded Compressed Sensing (ST-CS), a hybrid framework integrating 1-bit compressed sensing with K-Medoids clustering. Unlike conventional methods relying on manual thresholds, ST-CS automates feature selection by dynamically partitioning coefficient magnitudes into discriminative biomarkers and noise. Evaluations on simulated and real-world proteomic datasets demonstrated ST-CS’s superiority in feature selection capability and classification performance. In simulations, ST-CS achieved feature selection robustness with balanced sensitivity (> 80

This study investigated the role of the Composite Dietary Antioxidant Index (CDAI) in cardiovascular-kidney-metabolic (CKM) syndrome staging and mortality using NHANES 2001–2018 data from 25,155 U.S. adults. Higher CDAI quartiles demonstrated progressively reduced odds of advanced CKM stages versus Stage 0 (Q4 vs. Q1 ORs: Stage 1: 0.71 (0.56–0.91); Stage 2: 0.58 (0.45–0.74); Stage 3: 0.30 (0.20–0.47); Stage 4: 0.46 (0.35–0.60); all P < 0.05). Weighted Quantile Sum regression identified a protective effect of the antioxidant mixture against advanced CKM (OR: 0.82 (0.76–0.88); P < 0.001), primarily driven by vitamins A (weight = 0.357), C (0.290), and selenium (0.212). In CKM patients, higher CDAI was associated with significantly lower all-cause (Q4 vs. Q1 HR: 0.63 (0.57–0.70)), cardiovascular (HR: 0.63 (0.51–0.78)), and non-cardiovascular mortality (HR: 0.63 (0.56–0.72); all P < 0.001). Nonlinear analyses revealed threshold effects for all-cause and non-CVD mortality at CDAI ≈ 0. These findings indicate that elevated CDAI is robustly associated with less severe CKM staging and reduced mortality, supporting dietary antioxidant optimization for CKM management and risk stratification.

The study aimed to assess the effect of lymph node dissection on survival outcomes in patients presenting with early-stage epithelial ovarian cancer and to delineate patient characteristics that may indicate a greater benefit from pelvic lymph node dissection. A retrospective analysis was performed on individuals diagnosed with clinical stage I-II epithelial ovarian cancer who received primary cytoreductive surgery at the Cancer Hospital Affiliated with Harbin Medical University from January 1, 2010, to January 1, 2018. The investigation encompassed an examination of demographic data, clinicopathological profiles, perioperative complications, and survival outcomes. A total of 315 patients diagnosed with ovarian cancer were incorporated into the study and were segregated into two distinct cohorts: 217 patients who underwent lymphadenectomy (Group A) and 98 patients who did not undergo the procedure (Group B). The disparities in progression-free survival and overall survival between the two cohorts did not attain statistical significance (p > 0.05). Upon conducting a subgroup analysis, it was discerned that patients characterized by clear cell carcinoma as the pathological subtype demonstrated a significantly extended progression-free survival post-lymphadenectomy (p = 0.02). Additionally, the operative duration for the patients in Group A was significantly protracted in comparison to Group B (146.15 ± 39.132 min vs. 133.49 ± 35.308 min, P = 0.043). For patients with early-stage ovarian cancer, lymph node dissection does not significantly improve progression-free or overall survival rates. Our findings suggest that individuals with clear cell carcinoma pathology have a higher probability of benefiting in terms of survival following lymph node dissection.

Vascular Electrical Stimulations Hong Li, Liming Yang, and co-workers used battery-free implants and surgically mounted them on the abdominal aorta of high-fat-fed ApoE-/- mice, which were electrically stimulated using a wireless electrical stimulation device for four weeks to observe changes in atherosclerotic plaques. Direct vascular electrical stimulation has emerged as a promising therapeutic strategy for atherosclerosis by reducing atherosclerotic plaque formation through the activation of Sirt1/Atg5 pathway-mediated autophagy. More details can be found in article number 2300584.

Abstract Background Diabetes mellitus (DM) is a chronic metabolic disease that could produce severe complications threatening life. Its early detection is thus quite important for the timely prevention and treatment. Normally, fasting blood glucose (FBG) by physical examination is used for large-scale screening of DM; however, some people with normal fasting glucose (NFG) actually have suffered from diabetes but are missed by the examination. This study aimed to investigate whether common physical examination indexes for diabetes can be used to identify the diabetes individuals from the populations with NFG. Methods The physical examination data from over 60,000 individuals with NFG in three Chinese cohorts were used. The diabetes patients were defined by HbA1c ≥ 48 mmol/mol (6.5%). We constructed the models using multiple machine learning methods, including logistic regression, random forest, deep neural network, and support vector machine, and selected the optimal one on the validation set. A framework using permutation feature importance algorithm was devised to discover the personalized risk factors. Results The prediction model constructed by logistic regression achieved the best performance with an AUC, sensitivity, and specificity of 0.899, 85.0%, and 81.1% on the validation set and 0.872, 77.9%, and 81.0% on the test set, respectively. Following feature selection, the final classifier only requiring 13 features, named as DRING (diabetes risk of individuals with normal fasting glucose), exhibited reliable performance on two newly recruited independent datasets, with the AUC of 0.964 and 0.899, the balanced accuracy of 84.2% and 81.1%, the sensitivity of 100% and 76.2%, and the specificity of 68.3% and 86.0%, respectively. The feature importance ranking analysis revealed that BMI, age, sex, absolute lymphocyte count, and mean corpuscular volume are important factors for the risk stratification of diabetes. With a case, the framework for identifying personalized risk factors revealed FBG, age, and BMI as significant hazard factors that contribute to an increased incidence of diabetes. DRING webserver is available for ease of application ( http://www.cuilab.cn/dring ). Conclusions DRING was demonstrated to perform well on identifying the diabetes individuals among populations with NFG, which could aid in early diagnosis and interventions for those individuals who are most likely missed.

Additional file 1: Fig. S1. Training and validation loss of DNN. Fig. S2. The other 11 characteristics with significant differences between diabetic and non-diabetic individuals with normal fasting glucose. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Fig. S3. Correlation of all features in the training set. Fig. S4. Feature importance ranking of the models constructed by mRMR-selected features. Fig. S5. Number of diabetic patients towards different thresholds of normal fasting glucose. Orange point is a turning point that the number of individuals with diabetes has halved when using 5.69 as the threshold of normal fasting glucose.

Electrical stimulation (ES) is a safe and effective procedure in clinical rehabilitation with few adverse effects. However, studies on ES for atherosclerosis (AS) are scarce because ES does not provide a long-term intervention for chronic disease processes. Battery-free implants and surgically mounted them in the abdominal aorta of high-fat-fed Apolipoprotein E (ApoE(-/-)) mice are used, which are electrically stimulated for four weeks using a wireless ES device to observe changes in atherosclerotic plaques. Results showed that there is almost no growth of atherosclerotic plaque at the stimulated site in AopE(-/-) mice after ES. RNA-sequencing (RNA-seq) analysis of Thp-1 macrophages reveal that the transcriptional activity of autophagy-related genes increase substantially after ES. Additionally, ES reduces lipid accumulation in macrophages by restoring ABCA1- and ABCG1-mediated cholesterol efflux. Mechanistically, it is demonstrated that ES reduced lipid accumulation through Sirtuin 1 (Sirt1)/Autophagy related 5 (Atg5) pathway-mediated autophagy. Furthermore, ES reverse autophagic dysfunction in macrophages of AopE(-/-) mouse plaques by restoring Sirt1, blunting P62 accumulation, and inhibiting the secretion of interleukin (IL)-6, resulting in the alleviation of atherosclerotic lesion formation. Here, a novel approach is shown in which ES can be used as a promising therapeutic strategy for AS treatment through Sirt1/Atg5 pathway-mediated autophagy.

Background and aims The misconception of the purpose of strabismus treatment has, on the one hand, affected the motivation of strabismus patients to seek care and, on the other hand, has resulted in strabismus not being covered by health insurance, both of which interact to limit the motivation of strabismus patients and also impose a financial burden on strabismus patients. Previous studies on the cost of strabismus had only addressed the cost utility and functional and psychosocial benefits of strabismus surgery. The aim of this study was to estimate the direct medical expenditure incurred for strabismus surgery and analyze the trend for the period 2014-2019 using the data collected by local eye hospitals in northeast China. Methods This study was based on 6-year strabismus medical expenditure data collected from the eye hospital of the first affiliated hospital of Harbin medical university, covering 3596 strabismus patients who had strabismus surgery. All medical expenditure data were adjusted to 2014 using China's annual consumer price index to remove the effects of inflation. Results The average direct medical expenditure for strabismus cares (in 2014) was 5309.6 CNY (US$870.4), and the annual growth rates from 2015 to 2019 (compared with the previous year) were 9.3, 7.7, 21.7, 14.5, and 4.3%, respectively. Surgical expenses accounted for the highest proportion (33.1%) of the total medical expenses followed by examinations expenses (19.7%) and medical consumables expenses (18.7%). The regression coefficient for general anaesthesia was 1804.5 and age was less than 0. Conclusion The average direct medical expenditure for strabismus increases year by year, and the growth rate is rapid. Anesthesia was the most important factor increasing medical cost, and age was negatively correlated with cost.

Objectives To assess the associations of sensitisation to common allergens with atopic dermatitis, allergic rhinitis and allergic asthma in adults. Design Case–control study. Setting Data were collected from the First Affiliated Hospital of Harbin Medical University in Harbin, China. Participants Cases were 5111 patients with physician-diagnosed atopic dermatitis (n=2631), allergic asthma (n=1320) and allergic rhinitis (n=1160) recruited from the department of allergy from March 2009 to December 2017. Controls were 2576 healthy adults who underwent physical examination at the same hospital during the same period. Main outcome measures Specific IgE levels to 16 common food, indoor and outdoor allergens were assessed in all participants. Adjusted ORs and 95% CIs for the association between allergen sensitisation and allergic diseases were estimated using multivariate logistic regression. Results The prevalence of allergen sensitisation was higher in patients with atopic dermatitis (indoor=17.14%, outdoor=12.85%, food=21.44%), allergic rhinitis (indoor=23.18%, outdoor=26.81%, food=8.94%) and allergic asthma (indoor=24.65%, outdoor=16.46%, food=14.31%) compared with controls (indoor=11.03%, outdoor=6.84%, food=5.83%). After adjustment for potential confounding variables, there was a dose–response relevance between the levels of allergen-specific IgE and allergic diseases (p trend <0.0001). The number of allergens to which a patient was sensitised increased the risk of allergic diseases (atopic dermatitis: highest adjusted OR=4.28, 95% CI 2.57 to 7.11; allergic rhinitis: highest adjusted OR=13.00, 95% CI 3.76 to 45.00; allergic asthma: OR=2.37, 95% CI 1.67 to 3.37). Conclusion There was a dose–response relevance between levels of allergen-specific IgE and allergic diseases’ prevalence, and multiple sensitisations increased the risk of allergic diseases. This study provides evidence for the prophylaxis of allergic diseases.

目的 应用蛋白质组学技术,基于sigFeature变量筛选方法,获得小麦不耐受患者血清差异表达蛋白;利用富集分析获得差异蛋白生物学解释,为小麦不耐受发病机制的研究提供依据.方法 收集小麦不耐受患者和对照组血清样本;应用TMT标记定量蛋白质组学技术获得蛋白表达数据、sigFeature方法筛选差异表达蛋白;进行差异蛋白GO功能注释和KEGG富集分析,外部数据集进行差异蛋白验证.结果 TMT技术鉴定蛋白849个,sigFeature筛选获得差异蛋白22个.富集分析结果:GO富集分析发现差异蛋白参与血小板脱颗粒、急性期反应等生物学过程;KEGG富集分析发现差异蛋白参与补体与凝血级联通路.外部验证结果:ITIH2蛋白的ROC曲线下面积最大,AUC值为0.8673.结论 补体系统抑制和脂质代谢过程的改变是小麦不耐受发生的重要环节;ITIH2蛋白可能是小麦不耐受的关键蛋白;本研究从人体血清蛋白质组学的角度,为探究小麦不耐受的发生和调控机制提供依据.

Evidence has demonstrated that enhancer RNAs (eRNAs) play a vital role in the progression and prognosis of cancers, but few studies have focused on the prognostic ability of eRNA-regulated genes (eRGs) for hepatocellular carcinoma (HCC). Using gene expression profiles of HCC patients from the TCGA-LIHC and eRNA expression profiles from the enhancer RNA in cancers (eRic) data portal, we developed a novel and robust prognostic signature composed of 10 eRGs based on Lasso-penalized Cox regression analysis. According to the signature, HCC patients were stratified into high- and low-risk groups, which have been shown to have significant differences in tumor immune microenvironment, immune checkpoints, HLA-related genes, DNA damage repair-related genes, Gene-set variation analysis (GSVA), and the lower half-maximal inhibitory concentration (IC50) of Sorafenib. The prognostic nomogram combining the signature, age, and TNM stage had good predictive ability in the training set (TCGA-LIHC) with the concordance index (C-index) of 0.73 and the AUCs for 1-, 3-, and 5-year OS of 0.82, 0.77, 0.74, respectively. In external validation set (GSE14520), the nomogram also performed well with the C-index of 0.71 and the AUCs for 1-, 3-, and 5-year OS of 0.74, 0.77, 0.74, respectively. In addition, an important eRG (AKR1C3) was validated using two HCC cell lines (Huh7 and MHCC-LM3) in vitro, and the results demonstrated the overexpression of AKR1C3 is related to cell proliferation, migration, and invasion in HCC. Altogether, our eRGs signature and nomogram can predict prognosis accurately and conveniently, facilitate individualized treatment, and improve prognosis for HCC patients.

Background: Wheat intolerance has various systemic manifestations that can affect people’s quality of life, and few studies have focused on the mechanism of wheat intolerance and the signaling pathways involved in wheat intolerance have not been fully identified.Methods: We compared the protein profiles of patients with wheat intolerance with those of healthy controls using LASSO (least absolute shrinkage and selection operator) and PLS (partial least squares regression) to obtain DEPs for Gene Ontology enrichment analysis, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis, and protein–protein interaction network analysis. Internal validation and external validation were conducted for target proteomics testing. The correlation between differently expressed protein and the wheat-specific IgG antibody concentration was analyzed. Then receiver operating characteristic (ROC) curves was generated to validate the differentially expressed proteins.Findings: We identified 30 DEPs as significant candidate proteins of wheat intolerance. These proteins were enriched in complement and coagulation cascade pathways, regulated exocytosis, immune activation, and immune response-related pathways. After internal and external target proteomics validation, CFHR3 (complement factor H-related protein 3) was identified as a key protein that may have an important role in wheat intolerance. We found CFHR3 protein expression abundance and the wheat-specific IgG antibody concentration were significantly negatively correlated ( P = 0.035; Spearman correlation coefficient r = −0.565). The median area under the ROC curve (AUC) of CFHR3 is 0.857 in external verification data.Interpretation: This study provides insights into wheat intolerance that can be used to further explore the pathogenesis of this condition.Funding Statement: This study was funded by the National Science and Technology Major Project of the Ministry of Science and Technology of China (2016ZX08011005), the National Natural Science Foundation of China (82073666), and the Youth Science Foundation Project of National Natural Science Foundation of China (82003556).Declaration of Interests: None declared.Ethics Approval Statement: This study was approved by Harbin Medical University’s Ethical Review Committee.

Ischemic heart disease (IHD) is a considerable health burden worldwide with high mortality and morbidity. Treatments for IHD are mainly focused on decreasing oxygen demand or increasing myocardial oxygen supply, including pharmacological, interventional, and surgical treatment, but there are also some limitations. Therefore, it is important to find a simple, effective, and economical treatment. As non-invasive and safe physiotherapy, electrical stimulation (ES) has a promising application in the treatment of IHD. Current studies suggest that ES can affect the occurrence and development of IHD by promoting angiogenesis, regulating autophagy and apoptosis, inhibiting the inflammatory response and oxidative stress. In this review, we focus predominantly on the mechanism of ES and the current progress of ES therapy in IHD, furthermore, give a brief introduction to the forms of ES in clinical application.

Atherosclerosis, predominantly characterized by the disturbance of lipid homeostasis, has become the main causation of various cardiovascular diseases. Therefore, there is an urgent requirement to explore efficacious targets that act as lipid modulators for atherosclerosis. Transcription factor EB (TFEB), whose activity depends on post-translational modifications, such as phosphorylation, acetylation, SUMOylation, ubiquitination, etc., is significant for normal cell physiology. Recently, increasing evidence implicates a role of TFEB in lipid homeostasis, via its functionality of promoting lipid degradation and efflux through mediating lipophagy, lipolysis, and lipid metabolism-related genes. Furthermore, a regulatory effect on lipid transporters and lipid mediators by TFEB is emerging. Notably, TFEB makes a possible therapeutic target of atherosclerosis by regulating lipid metabolism. This review recapitulates the update and current advances on TFEB mediating lipid metabolism to focus on two intracellular activities: a) how cells perceive external stimuli and initiate transcription programs to modulate TFEB function, and b) how TFEB restores lipid homeostasis in the atherosclerotic process. In-depth research is warranted to develop potent agents against TFEB to alleviate or reverse the progression of atherosclerosis.

Atherosclerosis is a chronic inflammatory disease that commonly affects the elderly and is characterized by vascular damage, macrophage infiltration, and plaque formation. Moreover, it increases the risk of cardiovascular disease. The pathogenesis of atherosclerosis involves an interplay between macrophage autophagy and apoptosis. A recently discovered transcription factor, transcription factor EB (TFEB) is known to activate autophagy in macrophages. Sirtuin deacetylase 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase, activates several transcription factors, including TFEB. We studied the effects of berberine on the NAD+ synthesis pathway and interactions between SIRT1 and TFEB. We also studied the effects of berberine-induced TFEB activation via SIRT1 on autophagy and apoptosis of peritoneal macrophages. We found that berberine promoted autophagy of peritoneal macrophages by activating SIRT1 via the NAD+ synthesis pathway and, in turn, promoting TFEB nuclear translocation and deacetylation. The functional regulation of SIRT1 and TFEB by berberine could be exploited as a potential therapeutic strategy for atherosclerosis.

Background The admission time of patients with ST-segment elevation myocardial infarction (STEMI) may affect the quality of care they receive. This study aimed to explore the pattern and magnitude of variation in quality of care for patients with STEMI in both the process and outcome domains. Methods We performed a retrospective study based on STEMI data from China. We estimated the adjusted ORs of six process indicators and one outcome indicator of STEMI care quality by fitting multilevel multivariable regression models across 42 4hour time periods per week. Results The study cohort comprised 98 628 patients with STEMI. Care quality varied by time of arrival to the emergency department. We identified three main patterns of variation, which were consistent across days of the week. In the first pattern, which applied to electrocardiographic examination within 10 min of arrival and to aspirin or clopidogrel use within 10 min of arrival, quality was lowest for arrivals between 08:00 and 12:00, rose through the day and peaked for arrivals between 24:00 and 04:00. Percutaneous transluminal coronary intervention treatment within 90 min showed the same pattern but with maximal performance for those arriving 20:00-24:00. In the third pattern, applying to lipid function evaluation within 24 hours and beta blocker use within 24 hours, quality was best for arrivals between 04:00-08:00 and 16:00-19:00 and worst for arrivals between 24:00-04:00 and 12:00-16:00. Conclusions The quality of care for STEMI shows three patterns of diurnal variation. Detecting the times at which quality is relatively low may lead to quality improvement in healthcare. Quality improvement should focus on reducing the weekend effect and off-hour effect and the diurnal temporal variation.

内质网(endoplasmic reticulum,ER)是真核细胞中最大的膜状细胞器,由跨越细胞质的连续片状或管状结构组成,参与蛋白质合成、修饰和转运,脂质和类固醇合成,Ca2+平衡及分泌的调节等[1].ER是一种高度动态化的细胞器,其膜蛋白及脂质的半衰期约为3～5 d,需要经过不断地翻新以维持其结构和功能的完整性.除了基础的循环周转外,在Ca2+平衡失调、缺氧、生物合成需求量增大、未折叠蛋白丰度增加、蛋白超聚积或者药物作用等情况时,ER会发生应激,其中积累的大量未折叠或错误折叠蛋白,超出ER负荷,致使ER扩张,此时ER必须为适应各种应激源而更活跃地周转,以防止过度扩张,维持ER稳态.

目的 基于加权基因共表达网络分析(weighted gene co-expression network analysis,WGCNA)方法识别IgG介导的西红柿不耐受相关蛋白质共表达模块及枢纽蛋白,为其发生机制研究提供依据.方法 收集IgG介导的西红柿不耐受患者及健康对照血清样本,使用DIA全扫描蛋白质组学定性定量技术获得蛋白质表达数据;利用WGCNA方法构建共表达网络,识别与IgG介导的西红柿不耐受相关的模块,并进行模块GO功能注释及KEGG通路富集分析;利用Cytoscape获得IgG介导的西红柿不耐受相关模块的枢纽蛋白.结果 获得IgG介导的西红柿不耐受相关的蛋白质模块两个,分别为blue模块和turquoise模块.blue模块与IgG介导的西红柿不耐受相关系数为-0.90;GO富集分析发现,该模块中蛋白主要参与脂蛋白重构、脂质代谢等相关生物过程以及蛋白质级联激活、补体激活等免疫调节过程;KEGG分析富集到5条通路,包括胆固醇代谢通路、PPAR信号通路、补体和凝血级联通路、类维生素A代谢和运输通路、维生素和辅酶因子代谢通路.turquoise模块与IgG介导的西红柿不耐受相关系数为0.72;GO富集分析发现,该模块主要与蛋白质级联激活、补体激活经典途径、体液免疫应答、受体介导的内吞,血小板脱颗粒、抗氧化活性等生物过程有关;KEGG分析富集到2条通路,补体和凝血级联通路、吞噬体通路.筛选出IgG介导的西红柿不耐受相关模块中的枢纽蛋白为APOA1、APOA4、APOC3、APOA2、APOC1、C3、HRG、FGB、HP、TF.结论 WGCNA方法进行IgG介导的西红柿不耐受蛋白质表达数据分析发现:脂质、胆固醇代谢等过程的改变可能是其发生的重要环节;获得的载脂蛋白类蛋白质及其他枢纽蛋白是其潜在关键调控蛋白;本研究从系统生物学的角度,为IgG介导的西红柿不耐受发生机制探索提供了依据和研究方向.

Objectives This study aimed to set a data-driven achievable performance benchmark, explore the process–outcome association and speculate about the net gain in quality improvement with benchmarking.Design Observational study.Setting Patient survey conducted at 466 secondary and tertiary hospitals across 31 provinces, autonomous regions and municipalities in China.Participants 183 334 patients diagnosed with chronic heart failure (CHF) who were treated at 466 Chinese hospitals from January 2011 through May 2017.Primary independent variables Hospital process composite performance (HPCP).Secondary independent variables Patient-level and hospital-level characteristics.Primary outcome measure Patients getting better or recovered after treatment, in-hospital mortality, length of hospital stay (LOS) and medical cost.Methods HPCP was calculated using denominator-based weights. Mixed random-intercept models were used to evaluate the contributions of HPCP on patient outcomes and to speculate quality improvement after adjusting HPCP to benchmark level.Results When all hospitals were to operate at the benchmark level, the proportion of patients getting better or recovered after treatment would increase in most hospitals, particularly those with low baseline rates. However, there was no evidence for lowering in-hospital mortality, significant savings in cost or shortening LOS.Conclusions Increasing the adherence rate of CHF care and closing the gap in HPCP between hospitals have important implications for improving patient condition.