Despite the increasing prevalence of hypertension (HTN) in China, the rates of treatment and control remain uncertain. This study aims to evaluate the prevalence, awareness, treatment, and control rates of HTN in selected townships. From May 1, 2024, to July 31, 2024, a random sampling survey was conducted involving 11,600 adult residents across seven community health service centers in Lingcheng District, Dezhou City, Shandong Province, China. Following a standardized rest period of 5 to 10 min, trained healthcare professionals measured blood pressure using a validated oscillometric monitor. According to the 2024 Chinese guidelines for HTN, HTN is defined as a systolic blood pressure (SBP) of ≥ 140 mmHg or a diastolic blood pressure (DBP) of ≥ 90 mmHg, as well as individuals with a self-reported history of HTN who are currently taking antihypertensive medication. Normal-high blood pressure (NHBP) is characterized by an SBP of 120 to 139 mmHg or a DBP of 80 to 89 mmHg in the absence of antihypertensive medication. HTN control is defined as blood pressure readings of < 140/90 mmHg. Additionally, the prevalence and control rate of HTN were estimated using a cutoff of 130/80 mmHg, in accordance with the 2025 American Heart Association/American College of Cardiology High Blood Pressure Guideline. The age-adjusted prevalence of HTN was 32.2%, while the age-adjusted prevalence of NHBP was 30.9%. Among patients diagnosed with HTN, the age-adjusted awareness rate was 57.4%, the treatment rate was 50.0%, and the control rate was 38.0%. Of those receiving treatment, 56.1% were prescribed a single antihypertensive medication, 31.7% required a combination of two drugs, and 12.2% needed three or more antihypertensive medications. According to the 2025 American Heart Association/American College of Cardiology guideline, the age-adjusted prevalence of HTN was 57.3%, with a control rate of only 14.7%. This cross-sectional study indicated a high prevalence of HTN in selected townships of Lingcheng District. Although the awareness, treatment, and control rates of HTN have improved, they remain significantly below the desired levels. This finding underscores the substantial challenges associated with HTN management at the grassroots level.

Background:Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the most prevalent chronic liver disease globally, significantly impairing patients' quality of life (QOL) through complex interactions with metabolic comorbidities, psychological factors, and disease progression. Despite growing research interest, a comprehensive bibliometric analysis of QOL studies in MAFLD remains lacking. Methods:Publications focusing on MAFLD and QOL were retrieved from the Web of Science Core Collection and Scopus. Bibliometric data, including titles, authors, institutions, countries, keywords, and citations, were extracted and analyzed using Bibliometrix (R-package) and VOSviewer. Annual publication trends, geographical contributions, institutional collaborations, journal influence, author networks, and keyword evolution were visualized. Results:A total of 1,347 publications (2004-2025) were included, with an annual growth rate of 18.76%. The United States (n = 368, 27.3%) was the most productive country, followed by China (n = 171, 12.7%) and Italy (n = 94, 7.0%). Leading institutions included the University of California System (n = 67) and Harvard University (n = 54). Key journals included Hepatology (n = 27) and Journal of Hepatology (n = 15). Keyword analysis identified five clusters: obesity management, metabolic health, MAFLD pathology, health impacts, and risk factors. Emerging trends focused on drug therapy, lifestyle interventions, and psychosocial support. Conclusion:Research on MAFLD patients' QOL is growing fast. Effective management needs integrated strategies (lifestyle, psychological support, multidisciplinary management, precision pharmacology) tailored to individuals. Future research should prioritize long-term data, clarity of mechanisms, and equitable interventions for patients' holistic well-being.

Background:The aim of the present study was to explore the value of coronary artery calcium score (CACS) using non-gated, non-contrast chest computed tomography (NCCT) to predict coronary artery disease (CAD) in airline pilots. Methods:Pilots with coronary calcification found on NCCT were consecutively enrolled into this study. All received a coronary computed tomography angiography (CCTA) examination. The coronary artery calcium score (CACS) was evaluated on NCCT using the Agatston method. CCTA images were analyzed using a semi-automated software. Coronary Artery Disease Reporting and Data System (CAD-RADS) scoring categorized coronary stenosis. Results:A total of 217 male pilots were included, of which 49 were diagnosed with significant CAD (CAD-RADS category 3 or higher). Pilots with significant CAD had much higher CACS (324.28 ± 389.02 vs. 39.16 ± 68.88; p < 0.001). Plaque volumetric measurements showed that total plaque volume (1,103.50 ± 285.51 mm3 vs. 913.18 ± 277.45 mm3; p < 0.001) and calcified plaque volume (149.77 ± 160.71 mm3 vs. 36.42 ± 26.86 mm3; p < 0.001) were more pronounced in individuals in the significant CAD group than those in the non-significant CAD group. A multivariate analysis demonstrated that CACS (odds ratio 1.01; 95% confidence interval 1.005-1.014; p < 0.001) was the only independent risk factor of significant CAD but traditional cardiovascular risk factors, pre-existing medication regimens, or prolonged flight duration were not. CACS positively correlated with total plaque volume (r = 0.156; p = 0.027) and calcified plaque volume (r = 0.434; p < 0.001). Receiver operating characteristic curve analysis showed the area under the curve for the CACS in diagnosing significant CAD was 0.891 (p < 0.001). Conclusions:CACS assessed using NCCT was significantly associated with CAD-RADS category 3 or higher, as confirmed by CCTA, which indicates that it may serve as a robust predictor for diagnosing significant CAD among airline pilots.

Fructose-1,6-bisphosphatase (FBPase) is a rate-limiting enzyme in gluconeogenesis, and its inhibition has the potential to improve glucose homeostasis. We characterize Cpd96, a novel inhibitor of FBPase, and demonstrate its multifaceted antidiabetic effects. In vivo, Cpd96 significantly improved glucose tolerance, enhanced insulin sensitivity, and promoted insulin secretion in type 2 diabetic (db/db and KKAy) mice. In vitro, Cpd96 potentiated insulin secretion in MIN6 cells and primary pancreatic islets by facilitating glucose uptake, elevating the ATP/ADP ratio, and activating the cAMP and AMPK/mTORC1/S6K signaling pathways. Notably, the insulinotropic effect of Cpd96 was FBPase-dependent, as it failed to promote insulin secretion in primary islets from β-cell-specific FBPase knockout mice. These findings suggest that Cpd96 improves insulin secretion through the metabolic reprogramming of β-cells and highlight its potential as a novel therapeutic strategy for diabetes treatment.

Objective: This study aims to establish DKD early screening model through different machine learning algorithms according to the clinical characteristics and biological indicators of type 2 diabetes patients, and compare its predictive value for DKD. Methods: We selected 74,982 type 2 diabetes patients hospitalized in Beijing Tongren Hospital from 2013 to 2022. The collected-data included common clinical characteristics and biological indicators. 625 DKD cases was diagnosed with the increase of urine microalbumin or the decrease of eGFR and diabetes retinopathy, and 1336 cases were diagnosed as Non-DKD. Establish DKD early screening models through 7 machine learning algorithms: Deep Neural Network(DNN), RF, SVM, XGBoost, GMB, DRF, Naive Bayes. Result: DNN were established for different feature dimensions: D0: blood routine, AUC=0.6911; D1: blood routine, DBP, SBP, WHR, AUC=0.7919; D2 : D1 dataset, biochemical indicators, AUC=0.8517. Evaluating the accuracy of the model, AUC of DNN is 0.902, while other algorithms have AUC between 0.81 and 0.88. Conclusion: The best prediction result is D2 dataset, which is the most effective combined with biochemical indicators to predict DKD; The single blood routine index also has important value in predicting the development of DKD. DNN is the the best model compared to other machine learning algorithms. Disclosure L. Zhang: None.

Nuclear factor erythroid 2-related factor 2 (NRF2) is a redox-sensitive transcriptional factor that enables cells to resist oxidant responses, ferroptosis and inflammation. Here, we set out to probe the effects of NRF2 on cardiomyocyte injury under acute myocardial infarction (AMI) condition and its potential mechanism. Human cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) to induce cell injury. qRT-PCR and western blot assays were used to detect the levels of mRNAs and proteins. Cardiomyocyte injury was determined by detecting the levels of lactate dehydrogenase and creatine Kinase MB (CK-MB). Cell apoptosis was investigated by flow cytometry and related markers. Levels of IL-6, IL-10, and TNF-α were measured by ELISA. Cell ferroptosis was assessed by detecting the production of reactive oxygen species (ROS), malonaldehyde (MDA), reduced glutathione/oxidized glutathione disulfide (GSH/GSSG) ratio, Fe + content, and related regulators. The interaction between NRF2 and the suppressor of zest 12 (SUZ12) was analyzed by using dual-luciferase reporter and RNA immunoprecipitation assays. AMI rat models were established for in vivo analysis. NRF2 was lowly expressed in AMI patients and H/R-induced cardiomyocytes. Forced expression of NRF2 reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis. Moreover, NRF2 overexpression improved cardiac function and injury in vivo. Mechanistically, SUZ12 bound to the promoter of NRF2 and promoted its expression. Further functional analyses showed that SUZ12 overexpression reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis, which were reversed by NRF2 silencing. SUZ12-increased NRF2 suppressed H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis in vitro and improved cardiac functions in rats with I/R injury, suggesting the potential cardioprotective effect of NRF2 in cardiac injury during AMI.

Background: As a disease, insomnia is often ignored by the general public. Insomnia, which not directly fatal, may be equivalent to chronic suicide if it is not paid attention to. However, there are many theories on how to treat insomnia, and researchers have been searching for a cure. Chinese herbal medicine (CHM) and exercise therapy (ET) are relatively effective, and have been used since ancient times to treat insomnia. This study aimed to examine the effect of CHM combined with ET (CHM-ET) on patients with insomnia. Methods: We searched eight electronic databases including PubMed, Web of Science, EMBASE, the Cochrane Library, the China National Knowledge Infrastructure (CNKI), the China Biology Medicine disc (CBMdisc), the China Science and Technology Journal Database (VIP), the Wanfang Database to find randomized controlled trials (RCTs) evaluating CHM-ET in the treatment of insomnia patients up to September 13, 2022. Two researchers read and screened the publications to extract data. We used the pittsburgh sleep quality index (PSQI) as the evaluation indicators for each study, and the other was the total effective rate (TER). The Cochrane risk-of-bias assessment tool was used to assess the risk of bias of the included literature. The level of evidence for this result was assessed by GARDE method. The meta-analysis was performed using STATA 14 software and RevMan 5.3. The research method was registered with PROSPERO (CRD42022350926). Results: We included fourteen randomized controlled trials, which including a total of 1,126 participants. Compared with the control group, the experimental group showed significantly improvements in sleep effect as reflected by the reduced PSQI score [mean difference (MD) = −2.47, 95% confidence interval (CI) (−3.15, −1.78), I 2 = 92%] with low quality of evidence, and increased TER [risk ratio (RR) = 1.23, 95% CI (1.14, 1.33), I 2 = 40%] with moderate quality of evidence. Compared with hypnotic drugs, CHM-ET significantly reduced the PSQI score [mean difference (MD) = −3.18, 95% CI (−5.48, −0.89), I 2 = 73%] with low quality of evidence. The PSQI of CHM-ET significantly decreased compared with single CHM [mean difference (MD) = −3.04, 95% CI (−5.84, −0.25), I 2 = 98%] with low quality of evidence, and ET [mean difference (MD) = −2.44, 95% CI (−2.87, −2.02), I 2 = 0%] with moderate quality of evidence. No serious adverse reactions were observed. Conclusion: This review suggested that CHM-ET may be an effective treatment for insomnia. However, given the limited quality of the studies and methodologies included in the trials, further rigorous randomized controlled trials are needed for more accurate results.

Background:Morus alba L. (Sangzhi) alkaloid (SZ-A) is a new antidiabetic drug approved by the China National Medical Products Administration in 2020. Diabetic nephropathy (DN) is a common diabetic complication and an important cause of morbidity and mortality in patients with diabetes. The effects of SZ-A on DN remain unknown.Purpose:This study evaluated the effects of SZ-A on DN in Zucker diabetic fatty (ZDF) rats and explored the underlying mechanisms based on nitrosative stress, inflammation, and fibrosis.Methods:Diabetic ZDF rats were orally administered 100 and 200 mg/kg of SZ-A once daily for 9 weeks. The glucose metabolism and kidney function were assayed. The pathological injury and fibrosis of the kidneys were separately evaluated using hematoxylin and eosin staining and Masson's staining. The oxidative and nitrosative stress and inflammation were assayed by determining the levels of related indices in the blood and kidneys and quantifying the related gene and protein expression. The expression of transforming growth factor β1 (TGFβ1) gene and protein were assayed by quantitative real-time PCR and immunohistochemistry, respectively. The renal transcriptomics was analyzed using RNA sequencing.Results:Repeated treatment with SZ-A significantly improved glucose metabolism, dose-dependently decreased the levels of blood urea nitrogen, urinary albumin, and β2-microglobulin, and evidently relieved the renal injury in diabetic ZDF rats. As for the mechanisms, SZ-A remarkably ameliorated systemic nitrosative stress through lowering the levels of blood inducible nitric oxide synthase and nitric oxide, and significantly relieved systemic and renal inflammation by reducing the levels of blood interleukin-1β and monocyte chemoattractant protein-1 (MCP-1) and decreasing the levels of renal C-reactive protein content and expression of tumor necrosis factor-α in the kidneys. SZ-A also improved renal fibrosis by lowering the expression of TGFβ1 in the kidneys. Additionally, SZ-A significantly lowered the expression of stimulator of chondrogenesis 1 in the kidneys.Conclusion:Repeated treatments with SZ-A significantly ameliorates DN by regulating systemic nitrosative stress, renal inflammation, and renal fibrosis partially through inhibition of the cytokine-NO and TGF-β1 signaling in ZDF rats, providing evidence for the additional application of SZ-A in clinical use for the treatment of DN.

Aims To explore the effect of liraglutide treatment on serum adropin and its relationship to the liver fat content in newly diagnosed patients with type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated fatty liver disease (MAFLD). Methods Serum adropin level and liver fat content were assessed in patients with T2DM and MAFLD (n = 22), along with healthy controls (n = 22). Afterward, the patients received liraglutide treatment for 12 weeks. Serum adropin levels were examined by a competitive enzyme-linked immunosorbent assay. Liver fat content was quantified via magnetic resonance imaging-estimated proton density fat fraction (MRI-PDFF). Results We found that patients with newly diagnosed T2DM and MAFLD had lower serum adropin levels [2.79 ± 0.47 vs. 3.27 ± 0.79 ng/mL, P < 0.05] and higher liver fat content [19.12 ± 9.46 vs. 4.67 ± 0.61%, P < 0.001], compared to healthy controls. Following 12-week liraglutide treatment, serum adropin levels increased from 2.83(2.44, 3.24) to 3.65(3.20, 3.85) ng/mL ( P < 0.001), and liver fat content decreased from 18.04(11.08, 27.65) to 7.74(6.42, 13.49) % ( P < 0.001) in patients with T2DM and MAFLD. Furthermore, increases in serum adropin were strongly associated with decreases in liver fat content (β = − 5.933, P < 0.001), liver enzyme and glucolipid metabolism parameters. Conclusion The increase in serum adropin level following liraglutide treatment was strongly correlated with the reduction in liver fat content and glucolipid metabolism. Hence, adropin might be a potential marker for the beneficial effects of liraglutide on treating T2DM and MAFLD.

We aimed to evaluate the impact of new Murray law-based QFR of jailed left circumflex coronary artery (LCx) on long-term clinical outcomes after left main coronary artery (LM) simple crossover stenting. 164 patients who underwent LM-to-left anterior descending coronary artery simple crossover stenting and had appropriate angiographic view of LCx for QFR computation were enrolled. The primary clinical outcome was the 5-year target lesion failure (TLF), defined as a composite of cardiac death, a target vessel myocardial infarction or target lesion repeat revascularization. The mean QFR of the LCx after LM stent implantation was 0.88 ± 0.09, and 29 patients (17.7%) had a low QFR (< 0.80), which was significantly associated with a higher 5-year rate of TLF when compared with the high QFR group (27.6% vs. 6.7%; HR: 4.235; 95% CI 1.21–14.95; p = 0.0015). The 5-year LCx ostium-related TLR rate in the low QFR group was also higher (17.2% vs. 3.0% in the high QFR group; HR: 6.07, 95% CI 1.63–22.59, p = 0.002). In a multivariate Cox regression analysis, a low QFR in the LCx after LM stenting was an independent predictor of the 5-year TLF rate (HR: 3.21, 95% CI 1.21–8.53; p = 0.019). ROC analysis showed that QFR a negative predictive value (NPV) of 89.6% ([AUC] 0.73, 95% CI 0.58–0.88, p < 0.05), the cutoff point is 0.85. The patients with a low QFR (< 0.80) in jailed LCX after LM simple crossover stenting had worse 5-year outcomes than those with a high QFR. Conversely, a QFR ≥ 0.85 of jailed LCx could serve as a good predictor of low risk of adverse outcome in LCx ostium. The QFR computation of the jailed LCx may be helpful to determine whether an additional procedure is required for the jailed side branch.

Background:This study intended to investigate the independent effect of admission heart rate (HR) on the risk of major adverse cardiovascular events (MACEs) in acute myocardial infarction (AMI) patients with different left ventricular ejection fraction (LVEF) levels. Methods:The study was a secondary analysis of the Acute Coronary Syndrome Quality Improvement in Kerela Trial. The relationship between admission HR and 30-day adverse outcomes in AMI patients with different LVEF levels was detected using a Logistic regression model. Interaction tests were used to compare the effects of different subgroups on HR and MACEs. Results:Our study enrolled 18,819 patients. In both partially and fully adjusted models (Model1 and Model2), the risk of MACEs was highest in patients with HR > 120 (OR: 1.62, 95%CI: (1.16, 2.26), P = 0.004, Model1; OR: 1.46, 95%CI: (1.00, 2.12), P = 0.047, Model2). There was a significant interaction between LVEF and HR (P for interaction = 0.003). Meanwhile, the trend test for this association showed that HR was positively and significantly associated with the MACEs in LVEF>40% group (OR (95%CI): 1.27 (1.12, 1.45), P < 0.001). However, in LVEF<40% group, the trend test was not statistically significant (OR (95%CI): 1.09 (0.93, 1.29), P = 0.269). Conclusion:This study found that elevated admission HR was associated with a significantly higher risk for MACEs in patients admitted with AMI. Elevated admission HR was significantly associated with the risk of MACEs in AMI patients without low LVEF but not those with low LVEF (<40%). LVEF levels should be considered when evaluating the association between admission HR and the prognosis of AMI patients in the future.

Voglibose is an α-glycosidase inhibitor that improves postprandial hyperglycemia and increases glucagon-like peptide-1 (GLP-1) secretion in patients with type 2 diabetes. Recently, there has been increasing interest in the anti-inflammatory effects of voglibose on the intestine, but the underlying mechanism is not clear. This study evaluated the effects and mechanisms of voglibose on glycemic control and intestinal inflammation. Type 2 diabetic KKAy mice were treated with voglibose (1 mg/kg) by oral gavage once daily. After 8 weeks, glucose metabolism, levels of short-chain fatty acids (SCFAs), systematic inflammatory factors, intestinal integrity and inflammation were evaluated using hematoxylin and eosin staining, immunohistochemistry, immunofluorescence and Western blot analysis. Voglibose ameliorated glucose metabolism by enhancing basal- and glucose-dependent GLP-1 secretion. Several beneficial SCFAs, such as acetic acid and propionic acid, were increased by voglibose in the fecal sample. Additionally, voglibose notably decreased the proportion of pro-inflammatory macrophages and the expression of nuclear factor kappa B but increased the expression of tight junction proteins in the ileum, thus markedly improving intestinal inflammatory damage and reducing the systematic inflammatory factors. Ileal genomics and protein validation suggested that voglibose attenuated inositol-requiring protein 1α-X-box binding protein 1-mediated endoplasmic reticulum stress (ERS). Together, these results showed that voglibose enhanced the secretion of GLP-1, which contributed to the glycemic control in KKAy mice at least in part by regulating intestinal inflammation and the expression of ERS factors.

Background:The aim of this study was to evaluate the capability of different magnetic resonance imaging (MRI) parameters for distinguishing between hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD).Methods:Thirty-eight patients with HCM, 35 patients with HHD, and 29 healthy controls subjects were enrolled in this study. All subjects underwent cardiac MRI to measure T1 values and extracellular volume (ECV), as well as the extent and patterns of late gadolinium enhancement (LGE). Myocardial segments were categorized as non-hypertrophic, mild-hypertrophic, moderate-hypertrophic, and severe-hypertrophic based on end-diastolic wall thickness (EDWT). The differences in native T1 values between all four groups were evaluated.Results:Native T1 values were significantly higher in patients with HCM than in patients with HHD and in healthy controls (both P < 0.001). Moreover, significantly increased ECV was shown in patients with HCM than in patients with HHD and in healthy controls (both P = 0.001). Native T1 values in the basal slice and apex slice were significantly higher in patients with HCM than in patients with HHD (P < 0.01). In patients with HCM, the non-hypertrophic myocardial segments demonstrated significantly elevated T1 values compared with patients with HHD (both P < 0.001). Using a cut-off value of 28.8% for ECV, it could differentiate between HCM and HHD with 85% sensitivity, 62.07% specificity, and an area under the curve of 0.772.Conclusion:In patients with HCM, T1 tissue remodeling occurs in the normal-appearing myocardial segments, but not in patients with HHD. Both native T1 values and ECV can support clinically relevant discrimination between HCM and HHD, although ECV had better diagnostic efficacy.

Objectives: To determine the association between radiomics signature (Rad-signature) of pericoronary tissue (PCT) in coronary computed tomography angiography (CCTA) and CT-derived fractional flow reserve (CT-FFR), and explore the influential factors of functional ischemia.Methods: We retrospectively included 350 patients who underwent CCTA from 2 centers, consisting of the training (n = 134), validation (n = 66), and testing (with CCTA and invasive coronary angiography, n = 150) groups. After evaluating coronary stenosis level in CCTA (anatomical CT), pericoronary fat attenuation index (FAI), and CT-FFR, we extracted 1,691 radiomic features from PCT. By accumulating and weighting the most contributive features to functional ischemia (CT-FFR ≤ 0.8) the Rad-signature was established using Boruta integrating with a random forest algorithm. Another 45 patients who underwent CCTA and invasive FFR were included to assure the performance of Rad-signature.Results: A total of 1046 vessels in 350 patients were analyzed, and functional ischemia was identified in 241/1046 (23.0%) vessels and 179/350 (51.1%) patients. From the 47 features highly relevant to functional ischemia, the top-8 contributive features were selected to establish Rad-signature. At the vessel level, the area under the curve (AUC) of Rad-signature to discriminate functional ischemia was 0.83, 0.82, and 0.82 in the training, validation, and testing groups, higher than 0.55, 0.55, and 0.52 of FAI (p < 0.001), respectively, and was higher than 0.72 of anatomical CT in the testing group (p = 0.017). The AUC of the combined model (Rad-signature + anatomical CT) was 0.86, 0.85, and 0.83, respectively, significantly higher than that of anatomical CT and FAI (p < 0.05). In the CCTA-invasive FFR group, using invasive FFR as the standard, the mean AUC of Rad-signature was 0.83 ± 0.02. At the patient level, multivariate logistic regression analysis showed that Rad-signature of left anterior descending (LAD) [odds ratio (OR) = 1.72; p = 0.012] and anatomical CT (OR = 3.53; p < 0.001) were independent influential factors of functional ischemia (p < 0.05). In the subgroup of nonobstructive (stenosis <50% in invasive coronary angiography) and obstructive (≥50%) cases of the testing group, the independent factor of functional ischemia was FAI of LAD (OR = 1.10; p = 0.041) and Rad-signature of LAD (OR = 2.45; p = 0.042), respectively.Conclusion: The machine-learning-derived Rad-signature of PCT in CCTA demonstrates significant association with functional ischemia.

BACKGROUND There is scarce data on the long-term mortality and associated prognostic factors in patients with dilated cardiomyopathy (DCM). The study aimed to investigate the all-cause mortality up to 15 years (mean 7.9 ± 5.7 years) in such patients, and the independent prognostic factors influencing their long-term mortality. METHODS One hundred and sixty-six consecutive patients with DCM were prospectively enrolled from 2002 to 2003. The mean age of patients was 59.5 ± 10.4 years, and approximately 57% were male. They were followed up by telephone or outpatient visit at least every three months until 2019 or all-cause death occurred. Predictors of mortality were identified using multivariate logistic regression analysis. RESULTSDuring the 15 years of follow-up, five patients were lost to follow-up, and the complete data records of 161 patients were included in the analysis. Patients were treated with angiotensin-converting-enzyme inhibitors (ACEI) or angiotensin-receptor blocker (ARB), β-blockers, mineralocorticoid receptor antagonist (MRA), diuretics and digitalis from 2002 to 2004, and maintained at the maximum tolerated doses between 2004 and 2019. Our safety targets to maintain heart rate and blood pressure at 60-80 beats/min and 90-120/60-80 mmHg, respectively. All-cause mortality in the first five years was 55.9%. The independent risk factors for the 5-year mortality were age ≥ 70 years old (OR = 5.45, P = 0.006), systolic blood pressure (SBP) > 120 mmHg (OR = 3.63, P = 0.004), 6-minute walk distance (6MWD) < 450 m (OR = 3.84, P = 0.001). 15-year all-cause mortality was 65.8%. The independent risk factors for 15-year mortality were age ≥ 70 years old (OR = 16.07, P = 0.009), LVEF ≤ 35% (OR = 5.69, P = 0.003), and SBP > 120 mmHg (OR = 9.56, P < 0.001). CONCLUSIONSThis study was the first to demonstrate the 15-year survival rate of 34% in DCM patients. The DCM patients’ first five-year all-cause mortality decreased significantly after continuous standardized treatment and intensive management. The mortality then plateaued in the following 10 years. Age ≥ 70 years, LVEF ≤ 35%, and SBP > 120 mmHg were independent predictors of 15-year all-cause mortality.

Background Obesity can influence thyroid function through multiple routes, even in people who are euthyroid. The correlation between weight and thyroid function is a matter of debate. The present study investigated the relationship between body weight and thyroid function in euthyroid Chinese adults. Material/Methods A total of 1564 participants with serum thyrotropin (TSH) and thyroid hormone levels within the reference range were included. All of them were tested for thyroid function parameters and categorized, based on body mass index (BMI), into 3 groups: normal weight, overweight, and obese. The effects of BMI on thyroid function were examined using linear (continuous values) and logistic (dichotomous levels according to medians or means) regression and controlling for age and sex. Results There were significant differences in free triiodothyronine (FT3) levels and FT3/free thyroxine (FT4) ratios among participants who were normal weight, overweight, and obese (both P<0.001). Multivariable regression analysis (P<0.001) showed that BMI was positively associated with FT3 levels and FT3/FT4 ratios. Compared with the normal weight group, the patients who were overweight or obese had significantly higher FT3 levels and FT3/FT4 ratios that were higher than average, according to logistic regression analyses. Conclusions We found that Chinese adults who are obese may have higher FT3 levels and FT3/FT4 ratios than those who are of normal weight, even if their thyroid function values are within the normal range.

Objective: Prolactin (PRL) is a polypeptide hormone named for its crucial role in lactation. Recently, PRL has been recognized as a metabolic hormone that regulates energy metabolism. The current study aimed to investigate the relationship between circulating PRL and metabolic alterations in overweight/obese patients and the effect of weight loss through bariatric surgery on circulating PRL. Methods: A total of 448 overweight/obese patients aged between 18 and 40 years and 120 age- and sex-matched healthy controls with normal weight were enrolled. Among all participants, 156 obese patients underwent bariatric surgery. Results: Circulating PRL levels were significantly increased in the overweight (15.27 +/- 9.58 mg/L) and obese (17.75 +/- 9.15 mg/L) groups compared with the normal weight (13.57 +/- 9.03 mg/L) group. Multiple regression analyses demonstrated that the adipose tissue insulin resistance (adipo-IR) level was an independent predictor for PRL (beta = -0.451, P <.01). Despite comparable anthropometric parameters, the overweight/obese patients with a higher PRL tertile had decreased levels of triglycerides, nonesterified fatty acids, homeostasis model assessment of insulin resistance, and adipo-IR compared with the patients in the moderate and lower PRL tertiles. Serum PRL levels were significantly decreased following the alleviation of metabolic parameters after bariatric surgery (from 17.12 +/- 8.27 to 13.00 +/- 5.78 mu g/L, P <.05), and the decrease in PRL levels was significantly greater in the lower adipo-IR group than in the higher adipo-IR group (P <.01). Conclusion: An increased serum PRL level might be an adaptive response for protecting against metabolic disorders in obesity. (C) 2021 AACE. Published by Elsevier Inc. All rights reserved.

Abstract Objective Prolactin (PRL) is a polypeptide hormone named for its crucial role in lactation. Recently, PRL has been recognized as a metabolic hormone that regulates energy metabolism. The current study aimed to investigate the relationship between circulating PRL and metabolic alterations in overweight/obese patients, and the effect of weight loss through bariatric surgery on circulating PRL. Methods A total of 448 overweight or obese patients aged between 18 and 40 years, and 120 age- and sex-matched healthy controls with a normal weight were enrolled. Among all participants, 156 obese patients underwent bariatric surgery. Results Circulating PRL levels were significantly increased in the overweight (15.27 ± 9.58 ng/mL) and obese groups (17.75 ± 9.15 ng/mL) compared with the normal weight group (13.57 ± 9.03 ng/mL). Multiple regression analysis demonstrated that the adipo-IR level was an independent predictor for PRL (β = -0.451, P Conclusions An increased serum PRL level might be an adaptive response for protecting against metabolic disorders in obesity.

Objective Prolactin (PRL) has been demonstrated as a metabolic hormone to regulate energy metabolism recently. The present study aims to investigate the association between PRL and metabolic alterations in different obesity phenotypes. Methods A total of 451 drug-naive participants were recruited, comprising 351 obese patients and 100 age- and sex-matched healthy participants with normal weight. PRL, anthropometric, and clinical parameters were measured. Results In the obesity group, 15.1% (53/351) were categorized as 'metabolically healthy obesity (MHO)'. Besides favorable blood pressure, glucose, and lipids profiles, the MHO group exhibited increased PRL, and lower levels of high-sensitivity C-reactive protein (hsCRP), homeostasis model assessment of insulin resistance (HOMA-IR), and adipose tissue insulin resistance (adipo-IR) than the metabolically unhealthy obesity (MUHO) group (PRL, HOMA-IR, and adipo-IR: P < 0.01; hsCRP: P < 0.05). The severe MUHO group showed significantly decreased PRL levels than the mild MUHO group (P < 0.05). Multivariate linear regression analysis indicated that fasting plasma glucose (FBG) and adipo-IR were significantly associated with PRL (FBG: β = −0.263, P < 0.05; adipo-IR: β = −0.464, P < 0.01). Multivariable logistic regression analysis showed that hsCRP (OR = 0.824) and PRL (OR = 1.211) were independent predictors of MHO (all P < 0.01). Conclusion The MHO group had significantly increased circulating PRL levels when compared with the control and MUHO groups, and multivariable logistic regression analysis showed that PRL was independent predictors of MHO. Our findings suggested that increased circulating PRL might be a compensatory response for favoring energy metabolism during obesity.