Acta Diabetologica最新文献

{"title":"Myeloid myeloid PRDM16 restrains macrophage inflammatory remodeling and renal fibrosis in diabetic kidney disease by limiting PI3K/AKT activation.","authors":"Shanshan Wang, Tao Zhang, Miao He","doi":"10.1007/s00592-026-02779-1","DOIUrl":"https://doi.org/10.1007/s00592-026-02779-1","url":null,"abstract":"<p><strong>Background: </strong>Diabetic kidney disease (DKD) is driven by persistent metabolic stress, immune dysregulation and progressive renal fibrosis. PRDM16 is a metabolic transcriptional regulator involved in adipose remodeling, mitochondrial activity and tissue homeostasis, but whether myeloid PRDM16 links diabetic metabolic stress to macrophage polarization and renal fibrosis remains unclear.</p><p><strong>Methods: </strong>Public DKD transcriptomic datasets were analyzed to identify PRDM16-associated immune and macrophage signatures. Myeloid PRDM16-deficient mice and littermate controls were used to establish experimental DKD. Renal injury, fibrotic remodeling, macrophage polarization and PI3K/AKT signaling were evaluated by histological staining, immunostaining, ELISA, qRT-PCR and western blotting. High glucose-stimulated BMDMs and THP-1-derived macrophages were used for mechanistic validation, and LY294002 was applied to inhibit PI3K/AKT signaling.</p><p><strong>Results: </strong>Bioinformatic analysis linked PRDM16 expression with macrophage-related immune features in DKD. In vivo, myeloid PRDM16 deficiency aggravated renal matrix accumulation, collagen deposition and α-SMA/Collagen-I expression. PRDM16 loss promoted a shift from M2-like macrophages toward M1-like inflammatory macrophages, characterized by increased CD80, CD86, NOS2, TNF-α and IL-1β, together with reduced CD206, Arg1, Fizz1, IL-10 and IL-4. Mechanistically, PRDM16 deficiency enhanced PI3K/AKT phosphorylation in macrophages, whereas LY294002 partially reversed M1-like polarization and attenuated renal inflammation and fibrosis.</p><p><strong>Conclusion: </strong>Myeloid PRDM16 acts as a metabolic-immune regulator that restrains M2-to-M1 macrophage polarization and limits renal fibrotic progression in DKD. Loss of PRDM16 aggravates macrophage-driven inflammation and fibrosis partly through PI3K/AKT activation, suggesting that the PRDM16-PI3K/AKT axis may represent a potential target for macrophage-directed intervention in diabetic kidney disease.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictors of first-ever major adverse cardiovascular events in newly diagnosed type 2 diabetes: a 5-year prospective cohort study.","authors":"Carmine Gazzaruso, Pietro Gallotti, Colomba Falcone, Livio Luzi, Adriana Coppola","doi":"10.1007/s00592-026-02786-2","DOIUrl":"https://doi.org/10.1007/s00592-026-02786-2","url":null,"abstract":"<p><strong>Aims: </strong>Cardiovascular risk stratification at the time of type 2 diabetes diagnosis remains challenging. We evaluated the incidence and baseline predictors of first-ever major adverse cardiovascular events (MACE) in patients with newly diagnosed type 2 diabetes without overt complications.</p><p><strong>Methods: </strong>We conducted a prospective cohort study of 937 consecutive adults with newly diagnosed type 2 diabetes, free of overt diabetic complications and pre-existing cardiovascular disease at baseline, followed for a mean of 62.7 ± 21.5 months. Baseline assessment included fasting C-peptide, transcutaneous oxygen tension (TcPO2), structured therapeutic patient education (TPE), and conventional metabolic and cardiovascular variables. Incident MACE was analyzed using Cox proportional hazards regression, and receiver operating characteristic analysis was used to derive an exploratory C-peptide cut-off.</p><p><strong>Results: </strong>During follow-up, 42 participants (4.5%) experienced a first MACE (0.86 per 100 person-years). In multivariable Cox analysis, higher fasting C-peptide (HR:4.70, 95%CI: 2.47-8.93, p < 0.001), lower TcPO2 (HR:15.15, 95%CI: 7.00-32.80, p < 0.001) were independently associated with MACE; non-participation in structured TPE was also associated with MACE (HR:0.26, 95%CI: 0.14-0.49, p < 0.001), but this finding should be interpreted cautiously given the observational design. The optimal C-peptide cut-off was 3.1 ng/mL (AUC 0.73). As a secondary endpoint, all-cause mortality occurred in 99 of 937 participants (10.6%; 2.02 per 100 person-years) and was independently associated with older age and lower TcPO2.</p><p><strong>Conclusions: </strong>In newly diagnosed type 2 diabetes without overt complications, higher fasting C-peptide and lower TcPO2 were associated with increased cardiovascular risk. These findings are hypothesis-generating and warrant external validation.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial structural and functional aberrations in diabetic bladder dysfunction: underlying mechanisms and therapeutic landscapes.","authors":"Junchao Wu, Huitao Wang, Rui Xu, Fei Song, Chunlei Dai, Yuanzhi Li, Wu Tang, Tao Yang, Kewei Fang","doi":"10.1007/s00592-026-02782-6","DOIUrl":"https://doi.org/10.1007/s00592-026-02782-6","url":null,"abstract":"<p><p>Diabetic bladder dysfunction (DBD) is a prevalent complication of diabetes mellitus (DM), characterized by heterogeneous urological impairments including altered bladder sensation, decreased compliance, and voiding difficulties. Emerging evidence highlights mitochondrial structural and functional aberrations as pivotal drivers of DBD pathogenesis. Chronic hyperglycemia induces excessive mitochondrial reactive oxygen species (ROS) generation, cristae disruption, impaired fission-fusion dynamics, defective mitochondrial quality control, and calcium dysregulation, collectively impairing bladder smooth muscle cell (BSMCs) bioenergetics and promoting apoptosis, inflammation, and fibrotic remodeling. These processes culminate in progressive bladder dysfunction, transitioning from compensatory hyperactivity to decompensated underactivity. Mitochondria-targeted therapeutic architectures fall into two complementary categories: repurposed guideline-based pharmacological agents and conceptual prospective interventions, the latter encompassing molecular reprogramming, cell-based therapies, and cell-free regenerative platforms. This review synthesizes current mechanistic insights into mitochondrial involvement in DBD and explores potential therapeutic landscapes, emphasizing the need for integrated, mechanism-driven interventions to advance clinical management of this condition.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of diabetes complications on body composition, dietary intake, and metabolic parameters","authors":"Tuba Tekin,&nbsp;Başak İkra Yıldız,&nbsp;Şaziye Yoldaş,&nbsp;Mustafa Asım Gedikli","doi":"10.1007/s00592-026-02783-5","DOIUrl":"10.1007/s00592-026-02783-5","url":null,"abstract":"<div><h3>Aim</h3><p>Diabetes is a metabolic disease characterized by hyperglycemia resulting from deficiencies in the effect or secretion of insulin. Diabetes leads to various acute and chronic complications. This study investigated the impact of complications on body composition, dietary habits, and biochemical parameters in individuals with type 2 diabetes.</p><h3>Methods</h3><p>The study included 42 diabetes patients with complications and 45 diabetic individuals without complications. A 24-hour dietary recall was conducted to assess nutritional status. The results of routine blood tests were analyzed to measure metabolic control. Measurements of participants’ body weight, height, body composition, and waist and hip circumferences were recorded. Body composition was assessed utilizing a portable bioelectrical impedance analyzer. Body composition was examined using body fat percentage, body water percentage, visceral fat percentage, muscle mass, and basal metabolic rate.</p><h3>Results</h3><p>Individuals with complications of diabetes had elevated body mass index (BMI), body fat percentage, visceral fat percentage, and waist and hip circumference (<i>p</i> &gt; 0.05). They exhibited increased consumption of carbohydrates, dietary cholesterol, and saturated fats (<i>p</i> &gt; 0.05). Additionally, HbA1c concentrations were higher and albumin concentrations were lower in individuals with diabetic complications (<i>p</i> &lt; 0.05).</p><h3>Conclusıon</h3><p>The study findings indicate that complications in individuals with type 2 diabetes negatively impact metabolic parameters, body composition, and nutritional consumption. To mitigate the risk of complications in individuals with type 2 diabetes, dietary treatments should be implemented to enhance metabolic parameters and body composition.</p></div>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":"63 11","pages":"1983 - 1990"},"PeriodicalIF":3.1,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal-fetal lipid metabolic profiling by tandem mass spectrometry in gestational diabetes mellitus: implications for pathogenic mechanisms.","authors":"Yuqi Yang, Xia Li, Fang Guo, Jian Zhang, Jiuxiang Fan, Wei Zhu, Bin Yu","doi":"10.1007/s00592-026-02790-6","DOIUrl":"https://doi.org/10.1007/s00592-026-02790-6","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to characterize lipid profiles in maternal serum, placenta, and umbilical cord serum from patients with gestational diabetes mellitus (GDM), clarify lipid metabolic disturbances at the maternal-fetal interface, and identify key molecules associated with the intergenerational metabolic inheritance of GDM.</p><p><strong>Method: </strong>Lipidomic profiling was performed using tandem mass spectrometry (MS/MS) in maternal serum, placental tissue, and umbilical cord serum. Orthogonal partial least squares discriminant analysis (OPLS-DA) was applied to compare lipid metabolic differences between GDM and control groups. Potential biomarkers were screened using combined multivariate and univariate analyses. Partial least squares structural equation modeling (PLS-SEM) was further used to evaluate lipid transmission and correlative associations across the maternal-fetal interface.</p><p><strong>Result: </strong>In total, 331, 246, and 301 lipid species were identified in maternal serum, placental tissue, and umbilical cord blood, respectively. OPLS-DA revealed distinctly different lipid profiles between groups in all three compartments, with the most pronounced separation in maternal serum. Thirteen, eight, and five differential lipids serving as potential biomarkers were identified in the three sample types, respectively. KEGG analysis showed that these differential lipids were significantly enriched in glycerophospholipid metabolism. PLS‑SEM results indicated that most maternal lipids showed no significant correlation with fetal lipid levels, and only phosphatidylinositol (PI) exhibited a significant positive correlation between maternal serum and umbilical cord blood. Lysophosphatidylethanolamine (LPE) exerted a significant positive correlation in the placental‑to‑fetal pathway. In addition, phosphatidylcholine (PC, C18), sphingomyelin (SM), phosphatidylglycerol (PG), and phosphatidylethanolamine (PE) exhibited significant positive correlations in the maternal‑to‑placental pathway.</p><p><strong>Conclusion: </strong>After adjustment for blood glucose levels, persistent lipid metabolic abnormalities were observed in mothers, fetuses, and at the maternal-fetal interface. These findings suggest a potential regulatory role of the placenta in the transmission of maternal lipid disturbances to the fetus, which may serve as a key organ associated with GDM-related fetal metabolic dysregulation.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early-onset transient neonatal diabetes: safe use of continuous glucose monitoring and sensor-integrated insulin pump therapy","authors":"Carolina Jesus e Sá,&nbsp;Clara Picão de Carvalho,&nbsp;Rita Ribeiro Martins,&nbsp;Sara Martins,&nbsp;Ana Raquel Henriques,&nbsp;Brígida Robalo,&nbsp;Carla Pereira,&nbsp;Lurdes Sampaio","doi":"10.1007/s00592-026-02789-z","DOIUrl":"10.1007/s00592-026-02789-z","url":null,"abstract":"","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":"63 10","pages":"1819 - 1823"},"PeriodicalIF":3.1,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Nutrient intake order on metabolic outcomes in type 2 diabetes: a systematic review and meta-analysis","authors":"Luisa M. Saldarriaga-Callejas,&nbsp;Piyush Ratan,&nbsp;Eric Pasqualotto,&nbsp;Sena Kodalak,&nbsp;Ticiane Bovi,&nbsp;Talita Trevisan","doi":"10.1007/s00592-026-02788-0","DOIUrl":"10.1007/s00592-026-02788-0","url":null,"abstract":"","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":"63 10","pages":"1817 - 1817"},"PeriodicalIF":3.1,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unrecognized mitochondrial diabetes cases in a group of patients with type 2 diabetes","authors":"Sebastian Skoczylas,&nbsp;Tomasz Płoszaj,&nbsp;Natalia Kapelan,&nbsp;Julia Grzybowska-Adamowicz,&nbsp;Katarzyna Piekarska,&nbsp;Julia Gonciarz,&nbsp;Katarzyna Nalepa,&nbsp;Ewa Zmysłowska-Polakowska,&nbsp;Maciej Borowiec,&nbsp;Katarzyna Cypryk,&nbsp;Agnieszka Zmysłowska","doi":"10.1007/s00592-026-02773-7","DOIUrl":"10.1007/s00592-026-02773-7","url":null,"abstract":"<div><h3>Background/Objectives</h3><p>Maternally Inherited Diabetes and Deafness (MIDD) is a unique form of diabetes caused by β-cell dysfunction. Due to the highly variable symptoms of MIDD, it can be misdiagnosed as either type 1 or type 2 diabetes (T2D). The aim of this study was to identify pathogenic mtDNA variants (m.3243 A &gt; G, m.8344 A &gt; G, m.3271T &gt; C, and m.12278T &gt; C) in patients with initially diagnosed T2D.</p><h3>Methods</h3><p>A total of 102 patients diagnosed with T2D with their mean age of 64 ± 12.5 years, and BMI (body mass index) of 29.1 ± 5.8 kg/m² were recruited. DNA was isolated from the urine sediment and analyzed using real-time PCR with TaqMan probes. Next, positive results were confirmed by next-generation sequencing (NGS).</p><h3>Results</h3><p>The m.3243 A &gt; G variant was detected in 3/102 patients, accounting for 2.94% of the cohort. Patients with MIDD had a lower BMI (median 19.3 vs. 29.1 kg/m²) and an earlier age at diabetes onset (median 26 vs. 50 years) than the non-carrier group. In addition, all MIDD patients exhibited hearing impairment and a positive maternal history of hyperglycemia/diabetes and hearing loss. </p><h3>Conclusions</h3><p>Urine sediment testing appears to be an effective and non-invasive method for identifying previously undiagnosed cases of MIDD in patients with type 2 diabetes. Key diagnostic indicators include early onset of diabetes (average age of onset around 27), low BMI, and accompanying hearing loss. These factors are combined with a maternal history of other symptoms, such as hyperglycemia/diabetes and hearing impairment.</p></div>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":"63 11","pages":"1977 - 1982"},"PeriodicalIF":3.1,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s00592-026-02773-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of phenotypic aging with dementia-free life expectancy among 45,608 participants with prediabetes: a prospective cohort study","authors":"Zheng Zhang,&nbsp;Han Zhou,&nbsp;Bi-Xia Liu,&nbsp;Xi-Jian Dai","doi":"10.1007/s00592-026-02751-z","DOIUrl":"10.1007/s00592-026-02751-z","url":null,"abstract":"<div><h3>Objective</h3><p>Prediabetes is a well-established risk factor for late-life dementia, and phenotypic age acceleration (PhenoAgeAccel) serves as a reliable biomarker reflecting cumulative biological aging burden. Few population-based cohorts have clarified their combined correlation with dementia-free survival among prediabetic adults. This study intended to explore the association between PhenoAgeAccel and dementia-free life expectancy in individuals with prediabetes.</p><h3>Methods</h3><p>We enrolled 45,608 prediabetic participants from UK Biobank with a median follow-up of 14.39 years. PhenoAgeAccel values were computed and categorized into three tertiles from low to high aging acceleration. Royston-Parmar parametric models were adopted to calculate dementia-free life expectancy at age 45 and 65. Competing risk analysis and five independent sensitivity analyses were performed to verify result stability.</p><h3>Results</h3><p>A total of 1,161 incident dementia events were documented during follow-up. Participants with lower PhenoAgeAccel presented significantly longer dementia-free survival at both baseline ages. At age 45, the lowest tertile gained an extra 1.99 dementia-free years (95%CI 0.95–3.03). Elevated PhenoAgeAccel predicted higher cumulative risks of dementia and all-cause mortality, with Gray’s test P values of 0.008 and &lt;0.001, respectively. All stratified and sensitivity analyses showed consistent findings.</p><h3>Conclusions</h3><p>Higher biological aging is independently associated with prolonged dementia-free life expectancy in prediabetic populations. PhenoAgeAccel can facilitate dementia risk stratification and guide early preventive interventions for prediabetic groups.</p></div>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":"63 11","pages":"1969 - 1975"},"PeriodicalIF":3.1,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating C-peptide as an independent predictor of HFpEF: influence of cardiometabolic risk beyond diabetes","authors":"Susanna Longo,&nbsp;Alessandro Nucera,&nbsp;Giacomo Piciucchi,&nbsp;Alberto Sulpizio,&nbsp;Gianluigi Ferrazza,&nbsp;Tommaso Rinaldi,&nbsp;Sara Martina,&nbsp;Andrea Quatrana,&nbsp;Marina Cardellini,&nbsp;Stefano Rizza,&nbsp;Massimo Federici","doi":"10.1007/s00592-026-02784-4","DOIUrl":"10.1007/s00592-026-02784-4","url":null,"abstract":"<div><p>Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndromecharacterized by diastolic dysfunction, preserved left ventricular ejection fraction, and arange of myocardial structural and metabolic abnormalities1. Rather than representingan isolated cardiac disorder, HFpEF is increasingly recognized as a multisystemdisorder, driven by multiple comorbidities, and manifesting as diverse clinicalphenotypes defined by differences in comorbidity burden, disease severity, cardiacstructure, biomarkers, and prognosis. Metabolic comorbidities such as obesity,dyslipidemia, type 2 diabetes (T2D), and hypertension are highly prevalent in HFpEFand may define a distinct cardiometabolic HFpEF (cmHFpEF) phenotype, marked bymore severe symptoms and poorer quality of life2. The coexistence of metaboliccomorbidities drives multisystem pathophysiological changes, worsening prognosis,and limiting the effectiveness of current therapies3.This study aimed to investigate the pathophysiological mechanisms of HFpEF, with afocus on cardiometabolic risk burden as a major contributor to HFpEF phenotypicheterogeneity, to inform future phenotyping strategies and therapeutic approaches.</p></div>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":"63 10","pages":"1811 - 1815"},"PeriodicalIF":3.1,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148786832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}