Life sciences最新文献

{"title":"Tuberous sclerosis complex 2 deficiency in cardiomyocytes exacerbates cardiac remodeling in diabetic mice","authors":"Rui-xue Yang ,&nbsp;Zhan-hui Du ,&nbsp;Xiu-hui Song ,&nbsp;Xiang-Jiu Ding ,&nbsp;Yan Liu ,&nbsp;Er-shun Liang ,&nbsp;Xue Liu","doi":"10.1016/j.lfs.2025.123891","DOIUrl":"10.1016/j.lfs.2025.123891","url":null,"abstract":"<div><h3>Background</h3><div>Based on gene expression profiles from the BioGPS database, Tuberous sclerosis complex 2 (Tsc2) exhibited the highest expression in mouse cardiac tissues. Herein, we investigated the potential functional role of Tsc2 in diabetic cardiomyopathy.</div></div><div><h3>Methods and results</h3><div>Cardiac-specific Tsc2 deletion exacerbated myocardial fibrosis and cardiac dysfunction in streptozotocin-induced diabetic mice. Whole-transcriptomic analysis combined with single cell-sequencing analysis from the Human Protein Atlas database demonstrated that Tsc2 deletion enhanced Angiopoietin-like protein 7 (Angptl7) expression in cardiomyocytes under hyperglycemia. Recombinant adeno-associated virus serotype 9 carrying Angptl7 shRNA under cardiac troponin T promoter substantially reversed Tsc2 deletion-induced cardiac remodeling and dysfunction in diabetic mice. Mechanistically, the study demonstrated that cardiomyocyte-released Angptl7 activated β-Catenin in fibroblasts and promoted cardiac fibrosis through a paracrine mechanism. Furthermore, chronic supplementation with leucine, an essential branched-chain amino acid, led to adverse cardiac remodeling and dysfunction through Angptl7 activation in diabetic mice.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrate that Tsc2 deficiency in cardiomyocytes disrupts cardiac homeostasis and contributes to the progression of diabetic cardiomyopathy. The results also suggest that targeting Angptl7 represents a potential therapeutic strategy for diabetic cardiomyopathy, particularly in patients with Tsc2 mutation.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123891"},"PeriodicalIF":5.1,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FGA139, a novel cysteine protease inhibitor, exhibits anti-inflammatory and neuroprotective activity and reveals microglial modulation via multi-omics profiling","authors":"Ania Canseco-Rodríguez ,&nbsp;Florenci V. González ,&nbsp;Ana María Sánchez-Pérez","doi":"10.1016/j.lfs.2025.123880","DOIUrl":"10.1016/j.lfs.2025.123880","url":null,"abstract":"<div><div>Neuroinflammation is a key driver in the progression of numerous brain disorders, with cysteine proteases such as calpains, caspases, and cathepsins playing central roles in inflammatory signaling.</div><div>This study investigates FGA139, a novel irreversible inhibitor targeting cysteine proteases. We evaluated the anti-inflammatory properties of FGA139 in lipopolysaccharide (LPS)-activated macrophages (RAW264.7) and microglia (HMC3). In addition, its neuroprotective effects were assessed in differentiated SH-SY5Y neuron-like cells exposed to conditioned media (CM⁺) derived from the activated immune cells.</div><div>FGA139 exhibited a favorable safety profile and robust anti-inflammatory activity, significantly reducing nitric oxide (NO) production in macrophages and TNFα levels in microglia. Conditioned media from both LPS-stimulated immune cells lines (CM⁺) reduced neurite length in neuronal cells. However, CM⁺ from HMC3 cells impaired neuronal viability, whereas CM⁺ from RAW264.7 cells elevated reactive oxygen species (ROS) and NO levels—indicating distinct neurotoxic signatures. Preincubation of neuron-like cells with FGA139 effectively mitigated most of these adverse effects.</div><div>Metabolomic analysis of the activated microglia supernatant revealed that FGA139 increased extracellular levels of neuroprotective metabolites, including purines, linoleic acid, and phenyllactic acid. Proteomic data confirmed that FGA139 attenuated M1-like microglial polarization, likely through modulation of pathways associated with zinc transport and vesicle trafficking.</div><div>In conclusion, FGA139 demonstrates potent neuroprotective effects and modulates microglial activation. These findings uncover novel mechanisms underlying the beneficial effects of cysteine protease inhibition and support the therapeutic potential of FGA139 in treating neuroinflammatory conditions, positioning it as a promising modulator of microglial function.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123880"},"PeriodicalIF":5.1,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"M6A modification of RRM2 drives B cell hyperactivity in primary Sjögren's syndrome","authors":"Yiying Yang ,&nbsp;Ke Liu ,&nbsp;Huali Zhang ,&nbsp;Yisha Li ,&nbsp;Muyao Guo","doi":"10.1016/j.lfs.2025.123884","DOIUrl":"10.1016/j.lfs.2025.123884","url":null,"abstract":"<div><h3>Background</h3><div>The mechanisms underlying B cell dysfunction in primary Sjögren's syndrome (pSS) remain unclear. This study investigates the expression and role of ribonucleotide reductase M2 (RRM2) in pSS B cells, focusing on its contribution to B cell hyperreactivity and potential as a biomarker for disease activity.</div></div><div><h3>Methods</h3><div>Transcriptomic data (GSE199868) of pSS B cells were analyzed to identify differentially expressed genes, with a focus on RRM2. The expression of RRM2 in B-cell subsets and salivary glands (SGs) from pSS patients was validated using flow cytometry and immunohistochemistry. <em>In vitro</em>, the role of RRM2 in B cell activation, differentiation, and antibody production was assessed by treating cells with the RRM2 inhibitor Osalmid. Additionally, the involvement of METTL3-mediated m6A modification in regulating RRM2 expression was explored using m6A-RIP-qPCR and actinomycin D assays.</div></div><div><h3>Results</h3><div>RRM2 expression was significantly upregulated in pSS B cells and SGs. Higher RRM2 levels correlated with increased disease activity (ESSDAI score), elevated IgG levels, and reduced salivary flow rate. Functionally, RRM2 promoted B cell activation, enhanced differentiation into CD38⁺CD27⁺ plasma cells, and increased production of IgG, IgM, and antinuclear antibodies. Mechanistically, METTL3-mediated m6A modification enhanced RRM2 mRNA stability, which contributed to its increased expression in B cells.</div></div><div><h3>Conclusion</h3><div>RRM2 is upregulated in pSS B cells and SGs, and correlates with disease activity. METTL3-mediated m6A modification regulates RRM2 expression, providing new insights into the molecular mechanisms driving the immune dysfunction in pSS. RRM2 may serve as a potential biomarker and a novel therapeutic target for modulating B-cell hyperactivity in pSS.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123884"},"PeriodicalIF":5.1,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144749140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling neutrophil extracellular traps: A new frontier in kidney disease therapy","authors":"Yiqiong Zhang ,&nbsp;Chaofu Li ,&nbsp;Qiuyan Jiang ,&nbsp;Yingying Jiang ,&nbsp;Gang Xu ,&nbsp;Guoying Kao ,&nbsp;Yanpeng Yang ,&nbsp;Bingbing Shen ,&nbsp;Jun Xiao ,&nbsp;Zhengmeng Ye ,&nbsp;Chuanwei Li","doi":"10.1016/j.lfs.2025.123892","DOIUrl":"10.1016/j.lfs.2025.123892","url":null,"abstract":"<div><div>Kidney disease, a formidable global public health challenge, critically demands the discovery of novel biomarkers and development of innovative therapeutic approaches. Although the clinical diagnosis and treatment system is improving, there are still big challenges in controlling disease progression and improving patient outcomes. Neutrophil extracellular traps (NETs), as a new pattern of neutrophil function, have gained attention in kidney disease research. Studies have shown that NETs, composed of chromatin fibers and antimicrobial proteins, contribute to kidney disease progression by mediating inflammatory responses and promoting thrombosis, and their potential as a therapeutic target is becoming more evident. Here, we comprehensively analyze the molecular regulatory mechanisms of NETs and their involvement in different kidney diseases, highlighting their significance as diagnostic and therapeutic targets.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123892"},"PeriodicalIF":5.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144749142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The silent invaders: Biofilms in neurological, cardiovascular, and metabolic diseases","authors":"Vinay Kumar ,&nbsp;Anuradha Tyagi","doi":"10.1016/j.lfs.2025.123886","DOIUrl":"10.1016/j.lfs.2025.123886","url":null,"abstract":"<div><div>Biofilms, intricate microbial communities enclosed in a protective extracellular matrix, are conventionally linked to localized illnesses. Emerging data indicates that biofilms significantly contribute to systemic disorders beyond traditional infections. Bacterial biofilms may induce neuroinflammation and impair the blood-brain barrier in neurodegenerative illnesses including Alzheimer's and Parkinson's. In cardiovascular illnesses, biofilms from oral and gut microbes play a role in atherosclerosis, endocarditis, and hypertension. In metabolic illnesses, biofilms affect insulin resistance and metabolic endotoxemia, worsening conditions such as obesity and type 2 diabetes. Moreover, biofilms are associated with cancer progression, especially in colorectal and gastric malignancies, as they provide a tumor-promoting milieu via chronic inflammation and the generation of bacterial metabolites. Biofilms advance disease development by increasing chronic inflammation, evading immunological responses, and allowing microbial translocation, aspects that have been previously underestimated. Identifying biofilms as significant contributors to systemic disease presents novel avenues for innovative therapies and enhanced patient outcomes across various chronic illnesses. Thus, this review examines the increasing influence of biofilms on chronic inflammatory diseases, neurological disorders, cardiovascular diseases, metabolic syndromes, and cancer.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123886"},"PeriodicalIF":5.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144738578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dopamine and its effects on the respiratory system: A narrative literature review","authors":"Vincenzo Bellitto ,&nbsp;Demetris Savva ,&nbsp;Niccolò Fagni ,&nbsp;Giulio Procelli ,&nbsp;Marco Maria Dima ,&nbsp;Giulio Nittari","doi":"10.1016/j.lfs.2025.123888","DOIUrl":"10.1016/j.lfs.2025.123888","url":null,"abstract":"<div><div>Dopamine is a neuromodulator molecule that is involved in several systems in the human body. As a neurotransmitter, it plays a role in regulating reward, pleasure, and motor control in the brain. Beyond its well-known central nervous system functions it significantly influences peripheral systems including kidneys, circulatory system, and notably, immune system. It increases glomerular filtration rate and renal blood flow in the kidneys, while it increases aortic pressure and cardiac output in the circulatory system. Crucially, dopamine and its receptors have been identified on various immune cells, playing a significant immunomodulatory role that contributes to balanced immune responses and has implications in autoimmune diseases and conditions like sepsis. Moreover, in the respiratory system, dopamine plays a significant role in the pathophysiology of major respiratory disorders such as asthma, cystic fibrosis, chronic obstructive pulmonary disease, and lung cancer. Depending on the type of receptor, dopaminergic receptors contribute to the pathophysiology of lung disease. As part of the narrative review, we have identified dopaminergic receptors in the respiratory system, their anatomic locations, and their specific mechanisms of action in the pathophysiology of major respiratory disorders. We have also identified and summarized molecular therapy protocols that can be used in the treatment of these disorders, considering the evolving understanding of dopamine's broad systemic effects.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123888"},"PeriodicalIF":5.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of impaired mitochondrial dynamics and mitophagy in cardiovascular diseases: Possible therapeutic approaches","authors":"Sarmistha Sarkar ,&nbsp;Aindrila Chattopadhyay ,&nbsp;Debasish Bandyopadhyay","doi":"10.1016/j.lfs.2025.123890","DOIUrl":"10.1016/j.lfs.2025.123890","url":null,"abstract":"<div><div>High mortality rates due to cardiovascular diseases (CVDs) fascinate the scientists worldwide in the past few decades to discover potent therapeutic strategies to save the victims. The myocardium being a highly active tissue, mitochondrial homeostasis and mitochondrial quality control system are crucial for maintaining optimal cardiac performance. Mitochondrial quality control mechanism is a finely tuned regulatory network encompassing mitochondrial biogenesis, mitochondrial dynamics and mitophagy and is an integral component of the mitochondrial response to stressor stimuli. Mitochondrial dynamics including the fusion and fission of mitochondrial membranes is regulated by an extensively conserved mechanism comprising a group of mitochondrial membrane proteins belonging to the dynamin family of GTPases. Emerging evidences indicate that defects in mitochondrial fusion or fission are intrinsically correlated with the pathophysiology of CVDs. Mitophagy is a kind of selective autophagy which removes damaged or redundant mitochondria. Experimental findings demonstrated that impairment of mitophagy in cardiomyocytes induces the accumulation of dysfunctional mitochondria, leading to the disruption of cellular homeostasis and consequently precipitating various CVDs. These findings speculate that pharmacological modulation of mitochondrial homeostasis including mitochondrial dynamics and mitophagy may represent a potential therapeutic approach in restoring cardiac physiology. This review summarizes the prevailing insight into the impact of disturbed mitochondrial dynamics and mitophagy in the pathogenesis of CVDs and also delineates the therapeutic potential of several relevant regulatory drugs that target mitochondrial function and quality control in alleviating mitochondrial impairment-related cardiac dysfunction.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123890"},"PeriodicalIF":5.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144749141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the effect of the Mediterranean diet on fecal bile acids and their mediating role on biomarkers of intestinal barrier function: An exploratory analysis of a randomized controlled trial","authors":"Benjamin Seethaler ,&nbsp;Audrey M. Neyrinck ,&nbsp;Maryam Basrai ,&nbsp;Marion Kiechle ,&nbsp;Nathalie M. Delzenne ,&nbsp;Stephan C. Bischoff","doi":"10.1016/j.lfs.2025.123855","DOIUrl":"10.1016/j.lfs.2025.123855","url":null,"abstract":"<div><h3>Background</h3><div>Recent preclinical studies have suggested that gut microbiota-derived secondary bile acids affect intestinal barrier function. In this exploratory analysis, we studied the effect of the Mediterranean diet on fecal bile acid levels and their role in intestinal barrier regulation.</div></div><div><h3>Methods</h3><div>Data from women with impaired intestinal barrier function following the Mediterranean diet (intervention group, <em>n</em> = 33) or standard diet (control group, <em>n</em> = 35) were assessed in a randomized controlled trial (<span><span>ClinicalTrials.gov</span><svg><path></path></svg></span>: <span><span>NCT02087592</span><svg><path></path></svg></span>). Evaluations comprised baseline (BL), month 3 (V1), and month 12 (V2). Adherence to the Mediterranean diet was assessed using questionnaires, intestinal barrier function using validated biomarkers (plasma lipopolysaccharide binding protein (LBP) and fecal zonulin), and fecal bile acids using gas chromatography–mass spectrometry.</div></div><div><h3>Results</h3><div>As described before, the intervention group showed increased adherence to the Mediterranean diet and reduced plasma LBP and fecal zonulin levels over the entire observation period (BL-V1 and BL-V2, <em>P</em> &lt; 0.01), whereas the control group did not. In the intervention group, the fecal levels of the secondary bile acids deoxycholic acid (DCA) and lithocholic acid (LCA) decreased, whereas the levels of the tertiary bile acid ursodeoxycholic acid increased (BL-V1 and BL-V2, <em>P</em> &lt; 0.01). Multivariate analyses confirmed that the Mediterranean diet was inversely associated with DCA, LCA, LBP, and zonulin levels. Mediation analyses showed that decreases in DCA and LCA mediated the beneficial effects of the Mediterranean diet on LBP.</div></div><div><h3>Conclusion</h3><div>Consistent with previous pre-clinical studies, we found that the Mediterranean diet altered fecal secondary bile acid levels and that this alteration was associated with improved intestinal barrier function.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123855"},"PeriodicalIF":5.1,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144722322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SNHG8/miR-873-3p/CDK6 axis triggers proliferation and migration of smooth muscle cells in intimal hyperplasia","authors":"Jiaying Sun ,&nbsp;Jing Qi ,&nbsp;Jianyao Su ,&nbsp;Jiye Wan","doi":"10.1016/j.lfs.2025.123878","DOIUrl":"10.1016/j.lfs.2025.123878","url":null,"abstract":"<div><h3>Aim</h3><div>Long-strand non-coding RNAs play a crucial role in intimal hyperplasia. Nevertheless, the mechanism by which small nucleolar RNA host gene 8 affects intimal hyperplasia remains unknown.</div></div><div><h3>Materials and methods</h3><div>The expression levels of SNHG8, miR-873-3p, and CDK6 were detected by qRT-PCR or Western blotting. Cell proliferation was measured using 5-ethynyl-2′-deoxyuridine and cell counting kit-8 assay. Cell migration was detected by Transwell and scratch assay. The binding roles and sites of miR-873-3p to SNHG8 and CDK6 were detected by dual luciferase reporter gene assay. The binding role of miR-873-3p and SNHG8 was detected by RNA immunoprecipitation assay. Vascular injury was simulated by ligation of the left common carotid artery.</div></div><div><h3>Key findings</h3><div>This study suggests that the high expression of SNHG8 in intimal hyperplasia vascular smooth muscle cells can function as a competitive endogenous RNA. By specifically binding to miR-873-3p, which is weakened, SNHG8 acts as a negative regulator of CDK6 target genes, leading to upregulation of CDK6 expression. This interaction was also shown to promote vascular smooth muscle cells proliferation and migration.</div></div><div><h3>Significance</h3><div>This study revealed a novel regulatory mechanism of action of the SNHG8/miR-873-3p/CDK6 axis in the progression of intimal hyperplasia and points to the potential of SNHG8, miR-873-3p, and CDK6 as novel targets for the diagnosis and treatment of intimal hyperplasia.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"379 ","pages":"Article 123878"},"PeriodicalIF":5.1,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"Decrypting the potential role of α-lipoic acid in Alzheimer's disease\" [Life Sci. 284 (2021) 119899].","authors":"Dapinder Kaur, Tapan Behl, Aayush Sehgal, Sukhbir Singh, Neelam Sharma, Sridevi Chigurupati, Ahmed Alhowail, Ahmed Abdeen, Samah F Ibrahim, Celia Vargas-De-La-Cruz, Monika Sachdeva, Saurabh Bhatia, Ahmed Al-Harrasi, Simona Bungau","doi":"10.1016/j.lfs.2025.123857","DOIUrl":"10.1016/j.lfs.2025.123857","url":null,"abstract":"","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":" ","pages":"123857"},"PeriodicalIF":5.2,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}