Life sciences最新文献

{"title":"Tryptase-like proteases: A novel perspective for fibrosis","authors":"Hui-Juan Zhang ,&nbsp;Nan Li ,&nbsp;Meng-Qi Li ,&nbsp;Ya-Ning Chen ,&nbsp;Shi-Yu Yin ,&nbsp;Ting-Ting Chen ,&nbsp;Na-Na Xu ,&nbsp;Wen-Xuan Liu ,&nbsp;Yu-Qian Xu ,&nbsp;Hua Wang ,&nbsp;Wu-Yi Sun","doi":"10.1016/j.lfs.2025.123970","DOIUrl":"10.1016/j.lfs.2025.123970","url":null,"abstract":"<div><div>Fibrosis, as a chronic disease, is affecting people's health. The main pathological characteristic is the deposition of fibrous connective tissue, such as collagen and fibronectin, which are components of the extracellular matrix (ECM). When fibrosis is not treated in time, it can lead to permanent scarring, organ dysfunction, and eventually death. Recent reports indicated that fibrosis may be reversible. Therefore, it is considerable significance to find potential gene targets or biomarkers for anti-fibrosis treatment. Trypsin-like proteases (TLPs), a family of serine enzymes predominantly specific for basic residues such as lysine and arginine in the P1 position, are widely distributed in the body. TLPs play crucial role in various physiological processes, including digestion, blood coagulation, wound healing, and immunity. They could promote the proliferation, differentiation, and activation of fibroblasts, as well as collagen production, either by cleaving and activating PARs receptors or by directly hydrolyzing collagen during fibrotic diseases. This review aims to clarify the connection between TLPs and fibrotic diseases through recent studies. There is an increasing agreement that TLPs play a potential therapeutic target for various fibrotic conditions.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"381 ","pages":"Article 123970"},"PeriodicalIF":5.1,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081039","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 the P2X7 receptor in intestinal inflammation due to infection with the oral pathogen Porphyromonas gingivalis","authors":"Lorraine Oliveira-Cruz ,&nbsp;Nayara Carvalho-Barbosa ,&nbsp;Fabiana Cristina-Rodrigues ,&nbsp;Thaís N. Côrtes ,&nbsp;Kamila Guimarães-Pinto ,&nbsp;André L. Amorim da Costa ,&nbsp;Isadora S. de Lima ,&nbsp;Talita G.B. Lourenço ,&nbsp;Archimedes B. Castro-Junior ,&nbsp;Alessandra D. Almeida Filardy ,&nbsp;Ana Paula V. Colombo ,&nbsp;Heitor S.P. de Souza ,&nbsp;Christina M. Takiya ,&nbsp;David M. Ojcius ,&nbsp;Luiz Eduardo B. Savio ,&nbsp;Robson Coutinho-Silva","doi":"10.1016/j.lfs.2025.123971","DOIUrl":"10.1016/j.lfs.2025.123971","url":null,"abstract":"<div><div><em>Porphyromonas gingivalis</em> (<em>P</em>. <em>gingivalis</em>), a Gram-negative bacterium present in the oral cavity, is one of the primary pathogens associated with periodontitis. <em>P</em>. <em>gingivalis</em> has also been linked to other non-oral pathologies, such as diabetes, colorectal cancer, and inflammatory bowel disease. The P2X7 receptor plays a role in resolving oral infection with <em>P</em>. <em>gingivalis</em>, and, separately, is associated with increased damage in colitis. This study investigated whether ingestion of <em>P</em>. <em>gingivalis</em> could aggravate colitis and whether the P2X7 receptor could play a role in this effect. Wild-type (WT) and P2X7-deficient mice were orally inoculated by gavage with <em>P</em>. <em>gingivalis</em>, and colitis was induced by intrarectal injection with 2,4,6-trinitrobenzene sulfonic acid (TNBS). <em>P</em>. <em>gingivalis</em> ingestion upregulated P2X7 receptor immunoreactivity in the colon of WT mice. <em>P</em>. <em>gingivalis</em> also triggered intestinal inflammation and reduced the colon length in WT mice but not P2X7-deficient mice. The balance of regulatory T (T_reg) cells and Th17 cells of the mesenteric lymph node was perturbed in WT mice that had been administered <em>P</em>. <em>gingivalis</em> and TNBS, while this was not observed in P2X7-deficient mice. Th17 cells were increased in WT mice in response to <em>P</em>. <em>gingivalis</em>, while P2X7-deficient mice showed an increase in T_reg cells. <em>P</em>. <em>gingivalis</em> ingestion induced liver injury in WT mice, but not in P2X7-deficient mice. Furthermore, the liver from WT mice that had been administered <em>P</em>. <em>gingivalis</em> and TNBS showed higher levels of bacteria than P2X7-deficient mice. Our findings suggest that the P2X7 receptor contributes to the deleterious effects of <em>P</em>. <em>gingivalis</em> on gut inflammation and liver damage.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123971"},"PeriodicalIF":5.1,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069968","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 “Calpain silencing alleviates myocardial ischemia-reperfusion injury through the NLRP3/ASC/Caspase-1 axis in mice” [Life Sci. 233 (2019) 116631]","authors":"Rong-Chuan Yue ,&nbsp;Sheng-Zhong Lu ,&nbsp;Yu Luo ,&nbsp;Tao Wang ,&nbsp;Hao Liang ,&nbsp;Jing Zeng ,&nbsp;Jie Liu ,&nbsp;Hou-Xiang Hu","doi":"10.1016/j.lfs.2025.123964","DOIUrl":"10.1016/j.lfs.2025.123964","url":null,"abstract":"","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123964"},"PeriodicalIF":5.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058454","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":"Commentary: Towards multi-targeting approaches in intestinal fibrosis – Emerging clues from prim-O-glucosylcimifugin","authors":"Giovanni Santacroce ,&nbsp;Marco Vincenzo Lenti ,&nbsp;Antonio Lo Bello ,&nbsp;Antonio Di Sabatino","doi":"10.1016/j.lfs.2025.123968","DOIUrl":"10.1016/j.lfs.2025.123968","url":null,"abstract":"","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123968"},"PeriodicalIF":5.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058426","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":"Cardiovascular and renal effects of 5-aminoimidazole-4-carboxyribonucleoside (AICAR) in the deoxycorticosterone acetate (DOCA)-salt rat model of hypertension","authors":"Melissa R. Dennis ,&nbsp;Lizetta Zozobrado ,&nbsp;Dakota M. Reinartz ,&nbsp;Thaiane Foster ,&nbsp;Madeline M. Gauthier ,&nbsp;Justin E. Wilson ,&nbsp;Christopher T. Banek","doi":"10.1016/j.lfs.2025.123969","DOIUrl":"10.1016/j.lfs.2025.123969","url":null,"abstract":"<div><div>Previous studies suggest that exercise training mitigates blood pressure in hypertensive animal models. While exercise training may be an effective therapeutic for hypertension treatment and prevention, many patients diagnosed with hypertension can be noncompliant with lifestyle modifications that involve physical activity or are unable to participate in strenuous activity due to the severity of their hypertension. AMP-activated protein kinase (AMPK) is responsive during metabolic stressors, plays a vasoprotective role in endothelial function, and is stimulated during exercise training. Studies have suggested that signaling pathways activated by AMPK may play a protective role in hypertensive models given AMPK's involvement in redox balancing. The purpose of this study is to determine the therapeutic potential of AICAR (5-aminoimidazole-4-carboxamide-3-ribonucleoside), a potent AMPK stimulator, for ameliorating hypertension. Uninephrectomized Sprague Dawley rats received DOCA-salt treatment and daily administration of either AICAR (100 mg/kg/day) or vehicle (20 % DMSO) subcutaneously for 21 days. Cardiovascular and renal function were assessed by radiotelemetry, tail cuff, proteinuria, and GFR. No differences in final MAP were detected in AICAR and vehicle treated DOCA-salt groups, respectively (183.6 ± 26.2 and 179.4 ± 26.5 mmHg). Notably, no changes in renal injury or function were detected with AICAR treatment as shown by the final GFR and proteinuria. From these findings we concluded that exogenous administration of AICAR does not attenuate hypertension in the DOCA-salt model despite increased AMPK activation.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123969"},"PeriodicalIF":5.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065339","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 “Combined apocynin and carvedilol protect against cadmium-induced testicular damage via modulation of inflammatory response and redox-sensitive pathways” [Life Sci. 311 (2022) 121152]","authors":"Adel G. Bakr,&nbsp;Emad H.M. Hassanein,&nbsp;Fares E.M. Ali,&nbsp;Ehab A.M. El-Shoura","doi":"10.1016/j.lfs.2025.123963","DOIUrl":"10.1016/j.lfs.2025.123963","url":null,"abstract":"","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123963"},"PeriodicalIF":5.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058469","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":"Cisplatin transported by COX17 induces cochlear damage by binding Myosin IIA to regulate cell pyroptosis induced by mitochondrial dysfunction","authors":"Jiahui Peng ,&nbsp;Guofang Tao ,&nbsp;Xubo Chen ,&nbsp;Yufeng Ai ,&nbsp;Ruosha Lai ,&nbsp;Wei Liu ,&nbsp;Bing Hu ,&nbsp;Yingying Xu ,&nbsp;Bingbin Xie ,&nbsp;Lihua Li","doi":"10.1016/j.lfs.2025.123961","DOIUrl":"10.1016/j.lfs.2025.123961","url":null,"abstract":"<div><h3>Aims</h3><div>Cytochrome c oxidase copper chaperone 17 (COX17) could transport cisplatin to cancer cell mitochondria. Whether COX17 transports cisplatin to cochlear mitochondria and induces pyroptosis to participate in cisplatin-induced ototoxicity remains unknown.</div></div><div><h3>Materials and methods</h3><div>A cisplatin-induced hearing loss model was constructed in rats, and the role of COX17 and Myosin IIA in cisplatin-induced hearing loss and cochlear injury was evaluated by auditory brainstem response test and H&amp;E staining. Cisplatin binding to Myosin IIA was verified through cisplatin agar-pull-down assays and drug affinity responsiveness target stability. The interaction between Myosin IIA and F-actin was verified using co-immunoprecipitation. Various techniques were used to study how cisplatin causes damage to cochlear hair cells and induces pyroptosis, including immunofluorescence staining, and flow cytometry.</div></div><div><h3>Key findings</h3><div>Our findings indicated that downregulating COX17 inhibits cisplatin accumulation in mitochondria, leading to improved cell survival, and inhibits pyrodeath. Upon entering the mitochondria, cisplatin transported by COX17 binds to Myosin IIA, enhancing its expression and subsequently promoting the expression of F-actin and p-DRP1 while inhibiting the expression of Mfn1, Mfn2, and OPA1. Furthermore, the interaction between Myosin IIA and F-actin was determined. Downregulation of Myosin IIA or treatment with mitochondrial fission inhibitors resulted in reduced mitochondrial ROS release and increased pyroptosis. In vivo studies demonstrated that downregulating COX17 or Myosin IIA improved cisplatin-induced hearing loss and cochlear damage in rats.</div></div><div><h3>Significance</h3><div>These findings offer new insights and potential targets for the preventing and treatment of cisplatin-induced ototoxicity.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123961"},"PeriodicalIF":5.1,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058458","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":"Glycoprotein Ib-CD11b + monocyte-derived macrophages mediate atherosclerosis-exacerbated psoriatic inflammation","authors":"Canbin Dong ,&nbsp;Wenjing Yang ,&nbsp;Lianxi Sun ,&nbsp;Jui-Ming Lin ,&nbsp;Jie Wang ,&nbsp;Yilun Wang ,&nbsp;Lanmei Lin ,&nbsp;Xinyi Zhu ,&nbsp;Jia Huang ,&nbsp;Xiaonian Lu ,&nbsp;Junhao Zhu ,&nbsp;Jinhua Xu ,&nbsp;Jinyun Tan ,&nbsp;Ningwen Zhu ,&nbsp;Juan Du","doi":"10.1016/j.lfs.2025.123960","DOIUrl":"10.1016/j.lfs.2025.123960","url":null,"abstract":"<div><h3>Background</h3><div>Psoriasis is a systemic inflammatory skin disease affecting 2–3 % of the global population, with significant cardiovascular comorbidities. A complex inflammatory interaction exists between psoriasis and atherosclerosis, but the exact mechanism remains unclear.</div></div><div><h3>Methods</h3><div>To elucidate this relationship, we collected skin biopsies from treatment-naïve patients with comorbid psoriasis and atherosclerosis underwent single-cell RNA sequencing, integrated with public atherosclerosis datasets. Bioinformatics analysis identified cell populations and interactions. Validation included immunohistochemistry, immunofluorescence, in vitro functional assays with isolated patient macrophages and platelets, and an in vivo imiquimod-induced psoriasis mouse model treated with a CD11b agonist.</div></div><div><h3>Results</h3><div>Single-cell RNA sequencing identified significantly increased CD11b + monocyte-derived macrophages in psoriasis lesions comorbid with atherosclerosis, exhibiting proinflammatory M1 polarization and enriched IL-17/chemokine signaling. These macrophages shared transcriptional signatures with monocytes in atherosclerotic plaques. In vivo, CD11b agonism (ADH-503) exacerbated imiquimod-induced psoriatic inflammation. Mechanistically, platelet-derived GPIb promoted macrophage M1 polarization via the GPIb-CD11b axis, evidenced by GPIb upregulation correlating with psoriasis severity (PASI), spatial co-localization in perivascular regions, and dose-dependent M1 marker induction by recombinant GPIb. GPIb^hi monocytes from atherosclerotic patients showed enhanced proinflammatory pathways, revealing a shared mechanism driving inflammation in both diseases.</div></div><div><h3>Conclusions</h3><div>Collectively, CD11b + monocyte-derived macrophages are central to the interplay between atherosclerosis and psoriasis through the GPIb-CD11b axis. Targeting GPIb with specific drugs to control atherosclerosis may enhance the efficacy of inflammatory control in psoriasis.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123960"},"PeriodicalIF":5.1,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058407","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 left and right vagus nerves in linking peripheral adrenergic signals to contextual fear memory","authors":"João Munhoz ,&nbsp;Ana Oliveira ,&nbsp;Márcia Azevedo ,&nbsp;Rafaela Seixas ,&nbsp;Iara Rodrigues-de-Castro ,&nbsp;Paula Serrão ,&nbsp;Mónica Moreira-Rodrigues","doi":"10.1016/j.lfs.2025.123946","DOIUrl":"10.1016/j.lfs.2025.123946","url":null,"abstract":"<div><div>Stress-induced physiological changes are crucial for adaptive responses to threats. Catecholamines, specifically epinephrine, activate peripheral β-adrenergic receptors, facilitating contextual fear memory consolidation. The vagus nerve is thought to be essential in transmitting physiological signals to the brain, influencing emotional memory consolidation. We aimed to evaluate the vagus nerve's role in contextual fear memory strengthening induced by epinephrine.</div><div>Male 129 × 1/SvJ mice underwent bilateral subdiaphragmatic vagotomy, right or left cervical vagotomy, or sham surgeries. After a seven-day recovery, mice were subjected to the fear conditioning paradigm, receiving three foot shocks on conditioning day, followed by contextual reminder exposure. Epinephrine (0.1 mg/kg, intraperitoneal, i.p.) was administered to a subset of left cervically vagotomized mice 3 min before each session. Freezing behavior was evaluated. Catecholamines were quantified by reverse-phase high-performance liquid chromatography (HPLC) with electrochemical detection.</div><div>Subdiaphragmatic vagotomy did not alter freezing behavior on both days. In cervical vagotomies, while no differences were observed on the conditioning day, a significant decrease in freezing behavior was observed on the context day. In left cervically vagotomized mice, epinephrine administration significantly increased freezing behavior.</div><div>In conclusion, unilateral left or right cervical vagotomy impaired contextual fear memory, contrary to subdiaphragmatic vagotomy. Impaired contextual fear memory in left cervical vagotomy was reversed by exogenous epinephrine, possibly due to the intact right cervical vagus. We suggest that stress-induced catecholamine release may activate thoracic peripheral β-adrenergic receptors and elevate systolic blood pressure, signals that are transmitted through the vagus nerve, influencing the hippocampus and facilitating contextual fear memory consolidation.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123946"},"PeriodicalIF":5.1,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054325","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":"Reprogramming cysteine metabolism via METTL14-SLC7A11 axis promotes the progression of NAFLD and hepatocellular carcinoma","authors":"Xing He ,&nbsp;Yuqin Gu ,&nbsp;Guangyu Lu ,&nbsp;Linxue Zhang ,&nbsp;Xue Yang ,&nbsp;Ziheng Kan ,&nbsp;Yuwei Li ,&nbsp;RuiJi Liu ,&nbsp;Xianjun Zhu ,&nbsp;Zhenglin Yang ,&nbsp;Ziyan Wang","doi":"10.1016/j.lfs.2025.123965","DOIUrl":"10.1016/j.lfs.2025.123965","url":null,"abstract":"<div><div>Non-alcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC) constitute significant global health challenges, with their prevalence exacerbated by shifts in lifestyle and dietary habits. Cysteine metabolism is intricately linked to the synthesis of reductive glutathione (GSH) and the maintenance of redox homeostasis, both of which are essential for cellular viability. N6-methyladenosine (m6A) methylation has emerged as a critical regulatory mechanism influencing metabolic pathways and redox balance in the context of NAFLD and HCC. This study aimed to elucidate the role of METTL14 in cysteine metabolism and the progression of NAFLD and HCC in vivo by examining the amino acid metabolic profile of NAFLD-affected livers using a hepatocyte-specific METTL14 knockout mouse model. Our results demonstrate that deletion of METTL14 reduces m6A methylation of SLC7A11 mRNA, thereby impairing cystine uptake, disrupting cysteine-dependent GSH synthesis, and compromising mitochondrial structure and function. These alterations culminate in the accumulation of reactive oxygen species, enhanced lipid peroxidation, increased cell death, and the accelerated progression of NAFLD and diethylnitrosamine-induced HCC. Collectively, these findings suggest that targeting the METTL14-SLC7A11-cysteine-GSH axis may offer a novel therapeutic approach for mitigating the advancement of NAFLD and HCC.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123965"},"PeriodicalIF":5.1,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054344","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}