Life metabolism最新文献

{"title":"Intestinal epithelial formyl peptide receptor 2 contributes to intestinal epithelium homeostasis and injury repair by regulating intestinal stem cell and transit-amplifying cell proliferation and differentiation.","authors":"Shuting Yu, Lele Song, Wunier, Shuyu Ouyang, Youpeng Ding, Lixing Zhan, Yi Arial Zeng, Yingying Le","doi":"10.1093/lifemeta/loaf045","DOIUrl":"10.1093/lifemeta/loaf045","url":null,"abstract":"<p><p>Intestinal stem cells (ISCs) play critical roles in the self-renewal and regeneration of the intestinal epithelium under physiological conditions and after injury, respectively. However, the underlying mechanisms are not fully understood. In this study, we investigate the role of the G protein-coupled receptor formyl peptide receptor 2 (FPR2) in intestinal epithelium homeostasis and regeneration. In mice, knocking out <i>Fpr2</i> in either intestinal epithelial cells (IECs) or ISCs significantly reduces villus height and crypt depth by impairing ISC and transit-amplifying (TA) cell proliferation and differentiation, primarily TA cell differentiation. Mechanistic studies using intestinal organoid culture and bulk and single-cell RNA sequencing revealed that activation of FPR2 promotes proliferation and differentiation of ISCs and TA cells by activating the wingless/integrated (Wnt), Notch, and Hippo signaling pathways via protein kinase C (PKC)-extracellular signal-regulated kinase (ERK). Under physiological conditions, the Wnt and Notch signaling pathways mediate the regulation of ISC proliferation and differentiation by FPR2. <i>Fpr2</i> deficiency in mouse IECs exacerbates X-ray- and 5-fluorouracil-induced villus and crypt injury, and delays intestinal epithelium regeneration by reducing ISC and TA cell proliferation. Administering an FPR2 agonist to mice significantly increases survival rates and accelerates intestinal epithelium regeneration after irradiation. Taken together, these results demonstrate that intestinal epithelial FPR2 plays a key role in intestinal epithelium homeostasis and regeneration by promoting ISC and TA cell proliferation and differentiation. FPR2 is a potential therapeutic target against chemotherapy- and radiotherapy-induced intestinal injury.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 3","pages":"loaf045"},"PeriodicalIF":6.3,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycine-GLRA1-calmodulin signaling regulates endoplasmic reticulum calcium to sustain insulin secretion and β-cell function.","authors":"Jiarui Zhang, Zehui Cao, Jinbao Yang, Kuo Zhu, Shuai Liu, Weijie Liu, Jin Lu, Hongfang Zhao, Wei Dai, Chunmei Chang, Haobin Ye, Xingrong Du, Qi Wang, Binghua Jiang, Sijia Wang, Li Jin, Tongjin Zhao, Peng Li, Antonio Vidal-Puig, Yuanting Zheng, Leming Shi, Linzhang Huang","doi":"10.1093/lifemeta/loaf044","DOIUrl":"10.1093/lifemeta/loaf044","url":null,"abstract":"<p><p>Glycine, a non-essential amino acid, has been linked to improved metabolic health and enhanced insulin secretion, yet its mechanistic role in β-cell function remains poorly defined. Here, we identify a glycine-GLRA1-calmodulin signaling axis that regulates endoplasmic reticulum (ER) calcium homeostasis to support insulin biosynthesis and β-cell survival. Dietary glycine deficiency impairs insulin secretion, reduces islet mass, and worsens glucose intolerance, while overexpression of serine hydroxymethyltransferase 2 (<i>Shmt2</i>), a key glycine biosynthetic enzyme, increases circulating glycine, enhances insulin output, and improves glucose control. Conversely, β-cell-specific deletion of <i>Glra1</i> phenocopies glycine deficiency, disrupting ER calcium dynamics, amplifying ER stress, and impairing insulin gene expression and secretion. Mechanistically, GLRA1 interacts with calmodulin to sustain ER calcium levels and alleviate ER stress, preserving β-cell viability under metabolic stress. Human genetic and transcriptomic analyses reveal that <i>GLRA1</i> expression and variants are associated with insulin secretion and glycemic traits, underscoring clinical relevance. These findings establish glycine as a signaling metabolite that activates a receptor-calcium axis to maintain β-cell function, offering a mechanistic rationale for targeting GLRA1 or dietary glycine in diabetes therapy.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 2","pages":"loaf044"},"PeriodicalIF":6.3,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocyte-specific DDAH1 regulates fasting-induced hepatic lipid metabolism via modulating FABP1 expression and AMPK/mTOR-mediated autophagy.","authors":"Kai Luo, Xiyue Shen, Siyu Wang, Fang Li, Yierxiati Jianggewaer, Weiping Sun, Zhongbing Lu","doi":"10.1093/lifemeta/loaf042","DOIUrl":"10.1093/lifemeta/loaf042","url":null,"abstract":"<p><p>Under nutrient deprivation conditions, the liver maintains systemic energy homeostasis by mobilizing lipid reserves, a process often accompanied by hepatic lipid accumulation. Dimethylarginine dimethylaminohydrolase 1 (DDAH1), a key metabolizing enzyme for asymmetric dimethylarginine (ADMA), has been demonstrated to exert a protective effect in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), yet its role in fasting-induced hepatic metabolic adaptation remains incompletely elucidated. In this article, we explored the function of DDAH1 in fasting-induced liver lipid accumulation using hepatocyte-specific <i>Ddah1</i> knockout (<i>Ddah1</i> ^HKO) mice. Compared with control mice (<i>Ddah1</i> ^f/f), <i>Ddah1</i> ^HKO mice exhibited significantly attenuated hepatic steatosis after fasting. Lipidomic analysis of the liver revealed decreased levels of most lipid species (e.g., triglycerides and free fatty acids) in <i>Ddah1</i> ^HKO mice. Further mechanistic studies demonstrated that <i>Ddah1</i> deletion downregulated the protein level of hepatic fatty acid binding protein 1 (FABP1) and activated the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway, thereby enhancing autophagic flux and promoting lipid droplet degradation under fasting conditions. Hepatic overexpression of FABP1 reversed the anti-steatotic phenotype of <i>Ddah1</i> ^HKO mice, while treatment with the AMPK inhibitor Compound C suppressed autophagy and increased hepatic lipid accumulation. In addition, overexpression of DDAH1 in hepatocytes exacerbated hepatic steatosis in fasted mice, coinciding with FABP1 upregulation and autophagy inhibition. Collectively, this article reveals that DDAH1 plays a critical role in hepatic lipid metabolism under fasting conditions by modulating FABP1 expression and AMPK/mTOR-mediated autophagy.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 2","pages":"loaf042"},"PeriodicalIF":6.3,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urate metabolism in the gut.","authors":"Riccardo Percudani","doi":"10.1093/lifemeta/loaf041","DOIUrl":"10.1093/lifemeta/loaf041","url":null,"abstract":"","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 1","pages":"loaf041"},"PeriodicalIF":6.3,"publicationDate":"2025-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P5CS-coupled proline metabolism manipulates metabolic dysfunction-associated steatotic liver disease.","authors":"Zan Lyu, Sike Yu, Chang Peng, Wenbiao Wu, Wenhua Yang, Huan Ma, Yan Sun, Liya Jing, Hongyu Gu, Erjiang Tang, Xuemei Zhang, Huihong Jiang, Haowen Jiang, Jia Li","doi":"10.1093/lifemeta/loaf040","DOIUrl":"10.1093/lifemeta/loaf040","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD), characterized by hepatic steatosis, inflammation, and fibrosis, has reached epidemic proportions globally. Emerging evidence highlights a close association between amino acid metabolic dysregulation and MASLD pathogenesis, however, the precise mechanisms remain elusive. In this study, we identify pyrroline-5-carboxylate synthase (P5CS), a pivotal enzyme in proline biosynthesis, as a critical regulator of hepatic proline production and a key driver of MASLD progression. Based on comprehensive analysis of clinical samples from MASLD patients and experimental mouse models, we demonstrate that elevated hepatic and plasma proline levels, resulting from increased P5CS expression, are strongly correlated with disease severity. Genetic overexpression of P5CS in the livers of mice exacerbates diet-induced MASLD, whereas its knockdown exhibits protective profiles. Notably, proline supplementation abolishes the beneficial effects of P5CS knockdown, confirming the causal role of proline overproduction in MASLD pathogenesis. Mechanistically, P5CS-mediated proline accumulation impairs mitochondrial function, thereby disrupting fatty acid oxidation and promoting hepatic lipid accumulation. Pharmacological inhibition of P5CS activity could restore mitochondrial capacity. Thus, our findings establish P5CS-regulated proline metabolism as a novel pathogenic mechanism of MASLD and provide a potential approach for MASLD therapy.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 2","pages":"loaf040"},"PeriodicalIF":6.3,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive value of 1-hour postprandial SPARC levels on metabolic outcomes from Mediterranean diet adherence: results from a randomized controlled feeding study.","authors":"Yanru Chen, Mengshan Ni, Yufei Chen, Chongrong Shen, Yaogan Luo, Huibin Lin, Juan Zhang, Huajie Dai, Aibo Gao, Muye Tong, Yinmeng Zhu, Yan Lu, Jie Hong, Weiqiong Gu, Rong Zeng, Weiqing Wang, Xu Lin, Min Xu, Ruixin Liu, Guang Ning, Jiqiu Wang","doi":"10.1093/lifemeta/loaf039","DOIUrl":"10.1093/lifemeta/loaf039","url":null,"abstract":"<p><p>Precision nutrition is pivotal to preventing cardiometabolic diseases. However, almost no single blood biomarker capable of predicting the metabolic benefits of specific dietary patterns has yet been identified. Here, we revealed the associations of plasma levels of the secreted protein acidic and rich in cysteine (SPARC), an inflammatory factor highly expressed in fat tissues, and insulin sensitivity improvement in a 6-month randomized controlled, calorie-restricted feeding trial recruiting 235 Chinese adults with overweight/obesity and prediabetes: the Mediterranean diet (MD) group (<i>n </i>= 81), the traditional Jiangnan diet (TJD) group (<i>n </i>= 81), and the control diet (CD) group (<i>n </i>= 73). The 1-h post-glucose loading plasma SPARC levels (SPARC-1H) decreased significantly from baseline to 3 months and 6 months in the MD group, whereas no significant changes were observed in the TJD or CD groups. Further analyses revealed that the individuals with higher baseline SPARC-1H levels were associated with fewer improvements in fasting insulin (β ± SE: 1.54 ± 0.43; <i>P </i>= 0.002), fasting glucose (0.10 ± 0.04; <i>P </i>= 0.049), the homeostasis model assessment of insulin resistance (HOMA-IR, 0.47 ± 0.12; <i>P </i>= 0.0005), and the homeostasis model assessment of β-cell function (HOMA-β, 7.63 ± 3.27; <i>P </i>= 0.047) after 6 months in the MD group. Moreover, baseline SPARC-1H levels were positively correlated with changes in lipidomic profiles, including three alkenylphosphatidylethanolamines, which potentially mediate the cardiometabolic benefits of MD. No significant associations were observed in the other two diet groups. Our findings suggest postprandial SPARC as a predictor for the metabolic benefits of MD, offering a potential biomarker for individualized nutrition intervention against cardiometabolic diseases.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 2","pages":"loaf039"},"PeriodicalIF":6.3,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant miR-378 expression promotes hepatic lipid accumulation via hijacking the bile acid-regulated autophagy.","authors":"Zhoumin Niu, Ying Yan, Wei Liu, Qiuming Yao, Jingjing Chen, Siyi Shen, Jing Yu, Mei Ma, Zhuoyang Li, Yuting Wu, Yan Li, Cheng Hu, Hailuan Zeng, Xin Gao, Yuying Li, Jingjing Jiang, Hao Ying","doi":"10.1093/lifemeta/loaf038","DOIUrl":"10.1093/lifemeta/loaf038","url":null,"abstract":"<p><p>Dysregulated autophagy contributes to liver steatosis, yet its regulation under distinct metabolic contexts remains poorly defined. Here, we identify bile acids (BAs) as critical modulators of hepatic autophagy. Circulating BA levels are elevated in human subjects with liver steatosis and independently associated with increased hepatic steatosis risk. High-fat diet (HFD) feeding increases circulating BA levels, while simultaneously reducing hepatic autophagic flux in mice, whereas pharmacological inhibition of farnesoid X receptor (FXR) enhances autophagy and alleviates steatosis in the livers of HFD-fed mice. Mechanistically, circulating BAs promote hepatic acetyl-CoA production through FXR-induced acyl-CoA oxidase 1 (ACOX1), which in turn suppresses autophagy by increasing the mechanistic target of rapamycin complex 1 (mTORC1) signaling. Similar to HFD feeding, prolonged fasting elevates BA levels and hepatic lipid accumulation, while concurrently upregulating hepatic miR-378, a positive regulator of BA synthesis. Although miR-378 exerts a cell-autonomous pro-autophagic effect during short-term fasting, it paradoxically drives lipid accumulation by suppressing hepatic autophagy via BA/FXR/ACOX1/acetyl-CoA axis in a non-cell-autonomous manner during either HFD feeding or prolonged fasting when BA action becomes considerable. Together, our study uncovers BAs as a previously unrecognized class of inhibitors of hepatic autophagy during prolonged fasting and in metabolic dysfunction-associated steatotic liver disease (MASLD), providing novel insights into context-dependent autophagic regulation of hepatic lipid metabolism and potential therapeutic strategies for MASLD.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 1","pages":"loaf038"},"PeriodicalIF":6.3,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deletion of hepatic growth hormone receptor contributes to the pathogenesis of lean MAFLD by elevating CD36.","authors":"Dong Yu, Xiao Yang, Xiaonan Zhang, Xiaoxin Wang, Zicheng Pu, Ai Mi, Liyuan Ran, Fang Zhang, Bin Liang, Yingjie Wu","doi":"10.1093/lifemeta/loaf037","DOIUrl":"10.1093/lifemeta/loaf037","url":null,"abstract":"<p><p>Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the most prevalent chronic liver disease worldwide, affecting both obese and non-obese individuals. While the reduced levels of circulating growth hormone (GH) and insulin-like growth factor 1 (IGF-1) have been consistently observed in patients with hepatic steatosis, the molecular role of hepatic growth hormone receptor (GHR) in MAFLD pathogenesis remains unclear. In this study, we established a liver-specific <i>Ghr</i> knockout (LGHRKO) mouse model that faithfully recapitulates non-obese MAFLD, characterized by hepatomegaly, elevated serum lipids and transaminases, and pronounced hepatic lipid accumulation, all occurring in the absence of obesity or increased adiposity. Mechanistically, LGHRKO livers displayed enhanced lipogenesis, impaired lipolysis, and upregulated cluster of differentiation 36 (CD36) expression, thereby driving hepatic lipid deposition. Single-cell RNA sequencing (scRNA-seq) further revealed hepatocyte-specific transcriptional alterations, including activation of lipid metabolic pathways and dysregulation of autophagy-related processes, providing insights into the cellular mechanisms underlying disease progression. Complementary human genetic analyses, including two-sample Mendelian randomization (MR) and genome-wide association studies (GWASs), demonstrated a causal relationship between impaired GH-IGF signaling and susceptibility to MAFLD, thereby bridging experimental observations with human disease risk. Collectively, our findings identify hepatic GHR deficiency as a key driver of non-obese MAFLD, establish LGHRKO mice as a valuable model for mechanistic and therapeutic studies, and underscore the translational significance of GH-IGF signaling in metabolic liver disease.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 1","pages":"loaf037"},"PeriodicalIF":6.3,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Propionic acid secreted by <i>Akkermansia muciniphila</i> alleviates hepatic fibrosis by antioxidant regulation across the gut-liver axis.","authors":"Lu Zhang, Jing Chen, Si-Jia Ge, Tian-Yi Huang, Xiang Shi, Yu-Yan Chen, Cui-Hua Lu","doi":"10.1093/lifemeta/loaf036","DOIUrl":"10.1093/lifemeta/loaf036","url":null,"abstract":"<p><p>The gut commensal bacterium <i>Akkermansia muciniphila</i> (AKK) has emerged as a candidate for treating liver disorders, yet its therapeutic potential in liver fibrosis remains poorly defined. Here, using a carbon tetrachloride (CCl₄)-induced murine model, we show that AKK administration markedly attenuates collagen deposition, inflammation, and hepatic injury. AKK restored intestinal barrier integrity, reshaped microbial composition, and enhanced propionic acid transport from the gut to the liver, leading to suppression of hepatic stellate cell activation. Multi-omics profiling revealed that AKK enriched propionate-producing taxa and upregulated key metabolic enzymes, thereby elevating hepatic propionate levels. Supplementation with propionic acid alone recapitulated AKK's benefits, improving liver function, alleviating extracellular matrix accumulation, and activating the Keap1-Nrf2 antioxidant pathway. Together, our findings identify a microbiota-metabolite axis in which AKK counters liver fibrosis by enhancing propionate-mediated antioxidant regulation, highlighting its therapeutic promise for chronic liver disease.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 1","pages":"loaf036"},"PeriodicalIF":3.4,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12857572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146109030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage sensing of the acidic milieu: BRD4 condensates in focus.","authors":"Dan Zhang, Vini Tiwari, Christopher K Glass","doi":"10.1093/lifemeta/loaf035","DOIUrl":"10.1093/lifemeta/loaf035","url":null,"abstract":"","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"5 1","pages":"loaf035"},"PeriodicalIF":6.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}