npj Gut and Liver最新文献

{"title":"Cirrhosis severity modulates proteomic and immune landscapes in hepatocellular carcinoma.","authors":"Raksha K R Shastry, Adithya Kale, Sui Seng Tee","doi":"10.1038/s44355-026-00079-7","DOIUrl":"10.1038/s44355-026-00079-7","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) most often arises in cirrhotic livers, yet the biological impact of cirrhosis severity on the tumor proteome remains poorly understood. We performed a quantitative proteomic analysis of 141 HCC tumors from a publicly available mass spectrometry dataset (Xing et al. Cell Reports Medicine, 2023), stratified by cirrhosis severity to delineate fibrosis-related molecular heterogeneity. Principal component analysis revealed substantial overlap between groups, indicating that increasing cirrhosis severity produces incremental rather than global proteomic shifts. Nevertheless, 295 proteins showed significant differential abundance (Hedges' <i>g</i> > 0.3, <i>p</i> < 0.05), including upregulation of HMOX1 and LRSAM1 and downregulation of CYP27A1 in Medium/High cirrhosis. Pathway enrichment highlighted alterations in organelle assembly, heme metabolism, and extracellular-matrix disassembly, alongside reduced cytoskeletal and focal-adhesion integrity. Exploratory immune deconvolution suggested proportional remodeling of natural-killer and B-cell subsets with advancing cirrhosis. A five-gene signature (HMOX1, LRSAM1, MAP2, EDEM3, RFC3) was associated with significantly worse overall survival in TCGA-LIHC (HR 1.8, <i>p</i> = 0.0021); cirrhosis severity alone did not predict survival (log-rank <i>p</i> = 0.248), supporting the tumor-intrinsic prognostic relevance of the signature. These findings demonstrate that cirrhosis severity subtly but measurably reshapes the HCC tumor proteome and immune landscape, with implications for risk stratification and precision therapy design.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"3 1","pages":"30"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13538045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890055","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":"Closing the screening gap but not the writing gap: a two-topic evaluation of LLMs for systematic reviews and meta-analyses in hepatology.","authors":"Yuntao Zou, Iris Kim, Nan Gao, Michelle Li, Mi-Ok Kim, Jin Ge","doi":"10.1038/s44355-026-00068-w","DOIUrl":"10.1038/s44355-026-00068-w","url":null,"abstract":"<p><p>Systematic reviews are essential but labor-intensive. We evaluated LLM-assisted literature screening and drafting in two hepatology topics: carvedilol in compensated cirrhosis and anticoagulation in portal vein thrombosis. For each topic, we searched PubMed, Cochrane, and EMBASE. A few-shot prompt with explicit inclusion/exclusion criteria was used to screen titles and abstracts, with results compared to manual review. Included studies were then processed using a retrieval-augmented LLM to generate ten automated systematic review and meta-analysis drafts per topic, which were evaluated by a separate judge LLM for PRISMA 2020 compliance against human reviews. Screening performance: After deduplication (703 and 370 records), LLM-assisted screening showed high agreement with manual review (sensitivity 86-93%, specificity 96-99%) while reducing screening time to 3 and 2 h versus 62 and 30 h manually. Drafting performance: RAG-enabled LLMs generated structured manuscripts with variable PRISMA 2020 compliance: 100% for titles, 91% for introductions, 75-80% for methods, and 68-75% for results, with downstream weaknesses in abstracts and discussions (<65%). LLM-based PRISMA scoring closely matched human review (ICC ≈ 0.90). LLM-assisted screening was highly accurate, reducing workload by >90%, but automated drafting was reliable mainly for titles and introductions, requiring human oversight to prevent errors and hallucinations.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"3 1","pages":"21"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13287001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148321436","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":"Optimising the induction of inflammation within preterm infant-derived intestinal epithelial organoids.","authors":"Jonathan A Chapman, Andrew M Frey, Maria Emilia Dueñas, Jeremy M Palmer, Andrea C Masi, Nicholas D Embleton, Matthias Trost, Janet E Berrington, Christopher J Stewart","doi":"10.1038/s44355-026-00054-2","DOIUrl":"10.1038/s44355-026-00054-2","url":null,"abstract":"<p><p>Preterm infants born <32 weeks gestation have abnormal microbial colonisation and dysregulated inflammation within the gut. Preterm infant-derived intestinal organoids (PIOs) represent a valuable model for investigating gut microbiome-host interactions and inflammatory responses. We optimised an inflammation model in PIO monolayers incubated within an anaerobic co-culture system that recreates the physiological oxygen gradient of the intestinal epithelium. We trialled multiple stimuli, including live and heat-killed pathobiont consortia, lipopolysaccharide (LPS) and flagellin. We found that a combination of apical LPS and basolateral flagellin, incubated for 3 h, elicited the most robust response. This was characterised by enhanced pro-inflammatory cytokine secretion, the potential for chemokine-driven immune recruitment, TNFα and IL17C pathway signalling, shifts from NF-κB to AP-1-mediated responses, and signs of tissue remodelling. This provides a framework for appropriate study design to disentangle the impacts of microbiome-host interactions in health and disease using intestinal organoids.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"3 1","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146121708","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":"Secondary Immune Surveillance via upregulation of C-type lectin receptors.","authors":"Farhin Patel, Emmanuel Boafo, Yurui Zheng, Colin Varnet, Adam Kim","doi":"10.1038/s44355-026-00067-x","DOIUrl":"10.1038/s44355-026-00067-x","url":null,"abstract":"<p><p>C-type lectin receptors (CLRs) are a family of pattern recognition receptors that sense diverse microbial and damage-associated molecular patterns. Many CLRs, like Mincle and Dectin-3, are upregulated by TLR4 signaling. In Alcohol-associated Hepatitis (AH), where alcohol consumption leads to leakage of bacterial LPS, TLR4 upregulates CLR expression and increases the diversity of what the immune system can detect, which we call \"secondary immune surveillance\". Previously, we found human monocytes upregulate CLRs in response to LPS/TLR4 signaling with much higher expression in AH. In this study, we broaden our understanding of secondary immune surveillance. We find that CLRs are upregulated by many kinds of TLR signaling. Additionally, mouse monocytes and microglia also upregulated CLRs in response to LPS/TLR4 signaling. We used Mincle-KO mice to dissect how loss of one CLR impacts tissue inflammation. Mincle-KO mice were protected from liver inflammation caused by LPS, but experienced worse adipose tissue inflammation, suggesting a shift in the site of injury. Bulk RNA-seq revealed extensive alternative splicing of many CLR genes, with only translatable mRNA detected after LPS. Finally, using bulk RNA-seq data of livers from patients with AH, we observe extensive expression of CLRs, suggesting these receptors may betargets for therapies to reduce inflammation.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"3 1","pages":"17"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13229920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148166373","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":"Illustration of the gut-immune-liver axis in early-stage alcohol-related liver disease: role and non-invasive potentiation of biomarkers and peptidomic signatures.","authors":"Anjali Kumari, Mukesh Sriwastva, Michael Merchant, Christine Dolin, Gavin Arteel, Sabine Waigel, Maiying Kong, Melanie L Schwandt, Joris Verster, Ashwani K Singal, Venkatakrishna R Jala, Craig J McClain, Vatsalya Vatsalya","doi":"10.1038/s44355-026-00072-0","DOIUrl":"10.1038/s44355-026-00072-0","url":null,"abstract":"<p><p>Alcohol use disorder (AUD) can progress to alcohol-associated liver disease (ALD), yet early-stage ALD (eALD) remains poorly defined at the molecular level. We performed plasma proteomic and peptidomic analysis in 42 adults (AUD <i>n</i> = 10, eALD <i>n</i> = 26, healthy volunteers <i>n</i> = 6) using LC-MS/MS and pathway enrichment. Individuals with eALD exhibited greater alcohol burden, elevated liver injury markers (AST and ALT), and increased gut-immune dysfunction markers, including lipopolysaccharide, TNF-α, and K18M65, compared with AUD. Proteomic profiling identified 23 dysregulated peptides, with fibrinogen alpha (FIBA), fibrinogen beta (FIBB), COL1A1, and ITIH4 as key candidates. FIBB and COL1A1 were associated with AST, while FIBA and COL1A1 distinguished eALD from AUD. These findings identify circulating peptide biomarkers reflecting gut-immune-liver axis dysfunction and support their potential utility for non-invasive detection of early alcohol-associated liver disease.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"3 1","pages":"22"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13318631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148379232","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":"Single-cell insights into hepatic fibroblasts and stellate cells: heterogeneity in matrix remodelling in development, health, and disease.","authors":"Sara Campinoti, Kavitha Kirubendran, Lai Wei, Maya Medic, Omkar Pravin Joshi, Luca Urbani","doi":"10.1038/s44355-026-00075-x","DOIUrl":"10.1038/s44355-026-00075-x","url":null,"abstract":"<p><p>Hepatic fibroblasts and hepatic stellate cells (HSCs) are dynamic regulators of liver development, homeostasis, and disease beyond structural roles. Advances in single-cell transcriptomics have provided new evidence on their heterogeneity, plasticity, and diverse functions across developmental and pathological contexts. This review synthesises contribution from single-cell and single-nuclei RNA sequencing studies to the understanding of the ontogeny, transcriptional diversity, and roles of hepatic stromal populations in foetal and adult liver. We highlight distinct fibroblast and HSC subpopulations identified across development and disease, characterised by extracellular matrix programmes and markers associated with shaping the hepatic microenvironment. We further examine their activation in chronic liver disease and reprogramming into cancer-associated fibroblasts in hepatobiliary cancers, and discuss how single-cell approaches are contributing to the re-evaluation of stromal plasticity by revealing cell-state transitions and informing in vitro modelling and targeted therapies.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"3 1","pages":"27"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13391356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581974","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":"Silencing of S100A11 attenuates murine metabolic dysfunction-associated steatohepatitis.","authors":"P V Daniel, Gyanendra Puri, Yixing Luo, Naresh Golla, Takahito Nishihara, Hanna Erickson, George Marek, Nagaswaroop Kengunte Nagaraj, Davide Povero, Amy S Mauer, Jun Liu, Harmeet Malhi","doi":"10.1038/s44355-025-00044-w","DOIUrl":"10.1038/s44355-025-00044-w","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by insulin resistance and impaired hepatic metabolism, which lead to steatosis and lipotoxicity. S100A11, an alarmin upregulated in MASH, promotes steatosis in vitro, but its role in vivo remains unclear. We hypothesized that S100A11 drives MASH by upregulating hepatic lipid synthesis. Using whole-body <i>S100a11</i> knockout (<i>S100a11</i> ^<i>-/-</i> ) mice on a MASH-inducing diet, we found <i>S100a11</i> deficiency reduced steatosis, inflammation, and fibrosis. Hepatotropic AAV8-mediated silencing of <i>S100a11</i> confirmed these findings. Bulk RNA sequencing with Ingenuity Pathway Analysis revealed dysregulated carbohydrate and lipid metabolism in <i>S100a11</i> ^<i>-/-</i> livers, including downregulation of hexokinase 2 (<i>Hk2</i>). Since hexokinases regulate glucose flux into downstream metabolic processes, we overexpressed HK2 in <i>S100a11</i> ^<i>-/-</i> mice, which was sufficient to increase steatosis. Further, palmitate-induced HK2 upregulation required S100A11 in a human hepatocyte cell line. These studies identify HK2 as a downstream target of S100A11, both of which are potential therapeutic targets for MASH.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"2 1","pages":"32"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12675283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145703669","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":"Unlocking therapeutic potential of amlexanox in MASH with insights into bile acid metabolism and microbiome.","authors":"Wenjing You, Jianfei Ji, Danwan Wen, Chen Wang, Xiaoli Sun, Peng Zhao","doi":"10.1038/s44355-024-00015-7","DOIUrl":"10.1038/s44355-024-00015-7","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatohepatitis (MASH) has become a global health issue associated with obesity and diabetes. It is becoming a leading cause of end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). Despite its increasing prevalence, effective pharmacotherapies for MASH remain limited, underscoring the urgent need for novel interventions. Amlexanox, an inhibitor of noncanonical IκB kinases, has demonstrated potential in restoring insulin sensitivity and glucose homeostasis in obese mice and human patients, as shown in our earlier studies. Here, we aimed to assess the therapeutic potential of amlexanox in dyslipidemia-associated diseases, particularly MASH and HCC, and to elucidate the underlying mechanism. We employed GAN diet-fed <i>Ldlr</i> ^-<i>/</i>- mice, which simultaneously develop obesity, MASH, and atherosclerosis, to recapitulate human metabolic syndrome and associated complications. Amlexanox was administrated orally to these mice after disease onset to examine its therapeutic efficacy. Our study demonstrates that even a low dose of amlexanox significantly reversed MASH and nearly completely prevented the progression from MASH to HCC. Both phenotypic and transcriptomic studies revealed that amlexanox markedly improved MASH-related dyslipidemia, hepatic steatosis, inflammation, liver injury, and hepatic fibrosis. Furthermore, multi-omics analysis revealed that amlexanox enhances hepatic bile acid synthesis and promotes fecal bile acid excretion. Notably, amlexanox reprogrammed gut microbiota, robustly increasing the abundance of <i>Akkermansia muciniphila</i>, a probiotic known to improve metabolic dysfunction. These findings uncover the multifaceted therapeutic potential of amlexanox in treating MASH and atherosclerosis by targeting bile acid metabolism, gut microbiota, hepatic inflammation, and fibrosis. Our study highlights amlexanox as a promising candidate for clinical applications.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"2 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12165453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144304230","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":"Steatotic liver disease is a marker of multimorbidity, not underlying cirrhosis, in older adults.","authors":"O Oduwole, C Ding, N Bitar, D Nair, S Salter, M Silverman, R Allen, L Ng Fat, E Tsochatzis, S Bell, G Mehta, A Britton","doi":"10.1038/s44355-025-00024-0","DOIUrl":"https://doi.org/10.1038/s44355-025-00024-0","url":null,"abstract":"<p><p>Steatotic liver disease (SLD) prevalence in adults is estimated at 30%, but older populations are understudied. Here, SLD prevalence and associated risk factors were assessed 1,021 Whitehall II study participants (mean age 72.5) using transient elastography (FibroScan). SLD was present in 33.3% (CAP ≥ 275 dB/m), with most classified as metabolic dysfunction-associated SLD. Only 2.4% had significant fibrosis ( ≥ 7.9 kPa). Adjusted for age and sex, SLD was associated with low physical activity (OR 1.60, 95% CI 1.13-2.27), poorer motor function (SF-36 PCS OR 1.21, 95% CI 1.05-1.40), difficulties in activities of daily living (OR 3.19, 95% CI 1.17-8.64), and multimorbidity (OR 1.45, 95% CI 1.22-1.73). These associations persisted after adjustment for socioeconomic, behavioural, and cardiometabolic risk factors. Frailty was associated with SLD at higher CAP thresholds ( ≥ 290 dB/m). In this older adult sample, SLD is common and appears more as a marker of multimorbidity and low physical activity than significant fibrosis.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"2 1","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12052588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061038","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":"Scores to predict steatotic liver disease - correlates and outcomes in older adults.","authors":"Daniel Clayton-Chubb, Isabella Commins, Stuart K Roberts, Ammar Majeed, Robyn L Woods, Joanne Ryan, Hans G Schneider, John S Lubel, Alexander D Hodge, John J McNeil, William W Kemp","doi":"10.1038/s44355-025-00021-3","DOIUrl":"https://doi.org/10.1038/s44355-025-00021-3","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant cause of chronic liver disease globally, and the rising prevalence of MASLD is occurring in parallel with the global aging population. The use of non-invasive biomarker tools to rule-in or rule-out hepatic steatosis is important in large epidemiological studies in this field. While the Fatty Liver Index (FLI) is the best validated tool in older adults, not all studies will have the necessary parameters for steatosis identification. This retrospective post-hoc analysis of the ASPirin in Reducing Events in the Elderly (ASPREE) study involved 16,703 Australian adults aged ≥70 years. Using the FLI as the 'gold standard' index, we evaluated the correlation with other indices: the Dallas Steatosis Index (DSI), Framingham Steatosis Index, ZJU index (ZJU), Hepatic Steatosis Index (HSI), Lipid Accumulation Product (LAP), and Visceral Adiposity Index (VAI), as well as age- and sex-adjusted outcome measures including mortality, major adverse cardiovascular events (MACE), atrial fibrillation (AF), and persistent physical disability. Of the non-FLI indices, the DSI and FSI had the highest percentage of participants correctly classified as having MASLD (97.7% and 93.8% respectively). The FSI, LAP, and VAI were associated with MACE. The FSI and FLI were predictive of incident AF. The FLI, DSI, FSI, LAP and VAI were associated with physical disability. No MASLD score was associated with increased mortality. Indeed, MASLD defined by the ZJU and HSI were both inversely associated with mortality. As such, we've demonstrated that the FSI and DSI are the most accurate scores for identifying MASLD in older adults when compared to the FLI as the gold standard. The FSI is associated with MACE, AF, and persistent physical disability, lending support to its use in identifying older persons with MASLD when the FLI is unable to be calculated.</p>","PeriodicalId":501708,"journal":{"name":"npj Gut and Liver","volume":"2 1","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12009214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061434","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}