JHEP Reports最新文献

{"title":"Paediatric autoimmune liver disease in Europe, the prospective ERN R-LIVER registry","authors":"Mikkel Malham,&nbsp;Gema Muñoz Bartolo,&nbsp;Antal Dezsöfi-Gottl,&nbsp;Steffen Hartleif,&nbsp;Loreto Hierro Llanillo,&nbsp;Daniel Teglmeyer,&nbsp;Alessio Gerussi,&nbsp;Virag Hives,&nbsp;Norman Junge,&nbsp;Andrea Briem-Richter,&nbsp;Marianne Hørby Jørgensen,&nbsp;ERN RARE-LIVER","doi":"10.1016/j.jhepr.2026.101855","DOIUrl":"10.1016/j.jhepr.2026.101855","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Most literature on paediatric autoimmune liver disease (P-AILD) comprises single-centre, retrospective studies. This study aims to describe robust, real-world data for P-AILD during the first year following diagnosis, utilising data from the prospective European Reference Network (ERN) R-LIVER registry.</div></div><div><h3>Methods</h3><div>All patients younger than 18 years with autoimmune hepatitis (AIH) or autoimmune sclerosing cholangitis (ASC) enrolled in the ERN R-LIVER registry from January 2017 to October 2023 and with &gt;12 months of follow-up were included. Each participating centre recorded data from three time points: diagnosis, 6 and 12 months.</div></div><div><h3>Results</h3><div>A total of 116 patients with P-AILD were enrolled. Seventy-one patients had AIH1, eight had AIH2, and 37 had ASC. At diagnosis, 27% had cirrhosis. Large duct disease was diagnosed in 45% of ASC. Inflammatory bowel disease was present in 14% at diagnosis. No differences were found in presentation and outcome between AIH1 and 2. Most patients (94%) began treatment with standard therapy (prednisolone with/without thiopurines), and 80% were kept on it during the first year. Complete biochemical remission was achieved by 44 (42%) at 6 months and by 45 (42%) at 1 year, while normal ALT (&lt;45) and IgG (age dependent) levels were observed in 81 (72%) and 53 (51%), respectively, at 12 months. All patients were alive at the end of follow-up, and two required liver transplantation.</div></div><div><h3>Conclusions</h3><div>Short-term survival in P-AILD is excellent. However, less than half of patients with P-AILD patients achieved complete biochemical remission at 1 year, with ASC and cirrhosis as main predictors of failure. These findings emphasise the need for improved therapeutic strategies.</div></div><div><h3>Impact and implications</h3><div>This prospective registry study supports current treatment strategies in paediatric autoimmune liver disease by describing real-world immunosuppression use and remission outcomes. These observations are important for paediatric hepatologists and researchers, as they provide contemporary insights into treatment response and also highlight variability in clinical practice. In practice, the results can inform clinical counselling, guide follow-up intensity, and help identify areas where harmonised care pathways and further collaborative research are needed to improve outcomes.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101855"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Copyright and information","authors":"","doi":"10.1016/S2589-5559(26)00221-1","DOIUrl":"10.1016/S2589-5559(26)00221-1","url":null,"abstract":"","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101950"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148523526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting RuvBL1 disrupts mitochondrial metabolism and structure in hepatocellular carcinoma","authors":"Tommaso Mello,&nbsp;Irene Simeone,&nbsp;Alice Guida,&nbsp;Dimitri Papini,&nbsp;Francesca Begnozzi,&nbsp;Alice Santi,&nbsp;Daniele Guasti,&nbsp;Patrizia Nardini,&nbsp;Simone Polvani,&nbsp;Matteo Lulli,&nbsp;Oxana Bereshchenko,&nbsp;Elisabetta Ceni,&nbsp;Armando Curto,&nbsp;Paolo Pinton,&nbsp;Massimo Bonora,&nbsp;Andrea Galli","doi":"10.1016/j.jhepr.2026.101858","DOIUrl":"10.1016/j.jhepr.2026.101858","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background &amp; Aims&lt;/h3&gt;&lt;div&gt;The AAA+ ATPase RuvBL1 takes part in several biological processes, including chromatin remodelling and DNA repair, ribosome biogenesis, mTOR signalling, and oncogenic transformation. RUVBL1 overexpression correlates with poor survival in patients with hepatocellular carcinoma (HCC). We previously found that RuvBL1 is a key regulator of liver glucose metabolism in mice. Here, we aimed at disentangling the metabolic function of RuvBL1 in HCC cells.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Non-transformed AML-12, primary mouse hepatocytes, HCC cell lines, and RuvBL1&lt;sup&gt;hep-/-&lt;/sup&gt; mice were used (n = 3). RuvBL1 was targeted by RNAi and by inhibition with CB-6644. Metabolomic profiling and mitochondrial functions were assessed by targeted GC/MS, Seahorse analysis, and ATP synthase activity. Mitochondrial morphology and membrane potential were investigated by fluorescence microscopy, high-content imaging, and transmission electron microscopy. Mitochondrial RuvBL1 was detected by WB, super-resolution microscopy, transmission electron microscopy, and proximity ligation assay. Human HCC and normal liver samples from The Cancer Genome Atlas and GTEx databases were used for &lt;em&gt;in-silico&lt;/em&gt; analysis (T = 369, N = 160).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Targeting RuvBL1 impairs mitochondria-centred metabolic processes, including amino acid metabolism, TCA cycle, and oxidative phosphorylation. Inhibition of RuvBL1/2 activity induces loss of cristae integrity, mitochondrial hyperpolarisation and fragmentation, a phenotype paralleled by the hepatocytes of RuvBL1&lt;sup&gt;hep-/-&lt;/sup&gt; mice. We detected RuvBL1 in proximity to mitochondrial ATP synthase, a previously unreported localisation for this protein. Mechanistically, CB-6644 reduces ATP synthase-RuvBL1 interaction and impairs complex V activity even under a fuelled TCA cycle. In human HCC, higher RUVBL1 expression correlates with gene signatures associated with mitochondrial oxidative phosphorylation (FDR = 5.64e&lt;sup&gt;-03&lt;/sup&gt;), ATP synthase complex (FDR = 6.03e&lt;sup&gt;-03&lt;/sup&gt;), and poorer outcome (&lt;em&gt;p&lt;/em&gt; = 2e&lt;sup&gt;-07&lt;/sup&gt;).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Targeting RuvBL1 impairs complex V activity, disrupting mitochondrial metabolic functions and structural integrity. The mitochondrial functions of RuvBL1 may inform novel therapeutic strategies in the fight against hepatocellular carcinoma.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Impact and implications&lt;/h3&gt;&lt;div&gt;Metabolic reprogramming is a key feature driving HCC onset, progression, and plasticity, contributing to treatment resistance and poor prognosis. RUVBL1 overexpression correlates with reduced survival of patients with HCC and has emerged as a potential metabolic modulator. In this study, we found that targeting RuvBL1 impairs its interaction with mitochondrial ATP synthase, disrupting mitochondrial metabolism and cristae structure. In human HCC samples, RUVBL1 expression correlates with hallmark mitochondrial metab","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101858"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147723022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemodiafiltration improves performance of 24 hour ex situ normothermic liver machine perfusion","authors":"Jordi Vengohechea,&nbsp;Amelia J. Hessheimer,&nbsp;Javier Muñoz,&nbsp;Joaquim Albiol,&nbsp;Marina Vendrell,&nbsp;Josep M. Sanahuja,&nbsp;Javier Salinas,&nbsp;Carlota Largo,&nbsp;Paula Patricia Burgos,&nbsp;Soraya Rodríguez,&nbsp;Aida Vaquero,&nbsp;Mingju Liang,&nbsp;Fen Huo,&nbsp;Constantino Fondevila","doi":"10.1016/j.jhepr.2026.101811","DOIUrl":"10.1016/j.jhepr.2026.101811","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background &amp; Aims&lt;/h3&gt;&lt;div&gt;Performing &lt;em&gt;ex situ&lt;/em&gt; normothermic machine perfusion (NMP) for ≥24 h represents an opportunity to evaluate and treat livers, but is limited by the lack of support from relevant extrahepatic organs. Incorporation of systems of renal replacement therapy, including hemodiafiltration (HDF), appears useful in this regard during prolonged &lt;em&gt;ex situ&lt;/em&gt; liver NMP. This study aimed to demonstrate the impact and benefits associated with incorporation of continuous HDF during 24-h &lt;em&gt;ex situ&lt;/em&gt; NMP in a relevant preclinical model, including transplantation and post-transplant follow-up.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Porcine livers (n = 28) underwent 24-h &lt;em&gt;ex situ&lt;/em&gt; NMP with either partial perfusate exchange at 12 h and no HDF (NHDF, n = 11) or HDF initiated 2 h after NMP start (n = 17). Biochemical, histological, endothelial, and metabolomic parameters were assessed. A subset of grafts undergoing NMP + HDF (n = 8) were transplanted into recipients.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Incorporation of HDF during NMP maintained stable pH and electrolyte levels, effectively preventing hypernatremia, hypochloremia, and hypocalcemia developing without HDF. HDF cleared metabolic wastes (&lt;em&gt;e.g.&lt;/em&gt; urea) and inflammatory cytokines (IL-1B, IL-2, IL-6, IL-8, and IL-18), resulting in reduced injury and oxidative stress markers after 24 h (Suzuki score 0.8 ± 0.4 HDF &lt;em&gt;vs.&lt;/em&gt; 2.7 ± 1.3 NHDF, &lt;em&gt;p&lt;/em&gt; &lt;0.001). Vasoprotective endothelial response mechanisms, including KLF2 and eNOS gene and protein expression, were upregulated, whereas stellate cell activation and sinusoidal contraction were reduced among HDF-treated grafts. HDF reduced metabolomic alterations arising in livers during 24-h NMP, and adequate graft maintenance using NMP + HDF was demonstrated by full functional and metabolic recovery during post-transplant follow-up.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Continuous HDF promotes a more physiological biochemical and metabolic environment, reduces inflammation and oxidative stress, and preserves homeostatic endothelial response mechanisms in livers undergoing 24-h &lt;em&gt;ex situ&lt;/em&gt; NMP, facilitating successful transplantation in a complex preclinical model.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Impact and implications&lt;/h3&gt;&lt;div&gt;In this preclinical study, livers were normothermically perfused for 24 h &lt;em&gt;ex situ&lt;/em&gt;, both with and without continuous HDF. Incorporation of HDF offered relevant improvements in numerous on-device measures, including the maintenance of physiological biochemical parameters; removal of injurious metabolic wastes; and improvement of injury and stress responses in parenchymal and nonparenchymal cells. A subset of livers were successfully transplanted and demonstrated full functional and metabolic recovery during follow-up. These findings indicate that advanced renal replacement therapies, such as HDF, are a key aspect of improving and prolonging &lt;em&gt;ex situ&lt;/em&gt; normotherm","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101811"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial Board page","authors":"","doi":"10.1016/S2589-5559(26)00218-1","DOIUrl":"10.1016/S2589-5559(26)00218-1","url":null,"abstract":"","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101947"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148524953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc finger protein 544 promotes hepatocellular carcinoma by generating an immunosuppressive tumor microenvironment","authors":"Jie Tang,&nbsp;Ming Xu,&nbsp;Xilong Ou","doi":"10.1016/j.jhepr.2026.101845","DOIUrl":"10.1016/j.jhepr.2026.101845","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>This study identified zinc finger protein 544 (ZNF544) as a biomarker in hepatocellular carcinoma (HCC) and aims to delineate its functional role.</div></div><div><h3>Methods</h3><div>The correlation between ZNF544 expression and clinical parameters of patients with HCC (n = 50) and the malignant biological behavior of HCC cells was analyzed <em>in vitro</em> (n = 5/group) and <em>in vivo</em> (n = 10/group).</div></div><div><h3>Results</h3><div>ZNF544 was elevated in tumors of patients with HCC (<em>p</em> = 0.0006). Patients with HCC exhibiting high ZNF544 expression was associated with a more advanced clinical stage (<em>p</em> = 0.0026) and showed greater infiltration of M2 macrophages (<em>p</em> = 0.0031) and Tregs (<em>p</em> = 0.0094). ZNF544 knockdown inhibited the pro-angiogenic ability of HCC cells (<em>p</em> &lt;0.01). Increased ZNF544 expression accelerated the growth of orthotopic tumors (increased &gt;80%, <em>p</em> &lt;0.0001) and the infiltration of M2 macrophages (increased &gt;60%, <em>p</em> = 0.0008) and Tregs (increased &gt;80%, <em>p</em> = 0.0029) within the orthotopic tumors, and accelerated lung metastasis (number of mice with lung metastasis increased &gt;160%). ZNF544 bound to the spermatogenesis-associated serine-rich protein 2 (SPATS2) promoter and activated its transcription, whereas SPATS2 enhanced the triosephosphate isomerase (TPI1) mRNA stability. ZNF544 promoted glycolysis in HCC cells in a SPATS2-dependent manner. SPATS2 knockdown suppressed glycolysis in HCC cells and inhibited orthotopic tumor growth, which was rescued by TPI1 overexpression. Ivermectin was identified as a pharmacological inhibitor of ZNF544, effectively suppressing the progression of HCC.</div></div><div><h3>Conclusions</h3><div>ZNF544 accelerates HCC by activating SPATS2/TPI1 and promoting glycolysis and immune escape. Targeting ZNF544, including compounds such as ivermectin, may offer a preliminary avenue for further investigation in HCC.</div></div><div><h3>Impact and implications</h3><div>This research underscores the role of ZNF544-SPATS2 as a pivotal regulator of TPI1 expression in HCC. TPI1 shapes the immunosuppressive TME and accelerates growth and metastasis by promoting glycolysis and facilitating the infiltration of M2 macrophages and Tregs. Our research suggests that ZNF544 could serve as a novel biomarker for HCC, and the pharmacological inhibitor of ZNF544, ivermectin, emerges as a promising therapeutic option for HCC treatment.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101845"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Actin-specific smooth muscle antibodies bridge adult and juvenile autoimmune hepatitis diagnosis","authors":"Alessandro Granito,&nbsp;Paolo Muratori,&nbsp;Georgios Pappas,&nbsp;Albert J. Czaja","doi":"10.1016/j.jhepr.2026.101814","DOIUrl":"10.1016/j.jhepr.2026.101814","url":null,"abstract":"","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101814"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to: “Actin-specific smooth muscle antibodies bridge adult and juvenile autoimmune hepatitis diagnosis”","authors":"Bastian Engel,&nbsp;Theresa Kirchner,&nbsp;Richard Taubert","doi":"10.1016/j.jhepr.2026.101895","DOIUrl":"10.1016/j.jhepr.2026.101895","url":null,"abstract":"","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101895"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the stromal and immune microenvironment in intrahepatic cholangiocarcinoma","authors":"Silvia Affo,&nbsp;Daniela Sia","doi":"10.1016/j.jhepr.2026.101850","DOIUrl":"10.1016/j.jhepr.2026.101850","url":null,"abstract":"<div><div>Intrahepatic cholangiocarcinoma (iCCA) is one of the deadliest malignancies, with an overall 5-year survival rate of approximately 10%. For decades, surgery and chemotherapy have represented the only treatment options for early- and late-stage disease, respectively. More recently, characterisation of the genomic landscape of iCCA has identified several “druggable” oncogenic drivers and led to the FDA approval of the first targeted therapies, including FGFR and IDH inhibitors, for second-line treatment in genetically defined patient subsets. Nonetheless, most patients treated with these therapies rapidly develop resistance and eventually experience disease progression. At a time when immune checkpoint inhibitors (ICIs) are profoundly reshaping cancer treatment, their use in combination with chemotherapy has yielded only modest survival benefits in iCCA, with more than two-thirds of patients exhibiting intrinsic resistance. The aggressive and refractory nature of this cancer is often attributed to its intricate tumour microenvironment (TME); however, the complex interplay between tumour cells and other TME components (<em>i.e</em>. immune cells, cancer-associated fibroblasts, and endothelial cells), as well as the molecular and cellular mechanisms driving tumour progression and therapeutic resistance, remain poorly understood. In this review, we discuss the critical role of the stromal and immune TME in iCCA and how its characterisation has informed patient stratification and molecular classification. We also describe recent findings supporting distinct genotype–immunophenotype relationships in iCCA, as well as the existence of functionally heterogeneous subsets of cancer-associated fibroblasts. Ultimately, this review aims to provide a comprehensive overview of current knowledge while stimulating discussion on therapeutic implications and future research directions.</div></div>","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 7","pages":"Article 101850"},"PeriodicalIF":8.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANTICIPATE-ing a future without liver biopsy in MASH. Ready for prime time?","authors":"Harendran Elangovan,&nbsp;Jacob George","doi":"10.1016/j.jhepr.2026.101836","DOIUrl":"10.1016/j.jhepr.2026.101836","url":null,"abstract":"","PeriodicalId":14764,"journal":{"name":"JHEP Reports","volume":"8 6","pages":"Article 101836"},"PeriodicalIF":7.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}