Journal of Clinical Investigation最新文献_第5页

Interferon-γ is a direct driver of crypt hyperplasia in celiac disease. 干扰素-γ是乳糜泻隐窝增生的直接驱动因子。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-19 DOI: 10.1172/JCI194858

Jorunn Stamnaes, Daniel Stray, M Fleur du Pré, Louise F Risnes, Alisa E Dewan, Jakeer Shaik, Maria Stensland, Knut Ea Lundin, Ludvig M Sollid

引用次数: 0

SAA1/FPR2 signaling between keratinocytes and neutrophils sustains chronic inflammation in Sweet syndrome. 角化细胞和中性粒细胞之间的SAA1/FPR2信号传导维持Sweet综合征的慢性炎症。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-19 DOI: 10.1172/JCI193566

Jianhe Huang, Satish Sati, Olivia Ahart, Emmanuel Rapp-Reyes, Linda Zhou, Robert G Micheletti, William D James, Misha Rosenbach, Thomas H Leung

{"title":"SAA1/FPR2 signaling between keratinocytes and neutrophils sustains chronic inflammation in Sweet syndrome.","authors":"Jianhe Huang, Satish Sati, Olivia Ahart, Emmanuel Rapp-Reyes, Linda Zhou, Robert G Micheletti, William D James, Misha Rosenbach, Thomas H Leung","doi":"10.1172/JCI193566","DOIUrl":"10.1172/JCI193566","url":null,"abstract":"Sweet syndrome (also known as acute febrile neutrophilic dermatosis) is a rare inflammatory skin disorder characterized by erythematous plaques with a dense dermal neutrophilic infiltrate. First-line therapy remains oral corticosteroids, which suppresses inflammation non-specifically. Although neutrophils are typically short-lived, how they persist in Sweet syndrome skin and contribute to disease pathogenesis remains unclear. Here, we identify a previously unrecognized population of antigen-presenting cell (APC)-like neutrophils expressing MHC class II genes that are uniquely present in Sweet syndrome skin but absent from healthy tissue and circulation. Keratinocytes extended neutrophil lifespan 10-fold in co-culture experiments and drove the emergence of an APC-like phenotype in approximately 30% of neutrophils, mirroring observations in patient lesions. Mechanistically, keratinocyte-derived serum amyloid A1 (SAA1) signals through the formyl peptide receptor 2 (FPR2) on neutrophils to promote their survival. These long-lived neutrophils actively orchestrate local immune responses by recruiting T cells and inducing cytokine production. Strikingly, dual blockade of SAA1-FPR2 signaling restores neutrophil turnover to baseline levels, with efficacy comparable to high-dose corticosteroids. These findings uncover a keratinocyte-neutrophil-T cell axis that sustains chronic inflammation in Sweet syndrome and highlight the SAA1/FPR2 pathway as a promising target for precision therapy.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":" ","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882961","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}

引用次数: 0

Loss of tumor cell MHC Class II drives MAPK-inhibitor insensitivity of BRAF-mutant anaplastic thyroid cancers. 肿瘤细胞MHC II类缺失驱动mapk抑制剂对braf突变间变性甲状腺癌不敏感。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-19 DOI: 10.1172/JCI191781

Vera Tiedje, Jillian Greenberg, Tianyue Qin, Soo-Yeon Im, Gnana P Krishnamoorthy, Laura Boucai, Bin Xu, Jena D French, Eric J Sherman, Alan L Ho, Elisa de Stanchina, Nicholas D Socci, Jian Jin, Ronald A Ghossein, Jeffrey A Knauf, Richard P Koche, James A Fagin

{"title":"Loss of tumor cell MHC Class II drives MAPK-inhibitor insensitivity of BRAF-mutant anaplastic thyroid cancers.","authors":"Vera Tiedje, Jillian Greenberg, Tianyue Qin, Soo-Yeon Im, Gnana P Krishnamoorthy, Laura Boucai, Bin Xu, Jena D French, Eric J Sherman, Alan L Ho, Elisa de Stanchina, Nicholas D Socci, Jian Jin, Ronald A Ghossein, Jeffrey A Knauf, Richard P Koche, James A Fagin","doi":"10.1172/JCI191781","DOIUrl":"10.1172/JCI191781","url":null,"abstract":"Cancer cells present neoantigens dominantly through MHC class I (MHCI) to drive tumor rejection through cytotoxic CD8+ T-cells. There is growing recognition that a subset of tumors express MHC class II (MHCII), causing recognition of antigens by TCRs of CD4+ T-cells that contribute to the anti-tumor response. We find that mouse BrafV600E-driven anaplastic thyroid cancers (ATC) respond markedly to the RAF + MEK inhibitors dabrafenib and trametinib (dab/tram) and that this is associated with upregulation of MhcII in cancer cells and increased CD4+ T-cell infiltration. A subset of recurrent tumors lose MhcII expression due to silencing of Ciita, the master transcriptional regulator of MhcII, despite preserved interferon gamma signal transduction, which can be rescued by EZH2 inhibition. Orthotopically-implanted Ciita-/- and H2-Ab1-/- ATC cells into immune competent mice become unresponsive to the MAPK inhibitors. Moreover, depletion of CD4+, but not CD8+ T-cells, also abrogates response to dab/tram. These findings implicate MHCII-driven CD4+ T cell activation as a key determinant of the response of Braf-mutant ATCs to MAPK inhibition.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":" ","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882960","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}

引用次数: 0

Hypertension promotes bone loss and fragility by favoring bone resorption in mouse models. 在小鼠模型中，高血压通过促进骨吸收来促进骨质流失和脆弱性。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-19 DOI: 10.1172/JCI184325

Elizabeth M Hennen, Sasidhar Uppuganti, Néstor de la Visitación, Wei Chen, Jaya Krishnan, Lawrence A Vecchi Iii, David M Patrick, Mateusz Siedlinski, Matteo Lemoli, Rachel Delgado, Mark P de Caestecker, Wenhan Chang, Tomasz J Guzik, Rachelle W Johnson, David G Harrison, Jeffry S Nyman

{"title":"Hypertension promotes bone loss and fragility by favoring bone resorption in mouse models.","authors":"Elizabeth M Hennen, Sasidhar Uppuganti, Néstor de la Visitación, Wei Chen, Jaya Krishnan, Lawrence A Vecchi Iii, David M Patrick, Mateusz Siedlinski, Matteo Lemoli, Rachel Delgado, Mark P de Caestecker, Wenhan Chang, Tomasz J Guzik, Rachelle W Johnson, David G Harrison, Jeffry S Nyman","doi":"10.1172/JCI184325","DOIUrl":"10.1172/JCI184325","url":null,"abstract":"Inflammatory diseases contribute to secondary osteoporosis. Hypertension is a highly prevalent inflammatory condition that is clinically associated with reduced bone mineral density and increased risk for fragility fracture. In this study, we showed that a significant loss in bone mass and strength occurs in two pre-clinical models of hypertension. This accompanied increases in immune cell populations, including monocytes, macrophages, and IL-17A-producing T cell subtypes in the bone marrow of hypertensive mice. Neutralizing IL-17A in angiotensin (ang) II-infused mice blunted hypertension-induced loss of bone mass and strength due to decreased osteoclastogenesis. Likewise, the inhibition of the CSF-1 receptor blunted loss of bone mass and prevented loss of bone strength in hypertensive mice. In an analysis of UK Biobank data, circulating bone remodeling markers exhibited striking associations with blood pressure and bone mineral density in > 27,000 humans. These findings illustrate a potential mechanism by which hypertension activates immune cells in the bone marrow, encouraging osteoclastogenesis and eventual loss in bone mass and strength.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":" ","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882958","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}

引用次数: 0

Chronic diseases alter the platelet rheostat to promote hyperreactivity and thrombosis. 慢性疾病改变血小板变阻器，促进高反应性和血栓形成。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-15 DOI: 10.1172/JCI194082

Roy L Silverstein

{"title":"Chronic diseases alter the platelet rheostat to promote hyperreactivity and thrombosis.","authors":"Roy L Silverstein","doi":"10.1172/JCI194082","DOIUrl":"10.1172/JCI194082","url":null,"abstract":"Platelet hyperreactivity, defined as enhanced sensitivity to activation in response to classical agonists, contributes to the increased risk of arterial thrombosis associated with chronic inflammatory diseases. In this issue of the JCI, Kong and colleagues used an unbiased proteomic approach to identify elevated SEC61B in platelets from patients with diabetes and from hyperglycemic mice. Typically, SEC61B participates in protein transport within the endoplasmic reticulum (ER), but it can also act as an ion channel that allows calcium to leak from ER to cytoplasm. The authors showed that elevated SEC61B expression caused increased calcium leak, elevated basal cytoplasmic calcium concentrations, and platelet hyperreactivity. In vitro and in vivo pharmacological interventions to alter calcium homeostasis through this pathway affected platelet reactivity. The results of this work are consistent with those of previous studies showing that platelets from patients with chronic diseases behaved differently than those from healthy participants. These findings identify potential disease-specific targets to prevent and treat arterial thrombosis.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 16","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882964","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}

引用次数: 0

Pharmacological targeting of the IL-17/neutrophil axis attenuates calcific deposits in rat models of calciphylaxis. IL-17/中性粒细胞轴的药理靶向可减轻大鼠钙化反应模型中的钙化沉积。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-15 eCollection Date: 2025-10-01 DOI: 10.1172/JCI190369

Bo Tao, Edward Z Cao, James Hyun, Sivakumar Ramadoss, Juan F Alvarez, Lianjiu Su, Qihao Sun, Zhihao Liu, Linlin Zhang, Alejandro Espinoza, Yiqian Gu, Feiyang Ma, Shen Li, Matteo Pellegrini, Arjun Deb

{"title":"Pharmacological targeting of the IL-17/neutrophil axis attenuates calcific deposits in rat models of calciphylaxis.","authors":"Bo Tao, Edward Z Cao, James Hyun, Sivakumar Ramadoss, Juan F Alvarez, Lianjiu Su, Qihao Sun, Zhihao Liu, Linlin Zhang, Alejandro Espinoza, Yiqian Gu, Feiyang Ma, Shen Li, Matteo Pellegrini, Arjun Deb","doi":"10.1172/JCI190369","DOIUrl":"10.1172/JCI190369","url":null,"abstract":"Calciphylaxis is a rare but life-threatening disorder characterized by ectopic calcification affecting the subcutaneous tissues and blood vessels of the skin. Survival rates are less than a year after diagnosis, and yet despite the severity of the condition, the pathobiology of calciphylaxis is ill understood. Here, we created animal models of calciphylaxis that recapitulated many characteristics of the human phenotype. We demonstrate that cutaneous calcification is preceded by inflammatory cell infiltration. We show that increased local skin inflammation, regardless of the inciting cause, in the presence of hypercalcemia and hyperphosphatemia contributes to cutaneous ectopic calcification. Genetically modified rodents lacking immune activation of T and B cells or NK cells are resistant to developing cutaneous calcification. Consistent with this, administration of the immunosuppressive cyclophosphamide reduced calcific deposits, as did T cell suppression with cyclosporine. We demonstrate that IL-17 is upregulated in calcific skin and neutrophils are the predominant cell type expressing IL-17 and tissue-nonspecific alkaline phosphatase (TNAP) that are necessary for ectopic calcification. Targeting IL-17 with a monoclonal antibody or using a myeloperoxidase inhibitor to blunt neutrophil activation notably attenuated calcific deposits in vivo. Taken together, these observations provide fresh insight into the role of the immune system and the IL-17/neutrophil axis in mediating ectopic calcification in rodent models of calciphylaxis.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 19","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199632","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}

引用次数: 0

Experimental models of pancreas cancer: what has been the impact for precision medicine? 胰腺癌实验模型：对精准医学有何影响？

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-15 DOI: 10.1172/JCI191945

Vasiliki Pantazopoulou, Casie S Kubota, Satoshi Ogawa, Kevin Christian Montecillo Gulay, Xiaoxue Lin, Hyemin Song, Jonathan R Weitz, Hervé Tiriac, Andrew M Lowy, Dannielle D Engle

{"title":"Experimental models of pancreas cancer: what has been the impact for precision medicine?","authors":"Vasiliki Pantazopoulou, Casie S Kubota, Satoshi Ogawa, Kevin Christian Montecillo Gulay, Xiaoxue Lin, Hyemin Song, Jonathan R Weitz, Hervé Tiriac, Andrew M Lowy, Dannielle D Engle","doi":"10.1172/JCI191945","DOIUrl":"10.1172/JCI191945","url":null,"abstract":"Pancreatic cancer has a 5-year survival rate of approximately 13% and is projected to become the second-leading cause of cancer-related deaths by 2040. Despite advances in preclinical research, clinical translation remains challenging, and combination chemotherapy remains the standard of care. The intrinsic heterogeneity of pancreas cancer underscores the potential of precision medicine approaches to improve patient outcomes. However, clinical implementation faces substantial challenges, including patient performance status, metastatic disease at diagnosis, intrinsic drug resistance, and a highly complex tumor microenvironment. Emerging targeted therapies, such as RAS inhibitors, offer promise for personalized treatment. These developments have prompted precision medicine-focused clinical trials using molecular subtyping for patient stratification. Effective development of precision medicine therapies depends heavily on robust preclinical models capable of accurately recapitulating the complexities of the pancreatic tumor microenvironment. Two-dimensional, air-liquid interface, and patient-derived organoid cultures combined with in vivo genetically engineered mouse models and patient-derived xenografts represent valuable experimental systems. This Review critically examines the strengths and limitations of these experimental model systems. We highlight their relevance and utility for advancing precision medicine strategies in pancreas cancer.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 16","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882966","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}

引用次数: 0

Targeting LAIR1-mediated immunosuppression adds a new weapon to our immunotherapy arsenal. 靶向lair1介导的免疫抑制为我们的免疫治疗武器库增加了新的武器。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-15 DOI: 10.1172/JCI194924

Ezri P Perrin, Hannah K Dorando, Jacqueline E Payton

引用次数: 0

KRAS: the Achilles' heel of pancreas cancer biology. KRAS：胰腺癌生物学的致命弱点。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-15 DOI: 10.1172/JCI191939

Kristina Drizyte-Miller, Taiwo Talabi, Ashwin Somasundaram, Adrienne D Cox, Channing J Der

{"title":"KRAS: the Achilles' heel of pancreas cancer biology.","authors":"Kristina Drizyte-Miller, Taiwo Talabi, Ashwin Somasundaram, Adrienne D Cox, Channing J Der","doi":"10.1172/JCI191939","DOIUrl":"10.1172/JCI191939","url":null,"abstract":"The genetic landscape of pancreatic ductal adenocarcinoma (PDAC) is well-established and dominated by four key genetic driver mutations. Mutational activation of the KRAS oncogene is the initiating genetic event, followed by genetic loss of function of the CDKN2A, TP53, and SMAD4 tumor suppressor genes. Disappointingly, this information has not been leveraged to develop clinically effective targeted therapies for PDAC treatment, where current standards of care remain cocktails of conventional cytotoxic drugs. Nearly all (~95%) PDAC harbors KRAS mutations, and experimental studies have validated the essential role of KRAS mutation in PDAC tumorigenic and metastatic growth. Identified in 1982 as the first gene shown to be aberrantly activated in human cancer, KRAS has been the focus of intensive drug discovery efforts. Widely considered \"undruggable,\" KRAS has been the elephant in the room for PDAC treatment. This perception was shattered recently with the approval of two KRAS inhibitors for the treatment of KRASG12C-mutant lung and colorectal cancer, fueling hope that KRAS inhibitors will lead to a breakthrough in PDAC therapy. In this Review, we summarize the key role of aberrant KRAS signaling in the biology of pancreatic cancer; provide an overview of past, current, and emerging anti-KRAS treatment strategies; and discuss current challenges that limit the clinical efficacy of directly targeting KRAS for pancreatic cancer treatment.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 16","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882968","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}

引用次数: 0

Quantitative functional profiling of ERCC2 mutations deciphers cisplatin sensitivity in bladder cancer. ERCC2突变的定量功能分析揭示了膀胱癌中顺铂的敏感性。

IF 13.6 1区医学

Journal of Clinical Investigation Pub Date : 2025-08-15 DOI: 10.1172/JCI186688

Judit Börcsök, Diyavarshini Gopaul, Daphne Devesa-Serrano, Clémence Mooser, Nicolas Jonsson, Matteo Cagiada, Dag R Stormoen, Maya N Ataya, Brendan J Guercio, Hristos Z Kaimakliotis, Gopa Iyer, Kresten Lindorff-Larsen, Lars Dyrskjøt, Kent W Mouw, Zoltan Szallasi, Claus S Sørensen

{"title":"Quantitative functional profiling of ERCC2 mutations deciphers cisplatin sensitivity in bladder cancer.","authors":"Judit Börcsök, Diyavarshini Gopaul, Daphne Devesa-Serrano, Clémence Mooser, Nicolas Jonsson, Matteo Cagiada, Dag R Stormoen, Maya N Ataya, Brendan J Guercio, Hristos Z Kaimakliotis, Gopa Iyer, Kresten Lindorff-Larsen, Lars Dyrskjøt, Kent W Mouw, Zoltan Szallasi, Claus S Sørensen","doi":"10.1172/JCI186688","DOIUrl":"10.1172/JCI186688","url":null,"abstract":"Tumor gene alterations can serve as predictive biomarkers for therapy response. The nucleotide excision repair (NER) helicase ERCC2 carries heterozygous missense mutations in approximately 10% of bladder tumors, and these may predict sensitivity to cisplatin treatment. To explore the clinical actionability of ERCC2 mutations, we assembled a multinational cohort of 2,012 individuals with bladder cancer and applied the highly quantitative CRISPR-Select assay to functionally profile recurrent ERCC2 mutations. We also developed a single-allele editing version of CRISPR-Select to assess heterozygous missense variants in their native context. From the cohort, 506 ERCC2 mutations were identified, with 93% being heterozygous missense variants. CRISPR-Select pinpointed deleterious, cisplatin-sensitizing mutations, particularly within the conserved helicase domains. Importantly, single-allele editing revealed that heterozygous helicase-domain mutations markedly increased cisplatin sensitivity. Integration with clinical data confirmed that these mutations were associated with improved response to platinum-based neoadjuvant chemotherapy. Comparison with computational algorithms showed substantial discrepancies, highlighting the importance of precision functional assays for interpreting mutation effects in clinically relevant contexts. Our results demonstrate that CRISPR-Select provides a robust platform to advance biomarker-driven therapy in bladder cancer and supports its potential integration into precision oncology workflows.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 16","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882969","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}

引用次数: 0