American Journal of Pathology最新文献_第7页

Current Clinical Trials for Alcohol-Associated Hepatitis. 当前酒精相关性肝炎的临床试验

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-18 DOI: 10.1016/j.ajpath.2025.03.009

Elias D Rady, Ahmad Anouti, Mack C Mitchell, Thomas G Cotter

{"title":"Current Clinical Trials for Alcohol-Associated Hepatitis.","authors":"Elias D Rady, Ahmad Anouti, Mack C Mitchell, Thomas G Cotter","doi":"10.1016/j.ajpath.2025.03.009","DOIUrl":"10.1016/j.ajpath.2025.03.009","url":null,"abstract":"<p><p>Alcohol-associated hepatitis (AH) is a severe form of alcohol-associated liver disease characterized by acute-onset jaundice and liver failure. AH carries a high mortality risk, particularly in severe cases. Although glucocorticoids have been the primary pharmacologic intervention for decades, their use is limited by a lack of long-term efficacy and significant side effects and relative contraindications. For patients who do not respond to glucocorticoids, early liver transplantation is a life-saving option; only a few patients qualify for this intervention, however. In recent years, advances in translational medicine have uncovered key mechanisms in AH pathophysiology, including microbiome interactions, proinflammatory signaling, and disruptions in hepatocyte function. These insights have led to the exploration of innovative pharmacologic treatments, targeting pathways such as the gut-liver axis, oxidative stress, inflammation, and liver regeneration. Despite promising results from ongoing clinical trials, several challenges persist, including low patient recruitment and retention rates, heterogeneity in trial design, and the lack of standardized endpoints. This review assesses the current pharmacologic landscape of AH, emphasizing emerging therapies and the ongoing challenges in AH clinical trials.</p>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

How Alcohol Induces Human Acute Alcoholic Pancreatitis-Problem Solved? 酒精是如何诱发急性酒精性胰腺炎的？

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-18 DOI: 10.1016/j.ajpath.2025.03.008

Isto Nordback, Hannu Paajanen, Stephen Pandol

引用次数: 0

Multiple Roles for Neuregulins and Their ERBB Receptors in Neurodegenerative Disease Pathogenesis and Therapy. 神经调节蛋白及其ERBB受体在神经退行性疾病发病机制和治疗中的多重作用。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-18 DOI: 10.1016/j.ajpath.2025.03.012

Brittany Turner-Ivey, Dorea P Jenkins, Steven L Carroll

{"title":"Multiple Roles for Neuregulins and Their ERBB Receptors in Neurodegenerative Disease Pathogenesis and Therapy.","authors":"Brittany Turner-Ivey, Dorea P Jenkins, Steven L Carroll","doi":"10.1016/j.ajpath.2025.03.012","DOIUrl":"https://doi.org/10.1016/j.ajpath.2025.03.012","url":null,"abstract":"<p><p>The role that neurotrophins, such as nerve growth factor, play in the pathogenesis of neurodegenerative diseases has long been appreciated. However, the neuregulin (NRG) family of growth factors and/or their v-erb-B2 avian erythroblastic leukemia viral oncogene homolog (ERBB) receptors have also been implicated in the pathogenesis of conditions, such as Alzheimer disease (AD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). In this review, we consider i) the structural variability of NRG isoforms generated by alternative RNA splicing, the use of multiple promoters and proteolysis, and the impact that this structural variability has on neuronal and glial physiology during development and adulthood. We discuss ii) the NRG receptors ERBB2, ERBB3, and ERBB4, how activation of each of these receptors further diversifies NRG actions in the central nervous system, and how dementia-related proteins, such as γ-secretase modulate the action of NRGs and their ERBB receptors. We then iii) turn to the abnormalities in NRG and ERBB expression and function evident in human AD and mouse AD models, how these abnormalities affect brain function, and attempts to use NRGs to treat AD. Finally, iv) we discuss NRG effects on the survival and function of neurons relevant to FTLD and ALS, alterations in NRG/ERBB signaling identified in these conditions, and the recent discovery of multiple human pedigrees in which autosomal dominant FTLD/ALS potentially results from point mutations in ERBB4.</p>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond. IL-22治疗酒精相关肝病及其他疾病的最新进展

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-18 DOI: 10.1016/j.ajpath.2025.03.010

Lihong Fu, Burhan Yokus, Bin Gao, Pal Pacher

{"title":"An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond.","authors":"Lihong Fu, Burhan Yokus, Bin Gao, Pal Pacher","doi":"10.1016/j.ajpath.2025.03.010","DOIUrl":"https://doi.org/10.1016/j.ajpath.2025.03.010","url":null,"abstract":"<p><p>Excessive alcohol consumption drives the development of alcohol-associated liver disease (ALD), including steatohepatitis, cirrhosis, and hepatocellular carcinoma, and its associated complications, such as hepatorenal syndrome. Hepatocyte death, inflammation, and impaired liver regeneration are key processes implicated in the pathogenesis and progression of ALD. Despite extensive research, therapeutic options for ALD remain limited. IL-22 has emerged as a promising therapeutic target because of its hepatoprotective properties mediated through the activation of the STAT3 signaling pathway. IL-22 enhances hepatocyte survival by mitigating apoptosis, oxidative stress, and inflammation while simultaneously promoting liver regeneration through the proliferation of hepatocytes and hepatic progenitor cells and the up-regulation of growth factors. Additionally, IL-22 exerts protective effects on epithelial cells in various organs affected by ALD and its associated complications. Studies from preclinical models and early-phase clinical trials of IL-22 agonists, such as F-652 and UTTR1147A, have shown favorable safety profiles, good tolerability, and encouraging efficacy in reducing liver injury and promoting regeneration. However, the heterogeneity and multifactorial nature of ALD present ongoing challenges. Further research is needed to optimize IL-22-based therapies and clarify their roles within a comprehensive approach to ALD management. This review summarizes the current understanding of IL-22 biology and its role in ALD pathophysiology and ALD-associated complications along with therapeutic application of IL-22, potential benefits, and limitations.</p>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Shared Mechanisms of Blood-Brain Barrier Dysfunction and Neuroinflammation in Coronavirus Disease 2019 and Alzheimer Disease. 2019冠状病毒病和阿尔茨海默病中血脑屏障功能障碍和神经炎症的共同机制

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-18 DOI: 10.1016/j.ajpath.2025.03.011

Meredith G Mayer, Tracy Fischer

{"title":"Shared Mechanisms of Blood-Brain Barrier Dysfunction and Neuroinflammation in Coronavirus Disease 2019 and Alzheimer Disease.","authors":"Meredith G Mayer, Tracy Fischer","doi":"10.1016/j.ajpath.2025.03.011","DOIUrl":"https://doi.org/10.1016/j.ajpath.2025.03.011","url":null,"abstract":"<p><p>The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has highlighted the virus's impact on the central nervous system and its potential to exacerbate neurodegenerative diseases, like Alzheimer disease (AD). Emerging evidence suggests that SARS-CoV-2 infection contributes to chronic neuroinflammation, a key driver in the etiopathogenesis of AD. Shared mechanisms, including blood-brain barrier (BBB) dysfunction, systemic inflammation, and activation of immune pathways, may link SARS-CoV-2 infection to AD onset and/or progression, particularly among vulnerable individuals, such as those of advanced age. This review explores convergent pathways involving the renin-angiotensin-aldosterone system, Wnt/β-catenin signaling, NF-κB activation, and interferon signaling, focusing on their roles in BBB integrity and neuroinflammation. SARS-CoV-2-mediated angiotensin-converting enzyme 2 depletion disrupts renin-angiotensin-aldosterone system homeostasis, favoring proinflammatory signaling that parallels vascular dysfunction in AD. Dysregulation of Wnt/β-catenin signaling exacerbates BBB permeability, whereas NF-κB and interferon pathways contribute to BBB breakdown and propagate central nervous system inflammation via endothelial and immune cell activation. These interactions may amplify prodromal AD pathology and/or initiate AD pathogenesis. By identifying mechanistic overlaps between COVID-19 and AD, this review underlines the need for therapeutic strategies targeting shared pathways of inflammation and BBB dysfunction. Understanding these connections is critical for mitigating the long-term neurologic sequelae of COVID-19 and reducing the burden of AD.</p>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Disintegrin and Metalloproteinase 10 Regulates Ephrin B2–Mediated Endothelial Cell Sprouting and Ischemic Retinopathy 崩解素和金属蛋白酶10调控Ephrin b2介导的内皮细胞发芽和缺血性视网膜病变。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-17 DOI: 10.1016/j.ajpath.2025.03.007

Shivantika Bisen , Purnima Gogoi , Anamika Sharma , Chandra S. Mukhopadhyay , Nikhlesh K. Singh

{"title":"A Disintegrin and Metalloproteinase 10 Regulates Ephrin B2–Mediated Endothelial Cell Sprouting and Ischemic Retinopathy","authors":"Shivantika Bisen , Purnima Gogoi , Anamika Sharma , Chandra S. Mukhopadhyay , Nikhlesh K. Singh","doi":"10.1016/j.ajpath.2025.03.007","DOIUrl":"10.1016/j.ajpath.2025.03.007","url":null,"abstract":"<div><div>Retinal neovascularization is the leading cause of visual impairment in diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration. The extracellular matrix breakdown by metalloproteinase leads to vascular complications in various proliferative retinopathies. A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) is involved in physiological angiogenesis. However, limited information exists regarding the role of ADAM10 in proliferative retinopathies. In this study, the levels of active ADAM10 were significantly up-regulated in the ischemic retina, and down-regulation or inactivation of ADAM10 significantly inhibited the proliferation, sprouting, migration, and tube formation of human retinal microvascular endothelial cell. Furthermore, the endothelial cell (EC)–specific deletion of <em>ADAM10</em> (<em>ADAM10</em><sup><em>iΔEC</em></sup>) significantly attenuated vascular leakage, edema, endothelial cell sprouting, and retinal neovascularization in ischemic retinas of mice exposed to oxygen-induced retinopathy. In experiments investigating the mechanisms through which ADAM10 regulated pathologic angiogenesis, ADAM10 regulated ephrin B2 (EfnB2) expression in endothelial cells. Down-regulation of EfnB2 expression influenced human retinal microvascular endothelial cell proliferation, migration, sprouting, and tube formation. In addition, a significant up-regulation of EfnB2 expression in the ischemic retina was detected. EC-specific depletion of <em>ADAM10</em> significantly reduced EfnB2 expression, suggesting its involvement in ADAM10-regulated retinal neovascularization. The findings demonstrate how EC-specific <em>ADAM10</em> regulates pathologic retinal neovascularization in the ischemic retina, indicating its significance as a potential therapeutic target for proliferative retinopathies.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 7","pages":"Pages 1311-1327"},"PeriodicalIF":4.7,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Laminin-γ2–NR6A1 Fusion Protein Promotes Metastatic Potential in Non–Small-Cell Lung Carcinoma Cells without Epidermal Growth Factor Receptor Mutation 层粘连蛋白-γ - 2- nr6a1融合蛋白促进无表皮生长因子受体突变的非小细胞肺癌细胞的转移潜能

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-17 DOI: 10.1016/j.ajpath.2025.03.006

Ryo Kaneko , Yuri Kishimoto , Ozora Ishikawa , Nobuaki Funahashi , Naohiko Koshikawa

{"title":"Laminin-γ2–NR6A1 Fusion Protein Promotes Metastatic Potential in Non–Small-Cell Lung Carcinoma Cells without Epidermal Growth Factor Receptor Mutation","authors":"Ryo Kaneko , Yuri Kishimoto , Ozora Ishikawa , Nobuaki Funahashi , Naohiko Koshikawa","doi":"10.1016/j.ajpath.2025.03.006","DOIUrl":"10.1016/j.ajpath.2025.03.006","url":null,"abstract":"<div><div>Laminin-γ2 fusion gene (<em>Lm-γ2F</em>), formed by translocation between <em>LAMC2</em> and <em>NR6A1</em>, functions as an epidermal growth factor receptor (EGFR) ligand. However, its expression and impact on cancers beyond the initially studied contexts remain unclear. This study focused on Lm-γ2F protein secretion and its role in non–small-cell lung carcinoma (NSCLC), where EGFR signaling plays a pivotal role in malignancy progression. Lm-γ2F secretion was confirmed in serum-free conditioned medium from six NSCLC cell lines by Western blot analysis and further validated in NCI-H1650 cells. Hypothesizing that Lm-γ2F functions as an EGFR ligand, its effects in NSCLC cells lacking EGFR mutations were explored. In EKVX and RERF-LC-KJ cell lines, Lm-γ2F overexpression significantly enhanced cell growth, survival, motility, and invasiveness through EGFR signaling activation compared with controls. Conversely, no effects were observed in VMRC-LCD cells lacking EGFR expression. Additionally, increased membrane-type 1 matrix metalloproteinase expression was detected in Lm-γ2F–expressing EKVX cells. <em>In vivo</em>, these cells exhibited elevated metastatic activity in a lung metastasis model. These findings suggested that ectopic Lm-γ2F expression contributes to malignant progression in NSCLC cells without EGFR mutations. Furthermore, EGFR tyrosine kinase inhibitors may suppress metastasis in these contexts. This study provides novel insights into the oncogenic role of Lm-γ2F in NSCLC, highlighting its potential as a therapeutic target to mitigate tumor progression and metastasis.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 7","pages":"Pages 1328-1339"},"PeriodicalIF":4.7,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

This Month in AJP 本月在AJP

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-15 DOI: 10.1016/j.ajpath.2025.04.001

引用次数: 0

Macrophage Migration Inhibitory Factor Contributes to Adverse Outcomes of Experimental Gestational Malaria across Pregnancy Stages 巨噬细胞迁移抑制因子与实验性妊娠期疟疾的不良结局有关。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-07 DOI: 10.1016/j.ajpath.2025.03.004

Andrea Tatiana Durán-Rodriguez , Marcos Paulo O. Almeida , Flávia Batista Ferreira , Laura Alejandra Lozano-Trujillo , Angelica Oliveira Gomes , Yusmaris Cariaco , Neide Maria Silva

{"title":"Macrophage Migration Inhibitory Factor Contributes to Adverse Outcomes of Experimental Gestational Malaria across Pregnancy Stages","authors":"Andrea Tatiana Durán-Rodriguez , Marcos Paulo O. Almeida , Flávia Batista Ferreira , Laura Alejandra Lozano-Trujillo , Angelica Oliveira Gomes , Yusmaris Cariaco , Neide Maria Silva","doi":"10.1016/j.ajpath.2025.03.004","DOIUrl":"10.1016/j.ajpath.2025.03.004","url":null,"abstract":"<div><div>Malaria infection during pregnancy, particularly caused by <em>Plasmodium falciparum</em>, poses significant risks, such as maternal anemia, low birth weight, preterm delivery, and increased infant mortality. This study investigated the role of macrophage migration inhibitory factor (MIF) in modulating pregnancy outcomes in a mouse model of gestational malaria. Herein, <em>Mif</em>-deficient (<em>Mif</em><sup>–/–</sup>) and <em>Mif</em>-sufficient (wild-type) mice were used to evaluate the impact of MIF on maternal-fetal immune interactions during <em>Plasmodium</em> infection in three different stages of pregnancy. <em>Mif</em><sup>–/–</sup> mice exhibited lower embryo resorption rates, preserved decidualization, and improved spiral artery remodeling compared with wild-type counterparts. Notably, although <em>Mif</em> deficiency was associated with increased parasitemia levels in late gestation, a shift toward a more anti-inflammatory phenotype in the uteroplacental tissues of infected mice contributed to better pregnancy outcomes. These results highlight the complex interplay between immune regulation and pregnancy in the context of malaria, indicating that targeting <em>Mif</em> may offer a therapeutic strategy to mitigate adverse pregnancy effects in infected individuals.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 7","pages":"Pages 1223-1241"},"PeriodicalIF":4.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Constitutive Hepatic mTORC1 Activation Aggravates Alcohol-Induced Liver Injury via Endoplasmic Reticulum Stress–Mediated Ferroptosis 组成性肝mTORC1激活通过内质网应激介导的铁下沉加重酒精诱导的肝损伤。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2025-04-07 DOI: 10.1016/j.ajpath.2025.03.005

Lin Xu , Yuanyuan Zhao , Yang Yang , Enbo Qi , Boao Liu , Peili Zhuang , Shiyi Song , Tingmin Chang , Zhiguo Chen , Xiaohong Kang , Xiwen Xiong

{"title":"Constitutive Hepatic mTORC1 Activation Aggravates Alcohol-Induced Liver Injury via Endoplasmic Reticulum Stress–Mediated Ferroptosis","authors":"Lin Xu , Yuanyuan Zhao , Yang Yang , Enbo Qi , Boao Liu , Peili Zhuang , Shiyi Song , Tingmin Chang , Zhiguo Chen , Xiaohong Kang , Xiwen Xiong","doi":"10.1016/j.ajpath.2025.03.005","DOIUrl":"10.1016/j.ajpath.2025.03.005","url":null,"abstract":"<div><div>Alcohol-related liver disease (ALD), a consequence of excessive alcohol use, manifests across a broad spectrum of liver damage, ranging from steatosis to cirrhosis. DEPDC5 (DEP domain–containing protein 5) is a component of the GATOR1 (gap activity towards rags 1) complex, which functions as a repressor of the amino acid–sensing branch of the mammalian target of rapamycin complex 1 (mTORC1) pathway. In this study, hepatocyte-specific <em>Depdc5</em> knockout mice (Depdc5<sup>△Hep</sup>) were generated. Aberrant activation of mTORC1 caused by <em>Depdc5</em> deletion led to exacerbated endoplasmic reticulum (ER) stress and hepatocyte ferroptosis in the livers of ethanol-fed mice. Torin-1, an ATP-competitive mTOR inhibitor, suppressed the mTORC1 activity and reversed the effects of <em>Depdc5</em> deletion on ER stress and ferroptosis in ethanol-fed mouse livers. Furthermore, pharmacologic relief of ER stress using tauroursodeoxycholic acid or inhibition of ferroptosis with liproxstatin-1 both alleviated the liver abnormalities induced by <em>Depdc5</em> ablation in ethanol-fed mice. In addition, ER stress was shown to function as an upstream signal of ferroptosis in the progression of ALD. These findings provide novel <em>in vivo</em> evidence that sustained mTORC1 activation leads to alcoholic liver injury by inducing ER stress and ferroptosis, suggesting that targeting these pathways may represent a potential therapeutic strategy for ALD.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 7","pages":"Pages 1209-1222"},"PeriodicalIF":4.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0