Journal of autoimmunity最新文献

{"title":"Comparison of circulating and excreted metals and of autoimmunity between two Great Plains Tribal communities","authors":"Esther Erdei ,&nbsp;Elena R. O'Donald ,&nbsp;Li Luo ,&nbsp;Kendra Enright ,&nbsp;Marcia O'Leary ,&nbsp;Debra MacKenzie ,&nbsp;John Doyle ,&nbsp;Margaret Eggers ,&nbsp;Deborah Keil ,&nbsp;Johnnye Lewis ,&nbsp;Jeffrey A. Henderson ,&nbsp;Robert L. Rubin","doi":"10.1016/j.jaut.2023.103117","DOIUrl":"10.1016/j.jaut.2023.103117","url":null,"abstract":"<div><div>Metals contaminants of the environment from mine waste have been implicated as contributing agents in autoimmune disease. The current study compares metals and autoimmunity in two Tribal communities residing in the Black Hills and the Bighorn Mountains geographical regions that are scattered with extant hard rock mines. With documented drinking water contamination in both communities, <em>in vivo</em> levels of more than half of the measured serum and urine metals differed between the two communities and were substantially different from their national median values. Serum autoantibodies associated with systemic autoimmune disease were rare or at low-level, but antibodies to denatured (single-stranded) DNA and thyroid-specific autoantibodies were commonly elevated, especially in women. A three-tier statistical modeling process was carried out to examine individual metals exposure as predictors of autoantibody levels. For the most part only weak positive associations between individual metals and systemic autoantibodies were found, although univariate quantile regression analysis showed positive statistical associations of serum lead and antimony with anti-chromatin and anti-histone autoantibodies. Using age and gender-adjusted multivariable statistical models, metals did not predict anti-thyroglobulin or -thyroid peroxidase significantly and metals were generally negative predictors of the other autoantibodies. Overall these results suggest that elevated levels of environmental metals and metalloids in these communities may result in suppression of autoantibodies associated with systemic autoimmune disease.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103117"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182635","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}

{"title":"High-content multimodal analysis supports the IL-7/IL-7 receptor axis as a relevant therapeutic target in primary Sjögren's syndrome","authors":"Emiko Desvaux ,&nbsp;Patrice Hemon ,&nbsp;Perrine Soret ,&nbsp;Christelle Le Dantec ,&nbsp;Loukas Chatzis ,&nbsp;Divi Cornec ,&nbsp;Valérie Devauchelle-Pensec ,&nbsp;PRECISESADS clinical consortium ,&nbsp;Sahar Elouej ,&nbsp;Fanny Duguet ,&nbsp;Laurence Laigle ,&nbsp;Nicolas Poirier ,&nbsp;Philippe Moingeon ,&nbsp;Sylvie Bretin ,&nbsp;Jacques-Olivier Pers","doi":"10.1016/j.jaut.2023.103147","DOIUrl":"10.1016/j.jaut.2023.103147","url":null,"abstract":"<div><h3>Objective</h3><div>While the involvement of IL-7/IL-7R axis in pSS has been described in relation to T cells, little is known about the contribution of this pathway in relationship with other immune cells, and its implication in autoimmunity. Using high-content multiomics data, we aimed at characterizing IL-7R expressing cells and the involvement of IL-7/IL-7R pathway in pSS pathophysiology.</div></div><div><h3>Methods</h3><div>An <em>IL-7 signature</em> established using RNA-sequencing of human PBMCs incubated with IL-7 was applied to 304 pSS patients, and on RNA-Seq datasets from tissue biopsies. High-content immunophenotyping using flow and imaging mass cytometry was developed to characterize peripheral and <em>in situ</em> IL-7R expression.</div></div><div><h3>Results</h3><div>We identified a blood 4-gene IL-7 module (<em>IKZF4</em>, <em>KIAA0040</em>, <em>PGAP1</em> and <em>SOS1</em>) associated with anti-SSA/Ro positiveness in patients as well as disease activity, and a tissue 5-gene IL-7 module (<em>IL7R, PCED1B, TNFSF8, ADAM19, MYBL1)</em> associated with infiltration severity. We confirmed expression of IL-7R on T cells subsets, and further observed upregulation of IL-7R on double-negative (DN) B cells, and especially DN2 B cells. IL-7R expression was increased in pSS compared to sicca patients with variations seen according to the degree of infiltration. When expressed, IL-7R was mainly found on epithelial cells, CD4⁺ and CD8⁺ T cells, switched memory B cells, DN B cells and M1 macrophages.</div></div><div><h3>Conclusion</h3><div>This exhaustive characterization of the IL-7/IL-7R pathway in pSS pathophysiology established that two IL-7 gene modules discriminate pSS patients with a high IL-7 axis involvement. Their use could guide the implementation of an anti-IL-7R targeted therapy in a precision medicine approach.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103147"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138743619","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}

{"title":"Infectious and non-infectious precipitants of sarcoidosis","authors":"Ozioma S. Chioma ,&nbsp;ZaDarreyal Wiggins ,&nbsp;Samantha Rea ,&nbsp;Wonder P. Drake","doi":"10.1016/j.jaut.2024.103239","DOIUrl":"10.1016/j.jaut.2024.103239","url":null,"abstract":"<div><div><span><span>Sarcoidosis is a chronic </span>inflammatory disease that can affect any organ in the body. Its exact cause remains unknown, but it is believed to result from a combination of genetic and </span>environmental factors<span>. Some potential causes of sarcoidosis include genetics, environmental triggers, immune system dysfunction, the gut microbiome<span><span>, sex, and race/ethnicity. Genetic mutations are associated with protection against </span>disease progression<span> or an increased susceptibility to more severe disease, while exposure to certain chemicals, bacteria, viruses, or allergens can trigger the formation of immune cell<span><span><span><span> congregations (granulomas) in different organs. Dysfunction of the immune system, including autoimmune reactions, may also contribute. The gut microbiome and factors such as being female or having African American, Scandinavian, Irish, or Puerto Rican heritage are additional contributors to disease outcome. Recent research has suggested that certain drugs, such as anti-Programmed Death-1 (PD-1) and </span>antibiotics such as tuberculosis (TB) drugs, may raise the risk of developing sarcoidosis. Hormone levels, particularly higher levels of estrogen and </span>progesterone in women, have also been linked to an increased likelihood of sarcoidosis. The diagnosis of sarcoidosis involves a comprehensive assessment that includes </span>medical history, physical examination, laboratory tests, and imaging studies. While there is no cure for sarcoidosis, the symptoms can often be effectively managed through various treatment options. Treatment may involve the use of medications, surgical interventions, or lifestyle changes. These disparate factors suggests that sarcoidosis has multiple positive and negative exacerbants on disease severity, some of which can be ameliorated and others which cannot.</span></span></span></span></div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103239"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141183717","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}

{"title":"Extrapulmonary sarcoidosis","authors":"Paolo Spagnolo ,&nbsp;Vasileios Kouranos ,&nbsp;Victoria Singh-Curry ,&nbsp;Thomas El Jammal ,&nbsp;Misha Rosenbach","doi":"10.1016/j.jaut.2024.103323","DOIUrl":"10.1016/j.jaut.2024.103323","url":null,"abstract":"<div><div>Sarcoidosis is a chronic disease of unknown origin that develops when a genetically susceptible host is exposed to an antigen, leading to an exuberant immune response characterized by granulomatous inflammation. Although lung involvement is almost universal as well as the leading cause of morbidity and mortality, virtually any organ can be affected. In particular, sarcoidosis of the heart, nervous system, and eyes can be devastating, leading to death, debilitation and blindness, and a multidisciplinary approach involving expert specialists is required for prompt diagnosis and appropriate treatment. Sarcoidosis of the skin can be disfiguring, thus posing a substantial psychologic and social impact on the patients. The diagnosis is often straightforward in the presence of compatible clinical manifestations in patients with biopsy-proven sarcoidosis, but is challenging when extrapulmonary signs/symptoms occur in isolation.</div><div>Corticosteroids remain the first line therapy, with immunosuppressive or biologic agents being reserved to patients failing or experiencing side effects from steroids or developing refractory disease.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103323"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380945","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":"Lung transplantation in pulmonary sarcoidosis","authors":"Jin Sun Kim,&nbsp;Rohit Gupta","doi":"10.1016/j.jaut.2023.103135","DOIUrl":"10.1016/j.jaut.2023.103135","url":null,"abstract":"<div><div><span><span><span>Sarcoidosis is a systemic </span>inflammatory disease of unknown etiology and variable </span>clinical course. </span>Pulmonary sarcoidosis<span><span> is the most common presentation and accounts for most morbidity and mortality related to sarcoidosis. While sarcoidosis generally has good outcomes, few patients experience chronic disease. A minority of patients progress to a specific phenotype of sarcoidosis referred to advanced pulmonary sarcoidosis (APS) which includes advanced </span>fibrosis<span><span><span>, pulmonary hypertension and respiratory failure, leading to high morbidity and mortality. In patients with advanced disease despite medical therapy, </span>lung transplantation may be the last viable option for improvement in </span>quality of life<span>. Though post-transplant survival is similar to that of other end-stage lung diseases, it is imperative that patients are evaluated and referred early to transplant centers with experience in APS. A multidisciplinary approach and clinical experience are crucial in detecting the optimal timing of referral, initiating comprehensive transplantation evaluation and listing, discussing surgical approach, and managing perioperative and post-transplant care. This review article seeks to address these aspects of lung transplantation in APS.</span></span></span></div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103135"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71481939","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}

{"title":"A framework for exclusion of alternative diagnoses in sarcoidosis","authors":"Logan J. Harper ,&nbsp;Carol F. Farver ,&nbsp;Ruchi Yadav ,&nbsp;Daniel A. Culver","doi":"10.1016/j.jaut.2024.103288","DOIUrl":"10.1016/j.jaut.2024.103288","url":null,"abstract":"<div><div>Sarcoidosis is a multisystem granulomatous syndrome that arises from a persistent immune response to a triggering antigen(s). There is no “gold standard” test or algorithm for the diagnosis of sarcoidosis, making the diagnosis one of exclusion. The presentation of the disease varies substantially between individuals, in both the number of organs involved, and the manifestations seen in individual organs. These qualities dictate that health care providers diagnosing sarcoidosis must consider a wide range of possible alternative diagnoses, from across a range of presentations and medical specialties (infectious, inflammatory, cardiac, neurologic). Current guideline-based diagnosis of sarcoidosis recommends fulfillment of three criteria: 1) compatible clinical presentation and/or imaging 2) demonstration of granulomatous inflammation by biopsy (when possible) and, 3) exclusion of alternative causes, but do not provide guidance on standardized strategies for exclusion of alternative diagnoses. In this review, we provide a summary of the most common differential diagnoses for sarcoidosis involvement of lung, eye, skin, central nervous system, heart, liver, and kidney. We then propose a framework for testing to exclude alternative diagnoses based on pretest probability of sarcoidosis, defined as high (typical findings with sarcoidosis involvement confirmed in another organ), moderate (typical findings in a single organ), or low (atypical/findings suggesting of an alternative diagnosis). This work highlights the need for informed and careful exclusion of alternative diagnoses in sarcoidosis.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103288"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141859866","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":"Genetic predisposition to sarcoidosis","authors":"Shu-Yi Liao ,&nbsp;Tasha Fingerlin ,&nbsp;Lisa Maier","doi":"10.1016/j.jaut.2023.103122","DOIUrl":"10.1016/j.jaut.2023.103122","url":null,"abstract":"<div><div>Sarcoidosis is a complex systemic disease with clinical heterogeneity based on varying phenotypes and natural history. The detailed etiology of sarcoidosis remains unknown, but genetic predisposition as well as environmental exposures play a significant role in disease pathogenesis. We performed a comprehensive review of germline genetic (DNA) and transcriptomic (RNA) studies of sarcoidosis, including both previous studies and more recent findings. In this review, we provide an assessment of the following: genetic variants in sarcoidosis susceptibility and phenotypes, ancestry- and sex-specific genetic variants in sarcoidosis, shared genetic architecture between sarcoidosis and other diseases, and gene-environment interactions in sarcoidosis. We also highlight the unmet needs in sarcoidosis genetic studies, including the pressing requirement to include diverse populations and have consistent definitions of phenotypes in the sarcoidosis research community to help advance the application of genetic predisposition to sarcoidosis disease risk and manifestations.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103122"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49677872","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}

{"title":"Pulmonary sarcoidosis: A comprehensive review: Past to present","authors":"John A. Belperio ,&nbsp;Michael C. Fishbein ,&nbsp;Fereidoun Abtin ,&nbsp;Jessica Channick ,&nbsp;Shailesh A. Balasubramanian ,&nbsp;Joseph P. Lynch III","doi":"10.1016/j.jaut.2023.103107","DOIUrl":"10.1016/j.jaut.2023.103107","url":null,"abstract":"&lt;div&gt;&lt;div&gt;Sarcoidosis is a sterile non-necrotizing granulomatous disease without known causes that can involve multiple organs with a predilection for the lung and thoracic lymph nodes. Worldwide it is estimated to affect 2–160/100,000 people and has a mortality rate over 5 years of approximately 7%. For sarcoidosis patients, the cause of death is due to sarcoid in 60% of the cases, of which up to 80% are from advanced cardiopulmonary failure (pulmonary hypertension and respiratory microbial infections) in all races except in Japan were greater than 70% of the sarcoidosis deaths are due to cardiac sarcoidosis.&lt;/div&gt;&lt;div&gt;Scadding stages for pulmonary sarcoidosis associates with clinical outcomes. Stages I and II have radiographic remission in approximately 30%–80% of cases. Stage III only has a 10%–40% chance of resolution, while stage IV has no change of resolution. Up to 40% of pulmonary sarcoidosis patients progress to stage IV disease with lung parenchyma fibroplasia, bronchiectasis with hilar retraction and fibrocystic disease. These patients are at highest risk for the development of precapillary pulmonary hypertension, which may occur in up to 70% of these patients. Sarcoid patients with pre-capillary pulmonary hypertension can respond to targeted pulmonary arterial hypertension medications. Stage IV fibrocytic sarcoidosis with significant pulmonary physiologic impairment, &gt;20% fibrosis on HRCT or pre-capillary pulmonary hypertension have the highest risk of mortality, which can be &gt;40% at 5-years.&lt;/div&gt;&lt;div&gt;First line treatment for patients who are symptomatic (cough and dyspnea) with parenchymal infiltrates and abnormal pulmonary function testing (PFT) is oral glucocorticoids, such as prednisone with a typical starting dose of 20–40 mg daily for 2 weeks to 2 months. Prednisone can be tapered over 6–18 months if symptoms, spirometry, PFTs, and radiographs improve. Prolonged prednisone may be required to stabilize disease. Patients requiring prolonged prednisone ≥10 mg/day or those with adverse effects due to glucocorticoids may be prescribed second and third line treatements. Second and third line treatments include immunosuppressive agents (e.g., methotrexate and azathioprine) and anti-tumor necrosis factor (TNF) medication; respectively. Effective treatments for advanced fibrocystic pulmonary disease are being explored. Despite different treatments, relapse rates range from 13% to 75% depending on the stage of sarcoid, number of organs involved, socioeconomic status, and geography.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;The mortality rate for sarcoidosis over a 5 year follow up is approximately 7%. Unfortunately, 10%–40% of patients with sarcoidosis develop progressive pulmonary disease, and &gt;60% of deaths resulting from sarcoidosis are due to advance cardiopulmonary disease. Oral glucocorticoids are the first line treatment, while methotrexate and azathioprine are considered second and anti-TNF agents are third line treatments","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103107"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49677873","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":"Quality of life in sarcoidosis","authors":"Catharina C. Moor ,&nbsp;Ogugua Ndili Obi ,&nbsp;Vivienne Kahlmann ,&nbsp;Katharina Buschulte ,&nbsp;Marlies S. Wijsenbeek","doi":"10.1016/j.jaut.2023.103123","DOIUrl":"10.1016/j.jaut.2023.103123","url":null,"abstract":"<div><div>Having sarcoidosis often has a major impact on quality of life of patients and their families. Improving quality of life is prioritized as most important treatment aim by many patients with sarcoidosis, but current evidence and treatment options are limited. In this narrative review, we describe the impact of sarcoidosis on various aspects of daily life, evaluate determinants of health-related quality of life (HRQoL), and provide an overview of the different patient-reported outcome measures to assess HRQoL in sarcoidosis. Moreover, we review the current evidence for pharmacological and non-pharmacological interventions to improve quality of life for people with sarcoidosis.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103123"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182636","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":"Kidney manifestations of sarcoidosis","authors":"Francesco Bonella ,&nbsp;Adriane DM Vorselaars ,&nbsp;Benjamin Wilde","doi":"10.1016/j.jaut.2024.103207","DOIUrl":"10.1016/j.jaut.2024.103207","url":null,"abstract":"<div><div>Renal involvement is a clinically relevant organ manifestation of sarcoidosis, leading to increased morbidity and complications. Although the exact incidence remains unknown, renal disease is likely to occur in up to one third of all sarcoidosis patients. Every patient with newly diagnosed sarcoidosis should receive a renal work-up and screening for disrupted calcium metabolism.</div><div>Amid various forms of glomerulonephritis, granulomatous interstitial nephritis is the most common one, but it rarely leads to renal impairment. Histologically, granulomas can be absent. Nephrocalcinosis and nephrolithiasis are frequent forms when hypercalcaemia or hypercalciuria occur. Drugs used for treatment of systemic sarcoidosis can also cause renal damage.</div><div>Due to its high heterogeneity, renal sarcoidosis can be difficult to treat. Glucocorticoids and various immunosuppressive treatments have been proven to be effective based on case series, but clinical trials are lacking. A treatment guideline for renal sarcoidosis is urgently needed.</div><div>In this review article, we present an overview of the different forms of renal sarcoidosis and the diagnostic steps to confirm renal involvement; in addition, we provide insights on the management and available treatments. A better understanding regarding the pathogenesis of sarcoidosis is the key for the development of more specific, targeted therapies.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103207"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140193881","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}