Experimental and molecular pathology最新文献

{"title":"Experimental models in Familial Mediterranean Fever (FMF): Insights into pathophysiology and therapeutic strategies","authors":"Nawal Mezher ,&nbsp;Ola Mroweh ,&nbsp;Louna Karam,&nbsp;José-Noel Ibrahim,&nbsp;Philippe Hussein Kobeissy","doi":"10.1016/j.yexmp.2024.104883","DOIUrl":"10.1016/j.yexmp.2024.104883","url":null,"abstract":"<div><p>Familial Mediterranean Fever (FMF) is a recurrent polyserositis characterized by self-limiting episodes or attacks of fever along with serosal inflammation. It mainly impacts people of the Mediterranean and Middle Eastern basin. FMF is a recessive autoinflammatory condition caused by mutation in the <em>MEFV</em> gene located on chromosome 16p13. <em>MEFV</em> mutations lead to the activation of the pyrin inflammasome resulting in an uncontrolled release of IL-1β. Various <em>in vitro</em>, <em>in vivo</em> and <em>ex vivo</em> experimental models have been developed to further comprehend the etiology and pathogenesis of FMF. These models have been proven to be clinically relevant to human FMF and can provide significant information about biological systems with respect to this condition. Additionally, these models have provided pertinent contributions to the development of potent therapeutic strategies against FMF. In this review, we describe the different experimental models utilized in FMF and we focus primarily on the most widely used models that have produced prominent insights into the pathophysiology of the disease.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480024000029/pdfft?md5=bb58ddaf7c248d2031ad07c65c126e39&pid=1-s2.0-S0014480024000029-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139546020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD10 expression as a potential predictor of pathological complete response in ER-negative and triple-negative breast cancer patients treated with anthracycline-based neoadjuvant chemotherapy","authors":"George Dimitrov ,&nbsp;Sami Shousha ,&nbsp;Petranka Troianova","doi":"10.1016/j.yexmp.2024.104885","DOIUrl":"10.1016/j.yexmp.2024.104885","url":null,"abstract":"<div><h3>Background</h3><p>Neoadjuvant chemotherapy (NCT) can induce a pathological complete response (pCR) in breast cancer patients, leading to improved outcomes. However, predicting which patients will achieve pCR remains a challenge. CD10, a myoepithelial marker, has shown diagnostic and prognostic value in metastatic tumors. Its potential as a predictor of chemosensitivity to anthracycline-based NCT in breast cancer is unknown.</p></div><div><h3>Aim</h3><p>This retrospective study aimed to investigate the potential of CD10 cancer cell expression as a predictive marker of chemosensitivity in breast cancers treated with anthracycline-based neoadjuvant chemotherapy.</p></div><div><h3>Methods</h3><p>We analyzed 130 patients with invasive ductal carcinoma who received anthracycline-based NCT. CD10 expression was assessed by immunohistochemistry on pre-treatment biopsies. Statistical analysis evaluated the association between CD10 expression and pCR rates.</p></div><div><h3>Results</h3><p>Univariate analysis revealed that ER-positive and CD10-negative tumors had lower pCR rates [OR 7.4830 (95% CI 2.7762–20.1699); <em>p</em> = 0.0001]. Multivariate analysis confirmed ER status as a strong predictor of poor response [OR 0.085 (95% CI 0.024–0.30); <em>p</em> &lt; 0.001] and CD10 expression as a predictor of a favourable response [OR 0.11 (0.8–0.19); <em>p</em> = 0.049]. CD10 expression significantly predicted pCR in ER-negative cases [OR 0.1098 (0.0268–0.4503); <em>p</em> = 0.0022] and triple-negative breast cancer [OR 0.0966 (95% CI 0.0270–0.3462); <em>p</em> = 0.0003]. Concordance was observed between core biopsies and excised samples.</p></div><div><h3>Conclusion</h3><p>Positive CD10 cancer cell expression may predict increased response to anthracycline-based neoadjuvant chemotherapy in ER-negative and triple-negative breast cancer cases. Further research is needed to validate these findings in larger cohorts and determine the clinical utility of CD10 as a predictive marker.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480024000042/pdfft?md5=aefb1618026e0da730b2791cf9888988&pid=1-s2.0-S0014480024000042-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139569804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interleukin 6 polymorphisms are associated with cardiovascular risk factors in premature coronary artery disease patients and healthy controls of the GEA Mexican study","authors":"Rosalinda Posadas-Sánchez ,&nbsp;Ángel Rene López-Uribe ,&nbsp;José Manuel Fragoso ,&nbsp;Gilberto Vargas-Alarcón","doi":"10.1016/j.yexmp.2024.104886","DOIUrl":"10.1016/j.yexmp.2024.104886","url":null,"abstract":"<div><h3>Background and aims</h3><p>Interleukin-6 (IL-6) is an acute-phase protein that plays an important role in the inflammatory response, vascular inflammation, and atherosclerosis process. The study aimed to establish whether <em>IL-6</em> gene polymorphisms and IL-6 concentrations are associated with premature coronary artery disease (pCAD) and cardiovascular risk factors.</p></div><div><h3>Methods</h3><p>The IL-6 concentrations and the rs2069827, rs1800796, and rs1800795 IL-6 polymorphisms were determined in 1150 pCAD patients and 1083 healthy controls (coronary artery calcium equal to zero determined by tomography).</p></div><div><h3>Results</h3><p>The <em>IL-6</em> polymorphisms studied were not associated with pCAD, but they were associated with cardiovascular risk factors in patients and controls. In controls, under the dominant model, the rs1800795 <em>C</em> allele and the rs2069827 <em>T</em> allele were associated with a low risk of central obesity (OR = 0.401, <em>p</em> = 0.017 and OR = 0.577, <em>p</em> = 0.031, respectively), hypoalphalipoproteinemia (OR = 0.581, <em>p</em> = 0.027 and OR = 0.700, <em>p</em> = 0.014, respectively) and hypertriglyceridemia (OR = 0.575, <em>p</em> = 0.030 and OR = 0.728, <em>p</em> = 0.033, respectively). In pCAD, the rs1800795 <em>C</em> allele was associated with an increased risk of hypoalphalipoproteinemia (OR = 1.370, <em>p</em>_additive = 0.025) and increased C-reactive protein (CRP) concentrations (OR = 1.491, <em>p</em>_additive = 0.007). pCAD patients had significantly higher serum IL-6 concentrations compared to controls (<em>p</em> = 0.002). In the total population, individuals carrying the rs1800795 <em>GC + CC</em> genotypes had higher levels of IL-6 than carriers of the <em>GG</em> genotype (<em>p</em> = 0.025). In control individuals carrying the <em>C</em> allele (<em>CG + CC</em>), an inverse correlation was observed between IL-6 and HDL-cholesterol levels (<em>p</em> = 0.003).</p></div><div><h3>Conclusions</h3><p>In summary, the <em>IL-6</em> polymorphisms were not associated with pCAD, however, they were associated with cardiovascular risk factors in pCAD patients and healthy controls. Individuals carrying the rs1800795 <em>GC + CC</em> genotypes had higher levels of IL-6 than carriers of the <em>GG</em> genotype.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480024000054/pdfft?md5=cca370e10e0d5fbb3a699bf21646d904&pid=1-s2.0-S0014480024000054-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139641949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental physical factors produce mitotic aberration and multicellularity in the ovarian cancer cell line SKOV3.","authors":"N Lujea, F Chiola, M De Leon Rodriguez, C Acosta, P Kunda","doi":"10.1016/j.yexmp.2024.104884","DOIUrl":"https://doi.org/10.1016/j.yexmp.2024.104884","url":null,"abstract":"<p><p>The spread of ovarian cancer (OC) to the coelomic cavity triggers the secretion and accumulation of ascitic fluid (AF). Although its biochemical composition has been well studied, less is known about the implications of physical factors such as the pH and the mechanical properties of the AF for the malignancy of tumor cells. In this work, we investigated the effect of pH and the mechanical properties of AF on cell proliferation and mitotic morphology. We employed biopsies from patients with OC and the SKOV3 cell line as an in vitro model of OC with HeLa cells as controls. Sections of each tumor were stained with HE, analyzed, and related to clinical data. AF from patients with OC exhibited an alkaline pH (ranging from 7.3 to 7.8). Compared to control conditions, the 3 AFs significantly enhanced the proliferation of SKOV3 and HeLa cells. These effects were more pronounced at a more alkaline pH. In addition, we found that AFs have different densities that correlated with a significant increase in multinucleated tumor cells and severe morphological defects in cells undergoing mitosis. In agreement with these data, we found that higher concentrations of soft agar provoked significantly higher numbers of multinucleated and morphologically abnormal SKOV3 cells with no effect on HeLa cells. We conclude that an alkaline pH and greater rigidity could enhance the metastatic potential of OC cells. We propose that these two physical factors could be parameters of clinical importance as predictors of malignancy.</p>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139575028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An in-silico analysis reveals further evidence of an aggressive subset of lung carcinoids sharing molecular features of high-grade neuroendocrine neoplasms","authors":"Giuseppe Pelosi ,&nbsp;Valentina Melocchi ,&nbsp;Elisa Dama ,&nbsp;Paul Hofman ,&nbsp;Marco De Luca ,&nbsp;Adriana Albini ,&nbsp;Maria Gemelli ,&nbsp;Riccardo Ricotta ,&nbsp;Mauro Papotti ,&nbsp;Stefano La Rosa ,&nbsp;Silvia Uccella ,&nbsp;Sergio Harari ,&nbsp;Angelica Sonzogni ,&nbsp;Michael K. Asiedu ,&nbsp;Dennis A. Wigle ,&nbsp;Fabrizio Bianchi","doi":"10.1016/j.yexmp.2024.104882","DOIUrl":"10.1016/j.yexmp.2024.104882","url":null,"abstract":"<div><p>Little is known as to whether there may be any pathogenetic link between pulmonary carcinoids and neuroendocrine carcinomas (NECs). A gene signature we previously found to cluster pulmonary carcinoids, large cell neuroendocrine carcinoma (LCNEC) and small cell lung carcinoma (SCLC), and which encompassed <em>MEN1, MYC, MYCL1, RICTOR, RB1, SDHA, SRC</em> and <em>TP53 mutations or</em> copy number variations (CNVs), was used to reclassify an independent cohort of 54 neuroendocrine neoplasms (NENs) [31 typical carcinoids (TC), 11 atypical carcinoids (AC) and 12 SCLC], by means of transcriptome and mutation data. Unsupervised clustering analysis identified two histology-independent clusters, namely CL1 and CL2, where 17/42 (40.5%) carcinoids and all the SCLC samples fell into the latter. CL2 carcinoids affected survival adversely, were enriched in T to G transversions or T &gt; C/C &gt; T transitions in the context of specific mutational signatures, presented with at least 1.5-fold change (FC) increase of gene mutations including <em>TSC2</em>, <em>SMARCA2</em>, <em>SMARCA4</em>, <em>ERBB4</em> and <em>PTPRZ1</em>, differed for gene expression and showed epigenetic changes in charge of <em>MYC</em> and <em>MTORC1</em> pathways, cellular senescence, inflammation, high-plasticity cell state and immune system exhaustion. Similar results were also found in two other independent validation sets comprising 101 lung NENs (24 carcinoids, 21 SCLC and 56 LCNEC) and 30 carcinoids, respectively. We herein confirmed an unexpected sharing of molecular traits along the spectrum of lung NENs, with a subset of genomically distinct aggressive carcinoids sharing molecular features of high-grade neuroendocrine neoplasms.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480024000017/pdfft?md5=8e18b58028ce704033d84572f79c139a&pid=1-s2.0-S0014480024000017-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139490897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Overexpression of cortistatin alleviates oxygen/glucose-deprivation-induced ER stress and prompts neural stem cell proliferation via SSTR2” [Experimental and Molecular Pathology 113 (2020) 104351]","authors":"Xiulin Liang ,&nbsp;Qing Mao ,&nbsp;Donghong Huang ,&nbsp;Jian Tang ,&nbsp;Jinou Zheng","doi":"10.1016/j.yexmp.2023.104878","DOIUrl":"10.1016/j.yexmp.2023.104878","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000291/pdfft?md5=0797031bcbde4b163b182d3b0d74ee57&pid=1-s2.0-S0014480023000291-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “RAB5A effect on metastasis of hepatocellular carcinoma cell line via altering the pro-invasive content of exosomes” [Experimental and Molecular Pathology 120 (2021) 104632]","authors":"Gilar Gorji-bahri ,&nbsp;Hamid Reza Moghimi ,&nbsp;Atieh Hashemi","doi":"10.1016/j.yexmp.2023.104875","DOIUrl":"10.1016/j.yexmp.2023.104875","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000266/pdfft?md5=45747e089facf4745939789bb527ce74&pid=1-s2.0-S0014480023000266-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71479852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roots remain","authors":"Marco Giudici","doi":"10.1016/j.yexmp.2023.104868","DOIUrl":"10.1016/j.yexmp.2023.104868","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000199/pdfft?md5=c0749998321ac7271527465891af5bc8&pid=1-s2.0-S0014480023000199-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary exosomes from patients with diabetic kidney disease induced podocyte apoptosis via microRNA-145-5p/Srgap2 and the RhoA/ROCK pathway","authors":"Lulu Han ,&nbsp;Shenghai Wang ,&nbsp;Juan Li ,&nbsp;Lulu Zhao ,&nbsp;Hong Zhou","doi":"10.1016/j.yexmp.2023.104877","DOIUrl":"10.1016/j.yexmp.2023.104877","url":null,"abstract":"<div><p>Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease without early diagnostic and specific therapeutic approaches. Podocyte apoptosis and loss play important roles in the pathological process of DKD. This study aimed to explore whether urinary exosomes from type 2 diabetes patients with DKD could induce podocyte apoptosis and the underlying pathological mechanisms. The exosomes were isolated from the urine samples of patients with DKD (DKD-Exo). Later, they were taken up and internalized by MPC5 cells. MPC5 cells were co-cultured with DKD-Exo (45 μg/ml) for 24 h in the presence or absence of microRNA-145-5p (miR-145-5p) inhibitor, fasudil and pcDNA-Srgap2 transfection. MiR-145-5p and Srgap2 expression was evaluated using real-time quantitative PCR. The protein levels of Srgap2, Bcl-2, Bax, and cleaved caspase-3, as well as ROCK activity were determined using Western blotting. Cell apoptosis was measured using flow cytometry and the TUNEL assay. miR-145-5p expression in MPC5 cells exposed to DKD-Exo was markedly upregulated. miR-145-5p negatively regulated Srgap2 levels. Exposure of MPC5 cells to DKD-Exo reduced Srgap2 expression and activated ROCK, which was partly reversed by the presence of the miR-145-5p inhibitor or Srgap2 overexpression. The apoptosis of MPC5 cells exposed to DKD-Exo increased significantly, which was counteracted by the addition of the miR-145-5p inhibitor and fasudil. The results showed that urinary exosomal miR-145-5p from patients with DKD induced podocyte apoptosis by inhibiting Srgap2 and activating the RhoA/ROCK pathway, suggesting that urinary exosomal miR-145-5p is involved in the pathological process of DKD and could become a noninvasive diagnostic biomarker for DKD.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S001448002300028X/pdfft?md5=a627243501fc25972111af7d28ece93a&pid=1-s2.0-S001448002300028X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89717564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The MC160 protein of the molluscum contagiosum virus dampens cGAS/STING-induced interferon-β activation","authors":"Brian T. Reiss,&nbsp;Lissette Bouza,&nbsp;Swagath Thomas,&nbsp;Catherine D. Suarez,&nbsp;Erik R. Hill,&nbsp;Daniel Brian Nichols","doi":"10.1016/j.yexmp.2023.104876","DOIUrl":"10.1016/j.yexmp.2023.104876","url":null,"abstract":"<div><p>Molluscum contagiosum virus (MCV) is a poxvirus that causes benign, persistent skin lesions. MCV encodes a variety of immune evasion molecules to dampen host immune responses. Two of these proteins are the MC159 and MC160 proteins. Both MC159 and MC160 contain two tandem death effector domains and share homology to the cellular FLIPs, FADD, and procaspase-8. MC159 and MC160 dampen several innate immune responses such as NF-κB activation and mitochondrial antiviral signaling (MAVS)-mediated induction of type 1 interferon (IFN). The type 1 IFN response is also activated by the cytosolic DNA sensors cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING). Both cGAS and STING play a vital role in sensing a poxvirus infection. In this study, we demonstrate that there are nuanced differences between both MC160 and MC159 in terms of how the viral proteins modulate the cGAS/STING and MAVS pathways. Specifically, MC160 expression, but not MC159 expression, dampens cGAS/STING-mediated induction of IFN in HEK 293 T cells. Further, MC160 expression prevented the K63-ubiquitination of both STING and TBK1, a kinase downstream of cGAS/STING. Ectopic expression of the MC160 protein, but not the MC159 protein, resulted in a measurable decrease in the TBK1 protein levels as detected via immunoblotting. Finally, using a panel of MC160 truncation mutants, we report that the MC160 protein requires both DEDs to inhibit cGAS/STING-induced activation of IFN-β. Our model indicates MC160 likely alters the TBK1 signaling complex to decrease IFN-β activation at the molecular intersection of the cGAS/STING and MAVS signaling pathways.</p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480023000278/pdfft?md5=33bae6cd6c463817b8ba12cb4dd26e62&pid=1-s2.0-S0014480023000278-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61561763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}