Pathology, research and practice最新文献

{"title":"CircRNA hsa_circ_0001946 promotes hypertrophic scar pathogenesis via the miR-514a-3p/COL5A2 axis.","authors":"Yi Shi, Yajuan Song, Tong Wang, Yan Jiao, Yufei Zhang, Shu'ao Xiao, Baoqiang Song, Zhou Yu","doi":"10.1016/j.prp.2026.156641","DOIUrl":"10.1016/j.prp.2026.156641","url":null,"abstract":"<p><p>Hypertrophic scars (HSs) represent a fibroproliferative disorder characterized by excessive extracellular matrix deposition. However, the underlying regulatory mechanisms involving circular RNAs (circRNAs) have not yet been fully elucidated. This study aimed to delineate the circRNA expression landscape in HS and reveal the functional roles of a specific candidate circRNA through the competing endogenous RNA (ceRNA) network. Eighty-one differentially expressed circRNAs (DEcircRNAs) were identified in five paired HS and normal skin samples by high-throughput sequencing. Functional enrichment analysis of host genes highlighted pathways involving cell proliferation and ECM-receptor interactions. CircRNA-miRNA-mRNA network analysis revealed hsa_circ_0001946 as a significantly upregulated candidate circRNA. Subsequent RT-qPCR validated its elevation in human HS tissues and hypertrophic scar fibroblasts (HSFs). Subcellular fractionation and RNase R assays confirmed its cytoplasmic localization and circular stability. Functionally, knockdown of hsa_circ_0001946 significantly inhibited HSF proliferation, migration, and collagen gel contraction. Mechanistically, dual-luciferase reporter assays demonstrated that hsa_circ_0001946 acts as a sponge for miR-514a-3p; notably, silencing hsa_circ_0001946 attenuated the pro-fibrotic effects induced by miR-514a-3p inhibition. Furthermore, miR-514a-3p was shown to directly target and suppress COL5A2. Collectively, these findings establish that hsa_circ_0001946 promotes HS development by sequestering miR-514a-3p to derepress COL5A2 expression. This study identifies the hsa_circ_0001946/miR-514a-3p/COL5A2 axis as a novel pathogenic mechanism contributing to HS formation, suggesting hsa_circ_0001946 as a promising intervention target for mitigating pathological scarring.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"286 ","pages":"156641"},"PeriodicalIF":3.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685371","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":"Association of myocardial injury with adverse long-term survival among patients with sarcopenia.","authors":"Wenyuan Ding, Yilu Hou, Shanbo Ma, Hui Qu","doi":"10.1016/j.prp.2026.156682","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156682","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is an age-related progressive syndrome characterized by reductions in skeletal muscle mass, decreased muscle strength, and impaired physical performance. Although sarcopenia has been correlated with elevated CVD risk, the prognostic impact of myocardial injury, measured by high‑sensitivity cardiac troponin (hs‑cTn), on extended outcomes in individuals with sarcopenia remains unclear. This study sought to determine the extent to which myocardial injury is associated with all‑cause and CVD mortality among adults with sarcopenia.</p><p><strong>Methods: </strong>We obtained data from NHANES 1999-2004. Sarcopenia was defined as an appendicular lean mass (ALM)-to-body mass index (BMI) ratio of < 0.789 for men and < 0.512 for women. Myocardial injury was defined as any hs‑cTn assay result above the sex‑specific 99th percentile across the Roche hs‑cTnT, Abbott hs‑cTnI, Siemens hs‑cTnI, and Ortho hs‑cTnI platforms. Weighted Cox models yielded hazard ratios (HRs) and 95%CI, and Fine‑Gray models accounted for competing non‑CVD deaths. Sensitivity analyses were run to exclude baseline CVD cases or deaths within two years of enrollment. Sex, race, income, smoking, drinking, BMI, and education were used as stratification variables in subgroup analyses.</p><p><strong>Results: </strong>Among 1061 sarcopenic adults, 306 had myocardial injury. These individuals were older with higher burdens of hypertension, diabetes, and prior CVD. Over median 188‑month follow‑up, the myocardial injury group showed lower survival probability (P < 0.001). After full adjustment, myocardial injury was independently associated with all‑cause (HR=1.88; 95%CI:1.41, 2.49) and CVD mortality (HR=2.19; 95%CI:1.34, 3.59). Excluding baseline CVD raised the CVD‑death HR to 2.64(1.48, 4.71); excluding 2‑year deaths yielded all‑cause HR = 1.68 (1.12, 2.53) and CVD‑death HR = 2.49 (1.33, 4.67). Subgroup analyses showed consistent effects across most strata (all P for interaction > 0.05), except for education (P for interaction=0.031).</p><p><strong>Conclusions: </strong>Myocardial injury was present in approximately 27% of sarcopenic adults and was independently associated with increased risks of all-cause and cardiovascular mortality. The associations remained robust across sensitivity analyses and were generally consistent across subgroups. These findings suggest that myocardial injury may provide prognostic information beyond conventional risk factors in adults with sarcopenia.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"288 ","pages":"156682"},"PeriodicalIF":3.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897635","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":"Pan-cancer landscape of APEX1 expression and genomic alterations: Associations with clinical outcomes and functional validation in lung cancer.","authors":"Wen-Ping Kong, Yan Ye, Yuan-Hui Ren, Li-Ting Lai","doi":"10.1016/j.prp.2026.156666","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156666","url":null,"abstract":"<p><p>This pan-cancer study systematically evaluated APEX1 expression, genomic alteration status, and prognostic value across 13,270 tumors and 2544 normal tissues from TCGA and GTEx. APEX1 overexpression was prominent in bladder, breast, and colon adenocarcinomas and correlated with advanced tumor stages and survival outcomes in a cancer-type-specific manner, with unfavorable associations in selected tumor contexts and an opposite favorable association in KIRC. Low-frequency APEX1 genomic alterations require cautious interpretation and may be associated with adverse outcomes in selected tumor contexts. Statistical methods including t-tests, ANOVA, Cox regression, Benjamini-Hochberg false-discovery rate correction for cohort-wise OS analyses, and log-rank tests were used to correlate APEX1 expression or alteration status with survival outcomes. The findings suggest that APEX1 expression and low-frequency genomic alterations are associated with tumor progression and worse patient outcomes in selected cancer contexts. This study supports APEX1 as a candidate prognostic indicator requiring further validation and suggests its potential value for future clinical stratification research. The pan-cancer approach improves contextual breadth, and the large sample size adds robustness. The observed relevance of APEX1 across malignancies supports further evaluation of its value for risk stratification and treatment planning. Future prospective studies are needed to validate its clinical utility. This work contributes to the growing field of DNA repair-related biomarkers and may inform future studies of APEX1-targeted therapeutic strategies.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"288 ","pages":"156666"},"PeriodicalIF":3.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892326","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":"Corrigendum to \"Low-frequency pulsed electromagnetic fields inhibit the NETs/PADI4/MFN2 axis to ameliorate BMSC senescence in the treatment of rheumatoid arthritis\" [Pathol. - Res. Pract. 286 (2026) 156620].","authors":"Qinfeng Lyu, Gang Chen, Longfei Chen, Yun Fan","doi":"10.1016/j.prp.2026.156664","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156664","url":null,"abstract":"","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":" ","pages":"156664"},"PeriodicalIF":3.7,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759837","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":"Corrigendum to \"An MRI radiomics approach to predict the efficacy of chemotherapy for osteosarcoma\", [Pathol. - Res. Pract., 277(2026) /156279].","authors":"Danna Liu, Xue Zhou, Yixiong Liu, Hong Wang, Jixin Liu, Zhengyuan Li, Yanfei Liu, Xin Hou, Yuewen Hao","doi":"10.1016/j.prp.2026.156632","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156632","url":null,"abstract":"","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":" ","pages":"156632"},"PeriodicalIF":3.7,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584659","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":"B4GALNT4 promotes lung cancer progression by suppressing ferroptosis through glycosylation of SLC7A11","authors":"Song Wu ,&nbsp;Rongrong Shen ,&nbsp;Shaofei Cheng ,&nbsp;Zhengyang Fan ,&nbsp;Hongyang Sang ,&nbsp;Qianping Li","doi":"10.1016/j.prp.2026.156548","DOIUrl":"10.1016/j.prp.2026.156548","url":null,"abstract":"<div><div>β-1,4-N-acetylgalactosaminyltransferase 4 (B4GALNT4) catalyzes LacdiNAc glycan synthesis and is implicated in multiple cancers; however, its role in lung cancer remains unclear. This study aimed to investigate the clinical relevance, biological impact, and regulatory pathways of B4GALNT4 in lung cancer. B4GALNT4 expression across 33 cancers was analyzed using Gene Expression Profiling Interactive Analysis, and its level, prognostic relevance, and pathways enrichment in lung cancer were further assessed. Its effects on cell viability, cell cycle, and ferroptosis were evaluated with gain- and loss-of-function assays. Co-immunoprecipitation, protein stability assays, immunofluorescence, and Western and lectin blotting were performed to identify whether B4GALNT4 regulates solute carrier family 7 member 11 (SLC7A11) glycosylation. Rescue experiments were conducted to verify whether B4GALNT4 affected the malignant proliferation phenotype via the SLC7A11-mediated ferroptosis pathway. B4GALNT4 is upregulated, and its upregulation is associated with a worse prognosis in lung cancer. Gene Set Enrichment Analysis demonstrated enrichment of proliferation and cell cycle pathways, alongside ferroptosis suppression in B4GALNT4 high-expression samples. Functional experiments revealed that B4GALNT4 knockdown significantly inhibited lung cancer cell viability by 25.6% and induced a 1.92-, 2.03-, 1.76-, and 4.29-fold increase in the cell proportion in G1 phase, intracellular Fe²⁺, malondialdehyde levels, and lipid reactive oxygen species production (<em>P</em> &lt; 0.001), respectively, which were reversed by Fer-1 <em>in vitro</em> (<em>P</em> &lt; 0.001) and <em>in vivo</em> (<em>P</em> &lt; 0.05). Conversely, B4GALNT4 overexpression improved the resistance of cells to ferroptosis (<em>P</em> &lt; 0.001). Mechanistically, we discovered that B4GALNT4 interacted with SLC7A11 and glycosylated it at residue N314. This N-glycosylation stabilized SLC7A11 and promoted membrane localization by blocking its degradation, which promoted cell viability and cell cycle progression and inhibited ferroptosis. Our findings establish B4GALNT4 as a critical regulator of lung cancer through SLC7A11 glycosylation, indicating that B4GALNT4 and SLC7A11 serve as potential therapeutic targets for lung cancer.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"285 ","pages":"Article 156548"},"PeriodicalIF":3.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148000389","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":"YAP-induced BICD1 promotes hepatocellular carcinoma cell proliferation, stemness, and migration by facilitating the nuclear translocation of HIF-1α.","authors":"Yezhen Jiang, Siying Jia, Chengquan Zhang, Lei Zhang, Kangsheng Tu, Qingguang Liu","doi":"10.1016/j.prp.2026.156540","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156540","url":null,"abstract":"<p><p>Treatment options for hepatocellular carcinoma (HCC) remain limited, and patient prognosis is generally poor. Therefore, elucidating the molecular mechanisms underlying HCC initiation and progression is critical for identifying novel therapeutic targets. Our previous study demonstrated that BICD cargo adaptor 1 (BICD1) was upregulated in HCC and functioned as a tumor promoter. However, the upstream regulators of BICD1 expression and the molecular basis of its pro-tumorigenic effects remain unclear. In this study, we identified Yes-associated protein (YAP) as a positive regulator of BICD1 in HCC. Mechanistically, YAP directly bound to the BICD1 promoter and enhanced its transcriptional activity. BICD1 expression was positively correlated with YAP, connective tissue growth factor (CTGF), and cysteine-rich angiogenic inducer 61 (CYR61) in HCC tissues. Functionally, BICD1 knockdown significantly attenuated hypoxia-induced proliferation, sphere formation, and migration of HCC cells, whereas BICD1 overexpression enhanced these phenotypes. In addition, BICD1 depletion markedly suppressed tumor initiation and growth in a nude mouse model. Further mechanistic investigations revealed that BICD1 interacted with hypoxia-inducible factor-1α (HIF-1α) via its C-terminal CC3 domain, thereby promoting HIF-1α nuclear translocation and transcriptional activity in HCC cells. Notably, AKT activation or knockdown of glycogen synthase kinase 3β (GSK3β) significantly enhanced the interaction between BICD1 and HIF-1α, thereby increasing HIF-1α transcriptional activity. Collectively, these findings demonstrate that YAP-driven BICD1 expression facilitates HIF-1α nuclear translocation and activation of downstream target genes, thereby promoting hypoxia-induced proliferation, stemness, and migration in HCC. This study highlights the YAP-BICD1-HIF-1α axis as a potential therapeutic target in HCC.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":" ","pages":"156540"},"PeriodicalIF":3.2,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974585","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":"Granulocytic myeloid derived suppressor cells derived extracellular vesicles ameliorate DSS-induced colitis via modulation of Th17/Treg balance","authors":"Juan Liu ,&nbsp;Chinenye Jane Ugwah-Oguejiofor ,&nbsp;Ling Zhu","doi":"10.1016/j.prp.2026.156405","DOIUrl":"10.1016/j.prp.2026.156405","url":null,"abstract":"<div><div>Colitis is closely associated with immune system dysregulation in the gastrointestinal tract. The present study aimed to evaluate the impact of Granulocytic Myeloid-Derived Suppressor Cells (G-MDSCs)-derived extracellular vesicles (EVs) on disease activity and the immunologic profile in a murine model of colitis. G-MDSCs-EVs were administered to colitis-bearing mice and were evaluated for changes in body weight, disease activity index, colon histopathology, frequencies of Th17 and Tregs, and cytokine release from lymphocytes. The impact of G-MDSCs-EVs was also evaluated on the expression of immune-response-related genes and the intestinal microbiome. G-MDSCs-EVs prevented body weight loss and controlled the disease activity index on day 10. This treatment improved the Treg population along with a decrease in the release of IL-6, IL-17A, and IFN-γ from lymphocytes. Treatment with G-MDSCs-EVs modulated immune-response-related gene expression and influenced the gut microbiota and colon histopathology. G-MDSCs-EVs demonstrated a preliminary potential in expanding the Treg population and upregulating immunoregulatory cytokines, which contributed to improvements in disease activity index and histopathology of the affected tissue.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"281 ","pages":"Article 156405"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146196842","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":"Modulation of AKT/GSK-3β signaling by ambrisentan alleviates chronic kidney disease","authors":"Rohan Bhadange,&nbsp;Anil Bhanudas Gaikwad","doi":"10.1016/j.prp.2026.156402","DOIUrl":"10.1016/j.prp.2026.156402","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is a progressive disease leading to severe health complications. Repurposing of existing drugs offers an attractive avenue for advancing drug development in CKD. Ambrisentan (AMB), a selective ET-1_A receptor antagonist used in pulmonary arterial hypertension, holds promise in CKD management. Hence, we aimed to investigate the potential of AMB in unilateral ureteral obstruction (UUO)-induced kidney fibrosis in Sprague-Dawley rats and in recombinant human-transforming growth factor-β1 (rh-TGF-β1)-induced fibrosis in NRK-52E cells. Animals were randomly assigned to the sham, UUO, and UUO + AMB (0.5 mg/kg, <em>p.o., o.d.</em>) groups for 21 days. Animals were sacrificed post-treatment, and plasma, urine, and kidney specimens were collected for biochemistry, histology, immunohistochemistry and qRT-PCR. Moreover, NRK-52E cells were exposed to AMB (100 µM) for 48 h and cell samples were collected for cell viability, morphology, immunocytochemistry, immunoblotting, and flow cytometry assays. AMB treatment significantly improves the left kidney weight, kidney mass ratio, kidney function parameters, and plasma protein levels of TGF-β1 and collagen I. Histopathology revealed that AMB treatment significantly preserved kidney histoarchitecture and interstitial fibrosis in UUO kidneys. Mechanistically, AMB suppressed phosphorylation of AKT and GSK-3β, downregulated α-SMA, vimentin and restored E-cadherin expression as shown by immunocytochemistry, immunohistochemistry and immunoblotting assay. Furthermore, AMB mitigated rh-TGF-β1-induced apoptosis, as assessed by flow cytometry, and modulated Bax, Bcl-2, and cleaved caspase-3 expression, as revealed by qRT-PCR and immunohistochemistry. Collectively, the findings indicate that the AMB modulates the AKT/GSK-3β axis, halting fibrotic progression in CKD, suggesting its clinical potential.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"281 ","pages":"Article 156402"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146196841","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":"TFAP2A facilitates aerobic glycolysis and metastasis of pancreatic cancer via IGF2BP2-mediated LDHA m6A modification","authors":"Zhiying Xu,&nbsp;Xingyang Zhong,&nbsp;Zhishi Yang,&nbsp;Zhuangzhi Cong,&nbsp;Lianwei Peng,&nbsp;Qifei Zou","doi":"10.1016/j.prp.2026.156387","DOIUrl":"10.1016/j.prp.2026.156387","url":null,"abstract":"<div><div>The hallmark of aerobic glycolysis in cancer progression is well-established, yet its specific role in pancreatic cancer (PC) remains elusive. Here, we reported that TFAP2A is upregulated in PC tissues, and elevated TFAP2A expression correlates with poor prognosis in patients. Functionally, we found that TFAP2A boosted the viability, invasion, and migration of PC cells <em>in vitro</em>, whereas TFAP2A depletion restrained tumor growth <em>in vivo</em>. Moreover, TFAP2A knockdown hindered aerobic glycolysis of PC cells. Further investigation revealed that TFAP2A deletion decreased LDHA expression in PC cells. LDHA overexpression counteracted the impacts of TFAP2A deletion on cell viability, migration, invasion, and aerobic glycolysis. Mechanistically, TFAP2A was directly bound to the promoter of IGF2BP2, upregulating its expression. Additionally, IGF2BP2 was found to bind to the m⁶A site in LDHA mRNA, thereby enhancing its stability. Overall, TFAP2A facilitated aerobic glycolysis and PC progression via IGF2BP2-mediated stabilization of LDHA mRNA, providing novel insights for PC therapy.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"280 ","pages":"Article 156387"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146132634","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}