The Kaohsiung journal of medical sciences最新文献

{"title":"Disulfidptosis- and Ferroptosis-Related Gene Signatures in Rheumatoid Arthritis: Association Analysis and Diagnostic Model Construction.","authors":"Ting-Ting Wang, Dong-Mei Wang, Xue Li, Yuan-Li Wei, Ping-Dan Liu, Shi-Lin Li, Si-Ying Xiong, Cai-Zhen Liu, Fan-Xin Zeng, Jian-Hong Wu, Lin Tang","doi":"10.1002/kjm2.70287","DOIUrl":"10.1002/kjm2.70287","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint damage. Although ferroptosis has been implicated in RA progression, the role of disulfidptosis and its interaction with ferroptosis remains unclear. This study aimed to identify Disulfidptosis- and Ferroptosis-Related Genes (DFRGs) associated with RA and construct a candidate diagnostic model. Blood transcriptomic data from 154 RA patients and 43 healthy controls were analyzed. Differentially expressed DFRGs were identified, and immune infiltration was assessed using single-sample Gene Set Enrichment Analysis (ssGSEA). Feature genes were selected through correlation analysis and logistic regression, followed by construction of a diagnostic nomogram. External validation was performed using independent datasets. Potential regulatory miRNAs and therapeutic agents were predicted, and single-cell eQTL-based Mendelian randomization (MR) was used to evaluate genetic associations between core gene expression and RA risk. Eleven DFRGs were identified and were enriched in p53, mTOR, and immune-related pathways. Five feature genes, DUOX1, DRD4, ATP6V1G2, ASNS, and CDKN1A, were used to establish a diagnostic model with favorable performance in the training cohort and external validation datasets. Five key miRNAs and 61 potential therapeutic agents were predicted. MR suggested that ASNS expression may be protective, whereas ATP6V1G2 expression may increase RA risk. These findings suggest that DFRGs-related signatures may be involved in RA pathogenesis and immune dysregulation, although further in vitro and in vivo validation is required.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70287"},"PeriodicalIF":3.1,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a Nomogram-Based Clinical Estimation Model for Pathological Upstaging in Patients With Preoperative Ductal Carcinoma In Situ.","authors":"Yu-Hua Chen, Chung-Liang Li, Ping-Fu Yang, Hui-Hua Hsiao, Fang-Ming Chen, Sin-Hua Moi","doi":"10.1002/kjm2.70282","DOIUrl":"10.1002/kjm2.70282","url":null,"abstract":"<p><p>Preoperative diagnosis of ductal carcinoma in situ (DCIS) may be followed by pathological upstaging to invasive ductal carcinoma (IDC) upon surgical excision, a discrepancy that significantly impacts surgical planning and decisions regarding sentinel lymph node biopsy (SLNB). This retrospective study aimed to evaluate clinical indicators associated with such upstaging and develop a nomogram-based clinical estimation model for risk stratification. We reviewed medical records of all consecutively diagnosed patients (n = 445) initially diagnosed with DCIS via core needle biopsy (CNB) or vacuum-assisted biopsy (VAB) between 2013 and 2022 at a single institution. Demographic, imaging, clinicopathological, immunohistochemical, and blood-based biomarkers were categorized and analyzed. Logistic regression analysis was employed to identify independent predictors, from which a visual risk estimation tool was constructed. Among the 445 patients, 137 (30.8%) were upstaged to IDC. In the multivariable analysis, clinical tumor size > 1.5 cm, biopsy modality, and high histologic grade at biopsy emerged as independent predictors of pathological upstaging. Notably, VAB was associated with a lower rate of underestimation than CNB. Subgroup analyses revealed that age > 50 years, larger lesion size, and high grade were associated with upstaging in the CNB group, whereas histologic grade was the primary predictor in the VAB group. The nomogram demonstrated modest discriminative performance (AUC = 0.690) for individualized preoperative assessment. In conclusion, clinical tumor size, biopsy method, and histologic grade provide valuable information for estimating the likelihood of occult invasive disease in patients with preoperative DCIS.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70282"},"PeriodicalIF":3.1,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of RNA-Binding Protein ELAVL1 in Promoting Th2 Cell Differentiation Through Stabilizing CPA3 mRNA in Allergic Rhinitis.","authors":"Meng-Ya Liu, Hong-Bing Yao, Cheng Chen","doi":"10.1002/kjm2.70281","DOIUrl":"10.1002/kjm2.70281","url":null,"abstract":"<p><p>This study aimed to elucidate the role of the RNA-binding protein embryonic lethality abnormal vision-like protein 1 (ELAVL1) in the pathogenesis of allergic rhinitis (AR), specifically by investigating its potential to promote T helper 2 (Th2) cell differentiation by regulating the stability of carboxypeptidase A3 (CPA3) mRNA. Differentially expressed genes associated with AR were screened via bioinformatic analysis. Nasal mucosal tissues were collected from 42 children with AR and 42 healthy controls. CPA3 was significantly upregulated in the nasal mucosal tissues of AR patients. CD4⁺ T cells were isolated from the peripheral blood of healthy volunteers, polarized toward Th2 differentiation, and subjected to cell transfection experiments to examine the effect of CPA3 on Th2 differentiation. An ovalbumin (OVA)-induced AR mouse model was established. Knockdown of CPA3 alleviated nasal symptoms (e.g., scratching and sneezing), attenuated pathological damage in the nasal mucosa (characterized by reduced edema and inflammatory cell infiltration), and suppressed Th2 immune responses (decreased interleukin-4 and immunoglobulin E levels, reduced Th2 cell proportion, and downregulated GATA binding protein 3 expression) in AR mice. ELAVL1 bound to CPA3 mRNA and enhanced its stability, thereby upregulating CPA3 expression; a positive correlation was observed between their expression levels in AR. Overexpression of CPA3 reversed the alleviating effects of ELAVL1 knockdown on nasal symptoms and Th2 immune responses in AR mice. Taken together, these results demonstrate that targeting the ELAVL1/CPA3 axis may provide a novel therapeutic strategy for AR.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70281"},"PeriodicalIF":3.1,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13538276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148882339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomics-Based Identification of the Pyroptosis-Related Biomarker PCSK9 and Its Association With the Pathogenesis of Rheumatoid Arthritis.","authors":"Lei Wang, Hao-Jie Chen, Ting-Ting Wu, Xin-Yi Shen, Ying-Ying Gao, Yu-Feng Yin, Tian Ren, Xin Chu, Jing Cao, Tao Cheng, Ming-Jun Wang","doi":"10.1002/kjm2.70183","DOIUrl":"10.1002/kjm2.70183","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a common autoimmune disease, and early diagnosis is critical for effective treatment. This study aims to identify potential biomarkers related to pyroptosis through serum proteomics analysis, offering new insights for the early diagnosis of RA. We enrolled 100 participants, including 50 patients with RA and 50 healthy controls. Serum samples were collected and analyzed using high-resolution liquid chromatography-tandem mass spectrometry (LC-MS/MS) for proteomics profiling. Differential protein expression analysis and functional annotation revealed significant upregulation of pyroptosis-related proteins in the serum of patients with RA. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, along with protein-protein interaction (PPI) network analysis, showed that these proteins are involved in inflammation and immune pathways, particularly the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome. Enzyme-linked immunosorbent assay (ELISA) validation confirmed a significant increase in PCSK9 levels in patients with RA, suggesting that PCSK9 may play a key role in the pathogenesis of RA. This study provides new directions for biomarker research in RA, particularly regarding the potential involvement of the pyroptosis pathway, with significant clinical application prospects.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70183"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing Voice Outcomes After Recurrent Laryngeal Nerve Transection: The Role of Early and Supplemental Injection Laryngoplasty.","authors":"Luo-Wei Chan, Hsin-Yi Tseng, Che-Wei Wu, Tzu-Yen Huang","doi":"10.1002/kjm2.70185","DOIUrl":"10.1002/kjm2.70185","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70185"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399622/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147392180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBMX Transcriptionally Repressed by EZH2-Associated H3K27me3 Modification Attenuates Pyroptosis in Renal Ischemia/Reperfusion Injury via Regulating SIRT3/NLRP3 Inflammasome Activation.","authors":"Yi-Han Wang, Yan Teng, Fang-Lan Yao, Shu-Qi Wei, Yan Li","doi":"10.1002/kjm2.70188","DOIUrl":"10.1002/kjm2.70188","url":null,"abstract":"<p><p>Ischemic reperfusion injury (IRI) to kidney is a significant clinical factor in acute kidney injury (AKI). This study aimed to investigate the new role of RNA-binding motif protein X-linked (RBMX), a modulator of m6A methylation, in renal IRI and to examine the associated regulatory mechanisms. An in vitro renal IRI model was established using HK-2 cells subjected to hypoxia-reoxygenation (H/R) treatment. To investigate the role of RBMX, RBMX-overexpressing cells were transfected with pcDNA/RBMX. The viability of HK-2 cells was evaluated using the CCK-8 assay. EdU was utilized to evaluate cell proliferation in HK-2 cells. Western blot analysis was conducted to determine the expression levels of proteins involved in NLRP3 inflammasome activation. ELISA was used to measure the secretion of inflammatory cytokines linked to pyroptosis. LDH and PI staining were used to investigate pyroptosis. IP, RIP, and MeRIP assays were performed to detect NLRP3 acetylation and the interaction between NLRP3 and SIRT3. An in vivo IRI mouse model was established to further validate the renoprotective effect of RBMX. Our results showed that RBMX expression was significantly downregulated in IRI mice and in vitro H/R-treated HK-2 cells. In H/R-induced HK-2 cells, RBMX overexpression attenuated NLRP3 inflammasome activation and pyroptosis, shown by reduced expression levels of NLRP3, ASC, cleaved caspase-1, and GSDMD-N, along with decreased levels of IL-18, IL-1β, TNF-α, and IL-6. Additionally, RBMX is associated with the m6A methylation of SIRT3, which is involved in the control of NLRP3 acetylation and activation in H/R-exposed HK-2 cells. SIRT3 knockdown reversed the impacts of RBMX on cell proliferation, NLRP3 inflammasome activation, and pyroptosis. Moreover, EZH2 may be involved in an upstream gene that mediates the H3K27me3 modification of RBMX. Finally, in vivo assays provided evidence suggesting that RBMX overexpression improved renal injury in mice. Taken together, our data support a potential role of the m6A regulator RBMX in suppressing NLRP3 inflammasome activation and pyroptosis possibly through the regulation of m6A methylation of SIRT3 in renal IRI. We hypothesized that targeting the EZH2/RBMX/SIRT3 axis might represent a new therapeutic approach to impede the progression of renal IRI.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70188"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRDM1 Knockdown Promotes Ferroptosis and Sunitinib Sensitivity by Modulating the PI3K/Akt Signaling Through Inhibition of ESM1 Transcription in Renal Cell Carcinoma.","authors":"Yi-Shuai Zhang, Xin-Qi Pei, Ji-Ping Sun, Chen-Hui Ma, Xin-Yang Wang, Xu-Dong Li","doi":"10.1002/kjm2.70187","DOIUrl":"10.1002/kjm2.70187","url":null,"abstract":"<p><p>Renal cell carcinoma (RCC) is a commonly occurring and considerable burden on public health. Although chemotherapy benefits patients with advanced RCC, sunitinib resistance leads to a poor prognosis. Ferroptosis is also involved in sunitinib resistance in RCC. PR domain-containing protein 1 with a zinc finger domain (PRDM1) is a tumor regulator in many types of cancer. However, its biological function in RCC has not been reported. This study aimed to investigate the role of PRDM1 in ferroptosis and sunitinib resistance in RCC and explore the underlying mechanisms. Bioinformatics analysis was performed to analyze the expression of related genes in RCC. PRDM1-silencing and overexpressing cells were constructed to confirm the role of PRDM1 in RCC in vitro. Our results showed that PRDM1 expression was markedly upregulated in RCC tissues and cell lines. PRDM1 knockdown significantly induced ferroptosis in RCC cells. Furthermore, knockdown of PRDM1 elevated the sensitivity of RCC cell lines to Mechanistically, PRDM1 directly bound to ESM1 and regulated its transcription. Subsequently, ESM1 overexpression reversed the effects of si-PRDM1 on ferroptosis and sunitinib sensitivity in RCC cells, and these effects were mitigated by a PI3K inhibitor. Finally, PRDM knockdown exhibited anti-tumor effects in a xenograft animal model. Taken together, our study shows that PRDM1 silencing promotes ferroptosis and sunitinib sensitivity by inhibiting ESM1 transcription and modulating PI3K/Akt signaling in RCC. Our findings thus provide novel insights for therapeutically targeting RCC.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70187"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146204320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncogenic KRAS Rewires Stress Granule Dynamics: Mechanisms and Therapeutic Opportunities.","authors":"Msimisi Ndzinisa, Birhanetensay Masresha Altaye, Yuh-Pyng Sher","doi":"10.1002/kjm2.70196","DOIUrl":"10.1002/kjm2.70196","url":null,"abstract":"<p><p>Stress granules (SGs) are dynamic, membrane-less structures that form in response to various cellular stresses, including metabolic, oxidative, and therapeutic challenges. They function as adaptive hubs and reorganize protein synthesis and signaling networks to help cells survive under stress. In cancer, these condensates are often hijacked to support survival and therapy resistance. SGs can sequester proapoptotic factors, buffer metabolic- and treatment-induced stress, and stabilize transcripts that promote cell survival, collectively contributing to tumor aggressiveness and resistance to therapy. Their formation relies on protein-RNA interactions, phase separation, and posttranslational modifications, which tumor cells exploit to maintain SGs even when normal stress conditions trigger their disassembly. This creates a protective pool of mRNAs and proteins that allows rapid adaptation to stress. Emerging therapeutic strategies that disrupt SG assembly, interfere with the adaptive functions of SGs, or accelerate SG clearance have shown promise in sensitizing tumors to treatment. This review summarizes the current understanding of SG dynamics, illustrating how cancer cells exploit these structures to survive stress. We focus specifically on KRAS-driven cancers, where persistent oncogenic signaling enhances SG formation and stability, making these condensates critical mediators of tumor adaptation. Targeting SG formation, maintenance, or associated stress-response pathways represents a promising approach to enhance therapeutic efficacy and improve long-term outcomes in cancers driven by sustained cellular stress.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70196"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent Pulmonary Atelectasis After Tracheoesophageal Fistula Repair: Diagnostic Challenge of a Communicating Bronchopulmonary Foregut Malformation Group 1a in a Neonate With VACTERL Association.","authors":"Tien-Pai Huang, Twei-Shiun Jaw, Yu-Tang Chang, Yu-Han Chen","doi":"10.1002/kjm2.70184","DOIUrl":"10.1002/kjm2.70184","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70184"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL14 Ameliorates Mitochondrial Dysfunction and Autophagy in Lens Epithelial Cells of Diabetic Cataracts via m6A Modification of RPL3.","authors":"Rui Li, Xue Wang, Wei Du, Qian Li, Hong-Ping Cui","doi":"10.1002/kjm2.70194","DOIUrl":"10.1002/kjm2.70194","url":null,"abstract":"<p><p>Diabetic cataracts are a leading cause of blindness, with lens epithelial cells (LECs) exhibiting mitochondrial dysfunction and autophagy inhibition under high glucose (HG) conditions. Methyltransferase-like 14 (METTL14), an RNA methyltransferase, regulates N6-methyladenosine (m6A) RNA modification; however, its role in modulating mitochondrial function and autophagy in LECs under diabetic conditions remains poorly understood. This study aims to explore the effects of METTL14 on mitochondrial dysfunction and autophagy in LECs under HG conditions and to investigate the underlying mechanism involving m6A modification of ribosomal protein L3 (RPL3). Primary LECs exposed to HG showed reduced viability, increased reactive oxygen species (ROS), decreased adenosine triphosphate (ATP) levels, and loss of mitochondrial membrane potential (MMP), alongside suppressed autophagy. Knockdown of METTL14 worsened these deficits, while METTL14 overexpression alleviated them. Mechanistically, METTL14 increased m6A modification on RPL3 mRNA, enhancing RPL3 expression. Overexpressing RPL3 improved mitochondrial function, whereas knocking down RPL3 abolished the protective effects of METTL14 overexpression. In diabetic mouse models, adeno-associated virus (AAV)-mediated METTL14 overexpression improved lens transparency and reduced oxidative stress, benefits that were reversed by concurrent RPL3 knockdown. In conclusion, METTL14 mitigates HG-induced mitochondrial dysfunction and autophagy inhibition in LECs by promoting m6A-dependent upregulation of RPL3, identifying the METTL14/RPL3 axis as a promising target for diabetic cataract therapy.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70194"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147825382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}