{"title":"IRF3 Promotes Asthma Pathogenesis by Regulating Type 2 Innate Lymphoid Cells.","authors":"Zihao Liang, Zixin Chen, Jinwei Chen, Yunfan Zhou, Hua Chen, Meimei Gu, Dehong Yan, Qiong Yang","doi":"10.1080/08820139.2024.2418935","DOIUrl":"10.1080/08820139.2024.2418935","url":null,"abstract":"<p><strong>Background: </strong>Allergic asthma is characterized by airway hyperresponsiveness triggered by inhaled allergens. Type 2 innate lymphoid cells (ILC2s) have been demonstrated to play a crucial role in promoting airway inflammation through the secretion of type 2 effector cytokines. However, the mechanisms underlying the functions of lung ILC2s remain unclear.</p><p><strong>Methods: </strong>In this study, we investigated the expression of <i>IRF3</i> in ILC2s in both human patients and mouse models of asthma. We utilized <i>IRF3</i>-deficient mice to assess the impact of <i>IRF3</i> deficiency on ILC2 function in a model of IL33-induced asthma. Additionally, we explored the mechanisms underlying <i>IRF3</i>-mediated regulation of ILC2s, focusing on the involvement of the transcription factor Gata3.</p><p><strong>Results: </strong>Our findings revealed elevated expression of <i>IRF3</i> in ILC2s of patients and mice with asthma, suggesting a potential role for <i>IRF3</i> in the pathogenesis of allergic asthma. Furthermore, we demonstrated that <i>IRF3</i> deficiency impairedthe expansion and function of ILC2s in IL33-induced asthma, highlighting the importance of <i>IRF3</i> in regulating ILC2-mediated responses. Importantly, we showed that the regulation of ILC2s by <i>IRF3</i> was independent of Th2 cells and mediated by the transcription factor Gata3.</p><p><strong>Conclusion: </strong>This study identifies <i>IRF3</i> as a novel regulator of lung ILC2s and suggests its potential as a promising immunotherapeutic target for allergic asthma. These findings shed light on the intricate mechanisms underlying asthma pathogenesis and provide insights into potential strategies for the development of targeted therapies for this prevalent airway disease.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"83-96"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521815","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":"The Physiological and Therapeutic Role of CD47 in Macrophage Function and Cancer.","authors":"Shelby N Bess, Matthew J Igoe, Timothy J Muldoon","doi":"10.1080/08820139.2024.2415409","DOIUrl":"10.1080/08820139.2024.2415409","url":null,"abstract":"<p><strong>Background: </strong>Immunotherapy is an emerging strategy in cancer therapeutics aimed at modulating the immune system to inhibit pro-tumor pathways and increase a tumor's sensitivity to chemotherapy. Several clinically approved immunotherapy treatments, such as monoclonal antibody treatments, have been successful in solid tumors such as breast, colorectal, and pancreatic. However, an outstanding challenge of these strategies is tumor cell resistance. One target of interest for immune cell modulation is targeting macrophages that enter the tumor microenvironment. More specifically, an immune checkpoint of interest is CD47. CD47 is a transmembrane protein that inhibits phagocytic activity by acting as a \"don't eat me\" signal. In both mice and humans, healthy cells can express CD47, while solid malignancies like colorectal and breast cancer express it most strongly.</p><p><strong>Methods: </strong>Analysis of literature data on the physiological and functional roles of tissue-resident macrophages, along with the structure and mechanisms of action of the CD47 pathway was explored. We also explored how CD47 can influence different aspects of the tumor microenvironment (i.e. cellular metabolism and hypoxia) in addition to current clinical strategies and challenges associated with targeting CD47.</p><p><strong>Results: </strong>Overall, it was discovered that CD47 is overexpressed in a variety of cancer types in addition to normal tissue, making it a promising treatment regimen to enhance the capability of macrophages to phagocytose tumor cells. However, treatment efficacy is varied in pre-clinical and clinical models due to various challenges such as off-target effects.</p><p><strong>Conclusion: </strong>This review emphasizes the diverse functionality of macrophages in normal and cancerous tissue, while also emphasizing the importance of macrophage targeting and their clinical significance.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"112-146"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464242","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":"Cordycepin Alleviates Lipopolysaccharides-Induced Preeclampsia-Like Impairments in Rats.","authors":"Feng Jian, Xiao Zhang","doi":"10.1080/08820139.2024.2418572","DOIUrl":"10.1080/08820139.2024.2418572","url":null,"abstract":"<p><strong>Introduction: </strong>Preeclampsia is a serious pregnancy complication that can lead to life-threatening conditions such as seizures, strokes, and even death. A dysregulated inflammatory response in the placenta plays a crucial role in the development of preeclampsia. Cordycepin, known for its anti-inflammatory and antioxidant properties, was the focus of this study, which aimed to investigate its effects on preeclampsia.</p><p><strong>Methods: </strong>A preeclampsia-like rat model was established via tail vein injection of lipopolysaccharides (LPS) at a dose of 1 μg/kg in pregnant rats. These rats were then treated with cordycepin at doses of 5, 25, or 50 mg/kg from embryonic day 6 (E6) today 18 (E18). Systolic blood pressures and urinary protein levels were monitored, and pregnancy outcomes, such as fetal body length and weight, were measured. The expression of target genes or proteins was assessed by qPCR, ELISA, and Western blot.</p><p><strong>Results: </strong>Our findings revealed that cordycepin significantly reduced systolic blood pressure and proteinuria in preeclampsia-like rats. Additionally, cordycepin improved pregnancy outcomes, as shown by increased fetal body length and weight. The treatment also lowered serum sFlt-1 levels, elevated PIGF levels, decreased placental pro-inflammatory cytokine levels (IL-1β, TNF-α, IL-6, MCP-1, and MIP-2), and raised levels of anti-inflammatory cytokine IL-10 level in preeclampsia-like rats. Furthermore, cordycepin helped restore macrophage population imbalances, increasing M1-type macrophage markers (iNOS, TNF-α, and IL-1β) and reducing M2-type macrophage markers (Arg 1, IL-10, and TGF-β).</p><p><strong>Conclusion: </strong>This study suggests that cordycepin alleviates LPS-induced preeclampsia by reducing placental inflammation and correcting the M1/M2 macrophage imbalance, offering potential therapeutic benefits for managing preeclampsia.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"68-82"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568165","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}
Zahra Mozooni, Fatemeh Faraji, Sara Minaeian, Leyla Bahadorizadeh
{"title":"The Relationship Between Serum IgE Level and IL-4 and IL-13 Cytokines in Colorectal Cancer Patients.","authors":"Zahra Mozooni, Fatemeh Faraji, Sara Minaeian, Leyla Bahadorizadeh","doi":"10.1080/08820139.2024.2414091","DOIUrl":"10.1080/08820139.2024.2414091","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is the most common malignancy of the digestive system in the world. Immune cells and molecules in tumor microenvironment are crucial.Identifying immune system components in cancer aids in biomarker discovery. This study investigated the serum IgE levels and expression of IL-4 and IL-13 in the tissue and serum of CRC patients and explored their possible association with pathological and clinical factors.</p><p><strong>Materials and methods: </strong>Thirty-six patients with CRC and 36 healthy individuals were involved in the study. Tissues and blood samples were collected. Serum levels of IgE and IL-4 and IL-13 were analyzed using the ELISA method. The quantitative Real-Time PCR (qRT-PCR) technique was used to assess the expression levels of the cytokines in CRC tissue samples in comparison with the adjacent control tissue.</p><p><strong>Results: </strong>Our results revealed that the serum level of IL-4 and IL-13 and also their gene expression levels were significantly decreased in CRC patients compared to the controls. The results of this study revealed that there is no significant difference in the serum levels of IgE between CRC patients and the control group.</p><p><strong>Conclusion: </strong>All in all, the results of the current research suggest that the expression levels of IL-13, IL-4, and IgE vary between CRC tissue.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"34-45"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400149","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}
Eman Abd Allah Fouda, Alshimaa Mohamed Elmalawany, Eman Masoud Abd El Gayed, Salah Mohamed El-Kousy, Heba Saber Mohamed, Ahmed B Zaid, Mohamed Farag Ali Assar
{"title":"Up Regulation of <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 Single Nucleotide Polymorphisms as a Genetic Risk Factor in Egyptian Patients with Rheumatoid Arthritis.","authors":"Eman Abd Allah Fouda, Alshimaa Mohamed Elmalawany, Eman Masoud Abd El Gayed, Salah Mohamed El-Kousy, Heba Saber Mohamed, Ahmed B Zaid, Mohamed Farag Ali Assar","doi":"10.1080/08820139.2024.2418569","DOIUrl":"10.1080/08820139.2024.2418569","url":null,"abstract":"<p><strong>Introduction: </strong>The protein <i>SCUBE3</i> has been observed to exhibit an association with various autoimmune conditions, including psoriasis and rheumatoid arthritis. Genetic experiments have revealed that changes in Zinc finger protein-coding sequences correlate with an increased vulnerability to developing autoimmune diseases, so we aimed to study investigates the involvement of <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 gene expression in individuals diagnosed with Rheumatoid Arthritis.</p><p><strong>Methods: </strong>In a case-control study conducted from January 2022 to March 2023, 80 adults with RA from Menoufia University Hospital were compared with 80 age- and gender-matched healthy controls. Single nucleotide polymorphisms (SNPs) <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 were analysed using real-time polymerase chain reaction (PCR).</p><p><strong>Results: </strong>ZNF76 rs10947540 demonstrated a 7.125-fold increased risk for RA in CC genotype individuals and a 2.958-fold risk associated with the C allele. Those with the TC genotype had a 2.523-fold increased risk. Similarly, <i>SCUBE3</i> rs1888822 showed a 6.364-fold risk for RA in TT genotype individuals and a 3.065-fold risk for T allele carriers. GT genotype individuals had a 2.765-fold risk.</p><p><strong>Discussion: </strong>Our study suggests that <i>ZNF76</i> rs10947540 and <i>SCUBE3</i> rs1888822 polymorphisms may be risk factors for RA in Egyptian patients. Understanding the genetic variations associated with higher risk underscores the role of genetics in RA progression.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"46-67"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853995","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":"Tectochrysin Alleviates Periodontitis by Modulating M2/M1 Macrophage Ratio and Oxidative Stress Via Nuclear Factor Kappa B/Heme Oxygenase-1/Nuclear Factor Erythroid 2-Related Factor 2 Pathway.","authors":"Ye Yin, Yanming Weng, Zeyu Ma, Li Li","doi":"10.1080/08820139.2024.2418938","DOIUrl":"10.1080/08820139.2024.2418938","url":null,"abstract":"<p><strong>Background: </strong>Tectochrysin suppresses several diseases. In this study, we aimed to explore the effects of tectochrysin ona rat model of periodontitis PDS).</p><p><strong>Methods: </strong>Male Sprague-Dawley (SD) rats were subjected to ligature to induce periodontitis. Bone parameters were analyzed using micro-computed tomography and periodontal tissues were evaluated using Masson's, hematoxylin and eosin, and tartrate-resistant acid phosphatase staining. The expression of HO-1, Nrf2, CD206, Arg-1, and iNOS was evaluated using immunohistochemistry. Malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) levels and IL-1β, IL-6, and tumor necrosis factor (TNF)-α,and NF-κB and Nrf2/HO-1 were analyzed.</p><p><strong>Results: </strong>Tectochrysin reduced alveolar bone loss, promoted new bone formation, and inhibited osteoclast formation in periodontitis rats. It decreased the number of inflammatory cells and the levels of IL-1β, IL-6, and TNF-α, indicating a reduction in inflammation. Tectochrysin restored the Arg-1/iNOS ratio, indicating M2 macrophage polarization, and inhibited the NF-kB pathway. Tectochrysin restored GSH and SOD levels, inhibited MDA content, and activated the HO-1/Nrf2 pathway.</p><p><strong>Conclusion: </strong>Tectochrysin alleviates PDS in rats by modulating the M2/M1 macrophage ratio via the NF-kB pathway and suppressing oxidative stress via the HO-1/Nrf2 pathway.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"97-111"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521816","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":"Integration of Gut Mycobiota and Oxidative Stress to Decipher the Roles of C-Type Lectin Receptors in Inflammatory Bowel Diseases.","authors":"Liu Yang, Min Hu, Jing Shao","doi":"10.1080/08820139.2024.2388164","DOIUrl":"10.1080/08820139.2024.2388164","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis (UC) and Crohn's disease (CD) are two subtypes of inflammatory bowel disease (IBD) with rapidly increased incidence worldwide. Although multiple factors contribute to the occurrence and progression of IBD, the role of intestinal fungal species (gut mycobiota) in regulating the severity of these conditions has been increasingly recognized. C-type lectin receptors (CLRs) on hematopoietic cells, including Dectin-1, Dectin-2, Dectin-3, Mincle and DC-SIGN, are a group of pattern recognition receptors (PRRs) that primarily recognize fungi and mediate defense responses, such as oxidative stress. Recent studies have demonstrated the indispensable role of CLRs in protecting the colon from intestinal inflammation and mucosal damage.</p><p><strong>Methods and results: </strong>This review provides a comprehensive overview of the role of CLRs in the pathogenesis of IBD. Given the significant impact of mycobiota and oxidative stress in IBD, this review also discusses recent advancements in understanding how these factors exacerbate or ameliorate IBD. Furthermore, the latest developments in CLR-guided IBD therapy are examined to highlight the modulation of CLRs in fungal recognition and oxidative burst during the IBD process.</p><p><strong>Conclusion: </strong>This review emphasizes the importance of CLRs in IBD, offering new perspectives on the etiology and therapeutic approaches for this disease.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1177-1204"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906496","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":"Statement of Retraction: Prophylactic Effect of BIO-1211 Small-Molecule Antagonist of VLA-4 in the EAE Mouse Model of Multiple Sclerosis.","authors":"","doi":"10.1080/08820139.2024.2412450","DOIUrl":"10.1080/08820139.2024.2412450","url":null,"abstract":"","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1456"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390315","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":"LncRNAPVT1 is Associated with Cancer-Associated Fibroblasts Proliferation Through Regulating TGF-βin Oral Squamous Cell Carcinoma.","authors":"Zhen Meng, Tongjuan Li, Jun Li, Shuxin Ding, Yujiao Liu, Guoli Zhao, Cheng Chen, Peng Zhao, Longxun Zhou","doi":"10.1080/08820139.2024.2395874","DOIUrl":"10.1080/08820139.2024.2395874","url":null,"abstract":"<p><strong>Introduction: </strong>Human oral squamous cell carcinoma (OSCC) is the most common type of oral cancer and has a poor survival rate. Cell-cell communication between OSCC cells and cancer-associated fibroblasts (CAFs) plays important roles in OSCC progression. We previously demonstrated that CAFs promote OSCC cell migration and invasion. However, how OSCC cells influence CAFs proliferation is unknown.</p><p><strong>Methods: </strong>Knockdown of PVT1 was confirmed using lentivirus infection technique. CAFs in tissues were identified by staining the cells with α-SMA using immunohistochemical technique. CCK-8 assay was used to evaluate cell proliferation. The mRNA level of a gene was measured by qRT-PCR. Secreted TGF-β were detected using ELISA assay.</p><p><strong>Results: </strong>We found that knockdown of the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) was associated with a low density of CAFs in xenograft tumors in mice; further analysis revealed that PVT1 in OSCC cells induced CAF proliferation through transforming growth factor (TGF)-β.</p><p><strong>Discussion: </strong>Our results demonstrate that lncRNA PVT1 in tumor cells participates in CAF development in OSCC by regulating TGF-β. This study revealed a new mechanism by which PVT1 regulates OSCC progression and PVT1 is a potential therapeutic target in OSCC.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1250-1263"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072699","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}
Yang Zou, Zhaoyang Wang, Hangchu Shi, Jiong Hu, Weifeng Hu
{"title":"Soybean Isoflavones Alleviate Osteoarthritis Through Modulation of the TSC1/mTORC1 Signaling Pathway to Reduce Intrachondral Angiogenesis.","authors":"Yang Zou, Zhaoyang Wang, Hangchu Shi, Jiong Hu, Weifeng Hu","doi":"10.1080/08820139.2024.2410737","DOIUrl":"10.1080/08820139.2024.2410737","url":null,"abstract":"<p><strong>Background: </strong>The incidence of osteoarthritis (OA) is increasing, yet its pathogenesis remains largely unknown. Recent studies suggest that abnormal subchondral bone remodeling plays a crucial role in OA development, highlighting a gap in clinical treatments targeting this aspect. Soybean Isoflavone (SI) has shown potential in treating OA, although its mechanisms are not fully understood.</p><p><strong>Methods: </strong>This research investigated the effects of SI on subchondral bone remodeling in an OA rat model, assessing joint damage, OARSI scores, and type H vessel formation (CD31hiEmcnhi expression). Additionally, the expression of ALP, OCN, BMP, and TSC1 was evaluated to determine involvement of the mTORC1 pathway. In vitro studies on IL-1β-induced osteoblasts further examined the impact of SI on TSC1/mTORC1 signaling and related markers.</p><p><strong>Results: </strong>SI treatment reduced joint damage and OARSI scores in the rat OA model, significantly decreasing CD31hiEmcnhi expression, indicating a reduction in type H vessel formation. SI also downregulated ALP, OCN, and BMP expression while upregulating TSC1, suggesting inhibition of the mTORC1 signaling pathway and VEGF release. In vitro, SI increased TSC1 expression and decreased mTORC1 signaling, VEGF, ALP, OCN, and BMP levels in IL-1β-induced osteoblasts.</p><p><strong>Conclusion: </strong>SI targets the TSC1/mTORC1 signaling pathway to suppress osteoblast activation and VEGF release, inhibiting type H vessel formation and slowing abnormal subchondral bone remodeling. These findings provide a novel therapeutic approach for OA by focusing on subchondral bone remodeling mechanisms.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1439-1455"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365130","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}