European cytokine network最新文献

{"title":"Association between interleukin-6 promoter polymorphisms and osteoporosis in javanese postmenopausal women.","authors":"Sri Lestari Utami, Mohammad Hidayat, Diana Lyrawati, Loeki Enggar Fitri","doi":"10.1684/ecn.2025.0507","DOIUrl":"10.1684/ecn.2025.0507","url":null,"abstract":"<p><p>The expression of the interleukin-6 (IL-6) gene promoter and its variations in postmenopausal women of Javanese ethnicity remains unexplored. This study aimed to examine IL-6 promoter polymorphisms at positions -174G/C, -572G/C, -597A/G, and -634C/G and their associations to osteoporosis status in Javanese postmenopausal women. A cross-sectional study was conducted at an elderly integrated service post in Sidoarjo, Indonesia. Among 699 screened individuals, 66 postmenopausal women fulfilled the inclusion and exclusion criteria. Bone mineral density was assessed using dual-energy X-ray absorptiometry (DXA), and osteoporosis status was defined based on T-score values. IL-6 promoter polymorphisms were genotyped by sequencing PCR-amplified promoter regions. IL-6 mRNA expression was assessed using RT-PCR followed by densitometric analysis, and serum IL-6 concentrations were determined using enzyme-linked immunosorbent assay. Our study showed that osteoporosis and osteopenia were predominant (28.8% and 57.6%, respectively), and 13.6% of subjects had normal BMD. The IL-6 promoter variant genotypes and frequencies were as follows: at -174 GG (0.924), CC (0.045), and GC (0.030); at -572 GC (0.424), CC (0.406), and GG (0.167); at -597 GG (0.924) and GA (0.0758) GA (0.076); and at -634 CC (1). The IL-6 mRNA and protein level (median 6.06, IQR 5.0398 pg/mL) were not statistically different among individuals with different genotypes and with normal, osteopenia, or osteoporosis status. Ordinal regression showed that IL-6 promoter polymorphisms were not significantly associated with osteoporosis status. The polymorphisms of the IL-6 promoter were detected in Javanese postmenopausal women; however, such polymorphisms did not correlate with IL-6 mRNA and protein levels nor osteoporosis status. IL-6 promoter polymorphisms were present in Javanese postmenopausal women; however, these variants were not associated with IL-6 expression at the mRNA or protein level, nor with osteoporosis status.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 4","pages":"74-83"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149585","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":"Igniting the Tumor: Targeting Mitochondrial Stress to Prime Breast Cancer for Immunotherapy.","authors":"Hung-Yu Lin, Hsing-Ju Wu, Pei-Yi Chu","doi":"10.1684/ecn.2025.0504","DOIUrl":"10.1684/ecn.2025.0504","url":null,"abstract":"<p><p>Immunotherapy has demonstrated limited efficacy in immunologically \"cold\" breast cancers characterized by absent T-cell infiltration and inadequate interferon signaling. The purpose of this work is to propose and articulate a mechanistic and therapeutic framework in which mitochondrial stress is deliberately harnessed to convert immunologically \"cold\" breast tumors into \"hot,\" T cell-inflamed, immunotherapy-responsive lesions. This review synthesizes emerging evidence positioning mitochondrial stress as a strategic lever to transform these immune-excluded tumors into inflamed, therapy-responsive lesions. We examine how mitochondrial dysfunction triggers cytosolic release of mitochondrial DNA (mtDNA), a potent damage-associated molecular pattern that activates the cGAS-STING pathway, initiating type I interferon responses and secretion of T-cell-recruiting chemokines such as CCL5 and CXCL10. This axis functions as a \"double-edged sword\"-while acute activation converts \"cold\" tumors into \"hot\" immune-responsive states, chronic engagement drives immunosuppressive cytokine networks and therapeutic resistance, with outcomes varying across breast cancer subtypes. We explore six combination therapeutic strategies: mitochondrial poisons, radiotherapy/chemotherapy, PARP/ATR inhibitors, metabolic reprogramming agents, mitochondrial quality control modulators, and localized mitochondrial stress induction, each paired with immune checkpoint blockade. The review emphasizes \"controlled ignition\" as a paradigm whereby precisely dosed mitochondrial stress amplifies tumor antigenicity and favorable cytokine landscapes while avoiding chronic immunosuppression. Cytokine networks emerge as both integrators and therapeutic targets of mitochondrial-immune crosstalk. Future advances require mapping subtype-specific thresholds, developing tumor-restricted delivery systems, and implementing biomarker-guided trials to safely harness mitochondrial stress, potentially redefining these organelles as programmable immunological adjuvants in breast cancer therapy.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 3","pages":"24-37"},"PeriodicalIF":1.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997422","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":"Identification of proteases associated with glioblastoma and their modulation by interferon-gamma signaling.","authors":"Enrique Oropeza-Maetínez, Eva G Palacios-Serrato, Marina Macías-Silva, Angeles C Tecalco-Cruz","doi":"10.1684/ecn.2025.0503","DOIUrl":"10.1684/ecn.2025.0503","url":null,"abstract":"<p><p>Glioblastoma is a lethal primary brain tumor that is therapeutically challenging due to its rapid progression. Interferon-gamma (IFN-γ) signaling is altered in glioblastoma. Moreover, proteolytic enzymes, known as proteases, have been linked to the invasive growth of cancerous cells. In this study, we aimed to identify a glioblastoma-associated protease group and to determine its potential connection with IFN-γ signaling. Using cancer expression databases, we analyzed the differential expression of 35 proteases in glioblastoma and healthy brain tissue, and the relevance of their deregulation to patient survival. We also explored correlations between IFN-γ signaling element expression and upregulated proteases in glioblastoma. Additionally, we analyzed the effect of IFN-γ on the levels of these 35 proteases using a protein microarray and found that cathepsin L (CTSL) was upregulated by IFN-γ. Then, we analyzed the modulation of CTSL by IFN-γ in glioblastoma cells using dot blot, western blot, and immunofluorescence assays. We identified 11 proteases (cathepsin B, Z, C, S (CTSB, CTSZ, CTSC, CTSS), matrix metalloproteinase 2, 7, 9 (MMP2, MMP7, MMP9), a disintegrin and metalloproteinase 9 (ADAM9), urokinase-type plasminogen activator (PLAU), presenilin 1 (PSEN1), and CTSL that were upregulated in glioblastoma tissue compared to healthy brain tissue. The expression of specific elements of the IFN-γ pathway correlated with the expression of some of these proteases in glioblastoma samples. Moreover, IFN-γ affected the intracellular and extracellular levels of proteases (four were upregulated and six were downregulated) in glioblastoma-derived cells. Hence, IFN-γ signaling may play a role in glioblastoma by regulating the expression of some proteases. The CTSL protease was upregulated by IFN-γ and was associated with poor glioblastoma prognoses. Thus, we revealed a protease profile (ADAM9, CTSB, MMP7, CTSC, CTSL, MMP9, and PLAU) associated with glioblastoma progression and further demonstrated that CTSL is regulated by IFN-γ in glioblastoma cells. These results establish a link between IFN-γ signaling and protease regulation in glioblastoma.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 3","pages":"38-51"},"PeriodicalIF":1.5,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146061009","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":"Astilbin ameliorates propranolol-induced psoriasis-like lesions through restoring Th17/Treg immune homeostasis in lymph nodes.","authors":"Yayun Wu, Qi Xia, Dancai Fan, Ya Zhao, Lijuan Liu, Shigui Deng, Ruizhi Zhao","doi":"10.1684/ecn.2025.0505","DOIUrl":"10.1684/ecn.2025.0505","url":null,"abstract":"<p><p>Psoriasis is a challenging immune-mediated dermatological disorder with an urgent need for effective clinical therapeutics, while astilbin has shown considerable efficacy in suppressing psoriasis progression, its underlying mechanisms are not fully clarified. This study aimed to systematically investigate the anti-psoriatic effects of astilbin and to elucidate its potential mechanisms of action. A psoriasis-like mouse model was established via cold water swimming, dietary restriction, and topical application of 5% propranolol emulsion, followed by daily treatment with low- (25.6 mg/kg), middle- (51.2 mg/kg), or high-dose (76.8 mg/kg) astilbin for 6 consecutive days, with evaluations including PASI scoring, histopathological examination, Baker scoring, inflammatory cytokine detection, and flow cytometric analysis of lymphocyte populations in lymph nodes and spleen. Middle and high doses of astilbin significantly reduced skin lesions and erythema, with PASI scores decreasing by 23.6%, and 44.9% respectively, Baker scores significantly reduced by 23.1% and 24.1% in the middle- and high-dose groups, and astilbin also significantly suppressed skin IL-17A, IL-6, and IFN-γ levels; moreover, middle and high doses substantially downregulated Th1, Th17, and Treg cell populations in lymph nodes and effectively restored Th17/Treg balance. Astilbin effectively ameliorates psoriatic skin lesions through immunomodulatory mechanisms involving the correction of lymph node Th17/Treg imbalance, highlighting its potential as a therapeutic agent for psoriasis.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 3","pages":"52-63"},"PeriodicalIF":1.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149539","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 role of IL-33 in immunotherapy for breast cancer: targets and signalling pathways.","authors":"Fu Zhang, Miao Lin, Yuancong Jiang, Fangjian Zhou","doi":"10.1684/ecn.2025.0500","DOIUrl":"https://doi.org/10.1684/ecn.2025.0500","url":null,"abstract":"<p><p>Interleukin-33 (IL-33), a key member of the IL-1 family, plays a significant role in inflammation and cancer. Its classic receptors, ST2 and IL-1 receptor accessory protein (IL-1RAcP), are predominantly expressed in immune cells such as T helper 2 (Th2) cells and mast cells. Recent studies have highlighted the involvement of IL-33 in breast cancer, demonstrating its ability to exert dual functional effects by modulating both innate and adaptive immune responses within the tumour microenvironment. However, the precise molecular mechanisms linking IL-33 to breast cancer pathogenesis and its potential as a target for molecularly targeted therapies remain incompletely understood. This review aims to provide a comprehensive summary of the current understanding of IL-33 in breast cancer immunotherapy.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 1","pages":"1-5"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157566","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":"It’s in the blood: plasma as a source for biochemical identification and biological characterization of novel leukocyte chemoattractants.","authors":"Jo Van Damme, Stijn Van Damme, Sofie Struyf, Ghislain Opdenakker","doi":"10.1684/ecn.2025.0501","DOIUrl":"https://doi.org/10.1684/ecn.2025.0501","url":null,"abstract":"<p><p>Since their discovery, chemotactic cytokines or chemokines have been intensively studied for about half a century. Chemokines originate from tissue cells, leukocytes, blood platelets and plasma. Here, we review a number of seminal findings on plasma chemokines within an historical and international context. These aspects include how induction and purification protocols led to the discovery of a new family of mediators, named chemokines, on the basis of protein sequencing; how molecular cloning techniques facilitated discoveries of additional family members on the basis of conserved protein structures; how blood plasma and platelets were used as a source of inducible and constitutively expressed chemokines; how various forms of proteolytic reactions may convert precursor proteins into chemokines and either potentiate or inactivate their activity; how abundancy classes and synergism should be interpreted through critically considering plasma chemokine biology; and how other blood proteins, such as serum amyloid A, interact in functional terms with CXC and CC chemokines. The gradual dissection of all these elements not only reveals the complexity of chemokine actions, but also stimulates a more comprehensive interpretation of chemokine levels in plasma and serum, with future chemokinome analyses in mind.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 1","pages":"6-14"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157562","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":"Anti-inflammatory action and effects on carbohydrate and lipid metabolism: an understudied role of interleukin-6.","authors":"Francisco Javier Alarcón-Aguilar, Israel Domínguez de la Mora, Angeles Fortis-Barrera","doi":"10.1684/ecn.2024.0499","DOIUrl":"10.1684/ecn.2024.0499","url":null,"abstract":"<p><p>Interleukin-6 (IL-6) is a cytokine with pleiotropic effects that plays a significant role in the transition from the innate immune response to adaptive response. IL-6 is of interest due to its proinflammatory action, however, it also exhibits anti-inflammatory effects, supporting metabolism and suppressing associated diseases, such as obesity, diabetes mellitus and metabolic syndrome. The IL-6 receptor (IL-6R) is a type I transmembrane glycoprotein in the plasma membrane of only some cell types, such as macrophages, neutrophils, hepatocytes, and T cells. The function of IL-6R requires another transmembrane glycoprotein of 130 kDa (gp130) which, in contrast to IL-6R, is expressed in many cell types. In addition, a soluble form of the IL-6 receptor (sIL-6R) also plays a role in the function of IL-6. These receptors, gp130 and sIL-6R, are involved in the trans pathway of IL-6 signalling, the activation of which is associated with high IL-6 concentrations, promoting proinflammatory processes that are well known. In contrast, the physiological effects of IL-6 associated with increased insulin secretion, fatty acid oxidation and decreased adipose tissue, which occur due to activation of the IL-6 anti-inflammatory signalling pathway, have been poorly explored. Some studies using IL-6 knockout models suggest that some of the anti-inflammatory effects of IL-6 may be stimulated by low concentrations of IL-6, and are essential to suppressing metabolic alterations. This review seeks to highlight the importance of the anti-inflammatory role of IL-6 in metabolic diseases.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"35 4","pages":"48-55"},"PeriodicalIF":2.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729487","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":"Dynamics of serum cytokines in preeclampsia.","authors":"Almagul Kurmanova, Gulfairuz Urazbayeva, Laura Kayupova, Damilya Salimbaeva, Nurzhamal Dzhardemalieva","doi":"10.1684/ecn.2024.0497","DOIUrl":"https://doi.org/10.1684/ecn.2024.0497","url":null,"abstract":"<p><p>The aim of the present study was to evaluate the diagnostic significance of the dynamics of cytokines and growth factors during pregnancy with and without preeclampsia. The study included 168 pregnant women at risk of hypertensive disorders. The levels of biomarkers of all pregnant women were studied at 12-16 weeks, 28-30 weeks and 36-38 weeks. These included cytokines (tumour necrosis factor-α, interferon-, γinterleukin-4) and growth factors (placental growth factor, vascular endothelial growth factor). All pregnant women were divided into two groups: 124 patients with preeclampsia and 44 without preeclampsia (control group). In patients with preeclampsia, an increase in the level of tumour necrosis factorα- was observed, compared with the control group: a 6.1-fold increase at 12-16 weeks and a 5.9-fold increase at 36-38 weeks. The level of interferon-γ was also increased, by 44.3% in the first trimester of pregnancy and by 46.8% at 28-30 weeks, compared to the control group. The level of interleukin-4 did not significantly differ between the studied groups. The level of placental growth factor was reduced in pregnant women with preeclampsia at all stages of gestation, and at 28-30 weeks was reduced by 67.9% compared to the control group. The level of vascular endothelial growth factor was also reduced, by 75%, compared with the control group. An increase in the level of pro-inflammatory cytokines and decrease in growth factors may therefore be considered as potential predictors of the development of preeclampsia, and evaluation of these factors may be advocated in pregnant women with risk factors of preeclampsia.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"35 2","pages":"21-27"},"PeriodicalIF":2.2,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343955","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":"Effect of proinflammatory cytokines on blood-brain barrier integrity.","authors":"Małgorzata Gryka-Marton, Anna Grabowska, Dariusz Szukiewicz","doi":"10.1684/ecn.2024.0498","DOIUrl":"https://doi.org/10.1684/ecn.2024.0498","url":null,"abstract":"<p><p>The blood-brain barrier (BBB) consists of a unique system of brain microvascular endothelial cells, capillary basement membranes, and terminal branches (\"end-feet\") of astrocytes. The BBB's primary function is to protect the central nervous system from potentially harmful or toxic substances in the bloodstream by selectively controlling the entry of cells and molecules, including nutrients and immune system components. During neuroinflammation, the BBB loses its integrity, resulting in increased permeability, mostly due to the activity of inflammatory cytokines. However, the pathomechanism of structural and functional changes in the BBB caused by individual cytokines is poorly understood. This review summarizes the current state of knowledge on this topic, which is important from both the pathophysiological and clinical-therapeutic point of view. The structure and function of each of the components of the BBB are discussed with particular attention to phenotypic differences between brain microvascular endothelial cells and the vascular endothelium at other locations of the circulatory system. The protein composition of the inter-endothelial tight junctions in the context of regulating BBB permeability is presented, as is the role of the pericyte-BMEC interaction in the exchange of metabolites, ions, and nucleic acids. Finally, the documented actions of proinflammatory cytokines within the BBB are summarized.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"35 3","pages":"38-47"},"PeriodicalIF":2.2,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946694","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":"MALAT1 promotes epithelial-mesenchymal transition of pancreatic cancer cells through the miR-141-5p-TGF-ß-TGFBR1/TGFBR2 axis.","authors":"Zhenlu Li, Chao Yue, Shengzhong Hou, Xing Huang, Zihe Wang, Weiming Hu, Huimin Lu","doi":"10.1684/ecn.2024.0495","DOIUrl":"https://doi.org/10.1684/ecn.2024.0495","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is one of the leading causes of cancer deaths, associated with a high risk of metastasis and mortality. The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is highly expressed in multiple types of tumour tissues and may be associated with the growth of PC cells. In this study, we aimed to assess the role and possible mechanisms of MALAT1 in PC progression. Expression of MALAT1 was studied by quantitative real-time polymerase chain reaction (qRT-PCR) in PC tissues. The dual-luciferase assay was performed to validate binding between MALAT1 and miR-141-5p in HEK293 cells. Western blot analysis was performed to examine the expression of transforming growth factor beta (TGF-β) and its receptors, TGFBR1 and TGFBR2. Invasiveness and migration of cultured PANC-1 cells were studied using transwell invasion and migration assays, respectively. A high level of miR-141-5p and low level of MALAT1 were detected in PC tissues, and the level of MALAT1 was shown to significantly correlate with tumour growth and metastasis. In HEK293 cells, miR-141-5p overexpression inhibited the expression of TGFBR1 and TGFBR2, and this inhibition was reversed by overexpression of MALAT1. In PANC-1 cells, MALAT1 was shown to act as a competing endogenous RNA, as the direct target of miR-141-5p. Furthermore, in PANC-1 cells, miR-141-5p overexpression suppressed TGF-induced epithelial-mesenchymal transition (EMT), cell migration, and cell invasion through direct binding to the 3'UTR of TGFBR1 and TGFBR2. Our results indicate that, in PC cells, miR-141-5p suppresses TGFBR1 and TGFBR2 expression and further inhibits TGF-β-induced EMT, cell migration, and cell invasion, which are reversed by overexpression of MALAT1, demonstrating that MALAT1 and miR-141-5p may be important regulators in the initiation and metastasis of PC.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"35 3","pages":"28-37"},"PeriodicalIF":2.2,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946697","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}