Journal of Biomedical Research最新文献

{"title":"Phase separation and transcriptional regulation in cancer development.","authors":"Yan Gu, Ke Wei, Jun Wang","doi":"10.7555/JBR.37.20230214","DOIUrl":"10.7555/JBR.37.20230214","url":null,"abstract":"<p><p>Liquid-liquid phase separation, a novel biochemical phenomenon, has been increasingly studied for its medical applications. It underlies the formation of membrane-less organelles and is involved in many cellular and biological processes. During transcriptional regulation, dynamic condensates are formed through interactions between transcriptional elements, such as transcription factors, coactivators, and mediators. Cancer is a disease characterized by uncontrolled cell proliferation, but the precise mechanisms underlying tumorigenesis often remain to be elucidated. Emerging evidence has linked abnormal transcriptional condensates to several diseases, especially cancer, implying that phase separation plays an important role in tumorigenesis. Condensates formed by phase separation may have an effect on gene transcription in tumors. In the present review, we focus on the correlation between phase separation and transcriptional regulation, as well as how this phenomenon contributes to cancer development.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":"38 4","pages":"307-321"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901856","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":"Oxytocin ameliorates cognitive impairments by attenuating excitation/inhibition imbalance of neurotransmitters acting on parvalbumin interneurons in a mouse model of sepsis-associated encephalopathy.","authors":"Renqi Li, Qiuting Zeng, Muhuo Ji, Yue Zhang, Mingjie Mao, Shanwu Feng, Manlin Duan, Zhiqiang Zhou","doi":"10.7555/JBR.37.20230318","DOIUrl":"10.7555/JBR.37.20230318","url":null,"abstract":"<p><p>Inflammation plays a crucial role in the initiation and progression of sepsis and induces alterations in brain neurotransmission, thereby contributing to the development of sepsis-associated encephalopathy (SAE). Parvalbumin (PV) interneurons are pivotal contributors to cognitive processes and have been implicated in various central nervous system dysfunctions, including SAE. Oxytocin, known for its ability to augment the firing rate of gamma-aminobutyric acid (GABA)-ergic interneurons and directly stimulate inhibitory interneurons to enhance the tonic inhibition of pyramidal neurons, has prompted an investigation into its potential therapeutic effects on cognitive dysfunction in SAE. In the current study, we administered intranasal oxytocin to SAE mice induced by lipopolysaccharide. Behavioral assessments, including open field, Y-maze, and fear conditioning, were used to evaluate cognitive performance. Golgi staining revealed hippocampal synaptic deterioration, local field potential recordings showed weakened gamma oscillations, and immunofluorescence staining demonstrated decreased PV expression in the cornu ammonis 1 (CA1) region of the hippocampus following lipopolysaccharide treatment, all of which were alleviated by oxytocin administration. Furthermore, immunofluorescence staining of PV co-localization with vesicular glutamate transporter 1 or vesicular GABA transporter indicated a balanced excitation/inhibition effect of neurotransmitters on PV interneurons after oxytocin administration in the SAE mice, leading to an improved cognitive function. In conclusion, oxytocin treatment improved cognitive function by increasing the number of PV ⁺ neurons in the hippocampal CA1 region, restoring the balance of excitatory/inhibitory synaptic transmission on PV interneurons, and enhancing hippocampal CA1 local field potential gamma oscillations. These findings suggest a potential mechanism underlying the beneficial effects of oxytocin in SAE.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"132-145"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161648","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":"Genetic variants in <i>C1GALT1</i> are associated with gastric cancer risk by influencing immune infiltration.","authors":"Mengfan Guo, Jingyuan Liu, Yujuan Zhang, Jingjing Gu, Junyi Xin, Mulong Du, Haiyan Chu, Meilin Wang, Hanting Liu, Zhengdong Zhang","doi":"10.7555/JBR.37.20230161","DOIUrl":"10.7555/JBR.37.20230161","url":null,"abstract":"<p><p>Core 1 synthase glycoprotein-N-acetylgalactosamine 3-β-galactosyltransferase 1 (C1GALT1) is known to play a critical role in the development of gastric cancer, but few studies have elucidated associations between genetic variants in <i>C1GALT1</i> and gastric cancer risk. By using the genome-wide association study data from the database of Genotype and Phenotype (dbGAP), we evaluated such associations with a multivariable logistic regression model and identified that the rs35999583 G>C in <i>C1GALT1</i> was associated with gastric cancer risk (odds ratio, 0.83; 95% confidence interval [CI], 0.75-0.92; <i>P</i> = 3.95 × 10 ^-4). <i>C1GALT1</i> mRNA expression levels were significantly higher in gastric tumor tissues than in normal tissues, and gastric cancer patients with higher <i>C1GALT1</i> mRNA levels had worse overall survival rates (hazards ratio, 1.33; 95% CI, 1.05-1.68; <i>P</i> _log-rank = 1.90 × 10 ^-2). Furthermore, we found that <i>C1GALT1</i> copy number differed in various immune cells and that <i>C1GALT1</i> mRNA expression levels were positively correlated with the infiltrating levels of CD4 ⁺ T cells and macrophages. These results suggest that genetic variants of <i>C1GALT1</i> may play an important role in gastric cancer risk and provide a new insight for <i>C1GALT1</i> into a promising predictor of gastric cancer susceptibility and immune status.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"348-357"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161527","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":"Macrophage scavenger receptor A1 promotes skeletal muscle regeneration after hindlimb ischemia.","authors":"Siying Wang, Saiya Wang, Wenhan Cai, Jie Wang, Jianan Huang, Qing Yang, Hui Bai, Bin Jiang, Jingjing Ben, Hanwen Zhang, Xudong Zhu, Xiaoyu Li, Qi Chen","doi":"10.7555/JBR.38.20240117","DOIUrl":"10.7555/JBR.38.20240117","url":null,"abstract":"<p><p>The macrophage-mediated inflammatory response is crucial for the recovery of skeletal muscle following ischemia. Therefore, macrophage-based therapeutic targets need to be explored for ischemic disease. In the current study, we found that the mRNA levels of scavenger receptor A1 ( <i>Sr-a1</i>) were elevated in patients with critical limb ischemia, based on an analysis of the Gene Expression Omnibus data. We then investigated the role and underlying mechanisms of macrophage SR-A1 in a mouse hindlimb ischemia (HLI) model. Compared with the <i>Sr-a1</i> ^fl/fl mice, the <i>Lyz</i> ^Cre/+/ <i>Sr-a1</i> ^flox/flox ( <i>Sr-a1</i> ^ΔMΦ) mice showed significantly reduced laser Doppler blood flow in the ischemic limb on day seven after HLI. Consistently, histological analysis revealed that the ischemic limb of the <i>Sr-a1</i> ^ΔMΦ mice exhibited more severe and prolonged necrotic morphology, inflammation, fibrosis, decreased vessel density, and delayed regeneration than that of the control <i>Sr-a1</i> ^fl/fl mice. Furthermore, restoring wild-type myeloid cells to the <i>Sr-a1</i> knockout mice effectively improved the Doppler perfusion in the ischemic limb and mitigated skeletal muscle damage seven days after HLI. Consistent with these <i>in vivo</i> findings, co-cultivating macrophages with the mouse myoblast cell line C2C12 revealed that the <i>Sr-a1</i> ^-/- bone marrow macrophages significantly inhibited myoblast differentiation <i>in vitro</i>. Mechanistically, SR-A1 enhanced the skeletal muscle regeneration in response to HLI by inhibiting oncostatin M production <i>via</i> suppression of the NF-κB signaling activation. These findings indicate that SR-A1 may be a promising candidate protein to improve tissue repair and regeneration in peripheral ischemic arterial disease.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"23-35"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161620","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":"Cyclopeptide moroidin inhibits vasculogenic mimicry formed by glioblastoma cells <i>via</i> regulating β-catenin activation and EMT pathways.","authors":"Pengxiang Min, Yingying Li, Cuirong Wang, Junting Fan, Shangming Liu, Xiang Chen, Yamin Tang, Feng Han, Aixia Zhang, Lili Feng","doi":"10.7555/JBR.38.20240015","DOIUrl":"10.7555/JBR.38.20240015","url":null,"abstract":"<p><p>Glioblastoma (GBM) is a highly vascularized malignant brain tumor with poor clinical outcomes. Vasculogenic mimicry (VM) formed by aggressive GBM cells is an alternative approach for tumor blood supply and contributes to the failure of anti-angiogenic therapy. To date, there is still a lack of effective drugs that target VM formation in GBM. In the present study, we evaluated the effects of the plant cyclopeptide moroidin on VM formed by GBM cells and investigated its underlying molecular mechanisms. Moroidin significantly suppressed cell migration, tube formation, and the expression levels of α-smooth muscle actin and matrix metalloproteinase-9 in human GBM cell lines at sublethal concentrations. The RNA sequencing data suggested the involvement of the epithelial-mesenchymal transition (EMT) pathway in the mechanism of moroidin. Exposure to moroidin led to a concentration-dependent decrease in the expression levels of the EMT markers N-cadherin and vimentin in GBM cells. Moreover, moroidin significantly reduced the level of phosphorylated extracellular signal-regulated protein kinase (p-ERK) and inhibited the activation of β-catenin. Finally, we demonstrated that the plant cyclopeptide moroidin inhibited VM formation by GBM cells through inhibiting the ERK/β-catenin-mediated EMT. Therefore, our study indicates a potential application of moroidin as an anti-VM agent in the treatment of GBM.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"322-333"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161372","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":"Genetic variation of <i>circHIBADH</i> enhances prostate cancer risk through regulating HNRNPA1-related RNA splicing.","authors":"Yifei Cheng, Rongjie Shi, Shuai Ben, Silu Chen, Shuwei Li, Junyi Xin, Meilin Wang, Gong Cheng","doi":"10.7555/JBR.38.20240030","DOIUrl":"10.7555/JBR.38.20240030","url":null,"abstract":"<p><p>The current study aimed to investigate associations of circRNAs and related genetic variants with the risk of prostate cancer (PCa) as well as to elucidate biological mechanisms underlying the associations. We first compared expression levels of circRNAs between 25 paired PCa and adjacent normal tissues to identify risk-associated circRNAs by using the MiOncoCirc database. We then used logistic regression models to evaluate associations between genetic variants in candidate circRNAs and PCa risk among 4662 prostate cancer patients and 3114 healthy controls, and identified <i>circHIBADH</i> rs11973492 T>C as a significant risk-associated variant (odds ratio = 1.20, 95% confidence interval: 1.08-1.34, <i>P</i> = 7.06 × 10 ^-4) in a dominant genetic model, which altered the secondary structure of the corresponding RNA chain. In the <i>in</i> <i>silico</i> analysis, we found that <i>circHIBADH</i> sponged and silenced 21 RNA-binding proteins (RBPs) enriched in the RNA splicing pathway, among which HNRNPA1 was identified and validated as a hub RBP using an external RNA-sequencing data as well as the in-house (four tissue samples) and publicly available single-cell transcriptomes. Additionally, we demonstrated that HNRNPA1 influenced hallmarks including MYC target, DNA repair, and E2F target signaling pathways, thereby promoting carcinogenesis. In conclusion, genetic variants in <i>circHIBADH</i> may act as sponges and inhibitors of RNA splicing-associated RBPs including HNRNPA1, playing an oncogenic role in PCa.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"358-368"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161529","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":"Associations of diet with infectious diseases in UK Biobank.","authors":"Junlan Tu, Xuehong Cai, Yifan Wang, Xiangyu Ye, Meijie Yu, Sheng Yang, Rongbin Yu, Peng Huang","doi":"10.7555/JBR.37.20230319","DOIUrl":"10.7555/JBR.37.20230319","url":null,"abstract":"<p><p>The current study used multivariable logistic regression analysis to investigate associations between the intake frequencies of 13 food groups (or four diet groups) and infectious diseases. The analysis included 487849 participants from the UK Biobank, with 75209 participants diagnosed with infectious diseases. Participants reporting the highest intake frequency of processed meat (odds ratio [OR] = 1.0964, 95% confidence interval [CI]: 1.0622-1.1318) and red meat (OR = 1.0895, 95% CI: 1.0563-1.1239) had a higher risk of infectious diseases, compared with those with the lowest intake frequency. Consuming fish 2.0-2.9 times (OR = 0.8221, 95% CI: 0.7955-0.8496), cheese ≥ 5.0 times (OR = 0.882 2, 95% CI: 0.855 9-0.9092), fruit 3.0-3.9 servings (OR = 0.8867, 95% CI: 0.8661-0.9078), and vegetables 2.0-2.9 servings (OR = 0.9372, 95% CI: 0.9189-0.9559) per week were associated with a lower risk of infection. Low meat-eaters (OR = 0.9404, 95% CI: 0.9243-0.9567), fish-eaters (OR = 0.8391, 95% CI: 0.7887-0.8919), and vegetarians (OR = 0.9154, 95% CI: 0.8561-0.9778) had a lower risk of infectious diseases, compared with regular meat-eaters. The mediation analysis revealed that glycosylated hemoglobin, white blood cell count, and body mass index served as the mediators in the associations between diet and infectious diseases. The current study indicates that the intake frequency of food groups is a risk factor for infectious diseases, and fish-eaters have a lower risk of infection.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"597-612"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of pericyte in ocular vascular diseases.","authors":"Lianjun Shi, Huimin Ge, Fan Ye, Xiumiao Li, Qin Jiang","doi":"10.7555/JBR.37.20230314","DOIUrl":"10.7555/JBR.37.20230314","url":null,"abstract":"<p><p>Pericytes are located in the stromal membrane of the capillary outer wall and contain endothelial cells. They are pivotal in regulating blood flow, enhancing vascular stability, and maintaining the integrity of the blood-retina barrier/blood-brain barrier. The pluripotency of pericytes allows them to differentiate into various cell types, highlighting their significance in vascular disease pathogenesis, as demonstrated by previous studies. This capability enables pericytes to be a potential biomarker for the diagnosis and a target for the treatment of vascular disorders. The retina, an essential part of the eyeball, is an extension of cerebral tissue with a transparent refractive medium. It offers a unique window for assessing systemic microvascular lesions. Routine fundus examination is necessary for patients with diabetes and hypertension. Manifestations, such as retinal artery tortuosity, dilation, stenosis, and abnormal arteriovenous anastomosis, serve as typical hallmarks of retinal vasculopathy. Therefore, studies of ocular vascular diseases significantly facilitate the exploration of systemic vascular diseases.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"521-530"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161691","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":"GSDMD protects intestinal epithelial cells against bacterial infections through its N-terminal activity affecting intestinal immune homeostasis.","authors":"Honghui Li, Jie Pu, Dongxue Yang, Lu Liu, Yingchao Hu, Shuo Yang, Bingwei Wang","doi":"10.7555/JBR.38.20240041","DOIUrl":"10.7555/JBR.38.20240041","url":null,"abstract":"<p><p>The intestinal mucosal barrier serves as a vital guardian of the gut health, maintaining a delicate equilibrium between gut microbiota and host immune homeostasis. Gasdermin D (GSDMD), a key executioner of pyroptosis downstream of the inflammasome, has been found to play intricate roles in modulating colitis by influencing intestinal macrophages and regulating mucus secretion from goblet cells. However, the exact nature of the regulatory function of GSDMD in maintaining intestinal immune homeostasis and defending against pathogens remains to be elucidated. In the current study, by using the <i>Citrobacter rodentium</i> infection model, we found that GSDMD played a key role in the defense against intestinal <i>Citrobacter rodentium</i> infection, with high expression levels in intestinal epithelial and lamina propria myeloid cells. Our results showed that GSDMD acted specifically in intestinal epithelial cells to combat the infection, independently of its effects on antimicrobial peptides or mucin secretion. Instead, the resistance was mediated by the N-terminal fragment of GSDMD, highlighting its importance in intestinal immunity. However, the specific mechanism underlying the N-terminal activity of GSDMD in protecting against intestinal bacterial infections requires future investigation.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"585-596"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161522","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":"Novel anti-inflammatory peptide alleviates liver ischemia-reperfusion injury.","authors":"Xuejun Xu, Kaineng Sun, Hao Chang, Chunxiang Shen, Xiangdong Li, Yangyue Ni, Yuxiao Zhu, Huiquan Wang, Ruiyan Xiong, Jon Rob Padde, Zhipeng Xu, Lin Chen, Lu Chen, Min Hou, Liyong Pu, Minjun Ji","doi":"10.7555/JBR.38.20240020","DOIUrl":"10.7555/JBR.38.20240020","url":null,"abstract":"<p><p>Ischemia-reperfusion injury (IRI) remains an unavoidable challenge in liver surgery, with macrophages playing a critical role in its pathogenesis. However, the mechanisms by which macrophages regulate the pathogenesis of IRI are not well understood. Through a target-guided screening approach, we identified a small 3 kDa peptide (SjDX5-271) from various schistosome egg-derived peptides that induced M2 macrophage polarization. SjDX5-271 treatment protected mice against liver IRI by promoting M2 macrophage polarization, and this protective effect was abrogated when the macrophages were depleted. Transcriptomic sequencing showed that the TLR signaling pathway was significantly inhibited in macrophages from the SjDX5-271 treatment group. We further identified that SjDX5-271 promoted M2 macrophage polarization by inhibiting the TLR4/MyD88/NF-κB signaling pathway and alleviated hepatic inflammation in liver IRI. Collectively, SjDX5-271 exhibited some promising therapeutic effects in IRI and represented a novel therapeutic approach, potentially applicable to other immune-related diseases. The current study demonstrates the potential of new biologics from the parasite, enhances our understanding of host-parasite interplay, and provides a blueprint for future therapies for immune-related diseases.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"61-75"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161647","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}