Biomedical Journal最新文献

{"title":"miRNA-mediated regulation of clock gene expression in men and women with colorectal cancer and possible consequences for disease management.","authors":"Iveta Herichová","doi":"10.1016/j.bj.2024.100784","DOIUrl":"https://doi.org/10.1016/j.bj.2024.100784","url":null,"abstract":"<p><strong>Background: </strong>The incidence and mortality of colorectal cancer (CRC) are persistently higher in men than in women. CRC malignancy is strongly influenced by small non-coding RNAs (miRNAs). Moreover, deregulation of the circadian molecular oscillator has been associated with CRC facilitation. To analyse possible cumulative effects of the above-mentioned factors on CRC progression, we focused on functions of sex-biased miRNAs associated with the clock genes per2 and/or cry2, which are involved in the cell cycle control and DNA damage response.</p><p><strong>Major findings: </strong>We identified miR-24, miR-92a, miR-181a, and miR-21 associated with per2 that are up-regulated in transformed colon tissue of men. miR-93, miR-17, miR-20a, and miR-24 with higher expression in males compared to females were linked to cry2. All these miRNAs possess oncogenic potential and exert their effects mainly via inhibition of the tumour suppressors phosphatase and tensin homolog (PTEN) and/or p53. Down-regulation of PTEN and p53 in men was further strengthened by inhibition of tumour suppressor per2. Oncogenic up-regulated miRNAs associated with per2 or cry2 in the transformed colon tissue of women were not detected.</p><p><strong>Conclusion: </strong>We conclude that the cancer-promoting, sex-biased miRNAs miR-24, miR-92a, miR-181a, miR-93, miR-17, miR-20a, and miR-21 associated with clock genes per2 and/or cry2 can contribute to the sex-dependent development of CRC via inhibition of the PTEN and p53 pathways.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100784"},"PeriodicalIF":4.1,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141970576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Prognosis of Patients with Myocardial Infarction after Light Therapy: A Preliminary Study.","authors":"Wei-Chih Chin, Yu-Shu Huang, Lung-Sheng Wu, Kuang-Tso Lee, Chien-Te Ho, Chen Lin, Wei-Sheng Yang, I-Hang Chung, Pao-Hsien Chu","doi":"10.1016/j.bj.2024.100783","DOIUrl":"https://doi.org/10.1016/j.bj.2024.100783","url":null,"abstract":"<p><strong>Background: </strong>Patients with myocardial infarction (MI) can have disturbed sleep, but little is known about the efficacy of light therapy on sleep and prognosis of patients with MI. We conducted a randomized controlled study to investigate its efficacy.</p><p><strong>Material and methods: </strong>This preliminary study included 34 patients with MI. They were randomized into the blue light and the white light groups during their stay in intensive care unit. 17 age and gender matched healthy controls were also enrolled. Actigraphy was used to evaluate objective sleep since enrollment. Delirium scales were used to screen delirium. Lab work-up including vitamin D level was performed at the baseline and discharge. We used Mann-Whitney U test or Wilcoxon signed-rank test to compare the difference between the MI group and the healthy control group, and the group difference after receiving light therapy.</p><p><strong>Results: </strong>Patients with MI had significantly lower vitamin D level than healthy controls (p<0.001). They also had significantly poorer sleep, as indicated by actigraphy parameters including sleep onset latency (p=0.01), sleep efficiency (p=0.002), wake after sleep onset (p<0.001) and awake times (p=0.002). No significant group difference was found by actigraphy after light therapy except a non-significant higher relative amplitude of the blue light group (p=0.061). Besides, vitamin D level of the blue light group increased significantly (p1=0.047, p2=0.045).</p><p><strong>Conclusions: </strong>Patients with MI had poorer sleep, highlighting the needs to develop interventions. Significantly increased vitamin D level and a non-significant better rest-active rhythm after light therapy suggest its potential with sleep and prognosis which warrants further investigation.</p>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":" ","pages":"100783"},"PeriodicalIF":4.1,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141911577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ancient wisdom and modern innovations: Methods of administering healing","authors":"Aila Akosua Kattner","doi":"10.1016/j.bj.2024.100773","DOIUrl":"10.1016/j.bj.2024.100773","url":null,"abstract":"<div><p>This issue of the <em>Biomedical Journal</em> highlights major advancements in drug delivery, including aptamer-functionalized liposomes and nanozymes. A new biomarker combination shows promise for improved diagnosis of idiopathic pulmonary fibrosis. Mesenchymal stem cells are suggested to mitigate inflammation in systemic lupus erythematosus, and a potential positive feedback loop driven by a prevalent mRNA modification is suggested to enhance NSCLC progression. Additional articles explore a pathological impact on autophagy leading to muscle dysfunction, the benefits of integrating an orphan drug with standard therapy for glioblastoma patients, and the influence of transcriptional super-enhancers in early-stage esophageal squamous cell carcinoma. Finally, this issue provides insights into the roles of different <em>Blastocystis</em> subtypes, and the use of laser light for treating infantile hemangioma.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100773"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417024000763/pdfft?md5=23319b7a4c6c7b7b5a08dab54def82c3&pid=1-s2.0-S2319417024000763-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of infantile hemangioma growth and promotion of apoptosis via VEGF/PI3K/Akt axis by 755-nm long-pulse alexandrite laser","authors":"","doi":"10.1016/j.bj.2023.100675","DOIUrl":"10.1016/j.bj.2023.100675","url":null,"abstract":"<div><h3>Background</h3><p>Infantile hemangioma (IH) is a common vascular tumor in female infants, which can lead to aesthetic issues and facial scarring. This study aimed to investigate the inhibitory effects and underlying mechanisms of 755 nm long-pulsed alexandrite laser on IH.</p></div><div><h3>Methods</h3><p>Hemangioma endothelial cells (HemECs) were exposed to 755 nm long-pulsed alexandrite laser to evaluate its impact on cell proliferation and apoptosis. A patient-derived xenograft model was established to assess the inhibitory effects of laser treatment on IH <em>in vivo</em>.</p></div><div><h3>Results</h3><p><em>In vitro</em>, 755 nm long-pulsed alexandrite laser effectively suppressed the proliferation of HemECs and induced cell apoptosis. Laser treatment significantly inhibited the volume and weight of tumors, accompanied by significant downregulation of vascular endothelial growth factor A (VEGFA), vascular endothelial growth factor receptor 2 (VEGFR2), phosphatidylinositol 3-kinase (PI3K), and protein kinase B (Akt) expression levels in both hemangioma cells and tumors. Additionally, laser treatment resulted in the conversion of VEGFA_165a to VEGFA_165b. TUNEL staining demonstrated increased apoptosis in tumor cells after laser treatment, along with upregulation of cleaved caspase-3 and Bax, and downregulation of Bcl-2.</p></div><div><h3>Conclusion</h3><p>In addition to the principle of selective photothermal decomposition, modulation of the VEGF/PI3K/Akt axis may serve as a potential mechanism for IH treatment using a long pulse-width 755 nm laser. This sheds valuable light on the molecular mechanisms underlying IH pathogenesis and potential therapeutic targets while providing a theoretical basis for the safe and efficient management of proliferative IH using laser therapy.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100675"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417023001129/pdfft?md5=dc4d9893747f22df17b764f630012336&pid=1-s2.0-S2319417023001129-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72013337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Msi2 enhances muscle dysfunction in a myotonic dystrophy type 1 mouse model","authors":"","doi":"10.1016/j.bj.2023.100667","DOIUrl":"10.1016/j.bj.2023.100667","url":null,"abstract":"<div><h3>Background</h3><p>Myotonic dystrophy type 1 (DM1) is a rare neuromuscular disease caused by a CTG repeat expansion in the 3′ untranslated region of the <em>DM1 protein kinase</em> gene. Characteristic degenerative muscle symptoms include myotonia, atrophy, and weakness. We previously proposed an Musashi homolog 2 (MSI2)&gt;miR-7&gt;autophagy axis whereby MSI2 overexpression repressed miR-7 biogenesis that subsequently de-repressed muscle catabolism through excessive autophagy. Because the DM1 HSA^LR mouse model expressing expanded CUG repeats shows weak muscle-wasting phenotypes, we hypothesized that MSI2 overexpression was sufficient to promote muscle dysfunction <em>in vivo.</em></p></div><div><h3>Methods</h3><p>By means of recombinant AAV murine MSI2 was overexpressed in neonates HSA^LR mice skeletal muscle to induce DM1-like phenotypes.</p></div><div><h3>Results</h3><p>Sustained overexpression of the murine MSI2 protein in HSA^LR neonates induced autophagic flux and expression of critical autophagy proteins, increased central nuclei and reduced myofibers area, and weakened muscle strength. Importantly, these changes were independent of MBNL1, MBNL2, and Celf1 protein levels, which remained unchanged upon Msi2 overexpression.</p></div><div><h3>Conclusions</h3><p>Globally, molecular, histological, and functional data from these experiments in the HSA^LR mouse model confirms the pathological role of MSI2 expression levels as an atrophy-associated component that impacts the characteristic muscle dysfunction symptoms in DM1 patients.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100667"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S231941702300104X/pdfft?md5=1be53c3ab977b1e60a3e8df7bda4edd9&pid=1-s2.0-S231941702300104X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41101531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aptamer-functionalized liposomes for drug delivery","authors":"","doi":"10.1016/j.bj.2023.100685","DOIUrl":"10.1016/j.bj.2023.100685","url":null,"abstract":"<div><p>Among the various targeting ligands for drug delivery, aptamers have attracted much interest in recent years because of their smaller size compared to antibodies, ease of modification, and better batch-to-batch consistency. In addition, aptamers can be selected to target both known and even unknown cell surface biomarkers. For drug loading, liposomes are the most successful vehicle and many FDA-approved formulations are based on liposomes. In this paper, aptamer-functionalized liposomes for targeted drug delivery are reviewed. We begin with the description of related aptamers selection, followed by methods to conjugate aptamers to liposomes and the fate of such conjugates <em>in vivo</em>. Then a few examples of applications are reviewed. In addition to intravenous injection for systemic delivery and hoping to achieve accumulation at target sites, for certain applications, it is also possible to have aptamer/liposome conjugates applied directly at the target tissue such as intratumor injection and dropping on the surface of the eye by adhering to the cornea. While previous reviews have focused on cancer therapy, the current review mainly covers other applications in the last four years. Finally, this article discusses potential issues of aptamer targeting and some future research opportunities.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100685"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417023001221/pdfft?md5=5ba4cbfa95c2259f31ece7b9b52ed767&pid=1-s2.0-S2319417023001221-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138573412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAN008 prolongs overall survival in patients with newly diagnosed GBM characterized by high tumor mutational burden","authors":"","doi":"10.1016/j.bj.2023.100660","DOIUrl":"10.1016/j.bj.2023.100660","url":null,"abstract":"<div><h3>Background</h3><p>A previous phase 1 dose-escalation study in Taiwan indicated CAN008 (asunercept) with standard concurrent chemoradiotherapy (CCRT) improved progression-free survival (PFS) in newly diagnosed glioblastoma (GBM) patients. This study evaluates the efficacy of CAN008 in promoting overall survival (OS) and identifies genetic alterations associated with treatment responses.</p></div><div><h3>Methods</h3><p>We compared OS of 5-year follow-ups from 9 evaluable CAN008 cohort patients (6 received high-dose and 3 received low-dose) to a historical Taiwanese GBM cohort with 164 newly diagnosed patients. CAN008 treatment response-associated genetic alterations were identified by whole-exome sequencing and comparing variant differences between response groups. Associations among patient survival, tumor mutational burden (TMB), and genetic alterations were analyzed using CAN008 cohort and TCGA-GBM dataset.</p></div><div><h3>Results</h3><p>OS for high-dose CAN008 patients at 2 and 5 years was 83% and 67%, respectively, and 40.1% and 8.8% for the historical GBM cohort, respectively. Better OS was observed in the high-dose CAN008 cohort (without reaching the median survival) than the historical GBM cohort (median OS: 20 months; <em>p</em> = 0.0103). Five high-dose CAN008 patients were divided into good and poor response groups based on their PFS. A higher variant count and TMB were observed in good response patients, whereas no significant association was observed between TMB and patient survival in the newly diagnosed TCGA-GBM dataset, suggesting TMB may modulate patient CAN008 response.</p></div><div><h3>Conclusion</h3><p>CAN008 combined with standard CCRT treatment prolonged the PFS and OS of newly diagnosed GBM patients compared to standard therapy alone. Higher treatment efficacy was associated with higher TMB.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100660"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417023000975/pdfft?md5=9e796b4d31372a214ba91569ea5d855f&pid=1-s2.0-S2319417023000975-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41177949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"c-MYC/METTL3/LINC01006 positive feedback loop promotes migration, invasion and proliferation of non-small cell lung cancer","authors":"","doi":"10.1016/j.bj.2023.100664","DOIUrl":"10.1016/j.bj.2023.100664","url":null,"abstract":"<div><h3>Background</h3><p>This study aims to clarify the N6-methyladenosine (m6A) modification of <em>LINC01006</em>, which is involved in migration, invasion and proliferation of non-small cell lung cancer (NSCLC).</p></div><div><h3>Materials and methods</h3><p><em>LINC01006</em> and <em>METTL3</em> expressions were analyzed in TCGA-LUAD cohort. Colony formation assay, wound-healing assay and transwell assay were performed to evaluate the ability of colony formation, migration and invasion. Q-PCR and western blot analysis determined gene expressions. M6A-RNA immunoprecipitation and m6A quantification assay were used to evaluate m6A modification. qChIP assay was used to validate transcriptional target. Luciferase assay validated the miRNA targets and transcriptional targets. In-situ xenograft model were included to evaluate tumor proliferation <em>in vivo</em>.</p></div><div><h3>Results</h3><p><em>LINC01006</em> and METTL3 expressions were elevated in NSCLC cells and tissues. <em>LINC01006</em> promoted the migration and invasion of NSCLC via epithelial – mesenchymal transition (EMT). The expression of <em>LINC01006</em> was positively correlated to the expression of <em>METTL3</em>. METTL3 promoted tumor formation and proliferation in the in-situ xenograft model of NSCLC. The expression of <em>LINC01006</em> was increased by METTL3 via m6A modification. c-MYC directly induced <em>METTL3</em>. Both <em>c-MYC</em> and <em>LINC01006</em> were commonly targeted by miR-34a/b/c and miR-2682, and thereby c-MYC/METTL3/<em>LINC01006</em> formed a positive feedback loop through miRNA targets in NSCLC.</p></div><div><h3>Conclusions</h3><p><em>LINC01006</em> is an oncogenic lncRNA, which induces migration, invasion and proliferation of NSCLC. METTL3 increases <em>LINC01006</em> expression through stabilizing <em>LINC0</em>1006 mRNA. c-MYC, as a transcription factor, activates METTL3, which results in an elevated level of <em>LINC01006</em>. c-MYC, METTL3 and <em>LINC01006</em> form a positive feedback loop through multiple miRNA targets in NSCLC.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100664"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417023001014/pdfft?md5=0de141ccded89abb4cf91afb0ff9abb8&pid=1-s2.0-S2319417023001014-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41117696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal stem cell transplantation may be able to induce immunological tolerance in systemic lupus erythematosus","authors":"","doi":"10.1016/j.bj.2024.100724","DOIUrl":"10.1016/j.bj.2024.100724","url":null,"abstract":"<div><p>Systemic lupus erythematosus (SLE) is a common, potentially fatal autoimmune disease involving a significant inflammatory response. SLE is characterised by failure of self-tolerance and activation of autoreactive lymphocytes, leading to persistent disease. Although current treatments achieve some improvement in patients, some SLE patients are refractory and others relapse after drug withdrawal. The toxicity of current drug regimens, with recurrent infections, together with ongoing inflammation, contribute significantly to the progressive decline in organ function. Therefore, the clinical management of SLE requires more effective and less toxic treatments, ideally inducing complete remission and self-tolerance. In this context, recently developed cell therapies based on mesenchymal stem cells (MSCs) represent a promising and safe strategy in SLE. MSCs inhibit the activation of B cells, prevent the differentiation of CD4⁺ T cells into autoreactive T cells, reprogram macrophages with anti-inflammatory effects and inhibit dendritic cells (DCs), limiting their activity as antigen-presenting cells. In addition, MSCs could induce antigen-specific tolerance by enhancing anergy processes in autoreactive cells - by inhibiting the maturation of antigen-presenting DCs, blocking the T cell receptor (TcR) pathway and secreting inhibitory molecules -, increasing apoptotic activity to eliminate them, and activating regulatory T cells (Tregs) to enhance their proliferation and induction of tolerogenic DCs. Thus, induction of self-tolerance leads to immune balance, keeping inflammation under control and reducing lupus flares.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100724"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417024000271/pdfft?md5=903807a8be42cb2b8b6fcfafaa068ca8&pid=1-s2.0-S2319417024000271-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140770484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Idiopathic pulmonary fibrosis (IPF): Diagnostic routes using novel biomarkers","authors":"","doi":"10.1016/j.bj.2024.100729","DOIUrl":"10.1016/j.bj.2024.100729","url":null,"abstract":"<div><p>Idiopathic pulmonary fibrosis (IPF) diagnosis is still the diagnosis of exclusion. Differentiating from other forms of interstitial lung diseases (ILDs) is essential, given the various therapeutic approaches. The IPF course is now unpredictable for individual patients, although some genetic factors and several biomarkers have already been associated with various IPF prognoses. Since its early stages, IPF may be asymptomatic, leading to a delayed diagnosis. The present review critically examines the recent literature on molecular biomarkers potentially useful in IPF diagnostics. The examined biomarkers are grouped into breath and sputum biomarkers, serologically assessed extracellular matrix neoepitope markers, and oxidative stress biomarkers in lung tissue. Fibroblasts and complete blood count have also gained recent interest in that respect. Although several biomarker candidates have been profiled, there has yet to be a single biomarker that proved specific to the IPF disease. Nevertheless, various IPF biomarkers have been used in preclinical and clinical trials to verify their predictive and monitoring potential.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 4","pages":"Article 100729"},"PeriodicalIF":4.1,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417024000325/pdfft?md5=bf7e330e3608e63be9d0aa09104b9b27&pid=1-s2.0-S2319417024000325-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140793450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}