<?xml version="1.0" encoding="utf-8"?>
    <rss version="2.0">
      <channel xmlns:content="http://purl.org/rss/1.0/modules/content/">
        <title>Experimental Biology and Medicine | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine</link>
        <description>RSS Feed for Experimental Biology and Medicine | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-09-25T14:25:53.872+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10935</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10935</link>
        <title><![CDATA[CERKL-related inherited retinal dystrophy in a Brazilian cohort: genotype-phenotype correlation]]></title>
        <pubdate>2026-09-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>E. S. Yasaki</author><author>M. V. Salles</author><author>F. L. Motta</author><author>J. M. F. Sallum</author>
        <description><![CDATA[The purpose of this study was to analyze the genotype-phenotype of CERKL-related inherited retinal dystrophy in an outpatient clinic. For the study, 2841 medical records of Brazilian patients with a diagnosis of an inherited retinal dystrophy (IRD) registered at Instituto de Genética Ocular, Brazil, between January 2006 and July 2025 were retrospectively reviewed and 52 patients from 50 unrelated families with a molecular diagnosis of an IRD related to the CERKL gene were selected. Clinical data and molecular tests results were analyzed for genotype-phenotype correlation. Most patients (50/52) presented with the cone rod dystrophy (CORD) and two patients presented with the macular dystrophy (MD) phenotype. Age of presenting symptoms ranged from early childhood (7 years old) to adulthood (40 years old). BCVA Snellen measured at the first visit ranged from 20/25 to light perception, corresponding to 0.1 to 2.7 in log MAR visual acuity. Visual acuity data according to disease duration at the first visit of 37 double null (DN) alleles patients disclosed a Pearson coefficient R2 of 0.315 for the right eye and 0.405 for the left eye, respectively. A highly significant association between disease duration and visual acuity loss was found suggesting consistent and predictable visual deterioration in patients with complete CERKL loss-of-function over time. Twenty-four different variants described in the CERKL gene were identified. The c.847C>T (p.Arg283) nonsense variant in exon 6 was the most common variant in this cohort, identified in 24 homozygous out of 52 individuals and in 12 compound heterozygous. The phenotype of CERKL-related IRD is CORD with an early age of presentation and fast decrease in visual acuity. In addition to OMIM classifying this gene as an retinitis pigmentosa IRD, we believe CERKL has CORD phenotype, in concordance with evidence described in the literature.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10940</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10940</link>
        <title><![CDATA[Primary biliary cirrhosis and inflammatory bowel disease: a two-sample bidirectional Mendelian randomization study]]></title>
        <pubdate>2026-09-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mingyi Yang</author><author>Jiale Xie</author><author>Jing Hu</author><author>Pengfei Wen</author><author>Lin Liu</author><author>Zhi Yang</author><author>Ming Zhang</author><author>Changliang Zhu</author><author>Yani Su</author>
        <description><![CDATA[Observational studies have frequently reported an association between primary biliary cirrhosis (PBC) and inflammatory bowel disease (IBD). In this study, we leveraged summary-level data from genome-wide association studies (GWAS) to conduct a two-sample bidirectional Mendelian randomization (MR) analysis, with the primary objective of investigating the genetic causal relationship between PBC and IBD, comprising ulcerative colitis (UC) and Crohn’s disease (CD). Additionally, a validation analysis was performed by repeating the bidirectional MR framework, alternately defining PBC and IBD as the exposure and outcome variables to confirm the directionality of the observed associations. A comprehensive panel of sensitivity analyses was implemented to test the robustness of the findings. We first examined the genetic causality at the subtype level. In the forward MR, PBC exerted a significant positive causal effect on UC (P < 0.001, OR 95% CI = 1.081 [1.037–1.127]) and on CD (P = 0.002, OR 95% CI = 1.136 [1.047–1.232]). In the reverse MR, only UC showed a significant negative causal influence on PBC (P > 0.003, OR 95% CI = 0.788 [0.672–0.924]), whereas no significant effect was detected from CD on PBC (P = 0.431, OR 95% CI = 0.956 [0.856–1.068]). We then extended the analysis to the overall IBD phenotype. The forward MR demonstrated a significant positive genetic relationship between PBC on IBD (P < 0.001, OR 95% CI = 1.076 [1.042–1.110]). Conversely, the reverse MR did not support a causal effect of IBD on PBC (P = 0.357, OR 95% CI = 0.898 [0.714–1.129]). The robustness of all these findings was confirmed by comprehensive sensitivity analyses, which showed no evidence of heterogeneity, horizontal pleiotropy, or undue influence from individual instrumental variables. Our MR analysis demonstrates that PBC serves as a genetic determinant of IBD as a whole and of UC/CD separately, whereas reverse causation is limited to a protective effect of UC on PBC. This direction-dependent and subtype-specific causal architecture provides novel insights into the shared etiological pathways between PBC and IBD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11238</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11238</link>
        <title><![CDATA[The causal relationship between antibody-mediated immune responses to infections and Graves’ disease: a bi-directional Mendelian randomization analysis]]></title>
        <pubdate>2026-09-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xinwei Zhang</author><author>Wenyu Xu</author><author>Zhou Liu</author><author>Jinan Zhang</author><author>Xiaorong Yang</author>
        <description><![CDATA[The pathogenesis of Graves’ disease (GD) has not been fully elucidated, and antibody-mediated immune responses following microbial infection may be involved in its development. We conducted a bidirectional two-sample Mendelian randomization analysis using genetic variants associated with GD and 46 antibody-mediated immune-response phenotypes obtained from large-scale genome-wide association studies. In the forward analysis, none of the antibody-mediated immune-response phenotypes was significantly associated with GD risk after Bonferroni or false discovery rate (FDR) correction. Three Epstein–Barr virus antibody phenotypes showed nominal inverse associations with GD under the inverse-variance weighted method, but these findings did not survive multiple-testing correction and showed evidence of heterogeneity, with additional evidence of horizontal pleiotropy for the ZEBRA antibody phenotype. In the reverse analysis, several associations survived multiple-testing correction, although sensitivity analyses indicated heterogeneity or horizontal pleiotropy for the corrected associations except anti-polyomavirus 2 IgG seropositivity. After jointly considering multiple-testing correction and sensitivity analyses, genetic liability to GD was associated with higher anti-polyomavirus 2 IgG seropositivity (OR = 1.156, 95% CI: 1.050–1.273; P = 0.003), which remained significant after FDR correction but did not reach the Bonferroni-corrected threshold. Four additional associations—lower cytomegalovirus pp52 and pp150 antibody levels and higher Helicobacter pylori UreA antibody levels and anti-Merkel cell polyomavirus IgG seropositivity—were nominally significant and should be considered hypothesis-generating. Overall, this bidirectional MR study suggests that genetic liability to GD may influence selected humoral immune-response phenotypes. Notably, the association with anti-polyomavirus 2 IgG seropositivity remained significant after FDR correction, while additional suggestive associations were observed for antibody responses related to CMV, Helicobacter pylori, and Merkel cell polyomavirus. These findings provide new genetic insights into the potential relationship between GD and infection-related humoral immunity, while the potential influence of antibody-mediated immune responses on GD risk warrants further investigation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11023</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11023</link>
        <title><![CDATA[Causal effects of gut microbiota on functional gastrointestinal disorders: a bidirectional Mendelian randomization study]]></title>
        <pubdate>2026-09-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yutong Cheng</author><author>Qiuai Shu</author><author>Ziwei Wang</author><author>Jian Wu</author><author>Yuxin Peng</author><author>Jiale Xie</author><author>Xiru Liang</author><author>Zhiwei Tao</author><author>Haitao Shi</author><author>Zhongcao Wei</author><author>Jinhai Wang</author><author>Ning Xie</author>
        <description><![CDATA[Emerging evidence suggests that gut microbiota is associated with functional gastrointestinal disorders (FGIDs). However, findings regarding microbial alterations in FGIDs have been inconsistent across observational studies, and the direction and causality of these associations remain unclear. We conducted a bidirectional two-sample Mendelian randomization (MR) study to investigate potential causal associations between gut microbiota and two common FGIDs, irritable bowel syndrome (IBS) and functional dyspepsia (FD). Genome-wide association study (GWAS) summary statistics of gut microbiota, IBS, and FD were obtained from public databases and applied to our MR analysis. The inverse-variance-weighted method was used as the primary analysis, with weighted median and complementary sensitivity analyses used to assess the consistency and robustness of the findings. Higher genetically predicted abundances of order Bifidobacteriales (OR: 0.741, 95% CI: 0.570 to 0.963, P = 0.025) and genus Eubacterium ventriosum group (OR: 0.684, 95% CI: 0.524 to 0.893, P = 0.005) were associated with a lower risk of IBS. Genus Lachnospiraceae NK4A136 group (OR: 1.368, 95% CI: 1.086 to 1.722, P = 0.008) correlated to a high risk of FD while family Desulfovibrionaceae and order Desulfovibrionales (OR: 0.649, 95% CI: 0.471 to 0.893, P = 0.008) were protective for FD. In the reverse MR analysis, genetically predicted IBS risk was associated with lower abundances of Turicibacter and Slackia, whereas no robust reverse associations were observed for FD. These findings identify several microbial taxa as candidates for further mechanistic and clinical validation rather than established risk factors or therapeutic targets. Further experimental research to investigate the underlying mechanisms is warranted.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11199</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11199</link>
        <title><![CDATA[Maternal high-fat diet and risk of cardiovascular disease in offspring: a review of mechanisms, controversies, and interventions]]></title>
        <pubdate>2026-09-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Heyu Meng</author><author>Jianjun Ruan</author><author>Qing Wang</author><author>Fanbo Meng</author>
        <description><![CDATA[A high-fat diet (HFD) is a well-established risk factor for coronary artery disease (CAD). Accumulating evidence indicates that maternal nutritional status before and during pregnancy critically influences long-term cardiovascular outcomes in offspring. This review systematically synthesizes current mechanistic, epidemiological, and clinical evidence regarding the impact of HFD on CAD while also examining its effects on broader cardiovascular phenotypes that are integral to CAD pathogenesis, such as endothelial dysfunction, cardiac remodeling, and metabolic derangements. A particular focus is placed on the potential effects of maternal pre-pregnancy HFD exposure on offspring CAD risk in adulthood. Existing studies suggest that HFD induces coronary injury primarily through metabolic dysregulation, endothelial dysfunction, and epigenetic reprogramming. Notably, maternal exposure to HFD during the perinatal period may predispose offspring to coronary artery disease via these mechanisms. Conversely, appropriate maternal nutritional interventions during pregnancy have shown promise in mitigating these adverse effects, although their long-term efficacy and underlying molecular mechanisms remain to be fully elucidated. Future research should prioritize large-scale prospective cohort studies with extended follow-up to determine the optimal timing, mechanisms, and efficacy of dietary interventions. Such evidence would provide a scientific foundation for developing preventive and therapeutic strategies aimed at reducing cardiovascular disease risk from the earliest developmental stages.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11246</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11246</link>
        <title><![CDATA[Extracellular vesicles for abdominal aortic aneurysm: mechanisms, therapeutic potential, and translational challenges]]></title>
        <pubdate>2026-08-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Huibo Ma</author><author>Zongyou Xie</author><author>Yihang Cai</author><author>Fangda Li</author><author>Jianqiang Wu</author><author>Yuehong Zheng</author>
        <description><![CDATA[Abdominal aortic aneurysm (AAA) is a progressive and potentially fatal vascular disease for which no effective pharmacological therapy is currently available. While surgical repair remains the only definitive treatment for advanced aneurysms, patients with small AAAs are mainly managed by surveillance, highlighting the need for disease-modifying strategies. Extracellular vesicles (EVs) have emerged as promising cell-free therapeutic tools because of their biocompatibility, ability to transfer bioactive cargo, and capacity to regulate multiple pathological processes involved in AAA progression. This review summarizes recent advances in EV-based therapies for AAA, focusing on mesenchymal stromal cell-derived EVs, immune cell-derived EVs, and engineered EV platforms. Preclinical studies suggest that therapeutic EVs can attenuate aneurysm formation by suppressing macrophage-driven inflammation, regulating macrophage polarization, inhibiting neutrophil extracellular trap-associated injury, protecting vascular smooth muscle cells from senescence, ferroptosis, apoptosis, and mitochondrial dysfunction, and limiting extracellular matrix degradation. Engineered EVs, including cargo-enriched, peptide-targeted, magnetically guided, chemotaxis-enabled, and biomaterial-assisted systems, may further improve lesion targeting, vascular retention, and therapeutic potency. However, EV-based AAA therapy remains at an early preclinical stage. Key barriers include unclear biodistribution and clearance, insufficient evidence of lesion-specific target engagement, heterogeneous EV isolation and characterization methods, uncertain dosing strategies, and the need for standardized potency, safety, manufacturing, and regulatory frameworks. Overall, EVs offer a biologically rational platform for non-surgical AAA therapy, but clinical translation requires rigorous standardization and robust evidence linking EV delivery to vascular repair.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11146</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11146</link>
        <title><![CDATA[The interaction between oxidative stress and Schwann cells]]></title>
        <pubdate>2026-08-27T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Sihan Yang</author><author>Zijun Zhang</author><author>Qing Liao</author><author>Qipeng Ouyang</author><author>Yongyou Ye</author><author>Wei Lu</author><author>Zhendong Jiang</author>
        <description><![CDATA[After peripheral nerve injury (PNI), a moderate increase in reactive oxygen species (ROS) levels can promote the proliferation and differentiation of Schwann cells (SCs) and participate in signal transduction. However, excessive ROS can trigger oxidative stress, and its harmful effects can overshadow the beneficial ones, such as inducing apoptosis, activating inflammation, disrupting environmental stability, and severely hindering neural processes. Therefore, if the damage caused by oxidative stress to SCs can be effectively alleviated, it will provide a new approach for the precise regeneration between peripheral nerves and target organs, thereby reducing the complications of PNI. With the advancements in materials science and neural tissue engineering, functional and precisely designed neural scaffolds and conduits have emerged as highly promising therapeutic strategies. This article focuses on revealing the interaction between SCs and oxidative stress during nerve injury, as well as the innovative tissue engineering technologies and new paradigms for damage repair that have emerged based on this interaction. It aims to provide effective new methods for addressing temporary or permanent functional impairments of PNI/peripheral neuropathies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11144</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11144</link>
        <title><![CDATA[Altered serum interleukin-4 and monocyte chemoattractant protein-3 levels are associated with generalized anxiety disorder: a case-control study]]></title>
        <pubdate>2026-08-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Most. Humayra Binta Rashid</author><author>Mehedi Islam</author><author>Sardar Mohammad Ashraful Islam</author><author>Md. Rabiul Islam</author>
        <description><![CDATA[Generalized Anxiety Disorder (GAD) is a long-term mental health condition often associated with immune system dysregulation. While pro-inflammatory and anti-inflammatory cytokines are known to influence neuroinflammation, their specific roles in GAD remain less understood. This study investigates the relationship between serum levels of IL-4 and MCP-3 and GAD in a Bangladeshi population. This case-control study included 44 patients with GAD and 44 healthy controls (HCs). Participants were examined using the GAD-7 scale. Serum IL-4 and MCP-3 levels were measured using ELISA. Data were analyzed using t-tests, Spearman’s correlation, and Receiver Operating Characteristic (ROC) curve analysis to assess diagnostic performance. GAD patients had significantly lower serum IL-4 levels (11.82 ± 10.91 pg/mL) and higher MCP-3 levels (57.80 ± 19.85 pg/mL) compared to HCs (IL-4: 24.51 ± 15.36 pg/mL; MCP-3: 34.01 ± 15.75 pg/mL; p < 0.001). IL-4 levels showed a significant negative correlation with GAD-7 scores (r = −0.496, p < 0.001), while MCP-3 showed a positive correlation (r = 0.544, p < 0.001). ROC analysis indicated that MCP-3 had higher diagnostic accuracy (AUC = 0.848, sensitivity = 87.6%, specificity = 84.3%) compared to IL-4 (AUC = 0.782, sensitivity = 80.2%, specificity = 78.5%). Moreover, decreased IL-4 and elevated MCP-3 levels were found to be significantly associated with GAD severity, suggesting an immune imbalance. These cytokines may serve as promising diagnostic biomarkers and therapeutic targets for GAD. Further longitudinal studies are recommended to investigate this causal relationship and its underlying mechanisms.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10915</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10915</link>
        <title><![CDATA[The value of serum exosomal miRNA signature profiles for the early diagnosis of feline infectious peritonitis]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hongxia Gu</author><author>Huisheng Wu</author>
        <description><![CDATA[Feline Infectious Peritonitis (FIP) is a highly lethal disease in cats, and early differential diagnosis remains a significant clinical challenge. In this study, we analyzed differences in serum exosomal miRNA expression between FIP-affected cats and healthy control cats via high-throughput sequencing and identified five significantly differentially expressed miRNAs (miR-21-5p, miR-155-5p, miR-200c-3p, miR-486-5p, and miR-423-5p). A combined diagnostic model was constructed based on three key miRNAs (miR-21-5p, miR-155-5p, and miR-423-5p). ROC curve analysis showed that a combined model of these three key miRNAs had an area under the curve (AUC) of 0.93, with a sensitivity and specificity of 88.6% and 91.2%, respectively. These results indicate that the serum exosomal miRNA signature could be used as a novel biomarker for the early diagnosis of FIP, providing a non-invasive diagnostic tool in clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10902</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10902</link>
        <title><![CDATA[XPA confers ability of endonucleases to act processively and to incise damaged nucleosomal DNA]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Muriel W. Lambert</author><author>W. Clark Lambert</author>
        <description><![CDATA[Repair of damaged DNA is a complex process, particularly when it is compacted into nucleosomes. There are a number of genetic disorders with deficiencies in DNA repair. Knowledge of the genes and proteins involved in these repair deficiencies is critical in developing an understanding of the molecular mechanisms utilized by proteins in the DNA repair pathways. One of these genetic disorders is xeroderma pigmentosum (XP), which is defective in nucleotide excision repair (NER). Patients in XP complementation group A (XP-A) are among the most severely affected with the lowest levels of DNA repair. The XPA protein, which is defective in these patients, plays a number of roles in the DNA repair process. One particularly important role proposed is acting as a processivity factor enabling endonucleases (XPF and XPG) and the XPB/TFIIH translocase to localize to damage sites using a processive mechanism of action. Another proposed role is in interacting with chromatin-remodeling proteins so as to enhance accessibility of lesions in nucleosomal DNA to endonucleolytic incision and other DNA repair activities. In XP-A cells, the XPA protein is proposed to be defective in ability to act as a processivity factor; endonucleases localize damage sites by a distributive mechanism and are also defective in incision of damaged nucleosomal DNA. This defect is corrected by recombinant normal human XPA. Mutations in exons 3 and 5 in the DNA binding domain of the XPA gene lead to loss of ability of XPA to act as a processivity factor. The mutation in exon 5 was found in two XP-A patients with severe XP. These studies emphasize the importance of correlating specific mutations in an XP gene and the resulting defect in a particular repair protein with the clinical severity of XP and could lead to development of novel therapeutic approaches for this disorder.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11192</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11192</link>
        <title><![CDATA[The role and mechanism of neutrophils in oncolytic virus therapy]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Baixian Huang</author><author>Qixin Yang</author><author>Ruixue Wang</author><author>Chaochao Zhao</author>
        <description><![CDATA[Oncolytic viruses (OVs) are a class of viruses capable of specifically infecting and killing tumor cells. They exert antitumor effects through direct lysis of tumor cells, activation of the immune system, and disruption of tumor vasculature. Neutrophils, which originate from the bone marrow, are the most abundant leukocytes in peripheral blood and the immune system and play a dual regulatory role in oncolytic virotherapy. In different TME, neutrophils can polarize into two phenotypes: N1 and N2. N1 neutrophils, owing to their chemotaxis and tumor-homing capabilities, can serve as delivery vehicles for OVs, enhance the therapeutic efficacy of oncolytic virotherapy, and activate host immune responses. In contrast, N2 neutrophils impair the efficacy of OVs through their antiviral activity and immunosuppressive functions. Therefore, an in-depth understanding of the mechanisms underlying the role of neutrophils in oncolytic virotherapy is of great significance for optimizing OV-based therapies and improving their clinical application outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10958</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10958</link>
        <title><![CDATA[Correction: Protective effects of berberine-loaded chitosan/solid lipid nanoparticles in streptozotocin-induced gestational diabetes mellitus rats]]></title>
        <pubdate>2026-08-03T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>EBM Production Office </author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10923</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10923</link>
        <title><![CDATA[Causal association between clonal hematopoiesis indeterminate potential and cancer: a Mendelian randomization study]]></title>
        <pubdate>2026-07-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Juan Jin</author><author>Qian Pu</author><author>Chengrong Wu</author><author>Yu Lei</author><author>Yaxin Hu</author><author>Xiuju Yang</author><author>Jinghui Huang</author><author>Fangfang Wu</author><author>Li Xiao</author><author>Lei Yu</author>
        <description><![CDATA[Clonal hematopoiesis of indeterminate potential (CHIP) causes the expansion of mutated hematopoietic stem cells and produces immunophenotypically altered leukocytes, which induce a tumor-promoting inflammatory condition. However, the causal effect of CHIP on cancer remains unclear. We assessed the relationship of genetically predicted CHIP with the risk of 18 cancer types involving 612,576 cases using two-sample Mendelian randomization (MR). Genetic instruments for overall and sub-types of CHIP were obtained from the a large-scale genome-wide association study using independent (r2 < 0.001) SNPs at genome-wide significance (p < 5.0 × 10-8). Summary statistics for 18 cancers were obtained from the FinnGen, MVP, PLCO study, and large consortia. Inverse-variance weighted random-effects models were used as the primary method for estimating causal effects. Findings from independent datasets were combined using the fixed-effect model and Bonferroni corrections were applied for multiple testing. We found genetic predicted overall and DNMT3A CHIP was significantly associated with an increased risk of thyroid cancer, lung cancer, kidney cancer, brain cancer, basal cell carcinoma, and malignant melanoma after corrections. In addition, we found the causal estimate of CHIP varied across histological sub-types of cancer. Sensitivity analyses confirmed that these findings were robust. Strong associations were found between genetic predicted CHIP and an increased risk of a broad range of cancers, highlighting the importance of timely screening for CHIP in cancer early detection and prevention.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11114</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11114</link>
        <title><![CDATA[Novel perspective on immune cell regulation in gastrointestinal inflammation: the role of extracellular vesicles and therapeutic prospects]]></title>
        <pubdate>2026-07-17T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jianshu Wang</author><author>Junxuan Xu</author><author>Zilu Cui</author><author>Jing Wu</author>
        <description><![CDATA[Gastrointestinal inflammation is an inflammatory disease arising from immune imbalance in any segment of the digestive tract, triggered by various factors. Immune cells play important roles in both the onset and resolution of gastrointestinal inflammation. With the recent extensive research on extracellular vesicles, the mechanism by which immune cells regulate gastrointestinal inflammation through extracellular vesicles has gradually gained recognition within the scientific community. Extracellular vesicles derived from immune cells can communicate with other immune cells in the digestive tract and directly regulate digestive tract epithelial cells. Furthermore, with advances in biological nanotechnology, immune cell-derived extracellular vesicles may be used to treat inflammatory gastrointestinal diseases. This review focuses on delineating the role of immune cell-derived extracellular vesicles in gastrointestinal inflammation and exploring their potential applications in treating these inflammatory diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10948</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10948</link>
        <title><![CDATA[Genetic evidence for causal relationships between brain functional networks and domain-specific recovery after nondisabling ischemic stroke]]></title>
        <pubdate>2026-07-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Huan Cai</author><author>Zhenchun Huang</author><author>Jialin Liang</author><author>Hao Zhang</author><author>Zhonghua Liu</author>
        <description><![CDATA[Intrinsic brain networks are crucial for post-stroke recovery, but the causal relationships between specific networks and domain-specific recovery outcomes, as well as the role of lipid metabolism, remain unclear. This study leveraged Mendelian randomization (MR) to evaluate 191 resting-state functional magnetic resonance imaging (rs-fMRI) BOLD-derived phenotypes in relation to post-stroke recovery after nondisabling ischemic stroke. Genetic instruments for rs-fMRI phenotypes were derived from a UK Biobank genome-wide association study (n = 34,691). Outcomes included motor, cognitive, and global recovery after nondisabling ischemic stroke, assessed using longitudinal National Institutes of Health Stroke Scale subscales over 2 years (n = 1,270). Primary analyses used the multiplicative random-effects inverse-variance weighted method. A two-step MR analysis investigated whether brain networks mediate the effects of lipids on post-stroke outcomes. Higher BOLD-derived functional connectivity within the triple network (default mode network, central executive network, and salience network) was associated with better motor and cognitive outcomes. Higher genetically predicted orbitofrontal node amplitude in the limbic network correlated with better motor recovery, while stronger parieto-frontal connectivity was associated with cognitive recovery. Genetically proxied higher low-density lipoprotein cholesterol (LDL-C) was associated with poorer cognitive recovery, with evidence suggesting partial mediation through differences in BOLD-derived triple-network connectivity. This MR study supports a potential causal role of BOLD-derived functional network phenotypes, particularly the triple network, in motor and cognitive recovery, and further suggests that differences in triple-network connectivity act as a partial mediator linking elevated LDL-C liability to impaired cognitive recovery. These findings provide hypothesis-generating evidence for future mechanistic studies and for exploring whether specific brain network-targeted interventions could have a role in stroke recovery.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11058</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11058</link>
        <title><![CDATA[Gut microbiota and polyendocrine metabolic ovarian syndrome: an integrated gut–metabolism–endocrine–ovary axis]]></title>
        <pubdate>2026-07-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Shengyue Jin</author><author>Menglei Zhu</author><author>Yiyang Lu</author><author>Jia Zhao</author><author>Jiayi Zhu</author><author>Xiaohong Fang</author>
        <description><![CDATA[Polyendocrine metabolic ovarian syndrome (PMOS), previously known as polycystic ovary syndrome (PCOS), is a common endocrine and metabolic disorder in reproductive-age women, characterized by marked clinical and biological heterogeneity. Accumulating evidence suggests that gut microbiota dysbiosis is associated with metabolic disturbances, hormonal imbalance, and ovarian dysfunction in PMOS. However, the pathways linking gut microbiota alterations to PMOS pathogenesis remain incompletely understood, and most evidence remains associative. This review aims to summarize current evidence regarding interactions between gut microbiota and PMOS, clarify the roles of key microbiota-derived metabolites, and evaluate the potential and limitations of gut microbiota–targeted interventions. A major novelty is the proposal of an integrated gut–metabolism–endocrine–ovary axis incorporating phenotypic heterogeneity, methodological variability, and evidence grading across clinical and preclinical studies. A narrative review with a systematic literature search was conducted. PubMed, Web of Science, Embase, and CNKI were searched from inception to March 2026 using terms related to PMOS, gut microbiota, microbial metabolites, and microbiota-targeted interventions. Eligible studies included human observational or interventional studies, animal experiments exploring microbiota–PMOS mechanisms, and peer-reviewed full-text articles in English or Chinese. Case reports, letters, conference abstracts, non-English publications, and irrelevant studies were excluded. Duplicate records were removed. Two authors independently screened records and resolved disagreements by consensus. No meta-analysis was performed, and clinical registration was not applicable. Gut microbiota dysbiosis may contribute to PMOS through chronic low-grade inflammation, insulin resistance, and hyperandrogenism. Microbiota-derived metabolites link intestinal dysbiosis with metabolic and endocrine dysfunction. Bile acids and short-chain fatty acids exert regulatory effects, whereas amino acid disorders and LPS-mediated endotoxemia amplify metabolic and inflammatory abnormalities. Considerable heterogeneity exists across studies regarding obesity, insulin resistance, hyperandrogenism, diet, ethnicity, region, and methodology. Microbiota-targeted interventions show potential, although evidence quality varies and most findings remain associative. Gut microbiota dysbiosis is a critical regulatory node within the integrated gut–metabolism–endocrine–ovary axis in PMOS. This review highlights phenotypic stratification, evidence hierarchy, and clinical translation potential. Although microbiota-targeted strategies may serve as adjunctive therapies, their causal roles and long-term efficacy require confirmation in well-designed longitudinal and randomized controlled trials.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11099</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11099</link>
        <title><![CDATA[A whole-transcriptome analysis of differentially expressed genes, transcripts, and transcript usage in blood samples from Parkinson’s disease patients]]></title>
        <pubdate>2026-07-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sulev Koks</author><author>Mari Muldmaa</author><author>Jack Price</author><author>Luke Whiley</author><author>Maili Jakobson</author><author>Lewis Singleton</author><author>Denise Howting</author><author>Abigail L. Pfaff</author><author>Abha Chopra</author><author>Mark Watson</author><author>Katrin Sikk</author><author>Pille Taba</author>
        <description><![CDATA[Parkinson’s disease (PD) is a complex neurodegenerative disorder with diverse molecular signatures that extend beyond the central nervous system. Peripheral blood serves as a minimally invasive source of transcriptomic biomarkers reflecting systemic inflammation, mitochondrial dysfunction, lysosomal impairment, and disrupted RNA processing—key pathways involved in PD. Long-read RNA sequencing with Oxford Nanopore Technologies (ONT) offers unprecedented detail of full-length transcripts, alternative isoforms, and RNA modifications, enabling more accurate detection of disease-related transcriptional changes. We conducted high-throughput ONT long-read RNA sequencing on blood samples from 145 individuals, including PD patients and age-matched healthy controls. RNA libraries were prepared using a cDNA-based protocol optimised for high-accuracy PromethION sequencing. Transcriptomes were quantified with ONT-specific pipelines, and analyses of differential gene expression (DGE), differential transcript expression (DEX), differential transcript usage (DTU), and alternative splicing were performed using ONT-aware tools such as DRIMSeq, DEXSeq, and stageR. Pathway enrichment linked disease-related changes to mitochondrial, lysosomal, and vesicle-trafficking pathways. Our analysis identified highly significant PD-associated transcriptional signatures in peripheral blood (SNCA, VPS13C, LRRK2, GRN, STAU1, NPTN, PARK7). Long-read sequencing uncovered extensive isoform-level dysregulation, including novel transcript variants (e.g., BCL2L2-PABPN1, SQSTM1) in pathways relevant to PD, such as autophagy and endolysosomal trafficking. DTU analyses revealed shifts in isoforms of LRRK2 and GBA1, indicating widespread disturbances in RNA processing. Enrichment analysis showed activation of molecular pathways linked to neurodegeneration. This study provides the largest long-read blood transcriptomic dataset in PD to date, demonstrating that ONT sequencing can resolve isoform-level changes and reveal systemic molecular signatures of PD. Our findings support the development of blood-based RNA biomarkers and the establishment of long-read transcriptomics as a transformative approach for genomic pathology in PD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11060</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11060</link>
        <title><![CDATA[Transcriptomics-based identification of shared biomarkers across type 2 diabetes, mild cognitive impairment, and uric acid metabolism]]></title>
        <pubdate>2026-07-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yan Liu</author><author>Dongmei Kang</author><author>Yuan Lei</author>
        <description><![CDATA[Uric acid metabolism is associated with the development of type 2 diabetes mellitus (T2DM), cardiometabolic, and cardiovascular diseases. Additionally, T2DM patients often exhibit mild cognitive impairment (MCI). However, the underlying mechanisms remain unclear. This study aims to identify and validate biomarkers associated with uric acid metabolism in T2DM and MCI, with the goal of discovering potential diagnostic and therapeutic targets to improve the quality of life for T2DM patients. Transcriptomic data for T2DM, MCI and uric acid metabolism-related genes were sourced from public databases. Biomarkers were screened using machine learning and validated for expression. Subsequent analyses included functional enrichment, immune infiltration, subcellular localization, and drug prediction. Three biomarkers—HP, ITGB3, and SELP—were identified. All showed significantly elevated expression in the T2DM group (p < 0.05). HP and ITGB3 were primarily enriched in ribosome-related pathways, primary immunodeficiency, and adherens junction processes. Immune infiltration analysis revealed that immature B cells and plasmacytoid dendritic cells were significantly enriched in T2DM. HP showed the strongest positive correlation with plasmacytoid dendritic cells (cor = 0.65, FDR <0.05), while ITGB3 exhibited the strongest positive correlation with immature B cells (cor = 0.76, FDR <0.05). Several potential therapeutic drugs were predicted, including calcifediol (score = −99.93) and meclofenamic acid (score = −99.89). This study identified three candidate biomarkers co-dysregulated across T2DM and MCI transcriptomes and associated with uric acid metabolism. Given the exploratory sample sizes, these findings are considered hypothesis-generating and require validation in larger independent cohorts.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11128</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11128</link>
        <title><![CDATA[Mitochondrial transfer and mesenchymal stem cells in ophthalmology: current evidence and therapeutic implications]]></title>
        <pubdate>2026-06-30T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Xiaoli Liu</author><author>Mingqi Zhang</author><author>Zhuoshi Wang</author>
        <description><![CDATA[Mitochondrial dysfunction, driven by genetic mutations or oxidative stress, is a central contributor to the onset and progression of ophthalmic diseases. In recent years, intercellular mitochondrial transfer (MT) has emerged as a novel mechanism of cellular communication and repair in ocular tissues. MT occurs through tunneling nanotubes, extracellular vesicles (EVs), cell fusion, or transmitophagy, and has been shown to support photoreceptor survival, maintain retinal homeostasis, and protect against oxidative injury. Mesenchymal stem cells (MSCs), owing to their remarkable reparative and immunomodulatory properties, have attracted particular attention as efficient mitochondrial donors. Evidence from experimental models demonstrates that MSC-mediated MT can restore bioenergetics, mitigate oxidative stress, and rescue cellular function in inherited optic neuropathies, corneal injuries, retinal degenerative diseases, and ischemic retinopathies. This review summarizes current evidence of MT in ophthalmology, highlights the therapeutic contributions of MSCs, discusses the molecular and microenvironmental factors regulating MT efficiency, and outlines unresolved challenges. We further provide perspectives on how mitochondrial transfer may be translated into innovative therapies for ocular disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11069</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11069</link>
        <title><![CDATA[Advances in research on pharmacological mechanisms of anatabine: from nicotinic modulation to multitarget therapeutic potential]]></title>
        <pubdate>2026-06-29T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xiaonan Li</author><author>Xiaomin Liu</author><author>Huaquan Sheng</author><author>Jianfeng Guo</author><author>Leihao Zhang</author><author>Ting Fei</author><author>Yihan Gao</author>
        <description><![CDATA[Anatabine, a characteristic minor alkaloid derived from tobacco byproducts, exhibits unique structural analogy to nicotine but possesses a superior safety profile and lower addictive liability, rendering it a promising natural multi-target therapeutic candidate. Accumulating preclinical evidence has demonstrated that anatabine exerts neuroprotective, anti-inflammatory, and antioxidant effects mainly through modulating α7/α4β2 nicotinic acetylcholine receptors, suppressing NF-κB/STAT3 inflammatory signaling, and activating the Nrf2-mediated antioxidant pathway. It effectively ameliorates typical pathological alterations, including β-amyloid deposition, tau hyperphosphorylation, and microglial overactivation, thereby improving cognitive and behavioral deficits in neurodegenerative disease models. Additionally, anatabine displays broad pharmacological potentials in chronic inflammation, autoimmune thyroiditis, asthma, and hypertension. Differing from previous reviews that merely focused on single receptor regulation, the present work systematically summarizes the multi-target pharmacological characteristics of anatabine, comprehensively collates its preclinical efficacy across multiple disease categories, and highlights its advantages over nicotine in safety and addiction risk. Furthermore, we analyze the current limitations, druggability optimization challenges, and clinical translation prospects, and propose sustainable strategies for high-value utilization of tobacco byproducts. This review provides an updated and systematic theoretical basis for further mechanism exploration and therapeutic development of anatabine.]]></description>
      </item>
      </channel>
    </rss>