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        <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>2026-05-14T02:16:14.734+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10987</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10987</link>
        <title><![CDATA[Peripheral immune cells and glycation indices as potential diagnostic biomarkers in amyotrophic lateral sclerosis]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xue Yang</author><author>Jing Yang</author><author>Rui Li</author><author>Hui Dong</author><author>Yaling Liu</author>
        <description><![CDATA[The diagnosis of amyotrophic lateral sclerosis (ALS) mainly relies on clinical symptoms and the exclusion of other diseases, with a lack of specific biomarkers, leading to delayed diagnosis and a high rate of misdiagnosis. This study aims to explore the utility of peripheral immune cells and glycosylation indices as potential diagnostic biomarkers for ALS to enhance the accuracy and efficiency of early ALS diagnosis. This retrospective study included 54 ALS patients diagnosed in our hospital from June 2023 to October 2024, along with 54 healthy controls. Blood samples and laboratory data, including levels of peripheral immune cells and glycosylation indices, were collected from both groups. Through logistic regression, random forest models, receiver operating characteristic (ROC) curve analysis, and SHAP interpretability analysis, the predictive abilities and clinical significance of each candidate indicator were screened and evaluated. Notable disparities were detected in age, leukocyte count, monocyte levels, glycated haemoglobin A1c (HbA1c), and haemoglobin glycation index (HGI) between the control and ALS groups (all P < 0.05). Logistic regression analysis revealed that age (OR = 1.114) and monocyte (OR = 3.174) were risk factors for ALS, while leukocyte (OR = 0.533) and HbA1c (OR = 0.069) were protective factors. The random forest algorithm, ranked by decreasing importance, showed that leukocyte, HGI, monocyte, and HbA1c level all influenced ALS. Using these indicators to predict ALS resulted in a false-positive rate of 18% and a false-negative rate of 6%. ROC curve analysis indicated that the combined use of leukocyte, monocyte, HbA1c level, and HGI provided the highest diagnostic value for ALS (AUC = 0.774), which was higher than that of any individual indicator (all P < 0.05). SHAP analysis visualization demonstrated that increased monocyte and decreased leukocyte, HGI, and HbA1c level were all associated with an increased risk of ALS onset, ranked in descending order of feature importance as monocyte, leukocyte, HGI, and HbA1c. Peripheral blood white blood cells, monocytes, HbA1c, and HGI can serve as potential diagnostic biomarkers for ALS. Combined detection can improve the diagnostic accuracy of ALS, facilitating early diagnosis and intervention, and ultimately improving patient prognosis. Further validation in cohorts including disease controls is required to confirm specificity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10945</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10945</link>
        <title><![CDATA[Antibody-mediated immune responses and cardiovascular disease: a Mendelian randomization study]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yi Li</author><author>Jiuqi Fan</author><author>Lirong Wu</author>
        <description><![CDATA[Cardiovascular diseases represent the leading cause of global mortality and disability, posing a severe threat to human health. Accumulating evidence suggests that antigen–antibody–mediated immune responses may be involved in the pathogenesis of various cardiovascular conditions; however, whether these associations reflect causal relationships has long remained unclear. To address this question, we conducted a bidirectional two-sample Mendelian randomization study leveraging summary-level data from genome-wide association studies. In this analysis, 46 antibody-mediated immune traits were evaluated as exposures, and 11 cardiovascular outcomes, including aortic aneurysm, aortic valve stenosis, atrial fibrillation, coronary artery disease, dilated cardiomyopathy, atrioventricular block, heart failure with reduced ejection fraction, hypertrophic cardiomyopathy, infective endocarditis, myocarditis, and pericarditis, were examined as outcomes. Our results revealed several significant causal associations: genetically predicted higher levels of Epstein–Barr virus EBNA-1 antibodies were associated with increased risks of myocarditis and aortic valve stenosis, while elevated VCA p18 antibody levels were linked to a higher risk of myocarditis. Furthermore, increased antibody levels against BK polyomavirus VP1 were causally associated with greater risks of aortic valve stenosis and dilated cardiomyopathy. In contrast, higher levels of antibodies against varicella-zoster virus glycoproteins and human herpesvirus 6 IE1B were associated with reduced risks of myocarditis and aortic aneurysm, respectively. These findings not only help clarify the causal role of immune-mediated mechanisms in cardiovascular pathogenesis but also provide a theoretical foundation for the future development of immune-targeted strategies for prevention and treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10922</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10922</link>
        <title><![CDATA[Causal relationship between oral diseases and hypertension: a Mendelian randomization study]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Bofan Qian</author><author>Zhiwen Fang</author>
        <description><![CDATA[Current evidence supports the potential association between several common oral diseases and hypertension. The aim of the research is to clarify the causal relationship between these oral diseases and hypertension using Mendelian randomization (MR) analysis. Single nucleotide polymorphisms (SNPs) related to five oral traits (periodontitis, bleeding gums, loose teeth, periapical abscess and dental caries) were obtained from GWAS catalog, while those associated with hypertension (essential and secondary) were extracted from the FinnGen database. The SNPs were employed as instrumental variables (IVs) in the MR analysis. Assorted methods were applied, and inverse variance-weighted (IVW) analytical method was prioritized. Sensitivity analyses including MR-PRESSO method, MR Egger intercept test, Cochran’s Q test, leave-one-out analysis and MR Steiger test were conducted. Our analysis identified the potential causal relationship between dental caries and essential hypertension. The forward MR analysis demonstrated a significant causal effect of dental caries on essential hypertension (OR = 1.036, 95%CI: 1.012–1.059, P = 0.003). The reverse analysis also indicated a significant causal effect (OR = 1.160, 95%CI: 1.016–1.323, P = 0.028). Additionally, we observed a causal effect of bleeding gums on essential hypertension (OR = 1.145, 95%CI: 1.019–1.288, P = 0.023). These findings support the potential causality between specific oral diseases and essential hypertension.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10997</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10997</link>
        <title><![CDATA[Ferroptosis and futile recanalization after mechanical thrombectomy in acute ischemic stroke: mechanisms, risk factors, predictive models and therapeutic interventions]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yuexin Wu</author><author>Cuiying Zhang</author><author>Yangyang Peng</author><author>Longlong Liu</author>
        <description><![CDATA[Acute ischemic stroke (AIS) remains a leading cause of mortality and long-term disability worldwide. Endovascular mechanical thrombectomy (EVT) has revolutionized stroke treatment by enabling rapid recanalization of occluded cerebral vessels. However, a significant proportion of patients experience futile recanalization, where successful vessel reopening fails to translate into favorable functional outcomes. Emerging evidence highlights ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, as a critical mechanism contributing to neuronal damage in ischemic stroke, particularly during reperfusion injury. This comprehensive review examines the intricate relationship between ferroptosis and futile recanalization following mechanical thrombectomy. We systematically explore the molecular mechanisms underlying ferroptosis in the context of cerebral ischemia-reperfusion injury, including iron metabolism dysregulation, lipid peroxidation cascades, glutathione depletion, and mitochondrial dysfunction. Multiple factors contribute to futile recanalization, including patient demographics (age, comorbidities), stroke characteristics (severity, infarct volume, collateral status), procedural variables (time to treatment, recanalization quality), and post-procedural complications (hemorrhagic transformation, reperfusion injury). We review current predictive models, including nomograms and machine learning algorithms, that integrate clinical, radiological, and biomarker data to stratify patient risk. Importantly, we discuss potential therapeutic interventions targeting ferroptosis pathways, such as iron chelators, lipophilic antioxidants, and ferroptosis-specific inhibitors. The integration of ferroptosis biomarkers into predictive models may enhance risk stratification and guide personalized treatment strategies. Future research should focus on validating ferroptosis-targeted therapies in clinical trials, developing real-time monitoring techniques, and establishing standardized protocols for neuroprotective interventions during mechanical thrombectomy. A deeper understanding of ferroptosis mechanisms and their contribution to futile recanalization may pave the way for novel therapeutic approaches to improve stroke outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10946</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10946</link>
        <title><![CDATA[Sacubitril valsartan combined with bisoprolol reduces doxorubicin-induced cardiotoxicity in rats by attenuating oxidative stress]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ping Liu</author><author>Hui Yang</author><author>Runqi Li</author><author>Hui Huang</author><author>Min Xu</author>
        <description><![CDATA[Doxorubicin-induced cardiotoxicity remains a leading cause of mortality among cancer patients, with oxidative stress serving as a central pathogenic mechanism. This study investigated whether combination therapy with sacubitril valsartan and bisoprolol attenuates doxorubicin-induced cardiotoxicity through modulation of oxidative stress pathways. Sixty male Sprague-Dawley rats were randomized into five groups: control, doxorubicin (DOX), bisoprolol (1.0 mg/kg/d), sacubitril valsartan (30 mg/kg/d), and combination therapy. All groups except control received intraperitoneal DOX (2.5 mg/kg weekly for 5 weeks). Cardiac function was assessed by echocardiography, myocardial injury by histopathology and enzyme levels (CK-MB, cTnI, BNP), and oxidative stress by ROS fluorescence, MDA, and SOD. Protein expression of Nrf2, HO-1, and Keap1 was analyzed by Western blot. DOX administration significantly impaired cardiac function, induced myocardial structural damage, elevated cardiac enzymes and oxidative stress markers, and downregulated Nrf2 pathway proteins compared to controls (all P < 0.05). All treatment groups significantly attenuated these abnormalities versus DOX (all P < 0.05), with combination therapy demonstrating superior cardioprotection evidenced by greatest improvement in LVEF (68.74 ± 6.87% vs. 50.26 ± 6.11%, P < 0.05), lowest cardiac enzyme levels, and most robust restoration of Nrf2 pathway expression. These findings demonstrate that sacubitril valsartan combined with bisoprolol effectively reduces doxorubicin-induced cardiotoxicity in rats by activating Nrf2-mediated antioxidant responses, providing experimental evidence for a potentially synergistic prophylactic strategy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10988</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10988</link>
        <title><![CDATA[Training the next-generation of biomedical scientists through artificial intelligence-driven education and research in pharmacology and pharmaceutical sciences]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Santosh Kumar</author><author>Ritu Karwasra</author><author>Weinan Zhou</author><author>Jayaraman Seetharaman</author><author>Bhupesh Singla</author>
        <description><![CDATA[Artificial intelligence (AI)-driven graduate education and research in pharmacology and pharmaceutical sciences (AIPPS) aims to address the rapidly-growing role of AI and machine learning (ML) applications in biomedical sciences. This review provides perspectives on why and how the next-generation of biomedical scientists equip themselves with skills necessary to integrate AI and ML tools into their current fields of study, particularly pharmacology and pharmaceutical sciences. The AI-enabled approaches discussed in this article highlight opportunities for improving competitiveness in an evolving scientific landscape, that includes academia, pharmaceutical and biotech industries and regulatory science. Furthermore, this review discusses how graduate education and research can be enhanced through training in AI-driven disease prediction, molecular target identification drug design and discovery, drug repurposing and pharmacometric modelling. The knowledge outlined here may help graduate students and early career researchers navigate the challenges associated with applying AI-based methodologies in fundamental research, product and process development, service delivery, and regulatory policy and ethics. Overall, the insights provided in the review aim to support the development of skilled forward-thinking biomedical and pharmaceutical scientists capable of leveraging AI technologies in modern research environments.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10827</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10827</link>
        <title><![CDATA[Elevated ApoC3 levels in cerebrospinal fluid predict poor outcomes in patients with aneurysmal subarachnoid hemorrhage]]></title>
        <pubdate>2026-04-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Bin Tong</author><author>Junjie Wang</author><author>Jiarui Chen</author><author>Qia Zhang</author><author>Zhouhan Xu</author><author>Kaichuang Yang</author><author>Xiaomin Chen</author>
        <description><![CDATA[Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating condition associated with approximately 30% mortality and 20% severe disability among survivors. Delayed cerebral ischemia due to cerebral vasospasm and hydrocephalus significantly contribute to poor neurological outcomes. Currently, reliable biomarkers for early prediction of these complications remain lacking. In this study, 63 patients with a mean age of 59.7 ± 11.53 years were enrolled. Functional outcomes were assessed by the modified Rankin Scale (mRS). Cerebrospinal fluid (CSF) samples were obtained through lumbar drainage (LD) or external ventricular drainage (EVD) and analyzed by ELISA. The predictive value of biomarkers was evaluated using receiver operating characteristic (ROC) curve analysis. Elevated Apolipoprotein C-III (ApoC3) levels in CSF of aSAH patients were observed. Furthermore, increased ApoC3 concentrations were significantly associated with poor prognosis and an elevated risk of severe complications. At an optimal cutoff value of 4,463 ng/mL, patients with high ApoC3 levels exhibited significantly worse 3-month functional outcomes and a higher incidence of delayed cerebral ischemia and hydrocephalus. Monitoring ApoC3 levels in CSF may be beneficial for predicting complications such as delayed cerebral ischemia and hydrocephalus in patients with aSAH.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11021</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11021</link>
        <title><![CDATA[CAR T cell engineering approaches to minimise toxicities]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Elizabeth Hogben</author><author>Anna Schurich</author><author>Charlotte Graham</author>
        <description><![CDATA[For the treatment of many forms of cancer, cell- and gene-based therapies are showing promise in both pre-clinical data and clinical trials. In particular, CAR T cell therapies, of which there are now 7 FDA-approved products, have shown ground-breaking results in haematological cancers such as multiple myeloma and B cell malignancies. Recent research is also attempting to develop effective CAR T cell therapies for solid tumours, with varying success. One of the key challenges faced by CAR T cell therapy is balancing strong cytotoxic activity for an effective treatment with preventing severe and potentially lethal toxicities, such as Cytokine Release Syndrome and Immune Effector Cell-Associated Neurotoxicity Syndrome. This mini review discusses some of the potential solutions that scientists have devised to overcome toxicities and improve existing CAR T cell therapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10850</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10850</link>
        <title><![CDATA[Lymphatic pumping technique in mice alters blood parameters and metastatic melanoma in an age-dependent manner]]></title>
        <pubdate>2026-03-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Christopher Walsh</author><author>Matthew Kirstein</author><author>Elise Wagner</author><author>Emily Scott</author><author>Jerome Walsh</author><author>Shashank Reddy</author><author>Nathan Hoggard</author><author>Arshad Ahmad</author><author>Reetobrata Basu</author><author>Sam Mathes</author><author>Yanrong Qian</author><author>John J. Kopchick</author>
        <description><![CDATA[Therapeutic touch applied to primary tumors can increase metastasis. The goal of this project was to determine whether touch applied to metastatic tumors also increases metastasis. We evaluated touch on a mouse model of experimental metastasis using a manual treatment called Lymphatic Pumping Technique (LPT), which increases lymphatic fluid flow and is contraindicated in patients with cancer. The LPT, or a sham treatment, was administered for 5 minutes while the mice were anesthetized with vaporized isoflurane. Young adult (3 months old) and aged (20–24 months old) mice received daily sham or LPT treatments for 7 days prior to the injection of 200k B16F10-luc2 mouse melanoma cells into the tail vein, then treated every other day for 21 days. In middle-aged (9–11 months old) mice, we waited 8 days after tumor injection to start treatments and assessed the effect of LPT on immunotherapy efficacy. These mice also received either LPT or sham every other day, along with four doses of 200 µg anti–PD-1 or isotype control antibody. LPT did not increase tumor growth or spread in any of the experiments. Surprisingly, LPT was negatively associated with metastasis in young and middle-aged mice, without enhancing or diminishing the efficacy of immunotherapy. In mice without cancer, LPT rapidly elevated red blood cell, white blood cell, and platelet counts in young, but not middle-aged, animals. Taken together, these findings suggest that therapeutic touch near metastatic tumors does not worsen disease and may confer an age-dependent benefit.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10857</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10857</link>
        <title><![CDATA[Towards a standardized diabetic prolonged wound healing model in hairless SKH1 mice]]></title>
        <pubdate>2026-03-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Elle Koivunotko</author><author>Julia Monola</author><author>Chris S. Pridgeon</author><author>Jere Linden</author><author>Riina Harjumäki</author><author>Emrah Yatkin</author><author>Mari Madetoja</author><author>Marjo Yliperttula</author>
        <description><![CDATA[Chronic wounds, particularly those associated with diabetes, pose a significant clinical challenge due to their impaired healing dynamics and lack of reliable and standardized preclinical models. This pilot study aimed to establish a diabetogenic, immunocompetent, hairless mouse model (SKH1 strain) to simulate prolonged wound healing. Diabetes was induced by streptozotocin administration, followed by the creation of full-thickness dorsal skin wounds. Wounds were treated with either saline or nanofibrillated cellulose hydrogel as a model treatment. Wound healing progression and blood glucose were monitored, and histopathological assessments were performed after a 14-day experiment. In addition, for the first time, the Thermidas thermal imaging system was used in an in vivo mouse model to evaluate skin temperature. Results demonstrated that diabetes induction successfully prolonged wound closure by 5 days compared with the previously described acute wound model in the same strain with the identical protocol without streptozotocin (STZ) induction. Histopathological analyses showed increased macrophage activity (16.2% vs. 2.2% in the treatment groups and 10.2% vs. 0.3% in the control groups) and decreased collagen deposition (12.2% vs. 43.2% in the treatment groups and 17.6% vs. 27.4% in the control groups), suggesting prolonged wound healing. These findings support the use of hairless SKH1 mice as a viable model for studying prolonged diabetic wound healing and evaluating future therapeutic candidates.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10933</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10933</link>
        <title><![CDATA[Genetics of epilepsy]]></title>
        <pubdate>2026-03-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Kynen Piacentini</author><author>Athanasios Gaitatzis</author><author>Sulev Kõks</author>
        <description><![CDATA[Epilepsy is one of the most common neurological diseases in the world, but it is also complex and difficult to study. There is a significant genetic component to epilepsy and more information is being published frequently. It is difficult to group and summarise all of this information in a way that is beneficial for both researchers and clinicians. The aim of this paper is to create a summary of all currently known epilepsy associated genes in order to aid epilepsy research to better understand the aetiology of the disease. This was achieved through gathering genetic data from three databases: Online Mendelian Inheritance in Man (OMIM), Clincal Genome (ClinGen), and PubMed. Genes were filtered based on specific criteria and were summarised into three tables: Epilepsy genes, Epilepsy associated genes and Predicted epilepsy associated genes. A fourth table was produced to showcase all epilepsy genes that were identified in all three databases. A total of 2,536 genes were identified to have some level of association with epilepsy. A total of 238 genes were classified as Epilepsy genes, 1,317 genes were classified as Epilepsy associated genes and 981 genes were classified as Predicted epilepsy genes. Finally, 86 genes were identified to be epilepsy genes that were found in all three genetic databases and represent the highest confidence in association with epilepsy. The significance of this study involves the ability to give researchers an up-to-date list of genes that have an association to epilepsy and a summary of information about said genes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10907</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10907</link>
        <title><![CDATA[A novel platelet-rich plasma clinically induces reliable, rapid, long-term chronic peripheral neuropathic pain elimination]]></title>
        <pubdate>2026-03-13T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Damien P. Kuffler</author><author>Onix Reyes</author><author>Ivan J. Sosa</author><author>Christian A. Foy</author>
        <description><![CDATA[Peripheral nerve trauma results in 50%–84% of patients developing chronic neuropathic pain, which is eliminated when axons reinnervate targets. Autografts reduce pain by promoting target reinnervation. We hypothesized that applying a novel platelet-rich plasma (PRP) formulation to proximal stumps would permanently eliminate the pain. This prospective case series compared analgesia levels after bridging nerve gaps with an autograft (autograft repair) vs. a PRP-filled collagen tube (PRP repair). Autograft repairs were performed on 16 nerves with a 5.75-cm mean gap length, 2.0-year repair delay, 42.3-year age, and 8.6 chronic neuropathic pain. PRP repairs were performed on 10 nerves with a 6.0-cm gap length, 1-year repair delay, 36.7-year age, with 88% having 9.1 chronic neuropathic pain. For autograft repairs, the pain began to decrease when axons reinnervated targets, reaching a mean of 0.3 in 18.2% of patients, and was eliminated in 81.8%. Following PRP repairs, the pain reduction began within 2 weeks and was eliminated by 2 months. Thus, autografts contribute to pain reduction/elimination by promoting target reinnervation. However, PRP directly and rapidly induced long-term pain elimination in all patients, while axons were regenerating, and without target reinnervation. These results prove that platelet-released factors reliably and rapidly eliminate chronic neuropathic pain.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10796</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10796</link>
        <title><![CDATA[Enhanced oxidative stress resilience in C. elegans acox-1.1 mutants through CTL-3 and proteasomal regulation]]></title>
        <pubdate>2026-03-13T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Woori Bae</author><author>Mina Norman</author><author>Myon Hee Lee</author>
        <description><![CDATA[Oxidative stress is a primary driver of aging, necessitating robust cellular adaptation mechanisms. While peroxisomal β-oxidation and proteasomal degradation are known to influence stress responses, their functional crosstalk remains elusive. In this study, we show that C. elegans acox-1.1 mutants, despite having a shortened lifespan under normal conditions, exhibit a paradoxical resistance to mild chronic oxidative stress (1 mM paraquat, PQ) compared to wild-type worms. This PQ-induced resistance in acox-1.1 mutants was independent of the canonical SKN-1 pathway but required the peroxisomal catalase CTL-3. RNA-mediated knockdown of ctl-3 largely abolished the stress resistance of acox-1.1 mutants, leading to rapid mortality. Proteomic and biochemical analyses revealed that acox-1.1 mutants possess reduced levels of PAS-5, a core 20S proteasome subunit, resulting in impaired proteasomal assembly and accumulation of ubiquitinated (Ub) substrates under basal conditions. Intriguingly, exposure to 1 mM PQ significantly reduced the Ub-smear in acox-1.1 mutants, suggesting a metabolic shift where the cell prioritizes ROS scavenging over ATP-dependent protein degradation. Under oxidative stress, acox-1.1 mutants bypass defective proteasomal machinery and redirect energy toward CTL-3-mediated antioxidant defense. This study identified a peroxisomal adaptation mechanism whereby reduced proteasome complexity, coupled with enhanced ROS-regulatory machinery, confers survival advantages under specific oxidative challenges.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10679</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10679</link>
        <title><![CDATA[Low dose thirdhand smoke exposure enhances platelet functional responses in mice]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Precious O. Badejo</author><author>Ahmed B. Alarabi</author><author>Hamdy E. A. Ali</author><author>Lanam Millican</author><author>Reina De La Paz</author><author>Shelby S. Umphres</author><author>Sadia Kamal</author><author>Fatima Z. Alshbool</author><author>Fadi T. Khasawneh</author>
        <description><![CDATA[Although cigarette smoking is the most preventable cause of cardiovascular diseases, most researchers have focused on either direct/firsthand or secondhand smoke exposures. Recently though, attention has shifted to an emerging/indirect exposure trend-known as thirdhand smoke (THS)- which was previously “overlooked.” This phenomenon, which was/is thought to be harmless, has been identified as a serious health risk, including in the context of thrombogenesis/platelets. However, whether low dose THS exposure has the capacity to modulate platelets has not been investigated. Two sets of household materials were exposed to 20 cigarettes/day for a week on an alternating basis, with controls exposed to clean air. After the first set of exposed materials is placed in mice cages, exposure of the second set is initiated. The materials were interchanged weekly, for a total exposure duration of 1 month. Mice were then subjected to multiple platelet function assays. THS exposed mice exhibited shortened tail bleeding and occlusion times, indicating a prothrombotic phenotype. Moreover, we also observed that platelets from the exposed mice exhibited an enhanced aggregation response. However, we did not observe any gender differences in our in vivo as well as aggregation experiments; hence, subsequent characterization was carried out on male mice. It was also found that dense granules release, integrin activation, and PS exposure were also potentiated in the exposed platelets compared to the controls. Finally, we observed for the first time that the tobacco-specific nitrosamine and THS toxicant NNK enhanced platelet aggregation and thrombus formation. Collectively, we provide documentation that low dose of THS exposure is detrimental to health by increasing the risk of thrombosis through a hyperactive platelet phenotype that involves the toxicant NNK.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10867</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10867</link>
        <title><![CDATA[Metabolomics-guided identification of bioactive phytometabolites from South African plants targeting neuroblastoma]]></title>
        <pubdate>2026-03-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mmei Cheryl Motshudi</author><author>Clarissa Marcelle Naidoo</author><author>Chikwelu Lawrence Obi</author><author>Benson Chucks Iweriebor</author><author>Earl Prinsloo</author><author>Muhammad Sulaiman Zubair</author><author>Nqobile Monate Mkolo</author>
        <description><![CDATA[Neuroblastoma constitutes a solid tumor in pediatric populations, characterized by a dismal prognosis and a scarcity of effective therapeutic interventions. Medicinal flora from South Africa represents valuable sources of bioactive phytometabolites with potential relevance to neuroblastoma. This study employed an integrated workflow merging untargeted UPLC-MS/MS metabolomics, mitochondrial functional assays, and in silico absorption, distribution, metabolism, and excretion (ADME) prediction to systematically identify bioactive metabolites from Acorus calamus and Lippia javanica with activity against SH-SY5Y neuroblastoma cells. Cytotoxic effects were quantified utilizing the CCK-8 assay, while mitochondrial membrane potential (ΔΨm) was conducted through JC-1 flow cytometry. Untargeted UPLC-MS/MS profiling yielded metabolomic fingerprints, through PCA, PLS-DA, and OPLS-DA. ADME and drug-likeness were predicted using SWISSADME. Both plant extracts exhibited dose-dependent inhibition of SH-SY5Y cell viability, with IC50 values determined at 0.2886 μg/μL for A. calamus and 0.3066 μg/μL for L. javanica. The ΔΨm assessment indicated enhanced mitochondrial polarization (68.2% and 65.4% compared to 58.8% in untreated controls), implying modulation of mitochondrial functional status. Metabolomic profiling unveiled distinct phytochemical signatures, including flavonoids, phenolics, jasmonates, and alkaloids, exhibiting significant species-level differentiation (F = 936.71, R2 = 0.989, p = 0.005). Notable metabolites such as isopropyl β-glucoside, 6β-hydroxymethandienone, and 7-epi-12-hydroxyjasmonic acid demonstrated favorable ADME characteristics and permeability across the blood-brain barrier. This investigation elucidates that A. calamus and L. javanica possess potential efficacy against neuroblastoma, underscoring the translational potential of African medicinal flora in pediatric oncology and necessitating further preclinical exploration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10929</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10929</link>
        <title><![CDATA[Global MyoG research 2004–2024: a bibliometric analysis of trends and translational implications]]></title>
        <pubdate>2026-03-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Luoming Hu</author><author>Weizhong Zhuang</author><author>Weimin Chen</author><author>Song Yang</author><author>Shuo Chen</author><author>Xin Wang</author><author>Qiang Gao</author><author>Jimei Chen</author>
        <description><![CDATA[Myogenin (MyoG) is a core myogenic transcription factor that orchestrates myoblast differentiation and myofiber maturation and has been increasingly implicated in skeletal muscle degeneration and rhabdomyosarcoma, yet its global research landscape has not been systematically characterized. In this study, we performed a bibliometric analysis of MyoG-related publications from 2004 to 2024 retrieved from the Web of Science Core Collection. A total of 402 articles authored by 2,402 researchers from 1,148 institutions across 165 countries and regions were analyzed using VOSviewer, CiteSpace and R-based bibliometric tools. We quantified annual publication output, identified leading countries, institutions, authors and journals, and reconstructed collaboration, co-citation and keyword co-occurrence networks to delineate thematic evolution. The global pattern showed a multipolar structure dominated by the United States and China, with European institutions forming an additional hub and emerging countries contributing with growing but comparatively lower impact. Research hotspots exhibited a clear progression from early work on molecular mechanisms (DNA binding, MyoD family interactions, chromatin remodelling) toward regenerative biology (satellite cell regulation, muscle regeneration) and, more recently, disease-oriented studies focused on muscle atrophy, Duchenne muscular dystrophy and rhabdomyosarcoma. Landmark co-cited studies established MyoG as an indispensable regulator of skeletal muscle differentiation and highlighted its expanding relevance in pathological remodelling and therapeutic targeting. Future work is expected to concentrate on decoding MyoG-centred regulatory networks in degenerative muscle disease, integrating single-cell and spatial transcriptomics with functional genomics and multi-omics, and developing MyoG-based diagnostic and targeted therapeutic strategies. Despite the intrinsic limitations of single-database and citation-based approaches, this study provides a panoramic overview of two decades of MyoG research and offers a structured framework to guide future basic and translational investigations in muscle biology and oncology.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10701</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10701</link>
        <title><![CDATA[Ananalysis of the effects of Treg cell therapy intervention on the gut microbiota of type 1 diabetic mice using 16S rRNA gene sequencing]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mengyao Zhou</author><author>Kang Du</author><author>Hanmin Wang</author><author>Zhuxian Zhang</author><author>Rui Zhao</author><author>Chenghong Ma</author><author>Qionger Huang</author><author>Wei Zhang</author><author>Weiwen Chen</author>
        <description><![CDATA[This study established a type 1 diabetes (T1DM) mouse model via intraperitoneal injection of streptozotocin (STZ) and examined the effect of regulatory T (Treg) cells on the gut microbiota by comparing its composition and diversity across three groups: control, T1DM, and Treg-treated mice. Forty-one 8-week-old male C57BL/6 mice under specific pathogen-free conditions were divided into a healthy control group, an untreated T1DM group, and a Treg treatment group (receiving low, medium, or high doses). T1DM was induced by administering a low-dose STZ injection over five consecutive days, with diabetes confirmation defined as a blood glucose level ≥300 mg/dL. CD4+CD25+ Treg cells isolated from spleens of healthy mice were used for treatment. Fecal samples collected on days 0, 14, and 34 from three randomly selected mice per group were subjected to 16S rRNA gene sequencing targeting the V3-V4 regions. The results showed significant differences in both alpha and beta diversity among the groups. Dominant bacterial families varied: Ruminococcaceae and others were enriched in the Treg treatment group, Muribaculaceae in the control group, and Lactobacillaceae in the untreated T1DM group. Genus-level abundances also shifted over time. Firmicutes abundance positively correlated with Treg levels (r = 0.70, p = 0.0433) but negatively with IFN-γ, whereas Cyanobacteria exhibited the opposite correlation. The Firmicutes/Bacteroidetes ratio was higher in T1DM mice than in controls and lower in the Treg-treated group. Metabolic pathway analysis indicated that two-component systems and ABC transporters were more prevalent in T1DM mice. In summary, Treg cell treatment altered the diversity, composition, dominant taxa, and Firmicutes/Bacteroidetes ratio of the gut microbiota compared with untreated T1DM mice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10834</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10834</link>
        <title><![CDATA[A novel de novo ATP2B1 variant causes autosomal dominant intellectual developmental disorder 66 by disrupting calcium homeostasis via impaired membrane trafficking]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Huanhuan Zang</author><author>Xiaoyun Yang</author><author>Yucai Liu</author><author>Caiyun Ma</author><author>Dawei Yang</author>
        <description><![CDATA[Heterozygous pathogenic variants in ATP2B1 (encoding PMCA1) cause autosomal dominant intellectual developmental disorder 66 (MRD66; OMIM #619910). To date, only 12 pathogenic de novo ATP2B1 variants have been reported in MRD66. This study aimed to identify the genetic etiology in a Chinese infant with a neurodevelopmental disorder characterized by early-onset seizures and global developmental delay (GDD) and functionally characterize a novel ATP2B1 missense variant. Trio-based whole-exome sequencing revealed a heterozygous de novo ATP2B1 variant (c.2140A>C, p.Thr714Pro) in the proband. The proband presented with infantile spasms, GDD (Gesell Developmental Quotient: 65–74), and severe growth restriction (height/weight <−2 SD). To investigate the variant’s pathogenicity, the wild-type (WT) and mutant ATP2B1 constructs, N-terminally tagged with mScarlet, were transfected into HEK293T cells. Confocal imaging demonstrated profound cytoplasmic mislocalization of the p.Thr714Pro mutant protein, contrasting sharply with the characteristic plasma membrane localization of WT ATP2B1. Measurement of intracellular Ca2+ levels using Fluo-4 AM showed a significant 2.07-fold increase in basal Ca2+ levels in cells expressing the mutant compared to WT. This finding expands the spectrum of ATP2B1 variants associated with MRD66 and confirms calcium dyshomeostasis as the core pathomechanism. This case of MRD66 demonstrates a very early onset of seizures, consistent with the recognized phenotypic variability and the critical role of PMCA1 in early neurodevelopment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10835</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10835</link>
        <title><![CDATA[Skeletal muscle reprogramming in peripheral nerve injury: mechanisms, therapeutic roles, and complication management]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fuqiang Long</author><author>Xiaoru Pan</author><author>Anxin He</author><author>Xinlu Wang</author><author>Zairong Wei</author><author>Shaoying Gao</author>
        <description><![CDATA[Peripheral nerve injury (PNI) presents a significant clinical challenge, frequently leading to long-term neuromuscular dysfunction, muscle atrophy, fibrosis, and chronic pain. Traditional repair strategies, including microsurgical reconnection and neurotrophic support, often yield limited functional recovery, especially in cases of delayed or incomplete reinnervation. In this context, skeletal muscle reprogramming—defined as the intentional modulation of cellular fate, function, or metabolic state in muscle-resident cells—has emerged as a promising strategy to enhance regenerative outcomes. This process involves transcriptional, epigenetic, and metabolic interventions targeting myogenic progenitors, fibro-adipogenic progenitors (FAPs), satellite cells (MuSCs), and the broader muscle microenvironment. Recent studies demonstrate that reprogramming strategies can mitigate denervation-induced muscle atrophy, delay fibrotic remodeling, promote neuromuscular junction (NMJ) reconstruction, and even stimulate endogenous nerve regrowth via retrograde signaling. Mechanistic insights have uncovered pivotal roles for signaling pathways such as Wnt/β-catenin, TGF-β, Notch, and HDAC-regulated chromatin dynamics. Furthermore, innovations in small molecule cocktails, CRISPR-based transcriptional reactivation, and metabolic rewiring have expanded the therapeutic toolkit for muscle preservation and regeneration. This review comprehensively examines the molecular mechanisms, therapeutic roles, and translational challenges of skeletal muscle reprogramming in the context of PNI. We explore how muscle-targeted interventions can address complications of denervation, improve the efficacy of nerve repair, and offer a synergistic axis of regeneration when integrated with nerve-centric strategies. Finally, we identify key knowledge gaps and outline future research directions required to translate reprogramming-based therapies into clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10709</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10709</link>
        <title><![CDATA[Identification of potential hub genes related to ferroptosis and hypoxia in dilated cardiomyopathy: a bioinformatic analysis with preliminary experimental validation]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiqin Wang</author><author>Chrismis Novalinda Ginting</author><author>William Leslie</author>
        <description><![CDATA[The study aims to explore the potential role of ferroptosis and hypoxia in dilated cardiomyopathy (DCM). GSE120895, GSE17800, GSE112556, ferroptosis-related genes (FRGs), and hypoxia-related genes (HRGs) were downloaded from the public dataset. Ferroptosis- and hypoxia-related differentially expressed genes (DEGs) and DCM-related genes were obtained. Subsequentially, hub genes were identified, and their diagnostic values were assessed. Next, immune cell infiltration analysis, drug prediction and molecular docking were carried out based on the hub genes. Finally, the hub gene TGM2 was preliminarily verified in vitro. A total of 18 ferroptosis- and hypoxia-related DEGs and 315 DCM-related genes were acquired. Subsequently, 6 hub genes (PPP1R15A, TGM2, MAP3K5, USP7, SESN2, and ADAM23) were obtained and have potential diagnostic value. Immune infiltration analysis showed that CD56dim natural killer (NK) cells, macrophages, monocytes, NK cells, and NK T cells were significantly infiltrated in DCM patients. Furthermore, the lncRNA-miRNA-mRNA network was constructed. Moreover, 16 drugs were predicted, and the binding energy between atorvastatin and TGM2 was −2.79 kcal/mol. In vitro verification showed that TGM2, PPP1R15A and SESN2 were up-regulated in DOX-induced AC16 cardiomyocyte injury. After knocking down TGM2, the expressions of α-actinin and cTnT were increased, and the expression level of HIF-1α was inhibited. Dual luciferase assay showed that hsa-miR-291-5p exerted its regulatory effect by directly binding to TGM2. Flow cytometry results showed that TGM2 had no significant effect on the apoptosis of AC16 cells. Our findings may provide new ideas for the diagnosis and treatment of DCM.]]></description>
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