World journal of experimental medicine最新文献

{"title":"Double-edged role of N6-methyladenosine reader YTH structural domain family protein 2 in neurological disorders: Molecular mechanisms and translational prospects.","authors":"Yu-Meng Liu, Ming Liu, Hang Yuan, Bin Li","doi":"10.5493/wjem.v16.i1.116383","DOIUrl":"10.5493/wjem.v16.i1.116383","url":null,"abstract":"<p><p>N6-methyladenosine (m6A) is the most prevalent internal RNA modification in eukaryotic transcripts, and YTH structural domain family (YTHDF) 2 is a principal m6A reader that governs RNA stability and turnover. Accumulating evidence indicates that YTHDF2 exerts context-dependent and sometimes opposing functions across major neurological disorders, including Alzheimer's disease, Parkinson's disease, glioblastoma, epilepsy, and experimentally induced cognitive and neuropsychiatric conditions. By selectively promoting decay of m6A-marked transcripts - such as leucine rich repeat and immunoglobulin domain containing 2, axis inhibition protein 1, breast cancer type 1 susceptibility protein associated protein 1, mitogen-activated protein kinase kinase 4, family with sequence similarity 134 member B, and NOD-like receptor family pyrin domain-containing 3 - YTHDF2 modulates diverse processes including amyloid processing, Wnt signaling, ferroptosis, neuroinflammation, metabolic homeostasis, and autophagy. Its activity is further shaped by upstream regulatory pathways (<i>e.g.</i>, epidermal growth factor receptor-SRC proto-oncogene, non-receptor tyrosine kinase-extracellular signal-regulated kinase and protein arginine methyltransferase 6-cyclin-dependent kinase 9) and by dynamic interplay with m6A writers and erasers, including methyltransferase like 14 and fat mass and obesity-associated protein. This mini-review synthesizes recent mechanistic advances, emphasizes regional and cell-type heterogeneity of YTHDF2 function, and proposes a \"dose-target dependency\" framework to reconcile its bidirectional effects. We also outline emerging translational strategies aimed at evaluating YTHDF2 as a mechanistic biomarker and a selectively tractable therapeutic target in neurological disease.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"116383"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melanoma leptomeningeal disease: Advances in diagnosis and emerging therapeutic strategies.","authors":"Michael L Middleton, Brandon Lucke-Wold","doi":"10.5493/wjem.v16.i1.117938","DOIUrl":"10.5493/wjem.v16.i1.117938","url":null,"abstract":"<p><p>Melanoma leptomeningeal disease (LMD) is a rare and severe manifestation of advanced melanoma involving malignant infiltration of the leptomeninges and cerebrospinal fluid. Historically, survival was measured in weeks, but recent advances in diagnostics and therapy have begun to improve outcomes. This narrative review summarizes current evidence on the epidemiology, biology, diagnosis, and management of melanoma LMD, with emphasis on studies from the past five years. Emerging cerebrospinal fluid liquid biopsy methods, including circulating tumor cell and cell free DNA analysis, allow earlier detection, identification of actionable mutations, and real time monitoring of disease activity. Modern systemic therapies have extended median overall survival to approximately 8.4 months compared with historical outcomes of 2.9 months to 3.7 months. Immune checkpoint inhibitors and B-rapidly accelerated fibrosarcoma and mitogen-activated protein kinase targeted therapies both contribute to these improvements, and early studies of intrathecal immunotherapy show encouraging clinical activity. Additional innovations such as proton craniospinal irradiation and novel drug delivery strategies reflect an evolving treatment landscape. Continued progress will depend on dedicated clinical trials, broader inclusion of patients with LMD, and deeper understanding of the leptomeningeal immune microenvironment.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"117938"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence-based review and clinical practice recommendations for the diagnosis and management of common oral mucosal lesions.","authors":"Giath Gazal, Anas B Alsalhani, Bassel Tarakji, Mohammad Zakaria Nassani","doi":"10.5493/wjem.v16.i1.115535","DOIUrl":"10.5493/wjem.v16.i1.115535","url":null,"abstract":"<p><p>Oral mucosal lesions are a common but diagnostically complex clinical challenge in general dental practice, comprising conditions from benign ulcers to potentially malignant disorders and systemic presentations. Early diagnosis and evidence-based management are crucial to prevent complications, including malignant changes. This review provided a practical protocol for the diagnosis and management of oral mucosal lesions for general dental practitioners. Drawing from National Health Service guidelines and retrieved literature <i>via</i> PubMed and Scopus, the findings were synthesized into structured clinical tables outlining diagnostic pathways, first-line and escalated treatment options, and referral criteria. The framework enables classification by clinical appearance and anatomical site, integrating pharmacological therapies with validated herbal agents such as Nigella sativa, honey, chamomile, and <i>Aloe vera</i> for their mucosal healing properties. An emphasis was placed on differentiating clinically similar conditions and addressing neuropathic disorders like burning mouth syndrome with agents such as amitriptyline. The current review advocated for an evidence-based, stepwise approach that enhances diagnostic accuracy, optimizes treatment outcomes, and aids safe, timely referrals in the management of oral mucosal lesions.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"115535"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation profiling in central nervous system tumors: Where do we draw the line of clinical utility?","authors":"Sumanta Das","doi":"10.5493/wjem.v16.i1.115070","DOIUrl":"10.5493/wjem.v16.i1.115070","url":null,"abstract":"<p><p>DNA methylation profiling has emerged as a transformative tool in the epigenetic classification and diagnosis of central nervous system (CNS) tumors, offering unprecedented resolution in distinguishing morphologically overlapping entities. The advent of methylation-based classifiers has refined the diagnostic landscape, enabling improved tumor stratification, prognostication, and even therapeutic decision-making. In CNS malignancies, DNA methylation profiling offers tumor-specific epigenetic \"fingerprints\" that improve diagnostic accuracy and repeatability. It improves the classification of glioneuronal tumors, ependymomas, and juvenile gliomas, eliminates 9%-25% of histopathological discrepancies, improves grading in up to 18% of instances, and achieves > 70% concordance with integrated histo-molecular diagnosis. However, its application in routine neuropathology practice raises critical questions regarding necessity, accessibility, and cost-effectiveness. While methylation signatures have proven indispensable in diagnostically ambiguous or rare cases, their universal application to all CNS tumors remains debatable, especially in settings where robust histopathology, immunohistochemistry, and targeted molecular assays already provide reliable diagnostic accuracy. This editorial explores the strengths and limitations of DNA methylation profiling, examining its role as a complementary <i>vs</i> mandatory tool in routine practice. We argue for a balanced approach, where methylation is deployed selectively, prioritized for diagnostically challenging, morphologically ambiguous tumors or in the context of clinical trials rather than applied indiscriminately. Such an evidence-driven framework may optimize resource utilization while ensuring diagnostic precision in CNS tumor pathology.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"115070"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurobiological mechanisms linking vitamin d signaling to cognitive decline and neurodegeneration: Untangling epidemiology, pathophysiology, and evidence.","authors":"Neha Choudhary, Maheen Zahid, Muhammad Ahmad, Muneeba Shaukat, Muhammad Tariq, Soura Rajeshwara, Shermeen Usman, Taimoor Wajid, Ayoola Awosika","doi":"10.5493/wjem.v16.i1.118761","DOIUrl":"10.5493/wjem.v16.i1.118761","url":null,"abstract":"<p><p>Dementia is a leading cause of disability and dependence among older adults, and its prevalence is projected to increase sharply with age. While age and genetics remain the dominant risk factors, modifiable contributors are gaining attention, including vitamin D deficiency, which is highly prevalent worldwide. This integrated review synthesizes current evidence on the association between vitamin D status and dementia, spanning the epidemiological, mechanistic, and interventional domains. Epidemiological studies have consistently linked low serum 25-hydroxyvitamin D levels with poorer cognition, faster decline, and higher risk of Alzheimer's disease and vascular dementia, although causality cannot be inferred. Mechanistic data suggest that vitamin D regulates amyloid and tau pathology, reduces neuroinflammation and oxidative stress, supports cerebrovascular integrity, and preserves mitochondrial function. Translation into clinical benefit has proven difficult; large randomized trials in generally healthy older adults, including VITAL and D-Health, report null effects, whereas smaller studies in vitamin D-deficient or cognitively impaired populations suggest potential improvements. Meta-analyses confirm mixed findings, typically indicating small or non-significant effects, with possible benefit restricted to vulnerable groups. The limitations across the literature include residual confounding in observational studies, assay variability, seasonal influences, heterogeneous cognitive measures, and publication bias. Future priorities include adequately powered randomized trials with standardized vitamin D assessments and harmonized cognitive endpoints as well as investigations into genetic moderators and multi-domain interventions. In conclusion, although vitamin D deficiency is consistently associated with cognitive decline and dementia, definitive evidence of causality remains lacking. Clarifying whether supplementation can alter dementia trajectory is a pressing public health priority.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"118761"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Indocyanine green doped with chitosan nanoparticles based antimicrobial photodynamic therapy in periodontitis patients: A randomized clinical trial.","authors":"Subash Chandra Raj, Sudip Sen, Debajani Baral, Devapratim Mohanty, Shaheda Tabassum, Swoyangprava Sil, Mrutyunjaya Sahu","doi":"10.5493/wjem.v16.i1.117125","DOIUrl":"10.5493/wjem.v16.i1.117125","url":null,"abstract":"<p><strong>Background: </strong>Periodontitis is a chronic inflammatory disease triggered by a polymicrobial challenge to the periodontium. While scaling and root planing (SRP) is the gold standard for treatment, its efficacy is often limited by incomplete pathogen eradication and rising antimicrobial resistance. Antimicrobial photodynamic therapy (aPDT) has emerged as a potent adjunctive treatment, utilizing light-activated photosensitizers to induce targeted bacterial lysis. Specifically, the delivery of indocyanine green (ICG) <i>via</i> chitosan nanoparticles (CNPs) may enhance stability and penetration, offering a synergistic approach to improving clinical outcomes when combined with SRP.</p><p><strong>Aim: </strong>To evaluate the overall improvements in various clinical and microbiological periodontal parameters in periodontitis patients undergoing aPDT with CNPs-ICG.</p><p><strong>Methods: </strong>Thirty periodontitis patients having interdental clinical attachment loss (CAL) 'detectable' at ≥ 2 non-adjacent teeth, buccal or oral CAL ≥ 3 mm with pocketing > 3 mm detectable at ≥ 2 teeth were randomly assigned to aPDT with CNPs-ICG + SRP (test) group and conventional SRP + laser irradiation only (control) group in a split-mouth design. At baseline, 1-month and 3-months plaque index (PI), modified sulcular bleeding index, pocket probing depth (PPD) and relative clinical attachment level (RCAL) and microbiological tests were recorded.</p><p><strong>Results: </strong>The test group showed more improvement in PPD (7 mm to 3.26 mm in 1-month and 3.13 mm in 3-months) and RCAL (12 mm to 8.26 mm in 1 month and 8.4 mm in 3 months) than control group that showed PPD reduction from 6.7 mm (at baseline) to 3.73 mm at 1-month and 3.76 mm at 3 months and RCAL reduction from 12.23 mm (at baseline) to 8.7 mm at 1-month and 8.9 mm at 3-months with a statistically significant difference (<i>P</i> = 0.001). The test sites showed a statistically significant (<i>P</i> = 0.001) increase in negative microbiological test results (from 10% at baseline to 80% at 1 month and 3 months follow-up) compared to control sites (6.7% at both baseline and 1-month and 3-months follow-up).</p><p><strong>Conclusion: </strong>aPDT using CNPs-ICG + SRP can be considered as a better procedure in improving periodontal clinical parameters like PPD and RCAL and in reducing periodontal pathogens than conventional SRP alone.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"117125"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Experimental beneficial effect of rosuvastatin on burn wound healing in a rat model.","authors":"Alexandra G Marneri, Efstathios T Pavlidis, Kalliopi E Stavrati, Athanasios Kofinas, Christina Mouratidou, Ioannis Gkoutziotis, Serafeim-Chrysovalantis Kotoulas, Christina Marouda, Dimitra Psalla, Konstantinos D Ballas, Theodoros E Pavlidis","doi":"10.5493/wjem.v16.i1.115208","DOIUrl":"10.5493/wjem.v16.i1.115208","url":null,"abstract":"<p><strong>Background: </strong>In addition to their primary lipid-lowering effects, statins also exhibit pleiotropic properties, including anti-inflammatory, immunomodulatory, antimicrobial, antioxidative, and angiogenic effects, all of which promote wound healing. Rosuvastatin, a synthetic hydrophilic statin, has recently been proposed to enhance wound healing by stimulating angiogenesis and accelerating tissue regeneration. Its hydrophilic nature, longer half-life, greater hepatoselectivity, and better efficacy/safety than other statins are believed to contribute to its superior efficacy in wound repair, as suggested by promising preliminary results. However, current data on its use remain limited, necessitating further preclinical and clinical studies to thoroughly investigate this novel treatment option for burns.</p><p><strong>Aim: </strong>To investigate the effects of rosuvastatin and its mechanism of action on burn wound healing process in an experimental study.</p><p><strong>Methods: </strong>Ninety male Wistar albino rats aged 12-16 weeks were randomly assigned to three groups of 30, subjected to burn using specific stainless steel sealer. Burn eschar was removed the following day applying topical rosuvastatin cream (study), Eucerin cream (placebo), normal saline (control), and sterile wound dressing. Each group was divided into three subgroups of ten according to sacrifice day (3^rd, 6^th, 9^th). C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, digital assessment of burn healing, and histopathology were performed.</p><p><strong>Results: </strong>Using the value on the third day in the control group as the baseline, reductions were measured on the sixth and ninth days. Similarly, reduction values were recorded on the third, sixth, and ninth days in the study group. A statistically significant reduction was observed in the study group compared to the control group, with greater reductions corresponding to later sacrifice days (3^rd, 6^th, and 9^th) in CRP (<i>P</i> < 0.01), TNF-α (<i>P</i> < 0.01), IL-1β (<i>P</i> < 0.01), and IL-6 (<i>P</i> < 0.01) levels and burn size (<i>P</i> < 0.01). Histopathology revealed a statistically significant reduction in inflammatory infiltration, coagulative necrosis, and microhemorrhage (<i>P</i> < 0.01). Conversely, statistically significant increases in neovascularization (<i>P</i> = 0.012) and fibroblastic reactions (<i>P</i> = 0.023) were noted. No adverse effects or deaths were observed.</p><p><strong>Conclusion: </strong>Rosuvastatin reduces inflammation by lowering TNF-α, IL-1β, IL-6, CRP while increasing neo-angiogenesis, fibroblast reactions and microenvironmental protection in burn wounds. These effects promote repair and positively impact burn wound healing.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"115208"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences of immunohistochemical profiling of MOC-31, caveolin-1, connexin-43, Ki-67 in ameloblastic fibroma, ameloblastic fibrodentinoma, ameloblastic fibro-odontoma, and odontomas.","authors":"Natalia González Umpiérrez, Estefania Sicco, Felipe Silveira, Aurita Veronica Beovide, Ronell Bologna-Molina","doi":"10.5493/wjem.v16.i1.115508","DOIUrl":"10.5493/wjem.v16.i1.115508","url":null,"abstract":"<p><strong>Background: </strong>Odontogenic tumors are a heterogeneous group of lesions originating from tissues involved in odontogenesis. Mixed odontogenic tumors comprise a group of lesions characterized by the presence of ectodermal and mesenchymal odontogenic tissues with or without the formation of hard dental tissues.</p><p><strong>Aim: </strong>To determine and compare the expression of caveolin-1, MOC-31, connexin-43 (Cx-43), and Ki-67 in ameloblastic fibromas (AF), ameloblastic fibrodentinomas (AFD), ameloblastic fibro-odontomas (AFO), and odontomas (O).</p><p><strong>Methods: </strong>Immunohistochemical analysis for caveolin-1, MOC-31, Cx-43, and Ki-67 was performed on eight AF, one AFD, five AFO, and six O.</p><p><strong>Results: </strong>Variable protein expression was identified in the epithelium and mesenchyme of most AF, AFD, and AFO with lower expression observed in O. Immunohistochemical analysis revealed significant differences in protein expression between AF and O (<i>P</i> = 0.0085) and between AFO/AFD and O (<i>P</i> = 0.0250). When evaluating individual proteins, a significant difference in MOC-31 expression was observed between AF and O (<i>P</i> = 0.0310), while Cx-43 expression differed between AFO/AFD and O (<i>P</i> = 0.0022) and between AF and O (<i>P</i> = 0.0310). Additionally, protein expression decreased with increasing age (<i>P</i> ≤ 0.0100).</p><p><strong>Conclusion: </strong>This immunohistochemical study suggested that the similarity in protein expression between AFD, AFO, and AF compared with O may be due to the biological proximity among these lesions at the protein expression level. Further studies with larger sample sizes and complementary techniques are required to validate these findings.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"115508"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetic ketoacidosis in patients with type 2 diabetes: Risk factors for mortality and adverse outcomes.","authors":"Vishnu Chandrabalan, Timothy Howcroft, Mohammed Khalid Alkhalifah, Noorulanne Younis, Ebrahim Aldhafiri, Joseph M Pappachan","doi":"10.5493/wjem.v16.i1.117464","DOIUrl":"10.5493/wjem.v16.i1.117464","url":null,"abstract":"<p><strong>Background: </strong>Diabetic ketoacidosis (DKA) resulting from type 2 diabetes mellitus (T2DM) is less common, and the factors associated with adverse outcomes and mortality are not well established based on large-scale studies.</p><p><strong>Aim: </strong>To identify the risk factors for adverse outcomes and mortality in treated patients with DKA in T2DM.</p><p><strong>Methods: </strong>Retrospective analysis of patients admitted to a tertiary-care hospital in the United Kingdom with DKA and T2DM for inpatient management between January 2010 to September 2024 to identify the clinical profile, demographic features, and laboratory parameters impacting treatment outcomes and survival.</p><p><strong>Results: </strong>Four hundred and sixty-four patients were included. Of these 395 (85.13%) were White, 266 (57.3%) were males with a mean age at presentation of 61.3 (17.6) years, median inpatient hospital stay of 5 (interquartile range: 3-10.3) days, and a mean glycated HbA1c of 89.3 (30) mmol/mol. The 30-day and 90-day mortality were 13.4% and 11% respectively after the index DKA event. The long-term survival after the DKA event was only 58.6%. Presence of cerebrovascular disease [odds ratio (OR): 6.75; 95%CI: 0.76-12.74], use of sodium glucose cotransporter 2 inhibitors (OR: 5.8; 95%CI: 1.32-9.62), chronic obstructive pulmonary disease (OR: 3.6; 95%CI: 2.14-6.44), higher national early warning score 2 score (OR: 1.14; 95%CI: 0.10-2.18) and low systolic blood pressure (OR: -0.18; 95%CI: -0.32 to -0.04) at admission were the significant predictors of longer inpatient stay. Coexistent peripheral vascular disease (PVD; OR: 46.43) and congestive heart failure (CHF; OR: 30.83), and lower estimated glomerular filtration rate (eGFR; OR: 0.98) were the important predictors of mortality during the hospital treatment. The significant predictors on 30-day mortality were: Age (OR: 1.06), eGFR (0.97) and index of multiple deprivation (IMD) decile (0.74). The factors associated with long-term mortality risk were dementia (20.54-fold higher), continued use of sulfonylurea/metformin, and older age (4% higher with each additional year).</p><p><strong>Conclusion: </strong>DKA carries a serious risk of mortality in both the short and long term in T2DM patients. Factors such as older age, dementia, PVD, CHF, low eGFR define the riskiest groups. These groups of patients may benefit from closer follow-up and more aggressive metabolic and comorbidity management after discharge.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"117464"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unconventional mechanisms of resveratrol in atherosclerosis prevention and management.","authors":"Nadim Chaarani, Riyad Mroweh, Razan Moghnieh, Mohammad Kheir Chahine, Hassan Zaiter, Saleh-Yezan Abdulaal, Nazih Obeid, Mohamad Tlais, Joy Raheb, Hadi Farhat, Razan Abdulaal","doi":"10.5493/wjem.v16.i1.116771","DOIUrl":"10.5493/wjem.v16.i1.116771","url":null,"abstract":"<p><p>Atherosclerosis is a progressive inflammatory disease and a major contributor to cardiovascular disease. Resveratrol (RES), a polyphenolic compound found in grapes and red wine, has been widely investigated for its protective effects on cardiovascular health. This review summarizes the mechanisms through which RES attenuates atherosclerosis, including its anti-inflammatory, antioxidant, and lipid-modulating effects. Experimental evidence indicates that RES inhibits nuclear factor kappa-light-chain-enhancer of activated B cells signaling, thereby reducing the expression of adhesion molecules such as vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 and limiting immune cell infiltration into the arterial wall. Additionally, it counteracts oxidative stress by enhancing antioxidant enzyme activity and preventing low-density lipoprotein oxidation, a key event in foam cell formation. RES also promotes cholesterol efflux through adenosine triphosphate-binding cassette transporters, supporting high-density lipoprotein-mediated reverse cholesterol transport. Findings from <i>in vitro</i>, animal, and clinical studies suggest that RES can reduce atherosclerotic plaque development, improve endothelial function, and modulate lipid metabolism.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"16 1","pages":"116771"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}