World journal of experimental medicine最新文献

{"title":"Molecular insights from skin biopsies: Deciphering microvascular pathology in peripheral vascular diseases.","authors":"Maneesha Kumari, Narainder Kumar, Rahol Meghwar, Rahul Rai, Fnu Rahul, Muhammad Ali Hassan, Kapeel Kumar, Hanesh Kumar, Muhammad Hashir Naveed Chaudhary, Kainaat Zahid, Farah Alam, Inshal Jawed, Danaish Kumar, Shafaq Jabeen, Umair Qadir, Rabia Asim","doi":"10.5493/wjem.v15.i4.111043","DOIUrl":"10.5493/wjem.v15.i4.111043","url":null,"abstract":"<p><strong>Background: </strong>The heterogeneous group of disorders called peripheral vascular diseases (PVDs) occurs outside the heart and brain tissue to cause ischemia and severe health complications. Diagnosis accuracy is essential in starting appropriate patient management at the proper time. Modern medicine considers skin biopsies crucial diagnostic tools that yield histopathological and molecular evidence for examining PVD-related microvascular changes.</p><p><strong>Aim: </strong>To evaluate skin biopsy applications in PVD diagnostics through artistic analysis of technical processes and examination of pathological and innovative molecular indicators.</p><p><strong>Methods: </strong>A systematic review of randomized controlled trials and original studies about skin biopsy utility in PVD diagnosis used PubMed, Scopus, and EMBASE search platforms. The reviewed studies met specific entry requirements, while all case reports and review articles remained excluded.</p><p><strong>Results: </strong>A total of 22 studies suited the research criteria that were evaluated. Researchers emphasized the value of skin biopsies for identifying inflammatory from non-inflammatory PVDs. At the same time, they detect systemic sclerosis and diabetic vasculopathy abnormalities of micro-vessels and identify endothelial dysfunction through measurements of vascular endothelial growth factor and intercellular adhesion molecule-1 and endothelial nitric oxide synthase markers. Skin biopsies require further improvement because they cause patient discomfort and produce variable diagnostic results that specialists must interpret.</p><p><strong>Conclusion: </strong>Skin biopsies enable essential diagnostic findings about PVD and improve patient detection. The development of standardized biopsy procedures and molecular diagnosis techniques should be studied to advance PVD diagnoses in clinical practice.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"111043"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145913992","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":"<i>Ferula assafoetida</i> induced colon cancer cells differentiation through JNK/MAPK signalling pathway activation.","authors":"Hani M Abdelsalam, Aya M Abdelghany, Wafaa A Ahmed, Abdelaziz Abbas Diab, Mona S Abdellateif","doi":"10.5493/wjem.v15.i4.110757","DOIUrl":"10.5493/wjem.v15.i4.110757","url":null,"abstract":"<p><strong>Background: </strong>Colon cancer is a major health problem with increasing mortality rates worldwide.</p><p><strong>Aim: </strong>To evaluate the ability of <i>Ferula assafoetida</i> (<i>F. assafoetida</i>) to induce differentiation of colon cancer cells to function as normal cells.</p><p><strong>Methods: </strong>The cytotoxic effect of <i>F. assafoetida</i> was assessed against Caco cells using the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphe nyltetrazoliumbromide thiazolyl assay. Cell cycle analysis and apoptosis were assessed using Cytell^TM cell system. The total antioxidant (TA), glutathione (GSH), malondialdehyde (MDA) concentrations, and alkaline phosphatase (ALP) activity were also assessed. The c-Jun N-terminal kinases (JNKs) and mitogen-activated protein kinase (MAPK) expressions were evaluated using quantitative real-time polymerase chain reaction.</p><p><strong>Results: </strong>There was a significant increase in the cell number treated with <i>F. assafoetida</i> (53.85% ± 0.03%), and those treated with sodium butyrate (NaBT) (54.6% ± 0.10%) in sub-G1 phase, compared to the untreated cells (0.78% ± 0.03%, <i>P</i> < 0.001). Apoptosis was significantly increased in the Caco cells treated with <i>F. assafoetida</i> (49.1% ± 0.14%) compared to those treated with NaBT (27.3% ± 0.10%, <i>P</i> < 0.001), and untreated cells (11.1% ± 0.02%, <i>P</i> < 0.001). DNA degradation was observed in Caco cells treated with <i>F. assafoetida</i> in a dose-dependent manner, where complete degradation occurred at the dose of IC₅₀ (342.9 μg/mL). <i>F. assafoetida</i> induced a significant increase in the TA concentration and GSH, while a significant decrease in the MDA levels (<i>P</i> < 0.001, for all). Also, there was a significant increase in ALP activity in Caco cells (0.53 ± 0.26 U/mL) compared to the control cells (0.05 ± 0.02 U/mL, <i>P</i> = 0.045). There was a significant upregulation of JNK and MAPK expression in Caco cells treated with <i>F. assafoetida</i> compared to the controls [2.59 ± 0.01 (<i>P</i> < 0.001), and 3.62 ± 0.01 (<i>P</i> < 0.001); respectively].</p><p><strong>Conclusion: </strong><i>F. assafoetida</i> is a potentially successful therapeutic and differentiating agent for colon cancer.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"110757"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145914218","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":"Sacubitril/valsartan as add-on to standard therapy in patients with heart failure: A randomized controlled trial.","authors":"Reevanshi Dhawan, Rakesh Mittal, Ashwani Kumar, Kuldip S Laller, Paramjeet S Gill, Adarsh Rag, Niti Mittal","doi":"10.5493/wjem.v15.i4.111542","DOIUrl":"10.5493/wjem.v15.i4.111542","url":null,"abstract":"<p><strong>Background: </strong>Sacubitril/valsartan is a first-in-class angiotensin receptor neprilysin inhibitor (ARNI) which combines an angiotensin receptor blocker (valsartan) with sacubitril, an inhibitor of the enzyme neprilysin. By virtue of combined effect of blocking the action of angiotensin-II and inhibiting the breakdown of natriuretic peptides, ARNIs have beneficial role in heart failure (HF).</p><p><strong>Aim: </strong>To evaluate the effect of sacubitril/valsartan on N-terminal pro-B-type natriuretic peptide (NT-pro BNP), inflammatory marker [high-sensitivity C-reactive protein (hs-CRP)], and quality of life when given as add-on to standard therapy in patients with HF.</p><p><strong>Methods: </strong>Sacubitril/valsartan as add-on therapy for improvement in HF study was a randomised controlled trial conducted from July 2023 to November 2024 in a public tertiary care hospital in India. Eligible patients were randomised in 1:1 ratio to either of the 2 study arms: (1) Group A (sacubitril/valsartan + standard treatment); and (2) Group B (standard treatment) for 12 weeks. Primary end point was change in NT-pro BNP levels at 12 weeks from baseline. Secondary endpoints included (1) Change in hs-CRP levels; (2) Change in World Health Organisation Quality of Life Questionnaire (WHOQOL-BREF) score; and (3) Incidence of treatment-related adverse events or worsening HF. Statistical analysis was done using Statistical Package for the Social Sciences trial version 29.0 and <i>P</i> < 0.05 was considered significant.</p><p><strong>Results: </strong>Out of 124 patients screened, 80 were enrolled of which 25 patients in each group were available for per-protocol analysis. At baseline, both the groups were comparable. Sacubitril/valsartan group exhibited a statistically significant greater reduction in NT-pro BNP (-35.91 ± 28.01 <i>vs</i> 24.68 ± 31.86; <i>P</i> < 0.0001) and hs-CRP (-2.87 ± 3.22 <i>vs</i> 0.76 ± 1.60; <i>P</i> < 0.0001) levels at 12 weeks compared to standard treatment group. There was also a greater improvement in quality of life with sacubitril/valsartan group (overall change in WHOQOL-BREF: 13.16 ± 8.73 in sacubitril/valsartan <i>vs</i> -4.12 ± 6.25 in standard treatment arm). No major adverse events were reported in two groups.</p><p><strong>Conclusion: </strong>Sacubitril/valsartan demonstrated significant improvements in HF biomarkers, inflammation, and quality of life without compromising safety supporting its role as an effective addition to standard HF therapy. Further research is needed to evaluate its long-term benefits on mortality and cardiac remodeling.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"111542"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145914113","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":"Chronotherapeutic optimization of radioactive iodine therapy in differentiated thyroid cancer: The rationale for evening administration.","authors":"Georgios Meristoudis, Christos Savvidis, Ioannis Ilias","doi":"10.5493/wjem.v15.i4.110893","DOIUrl":"10.5493/wjem.v15.i4.110893","url":null,"abstract":"<p><p>Radioactive iodine (RAI) therapy remains a cornerstone in the management of differentiated thyroid cancer (DTC). The therapeutic efficacy of RAI depends on thyroid-stimulating hormone (TSH)-driven uptake <i>via</i> the sodium-iodide symporter (NIS). Although elevated TSH levels are routinely achieved before RAI administration, the circadian rhythm of TSH, which peaks overnight, is largely overlooked in treatment protocols. Aligning RAI administration with this physiological peak, particularly through evening dosing, may enhance iodine uptake, improve therapeutic efficacy, and reduce systemic exposure. Preclinical data and the known circadian regulation of TSH and NIS support this approach, although clinical validation is lacking. Evening dosing may also improve patient convenience and clinic workflow. However, logistical challenges and the absence of human trials present barriers to implementation. In this narrative review, we synthesize current evidence and tentatively propose the chronotherapeutic alignment of RAI timing as a novel, potentially impactful optimization strategy in DTC management. Prospective studies are needed to evaluate its clinical benefits and feasibility.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"110893"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145914180","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":"Gut microbiota and metabolic-associated steatosis liver disease: Unveiling mechanisms and opportunities for therapeutic intervention.","authors":"Resha Dermawansyah Rusman, Fardah Akil, Muhammad Luthfi Parewangi, Nu'man As Daud, Rini Bachtiar, Susanto Hendra Kusuma, Amelia Rifai","doi":"10.5493/wjem.v15.i4.107316","DOIUrl":"10.5493/wjem.v15.i4.107316","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) has become a leading cause of chronic liver disease, closely linked with metabolic syndrome. Recent evidence spotlights the gut-liver axis as a major player in MASLD pathogenesis. Dysbiosis of gut microbiota alters the intestinal barrier and enhances endotoxemia, hepatic inflammation, insulin resistance and fibrosis. Microbial metabolites including short-chain fatty acids, bile acids and ethanol impact host metabolism and immunity, and their dysregulation contributes to disease progression. This review summarises the mechanistic associations between dysbiosis and MASLD involving altered microbial composition, leaky gut, toll-like receptor signalling and immune dysregulation. It also reviews microbially targeted therapeutic strategies, such as probiotics, prebiotics, synbiotics, faecal microbiota transplantation, diet changes, and postbiotic metabolites. Although these interventions may have clinical potential, the heterogeneity of outcomes highlights the interindividual nature of the microbiome and warrant personalized interventions. Developments in multi-omics and precision medicine provide possibilities to discover microbial biomarkers and customize therapeutic approach. Resolving methodological heterogeneity and providing a clear definition of MASLD-related dysbiosis are key for translating microbiome science into the clinic. In conclusion, modulation of gut microbiota is an emerging strategy for the adjunctive treatment of MASLD alongside lifestyle and pharmacologic therapies.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"107316"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145913621","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":"Short-term blood pressure variability as an indicator of the adaptive capacity of patients with chronic heart failure.","authors":"Natalia S Akimova, Larisa E Konshina, Anastasiya E Runnova, Maksim O Zhuravlev, Tatyana M Bogdanova, Anton R Kiselev, Yury G Shvarts","doi":"10.5493/wjem.v15.i4.110904","DOIUrl":"10.5493/wjem.v15.i4.110904","url":null,"abstract":"<p><strong>Background: </strong>The six-minute walk test (6MWT) allows to determine, in addition to the main parameters, the time of heart rate recovery (THRR), cardiac function, adaptation index (AI), which characterize the compensatory reserve of patients with chronic heart failure (CHF). At the same time, the significance of these parameters in patients taking beta-blockers for CHF is insufficiently studied, taking into account the negative chronotropic effect of drugs. In this regard, it is relevant to identify factors that can characterize the compensatory capabilities of a patient with CHF during 6MWT, not related to the calculation of heart rate.</p><p><strong>Aim: </strong>To identify hemodynamic indicators of the adaptive capabilities of patients with CHF during paired 6MWT depending on their intake of beta-blockers.</p><p><strong>Methods: </strong>Seventy-four patients with compensated CHF due to coronary heart disease and/or hypertension formed the main group, comprising 46 individuals who were taking beta-blockers, and a comparison group comprising 28 individuals who had not been taking beta-blockers for at least one month before 6MWT. All participants underwent Doppler echocardiography (DECG), paired 6MWT, with assessment of hemodynamic parameters before and after both the first and second test. AI, THRR, blood pressure variability (BPV) were calculated. Multivariate, correlation analyses, univariate analysis of variance were used.</p><p><strong>Results: </strong>There were no significant associations between adaptation characteristics and DECG parameters or functional class (FC) of CHF in patients of the main group. In the comparison group, the indicators of compensatory reserve were significantly and directly associated with left ventricular ejection fraction (LVEF), and inversely with FC CHF and cardiac cavity size. In both groups, a greater difference in systolic blood pressure between the end of the first and the beginning of the second 6MWT was significantly associated with a higher index of right ventricular systolic dysfunction (Tricuspid annular plane systolic excursion) and LVEF, as well as a smaller left ventricular size and mass, and a lower pulmonary artery systolic pressure in patients in the main group.</p><p><strong>Conclusion: </strong>Systolic BPV, measured immediately after 6MWT and 20 minutes after its completion, can indirectly characterize the compensatory reserve in patients with CHF, regardless of their beta-blocker intake.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"110904"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145914121","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":"Lack of cytoplasmic expression of a new marker programmed cell death ligand-1 in tumor cells is significant.","authors":"Marina A Senchukova, Evgeniya Yu Zubareva, Natalia V Saidler, Lyubov V Krivolapova","doi":"10.5493/wjem.v15.i4.110890","DOIUrl":"10.5493/wjem.v15.i4.110890","url":null,"abstract":"<p><strong>Background: </strong>Recent studies have indicated that an antibody against programmed cell death protein 1-ligand 1 (PDCD1-LG1), a new marker of programmed cell death-ligand 1 expression, is promising for studying the mechanisms of breast cancer (BC) progression and resistance to chemotherapy.</p><p><strong>Aim: </strong>To compare the features of PDCD1-LG1 expression in chemoresistant luminal A BC and BC with high Ki67 indices.</p><p><strong>Methods: </strong>This prospective single-center observational cohort study included 148 patients with newly diagnosed primary resectable BC. The tumor sections were stained with antibodies against PDCD1-LG1. The statistical calculations were performed using Statistica software version 12.0. <i>P</i> < 0.05 was considered statistically significant.</p><p><strong>Results: </strong>Cytoplasmic PDCD1-LG1 (cPDCD1-LG1) expression was detected in the nonneoplastic epithelium, tumor cells (TCs) and immune cells (ICs). A lack of cPDCD1-LG1 expression in ≥ 20% of TCs and a PDCD1-LG1+ IC score ≥ 10% were associated with aggressive BC characteristics, including tumor G3, estrogen receptor-negative status, overexpression of human epidermal growth factor receptor 2 (HER2+), luminal B HER2+ BC, nonluminal HER2+ BC and triple-negative BC. The lack of cPDCD1-LG1 expression in < 20% of the TCs, in combination with a PDCD1-LG1+ IC score < 10% and G1, was characteristic of chemoresistant luminal A BC, whereas the lack of cPDCD1-LG1 expression in ≥ 20% of the TCs, combined with a PDCD1-LG1+ IC score ≥ 10%, was a predictor of high BC sensitivity to chemotherapy.</p><p><strong>Conclusion: </strong>These results indicate that both the lack of cPDCD1 LG1 in TCs and the PDCD1 LG1 IC score and their combination may be important for assessing BC prognosis and sensitivity to chemotherapy.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"110890"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145914000","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":"Psoriasis and atrial fibrillation: Exploring the intersection.","authors":"Hitaishi Mehta, Smriti Gupta, Juniali Hatwal, Aalam Sohal, Akash Batta, Bishav Mohan","doi":"10.5493/wjem.v15.i4.107425","DOIUrl":"10.5493/wjem.v15.i4.107425","url":null,"abstract":"<p><p>This review explores the emerging connection between psoriasis and atrial fibrillation (AF), focusing on shared inflammatory mechanisms, clinical implications, and research gaps. Psoriasis, characterized by chronic systemic inflammation, has been associated with increased AF risk, driven by elevated pro-inflammatory cytokines such as interleukin (IL)-6, IL-17, and tumor necrosis factor-alpha. These inflammatory mediators contribute to atrial remodeling, fibrosis, and conduction abnormalities, evidenced by prolonged P-wave dispersion and atrial electromechanical delay in psoriasis patients. Severe psoriasis further exacerbates atrial dysfunction, increasing susceptibility to AF. This review synthesizes existing epidemiological and biological data, highlighting the need for interdisciplinary management of psoriasis patients to mitigate cardiovascular risks. However, the reliance on observational studies limits definitive conclusions about causality. We emphasize the necessity for large-scale, multicenter research to validate these findings, investigate genetic predispositions, and evaluate lifestyle factors and AF burden. Future research should aim to delineate the pathophysiological link between psoriasis and AF. By examining the interplay of systemic inflammation, electrophysiological changes, and clinical outcomes, this review aims to advance understanding of the psoriasis-AF link and guide strategies for early detection, prevention, and management of AF in psoriasis patients. Comprehensive care integrating dermatology and cardiology is essential for improving patient outcomes.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"107425"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145913995","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":"Immunohistochemical expression of epithelial mesenchymal transition proteins ZEB1 and E-cadherin in oral leukoplakia and oral squamous cell carcinoma.","authors":"Gouri S Panchannavar, Punnya V Angadi","doi":"10.5493/wjem.v15.i4.110372","DOIUrl":"10.5493/wjem.v15.i4.110372","url":null,"abstract":"<p><strong>Background: </strong>Oral squamous cell carcinoma (OSCC) is a frequent cancer affecting the oral cavity. OSCC is usually preceded by occurrence of precursor lesions, which demonstrate a varying degree of malignant transformation potential. Epithelial-mesenchymal transition is a significant biological phenomenon that facilitates tumor growth and metastasis through the involvement of diverse epithelial and mesenchymal proteins. E-cadherin down regulation and over-expression of zinc-finger E-box-binding homeobox 1 (ZEB1) has been reported in several cancers.</p><p><strong>Aim: </strong>To evaluate the role of E-cadherin and ZEB1 in oral leukoplakia and OSCC.</p><p><strong>Methods: </strong>A total of 60 cases <i>i.e.</i>, oral leukoplakia/oral epithelial dysplasia (OED) (<i>n</i> = 30) and OSCC (<i>n</i> = 30) were included. Immunohistochemistry was performed utilizing two markers: E-cadherin and ZEB1. The Mann-Whitney <i>U</i> test was employed to compare individual markers across the study groups. Spearman's correlation was done followed by discriminant function analysis.</p><p><strong>Results: </strong>Reduction in the expression E-cadherin and altered localization were noted from OED to OSCC. Overexpression of ZEB1 along with cytoplasmic accumulation was noted in OED, with marked expression in OSCC. ZEB1 epithelium intensity and ZEB1 connective tissue percentage contributed to the discriminant function with an accuracy of 85% for the classification of OED from OSCC.</p><p><strong>Conclusion: </strong>Loss of E-cadherin and up-regulation of ZEB1 from OED to OSCC, predisposes to induction of epithelial-mesenchymal transition. Discriminant formulas are developed to classify cases of OED and OSCC with 85% accuracy.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"110372"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145913585","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":"Proneurogenic and microglial modulatory properties of botulinum neurotoxin in the hippocampus of aging experimental mice.","authors":"Jerly Helan Mary Joseph, Mercy Priyadharshini Babu Deva Irakkam, Mahesh Kandasamy","doi":"10.5493/wjem.v15.i4.108187","DOIUrl":"10.5493/wjem.v15.i4.108187","url":null,"abstract":"<p><strong>Background: </strong>Botulinum neurotoxin (BoNT) is widely recognized as an effective therapeutic agent for managing various neurological disorders, characterized by motor impairments and neuromuscular deficits. BoNT works by modulating the release of acetylcholine at the neuromuscular junction. Recently, BoNT has been shown to enhance spatial memory and attenuate anxiety in experimental aging animals. While neurogenesis in the hippocampus contributes to cognitive properties, BoNT treatment could potentially influence the regulation of adult neurogenesis. As aging-associated microglial activation impairs neurogenesis, the anti-inflammatory properties of BoNT could be associated with the modulation of microglial activity, thereby enhancing cognitive function.</p><p><strong>Aim: </strong>To investigate the neurogenic and microglial modulatory properties of BoNT in the hippocampus of aging experimental mice.</p><p><strong>Methods: </strong>Experimental aging mice were administered BoNT and after four weeks, the animals were sacrificed. The brains were subjected to cryosections followed by immunohistochemical analysis to quantify doublecortin (DCX)-positive immature neurons, bromodeoxyuridine (BrdU)-neuronal nuclei (NeuN) double positive newly matured neurons and ionized calcium-binding adapter molecule 1 (Iba1)-positive microglia in the hippocampal dentate gyrus. In parallel, an additional set of animals was used to evaluate BoNT-mediated alterations in key inflammatory markers such as cyclooxygenase (COX)-2, and nitric oxide (NO) in hippocampal tissues.</p><p><strong>Results: </strong>The results revealed a significant increase in the number of DCX-positive immature neurons and BrdU-NeuN positive differentiated neurons in the hippocampus of the BoNT-treated group compared to the control. This enhancement in neurogenesis was accompanied by a marked reduction in the activated form of microglial cells, coupled with decreased mRNA expression of COX-2 and reduced NO levels in the hippocampus of BoNT-treated animals.</p><p><strong>Conclusion: </strong>This study validates the proneurogenic and anti-neuroinflammatory properties of BoNT, which may underlie its procognitive effects. Hence, BoNT could be a promising therapeutic agent for treating various neurocognitive disorders.</p>","PeriodicalId":75340,"journal":{"name":"World journal of experimental medicine","volume":"15 4","pages":"108187"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12767248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145914003","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}