Multidrug-resistant Gram-negative pathogens, including Escherichia coli (E.coli) and Klebsiella pneumoniae (K.pneumoniae) represent major clinical concerns due to their potent biofilm-forming ability and associated virulence traits that contribute to persistent infections and antibiotic failure.In response to the growing limitations of conventional antibiotics against biofilm-associated infections, the present study evaluated the antibiofilm potential of the ethanolic leaf extract of Ruellia tuberosa L. (R. tuberosa L.) using in vitro assays and gas chromatography-mass spectrometry-guided molecular docking analysis.The extract demonstrated antibacterial activity at the minimum inhibitory concentration (MIC) level and effectively inhibited biofilm formation at sub-MIC concentrations, achieving 55% inhibition in E. coli at 10 mg/ml and 67.81% inhibition in K. pneumoniae at 20 mg/ml, without significantly affecting planktonic growth.Phytochemical profiling revealed a diverse compound composition, with diethyl phthalate identified as the major constituent.Molecular docking demonstrated stable interactions of this compound with key biofilm-and virulence-associated targets in both pathogens, suggesting interference with bacterial adhesion, biofilm development, and persistence.Overall, these findings highlight R. tuberosa L. as a promising natural source of antibiofilm agents capable of attenuating biofilm formation in multidrug-resistan Gram-negative pathogens.These plant-derived compound may serve as adjunct strategies for managing biofilm-associated infections caused by E. coli and K. pneumoniae, warranting further in vivo and molecular validation.

Periodontitis is characterized by dysregulated host immune responses to Gram-negative anaerobes, resulting in local tissue destruction and systemic inflammatory spill-over.In parallel, neurovascular inflammation potentially influenced by mediators, such as interleukin-1 (IL-1), calcitonin gene-related peptide (CGRP) and pentraxin-3 (PTX-3) is associated with migraine chronification.Given the biological overlap between mucosal and systemic inflammatory pathways, the present study assessed serum and salivary IL-1, CGRP and PTX-3 levels in 96 individuals allocated to four groups as follows: Healthy controls, patients with chronic migraines without periodontitis, periodontitis without migraines, and patients with chronic migraines with periodontitis.Biomarker levels were quantified using validated ELISA protocols, and the periodontal status was evaluated using the plaque index, modified sulcular bleeding index, probing depth and clinical attachment level.Individuals with co-existing chronic migraines and periodontitis exhibited the highest salivary and serum biomarker concentrations.The salivary IL-1 level was consistently higher than the serum levels, whereas CGRP and PTX-3 levels were predominantly elevated in serum.Significant correlations were observed between the salivary and serum concentrations of all markers, and between biomarker levels and periodontal parameters.These findings indicate an amplified inflammatory burden in individuals with both conditions and support the concept of a shared neurovascular-immune axis.Although the cross-sectional design precludes causal inference, the results of the present study highlight the potential relevance of periodontal status in the inflammatory profile of chronic migraine.

The present study was carried out to determine the efficacy of the apex preservation technique in the management of benign prostatic hyperplasia (BPH) complications following surgery.For this purpose, the PubMed, Embase and Cochrane Library electronic databases were widely searched for controlled trials published up to 2025.The ROBINS-I tool was used to assess the risk of bias in the included studies.Funnel plots and Egger's regression test were applied for publication bias in the present study.GRADEpro was used to assess the quality of evidence.The results revealed that the surgery duration of the preserving technique was significantly shorter [mean difference (MD), -9.82; 95% confidence interval (CI), -13.91 to -5.73; P<0.00001].The preserving technique method was associated with a lower incontinence rate (relative risk, 0.18; 95% CI, 0.07 to 0.46; P=0.0004).Blood loss in the preserving technique group was also less (MD, -65.37; 95% CI, -121.97 to -8.77; P=0.02).On the whole, as demonstrated herein, preserving the prostatic apex is also more time-efficient, leading to a markedly lower risk of developing complications such as blood loss and quicker urinary continence recovery following catheter removal.This leads to improved patient satisfaction, while maintaining similar International Prostate Symptom Score, quality of life and peak urinary flow rate values.Therefore, further research is required in order to fully determine the clinical effects of prostatic apex preservation in BPH surgery in minimizing the rate of complications.

Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer with a good prognosis.However, in rare cases, it can behave aggressively and exhibit unusual features such as squamous differentiation, where squamous cells appear alongside typical PTC cells.PTC with squamous differentiation (PTC-SD) is extremely rare and is thus not well understood.The present study reports two cases of PTC-SD.The first case was that of a 28-year-old female patient who presented with a neck mass and hoarseness, and another that of a 49-year-old male patient who presented with an incidental finding of a thyroid lesion during a neck ultrasound for a dental issue.Upon investigations, both patients had suspicious thyroid nodules.A total thyroidectomy was performed for both cases.A histopathological examination confirmed PTC-SD.Levothyroxine was prescribed for both patients, and radioactive iodine ablation was scheduled for the first case.Squamous epithelium in the thyroid is rare and can result from various causes, including primary thyroid squamous cell carcinoma, anaplastic transformation, metastasis, or PTC-SD.Although the available data are limited, they indicate that PTC-SD may be associated with a poorer prognosis compared to conventional PTC.Herein, in a review of 4 cases reported in the literature, it was found that 1 patient succumbed and another experienced recurrence.Despite its rarity, recognizing this variant is crucial for an accurate diagnosis and appropriate treatment planning.Patients with PTC-SD require careful monitoring, with the majority undergoing surgical resection.Though rare, clinicians should recognize that PTC can undergo squamous differentiation.

Oral squamous cell carcinoma (OSCC) is a prevalent malignancy with a poor prognosis due to late diagnosis, with a 5-year survival rate of 35-50%.Patients with Fanconi anemia (FA) exhibit a 500-700-fold increased risk of developing OSCC at younger ages.Non-invasive biomarkers are critical for early detection in high-risk groups.The present study investigated the salivary expression levels of miR-34a and the serum levels of survivin, both of which are associated with the PI3K signaling pathway, in patients with OSCC (n=24), patients with FA (n=24) and healthy controls (n=40).The miRNA levels were quantified using reverse transcription-quantitative PCR, and protein levels were measured using ELISA.Compared to the controls, the patients with OSCC exhibited significantly lower miR-34a levels (P=0.012), and patients with FA exhibited a reduced expression of miR-34a (P=0.014).Survivin levels were elevated in patients with OSCC (P=0.04) and FA (P=0.01)compared to the controls.A negative correlation was identified between miR-34a and surviving levels (=-0.52,P=0.005) in patients with OSCC.These findings suggest that miR-34a and survivin are promising non-invasive biomarkers for assessing the risk of developing OSCC in patients with FA and OSCC.However, multicenter studies with larger cohorts are warranted to validate these results for clinical surveillance protocols.

Urinary incontinence, the involuntary leakage of urine, is a common, yet underreported issue among older adults, with its prevalence markedly increasing with age and often leading to a loss of independence, social withdrawal and psychological distress.Diabetes mellitus is considered to aggravate urinary incontinence via neuropathy, impaired bladder innervation and detrusor dysfunction.Although random blood glucose (RBG) and glycated hemoglobin (HbA1c) are widely used markers of glycemic control, their direct association with incontinence severity has not yet been fully established, particularly in elderly Asian populations.The present observational, cross-sectional and correlation-based study evaluated the association between RBG, HbA1c and the severity of urinary incontinence using the International Consultant Incontinence Questionnaire-Urinary Incontinence Short Form (ICIQ-UISF).A total of 100 elderly patients (60 years of age; 52 males and 48 females; median age, 66 years) were recruited for the present study.The median RBG level was 274 mg/dl and the median HbA1c level was 8.50%.Among the participants, 82% reported urinary incontinence (36% patients had severe incontinence, 24% had moderate incontinence, 12% had mild incontinence and 10% had very severe incontinence).Small-volume leakage was most common (55%), and 36% of patients rated their quality-of-life impact as maximal (score, 10).Spearman's correlation analysis did not reveal any significant correlation between RBG and ICIQ-UISF scores (=-0.016,P=0.877) or between HbA1c and ICIQ-UISF scores (=0.047,P=0.641), whereas age demonstrated a weak, yet significant positive correlation with ICIQ-UISF scores (=0.242,P=0.015).On the whole, these findings suggest that urinary incontinence in older adults is influenced to a greater extent by an age-related physiological decline than glycemic markers, underscoring the multifactorial nature

AMP‑activated protein kinase (AMPK) and mechanistic target of rapamycin complexes (mTORCs; mTORC1 and mTORC2) have critical functions in controlling tumor cell metabolism, reciprocally affecting the anabolic and catabolic pathways that control cell growth, proliferation and survival. AMPK serves as a key energy sensor, activated in response to low cellular energy levels, while the action of mTORCs becomes evident under conditions with high nutrient and growth factors. The dysregulation of these cascades is notably detected in a number of types of cancer, where reduced AMPK activity and unrestrained mTOR signaling pathways accelerate metabolic shifts that support carcinogenesis. The connection between AMPK and mTOR is significant. AMPK plays a role in hindering mTOR signaling, thus diminishing protein biosynthesis and stimulating autophagy. This strengthens cellular homeostasis, progression and survival during severe metabolic distress. Nevertheless, the function of AMPK in tumors is multifaceted. At the same time, it commonly functions as a tumor suppressor; evidence suggests that in specific environments, AMPK may stimulate tumor development by supporting the survival of tumor cells under adverse conditions, such as metabolic deprivation. This dualism highlights that the therapeutic targeting of AMPK/mTOR signaling pathways needs to be addressed carefully, as the consequences may vary, depending on the specific cancer microenvironment and nutrient state. The present review summarizes evidence from the literature in an aim to shed light onto the complex balance of the actions, regulation and critical role of AMPK and mTORCs in cancer cell metabolism. The present review aimed to provide insight that may lead to the development of novel targeted therapies that diminish the threat of unfavorable consequences associated with modified metabolic control.

Colorectal cancer (CRC) is a major global health burden, and oxaliplatin is a cornerstone of its treatment. However, oxaliplatin‑induced neurotoxicity, particularly chronic cumulative neurotoxicity (CN), poses a significant clinical challenge, often severely compromising the quality of life of patients. Genetic polymorphisms in glutathione S‑transferase pi‑1 (<em>GSTP1</em>) may influence individual susceptibility to oxaliplatin‑induced neurotoxicity. The present study investigated the association between <em>GSTP1</em> polymorphisms (rs1695 and rs1138272) and CN in patients with CRC receiving oxaliplatin‑based chemotherapy. For this purpose, a prospective observational cohort study was conducted across two oncology centers, enrolling 120 patients with CRC. <em>GSTP1</em> polymorphisms were genotyped using polymerase chain reaction and Sanger sequencing. CN severity was assessed using the National Cancer Institute Common Terminology Criteria for Adverse Events. Logistic regression analysis was used to assess the association between GSTP1 genotypes and neurotoxicity onset and severity. Significant associations were observed between <em>GSTP1</em> polymorphisms and the risk of developing CN. The rs1695 GG genotype conferred a 7.7‑fold increased risk of developing CN at oxaliplatin doses &lt;1,000 mg/m2 (P=0.012) and a 5.5‑fold risk at doses &gt;1,000 mg/m2 (P&lt;0.001). The rs1138272 CT genotype was found to be associated with an elevated risk of developing CN [odds ratio (OR), 4.05; P=0.004], implicating the T allele in susceptibility. The GG genotype was strongly associated with progressive CN severity, exhibiting a 5‑fold risk for grade 2 (P=0.031) and a 6.2‑fold risk for grade 3 CN (P=0.029). Similarly, the CT genotype was associated with grade 3 CN. (OR, 3.43; P=0.043). To the best of our knowledge, the present study is the first to demonstrate a link between the rs1695 and rs1138272 polymorphisms and the onset and severity of CN. On the whole, the present study demonstrates that <em>GSTP1</em> polymorphisms significantly affect the oxaliplatin‑induced risk of developing CN in patients with CRC. These findings advocate genetic screening as part of personalized treatment strategies and underscore the need for further mechanistic and validation studies.

Melanoma is an aggressive type of skin cancer with a high metastatic potential and resistance to therapy. Through its core effectors, yes‑associated protein (YAP) and transcriptional coactivator with PDZ‑binding motif (TAZ), the Hippo signaling pathway has emerged as a key regulator of tumorigenesis in melanoma. However, the roles of these effectors remains incompletely understood. The present scoping review systematically synthesized the currently available knowledge on the function of YAP/TAZ in the progression of melanoma, resistance to therapy and potential therapeutic interventions. The present study conducted a scoping review and reported the results based on the Preferred Reporting Items for Systematic Reviews and Meta‑Analyses Extension for Scoping Reviews guidelines. A comprehensive literature search was performed across the PubMed and Cochrane Central databases, incorporating peer‑reviewed articles published up to June, 2024. The inclusion criteria encompassed studies investigating YAP/TAZ activity in melanoma models, including <em>in vitro</em>, <em>in vivo</em> and patient‑derived datasets. A total of 37 articles were identified, discussing YAP/TAZ in melanoma. The present scoping review highlights that the overexpression of YAP/TAZ promotes melanoma proliferation, metastasis, immune evasion and resistance to targeted therapy. These factors contribute to therapeutic failure and disease recurrence. YAP/TAZ activation occurs independently of the suppression of the Hippo pathway, involving MAPK‑driven phosphorylation, PI3K/AKT stabilization and extracellular matrix remodeling. Additionally, YAP/TAZ affects the tumor microenvironment and facilitates immune evasion. Targeting YAP/TAZ through verteporfin, bromodomain and extraterminal domain/histone deacetylase inhibitors and ibrutinib has demonstrated promise in preclinical studies. However, compensatory pathways and clinical translation remain a key challenge. YAP/TAZ are central mediators of melanoma pathogenesis, metastasis and therapeutic resistance by integrating multiple oncogenic pathways. While therapeutic strategies targeting YAP/TAZ are emerging, clinical translation remains limited. Future research is thus required to focus on developing selective inhibitors, patient stratification, elucidating the role of YAP/TAZ in melanoma, and combining therapies to improve melanoma treatment outcomes.