Platelet-rich plasma (PRP) has become an increasingly valuable biologic approach for personalized regenerative medicine because of its potent anti-inflammatory/healing effects. It is thought to be an excellent source of growth factors that can promote tissue healing and lessen fibrosis. Although this treatment has demonstrated effectiveness in numerous disease areas, its impact on pulmonary fibrosis (PF) caused by silver nanoparticles (AgNPs) via its antiapoptotic effects remains to be explored. AgNPs were synthesized biologically by Bacillus megaterium ATCC 55000. AgNP characterization was carried out via UV–Vis spectroscopy, X-ray diffraction (XRD), dynamic light scattering (DLS), transmission electron microscopy (TEM), and scanning electron microscopy (SEM) imaging to reveal monodispersed spheres with a mean diameter of 45.17 nm. A total of 48 male Wistar rats divided into six groups, with 8 rats per group, were used in the current study on the basis of sample size and power. The groups used were the PRP donor, control, AgNP, AgNP + PRP, AgNP + dexamethasone (Dexa) rat groups, and a recovery group. Body weights, hydroxyproline (HP) levels, and CASP3 and TWIST1 gene expression levels were assessed. H&E and Sirius Red staining were performed. Immunohistochemical studies for inducible nitric oxide synthase (iNOS) and cluster of differentiation 68 (CD68) with histomorphometry were conducted. A significant reduction in body weight (BWt) was noted in the AgNP group compared with the AgNP + PRP group (p < 0.001). HP, CASP3, and TWIST1 expression levels were significantly increased by AgNPs but decreased upon PRP (p < 0.001) treatment. Compared with those in the control group, the adverse effects of AgNPs included PF, lung alveolar collapse, thickening of the interalveolar septa, widespread lymphocytic infiltration, increased alveolar macrophage CD68 expression, and iNOS positivity in the cells lining the alveoli. This work revealed that PRP treatment markedly improved the histopathological and immunohistochemical findings observed in the AgNP group in a manner comparable to that of the Dexa. In conclusion, these results demonstrated the therapeutic potential of PRP in a PF rat model induced via AgNPs. This study revealed that PRP treatment significantly improved the histopathological and immunohistochemical alterations observed in the AgNP-induced group, with effects comparable to those of the Dexa. In conclusion, these findings highlight the therapeutic potential of PRP in a rat model of AgNP-induced PF.

Background: Accurate diagnosis, early detection, and differentiation of lung adenocarcinoma from mesothelioma; particularly the epithelioid subtype is needed to allow better management thus to improve their prognosis. Aim of our study was to assess applicability of CPA4, UHRF1, glypican-1 and CD90 expression by immunohistochemistry to differentiate between lung adenocarcinoma and epithelioid mesothelioma in addition to detection of their prognostic roles and relation to patients’ survival. Methods: We collected samples from 30 patients diagnosed with lung adenocarcinoma and 30 patients diagnosed with epithelioid mesothelioma. For the immunohistochemistry, sections of all collected samples were incubated with CPA4, UHRF1, glypican-1 and CD90 to assess their diagnostic accuracy. RESULTS: A highly significant association was detected between positive CPA4, UHRF1 expression in lung adenocarcinoma and their diagnostic accuracy (p value <0.001). Also, highly significant association was detected between positive CD90, Glypican 1 expression in epithelioid mesothelioma and their diagnostic accuracy (p value <0.001). CPA4 expression was associated with shorter OS rate (P value 0.019, 0.009) UHRF1 expression was associated with shorter OS rate (P value=0.009) Conclusions: CPA4, UHRF1, glypican-1 and CD90 were considered novel biomarkers that have important roles in differentiation between epithelioid malignant mesothelioma and adenocarcinoma of the lung with high sensitivity and specificity.

Background: Chronic obstructive pulmonary disease (COPD) and heart failure (HF) are highly prevalent chronic conditions that frequently coexist and share common risk factors, including smoking, aging, and physical inactivity. COPD is associated with a two- to fivefold increased risk of HF, yet estimates of COPD prevalence among HF patients vary widely, and the impact of this coexistence on morbidity and mortality remains uncertain. Reliable long-term, real-world data—particularly from the Gulf region—are limited. This systematic review and meta-analysis aimed to evaluate the relationship between COPD and HF and to assess the impact of their coexistence on clinical outcomes. Methods: A systematic review and meta-analysis were conducted in accordance with PRISMA guidelines. Major electronic databases (PubMed, EMBASE, Cochrane Library, and Scopus) were searched for studies published in English involving adults (≥18 years) with both COPD and HF. Observational studies and randomized controlled trials reporting morbidity and/or mortality outcomes were included. Pediatric studies, case reports, editorials, and studies lacking clear diagnostic criteria for COPD or HF were excluded. Data were synthesized qualitatively and quantitatively where applicable. Results: Ten studies published between 1990 and 2023 were included, encompassing prospective registries, retrospective cohorts, cross-sectional studies, physician surveys, and one meta-analysis, primarily from Saudi Arabia and the Gulf region [4–13]. COPD prevalence among HF patients was approximately 10% in acute HF cohorts, while primary-care screening revealed a COPD prevalence of 14.2% among smokers aged ≥40 years, indicating substantial underdiagnosis [4,13]. Patients with COPD–HF overlap were generally older and had higher rates of cardiometabolic and systemic comorbidities. COPD was associated with increased hospital length of stay, ICU admission (12.4%), and higher 30- and 90-day readmission rates (up to 39%) [5,6,12]. However, COPD was not independently associated with increased in-hospital or one-year mortality in acute HF populations [4]. Subclinical cardiac dysfunction was frequently observed in COPD patients and was not correlated with airflow limitation severity [7]. Conclusion: COPD and heart failure commonly coexist and significantly increase healthcare utilization, ICU admission, and hospital readmissions in the Gulf region. Although COPD does not independently increase short-term mortality in heart-failure populations, it substantially contributes to morbidity and post-discharge burden. Rising COPD prevalence, persistent underdiagnosis, and variability in multidisciplinary management highlight the need for early detection, integrated cardiopulmonary care models, and targeted interventions to reduce readmissions and improve outcomes.

Laryngeal cancer, particularly the squamous cell carcinoma subtype, is prevalent all over the world and is characterized by a poor prognosis and high mortality rates. Currently, no definitive prognostic markers exist for predicting the behavior of the tumor. The aim of this study is to examine the correlation between cyclin D1 and E-cadherin expression with some clinicopathological parameters in laryngeal squamous cell carcinoma (LSCC). 60 cases of LSCC were retrospectively studied concerning the clinicopathological features and the potential prognostic role of cyclin D1 and E-cadherin expression in laryngeal carcinoma, using immunohistochemical staining scores on paraffin-embedded cancer tissues from patients who were treated with surgical excision. Reduced E-cadherin expression was significantly correlated with tumor grade (p = 0.0288), T stage (p = 0.041), and lymph node metastasis (p = 0.003). Regarding Cyclin D1, a statistically significant correlation was found with lymph node metastasis (p=0.019). In contrast, cyclin D1 expression was not significantly correlated with TNM stage or tumor grade (p=0.99 and 0.66, respectively). Evaluating expression of cyclin D1 in conjunction with E-cadherin expression in laryngeal squamous cell carcinoma may prove beneficial in identifying patients with lymph node metastasis. Tumor grade, stage, and nodal metastasis can significantly affect E-cadherin expression in patients with LSCC. However, further studies using genetic testing are recommended to assess the role of E-cadherin in tumor progression.