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This study aimed to assess the potential antifibrotic impact of zinc sulfate in chronic Hepatitis C Virus (HCV) patients receiving direct-acting antiviral therapy. This randomized controlled study included 50 chronic HCV-infected patients with fibrosis stage (F1 & F2). Participants were randomly assigned to two groups: Group 1 (Control group, n = 25) received standard direct-acting antiviral therapy for 3 months, while Group 2 (Zinc group, n = 25) received 50 mg/day of zinc sulfate in addition to the standard direct-acting antiviral therapy for the same duration. Baseline and 3-month post-intervention assessments included evaluating serum levels of hyaluronic acid, transforming growth factor beta-1, and fibronectin. Furthermore, indices of liver fibrosis, such as the Fibrosis Index based on the 4 factors (FIB-4) and the Aspartate Transaminase-to-Platelet-Ratio Index (APRI), were calculated during these assessments. At baseline, the two studied groups had no statistical difference in demographic and laboratory data. After treatment, serum zinc levels significantly increased in the zinc-treated group compared to the control group. Additionally, serum fibronectin and hyaluronic acid levels were significantly reduced in group 2 (zinc group) compared to group 1 (control group). Moreover, zinc group showed lower APRI scores than the control group after a 3-month follow-up period, but there was non-significant difference in FIB-4 scores between the two groups after treatment. Furthermore, total bilirubin levels were reduced after zinc therapy for 3 months. Administering zinc sulfate could potentially serve as a safe and efficient therapeutic strategy for the management of hepatic fibrosis in individuals with chronic hepatitis C virus. ClinicalTrials.gov identifier: NCT05465434, On 19/7/2022.

Objective This study aimed to assess the potential antifibrotic impact of zinc sulfate in chronic Hepatitis C Virus (HCV) patients receiving direct-acting antiviral therapy. Methods This randomized controlled study included 50 chronic HCV-infected patients with fibrosis stage (F1 & F2). Participants were randomly assigned to two groups: Group 1 (Control group, n  = 25) received standard direct-acting antiviral therapy for 3 months, while Group 2 (Zinc group, n  = 25) received 50 mg/day of zinc sulfate in addition to the standard direct-acting antiviral therapy for the same duration. Baseline and 3-month post-intervention assessments included evaluating serum levels of hyaluronic acid, transforming growth factor beta-1, and fibronectin. Furthermore, indices of liver fibrosis, such as the Fibrosis Index based on the 4 factors (FIB-4) and the Aspartate Transaminase-to-Platelet-Ratio Index (APRI), were calculated during these assessments. Results At baseline, the two studied groups had no statistical difference in demographic and laboratory data. After treatment, serum zinc levels significantly increased in the zinc-treated group compared to the control group. Additionally, serum fibronectin and hyaluronic acid levels were significantly reduced in group 2 (zinc group) compared to group 1 (control group). Moreover, zinc group showed lower APRI scores than the control group after a 3-month follow-up period, but there was non-significant difference in FIB-4 scores between the two groups after treatment. Furthermore, total bilirubin levels were reduced after zinc therapy for 3 months. Conclusions Administering zinc sulfate could potentially serve as a safe and efficient therapeutic strategy for the management of hepatic fibrosis in individuals with chronic hepatitis C virus. Trial Registration ClinicalTrials.gov identifier: NCT05465434, On 19/7/2022.

Phthalates are widely distributed in our environment due to their usage in many industries, especially in plastic production, which has become an essential part of daily life. This investigation aimed to assess the potential remedial influence of lutein, a naturally occurring carotenoid, on phthalate-triggered damage to the liver and kidneys. When di-(2-ethylhexyl) phthalate (DEHP) was administered to male albino rats over sixty straight days at a dosage of 200 mg/kg body weight, it resulted in a significant increase in the serum activity of liver enzymes (AST, ALT, and GGT), alpha-fetoprotein, creatinine, and cystatin-C, as well as disruptions in the serum protein profile. In addition, intoxication with DEHP affected hepato-renal tissues’ redox balance. It increased the content of some proinflammatory cytokines, nuclear factor kappa B (Nf-κB), and apoptotic marker (caspase-3); likewise, DEHP-induced toxicity and decreased the level of anti-apoptotic protein (Bcl-2) in these tissues. Lutein administration at a dose level of 40 mg/kg b.w efficiently facilitated the changes in serum biochemical constituents, hepato-renal oxidative disturbance, and inflammatory, apoptotic, and histopathological alterations induced by DEHP intoxication. In conclusion, it can be presumed that lutein is protective as a natural carotenoid against DEHP toxicity.

Background Pediatric pulmonary embolism is a rare yet potentially life-threatening condition, presenting significant diagnostic and therapeutic challenges owing to its nonspecific symptoms and diverse underlying risk factors. This systematic review aims to consolidate data from case series and case reports to provide a comprehensive overview of pediatric pulmonary embolism, focusing on clinical characteristics, diagnostic approaches, treatment strategies, and outcomes. Methods This systematic review was conducted in adherence to the Preferred Reporting Items for Systematic Reviews and Meta-analysis guidelines and the Cochrane Handbook for Systematic Reviews of Interventions, version 6.3. The study protocol was registered with PROSPERO (ID: CRD42024532471). We utilized the Covidence systematic review software for deduplication and screening of search results. The literature search was developed with a subject specialist and included Medical Subject Headings terms and free-text keywords such as “pulmonary embolism,” “pediatric,” and “case reports.” Databases searched included PubMed, Scopus, Web of Science, and the Cochrane Library up to April 2024, limited to English-language publications. Reference lists of relevant articles were also reviewed. Results Pulmonary embolism affected males and females with age ranging from 1 to 18 years. Common underlying conditions included malignancies (for example, Wilms tumor), chronic diseases (for example, nephrotic syndrome), and recent surgical interventions. Diagnostic practices primarily relied on computed tomography pulmonary angiography, supplemented by chest X-ray and ultrasound. Treatment typically involved anticoagulation therapy with unfractionated heparin and low-molecular-weight heparin, transitioning to oral anticoagulants for long-term management. Thrombolytic therapy was used in severe cases. Outcomes varied, with many patients recovering well, though complications such as recurrent embolism and pleural effusion were observed. Fatal cases underscored the critical need for early detection and prompt treatment. Conclusion This systemic review underscores the rarity and complexity of pediatric pulmonary embolism, highlighting the necessity for increased clinical vigilance given its nonspecific presentation and diverse underlying risk factors. Accurate diagnosis, primarily via computed tomography pulmonary angiography, with the prompt initiation of anticoagulation therapy are essential for optimal outcomes. Despite favorable recovery rates for most patients, the potential for severe complications and fatalities reinforces the value of timely diagnosis and personalized management approaches. Further research is essential to refine diagnostic protocols, optimize treatment approaches, establish evidence-based guidelines, and improve long-term outcomes for children with pulmonary embolism.

Phthalates are widely distributed in our environment due to their usage in many industries, especially in plastic production, which has become an essential part of daily life. This investigation aimed to assess the potential remedial influence of lutein, a naturally occurring carotenoid, on phthalate-triggered damage to the liver and kidneys. When di-(2-ethylhexyl) phthalate (DEHP) was administered to male albino rats over sixty straight days at a dosage of 200 mg/kg body weight, it resulted in a significant increase in the serum activity of liver enzymes (AST, ALT, and GGT), alpha-fetoprotein, creatinine, and cystatin-C, as well as disruptions in the serum protein profile. In addition, intoxication with DEHP affected hepato-renal tissues’ redox balance. It increased the content of some proinflammatory cytokines, nuclear factor kappa B (Nf-κB), and apoptotic marker (caspase-3); likewise, DEHP-induced toxicity and decreased the level of anti-apoptotic protein (Bcl-2) in these tissues. Lutein administration at a dose level of 40 mg/kg b.w efficiently facilitated the changes in serum biochemical constituents, hepato-renal oxidative disturbance, and inflammatory, apoptotic, and histopathological alterations induced by DEHP intoxication. In conclusion, it can be presumed that lutein is protective as a natural carotenoid against DEHP toxicity.