Mohammed Merza

Background and objective: Acute lung injury (ALI) it considered as a very serious illness characterized by inflammatory lung swelling, leading to acute hypoxic respiratory failure. c-Raf G-protein has been shown to regulate inflammation we predicted that c-Raf could regulate neutrophil infiltration in LPS induced sepsis in mice model. Methods: 18 albino mice (6 weeks age, weighing 26±2 grams) were randomly assigned to three groups: the control group (they were injected by normal saline intraperitoneally, n=6), the LPS (lipopolysaccharide) group (50 mg/kg LPS Were injected intraperitoneally, n=6), the GW5074 + LPS group (2 mg/kg of the selective c-Raf inhibitor GW5074 were given intraperitoneally 15 minutes before LPS injection, n=6). After 24 hours, the mice were sacrificed, then inflammatory cell counts, proinflammatory cytokines (TNF-α, IL-1β, MPO activity, CXCL-2, IL-6) were measured. The lungs were then isolated for molecular target analysis, histopathological, and immunohistochemical evaluations. Results: Resemble to the LPS group, pretreatment of mice with c-Raf inhibitor significantly decreased MPO, CXCL-2, TNF-α, IL-1β and IL-6, activity. GW5074 weakened migration and infiltration of inflammatory cells, showing a marked reduce in MPO (6.0 ±0.2 vs. 2.2±2.0 P <0.05) as well as CXCL-2(132.8± 2.0 vs. 80.4±6.0 P <0.05) in the sham, LPS, and GW5074 + LPS. Additionally, IL-6 levels in treatment group significantly decrease compared with LPS group (123 ± 4.0 vs. 71.2 ± 6.0 P <0.05). Conclusion: The conclusions of this research propose that c-Raf may have anti-inflammatory and protective effects against LPS-stimulated ALI in mice.

Being overweight is a growing concern worldwide, characterized by a body mass index (BMI) ranging from 25 to 29.9 kg/m2. This condition can arise from vari

Diabetes mellitus (DM) is a prevalent cause of platelet (PLT) activation. Inflammation-induced dysregulation of PLT function adds to chronic complications. Ras-related C3 botulinum toxin substrate 1 (Rac1), a 21 kDa G-protein, has been shown to modulate many PLT activities. We hypothesized that Rac1 may influence the PLT release of CXCL4 and CCL5, thereby contributing to macrovascular and microvascular problems in DM. The study included Swiss albino male mice pretreated with the Rac1 inhibitor NSC23766 and streptozotocin (STZ) to induce diabetes. A sample of 150 diabetic patients and 50 healthy controls was also analyzed. Statistical analyses were performed using Mann-Whitney tests on one hundred fifty confirmed diabetic patients who visit Layla Qasim health center for diabetes management, and 50 healthy individuals were included in this study. The serum CXCL4 and CCL5 in diabetic patients and healthy volunteer were measured. Swiss albino male mice received pretreatment of 5 mg/kg of the Rac1 inhibitor NSC23766, followed by injection of streptozotocin at a dosage of 45 mg/kg body weight, twice daily for five days. Rac1 activity in the PLT was measured using pulldown assay and Western blot method. Blood chemokine concentrations were also assessed using ELISA, and histological scores for the kidney, liver, pancreas, and lung were evaluated. CXCL4 and CCL5 levels were markedly elevated in DM patients compared to healthy individuals. Our findings indicated that streptozotocin induced diabetes mellitus in mice. GTP-Rac1 was induced in diabetic mice, and pretreatment with NSC23766 was significantly lower compared to vehicle group. Furthermore, diabetic mice showed significantly greater levels of CXCL4 and CCL5 (P <0.05) compared to the sham group. CXCL4 levels were reduced by 80% following Rac1 inhibition (P <0.05), while CCL5 levels decreased by 55.5% (P <0.05). The current study indicates that Rac1 plays a pivotal role in releasing PLT chemokines due to diabetes-induced inflammation in several organs, and inhibiting Rac1 may represent a novel therapeutic approach to managing inflammation in diabetic individuals.

Background: ketogenic diet refers to the diet plan that emphasizes foods that are high in fats, moderate proteins and very low carbohydrates to consume more calories from fat rather than carbohydrates and is commonly used as a weight-loss plan and in rare cases, as a treatment for some diseases. Objective: The aim of this study was to evaluate or assess organ functions in the individuals following ketogenic diet. Patients and methods: A total 31 samples were collected from individuals following ketogenic diet in male and femal aged from 20 to 55, and a control group which composed of 10 healthy individuals without ketogenic diet, and the diet duration was from 2 to 44 weeks. The sample were collected from Dec 2021 to Mar 2021 at Rozhalat emergency laboratory. We have measured serum urea, creatinine and hepatic enzymes in those individuals. We measured it statistically and regarded p-value for significance for less than 0.05. Result: Our result showed that ketogenic diet reduced the estimated glomerular filtration rate (eGFR) and induced Alanine transaminase(ALT) compared to control group (individual without ketogenic diet), moreover, there is no statistically difference in serum Aspartate transaminase(AST) and bilirubin compared to control group. The mean value of eGFR, ALT, AST, and bilirubin in ketogenic group are (79.3±5.7), (22.7± 3.6), (24.87±3.73), (0.72±0.05) respectively. Conclusion: We have observed that ketogenic diet affects the kidney function, the function of other organs like liver and induce hypercholesterolemia

The emergence of the novel coronavirus and then pandemic outbreak was coined 2019- nCoV or COVID-19 (or SARS-CoV-2 disease 2019). This disease has a mortality rate of about 3·7 percent, and successful therapy is desperately needed to combat it. The exact cellular mechanisms of COVID-19 need to be illustrated in detail. This study aimed to evaluate serum cytokines in COVID-19 patients. In this study, serum was collected from volunteer individuals, moderate COVID-19 patients, severe cases of COVID-19 patients, and patients who recovered from COVID-19 (n = 122). The serum concentrations of interleukins such as IL-1, IL-4, IL-6, IL-8, IL-10, and tumor necrosis factor-alpha (TNF-α), were measured by enzyme-linked immunosorbent assays (ELISA). The concentrations of IL-1 and TNF-α were did not differ significantly among groups. However, the concentration of IL-6 was significantly higher in moderate COVID-19 and severe cases of COVID-19 groups compared to control and recovered groups indicating it to be an independent predictor in the coronavirus disease. The levels of IFN-γ and IL-4 were significantly lower in the recovery group than the severe case of the COVID-19 group. In contrast, the level of IL-10 in recovered COVID-19 patients was significantly higher in compare to severe cases, COVID-19 patients. Varying levels of cytokines were detected in COVID-19 group than control group suggesting distinct immunoregulatory mechanisms involved in COVID-19 pathogenesis. However, additional investigations are needed to be to be performed to understand the exact cellular mechanism of this disease.