Background and Objective: Stridor is considered as a serious adverse complication of intubation that may lead to respiratory distress, reintubation, and further complications. Intravenous steroids including dexamethasone are assumed as an effective therapy. However, their associated side effects pose a limit on their usage. This study was carried out to elucidate the effect of intravenous dexamethasone with inhaled budesonide on the reduction of post-extubation stridor in ICU patients. Materials and Methods: This randomized clinical trial study included 80 intubated patients with extubation during their stay in the ICU ward. Prior to the extubation, a cuff-leak test was performed for all patients, and those with either negative test results or less than expected were randomly assigned to two groups of A or B (n= 40 each). Group A received 8 mg/8 hr of intravenous dexamethasone, while group B received aerosolized budesonide (0.5 mg/6 hr). Both groups received their medications starting 24 hours prior to the extubation until 24 hours afterwards. All of the patients were examined for stridor for 24 hours following the extubation. The data were collected and analyzed by SPSS-16 software using t-test, Chi-square, Fisher, and Mann-Whitney tests. Results: Post-extubation stridor occurred in 62.5% of the patients in the dexamethasone group vs. 52.5% of the budesonide group. However, this difference is not statistically significant (P= 0.36). Similarly, the difference between the stridor scores for the two groups was not significant either (P= 0.26). Conclusion: Our results show that the effect of intravenous dexamethasone vs. inhaled budsonide was similar on the restriction of post-extubation stridor. Nonetheless, using aerosolized budesonide is recommended due to its fewer associated side effects.

Background and Objective: Compelling evidence exists in favor of the effectiveness of herbal plant-derived components in cancer treatment; however their exact mechanisms of action are not well understood. Since the alteration of mitogen-activated protein kinase enzymes (MAPKs) has been reported in different cancer types, the present study aimed to investigate the effects of soy isoflavonoid genistein on the inhibition of cell viability and proliferation of AGS gastric cancer cell line by determining p38MAPK gene expression and also protein levels.
Materials and Methods: Cell viability was determined by MTT assay at different genistein concentrations (0, 50, 70, and 90 µM) after 24 hours of incubation. Quantitative Real-time PCR was carried out to obtain p38MAPK gene expression levels and its active phosphorylated protein (p-p38MAPK) was measured by flow cytometry.
Results: Genistein significantly reduced cell viability in a concentration and time-dependent manner.  Exposure of gastric cancer cells to 0, 50, 70, and 90 µM genistein down-regulated p38MAPK gene expression by 83, 56, and 57%, and reduced cell proliferation by 35, 52, and 67%, respectively.  In addition, a great reduction was observed in p-p38MAPK protein levels in treated cells compared to untreated control cells.
Conclusion: Since different concentrations of genistein reduced p38MAPK gene expression and lowered proliferation of AGS gastric cancer cells, it might be a potent candidate for a therapeutic plant-derived agent for combination therapy in gastric cancer.

Coronavirus disease (COVID-19) can induce coagulopathy at the base of sepsis-induced coagulopathy (SIC), which is an important cause of death in these patients. Cytokine storm causes imbalance in coagulation and fibrinolytic system. A combination of hypercoagulability state, decrease or inhibition of fibrinolysis and endotheliopathy causes thromboembolic events. Underlying diseases such as diabetes and hypertension with a high rate of mortality in COVID-19 and some conditions like aging and obesity are the main disorders with hemostatic disturbance and increase of coagulopathy. Therefore, it seems that the combination of COVID-19 infection and these risk factors increase the risk of thromboembolic complications all together.

Background and Aims: Familial Mediterranean fever (FMF) is caused by mutations in the MEFV (Mediterranean fever) gene and is characterized by recurrent, self-limiting attacks of fever with polyserositis. This study aimed to identify MEFV gene variants in suspected FMF patients in the southwest of Iran.
Methods: We obtained whole blood samples from 40 unrelated pediatric patients suspected to have FMF between 2020 and 2024. The entire coding and flanking regions of the MEFV gene were sequenced using genomic DNA. We employed in-silico tools to detect the pathogenicity predictions of the rare mutation. Further, the clinical symptoms experienced by the patients were recorded and evaluated.
Results: We identified eight different mutations, including six common mutations (p.E148Q, p.M694I, p.M694V, p.A744S, p.M680I (c.2082G>A), p.V726A), one uncommon mutation (p. R202Q), and one rare mutation located in exon 3 (p.S339F). The most frequently reported mutant allele was p.E148Q (50%), followed by p.R202Q (43.75%). We reported the rare mutation p.S339F for the first time in Iranian FMF patients. Bioinformatics prediction tools confirmed the pathogenicity of this mutation, and for the first time, we used the I-mutant website for this mutation. Fever and abdominal pain were the most prevalent clinical symptoms.
Conclusion: These findings can be used to develop the genetic database of MEFV gene mutations and help in detection of hotspot regions in the Iranian population, especially in the southwest. Our results can be helpful in early diagnosis and pharmacotherapy for patients suspected of having FMF.