Tahmine Tavakoli

Background: Functional dyspepsia is a chronic gastrointestinal disorder with uncertain causes, often linked to anxiety and depression, which can worsen symptoms and hinder treatment success. Although psychological therapies and antidepressants have shown some benefit, the role of anti‐anxiety medications remains unclear. This study aims to evaluate the effectiveness of buspirone and mirtazapine in reducing symptoms and improving the quality of life for patients with functional dyspepsia. Methods: In a semi experimental study, 71 patients with functional dyspepsia were randomized to receive either buspirone 15 mg, mirtazapine 7.5 mg, or pantoprazole 40 mg once daily for 12 weeks. Outcomes—anxiety severity, dyspepsia symptom score, quality of life, and adverse events—were assessed at baseline and monthly. Efficacy was analyzed by repeated‐measures ANOVA and adverse event rates by chi‐square tests. Results: Both buspirone and mirtazapine significantly outperformed pantoprazole alone in reducing anxiety (buspirone vs. control at 3 months, p = 0.01; both active treatments vs. control, p < 0.05) and in alleviating functional dyspepsia symptoms by Week 12 (both vs. control, p < 0.05), with no difference between the two active drugs. Conclusions: This study suggests that buspirone and mirtazapine are effective in reducing anxiety and improving symptoms in patients with functional dyspepsia. These findings highlight the potential role of anti‐anxiety medications in managing both the psychological and gastrointestinal aspects of this disorder.

Background & Objective: Colorectal cancer contributes substantially to global cancer mortality, ranking among the leading causes of cancer-related deaths. Studies have linked its development to diminished expression of the SLC4A4 gene alongside elevated levels of the microRNAs hsa-miR-223-3p and hsa-miR-106a-5p. This study examines hsa-circRNA-001587 and hsa-circ-0004872 to determine their utility ...

Background: Since the early diagnosis of celiac disease (CD) is crucial, understanding its epidemiological characteristics can facilitate timely diagnosis and treatment. This study investigated CD's epidemiological, clinical, and laboratory characteristics in South Khorasan Province, Iran. Objectives: This study aimed to clarify the epidemiological characteristics, clinical manifestations, and laboratory findings of patients with CD in South Khorasan Province. Methods: This descriptive epidemiological research was conducted on 110 individuals with CD referred to the Gastroenterology Clinic from March to August 2019. The data were acquired via a comprehensive questionnaire, encompassing the participants' demographic specifications, medical records, the symptoms of the disease, laboratory diagnostic evaluations, and biopsy results. The data were employed for epidemiological inquiry, and the corresponding analyses were performed in SPSS v. 22. Results: The participants' mean age was 28.38 ± 15.25 years,78 (70.9%) were men, and 32 (29.1%) were women. The most common clinical gastrointestinal symptoms included abdominal pain in 70 (63.6%), diarrhea in 44 (40%), constipation in 43 (39.1%), and nausea in 35 (31.8%). Of the 83 biopsy cases, 3 (3.6%), 4 (4.8%), 9 (10.8%), 21 (25.3%), and 43 (55.4%) belonged to Marsh-I, Marsh-II, Marsh-IIIa, Marsh-IIIb, Marsh-IIIc categories, respectively. Conclusions: Most participants were male and aged 10 to 20 years. Abdominal pain was the most common clinical symptom. All the pathologically examined patients showed evidence of CD, while approximately two-thirds were serologically positive.

Nonalcoholic fatty liver disease (NAFLD) is a prevalent chronic liver disease with a global prevalence, and modulation of ANGPTL8 expression has emerged as a promising predictor of NAFLD susceptibility. This research was conducted to scrutinize ANGPTL8 protein expression in NAFLD patients and elucidate the interplay between ANGPTL8 gene polymorphisms and their lipid profiles, thus shedding new light on the pathophysiology of this complex disease. The study comprised 423 unrelated participants, including 222 healthy controls and 201 individuals with NAFLD, screened using FibroScan/ultrasonography and laboratory tests. The main goal focused on the genotype and allele frequency distribution in the ANGPTL8 gene, specifically analyzing two genetic variations: rs737337 (T/C) and rs2278426 (C/T). The participants diagnosed with NAFLD were slightly younger (P ≥ 0.05) and had a higher body mass index (BMI) than the individuals in the control group. Notably, there was a significant difference in the occurrence of the rs737337 polymorphism between the NAFLD and control groups, with a lower frequency observed in the NAFLD group. Our results indicated that individuals with the TC + CC genotype and C allele of rs737337 (T/C) had a decreased risk of higher levels of ALT and AST. Conversely, those with the CT, CT + TT genotype, and T allele of rs2278426 (C/T) exhibited an increased risk of higher levels of ALT and AST. The results imply that the rs2278426 (C/T) variant of the ANGPTL8 gene is more strongly linked to an increased risk of NAFLD compared to the rs737337 polymorphism. However, additional research is needed to understand the specific molecular mechanisms responsible for the upregulation of ANGPTL8 in individuals with NAFLD.

Background and Methods: Colorectal cancer (CRC) is considered one of the most common malignancies worldwide. The diagnosis and prognosis of the patients are very poor. In this study, we used in‐silico analysis and experimental techniques to investigate novel co‐expression genes and their associated miRNA networks in CRC. For this purpose, we conducted a comprehensive transcriptome analysis using online bulk and single‐cell RNA‐seq datasets. We then validated the results on tissue samples from cancerous and adjacent normal tissues from CRC patients by RT‐qPCR.Results: Using a weighted gene co‐expression network algorithm, we identified SLC4A4 as a significantly downregulated hub gene in the CRC. The single‐cell analysis indicated that the expression level of SLC4A4 in Paneth cells is higher than in other cell populations. Further computational analysis suggested hsa‐miR‐223‐3p and hsa‐miR‐106a‐5p as two specific hub‐miRNAs for the SLC4A4 gene. RT‐qPCR analysis showed a 2.60‐fold downregulation of SLC4A4. Moreover, hsa‐miR‐223‐3p and hsa‐miR‐106a‐5p showed an increased expression level of 5.58‐fold and 9.66‐fold in CRC samples, respectively. Based on the marginal model analysis, by increasing the expression of hsa‐miR‐106a‐5p, the average expression of the SLC4A4 gene significantly decreased by 103 units. Furthermore, ROC curves analysis indicated statistically significant for diagnostic ability of SLC4A4 (AUC: 0.94, Sensitivity: 95.5%, Specificity: 95.5%) and hsa‐miR‐106a‐5p (AUC: 0.72, Sensitivity: 72.7%, Specificity: 100%).Conclusion: This study provides a framework of co‐expression gene modules and miRNAs of CRC, which identifies some important biomarkers for CRC pathogenicity and diagnosis. Further experimental evidence will be required to support this study and validate the precise molecular pathways.

Background: Meteorin-like (Metrnl) is an adipokine with insulin sensitizing and anti-inflammatory properties that has been discovered recently. The relation among Metrnl, Inflammatory Bowel Disease (IBD), and obesity has been unexplored yet. Methods: The present study was conducted on 54 healthy control, 42 Ulcerative Colitis (UC), and 43 Crohn’s disease (CD) patients who were diagnosed by pathological examination. In all participants, serum levels of adiponectin, Metrnl, interleukin (IL)-6, and Tumor necrosis factor (TNF-α) were measured using ELISA kits. Results: Metrnl concentration was considerably lower in both UC (85.25 ± 36.55 pg/mL) and CD (76.93 ± 27.92 pg/mL) patients in comparison to control (107.52 ± 35.33 pg/mL). In addition, it was seen that both patient groups have a decreased level of adiponectin compared to the controls. Besides that, the level of IL-6 and TNF-α were significantly greater in the patient groups. Moreover, the result showed that the level of Metrnl is inversely correlated with body mass index (BMI) in the controls and the patients. Metrnl levels are also inversely associated with IL-6, and TNF-α in both of the patient groups. Conclusions: The current study is the first one reporting the decreased levels of Metrnl in serum among patients with IBD, which is inversely related with BMI, TNF-α, and IL-6. These results suggested a possible relation of Metrnl with the pathogenesis of IBD, particularly through inflammatory process, although further studies are warranted to dissect the possible mechanism.

Ulcerative colitis (UC) and Crohn's disease (CD) are two major forms of inflammatory bowel disease (IBD), which is an inflammatory disease. Studies have shown that adipose tissue and inflammation play important roles in the pathogenesis of IBD. C1q/TNF‐related protein‐3 (CTRP3) is a newly discovered adipokine playing a substantial role during inflammatory process, and for the first time in the present study, serum levels of this adipokine were measured in the UC and CD patients. This case–control study included 70 control, 50 UC, and 50 CD patients who were diagnosed by standard criteria. Serum levels of adiponectin, IL‐6, TNF‐α, TGF‐β, and CTRP3 were evaluated using ELISA kits. Serum levels of IL‐6, TNF‐α, and TGF‐β elevated in the UC and CD patients compared with the controls while adiponectin and CTRP3 diminished in the patient's groups compared with the control. Furthermore, decrease in CTRP3 serum levels was associated with the risk of UC and CD diseases. Moreover, CTRP3 indicated negative correlation with BMI, FBS, insulin, homeostasis model assessment of insulin resistance, IL‐6, TNF‐α, and TGF‐β and also a positive correlation with adiponectin in both the UC and CD patients. For the first time, the present study demonstrated lower levels of CTRP3 in the UC and CD patients. Decreased serum levels of CTRP3 and its inverse relationship with inflammatory cytokines and TGF‐β levels suggested a possible role for CTRP3 in the pathogenesis of UC and CD diseases.

MicroRNAs (miRNAs) are a novel class of single-stranded RNAs with a key role in the regulation of gene expression. miRNA main mechanism of action involves interaction with the mRNA transcribed from the genes, leading to the target mRNA silencing and degradation. Indeed, it is easy to conceive that a defective miRNA-based mRNA regulation may compromise normal cell function and cause genetic diseases. A wide spectrum of studies has focused on the identification and introduction of regulatory diseases-specific miRNAs for the past decade. Overexpression or downregulation of several miRNAs can potentially stimulate or inhibit pathways related to the pathogenesis of celiac disease (CD). CD is a chronic inflammatory disease characterized by small intestinal mucosal injury and nutrient malabsorption in genetically susceptible individuals after the dietary ingestion of gluten. The disease is characterized by villous atrophy, intraepithelial lymphocyte infiltration, and chronic inflammation and activation of lamina propria T cells. The common genetic background in CD is the presence of heterodimeric human leukocyte antigen class II molecules DQ2 or DQ8 that account for ∼40% of the genetic predisposition in this disease. In fact, by minute identification of these miRNAs and related targets and mechanisms, specific therapeutics can be developed to suppress these pathophysiological pathways through the enhancement or inhibition of miRNAs. This development can open a new prospect for personalized medicine.