Iranian Journal of Medical Sciences最新文献

Background: Inadequate pulmonary blood flow in tetralogy of Fallot (TOF) can lead to the development of major aortopulmonary collateral arteries (MAPCA), which interferes with surgical repair. The present study evaluated the features of MAPCAs among patients with TOF and their treatment approaches. Besides, perioperative parameters and mortality rates of our TOF patients with and without MAPCA were compared.

Methods: This retrospective case-control study was conducted from 2011 to 2020 at Namazi and Shahid Faghihi Hospitals, affiliated with Shiraz University of Medical Sciences, Shiraz, Iran. The significant aspects of MAPCAs, including their quantity, the presence of dual or single supply lung segments, and the employed devices for closure were evaluated. The patients were divided into three groups: TOF patients without MAPCAs as the control group, those with preoperative percutaneous MAPCA closure (Closed MAPCA), and those with small MAPCAs deemed unsuitable for percutaneous closure (Open MAPCA). A comparative analysis, encompassing hospital and surgical data, such as the presence of MAPCA, blood transfusion volume, intubation time, ICU stay, and mortality rates during and post-surgery, was performed among the aforementioned groups. The Chi square, Mann-Whitney, and Kruskal-Wallis tests were used to analyze the data.

Results: 59 patients were enrolled, with a mean age of 27.98±24.19 months. The control group included 34 patients with no collaterals, the closed MAPCA group had 12 patients with occluded collaterals, and the open MAPCA group had 13 patients with small collaterals unsuitable for closure. Blood transfusion volume and intensive care unit (ICU) stay were significantly higher in the open MAPCA group than the control group (P=0.01 and P=0.04, respectively). The highest mortality rate was seen in the Iranian Journal of Medical Sciences group (P<0.001).

Conclusion: In TOF patients, percutaneous MAPCA closure prior to surgical repair was recommended. This approach could potentially decrease the occurrence of complications both during and post-surgery.

Background: In approximately 80% of colorectal cancer cases, mutations in the adenomatous polyposis coli (APC) gene disrupt the Wingless-related integration site (Wnt)/β-catenin signaling pathway, a crucial factor in carcinogenesis. This disruption may result in consequences such as aberrant spindle segregation and mitotic catastrophe. This study aimed to analyze the effectiveness of the ethanolic extract of red okra (Abelmoschus esculentus) pods (EEROP) in inducing apoptosis in colorectal cancer cells (SW480) by inhibiting the Wnt/β-catenin signaling pathway.

Methods: The IC₅₀ of EEROP in SW480 cells was determined by treating the cells with varying doses of EEROP, ranging from 0 to 1000 µg/mL. Apoptosis assay and signaling pathway analysis were performed through immunofluorescence staining and Western Blotting on SW480 cells treated with 250 µg/mL of EEROP for 72 hours.

Results: EEROP treatment induced apoptosis in SW480 cells, marked by elevated levels of active caspase-3 (P<0.001) and cleaved poly-(ADP-ribose) polymerase (PARP)-1. Moreover, it notably decreased β-catenin protein levels, resulting in an augmented occurrence of cells displaying abnormal spindle segregation during mitosis (P=0.04).

Conclusion: EEROP treatment reduces β-catenin protein levels, promotes abnormal spindle apparatus segregation, and finally leads to apoptotic cell death in CRC cells.

Background: The risk of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) is estimated to be far greater than that in the general population. Adropin regulates endothelial function and may play a role in the pathogenesis of CVD. Angiotensin-converting enzyme inhibitor (ACEI) treatment was reported to have a protective effect on both renal and cardiovascular function. This study investigated whether adropin is associated with renal and cardiovascular outcomes after using ACEI treatment in CKD rats.

Methods: In 2021, in Zagazig, Egypt, rats were assigned to: GI, control group (n=8); GII, CKD group (n=8), and GIII, CKD+captopril group (n=8), in which CKD rats received 100 mg/Kg/day captopril orally. Adropin levels, renal function, blood pressure, and various CVD risk factors were measured. Renal, cardiac, and aortic tissues were examined histologically and immunohistochemically to detect the expression of vascular endothelial growth factor receptor-2 (VEGFR-2). To analyze data, ANOVA and Pearson's correlation tests were used (SPSS version 18, P<0.05 is significant).

Results: Adropin was significantly lower in GII than in GI and GIII (P<0.001). Adropin in GII and GIII was negatively correlated with atherogenic index (P=0.019 and P=0.001, respectively), atherogenic co-efficient (P=0.012 and P=0.013, respectively), troponin I (P=0.021 and P=0.043, respectively), and nitric oxide (P=0.025 and P=0.038, respectively). VEGFR-2 expression decreased in GII and was elevated in GIII (P<0.001).

Conclusion: Adropin levels were significantly correlated with most CVD risk factors in CKD and captopril-treated CKD rats, indicating a role for adropin in the pathogenesis of CVD in CKD. It also refers to its implication in the ameliorative effect of ACEI treatment, possibly by affecting VEGFR-2 and nitric oxide release.

Rupture of a hydatid cyst can lead to the development of a disseminated form of intra-abdominal cystic echinococcosis if not diagnosed and treated promptly. Anaphylactic shock is a definite indication of cyst rupture. The presented clinical case was a young athlete with a disseminated form of cystic echinococcosis, which was investigated in 2023 at the Syzganov National Scientific Center for Surgery of Kazakhstan. The disease developed gradually following a sports injury to the abdomen during sports training and was accompanied by blurred signs of anaphylactic shock. In the next 2 years, echinococcosis of the abdominal cavity was asymptomatic. The clinical manifestation of cystic echinococcosis developed gradually over the last 10-12 weeks, in the form of dull, painful abdominal pain, malaise, weakness, sweating, nausea, poor appetite, and weight loss. Subacute manifestations of the disease resembled those of acute appendicitis. A diagnostic laparotomy revealed an abundance of cystic formations in the abdominal cavity, necessitating a differential diagnosis between a disseminated form of abdominal tuberculosis with damage to the mesenteric lymph nodes. However, instrumental verification of the parasite, together with the morphological exclusion of the extrapulmonary form of tuberculosis, made it possible to establish a disseminated form of cystic echinococcosis. The patient underwent a cystectomy, was discharged in satisfactory condition, and was informed about the possibility of disease recurrence. In conclusion, in hyperendemic zones, it is recommended to carry out immunological testing for echinococcosis on all abdominal sports injuries, independent of the presence of anaphylactic shock symptoms.

Aggressive periodontitis is an inflammation of the periodontal tissue that usually affects adolescents and young adults aged <30 years, caused by attachment loss and fast bone degradation. The correlation between the epigenetic status and the initiation and progression of numerous acquired diseases was documented. Consequently, targeting epigenetic factors within periodontal tissues stands as an appealing prospect for both the diagnosis and treatment of periodontitis. In addition to the role of pathogenic bacteria and their products, alterations in gene expression due to extrinsic and intrinsic factors can cause disturbances in the host's immune response. Epigenetic changes, whether DNA methylation or microRNA (miRNA) dysregulation, can cause changes in gene expression in aggressive periodontitis and lead to more severe and rapid loss of the periodontal tissues. This study aimed to elucidate the relationships between oral hygiene, pathogenic bacteria, and genetics in periodontitis development to promote targeted prevention and treatment for enhanced oral health in individuals at risk of aggressive periodontitis. The method employed in this study entailed a comprehensive review and analysis of scholarly literature on the relationship between epigenetic mechanisms and the development of aggressive periodontitis. In conclusion, epigenetic regulation plays an important role in the pathogenesis of periodontitis through DNA methylation mechanisms that begin with Toll-like receptors (TLRs), cytokine signaling pathways, promoter genes, and progress to pro-inflammatory cells. When periodontal tissue inflammation occurs, miRNA inhibits protein translation from messenger ribonucleic acid (mRNA), which contributes to its aggressiveness.

Background: The therapeutic effect of mesenchymal stem cells (MSCs) in liver cirrhosis is limited by their entrapment in the pulmonary vessels. Thus, the use of MSC-derived exosomes has become a promising strategy. The current work aimed to compare the role of human umbilical cord blood-MSCs (hUCB-MSCs) and their derived exosomes in the alleviation of liver cirrhosis focusing on the role of miR-23b and miR-221 and their direct effectors in inflammatory and autophagic pathways.

Methods: Rats were divided into six groups normal controls (negative control), liver cirrhosis group (positive control), liver cirrhotic rats that received conditioned media, liver cirrhotic rats that received hUCB-MSCs, cirrhotic rats that received exosomes, and cirrhotic rats that received both hUCB-MSCs and exosomes. The messenger RNA expression of transforming growth factor-β (TGF-β), Matrix metalloproteinase 9 (MMP 9), fibronectin, collagen type-1 (col1), alpha-smooth muscle actin (α-SMA), Suppressor of Mothers Against Decapentaplegic (SMAD) 2 and 7, Beclin, P62, and light chain 3 (LC3) were evaluated by quantitative real-time polymerase chain reaction. Immunohistochemical staining for Beclin, P62, and LC3 was performed.

Results: The treatment of cirrhotic rats with hUCB-MSCs, exosomes, or the combination of them significantly downregulated miRNA-221, fibronectin, collagen I, α-SMA, Smad2 (P<0.001, for each), and P62 (P=0.032, P<0.001, P<0.001, respectively). Additionally, the treatment of cirrhotic rats with hUCB-MSCs, exosomes, or the combination of them significantly upregulated mTOR, Beclin, LC3, and Smad7 (P<0.001, for each) and miRNA-23 (P=0.021, P<0.001, P<0.001, respectively).

Conclusion: hUCB-MSCs and their derived exosomes ameliorated liver cirrhosis by anti-inflammatory and anti-fibrotic effects besides modulation of autophagy. The exosomes had a better improvement effect either alone or combined with hUCB-MSCs, as proved by improvement in liver function tests, and molecular, histopathological, and immunohistochemical profiles.

Background: Myocardial infarction causes mitochondrial atrophy and loss of function by reducing mitochondrial volume. Therefore, researchers are interested in finding a way to reduce the injuries and treat them. The study aims to evaluate the effect of 8 weeks of high-intensity interval training on follistatin (FST) gene expression in the fast and slow twitch muscles of rats with myocardial infarction.

Methods: The study was conducted in 2020 at the Cardiac Research Center, Shahid Rajaei University of Medical Sciences (Tehran, Iran). For this purpose, 12 male Wistar rats with myocardial infarction were assigned to the experimental group high-intensity interval training (3 days a week for 30 min, each interval consisting of 4 min of running with 85-90% VO_2max intensity and 2 min of active recovery with intensity of 50-60% VO_2max for 8 weeks) and a control group. Then, the expression of follistatin in fast and slow twitch muscle contraction genes was investigated as triggers and inhibitors of muscle atrophy. Statistical data were analyzed with SPSS18 (α≥0.05). To determine the normality of the data, the Kolmogorov-Smirnov test was used, and in the case of normality of the data distribution, the independent samples t test was used.

Results: Independent t test results showed that FST gene expression in the slow twitch (ST) muscle contraction group was significantly decreased compared with the control group (P<0.001). Moreover, the expression of the FST gene in fast twitch muscles was significantly increased in the severe exercise group compared with the control group (P<0.001).

Conclusion: Overall, 8 weeks of intense intermittent exercise decreased FST gene expression in slow and fast twitch muscles in rats with myocardial infarction.

Background: Acute renal colic has been challenging and has brought many concerns for physicians and patients for centuries. This study aimed to evaluate the analgesic effect and safety of a combination of papaverine and ketorolac against ketorolac and placebo in treating acute renal colic.

Methods: This randomized clinical trial was performed in patients with renal colic from May 2018 to May 2020 in Ahvaz, Iran. Patients with colic pain due to sand or kidney stones underwent clinical examination. The pain intensified based on the visual analog scale (VAS) and the patients' need for rescue analgesia are considered as primary outcomes at various times after treatment. Patients were equally divided into two groups: A (ketorolac plus papaverine) and B (ketorolac plus placebo) by block balanced randomization method. Student t test, the Chi square, and ANOVA tests were used for statistical analyses, which were performed by SPSS 19.0. P<0.05 was considered significant.

Results: A significant difference was observed in 280 patients (140 patients in each group) in pain intensity between both groups at 45 and 60 min. VAS scores in groups A and B were 5.08±1.23 and 5.56±1.11 in 45 min and 3.35±1.47 and 3.92±1.31 in 60 min (P=0.001, P=0.002), respectively. In subgroup analysis, the VAS score significantly decreased after taking the drug for middle and proximal ureteral stones at 45 and 60 min (P<0.001). Rescue analgesics were required in 7 (5%) and 21 (15%) patients in groups A and B, respectively (P=0.005). Side effects were similar in the two groups.

Conclusion: In this study, ketorolac, along with papaverine, was effective in acute renal colic control, and combination therapy with ketorolac and papaverine was associated with reduced use of other rescue analgesics.Trial Registration Number: IRCT20190217042738N1.