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      • KCI등재후보

        Single-dose intravenous sodium valproate (Depakine) versus dexamethasone for the treatment of acute migraine headache: a double-blind randomized clinical trial

        Narges Karimi,Mahdiye Tavakoli,Jamshid Yazdani Charati,Mastoureh Shamsizade 대한응급의학회 2017 Clinical and Experimental Emergency Medicine Vol.4 No.3

        Objective Migraine headache is a chronic and disabling condition in adults. Some studies have investigated the efficacy of sodium valproate in the treatment of acute migraine, but the effectiveness and tolerability of intravenous valproate as abortive therapy remains unclear. This study aimed to evaluate the effects of sodium valproate and dexamethasone in the treatment of acute migraine. Methods We conducted a double-blind randomized clinical trial including 90 patients aged 18 to 65 years with acute migraine headache but no aura. Patients were randomized to receive intravenous dexamethasone (8 mg) or sodium valproate (400 mg) diluted into 4 mL of normal saline. The primary outcome measure was pain relief after 0.5, 1, 3, or 6 hours after administration. The secondary outcome criteria were the associated symptom recovery, rate of headache recurrence after 24 hours, and medication side effects. Pearson’s chi square and the t-test were employed in the data analysis. Results Of the 90 patients, 80 were investigated. The percentage of headache improvement at 0.5 hours after treatment was 55% and 67.5% in the sodium valproate and dexamethasone groups, respectively. Before-treatment and 0.5 hour after treatment pain severity visual analog scale scores were 9.05±0.90 and 3.8±3.09 in the sodium valproate group and 8.92±0.79 and 3.10±2.73 in the dexamethasone group, respectively. There were no significant intergroup differences. Conclusion This randomized clinical trial showed that the intravenous injection of sodium valproate 400 mg has similar effects to those of dexamethasone for improving acute migraine headache.

      • KCI등재

        Ameliorative Effects of Nilotinib on CCl4 Induced Liver Fibrosis Via Attenuation of RAGE/HMGB1 Gene Expression and Oxidative Stress in Rat

        Vahid Khanjarsim,Jamshid Karimi,Iraj Khodadadi,Adel Mohammadalipour,Mohammad Taghi Goodarzi,Ghasem Solgi,Mohammad Hashemnia 전남대학교 의과학연구소 2017 전남의대학술지 Vol.53 No.2

        Nilotinib as a tyrosine kinase inhibitor has been recently used to improve the liver fibrosis process, but the exact mechanisms still require further clarification. In this study, we investigated the anti-fibrotic effects of Nilotinib via RAGE/HMGB1axis and antioxidant mechanisms. This experimental study was performed in the Hamadan University of Medical Sciences, Iran, from May 2015 to December 2016. Liver fibrosis was induced in Wistar male rats by CCL4. Rats were gavaged daily with Nilotinib (10 mg/kg). RAGE, HMGB1, TNF-a and TGF-b mRNA expression were evaluated by quantitative RT-PCR. TNF-a protein levels were measured using the immunoassay method. Thiol groups, carbonyl groups, nitric oxide levels and glutathione peroxidase activity were measured by spectrophotometric methods.The results showed that Nilotinib decreased TNF-a, TGF-b, RAGE and HMGB1 mRNA expression (p<0.001) in the liver tissues of the fibrosis group. Nilotinib also decreased carbonyl groups and nitric oxide levels and increased thiol groups and glutathione peroxidase activity in the fibrosis groups. The histopathological changes were found to be attenuated by Nilotinib. In conclusion, Nilotinib can improve liver fibrosis and open new mechanisms of the anti-fibrotic properties of Nilotinib.

      • KCI등재

        The Association of COVID-19 and Reactive Oxygen Species Modulator 1 (ROMO1) with Oxidative Stress

        Mohammad Amin Amini,Jamshid Karimi,Seyed Saman Talebi,Hosein Piri 전남대학교 의과학연구소 2022 전남의대학술지 Vol.58 No.1

        There is no denying that the massive spread of COVID-19 around the world has worried everyone. The virus can cause mild to severe symptoms in various organs, especially the lungs. The virus affects oxidative stress in the cells. Reactive Oxygen Species modulator 1 (ROMO1) is one of the most important mitochondrial proteins that plays a critical regulatory role in the production of Reactive Oxygen Species (ROS). According to the studies, COVID-19 can promote oxidative stress through some important pathways, for instance, TNF-a and NF-kB routes. Furthermore, ROMO1 is closely related to these pathways and its dysfunction may affect these routes, then promote oxidative stress, and ultimately cause tissue damage, especially in the lungs. Another factor to consider is that the TNF-a and NF-kB pathways are associated with ROMO1, COVID-19, and oxidative stress. To summarize, it is hypothesized that COVID-19 may increase oxidative stress by affecting ROMO1. Understanding the exact molecular mechanisms of ROMO1 in the pathogenesis of COVID-19 can pave the way to find better therapeutic strategies.

      • KCI등재

        The Association of Oxidative Stress and Reactive Oxygen Species Modulator 1 (ROMO1) with Infertility: A Mini Review

        Mohammad Amin Amini,Masoud Karimi,Seyed Saman Talebi,Hossein Piri,Jamshid Karimi 전남대학교 의과학연구소 2022 전남의대학술지 Vol.58 No.3

        Infertility is one of the disorders that worries many couples around the world, although novel and molecular methods can be used to cure this disease in different stages. One of the factors that causes infertility in men and women is the increased oxidative stress within the cells, which can lead to damage in zygote formation. ROMO1 is one of the most important proteins in the production of reactive oxygen species. This protein can enhance oxidative stress in the cells and body through cellular pathways, such as TNF-a and NF-kB routes, which will eventually lead to many diseases, especially infertility. We engage several international databases by using keywords; ROMO1, Infertility, and Reactive Oxygen Species, and gained a great quantity of information about ROMO1, Infertility, and Oxidative Stress. Although not proven, it is hypothesized that ROMO1 might elevate oxidative stress by activating NF-kB pathway in the cells, furthermore, TNF-a can arouse ROMO1 that can end up with apoptosis and cell death, which consequently can have a lot of disturbing effects on the body, especially the reproductive system. To sum up, revealing the exact cellular and molecular mechanisms of ROMO1-dependent TNF-a and NF-kB pathways in the pathogenesis of infertility might find interesting therapeutic and management strategies for this disorder.

      • KCI등재

        Reactive Oxygen Species Modulator 1 (ROMO1), a New Potential Target for Cancer Diagnosis and Treatment

        Mohammad Amin Amini,Seyed Saman Talebi,Jamshid Karimi 전남대학교 의과학연구소 2019 전남의대학술지 Vol.55 No.3

        Today, the incidence of cancer in the world is rising, and it is expected that in the next several decades, the number of people suffering from cancer or (the cancer rate) will double. Cancer is defined as the excessive and uncontrolled growth of cells; of course (in simple terms), cancer is considered to be a set of other diseases that ultimately causes normal cells to be transformed into neoplastic cells. One of the most important causes of the onset and exacerbation of cancer is excessive oxidative stress. One of the most important proteins in the inner membrane of mitochondria is Reactive Oxygen Species (ROS) Modulator 1 (ROMO1) that interferes with the production of ROS, and with increasing the rate of this protein, oxidative stress will increase, which ultimately leads to some diseases, especially cancer. In this overview, we use some global databases to provide information about ROMO1 cellular signaling pathways, their related proteins and molecules, and some of the diseases associated with the mitochondrial protein, especially cancer.

      • KCI등재

        Circulating Betatrophin Levels Are Associated with the Lipid Profile in Type 2 Diabetes

        Hassan Ghasemi,Heidar Tavilani,Iraj Khodadadi,Massoud Saidijam,Jamshid Karimi 전남대학교 의과학연구소 2015 전남의대학술지 Vol.51 No.3

        Betatrophin is a newly characterized circulating hormone that is produced in tissuessuch as adipose tissue and liver and stimulates pancreatic beta-cell proliferation. Thepurpose of the current study was to examine circulating betatrophin levels in Iranianpatients with type 2 diabetes mellitus (T2DM) and in normal controls. Seventy-five subjectswere enrolled in this case-control study in the following two groups: T2DM patients(n=40) and a group of age-, sex-, and BMI-matched normal control subjects (n=35). Circulating betatrophin concentrations as well as the blood lipid profile, body mass index(BMI), fasting blood sugar (FBS), glycated hemoglobin (HbA1c), and insulin resistancewere determined. Circulating betatrophin levels were significantly higher in patientswith T2DM than in the normal subjects (4.79±1.53 ng/mL vs. 2.79±1.11 ng/mLrespectively; p=0.001). Serum triacylglycerol and total cholesterol were also significantlyhigher in patients with T2DM than in the control group. In the patients withT2DM, serum betatrophin was positively correlated with age, FBS, TG, total cholesterol,and HbA1c. The results of this initial study in Iran have shown that circulating betatrophinlevels are significantly increased in Iranian patients with T2DM comparedwith a control group. Additionally, it is postulated that betatrophin as a novel hormonemay be involved in the generation of an atherogenic lipid profile.

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