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ABSTRACT Objective: This study investigates the relationship between serum nitric oxide, asymmetrical dimethylarginine and symmetrical dimethylarginine levels and Total Antioxidant Capacity, and cognitive function in patients with bipolar disorder. Method: The study included 42 bipolar patients, diagnosed and assessed according to the DSM-V criteria, and 30 healthy controls. The Sociodemographic Questionnaire was used for the collection of data, and a bivariate Pearson correlation analysis was carried out. Results: The patient scores from a Rey Auditory Verbal Learning Test (RAVLT), Auditory Consonant Trigram (ACT), Digit Span Test (DST), Wisconsin Card Sorting Test (WCST), Trail Making-B (TMT-B) and Stroop Tests (ST) were found to be impaired in patients with BD when compared to the healthy controls. The SDMA level of the patient group was significantly higher in the control group, while the ADMA level was lower. The SDMA value was found to be positively correlated with ST-1,2,5 duration; and the NO value was positively correlated with ST-3 duration. Conclusions: The presence of neurobiological markers may serve to predict the severity of neurocognitive deficits, and can provide information about the progress of the disease.
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Aging-related ED is predominantly attributed to neurovascular dysfunction mediated by NO suppression and increased oxidative stress in penis. The alterations of protein arginine methyltransferases 1 (PRMT1)/dimethylarginine dimethylaminohydrolase (DDAH)/asymmetrical dimethylarginine (ADMA)/NO synthase (NOS) pathway regulate NO production in the vascular endothelium. Epigallocatechin-3-gallate (EGCG) is one of the most abundant and antioxidative ingredients isolated from green tea. In the present study, 40 Sprague-Dawley rats were randomly distributed into four groups: one young rat group and three aged rat groups treated with daily gavage feedings of EGCG at doses of 0, 10 mg kg-1 and 100 mg kg-1 for 12 weeks, respectively. Erectile function was assessed by electrical stimulation of the cavernous nerves with intracavernous pressure (ICP) measurement. After euthanasia, penile tissue was investigated using Western blot and ELISA to assess the PRMT1/DDAH/ADMA/NOS metabolism pathway. Superoxide dismutase (SOD) and malondialdehyde (MDA) levels were detected by colorimetry. We also evaluated smooth muscle contents. The ratio of maximal ICP and mean systemic arterial pressure (MAP) was markedly higher in EGCG-treated aged rats than in untreated aged rats. We found that DDAH1 and DDAH2 were expressed in cavernosal tissue, and they were downregulated in corpora of aged rats. The administration of EGCG upregulated the expression and activity of DDAH. In contrast, EGCG treatment downregulated the expression of PRMT1 and ADMA content. Moreover, EGCG-treated rats showed an improvement in smooth muscle expression, the ratio of smooth muscle cell/collagen fibril, SOD activity, and MDA levels when compared with untreated aged rats.
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Objective To investigate the serum asymmetric dimethylarginine (ADMA)expression in patients with acute cerebral infarction. Methods A total of 100 patients with acute cerebral infarction admitted to the Department of Neurology,the First Affiliated Hospital of Xi′an Medical College from March 2013 to August 2015 were enrolled retrospectively. According to the National Institutes of Health Stroke Scale (NIHSS)scores,they were divided into three groups:mild infarction (n =21; 15);100 healthy subjects without cerebrovascular disease in the same period were used as a control group. Enzyme linked immunosorbent assay was used to detect the plasma ADMA concentration,and the levels of plasma ADMA among the groups were compared. Results The concentrations of plasma ADMA of the mild,moderate,severe cerebral infarction,and the control groups were 0. 80 ± 0. 16,1. 14 ± 0. 28,1. 33 ± 0. 33,and 0. 52 ± 0. 16 μmol/ L,respectively. There were significant differences among the groups (F = 2. 32,P < 0. 05). Multivariate logistic regression analysis suggested that ADMA was an independent risk factor for cerebral infarction (OR,1. 140,95% CI 1. 078 -1. 212,P = 0. 045). Conclusions The expression levels of plasma ADMA increased gradually in patients with mild,moderate,and severe cerebral infarction. The higher the ADMA levels,the severe the neurological deficit would be. ADMA might be an independent risk factor for cerebral infarction.