排序方式: 共有87条查询结果,搜索用时 15 毫秒
1.
Soares Mayara Sandrielly Pereira Viau Cassiana Macagnan Saffi Jenifer Costa Marcelo Zanusso da Silva Tatiane Morgana Oliveira Pathise Souto Azambuja Juliana Hofstatter Barschak Alethéa Gatto Braganhol Elizandra S Wyse Angela T Spanevello Roselia Maria Stefanello Francieli Moro 《Metabolic brain disease》2017,32(5):1693-1703
Metabolic Brain Disease - High plasma levels of methionine (Met) and its metabolites such as methionine sulfoxide (MetO) may occur in several genetic abnormalities. Patients with hypermethioninemia... 相似文献
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Daniella de S. Moreira Paula W. Figueiró Cassiana Siebert Caroline A. Prezzi Francieli Rohden Fatima C. R. Guma Vanusa Manfredini Angela T. S. Wyse 《Neurotoxicity research》2018,33(3):580-592
Homocysteine is a sulfur-containing amino acid derived from methionine metabolism. When plasma homocysteine levels exceed 10–15 μM, there is a condition known as hyperhomocysteinemia, which occur as a result of an inborn error of methionine metabolism or by non-genetic causes. Mild hyperhomocysteinemia is considered a risk factor for development of neurodegenerative diseases. The objective of the present study was to evaluate whether acetylsalicylic acid has neuroprotective role on the effect of homocysteine on inflammatory, oxidative/nitrative stress, and morphological parameters in cerebral cortex of rats subjected to chronic mild hyperhomocysteinemia. Wistar male rats received homocysteine (0.03 μmol/g of body weight) by subcutaneous injections twice a day and acetylsalicylic acid (25 mg/Kg of body weight) by intraperitoneal injections once a day from the 30th to the 60th postpartum day. Control rats received vehicle solution in the same volume. Results showed that rats subjected to chronic mild hyperhomocysteinemia significantly increased IL-1β, IL-6, and acetylcholinesterase activity and reduced nitrite levels. Homocysteine decreased catalase activity and immunocontent and superoxide dismutase activity, caused protein and DNA damage, and altered neurons ultrastructure. Acetylsalicylic acid totally prevented the effect of homocysteine on acetylcholinesterase activity and catalase activity and immunocontent, as well as the ultrastructural changes, and partially prevented alterations on IL-1β levels, superoxide dismutase activity, sulfhydryl content, and comet assay. Acetylsalicylic acid per se increased DNA damage index. In summary, our findings showed that chronic chemically induced model of mild hyperhomocysteinemia altered some parameters and acetylsalicylic acid administration seemed to be neuroprotective, at least in part, on neurotoxicity of homocysteine. 相似文献
3.
Monteiro SC Stefanello FM Vianna LP Matte C Barp J Belló-Klein A Trindade VM Wyse AT 《Metabolic brain disease》2005,20(1):35-44
In the present work we investigated the effect of ovariectomy on acetylcholinesterase (AChE) activity and ganglioside content in cerebral cortex of female rats. We also studied the activity of butyrylcholinesterase (BuChE) in serum of these animals. Adult Wistar rats were divided into three groups: (1) naive females (control), (2) sham-operated females and (3) castrated females (ovariectomy). Thirty days after ovariectomy, rats were sacrificed by decapitation without anaesthesia. Blood was collected and the serum used for BuChE determination. Cerebral cortex was homogenized to determine AChE activity and extracted with chlorophorm:methanol for ganglioside evaluation. Results showed that rats subjected to ovariectomy presented a significant increase of AChE activity, but did not change the content and the profile of gangliosides in cerebral cortex when compared to sham or naive rats. BuChE activity was decreased in serum of rats ovariectomized. Our findings suggest that the alteration in the activity of brain AChE, as well as serum BuChE activity caused by ovariectomy may contribute to the impaired cognition and/or other neurological dysfunction found in post-menopausal women. 相似文献
4.
Luduvico Karina Pereira Spohr Luiza de Aguiar Mayara Sandrielly Soares Teixeira Fernanda Cardoso Bona Natália Pontes de Mello Julia Eisenhardt Spanevello Roselia Maria Stefanello Francieli Moro 《Metabolic brain disease》2022,37(6):2133-2140
Metabolic Brain Disease - Acetylcholine is an excitatory neurotransmitter that modulates synaptic plasticity and communication, and it is essential for learning and memory processes. This... 相似文献
5.
Flavia R. Toledo Aline A. Antunes Francieli C. D. Vannini Liciana V. A. Silveira Luis C. Martin Pasqual Barretti Jacqueline C. T. Caramori 《International urology and nephrology》2013,45(6):1747-1752
Purpose
Malnutrition is a strong predictor of mortality in hemodialysis patients. Several scoring systems for evaluating nutritional status have been proposed. However, they rely on different sets of anthropometric and laboratory markers to make a diagnosis of malnutrition and assess its impact on prognosis. To validate them, nutritional scores should be compared with clinical outcomes. Thus, the purpose of this study was to assess malnutrition by three different nutrition scoring systems and determine which best predicts mortality in hemodialysis patients.Methods
This prospective study included 106 adult chronic hemodialysis patients. Their mean age was 56.3 ± 14.9 years and mean body mass index 24.8 (21.8–28.9); 52 % were men and they had been on dialysis for 24 (5–55) months. Nutritional status was classified according to the diagnostic systems proposed by Wolfson et al. (Am J Clin Nutr 39(4):547–555, 1984), International Society of Renal Nutrition and Metabolism (ISRNM) (Fouque et al. in Kidney Int 73(4):391–398, 2008), and Beberashvili et al. (Nephrol Dial Transplant 25(8):2662–2671, 2010). During about 2 years of follow-up, mortality was assessed by Kaplan–Meier curves, log-rank, and Cox’s models adjusted for diabetes, sex, C-reactive protein, time on dialysis, age, and fractional urea clearance.Results
Twenty-three deaths (21.5 %) occurred during the study period. According to the systems of Wolfson, Beberashvili, and the ISRNM, 54, 32, and 20 % of patients, respectively, had malnutrition. Both univariate and multivariate analyses showed that the ISRNM system was the only one that predicted poorer survival (fourfold higher death risk) in malnourished patients.Conclusions
The scoring system proposed by the ISRNM most accurately identifies patients at higher risk of death. 相似文献6.
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ngela M. Sgaravatti Bethnia A. Vargas Bernardo R. Zandon Ktia B. Deckmann Francieli J. Rockenbach Tarsila B. Moraes Jos M. Monserrat Mirian B. Sgarbi Carolina D. Pederzolli Angela T.S. Wyse Clvis M.D. Wannmacher Moacir Wajner Carlos Severo Dutra-Filho 《International journal of developmental neuroscience》2008,26(6):551-559
Tyrosine accumulates in inborn errors of tyrosine catabolism, especially in tyrosinemia type II, where tyrosine levels are highly elevated in tissues and physiological fluids of affected patients. In tyrosinemia type II, high levels of tyrosine are correlated with eyes, skin and central nervous system disturbances. Considering that the mechanisms of brain damage in these disorders are poorly known, in the present study, we investigated whether oxidative stress is elicited by l-tyrosine in cerebral cortex homogenates of 14-day-old Wistar rats. The in vitro effect of 0.1-4.0mM l-tyrosine was studied on the following oxidative stress parameters: total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR), ascorbic acid content, reduced glutathione (GSH) content, spontaneous chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS), thiol-disulfide redox state (SH/SS ratio), protein carbonyl content, formation of DNA-protein cross-links, and the activities of the enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glucose-6-phosphate dehydrogenase (G6PDH). TRAP, TAR, ascorbic acid content, SH/SS ratio and CAT activity were significantly diminished, while formation of DNA-protein cross-link was significantly enhanced by l-tyrosine in vitro. In contrast, l-tyrosine did not affect the other parameters of oxidative stress evaluated. These results indicate that l-tyrosine decreases enzymatic and non-enzymatic antioxidant defenses, changes the redox state and stimulates DNA damage in cerebral cortex of young rats in vitro. This suggests that oxidative stress may represent a pathophysiological mechanism in tyrosinemic patients, in which this amino acid accumulates. 相似文献
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Cíntia dos Santos Costa Thais Ortiz Hammes Francieli Rohden Rogério Margis Josiane Woutheres Bortolotto Alexandre Vontobel Padoin Cláudio Cora Mottin Regina Maria Guaragna 《Obesity surgery》2010,20(5):633-639
Background
Visceral adipose tissue is known to release greater amounts of adipokines and free fatty acids into the portal vein, being one of the most predictive factors of nonalcoholic fatty liver disease (NAFLD). Our study has the purpose to evaluate sirtuin 1 (SIRT1), adiponectin, Forkhead/winged helix (FOXO1), peroxisome proliferator-activated receptor (PPAR)γ1–3, and PPARβ/δ mRNA expression in morbidly obese patients in three different lipid depots: visceral (VAT), subcutaneous (SAT), and retroperitoneal (RAT). Recent studies suggest that SIRT1, a NAD+-dependent deacetylase, protects rats from NAFLD. 相似文献10.
Cristiane Matté Eduardo Durigon Francieli M Stefanello Franciele Cipriani Moacir Wajner Angela T S Wyse 《International journal of developmental neuroscience》2006,24(1):3-8
The main objective of the present study was to evaluate the effect of folic acid pretreatment on parietal cortex Na(+),K(+)-ATPase and serum butyrylcholinesterase activities in rats subjected to acute hyperhomocysteinemia. Animals were pretreated daily with an intraperitoneal injection of folic acid (5 mg/kg) or saline from the 22th to the 28th day of age. Twelve hours after the last injection of folic acid or saline, the rats received a single subcutaneous injection of homocysteine (0.6 micromol/g of weight body) or saline and were killed 1h later. Serum was collected and the brain was quickly removed and parietal cortex dissected. Results showed that acute homocysteine administration significantly decreased the activities of Na(+),K(+)-ATPase and butyrylcholinesterase on parietal cortex and serum, respectively. Furthermore, folic acid pretreatment totally prevented these inhibitory effects. We also evaluated the effect of acute homocysteine administration on some parameters of oxidative stress, namely thiobarbituric acid-reactive substances and total thiol content in parietal cortex of rats. No alteration of these parameters were observed in parietal cortex of homocysteinemic animals, indicating that these oxidative stress parameters were probably not responsible for the reduction of Na(+),K(+)-ATPase and butyrylcholinesterase activities. The presented results confirm previous findings that acute hyperhomocysteinemia produces an inhibition of Na(+),K(+)-ATPase and butyrylcholinesterase activities and that pretreatment with folic acid prevents such effects. Assuming that homocysteine might also reduce the activities of these enzymes in human beings, our results support a new potential therapeutic strategy based on folic acid supplementation to prevent the neurological damage found in hyperhomocysteinemia. 相似文献