990 resultados para Ast-3V-45


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0-meridiaani : Helsinki

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We studied the alterations in the metabolism of liver mitochondria in rats with acute pancreatitis. Male Wistar rats were allocated to a control group (group I) and to five other groups corresponding to 2, 4, 12, 24 and 48 h after the induction of acute pancreatitis by the injection of 5% sodium taurocholate into the pancreatic duct. Sham-operated animals were submitted to the same surgical steps except for the induction of acute pancreatitis. Mitochondrial oxidation and phosphorylation were measured polarographically by determining oxygen consumption without ADP (basal respiration, state 4) and in the presence of ADP (activated respiration, state 3). Serum amylase, transaminases (ALT and AST) and protein were also determined. Ascitic fluid, contents of amylase, trypsin and total protein were also determined and arterial blood pressure was measured in all groups. In ascitic fluid, trypsin and amylase increased reaching a maximum at 2 and 4 h, respectively. Serum amylase increased at 2 h reaching a maximum at 4 h. Serum transaminase levels increased at 12 and 24 h. After 2 h (and also 4 h) there was an increase in state 4 respiration (45.65 ± 1.79 vs 28.96 ± 1.50) and a decrease in respiration control rate (3.53 ± 0.09 vs 4.45 ± 0.08) and in the ADP/O ratio (1.77 ± 0.02 vs 1.91 ± 0.01) compared to controls (P<0.05). These results indicate a disruption of mitochondrial function, which recovered after 12 h. In the 48-h groups there was mitochondrial damage similar to that occurring in ischemic lesion. Beat-to-beat analysis (30 min) showed that arterial blood pressure remained normal up to 24 h (111 ± 3 mmHg) while a significant decrease occurred in the 48-h group (91 ± 4 mmHg). These data suggest biphasic damage in mitochondrial function in acute pancreatitis: an initial uncoupled phase, possibly secondary to enzyme activity, followed by a temporary recovery and then a late and final dysfunction, associated with arterial hypotension, possibly related to ischemic damage.

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Kartta kuuluu A. E. Nordenskiöldin kokoelmaan

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Kartta kuuluu A. E. Nordenskiöldin kokoelmaan

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The aim of the present study was to assess the influence of hyperbaric oxygenation (HBO) on rat liver regeneration before and after partial hepatectomy. Rats were sacrificed 54 h after 15% hepatectomy, liver and body weights were measured, and serum alanine transaminase (ALT) and aspartate transaminase (AST) activity and albumin levels were determined. The lipid peroxide level, as indicated by malondialdehyde production in the remnant liver was measured, and liver sections were analyzed by light microscopy. Five groups of 10 rats in each group were studied. The preHBO and pre-hyperbaric pressure (preHB) groups were treated before partial hepatectomy with 100% O2 and 21% O2, respectively, at 202,650 pascals, daily for 3 days (45 min/day). The control group was not treated before partial hepatectomy and recovered under normal ambient conditions after the procedure. Groups postHBO and postHB were treated after partial hepatectomy with HBO and HB, respectively, three times (45 min/day). The preHBO group presented a significant increase in the initiation of the regeneration process of the liver 54 h postoperatively. The liver/body weight ratio was 0.0618 ± 0.0084 in the preHBO compared to 0.0517 ± 0016 g/g in the control animals (P = 0.016). In addition, the preHBO group showed significant better liver function (evaluated by the lowest serum ALT and AST activities, P = 0.002 and P = 0.008, respectively) and showed a significant decrease in serum albumin levels compared to control (P < 0.001). Liver lipid peroxide concentration was lowest in the preHBO group (P < 0.001 vs control and postHBO group) and light microscopy revealed that the composition of liver lobules in the preHBO group was the closest to normal histological features. These results suggest that HBO pretreatment was beneficial for rat liver regeneration after partial hepatectomy.

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The aim of the present study was to investigate the effects of daily intragastric administration of bullfrog oil (oleic, linoleic and palmitoleic acid-rich oil), corresponding to 0.4% of body weight for four weeks, on fatty acid composition and oxidative stress (lipid peroxidation and catalase activity) in mouse liver. The activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), and gamma-glutamyltransferase (GGT), biomarkers of tissue injury, were determined in liver homogenates and serum. The proportions of 18:2n-6, 20:4n-6, 20:5n-3, and 22:6n-3 (polyunsaturated fatty acids, from 37 to 60%) in the total fatty acid content were increased in the liver of the bullfrog oil-treated group (P < 0.05) compared to control. At the same time, a significant decrease in the relative abundance of 14:0, 16:0, and 18:0 (saturated fatty acids, from 49 to 25%) was observed. The hepatic content of thiobarbituric acid reactive substances (TBARS) was increased from 2.3 ± 0.2 to 12.3 ± 0.3 nmol TBA-MDA/mg protein and catalase activity was increased from 840 ± 32 to 1110 ± 45 µmol reduced H2O2 min-1 mg protein-1 in the treated group. Bullfrog oil administration increased AST and ALP activities in the liver (from 234.10 ± 0.12 to 342.84 ± 0.13 and 9.38 ± 0.60 to 20.06 ± 0.27 U/g, respectively) and in serum (from 95.41 ± 6.13 to 120.32 ± 3.15 and 234.75 ± 11.5 to 254.41 ± 2.73 U/l, respectively), suggesting that this treatment induced tissue damage. ALT activity was increased from 287.28 ± 0.29 to 315.98 ± 0.34 U/g in the liver but remained unchanged in serum, whereas the GGT activity was not affected by bullfrog oil treatment. Therefore, despite the interesting modulation of fatty acids by bullfrog oil, a possible therapeutic use requires care since some adverse effects were observed in liver.

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Tutkimuksen tarkoituksena oli selvittää, mitä positiivisia ja negatiivisia psykososiaalisia kuormitustekijöitä oli kirjattu yli 45-vuotiaiden hoito- ja opetusalan työntekijöiden terveystarkastuskirjauksissa. Lisäksi tarkoituksena oli selvittää, kuinka paljon kuormitustekijöitä oli kirjattu ja miten ne olivat yhteydessä itsearvioituun sen hetkiseen työkykyyn, jota mitattiin työkykyindeksimittarilla. Tutkimuksen kohderyhmänä olivat ikääntyneet, valtakunnallisesti toimivan yksityisen lääkäriasemaketjun työterveyshuollon asiakkaat (N=106). Tutkimusaineiston muodostivat työntekijöiden elektronisessa muodossa olevat terveystarkastusdokumentit (N=147). Aineisto kerättiin kesäkuussa 2014. Tutkimusmenetelmänä oli annotointi, jossa etukäteen määritellyt psykososiaaliset positiiviset ja negatiiviset kuormitustekijät tunnistettiin ja poimittiin terveystarkastuskirjauksista. Aineisto analysoitiin tilastollisilla menetelmillä ja deduktiivisella sisällön analyysillä. Kuormitustekijöiden osuuksia sisällön analyysimenetelmällä tarkasteltaessa, erottuivat selkeästi kuormittavimmat riskitekijät: työn määrä ja työtahti (neg. n=116, pos. n=32), työympäristö ja välineet (neg. n=68, pos. n=73), sosiaaliset suhteet (neg. n=43, pos. n=73). Tilastollisen analyysin tulokset osoittivat kuormitustekijöiden yhteyden huono/kohtalaiseen työkykyindeksiin. Tilastollisesti merkitsevin yhteys oli sosiaalisilla suhteilla, sen jälkeen tulivat työmäärä ja -tahti sekä työympäristö ja välineet. Tutkimuksen tuloksia voidaan hyödyntää ikääntyvien työntekijöiden terveystarkastusten suunnittelussa ja kehittämisessä. Lisäksi tutkimustulokset auttavat sekä terveydenhuolto- että koulutusorganisaatioita tukemaan työntekijöidensä työhyvinvointia ja työkykyä. Työn kuormitustekijöiden yksilöllinen kartoitus antaa mahdollisuuden käyttää joustavia interventioita, jotka voidaan kohdistaa sekä organisaatiotasolle että psykososiaalisiin tekijöihin.