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The aim of the study was to evaluate blood serum ascorbic acid levels in patients with hepatic cirrhosis, acute and chronic pancreatitis and in the liver, heart, kidneys and lungs of rats intoxicated with CCl₄ and galactosamine. The results revealed statistically significant increases in the blood plasma ascorbic acid levels in patients with acute and chronic pancreatitis and hepatic cirrhosis. In the group of patients with chronic pancreatitis, however, the blood plasma ascorbic acid levels were not different from the controls. In the group of control rats the highest ascorbic acid levels were observed in the liver and the lowest in the heart. In the intoxicated rats with CCl₄ and galactosamine the kidneys’ ascorbic acid contents increased significantly after administration of both toxins in single doses but decreased after 3-days of administration of CCl₄. In the liver, decreased ascorbic acid contents were observed after single doses of CCl4 and galactosamine, but after the 3-day administration its contents were increased. The content of ascorbic acid in the lung increased after each of the toxins used. In the heart, ascorbic acid contents decreased considerably after single and three-day CCl₄ and galactosamine administration as well.
Recent studies indicate the involvement of peroxisone proliferator-activated receptor- (PPAR-) in the inflammatory reaction. The exact mechanism of PPAR- action has not been elucidated. It is supposed that PPAR- regulates transcription of genes responsible for encoding cytokines involved in the inflammatory response. The latest studies, carried out to explain the pathogenesis of non-specific colitis, confirm beneficial effects of PPAR- agonists on attenuation of colon inflammation. The aim of the present study was to assess the effects of nuclear PPAR- activity on the course of experimental acute colitis induced by intragastric administration of dextran sodium sulphate (DSS) using the PPAR- agonist rosiglitazone and the antagonist BADGE in rats. Colitis in Wistar rats was induced by 1.5% DSS administered in drinking water for 8 days. Animals with induced colitis received rosiglitazone, bisphenol A diglycidyl ether (BADGE) or both substances. After decapitation, colons were macroscopically and histopathologically evaluated. Levels of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor- (TNF-) and myeloperoxidase (MPO) were determined in serum and colon homogenates using ELISA. In rats with experimentally induced colitis receiving rosiglitazone, the inflammatory reaction was found to be markedly limited; ulceration, oedema and infiltration activity were reduced. The activated PPAR- inhibit the expression of proinflammatory factors, such as IL-6, TNF-, and neutrophil chemotaxis, which was evidenced by MPO reduction in serum and colon homogenates mediated by rosiglitazone. The positive effects of rosiglitazone on expression of IL-10 were also demonstrated. During the short period of observation, BADGE did not increase histopathological inflammatory markers.
Chronic pancreatitis (CP) is a progressive disease, in which the exocrine function of the gland is gradually lost and fibrosis develops due to repeated episodes of acute pancreatitis. The detection of the renin-angiotensin system (RAS) brings us closer to understanding the pathogenesis of CP. It has been observed that the use of RAS inhibitors reduces hepatic fibrosis. The aim of the study was to examine the effects of RAS inhibitors on fibrotic processes in the course of experimental chronic pancreatitis induced by dibutyltin dichloride (DD). Chronic pancreatitis was induced by administering dibutyltin dichloride to the femoral vein and, simultaneously, captopril, losartan and enalapril which were administered intraperitoneally. The rats were decapitated after 60 days and pancreas tissue was collected for histopathology examination. No pathological changes were observed in the control group. Rats treated by dibutyltin dichloride displayed features of focal inflammatory infiltration, ductal lumen dilatation, fibrosis in the periductal spaces and slight interstitial fibrosis. Animals treated by RAS inhibitor displayed less severe inflammatory changes and fibrosis - particularly those rats treated by enalapril. The findings suggest that enalapril most effectively inhibits inflammatory changes and fibrosis.
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Non-variceal upper gastrointestinal bleeding-guidelines on management

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In gastroenterology non-variceal upper gastrointestinal bleeding is health hazard. Frequency of occurrence accounts for 40-150 cases per 100000 inhabitants with death rate of 7-14%. Researches which goal is to improve treatment effectiveness as well as to establish standardized procedures for managing patients with symptoms of non-variceal upper gastrointestinal bleeding; have been conducted since many years. At the moment of admission, designed standards enable appropriate elaboration of patients’ health state, referral to the right clinic and implementation of the most accurate treatment methods. Increase of suppression of primary bleeding as well as prevention of recurrence is associated with dynamic development of endoscopic treatment methods as well as with optimization of pharmacological treatment. In significant percentage, efficiency of non – variceal bleedings treatment depends on clinic’s character (availability of equipment, experience of personnel) and on cooperation between several specialists (including gastroenterologist, surgeon, anesthetist, operative radiologist). Aim of the work is to present the latest evaluation of the mentioned subject, based on accessible literature. This work includes the basic principles for determination of bleeding intensity and risk of its recurrence as well as directions referring to fluids resuscitation and to monitoring of patients. Information on currently applied endoscopic methods for inhibition of non variceal upper gastrointestinal bleeding (injection, mechanical and thermo-coagulation techniques), comparison of their efficiency and possibility of application is provided in the work. The paper work also presents the newest directives for pharmacological treatment and guidelines for possible surgical treatment.
Chronic pancreatitis (CP) is a progressive disease, in which the exocrine function of the gland is gradually lost and fibrosis develops due to repeated episodes of acute pancreatitis. The aim of the study was to investigate the effects of RAS inhibitors on the apoptosis of acinar cells and pancreatic stellate cells (PSCs) elimination in experimental CP induced by dibutyltin dichloride (DBTC). CP was induced by administration of DBTC to the femoral vein. Simultaneously captopril, losartan, enalapril and lisinopril were administered intraperitoneally. The rats were decapitated after 60 days and tissue of pancreas was collected. In rats treated by DBTC the features of inflammatory infiltration, ductal lumen dilatation, fibrosis were found. Strong reactivity with capsase2L and clusterin-ß antibodies was observed in areas of fibrosis. In animals treated with RAS inhibitors inflammatory changes and fibrosis were less severe. In groups of rats treated with DBTC and RAS inhibitors immunoreactivity of capsase2L and clusterin-ß was weak. Positive immunostaining against smooth muscle actine and desmin was observed in the elongated cells (PSC-s). This reaction was weak in groups of rat treated with DBTC and RAS inhibitors. Treatment of CP rats with RAS inhibitors alleviate apoptosis of pancreatic acinar cells and induces PSCs elimination.
The aim of the study was to analyse the prevalence of H. pylori infection in adult inhabitants of Lublin Province. The effects of living conditions and lifestyle on the infection frequency were evaluated. The study included 585 adults randomly chosen for the epidemiological analysis of H. pylori infection in the Lublin region within the project commissioned by the Ministry of Health (PCZ 08-09) and State Committee for Scientific Research (C007/P05/2000). The study was based on a personal questionnaire and determinations of anti/Hp antibodies in IgG class using the ELISA method. High titres of anti/Hp antibodies (>24 IU/ml) were demonstrated in 78.5% of the subjects. In Lublin Province the infected individuals constitute 72% of inhabitants, in the big towns - 74% and in small towns - 95%. According to the place of birth: among those born in the country 87% are infected, compared to 78.4% in the small towns and 64% in the big towns, respectively. Positive test results were observed in 79% of farmers, 78% of manual workers and 75% of mental workers. The percentage of the affected neglecting basic hygienic rules exceeded 90%. With increased frequency of hygienic measures the number of the H. pylori infected individuals decreased to 65%. The prevalence of H. pylori infection among the inhabitants of the Lublin region is lower than that found in town inhabitants. Lublin Province shows the lowest level of H. pylori infection in Poland. The H. pylori infection is strongly affected by the lack of basic rules of personal hygiene and improper diet.
In the course of acute pancreatitis the liver is an organ that is especially exposed to damage. The presence of adenosine receptors was observed in the whole digestive system. The aim of the experiment was to define the correlation between the extinction of cytochrome P450 in the liver of rats and adenosine receptor agonists and antagonists in the course of necrotizing acute pancreatitis. The experiments were carried out on Wistar male rats weighing 250 g. Acute pancreatitis was induced injecting 5% sodium taurocholate to the biliary-pancreatic duct. Prior to the induction of acute pancreatitis the animals were injected intraperitoneally with selective agonists and antagonists: CGS 21680 (selective A2 agonist), 3 mg/kg, ZM 241385 (selective A2a antagonist), 3 mg/kg, DPCPX (A1 antagonist), 1 mg/kg, 1.3-Dipropyl-8-phenylxantine (selective A1 antagonist), 3 mg/kg, IB-MECA (A3 agonist), 0.75 mg/kg. The determinations were performed in hepatic microsomes obtained according to Guegenrichs method Cytochrome P450 extinction was determined by Matsubars technique. The results obtained reveal statistically significantly decreased cytochrome P450 extinction after sodium taurocholate administration. Decreased levels of extinction were also observed after combined administration of sodium taurocholate + Phenylxantine and sodium taurocholate + ZM. The level of IB-MECA remained unchanged in comparison to the controls. However DPCPX and CGS administration increased the extinction of cytochrome P450. The diverse influence of adenosine receptor agonists and antagonists used in the experiment on cytochrom P450 extinction seems to modify the course of the inflammatory process after using 5% sodium taurocholate.
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