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Therapeutic endoscopy in gastroenterology

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The purpose of our study was to analyze hospitalizations for inflammatory bowel disease noted in the Department of Gastroenterology, Medical University of Lublin. Cases of patients hospitalized in the Department of Gastroenterology, Medical University of Lublin in 1997-2007 were retrospectively analyzed. The material studied included patients’ case histories and medical records that were used to select such patients whose hospitalizations were caused by ulcerative colitis and Crohn’s disease. Analysis distinguished two groups: rural and urban inhabitants. In 1997-2007 there were 1,825 hospitalizations for the inflammatory bowel disease noted at our clinic, which was 12.15% of all hospitalizations: 8.54% patients with ulcerative colitis and 3.61% with Crohn’s disease. Among them, 30.47% were rural inhabitants while 69.53% of patients lived in towns. The observation data demonstrated that there has been a significant increase of patients with inflammatory bowel disease in the last decade, and the patients originating in urban areas were more frequent than those from rural regions. This may be related to environmental differences between these two population groups.
Four cpDNA regions were analyzed with the use of PCR-RFLP technique and nucleotide sequences of two mtDNA regions were characterized in order to find P. sylvestris and P. mugo species specific markers useful for studies of the species hybridization. The difference in the restriction fragment patterns of trnV-rbcL region after digestion with MvaI endonuclease was detected. The analyses of the species representatives from various geographic regions revealed that the observed polymorphism is species specific. No differences have been disclosed in the analyzed trnS-trnT, trnK1-trnK2, trnC-trnD cpDNA regions. The P. sylvestris and P.mugo mtDNA sequences of orf25 and coxI regions proved to be identical.
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Pathophysiology of portal hypertension

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In last years significant progress in recognizing mechanisms of portal hypertension pathophysiology was done. However, some unclear topics in this disease still exist. Portal hypertension is primarily caused by the increase in resistance to portal outflow and secondly by an increase in splanchnic blood flow. Portal hypertension is associated with changes in the intrahepatic, systemic, and portosystemic collateral circulation. Alterations in vasoreactivity (vasodilation and vasoconstriction) play a central role in the pathophysiology of portal hypertension by contributing to increased intrahepatic resistance, hyperdynamic circulation, and expansion of the collateral circulation. Among vasoactive substances which are activated in portal hypertension nitric oxide (NO) is considered as the most important vasodilator. Endothelin-1 and cyclooxygenase-derived prostaglandins are the main vasoconstrictor factors. The imbalance between the hyperresponsiveness and overproduction of vasoconstrictors and the hyporesponsiveness and impaired production of vasodilators are the mechanisms responsible of the increased vascular tone in the sinusoidal area of the liver. New concepts in the pathophysiology of portal hypertension find the significant role of hepatic stellate cells activated by endothelial factors which cause vascular remodeling as an adaptive response of the portal vessels wall. The most frequent causes of portal hypertension include portal vein thrombosis, storage diseases of the liver, hepatic cirrhosis (independent of etiology), hepatic veins thrombosis and schistosomiasis. Understanding the pathophysiology of portal hypertension could be of great utility in preventing and curing the complications of portal hypertension, such as esophageal varices, hepatic encephalopathy, ascites.
The aim of this study was to: 1) describe the genetic structure of the population of old Picea abies trees in the Białowieża Primeval Forest and 2) design the genetic database for every examined tree in scope of 26 isoenzymatic loci containing: the genotype pattern, the number of stated alleles and the level of individual heterozygosity. We found that 101 out of 117 trees are characterized by a unique genotype pattern and 20 ones are completely homozygous individuals. The oldest Norway spruces in the Białowieża Primeval Forest are characterized by rather low level of genetic variation and their homozygous genotypes that are well adapted to their environment let them live to a ripe old age.
The aim of this study was to compare the most commonly-used experimental models and to assess the microscopic renal changes in different models of cyclosporine A (CsA) nephrotoxicity. Wistar male rats were divided into five groups, eight animals in each. CsA was given in doses of 15 mg/kg, 25 mg/kg, and 100 mg/kg, respectively. The blood was collected for creatinine, urea, and uric acid levels analysis in the serum and the kidneys were sampled for microscopic examination on the 11th and 29th d of the experiment. CsA induced nephrotoxicity was characterised by increased serum levels of creatinine, urea, and uric acid. Microscopic features of CsA nephrotoxicity in all CsA experimental groups were observed. We would recommend the use of low doses of CsA for approximately 28 d as the most relevant experimental procedure for achieving the features of chronic CsA nephrotoxicity.
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.
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