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The aim of the study was evaluation of the correlation between the level of clinical activity of Crohn’s disease (CD) and the number of Faecalibacterium prausnitzii, total number of bacteria and the concentration of selected short chain fatty acids (SCFA) in stool. 34 individuals diagnosed with Crohn’s disease participated in this study in 2011. The disease activity was determined according to the Crohn Disease Activity Index (CDAI). The number of Faecalibacterium prausnitzii and total number of bacteria were monitored by RT-PCR. The concentrations of SCFA were determined by gas chromatography. In CD patients, Faecalibacterium prausnitzii number and percentage of the total number of bacteria were greatly reduced. In patients with CD the percentage of acetate was elevated (70%), while the percentages of propionate and butyrate were significantly reduced (14.9% and 7.99%, respectively).
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Etiopathogenesis of allergic diseases

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Allergic diseases are the most common chronic diseases, particularly widely spread among children, adolescents and young adults. The problem is that there is an increasing incidence of allergic diseases. The causes of such a sudden increase of incidence rate are not well known. Complex interactions of environmental factors seem to play their role in the phenomenon. These include: change in the dietary and hygienic habits, progressing industrialization and increased use of numerous chemical agents. It was shown that inhabitants of highly industrialised nations, as compared to those from the developing countries, suffer from allergic diseases more frequently (most often in USA, Australia, Great Britain, Ireland and New Zealand, least frequently in Eastern Europe, Russia, China, India and Ethiopia), inhabitants of cities rather than those of rural areas, children who have no siblings rather than those from large families [1]. Knowledge of the factors that cause or influence the course of allergy is significant as it can help prevent and properly treat this disorder. It seems especially vital as in some patients allergy can manifest itself in the form of severe anaphylactic reactions, including an anaphylactic shock burdened with high risk of death.
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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.
Helicobacter pylori is thought to represent a significant etiopathogenic factor in diseases of the upper gastrointestinal tract. It seems, therefore, important to elaborate effective techniques for its detection. The aim of the present study was to evaluate the effectiveness of Helicobacter pylori detection using the PCR technique on paraffin sections with various pairs of primers and to compare the results with those of a histological appraisal. Material for the studies involved 50 paraffin blocks with gastric mucosa biopsies fixed in 4% buffered formalin. In this material 4 tests were performed with the aim of diagnosing Helicobacter pylori infection: 1) H+E staining, 2) staining by the Giemsa technique, 3) an immunocytochemical technique with antibodies against H. pylori and 4) the PCR technique with various primers. In the present study the most reliable results for H. pylori detection as well as the most pronounced correlation were obtained by using the PCR technique with primers for the ureC gene, immunohistochemistry and staining according to Giemsa. Less compatible results were obtained employing the two PCR techniques which utilise various primers. The experiments confirmed the usefulness of the PCR technique in the detection of Helicobacter pylori in paraffin sections by using a suitable pair of primers, and also indicated that Giemsa staining and immunohistochemistry should be taken into account.
The incidence of diabetes type 1, a chronic autoimmune disease, may reach the status of an epidemic in the 21st century. The highest incidence of diabetes in the world is observed in Finland. However, in the last 8 years a dynamic rise has been observed in Poland, moving the country toward an intermediate level incidence classification. Environmental factors seem to play a part in the observed increase in diabetes incidence both in Poland and in the world since, by acting on genetically predisposed ground prompt to auto-aggression, they may provoke disease occurrence. The study was carried out on a group of 511 children aged 0-15 years (255 girls and 256 boys). During the period of analysis (1998-2005) almost a two-fold increase in the diabetes incidence rate was observed (1998-10.4 vs 2005-20.4). The identification of all the factors increasing the risk of diabetes mellitus type 1 shall allow for understanding of diabetes ethiopathogenesis, and thus might create a chance for development of new prevention strategies.
Recent fi ndings in experimental models and in the clinical setting highlight the possibility that infl ammatory processes in the brain contribute to the etiopathogenesis of seizures and to the establishment of a chronic epileptic focus. Prototypical infl ammatory cytokines such as IL-1β and TNF-α are overexpressed in epileptogenic brain areas, prominently by glia and to a lesser extent by neurons and endothelial cells of the blood brain barrier. Cytokine receptors are also upregulated, and the related intracellular signalling is activated, highlighting both autocrine and paracrine actions of cytokines in diseased brain. Cytokines can profoundly affect neuronal network excitability, and the recent demonstration of molecular and functional interactions between cytokines and classical neurotransmitters, such as glutamate and GABA, provides one mechanism by which cytokines affect neuronal activity. These interactions may result in increased tissue excitability leading to seizures and cell loss. These fi ndings describe novel communications between glia and neurons which may contribute to pathological conditions (e.g. seizures, neurodegeneration) characterized by the activation of infl ammatory processes, thus highlighting potential new targets for therapeutic intervention.
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