Kinins are a set of peptides present in tissues that are involved in the inflammatory response and cancer progression. However, studies showing the expression of kinin receptors in human glioma samples are still incomplete and contradictory. The aim of the present study was to ascertain the expression of and genes, as well as the level of B1R and B2R proteins in human gliomas, depending on the degree of malignancy.
View Article and Find Full Text PDFBackground/aim: The aim of this study was to compare high-resolution manometry (HRM) and upper gastrointestinal (GI) endoscopy as diagnostic utilities in detecting a sliding hiatus hernia in patients with gastro-oesophageal reflux disease (GORD) symptoms.
Material And Methods: For both diagnostic modalities, the data obtained from 31 patients (20 females; mean age 48.2) who qualified for Nissen fundoplication were analysed using oesophageal pressure topography in line with the Chicago Classification.
World J Gastroenterol
October 2021
The risk of thromboembolism (TE) is increased in patients with inflammatory bowel disease (IBD), mainly due to an increased risk of venous TE (VTE). The risk of arterial TE (ATE) is less pronounced, but an increased risk of cardiovascular diseases needs to be addressed in IBD patients. IBD predisposes to arterial and venous thrombosis through similar prothrombotic mechanisms, including triggering activation of coagulation, in part mediated by impairment of the intestinal barrier and released bacterial components.
View Article and Find Full Text PDFKallikreins cleave kininogens to release kinins. Kinins exert their biological effect by activating constitutive bradykinin receptor-2 (BR2) and inducible by inflammatory cytokines bradykinin receptor-1 (BR1). Studies in animal models and some clinical observations indicate tat the activation of kallikrein - kinin system may have relevance to central nervous system (CNS) diseases, including multiple sclerosis, Alzheimer's disease, epilepsy as well as cerebral ischemia and neoplasmatic tumors.
View Article and Find Full Text PDFBackground/aims: The study aimed to determine pre- and post-fundoplication esophagogastric junction (EGJ) pressure and esophageal peristalsis by high-resolution manometry (HRM) in patients with gastroesophageal reflux disease (GERD).
Methods: Pre-operative and post-operative HRM data from 25 patients with GERD were analyzed using ManoView version 2.0.
The skin is one of the most common extraintestinal organ system affected in patients with inflammatory bowel disease (IBD), including both Crohn's disease and ulcerative colitis. The skin manifestations associated with IBD are polymorphic and can be classified into 4 categories according to their pathophysiology: (1) specific, (2) reactive, (3) associated, and (4) induced by IBD treatment. Cutaneous manifestations are regarded as specific if they share with IBD the same granulomatous histopathological pattern: perianal or metastatic Crohn's disease (commonly presenting with abscesses, fistulas or hidradenitis suppurativa-like features) is the prototype of this setting.
View Article and Find Full Text PDFJ Pediatr Gastroenterol Nutr
April 2013
Introduction: Doctors claim that salt intake should be reduced, which, taking into consideration the popularity of salt-rich food, can be a real challenge. So far it has not been determined what makes the reduction of salt intake so difficult, especially in elderly people.
Materials And Methods: The subject of the study was a group of 239 persons (107 women, 132 men), aged 18-34, and a group of 100 persons (54 women and 46 men), aged 51-73.
Ezetimibe is the first agent used in hypercholesterolemia treatment known to lower intestinal cholesterol uptake that is able to inhibit NPC1L1 transport proteins in the brush boarder of enterocytes and macrophages. Furthermore, it demonstrates anti-inflammatory and immunomodulatory properties and influences the expression of certain antigens. The drug is rapidly absorbed from the gastrointestinal tract and is then glucuronidated to form the active metabolite.
View Article and Find Full Text PDFCurr Vasc Pharmacol
September 2012
Inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis (UC) are idiopathic, intestinal and systemic inflammatory disorders which are immunologically mediated with the activation of plasma proteolytic cascades. The activation of coagulation in IBD is related to the activity and colonic extension of the disease, but may still be persistent in a quiescent stage. Factor XIII seems to be as much a coagulation factor as a connective tissue factor which may contribute to intestinal healing.
View Article and Find Full Text PDFVascular endothelial grow factor (VEGF) promotes angiogenesis by activating the specific receptors KDR and Flt-1. We investigate the expression of genes encoding VEGF and its receptors KDR and Flt- 1 by RT-QPCR reaction using Quanti Tect SYBR Green RT-PCR in patients with active and inactive ulcerative colitis (UC) and control subjects. The localization and level of VEGF protein and its receptors protein in intestinal tissue were estimated by immunohistochemistry.
View Article and Find Full Text PDFInflamm Bowel Dis
February 2011
Tissue kallikrein cleaves kininogens to release kinins. Kinins mediate inflammation by activating constitutive bradykinin receptor-2 (BR2), which are rapidly desensitized, and induced by inflammatory cytokines bradykinin receptor-1 (BR1), resistant to desensitization. Intestinal tissue kallikrein (ITK) may hydrolyze growth factors and peptides, whereas kinins are responsible for capillary permeability, pain, synthesis of cytokines, and adhesion molecule-neutrophil cascade.
View Article and Find Full Text PDFTransforming growth factor-beta1 (TGF-beta1) plays a role in the pathogenesis of ulcerative colitis (UC) by activating its specific receptors (T beta RI-T beta RIII). We investigated the expression of genes encoding for TGF-beta1 and T beta RI-III using RT-QPCR in patients with active and inactive UC and non-IBD controls. The localization and level of TGF-beta1 protein in intestinal tissue was estimated by immunohistochemistry, and serum TGF-beta1 concentrations were determined using ELISA.
View Article and Find Full Text PDFNon-steroidal anti-inflammatory drugs (NSAID), including acetylsalicylic acid, are the most commonly applied in the world, however at the same time they constitute a risk factor for gastrointestinal complications. The main mechanism of action of NSAID is based on reducing the synthesis of prostaglandins by means of inhibiting the activity of cyclooxygenase (COX), namely, of COX-1, which generates gut protective prostaglandins, and COX-2, induced at the sites of inflammation, tissue lesions and certain neoplasm. Complications caused by NSAID within the upper gut are subject to numerous studies; however those affecting the intestines are considerably less known.
View Article and Find Full Text PDFNeurol Med Chir (Tokyo)
December 2005
A 61-year-old man with severe factor XII deficiency presented with a subdural hematoma appearing as mixed but mainly high density by computed tomography in the left frontotemporoparietal region. No cranial injury was reported in the medical history of the patient. Clotting system study showed less than 1% functional activity of factor XII, whereas the levels of the other clotting factors were within the normal ranges.
View Article and Find Full Text PDFKallikreins are serine proteases, which are divided into plasma kallikrein and tissue kallikrein. Kallikreins cleave kininogen, theirs main substrate to release bradykinin, a potent inflammatory mediator. Kinins act directly by B2 and B1 receptors, or indirectly stimulating synthesis of nitric oxide, prostanoids and cytokinines by epithelial cells, smooth muscle cells, endothelial cells and fibroblasts.
View Article and Find Full Text PDFKinins are mediators of inflammation and proliferation and act by activating their specific B1 and B2 receptors. In the present study we evaluate the tissue kallikrein-kinin system during cyclosporine A treatment in patients with ulcerative colitis (UC). Six severe active UC patients were treated with cyclosporine A, i.
View Article and Find Full Text PDFAm J Physiol Gastrointest Liver Physiol
August 2005
Bradykinin is a mediator of inflammation, responsible for pain, vasodilation, and capillary permeability. Bradykinin receptor 1 (B(1)R) and bradykinin receptor 2 (B(2)R) are G protein-coupled receptors that mediate kinin effects. The latter is constitutive and rapidly desensitized; the former is induced by inflammatory cytokines and resistant to densensitization.
View Article and Find Full Text PDFWe have analyzed the prothrombotic risk factors in 124 patients with ulcerative colitis (UC) as compared with control subjects with other gastrointestinal disorders. The patients were hospitalized from 1991 to 2000 in the Department of Internal Medicine. Platelets level was significantly higher (p < 0.
View Article and Find Full Text PDFThe etiology and pathogenesis of inflammatory bowel disease (IBD) remains unsolved, but improved experimental models of enterocolitis have led to progress. Intestinal inflammation and experimental IBD can be induced by chemical or dietary factors or by microbial products. Many animal models of IBD can be used to evaluate new anti-inflammatory drugs.
View Article and Find Full Text PDFThe profile of tissue kallikrein (TK) and its inhibitor, kallistatin was evaluated in patients with active ulcerative colitis (UC) and Crohn's disease (CD). Tissue kallikrein is mainly localized to goblet cells and kallistatin to epithelial cells of human intestine. Intestinal tissue kallikrein (ITK) and kallistatin are significantly decreased in inflamed intestine compared to noninflammatory controls.
View Article and Find Full Text PDFThe distribution of tissue kallikrein (TK) and its plasma inhibitor, kallistatin in plasma and intestinal tissue, was studied in patients with active ulcerative colitis (UC) and Crohn's disease (CD). TK was localized to goblet cells and kallistatin to epithelial cells of normal human intestine. Both proteins are visualized in macrophages inside granulomas in CD as well as in plasmocytes in both CD and UC.
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