Jerzy Mrowicki

Effects of whole-body cryotherapy on a total antioxidative status and activities of antioxidative enzymes in blood of depressive multiple sclerosis patients.

Abstract Objectives. Oxidative stress (OS) plays an important role in the pathogenesis of multiple sclerosis (MS). In MS patients depression is often observed. Cryotherapy might have an effect on OS. The aim of this study was to compare the effects of whole body cryotherapy (WBCT) on changes in total antioxidative status (TAS) of plasma and activities of antioxidative enzymes in erythrocytes from depressive and non depressive MS patients. Methods. Twenty-two MS patients with secondary progressive disease course (12 depressive and 10 non depressive) were treated with 10 exposures in a cryochamber. Before and after WBCT the plasma TAS and the activities of superoxide dismutase (SOD) and catalase (CAT) in the erythrocytes were measured. Results. The level of TAS in depressive MS group was significantly lower than in non depressive MS (P < 0.0003). WBCT increased the level of TAS in depressive (P < 0.002) more than in non depressive MS patients (P < 0.01). WBCT treatment of MS patients resulted in the significant increase of TAS level in plasma but had no effects on activities of SOD and CAT. Conclusions. Our results indicate that WBCT suppresses OS in MS patients, especially in depressive patients.

The role of polymorphisms of genes CXCL12/CXCR4 and MIF in the risk development IBD the Polish population

AbstractInflammatory bowel disease (IBD) are characterized recurrent inflammation of gastrointestinal tract. The etiology and pathogenesis this disease is currently unclear, but it has become evident that immune and genetic factors are involved in this process. The aim of this study was to determine whether gene polymorphisms: MIF-173 G/C; CXCL12-801 G/A and CXCR4 C/T exon 2 position of rs2228014 is associated with susceptibility to IBD. A total of 286 patients were examined with IBD, including 152 patients with ulcerative colitis and 134 with Crohn’s disease (CD) and 220 healthy subjects were recruited from the Polish population. Genotyping for polymorphisms in CXCL12/CXCR4 and MIF was performed by RFLP-PCR. Statistical significance was found for polymorphisms CXCR4, a receptor gene for CXCL12 genotypes and alleles in CD and for genotype C/T and T allele in ulcerative colitis with respect to control. This confirms the effect of CXCL12 gene. The interplay between CXCL12 and its receptor CXCR4 affects homeostasis and inflammation in the intestinal mucosa. Three-gene analysis in CD confirmed the association of genotype GGGGCT. Statistical analysis of clinical data of patients with ulcerative colitis showed significant differences in the distribution of genotype C/T and T allele for CXCR4 in the left-side colitis. Having CXCR4/CXCL12 chemokine axis polymorphisms may predispose to the development of IBD. Activation can also be their defensive reaction to the long-lasting inflammation.

Association of the-801G/A Polymorphism of CXCL12 Gene with the Risk of Inflammatory Bowel Diseases Development in a Polish Population

UNLABELLED Inflammatory bowel diseases (IBDs), mainly ulcerative colitis (UC) and Crohns disease (CD), are characterized by chronic and idiopathic inflammatory conditions of gastrointestinal tract that are immunologically mediated. Stromal cell-derived factor 1 (CXCL12) has been demonstrated to be involved in the pathophysiology of IBD.The aim of the study was to investigate whether the CXCL12 -G/A polymorphism (rs1801157) is associated to IBD in a sample of Polish population. MATERIAL AND METHODS A total of 188 patients with IBD including 103 patients with CU and 72 patients with CD and 184 controls were enrolled in the study. Both groups came from the Polish population. The G/A polymorphism of CXCL12 was determined by PCR-RFLP analysis. RESULTS There was no association between G/A polymorphism at position -801 promoter region of CXCL12 gene and increased risk of IBD. The study population was not found a difference in genotype distribution between the control group and with both CD and CU patients. CONCLUSIONS These results suggest that G/A polymorphism at position -801 promoter region of CXCL12 gene relates neither to the risk of the development of inflammatory bowel disease nor to the clinical subtypes of IBD in the Polish population. Whether this polymorphism truly contributes to disease susceptibility needs to be further addressed, and should stimulate additional studies in other populations.

Evaluation of Effect CAT -262C/T, SOD + 35A/C, GPx1 Pro197Leu Polymorphisms in Patients with IBD in the Polish Population.

Inflammatory bowel disease (IBD) are a heterogeneous group of disorders in the course dominated by chronic, recurrent gastrointestinal inflammation. It is believed that the activation of IBD occurs in patients with a genetic predisposition to their development. Chronic inflammation develops as a result of an excessive reaction of the immune system principally under the influence of environmental risk factors. Among them, it has been shown that the mechanism of oxidative stress is associated with the pathophysiology of inflammatory bowel disease, responsible for the commencement and progress of these diseases. The aim of the study was the relationship between single nucleotide polymorphisms (SNPs) of individual antioxidant enzymes, and the prevalence of inflammatory bowel disease that may be associated with increased levels of oxidative stress. MATERIAL AND METHODS A total of 111 IBD patients, including 65 patients with ulcerative colitis (UC) and 46 with Crohns disease (CD) and 125 healthy controls recruited from the Polish population, were genotyped for CAT -262C / T (rs1001179), SOD + 35A / C (rs2234694), GPx Pro 197 Leu polymorphisms. Genotyping of CAT, SOD, GPx gene polymorphism was performed by a RFLP-PCR. RESULTS The performed analysis of genetic polymorphisms of antioxidant enzymes showed that polymorphic variant of the CAT -262 C / T may have protective effects in patients with ulcerative colitis in the range of genotype C / T; OR = 0.49 (0.25-0.99), p = 0.044. Trend protective, but statistically unrelated, it was also observed for genotype T / T and T allele of the same polymorphism and genotypes and alleles + 35A / C SOD1 in UC as well as polymorphic variants CAT -262 C / T, Pro197Leu of GPx1, + 35A / C SOD1 in CD. The results were compared with a control group of potentially healthy individuals without such diseases. CONCLUSIONS It has been shown that the polymorphism of antioxidant enzymes CAT gene -262 C / T may have protective effects in patients who are carriers of a genotype C / T at the UC. The potential protective effect without statistical relationships were also observed for other genotypes and alleles studied polymorphic variants of antioxidant enzymes in CD and CAT- 262C / T and + 35 A / C SOD1 in UC. Conducted our audit should be extended to more group of patients in order to assess whether or not to confirm the observed during analysis, the protective effect of CAT-262 C / T in ulcerative colitis and other trends observed for other polymorphic variants tested genes.

Analysis of antioxidative factors related to AMD risk development in the polish patients

Age‐related macular degeneration (AMD) is a major cause of blindness in developed countries. Oxidative mechanisms may play a key role in the aetiology of AMD. The main aim of this study was to investigate antioxidative markers in the pathogenesis of AMD.

Etiopathogenesis of Inflammatory Bowel Diseases

Non-specific Inflammatory Bowel Diseases (IBD) are particularly troublesome diseases affecting the human digestive tract, in particular the intestine. These diseases manifest themselves in chronic intestinal inflammation that is difficult to control, with periods of uncontrolled exacerbations and self-reminiscent occurrences. Depending on the symptoms and their location in the human gastrointestinal tract, these diseases may occur in various forms. Among the two most common forms of these diseases, Ulcerative Colitis (UC), and Crohns Disease (CD) can be distinguished. Although the underlying cause of activation as well as the subsequent development of these diseases is not clearly defined, these disorders are known to have autoimmune background. The pathogenesis of IBD is associated with chronic idiopathic, recurrent, inflammatory-mediated gastrointestinal inflammation. The disease may be caused by changes in genes caused by various factors or family genetic predisposition. Exposure to a range of environmental risk factors may lead to disease activation in susceptible individuals. Many of the various factors mentioned in the article, which people are exposed to in their lives, may influence the development of these diseases.