The regulative role of adenine nucleotide translocators (ANTS) in oxidative phosphorylation has been estimated by the titration of respiration of isolated rabbit heart mitochondria with carboxyatractyloside in the presence of a non-rate limiting creatine phosphokinase ADP-regenerating system. It has been established that the respiration rate is not controlled by ANTS in the two extreme states, state 3 and state 4. On the other hand, at an intermediate respiration rate (30-70s of the state 3 respiration, which roughly corresponds to that under physiological conditions) the ANT control coefficient had a value of 0.62-0.75. Thus, ANTS seem to play a key role in the regulation of oxidative phosphorylation.

Objective. Perturbed immune homeostasis elicited by misbalanced production of proinflammatory and anti-inflammatory cytokines is characteristic of inflammatory bowel disease. The aim of this study was to evaluate cytokine profile in patients with different forms of inflammatory bowel disease – ulcerative colitis and Crohn’s disease – during clinical remission phase. Material and methods. Production of proinflammatory Th1 cytokines (tumor necrosis factoralpha (TNF-a), interferon-gamma (IFN-g)) and anti-inflammatory Th2 cytokines (interleukin- 10 (IL-10) and interleukin-13 (IL-13)) was analyzed in peripheral blood mononuclear cells of patients with inflammatory bowel disease (9 with ulcerative colitis and 9 with Crohn’s disease) and control subjects (n=11) by enzyme-linked immunosorbent assay (two-site ELISA). Results. The results of the study revealed that the level of TNF-a after stimulation with phytohemagglutinin in patients with Crohn’s disease was significantly higher in comparison to both patients with ulcerative colitis and controls (P<0.001 and P<0.01, respectively). The secretion of IFN-g both in patients with Crohn’s disease and ulcerative colitis was lower than that in controls (P=0.05 and P<0.01, respectively), but it normalized after stimulation with phytohemagglutinin. The levels of IL-10 and IL-13 were significantly (P<0.01) higher in patients with Crohn’s disease than in patients with ulcerative colitis and control group before and after stimulation with phytohemagglutinin. Conclusions. The results of our study provide evidence that in patients with inflammatory bowel disease, the imbalance between production of proinflammatory Th1 and anti-inflammatory Th2 cytokines persists even during remission of the disease, and disturbances of immune homeostasis are significantly more expressed in patients with Crohn’s disease than in patients with ulcerative colitis.

Objective. Clinical outcome of Helicobacter pylori (H. pylori) infection might be associated with specific virulence-associated bacterial genotypes. The distribution of different bacterial genotypes varies geographically. The aim of this study was to assess the relationship between cagPAI, vacA, and iceA status and severity of the disease in patients from Lithuania, infected by H. pylori. Material and methods. H. pylori from 81 patients (37 with duodenal ulcer and 44 with chronic gastritis) was isolated from gastric biopsy specimens and cultured. Bacterial genotypes cagPAI, vacA (s and m subtypes) and iceA were analyzed by polymerase chain reaction using specific primers. Results. The cagPAI was identified in 59.3% of Lithuanian H. pylori strains investigated. H. pylori strains cultured from duodenal ulcer (DU) patients more frequently (P<0.01) contained cagPAI and vacA s1 genotypes (75.7% and 75.7%, respectively) in comparison to isolates from chronic gastritis (CG) patients (45.5% and 40.9%, respectively). Evaluation of nucleotide sequence of the vacA middle-region revealed that vacA s2/m2 genotype was more frequent in CG than in DU patients (56.8% and 24.3%, respectively; P<0.05). We have not found any differences in the frequency of iceA1 genotype between the DU and CG patients (46.0% and 40.9%, respectively; P>0.05). Conclusion. Our study suggests that cagPAI and vacA s1 genotypes are associated with peptic ulceration in Lithuanian patients infected by H. pylori.

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