The role of T-system immunity in reparatory regeneration of the bone tissue in animals

It has been demonstrated in experiments on mice (CBA X C57BL) X F1, thymectomized and irradiated by 800 R, with the haemopoietic system restored by bone marrow (B-mice) that in these animals, as compared with the controls, the changes in cellular immunity (inhibition of natural killer cells and stimulation of individual functions of the phagocytizing cells) are accompanied by considerable inhibition of osteogenesis. Compensatory regeneration of broken thigh-bone in B-mice is delayed by 5--10 days in various elements of the regenerated tissue in comparison with normal mice. Anatomical formation of the provisional callus in B-mice is not completed on day 21 and approaches a 14-day regenerate of the controls. The obtained results suggest the participation of T-system immunity in the reparatory regeneration of bone tissue.     

Study of the role of type-specific antigen in the process of Shigella flexneri interaction with epithelial cell and macrophage cultures]

Epithelial cells of the HEp-2 line infected in parallel by genetically connected strains of Sh. flexneri, differing in the capacity to synthesize the type antigen were studied morphologically. The type antigen proved to show no significant influence on the penetration of dysentery bacilli into the cell. A study of the process of phagocytosis of the mentioned strains by a culture of peritoneal macrophages of guinea pig demonstrated that the presence of a type antigen communicated to the bacteria some selective advantages within the macrophages increasing their resistance to the action of the digestive enzymes.     

The detection of a choleriform thermolabile enterotoxin in clinical strains of Proteus isolated in different infections

The capacity of Proteus strains, isolated from patients with purulent inflammatory, urological and enteric infections, for the production of choleriform thermolabile enterotoxin was studied by means of the enzyme immunoassay (EIA) with the use of antitoxic serum to Escherichia coli enterotoxin. Out of 125 strains, 27 (21.6%) showed the capacity for producing choleriform thermolabile enterotoxin in EIA experiments. The results thus obtained indicate that EIA techniques can be used, in principle, for detecting the capacity of Proteus for the production of choleriform thermolabile enterotoxin.     

Age-related characteristics of the effects of epithalamin on serotonin metabolism in the pineal gland of rats]

The biosynthesis of serotonin into melatonin was decreased in old (18-20-month) in comparison to young (4-5-month) male Wistar rats. 5-day morning injections to young and old rats with polypeptide pineal preparation (epithalamin) in a dose of 2.5 mg/kg of body weight induced the increase in the night peak of serotonin, N-acetylserotonin and melatonin in young and melatonin alone in old rats and did not influence 5-methoxytryptamine, 5-oxy- and 5-methoxyindoleacetic acids level. These data support suggestion of ultrashort loop between pineal peptides and indoles and that epithalamin increases the metabolism of serotonin into melatonin.     

Effects of excess and deficiency of thyroid hormones in the body upon blood melatonin in pubertal male rats

Experiments have been carried out on Wistar line pubertal male rats in Winter. Radioimmunological method showed, that in intact animals the night peak of melatonin in blood was 994,36 +/- 195,99 pM/l, following ten-days intramuscular thyroxin injection (100 mg/100 g body mass)--2560,52 +/- 322,04 pM/1 and 20 days after, following bilateral thyroidectomy--117,13 +/- 16,35 pM/l, that totals 257,5% and 11,8%, respectively. Thus, the night peak of melatonin depends upon thyroid hormones concentration in blood.     

Effect of acidosis on the membrane potential of intact guinea pig aortic endothelial cells

The effects of a decrease in the extracellular pH from 7.4 to 6.9 on the membrane potential (MP) of intact non-stimulated guinea pig aortic endothelial cells and their ATP-induced electrical responses were studied using a whole-cell mode of the patch-clamp technique. Superfusion of the strip with CO₂-−HCO ₃ ⁻ -buffered acidic solution evoked endothelial depolarization of 6.1±1.0 mV. In Ca²⁺-free medium, after the MP had been stabilized at a depolarized value, there was no shift in the MP due to extracellular acidification to pH 6.9. In the case of using tris-buffered solution, the same drop in the extracellular pH in Ca²⁺-containing medium induced no change in the endothelial MP. Subsequent superfusion with CO₂−HCO ₃ ⁻ -buffered solution with pH 6.9 evoked endothelial depolarization of 7.3±1.5 mV. Changing from tris-buffered to CO₂−HCO ₃ ⁻ -buffered solution at a constant buffer pH 7.4 also induced endothelial depolarization, suggesting that intracellular pH is a possible factor that modulates leak Ca entry. The duration of ATP-induced endothelial hyperpolarization at pH 6.9 significantly dropped (76±5 sec, on average) compared with that at pH 7.4 (121±14 sec). It is concluded that modulatory effect of acidosis on the MP of endothelial cells and their ATP-induced electrical responses are caused by inhibition of leak and ATP-stimulated calcium entry into these cells.     

Caffeine-induced electrical responses of intact endothelial cells

The mechanism of caffeine-induced endothelial-dependent relaxation of vascular smooth muscle cells has been studied by recording caffeine application-induced electrical responses from intact guinea pig aortic endothelial cells. Depending on the values of the membrane potential, caffeine evoked either hyperpolarizing responses (V _m<−45 mV, 88.9% of the cells tested), or depolarizing reactions (V _m>−45 mV). The mean amplitude of caffeine-induced hyperpolarization of endothelial cells was 11.2±5.5 mV, which is comparable with the amplitude of ATP-induced hyperpolarization. The amplitude of caffeine-induced depolarization was 8.9±3.4 mV, on average. It was shown that caffeine-induced hyperpolarization of endothelial cells is a result of calcium release from the intracellular stores with subsequent activation of calcium-dependent potassium channels. Intracellular calcium stores involved in caffeine-induced responses are different from those involved in ATP responses. It is concluded that calcium mobilization from the intracellular stores of endothelial cells and, possibly, activation of calcium entry contributes to the caffeine-induced endothelial-dependent relaxation of vascular smooth muscle cells.