Binding of cholera toxin B subunit to intestinal epithelial cells.

We have prepared I-labeled cholera toxin B subunit (I-labeled CT-B, a specific activity of 98Ci/mmol) and found that it binds to rat IEC-6 and human Caco-2 intestinal epithelial cells with high affinity (K 3.6 and 3.7nM, respectively).

Interaction of Cholera Toxin B-subunit with Human T-lymphocytes.

In this work, I-labeled cholera toxin B-subunit (CT-B) (specific activity 98 Ci/mmol) was prepared, and its high-affinity binding to human blood T-lymphocytes (K = 3.3 nM) was determined. The binding of the I-labeled CT-B was inhibited by unlabeled interferon-α (IFN-α), thymosin-α (TM-α), and by the synthetic peptide LKEKK, which corresponds to sequences 16-20 of human TM-α and 131-135 of IFN-α (K 0.

Interaction of cholera toxin B subunit with T and B lymphocytes.

We have prepared I-labeled cholera toxin B subunit (I-labeled CT-B, a specific activity of 98Ci/mmol) and found that its binding to T and B lymphocytes from the blood of healthy donors was high-affinity (K 2.8 and 3.0nM, respectively).

Synthetic peptide octarphin (TPLVTLFK), a selective agonist of nonopioid β-endorphin receptor, stimulates nitric oxide synthesis in macrophages.

Synthetic peptide octarphin (TPLVTLFK, a selective agonist of nonopioid β-endorphin receptor) was able to activate in a dose-dependent manner murine macrophages to express nitric oxide (NO) synthase and to produce NO. Octarphin required lipopolysacharide for the optimal induction of NO production. Octarphin-dependent NO production was sensitive to inhibition by dexamethasone and the NO synthase specific inhibitor NG-monomethyl-L-arginine.

The ATP permeability of pannexin 1 channels in a heterologous system and in mammalian taste cells is dispensable.

Afferent output in type II taste cells is mediated by ATP liberated through ion channels. It is widely accepted that pannexin 1 (Panx1) channels are responsible for ATP release in diverse cell types, including taste cells. While biophysical evidence implicates slow deactivation of ion channels following ATP release in taste cells, recombinant Panx1 activates and deactivates rapidly.

[Hepatoprotective effect of deanol aceglumate on experimental stress-induced gastropathy and diabetes mellitus].

Experiments on mice with streptozotocin-induced diabetes mellitus and stress-induced erosive ulcerous damage of the mucous membrane of stomach showed evidence of the preventive activity of deanol aceglumate in the course of peroral introduction at a dose of 250 mg/kg per 24 h during 4 days. This effect is accompanied by activation of the peristalsis of bowels and by an increase in the blood flow in the wall of stomach.

[Cardiotropic activity of synthetic peptide CH3CO-Lys-Lys-Arg-Arg-NH2 (protectin)].

Peptide CH3CO-Lys-Lys-Arg-Arg-NH2 (protectin) was synthesized and its activity was studied on the model of experimental myocardial infarction in rats in comparison to the reference antihypoxant drug riboxin. Intranasal injections ofprotectin at doses within 2-20 microg/kg once a day by course of 7 days produced a pronounced anti-ischemic action, improved coronary circulation of the blood, increases contractile activity of myocardium, reduced intensity of lipid peroxidation, and improved antioxidant protection. In some respects (improved coronary circulation of the blood, increased antioxidant protection), protectin was more effective than riboxin.

Immunostimulating effect of the synthetic peptide octarphin corresponding to β-endorphin fragment 12-19.

We have synthesized the peptide TPLVTLFK corresponding to β-endorphin fragment 12-19 (dubbed octarphin) and its analogs (LPLVTLFK, TLLVTLFK, TPLVLLFK, TPLVTLLK, TPLVTLFL). The octarphin peptide was labeled with tritium (specific activity 28 Ci/mol), and its binding to murine peritoneal macrophages was studied. [3H]Octarphin was found to bind to macrophages with high affinity (K(d) = 2.

[Effects and mechanism of action of synthetic peptide octarphin].

We have synthesized the peptide TPLVTLFK corresponding to the β-endorphin fragment 12-19 (the name given by the authors - octarphin), and its analogs (LPLVTLFK, TLLVTLFK, TPLVLLFK, TPLVTLLK, TPLVTLFL). The peptide octarphin was labeled with tritium (the specific activity of 28 Ci/mmol) and its binding to the murine peritoneal macrophages has been studied. [(3)H]Octarphin was found to bind to macrophages with high affinity (K(d) = 2.

Binding of synthetic peptide TPLVTLFK to nonopioid beta-endorphin receptor on rat brain membranes.

The synthetic peptide TPLVTLFK corresponding to the sequence 12-19 of beta-endorphin (referred to as octarphin) was found to bind to high-affinity naloxone-insensitive binding sites on membranes isolated from the rat brain cortex (K(d) = 2.6 +/- 0.2 nM).

[Antitumor effect of low-intensity extremely high-frequency electromagnetic radiation on a model of solid Ehrlich carcinoma].

The influence of different exposure regimes of low-intensity extremely high-frequency electromagnetic radiation on the growth rate of solid Ehrlich carcinoma in mice has been studied. It was shown that, at an optimum repetition factor of exposure (20 min daily for five consecutive days after the tumor inoculation), there is a clearly pronounced frequency dependence of the antitumor effect. The analysis of experimental data indicates that the mechanisms of antitumor effects of the radiation may be related to the modification of the immune status of the organism.

[Changes in the antigenic properties of proteins of laboratory mice during oxidative stress].

Changes in the level of oxidative damage to proteins in CD1 outbred mice gamma irradiated with a dose of 3 Gy have been studied. The changes were estimated from the amount of carbonyl groups (CG) in the proteins. It was found that two hours after exposure to gamma radiation, the amount of CG in the cytoplasmic and nuclear fractions of the liver, heart, brain, and spleen sharply increased.

[Stress-protective activity of the CH3CO-Lys-Lys-Arg-Arg-NH2 synthetic peptide (protektin)].

The CH3CO-Lys-Lys-Arg-Arg-NH2 peptide (the author has named it protectin) was synthesized, and its activity was studied during different stress actions. Protectin was found to normalize the content of corticosterone and adrenalin in adrenal glands and blood after its intranasal administration to rats one day before a cold or heat shock, or hypobaric hypoxia at doses of 1-10 microg/animal and after its intravenous administration just after acute hemorrhage at doses of 0.5-2 microg/animal.

[Stress-protective effect of the KKRR synthetic peptide corresponding to the 15-18 sequence of human adrenocorticotropic hormone].

The activity of the KKRR synthetic peptide corresponding to the 15-18 sequence of human adrenocorticotropic hormone (ACTH) and its analogues KKKK, RRRR, RRKK, kKRR, KkRR, KKrR, and KKRr (amino acid residues of the D configuration are designated by small letters) was studied in vivo on rats under cold and heat shock. Intranasal administration of the KKRR peptide at doses of 2-10 microg/animal 1 day before the shock was found to prevent a dramatic increase in the level of corticosterone in rat adrenal glands and blood plasma caused by the temperature effect. Amino acid substitutions in the KKRR peptide were shown to result in an abrupt decrease in its activity.

Binding of synthetic fragments of beta-endorphin to nonopioid beta-endorphin receptor.

Selective agonist of nonopioid beta-endorphin receptor decapeptide immunorphin (SLTCLVKGFY) was labeled with tritium (the specific activity of 24 Ci/mmol). [3H]Immunorphin was found to bind to nonopioid beta-endorphin receptor of mouse peritoneal macrophages (Kd = 2.0 +/- 0.

[Binding of beta-endorphin and its fragments to the non-opiod receptor of murine peritoneal macrophages].

The tritium-labeled selective agonist of the nonopioid beta-endorphin receptor the decapeptide immunorphin ([3H]SLTCLVKGFY) with a specific activity of 24 Ci/mmol was prepared. It was shown that [3H]immunorphin binds with a high affinity to the non-opioid beta-endorphin receptor of mouse peritoneal macrophages (Kd 2.4 +/- 0.

[Synthetic peptide KKRR corresponding to the human ACTH fragment 15-18 is an antagonist of the ACTH receptor].

Tritium-labeled synthetic fragments of human adrenocorticotropic hormone (ACTH) [3H]ACTH (11-24) and [3H]ACTH (15-18) with a specific activity of 22 and 26 Ci/mmol, respectively, were obtained. It was found that [3H]ACTH (11-24) binds to membranes of the rat adrenal cortex with high affinity and high specificity (Kd 1.8 +/- 0.

Interaction of ACTH synthetic fragments with rat adrenal cortex membranes.

Synthetic peptide, corresponding to the amino acid sequence 11-24 of human adrenocorticotropic hormone (ACTH), was labeled with tritium (specific activity of 22 Ci/mmol). [(3)H]ACTH (11-24) was found to bind to rat adrenal cortex membranes with high affinity and specificity (K(d) = 1.8 +/- 0.

[An ACTH-like peptide immunocortin: effect on the activity of cells from the rat adrenal cortex].

The effect of immunocortin, an ACTH-like decapeptide VKKPGSSVKV corresponding to the 11-20 sequence of the variable part of the human IgG1 heavy chain on the content of 11-hydroxycorticosteroids (CS) in rat adrenal glands and blood serum in vivo was studied. An intramuscular injection of immunocortin at a dose of 10 microg/kg was found in an hour to induce a twofold decrease in CS content in the adrenal glands and a 1.8-fold increase in the blood serum CS content.

Effects of low-intensity ultrahigh frequency electromagnetic radiation on inflammatory processes.

Low-intensity ultrahigh frequency electromagnetic radiation (42 GHz, 100 microW/cm(2)) reduces the severity of inflammation and inhibits production of active oxygen forms by inflammatory exudate neutrophils only in mice with inflammatory process. These data suggest that some therapeutic effects of electromagnetic radiation can be explained by its antiinflammatory effect which is realized via modulation of functional activity of neutrophils in the focus of inflammation.

[Decrease in the intensity of the cellular immune response and nonspecific inflammation upon exposure to extremely high frequency electromagnetic radiation].

The effect of low-intensity extremely high-frequency electromagnetic radiation (EHF EMR, 42.0 GHz, 0.1 mW/cm2, 20 min daily) on cell-mediated immunity and nonspecific inflammatory response in mice was studied.

[Effects of low-intensity extremely high frequency electromagnetic radiation on chromatin structure of lymphoid cells in vivo and in vitro].

Using a comet assay technique, it was shown for the first time that low-intensity extremely high-frequency electromagnetic radiation (EHF EMR) in vivo causes oppositely directed effects on spatial organization of chromatin in cells of lymphoid organs. In 3 hrs after single whole-body exposure of NMRI mice for 20 min at 42.0 GHz and 0.

Functional peculiarities of MAP2 in DBA/2J inbred mice as a component of genetic predisposition to seizures.

We compared the content of high molecular microtubule-associated protein-2 and its phosphorylation by cAMP- and Ca(2+)/calmodulin-dependent protein kinases in the brain of DBA/2J and C57Bl/6 inbred mice. The revealed differences in protein content and phosphorylation can be attributed to the mechanisms mediating audiogenic seizures in DBA/2J mice and to differential sensitivity of these inbred lines to seizure-inducing factors.

[Suppression of nonspecific resistance of the body under the effect of extremely high frequency electromagnetic radiation of low intensity].

The dynamics of leukocyte number and functional activity of peripheral blood neutrophils under whole-body exposure of healthy mice to low-intensity extremely-high-frequency electromagnetic radiation (EHF EMR, 42.0 GHz, 0.15 mW/cm2, 20 min daily) was studied.