PubMed Health⌕ Search

Biomedical subjects

T L Krasnikova

Publications and source records attributed to T L Krasnikova.

At least 19 recordsLinked to original sources
PubMed2006

[Markers of inflammation--monocyte chemoattractant protein-1 (MCP-1) and C-reactive protein--in blood of patients with unstable angina pectoris and stable effort angina].

AIM: To estimate concentrations of C-reactive protein (CRP) and MCP-1 in blood plasma of patients with unstable angina (UA) and stable effort angina (SEA). MATERIAL AND METHODS: Multiprojection coronaroangiography was performed in 12 patients with UA and 11 patients with SEA. Hemodynamically significant stenosis (50% and more) at least in one major coronary artery was confirmed in all the patients. CRP and MCP-1 were measured with latex agglutination and enzyme immunoassay (Biosource kits), respectively. RESULTS: UA patients had significantly higher plasma levels of MCP-1 and CRP than those with SEA (107.25 +/- 16.19 vs. 63.0 +/- 16.16 pg/ml and 1.99 +/- 1.64 vs 0.44 +/- 0.28 mcg/ml, respectively). CONCLUSION: Estimation of MCP-1, as a marker of vascular wall inflammation, can be used, in line with other indices, for verification of UA.

Acute Disease↗
PubMed2005

Intracellular signal cascade in CD4+ T-lymphocyte migration stimulated by interferon-gamma-inducible protein-10.

The intracellular signal cascades involved in chemokine-stimulated migration of in vitro activated human peripheral blood CD4+ T-lymphocytes were investigated. IP-10-mediated chemotactic response of lymphocytes was decreased in the presence of selective inhibitors of Src-kinases (by 40-45%), PI3-kinases (35-40%), and MAP-kinases ERK1/2 (35-40%) and p38 (20%). Combined addition of specific inhibitors of Src-kinases and PI3-kinases and inhibitors of Src-kinases and ERK1/2 MAP-kinases did not result in the further increase of the inhibitory effect, while the combined addition of specific inhibitors of PI3-kinases and ERK1/2 MAP-kinases decreased migration of CD4+ T-lymphocytes more effectively (by 55-60%) than any individual inhibitor. Immunoblotting analysis of activation of MAP-kinases ERK1/2 and p38 revealed increased level of phosphorylation of ERK1/2 and p38 MAP-kinases in the presence IP-10. Selective inhibitors of Src-kinases and PI3-kinases significantly inhibited phosphorylation of p38 but did not influence phosphorylation of ERK1/2 MAP-kinases. Our results suggest that Src-kinases, PI3-kinases, and ERK1/2 MAP-kinases are involved in intracellular signal cascade activated during IP-10-stimulated migration of T-lymphocytes, whereas p38 MAP-kinases do not participate in the migration process, although its activation induced by IP-10 depends on Src-kinases and PI3-kinases.

CD4-Positive T-Lymphocytes↗
PubMed2005

[Primary pulmonary hypertension: activation of sympathico-adrenal system and free radical oxidation. Positive effects of carvedilol therapy].

AIM: To study the condition of the sympathico-adrenal system (SAS), synthesis of cAMP dependent on beta2-adrenoreceptors and parameters of free radical oxidation in patients with primary pulmonary hypertension (PPH); to examine efficacy of non-selective beta- and alpha1-adrenoblocker carvedilol in PPH patients. MATERIAL AND METHODS: Twenty patients with PPH had 6-minute walk test, ECG monitoring with assessment of heart rhythm variability (HRV). Tests for noradrenalin and adrenalin concentration in blood plasma, cAMP synthesis by blood lymphocytes in basal conditions and under stimulation with isoproterenol and forskolin, free radical oxidation were made initially, 1 and 6 months later. Ten patients received carvedilol in addition to standard therapy, 10 patients served control. RESULTS: PPH patients had higher NA in the blood, low cAMP synthesis, high malonic aldehyde, low activity of glutathionperoxidase, increased activity of superoxidedismutase and catalase of erythrocytes. The most pronounced changes in the above parameters were observed in patients with PPH FC III-IV. HRV declined in progression of cardiac failure. 6-months of combined treatment with carvedilol increased the distance of 6-min walk. Carvedilol had no effect on HRV, it reduced NA, stimulated cAMP synthesis, demonstrated no antioxidant activity. CONCLUSION: In PPH there is activation of SAS and desensitization of beta2-AR cells, oxidative stress develops. Addition of carvedilol to standard therapy with PPH improves clinical condition due to adrenoblocking properties of the drug.

Adrenergic Agents↗
PubMed2003

[Effect of the mitogen-activated kinase inhibitors on monocyte protein-1-stimulated chemotaxis of cells].

Monocyte chemoattractant protein (MCP-1) is a major chemoattractant for monocytes and T-lymphocytes although it can cause migration of the HUVECs. We used monocytic cell line THP-1, monocytes of human peripheral blood, and HUVECs to study MCP-1 receptor-mediated cell migration. We showed that THP-1 and the monocytes chemotaxis was decreased in presence of specific inhibitors of p 38 MAP-kinase. Furthermore, it was almost completely diminished by inhibitor of tyrosine kinases. In contrast, MCP-1-stimulated migration of HUVECs was abrogated by specific inhibitor of ERK1/2 MAP-kinases and, to a lesser extent, by blocking tyrosine kinases. These results suggest that intracellular signal pathways activated by MCP-1 in monocytes and HUVECs, are distinct.

Cell Line↗
PubMed2003

[Effect of matrix composition on chemotaxis response of monocytes stimulated by monocyte chemoattractant protein-1].

MCP-1-stimulated chemotaxic response of monocytic cell line THP-1 and peripheral blood monocytes were investigated through extra cellular matrix proteins fibronectin, fibrinogen and fibrinogen degradation products. Cellular migration was significantly decreased in the presence of fibrinogen as compared with fibronectin. Fibrinogen proteolysis with plasmin generating D and E degradation products, resulted in increase of the chemotaxic response.

Cell Line↗
PubMed2002

[Increased expression of monocytic cell adhesion molecules and formation of monocyte-thrombocyte aggregates in coronary restenosis].

AIM: To examine expression of superficial antigens by blood monocytes and granulocytes as well as the number of leukocyte-platelet complexes forming in in vitro activation in patients subjected to coronary angioplasty; to analyse changes in these parameters in coronary restenosis. MATERIAL AND METHODS: Membrane expression of leukocytic antigens and the number of leukocyte-platelet complexes after activation in the whole blood were measured by direct immunofluorescence and flow cytometry in 24 patients who have undergone stenting of coronary arteries. 14 of them had angiographically confirmed restenosis. RESULTS: The tests discovered high expression of integrins Mac-1 and VLA-4 by monocytes and elevated relative number of monocyte-platelet complexes in patients with restenosis vs those free of stenosis (1425 +/- 76 and 1195 +/- 71 r.u. for Mac-1, 87 +/- 7 and 65 +/- 6 r.u. for VLA-4, 47 +/- 4 and 29 +/- 3%, respectively, for monocyte-platelet complexes; p < 0.05 for all the indices). CONCLUSION: Coronary restenosis may result from elevated expression of adhesion molecules by monocytes manifest in activation of the cells in vitro.

Angioplasty, Balloon, Coronary↗
PubMed2002

[Catecholamine levels in plasma and beta2-adrenoreceptor-dependent synthesis of cAMP in lymphocytes of patients with primary pulmonary hypertension].

AIM: To evaluate norepinephrine (NE) and epinephrine (E) plasma concentration and lymphocyte beta-2-adrenoceptor dependent cAMP synthesis in primary pulmonary hypertension (PPH) patients in comparison with healthy controls. MATERIAL AND METHODS: Seven volunteers and fifteen patients with PPH were included in the study. NE and E plasma levels were measured by high performance liquid chromatography. Basal and stimulated (isoproterenol and forskolin) adenylyl cyclase activity in lymphocytes was measured by cAMP production using an enzyme immunoassay (Biotrak, Amersham UK). RESULTS: There was a 110% (p = 0.001) NE level increase in PPH patients. In systolic pulmonary artery pressure (SPAP) > 95 mm Hg lymphocyte cAMP production associated with adenylyl cyclase catalytic subunit was decreased by 170% and 70% vs PPH patients with SPAP < 95 mm Hg and healthy controls, respectively (p < 0.05). A significant negative correlation between forskolin cAMP production by lymphocytes and SPAP level was observed in PPH patients (k = -0.810, p = 0.011 by Kendell; k = -0.893, p = 0.007 by Spirman). Heart failure progressing from I-II to III NYHA functional classes was accompanied by plasma NE enhance and lymphocyte beta-2-adrenoreceptor-activated cAMP production decrease. CONCLUSION: The data demonstrate sympathoadrenal system activation and lymphocyte beta-2-adrenoceptor desensitization in PPH patients.

Adolescent↗
PubMed2002

[Carvedilol in treating primary pulmonary hypertension patients: effect on severity of cardiac failure, degree of pulmonary hypertension, concentration of catecholamines in blood plasma and dependence of cyclic AMP synthesis in lymphocytes on beta-adrenergic receptors].

AIM: To evaluate carvedilol effect on clinical state, norepinephrine (NE) and epinephrine (E) plasma concentration and lymphocyte beta 2-adrenoreceptor dependent cAMP synthesis in patients with primary pulmonary hypertension (PPH). MATERIAL AND METHODS: 14 patients with PPH were included in the study; 9 patients were treated by carvedilol; 5 patients were in the control group. The primary efficiency parameters were submaximal exercise measured by 60 min walk test, systolic pulmonary artery pressure (SPAP) measured by Doppler echocardiography, heart rate (HR) measured by 24-hour ECG-monitoring. RESULTS: One month carvedilol treatment of PPH patients resulted in a significant HR reduction. There was a tendency to SPAP decrease, the 6-minute walk test results improved in IIINYHA patients. CONCLUSION: Carvedilol therapy improves clinical state and evoked lymphocyte beta 2-adrenoceptor resensitization in PPH patients.

Adolescent↗
PubMed2001

Monocytic cell adhesion to intact and plasmin-modified fibrinogen: possible involvement of Mac-1 (CD11b/CD18) and ICAM-1 (CD54).

beta(2)-integrin Mac-1 and immunoglobulin-like ICAM-1 adhesion molecules are expressed by monocytes and both known to bind fibrinogen and its degradation products. Here, we investigated whether fibrinogen cleavage with plasmin modulates the adherence of monocytic cells and what types of adhesion molecules are involved. Using several cell types, characterized by different patterns of Mac-1 and ICAM-1 expression, and monoclonal antibodies against beta(2)-integrins and ICAM-1 we demonstrate, that fibrinogen cleavage evokes gradual decrease in beta(2)-integrin-dependent cell adhesion. Furthermore, generation of the early degradation products, fragments X and Y, by minimum cleavage of fibrinogen stimulates cell adhesion, mediated by ICAM-1.

Cell Adhesion↗
PubMed2001

Monocyte integrin expression and monocyte-platelet complex formation in humans with coronary restenosis.

1. In the present study, we sought to determine whether patients with restenosis after coronary stenting possess increased monocyte reactivity, as manifested by a higher level of adhesion molecule expression and an enhanced propensity to form monocyte-platelet aggregates after activation in vitro. 2. Anti-coagulated peripheral venous blood from 24 patients, 10 with and 14 without angiographically verified restenosis, was obtained. Leucocyte antigen expression and the number of leucocyte-platelet complexes were measured by flow cytometry after activation in whole blood. 3. Surface integrin Mac-1 (CD11b/CD18) and VLA-4 (CD49d/ CD29) expression on monocytes and the relative number of monocyte-platelet complexes after in vitro activation were significantly elevated in patients with restenosis compared with patients without restenosis (fluorescence intensities of 1425 +/- 76 vs 1195 +/- 71, 87 +/- 7 vs 65 +/- 6 and 47 +/- 4 vs 29 +/- 3% for for Mac-1, VLA-4 and monocyte-platelet complexes, respectively; P < 0.05 for each parameter). 4. The results suggest that restenosis is associated with increased monocyte VLA-4 and Mac-1 integrin expression and monocyte-platelet complex formation, which can be revealed after activation in vitro.

Blood Platelets↗
PubMed2001

[The role of Mac-1 and ICAM-1 molecules in adhesion of cells on fibronogen and its degradation products].

Monocytic cell adhesion to immobilized fibrinogen and fibrinogen degradation products, and involvement of integrins Mac-1 and immunoglobulin-like ICAM-1 adhesion molecules in these processes were investigated. Fibrinogen cleavage with plasmin down-regulated adhesion of cells with predominant Mac-1 expression; in contrast, the attachment of ICAM-1-expressing was up-regulated. By means of function-blocking anti-Mac-1 and anti-ICAM-1 antibodies, and immobilization of known fibrinogen degradation products, it was shown that Mac-1 molecules mediated cell adhesion predominantly to fibrinogen, and its early degradation products, fragments X and Y, while ICAM-1 participated in cell attachment to X- and Y-fragments, rather than to intact fibrinogen or late degradation products, fragments D and E.

Cell Adhesion↗
PubMed1999

Urokinase plasminogen activator system in humans with stable coronary artery disease.

1. The present study compares plasma urokinase plasminogen activator (uPA) peptide levels, plasma plasminogen inhibitor (PAI-1) activity and urokinase receptors (uPAR) on peripheral blood monocytes of patients with stable coronary artery disease (SCAD) and healthy volunteers. 2. Urokinase plasminogen activator levels were analysed by ELISA and PAI-1 activity was determined by a plasmin generation method using the chromogenic substrate S2390. Relative uPAR numbers and the adhesion molecules CD11b/CD18 on peripheral blood monocytes were estimated using specific antibodies and flow cytometry. 3. Patients with SCAD were found to have higher plasma uPA peptide levels than age-matched healthy subjects (10.40 +/- 0.99 vs 8.25 +/- 0.53 pmol/L, respectively; P < 0.05). 4. Plasma PAI-1 activity was also higher in patients with SCAD than in healthy subjects (13.6 +/- 2.5 vs 5.2 +/- 1.0 IU/mL, respectively; P < 0.05). 5. Relative uPAR and CD11b/CD18 adhesion molecules were similar on peripheral blood monocytes of patients with SCAD and in healthy subjects. 6. The data indicate a pattern of expression/activity of uPA and PAI-1 in patients with SCAD suggestive of an impaired fibrinolytic ability.

Adult↗