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Biomedical subjects

V Dotsenko

Publications and source records attributed to V Dotsenko.

6 recordsLinked to original sources
PubMed2001

Observation of dynamical ordering in a confined Wigner crystal.

We present measurements of the conduction of nondegenerate free electrons along a low-dimensional channel at low temperatures, using surface-state electrons on liquid helium in novel microelectronic devices. Above 1 K, the electrons form an ideal classical Drude conductor. Below 1 K, Coulomb interactions produce electronic spatial order, leading to strong non-Ohmic effects and negative differential conductivity. Evidence is presented for self-organized current filaments in the channel, created by a nonequilibrium phase transition. Periodic conductance oscillations suggest an anisotropic spatial order with lines of electrons along the channel edges.

Journal Article↗
PubMed1999

The possible role of plasma kallikrein-kinin system and leukocyte elastase in pathogenesis of schizophrenia.

The main purpose of this paper is to study the possible causes of blood-brain barrier (BBB) damage during the acute condition of schizophrenia (Sch), which makes brain antigens accessible to the immunocompetent cells. The development of autoimmune reactions in this disease has to be preceded by the damage of BBB. We have studied the level of activity of plasma kallikrein-kinin (KKS) and complement systems, C-reactive protein (CRP) concentration, proteinase inhibitory potential as well as the oxidized and degranulating activity of neutrophils as the main factors affected the permeability of tissue-blood barrier. Our results suggested that the acute stage of Sch was accompanied by the activation of KKS on the background of enhance in the functional activity of the alpha-1-proteinase inhibitor. The increased level of CRP, the high haemolytic activity of complement and significant degranulating activity of polymorphonuclear leukocytes testified to inflammatory character of Sch. The treatment with psychotropic drugs have led to decrease of polymorphonuclear elastase (PMN-E) activity in patient's plasma. Our in vitro study indicates that Haloperidol causes the lowering of PMN-E activity in the dose-dependent fashion.

Adult↗
PubMed1996

Molecular and functional aspects of alterations in the kallikrein-kinin system activity in human blood plasma at different stages of peritonitis and chronic renal failure.

We are concerned with the investigation of dynamics of the plasma kallikrein-kinin system, elastase-like activity and some serpins, alpha 1-protease inhibitor, alpha 2-macroglobulin and antithrombin III, in patients suffering from general peritonitis and chronic renal failure. The results indicate that activation of the kallikrein-kinin system, as well as elastase-like activity are elevated and while decreased inhibitory potential becomes more intensive with disease progression. However, sharply decreased levels of kallikrein, prekallikrein and serpins were seen in patients a few days before death. We suggest that exhaustion of these components during the end-stage of general peritonitis and chronic renal failure (in the cases with lethal outcome) may be produced by leukocyte elastase release. Evidence is presented for the destructive action of leukocyte elastase on components of the kallikrein-kinin system.

Adult↗
PubMed1996

Hageman factor and kallikrein in pathogenesis of senile cataracts and the pseudoexfoliation syndrome.

It is thought that dystrophic changes in the human aging anterior eye are due to lipid peroxidation in both the cortical and nuclear structures of the lens under the conditions of ischemia. These changes are often accompanied by only lens opacification (senile cataract-SC) or by formation of amorphous or fibrillar deposits in anterior eye, disturbances of eye hydrodynamics and lens opacification (pseudoexfoliation syndrome-PES). Our results suggest that the main reason of dystrophic changes in the tissues of the aging anterior eye is the disturbance of the haemato-ophthalmic barrier and that the plasma kallikrein-kinin system takes part in this disturbance. Penetration of plasma proteins, such as C-reactive protein, complement components, immunoglobulins and coagulation factors, from plasma into the aqueous humor is responsible for damaging epithelial structures of anterior eye and formation of pseudoexfoliative material. Using ELISA, the C-reactive protein, IgG and IgM antigens have been shown to localize on the surface of the opaque lenses. Presence of these complement binding proteins in the superficial lens structures as well as the high C3a concentration in the aqueous humor substantiates the pathogenic role of complement activation in the lenticular epithelium upon cataract and PES formation.

Age Factors↗
PubMed1996

Activity of leukocyte elastase in patients' plasma is a significant indicator of atopic diseases.

It is commonly known that activation of plasma kallikrein-kinin system is of great importance in the pathogenesis of atopic diseases. Plasma kallikrein most likely activates other arginine-esterases in human plasma. Diagnostic and prognostic values of the total arginine-esterase activity and the activity of leukocyte elastase (LE) in plasma of patients with allergic rhinitis (AR), atopic bronchial asthma (ABA) and atopic dermatitis (AD) were examined in this study. Our results demonstrate that the level of arginine-esterase activity was slightly elevated only in plasma of patients with ABA (424 +/- 24; N-360 +/- 20 mU/ml), but not with AR and AD. Elastase-like activity in human plasma proved to be a far more informative indicator of the atopic states than arginine-esterase activity. In plasma of patients with AR, ABA and AD the activity of LE exceeded the normal level in 1.7, 1.8, and 2.4 times, respectively. Treatment of these atopic states with Ditec (Boehringer Ingelheim) led to some improvements of the patient' states. The main component of this drug (disodium chromoglycate) inhibited the activity of leukocyte elastase in experiments in vitro.

Adolescent↗