PubMed Health⌕ Search

Biomedical subjects

A V Semenova

Publications and source records attributed to A V Semenova.

7 recordsLinked to original sources
PubMed2006

[Elimination of neurospecific proteins from CNS: pathogenetic and methodical aspects].

Appearance of neurospecific proteins (NSP) outside the brain plays a certain pathogenetic role in the development of autosensitization occurring in many kinds of CNS injuries and diseases. Analysis of modern views of cerebrospinal fluid (CSF) exchange allows us to suppose that NSP are eliminated from the brain tissue within CSF, moving from the subarachnoid space into cranial veins, and by lymphatic way, into deep cervical lymph nodes. Elevation of NSP level in CSF indicates an actual neudegenerative process. Serum levels of NSP are determined by the balance between the elimination of NSP from the brain, on the one hand, and their metabolism and the response of the immune system to the appearance of these autoantigenes in the blood stream, on the other. Basing on their own data on the dynamics of NSP (NSE, GFAR, and MBP) concentrations and the proportions of these proteins in CSF and serum (coefficient of elimination) in rats after ischemic, hypoxic, and autoimmune cerebral lesions, the authors offer an algorithm of pathogenetic evaluation, including, on the one part, a conclusion on the presence or absence of a neurodegenerative process, and, on the other, a conclusion on a normal or lowered rate of NSP elimination (metabolism). The results of such an analysis may have a clinical significance in terms of the development of a pathogenetic therapy, including, in every individual case, not only neuroprotectors, but also pharmaceuticals directed towards correction of the functional condition of the immune system.

Animals↗
PubMed2003

Enzyme immunoassay of NSE and GFAP as the criterion of dynamic evaluation of the rat blood-brain barrier in perinatal hypoxic ischemic injury of the CNS.

Enzyme immunoassay of the serum neurospecific antigens (gliofibrillar acid protein and neurospecific enolase) was used for evaluation of the resistance of the blood-brain barrier in Wistar rats with perinatal hypoxia and ischemia of the CNS. Perinatal hypoxia and ischemia of the CNS was modeled by two methods: ligation of the common carotid artery in 7-day-old rats followed by 3.5-h hypoxic hypoxia or 15-min anoxic exposure of fetuses isolated via hysterectomy on day 21 of gestation. Enzyme immunoassay of serum gliofibrillar acid protein and neurospecific enolase in control an experimental rat pups was carried out once a week during 3 months. In controls serum levels of gliofibrillar acid protein and neurospecific enolase virtually did not change during postnatal development, while in animals with cerebral hypoxia and ischemia induced in fetuses by both methods serum concentration of neurospecific enolase sharply increased 1 week after the injury and increased on weeks 6 and 10. The content of gliofibrillar acid protein was maximum on week 1 and later considerably varied, the peaks of its concentrations observed on weeks 3 and 8 preceded the increase in neurospecific enolase activity in peripheral blood.

Animals↗
PubMedDate not supplied

[Myelin basic protein. Structure, properties, function and role in diagnosing demyelinating diseases].

Physico-chemical properties and biological role of myelin basic protein (MBP)--one of the main myelin membrane proteins are reviewed. The data on MBP phosphorylation, methylation, fatty acid acylation and on interaction with lipid molecules in the human and animals bodies are presented. Much attention has been paid to the discussion of the diagnostic and clinical significance of the MBP, as the marker of demyelinating process in the central and peripheral nervous system.

Demyelinating Diseases↗
PubMedDate not supplied

[Production and characteristics of PEGylated immunoliposome transport vectors specific for neural tissue astrocytes].

PEGylated (stealth) immunoliposomes covalently linked to antibodies against human gliofibrillary acidic protein (GFAP) were prepared by coupling the thiolated monoclonal anti-GFAP antibodies, D4, with a maleimide derivative of the phosphatidyl ethanolamine of the liposomal membrane. Depending on the initial protein-to-lipid ratios, the immunoliposomes prepared (with a diameter of about 70 nm) were coupled with 60 to 240 molecules of the antibodies. In vitro experiments with cultures of the embryonic rat brain astrocytes demonstrated a specific binding of these immunoliposomes, which could be inhibited by the preincubation of the cells with free non-coupled D4 but not with non-specific antibodies. Administered intravenously into rats, the immunoliposomes exhibited a kinetic behaviour typical for the PEGylated liposomes: after 24 h, approximately 20% of the doses injected were still present in the blood; the elimination rate constants were 0.05-0.09 h(-1), the elimination half-lives were 8-15 h. With such a systemic longevity, as well as with such a specificity, these immunoliposomes, non-penetrating through intact blood-brain barrier (BBB), should be useful in delivering pharmacological agents to glial brain tumours (which continue to express GFAP) or to other pathological loci in the brain with a partially disintegrated BBB.

Animals↗
PubMedDate not supplied

[Myelin oligodendrogliocyte glycoprotein: the structure, functions, role in pathogenesis of demyelinating disorders].

Myelin oligodendrocyte glycoprotein (MOG) is a myelin-specific protein of the central nervous system (CNS). It is a member of the immunoglobulin superfamily. The contents of this protein in oligodendrogliocyte membrane is very low (approximately 0.1% total proteins). Functions of MOG are still unknown. It is considered that MOG is an autoantigen capable to produce a demyelinating multiple sclerosis-like disease in experimental animals. The structure, membrane topology, putative functions and role in demyelinating diseases are considered in this review.

Alternative Splicing↗
PubMedDate not supplied

[The role of nitric oxide in fertility disorders in men].

The aim of the study was investigation of NO influence on fertility properties of ejaculate in the diseases of male sex organs. A total of 73 males aged 20-55 years with different sexual disorders were examined. Potentiometric assay for nitrates in ejaculate, size and shape of spermatosoa were studied. NO3 was present in all sperma samples. In the control group nitrates levels were 0.662 +/- 0.147 mmol/l. In men with sexual diseases nitrates levels in ejaculate ranged from 0.114 mmol/l to 1.530 mmol/l). In normozoospermia nitrates occurred in "mean" levels (0.295 mmol/l to 0.900 mmol/ 1). In pathospermia nitrates level was high. NO produces a protective action if it was in adequate quantity. Spermatozoid concentration and a relative number of progressive-mobile forms correlated negatively with nitrates of spermatic plasma (r = -0.40) while dead spermatozoa percentage correlated positively. Thus, low NO3 content in ejaculate may result from microcirculatory disorders and endothelial dysfunction in testicular parenchyma and epididimus. NO hyperproduction occurs in inflammatory urogenital diseases. It probably induces pathospermia via direct toxic effects of NO and stimulation of lipid peroxidation.

Adult↗