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G I Fokina

Publications and source records attributed to G I Fokina.

At least 19 recordsLinked to original sources
PubMed1995

[The Gerstmann-Sträussler syndrome: new diagnostic possibilities].

On the basis of clinical picture of the disease, data of CT, MRT, psychological study, original laboratory investigation aimed at indication of changes in transposed neuroglia cells induced by the causal agent of subacute spongious transmissible encephalopathies, the diagnosis of patient K., 49 years old, was considered to be: syndrome of Gertsmann-Sträussler [correction of Herstmann Streussler]. Duration of the disease was 2 years. The case was sporadic. The history of the problem, modern views on etiology, pathogenesis of preventive measures are presented.

Animals↗
PubMed1991

[Antibodies to the structural elements of the neuron in patients with amyotrophic lateral sclerosis and in their healthy relatives].

The results of determining antibodies to the structural elements of neuron in the serum and CSF of 100 patients with lateral amyotrophic sclerosis (LAS), in the serum of their relatives (n-67), and in biological fluids of 50 patients suffering from other neurologic diseases allowed the following conclusions to be made. The predominance of antibody demonstration in the CSF of LAS patients over that in the serum may attest to the immune response on the part of the CNS. The presence of antibodies in the relatives (not-blood ones for the most part) of LAS patients suggests an infectious nature of the disease.

Adult↗
PubMed1991

Development of antibodies to axonal neurofilaments in the progression of chronic tick-borne encephalitis.

We followed the presence of autoantibodies to neurofilaments (NF) in the sera of patients with acute tick-borne encephalitis (TBE), chronic TBE, amyotrophic lateral sclerosis (ALS), and other diseases of CNS. The diagnosis was made according to clinical signs and based on virus neutralizing antibodies. Autoantibodies to NF were found in the majority of chronic TBE patients during disease progression, but were neither present in acute TBE nor in chronic TBE cases during the stabilization phase. Autoantibodies to NF found in a patient with acute TBE showed subsequent progression to a prolonged course. The data are discussed in order to assess the mechanisms of the chronic TBE process and its role in impairing the slow axonal transport.

Amyotrophic Lateral Sclerosis↗
PubMed1990

Alterations of arginase activity in scrapie-infected mice and in amyotrophic lateral sclerosis.

We followed the dynamics of arginase activity, the ultrastructural changes, and accumulation of the scrapie agent in the CNS of scrapie-infected mice. The arginase activity has been shown to increase 5-fold within the first 3-4 months of the incubation period followed by subsequent fall at its end. The peak of increased arginase activity coincided with appearance of multilayer membranes, whereas the decrease of this activity was associated with the greatest development of status spongiosus, synaptic degeneration, accumulation of five-layer membranes as well as with maximal accumulation of the scrapie agent in the CNS. Examination of 100 patients with different forms of amyotrophic lateral sclerosis (ALS) revealed a 2-8-fold increase of arginase levels in the cerebrospinal fluid (CSF) as compared with the background levels in the comparative groups of control patients. Similar enzyme alterations in scrapie--and in ALS--are discussed in terms of possible resemblance of their pathogenesis.

Amyotrophic Lateral Sclerosis↗
PubMed1988

[Anti-neurofilament antibodies in slow infections of the nervous system].

Twenty-six patients including 12 with lateral amyotrophic sclerosis, 7 with multiple sclerosis, 5 with the Creutzfeld-Jakob disease and 2 with Alzheimer's disease were examined. Antibodies to neurofilaments in the blood serum were detected in all cases of the Creutzfeld-Jakob disease and Alzheimer's disease and in 8 patients with lateral amyotrophic sclerosis with clinical evidence of supranuclear structure involvement. A conclusion is drawn about a certain similarity of pathogenic mechanisms of these diseases, as well as about heterogeneity of the cytoskeleton of neurons in the brain and the spinal cord.

Adolescent↗
PubMed1987

Persistence of the scrapie agent in glial cells from rat Gasserian ganglion.

Persistence of the scrapie agent in glial cell monolayers from rat Gasserian ganglion have been studied by electron microscopy, virologic and histologic methods. Under chosen experimental conditions the scrapie agent had been shown to persist in cells for over 2 years. The infected cells appeared to be infectious for BALB/c mice throughout. Persistence of the scrapie agent was associated with development of a marked proliferative effect with increasing mitotic index of the cells. Changes similar to those observed in the CNS in vivo were found by means of electron microscopy. The decreased number of oncovirus-containing cells seems to indicate the decreased proportion of such cells in the culture infected with scrapie agent.

Animals↗
PubMed1984

Effect of hyperbaric oxygenation on experimental scrapie in mice.

The effect of hyperbaric oxygenation upon experimental infection of BALB/c mice with the scrapie agent was investigated by virological methods, histology and electron microscopy. A multiple exposure of scrapie-infected mice to hyberbaric oxygenation during the incubational period led to a certain aggravation of infection as evidenced by a greater accumulation of the agent in the central nervous system (CNS) and spleen, as well as by more pronounced ultramicroscopic changes in CNS. A single exposure to hypoxia failed to alter any manifestations of infection.

Animals↗
PubMed1984

Influence of aminasine on experimental scrapie in mice.

The influence of long-term treatment with aminasine--an inhibitor of monoamine oxidase--on duration of the incubation period, morbidity and on accumulation of the agent in the brain was followed in experimental scrapie of mice. Aminasine administration after intracerebral (i.c.) but not after intraperitoneal (i.p.) inoculation of the agent markedly prolonged the incubation period and slightly reduced the morbidity. The accumulation of the scrapie agent and the degree of histological lesions in the CNS detected 6 months post-inoculation (p.i.) were equal in both groups compared. The significance of these results is discussed from the viewpoint of the role of biogenic monoamines in the pathogenesis of scrapie.

Animals↗
PubMed1983

Study on West Nile virus persistence in monkeys.

Experiments in M. rhesus showed persistence to be a typical property of West Nile virus. This property was exhibited by strains belonging to different antigenic types, and varying in virulence and in the isolation area (U.S.S.R., Uganda, India). The duration of persistence was at least 5 1/2 months in asymptomatic infection and in convalescence after encephalitis or a febrile disease. The virus isolated within the first 2 weeks after inoculation of monkeys has the standard properties. The virus persisting for 2 months retains its cytopathic and antigenic activity, however, is non-pathogenic for white mice. After 5 1/2 months of persistence the virus has no neurovirulence or cytopathic properties but is capable of infecting the susceptible cells and induces in them the synthesis of virus-specific antigen detectable by immunofluorescence. The persisting virus has been isolated by cocultivation of trypsinized monkey organ cells and cells of the indicator culture. This virus was located mostly in the cerebellum, cerebral subcortical ganglia, lymph nodes, and kidneys. The monkeys experiencing encephalitis, febrile, or asymptomatic infection showed in morphological examinations a subacute inflammatory-degenerative process in the central nervous system. The results suggest that West Nile virus, one of the most widely spread arboviruses in Africa, Asia, and Europe, may be implicated in the etiology of subacute diseases of the CNS.

Animals↗
PubMed1983

Study of early stages of the pathogenesis of scrapie in experimentally infected mice.

Virological, histological, and electron microscopic methods were used to study the early manifestations of infection in brains and spleens of mice experimentally infected with the scrapie agent. A statistically significant increase in the spleen weight was demonstrated during the incubation period; this occurred only after intracerebral (i.c.) inoculation of the scrapie-containing brain suspensions and subcutaneous (s.c.) inoculation of the scrapie-containing spleen suspensions. No differences were observed between the scrapie agents replicating in the brain or spleen. In the brain at early stages of the incubation period, ultrastructural changes were observed in pre- and post-synaptic areas. The importance of these findings for understanding of the pathogenesis of subacute transmissible spongiform encephalopathy (STSE) is discussed.

Animals↗
PubMed1983

Reaction of mouse CNS cells to the scrapie agent in early stages of experimental infection.

Accumulation of the scrapie agent, histological lesions and cytometric parameters in layers III and V of the cerebral cortex and caudate nucleus were investigated in BALB/c mice during the incubation period of scrapie after intracerebral (i.c.) inoculation of the agent. The following cell parameters were determined: areas of the body, nucleus, and cytoplasm of neurons, concentration and amount of protein within the nucleus and cytoplasm. One month after i.c. inoculation, titre of the agent in the brain was 6.3 log LD50/g. Histological examinations of the infected brains revealed no lesions. Cytointerferometric studies showed a statistically significant increase in the size of the body, nucleus and cytoplasm of neurons, namely in the layer III of brain cortex. Increased amounts of protein were observed only in the nuclei of these cells. No such changes were found following i.c. inoculation of normal brain tissue used as a substrate for the agent.

Animals↗
PubMed1982

Persistence of tick-borne encephalitis virus IV. Virus localization after intracerebral inoculation.

Tick-borne encephalitis (TBE) virus was isolated from the brains and spinal cords, blood, livers, lymph nodes and kidneys from Macaca rhesus monkeys showing acute and subacute fatal encephalitis. In subacute encephalitis, virus titres in the CNS were lower than in acute disease (3.0--6.2 against 3.8--8.3 log LD50/ml). TBE virus localization in chronic encephalitis was largely the same as in acute and subacute disease. In monkeys with a chronic course and stable paralysis of the upper extremity, infectious TBE virus was isolated on day 383 from subcortical ganglia and spinal cord. In lymph nodes and spleen, it could be detected only by a combination of methods (co-cultivation in association with fluorescent antibody technique and complement-fixation test, explantation of organ fragments) more sensitive than is the inoculation of mice with organ homogenates. TBE virus was detected by the same methods on day 90 in the CNS and internal organs of a monkey with chronic encephalitis in the stage of remission.

Animals↗
PubMed1982

Persistence of tick-borne encephalitis virus in monkeys. V. Virus localization after subcutaneous inoculation.

In 28 Macaca rhesus monkeys inoculated subcutaneously (s.c.) with different strains and mutants of tick-borne encephalitis (TBE) virus and developing asymptomatic infection, TBE virus and the virus-specific antigen were found at different intervals up to 302 days post inoculation (p.i.) in the CNS and internal organs (liver, spleen, lymph nodes, kidneys). When cyclophosphane (CP) was used as an immunosuppressor, no significant changes in virus distribution were observed with the exception of more frequent isolations at early intervals from kidneys and at late intervals from spleen. With or without CP administration virus was found in the spinal cord at 3--6 days, in the cerebellum and subcortical ganglia at 11--14 days, in the cerebral cortex at 19 days p.i. Early after inoculation the virus was more frequently isolated from the CNS than from the internal organs; later (93--302 days p.i.) the persisting virus or virus-specific antigen were predominantly found in internal organs. The set of sensitive methods used facilitated to detect the persistence of TBE virus in noninfectious form in monkeys with asymptomatic infection.

Animals↗
PubMed1981

Persistence of tick-borne encephalitis virus in monkeys. I. Features of experimental infection.

Sixty-seven Macaca rhesus monkeys were inoculated with 2 mutants and 3 virulent strains of tick-borne encephalitis (TBE) virus including strains isolated from patients with a chronic form of TBE. A model of the clinical course of acute, subacute, and chronic encephalitis was produced by intracerebral inoculation and that of asymptomatic infection was produced by subcutaneous inoculation [with or without administration of cyclophosphane (CP)]. Virus persistence developed after inoculation with all the strains, after non-fatal encephalitis and inapparent infection irrespective of CP administration. In monkeys recovering from encephalitis the virus persisted for at least 783 days. After asymptomatic infection, it persisted for 302 days; neither virus nor virus-specific antigen was detected at 356, 367, and 620 days.

Animals↗
PubMed1981

Persistence of tick-borne encephalitis virus in monkeys. II. Effectiveness of methods used for virus detection.

Fifty monkeys (Macaca rhesus) inoculated with tick-borne encephalitis (TBE)virus intracerebrally or subcutaneously were examined. The efficiencies of different virus detection methods at 90 to 783 days after inoculation were: explantation of organs - 41.2%; co-cultivation of trypsinized organ cells and indicator cells in the presence of 5-bromo-2-iododeoxyuridine with detection of the virus-specific antigen by immunofluorescence - 43.7%, detection of infectious virus and complement-fixing antigen - 13.6%; immunofluorescence examination of organ impression smears - 29.3%; and examination of organ homogenates with detection of virus pathogenic for mice - 1.7%. the latter method was the least sensitive for the detection of persisting TBE virus, in spite of that in the first 3 weeks of infection its efficacy was 88.1% in examinations of clinically ill monkeys and 23.8% in the inapparent form of the infection.

Animals↗
PubMed1981

Persistence of tic-borne encephalitis virus in monkeys. III. Phenotypes of the persisting virus.

The properties of tick-borne encephalitis (TBE) virus persisting for 90-383 days after intracerebral and subcutaneous inoculation of Macaca rhesus monkeys were studied, namely (1) the type of infection produced directly in the tissues of the experimental monkeys; (2) the activating effect of co-cultivation and explantation procedures; and (3) the phenotype of the isolates by a set of markers. The virus was detected and analysed in 52 instances. Directly in monkey tissues the virus induced a productive infection rarely (5.8%) but more frequently (71.2%) an abortive infection detectable by immunofluorescence (presence of virus-specific antigen). In 23% of instances a nonproductive infection was observed in monkey tissues. Like abortive infection it could be activated by the co-cultivation of cells and explantation procedures. The latter exerted a more marked activating effect than co-cultivation. The strains isolated from monkey tissues in productive infection or activated by explanation or co-cultivation were heterogeneous in their properties. The following virus phenotypes were found: virus highly virulent for mice, cytocidal and antigenically complete; a cytocidal virus of low virulence, possessing haemagglutinin; and a cytocidal virus apathogenic for mice, devoid of haemagglutinin but synthesizing complement-fixing antigen and an antigen detectable by immunofluorescence.

Animals↗
PubMed1977

[Interaction of the Sindbis virus and Rauscher and Friend leukoviruses in primary cultures and subcultures of mouse fibroblasts in the early stages of persistence].

The interaction between Friend and Raucher leukoviruses and Sindbis togavirus was studied in primary cultures of mouse fibroblasts and subcultures passaged for 77 days. In primary cultures, two types of virus interactions were observed: neutralism and interference. In interference, the release of the infectious Sindbis virus from the cells is blocked. According to electron microscopic observations, its reproduction terminates by formation of virus nucleocapsid. The blocking of the togavirus maturation is stable in primary cultures but reversible upon subcultivation of the cells infected with oncorna- and togavirus. Rauscher and Sindbis viruses are capable of joint persistence in subcultures with a gradual decrease of the infectivity of togavirus and the leukemogenic activity of oncornavirus.

Animals↗