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Biomedical subjects

S A Ivanova

Publications and source records attributed to S A Ivanova.

At least 19 recordsLinked to original sources
PubMed2006

[Apoptosis of immunocompetent cells in patients with depressive disorders].

A comprehensive evaluation of biological indices has been carried out in 26 patients with depressive disorders and in 20 age- and sex-matched controls. Indices of programmed cell death (apoptosis) in subpopulations of blood lymphocytes and concentration of cortisone in blood serum were determined. Significantly enhanced apoptosis was observed in the lymphocytes of depressive patients as shown by increased percentage of lymphocytes expressing FAS-receptor and cells with morphological changes characteristic of apoptosis (nuclear condensation, vacuolation. Clinical symptoms of depression were concomitant with alterations of cellular link of immunity expressing in the decrease of the total T-lymphocytes (CD3+) number, T-helpers (CD4+) and natural killers (CD16+) as compared to healthy persons. The level of blood serum cortisone was increased in patients with depression. High cortisone values correlated with suppression of cellular CD4+ population and an increase of FAS-receptors expression in patients with depression.

Apoptosis↗
PubMed2003

Comparative efficiency of Proproten-100 during the therapy of patients with alcoholism in the stage of therapeutic remission.

An open comparative clinical study evaluated the efficiency of Proproten-100 in reliving affective, somatovegetative, behavioral, and cognitive post-withdrawal disorders and manifestations of primary pathological alcohol addiction in patients with alcohol dependence in the stage of therapeutic remission. We compared the efficiency of Proproten-100 and standard symptomatic drugs. The preparation possessed anxiolytic, antidepressant, and vegetostabilizing properties, produced a moderate soporific effect, and had no sedative activity in patients with dysphoric depressions and psychopathic disorders. Proproten-100 was more effective during the therapy of patients with anxious and wistful depressions. Proproten-100 increased the contents of IgG and natural antibodies against S100 protein in the blood from patients. The preparation did not cause side effect or development of tolerance. Proproten-100 has psychotropic properties and holds much promise for long-term treatment of patients with alcohol dependence to reduce the incidence of recurrences.

Adult↗
PubMed2003

Changes in immunological parameters in patients with opium abuse receiving ANAR therapy.

We studied the effects of ANAR containing antibodies to morphine in ultralow doses on immunological parameters in patients with opium abuse. Changes in blood content of immunocompetent CD3+, CD16+, and HLA-DR+ cells, lymphocytes carrying receptors for serotonin and dopamine, and humoral immune factors were evaluated. As differentiated from standard preparations, ANAR possessed immunomodulatory properties, increased the content of HLA-DR+ lymphocytes and immunoglobulins in the blood, and normalized the number of CD16+ cells.

Adolescent↗
PubMed1999

Group II metabotropic glutamate receptor activation attenuates traumatic neuronal injury and improves neurological recovery after traumatic brain injury.

We examined the effects of modulating group II metabotropic glutamate receptors (mGluRs) on traumatic neuronal injury using both in vitro and in vivo models. Treatment with various selective group II mGluR agonists significantly decreased lactate dehydrogenase release, a marker of cell death, after traumatic injury to rat neuronal-glial cultures; injury-induced increases in cyclic AMP and glutamate levels were also significantly reduced by a group II agonist. The neuroprotective effects of group II agonists were markedly attenuated by coadministration of a group II antagonist or a membrane-permeable cyclic AMP analog and were additive to those provided by an N-methyl-D-aspartate receptor antagonist or a selective group I mGluR antagonist. Administration of a group II mGluR agonist 30 min after lateral fluid percussion-induced brain injury in rats significantly improved subsequent behavioral recovery as compared with vehicle-treated controls. Together these studies indicate that group II mGluR agonists protect against traumatic neuronal injury by attenuating glutamate release and cAMP levels and suggest a potential role for these agents in the treatment of clinical neurotrauma.

Animals↗
PubMed1998

Mechanical injury to neuronal/glial cultures in microplates: role of NMDA receptors and pH in secondary neuronal cell death.

In vitro models of traumatic injury are useful adjuncts to animal models for studying mechanisms of post-traumatic cell death. Here we describe a new in vitro model in which reproducible levels of injury are delivered by a punch device that produces 28 parallel cuts in individual wells of 96-well microplates. Cell loss is measured by LDH assay or quantitative fluorometric assay for ethidium homodimer staining. Glial cultures show cell death restricted to the initial injury site, whereas neuronal/glial cultures demonstrate substantial spread of cell loss over time. We used this model to examine the role of pH and NMDA receptors in delayed post-traumatic injury. NMDA receptor blockade by dizocilpine (MK-801) or treatment with antisense oligodeoxynucleotides directed against NMDAR1 was neuroprotective. Decreased cell death was observed under acidic conditions whereas increased extracellular pH was associated with increased, MK-801 sensitive cell loss. Advantages of our model include: reproducible trauma induction; rapid measurements of cell injury; and use of 96-well microplates which reduce time and cost. This model appears to be well-suited for the study of selected mechanisms of post-traumatic neuronal injury as well as for screening potential neuroprotective agents.

Animals↗
PubMed1997

mGluR modulation of post-traumatic neuronal death: role of NMDA receptors.

The potential interaction between group I metabotropic glutamate receptors (mGluR) and NMDA receptors in mediating of post-traumatic neuronal death was studied using an in vitro trauma model. Treatment with group I mGluR antagonists provided significant neuroprotection either in the presence or absence of an NMDA receptor antagonist. In contrast, treatment with a group I mGluR agonist alone significantly exacerbated injury; this exacerbation was significantly, but incompletely, reduced in the presence of an NMDA receptor antagonist. These findings are consistent with the conclusion that the effects of group I mGluR activation on post-traumatic cell death are mediated only in part through NMDA receptor modulation and suggest that group I mGluR antagonists may have important therapeutic potential.

Animals↗
PubMed1997

New in vitro model of traumatic neuronal injury: evaluation of secondary injury and glutamate receptor-mediated neurotoxicity.

The multiplicity and complexity of secondary injury processes following brain trauma in vivo make it difficult to elucidate the roles of specific injury mechanisms. As with other areas of CNS injury, such as ischemia, this has led to the development of in vitro models. Here we describe a new trauma model, in which standardized trauma is delivered to neuronal/glial cultures using a special mechanical device that produces concentric circular cuts in the cell layer. Changes in the number of circles (from 1 to 6) allows variation of injury severity. Comparison studies of cell death induced by such trauma in glial and neuronal/glial cultures demonstrated that glial cells are relatively resistant to this injury, and that the cell death after trauma to neuronal/glial cultures reflects primarily neuronal death. Consistent with other in vivo and in vitro studies, glutamate receptor antagonists MK 801 and MCPG were neuroprotective. Thus, this model appears useful for studying glutamatergic mechanisms involved in secondary injury, and may prove useful for evaluating certain pharmacological strategies for CNS trauma.

Animals↗
PubMed1997

Neuroprotective effects of group III mGluR in traumatic neuronal injury.

We have used an in vitro trauma model to examine the effects of modulation of group III metabotropic glutamate receptors (mGluR) on post-traumatic neuronal cell death. Rat cortical neuronal/glial cultures were subjected to standardized mechanical injury using a punch that delivers 28 parallel cuts to 96-well culture plates, resulting in approximately 50% neuronal cell loss in untreated cultures. RT-PCR demonstrated expression of mRNA for mGluR4, mGluR6, mGluR7, and mGluR8 in uninjured cultures as well as in adult rat brain. Treatment with the group III agonists L-(+)-2-amino-4-phosphonobutyric acid (L-AP4) or L-serine-O-phosphate (L-SOP) resulted in dose-dependent neuroprotection. In contrast, treatment with the group III antagonists alpha-methyl-AP4 (MAP4) or (RS)-alpha-methylserine-O-phosphate (MSOP) caused dose-dependent exacerbation of injury, which was significantly attenuated by L-AP4 or L-SOP. The neuroprotective actions of L-AP4 or L-SOP were markedly reduced by the cyclic AMP analog 8-CPT-cAMP (500 microm), which by itself had no effects at this concentration. Moreover, treatment with L-AP4 or L-SOP reduced basal cyclic AMP levels. Treatment with the NMDA antagonist MK 801 decreased post-traumatic cell death by 45% at optimal concentrations; combined treatment with MK 801 and group III agonists showed a significant enhancement of neuroprotection as compared to treatment with the NMDA antagonist alone. Our findings indicate a clear neuroprotective action for group III agonists in this model and suggest that group III mGluR are endogenously activated in response to trauma. The neuroprotective effects of group III agonists appear to result in part from modulation of adenylyl cyclase activity and are additive to those of an NMDA receptor antagonist.

Animals↗
PubMed1990

[Sensitization to fungi of the genus Candida in tuberculosis patients].

Allergic diseases in patients with tuberculosis occur three times more frequent than in the nontubercular population. Drug-related allergy is most frequent. The causes of allergy in this contingent of patients are diverse. Of one them is, apparently, high frequency of sensibilization to Candida fungi determined by skin tests and immunothermistography. This problem deserves a more detailed investigation.

Allergens↗
PubMed1989

[Phagocytosis of immune complexes by leukocytes in patients with schizophrenia].

Comparative investigation of the leukocytes' in vitro capabilities of attacking the immune complexes was performed in 20 schizophrenic patients and 20 healthy individuals. The patients' leukocytes were considerably less active against the immune complexes that those of healthy persons that was probably related to both primary defect in the phagocytic cells and their overload (block) by different biologically active factors. Levamisole in vitro stimulated these events.

Adjuvants, Immunologic↗
PubMed1987

[Characteristics of the influenza type A (H3N2) epidemic in Omsk in January 1985].

The work presents the data obtained in analysis of the epidemic situation among the population of Omsk in January-February 1985 and the characterization of the isolated strains of influenza A (H3N2) virus, determines the specific features of the course of the influenza epidemic process among different social and age groups, evaluates anti-influenza measures.

Age Factors↗
PubMed1987

[Antibody formation in the blood and respiratory tract secretions following one-time and repeat immunization with an inactivated influenza vaccine].

Eighty nine volunteers were under study. They were immunized by inactivated vaccine from influenza viruses A(H1N1)+A(H3N2) one time or every year during 4 to 6 years. Vaccine in dosage of 0.2 ml was applied intracutaneously. Under detailed clinical study deflections of health were not over standard. Accumulation of antibodies was determined to immunogens of the vaccine and to virus A/Leningrad/X/83(H3N2), which was in epidemic circulation 3 years later. Intensity of relative increase of antibodies with repeated immunization was 1.5 to 2 times lower. Maximum concentrations of antibodies were found in a week after vaccination. Immunization didn't cause change of titres of secretory antibodies and concentration of immunoglobulin isotopes G, M, A and E in sera and secretions.

Adult↗
PubMed1986

[Sensitivity of fungi in the genus Candida to antimicrobial preparations].

Sensitivity of 50 Candida fungus strains isolated from patients with chronic intestine diseases was studied with respect to amphotericin B, levorin, enteroseptol, intestopan and decamethoxin. The rate of forming resistant variants of the strains with respect to decamethoxin and development of their cross resistance to levorin was estimated. It was shown that decamethoxin was the most active antifungal drug among the drugs tested. Estimation of sensitivity of the Candida strains to enteroseptol and intestopan revealed that the fungicidal concentration of enteroseptol for 78 per cent of the strains ranged within 3.9-7.8 micrograms/ml. It was demonstrated that development of resistance to decamethoxin in the strains of Candida albicans was slow and did not reach high levels. No cross resistance between decamethoxin and levorin was detected.

Amphotericin B↗
PubMed1983

[Role of genetic factors in the epidemic process in respiratory viral infections].

Observations carried out during 1973-1979 indicate that persons, who are frequently ill, determine the incidence of influenza and acute respiratory diseases among various groups of adult population at all epidemic periods. In constantly observed groups of different ages such persons were the source of 60-85% of the outbreaks of acute respiratory diseases. The correlation between genotypic blood markers (the ABO and HLA systems) and susceptibility to respiratory viruses has been established.

ABO Blood-Group System↗