[The technologies of inpatient care substitution in surgery]. / Statsionarzameshchayushchie tekhnologii v khirurgii.

It was analyzed the introduction of inpatient care substitution technologies in multi-disciplinary Polyclinic OAO «Gazprom¼. Organizational principles of outpatient surgical interventions under general and combined anesthesia are represented. Also it was described surgical features to decrease incidence of intra- and postoperative complications. System of active postoperative management was presented to define early different features of disease. Also main directions of development of this technology were suggested.

[Characteristics of heritability and effect of selection on prevalence of diffuse-toxic goiter in population].

On genealogic data about 242 Gravers disease patients, fertility parameters of 2105 healthy and 369 Grave's disease women peculiarities of genetic determination and natural selection of disease were studied. Results of the genetic analysis have revealed conformity of Grave's disease inheritance to alternative model parameters. Homozygote penetrance within the framework of this model was 78.8%, heterozygote--17.3%. For one generation in the Kharkov area population frequency of a gene to Grave's disease predisposition increases 0.8%.

Material equations for electromagnetism with toroidal polarizations.

With regard to the toroid contributions, a modified system of equations of electrodynamics moving continuous media has been obtained. Alternative formalisms to introduce the toroid moment contributions in the equations of electromagnetism has been worked out. The two four-potential formalism has been developed. Lorentz transformation laws for the toroid polarizations has been given. Covariant form of equations of electrodynamics of continuous media with toroid polarizations has been written.

Animal model and in vitro studies of anti neurofilament antibodies mediated neurodegeneration in Alzheimer's disease.

Alzheimer's disease (AD) is associated with serum antibodies directed specifically against phosphorylated epitopes highly enriched in the heavy neurofilament protein NF-H of cholinergic neurons. Prolonged immunization of rats with these molecules but not with other NF-H isoforms results in cognitive impairments. This animal model, termed experimental autoimmune dementia (EAD), supports a role for such antibodies in neurodegeneration in AD. In the present study we investigated the cellular and immunological mechanisms underlying the cognitive defects in EAD. Immunohistochemical studies revealed that IgG accumulate in the septum, hippocampus and in the entorhinal cortex of the EAD rats. This is accompanied by a marked reduction in the density of septal cholinergic neurons. An inverse correlation was observed between the level of IgG in the septum of individual EAD rats and the density of their septal cholinergic neurons. Time course studies revealed that the decrease in the density of cholinergic neurons in the septum of EAD rats and the accumulation of IgG in this brain area have the same time course and are both significant by three to four months following the initiation of immunization with cholinergic NF-H. The cognitive deficits of the EAD rats evolve more slowly and are pronounced only after six months following the initation of immunization. In vitro studies revealed that anti NF-H IgG bind to the outer surface of neurons in tissue cultures of rat forebrain and can affect neuronal viability. These AD and in vitro findings provide model systems for studying the mechanisms underlying the neuropathological effects of specific anti NF-H antibodies.

Disintegration of the spatial organization of behavior in experimental autoimmune dementia.

Experimental autoimmune dementia is a rat model designed to examine the potential role of anti-cholinergic neurons antibodies in neuronal degeneration in dementia and Alzheimer's disease. We have previously shown that sera of patients with Alzheimer's disease contain antibodies which bind specifically to the high molecular weight neurofilament protein of the purely cholinergic electromotor neurons of Torpedo. Production of such antibodies in experimental autoimmune dementia rats by prolonged immunization with the Torpedo cholinergic high molecular weight neurofilament subunit results in accumulation of antibodies in the septum and hippocampus of the immunized rats, in a marked decrease in the density of forebrain cholinergic neurons, and in memory deficits. In the present study we characterized the open-field behavior of experimental autoimmune dementia rats, and examined whether, like in dementia, the spatiotemporal organization of their behavior is impaired. The results obtained revealed that experimental autoimmune dementia rats travel shorter distances; explore a smaller part of the open-field; and perform less round-trips to the key location--the home base--in reference to which their behavior is normally organized. The shrinkage of the explored space and the reduced number of round trips are independent of the amount of locomotion and represent a deterioration in the organization of behavior in time and space. These behavioral changes are specific to the anti-cholinergic immune response of experimental autoimmune dementia rats as they are not observed in rats which were immunized with chemically heterogeneous high molecular weight neurofilament subunit.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased density of forebrain cholinergic neurons in experimental autoimmune dementia.

Sera of Alzheimer's disease and Down's syndrome patients contain antibodies which bind specifically to the high molecular weight neurofilament protein of Torpedo cholinergic neurons. We have recently shown that prolonged immunization of rats with this antigen results in the accumulation of IgG in neurons in the septum and hippocampus of the immunized rats and in cognitive impairments. This animal model is termed experimental autoimmune dementia. In the present study we examined whether the anti-cholinergic high molecular weight neurofilament subunit immune response of the experimental autoimmune dementia rats affects forebrain cholinergic neurons. This was performed immunohistochemically utilizing a monoclonal antibody to nerve growth factor receptor, a specific marker of cholinergic neurons in the forebrain. The results obtained revealed significant decreases in the density of cholinergic neurons in the medial septal nucleus and diagonal band of the experimental autoimmune dementia rats. These decreases are specific to the anti-cholinergic high molecular weight neurofilament subunit immune response of the experimental autoimmune dementia rats and are not observed in control rats which were immunized with chemically heterogeneous high molecular weight neurofilament subunit. The decrease in density of forebrain cholinergic neurons in experimental autoimmune dementia rats may mimic pathogenic processes in Alzheimer's disease and supports a role for anti-cholinergic high molecular weight neurofilament subunit antibodies in the degeneration of cholinergic neurons in the disease.

Decreased density of forebrain cholinergic neurons and disintegration of the spatial organization of behavior in experimental autoimmune dementia (EAD).

Experimental autoimmune dementia (EAD) is a rat model designed to examine the potential role of anti-cholinergic neurons antibodies (Abs) in the neuropathology of Alzheimer's disease (AD) and dementia. We have previously shown that sera of AD and Down's syndrome patients contain Abs which bind specifically to the high molecular weight neurofilament protein (NF-H) of the purely cholinergic electromotor neurons of Torpedo. Production of such Abs in EAD rats by prolonged immunization with Torpedo cholinergic NF-H results in the accumulation of IgG in the septum and hippocampus of the immunized rats and in memory deficits. In the present study, we examined immunohistochemically whether the anti-cholinergic NF-H immune response of the EAD rats affects their brain cholinergic neurons. In addition, since dementia is associated with severe deterioration in the spatio-temporal organization of behavior, we examined whether EAD rats also mimic this important feature of dementia. The results obtained show that production in EAD rats of anti-cholinergic NF-H Abs similar to those found in AD patients results in a marked decrease in the density of forebrain cholinergic neurons and in derangements in the spatio-temporal organization of their behavior. These findings may replicate pathogenic processes in AD and support a role for anti-cholinergic NF-H Abs in the degeneration of cholinergic neurons in the disease.

[Antiheparin properties of synthetic polycations]. / Antigeparinovye svoistva sinteticheskikh polikationov

The toxicity of differently structured polymeric compounds for mice (intravenously) and their antiheparin properties in in vitro and in vivo tests were studied. The antiheparin activity display polymers containing amino groups or onium atoms of nitrogen, sulphur and phosphorus in various structures. The antagonism to heparin is due to the polymers being endowed with polycationic properties.