Respiratory moisture loss and possible pathways of its regulation

Examination of healthy men and those suffering from nonspecific pulmonary diseases has shown that respiratory moisture loss is induced by situation and While "lifting" examinees in the altitude chamber 5000 m upwards intensity of the moisture loss increases to 158%. Essential individual variations of the response are shown. Pulmonary diseases (chronic bronchitis, pneumonia, lecithin synthesis disturbances) make the moisture loss higher. It is concluded that lung surfactants participate in regulation of the respiratory moisture loss. participate in regulation of the respiratory moisture loss.     

Identification of pathological states based on luminescent analysis of immunocompetent blood cells]

The immune status and state of health of individuals were estimated by luminescence microspectral analysis of immunocompetent blood cells were estimated. The approach consists in the computer analysis of the distribution of luminescent characteristics of nuclear blood cells stained with acridine orange on a phase plane in the coordinates of intensities of green and red fluorescence bands. The method provides information on the tension of the immune system and types of pathological processes. The following pathological processes can be identified: acute, progressing and prolonged chronic pathologies, neuroendocrine and oncologic diseases, allergic and autoimmune disorders.     

Noncytopathic replication of Venezuelan equine encephalitis virus and eastern equine encephalitis virus replicons in Mammalian cells

Venezuelan equine encephalitis (VEE) and eastern equine encephalitis (EEE) viruses are important, naturally emerging zoonotic viruses. They are significant human and equine pathogens which still pose a serious public health threat. Both VEE and EEE cause chronic infection in mosquitoes and persistent or chronic infection in mosquito-derived cell lines. In contrast, vertebrate hosts infected with either virus develop an acute infection with high-titer viremia and encephalitis, followed by host death or virus clearance by the immune system. Accordingly, EEE and VEE infection in vertebrate cell lines is highly cytopathic. To further understand the pathogenesis of alphaviruses on molecular and cellular levels, we designed EEE- and VEE-based replicons and investigated their replication and their ability to generate cytopathic effect (CPE) and to interfere with other viral infections. VEE and EEE replicons appeared to be less cytopathic than Sindbis virus-based constructs that we designed in our previous research and readily established persistent replication in BHK-21 cells. VEE replicons required additional mutations in the 5' untranslated region and nsP2 or nsP3 genes to further reduce cytopathicity and to become capable of persisting in cells with no defects in alpha/beta interferon production or signaling. The results indicated that alphaviruses strongly differ in virus-host cell interactions, and the ability to cause CPE in tissue culture does not necessarily correlate with pathogenesis and strongly depends on the sequence of viral nonstructural proteins.     

Analysis of DNA Interband Regions 3A5/A6, 3C5-6/C7, and 60E8-9/E10 in Polytene Chromosomes of Drosophila melanogaster

Using electron microscopic (EM) data on the formation of a novel band from theP-element material after its insertion in the interband and the procedure of P-target rescue, DNA interband regions 3A5/A6, 3C5-6/C7, and 60E8-9/E10 of Drosophila melanogasterpolytene chromosomes were cloned and sequenced. EM analysis of the 3C region have shown that the formation of the full-size 3C5-6/C7 interband requires a 880-bp DNA sequence removed by deletion Df(1)fa ^swb. A comparison of DNA sequences of six bands, two of which were obtained in the present work and four were described earlier, demonstrated the uniqueness of each of them in the Drosophilagenome and heterogeneity of their molecular organization. Interband 60E8-9/E10 contains gene rpl19transcribed throughout the development, in particular in salivary glands. In the other interbands examined 5" and 3" nontranslated gene regions are located. These results suggest that Drosophilainterbands may contain both housekeeping genes and regulatory sequences of currently inactive genes from adjacent bands.     

Creation of a convenient vector for transformation of Drosophila with functional FRT-pFRT sites

Modification of Drosophila transformation vector pCaSper3 with the P element was used to construct a new vector, pFRT. The vector contains two tandem FRT sites flanked with several unique restriction sites and separated by a polylinker of five restriction sites, and allows easy cloning of DNA fragments between or close to the FRT sites. FRT-mediated excision of DNA sequences cloned between the FRT sites was demonstrated in vivo. The vector was proposed for molecular genetic studies of the position effect variegation, structural and molecular organization of Drosophila polytene chromosomes, etc.     

Hemo- and lymphomicrocirculatory bed of the broad ligament of the uterus in the presence of collateral circulation

Structural adaptation of the vascular bed in the broad ligament of the dog uterus has been studied at various time of the experimental phlebohypertension. Restitution of the circulation after the posterior vena cava occulsion occurs phasically. The venous collateralies are not formed at one time and it is connected with the venous pressure level in the inferiocaval system and with some changes in the construction of the microcirculatory bed. Basing on the morphometry data, a general equation has been derived which reflects dynamics of the microangiological parameters and demonstrates unidirectionness of the adaptive reactions in the vascular bed at the disturbed venous circulation. Using principles of the system-structural analysis and the mathematical graph theory, we consider the microcirculatory system of the broad ligament of the uterus as a graph-system and study the reorganization of the microcirculatory network at a venous congestion. Realization of the compensatory possibilities is reached in the microcirculatory bed by a changed relationships in the number of the intervascular connections. The latter are estimated according to the graph-schemes of the microvascular bed. Morphokinetics of the connections between the vessels is characterized by widening or narrowing the borders of the "adaptive norm" and by changing the microangioarchitectonics. At the same time, there is noted formation of specialized microhemoangioconstructions. Morphofunctional state of the lymphatic system is connected with reorganization of the angioarchitectonics. This is certain manifestation of the law of the lymphatic and blood beds "synergism". Thus, the structural changes of the vascular bed are aimed to support a certain hemodynamic level.     

PKR-dependent and -independent mechanisms are involved in translational shutoff during Sindbis virus infection

The replication of Sindbis virus (SIN) profoundly affects the metabolism of infected vertebrate cells. One of the main events during SIN infection is the strong inhibition of translation of cellular mRNAs. In this study, we used a combination of approaches, including the study of SIN replication in PKR(-/-) mouse embryo fibroblasts or in the presence of an excess of catalytically inactive PKR. We show that the PKR-dependent inhibition of translation is not the only and most likely not the major pathway mediating translational shutoff during SIN infection. The PKR-independent mechanism strongly affects the translation of cellular templates, whereas translation of SIN subgenomic RNA is resistant to inhibition, and this leads to a benefit for viral replication. Our findings suggest that both PKR-dependent and non-PKR-dependent mechanisms of SIN-induced translational shutoff can be manipulated by using SIN replicons expressing mutated SIN nsP2 or kinase-defective PKR. Specifically, we show that expression of heterologous genes from SIN-based and most likely other alphavirus-based replicons can be increased by downregulating both the PKR-dependent and PKR-independent translational shutoffs.     

Possibility of directed changes in the surface activity of rat pulmonary surfactants by means of exposure to antibodies specific to them]

The experiments were performed on Wistar rats with weight of 150-200 g. Antibodies were prepared by immunization of rabbits with pure surfactants of rat lungs and were intravenously injected into rats three times within 3 days intervals. These antibodies were shown to influence the superficial activity of lung surfactants and the alveolar lung cells activity. The low doses of antibodies (0.06 micrograms of protein per 100 g of body mass) stimulated the superficial activity of lung surfactants, while higher doses (3 mg of protein per 100 g of body mass) inhibited it.