Cytological study of a continuous swine embryonic kidney cell line with a persistent Toxoplasma infection]

Invasion of the PEK cell culture by toxoplasma did not cause any sharp disruption of the vital activity of the cells and failed to lead to their rapid degeneration. The observed changes in the morphology of the host cells were apparently chiefly the result of a purely mechanical pressure of the vacuoles on the nucleus and the cytoplasm, although the extreme forms of disturbances of the cell morphology were possibly associated with their greater injury. No complete "selfpurification" of the cells apparently occurred, since despite the marked reduction in the number of parasites a possibility of reinfection with toxoplasma of the culture at the later periods after the infection could not be excluded.     

Long non‐coding RNAs in melanoma

Melanoma is the most lethal cutaneous cancer with a highly aggressive and metastatic phenotype. While recent genetic and epigenetic studies have shed new insights into the mechanism of melanoma development, the involvement of regulatory non‐coding RNAs remain unclear. Long non‐coding RNAs (lncRNAs) are a group of endogenous non‐protein‐coding RNAs with the capacity to regulate gene expression at multiple levels. Recent evidences have shown that lncRNAs can regulate many cellular processes, such as cell proliferation, differentiation, migration and invasion. In the melanoma, deregulation of a number of lncRNAs, such as HOTAIR, MALAT1, BANCR, ANRIL, SPRY‐IT1 and SAMMSON, have been reported. Our review summarizes the functional role of lncRNAs in melanoma and their potential clinical application for diagnosis, prognostication and treatment.     

Interactions between adsorbed layers of alphaS1-casein with covalently bound side chains: a self-consistent field study

The effect on the adsorbed layer properties of the modification of alpha S1-casein by covalent bonding with an uncharged polysaccharide side chain has been investigated using lattice-based self-consistent field (SCF) theory. Interactions between two hydrophobic planar surfaces coated by a layer of adsorbed modified alpha S1-casein have been studied as a function of pH and ionic strength. While the interactions of the unmodified alpha S1-casein layers become attractive at high ionic strength, it has been shown that the presence of polysaccharide attachment to the alpha S1-casein molecule can confer net repulsive interactions over a wide range of salt concentration. The disordered protein is represented as a linear flexible polyampholyte with a sequence of hydrophobic, polar, and charged units based on the known alpha S1-casein primary structure. The hydrophilic side chain is attached at various fixed positions along the casein backbone. Different lengths and locations of the attached polysaccharide side chain are examined. Interfacial structures and colloidal stability properties of the system are determined, including the surface-surface interaction potential, the extent of protein bridging, and the distribution of protein segments from the surface under different conditions of pH and ionic strength. It has been found that the covalent bonding of short hydrophilic chains may not only enhance but can also worsen the colloidal stabilizing properties of the modified protein, depending on the position of the attachment.     

Protective effect of bixin on carbon tetrachloride-induced hepatotoxicity in rats

Background

The liver is an important organ for its ability to transform xenobiotics, making the liver tissue a prime target for toxic substances. The carotenoid bixin present in annatto is an antioxidant that can protect cells and tissues against the deleterious effects of free radicals. In this study, we evaluated the protective effect of bixin on liver damage induced by carbon tetrachloride (CCl₄) in rats.

Results

The animals were divided into four groups with six rats in each group. CCl₄ (0.125 mL kg^-1 body wt.) was injected intraperitoneally, and bixin (5.0 mg kg^-1 body wt.) was given by gavage 7 days before the CCl₄ injection. Bixin prevented the liver damage caused by CCl₄, as noted by the significant decrease in serum aminotransferases release. Bixin protected the liver against the oxidizing effects of CCl₄ by preventing a decrease in glutathione reductase activity and the levels of reduced glutathione and NADPH. The peroxidation of membrane lipids and histopathological damage of the liver was significantly prevented by bixin treatment.

Conclusion

Therefore, we can conclude that the protective effect of bixin against hepatotoxicity induced by CCl₄ is related to the antioxidant activity of the compound.     

Criteria of the epidemiological surveillance of meningococcal infection

The results of studies carried out with the use of the unified, specially developed methods in eight regions of the USSR are generalized. Basing on the analysis of the results, the leading role of serogroup A meningococci in the rise of morbidity is emphasized, the relation of the morbidity level to the serogroup composition of meningococci circulating among healthy population is revealed, the necessity of carrying out selective bacteriological surveys with a view to establish the serogroups of meningococci circulating among the population is shown. The expedient criteria to be used in the system of epidemiological surveillance of meningococcal infection are presented.     

The relationship between the fate of the agent of toxoplasmosis, Toxoplasma gondii, in macrophages cultivated in vitro and the virulence of the parasites]

Comparative light microscopic and electron microscopic studies of development of a highly-virulent RH strain and a less virulent Lagrave strain of Toxoplasma cultivated in macrophages in vitro were made. Contrary to active multiplication of the highly virulent strain most of toxoplasmas of a less virulent strain disintegrated the first hours, degenerating completely in 24-48 hours after the penetration into the macrophages. Submicroscopic study showed no marked cytological changes of macrophages infected with a less virulent strain in comparison with the marked changes of the nuclei in macrophages infected with the RH strain. Disintegration of parasites within the phagosome was accompanied by a gradual transformation of an originally double (or triple) vacuolar membrane to a single membrane and by the disappearance of an additional layer of mitochondria and endoplasmic reticulum elements surrounding the vacuolar membrane. It is likely that the capacity of toxoplasma to develop in macrophages in vitro could become an additional marker to its virulence for albino mice.     

Mitochondrial ND5 gene variation associated with encephalomyopathy and mitochondrial ATP consumption

Mitochondrial encephalomyopathy and lactic acidosis with strokelike episodes (MELAS) is a severe young onset stroke disorder without effective treatment. We have identified a MELAS patient harboring a 13528A-->G mitochondrial DNA (mtDNA) mutation in the Complex I ND5 gene. This mutation was homoplasmic in mtDNA from patient muscle and nearly homoplasmic (99.9%) in blood. Fibroblasts from the patient exhibited decreased mitochondrial membrane potential (Deltapsim) and increased lactate production, consistent with impaired mitochondrial function. Transfer of patient mtDNA to a new nuclear background using transmitochondrial cybrid fusions confirmed the pathogenicity of the 13528A-->G mutation; Complex I-linked respiration and Deltapsim were both significantly reduced in patient mtDNA cybrids compared with controls. Inhibition of the adenine nucleotide translocase or the F1F0-ATPase with bongkrekic acid or oligomycin caused a loss of potential in patient mtDNA cybrid mitochondria, indicating a requirement for glycolytically generated ATP to maintain Deltapsim. This was confirmed by inhibition of glycolysis with 2-deoxy-D-glucose, which caused depletion of ATP and mitochondrial depolarization in patient mtDNA cybrids. These data suggest that in response to impaired respiration due to the mtDNA mutation, mitochondria consume ATP to maintain Deltapsim, representing a potential pathophysiological mechanism in human mitochondrial disease.     

Use of the common winter wheat homozygous population for genetic analysis of beta-amylase and evaluation of its aggregation ability

We investigated a self-pollinated homozygous population of common winter wheat, F→∞ 24/04 × Odesskaya krasnokolosaya, for variants of beta-amylase and the aggregation ability of the protein complex of seed via disulfide bonds. It was found that variation in the electrophoretic types of this enzyme was due to four isoenzymes. Two of them (a and b) are doubled and controlled by separate loci with independent inheritance. Isoenzyme c was due to three dominant factors, and four loci were responsible for d. Analysis of the number of -S-S- bonds of five genotypes, which were harvested in 2013 and differed in the types of beta-amylase, showed that some of them were significantly different from others in this indicator. In general, the samples were grouped by the type of this enzyme, forming the following continuous series with respect to aggregation ability: I ≥ B ≥ F ≥ D ≥ G or 59.13 ± 3.18 ≥ 56.65 ± 2.46 ≥ 52.54 ± 2.24 ≥ 50.16 ± 1.67 ≥ 48.63 ± 6.25 of cond. units. Significant differences were observed for this property between groups B > D and I > D. Therefore, genotypes having types I and B have a positive influence on the rheological properties of dough.     

Genetic control of several alpha-amylase isozymes in winter hexaploid wheat

alpha-Amylase isozymes were detected via electrophoretic separation in a Tris-glycine polyacrylamide gel system (pH 8.4). Three chromosome 6B loci controlling the alpha-amylase isozyme composition were identified by studying the grain alpha-amylase patterns in an F --> infinity self-pollinating population of winter common wheat (Donskoi Mayak). The loci were found to take the following order in the long arm of chromosome 6B: cen.-alpha-Amy-B3-alpha-Amy-B6-alpha-Amy-B1-.