PubMed Health⌕ Search

Biomedical subjects

N G Kharlanova

Publications and source records attributed to N G Kharlanova.

At least 19 recordsLinked to original sources
PubMed2004

Ultrastructural evidence of invasive activity of Vibrio cholerae.

The development of experimental cholera in suckling rabbits is associated with typical cholerogenic syndrome: the presence of Vibrio cholerae in the blood, bile (in 60 and 70% cases, respectively), small and large intestine (in 100% cases). Simultaneously with enterocyte desquamation and increased permeability of the blood-enterocyte barrier, the vibrios are released into villous stroma and then into the microcirculatory bed. the zot toxin is involved in the mechanism of Vibrio cholerae invasion, the corresponding gene is present in the genome of the studied strain.

Animals↗
PubMed2004

Ultrastructural changes in small intestinal lipofibroblasts of suckling rabbits with experimental cholera.

Ultrastructural analysis of the jejunum in suckling rabbits showed that lipofibroblasts localized in the submucosa and adjacent to crypts contain lipid inclusions (granules) with typical "melting" surface. Lipofibroblasts contained moderately widened cisternae of the granular endoplasmic reticulum and few mitochondria with dense matrix and poorly developed cristae. Experimental cholera was usually accompanied by a decrease in the number of lipid inclusions, and only in some cases by accumulation of lipid material. Our results suggest that the material accumulated in granules plays a role in the pathogenesis of cholera.

Animals↗
PubMed2003

Ultrastructural changes in smooth muscle cells of the small intestine in suckling rabbits with experimental cholera.

Ultrastructural study of the small intestine in suckling rabbits with experimental cholera revealed involvement of the inner and outer smooth muscle layers into the pathological process. Smooth muscle cells were characterized by vacuolar and fatty degeneration and focal colliquative necrosis. Apoptosis played little role in gastrointestinal motility disturbances. The presence of considerable amounts of fluid in intestinal loops reflects peristaltic dysfunction due to generalized damage to smooth muscle cells.

Animals↗
PubMed2003

[Coccoid forms of Helicobacter pylori and their role in human pathology].

Most helocobacteria die as a result of eradication therapy. However, a negligible amount of them revert to the non-cultivated state and remain in the form of coccoids. Based on the literature analysis it has been proved that coccoid forms of H. pylori are viable and their basic properties are similar to those of vegetative helocobacteria forms. It has been suggested for the first time that it is necessary to find therapeutic means for having an impact on helocobacteria, which are in the coccoid form, in addition to standard methods of treatment of helicobacteriosis and its consequences.

Bacterial Adhesion↗
PubMed2002

Ultrastructural peculiarities of intranuclear inclusions in some target cells during endotoxin shock.

Intranuclear inclusions detected in hepatic, renal, and cerebral cells during endotoxemia can be subdivided into true and pseudo inclusions. True inclusions have filamentous and crystalline structure and are rarely found in control animals. However, the number of true inclusions increases during pathology and can serve as a marker of molecular pathology in the cells provoked by endotoxin.

Animals↗
PubMed2002

[Role of genetic features of Helicobacter pylori in development of inflammation of the gastric mucosa in chronic gastritis and ulcer disease].

This review, which is devoted to the analysis of current data on genetic properties of Helicobacteria, is the first work in the Russian literature summarizing the research results published before and after the sequencing of the genome of two Helicobacter pylori pathogenic strains--26695 and J99. It discloses information about the genetic control of pathogenecity factors and their localization on the chromosome. There is a review of genes participating in the colonization of Helicobacteria, lipopolysaccharide biosynthesis, urease synthesis, and pH control. Special attention is focused on the problem of so-called "viable" but non-cultured forms of Helicobacter pylori.

Chronic Disease↗
PubMed2001

Ultrastructural changes in the nephron and renal protein cleaving function in suckling rabbits with experimental cholera.

Immature nephrons and the presence of a proteolytic system mediating extracellular protein digestion in the epithelium of proximal tubules are characteristic features of renal cortical ultrastructure in intact 10-12-day-old suckling rabbits. Cholera infection is accompanied by intensive cleavage of exogenous protein, which starts in podocytes and is completed in the cytoplasm of the proximal tubule epitheliocytes. Overload to nephron associated (in addition to urine production) with intensive extracellular hydrolysis impairs nephrothelium reactivity and increases its vulnerability to cholera exo- and endotoxins and their mediators.

Animals↗
PubMed1996

[Ultrastructural changes in the interstitial cells of the kidney medullary substance in suckling rabbits with experimental cholera].

A culture of virulent selection of cholera vibrios L-top 5879 was introduced through the probe to suckling rabbits-pups 10 to 12 days old. Ultrastructural changes of interstitial cells and capillaries of kidney medulla were studied. During vibrio adhesion (4 hrs after the inaction) interstitial cells acquire dystrophic changes, lipid granules content reduces, while vascular permeability grows higher which suggests the presence of prostaglandin precursors elimination into blood flow. Cholera development (1-2 days later) is accompanied with progressing of signs of prostaglandin synthesis activation and their precursors passage into the vascular bed.

Animals↗
PubMed1996

[The effect of myelopid on the ultrastructural changes in the rat myocardium induced by an endotoxin].

Ultrastructural changes in the myocardial atria and ventricles have been studied in experiments on rats in the intermediate period of the endotoxin shock, on the stage of late endotoxemia and its correction with myelopid. It was established that 5 hours after endotoxin injection contractile disturbances and intracellular myocytolysis take place and growth of secretory activity is observed in atrial cardiomyocytes. Simultaneously vascular permeability increases. Only the endocrine heart function is restored 3 days later, while dystrophic changes and glycogen depletion are maintained. The myelopid administration beginning from the intermediate period of the endotoxin shock and then once during 3 days, removes most of ultrastructural damages or attenuates their expression.

Activins↗