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Biomedical subjects

R A Ivanchenkova

Publications and source records attributed to R A Ivanchenkova.

At least 19 recordsLinked to original sources
PubMed2002

[Pathogenesis of gallbladder cholesterolemia].

Disturbances in cholesterol metabolism may be essential in pathogenesis of gallbladder cholesterosis (GBC). HDL cholesterol in the blood is subnormal. Physicochemical changes in the superficial layer of HDL induce impairment of free cholesterol esterification. Blood lipids and their apoprotein component are important for bile cholesterol level. In gallbladder contractile dysfunction but unaffected absorption there is enhanced passive and active cholesterol transport from the supersaturated bile to the cytoplasm of the epithelial cells from the bladder mucosa. Mechanism of intensive absorption of the lipids by macrophages operates primarily via modification of their apoprotein component. Modification of apoprotein occurs both in blood and gallbladder. Modified apoprotein is recognized by the macrophage and is absorbed by it together with transported lipids. In accumulation of great quantities of lipids in the macrophage it becomes big, slow, stays in the mucous or submucous layer of the wall and finally transforms into the foam cell. Moreover, deterioration of HDL cholesterol acception in GBC leads to slow discharge of cholesterol from the bladder wall.

Adult↗
PubMed2001

[Immunomorphologic detection of apoprotein B antigenic determinants in the gallbladder wall in cholesterosis and cholelithiasis].

The presence and location of apoprotein B (Apo B) antigenic determinants in cholesterosis and cholelithiasis in gall bladder wall were detected for elaboration of modified Apo B role in pathogenesis of these diseases. Macroscopically changed parts of gall bladder (GB) wall of patients with gall bladder cholesterosis (GBC), and also macroscopically unchanged parts of GB wall of patients with cholelithiasis (CL) after cholecystectomy were studied. Macroscopically unchanged parts of GB wall obtained during autopsy of persons without symptoms of GB pathology were used as a control. Apo B location was studied with monoclonal (MAB 5F8 to Apo B) and polyclonal (PAB) antibodies; Apo B modified by malonic dialdehyde and oxidized by Cu2+ (4C11), Apo A with MAB1C5. Antibodies to CD 68 (specific marker of macrophages) was positive control, antibodies to trichinella--negative control. The most intensive accumulation of modified Apo B was revealed in foam cells region with accumulate lipids and form polyps that testifies to connection of apoproteins with lipids and foam cells and suggests their role in pathogenesis of GBC. More intensive staining of GB epithelial cells, particularly on GB peripheral parts by antibodies to apoproteins compared with surrounding tissues shows that bile is the source of detected modified apoproteins. Increase of absorption and accumulation of apoproteins in GB wall were also revealed in CL but these processes are less intensive than in GBS.

Adult↗
PubMed2000

[High-density lipoproteins in cholesterosis of the gall bladder].

The composition of serum high-density lipoproteins (HDL) was studied in 64 patients with polypous cholesterosis (PC). The spectrum of serum lipids in patients with PC was characterized by the lower concentrations of HDL cholesterol (42.0 +/- 2.5 mg/dl; p < 0.05) and higher concentrations of low-density lipoproteins (LDL) cholesterol (169.9 +/- 6.9 mg/dl; p < 0.01) than those in the controls. The decreased HDL cholesterol, or hypoalphacholesterolemia was associated with quantitative changes in HDL phospholipids (PL) (66.48 +/- 3.4; p < 0.01) and with changes in the composition of individual PL by lowering the proportion of lecithin (47.13 +/- 2.19 mg/dl; p < 0.01). It may be suggested that the lower amount of HDL cholesterol is caused by the decreased HDL acception of free cholesterol from the peripheral cell membranes due to the impaired complexation of PL with free cholesterol and associated the altered PL composition of the superficial monolayer of a lipoprotein particle. At the same time the physicochemical changes in Hdl superficial layer are a cause of abnormal free cholesterol esterification and the impaired plunge of esterified cholesterol into the nucleus of a HDL particle, which facilitates the conversion of HDL to LDL and may explain elevated LDL levels in cholesterosis. The findings suggest that serum lipids are involved in the development of cholesterosis.

Adolescent↗
PubMed1990

[Diagnostic possibilities of mathematical analysis in the evaluation of lithogenicity of the bile].

A simple modification of the triangulation system is suggested for determination of lithogenous potential of bile. Basing on correlation analysis the regression equation is derived for quantitation of total bile acids. This makes time-consuming chromatographic evaluation of bile needless. It is believed sufficient to specify only two parameters (bile acids and cholesterol) as their correlation in a coordinate system allows one to define the zone of cholesterol saturation of bile. A table is presented to simplify calculations.

Bile↗
PubMed1989

[Lithogenic properties of bile in cholelithiasis].

To specify lithogenic properties of bile in cholelithiasis as well as the effect of cholecystectomy on biochemical composition of bile, 168 patients with cholelithiasis have been examined. Fifty patients underwent preoperative investigation, some of them were followed up for 1-2 years after cholecystectomy (group 1). The rest postcholecystectomy patients were followed up for 10 years (group 2). Bile levels of cholesterol were evaluated by absolute and relative lipid concentrations. The conclusion is made on the absence of a direct correlation between bile cholesterol supersaturation and cholelithiasis as the above supersaturation occurs in healthy subjects as well. It is noticed that cholecystectomy does not warrant discontinuation of cholesterol supersaturation of bile.

Bile↗