Biomedical subjects
Publications and source records attributed to N A Nikitina.
In vitro experiments showed that copper-oxidized low-density lipoproteins activate factors of the prothrombin complex in the whole blood and inhibit fibrin generation in both blood and plasma. Moreover, oxidized low-density lipoproteins inhibit fibrinolysis and impair the structure of fibrin clot, which results in hypercoagulation.
Before starting treatment of chronic glomerulonephritis it is desirable to determine the patient's drug sensitivity in vitro because in the absence of such sensitivity chemotherapy should be preceded by immunomodulation with tactivin or thymalin and 3-5 sessions of plasmapheresis to stimulate drug sensitivity. Further measures include prednisolone or cyclophosphamide intravenously for 3-5 days in a dose 300-500 followed by oral administration. Active treatment lasts for 4-8 weeks. After that the patients receive maintenance for 1-2 years.
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30 untreated patients with membranoproliferative glomerulonephritis (MPGN) with isolated urinary syndrome were examined for cellular and humoral immunity. There was a significant (p < 0.05) reduction of the number of T-helpers/inductors (T4/4B4) and early undifferentiated lymphoid precursors with the marker enzyme. T-lymphocytes with markers T1, T3, T11, T12 as well as T-suppressors/cytotoxic cells (T8/2H4) occurred in normal quantities. IL-1 and IL-2 production was inhibited. Mature T-lymphocytes with markers T11, suppressors T8, early precursors of T-cells (T6) were higher in number in development of dystrophic changes in tubular epithelium. It is suggested that T-cell factor may be involved in nephron impairment observed in MPGN patients. Humoral immunity disorders are of the secondary nature.
Phenbutol, a Russian analogue of probucol, was studied by the single blind method by using placebo in 30 patients aged 36 to 65 years whose total serum cholesterol levels were more than 250 mg/dl after a month placebo therapy. The patients were divided into two groups: (1) 15 patients on placebo and (2) 15 patients on phenbutol, 500 mg twice a day for 5 months. Blood lipid parameters were monthly determined. The findings are in agreement with the data on the effects of probucol on lipids and its adverse effects. During the follow-up, phenbutol showed 17%, 14% and 10% decreases in total cholesterol and low density lipoprotein cholesterol and high density lipoprotein cholesterol, respectively, as compared with the baselines. These changes were greater than those in patients on placebo. In the first week of therapy with phenbutol, vomiting, appetite decrease, digestive disturbances were observed in 73% of patients. These adverse reactions did not require its withdrawal. Resting ECG Q-T interval became prolonged in 7 out of 15 patients receiving phenbutol (maximum 500 msec).
The lipoprotein (LP) fractions VLDL, LDL, HDL2 and HDL3 were prepared by ultracentrifugation of plasma from healthy volunteers and from patients with coronary heart disease (CHD). We investigated the capacity of platelets from healthy volunteers and patients with atherosclerosis to generate thromboxane A2 (TXA2) during spontaneous clotting of whole blood under the influence of the lipoprotein fractions. In our experiments the serum concentration of TXB2, reflecting the capacity of platelets to generate TXA2 during clotting, depends on several factors: the type of LP fraction used, the blood used for generation of TXA2, and for the same LP fraction whether it was taken from plasma of healthy volunteers or patients with CHD. VLDL prepared from plasma of healthy volunteers inhibited but VLDL prepared from plasma of patients with CHD enhanced the TXA2 formation of platelets from healthy volunteers (p less than 0.05, resp.). LDL from CHD patients inhibited the TXA2 formation of platelets from atherosclerotic patients (p less than 0.01). The HDL subfractions HDL2 and HDL3 from healthy volunteers inhibited TXA2 formation by platelets from healthy volunteers as well as those from atherosclerotic patients (p less than 0.05; p less than 0.01, respectively). HDL2 from patients with CHD inhibited only the TXA2 formation of platelets from healthy volunteers (p less than 0.01), whereas HDL3 from CHD patients inhibited only the TXA2 formation of platelets from atherosclerotic patients (p less than 0.01).
Human and mouse peritoneal macrophages cultured in the presence of the blood serum of patients with documented coronary heart disease showed a 2- to 3-fold rise in levels of intracellular cholesterol ester and a 1.5- to 2-fold increase in those of free cholesterol and triglycerides. This effect was observed in 83% of cases, whereas the serum of healthy subjects induced the accumulation of lipids in macrophages only in 28% of cases. These data accord with previously published observations obtained on smooth muscle cells of human aortic intima. A direct correlation was found between the accumulation of cholesterol in macrophages and in cultured smooth muscle cells of human aortic intima. The accumulation of lipids in macrophages was dose dependent and increased with time. It is assumed that a culture of peritoneal macrophages may serve as a model for identifying an atherogenic potential of patients' blood serum.
The sera of coronary patients with angiographically-documented stenosis of 1 to 3 coronary arteries caused a two-to-fivefold accumulation of intracellular cholesterol in intact human aortic intimal cell culture. This property, qualified as "atherogenic", was exhibited by the sera of 90% of the coronary patients examined (97 males and females, aged 29 to 55 years). Only 20% of normal subjects revealed atherogenic properties in cell cultures. The capacity of the sera to accumulate intracellular cholesterol was unrelated to the levels of total cholesterol, high density lipoprotein cholesterol, apo-B or apo-AI, taken separately, but showed a weak correlation to the apo-B/apo-AI ratio. The sera of coronary patients caused lipid accumulation in human aortic medial smooth-muscle cells and blood mononuclear cells, in human and mouse peritoneal macrophages, but never in human aortic or umbilical vein endothelial cells, nor human embryo fibroblasts.
Coronary angiography and the assessment of blood lipoproteins were carried out in 43 patients with recent (not more than three months old) angina. A rise in cholesterol above 270 mg/dl and/or triglycerides above 200 mg/dl was demonstrated in 19. The level of alpha-cholesterol was below 35 mg/dl in 11 of 24 normolipidemic patients. The apoprotein B/apoprotein AI ratio was above 1.0 in 7 of 13 patients with normal cholesterol levels. Plasma phospholipid composition was disturbed in 4 of 6 patients with normal apoprotein B/apoprotein AI rations. Therefore, atherogenic changes in plasma lipoprotein composition were found in 95% of patients with recent angina.
A combined study of possible atherogenic factors was carried out in 213 males subjected to clinical investigation including selective angiography of the heart's coronary arteries. Two sets of biochemical tests were used: the routine set including the measurement of the plasma lipid spectrum, and a more sophisticated procedure (93 cases) where plasma apoproteins A1 and B, and high-density lipoprotein phospholipid composition were assessed as well. A correlation of biochemical disorders to coronary atherosclerosis could be demonstrated in 68% of cases, using the first set, and in 98% with the second set. Abnormal apoprotein levels and high-density lipoprotein phospholipid composition were found to contribute significantly to lipoprotein atherogenesis even in cases of normolipidemia.
Apoprotein C-II was isolated from human blood plasma by means of column chromatography-gel filtration and DEAE ion exchange chromatography by modified method of Brown et al (1969). Production of antiserum to apoprotein C-II as well as a procedure for rocket immunoelectrophoresis are described for estimation of the apoprotein in blood plasma of men and women of various age, exhibiting different lipid spectra. Content of the apoprotein C-II in blood plasma, estimated by the immunoelectrophoretic procedure, was higher in men as compared with women and correlated with concentration of triglycerides in blood plasma.
The pattern of contact between small terrestrial mammals and tick-borne encephalitis virus was studied in dependence on year, yearly season and the age of the largest animal populations. The animal-virus contact was assessed by the appearance, persistence and loss of antibodies in the animals examined. A total of 9256 sera of small rodents were collected and tested in this study.
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By way of gel double immunodiffusion a certain heterogeneity of low density lipoproteins was observed to manifest itself in an additional band of immunoprecipitation. The incidence of this additional band does not exceed 1/3 of the cases of low density lipoproteins studies in normal individuals, while in those with ischaemic heart disease the additional band is found twice-thrice as often, the highest incidence being noted in patients with ischaemic heart disease and Type IIb hyperlipoproteinemia (93% of cases). The revealed immunochemical heterogeneity of low density lipoproteins was shown to be not connected with the appearance of any new, additional antigen in their structure. Most probably it is attributable to the presence of lipoprotein particles with a quantitatively different protein and lipid composition, probably of intermediate lipoprotein metabolites in blood plasma, or conformation changes in the structure of low density lipoproteins.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.