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Biomedical subjects

L V Kuznetsova

Publications and source records attributed to L V Kuznetsova.

At least 55 records · Page 3Linked to original sources
PubMed1985

[Mutagenic effect of o-methylhydroxylamine on the prophage and extracellular phage lambda].

Induction of c-mutations in extracellular bacteriophage and prophage lambda cI857 ind-treated with 1 M O-methylhydroxylamine (OMHA) at 32 degrees and pH 5.6 has been studied. The frequency of c-mutations increases proportionally to the time of treatment of extracellular phage and does not depend on cellular recA+ or polA+ functions and on induction of SOS-repair system caused by UV-irradiation of host cells. Prophage is inactivated and mutagenized approximately 10-fold faster than extracellular phage immediately after treatment of lysogenic cells during prophage induction. Thus, prophage survival does not depend on repair functions of the host cells, and the frequency of c-mutations in recA and, especially, in polA lysogens is significantly lower, than in the wild-type cells. Delayed thermoinduction (90 min) of prophage causes significant enhancement of survival and decreases the frequency of c-mutations in all strains studied. Preliminary treatment of non-lysogens with OMHA does not increase the frequency of c-mutations in undamaged phage or in phage treated with OMHA in vitro.

Bacteriophage lambda↗
PubMed1985

[Assessment of peripheral blood monocyte function in pulmonary tuberculosis patients].

As the result of the study of the peripheral blood monocyte function in patients with pulmonary tuberculosis, the ingestive capacity of monocytes has been found to be suppressed, which indicates the pathological state of oxygen-dependent mechanisms governing the bactericidal activity of cells, the most pronounced disturbances of monocyte functions being observed in patients with fibrous-cavernous and disseminated tuberculosis.

Adult↗
PubMed1984

[Mutagenic action of alkylating agents on prophage lambda].

The lethal and mutagenic effects of 7 alkylating agents: N-nitroso-N-methylurea (NMU), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), methyl methanesulfonate (MMS), ethyl methanesulfonate (EMS), nitrogen mustard (HN2), mitomycin C (MC), bifunctional acridine mustard (AM)--and of cyanate (KNCO) on heat inducible lambda cI857 prophage were studied. After treatment of lysogenic cells with mutagens, prophage was heat-induced either immediately or after 90 min incubation in nutrient broth and c mutants forming clear plaques at 32 degrees C were scored. NMU (0.02 M) when immediately induced with heat, induces c mutants very efficiently (maximal yield 10%) not only in the wild-type cells but also in repair-deficient mutants recA13, lexA102, uvrA6 umuC36, recF143, xthA9, polA1, uvrD3 and uvrD502. These data show that NMU-induced mutations are fixed as replication errors due to mispairing modified bases. After delayed heat induction, the prophage survival enhances and the frequency of c mutations declines considerably in host cells of all repair genotypes tested. Carbamoylation is not involved in the mutagenic action of NMU, because KNCO (0.02 M) has a very slight lethal effect and does not induce mutations. MNNG (100 micrograms/ml) and EMS (0.1 M) also induce mutations by replicative mechanism, because maximal yield of c mutations does not depend on RecA+ and is about 15 and 2%, respectively. MMS is a mutagen of the repair type, since its mutagenic action is suppressed by recA mutation of the host. NH2 only inactivates prophage, but does not induce mutations. MC (50 micrograms/ml) and AM (150 micrograms/ml) induce mutations rather inefficiently (the maximal yield 0.1 and 0.3%, respectively) both in recA+ and recA- hosts. The mutagenic action of these agents is probably due to intercalation.

Alkylating Agents↗
PubMed1984

[Determination of alveolar macrophage function in nonspecific lung diseases by the simultaneous estimation of phagocytosis and acid phosphatase activity].

The aim of this investigation was to increase the accuracy of the determination of the functional activity of alveolar macrophages with phagocytic functions, isolated from bronchial washings, to reduce the time necessary for this determination and to compare the results thus obtained with the clinical signs of the disease. 46 patients with nonspecific pulmonary diseases were examined. The method of the simultaneous evaluation of the phagocytic activity of alveolar macrophages and the level of acidic phosphatase activity during phagocytosis was found to ensure greater accuracy in the determination of the functional activity of alveolar macrophages and to reduce the time necessary for the evaluation of the reaction by 1.5 hours. In patients with non-specific pulmonary diseases the phagocytic activity of alveolar macrophages decreased, which was accompanied by a lower level of acidic phosphatase consumption.

Acid Phosphatase↗
PubMed1982

[Mutagenic action of nitrous acid on prophage lambda].

The lethal and mutagenic effects of nitrous acid (0,1 M NaNO2 in 0,1 M acetate buffer, pH 4.6) on prophage lambda cI857 ind- were studied in the wild-type cells of Escherichia coli and in 9 repair-deficient mutants: uvrA6, uvrA6 umuC36, uvrD3, uvrE502, polA1, recA13, lexA102, recF143 and xthA9. After treatment with HNO2, the prophage was heat-induced either immediately or after 90 min incubation in broth at 32 degrees C. The prophage survival after delayed induction was considerably higher than after immediate induction. The lethal action of HNO2 was highly expressed in uvrA- and uvrE- lysogens after delayed induction. The frequency of temperature-independent c mutants forming clear plaques at 32 degrees C reached 4% in the wild-type host after immediate induction, this value being 10-15% in uvrA, uvrA umuC, uvrD, uvrE, polA and xthA mutants, 0,8% in recF- lysogen and only 0,2-0,3% in recA and lexA mutants. Under these conditions, about 90% of c mutants are generated by recA+, lexA+-dependent repair mechanism (most probably, due to W-mutagenesis). After delayed induction, mutation frequency in the wild-type host declines considerably (down to 0,1%). Analogous phenomenon of mutation frequency decline was registered in uvrA, xthA, recF, polA, uvrE and uvrD lysogens. Under conditions of delayed induction, the frequency of HNO2-induced c mutations only slightly depends on the recA+ and lexA+ gene products and mutations are, apparently, fixed by replication.

Bacteriophage lambda↗
PubMed1982

[Functional maturation of the human corticotropin releasing factor-adrenocorticotropic hormone system during intrauterine life. An in vitro study].

Radioimmunoassay was used to determine ACTH secretion by cultured hypophyses of human fetuses from the 6th to the 30th week of intrauterine life and their responsiveness to hypothalamic extracts obtained from adult animals. CRF-like activity in the human hypothalamus was measured within the 6th to the 32nd week of prenatal development from changes in ACTH release by cultured cells of the adult rat hypophysis. It was established that starting from weeks 6-7 of embryogenesis, the human fetal hypophysis is capable of synthesizing and secreting immuno-reactive ACTH in vitro. The human fetus hypothalamus of the first trimester of gestation contained no CRF-like substance. The fetus hypothalamus of the second and third trimesters of pregnancy manifested a considerable amount of CRF-like substance. It is suggested that CRF appears at the end of the first trimester of pregnancy.

Adrenocorticotropic Hormone↗
PubMed1981

[Level of immunoreactive adrenocorticotropic hormone in the pituitary gland and blood of humans during prenatal development].

The levels of immunoreactive ACTH were determined in 109 pituitaries and in serum of human fetuses from the 7th to the 34th week of intrauterine life, and in serum of 7 infants. ACTH in the pituitary is detectable for the first time in a 7-week-old embryo. The mean content and concentration of ACTH in the pituitary significantly increases twice: between weeks 7-13 and between weeks 17-34, with a peak at the 34th week. Immunoreactive ACTH is detectable in serum from the 12th week of gestation. A significant rise was recorded at the 24th week, with maximum being reached by the 34th week. Serum ACTH decreases more than 10-fold by the time of the term as compared with that by the 34th week. The data obtained suggest that the pituitary of man starts ACTH synthesis from the 7th week and secrets it into fetal blood from the 12th week of prenatal development.

Adrenocorticotropic Hormone↗