Length-independent voltage fluctuations in small devices.
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Biomedical subjects
Publications and source records attributed to A Benoit.
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Treatment of monkey kidney cells with mitomycin C (MMC) 24 h prior to infection with UV-irradiated simian virus 40 (SV40) enhanced both virus survival and virus mutagenesis. The use of SV40 as a biological probe has been taken as an easy method to analyse SOS response of mammalian cells to the stress caused by DNA damage or inhibition of DNA replication. The mutation assay we used was based on the reversion from a temperature-sensitive phenotype (tsA58 mutant) to a wild-type phenotype. The optimal conditions for producing enhanced survival and mutagenesis in the virus progeny were determined with regard to the multiplicity of infection (MOI). Results showed that the level of enhanced mutagenesis observed for UV-irradiated virus grown in MMC-treated cells was an inverse function of the MOI, while enhanced survival was observed at nearly the same level regardless of the MOI. For the unirradiated virus, almost no increase in the mutation of virus progeny issued from MMC-treated cells was observed, while a small amount of enhanced virus survival was obtained. These results show that enhanced virus mutagenesis and enhanced virus survival can be dissociated under some experimental conditions. Enhanced virus mutagenesis, analogous to the error-prone replication of phages in SOS-induced bacteria, was observed, at least for SV40, only when DNA of both virus and host cells was damaged and when infection occurred with a small number of viral particles. We therefore hypothesize that an error-prone replication mode of UV-damaged templates is observed in induced monkey kidney cells.
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Mammalian cells are constantly facing various types of mutagens. However, due to the high complexity of the cell genome, the molecular analysis of mutagenesis has not yet been possible. Therefore, we have used simian virus 40 (SV40) as a biological and molecular probe to characterize mutagenesis at the nucleotide level. By using a reversion assay from a temperature-sensitive phenotype towards a wild-type phenotype, we have analysed mutagenesis induced by u.v.-light and by apurinic sites (Ap sites). We report here experiments allowing us to quantify and to compare the mutagenic efficiency of various DNA lesions measured on the SV40 genome. The Ap sites are very mutagenic in this type of assay. The molecular analysis of u.v.-induced mutagenesis reveals that mutations correspond to single base-pair substitutions always located opposite Py-Py lesions. The mutations are almost equally distributed between transition and transversion types, and between the 5' and the 3' side of the Py-Py targets. These results demonstrate for the first time in animal cells the existence of targeted mutations induced by u.v.-light. We propose therefore, the use of SV40 as an efficient biological and molecular probe for assaying mutagenic pathways in mammalian cells.
In a canine model of acute respiratory failure, the authors investigated acute cardiopulmonary effects of nitroglycerin (TNG) and compared the results with those obtained after phlebotomy. Oleic acid increased intrapulmonary shunt (Qs/Qt) from 7.4 to 31% (P less than 0.001) and decreased (P less than 0.01) cardiac output (CO). In the presence of assumed low-pressure pulmonary edema, TNG was infused to decrease mean blood pressure (BP) by 40%; this was associated with a 26% decrease (P less than 0.05) in CO. Qs/Qt increased from 31 to 42% (P less than 0.01). There was a slight increase (P less than 0.01) in pulmonary vascular resistance (PVR) with TNG, and mean pulmonary artery pressure (PAP) decreased (P less than 0.05). In contrast, when CO was decreased by a similar amount with phlebotomy, mean Qs/Qt did not significantly change. There were similar changes in PVR and PAP and mixed venous O2 tension with TNG and phlebotomy. Accordingly, current results rule out increased flow, increased PVO2, and mechanical alterations in pulmonary vascular pressures as contributory to the increase in Qs/Qt with TNG. Alternatively, the increase in Qs/Qt with TNG may be explained by a direct pharmacologic decrease in pulmonary hypoxic vasoconstriction and/or by nonspecific pharmacologic effects.
Maternal toxoplasma infection was responsible for congenital toxoplasmosis with ocular and cerebral manifestations in the infant. The acquired character of the toxoplasmosis in the 5th month of pregnancy was confirmed by serologic data and isolation of the parasite from the placenta. Five years later, an evolutive chorioretinitis was found in the mother. The toxoplasma origin of the ocular injury was proven by the study of aqueous humor. This case report is compared with the rare similar cases in the literature. The late discovery of ocular impairment is discussed.
The prevention of symblepharon formation in severe ocular burns can be achieved simply, innocuously and economically, by the application of hen's egg allantoic membrane. Three cases of burns caused by tear gas, sulphuric acid and quicklime were treated by this procedure. The operative procedures, including the membrane preparation and dissection techniques, and methods of applying this membrane to the eye are described. The various advantages of this very old technique, which is apparently not very well-known, are discussed.
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An 87-year-old woman underwent surgery for a dermato-fibrosarcoma of the thigh, responsible for hypoglycaemic episodes. There was a high level of NSILP contrasting with a low level of NSILAs. This is the second case where such a finding has been made in a patient suffering from an extra-pancreatic tumour causing hypoglycaemia. The possible aetiological role of NSILP in extra-pancreatic tumours causing hypoglycaemia is discussed.
The survival of UV-irradiated simian virus 40 (SV40) on UV-irradiated monkey kidney CV-1P cells at 33 degrees was increased over survival on unirradiated cells. During this process - called induced-virus reactivation - the progeny virus yielded by UV-irradiated cells had a much higher mutation frequency than did the progeny from unirradiated cells. Mutation rates were quantified by using phenotypic reversion towards wild-type growth of an early (tsA 58) or a late (tsB 201) temperature-sensitive SV40 mutant. Analysis of SV40 revertant genomes indicated that no detectable deletions of additions were responsible for the reversion process. These results suggest that enzymes from UV-irradiated cells are able to replicate UV-irradiated DNA by an error-prone mode of DNA repair. Induced virus reactivation and error-prone replication are probably one of the expressions of SOS functions in mammalian cells.
We report our experience of medical treatment, chiefly based on prolonged artificial ventilation, of 33 preterm infants with PDA and heart failure whose survival rate was 88%. All of them had clinical criteria used by others to indicate surgical ligation of the ductus arteriosus. This conservative approach seems to give better results than surgical ligation, despite a high frequency of bronchopulmonary dysplasia among survivors.
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From this study carried out under sufficiently strict conditions to analyze normal common bile ducts of the third to the tenth decade, with radio-geometric measurement redusurement reducing errors as far as possible, it appears that: a) there is no difference in the frequency and the density of opacification of the bile duct in young or elderly subjects, b) that the radiological diameter of the normal bile duct becomes enlarged with time, according to the formula: (see article) which may be considered in routine clinical practice as a true increase in diameter of about 1 mm per decade. The limits of true diameter of the bile duct, in our experience, were +/- 3 mm at 30 years to +/- 7 mm after 80 years.
The organophosphorus insecticide ethyl-parathion was transformed by rat liver microsomes into metabolites which were bound to calf thymus DNA, in large amount. When the rats were treated by phenobarbital or 3-methylcholanthrene, the metabolite binding to DNA was increased two-fold. By contrast, in the same conditions, the organochlorine insecticides, aldrin, dieldrin and gamma hexachlorocyclohexane (lindane), did not yield metabolites able to bind to DNA and to proteins.
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To analyze the molecular mechanism of mutagenesis in carcinogen-treated mammalian cells, we developed a model system composed of various simian virus 40 (SV40) mutants as a biological probe to detect inducible DNA repair and mutagenesis in carcinogen-treated monkey kidney cells (CV1-P). Results have shown that treatment of cells with UV-light, acetoxy-acetyl-aminofluorene, or mitomycin C, increases the mutagenesis of UV-irradiated SV40 ts mutant measured as a reversion frequency from a thermosensitive phenotype toward a thermoresistant phenotype. This increased mutagenesis is not observed in the case of undamaged virus indicating that we are looking at targeted mutagenesis. The molecular analysis of several revertant genomes indicates that some DNA rearrangements may occur in the revertant genomes but in some cases the reversion site is a single basepair substitution located at positions different from the original thermosensitive mutation, which is still present. The general interpretation of our results leads to the conclusion that carcinogen treatment of monkey cells activates some kind of error-prone replication mode able to better replicate UV-damaged templates but leading to a higher level of mutagenesis. This activity may represent a SOS-like function in mammalian cells.