Etude theorique et methodologique du phenomene de demande biologique en oxygene

We establish a Biological Oxygen Demand, BOD, model in a pure culture during growing phases. This model, exprimed in reduced coordinates, is used to do a methodologic study of the BOD measure on urban and industrial effluents and on river waters. The different types of curves observed are described using dimensionless numbers. We study the influence of the method used and of the initial concentration in present or introduce micro-organisms on the numerical value of result obtained for a limited period (5 days).

We show that this model corresponds for weak values of the dimensionless number n, to the FAIR's model of first pseudo order. The dimensionless number n represent the ratio between the initial substrate concentration and the substrate equivalent of the biomass initially present.     

Kainate-induced hippocampal DNA damage is attenuated in superoxide dismutase transgenic mice

Peripheral administration of kainic acid (KA) can cause cell death in the hippocampus of rodents. This is thought to involve oxidative stress. In the present study, we tested the possibility that KA-induced neuronal cell death might be attenuated in CuZn superoxide dismutase transgenic (SOD-Tg) mice. Acute administration of KA causes animal death in a dose-dependent fashion; this was attenuated in SOD-Tg mice. Similarly, KA caused dose-dependent neuronal cell death in the hippocampus of wild-type mice; this cell death was attenuated in the SOD-Tg mice, in a gene-dosage-dependent fashion, with homozygous mice showing complete protection even at the highest dose (45 mg/kg) of KA used in this study. These results provide further support for the involvement of oxygen-based radicals in the toxic effects of KA.     

Oxidatively generated damage to the guanine moiety of DNA: mechanistic aspects and formation in cells

Nuclear DNA and other molecules in living systems are continuously exposed to endogenously generated oxygen species. Such species range from the unreactive superoxide radical (O2*-)the precursor of hydrogen peroxide (H2O2)to the highly reactive hydroxyl radical (*OH). Exogenous chemical and physical agents, such as ionizing radiation and the UVA component of solar light, can also oxidatively damage both the bases and the 2-deoxyribose moieties of cellular DNA. Over the last two decades, researchers have made major progress in understanding the oxidation degradation pathways of DNA that are most likely to occur from either oxidative metabolism or exposure to various exogenous agents. In the first part of this Account, we describe the mechanistic features of one-electron oxidation reactions of the guanine base in isolated DNA and related model compounds. These reactions illustrate the complexity of the various degradation pathways involved. Then, we briefly survey the analytical methods that can detect low amounts of oxidized bases and nucleosides in cells as they are formed. Recent data on the formation of oxidized guanine residues in cellular DNA following exposure to UVA light, ionizing radiation, and high-intensity UV pulses are also provided. We discuss these chemical reactions in the context of *OH radical, singlet oxygen, and two-quantum photoionization processes.     

Effect of dopamine receptor antagonists on cocaine subjective effects: a naturalistic case study

Schizophrenic patients on neuroleptic medications abuse cocaine and report cocaine-induced euphoria. This study was undertaken to provide better clinical characterization of these phenomena by administering the POMS and a custom-designed questionnaire. A group of heavy cocaine users who were not mentally ill served as the control group. The results clearly suggest that schizophrenic patients report cocaine-induced euphoria and post-use craving despite being treated with therapeutic doses of haloperidol or fluphenazine. The responses of the control group were similar to that of the schizophrenic group except that the latter subjects reported a greater degree of anxiety. These results suggest that blockade of D2 receptors is not sufficient to block cocaine-induced subjective effects in humans.     

Isolation and characterization of a new product produced by ionizing irradiation and type I photosensitization of 2'-deoxyguanosine in oxygen-saturated aqueous solution: (2S)-2,5'-ANHYDRO-1-(2'-deoxy-beta-D-erythro-pentofuranosyl)-5-guanidin ylidene- 2-hydroxy-4-oxoimidazolidine

A major product of the radiation-induced decomposition of 2'-deoxyguanosine in oxygen-saturated aqueous solution has been isolated by reverse phase high performance liquid chromatography and characterized by carbon and proton NMR spectroscopy, fast-atom bombardment mass spectrometry, and chemical analysis as (2S)-2,5'-anhydro-1-(2'-deoxy-beta-D-erythro-pentofuranosyl)-5-guanid inylidene- 2-hydroxy-4-oxoimidazolidine(d < G). This compound is stable in aqueous solution at room temperature but decomposes upon heating (45 degrees C). The lesion is also observed following type I (riboflavin, benzophenone, and acetophenone) photosensitized irradiation of 2'-deoxyguanosine at 350 nm in oxygen-saturated aqueous solution. A similar reaction mechanism, involving a neutral guanine radical intermediate, is proposed to explain the generation of d < G following both types of irradiation.     

Tensile Behavior of Air Plasma Spray MCrAlY Coatings: Role of High Temperature Agings and Process Defects

Metallurgical and Materials Transactions A - $$\beta $$-$$\gamma $$ MCrAlY coatings generally exhibit a brittle mechanical behavior below 600 °C. When exposed at elevated temperatures, the...     

Ductile fracture of materials with randomly distributed voids

International Journal of Fracture - A reliable determination of the onset of void coalescence is critical to the modelling of ductile fracture. Numerical models have been developed but rely mostly...     

Synthesis and enzymatic processing of oligodeoxynucleotides containing tandem base damage

Several studies have shown that ionizing radiation generates a wide spectrum of lesions to DNA including base modifications, abasic sites, strand breaks, crosslinks and tandem base damage. One example of tandem base damage induced by @OH radical inX-irradiated DNA oligomers is N -(2-deoxy-beta-d- erythro -pentofuranosyl)-formylamine/8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo). In order to investigate the biological significance of such a tandem lesion, both 8-oxo-7,8-dihydroguanine and formylamine were introduced into synthetic oligonucleotides at vicinal positions using the solid phase phosphoramidite method. For this purpose, a new convenient method of synthesis of 8-oxodGuo was developed. The purity and integrity of the modified synthetic DNA fragments were assessed using different complementary techniques including HPLC, polyacrylamide gel electrophoresis, electrospray and MALDI-TOF mass spectrometry. The piperidine test applied to the double modified base-containing oligonucleotides revealed the high alkaline lability of formylamine in DNA. In addition, various enzymatic experiments aimed at determining biochemical features of such multiply damaged sites were carried out using the synthetic substrates. The pro-cessing of the vicinal lesions by nuclease P1, snake venom phosphodiesterase, calf spleen phospho-diesterase and repair enzymes including Escherichia coli endonuclease (endo) III and Fapy-glycosylase was studied and is reported.     

Effects of toxic doses of methamphetamine (METH) on dopamine D1 receptors in the mouse brain

Methamphetamine (METH) is a drug of abuse that causes marked DA depletion in the mammalian dopaminergic systems. These are characterized by marked decreases in presynaptic markers including dopamine (DA) levels and DA transporters. Very little research has been carried out to evaluate possible postsynaptic effects of this drug. In the present study, we assessed the status of METH on striatal DA D1 receptors labeled with [3H]SCH23390 after toxic doses of METH that were shown to cause marked depletion of various markers of presynaptic DA systems in mice [J. Neurochem. 69 (1997) 780]. Our results show that these doses of METH caused 30% decrease in striatal DA D1 receptors. In contrast, p53 knockout mice that show protection against the toxic effects of METH show no significant decreases in DA D1 receptors. These results suggest that toxic doses of METH that cause loss of presynaptic DA markers might also affect postsynaptic elements. We discuss the possibility that these changes might be secondary to toxic effects of METH on intrinsic striatal cell bodies.