Time calibration of the ANTARES neutrino telescope

The ANTARES deep-sea neutrino telescope comprises a three-dimensional array of photomultipliers to detect the Cherenkov light induced by upgoing relativistic charged particles originating from neutrino interactions in the vicinity of the detector. The large scattering length of light in the deep sea facilitates an angular resolution of a few tenths of a degree for neutrino energies exceeding 10 TeV. In order to achieve this optimal performance, the time calibration procedures should ensure a relative time calibration between the photomultipliers at the level of similar to 1 ns. The methods developed to attain this level of precision are described

The positioning system of the ANTARES Neutrino Telescope

The ANTARES neutrino telescope, located 40km off the coast of Toulon in the Mediterranean Sea at a mooring depth of about 2475m, consists of twelve detection lines equipped typically with 25 storeys. Every storey carries three optical modules that detect Cherenkov light induced by charged secondary particles (typically muons) coming from neutrino interactions. As these lines are flexible structures fixed to the sea bed and held taut by a buoy, sea currents cause the lines to move and the storeys to rotate. The knowledge of the position of the optical modules with a precision better than 10cm is essential for a good reconstruction of particle tracks. In this paper the ANTARES positioning system is described. It consists of an acoustic positioning system, for distance triangulation, and a compass-tiltmeter system, for the measurement of the orientation and inclination of the storeys. Necessary corrections are discussed and the results of the detector alignment procedure are described

Genotoxicity produced by disease and drugs

In humans, DNA damage or genotoxicity may be caused by exposure to outsideagents like radiation, pesticides, combustion of hydrocarbons products as well asantineoplastic drugs. But also DNA damage could be come from inside of the body,determined mainly for excessive free radicals production generated by some diseaseprocess and that their increase exceed the natural defense systems responsible forremoving free radicals. In either case, the important thing is to identify the genotoxicityand try to protect the body, this may as simply as removing the source of exposure orprovide protection against such agents. In this chapter, we address some ways of how it has been identified genotoxiccompounds by direct analyses, basically micronucleogenics ones expressed quantitativelyby number of micronuclei in peripheral blood erythrocytes and micronucleated cells fromoral mucosa, the genotoxicity of some antineoplastic drugs as well as the identification ofsome diseases that are "genotoxic" to the individual that suffers it and that under certainconditions can also result in potentially teratogenic for children to mothers who hadsuffered some of these disorders. © 2009 Nova Science Publishers, Inc. All rights reserved

Genotoxicity produced by disease and drugs

In humans, DNA damage or genotoxicity may be caused by exposure to outsideagents like radiation, pesticides, combustion of hydrocarbons products as well asantineoplastic drugs. But also DNA damage could be come from inside of the body,determined mainly for excessive free radicals production generated by some diseaseprocess and that their increase exceed the natural defense systems responsible forremoving free radicals. In either case, the important thing is to identify the genotoxicityand try to protect the body, this may as simply as removing the source of exposure orprovide protection against such agents. In this chapter, we address some ways of how it has been identified genotoxiccompounds by direct analyses, basically micronucleogenics ones expressed quantitativelyby number of micronuclei in peripheral blood erythrocytes and micronucleated cells fromoral mucosa, the genotoxicity of some antineoplastic drugs as well as the identification ofsome diseases that are "genotoxic" to the individual that suffers it and that under certainconditions can also result in potentially teratogenic for children to mothers who hadsuffered some of these disorders. � 2009 Nova Science Publishers, Inc. All rights reserved

The TP53 16-bp duplication polymorphism is enriched in endometriosis patients

Background/Aim: The TP53 tumor suppressor gene encodes the nuclear phosphoprotein p53, which plays an important role in cell cycle regulation, apoptosis, DNA repair and angiogenesis. The TP53 gene contains common genetic polymorphisms that influence gene activity. Clinical implications of TP53 polymorphisms have been reported for several diseases, including a variety of solid tumors and endometriosis. We evaluated the association of a TP53 duplication polymorphism with endometriosis. Methods: We evaluated the role of the TP53 16-bp duplication polymorphism by comparing the genotypes of 204 healthy women (controls with surgically excluded endometriosis) to the genotypes of 151 women with endometriosis in the Mexican population. Results: The observed genotype frequencies for controls and endometriosis patients were 0.5 and 5% for 16 bp+/+, 11 and 21% for 16 bp+/-, and 88.5 and 77% for 16 bp-/-, respectively. The odds ratio (OR) was 9.8 (95% CI 1.2-446.8; p = 0.01). The association was more evident when we compared the distribution of genotype 16 bp+/+ to genotype 16 bp+/-. In patients with moderate/severe endometriosis, the OR was 4.0 (95% CI 1.6-9.8; p = 0.003). Conclusion: Our data suggest that the 16-bp duplication polymorphism in TP53 contributes significantly to endometriosis susceptibility in the Mexican population. Copyright � 2012 S. Karger AG, Basel

Determination of diesel genotoxicity in firebreathers by micronuclei and nuclear abnormalities in buccal mucosa

Diesel or its derivatives could have aneuploidogenic and/or clastogenic activity. Hence, the genotoxicity of diesel gases has been studied, considering exposure to them as potentially carcinogenic. The results obtained by different authors suggest the need to know the effects of direct and chronic exposure to diesel in humans, as in the case of the street workers called 'firebreathers' who fill their buccal cavity with diesel and then spread it to a burning torch many times during the day in order to give a 'dragon show' for 5 h a day and 6 days a week. The buccal samples of eight firebreathers were collected, processed and scared according to the criterion established by Tolbert et al., 1992 and then compared with positive and negative control groups. The results revealed that diesel was not micronucleogenic although it induces some nuclear abnormalities

Association between the Xba I polymorphism of APOB gene and plasma lipid level in Mexican patients with coronary artery disease

Some studies, that consider polymorphisms of the apolipoprotein B (APOB) gene as risk factors for coronary artery disease (CAD), have reported discordant results. The aim of the present study was to search for associations between plasma lipid profiles with the DNA Xba I polymorphism of the APOB gene in CAD patients diagnosed by angiography (CAD+). In the present study we compared 114 Mexican patients (80 men and 34 women) with CAD+ and 132 control patients (59 men and 73 women) without evidence of ischemia or arterial damage (CAD The frequency of X+/X+ genotype of Xba I polymorphism, in CAD+ group, was 23% (26/114) compared with 8% (11/132) in the CAD- (OR 3.25, p = 0.002). The patients with X+/X+ for the Xba I genotype APOB gene had higher concentration of triglycerides (TG) and VLDL in plasma than CAD- (p < 0.05). The genotype X+/X+ in the CAD had an effect increasing the TG and VLDL plasma levels when compared with individuals with X-/Xand X-/X+ genotypes. The present study indicated that the X+X+ genotype of Xba I polymorphism is associated with CAD+ patients and high plasma levels of TG and VLDL, in the Mexican population

Spontaneous micronuclei in peripheral blood erythrocytes from 35 mammalian species

In this paper we report the results of a study to determine the frequencies of spontaneous micronucleated erythrocytes (MNE) in peripheral blood of 35 mammalian species. The main goal was to find mammals with a high spontaneous frequency of MNE that could, therefore, be good candidates for biomonitoring genotoxic agents in their natural habitat. We obtained 187 peripheral blood samples, but in 13 of the species we could only sample one individual. A wide range in the number of MNE (1/434 to 0/40000 erythrocytes) was observed. Since the number of individuals per species is not high enough, this results should be cautiously considered. The cat, mouse, giraffe, pig, opossum and capuchin monkey seem to be suitable species for biomonitoring for genotoxic events

Association between the Xba I polymorphism of APOB gene and plasma lipid level in Mexican patients with coronary artery disease

Some studies, that consider polymorphisms of the apolipoprotein B (APOB) gene as risk factors for coronary artery disease (CAD), have reported discordant results. The aim of the present study was to search for associations between plasma lipid profiles with the DNA Xba I polymorphism of the APOB gene in CAD patients diagnosed by angiography (CAD+). In the present study we compared 114 Mexican patients (80 men and 34 women) with CAD+ and 132 control patients (59 men and 73 women) without evidence of ischemia or arterial damage (CAD The frequency of X+/X+ genotype of Xba I polymorphism, in CAD+ group, was 23% (26/114) compared with 8% (11/132) in the CAD- (OR 3.25, p = 0.002). The patients with X+/X+ for the Xba I genotype APOB gene had higher concentration of triglycerides (TG) and VLDL in plasma than CAD- (p < 0.05). The genotype X+/X+ in the CAD had an effect increasing the TG and VLDL plasma levels when compared with individuals with X-/Xand X-/X+ genotypes. The present study indicated that the X+X+ genotype of Xba I polymorphism is associated with CAD+ patients and high plasma levels of TG and VLDL, in the Mexican population