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Embrotoxic and teratogenic effects of carbendazim were examined in Wistar rats for the product containing 98% a.i. of carbendazim and diaminophenazine contamination level of 1,1 ppm. The compound was administered by the oral route to pregnant rats during the organogenetic phase of gestation at doses: 0; 15, 30, 45 mg/kg b.w. and in the other group in diets at the concentration 2000 ppm. We found that carbendazim was teratogenic in rats if administered by the oral route but no incidence of fetuses malformations was observed when carbendazim was given in the diet.
Effects of thiram on the process of disturbances of development in consequence of transplacentar exposure were studied in rats. Analysis was performed in descendants born by females exposed to thiram (orally by gavage) for the first time pregnancy and born by females from third generation exposed to the fungicide (multigeneration exposure by food with thiram). In the conditions of two experiments no defects of development were found, only at highest doses embriotoxic effect of the examined compound was observed.
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WWOX, the tumour suppressor gene affected in multiple cancers

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WWOX is a tumour suppressor gene affected in multiple cancers, especially in breast, prostate and ovary. This gene is located at the chromosomal area 16q23.3-24.1, which was identified as a common chromosomal fragile site FRA16D. WWOX turned out to possess tumour suppressor features despite the fact that the most basic (classical) way of tumour suppressor gene inactivation involves both alleles (e.g. through deletions, point mutations and promoter methylation), which is very rare event in a case of WWOX, occurring only in few cell lines. A large number of papers corroborate the phenomenon of correlation between the loss of WWOX expression and more aggressive/worse prognosis in many different types of tumours, for example breast cancer, non-small cell lung cancer, bladder cancer, gastric cancer or sporadic meningiomas. Ectopically increased WWOX expression promotes migration through basal membrane, however suppresses anchorage independent growth and induces normal-like colony formation in matrigel.
The molecular determination of viral load in the serum represents the most valuable prognostic marker of HBV infection. In this paper, a new molecular assay for the quantitative measurement of HBV presence is described. It is based on PCR performing with a HBV-specific competitor DNA template. For the construction of the DNA template, a HBV DNA-originated 436 bp DNA fragment was modified by introducing a 110 bp deletion and cloned into pUC19. The resulting vector serves as the competitor DNA template in the competitive PCR. Post-PCR, the competitor DNA generates an amplified fragment of 306 bp; it could be easily distinguished from the product generated from the viral-originated DNA product (416 bp) when the same primers are used. The quantitative ratio between the two products enables the quantitative determination of viral load. The range of the HB-PCR assay is from 3 x 104 to 6 x 1010 particles/ml. A serum HBV load determination performed by HB-PCR assay indicated a close correlation with the results of the Quantiplex HBV DNA assay (bDNA). The HB-PCR assay is cheap, reliable and easy to use in any laboratory working with PCR methods.
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