The kinetics of inactivation of six enteric viruses plus simian virus 40 and Kilham rat virus by free available chlorine was studied under carefully controlled laboratory conditions. It was found that the different virus types demonstrated a wide range of susceptibility to chlorine disinfection. The rate of inactivation was greater at pH 6 than at pH 10; however, the relative susceptibilities of the different viruses were affected differently by a change in pH, suggesting that the pH influenced both the species of chlorine present and the susceptibility of the different viruses to chlorine. The presence of potassium chloride also affected the susceptibility of viruses to chlorine.
In order to evaluate the prevalence of human herpesvirus type 7 (HHV-7) in adult blood donors oral lavage fluid, buffy coat, and urine samples from 112 persons were examined by the polymerase chain reaction (PCR) at one time point. In addition, 11 donors were studied longitudinally over 11 weeks. When the results of the initial and the longitudinal study were combined HHV-7 DNA was found in samples from 109 of 112 (97.3%) adult blood donors. On the basis of different sensitivity levels of the first and the nested PCR differences were detected in the viral DNA load in the samples. It was found that lavage fluid regularly carried significantly higher DNA concentrations than buffy coat. Out of 112 donors, 102 (91.1%) and 8 (7.1%) were positive in the first, less sensitive PCR in lavage fluid and buffy coat, respectively (P < .0001). After nested PCR, 107 (95.5%) and 74 (66.1%) were positive in lavage fluid and buffy coat, respectively (P < .0001). Urine samples were found positive only sporadically. The longitudinal study showed that the oral lavage fluid of most of the donors consistently carried HHV-7 over up to 53 weeks, whereas buffy coat samples were positive less often. In conclusion, HHV-7 is found frequently in adult blood donors in the oral lavage fluid and buffy coat, which are, therefore, potential sources of HHV-7 transmission.
Cells of a patient with Turcot's syndrome and of her parents were evaluated for the presence of molecular alterations in the p53 and the Ki-ras gene. Deletions on chromosome 17p, overexpression and point mutations of the p53 gene as well as mutations of the Ki-ras gene were detected in primary and metastatic tumour but not in the germline of the patient nor in her parents.
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