[en] Energy needs and concerns in the construction industry are mainly focused on energy savings, characterized by research for new insulation products. Automotive industry, for example, has already overgrown this level of energy performance of their products and fuel economizing is not carried out only through new engine design but also through new aerodynamic lines of vehicles aimed at reducing air resistance. The construction product industry, which, in financial terms, is quite capable to address the issue of energy savings and which benefits from these inventions, has no possibility to interfere in the form of buildings and relations between them. This is something architects and urban planners deal with. This is the subject of this paper, with emphasis on what has been accomplished so far in this regard in the so called developed countries, in comparison with others, where the issues of energy saving are even more difficult to tackle. (author)

[en] Eighty-four biopsies derived from cervical tissues were analyzed for the presence of human papillomavirus (HPV) DNA types 6, 16 and 18 using Southern blot hybridization. HPV 6 was found in none of the cervical biopsies, and HPV types 16 and 18 were found in 44% of them. The rate of HPV 16/18 positive samples increased proportionally to the severity of the lesion. In normal tissue there were no positive samples, in mild and moderate dysplasia HPV 16/18 was present in 20% and in severe dysplasia and invasive carcinomas in 37 and 50%, respectively. In biopsies from 13 cases with squamous cell carcinoma of the uterine cervix and CIN III lesions HPV 16 was integrated within the host genome. It was concluded that the virus could be integrated at variable, presumably randomly selected chromosomal loci and with different number of copies. Transcription of HPV 16 and 18 was detected in one cervical cancer in HeLa cells, respectively. These results imply that HPV types 16 and 18 play an etiological role in the carcinogenesis of human cervical epithelial cells. (author)

[en] Multiple fractions of gamma rays (0.5 Gy daily, 30 fractions) had previously been found to change the sensitivity of human cervical carcinoma HeLa cells to anticancer drugs. Preirradiated cells became resistant to cisplatin, methotrexate and vincristine but retained the same sensitivity to gamma rays and ultraviolet light. Some mechanisms involved in the resistance of preirradiated cells to cisplatin and vincristine were determined, i.e. the increased levels of metallothioneins and increased expression of plasma membrane P glycoprotein. As recent reports indicated that the resistance to cisplatin and ionizing radiation may involve the expression of oncogenes, the problem was studied whether multiple fractions of gamma rays can change the expression of c-myc and c-Ki-ras oncogenes in HeLa cells and whether there is a correlation between the expression of these oncogenes and the sensitivity of preirradiated cells to cisplatin and gamma rays. The expression of c-myc and c-Ki-ras oncogenes was examined using the DNA dot blot, the RNA dot blot and Northern blot analysis. The results show that preirradiation induced neither amplification nor elevated expression of c-myc and c-Ki-ras oncogenes. Furthermore, there is no correlation between the expression of c-myc and c-Ki-ras oncogenes and the acquired resistance to cisplatin. (author) 3 figs., 32 refs

[en] Cell-radioresistance has two important practical aspects. In radiation protection, radiation resistance is welcome and beneficial. Contrary to that, the radioresistance of tumor cells is negative, because it cause the failure in radiotherapy. Although this phenomenon has been known for a long period of time, molecular, cellular and biological basis of radioresistance has not still been elucidated. The aim of present study was to examine some of the potential molecular mechanisms that could be involved in resistance of human larynx carcinoma cells to gamma rays. For this purpose five cell lines were used: parental HEp2 and CK2 cells, which exert similar radiosensitivity, radioresistant CA3 cells and radiosensitive VA3 and VK cells. In these cells the expression of c-myc and c-Ki-ras oncogenes was determined due to RNA dot blot and Northern blot analyses. The relative content of metallothioneins was determined indirectly due to cell-survival after the treatment with cadmium. Our results show that the expression of c-myc and c-Ki-ras oncogenes was similar in all five cells lines, independent on their radiosensitivity. Similarly, the relative content of metallothioneins did not correlate with the radiosensitivity of examined cell lines. Therefore we can conclude, that neither c-myc and c-Ki-ras oncogenes nor metallothioneins are the cause of radioresistance, at least in examined cell lines. Further investigations are needed to elucidate the mechanisms responsible for radioresistance of CA3 cells. (author)