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Side bands in ¹⁷² Hf
(1977)
In-beam study of ¹⁴⁴ Gd
(1977)
Side bands in ¹⁷² Hf
(1978)
High-spin isomer in ¹³⁷ Ce
(1978)
Band structure in ¹⁹⁰,¹⁹² Au
(1978)
Side bands in ¹⁷² Hf
(1978)
Band structure in ¹⁹⁰,¹⁹² Au
(1978)
In-beam study of ¹⁴⁴ Gd
(1978)
In-beam study of ¹⁴⁴ Gd
(1978)
It has been observed that carcinogenic polycyclic aromatic hydrocarbons (PAH) are present in the atmosphere. Combustion processes are considered the most important sources for PAH. Among these, the burning of coal produces the highest emission, but in cities with high traffic density and low meteorological exchange activities, vehicle emissions determine the immission situation, especially in narrow streets. For estimating the potential health effects caused by PAH, it is sufficient to characterize the emission of PAH with respect to their physical state, concentrations, and, as far as the particulate phase is concerned, size distribution. The size distribution is important for transport phenomena, inhalation, and deposition in the respiratory tract. These parameters mainly depend on the combustion system, on system operating conditions, on the exhaust system, and on exhaust cooling conditions. At exhaust-gas temperatures in the range of ambient air temperatures, almost the whole emission of PAH is made up of particulate matter.
Synthesis of derivatives of the peptide sequence L-pyroglutamyl-L-phenylalanyl-L-aspartyl-glycyl-L-lysyl-glycyl-glycyl-glycine as the antigenic determinant representing the N-terminal non-helical region of the α-2-chain of rabbit skin collagen, and conjugation to two different polypeptide carriers, are described.
Tumour cell death can be evaluated in the living mouse by externally measuring the rate of loss of tumour-bound DNA tracer. By sequentially labelling the tumour-bearing animals with ¹²⁵IUdR and ¹³¹IUdR 50 h apart, the average tumour cells at the time of the second injection are labelled by ¹²⁵IUdR and the euoxic tumour cells are specifically labelled with ¹³¹IUdR. Tumour treatment at this stage of labelling permits the observation of the reaction of euoxic cells and average tumour cells and finally yields data on hypoxic cells and thus on the oxygen enhancement ratio. This information adds to results from tumour control and growth delay.
With this technique effects were analysed of 60-Co γ-rays, cyclotron neutrons (E = 6 MeV), misonidazole (500 mg/kg body wt) and hyperthermia (42°C water-bath), or combinations of these.
Misonidazole (15 min before irradiation) altered the oxygen enhancement ratio by a factor of 1·5 for γ-rays and of 1·1 for neutrons; when evaluated from tumour-growth delay and TCD-50 misonidazole gave a dose modifying factor of 1·47 for γ-rays and of 1·2-1·3 for neutrons.
Based on percentage tumour regression 100 days after treatment, the enhancement ratio from hyperthermia (after irradiation) was 2·75 for γ-rays (at 10 Gray) and 2·2 for neutrons (at 3·2 Gray). For neutrons combined with misonidazole and hyperthermia the ratio was 2·4.
These results demonstrate that effects of neutron irradiation may be modified by electron-affinic substances and/or hyperthermia.