[Nonverbal mention communication 1 (author's transl)].
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Two different hypotheses in modern physics according to which protons might disappear are discussed: Gravitational collapse of matter into black holes, and proton decay according to Unified Gauge Theories. The latter might soon be observed in experiments in which sensitive detectors are placed in a mass of 1000 tons of matter (10(33) protons) in a deep tunnel or mine. One hundred observed decays per year would correspond to an "expected lifetime" of 10(31) years for an individual proton, as predicted by these theories.
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Using a specially designed program, the authors managed to obtain dose distributions in irradiation by a rotation method in two planes of small intracranial targets with narrow photon beams (up to 1cm) with the energy of 0.2; 1.25; 15MeV. It has been shown that though these distributions less correspond to clinical requirements than those for proton beams the use of narrow photon beams seems promising in this field of radiology.
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The assumption that the formation of pyrimidine dimers in E. coli cells, placed in a transient aqueous medium exposed to gamma-quanta, is conditioned by Cerenkov radiation laid the basis for the development of a biophysical model to explain the photoreactivation effect observed. The dependence of the effect upon gamma-radiation energy and the volume of the exposed suspension is predicted and compared with experimental data.
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A variety of prostaglandins (PG) protect the gastric and intestinal mucosa when given before damaging agents such as absolute ethanol, acidified taurocholate, boiling water, or nonsteroidal anti-inflammatory agents (NSAI). A synthetic prostaglandin, 16, 16-dimethyl PGE2, shown to be cytoprotective at physiologic levels to the above agents was given to mice 1 hr before or 15 min after 137Cs gamma (gamma) whole-body irradiation. The survival of intestinal stem cells measured by their ability to form in situ colonies of regenerating epithelium was increased when 16, 16-dimethyl PGE2 was given before but not after 137Cs gamma irradiation. The maximum degree of 16, 16-dimethyl PGE2-induced radioprotection was seen when the drug was given 1 hr before irradiation. No radioprotection was seen when the interval between drug and irradiation was 3 hr or longer. When the time between 16, 16-dimethyl PGE2 and irradiation was kept at 1 hr, the degree of radioprotection was dependent on the PG drug dose. There was a steep rise in the number of surviving cells at low doses of PG. These results imply that tumors which secrete PGE2 may in part be protected from the lethal effects of ionizing photon radiation.
Two different sets of Monte Carlo computations were carried out for the study of dose penetration of monoenergetic, low-energy (10 to 100 keV) photon beams incident on slabs of tissue. One program took into account coherent scattering and considered electron binding when finding the angle of scattering during incoherent scattering; the other simpler program, customarily used at higher energies, largely ignored these effects. For calculations at the source photon energy of 100 keV, it was found that there was negligible difference in dose distribution in the slab between the more and less complex type of calculations. The same thing was found to be true for the 30 and 10-keV source photon energies only for shallow penetration distances; and at deeper penetrations the simple approach tended to overestimate the dose appreciably. It is concluded that for penetration of low-energy photon beams into tissue, accurate calculational results cannot be assured with the neglect of coherent scattering effects and electron binding considerations in determining the scattering angles except for shallow depths of penetration.
Between 1974 and 1981 a group of 234 patients with generally advanced regional cancers were treated with pions at the Los Alamos Meson Production Facility (LAMPF). As of May 1983, 53 patients remained alive of which 31 were examined. Records on these and others were reviewed in order to assess some late effects of pion therapy. In judging clinical RBE values there appeared to be no difference between acute and late effect RBE's. Complications were clearly dose-related and significantly greater in patients who received additional local photon irradiation and/or surgery. Tumor control also appeared dose related but difficult to assess because of a wide range of fractionation numbers.
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Responses to photon irradiation of xenografted human colon tumors derived from the heterogeneous DLD-1 line or its derivative A and D subpopulations were determined using excision assay and tumor regrowth delay assays. Differential responses among the three xenografted carcinomas were demonstrated. Clone A tumors treated with up to 17.5 Gy showed no actual regression below pretreatment volume. In contrast, clone D tumors were sensitive to doses as low as 3.5 Gy, and tumor volumes were reduced by 65% with a dose of 17.5 Gy. The responses of DLD-1 tumors were intermediate between the clone A and clone D tumor responses. The survival parameters obtained in the excision assay studies for the DLD-1, clone A, and clone D tumors were, respectively: n = 3.3, 1.4, and 1.0; D0 (Gy) = 2.1, 2.2, and 2.7; and DQ (Gy) = 2.6, 0.6, and 0.0. These data indicate that the DLD-1 tumors were the most resistant, with clone A of intermediate sensitivity, clone D being the most sensitive tumor. In addition to the interclonal diversity among xenograft lines, intraclonal variation was also observed with clone A (but not clone D or DLD-1) tumors. A biphasic survival curve of cells from clone A xenografts irradiated in air-breathing hosts clearly indicated a minority (approximately 3%) subpopulation of hypoxic cells. Similar results indicating a small percentage of hypoxic cells in clone A solid tumors were obtained from the tumor regrowth delay studies. Also, excision assay data from experiments in which the heterografted carcinomas were irradiated under anoxic conditions support the interpretation that clone A tumors contain a small fraction of hypoxic cells. This study indicates that: (a) heterogeneity in vivo to ionizing radiation exists in the DLD-1 system; and (b) intraclonal variation occurs in vivo due to extrinsic (e.g., environmental hypoxia) factors, such that the intrinsic radioresistance of a subpopulation (clone A) of a heterogeneous human tumor can be further increased.
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