[Prostatic brachytherapy indications and technique]. / Indicaciones y técnica de la braquiterapia prostática.

Prostate cancer is an important health problem, mainly in elderly men. It is the second cause of death among men in USA ant the third at the "Registro del Cáncer de Tarragona", behind both the lung and colorectal cancer. About the 58% of the newly diagnosed cancers are localized, therefore, they have to be treated with curative intention. Radical prostatectomy is considered the gold standard treatment for organ confined prostate cancer in our country. On basis to the experience of American groups and the improvement of both, image techniques and dosimetric calculation, brachytherapy has been brought in as a new option in the treatment of localized prostate cancer. We started our program of brachytherapy for prostate cancer on May 2000. We have performed 51 procedures by now. Our protocol and the technique to perform a prostatic brachytherapy are described following.

Selective c-Jun overexpression is associated with ionizing radiation-induced apoptosis in the developing cerebellum of the rat.

Immunohistochemistry to Bcl-2, Bax, c-Myc, c-Fos, Fos-related, c-Jun, Jun B and Jun D was used to study the involvement of these factors in ionizing radiation-induced apoptosis in the cerebellum of the developing rat. Selective c-Jun overexpression was observed during the whole process of radiation-induced cell death. Furthermore, c-Jun overexpression was restricted to apoptotic cells, as shown by double labeling with the method of in situ labeling of nuclear DNA fragmentation and c-Jun immunohistochemistry. This is the first in vivo evidence that selective c-Jun overexpression is associated with apoptotic cell death in the developing nervous system following ionizing radiation.

Cell death induced by gamma irradiation of developing skeletal muscle.

Newborn Sprague-Dawley rats were exposed to a single dose of 2 Gy gamma rays and killed from 6 h to 5 d later. Increased numbers of dying cells, characterised by their extreme chromatin condensation and often nuclear fragmentation were seen in skeletal muscle 6 h after irradiation. Dying cells decreased to nearly normal values 48 h later. In situ labelling of nuclear DNA fragmentation identified individual cells bearing fragmented DNA. The effects of gamma rays were suppressed following cycloheximide i.p. at a dose of 1 microgram/g body weight given at the time of irradiation. Taken together, the present morphological and pharmacological results suggest that gamma ray induced cell death in skeletal muscle is apoptotic, and that the process is associated with protein synthesis. Finally, proliferating cell nuclear antigen-immunoreactive cells, which were abundant in control rats, decreased in number 48 h after irradiation. However, a marked increase significantly above normal age values was observed at the 5th day, thus suggesting that regeneration occurs following irradiation-induced cell death in developing muscle.

Amoeboid microglial response following X-ray-induced apoptosis in the neonatal rat brain.

The phagocytic response following X-ray-induced apoptosis in the neonatal rat brain was examined by immunohistochemistry with the antibodies OX-6 and OX-42 which recognize MHC class II antigens and the CR3 complement receptor, respectively. Few OX-6-immunoreactive cells were observed in control rats, and in rats irradiated at postnatal day 2 and examined during the first 2 postnatal weeks. However, a transient increase in the number of OX-42-immunoreactive amoeboid microglia, containing large numbers of apoptotic cells, occurred at 6, 24 and 48 h after irradiation when compared with age-matched controls. These results show that X-ray-induced apoptosis promotes a short-lasting phagocytic response.

Evidence of internucleosomal DNA fragmentation and identification of dying cells in X-ray-induced cell death in the developing brain.

Newborn Sprague-Dawley rats received a single dose of 2 Gy X-rays and were killed 6 hr later. Dying cells were characterized by extreme chromatin condensation and nuclear fragmentation. Dying cells were distributed in the primary and secondary germinal zones and in other brain regions. Among these latter, dying cells occurred in the cortical layers of the olfactory bulb, layers II-III and VIb of the neocortex, piriform and entorhinal cortex, stratum oriens and pyramidale of the hippocampus, striatum, thalamus, amygdala, brainstem, internal granular layer of the cerebellum, and cerebral and cerebellar white matter. Dying cells were immature cells, neurons and glial cells (including radial glia). In-situ labeling of nuclear DNA fragmentation identified individual cells bearing fragmented DNA. Since the number of cells stained with this method was larger than the number of dying cells, as revealed with current histological techniques, it is suggested that nuclear DNA fragmentation precedes chromatin condensation and nuclear fragmentation in X-ray-induced apoptosis. Furthermore, agarose gel electrophoresis of extracted DNA from irradiated brains showed a "ladder" pattern which is typical of internucleosomal DNA fragmentation and endonuclease activation.

Structure and pathogenesis of cortical nodules induced by prenatal X-irradiation in the rat.

Segmentation of the cerebral cortex with formation of nodules, predominating in the upper cortical levels, was found in the rat after 200 cGy X-ray exposure at embryonic days 15, 17 or 19. Nodules were composed of pyramidal and nonpyramidal neurons occupying normal positions at different levels of the cerebral cortex as revealed with parvalbumin and calbindin D-28k immunocytochemistry. The nodules, which were large in animals irradiated at embryonic day 15 but reduced to groups of a few cells in rats irradiated at embryonic day 19, were separated by low cell density zones. Autoradiographic studies using tritiated methylthymidine injections given to pregnant irradiated rats at different days of gestation further demonstrated a preserved inside-out gradient of cortical neurogenesis in this cortical malformation. Morphological studies of irradiated embryos disclosed that groups of dead cells were separated by patches of preserved cells in the germinal layer 6 h after irradiation. Columns of migrating neuroblasts separated by low cell density zones were seen 24 h later. These features suggest that cortical nodules observed after prenatal X-irradiation were the result of multifocal cell death in vulnerable (at the moment of X-ray exposure) proliferative units of the germinal neuroepithelium, combined with normal neurogenesis and migration of neuroblasts from the preserved germinal zones. These findings also suggest that cell proliferation is not uniform through the germinal layer but occurs synchronously in alternate proliferative units. These proliferative units probably co-generate pyramidal and nonpyramidal cells.

Neuronal ectopic masses induced by prenatal irradiation in the rat.

Ectopic neuronal masses below the subcortical white matter were seen in the brains of postnatal rats after 200 cGy irradiation at embryonic day 14. In contrast with the laminated organisation of the cortex located above the subcortical white matter, the ectopic masses were formed of confluent nodules composed of pyramidal and non-pyramidal neurons distributed at random, with no laminar organisation. Afferent and efferent fibres to/from the ectopic masses running together with fibres passing the subcortical white matter indicated that the ectopic masses were heavily connected to neighbouring structures. Examination of irradiated embryos revealed that the ectopic masses originated from ectopic periventricular rosettes, composed of germinal cells, which were formed shortly after irradiation. Neuronogenesis in these rosettes did not follow an inside-out gradient, as seen in the laminated cortex; however, early-generated neurons predominated in the external regions, whereas late-generated neurons were mainly located in the middle and internal regions of the ectopic masses.

Total perturbation correction factor for PTW and NACP plane parallel chambers in electron beams.

The international protocols of electron dosimetry published by the Nordic Association of Clinical Physics and the Sociedad Española de Física Médica recommend the use of a total perturbation correction factor pu, pp which is constant for all plane parallel chambers. In this work we have compared the dose measured with the PTW-Markus and NACP plane parallel chambers in respect to a cylindrical one. The obtained results indicate that for the ionization chamber NACP the value of pu, pp = 1.000 +/- 0.005 is adequate while for the ionization chamber PTW the observed difference is explained by considering an individual total perturbation correction factor variable with the mean energy at depth z, Ez, as the fluence perturbation correction factor pf is usually given for cylindrical chambers.