PubMed · 8949034
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J Espeillac, J Yvon. 1996. [Guiding care plan. Steps in learning].. https://pubmed.ncbi.nlm.nih.gov/8949034/
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There is a familial aggregation of prostate cancer, and 5 to 10% of all prostate cancers are estimated to be inherited in an autosomal-dominant mode. A population-based cohort study was performed in order to study familial prostate cancer and associated malignancies. A nation-wide register cohort study was conducted using an unselected study population. The cohort of 5,595 sons and 5,089 daughters of Swedish men found to have prostate cancer between 1959 and 1963 was identified. All types of cancer reported between 1958 and 1992 in this cohort were identified through linkage to the Swedish Cancer Registry. The expected number of different cancers was calculated using incidence rates obtained from the Registry. A highly significant increased overall standardized incidence ratio (SIR) of 1.65 (95% CI, 1.49-1.83) was obtained for prostate cancer, with 370 observed cases compared with 224 expected prostate cancers. The SIR was 3.18 among cases 45 to 49 years old at diagnosis, with the risk gradually decreasing to a SIR of 1.45 among cases over 80 years of age. Among sons and daughters with a father whose prostate cancer was diagnosed at an early age (<70 years), an increased risk for colorectal cancer SIR 1.48 (1.10-1.95) was observed. No significant difference in cancer risk for other sites was observed among the daughters and sons of men with prostate cancer. This cohort study confirms earlier studies that a positive family history of prostate cancer is an important risk factor for developing this disease. Though increased risk was found for all ages, it was more pronounced in younger men. Since no other malignancy was significantly associated with prostate cancer, it is most likely that familial prostate cancer is "site-specific".
Recent molecular studies have noted the affinity among cephalochordates and vertebrates. In particular, a cluster of vertebrate-like homeobox genes regulates the development of the lancelet Branchiostoma lanceolatum. A previous study has outlined the expression pattern of the pituitary-specific transcription factor Pit-1 in adult lancelets. Pit-1 belongs to the POU family of transcription factors, which, like homeotic proteins, are members of the helix-turn-helix superfamily of proteins. POU is an acronym for Pit-1, Oct-1 and Oct-2, and Unc-86. In the present work, we investigated the head region of premetamorphic larvae of B. lanceolatum, by means of scanning electron microscopy, wholemount and tissue sections immunocytochemistry, and Western blotting assay, to verify the presence and distribution of Pit-1. Immunoreactive Pit-1 protein was detected in the rostral nerves and in a cluster of photoreceptor cells of the frontal eye. At the same time, an electrophoretic band of 33 kDa was shown from extracts of premetamorphic larvae and recognized by a monoclonal antibody to rat Pit-1. On the basis of the immunocytochemical and electrophoretic results, we can assume that Pit-1 may play a neuromodulatory role in the larval central nervous system. Moreover, the spatial and temporal distribution of Pit-1 protein in larva and adult lancelets agrees only in part with that described in embryonic and adult mice, suggesting different molecular controls of regional identity in the nervous system of cephalochordates and vertebrates.
Following specific neonatal brain lesions in rodents and ferrets, retinal axons have been induced to innervate the medial geniculate nucleus (MGN). Previous studies have suggested that reduction of normal retinal targets along with deafferentation of the MGN are two concurrent factors required for the induction of novel retino-MGN projections. We have examined, in ferrets, the relative influence of these two factors on the extent of the novel retinal projection. We first characterized the inputs to the normal MGN, and the most effective combination of neonatal lesions to deafferent this nucleus, by injecting retrograde tracers into the MGN of normal and neonatally operated adult ferrets, respectively. In a second group of experiments, newborn ferrets received different combinations of lesions of normal retinal targets and MGN afferents. The resulting extent of retino-MGN projections was estimated for each case at adulthood, by using intraocular injections of anterograde tracers. We found that the extent of retino-MGN projections correlates well with the extent of MGN deafferentation, but not with extent of removal of normal retinal targets. Indeed, the presence of at least some normal retinal targets seems necessary for the formation of retino-MGN connections. The diameters of retino-MGN axons suggest that more than one type of retinal ganglion cells innervate the MGN under a lesion paradigm that spares the visual cortex and lateral geniculate nucleus. We also found that, after extensive deafferentation of MGN, other axonal systems in addition to retinal axons project ectopically to the MGN. These data are consistent with the idea that ectopic retino-MGN projections develop by sprouting of axon collaterals in response to signals arising from the deafferented nucleus, and that these axons compete with other sets of axons for terminal space in the MGN.