PubMed · 7095427
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S Kent. 1982. Determining biologic age.. https://pubmed.ncbi.nlm.nih.gov/7095427/
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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".
The lithium-pilocarpine model of status epilepticus (SE) was used to study the type and distribution of seizure-induced neuronal injury in the rat and its consequences during development. Cell death was evaluated in hematoxylin- and eosin-stained sections and by electron microscopy. Damage to the CA1 neurons was maximal in the 2- and 3-week-old pups and decreased as a function of age. On the other hand, damage to the hilar and CA3 neurons was minimal in the 2-week-old rat pups but reached an adult-like pattern in the 3-week-old animals, and damage to amygdalar neurons increased progressively with age. The 3-week-old animals also demonstrated vulnerability of the dentate granule cells. To evaluate neuronal apoptosis, we used terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) stain, confocal fluorescence microscopy of ethidium bromide-stained sections, electron microscopy, and DNA electrophoresis. Neurons displaying all of those features of apoptotic death in response to SE were seen in the CA1 region of the 2-week-old pups and in the hilar border of the dentate granule cells of the 3-week-old animals. Some (3/11) of the animals that underwent SE at 2 weeks of age and most of the animals that underwent SE at 3 or 4 weeks of age (8/11 and 6/8, respectively) developed spontaneous seizures later in life; the latter showed SE-induced synaptic reorganization as demonstrated by Timm methodology. These results provide strong evidence for the vulnerability of the immature brain to seizure-induced damage, which bears features of both necrotic and apoptotic death and contributes to synaptic reorganization and the development of chronic epilepsy.
Angelman syndrome (AS) is a severe neurodevelopmental disorder resulting from a deletion/mutation in maternal chromosome 15q11-13. The genes in 15q11-13 contributing to the full array of the clinical phenotype are not fully identified. This study examines whether a loss or reduction in the GABAA receptor beta3 subunit (GABRB3) gene, contained within the AS deletion region, may contribute to the overall severity of AS. Disrupting the gabrb3 gene in mice produces electroencephalographic abnormalities, seizures, and behavior that parallel those seen in AS. The seizures that are observed in these mice showed a pharmacological response profile to antiepileptic medications similar to that observed in AS. Additionally, these mice exhibited learning and memory deficits, poor motor skills on a repetitive task, hyperactivity, and a disturbed rest-activity cycle, features all common to AS. The loss of the single gene, gabrb3, in these mice is sufficient to cause phenotypic traits that have marked similarities to the clinical features of AS, indicating that impaired expression of the GABRB3 gene in humans probably contributes to the overall phenotype of Angelman syndrome. At least one other gene, the E6-associated protein ubiquitin-protein ligase (UBE3A) gene, has been implicated in AS, so the relative contribution of the GABRB3 gene alone or in combination with other genes remains to be established.