PubMed · 11838141
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Osamu Ishikawa, Kazunori Ohnishi. 2002. [Systemic sclerosis (SSc)].. https://pubmed.ncbi.nlm.nih.gov/11838141/
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Cataract prevalence increases with age. As the world's population ages, cataract-induced visual dysfunction and blindness is on the increase. This is a significant global problem. The challenges are to prevent or delay cataract formation, and treat that which does occur. Genetic and environmental factors contribute to cataract formation. However, reducing ocular exposure to UV-B radiation and stopping smoking are the only interventions that can reduce factors that affect the risk of cataract. The cure for cataract is surgery, but this is not equally available to all, and the surgery which is available does not produce equal outcomes. Readily available surgical services capable of delivering good vision rehabilitation must be acceptable and accessible to all in need, no matter what their circumstances. To establish and sustain these services requires comprehensive strategies that go beyond a narrow focus on surgical technique. There must be changes in government priorities, population education, and an integrated approach to surgical and management training. This approach must include supply of start-up capital equipment, establishment of surgical audit, resupply of consumables, and cost-recovery mechanisms. Considerable innovation is required. Nowhere is this more evident than in the pursuit of secure funding for ongoing services.
The widespread use of organophosphate insecticides has raised concern about neurotoxic effects of fetal and childhood exposures. Studies in rats show that chlorpyrifos (CPF) elicits CNS cell damage, in part, through noncholinergic mechanisms that involve alterations in the expression and function of nuclear transcription factors that control cell replication, differentiation, and apoptosis. In the current study, we examined mRNAs encoding c-fos and p53, in order to determine if changes in these factors correspond to the differential susceptibility of forebrain neurons and glia, when exposure is shifted from the early neonatal period (postnatal days 1-4) to a later period (days 11-14). The early treatment paradigm elicited a significant elevation of c-fos whereas the later treatment suppressed c-fos. Neither regimen altered forebrain p53 expression, but values were elevated in the cerebellum following the later treatment; the cerebellum develops later than the forebrain and has its peak of neurogenesis postnatally. Our results suggest that a wider profiling of mRNAs using genomic arrays would enable screening for developmental neurotoxicants, but that regional and temporal profiles will be required in order to draw mechanistic conclusions or to identify critical periods of vulnerability.
We present the first quantitative gene expression analysis of cardiac aging under conditions of sedentary and active lifestyles using high-density oligonucleotide arrays representing 11,904 cDNAs and expressed sequence tags (ESTs). With these data, we test the hypothesis that exercise attenuates the gene expression changes that normally occur in the aging heart. Male mice (Mus domesticus) were sampled from the 16th generation of selective breeding for high voluntary exercise. For the selective breeding protocol, breeders were chosen based on the maximum number of wheel revolutions run on days 5 and 6 of a test at 8 wk of age. For the colony sampled herein, mice were housed individually over their entire lifetimes (from weaning) either with or without access to running wheels. The hearts of these two treatment groups (active and sedentary) were assayed at middle age (20 mo) and old age (33 mo). Genes significantly affected by age in the hearts of the sedentary population by at least a 50% expression change (n = 137) were distributed across several major categories, including inflammatory response, stress response, signal transduction, and energy metabolism. Genes significantly affected by age in the active population were fewer (n = 62). Of the 42 changes in gene expression that were common to both treatment groups, 32 (72%) displayed smaller fold changes as a result of exercise. Thus exercise offset many age-related gene expression changes observed in the hearts of the sedentary animals. These results suggest that adaptive physiological mechanisms that are induced by exercise can retard many effects of aging on heart muscle at the transcriptional level.