PubMed · 6862836
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M Hyland. 1983. Prescribing for the elderly.. https://pubmed.ncbi.nlm.nih.gov/6862836/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
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 unique maturational period of adolescence is replete with numerous changes in anatomy and function that may yield clues as to why drug abuse emerges at this stage. The behavioral effects of amphetamine are diminished during periadolescence (35 days) relative to younger (21 days) and older (>60 days) rats, prompting us to examine amphetamine effects on neuronal activation with the immediate early gene, c-fos. Amphetamine (1 and 5 mg/kg, i.p.) increased c-fos immunoreactivity in rats 21, 35, and 60 days of age in a dose-dependent manner. When expressed as a percentage of vehicle for each age, amphetamine-induced effects on c-fos immunoreactivity were higher at 21 days of age compared with the effects at 35 and 60 days of age in the nucleus accumbens core and shell, striatum, and prefrontal cortex. These data provide a possible reason as to why stimulants produce dysphoria in children, before transitioning to euphoria during adolescence. Implications of these results are discussed for stimulant use in a pediatric population and the development of drug abuse.
Neonatal exposure to low doses of nicotine has been shown to disturb the development of low-affinity nicotinic binding sites in the cerebral cortex and to elicit a deviant behavioural response to nicotine in adult mice. In this study, 10-day-old male NMRI mice were exposed to one of three different doses of nicotine (3.3, 33, or 66 microg nicotine-base/kg body wt.) s.c. twice daily on 5 consecutive days to study dose-response effects of nicotine on adult spontaneous and nicotine-induced motor behaviour. The nicotine-induced behaviour test revealed a hypoactive response to nicotine in 4-month-old mice neonatally exposed to 33 or 66 microg nicotine-base, whereas the response to nicotine in control animals and mice exposed to 3.3 microg nicotine-base was an increased activity. Learning and memory functions were also investigated in adult animals neonatally exposed to 66 microg nicotine-base/kg body wt. in the same manner, in the Morris water maze and in the Radial arm maze. In the swim maze and the Radial arm maze tests, no significant differences were observed between nicotine-treated and control animals at the age of 4 months. At 7 months, however, a significant difference in performance was evident, indicating a time-response/time-dependent effect. Furthermore, it was shown that in mice exposed neonatally to a nicotine dose known to inhibit the development of the nicotinic low affinity-binding site (LA), the response to nicotine could not cause any increase in spontaneous motor activity as seen in controls.