Biomedical subjects
Publications and source records attributed to H McIntosh.
The localization of GAP-43-like immunoreactivity has been determined in retinas from adult toad, snake, rat, rabbit, cow and human. Specific labeling was conspicuous in discrete sublaminae within the inner plexiform layer of all mammalian species tested. In contrast, the toad retina exhibited punctate labeling in the outer plexiform layer, while the snake retina had little or no GAP-43-like immunoreactivity.
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GAP-43 was purified from cat brain by a rapid isolation procedure and was used to raise highly specific polyclonal antibodies in rabbits. Immunoblots of proteins from adult cat, monkey and human visual cortex as well as bovine cortex also showed specific staining of a single protein that was present in both soluble and membrane fractions. Immunocytochemistry of both cat and human adult visual cortex showed that GAP-43 has a laminar distribution.
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GAP-43 levels have been determined by immunoassay in cat visual cortex during postnatal development to test the idea that GAP-43 expression could be related to the duration of the critical period for plasticity. For comparison, GAP-43 levels have also been assayed in primary motor cortex, primary somatosensory cortex, and cerebellum at each age. GAP-43 levels were high in all regions at 5 d (with concentrations ranging from 7-10 ng/microgram protein) and then declined 60-80% by 60 d of age. After 60 d of age, GAP-43 concentrations in each region continued a slow decline to adult values, which ranged from 0.5-2 ng/microgram protein. To test for the involvement of GAP-43 in ocular dominance plasticity during the critical period, the effect of visual deprivation on GAP-43 levels was investigated. Monocular deprivation for 2-7 d, ending at either 27 or 35 d of age, had no effect on total membrane levels of GAP-43. The concentrations of membrane-associated GAP-43 prior to 40 d of age correlate with events that occur during postnatal development of the cat visual cortex. However, the slow decline in membrane-associated GAP-43 levels after 40 d of age may be an index of relative plasticity remaining after the peak of the critical period.
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We have purified a protein that changes in relative concentration during the development of the kitten visual cortex. It resembles GAP-43 (a neuronal protein that is expressed at elevated levels during periods of development and regenerative axon growth) in the following respects: (1) it is an acidic protein (pI = 4.7) whose electrophoretic mobility on SDS-PAGE is similar to, but lower than rat GAP-43, suggesting that the cat protein is larger; (2) its electrophoretic mobility varies with the acrylamide concentration in a manner that is characteristic of GAP-43; (3) its concentration in kitten forebrain is elevated during early postnatal development; (4) the sequence of ten consecutive amino acids from a chemically generated fragment matches the expected sequence from GAP-43; and (5) its amino-acid content also matches GAP-43. We conclude that our purified protein is cat GAP-43. Immunoblots with an antibody prepared against rat GAP-43 suggested that the concentration of GAP-43 in the visual cortex declines with age.
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Throughout 1981 and 1982 all deaths of infants aged 8-365 days (post-perinatal infant mortality, PPIM) in Scotland were studied. During this period there were 135 250 live births and 1533 infant deaths (infant mortality rate 11.3), including 763 PPIM deaths (5.6 per 1000 live births). These 763 deaths fell into three main categories: birth-determined (329), accident or acquired disease (65), and cot deaths (369). Birth-determined deaths included 109 preterm, 199 congenital disorders, and 21 miscellaneous deaths. 61 of the cot deaths were fully explained on necropsy, in 141 an associated finding which might or might not be relevant was found, and in the remaining 167 no explanation was found. The cot death rate was 2.7 per 1000 live births overall (3.3 for boys, 2.1 for girls), and more second-born than first-born children died (approximately 3:2). Excluding "explained" cot deaths the rate was 2.3 per 1000 live births.
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Post-perinatal infant mortality (PPIM; deaths from the 8th day to the end of the 1st year of life) was studied in Glasgow over the 3-year period 1979-81. The 244 deaths were divided into three main categories--those determined at birth, those due to accidents and acquired disease, and cot deaths. 50% of deaths were determined at birth, and of these 46% were due to prematurity and 49% to congenital disorder. Cot deaths accounted for 44% of the total (88% of deaths not determined at birth) and a definite cause could be identified in only 10% of these. The PPIM rate was 6.1 per 1000 livebirths, a significant part of the infant mortality rate of 12.6. The significance of these findings is discussed in relation to the possible reduction of these figures.