Wound care. Pressure ulcers: stop don't yield.
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Biomedical subjects
Publications and source records attributed to Y Parsons.
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Integrons are genetic elements which are capable of acquiring genes by site-specific recombination. The most common integron structure consists of two conserved segments flanking a variable region where many different antibiotic resistance genes have been found. The integrons In6 and In7, present in the plasmids pSa and pDGO100, respectively, are unusual in that they include a duplication of the sulI gene which is located within the integron 3'-conserved segment. To further investigate the structure of these integrons, the DNA sequence of the segment located between the two sulI genes was determined. In In7 this segment is 2822 bases long and includes a trimethoprim resistance gene, dhfrX, at one end. The corresponding region in In6 is 4.5 kb and is nearly identical to the In7 segment over the first 2105 bases. In the region unique to In6, a cat gene, conferring chloramphenicol resistance, has replaced the dhfrX gene of In7. This location thus represents a second variable region where different antibiotic resistance genes are found, but the way in which genes become associated with this second variable region is not known. The overall similarity of the structures of In6 and In7 suggests that the additional DNA segments found in these integrons have a common origin, and a possible mechanism for the origin of integrons with partial 3'-conserved segment duplications is presented.
A new trimethoprim resistance determinant, designated dhfrX, was identified in the In7 integron of pDGO100. The sequence of the dhfrX dihydrofolate reductase is up to 28% identical to the sequences of several known dihydrofolate reductase proteins. The dhfrX gene is adjacent to the second 3'-conserved segment of the In7 integron, but the first 77 bases of this segment are not present.
Stereotaxic surgery was performed on sheep fetuses at 108 to 110 days of gestation to investigate hypothalamic influences on fetal growth hormone (GH) release. In 5 fetuses the median eminence was destroyed, in 6 damage was confined to the medial basal hypothalamus without total destruction of the median eminence, 6 had misplaced lesions and 4 were sham operated controls. Destruction of the median eminence led to a marked fall in GH secretion and an abolition of pulsatile GH release. Following lesioning of the median eminence, GH values are comparable to resting levels in the infant lamb. Pituitary infarction was excluded in these fetuses both histologically and by a maintained GH response to exogenous growth hormone releasing factor. Lesions of the medial basal hypothalamus without destruction of the median eminence led to a significant but lesser fall in GH secretion and a reduction in the pulsatility of GH release. Sham operated fetuses and those with lesions misplaced outside the endocrine hypothalamus showed maintained high circulating GH concentrations with marked pulsatility of GH release. These studies demonstrate that fetal GH release is solely dependent upon hypothalamic stimulation presumably mediated by growth hormone releasing factor. There is no evidence for pituitary autonomy or for direct extrahypothalamic stimulation of the fetal somatotrope.
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