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Biomedical subjects

S A Jordan

Publications and source records attributed to S A Jordan.

41 records · Page 3Linked to original sources
PubMed1991

Autosomal dominant retinitis pigmentosa: localization of a disease gene (RP6) to the short arm of chromosome 6.

DNA from members of an Irish pedigree presenting with late onset autosomal dominant retinitis pigmentosa (ADRP) have been typed with a series of genetic markers from chromosome 6p. Positive two-point lod scores have been obtained with five markers (D6S89: theta = 0.10, Z = 3.338; D6S109: theta = 0.10, Z = 3.932; D6S105: theta = 0.00, Z = 6.081; HLA-DRA: theta = 0.00, Z = 4.364; and RDS: theta = 0.00, Z = 5.376). In a series of overlapping multipoint analyses a lod score of 6.6 was obtained, maximizing at HLA-DRA and hence localizing the ADRP gene (RP5) segregating in this pedigree to 6p. These data provide direct evidence for an additional autosomal dominant RP locus and strongly implicate the human equivalent of the mouse retinal degeneration slow (rds) gene, peripherin-rds, as a candidate for autosomal dominant retinitis pigmentosa.

Base Sequence↗
PubMed1991

Understanding and treating motivation difficulties in ventilator-dependent SCI patients.

Motivation for spinal cord injury rehabilitation is a difficult management task for clinicians. Ventilator-dependent quadriplegics experience conditions which are particularly likely to lead to motivational problems. The following article provides a theoretical model with which to understand patient motivation. The model conceptualizes patient motivation as a patient-rehabilitation environment fit problem and employs concepts from social learning theory to facilitate understanding and intervention with such difficulties. The model is applied to two ventilator-dependent rehabilitation cases. Recommendations for clinical practice are provided.

Humans↗
PubMed1989

Combined nephrotoxicity of methylmercury, lead, and cadmium in Pekin ducks: metallothionein, metal interactions, and histopathology.

This report describes the metallothionein (MT) levels and accumulation of mercury, lead, and cadmium, as well as their interaction with tissue zinc, copper, and iron, and the histopathological changes in kidneys of ducks exposed to methylmercury chloride (MeHgCl), lead acetate (PbAc), and cadmium chloride (CdCl2), singly or in combination for 13 wk. Forty-eight female Pekin ducks, divided into 8 groups of 6 birds each, were fed diets containing no added metals (control), 8 mg MeHgCl/kg feed, 80 mg PbAc/kg feed, 80 mg CdCl2/kg feed, 8 mg MeHgCl + 80 mg PbAc/kg feed, 8 mg MeHgCl + 80 mg CdCL2/kg feed, 80 mg PbAc + 80 mg CdCl2/kg feed, and 8 mg MeHgCl + 80 mg PbAc + 80 mg CdCL2/kg feed. Cadmium (Cd) when administered alone or in combination caused a 60-fold increase in kidney MT levels, while methylmercury (MeHg) or lead (Pb) administration caused a threefold increase in kidney MT levels. No significant changes in kidney MT levels were observed when metals were administered concurrently when compared with single-treatment groups. Residue analysis revealed accumulation of administered metals in kidney tissue. However, lead administration resulted in accumulation of small amounts of this element in kidney tissue. Simultaneous administration of MeHgCl and PbAc significantly increased the accumulation of lead in kidney when compared with PbAc-treated group. Cadmium when administered alone or in combination caused an increase in the levels of zinc and copper in kidney. Administration of MeHgCl or PbAc either alone or in combination caused increased iron levels in kidney, while cadmium administration either alone or in combination caused decreased iron levels. Administration of cadmium either alone or in combination caused degenerative changes in kidney proximal tubules. The severity of degenerative lesions increased when cadmium was simultaneously administered with other metals. These results indicate that combined administration of MeHg, Pb, and Cd has no significant effect on kidney MT levels or on essential elements in kidney tissue when compared with single metal groups. However, there appears to be an increase in the severity of histopathologic changes.

Animals↗
PubMed1989

Ultrastructure of kidney of ducks exposed to methylmercury, lead and cadmium in combination.

Ultrastructural alterations in the kidneys of Pekin ducks exposed to various combinations of methylmercury chloride (MeHgCl), lead acetate (PbAC) and cadmium chloride (CdCl2 for 12 weeks were studied. Eight groups (Gr), each consisting of 6 female ducks, were fed diets containing no heavy metals (control), 8 mg of methylmercury chloride (MeHgCl)/kg of feed (GrII), 80 mg of lead acetate (PbAC)/kg of feed (GrIII), 80 mg of cadmium chloride (CdCl2)/kg of feed (GrIV), 8 mg of MeHgCl + 80 mg of PbAC/kg of feed (GrV), 8 mg of MeHgCl + 80 mg of CdCl2/kg of feed (GrVI), 80 mg of PbAC + 80 mg of CdCl2/kg of feed (GrVII), and 8 mg of MeHgCl + 80 mg of PbAC + 80 mg of CdCl2/kg of feed (GrVIII). Renal corpuscles of the ducks treated with methylmercury (MdHg), lead (Pb), the cadmium (Cd), either alone or in two way combinations exhibited minor ultrastructural changes. The thickness of the glomerular basement membrane was significantly different from control only in Grs II, IV, V and VI. Crystallization of granules in the juxtaglomerular cells was also observed in Cd and Pb treated birds. Administration of the three metals in combination caused marked changes in podocytes with fusion of secondary processes and no pedicle differentiation. The proximal tubule cells approximately (PT) accumulated lipid droplets, lysosomal bodies and membrane bound vacuoles in methylmercury treated birds. Lead exposed birds had a large number of secondary lysosomes and swollen mitochondria in PT cells. Cadmium administration caused degenerative changes in PT cells which included accumulation of lysosomal bodies containing degenerating organelles, lipid droplets and vacuoles containing myelin figures. Marked degenerative changes in PT cells and interstitial fibrosis was prominent when cadmium was concomitantly administered with the other metals. Concurrent administration of all three metals caused enhancement of degenerative changes in proximal tubule cells and collecting duct cells. These observations suggest that the combined administration of metals causes renal damage that appears to be additive.

Animals↗