Biomedical subjects
L A James
Publications and source records attributed to L A James.
Clinical and pathologic features of chromosome 21-linked familial Alzheimer's disease.
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Research, career development and training opportunities at the National Center for Nursing Research.
Research, career development, and training grant mechanisms available at the National Center for Nursing Research are described. Funding is available for applications using any of these grant mechanisms. Submission of high-quality applications focusing on gastroenterology nursing issues is encouraged.
Physical mapping around the Alzheimer disease locus on the proximal long arm of chromosome 21.
Evidence from linkage studies suggests that familial Alzheimer disease (AD) can be caused by a defect in a gene on the proximal long arm of chromosome 21. We have constructed a physical map spanning 10 megabases of this region of the chromosome by means of pulsed-field gel electrophoresis and analysis of somatic cell hybrids. Our data have allowed us to establish the order of chromosome 21 loci--cen-(S16,S48)-S13-S46-S4-(S52,S110)-(S1,S1 1)--and are thus of immediate relevance both to multipoint linkage analysis in families affected by AD and for moving from this linkage to the isolation of the genetic defect. We have also been able to identify several CpG-rich sequences close to the four most centromeric loci, suggesting the location of genes in this region. These probes, which are all within 1.5 megabases of one another, are currently the markers most tightly linked to the AD locus. Genes identified in this region can therefore be considered as candidates for the disease locus.
Predisposing locus for Alzheimer's disease on chromosome 21.
Linkage between Alzheimer's disease and markers on the long arm of chromosome 21 was investigated in six families affected by disease of early onset. Linkage was confirmed and the disease locus shown to be centromeric to the locus D21S1/S11 on the long arm of the chromosome. It is argued that the data are consistent with the notion that all patients with Alzheimer's disease of genetic aetiology have a predisposing locus on chromosome 21.
Molecular genetics of Alzheimer's disease.
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Primary structure around the lipoate-attachment site on the E2 component of bovine heart pyruvate dehydrogenase complex.
Bovine heart pyruvate dehydrogenase complex was acetylated by using [3-14C]pyruvate in the presence of N-ethylmaleimide, with approx. 1 mol of acetyl groups being incorporated per mol of E2 polypeptide. After peptic digestion, lipoate-containing peptides were purified by high-voltage electrophoresis and ion-exchange and reverse-phase h.p.l.c. The amino acid sequence around the lipoic acid-attachment site of E2 was determined by automated Edman degradation. Acetylation of a lipoate cofactor bound to a lysine residue was verified by fast-atom-bombardment m.s.
Protein phosphorylations in poliovirus infected cells.
In vivo phosphorylation of proteins that are associated with polysomes of poliovirus-infected VERO (African green monkey kidney) and HeLa (Henrietta Lacks) cells differed from phosphorylations observed with uninfected cells that were fed fresh medium. With both types of cells infection stimulated phosphorylation of proteins with molecular weights of 40 000-41 000, 39 000, 34 000, 32 000, and 24 000. Similarities of phosphorylations in VERO and HeLa cells suggest that they are a specific consequence of infection and might serve a regulatory function during protein synthesis.
Fatigue behavior of type 316 stainless steel under simulated body conditions.
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Effectiveness of low dose erythropoietin: a possible advantage of high flux hemodialysis.
Recombinant human erythropoietin (EPO) was administered to 32 stable out-patients with end-stage renal disease (ESRD) on a priority basis three times a week. All patients underwent dialysis with polysulfone hollow fiber dialyzers. Mean time-averaged blood urea nitrogen (BUN) value was 50 +/- 12 mg/dl, and Kt/V for urea was 1.20 +/- 0.34/dialysis. The initial dose of EPO was 2,800 +/- 950 U/dialysis (45 +/- 17 U/kg/dialysis). The maintenance dose averaged 2,500 U/dialysis. Within the mean time of observation, 15 +/- 4 weeks, all but one patient responded to EPO by eliminating transfusion requirements, and 29 of 32 achieved the target hematocrit of 30-33%. For patients with hematocrits below 25% before EPO, the increase averaged 1.6 +/- 0.8%/week. The dose of EPO was lower and the hematocrit response was higher than reported previously. The rate of increase in hematocrit did not correlate with small molecular weight solute removal. Mean red blood cell survival was 52 +/- 18 days. No adjustments in blood pressure (BP) medications or dry weight were required to control BP. These data and earlier experiences with recovery from the anemia of ESRD after more effective dialysis suggest that the bone marrow response to EPO may be augmented by high flux hemodialysis.