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Biomedical subjects

A Tate

Publications and source records attributed to A Tate.

16 recordsLinked to original sources
PubMed1996

Genetic linkage of familial granulomatous inflammatory arthritis, skin rash, and uveitis to chromosome 16.

Blau syndrome (MIM 186580), first described in a large, three-generation kindred, is an autosomal, dominantly inherited disease characterized by multiorgan, tissue-specific inflammation. Its clinical phenotype includes granulomatous arthritis, skin rash, and uveitis and probably represents a subtype of a group of clinical entities referred to as "familial granulomatosis." It is the sole human model with recognizably Mendelian inheritance for a variety of multisystem inflammatory diseases affecting a significant percentage of the population. A genomewide search for the Blau susceptibility locus was undertaken after karyotypic analysis revealed no abnormalities. Sixty-two of the 74-member pedigree were genotyped with dinucleotide-repeat markers. Linkage analysis was performed under a dominant model of inheritance with reduced penetrance. The marker D16S298 gave a maximum LOD score of 3.75 at theta = .04, with two-point analysis. LOD scores for flanking markers were consistent and placed the Blau susceptibility locus within the 16p12-q21 interval.

Adolescent↗
PubMed1994

N-acetylgalactosaminyl GD1a is a target molecule for serum antibody in Guillain-Barré syndrome.

Serum antibodies against such major glycolipids as GM1, GD1b, and LM1 have been reported in patients in the acute phase of Guillain-Barré syndrome (GBS). Because minor unidentified glycolipids also may be targets of antibodies in GBS sera, we assayed serum antibody against a crude ganglioside fraction using thin-layer chromatogram immunostaining. Antibody activity was detected against a band that migrated just below GD1a in 6 of the 50 patients with GBS tested. Antibody titer, as determined by enzyme-linked immunosorbent assay, decreased during the course of the disease. All 6 patients had suffered gastrointestinal infection before the neurological onset of GBS and showed low amplitudes for the compound muscle action potentials and normal or only slightly decreased nerve conduction velocities. Thin-layer chromatogram immunostaining did not show this antibody activity in any of the 16 normal and 119 disease controls. The unidentified glycolipid was isolated by DEAE-Sephadex A-25 column chromatography, sialidase treatment, and Iatrobeads column chromatography. Fast atom bombardment-mass spectra showed it to be N-acetyl-galactosaminyl GD1a.

Adult↗
PubMed1992

Molecular computing for edge-enhanced laser imaging.

In order to illustrate the self-assembly capability, we consider a laser imaging experiment on a wet film that is made of bacteriorhodopsin (BR) molecules suspended in a diffusion-limited viscous medium. BR wet film is similar to a wet photograph film but having a finer resolution and adaptive pixel locations due to laser-induced thermal diffusion. The synergism between thermal diffusion of BR molecules (induced externally by a write-laser) and molecular photochromism (generated internally by a read-laser) is exploited naturally for edge-enhanced image applications.

Bacteriorhodopsins↗
PubMed1979

Expanded linkage map of Vibrio cholerae.

An expanded linkage map of the Vibrio cholerae classical strain 162 chromosome has been prepared using a variety of new auxotrophic mutants. The chromosome consists of a single, linear linkage group. The map consists of 17 markers, which have been ordered; 20 mutational sites, which are tentatively ordered; five markers (ura-1, ser-2, mal-1, man-1, suc-1), which are linked but unordered; and three mutations (aro-2, cys-2 and cys-6) which showed little or no linkage. A proposal is made to standardize genetic nomenclature in V. cholerae genetic studies.

Chromosome Mapping↗
PubMed1976

A study of the transmission and structure of double stranded RNAs associated with the killer phenomenon in Saccharomyces cerevisiae.

Killer strains contain two double stranded RNAs, L and M. The M dsRNA appears to be necessary for production of a toxin and for resistance to that toxin. Mutant strains have been found that are defective in their ability to kill and in their resistance to toxin. These sensitive, non-killer strains have altered dsRNA composition. One class has no M dsRNA. Another class of sensitive, non-killers called suppressives has no M dsRNA but instead has smaller dsRNAscalledS. Indiploidsresulting from a cross of a wild-type killer by a suppressive the transmission of the M dsRNA is suppressed by the S dsRNA. When a suppressive is crossed by a strain with no M dsRNA, the diploids and all four meiotic spores have the S dsRNA characteristic of the parental suppressive strain. Suppressive strains do not suppress each other. Intercrosses between two different suppressives yields diploids with both parental S dsRNAs. These two S dsRNAs are transmitted to all 4 meiotic progeny. Another class of mutants has been found which is defective for one of the traits but retains the other. One type, temperature-sensitive killers, has a normal dsRNA composition but is unable to kill at 30 degrees. The other type, immunity-minus, has a complex dsRNA pattern. The immunity-minus strain is extremely unstable during mitotic growth and segregates several different types of non-killers. Analysis of the dsRNAs from wild type and the mutants by electron microscopy shows that the L, M, and S dsRNAs are linear. All strains regardless of killer phenotype appear to have the same size L dsRNA.

Cell Division↗
PubMed1973

Mitochondrial proliferation within the nephron. I. Comparison of mitochondrial hyperplasia of tubular regeneration with compensatory hypertrophy.

MITOCHONDRIAL PROLIFERATION IN THE RENAL PROXIMAL TUBULAR EPITHELIUM IN RESPONSE TO TISSUE LOSS HAS BEEN QUANTITATED BY TWO DIVERSE MODELS: acute tubular necrosis induced by mercuric chloride and unilateral nephrectomy. The increased work demand on the remaining tubular mass in both models has probably stimulated both cell hyperplasia and hypertrophy. In both instances, cell hyperplasia preceeds hypertrophy. During the cellular hypertrophy, mitochondria first proliferate in number and then increase in size; presumably to satisfy the greater need for energy metabolism necessary during increased active transtubular solute transport.

Animals↗