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Biomedical subjects

A S Williams

Publications and source records attributed to A S Williams.

13 recordsLinked to original sources
PubMed1992

Histologic study of healing after ab interno laser sclerostomy.

We examined the histologic characteristics of healing after ab interno laser sclerostomy in a human eye. A KTP 532 green laser coupled to a 300-microns quartz fiberoptic probe was used to create an ab interno sclerostomy in a terminally ill patient with pigmentary glaucoma. The intraocular pressure increased five days postoperatively and did not respond to medical treatment. The patient died six weeks postoperatively of metastatic lung cancer. Histopathologic analysis showed a patent 150-microns scleral lumen from the anterior chamber to the episclera, surrounded by a 300-microns zone of acellular thermal damage. There was no healing of the lumen. The subconjunctival end of the lumen was capped with a thick episcleral scar, which caused the failure of the operation.

Cicatrix↗
PubMed1989

Acute comitant esotropia in children with brain tumors.

If acute onset of esotropia is comitant, its cause is generally believed to be benign. Although this is, by and large, true, it is now clear that acute comitant esotropia may be associated infrequently with central nervous system illness. We describe six children who presented with acute onset of comitant esotropia, and who were found to have tumors of the brain stem or cerebellum. Four of the patients underwent strabismus surgery after appropriate neurologic and neurosurgical treatment was completed. In none of these patients was ocular motor fusion reestablished.

Acute Disease↗
PubMed1988

The cdc30 mutation in Saccharomyces cerevisiae affects phosphoglucose isomerase, the cell cycle and sporulation.

Spontaneous revertants of the cdc30 mutation in Saccharomyces cerevisiae simultaneously regained the ability to grow and divide at 36.5 degrees C on glucose-containing media along with a more thermostable phosphoglucose isomerase (PGI). An independently isolated allele of cdc30 gave a similar phenotype to that previously described including temperature-sensitivity of PGI. Isoelectric focussing allowed the separation of two isoenzymes of PGI. These results all support the idea that two genes--PGI1 and CDC30--are responsible for PGI activity in yeast. Diploid strains homozygous for the cdc30 mutation sporulated poorly in potassium acetate irrespective of whether the cells had previously been cultured at a temperature that was permissive or restrictive for cell cycle progression. This was not surprising because a strain defective in PGI would not be expected to be able to complete the gluconeogenic events of sporulation.

Alleles↗
PubMed1987

The cdc30 mutation in Saccharomyces cerevisiae results in a temperature-sensitive isoenzyme of phosphoglucose isomerase.

The cdc30 mutation in the yeast Saccharomyces cerevisiae causes cell cycle arrest late in nuclear division when cells are shifted from the permissive temperature of 25 degrees C to the restrictive temperature of 36.5 degrees C. Cell cycle arrest at 36.5 degrees C is dependent upon the carbon source used: a shift-up in glucose containing media results in cell cycle blockade, whereas a shift-up in ethanol, fructose, glycerol, glycerol plus ethanol, or mannose does not. Metabolite analyses showed accumulation of glucose 6-phosphate in a cdc30-bearing strain after a temperature shift-up in glucose-containing medium. Thermal denaturation studies and kinetic measurements indicate the existence of two isoenzymes of phosphoglucose isomerase (EC 5.3.1.9); one of which is apparently altered in the temperature-sensitive cell cycle mutant. We propose that the gene products of both the CDC30 and PG11 genes are required for cell cycle progression in glucose media and that the PGI1 gene product has a regulatory function over the CDC30 gene product.

Cell Division↗
PubMed1986

Fat--again.

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Body Image↗
PubMed1986

A genetic and biochemical analysis of the role of gluconeogenesis in sporulation of Saccharomyces cerevisiae.

The requirement for gluconeogenesis and the pentose phosphate pathway in sporulation of Saccharomyces cerevisiae was investigated using homozygous diploids with mutations in selected portions of the respective metabolic pathways. Mutations affecting the genes FBA1 (fructose-1,6-bisphosphate aldolase), GPM1 (phosphoglycerate mutase) and ZWF1 (glucose-6-phosphate dehydrogenase) were used. Homozygous diploids bearing either fba1-11 or gpm1 mutations were asporogenous, indicating an absolute requirement for gluconeogenesis in sporulation. A strain homozygous for the zwf1 mutation sporulated, but at a reduced level compared to the wild-type. Homozygous spd1-1 mutations restored the ability to sporulate in fba1-11 homozygous diploids; this is believed to occur as a consequence of reduced NH+4 levels in spd1-1-bearing strains, the reduced intracellular NH+4 content serving to promote gluconeogenesis via the residual low levels of enzyme activity present in such mutants.

Fructose-Bisphosphate Aldolase↗