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Biomedical subjects

C W Adams

Publications and source records attributed to C W Adams.

At least 55 records · Page 3Linked to original sources
PubMed1982

DNA sequence fine-structure analysis of ilvG (IlvG+) mutations of Escherichia coli K-12.

Six ilvG (IlvG+) mutations of Escherichia coli K-12 were transferred to recombinant plasmids, and the DNA sequence of each mutation was determined. This analysis confirmed that expression of the ilvG gene product (acetohydroxy acid synthase II) requires the deletion of a single base pair or the addition of two base pairs within ilvG to displace a frameshift site present in wild-type E. coli K-12. This system should be useful in the analysis of potential frameshift mutagens.

Acetolactate Synthase↗
PubMed1982

Macroscopic enzyme histochemistry in myocardial infarction: artefactual nature of the creatine phosphokinase reaction.

The histochemical creatine phosphokinase (CPK) tetrazolium test has been evaluated to detect recent human myocardial infarction in gross slices of the heart at necropsy. The demonstration of the lesion with this method has been assumed to result from local loss of CPK from the damaged myocardium. However, the present study indicates that the mechanism involved depends on localising NADPH tetrazolium reductase and not CPK. Phenazine methosulphate (PMS), when added to the incubating medium as an electron-acceptor to circumvent the tetrazolium-reductase (diaphorase) system, resulted in generalised false staining of the heart slice.

Aged↗
PubMed1982

Macroscopic enzyme histochemistry in myocardial infarction: use of coenzyme, cyanide, and phenazine methosulphate.

Transversely sectioned human heart slices, obtained at necropsy from normal subjects and from cases of recent myocardial infarction, were stained with the nitroblue tetrazolium (NBT) dehydrogenase macroreaction for the gross identification of recent myocardial infarction. The addition of nicotinamide adenine dinucleotide (NAD) to the incubating medium greatly improved the sensitivity of the method, while addition of cyanide caused just a modest improvement. Addition of the electron transfer mediator phenazine methosulphate (PMS) resulted in false non-selective staining and obscured areas of recent myocardial damage.

Clinical Enzyme Tests↗
PubMed1981

Different nucleotide changes in the large rRNA gene of the mitochondrial DNA confer chloramphenicol resistance on two human cell lines.

The nucleotide sequence of the mitochondrial DNA (mtDNA) in the region coding for the 3' end of the large rRNA has been determined for two human cell lines bearing independent cytoplasmic chloramphenicol-resistant (CAP-r) mutations. Comparison of the sequences of these two phenotypically different CAP-r mutants with their CAP-sensitive (CAP-s) parental cell lines has revealed a single base change for each in a region which is highly conserved among species. One CAP-r mutation is associated with an A to G transition on the coding strand while the second contains a G to T transversion 52 nucleotides away. Comparable sequence changes in this region had previously been found for mouse and yeast cell mitochondrial CAP-r mutants. Thus, changes in the large rRNA gene eliminate the inhibition of the ribosome by CAP and different nucleotide changes may result in variations in the drug-r phenotype.

Base Sequence↗
PubMed1981

Mutational specificity of the base analogue, 2-aminopurine, in Escherichia coli.

2-Aminopurine (2-AP) is a base analogue of adenine which mispairs with cytosine and causes base-pair substitutions of the transition type. By analyzing the reversion patterns of defined trpA alleles in Escherichia coli we confirm that 2-AP causes both A:T leads to G:C and G:C leads to A:T transitions with the former induced more frequently than the latter. We also find that 2-AP enhances transversions at 3 sites and frameshift mutations at 1 other site. It is unlikely that 2-AP can cause transversions and frameshifts solely by a mispairing mechanism. However, 2-AP-induced transversion and frameshift mutagenesis was not abolished by the presence of an inactive recA allele, indicating this mutagenic activity is not dependent upon recA-directed misrepair.

2-Aminopurine↗
PubMed1981

Molecular basis of valine resistance in Escherichia coli K-12.

The relationship of valine resistance to the expression of the ilvGEDA operon of Escherichia coli K-12 has been determined. DNA sequence and in vivo protein analyses indicate that in wild-type E. coli K-12 there is a frameshift site within the gene (ilvG) for valine resistance. The ilvG+2096 (formerly designated ilv02096) mutation displaces this frameshift site, resulting in the expression of ilvG and the relief of transcriptional polarity on the distal genes of this operon. Thus, the "ilv0" mutation, which concomitantly confers valine resistance and increased expression of the ilvEDA genes, is, in fact, the "reversion" of a polar site within the first structural gene of the ilvGEDA operon.

Base Sequence↗
PubMed1980

Preliminary oxidation in histochemical staining methods for cholesterol.

The need for preliminary oxidation with histochemical methods for cholesterol was investigated on silica-coated sheets and in tissue sections. The techniques used were the Schultz reaction, perchloric acid-naphthoquinone (PAN), Lewis & Lobban's ferric alum-sulphuric acid reagent and Okamoto's iodine-sulphuric acid. The oxidants assessed were ferric chloride, ferric alum, potassium permanganate, ammonium sulphamate and ultraviolet light. The best combinations amongst those tested in order of reactivity were FeCl3-PAN, ferric alum-Schultz, Lewis-Lobban (no additional oxidant), iodine-sulphuric acid (no additional oxidant). Authentic preparations of cholesterol oxidation products were stained with these methods, but the nature of the oxidized product in the preliminary stage could not be determined.

Cholesterol↗
PubMed1979

The pH dependence of borohydride as an aldehyde reductant.

The aldehyde-reducing capacity of borohydride has been investigated in the sequence periodic acid-borohydride-periodic acid-Schiff and variants. Densitometric studies on rat colonic mucins show that borohydride incompletely blocks periodate-engendered aldehydes unless the pH is above 8.2. Below this value, some aldehydes are not reduced and continue to be Schiff-stainable, while others are subsequently gerenated by the second exposure to periodic acid. The effect is more pronounced in paraffin than in cryostat sections, but does not apply to human colonic mucins.

Aldehydes↗
PubMed1979

The non-specific nature of the myocardial wavy fibre.

Wavy myocardial fibres were found in about half each of a series of 28 normal and 31 infarcted human hearts, as well as in the normal heart of an infant. Such fibres were also seen in rather more than half of a series of normal rat hearts. Thus, the wavy fibre is not a specific feature of acute ischaemic heart disease. Some experimental evidence was obtained that patchy loss or preservation of ATP promotes the formation of wavy fibres.

Adolescent↗
PubMed1978

The action of human high density lipoprotein on cholesterol crystals. Part 1. Light-microscopic observations.

High density lipoprotein (HDL) was found in vitro to form myelin buds (liposomes) from washed crystals of free cholesterol (commercial or atheroma sources). This activity led to the progressive destruction and solubilization of the crystals. Low density and very low density lipoproteins did not have any effect. Liposome formation and solubilization were accelerated by calcium ions, phospholipase A and polyunsaturated lecithin (Lipostabil). Cholesterol crystals were nearly completely destroyed after 18 h incubation with HDL-Lipostabil.

Arteriosclerosis↗
PubMed1978

The action of human high density lipoprotein on cholesterol crystals. Part 2. Biochemical observations.

Electron microscopy of the reaction product between human pooled high density lipoprotein (HDL) and cholesterol shows that characteristic liposome macromicellar bodies are formed. These bodies vary in size between 30 and 1200 nm. In comparison with HDL, they contain markedly more cholesterol, but less protein and phospholipid. Their phospholipid pattern shows enrichment with sphingomyelin and phosphatidyl serine in comparison with HDL.

Cholesterol↗
PubMed1978

The antiocclusive effect of coronary dilatation with age.

Human coronary arteries were perfusion-fixed; sectioned and their external and lumenal circumferences measured by microscopic planimetry. They were found to dilate with increasing age, and this change seems to be more a degenerative process than a response to increasing heart weight. It is inferred that a moderate degree of coronary dilatation compensates for the tendency of atherosclerosis to occlude the lumen. Absence of any coronary dilatation might be hazardous in that the stenosing effects of atherosclerosis would be enhanced. By contrast over-dilatation (ectasia) is dangerous in that it causes a reduced flow-rate and, hence, promotes thrombosis.

Adult↗
PubMed1978

Nitroblue tetrazolium test: early gross detection of human myocardial infarcts.

The hearts from 81 cases of suspected myocardial infarction were stained with the nitroblue tetrazolium (NBT) test to show damaged heart muscle in the gross at necropsy. Thirty-seven cases were of stated clinical age less than 12 h and 27 of these were less than 5 h. Seven out of 17 cases under 1 h were negative with NBT, but all other cases showed either focal diminution of staining with the dark blue diformazan or patchy red staining with the monogormazan of NBT. Thus the method may be of diagnostic value at necropsy from 1 h onwards after the time of apparent infarction (stated clinical onset). Satisfactory results were obtained up to 3 days at ambient temperature after death and for longer when the corpse was stored at 4 degrees C.

Humans↗
PubMed1977

Permeability in atherosclerosis: fluorescence test in green light with trypan blue.

A new microscopic fluorescence method for trypan blue at 570 nm has been used to follow the entry of albumin into the atheromatous rabbit aorta. Permeability into the inner aortic wall increases before the onset of gross lesions and seems just to precede intraendothelial deposition of lipid. Thereafter, permeability of the inner wall progressively increases until streaks or small plaques develop. These raised lesions stain and fluoresce variably, some intensely so while others are almost unreactive. This variability might reflect the difference between progressive and quiescent lesions. However, a zone of increased permeability surrounds many raised lesions, suggesting that the edge is a major site of growth and progression.

Animals↗