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Biomedical subjects

A H Jackson

Publications and source records attributed to A H Jackson.

At least 19 recordsLinked to original sources
PubMed1988

The isolation and identification of indigoid pigments from urine.

A purple pigment, phyriaviolin, and a blue pigment, phyriaazulin, have been found in relatively large amounts in the urine of patients suffering from two diverse pathological conditions, porphyria cutanea tarda and Crohn's disease. The two pigments have been characterised by chemical, spectroscopic, and chromatographic studies and identified to be indirubin and indigo (indigotin). Possible reasons for their formation are discussed.

Chromatography, Thin Layer↗
PubMed1987

The synthesis of stereoselectively labelled porphobilinogen and its incorporation into protoporphyrin-IX.

11-(R)-2H porphobilinogen, stereospecifically labelled with deuterium in the aminomethylene group has been incorporated into protoporphyrin-IX by haemolysates of chicken erythrocytes. High field NMR spectroscopy confirms that the overall biochemical process is stereospecific, deuterium being retained at the alpha-, gamma- and delta-meso positions and lost from the beta-meso position.

Animals↗
PubMed1984

Sputum sol-phase proteins and elastase activity in patients with cystic fibrosis.

Sputum and serum samples were obtained from 38 patients with cystic fibrosis seen as out-patients at routine follow-up, or from patients admitted with acute pulmonary exacerbations of their disease. Elastolytic activity was measurable in the sputum of 13 of 16 out-patient samples and detectable in 21 of 22 patients admitted with pulmonary exacerbation. The enzyme activity was inhibited by soy bean trypsin inhibitor and alpha 1 antitrypsin, but not by ethylenediamine tetracetic acid, suggesting that it was predominantly a serine proteinase, probably leucocyte elastase. The mean sputum/serum albumin ratio was 2.53 X 10(-2) (SD +/- 2.4) for the out-patients and this was not significantly different from those of patients admitted with pulmonary exacerbation. However, those patients admitted with fever had increased sputum/serum albumin ratios (mean = 4.66 X 10(-2); SD +/- 3.19) compared with those admitted with a normal temperature (mean = 1.52 X 10(-2); SD +/- 0.41. 2p less than 0.01). The albumin ratios of the pyrexial group fell with antibiotic therapy. The sputum/serum alpha 1 antitrypsin ratios were generally greater than expected (by comparison with albumin) and evidence is presented suggesting that this is due to immunological over-estimation.

Adolescent↗
PubMed1984

Apnea documentation for determination of brain death in children.

Discontinuing ventilatory support for determination of respiratory drive is a recognized means of assessing clinical brain death. Methodology must include a means for assuring adequate oxygenation during the test as well as providing sufficient duration for appropriate hypercarbia. Nine patients with other findings of clinical brain death were prospectively assessed with a standardized apnea test protocol. None demonstrated spontaneous respirations. Whereas adequate oxygenation was maintained in each case, wide variability was evident in degree of hypercarbia and acidosis.

Apnea↗
PubMed1983

Psychiatrists' responses to violence: pharmacologic management of psychiatric inpatients.

Court decisions setting limits on the use of medication in psychiatric hospitals often assume that psychiatrists use medications inappropriately in response to patients' violent acts. No empirical data have existed to support or refute this assumption. The authors examined the types and doses of antipsychotic medications received by 45 violent patients and 48 control subjects. They found no significant differences in type and dose of medication before the violent act and no significant changes afterward. Violent patients tended to be on somewhat higher doses at discharge than control patients. The judicial concern that psychotropic medications will automatically be abused or overused is not supported by these results.

Antipsychotic Agents↗
PubMed1978

Factors determining the sequence of oxidative decarboxylation of the 2- and 4-propionate substituents of coproporphyrinogen III by coproporphyrinogen oxidase in rat liver.

Coproporphyrinogen oxidase (EC 1.3.3.3) catalyses the oxidative decarboxylation of the 2- and 4-propionate substituents of coproporphyrinogen III to form protoporphyrinogen IX. A 4-propionate-substituted porphyrinogen, harderoporphyrinogen, which is also a substrate for coproporphyrinogen oxidase, is formed during the reaction. Synthetic [(14)C]coproporphyrinogens III, specifically labelled in the carboxyl carbon atoms of either the 2- or 4-propionate substituents, were used to measure the rate of decarboxylation of each substituent by rat liver coproporphyrinogen oxidase. The experimental results, together with the recognition that in all known substrates of coproporphyrinogen oxidase only those propionate groups flanked by a specific arrangement of substituents are decarboxylated, indicate that the 4-propionate group of coproporphyrinogen III cannot be attacked until the 2-propionate group has been decarboxylated. Production of (14)CO(2) from the substrate labelled in the 2-propionate group therefore measures the formation of harderoporphyrinogen, whereas (14)CO(2) from the 4-propionate-labelled substrate measures protoporphyrinogen IX formation. The rate of harderoporphyrinogen formation is about twice that of protoporphyrinogen, and this ratio is unchanged by varying the concentration of coproporphyrinogen III or by competitive inhibition of the enzyme. When coproporphyrinogen III is present in an excess, two fractions of harderoporphyrinogen can be distinguished. One accumulates during the reaction, and the other, which is destined to become protoporphyrinogen IX, does not equilibrate with added harderoporphyrinogen. It is suggested that both decarboxylations take place at the same active centre, which becomes temporarily inaccessible to coproporphyrinogen III and added harderoporphyrinogen, and that the molecule rotates after the first decarboxylation to allow the second to take place.

Animals↗