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Biomedical subjects

T Marshall

Publications and source records attributed to T Marshall.

At least 163 records · Page 9Linked to original sources
PubMed1991

Drug interference in the Bradford and 2,2'-bicinchoninic acid protein assays.

The interference of a range of drugs and related substances has been investigated in the Bradford Coomassie brilliant blue (CBB) protein dye-binding assay and the 2,2'-bicinchoninic acid (BCA) protein assays. Chlorpromazine was the only substance to interfere in the CBB assay but the interference was slight. In contrast, the BCA reagent interacted strongly with chlorpromazine, the penicillins, vitamin C, and paracetamol and the mode of interference varied with the test substance. The chlorpromazine produced turbidity and an atypical color. The penicillins show a slow but normal color response while vitamin C and paracetamol gave an immediate and intense response.

Drug Interactions↗
PubMed1991

Electrophoresis of serum isoenzymes and proteins following acute myocardial infarction.

The clinical significance of the serum enzymes creatine kinase (CK, EC 2.7.3.2), lactate dehydrogenase (LD, EC 1.1.1.27) and aspartate aminotransferase (EC 2.6.1.1), and the isoenzymes CK 1-3 and LD 1-5, in acute myocardial infarction (AMI) is reviewed. Particular attention is given to electrophoretic analysis of the isoenzymes (and the CK isoforms/subforms) following AMI and thrombolytic therapy. Other protein markers for the monitoring of AMI, including myoglobin and muscle contractile proteins, are also discussed and the potential for the detection of new marker proteins using high-resolution two-dimensional electrophoretic methods is demonstrated. Whilst emphasis is placed upon electrophoretic methods the value of complementary immunoassays is acknowledged in order to maintain a balanced perspective.

Aspartate Aminotransferases↗
PubMed1991

Simplification of the initiation of bromocriptine in elderly patients with advanced Parkinson's disease.

One hundred and seventy-three parkinsonian patients treated with levodopa entered a randomized multicentre comparison between two introductory schedules for adjuvant bromocriptine. A 2-week placebo run-in was followed by a double-blind 8-week titration phase of bromocriptine up to 15 mg daily, according to the standard seven-step, or a simpler three-step, regimen. They were maintained on this dose for a further 8 weeks and then followed for a further 12 weeks. One hundred and fifty-nine patients completed the placebo run-in period, and 132 completed 16 weeks. No significant differences were found between the standard and simplified regimens for efficacy, side-effects, withdrawals or deaths, nor for any of the clinical or functional assessments. The Webster score improved by 29% and the Cape ADL by 32%. The simpler schedule offers advantages to those elderly parkinsonian patients in whom bromocriptine is added to optimal levodopa dosage.

Aged↗
PubMed1991

Developmental profile of plasma proteins in human fetal cerebrospinal fluid and blood.

Total protein, alphafetoprotein, albumin, prealbumin, alpha-1-antitrypsin, transferrin and ceruloplasmin levels were measured in samples of human fetal and neonatal cerebrospinal fluid (CSF) (97 cases), obtained between 12 and 41 weeks of gestation. In 39 of these cases (13 to 40 weeks gestation) plasma was also available for comparative analysis. CSF was collected from lateral ventricles in the first half of gestation and from the lumbar region in the second. Since these CSF samples were obtained from different sites, the protein levels in the lateral ventricle (early) samples could not be compared directly with those in the lumbar (later) samples. However, the mean protein levels in the lumbar samples were lower than those in the ventricular samples, which is in accord with the decline in CSF protein levels described in maturing animal fetuses. Despite a wide scatter of results, particularly in the first half of gestation, significant decline in the level of CSF alphafetoprotein was demonstrated during both first and second halves of gestation, and of albumin and prealbumin in the second half. No sex differences were found except for ceruloplasmin in lumbar CSF later in gestation, when males had higher levels than females. In fetal plasma, protein levels increased with increasing gestation apart from alphafetoprotein and prealbumin which both declined progressively. CSF/plasma ratios were dissimilar for different proteins, and changed with increasing gestation. These findings support the concept that the human fetal blood brain barrier matures early.

Blood Proteins↗
PubMed1991

Clinical investigation of females with the Martin-Bell syndrome and risk assessment for carrier status.

Anthropometric measurements were made on a series of females heterozygous for the fragile-X syndrome. It was found that there were no simple series of discriminating features separating those of normal IQ from the mentally handicapped, but rather that the carriers studied represented a wide spectrum of phenotype. When measurements performed on 15 FRAXA negative, obligate carriers of normal IQ were considered separately, it was found that there were certain common phenotypic features allowing risk figures to be amended for those females at 50% risk of being a carrier but who are also FRAXA negative.

Adolescent↗
PubMed1991

Motor development and nutritional status of young children in Madang, Papua New Guinea.

The relationship between nutritional status and motor development was investigated in a cross-sectional study of 457 0-2 year old children in Madang, Papua New Guinea. The median ages at which the major motor developmental milestones are attained are almost comparable to western populations up to 6 months of age. However, crawling and independent walking are slower to develop. At any given age children of higher nutritional status by weight for age (W/A), length for age (L/A) or weight for length (W/L) are more likely to have attained a given developmental stage than children of lower nutritional status.

Age Factors↗
PubMed1991

Changes in the postenteropathic form of the hemolytic uremic syndrome in children.

An analysis was made of clinical and laboratory findings in children with the diarrheal form of the hemolytic uremic syndrome (HUS) treated at The Children's Hospital, Birmingham between 1970 und 1987. From 1982 the rate of referral increased, the prodromal illness more often consisted of bloody diarrhea, and the mean age at presentation doubled from 2 to 4 years. For patients with a good outcome there was an excess of males in the period 1970-81, and females in the period 1982-87. Moreover, in the years 1982-87 the disorder was distinguished from that of the earlier time by a positive correlation between adverse outcome and both neutrophil leukocytosis and a higher hemoglobin concentration at presentation. Prognostic scores obtained by logistic regression analysis were specific for each period. From July 1983 stool samples were analyzed for verocytotoxin-producing Escherichia coli (VTEC) and neutralizable verotoxin. Positive results were obtained in 39% of cases. The nature of HUS has changed and the new form of the disorder is associated with VTEC infection.

Acute Disease↗
PubMed1990

Safety at work for railway staff in Britain.

The recent series of railway accidents raised questions about the safety of British Railways. We have studied trends in accidents to railway staff over a 33-year period, 1954-86, which time has covered the pre- and post-modernization of the railways, in conjunction with large reductions in both staffing and traffic volume. The Railway Inspectorate, which has the duty of investigating and reporting on accidents occurring on railway premises, defines three kinds of accident: train, movement and non-movement. The numbers of railway staff killed and injured in each kind of accident have been studied in relation to the number of staff employed and train-miles run. Trends in the three accident rates derived thereby show quite different patterns: for most of the period under study, train accident rates have shown a linear increase and movement accident rates a linear decrease, whilst non-movement accidents exhibited no particular trend at all. In the last 5 years, however, both movement and non-movement accident rates have decreased sharply, whilst train accident rates have increased above the generally rising trend. Explanations for some of these trends and changes are suggested, but the reasons for others remain obscure.

Accidents, Occupational↗
PubMed1990

heterogeneity of creatine kinase isoenzyme MM in serum in myocardial infarction: interconversion of the "normal" and "abnormal" sub-bands by glutathione.

We used isoelectric focusing (IEF) in polyacrylamide gels to investigate the effects of glutathione on the sub-bands of serum creatine kinase (CK; EC 2.7.3.2) isoenzyme MM in acute myocardial infarction. The intensity of the "abnormal" sub-bands c (pI 7.25), e (pI 6.85), and g (pI 6.50) increased, and that of the "normal" sub-bands 1 (pI 6.91), 2 (pI 6.65), and 3 (pI 6.35) decreased, following serum incubation with reduced glutathione (GSH, final concentration 1.25 mmol/L). Further incubation with oxidized glutathione (GSSG, final concentration 5 mmol/L) reversed this change and restored the original pattern, whereas GSSG at 7.5 mmol/L caused sub-bands c, e, and g to disappear and sub-bands 1, 2, and 3 to be enhanced. Sequential incubation of serum with 2.5 mmol of GSSG and 7.5 mmol of GSH per liter produced the opposite sequence of events; i.e., the "abnormal" sub-bands disappeared then reappeared (and GSH at 10 mmol/L enhanced their reappearance). At higher concentrations, glutathione (GSH or GSSG) impaired the detection of the CK-MM sub-bands after IEF, an effect that was "quenched" by heat-inactivated serum of low CK activity. Likewise, the intensity of tissue CK-MM (corresponding to myocardium extracted into 100 mmol/L Tris HCl buffer, pH 7.4) was greatly enhanced by adding heat-inactivated serum to the tissue extract before IEF. We discuss the significance of these findings for the diagnosis of myocardial infarction.

Creatine Kinase↗