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Biomedical subjects

M Crook

Publications and source records attributed to M Crook.

At least 55 records · Page 3Linked to original sources
PubMed1994

Raised concentration of plasma creatine kinase BB isoenzyme in myelodysplasia.

A 72 year old woman presented with a suspected myocardial infarction. An echocardiograph showed no acute changes but her plasma creatine kinase (CK) activity was increased at 343 U/l (< 175 normal range). The apparent creatine kinase-MB activity by a CK-M subunit immunoinhibition assay was 350 U/l. In view of the discrepancy between the total creatine kinase and CK-MB activity plasma creatine kinase electrophoresis studies were performed which showed not only a band of creatine kinase-MM but also a band of creatine kinase-BB, 53% of the total creatine kinase activity. No band of CK-MB was seen. It later transpired that the woman had myelodysplasia. It is suggested that premalignant and malignant haematological conditions should be considered in patients with an unexplained increase in plasma CK-BB.

Aged↗
PubMed1994

Plasma sialic acid and acute-phase proteins in patients with myocardial infarction.

Plasma total sialic acid (TSA) and lipid-associated sialic acid (LASA) were measured in 19 patients with a myocardial infarction (MI) on days 1, 2, and 5 and in 19 normal subjects. On each day plasma TSA was elevated in the MI patients as compared with that of normal subjects, although no significant difference was seen in the plasma LASA between the two groups. The following plasma acute-phase proteins were also assayed in the MI patients and the normal subjects: C-reactive protein (CRP), alpha-1 acid glycoprotein (AGP), alpha-1 antichymotrypsin (ACT), alpha-2 macroglobulin (AMG), and fibrinogen (FIB). Significantly elevated plasma concentrations were found in the MI patients as compared with normal subjects. Furthermore, a significant correlation was found between some of these plasma acute-phase proteins (ACT, AMG, and FIB) and plasma TSA in the MI patients and also in normal subjects (ACT, AMG, CRP, and FIB). However, no significant difference was noted in any of the plasma acute-phase proteins, or plasma TSA, or plasma LASA between survivors and patients who died of their MI.

Acute-Phase Proteins↗
PubMed1994

Serum lipids, acute phase proteins and serum cholinesterase in normal subjects.

Although serum cholinesterase (CHE) is elevated in some hyperlipidaemic subjects, the relationship between serum CHE and lipids in normolipidaemic subjects is scanty. Furthermore, serum CHE is reduced in conditions in which there is an acute phase response. Serum CHE activity was measured in 46 normal individuals (22 males and 24 females). There was no significant difference between the activity of serum CHE in males or females being 6.2 +/- 1.8 U1(-1) vs. 6.4 +/- 1.5 U1(-1) respectively (mean +/- SD). There was, however, a significant correlation between serum CHE and subject age (Spearman rho 0.35, p < 0.05). There was also a significant correlation between serum CHE and serum nonfasting triglyceride concentration (rho 0.34, p < 0.05) and also apolipoprotein B (rho 0.38, p < 0.05) but not serum cholesterol or HDL-cholesterol. Five serum acute phase proteins were measured namely serum alpha-1 antichymotrypsin (ACT), alpha-1-acid-glycoprotein (AGP), alpha-2-macroglobulin (AMG), C-reactive protein (CRP), haptoglobin (HAP). Only serum AGP showed a significant negative correlation with serum CHE (rho - 0.43, p < 0.02).

Acute-Phase Proteins↗
PubMed1994

Erythrocyte, plasma total, ultrafiltrable and platelet magnesium in type 2 (non-insulin dependent) diabetes mellitus.

We studied plasma magnesium, plasma ultrafiltrable magnesium, erythrocyte and platelet magnesium in 28 non-insulin dependent (NIDDM) patients and 28 age and sex matched non-diabetic control subjects. The plasma magnesium concentration was significantly lower in the diabetic subjects as compared with the control subjects (0.67 +/- 0.09 mmol/l versus 0.72 +/- 0.07 mmol/l, P < 0.05) as was plasma ultrafiltrable magnesium (0.43 +/- 0.06 mmol/l versus 0.47 +/- 0.05 mmol/l, P < 0.01. Similarly, erythrocyte magnesium was lower in the diabetic subjects than the non diabetic controls, (0.17 +/- 0.03 nmol/10(6) cells versus 0.19 +/- 0.02 nmol/10(6) cells, P < 0.01. Platelet magnesium was higher in the diabetic subjects (48.3 +/- 19.1 umol/g platelet protein versus 36.6 +/- 22.2 umol/g platelet protein, P < 0.01). There was no significant difference between the % plasma ultrafiltrable magnesium with respect to total plasma levels between the diabetic and normal subjects (64.7 +/- 4.7% versus 65.8 +/- 3.2% respectively). There was no significant correlation between any of these parameters and systolic or diastolic blood pressure of HbA1C in the diabetics. Nor were there any significant differences in these magnesium parameters in patients with or without diabetic complications.

Age Factors↗
PubMed1993

Alpha 2-adrenoreceptor status of human platelet subpopulations separated by continuous flow electrophoresis.

Human platelets were separated into subpopulations using continuous flow electrophoresis, which uses electrophoretic mobility as the separative parameter. The platelets with the greatest electrophoretic mobility showed higher amounts of total sialic acid than the less electrophoretically mobile subpopulation (74.3 +/- 18.2 nmol/10(9) platelets vs. 49.2 +/- 20.1 nmol/10(9) platelets, p < 0.05 paired Student's t-test). Furthermore, neuraminidase-labile sialic acid was also elevated in the more electrophoretically mobile platelet subpopulation (29.1 +/- 6.0 nmol/10(9) platelets vs. 21.8 +/- 10.4 nmol/10(9) platelets, p < 0.05 paired Student's t-test). We also found that the sialic acid enriched platelet subpopulation had more alpha 2-adrenoreceptors than the less electrophoretically mobile platelets (457 +/- 104 vs. 302 +/- 164 receptors per cell, p < 0.05 paired Student's t-test).

Blood Platelets↗
PubMed1993

Evaluation of three assays for the determination of serum total sialic acid.

There is increasing clinical interest in the measurement of serum total sialic acid (TSA). There are a number of methods available but with little data suggesting the preferred technique. We evaluated three serum sialic acid assays: the Warren assay, the Svennerholm assay, and a commercially available enzymatic method. The analytical performances of the three assays were similar, except that the enzymatic assay had a greater analytical range than the other assays and better precision at low and high serum sialic acid concentrations. The enzymatic assay was readily automated for use on a Cobas Bio analyser but was substantially more expensive than the other two methods.

Chemistry, Clinical↗
PubMed1993

The determination of plasma or serum sialic acid.

Plasma or serum sialic acid has been established as a potential tumour marker. More recently it has been shown that elevated serum sialic acid is a risk factor for cardiovascular mortality. A variety of assays are available to measure serum or plasma sialic acid and are discussed in this review, along with other clinical conditions in which serum or plasma sialic acid may be of relevance. Other factors influencing serum or plasma sialic acid concentrations are also discussed.

Biomarkers↗
PubMed1993

Serum sialic acid and acute-phase proteins in hypertriglyceridaemic patients showing the Frederickson's type IIB phenotype.

1. We have shown that serum total sialic acid is elevated in hypertriglyceridaemic patients showing the Frederickson's type IIB phenotype in comparison with normal subjects (2.30 +/- 0.34 versus 1.92 +/- 0.32 mmol/l, P < 0.02). Lipid-associated sialic acid was also elevated in the hypertriglyceridaemic group in comparison with the normal subjects (0.60 +/- 0.09 versus 0.35 +/- 0.04 mmol/l, P < 0.001). 2. We measured five serum acute-phase proteins in the hypertriglyceridaemic patients and the normal subjects, namely alpha 1-antichymotrypsin, alpha 1-acid glycoprotein, alpha 2-macroglobulin, C-reactive protein and haptoglobin. Serum alpha 2-macroglobulin was significantly elevated in the hypertriglyceridaemic patients compared with the normal subjects (2.1 +/- 1.0 versus 1.5 +/- 0.55 g/l, P < 0.05) as was serum C-reactive protein (5.9 +/- 3.5 versus 3.5 +/- 1.9 mg/l, P < 0.05). There were, however, no significant differences in the serum concentrations of alpha 1-antichymotrypsin, alpha 1-acid glycoprotein or haptoglobin between the two groups. 3. There was a significant correlation between serum total sialic acid and serum alpha 1-antichymotrypsin, alpha 1-acid glycoprotein and haptoglobin (Spearman correlation coefficients 0.74, 0.50 and 0.76, respectively) in the normal subjects, and there was a significant correlation between serum total sialic acid and serum alpha 1-antichymotrypsin and alpha 1-acid glycoprotein (Spearman correlation coefficients 0.72 and 0.84, respectively) in the hypertriglyceridaemic patients.

Acute-Phase Proteins↗
PubMed1993

Serum total sialic acid and lipid-associated sialic acid in normal individuals and patients with myocardial infarction, and their relationship to acute phase proteins.

Serum total sialic acid (TSA) has gained medical interest, particularly as a cardiovascular risk factor and it has been hypothesized that serum levels relate to serum acute phase proteins, some of which are sialylated. We assayed serum TSA and also lipid associated sialic acid (LASA) in 50 normal individuals (24 male) and 15 subjects (12 male) who had experienced a myocardial infarct. The mean serum TSA in the normal individuals was 2.05 SD 0.38 mmol/L (range 1.16-2.74) and the mean serum LASA was 0.70 SD 0.19 mmol/L (range 0.23-1.03). We also measured five serum acute phase proteins and found a good correlation between these and serum TSA: C-reactive protein, r = 0.52, P < 0.001, alpha-1-antichymotrypsin, r = 0.79, P < 0.0001, alpha-2-macroglobulin, r = 0.38, P < 0.01 and alpha-1-acid glycoprotein, r = 0.32, P < 0.05. A significant correlation between plasma TSA and plasma C-reactive protein (r = 0.47, P < 0.04) and also fibrinogen (r = 0.53, P < 0.04) was noted on day one following the myocardial infarction, whereas a significant correlation between plasma TSA and plasma alpha-1-antichymotrypsin (r = 0.51, P < 0.03) and also plasma alpha-1-acid glycoprotein (r = 0.64, P < 0.05) was found on day two following the infarction. Thus it would seem that serum TSA is at least in part related to some of the acute phase proteins in both healthy individuals and those having had a myocardial infarction.

Acute-Phase Proteins↗
PubMed1993

Hypouricaemia in a hospital population.

The prevalence of hypouricaemia in a hospital population was studied. Hypouricaemia in females, defined as less than 0.14 mmol l-1 was found in 4.8% of all urate requests. Similarly, the prevalence in males, defined as less than 0.20 mmol l-1 was 6.5%. The largest group displaying hypouricaemia was intensive care patients. Oncology patients, particularly those with haematological malignancies also exhibited hypouricaemia. Another patient group in which hypouricaemia was prevalent were those with diabetes mellitus treated with insulin.

Diabetes Mellitus↗
PubMed1992

Serum sialic acid concentration in patients with hypertriglyceridaemia showing the Frederickson's IIB phenotype.

1. Serum total sialic acid concentration, recently shown to be a cardiovascular risk factor, and also serum lipid-associated sialic acid concentration were measured in 15 patients with hypertriglyceridaemia (fasting serum triacyglycerol concentration > 2.3 mmol/l) showing a Frederickson's type IIB phenotype, 15 patients with hypercholesterolaemia showing a IIA phenotype and 15 age- and sex-matched normal control subjects. 2. Total serum sialic acid concentration was significantly raised in the hypertriglyceridaemic group (84.9 +/- 21.5 versus 64.9 +/- 20.8 mg/dl, P < 0.03, Mann-Whitney U-test) compared with the normal control group, as was serum lipid-associated sialic acid concentration (23.0 +/- 4.3 versus 12.0 +/- 3.2 mg/dl, respectively, P < 0.001, Mann-Whitney U-test). 3. Serum total sialic acid concentration was also significantly elevated in the hypertriglyceridaemic group as compared with the IIA phenotype hypercholesterolaemic group (84.9 +/- 21.5 versus 58.4 +/- 11.7 mg/dl, P < 0.03, Mann-Whitney U-test), as was serum lipid-associated sialic acid concentration (23.0 +/- 4.3 versus 14.9 +/- 4.7 mg/dl, P < 0.001, Mann-Whitney U-test). 4. We suggest that serum concentrations of both total sialic acid and lipid-associated sialic acid may be useful markers of cardiovascular risk which could, in part, be related to hypertriglyceridaemia.

Biomarkers↗
PubMed1992

Electrokinetic behaviour and surface sialic acid status of blood platelets in essential thrombocythaemia (ET).

We have previously reported, for platelets from patients with idiopathic thrombocytopenic purpura, that there was in increased electrophoretic mobility that was related to their increased sialic acid content. Heterogeneity in the circulating platelet pool of patients with essential thrombocythaemia (platelet counts 600-1000 x 10(9)/l) has also been investigated by preparative continuous flow electrophoresis (CFE). The surface charge-dependent separation profiles of all the patients' platelets showed marked anodal shifts compared with the profiles of platelets from age- and sex-matched control subjects separated under identical conditions. The increase above normal in the net electronegativity of the patients' platelets could not be accounted for by differences in surface neuraminidase-labile or total platelet sialic acid content.

Blood Platelets↗
PubMed1992

Hypophosphataemia in a hospital population and the incidence of concomitant hypokalaemia.

There have been few recent studies describing the incidence and causes of hypophosphataemia in a hospital population and the frequency of concomitant hypokalaemia. In this study a majority (53%) of patients with hypophosphataemia had been on a glucose infusion at the time of their low plasma phosphate. The largest patient group found to show hypophosphataemia (less than 0.8 mmol/L) were in the Intensive Therapy Unit (ITU), and this was also the largest patient group manifesting severe hypophosphataemia (less than 0.3 mmol/L). Approximately, 11% of patients with hypophosphataemia (less than 0.8 mmol/L) had a plasma potassium equal to or less than 3.5 mmol/L, compared with 5.7% of hospital patients without hypophosphataemia. Furthermore, 20% of patients with severe hypophosphataemia (less than 0.3 mmol/L) had hypokalaemia as similarly defined.

Hospitalization↗