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Biomedical subjects

M E Cooper

Publications and source records attributed to M E Cooper.

At least 199 records · Page 11Linked to original sources
PubMed1987

The development of Cushing's syndrome from a previously silent pituitary tumour.

A 60 year old woman originally presented with headache. Investigations revealed a pituitary tumour and endocrine investigations at that time showed normal plasma cortisol levels. Seven years after removal of this tumour, the patient developed the clinical and biochemical features of Cushing's disease. Immunoperoxidase staining of the original tumour was positive for adrenocorticotrophic hormone. This report suggests that immunocytochemistry may have an important role in the routine evaluation of pituitary tumours.

Adenoma↗
PubMed1986

Nuclear scanning in the diagnosis and localization of parathyroid adenomas.

Technetium-thallium nuclear scanning was performed in 17 patients whose clinical and biochemical findings were suggestive of the presence of hyperparathyroidism. An adenoma was located by scanning in 12 patients. Ten of these 12 patients underwent surgery; the scan had located the adenoma correctly in all these patients. One patient with a negative result of a scan examination subsequently had an adenoma removed at operation. Thyroid pathology interfered with the interpretation of the scan. This technique is recommended as a useful preoperative procedure for the detection of parathyroid adenomas, and its role in the rapid evaluation of hypercalcaemia seems promising. A prospective study to compare the sensitivity and specificity of this technique with computerized tomographic scanning and ultrasound is warranted.

Adenoma↗
PubMed1986

Identification and characterization of both the cytosolic and particulate forms of cyclic GMP-stimulated cyclic AMP phosphodiesterase from rat liver.

Two enzymes displaying cyclic GMP-stimulated cyclic AMP phosphodiesterase activity were purified from rat liver to apparent homogeneity: a 'particulate enzyme' found as an integral membrane protein associated with the plasma membrane, and a 'soluble' enzyme found in the cytosol. The physical properties of these enzymes were very similar, being dimers of Mr 134,000, composed in each instance of two subunits of Mr = 66,000-67,000. Both enzymes showed similar kinetics for cyclic AMP hydrolysis. They are both high-affinity enzymes, with kinetic constants for the particulate enzyme of Km = 34 microM and Vmax. = 4.0 units/mg of protein and for the cytosolic enzyme Km = 40 microM and Vmax. = 4.8 units/mg of protein. In both instances hydrolysis of cyclic AMP appeared to show apparent positive co-operativity, with Hill coefficients (happ.) of 1.5 and 1.6 for the particulate and cytosolic enzymes respectively. However, in the presence of 2 microM-cyclic GMP, the hydrolysis of cyclic AMP obeyed Michaelis kinetics (happ. = 1) for both enzymes. The addition of micromolar concentrations of cyclic GMP had little effect on the Vmax. for cyclic AMP hydrolysis, but lowered the Km for cyclic AMP hydrolysis to around 20 microM in both cases. However, at low cyclic AMP substrate concentrations, cyclic GMP was a more potent activator of the particulate enzyme than was the soluble enzyme. The activity of these enzymes could be selectively inhibited by cis-16-palmitoleic acid and by arachidonic acid. In each instance, however, the hydrolysis of cyclic AMP became markedly more sensitive to such inhibition when low concentrations of cyclic GMP were present. Tryptic peptide maps of iodinated preparations of these two purified enzyme species showed that there was considerable homology between these two enzyme forms.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1986

Accelerated progression of diabetic nephropathy in the spontaneously hypertensive streptozotocin diabetic rat.

Streptozotocin (STZ)-diabetes was induced in spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats with their litter mates serving as controls. The animals were studied for 6 months and blood pressure, weight, urinary and serum glucose, creatinine clearance, total proteinuria and albuminuria were measured monthly. With induction of diabetes, there was a significant rise in creatinine clearance in the hypertensive diabetic animals (SHR-STZ). SHR-STZ (n = 6) developed higher levels of total proteinuria than WKY-STZ (n = 5) although the rise from basal levels was only apparent after 20 weeks of diabetes. All SHR-STZ developed albustix positive proteinuria after 6 months of diabetes. In the first 12 weeks after onset of diabetes, albuminuria increased to a greater degree in SHR-STZ than in WKY-STZ. This occurred before there was a detectable rise in total proteinuria. The SHR-STZ model of genetic hypertension and diabetes may be suitable for the evaluation of antihypertensive therapy in human diabetic renal disease.

Albuminuria↗
PubMed1983

The Zoo Licensing Act 1981.

The Zoo Licensing Act 1981 introduces a system of licensing and inspection for zoos and other collections of nondomesticated species to which the public has access. The requirements of the Act are outlined with particular reference to the various forms of inspection, some of which involve the veterinary profession. This legislation is a new concept for Britain and heralds a new era in the management and recognition of zoological collections.

Animal Husbandry↗
PubMed1979

The determination of aluminium in antacid formulations by Gran's Plot titration with sodium fluoride.

The aluminium content of a number of proprietary antacid formulations has been determined by titration with sodium fluoride, using the fluoride activity electrode as an end-point detector. Results compared favourably with the official method. The fluoride titration, however, involved less sample manipulation and was more rapid to carry out. End-point detection was made easier by treating titration data by the Gran's Plot method.

Aluminum↗
PubMedDate not supplied

Glomerular filtration rate in early experimental diabetes.

A noninvasive single injection technique for the measurement of glomerular filtration rate (GFR) using technetium99m diethylene triamine pentaacetic acid (DTPA) was developed for use in the rat. GFR measurements obtained by the technique correlated well with those obtained by Cr51 EDTA infusion (R = 0.95, n = 7). The coefficient of variation was 8.4%. GFR was measured over 4 weeks in diabetic and control rats. GFR increased with time in both groups, with no difference between the groups; however, when corrected for body weight, diabetes was associated with an increased GFR (diabetic 13.6 +/- 1.7 vs. control 10.4 +/- 0.1 ml/min/kg p less than 0.001). Insulin treated rats had higher GFRs than untreated diabetics (p less than 0.05), but GFR/kg was reduced to that of nondiabetic controls. High protein intake in diabetic rats caused an increase in GFR after 1 week of diabetes, but this was not sustained by the fourth week. Genetic hypertension and angiotensin converting enzyme (ACE) inhibition with ramipril had no effect on GFR in diabetic rats. We conclude that serial measurement of GFR in the diabetic rat is accurate and reproducible. Genetic hypertension, high protein intake, and ACE inhibition have little effect on GFR in experimental diabetes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Intermittent diabetic microalbuminuria: association with blood pressure, glycemic control, and protein intake.

The factors associated with intermittent microalbuminuria were studied over 7 years in 49 Type I and 53 Type II diabetics who had normal initial albumin clearance. Fasting plasma glucose, HbA1, 24 hour urinary glucose, blood pressure, protein intake (24 hour urinary urea), and the renal clearance of albumin, transferrin, and IgG, as well as total proteinuria, were assessed every 3-6 months. Fifteen Type I and 11 Type II diabetics had 40 and 31 episodes, respectively, of intermittent microalbuminuria, defined as an albumin clearance greater than 11 nl/sec, without progressing to persistent microalbuminuria. Rises in transferrin and IgG clearance paralleled albumin clearance in both Type I and Type II diabetics. There were no significant changes in blood pressure or glycemic control during episodes of intermittent microalbuminuria. However, in Type I diabetics, intermittent microalbuminuria was associated with higher levels of urinary urea excretion. This study raises the possibility that increased protein intake may participate in the development of nephropathy in Type I diabetes.

Adult↗
PubMedDate not supplied

Prediction of persistent microalbuminuria in patients with diabetes mellitus.

Persistent microalbuminuria [albumin excretion rate (AER): 30-300 micrograms/min] is predictive of clinical nephropathy in patients with insulin-dependent diabetes mellitus (IDDM) and cardiovascular mortality in addition to nephropathy in patients with non-insulin-dependent diabetes. The clinical significance of intermittent microalbuminuria, however, is unknown. We performed serial measurements of urinary albumin excretion at intervals of approximately 6 months in 139 diabetic patients who at entry did not have persistent microalbuminuria to determine whether intermittent microalbuminuria occurs more frequently in those patients who subsequently develop persistent microalbuminuria. The relative risk for the development of persistent microalbuminuria in diabetic patients with a greater proportion than 3 out of 20 determinations in the microalbuminuric range was 17.4 (95% confidence interval, 3.92-77.2) in those with IDDM and 2.78 (0.99-7.8) in those with non-insulin-dependent diabetes when compared with matched diabetic patients with fewer elevated measurements. These data suggest that frequent intermittent microalbuminuria predicts the future development of persistent microalbuminuria particularly in IDDM patients and that AER should be assessed by serial rather than single measurements.

Adolescent↗
PubMedDate not supplied

Extracellular matrix and its interactions in the diabetic kidney: a molecular biological approach.

Increased extracellular matrix (ECM) is the ultrastructural hallmark of diabetic microangiopathy. Its accumulation within the kidney is directly linked to the clinical manifestations of diabetic nephropathy, namely proteinuria and declining renal function. The pathogenesis of ECM changes in diabetes is not well understood, but is likely to involve interaction between cells, growth factors, structural proteins, and cell receptors for these molecules. Molecular biological techniques may offer the necessary tools for gaining insight into the pathogenetic processes that eventually lead to renal failure in diabetes.

Animals↗
PubMedDate not supplied

Vascular changes in the diabetic kidney: effects of ACE inhibition.

The effects of angiotensin-converting enzyme (ACE) inhibition with perindopril on renal vascular structure were studied in control and streptozotocin diabetic male Sprague-Dawley rats after 3 weeks. After kidneys were perfusion-fixed at systolic blood pressure, morphometric analysis of vascular structural changes in the media of the renal vasculature at the cortico-medullary junction was performed. Vascular hypertrophy was present in the diabetic vessels, as assessed by an increase in medial cross-sectional area for a given lumen size. This relative increase in medial area was prevented by perindopril treatment, consistent with an antitrophic effect on diabetic kidney vessels by ACE inhibition. The diabetic kidney had an increased proportion of small vessels less than 50 microns diameter at the cortico-medullary junction, perhaps representing diabetes induced angiogenesis. This subpopulation of vessels was reduced in number after perindopril treatment. Our data support a role for increased activity of angiotensin converting enzyme as a mechanism for vascular hypertrophy, which may be involved in the pathogenesis of diabetic vasculopathy and nephropathy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Natural history of early diabetic nephropathy: what are the effects of therapeutic intervention? Melbourne Diabetic Nephropathy Study Group.

Several studies have shown that lowering of blood pressure slows the rate of progression of diabetic renal disease. Some placebo-controlled studies have also shown that angiotensin-converting enzyme (ACE) inhibitors decrease or stabilize albuminuria in incipient nephropathy and slow the rate of progression of advanced nephropathy. However, it is not yet clear if prolonged treatment with ACE inhibitors or with other agents exerts a specific renoprotective effect in incipient diabetic nephropathy. It is proposed that such an effect should be independent from changes in systemic blood pressure and should be characterized by amelioration of the rate of rise of albumin excretion rate (AER) and the rate of fall of glomerular filtration rate (GFR) and independence from changes in other parameters known to influence AER (glycemic control, protein intake, sodium intake). In addition, there should be evidence that the potentially reversible effects of therapeutic intervention on AER and GFR are translated to long-term changes in renal function and structure. This paper reviews the evidence on which the concept of renoprotection is based, with particular reference to choice of end points, heterogeneity of study groups, and complexities of the disease process, and relates this evidence to the natural history of nephropathy in type I and type II diabetes. Based on the above, an assessment is made of the comparative effects of ACE inhibitors and other antihypertensive agents on AER and GFR. It is suggested that longitudinal intra-individual analysis of both variables may be necessary in order to determine whether ACE inhibitors exert greater renoprotection than calcium channel blockers or other antihypertensive agents.

Albuminuria↗
PubMedDate not supplied

Diabetic vascular hypertrophy and albuminuria: effect of angiotensin converting enzyme inhibition.

The role of angiotensin-converting enzyme (ACE) inhibition with ramipril on mesenteric vascular hypertrophy and urinary albumin excretion was explored in a normotensive model of experimental diabetes. Serial measurements of albuminuria were performed in Sprague-Dawley control, diabetic rats, and diabetic rats treated with ramipril. Over 24 weeks, urinary albumin excretion showed a continuous rise in the untreated diabetic rats. Ramipril prevented the increase in albuminuria over the whole study period. After 6 months, animals were perfused with glutaraldehyde and sacrificed for measurement of mesenteric vessel wall/lumen ratio and kidney weight. Diabetes was associated with increased mesenteric wall/lumen ratio and kidney weight. ACE inhibition, despite no effect on glycemic control, attenuated mesenteric vascular hypertrophy but did not decrease kidney weight. In addition to the well-described renoprotective effects of ACE inhibition in diabetes, this class of agents may have a favorable effect on diabetic vascular disease.

Albuminuria↗