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Biomedical subjects

C Chapman

Publications and source records attributed to C Chapman.

At least 37 records · Page 2Linked to original sources
PubMed1991

Transferrinuria in type 2 diabetes: the effect of glycaemic control.

Urinary excretion rates of transferrin, albumin, N-acetyl-beta-D-glucosaminidase (NAG) and alpha-1-microglobulin (A1M) were measured in type 2 (non-insulin-dependent) diabetic patients at diagnosis and after 6 and 12 weeks treatment. Initially 21 (53%) patients had elevated transferrin excretion rates. The proportion of patients with raised transferrin excretion rates fell to 30% at 6 weeks and 20% at 12 weeks with treatment of diabetes. At diagnosis 11 (28%) patients had elevated albumin excretion rates and 10 of these had elevated transferrin excretion rates. After 6 weeks treatment only six (15%) had elevated albumin excretion rates and by 12 weeks this number had fallen to four (10%). NAG and A1M levels also fell with treatment of diabetes. There were correlations between the transferrin excretion rate and albumin excretion rate (r = 0.86, P less than 0.0001), transferrin excretion rate and NAG (r = 0.46, P less than 0.0001), and transferrin excretion rate and A1M (r = 0.55, P less than 0.0001) at each visit. There were weaker correlations between the albumin excretion rate and A1M and NAG at each visit. The correlations between the transferrin excretion rate and markers of tubular function (NAG and A1M) suggest that tubular dysfunction may play a part in renal loss of transferrin in diabetes mellitus. There were no differences in transferrin excretion rates between patients with and without evidence of complications.

Adult↗
PubMed1991

Increased urinary transferrin excretion in exercising normoalbuminuric insulin-dependent diabetic patients.

The median rate of urinary transferrin excretion is greatly increased by exercise in subjects with uncomplicated type 1 (insulin-dependent) diabetes. This increase is proportionally far greater than that seen in urinary albumin excretion rate after the same exercise. Non-diabetic control subjects showed no rise in urinary transferrin excretion rate following exercise. N-acetyl-beta-D-glucosaminidase excretion rate was higher in diabetic than control groups but did not rise with exercise. Our results suggest that patients with apparently uncomplicated diabetes have abnormal renal function. In this group an elevated urinary transferrin excretion rate appears to be a more sensitive indicator of altered renal function than is elevated albumin excretion rate. The mechanism underlying exercise-induced urinary loss of transferrin remains to be elucidated.

Acetylglucosaminidase↗
PubMed1991

The use of vidarabine in the treatment of human polyomavirus associated acute haemorrhagic cystitis.

The human BK and JC polyomaviruses are known to be reactivated and excreted in the urine following bone marrow transplantation (BMT). A proportion of patients who excrete BK virus following BMT experience a haemorrhagic cystitis (HC), which may persist for many months. We report a case of human polyomavirus-associated HC, in whom treatment with vidarabine was associated with a dramatic response.

Acute Disease↗
PubMed1990

Long-term prognostic value of serum beta 2 microglobulin in myelomatosis.

The prognostic value of serum beta 2 microglobulin (s beta 2m) measured at entry, at plateau and at 3-monthly follow-up times has been assessed for patients in the Medical Research Council's 4th and 5th Myelomatosis Trials. Analysis of 1014 patients confirmed the value of presentation s beta 2m of predicting survival in the short term but showed that predictive value was lost for subsequent survival in those patients who had survived for at least 2 years. However, measurements of s beta 2m taken during follow-up were predictive of subsequent survival. The predictive power of these follow-up measurements was very similar to that for the presenting measurement, and again they were only of value in predicting survival in the next 2 years.

Calcium↗
PubMed1990

Increased urinary excretion of transferrin in children with type 1 diabetes mellitus.

Urinary transferrin excretion was measured by radioimmunoassay in 74 children with Type 1 diabetes mellitus and in 40 normal children, and compared with urinary excretion of albumin, alpha-1-microglobulin, and N-acetyl-beta-D-glucosaminidase. Urinary transferrin excretion was significantly elevated in diabetic (median (range) 186 (18-1671) mg mol-creatinine-1) compared with normal (85 (27-668) mg mol-creatinine-1) children (p less than 0.001). Seventeen diabetic children had transferrin excretion above the 95th centile for normal children. In contrast there was no significant increase in urinary albumin excretion in the diabetic children although 8 had urinary albumin excretion which exceeded the 95th centile for normal children (6 of these 8 patients having coexistent urinary hyperexcretion of transferrin). Urinary transferrin excretion correlated significantly with urinary albumin excretion in both normal (rs = 0.62, p less than 0.001) and diabetic (rs = 0.61, p less than 0.001) children. The indices of proximal renal tubular function (urinary excretion of alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase) correlated significantly with transferrin excretion in both diabetic (rs = 0.43 and rs = 0.41, p less than 0.001) and normal (rs = 0.40, p less than 0.02 and rs = 0.53, p less than 0.001) children, but not with albumin excretion (rs = 0.20, p greater than 0.05 and rs = 0.22, p greater than 0.05). In addition urinary transferrin excretion significantly correlated with urinary glucose concentration (rs = 0.34, p less than 0.007) in Type 1 diabetic children. The discrepancy in urinary excretion of transferrin and albumin may reflect impaired proximal renal tubular reabsorption of transferrin and/or altered glomerular basement membrane selectivity for the two proteins.

Acetylglucosaminidase↗
PubMed1990

A novel T-cell protein which recognizes a palindromic sequence in the negative regulatory element of the human immunodeficiency virus long terminal repeat.

Two major protein-binding sites within the negative regulatory element of the human immunodeficiency virus type 1 long terminal repeat have been identified. One (site B) contained a palindromic sequence with homology to steroid/thyroid hormone response elements but was distinct from previously described binding sites of this class. A novel T-cell protein recognized the palindromic sequence within site B and also bound estrogen- or thyroid hormone-response elements with lower affinity. A 7-base-pair mutation in the site B palindrome, which destroyed protein binding, resulted in increased expression from the human immunodeficiency virus type 1 long terminal repeat in T cells.

Base Sequence↗
PubMed1990

Microbumintest and non-albumin proteinuria in diabetes.

Bedside methods for the detection of microalbuminuria such as Microbumintest (TM) have the advantage of simplicity but not the specificity of radio-immunoassay. In the present study we assessed whether apparently inappropriate positive Microbumintest results in the presence of low urinary albumin concentrations could be accounted for by non-albumin proteinuria of glomerular or renal tubular origin. Urinary albumin and transferrin were considered to indicate glomerular proteinuria, and alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase to reflect tubular proteinuria. Microbumintest had a sensitivity of 100% and specificity of 67% to detect a urinary albumin concentration of 40 mg/l. Samples with albumin concentration less than 40 mg/l contained more total protein: 110 (78-155) v 60 (35-104) mg/l p less than 0.0001 (geometric means with 1 SD range), more albumin: 11.7 (5.1-26.8) v 5.4 (2.8-10.4) mg/l p less than 0.005 and more transferrin: 496 (191-1284) v 174 (78-389) micrograms/l p less than 0.001, in those testing positive with Microbumintest than in those testing negative. Microbumintest had a sensitivity of 82% and specificity of 75% to detect an albumin concentration of 20 mg/l. In samples containing less than or equal to 20 mg/l albumin, the mean albumin concentration was no greater in those testing positive compared with those testing negative. However, total protein: 108 (72-161) v 60 (34-105) mg/l p less than 0.001, and transferrin: 326 (148-715) v 157 (78-316) micrograms/l p = 0.01 both remained increased in samples testing positive compared with those testing negative.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1988

Functional kappa-opioid receptors on oxytocin and vasopressin nerve terminals isolated from the rat neurohypophysis.

Opioids intrinsic to the rat neurohypophysial system act to inhibit secretion from the terminals of magnocellular neurones. Opioid receptors in the neurohypophysis are predominantly of the kappa-subtype and selective kappa-agonists suppress electrically evoked release of oxytocin (OXT) and vasopressin (AVP). We have looked for the presence of functional kappa-receptors on neurohypophysial nerve terminals by examining effects of kappa-agonists on secretion from suspensions of isolated neurohypophysial nerve terminals (neurosecretosomes) retained on filters in a perifusion system. Release of both OXT and AVP evoked by K+-depolarisation was inhibited by the kappa-agonists U-50,488H (34% and 45% respectively) and dynorphin A1-13 (68% and 51% respectively). Inhibition by dynorphin A was only observed in the presence of peptidase inhibitors. The actions of both kappa-agonists were prevented by the opioid receptor antagonist naloxone. The experiments indicate the presence of kappa-receptors on terminals of OXT and AVP neurones. This receptor population is in addition to those previously described on pituicytes and those influencing release of neurohypophysial noradrenaline.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1988

Microdialysis measurement of oxytocin, aspartate, gamma-aminobutyric acid and glutamate release from the olfactory bulb of the sheep during vaginocervical stimulation.

Concentrations of oxytocin and amino acids were measured in microdialysis samples taken from the olfactory bulbs of 5 conscious, oestrogen-treated ewes before, during and after a 10-min period of vaginocervical stimulation. Results showed that vaginocervical stimulation induced significant increases in concentrations of oxytocin, aspartate, gamma-aminobutyric acid (GABA) and glutamate in dialysis samples. Concentrations of other amino acids measured were not affected. These findings show that vaginocervical stimulation produces significant changes in neurochemical release in the olfactory bulbs of sheep. Such changes may be involved in the induction of maternal behaviour of the olfactory recognition of offspring.

Animals↗
PubMed1988

Opioid-noradrenergic interactions in the neurohypophysis. I. Differential opioid receptor regulation of oxytocin, vasopressin, and noradrenaline release.

The actions of opioids on electrically evoked release of oxytocin, vasopressin, and noradrenaline-using the [3H]-noradrenaline technique-from the rat neurohypophysis were examined in vitro. Antagonism of the action of endogenous neurohypophysial opioids with naloxone enhanced release of peptides and [3H]-noradrenaline differentially. Naloxone enhanced oxytocin release by 100 and 173% in two series of experiments (ED50 7 x 10(-7) M), whilst vasopressin release was enhanced by only 30 and 20%, respectively. [3H]-noradrenaline release was maximally enhanced by 41% (ED50 2 x 10(-7) M). We examined the opioid receptor subtypes mediating these effects using selective receptor agonists. The kappa-agonist U-50,488H inhibited oxytocin and vasopressin release to a similar extent, but did not modify [3H]-noradrenaline release. The effects of U-50,488H were completely prevented by a tenfold molar excess of naloxone. The mu-agonist (D-Ala2, MePhe5 Gly-ol)-enkephalin also failed to inhibit [3H]-noradrenaline release and caused only a minor inhibition of oxytocin and vasopressin secretion. The delta-agonist (D-Pen2, D-Pen5)-enkephalin was without effect. We conclude that (1) kappa-receptors sensitive to U-50,488H mediate opioid inhibition of secretion from oxytocin and vasopressin nerve terminals; (2) when opioid actions are blocked by naloxone, opioid peptides within the neurohypophysis are shown to exert a much greater influence over oxytocin compared to vasopressin terminals; (3) neurohypophysial opioids also regulate release from noradrenergic terminals, although the nature of the receptors involved remains unclear, and (4) kappa-receptors can mediate inhibition of neurohormone secretion by an action independent of the neurohypophysial noradrenergic innervation.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1988

Opioid-noradrenergic interactions in the neurohypophysis. II. Does noradrenaline mediate the actions of endogenous opioids on oxytocin and vasopressin release?

The function of noradrenaline in the rat neurohypophysis was investigated by examining the effects of selective adrenergic receptor agents on electrically evoked release of oxytocin, arginine vasopressin, and noradrenaline using the [3H]-noradrenaline technique. Since endogenous opioids in the neurohypophysis suppress release of both neurohormones and of noradrenaline, we assessed the role of noradrenaline in mediating opioid actions on neurohormone secretion by examining modification of the action of the opioid antagonist naloxone by adrenergic receptor agents. The data suggest (1) that in addition to opioid receptors, 'presynaptic' alpha 2-receptors regulate release from neurohypophysial noradrenaline terminals; (2) noradrenaline released from neurohypophysial terminals acts on beta- and alpha 1-receptors to facilitate both oxytocin and arginine vasopressin release: this action only becoming evident at elevated levels of endogenous noradrenaline release attained following removal of presynaptic opioid or alpha 2-regulation, and (3) opioid peptides within the neurohypophysis act to inhibit oxytocin and, to a lesser extent, arginine vasopressin secretion, partly through inhibiting release of facilitatory noradrenaline. We propose a model in which opioids act in the neurohypophysis both independently of noradrenaline via kappa-receptors on neurosecretory terminals or pituicytes and also via interaction with the noradrenaline system.

Animals↗
PubMed1988

Percutaneous balloon aortic valvuloplasty in pregnancy.

Severe symptomatic aortic stenosis in pregnancy carries a poor prognosis. Although cardiopulmonary bypass and surgical repair has been reported to have a low maternal mortality, the fetal risk remains substantial. We report a case in which percutaneous balloon valvuloplasty was performed successfully at 19 weeks' gestation. The procedure restored physiologic left ventricular outflow and improved the aortic valve peak systolic pressure gradient. This allowed progression of the pregnancy to term and an uneventful delivery of a healthy infant, with no maternal complications. Although the long-term efficacy of percutaneous balloon aortic valvuloplasty has not been established, this case report has shown it to be useful as a palliative procedure.

Adolescent↗
PubMed1986

Remission of diarrhoea due to cryptosporidiosis in an immunodeficient child treated with hyperimmune bovine colostrum.

A boy aged 6 months who presented with poor weight gain, diarrhoea, and infection with Pneumocystis carinii was found to have congenital hypogammaglobulinaemia, which did not improve despite monthly treatment with intravenous gammaglobulin. At the age of 3 years and 2 months he developed severe vomiting and diarrhoea due to cryptosporidiosis, which failed to respond to conventional treatment. Infusion of hyperimmune bovine colostrum produced against parasite antigen, given by nasogastric tube, was started after symptoms had persisted for three weeks. His vomiting and diarrhoea resolved within five days of treatment, and oocysts were no longer seen in the stools after eight days. Later, however, he developed a rare complication, and oocysts were found in the common bile duct. Hyperimmune bovine colostrum may be useful in the treatment of many patients with immunodeficiency disorders.

Agammaglobulinemia↗
PubMed1986

Hypogonadism in chronic liver disease: impaired release of luteinising hormone.

Alcohol abuse leads to impotence, infertility, and feminisation. Patients with chronic alcoholism may have impaired hypothalamic-pituitary function. The release of luteinising hormone was investigated in men with alcoholic cirrhosis with and without hypogonadism and controls. Blood was sampled every 15 minutes for six or eight hours and luteinising hormone concentrations measured by radioimmunoassay. Data were analysed by iterative computerised analysis and spectral analysis to assess pulsatile release and the length of the cycle, respectively. Pulsatile release of luteinising hormone was shown in all the control subjects; in the men with alcoholic liver disease it was normal in those with subclinical primary testicular failure but absent or grossly attenuated in those with overt combined central and primary gonadal failure. The impaired release of luteinising hormone in the men with overt gonadal failure might be due to a hypothalamic defect.

Adult↗