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Biomedical subjects

M B Allen

Publications and source records attributed to M B Allen.

At least 73 records · Page 4Linked to original sources
PubMed1986

Skin necrosis following Haemaccel.

Haemaccel is a plasma substitute in frequent clinical use with a low incidence of side effects. I report a patient who developed necrotic blisters following two Haemaccel-insulin infusions, a previously undescribed complication. The rationale behind carrier solutions for insulin therapy is discussed and some of the problems associated with Haemaccel use are considered. I conclude by urging caution in the use of Haemaccel as a carrier solution for insulin therapy.

Humans↗
PubMed1984

Acute anterior spinal epidural abscess.

We have reported a case of acute spinal epidural abscess, an uncommon cause of pain in the neck and back. The typical progression from spinal ache to paralysis may be halted if the diagnosis is suspected and prompt radiologic and surgical interventions are initiated.

Abscess↗
PubMed1982

Effect of neonatal androgenization on the LHRH response of dispersed pituitary cell cultures.

To determine if neonatal androgenization affects pituitary luteinizing hormone releasing hormone (LHRH) response, female rats were androgenized 24-48 hr following birth. Intact male and female litter mates were maintained for comparison. At 83 days of age, randomly selected males and androgenized females were gonadectomized. At 90 days of age, pituitary cell cultures were begun. On day 3 the cells were challenged with LHRH. Gonadotropin response was determined by radioimmunoassay (RIA). Basal gonadotropin release from androgenized female cells was similar to male cells, while the pattern and magnitude of the LHRH response was similar to intact female cells. After castration, the pattern and magnitude of the LHRH response of the androgenized female pituitary was most like the male. Androgenized female cells exhibited mixed male and female LHRH response.

Animals↗
PubMed1982

Effect of pressure on cerebrospinal fluid absorption in cats, baboons, and humans: comparison of the linear and logarithmic models.

To circumvent time constraints inherent in indicator clearance measurements of cerebrospinal fluid absorption, investigators have used the relationship between CSF pressure at steady state and the rate of infusion of mock CSF, in both patients and experimental animals, to evaluate the bulk absorption rate of CSF. This latter approach required mathematical model of the effect of CSF pressure on CSF bulk flow. Two such models--a fixed resistance and a variable resistance model of CSF flow through arachnoid villi--have been used in both clinical and laboratory settings. In this study, the relationship between steady state CSF pressure and mock CSF infusion rate was assessed using both mathematical models. We studied two patients, three cats, and seven baboons. Values of CSF outflow resistance calculated according to both models as well as other parameters of CSF bulk flow estimated on the basis of both models were all in the range expected from other studies. The data from these experiments do not provide justification for preferring one model over the other. Depending on the experimental or clinical situation, some of the assumptions behind both models may not be valid. Multiple direct measurements of the rates of CSF absorption and formation over a wide range of CSF pressures in individual subjects will be necessary to validate either the variable or the fixed resistance model or to suggest a more appropriate model. Until such information is available, it is probably reasonable to use both approaches for the analysis of mock CSF infusion data. CSF bulk flow parameters calculated on the basis of either the variable or the fixed resistance model should never be taken as absolute, but should be evaluated critically in the context of the clinical or experimental situation.

Absorption↗
PubMed1981

Transsphenoidal surgery on the pituitary.

Transseptal transsphenoidal hypophysectomy has evolved into a low mortality/morbidity procedure in properly selected patients. Preoperative evaluation is becoming increasingly accurate with the rapid advances in computerized axial tomography. With the lowering of operative morbidity, indications for the transsphenoidal approaches to the sella are broadening. Caution must be used when approaching pituitary tumors with extensive suprasellar components by the transsphenoidal route.

Adolescent↗
PubMed1980

Apparent 'glucokinase' activity in non-hepatic tissues due to N-acetyl-D-glucosamine kinase.

1. Electrophoretic examination of tissue extracts from rat intestinal mucosa, kidney, lung, spleen, mammary gland, adipose tissue, heart muscle and placenta in agarose gels did not reveal the presence of any glucokinase (ATP:D-glucose 6-phosphotransferase, EC 2.7.1.2) activity corresponding to that present in rat liver. 2. All these tissues do contain an enzyme that possesses very high-Km glucose-phosphorylating activity but which has a slightly lower electrophoretic mobility than glucokinase and can be separated from it by various means. 3. This phosphotransferase activity is due to N-acetyl-D-glucosamine kinase (ATP:2-acetamido-2-deoxy-D-glucose 6-phosphotransferase, EC 2.7.1.59), which has been partialyy purified from intestinal mucosa tissue and shown to have similar kinetic properties to the same enzyme previously purified more extensively from liver and kidney. 4. It is suggested that many of the effects reported in the literature of 'glucokinase' activity in non-hepatic tissues are probably due to N-acetyl-D-glucosamine kinase.

Animals↗
PubMed1980

Factors that prevent the premature appearance of glucokinase in neonatal rat liver.

1. The physiological factors that prevent the precocious appearance of glucokinase activity in the 13-day-old rat that can be induced by oral glucose administration were explored. 2. Evidence is presented that the galactose component of milk sugar is inhibitory. In the absence of this inhibitory galactose, the amount of glucose necessary to effect appreciable induction is greater than that present in milk. 3. The induction is prevented both by administration of mannoheptulose, which inhibits insulin release, and by excess insulin; the amount of insulin available therefore seems to be critical. 4. The inhibition of induction by galactose does not appear to be via competition with glucose but by enhancing insulin release and thereby making this excessive. The relative amounts of glucose and insulin appear to be important in regulating glucokinase induction. 5. The precocious induction of glucokinase by glucose is inhibited by simultaneous treatment with approriate amounts of adrenaline, glucagon, dibutyryl cyclic AMP or isoprenaline but not by vasopressin or angiotensin II. 6. No single cause of glucokinase induction in neonatal rat liver can be recognized. The process is subject to regulation by many factors at a time subsequent to when competence to synthesize the enzyme has been established.

Animals↗
PubMed1980

The isolation and preliminary characterization of N-acetyl-D-glucosamine kinase from rat kidney and liver.

1. Procedures for the extensive purification in high yield of N-acetyl-D-glucosamine kinase from rat liver and kidney are described. The separation of this enzyme from hepatic glucokinase depended primarily on their differing behaviour on an affinity column of Sepharose--N-(6-aminohexanoyl)-2-amino-2-deoxy-D-glucopyranose. 2. This N-acetyl-D-glucosamine kinase also catalyses the phosphorylation of N-acetyl-D-mannosamine and, at a lower rate, several other sugar analogues, including D-glucose. 3. A comparison of the behaviour of the enzyme during gel filtration and electrophoresis in sodium dodecyl sulphate/polyacrylamide gels suggests that N-acetyl-D-glucosamine kinase is a symmetrical dimer of mol.wt. 80000.

Acetylglucosamine↗
PubMed1980

Kinetic characterization of N-acetyl-D-glucosamine kinase from rat liver and kidney.

1. Under normal assay conditions the N-acetyl-D-glucosamine kinases from rat liver and kidney show a pH-dependent lag phase before reaching a steady state, which is probably due to reversible dissociation of the dimeric enzyme. 2. The enzyme catalyses the phosphorylation of N-acetyl-D-glucosamine, N-acetyl-D-mannosamine and D-glucose at pH 7.5, with apparent Km values of 0.06, 0.95 and 600 mM respectively for the enzyme from liver and 0.04, 1.0 and 410 mM respectively for the kidney enzyme. It is strongly inhibited by ADP. 3. The interaction between the enzymes and acceptor substrates shows non-Michaelian kinetics with respect to N-acetyl-D-glucosamine but normal behaviour towards N-acetyl-D-mannosamine and D-glucose. 4. Both N-acetyl-D-glucosamine and N-acetyl-D-mannosamine inhibit the phosphorylation of D-glucose; this inhibition appears to be mixed in character. 5. The facts that the enzymes catalyse the phosphorylation of N-acetyl-D-mannosamine and D-glucose do not detract from the designation of the enzymes as N-acetyl-D-glucosamine kinase. Phosphorylation of glucose in vivo by these kinases is unlikely.

Acetylglucosamine↗
PubMed1979

Thyroid hormones and the precocious induction of hepatic glucokinase in the neonatal rat.

1. Oral intubation of glucose is more effective than intraperitoneal injection in inducing the premature appearance of hepatic glucokinase in suckling rats. 2. The inducing effect of glucose is enhanced by treatment of the animals 12 h or more earlier with 1 microgram triiodothyronine/g body weight. 3. Low but significant activities of glucokinase appear at the normal time of development in hypothyroid neonatal rats. Intubation of glucose into 13-day-old and 24-day-old hypothyroid results in the rapid appearance of glucokinase similar to that in normal animals treated likewise. 4. The enhancing effect of thyroid hormones on glucokinase induction by glucose does not necessarily mean that the normal postnatal increase in plasma thyroid hormones is essential for the normal appearance of glucokinase activity at the time of weaning. Other possible explanations are discussed.

Animals↗
PubMed1979

Evaluation of in vitro incubation systems for the study of gonadotropin release.

A detailed study was undertaken in order to determine if a pituitary-half incubation system were a suitable model for the study of anterior pituitary response to estradiol and LHRH. Considerable variation in the gonadotropin content of randomized pituitary halves was observed. Much less variation was found in matched halves. During the initial thirty minutes incubation of pituitary halves, a large spontaneous release of gonadotropins was observed. Time course secretion studies indicated that by four hours incubation, in the presence of 50 ng/ml LHRH, cumulative secretion of LH and FSH had far exceeded that of controls. Elevations in both cumulative secretion and rate of secretion were evident within 15-30 minutes of incubation. Regardless of LHRH dose, only 2-4% of either gonadotropin was secreted. Estradiol in the range of 10, 100, 500, 1,000 and 50,000 pg/ml had no significant effect on pituitary response to LHRH or on basal release, tissue levels or total gonadotropin. Based on these results, it was concluded that while the pituitary-half incubation system may be suitable for studying LHRH induced gonadotropin secretion, it is apparently of insufficient sensitivity to allow the collection of meaningful data concerning the effects of estradiol alone on gonadotropin secretion or estradiol modulation of LHRH induced gonadotropin secretion.

Animals↗