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M J Cook

Publications and source records attributed to M J Cook.

At least 55 records · Page 3Linked to original sources
PubMed1992

Hippocampal volumetric and morphometric studies in frontal and temporal lobe epilepsy.

The most common temporal lobe pathology is Ammons Horn sclerosis (AHS), and several different imaging techniques have been utilized to detect this with varying success. We describe the clinical application of magnetic resonance imaging (MRI) using a three-dimensional volume technique which allows total hippocampal volume to be measured and symmetry evaluated. Hippocampal surface area was calculated in sequential 1.5 mm thick contiguous images, using a GE IC workstation. Total volumes and surface areas were calculated. The cross-sectional surface area at 1.5 mm intervals was displayed graphically, permitting morphometric analysis of the hippocampus throughout its length. Focal atrophy within any part of the hippocampal formation (HF) and its extent could thus be assessed. Patients with well-lateralized temporal lobe epilepsy (TLE) (n = 20) and well-defined frontal lobe epilepsy (FLE) (n = 20) were studied, and volumes compared with normal values derived from 10 neurologically normal controls. Asymmetric hippocampal volume loss was demonstrated in all 20 patients with clinically typed TLE, but not in normal controls or patients with FLE. Volume loss distribution was anterior in 12 patients, posterior in one patient and widespread in seven patients. Secondarily generalized seizures were strongly associated with widespread loss. This method of surface area and volumetric analysis of the hippocampus in TLE can demonstrate asymmetry and focal involvement, and help distinguish between hippocampal and frontal pathologies.

Adult↗
PubMed1991

Comparison of plasma oxytocin and catecholamine concentrations with uterine activity in pregnant rhesus monkeys.

Pregnant rhesus monkeys exhibit diurnal changes in uterine activity (UA), with episodes of increased UA during the early hours of darkness. The estrogenic environment during late pregnancy serves a permissive role in the maintenance of nocturnal UA episodes and may involve myometrial interactions with oxytocin (OT) and/or alpha-adrenergic stimuli. In the present study we have used chronically catheterized pregnant rhesus monkeys to measure diurnal changes in maternal plasma OT, epinephrine, norepinephrine, and dopamine. We also determined the effects of infusing an OT antagonist (ORF 22164) and the alpha-adrenergic antagonist phentolamine on nocturnal UA episodes. Animals were exposed to a 16-h light, 8-h dark photo-period, with the hours of darkness between 2300-0700 h. Maternal plasma samples were collected at 3-h intervals for 36 h and analyzed by RIA for OT and by high performance liquid chromatography for catecholamines. Plasma OT was correlated with UA in animals that displayed nocturnal UA episodes (r = 0.76; P less than 0.01). Maximal OT concentrations occurred at 2400 h in these animals; plasma OT was higher during the hours of darkness compared to levels during the light phase (10.4 +/- 1.9 and 3.0 +/- 0.3 pmol/L, respectively; n = 4). Some animals did not display nocturnal episodes of increased UA and showed no increase in OT concentrations during the hours of darkness. Maternal plasma catecholamine concentrations were not correlated with nocturnal UA and were maximal during the light phase. Nocturnal UA was abolished within 30 min of infusion of the OT antagonist, but phentolamine infusions had no effect on nocturnal UA. We conclude that 1) changes in maternal plasma catecholamine concentrations are not involved in the generation of nocturnal UA; 2) the presence of episodes of increased UA at night results from increased maternal plasma OT concentrations; and 3) the absence of nocturnal UA in some animals can be explained by a reduced level of OT secretion.

Animals↗
PubMed1991

Antagonism of oxytocin in rats and pregnant rhesus monkeys by the novel cyclic hexapeptides, L-366,682 and L-366,948.

Two cyclic hexapeptides unrelated in chemical structure to oxytocin (OT) were shown in vivo to be antagonists of the contractile action of OT on the uterus. In anesthetized rats challenged with OT (1 micrograms/kg) administered as an i.v. bolus, L-366,682 [cyclo-(L-Pro-D-Trp-L-Ile-D-pipecolic acid-L-pipecolic acid-D-His)] and L-366,948 (D-2-naphthyl-alanine in place of D-Trp) were equipotent with AD50 values of about 100 micrograms/kg i.v. At doses of L-366,682 or L-366,948 causing approximately 90 to 95% block (approximately the AD95 dose) of OT, the duration of action of the antagonists exceeded 145 min. Both compounds exhibited selectivity in the rat, as a dose of either at 300 micrograms/kg i.v. shifted the dose-response for OT-induced uterine contraction to the right by approximately 5-fold but did not affect the dose-response to prostaglandin F2 alpha. Furthermore, neither compound, at a dose of 3 mg/kg i.v., antagonized the action of arginine vasopressin acting at V-1 (pressor effect in pithed rats) or V-2 (antidiuretic) receptors. In conscious, freely moving, pregnant rhesus monkeys, L-366,948 or L-366,682 given i.v. or s.c. were effective antagonists of uterine contractions elicited by an infusion of OT. OT- or arginine vasopressin-like agonist activity was not observed in any of the in vivo models. It is concluded that L-366,682 and L-366,948 act in vivo as reasonably potent, long-acting and selective antagonists at OT receptors in the rat and rhesus uterus.

Animals↗
PubMed1989

Half-life of plasma sex steroid-binding protein (SBP) in the primate.

We have recently shown that the metabolic clearance of testosterone in plasma is directly dependent on sex steroid-binding protein (SBP or SHBG) levels [J. steroid. Biochem. 22, 739 (1986)]. In order to further understand the relationship between these two parameters, we have measured the half-life of SBP in plasma of female rhesus monkeys. SBP was purified to homogeneity from pooled Macaca nemestrina serum, and iodinated with 125I. The labeled protein ([125I]nSBP) was purified by chromatography on DEAE-agarose and fractions identified as immunologically reactive against anti-human SBP were collected. Protein purity of [125I]nSBP was established by SDS gel electrophoresis using an unlabelled Macaca nemestrina SBP as standard. The labeled protein was infused intravenously into two different adult female Macaca mulatta (rhesus) monkeys. Plasma samples were collected at short intervals during the first 24 h after infusion, and then daily for 7-9 days. The clearance profile of labeled SBP in plasma was quantitated by radioactivity measurement and immunoprecipitation. Analysis of the results indicate that the rate of SBP clearance in plasma has two components, the t1/2 (app) of the first component is 7.5 h (r = 0.94), and the t1/2 (app) of the second component is 3.95 days (r = 0.95). Over 90% of the injected 125I-nSBP was removed from plasma within 24 h at a rate corresponding to the t1/2 (app) of the first component. The data indicate that most of the SBP rapidly distributes into extravascular spaces during the first 24 h following infusion, and are consistent with the hypothesis that SBP may be directly involved in sex steroid hormone transport into tissues.

Animals↗
PubMed1987

Temporal changes in uterine activity and prostaglandin response to RU486 in rhesus macaques in late gestation.

Progesterone withdrawal as a mechanism of parturition in primates is controversial because maternal, fetal, and amniotic fluid progesterone concentrations do not decrease before parturition. We therefore studied the effects of RU486 on uterine activity and amniotic fluid prostaglandins in four rhesus macaques implanted with amniotic fluid and maternal vascular catheters and with fetal electrocardiogram and uterine electromyogram electrodes at 119 to 124 days' gestation (term = 168 days). Uterine electromyogram, intra-amniotic pressure (hourly contraction area, mm Hg.sec/hr), and fetal electrocardiogram were monitored continuously. After a stabilization period (6 to 9 days) RU486 was administered orally (20 mg/kg/day) at 1000 hours for 3 days. Uterine activity increased from basal levels (less than 4000 mm Hg.sec/hr) 8 hours after the first dose of RU486, reaching levels of 12,000 mm Hg.sec/hr. A sustained increase in uterine activity (13,000 to 30,000 mm Hg.sec/hr) was observed for 48 hours before cesarean section with little or no cervical effacement or dilatation. Increases in amniotic fluid prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, 13,14-dihydro-15-keto-prostaglandin F2 alpha, and 11-deoxy-13,14-dihydro-15-keto-11 beta, 16 epsilon-cycloprostaglandin E2 occurred 40 hours after the onset of increased uterine activity. In contrast, amniotic fluid prostaglandins in the control animals delivering at term (n = 4) increased 24 to 48 hours before significant increases in uterine activity occurred. Control animals but not those given RU486 demonstrated a progressive nocturnal peak in uterine activity before delivery. Progesterone receptor blockade stimulates intense preterm uterine activity but not the orderly sequence of changes in prostaglandins and cervical status observed during normal parturition.

Amniotic Fluid↗
PubMed1983

Circadian patterns and dexamethasone-induced changes in uterine activity in pregnant rhesus monkeys.

Five monkeys with amniotic pressure catheters were placed in restraining chairs on days 127 to 131 of gestation (term = 167 days) for examination of circadian patterns in uterine activity. Uterine activity (total area under the contraction curve) was recorded continuously for 3- to 9-day intervals while the animals were exposed to a 16-hour:8-hour light:dark photoperiod. A ratio of hourly contraction area to mean hourly contraction area was established for each individual, and a circadian pattern was observed, with the occurrence of peak uterine activity between 2200 and 0200 hours (analysis of variance, P less than 0.01). An unrestrained animal equipped with a telemetry device and monitored for 23 days demonstrated a similar pattern. Four other catheterized, chair-restrained, pregnant monkeys were used to examine the effects of dexamethasone on uterine activity rhythms. After a 48-hour control period, dexamethasone (0.1 mg/hr) was infused via a maternal venous catheter for 48 hours. Fetal and maternal estrone and estradiol levels and total uterine activity were significantly reduced during dexamethasone infusion (P less than 0.05). In the 48 hours after dexamethasone infusion, mean uterine activity returned to preinfusion levels but the nocturnal peak remained ablated. Therefore, dexamethasone, alters the magnitude, as well as the circadian pattern, of uterine activity in association with reduced estrogen biosynthesis by the fetoplacental unit. Since the effect on uterine activity is biphasic, dexamethasone probably acts by more than one mechanism.

Animals↗
PubMed1982

Cell-surface discoidin in aggregating cells of Dictyostelium discoideum.

Both discoidin I and discoidin II have been detected on the surface of aggregating (10 h developmental stage) cells of Dictyostelium discoideum NC4 by radioiodination of the cell-surface followed by immunoprecipitation and sodium dodecyl sulphate/polyacrylamide-gel-electrophoretic analysis. Approx. 92% of cell-surface discoidin I and 72% of cell-surface discoidin II can be eluted with 0.5 M-galactose, showing that most of each endogenous lectin is not present as integral membrane protein but rather is bound to cell-surface discoidin receptors. Two-dimensional polyacrylamide-gel-electrophoretic analysis of discoidin I suggests that the native tetramer may be a hetero-multimer composed of both Ia and Ib subunits. Cell-surface discoidin I also contains both types of subunit, but it is not clear whether both subunits have corresponding cell-surface receptors.

Carrier Proteins↗
PubMed1980

Materno-fetal pharmacokinetics and fetal distribution of valproic acid in a pregnant rhesus monkey.

Chronic indwelling catheters in the maternal femoral artery and vein, fetal carotid artery and jugular vein, and amniotic cavity of a pregnant rhesus monkey permitted administration of sodium valproate (NaVPA) and collection of timed samples of maternal and fetal blood and amniotic fluid. After a single IV dose (50 mg/kg) to the mother, a rapid distribution phase (t1/2 alpha = 0.5 minute) was followed by a biphasic decline in concentration in maternal blood (t1/2 beta = 31 minutes, t1/2 gamma = 390 minutes). VPA appeared rapidly in fetal blood, reached a concentration slightly higher than in maternal blood by 15 minutes, and thereafter declined in parallel with the concentration in maternal blood. Terminal fetal/maternal ratios of blood concentration of VPA were about 1.3. Similar patterns of decline were observed after NaVPA was given IV to the fetus. A multicompartment first-order materno-fetal pharmacokinetic model is presented. Tissue distribution studies in the fetus showed that VPA concentration was highest in blood; moderate in heart, liver, spleen, kidney, and skeletal muscle; and low in brain.

Amniotic Fluid↗
PubMed1970

Practical examining. 1.

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Education, Nursing, Diploma Programs↗