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J S Cowan

Publications and source records attributed to J S Cowan.

At least 19 recordsLinked to original sources
PubMed2006

Elongational flow induced ordering in surfactant micelles and mesophases.

We have used small angle neutron scattering, SANS, to investigate the elongational flow induced ordering in surfactant micelles and mesophases. Spatially resolved SANS measurements have been used to determine the distribution of orientational ordering over the flow velocity pattern in an elongational flow cell, and comparison with the effects of shear flow are made. Two different surfactant systems have been studied, the charged wormlike mixed micelles of hexaethylene monododecyl ether, C16E6/hexadecyl trimethylammonium bromide, C16TAB (3% C16E(6)/5 mol% C16TAB), and the Lalpha lamellar phase of C16E6 (50.6 wt% C16E6 at 55 degrees C), and a substantially different response is observed. The orientational distribution of the Lalpha lamellar phase of C16E6 reflects the flow velocity pattern distribution within the cell, whereas for the wormlike mixed micelles of C16E6/C16TAB this is not the case, and this is associated with the shear thinning behavior of that system.

Journal Article↗
PubMed2001

The prevention of shaken baby syndrome.

Shaken Baby Syndrome may have life-long consequences, but it can be prevented. It is far too common and usually arises when the parent or caretaker gets angry, frustrated or impatient, but it can also be caused by inappropriate play. There are pathognomonic signs but suspicion must be high to suspect it. Physicians play an important role in diagnosis, management and most importantly, prevention.

Adult↗
PubMed1988

Failure of growth hormone (GH) to feed back at the level of the pituitary to alter the response of the somatotrophs to GH-releasing factor.

GH feeds back at the level of the central nervous system to alter the release of somatostatin and GRF, resulting in altered GH release. The purpose of this study was to see whether the concentration of GH, impinging directly on the somatotrophs of the adenohypophysis, would alter the responsiveness of the somatotrophs to GRF. Using a perifusion system and dispersed pituitary cells, we found that the GH response to a pulse of GRF is unaltered over a wide range of GH concentrations. We conclude that GH does not feed back at the level of the adenohypophysis to alter the responsiveness of the somatotrophs to GRF.

Animals↗
PubMed1988

Effect of withdrawal of somatostatin and growth hormone (GH)-releasing factor on GH release in vitro.

The secretion of GH, in vivo, is pulsatile. We have proposed that the timing of the episodic bursts of GH secretion is set by somatostatin (SRIF) withdrawal, while the magnitude of the bursts is set by the amount of GH-releasing factor (GRF) impinging on the somatotrophs, before and during SRIF withdrawal. We have now used an in vitro model of perifused rat pars distalis cells to further examine the interaction between GRF and SRIF on the magnitude of the burst of GH release that follows SRIF withdrawal. We first characterized the GH response, with time, to constant perifusion with GRF. The initial burst, followed by a rapid decrease in GH release induced by constant perifusion is due to a loss of GRF bioactivity in the perifusion medium and not to a decreasing responsiveness of the somatotrophs. This was followed by studies on the interaction between GRF and SRIF. The burst of GH release after cessation of perifusion with SRIF (10(-9) M) plus GRF (10(-10) M) can be blocked by the administration of SRIF during the burst. Also, the magnitude of the burst is proportional to the concentration of GRF preceding the withdrawal of SRIF. It is likely that similar relations apply in vivo, where SRIF withdrawal sets the timing and duration of the episodic burst of GH release, while GRF sets the magnitude.

Animals↗
PubMed1986

Effect of somatostatin withdrawal and growth hormone (GH)-releasing factor on GH release in vitro: amount available for release after disinhibition.

The secretion of GH is strikingly episodic. We have suggested that the timing of the episodic bursts of GH secretion is set by somatostatin (SRIF) withdrawal, whereas the magnitude of the bursts is determined by the amount of GH-releasing factor (GRF) impinging on the somatotrophs before and during SRIF withdrawal. We have now used an in vitro model of perifused rat pars distalis cells to examine the interaction of SRIF and GRF on GH release and, in particular, to examine the effect of GRF on the magnitude of the burst of GH release that follows SRIF withdrawal. After 30 min of perifusion with SRIF (10(-9) M), there follows an immediate but small burst of GH release. The burst of GH release following concurrent perifusion with SRIF plus GRF (10(-10) M) is increased, with a 7.5- to 9.5-fold increase in the peak secretion rate. When GRF is maintained after the withdrawal of SRIF, the peak secretion rate is not different from that seen after simple withdrawal of both SRIF and GRF, but the duration of the burst is increased. These data demonstrate that the presence of GRF during SRIF perifusion, while not altering basal release, does strikingly increase the post-SRIF release of GH. We propose that a similar relation applies in vivo, where SRIF withdrawal sets the timing of the episodic bursts of GH release, whereas GRF determines the magnitude.

Animals↗
PubMed1984

Secretory bursts of growth hormone secretion in the dog may be initiated by somatostatin withdrawal.

In 28 6-h experiments on 10 conscious resting trained male dogs, plasma growth hormone (GH) was determined at 5-min intervals by radioimmunoassay. For all experiments, the basal GH concentration in plasma was 0.80 +/- 0.06 ng mL-1. In each experiment, 1-3 secretory bursts of GH occurred, raising plasma GH 2.4 to 15.3 times basal concentrations (for all 43 bursts, 6.6 +/- 0.4 times the basal value). Metabolic clearance rates (MCR) and apparent distribution volumes (V) were determined, using stepwise infusions of canine GH. The MCR (3.99 +/- 0.30 mL kg-1 min-1) and V (57.9 +/- 5.5 mL kg-1) were used to transform the GH concentration versus time data into GH secretion rates, using a single compartment approach. Basal GH secretion rates for all 28 experiments were 3.12 +/- 0.24 ng kg-1 min-1. The secretory bursts yield peak GH secretion rates of 9.4 +/- 0.8 times basal secretion and these steep-sloped bursts last 25.1 +/- 1.2 min. Six-hour infusions of 0.15 microgram kg-1 min-1 of somatostatin (SRIF) abolished all secretory bursts but did not lower basal secretion rates. In five of seven SRIF infusion experiments in which samples were taken after the infusion ceased a secretory burst was seen in the hour following cessation of infusion (in four cases within 10 min). These secretory bursts lasted 23.0 +/- 2.9 min and were similar to those seen in control experiments. Infusions of SRIF at 0.05 microgram kg-1 min-1 had no effect. These results imply that during basal GH secretion, a surfeit of SRIF impinges on the somatotrophs, as extra SRIF does not further lower basal secretion. However, during secretory bursts, very little SRIF must be present, as exogenous SRIF blocks these bursts. The bursts are similar in duration to overshoots provoked in perifused dispersed rat somatotrophs by removal of an SRIF signal. It seems likely that their cause in vivo is similar. (All values are means +/- SEM.)

Adrenocorticotropic Hormone↗
PubMed1983

Feedback suppression of ACTH secretion by cortisol in dogs: lags after large signals equal those following very small signals.

Previously, low stepwise infusions of cortisol in resting adrenalectomized dogs (plateaux less than or equal to 6 micrograms/dL) were shown to reduce ACTH secretion only after 20 min. In the present study, large, steep-sloped cortisol signals were used to try to evoke faster feedback. Adrenalectomized male mongrel dogs were maintained on exogenous steroids until 48 h before the experiment. Of the 23 experiments on 15 dogs (under light pentobarbital anesthesia), 12 were on resting dogs, 7 on dogs stressed by variable insulin infusion (keeping plasma glucose at 18-40 mg/dL), and 4 stressed as above but with 4 h of low cortisol infusion (plasma congruent to 5 micrograms/dL) before applying the feedback signal. After a 50-min control period, a 30-min feedback period was initiated by one of two i.v. cortisol signals: (a) injection of 0.3 mg/kg or (b) infusion of 46 micrograms kg-1 min-1. Both raised plasma cortisol above physiological limits (within 2 and 6 min, respectively). In each experiment, 23 timed venous blood samples were assayed for plasma ACTH and cortisol. ACTH secretion rates were calculated continuously using a validated single-compartment method. Results from both types of cortisol signals were indistinguishable, and were thus pooled. In the unstressed dogs, control-period ACTH secretion of 0.97 +/- 0.12 mU kg-1 min-1 showed no significant decline due to the feedback signal for 20.3 +/- 1.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1983

Characteristics of the post-somatostatin rebound in growth hormone secretion from perifused somatotrophs.

Dispersed rat somatotrophs were perifused with repeated step SRIF signals of 10 or 60 min (100 ng/ml) separated by 45-min control periods. Effluent was assayed for rat GH (RIA). Maximum suppression of GH secretion (on signal) or complete recovery (off signal) occurred within 1 min. Repeated signals evoked identical normalized responses. GH release fell to 67 +/- (SE) 2% of control with 10-min SRIF signals and 59 +/- 4% of control with 60-min SRIF signals. After SRIF removal, major overshoots of GH secretion were observed, lasting 21 +/- 2 min (after 10-min or 60-min SRIF steps). Peak secretion rates and total secretion due to the overshoot were greater after longer SRIF signals, despite the constant duration of the overshoot. However, the extra secretion during overshoots after 60-min SRIF exposure contained only 23 +/- 3% of the secretion suppressed by SRIF, whereas the extra secretion after 10-min SRIF exposure contained 79 +/- 12% of the amount suppressed by the SRIF exposure, suggesting an intracellular feedback which slows accumulation of readily releasable GH after a period of SRIF exposure. During overshoot, peak secretion rates of twice the control rate (and 3.5 times the SRIF-inhibited rate) were observed. Similarities between these overshoots and in vivo bursts of GH secretion are noted.

Animals↗
PubMed1981

Effect of cooling on the glucoregulation of anaesthetized and non-anaesthetized newborn dogs.

UNLABELLED: When newborn dogs 2-14 days of age, anaesthetized with Nembutal, were cooled to 30 degrees C body core temperature, their rate of CO2 production (QCO2) decreased as predicted by van't Hoff's law, but the rates of hepatic glucose production and overall glucose utilization were decreased to a lesser degree, indicating an increase in the percentage contribution of plasma glucose to the overall energy turnover. In different litters of pups cooled to 32 degrees C, QCO2 and the rate of glucose production and utilization were decreased as predicted by van't Hoff's law. The metabolic clearance rate of glucose was decreased by cooling in all pups. These changes were wholly or partially reversible upon rewarming. Because of the approximate parallelity in the changes in the rates of production and utilization of glucose, no consistent change in blood glucose was observed during cooling. When non-anaesthetized pups less than 6 days old were exposed to cold until their core temperature was decreased to 32 degrees C QCO2 increased transiently during cooling. A small and transient elevation in plasma glucose concentration was observed due to a small increase in hepatic glucose production. Older pups fell into two categories: those which were able to maintain their body temperature by increasing their metabolic rate did not react with any change in their rates of glucose production and utilization. On the other hand pups which, during cooling, failed to raise their metabolic rate became hyperglycaemic because of an increased rate of glucose production and a decrease in glucose clearance. IN CONCLUSION: in anaesthetized pups QCO2 and the rates of hepatic glucose production and utilization follow approximately van't Hoff's law, indicating the absence of significant regulatory responses. Non-anaesthetized pups, if they are able to maintain their body temperature during cooling by an increase of their metabolic rate, show no significant changes in glucose production and utilization. Hyperglycaemia developed only in those pups which failed to increase their metabolic rate and consequently became severely hypothermic. In no case did hypothermia lead to hypoglycaemia.

Aging↗
PubMed1978

Validation of a single-compartment approach to the calculation of secretion rates of ACTH.

A single-compartment model used in this laboratory for continuously calculating ACTH secretion rates from measured plasma ACTH concentrations has been tested for its ability to follow changing rates of ACTH entry (rapid departure from steady state). ACTH was infused at known moderately high but physiological rates into anaesthetized dogs (Nembutal). Under such conditions endogenous secretion is initially less than 5% of infused rates. Orthogonal polynomials (ACTHt) were fitted to plasma ACTH vs. time data. Then secretion ratet = (ACTHt X MCR) + (dACTHt/dt X V) where it was previously shown that the metabolic clearance rate of ACTH (MCR) lacked significant inter-animal or concentration-dependent variation, and its distribution volume (V) was also constant. The calculated ACTH entry rate curves (a) followed a 10-fold increase in infusion rate over 4 min and subsequent rapid decline with a lag of only about 1 min and, despite some blurring, gave an integrated response equal to 94 +/- 5.5% of the known signal, and (b) followed a sinusoidal change in infusion rate (amplitude, 1.7 X base rate; period, 40 min) with a few percent error and negligible lag. These signals imitate (a) an abrupt stress response, and (b) other rapid departures from steady state.

Adrenocorticotropic Hormone↗
PubMed1978

Progressive suppression of adrenocorticotropin secretion in resting adrenalectomized dogs by low stepwise infusions of cortisol.

Ten male mongrel dogs of 8.3-14.3 kg were bilaterally adrenalectomized and maintained on replacement steroids for 1 week. No exogenous steroids were detectable at the time of the experiment. Each dog, under light Nembutal anesthesia, received two stepwise primed constant infusions of cortisol (iv), each lasting 90 min (except in one dog with three infusions of 60 min). A recovery period of 80 min without cortisol infusion followed. Twenty-three venous blood samples were withdrawn for determination of plasma ACTH by adrenal cell suspension bioassay and 25 were withdrawn for plasma cortisol by fluorimetry at various times before, during, and after the cortisol infusions. ACTH secretion rates were calculated continuously from functions fitted to ACTH concentration and time data, using a validated single compartment approach with previously determined clearances and volumes. Initial high ACTH secretion rates of 1.0 +/- 0.2 mU/kg . min (range, 0.3-2.4) were reduced by 67.4 +/- 4.6% and 94.6 +/- 2.1% by the two cortisol infusions, which yielded cortisol plateau concentrations in plasma of 4.24 +/- 0.41 and 6.09 +/- 0.68 microgram/100 ml, respectively. This sensitive feedback response to low cortisol concentrations was delayed, with no effect for about 20 min and maximal effect reached within 1 h. There was no evidence of a fast rate-sensitive feedback. Some increases in ACTH secretion were seen during the recovery period (errors are +/- SEM).

Adrenalectomy↗
PubMed1975

Adrenocorticotropin secretion rates following histamine injection in adult and newborn dogs.

The metabolic clearance rate (MCR) for ACTH in adult dogs was previously shown not to vary significantly with varying plasma ACTH concentrations or among dogs. This is confirmed here for pups aged 1-7 days. Hence, ACTH secretion rates can be continuously calculated from a continuous function of plasma ACTH vs. time. Each of seven adult dogs under Nembutal anesthesia received two or three intravenous (i.v.) injections of histamine with increasing doses. The first injections in each dog ranged from 7 to 50 mug/kg, while the last dose was 62-108 mug/kg. A total of 16 injections were given. Twelve pups (two litters of six) aged 1-7 days each received one injection of histamine of 76-116 mug/kg (i.v.). ACTH concentrations in plasma were determined by an adrenal cell suspension bioassay before, and 6 times after each injection. Nine pups also underwent determinations of their MCR for ACTH, with plateau concentrations determined at three times during an ACTH infusion. Continuous curves of ACTH secretion rates were calculated for all 28 histamine injections, showing that all except the 1-day-old pups secrete considerable ACTH when stressed. Compared to adult dogs, the pups show lower secretion rate peaks and shorter periods of rapid secretion. Changes in plasma glucocorticoids also suggest that the adrenal cortex of newborn dogs can respond to ACTH by increased glucocorticoid secretion.

Adrenocorticotropic Hormone↗
PubMed1975

Effects of arterial or portal ischemia on survival and metabolism of partially and totally depancreatized dogs.

The role of arterial blood flow in hepatic metabolic functions was compared to that of portal flow in two groups of totally depancreatized dogs. Survival times and glucose and nitrogen excretion were significantly greater in dogs with ligation of the hepatic artery than in dogs with an Eck fistula. The dogs with ligated hepatic arteries also showed a significantly slower rise in plasma ketones. The course of diabetes was compared in three additional groups of partially depancreatized dogs consisting of a) dogs with ligated hepatic arteries, b) dogs with Eck fistulas, and c) controls. Hepatic arterial ischemia: 1) increased survival, without insulin treatment (a--650, b--167, c--124 days) 2) did not decrease tracer-determined rate of glucose production 3) led to a greater urinary excretion of glucose, ketone bodies and nitrogen than portal ischemia. Partially depancreatized dogs with either arterial or portal hepatic ischemia maintained a high rate of glucose disappearance on acute deprivation of endogenous insulin (clamping of vessels of their pancreatic remnant) due probably to decreased insulin degradation by the ischemic liver. The dogs died in coma after losing all fat depots. There was severe fatty change in the livers of dogs with hepatic artery ligation, slight in those with Eck fistulas and no fat in the livers of controls.

Animals↗