PubMed Health⌕ Search

Biomedical subjects

B A Baldwin

Publications and source records attributed to B A Baldwin.

At least 19 recordsLinked to original sources
PubMed2003

Monitoring hydrate formation and dissociation in sandstone and bulk with magnetic resonance imaging.

Magnetic resonance imaging (MRI) has been shown to be a very effective tool for monitoring the formation and dissociation of hydrates because of the large intensity contrast between the images of the liquid components and the solid hydrate. Tetrahydrofuran/water hydrate was used because the two liquid components are miscible and form hydrate at ambient pressure. These properties made this feasibility study proceed much faster than using methane/water, which requires high pressure to form the hydrate. The formation and dissociation was monitored first in a THF/water-saturated Berea sandstone plug and second in the bulk. In both cases it appeared that nucleation was needed to begin the formation process, i.e., the presence of surfaces in the sandstone and shaking of the bulk solution. Dissociation appeared to be dominated by the rate of thermal energy transfer. The dissociation temperature of hydrate formed in the sandstone plug was not significantly different from the dissociation temperature in bulk.

Chemical Phenomena↗
PubMed1999

Activators of phosphorylase kinase alter the cross-linking of its catalytic subunit to the C-terminal one-sixth of its regulatory alpha subunit.

Phosphorylase kinase, a regulatory enzyme of glycogenolysis in skeletal muscle, is a hexadecameric oligomer consisting of four copies each of a catalytic subunit (gamma) and three regulatory subunits (alpha, beta, and delta, the last being endogenous calmodulin). The enzyme is activated by a variety of effectors acting through its regulatory subunits. To probe the quaternary structure of nonactivated and activated forms of the kinase, we used the heterobifunctional, photoreactive cross-linker N-5-azido-2-nitrobenzoyloxysuccinimide. Mono-derivatization of the holoenzyme with the succinimidyl group, followed by photoactivation of the covalently attached azido group, resulted in intramolecular cross-linking to form two distinct heterodimers: a major (alphagamma) and a minor (betadelta) conjugate. Formation of both conjugates was significantly altered in activated conformations of the enzyme induced by phosphorylation, alkaline pH, and several allosteric activators (ADP, exogenous calmodulin/Ca2+, and Ca2+ alone). Of these activating mechanisms, all increased formation of alphagamma, except Ca2+ alone, which inhibited its formation. When cross-linking was carried out at alkaline pH or in the presence of ADP or exogenous calmodulin/Ca2+, the cross-linked enzyme remained activated following removal of the activators; however, cross-linking in the presence of Ca2+ resulted in sustained inhibition. The results indicate that perturbations in the subunit cross-linking forming the alphagamma dimer reflect the subsequent extent of sustained activation of the holoenzyme that is measured. The region cross-linked to the catalytic gamma subunit was confined to the C-terminal 1/6th of the alpha subunit, which contains known regulatory regions. These results suggest that activators of the phosphorylase kinase holoenzyme perturb interactions between the C-terminal region of the inhibitory alpha subunit and the catalytic gamma subunit, ultimately leading to activation of the latter.

Animals↗
PubMed1999

Pseudoephedrine, a sympathomimetic agent, induces Fos-like immunoreactivity in rat nucleus accumbens and striatum.

The pharmacological properties of the ephedrine derivative pseudoephedrine were investigated at the nuclear level. Following intraperitoneal injection of Sprague Dawley rats with pseudoephedrine, Fos induction was measured in various brain areas by Western blots and immunocytochemistry. Pseudoephedrine induced Fos-like immunoreactivity in the nucleus accumbens and striatum in a time and concentration-dependent manner with maximal effect at 60 mg/kg 2 h after injection. Immunocytochemical studies confirmed that the majority of the signal was detectable in the nucleus accumbens and striatum. Pre-injection with the D1 dopamine receptor antagonist SCH23390 partially and completely blocked pseudoephedrine-induced Fos-like immunoreactivity in the striatum and nucleus accumbens, respectively, suggesting that the action of pseudoephedrine is mediated via dopamine release and results in the activation of D1 dopamine receptors. With the exception of the higher doses required, the actions of pseudoephedrine were similar to those previously described for the psychostimulant amphetamine.

Amphetamine↗
PubMed1998

Drug discrimination analysis of pseudoephedrine in rats.

Rats were trained to discriminate amphetamine, 1 mg/kg given intraperitoneally, from saline injection in a two-lever operant drug discrimination task. Pseudoephedrine (a sympathomimetic drug with central and peripheral actions) at doses of 10 mg/kg failed to substitute for amphetamine, at 20 mg/kg partial substitution occurred, while at a 40 mg/kg full substitution was seen. The specificity of the amphetamine cue at the training dose used (1 mg/kg) was shown by the finding that a peripherally acting sympathomimetic drug phenylephrine at doses from 0.2 to 0.8 mg/kg failed to substitute for amphetamine. The potential for abuse of pseudoephedrine administered at high doses is discussed.

Adrenergic alpha-Agonists↗
PubMed1998

Food for thought: a critique on the hypothesis that endogenous cholecystokinin acts as a physiological satiety factor.

This review evaluates the various lines of evidence supporting the hypothesis that cholecystokinin (CCK) released from the small intestine during feeding plays a physiological satiety. Issues considered include, the effects of systemic injection of CCK on consummatory and operant feeding, the role of the vagus nerve, the effects of CCKB receptor antagonists, and the neuroendocrine responses to exogenous CCK. A critical appraisal of this research indicates that while it is clearly demonstratable that exogenous peripheral CCK can alter food intake by acting on CCKA receptors, the mechanism involved may be more closely related to the induction if aversion and nausea, rather than satiety. With regard to peripheral endogenous CCK, the available evidence also does not seem to support a role for the hormone in satiety. In particular, it is doubtful whether plasma concentrations of CCK following a meal are sufficiently high to inhibit feeding. Moreover, CCKA receptor antagonist which do not cross the blood brain barrier fail to increase meal size, as would be expected if peripheral CCK was an effective satiety factor. In addition, the recent literature concerned with the possibility that CCK may have a direct action within the brain in the control of food intake has been reviewed. These studies show that CCK administered intracerebroventicularly, or by micoinjection into discrete brain regions, also inhibits feeding via a CCKA receptor mechanism. However, the physiological relevance of these findings have yet to be determined.

Amino Acid Sequence↗
PubMed1996

Ethanol alone or with dexamethasone alters the kinetics of choline acetyltransferase.

Choline acetyltransferase activity was measured in rats treated with daily injections of ethanol (0.1 g/kg body wt) and or dexamethasone (1 mg/kg body wt) for 5 consecutive days. Ethanol produced a biphasic reduction of choline acetyltransferase activity in rat cerebral cortex, which at most time points was further decreased by simultaneous injection of dexamethasone. Kinetic studies of cortex choline acetyltransferase activity in rats that had received 5 daily injections of ethanol or ethanol and dexamethasone indicated that the observed reduction in enzyme activity was due to an apparent reduction in affinity (K(m)) of the enzyme for acetyl coenzyme A with no significant change in the total amount of enzyme present (Vmax). This finding has implications with respect to the use of choline acetyltransferase as a marker for cholinergic neurons, and for the understanding of the regulation of choline acetyltransferase activity in the brain.

Animals↗
PubMed1996

Postingestive factors influencing operant sugar intake in pigs.

Intravenous injections of glucose, which increased plasma glucose levels to approximately 10 times the normal level, had no significant effects on the amount of glucose consumed in operant tests carried out immediately after the injection. The importance of gastrointestinal factors in regulating glucose intake was demonstrated in experiments in which pigs with gastric cannulae sham drank significantly (p < 0.01) more glucose over a 1-h period than control sessions with the cannula closed. Intraduodenal injection of glucose or mannitol significantly reduced glucose intake, with glucose significantly (p < 0.05) more effective than mannitol and both significantly (p < 0.01) more effective than water. Gastrointestinal factors are important in regulating sugar intake whereas blood sugar levels are not. The pig is a good experimental animal for the study of sugar appetite.

Animals↗
PubMed1996

Intracerebroventricular injection of CCK reduces operant sugar intake in pigs.

Pigs have a strong appetite for sugar solutions and readily learn to perform operant responses (pressing a panel with their snouts) to obtain glucose solution. Intracerebroventricular (ICV) injection of 1 microgram CCK produced a significant (p < 0.01) reduction in the amount of glucose consumed compared with saline in the 30 min following injection. The reduction was a central effect as the same dose of CCK was ineffective given intravenously. The inhibition of intake was completely abolished by prior dosing with 100 micrograms of the CCKA receptor antagonist Devazepide given ICV. Devazepide itself had no effect on intake. The pig is a good experimental animal for the study of the regulation of sugar intake.

Animals↗
PubMed1995

Effects of the 5-HT1A agonist 8-OH-DPAT on operant feeding in pigs.

The effect of intravenous (i.v.) injection of 8-OH-DPAT on operant food intake in pigs has been examined in animals with food available ad lib and in pigs feeding after 4 h deprivation of food. Operant methods were used to ascertain whether any increases in food intake were due to increased motivation to feed rather than stereotypic chewing movements. In nondeprived animals i.v. injection of 8-OH-DPAT at doses of 10, 30, and 50 micrograms/kg significantly increased food intake in the 45 min following injection. In pigs feeding after 4 h deprivation, i.v. injection of 8-OH-DPAT at doses of 30 and 50 micrograms/kg, given 5 min before feeding commenced, had no effect on food intake.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

2-Naphthalenesulphanyl-L-aspartyl-2-(phenethyl) amide (2-NAP) and food intake in rats: evidence that endogenous peripheral CCK does not play a major role as a satiety factor.

1. The demonstration that systemic administration of the CCKA receptor antagonist, devazepide, increases food intake in rats has provided the strongest support for the hypothesis that endogenous peripherally released cholecystokinin (CCK) acts as a satiety factor. However, interpretation of these results has been confounded by the fact that devazepide can enter the brain from the systemic circulation and may increase food intake by a central action. The present study was therefore undertaken to confirm the hypothesis that endogenous peripheral CCK is a satiety factor by investigating the effects of a novel CCKA receptor antagonist, 2-NAP, which is unlikely to cross the blood brain barrier, on food intake in rats. 2. 2-NAP (1-16 mg kg-1, i.p.) had no significant effects on the intake of a test meal in rats. 3. Pretreatment of rats with 2-NAP (2 mg kg-1, s.c.) abolished the inhibitory effects of exogenous peripheral CCK (5 micrograms kg-1, i.p.) on food intake. 4. In agreement with previous results, devazepide (50-200 micrograms kg-1, i.p.) significantly increased the intake of a test meal in rats. 5. The observations that 2-NAP, which is unlikely to penetrate the blood brain barrier, had no effect on food intake, but that 2-NAP abolished the suppressant effect of exogenous peripheral CCK, suggest that endogenously released peripheral CCK is not important as a satiety factor in rats.

Animals↗
PubMed1995

Intravenous administration of cholecystokinin (CCK) stimulates prolactin and growth hormone release in the pig.

Blood samples were taken from prepubertal pigs (n = 7) surgically prepared with venous catheters before, and at intervals during the 30 min period after, administration of physiological saline (vehicle) or sulphated cholecystokinin octapeptide (CCK) (0.3, 0.7 and 1.3 mu g/kg). Plasma concentrations of prolactin and growth hormone were measured by radioimmunoassay. Statistically significant dose-related increases in prolactin occurred mainly in the first 10-min period following CCK administration. The peptide also stimulated growth hormone secretion although in a less consistent manner, with the increases tending to occur over a longer time period. Together with earlier reports showing that CCK induces cortisol release in pigs, these results suggest that the peptide's effect on anterior pituitary function could be indicative of a stress response.

Animals↗
PubMed1994

Effect of a novel CCKA receptor antagonist (2-NAP) on the reduction in food intake produced by CCK in pigs.

The effect of a novel CCKA receptor antagonist 2-naphthalene sulphonyl-L-aspartyl-2-(phenethyl)amide, sodium salt (2-NAP) on the reduction of food intake induced by exogenous CCK, administered centrally or peripherally, has been examined in pigs. 2-NAP is hydrophilic and should not readily cross the blood-brain barrier. Intravenous (IV) 2-NAP (20 or 40 mg/kg) injected prior to IV CCK-8S (1 microgram/kg) abolished the inhibitory effect of CCK-8S on operant food intake in hungry pigs. Intravenous injections of 2-NAP (20 and 30 mg/kg) prior to the administration of intracerebroventricular (ICV) injection of CCK-8S (1 microgram) did not affect the inhibitory action of ICV CCK-8S on food intake. ICV injection of 2-NAP (5 mg) abolished the inhibitory effect on food intake of ICV CCK-8S (1 microgram). The results indicate that 2-NAP does not cross the blood-brain barrier readily and that central and peripheral administration of CCK-8S inhibits feeding by different mechanisms. Neither ICV nor IV injection of 2-NAP altered food intake when injected alone.

Animals↗
PubMed1993

Family caregivers of institutionalized and noninstitutionalized elderly individuals.

This article provides an overview of the literature that has examined the issues of institutionalization and community care of elderly persons. Specifically, those studies are discussed that report on the family's decision to institutionalize the elderly person and those that report on the effect of institutionalization of the family. Studies about community caregiving that report on caregiver characteristics, the stress of caregiving, and interventions to manage care issues and caregiver stress also are detailed. Implications for nursing research and practice can be derived from the article.

Adaptation, Psychological↗
PubMed1991

GABA release in the zona incerta of the sheep in response to the sight and ingestion of food and salt.

In order to establish which neurotransmitters may influence the activity of zona incerta neurones in the sheep which respond selectively to the sight or ingestion of food, we have measured the release of amino acid and monoamine neurotransmitters from this region using microdialysis sampling. Co-ordinates for the placement of microdialysis probes in regions of the zona incerta where cells respond to the sight or ingestion of food were first established by making single-unit extracellular recordings. When animals were food-deprived results showed that release of gamma-aminobutyric acid (GABA) was increased in response to the sight and ingestion of food but not of aspartate, glutamate, taurine, noradrenaline, dopamine or serotonin. This release of GABA was absent when the animals were shown non-food objects or saw or ingested salt solutions. When the same animals were physiologically sodium-depleted GABA release was evoked by the sight and ingestion of salt solutions and release following the sight and ingestion of food was significantly reduced. These results provide further evidence that GABA is an important neurotransmitter in neural circuits controlling the regulation of food intake.

Analysis of Variance↗
PubMed1991

Central and peripheral doses of cholecystokinin that inhibit feeding in pigs also stimulate vasopressin and cortisol release.

The effects on vasopressin and cortisol secretion of centrally and peripherally administered cholecystokinin octapeptide (CCK) were investigated in conscious prepubertal pigs. Injection of 1.3 micrograms CCK into the lateral cerebral ventricle resulted in a sustained increase in plasma vasopressin after a latency of 5 min but no change in cortisol concentrations. Intravenous injection of 0.7 and 1.3 micrograms/kg CCK initiated a rapid surge (within 2 min) in plasma vasopressin and a later increase in cortisol secretion. The time course of the vasopressin response to the central injection of CCK was found to be similar to the period of behavioural inhibition induced when an equivalent dose of the peptide was given by the same route in an earlier feeding experiment. An analogous situation was also observed when CCK was given peripherally and, in this case, the threshold dose at which the behavioural and endocrine responses were induced was found to be the same.

Animals↗
PubMed1991

Hormonal effects of apomorphine and cholecystokinin in pigs: modification of the response to cholecystokinin by a dopamine antagonist (metoclopramide) and a kappa opioid agonist (PD117302).

Three experiments were carried out to investigate some of the mechanisms involved in the endocrine responses of pigs to the emetic agents apomorphine and cholecystokinin. In Experiment 1, plasma levels of vasopressin and cortisol were measured in prepubertal pigs (N = 5) treated with i.v. apomorphine (25 micrograms/kg) or saline vehicle. In Experiment 2, concentrations of vasopressin and cortisol were determined in pigs given iv sulphated cholecystokinin octapeptide (1.3 micrograms/kg), metoclopramide (300 micrograms/kg), metoclopramide + cholecystokinin, and an oral dose of the kappa opioid agonist PD 117302 (20 micrograms) alone, or followed by i.v. cholecystokinin. In Experiment 3, operant feeding behaviour was quantified in pigs (N = 4) given cholecystokinin (1 microgram/kg) or cholecystokinin preceded by oral PD 117302. Following apomorphine injection in Experiment 1, there was a rapid, transient, rise in plasma vasopressin. Cholecystokinin had a similar effect on vasopressin secretion in Experiment 2 and also induced a later rise in plasma cortisol. Pre-treatment with metoclopramide appeared to reduce both of these effects of cholecystokinin, but only the decrease in cortisol was statistically significant. However, oral administration of PD 117302 abolished the effect of cholecystokinin on vasopressin release and reduced the subsequent rise in cortisol. The inhibitory effect of cholecystokinin on feeding was unaltered by PD 117302 treatment in Experiment 3. The results obtained with apomorphine and metoclopramide, together, suggest that the neuroendocrine effects of cholecystokinin in the pig may involve an action on central dopamine receptors while the effects of PD 117302 indicate that kappa opioids may modify the hormonal responses to cholecystokinin by a peripheral action.

Animals↗
PubMed1990

Brain isozyme of glycogen phosphorylase: immunohistological localization within the central nervous system.

An antibody specific for the predicted carboxyterminal sequence of the human brain isozyme of glycogen phosphorylase (alpha-1,4-D-glucan:orthophosphate D-glucosyltransferase, EC 2.4.1.1) was generated to verify the carboxyterminal amino acid sequence of this protein. The isozyme-specific antibody was used to examine the localization of this protein in primate and non-primate brain. The highest levels of the brain isozyme in cerebrum and cerebellum were found in fibrous astrocytes, many with glial processes that appear to terminate upon blood vessels.

Animals↗