Search PubMed⌕ Search

Biomedical subjects

J W Chambers

Publications and source records attributed to J W Chambers.

35 records · Page 2Linked to original sources

The compression block technique: use and misuse in the study of motor skills.

Laszlo and Bairstow (1971b) claim that the compression block technique eliminates kinesthetic feedback prior to motor impairment and loss of motor control. They use evidence from studies employing the block to infer the nature of motor-skills processing. The present study, using two-point threshold, pro-prioceptive sensitivity, and hand and finger strength measures, yielded no evidence that afferent loss preceded loss of motor control.

Journal Article↗

Determination of N-acetylserotonin and melatonin activities in the pineal gland, retina, harderian gland, brain and serum of rats and chickens.

An N-acetylserotonin/melatonin radioimmunoassay (NAS/Mel RIA) and a Mel RIA were developed to measure NAS and Mel contents in tissues of rats and chickens. Anti-NAS and anti-Mel sera were produced by immunization of rabbits with NAS-M-bovine serum albumin (BSA) and Mel-M-BSA, respectively. Anti-NAS serum used in the NAS/Mel RIA reacts equally well with NAS and Mel, while anti-Mel serum used in the Mel/RIA reacts specifically with Mel. The NAS and Mel levels in the pineal and Harderian gland, the retina and the brain of rats and chickens and Mel levels in chicken serum were determined using these RIAs. Levels of NAS and Mel in the rat pineal demonstrated diurnal rhythms with high levels during the dark period and low levels during the light period. The indole levels determined in this study correlate well with those obtained by other methods.

Animals↗

Neurotransmitter regulation of growth hormone and ACTH in the rhesus monkey: effects of biogenic amines.

In an attempt to clarify the role of central neurotransmitters in GH and ACTH regulation, chair-adapted unanesthetized adult male rhesus monkeys and chronic indwelling intratrial cannulae were given 30 min infusions of various agonists known to affect central amines, and plasma samples were withdrawn for GH and cortisol determinations. Infusion of acid-saline vehicle alone had no significant effect on plasma GH or cortisol (P less than 0.05). L-Dihydroxyphenylalanine (L-Dopa) (4.5 and 45 mg/kg), but not apomorphine (7 mug/kg), a specific dopaminergic agonist, produced significant elevations of GH. Both noradrenergic (clonidine HCl, 1.5, 15, and 150 mug/kg, and D,L-threodihydroxyphenylserine (D,L-threodops) 90 mg/kg) and serotoninergic (5-hydroxy-L-tryptophan (5-HTP), 45 mg/kg) agonists induced significant GH responses. These findings suggest that GH is regulated in the rhesus monkey by noradrenergic and serotoninergic neurons, whereas participation of dopaminergic neurons has not been established. Significant cortisol responses were only observed following infusion of 5HTP (45 mg/kg). Dopaminergic and noradrenergic agonists not only failed to alter resting cortisol levels but also did not affect the cortisol response to 5-HTP. In the rhesus monkey serotoninergic mechanisms appear to be responsible for the regulation of resting cortisol levels. A catecholamine inhibitory mechanism was not demonstrated in this species.

5-Hydroxytryptophan↗

Stimulation of rhesus monkey GH release: arginine vs plasma volume expansion.

Plasma GH and cortisol responses were examined in unanesthetized adult male rhesus monkeys infused with approximately 30 ml (8.3 ml/kg) of arginine monohydrochloride (Arg 0.5 g/kg), 0.9% saline (NS) or Dextran 75 and following 15 ml infusions of acid-saline (AS), or somatostatin (GHRIH 30 mug/kg). None of the infusions were accompanied by GH elevations. Rebound GH elevations occurred after each 30 ml infusion and after GHRIH but not after 15 ml AS. Although the amplitude of GH responses were not significantly different (p greater than 0.05), responses to Arg and dextran were significantly delayed as compared to responses following NS and GHRIH which did not differ from each other. Both of the latter responses occurred within 15 min of infusion completion. The delay following dextran was significantly longer than that following Arg (p less than 0.05). Since the volume of saline and the dosage of Arg were equivalent to those used in the standard intravenous Arg test, results suggest that effects of infusion volume upon GH secretion and upon GH responses to Arg warrant examination in the human. In addition, it is suggested that GH responses to NS and to dextran are mediated via an intravascular volume control mechanism and that GHRIH may be released upon activation of such a mechanism. GH elevations may represent rebound responses upon termination of GHRIH secretion.

Animals↗

Inhibition of hepatic uptake of alpha aminoisobutyric acid by ethanol: effects of pyrazole and metabolites of ethanol.

Ethanol inhibits the uptake of AIB by the isolated perfused rat liver. However, if the metabolism of ethanol is blocked by pyrazole, there is no reduction in accumulation of AIB by the liver. Acetaldehyde and acetate, metabolites of ethanol have no effect on AIB uptake by the liver. The inhibition of urea synthesis by ethanol is also prevented by pyrazole. Neither of the metabolites of ethanol inhibit urea synthesis in the isolated liver.

Acetaldehyde↗