Human factors in chemical containment laboratory design

A human factors engineering analysis of a chemical containment laboratory was performed to develop appropriate standards for future laboratory design. In order to perform this evaluation, a state-of-the-art facility was studied in depth. Measurements and observations were made of key operating areas. In addition, technicians were observed and interviewed as they performed various tasks. Compiled data were compared to existing ergonomic standards. The occupational implications of instituting ergonomically developed laboratory design standards are as follows: increased worker health, safety and productivity, improved work quality and reduced stress.     

The growth and development of Echinococcus granulosus of sheep origin in dogs and foxes in Britain

Four separate experiments were carried out by dosing dogs (Beagles and Border collies) and red foxes with protoscoleces obtained from hydatid cysts in sheep from mid-Wales. The dogs and foxes were killed at intervals over a period from 34-180 days after infection and the intestines were examined for Echinococcus granulosus. Border collie dogs were efficient hosts in that large numbers of worms developed, with gravid segments present by 55 days after infection; but Beagle dogs were poor hosts in that only small numbers of immature worms developed. Foxes were poor hosts in that few or no worms developed, but gravid segments were seen in three of 29 foxes. The worms showed morphological features similar to the 'sheep' rather than the 'horse' strain.     

Neurophysiological investigation of effects of the D-1 agonist SKF 38393 on tonic activity of substantia nigra dopamine neurons

The effects of the D-1 agonist SKF 38393 on tonic activity of rat substantia nigra pars compacta dopamine neurons were studied using extracellular, single-unit recording techniques. Unlike nonselective D-1/D-2 dopamine agonists or the D-2 agonist quinpirole, SKF 38393 did not inhibit dopamine neuronal activity when applied iontophoretically or when administered intravenously in doses up to 20 mg/kg to chloral hydrate-anesthetized rats. Moreover, pretreatment with SKF 38393 did not alter the inhibitory response of these neurons to apomorphine or the D-2 agonist quinpirole. However, in locally anesthetized, gallamine-treated, artificially respired rats, dopamine cell activity was significantly altered by i.v. administration of SKF 38393; firing rate increases and decreases were observed. Administration of the inactive enantiomer of SKF 38393, S-SKF 38393, did not induce similar changes in parallel experiments. These results support the idea that unlike D-2 autoreceptor stimulation, D-1 receptor stimulation does not exert a direct local effect on dopamine neurons in the substantia nigra pars compacta and suggest that D-1 receptor stimulation at sites postsynaptic to the dopamine cells may indirectly affect the activity of some dopamine neurons through long-loop feedback mechanisms.     

Unilateral lesion of the nigrostriatal pathway decreases the firing rate and alters the firing pattern of globus pallidus neurons in the rat

Activities of spontaneously firing neurons in the globus pallidus of intact rats and rats that survived unilateral lesions of the nigrostriatal pathway for 3 days, 1 week, or 6-11 weeks were compared. No significant differences in neuronal firing rate, firing pattern, and number of cells per pass were observed between chloral hydrate-anesthetized control and lesioned animals. However, in locally anesthetized animals, pallidal cells fired significantly faster than in chloral hydrate-anesthetized animals, and the lesion caused a decrease in the firing rates of pallidal cells 1 week and 6-9 weeks postlesion. In addition, significant differences in the firing pattern of pallidal cells, as determined by the ratio of the mean to median interspike intervals, were seen between locally anesthetized controls and animals surviving 3 days, 1 week, and 6-9 weeks postlesion. This altered firing pattern tended to return to normal with time. The number of cells per pass was not significantly altered by the lesion. Data from this study suggest that, in locally anesthetized animals, the removal of the tonic dopaminergic input to the basal ganglia causes pallidal cells to decrease their firing rates in a time-dependent fashion and causes reversable firing pattern changes. This suggests that tonically active dopamine neurons, probably acting through the striatopallidal pathway, regulate the firing rate and mechanisms controlling the temporal ordering of spontaneous discharges of globus pallidus neurons.     

Effect of a gonadotropin releasing hormone analog on cerebral hemodynamics in premenopausal women.

BACKGROUND: Impaired reactivity of cerebral blood vessels is associated with increased risk of stroke. Female sex hormones have vasoactive effects in a number of vascular beds but their effects upon the cerebral circulation are not well understood. Ultrasound techniques allow us to examine the ability of intracranial vessels to dilate in response to a pharmacological stimulus (the carbonic anhydrase inhibitor acetazolamide). We studied intracranial hemodynamics in a group of premenopausal women before and after induction of a temporary hypoestrogenic state. METHODS: We examined middle cerebral artery mean flow velocity, common and internal carotid artery pulsatility index and cerebrovascular reactivity to acetazolamide (CVR) in a group of women undergoing treatment for menstrual disorders. Volunteers underwent ultrasound examination during the follicular phase of the menstrual cycle and after completing treatment with gonadotropin releasing hormone (GnRH, goserelin 3.6 mg) administered subcutaneously every 28 days for 12 weeks. The study was conducted in a prospective, single-blind fashion and analyzed using parametric comparisons of means to examine change in intracranial hemodynamic parameters between pre- and postmenopausal states. RESULTS: Twelve premenopausal women aged 37.2+/-7 years and without overt vascular disease completed the protocol. GnRH reduced serum estrogen concentration (215.6+/-122 pg/ml vs. 82.4+/-12 pg/ml, p=0.0047) but this was not associated with a change in CVR (145+/-19% and 146+/-14% for follicular and post-GnRH studies, respectively (p=0.6). No significant changes in blood pressure, internal carotid or middle cerebral artery pulsatility or mean flow velocity were observed between time points. CONCLUSION: Neither resting cerebral hemodynamics nor reactivity of cerebral resistance vessels to a potent vasodilatory stimulus changed when the circulating concentration of estradiol was artificially decreased using a GnRH agonist. Induction of a hypoestrogenic state does not appear to influence cerebral vasodilatory capacity in the short term.