A comprehensive model of a novel rotating spool compressor

A comprehensive simulation model of a novel rotating spool compressor is presented. The spool compressor provides a new rotary compression mechanism with easily manufactured components. A detailed analytical geometry model of the spool compressor is presented, which includes the geometry of the vane. This geometry model is included in an overall comprehensive compressor model that includes sub-models for friction, leakage, and heat transfer. The results of the comprehensive model were validated using experimental data from a prototype compressor. The prototype compressor has an overall displacement of 23.9 cm³, and was operated using R410A as the working fluid. The model predicts the volumetric efficiency, discharge temperature, and shaft power of the prototype compressor to within 3.13% MAE, 16.5 K and ?13.2 W average deviation, respectively. The trends and spread in the data indicate that additional effort should be focused on the operation of the active sealing elements within the compressor.     

Further studies on the role of the adrenal hormones in responses of rats to meal-feeding

The importance of the adrenal hormones in the lipogenic responses to meal-feeding or starvation-refeeding was studied. In experiment 1, intact or adrenalectomized (ADX) rats were either ad libitum-fed or meal-fed a 65% glucose diet for 21 days or until moribund (ADX rats only). Serum glucose and electrolytes (Ca++, Mg++, Na+, K+), hepatic glycogen and glucose-6-phosphate dehydrogenase (G6PD) and malic enzyme (ME) were determined. ADX rats died within 10 days after the initiation of meal-feeding and were hypoglycemic with low liver glycogen levels and low enzyme activities. No differences in serum electrolytes were observed. In the second experiment, ADX and intact rats of varying initial weights were weight paired and meal-fed. When the ADX rat died, his intact control was killed and both carcasses assayed for fat content. Heavier rats with presumably more carcass fat survived meal-feeding longer than the lighter rats. Rats died when they had lost all but 2 to 3 g carcass lipid. In experiments 3 and 4, ADX and intact rats were subjected to starvation-refeeding. In experiment 4, additional ADX groups were given supplemental doses of cortisol (0.75 mg/kg, subcutaneous, 2 times daily) during either the starvation period, the refeeding period or during both periods. The activities of hepatic G6PD and ME were determined as well as the levels of liver lipid in experiment 4. Intact starved-refed rats had the usual enzyme overshoot, whereas ADX starved-refed rats did not. Cortisol-treated ADX starved-refed rats had as great an enzyme overshoot as the intact rats and as great an increase in liver lipid. These results suggest that ADX rats die when meal-fed the glucose diet, because they are unable to store sufficient metabolic fuel for use during the starvation phase of the meal-feeding cycle. Further, the results show that glucocorticoids are required for the induction of de novo enzyme synthesis.     

Overselectivity, developmental level, and overtraining in autistic and normal children

Thirteen autistic children were compared to 13 normal children matched to them in mental age, on performance of a visual discrimination task. Form, color, and size were relevant and redundant cues. The groups did not differ significantly in mean trials to reach criterion or in breadth of learning, and both groups increased their breadth of learning after 50 trials of overtraining. Form was preferred to color and size by both autistic and normal children. Within each group, rank on mental age was highly correlated with rank in breadth of learning. Verbal and nonverbal autistic children did not differ in breadth of learning or in dimensional preference. Even nonverbal autistics equaled the performance of their normal controls. Our results suggest that overselective attention is better understood as part of a general developmental lag in cognition in autistic children than as a specific deficit underlying psychotic behavior.     

Subclavian steal syndrome. A 12-year experience

Over a 12-year period, 43 operations were performed on 40 patients for correction of the subclavian steal syndrome. Eleven of these patients also underwent endarterectomy for coexisting carotid artery disease. There were 16 transthoracic procedures and 27 transcervical procedures. Graft failure in two patients was corrected by a second operation. There was one early death and one late death. The remaining 38 patients have been carefully studied for up to 12 years, with an average follow-up period of 60 months. These 38 patients have remained asymptomatic and their revascularization procedures have remained functional, as determined by blood pressure determinations in the involved extremity and, in some cases, by arteriography.     

Cost of management of patients with haemophilia

The cost of managing 114 adult haemophiliacs in the west of Scotland was assessed for the period 1 March 1971 to 28 February 1974. Altogether 23 of them (20%) accounted for 80% of the resources used. The cost of hospital treatment of these patients during the period was compared with the predicted cost of home treatment, given the availability of freeze-dried factor VIII concentrate in sufficient amounts. We calculate that adequate on-demand home treatment would cost only 16% more than the present treatment, which is substantially less efficient.     

The relationship between striatal and mesolimbic dopamine dysfunction and the nature of circling responses following 6-hydroxydopamine and electrolytic lesions of the ascending dopamine systems of rat brain

The importance of extrapyramidal and mesolimbic function for circling behaviour was investigated by placing 6-hydroxydopamine (6-OHDA) and electrolesions in the cell bodies, axons and terminals of each system. Circling behaviour was weak when 6-OHDA was placed at the centre of the substantia nigra (SN), but the characteristic contralateral/ipsilateral turning to apomorphine/amphetamine were recorded. Circling was more marked when 6-OHDA was placed anterior to the SN but was generally absent following injections posterior to the SN. However, 6-OHDA placed in the medial forebrain bundle in the lateral hypothalamus resulted in intense contralateral/ipsilateral turning to apomorphine/amphetamine. Generally, the intensity of circling responses was related to the degree of striatal dopamine (DA) depletion but the more effective lesions also caused reductions in mesolimbic DA content. However, circling was not observed following any 6-OHDA injection into the mesolimbic DA system and it is concluded that mesolimbic DA function is not essential for the initiation of circling. In contrast to the 6-OHDA lesions, rats circled ipsilateral to both apomorphine and amphetamine when the SN was damaged by electrocoagulation to cause marked depletion of striatal dopamine. Lesser depletions of striatal dopamine after electrocoagulation in different regions of the medial forebrain bundle were associated with a lower intensity of ipsilateral circling to both drugs. In general, the differences between 6-OHDA and electrolesions could not be explained by additional damage to ascending noradrenaline or 5-hydroxytryptamine pathways. Lower doses of apomorphine were effective in the 6-OHDA circling rats, and the ipsilateral striatum of such rats was more sensitive to directly applied DA. Higher doses of apomorphine were required to produce circling after chronic electrolesions which rendered the ipsilateral striatum insensitive to DA. The contralateral circling to apomorphine after 6-OHDA lesions was abolished by chronic but not by acute electrolesion of the SN. It is suggested that electrolesions of the SN cause different effects to 6-OHDA because they destroy neuronal pathways in addition to the dopaminergic nigrostriatal tract. These appear to be required for the expression of circling behaviour caused by stimulation of the denervated striatum. Whereas 6-OHDA lesions result in super-sensitivity of the denervated strital DA receptors, electrolesions may cause a hypo-sensitivity of the same receptor sites.