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In chronic gastric fistula rats hourly gastric juice collections were made before and after subcutaneous injections of histamine and insulin. Linear relationships were obtained between gastric juice osmolality and H + and Cl − ion concentrations. These relationships were independent of the type of the stimulant used. The osmotic effects of the individual gastric juice electrolytes were calculated. The contribution of the non-electrolyte component was greater than 50% of the total gastric juice osmolality. Apart from the first hour after stimulation, close correlation existed between the Na + and H + ion concentrations. Close correlation was apparent between the H + ion concentration and that of total and neutral chloride at all time periods.

1. 1. The auditory averaged evoked response (AER) was measured at the vertex in twelve 6–12-month-old normal babies during Stage 2 and rapid eye movement (REM) sleep and during the ocular quiescent and eye movement burst phases of REM sleep. Amplitudes and latencies of wave N 2 of the auditory AER were compared during the different sleep stages and to previously reported values for normal and autistic children. 2. 2. The latencies of wave N 2 in the babies were similar to those of the normal children during Stage 2. However, latencies during REM sleep and during both the eye movement burst and ocular quiescent epochs of REM sleep were significantly longer in the babies. 3. 3. The babies showed a tendency toward greater amplitudes of wave N 2 during both the eye movement burst and ocular quiescent phases of REM sleep than during Stage 2 sleep. In the group of babies, the relative amplitudes of wave N 2 during both REM sleep and the eye movement bursts of REM sleep (relative to Stage 2 sleep) were significantly greater than in a group of normal children, but were similar to those of a group of young autistic children. 4. 4. These findings suggest that the normal phasic inhibition of evoked responses accompanying the ocular activity of REM sleep may not be present in the very young organism and that the development of phasic inhibition may be related to maturational factors underlying the post-natal reduction of REM sleep time.

During a 7 year period from January, 1965 to December, 1962, 364 patients were operated on for pulmonary tuberculosis, resection in 249 patients and thoracoplasty in 115 cases. The operative mortality for resection was 2.8% and that for thoracoplasty 1.7%. Of these, 207 patients, 147 resection cases and 60 thoracoplasty cases, were followed for a period of 10 months to 6 years. Of the 147 cases of resection, 129 cases oir 87.8% became inactive following the surgery, while, of the 60 cases of thoracoplasty, 49 cases or 81.7% were converted inactive following the surgery. Of the resection cases, 25 patients had pneumonectomy and all remained inactive following the surgery. One hundred and eight cases had lobectomy or lobectomy plus segmental resection and 16 cases or 14.8% remained active following the surgery. Fourteen cases had a segmental resection only and 2 cases or 14.3% remained active following resection. Of the cases with moderately advanced and far advanced tuberculosis, the reactivation rate was 13.4% and 13.5% respectively following resection while none of those who had only minimal disease had reactivation following resection. Those who had positive sputum preoperatively showed a reactivation rate of 15.4 % following resectrion. On the other hand, none of those who had negative sputum preoperatively had a reactivation of the disease following resection. Those who had unilateral disease showed a reactivation rate of 8.9% and those who had fibrosis or small nodular diseases on the contralateral side on X-Ray at the time of resection had a reactivation rate of 21.4%

1. 1. The auditory averaged evoked response (AER) was measured at the vertex in age-matched groups of normal and autistic children during Stage 2 and REM sleep and during the ocular quiescent and eye movement burst phases of REM sleep. Amplitudes and latencies of wave N2 of the auditory AER were compared during these different sleep stages. 2. 2. In a group of sixteen autistic children under 5 years 1 month old, the relative amplitude of wave N2 during REM sleep (relative to Stage 2 sleep) was significantly greater than in a group of sixteen normal children. 3. 3. In a group of seventeen autistic children under 61 months old, the relative amplitude of wave N2 during the eye movement bursts (relative to ocular quiescence) was greater than that measured in a group of eighteen normal children. 4. 4. In a group of ten normal children under 61 months old, there was no appreciable difference between amplitudes of wave N2 obtained during the ocular quiescent phase of REM sleep and Stage 2 sleep. In contrast, amplitudes of wave N2 obtained during the eye movement burst phase of REM sleep were significantly smaller than during Stage 2. 5. 5. A group of eleven autistic children showed significantly larger relative amplitudes of wave N2 during both the ocular quiescent and the eye movement burst phases of REM sleep (relative to Stage 2 sleep) than did the group of ten normal children. The relative reduction of response amplitude during the eye movement bursts in normals was markedly overridden in these autistic subjects. 6. 6. The finding that relative reduction of response amplitude during REM sleep in normals is confined to the eye movement burst phase was related to the concept of phasic inhibition distinct from tonic inhibition during REM sleep. The phasic inhibition has been shown to be mediated by vestibular nuclei. The overriding of phasic inhibition in the autistic children was related to clinical observations suggesting vestibular dysfunction and faulty registration of the significance of sensory input.

Gastric secretion was studied hourly for five hours in chronic gastric fistula male rats (300–400 g). Following a control hour collection gastric secretion was stimulated by histamine 10.0 mg base/kg, ICI-50123 40 μg/kg and insulin 0.4 unit/kg SC-15396, 2-phenyl-2-(2-pyridyl) thioacetamide, a recently introduced anti-ulcer compound significantly (P < 0.01 to < 0.001) reduced gastric juice volume, acidity and total acidity in doses of 25 mg/kg and 50 mg/kg subcutaneously with all 3 secretagogues. Inhibition occurred when SC-15396 was given before or after the secretagogues, however, if it was given before the secretagogue acidity was depressed to a greater degree than volume; the reverse occurred if SC-15396 w was given after the secretagogue.

The anti-secretory and anti-ulcer effects of prostaglandin E 2 (PGE 2 ) using iso-osmotic buffer as a vehicle have been investigated in several types of laboratory animals. Orally administered PGE 2 was found to be highly effective in preventing formation of ulcers in several experimental models -- pylorus ligated induced ulcers in rats, histamine induced ulcers in guinea pigs, reserpine induced ulcers in rats and pentagastrin induced ulcers in guinea pigs and cats. PGE 2 also suppressed acid secretion but not pepsin activity. It was concluded that the anti-ulcer effects of PGE 2 were due to its anti-secretory activity rather than antipepsin activity. In view of PGE 2 's activity in preventing ulceration induced by histamine and reserpine in addition to pentagastrin, it is suggested that the anti-pentagastrin activity of PGE 2 is not specific.