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SUMMARY1. One hundred and seventeen healthy new-born babies weighing between 0 9 and 4-8 kg at delivery have been studied during the first ten days of life, and sixteen of these babies have been studied serially for 6 weeks after birth. The babies lay supine in a draught-free environment (air speed 4-5 cm/sec) of moderate humidity. The operative temperature was between 26 and 380 C for the babies who were studied naked.2. Total non-evaporative heat loss was calculated from simultaneous measurements of oxygen consumption, evaporative water loss and the concomitant change in mean body temperature.3. Approximately 10 % of the total body surface area was in contact with the mattress or floor. Conductive heat loss accounted for only about 5 % of all non-evaporative heat loss when the naked baby was lying on a thick foam mattress, but for as much as 25 % when the baby was lying in a water-jacketed chamber with a floor of clear plastic 5 mm thick.4. Insulation to heat loss by convection and radiation varied with environmental temperature. Total specific insulation was low in a warm environment when the naked baby vasodilated, and rose by between 16 and 25 % to a maximum in an environment of 310 C. It decreased significantly when the baby became physically active in environments with a temperature less than this.5. Total specific insulation in an environment of 310 C varied with body size: it averaged 0.1560 C.m2. hr/kcal in seven naked babies weighing 0 9-1*2 kg, rose to 0-190°C. m2 . br/kcal in twelve babies weighing 1-8-2 2 kg, and averaged 0-201' C. m2.hr/kcal in the thirty-four babies who weighed over 3 kg. Tissue insulation accounted for 23 % of this total specific insulation in the smaller babies, and about 28 % of the total in babies weighing over 3 kg.6. Clothing ten babies in a vest, napkin and long cotton nightdress increased the total specific insulation by an average of 0 230 C . m2 . hr/kcal.

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Neuropathological studies of rats were made after seizures of different durations. Seizures were produced by mercaptopropionic acid in paralyzed, ventilated rats that were perfusion-fixed immediately (acute) or after 2-7 days of recovery (chronic). Analysis of chronic rats, which had only 20-min seizures, showed that damage occurred to several structures including: the substantia nigra pars reticulata, the hypothalamus, the diagonal band of Broca, and the globus pallidus; the damage was worse with longer seizures. In rats perfused acutely no changes were detected in paraffin sections in the aforementioned structures if the length of seizures was 45 min or less. It was concluded that: (1) mercaptopropionic acid-induced seizures cause permanent lesions to specific brain areas, with the most pronounced effect in the substantia nigra pars reticulata; (2) the lesions result from the seizures, and they are roughly proportional to the seizures duration; and (3) permanent lesions may begin within 20 min but require longer times to become visible on light microscopy.

Two babies are described whose mothers were given large doses of diazepam during labour. One mother had eclampsia, and the other had severe pre-eclampsia. Both babies were severely asphyxiated at birth, and one showed depressed respirations and reflexes for four days. The blood levels of diazepam in both babies rose for 40 hours after birth and then fell suddenly but remained detectable until the seventh day of life. The metabolism of the drug in the perinatal period is discussed.

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Light microscopic and ultrastructural changes of substantia nigra were studied in paralyzed ventilated rats with status epilepticus induced by mercaptopropionic acid. Some rats were killed at the end of seizure activity and others were examined in varying intervals after the arrest of seizure. The earliest changes were reduction in the size of the neuronal nuclei and chromatin clumping followed by simultaneous distention of axons and dendrites. There was also enlargement of the neuronal perikarya associated with microvacuolation. This neuronal microvacuolation corresponded ultrastructurally to swollen mitochondria with disrupted cristae. These changes were followed by progressive neuronal shrinkage and astrocytic swelling. The swollen astrocytic processes together with swollen neurites gave a spongy appearance to the involved area. The lesion thereafter progressively enlarged and evolved into an area of frank necrosis containing abundant macrophages. This lesion is morphologically different from that produced in cortex and hippocampus by seizure activity or due to the direct effect of excitotoxins. The significance of substantia nigra pars reticularis changes and their pathogenesis are discussed.