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Biomedical subjects

K Sainio

Publications and source records attributed to K Sainio.

8 recordsLinked to original sources

Gyrate atrophy of the choroid and retina with hyperornithinemia: tubular aggregates and type 2 fiber atrophy in muscle.

We studied 21 patients with gyrate atrophy of the choroid and retina and hyperornithinemia. Although the patients were not weak, type 2 muscle fibers were almost universally atrophic and had tubular aggregates. Gyrate atrophy is the first disease in which females are shown to have tubular aggregates; the sexes were affected equally. In gyrate atrophy the number of type 2 fibers decreases with age. The muscle and eye changes are probably related to abnormal creatine synthesis, caused, in gyrate atrophy, by the increased body pool of ornithine; muscle abnormalities may also be present in other tapetoretinal dystrophies.

Adolescent

Electroencephalographic changes during experimental hangover.

The EEG was recorded in 27 subjects during hangover. Male healthy volunteers drank 1.75 g/kg body weight of ethanol in 3 h and the EEG was recorded 14-16 h later when the degree of hangover was highest. For control purposes a second EEG was recorded after a similar session when subjects drank water instead of ethanol. A third record was taken in normal laboratory conditions. T5-A1 and O1-A1 derivations were subjected to computer analysis from which spectral and frequency parameters were calculated. Visual analysis of the EEG during hangover showed a decrease and slowing of alpha activity and an increase in theta activity. Spectral analysis of the EEG gave a statistically significant increase in 7-8 c/sec activity during hangover. The EEG change could not be explained in terms of blood alcohol level, hypoglycaemia or acidosis. Also fatigue could be excluded as a cause of EEG change by means of "water controls". The conclusion is that the slowing of the EEG during hangover is caused by the depressant action of ethanol, or its metabolites, on cortical function.

Adolescent

Sleep-waking cycle in rabbits after cerebral ischemia.

In rabbits experimental cerebral ischemia of 4-6 min was followed by degradation of the electroencephalographic sleep-waking cycle, as determined from 3 h afternoon records: I. Hyposomnia i.e., reduction of slow wave and paradoxical sleep lasting for about 2 days, was seen, with gradual normalization in case of survival. II. In the first postischemic days abundant 14-17 c/sec spindles appeared in the motor cortex against a low voltage desynchronized background, making the EEG of waking qualitatively different from control records. The results are discussed with reference to polygraphic studies in comatose patients, EEG phenomenology of drowsiness, and cerebral monoamines.

Animals