One hundred eighty-one dissected hands were examined to study the pattern of extensor tendons on the dorsum of the hand. Extensor digitorum often had multiple tendons for the middle and ring fingers. Its contribution to the little finger was usually by a bifurcating tendon common with that of the ring finger. The index finger always received a single tendon. Intertendinous connections between the various tendons of the extensor digitorum were variable but were most frequent between ring and middle fingers. Extensor indicis had one tendon in most of the specimens and it was always on the ulnar side of the extensor digitorum tendon. This remained true even when there were multiple tendons. Extensor digiti minimi had two tendons in most cases. It was always linked to extensor digitorum either by receiving one or part of its tendon or by an intertendinous connection. Two accessory muscles were seen, one was extensor indicis brevis replacing the proper muscle. The other, the extensor medii brevis, was distributed to the middle finger.

Six girls between 2 years 9 months and 15 years of age with Rett syndrome were thoroughly investigated. Blood ammonia levels varied between 42 and 123 mumol/L, and serum lactate concentration was slightly elevated in two girls. Electroencephalograms showed a dysrhythmic pattern during wakefulness; during drowsiness and light sleep, bilateral bursts of spike or multispike-and-wave activity were seen in all but the oldest girl. In one of the younger girls, slight cortical atrophy was found on computed tomographic scan. Muscle biopsy was performed on all girls, and electron microscopy revealed abnormal mitochondria. Physical signs such as somatic hypotrophy with extremely small muscle mass, and unsatisfactory weight gain in spite of good appetite are found in Rett syndrome. These attributes, as well as reports of ornithine carbamoyltransferase deficiency, may support a mitochondrial dysfunction. The mitochondrial changes indicate either a mitochondrial mutation or more probably an X-borne modulator gene mutation. Another genetic possibility discussed is the "metabolic interference" of an X-borne allele. Further delineation of such mitochondrial changes may clarify the causal metabolic defect in Rett syndrome.

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The objective of this investigation was to find out the histopathological changes of the placenta and to correlate them with fetal malformations and growth retardation in experimental diabetes. Diabetes was induced in Wistar rats at different stages of gestation by intraperitoneal injection of streptozotocin (STZ). The controls were either buffer treated or injected with STZ followed by 2-6 IU insulin until term. All fetuses and placentae were collected on day 20 of gestation. Fetuses of diabetic rats were significantly growth retarded. Maxillary hypoplasia, edema, gastroschisis, exencephaly and septa1 defects of the heart were the major malformations. Most of the experimental placentae weighed heavier relative to their body mass. Toluidine blue stained sections of the placentae revealed severe histological abnormalities. The unusually large sized placentae had extensive cystic degeneration, often with an increased population of leucocytes. Giant cells were very numerous. Perivascular fibrosis, persistence of fetal mesenchyme, edema, infarcts and vacuolisation were observed in the labyrinths. In the small placentae, the glycogen cells were fewer and the glycogen in them remained unutilized. Reduction of labyrinthine zone, hypovascularity, constriction of vessels, perivascular edema and platelet aggregation characterized these placentae. The placentae of externally malformed fetuses showed cystic degeneration; their labyrinths contained constricted and less extensive vascular network. Phagocytic giant cells, polymorphs and platelet aggregation were also marked. Placentae of externally normal looking fetuses also presented cystic degeneration, reduction in fetal vasculature, dilated maternal sinusoids and giant cell proliferation. Insulin treatment resulted in the preservation of most of the normal histology of the placenta which correlated well with the reduced fetal malformations.

The ultrastructure of HeLa cells arrested in the G2 phase of the cell cycle by the antineoplastic agent cis-acid was studied and compared with that of normal G2-phase-synchronized cells. The results demonstrate that the chromatin of drug-treated cells was fragmented and clumped, the membranous structures had degenerated or were destroyed and the polyribosomes were decreased. The mitochondria were swollen and vacuolated, suggesting that energy production might have been impaired.

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