Paroxysmal kinesigenic choreoathetosis (PKC), the most frequently described type of paroxysmal dyskinesia, is characterized by recurrent, brief attacks of involuntary movements induced by sudden voluntary movements. Some patients with PKC have a history of infantile afebrile convulsions with a favorable outcome. To localize the PKC locus, we performed genomewide linkage analysis on eight Japanese families with autosomal dominant PKC. Two-point linkage analysis provided a maximum LOD score of 10.27 (recombination fraction [theta] =.00; penetrance [p] =.7) at marker D16S3081, and a maximum multipoint LOD score for a subset of markers was calculated to be 11.51 (p = 0.8) at D16S3080. Haplotype analysis defined the disease locus within a region of approximately 12.4 cM between D16S3093 and D16S416. P1-derived artificial chromosome clones containing loci D16S3093 and D16S416 were mapped, by use of FISH, to 16p11.2 and 16q12.1, respectively. Thus, in the eight families studied, the chromosomal localization of the PKC critical region (PKCR) is 16p11.2-q12.1. The PKCR overlaps with a region responsible for "infantile convulsions and paroxysmal choreoathetosis" (MIM 602066), a recently recognized clinical entity with benign infantile convulsions and nonkinesigenic paroxysmal dyskinesias.

Objective: To investigate the arthritis inhibiting effect of endostatin, known to have potent antiangiogenic activity, systemically given to animal models of rheumatoid arthritis (RA). Methods: Four kinds of monoclonal anti-type II collagen antibody followed by lipopolysaccharide (LPS) three days later were given to 6 week old, female Balb/c mice to induce arthritis. Three groups of mice received 0.2 mg/kg/day, 2 mg/kg/day, and 10 mg/kg/day of endostatin, respectively, whereas a control group received phosphate buffered saline (PBS). Endostatin or PBS was given for 13 days, starting before the development of arthritis. Arthritis was evaluated by arthritis scores and hind paw thicknesses. Mice were killed for histological examination on the 22nd day after the administration of monoclonal anti-type II collagen antibody. Results: Arthritis developed within three days after LPS administration in both the control and endostatin treatment groups. No difference in the development rate of arthritis was noted between the control and endostatin treatment groups. Arthritis scores remained significantly lower in the endostatin 10 mg/kg/day group than in the control group. Hind paw thicknesses also remained significantly smaller in the endostatin 10 mg/kg/day group than in the control group. Histopathological examination showed that synovial thickening and subchondral bone erosion improved more in the endostatin treatment groups than in the control group. Conclusion: The systemic administration of endostatin had an arthritis inhibiting effect in RA animal models. Endostatin inhibited, in particular, pannus formation and bone destruction.

The effect of estrogen on the sleep‐wakefulness circadian rhythm was examined in ovariectomized rats. Implantation of crystalline estradiol benzoate (EB) into the third cerebral ventricle reduced the slow wave sleep (SWS) and paradoxical sleep (PS) appearances within the dark period. This result was similar to that obtained by a systemic administration of 20 μg of EB. The inhibition of sleep during the nighttime was more remarkable in PS than in SWS. The reduction of SWS was due to a shorter duration of SWS episodes and the reduction of PS to a fewer number of PS episodes. These results indicate that ovariectomized rats treated with estrogen develop an inability to sustain episodes of SWS and initiate PS episodes.

Nerve terminals in the lateral septum were studied by electron microscopy in the rat after lesions of the suprachiasmatic nuclei (SCN). The results were as follows: 1) The electron‐lucent degenerations showed a reduction in the number of vesicles and the swelling of terminals and/or vesicles. These degenerating terminals predominated at two days of survival period. The electron‐dense degenerations which showed a darkening and shrinkage of the terminals mainly appeared at four days of survival period. 2) Most of the degenerating terminals contained large core vesicles of a diameter in the range of 800–1500 A. 3) The percentage of the degenerating terminals to all the terminals on the electron micrographs was about 7%. 4) The F‐type synapses were not found in the lateral septum of the normal and SCN lesion rats. These data confirmed the existence of the projection which reached the lateral septum from the SCN and suggested to us that these synapses were so‐called peptidergic synapses.

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