PubMed · 6551155
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1983. Sample shows decrease in median age of RNs.. https://pubmed.ncbi.nlm.nih.gov/6551155/
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In order to detect the dysfunction of central and peripheral nervous systems among rats with varied duration of hypothyroidism and to elucidate the pattern of recovery after thyroxine replacement, a series of BAEP and PNCS (Peripheral Nerve Conduction Study) were conducted and compared with age-matched controls. BAEP and PNCS were performed in three groups of hypothyroid animals 1, 3 and 5 months after thyroidectomy, respectively. Following initial electrophysiological assessment, thyroxine replacement was administered to each group of hypothyroid rats, and BAEP and PNCS were performed at two month intervals, up to two successive normal studies, or six months after the initiation of therapy, whichever came first. For BAEP, prolonged I-V interpeak latency was the most consistent abnormal finding in all groups of hypothyroid rats, and longer hypothyroid states correlated well with more severe central conduction disorder. Nevertheless, these abnormalities usually returned to normal after thyroxine replacement if the duration of hypothyroidism was less than 5 months. Regarding PNCS, all groups of thyroidectomized rats showed normal conduction before and after thyroxine therapy. The present study indicates that, in rats: (1) the peripheral nervous system seems to be more resistant to hypothyroidism than the central nervous system, or (2) the pathogenesis of central and peripheral nerve dysfunction in hypothyroid rats may occur through different mechanisms.
Delayed neuronal death is produced at about the 4th day following global forebrain ischemia. This study investigates whether L-deprenyl, an irreversible and selective MAO-B inhibitor, reduces brain damage following global forebrain ischemia in adult gerbils. For this purpose, global forebrain ischemia was induced in adult gerbils by occlusion for 5 min of both common carotid arteries. L-Deprenyl, 10 mg/kg weight in saline (10 mg/ml) i.p., was administered 1 h after or 2 h before occlusion, followed by daily administration for 4 days. Treated animals were processed in parallel with ischemic animals receiving saline alone, and with sham-operated controls. Counts of viable neurons were made in the pyramidal cell layer of the CA1 region of the hippocampus at the 4th day after the ischemic episode. The number of viable neurons in the pyramidal cell layer of CA1 was similar in animals treated with L-deprenyl or saline alone (Mann-Whitney U-test, alpha=0.05 two-tailed). The present results show that L-deprenyl does not prevent neuronal cell death following global forebrain ischemia in the adult gerbil when the administration of the drug is started shortly after or shortly before the ischemic episode.
Mouse TCR gamma genes in the gamma1 cluster are arranged in the order of Vgamma5, Vgamma2, Vgamma4, Vgamma3, Jgamma1, and Cgamma1 on the chromosome. During thymic ontogeny, each Vgamma gene recombines with the Jgamma1 gene in the order of proximity to Jgamma1. To explore the mechanism of the ordered recombination, we generated Vgamma4-deficient mice by gene targeting and the Cre/loxP system, by deleting the 4.8-kb DNA region between 3' of the Vgamma2 and 3' of the Vgamma4. In semiquantitative PCR analysis, Vgamma2-Jgamma1 recombination was detected frequently in adult thymus, while Vgamma3-Jgamma1 recombination preferentially occurred in fetal thymus of the mutant mice. There was no difference in the frequency of V-J recombinations between control and mutant mice. Southern blot analysis also revealed that recombination of the Vgamma2 gene occurred as frequently as in control mice. In addition, there was no difference in the levels of germline transcripts of Vgamma2 and Vgamma3 genes between control and mutant mice. Therefore, regulation of the Vgamma-Jgamma recombination was not affected by deletion of the Vgamma4 gene. These results suggest that the ordered recombination is controlled by regulatory elements near each Vgamma gene.