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Over 50% of men having paraplegia due to traumatic lesions of the spinal cord or cauda equina show decreased spermatogenesis in varying degrees (Paulsen, 1968). The commonest pathology is arrested spermatogenesis with generalized hypoplasia of the germinal epithelium. Leydig cells usually appear normal, but the presence of nodular hyperplasia has been reported (Horne, Paull & Munro, 1948; Keye, 1956). Androgen production has been considered essentially normal judging from clinical symptoms, though most testes become smaller. Although urinary gonadotrophin excretion is reported to be low or absent in the majority of paraplegic men (Paulsen, 1968) and women (Durkan, 1968), there are no reports of plasma androgen concentrations. The concentration of testosterone in peripheral plasma from 51 paraplegic men after spinal cord injuries was therefore measured and compared with that of normal men.

The patients studied (aged 18–66 yr, average 37 yr) had been admitted to Osaka Labour Injury Hospital and the

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K Kashimada, T Yamashita, K Tsuji, A Nifuji, S Mizutani, Y Nabeshima, and M Noda

Klotho mutant (kl/kl) mice exhibit growth retardation after weaning, and previous electron microscopic examination of GH-producing cells in pituitary glands revealed a reduction in GH granules. However, it has not been known whether growth retardation in klotho mutant mice is related to the loss of GH function. We therefore examined whether treatment with GH could rescue the retardation of growth. At the end of 3 weeks of treatment with human GH, the body weight of wild-type (WT) mice was increased. In contrast, body weight was not increased in klotho mutant mice even after the treatment with human GH. Another feature of klotho mutant mice is the presence of osteopetrosis in the epiphyses of long bones and vertebrae. Treatment with human GH increased trabecular bone volume in the epiphyseal region of WT tibiae. Interestingly, increase in trabecular bone volume by GH treatment was also observed in klotho mutant mice and, therefore, the phenotype of high bone volume in the klotho mice was further enhanced. These findings indicate that a GH receptor system in cancellous bones could operate in mutant mice. Thus, growth retardation in the klotho mutant mice is resistant against GH treatment even when these mice respond to GH treatment in terms of cancellous bone volume.