The effect on testicular steroidogenesis after lindane (δ-isomer of hexa-cholorocyclohexane) administration of 4 and 8 mg/kg, i. p. daily for 45 days to male mature rats was investigated. A significant decline in testicular weight of both test groups was observed. Celluler degeneration in Leydig cells of the 8 mg/kg treated group was conspicuous. A sharp decline in the Leydig cell's population and morphological deformation were supported by the decreased activities of testicular hyaluronidase and 3βΔ5-hydroxy-steroid dehydrogenase. A high level of testicular cholesterol and depletion of ascorbic acid were also responsible for steroidogeneic impairment in the treated groups. These impairments also led to a significant diminution in serum testosterone.

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Carcinogenesis in the rat intestine induced with 1,2-dimethylhydrazine (DMH), N-methyl-N-nitrosourea (MNU), and their combinatorial use was studied. Intestinal tumors, including both adenoma and adenocarcinoma, were induced in all the rats given the carcinogens. The tumor frequently occurred in the intestinal tract extending from the duodenum to the colon in the DMH treated group. In the MNU treated group, the tumor occurred in the colon, especially on the distal side. Distribution of tumors in the group treated with both carcinogens was similar to that seen in the MNU-treated group. Neither obvious macroscopic nor histological differences were observed between groups treated with these carcinogens. In addition, we investigated the effect of carcinogens on ornithine decarboxylase (ODC) activity in rat colon. Tumor tissues showed a remarkably high level of enzyme activity compared with the normal-appearing mucosa, and there was a correlation between the level of the ODC activity and the histological grade of malignancy. ODC activity in the normal-appearing mucosa of the carcinogens-treated rats was significantly higher than that of control rats, and the number of tumors per rat was correlated with the level of ODC activity. These results indicate that mucosal ODC may be a pertinent biological marker for local carcinogenic activity.

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The levels of pseudouridine (ψrd), uridine (Urd), hypoxanthine (Hyp), xanthine (Xan) and uric acid (UA) in both blood and urine samples were assayed by a reversed-phase high performance liquid chromatographic (HPLC) method. The evaluation of the sampling procedures showed that the levels of plasma oxypurines were overestimated by more than 15% for Hyp and 35% for Xan when heparinized plasma separation was delayed for 5 minutes after sampling. The fact that oxypurines levels of serum were significantly higher than those of plasma was also documented. Hence, for the accurate measurement of plasma oxypurines, plasma should be immediately separated from the blood with anticoagulants after it is collected. Physiological variation under a suitable sample preparation was also studied in 6 healthy male volunteers after their usual and a low purine diet for 4 days. The mean plasma levels for 6 male volunteers on a usual diet were 2.52 ± 0.19 μmol/ℓ for ψrd, 290.1 ± 88.8 for UA, 49.4 ± 1.24 for Urd, 0.82 ± 0.30 for Hyp and 0.49 ± 0.12 for Xan. On a low purine diet, the declines in the plasma oxypurine concentrations and the renal excretions of UA as well as oxypurine were demonstrated. When a dietary purine intake was restricted, the reference range of the Hyp level in plasma was 0.48 ± 0.26, and Xan was 0.36 ± 0.17 μmol/ℓ. Dietary influences on purine-pyrimidine metabolites should also be considered for the accurate measurement of their concentrations in blood and urine.

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A 35-year-old man with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with acute bilateral optic neuritis is described. At age 33, he noticed a tingling sensation in his toes followed by weakness in the lower limbs. He was admitted to our hospital because he became unable to walk without support. His motor and sensory symptoms gradually resolved during 7 months admission only with physical rehabilitation. At age 35, in July 1988, he noticed a tingling sensation in his toes and fingers, which reached to the knees and elbows in October 1988, when he developed weakness in the lower limbs. Motor and sensory symptoms were almost stationary thereafter and in March 1989, he experienced bilateral blurred vision of acute onset without ocular pain. He was readmitted to our hospital in April 1989. The neurological examination revealed decreased visual acuity of both eyes without any abnormality of the optic disks, mild weakness on flexion and extension of toes, an absence of Achilles reflex, and distal impairment of pain and touch sensations in the upper limbs, and of pain, touch and vibration sensations in the lower limbs. After laboratory examinations, CSF protein was elevated (122 mg/dl), and sensory nerve conduction velocity of the right median nerve was decreased (37.1 m/sec). The sural nerve action potential was not elicited on electrical stimulation. Central scotoma was found in both eyes by the visual field examination. P100 latency was seen to be normal by repeated pattern-reversal visual evoked potential (VEP) studies. CT and MRI of the brain were unremarkable. On sural nerve biopsy, axonal degeneration and segmental demyelination with a moderate decrease in the density of the myelinated fibers and onion-bulb formation at low frequency were found. After two months treatment with prednisolone (40 to 60 mg on alternate days), visual acuity was markedly improved and central scotoma disappeared. Motor and sensory symptoms in both limbs were also improved. CSF protein was normalized and sensory nerve conduction velocity of the right median nerve was definitely improved. In this patient, pattern-reversal VEP studies were normal and failed to support the presence of demyelinating lesions in the visual pathway, which was strongly suggested by the neurologic findings. However, steroid treatment resulted in a marked improvement of neurologic symptoms and signs, including visual acuity and laboratory findings. Therefore, we concluded optic neuritis was one of the signs of CIDP in this patient.

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Parasitic helminths can not choose a strategy for fighting against their hosts but can only compromise with them. They do not kill their hosts because the host is necessary for their survival. Schistosoma haematobium, one of the main causes of tropical parasitic diseases, is a parasitic helminth whose only host is human beings and therefore is considered to evolve fully while adapting to humans. In a human community, the peak intensity and peak prevalence of S. haematobium infection occur in adolescence and suddenly decline thereafter. This is advantageous for the hosts and could be explained as a typical strategy of parasitic helminths. The possible mechanisms of maintaining this host-parasite relationship are the development of acquired protective immunity and the change of human water-contact behavior by age. However, our study in Kenya indicates that the worm burden is regulated mainly by the change of human water-contact behavior. Since human behavior depends on the cultural background of the society, the relation between humans and S. haematobium is an example of the great influence that the human culture has on the host-parasite relationship. For any further investigation of tropical infectious diseases, socio-cultural research is indispensable.

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