Japan 1 We investigated the effects of intraplantar (i.pl.) administration of L-arginine and N0-nitro-L-arginine methyl ester (L-NAME) on formalin-induced behavioural nociception in the mouse. 2 L-but not D-arginine, at 0.1-1 -g per paw, coadministered with i.pl. formalin, enhanced the secondbut not the first-phase nociceptive responses, whereas it was without significant effects at 3 fg per paw, and conversely, produced antinociception at 10 tLg per paw, resulting in a bell-shaped dose-response curve.3 L-NAME at 0.1-1 fig per paw, when administered i.pl., exhibited antinociceptive activity in the second phase in a dose-dependent manner, although its D-enantiomer produced no effect. 4 An antinociceptive dose (1 pg per paw) of L-NAME (i.pl.) considerably reduced the increase in second-phase nociception elicited by low doses (1 fg per paw) of i.pl. L-arginine. The second-phase nociception decrease induced by a large dose (10 pg per paw) of i.pl. L-arginine was markedly reversed by i.pl. L-NAME at 0.1 pg per paw, raising it to a level above that of the control (formalin only). 5 These results suggest that peripheral NO plays a dual role in nociceptive modulation, depending on the tissue level, inducing either nociceptive or antinociceptive responses.

Intracerebroventricular (i.c.v.) or intracisternal (i.cist.) administration of kyotorphin (KTP), an endogenous Met‐enkephalin releaser, at 5 μg per mouse, and l‐arginine (l‐Arg), a possible KTP precursor, at 30 μg per mouse, elicited antinociception in mice to a similar extent, as assessed by the tail‐flick test. Intracisternal preadministration of anti‐KTP serum abolished the effects of i.cist. KTP and i.c.v. or i.cist. l‐Arg, but not of i.c.v. KTP. The antinociceptive effects of i.cist. KTP and of i.c.v. or i.cist. l‐Arg disappeared in reserpinized mice, whereas the effect of i.c.v. KTP was unaffected by treatment of mice with reserpine. Intrathecal (i.t.) phentolamine markedly reduced the antinocieption induced by i.cist. KTP and by i.c.v. or i.cist. l‐Arg, but not by i.c.v. KTP. Intrathecal methysergide attenuated the antinociceptive effects of i.cist. KTP, but not of i.c.v. KTP and i.c.v. or i.cist. l‐Arg. These results suggest that the antinociception produced by i.cist. KTP, but not by i.c.v. KTP, is mediated by the brainstem‐spinal noradrenergic and 5‐hydroxytryptaminergic systems, and that l‐Arg given i.c.v. or i.cist. increases KTP formation in the lower brain, possibly the brainstem, resulting in antinociception mediated by the descending noradrenergic system. Therefore, the regional distribution of KTP receptors and KTP synthetase in the brain does not appear to be common.

We examined the characteristics and usefulness of a third generation anti-HCV test kit, SYNPEPTM HCV-EIA II (Kyokuto Pharmaceutical Inca, Tokyo, Japan). The sera of inhabitants from a hepatitis C virus (HCV) hyperendemic area were used. The kit had even or more anti-HCV detection sensitivity and reproducibility than ORTHO HCVIII ELISA Test SystemTM (Ortho-Clinical Diagnostic K.K., Tokyo, Japan) or HCV PHA 2nd GenerationTM (Dinabot Co., Ltd., Tokyo, Japan). SYNPEPTM HCV-EIA II needed less total reaction time than other EIA kits, resulting in a simple procedure. Also, HCV RNA was detected in 90% of subjects who had a 7.5 or greater cutoff index (COl) of SYNPEPTM HCV-EIA II kit. In conclusion, SYNPEPTM HCV-EI'A II require cheap cost and simple procedure and it could be applied to mass screening to find out HCV RNA positive persons who may need clinical care.