BACKGROUND: A randomized, controlled clinical trial was conducted in 1991 to compare an intravenous megadose of methylprednisolone with a control drug (mecobalamin) for treating acute idiopathic optic neuritis. CASES: Sixty-six cases from 22 clinical centers throughout Japan were examined to evaluate the treatment on visual function parameters, such as visual acuity, visual field, color vision, contrast sensitivity, and critical flicker frequency. OBSERVATIONS: The methylprednisolone pulse treatment group showed faster recovery of visual function, particularly the visual acuity at 1 week (P<.05), Humphrey field analyzer mean deviation at 3 weeks (P<.05), and color vision at 1 week (P<.05). Recovery of contrast sensitivity at several different spatial frequencies was significant in the pulse treatment group at 1 (P<.01), 2 (P<.05), and 4 weeks (P<.05) after the start of treatment. Visual function test results at 12 weeks and 1 year were essentially the same in the two treatment groups. Side effects appeared more frequently in the pulse treatment group than in the control (P<.05). CONCLUSIONS: Pulse treatment does not appear effective for idiopathic optic neuritis even though visual function in the pulse treatment group of this trial recovered more quickly during the initial phase compared to the controls. More effective and specific treatment should be established for optic neuritis.

Adolescent↗

PubMedDate not supplied

Presynaptic effects of botulinum toxin type A on the neuronally evoked response of albino and pigmented rabbit iris sphincter and dilator muscles.

PURPOSE: To investigate the effects of botulinum toxin type A (botulinum A toxin) on the autonomic and other nonadrenergic, noncholinergic nerve terminals. METHODS: The effects of botulinum A toxin on twitch contractions evoked by electrical field stimulation (EFS) were studied in isolated albino and pigmented rabbit iris sphincter and dilator muscles using the isometric tension recording method. RESULTS: Botulinum A toxin inhibited the fast cholinergic and slow substance P-ergic component of the contraction evoked by EFS in the rabbit iris sphincter muscle without affecting the response to carbachol and substance P. These inhibitory effects were more marked in the albino rabbit than in the pigmented rabbit. Botulinum A toxin (150 nmol/L) did not affect the twitch contraction evoked by EFS in the rabbit iris dilator muscle. CONCLUSIONS: These data indicated that botulinum A toxin may inhibit not only the acetylcholine release in the cholinergic nerve terminals, but also substance P release from the trigeminal nerve terminals of the rabbit iris sphincter muscle. However, the neurotoxin has little effect on the adrenergic nerve terminals of the rabbit iris dilator muscle. Furthermore, the botulinum A toxin binding to the pigment melanin appears to influence the response quantitatively in the two types of irides.

Albinism↗

PubMedDate not supplied

Flow cytometric and fluorescence microscopic analysis of ethanol-induced G2+M block: ethanol dose-dependently delays the progression of the M phase.

We found previously that short-term (3 and 6 h) exposure to ethanol (100 and 200 mM) induced the transient arrest of L929 cells at the G2+M phase. To identify the exact site blocked during the G2+M phase, we carried out flow cytometry and microscopic analysis with asynchronous L929 cells exposed to ethanol (12.5-330 mM) for 3, 6 or 24 h. Flow cytometry (the simultaneous analysis of cellular DNA and cyclin B1 content) revealed that the percentage of 4c (tetraploid) cells with a high level of cyclin B1 increased after continuous 6 h exposure to ethanol (> or =82.5 mM) and decreased after 24 h exposure, which supports the idea of a transient M-phase block. To determine the sub-M phase of 4c cells with high levels of cyclin B1 based on spindle microtubules and their karyotype, we viewed immunofluorescent images by double staining with Hoechst 33258 (bis-benzimide trihydrochloride) for DNA and with fluorescein isothiocyanate-labelled antibody for cyclin B1 or beta-tubulin. A 6 h exposure to intermediate concentrations (50-100 mM) of ethanol increased the number of early-anaphase cells, compared with the control, suggesting an inhibition of the elongation of polar microtubules. Both 6 and 24 h exposure to higher concentrations (100-200 mM) of ethanol increased metaphase cells, indicating an arrest at the spindle assembly checkpoint and suggesting an inhibition of the shortening of kinetochore microtubules and/or the degradation of cyclin B . Moreover, 6 h exposure to 330 mM ethanol increased round, probably early-prophase, cells, suggesting inhibition of the formation of spindle microtubules. Thus, it is likely that higher concentrations of ethanol affect the elongation, contraction, and formation of the spindle microtubules of L929 cells dose-dependently and also disrupt the correlation between microtubule organization and the synthesis and degradation of cyclin B1, thereby delaying the progress of karyokinesis, which may lead to an ethanol-induced G2+M block.

Cell Division↗