Treatment of acute nonlymphocytic leukemia in adults: response to 2,2-anhydro-1-B-D-arabinofuranosyl-5-fluorocytosine and thioguanine on the L-12 protocol

Fifty-one adult patients with acute nonlymphocytic leukemia (excluding acute promyelocytic leukemia) were treated on the L-12 protocol. The L-12 differed from the preceding L-6 in that 2,2-anhydro-1-B-D-arabinofuranosyl-5-fluorocytosine (AAFC), replaced arabinosylcytosine (ara-C) together with 6-thioguanine (TG) for remission induction. Achievement of remission was followed by an extended 14-week multi-drug consolidation program. With this more intense regimen, an overall complete remission rate of 49% and a median remission duration of 23.7 months were achieved; these results were not significantly better than the 57% complete remission rate and 8.6 months median remission duration obtained with the L-6 regimen. Four year disease-free survival was 22% on the L-12 compared with 16% on the L-6 protocol. No relationship between prognosis and FAB classification was found on either the L-6 or the L-12 protocol.     

Mycoplasma antibody in guillain-barré syndrome and other neurological disorders

Counterimmunoelectrophoresis (CIEP) was used to determine precipitating antibodies to Mycoplasma pneumoniae retrospectively in sera from 100 patients with Guillain-Barré syndrome (GBS), 125 medical and neurological controls, and 40 normal individuals. Sera from 7 patients produced precipitin lines. These positive cases included 5 patients with GBS, 1 with acute cerebellar ataxia, and 1 with acute disseminated encephalomyelitis. A complement-fixation test performed with the same antigen showed titers to M. pneumoniae of 1:512 or greater in these 7 sera. In contrast, sera from other patient controls and normal individuals were negative by CIEP and had only low mycoplasma complement-fixation antibody titers. No distinguishing clinical features separated the 5 seropositive GBS patients from the whole group except for their young age, which parallels that for human mycoplasma infection in general. Additional laboratory findings consistent with acute mycoplasma infection were demonstrated in 6 of the 7 seropositive patients.     

Fluorescence and electron microscopical observations on the amine-accumulating neurons of the cebus monkey retina

The organization of the Cebus monkey regina was analysed after the intraocular injection of 5,6-dihydroxytryptamine. This amine was taken up not only by the previously known dopaminergic neurons, but also by a set of indoleamine-accumulating neurons, whose processes are confined to the inner plexiform layer. The synaptic contacts of the dopaminergic neurons were analysed in the electron microscope after the processes of the indoleamine-accumulating neurons were destroyed by the intravitreal injection of the neurotoxic indoleamine, 5,7-dihydroxytryptamine. The subsequent injection of 5,6-dihydroxytryptamine induces certain changes in the dopaminergic neurons which accumulate the substance: electron-dense cores appear in the synaptic vesicles, and increased electron-density of mitochodrial and cellular membranes is often observed. The dopaminergic neurons were found to be presynaptic to amacrine cell perikarya and processes in the inner plexiform layer. In the outer plexiform layer they were presynaptic to both bipolar and horizontal cells, but they did not contact photoreceptors. The dopaminergic neurons received synapses only in the inner plexiform layer, from amacrine cell processes. It is inferred that in Cebus most dopaminergic neurons belong to a special class of retinal neuron, the interplexiform cells, which appear to transmit information centrifugally within the retina, from the inner to the outer plexiform layers. There are considerable similarities between the synaptology of the dopaminergic interplexiform neurons in the Cebus monkey and the goldfish retina, and the function of interplexiform neurons may therefore be similar in these two species.     

Acoustic neuroma causing subarachnoid haemorrhage.

The case reported in this paper appears to be the first example of spontaneous subarachnoid haemorrhage complicating an acoustic tumour. The only comparable case is one of a pontocerebellar angle tumour, but its histological nature is unstated. The excellent response to surgical management has been gratifying, and the patient has remained well over an extended period of surveillance.     

Localization of cyclic adenosine monophosphate in the teleost retina: effects of dopamine and prolonged darkness

Localization of cyclic adenosine monophosphate (cAMP) in the white perch retina was carried out with immunohistochemical and autoradiographic methods. Following exposure to dopamine or prolonged darkness, cAMP staining was observed by immunohistochemistry in the distal part of the inner nuclear layer, i.e. in the horizontal cells. After exposure to dopamine, increased levels of cAMP were also observed by autoradiography in many horizontal cells. Finally, increased levels of cAMP staining were observed immunohistochemically following incubation with dopamine in all types of cone-related horizontal cells that had been isolated and maintained in culture.     

Effects of d-aspartate on excitatory amino acid-induced release of [H]GABA from goldfish retina

The rate of release of [³H]GABA from isolated intact goldfish retinas was studied. Release of [³H]GABA is markedly stimulated by the inclusion in the incubation medium of the photoreceptor neurotransmitter candidates l-glutamate (l-Glu) and l-aspartate (l-Asp), and the glutamate analogs, kainate and quisqualate. At micromolar concentrations, kainate and quisqualate are effective releasers of [³H]GABA, whereas millimolar concentrations of l-Glu and l-Asp are required to release comparable amounts of [³H]GABA. The d-isomers of aspartate (d-Asp) and glutamate (d-Glu) are able to release [³H]GABA, but only when applied at high concentrations (3–30 mM). In the presence of 5 mM d-Asp, the effect of l-Glu in releasing [³H]GABA was markedly potentiated. This dose-response curve of l-Glu was shifted to the left in the presence of d-Asp, although the maximal amount of release was unchanged. d-Asp at 5 mM only slightly increased the GABA release induced by quisqualate, and it did not increase the GABA release induced by kainate. Finally, low concentrations of l-Asp were potentiated by d-Asp, but higher concentrations of l-Asp (3–10 mM) were clearly inhibited by this agent. This biphasic effect of d-Asp on l-Asp-induced release of [³H]GABA is a possible explanation for previously conflicting reports of d-Asp's effect on l-Asp action^2,8,29. Our data suggest that d-Asp has both pre- and postsynaptic sites of action.