Effect of multiple sclerosis materials on polymorphonuclear neutrophils of miceMackay, I. R.; Godycki, L.; Tourtelotte, W. W.
doi: 10.1111/j.1600-0404.1980.tb02990.xpmid: 7395453
An assessment was made of a bioassay for a multiple sclerosis (MS)‐associated agent claimed to cause a depression in the proportion of circulating polymorphonuclear neutrophils (PMN) in mice. Serum (1 sample), supernate from brain homogenates (four samples) and cerebrospinal fluid (four samples), and corresponding control materials, were tested under code by intraperitoneal injection into BALB/c mice. Results were plotted of proportions and absolute numbers of PMN over observation periods up to 2 weeks. Handling, injection and bleeding of mice did not significantly influence “baseline”counts of PMN. However, all samples from MS patients and controls caused an initial increase in PMN over 1–4 days, and then a later fall towards baseline. The claimed effect of MS materials in depressing counts of PMN in mice was not observed in these experiments, and variations in counts of PMN did not discriminate between samples from MS patients and controls.
Optic atrophy in experimental vitamin B 12 deficiency in monkeysChester, Edward M.; Agamanolis, Dimitris P.; Harris, John W.; Victor, Maurice; Hines, John D.; Kark, John A.
doi: 10.1111/j.1600-0404.1980.tb02991.xpmid: 6771960
The clinical findings and pathological changes of the visual pathway of vitamin B12 deficient monkeys have been described. The cellular morphology and counts of the peripheral blood and bone marrow remained normal during the study (nine deficient, three controls: one still alive in each group). Visual impairment was noted in all seven of the deficient animals that were evaluated by clinical observations. Ophthalmoscopic examination disclosed optic atrophy in six of the seven deficient monkeys. Degeneration of the visual pathway was demonstrated by pathological examination in eight of the deficient group of nine (one is still alive). Loss of ganglion cells was noted in the maculae of two of three deficient animals with completed studies. In the three control animals there were neither visual disturbances nor ophthalmoscopic changes and in two animals autopsies disclosed no lesions in the visual pathways. The third animal is still alive and well.
Uptake of 5‐HT by blood platelets of patients with myoclonus epilepsyTukiainen, Erkki; Leino, Eeva
doi: 10.1111/j.1600-0404.1980.tb02992.xpmid: 6771959
5‐HT uptake by blood platelets was tested in patients with PME with no Lafora bodies. Blood platelets from patients with myoclonus epilepsy and those from healthy sex and age matched controls were incubated for 5 min with 0.1 μM 3H‐5‐HT in Krebs‐Henseleit buffer at 37°C. The radioactivity taken up by platelets was assayed by liquid scintillation counting. 5‐HT uptake in platelets from patients tended to be slightly higher (19 %, n = 18, P > 0.05). The kinetic pattern as revealed by the Lineweaver‐Burk plot, was very similar in the two groups. All patients were on antiepileptic drugs (sodium valproate, clonazepam and phenobarbital), but no evidence was found in vitro that these drugs would have any direct effect on the uptake.
Late onset spinal muscle atrophy ‐ a sex linked variant of Kugelberg‐WelanderPaulson, George W.; Liss, Leopold; Sweeney, Patrick J.
doi: 10.1111/j.1600-0404.1980.tb02995.xpmid: 7395454
A syndrome of progressive muscular atrophy is reported in male members of a Caucasian family. Two affected members were examined in detail, one with post mortem. Fasciculations and atrophy of tongue as well as of the proximal limb muscles were observed, and there was profound weakness of the proximal muscles. The EMG and muscle biopsy were consistent with a neurogenic disease. The most pronounced lesion was in the lateral part of the anterior horn, with minimal involvement of the ventral portion of the anterior horns and sparing of the neurons of Clarke's column. Two earlier families with possible Kugelberg‐Welander syndrome have been reported in which a sex‐linked form also seems probable, and the varied inheritance pattern and uncertain pathological correlations suggest that the Kugelberg‐Welander and familial amyotrophic lateral sclerosis both represent heterogenous neurological disorders.