50ppm MnBK subclinical neuropathy in rats.
40 rats were subjected daily for 6 months to an atmosphere containing 50ppm MnBK. 32 of the rats presented with demyelination of the sciatic nerve and 2 of these with axonal hypertrophy.
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Publications and source records attributed to S Duckett.
40 rats were subjected daily for 6 months to an atmosphere containing 50ppm MnBK. 32 of the rats presented with demyelination of the sciatic nerve and 2 of these with axonal hypertrophy.
Elemental tellurium (TE) was included in the normal diet of 15-day-old rats and every day thereafter for 35 days. Within 24 hours a segmental demyelination was seen in the sciatic nerve. On the 2nd day, Te was localized in the cytoplasm of the Schwann cells. On the 3rd day paralysis of the hind legs appeared which lasted 7--10 days. The papralysis then disappeared and demyelination ceased, although the rats were still ingesting Te. After one week there was also slight demyelination in the brachial plexus. Motor nerve conduction velocities were reduced below the normal control range, but only after the rats had taken Te for a least 7 days. This peripheral neuropathy can only be induced in the rat by Te ingestion between the 15th and 35th days of post-natal life, not before or after this period of time.
Preliminary electron microprobe studies of a small number of meningiomas, oligodendrogliomas, glioblastoma multiformae, craniopharyngiomas, and metastatic epithelioma of the breast suggest that the elemental composition of the deposits associated with these tumors is characteristic for each type of tumor.
The omentum of 13 rats were removed from the abdomen and placed directly on the brain. 5-14 days later the omentum and the underlying brain were joined by numerous vascular anastomoses in 9 rats. The purpose of this work was to study the use of omentum to establish extracranial vascularization of the brain.
SPD calcifications from four cases of Fahr's disease were studied with an electron microprobe of Castaing, and found to contain different elements, among them Zn, Al, Mg. The presence of the elements is underlined not because of presumption as to their importance on the pathogenesis of this disease, but because of their rare identification in cerebral calcifications. A1 and Mg have been localized previously in cerebral calcification, but this is the first report of morphological localization of a high concentration of zinc in the brain. Two of these cases had hypoparathyroidism.
The localization of calcium (Ca) and phosphorus (P) by scanning with the electron microprobe of Casting, provides a morphological outline of the normal nerve which can be used qualitatively and quantitatively for comparison with abnormal nerves. The normal saphenous nerves of eight cadavers and the abnormal saphenous nerves of two cases of diabetic neuropathy, were scanned and the results compared.
Vascular siderosis (VS) refers to the presence of mineralized small and medium-sized arteries in the globus pallidus, usually regarded as reflecting an aging process. The electron probe analysis of deposits in vascular siderosis in 10 patients dying of parkinsonism and in 8 other patients without parkinsonism is reported here. The microprobes identified a total of 11 elements in the VS in these 18 patients. Five elements--lead, aluminum, sulfur, manganese, and barium--were present only in VS associated with parkinsonism. Statistically, the association of lead was highly significant while that of aluminum and sulfur in 4. The significance of the presence of sulfur is difficult to assess since its compounds are normally present in large quantities in the brain. These findings raise the question whether lead and aluminum may be associated in some way with the pathogenesis of certain forms of Parkinson disease.
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Electron probe microanalysis demonstrates the presence of aluminium, magnesium, iron, calcium, phosphorus in and around blood vessels in the pallidum (vascular siderosis) and in the putaminal parenchyma in five out of six cases of striatonigral degeneration, associated with orthostatic hypotension in two of these cases. These results suggest that striatonigral degeneration could be the result of a vascular disease, the result of an elemental intoxication of unknown cause.
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Three groups of dogs underwent total occlusion of the right middle cerebral artery close to its junction with the internal carotid artery. Dogs that had omentum placed on the brain prior to occlusion of the middle cerebral arterial withstood this deprivation of normal cerebral blood flow in a statistically significant manner when compared with dogs that had no omental protection or had omental placement on the brain simultaneous with middle cerebral artery occlusion. These results raise the possibility that use of the intact omentum might be another technic for revascularization of the brain in patients with transient cerebral ischemic attacks or brain dysfunctions secondary to diminished cerebral blood flow who presently are not candidates for routine surgical procedures for cerebral revascularization.
A 2 year old girl develops a fever, anorexia and a cough which last three weeks. Following this event, she presented with intention tremor and increasing difficulty with crawling. At the age of 3, a nerve biopsy was done which made the diagnosis of metachromatic leukodystrophy. EM examination of the nerve biopsy revealed large quantitites of abnormal structures in the cytoplasm of Schwann and phagocytic cells. Virus like spheroid bodies were present in a few axons and cytoplasm of Schwann cells.
A man presented at 27 years of age, the first signs of a progressive neurological and mental deterioration which eventually lead to his death at 37, from an intercurrent pulmonary infection. He was a severe alcoholic. The pathological examination of the brain revealed patchy demyelination and deposits of crystalline material, resembling so called calcifications. The biophysical examination showed the presence in the brain and other organs, of aluminum and phosphorus in all deposits, sometimes associated with iron, sulfur and calcium. Nothing in his past history suggests any contact with aluminum. Presumably this is a case of "generalized aluminosis", with the main clinical and pathological features manifesting in the central nervous system.
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