Transport for community nurses. 7. Small cars.
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Biomedical subjects
Publications and source records attributed to T Scott.
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Myelin fractionation and subsequent lipid isolation have been carried out on a brain from a patient who suffered from a cellular deficiency of the adenosylcobalamin and methylcobalamin co-enzyme forms of vitamin B12. Examination of the fatty acid composition of choline and ethanolamine glycerophospholipids indicated a relative enrichment of odd-chain fatty acids which were identified by gas-liquid chromatography-mass spectroscopy as C15, C15:1, C17 and C17:1. A mixture of methyl branched C17 fatty acids was also identified. Odd-chain fatty acids accounted for 9.8% of the total fatty acid in the myelin choline phospholipid conpared to control values of 1.2%. The affected brain myelin phospholipids had a lower unsaturated fatty acid content. Examination of the myelin sphingolipids, sphingomyelin, cerebroside and sulfatide, yielded abnormal fatty acid profiles. The sphingomyelin contained only small amounts of C24:1 fatty acid. Both normal and hydroxy fatty acid containing cerebroside and sulfatide had reduced levels of C24 fatty acid. Determination of the relative hydroxy and normal fatty acid content of the galactolipids indicated an abnormally high hydroxy fatty acid level. Abnormal fatty acid profiles of brain cerebral sphingolipids have not been previously described in cases of vitamin B12 deficiency. Whether or not these alterations are characteristic will only be established by estimating sphingolipids in other such cases.
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The results of neurochemical examination of brain tissue derived from 2 cases of adreno-leukodystrophy have been presented. Both white and grey matter contained suadanophilic material. Although free fatty acid was also present, cholesteryl ester accounted for the bulk of the sudanophilic material. Total cholesterol, galactolipid and phospholipid content was reduced in both white and grey matter. The lipid loss was particularly severe from white matter indicative of considerable demyelination. Cholesterol was found to be the only major sterol present in white or grey matter. Subcellular fractionation of the diseased white matter resulted in myelin and two related fractions, one of which was very fatty and was rich in steryl ester. Morphological examination of myelin indicated loosely-packed lamellae. All of 3 fractions had adenosine 2',6'-cyclic nucleotide-3'-phosphohydrolase activity. Myein and the fraction not rich in cholesteryl ester had discernable basic protein bands when examined by polyacrylamide gel electrophoresis. Analysis of the fatty acid composition of choline and ethanolamine glycerophospholipids indicated a general increase of saturated fatty acids, relative to control values and a decrease in long-chain fatty acids. Examination of sphingomyelin fatty acids also demonstrated a loss of long-chain fatty acids. The fatty acid composition of the cholesteryl esters from white and grey matter differed. The findings indicate generalized damage to the brain, both of white and grey matter, with the damage to the white matter being much more severe. No abnormal sterol or other lipid was isolated.
Neurochemical and neuropathological studies have been made of a 10-day-old child who suffered from a sudanophilic leukodystrophy. The brain white matter contained abundant sudanophilic material. The patient's grey matter total cholesterol content was 30% higher than whole brain tissue derived from a comparable control. White matter cholesterol content was more than double the control value. Nearly 80% of the white matter cholesterol was esterified. Subcellular fractionation of the white matter resulted in a "floating fraction" rich in cholesteryl ester. The steryl ester fatty acid composition was not typical of control tissue or demyelinating tissue. Patient phospholipid fatty acid composition patterns differed from control, but white matter galactolipid fatty acid composition appeared normal. Cholesteryl ester hydrolase activity appeared normal. Myelin and myelin-like fractions, isolated from diseased and normal brain tissue, were of a primitive developing nature but appeared to be comparable. The findings indicate a neonatal sudanophilic leukodystrophy which doubtless began in prenatal life and which was rich in cholesteryl ester. The aetiology of the leukodystrophy is unknown.
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A study of eighteen cases of primary lymphoreticular tumours in the brain is described. In four of these there were extraneural lesions and in one macroglobulinaema. The use of whole brain sections embedded in celloidin, and of metallic impregnation methods, revealed certain constant patterns of proliferation. The tumours were diffuse and multicentric; the leptomeninges and perivascular spaces especially in the subependymal regions were frequently involved. Mature microglia were active both in infiltrated and in apparently tumour-free regions.
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ECG changes have been recorded in 11 monkeys following experimental head injury. The principal changes include bradycardia, shortening of the Q-Tc interval, prolongation of the Q-T interval, and alterations of rhythm. The changes last from a few seconds to approximately 2 hours. It is concluded that the changes result from a massive autonomic out-flow from the injured brain and in occasional instances may result in death due to cardiac arrest.
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