Estimation of hydroxyproline in urine.
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Biomedical subjects
Publications and source records attributed to C A Pennock.
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Three turbidometric methods and one method using ultraviolet spectrophotometry for estimating total cerebrospinal fluid protein have been examined. The necessity for preliminary dialysis renders the ultraviolet method unsuitable for routine use. The turbidometric method of Meulemans (1960) using a sulphosalicylic acid-sodium sulphate precipitating fluid is better than a method using sulphosalicylic acid alone which is affected by the albumin-globulin ratio, and has a greater sensitivity and better reproducibility than a method using trichloracetic acid as a precipitant. Turbidity may be measured with a spectrophotometer or an MRC grey wedge photometer with human or bovine albumin as a standard. This method deserves wider acceptance.
Sections of liver and spleen from six cases of secondary amyloidosis have been examined, by various improved histochemical methods, for acidic mucosubstances. The results indicate a complex in amyloid deposits of protein and sulphated mucopolysaccharides in which the principal substance is heparan sulphate with traces of chondroitin sulphates. Deposits also contain sialic acid. The results are compared with chemical analyses of the same tissues and isolated fibrils which confirm the presence of heparan sulphate, chondroitin sulphates, and a sialic acid containing protein.
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The effect of varying concentrations of ethylene-diamine-tetra-acetic acid (E.D.T.A.) (dipotassium salt) and heparin on the estimation of packed cell volume has been studied using a microhaematocrit method. Varying concentrations of E.D.T.A. can produce serious errors in estimation of packed cell volume (P.C.V.) and reliable results are only obtained within the range of 1 to 2 mg./ml. Heparin is a more suitable anticoagulant for this investigation as varying the concentration has little effect. Storage with either anticoagulant at suitable concentrations for 24 hours at room temperature has little influence on the results.
This paper describes the clinical, morphological and biochemical features of three cats with a progressive neurological disorder. Clinical features were ataxia and progressive tremor. The morphological characteristics were those of lysosomal storage disease affecting neurones of the central nervous system and autonomic ganglia; membranous cytoplasmic bodies were demonstrated by electron microscopy in cerebral neurones. Chemical analysis of brain from two of the cats revealed an increased content of total gangliosides, sialic acid and a specific increase in GMI ganglioside. Enzyme analysis of homogenates of leucocytes, spleen and brain showed less than 5% or normal 4-methylumbelliferyl-beta galactosidase (4MU-beta gal) activity. In liver, activity was markedly reduced at pH values below 4.2, but there was considerable activity above this value. The properties of 4MU-beta gal in normal and diseased feline livers were investigated. Sephadex gel filtration of diseased liver homogenates showed an absence of two thermolabile "acid' components, and reduced activity of a third thermostable "neutral' component. The biochemical abnormalities found in the diseased cats are similar to those found in human juvenile GMI gangliosidosis (type 2).