Oregon Health & Science University
Publishes on Amyloidosis: Diagnosis, Treatment, Outcomes, Alzheimer's disease research and treatments, Rheumatoid Arthritis Research and Therapies. 112 papers and 4.8k citations.
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A simple and reproducible histochemical method for distinguishing different chemical types of amyloid is described. The method is based on the affinity of amyloid for Congo red dye after exposure to potassium permangenate and dilute sulfuric acid. The permanganate method represents a modification of the Romhanyi trypsin technique. It yields comparable results while obviating some of the technical difficulties associated with the latter method. The permanganate reaction was applied to a series of amyloid samples of known amino acid composition, to amyloid samples fixed in a variety of different preservatives, and to tissues obtained at autopsy from 67 amyloidosis patients whose disease had been previously subclassified on the basis of clinical presentation and autopsy observations. This method distinguished amyloid protein AA from other varieties of amyloid and proved effective when applied to amyloid samples preserved in any of several commonly used fixatives. This simple histochemical method proved useful in subclassifying amyloid type in the patient series particularly when used in conjunction with the available clinical history and the organ distribution of amyloid accumulation.
The enzyme tyrosinase, which catalyzes the aerobic oxidation of tyrosine to produce the pigment melanin, is found widely distributed in nature.Much has been reported (1, 2) on tyrosinase obtained from plant, insect, and marine animal sources, but relatively little is known concerning mammalian tyrosinase.Some years ago, Bloch and his coworkers proposed, on the basis of histochemical evidence, that melanin formation in mammalian skin was attributable to the presence of a specific enzyme whose substrate was not tyrosine but dihydroxyphenyl-n-alanine (dopa) (3).This enzyme was given the name "dopa oxidase."Largely as the result of this work, which has been amply confirmed, the concept has arisen that the primary amino acid precursor of mammalian melanin is not tyrosine but dopa, and there has even been some question as to the actual existence of a mammalian tyrosinase, although it is generally agreed that the enzyme from other sources is a true tyrosinase.In 1903 Gessard (4) found that extracts from a horse melanoma were able to catalyze the conversion of tyrosine to melanin.This was confirmed by de Coulon in 1920 (5).In 1907 Alsberg (6) prepared an extract from a human melanoma which could catalyze the formation of black pigment from catechol and possibly from tyrosine.In the following year Neuberg (7) showed that dilute extracts from a human melanoma accelerated pigment formation from tyramine and adrenalin but not from tyrosine.Recently Hogeboom and Adams (8) demonstrated that extracts from the Harding-Passey mouse melanoma possess both tyrosinase and dopa oxidase activity.They reported the separation of these two activities by ammonium sulfate precipitation.Similar results were reported by Green-
Muscle function and functional performance are limited in patients with osteoarthritis (OA). Although aerobic exercise can increase aerobic power and reduce fatigue, it does not appear to improve muscle function. The purpose of this study was to demonstrate the effect of a muscle rehabilitation program on muscle strength, endurance, speed, and function for patients with OA of the knees. Fifteen men (67.6 +/- 6.1 years) with OA of the knees underwent a four-month exercise program, three times per week. Muscle strength, endurance, and speed were 50% less in OA patients than in controls. After rehabilitation, there was a significant increase in strength (35%), endurance (35%), and speed (50%). Deficiencies and improvements in the muscles were greater at longer muscle lengths. Increases in muscle function were associated with decreased dependency (10%), difficulty (30%), and pain (40%). The average increase in all measured parameters was 10% and 25% after two and four months of rehabilitation, respectively. Improvements were sustained for eight months after rehabilitation. The muscle rehabilitation program was designed specifically to improve function; the improved muscle function was translated into improved functional performance.