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Biomedical subjects

R Harrison

Publications and source records attributed to R Harrison.

At least 217 records · Page 12Linked to original sources
PubMed1981

Dehydrogenation by gluconate 6-phosphate dehydrogenase of an isosteric phosphonate substrate analogue.

6,7-Dideoxy-D-gluco-heptonic-7-phosphonic acid, the isosteric phosphonate analogue of gluconate 6-phosphate, was prepared by incubation of the corresponding analogue of glucose 6-phosphate with glucose 6-phosphate dehydrogenase and NADP+ in the presence of an enzyme NADPH-NADP+ recycling system. The analogue of gluconate 6-phosphate is a substrate for yeast gluconate 6-phosphate dehydrogenase, showing Michaelis-Menten kinetics at pH 7.5 and 8.0. At both pH values the Km values are approx. 3-fold higher and the Vmax. values approx. 7-fold lower than those of the natural substrate.

Gluconates↗
PubMed1981

The isolation and characterisation of the nicotinic acetylcholine receptor from human skeletal muscle.

Nicotinic acetylcholine receptor protein has been purified from human skeletal muscle by a procedure involving extraction in non-ionic detergent followed by affinity purification on immobilised alpha-toxin. Purified receptor preparations had specific activities of 0.5-3.5 mumol alpha-bungarotoxin binding sites/g protein and sedimented as a single 125I-alpha-bungarotoxin-binding species in sucrose-density-gradient centrifugation with s20,w = 9.5 S. The purified protein focussed as a single sharp band at pH 5.1 when complexed to 125I-alpha-bungarotoxin. Polyacrylamide gel electrophoresis of the purified receptor under denaturing conditions showed two major protein bands with Mr 42 000 and 66 000 respectively with the occasional appearance of minor components of Mr 56 000 and 85 000. Only the 42 000-Mr band was labelled with the affinity reagent, 4-(N-maleimido)[3H]-benzyltrimethylammonium. The purified receptor bound 125I-alpha-bungarotoxin and d-tubocurarine with Kd values of 0.5 nM and 0.25 microM respectively. It behaved similarly to unpurified detergent-extracted human receptor in the radioimmunoassay for anti-(human acetylcholine receptor) antibodies and when injected into rabbits caused increased levels of the latter antibodies but did not cause experimental autoimmune myasthenia gravis.

Animals↗
PubMed1981

An assessment of radioimmunoassay procedures for determination of anti-acetylcholine receptor antibodies in the sera of patients with myasthenia gravis.

A reproducible radioimmunoassay procedure for the determination of anti-acetylcholine receptor antibodies in the sera of patients with myasthenia gravis is described and examined in detail. The assay combines features of a number of methods previously outlined and allows repeat determinations of antibody titre in a given myasthenic serum sample with coefficient of variation 6%. The mean +/- standard deviation for normal human serum anti-acetylcholine receptor antibodies was found by this procedure to be 0.024 +/- 0.033 nmol/l alpha-bungarotoxin binding sites whereas the range for myasthenic patients was 0-139.14 nmol/l with a mean value of 7.55 nmol/l alpha-bungarotoxin binding sites.

Acetylcholine↗
PubMed1981

A roentgenographic technique to evaluate and document hindfoot position.

The position of the posterior portion of the foot is difficult to evaluate and document on the basis of clinical examination. Conventional roentgenographic techniques also do not allow objective determination of hindfoot position. A new roentgenographic technique utilizing a double-exposure has been developed to allow accurate documentation of the position of the calcaneus relative to the ankle. Normal adult values for this technique have been determined from 60 normal feet.

Ankle↗
PubMed1980

Factors affecting the acquisition of resistance against Schistosoma mansoni in the mouse. The effect of varying the route and the number of primary infections, and the correlation between the size of the primary infection and the degree of resistance that is acquired.

Mice given primary infections of Schistosoma mansoni by percutaneous or subcutaneous routes were found to acquire a higher degree of resistance against homologous challenge after 7--8 weeks than mice infected intraperitoneally. Mice infected by the intraperitoneal route tended to have smaller worm burdens than those infected with the same number of cercariae by the other two routes and this may, in part, have contributed to the relative lack of efficacy of intraperitoneal infections in inducing resistance to re-infection. The same degree of resistance was acquired after primary percutaneous infection irrespective of whether it was administered in 3 equivalent weekly doses, or the same total number of cercariae was administered as a single infection. The same degree of resistance was also observed when a percutaneous challenge was administered on the same or a different skin site to that which received the percutaneous primary infection. The degree of resistance to re-infection acquired after a percutaneous primary infection correlated well with the size of the primary worm burden and the number of eggs in the intestine and liver, but did not correlate with the number of eggs in the lungs.

Animals↗
PubMed1980

Interrelationship of concanavalin-A-binding and antigenic sites on the acetylcholine receptor from Torpedo marmorata.

A preparation of purified 125I-labelled acetylcholine receptor was shown to bind to concanavalin A and to be totally bound by rabbit antiserum to Torpedo acetylcholine receptor. Pre-incubation of the receptor with F(ab')2 and Fab fragments from antibodies against Torpedo acetylcholine receptor, or with corresponding fragments from control immunoglobulin G showed that subsequent binding of the receptor to concanavalin A was specifically inhibited to a maximum of approximately 25% by the immune fragments. Treatment of acetylcholine receptor with periodate or with glycosidases apparently destroyed or removed carbohydrate residues without affecting the antigenicity of the receptor as assessed by radioimmunoassay. These results suggest that although there is a steric interrelatonship between the antigenic and concanavalin-A-binding sites of the receptor the latter sites do not contain its major antigenic determinants.

Acetylcholine↗
PubMed1980

Patient-specific anti=acetylcholine receptor antibody patterns in myasthenia gravis.

Anti-acetylcholine receptor (AChR) antibodies have been determined in the sera of ten myasthenic patients over a period of several months which in each case included a series of plasma-exchanges coupled with immunosuppressive therapy. The ratio of anti-(extra-junctional rat AChR): anti-(human AChR) antibody titres was found to vary with the patient but to be constant for a given patient over the period of study. Similar indications of a patient-specific anti-AChR antibody pattern were obtained by using junctional as well as extra-junctional rat AChR and also by precipitation of human AChR in the presence of excess antiserum. Individual anti-AChR antibody patterns may have relevance to the varying courses taken by myasthenia gravis in different patients.

Acetylcholine↗
PubMed1980

Anti-acetylcholine receptor antibody titres in the sera of myasthenia patients treated with plasma exchange combined with immunosuppressive therapy.

Anti-acetylcholine receptor antibody titres have been monitored in the sera of 19 myasthenic patients treated with plasma exchange combined with a three month period of immunosuppressive therapy. In general the post-exchange titres stabilised at below pre-exchange levels for prolonged periods which were associated with clinical improvement. In seven instances recurrence of symptoms occurred and in six of these cases relapse was shown to be associated with a rise in anti-acetylcholine receptor antibody titre.

Acetylcholine↗