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G T Patterson

Publications and source records attributed to G T Patterson.

48 records · Page 3Linked to original sources
PubMed1982

Regulation of acetylcholinesterase forms in quail and chicken muscle cultures.

High molecular forms of acetylcholinesterase (AChE) have been difficult to obtain in primary cultures of muscle from mammals and birds. This research used pectoral muscle cultures from Japanese quail and chick embryos grown in medium containing embryo extract and horse serum to study the growth and extraction conditions necessary for study of high molecular weight 20S AChE forms found in these birds. The results confirmed the presence of a 20S AChE form in quail muscle cultures and showed that its extraction from the cells was considerably improved by using a Mg-cholate extraction buffer rather than the more commonly used NaCl-Triton X buffer. A striking finding was that removal of serum from the medium for 1-2 days caused the preferential increase in a 20S form in the quail and the resolution of one from background activity in chick muscle cultures. Removal of embryo extract had no effect on levels of the AChE forms. The results suggest that serum factors inhibit the formation of the high molecular weight, motor end plate associated form of AChE in aneural cultures of avian muscle, and that effects of factors such as neural extracts and nerves on AChE forms in cultured muscle should be examined using a defined basal media.

Acetylcholinesterase↗
PubMed1981

Osteomyelitis of a bone graft of the mandible with Acanthamoeba castellanii infection.

An ameloblastoma of the right side of the mandible was resected in a 32 year old prediabetic female. An iliac crest autograft became infected and a sequestrum was removed seven weeks later. Pathologic examination of this tissue demonstrated a mixed infection, including Acanthamoeba castellanii. This is the first recorded instance of invasion of bone by a free living ameba.

Adult↗
PubMed1977

Avian muscular dystrophy: functional and biochemical improvement with diphenylhydantoin.

Chicks affected with hereditary muscular dystrophy were injected twice daily with 20 milligrams of diphenylhydantoin per kilogram of body weight on days 1 to 40 after hatching. The righting ability of dystrophic chicks treated with diphenylhydantoin was improved compared to that of untreated dystrophic chicks, and acetylcholinesterase activity was reduced to normal levels in the posterior latissimus dorsi muscles.

Acetylcholinesterase↗
PubMed1976

Acetylcholinesterase in abnormal human muscle.

Fifty human muscle biopsies were examined for histochemical localization of acetylcholinesterase (AChE) activity. Six normal muscle samples had AChE at the myoneural junctions and around the periphery of many fibers. The AChE within the sarcoplasm itself was found in only a few atrophied fibers. However, 21 of 44 biopsies of abnormal muscles had sarcoplasmic AChE in more than 10% of their fibers. Such cases included Duchenne, limb-girdle and facio-scapulo-humeral dystrophy, neurogenic and spinal muscle atrophy, spinal cord injury, peripheral nerve injury, Schwartz-Jampel syndrome and myasthenic syndrome. Sarcoplasmic AChE is found in embryo muscle and usually declines after birth. It appears after denervation in the chicken but not the rat and remains in muscles of chickens with an inherited muscular dystrophy. The results of the human muscle study support the idea that in the human, as in the chicken, interruption of a neurally-mediated regulation of AChE results in the reappearance of high AChE activity in the sarcoplasm of the muscle fibers.

Acetylcholinesterase↗
PubMed1975

Incidence of acetylcholinesterase in the sarcoplasm of human and chicken muscles.

Fifty-nine biopsies of human muscle, 53 of them abnormal, 6 normal, were studied for the histochemical localization of acetylcholinesterase (AChE) using frozen sections and light microscopy. In addition to AChE which was found at the myoneural and myotendon junction, specific staining was found around the periphery of many fibers from normal and abnormal muscles. Moreover, AChE activity was found to be high in the sarcoplasm of more than 10% of the fibers from 28 biopsies of abnormal muscle including cases of hemiplegia, spinal cord injury, denervation and neuropathy, infantile spinal muscle atrophy, Duchenne, limb-girdle and facioscapulohumeral dystrophies, Schwartz-Jampel syndrome and a myasthenic syndrome. Of the muscles from experimental animals examined, only the Rhesus monkey exhibited AChE around the periphery of the fibers, and only the dystrophic chicken and not the dystrophic mouse or hamster, showed extensive sarcoplasmic AChE. Histograms of muscle fiber diameters indicated that AChE in the sarcoplasm was associated with fibers of all sizes, depending on the nature of the disorder examined. Fibers containing AChE were smaller than unstained fibers in dystrophic chicken muscle. The results suggest that in the human, sarcoplasmic AChE is reversibly repressed during muscle maturation and that its mode of regulation by motor neurons is similar to that found in the chicken.

Acetylcholinesterase↗