G

Graeme B. Ryan

The Royal Melbourne Hospital

Publishes on Renal Diseases and Glomerulopathies, Birth, Development, and Health, Renin-Angiotensin System Studies. 44 papers and 3k citations.

44Publications
3kTotal Citations

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Top publicationsby citations

Human smooth muscle autoantibody. Its identification as antiactin antibody and a study of its binding to "nonmuscular" cells.
Cited by 258Open Access

When human serum containing smooth muscle autoantibodies (SMA) is incubated with extracts containing thrombosthenin (the contractile material of platelets) or thrombosthenin-A (the actin-like moiety of thrombosthenin), it loses its ability to bind to smooth muscle. Such binding is also diminished when SMA serum is incubated with lysed platelets; this effect is not seen if the SMA serum is incubated with intact platelets. The incubation of other autoantibodies (such as antimitochondrial or antinuclear antibodies) with thrombosthenin does not affect their binding to the specific antigens. It appears that SMA is directed against the actin fraction of thrombosthenin-ie, SMA is an antiactin antibody. Hence the name of antiactin autoantibody (AAA) seems more appropriate than smooth muscle autoantibody (SMA). A study of the distribution of antiactin autoantibody binding in rat, rabbit and man shows that several "nonmuscular" structures contain actin under normal conditions; these include megakaryocytes and platelets, normal rat hepatocytes, the brush borders of renal tubules, the periphery of epithelial cells of the intestine, polymorphs and lymphocytes in lymph nodes (but not thymic cortical lymphocytes). In addition, certain cell types (such as granulation tissue fibroblasts, cultivated fibroblasts, hepatocytes or regenerating liver and epidermal cells growing over a skin wound) can reversibly acquire a massive network of actin-containing microfilaments resembling those in smooth muscle.

Mesothelial injury and recovery.
Cited by 200Open Access

This paper describes the cytologic effects of drying or wetting of visceral peritoneum and the course of mesothelial regeneration. Using en face silver staining and electron microscopy, it was found that mesothelial cells disappeared from the surface after the cecum was either briefly dried or kept wet with isotonic saline for 30 minutes; the fibrin-slide technic showed that such injury caused a loss of the normal serosal fibrinolytic activity. In following the course of mesothelial regeneration using the same technics, it was apparent that free-floating peritoneal mononuclear cells settled on the denuded surface where they spread out, attached to one another, and developed features (eg, microvilli) typical of mature mesothelial cells; such new mesothelium showed a greatly enhanced fibrinolytic activity.