Biomedical subjects
R Woodbury
Publications and source records attributed to R Woodbury.
The hairless mouse model for assaying the atrophogenicity of topical corticosteroids.
The daily application of corticosteroids for 18 days to the dorsal skin of hairless mice resulted in loss of volume of all the cutaneous compartments. The epidermis thinned, sebaceous glands regressed, dermal thickness was reduced, horn-filled cysts shrunk, subcutaneous fat disappeared, and regression of the muscular layer occurred. The magnitude of these changes correlated strongly with the accepted potency ranking of these agents by clinical efficacy. Thus, atrophogenicity predicts anti-inflammatory activity. This model furnishes a simple screening method for assaying corticosteroid activity and for optimizing proprietary formulations.
An overview and critical analysis of breast cancer screening.
From October 1973 through September 1979, 10,000 women were screened for breast cancer as part of a national project. In this follow-up analysis, we evaluate the current status of 166 women whose tumors were detected by this screening project (women with bilateral malignant neoplasms have been excluded). Mammogram abnormalities only were present in 55 women and abnormal physical findings with or without an abnormal mammogram were present in 111 women. Overall, 75% of patients were diagnosed with stage I (n = 86) or stage II (n = 39) disease. Median follow-up was 117 months. Only eight women (14.5%) whose tumors were detected by mammogram have suffered a relapse. Recurrences have developed in 27 women (24.3%) in the group with abnormal physical findings with or without an abnormal mammogram. Disease-free and relative survival at ten years' follow-up are 79.6% and 83.7%, respectively, for the 166 women whose cancer was detected by mammography only and by physical examination with or without an abnormal mammogram. Further follow-up will be required to determine the impact of screening detection on the natural history of breast cancer.
Isolation and expression of cDNAs encoding human factor VII.
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Stimulation of mucosal mast cell growth in normal and nude rat bone marrow cultures.
Mast cells with the morphological and biochemical properties of mucosal mast cells (MMC) appear and proliferate to form the predominant cell type in rat bone marrow cultures stimulated with factors from antigen- or mitogen-activated lymphocytes. Conditioned media causing a selective proliferation of MMC were derived from mesenteric lymph node cells of Nippostrongylus brasiliensis-infected rats restimulated in vitro with specific antigen or from normal or infected rat mesenteric lymph node cells stimulated with concanavalin A. MMC growth factor is not produced by T-cell-depleted mesenteric lymph node cells or by the mesenteric lymph node cells of athymic rats. By contrast, MMC precursors are present in the bone marrow of athymic rats and are normally receptive to the growth factor produced by the lymphocytes of thymus-intact rats. The thymus dependence of MMC hyperplasia is thus based on the requirement of a thymus-independent precursor for a T-cell-derived growth promoter.
Generation of mucosal mast cells is stimulated in vitro by factors derived from T cells of helminth-infected rats.
The connective tissue of rats, and several other species of mammals, contains two distinct types of mast cells that differ in morphology, histochemical staining properties and location1. One type, frequently called the normal connective tissue mast cell, can be obtained in nearly homogeneous preparation from a mixed cell population in the peritoneal cavity and forms the basis of our knowledge of mast cells. The other type is referred to as the mucosal mast cell because in normal rats it has been observed only in mucosal tissue. Infection with helminth parasites induces an exteNsive accumulation of mast cells and eosinophils in the tissues, and parasites of mucous surfaces, in particular, stimulate a rapid hyperplasia of mucosal mast cells. However, the origin of mucosal mast cells, and their relationship to the connective tissue mast cells is uncertain. We now slow that lymphocytes of helminth-infected rats, on in vitro stimulation with specific antigen, release factors causing pronounced mucosal mastocytosis in normal rat bone marrow cultures.
Delinquents' attitudes toward the juvenile justice system.
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Expression of active human factor IX in transfected cells.
Factor IX is the precursor of a serine protease that functions in the intrinsic blood clotting pathway. Deficiencies in this plasma glycoprotein result in haemophilia B (or Christmas disease) and occur in about 1 in 30,000 males. Patients are currently treated with fresh frozen plasma or prothrombin complex concentrates prepared from pooled plasma from normal individuals. There are several problems with this method of treatment, including the probable exposure of the patients to contaminants such as the viral agents responsible for hepatitis and AIDS (acquired immune deficiency syndrome). As a first step towards an alternative source of pure human factor IX, we report here on the use of recombinant DNA techniques to produce biologically active factor IX in cultured mammalian cells. Stable cell lines were produced by cotransfecting a baby hamster kidney (BHK) cell line with a plasmid containing a gene for factor IX and a plasmid containing a selectable marker. Protein secreted by these cell lines reduces the clotting time of plasma from factor IX-deficient patients. We present additional evidence that this protein is authentic human factor IX.