Extrachromosomal bovine papillomavirus type 1 DNA in hamster fibromas and fibrosarcomas.
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Biomedical subjects
Publications and source records attributed to C Thomas.
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The aggregation of human platelets is enhanced after preincubations with lithium salts. Previously it was shown that lithium inhibits adenylate cyclase activity in human platelets. Enhancement of aggregation and inhibition of adenylate cyclase by lithium was not observed in rabbit platelets. In this paper it is shown that in human platelets lithium enhances considerably the synthesis of thromboxane B2, whereas the synthesis of PGE2 and PGF2 alpha was enhanced to a lesser extent. In rabbit platelets lithium had no effect on prostaglandin synthesis. It is concluded that lithium specifically stimulates the synthesis of thromboxanes in human platelets, probably due to the previously reported inhibition of adenylate cyclase activity, resulting in an increased aggregability.
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Using a panel of monoclonal antibodies and rabbit heteroantisera, we have studied the cell surface markers of peripheral blood (PB) Sezary cells from six patients with mycosis fungoides or Sezary syndrome, disease grouped within the spectrum of cutaneous T cell lymphomas (CTCL). Furthermore, we have studied two cell lines (Hut 78 and Hut 102) derived from malignant Sezary T cells from CTCL patients. The monoclonal antibody 3A1 defines a major human PB T cell subset (85% of PB T cells) while the antigen defined by the monoclonal antibody 4F2 is present on a subset (70%) of activated PB T cells and on circulating PB monocytes. In contrast to normal subjects in whom 60-70% of circulating PB mononuclear cells were 3A1(+) T cells, PB mononuclear cells from six CTCL patients studied had an average of only 10.6+/-3.2% 3A1(+) T cells. Whereas 85% of E-rosette positive cells from normal individuals were 3A1(+), virtually all E-rosette positive T cells from the Sezary patients were 3A1(-). Two patients with high numbers of circulating Sezary T cells had both aneuploid and diploid PB T cell populations present; after separation of PB T cells into 3A1(+) and 3A1(-) cell suspensions, all 3A1(-) cells were found to be aneuploid. In contrast to normal resting PB T cells which were 4F2(-), all PB Sezary cells were 4F2(+), suggesting a state of activation. The 3A1 antigen was on a variety of acute lymphoblastic leukemia T cell lines (HSB-2, RPMI-8402, MOLT4, CEM) but was absent on the Hut 78 and Hut 102 Sezary T cell lines. Using rabbit anti-human T and anti-human Ia (p23, 30) antisera, we found that all malignant Sezary PB cells tested were killed by anti-T cell antiserum plus complement but not by anti-Ia plus complement. In contrast, Sezary cell lines Hut 78 and 102, were killed by both anti-T cell antiserum and anti-Ia plus complement. Similar to 3A1(-) normal PB T cells, 3A1(-) Sezary PB T cells proliferated poorly to phytohemagglutinin and concanavalin A. However, 3A1(-) Sezary T cells were able to provide T cell help towards pokeweed mitogen-induced in vitro B cell immunoglobulin synthesis, an immunoregulatory function limited to 3A1(+) T cells in normal subjects.Thus, the 3A1 antigen is present on 85% of normal PB T cells, and on most T-acute lymphoblastic leukemia lines tested; in contrast the 3A1 antigen is not present on the majority of circulating malignant Sezary PB T cells nor on T cell lines derived from malignant Sezary T cells. The lack of expression of the 3A1 antigen may be associated with malignant transformation of T cells in CTCL and may be an important marker for tracing the clonal origin of the malignant Sezary T cell.
According to the WHO (1964) about 80% of human malignant tumours are supposed to be the result of an exogenous effect. Beside the exposition also an inherited or acquired disposition (genetical defect or basic condition with increased regenerative hyperplasia) as well as the age may play a role in the promotion of cancerogenesis. The significance of the advanced age is expressed in the cumulative effect of different exogenous cancerogens with the scope of syncancerogenesis.
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A controlled trial was conducted to determine whether counselling by a specialist nurse prevented the psychiatric morbidity associated with mastectomy and breast cancer. Seventy-five patients were counselled by the nurse and monitored during follow-up, while 77 patients received only the care normally given by the surgical unit. Counselling failed to prevent morbidity, but the nurse's regular monitoring of the women's progress led her to recognise and refer 76% of those who needed psychiatric help. Only 15% of the control group whose condition warranted help were recognised and referred. Consequently, 12 to 18 months after mastectomy there was much less psychiatric morbidity in the counselled group (12%) than in the control group (39%). These findings highlight the high degree of psychiatric morbidity in patients who have undergone mastectomy and indicate the need to find ways of reducing this morbidity.
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A simple quantitative test is described for measuring the duration of post-traumatic amnesia. It was used in a study of 336 patients with closed head injury; and the results matched closely the independent estimates of experienced neurosurgeons. A systematic procedure of this kind is clinically useful in its sensitivity to fluctuations or deterioration in the patient's mental state. It could also be used with advantage in multi-centre research by providing a standard criterion for the assessment of post-traumatic amnesia.
A monospecific antibody to purified human skin chemotactic proteinase was raised in rabbits and shown to produce a single line of identity against crude and purified human proteinase. The antibody was used to localize the proteinase in human fibroblasts, polymorphonuclear leukocytes, lymphocytes, and sections of whole skin. All cells demonstrated particulate extranuclear staining. Whole human skin demonstrated staining of the epidermis, especially in the granular layer; particulate staining was also found in the dermis. Staining could be blocked by preincubation of the rabbit anti-human neutral proteinase with purified proteinase antigen. These data indicate that neutral proteinase is located in a number of different human cells in a particulate distribution.