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Biomedical subjects

T M Walker

Publications and source records attributed to T M Walker.

45 records · Page 3Linked to original sources
PubMed1977

The value of urography following lymphography in malignant diseases.

The need for urography following ascending pedal lymphography in malignant disease has been studied in 298 consecutive patients. Forty per cent of the urograms were abnormal. Urographic abnormalities due to the disease being investigated were heralded by abnormal lymphography except in four patients, three with carcinoma of the bladder and one with carcinoma of the cervix. The majority of abnormalities unrelated to the disease being investigated were of no significance. In a small number there was congenital malposition of the kidney so that it fell within the proposed field of treatment. It is concluded that it is unnecessary to do routine urography with every lymphogram. Indications for urography are abnormality or suspected abnormality of the lymphogram, failure to locate the kidneys on plain films and clinical indications such as carcinoma of the bladder or carcinoma of the cervix.

Adolescent↗
PubMedDate not supplied

Tumor growth alters macrophage responsiveness to macrophage colony-stimulating factor during reactivity against allogeneic and syngeneic MHC class II molecules.

Tumor-induced changes in macrophage (M phi)2 accessory activities significantly suppress T-cell recognition of allogeneic and syngeneic major histocompatibility complex (MHC) class II molecules. Because these changes are often associated with altered responses to stimulatory and inhibitory cytokines, we investigated the possibility that tumor growth alters the contribution of a macrophage regulatory cytokine, macrophage colony-stimulating factor (M-CSF), during reactivity against allogeneic and syngeneic MHC class II molecules. T-cell reactivity against allogeneic MHC class II molecules was significantly suppressed by tumor-bearing host (TBH) M phi in the presence of M-CSF. M-CSF-induced suppression was independent of TBH M phi prostaglandin E2 (PGE2) synthesis. T-cell reactivity against syngeneic MHC class II molecules increased in the presence of M-CSF when normal host (NH) M phi served as the source of syngeneic molecules. However, T-cell reactivity against syngeneic MHC class II molecules in the presence of M-CSF did not change when TBH M phi served as stimulator/accessory cells. Although T-cell reactivity against NH syngeneic MHC class II molecules was additively increased by M-CSF and indomethacin (a PGE2 synthesis inhibitor) treatment, reactivity against TBH syngeneic MHC class II molecules increased solely through PGE2 synthesis inhibition. Admixtures of both NH and TBH M phi in the absence or presence of M-CSF suggest that tumor-induced suppression was not strictly due to decreased expression of MHC class II molecules. Collectively, these data suggest that TBH M phi are partly suppressive through altered responsiveness to M-CSF.

Animals↗