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At least 55 records · Page 3Linked to original sources
PubMed1978

Prostaglandin-mediated hyperemia and renin-mediated hypertension during acute ureteral obstruction.

Acute elevation of ureteral pressure to 100 mm Hg in anesthetized dogs (n=7) resulted in an increase (P less than 0.005) in systemic blood pressure form 151 +/- 7 to 163 +/- 7 mm Hg, a transient (approximately 15 min) increase (P less than 0.05) in renal blood flow from 413 +/- 27 to 465 +/- 27 ml/min and a rise (P less than 0.05) in plasma renin activity from 6.0 +/- 1.6 to 10.3 +/- 2.1 ng/ml/hr. Pretreatment with a competitive inhibitor of angiotensin II, i.e. sar1gly8AII, abolished the hypertensive response to acute ureteral obstruction, and pretreatment with 2 mg/kg of either indomethacin (n=6) or meclofenamate (n=3), 15 min before obstruction, prevented the hyperemic response. These results suggest that acute ureteral obstruction leads to hypertension via activation of the renin-angiotensin system and hyperemia via a prostaglandin-initiated mechanism.

Acute Disease↗
PubMed1976

Cell-mediated immunity to herpes simplex virus in man. V. Antibody-mediated cell-dependent immune lysis of herpes virus-infected target cells.

Thirty-four patients, subject to recurrent herpes labialis, have been studied. They have all been shown to have high serum levels of an antibody to HSV1. This antibody has the property of sensitizing HSV1-infected target cells to lysis by nonimmune effector lymphocytes. Of 23 subjects who gave no history of herpes labialis, only four had antibody demonstrable by this technique. The level of antibody remains essentially unchanged despite recrudescenes of herpes labialis in the susceptible subjects. Effector cell activity was present in all of these and other subjects tested except for two who were suffering from chronic lymphatic leukemia. We have positive evidence that the effector cells in this system are neither T cells nor macrophages. Additional evidence suggests that the effector cells may be "null" cells.

Antibody Specificity↗
PubMed1979

Ionophore-mediated cation translocation in artificial systems. I. A23187-mediated calcium translocation.

The inophore A23187 stimulates the translocation of calcium from an aqueous Hepes buffer into an organic immiscible phase. At saturating calcium concentrations, 2 molecules of ionophore seem to complex each atom of calcium. Consistent with such a stoichiometric behaviour, the apparent ratio of calcium-ionophore association to dissociation rate constants increases as the concentration of ionophore is raised. As a result, at low calcium concentrations, the amount of translocated calcium increases as a power function of A23187 concentration. When allowance is made for such a phenomenon, the relation between calcium translocation and concentration is characterized by usual substrate-receptor binding kinetics.

Anti-Bacterial Agents↗
PubMed1978

Cell-mediated responses in dogs with spontaneous neoplasms. I. Detection of cell-mediated cytotoxicity by the chromium-51 release assay.

A series of 43 dogs with spontaneous melanomas, sarcomas, or mammary carcinomas were tested for peripheral blood lymphocytotoxicity against a range of allogeneic tumor cells in vitro on one or more occasions during therapy. All tumor-bearer groups contained a proportion of dogs showing a significant 51Cr release with increasing effector-to-target cell ratios. However, cytotoxicity was not restricted for target cells of the same histologic type as that of the effector cell donor. Some unrelated target cells more sensitive to nonspecific effects showed a greater cytotoxicity in some instances. Control effector cells from healthy dogs were nonspecifically cytotoxic for a range of tumor target cells in a similar proportion of instances. Short-term cultures of autochthonous tumor target cells were resistant to lysis in the 51Cr release assay. The findings did not provide evidence for the existence of specific tumor antigens operative to allogeneic 51Cr release cytotoxicity assays.

Animals↗