Vasopressin (AVP) and some of its synthetic analogues, for example 1 desamino 8-D-AVP (DDAVP), induce plasminogen activator (PA) release in vivo. It has been proposed that this occurs via the release from the central nervous system of a plasminogen activator releasing hormone (PARH). The present study shows that a crude extract of bovine posterior pituitary, but not of the anterior pituitary or of the hypothalamus, induces a marked increase of circulating PA in anaesthetized rats. PA release appears to be caused by AVP because no other PA releasing activities could be identified in or isolated from the extract. In addition, no PA-releasing activity was found in extracts of pituitary glands of rats congenitally deficient in vasopressin. The following experiments did not reveal central nervous system involvement in the PA-release caused by AVP or DDAVP. Perfusion of isolated organs (rat heart and rat liver) with AVP resulted in PA-release. In squirrel monkeys, comparable PA levels were found in the venous return following intrafemoral or intracarotid injection of AVP. Moreover, when plasma obtained 2 min following AVP or DDAVP injection was transfused to a receiving animal no PA release was observed. Thus our present findings do not support the hypothesis that the fibrinolytic response to AVP is mediated by the release of a specific peptide hormone from the central nervous system.
Eleven analogues of the laminin pentapeptide amide fragment Tyr-Ile-Gly-Ser-Arg-NH2 (YIGSR-NH2) corresponding to a B1 chain fragment of the glycoprotein laminin have been synthesized by the solid phase method, and their biological activity has been studied in vitro by a cell adhesion assay: all of them inhibited the adhesion of LLC tumor cells to laminin. The analogues were found to be more resistant to enzymatic degradation in human serum than YIGSR-NH2 itself. Analogue DatIGSHar-NH2 was selected for an experimental pulmonary metastasis assay in vivo: it had higher antimetastatic activity than YIGSR-NH2.
The cytotoxicity of NK cells and lymphocytes derived from nonadherent splenocytes (SPL) and regional lymph node cells (LNC) from complete Freund's adjuvant (CFA)‐treated athymic nude young (4–6 weeks) and aged (over 1 year) BALB/c nu/nu mice in vitro activated with rIL‐2, anti‐CD3 mAb or PPD was analyzed and compared to SPL and LNC from age‐matched euthymic BALB/c mice. The high natural cytotoxicity to YAC‐1 target cells of SPL or LNC could be augmented by 48 h stimulation in vitro with rIL‐2, especially when derived from young nude BALB/c mice. The increase in cytotoxic activity was accompanied by increased proliferative activity of both SPL and LNC, which showed statistically significant differences between the rates of stimulation of cells from the young and aged groups. Anti‐CD3 mAb strongly activated the cytotoxicity of BALB/c euthymic donor effector cells against P‐815 target cells, corresponding to a very high proliferative activity of these cells, but anti‐CD3 mAb did not lead to activation of effector cells from nude donors. FACS analyses of antigenic markers similarly showed an increased number of T cells in LNC from aged BALB/c nude donors, which, however, never reached the levels of those of euthymic animals.
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