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Biomedical subjects

K Long

Publications and source records attributed to K Long.

At least 37 records · Page 2Linked to original sources
PubMed1993

Effects of glaucocalyxin A on aggregation and cAMP levels of rabbit platelets in vitro.

Glaucocalyxin A (Gla A) is a new diterpenoid isolated from ethereal extract of the leaves of Rabdosia japonica (Burm f) Hara var glaucocalyx (Maxim) Hara (Labiatae) collected in Northeastern China. When incubated with washed rabbit platelets, Gla A inhibited ADP-, AA-, and PAF-induced aggregation of rabbit platelets with IC50 values of 3.44, 13.32, and 7.74 mumol.L-1, respectively. Gla A 10 and 100 mumol.L-1 increased the cAMP levels in platelets. In combination with imazodan hydrochloride, Gla A (1-100 mumol.L-1) caused a marked increase of platelet cAMP levels, while no effect with PGE1.

Animals↗
PubMed1993

Tamoxifen.

Explore the source record for details and available documents.

Breast Neoplasms↗
PubMed1992

Emergent leadership and female sex role identity.

The effects of female sex role identity on self- and rater evaluations of emergent leadership behavior were compared in two studies. We used the same consensus-seeking procedure in both studies to collect the data; only the biological sex composition of the groups in the second study was changed. Study 1 examined 15 mixed-sex groups of 39 female and 21 male students; Study 2 contained 96 female students in 22 same-sex groups. Sex role orientation was measured with the Bem Sex Role Inventory (BSRI: Bem, 1974). Androgynous and feminine-oriented self-ratings of leadership were significantly higher than peer ratings and were also significantly higher than the undifferentiated self-ratings. The self-ratings of masculine-oriented women agreed most closely with peer ratings. Contrary to research and theory, peer evaluation of leadership behavior by sex role orientation did not differ.

Adult↗
PubMed1991

[Effects of econazole and clotrimazole on TXB2 and PGE2 production in calcimycin-stimulated neutrophils and arachidonic acid-stimulated platelets].

The effects of econazole and clotrimazole which are used as antifungal agents, on TXB2 and PGE2 production in calcimycin (A-23187)-stimulated rat pleural neutrophils and arachidonic acid (AA)-stimulated washing rabbit platelets were examined by radioimmunoassay. Econazole and clotrimazole 0.05-100 mumol.L-1 inhibited TXB2 production both in rat pleural neutrophils and in rabbit platelets with a dose-dependent manner. The most potent inhibition was found in rabbit platelets. At the concentration of 50 mumol.L-1, econazole and clotrimazole were sufficient to inhibit TXB2 production in rabbit platelets by up to 99% and 98% respectively. Econazole and clotrimazole 0.05-5 mumol.L-1 also increased PGE2 biosynthesis in rabbit platelets. But econazole and clotrimazole 50 mumol.L-1 reduced the PGE2 production in rabbit platelets to 11% and 37% of the amounts of 5 mumol.L-1 econazole and clotrimazole respectively. The results suggest that econazole and clotrimazole at lower concentration may have a selective inhibitory effect on thromboxane synthetase, at higher concentration they also inhibit cyclooxygenase.

Animals↗
PubMed1991

Effects of CI-930 on hemostasis, thrombosis, and AA-induced hemodynamic reaction.

In mice, CI-930 0.5-2 mg.kg-1 ip not only prolonged the tail bleeding time but also protected the mice from sudden thromboembolic death induced by arachidonic acid (AA, 100 mg.kg-1, i.v.) or TXA2/PGH2 mimetic U46619 (200 micrograms.kg-1, i.v.). CI-930 0.625 and 2.5 mg.kg-1 i.v. exhibited a dose-dependent inhibitory effect on thrombus formation in rat arteriovenous shunt. All these effects of CI-930 were more potent than those of dazoxiben, a known antiplatelet drug. In rabbit, AA 0.75 mg.kg-1 i.v. caused a rapid and marked increase in pulmonary vascular resistance and a concomitant sharp decrease in cardiac output and carotid arterial pressure. CI-930 itself 0.5 mg.kg-1 i.v. resulted in a long-lasting fall in carotid arterial pressure, systemic vascular resistance, and a slight decrease in cardiac output. In addition, CI-930 protected rabbit from all the harmful hemodynamic responses to the occlusion of pulmonary microcirculation, which was induced by AA. The results suggest that CI-930 possess a potent anti-hemostatic, antithrombotic, and probably antihypertensive effects on experimental animals.

Animals↗
PubMed1990

Effects of CI-930, a novel phosphodiesterase III inhibitor, on platelet aggregation and arachidonic acid metabolism.

In the platelet-rich plasma of rabbits, 4,5-dihydro-6-[4-(1H-imidazol-1-yl)phenyl]-5-methyl-3(2H)-pyridazinone (CI-930) inhibited platelet aggregation triggered by AA, U-46619, ADP, collagen and PAF, with the IC50 values of 0.91, 0.73, 2.12, 2.35 and 7.15 mumols/L, respectively. The inhibitory effect of CI-930 on AA-induced aggregation was potentiated by PGE1, an adenylate cyclase activator, and antagonized by SQ-22536, an adenylate cyclase inhibitor. The contents of cAMP in washed rabbit platelets were increased by CI-930 5-50 mumols/L. In the concentration range of 0.5-500 mumols/L, CI-930 reduced the synthesis of TXB2 by either washed rat or rabbit platelets or rat pleural neutrophils. At the same time, CI-930 induced a dose-dependent increase of PGE2, PGF2a, and PGD2 biosynthesis by rat platelets and had no significant influence on the formation of 6-keto-PGF1a by the neutrophils. It is showed that CI-930 is an anti-platelet agent with a wide-spectrum activity and its anti-aggregating action may be exerted by dual mechanisms, both increasing cAMP contents and selectively inhibiting TXA2 synthesis in platelets.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

[Selective inhibition of CI-914 on the production of TXA2 and HHT].

The effects of CI-914, a novel cardiotonic agent, on AA metabolism in rat neutrophils and platelets in vitro were investigated. Using washed rat platelets, the formation of HHT (measured by HPLC), a product of AA metabolism via cyclooxygenase and TXA2 synthetase, was found to be inhibited by the agent in a dose-dependent manner, with IC50 value of 78.6 mumol/L. Only at higher concentration (500 mumol/L) of CI-914, was the production of 12-HETE (measured by HPLC), a lipoxygenase product in platelets, shown to be inhibited. These indicate that CI-914 mainly inhibits the metabolism of AA via cyclooxygenase and TXA2 synthetase rather than via lipoxygenase. In rat platelets and A23187-stimulated pleural neutrophils, CI-914 caused a dose-related decrease of TXA2 production (measured by RIA), with IC50 values of 28.6 and 51.3 mumol/L, respectively. Meanwhile, significant increases of PGE2 synthesis in the platelets and 6-keto-PGF1 alpha synthesis in the pleural neutrophils were observed when CI-914 was preincubated with these cells. It is suggested that CI-914 might selectively inhibit the activity of TXA2 synthetase in rat platelets and pleural neutrophils.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[Effects of imazodan and dazoxiben on cAMP levels and PGI2 production in cultured bovine aortic endothelial cells].

We have investigated the effects of imazodan, a potent inhibitor of phosphodiesterase III (PDE III) and dazoxiben, a selective inhibitor of thromboxane synthetase on cAMP levels and PGI2 production in cultured bovine aortic endothelial cells by radioimmunoassay. When cultured endothelial cells were incubated with imazodan, intracellular levels of cAMP were increased in a dose-dependent manner. PGI2 production induced by arachidonic acid (AA) was not affected by imazodan 0.1-10 mumol/L. But imazodan 100 mumol/L caused a 35% inhibition of PGI2 production. In the presence of AA, dazoxiben could also elevate intracellular levels of cAMP. Furthermore, dazoxiben 1-10 mumol/L caused a marked increase in PGI2 production, but 1000 mumol/L inhibited PGI2 production.

Animals↗