ABSTRACT
An angiogenic factor from human transitional cell cancer of bladder has been purified by protein extraction, cation exchange chromatography, gel filtration high-performance liquid chromatography (GE-HPLC) and reversed-phase high-performance liquid chromatography (RP-HPLC). The purified substance was named bladder cancer angiogenic factor (BCAF). Biological activity of the BCAF was assessed by the method of chick embryo chorioallantoic membrane (CAM) assay and 3H-TdR incorporation into DNA in Balb/C 3T3 cells. The BCAF displayed the potent activities of neovascularization in CAM and DNA synthesis in Balb/C 3T3 cells. The ultrastructural features of blood vessels induced by the BCAF were similar to the blood vessels in tumors. The BCAF contained a protein with an approximate molecular weight of 15,000 D which was identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and silver staining. Amino acid compositions of the BCAF were also analysed by acid hydrolysis.
Subject(s)
Angiogenesis Inducing Agents/isolation & purification , Carcinoma, Transitional Cell/chemistry , Urinary Bladder Neoplasms/chemistry , 3T3 Cells , Angiogenesis Inducing Agents/pharmacology , Animals , Chick Embryo , DNA/biosynthesis , Humans , Mice , Mice, Inbred BALB C , Neovascularization, PathologicABSTRACT
In this paper, the synthesis of a series of aminoketone derivatives are reported. Compounds I1-9 and II1-10 were synthesized from substituted chloroacetophenone with various amines. Compounds I10-12 and II11-12 were synthesized from substituted acetophenones with corresponding amines through Mannich reaction. The 1HNMR and MS were discussed. Pharmacological study showed that the vascular contraction of dog mesenteric and basilar arteries induced by serotonine and calcium in vitro could not be antagonized by this kind of compounds and the known compound 3,4-dihydroxy acetophenone (I0). Except I10, the vasodilator effects of all compounds as shown by measurement of arterial blood flow after injection into femoral artery in dogs are weaker than I0. After intravenous injection in anesthetized dogs, I10 showed the same effect as I0 to increase coronary blood flow and myocardial contraction. Furthermore, the ventricular arrhythmia induced by aconitine and chloroform could also be protected by compound I10, but compound I0 was not effective.
Subject(s)
Norepinephrine/analogs & derivatives , Animals , Arrhythmias, Cardiac/prevention & control , Chemical Phenomena , Chemistry , Coronary Circulation/drug effects , Dogs , Muscle Contraction/drug effects , Muscle, Smooth, Vascular/drug effects , Myocardial Contraction/drug effects , Norepinephrine/chemical synthesis , Norepinephrine/pharmacologyABSTRACT
PIP: To investigate the effect of steroids on the level of sex hormone binding globulin (SHBG), 24 women between ages 25 and 35 received one injection of 200 mg norethisterone enanthate (NET-EN). The mean serum SHBG level before the injection was 53.23 mnol/L, with a standard deviation of 23.23 mnol/L. Five days after the injection, the serum SHBG level was reduced to 41.99 +or- 17.06 nmol/L (P.05). 21 days after the injection, the serum SHBG level reached the lowest point of 14.72 +or- 10.01 nmol/L. The SHBG level gradually increased afterwards and did not recover to the premedication level at 84 days with 34.46 +or- 20.39 nmol/L. Two groups of women received oral administration of levonorgestrel (LNG) including one group of 10 women who received a single dose of 6 mg LNG plus 3 mg quinestrol (CEE) and another group of 8 women who received 3 doses of the same regimen as the single-dose group at an interval of 23 days between each dose. The mean premedication SHBG level of the single-dose group was 42.76 +or- 13.89 nmol/L, and it rose to 62.53 +or- 10.9 nmol/L on the seventh day after the administration (p.01). The serum SHBG level peaked at 71.33 +or- 5.77 days after the administration and this high level was sustained until 56 days. For the three doses group, the serum SHBG level prior to medication was 44.94 +or- 15.36 nmol/L. 9 days after the first administration, it reached 83.46 +or- 10.08 nmol/L and peaked at 16 days with 91.74 +or- 2.28 nmol/L. The high serum SHBG level sustained until 30 days after the third administration. The second and third administration of levonorgestrel did not have a significant effect on the SHBG level, as it had already reached a high level. The peak value of LNG blood concentration after the second and third administration was 6 times higher than the peak after the first administration.^ieng