In order to obtain novel genes related to the human craniofacial development, molecular cloning and sequencing, and in situ hybridization using craniofacial tissue sections were performed and followed by protein structure simulation. Totally 231 clones were obtained from the subtracted craniofacial tissue cDNA library of human embryo. Random cloning using the non-redundant clones from the craniofacial tissue of human embryo was done and obtained 398 clones from the premade human chondrocyte cDNA library. Their partial sequence data showed that 214 clones of subtracted cDNA library of craniofacial tissue were still non-redundant in Genebank search. And 20 clones among 498 clones of premade chondrocyte cDNA library were known to be undefined genes. Through in situ hybridization screening in the craniofacial tissue sections of 10 weeks old human embryo 36 clones were found to be positive in specific tissues. Depending on the cell types of sirnilar developmental origin, the positive reactions could be divided into five groups. Among the 20 clones of undefined genes from human chondrocyte cDNA library, 7 clones showed characteristic positive reaction in human cartilage tissue by in situ hybridization. From the simulated protein structure, motif analysis and in situ hybridization studies for the 7 undefined clones, Ch89, Ch96, Ch129, Ch285 clones may function in the outer space of the cell constituting a part of matrix protein complex, and Ch276 as a transmembrane protein which might partic ipate in matrix calcification around chondrocytes. Ch153 is a kind of antirnicrobial protein also acting as an inflammation mediator, and Ch334 clone is a zinc finger protein, of which expression increases in human adult tissues We presume these novel genes from human chondrocytes may provide a new path of chondrocyte development and functions of human craniofacial tissues

We investigated the antiplatelet effect of a newly synthesized guanidine derivative KR-32558, a sodium-hydrogen exchanger-1 (NHE-1) inhibitor, together with the elucidation of the possible mechanisms of action. KR-32558 concentration -dependently inhibited the aggregation of washed rabbit platelets induced by collagen (10 μg/ml) with an IC_(50) value of 85.9 μM, but with much weaker potency against aggregation induced by thapsigargin (0.5 μM) or A23187 (5 μM). And had no effect on platelet aggregation induced by arachidonic acid (100 μM), thrombin (0.05 U/ml) and U46619 (1 μM) up to 100 μM. KR-32558 completely inhibited the [Ca^(2+)] mobilization induced by collagen at concentration of 100μiM. Taken together, these observations suggest that KR-32558 selectively inhibited collagen-mediated platelet aggregation by blocking the cytoplasmic calcium mobilization in addition to NHE-1 inhibition.

Ultra fine titanium carbide particles were synthesized by novel metallic thermo-reduction process. The vaporized TiC1+ gases were reacted with liquid magnesium and the fine titanium carbide particles were then produced by combining the released titanium and carbon atoms. The vacuum treatment was followed to remove the residual phases of MgC1 and excess Mg. The stoichiometry, microstructure, fixed and carbon contents and lattice parameter were investigated in titanium carbide powders produced in various reaction parameters.