Type X collagen synthesis by cultured chondrocytes derived from the permanent cartilaginous region of chick embryo sternum.

In the developing chick embryo sternum, type X collagen is synthesized by chondrocytes from the cephalic region (presumptive mineralization zone) but not by chondrocytes from the caudal region (permanent cartilaginous zone) (Gibson et al., 1984, J. Cell Biol. 99, 208-216). To distinguish between two possibilities, the presence of a nonpermissive microenvironment in the permanent cartilage or the intrinsic inability of caudal chondrocytes to become hypertrophic, type X-producing cells, we have isolated chondrocytes from the caudal third of stage 44 chick embryo sterna and grown them in suspension on agarose-coated dishes. We have found that in these conditions chondrocytes from the caudal zone differentiate to hypertrophic chondrocytes and synthesize large amount of type X collagen, as revealed by the electrophoretic pattern of labeled proteins made in vitro and by slot blot analysis of mRNAs with specific cDNA probes.

Evidence for an adenosine A2/Ra receptor on human basophils.

5'-N-ethylcarboxamideadenosine (NECA) greater than 2-chloroadenosine greater than adenosine greater than (-)-N6-(R-phenyl-isopropyl)-adenosine greater than (+)-N6-(S-phenylisopropyl)-adenosine, in that order of potency, inhibited in vitro antigen-induced histamine release from human basophils in a dose-dependent fashion. Inhibition occurred only during the first stage of antigen-induced histamine release and the nucleosides failed to inhibit the release caused by the Ca2+ ionophore, A23187. 6-nitrobenzylthioinosine and dipyridamole, which inhibit adenosine uptake, and erythro-9-(2-hydroxy-3-nonyl)adenine, which blocks adenosine metabolism, did not impair the inhibition caused by NECA and adenosine. 8-phenyltheophylline and theophylline, two competitive antagonists of adenosine receptors, blocked the inhibition caused by NECA and adenosine. These data suggest that NECA and other adenosine analogs activate a specific cell surface adenosine receptor which possesses properties similar to those of an adenosine A2/Ra receptor.

Possible role of arachidonic acid and of phospholipase A2 in the control of lysosomal enzyme release from human polymorphonuclear leukocytes.

We have studied the role of arachidonic acid (AA) metabolism in the release of lysosomal enzymes (beta-glucuronidase and lysozyme) from human polymorphonuclear leukocytes (PMNs). 5,8,11,14-Eicosatetraenoic acid (ETYA), which inhibits both the cyclo-oxygenase and the lipoxygenase pathways of AA metabolism, was found to cause a dose-dependent inhibition of lysosomal enzyme release from human PMNs induced by immunological (i.e., serum-treated zymosan: Zx) and nonimmunological stimuli (i.e., formyl methionine-containing peptide and the Ca2+ ionophore A23187). In contrast, the non-steroidal anti-inflammatory drugs (indomethacin, meclofenamic acid and aspirin), which only block the cyclo-oxygenase pathway of AA metabolism, had little effect on enzyme release from PMNs induced by the same stimuli. 5,8,11-Eicosatriynoic acid (ETI), a selective inhibitor of the lipoxygenase pathway of AA metabolism, caused a dose-dependent inhibition of lysosomal enzyme release elicited by Zx, f-met peptide, and A23187. p-Bromophenacyl bromide (BPB), which inhibits the phospholipase A2 (PLA2) activity in several tissues, was found to cause a dose-dependent inhibition of lysosomal enzyme release induced by the same immunological and non-immunological stimuli. The inhibitory effect of BPB on enzyme release was irreversible and extremely rapid. It appears that activation of PLA2 and the products of the AA metabolism, generated via a lipoxygenase pathway, play an essential role in the biochemical control of human PMNs activation and secretion.

[Comparison between spontaneous changes in circulating triiodothyronine (T3 and reverse-T3) and those induced by acute intravenous administration of thyroliberin]. / Confronto tra le variazioni spontanee delle triiodotironine circolanti (T3 e rT3) e quelle indotte da carico endovenoso acuto di tiroliberina (TRH).

Some of the Authors had previously observed a slight-non significant decrease in T3 serum levels 10 minutes after TRH intravenous administration. On the other hand, it is now well known that reverse T3 (rT3) inhibits T4 conversion to T3. We therefore investigated the changes in T3 and rT3 serum levels within the first ten minutes of a 200 micrograms TRH test in a group of 10 healthy women in fertile age. No significant change in T3 was demonstrated. On the other hand, rT3 showed a significant-yet slight-decrease 6 minutes after TRH injection (from 0,27 to 0,21 ng/ml, p less than 0,05). Some feasible explanations for this phenomenon are given in the text.

[Behavior of triiodothyronine, tetraiodothyronine and thyrotropin during the TRH test]. / Comportamento della triiodotironina, della tetraiodotironina e della tireotropina in corso di TRH test.

Much confusion seems to exist on the timing and intensity of thyroid hormones (T4 and T3) response to TRH. As a first approach to the problem, the Authors performed TRH test in 5 healthy women. TSH showed a significant increase immediately after the TRH injection and kept high until the 90th minute. T3 decreased at first-still not significantly--then increased steadily and at 60 min it reached values significantly higher than the basal ones. Some increase was seen for T4 too, but it did not show to be statistically significant within 180 minutes. The Authors give revelance to the significance of precious (60 min) T3 increase in such a small casuistry.

[Changes in blood prolactin in relation to the menstrual cycle]. / Comportamento della prolattinemia in rapporto al ciclo mestruale.

Scientists are in general agreement on the hypothesis of a prolactin surge at midcycle. In order to test this hypothesis the Authors measured radioimmunoassayable circulating prolactin in the follicular phase and at midcycle in 15 normally menstruating health women. Due to the well known individual variability, mean prolactin values showed statistically poor differences in the two phases of the cycle. Though, a very good positive correlation (r = 0.72, p less than 0.01) was shown when individual follicular values were plotted against the corresponding midcycle values. The Authors conclude that at midcycle prolactin increases significantly and discuss physiological significance of this phenomenon.