Skeletal tumor formations in the massive coral Pavona clavus were investigated for 3 yr on the northern Pacific coast of Costa Rica in a reef composed almost exclusively of this species. A field survey of tumor incidence showed that more than half of the population presented this phenomenon and that frequencies increased with depth. Up to 37 tumors per colony were recorded, and the largest tumor size was 37.5 m 2 , covering the whole colony surface area. Tumors and healthy skeletons and tissues were studied by scanning and transmission electron microscopy, histology, in situ alizarin marking for growth rates, and x-ray radiographs of skeletal slabs. Macroscopic and microscopic analyses of skeletons revealed the presence of 3 types of tumors (Types I to III). No cytological changes or intracellular infection by parasitic agents were recorded. The only cellular change observed was the reduced numbers of zooxanthellae in tumorigenic tissues. Tumors begin their growth as a single polyp and develop for scores of years without any sign of cellular necroses. Tumors grew faster than healthy parts; however, their skeletal density was lower, with a higher Mg content making it less resistant to bioerosion. Two yr of in situ isogeneic and allogeneic contacts between healthy and tumor fragments revealed no infection or transfer of the tumor to the healthy tissue, even following isogeneic fusion combinations of healthy versus tumor fragments. We suggest that the terminology often used to characterize tumors in hard corals ('tumor', 'neoplasm', 'hyperplasia') does not reflect the pathogenesis and etiology of this phenomenon. The terms 'skeletal tumor' or 'calicoblastic epithelioma' seem more fitting for this de novo genesis.

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During the Early and Middle Jurassic, the Iberian Basin (East of Spain) recorded the transition from a generally magma-poor passive margin, which operated during the latest Triassic and most of Early Jurassic, to a magma-rich passive margin, developed from Pliensbaextensional fault zones. One of these zones of weakness, from which the volcanic deposits were expelled to the sea bottom, was the Caudiel -formations. So far, the accurate age of these volcanisms, critical in the knowledge of the palaeogeographical and geodynamical evolution of the Iberian Basin, has remained uncertain. The ammonite content of the carbonate successions, with which these rocks are interbedded, allows precise biostratigraphical dating at the chronozone scale. For this purpose, 9 sections have been measured and 360 specimens of ammonites were collected and determined. The obtained data indicate that the Middle Jurassic volcanic deposits that are linked to the Caudiel Fault Zone and included into the El Pedregal Formation show a slight diachrony. They were deposited around the boundary between the Late Aalenian Concavum and the Early Bajocian Discites chronozones. However, in very restricted areas of the Caudiel Fault Zone, an older intra-Murchisonae volcanism was recorded.Keywords: Volcanism, Biochronostratigraphy, Ammonites, Middle Jurassic, Iberian Range ResumenDurante el Jurásico Inferior y Medio, la Cuenca Ibérica (Este de España) registró la transición de un margen pasivo pobre en magmatismo, que operó durante el Triásico terminal y la mayor parte del Jurásico Inferior, a un margen pasivo rico en actividad magmática, que se desarrolló desde el Pliensbachiense hasta el comienzo del Jurásico Medio. El volcanismo submarino, fundamentalmente piroclástico y con volcánicas que tuvieron lugar a lo largo del Jurásico Medio en relación con esta línea de debilidad. La fase principal se manifestó mientras y geodinámica de la Cuenca Ibérica, ha permanecido incierta. El contenido en ammonites de las sucesiones de carbonatos, entre los que del Jurásico Medio que están asociados a la Zona de Falla de Caudiel e incluidos en la Formación El Pedregal muestran una sincronía casi perfecta. Se depositaron hacia el límite entre la Cronozona Concavum del Aaleniense Superior y la Cronozona Discites del Bajociense Inferior. Con anterioridad, un volcanismo de edad intra-Murchisonae quedó registrado en áreas muy localizadas de la Zona de Falla de Caudiel.

The in vitro and in vivo effects of lovastatin on fatty acid metabolism were studied in isolated rat hepatocytes. When added in vitro to cell incubations, lovastatin stimulated de novo fatty acid synthesis and acetyl-CoA carboxylase activity, whereas fatty acid synthase activity was unaffected. Lovastatin depressed palmitate, but not octanoate, oxidation. This may be attributed to the lovastatin-induced increase in intracellular malonyl-CoA levels, as no concomitant change of carnitine palmitoyltransferase I (CPT-I) specific activity was detected. Lovastatin had no effect on the synthesis and secretion of triacylglycerols and phospholipids in the form of very low density lipoproteins (VLDL). When rats were fed a diet supplemented with 0.1% (w/w) lovastatin for one week, both acetyl-CoA carboxylase activity and de novo fatty acid synthesis were reduced compared to pair-fed controls, whereas fatty acid synthase activity was unaffected. Palmitate oxidation was enhanced in the lovastatin-fed group. There was an increase in CPT-I activity but no change in intracellular concentration of malonyl-CoA. Lovastatin feeding had no significant effect either on the esterification of exogenous palmitic acid into both cellular and VLDL triacylglycerols and phospholipids or on hepatic lipid accumulation. The in vitro and in vivo effects of lovastatin were not significantly different between periportal and perivenous hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

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