Infections associated with Vibrio parahaemolyticus on the coast of Galicia (in northwestern Spain) were reported to be linked to large outbreaks of illness during 1999 and 2000. Little information is available about the ecological factors that influence the emergence of V. parahaemolyticus infections in this temperate region. We carried out a 3-year study to investigate the occurrence and distribution of V. parahaemolyticus at 26 sites located in the four main rias of Galicia in association with environmental and oceanographic variables. V. parahaemolyticus was detected in all the areas investigated and throughout the complete period of study with an overall incidence of 12.5%. Salinity was the primary factor governing the temporal and spatial distribution of V. parahaemolyticus, whereas seawater temperature had a secondary effect and only modulated the abundance in periods and areas of reduced salinities. Higher occurrence of V. parahaemolyticus was observed during periods of lower salinity in autumn, with a total of 61 positive samples (18%) and a mean density of 1,234 most probable number/100 g. V. parahaemolyticus was primarily detected in areas of reduced salinity close to freshwater discharge points, where it was found in up to 45% of the samples. Characterization of the isolates obtained from the study resulted in the first identification of two pathogenic tdh-positive strains of V. parahaemolyticus recovered from the marine environment in Galicia. These isolates showed serotypes identical to and DNA profiles indistinguishable from those of the clinical clone of V. parahaemolyticus dominant in infections in Spain in the last 10 years.Vibrio parahaemolyticus is a natural inhabitant of the marine environments of coastal areas and estuaries worldwide. The presence of the organism has traditionally been confined to warm and temperate geographical areas (11). However, in recent years, the emergence of infections caused by V. parahaemolyticus in remote areas of Europe and America (14,15,23,24) has revealed the presence of the organism in regions where it had never previously been reported. The progressive spread of V. parahaemolyticus and its colonization of new areas has been related to an unusual increase in seawater temperatures in coastal zones (5,15,24). However, little information is available about the environmental variables governing the dynamics of V. parahaemolyticus populations in these areas of recent emergence.V. parahaemolyticus infections were rarely reported in Europe before 1998 (2). The presence of V. parahaemolyticus was reduced to sporadic cases reported in different countries without any evidence of epidemiological connection. The epidemiology of the organism in Europe changed significantly when a large number of illnesses associated with V. parahaemolyticus were reported in Galicia (in northwestern Spain) in 1999 and 2000. Isolates obtained from the outbreaks in Galicia and from hospitals in other regions of Spain were characteristically tdh positive, serotype O4:K11, and belonged to a di...

During the Galicia X cruise, from May to October 1989 an intensive collection of hydrographic data was carried out at a single station on the shelf off the western coast of Galicia. It allows us to follow the response of the water column to the intermittent equatorward wind stress during the upwelling season. Upwelling events occur with biweekly periodicity, bringing Eastern North Atlantic Water (ENAW) to the subsurface layer at our station. A trend of the thermohaline properties of the upwelled water to increase in time was observed. This seems to be mostly due to the southwestward displacement of the origin of this water mass during the year. Although the saltier and warmer ENAW is less nutrient-rich, nutrient levels increase because of the rapid remineralization of organic matter from the Rias, which takes place in the bottom water on the shelf.

The role of obestatin, a 23-amino-acid peptide encoded by the ghrelin gene, on the control of the metabolism of pre-adipocyte and adipocytes as well as on adipogenesis was determined. For in vitro assays, pre-adipocyte and adipocyte 3T3-L1 cells were used to assess the obestatin effect on cell metabolism and adipogenesis based on the regulation of the key enzymatic nodes, Akt and AMPK and their downstream targets. For in vivo assays, white adipose tissue (WAT) was obtained from male rats under continuous subcutaneous infusion of obestatin. Obestatin activated Akt and its downstream targets, GSK3α/β, mTOR and S6K1, in 3T3-L1 adipocyte cells. Simultaneously, obestatin inactivated AMPK in this cell model. In keeping with this, ACC phosphorylation was also decreased. This fact was confirmed in vivo in white adipose tissue (omental, subcutaneous and gonadal) obtained from male rats under continuous sc infusion of obestatin (24 and 72 hrs). The relevance of obestatin as regulator of adipocyte metabolism was supported by AS160 phosphorylation, GLUT4 translocation and augment of glucose uptake in 3T3-L1 adipocyte cells. In contrast, obestatin failed to modify translocation of fatty acid transporters, FATP1, FATP4 and FAT/CD36, to plasma membrane. Obestatin treatment in combination with IBMX and DEX showed to regulate the expression of C/EBPα, C/EBPβ, C/EBPδ and PPARγ promoting adipogenesis. Remarkable, preproghrelin expression, and thus obestatin expression, increased during adipogenesis being sustained throughout terminal differentiation. Neutralization of endogenous obestatin secreted by 3T3-L1 cells by anti-obestatin antibody decreased adipocyte differentiation. Furthermore, knockdown experiments by preproghrelin siRNA supported that obestatin contributes to adipogenesis. In summary, obestatin promotes adipogenesis in an autocrine/paracrine manner, being a regulator of adipocyte metabolism. These data point to a putative role in the pathogenesis of metabolic syndrome.