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Luis Valdés

Publications and source records attributed to Luis Valdés.

4 recordsLinked to original sources
PubMed2005

The effect of the "Prestige" oil spill on the plankton of the N-NW Spanish coast.

Chlorophyll, primary production, zooplankton biomass and the species composition of phytoplankton and zooplankton were studied in 2003, after the Prestige shipwreck. The information obtained was compared to previous data series available for the area affected by the spill. A large data series on plankton variables for the N-NW Spanish coast existed, and therefore a realistic evaluation of the effects by comparison with the range of natural variability could be carried out. We emphasized the evaluation of impact during the spring bloom, the first important biological event after the spill. Some minor changes were observed occasionally, but they did not show any clear pattern and were more related to the natural variability of the ecosystem than to effect of the spill. Plankton community structure did not undergo any changes. Only a few species were more abundant during spring 2003 than in previous years. No significant changes were detected in the planktonic community during productive periods, such as the spring bloom and the summer blooms related to intrusions of East North Atlantic Central Waters. The lack of evidence of the effects of the spill on planktonic communities is discussed in terms of the characteristics of the fuel, the high dynamics of the water masses, the biological mechanisms through which the fuel from the surface waters is transferred to the sea floor and, particularly, the influence of the natural variability by means of large and meso-scale hydrographic processes in the area under study. At the present time it is not possible to determine any minor effects the spill may have had on the plankton owing to the great variability of the planktonic cycles and the short-term impact of the oil from the Prestige on the pelagic system.

Animals↗
PubMed2003

Tuberculous pleural effusions.

Tuberculosis is the most frequent cause of death due to infectious diseases. In Europe, it is one of the most frequent types of pleural effusions in young patients. Tuberculosis is caused by the rupture of a pulmonary subpleural caseous focus, which releases mycobacterium into the pleural cavity, thereby triggering an immune response involving mainly macrophages, CD4+ T lymphocytes, and the cytokines released by these cells (especially interleukin 1, interleukin 2, and ?-interferon). In recent years, classical microbiological and histological methods of diagnosis have been joined by biochemical analyses of pleural fluid, which are faster and can be more sensitive. In particular, tuberculous effusions have high adenosine deaminase (ADA) activity, apparently due to high levels of the ADA isoenzyme ADA2, which is only found in monocytes and macrophages (although certain data suggest the possible involvement of activated T cells, too). It has been recommended that treatment for tuberculosis be initiated if analysis of pleural fluid shows high ADA activity, a lymphocyte/neutrophil ratio greater than 0.75, and no malignant cells. Another highly efficient marker is ?-interferon, which is released by activated CD4+ T cells, but its high price is an obstacle to its routine determination in clinical practice. Identification of mycobacterial DNA by means of the polymerase chain reaction (PCR) is less efficient, apparently because its sensitivity depends heavily on mycobacterium concentration. No other biochemical parameters currently appear to be of marked relevance for the diagnosis of tuberculous pleural effusion (TPE). TPE responds well to the standard treatment for tuberculosis. However, 50% of TPE patients have a thickened pleura as a result of the accumulation of fluid, and in 16% the quantity of effusion increases during treatment, even if corticosteroids are administered. It therefore seems reasonable for treatment with antituberculous drugs to be preceded by therapeutic thoracocentesis to remove as much fluid as possible.

Journal Article↗
PubMed2002

Enhanced severity of secondary dengue-2 infections: death rates in 1981 and 1997 Cuban outbreaks.

OBJECTIVE: To understand the possible effect that length of time has on disease severity with sequential dengue infections. METHODS: Death and hospitalization rates for dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) per 10,000 secondary dengue-2 infections were compared in the same age group for two dengue-2 (DEN-2) epidemics in Cuba. The first DEN-2 epidemic affected all of Cuba in 1981; the second one, in 1997, impacted only the city of Santiago de Cuba. The sensitizing infection for DHF/DSS for each of the DEN-2 epidemics was dengue-1 (DEN-1) serotype virus, which was transmitted in 1977-1979, that is, 4 years and 20 years before the two DEN-2 epidemics. Using published seroepidemiological data from the cities of Havana and Santiago de Cuba, we estimated the rates at which persons aged 15-39 years old and those 40 years and older were hospitalized or died of DHF/DSS in Havana and in all of Cuba in 1981 and in just Santiago de Cuba in 1997. RESULTS: Among adults 15-39 years old the death rate per 10,000 secondary DEN-2 infections was 38.5 times as high in Santiago de Cuba in 1997 as in Havana in 1981. As a further indication of the increased severity coming with a longer period between the initial DEN-1 infection and the secondary DEN-2 infection, the case fatality rate for that same age group was 4.7 times as high in Santiago in 1997 as it was in Havana in 1981. CONCLUSION: We found a marked increase in severity with the longer of the two intervals (20 years) between an initial DEN-1 infection and a secondary DEN-2 infection. Such a difference may be due to subtle shifts in causative dengue strains or to changes with the passage of time in the circulating population of human dengue antibodies. These observations have important implications for dengue control, pathogenic mechanisms, and vaccine development.

Adolescent↗