La vegetación de la Comunidad Autónoma del País Vasco. Leyenda del mapa de series de vegetación a escala 1:50.000

Índice: 1. Marco geográfico. El medio físico: - Situación, extensión y límites. - Estructura, morfología y relieve. - Rasgos generales de los Pirineos. - Los Montes Vasco-Cantábricos. - La depresión del Ebro. 2. Los cambios de la vegetación en el tiempo: paleogeobotánica o geobotánica histórica: - Introducción. Las glaciaciones del Cuaternario. - La vegetación de Europa en el Terciario. - El tránsito Plioceno-Pleistoceno y el Pleistoceno antiguo. - El Pleistoceno medio y reciente. - El Tardiglaciar y el Holoceno. - La expansión de Fagus sylvatica en el Holoceno. - La Península Ibérica. 3. El clima actual del la Comunidad Autónoma del País Vasco y regiones limítrofes: - El régimen climático general del territorio noribérico. - La ubicación geográfica. - Centros de acción. - El contexto geográfico. - La clasificación bioclimática. - El paisaje vegetal a través de las unidades bioclimáticas: macroclimas, bioclimas y pisos bioclimáticos. - El macroclima Templado. - El macroclima Mediterráneo. 4. Biogeografía: - Biogeografía: definición y concepto. - Corionomía. - Biogeografía del norte-centro de la Península Ibérica. - Descripción y caracterización de las principales unidades biogeográficas. 5. Flora de la CAPV y territorios limítrofes: - La flora eurosiberiana. - La flora mediterránea. - La flora endémica. 6. Series, Geoseries y Geopermaseries de Vegetación de la Comunidad Autónoma del País Vasco: - Los cambios de la vegetación en escala temporal reducida: dinamismo y sucesión. Concepto de Serie, Geoserie y Geopermaserie de Vegetación - Series climatófilas y temporihigrófilas. - Geoseries fluviales. - Halogeopermaseries (Geopermaseries costeras): los sistemas costeros. - Saxigeopermaseries (Geopermaseries rupícolas): crestas, acantilados y gleras. - Higrogeopermaseries (Geopermaseries higrófilas): turberas, charcas y lagunas.

Novel equation to determine the hepatic triglyceride concentration in humans by MRI: diagnosis and monitoring of NAFLD in obese patients before and after bariatric surgery

Background: Non-alcoholic fatty liver disease (NAFLD) is caused by abnormal accumulation of lipids within liver cells. Its prevalence is increasing in developed countries in association with obesity, and it represents a risk factor for non-alcoholic steatohepatitis (NASH), cirrhosis and hepatocellular carcinoma. Since NAFLD is usually asymptomatic at diagnosis, new non-invasive approaches are needed to determine the hepatic lipid content in terms of diagnosis, treatment and control of disease progression. Here, we investigated the potential of magnetic resonance imaging (MRI) to quantitate and monitor the hepatic triglyceride concentration in humans. Methods: A prospective study of diagnostic accuracy was conducted among 129 consecutive adult patients (97 obesity and 32 non-obese) to compare multi-echo MRI fat fraction, grade of steatosis estimated by histopathology, and biochemical measurement of hepatic triglyceride concentration (that is, Folch value). Results: MRI fat fraction positively correlates with the grade of steatosis estimated on a 0 to 3 scale by histopathology. However, this correlation value was stronger when MRI fat fraction was linked to the Folch value, resulting in a novel equation to predict the hepatic triglyceride concentration (mg of triglycerides/g of liver tissue = 5.082 + (432.104 * multi-echo MRI fat fraction)). Validation of this formula in 31 additional patients (24 obese and 7 controls) resulted in robust correlation between the measured and estimated Folch values. Multivariate analysis showed that none of the variables investigated improves the Folch prediction capacity of the equation. Obese patients show increased steatosis compared to controls using MRI fat fraction and Folch value. Bariatric surgery improved MRI fat fraction values and the Folch value estimated in obese patients one year after surgery. Conclusions: Multi-echo MRI is an accurate approach to determine the hepatic lipid concentration by using our novel equation, representing an economic non-invasive method to diagnose and monitor steatosis in humans.

Alcohol-Related Brain Damage in Humans

Chronic excessive alcohol intoxications evoke cumulative damage to tissues and organs. We examined prefrontal cortex (Brodmann's area (BA) 9) from 20 human alcoholics and 20 age, gender, and postmortem delay matched control subjects. H & E staining and light microscopy of prefrontal cortex tissue revealed a reduction in the levels of cytoskeleton surrounding the nuclei of cortical and subcortical neurons, and a disruption of subcortical neuron patterning in alcoholic subjects. BA 9 tissue homogenisation and one dimensional polyacrylamide gel electrophoresis (PAGE) proteomics of cytosolic proteins identified dramatic reductions in the protein levels of spectrin beta II, and alpha- and beta-tubulins in alcoholics, and these were validated and quantitated by Western blotting. We detected a significant increase in a-tubulin acetylation in alcoholics, a non-significant increase in isoaspartate protein damage, but a significant increase in protein isoaspartyl methyltransferase protein levels, the enzyme that triggers isoaspartate damage repair in vivo. There was also a significant reduction in proteasome activity in alcoholics. One dimensional PAGE of membrane-enriched fractions detected a reduction in beta-spectrin protein levels, and a significant increase in transmembranous alpha 3 (catalytic) subunit of the Na+, K+-ATPase in alcoholic subjects. However, control subjects retained stable oligomeric forms of a-subunit that were diminished in alcoholics. In alcoholics, significant loss of cytosolic alpha-and beta-tubulins were also seen in caudate nucleus, hippocampus and cerebellum, but to different levels, indicative of brain regional susceptibility to alcohol-related damage. Collectively, these protein changes provide a molecular basis for some of the neuronal and behavioural abnormalities attributed to alcoholics