University of Alcalá

About: University of Alcalá is a education organization based out in Alcalá de Henares, Spain. It is known for research contribution in the topics: Population & Context (language use). The organization has 10795 authors who have published 20718 publications receiving 410089 citations. The organization is also known as: University of Alcala & University of Alcala de Henares.

Analysing forest recovery after wildfire disturbance in Boreal Siberia using remotely sensed vegetation indices

Abstract: Wildfires have major effects on forest dynamics, succession and the carbon cycle in the boreal biome. They are a significant source of carbon emissions, and current observed changes in wildfire regimes due to changes in climate could affect the balance of the boreal carbon pool. A better understanding of postwildfire vegetation dynamics in boreal forests will help predict the future role of boreal forests as a carbon sink or source. Time series of Normalized Difference Vegetation Index (NDVI) and Normalized Difference Shortwave Infrared Index (NDSWIR) derived from Moderate Resolution Imaging Spectroradiometer (MODIS) aboard the Terra satellite were used to investigate whether characteristic temporal patterns exist for stands of different ages in the Siberian boreal forests and whether their postwildfire dynamics are influenced by variables such as prewildfire vegetation cover. Two types of forests, evergreen needle-leaf (ENF) and deciduous needle-leaf (DNF), were studied by analysing a sample of 78 burned forest areas. In order to study a longer time frame, a chronosequence of burned areas of different ages was built by coupling information on location and age provided by a forest burned area database (from 1992 to 2003) to MODIS NDVI and NDSWIR time series acquired from 2001 to 2005. For each of the burned areas, an adjacent unburned control plot representing the same forest type was selected, with the aim of separating the interannual variations caused by climate from changes in NDVI and NDSWIR behaviour due to a wildfire. The results suggest that it takes more than 13 years for the temporal NDVI and NDSWIR signal to recover fully after wildfire. NDSWIR, which is associated to canopy moisture, needs a longer recovery period than NDVI, which is associated to vegetation greenness. The results also suggest that variability observed in postwildfire NDVI and NDSWIR can be explained partially by the dominant forest type: while 13 years after a fire NDVI and NDSWIR are similar for ENF and DNF, the initial impact appears to be greater on the NDVI and NDSWIR of ENF, suggesting a faster recovery by ENF.

Role of chemokines and their receptors in viral persistence and liver damage during chronic hepatitis C virus infection.

Abstract: Chemokines produced in the liver during hepatitis C virus (HCV) infection induce migration of activated T cells from the periphery to infected parenchyma. The milieu of chemokines secreted by infected hepatocytes is predominantly associated with the T-helper cell/Tc1 T cell (Th1/Tc1) response. These chemokines consist of CCL3 (macrophage inflammatory protein-1 alpha; MIP-1 alpha), CCL4 (MIP-1 beta), CCL5 (regulated on activation normal T cell expressed and secreted; RANTES), CXCL10 (interferon-gamma-inducible protein-10; IP-10), CXCL11 (interferon-inducible T-cell alpha chemoattractant; I-TAC), and CXCL9 (monokine induced by interferon gamma; Mig) and they recruit T cells expressing either CCR5 or CXCR3 chemokine receptors. Intrahepatic and peripheral blood levels of these chemokines are increased during chronic hepatitis C. The interaction between chemokines and their receptors is essential in recruiting HCV-specific T cells to control the infection. When the adaptive immune response fails in this task, non-specific T cells without the capacity to control the infection are also recruited to the liver, and these are ultimately responsible for the persistent hepatic damage. The modulation of chemokine receptor expression and chemokine secretion could be a viral escape mechanism to avoid specific T cell migration to the liver during the early phase of infection, and to maintain liver viability during the chronic phase, by impairing non-specific T cell migration. Some chemokines and their receptors correlate with liver damage, and CXCL10 (IP-10) and CXCR3 levels have shown a clinical utility as predictors of treatment response outcome. The regulation of chemokines and their receptors could be a future potential therapeutic target to decrease liver inflammation and to increase specific T cell migration to the infected liver.