37 research outputs found
The Aragonian and Vallesian high-resolution micromammal succession from the Calatayud-MontalbĂĄn Basin (AragĂłn, Spain)
We present an updated taxonomy and faunal distribution of the micromammal fossil record from the Aragonian and lower Vallesian of the Calatayud-MontalbĂĄn Basin. The analysed record includes the orders Rodentia, Eulipotyphla, and Lagomorpha. The pattern of species turnover showsseven major faunal events,which are correlated to major climate changes based on marine stable oxygen and carbon isotope records. The episodesÎŽ 18OMi-2 and Mi-3 are significantly correlated with major micromammal turnover at the boundaries between lower and middle Aragonian and middle and upper Aragonian, respectively. Our resultssupport the existence of a selective turnover during the Aragonian and lower Vallesian
Inside-Out Regulation of ICAM-1 Dynamics in TNF-α-Activated Endothelium
Background: During transendothelial migration, leukocytes use adhesion molecules, such as ICAM-1, to adhere to the endothelium. ICAM-1 is a dynamic molecule that is localized in the apical membrane of the endothelium and clusters upon binding to leukocytes. However, not much is known about the regulation of ICAM-1 clustering and whether membrane dynamics are linked to the ability of ICAM-1 to cluster and bind leukocyte integrins. Therefore, we studied the dynamics of endothelial ICAM-1 under non-clustered and clustered conditions. Principal Findings: Detailed scanning electron and fluorescent microscopy showed that the apical surface of endothelial cells constitutively forms small filopodia-like protrusions that are positive for ICAM-1 and freely move within the lateral plane of the membrane. Clustering of ICAM-1, using anti-ICAM-1 antibody-coated beads, efficiently and rapidly recruits ICAM-1. Using fluorescence recovery after photo-bleaching (FRAP), we found that clustering increased the immobile fraction of ICAM-1, compared to non-clustered ICAM-1. This shift required the intracellular portion of ICAM-1. Moreover, biochemical assays showed that ICAM-1 clustering recruited beta-actin and filamin. Cytochalasin B, which interferes with actin polymerization, delayed the clustering of ICAM-1. In addition, we could show that cytochalasin B decreased the immobile fraction of clustered ICAM-1-GFP, but had no effect on non-clustered ICAM-1. Also, the motor protein myosin-II is recruited to ICAM-1 adhesion sites and its inhibition increased the immobile fraction of both non-clustered and clustered ICAM-1. Finally, blocking Rac1 activation, the formation of lipid rafts, myosin-II activity or actin polymerization, but not Src, reduced the adhesive function of ICAM-1, tested under physiological flow conditions. Conclusions: Together, these findings indicate that ICAM-1 clustering is regulated in an inside-out fashion through the actin cytoskeleton. Overall, these data indicate that signaling events within the endothelium are required for efficient ICAM-1-mediated leukocyte adhesio
Rapport ESBL-Attributieanalyse (ESBLAT) : Op zoek naar de bronnen van antibioticaresistentie bij de mens
Samenvatting ESBL-Attributieanalyse (ESBLAT) : Op zoek naar de bronnen van antibioticaresistentie bij de mens
Samenvatting over een project rondom ESBL's. Doelstellingen waren: vaststellen wat de bijdrage is van alle ESBL-reservoirs aan het dragerschap en infecties bij mensen en vaststellen wat de transmissieroutes zijn vanuit deze reservoirs naar de (geĂŻnfecteerde) mens
Biostratigraphical and palaeoecological implications of the small mammal assemblage from the late early Miocene of Montalvos2, Teruel Basin, Spain
Biostratigraphy or biochronology? Lessons from the Early and Middle Miocene small Mammal Events in Europe
Quantitative High-Pressure Liquid Chromatography-Fluorescence Determination of Some Important Lower Fatty Acids in Lake Sediments
For the quantitative determination of traces of fatty acids in pore water, several gas and liquid chromatographic methods were tested and discussed. Direct determination by gas-liquid chromatography with the use of formic acid-saturated carrier gas was found to be the least laborious method, but it is only recommended for the determination of volatile acids such as acetate and higher homologs. For the determination of lactate and formate, a derivatization procedure is necessary. The determination of these acids as phenacyl or benzyl esters was complicated by contaminants in the reagents. For this reason, a high-pressure liquid chromatography procedure with 4-bromomethyl-7-methoxycoumarin as a fluorescent labeling reagent is preferred. With this method, lactic, acetic, and formic acids could be demonstrated simultaneously at the nanogram level in 5-ml samples. Profiles of these acids in the sediment of Lake Vechten were measured, and they showed correlations with sulfate-reducing and methanogenic bacterial activities
Calcium signaling regulates translocation and activation of Rac
Rac is activated in response to various stimuli including growth factors and by adhesion to the extracellular matrix. However, how these stimuli ultimately result in Rac activation is poorly understood. The increase in intracellular calcium [Ca2+]i represents a ubiquitous second messenger system in cells, linking receptor activation to downstream signaling pathways. Here we show that elevation of [Ca2+]i, either artificially or by thrombin receptor activation, potently induces Rac activation. Lamellipodia formation induced by artificial elevation of [Ca2+]i is blocked by inhibition of Rac signaling, indicating that calcium-induced cytoskeletal changes are controlled by the activation of Rac. Calcium-dependent Rac activation was dependent on the activation of a conventional protein kinase C. Furthermore, both increased [Ca2+]i and protein kinase C activation induce phosphorylation of RhoGDI alpha and induce the translocation of cytosolic Rac to the plasma membrane. Intracellular calcium signaling may thus contribute to the intracellular localization and activation of Rac to regulate the cytoskeletal changes in response to receptor stimulatio