Image processing mini manual

The intent is to provide an introduction to the image processing capabilities available at the Langley Research Center (LaRC) Central Scientific Computing Complex (CSCC). Various image processing software components are described. Information is given concerning the use of these components in the Data Visualization and Animation Laboratory at LaRC

Carbonic anhydrase inhibition selectively prevents amyloid b neurovascular mitochondrial toxicity

Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer’s disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid b (Ab)-mediated onset of apoptosis in the mouse brain. In this study, we used MTZ and, for the first time, the analog CAI acetazolamide (ATZ) in neuronal and cerebral vascular cells challenged with Ab, to clarify their protective effects and mitochondrial molecular mechanism of action. The CAIs selectively inhibited mitochondrial dysfunction pathways induced by Ab, without affecting metabolic function. ATZ was effective at concentrations 10 times lower than MTZ. Both MTZ and ATZ prevented mitochondrial membrane depolarization and H2O2 generation, with no effects on intracellular pH or ATP production. Importantly, the drugs did not primarily affect calcium homeostasis. This work suggests a new role for carbonic anhydrases (CAs) in the Ab-induced mitochondrial toxicity associated with AD and cerebral amyloid angiopathy (CAA), and paves the way to AD clinical trials for CAIs, FDA-approved drugs with a well-known profile of brain delivery

Protective action of n-3 fatty acids on benzo[a]pyrene-induced apoptosis through the plasma membrane remodeling-dependent NHE1 pathway

International audiencePlasma membrane is an early target of polycyclic aromatic hydrocarbons (PAH). We previously showed that the PAH prototype, benzo[a]pyrene (B[a]P), triggers apoptosis via DNA damage-induced p53 activation (genotoxic pathway) and via remodeling of the membrane cholesterol-rich microdomains called lipid rafts, leading to changes in pH homeostasis (non-genotoxic pathway). As omega-3 (n-3) fatty acids can affect membrane composition and function or hamper in vivo PAH genotoxicity, we hypothesized that addition of physiologically relevant levels of polyunsaturated n-3 fatty acids (PUFAs) might interfere with B[a]P-induced toxicity. The effects of two major PUFAs, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), were tested on B[a]P cytotoxicity in the liver epithelial cell line F258. Both PUFAs reduced B[a]P-induced apoptosis. Surprisingly, pre-treatment with DHA increased the formation of reactive B[a]P metabolites, resulting in higher levels of B[a]P-DNA adducts. EPA had no apparent effect on B[a]P metabolism or related DNA damage. EPA and DHA prevented B[a]P-induced apoptotic alkalinization by affecting Na(+)/H(+) exchanger 1 activity. Thus, the inhibitory effects of omega-3 fatty acids on B[a]P-induced apoptosis involve a non-genotoxic pathway associated with plasma membrane remodeling. Our results suggest that dietary omega-3 fatty acids may have marked effects on the biological consequences of PAH exposure

Modelling of early diagenesis of lacustrine carbonates associated with Mg-silicates

International audienceDiagenetic processes occuring in time and space are critical in the evolution of sedimentary rocks. They need to be assessed to improve our abilities for palaeoenvironmental interpretations. A numerical model was developed with the reactive transport code CrunchFlow to assess the chemical and physical processes occurring during the early diagenesis of lacustrine carbonates formed in rift settings, using as a case study the carbonate sediments associated with Mg-silicates of the alkaline volcanic crater lake, Dziani Dzaha. The model relies on the solid phase compositions of the first meter of sediments, the porosity, the pore water chemistry and an age model for the sediment based on radiocarbon measurements. Chemical and isotope analyses reveal the inflow of magmatic CO 2 and intense microbial methanogenesis activity in the lake. The alkaline pH of the lake induce oversaturation of porewaters relative to aragonite, hydromagnesite and saponite. Carbonates form close to equilibrium and dominate the mineralogy of the shallow sediment while kinetic effects inhibit the formation of saponite that precipitate only at depth. Magmatic CO 2 inflow and microbial degradation of organic matter cause a decrease of pH that destabilized hydromagnesite. The model brings new insights on the palaeoenviroments and on the early diagenetic processes leading to the lacustrine carbonates formed in rift settings. It quantifies the mechanisms involved in the early diagenetic processes (e.g. input of mantellic CO 2) without which minerals reactivity, pH and porosity would not be described over the sediment depth. This study represents a first step towards the forward modeling of the evolution of the solid and fluid phases of carbonate sediments from their deposition at sediment surface to their current settings in the sedimentary column