Mixed lipid bilayers with locally varying spontaneous curvature and bending

A model of lipid bilayers made of a mixture of two lipids with different average compositions on both leaflets, is developed. A Landau hamiltonian describing the lipid-lipid interactions on each leaflet, with two lipidic fields $\psi_1$ and $\psi_2$, is coupled to a Helfrich one, accounting for the membrane elasticity, via both a local spontaneous curvature, which varies as $C_0+C_1(\psi_1-\psi_2)/2$, and a bending modulus equal to $\kappa_0+\kappa_1(\psi_1+\psi_2)/2$. This model allows us to define curved patches as membrane domains where the asymmetry in composition, $\psi_1-\psi_2$, is large, and thick and stiff patches where $\psi_1+\psi_2$ is large. These thick patches are good candidates for being lipidic rafts, as observed in cell membranes, which are composed primarily of saturated lipids forming a liquid-ordered domain and are known to be thick and flat nano-domains. The lipid-lipid structure factors and correlation functions are computed for globally spherical membranes and planar ones. Phase diagrams are established, within a Gaussian approximation, showing the occurrence of two types of Structure Disordered phases, with correlations between either curved or thick patches, and an Ordered phase, corresponding to the divergence of the structure factor at a finite wave vector. The varying bending modulus plays a central role for curved membranes, where the driving force $\kappa_1C_0^2$ is balanced by the line tension, to form raft domains of size ranging from 10 to 100~nm. For planar membranes, raft domains emerge via the cross-correlation with curved domains. A global picture emerges from curvature-induced mechanisms, described in the literature for planar membranes, to coupled curvature- and bending-induced mechanisms in curved membranes forming a closed vesicle

Physical and Mechanical Properties of Thermally Cracked Andesite Under Pressure

International audienceThe efects of thermal crack damage on the physical properties and rupture processes of andesite were investigated under triaxial deformation at room temperature. Thermal cracking was induced by slowly heating and cooling samples. The efects of heat treatment temperatures ranging between 500 °C and 1100 °C on the P-wave velocities and on the microstructure were investigated. Then, the mechanical properties of andesite samples treated at 930 °C were investigated under triaxial stress at room temperature using constant strain rate tests and conining pressures ranging between 0 and 30 MPa. Similar triaxial experiments were conducted on non-heat-treated samples. Our results show that: (1) for heat treatments at temperatures below 500 °C, no signiicant changes in the physical properties are observed; (2) for heat treatments in the temperature range of 500-1100 °C, crack density increases; and (3) thermal cracking has no inluence on the onset of dilatancy but increases the strength of the heat-treated samples. This last result is counterintuitive, but seems to be linked with the presence of a small fraction of clay (3%) in the non-heat-treated andesite. Indeed, for heat treatment above 500 °C, some clay melting is observed and contributes to sealing the longest cracks

Steroid modulation of neurogenesis: Focus on radial glial cells in zebrafish

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Implementation of an image recognition algorithm on the DM6446 DaVinci Processor

We are developing an Alternative and Augmentative Communication (AAC) portable device called PictoBar which is used in speech rehabilitation therapy. PictoBar recognizes barcodes and images, such as pictograms and pictures. Then it plays a sound message associated with the recognized barcode or image. This paper describes the development of the image recognition algorithm and its implementation using Codec Engine framework on a DM6446 DaVinci processor

Portable augmentative and alternative communication device with pictogram recognition functionality

The field of electronic aid for disabled people has been growing constantly with many new innovations being added every year. The need for electronic aid in alternative and augmentative communication (ACC) is becoming increasingly important. Devices which describe extra ways of helping people who find it hard to communicate by speech or writing are being introduced into the market every year. A next generation device for alternative and augmentative communication which shall be used in rehabilitation therapies for speech-impaired people is being developed at EPFL-IMT. This device includes smart image processing capabilities to offer new possibilities to train users and to let them express in a more intuitive and interactive manner. The user acquires an image (pictogram, picture or barcode). The device recognizes the image and plays its corresponding pre-recorded audio sequence. This device is intended to be used by language re-education professionals and specialized educators in the treatment of people affected by pathologies such as aphasia, autism, trisomy or mental handicaps

Mitochondrial dysfunction and pathophysiology of Charcot-Marie-Tooth disease involving GDAP1 mutations

Charcot-Marie-Tooth (CMT) disease represents a large group of clinically and genetically heterogeneous disorders leading to inherited peripheral neuropathies affecting motor and sensory neurons. Mutations in the ganglioside-induced differentiation-associated-protein 1 gene (GDAP1), which encodes a protein anchored to the mitochondrial outer membrane, are usually associated with the recessive forms of CMT disease and only rarely with the autosomal dominant forms. The function of GDAP1 is not fully understood but it plays a role in mitochondrial dynamics by promoting fission events. We present an overview of GDAP1 and the corresponding protein together with the complete spectrum of the 41 gene mutations described so far. We examine the relationship between the genotype and the phenotype in the various forms of CMT disease related to GDAP1 mutations, and discuss the pathophysiological hypotheses that link peripheral neuropathies to mitochondrial dysfunction and GDAP1 mutations. The meta-analysis of the literature reveals the great heterogeneity of phenotypic presentations and shows that the recessive forms of CMT disease, i.e. CMT4A and AR-CMT2, are far more severe than the dominant form, i.e. CMT2K. Among patients with recessive forms of the disease, those carrying truncating mutations are more seriously affected, often becoming wheelchair-bound before the end of the third decade. At the neuronal level, GDAP1 mutations may lead to perturbed axonal transport and impaired energy production as in other neurodegenerative diseases due to mutations in genes involved in mitochondrial dynamics

A Universal Bleeding Risk Score in Native and Allograft Kidney Biopsies: A French Nationwide Cohort Study

BackgroundThe risk of bleeding after percutaneous biopsy in kidney transplant recipients is usually low but may vary. A pre-procedure bleeding risk score in this population is lacking.MethodsWe assessed the major bleeding rate (transfusion, angiographic intervention, nephrectomy, hemorrhage/hematoma) at 8 days in 28,034 kidney transplant recipients with a kidney biopsy during the 2010-2019 period in France and compared them to 55,026 patients with a native kidney biopsy as controls.ResultsThe rate of major bleeding was low (angiographic intervention: 0.2%, hemorrhage/hematoma: 0.4%, nephrectomy: 0.02%, blood transfusion: 4.0%). A new bleeding risk score was developed (anemia = 1, female gender = 1, heart failure = 1, acute kidney failure = 2 points). The rate of bleeding varied: 1.6%, 2.9%, 3.7%, 6.0%, 8.0%, and 9.2% for scores 0 to 5, respectively, in kidney transplant recipients. The ROC AUC was 0.649 (0.634-0.664) in kidney transplant recipients and 0.755 (0.746-0.763) in patients who had a native kidney biopsy (rate of bleeding: from 1.2% for score = 0 to 19.2% for score = 5).ConclusionsThe risk of major bleeding is low in most patients but indeed variable. A new universal risk score can be helpful to guide the decision concerning kidney biopsy and the choice of inpatient vs. outpatient procedure both in native and allograft kidney recipients

Methyl donor deficiency impairs fatty acid oxidation through PGC-1α hypomethylation and decreased ER-α, ERR-α, and HNF-4α in the rat liver

BACKGROUND & AIMS: Folate and cobalamin are methyl donors needed for the synthesis of methionine, which is the precursor of S-adenosylmethionine, the substrate of methylation in epigenetic, and epigenomic pathways. Methyl donor deficiency produces liver steatosis and predisposes to metabolic syndrome. Whether impaired fatty acid oxidation contributes to this steatosis remains unknown.METHODS: We evaluated the consequences of methyl donor deficient diet in liver of pups from dams subjected to deficiency during gestation and lactation. RESULTS: The deprived rats had microvesicular steatosis, with increased triglycerides, decreased methionine synthase activity, S-adenosylmethionine, and S-adenosylmethionine/S-adenosylhomocysteine ratio. We observed no change in apoptosis markers, oxidant and reticulum stresses, and carnityl-palmitoyl transferase 1 activity, and a decreased expression of SREBP-1c. Impaired beta-oxidation of fatty acids and carnitine deficit were the predominant changes, with decreased free and total carnitines, increased C14:1/C16 acylcarnitine ratio, decrease of oxidation rate of palmitoyl-CoA and palmitoyl-L-carnitine and decrease of expression of novel organic cation transporter 1, acylCoA-dehydrogenase and trifunctional enzyme subunit alpha and decreased activity of complexes I and II. These changes were related to lower protein expression of ER-α, ERR-α and HNF-4α, and hypomethylation of PGC-1α co-activator that reduced its binding with PPAR-α, ERR-α, and HNF-4α. CONCLUSIONS: The liver steatosis resulted predominantly from hypomethylation of PGC1-α, decreased binding with its partners and subsequent impaired mitochondrial fatty acid oxidation. This link between methyl donor deficiency and epigenomic deregulations of energy metabolism opens new insights into the pathogenesis of fatty liver disease, in particular, in relation to the fetal programming hypothesis

The Fourteenth Data Release of the Sloan Digital Sky Survey: First Spectroscopic Data from the extended Baryon Oscillation Spectroscopic Survey and from the second phase of the Apache Point Observatory Galactic Evolution Experiment

The fourth generation of the Sloan Digital Sky Survey (SDSS-IV) has been in operation since July 2014. This paper describes the second data release from this phase, and the fourteenth from SDSS overall (making this, Data Release Fourteen or DR14). This release makes public data taken by SDSS-IV in its first two years of operation (July 2014-2016). Like all previous SDSS releases, DR14 is cumulative, including the most recent reductions and calibrations of all data taken by SDSS since the first phase began operations in 2000. New in DR14 is the first public release of data from the extended Baryon Oscillation Spectroscopic Survey (eBOSS); the first data from the second phase of the Apache Point Observatory (APO) Galactic Evolution Experiment (APOGEE-2), including stellar parameter estimates from an innovative data driven machine learning algorithm known as "The Cannon"; and almost twice as many data cubes from the Mapping Nearby Galaxies at APO (MaNGA) survey as were in the previous release (N = 2812 in total). This paper describes the location and format of the publicly available data from SDSS-IV surveys. We provide references to the important technical papers describing how these data have been taken (both targeting and observation details) and processed for scientific use. The SDSS website (www.sdss.org) has been updated for this release, and provides links to data downloads, as well as tutorials and examples of data use. SDSS-IV is planning to continue to collect astronomical data until 2020, and will be followed by SDSS-V.Comment: SDSS-IV collaboration alphabetical author data release paper. DR14 happened on 31st July 2017. 19 pages, 5 figures. Accepted by ApJS on 28th Nov 2017 (this is the "post-print" and "post-proofs" version; minor corrections only from v1, and most of errors found in proofs corrected