128 research outputs found

    Do Loading Path and Specimen Thickness Affect the Brittle Compressive Failure of Ice?

    Get PDF
    Compressive experiments were performed on square (160 mm × 160 mm) prismatic specimens of columnar-grained, S2 freshwater ice, biaxially loaded across the columns at −10°C. The work focused on brittle behavior, achieved by deforming the specimens at an applied strain rate of 4.5 ± 1.2 × 10 3s 1 in the direction of shortening. The results show that the specimen thickness (25–150 mm) has no detectable effect on the terminal failure strength of the ice. Likewise, the strength of the ice when loaded under proportional loading, where the minor stress varies during the test, was similar to that when loaded under a constant minor stress, implying that terminal failure depends only on the stress state and not on the path taken

    Does the Normal Stress Parallel to the Sliding Plane Affect the Friction of Ice upon Ice?

    Get PDF
    Sliding experiments were performed at –10 degrees C on smooth surfaces of freshwater columnar-grained S2 ice sliding against itself at a velocity of 8X10 –4 ms –1, with the purpose of examining whether normal stress parallel to the sliding plane affects frictional resistance. This component of the stress tensor was varied (0.20–1.83 MPa) using a loading system operated under biaxial compression, by orienting the sliding plane at two different angles, 26 degrees and 64 degrees, with respect to the principal loading direction. Under these conditions, no evidence was found to indicate that the normal stress in the direction of sliding affects the friction coefficient

    Comparative Genomics Analysis of a New Exiguobacterium Strain from Salar de Huasco Reveals a Repertoire of Stress-Related Genes and Arsenic Resistance

    Get PDF
    Indexación: Web of Science; Scopus.The Atacama Desert hosts diverse ecosystems including salt flats and shallow Andean lakes. Several heavy metals are found in the Atacama Desert, and microorganisms growing in this environment show varying levels of resistance/tolerance to copper, tellurium, and arsenic, among others. Herein, we report the genome sequence and comparative genomic analysis of a new Exiguobacterium strain, sp. SH31, isolated from an altiplanic shallow athalassohaline lake. Exiguobacterium sp. SH31 belongs to the phylogenetic Group II and its closest relative is Exiguobacterium sp. S17, isolated from the Argentinian Altiplano (95% average nucleotide identity). Strain SH31 encodes a wide repertoire of proteins required for cadmium, copper, mercury, tellurium, chromium, and arsenic resistance. Of the 34 Exiguobacterium genomes that were inspected, only isolates SH31 and S17 encode the arsenic efflux pump Acr3. Strain SH31 was able to grow in up to 10 mM arsenite and 100 mM arsenate, indicating that it is arsenic resistant. Further, expression of the ars operon and acr3 was strongly induced in response to both toxics, suggesting that the arsenic efflux pump Acr3 mediates arsenic resistance in Exiguobacterium sp. SH31.http://journal.frontiersin.org/article/10.3389/fmicb.2017.00456/ful

    Critical slip and time dependence in sea ice friction

    Get PDF
    Recent research into sea ice friction has focussed on ways to provide a model which maintains much of the clarity and simplicity of Amonton's law, yet also accounts for memory effects. One promising avenue of research has been to adapt the rate- and state- dependent models which are prevalent in rock friction. In such models it is assumed that there is some fixed critical slip displacement, which is effectively a measure of the displacement over which memory effects might be considered important. Here we show experimentally that a fixed critical slip displacement is not a valid assumption in ice friction, whereas a constant critical slip time appears to hold across a range of parameters and scales. As a simple rule of thumb, memory effects persist to a significant level for 10 s. We then discuss the implications of this finding for modelling sea ice friction and for our understanding of friction in general

    Understanding the limits to ethnic change: lessons from Uganda's “lost counties”

    Get PDF
    The historically constructed nature of ethnicity has become a widely accepted paradigm in the social sciences. Scholars have especially have focused on the ways modern states have been able to create and change ethnic identities, with perhaps the strongest case studies coming from colonial Africa, where the gap between strong states and weak societies has been most apparent. I suggest, however, that in order to better understand how and when ethnic change occurs it is important to examine case studies where state-directed ethnic change has failed. To rectify this oversight I examine the case of the “lost counties” of Uganda, which were transferred from the Bunyoro kingdom to the Buganda kingdom at the onset of colonial rule. I show that British attempts to assimilate the Banyoro residents in two of the lost counties were an unmitigated failure, while attempts in the other five counties were successful. I claim that the reason for these differing outcomes lies in the status of the two lost counties as part of the historic Bunyoro homeland, whereas the other five counties were both geographically and symbolically peripheral to Bunyoro. The evidence here thus suggests that varying ethnic attachments to territory can lead to differing outcomes in situations of state-directed assimilation and ethnic change

    The novel choline kinase inhibitor ICL-CCIC-0019 reprograms cellular metabolism and inhibits cancer cell growth.

    Get PDF
    The glycerophospholipid phosphatidylcholine is the most abundant phospholipid species of eukaryotic membranes and essential for structural integrity and signaling function of cell membranes required for cancer cell growth. Inhibition of choline kinase alpha (CHKA), the first committed step to phosphatidylcholine synthesis, by the selective small-molecule ICL-CCIC-0019, potently suppressed growth of a panel of 60 cancer cell lines with median GI50 of 1.12 μM and inhibited tumor xenograft growth in mice. ICL-CCIC-0019 decreased phosphocholine levels and the fraction of labeled choline in lipids, and induced G1 arrest, endoplasmic reticulum stress and apoptosis. Changes in phosphocholine cellular levels following treatment could be detected non-invasively in tumor xenografts by [18F]-fluoromethyl-[1,2–2H4]-choline positron emission tomography. Herein, we reveal a previously unappreciated effect of choline metabolism on mitochondria function. Comparative metabolomics demonstrated that phosphatidylcholine pathway inhibition leads to a metabolically stressed phenotype analogous to mitochondria toxin treatment but without reactive oxygen species activation. Drug treatment decreased mitochondria function with associated reduction of citrate synthase expression and AMPK activation. Glucose and acetate uptake were increased in an attempt to overcome the metabolic stress. This study indicates that choline pathway pharmacological inhibition critically affects the metabolic function of the cell beyond reduced synthesis of phospholipids

    The novel choline kinase inhibitor ICL-CCIC-0019 reprograms cellular metabolism and inhibits cancer cell growth

    Get PDF
    The glycerophospholipid phosphatidylcholine is the most abundant phospholipid species of eukaryotic membranes and essential for structural integrity and signaling function of cell membranes required for cancer cell growth. Inhibition of choline kinase alpha (CHKA), the first committed step to phosphatidylcholine synthesis, by the selective small-molecule ICL-CCIC-0019, potently suppressed growth of a panel of 60 cancer cell lines with median GI50 of 1.12 μM and inhibited tumor xenograft growth in mice. ICL-CCIC-0019 decreased phosphocholine levels and the fraction of labeled choline in lipids, and induced G1 arrest, endoplasmic reticulum stress and apoptosis. Changes in phosphocholine cellular levels following treatment could be detected non-invasively in tumor xenografts by [18F]-fluoromethyl-[1,2–2H4]-choline positron emission tomography. Herein, we reveal a previously unappreciated effect of choline metabolism on mitochondria function. Comparative metabolomics demonstrated that phosphatidylcholine pathway inhibition leads to a metabolically stressed phenotype analogous to mitochondria toxin treatment but without reactive oxygen species activation. Drug treatment decreased mitochondria function with associated reduction of citrate synthase expression and AMPK activation. Glucose and acetate uptake were increased in an attempt to overcome the metabolic stress. This study indicates that choline pathway pharmacological inhibition critically affects the metabolic function of the cell beyond reduced synthesis of phospholipids
    corecore