Lateral deformation and defect resistance of compacted silica glass: Quantification of the scratching hardness of brittle glasses

Human interaction with multimedia devices occurs predominantly over inorganic glass surfaces. Scratch-induced damage is a primary limitation in the suitability of brittle glasses for this purpose. However, neither truly quantitative data nor a topo-chemical understanding of the underlying deformation process which would allow for the development of improved materials is presently available. Here, we present lateral nano-indentation experiments for determining the work of deformation which is involved in the process of glass scratching. Using a series of hot-compressed vitreous silica with mild degrees of structural densification, we derive relations between quantitative scratch hardness and the underlying glass structure. We show that Young's modulus provides a clear rational for the observed variations in scratching hardness. In the specific case of silica, the energy needed to generate a certain scratch volume corresponds to roughly one tenth of Young's modulus. This relationship formally indicates that only about one tenth of the bonds which are involved in the deformation process are broken in its course. However, comparison with a more complex glass material with a certain fraction of two dimensional structural units and a strong ability for topological adaption to local stress clearly indicates a deviation from this behavior. This opens a pathway to topo-chemical engineering of scratch-resistant glasses

The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J-SSCG 2016)

Background and purposeThe Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J-SSCG 2016), a Japanese-specific set of clinical practice guidelines for sepsis and septic shock created jointly by the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine, was first released in February 2017 and published in the Journal of JSICM, [2017; Volume 24 (supplement 2)] https://doi.org/10.3918/jsicm.24S0001 and Journal of Japanese Association for Acute Medicine [2017; Volume 28, (supplement 1)] http://onlinelibrary.wiley.com/doi/10.1002/jja2.2017.28.issue-S1/issuetoc.This abridged English edition of the J-SSCG 2016 was produced with permission from the Japanese Association of Acute Medicine and the Japanese Society for Intensive Care Medicine.MethodsMembers of the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine were selected and organized into 19 committee members and 52 working group members. The guidelines were prepared in accordance with the Medical Information Network Distribution Service (Minds) creation procedures. The Academic Guidelines Promotion Team was organized to oversee and provide academic support to the respective activities allocated to each Guideline Creation Team. To improve quality assurance and workflow transparency, a mutual peer review system was established, and discussions within each team were open to the public. Public comments were collected once after the initial formulation of a clinical question (CQ) and twice during the review of the final draft. Recommendations were determined to have been adopted after obtaining support from a two-thirds (> 66.6%) majority vote of each of the 19 committee members.ResultsA total of 87 CQs were selected among 19 clinical areas, including pediatric topics and several other important areas not covered in the first edition of the Japanese guidelines (J-SSCG 2012). The approval rate obtained through committee voting, in addition to ratings of the strengths of the recommendation, and its supporting evidence were also added to each recommendation statement. We conducted meta-analyses for 29 CQs. Thirty-seven CQs contained recommendations in the form of an expert consensus due to insufficient evidence. No recommendations were provided for five CQs.ConclusionsBased on the evidence gathered, we were able to formulate Japanese-specific clinical practice guidelines that are tailored to the Japanese context in a highly transparent manner. These guidelines can easily be used not only by specialists, but also by non-specialists, general clinicians, nurses, pharmacists, clinical engineers, and other healthcare professionals

Comparison of Thermal Stability of Epitaxially Grown (La0.5Sr0.5)CoO3 and (La0.6Sr0.4)MnO3 Thin Films Deposited on Si Substrate

Thermal stability of bottom electrode thin films (La0.5Sr0.5)CoO3 (LSCO) and (La0.6Sr0.4)MnO3 (LSMO) were investigated. The crystallization and surface morphology of the heterostructure were characterized using x-ray diffraction and atomic force microscopy. Resistivity of the LSCO thin film was 25 cm. However, the resistivity of LSCO thin film increases sharply with annealing temperature. The LSMO thin film has high resistivity (100 mcm). The film does not decompose after thermal processing at 900 °C. To confirm thermal stability, we examined the effect of post annealing at various temperatures on the morphology and resistivity. Results showed that LSMO has higher thermal stability than that of LSCO.autho

The juvenile myoclonic epilepsy-related protein EFHC1 interacts with the redox-sensitive TRPM2 channel linked to cell death.

The transient receptor potential M2 channel (TRPM2) is the Ca(2+)-permeable cation channel controlled by cellular redox status via β-NAD(+) and ADP-ribose (ADPR). TRPM2 activity has been reported to underlie susceptibility to cell death and biological processes such as inflammatory cell migration and insulin secretion. However, little is known about the intracellular mechanisms that regulate oxidative stress-induced cell death via TRPM2. We report here a molecular and functional interaction between the TRPM2 channel and EF-hand motif-containing protein EFHC1, whose mutation causes juvenile myoclonic epilepsy (JME) via mechanisms including neuronal apoptosis. In situ hybridization analysis demonstrates TRPM2 and EFHC1 are coexpressed in hippocampal neurons and ventricle cells, while immunoprecipitation analysis demonstrates physical interaction of the N- and C-terminal cytoplasmic regions of TRPM2 with the EFHC1 protein. Coexpression of EFHC1 significantly potentiates hydrogen peroxide (H(2)O(2))- and ADPR-induced Ca(2+) responses and cationic currents via recombinant TRPM2 in HEK293 cells. Furthermore, EFHC1 enhances TRPM2-conferred susceptibility of HEK293 cells to H(2)O(2)-induced cell death, which is reversed by JME mutations. These results reveal a positive regulatory action of EFHC1 on TRPM2 activity, suggesting that TRPM2 contributes to the expression of JME phenotypes by mediating disruptive effects of JME mutations of EFHC1 on biological processes including cell death