Transient and steady state creep response of ice I and magnesium sulfate hydrate eutectic aggregates

Using uniaxial compression creep experiments, we characterized the transient and steady state deformation behaviors of eutectic aggregates of system ice I and MgSO4 • 11H2O (MS11; meridianiite), which has significance because of its likely presence on moons of the outer solar system. Synthetic samples of eutectic liquid bulk composition, which produce eutectic colonies containing 0.35–0.50 volume fraction MS11, were tested as functions of colony size and lamellar spacing, temperature (230–250 K), and confining pressure (0.1 and 50 MPa) to strains ≤ 0.2. Up to a differential stress of 6 MPa, the ice I‐MS11 aggregates display an order of magnitude higher effective viscosity and higher stress sensitivity than do aggregates of pure polycrystalline ice at the same conditions. The creep data and associated microstructural observations demonstrate, however, that the aggregates are additionally more brittle than pure ice, approaching rate‐independent plasticity that includes rupture of the hydrate phase at 6–8 MPa, depending on the scale of the microstructure. Microstructures of deformed samples reveal forms of semibrittle flow in which the hydrate phase fractures while the ice phase deforms plastically. Semibrittle flow in the icy shell of a planetary body would truncate the lithospheric strength envelope and thereby decrease the depth to the brittle‐ductile transition by 55% and reduce the failure limit for compressional surface features from 10 to ∼6 MPa. A constitutive equation that includes eutectic colony boundary sliding and intracolony flow is used to describe the steady state rheology of the eutectic aggregates

p50–NF-κB Complexes Partially Compensate for the Absence of RelB: Severely Increased Pathology in p50−/−relB−/−Double-knockout Mice

RelB-deficient mice (relB−/−) have a complex phenotype including multiorgan inflammation and hematopoietic abnormalities. To examine whether other NF-κB/Rel family members are required for the development of this phenotype or have a compensatory role, we have initiated a program to generate double-mutant mice that are deficient in more than one family member. Here we report the phenotypic changes in relB−/− mice that also lack the p50 subunit of NFκB (p50−/−). The inflammatory phenotype of p50−/−relB−/− double-mutant mice was markedly increased in both severity and extent of organ involvement, leading to premature death within three to four weeks after birth. Double-knockout mice also had strongly increased myeloid hyperplasia and thymic atrophy. Moreover, B cell development was impaired and, in contrast to relB−/− single knockouts, B cells were absent from inflammatory infiltrates. Both p50−/− and heterozygous relB−/+ animals are disease-free. In the absence of the p50, however, relB−/+ mice (p50−/−relB−/+) had a mild inflammatory phenotype and moderate myeloid hyperplasia. Neither elevated mRNA levels of other family members, nor increased κB-binding activities of NF-κB/Rel complexes could be detected in single- or double-mutant mice compared to control animals. These results indicate that the lack of RelB is, in part, compensated by other p50-containing complexes and that the “classical” p50-RelA–NF-κB activity is not required for the development of the inflammatory phenotype

Oral splints for patients with temporomandibular disorders or bruxism : a systematic review and economic evaluation

This project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 24, No. 7. See the NIHR Journals Library website for further project information.Peer reviewedPublisher PD

Oral splints for temporomandibular disorder or bruxism : a systematic review

Funded by: This project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment Programme (Project number: 16/146/06). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.Peer reviewedPublisher PD