Nuclear Anapole Moments

Nuclear anapole moments are parity-odd, time-reversal-even E1 moments of the electromagnetic current operator. Although the existence of this moment was recognized theoretically soon after the discovery of parity nonconservation (PNC), its experimental isolation was achieved only recently, when a new level of precision was reached in a measurement of the hyperfine dependence of atomic PNC in 133Cs. An important anapole moment bound in 205Tl also exists. In this paper, we present the details of the first calculation of these anapole moments in the framework commonly used in other studies of hadronic PNC, a meson exchange potential that includes long-range pion exchange and enough degrees of freedom to describe the five independent $S-P$ amplitudes induced by short-range interactions. The resulting contributions of pi-, rho-, and omega-exchange to the single-nucleon anapole moment, to parity admixtures in the nuclear ground state, and to PNC exchange currents are evaluated, using configuration-mixed shell-model wave functions. The experimental anapole moment constraints on the PNC meson-nucleon coupling constants are derived and compared with those from other tests of the hadronic weak interaction. While the bounds obtained from the anapole moment results are consistent with the broad ``reasonable ranges'' defined by theory, they are not in good agreement with the constraints from the other experiments. We explore possible explanations for the discrepancy and comment on the potential importance of new experiments.Comment: 53 pages; 10 figures; revtex; submitted to Phys Rev

Modern microwave methods in solid state inorganic materials chemistry: from fundamentals to manufacturing

No abstract available

Surface and Temporal Biosignatures

Recent discoveries of potentially habitable exoplanets have ignited the prospect of spectroscopic investigations of exoplanet surfaces and atmospheres for signs of life. This chapter provides an overview of potential surface and temporal exoplanet biosignatures, reviewing Earth analogues and proposed applications based on observations and models. The vegetation red-edge (VRE) remains the most well-studied surface biosignature. Extensions of the VRE, spectral "edges" produced in part by photosynthetic or nonphotosynthetic pigments, may likewise present potential evidence of life. Polarization signatures have the capacity to discriminate between biotic and abiotic "edge" features in the face of false positives from band-gap generating material. Temporal biosignatures -- modulations in measurable quantities such as gas abundances (e.g., CO2), surface features, or emission of light (e.g., fluorescence, bioluminescence) that can be directly linked to the actions of a biosphere -- are in general less well studied than surface or gaseous biosignatures. However, remote observations of Earth's biosphere nonetheless provide proofs of concept for these techniques and are reviewed here. Surface and temporal biosignatures provide complementary information to gaseous biosignatures, and while likely more challenging to observe, would contribute information inaccessible from study of the time-averaged atmospheric composition alone.Comment: 26 pages, 9 figures, review to appear in Handbook of Exoplanets. Fixed figure conversion error

Perspectives on Continental Rifting Processes From Spatiotemporal Patterns of Faulting and Magmatism in the Rio Grande Rift, USA

Analysis of spatiotemporal patterns of faulting and magmatism in the Rio Grande rift (RGR) in New Mexico and Colorado, USA, yields insights into continental rift processes, extension accommodation mechanisms, and rift evolution models. We combine new apatite (U‐Th‐Sm)/He and zircon (U‐Th)/He thermochronometric data with previously published thermochronometric data to assess the timing of fault initiation, magnitudes of fault exhumation, and growth and linkage patterns of rift faults. Thermal history modeling of these data reveals contemporaneous rift initiation at ca. 25 Ma in both the northern and southern RGR with continued fault initiation, growth, and linkage progressing from ca. 25 to ca. 15 Ma. The central RGR, however, shows no evidence of Cenozoic fault‐related exhumation as observed with thermochronometry and instead reveals extension accommodated through Late Cenozoic magmatic injection. Furthermore, faulting in the northern and southern RGR occurs along an approximately north‐south strike, whereas magmatism in the central RGR occurs along the northeast to southwest trending Jemez lineament. Differences in deformation orientation and rift accommodation along strike appear to be related to crustal and lithospheric properties, suggesting that rift structure and geometry are at least partly controlled by inherited lithospheric‐scale architecture. We propose an evolutionary model for the RGR that involves initiation of fault‐accommodated extension by oblique strain followed by block rotation of the Colorado Plateau, where extension in the RGR is accommodated by faulting (southern and northern RGR) and magmatism (central RGR). This study highlights different processes related to initiation, geometry, extension accommodation, and overall development of continental rifts.Plain Language SummaryWe identify patterns of faulting and volcanism in the Rio Grande rift (RGR) in the western United States to better understand how continental rifts evolve. Using methods for documenting rock cooling ages (thermochronology), we determined that rifting began around 25 million years ago (Ma) in both the northern and southern RGR. Rift faults continued to develop and grow for another 10 to 15 million years. The central RGR, however, shows that rift extension occurred through volcanic activity both as eruptions at the surface and as magma injection below the surface since ~15 Ma. Interestingly, RGR faulting in the north and south parts of the rift occurs on a north‐south line, while volcanism in the central RGR is along a northeast to southwest line. The differences in the location and orientation of faulting and volcanic activity may be related to the thickness of the lithosphere beneath different parts of the rift. Using these patterns of faulting and magmatism, we propose the RGR evolved through a combination of (1) oblique strain—extension diagonal to the rift and (2) block rotation—where the Colorado Plateau is the rotating block. This detailed study highlights different processes related to the accommodation of extension and the overall development of continental rifts.Key PointsInitiation of the Rio Grande rift appears to be synchronous ~25 Ma and does not support a northward propagation modelExtension is accommodated by faulting in the northern and southern Rio Grande rift and by magmatic injection in the central Rio Grande riftDifferent rift accommodation mechanisms may be controlled by preexisting weaknesses and lithospheric properties (i.e., thickness)Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/152704/1/tect21226.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/152704/2/wrcr21226-sup-00001-2019TC005635-SI.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/152704/3/tect21226_am.pd

Insulin Resistance Exacerbates Genetic Predisposition to Nonalcoholic Fatty Liver Disease in Individuals Without Diabetes

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149741/1/hep41353.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149741/2/hep41353_am.pd

T Cells from Programmed Death-1 Deficient Mice Respond Poorly to Mycobacterium tuberculosis Infection

Programmed Death-1 (PD-1; CD279) receptor molecule is widely believed to be a negative regulator predominantly expressed by exhausted/activated mouse T cells. Upon interaction with its ligands, PD-L1 and PD-L2, PD-1 inhibits activation of T cells and cytokine production, which has been documented in various viral and fungal infections as well as in vitro studies. Therefore, inhibition of T cell responses by PD-1 resulted in disease resistance in a variety of mouse infection models studied heretofore.Here, we report that PD-1 deficient (PD-1(-/-)) mice infected with Mycobacterium tuberculosis (M. tb) H37Rv by the aerosol route have increased susceptibility as compared with their wild type littermates. Surprisingly, M. tb antigen-specific T cell proliferation was dramatically reduced in PD-1 deficient animals compared with wild-type littermates, and this was due to increased numbers of regulatory T cells (Tregs) and recruitment of mesenchymal stem cells. Furthermore, PD-1(-/-) mice exhibited decreases in the autophagy-induced LC3-B marker protein in macrophages.Our findings suggest that PD-1 does not play an inhibitory role during M. tb infection and instead promotes mycobacterial clearance in mice

Evolution and diversity of Rickettsia bacteria

Background: Rickettsia are intracellular symbionts of eukaryotes that are best known for infecting and causing serious diseases in humans and other mammals. All known vertebrate-associated Rickettsia are vectored by arthropods as part of their life-cycle, and many other Rickettsia are found exclusively in arthropods with no known secondary host. However, little is known about the biology of these latter strains. Here, we have identified 20 new strains of Rickettsia from arthropods, and constructed a multi-gene phylogeny of the entire genus which includes these new strains.Results: We show that Rickettsia are primarily arthropod-associated bacteria, and identify several novel groups within the genus. Rickettsia do not co-speciate with their hosts but host shifts most often occur between related arthropods. Rickettsia have evolved adaptations including transmission through vertebrates and killing males in some arthropod hosts. We uncovered one case of horizontal gene transfer among Rickettsia, where a strain is a chimera from two distantly related groups, but multi-gene analysis indicates that different parts of the genome tend to share the same phylogeny.Conclusion: Approximately 150 million years ago, Rickettsia split into two main clades, one of which primarily infects arthropods, and the other infects a diverse range of protists, other eukaryotes and arthropods. There was then a rapid radiation about 50 million years ago, which coincided with the evolution of life history adaptations in a few branches of the phylogeny. Even though Rickettsia are thought to be primarily transmitted vertically, host associations are short lived with frequent switching to new host lineages. Recombination throughout the genus is generally uncommon, although there is evidence of horizontal gene transfer. A better understanding of the evolution of Rickettsia will help in the future to elucidate the mechanisms of pathogenicity, transmission and virulence

Biology of Francisella tularensis Subspecies holarctica Live Vaccine Strain in the Tick Vector Dermacentor variabilis

Background: The c-proteobacterium Francisella tularensis is the etiologic agent of seasonal tick-transmitted tularemia epizootics in rodents and rabbits and of incidental infections in humans. The biology of F. tularensis in its tick vectors has not been fully described, particularly with respect to its quanta and duration of colonization, tissue dissemination, and transovarial transmission. A systematic study of the colonization of Dermacentor variabilis by the F. tularensis subsp. holarctica live vaccine strain (LVS) was undertaken to better understand whether D. variabilis may serve as an inter-epizootic reservoir for F. tularensis. Methodology/Principal Findings: Colony-reared larva, nymph, and adult D. variabilis were artificially fed LVS via glass capillary tubes fitted over the tick mouthparts, and the level of colonization determined by microbial culture. Larvae and nymphs were initially colonized with 8.860.8610 1 and 1.160.03610 3 CFU/tick, respectively. Post-molting, a significant increase in colonization of both molted nymphs and adults occurred, and LVS persisted in 42 % of molted adult ticks at 126 days post-capillary tube feeding. In adult ticks, LVS initially colonized the gut, disseminated to hemolymph and salivary glands by 21 days, and persisted up to 165 days. LVS was detected in the salivary secretions of adult ticks after four days post intra-hemocoelic inoculation, and LVS recovered from salivary gland was infectious to mice with an infectious dose 50 % of 3 CFU. LVS in gravid female ticks colonized via the intra-hemocoelic route disseminated to the ovaries and then t