Bedrock Geology and Sea-Level History of Fayetteville Quadrangle, Washington County, Arkansas

A digital map depicting the detailed bedrock geology of Fayetteville Quadrangle, Washington County, Arkansas was produced at 1:24,000 scale. This map was developed utilizing state-of-the-art Geographic Information Systems technology and represents the most detailed map of the geology of Fayetteville Quadrangle that has been produced. In addition, the stratigraphy was interpreted to develop a regional sea-level history for the quadrangle. The bedrock geology of Fayetteville Quadrangle consists of sedimentary rocks of the Mississippian and Pennsylvanian systems. The Mississippian System is represented by (in ascending order) the Boone, Batesville, Fayetteville, and Pitkin Formations. The Pennsylvanian System is represented by (in ascending order) the Hale, Bloyd, and Atoka Formations. Each of these formations has members that were mapped at 1:24,000 scale, with the exception of the Hindsville Member of the Batesville Formation. Depositional environments represented by Fayetteville Quadrangle strata range from shallow marine to terrestrial and were interpreted to reflect the interplay of tectonics and eustasy during the Mississippian-Pennsylvanian Periods. Analysis of the apparent tempo and amplitude of sea-level variations suggests tectonic processes dominated over eustatic processes during these times. Within Fayetteville Quadrangle there are also several geologic structures that deserve further investigation. These structures include faults, fractures, domes, and so-called collapse or subsidence structures

Bedrock Geology of West Fork Quadrangle, Washington County, Arkansas

A digital geologic map of West Fork quadrangle was produced at 1:24,000 scale using the geographic information system (GIS) software Maplnfo. Data regarding stratigraphic relations observed in the field were digitized onto the United States Geological Survey (USGS) digital raster graphic (DRG) of West Fork quadrangle. The geology of West Fork quadrangle consists of sedimentary rocks of the Mississippian and Pennsylvanian systems. The Fayetteville Shale and Pitkin Formation represent the Mississippian system. The Hale, Bloyd, and Atoka Formations represent the Pennsylvanian System. Each of these formations consists of members that were mapped at 1:24,000 scale, and this mapping effort represents the first time stratigraphic members were mapped utilizing digital technologies at this scale in West Fork quadrangle. The Hale Formation consists of the Cane Hill Member and the Prairie Grove Member. The Bloyd Formation consists of the Brentwood Member, the Woolsey Member, the Dye Member, and the Kessler Member. The Atoka Formation in West Fork quadrangle includes the Trace Creek Member at its base. The overlying units of the Atoka Formation occur as unnamed alternating sandstone and shale units. The most prominent geologic structure in West Fork quadrangle is the Fayetteville Fault, which crosses the northwest quarter of the quadrangle. Several additional faults are associated with a fault zone surrounding the Fayetteville Fault. Another prominent normal fault was mapped striking east-west (downthrown to the south) in the southern part of the quadrangle

Probing the Planck Scale with Proton Decay

We advocate the idea that proton decay may probe physics at the Planck scale instead of the GUT scale. This is possible because supersymmetric theories have dimension-5 operators that can induce proton decay at dangerous rates, even with R-parity conservation. These operators are expected to be suppressed by the same physics that explains the fermion masses and mixings. We present a thorough analysis of nucleon partial lifetimes in models with a string-inspired anomalous U(1)_X family symmetry which is responsible for the fermionic mass spectrum as well as forbidding R-parity violating interactions. Protons and neutrons can decay via R-parity conserving non-renormalizable superpotential terms that are suppressed by the Planck scale and powers of the Cabibbo angle. Many of the models naturally lead to nucleon decay near present limits without any reference to grand unification.Comment: 11 pages,4 figures. Revised to drop the options y=-6, -7 that are not phenomenologically viable anyway, following the revision of hep-ph/0312012 this work is based on. Conclusions unchange

TEF, Vol. 1 No. 1

https://scholarworks.sfasu.edu/tef/1000/thumbnail.jp

Infrared alignment of SUSY flavor structures

The various experimental bounds on flavor-changing interactions severely restrict the low-energy flavor structures of soft supersymmetry breaking parameters. In this work, we show that with a particular assumption of Yukawa couplings, the fermion mass and sfermion soft mass matrices are simultaneously diagonalized by common mixing matrices and we then obtain an alignment solution for the flavor problems. The required condition is generated by renormalization group evolutions and achieved at low-energy scale independently of high-energy structures of couplings. In this case, the diagonal entries of the soft scalar mass matrices are determined by gaugino and Higgs soft masses. We also discuss possible realizations of this scenario and the characteristic sparticle spectrum in the models.Comment: 18 pages, 1 figur

Softening the Supersymmetric Flavor Problem in Orbifold GUTs

The infra-red attractive force of the bulk gauge interactions is applied to soften the supersymmetric flavor problem in the orbifold SU(5) GUT of Kawamura. Then this force aligns in the infra-red regime the soft supersymmetry breaking terms out of their anarchical disorder at a fundamental scale, in such a way that flavor-changing neutral currents as well as dangerous CP-violating phases are suppressed at low energies. It is found that this dynamical alignment is sufficiently good compared with the current experimental bounds, as long as the diagonalization matrices of the Yukawa couplings are CKM-like.Comment: 15 pages,4 figure

Influence of hyper-energetic, high-fat feeding on circulating hepatokines in healthy men: a randomised crossover study [Abstract]

No description supplie

Toll-like receptor signaling adapter proteins govern spread of neuropathic pain and recovery following nerve injury in male mice.

BackgroundSpinal Toll-like receptors (TLRs) and signaling intermediaries have been implicated in persistent pain states. We examined the roles of two major TLR signaling pathways and selected TLRs in a mononeuropathic allodynia.MethodsL5 spinal nerve ligation (SNL) was performed in wild type (WT, C57BL/6) male and female mice and in male Tlr2-/-Tlr3-/-, Tlr4-/-, Tlr5-/-, Myd88-/-, Triflps2, Myd88/Triflps2, Tnf-/-, and Ifnar1-/- mice. We also examined L5 ligation in Tlr4-/- female mice. We examined tactile allodynia using von Frey hairs. Iba-1 (microglia) and GFAP (astrocytes) were assessed in spinal cords by immunostaining. Tactile thresholds were analyzed by 1- and 2-way ANOVA and the Bonferroni post hoc test was used.ResultsIn WT male and female mice, SNL lesions resulted in a persistent and robust ipsilateral, tactile allodynia. In males with TLR2, 3, 4, or 5 deficiencies, tactile allodynia was significantly, but incompletely, reversed (approximately 50%) as compared to WT. This effect was not seen in female Tlr4-/- mice. Increases in ipsilateral lumbar Iba-1 and GFAP were seen in mutant and WT mice. Mice deficient in MyD88, or MyD88 and TRIF, showed an approximately 50% reduction in withdrawal thresholds and reduced ipsilateral Iba-1. In contrast, TRIF and interferon receptor null mice developed a profound ipsilateral and contralateral tactile allodynia. In lumbar sections of the spinal cords, we observed a greater increase in Iba-1 immunoreactivity in the TRIF-signaling deficient mice as compared to WT, but no significant increase in GFAP. Removing MyD88 abrogated the contralateral allodynia in the TRIF signaling-deficient mice. Conversely, IFNβ, released downstream to TRIF signaling, administered intrathecally, temporarily reversed the tactile allodynia.ConclusionsThese observations suggest a critical role for the MyD88 pathway in initiating neuropathic pain, but a distinct role for the TRIF pathway and interferon in regulating neuropathic pain phenotypes in male mice