The Geology of Switzerland Township, Monroe County, Ohio

Author Institution: Ohio Department of Natural Resources, Division of Geological Survey, Columbus 1

The decomposition of cyanate ions in aqueous solution

Not availabl

Postal card from Thomas Arkle Clark

Postal card concerning a copy of the catalogue for Utah Agricultural College

The geology of Switzerland Township, Monroe County, Ohio

Reprinted from the Ohio Journal of Science, vol. 53, no. 1, pp. 1-13, January 1953

Geothermometric Constraints on the Thermal Architecture, Metamorphism, and Exhumation of the Northern Range, Trinidad

The Northern Range of Trinidad is composed of Mesozoic passive margin sedimentary rocks that underwent ductile deformation and subgreenschist- to greenschist-facies metamorphism in the early Miocene. Previous studies suggested a two-stage formation of the Northern Range between the Caribbean and South American plates: an initial collision drove mountain building in the Miocene and subsequent strike-slip plate motion preferentially exhumed the western segment, producing a westward increase in the metamorphic thermal gradient. However, these studies were not able to resolve whether this gradient was discrete or continuous so the tectonic model awaits testing. In this study we use Raman spectroscopy on carbonaceous material (RSCM), an empirical geothermometer, to constrain peak temperatures across the Northern Range with a greater resolution than was available in previous studies. The RSCM temperatures show an abrupt increase from 337°C ± 10°C in the east to 442°C ± 16°C west of Chupara Point, where a range-cutting fault (Chupara Fault) had been inferred in previous geologic mapping campaigns. Thus, the discrete thermal discontinuity of ~100°C very likely represents the Chupara Fault. Our RSCM-derived peak metamorphic temperatures are 50°C to 100°C higher than those from previous estimates, requiring revision of tectonic models to account for deeper burial and greater exhumation. The peak metamorphic conditions determined here, and the deduced timing of faulting from published thermochronological data, are consistent with the two-stage tectonic model proposed in previous studies

Occupancy and Abundance of American Badgers and Piute Ground Squirrels in the Sagebrush-Steppe: Implications of the Fire-Cheatgrass Cycle

Sagebrush-steppe is experiencing vast changes due to biological invasions and changing fire characteristics. Understanding how these changes influence functionally important animals is essential for ecosystem management. American Badgers (Taxidea taxus) are an apex predator and ecosystem engineer within sagebrush ecosystems. Piute Ground Squirrels (Urocitellus mollis) are also an ecosystem engineer as well as an essential prey source for many predators.  Our objective was to evaluate the relative importance of large-scale changes, abiotic processes, and biotic processes on badgers and ground squirrels. We samples 163 1-ha plots across a gradient of burn histories within a 1,962 km2 area in Southern Idaho, USA. At each plot, we characterized ground squirrel and badger occupancy, ground squirrel relative abundance, and many environmental variables. We used information-theoretic approaches to evaluate competing hypotheses concerning occupancy of ground squirrels and badgers, and ground squirrel relative abundance. Results suggest that ground squirrel occupancy was positively associated with abiotic characteristics (e.g., higher precipitation and finer textured soil). Badger occupancy was positively associated with ground squirrel occupancy and agriculture. Relative abundance of ground squirrels was positively associated with finer textured soils, but negatively associated with cheatgrass (Bromus tectorum), fire frequency, agriculture and shrubs. Managers can focus restoration efforts on areas with high cheatgrass and shrub cover, if ground squirrels are a management objective. These results support previous hypotheses suggesting abiotic processes are important for herbivore occupancy. However, we provide support that a combination of abiotic, biotic and disturbance processes are important for mesocarnivore occupancy and herbivore abundance

A novel mechanism of autophagic cell death in dystrophic muscle regulated by P2RX7 receptor large-pore formation and HSP90

<div><p>P2RX7 is an ATP-gated ion channel, which can also exhibit an open state with a considerably wider permeation. However, the functional significance of the movement of molecules through the large pore (LP) and the intracellular signaling events involved are not known. Here, analyzing the consequences of P2RX7 activation in primary myoblasts and myotubes from the <i>Dmd^mdx</i> mouse model of Duchenne muscular dystrophy, we found ATP-induced P2RX7-dependent autophagic flux, leading to CASP3-CASP7-independent cell death. P2RX7-evoked autophagy was triggered by LP formation but not Ca²⁺ influx or MAPK1-MAPK3 phosphorylation, 2 canonical P2RX7-evoked signals. Phosphoproteomics, protein expression inference and signaling pathway prediction analysis of P2RX7 signaling mediators pointed to HSPA2 and HSP90 proteins. Indeed, specific HSP90 inhibitors prevented LP formation, LC3-II accumulation, and cell death in myoblasts and myotubes but not in macrophages. Pharmacological blockade or genetic ablation of <i>p2rx7</i> also proved protective against ATP-induced death of muscle cells, as did inhibition of autophagy with 3-MA. The functional significance of the P2RX7 LP is one of the great unknowns of purinergic signaling. Our data demonstrate a novel outcome—autophagy—and show that molecules entering through the LP can be targeted to phagophores. Moreover, we show that in muscles but not in macrophages, autophagy is needed for the formation of this LP. Given that P2RX7-dependent LP and HSP90 are critically interacting in the ATP-evoked autophagic death of dystrophic muscles, treatments targeting this axis could be of therapeutic benefit in this debilitating and incurable form of muscular dystrophy.</p></div

Store-operated calcium entry contributes to abnormal Ca²⁺ signalling in dystrophic mdx mouse myoblasts

Sarcolemma damage and activation of various calcium channels are implicated in altered Ca2+ homeostasis in muscle fibres of both Duchenne muscular dystrophy (DMD) sufferers and in the mdx mouse model of DMD. Previously we have demonstrated that also in mdx myoblasts extracellular nucleotides trigger elevated cytoplasmic Ca2+ concentrations due to alterations of both ionotropic and metabotropic purinergic receptors. Here we extend these findings to show that the mdx mutation is associated with enhanced store-operated calcium entry (SOCE). Substantially increased rate of SOCE in mdx myoblasts in comparison to that in control cells correlated with significantly elevated STIM1 protein levels. These results reveal that mutation in the dystrophin-encoding Dmd gene may significantly impact cellular calcium response to metabotropic stimulation involving depletion of the intracellular calcium stores followed by activation of the store-operated calcium entry, as early as in undifferentiated myoblasts. These data are in agreement with the increasing number of reports showing that the dystrophic pathology resulting from dystrophin mutations may be developmentally regulated. Moreover, our results showing that aberrant responses to extracellular stimuli may contribute to DMD pathogenesis suggest that treatments inhibiting such responses might alter progression of this lethal disease

Focused Exhumation Along Megathrust Splay Faults in Prince William Sound, Alaska

Megathrust splay faults are a common feature of accretionary prisms and can be important for generating tsunamis during some subduction zone earthquakes. Here we provide new evidence from Alaska that megathrust splay faults have been conduits for focused exhumation in the last 5 Ma. In most of central Prince William Sound, published and new low-temperature thermochronology data indicate little to no permanent rock uplift over tens of thousands of earthquake cycles. However, in southern Prince William Sound on Montague Island, apatite (U–Th)/He ages are as young as 1.1 Ma indicating focused and rapid rock uplift. Montague Island lies in the hanging wall of the Patton Bay megathrust splay fault system, which ruptured during the 1964 M9.2 earthquake and produced ∼9 m of vertical uplift. Recent geochronology and thermochronology studies show rapid exhumation within the last 5 Ma in a pattern similar to the coseismic uplift in the 1964 earthquake, demonstrating that splay fault slip is a long term (3–5 my) phenomena. The region of slower exhumation correlates with rocks that are older and metamorphosed and constitute a mechanically strong backstop. The region of rapid exhumation consists of much younger and weakly metamorphosed rocks, which we infer are mechanically weak. The region of rapid exhumation is separated from the region of slow exhumation by the newly identified Montague Strait Fault. New sparker high-resolution bathymetry, seismic reflection profiles, and a 2012 Mw4.8 earthquake show this feature as a 75-km-long high-angle active normal fault. There are numerous smaller active normal(?) faults in the region between the Montague Strait Fault and the splay faults. We interpret this hanging wall extension as developing between the rapidly uplifting sliver of younger and weaker rocks on Montague Island from the essentially fixed region to the north. Deep seismic reflection profiles show the splay faults root into the subduction megathrust where there is probable underplating. Thus the exhumation and extension in the hanging wall are likely driven by underplating along the megathrust décollement, thickening in the overriding plate and a change in rheology at the Montague Strait Fault to form a structural backstop. A comparison with other megathrust splay faults around the world shows they have significant variability in their characteristics, and the conditions for their formation are not particularly unique

P2X7 purinoceptor alterations in dystrophic mdx mouse muscles: Relationship to pathology and potential target for treatment.

Open AccessDuchenne muscular dystrophy (DMD) is a lethal inherited muscle disorder. Pathological characteristics of DMD skeletal muscles include, among others, abnormal Ca2 homeostasis and cell signalling. Here, in the mdx mouse model of DMD, we demonstrate significant P2X7 receptor abnormalities in isolated primary muscle cells and cell lines and in dystrophic muscles in vivo. P2X7 mRNA expression in dystrophic muscles was significantly up-regulated but without alterations of specific splice variant patterns. P2X7 protein was also up-regulated and this was associated with altered function of P2X7 receptors producing increased responsiveness of cytoplasmic Ca2 and extracellular signal-regulated kinase (ERK) phosphorylation to purinergic stimulation and altered sensitivity to NAD. Ca2 influx and ERK signalling were stimulated by ATP and BzATP, inhibited by specific P2X7 antagonists and insensitive to ivermectin, confirming P2X7 receptor involvement. Despite the presence of pannexin-1, prolonged P2X7 activation did not trigger cell permeabilization to propidium iodide or Lucifer yellow. In dystrophic mice, in vivo treatment with the P2X7 antagonist Coomassie Brilliant Blue reduced the number of degeneration–regeneration cycles in mdx skeletal muscles. Altered P2X7 expression and function is thus an important feature in dystrophic mdx muscle and treatments aiming to inhibit P2X7 receptor might slow the progression of this disease