A revised Litostragraphic Framework for the Southern Yucca Mountain Area, Nye County, Nevada

An informal, revised lithostratigraphic framework for the southern Yucca Mountain area, Nevada has been developed to accommodate new information derived from subsurface investigations of the Nye County Early Warning Drilling Program. Lithologies penetrated by recently drilled boreholes at locations between Stagecoach Road and Highway 95 in southern Nye County include Quaternary and Pliocene alluvium and alluvial breccia, Miocene pyroclastic flow deposits and intercalated lacustrine siltstone and claystone sequences, early Miocene to Oligocene pre-volcanic sedimentary rocks, and Paleozoic strata. Of the 37 boreholes currently drilled, 21 boreholes have sufficient depth, spatial distribution, or traceable pyroclastic flow, pyroclastic fall, and reworked tuff deposits to aid in the lateral correlation of lithostrata. Medial and distal parts of regional pyroclastic flow deposits of Miocene age can be correlated with the Timber Mountain, Paintbrush, Crater Flat, and Tram Ridge Groups. Rocks intercalated between these regional pyroclastic flow deposits are substantially thicker than in the central part of Yucca Mountain, particularly near the downthrown side of major faults and along the southern extent of exposures at Yucca Mountain

Economic Impact of Alternative Growth Promotant Strategies on the United States Beef Industry.

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Chronic tooth pulp inflammation induces persistent expression of phosphorylated ERK (pERK) and phosphorylated p38 (pp38) in trigeminal subnucleus caudalis

Background: Extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase are transiently phosphorylated (activated) in the spinal cord and trigeminal nucleus by acute noxious stimuli. Acute stimulation of dental pulp induces short-lived ERK activation in trigeminal subnucleus caudalis (Vc), and p38 inhibition attenuates short-term sensitization in Vc induced by acute pulpal stimulation. We have developed a model to study central changes following chronic inflammation of dental pulp that induces long-term sensitization. Here, we examine the effects of chronic inflammation and acute stimulation on the expression of phosphorylated ERK (pERK), phosphorylated p38 (pp38) and Fos in Vc. Results: Chronic inflammation alone induced bilateral expression of pERK and pp38 in Vc, but did not induce Fos expression. Stimulation of both non-inflamed and inflamed pulps significantly increased pERK and pp38 bilaterally; expression was greatest in inflamed, stimulated animals, and was similar following 10-min and 60-min stimulation. Stimulation for 60 min, but not 10 min, induced Fos in ipsilateral Vc; Fos expression was significantly greater in inflamed, stimulated animals. pERK was present in both neurons and astrocytes; pp38 was present in neurons and other non-neuronal, non-astrocytic cell types. Conclusions: This study provides the first demonstration that chronic inflammation of tooth pulp induces persistent bilateral activation of ERK and p38 within Vc, and that this activation is further increased by acute stimulation. This altered activity in intracellular signaling is likely to be linked to the sensitization that is seen in our animal model and in patients with pulpitis. Our data indicate that pERK and pp38 are more accurate markers of central change than Fos expression. In our model, localization of pERK and pp38 within specific cell types differs from that seen following acute stimulation. This may indicate specific roles for different cell types in the induction and maintenance of pulpitic and other types of pain