Paleotectonic Investigations of the Permian System in the United States

(A) Allegheny region, by Henry L. Berryhill, Jr (B) Gulf Coast region, by Eleanor J. Crosby (C) West Texas Permian basin region, by Steven S. Oriel, Donald A. Myers, and Eleanor J. Crosby (D) Northeastern New Mexico and Texas-Oklahoma Panhandles, by George H. Dixon (E) Oklahoma, by Marjorie E. MacLachlan (F) Central Midcontinent region, by Melville R. Mudge (G) Eastern Wyoming, eastern Montana, and the Dakotas, by Edwin K. Maughan (H) Middle Rocky Mountains and northeastern Great Basin, by Richard P. Sheldon, Earl R. Cressman, Thomas M. Cheney, and Vincent E. McKelvey (I) Western Colorado, southern Utah, and northwestern New Mexico, by Walter E. Hallgarth (J) Arizona and western New Mexico, by Edwin D. McKee (K) West Coast region, by Keith B. Ketner References cited (284pp) This professional paper is a supplementary volume to Paleotectonic Maps of the Permian System by McKee, Oriel, and others (1967), published by the U.S. Geological Survey as Miscellaneous Geologic Investigations Map I-450. The I-450 publication consists of 20 plates isopach and lithofacies maps, cross sections to accompany the maps, and interpretive and environmental maps and a summary of available geological information on each part of the Permian Period, an interpretation or reconstruction of Permian history, and brief discussions of environment, tectonics, and other significant features. The present volume explains and documents the maps and conclusions presented there. This study of the Permian System was made by 15 geologists, who were individually responsible for coverage of 18 regions. These authors are: Henry L. Berryhill, Jr. • Walter E. Hallgarth • Vincent E. McKelvey • Thomas M. Cheney • Keith B. Ketner • Melville R. Mudge • Earl R. Cressman • Marjorie E. MacLachlan • Donald A. Myers • Eleanor J. Crosby • Edwin K. Maughan • Steven S. Oriel • George H. Dixon • Edwin D. McKee • Richard P. Sheldon The Permian System of the 18 regions is described in 11 chapters. Each chapter presents an analysis of the basic data used, points out significant trends, and presents an interpretation, as well as alternative explanations where each occur, for the region concerned. The chapters and accompanying illustrations were coordinated and assembled by E. J. Crosby, E. D. McKee, W. W. Mallory, E. K. Maughan, and S. S. Oriel. Descriptive and documentary data are organized according to region, from east to west, and according to chronological sequence. Each chapter discusses, in order, rocks that underlie the Permian, the several intervals or divisions of the Permian (from oldest to youngest (table 1, in pocket)), and, finally, the rock units that directly overlie the Permian. Stratigraphic problems, the nature of contacts, trends in thickness and lithology, possible sources of sediment, environments of deposition, and paleotectonic implications of each interval are treated in that order

Reversal of cardiac hypertrophy and fibrosis from pressure overload by tetrahydrobiopterin - Efficacy of recoupling nitric oxide synthase as a therapeutic strategy

Background-Sustained pressure overload induces pathological cardiac hypertrophy and dysfunction. Oxidative stress linked to nitric oxide synthase (NOS) uncoupling may play an important role. We tested whether tetrahydrobiopterin (BH4) can recouple NOS and reverse preestablished advanced hypertrophy, fibrosis, and dysfunction. Methods and Results-C57/Bl6 mice underwent transverse aortic constriction for 4 weeks, increasing cardiac mass (190%) and diastolic dimension (144%), lowering ejection fraction (-46%), and triggering NOS uncoupling and oxidative stress. Oral BH4 was then administered for 5 more weeks of pressure overload. Without reducing loading, BH4 reversed hypertrophy and fibrosis, recoupled endothelial NOS, lowered oxidant stress, and improved chamber and myocyte function, whereas untreated hearts worsened. If BH4 was started at the onset of pressure overload, it did not suppress hypertrophy over the first week when NOS activity remained preserved even in untreated transverse aortic constriction hearts. However, BH4 stopped subsequent remodeling when NOS activity was otherwise declining. A broad antioxidant, Tempol, also reduced oxidant stress yet did not recouple NOS or reverse worsened hypertrophy/fibrosis from sustained transverse aortic constriction. Microarray analysis revealed very different gene expression profiles for both treatments. BH4 did not enhance net protein kinase G activity. Finally, transgenic mice with enhanced BH4 synthesis confined to endothelial cells were unprotected against pressure overload, indicating that exogenous BH4 targeted myocytes and fibroblasts. Conclusions-NOS recoupling by exogenous BH4 ameliorates preexisting advanced cardiac hypertrophy/fibrosis and is more effective than a less targeted antioxidant approach (Tempol). These data highlight the importance of myocyte NOS uncoupling in hypertrophic heart disease and support BH4 as a potential new approach to treat this disorder