Physiol. Genomics -- Table of Contents (October 2009, 39 [2])

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Editorial Focus:

Christina Runge-Samuelson and Michael Olivier: The rocky road toward clinical genetic testing: insights into the physio-genetic basis of hearing loss
Physiol. Genomics 39: 83-84, 2009. First published August 25, 2009; doi:10.1152/physiolgenomics.00125.2009 [Full Text] [PDF]

Call for Papers: Comparative Genomics:

M. Carey Satterfield, Gwonhwa Song, Kelli J. Kochan, Penny K. Riggs, Rebecca M. Simmons, Christine G. Elsik, David L. Adelson, Fuller W. Bazer, Huaijun Zhou, and Thomas E. Spencer: Discovery of candidate genes and pathways in the endometrium regulating ovine blastocyst growth and conceptus elongation
Physiol. Genomics 39: 85-99, 2009. First published August 18, 2009; doi:10.1152/physiolgenomics.00001.2009 [Abstract] [Full Text] [PDF] [Supplemental Tables]

Hunter Wessells, Chris J. Sullivan, Yoshiaki Tsubota, Karen L. Engel, Bryan Kim, N. Eric Olson, Daniel Thorner, and Kanchan Chitaley: Transcriptional profiling of human cavernosal endothelial cells reveals distinctive cell adhesion phenotype and role for claudin 11 in vascular barrier function
Physiol. Genomics 39: 100-108, 2009. First published July 21, 2009; doi:10.1152/physiolgenomics.90354.2008 [Abstract] [Full Text] [PDF] [Supplemental Figures and Tables]

Research Articles:

Lee D. Roberts, Sam Virtue, Antonio Vidal-Puig, Andrew W. Nicholls, and Julian L. Griffin: Metabolic phenotyping of a model of adipocyte differentiation
Physiol. Genomics 39: 109-119, 2009. First published July 14, 2009; doi:10.1152/physiolgenomics.90365.2008 [Abstract] [Full Text] [PDF]

Hirokazu Matsumura, Kiyoshi Kano, Caralina Marín de Evsikova, James A. Young, Patsy M. Nishina, Jürgen K. Naggert, and Kunihiko Naito: Transcriptome analysis reveals an unexpected role of a collagen tyrosine kinase receptor gene, Ddr2, as a regulator of ovarian function
Physiol. Genomics 39: 120-129, 2009. First published August 11, 2009; doi:10.1152/physiolgenomics.00073.2009 [Abstract] [Full Text] [PDF] [Supplemental Tables]

Cover Caption:

Cover

Cover: Experimental pulmonary embolism (PE) causes right ventricular heart strain and acute inflammation followed by tissue remodeling in rats. The right ventricular outflow tract of the heart appears translucent 6 wk after PE compared with the apex region (top inset). Histological changes, shown with Masson's trichrome stain, indicate a transition between heart muscle (red myocytes in cross section) and the remodeling tissue in the PE outflow region, where myofibroblast and monocyte cells are present (dark nuclei), fibrotic collagen deposition (blue) occurs, and few myocytes (red) remain (top). In contrast, the outflow tract and apex of the normal hearts are red throughout, and the heart (bottom inset) and histology show normal myocyte structure in cross section (red) with normal collagen (blue) distribution (bottom). DNA microarray analysis demonstrated major transcriptional changes that were focused in the outflow region compared with the apex of the PE hearts or the same regions of the normal heart (right; red and green indicate up- and downregulation of gene expression in normal apex, normal outflow, PE apex, and PE outflow; top 20 red genes, bottom 20 green genes, and 15 genes at the red-green boundary are shown). Consistent with myocyte depletion, genes for cellular respiration and energy metabolism were decreased, and genes for leukocyte cell adhesion, extracellular matrix proteins, and signal pathways for wound healing were increased in the PE outflow tract. For details, see Zagorski J, Obraztsova M, Gellar MA, Kline JA, and Watts JA. Transcriptional changes in right ventricular tissues are enriched in the outflow tract compared with the apex during chronic pulmonary embolism in rats. Physiol Genomics 39: 61–71, 2009.