Zobrazeno 1 - 10
of 35
pro vyhledávání: '"Richard H. Watkins"'
Autor:
Dawn J. Mazzatti, Jason M. Roper, Peter C. Keng, William M. Maniscalco, Michael A. O'Reilly, Richard H. Watkins
Publikováno v:
American Journal of Physiology-Lung Cellular and Molecular Physiology. 286:L1045-L1054
It is well established that hyperoxia injures and kills alveolar endothelial and type I epithelial cells of the lung. Although type II epithelial cells remain morphologically intact, it remains unclear whether they are also damaged. DNA integrity was
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d925c83762299b14689022426f83aa47
https://doi.org/10.1152/ajplung.00376.2003
https://doi.org/10.1152/ajplung.00376.2003
Publikováno v:
American Journal of Physiology-Renal Physiology. 284:F399-F410
Membrane-bound carbonic anhydrase (CA) facilitates acidification in the kidney. Although most hydratase activity is considered due to CA IV, some in the basolateral membranes could be attributed to CA XII. Indeed, CA IV is glycosylphosphatidylinosito
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::25856440ee0f57875c727e29e0abec76
https://doi.org/10.1152/ajprenal.00370.2001
https://doi.org/10.1152/ajprenal.00370.2001
Publikováno v:
American Journal of Physiology-Lung Cellular and Molecular Physiology. 283:L991-L1001
Coordinated proliferation of lung cells is required for normal lung growth and differentiation. Chronic injury to developing lung may disrupt normal patterns of cell proliferation. To examine patterns of cell proliferation in injured developing lungs
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9122f37a4e874ea50095f14346e6f309
https://doi.org/10.1152/ajplung.00050.2002
https://doi.org/10.1152/ajplung.00050.2002
Autor:
Richard H. Watkins, Gloria S. Pryhuber, Abhay J. Bhatt, William M. Maniscalco, Leon A. Metlay, Heidie Huyck
Publikováno v:
American Journal of Respiratory and Critical Care Medicine. 164:1971-1980
An abnormal pulmonary vasculature may be an important component of bronchopulmonary dysplasia (BPD). We examined human infant lung for the endothelial cell marker PECAM-1 and for angiogenic factors and their receptors. Lung specimens were collected p
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::35d6dc22ebf0ac7a9c82c34e47cca2c2
https://doi.org/10.1164/ajrccm.164.10.2101140
https://doi.org/10.1164/ajrccm.164.10.2101140
Autor:
Richard H. Watkins, George J. Schwartz, Ann M. Kittelberger, Cornelia A. Winkler, William M. Maniscalco
Publikováno v:
American Journal of Physiology-Renal Physiology. 280:F895-F903
Carbonic anhydrase (CA) IV facilitates renal acidification by catalyzing the dehydration of luminal H2CO3. CA IV is expressed in proximal tubules, medullary collecting ducts, and A-intercalated cells of the mature rabbit kidney (Schwartz GJ, Kittelbe
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::17828db95d688919bd77be7a34b94440
https://doi.org/10.1152/ajprenal.2001.280.5.f895
https://doi.org/10.1152/ajprenal.2001.280.5.f895
Autor:
Gloria S. Pryhuber, William M. Maniscalco, Michael B. LoMonaco, Carl T. D'Angio, Heidie Huyck, Raymond B. Baggs, Rhonda J. Staversky, Richard H. Watkins, Michael A. O'Reilly
Publikováno v:
Laboratory Investigation. 80:1845-1854
Exposure of the lung to severe hyperoxia induces terminal transferase dUTP end-labeling (TUNEL) indicative of DNA damage or apoptosis and increases expression of the tumor suppressor p53 and of members of the Bcl-2 gene family. Because cell survival
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4d2173e1bcf4a15c6a069a057a749328
https://doi.org/10.1038/labinvest.3780195
https://doi.org/10.1038/labinvest.3780195
Publikováno v:
Pediatric Research. 47:606-613
Although the endothelial cell is the most abundant cell type in the differentiated lung, little is known about regulation of lung developmental vasculogenesis. Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and angiogenic fa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::abbd0612c1b24e7eb9f76da6b1a2bd5b
https://doi.org/10.1203/00006450-200005000-00009
https://doi.org/10.1203/00006450-200005000-00009
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 19:777-785
Hyperoxic lung injury results in decreased cell proliferation, DNA damage, and cell death. Because the cyclin-dependent kinase inhibitor p21(Cip1/WAF1) (p21) inhibits cell proliferation in G1/S, enhances DNA repair, and regulates apoptosis in some ce
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11509a2cc4df517aa6cd66a2347bd832
https://doi.org/10.1165/ajrcmb.19.5.3200
https://doi.org/10.1165/ajrcmb.19.5.3200
Autor:
Stuart Horowitz, Stephen E. Welty, Marie Gamache, Bruno Piedboeuf, Carl J. Johnston, Patrice E. Poubelle, Sylvie Bélanger, Richard H. Watkins
Publikováno v:
Free Radical Biology and Medicine. 24:1446-1454
An important component of the pathophysiologic response to hyperoxia (O2) is pulmonary inflammation, although the roles of specific inflammatory mediators during pulmonary O2 toxicity are not completely known. Interleukin-1 (IL-1) is an early inflamm
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a1cd99c1df303e5c27daa17c34ba2cb5
https://doi.org/10.1016/s0891-5849(98)00002-1
https://doi.org/10.1016/s0891-5849(98)00002-1
Autor:
Robert A. Sinkin, Stuart Horowitz, William M. Maniscalco, Patricia R. Chess, Liana Toia, Richard H. Watkins
Publikováno v:
American Journal of Physiology-Lung Cellular and Molecular Physiology. 274:L599-L609
Cellular fibronectin (cFN) expression is characteristic of injured tissues. Unlike plasma FN, cFN mRNA often contains the EIIIA or EIIIB domains. We examined the lung cell-specific expression of total cFN mRNA and the EIIIA and EIIIB splice variants
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::42548f7564e0883865c967082c67a7d3
https://doi.org/10.1152/ajplung.1998.274.4.l599
https://doi.org/10.1152/ajplung.1998.274.4.l599