Zobrazeno 1 - 10
of 55
pro vyhledávání: '"William M. Hull"'
Autor:
Chong Jai Kim, Tinnakorn Chaiworapongsa, Roberto Romero, William M. Hull, Jeffrey A. Whitsett, Ricardo Gomez, Moshe Mazor, Joon-Seok Hong
Publikováno v:
The Journal of Maternal-Fetal & Neonatal Medicine. 21:652-659
The fetus is thought to play a central role in the onset of labor. Pulmonary surfactant protein (SP)-A, secreted by the maturing fetal lung, has been implicated in the mechanisms initiating parturition in mice. The present study was conducted to dete
Autor:
William M. Hull, Jeffrey A. Whitsett, Roberto Romero, Tinnakorn Chaiworapongsa, Joon Seok Hong
Publikováno v:
The Journal of Maternal-Fetal & Neonatal Medicine. 21:663-670
Pulmonary surfactant is a complex molecule of lipids and proteins synthesized and secreted by type II alveolar cells into the alveolar epithelial lining. Both lipid and protein components are essential for lung function in postnatal life. Infection i
Autor:
Susan E. Wert, William M. Hull, Kwon Sik Park, Yohei Matsuzaki, Yan Xu, Machiko Ikegami, Valérie Besnard, Jeffrey A. Whitsett
Publikováno v:
The Journal of Immunology. 177:527-537
The role of Stat3 in the maintenance of pulmonary homeostasis following adenoviral-mediated lung injury was assessed in vivo. Stat3 was selectively deleted from bronchiolar and alveolar epithelial cells in Stat3(DeltaDelta) mice. Although lung histol
Autor:
Lawrence M. Nogee, Frances V. White, Tami H Garmany, Michael Dean, Aaron Hamvas, Jeffrey A. Whitsett, William M. Hull, Michael A. Moxley
Publikováno v:
Pediatric Research. 59:801-805
Mutations in the gene encoding the ATP binding cassette transporter member A3 (ABCA3) are associated with fatal surfactant deficiency. ABCA3 lines the limiting membrane of lamellar bodies within alveolar type-II cells, suggesting a role in surfactant
Autor:
Shizuo Akira, William M. Hull, Machiko Ikegami, Anne-Karina T. Perl, Kiyoshi Takeda, Susan E. Wert, Jeffrey A. Whitsett, Isamu Hokuto, Mitsuhiro Yoshida
Publikováno v:
Journal of Clinical Investigation. 113:28-37
Acute lung injury syndromes remain common causes of morbidity and mortality in adults and children. Cellular and physiologic mechanisms maintaining pulmonary homeostasis during lung injury remain poorly understood. In the present study, the Stat-3 ge
Publikováno v:
Journal of Histochemistry & Cytochemistry. 50:651-660
Immunoreactive surfactant protein-D (SP-D) was assessed in human fetal, newborn, and adult tissues. In the fetal lung, SP-D was detected on airway surfaces by 10 weeks' gestation, staining increasing in the distal airways, decreasing in the proximal
Publikováno v:
American Journal of Physiology-Lung Cellular and Molecular Physiology. 281:L697-L703
Both surfactant protein (SP) D and granulocyte-macrophage colony-stimulating factor (GM-CSF) influence pulmonary surfactant homeostasis, with the deficiency of either protein causing marked accumulation of surfactant phospholipids in lung tissues and
Autor:
Lawrence M. Nogee, Robert P. Baughman, Joseph F. Tomashefski, Susan E. Wert, William M. Hull, Jeffrey A. Whitsett, Alan S. Brody, Raouf S. Amin
Publikováno v:
The Journal of Pediatrics. 139:85-92
Objective: To determine the contribution of surfactant protein abnormalities to the development of chronic lung injury in a familial form of interstitial lung disease. Study design: An 11-year-old girl, her sister, and their mother who were diagnosed
Publikováno v:
American Journal of Respiratory and Critical Care Medicine. 161:973-981
Inability to produce surfactant protein B (SP-B) causes fatal neonatal respiratory disease. A frame-shift mutation (121ins2) is the predominant but not exclusive cause of disease. To determine the range of mechanisms responsible for SP-B deficiency,
Autor:
Pierre Aymard, Claude Houdayer, M Tredano, Ruurd M. van Elburg, Jeffrey A. Whitsett, Matthias Griese, Michel Bahuau, Ageeth G. Kaspers, William M. Hull, Jacques Elion, Luc J I Zimmermann
Publikováno v:
Human mutation, 14(6), 502-509. Wiley-Liss Inc.
Several human respiratory disorders have been linked to an abnormality of pulmonary surfactant synthesis or turnover. Among those conditions, hereditary deficiency in the hydrophobic surfactant protein B (SP-B) has been recognized as a rare cause of