www.atsjournals.org/doi/pdf/10.1165/rcmb.2003-0290OC
www.atsjournals.org/doi/pdf/10.1165/rcmb.F296
www.atsjournals.org/doi/pdf/10.1513/pats.200904-017RM
Clara cell
They are also known by their descriptive name of "bronchiolar exocrine cells".[2] Name[edit] Club cells were previously called Clara cells as they were originally described by their namesake, Max Clara in 1937. One of the main functions of club cells is to protect the bronchiolar epithelium. Mechanism[edit] The respiratory bronchioles represent the transition from the conducting portion to the respiratory portion of the respiratory system. Role in disease[edit] Club cells contain tryptase, which is believed to be responsible for cleaving the hemagglutinin surface protein of influenza A virus, thereby activating it and causing the symptoms of flu.[7] When the l7Rn6 protein is disrupted in mice, these mice display severe emphysema at birth as a result of disorganization of the Golgi apparatus and formation of aberrant vesicular structures within clara cells.[8] Malignant club cells are also seen in bronchioalveolar carcinoma of the lung See also[edit] References[edit] External links[edit]
File:Hematopoiesis simple.svg
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Figure 1
Resolution: standard / high The distal airway epithelium contains alveolar type I and type II cells and Clara cells, which possess various pumps and channels that achieve clearance of edema fluid. Sodium is transported through channels on the apical membrane and extruded from the cell by the Na+/K+-ATPase located on the basolateral membrane. This transport generates a sodium gradient that drives the transport of water, which is accomplished in part through water channels. AQP, aquaporin; CFTR, cystic fibrosis transmembrane conductance regulator; CNG, cyclic nucleotide-gated; ENaC, epithelial Na+channel.
BIOL 210 Photo-montage
[Go to semester: Fall 2002, Fall 2003, Spring 2005, Spring 2006] The scanning electron microscope (SEM) is used to teach principles of electron optics and digital imaging for the study of surface morphology and microstructure of materials. The following micrographs were captured by students in BIOL 210. (below, left) Cleavage in a sample of citrine, a semi-precious stone. (below, left) Lumenal surface of murine intestine. (below, left) Specialized, dome-shaped Clara cells are visible in this micrograph of murine lung. (below, left) A posterior view of an aphid on leaf tissue. (below, left) A branching blood vessel found in a murine liver sample. (below, left) The aperature of an earthworm.
Quantitative assessment of markers for cell sen... [Exp Gerontol. 2010
Can ends justify the means?: Telomeres and the mechanisms of replicative senescence and immortalization in mammalian cells
John M. Sedivy Author Affiliations Contributed by George Klein Abstract Finite replicative lifespan, or senescence, of mammalian cells in culture is a phenomenon that has generated much curiosity since its description. A Historical Perspective of Senescence. Although mechanisms may differ, some form of replicative limit is probably operative in most living cells ( 1 ). Two major theories have been used to explain limited replicative capacity. How is senescence different from quiescence, the normal physiological withdrawal from the cell cycle that is displayed by almost all cells? We all know that senescence can be overcome, because many cell lines in common use are quite obviously immortal. At the cellular level, senescence is genetically a dominant trait. In contrast, normal human cells never have been observed to immortalize spontaneously. Bypass of Senescence and the Phenomenon of Crisis. What happens at the end of the extended lifespan? The Molecular Clock of Aging. Perspectives.