Abstract:
:In a number of recent studies, a lung tumor resistance locus designated either Par2 or Pas7 was mapped to distal chromosome 18 in crosses between susceptible A/J and more resistant BALB/c mice. This locus is important in that it accounts for as much as 60% of the difference in lung tumor susceptibility between the A/J and BALB/c mice, both of which contain the susceptible allele of Kras2, a marker and strong candidate for the major lung tumor susceptibility gene on mouse chromosome 6. We have now fine-mapped the Par2 locus by using congenic mice that were constructed by placing part of chromosome 18 from the susceptible A/J onto the genetic background of lung tumor-resistant BALB/c mice. After 7 generations of backcrossing, N7 mice that carried 28 cM of the A/J quantitative trait locus (QTL) region were crossed to the BALB/c to generate the N8 generation. Congenic strains (N8) that contain various QTL regions were generated. N9 mice, generated from N8 males x 3 BALB/c females, were genotyped in the region of the Par2 locus and treated with an initiating dose of urethane and allowed to form lung tumors over 6 months. The mice were killed and the lung tumors counted. With this cross the Par2 locus was narrowed to a 6-cM region. Potential candidate genes in this region include Smad4, Smad2, and Dcc. Previously, we excluded Smad4 and Smad2 as candidates for Par2 based on the lack of functional polymorphism(s) and differential expression in lungs from A/J and BALB/c mice. In this study, no polymorphism of the coding sequence of Dcc was observed between A/J and BALB/c mice. Further fine mapping and positional cloning are required for the identification of the Par2 gene.
journal_name
Exp Lung Resjournal_title
Experimental lung researchauthors
Zhang Z,Lin L,Liu G,Wang M,Hill J,Wang Y,You M,Devereux TRdoi
10.1080/01902140150216710subject
Has Abstractpub_date
2000-12-01 00:00:00pages
627-39issue
8eissn
0190-2148issn
1521-0499journal_volume
26pub_type
杂志文章abstract::The cigarette smoke-induced rat model of chronic bronchitis was used to study the time course of the return of cigarette smoke-induced secretory cell hyperplasia to the normal and the capacity of two non-steroidal anti-inflammatory drugs to speed this recovery. Cigarette smoke alone significantly increased (P less tha...
journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902148609061499
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abstract::Acute lung injury (ALI) is often associated with sepsis and is the most common cause of acute respiratory failure. The authors evaluated the role of the heme oxygenase (HO)/carbon monoxide (CO) system on lung injury in a cecal ligation and puncture (CLP)-induced mouse model of ALI. The authors established CLP-induced ...
journal_title:Experimental lung research
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journal_title:Experimental lung research
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journal_title:Experimental lung research
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abstract::Paraquat accumulation into rat lung slices was unaffected by hypoxia (PO2 = 645 mm Hg) but was inhibited by hypoxia. The IC50 (IC50 = partial pressure of O2 resulting in a 50% inhibition of paraquat accumulation) for paraquat accumulation was P02 = 50 mm Hg; significant accumulation could be observed after 1 or 2 hr o...
journal_title:Experimental lung research
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doi:10.3109/01902148009065463
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journal_title:Experimental lung research
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doi:10.3109/01902148909069608
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journal_title:Experimental lung research
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journal_title:Experimental lung research
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journal_title:Experimental lung research
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journal_title:Experimental lung research
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abstract::Because high partial pressures of oxygen (O2) can cause peroxidative cleavage of membrane lipids, it is plausible to hypothesize that hyperoxia alters the physical state and composition of lipids in the membranes of pulmonary endothelial cells and that manipulation of the lipid profile may modify endothelial cell tole...
journal_title:Experimental lung research
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journal_title:Experimental lung research
pub_type: 杂志文章,评审
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更新日期:1988-01-01 00:00:00
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journal_title:Experimental lung research
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更新日期:2017-01-01 00:00:00
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journal_title:Experimental lung research
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