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Thiamine entry into mammalian cells occurs by a saturable, high affinity transporter that is deficient in humans with thiamine-responsive megaloblastic anemia (TRMA) [ 7 8 9 10 11 12 ] . Thiamine uptake by mitochondria has been demonstrated [ 13 ] , yet thiamine diphosphokinase is cytosolic and mitochondria cannot convert thiamine to ThDP [ 14 15 16 ] . Barile and coworkers demonstrated saturable uptake of ThDP by rat liver mitochondria characterized by a K m of around 20 μM.
Sato and coworkers [ 8] studied the relationship between gastric wall P CO 2 and esophageal P CO 2 (Pe CO 2 ) before, during, and after reversal of hemorrhagic shock in five spontaneously breathing rats, using an ion-sensitive field-effect transistor.
Chess and coworkers have shown that transforming growth factor-α and hepatocyte growth factor increase the phosphorylation of p44/p42 MAPK in H441 cells [ 23 ] . Epidermal growth factor, which binds to the same receptor as transforming growth factor-α, increases SP-A content in human fetal lung [ 24 ] . Hepatocyte growth factor has also been shown to upregulate the synthesis of SP-A in rat type II cells [ 25 ] . Thus, phosphorylation of p44/42 MAPK may be involved in the up-regulation of SP-A gene expression, results consistent with our observation that inhibition of basal levels of p44/42 MAPK phosphorylation may decrease SP-A gene expression.
0020007) on the microarray analysis of tumors and one by Sarah Rowland-Jones and coworkers (found at DOI: 10.
Casciola-Rosen and coworkers have proposed that modifications of autoantigens during cell death, particularly proteolytic cleavage, might be crucial for the generation of autoantibodies in autoimmune diseases [ 23 37 ] . Unique proteolytic fragments of α-fodrin and type 3 muscarinic acetylcholine receptor have been implicated in the generation of autoantibody responses in primary Sjögren's syndrome [ 38 39 ] .
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