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FOR CENTURIES, people have known of the wreck of a Large vessel on or near the shores of Nehalem Spit, south of Neahkahnie Mountain in Tillamook County, Oregon. In addition [...]

AMPLE EVIDENCE OF A VAST SHIPWRECK on Oregon's north coast appeared from the very beginnings of the state's written historical record. John Ordway of the Lewis and Clark Expedition mentioned [...]

The adult proximal tubule is a low-resistance epithelium where there are high rates of both active transcellular and passive paracellular NaCl transport. We have previously demonstrated that the neonatal rabbit and rat proximal tubule have substantively different passive paracellular transport properties than the adult proximal tubule, which results in a maturational change in the paracellular passive flux of ions. Neonatal proximal tubules have a higher [P.sub.Na]/[P.sub.cl] ratio and lower chloride and bicarbonate permeabilities than adult proximal tubules. Claudins are a large family of proteins which are the gate keepers of the paracellular pathway, and claudin isoform expression determines the permeability characteristics of the paracellular pathway. Previous studies have shown that claudins 1, 2, 3, 4, 5, 7, 8, 10, 11, 12, 15, and 16 are expressed in the adult mouse kidney. To determine whether there are developmental claudin isoforms, we compared the claudin isoforms present in the neonatal and adult kidney using RT-PCR to detect mRNA of claudin isoforms. Claudin 6, claudin 9, and claudin 13 were either not expressed or barely detectable in the adult mouse kidney using traditional PCR, but were expressed in the neonatal mouse kidney. Using real-time RT-PCR, we were able to detect a low level of claudin 6 mRNA expression in the adult kidney compared with the neonate, but claudin 9 and claudin 13 were only detected in the neonatal kidney. There was the same maturational decrease in these claudin proteins with Western blot analysis. Immunohistochemistry showed high levels of expression of claudin 6 in neonatal proximal tubules, thick ascending limb, distal convoluted tubules, and collecting ducts in a paracellular distribution but there was no expression of claudin 6 in the adult kidney. Using real-time RT-PCR claudin 6 and 9 mRNA were present in 1-day-old proximal convoluted tubules and were virtually undetectable in proximal convoluted tubules from adults. Claudin 13 was not detectable in neonatal or adult proximal convoluted tubules. In summary, we have identified developmentally expressed claudin isoforms, claudin 6, claudin 9, and claudin 13. These paracellular proteins may play a role in the maturational changes in paracellular permeability. renal tubule; renal development; paracellular pathway; neonatal kidney

An introduction to a series of articles published within the issue is presented on topics including the shipwreck of Oregon's Manila galleon based on eyewitness accounts of the Nehalem-Tillamook people, the Beeswax Wreck Project, and journey of the ships Santo Cristo de Burgos and San Francisco Xavier.

At the start of the nineteenth century, Euro-American settlers along the Oregon coast learned of a shipwreck with a large cargo of beeswax blocks and candles that had foundered a century or more before their arrival. The wreck and its origin were a mystery, and some observers believed that no vessel could carry such a large cargo of beeswax and therefore the wax must be from a natural source of mineral wax. This paper summarizes archaeological, historical, and geomorphological data that demonstrate the wreck is that of a wayward Manila galleon that wrecked on the Oregon coast sometime after ad 1670 but before the last large Cascadia Subduction Zone earthquake and associated tsunami in ad 1700. An exhaustive search of Spanish shipping records revealed only one eastbound Manila galleon was lost during this time, suggesting that the Beeswax Wreck is actually the missing Manila galleon Santo Cristo de Burgos, which left the Philippines in July 1693 and was never seen again. [ABSTRACT FROM AUTHOR]

Autosomal recessive polycystic kidney disease, an inherited disorder characterized by the formation of cysts in renal collecting ducts and biliary dysgenesis, is caused by mutations of the polycystic kidney and hepatic disease 1 (PKHD1) gene. Expression of PKHD1 is tissue specific and developmentally regulated. Here, we show that a 2.0-kb genomic fragment containing the proximal promoter of mouse Pkhd1 directs tissue-specific expression of a lacZ reporter gene in transgenic mice. LacZ is expressed in renal collecting ducts beginning during embryonic development but is not expressed in extrarenal tissues. The Pkhd1 promoter contains a binding site for the transcription factor hepatocyte nuclear factor (HNF)-1β, which is required for activity in transfected cells. Mutation of the HNF-1β-binding site abolishes the expression of the lacZ reporter gene in renal collecting ducts. Transgenes containing the 2.0-kb promoter and 2.7 kb of additional genomic sequence extending downstream to the second exon are expressed in the kidney, intrahepatic bile ducts, and male reproductive tract. This pattern overlaps with the endogenous expression of Pkhd1 and coincides with sites of expression of HNF-1β. We conclude that the proximal 2.0-kb promoter is sufficient for tissue-specific expression of Pkhd1 in renal collecting ducts in vivo and that HNF-1β is required for Pkhd1 promoter activity in collecting ducts. Additional genomic sequences located from exons 1-2 or elsewhere in the gene locus are required for expression in extrarenal tissues. [ABSTRACT FROM AUTHOR]

P-glycoprotein (P-gp) plays a fundamental role in multidrug resistance. The quantity of P-gp relates to the degree of drug resistance. A comparison was made between P-gps in mouse and hamster cell lines in both Laemmli and modified Fairbanks gel systems. Both proteins are derived from precursors of similar size that undergo differential N-linked glycosylation. The electrophoretic mobility and the amount of P-gp are remarkably dependent on the conditions of analysis. Notably, boiling P-gp before Laemmli gel elec-trophoresis decreases its mobility by an amount that is equivalent to ≈15 kDa and results in an apparent diminution in the amount of protein. The latter effect can give a false impression concerning the quantity of P-gp in cells. [ABSTRACT FROM PUBLISHER]