Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1111/j.1749-6632.2009.04041.x http://scihub22266oqcxt.onion/10.1111/j.1749-6632.2009.04041.x 19538300!ä!19538300 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\19538300.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Ann+N+Y+Acad+Sci 2009 ; 1165 (ä): 148-51 Nephropedia Template TP {{tp|p=19538300|t=2009. Insights into driving forces and paracellular permeability from claudin-16 knockdown mouse |pdf=|usr=}}{{19538300}} gab.com Text Insights into driving forces and paracellular permeability from claudin-16 knockdown mouse JO: Ann N Y Acad Sci http://www.kidney.de/pget.php?&tw=1&pmid=19538300 #FOAvip Tight junction (TJ) properties are determined by membrane protein complexes of neighboring cells that form both a barrier and a selective pathway for paracellular substrate transport. Our previous work supports the view that paracellular permeability changes in the thick ascending limb (TAL) may underlie the mechanism for familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), a rare autosomal recessive disease linked to mutations in claudin-16 (CLDN16) and claudin-19 (CLDN19). CLDN16 knockdown (KD) mice are lacking CLDN16 expression by transgenic RNA interference. We observed that the transport defect for Mg(2+) and Ca(2+) in this animal model is caused by a loss of paracellular cation selectivity. The permeability ratio for Na(+) over Cl(-) in KD mice was lower by a factor of two without a change in paracellular conductance, compared to wild type (WT). This resulted in a collapse of the transepithelial voltage, which is the driving force for Mg(2+) and Ca(2+) absorption in TAL. Since CLDN16 KD mice revealed lower blood pressure and an increased aldosterone plasma concentration, we hypothesize that the reduction in paracellular selectivity could allow backflow of Na(+) and Cl(-) into the lumen of the TAL, thus enhancing the distal NaCl load and challenging the organism with a latent NaCl loss. Twit Text FOAVip Insights into driving forces and paracellular permeability from claudin-16 knockdown mouse ????Ann N Y Acad Sci http://www.kidney.de/pget.php?&tw=1&pmid=19538300 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19538300 #FOAvip English Wikipedia <ref>{{Cite pmid|19538300}}</ref> Insights into driving forces and paracellular permeability from claudin-16 knockdown mouse #MMPMID19538300 Shan Q; Himmerkus N; Hou J; Goodenough DA; Bleich M Ann N Y Acad Sci 2009[May]; 1165 (ä): 148-51 PMID19538300show ga Tight junction (TJ) properties are determined by membrane protein complexes of neighboring cells that form both a barrier and a selective pathway for paracellular substrate transport. Our previous work supports the view that paracellular permeability changes in the thick ascending limb (TAL) may underlie the mechanism for familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), a rare autosomal recessive disease linked to mutations in claudin-16 (CLDN16) and claudin-19 (CLDN19). CLDN16 knockdown (KD) mice are lacking CLDN16 expression by transgenic RNA interference. We observed that the transport defect for Mg(2+) and Ca(2+) in this animal model is caused by a loss of paracellular cation selectivity. The permeability ratio for Na(+) over Cl(-) in KD mice was lower by a factor of two without a change in paracellular conductance, compared to wild type (WT). This resulted in a collapse of the transepithelial voltage, which is the driving force for Mg(2+) and Ca(2+) absorption in TAL. Since CLDN16 KD mice revealed lower blood pressure and an increased aldosterone plasma concentration, we hypothesize that the reduction in paracellular selectivity could allow backflow of Na(+) and Cl(-) into the lumen of the TAL, thus enhancing the distal NaCl load and challenging the organism with a latent NaCl loss. |Animals[MESH] |Calcium/metabolism[MESH] |Cell Membrane Permeability/*genetics[MESH] |Claudins[MESH] |Magnesium/metabolism[MESH] |Membrane Proteins/*genetics/metabolism[MESH] |Mice[MESH] |Mice, Knockout[MESH] |RNA Interference[MESH] |Sodium/metabolism[MESH]Insights into driving forces and paracellular permeability from claudi(epmc).pdf DeepDyve Pubget Overpricing