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10.1038/ncomms9715 http://scihub22266oqcxt.onion/10.1038/ncomms9715 C4620584!4620584!26493500     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): ä Nephropedia Template TP {{tp|p=26493500|t=2015. Modelling kidney disease with CRISPR-mutant kidney organoids derived from human pluripotent epiblast spheroids |pdf=|usr=}}{{26493500}} gab.com Text Modelling kidney disease with CRISPR-mutant kidney organoids derived from human pluripotent epiblast spheroids JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26493500 #FOAvip Human-pluripotent-stem-cell-derived kidney cells (hPSC-KCs) have important potential for disease modelling and regeneration. Whether the hPSC-KCs can reconstitute tissue-specific phenotypes is currently unknown. Here we show that hPSC-KCs self-organize into kidney organoids that functionally recapitulate tissue-specific epithelial physiology, including disease phenotypes after genome editing. In three-dimensional cultures, epiblast-stage hPSCs form spheroids surrounding hollow, amniotic-like cavities. GSK3? inhibition differentiates spheroids into segmented, nephron-like kidney organoids containing cell populations with characteristics of proximal tubules, podocytes and endothelium. Tubules accumulate dextran and methotrexate transport cargoes, and express kidney injury molecule-1 after nephrotoxic chemical injury. CRISPR/Cas9 knockout of podocalyxin causes junctional organization defects in podocyte-like cells. Knockout of the polycystic kidney disease genes PKD1 or PKD2 induces cyst formation from kidney tubules. All of these functional phenotypes are distinct from effects in epiblast spheroids, indicating that they are tissue specific. Our findings establish a reproducible, versatile three-dimensional framework for human epithelial disease modelling and regenerative medicine applications. Twit Text FOAVip Modelling kidney disease with CRISPR-mutant kidney organoids derived from human pluripotent epiblast spheroids ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26493500 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26493500 #FOAvip English Wikipedia <ref>{{Cite pmid|26493500}}</ref> Modelling kidney disease with CRISPR-mutant kidney organoids derived from human pluripotent epiblast spheroids #MMPMID26493500 Freedman BS; Brooks CR; Lam AQ; Fu H; Morizane R; Agrawal V; Saad AF; Li MK; Hughes MR; Werff RV; Peters DT; Lu J; Baccei A; Siedlecki AM; Valerius MT; Musunuru K; McNagny KM; Steinman TI; Zhou J; Lerou PH; Bonventre JV Nat Commun 2015[]; 6 (ä): ä PMID26493500show ga Human-pluripotent-stem-cell-derived kidney cells (hPSC-KCs) have important potential for disease modelling and regeneration. Whether the hPSC-KCs can reconstitute tissue-specific phenotypes is currently unknown. Here we show that hPSC-KCs self-organize into kidney organoids that functionally recapitulate tissue-specific epithelial physiology, including disease phenotypes after genome editing. In three-dimensional cultures, epiblast-stage hPSCs form spheroids surrounding hollow, amniotic-like cavities. GSK3? inhibition differentiates spheroids into segmented, nephron-like kidney organoids containing cell populations with characteristics of proximal tubules, podocytes and endothelium. Tubules accumulate dextran and methotrexate transport cargoes, and express kidney injury molecule-1 after nephrotoxic chemical injury. CRISPR/Cas9 knockout of podocalyxin causes junctional organization defects in podocyte-like cells. Knockout of the polycystic kidney disease genes PKD1 or PKD2 induces cyst formation from kidney tubules. All of these functional phenotypes are distinct from effects in epiblast spheroids, indicating that they are tissue specific. Our findings establish a reproducible, versatile three-dimensional framework for human epithelial disease modelling and regenerative medicine applications. äModelling kidney disease with CRISPR-mutant kidney organoids derived f(epmc).pdf DeepDyve Pubget Overpricing