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.

10.1172/jci.insight.91042 http://scihub22266oqcxt.onion/10.1172/jci.insight.91042 C5374078!5374078!28405619     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight ä ; 2 (7): ä Nephropedia Template TP {{tp|p=28405619|t=ä. Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus |pdf=|usr=}}{{28405619}} gab.com Text Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405619 #FOAvip Psychiatric patients treated with lithium (Li+) may develop nephrogenic diabetes insipidus (NDI). Although the etiology of Li+-induced NDI (Li-NDI) is poorly understood, it occurs partially due to reduced aquaporin-2 (AQP2) expression in the kidney collecting ducts. A mechanism postulated for this is that Li+ inhibits adenylyl cyclase (AC) activity, leading to decreased cAMP, reduced AQP2 abundance, and less membrane targeting. We hypothesized that Li-NDI would not develop in mice lacking AC6. Whole-body AC6 knockout (AC6?/?) mice and potentially novel connecting tubule/principal cell?specific AC6 knockout (AC6loxloxCre) mice had approximately 50% lower urine osmolality and doubled water intake under baseline conditions compared with controls. Dietary Li+ administration increased water intake and reduced urine osmolality in control, AC6?/?, and AC6loxloxCre mice. Consistent with AC6?/? mice, medullary AQP2 and pS256-AQP2 abundances were lower in AC6loxloxCre mice compared with controls under standard conditions, and levels were further reduced after Li+ administration. AC6loxloxCre and control mice had a similar increase in the numbers of proliferating cell nuclear antigen?positive cells in response to Li+. However, AC6loxloxCre mice had a higher number of H+-ATPase B1 subunit?positive cells under standard conditions and after Li+ administration. Collectively, AC6 has a minor role in Li-NDI development but may be important for determining the intercalated cell?to?principal cell ratio. Twit Text FOAVip Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28405619 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28405619 #FOAvip English Wikipedia <ref>{{Cite pmid|28405619}}</ref> Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus #MMPMID28405619 Poulsen SB; Kristensen TB; Brooks HL; Kohan DE; Rieg T; Fenton RA JCI Insight ä[]; 2 (7): ä PMID28405619show ga Psychiatric patients treated with lithium (Li+) may develop nephrogenic diabetes insipidus (NDI). Although the etiology of Li+-induced NDI (Li-NDI) is poorly understood, it occurs partially due to reduced aquaporin-2 (AQP2) expression in the kidney collecting ducts. A mechanism postulated for this is that Li+ inhibits adenylyl cyclase (AC) activity, leading to decreased cAMP, reduced AQP2 abundance, and less membrane targeting. We hypothesized that Li-NDI would not develop in mice lacking AC6. Whole-body AC6 knockout (AC6?/?) mice and potentially novel connecting tubule/principal cell?specific AC6 knockout (AC6loxloxCre) mice had approximately 50% lower urine osmolality and doubled water intake under baseline conditions compared with controls. Dietary Li+ administration increased water intake and reduced urine osmolality in control, AC6?/?, and AC6loxloxCre mice. Consistent with AC6?/? mice, medullary AQP2 and pS256-AQP2 abundances were lower in AC6loxloxCre mice compared with controls under standard conditions, and levels were further reduced after Li+ administration. AC6loxloxCre and control mice had a similar increase in the numbers of proliferating cell nuclear antigen?positive cells in response to Li+. However, AC6loxloxCre mice had a higher number of H+-ATPase B1 subunit?positive cells under standard conditions and after Li+ administration. Collectively, AC6 has a minor role in Li-NDI development but may be important for determining the intercalated cell?to?principal cell ratio. äRole of adenylyl cyclase 6 in the development of lithium-induced nephr(epmc).pdf DeepDyve Pubget Overpricing