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.

10.1002/brb3.919 http://scihub22266oqcxt.onion/10.1002/brb3.919 C5893341!5893341!29670817     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Brain+Behav 2018 ; 8 (4): ä Nephropedia Template TP {{tp|p=29670817|t=2018. Dejerine?Sottas disease in childhood?Genetic and sonographic heterogeneity |pdf=|usr=}}{{29670817}} gab.com Text Dejerine Sottas disease in childhood Genetic and sonographic heterogeneity JO: Brain Behav http://www.kidney.de/pget.php?&tw=1&pmid=29670817 #FOAvip Introduction: The nerve sonographic features of Dejerine?Sottas disease (DSD) have not previously been described. Methods: This exploratory cross?sectional, matched, case?control study investigated differences in nerve cross?sectional area (CSA) in children with DSD compared to healthy controls and children with Charcot?Marie?Tooth disease type 1A (CMT1A). CSA of the median, ulnar, tibial, and sural nerves was measured by peripheral nerve ultrasound. The mean difference in CSA between children with DSD, controls, and CMT1A was determined individually and within each group. Results: Five children with DSD and five age? and sex?matched controls were enrolled. Data from five age?matched children with CMT1A was also included. Group comparison showed no mean difference in nerve CSA between children with DSD and controls. Individual analysis of each DSD patient with their matched control indicated an increase in nerve CSA in three of the five children. The largest increase was observed in a child with a heterozygous PMP22 point mutation (nerve CSA fivefold larger than a control and twofold larger than a child with CMT1A). Nerve CSA was moderately increased in two children?one with a heterozygous mutation in MPZ and the other of unknown genetic etiology. Conclusions: Changes in nerve CSA on ultrasonography in children with DSD differ according to the underlying genetic etiology, confirming the variation in underlying pathobiologic processes and downstream morphological abnormalities of DSD subtypes. Nerve ultrasound may assist in the clinical phenotyping of DSD and act as an adjunct to known distinctive clinical and neurophysiologic findings of DSD subtypes. Larger studies in DSD cohorts are required to confirm these findings. Twit Text FOAVip Dejerine Sottas disease in childhood Genetic and sonographic heterogeneity ????Brain Behav http://www.kidney.de/pget.php?&tw=1&pmid=29670817 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29670817 #FOAvip English Wikipedia <ref>{{Cite pmid|29670817}}</ref> Dejerine?Sottas disease in childhood?Genetic and sonographic heterogeneity #MMPMID29670817 Hobbelink SMR; Brockley CR; Kennedy RA; Carroll K; de Valle K; Rao P; Davis MR; Laing NG; Voermans NC; Ryan MM; Yiu EM Brain Behav 2018[Apr]; 8 (4): ä PMID29670817show ga Introduction: The nerve sonographic features of Dejerine?Sottas disease (DSD) have not previously been described. Methods: This exploratory cross?sectional, matched, case?control study investigated differences in nerve cross?sectional area (CSA) in children with DSD compared to healthy controls and children with Charcot?Marie?Tooth disease type 1A (CMT1A). CSA of the median, ulnar, tibial, and sural nerves was measured by peripheral nerve ultrasound. The mean difference in CSA between children with DSD, controls, and CMT1A was determined individually and within each group. Results: Five children with DSD and five age? and sex?matched controls were enrolled. Data from five age?matched children with CMT1A was also included. Group comparison showed no mean difference in nerve CSA between children with DSD and controls. Individual analysis of each DSD patient with their matched control indicated an increase in nerve CSA in three of the five children. The largest increase was observed in a child with a heterozygous PMP22 point mutation (nerve CSA fivefold larger than a control and twofold larger than a child with CMT1A). Nerve CSA was moderately increased in two children?one with a heterozygous mutation in MPZ and the other of unknown genetic etiology. Conclusions: Changes in nerve CSA on ultrasonography in children with DSD differ according to the underlying genetic etiology, confirming the variation in underlying pathobiologic processes and downstream morphological abnormalities of DSD subtypes. Nerve ultrasound may assist in the clinical phenotyping of DSD and act as an adjunct to known distinctive clinical and neurophysiologic findings of DSD subtypes. Larger studies in DSD cohorts are required to confirm these findings. äDejerine?Sottas disease in childhood?Genetic and sonographic heterogen(epmc).pdf DeepDyve Pubget Overpricing