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http://scihub22266oqcxt.onion/ 8981955/?report=reader!1712548!8981955     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 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 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Hum+Genet 1997 ; 60 (1): 121-32 Nephropedia Template TP {{tp|p=8981955|t=1997. Fine mapping of an imprinted gene for familial nonchromaffin paragangliomas, on chromosome 11q23 |pdf=|usr=}}{{8981955}} gab.com Text Fine mapping of an imprinted gene for familial nonchromaffin paragangliomas, on chromosome 11q23 JO: Am J Hum Genet http://www.kidney.de/pget.php?&tw=1&pmid=8981955 #FOAvip Hereditary nonchromaffin paragangliomas (PGL; glomus tumors; MIM 168000) are mostly benign, slow-growing tumors of the head and neck region, inherited from carrier fathers in an autosomal dominant fashion subject to genomic imprinting. Genetic linkage analysis in two large, unrelated Dutch families assigned PGL loci to two regions of chromosome 11, at 11q23 (PGL1) and 11q13.1 (PGL2). We ascertained a total of 11 North American PGL families and confirmed maternal imprinting (inactivation). In three of six families, linkage analysis provided evidence of linkage to the PGL1 locus at 11q23. Recombinants narrowed the critical region to an approximately 4.5-Mb interval flanked by markers D11S1647 and D11S622. Partial allelic loss of strictly maternal origin was detected in 5 of 19 tumors. The greatest degree of imbalance was detected at 11q23, distal to D11S1327 and proximal to CD3D. Age at onset of symptoms was significantly different between fathers and children (Wilcoxon rank-sum test, P < .002). Affected children had an earlier age at onset of symptoms in 39 of 57 father-child pairs (chi2 = 7.74, P < .006). However, a more conservative comparison of the number of pairs in which a child had > or = 5 years earlier age at onset (n = 33) vis-a-vis that of complementary pairs (n = 24) revealed no significant difference (chi2 = 1.42, P > .2). Whether these data represent genetic anticipation or ascertainment bias can be addressed only by analysis of a larger number of father-child pairs. Twit Text FOAVip Fine mapping of an imprinted gene for familial nonchromaffin paragangliomas, on chromosome 11q23 ????Am J Hum Genet http://www.kidney.de/pget.php?&tw=1&pmid=8981955 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=8981955 #FOAvip English Wikipedia <ref>{{Cite pmid|8981955}}</ref> Fine mapping of an imprinted gene for familial nonchromaffin paragangliomas, on chromosome 11q23 #MMPMID8981955 Baysal BE; Farr JE; Rubinstein WS; Galus RA; Johnson KA; Aston CE; Myers EN; Johnson JT; Carrau R; Kirkpatrick SJ; Myssiorek D; Singh D; Saha S; Gollin SM; Evans GA; James MR; Richard CW 3rd Am J Hum Genet 1997[Jan]; 60 (1): 121-32 PMID8981955show ga Hereditary nonchromaffin paragangliomas (PGL; glomus tumors; MIM 168000) are mostly benign, slow-growing tumors of the head and neck region, inherited from carrier fathers in an autosomal dominant fashion subject to genomic imprinting. Genetic linkage analysis in two large, unrelated Dutch families assigned PGL loci to two regions of chromosome 11, at 11q23 (PGL1) and 11q13.1 (PGL2). We ascertained a total of 11 North American PGL families and confirmed maternal imprinting (inactivation). In three of six families, linkage analysis provided evidence of linkage to the PGL1 locus at 11q23. Recombinants narrowed the critical region to an approximately 4.5-Mb interval flanked by markers D11S1647 and D11S622. Partial allelic loss of strictly maternal origin was detected in 5 of 19 tumors. The greatest degree of imbalance was detected at 11q23, distal to D11S1327 and proximal to CD3D. Age at onset of symptoms was significantly different between fathers and children (Wilcoxon rank-sum test, P < .002). Affected children had an earlier age at onset of symptoms in 39 of 57 father-child pairs (chi2 = 7.74, P < .006). However, a more conservative comparison of the number of pairs in which a child had > or = 5 years earlier age at onset (n = 33) vis-a-vis that of complementary pairs (n = 24) revealed no significant difference (chi2 = 1.42, P > .2). Whether these data represent genetic anticipation or ascertainment bias can be addressed only by analysis of a larger number of father-child pairs. |*Chromosome Mapping[MESH] |*Chromosomes, Human, Pair 11[MESH] |*Genomic Imprinting[MESH] |Adolescent[MESH] |Adult[MESH] |Age of Onset[MESH] |Aged[MESH] |Alleles[MESH] |Child[MESH] |Child, Preschool[MESH] |Crossing Over, Genetic[MESH] |Female[MESH] |Genes, Tumor Suppressor[MESH] |Genetic Heterogeneity[MESH] |Genetic Linkage[MESH] |Genotype[MESH] |Head and Neck Neoplasms/*genetics[MESH] |Humans[MESH] |Infant[MESH] |Infant, Newborn[MESH] |Male[MESH] |Middle Aged[MESH] |Molecular Sequence Data[MESH] |Paraganglioma, Extra-Adrenal/*genetics[MESH]Fine mapping of an imprinted gene for familial nonchromaffin paragangl(epmc).pdf DeepDyve Pubget Overpricing