LMNICE 1/2" x 132" Deck Belt for Hustler 600734

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After exclusion of chimeric fusion of CYP11B1/CYP11B2 or mutation in the AT1R gene (106165) in a mother and daughter with severe aldosteronism requiring total adrenalectomy, Charmandari et al. (2012) sequenced the candidate genes KCNK3 (603220), KCNK5 (603493), KCNK9 (605874), and KCNJ5, and identified heterozygosity for a missense mutation in the KCNJ5 gene (I157S; 600734.0006). The actual shade displayed/printed will depend on your system settings and should therefore be used for guidance only. Kokunai, Y., Nakata, T., Furuta, M., Sakata, S., Kimura, H., Aiba, T., Yoshinaga, M., Osaki, Y., Nakamori, M., Itoh, H., Sato, T., Kubota, T., Kadota, K., Shindo, K., Mochizuki, H., Shimizu, W., Horie, M., Okamura, Y., Ohno, K., Takahashi, M. P. The customer shall cooperate with VWR in all matters relating to the services, provide all such access and information as is necessary and obtain any licences permissions and consents required before commencement of the services. Where delivery or performance dates are stated by VWR these are estimates only and time is not of the essence; however, if VWR needs to change such dates it will do so only after providing information to the customer and having regards to the customer’s stated objectives.

Mulatero et al. (2012) described an Italian mother and daughter with primary hyperaldosteronism, in whom the presence of the chimeric gene responsible for GRA had been excluded. The mother, who had a history of polyuria in the first decade of life, was initially reported to be hypertensive at age 18 years. Primary aldosteronism was diagnosed at 27 years of age, when she presented with hypertension, hypokalemia, decreased plasma renin activity, and elevated aldosterone levels that did not normalize after dexamethasone administration. On electrocardiogram, QTc was slightly prolonged at 456 ms, even after normalization of potassium levels. The daughter had polyuria and polydipsia at 2 years of age, and evaluation revealed hypertension, hypokalemia, and severe hyperaldosteronism with hypotonic urine and hypercalciuria. CT scans of the adrenal glands were normal in both patients, and symptoms in both were controlled with medication. The iduronate sulfatase gene: isolation of a 1.2-Mb YAC contig spanning the entire gene and identification of heterogeneous deletions in patients with Hunter syndrome. Although the arg468-to-trp mutation ( 300823.0012) was associated with a mild form of MPS II, Whitley et al. (1993) found very severe MPS II ( 309900) manifestations in a boy who was found to have a mutation in the same codon: a G-to-A transition at nucleotide 1403 of the IDS gene resulted in substitution of glutamine for arginine-468 (R468Q). In a note added in proof, it was reported that fibroblast cultures showed a large acrocentric supernumerary marker chromosome, which presumably was responsible for the quantitatively and qualitatively atypical features of the proband's face. The proband died at the age of 23 months. Ricci et al. (2003) stated that more than 200 different mutations in the IDS gene had been reported in patients with Hunter syndrome. Sukegawa, K., Song, X.-Q., Masuno, M., Fukao, T., Shimozawa, N., Fukuda, S., Isogai, K., Nishio, H., Matsuo, M., Tomatsu, S., Kondo, N., Orii, T.

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Identification of critical residues controlling G protein-gated inwardly rectifying K+ channel activity through interactions with the beta-gamma subunits of G proteins. In a father and 2 daughters with hyperaldosteronism type III (HALD3; 613677), Choi et al. (2011) identified heterozygosity for an A-to-G transition in the KCNJ5 gene resulting in a threonine-to-alanine substitution at codon 158 (T158A). This mutation was present in affected family members and was not identified in 900 control alleles. All 3 patients had massive adrenal hyperplasia and required bilateral adrenalectomy in childhood. Threonine-158 is conserved among KCNJ5 orthologs and other inward rectifiers and lies in the loop between the selectivity filter and the second transmembrane domain. The T158A mutation eliminates hydrogen bonds that constrain the structure of the KCNJ5 potassium channel.Any additional or special terms included by VWR in its written acceptance shall form part of the contract. The terms and conditions of the contract apply equally to the supply of both products and services except where application to one or the other is specified. Kosuga, M., Mashima, R., Hirakiyama, A., Fuji, N., Kumagai, T., Seo, J.-H., Nikaido, M., Saito, S., Ohno, K., Sakuraba, H., Okuyama, T. Hunter disease in a girl caused by R468Q mutation in the iduronate-2-sulfatase gene and skewed inactivation of the X chromosome carrying the normal allele. The customer is required to ensure that the use of any products supplied by VWR does not infringe the intellectual property rights of any third party and the customer shall indemnify VWR against any claims made against VWR by any third party in relation to any such infringement or alleged infringement.