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98 Tang BS, Zhao GH, Luo W, et al Small heat-shock protein 22 mutated in autosomal dominant Charcot Marie Tooth disease type 2 L Hum Genet 2005;116(3): 222 224 99 Teunissen LL, Notermans NC, Fransen H, et al Difference between hereditary motor and sensory neuropathy type 2 and chronic idiopathic axonal neuropathy A clinical and electrophysiological study Brain 1997;120:955 962 100 Fabrizi GM, Cavallaro T, Angiari C, et al Charcot Marie Tooth disease type 2E, a disorder of the cytoskeleton Brain 2007;130(Pt 2):394 403 101 Hahn AF, Parkes AW, Bolton CF, et al Neuromyotonia in hereditary motor neuropathy J Neurol Neurosurg Psychiatry 1991;54:230 235 102 Vasilescu C, Marilena A, Dan A Neuronal type of Charcot Marie Tooth disease with a syndrome of continuous motor unit activity J Neurol Sci 1984;63:11 25 103 Schroder JM Neuropathology of Charcot Marie Tooth and related disorders Neuromol Med 2006;8(1 2):23 42 104 Zhao C, Takita J, Tanaka Y, et al Charcot Marie Tooth disease type 2 A caused by mutation in a microtubule motor KIF1Bbeta [erratum appears in Cell 2001;106(1):127] Cell 2001;105(5):587 597 105 Ben Othame K, Middleton LT, Loprest LJ Localization of a gene (CMT2 A) for autosomal dominant Charcot Marie Tooth type 2 to chromosome 1p and evidence for genetic heterogeneity Genomics 1993;17:370 375 106 Zuchner S, Mersiyanova IV, Muglia M, et al Mutations in the mitochondrial GTPase mitofusin 2 cause Charcot Marie Tooth neuropathy type 2A Nat Genet 2004;36(5):449 451 (Zucher 2004A) 107 Baloh RH, Schmidt RE, Pestronk A, Milbrandt J Altered axonal mitochondrial transport in the pathogenesis of Charcot Marie Tooth disease from mitofusin 2 mutations J Neurosci 2007;27(2):422 430 108 Kwon JM, Eliott JL, Yee W, et al Assignment of a second Charcot Marie Tooth type II locus to chromosome 3q Am J Hum Genet 1995;57:853 858 109 Kalaydjieva L, Gresham D, Gooding R, et al N-myc downstream-regulated gene 1 is mutated in hereditary motor and sensory neuropathy Lom Am J Hum Genet 2000;67:47 58 109a Delague V, Jacquier A, Hamadouche T, Poitelon Y, Baudot C, Boccaccio I, Chouery E, Chaouch M, Kassouri N, Jabbour R, Grid D, M garban A, Haase G, L vy N Mue e e tations in FGD4 encoding the Rho GDP/GTP exchange factor FRABIN cause autosomal recessive Charcot-MarieTooth type 4H Am J Hum Genet 2007 Jul;81(1):1 16 109b Stendel C, Roos A, Deconinck T, Pereira J, Castagner F, Niemann A, Kirschner J, Korinthenberg R, Ketelsen UP, Battaloglu E, Parman Y, Nicholson G, Ouvrier R, Seeger J, De Jonghe P, Weis J, Kr ttgen A, Rudnik-Sch neborn u o S, Bergmann C, Suter U, Zerres K, Timmerman V, Relvas JB, Senderek J Peripheral nerve demyelination caused by a mutant Rho GTPase guanine nucleotide exchange factor, frabin/FGD4 Am J Hum Genet 2007;81(1):158 164 110 Auer-Grumbach M, Strasser-Fuchs S, Robl T, Windpassinger C, Wagner K Late onset Charcot Marie Tooth.

The first line of code declares an array of four ints, setting myInts[0] to 10, myInts[1] to 20, myInts[2] to 30, and myInts[3] to 40. If you leave out the array dimension, the compiler makes it just large enough to contain the listed data. The second line of code includes a dimension but not enough data to fill the array. The first three array elements are filled with the specified values, but myFloats[3] and myFloats[4] are initialized to 0.0. Here s another example:

Serum CK levels are usually markedly elevated (usually 35 200 times normal) Because dysferlin is present on white blood cells, Western blot analysis on these cells for dysferlin represents a noninvasive method of con rming the diagnosis111

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Figure 24 11 LGMD 2B/Miyoshi myopathy Muscle biopsies often demonstrate endomysial in ammatory cell in ltrate that can lead to misdiagnosis as polymyositis An early observation is the demonstration of membrane attack complex on the sarcolemma of non-necrotic muscle bers in dysferlinopathies (also seen in FSHD) that is not appreciated in PM Immunoperoxidase with anti-MAC antibodies LGMD, limb-girdle muscular dystrophy; FSHD, facioscapulohumeral muscular dystrophy

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Mutations within the dysferlin gene are the cause of Miyoshi myopathy, LGMD 2B, and some distal myopathies with anterior tibial weakness13,105,115 A study of 407 muscle biopsies from patients with unclassi ed myopathies (nondystrophinopathy and nonsarcoglycanopathy) demonstrated that 65% had abnormal dysferlin by Western blot and immunostaining103 Dysferlinopathy accounted for 1% of patients with an unknown LGMD and 60% of patients with a distal myopathy The clinical phenotype of patients with dysferlinopathy broke down as follows: 80% manifest with distal weakness, 8% have LGMD phenotype, and 6% present with asymptomatic hyper-CK-emia Dysferlin shares amino acid sequence homology with C elegans spermatogenesis factor FER-1, thus the origin of its name Dysferlin is located predominantly on the subsarcolemmal surface of the muscle membrane, but it has small transmembrane spanning tail (Fig 24 1) It does not appear to have a signi cant interaction with the dystrophin glycoprotein complex, and immunostaining for dystrophin, dystroglycans, merosin, and the sarcoglycans is normal Recent studies have suggested that at least one role of dysferlin is patching defects in skeletal membrane and mutations in the gene result in defective membrane repair12

4 In the meteorInitonEnterFrame event handler, find the code for Mouseshow();

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