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termed D4Z4186 Most patients with autosomal-dominant FSHD carry one array of one to 10 units It is this decrease in the number of these KpnI units or 33 kB repeats that result in the decreased size of the FSHDassociated polymorphism Another interesting observation is the allelic variation of chromosome 4qter, designated 4qA and 4qB, which differ by a few insertion/deletion events in the region distal to D4Z4186 The 4qA allele contains a block of beta-satellite DNA directly distal to D4Z4 on 4qA, which is not present on the 4qB allele Although occurring in similar frequency in the normal population, FSHDcausing mutations are associated exclusively in the 4qA type of allele Similar reductions in D4Z4 in 4qB alleles are nonpathogenic or have a highly reduced penetrance There is an inverse correlation between the size of the D4Z4 repeat unit and the severity of the disease202,203 Patients carrying one to three units are usually severely affected and often represent isolated (de novo mutations) cases, whereas patients carrying four to 10 units typically have an affected parent185 Anticipation phenomena may occur in some families, although the size of the mutation appears stable and there can be extreme variability in phenotype even within families203 The mutation in FSHD is unlike other described genetic disorders, in which anticipation is associated with an increased size of a polymorphic trinucleotide repeat mutation FSHD may result from the inappropriate overexpression of certain genes, rather than the absence or underexpression of genes, as in most dystrophies The D4Z4 region normally contains a multiprotein complex

B 1 0 1 0

The diagnosis of FSHD is usually apparent on clinical grounds Genetic testing is particularly useful for con rmation in patients without family history or unusual clinical phenotypes as well as for genetic counseling, genetic testing is very useful As noted previously, over 95% of patients have deletions in D4Z4 region False positives may result from rare, nonpathogenic contractions on 4qB or complex 4q 10q rearrangements and false negatives from deletions that extend to involve the p13E 11 probe186

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A small open-label pilot study of prednisone 15 mg/ kg/d for 12 weeks resulted in no signi cant improvement in strength or muscle mass190 An open-label trial of albuterol in 15 patients with FSHD for 3 months demonstrated increased lean body mass and muscle strength206 However, a subsequent larger, longer, double-blinded, placebo-controlled study of albuterol revealed no clear bene t207 Modest improvement in strength has been reported in a small number of patients with FSHD treated with short courses of creatine monohydrate (5 10 g/d) Surgery to x the scapula to the thorax, thereby increasing range of motion, is bene cial in some patients208,209 However, they need to have suf cient strength of the deltoid muscles in order to bene t from the procedure Ankle foot orthotics are useful in patients with foot drop secondary to tibialis anterior and peroneal muscle weakness

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The previous examples assumed that a short is 2 bytes (16 bits) long. Of course, this makes for some implementation-dependent code. Here s a more portable example. This code sets the rightmost bit of myShort, no matter how many bytes are used to implement a short:

D4S2463 D4F104S1 (p13E-11)

Figure 24 17 Schematic representation of the facioscapulohumeral muscular dystrophy (FSHD) locus The polymorphic D4Z4 repeat array (arrowheads) in the subtelomere of chromosome 4 (blue) can vary between 11 and 100 units in the healthy population One inversed copy of D4Z4 (D4S2463) is located 37 Kb proximally Just preceding the D4Z4 repeat unit, probe p13E-11 (D4F104S1), used in the DNA diagnosis of FSHD, is situated Within each unit, a putative open reading frame designated DUX4 (block arrow) is located, but expression of this gene has never been established In a proximal direction, several additional genes have been identi ed (block arrows) including FRG2, TUBB4Q (a pseudogene), and FRG1 At a much larger distance, several other genes have been evaluated for their involvement in FSHD Most notably, these include ANT1 and PDLIM3 Distal to D4Z4, two allelic variants of 4qter have been identi ed: 4qA (dark blue) and 4qB (light blue) Both variants are almost equally common in the population and vary by a few insertion and deletion events FSHD alleles are exclusively linked with the 4qA variant The subtelomere of chromosome 10q is similarly organized as 4q due to an ancient duplication of the 4q subtelomere The homology between 4qter and 10qter extends from the telomere to 40 kb proximally to D4Z4 within an incomplete inverted copy of D4Z4 In contrast to 4qter, there is no B variant of the 10q subtelomere (With permission from Tawil R, Van Der Maarel SM Facioscapulohumeral muscular dystrophy Muscle Nerve 2006;34(1):1 15)

short myShort; myShort = (~1) & myShort;

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