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Here s a bit of sample code. Before you read on, try to guess what the output will look like when this code runs:

This myopathy is associated with prominent early weakness of the quadriceps and anterior tibial muscle groups and has mean age of onset of muscle weakness of 125 years127,128 Cases resembling Miyoshi myopathy (LGMD 2B) with calf weakness have also been described129 LGMD 2H and sarcotubular myopathy (discussed in 25 with the Congenital Myopathies) are now known to be allelic disorders caused by mutations in the gene that encodes for E3-ubiquitine ligase (also known as TRIM 32) located on chromosome 9q31 q33 was recently reported29 TRIM 32 may function by ubiquinating proteins that need degradation by proteosomes The mechanism by which this leads to muscle destruction is unclear, but one might speculate on the possible toxic accumulation of aged or otherwise abnormal proteins not cleared by proteasomes

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LGMD 2I was initially described in a large consanguineous Tunisian family with 13 affected members133 However, it subsequently has been demonstrated worldwide and is the most common form of LGMD in England, the Netherlands, and northern Europe The onset can range from infancy (MDC type 1C) to the fourth decade of life30,31 The pattern of weakness and course is variable Some individuals have more hip-girdle involvement, while others are weaker in the proximal arms and neck exors Calves are often hypertrophic Importantly, approximately one-half of patients develop a dilated cardiomyopathy and ventilatory muscle weakness134 136

int main (int argc, const char * argv[]) { int i; char s[ kArraySize ] = "Hello"; printf( "i before it is initialized: %d\n\n", i ); for ( i=0; i<kArraySize; i++ ) printf( "s[ i ]: %d\n", s[ i ] ); return 0; }

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Nonspeci c dystrophic features are evident on muscle biopsy Of note, immunohistochemistry demonstrates normal dystrophin and sarcoglycan staining However, -dystroglycan and occasional merosin are reduced or absent on immunostaining (Fig 24 12)

The LGMD 2I is caused by mutations in the gene that encodes for FKRP located on chromosome 19q133 Mutations in this gene are also responsible for MDC type 1C; FKRP is a glycosyltransferase and its de ciency is associated with abnormal glycosylation of alphadystroglycan, which apparently disrupts the dystrophin glycoprotein complex Abnormalities in glycosylation of -dystroglycan is recurring theme in the MDCs, as this is also causative mechanism in Fukuyama disease, MEB, WWS, and LARGE-related CMD (MDC 1D) There is a correlation between a reduction in alpha-dystroglycan, the mutation, and the clinical phenotype in MDC 1C and LGMD 2I32

This code defines an int, without initializing it, as well as a ten-element array of type char, initializing the array to the string "Hello". Here s the output:

Serum CKs are elevated 10 30 times normal in some younger patients who are affected but may be normal in older individuals

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Figure 24 12 LGMD 2I Muscle biopsies demonstrate reduced or patchy merosin staining (A), absent alpha-dystroglycan staining (B), but normal dystrophin staining (C) around the sarcolemma Immunoperoxidase

i before it is initialized: -1881141193 s[ s[ s[ s[ s[ s[ s[ s[ s[ s[ i i i i i i i i i i ]: ]: ]: ]: ]: ]: ]: ]: ]: ]: 72 101 108 108 111 0 0 0 0 0

FKRP localizes in rough endoplasmic reticulum, while fukutin localizes in the cis-Golgi compartment (ER)137 Fukutin and FKRP appear to be involved at different steps in O-mannosylglycan synthesis of alphadystroglycan, and FKRP is most likely involved in the initial step in this synthesis ER retention of mutant FKRP may play a role in the pathogenesis of these dystrophies and potentially explain why the allelic disorder LGMD 2I is milder, because the mutated protein is able to reach the Golgi apparatus138

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