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(eg, Jo-1 antibodies) may predict patterns of organ involvement in addition to skeletal muscle, particularly interstitial lung disease; response to treatment; and therefore prognosis Only those selected antibodies will be described here Autoantibodies to amino-acyl-tRNA synthetase appear to correlate with a constellation of symptoms known collectively as the antisynthetase syndrome Polymyositis, polyarthropathy, pulmonary brosis, Raynaud s phenomenon, and scaling and cracking of the lateral ngers constitute the major manifestations of this phenotype The presence of anti-tRNA synthetases predicts a chronic condition with moderate responsiveness to immunomodulating treatment126 One of these six antisynthetases, anti-histidyl-tRNA synthetase or Jo-1, is found in 20 30% of patients with polymyositis or dermatomyositis It correlates with the presence of interstitial lung disease in approximately 75% of these patients Anti-Jo-1 essentially precludes the diagnosis of inclusion body myositis, although this distinction is usually readily made by clinical and histological means Antibodies directed against signal recognition protein occur infrequently in patients with polymyositis but serve to identify a subgroup that is disproportionately black, with acute-onset, prominent cardiac involvement and poor responsiveness to immunomodulating treatment127 The presence of anti-Mi-2 antibodies conversely are seen predominantly if not exclusively in a small percentage of pediatric and adult dermatomyositis cases and typically predict treatment responsiveness128 Anti-PM-Scl and anti-Ku antibodies, unlike those already addressed, are myositis associated rather than myositis speci c These typically occur in individuals with other connective tissue diseases, with or without an associated myositis These are usually associated with good treatment responsiveness125

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antigens134 There is no recognized role for Western blotting in the setting of a negative ELISA screen Although providing speci city, Western blotting lacks perfect sensitivity The use of Western blotting alone without ELISA screening provides some risk of a false-negative result Polymerase chain reaction, C6 ELISA antigen detection in urine and detection of immune complex disruption, and B lymphocyte chemoattractant have either not been adequately tested or not achieved adequate levels of sensitivity and/or speci city to be routinely applied to either serum or CSF135 In the CSF, demonstrating IgG and IgM Lyme antibodies in concentrations greater than those found in serum is currently the recommended means to con rm central nervous system involvement The detection of Lyme antibodies in the spinal uid may lack sensitivity, and CSF pleocytosis and/or elevation of protein levels in the appropriate clinical context is considered suf cient by some to identify CNS Lyme disease136 138 Rare cases of seronegative CNS Lyme detectable only with CSF examination have been reported129 HIV is a neurotropic virus with a number of potential neuromuscular manifestations139 141 Serological testing is based on the detection of IgG antibodies directed against the p24 nucleocapsid and gp41 and 120 envelope proteins These antibodies appear within 6 weeks in the majority of infected individuals and within 6 months in 95% and persist for life142,143 A positive test requires detection of two of these three antigens and has a detected sensitivity and speci city of over 99%144 As in Lyme disease, serological testing for HIV typically consists of an ELISA screen followed by Western blot con rmation HIV antigens can be detected in the CSF in patients with CNS involvement145

Serum CK levels are markedly elevated In contrast to the dystrophinopathies, there are no signi cant intellectual impairments or cardiac abnormalities in the sarcoglycanopathies

As you can see, the three initializing values were wrapped in a pair of curly braces. This leaves myNums.i with a value of 1, myNums.j with a value of 2, and myNums.f with a value of 3.01. If you have a struct, union, or array embedded in your struct, you can nest a curlywrapped list of values inside another list, for example:

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Muscle biopsies demonstrate normal dystrophin; however, each of the sarcoglycans are absent or diminished on the sarcolemma, regardless of the primary sarcoglycan mutation

This genetically distinct LGMD was initially reported in families of Manitoba Hutterite origin29,132 Age of onset of weakness ranges from 8 to 27 years The myopathy is slowly progressive, and most affected individuals are still ambulatory, without assistance in the fourth decade of life

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LGMDs 2C, 2D, 2E, and 2F are caused by mutations in the -, -, -, and -sarcoglycan genes, respectively6,102,116, 117,119 125 The clinical phenotypes appear to correlate with the expression of the sarcoglycans The proteins of the sarcoglycan complex appear to function as a unit Mutations involving any of the sarcoglycans result in destabilization of the entire complex and reduced expression of the other proteins As apparent with the dystrophinopathies, the clinical severity of the sarcoglycanopathies may correlate with the type of mutation (ie, whether the reading frame is preserved) and subsequent level of functional protein expression

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Mutations in the sarcospan gene located on chromosome 12p112 are associated with congenital brosis of the extraocular muscles, a rare form of muscular dystrophy126 Muscle biopsies demonstrate typical dystrophic features In addition, many bers (mostly type 2) contain small vacuoles that immunostain for sarcoplasmic reticulumassociated ATPase These vacuoles abut T-tubules and appear to be membrane bound and appeared on EM

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