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been mapped to chromosome 4q12, of -sarcoglycan (35 DAG) to the pericentromeric region of chromosome 13q, and of -sarcoglycan (35 DAG) to chromosome 5q Primary defects in 43 DAG or 25 DAG, may in addition lead to a de ciency of adhalin, but the latter is incomplete and represents a secondary effect, possibly explained by the proximity of the defective genes to the adhalin gene From a practical point of view, despite clinical similarities, there is usually no serious dif culty in distinguishing these dystrophies (formerly termed SCARMD) from a dystrophinopathy In addition to the difference in inheritance, they can be readily diagnosed by showing a loss of sarcolemmal immunostaining for any of the dystrophin-associated glycoproteins but with preservation of staining for dystrophin itself However, it is not possible on clinical grounds to distinguish one sarcoglycanopathy from another; this can be accomplished only by speci c immunostaining.

There is no way of af rming or refuting this proposition The same can be said for the many suggestions that disturbed intrafamily relationships engender schizophrenic traits or possibly provoke psychosis in persons who are genetically vulnerable Behind all these suggestions was the notion that disturbed interpersonal relations in the family in some way interfered with the normal maturation of personality Adolf Meyer believed that schizophrenia was a reaction to a series of traumatic life situations a maladaptive response to some organic, psychologic, or sociologic factor Others have stressed the importance of disturbed interpersonal relationships However, with all these hypotheses, proof is lacking that such environmental factors are unique to the development of schizophrenia Furthermore, the extent to which these aberrations of family relationships are primary or secondary cannot be ascertained.

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Where substantial with data,the best curve-fitting strategy to derive is error is associated an approximatingfunction that fits the shapeor generaltrend of the datawithoutnecessarily matching the individual points. One approachto do this is to visually inspect the plotted data and then sketch a "best" line through the points. Although such"eyeball" calculaapproaches have commonsense appealand are valid for "back-ot'-the-envelope" tions, they are deficient becausethey are arbitrary.That is, unlessthe points defineaperfert would straightline (in which case,interpolationwould be appropriate), differentanalysts draw different lines. forthe To removethis subjectivity.somecriterion must be devisedto establish basis a fit. One way to do this is to derivea curve that minimizesthe discrepancy between data the points and the curve. To do this, we must first quantify the discrepancy. The simplest examrr p l e i s f i t t i n g a s t r a i g h t l i n e t o a s e t op a i r e d o b s e r v a t i o(n s,:) l ) . ( x z , y ) , . . . , ( . r , , ) n ) , f for The mathematical expression the straightline is y : a o* z t l x1 e (13.8)

Autosomal Recessive Muscular Dystrophy Linked to Chromosomes 15q and 2p (LGMD 2A and B; Calpain Mutation; See Table 50-1) These forms of limb-girdle dystrophy have been described in several large kindreds, in Indiana (among the Amish people), on the island of Reunion in the Indian Ocean, and in Brazil, affecting males and females equally Both the shoulder and pelvic girdles are involved The degree of weakness has varied considerably In one form of the disease, called LGMD 2A, the abnormal gene codes for a calcium-activated neutral protease, or calpain This calpainopathy is currently believed to account for about 40 percent of patients with LGMD Frequently, and early in the course of disease, there are Achilles tendon contractures and very high serum CK levels (at least 10 times normal) features that may permit distinction from the sarcoglycanopathies.

Yet another recessive limb-girdle dystrophy of slow progression has been identi ed in a Palestinian and Sicilian family and is due to a mutation in the gene for the protein dysferlin, which localizes to the muscle ber membrane Noteworthy is the fact that this same protein is involved in the distal form of Miyoshi muscular dystrophy described further on (page 1223) Early involvement of the gastrocnemius muscle (inability to walk on tiptoe) and extraordinarily high levels of CK, as in calpainopathy, are clues to the latter disease Autosomal Dominant Limb-Girdle Dystrophies (See Table 50-1) Several dystrophies with the LGMD phenotype are inherited as autosomal dominant traits For example, LGMDA 1A is an autosomal dominant limb-girdle dystrophy of late onset that was described in a large North Carolina family (49 affected members in a pedigree of 218 persons) The mean age at onset was 27 years.

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