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The histologic changes are readily overlooked in paraf n sections Cryostat sections show masses of material that is basophilic with hematoxylin and eosin and bright red with Gomori trichrome and shows an intense reaction with NADH dehydrogenase By electron microscopy, the bundles of tubular aggregates are sharply demarcated from myo brils Other Congenital Myopathies The foregoing congenital myopathies central core, nemaline, centronuclear, and tubular aggregate types are well-de ned clinicopathologic entities In addition, other far less common types have been described, each named according to a distinctive dysmorphic alteration of organelles in muscle bers in histochemical and electron microscopic preparations In none of these additional types has the pattern of inheritance or the gene locus been identi ed Some of these myopathies multicore (minicore), ngerprint body, sarcotubular have been reported in only a few cases, quite insuf cient to allow their categorization as disease entities Two other types congenital ber type disproportion and congenital ber type predominance originally designated as congenital myopathies, have proved to be nonspeci c histochemical alterations observed in many infants and children with congenital developmental abnormalities, delays in motor development, and other conditions Other putative congenital myopathies include so-called reducing body, trilaminar, and cap disease; zebra body; and familial myopathy with lysis in type 1 bers, among others They most likely represent nonspeci c reactions in muscle or xation artifacts; as yet there is no evidence that any one of them represents a clinicopathologic entity Myo brillar Myopathy Beyond the uncertain entities noted earlier, the eld of chronic myopathies has been muddied by a plethora of reports describing a variety of curious inclusions in muscle bers, under a bewildering array of terms: myopathy with inclusion bodies, atypical myopathy with myo brillar aggregates; autosomal dominant myopathy with myo brillar inclusions; cardioskeletal myopathy with intrasarcoplasmic dense granulo lamentous material; cytoplasmic body myopathy; spheroid body myopathy; myopathy with characteristic sarcoplasmic bodies and skeleton (desmin) laments; myopathy with Mallory-body-like inclusions; and familial cardiomyopathy with subsarcolemmal vermiform deposits Implied by these reports was the notion that each of these structural abnormalities represented a new and distinctive myopathy More recently, in a careful light microscopic evaluation of both published reports and their own cases, Nakano and Engel and their colleagues have convincingly demonstrated that the many reported structural changes were the consequence of a single pathologic process a focal dissolution of myo brils, followed by an accumulation of the products of the degradative process These authors proposed the term myo brillar myopathy to encompass the entire spectrum of these pathologic changes Mutations of one of the various proteins that relate to the Z-disc (the connection between adjacent sarcomeres, which are the structural units of the myo bril) of muscle seem to be the unifying feature Many of these abnormalities can be traced to a dominant mutation in the genes coding for the lament proteins myotilin and desmin and in the chaperone protein -crystallin, as described in the review by Selcen and colleagues cited later Presumably, mutations in either gene predispose to protein aggregation, the former by destabilizing desmin and the latter by altering the capacity of the -crystallin to facilitate normal desmin folding. convert text to barcode in excel 2016 Free Barcode Font Download Using Code 39 (3 of 9) With No ...
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