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vriesea friburgensis/atrofia

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The closer muscle of large-clawed decapod crustaceans undergoes a proecdysial (premolt) atrophy to facilitate withdrawal of the appendage at ecdysis. This atrophy involves the activation of both calcium-dependent (calpains) and ubiquitin (Ub)/proteasome-dependent proteolytic systems that break down

Focal dermal hypoplasia with exuberant fat herniations and skeletal deformities.

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Focal dermal hypoplasia or Goltz syndrome is a rare congenital and mesoectodermal dysplasia with multisystemic involvement. Although the genetic alterations responsible for focal dermal hypoplasia are not fully known, there is predominance in affected females, suggesting dominant X-linked

Molt cycle-dependent molecular chaperone and polyubiquitin gene expression in lobster.

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Lobster claw muscle undergoes atrophy in correlation with increasing ecdysteroid (steroid molting hormone) titers during premolt. In vivo molecular chaperone (constitutive heat shock protein 70 [Hsc70], heat shock protein 70 [Hsp70], and Hsp90) and polyubiquitin messenger ribonucleic acid (mRNA)

X-chromosomally inherited split-hand/split-foot anomaly in a Pakistani kindred.

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A Pakistani kindred comprising seven generations and 36 members with the split-hand/split-foot anomaly is described. The full expression of the trait, monodactylous or split hand and split foot, mainly of the lobster-claw type, was present in 33 males and 3 females. Other females showed a distinctly
The organization of skeletal muscles in decapod crustaceans is significantly altered during molting and development. Prior to molting, the claw muscles atrophy dramatically, facilitating their removal from the base of the claw. During development, lobster claw muscles exhibit fiber switching over
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