Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenital anomalies of the penis expressed in various forms of flexures can be associated with a rotation of the shaft. An asymmetrical insertion of the suspensory ligament on the dorsal surface of the tunica albuginea often accounts for corporal rotation. This distorts the spatial relationship between the corpora cavernosa and the pubic bone. The two corpora may overlap and the shaft is partially rotated. For the surgical treatment of these defects we proposed (1989) a technique of contrarotation of the tunica albuginea which was later abandoned because it was too invasive. We developed a technique based on the ipsilateral re-suspension of the suspensory ligament of the penis between the tunica of the lower corpus and the pubic symphysis to restore the true axis. The neurovascular adnexa, the corpora cavernosa, and the corpus spongiosum remain untouched.
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PMID:Modified corporopexy as a new approach to the treatment of congenital rotation of the penis. 795 98

Congenital anomalies of the penis expressed in various forms of flexures can be associated to a rotation of the shaft. An asymmetrical insertion of the suspensory ligament on the dorsal surface of the tunica albuginea often accounts for corporal rotation. This distorts the spatial relationship between the corpora cavernosa and the pubic bone. The two corpora may overlap and the shaft is partially rotated. For the surgical treatment of these defects we proposed (1989) a technique of contrarotation of the tunica albuginea which was later abandoned because it was too invasive. We developed a technique based on the ipsilateral re-suspension of the suspensory ligament of the penis between the tunica of the lower corpus and the pubic symphysis to restore the true axis. The neurovascular adnexa, the corpora cavernosa, and the corpus spongiosum remain untouched.
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PMID:Our treatment of congenital complicated penile deviations. 831 52

Congenital anomalies have complex etiologies involving both genetic and nongenetic components. Many are sporadic, without obvious evidence for heritability. An important model for these anomalies is a mutation in laboratory mice that is called "disorganization" (Ds), which functions as a variable autosomal dominant and leads to a wide variety of congenital anomalies involving many developmental processes and systems. Variable expressivity, asymmetrical manifestations, and low penetrance suggest that somatic events determine the location and nature of these anomalies. A statistical analysis suggests that occurrence of anomalies in mice with the Ds mutation follows a Poisson distribution. These results suggest that congenital anomalies in mice with the Ds mutation occur independently of each other. We propose that Ds causes a heritable predisposition to congenital anomalies and that Ds and appropriate somatic events combine to compromise normal development. We also propose that some sporadic, nonheritable congenital anomalies involve somatic mutations at Ds-like loci. Ds may therefore serve not only as a model for developmental anomalies in cell fate and pattern formation but also for complex developmental traits showing variable expressivity, low penetrance, and sporadic occurrence in mice and humans.
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PMID:Two-hit model for sporadic congenital anomalies in mice with the disorganization mutation. 848 37