Objective To describe the detailed anatomy of the urethral plate in relation to its controversial role in hypospadias surgery. Materials and methods A newborn penis with proximal penile hypospadias and two fetal penises with distal shaft hypospadias were included in the study; 30 normal fetal penises served as the control. Specimens were embedded in paraf®n and serially sectioned (6 mm) after formalin ®xation. Every 10th section was stained with haematoxylin and eosin.Immunohistochemical staining for nerves (S100), smooth muscles (a-actin), blood vessels (factor VIII) and epithelium (cytokeratins 7, 14 and 18) were used on selected sections, with particular attention to the urethral plate. Masson's trichrome and Sirius Red stains were used to localize collagen. Results There were extensive blood vessels, glands and smooth muscle under the urethral plate in the hypospadias specimens. These relatively well organized tissues corresponded to an abnormally formed corpus spongiosum. The glands underneath the urethral plate and adjacent to the normal urethra showed positive staining for cytokeratins 7 and 18, respectively (markers of endodermal origin) but were negative for cytokeratin 14 (a marker of ectodermal origin). Penile skin and urethral plate epithelium stained positively for cytokeratin 14 but not for cytokeratin 7 and 18. The urethral plate has a rich nerve supply, as determined by S100 staining.Collagen intensity under the urethral plate was no different from that in normal areas. Tunica albuginea stained intensely for type I and III collagen. Conclusion These results show that the urethral plate is well vascularized, has a rich nerve supply and an extensive muscular and connective tissue backing. These features may explain the lower complication rate with onlay¯aps than with tube¯aps. Therefore, from these anatomical ®ndings, we continue to advocate preservation of the urethral plate and the onlay island¯ap for hypospadias reconstruction.
In humans, trisomy 21 results in a specific phenotype known as Down syndrome (DS). The mechanism by which an extra copy of normal genes leads to the DS phenotype is unknown. Most studies in DS and other aneuploid organisms have shown that gene dose is proportional to gene expression. To date, most genes examined have encoded either metabolic enzymes or constitutively expressed products. In the trisomy 16 mouse, an animal model of DS, we found marked dysregulation of two developmentally regulated genes, App and Prn‐p. Dysregulation varied from tissue to tissue and during development in the same tissue. We conclude that abnormal phenotypes seen in aneuploid conditions may result in part from disordered expression of developmentally regulated genes.
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