Two C. elegans DM domain proteins, DMD-3 and MAB-3, function in late stages of male somatic gonad development.

To bring about sexual dimorphism in form, information from the sex determination pathway must trigger sex-specific modifications in developmental programs. DM-domain encoding genes have been found to be involved in sex determination in a multitude of animals, often at the level of male somatic gonad formation. Here we report our findings that the DM-domain transcription factors MAB-3 and DMD-3 function together in multiple steps during the late stages of C. elegans male somatic gonad development. Both mab-3 and dmd-3 are expressed in the linker cell and hindgut of L4 males and dmd-3 is also expressed in presumptive vas deferens cells. Furthermore, dmd-3, but not mab-3, expression in the linker cell is downstream of nhr-67, a nuclear hormone receptor that was previously shown to control late stages of linker cell migration. In mab-3; dmd-3 double mutant males, the last stage of linker cell migration is partially defective, resulting in aberrant linker cell shapes and often a failure of the linker cell to complete its migration to the hindgut. When mab-3; dmd-3 double mutant linker cells do complete their migration, they fail to be engulfed by the hindgut, indicating that dmd-3 and mab-3 activity are essential for this process. Furthermore, linker cell death and clearance are delayed in mab-3; dmd-3 double mutants, resulting in the linker cell persisting into adulthood. Finally, DMD-3 and MAB-3 function to activate expression of the bZIP transcription factor encoding gene zip-5 and downregulate the expression of the zinc metalloprotease ZMP-1 in the linker cell. Taken together, these results demonstrate a requirement for DM-domain transcription factors in controlling C. elegans male gonad formation, supporting the notion that the earliest DM-domain genes were involved in male somatic gonad development in the last common ancestor of the bilaterians.

Comparative Radiographic Analysis of the Width of the Lesser Digit Proximal Phalangeal Heads.

BACKGROUND: Digital deformities represent a common presenting abnormality and target for surgical intervention in podiatric medicine and surgery. The objective of this investigation was to compare the radiographic width of the heads of the lesser digit proximal phalanges. METHODS: One hundred fifty consecutive feet with a diagnosis of digital deformity and performance of weightbearing radiographs were analyzed. The maximum width of the heads of the lesser digit proximal phalanges were recorded from the radiographs using computerized digital software. RESULTS: The mean ± standard deviation of the head of the second digit proximal phalanx was 9.74 ± 0.87 mm (range, 7.94-11.78 mm); the head of the third digit proximal phalanx, 9.00 ± 0.91 mm (range,7.27-10.94 mm); the head of the fourth digit proximal phalanx, 8.49 ± 1.01 mm (range, 5.57-10.73 mm); and the head of the fifth digit proximal phalanx, 8.67 ± 0.89 mm (range, 6.50-11.75 mm). The width of the head of the proximal phalanx decreased from the second digit to the third digit (P < .001), decreased from the third digit to the fourth digit (P < .001), and then increased from the fourth digit to the fifth digit (P = .032). CONCLUSIONS: The results of this investigation provide evidence in support of an anatomical and structural contribution to digital deformities. The width of the heads of the lesser digit proximal phalanges decreased from the second to the third to the fourth toes, and then subsequently increased with the fifth proximal phalangeal head.

Shoe Dermatitis.

Shoe dermatitis is a type of contact dermatitis precipitated by allergens or irritants found in shoes. Potassium dichromate, commonly used in leather processing, is one of the most prevalent agents responsible for shoe dermatitis; however, it is not the only one. Shoe dermatitis caused by an allergen or an irritant may affect a person of any age, sex, or ethnicity. Numerous treatments exist for shoe dermatitis, the most simple yet important being avoidance of causative agents. Pharmaceutical agents commonly used are emollients, humectants, and topical corticosteroids. In more severe cases, topical calcineurin inhibitors and phototherapy may be used.