Follmann balanitis - A very rare presentation of primary syphilis.

Syphilis is a sexually transmitted infection caused by Treponema pallidum. The primary stage of the disease manifests as a chancre. Balanoposthitis as a presenting feature of primary syphilis is a very rare presentation. A 26-year-old male presented with asymptomatic erythematous plaques involving the glans and prepuce after unprotected intercourse with a known female. Routine investigations, serology, and dark field examination were normal. Fontana-Masson stain revealed spirochetes and a diagnosis of syphilitic balanitis of Follmann was entertained. This rare presentation accounts for only 0.3%-0.5% of cases of primary syphilis and hence is highlighted in this case report.

Early Surgical Intervention in Amniotic Band Sequence for Upper Extremity Motor Nerve Palsies: A Case Report.

Urgent surgical intervention for amniotic band sequence (ABS) is currently indicated for concerns of vascular compromise and progressive lymphedema. Peripheral motor nerve palsies are rare, and reports of surgical intervention in these cases describe persistent motor dysfunction. We report band release and ulnar, median, and radial nerve decompression in a 1-week-old with a severe upper extremity constriction band and signs of ulnar nerve motor dysfunction. A literature review on nerve exploration and outcomes of patients with motor nerve palsy from ABS was performed. Early evidence of ulnar motor function was observed at 5.5-month follow-up. Previous reports of nerve decompression for upper extremity constriction bands with motor nerve palsy document poor recovery after interventions beginning at 3 months of age. In this case, band release and nerve decompression were undertaken at 7 days of age, and we observed early motor recovery. This finding suggests that very early surgical intervention in the neonate may facilitate nerve recovery in appropriate candidates.

Enhanced Dendritic Actin Network Formation in Extended Lamellipodia Drives Proliferation in Growth-Challenged Rac1P29S Melanoma Cells.

Actin assembly supplies the structural framework for cell morphology and migration. Beyond structure, this actin framework can also be engaged to drive biochemical signaling programs. Here, we describe how the hyperactivation of Rac1 via the P29S mutation (Rac1P29S) in melanoma hijacks branched actin network assembly to coordinate proliferative cues that facilitate metastasis and drug resistance. Upon growth challenge, Rac1P29S-harboring melanoma cells massively upregulate lamellipodia formation by dendritic actin polymerization. These extended lamellipodia form a signaling microdomain that sequesters and phospho-inactivates the tumor suppressor NF2/Merlin, driving Rac1P29S cell proliferation in growth suppressive conditions. These biochemically active lamellipodia require cell-substrate attachment but not focal adhesion assembly and drive proliferation independently of the ERK/MAPK pathway. These data suggest a critical link between cell morphology and cell signaling and reconcile the dichotomy of Rac1's regulation of both proliferation and actin assembly by revealing a mutual signaling axis wherein actin assembly drives proliferation in melanoma.