RESUMO
INTRODUCTION AND IMPORTANCE: Schwannoma, a benign tumor originating from Schwann cells, is a rare case found intraorally. The tongue, palate and buccal mucosa are the most common sites of intraoral Schwannoma while it is very rarely found on the lips. Previous studies reported only twelve cases of Schwannoma on the upper lip. The etiology of Schwannoma is unknown, but in some literature, Schwannoma occurs due to a defect in the NF2 gene. Management of Schwannoma is excision of the capsule. The prognosis is good, and the recurrency is low. This article reports a rare case of upper lip Schwannoma in adolescent and its management with its histological, immunohistochemical and pathogenesis aspects. CASE PRESENTATION: A 16-years old female presented a painless, semi-solid, mobile lump on the upper lip measuring of approximately 1.5 × 3 cm that had similar color with the surrounding tissue. The lump appeared 7 years ago. CLINICAL DISCUSSION: Excision of the capsule and margins of the tumor. Histopathological examination showed a unique feature of Schwannoma, the Verocay bodies. Subsequent immunohistochemical examination of S100 protein showed a classic type of Schwannoma. CONCLUSION: Upper lip schwannoma is a very rare tumor, and this type of tumor cannot be distinguished from other benign soft tissue tumors based on clinical findings. Immunohistochemical results are in accordance with the Histopathological results for the final diagnosis of Schwannoma. Schwannoma can be used as a differential diagnosis in cases of lumps on the lips with sessile, similar color like surrounding tissue, painless, and movable features.
RESUMO
Pseudomonas aeruginosa infection is considered a high-risk nosocomial infection and is very difficult to eradicate because of its tolerance to antibiotic treatment. A new compound, autoinducer analog-1 (AIA-1), has been demonstrated to reduce antibiotic tolerance, but its mechanisms remain unknown. This study aimed to investigate the mechanisms of AIA-1 in the antibiotic tolerance of P. aeruginosa. A transposon mutant library was constructed using miniTn5pro, and screening was performed to isolate high tolerant mutants upon exposure to biapenem and AIA-1. We constructed a deletion mutant and complementation strain of the genes detected in transposon insertion site determination, pruR and PA0066-65-64, and performed killing assays with antibiotics and AIA-1. Gene expression upon exposure to biapenem and AIA-1 and their relationship to stress response genes were analyzed. High antibiotic tolerance was observed in Tn5-pruR and Tn5-PA0065 transposon mutants and their deletion mutants, ΔpruR and ΔPA0066-65-64. Complemented strains of pruR and PA0066-65-64 with their respective deletion mutants exhibited suppressed antibiotic tolerance. It was determined that deletion of PA0066-65-64 increased rpoS expression, and PA0066-65-64 affects antibiotic tolerance via the rpoS pathway. Additionally, antibiotics and AIA-1 were found to inhibit pruR and PA0066-65-64. This study proposed that pruR and PA0066-65-64 are members of the antibiotic tolerance suppressors.
