RESUMEN
Background: Acral persistent papular mucinosis (APPM) is a rare idiopathic subtype of localized lichen myxedematosus. To date, there have been less than 41 APPM cases reported worldwide, however, almost all patients were older than 18 years of age. A 7-year-old child was first reported in this paper. Case Description: A 7-year-old boy was admitted to our hospital with a solitary skin-colored papule on the radial side of the middle segment of his right index finger. The patient wanted to know the exact diagnosis and remove it because the flexion movement of the middle segment had been affected. Thus, a surgery was performed. Histopathological examination of a biopsy specimen obtained from the papule on the radial side of the middle segment of his right index finger showed a focal and well-circumscribed deposit of mucin in the papillary and middermis. The deposit never extended deeply into the reticular dermis. Mucin spared a subepidermal area in the papillary dermis. Alcian blue stains can highlight the mucin. The papule was histologically diagnosed as an APPM and excised surgically. The wound gradually healed after the operation, and no obvious recurrence, scar or other discomfort was observed during follow-up so far. Conclusions: To the best of our knowledge, this is the rare case of a child APPM presenting as a solitary papule affecting the flexion movement of the middle segment. Since it is a rare disease, we report this case to contribute to future research on the diagnosis and pathogenesis of APPM.
RESUMEN
Lipoma of the tongue is a rare benign tumor that accounts for approximately 1% to 5% of all oral cavity tumors while 0.3% of tumors are of the tongue. Notably, it is rarer in children. In this article, we report the case of a 4-year-old girl with lipomas of the tongue. The lipomas were found at age 1 year by her parents, located on the tip, ventro, and dorsum of the tongue, and presenting with a trend to increase gradually. At the time of presentation to the hospital at age 4 years, the articulatory function of the patient was partially affected, and surgical excision was performed. The surgery was uneventful, and no evidence of recurrence was noted at 3 month follow-up.
RESUMEN
Epithelialmesenchymal transition (EMT) serves an important regulatory role in obstructive nephropathy and renal fibrosis. As an intracellular energy sensor, AMPactivated protein kinase (AMPK) is essential in the process of EMT. The aim of the present study was to elucidate changes in the expression levels of AMPKα2 and which AMPKα2 genes play a role during EMT. TGFß1 was used to induce EMT in normal rat renal tubular epithelial (NRK52E) cells. The short hairpin AMPKα2 lentivirus was used to interfere with AMPKα2 expression levels in EMTderived NRK52E cells and AMPKα2 expression levels and EMT were detected. Differential gene expression levels following AMPKα2 knockdown in EMTderived NRK52E cells were assessed via gene microarray. Potential regulatory pathways were analyzed using ingenuity pathway analysis (IPA) and differentially expressed genes were partially verified by reverse transcriptionquantitative PCR (RTqPCR) and western blotting. AMPKα2 was upregulated in TGFß1induced EMTderived NRK52E cells. EMT progression was significantly inhibited following downregulation of expression levels of AMPKα2 by shAMPKα2 lentivirus. A total of 1,588 differentially expressed genes were detected following AMPKα2 knockdown in NRK52E cells in which EMT occurred. The ERK/MAPK pathway was significantly impaired following AMPKα2 knockdown, as indicated by IPA analysis. Furthermore, RTqPCR and western blot results demonstrated that the expression levels of AMPKα2, vets erythroblastosis virus E26 oncogene homolog1 (ETS1) and ribosomal protein S6 kinase A1 (RPS6KA1) were upregulated following EMT in NRK52E cells, whereas the expression levels of ETS1 and RPS6KA1 were downregulated following AMPKα2 knockdown. It was concluded that AMPKα2 plays a key role in the regulation of rat renal tubular EMT, which may be achieved by modulating ETS1 and RPS6KA1 in the ERK/MAPK pathway.