RESUMEN
Management of testicular rupture with a large tunical defect may not be feasible without excision of viable tissue. This study describes the use of a vascularized tunica vaginalis flap, without debridement of viable tissue, in four adolescents. Postoperative ultrasound showed good blood flow and 80% volume of the contralateral testis in two cases. Postoperative exam revealed normal exam and ultrasonographic appearance in three patients, the fourth was demonstrated to be small and undescended during evaluation of contralateral testicular torsion. This approach is recommended in cases of large tunical defects, as it avoids the debridement of viable testicular tissue.
Asunto(s)
Procedimientos de Cirugía Plástica , Rotura/cirugía , Colgajos Quirúrgicos , Testículo/lesiones , Testículo/cirugía , Adolescente , Humanos , MasculinoAsunto(s)
Colangitis/diagnóstico por imagen , Colangitis/patología , Colestasis Intrahepática/diagnóstico por imagen , Colestasis Intrahepática/patología , Absceso Hepático/diagnóstico por imagen , Absceso Hepático/patología , Anciano , Colangitis/etiología , Colestasis Intrahepática/etiología , Humanos , Absceso Hepático/etiología , Trasplante de Hígado/efectos adversos , Masculino , Radiografía , SíndromeRESUMEN
Nitrofen is a diphenyl ether herbicide that produces a spectrum of fetal abnormalities in rodents. To characterize the molecular mechanisms of nitrofen-mediated birth defects at the cellular level, we explored its effects on undifferentiated P19 teratocarcinoma cells. Nitrofen induces a time-dependent cell death of P19 cells that is associated with increases in TUNEL-positivity and caspase-3 cleavage suggesting that nitrofen induces P19 cell apoptosis. In addition, the increase in TUNEL-positive cells was inhibited with zVAD-fmk, suggesting that nitrofen induces a caspase-dependent apoptosis. Nitrofen treatment was associated with increased p38 MAP kinase activity, though pretreatment of cells with multiple p38 inhibitors did not affect nitrofen-mediated caspase-3 cleavage, suggesting caspase-3 cleavage is p38-independent. Nitrofen induced a dose-dependent increase in reactive oxygen species (ROS), which was accompanied by a decrease in the ratio of reduced/oxidized glutathione, indicating that nitrofen alters the cellular redox state of these cells. Furthermore, pretreatment of cells with N-acetyl cysteine gave a dose- and time-dependent reduction of caspase-3 cleavage, supporting the observations that caspase-3 cleavage is cell-redox-dependent. Therefore, nitrofen induces P19 cell apoptosis that is cell-redox-dependent and is associated with increases in p38 activity and ROS and may play a role in nitrofen-mediated birth defects.