A 32-year-old woman presented with a slow-growing, painless, subcutaneous lesion in the right inguinal and perineum regions. The mass was 24.0 cm × 10.5 cm × 5.0 cm in size, well circumscribed, mobile, and rubbery. Microscopically, the resected mass was mainly composed by a proliferation of small spindle or stellate cells, variably admixed with mature adipose tissue, embedded within an abundant myxoid and collagenized stroma. Immunohistochemically, the spindle and stellate cells were strongly positive for vimentin, CD34, and bcl-2 antibodies but not for smooth muscle actin and desmin. The tumor was diagnosed as dendritic fibromyxolipoma based on the typical findings of histology and immunohistochemistry. Clinical follow-up of 9 months after surgery revealed no evidence of recurrence. We report the first case of dendritic fibromyxolipoma in the right inguinal and perineum regions and discuss the different diagnosis.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1313680868103019.

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Objective. To investigate the role of oxidative stress, NF-κB activity, and its related cytokines in the pathogenesis of seawater immersion after open abdominal injury (SI-OAI) and whether UTI treatment can attenuate SI-OAI induced IMI. Methods. Wistar rats were randomly divided into three groups: C group, S group, and U group. The rats in C group only suffered from anesthesia and surgical operation, whereas the rats in S group and U group received caudal vein injection of normal saline without/with 50,000 U/kg body weight of UTI. The activities of TNF-α, IL-6, SOD, MDA, ROS, NF-κB, and IκB-β were monitored by ELISA, biochemical methods, EMSA, and Western blot, respectively. Results. The plasma inflammatory mediators and the contents of MDA, ROS, and NF-κB in intestine as well as the pathological scores in ileal mucosa were significantly increased in rats after SI-OAI, accompanied by a reduction in SOD activities and IκB-β levels. UTI treatment significantly attenuated intestinal histopathological changes with evidence of a decrease in all of the parameters, except for upregulation of the levels of SOD and IκB-β protein. Conclusion. UTI can attenuate SI-OAI induced IMI via inhibition of NF-κB activity, subsequently inhibiting the expression of inflammatory cytokines and by combating oxidative stress.