The origins and distribution of arteries of the celiac-mesenteric system were examined by dissection of 52 formalin-fixed human cadavers. Seventy-five percent of the cadavers exhibited the classic Michels' Type I hepatolienogastric pattern; 25% had different branching patterns. Multiple anomalies of the celiac-mesenteric arterial system were observed in one Caucasian female cadaver: a short lienogastric trunk; a common hepatic artery arising directly from the abdominal aorta; an anomalous course of the hepatic arteries; an accessory left hepatic artery arising from the left and right gastric arterial anastomosis along the lesser curvature of the stomach; a double cystic artery; a common inferior phrenic trunk arising from the celiac trunk; and an aberrant arterial channel connecting the proximal segments of the splenic and gastroduodenal arteries. A patent ductus venosus and an anomalous formation of the portal vein by the confluence of the splenic and superior and inferior mesenteric veins was also observed. Although single anomalies of the celiac-mesenteric arterial system are common, complex combinations, such as were observed in the present case, represent a significant deviation from the normal developmental pattern. There seems to be no report in the literature of such a combination of anomalies coexisting in one individual. The developmental and clinical significance of these anomalous vessels is discussed.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Ewing sarcomas/primitive neuroectodermal tumors (ES/PNET) of the kidney are rarely found high-grade malignant tumors, offering poor prognosis. Although established treatment guidelines for ES of kidney are scarce, a multi-modality treatment approached is typically implemented. Herein, we report a 14-year-old female patient with ES of right kidney. Post-nephrectomy disease recurrence was treated with chemotherapy (i.e., vincristine, doxorubicin and cyclophosphamide); marked reduction in tumor size (i.e., from 18.5 9 11.3 cm 2 to 3.7 9 2.2 cm 2 ; *96% reduction in size) as per computed tomography images was observed. We present our treatment experience and review from the available literature.

SRY-box 9 (SOX9) is the master regulator of the chondrocyte phenotype, which is essential for differentiating chondrogenic mesenchymal condensations into chondrocytes, and is involved in regulating every stage of chondrocyte differentiation. SOX9 deletion in chondrocytes at the late stages of cartilage development results in decreased chondrocyte proliferation; inhibited expression of cartilage matrix genes, including Indian hedgehog and the downstream parathyroid hormone-related protein; and premature conversion of proliferating chondrocytes into hypertrophic chondrocytes, which mineralize their matrix prematurely. Therefore, SOX9 is considered vital for the majority of phases of chondrocyte lineage, from early condensations to the differentiation of proliferating chondrocytes, leading to chondrocyte hypertrophy. It has been reported that SOX9 expression is decreased in osteoarthritis (OA) cartilage. Regeneration or repair of cartilage degradation in OA remains a challenge. Previous studies have indicated that overexpression of SOX9 can promote cartilage repair and can be used as a potential therapeutic agent at the early stages of human OA. The present study identified Scm-like with four malignant brain tumor domains 2 (SFMBT2) as a novel regulator of SOX9 expression in human chondrocytes. Our previous study revealed that SFMBT2 is negatively regulated in OA cartilage, and decreased levels of SFMBT2 contribute to the catabolic phenotype of chondrocytes. The present study detected increased expression levels of SFMBT2 in early cartilage development and during the early phases of chondrogenesis. Overexpression of SFMBT2 in c28/I2 cells upregulated SOX9 expression in a dose-dependent manner. Furthermore, SFMBT2 positively regulated c28/I2 cell proliferation and restored the decreased levels of SOX9 in chondrocytes following tumor necrosis factor-α treatment. Additional studies may reveal novel insights into the molecular mechanism involved and the potential role of SFMBT2 in cartilage repair and OA management.