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Squamous cell carcinoma (SCC) is well-known for its high rate of metastasis with poor prognosis. CD109 is a glycosylphosphatidylinositol-anchored cell-surface glycoprotein. Recently, CD109 emerges as a potential biomarker and a therapeutic target for SCCs. Accumulating studies have reported that CD109 is highly expressed in human SCCs of multiple organs, and may contribute to the progression of SCCs. In this review, we summarized the findings on expression pattern of CD109 in SCCs, and discussed the molecular mechanisms underlying the roles of CD109 in pathogenesis of SCCs.

Sepsis, the systemic inflammatory responses after infection, remains a serious cause of morbidity and mortality in critically ill patients. The anti-malarial agent dihydroartemisinin (DHA) has been shown to be anti-inflammatory. In this study, we examined the effects of DHA on sepsis-induced acute kidney injury (AKI) and explored the mechanism underlying its mode of action in AKI. In a lipopolysaccharide (LPS)-induced mouse model, we observed that DHA treatment ameliorated glomerular injury, and relieved elevation of the urine albumin to creatinine ratio (UACR) and serum creatinine. At a concentration of 25 μM, DHA had no effect on overall cellular viability or apoptosis in assays with human renal glomerular endothelial cells (HRGECs), but significantly inhibited the tumor necrosis factor-α (TNF-α)-induced hyperpermeability of HRGEC monolayers. We found that TNF-α decreases the expression of the junctional protein occludin in HRGECs, which is reversed by DHA. Taken together, our results demonstrate that DHA decreases permeability of the glomerular endothelium by maintenance of occludin expression. This suggests DHA may have therapeutic utility in sepsis-induced AKI.

Free flap transplantation is the most important plastic surgery treatment. Although free flap is an important tissue repair tool for plastic surgery, it is easy to happen due to the anastomotic stenosis or thrombosis, as well as the inflammatory reaction caused by ischemia-reperfusion injury of the flap and the inflammation caused by these inflammatory reactions. Microcirculation contracture or occlusion will lead to partial or complete flap necrosis, thus affecting the repair effect. Numerous studies show that neutrophils are closely involved in the process of ischemic injury of free flaps. The purpose of this experiment is to investigate the use of ulinastatin to inhibit the inflammatory infiltration of free flaps to improve the survival of the flap.