Renal cell carcinoma is one of the most common malignancy in adults, its prognosis is poor in an advanced stage and early detection is difficult due to the lack of molecular biomarkers. The identification of novel biomarkers for RCC is an urgent and meaningful project. Long non-coding RNA (lncRNA) is transcribed from genomic regions with a minimum length of 200 bases and limited protein-coding potential. Recently, lncRNAs have been greatly studied in a variety of cancer types. They participate in a wide variety of biological processes including cancer biology. In this review, we provide a new insight of the profiling of lncRNAs in RCC and their roles in renal carcinogenesis, with an emphasize on their potential in diagnosis, prognosis and potential roles in RCC therapy.

Laparoscopic partial nephrectomy and robot-assisted partial nephrectomy are attracting increased attention from urologists. They can achieve the same effect of oncology control as radical nephrectomy; moreover, they can offer better preservation of renal function, thus obtaining longterm living benefits. The indications are also expanding, making it possible for larger and more difficult tumors. Laparoscopic partial nephrectomy and robot-assisted partial nephrectomy can be performed by transperitoneal and retroperitoneal approaches, with their individual advantages and limitations. In addition, the renal tumor scoring systems have been widely used and studied in laparoscopic partial nephrectomy and robot-assisted partial nephrectomy. In order to better preserve renal function, the zero-ischemia technique is widely used. The application of intraoperative imaging technology provides convenience and greater benefits. Besides, whether minimal invasive partial nephrectomy can be performed without stop antiplatelet treatment is still disputed. Clinicians perform substantial exploration and practice to achieve the "trifecta" of surgery: complete resection of the tumor, maximum protection of renal function, and no complications.

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Background Exposure to glyoxal, the smallest dialdehyde, is associated with several diseases; humans are routinely exposed to glyoxal because of its ubiquitous presence in foods and the environment. The aim of this study was to examine the damage caused by glyoxal in human aortic endothelial cells. Methods Cell survival assays and quantitative fluorescence assays were performed to measure DNA damage; oxidative stress was detected by colorimetric assays and quantitative fluorescence, and the mitogen-activated protein kinase pathways were assessed using western blotting. Results Exposure to glyoxal was found to be linked to abnormal glutathione activity, the collapse of mitochondrial membrane potential, and the activation of mitogen-activated protein kinase pathways. However, DNA damage and thioredoxin oxidation were not induced by dialdehydes. Conclusions Intracellular glutathione, members of the mitogen-activated protein kinase pathways, and the mitochondrial membrane potential are all critical targets of glyoxal. These findings provide novel insights into the molecular mechanisms perturbed by glyoxal, and may facilitate the development of new therapeutics and diagnostic markers for cardiovascular diseases.