Previous studies have demonstrated that the expression of CARD10 is closely associated with the occurrence of tumors, and its role is mainly to promote tumor progression by activating the transcription factor NF-κB. However, the signaling pathway in renal cancer remains unclear. The objective of the present study was to investigate the ability of caspase recruitment domain 10 (CARD10) to regulate the NF-κB signaling pathway and promote the progression of renal cell carcinoma (RCC). Expression of CARD10 in ACHN, 786-O and HK-2 cells was evaluated via western blot analysis, as was the epidermal growth factor (EGF)-induced activation of NF-κB signaling pathway-related proteins in cells. The expression of CARD10 was inhibited by CARD10 short hairpin RNA transfection. Cell cycle analysis and MTT assays were used to evaluate cell proliferation. Cell apoptosis was analyzed via flow cytometry. The invasion of renal cell lines was detected via Transwell cell migration and invasion assays in vitro. The results showed that CARD10 expression was significantly higher in RCC cells than in normal renal tubular epithelial cells. CARD10 silencing inhibited the proliferation, invasion and migration of RCC cells. EGF stimulation upregulated the activation of the NF-κB pathway in RCC cells. Inhibition of CARD10 expression inhibited NF-κB activation in RCC cells. Taken together, these data suggested that CARD10 promotes the progression of renal cell carcinoma by regulating the NF-κB signaling pathway. Thus, this indicated that CARD10 may be a novel therapeutic target in RCC.

Surgical site infection (SSI) is one of the most common complications of emergency abdominal surgery. With the increase of drug-resistant bacteria, abdominal SSI cannot be effectively controlled by increasing the use of antibiotics. Nonchemical treatment as an alternative to antibiotics for abdominal SSI induced by drug-resistant bacteria is urgently needed. This study is aimed at exploring the effects of low-temperature atmospheric plasma (LTAP) exposure for 30 and 60 s on abdominal SSI in in vitro and in vivo experiments. In the in vitro experiment, the culture dishes with extended-spectrum beta-lactamase-producing Escherichia coli ( ESBL-E. coli) were exposed to LTAP and the changes in bacterial concentration and structure were observed by bacterial culture counting and transmission electron microscopy (TEM). In in vivo experiments, we established an abdominal SSI rat model induced by ESBL-E. coli and the infected surgical sites were exposed to LTAP. The infiltration of inflammatory cells, the proliferation of fibroblasts, and the regeneration of fibrous tissue were evaluated by histopathological examination. The in vitro bacterial experiment showed that the concentration of bacteria exposed to LTAP for 30 and 60 s was decreased, and the decline in bacterial concentration in the last 30 s was significantly higher than that in the first 30 s. TEM showed that the bactericidal effect of the LTAP exposure worked by damaging the morphology and intracellular structures of bacteria. In addition, our data suggested that reactive oxygen species are the key mediator of the bactericidal effect, and bacteria exposed to LTAP do not develop resistance to repeated exposure. The pathological results from in vivo experiments revealed that the inflammatory cells infiltrating into the infected site were inhibited. The proliferation of fibroblasts and the regeneration of fibers increased after exposure to LTAP for 30 and 60 s in abdominal SSI. In conclusion, our study indicated that LTAP was effective in wound sterilization, anti-inflammatory action, and healing promotion and holds promise as an alternative to antibiotics for treating abdominal SSIs.

Acute pancreatitis (AP), a sterile inflammation in local pancreas, is well-known as one of the most serious abdominal diseases. It could develop into a systemic inflammation if there is lack of instant supervision. Thus, it is important to find an effective method to solve this clinical challenge. The purpose of our work is to study the anti-inflammatory effect of low temperature atmospheric plasma (LTAP) on AP in vivo, and two treatment doses, namely, 30 s and 60 s, were used in our experiment. The optical emission spectroscopy assay proved that the LTAP produced by an arc discharge reactor contains reactive oxygen and nitrogen species. The histopathologic result showed that the LTAP treatment for 60 s can significantly mitigate AP as compared with the group treated for 30 s. Moreover, the quantity of inflammation cells treated by the LTAP treatment for 60 s and 30 s was markedly reduced, while the 60 s treatment displayed a better suppress effect on AP. Taken together, our study indicated that LTAP can be used as a promising strategy to alleviate AP.

Clear cell renal cell carcinoma is a common malignant tumor of the urinary system. The mechanism of its occurrence and development is unknown, and there is currently few effective comprehensive predictive markers for prognosis and treatment response. With the discovery of a new cell death process - cuproptosis drew the attention of researchers. We constructed a model for the prediction of clinical prognosis and immunotherapy response through integrative analysis of gene expression datasets from KIRC samples in the TCGA database. During the course of the study, we found that cuproptosis genes are significantly differentially expressed between clear cell renal cell carcinoma samples and normal samples. Based on this, we put forward the prognostic model for cuproptosis gene related-long non-coding RNA. And through various statistic and external independent cohorts, we proved that the model is accurate and stable, worthy of clinical application and further exploration and validation.