Colon cancer is one of the most common cancers in the world. To identify the candidate genes in the carcinogenesis and progression of colon cancer, the microarray datasets GSE10950, GSE44861 and GSE74602 were downloaded from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) were identified, and functional enrichment analyses were performed. A total of 176 DEGs were identified, consisting of 55 genes upregulated and 121 genes downregulated in colon cancer tissues compared to non-cancerous tissues. The DEGs were mainly enriched in mineral absorption, nitrogen metabolism and complement and coagulation cascades. By using STRING database analysis, we constructed a coexpression network composed of 140 nodes and 280 edges for the DEGs with a combined score >0.4 and a significant interaction relation. Thirteen hub genes were identified, and poor OS of patients was only associated with high expression of Matrix Metallopeptidase 7 ( MMP7 ), which may be involved in the carcinogenesis, invasion or recurrence of colon cancer. In conclusion, we propose that the DEGs and hub genes identified in the present study may be regarded as diagnostic biomarkers for colon cancer. Moreover, the overexpression of MMP7 may correlate with poor prognosis.

Glutamate excitotoxicity in cerebral ischemia/reperfusion is an important cause of neurological damage. The aim of this study was to investigate the mechanism of Na+, K+-ATPase (NKA) involved in l ow concentration of ouabain (Oua, activating NKA)-induced protection of rat cerebral ischemia-reperfusion injury. The 2,3,5triphenyltetrazolium chloride (TTC) staining and neurological deficit scores (NDS) were performed to evaluate rat cerebral injury degree respectively at 2 h, 6 h, 1 d and 3 d after reperfusion of middle cerebral artery occlusion (MCAO) 2 h in rats. NKA a1/a2 subunits and glutamate transporter-1 (GLT-1) protein expression were investigated by Western blotting. The cerebral infarct volume ratio were evidently decreased in Oua group vs MCAO/R group at 1 d and 3 d after reperfusion of 2 h MCAO in rats (*p ＜ 0.05 ). Moreover, NDS were not significantly different (p ＞ 0.05 ). NKA a1 was decreased at 6 h and 1 d after reperfusion of 2 h MCAO in rats, and was improved in Oua group. However, NKA a1 and a2 were increased at 3 d after reperfusion of 2 h MCAO in rats, and was decreased in Oua group. GLT-1 was decreased at 6 h, 1 d and 3 d after reperfusion of 2 h MCAO in rats, and was improved in Oua group. These data indicated that l ow concentration of Oua could improve MCAO/R injury through probably changing NKA a1/a2 and GLT-1 protein expression, then increasing GLT-1 function and promoting Glu transport and absorption, which could be useful to determine potential therapeutic strategies for patients with stroke. Low concentration of Oua improved rat MCAO/ R injury via NKA a1/a2 and GLT-1.

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Hereditary protein S deficiency is an autosomal dominant disorder associated with a high risk of venous thromboembolism (VTE) and usually results from mutations of PROS1. Historically heparin and warfarin have been applied as recommended treatment of VTE. Recent researches showed that rivaroxaban provided more consistent and predictable anticoagulation than warfarin. However, it is unknown whether rivaroxaban is effective for the treatment of VTE in patients with thrombophilia, including protein S deficiency, due to lack of evidence. Here, we report two cases of recurrent VTE in two patients with hereditary protein S deficiency, owing to the same nonsense mutation in PROS1, which were successfully treated by rivaroxaban monotherapy.