Oncol Lett
-
The effects of neoadjuvant chemotherapy on the minimum alveolar concentration (MAC) values of sevoflurane and desflurane in patients with hepatocellular carcinoma (HCC) complicated with jaundice were investigated. Eighty patients with HCC complicated with jaundice were selected. Forty patients underwent the neoadjuvant chemotherapy and were grouped into the desflurane group (Group D) and the sevoflurane group (Group S). ⋯ Logistic regression analyses were conducted, respectively, which revealed that the MAC of sevoflurane and desflurane were associated with whether patients received the neoadjuvant chemotherapy. MACLog of sevoflurane and desflurane were decreased in patients receiving the neoadjuvant chemotherapy. The results suggested that neoadjuvant chemotherapy can reduce MAC values of sevoflurane and desflurane in HCC patients complicated with jaundice and may improve these patients' sensitivity to sevoflurane and desflurane.
-
The incidence of complications and mortality following open-heart surgery with cardiopulmonary bypass (CPB) is associated with the severity of the myocardial injury that occurs during surgery. Hydrogen-rich solution (HRS) may prevent antioxidant stress and inhibit apoptosis and inflammation. The present study was designed to investigate the effects of HRS on CPB-induced myocardial injury, and to investigate its potential regulation of the Janus-activated kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway. ⋯ Additionally, the results demonstrated that the HRS treatment significantly increased the expression levels of p-JAK2, p-STAT3 and Bcl-2 in myocardial cells following hypoxia and decreased Bax expression in the control siRNA and CPB groups (P<0.05). In addition, JAK2 siRNA was determined to attenuate these effects of HRS (P<0.05 vs. control siRNA, HRS and CPB groups). Taken together, these results indicated that HRS may alleviate CPB-induced myocardial injury, inhibit myocardial cell apoptosis and protect myocardial cells through regulation of the JAK2/STAT3 signaling pathway.