RESUMO
BACKGROUND: In China, as the population grows older, the number of elderly people who have died from respiratory problems has increased. AIM: To investigate whether enhanced recovery after surgery (ERAS)-based respiratory function training may help older patients who had abdominal surgery suffer fewer pulmonary problems, shorter hospital stays, and improved lung function. METHODS: The data of 231 elderly individuals having abdominal surgery was retrospectively analyzed. Based on whether ERAS-based respiratory function training was provided, patients were divided into ERAS group (n = 112) and control group (n = 119). Deep vein thrombosis (DVT), pulmonary embolism (PE), and respiratory tract infection (RTI) were the primary outcome variables. Secondary outcome variables included the Borg score Scale, FEV1/FVC and postoperative hospital stay. RESULTS: The percentage of 18.75% of ERAS group participants and 34.45% of control group participants, respectively, had respiratory infections (P = 0.007). None of the individuals experienced PE or DVT. The ERAS group's median postoperative hospital stay was 9.5 d (3-21 d) whereas the control groups was 11 d (4-18 d) (P = 0.028). The Borg score decreased on the 4th d following surgery in the ERAS group compared to the 2nd d prior (P = 0.003). The incidence of RTIs was greater in the control group than in the ERAS group among patients who spent more than 2 d in the hospital before surgery (P = 0.029). CONCLUSION: ERAS-based respiratory function training may reduce the risk of pulmonary complications in older individuals undergoing abdominal surgery.
RESUMO
Chronic infection of hepatitis B virus (HBV) is one of the major causes of hepatocellular carcinoma (HCC) in the world. The hepatitis B virus X protein (HBx) is implicated in HCC development, although its oncogenic role remains controversial. HBx is a multifunctional regulator that modulates transcription, signal transduction, cell cycle progress, and DNA repair by directly or indirectly interacting with host factors. We constructed the HBx stably expressing HepG2 cell line to investigate the impact of HBx on intra-S-phase checkpoint induced by mitomycin C (MMC). The HBx transformed HepG2 cells are more sensitive to MMC treatment and showed defective radioresistant DNA synthesis compared to the control cell line transformed with empty vector. With DNA content assay, HBx transformed cells showed defective S phase arrest and a consequent G2/M arrest after MMC treatment. HBx impaired the ATR dependent phosphorylation of Chk1 and monoubiquitination of FANCD2. Overexpression of ATR reverted the MMC induced phenotype of Chk1 and FANCD2 in HBx transformed cells. The defect of intra-S-phase checkpoint resulted in accumulation of genomic instability. In conclusion, HBx disrupts intra-S-phase checkpoint induced by MMC through ATR-Chk1 and ATR-FANCD2 pathways.