Objective To observe the changes of pleth variability index ( PVI) and central venous pressure ( CVP) in patients undergo-ing resection operation of brain neoplasms,and the correlation of PVI with CVP was investigated. Methods Forty-two patients ( ASA Ⅱ~Ⅲ grade) undergoing elective resection operation of brain neoplasms were included in the study. PVI was monitored continously with Masio Radical-7 pulse oximeter after patient entering operative room. CVP was monitored after central venous catheterization placed with regional an-esthesia. Total intravenous anesthesia was chosen. CVP and PVI were recorded at the time of entering operative room,operation began,and 30 minutes,60 minutes,90 minutes,120 minutes after the beginning of operation. Results The correlation coefficient of PVI with CVP was 0. 201 under spontaneously breathing ( at patient entering operative room before anesthesia) and was 0. 237 under mechanical ventilation. Conclusion Correlation of PVI and CVP is lower. The value of PVI might need further research for guiding volume management.

Objective To observe the leading effect of end-tidal pressure of carbon dioxide in artery ( PET CO2 ) on mechanical ventila-tion in New Zealand white rabbits, and to establish parameters for medical animal experiments in terms of hemodynamics, blood gas, blood glucose, electrolyte. Methods 31 anesthetized New Zealand rabbits were practiced tracheostomy tube and mechanical ventilation. Respira-tion rate was 40 breaths/min and tidal volume was adjusted so that PET CO2 was 29 mmHg. Invasive blood pressure, electrocardiogram and PET CO2 were monitored. Blood gas analysis, electrolyte, hemoglobin and blood glucose were tested. Results When PET CO2 was maintained at 29 mmHg, the results were as follows:PH (7.42 ±0.07), 95% confidenceinterval (7.40~7.45);PaCO2(38.5 ±5.8) mmHg, 95%confidenceinterval (36. 4~40. 6) mmHg;BE (1. 45 ± 2. 80) mmol/L,95% confidenceinterval (0. 43~2. 48) mmHg. Conclusion Moni-toring of PET CO2 is good to guide mechanical ventilation in New Zealand white rabbits.

The definition and function of epidemiological investigation report on food safety accident is described and its impact on the business behavior,civil liability,administrative responsibility,and criminal responsibility of food producers,marketers,supervisory and management department is presented.It suggests that center for disease prevention and control should give attention to timeliness,authenticity,accuracy,normalization of epidemiological investigation report on food safety accidents and cases.The purpose is to avoid accountability on investigation of food safety accidents and ensure the epidemiological investigation report not been challenged in legal proceedings as evidence.

Hepatic stellate cells(HSCs)are essential drivers of fibrogenesis.Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis.18beta-glycyrrhetinic acid(18β-GA)is a natural com-pound that exists widely in herbal medicines,such as Glycyrrhiza uralensis Fisch,which is used for treating multiple liver diseases,especially in Asia.In the present study,we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs.18β-GA inhibited the expression of α-smooth muscle actin and collagen type Ⅰ alpha-1.Using a chemoproteomic approach derived from activity-based protein profiling,together with cellular thermal shift assay and surface plasmon reso-nance,we found that 18β-GA covalently targeted peroxiredoxin 1(PRDX1)and peroxiredoxin 2(PRDX2)proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities.18β-GA induced the elevation of reactive oxygen species(ROS),resulting in the apoptosis of activated HSCs.PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs.Collectively,our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis,highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis.

Ferroptosis is a form of regulated cell death, characterized by excessive membrane lipid peroxidation in an iron- and ROS-dependent manner. Celastrol, a natural bioactive triterpenoid extracted from Tripterygium wilfordii, shows effective anti-fibrotic and anti-inflammatory activities in multiple hepatic diseases. However, the exact molecular mechanisms of action and the direct protein targets of celastrol in the treatment of liver fibrosis remain largely elusive. Here, we discover that celastrol exerts anti-fibrotic effects via promoting the production of reactive oxygen species (ROS) and inducing ferroptosis in activated hepatic stellate cells (HSCs). By using activity-based protein profiling (ABPP) in combination with bio-orthogonal click chemistry reaction and cellular thermal shift assay (CETSA), we show that celastrol directly binds to peroxiredoxins (PRDXs), including PRDX1, PRDX2, PRDX4 and PRDX6, through the active cysteine sites, and inhibits their anti-oxidant activities. Celastrol also targets to heme oxygenase 1 (HO-1) and upregulates its expression in activated-HSCs. Knockdown of PRDX1, PRDX2, PRDX4, PRDX6 or HO-1 in HSCs, to varying extent, elevated cellular ROS levels and induced ferroptosis. Taken together, our findings reveal the direct protein targets and molecular mechanisms via which celastrol ameliorates hepatic fibrosis, thus supporting the further development of celastrol as a promising therapeutic agent for liver fibrosis.