Objective To investigate the influence of rutin on neuroinflammation in rats with hydraulic shock brain injury by regulating thioredoxin-interacting protein(TXNIP)/NOD-like receptor protein 3(NLRP3)signaling pathway.Methods Rats were randomly separated into model group and sham operation group;the rats in the model group were established by hydraulic impact method.After modeling,they were randomly separated into rutin low(rutin-L,25 mg·kg-1 rutin)and medium(rutin-M,50 mg·kg-1 rutin).D),high(rutin-H,100 mg·kg-1 rutin)dose groups,model group and positive control group(dexamethasone group,0.1 mg·kg-1 dexamethasone),18 animals/group.Each group was intervened with drugs and normal saline once a day,and after continuous intervention for 3 days,the neurological deficit(neurological severity score,NSS)of the rats was scored;the rats were sacrificed by decapitation,the cerebral edema was determined,the brain tissue around the contusion was separated,and the histological changes,inflammatory cytokine indicators-tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)levels and TXNIP,NLRP3 protein expression levels were measured.Results The rats in the sham operation group had no injury.The integrity of brain tissue in model group was damaged,cell wrinkly nuclei were deeply stained,interstitial edema was accompanied by holes and the TNF-α and IL-1β levels,NSS score,cerebral edema,TXNIP and NLRP3 protein expression levels were all increased compared with those in the sham operation group(P<0.05);after rutin intervention,the pathological injury of rat brain tissue was relieved,and the TNF-α and IL-1β levels,NSS score,cerebral edema,TXNIP,and NLRP3 protein expression levels were all lower than those in the model group(P<0.05),there was no significant difference between the rutin-H group and the dexamethasone group(P>0.05).Conclusion Rutin can inhibit the inflammatory response of hydraulic shock brain injury rats,improve brain tissue injury and edema,which may be related to the inhibition of TXNIP/NLRP3 signaling pathway.

Objective To investigate the influence of rutin on neuroinflammation in rats with hydraulic shock brain injury by regulating thioredoxin-interacting protein(TXNIP)/NOD-like receptor protein 3(NLRP3)signaling pathway.Methods Rats were randomly separated into model group and sham operation group;the rats in the model group were established by hydraulic impact method.After modeling,they were randomly separated into rutin low(rutin-L,25 mg·kg-1 rutin)and medium(rutin-M,50 mg·kg-1 rutin).D),high(rutin-H,100 mg·kg-1 rutin)dose groups,model group and positive control group(dexamethasone group,0.1 mg·kg-1 dexamethasone),18 animals/group.Each group was intervened with drugs and normal saline once a day,and after continuous intervention for 3 days,the neurological deficit(neurological severity score,NSS)of the rats was scored;the rats were sacrificed by decapitation,the cerebral edema was determined,the brain tissue around the contusion was separated,and the histological changes,inflammatory cytokine indicators-tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)levels and TXNIP,NLRP3 protein expression levels were measured.Results The rats in the sham operation group had no injury.The integrity of brain tissue in model group was damaged,cell wrinkly nuclei were deeply stained,interstitial edema was accompanied by holes and the TNF-α and IL-1β levels,NSS score,cerebral edema,TXNIP and NLRP3 protein expression levels were all increased compared with those in the sham operation group(P<0.05);after rutin intervention,the pathological injury of rat brain tissue was relieved,and the TNF-α and IL-1β levels,NSS score,cerebral edema,TXNIP,and NLRP3 protein expression levels were all lower than those in the model group(P<0.05),there was no significant difference between the rutin-H group and the dexamethasone group(P>0.05).Conclusion Rutin can inhibit the inflammatory response of hydraulic shock brain injury rats,improve brain tissue injury and edema,which may be related to the inhibition of TXNIP/NLRP3 signaling pathway.

Pharmacokinetics (PK) is the study of the absorption, distribution, metabolism, and excretion (ADME) processes of a drug. Understanding PK properties is essential for drug development and precision medication. In this review we provided an overview of recent research on PK with focus on the following aspects: (1) an update on drug-metabolizing enzymes and transporters in the determination of PK, as well as advances in xenobiotic receptors and noncoding RNAs (ncRNAs) in the modulation of PK, providing new understanding of the transcriptional and posttranscriptional regulatory mechanisms that result in inter-individual variations in pharmacotherapy; (2) current status and trends in assessing drug-drug interactions, especially interactions between drugs and herbs, between drugs and therapeutic biologics, and microbiota-mediated interactions; (3) advances in understanding the effects of diseases on PK, particularly changes in metabolizing enzymes and transporters with disease progression; (4) trends in mathematical modeling including physiologically-based PK modeling and novel animal models such as CRISPR/Cas9-based animal models for DMPK studies; (5) emerging non-classical xenobiotic metabolic pathways and the involvement of novel metabolic enzymes, especially non-P450s. Existing challenges and perspectives on future directions are discussed, and may stimulate the development of new research models, technologies, and strategies towards the development of better drugs and improved clinical practice.

Objective To summarize the experience of surgical treatment of ascending aortic aneurysms and aortic dissections. Methods From February 2001 to October 2005, 31 patients including 26 male, 5 female, aged 41.3 years old (range 14-72) received surgical management. Twenty cases were diagnosed as ascending aortic aneurysm and aortic root aneurysm, 8 as Standford A dissection, 3 as Stanford B dissection. Twenty-one patients underwent classic Bentall procedure in which VSD repair was carried out in 1 case, mitral valvoplasty in 2 and mitral valve replacement in 2; Four patients underwent modified Bentall procedure (coronary button technique); Three patients underwent Wheat procedure; The remaining 3 patients with Stanford B dissection underwent graft replacement of descending aorta. Results There was no death during hospital stay that lasted 13-46 d with an average of 16.4 d after operation. The mean clinical follow-up was (21?18.5) months (range 1-63 months). One patient died without describable cause two years later. One patient had ascending aorta-pulmonary artery fistula at color Doppler examination half a year later. One patient was detected rupture of distal anastomoses half a year after operation and underwent stent-graft, SG. Conclusion The surgical treatment of aortic aneurysms and aortic dissections could be carried out safely based on the accurate diagnosis, specific surgical strategy and fine technique.

Objective　Coronary artery bypass grafting (CABG)i n 13 patients was analyzed. Methods　9 patients were performed C ABG with cardiopulmonary bypass, 4 patients undergone off-pump coronary artery bypass(OPCAB). Among the 4 patients, 3 undergone transmyocardial laser revascula rization concomitantly. 2 patients with single-vessel disease, 3 with double-v essel disease, 7 with triple-vessel disease and 1 with left main coronary arter y disease. The average bypass per patient was 2.3. Results　All patients survived, 11 patients were angina free, 2 were angina relief. C onclusion　CABG is a safe operation, OPCAB may reduce blood transfusion and complication, patients recover more quickly after OPCAB compared with those with CABG.