ObjectiveTo explore the effects of propofol combined with remifentanil in different ratios for intravenous anesthesia. Methods63 patients were randomly divided into three groups,each group 21 cases,different target plasma concentration of propofol and remifentanil were dosed for every group.Hemodynamic parameters such as MAP,HR were recorded at different time.so as to stop time for the zero time of local anesthetic.The extubation time,the quality and time of awakening were compared as well. ResultsThe MAP and HR value of all patients after induction of general anesthesia were lower than that before intubation,which showed significant difference(all P＜0.05),and the MAP and HR value of all patients after intubation reseal and decannulation showed significant difference compared with that before intubation reseal.The resurgence time and decannulation time of group A were the shortest,and the postoperative detubation revive quality score was also the best when compared with that of group B and C. ConclusionThe target plasma concentration of propofol(2.5mg/L)and remifentanil(μg/L)was the best.With the increasing of target plasma concentration of remifentanil and the decreasing of target plasma concentration of propofol,the resurgence time,decannulation time and the postoperative detubation revive quality score were improved gradually.

Objective To investigate the role of recombinant Vibrio vulnificus cytolysin (rVvhA) in inducing THP-1 cells damage and study the pathway of associated calcium influx .Methods Inverted mi-croscope, CCK-8 cell proliferation kit, Fluo3/AM staining and caspase activity detection were performed to analyze the damage of THP-1 cells induced by rVvhA and the pathway of calcium influx .Results rVvhA had cytotoxic effects on THP-1 cells in a dose-dependent manner .The concentrations of extracellular K +and LDH were respectively up-regulated after 1 h and 6 h of 12 μg/ml rVvhA intervention .Verapamil , Mibe-fradil and SKF-96365 could not prevent the influx of free Ca 2+induced by rVvhA .The activities of caspase-3 and caspase-9 were singanificantly enhanced by rVvhA in a time-dependant manner .Conclusion rVvhA can induce THP-1 cells damage through triggering extracellular calcium influx via porous channel on cell membrane.Moreover, rVvhA might induce THP-1 cell apoptosis through activating caspase-9/3-dependent pathway .

Objective To investigate the factors associated with vision and hole closure for idiopathic macular hole (IMH) after vitrectomy surgery.Methods Eighty-nine eyes of 89 patients with IMH were enrolled in this retrospective study.There were 15 males and 74 females.The patients aged from 42 to 82 years,with the mean age of (64.13 ± 7.20) years.All subjects underwent best corrected visual acuity (BCVA) and optical coherence tomography (OCT) examinations.The BCVA ranged from 0.01 to 0.4,with the mean BCVA of 0.12 ± 0.09.The MH stages was ranged from 2 to 4,with the mean stages of 3.56 ± 0.77.The basal diameter ranged from 182 μm to 1569 μm,with the mean basal diameter of (782.52± 339.17) μm.The treatment was conventional 25G pars plana vitrectomy combined with phacoemulsification and intraocular implantation.Fortyone eyes received internal limiting membrane peeling and 48 eyes received internal limiting membrane grafting.The follow-up ranged from 28 to 720 days,with the mean follow-up of (153.73 ± 160.95) days.The visual acuity and hole closure were evaluated on the last visit and the possible related factors were analyzed.Results On the last visit,the BCVA ranged from 0.02 to 0.8,with the mean BCVA of 0.26±0.18.Among 89 eyes,vision improved in 45 eyes (50.56％) and stabled in 44 eyes (49.44％).Eighty-six eyes (96.63％) gained MH closure but 3 eyes (3.37％) failed.By analysis,patients of early stages of MH and smaller basal diameter of MH will gain better vision outcome (t=2.092,2.569;P＜ 0.05) and patients of early stage MH will gain high hole closure rate after surgery for IMH (t=-5.413,P＜0.05).However,gender,age,duration,preoperative BCVA,surgery technique,gas types and follow-up time had no relationship with the effect after surgery for IMH (P＞0.05).Conclusions Stages of MH and basal diameter of MH may be the factors associated with the visual outcome for idiopathic macular hole after surgery.However,age,gender,duration,surgery patterns,gas types and followup time showed no effects on operational outcomes.

Aim To investigate the apoptosis mechanism of human gastric cancer cell SGC-7901 induced by Omphalia lapidescens protein pPeOp.Methods CCK-8 and flow cytometry were used to detect the inhibitory effect of different concentrations of pPeOp(30, 60, 90 mg·L-1) on SGC-7901.The mRNA and protein expression of TNF-R1, Fas/FasL, Bcl-2, caspase-3 and caspase-8 were detected by qRT-PCR and Western blot.Results SGC-7901 cells were treated with different concentrations of pPeOp(30, 60, 90 mg·L-1) for 24 h.CCK-8 test showed that there was no significant difference between PVP group and the control group.The survival rate of the 5-Fu group was(53.71±7.34)% (P<0.05).The survival rates of pPeOp group(30, 60, 90 mg·L-1) were(80.95±6.25)%, (53.48±5.70)% and(44.61±6.50)%(r=0.984,P=0.016),respectively.Flow cytometry showed that the apoptosis rate of PVP group had no significant difference with control group, and the apoptosis rate of 5-Fu group was about(39.30±3.34)%(P<0.05).The apoptotic rates of pPeOp group(30, 60, 90 mg·L-1) were(10.90±1.25)%, (28.80±2.70)% and (32.00±3.50)%,respectively(P<0.05).The mRNA and protein expression levels of Bcl-2 were down-regulated,whereas the expression of TNF-R1, Fas/FasL, caspase-3 and caspase-8 were significantly up-regulated(P<0.05).Conclusions pPeOp can significantly inhibit the proliferation of gastric cancer cell line SGC-7901 and induce apoptosis in a dose-dependent manner.Death receptor pathway and mitochondrial pathway may be related to pPeOp-induced apoptosis of gastric cancer SGC-7901.

OBJECTIVE To investigate the change in antibiotic resistance of Burkholderia cepacia in hospital for reference of clinical antimicrobial strategy.METHODS Data were collected of the 859 bacteria strains isolated from clinical specimens from Jan 2004 to Dec 2006.Drug sensitivity tests were made for 22 antimicrobial agents.RESULTS All of the drug-resistance rates were higher than 90.00% including ampicillin,ampicillin/sulbactam,amoxicillin/clavulanic acid,cefazolin,gentamicin,tobramycin,amikacin,imipenem and nitrofurantoin.but that of the others such as ceftazidime(23.57%),cefepime(26.95%),ciprofloxacin(31.73%),cefoperazone/sulbactam(33.33%),and piperacillin/tazobactam(21.45%) were lower.The resistance rate to sulfamethoxazole/trimethoprim was 5.73% which was the lowest.CONCLUSIONS The isolation rate as well as the resistance to most of the antibiotics are increasing in clinical specimens.Antimicrobial treatment should be guided by drug sensitivity test.

Abstract: Kirsten rat sarcoma viral oncogene homolog (KRAS) gene is one of the most commonly mutated oncogenes. It has been found that KRAS inhibitors have the potential therapeutic effect on cancer patients with this gene mutation. In this study, machine learning was applied to develop a QSAR(quantitative structure-activity relationship) model for KRAS small molecule inhibitors. A total of 1857data points of IC50 and SMILES(simplified molecular input line entry system) for KRAS inhibitors were collected from three databases: ChEMBL, BindingDB, and PubChem. And nine different classifiers were constructed using three different feature screening methods combined with three machine learning models, namely, random forest, support vector machine, and extreme gradient boosting machine. The results showed that the SVM model combined with mutual information feature selection exhibited the best performance: AUCtest=0.912, ACCtest=0.859, F1test=0.890. Moreover, it also demonstrated good predictive performance on the external validation set(AUCExt=0.944, RecallExt=0.856, FPRExt=0.111). This study provides a new technical route for KRAS inhibitor screening in natural product databases using artificial intelligence methods.

Objective: To analyze serum HBV-RNA levels in patients with chronic hepatitis B whose serum HBV-DNA has dropped to undetected levels after treatment with entecavir, and to explore the correlation between HBV-RNA level and liver biochemical parameters, which lay the research foundation for the clinical significance of new serological marker HBV-RNA. Methods: HBeAg negatively detected 107 cases with chronic hepatitis B whose serum HBV-DNA test results were lower than detection level for six consecutive months after receiving standard nucleoside therapy for more than 12 months were included. HBV-RNA level was detected by Perkin-Elmer reagent. HBV-DNA level was detected by Roche Cobas. Hitachi automatic biochemical analyzer was used to detect ALT and AST. Architect chemiluminescence analyzer was used to detect HBsAg, HBeAg, anti-HBe and anti-HBc. RStudio software was performed to analyze the correlation between HBV-RNA level and liver biochemical parameters. Logistic regression was used to analyze the independent factors influencing HBV-RNA level. Results: The positive detection rate of serum HBV-RNA in patients with chronic hepatitis B whose serum HBV-DNA had dropped to undetected levels after ETV treatment was 22.43%. HBsAg, ALT and AST levels in HBV-RNA positive group were slightly higher than HBV-RNA negative group, while anti-HBc levels were slightly higher in HBV-RNA negative group. There was no difference in the level of anti-HBe between the HBV-RNA negative and the positive group. Logistic regression analysis showed that anti-HBc was an independent factor influencing the level of HBV-RNA detection (P = 0.021). Conclusion HBV-RNA can be detected in some patients with chronic hepatitis B whose serum HBV-DNA level has dropped to undetected levels after ETV treatment. Serum HBV-RNA only comes from the direct transcription of cccDNA, so it is better than HBV-DNA and HBsAg to reflect cccDNA level or activity. Anti-HBc, as an independent factor influencing the level of HBV-RNA, may be used in combination as a new marker to predict the efficacy of antiviral therapy.

OBJECTIVETo investigate the molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.

METHODSMTT assay was employed to detect the proliferation inhibition of Jurkat cells by triptolide, and the IC50 was calculated by OriginPro8. Flow cytometry was used to analyze apoptosis of Jurkat cells. Np9 mRNA levels were detected by RT-PCR and analyzed quantitatively by Kodak 1D 3.6 software. Correlation between the inhibition of Np9 transcription and the cell apoptosis was analyzed by SPSS 19.0.Western blotting was employed to determine Np9 downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 protein level in Jurkat cells after exposure to different concentrations of triptolide for 48 h.

RESULTSTriptolide treatment resulted in dose-dependent inhibition of Jurkat cells proliferation and its IC50 was 12.7 nmol/L. Triptolide induced apoptosis of Jurkat cells in dose- dependent manner. Furthermore, triptolide inhibited Np9 mRNA transcription level in Jurakt cells in a dose-dependent manner. There was a correlation between the triptolide-mediated the apoptosis and the inhibition of Np9 transcription of Jurkat cells (R(2)=0.907). Western blotting results displayed that triptolide inhibited transcription levels of Np9 mRNA with a concomitant decrease of its downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 at protein levels.

CONCLUSIONInhibition of HERV-K Np9 mRNA and its downstream signaling molecules c-myc, β-catenin, ERK, Akt and Notch1 protein might be one of important molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.

Apoptosis ; drug effects ; Diterpenes ; pharmacology ; Endogenous Retroviruses ; genetics ; Epoxy Compounds ; pharmacology ; Flow Cytometry ; Gene Products, env ; genetics ; Humans ; Jurkat Cells ; drug effects ; Phenanthrenes ; pharmacology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; pathology ; Transcription, Genetic

Objective To better understand the clinical features and the diagnosis of TAFRO syndrome.Methods The clinical data of a patient were analyzed and the related literatures were reviewed.Results A 51-year-old male characterized by fever,edema of the legs,serous cavity effusion,throm-bocyto-penia,and renal dysfunction;Kidney biopsy suggested a diagnosis of endocapillary proliferative glomerulon-ephritis and thrombotic microangiopathy.The pathology of lymph node biopsy supported the diagnosis of Castleman disease.After administering with glucocorticoids and supportive platelet transfusion,the clinical symptoms relieved.Conclusion Symptoms of patients with TAFRO syndrome are variable.The diagnosis relies on history and pathological examination.Currently,glucocorticoids can be used as first line therapy.TAFRO syndrome should be thoroughly investigated for differentiating with other diseases.