Objective To assess the safety and efficacy of an olive oil-based lipid emulsion for parenteral nutrition in patients after hepatectomy.Methods Thirty-one postoperative patients with elective hepateetomy were randomized to receive isonitrogenous,isocalorie parenteral nutrition over 6 days after liver lobectomy(48-72hours)with either olive oil-based lipid emulsion(study group,n=15)or standard soybean oil emulsion(control group,n=16).The liver function and plasma protoins were assessed using peripheral venous blood collected before surgery,one day after surgery,and 7 days after surgery.The safety profiles of emulsion supports and postoperative rehabilitation were also assessed.Results The preoperative serum levels of total bilirubin,direct bilirubin,alanine amiotransferase,aspartate aminotransferase,alkaline phosphatase,total protein,albumin,and prealbumin were comparable between the two groups(all P>0.05).Although the Postoperative safety profile and liver function were not significantly different between two groups(all P>0.05),plasma total proteins,albumin,and prealbumin returned to the normal levels significantly faster in the study group than in control group[(57.57±9.84)g/L vs.(47.76±6.53)g/L,P=0.000;(31.29±3.11)g/L vs.(26.34±4.87)g/L,P=0.000;(0.188±0.059)g/L vs.(0.103±0.037)g/L,P=0.000]on the 7th Postoperative day,and the Postoperative hospital stay was also significantly shorter in the study group[(13.1±1.2)d vs.(15.2±1.1)d,P=0.041].The incidence of postoperative complications in study group and control group was 26.7%and 31.3%.respectively.Conclusions Treatment with the new olive oil-based lipid emulsion is weU tolerated in hepatectomy patients.It can speed up plasma proteins recovery and may shorten postoperative hospital stay,although it does not remarkably decrease the incidence of postoperative complications.

From 1965 to 1986, 36 patients with Wilms' tumor were terated by nephrectomy,postoperative irradiation and chemotherapy. The radiation doses of 1540～3920cGy were given according to an age-medulated dose scheme. All except 4 Stage I received chemotherapy. The most commonly used chemotherapeutic agent was Act-D, VCR. The overall 5-year survival rate was 61.1%(22/36) and 10-year survival rate was 56%(14/25). The 5- and 10-year survival rates were 87.5% and 80% for Stage I, 63.2% and 61.5% for stage II,33.3% and 28.6% for stage III patents. The favorable factors which led to better results were: early stages(stages I,II) and aged under 5 years . The 5-year survival rates of Stages I,II and Stage III were 70.4%(19/27) and 33.3%(3/9), respectively(P

Objective To investigate the clinical efficacy of methotrexate and mifepristone in treatment of ectopic pregnancy. Methods 58 cases with ectopic pregnancy admitted in the Second People's Hospital in Putuo district of Zhoushan city from February 2010 to February 2012 were randomly divided into observation group and control group,each had 29 cases. Control group were received methotrexate 1 mg/kg or 50 mg/m2 once a day by intramuscular injection,observation group were given both methotrexate and mifepristone treatment,the mifepristone was given one piece a day and each piece is 75 mg. the treatment success,b-HCG returned to normal time,normal pregnancy and the occurrence of complications were compared between two groups. Results The treatment success and normal pregnancy rate in observation group were significantly higher than control group(P<0.05),b-HCG returned to normal time was significantly shorter than control group (P<0.05 ). There were no obvious adverse reactions in both two groups, observation group had one light nausea,and control group had one light nausea and one case with alanine aminotransferase (ALT)slightly increased phenomenon,those patients were all back to normal on their own without treatment,the difference of adverse reaction rate between two groups was not significant. Conclusions Methotrexate and mifepristone has good efficacy and are safe and reliable in,treatment of ectopic pregnancy.

The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulation-induced pancreatic acinar cellular injury and trypsinogen activation or NF-kappaB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-kappaB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10(-3) mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P < 0.01) following the treatment with a high concentration of carbachol (10(-3) mol/L) in vitro. The addition of 10(-2) mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10(-3) mol/L) in vitro (P > 0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-kappaB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.
Carbachol/*pharmacology ; Cholinergic Agonists/pharmacology ; NF-kappa B/*metabolism ; Pancreas/metabolism ; Pancreas/*pathology ; Rats, Wistar ; Receptor, Muscarinic M3/agonists ; Trypsinogen/*metabolism

“Acupoint characteristics” has a significant influence on the study of acupoints. The description pattern of “property of Chinese medicine - function - indication” of analogy TCM put forward the description pattern of “acupoint characteristics-function-indication axis”. The study was carried out from the following three aspects:sorting, forming and improving the theories on acupoint characteristics; determining the functions according to present theories and indications of acupoints, methodizing the indications of acupoints; through functions, gradually simplifying and supplementing. Therefore, the above would make great sense to further research and systematic study and memorizing of acupoints and promoting clinical thinking about acupuncture, with a purpose to better guide clinical application.

Objective: The impact of parenteral fish oil lipid emulsion on liver function and nutritional status of malignant tumors of the liver and gallbladder patients. Methods: From December 2007 to A-pril 2008, 32 post-operative hepatobiliary cancer patients were randomly divided into control and study groups. Two groups were treated with isocaloric, isonitrogenic parenteral nutrition and the study group was added fish oil lipid emulsion. Comparison of plasma protein, glucose, jaundice index, transaminase, ALP and the rate of infection complications was made betweent the two groups. Results: The blood glucose, transaminase and ALP levels were not significantly different between the two groups. But the plasma proteins and bilirubin levels were improved significantly (P < 0.05) with reduced infection complication in the study group. Conclusion : Fish oil lipid emulsion is conducive to the recovery of post-operative liver and gallbladder cancer patients in live function and nutritional status.

Objective Carbonic anhydrase 1 (CA1) not only enhances the hydration reaction but also promotes the formation of CaCO3,which is an essential step for new bone formation in vitro.However,there is no direct evidence to demonstrate the involvement of CA1 in bio-mineralization in cells and tissues.This study is aimed to evaluate the important role of CA1 in bio-mineralization and ossification in cultured cells.Methods Calcification in Saos-2 cells was induced using osteogenic medium (OM) and the calcification was determined by Alizarin Red-S staining.The expressions of ossification protein marker Runt-related transcription factor-2 (Runx2),osterix (OSX),alkaline phosphatase (ALP),osteocalcin (OCN) and bone sialoprotein (BSP) were detected in the process of bone formation by real-time PCR.The expression of CA 1 in the calcified cells were measured using real-time PCR and Western blotting.We also detected calcification in Saos-2 cells in the presence of acetazolamide,an anti-carbonic anhydrase drug to CA1,to determine the role of CA1 in biomineralization in culture cells.T test analysis was used to compare the two groups,M-ANOVA of repeated measurs was conducted for different time point.Results Following the stimulation of OM,Saos-2 cells produced a great amount of calcium-rich deposits [0.68±0.03 vs 2.76±0.13,P＜0.01].Increased transcriptions of ossification protein markers were also detected in these stimulated Saos-2 cells,indicating that the OM launched the process of bone formation in the cells.CA1 had a significantly increased expression during this process [0.25±0.03 vs 0.94±0.06,P＜0.01].Following treatment with acetazolamide,the expression of CA1 evidently declined [1.09±0.05 vs 0.55±0.07,P＜0.05],and the mineralized nodule formation was declined [2.76±0.13 vs 2.19±0.07,P＜0.01].Conclusion These findings indicate that CA1 participates in the biomineralization and ossification,and may play an important roles in bone formation.

To investigate TLR2 (Toll-like receptor 2) mRNA expression in ischemic hepatic lobes under the condition of partial hepatic ischemia/reperfusion injury in BALB/c mice and its relationship with liver function impairment. A partial ischemia/reperfusion injury model was established. The portal vein and hepatic artery supply to the median and left lobes of the liver were obstructed by an atraumatic artery micro-clip, with the obstruction lasting for about 60 min. Then reperfusion was fulfilled by removal of the clip. The liver samples were collected at the 4th h after the restoration of blood inflow. Total RNA was extracted from the liver samples and analyzed quantitatively by method of real-time PCR. At the same time, portal vein serum and plasma were taken respectively for further detection of the level of endotoxin, tumor necrosis factor alpha (TNF-alpha) and plasmic alanine aminotransferase (pALT). The results indicated that TLR2 mRNA in ischemic lobe was up-regulated markedly in mice partial liver ischemia/reperfusion injury model compared to that in sham operation group (deltaCt: 1.05 +/- 1.02 vs 5.08 +/- 1.36, P<0.001). The level of portal vein pALT and TNF-alpha increased significantly (112.32 +/- 17.56 pg/ml vs 6.07 +/- 5.33 pg/ml, P<0.01; 890 +/- 127 microm/L vs 30 +/- 5 microm/L, P<0.001) . However, the level of portal vein endotoxin remained below the normal line, suggesting a state of non-endotoxemia. TLR2 mRNA expression in ischemic lobe, as well as portal vein pALT and TNF-alpha, was up-regulated in the model of mice partial ischemia/reperfusion injury, suggesting the involvement of TLR2 in ischemia/reperfusion pathological process.
Liver/*blood supply ; Liver/metabolism ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; RNA, Messenger/physiology ; Reperfusion Injury/etiology ; Reperfusion Injury/*metabolism ; Toll-Like Receptor 2/*biosynthesis ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/physiology ; Up-Regulation

In order to construct an expression vector carrying small hairpin (sh) RNA (shRNA) for toll-like receptor 4 mRNA and a reporter gene of enhanced green fluorescence protein (EGFP) and study the inhibition of cytokine release by RAW264.7 cell induced by lipopolysaccharide (LPS) stimulation through transfection and expression of shRNA targeting TLR4 gene via the RNAi mechanism, the reporter gene plasmid pEGFP-C1 (4.7 kb) and psiRNA-hHlneo (2979 bp) were used. The H1 promotor and double Bbs I restrict endoenzyme site were cloned from plasmid psiRNA-hH1neo and reconstructed them into plasmid pEGFP-C1 in the Mlu I restrict endoenzymic site, forming plasmid pEGFP-H1/siRNA, which contained Bbs site and reporter EGFP gene. Then an oligonuclear hairpin sequence targeting TLR4 gene was designed by internet tool and inserted into the plasmid pEGFP-H1/siRNA forming plasmid pEGFP-H1/TLR4-siRNA. After transfection of pEGFP-H1/TLR4-siRNA into RAW264.7 cells, tumor necrosis factor-alpha (TNF-alpha) release by the cells after stimulation by LPS was detected. The results showed that the constructed pEGFP-H1/TLR4-siRNA carrying hairpin RNA for TLR4 gene and reporter EGFP gene were proven to be right by restriction endonuclease analysis. The expression of EGFP gene was (50.37+/-8.23) % and after transfection of the plasmid pEGFP-H1/ TLR4-siRNA the level of TNF-alpha released by RAW264.7 cell was down regulated. It was concluded that shRNA targeting TLR4 gene could inhibit the TNF-alpha release by RAW264.7 cells evoked by LPS.

The evolution of hepatocellular carcinoma (HCC) is a compound process which involves many kinds of genes and transductional pathways. The expression of the peptidyl-proplyl-isomerase PIN1 gene, the mutation in exon 3 of beta-catenin and its correspondent abnormal expression and their roles in the hepatocellular carcinogeneisis were investigated. Among 29 pair cases of HCC and non-carcinoma tissues, the expression of PIN1 gene was detected by immunochemical staining. Mutations in exon 3 of beta-catenin gene and differential expression of beta-catenin gene were investigated by the methods of PCR-SSCP, direct sequencing and immunohistochemical technique as well. The results indicated: (1) 44.8% (13/29) cases of HCC presented higher level of PIN1 gene expression than non-cancerous tissues (chi2=32.63, P<0.05), especially in cytoplasm and nucleus, while there was lower level of PIN1 expression in non-cancerous tissues; (2) 58.6% (17/29) HCC tissues showed beta-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated beta-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated beta-catenin protein accumulation with lower level or trace of PIN1 expression (chi2=0.00, P>0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of beta-catenin, and accompanied by beta-catenin protein accumulation. There was no mutation in non-cancerous tissues. All the mutation presented in tissues with low level of PIN1 expression. There was no mutation of beta-catenin gene in tissues with high PIN1 expression level (chi2=58.12, P<0.05). So it was postulated that the increase of PIN1 gene expression could promote hepatocellular carcinogenesis via a way different from beta-catenin gene mutation.