Objective To study the protective effect of glutamine on the intestinal mucosal antioxidation in endotoxemic rats. Methods　Twenty-eight male Wistar rats were randomly divided into three groups, group A:parenteral nutrition supplemented with glutamine, group B:TPN without glutamine,and group C:normal control. Endotoxemia was induced by continous intravenous infusion of lipopolysaccharide(LPS) at a dose of 2 mg/kg per day throughout the 5-day study period. The mucosal protein、DNA、ATP、SOD、MDA、GSH、sIgA were determined. Results The mucosal protein、DNA、ATP、SOD、GSH and sIgA content in endotoxic rats were markedly decreased, MDA was increased as compared with normal control(P＜0.05). The former indices in group A were improved and MDA content was decreased as compared with group B(P＜0.05). Conclusion　Glutamine can improve gut energy metabolism, decrease the extent of mucosal injury of free radicals, and give an protective effect on the mucosal probably by increasing GSH.

Objectives:To evaluate the effect of early enteral nutrition(EEN) on the structure and function of the gut, the bacterial and endotoxin translocation. Methods:SAP model was induced by injecting 1 ml/kg of combined solution of 5% sodium taurocholate and trypsin into the pancreas via pancreatic duct.15 dogs were divided into PN group and EEN group.Systemic plasma endotoxin levels was quantified.Both portal and systemic blood sample were obtained before and 1?4?7 d following SAP,and cultured for aerobic as well as anaerobic bacterial growth.Specimens of tissue from mesentery lymph nodes,lung and pulmonary portal nodes and pancreas were removed,weighed and homogenized at the 7th day. Results:The levels of systemic plasma endotoxin and the magnitude of bacterial translocation to the portal and cycle blood and distant organs were significantly reduced the protein and DNA content of the small intestine and colon increased,and the height of the villi and the thickness of mucosa and whole bowel wall of the intestinel and colon improved in EEN group as compared with those in PN group. Conclusions:We conclude that EEN can improve gut metabolism,decrease the extent of mucosal atrophy,and assist in the maintenance of the mucosal barrier function.It is effective touse EEN in severe acute pancreatitis.

Objective To study the effect of propofol used for outpatient painless enteroscope on cognitive function.Methods One hundred and twenty ASAⅠ~Ⅱpatients scheduled for enteroscope were randomly divided into three groups .Propofol was given 1.5mg/kg(groupⅠ), 2mg /kg (group Ⅱ) or 2.5 mg/kg ( group Ⅲ) intravenously .The enteroscope was inserted when patient showed unconsciousness and no reaction to dictation .SpO2 was kept above 95%96% throughout enteroscope .All patients received neurobehavioral cognitive status examination ( NCSE ) and mini-mental state examination ( MMSE ) test 1 hour before enteroscope examination and 5 minutes,30 minutes, 1 hour after enteroscope examination was o-ver and must finish it within 15 min.The enteroscope examination time , vital signs, analgesia effects and intraoperative awareness were record .Results The ability of memory and calculation at 5 minutes after en-teroscope examination showed a statistical difference between group Ⅰ and ⅡorⅢ( P <0.05),there was no significant difference between in group II and in group Ⅲ( P >0.05 ) , The ability of memory and calcu-lation at 30 minutes, 1 hour after enteroscope examination there was no significant difference in three groups ( P >0.05 ) .In all patients ,the MMSE scores at 5 minutes after enteroscope examination were significant-ly lower than the baseline value ( P <0.05).The MMSE scores at 30 minutes, 1 hour after enteroscope examination in Ⅲgroup patients were significantly lower than the baseline value ( P <0.05 ) .The MMSE scores at 30 minutes, 1 hour after enteroscope examination in I group patients were significantly higher than that inⅡor Ⅲgroup( P <0.05).The MMSE scores at 30 minutes, 1 hour after enteroscope examination there was no significant difference between in group II and in group Ⅲ( P >0.05 ) .The NCSE and MMSE scores at 3hour, 12 hour after enteroscope examination there was no significant difference between in group I and II or Ⅲ( P >0.05).Conclusion Propofol 1.5mg/kg used for painless enteroscope examination has no effect on cognitive function .MMSE and NCSE are suitable for evaluation of outpatient's cognitive func-tion.

Objective To explore the significance of urine deoxypyridinoline to diagnosis on osseous metastasis of lung neoplasms.Methods.182 cases with lung carcinoma was divided into two groups.One group was case with osseous metastasis,the other group was case without osseous metastasis,uDPD/uCr, uCa/Cr,sCa and sAKP in two groups were respectively compared.Sensitivity and specificity of these indexes to diagnosis on osseous metastasis of lung cancer were also acalculated and compared.80 cases without osseous metastasis were follow-up for 6 months.Results The ratio of uDPD/uCr with osseous metastasis group[(12.35?2.65)nmol/mmol]was significantly higher than that of without osseous metastasis group [(7.76?2.11)nmol/mmol](t=2.46,P

AIM:To study whether homocysteine (Hcy) inhibits the expression of ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) by microRNA-33 (miRNA-33) signaling, and reduces the efficiency of reverse cholesterol transport (RCT).METHODS:RAW264.7 macrophages were induced by oxidized low-density lipoprotein (ox-LDL) to establish foam cell model.Oil red O staining was used to determine whether the model was established successfully.miRNA-33 mimics and miRNA-33 inhibitor were transfected into the cells by Lipofectamine 2000, and the cells were exposed to Hcy at concentration of 5 mmol/L for 24 h.The intracellular lipid droplets were observed by Oil red O staining.The expression of ABCA1 and ABCG1 at mRNA and protein levels was determined by real-time PCR and Western blot.The cellular cholesterol content was analyzed by HPLC, and effluent rate of cholesterol was detected by the method of liquid scintillation counting.RESULTS:Compared with blank control group, the lipid content in miRNA-33 mimics group was increased, and the expression of ABCA1 and ABCG1 at mRNA and protein levels was decreased (P<0.05).The intracellular cholesterol content was increased gradually (P<0.05) , and the cellular cholesterol efflux rate was gradually decreased (P<0.05) in miRNA-33 mimics group.Compared with blank control group, the testing results in miRNA-33 inhibitor group were the opposition of those in miRNA-33 mimics group (P<0.05).No difference of the above indexes among blank control group, miRNA-33 mimics-NC group and miRNA-33 inhibitor-NC group was observed.CONCLUSION:Hcy inhibits the mRNA and protein expression of ABCA1 and ABCG1 through miRNA-33 signaling, and reduces the efficiency of RCT in RAW264.7 macrophage-derived foam cells.

OBJECTIVETo study the changes of inducible nitric oxide synthase (iNOS) activity and apoptosis-related genes Bcl-2, Bax and caspase-3 mRNA expressions in endotoxemia-induced rat diaphragm injury and analyze the related apoptosis mechanism.

METHODSThirty-two male SD rats were randomly divided into 4 groups (n = 8): control group (saline 0.5 ml ip), endotoxin 24 h, 48 h and 96 h group (endotoxin 12 mg/kg ip, animals were killed either 24, 48 or 96 h after injections). Body weight were measured, the ratio between diaphragm weight and body weight, activities of constitutive nitric oxide syntheses (cNOS), iNOS and succinate dehydrogenase (SDH) were also measured. The expressions of Bcl-2, Bax and caspase-3 mRNA were detected by RT-PCR analysis.

RESULTSEndotoxin induced significant reductions in diaphragm mass in endotoxin 96 h group (P < 0.05). Endotoxin increased diaphragm cNOS or iNOS activities, and they were significantly higher in endotoxin 96 h group than those in endotoxin 24 h and 48 h groups, diaphragm SDH activity was reduced, and it was lower in endotoxin 96 h group than that in endotoxin 24 h and 48 h groups (P < 0.01). Endotoxin significantly increased Bax and caspase-3 mRNA expressions, and they were higher in endotoxin 48 h and 96 h groups than those in endotoxin 24 h group (P < 0.01). Endotoxin significantly reduced Bcl-2 mRNA expression and the ratio of Bcl-2/Bax, and they were lower in endotoxin 48 h and 96 h groups than those in endotoxin 24 h group (P < 0.01).

CONCLUSIONiNOS is activated in endotoxemia-induced rat diaphragm injury. It damages mitochondria, upregulates Bax expression and downregulates Bcl-2 expression, then induces caspase-3 related apoptotic pathway. These changes may cause diaphragm injury and atrophy.

Animals ; Apoptosis ; Caspase 3 ; metabolism ; Diaphragm ; metabolism ; physiopathology ; Endotoxemia ; metabolism ; Gene Expression ; Male ; Nitric Oxide Synthase Type II ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; bcl-2-Associated X Protein ; metabolism

In this work, datasets of water and carbon fluxes measured with eddy covariance technique above a summer maize field in the North China Plain were simulated with artificial neural networks (ANNs) to explore the fluxes responses to local environmental variables. The results showed that photosynthetically active radiation (PAR), vapor pressure deficit (VPD), air temperature (T) and leaf area index (LAI) were primary factors regulating both water vapor and carbon dioxide fluxes. Three-layer back-propagation neural networks (BP) could be applied to model fluxes exchange between cropland surface and atmosphere without using detailed physiological information or specific parameters of the plant.
Agriculture ; Carbon ; metabolism ; Carbon Dioxide ; metabolism ; China ; Models, Biological ; Neural Networks (Computer) ; Seasons ; Volatilization ; Water ; metabolism ; Zea mays ; metabolism

OBJECTIVETo investigae the function of the glass colorant on the color of the machinable infiltrated ceramics(MIC).

METHODSFive kinds of glass with different colorant were infiltrated through the aluminous matrix by heating the components to 1 100 degrees C for 2 hours. The specimens surface was polished, and their thickness was 0.5 mm.

RESULTSThe refractive index of the MIC infiltration glass was 1.59691 (587.6 nm, nd) . The most different parameter of the MIC color were L*, then a*, and b* had little difference . The parameters of the color space of MIC were: L*(64.55-71.46), a*(3.35-7.38), b*(10.00-12.41), Ca*b*(11.38-13.95), ha*b*(54.07-73.00). These were almost close to the color parameters of Vita In-ceram.

CONCLUSIONThis experiment proved that the glass colorant was changed the MIC color parameters, and the main function was on L*, then a*. The ceramic color was up to the requirement of clinic.

Aluminum Oxide ; Ceramics ; Color ; Dental Materials ; Dental Porcelain ; Glass ; Humans

OBJECTIVETo investigate whether activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) and inhibition of mitochondrial permeability transition pore (mitoPTP) were involved in the cardioprotection of ethanol postconditioning in isolated rat heart.

METHODSHearts isolated from male Sprague-Dawley rats were perfused on a langendorff apparatus and subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. Infarct size was measured by TTC staining method and the expression of ALDH2 at mRNA level of left anterior myocardium was detected by RT-PCR.

RESULTIn contrast to ischemia and reperfusion, ethanol postconditioning improved the recovery of left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure during reperfusion, reduced LDH release and infarct size. The expression of ALDH2 mRNA level was increased. Administration of mitoPTP activator atractyloside attenuated the effect of ethanol postconditioning, LDH release and infarct size were increased, and the recovery of hemodynamic parameters was inhibited. The expression of ALDH2 mRNA was decreased.

CONCLUSIONEthanol postconditioning has cardioprotection effect, which may be associated with upregulating mitochondrial ALDH2 mRNA expression and inhibiting the opening of mitochondrial permeability transition pore.

Aldehyde Dehydrogenase ; drug effects ; genetics ; metabolism ; Aldehyde Dehydrogenase, Mitochondrial ; Animals ; Ethanol ; pharmacology ; In Vitro Techniques ; Ischemic Postconditioning ; L-Lactate Dehydrogenase ; metabolism ; Male ; Mitochondria, Heart ; drug effects ; metabolism ; Mitochondrial Membrane Transport Proteins ; drug effects ; metabolism ; Mitochondrial Proteins ; drug effects ; genetics ; metabolism ; Myocardial Reperfusion Injury ; metabolism ; pathology ; prevention & control ; Myocardium ; metabolism ; pathology ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate whether the release of nitric oxide (NO) was involved in the cardioprotection of ethanol postconditioning in isolated rat hearts.

METHODSHearts isolated from male SD rats were subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. Ethanol postconditioning was fulfilled through perfusion of 50 mmol/L ethanol for 15 min (at the end of cardiac ischemia for 5 min and at the beginning of reperfusion for 10 min). The rats were divided into five groups: normal, ischemia and reperfusion, ethanol postconditioning, ethanol postconditioning + L-nitro-arginine-methylester (L-NAME) and ethanol postconditioning + atractyloside. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. The infarct size was measured by TTC staining method and NO content was measured by nitric acid reductase method. The expressions of Bcl-2 and Bax mRNA were detected by RT-PCR analysis.

RESULTSIn contrast to ischemia and reperfusion, ethanol postconditioning improved left ventricular developed pressure, rate pressure product during reperfusion, reduced LDH release and infarct size. NO content was decreased. The ratio of Bcl-2/Bax was increased. Administration of nitric oxide synthase inhibitor L-NAME or mitochondrial permeability transition pore opener atractyloside both attenuated the role of ethanol postconditioning, which inhibited the recovery of hemodynamic parameters, the decreases of LDH and infarct size. NO content was decreased further. The ratio of Bcl-2/Bax was decreased.

CONCLUSIONThe cardioprotection of ethanol postconditioning may be associated with reducing nitric oxide release, inhibiting the opening of mitochondrial permeability transition pore and decreasing the happening of apoptosis.

Animals ; Ethanol ; therapeutic use ; In Vitro Techniques ; Ischemic Postconditioning ; Male ; Mitochondria, Heart ; metabolism ; Myocardial Ischemia ; metabolism ; prevention & control ; Myocardial Reperfusion Injury ; metabolism ; prevention & control ; Myocardium ; metabolism ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley