Adult ; Echinococcosis ; Heart Diseases ; parasitology ; Humans ; Male

Objective To evaluate the protective effect of leukocyte-depleted warm blood cardioplegia on immature myocardium in infant.Methods Thirty infants with congenital heart disease whose American Society of Anesthesiologists(ASA) were Ⅱ-Ⅲ,aortic clamping time and bypass time were more than 30,40 minutes were respectively selected and divided into 2 groups:Experimental group and control group.Experimental group were perfused with leukocyte-depleted warm blood cardioplegia while control group perfused with common warm blood cardiplegia.Under monitoring the hemodynamics at surgery,the serum levels of troponin I(cTnI) and intercellular adhesion molecule-1(ICAM-1) in heparinized anticoagulant blood samples from radial artery at different time points [anesthesia induction and before extracorporeal circulation(T1),30 min after aortic clamping(T2) and aortic declamping 5 min(T3),15 min(T4)]were detected.Three pieces of cardiac muscle were taken from right atrium at different time points and the levels of myeloperoxidase(MPO) were detected.Results 1.The serum cTnI and ICAM-1 levels after aortic declamping were higher than those before operation,and the levels in experimental group were lower than those in control group(t=2.358,2.533,2.30,2.639 Pa

OBJECTIVE: To determine ginsenoside Rg1 and ginsenoside Re in Jiangshen Capsules by HPLC simultaneously. METHODS: The separation was performed on Kromasil-C18 column, the mobile phase consisted of acetonitrile-0. 05% H3PO4 solution ( 21∶ 79) with flow rate of 1. 0mL? min-1 and detection wavelength of 203nm. RESULTS: The linear ranges of ginsenoside Rg1 and ginsenoside Re were 0. 502～ 4. 016? g( r=0. 999 7) and 1. 090～ 8. 720? g( r=0. 999 8) , respectively, with average recovery at 98. 8% ( RSD=1. 24% ) and 99. 4% ( RSD=1. 68% ) , respectively. CONCLUSION: This method is simple, rapid, accurate and reliable, and suitable for the quality control of Jiangshen Capsules.

Accidents, Occupational ; China ; epidemiology ; Humans ; Poisoning ; epidemiology

ObjectiveTo observe the effect of rat cerebral hemorrhage model via autologous blood injection.MethodsBlood extracted from rats' cardiac ventricles was injected into the right caudate nucleus via stereotactic method. Pathological examination,ultrastructural visualization and motor functional test were applied to validate the feasibility of this method.ResultsRats showed paralysis of left extremities rapidly after surgery. Pathological examination confirmed the formation of hematoma in caudate nucleus. The deviation of hematoma volume and location among individuals was significantly lower than that of rats made by collagenase injection. Transmission electron microscopy showed wide mylin degeneration in right caudate nucleus. Motor functional test revealed the dysfunction of left extremities with marked lower deviation among individuals compared with that of collagenase injection (P<0.05).ConclusionAutologous blood injection can result in significantly lower deviation of hematoma volume and location as well as dysfunctional degree compared with that of collagenase injection.

Glioblastoma is a malignant tumor in central nervous system, which has strong invasion, poor prognosis and short survival time. At present, the main treatment strategy of glioblastoma is surgical excision, supplemented by radiotherapy and chemotherapy. However, due to incomplete resection and high recurrence rate, it is urgent to find novel therapeutic method for glioblastoma. Photodynamic therapy, as a promising non-surgical treatment, provides a new strategy for postoperative adjuvant therapy of glioblastoma. This review summarizes the mechanism and clinical application of photodynamic therapy mediated by various photosensitizers in glioblastoma, in order to provide help for the treatment of glioblastoma.

The present is aimed at identifying the activation of TRAFs in n asopharyngeal carcinoma (NPC) in vitro. The differential expression of TRAF2\,TRAF3 was not detected in RN A and protein level, whereas the expression of TRAF1 in HNE2-LMP1 cell lines wa s much more abundant than that in HNE2 cell lines, suggesting that TRAF1 may be an inducible molecule; More importantly, TRAF1, TRAF2 or TRAF3 were activated in the HNE2-LMP1 cells, whereas TRAF1, TRAF2 or TRAF3 were not activated in HNE2 cells as detected by the immunoprecipitation-Western blotting assay. These data provide an experimental basis for our study beginning from the signal transduca tion pathway for the eluccidation of the mechanism of LMP1 carcinogenesis in NP C.

Objective:Increased reactive oxygen species (ROS) formation and by which in turn promotes cardiomyocytes apoptosis is associated with the pathogenesis and progression of various cardiac diseases. Small heat shock protein 27(Hsp27) could protect different cells from oxidative damage. By using tissue nonspecific overexpression Hsp 27 transgenic model, other investigators demonstrated that Hsp27 suppressed successfully kainate-induced seizures and hippocampal cell death in intact transgenic mice, and attenuated mimic ischemia/reperfusion injury in Langendorff-perfused isolated mice heart. As there are complicated and long distance neuro-humoral regulation associated with the development of cardiac diseases, it is better to choose a cardiac-specific overexpression transgenic model to study the effects of Hsp27 in hearts in vivo.Methods:A cDNA encoding human Hsp27 was subcloned into pBSII-SK+ containing the ?-myosin heavy chain (?-MHC) promoter (generously provided by Dr. J. Robbins, Children’s Hospital of Cincinnati, Ohio). BamHI-digested linear transgene consistent with the ?-MHC promoter, Hsp27 cDNA, and poly (A) of human growth hormone (hGH) was microinjected into the fertilized eggs from CBA/BL6 mice. Mice containing the transgene were identified by polymerase chain reaction. Founders revealed by this screening were used to establish independent transgenic lines. Following successful transmission, a range of tissues including heart, lung, liver, brain, skeleton muscle, spleen and kidney was screened by Western blot to confirm the cardiac specific expression of the transgene. Results and Discussion:Transgenic mice expressed Hsp27 under the control of a-MHC promoter. Cardiac tissues from independent TG line expressed abundant Hsp27, and as expected, Hsp27 expressed in cardiac tissues only, whereas none in liver, spleen, lung, kidney, brain and skeleton muscle. Surprisingly, Hsp25, the endogenous isoform of Hsp27 in murine, was downregulated by Hsp27 overexpression (data not shown), which is in contrast to the result of Hollander’s [1]. It needs to determine in future whether Hsp27 expression profile in heart could exert any effect on the regulation of Hsp25.Conclusion: The TG mice overexpression human Hsp27 specifically in the heart by using ?MHC- promotor were created. All TG mice expressed Hsp27 abundantly and cardiac-specifically. To our knowledge, it is the first report of creation of transgenic mice which overexpressing Hsp27 cardiac specifically. This current model suggests that the Hsp27 cardiac-specific over-expression of transgenic mouse remains a robust genetic tool for dissecting molecular and genetic events involving Hsp27, which could be a therapeutic target in heart failure.

The inhibitory ratio (1%) of artificial musk on cyclooxygenase-2 (COX-2) was determined by enzyme immunoassay (EIA). The dose-effect relationship between concentrations of artificial musk and 1% was established. It was found that artificial musk had obvious inhibitory action on COX-2. The concentration for 50% of maximum inhibitory effect (IC50) was about 2.26 mg x mL(-1). There was a good relationship between the logarithm concentrations of artificial musk and 1% when the concentrations of artificial musk ranged from 0.31-20.0 mg x mL(-1). The results indicated that this EIA method could be applied to evaluate the anti-inflammatory activity of artificial musk quickly, conveniently, sensitively and exactly. This paper provided a novel method and foundational research for the bioassay of artificial musk.

Objective To investigate the relatonahip between TNF-α and ventricular arrhythmias after acute myocardial infarction(AMI)and its mechanism.Method Both the clinical and animal experiments were done.(1)Clinical experiment:Eighty patients with AMI were included in Union Hospital,Tongji Medical College,Huazhong University of Science and Techology,from May 2005 to November 2006 according to the WHO diagnostic criteria.Co-infection of diseases such as severe upper respiratory infection,lung infection,high fever,cancer,et al were excluded.The relationship between the levels of TNF-α and arrhythmias were observed at different times after AMI.A straight line correlation,analysis Was done.(2)Animal experiment:Different concentrations of TNF-αwere added to isohted rat hearts for observing the arrhythrnia effects.The effect of TNF-α on intracellular Ca2+ concentration was detected by laser confocal technique.All data were analyzed by SNK-q test using SPSS 13.0 sofeware prograrn.Results(1)The plasma levels of TNF-α were significantly associated with the Lown class of PVC after AMI and they were higher in AMI of anterior wall[(46.41±10.34)pg/ml]than other positions [(28.25±6.35)pg/ml,P<0.05].2)The frequency of ventricular arrhythmias was interrelated with the concentralions of TNF-α.Using etanercept beforehand,TNF-α induced a slight increase of intracellular Ca2+ intensity (P<0.05).Conclusions There was a relationship between TNF-αlevels and ventricular arrhythmisa in patients with AMI.Animal experiments confirmed the isolated heart perfusion with TNF-α induced ventricular arrhytrnias.Expression of TNF-α after AMI was related with the occurrence of ventricular arrhythrnias.The effect might be associated with the increased inuaeellular Ca2+ intensity caused by TNF-α.