A rapid screening model for biosurfactant-producing strains is described in this paper, according as biosurfac-tant can make the blood-plate hemolysis and produce the blue cycles in blue-glue-plate. 12 microorganisms have been got from soil and water samples sampled from oil field and refinery using this model, and one of them can produce the glyco-lipid biosurfactant, which can depress the interfacial tension of water from 71. 3mN/m to 30. 5mN/m, and yield is 6.5 g/L.

OBJECTIVETo evaluate the value of double source multidetector computed tomography (MDCT) in visualization of cardiac veins in patients with chronic heart failure.

METHODSThirty-five patients with chronic heart failure (aged 65.4 ± 8.8, 21 males and 14 females) were enrolled in the study. In Group A, MDCT and retrograde coronary venography (RCV) were performed consecutively; in Group B anterograde visualization of the coronary venous and RCV were performed.

RESULTSCoronary sinus, GCV and MCV of all individuals were identified in MDCT. LVPV was observed in 65% patients of Group A, and 66.7% patients of Group B. The correlation coefficient between MDCT and RCV was 0.944, and that between CVG and RCV was 0.42.

CONCLUSIONNon-invasive evaluation of cardiac veins with double source CT is feasible and may be used in cardiac resynchronization therapy.

Aged ; Coronary Angiography ; methods ; Female ; Humans ; Male ; Middle Aged ; Phlebography ; methods ; Tomography, Spiral Computed ; methods

OBJECTIVETo investigate the effects of heme oxygenase 1 inducer hemin on protection of ischemia-reperfusion injury in rats and its mechanisms.

METHODSThe Langendorff model of isolated rat heart was used; the left anterior descending coronary artery was occluded for 30 min and subsequently reperfused for 2 h. Then the ventricular function and infarct size were measured.

RESULTHemin preconditioning prevented the increase in LVEDP, decrease in LVDP and +/- dp/dt(max) in the isolated ischemia-reperfusion rat hearts. The leakage of LDH and CK in the coronary effluent was significantly declined in hemin-treated rat hearts. And the infarct size was also reduced. Administration of a blocker of mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) 5-HD (5 mg/kg) before hemin preconditioning increased the LVEDP, and reduced the LVDP and +/- dp/dt(max). The leakage of LDH and CK in the coronary effluent and the infarct size were also increased compared with only hemin-treated rat hearts. Pretreatment of the rats with a blocker of sarcolemmal ATP-sensitive potassium channel (sarcK(ATP)) HMR-1098 (6 mg/kg) before hemin preconditioning also abolished the protective effect. Infusion of paxilline (1 micromol/L), a blocker of calcium activated potassium channel (K(Ca)) for 10 min before ischemia/reperfusion led to larger infarct size and poorer myocardial performance as compared with the hemin group. The leakage of LDH and CK in the coronary effluent was also increased.

CONCLUSIONBoth mitoK(ATP)and sarcK(ATP)channels activation are required for the delayed cardioprotection induced by hemin. The opening of K(Ca) channels-dependent mechanism may be involved in the protection.

Animals ; Cardiotonic Agents ; pharmacology ; Heme Oxygenase-1 ; biosynthesis ; Hemin ; pharmacology ; In Vitro Techniques ; Ischemic Preconditioning, Myocardial ; methods ; Male ; Myocardial Infarction ; metabolism ; Myocardial Reperfusion Injury ; metabolism ; physiopathology ; prevention & control ; Potassium Channel Blockers ; pharmacology ; Potassium Channels ; metabolism ; Potassium Channels, Calcium-Activated ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effects of metoprolol on electrophysiology of ischemic and anoxic myocardium in diabetic rats.

METHODSForty Sprague-Dawley (SD) rats were divided into 4 groups: diabetes group; diabetes and ablation of left sympathetic nerve group; diabetes and metoprolol group and sham group. The diabetes model was induced by intraperitoneal injection of streptozotocin (STZ, 60 mg/kg). The ventricular diastolic effective threshold (DET), effective refractive period (ERP), and Ventricular fibrillation threshold (VFT) were measured. The serum concentration of nerve growth factor (NGF) was measured.

RESULTSMetoprolol increased DET of ischemic and anoxic myocardium in diabetic rats. The ablation of the left sympathetic nerve increased VFT of diabetic rats. VFT in metoprolo group was significantly increased compared to diabetes group after ischemia. The concentrations of NGF in diabetic group and metoprolol group were higher than those in sham group. There were no difference in NGF levels between ablation of left sympathetic nerve group and sham group.

CONCLUSIONThe remodeling of sympathetic nerve affects the electrophysiology of ischemic myocardium of diabetic rats. Metoprolol can increase the VFT and decrease the excitation threshold of the ischemic myocardium in diabetic rats.

Animals ; Diabetes Mellitus, Experimental ; physiopathology ; Heart ; drug effects ; physiopathology ; Male ; Metoprolol ; pharmacology ; Myocardial Ischemia ; physiopathology ; Nerve Growth Factor ; blood ; Rats ; Rats, Sprague-Dawley ; Sympathectomy

OBJECTIVETo study the feasibility and cost-effectiveness of a case-finding program on tuberculosis (TB) in richer rural areas.

METHODSScreening was implemented every three months for a total period of 9 months, in rural areas with high case notification rates. Three villages, each with ten thousand population, were selected to carry out a household screening program. A suspect was defined as who coughed for more than 3 weeks. The suspect was then referred to further diagnosis in county TB dispensary to undergo chest X-ray and sputum test.

RESULTSOf the 86,168 community population screened, 26 TB patients were identified with 7 of them were smear positive. The ratio of effectiveness vs. cost decreased on the second but slightly increased on the third screening program. The direct costs for the 3 screening programs were 6,312,397 and 1637 RMB respectively. Of total direct cost, 5.9% was paid by TB patients, whereas 35.9% was through financing of the county itself.

CONCLUSIONThe community household screening program could achieve higher case detection rate than passive case-finding approach which could be used in richer areas with low case detection rate in China.

China ; Chronic Disease ; Cost-Benefit Analysis ; Cough ; etiology ; Family Characteristics ; Humans ; Mass Screening ; economics ; Radiography, Thoracic ; Rural Health ; Sputum ; microbiology ; Tuberculosis ; complications ; diagnosis

OBJECTIVETo investigate whether cyclooxygenase-2 (COX-2) and heme oxygenase-1 (HO-1) are involved in the bradykinin-induced delayed protection.

METHODSCardiac contractility, lactate dehydrogenase (LDH) and infarct area were analyzed in isolated rat hearts undergoing ischemia-reperfusion injury induced by Langendorff method.

RESULTConscious rats received bradykinin (40 microg/kg), and the isolated hearts were subjected to 30 min of regional ischemia and 120 min of reperfusion 24 h later. Bradykinin pretreatment would improve post-ischemic performance, and reduced the release of LDH and infarct size. COX-2 inhibitor celecoxib (3 mg/kg) abolished bradykinin-induced protection, leading to poorer myocardial performance, release of more LDH and larger infarct sizes. Administration of HO-1 inhibitor ZnPP IX(20 microg/kg) before bradykinin partially abrogated the delayed protection. Pretreatment with the mitochondrial ATP sensitive potassium channel(mitoK(ATP) antagonist 5-HD before or 24 h after bradykinin administration also abolished the effect of protection.

CONCLUSIONThe results indicate that activation of HO-1 and COX-2 might be involved in the delayed cardioprotection evoked by bradykinin, and mitoK(ATP) channel may serve as both a trigger and a mediator in the cardioprotection.

Animals ; Bradykinin ; pharmacology ; Celecoxib ; Cyclooxygenase 2 ; metabolism ; Cyclooxygenase Inhibitors ; pharmacology ; Heme Oxygenase-1 ; metabolism ; In Vitro Techniques ; Ischemic Preconditioning, Myocardial ; methods ; Male ; Myocardial Reperfusion Injury ; enzymology ; prevention & control ; Potassium Channels ; physiology ; Pyrazoles ; pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sulfonamides ; pharmacology

BACKGROUNDThere are few reports of a biological role for glycosyltransferases in the infiltration of osteoarthritic synovitis. The aim of this research was to investigate the expression and cellular location of β-1,4-galactosyltransferase I (β-1,4-GalT-I) in a surgically-induced rat model of knee osteoarthritis (OA), and explore the role of β-1,4-GalT-I in the pathogenesis of OA.

METHODSMale Sprague-Dawley rats were randomly divided into three groups: OA group, sham group and normal group. The model of OA was established in the right knees of rats by anterior cruciate ligament transaction (ACLT) with partial medial meniscectomy. Fibroblast-like synoviocytes (FLSs) obtained from normal rat synovial tissue were cultured. The expression of β-1,4-GalT-I mRNA in the synovial tissue, articular cartilage and FLSs treated with tumor necrosis factor-α (TNF-α) were assayed by real-time PCR. Western-blotting and immunohistochemisty were used to observe the expression of β-1,4-GalT-I at the protein level. Double immunofluorescent staining was used to define the location of the β-1,4-GalT-I with macrophage-like synoviocytes, FLSs, neutrophils, and TNF-α in the OA synovium. The alteration of TNF-α in FLSs which were treated with lipopolysaccharide (LPS) and β-1,4-GalT-I-Ab were detected by enzyme-linked immunosorbent assay (ELISA).

RESULTSThe mRNA and protein expression of β-1,4-GalT-I increased in synovial tissue of the OA group compared with the normal and sham groups at two and four weeks after the surgery, however, no significant difference appeared in the articular cartilage. Immunohistochemistry also indicated that the β-1,4-GalT-I expression in OA synovium at four weeks after surgery increased sharply compared with the control group. β-1,4-GalT-I co-localized with macrophage-like synoviocytes, FLSs, neutrophils and TNF-α in rat OA synovitis. Moreover, in vitro β-1,4-GalT-I mRNA in FLSs was affected in a dose- and time-dependent manner in response to TNF-α stimulation. ELISA revealed that the expression of TNF-α was attenuated in FLSs in vitro when treated with anti β-1,4-GalT-I antibody.

CONCLUSIONβ-1,4-GalT-I may play an important role in the inflammation process of rat OA synovial tissue which would provide the foundation for further researching into the concrete mechanism of β-1,4-GalT-I in OA synovitis.

Animals ; Blotting, Western ; Cells, Cultured ; Enzyme-Linked Immunosorbent Assay ; Galactosyltransferases ; genetics ; metabolism ; Immunohistochemistry ; Knee Joint ; enzymology ; pathology ; surgery ; Male ; Osteoarthritis, Knee ; enzymology ; genetics ; pathology ; Polymerase Chain Reaction ; Rats ; Rats, Sprague-Dawley ; Synovial Membrane ; enzymology ; Synovitis ; enzymology ; etiology

OBJECTIVETo explore the potential effects of anti-VEGF hairpin ribozyme gene to gene expression profiles in leukemia cell line K562.

METHODSThe lipofectamine mediation was used to transfect the recombinant eukaryotic expression plasmid (pcDNA3-RZ) containing anti-VEGF hairpin ribozyme gene and the non-recombinant vector as control into K562 cells. And the positive clones were screened by G418. Ribozyme gene in K562 cells was confirmed by PCR. Fluorescent real time reverse transcription-PCR(RT-PCR) and Western blotting were employed to detect the expression of VEGF mRNA and protein in leukemia cells. cDNA microarray was used to explore the alteration of gene expression profiles when decreasing VEGF gene expression in leukemia cells. Expression of PCNA and GSN genes were verified by semi-quantitative RT-PCR.

RESULTSThe pcDNA3-RZ and pcDNA3 had been transfected into the human leukemia cell line K562 and positive clones been screened by G418. Stable expression of the ribozyme gene in K562 cells was confirmed by PCR. The level of VEGF mRNA and protein decreased dramatically in K562-RZ cells when compared with K562 or K562-PC (K562 cell transfected with empty vector) cells. The gene expression profiles were changed by transfection of anti-VEGF hairpin ribozyme gene into K562 cells. Among 4096 gene clones on the microarray, 191 (4.86%) genes were detected to have the marked changes with 104 down-regulated and 87 up-regulated, that were functionally related to cell cycle progression, gene replication, metabolism, cell apoptosis, cell signal transduction, and oncogenes etc. An increased expression of GSN gene and a decreased expression of PCNA gene in K562/RZ cells have been detected by RT-PCR.

CONCLUSIONDown-regulation of VEGF gene by introducing anti-VEGF hairpin ribozyme gene can alter the gene expression profiles in K562 cells, leading to change of cell growth, differentiation and apoptosis in K562/RZ cells.

Down-Regulation ; drug effects ; Gene Expression ; drug effects ; Gene Expression Profiling ; Humans ; K562 Cells ; Leukemia ; genetics ; metabolism ; pathology ; RNA, Catalytic ; pharmacology ; Vascular Endothelial Growth Factor A ; antagonists & inhibitors ; genetics ; metabolism

OBJECTIVEThe study was designed to compare the antithrombotic property and safety between nadroparin and unfractionated heparin during percutaneous coronary intervention (PCI).

METHODSA prospective, single blind, randomized study was performed. A total of 98 patients (aged 65.1 +/- 8.6 years, female, 28.6%, diabetes, 7.1%) undergoing selective PCI were randomized to be administered intravenously either nadroparin (0.075 ml/10 kg) or unfractionated heparin (100U/kg) for procedural anticoagulation, in whom stable angina was 42.9%, unstable angina, 27.6%, myocardial infarction, 29.6%, two or three-vessel disease, 23.5%, stent, 100%. Blood samples for anti-Xa level were assayed in the first 22 patients of the nadroparin group before and after administration at the following intervals: 8 min, 1 h, 2 h and 4 h. Bleeding complications were classified according to Thrombolysis In Myocardial Infarction (TIMI) criteria. The bleeding index (change in hemoglobin) was calculated. All patients were monitored for adverse clinical events (i.e. death, myocardial infarction, need for revascularization) during the period of 30 days after PCI.

RESULTS(1) There were no significant differences in baseline characteristics between the two randomized groups. (2) Plasma anti-Xa activities were 0.10 +/- 0.00 IU/ml at the time just before the administration of nadroparin, 1.89 +/- 0.24 IU/ml, 0.96 +/- 0.24 IU/ml, 0.47 +/- 0.13 IU/ml, and 0.30 +/- 0.12 IU/ml at the time of 8 min, 1 h, 2 h and 4 h after the use of nadroparin (and the rate of > 0.5 IU/ml were 100%, 100%, 45% and 9% patients), respectively. (3) There were no significant differences in the mean bleeding index, post-PCI hemoglobin and hematocrit between nadroparin and unfractionated heparin group [(1.16 +/- 5.80) g/L vs (0.90 +/- 6.50) g/L, P = 0.858; (129.5 +/- 13.6) g/L vs (125.5 +/- 14.9) g/L, P = 0.175; (39.0 +/- 3.9)% vs (37.9 +/- 4.6)%, P = 0.205]. (4) None of the patients in two randomized groups were observed hemorrhagic events, which including TIMI major or minor bleeding complications, gross or microscopic hematuria, melena, positive stool occult blood. There were no blood transfusions and no hematoma at the vascular access site in either of the group. (5) No death, no recurrent angina pectoris, and no urgent revascularization occurred within 30 days in both groups. One patient in nadroparin group was observed "no reflow" phenomenon that was accompanied with an elevated ST segment and a risen serum level of cTnI. This patient was diagnosed as non-Q-wave myocardial infarction. Though no myocardial infarction was found in unfractionated heparin group, there was no significant difference in the rate of myocardial infarction between the two groups of the study (P = 0.970).

CONCLUSIONSThe administration of nadroparin before PCI seems effective and safe. Compared with unfractionated heparin, nadroparin was associated with neither an excess of bleeding nor an increase of clinical complications in this study.

Adult ; Aged ; Aged, 80 and over ; Angioplasty, Balloon, Coronary ; methods ; Antithrombins ; adverse effects ; therapeutic use ; Female ; Heparin ; adverse effects ; therapeutic use ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; therapy ; Nadroparin ; adverse effects ; therapeutic use ; Prospective Studies ; Single-Blind Method ; Treatment Outcome

The objective of study was to investigate whether U937 cells-loaded dendritic cells (DCs) could induce anti-leukemic immune activity. The apoptosis of U937 cells was induced by artesunate (ART). DCs derived from peripheral blood mononuclear cells of health donors were loaded with apoptotic U937 cells, and induced to maturation in the presence of TNF-alpha. Matured DCs were cocultured with autologous T-lymphocytes, and combined with IL-2 in order to induce the leukemia-specific CTL. The phenotypes of DCs and T lymphocytes were tested by flow cytometry. The ability of DC capturing antigens was measured by Dextran-FITC endocytosis. The IL-12p70 level was assayed by ELISA kit. The proliferation of CTL and CTL activity were measured by MTT assay. The results showed that the apoptotic rate of the U937 cells was 51.2% when U937 cells were induced by 1 microg/ml ART for 48 hours in vitro. DCs had the most powerful ability of endocytosis in its immature phase. Apoptotic U937 cells could not induce the features of DC maturation, and apoptotic U937 cell-pulsed immature DCs could be matured with TNF-alpha. The IL-12p70 level secreded by apoptotic U937 cell-loaded mature DCs (mDC-(Apo)U937) was higher than that of non-loaded mDC. The proliferation of autologous T lymphocytes co-cultured with mDC-(Apo)U937 was significantly remarkable and the content of CD8(+) CTL was significantly higher in comparison with any other groups. CTL induced by mDC-(Apo)U937 had stronger killing effect on U937 cells than NB4 (p < 0.01). It is concluded that the mDC-(Apo)U937 can effectively generate T cell-mediated dendritic antileukemic responses in vitro.
Antigens, Neoplasm ; immunology ; Apoptosis ; Artemisinins ; pharmacology ; Coculture Techniques ; Dendritic Cells ; cytology ; immunology ; Humans ; Leukemia ; immunology ; T-Lymphocytes, Cytotoxic ; immunology ; U937 Cells