Chemical constituents from Crepis crocea / 中国中药杂志

Thirteen compounds were isolated from the ethyl acetate fraction of Crepis crocea by column chromatographies on silica gel, Sephadex LH-20 and semi-preparative HPLC. The structures were elucidated on the basis of spectral analysis as tectorone I (1), 8β- (2-methyl- 2-hydroxy-3-oxobutanoyloxy) -glucozaluzanin C (2), tectoroside (3), luteolin-7-O-glucoside (4), cosmosiin (5), esculetin (6), 3,4-dihydroxybenzaldehyde (7), trans-4-hydroxycinnamic acid (8), Caffeic acid (9), methyl p-hydroxyphenyllactate (10), ethylp- hydroxyphenyllactate (11), cis-3,4-dihydroxy-β-ionion (12). All the compounds, except for compounds 4 and 9, were isolated from this plant for the first time, and tectorone I (1) is a new natural product.

Structural characterization of the polysaccharide CTP3-E from Crepis turczaniowii C. A. Mey / 中国药学杂志

OBJECTIVE: To characterize the chemical structure of a homogenous polysaccharide CTP3-E purified from Crepis turczaninowii C. A. Mey. METHODS: Sugar composition analysis, methylation analysis, IR and NMR (Dept, HMBC, HMQC, etc.) were used to elucidate the structure. RESULTS: The molecular weight of CTP3-E was 12182. CTP3-E was composed of mannose, rhamose, glucuronic acid, galacturonic acid, glucose, galactose, and arabinose. CONCLUSION: CTP3-E is a new acidic heteropolysaccharide and was isolated from this medicinal plant for the first time.

Effects of tetramethylpyrazine on thrombin-induced tissue factor expression in vascular endothelial cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effects of tetramethylpyrazine (TMP) on tissue factor (TF) expression induced by thrombin in human umbilical vein endothelium derived cell line ECV304.</p><p><b>METHODS</b>The changes in the total cellular procoagulant activity (PCA) of ECV304 cells exposed to thrombin were observed with one-stage clotting assay. TF mRNA expression in the exposed cells was examined using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>ECV304 cells stimulated with increasing concentrations of thrombin (1.25-20 U/ml) showed a gradual increase of PCA (r=0.9602, P<0.01). The application of FVII-deficient plasma and the monoclonal antibody of TF confirmed that the PCA of the cells mediated by TF activity. TMP at 125-1000 microg/ml alone did not affect TF expression in ECV304 cells (P>0.20), TMP administered 30 min prior to thrombin exposure showed a significant concentration-dependent inhibitory effect on the increments of PCA (r=-0.9644, P<0.01) and TF mRNA expression (r=-0.9576, P<0.05) in ECV304 cells, and 1000 microg/ml TMP produced the strongest effect. In ECV304 cells stimulated with thrombin for 4, 6, 8, 10 and 12 h, TMP administration significantly inhibited the thrombin-induced PCA, and the effect was especially obvious at 8 h following thrombin exposure (P<0.05).</p><p><b>CONCLUSION</b>Thrombin induces TF expression in vascular endothelial cells, and this effect can be inhibited by TMP at the mRNA level.</p>

Development of a digital EEG signal acquiring system based on virtual instrument technology / 中国医疗器械杂志

This paper introduces an 16-lead digital EEG signal acquisition system, which applies MCU MSP430 as central control unit with high performance analog devices and high speed multi-channel, multi-bit analog-to-digital converter as peripheral to retrench analog circuit. Data is transferred to PC by USART interface. Software on PC based on virtual instrument technology realizes real-time detection, display and storage. The system has many advantages such as high precision, stable performance, small volume and low power dissipation, thus provides a new means for digital EEG signal acquisition.

Establishment and evaluation of a rabbit model of arterial thrombosis by collagen encapsulated thread-drawing / 中南大学学报(医学版)

OBJECTIVE@#To establish and evaluate a rabbit model of arterial thrombosis by modified thread-drawing.@*METHODS@#Fifty-three rabbits were randomly divided into 6 groups: a normal group, a ligating group,a collagen encapsulated thread-drawing group,a aspirin group,a clopidogrel group, and an aspirin clopidogral group. The endovascular pathological changes in the rabbits were observed, and D-fructose-1,6-diphosphate trisodium salt octahydrate (FDP), D-Dimer and tissue factor (TF) were detected with enzyme linked immunosorbent assay.@*RESULTS@#In the thread-drawing group, thrombus was obvious, and the endovascular elastic membrane was injured seriously compared with the ligating group. After being treated with aspirin and clopidogrel, most arterial thrombus was softened, dissolved and absorbed. Compared with that in the modified thread-drawing group,wet and dry weight of thrombus increased,and the level of D-Dimer, FDP and TF also increased in the modified thread-drawing group (P<0.01). After being treated by aspirin and/or clopidogrel, the wet and dry weight of thrombus and the level of D-Dimer, FDP and TF decreased compared with the control (P<0.01). Aspirin plus clopidogral could obviously reduce the wet and dry weight of thrombus, and reduce the level of D-Dimer and FDP (P<0.01). Aspirin plus clopidogral could obviously inhibit the formation of TF compared with aspirin (P<0.05).@*CONCLUSION@#Arterial thrombosis model by collagen encapsulated thread-drawing which is visible, repeatable and effective is better than thread-drawing. It is suitable for screening anti-thrombosis drugs and evaluating their effect.

Value of plasma tissue factor, tissue factor pathway inhibitor and factor VII assessments in patients with acute myocardial and cerebral infarction / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the clinical implications of changes in plasma tissue factor (TF), tissue factor pathway inhibitor (TFPI) and factor VII (FVII) after the onset of acute myocardial infarction (AMI) and acute cerebral infarction (ACI).</p><p><b>METHODS</b>Sixty-nine patients with AMI, 71 with ACI and 50 age-matched healthy volunteers were enrolled in this study. Blood samples were obtained from the healthy subjects and from the patients at the early stage of AMI and ACI onset for examination of plasma TF and TFPI activity using chromogenic assay, and the plasma TF and TFPI antigens were measured by enzyme-linked immunosorbent assay (ELISA). The plasma FVII coagulation activity (FVII:C) was also measured, and the plasma FVIIa determined using soluble TF assay.</p><p><b>RESULTS</b>Compared with the healthy control group, AMI patients had significantly enhanced plasma TF and TFPI activities and elevated TF and TFPI antigen levels (P<0.05), with also markedly increased FVIIa (P<0.05) but comparable FVII:C (P>0.05). In ACI patients, the plasma TF activity and antigen were obviously increased in comparison with the control group (P<0.05), but plasma TFPI activity and antigen were lowered (P<0.05), and both the FVII:C and FVIIa were markedly higher (P<0.05). Significant differences were noted in plasma TF and TFPI activities and their antigen levels as well as in FVII:C, but not in FVIIa between AMI and ACI patients.</p><p><b>CONCLUSION</b>V Following the onset of AMI and ACI, TF pathway is initiated and the risk of thrombogenesis increases, and the assessment of TF pathway is therefore of value for understanding the development of the condition.</p>

Effects of insulin like growth factor-1 on cell viability and tissue factor in vascular endothelial cells / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the effects of insulin like growth factor-1 (IGF-1) on cell viability and tissue factor (TF) in angiotensin II (Ang II) induced vascular endothelial cells and to investigate its mechanisms.</p><p><b>METHODS</b>10(-6) mol/L Ang II was added to human vascular endothelial cells (HUVECs) culture media alone or 30 min after pretreatment with IGF-1 (0.1 microg/ml , 0.5 microg/ml, 2.5 microg/ml). Cell viability and AngII type 1 receptor (AT1-R) mRNA were evaluated after 24 h incubation with AngII. At the optimum concentration of IGF-1 affecting cell viability, the time dependent manner for 12 - 48 h incubation with Ang II was evaluated. TF, NOS and NO were investigated after 24 h incubation with Ang II. In addition, NO synthase inhibitor Nomega-nitro-1-arginine methylester(L-NAME) was added 30 min before addition of IGF-1 and Ang II, and cell viability, TF, AT1-R mRNA, NOS and NO were evaluated after 24 h incubation.</p><p><b>RESULTS</b>(1) Ang II induced a decrease in cell vitality, an upregulation of AT1-R mRNA, an increase in TF, and a decrease in the activity of NOS and content of NO. (2) Pretreatment with IGF-1 significantly inhibited the decreased cell viability and upregulation of AT1-R mRNA. IGF-1 at 0.5 microg/ml showed the most obvious effects. This effect of cell viability recovery was in a time dependent manner during 12 -48 h. (3) IGF-1 also inhibited the increased content of TF, the decreased activity of NOS and the decreased content of NO. (4) The beneficial effects of IGF-1 on cultured endothelial cells were completely abolished by L-NAME.</p><p><b>CONCLUSION</b>IGF-1 pretreatment could enhance the ang II injured cell viability and anti-thrombosis capacity, and the protective effects may be related to activation of NOS-NO signaling pathway which inhibited AT1-R.</p>

Effects of Tongxinluo on cell viability and tissue factor in AngII induced vascular endothelial cells / 中南大学学报(医学版)

OBJECTIVE@#To determine the effects of Tongxinluo on cell viability and tissue factor (TF) in AngII induced vascular endothelial cells and to investigate its mechanism.@*METHODS@#AngII(10(-6)mol/L) was added to human vascular endothelial cells (HUVECs) culture media alone or with various concentration of Tongxinluo drug containing plasma (5%,10%, and 20%) added 30 minutes before AngII. Cell viability was evaluated after 24-hour incubation with AngII in a dose manner. TF, AngII type 1 receptor (AT(1)) mRNA, NO synthase (NOS) and NO were observed after 24-hour incubation with AngII. In addition, NOS inhibitor nomega-nitro-larginine (L-NAME) was added 30 minutes before Tongxinluo and AngII. Cell viability, TF, AT(1)mRNA, the level of NOS and NO were evaluated after 24-hour incubation with Tongxinluo and AngII.@*RESULTS@#Tongxinluo significantly improved AngII induced endothelial cell viability and the effect was the most obvious at 10%. Tongxinluo (10%) decreased the TF and AT(1) mRNA while increased the NOS and NO levels. L-NAME obviously inhibited the effects of Tongxinluo on cell viability, TF, AT(1) mRNA, and NOS and NO levels.@*CONCLUSION@#Up-regulating NOS-NO signaling may be the mechanism of Tongxinluo on cell viability and TF in AngII induced vacular endothelial cells.

Study on platelet-associated tissue factor and its significance / 中华血液学杂志

<p><b>OBJECTIVE</b>To explore whether normal platelet contains tissue factor (TF), and the significance of platelet-associated TF (PATF).</p><p><b>METHODS</b>Platelets were isolated by Sepharose 2B gel column. ELISA was used to detect the TF content in the lysates of washed platelets. Procoagulant activity of PATF was measured by one stage clotting time assay. The mRNA of TF was detected by reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>A certain amount of TF antigen (16.37 +/- 6.39) ng/L was detected in the washed-platelet lysates. Upon activation by collagen, platelets released TF and caused a marked increase in TF level in plasma (P <0.05). Resting platelets had no TF procoagulant activity, while procoagulant activity of platelets activated by collagen increased significantly, which could be blocked by TF McAb and poor VII plasma. TF mRNA could not be detected in washed platelets. TF content in platelets from patients with coronary heart disease was significantly higher than that from normal controls (P < 0.05). Resting platelets from the patients showed a higher procoagulant activity, which could be inhibited by TF McAb.</p><p><b>CONCLUSION</b>Platelets contain TF and the latter released by activated platelet was functionally active. Platelet itself might not synthesize TF. Protein content and procoagulant activity of PATF in patients with coronary heart disease were higher than that in controls. All these indicate that platelet may be involved in coagulation and thrombosis by releasing TF.</p>

Changes of tissue factor and tissue factor pathway inhibitor in neonatal jaundice due to infection / 中华儿科杂志

<p><b>OBJECTIVE</b>Tissue factor (TF) is an important factor in extrinsic coagulation. Tissue factor pathway inhibitor (TFPI) is a negative regulator of coagulation mediated by TF. Studies on TF and TFPI focus mainly on adult objects, seldom have been done on newborns, especially on sick newborns. The aim of this study was to observe the changes of TF and TFPI in plasma of newborns with infection jaundice and to research the effect of jaundice and infection on the balance of TF and TFPI in newborns.</p><p><b>METHODS</b>The content of TF and TFPI in plasma of 21 jaundiced newborns with infection and 8 jaundiced newborns without infection as control was determined quantitatively with the enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>The content of TFPI and TF in plasma of jaundiced newborn with infection was significantly higher than that of controls [TFPI (21.0 +/- 4.3) vs. (16.2 +/- 1.9) microg/L, P < 0.01; TF (177 +/- 79) vs. (51 +/- 24) ng/L, P < 0.01]. The ratio of TFPI/TF was significantly lower in newborn with infection jaundice than the controls (137 +/- 61 vs. 319 +/- 67, P < 0.01). The 21 jaundiced newborns with infection were divided into the severe hyperbilirubinemia group (serum bilirubin > or = 205.2 micromol/L, n = 10) and the mild hyperbilirubinemia group (serum bilirubin < 205.2 micromol/L, n = 11). There was no significant difference of TFPI level between the severe hyperbilirubinemia group and mild hyperbilirubinemia group (P > 0.05). The TF content in the severe hyperbilirubinemia group was higher than that in the mild hyperbilirubinemia group (216 +/- 79 vs.141 +/- 63, P < 0.01), while the ration of TFPI/TF was lower in the severe hyperbilirubinemia group than in the mild hyperbilirubinemia group (100 +/- 30 vs. 171 +/- 74, P < 0.01).</p><p><b>CONCLUSION</b>Infection might induce imbalance between the coagulation inhibition and activation in newborns. Hyperbilirubinemia can aggravate the imbalance induced by the infection through increasing plasma TF level.</p>

Effect of angiotensin II on tissue factor expression in human peripheral blood monocytes and its mechanisms / 中华血液学杂志

<p><b>OBJECTIVE</b>To elucidate the effect of angiotensin II (AngII) on the expression of tissue factor (TF) by monocytes and its mechanisms.</p><p><b>METHODS</b>Monocytes were isolated from healthy volunteers by Ficoll-Hypaque gradient and Percoll, and cultured in RPMI-1640. Procoagulant activity (PCA) was determined by one-stage clotting method, TF antigen by ELISA. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the TF gene mRNA. The levels of IkappaBalpha was detected by Western blot. Electrophoretic mobility shift assays (EMSA) were performed to evaluate the activity of NF-kappaB.</p><p><b>RESULTS</b>AngII (10(-9) - 10(-7) mol/L) significantly increased monocyte PCA, TF antigen and TF mRNA expression in a dose and time dependent manner. Losartan (10(-6) - 10(-5) mol/L) significantly inhibited the effects of AngII on TF activity, antigen and mRNA expression in a dose-dependent effects. Staurosporine (2.5 x 10(-7) mol/L) and genistein (4 x 10(-5) mol/L) lowered TF level of monocytes (P < 0.05). Western blot analysis revealed that after exposure to AngII (10(-7) mol/L), IkappaBalpha level decreased at 15 min, reached nadir at 60 min, and recovered at 180 min. EMSA showed NF-kappaB binding activity increased at 15 min, reached peak at 60 min, and recovered at 180 min. Pyrrolidine dithiocarbamate (PDTC, 10(-4) mol/L), an inhibitor of NF-kappaB, or AT1R antagonist losartan (10(-5)mol/L) inhibited AngII-induced NF-kappaB translocation.</p><p><b>CONCLUSIONS</b>AngII could induce the expression of TF in human monocytes, and this effect was mediated by AT1R. The PKC pathway played the most important role in AngII-induced TF expression. The activation of NF-kappaB was involved in TF expression in monocytes.</p>