Test particles of medical devices by Coulter Multisizer / 中国医疗器械杂志

Introduced the "particles" item testing progress and some notes, using Coulter Multisizer, about medical devices and drugs wrapper, with an expectation of some help for the "particles" item tests in the solution in these area.

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>

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>