PubMed · 4184248
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B P Dunn, W R Livingstone, A I Macdougall, J B Rennie, D A Watt. 1969-08-09. Declotting Scribner shunts.. https://pubmed.ncbi.nlm.nih.gov/4184248/
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Tissue factor (TF), a transmembrane glycoprotein, initiates the extrinsic coagulation cascade. TF is known to play a major role in mediating thrombosis and thrombotic episodes associated with the progression of atherosclerosis. Macrophages at inflammatory sites, such as atherosclerotic lesions, release numerous cytokines that are capable of modulating TF expression. This study examined the role of oncostatin M (OSM), a macrophage/ T-lymphocyte-restricted cytokine, in the expression of TF in vascular smooth muscle cells (SMCs). It is reported here that OSM stimulated a biphasic and sustained pattern of TF messenger RNA (mRNA). The effect of OSM on TF mRNA expression was regulated at the transcriptional level as determined by nuclear run-offs and transient transfection of a TF promoter-reporter gene construct. OSM-induced TF expression was regulated primarily by the transcription factor NF-kappaB. Activation of NF-kappaB by OSM did not require IkappaB-alpha degradation. Inhibition of MEK activity by U0126 prevented OSM-induced TF expression by suppressing NF-kappaB DNA binding activity as determined by gel-shift analysis. Further, inhibition of Erk-1/2 protein by antisense treatment resulted in suppression of TF mRNA expression, indicating a role for Erk-1/2 in modulating NF-kappaB DNA binding activity. These studies suggest that the induced expression of TF by OSM is primarily through the activation of NF-kappaB and that activation of NF-kappaB is regulated in part by the MEK/Erk-1/2 signal transduction pathway. This study indicates that OSM may play a key role in promoting TF expression in SMCs within atherosclerotic lesions.
BACKGROUND: Virus inactivation of plasma can be achieved by photodynamic methods in the presence of phenothiazine dyes such as methylene blue (MB). Subsequent filtration may increase the efficacy of virus inactivation and reduce adverse effects of WBC contamination and MB. STUDY DESIGN AND METHODS: This study examined the effect of filtration with three different filters (MBF1, MBF2, and MBF3) on MB concentration, residual cells, coagulation factors, and activation measures of coagulation, fibrinolysis, and complement in MB-treated (1 microM/L) plasma units. RESULTS: Filtration reduced the concentration of MB by > or = 89 percent. WBCs were depleted by 92 percent (MBF1) and >99.9 percent (MBF2 and MBF3). Treatment with MB significantly decreased the coagulation potency from levels in untreated plasma, as measured by thromboplastin time ratio (112 +/- 18% vs. 95 +/- 11%), activated partial thromboplastin time (40 +/- 3 sec vs. 44 +/- 3 sec), thrombin time (16.9 +/- 1.1 sec vs. 18.6 +/- 1.5 sec), factor VIII (1.09 +/- 0.21 U/mL vs. 0.85 +/- 0.13 U/mL), and vWF (0.94 +/- 0.65 U/mL vs. 0.65 +/- 0.24 U/mL). Filtration did not further decrease these values, while factor XI (0.75 +/- 0.22 U/mL vs. 0.37 +/- 0.20 U/mL) and prekallikrein values decreased in MB plasma units filtered with the MBF3. In addition, activated factor XII (0.7 +/- 0.5 microg/L vs. 4.5 +/- 1.0 microg/L) increased. CONCLUSION: WBCs and MB can be eliminated from MB-treated plasma units by filtration. Differences in biocompatibility of the different filters, especially the influence on the contact phase of coagulation, must be taken into consideration.
Saturated and n-3 fatty acids, postprandial lipaemia, and the combined effects of fatty acids and lipid-lowering drugs have been of principal interest in recent studies in the field of dietary fats, lipids and haemostasis. The sex-specific effect of individual saturated fatty acids on coagulation factor VII activity has been discovered, and the significant effect of factor VII R353Q polymorphism on the postprandial response has also been found. An increased intake of n-3 fatty acids or fat reduction when combined with intensive lifestyle interventions may lead to reduced thrombotic potential in type 2 diabetic patients and obese individuals. Furthermore, positive effects on haemostasis by combined treatment with long-chain n-3 fatty acids and simvastatin indicate that n-3 fatty acids may be of some relevance with lipid-lowering drugs. The possible unfavourable effect of n-3 fatty acids on plasminogen activator inhibitor-1 activity is still a matter of dispute, but recent studies suggest that n-3 fatty acids, including alpha-linolenic acid, may have antithrombotic effects by enhancing protein C activity.