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Pàgina 1 des de 36 resultats
Renal transplantation in HIV-infected patients: the Paris experience.
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Kidney transplantation is now considered as a reasonable option for HIV-infected patients with end-stage renal disease. We describe here a retrospective study conducted in five transplantation centers in Paris. Twenty-seven patients were included. Immunosuppressive protocol associated an induction
Paris saponin I induces G₂/M cell cycle arrest and apoptosis in human gastric carcinoma SGC7901 cells.
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The aim of this study was to investigate the effect of Paris saponin I (PS I) on human gastric carcinoma cell growth and apoptosis and to explore the potential mechanisms. The proliferation of SGC7901 cells was monitored by the MTT cell viability assay, while the nuclear morphology of apoptotic
[Effects of Different AM Fungi on Quantity and Enzyme Activity of Rhizosphere Soil Microorganism of Paris polyphylla var. yunnanensis].
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To investigate the rhizosphere soil microorganism and enzyme activity after Paris polyphylla var. yunnanensis inoculated Arbuscular Mycorrhizal( AM) fungi,which provide the technological condition for artificial cultivation of Paris polyphylla var. yunnanensis.
By the method of combining the
Steroidal saponins from Paris polyphylla suppress adhesion, migration and invasion of human lung cancer A549 cells via down-regulating MMP-2 and MMP-9.
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BACKGROUND
Tumor metastases are the main reasons for oncotherapy failure. Paris polyphylla (Chinese name: Chonglou) has traditionally been used for its anti-cancer actions. In this article, we focus on the regulation of human lung cancer A549 cell metastases and invasion by Paris polyphylla
Effect of statins on platelet PAR-1 thrombin receptor in patients with the metabolic syndrome (from the PAR-1 inhibition by statins [PARIS] study).
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We investigated whether, in primary prevention patients with metabolic syndrome, statins affect the platelet protease-activated receptor-1 (PAR-1) thrombin receptor by performing serial measurements of its activity and the antigen expression level by flow cytometry before and during treatment.
The agonist of the protease-activated receptor-1 (PAR) but not PAR3 mimics thrombin-induced vascular endothelial growth factor release in human smooth muscle cells.
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Thrombin, a serine protease generated by the activation of the blood coagulation cascade following vessel injury, induces vascular endothelial growth factor-(VEGF) release. However, the molecular mechanism of thrombin-induced VEGF release is largely unknown. Anagonist of protease-activated
Peripheral deposition of alpha1-protease inhibitor using commercial inhalation devices.
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Patients with hereditary alpha1-proteinase inhibitor (alpha1-PI) deficiency are at risk of developing lung emphysema. To prevent the development of this disease, alpha1-PI replacement therapy via inhalation may be a more convenient and effective therapy than the intravenous administration of the
Sequence characterization of the protease and partial reverse transcriptase proteins of the NED panel, an international HIV type 1 subtype reference and standards panel.
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The NED panel (NIH-ENVA-DOD) was assembled by the Virology Quality Assurance Laboratory for use as an international HIV-1 subtype reference and standards panel. The panel contains 44 minimally cultured strains from diverse geographic areas donated by the Walter Reed Army Institute of Research and F.
Identification of a novel 33-kDa Ser/Thr kinase that phosphorylates the cytoplasmic tail of protease-activated receptor 1 (thrombin receptor) in human platelets.
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Stimulation of human platelets with thrombin or thrombin receptor agonist peptide (TRAP/ Ser-Phe-Leu-Leu-Arg-Asn) resulted in phosphorylation of the protease-activated receptor 1 (PAR1). However, protein kinase(s), capable of phosphorylating PAR1 upon activation of this receptor, has not been as yet
Activation of serpins and their cognate proteases in muscle after crush injury.
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Direct muscle injury was induced in rats in order to evaluate alterations in the balance of serine proteases and inhibitors (serpins) as a response to tissue damage. It was previously found that certain proteases, specifically urokinase-like plasminogen activator (uPA) and others, required
Protective effect of a thrombin receptor (protease-activated receptor 1) gene polymorphism toward venous thromboembolism.
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The human protease-activated receptor 1 (PAR-1) is activated by thrombin at the surface of platelets and endothelial cells, 2 cells that are implicated in hemostasis and thrombosis. We studied the PAR-1 gene in a large case-control study from the Paris Thrombosis Study (PATHROS), and the possible
Lopinavir/ritonavir-based antiretroviral therapy in human immunodeficiency virus type 1-infected naive children: rare protease inhibitor resistance mutations but high lamivudine/emtricitabine resistance at the time of virologic failure.
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BACKGROUND
Lopinavir/ritonavir (LPV/r) is now the protease inhibitor regimen of choice in the first-line antiretroviral therapy for children <6 years of age.
METHODS
We included all the human immunodeficiency virus (HIV) type 1-infected highly active antiretroviral therapy (HAART)-naive children who
Differentiation of conglutination activity and sugar-binding activity of conglutinin after removal of NH2-terminal 54 amino acid residues by endogenous serine protease(s).
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Bovine conglutinin, which is a serum lectin specific for N-acetylglucosamine, was purified from heat-inactivated bovine serum by Sepharose 4B-mannan affinity chromatography. Without prior heat inactivation, however, the same affinity chromatography yielded a modified conglutinin, which retained
[The revival of proteinases].
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In this article, which was presented at the meeting on proteases (organized by the French Society for Connective Tissue Studies and held in Paris in September 1989) current lines of research on proteases are analyzed. A few examples show that the current renewed interest in this field is the result
Molecular characterization of antithrombin III (ATIII) variants using polymerase chain reaction. Identification of the ATIII Charleville as an Ala 384 Pro mutation.
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The genes of seven structural mutants of antithrombin III (ATIII), presenting either defective serine protease reactivity or abnormal heparin binding, were analyzed. The polymerase chain reaction (PCR) was used to amplify the corresponding gene exon and the mutation was identified by either dot blot
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