leukopenia/protease

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Gabexate mesilate, a synthetic protease inhibitor, attenuates endotoxin-induced pulmonary vascular injury by inhibiting tumor necrosis factor production by monocytes.

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OBJECTIVE In order to determine whether gabexate mesilate, a synthetic protease inhibitor with anticoagulant properties, is useful for the treatment of adult respiratory distress syndrome, we examined its effect on endotoxin-induced pulmonary vascular injury in rats. METHODS Prospective, randomized,

Treatment of post-transfusion graft-versus-host disease with nafmostat mesilate, a serine protease inhibitor.

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BACKGROUND Cytotoxic T lymphocytes from donors are thought to injure the target organs in post-transfusion graft-versus-host disease (PT-GVHD) through perforin-granzyme- and Fas-dependent cell killings. The protease involved is a serine protease, and nafmostat mesilate (NM), a serine protease

Resistance-plasmid- and protease-independent murine virulence of a multiple-drug-resistant strain of Serratia marcescens.

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The multiple-drug-resistant Serratia marcescens isolate SH 186 (serotype 06/014:H12, bacteriocin type 18) carried a 44 megadalton, nonconjugative resistance (R-) plasmid as demonstrated with 'curing' experiments and the DNA agarose gel electrophoresis technique. 'Cured' variants, which had lost part

Gabexate mesilate, a synthetic protease inhibitor, prevents compression-induced spinal cord injury by inhibiting activation of leukocytes in rats.

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OBJECTIVE Gabexate mesilate is a synthetic protease inhibitor capable of inhibiting both coagulation and cytokine production by monocytes. To investigate whether gabexate mesilate is useful for the prevention of posttraumatic spinal cord injury, we examined its effect on compression trauma-induced

Toxic uveitis caused by pharmacodynamic interactions of Rifabutin and protease inhibitors: a case report.

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Toxic reactions (uveitis, arthritis and leucopenia) of Rifabutin at normal doses should always be considered because of pharmacokinetic interactions with other drugs (e.g. the protease inhibitors). This case demonstrates that this kind of uveitis is clinically significant as the diagnosis of

Absence of neutral protease and alkaline phosphatase in neutrophils of a case of hairy cell leukemia.

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Enzymaticaly homogeneous fractions of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from peripheral blood of a patient with hairy cell leukemia, or leukemic reticuloendotheliosis, LRE,(with leukopenia, neutropenia, lymphocytosis, and massive splenomegaly). To detect

Contribution of protein Z and protein Z-dependent protease inhibitor in generalized Shwartzman reaction.

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OBJECTIVE Sepsis, a leading cause of mortality in critically ill patients, is closely linked to the excessive activation of coagulation and inflammation. Protein Z, a cofactor for the protein Z-dependent protease inhibitor, enhances the inhibition of coagulation factor Xa, and protein Z-dependent

A phase I trial of the HIV protease inhibitor nelfinavir with concurrent chemoradiotherapy for unresectable stage IIIA/IIIB non-small cell lung cancer: a report of toxicities and clinical response.

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BACKGROUND The objective of this phase I trial was to determine dose-limiting toxicities (DLT) and the maximally tolerated dose of the radiosensitizer Nelfinavir in combination with concurrent chemoradiotherapy in locally advanced non-small cell lung cancer (NSCLC). METHODS Nelfinavir (dose level 1:

Proteomic profiling of blood-dialyzer interactome reveals involvement of lectin complement pathway in hemodialysis-induced inflammatory response.

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OBJECTIVE dialysis-induced inflammatory response including leukocyte and complement activation is considered a significant cofactor of chronic morbidity in long-term hemodialysis (HD) patients. The aim of this study was to provide better insight into its molecular background. METHODS in 16 patients,

Activated protein C reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation.

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We examined whether activated protein C (APC) reduces ischemia/reperfusion (I/R)-induced renal injury by inhibiting leukocyte activation. In a rat model, intravenous administration of APC markedly reduced I/R-induced renal dysfunction and histological changes, whereas intravenous administration of

Activated protein C prevents endotoxin-induced hypotension in rats by inhibiting excessive production of nitric oxide.

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BACKGROUND Excessive production of nitric oxide (NO) by the inducible isoform of NO synthase (iNOS) is critically involved in endotoxin (ET)-induced hypotension. Tumor necrosis factor-alpha (TNF-alpha) plays an important role in induction of iNOS. Because activated protein C (APC), a physiological

Activated protein C attenuates endotoxin-induced pulmonary vascular injury by inhibiting activated leukocytes in rats.

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We investigated the effect of activated protein C (APC) on lipopolysaccharide (LPS)-induced pulmonary vascular injury in rats to investigate the possible usefulness of APC as a treatment for adult respiratory distress syndrome. Intravenously administered LPS (5 mg/kg) significantly increased

Treatment of post transfusion graft-versus-host disease.

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OBJECTIVE In Japan, so many cases of post-transfusion graft-versus-host disease (PT-GVHD) have been reported, and no effective treatment has been reported. METHODS RESULTS Totally 61 cases of PT-GVHD have been collected, and their background were analyzed. A serine protease inhibitor, nafamostat

Nafamstat mesilate attenuates pulmonary hypertension in heparin-protamine reactions.

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Rapid protamine reversal of heparin anticoagulation in awake sheep caused, after 1 min, a approximately 15-fold increase of arterial plasma thromboxane B2 (TxB2) levels, a 4-fold rise of pulmonary vascular resistance (PVR), a 2-fold rise of pulmonary arterial pressure, and after 3 min, a 2-fold rise

Degradation of circulating von Willebrand factor and its regulator ADAMTS13 implicates secreted Bacillus anthracis metalloproteases in anthrax consumptive coagulopathy.

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Pathology data from the anthrax animal models show evidence of significant increases in vascular permeability coincident with hemostatic imbalances manifested by thrombocytopenia, transient leucopenia, and aggressive disseminated intravascular coagulation. In this study we hypothesized that anthrax

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