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PubMedDate not supplied

Current concepts of the mechanism of acute inflammation in gouty arthritis.

The acute gouty attack develops after free crystalline monosodium urate crystals appear in the joint cavity (1). Recent developments in the investigation of urate crystal-induced inflammation have led to a better understanding of the pathogenesis of acute gouty arthritis. The purpose of this review is to summarize present concepts concerning the mechanism of the acute gouty attack.

Acute Disease↗
PubMedDate not supplied

One-step preparation of Hageman factor fragment concentrate.

The Hageman factor fragment (HFf) concentrate was prepared from acetone and dextran sulphate activated human plasma by chromatography on a CM-Sephadex column. The preparation was free of the main kallikrein inhibitors--Cl-inactivator, alpha 2-macroglobulin, antithrombin III and alpha 1-antitrypsin. The HFf concentrate can serve as an activator of prekallikrein in patient plasma.

Blood↗
PubMed2003

Interactions of antithrombin and proteins in the plasma contact activation system with immobilized functional heparin.

The interactions of antithrombin (AT) and the contact phase clotting factors with two commercially available heparinized surfaces are reported. The Carmeda (CBAS) and Corline surfaces along with controls (a sulfonated polyethylene surface and a CBAS analog in which the heparin used was devoid of specific AT-binding sequences) were exposed to human plasma. Adsorbed proteins were eluted and examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. The CBAS and Corline surfaces adsorbed large amounts of AT, whereas adsorption on the controls was negligible. Immunoblots for the four contact phase clotting factors indicated less contact activation on the CBAS and Corline surfaces than on the controls. Determination of adsorbed functional AT using a FXa inhibition assay showed that the CBAS surface adsorbed about 4 times as much AT as the Corline surface. Adsorption of AT to the control surfaces was minimal. Assays for adsorbed FXII and FXIIa based on kallikrein generation showed that all four surfaces adsorbed similar amounts of FXII. However, on the controls, most of the FXII was in activated form, whereas on the CBAS and Corline surfaces very little activation occurred.

Antithrombins↗
PubMed2001

Contradictory functions of the sulfatide in the blood coagulation system.

It has long been controversial whether sulfatide stimulates blood coagulation or inhibits blood coagulation. In this paper, I demonstrated not only anticoagulant activity but also coagulant activity of sulfatide in vivo by using experimental animal models and presented the possibility that sulfatide may function contradictorily under physiological and/or pathological conditions. For instance, I presented possible involvement of sulfatide in thrombotic diseases associated with cancers.

Animals↗
PubMed1989

Hageman factor dependent kinin generation system in guinea pig skin: extravascular localization of the components, and prolonged vascular reaction in inhibitor-depleted animal of this system.

1. Monospecific antibodies against components of the guinea pig Hageman factor-dependent system, such as Hageman factor, prekallikrein and high-molecular-weight (HMW) kininogen were prepared. These antibodies demonstrated the presence of all of these components in the normal guinea pig skin extract with the properties identical to them in plasma on western immunoblotting analysis. 2. Guinea pig macroalbumin which is a major circulating inhibitor of activated Hageman factor was immunologically depleted from three animals. Duration of a vascular permeability reaction caused by an intradermal injection of activated Hageman factor was prolonged in all of these guinea pigs approximately twice as long as the control, indicating a presence of negative feedback regulation of the Hageman factor-dependent kinin generation cascade in dermal tissue via the circulating protease inhibitor.

Animals↗