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Biomedical subjects

M Aiach

Publications and source records attributed to M Aiach.

At least 199 records · Page 11Linked to original sources
PubMed1985

A functional abnormal antithrombin III (AT III) deficiency: AT III Charleville.

An antithrombin III (AT III) functional defect (AT III Charleville) was discovered in a patient presenting with recurrent venous thrombosis. Both anti-activated factor X (anti Xa) and antithrombin activity were decreased, in the absence and in the presence of heparin, while protein concentration was normal in an immunological assay. The abnormal AT III copurified with functional AT III using insolubilized heparin affinity chromatography. Polyacrylamide gel electrophoresis (PAGE) and high pressure liquid chromatography (HPLC) on a TSK column suggest that AT III Charleville forms unstable complexes with thrombin from which a modified protein is rapidly released.

Adult↗
PubMed1985

[Biological profile of the 1st 4 hours of a thrombolytic treatment combining urokinase with lysyl-plasminogen].

The authors study the biological variations which accompany an oral, thrombolytic treatment in which urokinase and lysyl-plasminogen are combined. Fibrinogen, the products of degradation of fibrinogen or fibrin, plasminogen and rapid alpha 2 antiplasmin are studied as a function of time. Two dimensional electrophoreses were carried out at precisely determined times. The combination of the two therapeutic agents causes the appearance of plasmin in the circulation, but it is neutralised by its rapid inhibitor. This therapeutic protocol entails moderate circulating fibrinolysis and may easily be monitored by determination of the circulating fibrinogen.

Acute Disease↗
PubMed1984

Involvement of hemostasis during an autoimmune glomerulonephritis induced by mercuric chloride in brown Norway rats.

Mercuric chloride (HgCl2) induces in Brown Norway (BN) rats an autoimmune disease characterized by a biphasic glomerulonephritis (GN). A transient nephrotic syndrome occurs during the third and fourth weeks after the first HgCl2 injection. Related to nephrotic syndrome, an hypercoagulable state develops with decreased factor XII and anti-thrombin III (AT III) levels and increased factor V activity and fibrinogen concentration. Moreover, during the same period, most of the rats were found thrombocytopenic. The presence of soluble fibrin monomer complexes and of fibrin degradation products (FDP) in the plasma of these rats associated with fibrin thrombi in glomerular capillary lumen proved the occurrence of disseminated intravascular coagulation (DIC). DIC was responsible for the death of several rats but most of these survived and clotting abnormalities were no longer found. Numerous factors can explain the occurrence of DIC in this model: anti glomerular basement membrane antibodies, circulating immune complexes, complement activation and/or glomerular endothelial cell detachment. The HgCl2 induced autoimmune disease appears as a good experimental model to study the relation between coagulation process and glomerulonephritis.

Animals↗
PubMed1984

[Intra-arterial thrombolysis with the combination of urokinase and lysyl-plasminogen. 27 cases of acute arterial obliteration of the lower limbs].

Twenty-five in situ thrombolysis using Lysyl Plasminogen and low doses of urokinase were performed on 25 acute, recent and severe arterial occlusion of lower limbs. Early success were 56% and 44% with a follow up of 5 months. Complications were very limited. Thus the thrombolytic treatment used in this study appears as effective as locally administered streptokinase but higher tolerated. It seems to be able to win one of the best places in the treatment of the arterial disease of the lower limbs.

Acute Disease↗
PubMed1984

Low molecular weight (LMW) heparin derivatives in experimental extra-corporeal circulation (ECC).

Low molecular weight (LMW) heparin has been shown to prevent experimental venous thrombosis. In order to investigate its biological action and its potential use in open heart surgery, we have conducted an experimental study using extracorporeal circulation (ECC) in sheep as an experimental model. 18 sheep were randomly selected to receive either LMW heparin (2 mg/kg), high dose heparin (HD; 160 U/kg), or low dose heparin (LD; 60 U/kg). The HD heparin yielded the same circulating anti-activated factor X (anti-Xa) activities as the LMW heparin and the LD heparin yielded the same anti-thrombin activity. LMW heparin and HD heparin were both effective in preventing blood clotting in the ECC circuit, demonstrating the antithrombotic activity of the LMW heparin. Clotting in the circuit was observed following LD heparin administration showing that the efficacy of LMW heparin does not only rely upon its weak anti-activated partial thromboplastin time (APTT) and anti-thrombin activity. Fibrinogen, fibrinogen degradation products (FDP), factor V (FV), platelet count, antithrombin III (AT III), fast acting antiplasmin (AP) were evaluated during and after ECC. The defects in hemostasis were similar in the three groups. Conclusions were: (1) heparin chain depolymerization diminishes the anti-APTT activity without altering the anti-thrombotic property; (2) LMW heparin is an effective alternative to heparin in cardiac surgery; (3) the absence of postoperative circulating anti-APTT activity might be associated with a reduced incidence of hemorrhagic complication, but we were not able to demonstrate it.

Animals↗
PubMed1983

Antithrombin III synthesis in rat liver parenchymal cells.

We have previously demonstrated by immunoperoxydase the presence of immunoreactive antithrombin III (AT III) in rat hepatocytes. We now present direct evidence that rat hepatocytes in culture synthesize AT III like immunoreactive material : 35S-methionine was added to the culture medium and incubated with hepatocytes. After incubation, AT III was immunologically characterized in the medium. We found significant amounts of 35S-AT III among the radioactive proteins synthesized and secreted by the cells.

Animals↗
PubMed1983

Albumin, fibrinogen, prothrombin and antithrombin III variations in blood, urines and liver in rat nephrotic syndrome (Heymann nephritis).

Albumin, fibrinogen, prothrombin and antithrombin III (AT III) variations have been studied in blood, urines and liver during an experimental nephrotic syndrome in rats (Heymann nephritis). A quantitative morphometric study (light microscopy) has been performed in the liver using an immunocytochemical technique--(PAP) method--to evaluate the protein synthesis by the number of protein-containing hepatocytes. Some sections were also studied by electron microscopy. The nephrotic animals were compared with control rats. In the blood of nephrotic rats, fibrinogen and prothrombin concentrations were increased and albumin and AT III concentrations were decreased. In the urines of nephrotic rats, albumin, prothrombin and AT III were lost, but no fibrinogen. The morphometric study in the liver has shown a significantly higher number of fibrinogen and prothrombin-containing hepatocytes in nephrotic rats than in controls, suggesting an increased synthesis of these proteins; no change was observed concerning albumin and AT III between nephrotic and control animals. In electron microscopy, albumin was demonstrated in Golgi apparatus, proving that the peroxidase-positive cells are related to protein synthesis. These results show that the mechanisms of regulation of the protein synthesis during nephrotic syndrome are different from one protein to another and, particularly, that their blood level is not the only regulating factor for their synthesis.

Albumins↗