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Biomedical subjects

M J Gallimore

Publications and source records attributed to M J Gallimore.

At least 55 records · Page 3Linked to original sources
PubMed1988

Parameters of the kallikrein-kinin, coagulation and fibrinolytic systems as early indicators of kidney transplant rejection.

In order to find early indicators of kidney transplant rejection before clinical symptoms were noticed, parameters of the coagulation, fibrinolytic and kallikrein-kinin systems were measured. Nineteen patients were followed before and daily after kidney transplantation during the first week and every second day in the following weeks. All patients received immunosuppressive therapy with cyclosporin and corticoids. Ten patients suffered from transplant rejection. The first rejection occurred on the 7th day after transplantation. Of all the parameters measured, kallikrein inhibition, beta-FXIIa inhibition, plasminogen and antithrombin III were early indicators of kidney transplant rejections. A rise in these parameters could be demonstrated 2-3 days before clinical signs were noticed. In the other 9 patients no significant rises in antithrombin III, plasminogen, kallikrein inhibition and beta-FXIIa inhibition could be found.

Adrenal Cortex Hormones↗
PubMed1986

Description and evaluation of a new chromogenic substrate assay kit for the determination of prekallikrein in human plasma.

Because of an increasing interest in the determination of prekallikrein a kit was made for the determination of this plasma proenzyme. The kit consists of 1) a prekallikrein activator of the cephalin-ellagic acid type containing Factor XII and HMW-kininogen to ensure a total activation of the prekallikrein even in pathological plasmas, 2) a buffer which is optimal for both activation and substrate hydrolysis and 3) the chromogenic substrate S-2302. A control plasma is also included. This kit was evaluated by thirteen research groups as well as by ourselves. Both normal and patient plasmas were analyzed. Good correlations were obtained for prekallikrein levels in plasma samples between the kit method and two other methods (immunochemical and functional). As well as in deficiency states the prekallikrein level was low in pancreatitis (n = 20), cancer (n = 16), early pregnancy with gestosis (n = 15), cirrhosis (n = 9) and cases with thromboembolic disorders (n = 5). The prekallikrein level was high in late pregnancy (n = 4).

Colorimetry↗
PubMed1986

Studies on synthetic peptide substrates for F XII enzymes.

Screening of chromogenic peptide substrates have shown that FXIIa readily splits substrates of D-Pro-Phe-Arg-pNA (S-2302) and -Gly-Arg-pNA (e.g. S-2222) types. The latter type is preferred in a system where kallikrein is present. By using the substrate S-2222 a method for the determination of beta FXIIa inhibitors has been designed. Chromatography data show that C1-esterase inhibitor is the major inhibitor of beta FXIIa in plasma. Preliminary studies have also been performed on the assay of FXII in human plasma. The procedure to obtain a complete activation of FXII has still to be studied.

Dipeptides↗
PubMed1982

Studies of components of the coagulation systems in normal individuals and septic shock patients.

Components of the coagulation system were determined in plasma samples from normal individuals and septic shock patients. The parameters measured included Hageman factor (HF), prekallikrein (PKK), high molecular weight kininogen (HMwK), antithrombin III (AT III), fibrinogen (Fg) and fibrin(ogen) degradation products (FDP's). The combined effects of factors II, VII & X were estimated using Normotest (NT). Plasma levels of HF, PKK, and HMwK and both immunochemical levels and functional activities of AT III were significantly lower in the septic shock patients. NT values were also significantly reduced. Fibrinogen levels varied from very low to very high indicating both Fg consumption and acute-phase synthesis. Elevated FDP levels were seen during septic shock, but no difference between survivors and fatal cases was found. Prekallikrein levels and functional AT III activities were significantly higher in the samples from patients who recovered following septic shock than in the samples from subjects who died. During treatment all the parameters gradually returned toward normal in the survivors, whereas continuous low values for HF, AT III, PKK, and NT were observed in the fatal cases.

Antithrombin III↗
PubMed1980

Studies on components of the plasma kallikrein-kinin system in plasma samples from normal individuals and patients with septic shock.

Components of the plasma kallikrein-kinin system were determined in plasma samples from ten healthy subjects and eight patients with septic shock. Five of the patients died. Low levels of Hageman factor, prekallikrein, and high molecular weight kininogen, together with significantly reduced concentrations of alpha 2-macroglobulin, were observed during septic shock both in patients who died and in the survivors. The patients who died also revealed a pronounced reduction of functional kallikrein inhibition determined by a chromogenic peptide substrate assay. In the survivors, however, functional kallikrein inhibition was very well preserved during septic shock, being within the range of values found in normals. Also plasma prekallikrein and C1-esterase inhibitor levels were slightly higher in the survivors than in those who died. Our results confirm that the plasma kallikrein-kinin system becomes activated during septicemia and that consumption of components of this protease system occurs. Because both C1-esterase inhibitor concentrations and functional kallikrein inhibitory activities were higher in patients who survived septic shock than in the fatal cases, our results suggest that functional inhibition of plasma kallikrein appears to play a major role in the outcome of this condition.

Complement C1 Inactivator Proteins↗