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Biomedical subjects

A M Freyria

Publications and source records attributed to A M Freyria.

30 records · Page 2Linked to original sources
PubMed1982

Contrast agents used for excretory urography impair platelet function in human patients.

The platelet function was investigated in 65 patients submitted to diagnostic excretion urography (injection of 60 ml contrast medium). Blood sampling was performed before (T0) 90 seconds after (T1) and 30 minutes after (T2) injection of the radiocontrast molecule (RCM). Five RCM of different osmolality ionicity and nature of the lateral chain have been tested. Platelet aggregation, platelet release of ATP, osmolality, total calcemia and ionized calcium level were determined on each plasma sample as well as RCM concentration at T1 and T2. Decrease (20 - 40%) of platelet aggregation occurred at T1, whichever platelet aggregating agent (ADP, collagen, Ristocetin or thrombin) were used (significant after Iopamidol 300 and Na Meg Ioxaglate). Platelet release of ATP induced by collagen was also decreased or delayed. These changes were rapidly reversible and a tendency to improvement was observed at T2. Among the five RCM tested, one (Na Diatrizoate) might be a proaggregating agent. No changes of osmolality occurred in the plasma and no correlation could be established between RCM concentration and platelet inhibition. A pathogenic hypothesis is suggested by the significant fall of total and ionized calcium level after RCM injection.

Adenosine Triphosphate↗
PubMed1981

Fractions of middle molecular weight responsible for immunodeficiency in malnourished and burnt patients.

Patients with protein calorie malnutrition (PCM) or burn injury have a high incidence of infection, partly related to a secondary deficiency of cell-mediated immunity. We have studied sera from 37 patients with PCM, 19 burns patients, and 8 uremic patients, and results were compared with those obtained in 12 healthy individuals. Chromatography on Sephadex G-25 fine revealed a high peak of so-called Middle Molecules. This fraction appeared to be almost superimposable on that separated from sera and urines of uremic patients, but even more concentrated especially in burns patients and in the severely hypoproteinemic patients with kwashiorkor. The proliferative responses of normal lymphocytes were inhibited by the patients' sera. A significantly more potent inhibition was obtained with middle molecular weight fractions from sera of these patients. Percentages of mixed lymphocyte reaction (MLR) inhibition were 69.38 +/- 21.69 (eluates from PCM patients), 67.05 +/- 21.75 (eluates from burnt patients), 66.37 +/- 31.38 (eluates from uremic patients), and 26.00 +/- 18.90 (eluates from control sera). Indirect evidence suggests that these inhibitory fractions may be responsible for several of the immunologic and hematologic disturbances found in PCM and in burnt patients.

Adult↗
PubMed1981

Effect of middle molecules on immunological functions.

The cell-mediated immunodeficiency secondary to renal failure is well established and is largely dependent on toxic or inhibitory serum factors. Our approach was to investigate the effect of so-called middle molecules (MM) on in vitro and in vivo immunological functions. A crude fraction of MM isolated from the serum or urines of uremic patients by chromatography on Sephadex G-25 fine was shown to markedly inhibit the lymphocyte proliferation induced in vitro by various phytomitogens or by allogeneic cells. A marked depression of the graft-versus-host reaction was demonstrated in vivo. When rats were continuously infused with MM, a significant delay of skin allograft rejection was obtained. From these results it is clear that the MM fraction contains a potent inhibitor of several T lymphocyte functions.

Animals↗
PubMed1980

[Specific measurement of alternate pathway activation of complement in human glomerulonephritides (GN): 125 cases (author's transl)].

C3 cleaving activity through alternate pathway, appreciated by native C3 antigen reduction in the presence of Mg EGTA, has been measured in sera of 40 controls and of 125 GN patients. The normal percentage of native C3 conversion ranged from 0 to 29 in controls (p less than 0.05). The number of positive samples is 0/30 in lupus GN (0%), 13/29 in acute GN (45%) and 26/66 in membranoproliferative GN (39%) with 7/8 in dense deposits subtype. The presence of alternate pathway activators of complement correlated with serum C3 level: their frequency is respectively 0, 0.32, and 0.48 if serum C3 is normal, low, and very low. Such activity correlated also well with alternate pathway C3 activation (low C3 and normal C4): the frequency of positive samples is respectively 0, 0.07, and 0.51 in the presence of No C3 activation, classical pathway activation (low C3 and low C4), and alternate pathway activation. The nature of such serum activators could be nephritic factor, bacterial polysaccharides, polymeric IgA, activated properdin, peculiar immune complexes, or other factors. Such measurement is an improvement immunopathological step in the investigation of human GN.

Complement Activation↗
PubMed1977

[Anticomplementary activity of a polyanion: polyanion: pentosan-poly-sulfoester. I. "In vitro" study and "in vivo" trial in human glomerulonephritis (author's transl)].

The drug, pentosan-poly-sulfoester (PPS), has an anticomplementary activity (ACA) on human serum both in vitro and in vivo, as judged by a reduction in total hemolytic complement activity (CH 50). In vitro, this ACA is very potent, immediate and temperature independent. In vivo this ACA obtained with a IV dose of 100 mg per 8 hours eg 300 mg/24 h, increases with the duration of treatment (mean time:30 days), suggesting a cumulative effect. Eleven patients with glomerulonephritis (GN) received such a treatment (8 with acute post-streptococcal GN and 3 with mesangio-proliferative GN). In patients with already marked hypocomplementemia, the ACA is difficult to establish, while in patients with normal complement activity or moderate hypocomplementemia, the decrease of CH 50 level in serum is obvious. There was no significant change inthe serum level of C3, C4, properdin factor B as measured by radial immunodiffusion technique. The clinical course of these GN was apparently not affected by this treatment. Neverthless, the in vivo ACA of PPS is firmly established and we can speculate that this functional depletion in complement may prevent or decrease the liberation of humoral mediators of inflammation.

Complement C3↗
PubMed1977

[Anticomplementary activity of a polyanion: pentosan-poly-sulfoester, II.--Mode of action and "in vitro " inhibition of human complement hemolytic activity (author's transl)].

The drug, pentosan-poly-sulfoester (PPS), is a potent in vitro inhibitor of the human complement hemolytic activity. This CH 50 inhibition represents a real anticomplementary activity (ACA), because this drug has no effect on sensitized sheep red blood cells (EA). The inhibition curve of human serum CH 50, by PPS is sigmoidal. The 50% inhibition is obtained for a 1: 650 dilution of PPS, which corresponds to a concentration of 0.08 mg/ml in normal human serum. Hemolytic titrations of C1, C4, C2, C3, and C5 showed a complete inhibition of C4, C2 and C3, and a partial inhibition of C1 (C1q, C1r, C1s, Ca++) and C5, by this drug. The mechanism of such functional inactivation of the different complement components is not yet elucidated.

Complement C2↗
PubMed1977

[Anticomplement activity of a polyanion: pentosan sulfuric polyester. III. Mechanism of functional inactivation of the different properdin and complement system fractions].

In vitro, the drug pentosan-poly-sulfoester (PPS) changes the electrophoretic migration of different proteins from the complement and properdin systems, such as native C3 (beta 1C globulin), C3c (beta-1A globulin), C3d (alpha-2D globulin), C1s inactivator (ClsINA), Clq and properdin factor B (B). Their more anodal migration is the consequence of a molecular alteration and persists after prolonged dialysis. These structural changes, yet undefined, explain the loss of functional activity of these proteins, and the anticomplementary activity of this drug. Moreover, PPS is able to block the alternate pathway activation by its action on properdin factor B (C3 proactivator). In fact, in presence of PPS, the activators of the properdin systems such as C3 nephritic factor are inactive. These altered mobilities are also responsible for the overestimation in the antigenic concentration of B (+ 45%), C4 (+27%) and C3/C3c (+ 14%), found in human serum containing 50 mg/ml of PPS. PPS has an original action upon the complement and properdin systems, which allows its clinical use as a potent inhibitor of the humoral mediators of inflammation.

Binding Sites↗
PubMedDate not supplied

Increased expression of tissue factor mRNA and procoagulant activity in ovine lentivirus-infected alveolar macrophages.

To link ovine lentivirus infection to lung tissue damage, we studied the procoagulant response in alveolar macrophages from experimentally infected lambs and in in vitro infected alveolar macrophages. We cloned ovine tissue factor cDNA and analysed its in vitro expression by Northern blotting. Visna-maedi virus induced tissue factor mRNA. In order to correlate this mRNA induction with its cellular function, we analysed macrophage procoagulant activity after in vitro and in vivo infection. The procoagulant activity was increased by interaction with the virus in both cases. Thus, visna-maedi virus-induced expression of tissue factor mRNA was associated with enhanced macrophage procoagulant activity. These findings indicate an active role of alveolar macrophages in the pathogenesis of these inflammatory lung lesions.

Animals↗