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A Aissaoui

Publications and source records attributed to A Aissaoui.

8 recordsLinked to original sources
PubMed2000

[Modulation of experimental myasthenia gravis by IVIg].

Myasthenia Gravis (MG) is an autoimmune disease mediated by antibodies directed against the acetylcholine receptor (AChR). Treatment by IVIg is effective in acute forms of myasthenia gravis. In order to determine the in vivo effects of the various fractions of human immunoglobulins, we used an experimental model of myasthenia gravis in SCID mice. To this end, thymic cells from MG patients are transferred to these mice according to a well defined protocol. When establishing of the model, we noticed the appearance of anti-AChR antibodies and the loss of AChR expression at the muscle level. After treatment with IVIgG or IVIgM, the mice displayed a lower anti-AChR antibody titer compared to control mice (albumin treated) and the loss of the AChR number at the muscle was significantly reduced. These results obtained from one MG patient indicate that the human immunoglobulin preparations induce significant effects on pathogenic parameters in the SCID mouse model. Therefore this model is interesting to approach the mechanisms of action of human immunoglobulins and deserves further investigation.

Acetylcholine↗
PubMed1999

Normal human immunoglobulin suppresses experimental myasthenia gravis in SCID mice.

Serum IgM has been shown to participate in the control of IgG autoreactivity in healthy subjects. We have recently shown that an immunoglobulin preparation of pooled normal human IgM (IVIgM) contains anti-idiotypic antibodies against disease-associated IgG autoantibodies in autoimmune patients and protects rats from experimental autoimmunity. The aim of the present study was to asses the in vitro and in vivo immunomodulatory effects of IVIgM in comparison with IgG, in SCID mice reconstituted with thymic cells from a myasthenia gravis patient. Non-leaky SCID mice were injected i.p. with 60 x 10(6) thymic cells from a patient with myasthenia gravis and 1 day later boosted with 10(6) irradiated acetylcholine receptor (AchR)-expressing TE671 cells. On days 14, 21 and 28, mice were treated with IVIgM or with equimolar amounts of human serum albumin. The level of anti-AchR antibodies in the sera of three out of four IgM-treated animals was less than 1 nM. Further, there was a significant decrease in the loss of endplate AchR on the diaphragms of IgM-treated SCID mice. These findings indicate that pooled normal IgM exerts an immunoregulatory role in experimental myasthenia gravis, and suggests that IgM may be considered as an alternative approach in the therapy of autommune diseases.

Animals↗
PubMed1999

Prevention of autoimmune attack by targeting specific T-cell receptors in a severe combined immunodeficiency mouse model of myasthenia gravis.

Myasthenia gravis (MG) is an autoimmune disease targeting the skeletal muscle acetylcholine receptor. We have previously demonstrated a selection bias of CD4+ T cells expressing the Vbeta5.1 T-cell receptor gene in the thymus of HLA-DR3 patients with MG. To evaluate the pathogenicity of these cells, severe combined immunodeficiency mice engrafted with MG thymic lymphocytes were treated with anti-Vbeta5.1 antibody. Signs of pathogenicity (eg, acetylcholine receptor loss and complement deposits at the muscle end plates of chimeric mice) were prevented in anti-Vbeta5.1-treated severe combined immunodeficiency chimeras. Pathogenicity was mediated by autoantibodies against acetylcholine receptor. Thymic cells depleted of Vbeta5.1-positive cells in vitro before cell transfer were nonpathogenic, indicating that Vbeta5.1-positive cells are involved in the production of pathogenic autoantibodies. Acetylcholine receptor loss was prevented by Vbeta5.1 targeting in HLA-DR3 patients only, demonstrating specificity for HLA-DR3-peptide complexes. The action of the anti-Vbeta5.1 antibody involved both the in vivo depletion of Vbeta5.1-expressing cells and an increase in the interferon-gamma/interleukin-4 ratio, pointing to an immune deviation-based mechanism. This demonstration that a selective and specific T-helper cell population is involved in controlling pathogenic autoantibodies in MG holds promise for the treatment of MG.

Adolescent↗
PubMed1994

Computing heart rate variability using spectral analysis techniques: HRVUAB, a ready-to-use program.

The application of spectral analysis techniques to study the nervous modulation of the vertebrate heart have given interesting results in clinical studies although nearly nothing is known in lower vertebrates. A program to compute this heart rate variability is described in detail and preliminary results are shown. Data is first statistically qualified and fragmented in smaller segments, each being further processed through linear trend removal and normalization before the application of the Fast Fourier Transform algorithm to estimate the interval spectrum. All consecutive periodograms are averaged and the interval spectrum plotted and saved.

Algorithms↗
PubMed1984

[Hodgkin's disease of the lung with cavitation and apparently primary. Apropos of a case].

The authors report a rare and diagnostically difficult clinical case of primary pulmonary Hodgkin's disease, with cavitation. They stress the diagnostic difficulties which they encountered: Indeed four stages are described in this case in which different diagnoses were considered as follows, a primary or secondary lung cancer, non-specific pulmonary suppuration, atypical hydated disease (as is frequently seen in Algeria) and finally pulmonary tuberculosis. The diagnosis of Hodgkin's disease was not considered until post-mortem. A review of the literature has called attention to the great rarity of cavitating Hodgkin's disease (only 53 cases in the world published). A clinical, radiological and anatomical study of the principal case published enhances the commentary on this rare case. In addition the pathogenesis of this granulomatous necrosis in Hodgkin's disease is discussed.

Hodgkin Disease↗
PubMedDate not supplied

Is the short-term modulation of heart rate in teleost fish physiologically significant? Assessment by spectral analysis techniques.

Heart rate is an important physiological variable in the control of cardiac output, even in fishes, where the importance of stroke volume has been overemphasized. Except for the myxinoids, the fish heart is innervated by cranial nerve X and the nature of this innervation is mainly inhibitory by parasympathetic fibers, although a sympathetic contribution has also been demonstrated. In mammals, cardiac innervation is not only responsible for the control of mean heart rate but it also modulates the beat-to-beat heart rate changes. These beat-to-beat changes are known as heart rate variability (HRV) and appear to be related to fluctuations in respiration and blood pressure. In this paper we demonstrate the link between cardiac innervation and HRV in several species of teleosts because HRV is greatly decreased after vagotomy or atropinization. In contrast, after abolishing the sympathetic influence with propranolol, only slight changes in total HRV are observed, indicating the restricted importance of the adrenergic innervation in determining phasic changes in HRV despite the significant tonic effect which has been demonstrated. Thus, it appears unlikely that the sympathetic influence will be present in any measured spectral component as suggested previously. Furthermore, clear spectral patterns do not always exist and this may be due to the erratic influence of respiration which is clearly faster than heart rate in all fish species studied. This differs from the slow ventilation frequency displayed by many mammalian species that exerts an influence on a beat-to-beat basis (respiratory sinus arrhythmia). Spectral patterns could also be affected by changing levels of circulating catecholamines, although this is still unproved.

Animals↗