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M Seddik

Publications and source records attributed to M Seddik.

16 recordsLinked to original sources
PubMed2006

Successful induction of tolerance to infliximab in patients with Crohn's disease and prior severe infusion reactions.

AIM: To appraise the tolerance and efficacy of an induction of tolerance protocol to infliximab permitting the re-administration of the drug to patients with Crohn's disease having had infusion reactions requiring suspension of treatment. METHODS: Fourteen patients were included in the induction of tolerance protocol. Each infusion of infliximab (5 mg/kg) was divided into 11 escalating 15 min increments over a 3-h time period. The induction of tolerance procedure was repeated for subsequent infusions. RESULTS: Ten patients (71.4%) received all the three infusions for the induction treatment. Nine (64.3%) had a significant response and six (48.8%) still benefited from infliximab infusions. Seven patients (50%) achieved a complete remission, after a mean of 2.5 (two to three) infusions. Four patients (28.6%) had no response and the protocol was stopped. Three patients (21.4%) experienced mild immediate hypersensitivity reactions, which were controlled, two patients (14.2%) experienced severe immediate hypersensitivity reactions, leading to interruption of the treatment and one patient developed a delayed hypersensitivity reaction. CONCLUSION: Our induction of tolerance protocol allows some patients who have experienced severe or repetitive infusion reactions to infliximab to be safely retreated with the drug in a hospitalized setting, with a clinical response achieved in a majority of these patients.

Adult↗
PubMed1995

Corrosion evaluation of recasting non-precious dental alloys.

The effect of recasting, up to four times, non precious Ni-Cr and Co-Cr commercial dental alloys on their corrosion behaviour in saliva and saline media was carried out. A potentiokinetic technique was utilised to analyse the electrochemical characteristics of the anodic polarisation curves of these alloys. A considerable anodic polarisation range (about 2.0 V vs SCE) was used to investigate the possibility of developing a passive regime at such high potential range. The most important feature noted was a rapid rise in current density above a certain critical potential called pitting potential, Ep. The experimental data show that the open circuit potential, Eoc does not enable differentiation between the corrosion resistance of the four alloys used in this study. However, Ep and the rupture potential Er does distinguish between them. Increasing the number of the successive recastings of Wirolloy leads to enhancing the pitting potential, thus, the corrosion resistance of Wirolloy (Ni-Cr) improves after remelting and recasting. It has been found that Wirolloy corrodes 26 times faster than Wironit alloy under the same solution. The alloys containing cobalt and molybdenum show higher corrosion resistance than those containing nickel. Additionally, their corrosion resistance was not affected by successive melting and recasting. In chloride solutions Ni-Cr alloys show a high susceptibility to pitting corrosion, while Co-Cr alloys show a noble behaviour. The corrosion resistance of the four non precious alloys were in the following order: Biocast > Wironit > Cobond > Wirolloy.

Chromium Alloys↗
PubMed1986

The graft-versus-host reaction and immune function. III. Functional pre-T cells in the bone marrow of graft-versus-host-reactive mice displaying T cell immunodeficiency.

Studies were performed to determine whether pre-T cells develop normally in the bone marrow of mice displaying thymic dysplasia and T cell immunodeficiency as a consequence of a graft-versus-host (GVH) reaction. GVH reactions were induced in CBAxAF1 mice by the injection of A strain lymphoid cells. To test for the presence of pre-T cells in GVH-reactive mice, bone marrow from GVH-reactive mice (GVHBM) was injected into irradiated syngeneic F1 mice and 30-40 days later thymic morphology and function were studied. Morphology studies showed nearly normal thymic architectural restoration; moreover, such glands contained normal numbers of Thy-1-positive cells. Functional pre-T cells were evaluated by transferring thymocytes from the irradiated GVHBM-reconstituted mice into T-cell-deprived mice. These thymocytes reconstituted allograft reactivity, T helper cell function and Con A and PHA mitogen responses of T-cell-deprived mice. These results suggest that the pre-T cell population in the bone marrow is not affected by the GVH reaction. Therefore, the T cell immunodeficiency associated with the GVH reaction is not due to a deficiency of pre-T cells in the bone marrow but is more likely associated with GVH-induced thymic dysplasia.

Animals↗
PubMed1986

The graft-versus-host reaction and immune function. IV. B cell functional defect associated with a depletion of splenic colony-forming units in marrow of graft-versus-host-reactive mice.

Studies were conducted to determine whether a functional B cell defect occurred in the bone marrow of mice experiencing a GVH reaction (GVHBM). GVH reactions were induced in AxCBA F1 adult mice by an injection of A strain lymphoid cells. The GVH reaction was confirmed by immunosuppression and thymus histology. At various intervals after GVH induction, GVHBM was tested for its ability to restore B cell function in adult thymectomized irradiated mice reconstituted with normal thymocytes. GVHBM cells obtained seven days after GVH induction restored but slightly the plaque forming cell (PFC) response to sheep erythrocytes and the mitogen response to lipopolysaccharide (LPS). GVHBM cells obtained 10 days or later failed to reconstitute the PFC or LPS responses. GVHBM cells suppressed neither the T or B cell function of normal spleen cells nor the LPS mitogen response of normal bone marrow cells. In addition, the splenic colony-forming units (CFU-s) in GVHBM were slightly decreased by day 10 after GVH induction and markedly depressed by day 22 after GVH induction. These results suggest that the GVH reaction may affect two different events in B cell differentiation. The early decrease in functional B cells that occurs before there is any change in the CFU-s population suggests a direct effect on B cell production, whereas the later absence of functional B cells could be due to the marked decline in stem cell production (CFU-s).

Animals↗
PubMed1985

The functional and histological basis for graft-versus-host-induced immunosuppression.

The GvH reaction resulting from the injection of parental strain cells into adult F1 hybrids suppresses both cell-mediated and humoral immune responses and is dependent on the donor-host combination and the number of parental cells used to induce the GvH reaction. The early suppression is due, at least in part, to the increased number of macrophages and the activation of suppressor macrophages which act directly on the T-helper cell and perhaps the B-cell as well. The macrophage suppression is associated with an increase in PGE production. The long-term T-cell immunodeficiency is mediated by GvH-induced thymic dysplasia resulting in a block or an arrest in T-cell differentiation and deficient IL-2 production. The B-cell immunodeficiency is associated with both a decrease in B-cell production from lymphoid progenitors and a decrease in CFU-s production. The GvH reaction induces 2 types of thymic lesion, a stress-related effect causing atrophy of the thymic cortex and a cytolytic process causing severe-to-moderate lesions in the thymic medulla as a consequence of injury to medullary epithelial cells and a loss of Hassall's corpuscles (thymic dysplasia). By employing the NK-cell-deficient beige mutation, it was shown that the severe-to-moderate thymic medullary lesions occurred in F1 mice only in those transplant situations in which the donor inoculum was of the +/bg genotype, regardless of the genotype of the recipient. It is proposed that activation of parental T cells may contribute to the early immunosuppressive events; however, the relatively permanent immunosuppression appears to be associated with NK-like effector cells which are capable of causing injury to lymphoid and epithelial tissue, especially epithelium of the thymic medulla. These studies raise the possibility that the GvH reaction may contribute to some T- and B-cell immunodeficiencies observed in the SCID and AIDS syndromes, as well as in patients following bone marrow transplantation.

Animals↗
PubMed1984

The graft-versus-host reaction and immune function. I. T helper cell immunodeficiency associated with graft-versus-host-induced thymic epithelial cell damage.

The injection of parental A strain lymphoid cells into adrenalectomized CBAxA F1 (BAF1) mice induced a chronic graft-versus-host (GVH) reaction resulting in T cell and B cell immunosuppression as well as thymic epithelial cell injury, but not stress-related thymic involution. Thymocytes from BAF1 mice undergoing a GVH reaction were studied for their ability to reconstitute T helper cell (TH) function and phytohemagglutinin (PHA) and concanavalin A (Con A) mitogen responses in thymectomized, irradiated, BAF1 mice reconstituted with normal syngeneic bone marrow (ATxBM). Thymocytes from BAF1 mice early after the induction of a GVH reaction (days 10-12) were as effective as normal thymocytes in reconstituting TH and mitogen responses. Thymocytes from BAF1 mice 40 or more days after the induction of a GVH reaction did not reconstitute either the TH function or PHA and Con A responses in ATxBM mice. The inability to reconstitute ATxBM mice was not due to the presence of suppressor cells contained in the thymocyte inoculum. It is proposed that GVH-induced thymic epithelial cell injury blocks or arrests normal T cell differentiation, resulting in a population of thymocytes that lack the potential to become competent T helper cells or mitogen-responsive cells when transferred into ATxBM mice. This thymic functional defect results in a permanent TH immunodeficiency in mice experiencing a chronic GVH reaction.

Adrenalectomy↗
PubMed1984

The graft-versus-host reaction and immune function. II. Recruitment of pre-T-cells in vivo by graft-versus-host-induced dysplastic thymuses following irradiation and bone marrow treatment.

The graft-versus-host (GVH) reaction induces thymic dysplasia and an arrest in T cell differentiation. Studies were performed to test the effect of irradiation and reconstitution with bone marrow on GVH-induced thymic dysplasia and T cell differentiation. GVH reactions were induced in CBAxAF1 adult mice by the injection of A strain lymphoid cells. All GVH-reactive mice were immunosuppressed by day 7 after GVH induction and thymic dysplasia was evident by day 24. Forty days after the induction of the GVH reaction the mice were irradiated (850 rads) and repopulated with 10-15 X 10(6) syngeneic or parental bone marrow cells. Thirty days after irradiation and bone marrow reconstitution, GVH-reactive mice were used for histological and functional studies. These mice displayed near-normal thymus morphology with scattered epithelial cells in the medulla, and normal numbers of Thy-1-positive cells. Donor cells had totally repopulated thymuses of irradiated bone marrow reconstituted mice by day 19 after irradiation. T helper cell function did not recover in the reconstituted mice. These results suggest that (1) the process responsible for GVH-induced thymic dysplasia is radiosensitive, and (2) the thymus has the potential to regenerate a normal structure, but fails to regain normal function.

Animals↗
PubMed1980

T cell functional defect associated with thymid epithelial cell injury induced by a graft-versus-host reaction.

The injection of parental strain cells into adrenalectomized (CBA x A)F1 mice induced a graft-versus-host (GVH) reaction which was morphologically characterized by thymus epithelial cell injury but not stress-related thymic involution. Thymocytes from mice undergoing a GVH reaction were studied for their ability to reconstitute allograft reactivity in thymectomized, irradiated, bone marrow reconstituted (ATxBM) (CBA x A)F1 mice. Thymocytes of mice experiencing a GVH reaction were theta-positive during the course of the reaction, however, by 40 days after GVH induction these thymocytes were unable to reconstitute allograft reactivity to H-2-incompatible skin grafts. It is proposed that GVH-induced thymic epithelial cell injury prevents or arrests normal T cell differentiation, resulting in a population of thymocytes which lack complete functional capability.

Animals↗