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Biomedical subjects

J Bentin

Publications and source records attributed to J Bentin.

18 recordsLinked to original sources
PubMed2000

Costs induced by hip fractures: a prospective controlled study in Belgium. Belgian Hip Fracture Study Group.

The economic burden of hip fractures is thought to be important, but the excess medical costs they induce remain largely unknown. We assessed the direct medical costs induced by hip fractures during and after hospitalization. Hospital costs of 170 consecutive Belgian women with hip fracture were gathered. During the year following discharge, all medical costs were collected for the 159 hip fracture women who survived the acute hospitalization stay. A similar collection of data was performed on a comparison group of 159 age-and residence-matched women without a history of hip fracture. The mean cost of the acute hospital stay was 8,667 Belgian francs and the mean 1-year hip-fracture-related extra costs after hospitalization was 6,636 Belgian francs. During the year following the acute hospital stay, 19% of the hip fracture women and 4% of the comparison women were newly admitted to nursing homes (p<0.001). Although health care costs increased with age, hip-fracture-related extra costs after hospitalization seemed similar in those below or above 81 years old. These extra costs amounted to 7,710 Belgian francs in women not living in nursing homes at the time of fracture, and to 3,479 Belgian francs in women who lived in nursing homes. Health or mental status before hip fracture seemed not to affect extra costs. Taking into account the higher mortality of women with hip fracture, the extra costs during the acute hospital stay and during the 1-year follow-up amounted to a mean 15,151 Belgian francs. In conclusion, both acute hospital stays and subsequent medical care contribute significantly to medical costs induced by hip fractures.

Age Factors↗
PubMed1995

Mechanism of action of cyclosporin in rheumatoid arthritis.

Heterogenous population of cells, including macrophages, synoviocytes and lymphocytes play important roles in the immunopathogenesis of rheumatoid arthritis (RA). T cells, however, seem to be a common thread throughout the disease process. In inhibiting T lymphocytes, cyclosporin A presents a more selective form of therapy in RA. The immunosuppressive action of cyclosporin is primarily due to the inhibition of antigen/mitogen-induced secretion of lymphokines at the transcriptional level from T cell. The inhibition of Ca2(+)-dependent signaling pathways by cyclophilin-cyclosporin complexes in T cell appears to shut down lymphokine-gene transcription.

Arthritis, Rheumatoid↗
PubMed1993

[Treatment of rheumatoid arthritis: current and future].

Rheumatoid arthritis (RA) is a chronic articular inflammatory disease of unknown aetiology. The therapeutic approach can be achieved at different levels: 1) symptomatic treatment with nonsteroidal anti-inflammatory drugs which can relieve articular pain and stiffness, 2) second-line drugs (or DMARD, for Disease Modifying Anti-Rheumatic Drug) selected for their capacity to slow the rheumatoid process. During this last decade, sulfasalazine and methotrexate became an alternative choice to the "classical" slow-acting antirheumatic drugs such as gold, D-penicillamine or antimalarials. The extensive progress in basic immunology and especially in the immunopathology of RA has allowed the elaboration of a new approach to immunotherapy, aimed at molecular targets on cells from the "specific immunity" system or against mediators of the inflammatory process, such as the cytokines.

Anti-Inflammatory Agents↗
PubMed1992

Relationship between magnetic resonance imaging and histologic findings by bone biopsy in nontraumatic osteonecrosis of the femoral head.

To attest the validity of magnetic resonance imaging (MRI) to evaluate the pathophysiology in nontraumatic osteonecrosis (ON) of the femoral head, we attempted to correlate the different MRI patterns with the histology in cases of early stages. We used not only the T1 and T2 pulse sequences, but also the T1 sequence after gadolinium-DTPA to demonstrate the presence of vascularization. Studying 24 core biopsies from 16 hips (9 patients), we explored the MRI presentations that corresponded to the main histologic findings of the different trabecular bone and bone marrow conditions. Histologic findings including trabecular bone necrosis and bone marrow necrosis represented by amorphous eosinophilic debris presented a low T1 signal intensity without enhancement after intravenous gadolinium injection and a low T2 signal intensity. Trabecular bone necrosis associated with mummified fat cells presented a normal T1 and T2 signal intensity. Trabecular bone necrosis with fibrosis filling the intertrabecular spaces had a low T1 signal intensity that was enhanced by gadolinium and had an intermediate T2 signal intensity. Bands of fibrosis without trabecular bone as seen in fracture zones showed a low T1 signal intensity that was enhanced by gadolinium with a high T2 signal intensity. Thickened trabecular bone with fibrosis as found in creeping substitution areas had also a low T1 signal enhanced by gadolinium, but the T2 signal intensity was low. Farther from the necrotic area, despite normal trabecular bone, we found some patchy necrosis of the bone marrow without any modification of the normal T1 and T2 MRI patterns.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Polymorphonuclear neutrophils enhance anti-CD3-induced T cell activation: the role of polymorphonuclear FC-receptors.

We investigated the effect of polymorphonuclear neutrophils (PMN) on anti-CD3 mAb (OKT3 and anti-Leu4)-mediated T cell activation. In the absence of monocytes, purified E-rosette-positive cells (further referred to as "T cells") require either solid-phase bound anti-CD3 or the combination of both a high concentration of soluble anti-CD3 and exogenous recombinant interleukin 2 (rIL-2) to proliferate. PMN cannot sustain T cell proliferation with soluble anti-CD3, but they markedly boost proliferation in the presence of soluble anti-CD3 and rIL-2. When PMN were added to T cell cultures stimulated with anti-CD3, this resulted in IL-2 receptor (IL-2R) expression and CD3 modulation. The mechanism of enhancement of anti-CD3-induced IL-2-responsiveness by PMN was further analyzed. A cellular T cell-PMN interaction was found to play a critical role and this was mediated through PMN Fc receptors (FcR). PMN bear two types of low-affinity FcR (FcRII and FcRIII). FcRII is known to bind mIgG1 (e.g., anti-Leu4) and FcRIII binds mIgG2a (e.g., OKT3). FcR involvement was demonstrated by two observations. Anti-FcRII mAb IV.3 inhibited the PMN signal for T cell activation with anti-Leu4. PMN bearing the second variant of FcRII which is unable to bind mIgG1 failed to promote anti-Leu4/IL-2-mediated T cell proliferation. Thus, PMN potentiate T cell responsiveness to IL-2 in the presence of anti-CD3 mAb and this potentiation by PMN requires interaction of anti-CD3 with PMN-FcR.

Animals↗
PubMed1991

Study of magnetic resonance imaging in transient osteoporosis of the hip.

To better define the magnetic resonance imaging (MRI) features during transient osteoporosis of the hip, we carried out sequential MRI of 8 patients with transient osteoporosis of the hip showing the typical radiographic pattern of diffuse osteoporosis of the femoral head. These cases displayed the same MRI changes in the femoral head and neck characterized by low signal intensity on the T1 weighted images and high signal intensity on the T2 weighted images. The MRI signal became normal within 11 months, but surprisingly, migration of the MRI abnormalities was observed during the course of the disease in 5 cases: abnormal MRI signals were first observed in the anterior area, then migrated to the posterior part, while a normal MRI signal reappeared in the anterior part. We conclude that MRI seems to show some particular features in transient osteoporosis of the hip, which normalize after a few months of evolution; this could represent a migration of MRI abnormalities. Such findings could help in the differential diagnosis of hip diseases such as aseptic bone necrosis.

Adult↗
PubMed1990

Chronic acquired immunodeficiency syndrome-associated arthritis: a synovial ultrastructural study.

We describe a patient who developed acquired immunodeficiency syndrome-related complex, complicated by chronic, symmetric polyarthritis. Synovial biopsy showed large areas of plasma cell infiltration subjacent to the synovial lining. Ultrastructural study demonstrated tubuloreticular structures within endothelial cells, crystal-like inclusions in plasma cells, and virus-like particles located around synoviocyte fragments. Although immunologic and morphologic studies did not permit classification of these virus-like structures, the role of these possible virions in the pathogenesis of the observed synovitis remains to be determined. Surprisingly, the patient's chronic arthritis resolved with anti-retroviral treatment (azidothymidine: AZT).

AIDS-Related Complex↗
PubMed1989

Impairment in T-lymphocyte responses during early infection with the human immunodeficiency virus.

Uncertainty has existed as to whether a T-cell deficiency exists in human immunodeficiency virus (HIV) infection different from that inherent in the reduced T-cell numbers characteristic of the disease. Heretofore, methods for measuring T-cell responses in patients have been carried out with systems requiring monocytes as accessory cells. In the presence of high concentrations of interleukin-2, however, highly purified T cells respond in a monocyte-independent fashion to antibody reactive with the CD3 component of the antigen receptor complex Ti/CD3. Highly purified T cells of HIV-infected patients responded subnormally in this anti-CD3/IL-2 system, even in the case of patients who were asymptomatic or had only lymphadenopathy. The defective T-cell responses occurred over a wide range of concentrations of the anti-CD3. Neither poor IL-2 receptor function as reflected by responses to limiting dilutions of IL-2 nor IL-1 receptor function as defined by incremental proliferation when IL-1 is added accounted for this defect, which also correlated poorly with T4 and T8 numbers. These results suggested that the T-cell abnormality was closely related to Ti/CD3 function, was not specifically or restrictively associated with T4 cells, and was not due to defective IL-2- or IL-1-receptor functions. The amount of HIV RNA in 10(5) T lymphocytes from the patients amounted to less than that found in one cell of a standard HIV infected laboratory cell line (CEM), using slot-blot hybridization. Thus the T-cell deficiency we have observed was not likely to be due directly to cell killing by HIV resident in the T4 cells. Other factors may be important in inducing the immunodeficiency, some of which are discussed.

AIDS-Related Complex↗
PubMed1988

T cell proliferation induced by anti-CD3 antibodies: requirement for a T-T cell interaction.

In the presence of interleukin 2 (IL2), soluble anti-CD3 monoclonal antibodies can stimulate highly purified normal T lymphocytes to proliferate. In these experiments HLADR+ T cells constituted 13 to 20% of the total cell population, and other HLADR+ cells, such as monocytes and B lymphocytes, constituted less than 1% of the population. When the HLADR+ T cells were removed from the total T cell population by cytofluorometric sorting, the residual HLADR- T cells failed to respond to soluble anti-CD3 plus IL2. When the separated HLADR+ T cells were recombined with the HLADR- T cells, a response was again found. This response was dependent on the dose of HLADR+ T cells added in the mixture. Irradiation individually of the HLADR+ and DR- T cells revealed that the proliferation in the cell mixture was predominantly, if not exclusively, by the HLADR- T cells. The ability of the HLADR+ T cells to provide a signal necessary to this proliferation was radioresistant. These data indicate that under the conditions of these experiments HLADR+ ("activated") T cells provide a signal necessary to the responsiveness of previously resting T cells.

Antibodies, Monoclonal↗
PubMed1987

Structural and functional characteristics of the CD3 (T3) molecular complex on human thymocytes.

The CD3 (T3) molecular complex is noncovalently associated with the antigen receptor molecule on T cells. The mitogenic properties of anti-CD3 antibodies have suggested that this complex may be the transducer of the antigenic signal to the intracellular environment. In the present investigation, we studied some of the structural and functional characteristics of the CD3 complex on human thymocytes. In 11 specimens tested, we found that anti-CD3 antibodies react with 50 to 76% of the thymocytes. Two-color immunofluorescence analysis revealed that the majority (greater than 50%) of thymocytes express both CD3 and CD1 on their surfaces. The latter is a marker of immature thymocytes. However, a distinct subpopulation comprising 13 to 19% of the total cells displays only CD3, while an approximately equal percentage of cells expresses only CD1. The mitogenic potential of anti-CD3 antibodies on peripheral T cells is dependent on the presence of monocytes. Anti-CD3 antibodies by themselves cannot activate thymocytes, indicating that functionally active monocytes are absent from the thymocyte population. Even the addition of peripheral monocytes does not allow a response of thymocytes to anti-CD3 antibodies. However, when the anti-CD3 antibody 64.1 is added in the presence of exogenous rIL 2, a strong antibody and lymphokine dose-dependent response ensues. Only CD1- CD3+ thymocytes are stimulated by the addition of antibody and IL 2. The mere expression of CD3 on the CD1+ CD3+ subpopulation of thymocytes apparently is not sufficient to render the cells responsive to the signals of anti-CD3 and IL 2.

Antibodies, Monoclonal↗
PubMed1985

Activation of resting T lymphocytes by anti-CD3 (T3) antibodies in the absence of monocytes.

The antigen receptor molecules on human T lymphocytes are noncovalently associated on the cell surface with the CD3 (T3) molecular complex. Perturbation of this complex with anti-CD3 monoclonal antibodies induces T cell activation. Previous studies have demonstrated that this process requires the participation of monocytes. In the present report, we demonstrate that purified, resting (G0 phase) T cells incubated with monoclonal anti-CD3 antibodies proliferate in response to purified interleukin 2 (IL 2), in a lymphokine dose-dependent fashion. Anti-CD3 antibody or IL 2 alone did not trigger cell division. The effect was specific for anti-CD3 antibodies because monoclonal antibodies reactive with other surface molecules (OKT4, OKT8, L368) were inactive. Furthermore, the same phenomenon was observed when anti-CD3 antibody Leu-4 (IgG1) was incubated with cells of individuals whose monocytes cannot process antibodies of the IgG1 subclass (Leu-4 nonresponders). In addition, both F(ab')2 and Fab fragments of anti-CD3 antibody OKT3 were also capable of rendering T cells receptive to the IL 2 growth signal. These data indicate that neither monocytes nor CD3 receptor cross-linking are required absolutely for resting T cell activation, provided that IL 2 is supplied exogenously. T lymphocytes treated with anti-CD3 antibodies proliferated in response to both purified mitogen-induced and recombinant IL 2. Antibodies to the IL 2 receptor (anti-Tac) inhibited the proliferation. Thus, the most likely mechanism for anti-CD3 antibody-mediated triggering is induction of IL 2 receptors.

Antibodies, Monoclonal↗
PubMed1983

Heterogeneity of immunoregulatory T cells in human thyroid autoimmunity: influence of thyroid status.

Monoclonal antibodies of the OKT series were used to identify circulating T lymphocytes (OKT3+), their helper-inducer (OKT4+) and suppressor-cytotoxic (OKT8+) subsets and cells bearing Ia antigen (OKIa+) in 75 patients with thyroid autoimmune disorders, including 14 Graves' disease, 21 myxoedema, 20 asymptomatic thyroiditis, 12 Hashimoto's thyroiditis and eight simple goitre with superimposed thyroiditis. In the whole population of patients, a negative correlation was observed between the percentage of OKT8+ cells and serum free thyroxine levels whatever the type of thyroiditis. The percentage of OKT8+ cells was decreased in Graves' disease and increased in myxoedema while it reversed after adequate treatment of the two diseases. However, a trend to a decrease in the proportion of OKT8+ cells was still observed in treated Graves' disease and in all the other groups of thyroiditis with euthyroidism. The minor modifications observed for OKT3+ and OKT4+ cells were in relation with those of OKT8+ cells. There was an increased percentage of Ia+ cells in Graves' disease and in Hashimoto's thyroiditis partly reflecting the presence of activated lymphocytes. In conclusion, these data suggest first of all a direct influence of serum T4 on the distribution of circulating OKT8+ cells in addition to documenting the heterogeneity of T cell immunoregulatory factors.

Adolescent↗