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Biomedical subjects

S Sohen

Publications and source records attributed to S Sohen.

12 recordsLinked to original sources
PubMed2001

Interleukin-4 reversed the Interleukin-1-inhibited proteoglycan synthesis through the inhibition of NO release: a possible involvement of intracellular calcium ion.

Interleukin-1 (IL-1) causes cartilage degradation through nitric oxide (NO) synthesis. Although Interleukin-4 (IL-4) antagonizes the IL-1-mediated cartilage degradation, the precise mechanisms are not clear. We examined the effect of IL-4 on NO synthesis in parallel with intracellular Ca levels ([Ca(2+)]i) and proteoglycan (PG) synthesis. IL-4-inhibited IL-1-enhanced NO release in a dose-dependent manner. IL-1-enhanced [Ca(2+)]i in the chondrocytes, and IL-4 attenuated this increase. IL-4 reversed IL-1-inhibited PG synthesis. Accordingly, IL-4 reversed the IL-1-inhibited PG synthesis through the inhibition of NO release. An increase in [Ca(2+)]i with IL-1 is possibly involved in this action.

Journal Article↗
PubMed2001

[Periarticular and generalized osteoporosis in rheumatoid arthritis].

Patients with rheumatoid arthritis (RA) develop both periarticular and generalized osteoporosis. Periarticular osteopenia in appendicular bones occurs early in the course of RA and is one of the earliest radiological signs of RA. Periarticular osteoporosis might be mediated through an increased productions of inflammatory cytokines and prostaglandins by synovium and bone marrow. Generalized osteoporosis is also common in RA and leads to increased risk of fractures. Generalized osteoporosis considered to be multifactorial. Corticosteroids and menopausal state are important risk factors for lumbar osteoporosis. Rheumatoid activity and reduced physical activity are also important determinants.

English Abstract↗
PubMed1997

A role for histamine receptors in rheumatoid arthritis.

Although neurotransmitters and various chemical mediators play an important role in the pathogenesis of rheumatoid arthritis (RA), precise underlying mechanisms have yet to be determined. Histamine is a classical mediator of inflammation and three types of receptors are known. We investigated the presence and functions of histamine receptors of lymphocytes, bone marrow cells, synovial fibroblasts, and chondrocytes in experimentally-induced arthritis and human RA. The function of H2 receptors in peripheral blood lymphocytes and bone marrow cells were down regulated as measured by increments of intracellular cAMP and IL-6 production. Synovial fibroblasts from RA patients did not respond to H2 agonist to synthesize hyaluronic acid. It is evident that H2 receptors are down-regulated in lymphocytes, bone marrow cells, and synovial fibroblasts. The reduced function of H2 receptors in collagen-induced arthritis was normalized by transfer of the receptor-bearing lymphocytes and bone marrow cells. These data suggest that histamine is involved in the pathogenesis of RA.

Animals↗
PubMed1993

Acrodysostosis associated with spinal canal stenosis.

An adult case of acrodysostosis with striking lumbar spinal canal stenosis is reported. She complained of numbness on the right arm, intermittent claudication with numbness on both legs and pain and weakness on the left leg. Although the reduced lumbar interpedicular distance has been reported, no adult case with neurologic symptoms has been reported.

Adult↗
PubMed1993

Abnormalities in bone marrow mononuclear cells in patients with rheumatoid arthritis.

We analyzed the cell surface phenotype and the function of mononuclear cells in peripheral blood and in bone marrow of patients with rheumatoid arthritis (RA). The monoclonal antibodies anti-CD45RA, anti-CD29 and anti-S6F1 identify the suppressor-inducer (CD4+CD45RA+), helper-inducer (CD4+CD29+) and killer-effector (CD8+S6F1+) subpopulations of lymphocytes, respectively. In patients with RA, peripheral blood samples showed the same percentage of CD4+CD45RA+, CD4+CD29+ and CD8+S6F1+ cells as seen in control subjects. In contrast, in the bone marrow of patients with RA we observed a significant decrease in CD4+CD45RA+ cells, a significant increase in CD8+S6F1+ cells compared with findings in peripheral blood and in bone marrow samples from control subjects. Consistent with the phenotypic changes observed, bone marrow T cells also showed functional abnormalities, since autologous mixed lymphocyte reaction-activated CD4 cells from bone marrow of patients with RA showed a decrease in suppressor-inducer activity and CD8+ cells activated by allogenic E- cell showed an increase in killer-inducer activity. The changes noted above may contribute to the immunologic abnormalities that occur in this disease and provide insight into the pathophysiology of RA.

Aged↗
PubMed1993

Effective treatment of mice with type II collagen induced arthritis with lethal irradiation and bone marrow transplantation.

We examined the effects of irradiation followed by bone marrow transplantation (BMT) on type II collagen induced arthritis (CIA) in mice. Either before or after the onset of arthritis, the mice were irradiated at levels lethal to cells, then given bone marrow cells from normal syngeneic or allogeneic mice. The BMT, especially allogeneic BMT, blocked the induction of CIA when administered before the onset of arthritis. When administered after CIA had begun, progression of the arthritis was significantly suppressed by allogeneic BMT.

Animals↗
PubMed1992

[Histamine receptors in arthritis].

Histamine H1 and H2 receptors in lymphocytes, bone marrow mononuclear cells, synovial fibroblasts and chondrocytes were measured by binding assay and pharmacological study. Histamine suppressed IgG production through H1 and H2 receptors and cytotoxic activity through H2 receptor in lymphocyte. Histamine increased the production of hyaluronic acid in synovial fibroblast through H1 and H2 receptors. In the production of keratan sulfate in the chondrocyte, histamine increased through H1 receptor and decreased through H2 receptor. In arthritis, the functions of H2 receptor in the lymphocyte, bone marrow mononuclear cell and synovial fibroblast were decreased, and the function of H1 receptor in the chondrocyte was decreased. On the other hand, histamine content was reported to increase in synovial fluid with RA. Our data indicate histamine had suppressive effects on IgG production and cytotoxic activity, but the functions of histamine receptors, especially H2 receptor, were decreased in RA. The beneficial effects of histamine in RA synovial fluid might therefore be decreased by hypofunction of the H2 receptor. These data suggest that abnormalities in histamine receptors in arthritis could be involved in perpetuating the inflammatory process in RA.

Arthritis, Rheumatoid↗
PubMed1991

Phenotypic abnormalities in CD8+ T lymphocyte subsets in patients with rheumatoid arthritis.

We analyzed the cell surface phenotype of CD8+ cells in both peripheral blood and synovial fluid (SF) of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Utilizing the monoclonal antibodies anti-CD45RA, anti-CD29 and anti-S6F1-, one can define both suppressor effector (CD45RA+CD29-S6F1-) and killer effector (CD45RA-CD29+S6F1+) cells within the CD8 population. In patients with OA, normal proportions of CD8+CD45RA+, CD8+CD29+ and CD8+S6F1+ cells were found in both peripheral blood and SF. The peripheral blood of patients with RA, in contrast, showed a decreased percentage of CD8+CD45RA+ cells (13.4 +/- 2.6) (p less than 0.05), but a normal percentage of CD8+CD29+ and CD8+S6F1+ cells. In the SF of patients with RA, we observed a more dramatic decrease in CD8+CD45RA+ suppressor effector cells (6.4 +/- 5.0) (p less than 0.001), a significant increase in killer effector cells as measured by both CD8 + CD29+ (35.5 +/- 9.9) (p less than 0.001) and CD8 + S6F1+ cells (28.2 +/- 11.4) (p less than 0.01). These changes may contribute to the immunologic abnormalities previously noted in this disease and may provide some insight into the pathophysiologic mechanisms of RA.

Adult↗
PubMed1990

The functional heterogeneity of CD8+ cells defined by anti-CD45RA (2H4) and anti-CD29 (4B4) antibodies.

The monoclonal antibodies, anti-2H4(CD45RA), and anti-4B4(CD29), along with UCHL1-(CD45RO), identify reciprocal populations of CD4 cells with distinct suppressor inducer (CD45RA+CD29-CD45RO-) and helper inducer (CD45RA-CD29+CD45RO+) functions. Although the CD8+ population is known to contain precytotoxic, cytotoxic, suppressor, and some natural killer cells, the exact phenotypic identities of these functional CD8 subsets has not been established. In this study, we tried to determine whether these monoclonal antibodies could distinguish functionally distinct subsets of cells within the CD8+ population. For this purpose, whole T cells or fractionated T cells were sensitized with irradiated allogeneic non-T cells for 6 days, following which, CD8+ or CD8+CD11b- cells were isolated and cellular functions such as suppressor, killer precursor, and killer effector activity were assessed. The results showed that both class I-restricted alloantigen-specific killer effector and killer precursor cells belonged to the CD8+CD11b-CD45RA-CD29+ population. Moreover, these killer effector cells expressed the CTL-associated S6F1 molecule, an epitope of the LFA-1 antigen. In contrast, suppressor effector cells belonged to the CD8+CD11b-CD45RA+CD29- cell population. Although the UCHL1 antigen has been reported to define the CD4+CD29+ helper inducer cell, over 90% of allo-activated CD8+ cells expressed this antigen, whereas only 40-60% of these cells expressed either CD45RA or CD29 antigens. These results suggest that anti-CD45RA and anti-CD29 antibodies may provide useful tools for distinguishing between suppressor effector versus killer effector and killer precursor cells within the CD8+CD11b- population.

Antibodies, Monoclonal↗
PubMed1990

CD4+CD45RA+ and CD4+CD45RA- T cell subsets in man maintain distinct function and CD45RA expression persists on a subpopulation of CD45RA+ cells after activation with Con A.

We have previously shown that Con A-induced suppressor T cells belong to the CD45RA+ subset. After unseparated T cells are activated with Con A, CD45RA expression increases to a maximum (Day 2), and then decreases significantly, but does not disappear entirely (Day 9), while CD29 expression increases steadily. In the present study, we examined the fate of these cell surface molecules on isolated CD4+CD45RA+ and CD4+CD45RA- cells following activation with Con A, and their relationship to the regulatory functions of these subsets. After activation of CD4+CD45RA+ cells with Con A, CD45RO and CD29 antigen expression rapidly increases (greater than 90%). While CD45RA expression is downregulated, approximately 40% of the cells continue to express low-density CD45RA in a stable fashion through Day 21. Despite these phenotypic changes, cells originally CD45RA+ continue to suppress IgG synthesis and provide only minimal B cell help. Furthermore, when cells originally CD45RA+ were sorted on the basis of continued presence, or loss of CD45RA antigen 14 days after activation, both populations demonstrated potent suppression and minimal help. In contrast, after activation with Con A, CD4+CD45A- cells maintain stable phenotype and provide significant help and minimal suppression. Immunoprecipitation of the CD45RA antigen from Day 14 activated CD4+CD45RA+ cells confirms the continued presence of the 205-kDa isoform, but reveals a significant decrease in the 220-kDa isoform. These results suggest that after activation with Con A, cells originally CD45RA+ remain functionally distinct from cells originally CD45RA-, and that CD45RA antigen persists on a subpopulation of CD45RA+ cells after activation with Con A.

Antigens, CD↗