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Biomedical subjects

L Mayer

Publications and source records attributed to L Mayer.

At least 163 records · Page 9Linked to original sources
PubMed1985

The use of Ender nails in fractures of the tibial shaft.

Between November 1979 and January 1983, we treated fifty-one severe fractures of the tibial shaft with multiple intramedullary Ender nails. Thirty-six fractures were treated within two weeks after injury. Forty-one fractures united in less than four months and eight, in four to eight months. Only two were not united after eight months. An anatomical reduction was maintained in all but three of the fractures, in which the tibia shortened. Two tibiae united with an angulation of 7 degrees and one with 6 degrees, as measured in two planes. There were two infections, both after an open fracture. It has been our experience that Ender nails provide excellent rotational stability, allow early full weight-bearing, and markedly decrease the duration of need for immobilization. Ender nailing was of value both for the acute management of complicated high-energy fractures of the tibial shaft with extensive soft-tissue damage and as a salvage procedure to maintain reduction of a fracture when other techniques had failed.

Adolescent↗
PubMed1984

Immunoregulatory lymphokines of T hybridomas from AIDS patients: constitutive and inducible suppressor factors.

Supernatants derived from peripheral blood mononuclear cell cultures of certain patients with the acquired immunodeficiency syndrome (AIDS) or its prodromes have the capacity to block T cell-dependent immune reactivity in vitro. T cells derived from a patient positive for antibody to the lymphadenopathy associated virus ( LAV ), and elaborating high titers of these soluble suppressor factors, were fused to a mutagenized clone of the human T lymphoblastoid cell line KE37 . Molecules capable of profoundly depressing T cell-dependent polyclonal antibody production and DNA synthetic responses, either directly or after incubation with normal adherent cells, were isolated from stable hybrid clones.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Regulation of B cell activation and differentiation with factors generated by human T cell hybridomas.

Human T cell hybridomas were generated by several techniques and the supernatants generated were screened for activity on human B cells. Three general activities were noted; B cell proliferation factor ( BCPF ), B cell differentiation factor (BCDF), and an IgA isotype-specific helper factor. BCPF acts on B cells to induce proliferation without differentiation and is distinct from conventional BCGF. This was documented by BCPF 's inability to synergize with anti-mu Ab in a standard BCGF assay ( Muraguchi & Fauci 1982, Howard et al. 1982, Sieckman et al. 1981), as well as its differential effect on a leukemic B cell preparation, when compared with BCGF. A possible schema for BCPF activity is depicted in Figures 3 and 4. In Figure 3, BCPF acts like Ag in vivo or like anti-mu in vitro, pre-activating B cells and rendering them responsive to BCGF. Figure 4 represents what our data depict, that is that BCPF bypasses the response to BCGF and induces cells to proliferate without pre-activation. The difference in the 2 mechanisms may be concentration-dependent and this possibility is currently being evaluated. It is interesting to speculate that T cells in vivo are capable of initiating B cell activation and may account for polyclonal responses seen with some Ag-specific reactions. BCDF(s) act on post-activated B cells (Figure 3) to induce differentiation to Ig-secreting cells. They appear to be heterogeneous and, therefore are capable of inducing varied responses depending on the B cell subpopulation affected. Figure 3 is deliberately complex demonstrating some of the possible as well as documented BCDF activities including polyclonal differentiation and isotype specific activity in IgA committed B cells. We cannot be certain of the frequency of these BCDF-secreting T cells, but the studies of cells from patients with common variable immunodeficiency and chronic lymphocytic leukemia have helped to dissect out these activities. These data would suggest that these BCDF subgroups are important, as deficiencies in one or more subgroups may result in disease.

Antibodies, Anti-Idiotypic↗
PubMed1984

Polyclonal immunoglobulin secretion in patients with common variable immunodeficiency using monoclonal B cell differentiation factors.

B cells from 25 patients with common variable immunodeficiency (CVI) were tested for their ability to differentiate under the influence of B cell differentiation factors (BCDF), derived from T cell hybridomas or T cell clones. 11 patients generated Ig plaque-forming cells in the range comparable to that of normal controls with supernatant from the T cell hybrid MOP 1L. With various hybrid or clone supernatants, differing response patterns emerged. Four patients who failed to respond to MOP 1L responded to T cell clone supernatant RAC. Another who failed to respond to both MOP 1L and RAC responded to T cell hybrid supernatant MTP 7. These results indicate that these supernatants contain different BCDFs and suggest heterogeneity in the differentiation states of B cells in CVI. In addition, three patients demonstrated exaggerated responses to BCDF, and evidence was obtained from B cells of these patients for increased BCDF receptor density. Thus, the accumulated evidence indicates that T cell defects may be a primary pathogenetic mechanism in common variable immunodeficiency, and purified BCDF may be of therapeutic value.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1983

IgA specific T-cell factor produced by a human T-T hybridoma.

A human T-T hybridoma was produced, which was a fusion product between and HGPRT-deficient T-cell line, Jurkat 3, and an OKT4+ activated peripheral blood T-cell. The hybrid expressed a receptor for IgM Fc and was negative for IgA Fc. It was shown to produce a factor capable of specifically enhancing IgA production and secretion by isolated human B-cells. The factor exerts its effect directly on B-cells and appears to be different from T-cell-replacing factors previously described.

Antibody Specificity↗
PubMed1982

Human T cell hybridomas secreting factors for IgA-specific help, polyclonal B cell activation, and B cell proliferation.

Human T-T hybridomas were established by fusion of concanavalin A-activated OKT-4+ T cells with hypoxanthine guanine phosphoribosyl transferase-deficient as well as nondeficient T cell lines. Four hybrids were selected for further study. Supernatant from hybrid clone J1.3 specifically enhanced IgA production and secretion by isolated human B cells, with increases in IgA plaque-forming cells approaching those seen with addition of autologous T cells and pokeweed mitogen. A monoclonal lymphocytic leukemia with membrane IgA also differentiated to IgA plasma cells by this supernatant. Evidence suggests that this hybrid supernatant acts on post-switch IgA-committed B cells. The other hybrids were not isotype specific; hybrid J2S1 enhanced polyclonal Ig secretion and hybrids K1 and K8 induced B cell proliferation without induction of Ig secretion.

B-Lymphocytes↗
PubMed1981

Occurrence of Clostridium difficile toxin during the course of inflammatory bowel disease.

Clostridium difficile toxin, the presumed mechanism of antibiotic-associated pseudomembranous colitis, has been suggested as a contributory factor to mucosal injury in inflammatory bowel disease. We evaluated its incidence and apparent role in 65 consecutive patients with diarrheal and inflammatory bowel diseases. Toxin was demonstrated in 3 of 18 patients with ulcerative colitis (17%), 1 of 26 with Crohn's colitis (4%), and 5 of 21 with a variety of diarrheal illnesses (24%). Toxin appeared only in those who had been exposed to antimicrobials within 2 mo. In inflammatory bowel disease, presence of toxin was not correlated with disease severity. We conclude that Clostridium difficile toxin appears only in patients exposed to antimicrobials and is unlikely to be a significant contributory factor in inflammatory bowel disease.

Anti-Bacterial Agents↗
PubMed1978

[Improvement of pathological glucose tolerance by bradykinin in diabetics and in surgical patients (author's transl)].

Intravenous glucose tolerance tests (GTT) were performed in 13 metabolically healthy patients at the first and second day after abdominal surgery. GTT were carried out during an additional infusion of bradykinin (BK) (80 microgram/h) in six of these patients at the first day (group A) and in seven patients at the second day (group B). Furthermore, GTT were performed in six patients with chemical diabetes with and without BK-infusion. In addition, the effect of BK on blood glucose concentration in the postabsorptive state was investigated in nine maturity onset diabetics and in five healthy volunteers. As a control, another nine diabetics received physiological saline. In both groups of surgical patients BK improved glucose tolerance (k-values: group A without BK 1.03 +/- 0.12, with BK 1.31 +/- 0.07; group B without BK 0.85 +/- 0.18, with BK 1.25 +/- 0.21). This was also true in chemical diabetics (without BK 0.81 +/- 0.03, with BK 1.08 +/- 0.04). While BK did not change blood glucose concentration in healthy volunteers, it reduced that of diabetics by 12.2 +/- 1.4% continuously during 100 min. No spontaneous drop of blood glucose was observed in diabetics receiving saline. These results are in good accord with the present view that kinins may play a role within the regulation of carbohydrate metabolism.

Blood Glucose↗
PubMed1978

Sulphydryl requirement for insulin release from the perfused pancreas. Studies with ethacrynic acid and dithiothreitol.

Using the isolated, perfused rat pancreas the importance of sulphydryl groups for the secretory process of insulin was investigated. It was found that ethacrynic acid (EA, 0.075-0.6 mmol/1) caused a dose-dependent, monophasic insulin release. Addition of EA to a glucose-stimulated (20 mmol/1) pancreas led to a sudden increase in hormone release, followed by a dose-dependent inhibition of release, which was not reversible after removal of EA. The same phenomenon was seen in the presence of 20 mmol/1 leucine. Dithiothreitol (DTT, 0.1 and 1 mmol/1) had no effect on basal insulin secretion. Added to a glucose-stimulated pancreas DTT (1 mmol/1) caused a reversible inhibition of insulin release. The persistent inhibitory action of EA on glucose-induced insulin release could be reversed by simultaneous perfusion of EA and DTT. Sequential exposure of a glucose-stimulated pancreas to EA and DTT led to a rapid release of insulin, due to DTT; however, the EA-induced inhibition of insulin secretion could not be prevented. Two kinds of thiol groups in the plasma membrane and in the beta cell might be responsible for the various kinetics of insulin release induced by EA and DTT.

Animals↗