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R H Vonderheide

Publications and source records attributed to R H Vonderheide.

9 recordsLinked to original sources
PubMed1998

Association of thrombocytopenia with the use of intra-aortic balloon pumps.

PURPOSE: The intra-aortic balloon pump has become an important tool in the management of patients with severe coronary artery disease. Although pump-induced thrombocytopenia was described more than 20 years ago, there has been no prospective study of this condition. PATIENTS AND METHODS: In a prospective study of consecutive adult intensive care patients admitted with acute coronary syndromes, we compared serial platelet counts in 58 patients treated with an intra-aortic balloon pump with 51 patients who were not. All patients received intravenous heparin. RESULTS: Clinical characteristics of the two groups were similar, except that unstable angina was more frequent among balloon pump patients. On each of 6 consecutive days, the mean platelet counts of patients treated with a balloon pump were significantly lower than those of non-pump patients. Platelet counts (mean +/- SD) of balloon pump patients decreased to a nadir of 63% +/- 4% of the initial count on day 4, but subsequently stabilized. There was only a slight, transient decrease in the platelet counts of non-pump patients. Overall, 47% of balloon pump patients developed thrombocytopenia (platelet count <150,000/mm3) compared with 12% of non-pump patients (P <0.01). Platelet counts dropped by at least half of initial counts in 26% of balloon pump patients compared with 4% of non-pump patients (P <0.01). Multivariate analysis demonstrated that the use of an intra-aortic balloon pump was independently associated with a substantial (> or =50%) decline in platelet count (odds ratio 7.2, 95% confidence interval 1.4 to 40, P = 0.03). Removal of the balloon pump was associated with a rapid increase in platelet count. CONCLUSIONS: The use of an intra-aortic balloon pump led to a steady and predictable decrease in platelet count, which recovered rapidly if the balloon pump was removed or slowly if the device remained in place.

Aged↗
PubMed1997

Angiosarcoma.

Explore the source record for details and available documents.

Adult↗
PubMed1994

Residues within a conserved amino acid motif of domains 1 and 4 of VCAM-1 are required for binding to VLA-4.

Vascular cell adhesion molecule 1 (VCAM-1), a member of the Ig superfamily originally identified on activated endothelium, binds to the integrin very late antigen-4 (VLA-4), also known as alpha 4 beta 1 or CD49d/CD29, to support cell-cell adhesion. Studies based on cell adhesion to two alternatively spliced forms of VCAM-1 or to chimeric molecules generated from them and intercellular adhesion molecule-1 (ICAM-1) have demonstrated two VLA-4 binding sites on the predominate form of VCAM-1. Here, we studied VLA-4-dependent adhesion of the lymphoid tumor cell line Ramos to cells expressing wild type and mutant forms of VCAM-1. Results based on domain deletion mutants demonstrated the existence and independence of two VLA-4-binding sites located in the first and fourth domains of VCAM-1. Results based on amino acid substitution mutants demonstrated that residues within a linear sequence of six amino acids found in both domain 1 and 4 were required for VLA-4 binding to either domain. Five of these amino acids represent a conserved motif also found in ICAM domains. We propose that integrin binding to these Ig-like domains depends on residues within this conserved motif. Specificity of integrin binding to Ig-like domains may be regulated by a set of nonconserved residues distinct from the conserved motif.

Amino Acid Sequence↗
PubMed1992

Lymphocyte adhesion through very late antigen 4: evidence for a novel binding site in the alternatively spliced domain of vascular cell adhesion molecule 1 and an additional alpha 4 integrin counter-receptor on stimulated endothelium.

Recent studies demonstrate that alternative splicing of mRNA from a single gene can produce two forms of vascular cell adhesion molecule 1 (VCAM-1): a six-immunoglobulin (Ig) domain form (VCAM-6D) and a seven-Ig domain form (VCAM-7D). Using a COS cell transient expression assay, we investigated whether VCAM-6D and VCAM-7D differ functionally in adhesion to the integrin VLA-4 (CD49d/CD29) on lymphoid cells. Binding of lymphoid cell lines and peripheral blood lymphocytes was completely blocked by VLA-4 monoclonal antibody (mAb) and one VCAM-1 mAb (4B9) to both VCAM-6D and VCAM-7D, whereas one VCAM-1 mAb (E1/6) completely blocked binding to VCAM-6D but only partially inhibited binding to VCAM-7D. We conclude that there is one VLA-4 binding site in the six Ig domains shared between VCAM-6D and VCAM-7D, and that the alternatively spliced domain 4 present in VCAM-7D provides a second VLA-4 binding site that is blocked by 4B9 but not the E1/6 mAb. We compared the inhibitory effects of anti-VCAM-1 and anti-VLA-4 mAbs on lymphoid cell adhesion to cultured human umbilical vein endothelial cells (HUVEC). The anti-VCAM-1 mAb 4B9 blocked the binding of PBL and lymphoid tumor cells to stimulated HUVEC better than the anti-VCAM-1 mAb E1/6. Because VCAM-7D is the predominant form of VCAM-1 expressed by stimulated endothelial cells, this difference in VCAM-1 mAb inhibition is attributed to lymphoid cell binding to VCAM-7D on stimulated HUVEC. Although the anti-VLA-4 mAb and anti-VCAM-1 mAb 4B9 equally inhibited PBL binding to stimulated HUVEC, mAb 4B9 inhibited the binding of two lymphoid cell lines significantly less than anti-VLA-4 mAb. Combination of 4B9 mAb with function-blocking antiserum to human fibronectin, a second known ligand for VLA-4, also failed to inhibit as much as anti-VLA-4 mAb. These findings suggest that adhesion of lymphoid cell lines through VLA-4 or other alpha 4 integrins may involve inducible counter-receptor(s) on endothelium distinct from either VCAM-1 or fibronectin. Time course experiments indicate that the fraction of alpha 4 integrin-dependent binding that can be blocked by anti-VCAM-1 mAb E1/6 rises and peaks within 2 h of tumor necrosis factor (TNF) stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Comparison of IgD+ and IgD- thoracic duct B lymphocytes as germinal center precursor cells in the rat.

Genetically marked thoracic duct B cell subpopulations rich in either IgD+ or IgD- B cells were transferred to non-irradiated, congenic rats in order to compare the capacities of IgD+ versus IgD- B cells to form germinal centers (GCs). This comparison was made quantitatively based on flow cytometric analyses of lymph node cells prepared from chimeric rats 7 days after s.c. immunization. Donor-origin and host-origin B cells were distinguished using anti-Igk antibodies, and GC B cells were distinguished from other B cells in suspension by their lack of labeling with the mAb HIS22. IgK+ HIS22- lymph node cells corresponded well to GC B cells: they contained many large cells, were IgM+ but mostly IgD-, expressed relatively lower levels of IgM than HIS22+ B cells, and increased in number and frequency in response to antigen. Results from flow cytometric analyses, corroborated by immunofluorescence histochemical studies, showed that cell-for-cell, IgD- B cells from GCs much more efficiently than IgD+ cells. B cell populations enriched for IgD- cells became relatively more distributed to GCs than to other lymph node B cell areas and gave rise to many more GC B cells of donor origin per transferred B cell than whole, unseparated thoracic duct B cells (for which greater than 97% were IgD+). IgD- B cells from rats primed deliberately with antigen also became relatively more distributed to GCs and gave rise to more GC B cells of donor origin than either IgD+ B cells from primed donors or IgD- B cells from unprimed donors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Immigration of thoracic duct B lymphocytes into established germinal centers in the rat.

Immigration of B lymphocytes into established germinal centers in the rat was studied by transferring genetically marked thoracic duct B cells to non-irradiated congenic hosts at various times between 3 days before and 6 days after host immunization. Seven days after host immunization, the distribution of donor B cells to lymph node germinal centers (relative to their distribution to non-germinal center lymph node areas) was measured by two-color flow cytometry in which (a) donor and host B cells were distinguished by their Ig kappa chain allotypes, and (b) germinal center B cells were distinguished by their lack of labeling with the monoclonal antibody HIS22. Thoracic duct B cells from long-term antigen-primed rats were found to immigrate into host germinal centers much better than B cells from unprimed donors. This effect was antigen specific: primed B cells only immigrated well into host germinal centers induced by the priming antigen. Although B cells localized in germinal centers most efficiently when injected before immunization, specifically primed donor B cells injected after immunization were still found to be at least as evenly distributed to germinal centers as to other lymph node areas, whereas unprimed B cells transferred after immunization localized poorly in host germinal centers. These findings are discussed in light of recent suggestions that memory B cell clones are maintained by continued antigenic stimulation within secondary lymphoid follicles.

Animals↗
PubMed1990

Does the availability of either B cells or CD4+ cells limit germinal centre formation?

To determine whether the availability of either B cells or T cells regulates the number and size of germinal centres observed following antigenic challenge, irradiated PVG rats were reconstituted with limiting numbers of thoracic duct B cells (with excess T cells) or with limiting numbers of thoracic duct CD4+ cells (with sufficient B cells). Germinal centre formation was measured histologically in the spleens of reconstituted rats 7 days after immunization with 2 x 10(9) sheep erythrocytes (at the height of the germinal centre reaction). Although reconstitution with B cells and antigen alone, or with thymocytes and antigen alone, produced no germinal centres, saturating numbers of germinal centres on the order observed for normal, non-irradiated rats were observed in irradiated rats reconstituted with only 10(7) B cells and 5 x 10(6) CD4+ cells. Germinal centres in the spleens of minimally reconstituted rats were also comparable in size to those observed in normal rats. Reconstitution with either 4 x 10(7) thoracic duct lymphocytes (including 2 x 10(7) B cells, as well as CD8+ and CD4+ cells) or with 4 x 10(7) thoracic duct lymphocytes and 2 x 10(8) thymocytes also led to saturating numbers of germinal centres. It is concluded therefore that (i) CD4+ cells are sufficient for the T-cell contribution required for germinal centre formation, and (ii) some factor other than the availability of B cells or CD4+ cells normally limits germinal centre formation.

Animals↗
PubMed1990

T lymphocytes in rat germinal centres belong to an ER3+ subpopulation of CD4+ cells.

Two-colour immunofluorescence histochemistry showed directly that greater than 90% of CD4+ germinal centre T cells in rat spleen or lymph node examined 7 days after immunization bear the antigen recognized by the monoclonal antibody (mAb) ER3. By contrast, only 30-40% of all thoracic duct or lymph node CD4+ cells were ER3+, as determined by two-colour flow cytometry. CD8+ cells were ER3+, but nearly all B cells were ER3-. Thus, germinal centre T cells belong to a subpopulation of CD4+ cells. Because only 25-30% of CD4+ cells that lack higher molecular weight forms of CD45 (i.e. mAb MRC OX32 cells, equivalent to MRC OX22 cells) express ER3, the CD4+ subpopulations defined by ER3 are neither identical nor complementary to the subsets defined by restricted expression of CD45 epitopes.

Animals↗