Gender, cholinesterase, platelet count and red cell count are main predictors of peripheral blood stem cell mobilization in healthy donors.

Background And Objectives: Mobilization of CD34 cells by stimulation with G-CSF shows considerable variation across stem cell donors. Upfront prediction of CD34 cell counts in peripheral blood based on easily available steady-state parameters would be helpful for the planning of apheresis and stem cell transplantation. Commonly accepted steady-state predictors for the mobilization are gender, body mass index and platelet count.

The Monoclonal Anti-CD157 Antibody Clone SY11B5, Used for High Sensitivity Detection of PNH Clones on WBCs, Fails to Detect a Common Polymorphic Variant Encoded by BST-1.

Background: CD157, encoded by BST-1, has been described as a useful flow cytometric marker for the analysis of paroxysmal nocturnal hemoglobinuria (PNH) as it is a glycosylphosphatidylinositol (GPI)-linked molecule highly expressed on normal monocytes and neutrophils. We and others observed isolated CD157 signal dropouts during intended PNH analysis. We hypothesize that these negative populations occur due to an antibody failure.

Peptide vaccination in the presence of adjuvants in patients after hematopoietic stem cell transplantation with CD4+ T cell reconstitution elicits consistent CD8+ T cell responses.

Patients receiving an allogeneic stem cell graft from cytomegalovirus (CMV) seronegative donors are particularly prone to CMV reactivation with a high risk of disease and mortality. Therefore we developed and manufactured a novel vaccine and initiated a clinical phase I trial with a CMV phosphoprotein 65 (CMVpp65)-derived peptide. Ten patients after allogeneic stem cell transplantation received four vaccinations at a biweekly interval.

Susceptibility to seizure-induced excitotoxic cell death is regulated by an epistatic interaction between Chr 18 (Sicd1) and Chr 15 (Sicd2) loci in mice.

Seizure-induced cell death is believed to be regulated by multiple genetic components in addition to numerous external factors. We previously defined quantitative trait loci that control susceptibility to seizure-induced cell death in FVB/NJ (susceptible) and C57BL/6J (resistant) mice. Two of these quantitative trait loci assigned to chromosomes 18 (Sicd1) and 15 (Sicd2), control seizure-induced cell death resistance.

Microarray-assisted fine mapping of quantitative trait loci on chromosome 15 for susceptibility to seizure-induced cell death in mice.

Prior studies with crosses of the FVB/NJ (FVB; seizure-induced cell death-susceptible) mouse and the C57BL/6J (B6; seizure-induced cell death-resistant) mouse revealed the presence of a quantitative trait locus (QTL) on chromosome 15 that influenced susceptibility to kainic acid-induced cell death (Sicd2). In an earlier study, we confirmed that the Sicd2 interval harbors gene(s) conferring strong protection against seizure-induced cell death through the creation of the FVB.B6-Sicd2 congenic strain, and created three interval-specific congenic lines (ISCLs) that encompass Sicd2 on chromosome 15 to fine-map this locus.