Accelerated death of megakaryocytes from Wiskott-Aldrich syndrome patients.

Wiskott-Aldrich syndrome (WAS) is an X-linked recessive disorder caused by WAS gene mutations resulting in haematopoietic/immune cell defects. Recent studies report accelerated death of WAS platelets and lymphocytes. Data on megakaryocyte (MK) maturation, viability and their possible role in thrombocytopenia development in WAS are limited.

The Nature and Clinical Significance of Atypical Mononuclear Cells in Infectious Mononucleosis Caused by the Epstein-Barr Virus in Children.

Atypical mononuclear cells (AM) appear in significant numbers in peripheral blood of patients with Epstein-Barr virus (EBV)-associated infectious mononucleosis (IM). We investigated the number and lineage-specific clusters of differentiation (CD) expression of atypical mononuclear cells in 110 children with IM using the anti-CD antibody microarray for panning leukocytes by their surface markers prior to morphology examination. The AM population consisted primarily of CD8+ T cells with a small fraction (0%-2% of all lymphocytes) of CD19+ B lymphocytes.

Simultaneous finding of chronic lymphocytic leukemia and residual hairy cell leukemia using a lymphocyte-binding anti-CD antibody microarray.

The morphologic diagnosis of hairy cell leukemia coexisting with another lymphoproliferative disorder is hindered by the small size of hairy cell population. It can be simplified by presorting peripheral blood mononuclear cell using an anti-CD antibody microarray on transparent support (including anti-CD11c, CD25, CD103, and CD123) before their morphology analysis.

Anti-CD antibody microarray for human leukocyte morphology examination allows analyzing rare cell populations and suggesting preliminary diagnosis in leukemia.

We describe a method for leukocyte sorting by a microarray of anti-cluster-of-differentiation (anti-CD) antibodies and for preparation of the bound cells for morphological or cytochemical examination. The procedure results in a "sorted" smear with cells positive for certain surface antigens localised in predefined areas. The morphology and cytochemistry of the microarray-captured normal and neoplastic peripheral blood mononuclear cells are identical to the same characteristics in a smear.

Tubulin heterodimers remain functional for one cell cycle after the inactivation of tubulin-folding cofactor D in fission yeast cells.

Tubulin-folding cofactor D plays a major role in the formation of functional tubulin heterodimers, the subunits of microtubules (MTs) that are essential for cell division. Previous work has suggested that, in Schizosaccharomyces pombe, cofactor D function is required during G(1) or S phases of the cell cycle, and when it fails to function due to the temperature-sensitive mutation alp1-t1, cells are unable to segregate their chromosomes in the subsequent mitosis. Here we report that another mutation in the cofactor D gene, alp1-1315, causes failures in either the first or second mitosis in cells synchronized in G(1) or G(2) phases, respectively.

Chromosome segregation in fission yeast with mutations in the tubulin folding cofactor D.

Faithful chromosome segregation requires the combined activities of the microtubule-based mitotic spindle and the multiple proteins that form mitotic kinetochores. Here, we show that the fission yeast mitotic mutant, tsm1-512, is an allele of the tubulin folding chaperone, cofactor D. Chromosome segregation in this and in an additional cofactor D mutant depends on growth conditions that are monitored specifically by the mitotic checkpoint proteins Mad1, 2, 3 and Bub3.