A laboratory model of toxin-induced hemolytic uremic syndrome.

Background: Verocytotoxin-producing (Shiga-like toxin-producing) Escherichia coli infection is the principal cause of hemolytic uremic syndrome (HUS). The pathogenesis is unclear, and there is a need for animal models. These are impeded by the different distribution of verocytotoxin receptors between species.

Susceptibility of AML cells to in vitro apoptosis correlates with heat shock protein 70 (hsp 70) expression.

Acute myeloid leukaemia (AML) cells from some individuals rapidly undergo apoptosis during in vitro culture. We have analysed this mode of cell death in AML cells harvested from patients at initial presentation and during subsequent treatment/relapse. Using flow cytometric analysis of propidium iodide-stained cells and quantitation of the subdiploid apoptotic peak, we observed that leukaemic cells from patients with AML displayed a heterogenous susceptibility to apoptosis in terms of the rate of accumulation of apoptotic cells.

Analysis of heat-shock protein expression in myeloid leukaemia cells by flow cytometry.

Expression of heat-shock proteins (hsp) was analysed in the leukaemic cells of 12 patients with acute myeloid leukaemia (AML) and nine patients with chronic myeloid leukaemia (CML). Using monoclonal antibodies to hsp70, hsp90 and hsp60 (ML30, a mycobacterial antigen with homology to human hsp60), we measured hsp levels by flow cytometry of permeabilized cells. Mononuclear cells from 10 healthy volunteers were also examined.