Subsequently, whole blood of human volunteers was incubated with 1, 2.3, 4 or 8 mu Ci Tc-99m-MIBI. After a 30-min incubation, the lymphocytes were stimulated with a mitogen to assay for micronuclei in cytokinesis-blocked binucleated cells. The frequency of micronuclei
in samples treated with this radiopharmaceutical up to 2-fold (8 mu Ci) the concentration of Tc-99m-MIBI normally found in the blood of patients was not more than in control lymphocyte cultures. We concluded that there is no increased induction of micronuclei in lymphocytes incubated with Tc-99m-MIBI at the radioactivity doses used for diagnostic purposes.”
“One of the goals of bone tissue engineering is to design delivery methods for skeletal ABT-737 datasheet stem/progenitor cells to repair or replace bone. Although the materials used to retain cells play a central role in the quality of the constructs, DMH1 the source of cells is key for bone regeneration. Bone marrow is the most common cell source, but other tissues are now being explored, such as the periosteum, fat, muscle, cord blood, and embryonic or induced pluripotent stem cells. The therapeutic effect of exogenous stem/progenitor cells is accepted, yet their contribution to bone repair is not well defined. The in vitro osteo- and/or chondrogenic potential of these skeletal progenitors
do not necessarily predict their differentiation potential in vivo and their function may be affected by their ability to home correctly to bone. This review provides an overview of animal models used to test the efficacy of cell-based approaches. We examine the mechanisms of endogenous cell recruitment during bone repair and compare the role of local versus systemic cell recruitment. We discuss how the normal repair process can help define efficacious
cell sources for bone tissue engineering and improve their methods of delivery.”
“Background: DB289, [2,5-bis(4-amidinophenyl) furan bis-O-methylamidoxime], is a broad spectrum anti-parasitic compound which has been shown to be effective against Staurosporine in vitro malaria in recent clinical trials. DB75, [2,5-bis(4-amidinophenyl) furan], is the active metabolite of this drug. The objective of this study was to determine the mechanism of action of DB75 in Plasmodium falciparum.
Methods: Live parasites were observed by confocal microscopy after treatment with organelle specific dyes and DB75, an inherently fluorescent compound. Parasites were exposed to DB75 and assessed for growth and morphological changes over time using blood smears and light microscopy. Also, to determine if DB75 affects gene transcription, real time PCR was used to monitor transcript levels over time for six developmentally expressed genes, including trophozoite antigen R45-like (PFD 1175w), lactate dehydrogenase (PF13_0141), DNA primase (PFI0530c), isocitrate dehydrogenase (PF13_0242), merozoite surface protein-1 (PF11475w), and merozoite surface protein-7 (PF13_0197).