The absorption peak at 809 [cm.sup.-1] assigned to Ara-C was found in ABMs-GP.
The release of Ara-C from BMs-based conjugates was assayed by suspending them in PBS (pH 7.4) to mimic pH of blood plasma [32].
In summary, Ara-C was immobilized on BMs efficiently by using GP, G, and direct absorption.
Caption: SCHEME 1: Graphical illustration showing the Ara-C immobilization on BMs through various methods and their resultant end products, (a) genipin (GP) cross-linker (ABMs-GP), (b) glutaraldehyde (G) cross-linker (ABMs-G), and (c) direct absorption method (ABMs).
Caption: FIGURE 2: The FTIR spectra of (a) Ara-C, (b) ABMs-GP, (c) ABMs-G, (d) ABMs, and (e) BMs.
Cell lines, peripheral blood, and bone marrow blasts were treated with 25 [micro]mol/L Ara-C for 30 min at 37 [degrees]C and 5% C[O.sub.2].
Ara-C toxicity was also assayed with a 3-day cytotoxicity assay using the Cell Titer-Glo[R] Luminescent Cell Viability Assay kit (Promega, www.promega.
(15), expressing the human dCK gene, exhibited reduced relative growth in the presence of Ara-C in minimal medium but not in a rich growth medium, due to incorporation of cytosine triphosphate instead of the toxic analog Ara-CTP into bacterial DNA.
To measure Ara-C response in a nutrient-rich intracellular environment, an alternative cdd-deficient mutant of a bioluminescent E.
2, A and B) is similar to that observed with Ara-C (Fig.
AML cell lines and leukemic cell samples from AML patients with known clinical outcome to Ara-C treatment were used to evaluate the assay outlined by the schematic in Fig.
The 3-day cytotoxicity test also showed that cells from patient sample CR were significantly more sensitive to Ara-C compared with cells from patient sample NR (Fig.
