Thermoluminescence emission on lead oxychloroborate glasses under UV exposure.

Glassy materials were prepared using two different systems: 50B2 O3 - (50 - x)PbO - xPbCl2, with x = 0, 2 and 5 in mol % (System BPCl-I) and 50BO1.5 - (50 - x)PbO - xPbCl2 with x = 0, 2, 5 and 7 in cationic % (System BPCl-II). Structural and optical characterization showed that PbCl when substituted for PbO changed the structure of the glass network by replacing nonbridging oxygens for chlorine ions. This substitution also caused a change in the number of defects responsible for thermoluminescence (TL) emission (electrons and hole trap centres). Thermoluminescence emissions were observed for the first time in lead oxychloroborate glasses after exposure to UV radiation. Sample BPCl-I-2 (x = 2 from System I) demonstrated better TL emission compared with other glass samples. One intense peak in the glow curve, centred at ~122°C followed by a shoulder at ~180°C, was highly sensitive to UV radiation. There were also good linear responses at dose range ~0.4 to ~2 J/cm2 for the first peak (low temperature) and ~0.4 to ~4 J/cm2 for the second peak (high temperature).

Role of new Immunophenotypic Markers on Prognostic and Overall Survival of Acute Myeloid Leukemia: a Systematic Review and Meta-Analysis.

Despite technological advances, the prognosis and survival of acute myeloid leukemia (AML) adult patients remain low, compared with other hematologic malignancies. Some antigens detected by immunophenotyping may soon play a significant role in the pathophysiologic, prognostic, and overall survival (OS) rate of AML patients. Therefore, we conducted a systematic review and meta-analysis of PubMed, Scopus, Science Direct, Web of Science, and the Cochrane Library (using PRISMA guidelines). We analyzed 11 studies and 13 antigens, detected through the immunophenotyping of 639 patients. From them, twelve exhibited a negative impact with AML prognosis. The meta-analysis demonstrated a high expression of AML markers, which have been associated with a decrease in survival over 10 months (RR 2.55; IC 95%; 1.49-4.37) and over 20 months (RR 2.46; IC 95%; 1.75-3.45). Knowing that the expression of immunophenotypic markers, which are not used on a routine basis, might be able to influence disease behavior, looks promising. However, they have been associated with a poor prognosis as well as a decrease in survival. This may allow for different chemotherapeutical protocols, including future studies for new therapeutic targets.

Effects of Bcl-2 modulation with G3139 antisense oligonucleotide on human breast cancer cells are independent of inherent Bcl-2 protein expression.

We have investigated the effects of transient Bcl-2 down-regulation induced by the Bcl-2 antisense oligodeoxynucleotide (ODN) G3139 (Genta Incorporated) in high Bcl-2 protein expressing, estrogen receptor (ER) positive MCF-7 and low Bcl-2 expressing, ER negative MDA435/LCC6 human breast cancer cells. Treatment with Bcl-2 antisense ODN in vitro caused > 80% reduction of Bcl-2 protein levels in a sequence specific manner for both cell lines. Maximum mRNA reduction was achieved within 24 h of the first antisense ODN exposure whereas full protein down-regulation required antisense exposure over 48 h. This Bcl-2 reduction was associated with 80-95% loss of viable cells compared to untreated cells. Similar cytotoxic effects were observed in both cell lines despite a nine-fold intrinsic difference in Bcl-2 protein expression suggesting that the relative degree of down-regulation of Bcl-2 is more important than the absolute reduction. Cell death associated with G3139 exposure exhibited properties indicative of apoptosis such as mitochondrial membrane depolarization and caspase activation. Combined treatment with G3139 and cytotoxic agents resulted in additive cytotoxicity in both cell lines. However, under most conditions studied, the direct cytotoxic activity of G3139 antisense was not synergistic with the cytotoxic agents. These results suggest that while Bcl-2 clearly constitutes an attractive therapeutic target due to its role in regulating apoptosis in breast cancer cells, additional mechanisms are important in the control of apoptosis arising from exposure to anticancer agents in vitro.