Cyclodextrin-complexed curcumin exhibits anti-inflammatory and antiproliferative activities superior to those of curcumin through higher cellular uptake (vol 80, vol 1021, 2010)

Retraction notice to “Cyclodextrin-complexed curcumin exhibits anti-inflammatory and antiproliferative activities superior to those of curcumin through higher cellular uptake” [Biochem. Pharmacol. 80 (2010) 1021–1032].Non peer reviewe

Trans-radial approach versus trans-femoral approach in patients with acute coronary syndrome undergoing percutaneous coronary intervention: An updated meta-analysis of randomized controlled trials.

IntroductionTrans-radial approach (TRA) is recommended over trans-femoral approach (TFA) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). We intended to study the effect of access on all-cause mortality.Methods and resultsWe searched PubMed and EMBASE for randomized studies on patients with ACS undergoing PCI. The primary outcome was all-cause mortality at 30-days. The secondary outcomes included in-hospital mortality, major adverse cardiac or cerebrovascular event (MACE) as defined by the study, net adverse clinical event (NACE), non-fatal myocardial infarction, non-fatal stroke, stent thrombosis, study-defined major bleeding, and minor bleeding, vascular complications, hematoma, pseudoaneurysm, non-access site bleeding, need for transfusion, access site cross-over, contrast volume, procedure duration, and hospital stay duration. We studied 20,122 ACS patients, including 10,037 and 10,085 patients undergoing trans-radial and trans-femoral approaches, respectively. We found mortality benefit in patients with ACS for the trans-radial approach [(1.7% vs. 2.3%; RR: 0.75; 95% CI: 0.62-0.91; P = 0.004; I2 = 0%). Out of 10,465 patients with STEMI, 5,189 patients had TRA and 5,276 had TFA procedures. A similar benefit was observed in patients with STEMI alone [(2.3% vs. 3.3%; RR: 0.71; 95% CI: 0.56-0.90; P = 0.004; I2 = 0%). We observed reduced MACE, NACE, major bleeding, vascular complications, and pseudoaneurysms. No difference in re-infarction, stroke, and serious bleeding requiring blood transfusions were noted. We noticed a small decrease in contrast volume(ml) {mean difference (95% CI): -4.6 [-8.5 to -0.7]}, small but significantly increase in procedural time {mean difference (95% CI) 1.2 [0.1 to 2.3]}and fluoroscopy time {mean difference (95% CI) 0.8 [0.3 to1.4] min} in the trans-radial group.ConclusionTRA has significantly reduced 30-day all-cause mortality among patients undergoing PCI for ACS. TRA should be the preferred vascular access in patients with ACS

Gossypol Induces Death Receptor-5 through Activation of the ROS-ERK-CHOP Pathway and Sensitizes Colon Cancer Cells to TRAIL*

Development of resistance to TRAIL, an apoptosis-inducing cytokine, is one of the major problems in its development for cancer treatment. Thus, pharmacological agents that are safe and can sensitize the tumor cells to TRAIL are urgently needed. We investigated whether gossypol, a BH3 mimetic that is currently in the clinic, can potentiate TRAIL-induced apoptosis. Intracellular esterase activity, sub-G1 cell cycle arrest, and caspase-8, -9, and -3 activity assays revealed that gossypol potentiated TRAIL-induced apoptosis in human colon cancer cells. Gossypol also down-regulated cell survival proteins (Bcl-xL, Bcl-2, survivin, XIAP, and cFLIP) and dramatically up-regulated TRAIL death receptor (DR)-5 expression but had no effect on DR4 and decoy receptors. Gossypol-induced receptor induction was not cell type-specific, as DR5 induction was observed in other cell types. Deletion of DR5 by siRNA significantly reduced the apoptosis induced by TRAIL and gossypol. Gossypol induction of the death receptor required the induction of CHOP, and thus, gene silencing of CHOP abolished gossypol-induced DR5 expression and associated potentiation of apoptosis. ERK1/2 (but not p38 MAPK or JNK) activation was also required for gossypol-induced TRAIL receptor induction; gene silencing of ERK abolished both DR5 induction and potentiation of apoptosis by TRAIL. We also found that reactive oxygen species produced by gossypol treatment was critical for TRAIL receptor induction and apoptosis potentiation. Overall, our results show that gossypol enhances TRAIL-induced apoptosis through the down-regulation of cell survival proteins and the up-regulation of TRAIL death receptors through the ROS-ERK-CHOP-DR5 pathway