Route of placebo administration: Robust placebo effects in laboratory and clinical settings.

Recent advances in laboratory and clinical research have greatly enhanced our understanding of placebo effects. However, little progress has been made in translational research that can well integrate these findings. This article examines pivotal role of placebo administration in subsequent placebo responses, providing a unified framework that accounts for robust placebo effects in both laboratory and clinical settings.

Inhibition of Glioblastoma Cell Growth In Vitro and In Vivo by Brucine, a Component of Chinese Medicine.

Glioblastoma multiforme (GBM) is one of the most common glial cell tumors and has drawn more and more attention in the clinic in recent years. Brucine has been reported to significantly suppress gastric cancer, lung cancer, and prostate cancer growth in vivo by inducing cell apoptosis. Here, the effects of brucine on U251 human glioma cell growth were investigated in vitro by cell proliferation assay, FACs, and qPCR in a xenograft tumor model.

Is acupuncture a placebo therapy?

Complementary therapies such as acupuncture are suggested to have enhanced placebo effects. Numerous high quality randomized controlled trials found that acupuncture is no better than its placebo control; however, patients in both real and sham acupuncture groups report clinically meaningful symptom improvements. A possible interpretation of these trials is that acupuncture acts entirely by engaging placebo mechanisms.

Postconditioning ameliorates mitochondrial DNA damage and deletion after renal ischemic injury.

Background: Reactive oxygen species (ROS) play a major role in causing injury in ischemia-reperfusion (I/R). Mitochondrial DNA (mtDNA) is particularly vulnerable to oxidative damage. We propose that increased mitochondrial ROS production is likely to damage mtDNA, causing further injury to mitochondria, and postconditioning (POC) may ameliorate kidney I/R injury by mitigating mitochondrial damage.

Stromal cell derived factor-1 enhances bone marrow mononuclear cell migration in mice with acute liver failure.

Aim: To evaluate the number of bone marrow mononuclear cells (BMMC) that are migrated to the liver following transplantation of murine BMMC into mice with acute liver injury.

Methods: BMMC were isolated from the bone marrow of mice in a lymphocyte separation medium and then labeled with PKH26. The labeled cells were subsequently infused into the caudal veins of BALB/c mice with hepatic injury induced by carbon tetrachloride and 2-acetylaminofluorene.