Etanercept Inhibits Pro-inflammatory Cytokines Expression in Titanium Particle-Stimulated Peritoneal Macrophages

Purpose: To investigate the inhibitory role of Etanercept in pro-inflammatory cytokines such as TNF-α, IL-1β and IL-6 production in titanium (Ti) particle stimulated macrophages.Methods: Peritoneal macrophages were stimulated with 1 × 109 Ti particles and treated simultaneously with or without 10, 100, or 1000 ng/mL Etanercept. The levels of TNF-α, IL-1β and IL-6 in the culture supernatants were measured using ELISA.Results: Titanium particles could stimulate TNF-α, IL-1β and IL-6 secretion in peritoneal macrophages. Etanercept inhibited Ti particle-induced TNF-α release by 29.7 % at 10 ng/ml (19.19 ± 4.72 pg/mL, p < 0.01), 49.3 % at 100 ng/mL (13.83 ± 3.72 pg/ml, p < 0.01) and 60.4 % at 1000 ng/mL (10.82 ± 3.87 pg/mL, p < 0.001), IL-1β release by 5.23 % at 10 ng/mL (34.79 ± 7.83 pg/mL, p > 0.05), 21.06 % at 100 ng/mL (28.98 ± 4.81 pg/mL, p < 0.01) and 29.83 % at 1000 ng/mL (25.76 ± 5.23 pg/ml, p < 0.001), and IL-6 release by 38.69 % at 10 ng/mL (256.8 ± 99.56 pg/mL, p < 0.01), by 42.13 % at 100 ng/mL (242.4 ± 33.26 pg/mL, p < 0.01) and 53.4 % at 1000 ng/ml (195.2 ± 48.82 pg/mL, p < 0.001).Conclusion: Etanercept has potent ability to prevent wear debris–induced osteolysis and may be valuable as a therapeutic agent for the treatment of prosthetic loosening in humans.Keywords: Etanercept; titanium particle; proinflammatory cytokines; peritoneal macrophage

Applying the scientific method to understand anomalous heat effect

Abstract only.Scientific methods in nuclear science are proposed to understand anomalous heat effect: (1) Neutrino Detection; (2) Internal Conversion Electrons; (3) RF emission and magnetic field fluctuation; (4) 3-Deuteron reaction; (5) Solid State Nuclear Track Detector(CR-39); (6) 6Li+p resonance at low energy. Each topic will be discussed in order

Receptor interactive protein kinase 3 promotes cisplatin-triggered necrosis in apoptosis-resistant esophageal squamous cell carcinoma cells

Cisplatin-based chemotherapy is currently the standard treatment for locally advanced esophageal cancer. Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that cisplatin induces necrotic cell death in apoptosisresistant esophageal cancer cells. This cell death is dependent on RIPK3 and on necrosome formation via autocrine production of TNFα. More importantly, we demonstrate that RIPK3 is necessary for cisplatin-induced killing of esophageal cancer cells because inhibition of RIPK1 activity by necrostatin or knockdown of RIPK3 significantly attenuates necrosis and leads to cisplatin resistance. Moreover, microarray analysis confirmed an anti-apoptotic molecular expression pattern in esophageal cancer cells in response to cisplatin. Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells. These data provide new insight into the molecular mechanisms underlying cisplatin-induced necrosis and suggest that RIPK3 is a potential marker for predicting cisplatin sensitivity in apoptosis-resistant and advanced esophageal cancer. © 2014 Xu et al

Obvious enhancement of the total reaction cross sections for 27,28^{27,28}P with 28^{28}Si target and the possible relavent mechanisms

The reaction cross sections of $^{27,28}$P and the corresponding isotones on Si target were measured at intermediate energies. The measured reaction cross sections of the N=12 and 13 isotones show an abrupt increase at $$. The experimental results for the isotones with $Z\leq 14$ as well as $$P can be well described by the modified Glauber theory of the optical limit approach. The enhancement of the reaction cross section for $^{28}$P could be explained in the modified Glauber theory with an enlarged core. Theoretical analysis with the modified Glauber theory of the optical limit and few-body approaches underpredicted the experimental data of $^{27}$P. Our theoretical analysis shows that an enlarged core together with proton halo are probably the mechanism responsible for the enhancement of the cross sections for the reaction of $^{27}$P+$^{28}$Si.Comment: 16 pages, 5 figures, to be published in Phys.Rev.

Anomalous heat induced by deuterium flux in a bunch of long-thin palladium tubes using PID method for calorimetry

PosterThis is a poster that was submitted to the 18th Annual International Conference on Cold Fusion (ICCF)