No abstract

A combination of hyperthermia with radiotherapy and chemotherapy for various solid tumors has been practiced clinically. However, hyperthermic therapy has side effects, such as thrombocytopenia. Up to now, the pathogenesis of hyperthermia-induced thrombocytopenia remains unclear. Previous studies have shown that hyperthermia induces platelet apoptosis. However, the signaling pathways and molecular mechanisms involved in hyperthermia-induced platelet apoptosis have not been determined. Here we show that hyperthermia induced intracellular reactive oxygen species (ROS) production and mitochondrial ROS generation in a time-dependent manner in platelets. The mitochondria-targeted ROS scavenger Mito-TEMPO blocked intracellular ROS and mitochondrial ROS generation. By contrast, inhibitors of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, nitric oxide synthase, cyclooxygenase and lipoxygenase did not. Furthermore, Mito-TEMPO inhibited hyperthermia-induced malonyldialdehyde production and cardiolipin peroxidation. We also showed that hyperthermia-triggered platelet apoptosis was inhibited by Mito-TEMPO. Furthermore, Mito-TEMPO ameliorated hyperthermia-impaired platelet aggregation and adhesion function. Lastly, hyperthermia decreased platelet manganese superoxide dismutase (MnSOD) protein levels and enzyme activity. These data indicate that mitochondrial ROS play a pivotal role in hyperthermia-induced platelet apoptosis, and decreased of MnSOD activity might, at least partially account for the enhanced ROS levels in hyperthermia-treated platelets. Therefore, determining the role of mitochondrial ROS as contributory factors in platelet apoptosis, is critical in providing a rational design of novel drugs aimed at targeting mitochondrial ROS. Such therapeutic approaches would have potential clinical utility in platelet-associated disorders involving oxidative damage.

Defect engineering is a strategy that is attracting widespread attention for the possibility of modifying battery active materials in order to improve the cycling stability of the electrodes. However, accurate investigation and quantification of the effect of the defects on the electrochemical energy storage performance of the cell are not trivial tasks. Herein, we report the quantification of vanadium-defective clusters (i.e., up to 5.7%) in the V2O3 lattice via neutron and X-ray powder diffraction measurements, positron annihilation lifetime spectroscopy, and synchrotron-based X-ray analysis. When the vanadium-defective V2O3 is employed as cathode active material in an aqueous Zn coin cell configuration, capacity retention of about 81% after 30,000 cycles at 5 A g−1 is achieved. Density functional theory calculations indicate that the vanadium-defective clusters can provide favorable sites for reversible Zn-ion storage. Moreover, the vanadium-defective clusters allow the storage of Zn ions in V2O3, which reduces the electrostatic interaction between the host material and the multivalent ions.

Coral-like NixCo1−xSe2 anode material with hierarchical architecture delivers ultralong cycle life and ultrahigh rate capability in SIBs.