Transition-metal oxides (TMOs) are one of the most promising kinds of p-doping materials for organic semiconductors. However, to be compatible with organic materials, low-temperature evaporable TMOs are highly desirable. Rhenium(VII) oxide with a very low melting temperature of only 225 °C, which is the lowest among all TMO dopants, is first investigated as a p-dopant in N,N′-bis(1-naphthyl)-N,N′-diphenyl-1,1′-biphenyl-4,4-diamine (NPB). Systematic studies are performed compared with ReO3, a different valence state oxide of rhenium. Hole mobility improvement from 5.38 × 10–4 to 5.88 × 10–3 cm2/(V s) at an electric field of 3 × 105 V/cm is achieved by doping Re2O7 into NPB. Lower valence states of Re species in Re2O7-doped NPB than ReO3 are observed by XPS study, indicating stronger charge transfer between Re2O7 and NPB. Temperature-dependent I–V study reveals lower hole injection barrier of Re2O7 than ReO3 in hole-only devices. Crystallinity of NPB films is found to be the same before and after doping by XRD study. Absorption spectrum study reveals higher stability of Re2O7-doped NPB than ReO3 in air. Hole current is enhanced by three orders of magnitude at 2 V when utilizing both rhenium-oxide-doped NPBs in hole-only devices. OLED devices with both rhenium-oxide-doped NPBs as hole injection layer (HIL) show a similar efficiency of 3.3 cd/A at 300 mA/cm2. Also, driving voltage is reduced from 2.6 V for pure NPB to 2.5 and 2.4 V for Re2O7 and ReO3 doped NPB, respectively.

Pain and depression comorbidity affect the patients’ both physical and mental health and quality of life seriously. The comorbid depressive symptoms in cancer pain severely affect the recognition and treatment of pain. Similarly, cancer pain patients with depression are inclined toward more despair and greater impairment. The mechanisms responsible for the comorbid depressive symptoms in cancer induced bone pain have not been fully delineated and the currently available therapeutics for this pathological pain is relatively limited. In the present study, we observed that carcinoma cells implantation induced pain and depression comorbidity resulted in the upregulation of major histocompatibility complex class I (MHC-I) in hippocampus associated with the activation of TREM2/DAP12-mediated microglial signaling pathways. These observations were reversed by a lentiviral vector harboring RNA interference sequence targeting MHC-I injected into the hippocampus of tumor bearing mice. Together, these results suggest that MHC-I involves in the cancer induced bone pain and depression comorbidity through regulating the TREM2/DAP12-mediated signals in microglia of hippocampus. Suppression of MHC-I could be a therapeutic target for cancer induced bone pain.

Background: Bone cancer pain (BCP) is a common chronic pain that is caused by a primary or metastatic bone tumor. It is refractory to currently available clinical treatment owing to its complicated underlying mechanisms. Methods: In this study, we used proteomics approaches to investigate expressional changes of the rat spinal cord proteome from 7 to 21 d after inoculation. Proteins from the rat L4-6 spinal cord homogenates of BCP and Sham animals were fractionated by two-dimensional (2-DE) gel electrophoresis to produce a high-resolution map of the spinal cord soluble proteins. Proteins showing altered expression levels between BCP and Sham were selected. Results: A total of 60 spots were obtained, and isolated proteins were in-gel trypsin-digested and the resulting peptides were analyzed by matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry. Using the mass spectrometric data, 34 differentially expressed proteins (DEPs) were identified. GO analysis of the identified proteins allowed us to explore the function of the represented proteins. Conclusions: Based on these results, the identified proteins may contribute to the maintenance of BCP, and may provided new or valuable information in the discovery of new therapeutic targets for BCP.