A cylindrical core-shell-like TiO2 nanotube array anode for flexible fiber-type dye-sensitized solar cells

A versatile anodization method was reported to anodize Ti wires into cylindrical core-shell-like and thermally crystallized TiO2 nanotube (TNT) arrays that can be directly used as the photoanodes for semi- and all-solid fiber-type dye-sensitized solar cells (F-DSSC). Both F-DSSCs showed higher power conversion efficiencies than or competitive to those of previously reported counterparts fabricated by depositing TiO2 particles onto flexible substrates. The substantial enhancement is presumably attributed to the reduction of grain boundaries and defects in the prepared TNT anodes, which may suppress the recombination of the generated electrons and holes, and accordingly lead to more efficient carrier-transfer channels

RXR negatively regulates ex vivo expansion of human cord blood hematopoietic stem and progenitor cells

Ex vivo expansion of human cord blood (CB) hematopoietic stem cells (HSCs) is one approach to overcome limited numbers of HSCs in single CB units. However, there is still no worldwide acceptable HSC ex vivo expansion system. A main reason is that we still have very limited knowldege regarding mechanisms underlying maintenance and expansion of CB HSCs. Here we report that retinoid X receptor (RXR) activity is of significance for CB HSC ex vivo expansion. RXR antagonist HX531 significantly promoted ex vivo expansion of CB HSCs and progenitor cells (HPCs). RXR agonist Bexarotene notably suppressed ex vivo expansion of CB HSCs. Activation of RXR by Bexarotene significantly blocked expansion of phenotypic HSCs and HPCs and expressed increased functional HPCs as assessed by colony formation induced by UM171 and SR1. In vivo transplantation experiments in immune-deficient mice demonstrated that HX531 expanded CB HSCs possess long-term reconstituting capacities, and Bexarotene treatment inhibited expansion of functional CB HSCs. RNA-seq analysis revealed that RXR regulates expression of FBP1 (a negative regulator of glucose metabolism) and many genes involved in differentation. ECAR analysis showed that HX531 significantly promoted glycolytic activity of CB CD34+ HSCs and HPCs. Our studies suggest that RXR is a negative regulator of ex vivo expansion of CB HSCs and HPCs

Covalent Heterojunctions Enhance Bi2S3/Reduced Graphene Oxide (rGO) Nanocomposite Performance as Aqueous Zinc Ion Battery Material

The shortage of lithium resources, safety and recycling difficulty has focused attention on alternative energy storage devices in recent years. The aqueous zinc-ion battery (ZIB) stands out against such a background because of its earth abundance, safety, and environmental friendliness.1 However, the limited choice of cathode materials hinders the development of advanced high-energy-density aqueous ZIBs. At present, manganese oxide2 and vanadium oxide3 are the two most widely studied zinc-ion battery cathodes, but the migration of Zn2+ in these materials is limited by the strong electrostatic interaction with lattice oxygen ions, resulting in poor reversible capacity. Metal sulfides, instead, may effectively improve the electrochemical performance reversibility of ZIBs. Layered metal sulfides have been extensively studied in monovalent cation (Li+, Na+, K+) rechargeable batteries.4 However, although limited studies with Bi2S35,6 as ZIB cathode material exist, their detailed electrochemical charge storage and transfer mechanisms are not well understood. In this work, we explore the effect of covalent anchoring Bi2S3 on reduced graphene oxide (rGO) on the stability and cycling performance as a cathode for aqueous ZIBs. During the hydrothermal synthesis, the reduced graphene oxide serves as the nucleation substrate enabling the formation of fine and uniformly sized Bi2S3 grains, Figure 1 (a). Raman and X-ray photoelectron spectroscopy (XPS) confirm the formation of Bi-O-C heterojunctions during hydrothermal synthesis. These oxygen bridges serve as efficient electron transfer channels in the Bi2S3/rGO composite for rapid charge compensation during Zn2+ incorporation/extraction. As a result, Bi2S3/rGO composite shows notably better rate performance and cycling stability compared with pristine Bi2S3. The specific capacity of Bi2S3-rGO8 composite is ~186 mAh g-1 at the current density of 500 mA g-1 after 150 cycles, considerably higher than unsupported Bi2S3. Additionally, the Bi2S3 nucleated on GO with smaller particle sizes can shorten the transport path of zinc ions, which is beneficial for fast charge transfer. Therefore, Bi2S3-rGO8 can deliver more than 100 mAh g-1 at 10 A/g charge/discharge current density, Figure 1 (b). Also, the zinc storage mechanism was analyzed by X-ray diffraction spectroscopy (XRD) and XPS, indicating a reversible conversion reaction of Zn2+ in the Bi2S3-rGO framework. During discharging, Zn2+ is embedded in Bi2S3-rGO frame to form ZnS and Bi wrapped in rGO. The process is accompanied by the dissolution of bismuth into electrolyte and the formation of (ZnSO4)[Zn(OH)2]3·5H2O (ZHS) on the electrode surface. Inhibition of these two processes may further increase the cycle stability of Bi2S3-rGO. Rotating ring disc electrode (RRDE) measurements, in which we detect dissolved Bi, indicate that Bi dissolution in the electrolyte during charging/discharging is mitigated in Bi2S3/rGO electrode, compared to pristine Bi2S3

Nanofat lysate ameliorates pain and cartilage degradation of osteoarthritis through activation of TGF-β–Smad2/3 signaling of chondrocytes

Introduction: Nanofat is an effective cell therapy for osteoarthritis (OA). However, it has clinical limitations due to its short half-life. We developed Nanofat lysate (NFL) to overcome the defect of Nanofat and explore its anti-OA efficacy and mechanism.Methods: Monoiodoacetate (MIA) was employed to establish rat OA model. For pain assessment, paw withdrawal latency (PWL) and thermal withdrawal latency (TWL) were evaluated. Degeneration of cartilage was observed by histopathological and immunohistochemical examination. Primary chondrocytes were treated with TNF-α to establish the cellular model of OA. MTT, wound healing, and transwell assays were performed to assess effects of NFL on chondrocytes. RNA-seq, qPCR and Western blot assays were conducted to clarify the mechanism of NFL.Results and Discussion: The animal data showed that PWL and TWL values, Mankin’s and OARSI scorings, and the Col2 expression in cartilage were significantly improved in the NFL-treated OA rats. The cellular data showed that NFL significantly improved the proliferation, wound healing, and migration of chondrocytes. The molecular data showed that NFL significantly restored the TNF-α-altered anabolic markers (Sox9, Col2 and ACAN) and catabolic markers (IL6 and Mmp13). The RNA-seq identified that TGF-β-Smad2/3 signaling pathway mediated the efficacy of NFL, which was verified by qPCR and Western blot that NFL significantly restored the abnormal expressions of TGFβR2, phosphorylated-Smad2, phosphorylated-Smad2/3, Col2, Mmp13 and Mmp3. After long-term storage, NFL exerted similar effects as its fresh type, indicating its advantage of storability. In sum, NFL was developed as a new therapeutic approach and its anti-OA efficacy and mechanism that mediated by TGF-β-Smad2/3 signaling was determined for the first time. Besides, the storability of NFL provided a substantial advantage than other living cell-based therapies