Abstract Chiral aminosulfonamides containing imidazolium group were used as ligands for the ruthenium(II)-catalyzed asymmetric transfer hydrogenation of prochiral ketones in ionic liquid, affording good to excellent conversions and enantiomeric excesses. The catalytic system could be easily recovered and reused several times.
Lead selenide (PbSe) is a candidate for harvesting infrared (IR) light, due to its narrow and controllable optical band gap which can be tuned by its grain size. However, there is still a challenge to assemble a photoelectrode with different cations of selenide and sulphide sensitizers, such as PbSe and cadmium sulphide (CdS), onto the same skeleton by a wet chemical route. In this work, we provide a chemical vapor deposition (CVD) method to assemble a PbSe and CdS nanoparticle (NP) co-sensitized nitrogen (N)-doped TiO2 nanorod array (PbSe/CdS/NT) photoelectrode. This hybrid photoanode showed an increased photoelectrochemical (PEC) performance under simulated sun light irradiation. Electrochemical analysis revealed that a presumable cascade structure of band-edge levels, in this photoanode, could be attributed to the enhanced photocurrent. In addition, the carrier multiplication in PbSe NPs via impact ionization, was also suggested to contribute to both the photo and dark current.
Recently, we have reported the self-assembly of nanobelts and microbelts originating from the organic–inorganic hybrid molecule hexakis-(4-(5-phenyl-1,3,4-oxazodiazol-2-yl)-phenoxy)-cyclotriphosphazene (HPCP) by a simple solution method. Inspired by [2 + 2] photodimerization, our group has further attempted to verify the proposed self-assembly mechanism of oxadiazole-containing cyclotriphosphazene by solid-state photochemical reaction. We modified the molecular structure of HPCP, introducing a vinyl group into it to obtain a new oxadiazole-containing cyclotriphosphazene, hexakis-(4-(5-styryl-1,3,4-oxazodiazol-2-yl)-phenoxy)-cyclotriphosphazene (HSCP). The microbelts and flower-like particles of HSCP were self-assembled through a simple solvent exchange process by exploiting the π–π interactions between neighboring HSCP molecules as the driving force. The as-prepared materials were capable of [2 + 2] photodimerization and shape maintenance, as well as forming insoluble fluorescent materials. The self-aggregating and photoreaction properties of HSCP were characterized by UV-vis, FESEM, TEM, 1H-NMR, etc.
Abstract Organic electrode materials (OEMs) featuring high abundance, structural designability, and eco‐friendliness, are considered promising candidates for rechargeable metal‐ion batteries. Nevertheless, the realization of efficient metal‐ion batteries based on OEMs is plagued by the poor intrinsic electronic conductivity and low insolubility of OEMs in common organic electrolytes. Herein, we present a systematic discussion of advancements in the design of OEMs from the perspective of molecular engineering and microstructure modulation, aiming at tuning the electrochemical, physical, and chemical properties of OEMs. Additionally, we elucidate the reaction mechanism of regulation strategies and provide new design directions for OEMs. This review offers essential concepts and perspectives on the development of advanced OEMs for rechargeable batteries.
Our previous study showed that miR-29 attenuates muscle wasting in chronic kidney disease. Other studies found that miR-29 has anti-fibrosis activity. We hypothesized that intramuscular injection of exosome-encapsulated miR-29 would counteract unilateral ureteral obstruction (UUO)-induced muscle wasting and renal fibrosis. We used an engineered exosome vector, which contains an exosomal membrane protein gene Lamp2b that was fused with the targeting peptide RVG (rabies viral glycoprotein peptide). RVG directs exosomes to organs that express the acetylcholine receptor, such as kidney. The intervention of Exo/miR29 increased muscle cross-sectional area and decreased UUO-induced upregulation of TRIM63/MuRF1 and FBXO32/atrogin-1. Interestingly, renal fibrosis was partially depressed in the UUO mice with intramuscular injection of Exo/miR29. This was confirmed by decreased TGF-β, alpha-smooth muscle actin, fibronectin, and collagen 1A1 in the kidney of UUO mice. When we used fluorescently labeled Exo/miR29 to trace the Exo/miR route in vivo and found that fluorescence was visible in un-injected muscle and in kidneys. We found that miR-29 directly inhibits YY1 and TGF-β3, which provided a possible mechanism for inhibition of muscle atrophy and renal fibrosis by Exo/miR29. We conclude that Exo/miR29 ameliorates skeletal muscle atrophy and attenuates kidney fibrosis by downregulating YY1 and TGF-β pathway proteins. Our previous study showed that miR-29 attenuates muscle wasting in chronic kidney disease. Other studies found that miR-29 has anti-fibrosis activity. We hypothesized that intramuscular injection of exosome-encapsulated miR-29 would counteract unilateral ureteral obstruction (UUO)-induced muscle wasting and renal fibrosis. We used an engineered exosome vector, which contains an exosomal membrane protein gene Lamp2b that was fused with the targeting peptide RVG (rabies viral glycoprotein peptide). RVG directs exosomes to organs that express the acetylcholine receptor, such as kidney. The intervention of Exo/miR29 increased muscle cross-sectional area and decreased UUO-induced upregulation of TRIM63/MuRF1 and FBXO32/atrogin-1. Interestingly, renal fibrosis was partially depressed in the UUO mice with intramuscular injection of Exo/miR29. This was confirmed by decreased TGF-β, alpha-smooth muscle actin, fibronectin, and collagen 1A1 in the kidney of UUO mice. When we used fluorescently labeled Exo/miR29 to trace the Exo/miR route in vivo and found that fluorescence was visible in un-injected muscle and in kidneys. We found that miR-29 directly inhibits YY1 and TGF-β3, which provided a possible mechanism for inhibition of muscle atrophy and renal fibrosis by Exo/miR29. We conclude that Exo/miR29 ameliorates skeletal muscle atrophy and attenuates kidney fibrosis by downregulating YY1 and TGF-β pathway proteins.
AIM:To observe the regional distributions and morphological features of nesfatin-1/nucleobindin-2 (NUCB2) immunoreactive (IR) cells in the rodent digestive system. METHODS:Paraffin-embedded sections of seven organs (pancreas, stomach, duodenum, esophagus, liver, small intestine and colon) dissected from sprague-dawley (SD) rats and institute of Cancer Research (ICR) mice were prepared.The regional distributions of nesfatin-1/NUCB2 IR cells were observed by immunohistochemical staining.The morphological features of the nesfatin-1/NUCB2 IR cells were evaluated by hematoxylin and eosin (HE) staining.Fresh tissues of the seven organs were prepared for Western blotting to analyze the relative protein levels of NUCB2 in each organ. RESULTS:Immunohistochemical staining showed that the nesfatin-1/NUCB2 IR cells were localized in the central part of the pancreatic islets, the lower third and middle portion of the gastric mucosal gland, and the submucous layer of the duodenum in SD rats and ICR mice.HE staining revealed that the morphological features of nesfatin-1/NUCB2 IR cells were mainly islet cells in the pancreas, endocrine cells in the stomach, and Brunner's glands in the duodenum.Western blotting revealed that NUCB2 protein expression was higher in the pancreas, stomach and duodenum than in the esophagus, liver, small intestine and colon (P = 0.000). CONCLUSION:Nesfatin-1/NUCB2 IR cells are expressed in the pancreas, stomach and duodenum in rodents.These cells may play an important role in the physiological regulation of carbohydrate metabolism, gastrointestinal function and nutrient absorption.
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