CdPbS quantum dots-sensitized TiO2 photoelectrode was prepared using chemical bath codeposition technique by dipping TiO2 film into a 0.5 M Cd(NO3)2-Pb(NO3)2 solution (molar ratio 9:1) and a 0.5 M Na2S methanol solution. The CdPbS quantum dots have the size about 4 to 6 nm and distribute homogeneously in the TiO2 film. The as-prepared electrode showed improved absorption spectra. The assembled quantum dots-sensitized solar cell (QDSSC) yielded a power conversion efficiency (nu) of 1.88% and a short-circuit current of 15.28 mA/cm2 under AM 1.5 illumination of 100 mW/cm2, far outperformed the single PbS, CdS QDSSC and the nu increased 49.2% than coupled PbS/CdS QDSSC. The solar cell presented IPCE peak value of 45.7% and the effective photovoltaic range covers the visible region and near infrared region.
Fragile X syndrome (FXS) is the leading inherited form of intellectual disability and the most common known cause of autism spectrum disorders. FXS patients exhibit severe syndromic features and behavioral alterations, including anxiety, hyperactivity, impulsivity, and aggression, in addition to cognitive impairment and seizures. At present, there are no effective treatments or cures for FXS. Previously, we have found the divergence of BDNF-TrkB signaling trajectories is associated with spine defects in early postnatal developmental stages of Fmr1 KO mice. Here, young fragile X mice were intraperitoneal injection of 7,8-Dihydroxy avone (7,8-DHF), which is a high a nity tropomyosin receptor kinase B (TrkB) agonist. 7,8-DHF ameliorated morphological abnormities in dendritic spine and synaptic structure, and rescued synaptic and hippocampus-dependent cognitive dysfunction in young FXS mice. These observed improvement of 7,8-DHF involved decreased protein levels of BDNF, p-TrkB Y816 , p-PLCγ, and p-CaMKII in the hippocampus. In addition, 7,8-DHF intervention in primary hippocampal neurons increased p-TrkB Y816 through activating the PLCγ1-CaMKII signaling pathway leading to improvement of neuronal morphology.This study is the rst to account for early life synaptic impairments, neuronal morphological and cognitive delays in FXS in response to the abnormal BDNF-TrkB pathway. Present studies provide novel evidences about the effective early intervention in FXS mice at developmental stages as a strategy to produce powerful impacts on neural development, synaptic plasticity and behaviors.
Both rosiglitazone and metformin have effects on blood glucose regulation and the proliferation of liver cancer cells. Combination therapy with these two drugs is common and effective for the treatment of diabetes in the clinic, however, the application of these two drugs is influenced by the poor dissolution of rosiglitazone and the gastrointestinal side-effect of metformin resulting from a high solubility. The formation of a multidrug crystal form (Rsg-Met) by a solvent evaporation method can solve the solubility issue. Crystal structure data and intramolecular hydrogen bonds were detected by X-ray diffraction and infrared spectroscopy. Surprisingly, Rsg-Met shortens the time spent in solubility equilibrium and multiplies the dissolution rate of Rsg. Finally, we found that a low concentration of Rsg-Met enhanced the proliferation inhibition effect on liver cancer cells (HepG2, SK-hep1) compared with rosiglitazone, without affecting the human normal cell line LO2.
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