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In the present study, we investigated the relationships among mothers' filial piety, mother-child discrepancy in perceived parental expectations, and children's academic achievement in 823 Chinese families. The results indicated that mothers' authoritarian filial piety hindered children's academic achievement, whereas reciprocal filial piety had no such effect. Compared to children whose reports of parental expectations were identical with their mothers, children whose reports were higher than their mothers had lower achievement. Mothers' reciprocal filial piety increased the odds of child-reported parental expectations that were lower than mother-reported parental expectations, while authoritarian filial piety increased the odds of child-reported parental expectations that were higher than mother-reported parental expectations. Furthermore, the indirect effect of authoritarian filial piety, via mother-child discrepancy, on academic achievement was significant. These findings highlight the importance of mothers' filial piety and mother-child discrepancy in perceived parental expectations in identifying culture-specific factors that influence academic achievement in China.

The achievement of dual-functional photocatalytic technology requires a photocatalyst with accelerated charge flow and purposeful active-site arrangement. In this study, we developed an oriented embedding strategy to induce ReS 2 growth at the S vacancy in twin-crystal Zn 0.5 Cd 0.5 S solid solution ( Sv -ZCS), obtaining an atomic-level heterostructure (ReS 2 / Sv -ZCS). The electronic structure calculations demonstrate that the charge density of the Zn atom around the S vacancy is higher than for other Zn atoms and the introduced S vacancy establishes a high-speed channel for electron transport via formed Zn-S-Re bonds at the interface between ReS 2 and Sv -ZCS. Photogenerated electrons and holes gathered on Re atoms and Sv -ZCS, respectively, which achieves spatial charge separation and separated arrangement for redox sites. As a result, the optimized ReS 2 / Sv -ZCS heterostructure possesses high efficiency of electron injection (2.6-fold) and charge separation (8.44-fold), as well as excellent conductivity capability (20.16-fold). The photocatalytic performance of the ReS 2 / Sv -ZCS composite exhibits highly improved dual-functional activity with simultaneous H 2 evolution and selective oxidation of benzyl alcohol. The reaction rate of benzaldehyde and H 2 evolution reaches 125 mmol g cat -1 h -1 and 159 mmol g cat -1 h -1 , which is the highest efficiency achieved so far for simultaneous coproduction of H 2 fuel and organic chemicals on ReS 2 -based composites. This work enriches the application of ReS 2 -modified composites in a dual-functional photoredox system and also gives insight into the role of defects in electronic structure modification and activity improvement.

Platelet-derived growth factor (PDGF) and transforming growth factor-β (TGF-β) signaling are required for hepatic stellate cell (HSC) activation under pathological conditions such as liver metastatic tumor growth. These two signaling pathways are functionally divergent; PDGF signaling promotes proliferation and migration of HSCs, and TGF-β induces transdifferentiation of quiescent HSCs into myofibroblasts. Although PDGF signaling is implicated in TGF-β-mediated epithelial mesenchymal transition of tumor cells, the role of PDGF receptors in TGF-β activation of HSCs has not been investigated. Here we report that PDGF receptor-α (PDGFR-α) is required for TGF-β signaling of cultured human HSCs although HSCs express both PDGF-α and -β receptors. PDGFR-α knockdown inhibits TGF-β-induced phosphorylation and nuclear accumulation of SMAD2 with no influence on AKT or ERK phosphorylation associated with noncanonical TGF-β signaling. PDGFR-α knockdown suppresses TGF-β receptor I (TβRI) but increases TβRII gene transcription. At the protein level, PDGFR-α is recruited to TβRI/TβRII complexes by TGF-β stimulation. PDGFR-α knockdown blocks TGF-β-mediated internalization of TβRII and induces accumulation of TβRII at the plasma membrane, thereby inhibiting TGF-β phosphorylation of SMAD2. Functionally, knockdown of PDGFR-α reduces paracrine effects of HSCs on colorectal cancer cell proliferation and migration in vitro. In mice and patients, colorectal cancer cell invasion of the liver induces upregulation of PDGFR-α of HSCs. In summary, our finding that PDGFR-α knockdown inhibits SMAD-dependent TGF-β signaling by repressing TβRI transcriptionally and blocking endocytosis of TGF-β receptors highlights a convergence of PDGF and TGF-β signaling for HSC activation and PDGFR-α as a therapeutic target for liver metastasis and other settings of HSC activation., (Copyright © 2014 the American Physiological Society.)