Chinese Parents’ Perceptions of Critical Thinking and Its Pedagogy

As a result of China’s education borrowing many Western educational values, such as critical thinking, became known to Chinese education practitioners and parents. However, Chinese parents’ perceptions of such educational values have not been studied. Three research questions centered on understanding Chinese parents’ perceptions of critical thinking and the role of schooling in the development of critical thinking. The conceptual framework comprised the established conceptualization of critical thinking from the Western research tradition and Confucian ideas of critical thinking. Qualitative data were collected from interviews with 12 participants and were coded to find emergent themes. The research results suggested that Chinese parents’ perceptions of critical thinking was in line with its Western definition and research tradition. The findings also suggested that there is a lack of communication between most public schools and parents in terms of the national educational goals. The findings indicated that most Chinese parents were actively engaged in building a positive family environment with the self-reported strategies for critical-thinking development. Participants’ self-reported beliefs in the efficiency of those strategies were confirmed by the empirical research regarding the indirect influence of parental involvement on students’ development of critical thinking. The findings may contribute to positive social change by encouraging school administrators to improve their communication to build a stronger partnership between schools and parents in developing students into creative and critical thinkers (i.e., the national educational goal)

Antagonistic Actions of Juvenile Hormone and 20-Hydroxyecdysone Within the Ring Gland Determine Developmental Transitions in \u3cem\u3eDrosophila\u3c/em\u3e

In both vertebrates and insects, developmental transition from the juvenile stage to adulthood is regulated by steroid hormones. In insects, the steroid hormone, 20-hydroxyecdysone (20E), elicits metamorphosis, thus promoting this transition, while the sesquiterpenoid juvenile hormone (JH) antagonizes 20E signaling to prevent precocious metamorphosis during the larval stages. However, not much is known about the mechanisms involved in cross-talk between these two hormones. In this study, we discovered that in the ring gland (RG) of Drosophila larvae, JH and 20E control each other’s biosynthesis. JH induces expression of a Krüppel-like transcription factor gene Kr-h1 in the prothoracic gland (PG), a portion of the RG that produces the 20E precursor ecdysone. By reducing both steroidogenesis autoregulation and PG size, high levels of Kr-h1 in the PG inhibit ecdysteriod biosynthesis, thus maintaining juvenile status. JH biosynthesis is prevented by 20E in the corpus allatum, the other portion of the RG that produces JH, to ensure the occurrence of metamorphosis. Hence, antagonistic actions of JH and 20E within the RG determine developmental transitions in Drosophila. Our study proposes a mechanism of cross-talk between the two major hormones in the regulation of insect metamorphosis

Long‐Range Cationic Disordering Induces two Distinct Degradation Pathways in Co‐Free Ni‐Rich Layered Cathodes

Ni-rich layered oxides are one of the most attractive cathode materials in high-energy-density lithium-ion batteries, their degradation mechanisms are still not completely elucidated. Herein, we report a strong dependence of degradation pathways on the long-range cationic disordering of Co-free Ni-rich Li1−m(Ni0.94Al0.06)1+mO2 (NA). Interestingly, a disordered layered phase with lattice mismatch can be easily formed in the near-surface region of NA particles with very low cation disorder (NA-LCD, m≤0.06) over electrochemical cycling, while the layered structure is basically maintained in the core of particles forming a “core–shell” structure. Such surface reconstruction triggers a rapid capacity decay during the first 100 cycles between 2.7 and 4.3 V at 1 C or 3 C. On the contrary, the local lattice distortions are gradually accumulated throughout the whole NA particles with higher degrees of cation disorder (NA-HCD, 0.06≤m≤0.15) that lead to a slow capacity decay upon cycling

Constructing a Thin Disordered Self‐Protective Layer on the LiNiO₂ Primary Particles Against Oxygen Release

One of the major challenges facing the application of layered LiNiO2 (LNO) cathode materials is the oxygen release upon electrochemical cycling. Here it is shown that tailoring the provided lithium content during synthesis process can create a disordered layered Li1-xNi1+xO2 phase at the primary particle surface. The disordered surface, which serves as a self-protective layer to alleviate the oxygen loss, possesses the same layered rhombohedral structure (R m) as the inner core of primary particles of the Li1-xNi1+xO2 (x ≈ 0). With advanced synchrotron-based x-ray 3D imaging and spectroscopic techniques, a macroporous architecture within the agglomerates of LNO with ordered surface (LNO-OS) is revealed after only 40 cycles, concomitant with the reduction of nickel on the primary particle surface throughout the whole secondary particles. Such chemomechanical degradation accelerates the deterioration of LNO-OS cathodes. Comparably, there are only slight changes in the nickel valence state and interior architecture of LNO with a thin disordered surface layer (LNO-DS) after cycling, mainly arising from an improved robustness of the oxygen framework on the surface. More importantly, the disordered surface can suppress the detrimental H2 ⇋ H3 phase transition upon cycling compared to the ordered one

RAGE Mediates Accelerated Diabetic Vein Graft Atherosclerosis Induced by Combined Mechanical Stress and AGEs via Synergistic ERK Activation

Aims/Hypothesis: Diabetes with hypertension rapidly accelerates vascular disease, but the underlying mechanism remains unclear. We evaluated the hypothesis that the receptor of advanced glycation end products (RAGE) might mediate combined signals initiated by diabetes-related AGEs and hypertension-induced mechanical stress as a common molecular sensor. Methods: In vivo surgical vein grafts created by grafting vena cava segments from C57BL/6J mice into the common carotid arteries of streptozotocin (STZ)-treated and untreated isogenic mice for 4 and 8 weeks were analyzed using morphometric and immunohistochemical techniques. In vitro quiescent mouse vascular smooth muscle cells (VSMCs) with either knockdown or overexpression of RAGE were subjected to cyclic stretching with or without AGEs. Extracellular signalregulated kinase (ERK) phosphorylation and Ki-67 expression were investigated. Results: Significant increases in neointimal formation, AGE deposition, Ki-67 expression, and RAGE were observed in the vein grafts of STZ-induced diabetic mice. The highest levels of ERK phosphorylation and Ki-67 expression in VSMCs were induced by simultaneous stretch stress and AGE exposure. The synergistic activation of ERKs and Ki-67 in VSMCs was significantly inhibited by siRNA-RAGE treatment and enhanced by over-expression of RAGE. Conclusion: RAGE may mediate synergistically increased ERK activation and VSMC proliferation induced by mechanica

High-performance infrared photodetectors based on InAs/InAsSb/AlAsSb superlattice for 3.5 µm cutoff wavelength spectra

High-performance infrared p-i-n photodetectors based on InAs/InAsSb/AlAsSb superlattices on GaSb substrate have been demonstrated at 300K. These photodetectors exhibit 50% and 100% cut-off wavelength of ∼3.2 µm and ∼3.5 µm, respectively. Under -130 mV bias voltage, the device exhibits a peak responsivity of 0.56 A/W, corresponding to a quantum efficiency (QE) of 28%. The dark current density at 0 mV and -130 mV bias voltage are 8.17 × 10−2 A/cm2 and 5.02 × 10−1 A/cm2, respectively. The device exhibits a saturated dark current shot noise limited specific detectivity (D*) of 3.43 × 109 cm·Hz1/2/W (at a peak responsivity of 2.5 µm) under -130 mV of applied bias

Reduced expression of N-Myc downstream-regulated gene 2 in human thyroid cancer

<p>Abstract</p> <p>Background</p> <p><it>NDRG</it>2 (N-Myc downstream-regulated gene 2) was initially cloned in our laboratory. Previous results have shown that <it>NDRG</it>2 expressed differentially in normal and cancer tissues. Specifically, <it>NDRG</it>2 mRNA was down-regulated or undetectable in several human cancers, and over-expression of <it>NDRG</it>2 inhibited the proliferation of cancer cells. <it>NDRG</it>2 also exerts important functions in cell differentiation and tumor suppression. However, it remains unclear whether <it>NDRG</it>2 participates in carcinogenesis of the thyroid.</p> <p>Methods</p> <p>In this study, we investigated the expression profile of human <it>NDRG</it>2 in thyroid adenomas and carcinomas, by examining tissues from individuals with thyroid adenomas (n = 40) and carcinomas (n = 35), along with corresponding normal tissues. Immunohistochemistry, quantitative RT-PCR and western blot methods were utilized to determine both the protein and mRNA expression status of Ndrg2 and c-Myc.</p> <p>Results</p> <p>The immunostaining analysis revealed a decrease of Ndrg2 expression in thyroid carcinomas. When comparing adenomas or carcinomas with adjacent normal tissue from the same individual, the mRNA expression level of <it>NDRG</it>2 was significantly decreased in thyroid carcinoma tissues, while there was little difference in adenoma tissues. This differential expression was confirmed at the protein level by western blotting. However, there were no significant correlations of <it>NDRG</it>2 expression with gender, age, different histotypes of thyroid cancers or distant metastases.</p> <p>Conclusion</p> <p>Our data indicates that <it>NDRG</it>2 may participate in thyroid carcinogenesis. This finding provides novel insight into the important role of <it>NDRG2 </it>in the development of thyroid carcinomas. Future studies are needed to address whether the down-regulation of <it>NDRG</it>2 is a cause or a consequence of the progression from a normal thyroid to a carcinoma.</p

An Efficient Method for Mapping High-Resolution Global River Discharge Based on the Algorithms of Drainage Network Extraction

River discharge, which represents the accumulation of surface water flowing into rivers and ultimately into the ocean or other water bodies, may have great impacts on water quality and the living organisms in rivers. However, the global knowledge of river discharge is still poor and worth exploring. This study proposes an efficient method for mapping high-resolution global river discharge based on the algorithms of drainage network extraction. Using the existing global runoff map and digital elevation model (DEM) data as inputs, this method consists of three steps. First, the pixels of the runoff map and the DEM data are resampled into the same resolution (i.e., 0.01-degree). Second, the flow direction of each pixel of the DEM data (identified by the optimal flow path method used in drainage network extraction) is determined and then applied to the corresponding pixel of the runoff map. Third, the river discharge of each pixel of the runoff map is calculated by summing the runoffs of all the pixels in the upstream of this pixel, similar to the upslope area accumulation step in drainage network extraction. Finally, a 0.01-degree global map of the mean annual river discharge is obtained. Moreover, a 0.5-degree global map of the mean annual river discharge is produced to display the results with a more intuitive perception. Compared against the existing global river discharge databases, the 0.01-degree map is of a generally high accuracy for the selected river basins, especially for the Amazon River basin with the lowest relative error (RE) of 0.3% and the Yangtze River basin within the RE range of &plusmn;6.0%. However, it is noted that the results of the Congo and Zambezi River basins are not satisfactory, with RE values over 90%, and it is inferred that there may be some accuracy problems with the runoff map in these river basins

The Role of Accounting in the Use of Employee Options

The determinants of the dramatic increase in the use of employee stock options in the 1990s and the subsequent decline in their popularity have been the subject of intense debate. Some have argued and found evidence to support that the discretion granted to firms to avoid recognizing the fair value of options as an expense led to their overuse for employee compensation. Others have argued and found evidence that the market “sees through” the accounting treatment for options and values firms as though options were expensed at fair value, regardless of financial statement treatment. We revisit this issue with the benefit of post-SFAS 123R data and the addition of controls for key economic and labor market factors that prior research has shown to influence option grants. Our analysis focuses on non-executive options, as such grants comprise almost 90% of employee option grants. We follow Carter et al. (2007) in measuring firm-level propensity to avoid expense recognition (financial reporting concerns). We do not find an association between financial reporting concerns and employee option grants after controlling for the relevant economic/labor market factors. Our analysis of change in option use over 1995-2007 shows that changes in option grants are associated with corresponding changes in economic determinants. Finally an examination of change in option use subsequent to the mandatory adoption of SFAS 123R shows that firms with a higher level of reporting concerns prior to adoption experienced a comparable reduction in options relative to firms with a lower level of reporting concerns. Overall, the results suggest that the role of accounting in influencing employee option grants has likely been overstated, and the dead-weight economic costs from overuse of options appear to be less than widely perceived