We report work progress on the growth of Si quantum dots in different matrices for future photovoltaic applications. The work reported here seeks to engineer a wide-bandgap silicon-based thin-film material by using quantum confinement in silicon quantum dots and to utilize this in complete thin-film silicon-based tandem cell, without the constraints of lattice matching, but which nonetheless gives an enhanced efficiency through the increased spectral collection efficiency. Coherent-sized quantum dots, dispersed in a matrix of silicon carbide, nitride, or oxide, were fabricated by precipitation of Si-rich material deposited by reactive sputtering or PECVD. Bandgap opening of Si QDs in nitride is more blue-shifted than that of Si QD in oxide, while clear evidence of quantum confinement in Si quantum dots in carbide was hard to obtain, probably due to many surface and defect states. The PL decay shows that the lifetimes vary from 10 to 70 microseconds for diameter of 3.4 nm dot with increasing detection wavelength.

SUMMARYCytokinins propagate signals via multiple phosphorelays in a mechanism similar to bacterial two-component systems. In Arabidopsis, signal outputs are determined by the activation state of transcription factors termed type-B Arabidopsis response regulators (ARRs); however, their regulatory mechanisms are largely unknown. In this study, we demonstrate that the proteolysis of ARR2, a type-B ARR, modulates cytokinin signaling outputs. ARR2-hemagglutinin (HA) is rapidly degraded by cytokinin treatment, but other type-B ARRs, such as ARR1-HA, ARR10-HA, ARR12-HA and ARR18-HA, are not. ARR2 degradation is mediated by the 26S proteasome pathway, and requires cytokinin-induced phosphorylation of Asp80 residue in the receiver domain. Through mutational analysis of amino acid residues in the receiver domain, we found that substitution of Lys90 with Gly inhibits ARR2 degradation. ARR2 K90G -HA in transgenic Arabidopsis conferred enhanced cytokinin sensitivity in various developmental processes, including primary root elongation, callus induction, leaf senescence and hypocotyl growth. ARR2 K90G -HA increased the expression of type-A ARRs, primary cytokinin-responsive genes and indicators of signaling output in two-component circuits. Expression of ARR2 K90G -HA from the native ARR2 promoter in the arr2-4 knock-out mutant also increased cytokinin sensitivity. In conclusion, ARR2 proteolysis is involved in the maintenance of the primary signaling output for normal developmental processes mediated by cytokinin in Arabidopsis.

OBJECTIVE Advances in neuroimaging techniques have led to the increased detection of asymptomatic intracranial meningiomas (IMs). Despite several studies on the natural history of IMs, a comprehensive evaluation method for estimating the growth potential of these tumors, based on the relative weight of each risk factor, has not been developed. The aim of this study was to develop a weighted scoring system that estimates the risk of rapid tumor growth to aid treatment decision making. METHODS The authors performed a retrospective analysis of 232 patients with presumed IM who had been prospectively followed up in the absence of treatment from 1997 to 2013. Tumor volume was measured by imaging at each follow-up visit, and the growth rate was determined by regression analysis. Predictors of rapid tumor growth (defined as ≥ 2 cm/year) were identified using a logistic regression model; each factor was awarded a score based on its own coefficient value. The probability (P) of rapid tumor growth was estimated using the following formula:[Formula: see text] RESULTS Fifty-nine tumors (25.4%) showed rapid growth. Tumor size (OR per cm 1.07, p = 0.000), absence of calcification (OR 3.87, p = 0.004), peritumoral edema (OR 2.74, p = 0.025), and hyperintense or isointense signal on T2-weighted MRI (OR 3.76, p = 0.049) were predictors of tumor growth rate. In the Asan Intracranial Meningioma Scoring System (AIMSS), tumor size was categorized into 3 groups of < 2.5 cm, ≥ 2.5 to < 4.0 cm, and ≥ 4.0 cm in diameter and awarded a score of 0, 3, and 6, respectively; the parameters of calcification and peritumoral edema were categorized into 2 groups based on their presence or absence and given a score of 0 or 2 and 1 or 0, respectively; and the signal on T2-weighted MRI was categorized into 2 groups of hypointense and hyperintense/isointense and given a score of 0 or 2, respectively. The risk of rapid tumor growth was estimated to be < 10% when the total score was 0-2, 10%-50% when the total score was 3-6, and ≥ 50% when the total score was 7-11 (Hosmer-Lemeshow goodness-of-fit test, p = 0.9958). The area under the receiver operating characteristic curve was 0.86. CONCLUSIONS The authors suggest a weighted scoring system (AIMSS) that predicts the specific probability of rapid tumor growth for patients with untreated IM. This scoring system will aid treatment decision making in clinical settings by screening out patients at high risk for rapid tumor growth.