Using refined kano model and decision trees to discover learners’ needs for teaching videos

Multimedia Tools and Applications - With the advancement of technology and the spread of the COVID19 epidemic, learning can no longer only be done through face-to-face teaching. Numerous digital...     

Substrate temperature-controlled precursor reaction mechanism of PEALD-deposited MoOx thin films

Journal of Materials Science - Molybdenum oxide (MoOx) films had been grown by using plasma-enhanced atomic layer deposition (PEALD) with Mo(CO)6 precursor and O2 plasma reactant in a substrate...     

Transgenerational Effects of Di(2-Ethylhexyl) Phthalate on Anogenital Distance,Sperm Functions and DNA Methylation in Rat Offspring

Di(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer in the manufacture of polyvinylchloride plastics and has been associated with concerns regarding male reproductive toxicity. In this study, we hypothesized that maternal exposure to DEHP induces transgenerational inheritance of adult-onset adverse reproductive outcomes through the male germline in the F1, F2, and F3 generations of male offspring. Pregnant rats were treated with 5 or 500 mg of DEHP/kg/day through gavage from gestation day 0 to birth. The offspring body weight, anogenital distance (AGD), anogenital index (AGI), sperm count, motility, and DNA fragmentation index (DFI) were measured for all generations. Methyl-CpG binding domain sequencing was performed to analyze sperm DNA methylation status in the F3. DEHP exposure at 500 mg/kg affected AGD, AGI, sperm count, mean DFI, and %DFI in the F1; AGD, sperm count, and mean DFI in the F2; and AGD, AGI, mean DFI, and %DFI in the F3. DEHP exposure at 5 mg/kg affected AGD, AGI, sperm count, and %DFI in the F1; sperm count in the F2; and AGD and AGI in F3. Compared with the control group, 15 and 45 differentially hypermethylated genes were identified in the groups administered 5 mg/kg and 500 mg/kg DEHP, respectively. Moreover, 130 and 6 differentially hypomethylated genes were observed in the groups administered 5 mg/kg and 500 mg/kg DEHP. Overall, these results demonstrated that prenatal exposure to DEHP caused transgenerational epigenetic effects, which may explain the observed phenotypic changes in the male reproductive system.     

Latchup-free ESD protection design with complementary substrate-triggered SCR devices

The turn-on mechanism of silicon-controlled rectifier (SCR) devices is essentially a current triggering event. While a current is applied to the base or substrate of an SCR device, it can be quickly triggered on into its latching state. In this paper, latchup-free electrostatic discharge (ESD) protection circuits, which are combined with the substrate-triggered technique and an SCR device, are proposed. A complementary circuit style with the substrate-triggered SCR device is designed to discharge both the pad-to-V/sub SS/ and pad-to-V/sub DD/ ESD stresses. The novel complementary substrate-triggered SCR devices have the advantages of controllable switching voltage, adjustable holding voltage, faster turn-on speed, and compatible to general CMOS process without extra process modification such as the silicide-blocking mask and ESD implantation. The total holding voltage of the substrate-triggered SCR device can be linearly increased by adding the stacked diode string to avoid the transient-induced latchup issue in the ESD protection circuits. The on-chip ESD protection circuits designed with the proposed complementary substrate-triggered SCR devices and stacked diode string for the input/output pad and power pad have been successfully verified in a 0.25-/spl mu/m salicided CMOS process with the human body model (machine model) ESD level of /spl sim/7.25 kV (500 V) in a small layout area.     

Biases of Success Rate Differences Shown in Binomial Effect Size Displays.

The intent of a binomial effect size display (BESD) is to show "the [real-world] importance of [an] effect indexed by a correlation [r]" (R. Rosenthal, 1994, p. 242) by reexpressing this correlation as a success rate difference (SRD) (e.g., treatment group success rate - control group success rate). However, SRDs displayed in BESDs generally overestimate real-world SRDs implied by correlations of (a) dichotomous X and Y variables (φ coefficients), (b) dichotomous X and continuous Y variables (point-biserial coefficients [rphs]). and (c) continuous X and Y variables (rxys). Furthermore, overestimation biases are larger for rxys than for rphs. Differences in the sizes of biases linked to different correlations suggest that BESD SRDs reported for different correlations are not comparable. The stochastic difference index (N. Cliff, 1993: A. Vargha & H. D. Delaney, 2000) is recommended as an alternative to the BESD. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Fixed-order H∞ compensator design

A method is presented for the construction of fixed-order compensators to provide H_∞ norm constraint for linear control systems with exogenous disturbances. The method is based on the celebrated bounded-real lemma that predicates the H_∞ norm constraint via a Riccati inequality. The synthesis of fixed-order controllers whose dimensions are less than the order of a given plant, is demonstrated by a set of sufficient conditions along with a numerical algorithm.     

Effects of the glucocorticoid agonist, RU28362, and the antagonist RU486 on lung phosphatidylcholine and antioxidant enzyme development in the genetically obese Zucker rat

The biochemical maturation of the lung in late gestation and in the young animal is regulated by glucocorticoids. The present study was aimed at dissociating the different glucocorticoid receptor sites involved in these regulatory functions. The obese Zucker rat was selected as a model for this study as it exhibits hypersensitivity to glucocorticoid hormone action by virtue of its elevated receptor numbers and activity. Two synthetic steroid analogues were administered to obese animals; RU28362, a specific type II receptor agonist, and the type II antagonist RU486. RU28362 promoted a strong catabolic effect, which was associated with reduced food intake and the abolition of growth in the rats. The agonist, RU28362, attenuated developmental increases in antioxidant enzyme activities, and altered the growth of the tissue. At the age studied, development of the lung phosphatidylcholine (PC) system was almost complete, but RU28362 increased disaturated PC 16:0/16:0 concentrations by almost 2-fold, and altered the molecular composition of total pulmonary PC. RU486 attenuated the growth of the rats and reduced their food intake. Treatment with the type II antagonist attenuated lung growth and increased the activities of pulmonary copper zinc (Cu/Zn) and manganese (Mn) superoxide dismutases. RU486 had no effect on lung PC concentrations and molecular composition. The data suggest a role for type I glucocorticoid receptors in the regulation of the antioxidant enzyme system in the lung, as type II antagonism will channel endogenous glucocorticoid binding to the type I site. Type II receptor binding would appear to play a role in regulating the lung PC content.