Electrical Breakdown Behaviors in Microgaps

The study of electrical breakdown behaviors in microgaps has drawn intensive attention around the world due to the miniaturization of electronic devices that allows electronic circuits to be packaged more densely, making possible compact computers, advanced radar and navigation systems, and other devices that use very large numbers of components. Therefore, a clear understanding of the electrical breakdown behaviors in microgaps is required to avoid the dielectric breakdown or to trigger the breakdown at microscale. This chapter introduces the significance of understanding breakdown characterization and reliability assessment for electrostatically actuated devices, magnetic recording devices, photomasks, RF MEMS switches, and micromachines and points out the derivation of the classical Paschen’s law at microscale. Then it summarizes the state-of-the-art research work on the methodology, influencing factors, dynamics, and physical mechanisms of electrical breakdown in microgaps, which is expected to expand the general knowledge of electrical breakdown to the microscale regime or more and benefits the reliability assessment and ESD protection of microscale and nanoscale devices

PON2 Deficiency Leads to Increased Susceptibility to Diet-Induced Obesity.

(1) Background: Paraoxonase 2 (PON2) is a ubiquitously expressed protein localized to endoplasmic reticulum and mitochondria. Previous studies have shown that PON2 exhibits anti-oxidant and anti-inflammatory functions, and PON2-deficient (PON2-def) mice are more susceptible to atherosclerosis. Furthermore, PON2 deficiency leads to impaired mitochondrial function. (2) Methods: In this study, we examined the susceptibility of PON2-def mice to diet-induced obesity. (3) Results: After feeding of an obesifying diet, the PON2-def mice exhibited significantly increased body weight due to increased fat mass weight as compared to the wild-type (WT) mice. The increased adiposity was due, in part, to increased adipocyte hypertrophy. PON2-def mice had increased fasting insulin levels and impaired glucose tolerance after diet-induced obesity. PON2-def mice had decreased oxygen consumption and energy expenditure. Furthermore, the oxygen consumption rate of subcutaneous fat pads from PON2-def mice was lower compared to WT mice. Gene expression analysis of the subcutaneous fat pads revealed decreased expression levels of markers for beige adipocytes in PON2-def mice. (4) Conclusions: We concluded that altered systemic energy balance, perhaps due to decreased beige adipocytes and mitochondrial dysfunction in white adipose tissue of PON2-def mice, leads to increased obesity in these mice

METHODS TO IMPROVE LIGNIN’S REACTIVITY AS A PHENOL SUBSTITUTE AND AS REPLACEMENT FOR OTHER PHENOLIC COMPOUNDS: A BRIEF REVIEW

Lignin is readily available as a by-product from the pulp and paper industry. It is considered to be a promising substitute for phenol in phenol-formaldehyde (PF) resin synthesis, given the increasing concerns of the shortage of fossil resources and the environmental impact from petroleum-based products. One hurdle that prevents the commercial utilization of lignin is its low reactivity due to its chemical structure. Many efforts have been made to improve its reactivity by modification and/or depolymerization of lignin molecules. Methylolation and phenolation are the two most studied modification approaches aimed at introducing reactive functional groups to lignin molecules. Modified lignin from these two methods could partially replace phenol in PF resin synthesis. Demethylation of lignin could effectively increase the reactivity of lignin by forming catechol moieties in the lignin macromolecule. Other methods, including reduction, oxidation, and hydrolysis, have also been studied to improve the reactivity of lignin as well as to produce phenolic compounds from lignin. Most current methods of lignin modification are not economically attractive. One can expect that efforts will be continued, aimed at improving the utilization of lignin for value-added products

Survival and self-renewing capacity of breast cancer initiating cells during fractionated radiation treatment

Abstract Introduction Recent data indicate a hierarchical organization of many solid cancers, including breast cancer, with a small number of cancer initiating cells (CICs) that have the ability to self-renew and exhibit multi-lineage potency. We, and others, have demonstrated that CICs in breast cancer and glioma are relatively resistant to ionizing radiation if compared to their non-tumorigenic counterparts. However, the extent of the remaining self-renewing capacity of CICs after fractions of radiation is currently unknown. We hypothesized that CICs, in contrast to their non-tumorigenic counterparts, not only survive fractions of ionizing radiation but also retain the CIC phenotype as defined by operational means. Methods We used two marker systems to identify breast CICs (CD24-/low/CD44high, or lack of proteasome activity) and performed sphere-forming assays after multiple clinical fractions of radiation. Lineage tracking was performed by membrane staining. Cell cycle distribution and RNA content were assessed by flow cytometry and senescence was assessed via β-galactosidase staining. Results We demonstrated that irradiated CICs survived and retained their self-renewal capacity for at least four generations. We show that fractionated radiation not only spared CICs but also mobilized them from a quiescent/G0 phase of the cell cycle into actively cycling cells, while the surviving non-tumorigenic cells were driven into senescence. Conclusions The breast CIC population retains increased self-renewal capacity over several generations and therefore, we conclude that increases in the number of CICs after sublethal doses of radiation have potential clinical importance. Prevention of this process may lead to improved clinical outcome

Molecular dynamics simulations of thermal evaporation and critical electric field of copper nanotips

Due to the miniaturization of microelectromechanical systems, nanoelectromechanical systems and molecular devices, the problem of vacuum insulation becomes more and more prominent. The nanoscale thermal effects caused by electron emission and electric current Joule heat under high electric fields lead to gasification and migration of material in the device. In this work, a coupled molecular dynamics-electrodynamics method is used to simulate the thermal evaporation of nanotips under high electric field. Moreover, Cu nanotips with different initial geometries and different macroscopic electric fields are modelled. The deformation and damage mechanisms of nanotips under high electric field are discussed. Our simulations show that the aspect ratio of nanotips has a significant influence on the thermal evaporation of nanotips. The thermal runaway occurring in picosecond time-scale plays an important role for the initiation of the vacuum breakdown. An empirical relationship is obtained between the on-set breakdown time and the macroscopic electric field and the geometry of nanotips by analysing the numerical results.Peer reviewe

Two CYP82D Enzymes Function as Flavone Hydroxylases in the Biosynthesis of Root-Specific 4′-Deoxyflavones in Scutellaria baicalensis

Baicalein, wogonin, and their glycosides are major bioactive compounds found in the medicinal plant Scutellaria baicalensis Georgi. These flavones can induce apoptosis in a variety of cancer cell lines but have no effect on normal cells. Furthermore, they have many additional benefits for human health, such as anti-oxidant, antiviral, and liver-protective properties. Here, we report the isolation and characterization of two CYP450 enzymes, SbCYP82D1.1 and SbCYP82D2, which function as the flavone 6-hydroxylase (F6H) and flavone 8-hydroxylase (F8H), respectively, in S. baicalensis. SbCYP82D1.1 has broad substrate specificity for flavones such as chrysin and apigenin and is responsible for biosynthesis of baicalein and scutellarein in roots and aerial parts of S. baicalensis, respectively. When the expression of SbCYP82D1.1 is knocked down, baicalin and baicalein levels are reduced significantly while chrysin glycosides accumulate in hairy roots. SbCYP82D2 is an F8H with high substrate specificity, accepting only chrysin as its substrate to produce norwogonin, although minor 6-hydroxylation activity can also be detected. Phylogenetic analysis suggested that SbCYP82D2 might have evolved from SbCYP82D1.1 via gene duplication followed by neofunctionalization, whereby the ancestral F6H activity is partially retained in the derived SbCYP82D2. We report the characterization of two CYP450 enzymes, which 6- and 8-hydroxylate chrysin to form the 4′-deoxyflavone bioactives in roots of Scutellaria baicalensis. Like the main 4′-deoxyflavone enzymes, these decorating enzymes have evolved their functionalities by convergence with the more ubiquitous 4′-hydroxyflavone pathway enzymes. Key words: Scutellaria baicalensis; Huangqin; baicalein; wogonin; flavone 6-hydroxylase; flavone 8-hydroxylas

Trimethylamine-N-Oxide, a Metabolite Associated with Atherosclerosis, Exhibits Complex Genetic and Dietary Regulation

SummaryCirculating trimethylamine-N-oxide (TMAO) levels are strongly associated with atherosclerosis. We now examine genetic, dietary, and hormonal factors regulating TMAO levels. We demonstrate that two flavin mono-oxygenase family members, FMO1 and FMO3, oxidize trimethylamine (TMA), derived from gut flora metabolism of choline, to TMAO. Further, we show that FMO3 exhibits 10-fold higher specific activity than FMO1. FMO3 overexpression in mice significantly increases plasma TMAO levels while silencing FMO3 decreases TMAO levels. In both humans and mice, hepatic FMO3 expression is reduced in males compared to females. In mice, this reduction in FMO3 expression is due primarily to downregulation by androgens. FMO3 expression is induced by dietary bile acids by a mechanism that involves the farnesoid X receptor (FXR), a bile acid-activated nuclear receptor. Analysis of natural genetic variation among inbred strains of mice indicates that FMO3 and TMAO are significantly correlated, and TMAO levels explain 11% of the variation in atherosclerosis