Quantum Transport in a Nanosize Silicon-on-Insulator Metal-Oxide-Semiconductor

An approach is developed for the determination of the current flowing through a nanosize silicon-on-insulator (SOI) metal-oxide-semiconductor field-effect transistors (MOSFET). The quantum mechanical features of the electron transport are extracted from the numerical solution of the quantum Liouville equation in the Wigner function representation. Accounting for electron scattering due to ionized impurities, acoustic phonons and surface roughness at the Si/SiO2 interface, device characteristics are obtained as a function of a channel length. From the Wigner function distributions, the coexistence of the diffusive and the ballistic transport naturally emerges. It is shown that the scattering mechanisms tend to reduce the ballistic component of the transport. The ballistic component increases with decreasing the channel length.Comment: 21 pages, 8 figures, E-mail addresses: [email protected]

Nonperturbative confinement in quantum chromodynamics:III. Improved gluon propagator

An ansatz is introduced for the three‐gluon vertex that is consistent with the Slavnov–Taylor identity in Landau gauge. It is shown that the gluon has a confining infrared singularity; but there is also a tachyon, indicating an insufficiency either of quarkless QCD or at least of our approximation to it

Neuronal network dysfunction in a model for Kleefstra syndrome mediated by enhanced NMDAR signaling

Kleefstra syndrome (KS) is a neurodevelopmental disorder caused by mutations in the histone methyltransferase EHMT1. To study the impact of decreased EHMT1 function in human cells, we generated excitatory cortical neurons from induced pluripotent stem (iPS) cells derived from KS patients. Neuronal networks of patient-derived cells exhibit network bursting with a reduced rate, longer duration, and increased temporal irregularity compared to control networks. We show that these changes are mediated by upregulation of NMDA receptor (NMDAR) subunit 1 correlating with reduced deposition of the repressive H3K9me2 mark, the catalytic product of EHMT1, at the GRIN1 promoter. In mice EHMT1 deficiency leads to similar neuronal network impairments with increased NMDAR function. Finally, we rescue the KS patient-derived neuronal network phenotypes by pharmacological inhibition of NMDARs. Summarized, we demonstrate a direct link between EHMT1 deficiency and NMDAR hyperfunction in human neurons, providing a potential basis for more targeted therapeutic approaches for KS

ICESTARS : integrated circuit/EM simulation and design technologies for advanced radio systems-on-chip

ICESTARS solved a series of critical issues in the currently available infrastructure for the design and simulation of new and highly-complex Radio Frequency (RF) front ends operating beyond 10 and up to 100 GHz. Future RF designs demand an increasing blend of analog and digital functionalities. The super and extremely high frequency (SHF, 3-30GHz, and EHF, 30-300GHz) ranges will be used to accomplish future demands for higher capacity channels. With todays frequency bands of approximately 1 to 3 GHz it is impossible to realize extremely high data transfer rates. Only a new generation of CAD and EDA tools will ensure the realization of complex nanoscale designs. It necessitates both new modeling approaches and new mathematical solution procedures for differential equations with largely differing time scales, analysis of coupled systems of DAEs (circuit equations) and PDEs (Maxwell equations for electromagnetic couplings) plus numerical simulations with mixed analog and digital signals. In ICESTARS new techniques and mathematical models working in highly integrated environments were developed to resolve this dilemma. The ICESTARS research area covered the three domains of RF design: (1) time-domain techniques, (2) frequency-domain techniques, and (3) EM analysis and coupled EM circuit analysis. The ICESTARS consortium comprised two industrial partners (NXP Semiconductors, Infineon Technologies AG), two SMEs (Magwel, AWR-APLAC) and five universities (Upper Austria, Cologne, Oulu, Wuppertal, Aalto), involving mathematicians, electronic engineers, and software engineers

Familial Longevity Is Marked by Lower Diurnal Salivary Cortisol Levels: The Leiden Longevity Study

BACKGROUND: Reported findings are inconsistent whether hypothalamic-pituitary-adrenal (HPA) signaling becomes hyperactive with increasing age, resulting in increasing levels of cortisol. Our previous research strongly suggests that offspring from long-lived families are biologically younger. In this study we assessed whether these offspring have a lower HPA axis activity, as measured by lower levels of cortisol and higher cortisol feedback sensitivity. METHODS: Salivary cortisol levels were measured at four time points within the first hour upon awakening and at two time points in the evening in a cohort comprising 149 offspring and 154 partners from the Leiden Longevity Study. A dexamethasone suppression test was performed as a measure of cortisol feedback sensitivity. Age, gender and body mass index, smoking and disease history (type 2 diabetes and hypertension) were considered as possible confounding factors. RESULTS: Salivary cortisol secretion was lower in offspring compared to partners in the morning (Area Under the Curve = 15.6 versus 17.1 nmol/L, respectively; p = 0.048) and in the evening (Area Under the Curve = 3.32 versus 3.82 nmol/L, respectively; p = 0.024). Salivary cortisol levels were not different after dexamethasone (0.5 mg) suppression between offspring and partners (4.82 versus 5.26 nmol/L, respectively; p = 0.28). CONCLUSION: Offspring of nonagenarian siblings are marked by a lower HPA axis activity (reflected by lower diurnal salivary cortisol levels), but not by a difference in cortisol feedback sensitivity. Further in-depth studies aimed at characterizing the HPA axis in offspring and partners are needed

Homocysteine and Familial Longevity: The Leiden Longevity Study

Homocysteine concentrations are a read-out of methionine metabolism and have been related to changes in lifespan in animal models. In humans, high homocysteine concentrations are an important predictor of age related disease. We aimed to explore the association of homocysteine with familial longevity by testing whether homocysteine is lower in individuals that are genetically enriched for longevity. We measured concentrations of total homocysteine in 1907 subjects from the Leiden Longevity Study consisting of 1309 offspring of nonagenarian siblings, who are enriched with familial factors promoting longevity, and 598 partners thereof as population controls. We found that homocysteine was related to age, creatinine, folate, vitamin B levels and medical history of hypertension and stroke in both groups (all p<0.001). However, levels of homocysteine did not differ between offspring enriched for longevity and their partners, and no differences in the age-related rise in homocysteine levels were found between groups (p for interaction 0.63). The results suggest that homocysteine metabolism is not likely to predict familial longevity

Fibrodysplasia Ossificans Progressiva: what have we achieved and where are we now? follow-up to the 2015 Lorentz Workshop

Fibrodysplasia ossificans progressiva (FOP) is an ultra-rare progressive genetic disease effecting one in a million individuals. During their life, patients with FOP progressively develop bone in the soft tissues resulting in increasing immobility and early death. A mutation in the ACVR1 gene was identified as the causative mutation of FOP in 2006. After this, the pathophysiology of FOP has been further elucidated through the efforts of research groups worldwide. In 2015, a workshop was held to gather these groups and discuss the new challenges in FOP research. Here we present an overview and update on these topics