Dielectric Breakdown in Chemical Vapor Deposited Hexagonal Boron Nitride

Insulating films are essential in multiple electronic devices because they can provide essential functionalities, such as capacitance effects and electrical fields. Two-dimensional (2D) layered materials have superb electronic, physical, chemical, thermal, and optical properties, and they can be effectively used to provide additional performances, such as flexibility and transparency. 2D layered insulators are called to be essential in future electronic devices, but their reliability, degradation kinetics, and dielectric breakdown (BD) process are still not understood. In this work, the dielectric breakdown process of multilayer hexagonal boron nitride (h-BN) is analyzed on the nanoscale and on the device level, and the experimental results are studied via theoretical models. It is found that under electrical stress, local charge accumulation and charge trapping/detrapping are the onset mechanisms for dielectric BD formation. By means of conductive atomic force microscopy, the BD event was triggered at several locations on the surface of different dielectrics (SiO2, HfO2, Al2O3, multilayer h-BN, and monolayer h-BN); BD-induced hillocks rapidly appeared on the surface of all of them when the BD was reached, except in monolayer h-BN. The high thermal conductivity of h-BN combined with the one-atom-thick nature are genuine factors contributing to heat dissipation at the BD spot, which avoids self-accelerated and thermally driven catastrophic BD. These results point to monolayer h-BN as a sublime dielectric in terms of reliability, which may have important implications in future digital electronic devices.Fil: Jiang, Lanlan. Soochow University; ChinaFil: Shi, Yuanyuan. Soochow University; China. University of Stanford; Estados UnidosFil: Hui, Fei. Soochow University; China. Massachusetts Institute of Technology; Estados UnidosFil: Tang, Kechao. University of Stanford; Estados UnidosFil: Wu, Qian. Soochow University; ChinaFil: Pan, Chengbin. Soochow University; ChinaFil: Jing, Xu. Soochow University; China. University of Texas at Austin; Estados UnidosFil: Uppal, Hasan. University of Manchester; Reino UnidoFil: Palumbo, Félix Roberto Mario. Comisión Nacional de Energía Atómica; Argentina. Universidad Tecnológica Nacional; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Lu, Guangyuan. Chinese Academy of Sciences; República de ChinaFil: Wu, Tianru. Chinese Academy of Sciences; República de ChinaFil: Wang, Haomin. Chinese Academy of Sciences; República de ChinaFil: Villena, Marco A.. Soochow University; ChinaFil: Xie, Xiaoming. Chinese Academy of Sciences; República de China. ShanghaiTech University; ChinaFil: McIntyre, Paul C.. University of Stanford; Estados UnidosFil: Lanza, Mario. Soochow University; Chin

A Role for Nanoparticles in Treating Traumatic Brain Injury

Traumatic brain injury (TBI) is one of the main causes of disability in children and young adults, as well as a significant concern for elderly individuals. Depending on the severity, TBI can have a long-term impact on the quality of life for survivors of all ages. The primary brain injury can result in severe disability or fatality, and secondary brain damage can increase the complexities in cellular, inflammatory, neurochemical, and metabolic changes in the brain, which can last decades post-injury. Thus, survival from a TBI is often accompanied by lifelong disabilities. Despite the significant morbidity, mortality, and economic loss, there are still no eective treatment options demonstrating an improved outcome in a large multi-center Phase III trial, which can be partially attributed to poor target engagement of delivered therapeutics. Thus, there is a significant unmet need to develop more eective delivery strategies to overcome the biological barriers that would otherwise inhibit transport of materials into the brain to prevent the secondary long-term damage associated with TBI. The complex pathology of TBI involving the blood-brain barrier (BBB) has limited the development of eective therapeutics and diagnostics. Therefore, it is of great importance to develop novel strategies to target the BBB. The leaky BBB caused by a TBI may provide opportunities for therapeutic delivery via nanoparticles (NP). The focus of this review is to provide a survey of NP-based strategies employed in preclinical models of TBI and to provide insights for improved NP based diagnostic or treatment approaches. Both passive and active delivery of various NPs for TBI are discussed. Finally, potential therapeutic targets where improved NP-mediated delivery could increase target engagement are identified with the overall goal of providing insight into open opportunities for NP researchers to begin research in TBI

Thalidomide-induced Teratogenesis : History and Mechanisms

Peer reviewedPublisher PD

Radiation damage effects on detectors and eletronic devices in harsh radiation environment

Radiation damage effects represent one of the limits for technologies to be used in harsh radiation environments as space, radiotherapy treatment, high-energy phisics colliders. Different technologies have known tolerances to different radiation fields and should be taken into account to avoid unexpected failures which may lead to unrecoverable damages to scientific missions or patient health

Studies on Pitting Corrosion of Al-Cu-Li Alloys Part III: Passivation Kinetics of AA2098-T851 Based on the Point Defect Model.

In this paper, the passivation kinetics of AA2098-T851 was investigated by a fundamental theoretical interpretation of experimental results based on the mixed potential model (MPM). The steady state passive layer formed on the AA2098-T851 in NaHCO3 solution in a CO2 atmosphere upon potentiostatic stepping in the anodic direction followed by stepping in the opposite direction was explored. Potentials were selected in a way that both anodic passive dissolution of the metal and hydrogen evolution reaction (HER) occur, thereby requiring the MPM for interpretation. Optimization of the MPM on the experimental electrochemical impedance spectroscopy (EIS) data measured after each potentiostatic step revealed the important role of the migration of Al interstitials in determining the kinetics of passive layer formation and dissolution. More importantly, it is shown that the inequalities of the kinetics of formation and dissolution of the passive layer as observed in opposite potential stepping directions lead to the irreversibility of the passivation process. Finally, by considering the Butler-Volmer (B-V) equation for the cathodic reaction (HER) in the MPM, and assuming the quantum mechanical tunneling of the charge carriers across the barrier layer of the passive film, it was shown that the HER was primarily controlled by the slow electrochemical discharge of protons at the barrier layer/solution (outer layer) interface

Reduction of leukocyte microvascular adherence and preservation of blood-brain barrier function by superoxide-lowering therapies in a piglet model of neonatal asphyxia

Background: Asphyxia is the most common cause of brain damage in newborns. Substantial evidence indicates that leukocyte recruitment in the cerebral vasculature during asphyxia contributes to this damage. We tested the hypothesis that superoxide radical (O2⋅_) promotes an acute post-asphyxial inflammatory response and blood-brain barrier (BBB) breakdown. We investigated the effects of removing O2⋅_ by superoxide dismutase (SOD) or C3, the cell-permeable SOD mimetic, in protecting against asphyxia-related leukocyte recruitment. We also tested the hypothesis that xanthine oxidase activity is one source of this radical.Methods: Anesthetized piglets were tracheostomized, ventilated, and equipped with closed cranial windows for the assessment of post-asphyxial rhodamine 6G-labeled leukocyte-endothelial adherence and microvascular permeability to sodium fluorescein in cortical venules. Asphyxia was induced by discontinuing ventilation. SOD and C3 were administered by cortical superfusion. The xanthine oxidase inhibitor oxypurinol was administered intravenously.Results: Leukocyte-venular adherence significantly increased during the initial 2 h of post-asphyxial reperfusion. BBB permeability was also elevated relative to non-asphyxial controls. Inhibition of O2⋅_ production by oxypurinol, or elimination of O2⋅_ by SOD or C3, significantly reduced rhodamine 6G-labeled leukocyte-endothelial adherence and improved BBB integrity, as measured by sodium fluorescein leak from cerebral microvessels.Conclusion: Using three different strategies to either prevent formation or enhance elimination of O2⋅_ during the post-asphyxial period, we saw both reduced leukocyte adherence and preserved BBB function with treatment. These findings suggest that agents which lower O2⋅_ in brain may be attractive new therapeutic interventions for the protection of the neonatal brain following asphyxia

Emerging insights into the genesis of cerebral ischaemia and stroke

Stroke is a global problem with increasing significance because of the ageing population. Except for age, hypertensionisbyfar themostimportantriskfactorfor stroke. Hypertensionpredisposes toanumberof intracerebral and extracerebral vascular lesions which may cause cerebrovascular events by different mechanisms. The high metabolic need and low energy reserve make the braiavery vulnerable to ischaemia. During the last decade a number of experimental studies - supported by PET studies in man - suggest the presence of a therapeutic window, i.e. the time during which the neurons can be saved. The penumbra is the zone surrounding the core of the infarct where the flow is decreased and the neurons are lethargic and may be electrically silent but still viable. The presumed role of calcium, excitatory amino acids, free radicals, platelet-activating factor, acidosis and brain temperature in the process of neuronal death is briefly reviewed.peer-reviewe

Electro-Magnetic Earthquake Bursts and Critical Rupture of Peroxy Bond Networks in Rocks

We propose a mechanism for the low frequency electromagnetic emissions and other electromagnetic phenomena which have been associated with earthquakes. The mechanism combines the critical earthquake concept and the concept of crust acting as a charging electric battery under increasing stress. The electric charges are released by activation of dormant charge carriers in the oxygen anion sublattice, called peroxy bonds or positive hole pairs (PHP), where a PHP represents an $O_3X/^{OO}\backslash YO_3$ with $X,Y = Si^{4+}, Al^{3+}...$, i.e. an $O^-$ in a matrix of $O^{2-}$ of silicates. We propose that PHP are activated by plastic deformations during the slow cooperative build-up of stress and the increasingly correlated damage culminating in a large ``critical'' earthquake. Recent laboratory experiments indeed show that stressed rocks form electric batteries which can release their charge when a conducting path closes the equivalent electric circuit. We conjecture that the intermittent and erratic occurrences of EM signals are a consequence of the progressive build-up of the battery charges in the Earth crust and their erratic release when crack networks are percolating throughout the stressed rock volumes, providing a conductive pathway for the battery currents to discharge. EM signals are thus expected close to the rupture, either slightly before or after, that is, when percolation is most favored.Comment: 17 pages with 3 figures, extended discussion with 1 added figure and 162 references. The new version provides both a synthesis of two theories and a review of the fiel