Electrical Measurement of the Direct Spin Hall Effect in Fe/In_xGa_{1-x}As Heterostructures

We report on an all-electrical measurement of the spin Hall effect in epitaxial Fe/In_{x}Ga_{1-x}As heterostructures with n-type channel doping (Si) and highly doped Schottky tunnel barriers. A transverse spin current generated by an ordinary charge current flowing in the In_{x}Ga_{1-x}As is detected by measuring the spin accumulation at the edges of the channel. The spin accumulation is identified through the observation of a Hanle effect in the Hall voltage measured by pairs of ferromagnetic contacts. We investigate the bias and temperature dependence of the resulting Hanle signal and determine the skew and side-jump contributions to the total spin Hall conductivity.Comment: 10 pages, submitted to Phys. Rev. Let

Spin Hall effect transistor

Spin transistors and spin Hall effects have been two separate leading directions of research in semiconductor spintronics which seeks new paradigms for information processing technologies. We have brought the two directions together to realize an all-semiconductor spin Hall effect transistor. Our scheme circumvents semiconductor-ferromagnet interface problems of the original Datta-Das spin transistor concept and demonstrates the utility of the spin Hall effects in microelectronics. The devices use diffusive transport and operate without electrical current, i.e., without Joule heating in the active part of the transistor. We demonstrate a spin AND logic function in a semiconductor channel with two gates. Our experimental study is complemented by numerical Monte Carlo simulations of spin-diffusion through the transistor channel.Comment: 11 pages, 3 figure

Queer(ed) Monstrous Embodiment

A brief poetry collection that explores themes around dehumanized, queer embodiment, mental illness, and inter-generational knowledges

House prices following Covid-19: A possible shift in demand?

Masteroppgave(MSc) in Master of Science in Business, Finance - Handelshøyskolen BI, 2022In this thesis, we study the house price growth in 2020 for different dwelling types and municipalities and compare it with its growth in 2015. The two years had one thing in common: both experienced a drop in the policy rate. We look at Oslo, and municipalities just outside Oslo, to see if there was a change in the geographical distribution in house price growth. We analyze how house prices have developed using a quantitative approach by studying the housing market between 2014 and 2021. Our research argues that there is an increased demand for detached houses in 2020 compared to 2015. Additionally, we discover that people have not moved out of Oslo, as analysts predicted, following the outbreak of Covid-19

Insulin down-regulates cardioprotective SUR2A in the heart-derived H9c2 cells:A possible explanation for some adverse effects of insulin therapy

Some recent studies associated insulin therapy with negative cardiovascular events and shorter lifespan. SUR2A, a KATP channel subunit, regulate cardioprotection and cardiac ageing. Here, we have tested whether glucose and insulin regulate expression of SUR2A/KATP channel subunits and resistance to metabolic stress in heart H9c2 cells. Absence of glucose in culture media decreased SUR2A mRNA, while mRNAs of Kir6.2, Kir6.1, SUR1 and IES SUR2B were increased. 2-deoxyglucose (50 mM) decreased mRNAs of SUR2A, SUR2B and SUR1, did not affect IES SUR2A and IES SUR2B mRNAs and increased Kir6.2 mRNA. No glucose and 2-deoxyglucose (50 mM) decreased resistance to an inhibitor of oxidative phosphorylation, DNP (10 mM). 50 mM glucose did not alter KATP channel subunits nor cellular resistance to DNP (10 mM). Insulin (20 ng/ml) in both physiological and high glucose (50 mM) down-regulated SUR2A while upregulating Kir6.1 and Kir6.2 (in high glucose only). Insulin (20 ng/ml) in physiological and high glucose decreased cell survival in DNP (10 mM). As opposed to Kir6.2, infection with SUR2A resulted in titre-dependent cytoprotection. We conclude that insulin decreases resistance to metabolic stress in H9c2 cells by decreasing SUR2A expression. Lower cardiac SUR2A levels underlie increased myocardial susceptibility to metabolic stress and shorter lifespan. Keywords: Insulin, Glucose, SUR2A, Hear

Design considerations for a hierarchical semantic compositional framework for medical natural language understanding

Medical natural language processing (NLP) systems are a key enabling technology for transforming Big Data from clinical report repositories to information used to support disease models and validate intervention methods. However, current medical NLP systems fall considerably short when faced with the task of logically interpreting clinical text. In this paper, we describe a framework inspired by mechanisms of human cognition in an attempt to jump the NLP performance curve. The design centers about a hierarchical semantic compositional model (HSCM) which provides an internal substrate for guiding the interpretation process. The paper describes insights from four key cognitive aspects including semantic memory, semantic composition, semantic activation, and hierarchical predictive coding. We discuss the design of a generative semantic model and an associated semantic parser used to transform a free-text sentence into a logical representation of its meaning. The paper discusses supportive and antagonistic arguments for the key features of the architecture as a long-term foundational framework

A non-cardiomyocyte autonomous mechanism of cardioprotection involving the SLO1 BK channel

Opening of BK-type Ca2+ activated K+ channels protects the heart against ischemia-reperfusion (IR) injury. However, the location of BK channels responsible for cardioprotection is debated. Herein we confirmed that openers of the SLO1 BK channel, NS1619 and NS11021, were protective in a mouse perfused heart model of IR injury. As anticipated, deletion of the Slo1 gene blocked this protection. However, in an isolated cardiomyocyte model of IR injury, protection by NS1619 and NS11021 was insensitive to Slo1 deletion. These data suggest that protection in intact hearts occurs by a non-cardiomyocyte autonomous, SLO1-dependent, mechanism. In this regard, an in-situ assay of intrinsic cardiac neuronal function (tachycardic response to nicotine) revealed that NS1619 preserved cardiac neurons following IR injury. Furthermore, blockade of synaptic transmission by hexamethonium suppressed cardioprotection by NS1619 in intact hearts. These results suggest that opening SLO1 protects the heart during IR injury, via a mechanism that involves intrinsic cardiac neurons. Cardiac neuronal ion channels may be useful therapeutic targets for eliciting cardioprotection

Expanding the Circle: Essays in Honor of Joan E. Hemenway

Reviewed by Sandee Yarlott

Uncoupling protein-1 (UCP1) contributes to the basal proton conductance of brown adipose tissue mitochondria

Proton leak pathways uncouple substrate oxidation from ATP synthesis in mitochondria. These pathways are classified as basal (not regulated) or inducible (activated and inhibited). Previously it was found that over half of the basal proton conductance of muscle mitochondria was catalyzed by the adenine nucleotide translocase (ANT), an abundant mitochondrial anion carrier protein. To determine whether ANT is the unique protein catalyst, or one of many proteins that catalyze basal proton conductance, we measured proton leak kinetics in mitochondria isolated from brown adipose tissue (BAT). BAT can express another mitochondrial anion carrier, UCP1, at concentrations similar to ANT. Basal proton conductance was measured under conditions where UCP1 and ANT were catalytically inactive and was found to be lower in mitochondria from UCP1 knockout mice compared to wild-type. Ablation of another abundant inner membrane protein, nicotinamide nucleotide transhydrogenase, had no effect on proton leak kinetics in mitochondria from liver, kidney or muscle, showing that basal proton conductance is not catalyzed by all membrane proteins. We identify UCP1 as a second protein propagating basal proton leak, lending support to the hypothesis that basal leak pathways are perpetrated by members of the mitochondrial anion carrier family but not by other mitochondrial inner membrane proteins