Founding quantum theory on the basis of consciousness

In the present work, quantum theory is founded on the framework of consciousness, in contrast to earlier suggestions that consciousness might be understood starting from quantum theory. The notion of streams of consciousness, usually restricted to conscious beings, is extended to the notion of a Universal/Global stream of conscious flow of ordered events. The streams of conscious events which we experience constitute sub-streams of the Universal stream. Our postulated ontological character of consciousness also consists of an operator which acts on a state of potential consciousness to create or modify the likelihoods for later events to occur and become part of the Universal conscious flow. A generalized process of measurement-perception is introduced, where the operation of consciousness brings into existence, from a state of potentiality, the event in consciousness. This is mathematically represented by (a) an operator acting on the state of potential-consciousness before an actual event arises in consciousness and (b) the reflecting of the result of this operation back onto the state of potential-consciousness for comparison in order for the event to arise in consciousness. Beginning from our postulated ontology that consciousness is primary and from the most elementary conscious contents, such as perception of periodic change and motion, quantum theory follows naturally as the description of the conscious experience.Comment: 41 pages, 3 figures. To be published in Foundations of Physics, Vol 36 (6) (June 2006), published online at http://dx.doi.org/10.1007/s10701-006-9049-

Spin-dependent (magneto)transport through a ring due to spin-orbit interaction

Electron transport through a one-dimensional ring connected with two external leads, in the presence of spin-orbit interaction (SOI) of strength \alpha and a perpendicular magnetic field is studied. Applying Griffith's boundary conditions we derive analytic expressions for the reflection and transmission coefficients of the corresponding one-electron scattering problem. We generalize earlier conductance results by Nitta et al. [Appl. Phys. Lett. 75, 695 (1999)] and investigate the influence of \alpha, temperature, and a weak magnetic field on the conductance. Varying \alpha and temperature changes the position of the minima and maxima of the magnetic-field dependent conductance, and it may even convert a maximum into a minimum and vice versa.Comment: 19 pages, 9 figure

Optoelectronic switching of addressable molecular crossbar junctions

This letter reports on the observation of optoelectronic switching in addressable molecular crossbar junctions fabricated using polymer stamp-printing method. The active medium in the junction is a molecular self-assembled monolayer softly sandwiched between gold electrodes. The molecular junctions are investigated through currentvoltage measurements at varied temperature (from 95 to 300 K) in high vacuum condition. The junctions show reversible optoelectronic switching with the highest on/off ratio of 3 orders of magnitude at 95 K. The switching behavior is independent of both optical wavelength and molecular structure, while it strongly depends on the temperature. Initial analysis indicates that the distinct binding nature of the molecule/electrode interfaces play a dominant role in the switching performance.Comment: 5 pages, 4 figures,original manuscript to be submitte

Integrative modeling identifies genetic ancestry-associated molecular correlates in human cancer

Cellular and molecular aberrations contribute to the disparity of human cancer incidence and etiology between ancestry groups. Multiomics profiling in The Cancer Genome Atlas (TCGA) allows for querying of the molecular underpinnings of ancestry-specific discrepancies in human cancer. Here, we provide a protocol for integrative associative analysis of ancestry with molecular correlates, including somatic mutations, DNA methylation, mRNA transcription, miRNA transcription, and pathway activity, using TCGA data. This protocol can be generalized to analyze other cancer cohorts and human diseases. For complete details on the use and execution of this protocol, please refer to Carrot-Zhang et al. (2020)

Measurements of 12C(→γ,pp) photon asymmetries for Eγ= 200–450 MeV

The 12C (→γ ,pp) reaction has been studied in the photon energy range 200-450 MeV at the Mainz microtron MAMI-C, where linearly polarised photons were energy-tagged using the Glasgow-Mainz Tagged Photon Spectrometer and protons were detected in the Crystal Ball detector. The photon asymmetry Σ has been measured over a wider Eγ range than previous measurements. The strongest asymmetries were found at low missing energies where direct emission of nucleon pairs is expected. Cuts on the difference in azimuthal angles of the two ejected protons increased the magnitude of the observed asymmetries. At low missing energies the Σ data exhibit a strong angular dependence, similar to deuteron photodisintegration

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

The Earth: Plasma Sources, Losses, and Transport Processes

This paper reviews the state of knowledge concerning the source of magnetospheric plasma at Earth. Source of plasma, its acceleration and transport throughout the system, its consequences on system dynamics, and its loss are all discussed. Both observational and modeling advances since the last time this subject was covered in detail (Hultqvist et al., Magnetospheric Plasma Sources and Losses, 1999) are addressed

A new strategy for enhancing imputation quality of rare variants from next-generation sequencing data via combining SNP and exome chip data

Background: Rare variants have gathered increasing attention as a possible alternative source of missing heritability. Since next generation sequencing technology is not yet cost-effective for large-scale genomic studies, a widely used alternative approach is imputation. However, the imputation approach may be limited by the low accuracy of the imputed rare variants. To improve imputation accuracy of rare variants, various approaches have been suggested, including increasing the sample size of the reference panel, using sequencing data from study-specific samples (i.e., specific populations), and using local reference panels by genotyping or sequencing a subset of study samples. While these approaches mainly utilize reference panels, imputation accuracy of rare variants can also be increased by using exome chips containing rare variants. The exome chip contains 250 K rare variants selected from the discovered variants of about 12,000 sequenced samples. If exome chip data are available for previously genotyped samples, the combined approach using a genotype panel of merged data, including exome chips and SNP chips, should increase the imputation accuracy of rare variants. Results: In this study, we describe a combined imputation which uses both exome chip and SNP chip data simultaneously as a genotype panel. The effectiveness and performance of the combined approach was demonstrated using a reference panel of 848 samples constructed using exome sequencing data from the T2D-GENES consortium and 5,349 sample genotype panels consisting of an exome chip and SNP chip. As a result, the combined approach increased imputation quality up to 11 %, and genomic coverage for rare variants up to 117.7 % (MAF < 1 %), compared to imputation using the SNP chip alone. Also, we investigated the systematic effect of reference panels on imputation quality using five reference panels and three genotype panels. The best performing approach was the combination of the study specific reference panel and the genotype panel of combined data. Conclusions: Our study demonstrates that combined datasets, including SNP chips and exome chips, enhances both the imputation quality and genomic coverage of rare variants

Loss-of-function mutations in UDP-Glucose 6-Dehydrogenase cause recessive developmental epileptic encephalopathy

Developmental epileptic encephalopathies are devastating disorders characterized by intractable epileptic seizures and developmental delay. Here, we report an allelic series of germline recessive mutations in UGDH in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia. UGDH encodes an oxidoreductase that converts UDP-glucose to UDP-glucuronic acid, a key component of specific proteoglycans and glycolipids. Consistent with being loss-of-function alleles, we show using patients’ primary fibroblasts and biochemical assays, that these mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not phenocopy the human disease. Our study defines UGDH as a key player for the production of extracellular matrix components that are essential for human brain development. Based on the incidence of variants observed, UGDH mutations are likely to be a frequent cause of recessive epileptic encephalopathy