Frustrated kinetic energy, the optical sum rule, and the mechanism of superconductivity

The theory that the change of the electronic kinetic energy in a direction perpendicular to the CuO-planes in high-temperature superconductors is a substantial fraction of the condensation energy is examined. It is argued that the consequences of this theory based on a rigorous $c$-axis conductivity sum rule are consistent with recent optical and penetration depth measurements.Comment: 4 pages (RevTeX) and 2 eps figure

Hybrid HVDC circuit breaker with self-powered gate drives

The ever increasing electric power demand and the advent of renewable energy sources have revived the interest in high-voltage direct current (HVDC) multi-terminal networks. However, the absence of a suitable circuit breaker or fault tolerant VSC station topologies with the required characteristics (such as operating speed) have, until recently, been an obstacle in the development of large scale multi-terminal networks for HVDC. This paper presents a hybrid HVDC circuit breaker concept which is capable of meeting the requirements of HVDC networks. Simulation results are presented which are validated by experimental results taken from a 2.5kV, 700A rated laboratory prototype

I Me Mine: on a Confusion Concerning the Subjective Character of Experience

In recent debates on phenomenal consciousness, a distinction is sometimes made, after Levine (2001) and Kriegel (2009), between the “qualitative character” of an experience, i.e. the specific way it feels to the subject (e.g. blueish or sweetish or pleasant), and its “subjective character”, i.e. the fact that there is anything at all that it feels like to her. I argue that much discussion of subjective character is affected by a conflation between three different notions. I start by disentangling the three notions in question, under the labels of “for-me-ness”, “me-ness” and “mineness”. Next, I argue that these notions are not equivalent; in particular, there is no conceptual implication from for-me-ness to me-ness or mineness. Empirical considerations based on clinical cases additionally suggest that the three notions may also correspond to different properties (although the claim of conceptual non-equivalence does not depend on this further point). The aim is clarificatory, cautionary but also critical: I examine four existing arguments from subjective character that are fuelled by an undifferentiated use of the three notions, and find them to be flawed for this reason

PTTG1 Attenuates Drug-Induced Cellular Senescence

As PTTG1 (pituitary tumor transforming gene) abundance correlates with adverse outcomes in cancer treatment, we determined mechanisms underlying this observation by assessing the role of PTTG1 in regulating cell response to anti-neoplastic drugs. HCT116 cells devoid of PTTG1 (PTTG1−/−) exhibited enhanced drug sensitivity as assessed by measuring BrdU incorporation in vitro. Apoptosis, mitosis catastrophe or DNA damage were not detected, but features of senescence were observed using low doses of doxorubicin and TSA. The number of drug-induced PTTG1−/− senescent cells increased ∼4 fold as compared to WT PTTG1-replete cells (p<0.001). p21, an important regulator of cell senescence, was induced ∼3 fold in HCT116 PTTG1−/− cells upon doxorubicin or Trichostatin A treatment. Binding of Sp1, p53 and p300 to the p21 promoter was enhanced in PTTG1−/− cells after treatment, suggesting transcriptional regulation of p21. p21 knock down abrogated the observed senescent effects of these drugs, indicating that PTTG1 likely suppresses p21 to regulate drug-induced senescence. PTTG1 also regulated SW620 colon cancer cells response to doxorubicin and TSA mediated by p21. Subcutaneously xenografted PTTG1−/− HCT116 cells developed smaller tumors and exhibited enhanced responses to doxorubicin. PTTG1−/− tumor tissue derived from excised tumors exhibited increased doxorubicin-induced senescence. As senescence is a determinant of cell responses to anti-neoplastic treatments, these findings suggest PTTG1 as a tumor cell marker to predict anti-neoplastic treatment outcomes

Genome-Wide Profiling of MicroRNAs in Adipose Mesenchymal Stem Cell Differentiation and Mouse Models of Obesity

In recent years, there has been accumulating evidence that microRNAs are key regulator molecules of gene expression. The cellular processes that are regulated by microRNAs include e.g. cell proliferation, programmed cell death and cell differentiation. Adipocyte differentiation is a highly regulated cellular process for which several important regulating factors have been discovered, but still not all are known to fully understand the underlying mechanisms. In the present study, we analyzed the expression of 597 microRNAs during the differentiation of mouse mesenchymal stem cells into terminally differentiated adipocytes by real-time RT-PCR. In total, 66 miRNAs were differentially expressed in mesenchymal stem cell-derived adipocytes compared to the undifferentiated progenitor cells. To further study the regulation of these 66 miRNAs in white adipose tissue in vivo and their dependence on PPARγ activity, mouse models of genetically or diet induced obesity as well as a mouse line expressing a dominant negative PPARγ mutant were employed

A bibliometric study of human–computer interaction research activity in the Nordic-Baltic Eight countries

Human–computer interaction (HCI) has become an important area for designers and developers worldwide, and research activities set in national cultural contexts addressing local challenges are often needed in industry and academia. This study explored HCI research in the Nordic-Baltic countries using bibliometric methods. The results show that the activity varies greatly across the region with activities dominated by Finland, Sweden, and Denmark, even when adjusting for differences in population size and GDP. Research output variations were larger for the top-tier conferences compared to entry-tier conferences and journals. Locally hosted conferences were associated with local increases in research activity. HCI research longevity appears to be an indicator of research maturity and quantity. HCI researchers typically collaborated either with colleagues within the same institution or with researchers from countries outside the Nordic-Baltic region such as US and the UK. There was less collaboration between national and Nordic-Baltic partners. Collaboration appeared especially prevalent for top-tier conference papers. Top-tier conference papers were also more frequently cited than regional-tier and entry-tier conferences, yet journal articles were cited the most. One implication of this study is that the HCI research activity gaps across the Nordic-Baltic countries should be narrowed by increasing the activity in countries with low research outputs. To achieve this, first-time authors could receive guidance through collaborations with experienced authors in the same institution or other labs around the world. More conferences could also be hosted locally. Furthermore, journals may be more effective than conferences if the goal is to accumulate citations.publishedVersio

Active and poised promoter states drive folding of the extended HoxB locus in mouse embryonic stem cells

Gene expression states influence the three-dimensional conformation of the genome through poorly understood mechanisms. Here, we investigate the conformation of the murine HoxB locus, a gene-dense genomic region containing closely spaced genes with distinct activation states in mouse embryonic stem (ES) cells. To predict possible folding scenarios, we performed computer simulations of polymer models informed with different chromatin occupancy features, which define promoter activation states or CTCF binding sites. Single cell imaging of the locus folding was performed to test model predictions. While CTCF occupancy alone fails to predict the in vivo folding at genomic length scale of 10 kb, we found that homotypic interactions between active and Polycomb-repressed promoters co-occurring in the same DNA fibre fully explain the HoxB folding patterns imaged in single cells. We identify state-dependent promoter interactions as major drivers of chromatin folding in gene-dense regions

p73: A Multifunctional Protein in Neurobiology

p73, a transcription factor of the p53 family, plays a key role in many biological processes including neuronal development. Indeed, mice deficient for both TAp73 and ΔNp73 isoforms display neuronal pathologies, including hydrocephalus and hippocampal dysgenesis, with defects in the CA1-CA3 pyramidal cell layers and the dentate gyrus. TAp73 expression increases in parallel with neuronal differentiation and its ectopic expression induces neurite outgrowth and expression of neuronal markers in neuroblastoma cell lines and neural stem cells, suggesting that it has a pro-differentiation role. In contrast, ΔNp73 shows a survival function in mature cortical neurons as selective ΔNp73 null mice have reduced cortical thickness. Recent evidence has also suggested that p73 isoforms are deregulated in neurodegenerative pathologies such as Alzheimer’s disease, with abnormal tau phosphorylation. Thus, in addition to its increasingly accepted contribution to tumorigenesis, the p73 subfamily also plays a role in neuronal development and neurodegeneration

Ultraconserved Elements in the Olig2 Promoter

. basal promoter and found that it represses expression in undifferentiated embryonic stem cells. expression during development