Matrix Product State for Higher-Order Tensor Compression and Classification

© 2017 IEEE. This paper introduces matrix product state (MPS) decomposition as a new and systematic method to compress multidimensional data represented by higher order tensors. It solves two major bottlenecks in tensor compression: computation and compression quality. Regardless of tensor order, MPS compresses tensors to matrices of moderate dimension, which can be used for classification. Mainly based on a successive sequence of singular value decompositions, MPS is quite simple to implement and arrives at the global optimal matrix, bypassing local alternating optimization, which is not only computationally expensive but cannot yield the global solution. Benchmark results show that MPS can achieve better classification performance with favorable computation cost compared to other tensor compression methods

Lasing oscillation in a three-dimensional photonic crystal nanocavity with a complete bandgap

We demonstrate lasing oscillation in a three-dimensional photonic crystal nanocavity. The laser is realized by coupling a cavity mode, which is localized in a complete photonic bandgap and exhibits the highest quality factor of ~38,500, with high-quality semiconductor quantum dots. We show a systematic change in the laser characteristics, including the threshold and the spontaneous emission coupling factor by controlling the crystal size, which consequently changes the strength of photon confinement in the third dimension. This opens up many interesting possibilities for realizing future ultimate light sources and three-dimensional integrated photonic circuits and for more fundamental studies of physics in the field of cavity quantum electrodynamics.Comment: 14 pages, 4 figure

Combinative effects of Thanh Hao Miet Giap Thang (sweetwormwood and tortoise shell decoction) ingredients on antioxidative activity in vitro

Background: Traditional formulae usually exhibit therapeutic effects through the combinations of different ingredients. The purpose of this study was to investigate in vitro anti-oxidative activity of Thanh Hao Miet Giap Thang (THMGT) (Sweet Wormwood and Tortoise Shell Decoction) formula and the interactions of its ingredients leading to the overall anti-oxidative effect.Materials and Methods: We prepared 31 combinations containing two to four of the five ingredients including Herba Artemisia apiacea L (HbA),Carapax Trionycis (Tryonix sinensis) (CT), Rhizoma Anemarrhenae (Anemarrhena asphodeloides) (RzA), Radix Rehmanniae (Rehmannia glutinosaLibosch) (RdR), Moutan Cortex (Paeonia suffruticosa) (MC). These  combinations were tested for anti-oxidative activity using DCFH-DA and DPPH assays on Hep G2 cells. We also analyzed changes in expression of genes involved in antioxidant defense system including Nuclear Factor Erythroid-Derived 2-Like 2 (NFE2L2), catalase (CAT), heme oxygenase-1 (HO-1), glutathione peroxidase (GPx), cytoplasmic superoxide dismutase (SOD1), mitochondrial superoxide dismutase (SOD2).Results: The complete formula and all combinations containing Moutan Cortex showed high antioxidant activity in both radical solution-basedchemical assay and cellular-based assay. On the contrary, Carapax Trionycis displayed inhibitory effect on the overall antioxidant activity whenpresent in a combination, an effect clearly emphasized in cellular-based assay. Hep G2 cells treated with the formula showed increased geneexpression of HO-1 and SOD2 while expression of CAT, SOD1, GPx was unchanged.Conclusion: Our results suggested that THMGT had anti-oxidative activity essentially through intrinsic reducing capacities and the overall activity ofthe formula resulted from enhancing and inhibiting interactions of  ingredients.Key words: Thanh Hao Miet Giap Thang, Sweet Wormwood and Tortoise Shell Decoction, antioxidant, traditional formulaAbbreviations: THMGT, Thanh Hao Miet Giap Thang; HbA, Herba Artemisia apiacea; CT, Carapax Tryonicis; RzA, Rhizoma Anemarrhenae; MC,Moutan Cortex; RdR, Radix Rehmanniae; ROS, Reactive oxygen species; NFE2L2, Nuclear Factor Erythroid-Derived 2-Like 2; CAT, catalase; GPx,glutathione peroxidase; SOD1, cytoplasmic superoxide dismutase; SOD2, mitochondrial superoxide dismutase; HO-1, heme oxygenase-1

Smc5/6 coordinates formation and resolution of joint molecules with chromosome morphology to ensure meiotic divisions

During meiosis, Structural Maintenance of Chromosome (SMC) complexes underpin two fundamental features of meiosis: homologous recombination and chromosome segregation. While meiotic functions of the cohesin and condensin complexes have been delineated, the role of the third SMC complex, Smc5/6, remains enigmatic. Here we identify specific, essential meiotic functions for the Smc5/6 complex in homologous recombination and the regulation of cohesin. We show that Smc5/6 is enriched at centromeres and cohesin-association sites where it regulates sister-chromatid cohesion and the timely removal of cohesin from chromosomal arms, respectively. Smc5/6 also localizes to recombination hotspots, where it promotes normal formation and resolution of a subset of joint-molecule intermediates. In this regard, Smc5/6 functions independently of the major crossover pathway defined by the MutLγ complex. Furthermore, we show that Smc5/6 is required for stable chromosomal localization of the XPF-family endonuclease, Mus81-Mms4Eme1. Our data suggest that the Smc5/6 complex is required for specific recombination and chromosomal processes throughout meiosis and that in its absence, attempts at cell division with unresolved joint molecules and residual cohesin lead to severe recombination-induced meiotic catastroph

GPER mediates the angiocrine actions induced by IGF1 through the HIF-1α/VEGF pathway in the breast tumor microenvironment

The G protein estrogen receptor GPER/GPR30 mediates estrogen action in breast cancer cells as well as in breast cancer-associated fibroblasts (CAFs), which are key components of microenvironment driving tumor progression. GPER is a transcriptional target of hypoxia inducible factor 1 alpha (HIF-1α) and activates VEGF expression and angiogenesis in hypoxic breast tumor microenvironment. Furthermore, IGF1/IGF1R signaling, which has angiogenic effects, has been shown to activate GPER in breast cancer cells. We analyzed gene expression data from published studies representing almost 5000 breast cancer patients to investigate whether GPER and IGF1 signaling establish an angiocrine gene signature in breast cancer patients. Next, we used GPER-positive but estrogen receptor (ER)-negative primary CAF cells derived from patient breast tumours and SKBR3 breast cancer cells to investigate the role of GPER in the regulation of VEGF expression and angiogenesis triggered by IGF1. We performed gene expression and promoter studies, western blotting and immunofluorescence analysis, gene silencing strategies and endothelial tube formation assays to evaluate the involvement of the HIF-1α/GPER/VEGF signaling in the biological responses to IGF1. We first determined that GPER is co-expressed with IGF1R and with the vessel marker CD34 in human breast tumors (n = 4972). Next, we determined that IGF1/IGF1R signaling engages the ERK1/2 and AKT transduction pathways to induce the expression of HIF-1α and its targets GPER and VEGF. We found that a functional cooperation between HIF-1α and GPER is essential for the transcriptional activation of VEGF induced by IGF1. Finally, using conditioned medium from CAFs and SKBR3 cells stimulated with IGF1, we established that HIF-1α and GPER are both required for VEGF-induced human vascular endothelial cell tube formation. These findings shed new light on the essential role played by GPER in IGF1/IGF1R signaling that induces breast tumor angiogenesis. Targeting the multifaceted interactions between cancer cells and tumor microenvironment involving both GPCRs and growth factor receptors has potential in future combination anticancer therapies

Cellular Radiosensitivity: How much better do we understand it?

Purpose: Ionizing radiation exposure gives rise to a variety of lesions in DNA that result in genetic instability and potentially tumorigenesis or cell death. Radiation extends its effects on DNA by direct interaction or by radiolysis of H2O that generates free radicals or aqueous electrons capable of interacting with and causing indirect damage to DNA. While the various lesions arising in DNA after radiation exposure can contribute to the mutagenising effects of this agent, the potentially most damaging lesion is the DNA double strand break (DSB) that contributes to genome instability and/or cell death. Thus in many cases failure to recognise and/or repair this lesion determines the radiosensitivity status of the cell. DNA repair mechanisms including homologous recombination (HR) and non-homologous end-joining (NHEJ) have evolved to protect cells against DNA DSB. Mutations in proteins that constitute these repair pathways are characterised by radiosensitivity and genome instability. Defects in a number of these proteins also give rise to genetic disorders that feature not only genetic instability but also immunodeficiency, cancer predisposition, neurodegeneration and other pathologies. Conclusions: In the past fifty years our understanding of the cellular response to radiation damage has advanced enormously with insight being gained from a wide range of approaches extending from more basic early studies to the sophisticated approaches used today. In this review we discuss our current understanding of the impact of radiation on the cell and the organism gained from the array of past and present studies and attempt to provide an explanation for what it is that determines the response to radiation

Brain structural concomitants of resting state heart rate variability in the young and old: evidence from two independent samples

Previous research has shown associations between brain structure and resting state high-frequency heart rate variability (HF-HRV). Age affects both brain structure and HF-HRV. Therefore we sought to examine the relationship between brain structure and HF-HRV as a function of age. Data from two independent studies were used for the present analysis. Study 1 included 19 older adults (10 male, age range 62-78 years) and 19 younger adults (12 male, age range 19-37). Study 2 included 23 older adults (13 males; age range 55-75) and 27 younger adults (19 males; age range 18-34). The rootmean- square of successive R-R-interval differences (RMSSD) from ECG recordings was used as timedomain measure of HF-HRV. MRI scans were performed on a 3.0-T Siemens Magnetom Trio scanner. Cortical reconstruction and volumetric segmentation were performed with the Freesurfer image analysis suite, including 12 regions as regions-of-interests (ROI). Zero-order and partial correlations were used to assess the correlation of RMSSD with cortical thickness in selected ROIs. Lateral orbitofrontal cortex (OFC) cortical thickness was significantly associated with RMSSD. Further, both studies, in line with previous research, showed correlations between RMSSD and anterior cingulate cortex (ACC) cortical thickness. Meta-analysis on adjusted correlation coefficients from individual studies confirmed an association of RMSSD with the left rostral ACC and the left lateral OFC. Future longitudinal studies are necessary to trace individual trajectories in the association of HRV and brain structure across aging

Thrombin-Fibrinogen In Vitro Flow Model of Thrombus Growth in Cerebral Aneurysms

Cerebral aneurysms are balloon-like structures that develop on weakened areas of cerebral artery walls, with a significant risk of rupture. Thrombi formation is closely associated with cerebral aneurysms and has been observed both before and after intervention, leading to a wide variability of outcomes in patients with the condition. The attempt to manage the outcomes has led to the development of various computational models of cerebral aneurysm thrombosis. In the current study, we developed a simplified thrombin-fibrinogen flow system, based on commercially available purified human-derived plasma proteins, which enables thrombus growth and tracking in an idealized cerebral aneurysm geometry. A three-dimensional printed geometry of an idealized cerebral aneurysm and parent vessel configuration was developed. An unexpected outcome was that this phantom-based flow model allowed us to track clot growth over a period of time, by using optical imaging to record the progression of the growing clot into the flow field. Image processing techniques were subsequently used to extract important quantitative metrics from the imaging dataset, such as end point intracranial thrombus volume. The model clearly demonstrates that clot formation, in cerebral aneurysms, is a complex interplay between mechanics and biochemistry. This system is beneficial for verifying computational models of cerebral aneurysm thrombosis, particularly those focusing on initial angiographic occlusion outcomes, and will also assist manufacturers in optimizing interventional device designs

Specific Inhibition of Phosphodiesterase-4B Results in Anxiolysis and Facilitates Memory Acquisition

Cognitive dysfunction is a core feature of dementia and a prominent feature in psychiatric disease. As non-redundant regulators of intracellular cAMP gradients, phosphodiesterases (PDE) mediate fundamental aspects of brain function relevant to learning, memory, and higher cognitive functions. Phosphodiesterase-4B (PDE4B) is an important phosphodiesterase in the hippocampal formation, is a major Disrupted in Schizophrenia 1 (DISC1) binding partner and is itself a risk gene for psychiatric illness. To define the effects of specific inhibition of the PDE4B subtype, we generated mice with a catalytic domain mutant form of PDE4B (Y358C) that has decreased ability to hydrolyze cAMP. Structural modelling predictions of decreased function and impaired binding with DISC1 were confirmed in cell assays. Phenotypic characterization of the PDE4BY358C mice revealed facilitated phosphorylation of CREB, decreased binding to DISC1, and upregulation of DISC1 and β-Arrestin in hippocampus and amygdala. In behavioural assays, PDE4BY358C mice displayed decreased anxiety and increased exploration, as well as cognitive enhancement across several tests of learning and memory, consistent with synaptic changes including enhanced long-term potentiation and impaired depotentiation ex vivo. PDE4BY358C mice also demonstrated enhanced neurogenesis. Contextual fear memory, though intact at 24 hours, was decreased at 7 days in PDE4BY358C mice, an effect replicated pharmacologically with a non-selective PDE4 inhibitor, implicating cAMP signalling by PDE4B in a very late phase of consolidation. No effect of the PDE4BY358C mutation was observed in the pre-pulse inhibition and forced swim tests. Our data establish specific inhibition of PDE4B as a promising therapeutic approach for disorders of cognition and anxiety, and a putative target for pathological fear memory