Lattice four-dimensional N=4 SYM is practical

We show that nonperturbative lattice studies of four-dimensional N=4 Super-Yang-Mills are within reach. We use Ginsparg-Wilson fermions to avoid gluino masses and an exact implementation of the (chiral) $R$-symmetry, which greatly limits the number of counterterms that must be fine-tuned. Only bosonic operators require fine tuning, so all tunings can be done ``offline'' by a Ferrenberg-Swendsen type reweighting. We show what measurables can be used to perform the tuning.Comment: 4 page

Lightweight XML-based query, integration and visualization of distributed, multimodality brain imaging data

A need of many neuroimaging researchers is to integrate multimodality brain data that may be stored in separate databases. To address this need we have developed a framework that provides a uniform XML-based query interface across multiple online data sources. The development of this framework is driven by the need to integrate neurosurgical and neuroimaging data related to language. The data sources for the language studies are 1) a web-accessible relational database of neurosurgical cortical stimulation mapping data (CSM) that includes patient-specific 3-D coordinates of each stimulation site mapped to an MRI reconstruction of the patient brain surface; and 2) an XML database of fMRI and structural MRI data and analysis results, created automatically by a batch program we have embedded in SPM. To make these sources available for querying each is wrapped as an XML view embedded in a web service. A top level web application accepts distributed XQueries over the sources, which are dispatched to the underlying web services. Returned results can be displayed as XML, HTML, CSV (Excel format), a 2-D schematic of a parcellated brain, or a 3-D brain visualization. In the latter case the CSM patient-specific coordinates returned by the query are sent to a transformation web-service for conversion to normalized space, after which they are sent to our 3-D visualization program MindSeer, which is accessed via Java WebStart through a generated link. The anatomical distribution of pooled CSM sites can then be visualized using various surfaces derived from brain atlases. As this framework is further developed and generalized we believe it will have appeal for researchers who wish to query, integrate and visualize results across their own databases as well as those of collaborators

RIPK1 is a critical modulator of both tonic and TLR-responsive inflammatory and cell death pathways in human macrophage differentiation

In this study, we took advantage of human-induced pluripotent stem cells (hiPSC) and CRISPR/Cas9 technology to investigate the potential roles of RIPK1 in regulating hematopoiesis and macrophage differentiation, proinflammatory activation, and cell death pathways. Knock-out of RIPK1 in hiPSCs demonstrated that this protein is not required for erythro-myeloid differentiation. Using a well-established macrophage differentiation protocol, knock-out of RIPK1 did not block the differentiation of iPSC-derived macrophages, which displayed a similar phenotype to WT hiPSC-derived macrophages. However, knock-out of RIPK1 leads to a TNFα-dependent apoptotic death of differentiated hiPSC-derived macrophages (iPS-MΦ) and progressive loss of iPS-MΦ production irrespective of external pro-inflammatory stimuli. Live video analysis demonstrated that TLR3/4 activation of RIPK1 KO hiPSC-derived macrophages triggered TRIF and RIPK3-dependent necroptosis irrespective of caspase-8 activation. In contrast, TLR3/4 activation of WT macrophages-induced necroptosis only when caspases were inhibited, confirming the modulating effect of RIPK1 on RIPK3-mediated necroptosis through the FADD, Caspase-8 pathway. Activation of these inflammatory pathways required RIPK3 kinase activity while RIPK1 was dispensable. However, loss of RIPK1 sensitizes macrophages to activate RIPK3 in response to inflammatory stimuli, thereby exacerbating a potentially pathological inflammatory response. Taken together, these results reveal that RIPK1 has an important role in regulating the potent inflammatory pathways in authentic human macrophages that are poised to respond to external stimuli. Consequently, RIPK1 activity might be a valid target in the development of novel therapies for chronic inflammatory diseases.España, MINECO/FEDER SAF2015-64171

3D N = 1 SYM Chern-Simons theory on the Lattice

We present a method to implement 3-dimensional N = 1 SUSY Yang-Mills theory (a theory with two real supercharges containing gauge fields and an adjoint Majorana fermion) on the lattice, including a way to implement the Chern-Simons term present in this theory. At nonzero Chern-Simons number our implementation suffers from a sign problem which will make the numerical effort grow exponentially with volume. We also show that the theory with vanishing Chern-Simons number is anomalous; its partition function identically vanishes.Comment: v2, minor changes: expanded discussion in section III c, typos corrected, 17 pages, 9 figure

Three Dimensional N=2 Supersymmetry on the Lattice

We show how 3-dimensional, N=2 supersymmetric theories, including super QCD with matter fields, can be put on the lattice with existing techniques, in a way which will recover supersymmetry in the small lattice spacing limit. Residual supersymmetry breaking effects are suppressed in the small lattice spacing limit by at least one power of the lattice spacing a.Comment: 21 pages, 2 figures, typo corrected, reference adde

Crossover from single-file to fickian diffusion in carbon nanotubes and nanotube bundles: pure components and mixtures

The diffusion mechanism of pure component Ar and binary mixtures of Ar/Kr and Ar/Ne confined in single-walled carbon nanotubes (SWNTs) and bundles was investigated by a combined Grand Canonical Monte Carlo and molecular dynamics study. For Ar confined in SWNTs, a crossover from single-file to Fickian diffusion existed when the density of Ar was a minimum as a function of the SWNT diameter. Argon diffused by a single-file mechanism in SWNTs smaller than an accessible diameter of 1.76σAr, corresponding to (7,7), (12,0) and (8,6) SWNTs but by a Fickian mechanism for SWNTs larger in diameter. Both components in Ar/Kr mixtures had a single-file diffusional mechanism in (6,6) and (7,7) SWNTs and a Fickain mechanism for SWNTs larger in diameter. Likewise, both components in a Ar/Ne mixtures had a single-file diffusional mechanism in a (6,6) CNT, and Ar had a single-file diffusional mechanism in a (7,7) SWCNT. However, Ne in the Ar/Ne mixture exhibited Fickian diffusion in the (7,7) SWNT , which indicated bi-modal diffusion. Larger diameters of SWNTs provided Fickian diffusion for both components in an Ar/Ne mixture. Argon diffused in a (25,0) SWNT bundle (with a bimodal pore size distribution) in a bimodal mechanism, with Ar diffusing in single-file in interstitial sites and in a Fickian mechanism in inner nanotube channels. In all cases of single-file diffusion the mean-squared displacement (MSD) of the fluid molecules had a square root of time dependence, while molecules diffusing by a Fickian mechanism had a MSD with a linear time dependence

Abnormal mineralization of the Ts65Dn Down syndrome mouse appendicular skeleton begins during embryonic development in a Dyrk1a-independent manner

The relationship between gene dosage imbalance and phenotypes associated with Trisomy 21, including the etiology of abnormal bone phenotypes linked to Down syndrome (DS), is not well understood. The Ts65Dn mouse model for DS exhibits appendicular skeletal defects during adolescence and adulthood but the developmental and genetic origin of these phenotypes remains unclear. It is hypothesized that the postnatal Ts65Dn skeletal phenotype originates during embryonic development and results from an increased Dyrk1a gene copy number, a gene hypothesized to play a critical role in many DS phenotypes. Ts65Dn embryos exhibit a lower percent bone volume in the E17.5 femur when compared to euploid embryos. Concomitant with gene copy number, qPCR analysis revealed a  ~1.5 fold increase in Dyrk1a transcript levels in the Ts65Dn E17.5 embryonic femur as compared to euploid. Returning Dyrk1a copy number to euploid levels in Ts65Dn, Dyrk1a+/− embryos did not correct the trisomic skeletal phenotype but did return Dyrk1a gene transcript levels to normal. The size and protein expression patterns of the cartilage template during embryonic bone development appear to be unaffected at E14.5 and E17.5 in trisomic embryos. Taken together, these data suggest that the dosage imbalance of genes other than Dyrk1a is involved in the development of the prenatal bone phenotype in Ts65Dn embryos

Metabolomic analysis of prostate cancer risk in a prospective cohort: The alpha‐tocolpherol, beta‐carotene cancer prevention (ATBC) study

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/113106/1/ijc29576.pd