833 research outputs found
A Parallel Solver for Graph Laplacians
Problems from graph drawing, spectral clustering, network flow and graph
partitioning can all be expressed in terms of graph Laplacian matrices. There
are a variety of practical approaches to solving these problems in serial.
However, as problem sizes increase and single core speeds stagnate, parallelism
is essential to solve such problems quickly. We present an unsmoothed
aggregation multigrid method for solving graph Laplacians in a distributed
memory setting. We introduce new parallel aggregation and low degree
elimination algorithms targeted specifically at irregular degree graphs. These
algorithms are expressed in terms of sparse matrix-vector products using
generalized sum and product operations. This formulation is amenable to linear
algebra using arbitrary distributions and allows us to operate on a 2D sparse
matrix distribution, which is necessary for parallel scalability. Our solver
outperforms the natural parallel extension of the current state of the art in
an algorithmic comparison. We demonstrate scalability to 576 processes and
graphs with up to 1.7 billion edges.Comment: PASC '18, Code: https://github.com/ligmg/ligm
Surface critical behavior in fixed dimensions : Nonanalyticity of critical surface enhancement and massive field theory approach
The critical behavior of semi-infinite systems in fixed dimensions is
investigated theoretically. The appropriate extension of Parisi's massive field
theory approach is presented.Two-loop calculations and subsequent Pad\'e-Borel
analyses of surface critical exponents of the special and ordinary phase
transitions yield estimates in reasonable agreement with recent Monte Carlo
results. This includes the crossover exponent , for which we obtain
the values and , considerably
lower than the previous -expansion estimates.Comment: Latex with Revtex-Stylefiles, 4 page
Development and validation of a gene expression test to identify hard-to-heal chronic venous leg ulcers
Background: Chronic venous leg ulcers pose a significant burden to healthcare systems, and predicting wound healing is challenging. The aim of this study was to develop a genetic test to evaluate the propensity of a chronic ulcer to heal. Methods: Sequential refinement and testing of a gene expression signature was conducted using three distinct cohorts of human wound tissue. The expression of candidate genes was screened using a cohort of acute and chronic wound tissue and normal skin with quantitative transcript analysis. Genes showing significant expression differences were combined and examined, using receiver operating characteristic (ROC) curve analysis, in a controlled prospective study of patients with venous leg ulcers. A refined gene signature was evaluated using a prospective, blinded study of consecutive patients with venous ulcers. Results: The initial gene signature, comprising 25 genes, could identify the outcome (healing versus non‐healing) of chronic venous leg ulcers (area under the curve (AUC) 0·84, 95 per cent c.i. 0·73 to 0·94). Subsequent refinement resulted in a final 14‐gene signature (WD14), which performed equally well (AUC 0·88, 0·80 to 0·97). When examined in a prospective blinded study, the WD14 signature could also identify wounds likely to demonstrate signs of healing (AUC 0·73, 0·62 to 0·84). Conclusion: A gene signature can identify people with chronic venous leg ulcers that are unlikely to heal
Surface critical exponents at a uniaxial Lifshitz point
Using Monte Carlo techniques, the surface critical behaviour of
three-dimensional semi-infinite ANNNI models with different surface
orientations with respect to the axis of competing interactions is
investigated. Special attention is thereby paid to the surface criticality at
the bulk uniaxial Lifshitz point encountered in this model. The presented Monte
Carlo results show that the mean-field description of semi-infinite ANNNI
models is qualitatively correct. Lifshitz point surface critical exponents at
the ordinary transition are found to depend on the surface orientation. At the
special transition point, however, no clear dependency of the critical
exponents on the surface orientation is revealed. The values of the surface
critical exponents presented in this study are the first estimates available
beyond mean-field theory.Comment: 10 pages, 7 figures include
Increased expression of Psoriasin is correlated with poor prognosis of bladder transitional cell carcinoma by promoting invasion and proliferation
Psoriasin, otherwise known as S100A7, is a member of the S100 protein family. With the key function of binding calcium, it is able to regulate a range of cellular functions. Altered Psoriasin expression is associated with poor clinical outcomes in several solid cancers. The present study aimed to examine the implication of Psoriasin in bladder cancer (BC). Expression of Psoriasin was examined in BC cell lines using PCR. Immunohistochemical (IHC) staining of Psoriasin was performed on a bladder disease spectrum tissue array. Plasmids were constructed to effectively knockdown and overexpress Psoriasin in BC cells and further utilized for in vitro BC cellular function assays. Association between Psoriasin expression and survival of patients with BC was evaluated using Kaplan‑Meier survival analysis. Psoriasin was revealed to be expressed by both bladder epithelia and cancer cells as determined by IHC. Increased expression of Psoriasin was significantly correlated with a poor overall BC patient survival. Overexpression of Psoriasin in the EJ138 cell line increased cellular proliferation, adhesion and invasion, whereas knockdown exhibited the opposite effect on cellular functions in RT112 cells. Matrix metalloprotease (MMP)9 appeared to be the most affected of the three MMPs examined in these two BC cell lines. The analysis revealed a positive correlation in BC tumours between Psoriasin and MMP9. Overall, high Psoriasin expression was correlated with poor overall survival in BC patients and promoted invasiveness of BC cells via upregulation of MMPs. Psoriasin possesses certain prognostic and therapeutic potential in BC which requires further exploration
Calcium-binding protein S100P promotes tumor progression but enhances chemosensitivity in breast cancer
Background: Chemoresistance remains one of the obstacles to overcome in the treatment of breast cancer. S100 calcium-binding protein P (S100P) has been observed to be overexpressed in several cancers and has been associated with drug resistance, metastasis, and prognosis. However, the role of S100P in chemoresistance in breast cancer has not been thoroughly determined. Methods: Immunohistochemistry was used to evaluate the expression level of S100P protein in 22 pairs (pre-chemo and post-chemo) of breast cancer tissue from patients who underwent neoadjuvant chemotherapy. The influence of S100P on the biological behavior and chemosensitivity of breast cancer cells was then investigated. Results: The protein level of S100P in breast cancer tissue was significantly higher than in benign fibroadenoma (p<0.001). The S100P expression level was shown to be decreased by 46.55% after neoadjuvant chemotherapy (p=0.015). Subgroup analysis revealed that S100P reduction (57.58%) was mainly observed in the HER2+ tumors (p=0.027). Our in-vitro experiments showed that the knockdown of S100P suppressed the proliferation, adhesion, migration and invasion abilities of T47D and SK-BR-3 breast cancer cells. We further demonstrated that this knockdown increased the chemoresistance to paclitaxel and cisplatin in SK-BR-3 cells. We found that S100P exerted its function by activating NF-κB, CCND1 and Vimentin, but downregulating E-cadherin. Conclusions: S100P promotes the aggressive properties of breast cancer cells and may be considered as a promising therapeutic target. Moreover, S100P can be used to predict the therapeutic effect of chemotherapy in HER2+ breast cancer patients
A Scheme to Numerically Evolve Data for the Conformal Einstein Equation
This is the second paper in a series describing a numerical implementation of
the conformal Einstein equation. This paper deals with the technical details of
the numerical code used to perform numerical time evolutions from a "minimal"
set of data.
We outline the numerical construction of a complete set of data for our
equations from a minimal set of data. The second and the fourth order
discretisations, which are used for the construction of the complete data set
and for the numerical integration of the time evolution equations, are
described and their efficiencies are compared. By using the fourth order scheme
we reduce our computer resource requirements --- with respect to memory as well
as computation time --- by at least two orders of magnitude as compared to the
second order scheme.Comment: 20 pages, 12 figure
Boundary critical behaviour at -axial Lifshitz points: the special transition for the case of a surface plane parallel to the modulation axes
The critical behaviour of -dimensional semi-infinite systems with
-component order parameter is studied at an -axial bulk
Lifshitz point whose wave-vector instability is isotropic in an -dimensional
subspace of . Field-theoretic renormalization group methods are
utilised to examine the special surface transition in the case where the
potential modulation axes, with , are parallel to the surface.
The resulting scaling laws for the surface critical indices are given. The
surface critical exponent , the surface crossover exponent
and related ones are determined to first order in
\epsilon=4+\case{m}{2}-d. Unlike the bulk critical exponents and the surface
critical exponents of the ordinary transition, is -dependent already
at first order in . The \Or(\epsilon) term of is
found to vanish, which implies that the difference of and
the bulk exponent is of order .Comment: 21 pages, one figure included as eps file, uses IOP style file
Motilitätsstörungen des Ösophagus
Zusammenfassung: Motilitätsstörungen des Ösophagus umfassen ein heterogenes Spektrum von Erkrankungen. Primäre Fehlbildungen des Ösophagus sind heute zwar einer verbesserten chirurgischen und gastroenterologischen Therapie zugänglich, führen jedoch zu langfristig persistierender ösophagealer Dysmotilität. Die Achalasie resultiert aus einer gestörten Relaxation des gastroösophagealen Sphinkters. Systemische Erkrankungen können mit einer sekundären ösophagealen Motilitätsstörung einhergehen. Zahlreiche neuromuskuläre Erkrankungen mit viszeraler Manifestation zeigen eine ösophageale Beteiligung. Selten kann eine Aganglionose bis in den Ösophagus reichen. Die wachsende Gruppe der Myopathien schließt metabolische und mitochondriale Störungen ein, deren zunehmende Charakterisierung genetischer Defekte vereinzelt bereits therapeutische Ansätze eröffnet. Infektbedingte Ösophagitiden zeigen besonders bei immunkompromittierten Patienten eine schwere Störung der Motilität. Immunologisch vermittelte Entzündungsprozesse im und um den Ösophagus werden allmählich besser verstanden. Schließlich können seltene Tumoren und tumorartige Läsionen eine Dysmotilität des Ösophagus verursache
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