604 research outputs found
The correspondence between augmentations and rulings for Legendrian knots
We strengthen the link between holomorphic and generating-function invariants
of Legendrian knots by establishing a formula relating the number of
augmentations of a knot's contact homology to the complete ruling invariant of
Chekanov and Pushkar.Comment: v2: 10 pages, 3 figures; minor revisions, to appear in Pacific J.
Mat
Invariants of Legendrian Knots and Coherent Orientations
We provide a translation between Chekanov's combinatorial theory for
invariants of Legendrian knots in the standard contact R^3 and a relative
version of Eliashberg and Hofer's Contact Homology. We use this translation to
transport the idea of ``coherent orientations'' from the Contact Homology world
to Chekanov's combinatorial setting. As a result, we obtain a lifting of
Chekanov's differential graded algebra invariant to an algebra over Z[t,t^{-1}]
with a full Z grading.Comment: 32 pages, 17 figures; small technical corrections to proof of Thm 3.7
and example 4.
Critical Fidelity
Using a Wigner Lorentzian Random Matrix ensemble, we study the fidelity,
, of systems at the Anderson metal-insulator transition, subject to small
perturbations that preserve the criticality. We find that there are three decay
regimes as perturbation strength increases: the first two are associated with a
gaussian and an exponential decay respectively and can be described using
Linear Response Theory. For stronger perturbations decays algebraically
as , where is the correlation dimension of the
critical eigenstates.Comment: 4 pages, 3 figures. Revised and published in Phys. Rev. Let
Deaths from acute abdominal conditions and geographical access to surgical care in India: a nationally representative spatial analysis
Background Few population-based studies quantify mortality from surgical conditions and relate mortality to access
to surgical care in low-income and middle-income countries.
Methods We linked deaths from acute abdominal conditions within a nationally representative, population-based
mortality survey of 1·1 million households in India to nationally representative facility data. We calculated total and
age-standardised death rates for acute abdominal conditions. Using 4064 postal codes, we undertook a spatial
clustering analysis to compare geographical access to well-resourced government district hospitals (24 h surgical and
anaesthesia services, blood bank, critical care beds, basic laboratory, and radiology) in high-mortality or low-mortality
clusters from acute abdominal conditions.
Findings 923 (1·1%) of 86 806 study deaths at ages 0–69 years were identifi ed as deaths from acute abdominal
conditions, corresponding to 72 000 deaths nationally in 2010 in India. Most deaths occurred at home (71%) and in
rural areas (87%). Compared with 567 low-mortality geographical clusters, the 393 high-mortality clusters had a nine
times higher age-standardised acute abdominal mortality rate and signifi cantly greater distance to a well-resourced
hospital. The odds ratio (OR) of being a high-mortality cluster was 4·4 (99% CI 3·2–6·0) for living 50 km or more
from well-resourced district hospitals (rising to an OR of 16·1 [95% CI 7·9–32·8] for >100 km). No such relation was
seen for deaths from non-acute surgical conditions (ie, oral, breast, and uterine cancer).
Interpretation Improvements in human and physical resources at existing government hospitals are needed to reduce
deaths from acute abdominal conditions in India. Full access to well-resourced hospitals within 50 km by all of India’s
population could have avoided about 50 000 deaths from acute abdominal conditions, and probably more from other
emergency surgical conditions
VisANT 3.0: new modules for pathway visualization, editing, prediction and construction
With the integration of the KEGG and Predictome databases as well as two search engines for coexpressed genes/proteins using data sets obtained from the Stanford Microarray Database (SMD) and Gene Expression Omnibus (GEO) database, VisANT 3.0 supports exploratory pathway analysis, which includes multi-scale visualization of multiple pathways, editing and annotating pathways using a KEGG compatible visual notation and visualization of expression data in the context of pathways. Expression levels are represented either by color intensity or by nodes with an embedded expression profile. Multiple experiments can be navigated or animated. Known KEGG pathways can be enriched by querying either coexpressed components of known pathway members or proteins with known physical interactions. Predicted pathways for genes/proteins with unknown functions can be inferred from coexpression or physical interaction data. Pathways produced in VisANT can be saved as computer-readable XML format (VisML), graphic images or high-resolution Scalable Vector Graphics (SVG). Pathways in the format of VisML can be securely shared within an interested group or published online using a simple Web link. VisANT is freely available at http://visant.bu.edu
VisANT 3.0: new modules for pathway visualization, editing, prediction and construction
With the integration of the KEGG and Predictome databases as well as two search engines for coexpressed genes/proteins using data sets obtained from the Stanford Microarray Database (SMD) and Gene Expression Omnibus (GEO) database, VisANT 3.0 supports exploratory pathway analysis, which includes multi-scale visualization of multiple pathways, editing and annotating pathways using a KEGG compatible visual notation and visualization of expression data in the context of pathways. Expression levels are represented either by color intensity or by nodes with an embedded expression profile. Multiple experiments can be navigated or animated. Known KEGG pathways can be enriched by querying either coexpressed components of known pathway members or proteins with known physical interactions. Predicted pathways for genes/proteins with unknown functions can be inferred from coexpression or physical interaction data. Pathways produced in VisANT can be saved as computer-readable XML format (VisML), graphic images or high-resolution Scalable Vector Graphics (SVG). Pathways in the format of VisML can be securely shared within an interested group or published online using a simple Web link. VisANT is freely available at http://visant.bu.edu
The impact of population-based disease management services for selected chronic conditions: the Costs to Australian Private Insurance - Coaching Health (CAPICHe) study protocol
A genome-wide association study for diabetic nephropathy genes in African Americans
A genome-wide association study was performed using the Affymetrix 6.0 chip to identify genes associated with diabetic nephropathy in African Americans. Association analysis was performed adjusting for admixture in 965 type 2 diabetic African American patients with end-stage renal disease (ESRD) and in 1029 African Americans without type 2 diabetes or kidney disease as controls. The top 724 single nucleotide polymorphisms (SNPs) with evidence of association to diabetic nephropathy were then genotyped in a replication sample of an additional 709 type 2 diabetes-ESRD patients and 690 controls. SNPs with evidence of association in both the original and replication studies were tested in additional African American cohorts consisting of 1246 patients with type 2 diabetes without kidney disease and 1216 with non-diabetic ESRD to differentiate candidate loci for type 2 diabetes-ESRD, type 2 diabetes, and/or all-cause ESRD. Twenty-five SNPs were significantly associated with type 2 diabetes-ESRD in the genome-wide association and initial replication. Although genome-wide significance with type 2 diabetes was not found for any of these 25 SNPs, several genes, including RPS12, LIMK2, and SFI1 are strong candidates for diabetic nephropathy. A combined analysis of all 2890 patients with ESRD showed significant association SNPs in LIMK2 and SFI1 suggesting that they also contribute to all-cause ESRD. Thus, our results suggest that multiple loci underlie susceptibility to kidney disease in African Americans with type 2 diabetes and some may also contribute to all-cause ESRD
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