Defect tolerance: fundamental limits and examples

This paper addresses the problem of adding redundancy to a collection of physical objects so that the overall system is more robust to failures. In contrast to its information counterpart, which can exploit parity to protect multiple information symbols from a single erasure, physical redundancy can only be realized through duplication and substitution of objects. We propose a bipartite graph model for designing defect-tolerant systems, in which the defective objects are replaced by the judiciously connected redundant objects. The fundamental limits of this model are characterized under various asymptotic settings and both asymptotic and finite-size systems that approach these limits are constructed. Among other results, we show that the simple modular redundancy is in general suboptimal. As we develop, this combinatorial problem of defect tolerant system design has a natural interpretation as one of graph coloring, and the analysis is significantly different from that traditionally used in information redundancy for error-control codes.©201

The Vehicle, Spring 1993

Table of Contents The Shape of Things to Come.Peter F. Essigpage 6 SaxophoneWalt Howardpage 6 Gravity BedSue Songerpage 7 UntitledJennifer Gutowskipage 8 uncertaintyWalt Howardpage 9 Ruth Ann, et. al.Susan Eisenhourpage 9 Failed IndustryScott Langenpage 10 UntitledKaren Wisspage 10 wanted:Walt Howardpage 10 Dida; 1978Diana Matijaspage 11 UntitledJennifer Gutowskipage 12 The Lesson in NovemberSue Songerpage 13 Coal MinerJames P. Tangpage 16 Christmas CrueltySue Songerpage 17 Astral ProjectionSusan Eisenhourpage 18 UntitledBen Hausmannpage 19 Into Zagreb\u27s Evening*Diana Matjaspage 20 UntitledJennifer Gutowskipage 22 The AnniversaryJennifer Moropage 23 NudeDan Trutterpage 24 death for saleWalt Howardpage 24 JudgedKevin St. Angelpage 25 Nature\u27s RefugeeScott Langenpage 25 Arrowhead Hunting at TippecanoeJennifer Moropage 26 UntitledKimberly Foxpage 27 TAINTED LOVESarah C. Patiencepage 28 cemeteryWalt Howardpage 28 Cow GameSusan Eisenhourpage 29 UntitledJennifer Gutowskipage 31 ReflectionsPeter F. Essigpage 32 Destination U.S.A.Dan Trutterpage 33 UntitledMario Letopage 33 Authors\u27 Pagepage 34https://thekeep.eiu.edu/vehicle/1061/thumbnail.jp

The Vehicle, Spring 1993

Table of Contents The Shape of Things to Come.Peter F. Essigpage 6 SaxophoneWalt Howardpage 6 Gravity BedSue Songerpage 7 UntitledJennifer Gutowskipage 8 uncertaintyWalt Howardpage 9 Ruth Ann, et. al.Susan Eisenhourpage 9 Failed IndustryScott Langenpage 10 UntitledKaren Wisspage 10 wanted:Walt Howardpage 10 Dida; 1978Diana Matijaspage 11 UntitledJennifer Gutowskipage 12 The Lesson in NovemberSue Songerpage 13 Coal MinerJames P. Tangpage 16 Christmas CrueltySue Songerpage 17 Astral ProjectionSusan Eisenhourpage 18 UntitledBen Hausmannpage 19 Into Zagreb\u27s Evening*Diana Matjaspage 20 UntitledJennifer Gutowskipage 22 The AnniversaryJennifer Moropage 23 NudeDan Trutterpage 24 death for saleWalt Howardpage 24 JudgedKevin St. Angelpage 25 Nature\u27s RefugeeScott Langenpage 25 Arrowhead Hunting at TippecanoeJennifer Moropage 26 UntitledKimberly Foxpage 27 TAINTED LOVESarah C. Patiencepage 28 cemeteryWalt Howardpage 28 Cow GameSusan Eisenhourpage 29 UntitledJennifer Gutowskipage 31 ReflectionsPeter F. Essigpage 32 Destination U.S.A.Dan Trutterpage 33 UntitledMario Letopage 33 Authors\u27 Pagepage 34https://thekeep.eiu.edu/vehicle/1061/thumbnail.jp

Falcipain Inhibitors Based on the Natural Product Gallinamide A Are Potent in Vitro and in Vivo Antimalarials

A library of analogues of the cyanobacterium-derived depsipeptide natural product gallinamide A were designed and prepared using a highly efficient and convergent synthetic route. Analogues were shown to exhibit potent inhibitory activity against the Plasmodium falciparum cysteine proteases falcipain 2 and falcipain 3 and against cultured chloroquine-sensitive (3D7) and chloroquine-resistant (W2) strains of P. falciparum. Three lead compounds were selected for evaluation of in vivo efficacy against Plasmodium berghei infection in mice on the basis of their improved blood, plasma, and microsomal stability profiles compared with the parent natural product. One of the lead analogues cured P. berghei-infected mice in the Peters 4 day-suppressive test when administered 25 mg kg–1 intraperitoneally daily for 4 days. The compound was also capable of clearing parasites in established infections at 50 mg kg–1 intraperitoneally daily for 4 days and exhibited moderate activity when administered as four oral doses of 100 mg kg–1.NHMR

BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations

Polycyclic Aromatic Hydrocarbons in Maternal and Umbilical Cord Blood from Pregnant Hispanic Women Living in Brownsville, Texas

Venous blood was drawn from 35 pregnant Hispanic women living in Brownsville, Texas, and matched cord blood was collected at birth. Gas chromatography/mass spectrometry was used to measure concentrations of 55 individual PAHs or groups of PAHs. Results indicate that these women and their fetuses were regularly exposed to multiple PAHs at comparatively low concentrations, with levels in cord blood generally exceeding levels in paired maternal blood. While the possibility of related adverse effects on the fetus is uncertain, these exposures in combination with socioeconomically-disadvantaged and environmentally-challenging living conditions raise legitimate public health concerns

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts