Sampling Hypergraphs with Given Degrees

There is a well-known connection between hypergraphs and bipartite graphs, obtained by treating the incidence matrix of the hypergraph as the biadjacency matrix of a bipartite graph. We use this connection to describe and analyse a rejection sampling algorithm for sampling simple uniform hypergraphs with a given degree sequence. Our algorithm uses, as a black box, an algorithm $\mathcal{A}$ for sampling bipartite graphs with given degrees, uniformly or nearly uniformly, in (expected) polynomial time. The expected runtime of the hypergraph sampling algorithm depends on the (expected) runtime of the bipartite graph sampling algorithm $\mathcal{A}$, and the probability that a uniformly random bipartite graph with given degrees corresponds to a simple hypergraph. We give some conditions on the hypergraph degree sequence which guarantee that this probability is bounded below by a constant

Diagnosing multiple faults.

Abstract Diagnostic tasks require determining the differences between a model of an artifact and the artifact itself. The differences between the manifested behavior of the artifact and the predicted behavior of the model guide the search for the differences between the artifact and its model. The diagnostic procedure presented in this paper is model-based, inferring the behavior of the composite device from knowledge of the structure and function of the individual components comprising the device. The system (GDE -General Diagnostic Engine) has been implemented and tested on many examples in the domain of troubleshooting digital circuits. This research makes several novel contributions: First, the system diagnoses failures due to multiple faults. Second, failure candidates are represented and manipulated in terms of minimal sets of violated assumptions, resulting in an efficient diagnostic procedure. Third, the diagnostic procedure is incremental, exploiting the iterative nature of diagnosis. Fourth, a clear separation is drawn between diagnosis and behavior prediction, resulting in a domain (and inference procedure) independent diagnostic procedure. Fifth, GDE combines modelbased prediction with sequential diagnosis to propose measurements to localize the faults. The normally required conditional probabilities are computed from the structure of the device and models of its components. This capability results from a novel way of incorporating probabilities and information theory into the context mechanism provided by AssumptionBased Truth Maintenance

Biocompatibility and degradation of the open-pored magnesium scaffolds LAE442 and La2

Porous magnesium implants are of particular interest for application as resorbable bone substitutes, due to their mechanical strength and a Young's modulus similar to bone. The objective of the present study was to compare the biocompatibility, bone and tissue ingrowth, and the degradation behaviour of scaffolds made from the magnesium alloys LAE442 (n= 40) and Mg-La2 (n= 40)in vivo. For this purpose, cylindrical magnesium scaffolds (diameter 4 mm, length 5 mm) with defined, interconnecting pores were produced by investment casting and coated with MgF2. The scaffolds were inserted into the cancellous part of the greater trochanter ossis femoris of rabbits. After implantation periods of 6, 12, 24 and 36 weeks, the bone-scaffold compounds were evaluated usingex vivo µCT80 images, histological examinations and energy dispersive x-ray spectroscopy analysis. The La2 scaffolds showed inhomogeneous and rapid degradation, with inferior osseointegration as compared to LAE442. For the early observation times, no bone and tissue could be observed in the pores of La2. Furthermore, the excessive amount of foreign body cells and fibrous capsule formation indicates insufficient biocompatibility of the La2 scaffolds. In contrast, the LAE442 scaffolds showed slow degradation and better osseointegration. Good vascularization, a moderate cellular response, bone and osteoid-like bone matrix at all implantation periods were observed in the pores of LAE442. In summary, porous LAE442 showed promise as a degradable scaffold for bone defect repair, based on its degradation behaviour and biocompatibility. However, further studies are needed to show it would have the necessary mechanical properties required over time for weight-bearing bone defects

Automatic systems diagnosis without behavioral models

Recent feedback obtained while applying Model-based diagnosis (MBD) in industry suggests that the costs involved in behavioral modeling (both expertise and labor) can outweigh the benefits of MBD as a high-performance diagnosis approach. In this paper, we propose an automatic approach, called ANTARES, that completely avoids behavioral modeling. Decreasing modeling sacrifices diagnostic accuracy, as the size of the ambiguity group (i.e., components which cannot be discriminated because of the lack of information) increases, which in turn increases misdiagnosis penalty. ANTARES further breaks the ambiguity group size by considering the component's false negative rate (FNR), which is estimated using an analytical expression. Furthermore, we study the performance of ANTARES for a number of logic circuits taken from the 74XXX/ISCAS benchmark suite. Our results clearly indicate that sacrificing modeling information degrades the diagnosis quality. However, considering FNR information improves the quality, attaining the diagnostic performance of an MBD approach

Tidal Heating: Lessons from Io and the Jovian System (Report from the KISS Workshop)

Summary of the Keck Institute for Space Studies workshop entitled "Tidal Heating: Lessons from Io and the Jovian System," held on October 15-19, 2018

Inhibition of CCN6 (WISP3) expression promotes neoplastic progression and enhances the effects of insulin-like growth factor-1 on breast epithelial cells

INTRODUCTION: CCN6/WISP3 belongs to the CCN (Cyr61, CTGF, Nov) family of genes that contains a conserved insulin-like growth factor (IGF) binding protein motif. CCN6 is a secreted protein lost in 80% of the aggressive inflammatory breast cancers, and can decrease mammary tumor growth in vitro and in vivo. We hypothesized that inhibition of CCN6 might result in the loss of a growth regulatory function that protects mammary epithelial cells from the tumorigenic effects of growth factors, particularly IGF-1. METHOD: We treated human mammary epithelial (HME) cells with a CCN6 hairpin short interfering RNA. RESULTS: CCN6-deficient cells showed increased motility and invasiveness, and developed features of epithelial-mesenchymal transition (EMT). Inhibition of CCN6 expression promoted anchorage-independent growth of HME cells and rendered them more responsive to the growth effects of IGF-1, which was coupled with the increased phosphorylation of IGF-1 receptor and insulin receptor substrate-1 (IRS-1). CONCLUSION: Specific stable inhibition of CCN6 expression in HME cells induces EMT, promotes anchorage-independent growth, motility and invasiveness, and sensitizes mammary epithelial cells to the growth effects of IGF-1

Expression of CCN family of genes in human skin in vivo and alterations by solar-simulated ultraviolet irradiation

The CCN family of proteins is involved in diverse biological functions such as cell growth, adhesion, migration, angiogenesis, and regulation of extracellular matrix. We have investigated expression of CCN family genes and alternations induced by solar-simulated ultraviolet irradiation in human skin in vivo. Transcripts of all six CCN genes were expressed in human skin in vivo. CCN5 was most abundantly expressed followed by CCN2>CCN3>CCN1>CCN4>CCN6. Solar-simulated ultraviolet irradiation increased mRNA expression of CCN1 and CCN2. In contrast, mRNA levels of CCN3, CCN4, CCN5, and CCN6, were reduced. Knowledge gained from this study provides the foundation to explore the functional roles of CCN gene products in cutaneous biology and responses to solar ultraviolet irradiation

Update on inflammatory breast cancer

Inflammatory breast cancer (IBC) is both the least frequent and the most severe form of epithelial breast cancer. The diagnosis is based on clinical inflammatory signs and is reinforced by pathological findings. Significant progress has been made in the management of IBC in the past 20 years. Yet survival among IBC patients is still only one-half that among patients with non-IBC. Identification of the molecular determinants of IBC would probably lead to more specific treatments and to improved survival. In the present article we review recent advances in the molecular pathogenesis of IBC. A more comprehensive view will probably be obtained by pan-genomic analysis of human IBC samples, and by functional in vitro and in vivo assays. These approaches may offer better patient outcome in the near future