Majority gates vs. general weighted threshold gates

In this paper we study small depth circuits that contain threshold gates (with or without weights) and parity gates. All circuits we consider are of polynomial size. We prove several results which complete the work on characterizing possible inclusions between many classes defined by small depth circuits. These results are the following:

Predicting fully plastic mode II crack growth from an asymmetric defect

Asymmetrically cracked specimens fail with considerably less ductility than symmetrically cracked ones, due to the crack progressing along a shear band into pre-damaged material. A formulation for the accumulation of damage ahead of an asymmetric crack is presented, based on strain increments following a power law relation. These results are integrated both numerically and approximately.The crack growth per unit displacement increases approximately as the logarithm of the total crack advance per inclusion spacing , and varies inversely as the critical fracture strain c. This provides a basis for predicting large-scale, fully plastic fracture from asymmetric weld defects, using small-scale laboratory specimens.

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Résumé Les éprouvettes fissurées de manière asymétrique se rompent avec beaucoup moins de ductilité que celles qui sont fissurées de manières symétrique, en raison du fait que la fissure se développe suivant une bande de cisaillement dans un matériau préendommagé. On Présente une formulation de l'accumulation du dommage en avant d'une fissure asymétrique, en se basant sur des gradients de déformations répartis selon une loi quadratique. L'interprétation des résultats est effectuée par voie numérique et par approximation.On constate que le croissance d'une fissure par unité de déplacement est sensiblement proportionnelle au logarithme de l'avancement total de la fissure rapporté à l'espacement entre deux inclusions , et en raison inverse de la déformation critique à la rupture c. Ceci fournt une base pour prédire une rupture à plus grande échelle et en conditions tout à fait plastiques, qui résulteront de défauts de soudage asymétriques, et ce en utilisant des éprouvettes réduites de laboratoire.

     

Ultrasonic crack characterization via a constrained inversion algorithm

The Kirchhoff approximation is used to show that the time domain impulse response of an isolated flat crack can be given a simple geometrical interpretation in terms of the derivative of a projected length function. For an elliptical crack, this derivative can be obtained explicitly to yield the two edge-diffracted waves which originate from the flashpoints of the crack. An explicit coordinate invariant expression is obtained from this elliptical crack solution which relates the time difference, t, between the arrival of these edge-diffracted waves and the crack size and orientation. Previously, we have proposed that this expression, together with t measurements in different scattering directions, could be used in a regression analysis as the basis for performing a constrained inversion of crack scattering data (i.e., where we attempt to obtain the best equivalent flat elliptical crack that fits the scattering measurements). Here we will demonstrate some results of applying the proposed algorithm using noisy synthetic data. The sensitivity of the results to both, number of measurements and transducer orientation, will be discussed.     

Textures in3He-A: Magnetic deformation in a narrow slab

A variational technique is used to analyze the deformed texture of superfluid³He-A in a narrow slab subject to a perpendicular magnetic field. Specific predictions are made for the anisotropy parameters and , averaged across the width.     

Dysregulated CD38 Expression on Peripheral Blood Immune Cell Subsets in SLE

Given its uniformly high expression on plasma cells, CD38 has been considered as a therapeutic target in patients with systemic lupus erythematosus (SLE). Herein, we investigate the distribution of CD38 expression by peripheral blood leukocyte lineages to evaluate the potential therapeutic effect of CD38-targeting antibodies on these immune cell subsets and to delineate the use of CD38 as a biomarker in SLE. We analyzed the expression of CD38 on peripheral blood leukocyte subsets by flow and mass cytometry in two different cohorts, comprising a total of 56 SLE patients. The CD38 expression levels were subsequently correlated across immune cell lineages and subsets, and with clinical and serologic disease parameters of SLE. Compared to healthy controls (HC), CD38 expression levels in SLE were significantly increased on circulating plasmacytoid dendritic cells, CD14⁺⁺CD16⁺ monocytes, CD56⁺ CD16^dim natural killer cells, marginal zone-like IgD⁺CD27⁺ B cells, and on CD4⁺ and CD8⁺ memory T cells. Correlation analyses revealed coordinated CD38 expression between individual innate and memory T cell subsets in SLE but not HC. However, CD38 expression levels were heterogeneous across patients, and no correlation was found between CD38 expression on immune cell subsets and the disease activity index SLEDAI-2K or established serologic and immunological markers of disease activity. In conclusion, we identified widespread changes in CD38 expression on SLE immune cells that highly correlated over different leukocyte subsets within individual patients, but was heterogenous within the population of SLE patients, regardless of disease severity or clinical manifestations. As anti-CD38 treatment is being investigated in SLE, our results may have important implications for the personalized targeting of pathogenic leukocytes by anti-CD38 monoclonal antibodies.     

Analysis of the Structure and Biosynthesis of the Lipopolysaccharide Core Oligosaccharide of Pseudomonas syringae pv. tomato DC3000

Lipopolysaccharide (LPS), the major component of the outer membrane of Gram-negative bacteria, is important for bacterial viability in general and host–pathogen interactions in particular. Negative charges at its core oligosaccharide (core-OS) contribute to membrane integrity through bridging interactions with divalent cations. The molecular structure and synthesis of the core-OS have been resolved in various bacteria including the mammalian pathogen Pseudomonas aeruginosa. A few core-OS structures of plant-associated Pseudomonas strains have been solved to date, but the genetic components of the underlying biosynthesis remained unclear. We conducted a comparative genome analysis of the core-OS gene cluster in Pseudomonas syringae pv. tomato (Pst) DC3000, a widely used model pathogen in plant–microbe interactions, within the P. syringae species complex and to other plant-associated Pseudomonas strains. Our results suggest a genetic and structural conservation of the inner core-OS but variation in outer core-OS composition within the P. syringae species complex. Structural analysis of the core-OS of Pst DC3000 shows an uncommonly high phosphorylation and presence of an O-acetylated sugar. Finally, we combined the results of our genomic survey with available structure information to estimate the core-OS composition of other Pseudomonas species.     

Cardioinotropic Effects in Subchronic Intoxication of Rats with Lead and/or Cadmium Oxide Nanoparticles

Subchronic intoxication was induced in outbred male rats by repeated intraperitoneal injections with lead oxide (PbO) and/or cadmium oxide (CdO) nanoparticles (NPs) 3 times a week during 6 weeks for the purpose of examining its effects on the contractile characteristics of isolated right ventricle trabeculae and papillary muscles in isometric and afterload contractions. Isolated and combined intoxication with these NPs was observed to reduce the mechanical work produced by both types of myocardial preparation. Using the in vitro motility assay, we showed that the sliding velocity of regulated thin filaments drops under both isolated and combined intoxication with CdO–NP and PbO–NP. These results correlate with a shift in the expression of myosin heavy chain (MHC) isoforms towards slowly cycling β–MHC. The type of CdO–NP + PbO–NP combined cardiotoxicity depends on the effect of the toxic impact, the extent of this effect, the ratio of toxicant doses, and the degree of stretching of cardiomyocytes and muscle type studied. Some indices of combined Pb–NP and CdO–NP cardiotoxicity and general toxicity (genotoxicity included) became fully or partly normalized if intoxication developed against background administration of a bioprotective complex.     

Interleukin 6 and Aneurysmal Subarachnoid Hemorrhage. A Narrative Review

Interleukin 6 (IL-6) is a prominent proinflammatory cytokine. Neuroinflammation in general, and IL-6 signaling in particular, appear to play a major role in the pathobiology and pathophysiology of aneurysm formation and aneurysmal subarachnoid hemorrhage (SAH). Most importantly, elevated IL-6 CSF (rather than serum) levels appear to correlate with delayed cerebral ischemia (DCI, “vasospasm”) and secondary (“vasospastic”) infarctions. IL-6 CSF levels may also reflect other forms of injury to the brain following SAH, i.e., early brain damage and septic complications of SAH and aneurysm treatment. This would explain why many researchers have found an association between IL-6 levels and patient outcomes. These findings clearly suggest CSF IL-6 as a candidate biomarker in SAH patients. However, at this point, discrepant findings in variable study settings, as well as timing and other issues, e.g., defining proper clinical endpoints (i.e., secondary clinical deterioration vs. angiographic vasospasm vs. secondary vasospastic infarct) do not allow for its routine use. It is also tempting to speculate about potential therapeutic measures targeting elevated IL-6 CSF levels and neuroinflammation in SAH patients. Corticosteroids and anti-platelet drugs are indeed used in many SAH cases (not necessarily with the intention to interfere with detrimental inflammatory signaling), however, no convincing benefit has been demonstrated yet. The lack of a robust clinical perspective against the background of a relatively large body of data linking IL-6 and neuroinflammation with the pathophysiology of SAH is somewhat disappointing. One underlying reason might be that most relevant studies only report correlative data. The specific molecular pathways behind elevated IL-6 levels in SAH patients and their various interactions still remain to be delineated. We are optimistic that future research in this field will result in a better understanding of the role of neuroinflammation in the pathophysiology of SAH, which in turn, will translate into the identification of suitable biomarkers and even potential therapeutic targets.