Sinusoidal fetal heart rate pattern

We describe 2 cases of term anemic fetuses with different sinusoidal pattern morphology, and possible mechanisms.nbspCasesmdashThe first patient noted sudden cessation of fetal movement on the day of presentation. She had a sinusoidal FHR pattern. The newborn had a hemoglobin of 3.7 g/dl, and umbilical artery pH was 7.10 and BE -7 mEq/l. The second patient noted decreased fetal movement for several days. She had a FHR pattern with absent FHR variability, and intermittent sinusoidal elements, with late decelerations. The newbornrsquos hemoglobin was 1.5 g/dl, umbilical artery pH was 7.07 and BE -10.2 mEq/l. Both cases had positive Kleihauer-Betke tests

Classification of KPZQ and BDP models by multiaffine analysis

We argue differences between the Kardar-Parisi-Zhang with Quenched disorder (KPZQ) and the Ballistic Deposition with Power-law noise (BDP) models, using the multiaffine analysis method. The KPZQ and the BDP models show mono-affinity and multiaffinity, respectively. This difference results from the different distribution types of neighbor-height differences in growth paths. Exponential and power-law distributions are observed in the KPZQ and the BDP, respectively. In addition, we point out the difference of profiles directly, i.e., although the surface profiles of both models and the growth path of the BDP model are rough, the growth path of the KPZQ model is smooth.Comment: 11 pages, 6 figure

Projectile interactions in granular impact cratering

We present evidence for the interactions between a ball and the container boundaries, as well as between two balls, that are mediated by the granular medium during impact cratering. The presence of the bottom boundary affects the final penetration depth only for low drop heights with shallow filling, in which case, surprisingly, the penetration becomes deeper. By contrast the presence of the side wall causes less penetration and also an effective repulsion. Repulsion is also found for two balls dropped side-by-side

Surface Scaling Analysis of a Frustrated Spring-network Model for Surfactant-templated Hydrogels

We propose and study a simplified model for the surface and bulk structures of crosslinked polymer gels, into which voids are introduced through templating by surfactant micelles. Such systems were recently studied by Atomic Force Microscopy [M. Chakrapani et al., e-print cond-mat/0112255]. The gel is represented by a frustrated, triangular network of nodes connected by springs of random equilibrium lengths. The nodes represent crosslinkers, and the springs correspond to polymer chains. The boundaries are fixed at the bottom, free at the top, and periodic in the lateral direction. Voids are introduced by deleting a proportion of the nodes and their associated springs. The model is numerically relaxed to a representative local energy minimum, resulting in an inhomogeneous, ``clumpy'' bulk structure. The free top surface is defined at evenly spaced points in the lateral (x) direction by the height of the topmost spring, measured from the bottom layer, h(x). Its scaling properties are studied by calculating the root-mean-square surface width and the generalized increment correlation functions C_q(x)= . The surface is found to have a nontrivial scaling behavior on small length scales, with a crossover to scale-independent behavior on large scales. As the vacancy concentration approaches the site-percolation limit, both the crossover length and the saturation value of the surface width diverge in a manner that appears to be proportional to the bulk connectivity length. This suggests that a percolation transition in the bulk also drives a similar divergence observed in surfactant templated polyacrylamide gels at high surfactant concentrations.Comment: 17 pages RevTex4, 10 imbedded eps figures. Expanded discussion of multi-affinit

Reversible Keap1 inhibitors are preferential pharmacological tools to modulate cellular mitophagy

Mitophagy orchestrates the autophagic degradation of dysfunctional mitochondria preventing their pathological accumulation and contributing to cellular homeostasis. We previously identified a novel chemical tool (hereafter referred to as PMI), which drives mitochondria into autophagy without collapsing their membrane potential (ΔΨm). PMI is an inhibitor of the protein-protein interaction (PPI) between the transcription factor Nrf2 and its negative regulator, Keap1 and is able to up-regulate the expression of autophagy-associated proteins, including p62/SQSTM1. Here we show that PMI promotes mitochondrial respiration, leading to a superoxide-dependent activation of mitophagy. Structurally distinct Keap1-Nrf2 PPI inhibitors promote mitochondrial turnover, while covalent Keap1 modifiers, including sulforaphane (SFN) and dimethyl fumarate (DMF), are unable to induce a similar response. Additionally, we demonstrate that SFN reverses the effects of PMI in co-treated cells by reducing the accumulation of p62 in mitochondria and subsequently limiting their autophagic degradation. This study highlights the unique features of Keap1-Nrf2 PPI inhibitors as inducers of mitophagy and their potential as pharmacological agents for the treatment of pathological conditions characterized by impaired mitochondrial quality control