Dendritic side-branching with anisotropic viscous fingering

We studied dendritic side-branching mechanism in the experiment of anisotropic viscous fingering. We measured the time dependence of growth speed of side-branch and the envelop of side-branches. We found that the speed of side-branch gets to be faster than one of the stem and the growth exponent of the speed changes at a certain time. The envelope of side-branches is represented as Y ~ X^1.47.Comment: 8 pages, 8 figures, to submited in J. Crystal Growt

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

Scaling of impact fragmentation near the critical point

We investigated two-dimensional brittle fragmentation with a flat impact experimentally, focusing on the low impact energy region near the fragmentation-critical point. We found that the universality class of fragmentation transition disagreed with that of percolation. However, the weighted mean mass of the fragments could be scaled using the pseudo-control parameter multiplicity. The data for highly fragmented samples included a cumulative fragment mass distribution that clearly obeyed a power-law. The exponent of this power-law was 0.5 and it was independent of sample size. The fragment mass distributions in this regime seemed to collapse into a unified scaling function using weighted mean fragment mass scaling. We also examined the behavior of higher order moments of the fragment mass distributions, and obtained multi-scaling exponents that agreed with those of the simple biased cascade model.Comment: 6 pages, 6 figure

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

Asymptotic function for multi-growth surfaces using power-law noise

Numerical simulations are used to investigate the multiaffine exponent $\alpha_q$ and multi-growth exponent $\beta_q$ of ballistic deposition growth for noise obeying a power-law distribution. The simulated values of $\beta_q$ are compared with the asymptotic function $\beta_q = \frac{1}{q}$ that is approximated from the power-law behavior of the distribution of height differences over time. They are in good agreement for large $q$. The simulated $\alpha_q$ is found in the range $\frac{1}{q} \leq \alpha_q \leq \frac{2}{q+1}$. This implies that large rare events tend to break the KPZ universality scaling-law at higher order $q$.Comment: 5 pages, 4 figures, to be published in Phys. Rev.

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