Numerical Modeling of the Coagulation and Porosity Evolution of Dust Aggregates

Porosity evolution of dust aggregates is crucial in understanding dust evolution in protoplanetary disks. In this study, we present useful tools to study the coagulation and porosity evolution of dust aggregates. First, we present a new numerical method for simulating dust coagulation and porosity evolution as an extension of the conventional Smoluchowski equation. This method follows the evolution of the mean porosity for each aggregate mass simultaneously with the evolution of the mass distribution function. This method reproduces the results of previous Monte Carlo simulations with much less computational expense. Second, we propose a new collision model for porous dust aggregates on the basis of our N-body experiments on aggregate collisions. We first obtain empirical data on porosity changes between the classical limits of ballistic cluster-cluster and particle-cluster aggregation. Using the data, we construct a recipe for the porosity change due to general hit-and-stick collisions as well as formulae for the aerodynamical and collisional cross sections. Simple coagulation simulations using the extended Smoluchowski method show that our collision model explains the fractal dimensions of porous aggregates observed in a full N-body simulation and a laboratory experiment. Besides, we discover that aggregates at the high-mass end of the distribution can have a considerably small aerodynamical cross section per unit mass compared with aggregates of lower masses. We point out an important implication of this discovery for dust growth in protoplanetary disks.Comment: 17 pages, 15 figures; v2: version to appear in ApJ (typos corrected

Electrostatic Barrier against Dust Growth in Protoplanetary Disks. I. Classifying the Evolution of Size Distribution

Collisional growth of submicron-sized dust grains into macroscopic aggregates is the first step of planet formation in protoplanetary disks. These grains are expected to carry nonzero negative charges in the weakly ionized disks, but its effect on their collisional growth has not been fully understood so far. In this paper, we investigate how the charging affects the evolution of the dust size distribution properly taking into account the charging mechanism in a weakly ionized gas as well as porosity evolution through low-energy collisions. To clarify the role of the size distribution, we divide our analysis into two steps. First, we analyze the collisional growth of charged aggregates assuming a monodisperse (i.e., narrow) size distribution. We show that the monodisperse growth stalls due to the electrostatic repulsion when a certain condition is met, as is already expected in the previous work. Second, we numerically simulate dust coagulation using Smoluchowski's method to see how the outcome changes when the size distribution is allowed to freely evolve. We find that, under certain conditions, the dust undergoes bimodal growth where only a limited number of aggregates continue to grow carrying the major part of the dust mass in the system. This occurs because remaining small aggregates efficiently sweep up free electrons to prevent the larger aggregates from being strongly charged. We obtain a set of simple criteria that allows us to predict how the size distribution evolves for a given condition. In Paper II (arXiv:1009.3101), we apply these criteria to dust growth in protoplanetary disks.Comment: 20 pages, 22 figures, accepted for publication in Ap

Electrostatic Barrier against Dust Growth in Protoplanetary Disks. II. Measuring the Size of the "Frozen" Zone

Coagulation of submicron-sized dust grains into porous aggregates is the initial step of dust evolution in protoplanetary disks. Recently, it has been pointed out that negative charging of dust in the weakly ionized disks could significantly slow down the coagulation process. In this paper, we apply the growth criteria obtained in Paper I to finding out a location ("frozen" zone) where the charging stalls dust growth at the fractal growth stage. For low-turbulence disks, we find that the frozen zone can cover the major part of the disks at a few to 100 AU from the central star. The maximum mass of the aggregates is approximately 10^{-7} g at 1 AU and as small as a few monomer masses at 100 AU. Strong turbulence can significantly reduce the size of the frozen zone, but such turbulence will cause the fragmentation of macroscopic aggregates at later stages. We examine a possibility that complete freezeout of dust evolution in low-turbulence disks could be prevented by global transport of dust in the disks. Our simple estimation shows that global dust transport can lead to the supply of macroscopic aggregates and the removal of frozen aggregates on a timescale of 10^6 yr. This overturns the usual understanding that tiny dust particles get depleted on much shorter timescales unless collisional fragmentation is effective. The frozen zone together with global dust transport might explain "slow" (\sim 10^6 yr) dust evolution suggested by infrared observation of T Tauri stars and by radioactive dating of chondrites.Comment: 14 pages, 13 figures, accepted for publication in Ap

Prolyl Isomerase Pin1 Suppresses Thermogenic Programs in Adipocytes by Promoting Degradation of Transcriptional Co-activator PRDM16

Summary: Non-shivering thermogenesis in adipocytes provides defense against low temperatures and obesity development, but the underlying regulatory mechanism remains to be fully clarified. Based on both markedly increased Pin1 expression in states of excess nutrition and resistance to obesity development in Pin1 null mice, we speculated that adipocyte Pin1 may play a role in thermogenic programs. Adipose-specific Pin1 knockout (adPin1 KO) mice showed enhanced transcription of thermogenic genes and tolerance to hypothermia when exposed to cold. In addition, adPin1 KO mice were resistant to high-fat diet-induced obesity and glucose intolerance. A series of experiments revealed that Pin1 binds to PRDM16 and thereby promotes its degradation through the ubiquitin-proteasome system. Consistent with these results, Pin1 deletion in differentiated adipocytes showed enhancement of thermogenic programs in response to the β3 agonist CL316243 through the upregulation of PRDM16 proteins. These observations indicate that Pin1 is a negative regulator of non-shivering thermogenesis. : Adipose Pin1 expression increases in obese mice. Pin1 associates with PRDM16 and promotes its degradation, resulting in the downregulation of UCP-1. Pin1 KO mice are resistant to obesity development and cold exposure-induced hypothermia. Thus, Pin1 is a negative regulator of thermogenesis and could be a target of obesity. Keywords: Pin1, PRDM16, UCP-1, thermogenesis, obesit