Are there higher pedestrian fatalities in larger cities?: A scaling analysis of 115 to 161 largest cities in the United States

<p><b>Objective</b>: In 2012, 4,743 pedestrians were killed in the United States, representing 14% of total traffic fatalities. The number of pedestrians injured was higher at 76,000. Therefore, 36 out of 52 of the largest cities in the United States have adopted a citywide target of reducing pedestrian fatalities. The number of cities adopting the reduction goal during 2011 and 2012 increased rapidly with 8 more cities. We examined the scaling relationship of pedestrian fatality counts as a function of the population size of 115 to 161 large U.S. cities during the period of 1994 to 2011. We also examined the scaling relationship of nonpedestrian and total traffic fatality counts as a function of the population size.</p> <p><b>Methods</b>: For the data source of fatality measures we used Traffic Safety Facts Fatality Analysis Reporting System/General Estimates System annual reports published each year from 1994 to 2011 by the NHTSA. Using the data source we conducted both annual cross-sectional and panel data bivariate and multivariate regression models. In the construction of the estimated functional relationship between traffic fatality measures and various factors, we used the simple power function for urban scaling used by Bettencourt et al. (<a href="#cit0006" target="_blank">2007</a>, <a href="#cit0008" target="_blank">2010</a>) and the refined STIRPAT (stochastic impacts by regression on population, affluence, and technology) model used in Dietz and Rosa (<a href="#cit0012" target="_blank">1994</a>, <a href="#cit0013" target="_blank">1997</a>) and York et al. (<a href="#cit0041" target="_blank">2003</a>).</p> <p><b>Results</b>: We found that the scaling relationship display diseconomies of scale or sublinear for pedestrian fatalities. However, the relationship displays a superlinear relationship in case of nonpedestrian fatalities. The scaling relationship for total traffic fatality counts display a nearly linear pattern. When the relationship was examined by the 4 subgroups of cities with different population sizes, the most pronounced sublinear scaling relationships for all 3 types of fatality counts was discovered for the subgroup of megacities with a population of more than 1 million.</p> <p><b>Conclusions</b>: The scaling patterns of traffic fatalities of subgroups of cities depend on population sizes of the cities in subgroups. In particular, 9 megacities with populations of more than 1 million are significantly different from the remaining cities and should be viewed as a totally separate group. Thus, analysis of the patterns of traffic fatalities needs to be conducted within the group of megacities separately from the other cities with smaller population sizes for devising prevention policies to reduce traffic fatalities in both megacities and smaller cities.</p

Effective Trapping of Lithium Polysulfides Using a Functionalized Carbon Nanotube-Coated Separator for Lithium–Sulfur Cells with Enhanced Cycling Stability

The critical issues that hinder the practical applications of lithium–sulfur batteries, such as dissolution and migration of lithium polysulfides, poor electronic conductivity of sulfur and its discharge products, and low loading of sulfur, have been addressed by designing a functional separator modified using hydroxyl-functionalized carbon nanotubes (CNTOH). Density functional theory calculations and experimental results demonstrate that the hydroxyl groups in the CNTOH provoked strong interaction with lithium polysulfides and resulted in effective trapping of lithium polysulfides within the sulfur cathode side. The reduction in migration of lithium polysulfides to the lithium anode resulted in enhanced stability of the lithium electrode. The conductive nature of CNTOH also aided to efficiently reutilize the adsorbed reaction intermediates for subsequent cycling. As a result, the lithium–sulfur cell assembled with a functional separator exhibited a high initial discharge capacity of 1056 mAh g^–1 (corresponding to an areal capacity of 3.2 mAh cm^–2) with a capacity fading rate of 0.11% per cycle over 400 cycles at 0.5 C rate

<em>Mig-6</em> Plays a Critical Role in the Regulation of Cholesterol Homeostasis and Bile Acid Synthesis

<div><p>The disruption of cholesterol homeostasis leads to an increase in cholesterol levels which results in the development of cardiovascular disease. Mitogen Inducible Gene 6 (<em>Mig-6</em>) is an immediate early response gene that can be induced by various mitogens, stresses, and hormones. To identify the metabolic role of <em>Mig-6</em> in the liver, we conditionally ablated <em>Mig-6</em> in the liver using the Albumin-Cre mouse model (<em>Alb^cre/+Mig-6^f/f</em>; <em>Mig-6^d/d</em>). <em>Mig-6^d/d</em> mice exhibit hepatomegaly and fatty liver. Serum levels of total, LDL, and HDL cholesterol and hepatic lipid were significantly increased in the <em>Mig-6^d/d</em> mice. The daily excretion of fecal bile acids was significantly decreased in the <em>Mig-6^d/d</em> mice. DNA microarray analysis of mRNA isolated from the livers of these mice showed alterations in genes that regulate lipid metabolism, bile acid, and cholesterol synthesis, while the expression of genes that regulate biliary excretion of bile acid and triglyceride synthesis showed no difference in the <em>Mig-6^d/d</em> mice compared to <em>Mig-6^f/f</em> controls. These results indicate that <em>Mig-6</em> plays an important role in cholesterol homeostasis and bile acid synthesis. Mice with liver specific conditional ablation of <em>Mig-6</em> develop hepatomegaly and increased intrahepatic lipid and provide a novel model system to investigate the genetic and molecular events involved in the regulation of cholesterol homeostasis and bile acid synthesis. Defining the molecular mechanisms by which <em>Mig-6</em> regulates cholesterol homeostasis will provide new insights into the development of more effective ways for the treatment and prevention of cardiovascular disease.</p> </div

Generation of conditional ablation of <i>Mig-6</i> in the liver.

<p>A. RT-PCR analysis of <i>Mig-6</i> mRNA expression level. 8 week old <i>Mig-6^f/f</i> and <i>Mig-6^d/d</i> male mice were sacrificed after 24 hrs of fasting and RNA was isolated from the liver, kidney, adrenal gland, lungs, muscle, and white adipose tissue. Five mice of each group were used for this experiment. The results represent the mean ± SEM of three independent RNA sets. ***, <i>p</i><0.001. B, Western blot analysis of MIG-6 in the liver of <i>Mig-6^f/f</i> and <i>Mig-6^d/d</i> mice. Liver tissue from <i>Mig-6^f/f</i> and <i>Mig-6^d/d</i> mice were lysed and equal amounts of protein were subjected to SDS-PAGE and Western blot analysis for MIG-6.</p

Concentration of bile acid in serum, liver, and feces.

<p>Serum and liver were collected from 8 week old <i>Mig-6^d/d</i> and <i>Mig-6^f/f</i> male mice after 24 hrs. of fasting. Feces were collected from individual mice for 3 days. 5 mice of each group were used for this experiment.</p>**<p>, <i>p</i><0.01.</p

Morphology of the liver of <i>Mig-6^f/f</i> and <i>Mig-6^d/d</i>

<p><b>mice.</b> A, Size of liver. Twelve mice of each group were used for this experiment. B, Weight of the liver adjusted to body weight. The results represent the mean ± SEM. The numbers in parentheses are the number of mice used. ***, p<0.001. C. Oil-Red-O staining. Liver tissue were fixed with 4% paraformaldehyde (vol/vol) and frozen in OCT. Sections were counterstained with hematoxylin and mounted with 15% glycerol. All of the photomicrographs are X400 magnification.</p

Serum lipid profile in <i>Mig-6 ^f/f</i> and <i>Mig-6^d/d</i> mice.

<p>Eight week old <i>Mig-6^d/d</i> and <i>Mig-6^f/f</i> male mice were sacrificed after 24 hrs of fasting and serum lipid profiles were analyzed. Five mice of each group were used for this experiment.</p>*<p>, <i>p</i><0.05;</p>**<p>, <i>p</i><0.01;</p>***<p>, <i>p</i><0.001.</p

Real-time RT-PCR analysis of metabolic genes in the liver.

<p>A, Bile acid metabolism related genes. B, Cholesterol synthesis related genes. C, Triglyceride metabolism related genes. 8 week old <i>Mig-6^d/d</i> and <i>Mig-6^f/f</i> male mice were sacrificed after 24 hrs fasting and RNA was isolated from the liver. 5 mice of each group were used for this experiment. The results represent the mean ± SEM of three independent RNA sets. *, <i>p</i><0.05; ***, <i>p</i><0.001.</p

Expression of ERK1/2 during <i>in vitro</i> decidualization of human endometrial stromal cells (hESCs).

<p>(A) Morphological change of hESCs was observed during <i>in </i><i>vitro</i> decidualization on day 0 (a), day 1 (b), day 3 (c) and day 6 (d). (B) Expression of decidualization marker genes, <i>IGFPB1</i> and PRL, was examined during <i>in </i><i>vitro</i> decidualization. (C) Level of total ERK1/2 and phospho-ERK1/2 proteins was measured by western blot. (D) Quantification of pERK1/2 protein levels during <i>in </i><i>vitro</i> decidualization. The results represent the mean ± SE. *, <i>p</i><0.05; **, <i>p</i><0.01; <i>***, p<0.001</i>. (E) Increased expression of phospho-ERK1/2 (a, b, c and d) was detected on day 3 by immunofluorescence during <i>in </i><i>vitro</i> decidualization. Images (i, j, k and l) were merged with DAPI staining (e, f, g and h).</p

Relationship between phospho-ERK1/2 and proliferation during early pregnancy.

<p>(A) Immunofluorescence analysis of phospho-ERK1/2 (green; a, b, c and d) and Ki67 (red: e, f, g and h) was performed in uteri of C57BL/6 mice on 2.5 (a, e, i and m), 3.5 (b, f, j and n), 4.5 (c, g, k and o) and 5.5 (d, h, l and p) dpc. Images (m, n, o and p) were merged with DAPI staining (i, j, k and l). (B) Higher magnification images of the insets. Arrowheads indicates positive phospho-ERK1/2 cells.</p