HTAP2 multi-model estimates of premature human mortality due to intercontinental transport of air pollution and emission sectors

Liang, Ciao-Kai,West, J. Jason,Silva, Raquel A.,Bian, Huisheng,Chin, Mian,Davila, Yanko,Dentener, Frank J.,Emmons, Louisa,Flemming, Johannes,Folberth, Gerd,Henze, Daven,Im, Ulas,Jonson, Jan Eiof,Keati Copernicus GmbH 2018 Atmospheric Chemistry and Physics Vol.18 No.14

<P><p><strong>Abstract.</strong> Ambient air pollution from ozone and fine particulate matter is associated with premature mortality. As emissions from one continent influence air quality over others, changes in emissions can also influence human health on other continents. We estimate global air-pollution-related premature mortality from exposure to PM<span class='inline-formula'>_2.5</span> and ozone and the avoided deaths due to 20<span class='thinspace'></span>% anthropogenic emission reductions from six source regions, North America (NAM), Europe (EUR), South Asia (SAS), East Asia (EAS), Russia-Belarus-Ukraine (RBU), and the Middle East (MDE), three global emission sectors, power and industry (PIN), ground transportation (TRN), and residential (RES), and one global domain (GLO), using an ensemble of global chemical transport model simulations coordinated by the second phase of the Task Force on Hemispheric Transport of Air Pollutants (TF HTAP2), and epidemiologically derived<span id='page10498'/> concentration response functions. We build on results from previous studies of TF HTAP by using improved atmospheric models driven by new estimates of 2010 anthropogenic emissions (excluding methane), with more source and receptor regions, new consideration of source sector impacts, and new epidemiological mortality functions. We estimate 290<span class='thinspace'></span>000 (95<span class='thinspace'></span>% confidence interval (CI): 30<span class='thinspace'></span>000, 600<span class='thinspace'></span>000) premature <span class='inline-formula'>O₃</span>-related deaths and 2.8 million (0.5 million, 4.6 million) PM<span class='inline-formula'>_2.5</span>-related premature deaths globally for the baseline year 2010. While 20<span class='thinspace'></span>% emission reductions from one region generally lead to more avoided deaths within the source region than outside, reducing emissions from MDE and RBU can avoid more <span class='inline-formula'>O₃</span>-related deaths outside of these regions than within, and reducing MDE emissions also avoids more PM<span class='inline-formula'>_2.5</span>-related deaths outside of MDE than within. Our findings that most avoided <span class='inline-formula'>O₃</span>-related deaths from emission reductions in NAM and EUR occur outside of those regions contrast with those of previous studies, while estimates of PM<span class='inline-formula'>_2.5</span>-related deaths from NAM, EUR, SAS, and EAS emission reductions agree well. In addition, EUR, MDE, and RBU have more avoided <span class='inline-formula'>O₃</span>-related deaths from reducing foreign emissions than from domestic reductions. For six regional emission reductions, the total avoided extra-regional mortality is estimated as 6000 (<span class='inline-formula'>−</span>3400, 15<span class='thinspace'></span>500) deaths per year and 25<span class='thinspace'></span>100 (8200, 35<span class='thinspace'></span>800) deaths per year through changes in <span class='inline-formula'>O₃</span> and PM<span class='inline-formula'>_2.5</span>, respectively. Interregional transport of air pollutants leads to more deaths through changes in PM<span class='inline-formula'>_2.5</span> than in <span class='inline-formula'>O₃</span>, even though <span class='inline-formula'>O₃</span> is transported more on interregional scales, since PM<span class='inline-formula'>_2.5</span> has a stronger influence on mortality. For NAM and EUR, our estimates of avoided mortality from regional and extra-regional emission reductions are comparable to those estimated by regional models for these same experiments. In sectoral emission reductions, TRN emissions account for the greatest fraction (26-53<span class='thinspace'></span>% of global emission reduction) of <span class='inline-formula'>O₃</span>-rela

<i>ITGB6</i> loss-of-function mutations cause autosomal recessive amelogenesis imperfecta

Wang, Shih-Kai,Choi, Murim,Richardson, Amelia S.,Reid, Bryan M.,Lin, Brent P.,Wang, Susan J.,Kim, Jung-Wook,Simmer, James P.,Hu, Jan C.-C. Oxford University Press 2014 Human Molecular Genetics Vol.23 No.8

<P>Integrins are cell-surface adhesion receptors that bind to extracellular matrices (ECM) and mediate cell–ECM interactions. Some integrins are known to play critical roles in dental enamel formation. We recruited two Hispanic families with generalized hypoplastic amelogenesis imperfecta (AI). Analysis of whole-exome sequences identified three <I>integrin beta 6</I> (<I>ITGB6</I>) mutations responsible for their enamel malformations. The female proband of Family 1 was a compound heterozygote with an <I>ITGB6</I> transition mutation in Exon 4 (g.4545G > A c.427G > A p.Ala143Thr) and an <I>ITGB6</I> transversion mutation in Exon 6 (g.27415T > A c.825T > A p.His275Gln). The male proband of Family 2 was homozygous for an <I>ITGB6</I> transition mutation in Exon 11 (g.73664C > T c.1846C > T p.Arg616*) and hemizygous for a transition mutation in Exon 6 of <I>Nance–Horan Syndrome</I> (<I>NHS</I> Xp22.13; g.355444T > C c.1697T > C p.Met566Thr). These are the first disease-causing <I>ITGB6</I> mutations to be reported. Immunohistochemistry of mouse mandibular incisors localized ITGB6 to the distal membrane of differentiating ameloblasts and pre-ameloblasts, and then ITGB6 appeared to be internalized by secretory stage ameloblasts. ITGB6 expression was strongest in the maturation stage and its localization was associated with ameloblast modulation. Our findings demonstrate that early and late amelogenesis depend upon cell–matrix interactions. Our approach (from knockout mouse phenotype to human disease) demonstrates the power of mouse reverse genetics in mutational analysis of human genetic disorders and attests to the need for a careful dental phenotyping in large-scale knockout mouse projects.</P>

Comparative global immune-related gene profiling of somatic cells, human pluripotent stem cells and their derivatives: implication for human lymphocyte proliferation

Chia-Eng Wu,Chen-Wei Yu,Kai-Wei Chang,Wen-Hsi Chou,Chen-Yu Lu,Elisa Ghelfi,Fang-Chun Wu,Pey-Shynan Jan,Mei-Chi Huang,Patrick Allard,Shau-Ping Lin,Hong-Nerng Ho,Hsin-Fu Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Human pluripotent stem cells (hPSCs), including embryonic stem cells (ESCs) and induced PSCs (iPSCs), represent potentially unlimited cell sources for clinical applications. Previous studies have suggested that hPSCs may benefit from immune privilege and limited immunogenicity, as reflected by the reduced expression of major histocompatibility complex class-related molecules. Here we investigated the global immune-related gene expression profiles of human ESCs, hiPSCs and somatic cells and identified candidate immune-related genes that may alter their immunogenicity. The expression levels of global immune-related genes were determined by comparing undifferentiated and differentiated stem cells and three types of human somatic cells: dermal papilla cells, ovarian granulosa cells and foreskin fibroblast cells. We identified the differentially expressed genes CD24, GATA3, PROM1, THBS2, LY96, IFIT3, CXCR4, IL1R1, FGFR3, IDO1 and KDR, which overlapped with selected immune-related gene lists. In further analyses, mammalian target of rapamycin complex (mTOR) signaling was investigated in the differentiated stem cells following treatment with rapamycin and lentiviral transduction with specific short-hairpin RNAs. We found that the inhibition of mTOR signal pathways significantly downregulated the immunogenicity of differentiated stem cells. We also tested the immune responses induced in differentiated stem cells by mixed lymphocyte reactions. We found that CD24- and GATA3-deficient differentiated stem cells including neural lineage cells had limited abilities to activate human lymphocytes. By analyzing the transcriptome signature of immune-related genes, we observed a tendency of the hPSCs to differentiate toward an immune cell phenotype. Taken together, these data identify candidate immune-related genes that might constitute valuable targets for clinical applications.

Effects of Neural Progenitor Cells on Sensorimotor Recovery and Endogenous Repair Mechanisms After Photothrombotic Stroke

Minnerup, Jens,Kim, Jeong Beom,Schmidt, Antje,Diederich, Kai,Bauer, Henrike,Schilling, Matthias,Strecker, Jan-Kolja,Ringelstein, E. Bernd,Sommer, Clemens,Schö,ler, Hans R.,Schä,bitz, Wolf-R&uu Ovid Technologies Wolters Kluwer -American Heart A 2011 Stroke Vol.42 No.6

Three-Dimensional Silicon Electronic Systems Fabricated by Compressive Buckling Process

Kim, Bong Hoon,Lee, Jungyup,Won, Sang Min,Xie, Zhaoqian,Chang, Jan-Kai,Yu, Yongjoon,Cho, Youn Kyoung,Jang, Hokyung,Jeong, Ji Yoon,Lee, Yechan,Ryu, Arin,Kim, Do Hoon,Lee, Kun Hyuck,Lee, Jong Yoon,Liu, American Chemical Society 2018 ACS NANO Vol.12 No.5

<P>Recently developed approaches in deterministic assembly allow for controlled, geometric transformation of two-dimensional structures into complex, engineered three-dimensional layouts. Attractive features include applicability to wide ranging layout designs and dimensions along with the capacity to integrate planar thin film materials and device layouts. The work reported here establishes further capabilities for directly embedding high-performance electronic devices into the resultant 3D constructs based on silicon nanomembranes (Si NMs) as the active materials in custom devices or microscale components released from commercial wafer sources. Systematic experimental studies and theoretical analysis illustrate the key ideas through varied 3D architectures, from interconnected bridges and coils to extended chiral structures, each of which embed n-channel Si NM MOSFETs (nMOS), Si NM diodes, and p-channel silicon MOSFETs (pMOS). Examples in stretchable/deformable systems highlight additional features of these platforms. These strategies are immediately applicable to other wide-ranging classes of materials and device technologies that can be rendered in two-dimensional layouts, from systems for energy storage, to photovoltaics, optoelectronics, and others.</P> [FIG OMISSION]</BR>

PHYLOGENY OF MADS-BOX GENES : ITS RELEVANCE FOR PLANT BREEDING AND THE EVOLUTION OF FLOWER DEVELOPMENT

Günter Theiβen,Annette Becker,Jorge Cacharron,Wim Deleu,Alexandra Di Rosa,Wolfram Faigl,Akira Kanno,Jan T. Kim,Charlotte Kirchner,Zheng Meng,Thomas Munster,Sunsane Werth,Luzie Ursula Wingen,Kai-U Plant molecular biology and biotechnology research 1998 Proceedings the 2nd Korean-Germany joint symposium Vol.1998 No.-

MADS-box genes (Schwarz-Sommer et al. 1990) contribute significantly to the development of inflorescences and flowers, e.g. by acting as floral meristem or organ identity genes (for recent reviews, see Thei?en and Saedler 1995; Thei?en et al. 1996;Riechmann and Meyerowitz 1997). Up to now, MADS-box genes have mainly been studied in the scientific context of developmental biology, and in eudicotyledonous model plants of little commercial value, such as Antirrhinum and Arabidopsis. The focus of our group is to apply our current knowledge about flower development to breeding research and evolutionary biology. Therefore, we are currently characterizing the MADS-box gene family in the important monocotyledonous crop plant maize (Zea mays ssp. mays), and in other phylogenetic informative taxa, such as the monocots lily (Lilium regale) and tulip (Tulipa gesneriana), the basal angiosperm Cabomba, and non-flowering plnats including the gymnosperm Gnetum gnemon and the ferns Ceratopteris and Ophioglossum.

The back contact modification in high-efficiency Cu₂ZnSn(S,Se)₄ solar cells by a thin MoO₃ layer

Septia KHOLIMATUSSADIAH,Cheng-Ying CHEN,Wei-Chao CHEN,Yi-Rung LIN,Shao-Hung LU,Meng-Chia HSIEH,Jan-Kai CHANG,Chih-I WU,Ruei-San CHEN,Kuei-Hsien CHEN,Li-Chyong CHEN 한국진공학회 2016 한국진공학회 학술발표회초록집 Vol.2016 No.8

Ultrathin Trilayer Assemblies as Long-Lived Barriers against Water and Ion Penetration in Flexible Bioelectronic Systems

Song, Enming,Li, Rui,Jin, Xin,Du, Haina,Huang, Yuming,Zhang, Jize,Xia, Yu,Fang, Hui,Lee, Yoon Kyeung,Yu, Ki Jun,Chang, Jan-Kai,Mei, Yongfeng,Alam, Muhammad A.,Huang, Yonggang,Rogers, John A. American Chemical Society 2018 ACS NANO Vol.12 No.10

<P>Biomedical implants that incorporate active electronics and offer the ability to operate in a safe, stable fashion for long periods of time must incorporate defect-free layers as barriers to biofluid penetration. This paper reports an engineered material approach to this challenge that combines ultrathin, physically transferred films of silicon dioxide (t-SiO<SUB>2</SUB>) thermally grown on silicon wafers, with layers of hafnium oxide (HfO<SUB>2</SUB>) formed by atomic layer deposition and coatings of parylene (Parylene C) created by chemical vapor deposition, as a dual-sided encapsulation structure for flexible bioelectronic systems. Accelerated aging tests on passive/active components in platforms that incorporate active, silicon-based transistors suggest that this trilayer construct can serve as a robust, long-lived, defect-free barrier to phosphate-buffered saline (PBS) solution at a physiological pH of 7.4. Reactive diffusion modeling and systematic immersion experiments highlight fundamental aspects of water diffusion and hydrolysis behaviors, with results that suggest lifetimes of many decades at physiological conditions. A combination of ion-diffusion tests under continuous electrical bias, measurements of elemental concentration profiles, and temperature-dependent simulations reveals that this encapsulation strategy can also block transport of ions that would otherwise degrade the performance of the underlying electronics. These findings suggest broad utility of this trilayer assembly as a reliable encapsulation strategy for the most demanding applications in chronic biomedical implants and high-performance flexible bioelectronic systems.</P> [FIG OMISSION]</BR>