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1

Owen, Caroline A. Monocyte adherence to fibronectin: Role of CD11/CD18 integrins and relationship to other monocyte functions. Birmingham: University of Birmingham, 1992.

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2

Moody, D. Branch, ed. T Cell Activation by CD1 and Lipid Antigens. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-69511-0.

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3

name, No. Ectopeptidases: CD13/aminopeptidase N and CD26/dipeptidylpeptidase IV in medicine and biology. New York, NY: Kluwer Academic/Plenum, 2003.

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4

Pumphrey, Nicholas Jonathan. Delineating the signalling potential of the cytoplasmic tail of CD31, and related protein CD66a. Birmingham: University of Birmingham, 2000.

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5

Roger, Knowles. Better by design?: A contractor's guide to the JCT standard form of buildingcontract with contractor's design (CD81). Knutsford: Knowles, 1990.

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6

David, Chappell, and Smith Mark, eds. Better by design?: A contractor's guide to the JCT standard form of building contract with contractor's design (CD81). 2nd ed. Knutsford: Knowles Publications, 1994.

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7

S, Jack Robert, ed. CD14 in the inflammatory response. Basel: Karger, 2000.

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8

Computer arts: CD101 : October 2004. Future, 2004.

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9

Jack, R. S., ed. CD14 in the Inflammatory Response. S. Karger AG, 1999. http://dx.doi.org/10.1159/isbn.978-3-318-00463-2.

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10

Bowen, P. Ellis M. Way Ahead 1 Tb Cdx1. Macmillan, 2010.

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11

GOICOECHEA, NESTOR, JOSE MANUEL SANCHEZ, ANDRES PASTOR, MANUEL OTERO, JOSE MARIA PORTELA, DAVID REPETO, JOSE LUIS VIGUERA, et al. DYNA NOTE BOOK #1: PROJECT MANAGEMENT. PUBLICACIONES DYNA, 2015. http://dx.doi.org/10.6036/cd1.

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12

Surgery Healing Cd1 (Healing after Surgery). Insight Audio, 2004.

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13

Jack, Robert S., ed. Cd14 In The Inflammatory Response (CHEMICAL IMMUNOLOGY (FORMERLY PROGRESS ALLERGY)). Karger, 2000.

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14

Various and Branch D. Moody. T Cell Activation by CD1 and Lipid Antigens. Springer, 2010.

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15

Branch, Moody D., ed. T cell activation by CD1 and lipid antigens. Berlin: Springer, 2007.

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16

Moody, Branch D. T Cell Activation by Cd1 and Lipid Antigens. Springer, 2008.

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17

B, Brenner M., ed. Antigen presentation by CD1 and NK T cells. London: Academic Press, 2000.

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18

Sjogren, Tove. Structural Plasticity and Function in Cytochrome Cd1 Nitrite Reductase. Uppsala Universitet, 2001.

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19

Haeryfar, S. M. Mansour, and Thierry Mallevaey, eds. CD1- and MR1-restricted T Cells in Antimicrobial Immunity. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-750-7.

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20

Langner, Jürgen, and Siegfried Ansorge. Ectopeptidases: CD13/Aminopeptidase N and CD26/Dipeptidylpeptidase IV in Medicine and Biology. Springer, 2012.

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21

Walsh, Ciaran J. The role of CD18 dependent neutrophil adhesion in septic acute lung injury. 1992.

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22

(Editor), Jürgen Langner, and Siegfried Ansorge (Editor), eds. Ectopeptidases: CD13/Aminopeptidase N and CD26/Dipeptidylpeptidase IV in Medicine and Biology. Springer, 2002.

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23

Ljutic, Belma. Characterization of lineage-specific expression and signaling function of mouse NKR-P1 (CD161). 2004.

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24

Carlyle, James Robert. Regulation of NK1.1 (NKR-P1/CD161) expression during lymphocyte lineage commitment in the fetal mouse. 1999.

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25

Iwabuchi, Kazuya, and Luc Van Kaer, eds. Role of CD1- and MR1-restricted T cells in Immunity and Disease. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-122-3.

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26

Kowalczuk, C. I. Teratological Effects of Exposure to 20 Mt, 50 Hz Magnetic Fields in Cd1 Mice. National Radiological Protection Board, 1992.

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27

T Cell Activation by CD1 and Lipid Antigens (Current Topics in Microbiology and Immunology Book 314). Springer, 2007.

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28

Tortora, Gerard J. Custom Introduction to Human Body 6th Edition with Black Microbiology & Cd1 Pkg for Georgian College (0471222798, 0470832681, 0471401625). Not Avail, 2003.

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29

Professional Ruby Collection: Mongrel, Rails Plugins, Rails Routing, Refactoring to REST, and Rubyisms CD1. Addison-Wesley Professional, 2007.

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30

Integrated Management Strategy for Arboviral Disease Prevention and Control in the Americas. Organización Panamericana de la Salud, 2020. http://dx.doi.org/10.37774/9789275120491.

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In recent years, conditions in the Region of the Americas have been highly favorable for the introduction and spread of arthropod-borne viral infections (arboviral diseases). Although dengue has been circulating for over 400 years, the number of cases reported since the year 2000 represents an unprecedented increase, with four serotypes in circulation. Since that year, 19.6 million cases of dengue have been reported to PAHO/WHO, including more than 800,000 severe cases and over 10,000 deaths. In 2015 and 2016 alone, more than 4.8 million cases were reported, 17,000 of them severe, resulting in 2,000 deaths. Despite a 23% reduction in the dengue case-fatality rate in the last six years (from 0.069% to 0.053%), the continued risk of severe disease and even death poses a serious public health problem in the Americas. Today, arboviruses present an extremely complex and unstable epidemiological situation, given the simultaneous epidemic circulation of three arboviral diseases and the risk that others could become epidemics, for example, Mayaro fever. Countries are aware that this complex situation can only be addressed with a comprehensive and multidisciplinary approach. The development of IMS-arbovirus is part of a history of technical cooperation between PAHO/WHO and the countries and territories of the Americas. It is based on the lessons learned during the development and implementation of national IMS-dengue programs in recent years. This history of cooperation is not new. It dates back to October 1947, with the adoption of Resolution CD1.R1 during the first Directing Council of PAHO. This resolution stated that the solution to the problem of urban yellow fever would be the eradication of Ae. aegypti in the entire hemisphere. The success of that campaign was demonstrated in 1962, with the eradication of this vector in 18 countries in the Region and several Caribbean islands.
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