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1

Ochieng, D. Damage caused by forest animals to farms adjacent to the south western side of Mount Kenya Forest Reserve. Nairobi: KIFCON, Karura Forest Station, 1993.

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2

Emerton, L. A survey to assess the damage caused by wild animals to farm households adjacent to the Aberdares Forest Reserve. Nairobi: KIFCON, Karura Forest Station, 1992.

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3

Great Britain. Department of the Environment. und Construction Research Communications Ltd, Hrsg. Damage to buildings caused by trees. London: Construction Research Communications, 1996.

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4

Koch, Bernhard A., Hrsg. Damage Caused by Genetically Modified Organisms. Berlin, New York: DE GRUYTER, 2010. http://dx.doi.org/10.1515/9783899498127.

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5

Pappel, Roland. Civil liability for damage caused by waste. Berlin: Duncker & Humblot, 1995.

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6

Service, United States Animal and Plant Health Inspection. Strategic plan: Animal Damage Control. Washington, D.C.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, 1989.

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7

Baumgartner, David M. Animal damage control in Washington. Pullman, Wash: Cooperative Extension, College of Agriculture & Home Economics, Washington State University, 1985.

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8

Bobath, Berta. Abnormal postural reflex activity caused by brain lesions. 3. Aufl. London: Heinemann Physiotherapy in association with The Chartered Society of Physiotherapy, 1985.

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9

Chartered Society of Physiotherapy (Great Britain), Hrsg. Abnormal postural reflex activity caused by brain lesions. 3. Aufl. London: W. Heinemann Medical Books, 1985.

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10

Marianne, Lipanovich, und Ortho Books, Hrsg. Protecting your garden from animal damage. San Ramon, CA: Ortho Books, 1994.

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11

Dempsey, Lynn. A quantification of concrete damage caused by alkali-silica reaction. [London]: Queen Mary and Westfield College, 1990.

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12

Hoverd, Tim. Blackfriars Monastery: Hereford : an assessment of damage caused by vandals. Hereford: City of Hereford Archaeology Unit, 1995.

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13

Dieting causes brain damage: How to lose weight without losing your mind. Kansas City, Mo: Andrews McMeel Pub., 2006.

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14

Kenkyūjo, Bōsai Kagaku Gijutsu. 2008-nen Iwate Miyagi nairiku jishin saigai chōsa hōkoku: Report on disasters caused by 2008 Iwate-Miyagi earthquake. Ibaraki-ken Tsukuba-shi: Bōsai Kagaku Gijutsu Kenkyūjo, 2010.

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15

Parola, Arthur C. Highway infrastructure damage caused by the 1993 Upper Mississippi River basin flooding. Washington, D.C: National Academy Press, 1998.

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16

Service, United States Animal and Plant Health Inspection. Animal Damage Control Program: Final environmental impact statement. Washington, DC: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, 1997.

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17

O'Toole, Randal. Audit of the USDA Animal Damage Control Program. Oak Grove, Or: Cascade Holistic Economic Consultants, 1994.

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18

District, United States Bureau of Land Management Casper. Environmental assessment: Animal damage control on public lands. Casper, Wyo: U.S. Department of the Interior, Bureau of Land Management, Casper District, 1994.

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19

United States. Animal and Plant Health Inspection Service. Animal Damage Control Program: Final environmental impact statement. Washington, D.C: United States Department of Agriculture, Animal and Plant Health Inspection Service, 1994.

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20

Bar, Christian von. Non-contractual liability arising out of damage caused to another (PEL liab. dam.). Oxford: Oxford University Press, 2009.

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21

Bar, Christian von. Non-contractual liability arising out of damage caused to another: (PEL Liab. Dam.). Munich: Sellier, 2009.

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22

Hegdal, Paul L. Prevention and control of animal damage to hydraulic structures. Denver, Colo: [Denver Wildlife Research Center], 1991.

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23

Hegdal, Paul L. Prevention and control of animal damage to hydraulic structures. Denver, Colo: [Denver Wildlife Research Center], 1991.

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24

J, Harbour A., Denver Wildlife Research Center, United States. Bureau of Reclamation. und United States. Animal and Plant Health Inspection Service., Hrsg. Prevention and control of animal damage to hydraulic structures. Denver, Colo: [Denver Wildlife Research Center], 1991.

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25

Administration, United States Maritime, Hrsg. Port damage assessment: Short-term action report-- April 2000 : Honduras : assessment of port infrastructure damage caused by Hurricane Mitch, 1998. [Washington, D.C.?]: The Administration, 2000.

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26

Administration, United States Maritime. Port damage assessment: Short-term action report-- April 2000 : Honduras : assessment of port infrastructure damage caused by Hurricane Mitch, 1998. [Washington, D.C.?]: The Administration, 2000.

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27

Administration, United States Maritime. Port damage assessment: Short-term action report-- April 2000 : Nicaragua : assessment of port infrastructure damage caused by Hurricane Mitch, 1998. [Washington, D.C.?]: The Administration, 2000.

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28

Administration, United States Maritime. Port damage assessment: Short-term action report-- April 2000 : Nicaragua : assessment of port infrastructure damage caused by Hurricane Mitch, 1998. [Washington, D.C.?]: The Administration, 2000.

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29

Administration, United States Maritime. Port damage assessment: Short-term action report-- April 2000 : Honduras : assessment of port infrastructure damage caused by Hurricane Mitch, 1998. [Washington, D.C.?]: The Administration, 2000.

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30

Administration, United States Maritime, Hrsg. Port damage assessment: Short-term action report-- April 2000 : Nicaragua : assessment of port infrastructure damage caused by Hurricane Mitch, 1998. [Washington, D.C.?]: The Administration, 2000.

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31

Rangen, Sheila A. A field guide to animal damage of Alberta's native trees. Vegreville, Alta: Alberta Research Council, 1997.

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32

Rai, Rajesh Kumar. Valuing the damage caused by invasive plant species in a low-income community in Nepal. Kathmandu: South Asian Network for Development and Environmental Economics, 2012.

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33

Linscombe, Greg. A survey of vegetative damage caused by nutria herbivory in the Barataria and Terrebonne basins. [Thibodaux, LA]: Barataria-Terrebonne National Estuary Program, 1997.

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34

Hawksworth, Frank G. Permanent plots for quantifying damage caused by western dwarf mistletoes and their spread and intensification. [Fort Collins, Colo.]: Rocky Mountain Forest and Range Experiment Station, 1990.

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35

Braathe, Peder. Birch dieback--caused by prolonged early spring thaws and subsequent frost. Ås, Norway: Forskningsparken i Ås AS, Infosenteret, 1995.

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36

Kenkyūjo, Bōsai Kagaku Gijutsu. 2010-nen 10-gatsu 20-nichi Amami Ōshima gōu saigai chōsa hōkoku: Report on disaster caused by the October 2010 heavy rainfall in Amami Oshima. Tsukuba-shi: Bōsai Kagaku Gijutsu Kenkyūjo, 2011.

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37

Thomson, M. Economic analysis of farm damage caused by wildlife along the south-western side of Mount Kenya. Nairobi: KIFCON, Karura Forest Station, 1993.

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38

Thomson, M. Economic analysis of plantation damage caused by wildlife along the south-western side of Mount Kenya. Nairobi: KIFCON, 1993.

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39

Commission, Ireland Law Reform. Report on the liability in tort of minors and the liability of parents for damage caused by minors. Dublin: The Commission, 1985.

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40

United States. President (1993-2001 : Clinton). Emergency appropriations for damage caused by Hurricane Georges: Communication from the President of the United States transmitting from the President, requesting emergency supplemental appropriations for the repair of damage caused by Hurricane Georges, pursuant to Pub. L. 105-277. Washington: U.S. G.P.O., 1998.

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41

Wolff, Pat. Waste, fraud & abuse in the U.S. Animal Damage Control Program: A special report. 2. Aufl. Tucson: Wildlife Damage Review, 1995.

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42

Klemm, Cyrille De. Compensation for Damage Caused by Wild Animals (Nature and Environment). Manhattan Pub. Co., 1996.

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43

Hone, Jim. Wildlife Damage Control. CSIRO Publishing, 2007. http://dx.doi.org/10.1071/9780643094390.

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The types of damage caused by wildlife are many and varied, and can be costly and far-reaching. Until now, there has been little effort to identify and evaluate generalities across that broad range of species, methods and topics. Wildlife Damage Control promotes principle-based thinking about managing impact. It documents and discusses the key principles underlying wildlife damage and its control, and demonstrates their application to real-life topics – how they have been used in management actions or how they could be tested in the future. It synthesises the wide but diffuse literature dealing with the impacts of vertebrate pests and encourages readers to adopt a more theoretical framework for thinking about pest impacts and ways to manage them. The book is organised around key principles that apply across species, rather than looking at individual species, and is damage-based not pest animal-based. Within each chapter there are exercises designed to help readers learn and evaluate key principles. Conservation biologists, ecologists and others involved in wildlife management will find the sections covering principles in biodiversity conservation, of production such as agriculture, and in human and animal health of real value.
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44

Fink, Mitchell P. Ischaemia-reperfusion injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0308.

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Ischaemia/reperfusion (I/R) injury contributes to the pathogenesis of many common clinical conditions, including stroke, myocardial damage after percutaneous intervention for acute coronary artery occlusion, primary graft dysfunction after solid organ transplantation. The mechanisms that are responsible for I/R injury remain incompletely understood, but damage caused by reactive oxygen species (ROS) and reactive nitrogen species clearly is important. A number of therapeutic approaches, such as administration of ROS scavengers, are effective in animal models of I/R injury, but for the most part, translation of these findings into strategies that can clearly benefit patients has yet to be achieved.
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45

Greive, Bradley Trevor. Dieting Causes Brain Damage. Andrews McMeel Publishing, 2006.

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46

Greive, Bradley Trevor. Dieting causes brain damage. Random House Australia, 2006.

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47

Cui, Zhao, Neil Turner und Ming-hui Zhao. Antiglomerular basement membrane disease. Herausgegeben von Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
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48

Animal-caused outages. Arlington, Va: National Rural Electri Cooperative Association, 1996.

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49

Koch, Bernhard A. Damage Caused by Genetically Modified Organisms. De Gruyter, Inc., 2010.

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50

Cattran, Daniel C., und Heather N. Reich. Membranous glomerulonephritis. Herausgegeben von Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
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