Livros: "Bird damage"

1

Blackbird and cowbird: Publications of the Section of Bird Damage Control. Denver, Colo: U.S. Fish and Wildlife Service, Denver Wildlife Research Center, 1985.

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2

Besser, Jerome F. A growers guide to reducing bird damage to U.S. agricutural [sic.] crops. Denver, Colo: Denver Wildlife Research Center, U.S. Fish and Wildlife Service, 1985.

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3

Boyce, Laurie. An economic analysis of bird damage in vineyards of the Marlborough Region. Palmerston North, N.Z: Centre for Applied Economics and Policy Studies, Dept. of Applied and International Economics, Massey University, 1999.

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4

), Wildlife Services (U S. Environmental assessment: Piscivorous bird damage management for the protection of juvenile salmonids on the Mid-Columbia River. Washington, D.C.]: Wildlife Services, U.S. Dept. of Agriculture, [2003, 2003.

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5

Hothem, Roger L. Bird damage to sunflower in North Dakota, South Dakota, and Minnesota, 1979-1981. Washington, D.C: U.S. Dept. of the Interior, Fish and Wildlife Service, 1988.

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6

Glahn, James F. A science-based initiative to manage double-crested cormorant damage to southern aquaculture. [Washington, D.C.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 2000.

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7

Glahn, James F. A science-based initiative to manage double-crested cormorant damage to southern aquaculture. [Washington, D.C.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 2000.

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8

Glahn, James F. A science-based initiative to manage double-crested cormorant damage to southern aquaculture. [Washington, D.C.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 2000.

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9

Glahn, James F. A science-based initiative to manage double-crested cormorant damage to southern aquaculture. [Washington, D.C.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 2000.

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10

Besser, Jerome F. Bird damage to ripening field corn increases in the United States from 1971 to 1981. Washington, D.C: U.S. Dept. of the Interior, Fish and Wildlife Service, 1986.

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11

Great, Plains Wildlife Damage Control Workshop (8th 1987 Rapid City S. D. ). Eighth Great Plains Wildlife Damage Control Workshop proceedings: April 28-30, 1987, Rapid City, South Dakota. Fort Collins, Colo: U.S. Dept. of Agriculture, Forest Service, Rocky Mountain Forest and Range Experiment Station, 1988.

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12

Office, General Accounting. Natural resources damage assessment: Information on study of seabirds killed by Exxon Valdez oil spill : report to the Honorable Frank H. Murkowski, U.S. Senate. Washington, D.C: The Office, 1991.

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13

Establishment, Building Research, ed. Bird bee and plant damage to buildings. Watford: Building Research Establishment, 1996.

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14

Center, Denver Wildlife Research, ed. Publications of the Denver Wildlife Research Center on birds and bird damage control. Denver, Colo: The Center, 1985.

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15

United States. Animal and Plant Health Inspection Service. Solutions through science: Reducing damage caused by cultures. 2^a ed. 2011.

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16

United States. National Marine Fisheries Service., U.S. Fish and Wildlife Service. e Washington (State). Dept. of Fish and Wildlife., eds. Environmental assessment: Piscivorous bird damage management for the protection of juvenile salmonids on the mid-Columbia River. [Washington, D.C.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, 2003.

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17

Hogg, Gary. I Heard of a Nerd Bird. Aro Books Inc., 1991.

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18

Controlling blackbird damage to sunflower and grain crops in the northern Great Plains. [Washington, D.C.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, 1997.

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19

Wounded Warriors: A Soldier's Story of Healing Through Birds. Potomac Books, Incorporated, 2015.

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20

Sonja, Meier. Ch.11 Plurality of obligors and of obligees, s.1: Plurality of Obligors, Introduction to Section 11.1 of the PICC. Oxford University Press, 2015. http://dx.doi.org/10.1093/law/9780198702627.003.0213.

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Section 11.1 of the UNIDROIT Principles of International Commercial Contracts (PICC) deals with the plurality of obligors in a contractual setting. Questions of a plurality of obligors arise in various circumstances. Several obligors may jointly bind themselves towards the obligee in a single promise or a single contract. If is only one obligor, a second party may bind itself towards the obligee to perform the same obligation. Several persons may be responsible for the same damage, or may have stood surety for the same debt. Section 11.1 describes two kinds of plurality, namely joint and several obligations, on the one hand, and separate obligations, on the other hand, with a default rule in favour of joint and several obligations. It also addresses rules for joint and several obligations, the relationship between obligors and obligee, and the internal relationship between the obligors.

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21

Goldberg, Jeff, e Doris Burke. Bird at the Buzzer: UConn, Notre Dame, and a Women's Basketball Classic. University of Nebraska Press, 2013.

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22

Cattran, Daniel C., e Heather N. Reich. Membranous glomerulonephritis. Editado por 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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23

J, Kittle Lewey, ed. The Washington State Department of Ecology marine resource damage assessment report for the ARCO Anchorage oil spill December 21, 1985 into Port Angeles Harbor and the Strait of Juan de Fuca. [Olympia?]: State of Washington Ecology, 1987.

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24

O’Connell, Sue. Lyme borreliosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0009.

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Lyme borreliosis is the most common vector-borne bacterial infection in the temperate northern hemisphere. In the United States of America over 35,000 confirmed or probable cases were reported by state health departments to the Centers for Disease Control and Prevention (CDC) in 2008. It is likely that well over 100,000 cases occur in Europe each year. Lyme borreliosis is caused by several genospecies of Borrelia burgdorferi sensu lato, which are transmitted by ticks of the Ixodes ricinus complex. The infection occurs most commonly in forested, woodland and heathland habitats that support the lifecycles of Ixodes ticks and the small mammals and birds that are reservoir-competent hosts for B burgorferi. The most common presenting feature of Lyme borreliosis is erythema migrans, a slowly spreading rash. The spirochaetes can disseminate through the bloodstream and lymphatics to other organs and tissues and cause later manifestations, most commonly affecting the nervous and musculoskeletal systems. The infection responds to appropriate antibiotic treatment at any stage of disease, with excellent outcomes in most cases, but patients with severe tissue damage from previously untreated late stage disease may recover incompletely. A small proportion of patients can have persistent non-specific symptoms following treatment, without evidence of continuing active infection. This has been termed “post-Lyme syndrome” and appears to be similar to other post-infection syndromes. Prevention relies mainly on personal protection measures against tick bites.

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25

Kneeland, Timothy W. Playing Politics with Natural Disaster. Cornell University Press, 2020. http://dx.doi.org/10.7591/cornell/9781501748530.001.0001.

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Hurricane Agnes struck the United States in June of 1972, just months before a pivotal election and at the dawn of the deindustrialization period across the Northeast. The response by local, state, and national officials had long-term consequences for all Americans. President Richard Nixon used the tragedy for political gain by delivering a generous relief package to the key states of New York and Pennsylvania in a bid to win over voters. After his landslide reelection in 1972, Nixon cut benefits for disaster victims and then passed legislation to push responsibility for disaster preparation and mitigation onto states and localities. The impact led to the rise of emergency management and inspired the development of the Federal Emergency Management Agency (FEMA). With a particular focus on events in New York and Pennsylvania, this book narrates how local, state, and federal authorities responded to the immediate crisis of Hurricane Agnes and managed the long-term recovery. The impact of Agnes was horrific, as the storm left 122 people dead, forced tens of thousands into homelessness, and caused billions of dollars in damage from Florida to New York. In its aftermath, local officials and leaders directed disaster relief funds to rebuild their shattered cities and reshaped future disaster policies. The book explains how the political decisions by local, state, and federal officials shaped state and national disaster policy and continues to influence emergency preparedness and response to this day.

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26

Pozio, Edoardo. Trichinellosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0068.

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Trichinellosis is caused by nematodes of the genus Trichinella. These zoonotic parasites show a cosmopolitan distribution in all the continents, but Antarctica. They circulate in nature by synanthropic-domestic and sylvatic cycles. Today, eight species and four genotypes are recognized, all of which infect mammals, including humans, one species also infects birds, and two other species infect also reptiles.Parasites of the genus Trichinella are unusual among the other nematodes in that the worm undergoes a complete developmental cycle, from larva to adult to larva, in the body of a single host, which has a profound influence on the epidemiology of trichinellosis. When the cycle is complete, the muscles of the infected animal contain a reservoir of larvae, capable of long-term survival. Humans and other hosts become infected by ingesting muscle tissuescontaining viable larvae.The symptoms associated with trichinellosis vary with the severity of infection, i.e. the number of viable larvae ingested, and the time after infection. The capacity of the worm population to undergo massive multiplication in the body is a major determinant. Progression of disease follows the biological development of the parasite. Symptoms are associated first with the gastrointestinal tract, as the worms invade and establish in the small intestine, become more general as the body responds immunologically, and finally focus on the muscles as the larvae penetrate the muscle cells and develop there. Although Trichinella worms cause pathological changes directly by mechanical damage, most of the clinical features of trichinellosis are immunopathological in origin and can be related to the capacity of the parasite to induce allergic responses.The main source of human infection is raw or under-cooked meat products from pig, wild boar, bear, walrus, and horses, but meat products from other animals have been implicated. In humans, the diagnosis of infection is made by immunological tests or by direct examination of muscle biopsies using microscopy or by recovery of larvae after artificial digestion. Treatment requires both the use of anthelmintic drugs to kill the parasite itself and symptomatic treatment to minimize inflammatory responses.Both pre-slaughter prevention and post-slaughter control can be used to prevent Trichinella infections in animals. The first involves pig management control as well as continuous surveillance programmes. Meat inspection is a successful post-slaughter strategy. However, a continuous consumer education is of great importance in countries where meat inspection is not mandatory.

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27

Karmali, Mohamed A., e Jan M. Sargeant. Verocytotoxin-producing Escherichia coli (VTEC) infections. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0008.

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Verocytotoxin (VT)-producing Escherichia coli (VTEC), also known as Shiga toxin producing E. coli (STEC), are zoonotic agents, which cause a potentially fatal illness whose clinical spectrum includes diarrhoea, haemorrhagic colitis, and the haemolytic uraemic syndrome (HUS). VTEC are of serious public health concern because of their association with large outbreaks and with HUS, which is the leading cause of acute renal failure in children. Although over 200 different OH serotypes of VTEC have been associated with human illness, the vast majority of reported outbreaks and sporadic cases of VTEC-infection in humans have been associated with serotype O157:H7.VTs constitute a family of related protein subunit exotoxins, the major ones implicated in human disease being VT1, VT2, and VT2c. Following their translocation into the circulation, VTs bind to endothelial cells of the renal glomeruli, and of other organs and tissues via a specific receptor globotriosylceramide (Gb 3), are internalized by a process of receptor-mediated endocytosis, and cause subcellular damage that results in the characteristic microangiopathic disease observed in HUS.The incubation period of VTEC-associated illness is about 3–5 days. After ingestion VTEC (especially of serotype O157:H7) multiply in the bowel and colonize the mucosa of probably the large bowel with a characteristic attaching and effacing (AE) cytopathology. Colonization is followed by the translocation of VTs into the circulation and the subsequent manifestation of disease.The majority of patients with uncomplicated VTEC infection recover fully with general supportive measures. Historically, the case-fatality rate was high for HUS. However, improvement in the treatment of renal failure and the attendant biochemical disturbances has substantially improved the outlook, although long-term sequelae may develop.Ruminants, especially cattle, are the main reservoirs of VTEC. Infection is acquired through the ingestion of contaminated food, especially under-cooked hamburger, through direct contact with animals, via contaminated water or environments, or via personto-person transmission.The occurrence of large outbreaks of food-borne VTEC-associated illness has promoted close scrutiny of this zoonoses at all levels in the chain of transmission, including the farm, abattoir, food processing, packaging and distribution plants, the wholesaler, the retailer and the consumer. While eradication of VTEC O157 at the farm may not be an option, interventions to increase animal resistance or to decrease animal exposure are being developed and validated. Hazard Analysis and Critical Control Programmes are being implemented in the processing sector and appear to be associated with temporal decreases in VTEC serotype O157 illness in humans. Education programmes targeting food handling procedures and hygiene practices are being advocated at the retail and consumer level. Continued efforts at all stages from the farm to the consumer will be necessary to reduce the risk of VTEC-associated illness in humans.

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