Relevant bibliographies by topics / Alpaca – Diseases

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  3. Books
  4. Book chapters
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Academic literature on the topic 'Alpaca – Diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Alpaca – Diseases"

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Rojas, Miguel, Alberto Manchego, Camila B. Rocha, Luz Alba Fornells, Raquel C. Silva, Gabriella S. Mendes, Helver G. Dias, Nieves Sandoval, Danilo Pezo, and Norma Santos. "Outbreak of diarrhea among preweaning alpacas (Vicugna pacos) in the southern Peruvian highland." Journal of Infection in Developing Countries 10, no. 03 (March 31, 2016): 269–74. http://dx.doi.org/10.3855/jidc.7398.

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Introduction: Infections, particularly diarrheal infections, are a major cause of neonatal death in South American camelids. The aim of this study was to identify the pathogens that could have caused the recent diarrhea outbreak among the alpacas in Silli, Cusco, located in the southern Peruvian highland. Methodology: Spleen, kidney, and intestine tissue along with fecal and intestinal lavage samples were obtained from 50 one- to five-week-old alpacas and analyzed for the presence of parasites, bacteria, and viruses. Results: Laboratory testing of the 50 crias included in this study revealed that 80% were infected with Eimeria spp., 40% with coronavirus, 34% with E. coli, 32% with rotavirus, 22% with Clostridium spp., and 20% with Cryptosporidium spp. Of these 50 alpaca crias, 20 presented with a single infection (19 positive for Eimeria spp. and 1 positive for rotavirus). Co-infections with up to four pathogens occurred in 60% of the samples. The significance of such infections is not clear, but it is noteworthy that the animals suffering from necrotic and/or hemorrhagic enteritis presented with quadruple infections. It is likely that co-infections increase the severity of the disease. Conclusions: These data show that multiple pathogens circulate among young alpaca crias and could be associated with diarrheal disease in these animals. The findings from this study warrant the provision of subsidies for future assessment of the potential economic impact of these infections on the productivity of the Peruvian alpaca industry.
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Sampaio, Natalia, Mark Gishen, Kevin Reed, Mel Brown, Daphne Gregory, and Kylie Munyard. "The occurrence and severity of grass toxicoses in Australian alpaca (Vicugna pacos) herds." Australian Journal of Experimental Agriculture 48, no. 8 (2008): 1099. http://dx.doi.org/10.1071/ea06325.

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A survey of 108 alpaca producers registered with the Australian Alpaca Association examined the occurrence and severity of ‘staggers’ (a colloquial term embracing various diseases of the nervous system in animals, characterised by neck tremors and head nodding in the milder alpaca cases and a lack of coordination in moving, a staggering gait and frequent falling in severe cases) in Australian alpaca and the presence of four pasture grasses, during three production seasons in 2004–2006. There have been few studies on the susceptibility of alpaca to staggers and its effect on productivity and animal welfare. The survey found that 23% of alpaca producers had observed staggering animals, with Victoria and South Australia being the most severely affected states. Clinical signs of staggers were most frequent in January–March, with a mean duration of 3 months. Some animals showed clinical signs lasting up to 12 months. A strong correlation was found between the presence of perennial ryegrass (P < 0.001) and phalaris (P < 0.003) and the occurrence of staggers. Based on grass presence and the timing when staggers was observed, it was concluded that perennial ryegrass toxicosis was the main cause of staggers in alpaca. About 12% and 9% of alpaca grazing pasture containing perennial ryegrass exhibited staggers in the two full seasons for which data were collected. Herds with staggering animals were correlated with those exhibiting possible subclinical effects – heat sensitivity and ill-thrift (P < 0.01) and reduced fertility (P < 0.05) – of perennial ryegrass endophyte toxins. Results indicate that weanlings and cria are more likely to stagger than adults. Thirteen of the 15 mixed farms with staggering alpaca did not observe staggers in other livestock, suggesting that alpaca may be more sensitive to the causal toxins than sheep and cattle.
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Björklund, Christina, Renée Båge, Jane Morrell, Kerstin de Verdier, Lisbeth Nisu Hartzell, Nanna Kjellinbro, Katinka Belák, Karin Bernodt, and Dolores Gavier-Widen. "Diseases and causes of death among alpacas in Sweden: a retrospective study." Veterinary Record Open 6, no. 1 (April 2019): e000239. http://dx.doi.org/10.1136/vetreco-2017-000239.

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BackgroundDue to increasing popularity in Sweden during the last decade, alpacas are frequently encountered by practising veterinarians and pathologists. Knowledge regarding their health and diseases under Swedish conditions is, however, limited.ObjectivesTo improve knowledge about the health of alpacas in Sweden by collecting information on diseases and health status.DesignA retrospective study was made of 93 necropsies conducted on alpacas in Sweden during the period 2001–2013.SettingData were obtained from the two major veterinary pathology centres in Sweden. The alpacas were hobby or farm animals and they were submitted by veterinarians in local practices or at a national animal healthcare organisation.ResultsThe digestive system was most frequently affected (29 per cent), with parasitic gastroenteritis (17 per cent) and hepatic disease being especially prevalent (15 per cent fascioliasis and 7 per cent hepatitis). Cardiovascular conditions (9 per cent), systemic diseases (7 per cent) and perinatal deaths were also common, including abortions (10 per cent) and fatal septicaemia (4 per cent). Wasting/emaciation was a frequent finding (26 per cent). Other diagnoses included dermatitis (8 per cent), diseases of the central nervous system (8 per cent), traumatic injuries (7 per cent), neoplasia (5 per cent), pneumonia (5 per cent) and nephritis (3 per cent).ConclusionsThis study identified areas of concern regarding diagnostic and pathological procedures, for which specific measures have been recommended. One particular cause for concern was the number of deaths from emaciation in weanling alpacas during late winter or early spring. For adult alpacas, infectious and non-infectious causes of death were approximately equally frequent. Many of the diseases were considered clinically acute but pathology often showed them to be chronic conditions that had eventually deteriorated and presented as acute cases in the late stages. This study revealed similarities in the health/disease status reported in other European countries and in North America. The results can be used by alpaca keepers and veterinary practitioners to improve management, diagnosis and treatment of alpacas.
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Küchler, Leonore, Isabelle Rüfli, Michel C. Koch, Melanie M. Hierweger, Ronja V. Kauer, Céline L. Boujon, Monika Hilbe, et al. "Astrovirus-Associated Polioencephalomyelitis in an Alpaca." Viruses 13, no. 1 (December 30, 2020): 50. http://dx.doi.org/10.3390/v13010050.

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An 8-year-old alpaca was admitted to the emergency service of the Clinic for Ruminants in Bern due to a reduced general condition and progressive neurological signs. Despite supportive treatment, its condition deteriorated and the animal had to be euthanized. Histopathological analysis revealed a severe non-suppurative polioencephalomyelitis with neuronal necrosis, most likely of viral origin. We detected abundant neuronal labelling with antibodies directed against two different epitopes of Bovine Astrovirus CH13/NeuroS1 (BoAstV-CH13/NeuroS1), which is a common viral agent associated with non-suppurative encephalitis in Swiss cattle. These findings were further verified by detection of viral RNA by use of in-situ hybridization and real-time RT-PCR. Next generation sequencing revealed that the detected virus genome had a pairwise identity of 98.9% to the genome of BoAstV-CH13/NeuroS1. To our knowledge, this is the first report of an astrovirus-associated polioencephalomyelitis in an alpaca. These results point to the possibility of an interspecies transmission of BoAstV-CH13/NeuroS1.
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Prkno, Almut, Donata Hoffmann, Matthias Kaiser, Daniela Goerigk, Martin Pfeffer, Karsten Winter, Thomas W. Vahlenkamp, Martin Beer, and Alexander Starke. "Field Trial Vaccination against Cowpox in Two Alpaca Herds." Viruses 12, no. 2 (February 20, 2020): 234. http://dx.doi.org/10.3390/v12020234.

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In Europe, cowpox virus (CPXV) infection in South American camelids occurs as a so-called spill-over infection. Although infected animals generally have a mild form of the disease and survive, cases of fatal generalised CPXV infection have also been described. Prevention by prophylactic vaccination is the only way to protect animals from disease. In the present study, modified vaccinia virus Ankara (MVA) vaccine, which has been successfully used in many animal species, was used in a prime-boost vaccination regimen in two alpaca herds with a history of CPXV infection. The focus of the study was the prevention of further clinical cases, and to determine the safety and immunogenicity of the MVA vaccine in alpacas. The MVA vaccine was well tolerated and safe in the 94 animals vaccinated. An indirect immunofluorescence assay (IFA) using MVA as an antigen showed that the seroprevalence of antibody after booster vaccination was 81.3% in herd I and 91.7% in herd II. Detectable antibody titres declined to 15.6% in herd I and 45.8% in herd II over a 12-month period after booster vaccination. Animals could be divided into four groups based on individual antibody titres determined over one year: Group 1 consisted of 19.3% of animals that were seropositive until the end of the trial period; Group 2 consisted of 58.0% of animals that were seropositive after booster vaccination, but seronegative one year later; Group 3 consisted of 14.7% of animals that were not seropositive at any time point; and Group 4 consisted of 7.9% of animals that were seropositive after initial immunisation, seronegative six months later, but seropositive or intermediate in IFA one year after immunisation, likely because of natural exposure. In new-born crias born to MVA-vaccinated mares, specific maternal antibodies were detected in 50.0% of animals up to 14 weeks of age. Our results confirm that MVA vaccination is a feasible tool for the prevention of CPXV disease in alpacas. Long-term studies are needed to verify future vaccination regimen in CPXV affected herds.
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Kumar, Chaudhary, Lu, Duff, Heffel, McKinney, Bedenice, and Marthaler. "Metagenomic Next-Generation Sequencing Reveal Presence of a Novel Ungulate Bocaparvovirus in Alpacas." Viruses 11, no. 8 (July 31, 2019): 701. http://dx.doi.org/10.3390/v11080701.

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Viruses belonging to the genus Bocaparvovirus (BoV) are a genetically diverse group of DNA viruses known to cause respiratory, enteric, and neurological diseases in animals, including humans. An intestinal sample from an alpaca (Vicugna pacos) herd with reoccurring diarrhea and respiratory disease was submitted for next-generation sequencing, revealing the presence of a BoV strain. The alpaca BoV strain (AlBoV) had a 58.58% whole genome nucleotide percent identity to a camel BoV from Dubai, belonging to a tentative ungulate BoV 8 species (UBoV8). Recombination events were lacking with other UBoV strains. The AlBoV genome was comprised of the NS1, NP1, and VP1 proteins. The NS1 protein had the highest amino acid percent identity range (57.89–67.85%) to the members of UBoV8, which was below the 85% cut-off set by the International Committee on Taxonomy of Viruses. The low NS1 amino acid identity suggests that AlBoV is a tentative new species. The whole genome, NS1, NP1, and VP1 phylogenetic trees illustrated distinct branching of AlBoV, sharing a common ancestor with UBoV8. Walker loop and Phospholipase A2 (PLA2) motifs that are vital for virus infectivity were identified in NS1 and VP1 proteins, respectively. Our study reports a novel BoV strain in an alpaca intestinal sample and highlights the need for additional BoV research.
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Severo, L. C., J. C. Bohrer, G. R. Geyer, and L. Ferreiro. "Invasive aspergillosis in an alpaca (Lama pacos)." Medical Mycology 27, no. 3 (January 1989): 193–95. http://dx.doi.org/10.1080/02681218980000261.

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Adney, Danielle, Lingshu Wang, Neeltje van Doremalen, Wei Shi, Yi Zhang, Wing-Pui Kong, Megan Miller, et al. "Efficacy of an Adjuvanted Middle East Respiratory Syndrome Coronavirus Spike Protein Vaccine in Dromedary Camels and Alpacas." Viruses 11, no. 3 (March 2, 2019): 212. http://dx.doi.org/10.3390/v11030212.

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MERS-CoV is present in dromedary camels throughout the Middle East and Africa. Dromedary camels are the primary zoonotic reservoir for human infections. Interruption of the zoonotic transmission chain from camels to humans, therefore, may be an effective strategy to control the ongoing MERS-CoV outbreak. Here we show that vaccination with an adjuvanted MERS-CoV Spike protein subunit vaccine confers complete protection from MERS-CoV disease in alpaca and results in reduced and delayed viral shedding in the upper airways of dromedary camels. Protection in alpaca correlates with high serum neutralizing antibody titers. Lower titers of serum neutralizing antibodies correlate with delayed and significantly reduced shedding in the nasal turbinates of dromedary camels. Together, these data indicate that induction of robust neutralizing humoral immune responses by vaccination of naïve animals reduces shedding that potentially could diminish the risk of zoonotic transmission.
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Haake, Christine, Sarah Cook, Nicola Pusterla, and Brian Murphy. "Coronavirus Infections in Companion Animals: Virology, Epidemiology, Clinical and Pathologic Features." Viruses 12, no. 9 (September 13, 2020): 1023. http://dx.doi.org/10.3390/v12091023.

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Coronaviruses are enveloped RNA viruses capable of causing respiratory, enteric, or systemic diseases in a variety of mammalian hosts that vary in clinical severity from subclinical to fatal. The host range and tissue tropism are largely determined by the coronaviral spike protein, which initiates cellular infection by promoting fusion of the viral and host cell membranes. Companion animal coronaviruses responsible for causing enteric infection include feline enteric coronavirus, ferret enteric coronavirus, canine enteric coronavirus, equine coronavirus, and alpaca enteric coronavirus, while canine respiratory coronavirus and alpaca respiratory coronavirus result in respiratory infection. Ferret systemic coronavirus and feline infectious peritonitis virus, a mutated feline enteric coronavirus, can lead to lethal immuno-inflammatory systemic disease. Recent human viral pandemics, including severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and most recently, COVID-19, all thought to originate from bat coronaviruses, demonstrate the zoonotic potential of coronaviruses and their potential to have devastating impacts. A better understanding of the coronaviruses of companion animals, their capacity for cross-species transmission, and the sharing of genetic information may facilitate improved prevention and control strategies for future emerging zoonotic coronaviruses. This article reviews the clinical, epidemiologic, virologic, and pathologic characteristics of nine important coronaviruses of companion animals.
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Gomez-Puerta, Luis A., Johan Carrasco, Katherine Robles, Ana Vargas-Calla, Nelly G. Cribillero, Gianfranco Arroyo, Hugo Castillo, Maria T. Lopez-Urbina, and Armando E. Gonzalez. "Coccidiosis in clinically asymptomatic alpaca (Vicugna pacos) crias from the Peruvian Andes." Parasitology International 85 (December 2021): 102438. http://dx.doi.org/10.1016/j.parint.2021.102438.

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Dissertations / Theses on the topic "Alpaca – Diseases"

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Suxo, Blanco Macario. "Brucellosis in alpacas (Lama pacos) in communities of the city Ulla Ulla, Franz Tomayo province, department of La Paz." BYU ScholarsArchive, 2005. https://scholarsarchive.byu.edu/etd/5436.

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This investigation was performed in the Altiplano Altoandino sub-humid region in the Ulla Ulla district, Pelechuco township, Franz Tomayo province, department of La Paz, Bolivia. The objective of this study was to quantify and compare the presence of Brucellosis in male and female alpacas (Lama pacos) at ages 2, 3, 4, 5, 6, and 7 years. Blood samples were taken from the jugular vein of 500 alpacas from the Hichucollo, Huacuchani, Ucha Ucha, and Ulla Ulla communities. The serum from each sample was separated and a serological diagnosis was performed by rapid agglutination with Rose Bengal chemical stain. In the Ulla Ulla district, 11.0% of alpacas were suspected of being infected. Of that 11.0%, 9.6% represented female alpacas while the remaining 1.4% represented male alpacas. By community, the overall results were 0.6%, 0.2%, 7.4%, and 2.8% for Hichucollo, Huacuchani, Ucha Ucha, and Ulla Ulla respectively. With regards to gender in each community, 1.4%, 1.6%, 13.3%, and 11.1% of female alpacas and 2.7%, 0.0%, 1.2%, and 1.9 % of male alpacas were suspected of being infected in Hichucollo, Huacuchani, Ucha Ucha, and Ulla Ulla, respectively. According to age, 0.8%, 2.6%, 3.8%, 2.0%, 11.8%, and 0.0% were suspected of Brucellosis in alpacas 2, 3, 4, 5, 6, and 7 years old, respectively in the Ulla Ulla district. The analysis of variance among the results does not present significant differences (p ≥ 0.05), failing to reject the given hypothesis. The final prevalence point found in the Ulla Ulla district was 11.0%. It was concluded that the prevalence of suspected cases of Brucellosis in alpacas is a consequence of the antigenic characteristics of each biotype. Furthermore, the results affirm that the poor management of livestock and livestock health lead to significant problems with alpaca health. It is therefore necessary to implement control strategies as well as disease monitoring in communities by following a detailed program of diagnostic tests for Brucellosis. Also, non-infected flocks must be protected against infection.
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Moualla, Dima. "The role of alpha synuclein in Parkinson's disease." Thesis, University of Bath, 2011. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555747.

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Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. It is characterized by the presence of intracellular inclusions termed Lewy bodies (LBs) and Lewy neuritis (LNs) in the brain, in which α-Syn aggregates constitute the main component. Therefore, α-Syn aggregation was implicated in the pathogenesis of PD. Structurally α-Syn is a disordered protein with little ordered structure under physiological conditions. However, research of α-Syn has provided substantial information about its structural properties. The precise function of α-Syn is still under investigation. Research has also shown that metals, such as copper and iron, accelerate α-Syn aggregation and fibrillation in vitro and are proposed to play an important role in vitro. In this study, isothermal titration calorimetry was used to determine iron binding properties to α-Syn revealing the presence of two binding sites for iron with an affinity of 1.06 x 105 M-1 and a dissociation constant of ~ 10μM which is physiologically relevant to iron content in the brain. In addition, α-Syn was found to reduce iron in the presence of copper. This property was demonstrated via ferrozine based assay. In vitro, thoflavin-T fluorescence assay was used to investigate the mechanism by which metals induce α-Syn aggregation and whether it is related to metal binding. Metals, mainly copper and iron, caused 2-fold increase in the aggregation rate of WT α-Syn and its metal binding mutants. Linking that to the increased metal content in the brain, α-Syn aggregation can cause changes in tissue composition, thus altering the normal functional environment in the brain. Moreover, western blotting analysis showed that copper increases the aggregate formation in mammalian dopaminergic cells over-expressing α-Syn.
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VanHoy, Grace M. "Safety and serologic response to a Haemonchus contortus vaccine in alpacas." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1554827479078096.

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Gooptu, Bibekbrata. "Alpha₁-antichymotrypsin : conformational transitions and disease." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621614.

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Elliott, P. R. "Alpha-antitrypsin conformations in health and disease." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598809.

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Alpha1-antitrypsin is the most abundant proteinase inhibitor in plasma and the archetypal member of a large family of serine proteinase inhibitors known as the serpins. All serpin members have a common molecular architecture which consists of three β-sheets surrounded by eight α-helixes with an exposed mobile reactive centre loop. In this thesis I show that it is possible to induce and purify an inactive latent α1-antitrypsin conformation which can be reactivated after denaturation and refolding. An inactive latent component was also shown to exist in commercial α1-antitrypsin pasteurised for use as replacement therapy in patients with α1-antitrypsin deficiency. Another consequence of the mobile reactive centre loop is the formation of inactive loop-sheet polymers which form when the reactive centre loop of one molecule is inserted into the β-sheet of another. This interaction accounts for the retention of Z (Glu342→Lys) α1-antitrypsin in the endoplasmic reticulum of hepatocytes with accompanying plasma deficiency. I show here that the plasma deficiency associated with the common S α1-antitrypsin allele (Glu 264→Val), which is present in 19% of individuals of Spanish descent, can also be attributed to loop-sheet polymerisation. The structural basis of this loop-sheet linkage was clarified by the solving here of the crystal structures of intact wildtype and a thermostable mutant of α1-antitrypsin. Both structures show the reactive centre loop in a canonical conformation that docks perfectly with its cognate proteinase. The rest of the reactive centre loop is held in a β-strand conformation via a stabilising salt bridge with the body of the molecule. In this conformation the reactive loop can be readily modelled into the A β-sheet of a second molecule, providing strong support for A β-sheet linkage as the mechanism for loop-sheet polymerisation. Finally, loop-sheet polymers of α1-antitrypsin have also been shown to occur within the small airways and alveoli of the lungs of Z α1-antitrypsin homozygotes. This findings provides another mechanism for the inactivation of α1-antitrypsin, thereby exacerbating the proteinase-antiproteinase imbalance in the lung disease emphysema.
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Senior, Steven L. "Functional analysis of alpha-synuclein." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670161.

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Munishkina, Larissa. "[alpha]-synuclein, its properties and connection to protein deposition diseases /." Diss., Digital Dissertations Database. Restricted to UC campuses, 2004. http://uclibs.org/PID/11984.

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Thakur, Garima. "Surface Chemistry and Spectroscopic Approach to Study Neurodegenerative Diseases." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/499.

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Accumulation or aggregation of amyloidogenic proteins in the brain plays a central role in neurodegenerative diseases. The most common and highly growing form of dementia in the elderly population is Alzheimer's disease (AD) followed by Parkinson's disease (PD). The major proteins associated are amyloid beta (Abeta) and alpha-synuclein (alpha-syn) in AD and PD, respectively. These proteins are released or found near the neuronal membranes in the brain. Consequently to understand the behavior of the proteins using a model membrane system becomes an important facet of understanding these diseases. Langmuir monolayer approach was used to study the surface chemistry and spectroscopy of Abeta (1-40), Abeta(1-42) and alpha-synuclein. Moreover, surface chemistry of a model protein namely, lysozyme was investigated. In recent times, quantum dots (QDs) are considered as potential probes for bio-imaging. These particles can be beneficial when it comes to the investigation of neurodegenerative diseases. The effect of nanoparticles, i.e., CdSe/ZnS QDs on Abeta (1-42) morphology was investigated. Nevertheless, it was observed that the capping ligand plays a significant role in the surface chemistry of QDs when mixed with or conjugated to Abeta (1-42). Surface pressure- and surface potential-area isotherms were used to characterize the lysozyme Langmuir monolayer. The compression-decompression cycles and stability measurements showed a homogeneous and stable monolayer at the air-water interface. Salt concentration in the subphase and pH of the subphase were parameters controlling homogeneity and stability of the Langmuir monolayer. In situ UV-vis and fluorescence spectroscopies were used to verify the homogeneity of the lysozyme monolayer, and to identify the chromophore residues in the lysozyme. Optimal experimental conditions were determined to prepare a homogeneous and stable lysozyme Langmuir monolayer. The surface chemistry and spectroscopy of the reduced lysozyme Langmuir monolayer were investigated at different pH values and were compared to a native lysozyme. It was established that the limiting molecular area of the reduced lysozyme was not subphase pH dependent as was found for the native one. To explain this result in terms of the conformation and orientation of the lysozyme Langmuir monolayer at various subphase pH values, we have used Infrared Reflection Absorption Spectroscopy (IRRAS). The interpretation of the results suggests a change in the conformation and orientation of the native lysozyme Langmuir monolayer with the subphase pH 3, 6 and 11. The surface chemistry of Abeta (1-40) and its interaction with the lipid raft Langmuir monolayer were examined where the stability of the lipid raft Langmuir monolayer came out as an essential parameter. Lipid raft Langmuir monolayer in the presence or absence of ganglioside GM1 having POPC as one of the phospholipids was found to be very unstable and collapsed within 26 min. Whereas, the phospholipid DPPG improved the stability of the monolayer significantly when cholesterol was used in excess. We have examined the surface and spectroscopic properties of Abeta (1-42) mixed with or conjugated to dihydrolipoic acid (DHLA)- and polyethylene glycol (PEG)- capped CdSe/ZnS QDs. Surface pressure-area isotherms, in situ UV-vis absorption, and fluorescence spectroscopy were used to characterize the Abeta (1-42) mixed with or conjugated to QDs at the air-water interface. The capping of QDs played a role in surface chemistry as was determined by surface pressure-area isotherms and spectroscopic properties of the Langmuir monolayer. Furthermore Abeta(1-42) was bioconjugated to DHLA-capped CdSe/ZnS QDs. Upon conjugation of Abeta (1-42) to DHLA-capped QDs, the sample was incubated at 37oC, the process of fibrillation was inhibited as compared with a sample where Abeta (1-42) was simply mixed with the QDs. Transmission electron microscopy (TEM) and atomic force microscopy (AFM) were employed for the analysis of the samples. The morphology of fibrils and reduction in number of fibrils was substantial in the case of Abeta(1-42) conjugated to QDs. Reduction in fibrillation was also confirmed using a Thioflavin T assay. Moreover, quenching of tyrosine signal was observed in presence of the QDs, which indicates an interaction of QDs to the tyrosine residue in Abeta (1-42). The Surface chemistry and spectroscopy of alpha-syn, which is a natively unstructured protein important in the neuropathology of PD was investigated. IRRAS was utilized to investigate its conformation, alpha-syn was found to form a Langmuir monolayer in alpha-helical conformation with its helical axis parallel to the air-water interface.
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吳惠茵 and Wai-yan Ng. "Pokemon and pak interactive exchange factor alpha in gestational trophoblastic diseases." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738322.

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Ng, Wai-yan. "Pokemon and pak interactive exchange factor alpha in gestational trophoblastic diseases." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40738322.

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Books on the topic "Alpaca – Diseases"

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Duncanson, G. R. Veterinary Treatment of Llamas and Alpacas. Wallingford: CABI, 2012.

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Moya, Viviana Ortíz de. En defensa de la carne de llama/alpaca. 2nd ed. Oruro [Bolivia]: Centro Diocesano de Pastoral Social, 1995.

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Fowler, Murray E. Medicine and surgery of camelids: Llama, alpaca, vicuña, guanaco, dromedary & Bactrian camels. 3rd ed. Ames, Iowa: Wiley-Blackwell, 2010.

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Medicine and surgery of South American camelids: Llama, alpaca, vicuña, guanaco. Ames: Iowa State University Press, 1989.

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Medicine and surgery of South American camelids: Llama, alpaca, vicuña, guanaco. 2nd ed. Ames: Iowa State University Press, 1998.

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Duncanson, Graham R. Veterinary treatment of llamas and alpacas. Wallingford, Oxfordshire, UK: CAB International, 2012.

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Symposium on Diseases of Small Ruminants (1990 Corvallis, Or.). American Association of Small Ruminant Practitioners ... , Western Regional Coordinating Committee-46 (Ram Epididymitis and Ovine Footrot), Oregon State University, College of Veterinary Medicine present Symposium on Diseases of Small Ruminants, Nendels Inn, Corvallis, Oregon, June 7,8,9, 1990. [S.l: s.n., 1990.

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Smith, Bradford B. Llama and alpaca medicine and surgery: Short course : March 22-28, 1994, College of Veterinary Medicine, Oregon State University. Corvallis, Or: Oregon State University, College of Veterinary Medicine, 1994.

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Periodontal disease. Basel: Karger, 2012.

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Foundation, Alpha-1. Welcome to Alphaville: Big fat reference guide for Alphas, their families, and their doctors : Alpha-1 disease management and prevention program. Coconut Grove, Fla: AlphaNet, 2004.

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Book chapters on the topic "Alpaca – Diseases"

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Lomas, David A., and David H. Perlmutter. "Alpha-1-Antitrypsin Deficiency." In Protein Misfolding Diseases, 403–23. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470572702.ch18.

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Feist, D. J. F. "Alpha-1-Antitrypsin Deficiency." In Inborn Metabolic Diseases, 361–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03147-6_33.

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Feist, D. "Alpha-1-Antitrypsin Deficiency." In Inborn Metabolic Diseases, 565–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-02613-7_41.

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Mukherjee, Amitava, Souvik Chakraborty, Yan Wang, Andy Chu, and David Perlmutter. "Liver Disease in α1-Antitrypsin Deficiency." In Alpha-1 Antitrypsin, 111–40. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23449-6_7.

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Setianingsih, Iswari, Alida Harahap, and Ita M. Nainggolan. "Alpha Thalassaemia in Indonesia: Phenotypes and Molecular Defects." In Tropical Diseases, 47–56. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0059-9_4.

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Sandhaus, Robert A. "Lung Disease of Alpha-1 Antitrypsin Deficiency." In Alpha-1 Antitrypsin, 99–110. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23449-6_6.

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Bright, Tamis M., and E. Chester Ridgway. "Alpha-Subunit Secreting Pituitary Tumors." In Diseases of the Pituitary, 273–82. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3954-3_13.

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Wallach, David, and Andrew Kovalenko. "Tumor Necrosis Factor Alpha (TNFalpha)." In Compendium of Inflammatory Diseases, 1273–82. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_38.

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North, Kathryn N., and Nigel G. Laing. "Skeletal Muscle Alpha-Actin Diseases." In Advances in Experimental Medicine and Biology, 15–27. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-84847-1_2.

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Perlmutter, David H. "Alpha-1 Antitrypsin Deficiency." In Schiff's Diseases of the Liver, 845–67. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119950509.ch31.

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Conference papers on the topic "Alpaca – Diseases"

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Schroer, Alison K., and W. David Merryman. "Integrin-Focal Adhesion Coupling and Substrate Stiffness Affect Smooth Muscle Alpha Actin Expression in Fibroblasts." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80887.

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Abstract:
Fibroblast cells play a key role in producing and maintaining connective tissue throughout the body. The ability of these cells to differentiate into a more active myofibroblastic phenotype is important during development and wound healing, but prolonged myofibroblast activation can lead to overproduction of extracellular matrix proteins and stiffening of the surrounding tissue. This stiffening can cause heightened differentiation of neighboring fibroblast through force transduction pathways and can lead to detrimental fibrotic pathologies in many organ systems. Atherosclerosis, interstitial lung disease, cirrhosis and heart valve disease are fibrotic diseases that cause significant cost and mortality in our society. Understanding the processes by which cells sense and respond to substrate stiffness is crucial to the treatment of connective tissue diseases. One primary indicator of the myofibroblastic phenotype is the production of α smooth muscle actin (αSMA) bundles called stress fibers which help transmit stress inside the cell and increases the contractility of the cells and their surrounding tissue [1].
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Madeb, Ralph, Joy Knopf, Dragan Golijanin, Patricia Bourne, and Erdal Erturk. "Evidence for Alpha Receptors in the Human Ureter." In RENAL STONE DISEASE: 1st Annual International Urolithiasis Research Symposium. AIP, 2007. http://dx.doi.org/10.1063/1.2723584.

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Fabris, M., L. Sinigaglia, S. Sacco, E. Di Poi, G. Favret, and GF Ferraccioli. "THU0008 Tnf-alpha gene polymorphism in severe and mild rheumatoid arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.111.

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Borodin, AG, AA Baranov, EL Nassonov, and NG Klukvina. "AB0014 Tumour necrosis factor-alpha in patients with systemic lupus erythematosus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.813.

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Wouters, C., F. Cornillie, and AD Billiau. "SAT0106 Anti-tnf-alpha therapy for systemic juvenile idiopathic arhtritis with polyarthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.499.

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Welcker, M., R. Hollatz, A. Werling, M. Emmlinger, and H. Franck. "AB0116 Treatment of systemic sclerosis with anti-tnf-alpha antibodies. a case report." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.264.

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Putterman, C., and B. Deocharan. "OP0071 A pathogenic anti-dna antibody binds to alpha-actinin in renal mesangial cells." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1235.

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Redlich, K., A. Maier, S. Hayer, G. Kollias, CR Dunstan, S. Lang, W. Woloszczuk, G. Steiner, J. Smolen, and G. Schett. "FRI0010 Effect of osteoprotegerin and pamidronate treatment in transgenic mice overexpressing human tnf-alpha." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1139.

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Bagnato, GG, C. Romano, C. Arrigo, and G. Chirico. "AB0009 Tnf alpha as a marker of articular involvement in patients infected with hiv." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.808.

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Choi, Jonggi, Sang Young Lee, Young-Suk Lim, Woochang Lee, and Sail Chun. "IDDF2018-ABS-0137 Longitudinal assessment of alpha-fetoprotein, lectin-reactive alpha-fetoprotein, and des-gamma-carboxy prothrombin for the early detection of hepatocellular carcinoma." In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.218.

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Reports on the topic "Alpaca – Diseases"

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Kowall, Neil W. Alpha Synuclein Aggregation in a Neurotoxic Model of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada393984.

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Kowall, Neil W. Alpha Synclein Aggreagation in a Neurotoxic Model of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada423207.

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Kowall, Neil W. Alpha Synuclein Aggregation in a Neurotoxic Model of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada397690.

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Kowall, Neil W. Alpha Synuclein Aggregation in a Neurotoxic Model of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada415870.

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Jeremiah Pate, Jeremiah Pate. Amelioration of Alpha-Synuclein in Parkinson's Disease through potentiated protein-protein interactions. Experiment, October 2016. http://dx.doi.org/10.18258/8102.

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Lee, Seung-Jae. Role of Oligomeric alpha-Synuclein in Mitochondrial Membrane Permeabilization and Neurodegeneration in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada427150.

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Lewis, James, Meenakshi Bewtra, Frank Scott, Colleen Brensinger, Shelby Reed, Jason Roy, Mark Osterman, et al. Patient Valued Comparative Effectiveness of Corticosteroids versus Anti-TNF Alpha Therapy for Inflammatory Bowel Disease. Patient-Centered Outcomes Research Institute (PCORI), November 2018. http://dx.doi.org/10.25302/11.2018.ce.12114143.

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