Academic literature on the topic 'Primates as carriers of disease'

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Journal articles on the topic "Primates as carriers of disease"

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Lerche, Nicholas W., and Kent G. Osborn. "Simian Retrovirus Infections: Potential Confounding Variables in Primate Toxicology Studies." Toxicologic Pathology 31, no. 1_suppl (January 2003): 103–10. http://dx.doi.org/10.1080/01926230390174977.

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Various species of nonhuman primates are natural hosts for 6 exogenous retroviruses, including gibbon-ape leukemia virus (GaLV), simian sarcoma virus, simian T-lymphotropic virus (STLV), simian immunodeficiency virus (SIV), simian type D retrovirus (SRV), and simian foamy virus (SFV). These viruses establish persistent infections with a broad spectrum of pathogenic potential, ranging from highly pathogenic to nonpathogenic, depending on various host, virus, and environmental factors. Latent or subclinical infections are common, and various procedures associated with experimental protocols may lead to virus reactivation and disease. Adverse effects on toxicologic research by undetected retroviral infections can occur in several ways, including loss of experimental subjects (and statistical power) due to increased morbidity and mortality. In addition, results may be confounded by virus-induced clinical abnormalities, histologic lesions, alteration of physiologic parameters and responses, and interference with in vitro assays and/or destruction of primary cell cultures. Key clinical and epidemiological features of several important retroviruses are reviewed, with emphasis on viruses infecting species of macaques most commonly used as research subjects in primate toxicology studies. Examples of actual and potential confounding of toxicologic studies by retroviruses are discussed, including altered cytokine profiles in healthy STLV carriers, and clinical and pathological abnormalities induced by SRV infection. Adequate prestudy viral screening is critical to exclude retrovirus-infected primates from toxicologic research protocols and prevent potential confounding of research results.
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Moura, Vandrielle Soares, and Mary Jane Tweedie de Mattos. "Zoonoses parasitárias que acometem primatas não humanos do gênero Alouatta nas regiões brasileiras - revisão sistemática no período de 2010-2021." Revista Agraria Academica 5, no. 1 (January 1, 2022): 1–15. http://dx.doi.org/10.32406/v5n1/2022/1-15/agrariacad.

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Non-human primates can be reservoirs and carriers of diseases transmitted to humans. The objective of this work was to carry out a systematic bibliographical review on parasitosis with zoonotic potential that affect the genus Alouatta. In the period 2010-2021 the genders were registered: Ascaris, Ancylostoma, Bertiella, Strongyloides, Oesophagostomum, Trichostrongylus and Trichuris, and Bertiella sp. was the zoonotic parasite with the most reports. The southeast region had the greatest diversity of helminths, with six of the seven (6/7) genera of helminths with zoonotic potential, in Alouatta. Knowledge of the epidemiology and biological cycle can contribute to the prevention of parasitic zoonoses transmitted by contact between non-human primates and humans.
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Mursel, Sena, Nathaniel Alter, Lindsay Slavit, Anna Smith, Paolo Bocchini, and Javier Buceta. "Estimation of Ebola’s spillover infection exposure in Sierra Leone based on sociodemographic and economic factors." PLOS ONE 17, no. 9 (September 1, 2022): e0271886. http://dx.doi.org/10.1371/journal.pone.0271886.

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Zoonotic diseases spread through pathogens-infected animal carriers. In the case of Ebola Virus Disease (EVD), evidence supports that the main carriers are fruit bats and non-human primates. Further, EVD spread is a multi-factorial problem that depends on sociodemographic and economic (SDE) factors. Here we inquire into this phenomenon and aim at determining, quantitatively, the Ebola spillover infection exposure map and try to link it to SDE factors. To that end, we designed and conducted a survey in Sierra Leone and implement a pipeline to analyze data using regression and machine learning techniques. Our methodology is able (1) to identify the features that are best predictors of an individual’s tendency to partake in behaviors that can expose them to Ebola infection, (2) to develop a predictive model about the spillover risk statistics that can be calibrated for different regions and future times, and (3) to compute a spillover exposure map for Sierra Leone. Our results and conclusions are relevant to identify the regions in Sierra Leone at risk of EVD spillover and, consequently, to design and implement policies for an effective deployment of resources (e.g., drug supplies) and other preventative measures (e.g., educational campaigns).
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Betts, Emma L., Eleni Gentekaki, Adele Thomasz, Vicki Breakell, Angus I. Carpenter, and Anastasios D. Tsaousis. "Genetic diversity of Blastocystis in non-primate animals." Parasitology 145, no. 9 (January 17, 2018): 1228–34. http://dx.doi.org/10.1017/s0031182017002347.

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AbstractBlastocystis is an anaerobic protist, commonly inhabiting the intestinal tract of both humans and other animals. Blastocystis is extremely diverse comprising 17 genetically distinct subtypes in mammals and birds. Pathogenicity of this enteric microbe is currently disputed and knowledge regarding its distribution, diversity and zoonotic potential is fragmentary. Most research has focused on Blastocystis from primates, while sampling from other animals remains limited. Herein, we investigated the prevalence and distribution of Blastocystis in animals held within a conservation park in South East England. A total of 118 samples were collected from 27 vertebrate species. The barcoding region of the small-subunit ribosomal RNA was used for molecular identification and subtyping. Forty one per cent of the species were sequence positive for Blastocystis indicating a high prevalence and wide distribution among the animals in the park. Six subtypes were identified, one of which is potentially novel. Moreover, the majority of animals were asymptomatic carriers, suggesting that Blastocystis is not pathogenic in animals. This study provides a thorough investigation of Blastocystis prevalence within a wildlife park in the UK and can be used as a platform for further investigations on the distribution of other eukaryotic gut microbes.
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Krucoff, Max O., Katie Zhuang, David MacLeod, Allen Yin, Yoon Woo Byun, Roberto Jose Manson, Dennis A. Turner, Laura Oliveira, and Mikhail A. Lebedev. "A novel paraplegia model in awake behaving macaques." Journal of Neurophysiology 118, no. 3 (September 1, 2017): 1800–1808. http://dx.doi.org/10.1152/jn.00327.2017.

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Lower limb paralysis from spinal cord injury (SCI) or neurological disease carries a poor prognosis for recovery and remains a large societal burden. Neurophysiological and neuroprosthetic research have the potential to improve quality of life for these patients; however, the lack of an ethical and sustainable nonhuman primate model for paraplegia hinders their advancement. Therefore, our multidisciplinary team developed a way to induce temporary paralysis in awake behaving macaques by creating a fully implantable lumbar epidural catheter-subcutaneous port system that enables easy and reliable targeted drug delivery for sensorimotor blockade. During treadmill walking, aliquots of 1.5% lidocaine with 1:200,000 epinephrine were percutaneously injected into the ports of three rhesus macaques while surface electromyography (EMG) recorded muscle activity from their quadriceps and gastrocnemii. Diminution of EMG amplitude, loss of voluntary leg movement, and inability to bear weight were achieved for 60–90 min in each animal, followed by a complete recovery of function. The monkeys remained alert and cooperative during the paralysis trials and continued to take food rewards, and the ports remained functional after several months. This technique will enable recording from the cortex and/or spinal cord in awake behaving nonhuman primates during the onset, maintenance, and resolution of paraplegia for the first time, thus opening the door to answering basic neurophysiological questions about the acute neurological response to spinal cord injury and recovery. It will also negate the need to permanently injure otherwise high-value research animals for certain experimental paradigms aimed at developing and testing neural interface decoding algorithms for patients with lower extremity dysfunction. NEW & NOTEWORTHY A novel implantable lumbar epidural catheter-subcutaneous port system enables targeted drug delivery and induction of temporary paraplegia in awake, behaving nonhuman primates. Three macaques displayed loss of voluntary leg movement for 60–90 min after injection of lidocaine with epinephrine, followed by a full recovery. This technique for the first time will enable ethical live recording from the proximal central nervous system during the acute onset, maintenance, and resolution of paraplegia.
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C. Ekezie, Joy, and Tanya Rogo. "Covid Reinfection versus Asymptomatic Carrier State: A Case Report." New Medical Innovations and Research 2, no. 5 (October 21, 2021): 01–03. http://dx.doi.org/10.31579/2767-7370/023.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), first discovered in China in December 2019, has been implicated in the current coronavirus disease 2019 (COVID-19) pandemic. Although much has been learned about the virus which peaked with the development of the vaccine, there is still a lot of unanswered questions. Maximum duration of positive SARS-CoV-2 real-time reverse transcriptase polymerase chain reaction (RT-PCR) from symptom onset may be up to 3 months [1], however it is not known if the continued detection of the viral genome implies prolonged infectivity or presence of a non-viable virus [2]. Most people with COVID-19 develop antibodies after resolution of acute infection [2]. The exact duration of these antibodies in the body is unknown, but some studies have shown that both memory T-cells and B-cells can persist up to 6 to 8 months after acute SARS-CoV-2 infection [3]. These SARS-CoV-2 antibodies may confer some immunity to the person after the acute infection and have been associated with protection against subsequent infection in nonhuman primates by the same viral strain during the early recovery phase [4]. In humans, however, it is unknown to what extent this immune response indicates a protective immunity to subsequent infection with SARS-CoV-2 [5]. Few cases of reinfection have been documented worldwide with varying symptom severity; the first case in the US was published in January 2021 (reinfection occurred in June 2020) [5]. None of the initial cases reported the presence of SARS-CoV-2 antibodies at the time of reinfection. We present a patient who tested positive to SARS-CoV-2 RT-PCR twice in 10 months (Table 1). At both times, she was asymptomatic and the second time, she had coexisting SARS-CoV-2 antibodies.
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Bausch, Birke, Ulrich Wellner, Dirk Bausch, Francesca Schiavi, Marta Barontini, Gabriela Sanso, Martin K. Walz, et al. "Long-term prognosis of patients with pediatric pheochromocytoma." Endocrine-Related Cancer 21, no. 1 (October 29, 2013): 17–25. http://dx.doi.org/10.1530/erc-13-0415.

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A third of patients with paraganglial tumors, pheochromocytoma, and paraganglioma, carry germline mutations in one of the susceptibility genes, RET, VHL, NF1, SDHAF2, SDHA, SDHB, SDHC, SDHD, TMEM127, and MAX. Despite increasing importance, data for long-term prognosis are scarce in pediatric presentations. The European-American-Pheochromocytoma–Paraganglioma-Registry, with a total of 2001 patients with confirmed paraganglial tumors, was the platform for this study. Molecular genetic and phenotypic classification and assessment of gene-specific long-term outcome with second and/or malignant paraganglial tumors and life expectancy were performed in patients diagnosed at <18 years. Of 177 eligible registrants, 80% had mutations, 49% VHL, 15% SDHB, 10% SDHD, 4% NF1, and one patient each in RET, SDHA, and SDHC. A second primary paraganglial tumor developed in 38% with increasing frequency over time, reaching 50% at 30 years after initial diagnosis. Their prevalence was associated with hereditary disease (P=0.001), particularly in VHL and SDHD mutation carriers (VHL vs others, P=0.001 and SDHD vs others, P=0.042). A total of 16 (9%) patients with hereditary disease had malignant tumors, ten at initial diagnosis and another six during follow-up. The highest prevalence was associated with SDHB (SDHB vs others, P<0.001). Eight patients died (5%), all of whom had germline mutations. Mean life expectancy was 62 years with hereditary disease. Hereditary disease and the underlying germline mutation define the long-term prognosis of pediatric patients in terms of prevalence and time of second primaries, malignant transformation, and survival. Based on these data, gene-adjusted, specific surveillance guidelines can help effective preventive medicine.
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Mabiaku TO, Mabiaku YO, Yovwin DG, and Anyanwu EB. "What a great blunder: Unknowingly disregarding the standard testing protocol for a patient exposed to a possible HIV infection." World Journal of Advanced Pharmaceutical and Medical Research 3, no. 1 (July 30, 2022): 001–5. http://dx.doi.org/10.53346/wjapmr.2022.3.1.0027.

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The world globally is presently saddled with a pandemic that started un-announced but subtly and progressively become a world-wide health concern. This is the general sequence of the Covid-19 pandemic that started locally in one city but had spread to affect all nations of the world with a loud roar. Human Immunodeficiency Virus (HIV) infection likewise started as a localized unexplained disease manifestation which was aggressively investigated and the causative virus was eventually identified and subsequently isolated. What initially seemed then to be a local disease was eventually reported gradually over-time to be seen all over the world. It was seen in both males and females and the original questions’ was to ascertain the routes of the spread of the virus between humans and possibly other primates, and to identify the reservoirs of the now known causative organism of the new human disease. On a regular basis, the sign and symptoms of the disease were manifesting and reported and several routes of transmission identified and reported. Among such numerous routes include but not excluding having unprotected sexual intercourse, transfusion of untested tainted blood donated by an active carrier of the virus, inadvertent needle pricks of a health worker, sharing of needles and syringes by drug abusing persons, unsterile tatooing instruments, use of common manicure/pedicure instruments. Rape or Sexual Assault (SA) is a problem that is reported from all nations of the world. It is probably grossly under reported, and can even be described as a pandemic because of its world-wide spread. The activities of SA has been known to be capable of transmitting disease from one person to the other, and HIV can be transmitted from the assailant to the victim and/or vice-versa of the victim is the infected one. It is based on this revelation of a potential transmission of HIV through this route that a protocol of testing of victims of this horrific crime was developed. So, what happens when a victim was not properly tested, the assailant not seen and not tested, the victim not placed on the available post-exposure prophylaxis but was re-assured and told “not to worry” that “all is well” and sent away.
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Davey, G. P., K. F. Tipton, and M. P. Murphy. "Uptake and accumulation of 1-methyl-4-phenylpyridinium by rat liver mitochondria measured using an ion-selective electrode." Biochemical Journal 288, no. 2 (December 1, 1992): 439–43. http://dx.doi.org/10.1042/bj2880439.

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The compound 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes selective destruction of nigrostriatal dopaminergic neurons in primates, giving rise to a condition resembling Parkinson's disease. The toxicity of MPTP is believed to be due to its metabolite 1-methyl-4-phenylpyridinium (MPP+). MPP+ is an inhibitor of mitochondrial respiration at the NADH-ubiquinone oxidoreductase site and this, together with its selective transport into dopaminergic nerve terminals, accounts for its neurotoxicity. In this paper an electrode selective for MPP+ was developed and used to measure the rate of uptake and the steady-state accumulation of MPP+ in rat liver mitochondria. The initial rates of MPP+ uptake were not saturable, confirming previous work that the transport of MPP+ is not carrier-mediated. The membrane potential of mitochondria respiring on succinate was decreased by MPP+ and the steady-state accumulation ratio of MPP+ did not come to equilibrium with the mitochondrial transmembrane potential gradient (delta psi). The effect of the cation exchanger tetraphenylboron (5 microM) was to increase the initial rate of MPP+ uptake by about 20-fold and the steady-state accumulation by about 2-fold. This suggests that there may be a mechanism of efflux of MPP+ from mitochondria which allows MPP+ to cycle across the membrane and thus decrease delta psi. These data indicate that MPP+ interacts with mitochondria independently of its inhibition of NADH-ubiquinone oxidoreductase, and these alternative interactions may be of relevance for its mechanism of neurotoxicity.
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McSweeny, Michelle J., Susan Montgomery, Kristen Danielle Whitaker, Mary Beryl Daly, and Michael J. Hall. "The protean phenotype of MSH6 pathogenic variants (PV) in Lynch syndrome (LS) patients (pts)." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 10537. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.10537.

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10537 Background: LS is among the most common hereditary cancer (CA) syndromes. PVs in MSH6 are 2-4 fold more common in the population (1/758) than those in MLH1 (1/1946) or MSH2 (1/2841), and are increasingly regarded as lower penetrance for CRC due to published data supporting later mean age of CRC onset and lower CRC risk. Unlike for MLH1/MSH2, NCCN 2020 CA risk estimates recognize only endometrial CA (EC) and CRC risks in MSH6+ carriers as clearly above SEER population estimates. Further, risks of other LS manifestations such as skin disease/Muir-Torre, ovarian CA (OC), and possible rare tumors in LS like sarcoma, have been minimally characterized in MSH6+ carriers. Methods: Pedigree data for 44 MSH6+ index (first-evaluated family member by our program) pts consecutively ascertained since 2009 at Fox Chase (FCCC) were reviewed. 1 pt w/a rare MSH6 uncertain variant w/personal history (PHx) of MSH6-expression deficient EC (age 50) and MSH6-deficient sebaceous skin CA (age 50) and a strong family history (FHx) c/w LS is also included here. 34% (15/44) index pts were referred to FCCC for cascade testing due to a known MSH6 PV in the family. Of the remaining 29 index pts, ascertainment included: 14% w/positive universal LS tumor screening, 21% w/early-onset or synchronous LS CA, 14% w/multi-gene panel for PHx of OC, 10% w/incidental MSH6+ result (2 had testing for PHx breast CA, 1 tumor genomic profiling), and 28% w/PHx and/or FHx of LS CA warranting genetic testing. Age of CA onset and path data were verified in > 90% index pts. Results: Index pts had a mean age of 55.5 yrs, and 77% were female. Overall, 11% (5/44) of MSH6+ index pts were found to have LS at diagnosis of synchronous primary CAs (3 EC/OC, 1 CRC/CRC, 1 CRC/EC), and 4/5 of these occurred <50 yrs. An additional 20% (9/44) index pts reported PHx of >2 metachronous LS CAs. OC was the presenting CA in 14% (6/44) female index pts; 2 additional index pts had rarer OC variants (Mullerian duct @ 41, primary peritoneal CA @ 50). Skin manifestations of LS were documented in 9.1% (4/44) index pts (3 sebaceous, 1 SCC in-situ/Bowen’s disease); 1 other family had documented sebaceous CAs in an FDR (father) but the 2 daughters seen @FCCC (both 30s) had yet to develop skin lesions. 2 index pts were found to have LS after developing early-onset breast CA (age 39) and contralateral breast CA (ages 50 and 54). Finally, 7% (3/44) index pts had a PHx of sarcoma: 2 were liposarcomas (ages 57 and 67), and 1 was a dermatofibrosarcoma. 2 other index pts had siblings w/childhood sarcomas. Conclusions: Our data, encompassing 44 MSH6+ pts evaluated in our clinic and consecutively ascertained, suggest MSH6 PV carriers develop synchronous primaries (11%), common and rare OC histologic types (18%), sarcomas (7%) and skin disease/Muir-Torre (9%). While common in the population and lower penetrance for CRC, MSH6 PV can behave in uncommon ways and may have significant extra-colonic CA risks such as OC, sarcoma and skin manifestations.
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Dissertations / Theses on the topic "Primates as carriers of disease"

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Romano, de Paula Valéria. "Social networks as a trade-off between optimal information transmission and reduced disease transmission." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ056/document.

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La structure sociale d'un groupe peut théoriquement réguler la transmission des informations et le risques de maladies via les contacts sociaux et la proximité. En théorie, les mêmes propriétés de réseau qui favorisent la transmission d'information favorisent également la transmission de pathogènes, créant de fait un potentiel compromis entre eux. Dans ma thèse, j'ai utilisé des données empiriques, des analyses de réseaux et modèle de simulation individuel afin de comprendre l'influence des structures sociales sur la transmission sociale chez les primates et dans des réseaux théoriques. Mes études ont montré que i) les macaques japonais centraux dans Je groupe transmettent les pathogènes plus rapidement mais sont également plus susceptibles d' être infectés; ii) le nombre d'individus infectés dans 40 groupes de primates est dépendant des propriétés globales du réseau et de l'étape de l'infection: iii) un pic d'efficacité de réseau à des valeurs intermédiaires de sous­ structure de groupe dans des réseaux empiriques et théoriques ; et iv) des variations dans les propriétés de réseaux sont la conséquence de décisions individuelles en fonction de compromise entre la collecte d'information et l'évitement de l'infection. Ainsi, ma thèse a démontré les mécanismes de transmission social et indiqué que les propriétés de réseau pourrait réflecter un compromise entre transmission de l'information et transmission de pathogène
Social structure can theoretically regulate information transmission and disease risk via social contact or proximity. In theory, the same network properties that favor information transmission also favor pathogen transmission creating a potential trade-off between them. In my thesis, I used empirical data, network analysis and individual-based modelling to understand the influence of social structure on social transmission in primate and theoretical networks. My studies show that i) central Japanese macaques transmit disease faster but are also more prone to acquiring infectious agents; ii) the number of infected individuals in 40 wild primate groups is dependent on global network properties and epidemic time; iii) network efficiency peaks with intermediate values of group substructure in theoretical and empirical networks; and, iv) variation in the network properties is a consequence of individual decisions given the trade-offs between collecting information and avoiding infection. Altogether, my thesis reveals the mechanisms of social transmission and indicates that network properties might reflect a trade-off between information and pathogen transmission
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Wu, Jinfang. "Alzheimer's disease (AD) like pathology following developmental lead exposure in primates and the role of aging in AD-related genes regulation in rodents and primates /." View online ; access limited to URI, 2008. http://0-digitalcommons.uri.edu.helin.uri.edu/dissertations/AAI3314462.

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Han, Pengcheng, Megan Nielsen, Melissa Song, Junxiang Yin, Michele R. Permenter, Julie A. Vogt, James R. Engle, et al. "The Impact of Aging on Brain Pituitary Adenylate Cyclase Activating Polypeptide, Pathology and Cognition in Mice and Rhesus Macaques." FRONTIERS MEDIA SA, 2017. http://hdl.handle.net/10150/624682.

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Pituitary adenylate cyclase activating polypeptide (PACAP) is associated with Alzheimer's disease (AD), but its age-related effects are unknown. We chose the rhesus macaque due to its closeness to human anatomy and physiology. We examined four variables: aging, cognitive performance, amyloid plaques and PACAP. Delayed nonmatching-to-sample recognition memory scores declined with age and correlated with PACAP levels in the striatum, parietal and temporal lobes. Because amyloid plaques were the only AD pathology in the old rhesus macaque, we further studied human amyloid precursor protein (hAPP) transgenic mice. Aging was associated with decreased performance in the Morris Water Maze (MWM). In wild type (WT) C57BL/ 6 mice, the performance was decreased at age 24-26 month whereas in hAPP transgenic mice, it was decreased as early as 9-12 month. Neuritic plaques in adult hAPP mice clustered in hippocampus and adjacent cortical regions, but did not propagate further into the frontal cortex. Cerebral PACAP protein levels were reduced in hAPP mice compared to age-matched WT mice, but the genetic predisposition dominated cognitive decline. Taken together, these data suggest an association among PACAP levels, aging, cognitive function and amyloid load in nonhuman primates, with both similarities and differences from human AD brains. Our results suggest caution in choosing animal models and in extrapolating data to human AD studies.
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Day, Brian Keith. "MICROELECTRODE ARRAY STUDIES OF NORMAL AND DISEASE-ALTERED L-GLUTAMATE REGULATION IN THE MAMMALIAN CENTRAL NERVOUS SYSTEM." UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/235.

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L-glutamate (Glu) is the major excitatory neurotransmitter in the mammalian central nervous system. Monitoring extracellular Glu is critical to understanding Glu regulation to discriminate physiological and pathological roles. To overcome the limitations of previous in vivo extracellular Glu studies, we developed Glu selective microelectrode arrays with better spatial and temporal resolutions than commonly used techniques like microdialysis. We used these microelectrode arrays to characterize basal and potassium-evoked Glu neurotransmission in the normal rat brain. We then investigated disease-related Glu alterations in a rat model of Parkinson's disease and normal Glu regulation in young and aged rhesus monkeys. In the normal anesthetized rat striatum and frontal cortex, basal Glu was regulated by active release and uptake mechanisms, fully TTX-dependent, and measured at ~2 micromolar levels. Potassium-evoked Glu kinetics were fast, concentration-dependent, and rapidly reproducible at 15-20 seconds intervals. In the unilateral 6-hydroxydopamine-lesioned rat, there were significant bilateral increases in potassium-evoked Glu release in the striatum and frontal cortex compared to hemisphere-matched non-lesioned rats. Ipsilateral striatal effects may have been related to DA loss, while contralateral striatal effects and the bilateral frontal corticaleffects may have resulted from parkinsonian neurotransmitter changes or bilateral neuranatomical connectivity, especially in the cortex. There were also alterations in Glu kinetics in the nucleus accumbens in both non-lesioned and lesioned rats. With appropriate technological and methodological modifications, we successfully recorded normal Glu signaling in anesthetized nonhuman primates in the operating room. Fast potassium-evoked Glu signals were recorded in the motor cortex of all monkeys, and Glu ejections showed robust Glu uptake in the motor and frontal cortices of all monkeys. These findings are comparable to initial rat studies. Slow evoked Glu kinetics and high basal Glu levels with oscillatory behavior were recorded in the frontal cortex. The primary age-related differences between monkeys were the nearly ten-fold increases in the volumes of Glu ejected needed in the aged monkey to achieve amplitude-matched signals in the motor and frontal cortices and a decreased uptake rate in the motor cortex. Preliminary work with excised human tissue and future plans for patient-oriented research and clinical applications are discussed.
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Li, Pui-lin Jennifer. "Aspects of bacteriology/virology of shellfish in relation to public health /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18734261.

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Pardanani, Neeta N. "Ecological determinants of lyme disease in an endemic community /." View online ; access limited to URI, 2004. http://wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3160034.

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Salgueiro, Sancha P. "Molecular studies on pea enation mosaic virus." Thesis, University of East Anglia, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317586.

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Chu, Ka-wing, and 朱嘉永. "Diversity and evolution of coronaviruses and astroviruses in bat, wildbirds and rodents." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47849733.

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Bats and birds are known to be the reservoirs of a number of zoonotic diseases. The capacity of flight and the diversity of these animals may make them special in maintaining and disseminating diverse viruses leading to instances of emerging zoonoses. In particular bats are increasingly recognized to be reservoirs of a wide range of viruses, including Nipah, Ebola and severe acute respiratory syndrome (SARS) coronaviruses. In most instances these viruses appear to establish long-term persistence in bats. In this thesis I report the identification of novel astroviruses from different insectivorous species of apparently healthy bats sampled in Hong Kong and in 11 provinces of Mainland China with high positive rates. Astroviruses are important causes of diarrhea in many animal species, including humans. This study revealed a remarkably high genetic diversity of bat astroviruses, which form novel distinct phylogenetic groups in the genus Mamastrovirus. Evidence for varying degrees of host restriction for bats astroviruses has been found. The finding of diverse astroviruses in Miniopterus bats captured within a single cave habitat in Hong Kong illustrates a very unusual virus host relationship between astroviruses and these bats. Surveillance of astroviruses in rodents, the only mammal with species numbers surpassing that of bats, has revealed a novel astrovirus in only 1.6 % of the faecal samples of urban brown rat (Rattus norvegicus) in Hong Kong in marked contrast with the prevalence and diversity of astroviruses in bats. Rat astrovirus was phylogenetically related to human astroviruses MLB1 which was detected from clinical samples from diarrhoeal patients in Hong Kong in this study. The unusually high positive rates of astroviruses in bats have been again highlighted. Avastroviruses were detected in 7.1% of the aquatic wild bird samples. Avastrovirus have also been detected in doves in Hong Kong, pond herons and a less whistling duck in Cambodia. A phylogenetic analysis of these novel astroviruses together with other previously known astroviruses revealed that avastrovirus can be divided into 3 monophyletic groups. On the other hand, avian coronaviruses was detected in 12.5% of the aquatic wild bird samples. Phylogenetic analysis of these avian coronaviruses has led us to suggest taxonomic separation of these viruses into two groups as gammacoronaviruses and deltacoronaviruses. Frequent interspecies transmissions of gammacoronaviruses between duck species were demonstrated. Analysis of the avian viral sequences and host mitochondrial DNA sequences suggested that some coronaviruses may have coevolved with birds from the same order. With the discoveries of coronaviruses and astroviruses in mammalian and birds, we now have a better understanding on the diversity and ecology of these two virus families in wildlife. These findings provide new insights into the ecology and evolution of these viruses in nature and have revealed possible inter-species transmissions of these viruses. The role of bats as a reservoir of viruses with potential to pose zoonotic threats to human health was also reinforced. Studies of the virus ecology in wildlife as demonstrated in this thesis will help formulating better strategies for controlling emerging diseases in the future.
published_or_final_version
Microbiology
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Doctor of Philosophy
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Edler, Melissa K. "Alzheimer's disease pathology in aged chimpanzees." Kent State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=kent1461401487.

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Dark, Michael James. "Comparative genomics of Anaplasma marginale : a preliminary examination of factors involved in tick transmission." Pullman, Wash. : Washington State University, 2008. http://www.dissertations.wsu.edu/Dissertations/Fall2008/m_dark_110708.pdf.

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Books on the topic "Primates as carriers of disease"

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Agents transmissible from Simians to man. Berlin: Springer-Verlag, 1987.

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Williams, Jean Balch. Parkinson's disease: Studies in nonhuman primates : a bibliography. Seattle: Primate Information Center, Regional Primate Research Center, University of Washington, 1989.

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Busvine, James R. Disease transmission byinsects. Berlin: Springer-Verlag, 1993.

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The vector- and rodent-borne diseases of Europe and North America: Their distribution and public health burden. Cambridge: Cambridge University Press, 2006.

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P, Lane Richard, and Crosskey Roger Ward, eds. Medical insects and arachnids. London: Chapman & Hall, 1993.

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Newman, Scott H. Investigating the role of bats in emerging zoonoses: Balancing ecology, conservation and public health interest. Rome: Food and Agriculture Organization of the United Nations, 2011.

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Valešová, Marie. Lymeská artritida. Praha: Grada Pub., 1999.

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Ginsberg, Howard S. Ecology and management of ticks and lyme disease at Fire Island National Seashore and selected Eastern National Parks. Denver, CO (P.O. Box 25287, Denver 80225-0287): U.S. Dept. of the Interior, National Park Service, 1992.

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Williams, Jean Balch. Parkinson's disease: studies in nonhuman primates: Annual update, March, 1992. A bibliography. Seattle: Primate Information Center, Regional Primate Research Center, University of Washington, 1992.

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McLean, Miriam. Parkinson's disease: Studies in nonhuman primates : a bibliography : annual update, September, 1993. Seattle, Wash: Primate Information Center, Regional Primate Research Center, University of Washington, 1993.

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Book chapters on the topic "Primates as carriers of disease"

1

Walker, Lary C. "Aged Non-Human Primates as Models of β-Amyloidoses." In Alzheimer Disease, 390–94. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_65.

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Shively, Carol A. "Social Stress and Cardiovascular Disease in Primates." In Stress and Cardiovascular Disease, 17–29. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84882-419-5_2.

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Harper, Kristin N., Molly K. Zuckerman, Bethany L. Turner, and George J. Armelagos. "Primates, Pathogens, and Evolution: A Context for Understanding Emerging Disease." In Primates, Pathogens, and Evolution, 389–409. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7181-3_13.

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Gomez, Felicia, Wen-Ya Ko, Avery Davis, and Sarah A. Tishkoff. "Impact of Natural Selection Due to Malarial Disease on Human Genetic Variation." In Primates, Pathogens, and Evolution, 117–60. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7181-3_5.

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Gaudieri, S., J. K. Kulski, and R. L. Dawkins. "MHC and Disease Associations in Nonhuman Primates." In Molecular Biology and Evolution of Blood Group and MHC Antigens in Primates, 464–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59086-3_21.

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Skelton-Stroud, P. N., and J. R. Glaister. "Naturally Occurring Renal Disease in Non-Human Primates." In Nephrotoxicity in the experimental and clinical situation, 189–210. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3367-5_6.

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Korting, Hans Christian, and Monika Schäfer-Korting. "Carriers in the Topical Treatment of Skin Disease." In Drug Delivery, 435–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00477-3_15.

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Kestenbaum, Meir, and Roy N. Alcalay. "Clinical Features of LRRK2 Carriers with Parkinson’s Disease." In Advances in Neurobiology, 31–48. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-49969-7_2.

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Capitanio, John P. "Nonhuman Primate Personality and Immunity: Mechanisms of Health and Disease." In Personality and Temperament in Nonhuman Primates, 233–55. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0176-6_9.

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Johnston, Tom M., and Susan H. Fox. "Symptomatic Models of Parkinson’s Disease and L-DOPA-Induced Dyskinesia in Non-human Primates." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 221–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/7854_2014_352.

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Conference papers on the topic "Primates as carriers of disease"

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Jacobs, Milou, Ellen P. Hart, Yuri Mejia Miranda, Geert Jan Groeneveld, Joop MA van Gerven, and Raymund AC Roos. "H56 Driving performance of huntington’s disease gene carriers." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.234.

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Martinez-Torteya, Antonio, Alejandro I. Trejo-Castro, Jose M. Celaya-Padill, and Jose G. Tamez-Pena. "Differences in the Progression from Mild Cognitive Impairment to Alzheimer's Disease between APOE4 Carriers and Non-Carriers." In 2019 IEEE 19th International Conference on Bioinformatics and Bioengineering (BIBE). IEEE, 2019. http://dx.doi.org/10.1109/bibe.2019.00043.

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Mahmood, Adil, Deborah Morris-Rosendahl, Matthew Edwards, Andrew Fleming, Tessa Homfray, Samantha Mason, Ellie Quinn, et al. "10 Disease penetrance in asymptomatic carriers of familial cardiomyopathy variants." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.10.

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Mahmood, Adil, Deborah Morris-Rosendahl, Matthew Edwards, Andrew Fleming, Tessa Homfray, Samantha Mason, Ellie Quinn, et al. "10 Disease penetrance in asymptomatic carriers of familial cardiomyopathy variants." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.10.

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Goldklang, M. P., K. F. Law, A. Gerber, J. Olsen, C. Henry, G. Wagener, and J. M. D'Armiento. "Increased Exacerbations of Chronic Obstructive Pulmonary Disease in Alpha-1 Antitrypsin Carriers." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1211.

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Goldklang, Monica, Kevin Law, Adam Gerber, Julie Olsen, Claudius Henry, Gebhard Wagener, and Jeanine D'Armiento. "Increased Exacerbations of Chronic Obstructive Pulmonary Disease in Alpha-1 Antitrypsin Carriers." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa3824.

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Nossent, Esther, David Montani, Barbara Girerd, Frederic Perros, Florent Soubrier, Eli Fadel, Katrien Grünberg, et al. "Pulmonary arterial lesions and interstitial remodeling patterns in histology differentiate EIF2AK4 mutation-carriers from non-carriers with pulmonary veno-occlusive disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa582.

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Baake, Verena, Erik van Duijn, and Raymund AC Roos. "F41 Huntington’s disease gene expansion carriers are aware of their degree of apathy." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.145.

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Turuelo, Miriam, Rocio Del Pino, Maria Ángeles Acera, María Díez-Cirarda, Tamara Fernández, Beatriz Tijero, Mar Carmona, et al. "F15 Visual-cognitive impairment in asymptomatic and symptomatic carriers of huntington’s disease (HD)." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.58.

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Castro, Marcelo A., Ji Hyun Lee, Ian Crozier, Jeffrey Solomon, Joseph Laux, Danny Ragland, James Logue, et al. "Evaluation of R2* as a noninvasive endogenous imaging biomarker for Ebola virus liver disease progression in nonhuman primates." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor S. Gimi and Andrzej Krol. SPIE, 2020. http://dx.doi.org/10.1117/12.2550405.

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Reports on the topic "Primates as carriers of disease"

1

Bercovier, Herve, and Ronald P. Hedrick. Diagnostic, eco-epidemiology and control of KHV, a new viral pathogen of koi and common carp. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7695593.bard.

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Abstract:
Original objectives and revisions-The proposed research included these original objectives: field validation of diagnostic tests (PCR), the development and evaluation of new sensitive tools (LC-PCR/TaqManPCR, antibody detection by ELISA) including their use to study the ecology and the epidemiology of KHV (virus distribution in the environment and native cyprinids) and the carrier status of fish exposed experimentally or naturally to KHV (sites of virus replication and potential persistence or latency). In the course of the study we completed the genome sequence of KHV and developed a DNA array to study the expression of KHV genes in different conditions. Background to the topics-Mass mortality of koi or common carp has been observed in Israel, USA, Europe and Asia. These outbreaks have reduced exports of koi from Israel and have created fear about production, import, and movements of koi and have raised concerns about potential impacts on native cyprinid populations in the U.S.A. Major conclusions-A suite of new diagnostic tools was developed that included 3 PCR assays for detection of KHV DNA in cell culture and fish tissues and an ELISA assay capable of detecting anti-KHV antibodies in the serum of koi and common carp. The TKPCR assay developed during the grant has become an internationally accepted gold standard for detection of viral DNA. Additionally, the ELISA developed for detecting serum anti-KHV antibodies is now in wide use as a major nonlethal screening tool for evaluating virus status of koi and common carp populations. Real time PCR assays have been able to detect viral DNA in the internal organs of survivors of natural and wild type vaccine exposures at 1 and 10³ genome equivalents at 7 months after exposure. In addition, vaccinated fish were able to transmit the virus to naive fish. Potential control utilizing hybrids of goldfish and common carp for production demonstrated they were considerably more resistant than pure common carp or koi to both KHV (CyHV-3). There was no evidence that goldfish or other tested endemic cyprinids species were susceptible to KHV. The complete genomic sequencing of 3 strains from Japan, the USA, and Israel revealed a 295 kbp genome containing a 22 kbp terminal direct repeat encoding clear gene homologs to other fish herpesviruses in the family Herpesviridae. The genome encodes156 unique protein-coding genes, eight of which are duplicated in the terminal repeat. Four to seven genes are fragmented and the loss of these genes may be associated with the high virulence of the virus. Viral gene expression was studies by a newly developed chip which has allowed verification of transcription of most all hypothetical genes (ORFs) as well as their kinetics. Implications, both scientific and agricultural- The results from this study have immediate application for the control and management of KHV. The proposal provides elements key to disease management with improved diagnostic tools. Studies on the ecology of the virus also provide insights into management of the virus at the farms that farmers will be able to apply immediately to reduce risks of infections. Lastly, critical issues that surround present procedures used to create “resistant fish” must be be resolved (e.g. carriers, risks, etc.). Currently stamping out may be effective in eradicating the disease. The emerging disease caused by KHV continues to spread. With the economic importance of koi and carp and the vast international movements of koi for the hobby, this disease has the potential for even further spread. The results from our studies form a critical component of a comprehensive program to curtail this emerging pathogen at the local, regional and international levels.
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