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

Author: Grafiati

Published: 4 June 2021

Last updated: 24 January 2023

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1

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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5

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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9

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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10

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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Ferreira da Silva, Maylane Tavares, Eric Carvalho Aquim, Tiago Paixão Ribeiro De Sousa, Naelson Railson de Sousa Gomes, Auan Rangel Oliveira De Vasconcelos, Camila Cristina de Oliveira Andrade Silveira, Franciso Michael Junior Costa, and Luanna Soares de Melo Evangelista. "Occurrence of Intestinal Parasites in Alouatta caraya of the Zoobotanical Park of Teresina, Piauí, Brazil." Acta Scientiae Veterinariae 46 (August 20, 2018): 5. http://dx.doi.org/10.22456/1679-9216.87478.

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Background: The animals of the genus Alouatta are popularly known as Bugios, barbados, roncadores and guaribas, being the neotropical primates better studied in the world. They originate in South America, with records in Argentina, Bolivia, Paraguay and Uruguay. Because of their migrations, many are found debilitated and taken to captivity until their rehabilitation and most cannot be reinserted in nature. They tend to live in extensive areas, having a low resistance against parasitic infections because of low exposure and when kept in captivity, the risks of these infections increase. Some diagnostic techniques can aid in the detection of parasites of zoo animals and can identify the parasitic fauna of these animals. The objective of this work was to investigate and report the presence of intestinal parasites in a female Bugio-preta (Alouatta caraya) captive of the Zoobotanical Park of the municipality of Teresina, Piauí, Brazil.Case: The animal presented a constipation signs before clinical signs of apathy, anorexia, diarrhea and weight loss, suggestive signs of parasitosis, Sterile papers were placed on the floor of the animal enclosure and collected fresh stools shortly after defecation, the feces were removed using gloves, stored in a capped containers, identified and taken to the Laboratory of Parasitology of the Department of Parasitology and Microbiology of the Federal University of Piauí, for further evaluation. The fecal samples were submitted to the techniques of spontaneous sedimentation (HPJ), centrifugation-flotation (Faust) and flotation method in hyper saturated sucrose solution (Willis-Mollay), obtaining slides that were analyzed under an optical microscope in the 10x and 40x objective, confirming the presence of ascarids and hookworms.Discussion: The results showed the presence of eggs of Ascaris sp. and Ancylostoma sp. in all of the analyzed techniques, thus maintaining an alert, since they are considered helminths of zoonotic character. The general state of the animal may have influenced considerably the result of mixed infection by helminths, since it had episodes of diarrhea and was skinny at the time of diagnosis. Diarrheal feces and slimming favor the encounter of mixed infection, since the parasites in large quantity can cause to their hosts a decrease in the absorption of nutrients and an intestinal peristalsis increase. Other works with primates also revealed the presence of parasites in animals, including protozoans. The collection moment and evaluation of the fecal samples of the Bugio coincided with the rainy period in the region. This fact can favor the increase of eggs and larvae of parasites in the environment and, consequently, can contaminate the animals. Regarding to sanitary management of zoos, areas full of plants and trees make it difficult to hygienize the enclosures and in these places is common the presence of other animals that can serve as carriers of pathogens. The available diagnostic great relevance to assess the degree of animal infection, the possibility of transmission and the sanitary conditions of the environment. It was concluded that the female Bugio of the Teresina Zoobotanical Park was parasitized by ascarids and hookworms and the techniques of parasitological exams performed represented great relevance for the early diagnosis and an appropriate treatment, being able to be used for the control of diseases parasites, mainly zoonoses.

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Rohaim, Mohammed A., and Muhammad Munir. "A Scalable Topical Vectored Vaccine Candidate against SARS-CoV-2." Vaccines 8, no. 3 (August 24, 2020): 472. http://dx.doi.org/10.3390/vaccines8030472.

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The severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) caused an ongoing unprecedented global public health crises of coronavirus disease in 2019 (CoVID-19). The precipitously increased death rates, its impact on livelihood and trembling economies warrant the urgent development of a SARS-CoV-2 vaccine which would be safe, efficacious and scalable. Owing to unavailability of the vaccine, we propose a de novo synthesized avian orthoavulavirus 1 (AOaV-1)-based topical respiratory vaccine candidate against CoVID-19. Avirulent strain of AOaV-1 was engineered to express full length spike (S) glycoprotein which is highly neutralizing and a major protective antigen of the SARS-CoV-2. Broad-scale in vitro characterization of a recombinant vaccine candidate demonstrated efficient co-expression of the hemagglutinin-neuraminidase (HN) of AOaV-1 and S protein of SARS-CoV-2, and comparable replication kinetics were observed in a cell culture model. The recombinant vaccine candidate virus actively replicated and spread within cells independently of exogenous trypsin. Interestingly, incorporation of S protein of SARS-CoV-2 into the recombinant AOaV-1 particles attributed the sensitivity to anti-SARS-CoV-2 antiserum and more prominently to anti-AOaV-1 antiserum. Finally, our results demonstrated that the recombinant vaccine vector stably expressed S protein after multiple propagations in chicken embryonated eggs, and this expression did not significantly impact the in vitro growth characteristics of the recombinant. Taken together, the presented respiratory vaccine candidate is highly attenuated in primates per se, safe and lacking pre-existing immunity in human, and carries the potential for accelerated vaccine development against CoVID-19 for clinical studies.

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Tokarew, Jacqueline M., Daniel N. El-Kodsi, Nathalie A. Lengacher, Travis K. Fehr, Angela P. Nguyen, Bojan Shutinoski, Brian O’Nuallain, et al. "Age-associated insolubility of parkin in human midbrain is linked to redox balance and sequestration of reactive dopamine metabolites." Acta Neuropathologica 141, no. 5 (March 10, 2021): 725–54. http://dx.doi.org/10.1007/s00401-021-02285-4.

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AbstractThe mechanisms by which parkin protects the adult human brain from Parkinson disease remain incompletely understood. We hypothesized that parkin cysteines participate in redox reactions and that these are reflected in its posttranslational modifications. We found that in post mortem human brain, including in the Substantia nigra, parkin is largely insoluble after age 40 years; this transition is linked to its oxidation, such as at residues Cys95 and Cys253. In mice, oxidative stress induces posttranslational modifications of parkin cysteines that lower its solubility in vivo. Similarly, oxidation of recombinant parkin by hydrogen peroxide (H2O2) promotes its insolubility and aggregate formation, and in exchange leads to the reduction of H2O2. This thiol-based redox activity is diminished by parkin point mutants, e.g., p.C431F and p.G328E. In prkn-null mice, H2O2 levels are increased under oxidative stress conditions, such as acutely by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxin exposure or chronically due to a second, genetic hit; H2O2 levels are also significantly increased in parkin-deficient human brain. In dopamine toxicity studies, wild-type parkin, but not disease-linked mutants, protects human dopaminergic cells, in part through lowering H2O2. Parkin also neutralizes reactive, electrophilic dopamine metabolites via adduct formation, which occurs foremost at the primate-specific residue Cys95. Further, wild-type but not p.C95A-mutant parkin augments melanin formation in vitro. By probing sections of adult, human midbrain from control individuals with epitope-mapped, monoclonal antibodies, we found specific and robust parkin reactivity that co-localizes with neuromelanin pigment, frequently within LAMP-3/CD63+ lysosomes. We conclude that oxidative modifications of parkin cysteines are associated with protective outcomes, which include the reduction of H2O2, conjugation of reactive dopamine metabolites, sequestration of radicals within insoluble aggregates, and increased melanin formation. The loss of these complementary redox effects may augment oxidative stress during ageing in dopamine-producing cells of mutant PRKN allele carriers, thereby enhancing the risk of Parkinson’s-linked neurodegeneration.

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Siddappa, Nagadenahalli B., Ruijiang Song, Victor G. Kramer, Agnès-Laurence Chenine, Vijayakumar Velu, Helena Ong, Robert A. Rasmussen, et al. "Neutralization-Sensitive R5-Tropic Simian-Human Immunodeficiency Virus SHIV-2873Nip, Which Carries env Isolated from an Infant with a Recent HIV Clade C Infection." Journal of Virology 83, no. 3 (November 19, 2008): 1422–32. http://dx.doi.org/10.1128/jvi.02066-08.

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ABSTRACT Human immunodeficiency virus clade C (HIV-C) accounts for >56% of all HIV infections worldwide. To investigate vaccine safety and efficacy in nonhuman primates, a pathogenic, R5-tropic, neutralization-sensitive simian-human immunodeficiency virus (SHIV) carrying HIV-C env would be desirable. We have constructed SHIV-2873Ni, an R5-tropic SHIV carrying a primary pediatric HIV-C env gene isolated from a 2-month-old Zambian infant, who died within 1 year of birth. SHIV-2873Ni was constructed using SHIV-1157ipd3N4 (R. J. Song, A. L. Chenine, R. A. Rasmussen, C. R. Ruprecht, S. Mirshahidi, R. D. Grisson, W. Xu, J. B. Whitney, L. M. Goins, H. Ong, P. L. Li, E. Shai-Kobiler, T. Wang, C. M. McCann, H. Zhang, C. Wood, C. Kankasa, W. E. Secor, H. M. McClure, E. Strobert, J. G. Else, and R. M. Ruprecht. J. Virol. 80:8729-8738, 2006) as the backbone, since the latter contains additional NF-κB sites in the long terminal repeats to enhance viral replicative capacity. The parental virus, SHIV-2873Ni, was serially passaged through five rhesus monkeys (RMs); SHIV-2873Nip, the resulting passaged virus, was reisolated from the fourth recipient about 1 year postinoculation. SHIV-2873Nip was replication competent in RM peripheral blood mononuclear cells of all random donors tested and was exclusively R5 tropic, and its env gene clustered with HIV-C by phylogenetic analysis; its high sensitivity to neutralization led to classification as a tier 1 virus. Indian-origin RMs were inoculated by different mucosal routes, resulting in high peak viral RNA loads. Signs of virus-induced disease include depletion of gut CD4+ T lymphocytes, loss of memory T cells in blood, and thrombocytopenia that resulted in fatal cerebral hemorrhage. SHIV-2873Nip is a highly replication-competent, mucosally transmissible, pathogenic R5-tropic virus that will be useful to study viral pathogenesis and to assess the efficacy of immunogens targeting HIV-C Env.

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Cohen, D. Walter, and Henry M. Goldman. "ORAL DISEASE IN PRIMATES." Annals of the New York Academy of Sciences 85, no. 3 (December 15, 2006): 889–909. http://dx.doi.org/10.1111/j.1749-6632.1960.tb50010.x.

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Peleg, L., A. Frisch, B. Goldman, M. Karpaty, R. Narinsky, S. Bronstein, and M. Frydman. "Lower frequency of Gaucher disease carriers among Tay-Sachs disease carriers." European Journal of Human Genetics 6, no. 2 (March 1998): 185–86. http://dx.doi.org/10.1038/sj.ejhg.5200176.

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Sou, Keitaro, Beth Goins, Michelle M. Leland, Eishun Tsuchida, and William T. Phillips. "Bone marrow-targeted liposomal carriers: a feasibility study in nonhuman primates." Nanomedicine 5, no. 1 (January 2010): 41–49. http://dx.doi.org/10.2217/nnm.09.78.

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Muller-Trutwin, Michaela C., Sylvie Corbet, Jan Hansen, Marie-Claude Georges-Courbot, Ousmane Diop, Jacques Rigoulet, Francoise Barre-Sinoussi, and Anders Fomsgaard. "Mutations in CCR5-Coding Sequences Are Not Associated with SIV Carrier Status in African Nonhuman Primates." AIDS Research and Human Retroviruses 15, no. 10 (July 1999): 931–39. http://dx.doi.org/10.1089/088922299310647.

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Groot, Colin, Carole H. Sudre, Frederik Barkhof, Charlotte E. Teunissen, Bart N. M. van Berckel, Sang Won Seo, Sébastien Ourselin, et al. "Clinical phenotype, atrophy, and small vessel disease in APOEε2 carriers with Alzheimer disease." Neurology 91, no. 20 (October 19, 2018): e1851-e1859. http://dx.doi.org/10.1212/wnl.0000000000006503.

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ObjectiveTo examine the clinical phenotype, gray matter atrophy patterns, and small vessel disease in patients who developed prodromal or probable Alzheimer disease dementia, despite carrying the protective APOEε2 allele.MethodsWe included 36 β-amyloid-positive (by CSF or PET) APOEε2 carriers (all ε2/ε3) with mild cognitive impairment or dementia due to Alzheimer disease who were matched for age and diagnosis (ratio 1:2) to APOEε3 homozygotes and APOEε4 carriers (70% ε3/ε4 and 30% ε4/ε4). We assessed neuropsychological performance across 4 cognitive domains (memory, attention, executive, and language functions), performed voxelwise and region of interest analyses of gray matter atrophy on T1-weighted MRI, used fluid-attenuated inversion recovery images to automatically quantify white matter hyperintensity volumes, and assessed T2*-weighted images to identify microbleeds. Differences in cognitive domain scores, atrophy, and white matter hyperintensities between ε2 carriers, ε3 homozygotes, and ε4 carriers were assessed using analysis of variance analyses, and Pearson χ2 tests were used to examine differences in prevalence of microbleeds.ResultsWe found that ε2 carriers performed worse on nonmemory domains compared to both ε3 homozygotes and ε4 carriers but better on memory compared to ε4 carriers. Voxelwise T1-weighted MRI analyses showed asymmetric (left > right) temporoparietal-predominant atrophy with subtly less involvement of medial–temporal structures in ε2 carriers compared to ε4 carriers. Finally, ε2 carriers had larger total white matter hyperintensity volumes compared to ε4 carriers (mean 10.4 vs 7.3 mL) and a higher prevalence of microbleeds compared to ε3 homozygotes (37.5% vs 18.3%).ConclusionAPOEε2 carriers who develop Alzheimer disease despite carrying the protective allele display a nonamnestic clinical phenotype with more severe small vessel disease.

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Ferson, Mark J. "Books as carriers of disease." Medical Journal of Australia 175, no. 11-12 (December 2001): 663–64. http://dx.doi.org/10.5694/j.1326-5377.2001.tb143769.x.

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Jones, Sir Keith. "Books as carriers of disease." Medical Journal of Australia 176, no. 4 (February 2002): 196. http://dx.doi.org/10.5694/j.1326-5377.2002.tb04368.x.

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Roche, John V. "Books as carriers of disease." Medical Journal of Australia 176, no. 9 (May 2002): 452. http://dx.doi.org/10.5694/j.1326-5377.2002.tb04497.x.

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23

Goker-Alpan, O. "Parkinsonism among Gaucher disease carriers." Journal of Medical Genetics 41, no. 12 (December 1, 2004): 937–40. http://dx.doi.org/10.1136/jmg.2004.024455.

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Haney, Matthew J., Hong Yuan, Steven T. Shipley, Zhanhong Wu, Yuling Zhao, Kelly Pate, Jonathan E. Frank, et al. "Biodistribution of Biomimetic Drug Carriers, Mononuclear Cells, and Extracellular Vesicles, in Nonhuman Primates." Advanced Biology 6, no. 2 (December 22, 2021): 2101293. http://dx.doi.org/10.1002/adbi.202101293.

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25

Riley, Brigit E., Jeff Boonsripisal, Alicia Goodwin, Dominique Cartier, Eudean Garces, Kate Nesbitt, Courtney Dwyer, et al. "Development of an Optimized rAAV2/6 Human Factor 8 cDNA Vector Cassette for Hemophilia a Gene Therapy." Blood 128, no. 22 (December 2, 2016): 1173. http://dx.doi.org/10.1182/blood.v128.22.1173.1173.

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Abstract Hemophilia A, which is caused by a mutation in the Factor 8 (F8) gene resulting in a deficiency or lack of the Factor VIII (FVIII) protein, is the most common inherited bleeding disorder in humans with an estimated worldwide incidence of half a million people. The disorder is X-linked and occurs in approximately 1 in 5,000 males; however there is also a growing appreciation of the impact on carrier females having a single mutant allele, with at least 10% of hemophilia A female carriers having less than normal clotting activity. Even modest increases in Factor V III activity (>1% of normal) can have a positive impact on patient lives, thus making the disease an ideal candidate for liver-directed gene therapy. Recombinant AAV (rAAV) has been used extensively for nearly 20 years as a gene therapy vector in preclinical and clinical studies where rAAV delivery to non-dividing tissues such as liver, brain and muscle affords stable, long-term transgene expression. However, there has been a lag in the clinical translation of a rAAV gene therapy approach for Hemophilia A/human F8 (hF8) compared to Hemophilia B/human Factor 9 due to poor yields of rAAV encoding a F8 transgene at clinical scale, and a requirement for large doses of rAAV F8 vector to achieve therapeutically relevant levels of circulating human FVIII (hFVIII), with the attendant risk of inducing an AAV-directed immune response requiring transient immunosuppression. To address these issues we optimized a rAAV F8 cDNA vector cassette to improve both virus yields and liver-specific hFVIII expression. The rAAV F8 cDNA vector cassette optimization required multi-factorial modifications to the liver-specific promoter module, hF8 transgene, synthetic polyadenylation signal and vector backbone sequence. This iterative process resulted in improved vector yields at research scale and greater than five-fold improvement in vector yields at clinical scale using our proven manufacturing process. Administration of the optimized rAAV hF8 cDNA packaged in serotype AAV2/6 at a dose of ~7.2E+12 vg/kg to both wild type and Hemophilia A mice resulted in robust circulating hFVIII levels and activity (levels in wild type mice were 241.6% of normal, and activity in Hemophilia A mice were 330.9% of normal). An analysis of hF8 mRNA levels in different tissues following dosage with our optimized vector demonstrated that hF8 expression from the modified promoter module was restricted to the liver. Notably there was a striking impact on hemostasis in the Hemophilia A mice treated with the optimized rAAV hF8 cDNA, with a reduction in bleeding time from 38.3 minutes to 2.5 minutes in treated mice (n = 12, p-value < 0.0001), which is in line with bleeding times in wild type mice. Initial studies in non-human primates (NHPs) resulted in supraphysiological levels of circulating hFVIII with mean peak values of 400-600% of normal levels. A follow up dose-ranging study was performed in NHPs with a rAAV2/6 F8 cDNA vector manufactured using our GMP clinical manufacturing process. Administration of vector doses ranging from 6E+11 vg/kg to 6E+12 vg/kg resulted in therapeutic circulating levels of hFVIII that were 5% - 229% of normal levels. The peak circulating hFVIII levels achieved in this dose-ranging study using GMP clinical-scale vector exceeds the levels previously reported in NHPs by several fold on an AAV vector dose basis. The high potency of this enhanced rAAV F8 cDNA cassette could significantly reduce the dose required to achieve therapeutically relevant levels in human subjects and reduce the potential of developing immune responses to AAV capsid requiring immunosuppression. Disclosures Riley: Sangamo BioSciences Inc: Employment. Boonsripisal:Sangamo BioSciences Inc: Employment. Goodwin:Sangamo BioSciences Inc: Employment. Garces:Sangamo BioSciences Inc: Employment. Ballaron:Sangamo BioSciences Inc: Employment. Tran:Sangamo BioSciences Inc: Employment. Kang:Sangamo BioSciences Inc: Employment. Zhang:Sangamo BioSciences Inc: Employment. Meyer:Sangamo BioSciences Inc: Employment. Greengard:Sangamo BioSciences Inc: Employment. Surosky:Sangamo BioSciences Inc: Employment. Ando:Sangamo BioSciences Inc: Employment. Lillicrap:bayer: Research Funding; biogen: Research Funding; CSL: Research Funding; Octapharma: Research Funding; Sangamo Biosciences Inc: Research Funding. Nichol:Sangamo BioSciences Inc: Employment. Holmes:Sangamo BioSciences Inc: Employment.

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Race, Brent, Kimberly D. Meade-White, Katie Phillips, James Striebel, Richard Race, and Bruce Chesebro. "Chronic Wasting Disease Agents in Nonhuman Primates." Emerging Infectious Diseases 20, no. 5 (May 2014): 833–37. http://dx.doi.org/10.3201/eid2005.130778.

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27

Cox, Laura A., Michael Olivier, Kimberly Spradling-Reeves, Genesio M. Karere, Anthony G. Comuzzie, and John L. VandeBerg. "Nonhuman Primates and Translational Research—Cardiovascular Disease." ILAR Journal 58, no. 2 (2017): 235–50. http://dx.doi.org/10.1093/ilar/ilx025.

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28

Reyes-Sandoval, A., J. C. Fitzgerald, R. Grant, S. Roy, Z. Q. Xiang, Y. Li, G. P. Gao, J. M. Wilson, and H. C. J. Ertl. "Human Immunodeficiency Virus Type 1-Specific Immune Responses in Primates upon Sequential Immunization with Adenoviral Vaccine Carriers of Human and Simian Serotypes." Journal of Virology 78, no. 14 (July 15, 2004): 7392–99. http://dx.doi.org/10.1128/jvi.78.14.7392-7399.2004.

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ABSTRACT Two triple immunization vaccine regimens with adenoviral vectors with E1 deleted expressing Gag of human immunodeficiency virus type 1 were tested for induction of T- and B-cell-mediated-immune responses in mice and in nonhuman primates. The vaccine carriers were derived from distinct serotypes of human and simian adenoviruses that fail to elicit cross-neutralizing antibodies expected to dampen the effect of booster immunizations. Both triple immunization regimens induced unprecedented frequencies of gamma interferon-producing CD8+ T cells to Gag in mice and monkeys that remained remarkably stable over time. In addition, monkeys developed Gag-specific interleukin-2-secreting T cells, presumably belonging to the CD4+ T-cell subset, and antibodies to both Gag and the adenoviral vaccine carriers.

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Löwy, Ilana. "Hidden Perils: Diagnosing Asymptomatic Disease Carriers." Medicine Anthropology Theory 8, no. 2 (July 16, 2021): 1–29. http://dx.doi.org/10.17157/mat.8.2.5106.

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COVID-19, a disease induced by SARS-CoV-2, became a worldwide pandemic while SARS, a disease induced by a closely related virus, SARS-CoV, was successfully contained. This is because COVID-19, unlike SARS, can be spread by people who do not display any symptoms of disease, either because they are in the early stages of the infection or because their infection remains clinically silent. This research article traces the complex history of the diagnosis of symptom-free (or asymptomatic) carriers of pathogens, a term inseparably linked to the rise of the laboratory diagnosis of pathogens. Only such a diagnosis can reveal that an apparently healthy individual harbours dangerous bacteria, parasites, or viruses. The article begins with the iconic story of ‘Typhoid Mary’, a New York cook found to be an asymptomatic carrier of typhoid fever microbes. It then discusses divergent approaches to the treatment of symptom-free carriers of hookworm and controversies around the screening of HIV carriers, especially before the development of anti-retroviral treatments. It concludes with a presentation of the debates on the role of asymptomatic carriers in the spread of COVID-19 and of the differences between the approaches of countries seeking to eliminate this disease, a goal that itself entails tracing and isolation of all asymptomatic carriers of coronavirus, and those trying to contain it, an approach that tolerates the presence of a limited number of ‘invisible’ virus carriers.

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Kawai, H., K. Yokoi, M. Akaike, M. Kunishige, M. Abe, Y. Tanouchi, H. Mine, Y. Mimura, and S. Saito. "Graves' disease in HTLV-I carriers." Journal of Molecular Medicine 73, no. 2 (February 1995): 85–88. http://dx.doi.org/10.1007/bf00270582.

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Floeter, Mary K., Bryan J. Traynor, Jennifer Farren, Laura E. Braun, Michael Tierney, Edythe A. Wiggs, and Tianxia Wu. "Disease progression in C9orf72 mutation carriers." Neurology 89, no. 3 (June 14, 2017): 234–41. http://dx.doi.org/10.1212/wnl.0000000000004115.

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Objective:To assess changes in 3 clinical measures, the Revised ALS Functional Rating Scale (ALSFRS-R), letter fluency, and Frontal Behavioral Inventory (FBI), over time in C9orf72 mutation carriers (C9+) with varied clinical phenotypes.Methods:Thirty-four unrelated participants with mutations in C9orf72 were enrolled in a prospective natural history study. Participants were classified as asymptomatic, amyotrophic lateral sclerosis (ALS), ALS–familial frontotemporal dementia (FTD), or behavioral-variant FTD by clinical diagnostic criteria. Diagnostic cognitive and motor tests were repeated at 6 and 18 months. The ALSFRS-R, letter fluency, and FBI were administered at baseline and follow-up visits at 6, 12, and 18 months.Results:The clinical diagnosis of most patients did not change over the follow-up. ALSFRS-R scores correlated with measures of motor function. Letter fluency correlated with FBI and cognitive tests. ALSFRS-R, letter fluency, and FBI differed among the C9+ diagnostic subgroups at enrollment and worsened over follow-up in symptomatic patients, with different slopes among the subgroups. Most patients survived to the 6-month time point after enrollment. Survival of C9+ patients with ALS and C9+ patients with ALS-FTD declined over the 12- and 18-month follow-up.Conclusions:The pattern of scores of the ALSFRS-R, letter fluency, and FBI distinguished between ALS, ALS-FTD, and FTD presentations of C9orf72 mutation carriers and asymptomatic carriers. Longitudinal changes in these measures occurred with disease progression in a manner consistent with presenting phenotype.

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Sugden, A. M. "ECOLOGY/EVOLUTION: Conquest by Disease Carriers." Science 299, no. 5615 (March 28, 2003): 1947c—1947. http://dx.doi.org/10.1126/science.299.5615.1947c.

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Race, Brent, Kimberly D. Meade-White, Michael W. Miller, Kent D. Barbian, Richard Rubenstein, Giuseppe LaFauci, Larisa Cervenakova, et al. "Susceptibilities of Nonhuman Primates to Chronic Wasting Disease." Emerging Infectious Diseases 15, no. 9 (September 2009): 1366–76. http://dx.doi.org/10.3201/eid1509.090253.

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34

Porras, G., Q. Li, and E. Bezard. "Modeling Parkinson's Disease in Primates: The MPTP Model." Cold Spring Harbor Perspectives in Medicine 2, no. 3 (December 22, 2011): a009308. http://dx.doi.org/10.1101/cshperspect.a009308.

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Muehlenbein, Michael P. "Primates on display: Potential disease consequences beyond bushmeat." American Journal of Physical Anthropology 162, S63 (January 2017): 32–43. http://dx.doi.org/10.1002/ajpa.23145.

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36

Mueller, Nicolas J., Rolf N. Barth, Shin Yamamoto, Hiroshi Kitamura, Clive Patience, Kazuhiko Yamada, David K. C. Cooper, David H. Sachs, Amitinder Kaur, and Jay A. Fishman. "Activation of Cytomegalovirus in Pig-to-Primate Organ Xenotransplantation." Journal of Virology 76, no. 10 (May 15, 2002): 4734–40. http://dx.doi.org/10.1128/jvi.76.10.4734-4740.2002.

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ABSTRACT Xenotransplantation of porcine organs carries the risk of reactivation of latent virus in donor and recipient tissues as well as transmission of viruses between species. We have investigated the activation of baboon cytomegalovirus (BCMV) and porcine CMV (PCMV) in a pig-to-primate model of xenotransplantation. Tissues originating from a series of six swine-to-baboon composite thymokidney xenotransplants were investigated. Four immunosuppressed baboons died (survival range, 7 to 27 days) with the graft in situ. Increases in BCMV DNA copy numbers occurred in three (75%) of these baboons and was thought to be responsible for pneumonitis and the death of one animal. In two baboons, disseminated intravascular coagulation was successfully treated by graftectomy and discontinuation of immunosuppression. PCMV was upregulated in five of six xenografts (83%). PCMV infection was associated with ureteric necrosis in one xenograft. Although significantly increased in native tissues, low levels of BCMV and PCMV were also detected in tissues other than that of the native viral host species. The cross-species presence of CMV did not appear to cause clinical or histological signs of invasive disease. Thus, viral infections with clinical disease were restricted to tissues of the native species of each virus. Intensive immune suppression currently required for xenotransplantation results in a significant risk of reactivation of latent infections by BCMV and PCMV. It is not yet known whether viral DNA detected across species lines represents cellular microchimerism, ongoing viral infection, or uptake of free virus. The observation of graft injury by PCMV demonstrates that CMV will be an important pathogen in immunosuppressed xenograft recipients. Strategies must be developed to exclude CMV from porcine organ donors.

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Deng, Xiao, Bin Xiao, John Carson Allen, Ebonne Ng, Jia Nee Foo, Yew-Long Lo, Louis C. S. Tan, and Eng-King Tan. "Parkinson’s disease GWAS-linked Park16 carriers show greater motor progression." Journal of Medical Genetics 56, no. 11 (February 27, 2019): 765–68. http://dx.doi.org/10.1136/jmedgenet-2018-105661.

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BackgroundData on the long-term motor outcomes of genome-wide association study (GWAS)-linked Parkinson disease (PD) carriers are useful for clinical management.ObjectivesTo characterise the association between GWAS-linked PARK16 gene variant and disease progression in PD over a 9-year time frame.MethodsOver a 9-year period, carriers of PARK16 rs11240572 variant and non-carriers were followed up and evaluated using the modified Hoehn and Yahr (H&Y) staging scale and Unified Parkinson’s Disease Rating Scale (UPDRS) part III. A longitudinal, linear mixed model was performed to compare the changes of H&Y staging scale, UPDRS motor score and UPDRS subscores between the two groups.ResultsA total of 156 patients (41 PARK16 carriers and 115 non-carriers) were evaluated and followed up for up to 9 years. Using longitudinal linear mixed model analysis, there was a greater rate of deterioration in the motor function as measured by the UPDRS scores compared with non-carriers after 5 years from the date of diagnosis (p=0.009). In addition, we demonstrated that PARK16 variant carriers had worse gait scores (p=0.043) and greater motor progression than non-carriers after 6 years based on the modified H&Y staging scale (p=0.040).ConclusionsIn a 9-year longitudinal study, we demonstrated that PD PARK16 variant carriers exhibited greater motor progression after 5 years of disease compared with non-carriers, suggesting that GWAS-linked gene variants may influence disease progression over time. Closer monitoring and management of these higher risk patients can facilitate a better quality of life.

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Lin, Ai-Ling, David Allan Butterfield, and Arlan Richardson. "mTOR: Alzheimer's disease prevention for APOE4 carriers." Oncotarget 7, no. 29 (June 30, 2016): 44873–74. http://dx.doi.org/10.18632/oncotarget.10349.

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Kotka, Maria, Agne Lieden, Sven Pettersson, Vito Trinchieri, Alessandra Masci, and Mauro DʼAmato. "Solute Carriers (SLC) in Inflammatory Bowel Disease." Journal of Clinical Gastroenterology 42 (September 2008): S133—S135. http://dx.doi.org/10.1097/mcg.0b013e31815f5ab6.

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ISHIKAWA, Koh-ichi, Yutaka TAKEBE, Rika KISHIMOTO, Takeshi KURATA, and Takashi KAWANA. "Sexually Transmitted Disease Infection in HIV Carriers." Journal of the Japanese Association for Infectious Diseases 68, no. 4 (1994): 474–78. http://dx.doi.org/10.11150/kansenshogakuzasshi1970.68.474.

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van Duijn, E., E. M. Kingma, and R. C. van der Mast. "Psychopathology in Verified Huntington’s Disease Gene Carriers." Journal of Neuropsychiatry and Clinical Neurosciences 19, no. 4 (October 2007): 441–48. http://dx.doi.org/10.1176/jnp.2007.19.4.441.

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Belkin, N. L. "Testing for carriers of Creutzfeldt-Jakob disease." Journal of Hospital Infection 55, no. 2 (October 2003): 153–54. http://dx.doi.org/10.1016/s0195-6701(03)00259-7.

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Belkin, Nathan L. "Creutzfeldt-Jakob Disease Identifying Prions and Carriers." AORN Journal 78, no. 2 (August 2003): 204–10. http://dx.doi.org/10.1016/s0001-2092(06)60771-0.

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Sekhon, L., Z. Luscher, T. G. Nazem, J. Lee, L. Grunfeld, and A. B. Copperman. "Gaucher’s disease carriers demonstrate improved art outcome." Fertility and Sterility 110, no. 4 (September 2018): e142. http://dx.doi.org/10.1016/j.fertnstert.2018.07.420.

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Vantaggiato, Lorenza, Enxhi Shaba, Alfonso Carleo, Daiana Bezzini, Giovanna Pannuzzo, Alice Luddi, Paola Piomboni, Luca Bini, and Laura Bianchi. "Neurodegenerative Disorder Risk in Krabbe Disease Carriers." International Journal of Molecular Sciences 23, no. 21 (November 4, 2022): 13537. http://dx.doi.org/10.3390/ijms232113537.

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Krabbe disease (KD) is a rare autosomal recessive disorder caused by mutations in the galactocerebrosidase gene (GALC). Defective GALC causes aberrant metabolism of galactolipids present almost exclusively in myelin, with consequent demyelinization and neurodegeneration of the central and peripheral nervous system (NS). KD shares some similar features with other neuropathies and heterozygous carriers of GALC mutations are emerging with an increased risk in developing NS disorders. In this work, we set out to identify possible variations in the proteomic profile of KD-carrier brain to identify altered pathways that may imbalance its homeostasis and that may be associated with neurological disorders. The differential analysis performed on whole brains from 33-day-old twitcher (galc −/−), heterozygous (galc +/−), and wild-type mice highlighted the dysregulation of several multifunctional factors in both heterozygous and twitcher mice. Notably, the KD-carrier mouse, despite its normal phenotype, presents the deregulation of vimentin, receptor of activated protein C kinase 1 (RACK1), myelin basic protein (MBP), 2′,3′-cyclic-nucleotide 3′-phosphodiesterase (CNP), transitional endoplasmic reticulum ATPase (VCP), and N-myc downstream regulated gene 1 protein (NDRG1) as well as changes in the ubiquitinated-protein pattern. Our findings suggest the carrier may be affected by dysfunctions classically associated with neurodegeneration: (i) alteration of (mechano) signaling and intracellular trafficking, (ii) a generalized affection of proteostasis and lipid metabolism, with possible defects in myelin composition and turnover, and (iii) mitochondrion and energy supply dysfunctions.

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Becker, Joanna G., Gregory M. Pastores, Alessandro Di Rocco, Marissa Ferraris, Jerome J. Graber, and Swati Sathe. "Parkinson’s disease in patients and obligate carriers of Gaucher disease." Parkinsonism & Related Disorders 19, no. 1 (January 2013): 129–31. http://dx.doi.org/10.1016/j.parkreldis.2012.06.023.

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Drozdzik, Marek, Maria Drozdzik, and Stefan Oswald. "Membrane Carriers and Transporters in Kidney Physiology and Disease." Biomedicines 9, no. 4 (April 14, 2021): 426. http://dx.doi.org/10.3390/biomedicines9040426.

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The growing information suggests that chronic kidney disease may affect expression and function of membrane carriers and transporters in the kidney. The dysfunction of carriers and transporters entails deficient elimination of uremic solutes as well as xenobiotics (drugs and toxins) with subsequent clinical consequences. The renal carriers and transporters are also targets of drugs used in clinical practice, and intentional drug–drug interactions in the kidney are produced to increase therapeutic efficacy. The understanding of membrane carriers and transporters function in chronic kidney disease is important not only to better characterize drug pharmacokinetics, drug actions in the kidney, or drug–drug interactions but also to define the organ pathophysiology.

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Verhoeven, AJ, ML van Schaik, D. Roos, and RS Weening. "Detection of carriers of the autosomal form of chronic granulomatous disease." Blood 71, no. 2 (February 1, 1988): 505–7. http://dx.doi.org/10.1182/blood.v71.2.505.505.

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Abstract The NADPH:O2 oxidoreductase catalyzing the respiratory burst in activated phagocytes from healthy individuals is not operative in phagocytes from patients with chronic granulomatous disease (CGD). In a microscopic slide test using the dye nitroblue tetrazolium (NBT), carriers of X-linked CGD can be recognized by a mosaic pattern of NBT- positive and NBT-negative cells, governed by the expression of an unaffected or an affected X chromosome, respectively. Until now, it has not been possible to detect carriers of the autosomal form of CGD (other than by family studies) because all cells of these carriers stain positive in the NBT test. We have investigated whether neutrophils from carriers of autosomal CGD can be recognized by measurement of the rate of oxygen uptake upon stimulation of the cells. It was found that with the phorbol ester PMA as a stimulus, the respiratory burst is significantly lower in autosomal CGD carriers. With serum-treated zymosan as a stimulus, no difference between controls and carriers was observed. The addition of f-Met-Leu-Phe (1 microM) to PMA-activated neutrophils of control donors caused a transient increase in oxygen consumption of about 40%. Under these conditions, an increase of more than 100% was observed in neutrophils from carriers of autosomal CGD. These findings provide a simple method for the detection of carriers of the autosomal form of CGD.

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Verhoeven, AJ, ML van Schaik, D. Roos, and RS Weening. "Detection of carriers of the autosomal form of chronic granulomatous disease." Blood 71, no. 2 (February 1, 1988): 505–7. http://dx.doi.org/10.1182/blood.v71.2.505.bloodjournal712505.

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The NADPH:O2 oxidoreductase catalyzing the respiratory burst in activated phagocytes from healthy individuals is not operative in phagocytes from patients with chronic granulomatous disease (CGD). In a microscopic slide test using the dye nitroblue tetrazolium (NBT), carriers of X-linked CGD can be recognized by a mosaic pattern of NBT- positive and NBT-negative cells, governed by the expression of an unaffected or an affected X chromosome, respectively. Until now, it has not been possible to detect carriers of the autosomal form of CGD (other than by family studies) because all cells of these carriers stain positive in the NBT test. We have investigated whether neutrophils from carriers of autosomal CGD can be recognized by measurement of the rate of oxygen uptake upon stimulation of the cells. It was found that with the phorbol ester PMA as a stimulus, the respiratory burst is significantly lower in autosomal CGD carriers. With serum-treated zymosan as a stimulus, no difference between controls and carriers was observed. The addition of f-Met-Leu-Phe (1 microM) to PMA-activated neutrophils of control donors caused a transient increase in oxygen consumption of about 40%. Under these conditions, an increase of more than 100% was observed in neutrophils from carriers of autosomal CGD. These findings provide a simple method for the detection of carriers of the autosomal form of CGD.

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Robins Wahlin, Tarja-Brita, Mary A. Luszcz, Åke Wahlin, and Gerard J. Byrne. "Non-Verbal and Verbal Fluency in Prodromal Huntington's Disease." Dementia and Geriatric Cognitive Disorders Extra 5, no. 3 (December 18, 2015): 517–29. http://dx.doi.org/10.1159/000441942.

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Abstract:

Background: This study examines non-verbal (design) and verbal (phonemic and semantic) fluency in prodromal Huntington's disease (HD). An accumulating body of research indicates subtle deficits in cognitive functioning among prodromal mutation carriers for HD. Methods: Performance was compared between 32 mutation carriers and 38 non-carriers in order to examine the magnitude of impairment across fluency tasks. The predicted years to onset (PYTO) in mutation carriers was calculated by a regression equation and used to divide the group according to whether onset was predicted as less than 12.75 years (HD+CLOSE; n = 16) or greater than 12.75 years (HD+DISTANT; n = 16). Results: The results indicate that both non-verbal and verbal fluency is sensitive to subtle impairment in prodromal HD. HD+CLOSE group produced fewer items in all assessed fluency tasks compared to non-carriers. HD+DISTANT produced fewer drawings than non-carriers in the non-verbal task. PYTO correlated significantly with all measures of non-verbal and verbal fluency. Conclusion: The pattern of results indicates that subtle cognitive deficits exist in prodromal HD, and that less structured tasks with high executive demands are the most sensitive in detecting divergence from the normal range of functioning. These selective impairments can be attributed to the early involvement of frontostriatal circuitry and frontal lobes.

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