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2. Therapeutic benefit of idebenone in patients with Leber hereditary optic neuropathy: The LEROS nonrandomized controlled trial

Author

Yu-Wai-Man, Patrick, Carelli, Valerio, Newman, Nancy J., Silva, Magda Joana, Linden, Aki, Van Stavern, Gregory, Szaflik, Jacek P., Banik, Rudrani, Lubiński, Wojciech, Pemp, Berthold, Liao, Yaping Joyce, Subramanian, Prem S., Misiuk-Hojło, Marta, Newman, Steven, Castillo, Lorena, Kocięcki, Jarosław, Levin, Marc H., Muñoz-Negrete, Francisco Jose, Yagan, Ali, Cherninkova, Sylvia, Katz, David, Meunier, Audrey, Votruba, Marcela, Korwin, Magdalena, Dziedziak, Jacek, Jurkutė, Neringa, Harvey, Joshua P., La Morgia, Chiara, Priglinger, Claudia, Llòria, Xavier, Tomasso, Livia, and Klopstock, Thomas

Published
2024
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3. SSBP1 mutations in dominant optic atrophy with variable retinal degeneration

Author

Jurkute, Neringa, Leu, Costin, Pogoda, Hans‐Martin, Arno, Gavin, Robson, Anthony G, Nürnberg, Gudrun, Altmüller, Janine, Thiele, Holger, Motameny, Susanne, Toliat, Mohammad Reza, Powell, Kate, Höhne, Wolfgang, Michaelides, Michel, Webster, Andrew R, Moore, Anthony T, Hammerschmidt, Matthias, Nürnberg, Peter, Yu‐Wai‐Man, Patrick, and Votruba, Marcela

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Pediatric, Neurosciences, Eye Disease and Disorders of Vision, Rare Diseases, Neurodegenerative, Genetics, 2.1 Biological and endogenous factors, Aetiology, Eye, Animals, Cell Differentiation, Cells, Cultured, DNA-Binding Proteins, Female, Gene Knockdown Techniques, Genetic Linkage, Genetic Predisposition to Disease, Humans, Male, Mice, Mitochondrial Proteins, Mutation, Missense, Optic Atrophy, Autosomal Dominant, Pedigree, RNA, Messenger, Retinal Degeneration, Zebrafish, Clinical Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveAutosomal dominant optic atrophy (ADOA) starts in early childhood with loss of visual acuity and color vision deficits. OPA1 mutations are responsible for the majority of cases, but in a portion of patients with a clinical diagnosis of ADOA, the cause remains unknown. This study aimed to identify novel ADOA-associated genes and explore their causality.MethodsLinkage analysis and sequencing were performed in multigeneration families and unrelated patients to identify disease-causing variants. Functional consequences were investigated in silico and confirmed experimentally using the zebrafish model.ResultsWe defined a new ADOA locus on 7q33-q35 and identified 3 different missense variants in SSBP1 (NM_001256510.1; c.113G>A [p.(Arg38Gln)], c.320G>A [p.(Arg107Gln)] and c.422G>A [p.(Ser141Asn)]) in affected individuals from 2 families and 2 singletons with ADOA and variable retinal degeneration. The mutated arginine residues are part of a basic patch that is essential for single-strand DNA binding. The loss of a positive charge at these positions is very likely to lower the affinity of SSBP1 for single-strand DNA. Antisense-mediated knockdown of endogenous ssbp1 messenger RNA (mRNA) in zebrafish resulted in compromised differentiation of retinal ganglion cells. A similar effect was achieved when mutated mRNAs were administered. These findings point toward an essential role of ssbp1 in retinal development and the dominant-negative nature of the identified human variants, which is consistent with the segregation pattern observed in 2 multigeneration families studied.InterpretationSSBP1 is an essential protein for mitochondrial DNA replication and maintenance. Our data have established pathogenic variants in SSBP1 as a cause of ADOA and variable retinal degeneration. ANN NEUROL 2019;86:368-383.

Published
2019

17. OPA1 mutation and late-onset cardiomyopathy: mitochondrial dysfunction and mtDNA instability.

Author

Chen, Le, Liu, Tingting, Tran, Alice, Lu, Xiyuan, Tomilov, Alexey A, Davies, Vanessa, Cortopassi, Gino, Chiamvimonvat, Nipavan, Bers, Donald M, Votruba, Marcela, and Knowlton, Anne A

Subjects
Mitochondria, Animals, Mice, Cardiomyopathies, Disease Models, Animal, Genomic Instability, Reactive Oxygen Species, GTP Phosphohydrolases, DNA, Mitochondrial, Blotting, Western, Polymerase Chain Reaction, Apoptosis, Mutation, OPA1, ROS, cardiomyopathy, mitochondrial fusion, mtDNA, Disease Models, Animal, DNA, Mitochondrial, Blotting, Western, Cardiorespiratory Medicine and Haematology
Abstract

BackgroundMitochondrial fusion protein mutations are a cause of inherited neuropathies such as Charcot-Marie-Tooth disease and dominant optic atrophy. Previously we reported that the fusion protein optic atrophy 1 (OPA1) is decreased in heart failure.Methods and resultsWe investigated cardiac function, mitochondrial function, and mtDNA stability in a mouse model of the disease with OPA1 mutation. The homozygous mutation is embryonic lethal. Heterozygous OPA(+/-) mice exhibit reduced mtDNA copy number and decreased expression of nuclear antioxidant genes at 3 to 4 months. Although initial cardiac function was normal, at 12 months the OPA1(+/-) mouse hearts had decreased fractional shortening, cardiac output, and myocyte contraction. This coincided with the onset of blindness. In addition to small fragmented mitochondria, aged OPA1(+/-) mice had impaired cardiac mitochondrial function compared with wild-type littermates.ConclusionsOPA1 mutation leads to deficiency in antioxidant transcripts, increased reactive oxygen species, mitochondrial dysfunction, and late-onset cardiomyopathy.

Published
2012

18. Real-World Clinical Experience With Idebenone in the Treatment of Leber Hereditary Optic Neuropathy

Author

Catarino, Claudia B., von Livonius, Bettina, Priglinger, Claudia, Banik, Rudrani, Matloob, Selma, Tamhankar, Madhura A., Castillo, Lorena, Friedburg, Christoph, Halfpenny, Christopher A., Lincoln, John A., Traber, Ghislaine L., Acaroglu, Gölge, Black, Graeme C. M., Doncel, Carlos, Fraser, Clare L., Jakubaszko, Joanna, Landau, Klara, Langenegger, Stefan J., Muñoz-Negrete, Francisco J., Newman, Nancy J., Poulton, Joanna, Scoppettuolo, Elisabetta, Subramanian, Prem, Toosy, Ahmed T., Vidal, Mariona, Vincent, Andrea L., Votruba, Marcela, Zarowski, Marcin, Zermansky, Adam, Lob, Felice, Rudolph, Günther, Mikazans, Oskars, Silva, Magda, Llòria, Xavier, Metz, Günther, and Klopstock, Thomas

Published
2020
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19. A clinical and molecular genetic study of dominant optic atrophy mapping to chromosome 3q28-qter

Author

Votruba, Marcela

Subjects
610, Eye defect genetics
Abstract

Dominant optic atrophy (DOA) is the commonest form of autosomally-inherited (non-glaucomatous) optic neuropathy. Patients present with bilateral visual loss, temporal optic nerve pallor, centro-caecal scotoma, and a colour vision deficit. A gene for dominant optic atrophy (OPAI) was mapped to within 12 cM on chromosome 3q28-qter in 1994. One hundred and fifty eight affected individuals from 41 families were recruited and blood collected for DNA analysis. The clinical, psychophysical, electrophysiological and neuro-ophthalmic features were investigated in affected individuals from pedigrees showing evidence of linkage to chromosome 3q28-qter. Electrophysiological studies suggest that the abnormalities are confined to the retinal ganglion cell. Psychophysical studies implicate magnocellular and parvocellular ganglion cells of the macula region of the retina. Genetic linkage, haplotype and linkage disequilibrium analysis was carried out. The critical disease interval has been substantially refined to a 1.4cM region between markers D3S3669 and D3S3562. No pedigrees mapped to a second locus on chromosome 18q 12.2-12.3. Haplotype analysis of 38 pedigrees revealed evidence of a founder effect in 36. This allowed for the prediction of the most likely position of the disease gene in the critical disease interval to within ca. 400 kb either side of the marker D3S1523. HRY, a positional and functional candidate gene for DOA, was screened by heteroduplex mutation screening and direct sequencing. No disease-associated abnormalities were found in the coding region of HRY. A physical map spanning the critical disease interval was constructed, comprising YAC and PAC clones. STS content mapping was carried out to confirm clone authenticity and establish overlaps to form a contig. A total of nine STSs, including five microsatellites, were used to allow integration with genetic maps of the region. A preliminary transcript map of the OPAI region was generated, with five ESTs mapping in the critical interval. The expression of these ESTs was studied by PCR of cDNA from a range of tissues. The insert of IMAGE clone EST SHGC374I4 was sequenced. Using the physical mapping data two further candidate genes, DAGK3 and GAP43 were excluded from the critical interval.

Published
2000

24. Common data elements for clinical research in mitochondrial disease: a National Institute for Neurological Disorders and Stroke project

Author

Karaa, Amel, Rahman, Shamima, Lombès, Anne, Yu-Wai-Man, Patrick, Sheikh, Muniza K., Alai-Hansen, Sherita, Cohen, Bruce H., Dimmock, David, Emrick, Lisa, Falk, Marni J., McCormack, Shana, Mirsky, David, Moore, Tony, Parikh, Sumit, Shoffner, John, Taivassalo, Tanja, Tarnopolsky, Mark, Tein, Ingrid, Odenkirchen, Joanne C., Goldstein, Amy, Abdenur, J. E., Anderson, Vernon, Balcells, Cristy, Bamberger, Mark, Barboni, Piero, Bindoff, Laurence, Camp, Kathryn, Carelli, Valerio, Chinnery, Patrick, Collins, Abigail, Copeland, William C., Fiorino, Kristin, Gai, Xiaowu, Goetz, Kerry, Goodpaster, Bret, Gropman, Andrea L., Gwinn, Katrina A., Haller, Ronald, Heuckeroth, Robert O., Hirano, Michio, Holder, Graham E., Kaufmann, Petra, Keller, Kierstin, Keltner, John L., Klein, Matthew, Klopstock, Thomas, Koene, Saskia, Koenig, Mary Kay, Koga, Yasutoshi, Krotoski, Danuta, Laforêt, Pascal, Lombès, Anne, McFarland, Robert, Milone, Margherita, Morgan, Philip, Sadun, Alfredo A., Saneto, Russel, Scaglia, Fernando, Scharfe, Curt, Sheldon, Claire, Smeitink, Jan, Stacpoole, Peter W., Stanley, Charles A., Thorburn, David, Vaurio, Rebecca, Votruba, Marcela, Wahbi, Karim, Willi, Steven M., Wolfe, Lynne A., Yang, Edward, Yeske, Philip, Züchner, Stephan, Zullo, Steven, and on behalf of the Mito Working Group Member Participants:

Published
2017
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32. Dysregulated mitophagy and mitochondrial organization in optic atrophy due to OPA1 mutations

Author

Liao, Chunyan, Ashley, Neil, Diot, Alan, Morten, Karl, Phadwal, Kanchan, Williams, Andrew, Fearnley, Ian, Rosser, Lyndon, Lowndes, Jo, Fratter, Carl, Ferguson, David J.P., Vay, Laura, Quaghebeur, Gerardine, Moroni, Isabella, Bianchi, Stefania, Lamperti, Costanza, Downes, Susan M., Sitarz, Kamil S., Flannery, Padraig J., Carver, Janet, Dombi, Eszter, East, Daniel, Laura, Matilde, Reilly, Mary M., Mortiboys, Heather, Prevo, Remko, Campanella, Michelangelo, Daniels, Matthew J., Zeviani, Massimo, Yu-Wai-Man, Patrick, Simon, Anna Katharina, Votruba, Marcela, and Poulton, Joanna

Published
2017
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34. Research priorities for mitochondrial disorders: Current landscape and patient and professional views

Author

Thomas, Rhys H., primary, Hunter, Amy, additional, Butterworth, Lyndsey, additional, Feeney, Catherine, additional, Graves, Tracey D., additional, Holmes, Sarah, additional, Hossain, Pushpa, additional, Lowndes, Jo, additional, Sharpe, Jenny, additional, Upadhyaya, Sheela, additional, Varhaug, Kristin N., additional, Votruba, Marcela, additional, Wheeler, Russell, additional, Staley, Kristina, additional, and Rahman, Shamima, additional

Published
2022
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39. Nicotinamide provides neuroprotection in glaucoma by protecting against mitochondrial and metabolic dysfunction

Author

Tribble, James R., primary, Otmani, Amin, additional, Sun, Shanshan, additional, Ellis, Sevannah A., additional, Cimaglia, Gloria, additional, Vohra, Rupali, additional, Jöe, Melissa, additional, Lardner, Emma, additional, Venkataraman, Abinaya P., additional, Domínguez-Vicent, Alberto, additional, Kokkali, Eirini, additional, Rho, Seungsoo, additional, Jóhannesson, Gauti, additional, Burgess, Robert W., additional, Fuerst, Peter G., additional, Brautaset, Rune, additional, Kolko, Miriam, additional, Morgan, James E., additional, Crowston, Jonathan G., additional, Votruba, Marcela, additional, and Williams, Pete A., additional

Published
2021
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40. Nicotinamide provides neuroprotection in glaucoma by protecting against mitochondrial and metabolic dysfunction

Author

Tribble, James R., Otmani, Amin, Sun, Shanshan, Ellis, Sevannah A., Cimaglia, Gloria, Vohra, Rupali, Jöe, Melissa, Lardner, Emma, Venkataraman, Abinaya P., Domínguez-Vicent, Alberto, Kokkali, Eirini, Rho, Seungsoo, Jóhannesson, Gauti, Burgess, Robert W., Fuerst, Peter G., Brautaset, Rune, Kolko, Miriam, Morgan, James E., Crowston, Jonathan G., Votruba, Marcela, Williams, Pete A., Tribble, James R., Otmani, Amin, Sun, Shanshan, Ellis, Sevannah A., Cimaglia, Gloria, Vohra, Rupali, Jöe, Melissa, Lardner, Emma, Venkataraman, Abinaya P., Domínguez-Vicent, Alberto, Kokkali, Eirini, Rho, Seungsoo, Jóhannesson, Gauti, Burgess, Robert W., Fuerst, Peter G., Brautaset, Rune, Kolko, Miriam, Morgan, James E., Crowston, Jonathan G., Votruba, Marcela, and Williams, Pete A.

Abstract

Nicotinamide adenine dinucleotide (NAD) is a REDOX cofactor and metabolite essential for neuronal survival. Glaucoma is a common neurodegenerative disease in which neuronal levels of NAD decline. We assess the effects of nicotinamide (a precursor to NAD) on retinal ganglion cells (the affected neuron in glaucoma) in normal physiological conditions and across a range of glaucoma relevant insults including mitochondrial stress and axon degenerative insults. We demonstrate retinal ganglion cell somal, axonal, and dendritic neuroprotection by nicotinamide in rodent models which represent isolated ocular hypertensive, axon degenerative, and mitochondrial degenerative insults. We performed metabolomics enriched for small molecular weight metabolites for the retina, optic nerve, and superior colliculus which demonstrates that ocular hypertension induces widespread metabolic disruption, including consistent changes to α-ketoglutaric acid, creatine/creatinine, homocysteine, and glycerophosphocholine. This metabolic disruption is prevented by nicotinamide. Nicotinamide provides further neuroprotective effects by increasing oxidative phosphorylation, buffering and preventing metabolic stress, and increasing mitochondrial size and motility whilst simultaneously dampening action potential firing frequency. These data support continued determination of the utility of long-term nicotinamide treatment as a neuroprotective therapy for human glaucoma.

Published
2021

44. Mutations in the m-AAA proteases AFG3L2 and SPG7 are causing isolated dominant optic atrophy

Author

Charif, Majida, Chevrollier, Arnaud, Gueguen, Naïg, Bris, Céline, Goudenège, David, Desquiret-Dumas, Valérie, Leruez, Stéphanie, Colin, Estelle, Meunier, Audrey, Vignal, Catherine, Smirnov, Vasily, Defoort-Dhellemmes, Sabine, Drumare Bouvet, Isabelle, Goizet, Cyril, Votruba, Marcela, Jurkute, Neringa, Yu-Wai-Man, Patrick, Tagliavini, Francesca, Caporali, Leonardo, La Morgia, Chiara, Carelli, Valerio, Procaccio, Vincent, Zanlonghi, Xavier, Meunier, Isabelle, Reynier, Pascal, Bonneau, Dominique, Amati-Bonneau, Patrizia, Lenaers, Guy, Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), Charif M., Chevrollier A., Gueguen N., Bris C., Goudenege D., Desquiret-Dumas V., Leruez S., Colin E., Meunier A., Vignal C., Smirnov V., Defoort-Dhellemmes S., Drumare Bouvet I., Goizet C., Votruba M., Jurkute N., Yu-Wai-Man P., Tagliavini F., Caporali L., La Morgia C., Carelli V., Procaccio V., Zanlonghi X., Meunier I., Reynier P., Bonneau D., Amati-Bonneau P., Lenaers G., Charif, Majida [0000-0003-3301-4305], Chevrollier, Arnaud [0000-0002-5135-6643], Jurkute, Neringa [0000-0002-3092-7451], Caporali, Leonardo [0000-0002-0666-4380], La Morgia, Chiara [0000-0002-4639-8929], Lenaers, Guy [0000-0003-2736-3349], and Apollo - University of Cambridge Repository

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, genetic structures, [SDV]Life Sciences [q-bio], DOA, 32 Biomedical and Clinical Sciences, Neurodegenerative, SPG7, Article, 3105 Genetics, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, optic atrophy, AFG3L2, Eye Disease and Disorders of Vision, ComputingMilieux_MISCELLANEOUS, 3212 Ophthalmology and Optometry, 2 Aetiology, FOS: Clinical medicine, Neurosciences, eye diseases, Brain Disorders, FOS: Biological sciences, Neurological, sense organs, 31 Biological Sciences
Abstract

Objective To improve the genetic diagnosis of dominant optic atrophy (DOA), the most frequently inherited optic nerve disease, and infer genotype-phenotype correlations.\ud\udMethods Exonic sequences of 22 genes were screened by new-generation sequencing in patients with DOA who were investigated for ophthalmology, neurology, and brain MRI.\ud\udResults We identified 7 and 8 new heterozygous pathogenic variants in SPG7 and AFG3L2. Both genes encode for mitochondrial matricial AAA (m-AAA) proteases, initially involved in recessive hereditary spastic paraplegia type 7 (HSP7) and dominant spinocerebellar ataxia 28 (SCA28), respectively. Notably, variants in AFG3L2 that result in DOA are located in different domains to those reported in SCA28, which likely explains the lack of clinical overlap between these 2 phenotypic manifestations. In comparison, the SPG7 variants identified in DOA are interspersed among those responsible for HSP7 in which optic neuropathy has previously been reported.\ud\udConclusions Our results position SPG7 and AFG3L2 as candidate genes to be screened in DOA and indicate that regulation of mitochondrial protein homeostasis and maturation by m-AAA proteases are crucial for the maintenance of optic nerve physiology.

Published
2020
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45. Real-World Clinical Experience With Idebenone in the Treatment of Leber Hereditary Optic Neuropathy

Author

Catarino, Claudia B, von Livonius, Bettina, Priglinger, Claudia, Banik, Rudrani, Matloob, Selma, Tamhankar, Madhura A, Castillo, Lorena, Friedburg, Christoph, Halfpenny, Christopher A, Lincoln, John A, Traber, Ghislaine L, Acaroglu, Gölge, Black, Graeme C M, Doncel, Carlos, Fraser, Clare L, Jakubaszko, Joanna, Landau, Klara, Langenegger, Stefan J, Muñoz-Negrete, Francisco J, Newman, Nancy J, Poulton, Joanna, Scoppettuolo, Elisabetta, Subramanian, Prem, Toosy, Ahmed T, Vidal, Mariona, Vincent, Andrea L, Votruba, Marcela, Zarowski, Marcin, Zermansky, Adam, Lob, Felice, Rudolph, Günther, Mikazans, Oskars, Silva, Magda, Lloria, Xavier, Metz, Günther, Klopstock, Thomas, Catarino, Claudia B, von Livonius, Bettina, Priglinger, Claudia, Banik, Rudrani, Matloob, Selma, Tamhankar, Madhura A, Castillo, Lorena, Friedburg, Christoph, Halfpenny, Christopher A, Lincoln, John A, Traber, Ghislaine L, Acaroglu, Gölge, Black, Graeme C M, Doncel, Carlos, Fraser, Clare L, Jakubaszko, Joanna, Landau, Klara, Langenegger, Stefan J, Muñoz-Negrete, Francisco J, Newman, Nancy J, Poulton, Joanna, Scoppettuolo, Elisabetta, Subramanian, Prem, Toosy, Ahmed T, Vidal, Mariona, Vincent, Andrea L, Votruba, Marcela, Zarowski, Marcin, Zermansky, Adam, Lob, Felice, Rudolph, Günther, Mikazans, Oskars, Silva, Magda, Lloria, Xavier, Metz, Günther, and Klopstock, Thomas

Abstract

BACKGROUND: Leber hereditary optic neuropathy (LHON) leads to bilateral central vision loss. In a clinical trial setting, idebenone has been shown to be safe and to provide a trend toward improved visual acuity, but long-term evidence of effectiveness in real-world clinical practice is sparse. METHODS: Open-label, multicenter, retrospective, noncontrolled analysis of long-term visual acuity and safety in 111 LHON patients treated with idebenone (900 mg/day) in an expanded access program. Eligible patients had a confirmed mitochondrial DNA mutation and had experienced the onset of symptoms (most recent eye) within 1 year before enrollment. Data on visual acuity and adverse events were collected as per normal clinical practice. Efficacy was assessed as the proportion of patients with either a clinically relevant recovery (CRR) or a clinically relevant stabilization (CRS) of visual acuity. In the case of CRR, time to and magnitude of recovery over the course of time were also assessed. RESULTS: At time of analysis, 87 patients had provided longitudinal efficacy data. Average treatment duration was 25.6 months. CRR was observed in 46.0% of patients. Analysis of treatment effect by duration showed that the proportion of patients with recovery and the magnitude of recovery increased with treatment duration. Average gain in best-corrected visual acuity for responders was 0.72 logarithm of the minimal angle of resolution (logMAR), equivalent to more than 7 lines on the Early Treatment Diabetic Retinopathy Study (ETDRS) chart. Furthermore, 50% of patients who had a visual acuity below 1.0 logMAR in at least one eye at initiation of treatment successfully maintained their vision below this threshold by last observation. Idebenone was well tolerated, with most adverse events classified as minor. CONCLUSIONS: These data demonstrate the benefit of idebenone treatment in recovering lost vision and maintaining good residual vision in a real-world setting. Together, these findings

Published
2020

46. New avenues for therapy in mitochondrial optic neuropathies

Author

Ng, Wing Sum Vincent, primary, Trigano, Matthieu, additional, Freeman, Thomas, additional, Varrichio, Carmine, additional, Kandaswamy, Dinesh Kumar, additional, Newland, Ben, additional, Brancale, Andrea, additional, Rozanowska, Malgorzata, additional, and Votruba, Marcela, additional

Published
2021
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47. The top ten research priorities for rare mitochondrial diseases: results of a patient/health professional priority setting partnership

Author

Votruba, Marcela, primary, Butterworth, Lyndsey, additional, Feeney, Catherine, additional, Graves, Tracey, additional, Holmes, Sarah, additional, Hunter, Amy, additional, Lowndes, Jo, additional, Rahman, Shamima, additional, Sharpe, Jenny, additional, Thomas, Rhys, additional, Upadhaya, Sheela, additional, Weaver, Lindsay, additional, and Wheeler, Russell, additional

Published
2021
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