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16 results on '"Vermaak, E."'

1. Association between age at disease onset of anti-neutrophil cytoplasmic antibody-associated vasculitis and clinical presentation and short-term outcomes

Author

Monti, S., Craven, A., Klersy, C., Montecucco, C., Caporali, R., Watts, R., Merkel, P. A., Luqmani, R., Achilleos, K., Adler, M., Alba, M. A., Albert, D. A., Alibaz-Oner, F., Allcoat, P., Amano, K., Amarasuriya, M., Amudala, N. A., Andrews, J., Archer, A. M., Arimura, Y., Atukorala, I., Azevedo, E., Bajad, S., Baldwin, C., Barra, L. J., Baslund, B., Basu, N., Baykal, M., Berger, C., Berglin, E., Besada, E., Bhardwaj, M., Bischof, A., Blockmans, D., Blood, J., Draibe, J. B., Brand, S., Brandao, M., Bruce, I. N., Butler, A., Calabrese, L. H., Ferrer, D. C., Carette, S., Carmona, D., Ceunen, H., Chakravarty, K., Chapman, P. T., Chocova, Z., Chung, S. A., Ci, W., Cid, M. C., Clark, T. M., Clarkson, M. R., De Jesus Contreras-Rodriguez, F., Conway, R., Cooke, K., Viros, X. C., Cordeiro, A., Costa, A., Culfear, K., Daikeler, T., Danda, D., Das, S. K., Dasgupta, B., De Castro, A. M., Dehghan, N., Devassy, R., Dhindsa, N., Diamantopoulos, A. P., Direskeneli, H., Dobashi, H., Juan, D., Durrani, M., Edelsten, C., Eifert, J., Elhayek, S., Elsideeg, S., Endo, T., Erden, A., Erer, B., Eriksson, P., Erturk, Z., Espigol-Frigole, G., Felicetti, M., Ferraro, A., Ferro, J. M., Fifi-Mah, A., Flores-Suarez, L. F., Flossmann, O., Flynn, D., Fonseca, J. E., Foot, J., Foote, M., Forbess, L., Fujimoto, S., Fukuoka, K., Furtado, C., Furuta, S., Gaffo, A. L., Gallagher, P., Gao, N., Gatenby, P., Gendi, N., Geraldes, R., Gerits, A., Gioffredi, A., Gomples, L., Goncalves, M. J., Gondo, P., Graham, A., Grainger, R., Gray, D. T., Grayson, P. C., Griffiths, L., Guo, Y., Gupta, R., Gylling, M., Hajj-Ali, R. A., Hammam, N., Harigai, M., Hartley, L., Haslett, J., Hassan, A., Hatemi, G., Hellmich, B., Henckaerts, L., Henes, J. C., Hepburn, J., Herd, V., Hess, C., Hill, C., Hinojosa-Azaola, A., Hirahashi, J., Hirano, F., Hocevar, A., Holle, J., Hollinger, N., Homma, S., Howard, T., Hoyles, R. K., Hruskova, Z., Hutcheon, G., Ignacak, M., Igney-Oertel, A., Ikeda, K., Ikegaya, N., Jagadeesh, S., Jaquith, J., Jayne, D. R. W., Jewell, T., Jones, C., Joshi, A., Kalyoncu, U., Kamall, S., Kamath, S., Lai, K. S., Kaname, S., Kanchinadham, S., Karadag, O., Karube, M., Kaszuba, M., Kaur, R., Kawakami, T., Kawashima, S., Khalidi, N., Khan, A., Kikuchi, M., Kilic, L., Kimura, M., King, M. J., Klapa, S., Klocke, R., Kobayashi, T., Kobayashi, S., Komagata, Y., Kronbichler, A., Kuczia, P., Kumar, M. S., Kurosawa, M., Lamprecht, P., Langford, C. A., Lanyon, P., Laversuch, C., Lee, S. J., Leoni, S., Li, J., Liang, K., Liang, P., Liao, H., Lee, L. A., Luqmani, R. A., Lyle, A., Macdonald, M., Mackie, S. L., Madden, L., Magliano, M., Makino, H., Makol, A., Malaiya, R., Malaviya, A., Manthri, R., Maritati, F., Da Silva, A. M., Mason, J. C., Matara, C., Matsui, K., Matteson, E. L., Mcbride, D., Mccullough, K., Mcgeoch, L., Mclaren, J., Mcmillian, C., Mendiratta, N., Menon, A., Merinopoulos, D., Merkel, P., Messier, S., Micheletti, R. G., Mills, K., Milman, N., Minoda, M., Minz, R. W., Mock, C., Mohammad, A. J., Moiseev, S., Moitinho, M., Molloy, E., Monach, P. A., Montgomery, M., Moosig, F., Moradizadeh, M., Morgan, M., Morgan, A. W., Morgan, A. -M., Muir, A., Mukhtyar, C., Muller, A., Muratore, F., Muso, E., Nada, R., Nakajima, H., Nakajima, T., Nakano, H., Nandagudi, A., Neumann, T., Y. F., Ng, K. H., Ng, Nogueira, E. L., Nolkha, N., Nordstrom, D., Novikov, P., Nugaliyadde, A., O'Donnell, J. L., O'Donoghue, J., O'Neill, L., O'Riordan, E., Oatley, M., Okubo, K., Oliva, E., Oshikawa, H., Ota, Y., Padoan, R., Pagnoux, C., Pan, L., Panaritis, K., Park, J. K., Patel, S., Patil, P., Pazzola, G., Peall, A., Pearce, F., Pehlevan, S., Pereira, L., Pettersson, T., Pineau, C. A., Pirila, L., Poglodek, B., Ponte, C., Prieto-Gonzalez, S., Priya, S. R., Purewal, B., Purschke, S., Putaala, J., Quickert, S., Quincey, V., Raghuvanshi, S., Rajasekhar, L., Ranganathan, D., Rathi, M., Rees, D., Rees, F., Renken, U., Restuccia, G., Rhee, R. L., Rice, B., Robins, D., Robson, J., Rodrigues, M., Romao, V. C., Rotar, C., Ruediger, C., Rutgers, A., A. C., Sa, Saavedra, M. J., Sada, K. -E., Sahbudin, I., Salvarani, C., Sandhu, N., Santos, E., Sato, Y., Schafer, V. S., Schiavon, F., Schmidt, W. A., Segelmark, M., Shahin, A., Sharma, A., Shotton, J., Silva, C., Singer, O. G., Sivasuthan, G., Smolen, S., Solanich-Moreno, X., Boixader, L. S., Song, Y. W., Springer, J., Sreih, A. G., Srivastava, R., Stamp, L. K., Stevens, R., Strbian, D., Sugino, K., Sunderkotter, C., Suppiah, R., Suzuki, K., Szekanecz, Z., Sznajd, J., Taimen, K., Tak, P. P., Takeuchi, T., Takizawa, N., Tames, L., Tan, B. E., Tanaka, M., Tang, M. W., Tatlisumak, T., Tesar, V., Thomas, A., Tian, X., Tokunaga, K., Tombetti, E., Tomsic, M., Toz, B., Tsukamoto, T., Uchida, S., Unal, A. U., Urban, M. L., Usui, J., Vaglio, A., Venkatachalam, S., Vermaak, E., Viswanath, V., Wada, T., Wagh, S., Wallace, D. J., Walters, G., Walz, B., Wan, J., Wang, T., Wang, G., Warrington, K. J., Watts, R. A., Wawrzycka-Adamczyk, K., Weeratunga, P., Weisman, M. H., Wickramasinghe, S., Williams, M., Wojcik, K., Woodruff, L., Xenitidis, T., Yamada, H., Yamagata, K., Yee, C. -S., Yoon, M., Yoshida, K., Yoshifuji, H., Ytterberg, S. R., Yumura, W., Zayed, H., Zeng, X., Zhao, M. -H., Zugaj, A., Zuk, J., İç Hastalıkları, Clinical Haematology, and Translational Immunology Groningen (TRIGR)

Subjects
Male, Outcome, Antineutrophil Cytoplasmic, 030232 urology & nephrology, 0302 clinical medicine, Risk Factors, 80 and over, Pharmacology (medical), Age of Onset, Young adult, Aged, 80 and over, education.field_of_study, age, anti-neutrophil cytoplasmic antibody-associated vasculitis, outcome, Adolescent, Adult, Aged, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Antibodies, Antineutrophil Cytoplasmic, Female, Humans, Middle Aged, Morbidity, Prognosis, Retrospective Studies, Risk Assessment, Survival Rate, United Kingdom, Young Adult, Vasculitis, Systemic vasculitis, medicine.medical_specialty, Population, anti-neutrophil cytoplasmic antibody–associated vasculitis, Antibodies, 03 medical and health sciences, Rheumatology, Internal medicine, medicine, education, Anti-neutrophil cytoplasmic antibody–associated vasculitis, Survival rate, Anti-neutrophil cytoplasmic antibody, 030203 arthritis & rheumatology, business.industry, Retrospective cohort study, medicine.disease, Age of onset, business
Abstract

Objectives ANCA-associated vasculitis (AAV) can affect all age groups. We aimed to show that differences in disease presentation and 6 month outcome between younger- and older-onset patients are still incompletely understood. Methods We included patients enrolled in the Diagnostic and Classification Criteria for Primary Systemic Vasculitis (DCVAS) study between October 2010 and January 2017 with a diagnosis of AAV. We divided the population according to age at diagnosis: Results A total of 1338 patients with AAV were included: 66% had disease onset at Conclusion Within 6 months of diagnosis of AAV, patients >65 years of age display a different pattern of organ involvement and an increased risk of significant damage and mortality compared with younger patients.

Published
2021

2. 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology Classification Criteria for Eosinophilic Granulomatosis With Polyangiitis

Author

Grayson, P. C., Ponte, C., Suppiah, R., Robson, J. C., Craven, A., Judge, A., Khalid, S., Hutchings, A., Luqmani, R. A., Watts, R. A., Merkel, P. A., Gatenby, P., Hill, C., Ranganathan, D., Kronbichler, A., Blockmans, D., Barra, L., Carette, S., Pagnoux, C., Dhindsa, N., Fifi-Mah, A., Khalidi, N., Liang, P., Milman, N., Pineau, C., Tian, X., Wang, G., Wang, T., Zhao, M. -H., Tesar, V., Baslund, B., Hammam, N., Shahin, A., Pirila, L., Putaala, J., Hellmich, B., Henes, J., Lamprecht, P., Neumann, T., Schmidt, W., Sunderkoetter, C., Szekanecz, Z., Danda, D., Das, S., Gupta, R., Rajasekhar, L., Sharma, A., Wagh, S., Clarkson, M., Molloy, E., Salvarani, C., Schiavon, F., Tombetti, E., Vaglio, A., Amano, K., Arimura, Y., Dobashi, H., Fujimoto, S., Harigai, M., Hirano, F., Hirahashi, J., Honma, S., Kawakami, T., Kobayashi, S., Kono, H., Makino, H., Matsui, K., Muso, E., Suzuki, K., Ikeda, K., Takeuchi, T., Tsukamoto, T., Uchida, S., Wada, T., Yamada, H., Yamagata, K., Yumura, W., Lai, K. S., Flores-Suarez, L. F., Hinojosa, A., Rutgers, B., Tak, P. -P., Grainger, R., Quincey, V., Stamp, L., Besada, E., Diamantopoulos, A., Sznajd, J., Azevedo, E., Geraldes, R., Rodrigues, M., Santos, E., Song, Y. -W., Moiseev, S., Hocevar, A., Cid, M. C., Moreno, X. S., Atukorala, I., Berglin, E., Mohammed, A., Segelmark, M., Daikeler, T., Direskeneli, H., Hatemi, G., Kamali, S., Karadag, O., Pehlevan, S., Adler, M., Basu, N., Bruce, I., Chakravarty, K., Dasgupta, B., Flossmann, O., Gendi, N., Hassan, A., Hoyles, R., Jayne, D., Jones, C., Klocke, R., Lanyon, P., Laversuch, C., Luqmani, R., Robson, J., Magliano, M., Mason, J., Maw, W. W., Mcinnes, I., Mclaren, J., Morgan, M., Morgan, A., Mukhtyar, C., O'Riordan, E., Patel, S., Peall, A., Venkatachalam, S., Vermaak, E., Menon, A., Watts, R., Yee, C. -S., Albert, D., Calabrese, L., Chung, S., Forbess, L., Gaffo, A., Gewurz-Singer, O., Grayson, P., Liang, K., Matteson, E., Springer, J., Sreih, A., and Translational Immunology Groningen (TRIGR)

Subjects
Adult, Male, Vasculitis, Myeloblastin, Immunology, Churg-Strauss Syndrome, Sensitivity and Specificity, General Biochemistry, Genetics and Molecular Biology, Antibodies, Antineutrophil Cytoplasmic, Diagnosis, Differential, Rheumatology, Risk Factors, Humans, Immunology and Allergy, anti-neutrophil cytoplasm antibody, Prospective Studies, Aged, Granulomatosis with Polyangiitis, Reproducibility of Results, Middle Aged, United States, Female, eosinophilic granulomatosis with polyangiitis, Eosinophilic Granuloma, Europe, classification, Societies
Abstract

ObjectiveTo develop and validate revised classification criteria for eosinophilic granulomatosis with polyangiitis (EGPA).MethodsPatients with vasculitis or comparator diseases were recruited into an international cohort. The study proceeded in five phases: (1) identification of candidate criteria items using consensus methodology, (2) prospective collection of candidate items present at the time of diagnosis, (3) data-driven reduction of the number of candidate items, (4) expert panel review of cases to define the reference diagnosis and (5) derivation of a points-based risk score for disease classification in a development set using least absolute shrinkage and selection operator logistic regression, with subsequent validation of performance characteristics in an independent set of cases and comparators.ResultsThe development set for EGPA consisted of 107 cases of EGPA and 450 comparators. The validation set consisted of an additional 119 cases of EGPA and 437 comparators. From 91 candidate items, regression analysis identified 11 items for EPGA, 7 of which were retained. The final criteria and their weights were as follows: maximum eosinophil count ≥1×109/L (+5), obstructive airway disease (+3), nasal polyps (+3), cytoplasmic antineutrophil cytoplasmic antibody (ANCA) or anti-proteinase 3–ANCA positivity (−3), extravascular eosinophilic predominant inflammation (+2), mononeuritis multiplex/motor neuropathy not due to radiculopathy (+1) and haematuria (−1). After excluding mimics of vasculitis, a patient with a diagnosis of small- or medium-vessel vasculitis could be classified as having EGPA if the cumulative score was ≥6 points. When these criteria were tested in the validation data set, the sensitivity was 85% (95% CI 77% to 91%) and the specificity was 99% (95% CI 98% to 100%).ConclusionThe 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology Classification Criteria for Eosinophilic Granulomatosis with Polyangiitis demonstrate strong performance characteristics and are validated for use in research.

Published
2022

3. A Ceratium hirundinella (O.F. Müller) bloom in Hartbeespoort Dam, South Africa

Author

Van Ginkel, CE, Hohls, BC, and Vermaak, E

Abstract

During the late winter to early spring of 1999 Ceratium hirundinella was recorded for the first time in the Hartbeespoort Dam, South Africa, and in bloom forming conditions. The C. hirundinella bloom started in July 1999 after complete mixing occurred and a Microcystis aeruginosa bloom disappeared. C. hirundinella occurred in chlorophyll a concentrations up to 4243 mg/l. The clogging of filters at water care works and a fish kill were encountered during the same period, in the area. This paper discusses the extent of the bloom, the possible causes and the water characteristics found in the Hartbeespoort Dam during the development of the bloom. WaterSA Vol.27(2) 2001: 269-276

Published
2004

4. Towards the assessment of the trophic status of South African impoundments for management purposes: Bon Accord Dam

Author

van Ginkel, CE, Hohls, BC, and Vermaak, E

Abstract

The 1mg/l phosphate effluent standard legislated in South Africa in 1980 in seven sensitive catchments, and ad hoc eutrophication-related requests, necessitated the monitoring of 53 impoundments throughout the country. Variables that were monitored, and are still being monitored in some cases, included nutrients, chlorophyll a, algal identification, suspended solids and other major inorganic constituents. The measurement of temperature and oxygen profiles was conducted on an ad hoc basis when the sites were visited. The results, as determined from data collected between 1989 and 1998, indicated a range of trophic states from oligotrophic to hyper-eutrophic in the sensitive catchments. The catchments that were covered in the survey are: the Vaal River, Crocodile River (North West Province), Pienaars River, Olifants River (Mpumalanga Province), Letaba River, Buffalo River, Berg River, White Mfolozi River, Mgeni River, Mlazi River and the Molopo River catchments. The objective of this paper is to discuss the methods, variables and presentation for determining the trophic status of an impoundment for management purposes by using findings in the Bon Accord Dam, a small reservoir near Pretoria. The trophic status of selected impoundments was determined by using the mean total phosphorus (TP) concentrations, the nitrogen to phosphorus ratio, the mean chlorophyll a concentration, the presence of cyanobacteria and the turbidity (measured by means of Secchi disc readings) of the system. The mean annual phosphorus concentrations dropped from more than 800µg/l to less than 100µg/l in three years, and have remained at that level since 1987. The authors suggest that further reductions in phosphorus input are necessary to prevent eutrophication in the reservoir. Keywords: eutrophication; trophic status; phosphorus; nitrogen; phytoplankton; cyanobacteria; Bon Accord Dam; South Africa (Afr J Aqua Sci: 2000 25: 211-218)

Published
2000

6. Muscle disorders * 111. The impact of fatigue in patients with idiopathic inflammatory myopathy: a mixed method study

Author

Campbell, R., primary, Hofmann, D., additional, Hatch, S., additional, Gordon, P., additional, Lempp, H., additional, Das, L., additional, Blumbergs, P., additional, Limaye, V., additional, Vermaak, E., additional, McHugh, N., additional, Edwards, M. H., additional, Jameson, K., additional, Sayer, A. A., additional, Dennison, E., additional, Cooper, C., additional, Salvador, F. B., additional, Huertas, C., additional, Isenberg, D., additional, Jackson, E. J., additional, Middleton, A., additional, Churchill, D., additional, Walker-Bone, K., additional, Worsley, P. R., additional, Mottram, S., additional, Warner, M., additional, Morrissey, D., additional, Gadola, S., additional, Carr, A., additional, Stokes, M., additional, Srivastava, R. N., additional, Sanghi, D., additional, Elbaz, A., additional, Mor, A., additional, Segal, G., additional, Drexler, M., additional, Norman, D., additional, Peled, E., additional, Rozen, N., additional, Goryachev, Y., additional, Debbi, E. M., additional, Haim, A., additional, Wolf, A., additional, Debi, R., additional, Cohen, M. S., additional, Igolnikov, I., additional, Bar Ziv, Y., additional, Benkovich, V., additional, Bernfeld, B., additional, Collins, J., additional, Moots, R. J., additional, Clegg, P. D., additional, Milner, P. I., additional, Ejtehadi, H. D., additional, Nelson, P. N., additional, Wenham, C., additional, Balamoody, S., additional, Hodgson, R., additional, Conaghan, P., additional, Wilkie, R., additional, Blagojevic, M., additional, Jordan, K. P., additional, Mcbeth, J., additional, Peffers, M. J., additional, Beynon, R. J., additional, Thornton, D. J., additional, Chapman, R., additional, Chapman, V., additional, Walsh, D., additional, Kelly, S., additional, Hui, M., additional, Zhang, W., additional, Doherty, S., additional, Rees, F., additional, Muir, K., additional, Maciewicz, R., additional, Doherty, M., additional, Snelling, S., additional, Davidson, R. K., additional, Swingler, T., additional, Price, A., additional, Clark, I., additional, Stockley, E., additional, Hathway, G., additional, Faas, H., additional, Auer, D., additional, Hirsch, G., additional, Hale, E., additional, Kitas, G., additional, Klocke, R., additional, Abraham, A., additional, Pearce, M. S., additional, Mann, K. D., additional, Francis, R. M., additional, Birrell, F., additional, Tucker, M., additional, Mellon, S. J., additional, Jones, L., additional, Price, A. J., additional, Dieppe, P. A., additional, Gill, H. S., additional, Ashraf, S., additional, Walsh, D. A., additional, McCollum, D., additional, McCabe, C., additional, Grieve, S., additional, Shipley, J., additional, Gorodkin, R., additional, Oldroyd, A. G., additional, Evans, B., additional, Greenbank, C., additional, Bukhari, M., additional, Rajak, R., additional, Bennett, C., additional, Williams, A., additional, Martin, J. C., additional, Abdulkader, R., additional, MacNicol, C., additional, Brixey, K., additional, Stephenson, S., additional, Clunie, G., additional, Andrews, R. N., additional, Clark, E. M., additional, Gould, V. C., additional, Carter, L., additional, Morrison, L., additional, Tobias, J. H., additional, Pye, S. R., additional, Vanderschueren, D., additional, O'Neill, T. W., additional, Lee, D. M., additional, Jans, I., additional, Billen, J., additional, Gielen, E., additional, Laurent, M., additional, Claessens, F., additional, Adams, J. E., additional, Ward, K. A., additional, Bartfai, G., additional, Casanueva, F., additional, Finn, J. D., additional, Forti, G., additional, Giwercman, A., additional, Han, T. S., additional, Huhtaniemi, I., additional, Kula, K., additional, Lean, M. E., additional, Pendleton, N., additional, Punab, M., additional, Wu, F. C., additional, Boonen, S., additional, Mercieca, C., additional, Webb, J., additional, Bhalla, A., additional, Fairbanks, S., additional, Moss, K. E., additional, Collins, C., additional, Sedgwick, P., additional, Parker, J., additional, Harvey, N. C., additional, Cole, Z. A., additional, Crozier, S. R., additional, Ntani, G., additional, Mahon, P. A., additional, Robinson, S. M., additional, Inskip, H. M., additional, Godfrey, K. M., additional, Dennison, E. M., additional, Bridges, M., additional, Ruddick, S., additional, Holroyd, C. R., additional, Mahon, P., additional, Godfrey, K., additional, McNeilly, T., additional, McNally, C., additional, Beringer, T., additional, Finch, M., additional, Coda, A., additional, Davidson, J., additional, Walsh, J., additional, Fowlie, P., additional, Carline, T., additional, Santos, D., additional, Patil, P., additional, Rawcliffe, C., additional, Olaleye, A., additional, Moore, S., additional, Fox, A., additional, Sen, D., additional, Ioannou, Y., additional, Nisar, S., additional, Rankin, K., additional, Birch, M., additional, Finnegan, S., additional, Rooney, M., additional, Gibson, D. S., additional, Malviya, A., additional, Ferris, C. M., additional, Rushton, S. P., additional, Foster, H. E., additional, Hanson, H., additional, Muthumayandi, K., additional, Deehan, D. J., additional, Birt, L., additional, Poland, F., additional, MacGregor, A., additional, Armon, K., additional, Pfeil, M., additional, McErlane, F., additional, Beresford, M. W., additional, Baildam, E. M., additional, Thomson, W., additional, Hyrich, K., additional, Chieng, A., additional, Gardner-Medwin, J., additional, Lunt, M., additional, Wedderburn, L., additional, Newell, K., additional, Evans, A., additional, Manning, G., additional, Scaife, C., additional, McAllister, C., additional, Pennington, S. R., additional, Duncan, M., additional, Moore, T., additional, Pericleous, C., additional, Croca, S. C., additional, Giles, I., additional, Alber, K., additional, Yong, H., additional, Midgely, A., additional, Rahman, A., additional, Rzewuska, M., additional, Mallen, C., additional, Strauss, V. Y., additional, Belcher, J., additional, Peat, G., additional, Byng-Maddick, R., additional, Wijendra, M., additional, Penn, H., additional, Roddy, E., additional, Muller, S., additional, Hayward, R., additional, Kamlow, F., additional, Pakozdi, A., additional, Jawad, A., additional, Green, D. J., additional, Hider, S. L., additional, Singh Bawa, S., additional, Bawa, S., additional, Turton, A., additional, Palmer, M., additional, Lewis, J., additional, Moss, T., additional, Goodchild, C. E., additional, Tang, N., additional, Scott, D., additional, Salkovskis, P., additional, Selvan, S., additional, Williamson, L., additional, Thalayasingam, N., additional, Higgins, M., additional, Saravanan, V., additional, Rynne, M., additional, Hamilton, J. D., additional, Heycock, C., additional, Kelly, C., additional, Norton, S., additional, Sacker, A., additional, Done, J., additional, Young, A., additional, Smolen, J. S., additional, Fleischmann, R. M., additional, Emery, P., additional, van Vollenhoven, R. F., additional, Guerette, B., additional, Santra, S., additional, Kupper, H., additional, Redden, L., additional, Kavanaugh, A., additional, Keystone, E. C., additional, van der Heijde, D., additional, Weinblatt, M. E., additional, Mozaffarian, N., additional, Liu, S., additional, Zhang, N., additional, Wilkinson, S., additional, Riaz, M., additional, Ostor, A. J., additional, Nisar, M. K., additional, Burmester, G., additional, Mariette, X., additional, Navarro-Blasco, F., additional, Oezer, U., additional, Kary, S., additional, Unnebrink, K., additional, Jobanputra, P., additional, Maggs, F., additional, Deeming, A., additional, Carruthers, D., additional, Rankin, E., additional, Jordan, A., additional, Faizal, A., additional, Goddard, C., additional, Pugh, M., additional, Bowman, S., additional, Brailsford, S., additional, Nightingale, P., additional, Tugnet, N., additional, Cooper, S. C., additional, Douglas, K. M., additional, Edwin Lim, C. S., additional, Bee Lian Low, S., additional, Joy, C., additional, Hill, L., additional, Davies, P., additional, Mukherjee, S., additional, Cornell, P., additional, Westlake, S. L., additional, Richards, S., additional, Rahmeh, F., additional, Thompson, P. W., additional, Breedveld, F., additional, Keystone, E., additional, Landewe, R., additional, McIlraith, M., additional, Dharmapalaiah, C., additional, Shand, L., additional, Rose, G., additional, Watts, R., additional, Eldashan, A., additional, Dasgupta, B., additional, Borg, F. A., additional, Bell, G. M., additional, Anderson, A. E., additional, Harry, R. A., additional, Stoop, J. N., additional, Hilkens, C. M., additional, Isaacs, J., additional, Dickinson, A., additional, McColl, E., additional, Banik, S., additional, Smith, L., additional, France, J., additional, Rutherford, A., additional, Scott Russell, A., additional, Smith, J., additional, Jassim, I., additional, Withrington, R., additional, Bacon, P., additional, De Lord, D., additional, McGregor, L., additional, Morrison, I., additional, Stirling, A., additional, Porter, D. R., additional, Saunders, S. A., additional, Else, S., additional, Semenova, O., additional, Thompson, H., additional, Ogunbambi, O., additional, Kallankara, S., additional, Baguley, E., additional, Patel, Y., additional, Alzabin, S., additional, Abraham, S., additional, Taher, T. E., additional, Palfeeman, A., additional, Hull, D., additional, McNamee, K., additional, Pathan, E., additional, Kinderlerer, A., additional, Taylor, P., additional, Williams, R. O., additional, Mageed, R. A., additional, Iaremenko, O., additional, Mikitenko, G., additional, Ferrari, M., additional, Kamalati, T., additional, Pitzalis, C., additional, Pearce, F., additional, Tosounidou, S., additional, Obrenovic, K., additional, Erb, N., additional, Packham, J., additional, Sandhu, R., additional, White, C., additional, Cardy, C. M., additional, Justice, E., additional, Frank, M., additional, Li, L., additional, Lloyd, M., additional, Ahmed, A., additional, Readhead, S., additional, Ala, A., additional, Fittall, M., additional, Manson, J., additional, Sibilia, J., additional, Marc Flipo, R., additional, Combe, B., additional, Gaillez, C., additional, Le Bars, M., additional, Poncet, C., additional, Elegbe, A., additional, Westhovens, R., additional, Hassanzadeh, R., additional, Mangan, C., additional, Fleischmann, R., additional, van Vollenhoven, R., additional, Huizinga, T. W. J., additional, Goldermann, R., additional, Duncan, B., additional, Timoshanko, J., additional, Luijtens, K., additional, Davies, O., additional, Dougados, M., additional, Hewitt, J., additional, Owlia, M., additional, Schiff, M., additional, Alten, R., additional, Kaine, J. L., additional, Nash, P. T., additional, Delaet, I., additional, Qi, K., additional, Genovese, M. C., additional, Clark, J., additional, Kardash, S., additional, Wong, E., additional, Hull, R., additional, McCrae, F., additional, Shaban, R., additional, Thomas, L., additional, Young-Min, S., additional, Ledingham, J., additional, Covarrubias Cobos, A., additional, Leon, G., additional, Mysler, E. F., additional, Keiserman, M. W., additional, Valente, R. M., additional, Abraham Simon Campos, J., additional, Porawska, W., additional, Box, J. H., additional, Legerton, C. W., additional, Nasonov, E. L., additional, Durez, P., additional, Pappu, R., additional, Teng, J., additional, Edwards, C. J., additional, Arden, N., additional, Campbell, J., additional, van Staa, T., additional, Housden, C., additional, Sargeant, I., additional, Choy, E., additional, McAuliffe, S., additional, Roberts, K., additional, Sarzi-Puttini, P., additional, Andrianakos, A., additional, Sheeran, T. P., additional, Choquette, D., additional, Finckh, A., additional, Desjuzeur, M.-L., additional, Gemmen, E. 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I., additional, Stafford, C., additional, Carolan, M., additional, and Ramakrishnan, S. A., additional

Published
2012
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9. The Culicoides sonorensis inhibitor of apoptosis 1 protein protects mammalian cells from apoptosis induced by infection with African horse sickness virus and bluetongue virus.

Author

Vermaak E, Maree FF, and Theron J

Subjects
African Horse Sickness Virus genetics, African Horse Sickness Virus growth & development, Animals, Apoptosis genetics, Bluetongue virus genetics, Bluetongue virus growth & development, Caspase 9 genetics, Caspase 9 metabolism, Cell Line, Ceratopogonidae metabolism, Ceratopogonidae virology, Gene Expression Regulation, Inhibitor of Apoptosis Proteins antagonists & inhibitors, Inhibitor of Apoptosis Proteins metabolism, Insect Proteins antagonists & inhibitors, Insect Proteins metabolism, Insect Vectors metabolism, Insect Vectors virology, Protein Domains, RNA, Small Interfering genetics, RNA, Small Interfering metabolism, Sheep, Signal Transduction, Ceratopogonidae genetics, Host-Pathogen Interactions, Inhibitor of Apoptosis Proteins genetics, Insect Proteins genetics, Insect Vectors genetics
Abstract

African horse sickness virus (AHSV) and bluetongue virus (BTV) are arboviruses of the genus Orbivirus that are transmitted to their vertebrate hosts by Culicoides biting midges. These orbiviruses exhibit lytic infection (apoptosis) in mammalian cells, but cause persistent infection with no cytopathic effects in Culicoides sonorensis cells. Although regulation of apoptosis could thus be integral for establishing persistent virus infection in midge cells, nothing is known about the presence and function of apoptosis pathways in Culicoides midges and their derived cell lines. Here, we report the cloning and functional characterization of an inhibitor of apoptosis protein (IAP), designated CsIAP1, from C. sonorensis cells. The CsIAP1 protein contains two baculoviral IAP repeat (BIR) domains and a RING domain. Silencing of the Cs iap1 gene in C. sonorensis cells caused apoptosis, indicating that CsIAP1 plays a role in cell survival. Stable expression of the CsIAP1 protein in BSR mammalian cells suppressed apoptosis induced by AHSV-4 and BTV-10 infection, and biochemical data indicated that CsIAP1 is an inhibitor of mammalian caspase-9, an initiator caspase in the intrinsic apoptotic pathway. Mutagenesis studies indicated that the BIR2 and RING domains are required for the anti-apoptotic activity of CsIAP1. The results suggest that the mechanism by which CsIAP1 suppresses apoptosis in insect cells may involve inhibition of a Culicoides caspase-9 homologue through a mechanism that requires both the BIR2 and RING domains. This study provides the first evidence that the CsIAP1 protein is a key negative regulator of apoptosis in C. sonorensis cells., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Published
2017
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10. Lack of diversity at innate immunity Toll-like receptor genes in the Critically Endangered White-winged Flufftail (Sarothrura ayresi).

Author

Dalton DL, Vermaak E, Smit-Robinson HA, and Kotze A

Subjects
Animals, Avian Proteins genetics, Avian Proteins immunology, Birds genetics, Birds immunology, Endangered Species, Genetic Variation, Immunity, Innate genetics, Toll-Like Receptors genetics, Toll-Like Receptors immunology
Abstract

The White-winged Flufftail (Sarothrura ayresi) population is listed as globally Critically Endangered. White-winged Flufftails are only known to occur, with any regularity, in the high-altitude wetlands of South Africa and Ethiopia. Threats to the species include the limited number of suitable breeding sites in Ethiopia and severe habitat degradation and loss both in Ethiopia and South Africa. Toll-like receptors (TLRs) are increasingly being studied in a variety of taxa as a broader approach to determine functional genetic diversity. In this study, we confirm low genetic diversity in the innate immune regions of the White-winged Flufftail similar to that observed in other bird species that have undergone population bottlenecks. Low TLR diversity in White-winged Flufftail indicates that this species is more likely to be threatened by changes to the environment that would potentially expose the species to new diseases. Thus, conservation efforts should be directed towards maintaining pristine habitat for White-winged Flufftail in its current distribution range. To date, no studies on immunogenetic variation in White-winged Flufftail have been conducted and to our knowledge, this is the first study of TLR genetic diversity in a critically endangered species.

Published
2016
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11. Diversity in the Toll-Like Receptor Genes of the African Penguin (Spheniscus demersus).

Author

Dalton DL, Vermaak E, Roelofse M, and Kotze A

Subjects
Animals, Genetic Loci genetics, Immunity, Innate, Phylogeny, Polymorphism, Single Nucleotide, Spheniscidae immunology, Genetic Variation, Spheniscidae genetics, Toll-Like Receptors genetics
Abstract

The African penguin, Spheniscus demersus, is listed as Endangered by the IUCN Red List of Threatened Species due to the drastic reduction in population numbers over the last 20 years. To date, the only studies on immunogenetic variation in penguins have been conducted on the major histocompatibility complex (MHC) genes. It was shown in humans that up to half of the genetic variability in immune responses to pathogens are located in non-MHC genes. Toll-like receptors (TLRs) are now increasingly being studied in a variety of taxa as a broader approach to determine functional genetic diversity. In this study, we confirm low genetic diversity in the innate immune region of African penguins similar to that observed in New Zealand robin that has undergone several severe population bottlenecks. Single nucleotide polymorphism (SNP) diversity across TLRs varied between ex situ and in situ penguins with the number of non-synonymous alterations in ex situ populations (n = 14) being reduced in comparison to in situ populations (n = 16). Maintaining adaptive diversity is of vital importance in the assurance populations as these animals may potentially be used in the future for re-introductions. Therefore, this study provides essential data on immune gene diversity in penguins and will assist in providing an additional monitoring tool for African penguin in the wild, as well as to monitor diversity in ex situ populations and to ensure that diversity found in the in situ populations are captured in the assurance populations., Competing Interests: The authors have declared that no competing interests exist.

Published
2016
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12. Pangolin genomes and the evolution of mammalian scales and immunity.

Author

Choo SW, Rayko M, Tan TK, Hari R, Komissarov A, Wee WY, Yurchenko AA, Kliver S, Tamazian G, Antunes A, Wilson RK, Warren WC, Koepfli KP, Minx P, Krasheninnikova K, Kotze A, Dalton DL, Vermaak E, Paterson IC, Dobrynin P, Sitam FT, Rovie-Ryan JJ, Johnson WE, Yusoff AM, Luo SJ, Karuppannan KV, Fang G, Zheng D, Gerstein MB, Lipovich L, O'Brien SJ, and Wong GJ

Subjects
Adaptation, Physiological, Animals, Endangered Species, Interferons genetics, Mammals anatomy & histology, Mammals classification, Mammals immunology, Receptors, Odorant genetics, Animal Scales anatomy & histology, Evolution, Molecular, Genome, Immunity, Innate genetics, Mammals genetics
Abstract

Pangolins, unique mammals with scales over most of their body, no teeth, poor vision, and an acute olfactory system, comprise the only placental order (Pholidota) without a whole-genome map. To investigate pangolin biology and evolution, we developed genome assemblies of the Malayan (Manis javanica) and Chinese (M. pentadactyla) pangolins. Strikingly, we found that interferon epsilon (IFNE), exclusively expressed in epithelial cells and important in skin and mucosal immunity, is pseudogenized in all African and Asian pangolin species that we examined, perhaps impacting resistance to infection. We propose that scale development was an innovation that provided protection against injuries or stress and reduced pangolin vulnerability to infection. Further evidence of specialized adaptations was evident from positively selected genes involving immunity-related pathways, inflammation, energy storage and metabolism, muscular and nervous systems, and scale/hair development. Olfactory receptor gene families are significantly expanded in pangolins, reflecting their well-developed olfaction system. This study provides insights into mammalian adaptation and functional diversification, new research tools and questions, and perhaps a new natural IFNE-deficient animal model for studying mammalian immunity., (© 2016 Choo et al.; Published by Cold Spring Harbor Laboratory Press.)

Published
2016
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13. African horse sickness virus infects BSR cells through macropinocytosis.

Author

Vermaak E, Conradie AM, Maree FF, and Theron J

Subjects
Actins metabolism, African Horse Sickness Virus ultrastructure, Animals, Cell Line, Cholesterol, Cricetinae, Dynamins metabolism, Endosomes metabolism, Endosomes virology, Hydrogen-Ion Concentration, African Horse Sickness virology, African Horse Sickness Virus physiology, Endocytosis, Virus Internalization
Abstract

Cellular pathways involved in cell entry by African horse sickness virus (AHSV), a member of the Orbivirus genus within the Reoviridae family, have not yet been determined. Here, we show that acidic pH is required for productive infection of BSR cells by AHSV-4, suggesting that the virus is likely internalized by an endocytic pathway. We subsequently analyzed the major endocytic routes using specific inhibitors and determined the consequences for AHSV-4 entry into BSR cells. The results indicated that virus entry is dynamin dependent, but clathrin- and lipid raft/caveolae-mediated endocytic pathways were not used by AHSV-4 to enter and infect BSR cells. Instead, binding of AHSV-4 to BSR cells stimulated uptake of a macropinocytosis-specific cargo and inhibition of Na(+)/H(+) exchangers, actin polymerization and cellular GTPases and kinases involved in macropinocytosis significantly inhibited AHSV-4 infection. Altogether, the data suggest that AHSV-4 infects BSR cells by utilizing macropinocytosis as the primary entry pathway., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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14. The evidence for immunotherapy in dermatomyositis and polymyositis: a systematic review.

Author

Vermaak E, Tansley SL, and McHugh NJ

Subjects
Azathioprine therapeutic use, Biological Products therapeutic use, Cyclosporine therapeutic use, Evidence-Based Medicine, Humans, Immunoglobulins, Intravenous therapeutic use, Methotrexate therapeutic use, Polymyositis therapy, Practice Guidelines as Topic, Rituximab therapeutic use, Treatment Outcome, Adrenal Cortex Hormones therapeutic use, Dermatomyositis therapy, Immunologic Factors therapeutic use, Immunosuppressive Agents therapeutic use, Leukapheresis, Plasmapheresis
Abstract

Dermatomyositis and polymyositis are rare chronic inflammatory disorders with significant associated morbidity and mortality despite treatment. High-dose corticosteroids in addition to other interventions such as immunosuppressants, immunomodulators, and more recently, biologics are commonly used in clinical practice; however, there are no clear guidelines directing their use. Our objective was to systematically review the evidence for immunotherapy in the treatment of dermatomyositis and polymyositis. Relevant studies were identified through Embase and PubMed database searches. Trials were selected using pre-determined selection criteria and then assessed for quality. Randomized controlled trials and experimental studies without true randomization and including adult patients with definite or probable dermatomyositis or polymyositis were evaluated. Any type of immunotherapy was considered. Clinical improvement, judged by assessment of muscle strength after 6 months, was the primary outcome. Secondary outcomes included IMACS definition of improvement, improvements in patient and physician global scores, physical function, and muscle enzymes. Twelve studies met eligibility criteria. Differences in trial design, quality, and variable reporting of baseline characteristics and outcomes made direct comparison impossible. Although no treatment can be recommended on the basis of this review, improved outcomes were demonstrated with a number of agents including methotrexate, azathioprine, ciclosporin, rituximab, and intravenous immunoglobulin. Plasmapheresis and leukapheresis were of no apparent benefit. More high-quality randomized controlled trials are needed to establish the role of immunosuppressive agents in the treatment of these conditions and the clinical context in which they are most likely to be beneficial.

Published
2015
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15. Virus uncoating is required for apoptosis induction in cultured mammalian cells infected with African horse sickness virus.

Author

Vermaak E and Theron J

Subjects
Animals, Capsid Proteins metabolism, Cell Line, Cricetinae, African Horse Sickness Virus physiology, Apoptosis, Host-Pathogen Interactions, Virus Uncoating
Abstract

Infection of cultured mammalian cells with African horse sickness virus (AHSV) is known to induce cell death. To date, the trigger(s) of this response, the apoptotic pathways activated during AHSV infection and the functional consequences of apoptosis on the virus replication cycle have yet to be characterized. This study demonstrated that extracellular treatment of BHK-21 cells with both of the AHSV4 outer capsid proteins, VP2 and VP5, was sufficient to trigger apoptosis. Whether steps in AHSV4 replication subsequent to viral attachment were required for AHSV4-induced apoptosis was also investigated. Apoptosis was induced in BHK-21 cells infected with UV-inactivated AHSV4 and in ribavirin-treated cells infected with AHSV4. However, both AHSV4- and VP2/VP5-stimulated apoptotic responses were inhibited in the presence of the endosomal acidification inhibitors ammonium chloride and chloroquine. These results indicated that uncoating of AHSV4 virions, but not viral transcription or subsequent steps in viral replication, was required for AHSV4 to induce apoptosis in BHK-21 cells. Furthermore, this study showed that both the extrinsic (caspase-8) and intrinsic (caspase-9) apoptotic pathways were induced following AHSV4 infection. The inhibition of caspase activity in AHSV4-infected cells did not diminish AHSV4 replication, but reduced the release and dissemination of progeny viral particles. Taken together, the data indicated that uncoating of AHSV virions was required for apoptosis induction, and that apoptosis enhanced virus spread and release.

Published
2015
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16. A surprise behind a case of winter vomiting virus.

Author

Panopoulou A, Vermaak E, and McHugh N

Subjects
Aged, Carcinoma, Bronchogenic diagnosis, Diagnosis, Differential, Granulomatosis with Polyangiitis complications, Granulomatosis with Polyangiitis diagnostic imaging, Granulomatosis with Polyangiitis pathology, Humans, Lung diagnostic imaging, Lung pathology, Lung Neoplasms diagnosis, Male, Radiography, Vomiting etiology, Caliciviridae Infections complications, Gastroenteritis complications, Granulomatosis with Polyangiitis diagnosis, Incidental Findings, Norovirus, Vomiting complications
Abstract

A 79-year-old man was admitted through the medical take with norovirus gastritis. Routine plain chest radiography demonstrated a right coin lesion. CT and subsequent positron emission tomography showed a right upper lobe mass consistent with primary bronchial carcinoma. The lesion was resected and histology revealed a granulomatous necrotising mass without evidence of dysplasia. Meticulous investigations for infectious and non-infectious causes of necrotising granulomatous diseases were repeatedly negative. His postoperative recovery was complicated by a hospital-acquired pneumonia and a pulmonary embolism. CT pulmonary angiography showed progression of the previously resected mass and repeat biopsy was similar to the initial. A clinical diagnosis of antineutrophil cytoplasmic antibody-negative vasculitis without extrapulmonary manifestations was made and immunosuppressive therapy was initiated with rapid clinical response.

Published
2013
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