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210 results on '"Almeida, Deepak"'

1. The Many Hosts of Mycobacteria 9 (MHM9): A conference report

Author

Klever, Abigail Marie, Alexander, Kathleen A., Almeida, Deepak, Anderson, Matthew Z., Ball, Ray L., Beamer, Gillian, Boggiatto, Paola, Buikstra, Jane E., Chandler, Bruce, Claeys, Tiffany A., Concha, Aislinn E., Converse, Paul J., Derbyshire, Keith M., Dobos, Karen M., Dupnik, Kathryn M., Endsley, Janice J., Endsley, Mark A., Fennelly, Kevin, Franco-Paredes, Carlos, Hagge, Deanna A., Hall-Stoodley, Luanne, Hayes, Don, Jr., Hirschfeld, Katherine, Hofman, Courtney A., Honda, Jennifer R., Hull, Natalie M., Kramnik, Igor, Lacourciere, Karen, Lahiri, Ramanuj, Lamont, Elise A., Larsen, Michelle H., Lemaire, Timothy, Lesellier, Sandrine, Lee, Naomi R., Lowry, Christopher A., Mahfooz, Najmus S., McMichael, Temet M., Merling, Marlena R., Miller, Michele A., Nagajyothi, Jyothi F., Nelson, Elizabeth, Nuermberger, Eric L., Pena, Maria T., Perea, Claudia, Podell, Brendan K., Pyle, Charlie J., Quinn, Fred D., Rajaram, Murugesan V.S., Mejia, Oscar Rosas, Rothoff, Michelle, Sago, Saydie A., Salvador, Liliana C.M., Simonson, Andrew W., Spencer, John S., Sreevatsan, Srinand, Subbian, Selvakumar, Sunstrum, James, Tobin, David M., Vijayan, K.K.Vidya, Wright, Caelan T.O., and Robinson, Richard T.

Published
2023
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7. Identification of 2-Aryl-Quinolone Inhibitors of Cytochrome bd and Chemical Validation of Combination Strategies for Respiratory Inhibitors against Mycobacterium tuberculosis

Author

Jeffreys, Laura N., primary, Ardrey, Alison, additional, Hafiz, Taghreed A., additional, Dyer, Lauri-Anne, additional, Warman, Ashley J., additional, Mosallam, Nada, additional, Nixon, Gemma L., additional, Fisher, Nicholas E., additional, Hong, W. David, additional, Leung, Suet C., additional, Aljayyoussi, Ghaith, additional, Bibby, Jaclyn, additional, Almeida, Deepak V., additional, Converse, Paul J., additional, Fotouhi, Nader, additional, Berry, Neil G., additional, Nuermberger, Eric L., additional, Upton, Anna M., additional, O’Neill, Paul M., additional, Ward, Stephen A., additional, and Biagini, Giancarlo A., additional

Published
2023
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15. ANTIBIOTICS: Targeting DnaN for tuberculosis therapy using novel griselimycins

Author

Kling, Angela, Lukat, Peer, Almeida, Deepak V., Bauer, Armin, Fontaine, Evelyne, Sordello, Sylvie, Zaburannyi, Nestor, Herrmann, Jennifer, Wenzel, Silke C., König, Claudia, Ammerman, Nicole C., Barrio, María Belén, Borchers, Kai, Bordon-Pallier, Florence, Brönstrup, Mark, Courtemanche, Gilles, Gerlitz, Martin, Geslin, Michel, Hammann, Peter, Heinz, Dirk W., Hoffinann, Holger, Klieber, Sylvie, Kohknann, Markus, Kurz, Michael, Lair, Christine, Matter, Hans, Nuermberger, Eric, Tyagi, Sandeep, Fraisse, Laurent, Grosset, Jacques H., Lagrange, Sophie, and Müller, Rolf

Published
2015

18. Quantitative analysis of the phase transition mechanism underpinning the systemic self-assembly of a mechanopharmaceutical device

Author

Dunne, Steven, Willmer, Andrew R., Swanson, Rosemary, Almeida, Deepak, Ammerman, Nicole C., Stringer, Kathleen A., Capparelli, Edmund V., Rosania, Gus R., Dunne, Steven, Willmer, Andrew R., Swanson, Rosemary, Almeida, Deepak, Ammerman, Nicole C., Stringer, Kathleen A., Capparelli, Edmund V., and Rosania, Gus R.

Abstract

Clofazimine (CFZ) is a poorly soluble, weakly basic, small molecule antibiotic clinically used to treat leprosy and is now in clinical trials as a treatment for multidrug resistant tuberculosis and COVID-19. CFZ exhibits complex, context-dependent pharmacokinetics that are characterized by an increasing half-life in long term treatment regimens. The systemic pharmacokinetics of CFZ have been previously represented by a nonlinear, 2-compartment model incorporating an expanding volume of distribution. This expansion reflects the soluble-to-insoluble phase transition that the drug undergoes as it precipitates out and accumulates within macrophages disseminated throughout the organism. Using mice as a model organism, we studied the mechanistic underpinnings of this increasing half-life and how the systemic pharmacokinetics of CFZ are altered with continued dosing. To this end, M. tuberculosis infection status and multiple dosing schemes were studied alongside a parameter sensitivity analysis (PSA) to further understanding of systemic drug distribution. Parameter values governing the sigmoidal expansion function that captures the phase transition were methodically varied, and in turn, the systemic concentrations of the drug were calculated and compared to the experimentally measured concentrations of drug in serum and spleen. The resulting amounts of drug sequestered were dependent on the total mass of CFZ administered and the duration of drug loading. This phenomenon can be captured by altering three different parameters of an expansion function corresponding to key biological determinants responsible for the precipitation and the accumulation of the insoluble drug mass in macrophages. Through this analysis of the context dependent pharmacokinetics of CFZ, a predictive framework for projecting the systemic distribution and self-assembly of precipitated drug complexes as intracellular mechanopharmaceutical devices of this and other drugs exhibiting similarly complex p

Published
2021

19. An adaptive biosystems engineering approach towards modeling the soluble-to-insoluble phase transition of clofazimine

Author

Willmer, Andrew R., Dunne, Steven, Swanson, Rosemary, Almeida, Deepak, Ammerman, Nicole C., Stringer, Kathleen A., Capparelli, Edmund V., Rosania, Gus R., Willmer, Andrew R., Dunne, Steven, Swanson, Rosemary, Almeida, Deepak, Ammerman, Nicole C., Stringer, Kathleen A., Capparelli, Edmund V., and Rosania, Gus R.

Abstract

Clofazimine (CFZ) is a weakly basic, small-molecule antibiotic used for the treatment of mycobacterial infections including leprosy and multidrug-resistant tuberculosis. Upon prolonged oral administration, CFZ precipitates and accumulates within macrophages throughout the host. To model the pharmacokinetics of CFZ, the volume of distribution (Vd) was considered as a varying parameter that increases with continuous drug loading. Fitting the time-dependent change in drug mass and concentration data obtained from CFZ-treated mice, we performed a quantitative analysis of the systemic disposition of the drug over a 20-week treatment period. The pharmacokinetics data were fitted using various classical compartmental models sampling serum and spleen concentration data into separate matrices. The models were constructed in NONMEM together with linear and nonlinear sigmoidal expansion functions to the spleen compartment to capture the phase transition in Vd. The different modeling approaches were compared by Akaike information criteria, observed and predicted concentration correlations, and graphically. Using the composite analysis of the modeling predictions, adaptive fractional CFZ sequestration, Vd and half-life were evaluated. When compared to standard compartmental models, an adaptive Vd model yielded a more accurate data fit of the drug concentrations in both the serum and spleen. Including a nonlinear sigmoidal equation into compartmental models captures the phase transition of drugs such as CFZ, greatly improving the prediction of population pharmacokinetics and yielding further insight into the mechanisms of drug disposition.

Published
2021

20. High incidence of the Beijing genotype among multidrug-resistant isolates of Mycobacterium tuberculosis in a tertiary care center in Mumbai, India

Author

Almeida, Deepak, Rodrigues, Camilla, Ashavaid, Tester F., Lalvani, Ajit, Udwadia, Zarir F., and Mehta, Ajita

Subjects
India -- Health aspects, Mycobacterium tuberculosis -- Risk factors, Mycobacterium tuberculosis -- Development and progression, Mycobacterium tuberculosis -- Research, Genotype -- Research, Health, Health care industry
Published
2005

27. Predicting nitroimidazole antibiotic resistance mutations in Mycobacterium tuberculosis with protein engineering

Author

Lee, Brendon, primary, Almeida, Deepak, additional, Afriat-Jurnou, Livnat, additional, Aung, Htin, additional, Forde, Brian, additional, Harold, Liam, additional, Hards, Kiel, additional, Pidot, Sacha, additional, Ahmed, Hafna, additional, Mohamed, Elaaf, additional, Taylor, Mathew, additional, West, Nicholas, additional, Stinear, Timothy, additional, Greening, Chris, additional, Beatson, Scott, additional, Cook, Gregory, additional, Nuermberger, Eric, additional, and Jackson, Colin, additional

Published
2020
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29. Predicting nitroimidazole antibiotic resistance mutations in Mycobacterium tuberculosis with protein engineering

Author

Lee, Brendon M., primary, Harold, Liam K., additional, Almeida, Deepak V., additional, Afriat-Jurnou, Livnat, additional, Aung, Htin Lin, additional, Forde, Brian M., additional, Hards, Kiel, additional, Pidot, Sacha J., additional, Ahmed, F. Hafna, additional, Mohamed, A. Elaaf, additional, Taylor, Matthew C., additional, West, Nicholas P., additional, Stinear, Timothy P., additional, Greening, Chris, additional, Beatson, Scott A., additional, Nuermberger, Eric L., additional, Cook, Gregory M., additional, and Jackson, Colin J., additional

Published
2020
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31. Evolution of extensively drug-resistant tuberculosis over four decades: whole genome sequencing and dating analysis of Mycobacterium tuberculosis isolates from KwaZulu-Natal

Author

Cohen, Keira A., Abeel, Thomas, McGuire, Abigail Manson, Desjardins, Christopher A., Munsamy, Vanisha, Shea, Terrance P., Walker, Bruce J., Bantubani, Nonkqubela, Almeida, Deepak V., Alvarado, Lucia, Chapman, Sinead B., Mvelase, Nomonde R., Duffy, Eamon Y., Fitzgerald, Michael G., Govender, Pamla, Gujja, Sharvari, Hamilton, Susanna, Howarth, Clinton, Larimer, Jeffrey D., Maharaj, Kashmeel, Pearson, Matthew D., Priest, Margaret E., Zeng, Qiandong, Padayatchi, Nesri, Grosset, Jacques, Young, Sarah K., Wortman, Jennifer, Mlisana, Koleka P., O'Donnell, Max R., Birren, Bruce W., Bishai, William R., Pym, Alexander S., and Earl, Ashlee M.

Subjects
Nucleotide sequencing -- Methods -- Genetic aspects, Drug resistance in microorganisms -- Genetic aspects, DNA sequencing -- Methods -- Genetic aspects, Mycobacterium tuberculosis -- Genetic aspects -- Methods, Biological sciences
Abstract

Background The continued advance of antibiotic resistance threatens the treatment and control of many infectious diseases. This is exemplified by the largest global outbreak of extensively drug-resistant (XDR) tuberculosis (TB) identified in Tugela Ferry, KwaZulu-Natal, South Africa, in 2005 that continues today. It is unclear whether the emergence of XDR-TB in KwaZulu-Natal was due to recent inadequacies in TB control in conjunction with HIV or other factors. Understanding the origins of drug resistance in this fatal outbreak of XDR will inform the control and prevention of drug-resistant TB in other settings. In this study, we used whole genome sequencing and dating analysis to determine if XDR-TB had emerged recently or had ancient antecedents. Methods and Findings We performed whole genome sequencing and drug susceptibility testing on 337 clinical isolates of Mycobacterium tuberculosis collected in KwaZulu-Natal from 2008 to 2013, in addition to three historical isolates, collected from patients in the same province and including an isolate from the 2005 Tugela Ferry XDR outbreak, a multidrug-resistant (MDR) isolate from 1994, and a pansusceptible isolate from 1995. We utilized an array of whole genome comparative techniques to assess the relatedness among strains, to establish the order of acquisition of drug resistance mutations, including the timing of acquisitions leading to XDR-TB in the LAM4 spoligotype, and to calculate the number of independent evolutionary emergences of MDR and XDR. Our sequencing and analysis revealed a 50-member clone of XDR M. tuberculosis that was highly related to the Tugela Ferry XDR outbreak strain. We estimated that mutations conferring isoniazid and streptomycin resistance in this clone were acquired 50 y prior to the Tugela Ferry outbreak (katG S315T [isoniazid]; gidB 130 bp deletion [streptomycin]; 1957 [95% highest posterior density (HPD): 1937-1971]), with the subsequent emergence of MDR and XDR occurring 20 y (rpoB L452P [rifampicin]; pncA 1 bp insertion [pyrazinamide]; 1984 [95% HPD: 1974-1992]) and 10 y (rpoB D435G [rifampicin]; rrs 1400 [kanamycin]; gyrA A90V [ofloxacin]; 1995 [95% HPD: 1988-1999]) prior to the outbreak, respectively. We observed frequent de novo evolution of MDR and XDR, with 56 and nine independent evolutionary events, respectively. Isoniazid resistance evolved before rifampicin resistance 46 times, whereas rifampicin resistance evolved prior to isoniazid only twice. We identified additional putative compensatory mutations to rifampicin in this dataset. One major limitation of this study is that the conclusions with respect to ordering and timing of acquisition of mutations may not represent universal patterns of drug resistance emergence in other areas of the globe. Conclusions In the first whole genome-based analysis of the emergence of drug resistance among clinical isolates of M. tuberculosis, we show that the ancestral precursor of the LAM4 XDR outbreak strain in Tugela Ferry gained mutations to first-line drugs at the beginning of the antibiotic era. Subsequent accumulation of stepwise resistance mutations, occurring over decades and prior to the explosion of HIV in this region, yielded MDR and XDR, permitting the emergence of compensatory mutations. Our results suggest that drug-resistant strains circulating today reflect not only vulnerabilities of current TB control efforts but also those that date back 50 y. In drug-resistant TB, isoniazid resistance was overwhelmingly the initial resistance mutation to be acquired, which would not be detected by current rapid molecular diagnostics employed in South Africa that assess only rifampicin resistance., Introduction The global burden of tuberculosis (TB) remains high, with an estimated 9 million active disease cases and 1.5 million deaths in 2013 [1]. Multidrug-resistant (MDR) TB, defined as Mycobacterium [...]

Published
2015
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33. The evolution of nitroimidazole antibiotic resistance in Mycobacterium tuberculosis

Author

Lee, Brendon M., primary, Almeida, Deepak V., additional, Afriat-Jurnou, Livnat, additional, Aung, Htin Lin, additional, Forde, Brian M., additional, Hards, Kiel, additional, Pidot, Sacha J., additional, Ahmed, F. Hafna, additional, Mohamed, A. Elaaf, additional, Taylor, Matthew C., additional, West, Nicholas P., additional, Stinear, Timothy P., additional, Greening, Chris, additional, Beatson, Scott A., additional, Cook, Gregory M., additional, Nuermberger, Eric L., additional, and Jackson, Colin J., additional

Published
2019
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34. Contribution of Pretomanid to Novel Regimens Containing Bedaquiline with either Linezolid or Moxifloxacin and Pyrazinamide in Murine Models of Tuberculosis

Author

Xu, Jian, primary, Li, Si-Yang, additional, Almeida, Deepak V., additional, Tasneen, Rokeya, additional, Barnes-Boyle, Kala, additional, Converse, Paul J., additional, Upton, Anna M., additional, Mdluli, Khisimuzi, additional, Fotouhi, Nader, additional, and Nuermberger, Eric L., additional

Published
2019
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38. Shorter-course treatment for Mycobacterium ulcerans disease with high-dose rifamycins and clofazimine in a mouse model of Buruli ulcer

Author

Converse, Paul J., primary, Almeida, Deepak V., additional, Tasneen, Rokeya, additional, Saini, Vikram, additional, Tyagi, Sandeep, additional, Ammerman, Nicole C., additional, Li, Si-Yang, additional, Anders, Nicole M., additional, Rudek, Michelle A., additional, Grosset, Jacques H., additional, and Nuermberger, Eric L., additional

Published
2018
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39. Impact of Clofazimine Dosing on Treatment Shortening of the First-Line Regimen in a Mouse Model of Tuberculosis

Author

Ammerman, Nicole C., primary, Swanson, Rosemary V., additional, Bautista, Elaine M., additional, Almeida, Deepak V., additional, Saini, Vikram, additional, Omansen, Till F., additional, Guo, Haidan, additional, Chang, Yong Seok, additional, Li, Si-Yang, additional, Tapley, Asa, additional, Tasneen, Rokeya, additional, Tyagi, Sandeep, additional, Betoudji, Fabrice, additional, Moodley, Chivonne, additional, Ngcobo, Bongani, additional, Pillay, Logan, additional, Bester, Linda A., additional, Singh, Sanil D., additional, Chaisson, Richard E., additional, Nuermberger, Eric, additional, and Grosset, Jacques H., additional

Published
2018
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41. Activity of 5-chloro-pyrazinamide in mice infected with Mycobacterium tuberculosis or Mycobacterium bovis

Author

Ahmad, Zahoor, Tyagi, Sandeep, Minkowski, Austin, Almeida, Deepak, Nuermberger, Eric L., Peck, Kaitlin M., Welch, John T., Baughn, Anthony D., Jacobs, Williams R., and Grosset, Jacques H.

Subjects
Mice, Mice, Inbred BALB C, pyrazinamide, Experimental chemotherapy, tuberculosis, Antitubercular Agents, Animals, Original Article, Female, Microbial Sensitivity Tests, Mycobacterium tuberculosis, Mycobacterium bovis, mouse
Abstract

Background & objectives: Pyrazinamide is an essential component of first line anti-tuberculosis regimen as well as most of the second line regimens. This drug has a unique sterilizing activity against Mycobacterium tuberculosis. Its unique role in tuberculosis treatment has lead to the search and development of its structural analogues. One such analogue is 5-chloro-pyrazinamide (5-Cl-PZA) that has been tested under in vitro conditions against M. tuberculosis. The present study was designed with an aim to assess the activity of 5-Cl-PZA, alone and in combination with first-line drugs, against murine tuberculosis. Methods: The minimum inhibitory concentration (MIC) of 5-Cl-PZA in Middlebrook 7H9 broth (neutral pH) and the inhibitory titre of serum from mice that received a 300 mg/kg oral dose of 5-Cl-PZA 30 min before cardiac puncture were determined. To test the tolerability of orally administered 5-Cl-PZA, uninfected mice received doses up to 300 mg/kg for 2 wk. Four weeks after low-dose aerosol infection either with M. tuberculosis or M. bovis, mice were treated 5 days/wk with 5-Cl-PZA, at doses ranging from 37.5 to 150 mg/kg, either alone or in combination with isoniazid and rifampicin. Antimicrobial activity was assessed by colony-forming unit counts in lungs after 4 and 8 wk of treatment. Results: The MIC of 5-Cl-PZA against M. tuberculosis was between 12.5 and 25 μg/ml and the serum inhibitory titre was 1:4. Under the same experimental conditions, the MIC of pyrazinamide was >100 μg/ml and mouse serum had no inhibitory activity after a 300 mg/kg dose; 5-Cl-PZA was well tolerated in uninfected and infected mice up to 300 and 150 mg/kg, respectively. While PZA alone and in combination exhibited its usual antimicrobial activity in mice infected with M. tuberculosis and no activity in mice infected with M. bovis, 5-Cl-PZA exhibited antimicrobial activity neither in mice infected with M. tuberculosis nor in mice infected with M. bovis. Interpretation & conclusion: Our findings showed that 5-Cl-PZA at doses up to 150 mg/kg was not active in chronic murine TB model. Further studies need to be done to understand the mechanism and mode of inactivation in murine model of tuberculosis.

Published
2012

42. Clofazimine has delayed antimicrobial activity againstMycobacterium tuberculosisbothin vitroandin vivo

Author

Ammerman, Nicole C., primary, Swanson, Rosemary V., additional, Tapley, Asa, additional, Moodley, Chivonne, additional, Ngcobo, Bongani, additional, Adamson, John, additional, Dorasamy, Afton, additional, Moodley, Sashen, additional, Mgaga, Zinhle, additional, Bester, Linda A., additional, Singh, Sanil D., additional, Almeida, Deepak V., additional, and Grosset, Jacques H., additional

Published
2016
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44. Clofazimine Contributes Sustained Antimicrobial Activity after Treatment Cessation in a Mouse Model of Tuberculosis Chemotherapy

Author

Swanson, Rosemary V., primary, Ammerman, Nicole C., additional, Ngcobo, Bongani, additional, Adamson, John, additional, Moodley, Chivonne, additional, Dorasamy, Afton, additional, Moodley, Sashen, additional, Mgaga, Zinhle, additional, Bester, Linda A., additional, Singh, Sanil D., additional, Almeida, Deepak V., additional, and Grosset, Jacques H., additional

Published
2016
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45. Direct Susceptibility Testing of Mycobacterium tuberculosis for Pyrazinamide by Use of the Bactec MGIT 960 System

Author

Demers, Anne-Marie, primary, Venter, Amour, additional, Friedrich, Sven O., additional, Rojas-Ponce, Gabriel, additional, Mapamba, Daniel, additional, Jugheli, Levan, additional, Sasamalo, Mohammed, additional, Almeida, Deepak, additional, Dorasamy, Afton, additional, Jentsch, Ute, additional, Gibson, Mara, additional, Everitt, Daniel, additional, Eisenach, Kathleen D., additional, and Diacon, Andreas H., additional

Published
2016
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46. Genomic and functional analyses of Mycobacterium tuberculosis strains implicate ald in D-cycloserine resistance

Author

Desjardins, Christopher A, primary, Cohen, Keira A, additional, Munsamy, Vanisha, additional, Abeel, Thomas, additional, Maharaj, Kashmeel, additional, Walker, Bruce J, additional, Shea, Terrance P, additional, Almeida, Deepak V, additional, Manson, Abigail L, additional, Salazar, Alex, additional, Padayatchi, Nesri, additional, O'Donnell, Max R, additional, Mlisana, Koleka P, additional, Wortman, Jennifer, additional, Birren, Bruce W, additional, Grosset, Jacques, additional, Earl, Ashlee M, additional, and Pym, Alexander S, additional

Published
2016
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47. Targeting DnaN for tuberculosis therapy using novel griselimycins

Author

Kling, Angela, primary, Lukat, Peer, additional, Almeida, Deepak V., additional, Bauer, Armin, additional, Fontaine, Evelyne, additional, Sordello, Sylvie, additional, Zaburannyi, Nestor, additional, Herrmann, Jennifer, additional, Wenzel, Silke C., additional, König, Claudia, additional, Ammerman, Nicole C., additional, Barrio, María Belén, additional, Borchers, Kai, additional, Bordon-Pallier, Florence, additional, Brönstrup, Mark, additional, Courtemanche, Gilles, additional, Gerlitz, Martin, additional, Geslin, Michel, additional, Hammann, Peter, additional, Heinz, Dirk W., additional, Hoffmann, Holger, additional, Klieber, Sylvie, additional, Kohlmann, Markus, additional, Kurz, Michael, additional, Lair, Christine, additional, Matter, Hans, additional, Nuermberger, Eric, additional, Tyagi, Sandeep, additional, Fraisse, Laurent, additional, Grosset, Jacques H., additional, Lagrange, Sophie, additional, and Müller, Rolf, additional

Published
2015
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48. Pharmacokinetics and Pharmacodynamics of Clofazimine in a Mouse Model of Tuberculosis

Author

Swanson, Rosemary V., primary, Adamson, John, additional, Moodley, Chivonne, additional, Ngcobo, Bongani, additional, Ammerman, Nicole C., additional, Dorasamy, Afton, additional, Moodley, Sashen, additional, Mgaga, Zinhle, additional, Tapley, Asa, additional, Bester, Linda A., additional, Singh, Sanil, additional, Grosset, Jacques H., additional, and Almeida, Deepak V., additional

Published
2015
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50. Evolution of extensively drug-resistant tuberculosis over four decades revealed by whole genome sequencing of Mycobacterium tuberculosis from KwaZulu-Natal, South Africa

Author

Cohen, Keira A., primary, Abeel, Thomas, additional, McGuire, Abigail Manson, additional, Desjardins, Christopher A., additional, Munsamy, Vanisha, additional, Shea, Terrance P., additional, Walker, Bruce J., additional, Bantubani, Nonkqubela, additional, Almeida, Deepak V., additional, Alvarado, Lucia, additional, Chapman, Sinead, additional, Mvelase, Nomonde R., additional, Duffy, Eamon Y., additional, Fitzgerald, Michael G., additional, Govender, Pamla, additional, Gujja, Sharvari, additional, Hamilton, Susanna, additional, Howarth, Clint, additional, Larimer, Jeffrey D., additional, Maharaj, Kasmheel, additional, Pearson, Matthew D., additional, Priest, Margaret E., additional, Zeng, Qiandong, additional, Padayatchi, Nesri, additional, Grosset, Jacques, additional, Young, Sarah K., additional, Wortman, Jennifer, additional, Mlisana, Koleka P., additional, O’Donnell, Max R., additional, Birren, Bruce W., additional, Bishai, William R., additional, Pym, Alexander S., additional, and Earl, Ashlee M., additional

Published
2015
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