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Thesis ; Online: Deconstructing Artemisinin Resistance in Plasmodium falciparum Using Genetic Crosses and Systems Biology Approaches

Davis, Sage Z.

2019

Abstract: In this thesis, I aim to understand the genetic and transcriptomic causes of artemisinin resistance and predict what drugs may prove effective in combination with artemisinin. Artemisinin resistance raises alarming concerns for the eradication efforts of ...

Abstract	In this thesis, I aim to understand the genetic and transcriptomic causes of artemisinin resistance and predict what drugs may prove effective in combination with artemisinin. Artemisinin resistance raises alarming concerns for the eradication efforts of malaria: if the resistance were to spread from Southeast Asia to Africa, as has previous anti-malarial resistances, the consequences are predicted to be dire. Further exacerbating the situation is the reports of resistance to artemisinin combination therapies, the frontline treatment as recommended by the World Health Organization, combining artemisinin with a long-lasting partner drug. To combat the spread of artemisinin and artemisinin combination therapy resistances, an understanding of artemisinin’s mechanism of action, the resistance mechanisms against artemisinin, and more rationally designed combination therapies are required. In the first section of my thesis, I take a genetic approach understand artemisinin resistance. Using a recently generated genetic cross whose parents have diverging artemisinin resistance phenotypes, I aim to determine the genetic loci controlling artemisinin resistance. What makes this approach unique is that the resistant parent harbors no K13 mutations, the genetic marker of resistance in the field. Although I find no suggestive or significant peak associated with artemisinin response, I do find two weaker peaks on chromosome 11 and 12, one which corresponds to pfmrp2, a gene involved in multitude of drug responses. I also attempt to develop a high throughput alternative to measure artemisinin response. In the second section of my thesis, I take a transcriptomic approach to understand artemisinin resistance. I collect transcription samples from 55 Southeast Asian isolates across two timepoints, two perturbations, and in replicate to understand how the biology of artemisinin resistant parasites has changed. Using gene co-expression networks and applying systems biology approaches, I find that gene co-expression networks illuminate known biology about artemisinin, including putative functions of K13. Additionally, I discover two genes, a putative DNA helicase MCM9 and an osmiophilic body protein G377 are two strong candidates whose functions are important for artemisinin response and resistance, with support of previously published data. I show how the functions of these two genes may have changed under differing conditions, highlighting DNA damage as a potentially important pathway in understanding artemisinin and its effect on malaria. In the third and final chapter of my dissertation I perturb three Southeast Asian isolates with thirty drugs/compounds of diverse targets and mechanisms, in addition to dihydroartemisinin, to determine what drugs may work best in combination with artemisinin. Transcriptional responses to drugs/compounds have previously proven to be a strong predictor of drug synergy in other models, and here I apply the same logic to malaria. I find that two drugs/compounds, namely epoxomicin and cisplatin seem to show high promise for more synergy than the currently used anti-malarials. Epoxomicin and cisplatin also seem to perturb G377 and MCM9 strongly and in the same manner as dihydroartemisinin, further encouraging their targets/mechanisms as potential combination therapy targets for future use.
Keywords	Parasitology\|Systematic biology\|Genetics
Subject code	572
Language	ENG
Publishing date	2019-01-01 00:00:01.0
Publisher	University of Notre Dame
Publishing country	us
Document type	Thesis ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Three-dimensional chromatin in infectious disease-A role for gene regulation and pathogenicity?

Davis, Sage Z / Hollin, Thomas / Lenz, Todd / Le Roch, Karine G

PLoS pathogens

2021 Volume 17, Issue 2, Page(s) e1009207

Abstract: The recent Coronavirus Disease 2019 pandemic has once again reminded us the importance of understanding infectious diseases. One important but understudied area in infectious disease research is the role of nuclear architecture or the physical ... ...

Abstract	The recent Coronavirus Disease 2019 pandemic has once again reminded us the importance of understanding infectious diseases. One important but understudied area in infectious disease research is the role of nuclear architecture or the physical arrangement of the genome in the nucleus in controlling gene regulation and pathogenicity. Recent advances in research methods, such as Genome-wide chromosome conformation capture using high-throughput sequencing (Hi-C), have allowed for easier analysis of nuclear architecture and chromosomal reorganization in both the infectious disease agents themselves as well as in their host cells. This review will discuss broadly on what is known about nuclear architecture in infectious disease, with an emphasis on chromosomal reorganization, and briefly discuss what steps are required next in the field.
MeSH term(s)	Animals ; COVID-19/genetics ; COVID-19/metabolism ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Chromatin/genetics ; Chromatin/metabolism ; Chromosomes/genetics ; Chromosomes/metabolism ; Communicable Diseases/genetics ; Communicable Diseases/metabolism ; Gene Expression Regulation ; Humans
Chemical Substances	Chromatin
Language	English
Publishing date	2021-02-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1009207
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Three-dimensional chromatin in infectious disease-A role for gene regulation and pathogenicity?

Sage Z Davis / Thomas Hollin / Todd Lenz / Karine G Le Roch

PLoS Pathogens, Vol 17, Iss 2, p e

2021 Volume 1009207

Abstract	The recent Coronavirus Disease 2019 pandemic has once again reminded us the importance of understanding infectious diseases. One important but understudied area in infectious disease research is the role of nuclear architecture or the physical arrangement of the genome in the nucleus in controlling gene regulation and pathogenicity. Recent advances in research methods, such as Genome-wide chromosome conformation capture using high-throughput sequencing (Hi-C), have allowed for easier analysis of nuclear architecture and chromosomal reorganization in both the infectious disease agents themselves as well as in their host cells. This review will discuss broadly on what is known about nuclear architecture in infectious disease, with an emphasis on chromosomal reorganization, and briefly discuss what steps are required next in the field.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	630
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genital cutaneous necrosis: a delayed sequela of intraperitoneal Mitomycin-c.

Vincent, Sage A / Maceyko, Meghan / Altshuler, Peter J / Davis, Zachary / Mark, J Ryan / Chung, Paul H / Bowne, Wilbur B

Pleura and peritoneum

2023 Volume 8, Issue 4, Page(s) 175–176

Language	English
Publishing date	2023-10-13
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2861909-2
ISSN	2364-768X ; 2364-7671
ISSN (online)	2364-768X
ISSN	2364-7671
DOI	10.1515/pp-2023-0021
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Article ; Online: The extended recovery ring-stage survival assay provides a superior association with patient clearance half-life and increases throughput.

Davis, Sage Z / Singh, Puspendra P / Vendrely, Katelyn M / Shoue, Douglas A / Checkley, Lisa A / McDew-White, Marina / Button-Simons, Katrina A / Cassady, Zione / Sievert, Mackenzie A C / Foster, Gabriel J / Nosten, François H / Anderson, Timothy J C / Ferdig, Michael T

Malaria journal

2020 Volume 19, Issue 1, Page(s) 54

Abstract: Background: Tracking and understanding artemisinin resistance is key for preventing global setbacks in malaria eradication efforts. The ring-stage survival assay (RSA) is the current gold standard for in vitro artemisinin resistance phenotyping. However, ...

Abstract	Background: Tracking and understanding artemisinin resistance is key for preventing global setbacks in malaria eradication efforts. The ring-stage survival assay (RSA) is the current gold standard for in vitro artemisinin resistance phenotyping. However, the RSA has several drawbacks: it is relatively low throughput, has high variance due to microscopy readout, and correlates poorly with the current benchmark for in vivo resistance, patient clearance half-life post-artemisinin treatment. Here a modified RSA is presented, the extended Recovery Ring-stage Survival Assay (eRRSA), using 15 cloned patient isolates from Southeast Asia with a range of patient clearance half-lives, including parasite isolates with and without kelch13 mutations. Methods: Plasmodium falciparum cultures were synchronized with single layer Percoll during the schizont stage of the intraerythrocytic development cycle. Cultures were left to reinvade to early ring-stage and parasitaemia was quantified using flow cytometry. Cultures were diluted to 2% haematocrit and 0.5% parasitaemia in a 96-well plate to start the assay, allowing for increased throughput and decreased variability between biological replicates. Parasites were treated with 700 nM of dihydroartemisinin or 0.02% dimethyl sulfoxide (DMSO) for 6 h, washed three times in drug-free media, and incubated for 66 or 114 h, when samples were collected and frozen for PCR amplification. A SYBR Green-based quantitative PCR method was used to quantify the fold-change between treated and untreated samples. Results: 15 cloned patient isolates from Southeast Asia with a range of patient clearance half-lives were assayed using the eRRSA. Due to the large number of pyknotic and dying parasites at 66 h post-exposure (72 h sample), parasites were grown for an additional cell cycle (114 h post-exposure, 120 h sample), which drastically improved correlation with patient clearance half-life compared to the 66 h post-exposure sample. A Spearman correlation of - 0.8393 between fold change and patient clearance half-life was identified in these 15 isolates from Southeast Asia, which is the strongest correlation reported to date. Conclusions: eRRSA drastically increases the efficiency and accuracy of in vitro artemisinin resistance phenotyping compared to the traditional RSA, which paves the way for extensive in vitro phenotyping of hundreds of artemisinin resistant parasites.
MeSH term(s)	Antimalarials/pharmacology ; Artemisinins/pharmacology ; Drug Resistance ; Erythrocytes/parasitology ; Flow Cytometry ; Fluorescent Dyes ; Half-Life ; Humans ; Malaria, Falciparum/diagnosis ; Malaria, Falciparum/drug therapy ; Organic Chemicals ; Parasitemia/diagnosis ; Parasitemia/drug therapy ; Plasmodium falciparum/drug effects ; Plasmodium falciparum/isolation & purification ; Povidone ; Real-Time Polymerase Chain Reaction/methods ; Silicon Dioxide
Chemical Substances	Antimalarials ; Artemisinins ; Fluorescent Dyes ; Organic Chemicals ; SYBR Green I (163795-75-3) ; Percoll (65455-52-9) ; artenimol (6A9O50735X) ; Silicon Dioxide (7631-86-9) ; artemisinin (9RMU91N5K2) ; Povidone (FZ989GH94E)
Language	English
Publishing date	2020-01-31
Publishing country	England
Document type	Journal Article
ISSN	1475-2875
ISSN (online)	1475-2875
DOI	10.1186/s12936-020-3139-6
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Article ; Online: Pairwise growth competitions identify relative fitness relationships among artemisinin resistant Plasmodium falciparum field isolates

Abigail R. Tirrell / Katelyn M. Vendrely / Lisa A. Checkley / Sage Z. Davis / Marina McDew-White / Ian H. Cheeseman / Ashley M. Vaughan / François H. Nosten / Timothy J. C. Anderson / Michael T. Ferdig

Malaria Journal, Vol 18, Iss 1, Pp 1-

2019 Volume 13

Abstract: Abstract Background Competitive outcomes between co-infecting malaria parasite lines can reveal fitness disparities in blood stage growth. Blood stage fitness costs often accompany the evolution of drug resistance, with the expectation that relatively ... ...

Abstract	Abstract Background Competitive outcomes between co-infecting malaria parasite lines can reveal fitness disparities in blood stage growth. Blood stage fitness costs often accompany the evolution of drug resistance, with the expectation that relatively fitter parasites will be more likely to spread in populations. With the recent emergence of artemisinin resistance, it is important to understand the relative competitive fitness of the metabolically active asexual blood stage parasites. Genetically distinct drug resistant parasite clones with independently evolved sets of mutations are likely to vary in asexual proliferation rate, contributing to their chance of transmission to the mosquito vector. Methods An optimized in vitro 96-well plate-based protocol was used to quantitatively measure-head-to-head competitive fitness during blood stage development between seven genetically distinct field isolates from a hotspot of emerging artemisinin resistance and the laboratory strain, NF54. These field isolates were isolated from patients in Southeast Asia carrying different alleles of kelch13 and included both artemisinin-sensitive and artemisinin-resistant isolates. Fluorescent labeled microsatellite markers were used to track the relative densities of each parasite throughout the co-growth period of 14–60 days. All-on-all competitions were conducted for the panel of eight parasite lines (28 pairwise competitions) to determine their quantitative competitive fitness relationships. Results Twenty-eight pairwise competitive growth outcomes allowed for an unambiguous ranking among a set of seven genetically distinct parasite lines isolated from patients in Southeast Asia displaying a range of both kelch13 alleles and clinical clearance times and a laboratory strain, NF54. This comprehensive series of assays established the growth relationships among the eight parasite lines. Interestingly, a clinically artemisinin resistant parasite line that carries the wild-type form of kelch13 outcompeted all other parasites in this ...
Keywords	Competitive growth ; Fitness ; Artemisinin resistance ; kelch13 ; Population genetics ; Arctic medicine. Tropical medicine ; RC955-962 ; Infectious and parasitic diseases ; RC109-216
Subject code	572
Language	English
Publishing date	2019-08-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Pairwise growth competitions identify relative fitness relationships among artemisinin resistant Plasmodium falciparum field isolates.

Tirrell, Abigail R / Vendrely, Katelyn M / Checkley, Lisa A / Davis, Sage Z / McDew-White, Marina / Cheeseman, Ian H / Vaughan, Ashley M / Nosten, François H / Anderson, Timothy J C / Ferdig, Michael T

Malaria journal

2019 Volume 18, Issue 1, Page(s) 295

Abstract: Background: Competitive outcomes between co-infecting malaria parasite lines can reveal fitness disparities in blood stage growth. Blood stage fitness costs often accompany the evolution of drug resistance, with the expectation that relatively fitter ... ...

Abstract	Background: Competitive outcomes between co-infecting malaria parasite lines can reveal fitness disparities in blood stage growth. Blood stage fitness costs often accompany the evolution of drug resistance, with the expectation that relatively fitter parasites will be more likely to spread in populations. With the recent emergence of artemisinin resistance, it is important to understand the relative competitive fitness of the metabolically active asexual blood stage parasites. Genetically distinct drug resistant parasite clones with independently evolved sets of mutations are likely to vary in asexual proliferation rate, contributing to their chance of transmission to the mosquito vector. Methods: An optimized in vitro 96-well plate-based protocol was used to quantitatively measure-head-to-head competitive fitness during blood stage development between seven genetically distinct field isolates from a hotspot of emerging artemisinin resistance and the laboratory strain, NF54. These field isolates were isolated from patients in Southeast Asia carrying different alleles of kelch13 and included both artemisinin-sensitive and artemisinin-resistant isolates. Fluorescent labeled microsatellite markers were used to track the relative densities of each parasite throughout the co-growth period of 14-60 days. All-on-all competitions were conducted for the panel of eight parasite lines (28 pairwise competitions) to determine their quantitative competitive fitness relationships. Results: Twenty-eight pairwise competitive growth outcomes allowed for an unambiguous ranking among a set of seven genetically distinct parasite lines isolated from patients in Southeast Asia displaying a range of both kelch13 alleles and clinical clearance times and a laboratory strain, NF54. This comprehensive series of assays established the growth relationships among the eight parasite lines. Interestingly, a clinically artemisinin resistant parasite line that carries the wild-type form of kelch13 outcompeted all other parasites in this study. Furthermore, a kelch13 mutant line (E252Q) was competitively more fit without drug than lines with other resistance-associated kelch13 alleles, including the C580Y allele that has expanded to high frequencies under drug pressure in Southeast Asian resistant populations. Conclusions: This optimized competitive growth assay can be employed for assessment of relative growth as an index of fitness during the asexual blood stage growth between natural lines carrying different genetic variants associated with artemisinin resistance. Improved understanding of the fitness costs of different parasites proliferating in human blood and the role different resistance mutations play in the context of specific genetic backgrounds will contribute to an understanding of the potential for specific mutations to spread in populations, with the potential to inform targeted strategies for malaria therapy.
MeSH term(s)	Antimalarials/pharmacology ; Artemisinins/pharmacology ; Drug Resistance/genetics ; Evolution, Molecular ; Genetic Fitness ; Genotype ; Genotyping Techniques ; Life Cycle Stages/genetics ; Microsatellite Repeats/genetics ; Mutation ; Plasmodium falciparum/drug effects ; Plasmodium falciparum/growth & development ; Protozoan Proteins/genetics
Chemical Substances	Antimalarials ; Artemisinins ; Protozoan Proteins ; artemisinin (9RMU91N5K2)
Language	English
Publishing date	2019-08-28
Publishing country	England
Document type	Journal Article
ISSN	1475-2875
ISSN (online)	1475-2875
DOI	10.1186/s12936-019-2934-4
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Article ; Online: Effects of N-phenylpropyl-N'-substituted piperazine sigma receptor ligands on cocaine-induced hyperactivity in mice.

Sage, Andrew S / Oelrichs, Clark E / Davis, Derick C / Fan, Kuo-Hsien / Nahas, Roger I / Lever, Susan Z / Lever, John R / Miller, Dennis K

Pharmacology, biochemistry, and behavior

2013 Volume 110, Page(s) 201–207

Abstract: The present study examined N-phenylpropyl-N'-substituted piperazine sigma receptor ligands on cocaine-induced changes in locomotor activity in mice. Previous reports indicate that N-phenylpropyl-N'-(4-methoxybenzyl)piperazine (Nahas-3h), N-phenylpropyl-N' ...

Abstract	The present study examined N-phenylpropyl-N'-substituted piperazine sigma receptor ligands on cocaine-induced changes in locomotor activity in mice. Previous reports indicate that N-phenylpropyl-N'-(4-methoxybenzyl)piperazine (Nahas-3h), N-phenylpropyl-N'-(4-methoxyphenethyl)piperazine (YZ-067), and N-phenylpropyl-N'-(3-methoxyphenethyl)piperazine (YZ-185) bind with high affinity (Ki values≈1 nM) to σ1 sigma receptors. YZ-067 and YZ-185 are known to attenuate cocaine-induced convulsions, while Nahas-3h has not been tested in behavioral studies. Nahas-3h significantly attenuated cocaine-induced hyperactivity. YZ-067 decreased the effect of cocaine in a dose-dependent manner. Interestingly, YZ-185 inhibited cocaine's effect at higher doses, but enhanced cocaine's effect at a low dose. The YZ-185 inhibition of cocaine-induced hyperactivity was not surmounted by increasing the cocaine dose. Overall, this study is consistent with previous work showing the ability of certain sigma receptor ligands to affect cocaine-induced hyperactivity. Further, subtle alterations of ligand structure and the specific dosage levels employed influence the behavioral effects observed, with a 3-methoxy substituent apparently conferring the ability of a ligand to enhance cocaine's locomotor stimulatory effects.
MeSH term(s)	Animals ; Cocaine/pharmacology ; Dose-Response Relationship, Drug ; Hyperkinesis/chemically induced ; Ligands ; Male ; Mice ; Piperazines/pharmacology ; Receptors, sigma/metabolism
Chemical Substances	Ligands ; Piperazines ; Receptors, sigma ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2013-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2013.07.006
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The extended recovery ring-stage survival assay provides a superior association with patient clearance half-life and increases throughput

Sage Z. Davis / Puspendra P. Singh / Katelyn M. Vendrely / Douglas A. Shoue / Lisa A. Checkley / Marina McDew-White / Katrina A. Button-Simons / Zione Cassady / Mackenzie A. C. Sievert / Gabriel J. Foster / François H. Nosten / Timothy J. C. Anderson / Michael T. Ferdig

Malaria Journal, Vol 19, Iss 1, Pp 1-

2020 Volume 9

Abstract: Abstract Background Tracking and understanding artemisinin resistance is key for preventing global setbacks in malaria eradication efforts. The ring-stage survival assay (RSA) is the current gold standard for in vitro artemisinin resistance phenotyping. ... ...

Abstract	Abstract Background Tracking and understanding artemisinin resistance is key for preventing global setbacks in malaria eradication efforts. The ring-stage survival assay (RSA) is the current gold standard for in vitro artemisinin resistance phenotyping. However, the RSA has several drawbacks: it is relatively low throughput, has high variance due to microscopy readout, and correlates poorly with the current benchmark for in vivo resistance, patient clearance half-life post-artemisinin treatment. Here a modified RSA is presented, the extended Recovery Ring-stage Survival Assay (eRRSA), using 15 cloned patient isolates from Southeast Asia with a range of patient clearance half-lives, including parasite isolates with and without kelch13 mutations. Methods Plasmodium falciparum cultures were synchronized with single layer Percoll during the schizont stage of the intraerythrocytic development cycle. Cultures were left to reinvade to early ring-stage and parasitaemia was quantified using flow cytometry. Cultures were diluted to 2% haematocrit and 0.5% parasitaemia in a 96-well plate to start the assay, allowing for increased throughput and decreased variability between biological replicates. Parasites were treated with 700 nM of dihydroartemisinin or 0.02% dimethyl sulfoxide (DMSO) for 6 h, washed three times in drug-free media, and incubated for 66 or 114 h, when samples were collected and frozen for PCR amplification. A SYBR Green-based quantitative PCR method was used to quantify the fold-change between treated and untreated samples. Results 15 cloned patient isolates from Southeast Asia with a range of patient clearance half-lives were assayed using the eRRSA. Due to the large number of pyknotic and dying parasites at 66 h post-exposure (72 h sample), parasites were grown for an additional cell cycle (114 h post-exposure, 120 h sample), which drastically improved correlation with patient clearance half-life compared to the 66 h post-exposure sample. A Spearman correlation of − 0.8393 between fold change and ...
Keywords	Ring-stage survival assay ; Artemisinin resistance ; kelch13 ; Arctic medicine. Tropical medicine ; RC955-962 ; Infectious and parasitic diseases ; RC109-216
Subject code	616
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Exploring UK medical school differences: the MedDifs study of selection, teaching, student and F1 perceptions, postgraduate outcomes and fitness to practise.

McManus, I C / Harborne, Andrew Christopher / Horsfall, Hugo Layard / Joseph, Tobin / Smith, Daniel T / Marshall-Andon, Tess / Samuels, Ryan / Kearsley, Joshua William / Abbas, Nadine / Baig, Hassan / Beecham, Joseph / Benons, Natasha / Caird, Charlie / Clark, Ryan / Cope, Thomas / Coultas, James / Debenham, Luke / Douglas, Sarah / Eldridge, Jack /

Hughes-Gooding, Thomas / Jakubowska, Agnieszka / Jones, Oliver / Lancaster, Eve / MacMillan, Calum / McAllister, Ross / Merzougui, Wassim / Phillips, Ben / Phillips, Simon / Risk, Omar / Sage, Adam / Sooltangos, Aisha / Spencer, Robert / Tajbakhsh, Roxanne / Adesalu, Oluseyi / Aganin, Ivan / Ahmed, Ammar / Aiken, Katherine / Akeredolu, Alimatu-Sadia / Alam, Ibrahim / Ali, Aamna / Anderson, Richard / Ang, Jia Jun / Anis, Fady Sameh / Aojula, Sonam / Arthur, Catherine / Ashby, Alena / Ashraf, Ahmed / Aspinall, Emma / Awad, Mark / Yahaya, Abdul-Muiz Azri / Badhrinarayanan, Shreya / Bandyopadhyay, Soham / Barnes, Sam / Bassey-Duke, Daisy / Boreham, Charlotte / Braine, Rebecca / Brandreth, Joseph / Carrington, Zoe / Cashin, Zoe / Chatterjee, Shaunak / Chawla, Mehar / Chean, Chung Shen / Clements, Chris / Clough, Richard / Coulthurst, Jessica / Curry, Liam / Daniels, Vinnie Christine / Davies, Simon / Davis, Rebecca / De Waal, Hanelie / Desai, Nasreen / Douglas, Hannah / Druce, James / Ejamike, Lady-Namera / Esere, Meron / Eyre, Alex / Fazmin, Ibrahim Talal / Fitzgerald-Smith, Sophia / Ford, Verity / Freeston, Sarah / Garnett, Katherine / General, Whitney / Gilbert, Helen / Gowie, Zein / Grafton-Clarke, Ciaran / Gudka, Keshni / Gumber, Leher / Gupta, Rishi / Harlow, Chris / Harrington, Amy / Heaney, Adele / Ho, Wing Hang Serene / Holloway, Lucy / Hood, Christina / Houghton, Eleanor / Houshangi, Saba / Howard, Emma / Human, Benjamin / Hunter, Harriet / Hussain, Ifrah / Hussain, Sami / Jackson-Taylor, Richard Thomas / Jacob-Ramsdale, Bronwen / Janjuha, Ryan / Jawad, Saleh / Jelani, Muzzamil / Johnston, David / Jones, Mike / Kalidindi, Sadhana / Kalsi, Savraj / Kalyanasundaram, Asanish / Kane, Anna / Kaur, Sahaj / Al-Othman, Othman Khaled / Khan, Qaisar / Khullar, Sajan / Kirkland, Priscilla / Lawrence-Smith, Hannah / Leeson, Charlotte / Lenaerts, Julius Elisabeth Richard / Long, Kerry / Lubbock, Simon / Burrell, Jamie Mac Donald / Maguire, Rachel / Mahendran, Praveen / Majeed, Saad / Malhotra, Prabhjot Singh / Mandagere, Vinay / Mantelakis, Angelos / McGovern, Sophie / Mosuro, Anjola / Moxley, Adam / Mustoe, Sophie / Myers, Sam / Nadeem, Kiran / Nasseri, Reza / Newman, Tom / Nzewi, Richard / Ogborne, Rosalie / Omatseye, Joyce / Paddock, Sophie / Parkin, James / Patel, Mohit / Pawar, Sohini / Pearce, Stuart / Penrice, Samuel / Purdy, Julian / Ramjan, Raisa / Randhawa, Ratan / Rasul, Usman / Raymond-Taggert, Elliot / Razey, Rebecca / Razzaghi, Carmel / Reel, Eimear / Revell, Elliot John / Rigbye, Joanna / Rotimi, Oloruntobi / Said, Abdelrahman / Sanders, Emma / Sangal, Pranoy / Grandal, Nora Sangvik / Shah, Aadam / Shah, Rahul Atul / Shotton, Oliver / Sims, Daniel / Smart, Katie / Smith, Martha Amy / Smith, Nick / Sopian, Aninditya Salma / South, Matthew / Speller, Jessica / Syer, Tom J / Ta, Ngan Hong / Tadross, Daniel / Thompson, Benjamin / Trevett, Jess / Tyler, Matthew / Ullah, Roshan / Utukuri, Mrudula / Vadera, Shree / Van Den Tooren, Harriet / Venturini, Sara / Vijayakumar, Aradhya / Vine, Melanie / Wellbelove, Zoe / Wittner, Liora / Yong, Geoffrey Hong Kiat / Ziyada, Farris / Devine, Oliver Patrick

BMC medicine

2020 Volume 18, Issue 1, Page(s) 136

Abstract: Background: Medical schools differ, particularly in their teaching, but it is unclear whether such differences matter, although influential claims are often made. The Medical School Differences (MedDifs) study brings together a wide range of measures of ...

Abstract	Background: Medical schools differ, particularly in their teaching, but it is unclear whether such differences matter, although influential claims are often made. The Medical School Differences (MedDifs) study brings together a wide range of measures of UK medical schools, including postgraduate performance, fitness to practise issues, specialty choice, preparedness, satisfaction, teaching styles, entry criteria and institutional factors. Method: Aggregated data were collected for 50 measures across 29 UK medical schools. Data include institutional history (e.g. rate of production of hospital and GP specialists in the past), curricular influences (e.g. PBL schools, spend per student, staff-student ratio), selection measures (e.g. entry grades), teaching and assessment (e.g. traditional vs PBL, specialty teaching, self-regulated learning), student satisfaction, Foundation selection scores, Foundation satisfaction, postgraduate examination performance and fitness to practise (postgraduate progression, GMC sanctions). Six specialties (General Practice, Psychiatry, Anaesthetics, Obstetrics and Gynaecology, Internal Medicine, Surgery) were examined in more detail. Results: Medical school differences are stable across time (median alpha = 0.835). The 50 measures were highly correlated, 395 (32.2%) of 1225 correlations being significant with p < 0.05, and 201 (16.4%) reached a Tukey-adjusted criterion of p < 0.0025. Problem-based learning (PBL) schools differ on many measures, including lower performance on postgraduate assessments. While these are in part explained by lower entry grades, a surprising finding is that schools such as PBL schools which reported greater student satisfaction with feedback also showed lower performance at postgraduate examinations. More medical school teaching of psychiatry, surgery and anaesthetics did not result in more specialist trainees. Schools that taught more general practice did have more graduates entering GP training, but those graduates performed less well in MRCGP examinations, the negative correlation resulting from numbers of GP trainees and exam outcomes being affected both by non-traditional teaching and by greater historical production of GPs. Postgraduate exam outcomes were also higher in schools with more self-regulated learning, but lower in larger medical schools. A path model for 29 measures found a complex causal nexus, most measures causing or being caused by other measures. Postgraduate exam performance was influenced by earlier attainment, at entry to Foundation and entry to medical school (the so-called academic backbone), and by self-regulated learning. Foundation measures of satisfaction, including preparedness, had no subsequent influence on outcomes. Fitness to practise issues were more frequent in schools producing more male graduates and more GPs. Conclusions: Medical schools differ in large numbers of ways that are causally interconnected. Differences between schools in postgraduate examination performance, training problems and GMC sanctions have important implications for the quality of patient care and patient safety.
MeSH term(s)	Female ; Humans ; Male ; Schools, Medical/standards ; Students, Medical/statistics & numerical data ; United Kingdom
Language	English
Publishing date	2020-05-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2131669-7
ISSN	1741-7015 ; 1741-7015
ISSN (online)	1741-7015
ISSN	1741-7015
DOI	10.1186/s12916-020-01572-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

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