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https://impactstory.org/u/0000-0003-0452-623X/activity
http://www.pnas.org/content/112/10/3020.abstract
To twist the analogy back to Alzheimer - all these scientists still agreed on the patient-level diagnosis of Alzheimer.
To make that claim for a single paper I would 1. have to be able to reproduce their p-value, and 2. spend enough time with the model to understand how/what assumptions were unfairly tweaked to get to that p-value.
Just running your own implementation of a model on your own dataset and getting an insignificant or different p-value is not enough. You might just have implemented the model wrongly.
I hope things like https://clojuriststogether.org/ or possibly patreon will make clojure open source projects more sustainable for developers.
If it is about the manifestation of the disease (the clinical symptoms), those we only know from historical descriptions and that is not something a model can change :-). So yeah, many infected people would still have had buboes. Buboes are also the expected result from plague acquired from fleas (whether they were human fleas or rat fleas).
What might be less known is that there is a pretty high chance (10-20%) that a person suffering from bubonic plague progresses to pneumonic plague. That basically is a death warrant for that person, but it also means that he/she might spread the disease further through air-droplets. If the conditions are right, you might get a pneumonic plague epidemic intermingled with a bubonic plague epidemic. Model-wise, that is one scenario we haven't looked into, but we have seen something like that play out in Madagascar last year.
I also put a popular science summary of the paper online here: https://medium.com/@boris.schmid/human-ectoparasites-and-the...
https://www.reddit.com/r/news/comments/7qopqf/black_death_sp...
We didn't use all of the cities for which we had outbreaks, but selected nine that covered a large part of the time period, and a large geographic region. Here is the list:
Givry, France, 1348. Florence, Italy, 1400. Barcelona, Spain, 1490. London, England, 1563-1564. Eyam, England, 1666. Gdansk, Poland, 1709. Stockholm, Sweden, 1710-1711. Moscow, Russia, 1771. Malta, Malta, 1813.
That said, there are some long-standing questions in plague research, one of which is why the first and second plague pandemic were that much more lethal than the third plague pandemic. Prior to the aDNA work, people speculated that medieval plague was a different pathogen altogether, but that hypothesis has been put to rest now. An alternative theory has been that plague could spread through human ectoparasites, and we found a novel way to test that theory. That resulted in this paper.
One of the groups that is doing most of the research on body lice as vectors of plague is the group of Didier Raoult. Michelle Ziegler made a nice summary of that work here:
https://contagions.wordpress.com/2016/11/17/the-case-for-lou...
Xavier Didelot did some work on testing mixed models for two cities, 17th century Eyam and 19th century Cairo. He did have to further simplify the models though - there are some restrictions on how many floating parameters you can have while the models are trying to converge to the parameter set that results in the best match with the observations.
Epidemiological analysis of the Eyam plague outbreak of 1665–1666: http://rspb.royalsocietypublishing.org/content/283/1830/2016...
Model-based analysis of an outbreak of bubonic plague in Cairo in 1801: http://rsif.royalsocietypublishing.org/content/14/131/201701...
Piarroux R, et al. (2013) Plague epidemics and lice, Democratic Republic of the Congo. Emerg Infect Dis 19:505–506.
Laudisoit A, et al. (2007) Plague and the human flea, Tanzania. Emerg Infect Dis 13: 687–693.
Ratovonjato J, Rajerison M, Rahelinirina S, Boyer S (2014) Yersinia pestis in Pulex irritans fleas during plague outbreak, Madagascar. Emerg Infect Dis 20:1414–1415.
What we have done is compare the rise and fall of daily or weekly mortality levels during plague outbreaks against three models of plague transmission - two that are generally accepted (rat-borne plague and pneumonic plague), and one that has been speculated about for a long time (human ectoparasites like body lice and fleas). We allowed the models to achieve the best fit they could within biological parameter constraints, and see how well each of these models could mimic the observed mortality curve.
There is a bit more detail in this interview: https://news.nationalgeographic.com/2018/01/rats-plague-blac...
The code/models we used are available online for one of the outbreaks (Barcelona 1490) https://zenodo.org/record/1043924
A pre-review version of the paper is available as a poster here: http://www.mn.uio.no/cees/english/people/phd/katharrd/kd_yer... Note that we changed the lice model a bit since then, on recommendation of one of the reviewers.
Do remember that Anglican is a partial language in clojure, so you can't use all clojure functions (and I think none of the macros) within anglican's defqueries.
I would suggest to enable import from ORCID. Seems to be the best initiative around to give a unique identifier to scientists.
From January 2 to September 10, 2016, 54 people from 16 states (Alabama,
Arizona,California, Colorado, Connecticut, Florida, Georgia, Hawaii, Illinois,
Massachusetts, Minnesota, New York, North Carolina, Tennessee, Texas, and Utah) were
reported to have measles.
It looks like that with "free" they mean that there is no self-sustainable epidemic possible anymore in the Americas, given the degree of vaccine coverage. Nice.http://czbiohub.org/projects/infectious-disease/
Looks like Chan and Zuckerberg's initiative on infectious diseases is focused on a rapid response once a disease establishes itself in humans. There is certainly a lot to win there, but it is still acting after the fact, rather than prevention. Would have liked part of the effort to be focused on monitoring wildlife to understand which diseases are at risk of jumping over.
Greger, M.Crit. Rev. Microbiol. 33, 243–299 (2007). https://www.ncbi.nlm.nih.gov/pubmed/18033595
Woolhouse, M .E.J. Trends Microbiol. 10, s3–s7 (2002). https://www.ncbi.nlm.nih.gov/pubmed/12377561
To put that into perspective - Y. pestis' main chromosome is a little over 4 million basepairs. So it is only broken pieces of code that they can recover, not the whole, intact bacterium. No risk here.
http://www.nature.com/nature/journal/v478/n7370/full/nature1...
https://goldin.shinyapps.io/Search_Pepys/
(enter plague as keyword, click on the tab marked histogram, or browse the entries)
That said, I would like these news articles to actually link to the scientific paper, or if the paper is not published yet/still under review, at least mention that.
http://eccmidlive.org/#resources/ancient-pathogen-genomics-w...
A big challenge is how to translate the genetic relatedness of plague strains spreading across Europe during successive pandemics to the actual location of its historic reservoirs. Location of the infected humans does not necessarily tell you much about the origin of that outbreak, especially with so much plague being moved by about ship.
There is a lively discussion about these papers on twitter, between a few of us spanning history, microbiology and computational biology, if you want to hear about these things earlier.
Ole Benedictow's chapter on Sweden (mainly discussing the lack of evidence, except for church donations) https://books.google.no/books?id=ZtjwPOB7aMkC&pg=PA170&dq=%2...
Stockholm in 1710-1711 had no problem in being rather brutally infected, with at its peak 1500 burials per week.
The Last plague in the Baltic Region from Frandsen: https://books.google.no/books?id=F3bNWrVRMb8C&pg=PA65&dq=%22...
For example, Givry is a tiny place somewhere in France, but for which by happenstance the parish registers at the time of the Black Death survived. They record the daily number of deaths, which end abruptly when presumably the priest died after recording ~620 deaths since the beginning of the epidemic in that town. The town's population is estimated at around 1170 people, based on the death rate in the earlier months, leading to a lower end estimate of 53% mortality (if the death of the priest was also the end of the epidemic).
(from page 306 of http://www.persee.fr/doc/bec_0373-6237_1939_num_100_1_449196)
[0 0 0 0 2 0 0 0 0 0 0 0 0 0 0 0 1 1 0 0 0 2 0 0 0 0 0 3 2 0 0] ;; jul. . approximate start of epidemic somewhere during jul.
[0 4 4 1 0 2 1 7 5 3 1 1 4 5 3 3 4 1 5 2 2 4 3 6 2 2 2 6 3 8 4 6 10] ;; aug.
[6 9 8 8 4 6 15 3 11 24 7 10 15 10 14 11 17 8 6 3 17 6 11 16 7 16 12 5 10 7] ;; sept
[7 6 7 7 8 7 6 6 9 4 7 9 3 14 5 5 4 8 6 7 3 2 5 4 4 2 3 1 3 0 6] ;; oct
[3 4 3 4 0 2 1 0 4 3 2 1 0 0 5 0 0 0 3] ;; nov, records end with the dead of the priest, worst of the epidemic is over.But the Black Death itself was special in that it was such a condensed and intense disaster. If you have the chance to read the eyewitness accounts, as collected by Rosemary Horrox it is quite impressive.
http://www.amazon.com/Black-Death-Manchester-Medieval-Source...
I enjoyed reading this paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2632865/
The paper highlights several aspects of plague that were different between the second and third plague pandemic, and which caused a scientific movement that searched for alternative explanations for the Black Death - that is, until the Yersinia pestis bacterium got sequenced from multiple Black Death mass graves.
Ran into a lot of examples like that when merging two existing georeferenced datasets of plague outbreaks in Europe. Had to do quite some manual checking, and made good use of the damerau-levenshtein distance between two strings to recognize alternative spellings.
end-result here: https://figshare.com/articles/plague_outbreaks_in_medieval_E...
The article is a bit old, and misses out on the large amount of genetic evidence since then sequenced and analyzed. Cui et al found that the closest living relatives to the Black Death stem from north-west China. That is about the only evidence we have on where the Black Death came from, and it does point to an origin in or near China.