As with many citizen science projects, our initial analyses efforts have been to demonstrate the quality and value of the project and data to the rest of the scientific community and other potential stakeholders resulting in the following papers.

• Citizen Science for Mining the Biomedical Literature. Citiz Sci. 2016;1(2). pii: 14. doi: 10.5334/cstp.56. Epub 2016 Dec 31.

• Aligning Needs: Integrating Citizen Science Efforts into Schools Through Service Requirements. Hum Comput (Fairfax). 2019;6(1):56-82

• Applying Citizen Science to Gene, Drug, and Disease Relationship Extraction from Biomedical Abstracts. Bioinformatics. 2019 Sep 3. pii: btz678. doi: 10.1093/bioinformatics/btz678.

We expect that further exploration of the data may lead to more insight on how to best leverage citizen science to facilitate biomedical discovery, and hope to invite you to join us on a new, improved platform in the future.

To get the latest updates on Mark2Cure, sign up for our mailing list.

The San Diego Citizen Science Expo

Who: Anyone who wants to do science
What: San Diego Citizen Science Day Expo
When: Saturday, April 13, 2018. 10:00 am – 2:00 pm
Where: North University Community Library
8820 Judicial Dr
San Diego, CA 92122

Cost: Free

This year, Mark2Cure super-contributor and StallCatcher extraordinaire, Tom Adams will be helping us run our in house StallCatchers event at the expo on behalf of the San Diego Public Libraries. The Megathon will happen at the San Diego Citizen Science Expo from 10:30 AM-12:30 PM. You can join us in person at the event or from the comfort of your own home (team name: 'SD library's Finest CITYzens').

Additionally, there will be a series of talks/demos from 1:00 PM - 2:00 PM in preparation for the City Nature Challenge:
1:00 – 1:20 pm – Safety and BioBlitzing (Cal. Dept of Fish and Wildlife)
1:20 – 1:40 pm – Spotting critters and what to look for (San Diego Tracking Team)
1:40 – 2:00 pm – How to take pictures and use iNat to participate in a bioblitz (San Diego Natural History Museum)

Other local citizen science groups that will be at this year's expo include:

• Organizer: La Jolla Public Library
• Organizer: Mark2Cure (Su Lab, The Scripps Research Institute)
• Organizer: Scripps Research Community Teaching Labs
• Presenter: California Dept of Fish and Wildlife
• Participant: Ocean Sanctuaries
• Presenter: San Diego Tracking Team
• Participant: Gut Instinct / Galileo
• Participant: San Diego County Department of Vector Control
• Participant: San Diego Mycological Society
• Participant: San Diego Barcode of Life
• Presenter: The San Diego Natural History Museum
• Participant: Escondido Creek Conservancy

We’ve been waiting with bated breath to hear back on a few submissions.

First, our manuscript submission for the Automated Knowledge Base Construction has completed the anonymous peer review process and has been accepted for the conference. We’ve uploaded the accepted submission to BioRxiv.

The manuscript along with the data and code used to generate the figures in the manuscript can be found at:
Most Important--Contributors to the data set used who gave us their permission to acknowledge them: https://mark2cure.org/blog/relation-paper-contributors/
Manuscript: https://www.biorxiv.org/content/10.1101/564187v1
Data: https://github.com/gtsueng/M2Crelnb/tree/master/data
Analysis code: https://github.com/gtsueng/M2Crelnb

Here are some key findings from the analysis of the data from the Relationship Extraction Module:
• Good relationship extraction is difficult without good Concept Recognition. When it comes to doing concept recognition, we often get asked the question, “Can’t machines do that?” And, as those of you who’ve been contributing to Mark2Cure know--yes, but there’s definitely room for improvement. A large part of error in the Relationship Extraction Module stems from concept recognition errors.
• Design issues also hamper user contributions. We’ve known all along that users are good, but that design issues can muck things up for them. Still, it can’t be stated to the scientific community enough! Data issues in citizen science are usually design issues.
• The relationships obtained via Mark2Cure are very different from those found using an algorithm, and we think that these two methods can complement one another nicely to cover gaps within each system.

The other submission we were waiting on was our funding application to combine Mark2Cure and active machine learning to identify diseases based on their clinical phenotypes. Unfortunately, this was not approved for funding. We are still investigating alternative applications for Mark2Cure in order to further its development and will let you know when we make progress on that end.

Rare Disease Day

Although we had high hopes for pushing this newsletter out on Rare Disease Day (yesterday) in order to acknowledge and thank our contributors from the rare disease community, we were unfortunately just not fast enough. Although we missed sending this out on Rare Disease Day, rare disease is not something that should be acknowledged just once a year. Rare disease patients and family live with the disease every day, and we are grateful to the rare disease folks in our community who have taken the time to share their stories with us, contribute to our efforts, and inspire researchers like us. We know that research on your disease is probably moving much more slowly than you’d like, and hope that in the future we’ll be able to speed things up (though we’re also pushing forward slowly right now.)

Some news from our friends about an upcoming event for Alzheimer’s Disease Citizen Science

StallCatchers, the citizen science project from our CitSciMedBlitz event last year, is aiming for a Guinness World Record and would love for you to take part in this effort. The goals is to surpass the world record for ‘largest practical science lesson (multiple venues)’ which currently held at 13,701 participants. If you’re local to San Diego, the San Diego Public Library (in particular, the La Jolla branch, whom we’ve partnered with for the San Diego Citizen Science Day Expo) is one of 9 cities in the U.S. where the libraries are engaged in the planning, preparation, and evaluation of this event.

If you’re interested in helping researchers to understand some of the circulatory underpinnings of Alzheimer’s disease, you can take part in this StallCatchers Megathon that happens between 10.30 am and 12.30pm on Saturday April 13th.

How you can take part:
• Sign up for at stallcatchers.com (https://stallcatchers.com/main#)
• If you’re in San Diego, make sure you and your friends join our online team after they sign up ('SD library's Finest CITYzens') so that the participation is credited to San Diego.
• Promote it in your community.
• Host a group event on April 13th.
• Use the project as a springboard for building community interest in other neighborhood science ideas of your own.
• Any age can take part. The project involves looking at scans of mice brains.

Thank you all for being a part of our research effort. We've submitted two manuscripts based on your contributions and have been selected to give three presentations on Mark2Cure for the CitSci2019 conference next year. The preprints for one of the papers is already available online at BioRxiv, and the other one will be uploaded as soon as it is out of the anonymous Peer review process (having the full version on BioRxiv kind of defeats the purpose of anonymizing it for peer review in an open reviews system).

PS- If you missed Andrew's webinar on Mark2Cure and Gene Wiki, it is now available online.

If you love science and enjoy learning, you're in for a treat! Andrew (the brains behind Mark2Cure) will be holding a webinar using two case studies (the Gene Wiki Project and Mark2Cure) to illustrate the use of crowdsourcing as it applies to knowledge management for translational research. Registration is free and open to anyone (we checked first). There may be some required questions on the registration form which may not necessarily be applicable to you, but they're only meant to inform, not exclude. So, if you're interested in the webinar but don't have an affiliation with an institute or department, feel free to select 'other' and type in 'Mark2Cure'.

Event Details

(View the original announcement)

Speaker: Andrew Su, PhD, Professor, Department of Integrative, Structural and Computational Biology, The Scripps Research Institute

Overview: Crowdsourcing involves the engagement of large communities of individuals to collaboratively accomplish tasks at massive scale. These tasks could be online or offline, paid or for free. But how can crowdsourcing science help your research? This webinar will describe two crowdsourcing projects for translational research, both of which aim to better organize biomedical information so that it can be more easily accessed, integrated, and queried:

First, the goal of the Gene Wiki project is to create a community-maintained knowledge base of all relationships between biological entities, including genes, diseases, drugs, pathways, and variants. This project draws on the collective efforts of informatics researchers from a wide range of disciplines, including bioinformatics, cheminformatics, and medical informatics.

Second, the Mark2Cure project partners with the citizen scientist community to extract structured content from biomedical abstracts with an emphasis on rare disease. Although citizen scientists do not have any specialized expertise, after receiving proper training, Mark2Cure has shown that in aggregate they perform bio-curation at an accuracy comparable to professional scientists.

The Digital Scholar Webinar Series introduces health researchers at USC, CHLA and beyond to digital approaches and tools relevant to their research. The series showcases the potential and limitations of digital approaches health researchers need to be aware of. All webinars will be accessible afterward on the Digital Scholar Program page.

Register for the webinar

We have been working on a preliminary analysis of the relationship extraction data generated by our fantastic Mark2Curators. This analysis is in the process of being written up into an academic paper and if your data was used for this paper, you will be given option of being credited on a page on our site dedicated to the contributors for this paper. We expect to have an email notifying contributors to the data set out by early next week, so keep an eye out for it.

San Diego Hackathon / Curation Jamboree

If you are in San Diego the week of October 14th, and have a background in software development, engineering, computational biology, bioinformatics, pathology, oncology, genomics, or biocuration--there is a hackathon/curation jamboree happening on October 15th-October 16th. The event is a joint event between the Griffith Labs, Su and Wu Labs and will cost $25 to register. Mark2Cure is a project of the Su Lab focusing on biomedical literature curation; while, the hackathon is focused on the CIViC resource from the Griffith labs. CIViC is an open access, open source, community-driven web resource for Clinical Interpretation of Variants in Cancer which aims to enable precision medicine by providing an educational forum for dissemination of knowledge and active discussion of the clinical significance of cancer genome alterations. You can learn more about this event at: https://www.eventbrite.com/e/cancer-variant-interpretation-hackathon-and-curation-jamboree-tickets-48287431006?aff=General

World Alzheimer Day

In case you missed it, September 21st is World Alzheimer’s day, and our friends at EyesOnAlz will be holding a world-wide Catchathon. Our very own TAdams organized a local team to participate in a previous Catchathon. If members of the Mark2Cure community are interested in teaming up and contributing with other Mark2Curators for this Catchathon, we would be happy to organize a Mark2Cure team for the event. Otherwise, if you are interested in contributing to Alzheimer’s research from the comfort of your own computer on an individual basis, we 100% encourage you to do so!

Science by the people and for the people—introducing a new Citizen Science project from the Knight Lab at UCSD

If you’ve ever wished that there was a citizen science project for answering questions about how nutrition and other habits affect health and other outcomes—there’s now a new platform to address your questions. This platform, Galileo, comes from the Knight Lab at the University of California, San Diego—the same lab that is responsible for the American Gut project!

Here’s how it works:
Learn more at gutinstinct.ucsd.edu/info

As mentioned earlier, kianic acid can cause behavioral changes and seizures. In a rats study, it has shown that the most common changes in behavior were strong immobility known as catatonia, ‘wet dog shake’, and generalized tonic-clonic convulsions. [3]. These behavioral changes had a rapid onset and lasted for long. [3]. After 3 hours of kainic acid injection, there was inflammation of dendrites and axons and a reduction of neuronal perikarya and these followed with inflammation signs of the entire brain. [3]. Chemically, there was a diminish level of noradrenaline levels and increased in levels of 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic acid and homovanillic acid. [3]. At times there were later reactions (after 24h) following kainic acid injection and in such case, there would be partial death of tissues with loss of nerve cells.[3]. And chemically, there was a reduce level of choline acetyltransferase. [3].

In a mice study, it has been demonstrated that interleukin-18 deficiency eases the activation of microglial in kainic acid-induced toxicity in the brain.[4]. It also showed that interleukin-18 is involved in kainic acid induced hippocampal degeneration. [4]. When there is over activation of glutamate receptors, there is an excess of calcium coming in and thus this leads to damage of neurons. [5]. Activated glial cells and inflammatory molecules can change the result of the disease. [5]. From an endocrinology perspective, kainic acid prevents prolactin production in male rats.[6]. This inhibition is caused by an increase in dopamine production and by a direct effect at the pituitary. [6].Kainic acid’s effect on prolactin production is to some extent reliant on endogenous nitric oxide.[6].

References:
1) https://www.ncbi.nlm.nih.gov/pubmed/10223631
“The activation of glutamate receptors by kainic acid and domoic acid.” Hampson DR1, Manalo JL.

Abstract
The neurotoxins kainic acid and domoic acid are potent agonists at the kainate and alphaamino-5-methyl-3-hydroxyisoxazolone-4-propionate (AMPA) subclasses of ionotropic glutamate receptors. Although it is well established that AMPA receptors mediate fast excitatory synaptic transmission at most excitatory synapses in the central nervous system, the role of the high affinity kainate receptors in synaptic transmission and neurotoxicity is not entirely clear. Kainate and domoate differ from the natural transmitter, L-glutamate, in their mode of activation of glutamate receptors; glutamate elicits rapidly desensitizing responses while the two neurotoxins elicit non-desensitizing or slowly desensitizing responses at AMPA receptors and some kainate receptors. The inability to produce desensitizing currents and the high affinity for AMPA and kainate receptors are undoubtedly important factors in kainate and domoate-mediated neurotoxicity. Mutagenesis studies on cloned glutamate receptors have provided insight into the molecular mechanisms responsible for these unique properties of kainate and domoate.

2) https://www.hindawi.com/journals/bmri/2011/457079/
“Kainic Acid-Induced Neurodegenerative Model: Potentials and Limitations.” Xiang-Yu Zheng,1,2 Hong-Liang Zhang,2,3 Qi Luo,1 and Jie Zhu2,3

Abstract
Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS. KA has been extensively used as a specific agonist for ionotrophic glutamate receptors (iGluRs), for example, KARs, to mimic glutamate excitotoxicity in neurodegenerative models as well as to distinguish other iGluRs such as α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors and N-methyl-D-aspartate receptors. Given the current knowledge of excitotoxicity in neurodegeneration, interventions targeted at modulating excitotoxicity are promising in terms of dealing with neurodegenerative disorders. This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.

3) https://www.ncbi.nlm.nih.gov/pubmed/6141539
“Kainic acid induced seizures: neurochemical and histopathological changes.” Sperk G, Lassmann H, Baran H, Kish SJ, Seitelberger F, Hornykiewicz O. Abstract
Behavioural, histopathological and neurochemical changes induced by systemic injection of kainic acid (10 mg/kg, s.c.) were investigated in rats. The most pronounced behavioural changes were strong immobility ("catatonia"), increased incidence of "wet dog shakes", and long-lasting generalized tonic-clonic convulsions. The behavioural symptoms were fast in their onset and lasted for several hours. Two distinct phases of histopathological and neurochemical changes were observed. (1) Early partially reversible changes were seen up to 3 h after kainic acid injection. They consisted of shrinkage and pyknosis of neuronal perikarya together with swelling of dendrites and axon terminals. These changes were accompanied by generalized signs of edema throughout the whole brain. Neurochemically, there was a marked decrease in noradrenaline levels (up to 70%) and an increase in levels of 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic acid and homovanillic acid (up to 200%) in all analysed brain regions, suggesting a strongly increased firing rate of aminergic neurones during the period of generalized seizures. These histological and neurochemical changes were found in all the brain regions examined; they were greatly reduced or only sporadically seen after 1-3 days, when the animals had recovered from the seizures. (2) Late irreversible changes developed 24 h and later following kainic acid injection. They consisted of incomplete tissue necrosis with loss of nerve cells and oligodendrocytes, demyelination, astroglial scar formation, small perivenous hemorrhages and extensive vascular sprouting. The changes were restricted to the pyriform cortex, amygdala, hippocampus (most pronounced in the CA1 sector), gyrus olfactorius lateralis, bulbus olfactorius and tuberculum olfactorium. Neurochemically, a selective decrease was seen in choline acetyltransferase activity (40%) of the amygdala/pyriform cortex area, and of glutamate decarboxylase activity in the dorsal hippocampus (45%) and amygdala/pyriform cortex (55%). No such changes were found in the frontal cortex and the striatum/pallidum. Since at these later time periods the widespread early changes in monoamine metabolism were mostly normalized, loss of acetylcholine and gamma-aminobutyric acid neurons in the affected brain regions represented a selective neurochemical change typical for this stage of kainic acid action. The observed neurochemical and histopathological changes may be directly related to the excitotoxic and convulsive properties of kainic acid. However, brain edema resulting in herniation damage of the basal portions of the brain in addition to disturbances of microcirculation and +

4)https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-7-26
“Kainic acid-induced microglial activation is attenuated in aged interleukin-18 deficient mice” Xing-Mei Zhang, Tao Jin, Hernan Concha Quezada, Eilhard Mix, Bengt Winblad and Jie Zhu.

Abstract
Background
Previously, we found that interleukin (IL)-18 deficiency aggravates kainic acid (KA)-induced hippocampal neurodegeneration in young C57BL/6 mice due to an over-compensation by IL-12. Additionally, IL-18 participates in fundamental inflammatory processes that increase during aging. In the present study, we were interested in the role of IL-18 in KA-induced neurodegeneration in aged female C57BL/6 mice.
Methods
Fifteen aged female IL-18 knockout (KO) and 15 age-matched wild-type (WT) mice (18 to 19 months old) were treated with KA at a dose of 25 mg/kg body weight intranasally. Seizure activities and behavioral changes were rated using a 6-point scoring system and open-field test, respectively. Seven days after KA treatment, degenerating neurons were detected by Nissl's method and Fluoro-Jade B staining; and microglial activation was analyzed by immunohistochemistry and flow cytometry.
Results
Aged female IL-18 KO and WT mice showed similar responses to treatment with KA as demonstrated by comparable seizure activities, behavioral changes and neuronal cell death. However, aged female IL-18 KO mice failed to exhibit the strong microglial activation shown in WT mice. Interestingly, even though the number of activated microglia was less in KA-treated IL-18 KO mice than in KA-treated WT mice, the proportion of microglia that expressed the cytokines tumor necrosis factor (TNF)-α, IL-6 and IL-10 was higher in KA-treated IL-18 KO mice.
Conclusion
Deficiency of IL-18 attenuates microglial activation after KA-induced excitotoxicity in aged brain, while the net effects of IL-18 deficiency are balanced by the enhancement of other cytokines, such as TNF-α, IL-6 and IL-10.

5) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131729/
“Kainic Acid-Induced Neurotoxicity: Targeting Glial Responses and Glia-Derived Cytokines.” Xing-Mei Zhang1 and Jie Zhu

Abstract
Glutamate excitotoxicity contributes to a variety of disorders in the central nervous system, which is triggered primarily by excessive Ca2+ influx arising from overstimulation of glutamate receptors, followed by disintegration of the endoplasmic reticulum (ER) membrane and ER stress, the generation and detoxification of reactive oxygen species as well as mitochondrial dysfunction, leading to neuronal apoptosis and necrosis. Kainic acid (KA), a potent agonist to the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate class of glutamate receptors, is 30-fold more potent in neuro-toxicity than glutamate. In rodents, KA injection resulted in recurrent seizures, behavioral changes and subsequent degeneration of selective populations of neurons in the brain, which has been widely used as a model to study the mechanisms of neurodegenerative pathways induced by excitatory neurotransmitter. Microglial activation and astrocytes proliferation are the other characteristics of KA-induced neurodegeneration. The cytokines and other inflammatory molecules secreted by activated glia cells can modify the outcome of disease progression. Thus, anti-oxidant and anti-inflammatory treatment could attenuate or prevent KA-induced neurodegeneration. In this review, we summarized updated experimental data with regard to the KA-induced neurotoxicity in the brain and emphasized glial responses and glia-oriented cytokines, tumor necrosis factor-α, interleukin (IL)-1, IL-12 and IL-18.

6) http://joe.endocrinology-journals.org/content/151/1/159
“Mechanisms of inhibitory action of kainic acid on prolactin secretion in male rats”. L Pinilla, D Gonzalez, M Tena-Sempere, R Aguilar and E Aguilar

Abstract
Activation of excitatory N-methyl-D-aspartate and kainate receptors evokes multiple and diverse neuroendocrine changes. We have previously shown that kainic acid (KA), an agonist of kainate receptors, inhibits prolactin (PRL) secretion in male rats when given systemically. In the present studies we have characterized this inhibitory action. KA inhibited in vivo PRL secretion in neonatal, prepubertal and adult male rats. This inhibition was independent of gonadal secretion and was evident in male rats whether intact, orchidectomized, or orchidectomized and treated with testosterone. In addition, KA inhibited PRL secretion in male rats rendered hyperprolactinaemic by neonatal administration of oestradiol benzoate. The decrease in serum PRL levels after KA administration was accompanied by an increase in pituitary concentrations of dopamine, and the KA effect on PRL disappeared in males pretreated with domperidone, an antagonist of dopaminergic receptors. These findings strongly suggest that an increase in dopamine release was involved in the effects of KA. Also, KA inhibited in vitro PRL secretion by adenohypophysial dispersed cells and this effect was blocked by 6,7-dinitroquinoxaline, a kainate receptor antagonist, which indicates that the pituitary is also a possible site of action of KA. Nw-nitro-L-arginine-methyl ester, a blocker of nitric oxide synthase, reduced the effects of KA in vivo and slightly stimulated PRL release in vitro.

Only two quests left in the Bip-part-two mission and the quests in the mission on pilocarpine-and-hypotonia only require submissions from two more Mark2Curators each. If you have some spare time and have unlocked the NER tasks, please consider contributing to these missions so that they can be closed out and analyzed.

Cochrane Crowd launches the PICO task

It's no secret, many Mark2Curators enjoy learning and have quickly built their biomedical knowledge arsenal just by reading. In Mark2Cure our contributors help to identify gene, treatment, and disease concepts in the text as well as how these concepts are related. These tasks can quickly become redundant even if the content of the abstracts can change wildly from abstract to abstract. Because Cochrane Crowd also works on biomedical literature, we've teamed up with Cochrane Crowd in the past and expect to do so in the future. In Cochrane Crowd, participants helped identify randomized controlled trials, but Cochrane Crowd has launched another biomedical literature task known as PICO--and this task has many similarities with what Mark2Curators have learned to do. PICO task participants will be actually be extracting information on Populations, Interventions, Comparators, and Outcomes from abstracts. Learn more about the PICO task.

Dazzle4Rare 2018 will happen the week of August 12th-18th.

"In 2016, an idea was born: to spread cross-community rare disease awareness via Twitter and other social platforms. It began in earnest but quickly gained momentum. With the summer approaching, it's time to take the #dazzle4rare mission to a larger audience here on Facebook and other platforms. We have been reaching out and asking for help to make this year's week-long online bigger than before and to connect people across various rare disease and undiagnosed populations. "

For us, #Dazzle4Rare is an opportunity to raise awareness about the the rare diseases that affect the selfless volunteers who make up the Mark2Cure community. To this end, we invite our contributors to tell us about the rare diseases they would like us to highlight during this event. We would be most honored to share your story on our blog or link your site or videos during #Dazzle4Rare. Learn more about #Dazzle4Rare or how to get involved here.

Call for Proposals now Open for #CitSci2019

If you have a professional interest in delving further into the practice of citizen science, consider submitting an abstract or proposal for the 2019 Citizen Science Association Conference. If you live in or near Raleigh, North Carolina, keep this conference in on your radar as there will be a public festival which will include various citizen science projects that you can get involved with.

References:
1.https://pubchem.ncbi.nlm.nih.gov/compound/pilocarpine#section=Top
2.https://www.drugs.com/cdi/pilocarpine-ophthalmic.html
3.https://www.drugs.com/cdi/pilocarpine-systemic.html
4.https://www.ngly1.org/about/
5.https://medical-dictionary.thefreedictionary.com/iontophoretic+pilocarpine+test
6.https://www.ncbi.nlm.nih.gov/pubmed/9927101
7.https://academic.oup.com/ijnp/article/15/7/957/639277
8.https://www.sciencedirect.com/science/article/pii/S0014488607002634
9.http://ard.bmj.com/content/62/12/1204
10. https://www.researchgate.net/publication/23699610-Autonomic-nervous-system-regulates-secretion-of-anti-inflammatory-prohormone-SMR1-from-rat-salivary-glands

As a citizen science effort, Mark2Cure is primarily driven by volunteers--and volunteers like you have brought us to where we are today. As of today, we have over 1.3 million annotations!!! We are currently busy with the analysis, so please accept my apologies for being a bit more slow to respond to your inquiries. Fortunately, you and your fellow volunteers continue to help us move forward. In fact, we are excited to share a new preprint on aligning citizen science opportunities with the needs of students fulfilling community service and service learning requirements. The research on these requirements was primarily performed by a volunteer with a marketing/business background and was inspired by a few high school Mark2Curators who have been kind enough to share their experience and needs as students and volunteers.

You can find the preprint on bioarxiv here, and it has been submitted for peer review in the journal Citizen Science Theory and Practice.

A designer has also wrapped up her work on making Mark2Cure more intuitive and user-friendly. A huge thanks to those of you who took the time to provide feedback on individual parts of her designs--although your feedback may not necessarily be incorporated in them here, we will definitely take your detailed and valuable suggestions into consideration.

Since this is citizen science and your voices are important--I'd like to share the designs with all of you. You can find the wire frames here. Note that the actual wording/content is subject to change (especially since we've received detailed content recommendations from some of you), and that the focus is more about the layout of the content. Please feel free to share your opinions about it with us!

For those of you who have joined us in last year's #MedLitBlitz or this year's #CitSciMedBlitz, you may be familiar with our friends at Cochrane Crowd. Like Mark2Cure, Cochrane Crowd is a citizen science project where volunteers help inspect biomedical abstracts. Cochrane crowd was also launched in May and are celebrating their anniversary with the #showyourscreen 2 Million annotations challenge. Learn more about the challenge here.

The challenge will run until 9am ET, April 21st and anyone interested in the challenge will have the opportunity to earn digital badges for just trying out (ie- registering or logging into) different citizen science projects. As Mark2Curators, you only need to log into your Mark2Cure account to earn a badge.

Learn more about this fun challenge at https://blog.eyesonalz.com/citsciday-hero/.

Citizen Science Day is on April 14th, this year and many citizen science organizations (including yours truly) are hosting citizen science events. Here in San Diego, we've teamed up with the San Diego Public Library and the Wet Lab group to put on the 3rd annual San Diego Citizen Science Day Expo. There are a lot of exciting new entrants into the San Diego citizen science scene, and we hope you will join us in learning about them at the expo. If you're in San Diego, please join us! The details are as follows:

Who: Anyone who wants to do science
What: San Diego Citizen Science Day Expo
When: Saturday, April 14, 2018. 1:00 PM – 5:00 PM
Where: North University Community Library (8820 Judicial Dr, San Diego, CA 92122)

Please note that the location has changed from the previous ones due to the limited availability of parking spots at the La Jolla Library. The North University Community Library has plentiful free parking, so please visit come if you're in the area! For the most up-to-date information about this event, visit SDCitSci.net.

If you're not in San Diego, there is probably an exciting Citizen Science Day event happening near you! To find a Citizen Science Day Event near you, visit Scistarter.com.

San Diego March for Science

The March for Science is also happening on April 14th in San Diego. It starts at the Waterfront park at 10:00am and ends at 1:00pm (right before our event!). If you want to show your love for science consider joining the march! If you want to DO science, be sure to join a Citizen Science Day event near you (or contribute to Mark2Cure, of course!).

Current Status of Mark2Cure

Development status and workarounds

Unfortunately, Mark2Cure no longer has a full time developer working on the project, so a lot of the issues and bugs that have been reported probably will not be fixed for a long, long time. We are very sorry for the frustration our system has caused our users and extremely grateful for the patience, graciousness, and encouragement our users have returned to us. Mark2Cure is really made up of a wonderful bunch of individuals, and we are thankful that this project has introduced us to you. Fortunately, many of you really put the science in the term citizen science and have systematically found ways to contribute productively in spite of all the issues in our system. You are all too amazing!

NER module issues: The most frustrating one has been the inability to highlight certain words, and the random highlighting/un-highlighting of words when users try to mark something. This has been reported by many users (many, many thanks to those of you who took the time to report this issue). Fortunately, one of your fellow volunpeers has found a workaround that appears to be quite robust. To get around a lot of these highlighting issues, AJ_Eckhart highlights the entire paragraph to remove the preannotations. These preannotations seem to be an important factor in this problem, and he has tested this workaround for the 'cannot-highlight-a-specific-term' bug, the 'highlighting-a-term-un-highlights-something-else', and the 'highlighting-a-term-highlights' something else' bugs.

RE module issues: A number of you have kindly taken the time to report issues with the RE module--the most common issue is the seemingly random inability to throw out an annotation. For this issue, two workarounds have been reported by our users. LadySteph has found that returning to the dashboard and then returning to the task will enable you to submit the response you wish (eg- throw out an annotation) and TAdams has reported that many of you have gravitated towards submitting 'Cannot be determined' in lieu of throwing out an annotation. We will take both workarounds into consideration when we analyze the data, so thank you all very much for contributing in spite of all these issues!

Data analysis and research status

Speaking of analyzing the data--we might not yet have enough abstracts annotated in order to generate ground-breaking, new hypotheses on NGLY1 deficiency, but we have enough for some initial analyses on the application of citizen science towards information extraction. We are working towards more scientific publications and look forward to sharing the results of your work and crediting you for your help. Note that many journal submission systems are not made to account for group names or a huge volume of names in the authorship; hence, we will continue to have our Mark2Cure contributors listed on a dedicated page which will be linked in the paper. As with our first paper, this will be an opt-in process because we respect your right to privacy. More details on opting-in will be sent via our mailing list.

We're all up and active now and looking forward to sharing a recap and the results of #CitSciMedBlitz with you.

First, a Recap

On February 21st, CitSciMedBlitz was kicked off with a webinar to introduce the three platforms that would be participating in CitSciMedBlitz

The first challenge, the StallCatchers challenge, was launched on February 26th at 7am PST. Within minutes of the launch, StallCatchers were hammering away at StallCatchers, including Cochrane Crowd's Anna.

Anna managed to get on the leaderboard but wasn't able to stay on there for very long because the competition was just too tough. At least she placed, though-- I never even made it!

By the end of the challenge, StallCatchers analyzed a whopping 18,348 real videos--the equivalent of two weeks worth of laboratory analysis!

While the EyesOnAlz team was still cooling off from their intense challenge, we were gearing up for the Mark2Cure arm--and NOT without a huge set of worries.

You can read more about the hiccups and snafu's that happened during the Mark2Cure 24hr challenge here. By the end of the challenge, CitSciMedBlitzers managed to submit ~300 doc annotations, and ~3000 relationship annotations--an impressive feat considering the increase in task difficulty, and the bugs and other technical issues that made the challenge--well, even more challenging!

While we were busy analyzing the results of our challenge, Cochrane crowd was preparing the last challenge of CitSciMedBlitz. This challenge started off right with 50 assessments within the first 2 minutes, and over 5000 in just the first 4 hours! This arm of the challenge would determine which of the top contenders from the previous challenges would win the trophy so the competition was intense! By the end of this challenge, over 46,000 classifications would be made--allowing our teams to determine the overall winner of #CitSciMedBlitz.

And now...the results of CitSciMedBlitz...

Of course, the biggest winner of the challenge goes to...

...biomedical and health evidence research! Everyone who has contributed (in the past) and continues to contributes to these efforts deserve a round of applause for being generous enough to donate their time towards helping with disease and health research.

The winner of the CitSciMedBlitz trophy is Michael Landau! Note, it was previously stated that Michael was also the top contributor to the EyesOnAlz challenge of CitSciMedBlitz. This is wrong.

Mike Capraro was the top contributor across all three measures of the EyesOnAlz challenge and the overall top contributor of that challenge for CitSciMedBlitz.

Editor's note #2: If you'd like to read more about CitSciMedBlitz from the EyesOnAlz team, check out their latest recap post here!

The top contributor to the Mark2Cure arm of CitSciMedBlitz was Kien Pong Yap, while the top contributor to the Cochrane Crowd arm of CitSciMedBlitz was Nikolaos. The top contributors to each platform will be receiving a platform-specific trophy.

Each platform will be awarding additional prizes to some of their top contributors and the notifications should be arriving via email (if they haven't already).

Editor's note #3, the recap from the Cochrane Crowd side of things is now available

Now that all the excitement of CitSciMedBlitz is over, I'd like to thank ALL the citizen scientists who contribute to projects like ours and make these platforms great. In citizen science, the people make the platform. And, as you can see--the people contributing to these platforms, do so with:

a collaborative spirit,

humor,

humility,

good spirit,

and grace,

Thank you all! Much respect for the work that you've done and the character you've shown!

Note this post was updated on 2018.03.12 to correct an error and on 2018.03.19 to add a link

What's exciting is that several of these names were also in the top 10 for the StallCatchers challenge so it'll be a tough competition in the Cochrane challenge to see who actually wins the CitSciMedBlitz triple challenge trophy.

Here are some random tidbits about the Mark2Cure arm of the CitSciMedBlitz triple challenge:

• The NER module was broken for the first few hours of the challenge, and we received emails and phone calls about it within the first hour of the challenge. THANK YOU for bringing it to our attention and providing so detailed information about the bugs. Max was able to solve it while on the airplane ride to San Diego for the Future of Genomic Medicine Conference.

• In spite of the NER module issues (a HUGE thanks to TAdams, JudyE, AJEckhart, and Itwontalwaysbelikethis for helping us troubleshoot), users doing this task still managed to climb the ranks even with the delayed start.

• A Mark2Curator created an introductory video about the relationship extraction task for the event while we were running around trying to ensure that everything was in place for the M2C challenge. THANK YOU for doing that, TAdams!

• One of the Mark2Curators joined the challenge as a personal challenge to raise awareness for dystonia on Rare Disease Day. Dystonia = loss of muscle control. There are many types, but you can imagine just how much more challenging that makes things! Read about her efforts here. And if you're curious how well she did--she made it to the top 5!

• I was worried about following StallCatchers because their task is so visually appealing while ours is text based and quite difficult. Indeed we got questions and suggestions-a-plenty about Mark2Cure on the StallCatchers forum, but there are plenty of very tenacious citizen scientists in stall catchers and they managed to climb pretty high in the ranks.

• The team behind StallCatchers is AMAZING!!!! Very generous with both support and humor! No wonder the StallCatchers are so ardent!

If you think it's all over--think again! The Cochrane crowd of the challenge has just started, and CitSciMedBlitzers who participate in all THREE challenges will get a digital badge on their StallCatchers profile. It's an awesome badge!

Now go take the cochrane challenge!