Stories, that persuade with data:On the research paper,

and the knowledge within

Anita de Waard, a.dewaard@elsevier.com Disruptive Technologies Director, Elsevier Labs

Scientific papers are stories, that persuade with data.The Story of Goldilocks and the Three Bears

Story Part Paper The AXH Domain of Ataxin-1 Mediates Neurodegeneration through Its Interaction with Gfi-1/Senseless Proteins

Once upon a time Time Setting Background The mechanisms mediating SCA1 pathogenesis are still not fully understood, but some general principles have emerged.

a little girl named Goldilocks Characters

Setting

Objects of study the Drosophila Atx-1 homolog (dAtx-1) which lacks a polyQ tract,

She went for a walk in the forest. Pretty soon, she came upon a house.

Location

Setting

Experimental setup

studied and compared in vivo effects and interactions to those of the human protein

She knocked and, when no one answered,

Goal Theme Researchgoal

Gain insight into how Atx-1's function contributes to SCA1 pathogenesis. How these interactions might contribute to the disease process and how they might cause toxicity in only a subset of neurons in SCA1 is not fully understood.she walked right in. Attempt

Theme

Hypothesis Atx-1 may play a role in the regulation of gene expression

At the table in the kitchen, there were three bowls of porridge.

Name Episode 1 Name dAtX-1 and hAtx-1 Induce Similar Phenotypes When Overexpressed in Files

Goldilocks was hungry. Subgoal

Episode 1

Subgoal test the function of the AXH domain

She tasted the porridge from the first bowl.

Attempt

Episode 1

Method overexpressed dAtx-1 in flies using the GAL4/UAS system (Brand and Perrimon, 1993) and compared its effects to those of hAtx-1.

This porridge is too hot! she exclaimed.

Outcome

Episode 1

Results Overexpression of dAtx-1 by Rhodopsin1(Rh1)-GAL4, which drives expression in the differentiated R1-R6 photoreceptor cells (Mollereau et al., 2000 and O'Tousa et al., 1985), results in neurodegeneration in the eye, as does overexpression of hAtx-1[82Q]. Although at 2 days after eclosion, overexpression of either Atx-1 does not show obvious morphological changes in the photoreceptor cellsSo, she tasted the porridge from the

second bowl.Activity

Episode 1

Data (data not shown),

This porridge is too cold, she said Outcome

Episode 1

Results both genotypes show many large holes and loss of cell integrity at 28 days

So, she tasted the last bowl of porridge.

Activity

Episode 1

Data (Figures 1B-1D).

Ahhh, this porridge is just right, she said happily and

Outcome

Episode 1

Results Overexpression of dAtx-1 using the GMR-GAL4 driver also induces eye abnormalities. The external structures of the eyes that overexpress dAtx-1 show disorganized ommatidia and loss of interommatidial bristles she ate it all up. Outcome

Episode 1

Data (Figure 1F),

Scientific papers are stories, that persuade with data.The Story of Goldilocks and the Three Bears

Story Part Paper The AXH Domain of Ataxin-1 Mediates Neurodegeneration through Its Interaction with Gfi-1/Senseless Proteins

Once upon a time Time Setting Background The mechanisms mediating SCA1 pathogenesis are still not fully understood, but some general principles have emerged.

a little girl named Goldilocks Characters

Setting

Objects of study the Drosophila Atx-1 homolog (dAtx-1) which lacks a polyQ tract,

She went for a walk in the forest. Pretty soon, she came upon a house.

Location

Setting

Experimental setup

studied and compared in vivo effects and interactions to those of the human protein

She knocked and, when no one answered,

Goal Theme Researchgoal

Gain insight into how Atx-1's function contributes to SCA1 pathogenesis. How these interactions might contribute to the disease process and how they might cause toxicity in only a subset of neurons in SCA1 is not fully understood.she walked right in. Attempt

Theme

Hypothesis Atx-1 may play a role in the regulation of gene expression

At the table in the kitchen, there were three bowls of porridge.

Name Episode 1 Name dAtX-1 and hAtx-1 Induce Similar Phenotypes When Overexpressed in Files

Goldilocks was hungry. Subgoal

Episode 1

Subgoal test the function of the AXH domain

She tasted the porridge from the first bowl.

Attempt

Episode 1

Method overexpressed dAtx-1 in flies using the GAL4/UAS system (Brand and Perrimon, 1993) and compared its effects to those of hAtx-1.

This porridge is too hot! she exclaimed.

Outcome

Episode 1

Results Overexpression of dAtx-1 by Rhodopsin1(Rh1)-GAL4, which drives expression in the differentiated R1-R6 photoreceptor cells (Mollereau et al., 2000 and O'Tousa et al., 1985), results in neurodegeneration in the eye, as does overexpression of hAtx-1[82Q]. Although at 2 days after eclosion, overexpression of either Atx-1 does not show obvious morphological changes in the photoreceptor cellsSo, she tasted the porridge from the

second bowl.Activity

Episode 1

Data (data not shown),

This porridge is too cold, she said Outcome

Episode 1

Results both genotypes show many large holes and loss of cell integrity at 28 days

So, she tasted the last bowl of porridge.

Activity

Episode 1

Data (Figures 1B-1D).

Ahhh, this porridge is just right, she said happily and

Outcome

Episode 1

Results Overexpression of dAtx-1 using the GMR-GAL4 driver also induces eye abnormalities. The external structures of the eyes that overexpress dAtx-1 show disorganized ommatidia and loss of interommatidial bristles she ate it all up. Outcome

Episode 1

Data (Figure 1F),

Story grammar of fairytales:

Story grammar of fairytales:

According to Propp, main characters (or dramatis personae) that are occuring in a fairy tale may be the following:1. Hero: a character that seeks something;2. Villain: opposes or actively blocks the heroʼs quest;3. Donor: provides the hero with an object of magical properties;4. Dispatcher: sends the hero on his/her quest via a message;5. False Hero: disrupts the heroʼs success by making false claims;6. Helper: aids the hero;7. Princess: acts as the reward for the hero and the object of the villainʼs plots;8. Her Father: acts to reward the hero for his effort.

Story grammar of fairytales:

According to Propp, main characters (or dramatis personae) that are occuring in a fairy tale may be the following:1. Hero: a character that seeks something;2. Villain: opposes or actively blocks the heroʼs quest;3. Donor: provides the hero with an object of magical properties;4. Dispatcher: sends the hero on his/her quest via a message;5. False Hero: disrupts the heroʼs success by making false claims;6. Helper: aids the hero;7. Princess: acts as the reward for the hero and the object of the villainʼs plots;8. Her Father: acts to reward the hero for his effort.

F. Peinado, P. Gervas, and B. Diaz-Agudo, ʻA description logic ontology for fairy tale generationʼ, in Procs LREC. ELRA, (5 2004)

Story grammar of fairytales:

According to Propp, main characters (or dramatis personae) that are occuring in a fairy tale may be the following:1. Hero: a character that seeks something;2. Villain: opposes or actively blocks the heroʼs quest;3. Donor: provides the hero with an object of magical properties;4. Dispatcher: sends the hero on his/her quest via a message;5. False Hero: disrupts the heroʼs success by making false claims;6. Helper: aids the hero;7. Princess: acts as the reward for the hero and the object of the villainʼs plots;8. Her Father: acts to reward the hero for his effort.

F. Peinado, P. Gervas, and B. Diaz-Agudo, ʻA description logic ontology for fairy tale generationʼ, in Procs LREC. ELRA, (5 2004)

Story analysis of scientific text: ORB vs. Medium-grained structure

See work at http://www.w3.org/wiki/HCLSIG/SWANSIOC

Story analysis of scientific text: ORB vs. Medium-grained structure

Episode-level access through Linked Data standards:

Episode-level access through Linked Data standards:

<ce:section id=#123>

Episode-level access through Linked Data standards:

<ce:section id=#123> mice like cheesethis says

Episode-level access through Linked Data standards:

<ce:section id=#123>

said @anita on April 5, 2011

mice like cheesethis says

but we all know she was deluded then

Episode-level access through Linked Data standards:

<ce:section id=#123>

said @anita on April 5, 2011

mice like cheesethis says

but we all know she was deluded then

Episode-level access through Linked Data standards:

<ce:section id=#123>

said @anita on April 5, 2011

the xml is fixed, but the structure is open!

mice like cheesethis says

allows for layers of annotation

but we all know she was deluded then

Episode-level access through Linked Data standards:

<ce:section id=#123>

said @anita on April 5, 2011

the xml is fixed, but the structure is open!

mice like cheesethis says

Satellite Format: LDR store for all our content

Satellites: Provenance

Information about an annotation:-Who created it?,When? By what (version of a) tool?-Has it been reviewed? If so, when and by whom? Was it approved or rejected?

Use pav:createdOn and createdBy instead of dc:date and creator to reduce confusion:<tag:TaggingAnnotation rdf:about="#anno-1"> <tag:annotatesStatement rdf:resource="#stmt-1"/> <tag:score>0.8939283</tag:score><pav:createdOn>2010-07-23T15:45:00Z</pav:createdOn> <pav:createdBy rdf:resource= "http://data.elsevier.com/enh-services/ProjectCode/version"/> <tag:status rdf:resource= "http://data.elsevier.com/namespace/LDR-Satellite/TagAnnot-1/

VendorChecked"/></tag:TaggingAnnotation>

Satellites: Fragments

Use XPointer for XML documents, Media Fragments for image, video, audio.XMLDocumentRegion, MediaRegion akin to Annotation Ontology Selectorsxpath1()* XPointer scheme so pointer can be dropped into any XPath engine and get back the section being annotated.Complex case – arbitrary string in document:

<rgn:XMLDocumentRegion rdf: about= "http://.../S0140-6736(95)90494-8#xpath-e(substring(id('sb-3')/p[2],15,6))">

<dct:isPartOf rdf:resource="http://.../S0140-6736(95)90494-8"/> <rgn:coveringXPath>id('sb-3')/p[2]</rgn:coveringXPath> <rgn:startingOffset>15</rgn:startingOffset> <rgn:stringLength>6</rgn:stringLength> <rgn:matchedString>biopsy</rgn:matchedString> <rgn:prefixString>Testing of the </rgn:prefixString> <rgn:suffixString>indicated nothing</rgn:suffixString></rgn:XMLDocumentRegion>

Both seminomas and the EC component of nonseminomas share features with ES cells. To exclude that the detection of miR-371-3 merely reflects its expression pattern in ES cells, we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004). In many of the m i R - 3 7 1 - 3 e x p r e s s i n g s e m i n o m a s a n d nonseminomas, miR-302a-d was undetectable (Figs S7 and S8), suggesting that miR-371-3 expression is a selective event during tumorigenesis.

Scientific papers are stories, that persuade with data.

Both seminomas and the EC component of nonseminomas share features with ES cells. To exclude that the detection of miR-371-3 merely reflects its expression pattern in ES cells, we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004). In many of the m i R - 3 7 1 - 3 e x p r e s s i n g s e m i n o m a s a n d nonseminomas, miR-302a-d was undetectable (Figs S7 and S8), suggesting that miR-371-3 expression is a selective event during tumorigenesis.

Both seminomas and the EC component of nonseminomas share features with ES cells.To exclude thatthe detection of miR-371-3 merely reflects its expression pattern in ES cells,we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004).In many of the miR-371-3 expressing seminomas and nonseminomas, miR-302a-d was undetectable (Figs S7 and S8),suggesting thatmiR-371-3 expression is a selective event during tumorigenesis.

Scientific papers are stories, that persuade with data.

Both seminomas and the EC component of nonseminomas share features with ES cells. To exclude that the detection of miR-371-3 merely reflects its expression pattern in ES cells, we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004). In many of the m i R - 3 7 1 - 3 e x p r e s s i n g s e m i n o m a s a n d nonseminomas, miR-302a-d was undetectable (Figs S7 and S8), suggesting that miR-371-3 expression is a selective event during tumorigenesis.

Both seminomas and the EC component of nonseminomas share features with ES cells.To exclude thatthe detection of miR-371-3 merely reflects its expression pattern in ES cells,we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004).In many of the miR-371-3 expressing seminomas and nonseminomas, miR-302a-d was undetectable (Figs S7 and S8),suggesting thatmiR-371-3 expression is a selective event during tumorigenesis.

Fact

Hypothesis

Method

Result

Implication

Goal

Reg-Implication

Scientific papers are stories, that persuade with data.

Both seminomas and the EC component of nonseminomas share features with ES cells. To exclude that the detection of miR-371-3 merely reflects its expression pattern in ES cells, we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004). In many of the m i R - 3 7 1 - 3 e x p r e s s i n g s e m i n o m a s a n d nonseminomas, miR-302a-d was undetectable (Figs S7 and S8), suggesting that miR-371-3 expression is a selective event during tumorigenesis.

Both seminomas and the EC component of nonseminomas share features with ES cells.To exclude thatthe detection of miR-371-3 merely reflects its expression pattern in ES cells,we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004).In many of the miR-371-3 expressing seminomas and nonseminomas, miR-302a-d was undetectable (Figs S7 and S8),suggesting thatmiR-371-3 expression is a selective event during tumorigenesis.

Fact

Hypothesis

Method

Result

Implication

Goal

Reg-Implication

Conceptual knowledge

Scientific papers are stories, that persuade with data.

Both seminomas and the EC component of nonseminomas share features with ES cells. To exclude that the detection of miR-371-3 merely reflects its expression pattern in ES cells, we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004). In many of the m i R - 3 7 1 - 3 e x p r e s s i n g s e m i n o m a s a n d nonseminomas, miR-302a-d was undetectable (Figs S7 and S8), suggesting that miR-371-3 expression is a selective event during tumorigenesis.

Both seminomas and the EC component of nonseminomas share features with ES cells.To exclude thatthe detection of miR-371-3 merely reflects its expression pattern in ES cells,we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004).In many of the miR-371-3 expressing seminomas and nonseminomas, miR-302a-d was undetectable (Figs S7 and S8),suggesting thatmiR-371-3 expression is a selective event during tumorigenesis.

Fact

Hypothesis

Method

Result

Implication

Goal

Reg-Implication

Conceptual knowledge

ExperimentalEvidence

Scientific papers are stories, that persuade with data.

Realms of persuasive experimental discourse:

(3) c. miR-371-3 expression is a selective event during tumorigenesis.

(1) Both seminomas and the EC component of nonseminomas share features with ES cells.

(2) b. the detection of miR-371-3 merely reflects its expression pattern in ES cells,

(2) c. we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004).

(3) a. In many of the miR-371-3 expressing seminomas and nonseminomas, miR-302a-d was undetectable (Figs S7 and S8),

(2) a. To exclude that (3) b. suggesting that

Realms of persuasive experimental discourse:

(3) c. miR-371-3 expression is a selective event during tumorigenesis.

(1) Both seminomas and the EC component of nonseminomas share features with ES cells.

(2) b. the detection of miR-371-3 merely reflects its expression pattern in ES cells,

(2) c. we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004).

(3) a. In many of the miR-371-3 expressing seminomas and nonseminomas, miR-302a-d was undetectable (Figs S7 and S8),

Concepts, models, ‘facts’

Experiment

Transitions(2) a. To exclude that (3) b. suggesting that

Realms of persuasive experimental discourse:

(3) c. miR-371-3 expression is a selective event during tumorigenesis.

(1) Both seminomas and the EC component of nonseminomas share features with ES cells.

(2) b. the detection of miR-371-3 merely reflects its expression pattern in ES cells,

(2) c. we tested by RPA miR-302a-d, another ES cells-specific miRNA cluster (Suh et al, 2004).

(3) a. In many of the miR-371-3 expressing seminomas and nonseminomas, miR-302a-d was undetectable (Figs S7 and S8),

Concepts, models, ‘facts’

Experiment

Transitions(2) a. To exclude that (3) b. suggesting that

Realms of persuasive experimental discourse:

‘State’ present tense

‘Narrative’ past tense

Fact creation through citations:

To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we...

Therefore, these results point to LATS2 as a mediator of the miR-372 and miR-373 effects on cell proliferation and tumorigenicity,

Voorhoeve et al, Cell, 2006:

Fact creation through citations:

To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we...

Therefore, these results point to LATS2 as a mediator of the miR-372 and miR-373 effects on cell proliferation and tumorigenicity,

Voorhoeve et al, Cell, 2006:

Hypothesis

Fact creation through citations:

To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we...

Therefore, these results point to LATS2 as a mediator of the miR-372 and miR-373 effects on cell proliferation and tumorigenicity,

Voorhoeve et al, Cell, 2006:

Hypothesis

Implication

... two miRNAs, miRNA-372 and-373, function as potential novel oncogenes in testicular germ cell tumors by inhibition of LATS2 expression, which suggests that Lats2 is an important tumor suppressor (Voorhoeve et al., 2006).

Raver-Shapira et.al, JMolCell 2007

Fact creation through citations:

To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we...

Therefore, these results point to LATS2 as a mediator of the miR-372 and miR-373 effects on cell proliferation and tumorigenicity,

Voorhoeve et al, Cell, 2006:

Hypothesis

Implication

... two miRNAs, miRNA-372 and-373, function as potential novel oncogenes in testicular germ cell tumors by inhibition of LATS2 expression, which suggests that Lats2 is an important tumor suppressor (Voorhoeve et al., 2006).

Raver-Shapira et.al, JMolCell 2007

Fact creation through citations:

To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we...

Therefore, these results point to LATS2 as a mediator of the miR-372 and miR-373 effects on cell proliferation and tumorigenicity,

Voorhoeve et al, Cell, 2006:

Hypothesis

Implication

Cited Implication

... two miRNAs, miRNA-372 and-373, function as potential novel oncogenes in testicular germ cell tumors by inhibition of LATS2 expression, which suggests that Lats2 is an important tumor suppressor (Voorhoeve et al., 2006).

Raver-Shapira et.al, JMolCell 2007

miR-372 and miR-373 target the Lats2 tumor suppressor (Voorhoeve et al., 2006)

Yabuta, JBioChem 2007:

Fact creation through citations:

To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we...

Therefore, these results point to LATS2 as a mediator of the miR-372 and miR-373 effects on cell proliferation and tumorigenicity,

Voorhoeve et al, Cell, 2006:

Hypothesis

Implication

Cited Implication

... two miRNAs, miRNA-372 and-373, function as potential novel oncogenes in testicular germ cell tumors by inhibition of LATS2 expression, which suggests that Lats2 is an important tumor suppressor (Voorhoeve et al., 2006).

Raver-Shapira et.al, JMolCell 2007

miR-372 and miR-373 target the Lats2 tumor suppressor (Voorhoeve et al., 2006)

Yabuta, JBioChem 2007:

Fact creation through citations:

To investigate the possibility that miR-372 and miR-373 suppress the expression of LATS2, we...

Therefore, these results point to LATS2 as a mediator of the miR-372 and miR-373 effects on cell proliferation and tumorigenicity,

Voorhoeve et al, Cell, 2006:

Hypothesis

Implication

Cited Implication

Fact

“[Y]ou can transform a fact into fiction or a fiction into fact just by adding or subtracting references [and data]”

– Bruno Latour, ‘Science in Action’,1987

“[Y]ou can transform a fact into fiction or a fiction into fact just by adding or subtracting references [and data]”

– Bruno Latour, ‘Science in Action’,1987

The logical structure of a scientific claim

The logical structure of a scientific claim

- A Proposition P is about entities, relations, events, actions…

The logical structure of a scientific claim

- A Proposition P is about entities, relations, events, actions…

- We define an Epistemic Evaluation of P to be EEs,v(P):

- S = Source = Holder, Basis:

- Holder: Author (A), Referent (N), Nameless referent (NN)

- Basis: Reasoning (R), Data (D), Unidentified (Ø)- V = Value = Certainly, Emphasis:

- Certainty: from 0 (uncertainty) to 3 (complete certainty)

- Emphasis: Focus (F: +/-), Surprise (S, +,-)

The logical structure of a scientific claim

- A Proposition P is about entities, relations, events, actions…

- We define an Epistemic Evaluation of P to be EEs,v(P):

- S = Source = Holder, Basis:

- Holder: Author (A), Referent (N), Nameless referent (NN)

- Basis: Reasoning (R), Data (D), Unidentified (Ø)- V = Value = Certainly, Emphasis:

- Certainty: from 0 (uncertainty) to 3 (complete certainty)

- Emphasis: Focus (F: +/-), Surprise (S, +,-)

- Nested evaluations, e.g. “We question X’s suggestion that P” can be written as: EEA(EE’N(P)).

The logical structure of a scientific claim

- A Proposition P is about entities, relations, events, actions…

- We define an Epistemic Evaluation of P to be EEs,v(P):

- S = Source = Holder, Basis:

- Holder: Author (A), Referent (N), Nameless referent (NN)

- Basis: Reasoning (R), Data (D), Unidentified (Ø)- V = Value = Certainly, Emphasis:

- Certainty: from 0 (uncertainty) to 3 (complete certainty)

- Emphasis: Focus (F: +/-), Surprise (S, +,-)

- Nested evaluations, e.g. “We question X’s suggestion that P” can be written as: EEA(EE’N(P)).

- If no explicit evaluation (“Water is wet”), of course, EE = Ø.

How is this rhetoric instantiated?Rhetorical goal

Utterance {Proposition} S = H, B

V = C, E

Indicate lack of knowledge

{The role of untranslated exons in the CCR3 gene} has not been studied.

NN 0

Evaluate other work

Recently, CCR3 has been shown to {be upregulated on neutrophils by interferons in vitro [..]}

N, D 3

Offer hypotheses

it is thought that {these transcription factors affect transcription of the gene through interactions with the RNA transcription complex.}

NN, R 2

Interpret results these data suggested that {5' untranslated exon 1 may have a regulatory function.}

A, D 2

Assess validity of interpretations

Since {this was not the case with other lines,} {we suspect {it is integration-site specific}}

A, D 1

State correspondence to expectations

While we expected {the transcript to be about 1 kb in size (Figure 4A),} {two bands ~4 and 5 kb were apparent.}

A, D 2, S+

Comparison to other work

It is important that {this data be viewed with {what is known about other myeloid-specific promoters,}}

A,R/NN/D

2, F+

One application: improve text mining:

insulin ::: GB000841

maintaining glucose homeostasis

... diabetes defect) to overcome insulin resistance in maintaining glucose homeostasis, hyperglycemia and glucose intolerance ...

improve glucose homeostasis

... in T2D is able to increase insulin secretion and improve glucose homeostasis.

improves glucose homeostasis

... SIRT1, whose administration to insulin-resistant animals improves glucose homeostasis.

is capable glucose homeostasis

S15511 is a novel insulin sensitizer that is capable of improving glucose homeostasis in nondiabetic rats.

maintains glucose homeostasis

Pancreatic beta-cells possess a well-regulated insulin secretory property that maintains systemic glucose homeostasis.

may be involved

glucose homeostasis

... similar way to those of insulin, PANDER may be involved in glucose homeostasis.

participates glucose homeostasis

Fine-tuning of insulin secretion from pancreatic beta-cells participates in blood glucose homeostasis.

One application: improve text mining:

insulin ::: GB000841

maintaining glucose homeostasis

... diabetes defect) to overcome insulin resistance in maintaining glucose homeostasis, hyperglycemia and glucose intolerance ...

improve glucose homeostasis

... in T2D is able to increase insulin secretion and improve glucose homeostasis.

improves glucose homeostasis

... SIRT1, whose administration to insulin-resistant animals improves glucose homeostasis.

is capable glucose homeostasis

S15511 is a novel insulin sensitizer that is capable of improving glucose homeostasis in nondiabetic rats.

maintains glucose homeostasis

Pancreatic beta-cells possess a well-regulated insulin secretory property that maintains systemic glucose homeostasis.

may be involved

glucose homeostasis

... similar way to those of insulin, PANDER may be involved in glucose homeostasis.

participates glucose homeostasis

Fine-tuning of insulin secretion from pancreatic beta-cells participates in blood glucose homeostasis.

When insulin secretion cannot be increased adequately (type I diabetes defect) to overcome insulin resistance in maintaining glucose homeostasis, hyperglycemia and glucose intolerance ensues. Insulin resistance and glucose intolerance has been well recognized in patients with advanced chronic kidney diseases (CKD).

.. Incretin metabolism is abnormal in T2D, evidenced by a decreased incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in T2D, and resistance to GIP. GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis.

SIRT1, a NAD(+)-dependent protein deacetylase that regulates transcription factors involved in key cellular processes, has been implicated as a mediator of the beneficial effects of calorie restriction. In a recent issue of Nature, Milne et al. (2007) describe novel potent activators of SIRT1, whose administration to insulin-resistant animals improves glucose homeostasis.

S15511 is a novel insulin sensitizer that is capable of improving glucose homeostasis in nondiabetic rats.... However, the mechanisms behind the insulin-sensitizing effect of S15511 are unknown. The aim of our study was to explore whether S15511 improves insulin sensitivity in skeletal muscles. S15511 treatment was associated with an increase in insulin-stimulated glucose transport in type IIb fibers, while type I fibers were unaffected.

Pancreatic beta-cells possess a well-regulated insulin secretory property that maintains systemic glucose homeostasis. Although it has long been thought that differentiated beta-cells are nearly static, recent studies have shown that beta-cell mass dynamically changes throughout the lifetime. In this article, recent progress of regenerative medicine of the pancreas is reviewed.

... Our results showed that glucose up-regulated PANDER mRNA and protein levels in a time- and dose-dependent manner in MIN6 cells and pancreatic islets. ...Because PANDER is expressed by pancreatic beta-cells and in response to glucose in a similar way to those of insulin, PANDER may be involved in glucose homeostasis.

Fine-tuning of insulin secretion from pancreatic beta-cells participates in blood glucose homeostasis. ... Our data identify miR124a and miR96 as novel regulators of the expression of proteins playing a critical role in insulin exocytosis and in the release of other hormones and neurotransmitters.

One application: improve text mining:

insulin ::: GB000841

maintaining glucose homeostasis

... diabetes defect) to overcome insulin resistance in maintaining glucose homeostasis, hyperglycemia and glucose intolerance ...

improve glucose homeostasis

... in T2D is able to increase insulin secretion and improve glucose homeostasis.

improves glucose homeostasis

... SIRT1, whose administration to insulin-resistant animals improves glucose homeostasis.

is capable glucose homeostasis

S15511 is a novel insulin sensitizer that is capable of improving glucose homeostasis in nondiabetic rats.

maintains glucose homeostasis

Pancreatic beta-cells possess a well-regulated insulin secretory property that maintains systemic glucose homeostasis.

may be involved

glucose homeostasis

... similar way to those of insulin, PANDER may be involved in glucose homeostasis.

participates glucose homeostasis

Fine-tuning of insulin secretion from pancreatic beta-cells participates in blood glucose homeostasis.

When insulin secretion cannot be increased adequately (type I diabetes defect) to overcome insulin resistance in maintaining glucose homeostasis, hyperglycemia and glucose intolerance ensues. Insulin resistance and glucose intolerance has been well recognized in patients with advanced chronic kidney diseases (CKD).

.. Incretin metabolism is abnormal in T2D, evidenced by a decreased incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in T2D, and resistance to GIP. GLP-1, on the other hand, when administered intravenously in T2D is able to increase insulin secretion and improve glucose homeostasis.

SIRT1, a NAD(+)-dependent protein deacetylase that regulates transcription factors involved in key cellular processes, has been implicated as a mediator of the beneficial effects of calorie restriction. In a recent issue of Nature, Milne et al. (2007) describe novel potent activators of SIRT1, whose administration to insulin-resistant animals improves glucose homeostasis.

S15511 is a novel insulin sensitizer that is capable of improving glucose homeostasis in nondiabetic rats.... However, the mechanisms behind the insulin-sensitizing effect of S15511 are unknown. The aim of our study was to explore whether S15511 improves insulin sensitivity in skeletal muscles. S15511 treatment was associated with an increase in insulin-stimulated glucose transport in type IIb fibers, while type I fibers were unaffected.

Pancreatic beta-cells possess a well-regulated insulin secretory property that maintains systemic glucose homeostasis. Although it has long been thought that differentiated beta-cells are nearly static, recent studies have shown that beta-cell mass dynamically changes throughout the lifetime. In this article, recent progress of regenerative medicine of the pancreas is reviewed.

... Our results showed that glucose up-regulated PANDER mRNA and protein levels in a time- and dose-dependent manner in MIN6 cells and pancreatic islets. ...Because PANDER is expressed by pancreatic beta-cells and in response to glucose in a similar way to those of insulin, PANDER may be involved in glucose homeostasis.

Fine-tuning of insulin secretion from pancreatic beta-cells participates in blood glucose homeostasis. ... Our data identify miR124a and miR96 as novel regulators of the expression of proteins playing a critical role in insulin exocytosis and in the release of other hormones and neurotransmitters.

Other application: improve citations

time = t+1

Model of phenomenon

!

Model of phenomenon

time = t

?

Domain Model

(C) Ed Hovy

Other application: improve citations

time = t+1

Model of phenomenon

!

Model of phenomenon

time = t

?

Domain Model

(C) Ed Hovy

Other application: improve citations

time = t+1

Model of phenomenon

!

Model of phenomenon

time = t

?

Domain Model

Citation: • ‘Lifts’ claim from previous paper and add it to current paper

• We need ‘rules for legal lifting’:• Express author’s claim truly• Maintain (experimental) content• Apply appropriately

(C) Ed Hovy

Other application: improve citations

time = t+1

Model of phenomenon

!

Model of phenomenon

time = t

?

Domain Model

Citation: • ‘Lifts’ claim from previous paper and add it to current paper

• We need ‘rules for legal lifting’:• Express author’s claim truly• Maintain (experimental) content• Apply appropriately

What does this mean?

(C) Ed Hovy

17

Eventually: trace roots of a claim: how many independent data points is it based on?

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

data 1

data 2 data 3

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

Paper B:

data 4

data 5 data 6

implication

results

method

goal

fact

fact

data 1

data 2 data 3

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

Paper B:

data 4

data 5 data 6

implication

results

method

goal

fact

fact

data 1

data 2 data 3

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

Paper B:

data 4

data 5 data 6

implication

results

method

goal

fact

fact

data 1

data 2 data 3

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

Paper B:

data 4

data 5 data 6

implication

results

method

goal

fact

fact

underpinning

data 1

data 2 data 3

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

Paper B:

data 4

data 5 data 6

implication

results

method

goal

fact

fact

data 1

data 2 data 3

17

PHC Growth arrestundergo

Eventually: trace roots of a claim: how many independent data points is it based on?

Paper A:implication

results

method

goal

fact

fact

Paper B:

data 4

data 5 data 6

implication

results

method

goal

fact

fact

data 1

data 2 data 3

method link

Scientific papers are stories, that persuade with data.

Scientific papers are stories, that persuade with data.

Scientific papers are stories, that persuade with data.

Sometimes the link to data is good:

And sometimes it’s not so good:

And sometimes it’s not so good:

And sometimes it’s not so good:

And sometimes it’s not so good:

Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne, Gully Burns and Cartic Ramakrishnan

Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne, Gully Burns and Cartic Ramakrishnan

1. Research: Each item in the system has metadata (including provenance) and relations to other data items added to it.

metadata

metadata

metadata

metadata

metadata

Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne, Gully Burns and Cartic Ramakrishnan

1. Research: Each item in the system has metadata (including provenance) and relations to other data items added to it.

metadata

metadata

metadata

metadata

metadata

2. Workflow: All data items created in the lab are added to a (lab-owned) workflow system.

Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne, Gully Burns and Cartic Ramakrishnan

1. Research: Each item in the system has metadata (including provenance) and relations to other data items added to it.

metadata

metadata

metadata

metadata

metadata

2. Workflow: All data items created in the lab are added to a (lab-owned) workflow system.

Rats were subjected to two grueling tests(click on fig 2 to see underlying data). These results suggest that the neurological pain pro-

3. Authoring: A paper is written in an authoring tool which can pull data with provenance from the workflow tool in the appropriate representation into the document.

Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne, Gully Burns and Cartic Ramakrishnan

1. Research: Each item in the system has metadata (including provenance) and relations to other data items added to it.

metadata

metadata

metadata

metadata

metadata

2. Workflow: All data items created in the lab are added to a (lab-owned) workflow system.

4. Editing and review: Once the co-authors agree, the paper is ‘exposed’ to the editors, who in turn expose it to reviewers. Reports are stored in the authoring/editing system, the paper gets updated, until it is validated.

Review

Edit

Revise

Rats were subjected to two grueling tests(click on fig 2 to see underlying data). These results suggest that the neurological pain pro-

3. Authoring: A paper is written in an authoring tool which can pull data with provenance from the workflow tool in the appropriate representation into the document.

5. Publishing and distribution: When a paper is published, a collection of validated information is exposed to the world. It remains connected to its related data item, and its heritage can be traced.

Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne, Gully Burns and Cartic Ramakrishnan

1. Research: Each item in the system has metadata (including provenance) and relations to other data items added to it.

metadata

metadata

metadata

metadata

metadata

2. Workflow: All data items created in the lab are added to a (lab-owned) workflow system.

4. Editing and review: Once the co-authors agree, the paper is ‘exposed’ to the editors, who in turn expose it to reviewers. Reports are stored in the authoring/editing system, the paper gets updated, until it is validated.

Review

Edit

Revise

Rats were subjected to two grueling tests(click on fig 2 to see underlying data). These results suggest that the neurological pain pro-

3. Authoring: A paper is written in an authoring tool which can pull data with provenance from the workflow tool in the appropriate representation into the document.

5. Publishing and distribution: When a paper is published, a collection of validated information is exposed to the world. It remains connected to its related data item, and its heritage can be traced.

Some other publisher

6. User applications: distributed applications run on this ‘exposed data’ universe.

Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne, Gully Burns and Cartic Ramakrishnan

1. Research: Each item in the system has metadata (including provenance) and relations to other data items added to it.

metadata

metadata

metadata

metadata

metadata

2. Workflow: All data items created in the lab are added to a (lab-owned) workflow system.

4. Editing and review: Once the co-authors agree, the paper is ‘exposed’ to the editors, who in turn expose it to reviewers. Reports are stored in the authoring/editing system, the paper gets updated, until it is validated.

Review

Edit

Revise

Rats were subjected to two grueling tests(click on fig 2 to see underlying data). These results suggest that the neurological pain pro-

3. Authoring: A paper is written in an authoring tool which can pull data with provenance from the workflow tool in the appropriate representation into the document.

One step: encouraging submission of structured workflows

Another step: ScienceDirect app store

Another step: ScienceDirect app store

- Eclipse SDK platform accessing all ScienceDirect/Scopus content

-Build applications on top of content-Offer to users in marketplace

A third step: Executable Paper ChallengeGoal: invite computer science community to help develop formats that:

- add executable files and reproducible data to computer science papers;

- handle storage and validation of very large files

- help validation of data and code, and decrease the reviewer’s workload

A third step: Executable Paper ChallengeGoal: invite computer science community to help develop formats that:

- add executable files and reproducible data to computer science papers;

- handle storage and validation of very large files

- help validation of data and code, and decrease the reviewer’s workload

In Summary:

In Summary:1. Stories:

- ORB, Satellite: link to any part of content - bring it on!

In Summary:1. Stories:

- ORB, Satellite: link to any part of content - bring it on!

2. Persuasion:

- Logical structure for biological propositions; trace a claim through successive citations

In Summary:1. Stories:

- ORB, Satellite: link to any part of content - bring it on!

2. Persuasion:

- Logical structure for biological propositions; trace a claim through successive citations

3. Data:

- Better data linking, better structuring of methods.

In Summary:1. Stories:

- ORB, Satellite: link to any part of content - bring it on!

2. Persuasion:

- Logical structure for biological propositions; trace a claim through successive citations

3. Data:

- Better data linking, better structuring of methods.

In conclusion: is the research paper going away?

In Summary:1. Stories:

- ORB, Satellite: link to any part of content - bring it on!

2. Persuasion:

- Logical structure for biological propositions; trace a claim through successive citations

3. Data:

- Better data linking, better structuring of methods.

In conclusion: is the research paper going away?

I don’t think so! But it will be:

- Structured better: authors will need to justify claims directly

- Connected better: more traceable, better links to data and workflow components, and to other work

Thank you!

W3C group on Discourse Structure: http://www.w3.org/wiki/HCLSIG/SWANSIOC SciVerse: http://developer.sciverse.comPangea project: http://bit.ly/98haOw Parsing rhetoric: http://elsatglabs.com/labs/anita/Fact creation demo: http://elsatglabs.com/labs/anita/demos/LATSDemo102007/Methods Navigator: http://www.methodsnavigator.comSciVerse APIs: http://developer.sciverse.comExecutable Paper Challenge: http://www.executablepapers.com

Or mail me at: Anita de Waard, a.dewaard@elsevier.com