Nell’iperspazio con Rocket: il Framework Web di Rust!
On the research paper, and the knowledge within
1. 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
2. Scientific papers are stories, that persuade with data.
The Story of Goldilocks and Story Part Paper The AXH Domain of Ataxin-1 Mediates
the Three Bears 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 Objects of study the Drosophila Atx-1 homolog (dAtx-1) which lacks a polyQ tract,
She went for a walk in the forest. Location Experimental studied and compared in vivo effects and interactions to those of the
Pretty soon, she came upon a house. setup human protein
She knocked and, when no one Goal Theme Research Gain insight into how Atx-1's function contributes to SCA1
answered, goal pathogenesis. How these interactions might contribute to the disease
process and how they might cause toxicity in only a subset of neurons in
she walked right in. Attempt Hypothesis SCA1 may play a role in the regulation of gene expression
Atx-1 is not fully understood.
At the table in the kitchen, there Name Episode 1 Name dAtX-1 and hAtx-1 Induce Similar Phenotypes When Overexpressed in
were three bowls of porridge. Files
Goldilocks was hungry. Subgoal Subgoal test the function of the AXH domain
She tasted the porridge from the Attempt Method overexpressed dAtx-1 in flies using the GAL4/UAS system (Brand and
first bowl. Perrimon, 1993) and compared its effects to those of hAtx-1.
This porridge is too hot! she Outcome Results Overexpression of dAtx-1 by Rhodopsin1(Rh1)-GAL4, which drives
exclaimed. 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
So, she tasted the porridge from the Activity Data (data not shown),
morphological changes in the photoreceptor cells
second bowl.
This porridge is too cold, she said Outcome Results both genotypes show many large holes and loss of cell integrity at 28
days
So, she tasted the last bowl of Activity Data (Figures 1B-1D).
porridge.
Ahhh, this porridge is just right, she Outcome Results Overexpression of dAtx-1 using the GMR-GAL4 driver also induces eye
said happily and abnormalities. The external structures of the eyes that overexpress
she ate it all up. Outcome Data dAtx-1 1F), disorganized ommatidia and loss of interommatidial bristles
(Figure show
3. Scientific papers are stories, that persuade with data.
The Story of Goldilocks and Story Part Paper The AXH Domain of Ataxin-1 Mediates
the Three Bears 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 Objects of study the Drosophila Atx-1 homolog (dAtx-1) which lacks a polyQ tract,
She went for a walk in the forest. Location Experimental studied and compared in vivo effects and interactions to those of the
Pretty soon, she came upon a house. setup human protein
She knocked and, when no one Goal Theme Research Gain insight into how Atx-1's function contributes to SCA1
answered, goal pathogenesis. How these interactions might contribute to the disease
process and how they might cause toxicity in only a subset of neurons in
she walked right in. Attempt Hypothesis SCA1 may play a role in the regulation of gene expression
Atx-1 is not fully understood.
At the table in the kitchen, there Name Episode 1 Name dAtX-1 and hAtx-1 Induce Similar Phenotypes When Overexpressed in
were three bowls of porridge. Files
Goldilocks was hungry. Subgoal Subgoal test the function of the AXH domain
She tasted the porridge from the Attempt Method overexpressed dAtx-1 in flies using the GAL4/UAS system (Brand and
first bowl. Perrimon, 1993) and compared its effects to those of hAtx-1.
This porridge is too hot! she Outcome Results Overexpression of dAtx-1 by Rhodopsin1(Rh1)-GAL4, which drives
exclaimed. 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
So, she tasted the porridge from the Activity Data (data not shown),
morphological changes in the photoreceptor cells
second bowl.
This porridge is too cold, she said Outcome Results both genotypes show many large holes and loss of cell integrity at 28
days
So, she tasted the last bowl of Activity Data (Figures 1B-1D).
porridge.
Ahhh, this porridge is just right, she Outcome Results Overexpression of dAtx-1 using the GMR-GAL4 driver also induces eye
said happily and abnormalities. The external structures of the eyes that overexpress
she ate it all up. Outcome Data dAtx-1 1F), disorganized ommatidia and loss of interommatidial bristles
(Figure show
5. 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.
6. Story grammar of fairytales:
F. Peinado, P. Gervas, and B. Diaz-Agudo, ʻA
description logic ontology for fairy tale
generationʼ, in Procs LREC. ELRA, (5 2004)
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.
7. Story grammar of fairytales:
F. Peinado, P. Gervas, and B. Diaz-Agudo, ʻA
description logic ontology for fairy tale
generationʼ, in Procs LREC. ELRA, (5 2004)
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.
13. Episode-level access through Linked Data standards:
said @anita
on April 5, 2011
this says
<ce:section id=#123> mice like cheese
14. Episode-level access through Linked Data standards:
but we all know
she was deluded then
said @anita
on April 5, 2011
this says
<ce:section id=#123> mice like cheese
15. Episode-level access through Linked Data standards:
the xml is fixed, but the structure is open!
but we all know
she was deluded then
said @anita
on April 5, 2011
this says
<ce:section id=#123> mice like cheese
16. Episode-level access through Linked Data standards:
the xml is fixed, but the structure is open! allows for layers of annotation
but we all know
she was deluded then
said @anita
on April 5, 2011
this says
<ce:section id=#123> mice like cheese
18. 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>
19. Satellites: Fragments
Use XPointer for XML documents, Media Fragments for image, video, audio.
XMLDocumentRegion, MediaRegion akin to Annotation Ontology Selectors
xpath1()* 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>
20. 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
miR-371-3 expressing seminomas and
nonseminomas, miR-302a-d was undetectable (Figs
S7 and S8), suggesting that miR-371-3 expression
is a selective event during tumorigenesis.
21. Scientific papers are stories,
that persuade with data.
Both seminomas and the EC component of
Both seminomas and the EC component of
nonseminomas share features with ES cells.
nonseminomas share features with ES cells. To
exclude thatthat detection of miR-371-3 merely
To exclude the
reflects its expression pattern in ES cells,reflects its
the detection of miR-371-3 merely we tested
by RPA miR-302a-d, another ES cells-specific
expression pattern in ES cells,
miRNA cluster RPA miR-302a-d, another ES cells-
we tested by (Suh et al, 2004). In many of the
m i R - 3 7 miRNAx p r e s s(Suh et e m2004). a s a n d
specific 1 - 3 e cluster i n g s al, i n o m
nonseminomas, miR-302a-d was undetectable (Figs
In many of the miR-371-3 expressing seminomas
S7 and S8), suggesting that miR-371-3undetectable
and nonseminomas, miR-302a-d was expression
is a selective event during tumorigenesis.
(Figs S7 and S8),
suggesting that
miR-371-3 expression is a selective event during
tumorigenesis.
22. Scientific papers are stories,
that persuade with data.
Both seminomas and the EC component of
Both seminomas and the EC component of Fact
nonseminomas share features with ES cells.
nonseminomas share features with ES cells. To
exclude thatthat detection of miR-371-3 merely
To exclude the Goal
reflects its expression pattern in ES cells,reflects its
the detection of miR-371-3 merely we tested Hypothesis
by RPA miR-302a-d, another ES cells-specific
expression pattern in ES cells,
miRNA cluster RPA miR-302a-d, another ES cells-
we tested by (Suh et al, 2004). In many of the
m i R - 3 7 miRNAx p r e s s(Suh et e m2004). a s a n d
specific 1 - 3 e cluster i n g s al, i n o m Method
nonseminomas, miR-302a-d was undetectable (Figs
In many of the miR-371-3 expressing seminomas
S7 and S8), suggesting that miR-371-3undetectable
and nonseminomas, miR-302a-d was expression Result
is a selective event during tumorigenesis.
(Figs S7 and S8),
suggesting that Reg-Implication
miR-371-3 expression is a selective event during
Implication
tumorigenesis.
23. Scientific papers are stories,
that persuade with data.
Conceptual
Both seminomas and the EC component of
Both seminomas and the EC component of knowledge
Fact
nonseminomas share features with ES cells.
nonseminomas share features with ES cells. To
exclude thatthat detection of miR-371-3 merely
To exclude the Goal
reflects its expression pattern in ES cells,reflects its
the detection of miR-371-3 merely we tested Hypothesis
by RPA miR-302a-d, another ES cells-specific
expression pattern in ES cells,
miRNA cluster RPA miR-302a-d, another ES cells-
we tested by (Suh et al, 2004). In many of the
m i R - 3 7 miRNAx p r e s s(Suh et e m2004). a s a n d
specific 1 - 3 e cluster i n g s al, i n o m Method
nonseminomas, miR-302a-d was undetectable (Figs
In many of the miR-371-3 expressing seminomas
S7 and S8), suggesting that miR-371-3undetectable
and nonseminomas, miR-302a-d was expression Result
is a selective event during tumorigenesis.
(Figs S7 and S8),
suggesting that Reg-Implication
miR-371-3 expression is a selective event during
Implication
tumorigenesis.
24. Scientific papers are stories,
that persuade with data.
Conceptual
Both seminomas and the EC component of
Both seminomas and the EC component of knowledge
Fact
nonseminomas share features with ES cells.
nonseminomas share features with ES cells. To
exclude thatthat detection of miR-371-3 merely
To exclude the Goal
reflects its expression pattern in ES cells,reflects its
the detection of miR-371-3 merely we tested Hypothesis
by RPA miR-302a-d, another ES cells-specific
expression pattern in ES cells,
miRNA cluster RPA miR-302a-d, another ES cells-
we tested by (Suh et al, 2004). In many of the
m i R - 3 7 miRNAx p r e s s(Suh et e m2004). a s a n d
specific 1 - 3 e cluster i n g s al, i n o m Method
Experimental
nonseminomas, miR-302a-d was undetectable (Figs
In many of the miR-371-3 expressing seminomas
Evidence
S7 and S8), suggesting that miR-371-3undetectable
and nonseminomas, miR-302a-d was expression Result
is a selective event during tumorigenesis.
(Figs S7 and S8),
suggesting that Reg-Implication
miR-371-3 expression is a selective event during
Implication
tumorigenesis.
26. Realms of persuasive experimental discourse:
(1) Both seminomas (2) b. the detection of (3) c. miR-371-3
and the EC component miR-371-3 merely expression is a
of nonseminomas share reflects its expression selective event during
features with ES cells. pattern in ES cells, tumorigenesis.
(2) a. To exclude that (3) b. suggesting that
(2) c. we tested by RPA (3) a. In many of the miR-371-3
miR-302a-d, another ES expressing seminomas and
cells-specific miRNA cluster nonseminomas, miR-302a-d was
(Suh et al, 2004). undetectable (Figs S7 and S8),
27. Realms of persuasive experimental discourse:
Concepts, models, ‘facts’
(1) Both seminomas (2) b. the detection of (3) c. miR-371-3
and the EC component miR-371-3 merely expression is a
of nonseminomas share reflects its expression selective event during
features with ES cells. pattern in ES cells, tumorigenesis.
(2) a. To exclude that Transitions (3) b. suggesting that
(2) c. we tested by RPA (3) a. In many of the miR-371-3
miR-302a-d, another ES expressing seminomas and
cells-specific miRNA cluster nonseminomas, miR-302a-d was
(Suh et al, 2004). undetectable (Figs S7 and S8),
Experiment
28. Realms of persuasive experimental discourse:
Concepts, models, ‘facts’ ‘State’ present tense
(1) Both seminomas (2) b. the detection of (3) c. miR-371-3
and the EC component miR-371-3 merely expression is a
of nonseminomas share reflects its expression selective event during
features with ES cells. pattern in ES cells, tumorigenesis.
(2) a. To exclude that Transitions (3) b. suggesting that
(2) c. we tested by RPA (3) a. In many of the miR-371-3
miR-302a-d, another ES expressing seminomas and
cells-specific miRNA cluster nonseminomas, miR-302a-d was
(Suh et al, 2004). undetectable (Figs S7 and S8),
Experiment ‘Narrative’ past tense
29. Fact creation through citations:
Voorhoeve et al, Cell, 2006:
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,
30. Fact creation through citations:
Voorhoeve et al, Cell, 2006:
To investigate the possibility that miR-372 and miR-373 suppress the Hypothesis
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,
31. Fact creation through citations:
Voorhoeve et al, Cell, 2006:
To investigate the possibility that miR-372 and miR-373 suppress the Hypothesis
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, Implication
32. Fact creation through citations:
Voorhoeve et al, Cell, 2006:
To investigate the possibility that miR-372 and miR-373 suppress the Hypothesis
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, Implication
Raver-Shapira et.al, JMolCell 2007
... 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).
33. Fact creation through citations:
Voorhoeve et al, Cell, 2006:
To investigate the possibility that miR-372 and miR-373 suppress the Hypothesis
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, Implication
Raver-Shapira et.al, JMolCell 2007 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).
34. Fact creation through citations:
Voorhoeve et al, Cell, 2006:
To investigate the possibility that miR-372 and miR-373 suppress the Hypothesis
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, Implication
Raver-Shapira et.al, JMolCell 2007 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).
Yabuta, JBioChem 2007:
miR-372 and miR-373 target the Lats2 tumor suppressor (Voorhoeve et al., 2006)
35. Fact creation through citations:
Voorhoeve et al, Cell, 2006:
To investigate the possibility that miR-372 and miR-373 suppress the Hypothesis
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, Implication
Raver-Shapira et.al, JMolCell 2007 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).
Yabuta, JBioChem 2007: Fact
miR-372 and miR-373 target the Lats2 tumor suppressor (Voorhoeve et al., 2006)
36. “[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
37. “[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
39. The logical structure of a scientific claim
- A Proposition P is about entities, relations, events, actions…
40. 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, +,-)
41. 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)).
42. 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.
43. How is this rhetoric instantiated?
Rhetorical Utterance {Proposition} S= V=
goal H, B C, E
Indicate lack of {The role of untranslated exons in the CCR3 gene} NN 0
knowledge has not been studied.
Evaluate other Recently, CCR3 has been shown to {be upregulated N, D 3
work on neutrophils by interferons in vitro [..]}
Offer it is thought that {these transcription factors affect NN, R 2
hypotheses transcription of the gene through interactions with the
RNA transcription complex.}
Interpret results these data suggested that {5' untranslated exon A, D 2
1 may have a regulatory function.}
Assess validity of Since {this was not the case with other lines,} {we A, D 1
interpretations suspect {it is integration-site specific}}
State While we expected {the transcript to be about 1 kb A, D 2, S+
correspondence in size (Figure 4A),} {two bands ~4 and 5 kb were
to expectations apparent.}
Comparison to It is important that {this data be viewed A,R/ 2, F+
other work with {what is known about other myeloid- NN/D
specific promoters,}}
44. One application: improve text mining:
insulin ::: maintaining glucose ... diabetes defect) to overcome
GB00084 homeostasis insulin resistance in maintaining
1 glucose homeostasis,
hyperglycemia and glucose
intolerance ...
improve glucose ... in T2D is able to increase
homeostasis insulin secretion and improve
glucose homeostasis.
improves glucose ... SIRT1, whose administration
homeostasis to insulin-resistant animals
improves glucose homeostasis.
is capable glucose S15511 is a novel insulin
homeostasis sensitizer that is capable of
improving glucose homeostasis
in nondiabetic rats.
maintains glucose Pancreatic beta-cells possess a
homeostasis well-regulated insulin secretory
property that maintains
systemic glucose homeostasis.
may be glucose ... similar way to those of
involved homeostasis insulin, PANDER may be
involved in glucose homeostasis.
participates glucose Fine-tuning of insulin secretion
homeostasis from pancreatic beta-cells
participates in blood glucose
homeostasis.
45. One application: improve text mining:
insulin ::: maintaining glucose ... diabetes defect) to overcome When insulin secretion cannot be increased adequately (type I diabetes
defect) to overcome insulin resistance in maintaining glucose homeostasis,
GB00084 homeostasis insulin resistance in maintaining hyperglycemia and glucose intolerance ensues. Insulin resistance and glucose
1 glucose homeostasis, intolerance has been well recognized in patients with advanced
hyperglycemia and glucose chronic kidney diseases (CKD).
intolerance ...
improve glucose ... in T2D is able to increase .. Incretin metabolism is abnormal in T2D, evidenced by a decreased
incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in
homeostasis insulin secretion and improve T2D, and resistance to GIP. GLP-1, on the other hand, when administered
glucose homeostasis. intravenously in T2D is able to increase insulin secretion and improve glucose
homeostasis.
improves glucose ... SIRT1, whose administration SIRT1, a NAD(+)-dependent protein deacetylase that regulates transcription
factors involved in key cellular processes, has been implicated as a mediator
homeostasis to insulin-resistant animals of the beneficial effects of calorie restriction. In a recent issue of Nature,
improves glucose homeostasis. Milne et al. (2007) describe novel potent activators of SIRT1, whose
administration to insulin-resistant animals improves glucose homeostasis.
is capable glucose S15511 is a novel insulin S15511 is a novel insulin sensitizer that is capable of improving glucose
homeostasis in nondiabetic rats.... However, the mechanisms behind the insulin-
homeostasis sensitizer that is capable of sensitizing effect of S15511 are unknown. The aim of our study was
improving glucose homeostasis to explore whether S15511 improves insulin sensitivity in skeletal
in nondiabetic rats. muscles. S15511 treatment was associated with an increase in insulin-
stimulated glucose transport in type IIb fibers, while type I fibers were
unaffected.
maintains glucose Pancreatic beta-cells possess a Pancreatic beta-cells possess a well-regulated insulin secretory property that
maintains systemic glucose homeostasis. Although it has long been
homeostasis well-regulated insulin secretory thought that differentiated beta-cells are nearly static, recent studies
property that maintains have shown that beta-cell mass dynamically changes throughout the
systemic glucose homeostasis. lifetime. In this article, recent progress of regenerative medicine of the
pancreas is reviewed.
may be glucose ... similar way to those of ... Our results showed that glucose up-regulated PANDER mRNA and
involved homeostasis insulin, PANDER may be protein levels in a time- and dose-dependent manner in MIN6 cells and
pancreatic islets. ...Because PANDER is expressed by pancreatic beta-cells
involved in glucose homeostasis. and in response to glucose in a similar way to those of insulin, PANDER may be
involved in glucose homeostasis.
participates glucose Fine-tuning of insulin secretion Fine-tuning of insulin secretion from pancreatic beta-cells participates in blood
homeostasis from pancreatic beta-cells glucose homeostasis. ... Our data identify miR124a and miR96 as novel
regulators of the expression of proteins playing a critical role in insulin
participates in blood glucose exocytosis and in the release of other hormones and neurotransmitters.
homeostasis.
46. One application: improve text mining:
insulin ::: maintaining glucose ... diabetes defect) to overcome When insulin secretion cannot be increased adequately (type I diabetes
defect) to overcome insulin resistance in maintaining glucose homeostasis,
GB00084 homeostasis insulin resistance in maintaining hyperglycemia and glucose intolerance ensues. Insulin resistance and glucose
1 glucose homeostasis, intolerance has been well recognized in patients with advanced
hyperglycemia and glucose chronic kidney diseases (CKD).
intolerance ...
improve glucose ... in T2D is able to increase .. Incretin metabolism is abnormal in T2D, evidenced by a decreased
incretin effect, reduction in nutrient-mediated secretion of GIP and GLP-1 in
homeostasis insulin secretion and improve T2D, and resistance to GIP. GLP-1, on the other hand, when administered
glucose homeostasis. intravenously in T2D is able to increase insulin secretion and improve glucose
homeostasis.
improves glucose ... SIRT1, whose administration SIRT1, a NAD(+)-dependent protein deacetylase that regulates transcription
factors involved in key cellular processes, has been implicated as a mediator
homeostasis to insulin-resistant animals of the beneficial effects of calorie restriction. In a recent issue of Nature,
improves glucose homeostasis. Milne et al. (2007) describe novel potent activators of SIRT1, whose
administration to insulin-resistant animals improves glucose homeostasis.
is capable glucose S15511 is a novel insulin S15511 is a novel insulin sensitizer that is capable of improving glucose
homeostasis in nondiabetic rats.... However, the mechanisms behind the insulin-
homeostasis sensitizer that is capable of sensitizing effect of S15511 are unknown. The aim of our study was
improving glucose homeostasis to explore whether S15511 improves insulin sensitivity in skeletal
in nondiabetic rats. muscles. S15511 treatment was associated with an increase in insulin-
stimulated glucose transport in type IIb fibers, while type I fibers were
unaffected.
maintains glucose Pancreatic beta-cells possess a Pancreatic beta-cells possess a well-regulated insulin secretory property that
maintains systemic glucose homeostasis. Although it has long been
homeostasis well-regulated insulin secretory thought that differentiated beta-cells are nearly static, recent studies
property that maintains have shown that beta-cell mass dynamically changes throughout the
systemic glucose homeostasis. lifetime. In this article, recent progress of regenerative medicine of the
pancreas is reviewed.
may be glucose ... similar way to those of ... Our results showed that glucose up-regulated PANDER mRNA and
involved homeostasis insulin, PANDER may be protein levels in a time- and dose-dependent manner in MIN6 cells and
pancreatic islets. ...Because PANDER is expressed by pancreatic beta-cells
involved in glucose homeostasis. and in response to glucose in a similar way to those of insulin, PANDER may be
involved in glucose homeostasis.
participates glucose Fine-tuning of insulin secretion Fine-tuning of insulin secretion from pancreatic beta-cells participates in blood
homeostasis from pancreatic beta-cells glucose homeostasis. ... Our data identify miR124a and miR96 as novel
regulators of the expression of proteins playing a critical role in insulin
participates in blood glucose exocytosis and in the release of other hormones and neurotransmitters.
homeostasis.
47. Other application: improve citations
!
Model of phenomenon
time = t+1
?
Model of phenomenon
time = t
Domain Model
(C) Ed Hovy
48. Other application: improve citations
!
Model of phenomenon
time = t+1
?
Model of phenomenon
time = t
Domain Model
(C) Ed Hovy
49. Other application: improve citations
!
Model of phenomenon
time = t+1
?
Citation:
Model of phenomenon • ‘Lifts’ claim from previous paper
and add it to current paper
time = t • We need ‘rules for legal lifting’:
• Express author’s claim truly
Domain Model • Maintain (experimental) content
• Apply appropriately
(C) Ed Hovy
50. Other application: improve citations
!
Model of phenomenon
time = t+1
?
Citation:
Model of phenomenon • ‘Lifts’ claim from previous paper
and add it to current paper
time = t • We need ‘rules for legal lifting’:
• Express author’s claim truly
Domain Model • Maintain (experimental) content
• Apply appropriately
What does this mean?
(C) Ed Hovy
52. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
17
53. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A:
implication
method fact
goal fact
results
17
54. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A:
implication
method fact
goal fact
results
data 1
data 2 data 3
17
55. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A: Paper B:
implication implication
method fact method fact
goal fact goal fact
results
results
data 1
data 4
data 2 data 3
data 5 data 6
17
56. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A: Paper B:
implication implication
method fact method fact
goal fact goal fact
results
results
data 1
data 4
data 2 data 3
data 5 data 6
17
57. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A: Paper B:
implication implication
method fact method fact
goal fact goal fact
results
results
data 1
data 4
data 2 data 3
data 5 data 6
17
58. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A: Paper B:
implication implication
g
nnin
method fact rpi method
de fact
un
goal fact goal fact
results
results
data 1
data 4
data 2 data 3
data 5 data 6
17
59. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A: Paper B:
implication implication
method fact method fact
goal fact goal fact
results
results
data 1
data 4
data 2 data 3
data 5 data 6
17
60. Eventually: trace roots of a claim:
how many independent data points is it based on?
PHC undergo Growth arrest
Paper A: Paper B:
implication implication
method method link
fact method fact
goal fact goal fact
results
results
data 1
data 4
data 2 data 3
data 5 data 6
17
69. Can we make data-driven papers? Work done with Ed Hovy, Phil Bourne,
Gully Burns and Cartic Ramakrishnan
70. 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
metadata (including provenance) and relations to other data items
metadata added to it.
metadata
metadata
metadata
71. 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
metadata (including provenance) and relations to other data items
metadata added to it.
2. Workflow: All data items created in the lab are added
metadata
to a (lab-owned) workflow system.
metadata
metadata
72. 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
metadata (including provenance) and relations to other data items
metadata added to it.
2. Workflow: All data items created in the lab are added
metadata
to a (lab-owned) workflow system.
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.
metadata
metadata
Rats were subjected to two grueling
tests
(click on fig 2 to see underlying
data). These results suggest that the
neurological pain pro-
73. 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
metadata (including provenance) and relations to other data items
metadata added to it.
2. Workflow: All data items created in the lab are added
metadata
to a (lab-owned) workflow system.
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.
metadata 4. Editing and review: Once the co-authors agree, the
paper is ‘exposed’ to the editors, who in turn expose it to
metadata reviewers. Reports are stored in the authoring/editing
system, the paper gets updated, until it is validated.
Rats were subjected to two grueling
tests
(click on fig 2 to see underlying
data). These results suggest that the
neurological pain pro-
Review
Revise
Edit
74. 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
metadata (including provenance) and relations to other data items
metadata added to it.
2. Workflow: All data items created in the lab are added
metadata
to a (lab-owned) workflow system.
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.
metadata 4. Editing and review: Once the co-authors agree, the
paper is ‘exposed’ to the editors, who in turn expose it to
metadata reviewers. Reports are stored in the authoring/editing
system, the paper gets updated, until it is validated.
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
Rats were subjected to two grueling data item, and its heritage can be traced.
tests
(click on fig 2 to see underlying
data). These results suggest that the
neurological pain pro-
Review
Revise
Edit
75. 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
metadata (including provenance) and relations to other data items
metadata added to it.
2. Workflow: All data items created in the lab are added
metadata
to a (lab-owned) workflow system.
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.
metadata 4. Editing and review: Once the co-authors agree, the
paper is ‘exposed’ to the editors, who in turn expose it to
metadata reviewers. Reports are stored in the authoring/editing
system, the paper gets updated, until it is validated.
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
Rats were subjected to two grueling data item, and its heritage can be traced.
tests
(click on fig 2 to see underlying 6. User applications: distributed applications run on this
data). These results suggest that the ‘exposed data’ universe.
neurological pain pro-
Some other publisher
Review
Revise
Edit
78. Another step: ScienceDirect app store
- Eclipse SDK platform accessing all
ScienceDirect/Scopus content
- Build applications on top of content
- Offer to users in marketplace
79. A third step: Executable Paper Challenge
Goal: 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
80. A third step: Executable Paper Challenge
Goal: 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
83. 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
84. 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.
85. 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?
86. 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
87. Thank you!
W3C group on Discourse Structure:
http://www.w3.org/wiki/HCLSIG/SWANSIOC
SciVerse: http://developer.sciverse.com
Pangea 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.com
SciVerse APIs: http://developer.sciverse.com
Executable Paper Challenge: http://www.executablepapers.com
Or mail me at:
Anita de Waard, a.dewaard@elsevier.com