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[don.git] / resume / research_statement.mdwn

diff --git a/resume/research_statement.mdwn b/resume/research_statement.mdwn
index 078bbe96abea73baddae92a07e0f7981d225d739..a2c382a409f7a98e5ec00ed3bb75d7f60b4667b8 100644 (file)
--- a/resume/research_statement.mdwn
+++ b/resume/research_statement.mdwn
@@ -51,18 +51,18 @@ I developed novel bioinformatic methods which increase
 
 likelihood of identifying reproducible genetic associations using
 prior knowledge from publicly available databases and expert
 
 likelihood of identifying reproducible genetic associations using
 prior knowledge from publicly available databases and expert

-information [#Armstrong2008:function2gene]. Using these methods, I
-was able to identify genes previously unassociated with SLE in a
-trio-based study [#Jacob2007:ar_lupus]. These genes were then
+information [^Armstrong2008:function2gene]. Using these methods, I was
+able to identify genes previously unassociated with SLE in a
+trio-based study [^Jacob2007:ar_lupus]. These genes were then

 replicated in a larger case-control study which was funded by the NIH
 replicated in a larger case-control study which was funded by the NIH

-on the basis of the original findings
-[#Jacob2009:sle_irak1],[#Armstrong2009:sle_gi]. Among other findings,
-this larger study identified a missense allele in NCF2 (H389Q,
-rs17849502) which was associated with SLE. Collaborative work
-indicated that H389Q altered the binding energy of NCF2 with VAV1
-using docking simulations, and in vitro experiments confirmed that
-H389Q altered NADPH oxidase function [#Jacob2012:sle_ncf2], thus
-identifying it as a causative SLE mutation.
+on the basis of the original findings [^Jacob2009:sle_irak1],[^Armstrong2009:sle_gi].
+Among other findings, this larger study
+identified a missense allele in NCF2 (H389Q, rs17849502) which was
+associated with SLE. Collaborative work indicated that H389Q altered
+the binding energy of NCF2 with VAV1 using docking simulations, and in
+vitro experiments confirmed that H389Q altered NADPH oxidase function
+[^Jacob2012:sle_ncf2], thus identifying it as a causative SLE
+mutation.

 
 ## Cancer Stem Cells in Glioblastoma
 
 
 ## Cancer Stem Cells in Glioblastoma
 


@@ -86,7 +86,7 @@ indentified multiple gene regulation pathways, many of them novel,
 including the Id1/Thsb1 inhibitory pathway. Additional experiments
 indicated that the *in vitro* pathology of endothelial cells could be
 partially rescued using extracellular Thsb1
 including the Id1/Thsb1 inhibitory pathway. Additional experiments
 indicated that the *in vitro* pathology of endothelial cells could be
 partially rescued using extracellular Thsb1

-[#Stapleton2011:thbs1].
+[^Stapleton2011:thbs1].

 
 # Future research directions
 
 
 # Future research directions
 


@@ -204,39 +204,41 @@ be able to build upon and improve my tools without being forced to
 reinvent them.
 
 
 reinvent them.
 
 

-[#Armstrong2009:sle_gi]: D L Armstrong et al. “Identification of new SLE-associated genes with a two-step
+[^Armstrong2009:sle_gi]: D L Armstrong et al. “Identification of new SLE-associated genes with a two-step

     Bayesian study design”. In: Genes Immun. 10.5 (July 2009), pp. 446–456. doi:
     Bayesian study design”. In: Genes Immun. 10.5 (July 2009), pp. 446–456. doi:

-    10.1038/gene.2009.38.
+    [10.1038/gene.2009.38](http://dx.doi.org/10.1038/gene.2009.38).

     
     

-[#Armstrong2008:function2gene]: Don L Armstrong, Chaim O Jacob, and Raphael Zidovetzki. “Function2Gene: a
+[^Armstrong2008:function2gene]: Don L Armstrong, Chaim O Jacob, and Raphael Zidovetzki. “Function2Gene: a

     gene selection tool to increase the power of genetic association studies by utilizing
     public databases and expert knowledge”. In: BMC Bioinformatics 9 (2008), p. 311.
     gene selection tool to increase the power of genetic association studies by utilizing
     public databases and expert knowledge”. In: BMC Bioinformatics 9 (2008), p. 311.

-    doi: 10.1186/1471-2105-9-311.
+    doi: [10.1186/1471-2105-9-311](http://dx.doi.org/10.1186/1471-2105-9-311).

     
     

-[#Jacob2009:sle_irak1]: Chaim O Jacob et al. “Identification of IRAK1 as a risk gene with critical role
-       in the pathogenesis of systemic lupus erythematosus”. In: Proc. Natl. Acad. Sci.
-        U.S.A. 106.15 (Apr. 2009), pp. 6256–6261. doi: 10.1073/pnas.0901181106.
+[^Jacob2009:sle_irak1]: Chaim O Jacob et al. “Identification of IRAK1 as a risk gene with critical role
+    in the pathogenesis of systemic lupus erythematosus”. In: Proc. Natl. Acad. Sci.
+    U.S.A. 106.15 (Apr. 2009), pp. 6256–6261. doi: [10.1073/pnas.0901181106](http://dx.doi.org/10.1073/pnas.0901181106).

 
 

-[#Jacob2007:ar_lupus]: Chaim O Jacob et al. “Identification of novel susceptibility genes in childhood-
+[^Jacob2007:ar_lupus]: Chaim O Jacob et al. “Identification of novel susceptibility genes in childhood-

     onset systemic lupus erythematosus using a uniquely designed candidate gene
     pathway platform”. In: Arthritis Rheum. 56.12 (Dec. 2007), pp. 4164–4173. doi:
     onset systemic lupus erythematosus using a uniquely designed candidate gene
     pathway platform”. In: Arthritis Rheum. 56.12 (Dec. 2007), pp. 4164–4173. doi:

-    10.1002/art.23060.
+    [10.1002/art.23060](http://dx.doi.org/10.1002/art.23060).

 
 

-[#Jacob2012:sle_ncf2]: Chaim O Jacob et al. “Lupus-associated causal mutation in neutrophil cytosolic
+[^Jacob2012:sle_ncf2]: Chaim O Jacob et al. “Lupus-associated causal mutation in neutrophil cytosolic

     factor 2 (NCF2) brings unique insights to the structure and function of NADPH
     oxidase”. In: Proc. Natl. Acad. Sci. U.S.A. 109.2 (Jan. 2012), pp. 59–67. doi:
     factor 2 (NCF2) brings unique insights to the structure and function of NADPH
     oxidase”. In: Proc. Natl. Acad. Sci. U.S.A. 109.2 (Jan. 2012), pp. 59–67. doi:

-       10.1073/pnas.1113251108.
+       [10.1073/pnas.1113251108](http://dx.doi.org/10.1073/pnas.1113251108).

 
 

-[#Stapleton2011:thbs1]: Christopher J Stapleton et al. “Thrombospondin-1 modulates the angiogenic phe-
-     notype of human cerebral arteriovenous malformation endothelial cells”. In: Neu-
-      rosurgery 68.5 (May 2011), pp. 1342–1353. doi: 10.1227/NEU.0b013e31820c0a68.
+[^Stapleton2011:thbs1]: Christopher J Stapleton et al.
+     “Thrombospondin-1 modulates the angiogenic phe- notype of human
+     cerebral arteriovenous malformation endothelial cells”. In:
+     Neurosurgery 68.5 (May 2011), pp. 1342–1353.
+     doi: [10.1227/NEU.0b013e31820c0a68](http://dx.doi.org/10.1227/NEU.0b013e31820c0a68).

 
 

-[survival_rate]: Only 4% of patients survive to 5 years after diagnosis
+[^survival_rate]: Only 4% of patients survive to 5 years after diagnosis

 
 

-[avm_definition]: Direct artery to vein connection without an
+[^avm_definition]: Direct artery to vein connection without an

     intervening capilary bed; leads to high pressure arterial flow in
     venous tissue and can lead to hemmorrhage and death.
 
     intervening capilary bed; leads to high pressure arterial flow in
     venous tissue and can lead to hemmorrhage and death.
 

-[extending_note]: and extending existing open source tools where they
+[^extending_note]: and extending existing open source tools where they

     exist
 
     exist