diff --git a/CNAME.sample b/CNAME.sample
new file mode 100644
index 0000000..3c1d59e
--- /dev/null
+++ b/CNAME.sample
@@ -0,0 +1 @@
+dyndna.github.io/lanyon-plus
diff --git a/Gemfile b/Gemfile
index c917492..9af5a4c 100644
--- a/Gemfile
+++ b/Gemfile
@@ -1,27 +1,14 @@
-source "https://rubygems.org"
+source 'https://rubygems.org'
-# Hello! This is where you manage which Jekyll version is used to run.
-# When you want to use a different version, change it below, save the
-# file and run `bundle install`. Run Jekyll with `bundle exec`, like so:
-#
-# bundle exec jekyll serve
-#
-# This will help ensure the proper Jekyll version is running.
-# Happy Jekylling!
-gem "jekyll", "3.5.1"
-
-# This is the default theme for new Jekyll sites. You may change this to anything you like.
-gem "minima", "~> 2.0"
-
-# If you want to use GitHub Pages, remove the "gem "jekyll"" above and
-# uncomment the line below. To upgrade, run `bundle update github-pages`.
-# gem "github-pages", group: :jekyll_plugins
-
-# If you have any plugins, put them here!
group :jekyll_plugins do
- gem "jekyll-feed", "~> 0.6"
+gem 'jekyll'
+gem 'jekyll-sitemap'
+gem 'jemoji'
+gem 'jekyll-redirect-from'
+gem 'jekyll-paginate'
+gem 'jekyll-compose'
end
-# Windows does not include zoneinfo files, so bundle the tzinfo-data gem
-gem 'tzinfo-data', platforms: [:mingw, :mswin, :x64_mingw, :jruby]
-
+gem 'font-awesome-sass'
+gem 'kramdown'
+gem 'rouge'
diff --git a/Gemfile.lock b/Gemfile.lock
index 41e9682..18f9584 100644
--- a/Gemfile.lock
+++ b/Gemfile.lock
@@ -1,58 +1,75 @@
GEM
remote: https://rubygems.org/
specs:
- addressable (2.5.1)
- public_suffix (~> 2.0, >= 2.0.2)
- colorator (1.1.0)
- ffi (1.9.18)
- forwardable-extended (2.6.0)
- jekyll (3.5.1)
- addressable (~> 2.4)
- colorator (~> 1.0)
+ activesupport (4.2.5)
+ i18n (~> 0.7)
+ json (~> 1.7, >= 1.7.7)
+ minitest (~> 5.1)
+ thread_safe (~> 0.3, >= 0.3.4)
+ tzinfo (~> 1.1)
+ colorator (0.1)
+ ffi (1.9.10)
+ font-awesome-sass (4.5.0)
+ sass (>= 3.2)
+ gemoji (2.1.0)
+ html-pipeline (2.2.2)
+ activesupport (>= 2, < 5)
+ nokogiri (>= 1.4)
+ i18n (0.7.0)
+ jekyll (3.0.1)
+ colorator (~> 0.1)
jekyll-sass-converter (~> 1.0)
jekyll-watch (~> 1.1)
kramdown (~> 1.3)
- liquid (~> 4.0)
+ liquid (~> 3.0)
mercenary (~> 0.3.3)
- pathutil (~> 0.9)
rouge (~> 1.7)
safe_yaml (~> 1.0)
- jekyll-feed (0.9.2)
- jekyll (~> 3.3)
- jekyll-sass-converter (1.5.0)
+ jekyll-compose (0.4.1)
+ jekyll (>= 2.5.0)
+ jekyll-paginate (1.1.0)
+ jekyll-redirect-from (0.9.1)
+ jekyll (>= 2.0)
+ jekyll-sass-converter (1.4.0)
sass (~> 3.4)
- jekyll-watch (1.5.0)
- listen (~> 3.0, < 3.1)
- kramdown (1.14.0)
- liquid (4.0.0)
- listen (3.0.8)
- rb-fsevent (~> 0.9, >= 0.9.4)
- rb-inotify (~> 0.9, >= 0.9.7)
- mercenary (0.3.6)
- minima (2.1.1)
- jekyll (~> 3.3)
- pathutil (0.14.0)
- forwardable-extended (~> 2.6)
- public_suffix (2.0.5)
- rb-fsevent (0.10.2)
- rb-inotify (0.9.10)
- ffi (>= 0.5.0, < 2)
- rouge (1.11.1)
+ jekyll-sitemap (0.9.0)
+ jekyll-watch (1.3.0)
+ listen (~> 3.0)
+ jemoji (0.5.1)
+ gemoji (~> 2.0)
+ html-pipeline (~> 2.2)
+ jekyll (>= 2.0)
+ json (1.8.3)
+ kramdown (1.9.0)
+ liquid (3.0.6)
+ listen (3.0.5)
+ rb-fsevent (>= 0.9.3)
+ rb-inotify (>= 0.9)
+ mercenary (0.3.5)
+ mini_portile2 (2.0.0)
+ minitest (5.8.3)
+ nokogiri (1.6.7.1)
+ mini_portile2 (~> 2.0.0.rc2)
+ rb-fsevent (0.9.7)
+ rb-inotify (0.9.5)
+ ffi (>= 0.5.0)
+ rouge (1.10.1)
safe_yaml (1.0.4)
- sass (3.5.1)
- sass-listen (~> 4.0.0)
- sass-listen (4.0.0)
- rb-fsevent (~> 0.9, >= 0.9.4)
- rb-inotify (~> 0.9, >= 0.9.7)
+ sass (3.4.21)
+ thread_safe (0.3.5)
+ tzinfo (1.2.2)
+ thread_safe (~> 0.1)
PLATFORMS
ruby
DEPENDENCIES
- jekyll (= 3.5.1)
- jekyll-feed (~> 0.6)
- minima (~> 2.0)
- tzinfo-data
-
-BUNDLED WITH
- 1.15.3
+ font-awesome-sass
+ jekyll
+ jekyll-compose
+ jekyll-paginate
+ jekyll-redirect-from
+ jekyll-sitemap
+ jemoji
+ kramdown
+ rouge
diff --git a/LICENSE.md b/LICENSE.md
new file mode 100644
index 0000000..af1b0ec
--- /dev/null
+++ b/LICENSE.md
@@ -0,0 +1,9 @@
+# Released under MIT License
+
+Copyright (c) 2014 Mark Otto.
+
+Permission is hereby granted, free of charge, to any person obtaining a copy of this software and associated documentation files (the "Software"), to deal in the Software without restriction, including without limitation the rights to use, copy, modify, merge, publish, distribute, sublicense, and/or sell copies of the Software, and to permit persons to whom the Software is furnished to do so, subject to the following conditions:
+
+The above copyright notice and this permission notice shall be included in all copies or substantial portions of the Software.
+
+THE SOFTWARE IS PROVIDED "AS IS", WITHOUT WARRANTY OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO THE WARRANTIES OF MERCHANTABILITY, FITNESS FOR A PARTICULAR PURPOSE AND NONINFRINGEMENT. IN NO EVENT SHALL THE AUTHORS OR COPYRIGHT HOLDERS BE LIABLE FOR ANY CLAIM, DAMAGES OR OTHER LIABILITY, WHETHER IN AN ACTION OF CONTRACT, TORT OR OTHERWISE, ARISING FROM, OUT OF OR IN CONNECTION WITH THE SOFTWARE OR THE USE OR OTHER DEALINGS IN THE SOFTWARE.
\ No newline at end of file
diff --git a/_config.yml b/_config.yml
index f2ea175..cebca3e 100644
--- a/_config.yml
+++ b/_config.yml
@@ -1,43 +1,102 @@
-# Welcome to Jekyll!
+# Permalinks
#
-# This config file is meant for settings that affect your whole blog, values
-# which you are expected to set up once and rarely edit after that. If you find
-# yourself editing this file very often, consider using Jekyll's data files
-# feature for the data you need to update frequently.
-#
-# For technical reasons, this file is *NOT* reloaded automatically when you use
-# 'bundle exec jekyll serve'. If you change this file, please restart the server process.
+# Use of `relative_permalinks` ensures post links from the index work properly.
+#permalink: pretty
+permalink: /blog/:year/:month/:day/:title/
+relative_permalinks: false
-# Site settings
-# These are used to personalize your new site. If you look in the HTML files,
-# you will see them accessed via {{ site.title }}, {{ site.email }}, and so on.
-# You can create any custom variable you would like, and they will be accessible
-# in the templates via {{ site.myvariable }}.
-title: Wild Toad
-email: your-email@example.com
-description: > # this means to ignore newlines until "baseurl:"
- Write an awesome description for your new site here. You can edit this
- line in _config.yml. It will appear in your document head meta (for
- Google search results) and in your feed.xml site description.
-baseurl: "" # the subpath of your site, e.g. /blog
-url: "" # the base hostname & protocol for your site, e.g. http://example.com
-twitter_username: jekyllrb
-github_username: jekyll
-
-# Build settings
+# Setup
+title: foo
+#tagline: 'foo's website
+description: Foo's blog...
+url: https://dyndna.github.io/lanyon-plus
+baseurl: "/lanyon-plus"
+urlimg: https://dyndna.github.io/lanyon-plus/images/
markdown: kramdown
-theme: minima
-plugins:
- - jekyll-feed
+paginate: 5
+paginate_path: "/blog/page:num"
+excerpt_separator:
+default_bg: sitelogo.png
+safe: false
+#timezone: America/Chicago
+future: true
-# Exclude from processing.
-# The following items will not be processed, by default. Create a custom list
-# to override the default setting.
-exclude:
- - Gemfile
- - Gemfile.lock
- - node_modules
-# - vendor/bundle/
-# - vendor/cache/
-# - vendor/gems/
- - vendor/ruby/
+gems:
+ - jekyll-paginate
+ - jemoji
+ - font-awesome-sass
+ - kramdown
+ - rouge
+
+include: [".htaccess"]
+exclude: ["lib", "config.rb", "Gemfile", "Capfile", "Gemfile.lock", "config", "log", "Rakefile", "Rakefile.rb", "rakefile", "README.md", "tmp", "less", "*.sublime-project", "*.sublime-workspace", "test", "spec", "Gruntfile.js", "package.json", "node_modules", "LICENSE", "vendor", "assets", "_plugins", "public/dormant"]
+
+# About/contact
+author:
+ name: Foo Boo
+ url: https://twitter.com/abcd
+ avatar: foo.png
+ #email:
+
+# Owner/author information
+owner:
+ name: Foo Boo
+ avatar: foo.png
+ #email:
+ # Use the coder's toolbox at http://coderstoolbox.net/string/#!encoding=xml&action=encode&charset=us_ascii to encode your description into XML string
+ description:
+ # Social networking links used in footer. Update and remove as you like.
+ twitter: abcd
+ facebook:
+ github: xyz123abc
+ stackexchange:
+ linkedin: https://www.linkedin.com/in/foo
+ instagram:
+ flickr:
+ tumblr:
+ google_plus: https://plus.google.com/+foo
+ # orcid and google scholar IDs are different than standard username.
+ orcid: xyz123abc
+ gscholar: xyz123abc
+
+## sidebar links:
+# For external links add external: true
+links:
+ - title: Home
+ url: /
+ - title: About
+ url: /about/
+ - title: Blog
+ url: /blog/
+ - title: Tags
+ url: /tags/
+ - title: Archive
+ url: /archive/
+ - title: Old Blog
+ url: https://foo.wordpress.com
+ external: true
+ - title: Contact
+ url: /contact/
+ - title: Twitter
+ url: https://twitter.com/abcd
+ external: true
+ - title: Feed
+ url: /feed.xml
+
+# Google Custom Search:
+#google_search: xyz123abc
+
+# Twitter stream widget:
+# Replace xyz123abc with your twitter widget id from https://twitter.com/settings/widgets
+#twitter_widget_id: xyz123abc
+
+# Add disqus username for Disqus comment board:
+disqus_shortname: foo
+
+# Analytics and webmaster tools stuff goes here
+#google_analytics: xyz123abc
+
+#### For dummy website only - remove if you wish ####
+github_repo: https://github.com/dyndna/lanyon-plus
+version: 1.1.0
+## END ##
diff --git a/_data/socialmedia.yml b/_data/socialmedia.yml
new file mode 100644
index 0000000..59e5b29
--- /dev/null
+++ b/_data/socialmedia.yml
@@ -0,0 +1,24 @@
+- name: Twitter
+ url: https://twitter.com/abcd
+ class: fa fa-twitter-square
+ title: "Follow me @foo"
+
+- name: Google Plus
+ url: https://plus.google.com/+foo
+ class: fa fa-google-plus-square
+ title: "Follow me +foo"
+
+- name: GitHub
+ url: https://github.com/xyz123abc
+ class: fa fa-github-square
+ title: Code repository
+
+- name: Contact
+ url: "/contact/"
+ class: fa fa-envelope-square
+ title: "Reach Us"
+
+- name: RSS
+ url: "/feed.xml"
+ class: fa fa-rss-square
+ title: "Subscribe to RSS"
diff --git a/_devconfig.yml b/_devconfig.yml
new file mode 100644
index 0000000..99aa90f
--- /dev/null
+++ b/_devconfig.yml
@@ -0,0 +1,102 @@
+# Permalinks
+#
+# Use of `relative_permalinks` ensures post links from the index work properly.
+#permalink: pretty
+permalink: /blog/:year/:month/:day/:title/
+relative_permalinks: false
+
+# Setup
+title: foo
+#tagline: 'foo's website
+description: Foo's blog...
+url: http://localhost:4000
+baseurl: ""
+urlimg: http://localhost:4000/images/
+markdown: kramdown
+paginate: 5
+paginate_path: "/blog/page:num"
+excerpt_separator:
+default_bg: sitelogo.png
+safe: false
+#timezone: America/Chicago
+future: true
+
+gems:
+ - jekyll-paginate
+ - jemoji
+ - font-awesome-sass
+ - kramdown
+ - rouge
+
+include: [".htaccess"]
+exclude: ["lib", "config.rb", "Gemfile", "Capfile", "Gemfile.lock", "config", "log", "Rakefile", "Rakefile.rb", "rakefile", "README.md", "tmp", "less", "*.sublime-project", "*.sublime-workspace", "test", "spec", "Gruntfile.js", "package.json", "node_modules", "LICENSE", "vendor", "assets", "_plugins", "public/dormant"]
+
+# About/contact
+author:
+ name: Foo Boo
+ url: https://twitter.com/abcd
+ avatar: foo.png
+ #email:
+
+# Owner/author information
+owner:
+ name: Foo Boo
+ avatar: foo.png
+ #email:
+ # Use the coder's toolbox at http://coderstoolbox.net/string/#!encoding=xml&action=encode&charset=us_ascii to encode your description into XML string
+ description:
+ # Social networking links used in footer. Update and remove as you like.
+ twitter: abcd
+ facebook:
+ github: xyz123abc
+ stackexchange:
+ linkedin: https://www.linkedin.com/in/foo
+ instagram:
+ flickr:
+ tumblr:
+ google_plus: https://plus.google.com/+foo
+ # orcid and google scholar IDs are different than standard username.
+ orcid: xyz123abc
+ gscholar: xyz123abc
+
+## sidebar links:
+# For external links add external: true
+links:
+ - title: Home
+ url: /
+ - title: About
+ url: /about/
+ - title: Blog
+ url: /blog/
+ - title: Tags
+ url: /tags/
+ - title: Archive
+ url: /archive/
+ - title: Old Blog
+ url: https://foo.wordpress.com
+ external: true
+ - title: Contact
+ url: /contact/
+ - title: Twitter
+ url: https://twitter.com/abcd
+ external: true
+ - title: Feed
+ url: /feed.xml
+
+# Google Custom Search:
+#google_search: xyz123abc
+
+# Twitter stream widget:
+# Replace xyz123abc with your twitter widget id from https://twitter.com/settings/widgets
+#twitter_widget_id: xyz123abc
+
+# Add disqus username for Disqus comment board:
+disqus_shortname: foo
+
+# Analytics and webmaster tools stuff goes here
+#google_analytics: xyz123abc
+
+#### For dummy website only - remove if you wish ####
+github_repo: https://github.com/dyndna/lanyon-plus
+version: 1.1.0
+## END ##
diff --git a/_drafts/2014-01-02-introducing-lanyon.md b/_drafts/2014-01-02-introducing-lanyon.md
new file mode 100644
index 0000000..c7e8e0f
--- /dev/null
+++ b/_drafts/2014-01-02-introducing-lanyon.md
@@ -0,0 +1,40 @@
+---
+layout: post
+title: Introducing Lanyon
+---
+
+Lanyon is an unassuming [Jekyll](http://jekyllrb.com) theme that places content first by tucking away navigation in a hidden drawer. It's based on [Poole](http://getpoole.com), the Jekyll butler.
+
+
+
+### Built on Poole
+
+Poole is the Jekyll Butler, serving as an upstanding and effective foundation for Jekyll themes by [@mdo](https://twitter.com/mdo). Poole, and every theme built on it (like Lanyon here) includes the following:
+
+* Complete Jekyll setup included (layouts, config, [404](/404), [RSS feed](/atom.xml), posts, and [example page](/about))
+* Mobile friendly design and development
+* Easily scalable text and component sizing with `rem` units in the CSS
+* Support for a wide gamut of HTML elements
+* Related posts (time-based, because Jekyll) below each post
+* Syntax highlighting, courtesy Pygments (the Python-based code snippet highlighter)
+
+### Lanyon features
+
+In addition to the features of Poole, Lanyon adds the following:
+
+* Toggleable sliding sidebar (built with only CSS) via **☰** link in top corner
+* Sidebar includes support for textual modules and a dynamically generated navigation with active link support
+* Two orientations for content and sidebar, default (left sidebar) and [reverse](https://github.com/poole/lanyon#reverse-layout) (right sidebar), available via `
` classes
+* [Eight optional color schemes](https://github.com/poole/lanyon#themes), available via `` classes
+
+[Head to the readme](https://github.com/poole/lanyon#readme) to learn more.
+
+### Browser support
+
+Lanyon is by preference a forward-thinking project. In addition to the latest versions of Chrome, Safari (mobile and desktop), and Firefox, it is only compatible with Internet Explorer 9 and above.
+
+### Download
+
+Lanyon is developed on and hosted with GitHub. Head to the GitHub repository for downloads, bug reports, and features requests.
+
+Thanks!
diff --git a/_includes/crosspost.html b/_includes/crosspost.html
new file mode 100644
index 0000000..60c83d2
--- /dev/null
+++ b/_includes/crosspost.html
@@ -0,0 +1 @@
+<hr><a href="https://twitter.com/share?text={{ post.title }}&url={{ post.url | prepend: site.baseurl | prepend: site.url }}&via={{ site.owner.twitter }} @rbloggers" target="_blank" title="tweet author @{{ site.owner.twitter }}">tweet author</a> | <a href="https://plus.google.com/share?url={{ post.url | prepend: site.baseurl | prepend: site.url }}" target="_blank" title="Share on Google+">share on Google+</a>{% if page.comments %} | <a href="{{ post.url | prepend: site.baseurl | prepend: site.url }}#disqus_thread" title="Comment at author's website">Comments</a>{% endif %}
diff --git a/_includes/disqus_comments.html b/_includes/disqus_comments.html
new file mode 100644
index 0000000..45ba4b3
--- /dev/null
+++ b/_includes/disqus_comments.html
@@ -0,0 +1,13 @@
+
+
diff --git a/_includes/feedfooter.html b/_includes/feedfooter.html
new file mode 100644
index 0000000..ff60362
--- /dev/null
+++ b/_includes/feedfooter.html
@@ -0,0 +1 @@
+<hr><a href="https://twitter.com/share?text={{ post.title }}&url={{ post.url | prepend: site.baseurl | prepend: site.url }}&via={{ site.owner.twitter }}" target="_blank" title="tweet author @{{ site.owner.twitter }}">tweet author</a> | <a href="https://plus.google.com/share?url={{ post.url | prepend: site.baseurl | prepend: site.url }}" target="_blank" title="Share on Google+">share on Google+</a>{% if page.comments %} | <a href="{{ post.url | prepend: site.baseurl | prepend: site.url }}#disqus_thread" title="Comment at author's website">Comments</a>{% endif %}
diff --git a/_includes/footer.html b/_includes/footer.html
new file mode 100644
index 0000000..a522b2d
--- /dev/null
+++ b/_includes/footer.html
@@ -0,0 +1,15 @@
+
diff --git a/_includes/gist_embed.html b/_includes/gist_embed.html
new file mode 100644
index 0000000..0466ecc
--- /dev/null
+++ b/_includes/gist_embed.html
@@ -0,0 +1,3 @@
+
+
+
diff --git a/_includes/head.html b/_includes/head.html
new file mode 100644
index 0000000..b8a1762
--- /dev/null
+++ b/_includes/head.html
@@ -0,0 +1,105 @@
+
+
+
+
+
+
+
+
+
+
+ {% if page.title == "Home" %}
+ {{ site.title }} · {{ site.tagline }}
+ {% else %}
+ {{ page.title }} · {{ site.title }}
+ {% endif %}
+
+
+
+
+{% if page.tags %}{% endif %}
+{% if page.noindex == true %}{% endif %}
+{% if page.nofollow == true %}{% endif %}
+{% if site.google_verify %}{% endif %}
+
+{% if site.owner.twitter %}
+ {% include twitter_card.html %}
+{% endif %}
+
+
+
+
+
+
+
+
+
+
+
+
+{% if page.imagefeature %}
+ {% if page.imagefeature contains 'http' %}
+ {% assign domain = '' %}
+ {% else %}
+ {% assign domain = site.urlimg %}
+ {% endif %}
+{% else %}
+{% endif %}
+{% if page.videofeature %}{% endif %}
+
+
+
+
+
+
+
+
+
+
+{% if page.category contains 'mypubs' or page.category contains 'myaoi' %}
+
+
+{% endif %}
+
+
+
+
+{% if page.style %}
+
+{% endif %}
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+{% capture canonical %}{{ site.url }}{% if site.permalink contains '.html' %}{{ page.url }}{% else %}{{ page.url | remove:'index.html' | strip_slash }}{% endif %}{% endcapture %}
+
+{% if site.owner.google_plus %}{% endif %}
+
+
+
+
+{% if page.mathjax %}
+ {% include mathjax_support.html %}
+{% endif %}
+
+
diff --git a/_includes/head_minimal.html b/_includes/head_minimal.html
new file mode 100644
index 0000000..3f03b0a
--- /dev/null
+++ b/_includes/head_minimal.html
@@ -0,0 +1,73 @@
+
+
+
+
+
+
+
+
+
+
+ {% if page.title == "Home" %}
+ {{ site.title }} · {{ site.tagline }}
+ {% else %}
+ {{ page.title }} · {{ site.title }}
+ {% endif %}
+
+
+
+
+
+{% if page.noindex == true %}{% endif %}
+{% if page.nofollow == true %}{% endif %}
+
+
+
+
+
+
+
+
+
+
+{% if page.category contains 'mypubs' or page.category contains 'myaoi' %}
+
+
+{% endif %}
+
+
+
+
+{% if page.style %}
+
+{% endif %}
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+{% if site.owner.google_plus %}{% endif %}
+
+
+
+
+
diff --git a/_includes/mathjax_support.html b/_includes/mathjax_support.html
new file mode 100644
index 0000000..c5446c0
--- /dev/null
+++ b/_includes/mathjax_support.html
@@ -0,0 +1,44 @@
+
+
+
+
+
diff --git a/_includes/meta_info.html b/_includes/meta_info.html
new file mode 100644
index 0000000..74f2129
--- /dev/null
+++ b/_includes/meta_info.html
@@ -0,0 +1,7 @@
+
+
+
+{% if page.comments %}{% endif %}
+{% if page.category contains "featured" %}{% endif %}
+
+
diff --git a/_includes/myaoi.html b/_includes/myaoi.html
new file mode 100644
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+
Visualizing the beginnings of melanoma
+In cancer biology‚ a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements‚ called super-enhancers‚ whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
+Science‚ this issue p. 10.1126/science.aad3867; see also p. 453
+Structured Abstract
+INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone‚ yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events‚ (ii) the difficulty of visiualizing initiating clones in living organisms‚ and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that‚ when inhibited‚ may prevent the cancer from ever starting.
+RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes‚ but they only rarely convert to melanoma. In an effort to define events that initiate cancer‚ we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background‚ these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors‚ making it an ideal candidate for tracking melanoma from initiation onward.
+RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient)‚ a single melanocyte reactivates the NCP state‚ and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity‚ and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors‚ including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation‚ whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas‚ identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
+CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus‚ in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development‚ the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful‚ and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks‚ capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP‚ whereas the rest of the fish remains EGFP-negative.
+The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation‚ but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient)‚ a single melanocyte reactivates the NCP state‚ revealing a fate change at melanoma initiation in this model. NCP transcription factors‚ including sox10‚ regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation‚ which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
TY - JOUR
+TI - A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation
+AU - Kaufman, Charles K.
+AU - Mosimann, Christian
+AU - Fan, Zi Peng
+AU - Yang, Song
+AU - Thomas, Andrew J.
+AU - Ablain, Julien
+AU - Tan, Justin L.
+AU - Fogley, Rachel D.
+AU - Rooijen, Ellen van
+AU - Hagedorn, Elliott J.
+AU - Ciarlo, Christie
+AU - White, Richard M.
+AU - Matos, Dominick A.
+AU - Puller, Ann-Christin
+AU - Santoriello, Cristina
+AU - Liao, Eric C.
+AU - Young, Richard A.
+AU - Zon, Leonard I.
+T2 - Science
+AB - Visualizing the beginnings of melanoma
+In cancer biology, a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements, called super-enhancers, whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
+Science, this issue p. 10.1126/science.aad3867; see also p. 453
+Structured Abstract
+INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone, yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events, (ii) the difficulty of visiualizing initiating clones in living organisms, and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that, when inhibited, may prevent the cancer from ever starting.
+RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes, but they only rarely convert to melanoma. In an effort to define events that initiate cancer, we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background, these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors, making it an ideal candidate for tracking melanoma from initiation onward.
+RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity, and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors, including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation, whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas, identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
+CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus, in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development, the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful, and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks, capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP, whereas the rest of the fish remains EGFP-negative.
+The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation, but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, revealing a fate change at melanoma initiation in this model. NCP transcription factors, including sox10, regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation, which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
+DA - 2016/01/29/
+PY - 2016
+DO - 10.1126/science.aad2197
+DP - science.sciencemag.org
+VL - 351
+IS - 6272
+SP - aad2197
+LA - en
+SN - 0036-8075, 1095-9203
+UR - http://science.sciencemag.org/content/351/6272/aad2197
+Y2 - 2016/01/29/T14:40:26Z
+KW - Development
+KW - SKCM
+KW - classics
+KW - epigenetics
+KW - evolution
+KW - melanoma
+KW - super_enhancer
+KW - zebrafish
+ER -
The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection‚ which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes‚ which have been extensively studied in evolutionary biology‚ limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.
@article{lipinski_cancer_2016,
+ title = {Cancer {Evolution} and the {Limits} of {Predictability} in {Precision} {Cancer} {Medicine}},
+ volume = {2},
+ issn = {2405-8033},
+ url = {http://www.sciencedirect.com/science/article/pii/S2405803315000692},
+ doi = {10.1016/j.trecan.2015.11.003},
+ number = {1},
+ urldate = {2016-01-30TZ},
+ journal = {Trends in Cancer},
+ author = {Lipinski, Kamil A. and Barber, Louise J. and Davies, Matthew N. and Ashenden, Matthew and Sottoriva, Andrea and Gerlinger, Marco},
+ month = jan,
+ year = {2016},
+ keywords = {classics, evolution, heterogeneity, resistance, review},
+ pages = {49--63}
+}
TY - JOUR
+TI - Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine
+AU - Lipinski, Kamil A.
+AU - Barber, Louise J.
+AU - Davies, Matthew N.
+AU - Ashenden, Matthew
+AU - Sottoriva, Andrea
+AU - Gerlinger, Marco
+T2 - Trends in Cancer
+AB - The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection, which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes, which have been extensively studied in evolutionary biology, limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.
+DA - 2016/01//
+PY - 2016
+DO - 10.1016/j.trecan.2015.11.003
+DP - ScienceDirect
+VL - 2
+IS - 1
+SP - 49
+EP - 63
+J2 - Trends in Cancer
+SN - 2405-8033
+UR - http://www.sciencedirect.com/science/article/pii/S2405803315000692
+Y2 - 2016/01/30/T22:58:32Z
+KW - classics
+KW - evolution
+KW - heterogeneity
+KW - resistance
+KW - review
+ER -
A revolution in cellular measurement technology is under way: For the first time‚ we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state‚ but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states‚ over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape‚ but illuminates the molecular mechanisms that shape the landscape itself. However‚ single-cell genomics is a field in its infancy‚ with many experimental and computational advances needed to fully realize its full potential.
TY - JOUR
+TI - Defining cell types and states with single-cell genomics
+AU - Trapnell, Cole
+T2 - Genome Research
+AB - A revolution in cellular measurement technology is under way: For the first time, we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state, but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states, over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape, but illuminates the molecular mechanisms that shape the landscape itself. However, single-cell genomics is a field in its infancy, with many experimental and computational advances needed to fully realize its full potential.
+DA - 2015/10/01/
+PY - 2015
+DO - 10.1101/gr.190595.115
+DP - genome.cshlp.org
+VL - 25
+IS - 10
+SP - 1491
+EP - 1498
+J2 - Genome Res.
+LA - en
+SN - 1088-9051, 1549-5469
+UR - http://genome.cshlp.org/content/25/10/1491
+Y2 - 2015/10/14/T06:07:23Z
+KW - Waddington
+KW - capacitance
+KW - chromatin
+KW - classics
+KW - epigenetics
+KW - evolution
+KW - genomics
+KW - ideas
+KW - oped
+KW - review
+KW - single-cell
+ER -
Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave‚ the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells‚ transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex‚ which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However‚ the identity of KZNF genes battling retrotransposons currently active in the human genome‚ such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1)‚ is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/’s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes‚ and this is followed by mutations in these retrotransposons to evade repression‚ a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.
TY - JOUR
+TI - An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons
+AU - Jacobs, Frank M. J.
+AU - Greenberg, David
+AU - Nguyen, Ngan
+AU - Haeussler, Maximilian
+AU - Ewing, Adam D.
+AU - Katzman, Sol
+AU - Paten, Benedict
+AU - Salama, Sofie R.
+AU - Haussler, David
+T2 - Nature
+AB - Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/'s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.
+DA - 2014/12/11/
+PY - 2014
+DO - 10.1038/nature13760
+DP - www.nature.com
+VL - 516
+IS - 7530
+SP - 242
+EP - 245
+J2 - Nature
+LA - en
+SN - 0028-0836
+UR - http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html
+Y2 - 2015/10/12/T21:07:51Z
+KW - classics
+KW - genereg
+KW - ideas
+KW - interactions
+KW - lncrna
+KW - network
+KW - transposon
+ER -
diff --git a/_includes/mypubs.html b/_includes/mypubs.html
new file mode 100644
index 0000000..1cc81fb
--- /dev/null
+++ b/_includes/mypubs.html
@@ -0,0 +1,297 @@
+
Visualizing the beginnings of melanoma
+In cancer biology‚ a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements‚ called super-enhancers‚ whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
+Science‚ this issue p. 10.1126/science.aad3867; see also p. 453
+Structured Abstract
+INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone‚ yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events‚ (ii) the difficulty of visiualizing initiating clones in living organisms‚ and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that‚ when inhibited‚ may prevent the cancer from ever starting.
+RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes‚ but they only rarely convert to melanoma. In an effort to define events that initiate cancer‚ we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background‚ these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors‚ making it an ideal candidate for tracking melanoma from initiation onward.
+RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient)‚ a single melanocyte reactivates the NCP state‚ and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity‚ and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors‚ including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation‚ whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas‚ identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
+CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus‚ in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development‚ the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful‚ and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks‚ capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP‚ whereas the rest of the fish remains EGFP-negative.
+The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation‚ but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient)‚ a single melanocyte reactivates the NCP state‚ revealing a fate change at melanoma initiation in this model. NCP transcription factors‚ including sox10‚ regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation‚ which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
TY - JOUR
+TI - A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation
+AU - Kaufman, Charles K.
+AU - Mosimann, Christian
+AU - Fan, Zi Peng
+AU - Yang, Song
+AU - Thomas, Andrew J.
+AU - Ablain, Julien
+AU - Tan, Justin L.
+AU - Fogley, Rachel D.
+AU - Rooijen, Ellen van
+AU - Hagedorn, Elliott J.
+AU - Ciarlo, Christie
+AU - White, Richard M.
+AU - Matos, Dominick A.
+AU - Puller, Ann-Christin
+AU - Santoriello, Cristina
+AU - Liao, Eric C.
+AU - Young, Richard A.
+AU - Zon, Leonard I.
+T2 - Science
+AB - Visualizing the beginnings of melanoma
+In cancer biology, a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements, called super-enhancers, whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
+Science, this issue p. 10.1126/science.aad3867; see also p. 453
+Structured Abstract
+INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone, yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events, (ii) the difficulty of visiualizing initiating clones in living organisms, and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that, when inhibited, may prevent the cancer from ever starting.
+RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes, but they only rarely convert to melanoma. In an effort to define events that initiate cancer, we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background, these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors, making it an ideal candidate for tracking melanoma from initiation onward.
+RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity, and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors, including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation, whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas, identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
+CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus, in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development, the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful, and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks, capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP, whereas the rest of the fish remains EGFP-negative.
+The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation, but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, revealing a fate change at melanoma initiation in this model. NCP transcription factors, including sox10, regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation, which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
+Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
+DA - 2016/01/29/
+PY - 2016
+DO - 10.1126/science.aad2197
+DP - science.sciencemag.org
+VL - 351
+IS - 6272
+SP - aad2197
+LA - en
+SN - 0036-8075, 1095-9203
+UR - http://science.sciencemag.org/content/351/6272/aad2197
+Y2 - 2016/01/29/T14:40:26Z
+KW - Development
+KW - SKCM
+KW - classics
+KW - epigenetics
+KW - evolution
+KW - melanoma
+KW - super_enhancer
+KW - zebrafish
+ER -
The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection‚ which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes‚ which have been extensively studied in evolutionary biology‚ limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.
@article{lipinski_cancer_2016,
+ title = {Cancer {Evolution} and the {Limits} of {Predictability} in {Precision} {Cancer} {Medicine}},
+ volume = {2},
+ issn = {2405-8033},
+ url = {http://www.sciencedirect.com/science/article/pii/S2405803315000692},
+ doi = {10.1016/j.trecan.2015.11.003},
+ number = {1},
+ urldate = {2016-01-30TZ},
+ journal = {Trends in Cancer},
+ author = {Lipinski, Kamil A. and Barber, Louise J. and Davies, Matthew N. and Ashenden, Matthew and Sottoriva, Andrea and Gerlinger, Marco},
+ month = jan,
+ year = {2016},
+ keywords = {classics, evolution, heterogeneity, resistance, review},
+ pages = {49--63}
+}
TY - JOUR
+TI - Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine
+AU - Lipinski, Kamil A.
+AU - Barber, Louise J.
+AU - Davies, Matthew N.
+AU - Ashenden, Matthew
+AU - Sottoriva, Andrea
+AU - Gerlinger, Marco
+T2 - Trends in Cancer
+AB - The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection, which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes, which have been extensively studied in evolutionary biology, limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.
+DA - 2016/01//
+PY - 2016
+DO - 10.1016/j.trecan.2015.11.003
+DP - ScienceDirect
+VL - 2
+IS - 1
+SP - 49
+EP - 63
+J2 - Trends in Cancer
+SN - 2405-8033
+UR - http://www.sciencedirect.com/science/article/pii/S2405803315000692
+Y2 - 2016/01/30/T22:58:32Z
+KW - classics
+KW - evolution
+KW - heterogeneity
+KW - resistance
+KW - review
+ER -
A revolution in cellular measurement technology is under way: For the first time‚ we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state‚ but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states‚ over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape‚ but illuminates the molecular mechanisms that shape the landscape itself. However‚ single-cell genomics is a field in its infancy‚ with many experimental and computational advances needed to fully realize its full potential.
TY - JOUR
+TI - Defining cell types and states with single-cell genomics
+AU - Trapnell, Cole
+T2 - Genome Research
+AB - A revolution in cellular measurement technology is under way: For the first time, we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state, but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states, over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape, but illuminates the molecular mechanisms that shape the landscape itself. However, single-cell genomics is a field in its infancy, with many experimental and computational advances needed to fully realize its full potential.
+DA - 2015/10/01/
+PY - 2015
+DO - 10.1101/gr.190595.115
+DP - genome.cshlp.org
+VL - 25
+IS - 10
+SP - 1491
+EP - 1498
+J2 - Genome Res.
+LA - en
+SN - 1088-9051, 1549-5469
+UR - http://genome.cshlp.org/content/25/10/1491
+Y2 - 2015/10/14/T06:07:23Z
+KW - Waddington
+KW - capacitance
+KW - chromatin
+KW - classics
+KW - epigenetics
+KW - evolution
+KW - genomics
+KW - ideas
+KW - oped
+KW - review
+KW - single-cell
+ER -
Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave‚ the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells‚ transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex‚ which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However‚ the identity of KZNF genes battling retrotransposons currently active in the human genome‚ such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1)‚ is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/’s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes‚ and this is followed by mutations in these retrotransposons to evade repression‚ a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.
TY - JOUR
+TI - An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons
+AU - Jacobs, Frank M. J.
+AU - Greenberg, David
+AU - Nguyen, Ngan
+AU - Haeussler, Maximilian
+AU - Ewing, Adam D.
+AU - Katzman, Sol
+AU - Paten, Benedict
+AU - Salama, Sofie R.
+AU - Haussler, David
+T2 - Nature
+AB - Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/'s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.
+DA - 2014/12/11/
+PY - 2014
+DO - 10.1038/nature13760
+DP - www.nature.com
+VL - 516
+IS - 7530
+SP - 242
+EP - 245
+J2 - Nature
+LA - en
+SN - 0028-0836
+UR - http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html
+Y2 - 2015/10/12/T21:07:51Z
+KW - classics
+KW - genereg
+KW - ideas
+KW - interactions
+KW - lncrna
+KW - network
+KW - transposon
+ER -
diff --git a/_includes/printmsgpages.html b/_includes/printmsgpages.html
new file mode 100644
index 0000000..29852d8
--- /dev/null
+++ b/_includes/printmsgpages.html
@@ -0,0 +1,16 @@
+
diff --git a/links.jsonp b/links.jsonp
new file mode 100644
index 0000000..930d872
--- /dev/null
+++ b/links.jsonp
@@ -0,0 +1,10 @@
+---
+---
+callback([
+{% for post in site.posts reversed | sort: title %}
+ {
+ "text": "{{post.title | replace:'"','\"'}}",
+ "href": "{{site.url}}{{post.url}}"
+ } {% unless forloop.last %},{% endunless%}
+{% endfor %}
+])
diff --git a/pages/about.md b/pages/about.md
new file mode 100644
index 0000000..0dec84a
--- /dev/null
+++ b/pages/about.md
@@ -0,0 +1,41 @@
+---
+layout: page
+title: About
+permalink: /about/
+show_meta: true
+# imagefeature path is relative to images/ directory.
+imagefeature: foo.png
+published: true
+description: "About example.com...."
+category: views
+comments: false
+mathjax: false
+noindex: false
+sitemap:
+ priority: 0.7
+ changefreq: 'monthly'
+ lastmod: 2016-02-13
+# tags will be used as html meta keywords.
+tags:
+ - "foo boo"
+ - "city tx"
+---
+
+
+
+
+
+
+
+
+
+
+Lorem ipsum dolor sit amet, consectetur adipiscing elit. In ornare lectus a purus rutrum, a hendrerit quam condimentum. Donec vel ante maximus, vulputate libero ac, rhoncus justo. Phasellus purus nisl, auctor id tristique eu, maximus quis leo. Mauris ultricies ante quis vehicula accumsan. Nulla facilisi. Lorem ipsum dolor sit amet, consectetur adipiscing elit. Ut mi elit, feugiat non scelerisque eget, ultrices nec est. Morbi a est iaculis, commodo quam congue, posuere quam. Phasellus venenatis finibus eros, vitae malesuada nisl gravida vitae.
+
+Praesent ac sem quis diam fermentum fermentum. Nullam turpis metus, elementum sit amet venenatis sed, placerat eget erat. Ut convallis ipsum vitae volutpat tristique. Cras a tempor lorem, quis aliquet dui. Nunc vel leo erat. Donec posuere massa sed justo luctus, accumsan porttitor ligula laoreet. Suspendisse sit amet nisi ultrices, venenatis lorem vel, posuere turpis. Fusce eget dictum nisi. Proin eu diam nisi. Quisque ut quam quis sem tincidunt efficitur vitae nec ex. Pellentesque ut dolor eros. Ut faucibus semper ultricies. Vestibulum nec nisl in magna porttitor dictum.
+
+Donec egestas eros arcu, id fermentum orci faucibus ac. Pellentesque facilisis elit eu tellus ultrices pulvinar. Cum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus. In ut eros et mi dapibus condimentum. Sed ante metus, porttitor ut aliquet vitae, ullamcorper quis ex. Donec ac efficitur arcu, a malesuada dolor. Nulla magna arcu, semper quis augue sed, rhoncus porta urna. Duis dictum dapibus diam, ac sodales ipsum lobortis vel. Nulla ac dictum metus. Morbi sollicitudin tortor eu diam tristique, ut tincidunt tortor euismod. Integer non tincidunt metus. In tempus sem dapibus, venenatis mi placerat, condimentum orci. Nunc et tellus diam.
+
+Nam imperdiet consequat lorem. Donec sagittis tortor eu dolor efficitur ullamcorper. Pellentesque dolor arcu, vestibulum quis laoreet at, tincidunt nec mauris. Praesent id laoreet arcu. Quisque blandit nunc at elit auctor, eget tempor nunc sodales. Cras venenatis lacinia tempus. Proin erat nisl, pharetra a massa volutpat, rhoncus pellentesque nisi. Mauris in elit dictum, egestas tellus et, laoreet velit. Nam auctor tempus augue sit amet fermentum. Nulla accumsan arcu quis efficitur aliquam. Nulla dapibus in neque eget facilisis. Nullam nisi augue, maximus at lectus sit amet, ornare malesuada ante. Morbi volutpat justo a urna pharetra elementum. Proin tempor ac felis ac consequat. Proin feugiat, nulla ac sagittis consequat, ante diam auctor tortor, in suscipit leo ante id dolor. Vivamus posuere pellentesque magna, sagittis blandit neque convallis sed.
+
+*[volutpat]: Tooltip for abbreviation.
diff --git a/pages/aoi.md b/pages/aoi.md
new file mode 100644
index 0000000..73107c9
--- /dev/null
+++ b/pages/aoi.md
@@ -0,0 +1,46 @@
+---
+layout: publ
+category: myaoi
+permalink: /about/aoi/
+title: "Articles of interest"
+published: true
+description: "Sample page showing bookmarked papers"
+tags:
+ - papers
+ - articles
+ - research
+ - starred
+comments: true
+modified: "2016-02-13"
+bibtex: "/files/myaoi.bib"
+#bibtex: "http://foo-alternate.com/files/myaoi.bib"
+show_meta: true
+noindex: false
+nofollow: true
+sitemap:
+ priority: 0.5
+ changefreq: 'monthly'
+ lastmod: 2016-02-13
+style: |
+ .container {
+ max-width: 48rem;
+ }
+---
+
+{% comment %}
+
+
+{% if page.bibtex %}
+ {% if page.bibtex contains 'http' %}
+ {% assign domain = '' %}
+ {% else %}
+ {% assign domain = site.url %}
+ {% endif %}
+ {% capture biburl %}{{ domain }}{{ page.bibtex }}{% endcapture %}
+
+{% endif %}
+
+{% endcomment %}
+
+If category is *myaoi*, then html content from bibtex file at `_includes/myaoi.html` will be shown below.
+
diff --git a/pages/contact.md b/pages/contact.md
new file mode 100644
index 0000000..6023cb3
--- /dev/null
+++ b/pages/contact.md
@@ -0,0 +1,53 @@
+---
+layout: page
+permalink: /contact/
+title: Contact
+show_meta: false
+published: true
+description: "Contact example.com"
+comments: false
+mathjax: false
+noindex: false
+sitemap:
+ priority: 0.5
+ changefreq: 'monthly'
+ lastmod: 2016-02-13
+tags:
+ - "foo boo"
+ - "driving directions"
+ - address
+---
+
+| | [@{{ site.owner.twitter }}](https://twitter.com/{{ site.owner.twitter }}) |
+| - | :- |
+| | foo XYZ 1234 ABC ST Washington, DC 11111 |
+| - | :- |
+| | [Driving directions]({{ site.url }}/directions) |
+| - | :- |
+| | foo@xyz |
+| - | :- |
+
+Tweet
+
+
+
+{% if site.twitter_widget_id %}
+
+{% else %}
+Twitter stream will show up here if `twitter_widget_id` is present is `_config.yml`
+{% endif %}
diff --git a/pages/cv.md b/pages/cv.md
new file mode 100644
index 0000000..d094d1c
--- /dev/null
+++ b/pages/cv.md
@@ -0,0 +1,36 @@
+---
+layout: page
+permalink: /cv/
+title: Curriculum Vitae
+category: base
+published: true
+description: "Curriculum Vitae / Resume"
+tags:
+ - cv
+ - resume
+ - "foo boo"
+comments: false
+imagesummary: foo.png
+modified: "2016-02-13"
+sitemap:
+ priority: 0.7
+ changefreq: 'monthly'
+ lastmod: 2016-02-13
+style: |
+ .container {
+ max-width: 48rem;
+ }
+---
+
+
+
+
+
+
+
+
+{:.text-center}
+[Publications]({{ site.url }}/about/publications/) \| [ORCID profile](https://orcid.org/{{ site.owner.orcid }}) \| [Google Scholar profile](https://scholar.google.com/citations?user={{ site.owner.gscholar }}&hl=en)
+
+
+
diff --git a/pages/disclosure.md b/pages/disclosure.md
new file mode 100644
index 0000000..69d53dc
--- /dev/null
+++ b/pages/disclosure.md
@@ -0,0 +1,56 @@
+---
+layout: page
+permalink: /disclosure/
+title: "Disclosure"
+description: "This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License"
+nofollow: false
+published: true
+modified: "2016-01-13"
+---
+
+This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
+
+### Theme Credit:
+
+* Base: [*lanyon*](https://github.com/poole/lanyon) by [Mark Otto](https://github.com/mdo)
+* Add-ons: [Samir B. Amin](https://twitter.com/sbamin) at [SBAmin.com](http://www.sbamin.com)
+
+{% highlight c %}
+Released under MIT License
+
+Copyright (c) 2014 Mark Otto.
+
+Permission is hereby granted, free of charge, to any person obtaining a copy of this software and associated documentation files (the "Software"), to deal in the Software without restriction, including without limitation the rights to use, copy, modify, merge, publish, distribute, sublicense, and/or sell copies of the Software, and to permit persons to whom the Software is furnished to do so, subject to the following conditions:
+
+The above copyright notice and this permission notice shall be included in all copies or substantial portions of the Software.
+
+THE SOFTWARE IS PROVIDED "AS IS", WITHOUT WARRANTY OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO THE WARRANTIES OF MERCHANTABILITY, FITNESS FOR A PARTICULAR PURPOSE AND NONINFRINGEMENT. IN NO EVENT SHALL THE AUTHORS OR COPYRIGHT HOLDERS BE LIABLE FOR ANY CLAIM, DAMAGES OR OTHER LIABILITY, WHETHER IN AN ACTION OF CONTRACT, TORT OR OTHERWISE, ARISING FROM, OUT OF OR IN CONNECTION WITH THE SOFTWARE OR THE USE OR OTHER DEALINGS IN THE SOFTWARE.
+{% endhighlight %}
+
+***
+
+### Credits for site features:
+
+* [Jekyll](https://jekyllrb.com){:target="_blank"}
+* [Footer social icons by Lauren Clark](http://codepen.io/Deadlymuffin/pen/hGiqo/){:target="_blank"}
+* [CSS and jekyll tips from HMFAYSAL OMEGA by HMFAYSAL](https://github.com/hmfaysal/hmfaysal-omega-theme){:target="_blank"}
+* Icons by [Font Awesome Icons](http://fortawesome.github.io/Font-Awesome/icons/){:target="_blank"} and [IcoMoon](https://icomoon.io){:target="_blank"}
+* [Responsive YouTube Playlist Embedding by John](http://avexdesigns.com/responsive-youtube-embed/){:target="_blank"}
+* [Related posts without plugin by Ross Gardler](http://rgardler.github.io/2015/07/28/adding-related-posts-to-jekyll-blog/){:target="_blank"}
+* [Archive page by Reyhan Dhuny and Michael Rowe](http://reyhan.org/2013/03/jekyll-archive-without-plugins.html){:target="_blank"}
+* [Print css by Pieter Beulque and David Walsh](http://www.webdesignerdepot.com/2010/01/10-tips-for-better-print-style-sheets/){:target="_blank"}
+* [Embed gists by Blair Vanderhoof](https://github.com/blairvanderhoof/gist-embed){:target="_blank"}
+* [code highlighting css from *jekyll-now* by Barry Clark](https://github.com/barryclark/jekyll-now){:target="_blank"}
+* CSS minify via [refresh-sf](http://refresh-sf.com){:target="_blank"}
+* Search box:
+ * By [Justin James](https://github.com/digitaldrummerj){:target="_blank"}
+ * By [Paula Borowska](https://twitter.com/paulaborowska){:target="_blank"} at [envato tuts+](http://webdesign.tutsplus.com/tutorials/css-experiments-with-a-search-form-input-and-button--cms-22069){:target="_blank"}
+ * By [Amit Agrawal](http://www.labnol.org/about/){:target="_blank"} at [Digital Inspiration](http://www.labnol.org/internet/google-custom-search-css/28360/){:target="_blank"}
+* Tag cloud:
+ * By [Tobias Sjosten](https://github.com/tobiassjosten/tobiassjosten.github.io){:target="_blank"}
+ * By [Thibaut Courouble](https://github.com/Thibaut){:target="_blank"} at [cssflow.com](http://www.cssflow.com/snippets/sliding-tags){:target="_blank"}
+ * By [Michael Lanyon](https://github.com/lanyonm){:target="_blank"} at [lanyonm.github.io](https://github.com/lanyonm/lanyonm.github.io){:target="_blank"}
+* Bibliography:
+ * [Zot/Bib/Web](https://github.com/davidswelt/zot_bib_web){:target="_blank"} by [David Reitter](https://github.com/davidswelt){:target="_blank"} for *jekyll* page layout and css
+ * [Zotero Reference Manager API](https://www.zotero.org){:target="_blank"} for bibliography management
+ * [BibBase.org](http://bibbase.org){:target="_blank"} for external linking over `http`
diff --git a/pages/publications.md b/pages/publications.md
new file mode 100644
index 0000000..d5a535f
--- /dev/null
+++ b/pages/publications.md
@@ -0,0 +1,44 @@
+---
+layout: publ
+category: mypubs
+permalink: /about/publications/
+title: "Sample Publications"
+published: true
+description: "Sample publication page"
+tags:
+ - papers
+ - articles
+ - research
+comments: true
+modified: "2016-02-13"
+bibtex: "/files/mypubs.bib"
+#bibtex: "http://foo-alternate.com/files/mypubs.bib"
+show_meta: true
+noindex: false
+nofollow: true
+sitemap:
+ priority: 0.5
+ changefreq: 'monthly'
+ lastmod: 2016-02-13
+style: |
+ .container {
+ max-width: 48rem;
+ }
+---
+
+{% comment %}
+
+
+{% if page.bibtex %}
+ {% if page.bibtex contains 'http' %}
+ {% assign domain = '' %}
+ {% else %}
+ {% assign domain = site.url %}
+ {% endif %}
+ {% capture biburl %}{{ domain }}{{ page.bibtex }}{% endcapture %}
+
+{% endif %}
+
+{% endcomment %}
+
+If category is *mypubs*, then html content from bibtex file at `_includes/mypubs.html` will be shown below.
diff --git a/pages/readme.md b/pages/readme.md
new file mode 100644
index 0000000..5e68714
--- /dev/null
+++ b/pages/readme.md
@@ -0,0 +1,100 @@
+---
+layout: page
+permalink: /readme/
+title: "README - How to set up lanyon-plus jekyll theme"
+description: "README for setting up lanyon-plus jekyll theme on github pages or custom domain having static website"
+---
+{% raw %}
+## lanyon-plus
+
+### Based on Jekyll theme: [Lanyon](http://lanyon.getpoole.com) by [Mark Otto](https://github.com/mdo)
+
+* add-ons by [Samir B. Amin](https://sbamin.com)
+* License: Open sourced under the [MIT license](LICENSE.md).
+
+### Required edits:
+
+#### _config.yml
+
+* Edit lines where text string `foo` is present with relevant information.
+* Add relevant author and owner information
+ * For proper sidebar, meta info below post title, and footer bar, add at least twitter, google plus info under `owner` and `sidebar` section.
+ * Uncomment and add relevant user names/keys to enable features, e.g., google analytics, disqus comments, twitter widget, google custom search.
+
+#### CNAME
+
+* Read [Using a custom domain with GitHub Pages](https://help.github.com/articles/using-a-custom-domain-with-github-pages/) for set-up details.
+* If you are hosting website on domain other than `github.io`, rename `CNAME.sample` file to `CNAME`, and add your custom domain name, e.g., `example.com` (only one domain is allowed), otherwise remove `CNAME` file if you want to host at default `github.io`.
+* If you are hosting website on `github.io`, replace `example.com` with `https://.github.io/` (for project site) or `https://.github.io` (for user site) under `site.url` and `site.urlimg` in `_config.yml` and `_prose.yml` file.
+
+#### .travis.yml
+* See more at [https://travis-ci.org/getting_started](https://travis-ci.org/getting_started)
+
+#### _prose.yml
+
+* [https://github.com/prose/prose/wiki/Getting-Started](https://github.com/prose/prose/wiki/Getting-Started)
+* Edit `example.com` with your domain name.
+* You may edit names for custom categories.
+
+#### robots.txt
+
+* replace `example.com` with your valid url.
+* Edit search engine inclusion/exclusion if desired.
+
+#### page specific edits
+
+* `_data/socialmedia.html`
+ * Replace user `foo` with appropriate username
+
+* `_includes/`
+ * Check if file paths for appropriate urls have valid css files, scripts, icons, and images in `head.html` and `head_minimal.html`, else comment html tags which are not being used.
+ * Also, check if variables (twitter, google plus, linkedin, google analytics key and disqus username, etc.) are specified in `_config.yml` located under root path.
+ * You may edit `meta_info.html`, `footer.html` and similar include files to add/remove elements in page meta bar, footer, etc.
+ * For publications page, `mypubs.html` and `myaoi.html` are trimmed outputs from [zot_bib_web](https://github.com/davidswelt/zot_bib_web). Github pages can not dynamically build these pages. Alternately, you may export `bib` format for publications under `/files/` directory which can be parsed dynamically using [bibbase.org](http://bibbase.org)
+ * `_includes/footer.html`: Edit copyright information as needed.
+* `_layouts`
+ * To add/remove/reorder page/post contents, edit `default.html` plus `page.html` or `post.html`.
+* `_posts`
+ * Live blog posts goes here with markdown formatted post. File name format must have following date-title format `yyyy-mm-dd-title.md` for jekyll to render blog post correctly.
+ * YAML sample header shows all available options. Minimal required elements are: layout, title and date. Date tag overrides date given in post file name.
+* `blog/index.html`
+ * Edit blog title and description.
+* `images/`
+ * Under `icons` directory, keep appropriate sized favicons and thumbnails as specified in `_includes/head.html` and `_includes/head_minimal.html`
+ * Also, keep `favicon.png` and `favicon.ico` in root directory.
+ * Final, `images/icons/` should have following images with exact filenames and image size as specified in respective filenames. These images can be generated using online *favicon generator*. Replace `foo` with your site title or other name if desired.
+
+~~~
+example.com/images/icons/apple-touch-icon-precomposed.png
+example.com/images/icons/apple-touch-icon-72x72-precomposed.png
+example.com/images/icons/apple-touch-icon-114x114-precomposed.png
+example.com/images/icons/apple-touch-icon-144x144-precomposed.png
+example.com/images/icons/apple-touch-icon-180x180.png
+example.com/images/icons/android-icon-192x192.png
+~~~
+
+* `pages/about.md`
+ * YAML variable `imagefeature` shoud have image path relative to `images/` directory, i.e., `foo.png` will link to `example.com/images/foo.png`
+ * Specify `site.owner.avatar` and `site.owner.twitter` along with other variables in `_config.yml`
+* `syspages/`:
+ * Edit page title and description in YAML front matter.
+ * For web search to work, specify [Google Custom Search Engine](https://cse.google.com) API key for `google_search` variable.
+ * Tag generation is experimental and dynamic size for tag box may need to be adjusted if you have more than 100 posts with one or two frequently occurring tags.
+ * All `{% for ... %}...{% endfor %}` loop operations will increase site build time, and remove such features (tags, meta info, related posts, etc.) under `_includes`, `_layouts` and `syspages` if required.
+* `pages/contact.md`
+ * Edit page title and description.
+ * Edit address, driving direction url, etc.
+* `pages/cv.md`
+ * Edit `_config.yml` to add twitter, google plus, linkedin, google scholar, ORCID profile info under owner heading.
+ * Add pdf at `{{ site.url }}/cv/cv.pdf`
+* `pages/publications.md`
+ * Add your publications at `/files/mypubs.bib` and `_includes/mypubs.html`. See above under `_includes` for more.
+* `pages/disclosure.md`
+ * Appreciated if you keep relevant credits in disclosure page.
+* `humans.txt`
+ * Replace `foo` with your name.
+* `rfeed.xml`
+ * Not required unless you are cross-posting about R language on blog aggregation site(s).
+
+END
+ {% endraw %}
diff --git a/public/css/addon.css b/public/css/addon.css
new file mode 100644
index 0000000..2e8b913
--- /dev/null
+++ b/public/css/addon.css
@@ -0,0 +1 @@
+/*CSS pending minification*/
diff --git a/public/css/iconmoon.css b/public/css/iconmoon.css
new file mode 100644
index 0000000..9e20cb4
--- /dev/null
+++ b/public/css/iconmoon.css
@@ -0,0 +1,131 @@
+@font-face {
+ font-family: 'icomoon';
+ src: url('../fonts/icomoon.eot?o6nkuq');
+ src: url('../fonts/icomoon.eot?o6nkuq#iefix') format('embedded-opentype'),
+ url('../fonts/icomoon.ttf?o6nkuq') format('truetype'),
+ url('../fonts/icomoon.woff?o6nkuq') format('woff'),
+ url('../fonts/icomoon.svg?o6nkuq#icomoon') format('svg');
+ font-weight: normal;
+ font-style: normal;
+}
+
+.headicons {
+ display: inline-block;
+ margin-left: 20px;
+}
+
+.masthead-title .headicons a {
+ color: #505050;
+ text-decoration: none;
+}
+
+i.iconm {
+ /* use !important to prevent issues with browser extensions that change fonts */
+ font-family: 'icomoon' !important;
+ speak: none;
+ font-style: normal;
+ font-weight: normal;
+ font-variant: normal;
+ text-transform: none;
+ line-height: 1;
+ padding: 0px 4px 0px 4px;
+
+ /* Better Font Rendering =========== */
+ -webkit-font-smoothing: antialiased;
+ -moz-osx-font-smoothing: grayscale;
+}
+
+i.iconside {
+ /* use !important to prevent issues with browser extensions that change fonts */
+ font-family: 'icomoon' !important;
+ speak: none;
+ font-style: normal;
+ font-weight: normal;
+ font-size: 1.0rem;
+ font-variant: normal;
+ text-transform: none;
+ line-height: 1;
+
+ /* Better Font Rendering =========== */
+ -webkit-font-smoothing: antialiased;
+ -moz-osx-font-smoothing: grayscale;
+}
+
+.iconm {
+ -o-transition:.5s;
+ -ms-transition:.5s;
+ -moz-transition:.5s;
+ -webkit-transition:.5s;
+ transition: .5s;
+ background-color: #ffffff;
+}
+
+.iconm:hover {
+ background-color: #999999;
+ border-radius: 30px;
+ color: white;
+}
+
+.iconm-home:before {
+ content: "\e900";
+}
+.iconm-pencil2:before {
+ content: "\e906";
+}
+.iconm-quill:before {
+ content: "\e907";
+}
+.iconm-blog:before {
+ content: "\e909";
+}
+.iconm-profile:before {
+ content: "\e923";
+}
+.iconm-envelop:before {
+ content: "\e945";
+}
+.iconm-location:before {
+ content: "\e947";
+}
+.iconm-compass2:before {
+ content: "\e94a";
+}
+
+.iconm-user:before {
+ content: "\e971";
+}
+.iconm-user-tie:before {
+ content: "\e976";
+}
+.iconm-embed2:before {
+ content: "\ea80";
+}
+.iconm-terminal:before {
+ content: "\ea81";
+}
+.iconm-google-plus:before {
+ content: "\ea88";
+}
+.iconm-twitter:before {
+ content: "\ea91";
+}
+.iconm-feed2:before {
+ content: "\ea94";
+}
+.iconm-github2:before {
+ content: "\eab2";
+}
+.iconm-wordpress:before {
+ content: "\eab6";
+}
+.iconm-linkedin2:before {
+ content: "\eac9";
+}
+.iconm-file-pdf:before {
+ content: "\eada";
+}
+.iconm-html5:before {
+ content: "\eadf";
+}
+
+/*END*/
diff --git a/public/css/publ.css b/public/css/publ.css
new file mode 100644
index 0000000..6d8da86
--- /dev/null
+++ b/public/css/publ.css
@@ -0,0 +1,123 @@
+/* The bibliography */
+div.bibliography
+ {
+ font-family: "PT Serif", Georgia, "Times New Roman", serif;
+ }
+
+/* Collection titles */
+div.bibliography h1, div.bibliography h2, div.bibliography h3, div.bibliography h4
+ {
+ font-family: "PT Sans", Helvetica, Arial, sans-serif;
+ font-weight:1000;
+ color:DarkSlateGray ;
+ }
+
+/* The entire bibliographic item */
+div.bib-item {
+}
+div.full-bib-section div.bib-item {
+ margin-bottom:25px;
+}
+/* the short format (selected works) */
+div.short-bib-section div.bib-item {
+ margin-bottom:5px;
+}
+
+/* The actual BibTeX record (when visible) */
+div.bib {
+ font-family:Menlo,Courier,monospaced;
+ color: #9A9A9A;
+ padding-left:30px;
+ padding-bottom:10px;
+}
+
+/* Text "bib" or "abstract" */
+
+/* Text "bib" or "abstract" */
+.blink a {
+ font-family:Arial,sans-serif;
+ font-variant: small-caps;
+ clear: both;
+ padding:0;
+ margin:0;
+}
+div.full-bib-section .blink a {
+ margin-bottom:-30px;
+}
+div.short-bib-section .blink {
+ display:inline-block; /* needed to make margin-top work (collapsed margins) */
+ margin-top:-5px;
+ margin-bottom:10px;
+}
+
+
+/* The actual abstract (when visible) */
+div.abstract {
+ color:black;
+ padding-left:30px;
+ padding-bottom:10px;
+}
+
+/* Document titles */
+.doctitle {
+ font-weight:700;
+}
+
+/* Document titles linking to a PDF or somewhere else */
+a.doctitle:link,a.doctitle:visited,a.doctitle,a.doctitle:hover,a.doctitle.active {
+ color:#3090D4;
+ font-weight:700;
+ text-decoration:none; /* do not underline */
+}
+
+/* Document titles where shorted, e.g. "selected works" */
+.doctitle-short {
+}
+
+/* Display publication titles in their own lines.
+Remove to disable. */
+a.doctitle,span.doctitle {
+ display:block;
+}
+
+/* Search box */
+#pubSearchButton {
+ /* border: 0 solid #d4d0ba; */
+ font-family: inherit;
+ padding: 0;
+}
+#pubSearchBox {
+ position:absolute;
+ right:10px; top:100px;
+ display:block;
+}
+
+
+/* Categories at top of the bibliography */
+.bib-cat {
+ display: inline;
+ list-style: none;
+ text-indent: 0;
+ margin: 0; padding: 0;
+}
+
+.bib-cat li {
+ display: inline;
+}
+.bib-cat li:after {
+ content: " | ";
+}
+.bib-cat li:last-child:after {
+ content: ""
+}
+
+@media print {
+ div.full-bib-section .blink {
+ display: none;
+ }
+ a.doctitle:link:after {
+ display: none;
+ }
+}
+
+/*END*/
diff --git a/public/css/style.min.css b/public/css/style.min.css
new file mode 100644
index 0000000..6600223
--- /dev/null
+++ b/public/css/style.min.css
@@ -0,0 +1 @@
+h2,h4,h5,h6{margin-top:1rem}dd,h1,h2,h3,h4,h5,h6{margin-bottom:.5rem}abbr,dt{font-weight:700}dl,ol,p,pre,ul{margin-top:0;margin-bottom:1rem}img,pre{display:block}.highlight .cm,.highlight .ge,.highlight .sd{font-style:italic}.wrap,hr{position:relative}*{-webkit-box-sizing:border-box;-moz-box-sizing:border-box;box-sizing:border-box}body,html{margin:0;padding:0}html{font-size:16px;line-height:1.5}@media (min-width:38em){html{font-size:20px}}body{color:#515151;background-color:#fff;-webkit-text-size-adjust:100%;-ms-text-size-adjust:100%}a{color:#268bd2;text-decoration:none}a strong{color:inherit}a:focus,a:hover{text-decoration:underline}.gsc-cursor,.related-posts li a:hover,.slidetags a,.social-icons a,.tag-box a,.tag-ts{text-decoration:none}h1,h2,h3,h4,h5,h6{line-height:1.25;text-rendering:optimizeLegibility}h1{font-size:2rem}h2{font-size:1.5rem}h3{margin-top:1.5rem;font-size:1.25rem}h4,h5,h6{font-size:1rem}abbr,code{font-size:85%}strong{color:#303030}hr{margin:1.5rem 0;border:0;border-top:1px solid #eee;border-bottom:1px solid #fff}abbr{color:#555;text-transform:uppercase}abbr[title]{cursor:help;border-bottom:1px dotted #e5e5e5}code,pre{font-family:Menlo,Monaco,"Courier New",monospace}code{padding:.25em;color:#bf616a;background-color:#f9f9f9;border-radius:3px}code.yelhglt{color:inherit;background:rgba(255,255,0,.17);font-family:inherit;border-radius:inherit;font-size:inherit}pre{padding:1rem;font-size:.8rem;line-height:1.4;white-space:pre;white-space:pre-wrap;word-break:break-all;word-wrap:break-word;background-color:#f9f9f9;page-break-inside:avoid}pre code{padding:0;font-size:100%;color:inherit;background-color:transparent}.highlight{padding:7px 7px 7px 10px;border:1px solid #ddd;-moz-box-shadow:3px 3px rgba(0,0,0,.1);-webkit-box-shadow:3px 3px rgba(0,0,0,.1);box-shadow:3px 3px rgba(0,0,0,.1);margin:20px 0;overflow:auto}.highlight pre,blockquote p:last-child{margin-bottom:0}.gist .gist-file{font-family:Menlo,Monaco,"Courier New",monospace!important}.gist .markdown-body{padding:15px}.gist code,.gist pre{padding:0;background-color:transparent}.gist .gist-file .gist-data{font-size:.8rem!important;line-height:1.4}.gist code{color:inherit;border-radius:0}.message,tbody tr:nth-child(odd) td,tbody tr:nth-child(odd) th{background-color:#f9f9f9}.gist .blob-code-inner{white-space:normal}blockquote{padding:.5rem 1rem;margin:.8rem 0;color:#7a7a7a;border-left:.25rem solid #e5e5e5}@media (min-width:30em){blockquote{padding-right:5rem;padding-left:1.25rem}}img{max-width:100%;margin:0 0 1rem;border-radius:5px;vertical-align:middle}.message,table{margin-bottom:1rem}table,td,th{border:1px solid #e5e5e5}table{width:100%;border-collapse:collapse}td,th{padding:.25rem .5rem}.lead{font-size:1.25rem;font-weight:300}.message{padding:1rem;color:#717171}.container{padding-left:3rem;padding-right:3rem;margin-left:auto;margin-right:auto;max-width:28rem}.highlight .hll{background-color:#ffc}.highlight .c{color:#999}.highlight .err{color:#a00;background-color:rgba(255,170,170,.34)}.highlight .k{color:#069}.highlight .o{color:#555}.highlight .cm{color:#09f}.highlight .cp{color:#099}.highlight .c1,.highlight .cs{color:#999}.highlight .gd{background-color:#fcc;border:1px solid #c00}.highlight .gr{color:red}.highlight .gh{color:#030}.highlight .gi{background-color:#cfc;border:1px solid #0c0}.highlight .go{color:#aaa}.highlight .gp{color:#009}.highlight .gu{color:#030}.highlight .gt{color:#9c6}.highlight .kc,.highlight .kd,.highlight .kn,.highlight .kp,.highlight .kr{color:#069}.highlight .kt{color:#078}.highlight .m{color:#f60}.highlight .s{color:#d44950}.highlight .na{color:#4f9fcf}.highlight .nb{color:#366}.highlight .nc{color:#0a8}.highlight .no{color:#360}.highlight .nd{color:#99f}.highlight .ni{color:#999}.highlight .ne{color:#c00}.highlight .nf{color:#c0f}.highlight .nl{color:#99f}.highlight .nn{color:#0cf}.highlight .nt{color:#2f6f9f}.highlight .nv{color:#033}.highlight .ow{color:#000}.highlight .w{color:#bbb}.highlight .mf,.highlight .mh,.highlight .mi,.highlight .mo{color:#f60}.highlight .s2,.highlight .sb,.highlight .sc,.highlight .se,.highlight .sh{color:#c30}.highlight .sd{color:#c30}.highlight .si{color:#a00}.highlight .sx{color:#c30}.highlight .sr{color:#3aa}.highlight .s1{color:#c30}.highlight .ss{color:#fc3}.highlight .bp{color:#366}.highlight .vc,.highlight .vg,.highlight .vi{color:#033}.highlight .il{color:#f60}.css .nt+.nt,.css .o,.css .o+.nt{color:#999}body,html{overflow-x:hidden}html{font-family:"PT Serif",Georgia,"Times New Roman",serif}.sidebar,h1,h2,h3,h4,h5,h6{font-family:"PT Sans",Helvetica,Arial,sans-serif}h1,h2,h3,h4,h5,h6{font-weight:400;color:#313131;letter-spacing:-.025rem}.wrap{width:100%}@media (min-width:38em){.container{max-width:32rem}}@media (min-width:56em){.container{max-width:38rem}}.masthead{padding-top:1rem;padding-bottom:1rem;margin-bottom:1rem;border-bottom:1px solid #eee}.masthead-title,.sidebar-item p:last-child{margin-bottom:0}.masthead-title{margin-top:0;color:#505050}.masthead-title a{color:#505050}.masthead-title small{font-size:75%;font-weight:400;color:silver;letter-spacing:0}@media (max-width:48em){.masthead-title{text-align:center}.masthead-title small{display:none}}.sidebar{position:fixed;top:0;bottom:0;left:-14rem;width:14rem;visibility:hidden;overflow-y:auto;font-size:.875rem;color:rgba(255,255,255,.6);background-color:#202020;-webkit-transition:all .3s ease-in-out;transition:all .3s ease-in-out}@media (min-width:30em){.sidebar{font-size:.75rem}}.sidebar a{font-weight:400;color:#fff;font-size:1rem}.sidebar-item{padding:1rem}.sidebar-nav{border-bottom:1px solid rgba(255,255,255,.1)}.sidebar-nav-item{display:block;padding:.5rem 1rem;border-top:1px solid rgba(255,255,255,.1)}.sidebar-nav-item.active,a.sidebar-nav-item:focus,a.sidebar-nav-item:hover{text-decoration:none;background-color:rgba(255,255,255,.1);border-color:transparent}@media (min-width:48em){.sidebar-item{padding:1.5rem}.sidebar-nav-item{padding-left:1.5rem;padding-right:1.5rem}}.sidebar-checkbox{position:absolute;opacity:0;-webkit-user-select:none;-moz-user-select:none;user-select:none}.sidebar-toggle{position:absolute;top:.8rem;left:1rem;display:block;padding:.25rem .75rem;color:#505050;background-color:#fff;border-radius:.25rem;cursor:pointer}.sidebar-toggle:before{display:inline-block;width:1rem;height:.75rem;content:"";background-image:-webkit-linear-gradient(to bottom,#555,#555 20%,#fff 20%,#fff 40%,#555 40%,#555 60%,#fff 60%,#fff 80%,#555 80%,#555 100%);background-image:-moz-linear-gradient(to bottom,#555,#555 20%,#fff 20%,#fff 40%,#555 40%,#555 60%,#fff 60%,#fff 80%,#555 80%,#555 100%);background-image:-ms-linear-gradient(to bottom,#555,#555 20%,#fff 20%,#fff 40%,#555 40%,#555 60%,#fff 60%,#fff 80%,#555 80%,#555 100%);background-image:linear-gradient(to bottom,#555,#555 20%,#fff 20%,#fff 40%,#555 40%,#555 60%,#fff 60%,#fff 80%,#555 80%,#555 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diff --git a/syspages/news.md b/syspages/news.md
new file mode 100644
index 0000000..39089a0
--- /dev/null
+++ b/syspages/news.md
@@ -0,0 +1,8 @@
+---
+title: "Redirecting to Blog"
+layout: redirect
+sitemap: false
+permalink: /news/
+redirect_to: /blog/
+#teaser: SYSTEM GENERATED PAGE FOR PAGE REDIRECT FUNCTION. DO NOT EDIT/RENAME/REMOVE THIS PAGE.
+---
diff --git a/syspages/pubs_redir.md b/syspages/pubs_redir.md
new file mode 100644
index 0000000..ed7bad6
--- /dev/null
+++ b/syspages/pubs_redir.md
@@ -0,0 +1,8 @@
+---
+title: "Redirecting to About/Publications"
+layout: redirect
+sitemap: false
+permalink: /publications/
+redirect_to: /about/publications/
+#teaser: SYSTEM GENERATED PAGE FOR PAGE REDIRECT FUNCTION. DO NOT EDIT/RENAME/REMOVE THIS PAGE.
+---
diff --git a/syspages/resume.md b/syspages/resume.md
new file mode 100644
index 0000000..8a1b24c
--- /dev/null
+++ b/syspages/resume.md
@@ -0,0 +1,8 @@
+---
+title: "Redirecting to Curriculum Vitae page"
+layout: redirect
+sitemap: true
+permalink: /resume/
+redirect_to: /cv/
+#teaser: SYSTEM GENERATED PAGE FOR PAGE REDIRECT FUNCTION. DO NOT EDIT/RENAME/REMOVE THIS PAGE.
+---
diff --git a/syspages/search.md b/syspages/search.md
new file mode 100644
index 0000000..4e2ae63
--- /dev/null
+++ b/syspages/search.md
@@ -0,0 +1,24 @@
+---
+layout: default_minimal
+title: "Search"
+description: "Search"
+permalink: /search/
+sitemap: false
+noindex: true
+nofollow: true
+category: base
+---
+
+{% if site.google_search %}
+
+
+
+
+
+
+{% else %}
+Google Custom Search key is not set in `_config.yml`
+{% endif %}
diff --git a/syspages/tags.md b/syspages/tags.md
new file mode 100644
index 0000000..3d68788
--- /dev/null
+++ b/syspages/tags.md
@@ -0,0 +1,39 @@
+---
+layout: page
+title: "Tag Cloud"
+permalink: "/tags/"
+description: "Browse website by tag based index"
+comments: false
+sitemap: false
+category: base
+---
+
+{:.text-center}
+## Featured Posts
+
+
+
+{% comment %}
+ Tag generation is experimental and dynamic size for tag box may need to be adjusted if you have more than 100 posts with one or two frequently occurring tags. Also,all for loop operations will increase site build time.
+{% endcomment %}
+
+{% capture site_tags %}{% for tag in site.tags %}{{ tag | first }}{% unless forloop.last %},{% endunless %}{% endfor %}{% endcapture %}
+{% assign tags_list = site_tags | split:',' | sort %}
+
+