Skip to main content
Advertisement
  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

  • Home
  • About this Journal
    • Editorial Board
    • General Statistics
    • Circulation Doodle
      • Doodle Gallery
      • Circulation Cover Doodle
    • → Blip the Doodle
    • Information for Advertisers
    • Author Reprints
    • Commercial Reprints
    • Customer Service and Ordering Information
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • AHA Guidelines and Statements
    • Bridging Disciplines
    • → Articles Bridging Discplines
    • Cardiovascular Case Series
    • Circulation Supplements
    • ECG Challenge
    • Hospitals of History
      • Hospital Santa Maria del Popolo, Naples, Italy
      • Minneapolis City Hospital
      • Pitié-Salpêtrière Hospital
      • Tufts Medical Center
      • Uppsala University Hospital
      • Vassar Brothers Medical Center (Poughkeepsie, NY)
      • Wroclaw Medical University
    • On My Mind
    • Podcast Archive
      • → Circulation on the Run, FIT Edition
    • → Subscribe to Circulation on the Run
  • Resources
    • Instructions for Authors
      • Accepted Manuscripts
      • Revised Manuscripts
    • → Article Types
    • → General Preparation Instructions
    • → Research Guidelines
    • → How to Submit a Manuscript
    • Journal Policies
    • Permissions and Rights Q&A
    • Submission Sites
    • Circulation CME
    • AHA Journals RSS Feeds
    • International Users
    • AHA Newsroom
    • Scientific Sessions 2017
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Cardiovascular Genetics
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association
  • Facebook
  • Twitter

  • My alerts
  • Sign In
  • Join

  • Advanced search

Header Publisher Menu

  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

Circulation

  • My alerts
  • Sign In
  • Join

  • Facebook
  • Twitter
  • Home
  • About this Journal
    • Editorial Board
    • General Statistics
    • Circulation Doodle
    • → Blip the Doodle
    • Information for Advertisers
    • Author Reprints
    • Commercial Reprints
    • Customer Service and Ordering Information
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • AHA Guidelines and Statements
    • Bridging Disciplines
    • → Articles Bridging Discplines
    • Cardiovascular Case Series
    • Circulation Supplements
    • ECG Challenge
    • Hospitals of History
    • On My Mind
    • Podcast Archive
    • → Subscribe to Circulation on the Run
  • Resources
    • Instructions for Authors
    • → Article Types
    • → General Preparation Instructions
    • → Research Guidelines
    • → How to Submit a Manuscript
    • Journal Policies
    • Permissions and Rights Q&A
    • Submission Sites
    • Circulation CME
    • AHA Journals RSS Feeds
    • International Users
    • AHA Newsroom
    • Scientific Sessions 2017
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Cardiovascular Genetics
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association

Search for author "Ron Simon"

  • Modify Search
  • Create Alert
  • Save Search

24 Results

Type a term to search within all articles in this journal: e.g., stem cell
Content Type
Select types of content to include in the results.
Citation
Citation-specific search information
e.g., 2009
e.g., 20
e.g., 3
e.g., 29
e.g., 10.9999/123XYZ456
Authors, Keywords
Search for specific authors and/or words and phrases.
e.g., Smith, JS
e.g., Smith, JS
Type any phrase that appears in the article title
Type any phrase that appears within article title or abstract
Type any phrase that appears within article body, title or abstract
e.g., Smith, JS
Book publisher name
Limit Results
Limit search results by date
e.g., 07/24/2017
e.g., 07/24/2017
Format Results
  • You have accessRestricted access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective PhenotypesA Speculative Synthesis
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King and Roger P. Simon
    Stroke. 2007;38:680-685, originally published January 29, 2007
    https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Download PDF
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 1. LPS and ischemic preconditioning alter the genomic response to stroke. Venn diagrams showing the percent of overlap in gene regulation 3 and...Show More
    Figure 1. LPS and ischemic preconditioning alter the genomic response to stroke. Venn diagrams showing the percent of overlap in gene regulation 3 and 24 hours after stroke in mice preconditioned with LPS (5 μg) or brief ischemia (15 minutes) vs control animals subjected to stroke without prior preconditioning. Preconditioning plus stroke represented by the yellow circles; stroke alone represented by the blue circles; overlap shown in green.Show Less
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 2. Ischemic preconditioning suppresses expression of genes involved in cellular metabolism and homeostasis. Ischemic preconditioning before str...Show More
    Figure 2. Ischemic preconditioning suppresses expression of genes involved in cellular metabolism and homeostasis. Ischemic preconditioning before stroke modulates the expression of a unique subset of genes that influence metabolism or transport/channels. Gene regulation is displayed from samples taken 24 hours after stroke in the presence or absence of ischemic preconditioning. Gene expression: red indicates increased expression; green indicates decreased expression; gray indicates no change in expression. Genes were assigned to Biological Function categories based on the Gene Consortium database and literature review. HDAC5 indicates histone deacetylase 5; Ptgds, prostaglandin D2 synthase; GluR1, glutamate receptor ionotropic AMPA1; GluR3, glutamate receptor ionotropic AMPA3; KA2, glutamate receptor ionotropic kainate5 γ2; Atpa1, ATPase Na+/K+ transporting α1 polypeptide.Show Less
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 3. LPS preconditioning alters the inflammatory response to stroke injury by suppressing pro-inflammatory and increasing anti-inflammatory media...Show More
    Figure 3. LPS preconditioning alters the inflammatory response to stroke injury by suppressing pro-inflammatory and increasing anti-inflammatory mediators. LPS preconditioning before stroke modulates the expression of a unique subset of genes associated with defense responses. Gene regulation is displayed from samples taken 24 hours after stroke in the presence or absence of LPS preconditioning. Gene expression: red indicates increased expression; green indicates decreased expression; gray indicates no change in expression. The shaded red area represents genes associated with type I interferons. Genes were assigned to Biological Function categories based on the Gene Consortium database and literature review. IL6 indicates interleukin 6; Mip1a, macrophage inflammatory protein 1α; IL1r, interleukin 1 receptor; Traf6, Tnf receptor-associated factor 6.Show Less
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 4. Osteopontin does not induce unique gene regulation in response to stroke. Venn diagram showing unique gene regulation (percentage) 24 hours...Show More
    Figure 4. Osteopontin does not induce unique gene regulation in response to stroke. Venn diagram showing unique gene regulation (percentage) 24 hours after stroke in mice treated with osteopontin vs mice given a stroke without osteopontin treatment. Osteopontin plus stroke and overlap shown in the green circle and stroke alone represented by the blue circle. Osteopontin treatment reduced the number of genes with changes in expression by 4-fold.Show Less
  • You have accessRestricted access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective PhenotypesA Speculative Synthesis
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King and Roger P. Simon
    Stroke. 2007;38:680-685, originally published January 29, 2007
    https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Download PDF
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 1. LPS and ischemic preconditioning alter the genomic response to stroke. Venn diagrams showing the percent of overlap in gene regulation 3 and...Show More
    Figure 1. LPS and ischemic preconditioning alter the genomic response to stroke. Venn diagrams showing the percent of overlap in gene regulation 3 and 24 hours after stroke in mice preconditioned with LPS (5 μg) or brief ischemia (15 minutes) vs control animals subjected to stroke without prior preconditioning. Preconditioning plus stroke represented by the yellow circles; stroke alone represented by the blue circles; overlap shown in green.Show Less
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 2. Ischemic preconditioning suppresses expression of genes involved in cellular metabolism and homeostasis. Ischemic preconditioning before str...Show More
    Figure 2. Ischemic preconditioning suppresses expression of genes involved in cellular metabolism and homeostasis. Ischemic preconditioning before stroke modulates the expression of a unique subset of genes that influence metabolism or transport/channels. Gene regulation is displayed from samples taken 24 hours after stroke in the presence or absence of ischemic preconditioning. Gene expression: red indicates increased expression; green indicates decreased expression; gray indicates no change in expression. Genes were assigned to Biological Function categories based on the Gene Consortium database and literature review. HDAC5 indicates histone deacetylase 5; Ptgds, prostaglandin D2 synthase; GluR1, glutamate receptor ionotropic AMPA1; GluR3, glutamate receptor ionotropic AMPA3; KA2, glutamate receptor ionotropic kainate5 γ2; Atpa1, ATPase Na+/K+ transporting α1 polypeptide.Show Less
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 3. LPS preconditioning alters the inflammatory response to stroke injury by suppressing pro-inflammatory and increasing anti-inflammatory media...Show More
    Figure 3. LPS preconditioning alters the inflammatory response to stroke injury by suppressing pro-inflammatory and increasing anti-inflammatory mediators. LPS preconditioning before stroke modulates the expression of a unique subset of genes associated with defense responses. Gene regulation is displayed from samples taken 24 hours after stroke in the presence or absence of LPS preconditioning. Gene expression: red indicates increased expression; green indicates decreased expression; gray indicates no change in expression. The shaded red area represents genes associated with type I interferons. Genes were assigned to Biological Function categories based on the Gene Consortium database and literature review. IL6 indicates interleukin 6; Mip1a, macrophage inflammatory protein 1α; IL1r, interleukin 1 receptor; Traf6, Tnf receptor-associated factor 6.Show Less
  • You have access
    Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes
    Mary P. Stenzel-Poore, Susan L. Stevens, Jeffrey S. King, Roger P. Simon
    Stroke February 2007, 38 (2) 680-685; DOI: https://doi.org/10.1161/01.STR.0000251444.56487.4c
    Figure 4. Osteopontin does not induce unique gene regulation in response to stroke. Venn diagram showing unique gene regulation (percentage) 24 hours...Show More
    Figure 4. Osteopontin does not induce unique gene regulation in response to stroke. Venn diagram showing unique gene regulation (percentage) 24 hours after stroke in mice treated with osteopontin vs mice given a stroke without osteopontin treatment. Osteopontin plus stroke and overlap shown in the green circle and stroke alone represented by the blue circle. Osteopontin treatment reduced the number of genes with changes in expression by 4-fold.Show Less

Pages

  • 1
  • 2
  • 3
  • Next Page
Back to top

Selected Facets

Selected Facets

  • Ischemic biology - basic studies (Subject)

Article Type

Article Type

  • Acute Cerebral Infarction 12
  • Animal models of human disease 12
  • Genomics of Ischemia: Introduction 10
  • Ischemic biology - basic studies 12
  • Original Contribution 7
  • Original Contributions 7
  • Original Contributions Original Contribution Original Contributions 7
  • Transient Ischemic Attacks 5
  • Show More
  • Show Less

Content Type

Resource Type

  • Articles 4
  • Tables & Figures 20
Advertisement
Advertisement

Circulation

  • About Circulation
  • Instructions for Authors
  • Circulation CME
  • Statements and Guidelines
  • Meeting Abstracts
  • Permissions
  • Journal Policies
  • Email Alerts
  • Open Access Information
  • AHA Journals RSS
  • AHA Newsroom

Editorial Office Address:
200 Fifth Avenue, Suite 1020
Waltham, MA 02451
email: circ@circulationjournal.org
 

Information for:
  • Advertisers
  • Subscribers
  • Subscriber Help
  • Institutions / Librarians
  • Institutional Subscriptions FAQ
  • International Users
American Heart Association Learn and Live
National Center
7272 Greenville Ave.
Dallas, TX 75231

Customer Service

  • 1-800-AHA-USA-1
  • 1-800-242-8721
  • Local Info
  • Contact Us

About Us

Our mission is to build healthier lives, free of cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question. Find Out More about the American Heart Association

  • Careers
  • SHOP
  • Latest Heart and Stroke News
  • AHA/ASA Media Newsroom

Our Sites

  • American Heart Association
  • American Stroke Association
  • For Professionals
  • More Sites

Take Action

  • Advocate
  • Donate
  • Planned Giving
  • Volunteer

Online Communities

  • AFib Support
  • Garden Community
  • Patient Support Network
  • Professional Online Network

Follow Us:

  • Follow Circulation on Twitter
  • Visit Circulation on Facebook
  • Follow Circulation on Google Plus
  • Follow Circulation on Instagram
  • Follow Circulation on Pinterest
  • Follow Circulation on YouTube
  • Rss Feeds
  • Privacy Policy
  • Copyright
  • Ethics Policy
  • Conflict of Interest Policy
  • Linking Policy
  • Diversity
  • Careers

©2017 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. The American Heart Association is a qualified 501(c)(3) tax-exempt organization.
*Red Dress™ DHHS, Go Red™ AHA; National Wear Red Day ® is a registered trademark.

  • PUTTING PATIENTS FIRST National Health Council Standards of Excellence Certification Program
  • BBB Accredited Charity
  • Comodo Secured