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Collaborations and Open Access Innovations – CHI, BioIT World, 4/29 – 5/1/2014, Seaport World Trade Center, Boston

Posted in Computational Biology/Systems and Bioinformatics, Curation, Interviews with Scientific Leaders, Technology Advance Assessment of, Theoretic convergence on February 7, 2014| Leave a Comment »

Collaborations and Open Access Innovations – CHI, BioIT World, 4/29 – 5/1/2014, Seaport World Trade Center, Boston

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #109: Collaborations and Open Access Innovations – CHI, BioIT World, 4/29 – 5/1/2014, Seaport World Trade Center, Boston. Published on 2/7/2014

WordCloud Image Produced by Adam Tubman

 

Track 11 explores best practices in collaboration and information sharing that helps to drive progress in translational research. Case studies will be presented to show new insights on key drivers, technology innovations, collaboration platforms, open-source frameworks, and other factors that are managing analytical data and empowering transformative changes through translation. Additional topics to be covered include portals (website, research, collaboration) and their applications, data liquidity, and technical and cultural obstacles.

Final Agenda

 

Download Brochure | Pre-Conference Workshops

 

TUESDAY, APRIL 29

 

7:00 am Workshop Registration and Morning Coffee

8:00 – 11:30 Recommended Morning Pre-Conference Workshops*

Analyzing NGS Data in Galaxy

12:30 – 4:00 pm Recommended Afternoon Pre-Conference Workshops*

Running a Local Galaxy Instance
The tranSMART Platform Today and Tomorrow
IT & Informatics in Support of Collaboration and Externalization

*Separate Registration Required. Click here for detailed information.

 

2:00 – 7:00 pm Main Conference Registration

4:00 Event Chairperson’s Opening Remarks

Cindy Crowninshield, RD, LDN, Conference Director, Cambridge Healthtech Institute

 

4:05 PLENARY KEYNOTE SESSION 

Click here for detailed information.

 

5:00 – 7:00 Welcome Reception in the Exhibit Hall with Poster Viewing

iPad® mini & Bose® QuietComfort 15 Noise Cancelling Headphones Raffle! Drawing held at 6:30pm!*

 

*Apple® & Bose® are not sponsors or participants in this program.

 

WEDNESDAY, APRIL 30

7:00 am Registration Open and Morning Coffee

8:00 Chairperson’s Opening Remarks

Phillips Kuhl, Co-Founder and President, Cambridge Healthtech Institute

 

8:05 PLENARY KEYNOTE SESSION 

Click here for detailed information.

 

9:00 Benjamin Franklin Award & Laureate Presentation

9:30 Best Practices Awards Program

9:45 Coffee Break in the Exhibit Hall with Poster Viewing

 

COLLABORATING IN CHRONIC AND RARE DISEASES 

10:50 Chairperson’s Remarks

Marcia Kean, Chairman, Strategic Initiatives, Feinstein Kean Healthcare

11:00 PANEL DISCUSSION: Data Liquidity: New “Surge” in the War against Cancer, Diabetes and MS

Marcia Kean, Chairman, Strategic Initiatives, Feinstein Kean Healthcare

Gwen Darien, Executive Vice President, Programs and Services, Cancer Support Community

Robert McBurney, Ph.D., neuroscientist; CEO, Accelerated Cure Project for MS

Kenneth Buetow, Ph.D., Director of Computational Sciences and Informatics, Complex Adaptive Systems Initiative (CASI), Arizona State University

Dave King, Founder and CEO, Exaptive, Inc.

Data that could be applied to fuel biomedical research has been siloed, inaccessible, and often incomprehensible across disciplines. New initiatives, often driven by patients, are demanding standards-based collection of data that can be facilely integrated, analyzed and shared. The Data Liquidity Coalition is a collaboration comprised of a wide spectrum of stakeholders in the biomedical community – including providers, payers, patients, researchers and others –who are deeply committed to actualizing a common vision of data liquidity to achieve personalized medicine. This panel of Coalition members will present three collaborative projects underway to combat killer and chronic diseases. Each project puts patients at the center, and uses open source technology to enable the seamless usage of data from multiple sources to accelerate basic, translational, clinical and psychosocial research, as well as to lay the groundwork for a national system of data liquidity in biomedicine.

12:00 pm Sponsored Presentations (Opportunities Available)

12:30 Luncheon Presentations (Sponsorship Opportunities Available) or Lunch on Your Own

1:50 Chairperson’s Remarks

1:55 Collaborating in Rare Diseases through Technology

Alex Sherman, Director, Strategic Development and Systems, Neurological Clinical Research Institute, Massachusetts General Hospital

Rare diseases have to self-organize to become attractive to pharma/biotech industry. Collaborative technology and methodology allow information to be aggregated and harmonized from heterogeneous sources, including patient registries, Electronic Health Records, biorepositories, and clinical and research databases. Global Patient Identifier helps to link it all together. Evolving crowd-sourcing and crowd-funding initiatives allow multiply number of people participating in medical research and data analyses.

2:25 Accelerating Rare and Chronic Disease Research with Transparent Informatics

Alexander Wait Zaranek, Ph.D., Research Fellow in Genetics, Harvard Catalyst at Harvard Medical School

2:55 Sponsored Presentation (Opportunity Available)

3:10 Accelrys ScienceCloud: A Hosted Strategies for Collaborative R&D

Matt Hahn, Ph.D., CTO, Accelrys

The life sciences industry has been undergoing dramatic changes and effective global collaboration has become a key success factor in this new age. Accelrys is providing a hosted and comprehensive solution stack for externalized, collaborative research for pharma/biotech and CROs to address these new challenges.

3:25 Refreshment Break in the Exhibit Hall with Poster Viewing

 

COLLABORATION AND EXTERNALIZATION IN R&D 

4:00 Informatics Paradox: Separating and Collaborating in Life Science

Sarah Blendermann, Senior Director, Chemistry & Pharmacology, Business Technology, Pfizer

The organization was running operations and discovery while separating data and systems. Collaboration and segregation were key components of the informatics required to successfully meet an IPO timeline. A long-term collaboration agreement means ties between the organizations will remain, requiring longer-term technical solutions for granular security, collaboration, and data sharing.

4:30 Towards the Intelligent and Automated Analytical Laboratory

Dave Hartsough, Ph.D., Executive Director, Sites, Benchtop, & Validation R&D Informatics, Amgen

This presentation will provide an update on the progress of the Allotrope Foundation towards delivering an open Framework solution for managing analytical data throughout its lifecycle and will include details on the deliverables, timelines, and results from completed proof-of-concept applications based upon the initial proposal and analysis presented in 2013.

5:00 Sponsored Presentations (Opportunities Available)

5:30 – 6:30 Best of Show Awards Reception in the Exhibit Hall

 

THURSDAY, MAY 1

7:00 am Registration Open

7:00 Breakfast Presentation (Sponsorship Opportunity Available) or Morning Coffee

8:00 Chairperson’s Opening Remarks

Kevin Davies, Ph.D., Vice President Business Development & Publisher C&EN, American Chemical Society; Founding Editor, Bio-IT World

 

8:05 PLENARY KEYNOTE SESSION 

Click here for detailed information.

 

10:00 Coffee Break in the Exhibit Hall and Poster Competition Winners Announced

 

COLLABORATIVE APPROACHES TO CLINICAL DATA 

10:30 Chairperson’s Opening Remarks

10:35 PANEL DISCUSSION: Forming a Collaborative Approach to Develop a Data and Technology Blueprint

Muzafar Mirza, Director, Information Strategy and Analytics, Clinical Informatics and Innovation, Pfizer, Inc.

Georgina Wood, Global Head, Technology Innovations, Novartis

Francis Kendall, Global Head, Statistical Programming and Analysis, Roche

Matt Smith, Director, Bristol-Myers Squibb

This panel is a read-out of a collaboration between several pharma companies with the prime objective of devising solutions to the challenges that we face as an industry. This cross-pharma consortium focused discussions on technology, standards and data with a view to creating a common framework for how we process data especially in the changing data landscape. Key focus areas included: Transition to CDSIC, Data Aggregation (including broad categories of data – Clinical Trial data, Payer databases, Registry data, Electronic Medical Records Genome data, Biomarker data and Legacy data), key technologies related to data warehousing/data reporting, validation of data analysis tools and open source approaches.

11:35 Sponsored Presentations (Opportunities Available)

12:05 pm Luncheon Presentations (Sponsorship Opportunities Available) or Lunch on Your Own

1:15 Dessert Refreshment Break in the Exhibit Hall with Poster Viewing

1:55 Chairperson’s Remarks

2:00 Interactive Medical Literature: ITN TrialShare for Open Access in Clinical Trials

Adam Asare, Ph.D., Senior Director, Bioinformatics, Immune Tolerance Network

The Immune Tolerance Network (ITN) recently achieved an unprecedented milestone in clinical trial transparency through a high profile publication in the New England Journal of Medicine that included links to the underlying clinical data and analysis code in the ITN TrialShare web portal (www.itntrialshare.org). This marks a significant advance in data sharing and transparency, allowing researchers the ability to access study data, confirm published conclusions and interactively perform their own exploratory analyses. The presentation includes lessons learned in creating interactive publications with embedded URL links and its impact on the manuscript development and review process. Metrics on system usage will also be highlighted along with scientific collaborations developed.

 

CONSORTIA EFFORTS: UPDATES, OPPORTUNITIES, DISCUSSION 

Speakers will give a 15-20 minute presentation about their consortia efforts and then convene for a panel discussion.

2:30 Open PHACTS: Practical Semantics for Drug Discovery

Lee Harland, Ph.D., CTO, Open PHACTS, Connected Discovery

The Open PHACTS project is a €20 Million collaboration between major pharma and a range of top academic institutes. Its mission it to create an open, pre-competitive, cloud-based data integration and analysis platform. This talk will describe the journey and the outcome of a major effort in applying semantic technologies to drug discovery and provide a vision for future collaboration across pharma and biotech in this area.

2:50 Enable Unified Analysis and Mining of Biological and Chemical Data from Various Sources

Daniel Stoffler, Ph.D., Senior Principal Scientist, Group Leader Cheminformatics & Statistics, F. Hoffmann-La Roche Ltd, Basel

Computational methods that rely on historical activity data such as target identification in phenotypic screens or virtual screenings based on biological profiles, compound repurposing or pathway identification have been limited due to the inaccessibility or fragmentation of the various data sources. This undertaking will capitalize on the IMI ‘OpenPHACTS’ initiative and will use novel approaches to allow scientist accessing internal and external Chemical and Biological data sources through one interface.

3:10 The European Translational Research Information and Knowledge Management Services (eTRIKS): 18 Months into a Novel IMI Project to Support Translational Research Data Management

Jay Bergeron, Director, Translational and Bioinformatics, Pfizer

eTRIKS has delivered substantial value to the translational data management community including acting as the key development partner for creating a fully open source version of the tranSMART platform (using PostgreSQL). eTRIKS has released (Nov 2013) a public server including clinical and molecular studies and is continuing to implement a tranSMART-based roadmap that includes emerging security, analytic and semantic capabilities.

3:30 tranSMART: Enabling Rapid Exploratory Analyses and Hypothesis Generation at Pfizer

Angela Gaudette, Business Analyst, Research Business Technology, Pfizer

Many organizations are seeking ways of supporting clinical endpoint and biomarker information generated by human studies and would benefit from a platform that consistently manages these data while allowing for collaborative information sharing and transfer both internally and externally. We will share our experience at Pfizer with our adoption of tranSMART, an open source platform. Learn how Pfizer has contributed to this open source initiative by enabling the search and visualization of Genome Wide Association Studies within the tranSMART platform and discover the potential of such a platform through a neuroscience case study.

3:50 PANEL DISCUSSION with Speakers

4:00 Conference Adjourns

Download Brochure | Pre-Conference Workshops

SOURCE

http://www.bio-itworldexpo.com/Open-Source-Solutions/

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Circulating Endothelial Progenitors Cells (cEPCs) as Biomarkers

Posted in Atherogenic Processes & Pathology, Best evidence, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, Bone marrow derived cells, Cardiovascular Research, Chemical Genetics, Circulating Progenitor Cells, Curation, Cytoskeleton, Diagnostic Immunology, Discovery process, Endothelial cells, Experimental validation, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Genomic Testing: Methodology for Diagnosis, Immunodiagnostics, Interviews with Scientific Leaders, Metabolomics, Nitric Oxide in Health and Disease, Nutrition, Origins of Cardiovascular Disease, Population Health Management, Nutrition and Phytochemistry, Proteomics, Technology Advance Assessment of, Translational Effectiveness, Translational Research, Translational Science, Umbilical cord cells, tagged CEC subtypes, cell function correlation, cell identification by labelling, Circulating Progenitor Endothelial Cells, endothelial cell, Endothelial progenitor cell, increased number of CECs, ischemic dardiac disease, myocardial infarction, target cell blockers on January 14, 2014| Leave a Comment »

Circulating Endothelial Progenitors Cells (cEPCs) as Biomarkers

Article Curator: Larry H. Bernstein, MD, FCAP

and

Topic Curator: Aviva Lev-Ari, PhD, RN

Article ID #105: Circulating Endothelial Progenitors Cells (cEPCs) as Biomarkers. Published on 1/14/2014

WordCloud Image Produced by Adam Tubman

Circulating progenitor cells have gained much interest rapidly in the past year primarily in identification of damaged tissue that has turnover of cells that are identifiable in the circulation.  This has to require a sensitivity for identification at one or two logs lower than circulating hematopoietic cells.  I mention this untested view only because cells of the circulation are detected routinely by automated hematology instruments like those of Beckman-Coulter and Siemens, with graphical presentation of results.  The Sysmex also reports immature granulocytes that are a small percent of the neutrophil count.  In the evaluation of leukemias, flow cytometry has been used for years, but require a preparative step.  Cell types have been identified by acidic and basic dye stains to identify basophilic, acidophilic and neutrophilic granulocyte series, and by size of the cell population, and nuclear features, differentiating mature and nucleated red cells, the granulocyte series, monocytes and lymphocytes, as well as platelets (aggregation gives an underestimate of platelet count).  But to detect cancer cells or damaged endothelial cells, the number of cells in the circulation requires and antibody to the surface with a visualizable ligand attached to an antibody for identification.  Visualization could be by a fluorophor, or perhaps a luciferase reaction.  Here are two articles that identify circulating endothelial cells, making them suitable for biomarkers of cardiovascular injury.  Whether they can detect early predictive ischemia, or frank AMI needs investigation.  The concept of piecemeal necrosis in the heart may be applicable to cardiomyocyte injury that is found unexpectedly at autopsy as “silent infarct”.

Circulating endothelial progenitors–cells as biomarkers

Rosenzweig, Anthony
N Engl J Med. 2005 Sep 8;353(10):1055-7

Comment on

Circulating endothelial progenitor cells and cardiovascular outcomes

[N Engl J Med. 2005]  PMID: 16148292 [PubMed – indexed for MEDLINE]

Endothelial injury and dysfunction are thought to be critical events in the  pathogenesis of atherosclerosis. Thus,

• understanding the mechanisms that  maintain and restore endothelial function
  • may have important clinical  implications.

A series of clinical and basic studies prompted by the discovery 

• of bone marrow derived endothelial progenitor cells1 have
• provided insights into these processes and
  • opened a door to the development of new therapeutic approaches.

Growing evidence suggests that bone marrow derived endothelial progenitor cells circulate in the blood and

• play an important role in the formation of new blood vessels as well as
• contribute to vascular homeostasis in the adult.

Circulating endothelial progenitor cells were initially identified

• through their expression of CD34
  (a surface marker common to hematopoietic stem cells and mature endothelial cells)
• and vascular endothelial cell growth-factor receptor 2
  (VEGFR2 or kinase-domain related [KDR] receptor),

but not of other markers seen on fully differentiated endothelial cells.1

Subsequent studies have also used other identifiers, such as

• the stem-cell marker CD133, and
• functional assays, including
  • the ability to form endothelial colonies.

Endothelial progenitor cells defined in these ways probably represent

• a heterogeneous population, which,
• in combination with the lack of a consensual definition,

complicates the interpretation of work in this field.

Nevertheless, numerous studies in animals have shown that endothelial  progenitor cells can integrate into new and existing blood vessels.2,3,4
Intravenous injection of cytokine-mobilized human endothelial progenitor cells

• improved myocardial neoangiogenesis and
• the recovery of functioning in a rat model of infarction.3

Repeated injection of bone marrow derived cells in a mouse model of atherosclerosis

• reduced the rate of plaque formation without altering serum lipids levels, and
• donor endothelial progenitor cells could subsequently be identified in the recipient’s blood vessels.4

Previous clinical studies have shown that

• traditional risk factors for coronary atherosclerosis
• are associated with low levels of circulating endothelial progenitor cells,5 whereas
• protective interventions, including statin therapy6 and exercise,7
  • appear to increase the supply of these cells.

Hill et al. found that even in healthy volunteers,

• levels of endothelial progenitor cells were inversely correlated with the Framingham risk score and
• actually appeared to predict vascular function better than the Framingham risk score.5

Together, these data suggest that circulating endothelial progenitor cells may participate

• not only in forming new blood vessels
• but also in maintaining the integrity and function of vascular  endothelium,

thereby mitigating disease processes such as atherosclerosis.

In this issue of the Journal, Werner and colleagues have further advanced our understanding of the clinical implications of endothelial progenitor cells.8 Endothelial progenitor cells were quantitated in 519 patients with coronary artery disease who

• were followed for one year after undergoing catheterization.

Patients with higher levels of endothelial progenitor cells had

• a reduced risk of death from cardiovascular causes and of
• the composite end point of major cardiovascular events.

These relationships were preserved even

• after adjustment for traditional risk factors and prognostic variables.

A similar relationship was seen

• whether endothelial progenitor cells were  identified by virtue of expression
  either of CD34 and KDR or of CD133 or
• because of their ability to form endothelial colonies,

further strengthening the authors’ conclusions. Repeated catheterization was not performed in this  cohort, so

• we do not know whether the reduction in clinical events reflected a slowed progression of atherosclerosis or some other clinical effect.

A  dissociation between anatomical measures of atherosclerosis and clinical events has been well documented in other settings.

Although this study is consistent with prior work suggesting that circulating endothelial progenitor cells may play a protective role in vascular homeostasis, other explanations

• for the association between endothelial progenitor number and outcome remain possible.

Changes in the number of endothelial progenitor cells and

• in clinical events might reflect a common underlying etiology,
  • • rather than a causal relation.

For example, a defect in the production of nitric oxide, which plays an important role

• in both the mobilization of endothelial progenitor cells9 and blood-vessel function, might account for both observations.

Similarly, the number of endothelial progenitor cells

• may mirror a person’s regenerative capacity more broadly and
• predict clinical events on that basis.

Even if endothelial progenitor cells are mechanistically linked to clinical cardiovascular events,

• such clinical studies do not distinguish between the possibility
• that the protection is mediated through the integration of endothelial  progenitor cells into blood vessels and

its possible mediation by other  mechanisms, such as the

• paracrine benefits of endothelial progenitor  cell secreted products.

Although such questions will undoubtedly continue to provide fertile ground  for fundamental investigation,

• the report by Werner and colleagues has more  immediate clinical implications.

First, it suggests that circulating cell  populations may represent a new class of biomarkers

• that naturally integrate  diverse genetic and environmental effects,
• thereby providing robust  physiological and prognostic insights.

Second, in the context of coronary  disease, the study shows that

• the number of endothelial progenitor cells is an independent predictor of hard clinical outcomes.

As with other biomarkers, a demonstration of clinical usefulness will ultimately require

• the examination of other patient populations, as well as
• a demonstration that clinical therapy can be guided and enhanced by this information.

Finally, the increased risk associated with reduced levels of endothelial progenitor cells

• supports the growing interest in the therapeutic potential of enhancing the level of these cells.

The most dramatic extension of this line of reasoning involves

transferring  bone marrow or peripheral blood cells that are likely to include endothelial  progenitor cells to patients with coronary artery disease. Although it would be premature to judge the clinical success of these strategies, early trials, including one randomized (though incompletely blinded) trial, have suggested

• at least short-term functional benefits of intracoronary infusion of bone marrow cells after acute infarction.10

Trials are planned to address more definitively the potential benefits of such cells

• in the settings of acute infarction and chronic ischemic cardiomyopathy.

Such efforts would be aided substantially by the identification of specific markers as well as

• an improved understanding of the role of subtypes of endothelial progenitor cells and
• of the mechanisms by which they work.

Ironically, the data presented by Werner and colleagues in combination with work showing

• the impaired functioning of endothelial progenitor cells in high-risk patients5 suggest
• that the patients most in need of endothelial progenitor cells may be
  • • those who are least able to donate them for autologous transplantation.

Whether these limitations can be overcome through

• ex vivo expansion or  genetic modification of endothelial progenitor cells is unclear.

In addition to possible cell-based therapies, work on endothelial progenitor cells provides yet another rationale

• for redoubling efforts to comply with established therapeutic guidelines,
• including lifestyle modifications and the use of statin therapy,
  • • both of which appear to enhance the number of circulating endothelial progenitor cells.

Whether there will be a downside to enhancing the number and function of  endothelial progenitor cells remains unclear,

• although obvious concerns  include exacerbating conditions that are characterized by adverse vessel  formation,
  • such as diabetic retinopathy and tumor angiogenesis.

Small studies have suggested an association between high levels of circulating endothelial progenitor cells and the risk of certain cancers, such as multiple myeloma.11 Moreover, studies in animals show that

• bone marrow derived endothelial progenitors participate in tumor angiogenesis, thereby
  • • enhancing tumor growth.12

In the study by Werner and colleagues,

• the number of deaths from cardiovascular causes among patients with high levels of endothelial progenitor cells
• was substantially lower than that among patients with lower levels of these cells,
• without a reduction in the risk of death overall.8

Although this finding could raise the specter of a counterbalancing adverse effect of endothelial progenitor cells,

• there was no apparent pattern in the deaths due to other causes,
• and no deaths from cancer were noted in this population.

It is possible that as we learn more about the biology of endothelial progenitor cells, there may be opportunities

• to target vessel formation more specifically.

In addition, therapeutic strategies

• tailored to individualized risk will undoubtedly help in practice.

For example, in the study by Werner et al.,

• patients in the group with the lowest baseline levels of endothelial progenitor cells
• had a risk of death from cardiovascular causes of 8.3 percent during one year of follow-up,
• suggesting that the benefits of enhancing the function and number of endothelial progenitor cells
  • • may well outweigh the risks in such high-risk populations.

Additional studies will be necessary to address these questions definitively. Larger studies

• of longer duration performed in different cohorts will be required to determine fully
  • the clinical usefulness of endothelial progenitor cells as a biomarker.

Rigorous interventional studies will indicate

• whether levels of endothelial progenitor cells can be used to guide therapy and
• whether cell transfer has a role in augmenting the levels of these cells.

Basic-science studies should help guide these clinical efforts by

• further defining the desirable subpopulations of endothelial progenitor cells and
• the mechanisms by which they mediate their effects.

By establishing a connection between circulating endothelial progenitor cells and hard clinical end points, Werner and colleagues

• provide a potent stimulus for clinical and basic studies to address these important issues.

Source Information

From the Program in Cardiovascular Gene Therapy, Massachusetts General  Hospital, and Harvard Medical School ― both in Boston.

References

Asahara T, Murohara T, Sullivan A, et al. Isolation of putative progenitor  endothelial cells for angiogenesis. Science 1997;275:964-967.

Takahashi T, Kalka C, Masuda H, et al. Ischemia- and cytokine-induced  mobilization of bone marrow-derived endothelial progenitor cells for  neovascularization. Nat Med 1999;5:434-438.

Kocher AA, Schuster MD, Szabolcs MJ, et al. Neovascularization of ischemic myocardium by human bone-marrow-derived angioblasts prevents cardiomyocyte apoptosis, reduces remodeling and improves cardiac function. Nat Med 2001; 7: 430-436.

Rauscher FM, Goldschmidt-Clermont PJ, Davis BH, et al. Aging, progenitor cell exhaustion, and atherosclerosis. Circulation 2003; 108: 457-463.

Hill JM, Zalos G, Halcox JPJ, et al. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med 2003;348:593-600.

Vasa M, Fichtlscherer S, Adler K, et al. Increase in circulating endothelial  progenitor cells by statin therapy in patients with stable coronary artery  disease. Circulation 2001; 103: 2885-2890.

Laufs U, Werner N, Link A, et al. Physical training increases endothelial  progenitor cells, inhibits neointima formation, and enhances angiogenesis.  Circulation 2004; 109: 220-226.

Werner N, Kosiol S, Schiegl T, et al. Circulating endothelial progenitor cells and cardiovascular outcomes. N Engl J Med 2005; 353: 999-1007.

Aicher A, Heeschen C, Mildner-Rihm C, et al. Essential role of endothelial nitric oxide synthase for mobilization of stem and progenitor cells. Nat Med  2003; 9: 1370-1376.

Wollert KC, Meyer GP, Lotz J, et al. Intracoronary autologous bone-marrow  cell transfer after myocardial infarction: the BOOST randomised controlled  clinical trial. Lancet 2004; 364: 141-148.

Zhang H, Vakil V, Braunstein M, et al. Circulating endothelial progenitor cells in multiple myeloma: implications and significance. Blood 2005; 105: 3286-3294.

Lyden D, Hattori K, Dias S, et al. Impaired recruitment of bone-marrow-derived endothelial and hematopoietic precursor cells blocks tumor angiogenesis and growth. Nat Med 2001;7:1194-1201.

Fluid phase biopsy for detection and characterization of circulating endothelial cells in myocardial infarction.

Kelly Bethel, Madelyn S Luttgen, Samir Damani, Anand Kolatkar, Rachelle Lamy, Mohsen Sabouri-Ghomi, Sarah Topol, Eric J Topol, Peter Kuhn

Physical Biology (Impact Factor: 2.62). 01/2014; 11(1):016002. http://dx.doi.org/10.1088/1478-3975/11/1/016002
Source: PubMed

Elevated levels of circulating endothelial cells (CECs) occur in response to various pathological conditions including myocardial infarction (MI). Here, we adapted

• a fluid phase biopsy technology platform that successfully detects circulating tumor cells in the blood of cancer patients (HD-CTC assay),
• to create a high-definition circulating endothelial cell (HD-CEC) assay for the detection and characterization of CECs.

Peripheral blood samples were collected from 79 MI patients, 25 healthy controls and six patients undergoing vascular surgery (VS). CECs were defined

• by positive staining for DAPI, CD146 and von Willebrand Factor
• and negative staining for CD45.

In addition, CECs exhibited distinct morphological features that

• enable differentiation from surrounding white blood cells.

1. CECs were found both as individual cells and as aggregates.
2. CEC numbers were higher in MI patients compared with healthy controls.
3. VS patients had lower CEC counts when compared with MI patients

but were not different from healthy controls.

Both HD-CEC and CellSearch® assays could discriminate

• MI patients from healthy controls with comparable accuracy

but the HD-CEC assay exhibited

• higher specificity while maintaining high sensitivity.

Our HD-CEC assay may be used as a robust diagnostic biomarker in MI patients.

MicroRNA function in endothelial cells

Solving the mystery of an unknown target gene using microRNA Target Site Blockers

Dr. Virginie Mattot

Dr. Virgine Mattot works in the team “Angiogenesis, endothelium activation and Cancer” directed by Dr. Fabrice Soncin at the Institut de Biologie de Lille in France where she studies the roles played by microRNAs in endothelial cells during physiological and pathological processes such as angiogenesis or endothelium activation. She has been using Target Site Blockers to investigate the role of microRNAs on putative targets which functions are yet unknown.

What is the main focus of the research conducted in your lab?

We are studying endothelial cell functions with a particular interest

• in angiogenesis and endothelium activation during physiological and tumoral vascular development.

How did your research lead to the study of microRNAs?

A few years ago, we identified in my team

• a new endothelial cell-specific gene which harbors a microRNA in its intronic sequence.

We have since been working on understanding

• the functions of both this new gene and
• its intronic microRNA in endothelial cells

What is the aim of your current project?

While we were searching for the functions of the intronic microRNA,

• we identified an unknown gene as a putative target.

The aim of my project was to investigate if this unknown gene was actually a genuine target and

• if regulation of this gene by the microRNA was involved in endothelial cell function.

We had already characterized the endothelial cell phenotype associated with the inhibition of our intronic microRNA.

We then used miRCURY LNA™ Target Site Blockers to demonstrate

• that the expression of this unknown gene is actually controlled by this microRNA.

Further, we also demonstrated that the microRNA regulates

• specific endothelial cell properties through regulation of this unknown gene.

How did you perform the experiments and analyze the results?

LNA™ enhanced target site blockers (TSB) for our microRNA were designed by Exiqon.
We transfected the TSBs into endothelial cells using our standard procedure and

• analysed the induced phenotype.

As a control for these experiments, a mutated version of the TSB was designed by Exiqon and

• transfected into endothelial cells.

We first verified that this TSB was functional by

• analyzing the expression of the miRNA target
  • • against which the TSB was directed in transfected cells.

Finally, we showed that the TSB induced similar phenotypes as those found when we inhibited the microRNA in the same cells. 

What were some specific challenges in your experiments and how did you overcome them?

The fact that the target gene for our microRNA was unknown was a major challenge. Without specific available tools, like antibodies,

• it becomes difficult to demonstrate the effect of the microRNA on the gene in question and
• to show that the unknown gene is indeed responsible for the functions of the microRNA.

However through the use of specific target site blockers, we were able to demonstrate

• that this unknown gene was associated with the phenotype observed
  • when the microRNA was inhibited in endothelial cells.

How do you feel about your results so far?

We are very pleased with the results of the TSB experiments and

• altogether these results demonstrate that our miRNA of interest
• is functional in endothelial cells
  • through the regulation of a target gene with a previously unknown role.

What do you find to be the main benefits/advantage of the LNA™ microRNA target site blockers from Exiqon?

Target Site Blockers are efficient tools to demonstrate the

• specific involvement of putative microRNA targets
• in the function played by this microRNA.

The use of LNA™ allows the design of short oligonucleotides that are very specific and easy to work with. 

What would be your advice to colleagues about getting started with microRNA functional analysis?

In order to address the role played by a microRNA,

• it is essential to perform both gain and loss of functions experiments.

What are the next steps in the current project and how do you plan to perform them?

We plan to use microRNA inhibitor libraries to identify

• more microRNAs specifically involved in the processes that we currently study.

When and where will be hear /read more about your studies?

We are currently in the process of submitting a manuscript regarding the function of my microRNA of interest.

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The Cost to Value Conundrum in Cardiovascular Healthcare Provision

Posted in Accountable Care Organizations, Affordable Care Act, Anemia, Atherogenic Processes & Pathology, Best evidence, Bio Instrumentation in Experimental Life Sciences Research, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, Ca2+ triggered activation, Ca2+ triggered activation, Calcium Signaling, Cardiac & Vascular Repair Tools Subsegment, Cardiac and Cardiovascular Surgical Procedures, Cardiac muscle regeneration, Cardiomyopathy, Cardiovascular Pharmacogenomics, Coagulation Therapy and Internal Bleeding, Computational Biology/Systems and Bioinformatics, Curation, Curation methodology, Cytoskeleton, Diabetes Mellitus, Electrophysiology, Evidence-based decision-making, Experimental validation, Federal Budget Appropriations, Frontiers in Cardiology and Cardiovascular Disorders, Health Economics and Outcomes Research, Health Law & Patient Safety, Healthcare costs and reimbursement, Healthcare Reform, Historical relevance, HTN, HTN in Youth, Indigent Nutrition, Interviews with Scientific Leaders, Ionic Transporters Na+, K, Medical Devices R&D and Inventions, Medical Imaging Technology, Image Processing/Computing, MRI, CT, Nuclear Medicine, Ultra Sound, Medicare and Medicaid, Na-K transport, Na-K-ATPase, Nephrology, Nitric Oxide in Health and Disease, Nutrition, Nutritional Supplements: Atherogenesis, lipid metabolism, Origins of Cardiovascular Disease, Pharmaceutical Analytics, Pharmacogenomics, Pharmacologic toxicities, Pharmacotherapy of Cardiovascular Disease, Population Health Management, Genetics & Pharmaceutical, Population Health Management, Nutrition and Phytochemistry, Prescription Drugs Costs, Regenerative Biology and Medicine, Resident-cell-based, Skilled Nursing Facilities, Stem Cells for Regenerative Medicine, Stents & Tools, Synaptic vesicle, Systematic Error (Bias), Systemic Inflammatory Response Related Disorders, Technology Advance Assessment of, Technology Capital Expenses, Technology Transfer: Biotech and Pharmaceutical, Translational Effectiveness, Translational Science, Uninsured and Underinsured, Valves & Tools, tagged acute myocardial infarct, American College of Cardiology ACC, Antiarrhythmic drugs, arrythmias, Artificial Biosensor, Artificial cardiac pacemaker, Artificial heart, Bare-metal stent, Cardiac & Vascular Repair, cardiac myocyte regeneration, Cardiogenic Shock, Cardiology, Cardiometabolic Syndrome, CHF, Content Curation, Coronary artery disease, Coronary stent, Curation methodology, Drug-eluting stents, gene expression, Hypertension, myocardial hypertrophy, nitric oxide, Nitric oxide synthase, RNA, Stem cell on January 1, 2014| Leave a Comment »

The Cost to Value Conundrum in Cardiovascular Healthcare Provision

Author: Larry H. Bernstein, MD, FCAP

Article ID #98: The Cost to Value Conundrum in Cardiovascular Healthcare Provision. Published on 1/1/2014

WordCloud Image Produced by Adam Tubman

I write this introduction to Volume 2 of the e-series on Cardiovascular Diseases, which curates the basic structure and physiology of the heart, the vasculature, and related structures, e.g., the kidney, with respect to:

1. Pathogenesis
2. Diagnosis
3. Treatment

Curation is an introductory portion to Volume Two, which is necessary to introduce the methodological design used to create the following articles. More needs not to be discussed about the methodology, which will become clear, if only that the content curated is changing based on success or failure of both diagnostic and treatment technology availability, as well as the systems needed to support the ongoing advances.  Curation requires:

• meaningful selection,
• enrichment, and
• sharing combining sources and
• creation of new synnthesis

Curators have to create a new perspective or idea on top of the existing media which supports the content in the original. The curator has to select from the myriad upon myriad options available, to re-share and critically view the work. A search can be overwhelming in size of the output, but the curator has to successfully pluck the best material straight out of that noise.

Part 1 is a highly important treatment that is not technological, but about the system now outdated to support our healthcare system, the most technolog-ically advanced in the world, with major problems in the availability of care related to economic disparities.  It is not about technology, per se, but about how we allocate healthcare resources, about individuals’ roles in a not full list of lifestyle maintenance options for self-care, and about the important advances emerging out of the Affordable Care Act (ACA), impacting enormously on Medicaid, which depends on state-level acceptance, on community hospital, ambulatory, and home-care or hospice restructuring, which includes the reduction of management overhead by the formation of regional healthcare alliances, the incorporation of physicians into hospital-based practices (with the hospital collecting and distributing the Part B reimbursement to the physician, with “performance-based” targets for privileges and payment – essential to the success of an Accountable Care Organization (AC)).  One problem that ACA has definitively address is the elimination of the exclusion of patients based on preconditions.  One problem that has been left unresolved is the continuing existence of private policies that meet financial capabilities of the contract to provide, but which provide little value to the “purchaser” of care.  This is a holdout that persists in for-profit managed care as an option.  A physician response to the new system of care, largely fostered by a refusal to accept Medicaid, is the formation of direct physician-patient contracted care without an intermediary.

In this respect, the problem is not simple, but is resolvable.  A proposal for improved economic stability has been prepared by Edward Ingram. A concern for American families and businesses is substantially addressed in a macroeconomic design concept, so that financial services like housing, government, and business finance, savings and pensions, boosting confidence at every level giving everyone a better chance of success in planning their personal savings and lifetime and business finances.

http://macro-economic-design.blogspot.com/p/book.html

Part 2 is a collection of scientific articles on the current advances in cardiac care by the best trained physicians the world has known, with mastery of the most advanced vascular instrumentation for medical or surgical interventions, the latest diagnostic ultrasound and imaging tools that are becoming outdated before the useful lifetime of the capital investment has been completed.  If we tie together Part 1 and Part 2, there is ample room for considering  clinical outcomes based on individual and organizational factors for best performance. This can really only be realized with considerable improvement in information infrastructure, which has miles to go.  Why should this be?  Because for generations of IT support systems, they are historically focused on billing and have made insignificant inroads into the front-end needs of the clinical staff.

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