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Archive for the ‘Disease Biology’ Category


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

Researchers have classified a brand-new organ inside human body. Known as the mesentery, the new organ is found in our digestive systems, and was long thought to be made up of fragmented, separate structures. But recent research has shown that it’s actually one, continuous organ. The evidence for the organ’s reclassification is now published in The Lancet Gastroenterology & Hepatology. Although we now know about the structure of this new organ, its function is still poorly understood, and studying it could be the key to better understanding and treatment of abdominal and digestive disease.

mesentery

J Calvin Coffey, a researcher from the University Hospital Limerick in Ireland, who first discovered that the mesentery was an organ. In 2012, Coffey and his colleagues showed through detailed microscopic examinations that the mesentery is actually a continuous structure. Over the past four years, they’ve gathered further evidence that the mesentery should actually be classified as its own distinct organ, and the latest paper makes it official. Mesentery is a double fold of peritoneum – the lining of the abdominal cavity – that holds our intestine to the wall of our abdomen. It was described by the Italian polymath Leanardo da Vinci in 1508, but it has been ignored throughout the centuries, until now. Although there are generally considered to be five organs in the human body, there are in fact now 79, including the mesentery. The heart, brain, liver, lungs and kidneys are the vital organs, but there are another 74 that play a role in keeping us healthy. The distinctive anatomical and functional features of mesentery have been revealed that justify designation of the mesentery as an organ. Accordingly, the mesentery should be subjected to the same investigatory focus that is applied to other organs and systems. This provides a platform from which to direct future scientific investigation of the human mesentery in health and disease.

References:

http://www.thelancet.com/journals/langas/article/PIIS2468-1253(16)30026-7/abstract

http://www.sciencealert.com/it-s-official-a-brand-new-human-organ-has-been-classified

http://www.bbc.com/news/health-38506708

http://www.independent.co.uk/news/science/new-organ-mesentery-found-human-body-digestive-system-classified-abdominal-grays-anatomy-a7507396.html

https://in.news.yahoo.com/scientists-discover-human-organ-064207997.html

https://en.wikipedia.org/wiki/Mesentery

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

MicroRNAs (miRNAs) are a group of small non-coding RNA molecules that play a major role in posttranscriptional regulation of gene expression and are expressed in an organ-specific manner. One miRNA can potentially regulate the expression of several genes, depending on cell type and differentiation stage. They control every cellular process and their altered regulation is involved in human diseases. miRNAs are differentially expressed in the male and female gonads and have an organ-specific reproductive function. Exerting their affect through germ cells and gonadal somatic cells, miRNAs regulate key proteins necessary for gonad development. The role of miRNAs in the testes is only starting to emerge though they have been shown to be required for adequate spermatogenesis. In the ovary, miRNAs play a fundamental role in follicles’ assembly, growth, differentiation, and ovulation.

 

Deciphering the underlying causes of idiopathic male infertility is one of the main challenges in reproductive medicine. This is especially relevant in infertile patients displaying normal seminal parameters and no urogenital or genetic abnormalities. In these cases, the search for additional sperm biomarkers is of high interest. This study was aimed to determine the implications of the sperm miRNA expression profiles in the reproductive capacity of normozoospermic infertile individuals. The expression levels of 736 miRNAs were evaluated in spermatozoa from normozoospermic infertile males and normozoospermic fertile males analyzed under the same conditions. 57 miRNAs were differentially expressed between populations; 20 of them was regulated by a host gene promoter that in three cases comprised genes involved in fertility. The predicted targets of the differentially expressed miRNAs unveiled a significant enrichment of biological processes related to embryonic morphogenesis and chromatin modification. Normozoospermic infertile individuals exhibit a specific sperm miRNA expression profile clearly differentiated from normozoospermic fertile individuals. This miRNA cargo has potential implications in the individuals’ reproductive competence.

 

Circulating or “extracellular” miRNAs detected in biological fluids, could be used as potential diagnostic and prognostic biomarkers of several disease, such as cancer, gynecological and pregnancy disorders. However, their contributions in female infertility and in vitro fertilization (IVF) remain unknown. Polycystic ovary syndrome (PCOS) is a frequent endocrine disorder in women. PCOS is associated with altered features of androgen metabolism, increased insulin resistance and impaired fertility. Furthermore, PCOS, being a syndrome diagnosis, is heterogeneous and characterized by polycystic ovaries, chronic anovulation and evidence of hyperandrogenism, as well as being associated with chronic low-grade inflammation and an increased life time risk of type 2 diabetes. Altered miRNA levels have been associated with diabetes, insulin resistance, inflammation and various cancers. Studies have shown that circulating miRNAs are present in whole blood, serum, plasma and the follicular fluid of PCOS patients and that these might serve as potential biomarkers and a new approach for the diagnosis of PCOS. Presence of miRNA in mammalian follicular fluid has been demonstrated to be enclosed within microvesicles and exosomes or they can also be associated to protein complexes. The presence of microvesicles and exosomes carrying microRNAs in follicular fluid could represent an alternative mechanism of autocrine and paracrine communication inside the ovarian follicle. The investigation of the expression profiles of five circulating miRNAs (let-7b, miR-29a, miR-30a, miR-140 and miR-320a) in human follicular fluid from women with normal ovarian reserve and with polycystic ovary syndrome (PCOS) and their ability to predict IVF outcomes showed that these miRNAs could provide new helpful biomarkers to facilitate personalized medical care for oocyte quality in ART (Assisted Reproductive Treatment) and during IVF (In Vitro Fertilization).

 

References:

 

http://link.springer.com/chapter/10.1007%2F978-3-319-31973-5_12

 

http://onlinelibrary.wiley.com/doi/10.1111/andr.12276/abstract;jsessionid=F805A89DCC94BDBD42D6D60C40AD4AB0.f03t03

 

http://www.sciencedirect.com/science/article/pii/S0009279716302241

 

http://link.springer.com/article/10.1007%2Fs10815-016-0657-9

 

http://www.nature.com/articles/srep24976

 

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Mitochondrial disease

 

Mitochondria are present in almost all human cells, and vary in number from a few tens to many thousands. They generate the majority of a cell’s energy supply which powers every part of our body. Mitochondria have their own separate DNA, which carries just a few genes. All of these genes are involved in energy production but determine no other characteristics. And so, any faults in these genes lead only to problems in energy production. Around 1 in 6500 children is thought to be born with a serious mitochondrial disorder due to faults in mitochondrial DNA.

 

Unlike nuclear genes, mitochondrial DNA is inherited only from our mothers. Mothers can carry abnormal mitochondria and be at risk of passing on serious disease to their children, even if they themselves show only mild or no symptoms. It is for such women who by chance have a high proportion of faulty mitochondrial DNA in their eggs for which the methods of mitochondrial replacement or “donation” have been developed. This technique is also referred as the three parent technique and it involves a couple and a donor.

 

Mitochondrial Donation

 

The most developed techniques, maternal spindle transfer (MST) and pro-nuclear transfer (PNT), are based on an IVF cycle but have additional steps. Other techniques are being developed.

 

In both MST and PNT, nuclear DNA is moved from a patient’s egg or embryo containing unhealthy mitochondria to a donor’s egg or embryo containing healthy mitochondria, from which the donor’s nuclear DNA has been removed.

 

mst

Maternal spindle transfer Bredenoord, A and P. Braude (2010) “Ethics of mitochondrial gene replacement: from bench to bedside” BMJ 341.

 

pnt

Pronuclear transfer Bredenoord, A and P. Braude (2010) “Ethics of mitochondrial gene replacement: from bench to bedside” BMJ 341.

 

Research Carried Out and Safety Issues

 

There have been many experiments conducted using MST and PNT in animals. PNT has been carried out since the mid-1980s in mice. MST has been carried out in a wide range of animals. More recently mice, monkeys and human embryos have been created with the specific aim of developing MST and PNT for avoiding mitochondrial disease.

 

  • There is no evidence to show that mitochondrial donation is unsafe
  • Research is progressing well and the recommended further experiments are expected to confirm this view.

 

The main area of research needed is to observe cells derived from embryos created by MST and PNT, to see how mitochondria behave.

 

Concerns about Mitochondrial Donation

 

The scientific evidence raises some potential concerns about mitochondrial donation. Just as we all have different blood groups, we also have different types of mitochondria, called haplotypes. Some scientists have suggested that if the patient and the mitochondria donor have different mitochondrial haplotypes, there is a theoretical risk that the donor’s mitochondria won’t be able to ‘talk’ properly to the patient’s nuclear DNA, which could cause problems in the embryo and resulting child. So, mitochondria haplotype matching in the process of selecting donors may be done to avoid problems.

 

Another potential concern is that a small amount of unhealthy mitochondrial DNA may be transferred into the donor’s egg along with the mother’s nuclear DNA. Studies carried out on MST and PNT show that some so-called mitochondrial ‘carry-over’ occurs. However, the carry-over is lower than 2% of the mitochondria in the resulting embryo, an amount which is very unlikely to be problematic for the children born.

 

References:

 

http://mitochondria.hfea.gov.uk/mitochondria/what-is-mitochondrial-disease/

 

http://mitochondria.hfea.gov.uk/mitochondria/what-is-mitochondrial-disease/new-techniques-to-prevent-mitochondrial-disease/

 

https://www.newscientist.com/article/2107219-exclusive-worlds-first-baby-born-with-new-3-parent-technique/

 

https://www.newscientist.com/article/2108549-exclusive-3-parent-baby-method-already-used-for-infertility/

 

http://www.frontlinegenomics.com/news/7889/ethical-concerns-raised-first-three-parent-ivf-baby/

 

http://www.hfea.gov.uk/docs/2011-04-18_Mitochondria_review_-_final_report.PDF

 

http://www.hfea.gov.uk/docs/Mito-Annex_VIII-science_review_update.pdf

 

http://www.hfea.gov.uk/docs/Third_Mitochondrial_replacement_scientific_review.pdf

 

https://pharmaceuticalintelligence.com/2014/02/26/three-parent-baby-making-practice-of-modifying-oocytes-for-use-in-in-vitro-fertilization-fda-hearing/

 

 

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LIVE 9/21 8AM to 10:55 AM Expoloring the Versatility of CRISPR/Cas9 at CHI’s 14th Discovery On Target, 9/19 – 9/22/2016, Westin Boston Waterfront, Boston

http://www.discoveryontarget.com/

http://www.discoveryontarget.com/crispr-therapies/

Leaders in Pharmaceutical Business Intelligence (LPBI) Group is a

Media Partner of CHI for CHI’s 14th Annual Discovery on Targettaking place September 19 – 22, 2016 in Boston.

In Attendance, streaming LIVE using Social Media

Aviva Lev-Ari, PhD, RN

Editor-in-Chief

http://pharmaceuticalintelligence.com

#BostonDOT16

@BostonDOT

 

COMMENTS BY Stephen J Williams, PhD

EXPLORING THE VERSATILITY OF CRISPR/Cas9

 

8:00 Chairperson’s Opening Remarks

TJ Cradick , Ph.D., Head of Genome Editing, CRISPR Therapeutics

 

@CRISPRTX

 

8:10 Functional Genomics Using CRISPR-Cas9: Technology and Applications

Neville Sanjana, Ph.D., Core Faculty Member, New York Genome Center and Assistant Professor, Department of Biology & Center for Genomics and Systems Biology, New York University

 

CRISPR Cas9 is easier to target to multiple genomic loci; RNA specifies DNA targeting; with zinc finger nucleases or TALEEN in the protein specifies DNA targeting

 

  • This feature of crisper allows you to make a quick big and cheap array of a GENOME SCALE Crisper Knock out (GeCKO) screening library
  • How do you scale up the sgRNA for whole genome?; for all genes in RefSeq, identify consitutive exons using RNA-sequencing data from 16 primary human tissue (alot of genes end with ‘gg’) changing the bases on 3’ side negates crisper system but changing on 5’ then crisper works fine
  • Rank sequences to be specific for target
  • Cloned array into lentiviral and put in selectable markers
  • GeCKO displays high consistency betweens reagents for the same gene versus siRNA; GeCKO has high screening sensitivity
  • 98% of genome is noncoding so what about making a library for intronic regions (miRNA, promoter regions?)
  • So you design the sgRNA library by taking 100kb of gene-adjacent regions
  • They looked at CUL3; (data will soon be published in Science)
  • Do a transcription CHIP to verify the lack of binding of transcription factor of interest
  • Can also target histone marks on promoter and enhancer elements
  • NYU wants to explore this noncoding screens
  • sanjanalab.org

 

@nyuniversity

 

8:40 Therapeutic Gene Editing With CRISPR/Cas9

TJ Cradick , Ph.D., Head of Genome Editing, CRISPR Therapeutics

 

NEHJ is down and dirty repair of single nonhomologous end but when have two breaks the NEHJ repair can introduce the inversions or deletions

 

    • High-throughput screens are fine but can limit your view of genomic context; genome searches pick unique sites so use bioinformatic programs  to design specific guide Rna
    • Bioinformatic directed, genome wide, functional screens
    • Compared COSMID and CCTOP; 320 COSMID off-target sites, 333 CCtop off target
    • Young lab GUIDESeq program genome wide assay useful to design guides
    • If shorten guide may improve specificity; also sometime better sensitivity if lengthen guide

 

  • Manufacturing of autologous gene corrected product ex vivo gene correction (Vertex, Bayer, are partners in this)

 

 

They need to use a clones from multiple microarrays before using the GUidESeq but GUIDEseq is better for REMOVING the off targets than actually producing the sgRNA library you want (seems the methods for library development are not fully advanced to do this)

 

The score sometimes for the sgRNA design programs do not always give the best result because some sgRNAs are genome context dependent

9:10 Towards Combinatorial Drug Discovery: Mining Heterogeneous Phenotypes from Large Scale RNAi/Drug Perturbations

Arvind Rao, Ph.D., Assistant Professor, Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center

 

Bioinformatics in CRISPR screens:  they looked at image analysis of light microscopy of breast cancer cells and looked for phenotypic changes

 

  • Then they modeled in a small pilot and then used the algorithm for 20,000 images (made morphometric measurements)
  • Can formulate training statistical algorithms to make a decision tree how you classify data points
  • Although their algorithms worked well there was also human input from scientists

Aggregate ranking of hits programs available on web like LINKS

 

@MDAndersonNews

 

10:25 CRISPR in Stem Cell Models of Eye Disease

Alexander Bassuk, M.D., Ph.D., Associate Professor of Pediatrics, Department of Molecular and Cellular Biology, University of Iowa

 

Blind athlete Michael Stone, biathlete, had eye disease since teenager helped fund and start the clinical trial for Starbardt disease; had one bad copy of ABCA4, heterozygous (inheritable in Ahkenazi Jewish) – a recessive inheritable mutation with juvenile macular degeneration

  • Also had another male in family with disease but he had another mutation in the RPGR gene
  • December 2015 paper Precision Medicine: Genetic Repair of retinitis pigmentosa in patient derived stem cells
  • They were able to correct the iPSCs in the RPGR gene derived from patient however low efficiency of repair, scarless repair, leaves changes in DNA, need clinical grade iPSCs, and need a humanized model of RPGR

@uiowa

10:55 CRISPR in Mouse Models of Eye Disease

Vinit Mahajan, M.D., Ph.D., Assistant Professor of Ophthalmology and Visual Sciences, University of Iowa College of Medicine

  • degeneration of the retina will see brown spots, the macula will often be preserved but retinal cells damaged but with RPGR have problems with peripheral vision, retinitis pigmentosa get tunnel vision with no peripheral vision (a mouse model of PDE6 Knockout recapitulates this phenotype)
  • the PDE6 is linked to the rhodopsin GTP pathway
  • rd1 -/- mouse has something that looks like retinal pigmentosa; has mutant PDE6; is actually a nonsense mutation in rd1 so they tried a crisper to fix in mice
  • with crisper fix of rd1 nonsense mutation the optic nerve looked comparible to normal and the retina structure restored
  • photoreceptors layers- some recovery but not complete
  • sequence results show the DNA is a mosaic so not correcting 100% but only 35% but stil leads to a phenotypic recovery; NHEJ was about 12% to 25% with large deletions
  • histology is restored in crspr repaired mice
  • CRSPR off target effects: WGS and analyze for variants SNV/indels, also looked at on target and off target regions; there were no off target SNVs indels while variants that did not pass quality control screening not a single SNV
  • Rhodopsin mutation accounts for a large % of patients (RhoD190N)
  • injection of gene therapy vectors: AAV vector carrying CRSPR and cas9 repair templates

CAPN mouse models

  • family in Iowa have dominant mutation in CAPN5; retinal degenerates
  • used CRSPR to generate mouse model with mutation in CAPN5 similar to family mutation
  • compared to other transgenic methods CRSPR is faster to produce a mouse model

To Follow LIVE CONFERENCE COVERAGE PLEASE FOLLOW ON TWITTER USING

Meeting #: #BostonDOT16

Meeting @: @BostonDOT

 

Overall good meeting #s:

#personalizedmedicine

#innovation

#cancer

#immunology

#immunooncology

#pharmanews

#CRSPR

#geneediting

#crisper

#biotech

 

AND FOLLOW these @

@pharma_BI

@AVIVA_1950

@BiotechNews

@CHI

@FierceBiotech

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Milestones in Physiology & Discoveries in Medicine and Genomics: Request for Book Review Writing on Amazon.com


physiology-cover-seriese-vol-3individualsaddlebrown-page2

Milestones in Physiology

Discoveries in Medicine, Genomics and Therapeutics

Patient-centric Perspective 

http://www.amazon.com/dp/B019VH97LU 

2015

 

 

Author, Curator and Editor

Larry H Bernstein, MD, FCAP

Chief Scientific Officer

Leaders in Pharmaceutical Business Intelligence

Larry.bernstein@gmail.com

Preface

Introduction 

Chapter 1: Evolution of the Foundation for Diagnostics and Pharmaceuticals Industries

1.1  Outline of Medical Discoveries between 1880 and 1980

1.2 The History of Infectious Diseases and Epidemiology in the late 19th and 20th Century

1.3 The Classification of Microbiota

1.4 Selected Contributions to Chemistry from 1880 to 1980

1.5 The Evolution of Clinical Chemistry in the 20th Century

1.6 Milestones in the Evolution of Diagnostics in the US HealthCare System: 1920s to Pre-Genomics

 

Chapter 2. The search for the evolution of function of proteins, enzymes and metal catalysts in life processes

2.1 The life and work of Allan Wilson
2.2  The  evolution of myoglobin and hemoglobin
2.3  More complexity in proteins evolution
2.4  Life on earth is traced to oxygen binding
2.5  The colors of life function
2.6  The colors of respiration and electron transport
2.7  Highlights of a green evolution

 

Chapter 3. Evolution of New Relationships in Neuroendocrine States
3.1 Pituitary endocrine axis
3.2 Thyroid function
3.3 Sex hormones
3.4 Adrenal Cortex
3.5 Pancreatic Islets
3.6 Parathyroids
3.7 Gastointestinal hormones
3.8 Endocrine action on midbrain
3.9 Neural activity regulating endocrine response

3.10 Genomic Promise for Neurodegenerative Diseases, Dementias, Autism Spectrum, Schizophrenia, and Serious Depression

 

Chapter 4.  Problems of the Circulation, Altitude, and Immunity

4.1 Innervation of Heart and Heart Rate
4.2 Action of hormones on the circulation
4.3 Allogeneic Transfusion Reactions
4.4 Graft-versus Host reaction
4.5 Unique problems of perinatal period
4.6. High altitude sickness
4.7 Deep water adaptation
4.8 Heart-Lung-and Kidney
4.9 Acute Lung Injury

4.10 Reconstruction of Life Processes requires both Genomics and Metabolomics to explain Phenotypes and Phylogenetics

 

Chapter 5. Problems of Diets and Lifestyle Changes

5.1 Anorexia nervosa
5.2 Voluntary and Involuntary S-insufficiency
5.3 Diarrheas – bacterial and nonbacterial
5.4 Gluten-free diets
5.5 Diet and cholesterol
5.6 Diet and Type 2 diabetes mellitus
5.7 Diet and exercise
5.8 Anxiety and quality of Life
5.9 Nutritional Supplements

 

Chapter 6. Advances in Genomics, Therapeutics and Pharmacogenomics

6.1 Natural Products Chemistry

6.2 The Challenge of Antimicrobial Resistance

6.3 Viruses, Vaccines and immunotherapy

6.4 Genomics and Metabolomics Advances in Cancer

6.5 Proteomics – Protein Interaction

6.6 Pharmacogenomics

6.7 Biomarker Guided Therapy

6.8 The Emergence of a Pharmaceutical Industry in the 20th Century: Diagnostics Industry and Drug Development in the Genomics Era: Mid 80s to Present

6.09 The Union of Biomarkers and Drug Development

6.10 Proteomics and Biomarker Discovery

6.11 Epigenomics and Companion Diagnostics

 

Chapter  7

Integration of Physiology, Genomics and Pharmacotherapy

7.1 Richard Lifton, MD, PhD of Yale University and Howard Hughes Medical Institute: Recipient of 2014 Breakthrough Prizes Awarded in Life Sciences for the Discovery of Genes and Biochemical Mechanisms that cause Hypertension

7.2 Calcium Cycling (ATPase Pump) in Cardiac Gene Therapy: Inhalable Gene Therapy for Pulmonary Arterial Hypertension and Percutaneous Intra-coronary Artery Infusion for Heart Failure: Contributions by Roger J. Hajjar, MD

7.3 Diagnostics and Biomarkers: Novel Genomics Industry Trends vs Present Market Conditions and Historical Scientific Leaders Memoirs

7.4 Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

7.5 Diagnosing Diseases & Gene Therapy: Precision Genome Editing and Cost-effective microRNA Profiling

7.6 Imaging Biomarker for Arterial Stiffness: Pathways in Pharmacotherapy for Hypertension and Hypercholesterolemia Management

7.7 Neuroprotective Therapies: Pharmacogenomics vs Psychotropic drugs and Cholinesterase Inhibitors

7.8 Metabolite Identification Combining Genetic and Metabolic Information: Genetic association links unknown metabolites to functionally related genes

7.9 Preserved vs Reduced Ejection Fraction: Available and Needed Therapies

7.10 Biosimilars: Intellectual Property Creation and Protection by Pioneer and by

7.11 Demonstrate Biosimilarity: New FDA Biosimilar Guidelines

 

Chapter 7.  Biopharma Today

8.1 A Great University engaged in Drug Discovery: University of Pittsburgh

8.2 Introduction – The Evolution of Cancer Therapy and Cancer Research: How We Got Here?

8.3 Predicting Tumor Response, Progression, and Time to Recurrence

8.4 Targeting Untargetable Proto-Oncogenes

8.5 Innovation: Drug Discovery, Medical Devices and Digital Health

8.6 Cardiotoxicity and Cardiomyopathy Related to Drugs Adverse Effects

8.7 Nanotechnology and Ocular Drug Delivery: Part I

8.8 Transdermal drug delivery (TDD) system and nanotechnology: Part II

8.9 The Delicate Connection: IDO (Indolamine 2, 3 dehydrogenase) and Cancer Immunology

8.10 Natural Drug Target Discovery and Translational Medicine in Human Microbiome

8.11 From Genomics of Microorganisms to Translational Medicine

8.12 Confined Indolamine 2, 3 dioxygenase (IDO) Controls the Homeostasis of Immune Responses for Good and Bad

 

Chapter 9. BioPharma – Future Trends

9.1 Artificial Intelligence Versus the Scientist: Who Will Win?

9.2 The Vibrant Philly Biotech Scene: Focus on KannaLife Sciences and the Discipline and Potential of Pharmacognosy

9.3 The Vibrant Philly Biotech Scene: Focus on Computer-Aided Drug Design and Gfree Bio, LLC

9.4 Heroes in Medical Research: The Postdoctoral Fellow

9.5 NIH Considers Guidelines for CAR-T therapy: Report from Recombinant DNA Advisory Committee

9.6 1st Pitch Life Science- Philadelphia- What VCs Really Think of your Pitch

9.7 Multiple Lung Cancer Genomic Projects Suggest New Targets, Research Directions for Non-Small Cell Lung Cancer

9.8 Heroes in Medical Research: Green Fluorescent Protein and the Rough Road in Science

9.9 Issues in Personalized Medicine in Cancer: Intratumor Heterogeneity and Branched Evolution Revealed by Multiregion Sequencing

9.10 The SCID Pig II: Researchers Develop Another SCID Pig, And Another Great Model For Cancer Research

Epilogue

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Keystone Symposia on Molecular and Cellular Biology – 2016-2017 Forthcoming Conferences in Life Sciences

Reporter: Aviva Lev-Ari, PhD, RN

2016-2017 Forthcoming Conferences in Life Sciences by topic:

DNA Replication and Recombination (Z2)
April 2 – 6, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: John F.X. Diffley, Anja Groth and Scott Keeney

Immunology

Translational Vaccinology for Global Health (S1)
October 25 – 29, 2016 | London, United Kingdom
Scientific Organizers: Christopher L. Karp, Gagandeep Kang and Rino Rappuoli

Hemorrhagic Fever Viruses (S3)
December 4 – 8, 2016 | Santa Fe, New Mexico, USA
Scientific Organizers: William E. Dowling and Thomas W. Geisbert

Cell Plasticity within the Tumor Microenvironment (A1)
January 8 – 12, 2017 | Big Sky, Montana, USA
Scientific Organizers: Sergei Grivennikov, Florian R. Greten and Mikala Egeblad

TGF-ß in Immunity, Inflammation and Cancer (A3)
January 9 – 13, 2017 | Taos, New Mexico, USA
Scientific Organizers: Wanjun Chen, Joanne E. Konkel and Richard A. Flavell

New Developments in Our Basic Understanding of Tuberculosis (A5)
January 14 – 18, 2017 | Vancouver, British Columbia, Canada
Scientific Organizers: Samuel M. Behar and Valerie Mizrahi

PI3K Pathways in Immunology, Growth Disorders and Cancer (A6)
January 19 – 23, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Leon O. Murphy, Klaus Okkenhaug and Sabina C. Cosulich

Biobetters and Next-Generation Biologics: Innovative Strategies for Optimally Effective Therapies (A7)
January 22 – 26, 2017 | Snowbird, Utah, USA
Scientific Organizers: Cherié L. Butts, Amy S. Rosenberg, Amy D. Klion and Sachdev S. Sidhu

Obesity and Adipose Tissue Biology (J4)
January 22 – 26, 2017 | Keystone, Colorado, USA
Scientific Organizers: Marc L. Reitman, Ruth E. Gimeno and Jan Nedergaard

Inflammation-Driven Cancer: Mechanisms to Therapy (J7)
February 5 – 9, 2017 | Keystone, Colorado, USA
Scientific Organizers: Fiona M. Powrie, Michael Karin and Alberto Mantovani

Autophagy Network Integration in Health and Disease (B2)
February 12 – 16, 2017 | Copper Mountain, Colorado, USA
Scientific Organizers: Ivan Dikic, Katja Simon and J. Wade Harper

Asthma: From Pathway Biology to Precision Therapeutics (B3)
February 12 – 16, 2017 | Keystone, Colorado, USA
Scientific Organizers: Clare M. Lloyd, John V. Fahy and Sally Wenzel-Morganroth

Viral Immunity: Mechanisms and Consequences (B4)
February 19 – 23, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Akiko Iwasaki, Daniel B. Stetson and E. John Wherry

Lipidomics and Bioactive Lipids in Metabolism and Disease (B6)
February 26 – March 2, 2017 | Tahoe City, California, USA
Scientific Organizers: Alfred H. Merrill, Walter Allen Shaw, Sarah Spiegel and Michael J.O.Wakelam

Bile Acid Receptors as Signal Integrators in Liver and Metabolism (C1)
March 3 – 7, 2017 | Monterey, California, USA
Scientific Organizers: Luciano Adorini, Kristina Schoonjans and Scott L. Friedman

Cancer Immunology and Immunotherapy: Taking a Place in Mainstream Oncology (C7)
March 19 – 23, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: Robert D. Schreiber, James P. Allison, Philip D. Greenberg and Glenn Dranoff

Pattern Recognition Signaling: From Innate Immunity to Inflammatory Disease (X5)
March 19 – 23, 2017 | Banff, Alberta, Canada
Scientific Organizers: Thirumala-Devi Kanneganti, Vishva M. Dixit and Mohamed Lamkanfi

Type I Interferon: Friend and Foe Alike (X6)
March 19 – 23, 2017 | Banff, Alberta, Canada
Scientific Organizers: Alan Sher, Virginia Pascual, Adolfo García-Sastre and Anne O’Garra

Injury, Inflammation and Fibrosis (C8)
March 26 – 30, 2017 | Snowbird, Utah, USA
Scientific Organizers: Tatiana Kisseleva, Michael Karin and Andrew M. Tager

Immune Regulation in Autoimmunity and Cancer (D1)
March 26 – 30, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: David A. Hafler, Vijay K. Kuchroo and Jane L. Grogan

B Cells and T Follicular Helper Cells – Controlling Long-Lived Immunity (D2)
April 23 – 27, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: Stuart G. Tangye, Ignacio Sanz and Hai Qi

Mononuclear Phagocytes in Health, Immune Defense and Disease (D3)
April 30 – May 4, 2017 | Austin, Texas, USA
Scientific Organizers: Steffen Jung and Miriam Merad

Modeling Viral Infections and Immunity (E1)
May 1 – 4, 2017 | Estes Park, Colorado, USA
Scientific Organizers: Alan S. Perelson, Rob J. De Boer and Phillip D. Hodgkin

Integrating Metabolism and Immunity (E4)
May 29 – June 2, 2017 | Dublin, Ireland
Scientific Organizers: Hongbo Chi, Erika L. Pearce, Richard A. Flavell and Luke A.J. O’Neill

Neuroinflammation: Concepts, Characteristics, Consequences (E5)
June 19 – 23, 2017 | Keystone, Colorado, USA
Scientific Organizers: Richard M. Ransohoff, Christopher K. Glass and V. Hugh Perry

Infectious Diseases

Translational Vaccinology for Global Health (S1)
October 25 – 29, 2016 | London, United Kingdom
Scientific Organizers: Christopher L. Karp, Gagandeep Kang and Rino Rappuoli

Hemorrhagic Fever Viruses (S3)
December 4 – 8, 2016 | Santa Fe, New Mexico, USA
Scientific Organizers: William E. Dowling and Thomas W. Geisbert

Cellular Stress Responses and Infectious Agents (S4)
December 4 – 8, 2016 | Santa Fe, New Mexico, USA
Scientific Organizers: Margo A. Brinton, Sandra K. Weller and Beth Levine

New Developments in Our Basic Understanding of Tuberculosis (A5)
January 14 – 18, 2017 | Vancouver, British Columbia, Canada
Scientific Organizers: Samuel M. Behar and Valerie Mizrahi

Autophagy Network Integration in Health and Disease (B2)
February 12 – 16, 2017 | Copper Mountain, Colorado, USA
Scientific Organizers: Ivan Dikic, Katja Simon and J. Wade Harper

Viral Immunity: Mechanisms and Consequences (B4)
February 19 – 23, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Akiko Iwasaki, Daniel B. Stetson and E. John Wherry

Malaria: From Innovation to Eradication (B5)
February 19 – 23, 2017 | Kampala, Uganda
Scientific Organizers: Marcel Tanner, Sarah K. Volkman, Marcus V.G. Lacerda and Salim Abdulla

Type I Interferon: Friend and Foe Alike (X6)
March 19 – 23, 2017 | Banff, Alberta, Canada
Scientific Organizers: Alan Sher, Virginia Pascual, Adolfo García-Sastre and Anne O’Garra

HIV Vaccines (C9)
March 26 – 30, 2017 | Steamboat Springs, Colorado, USA
Scientific Organizers: Andrew B. Ward, Penny L. Moore and Robin Shattock

Modeling Viral Infections and Immunity (E1)
May 1 – 4, 2017 | Estes Park, Colorado, USA
Scientific Organizers: Alan S. Perelson, Rob J. De Boer and Phillip D. Hodgkin

Metabolic Diseases

Mitochondria Communication (A4)
January 14 – 18, 2017 | Taos, New Mexico, USA
Scientific Organizers: Jared Rutter, Cole M. Haynes and Marcia C. Haigis

Diabetes (J3)
January 22 – 26, 2017 | Keystone, Colorado, USA
Scientific Organizers: Jiandie Lin, Clay F. Semenkovich and Rohit N. Kulkarni

Obesity and Adipose Tissue Biology (J4)
January 22 – 26, 2017 | Keystone, Colorado, USA
Scientific Organizers: Marc L. Reitman, Ruth E. Gimeno and Jan Nedergaard

Microbiome in Health and Disease (J8)
February 5 – 9, 2017 | Keystone, Colorado, USA
Scientific Organizers: Julie A. Segre, Ramnik Xavier and William Michael Dunne

Bile Acid Receptors as Signal Integrators in Liver and Metabolism (C1)
March 3 – 7, 2017 | Monterey, California, USA
Scientific Organizers: Luciano Adorini, Kristina Schoonjans and Scott L. Friedman

Sex and Gender Factors Affecting Metabolic Homeostasis, Diabetes and Obesity (C6)
March 19 – 22, 2017 | Tahoe City, California, USA
Scientific Organizers: Franck Mauvais-Jarvis, Deborah Clegg and Arthur P. Arnold

Neuronal Control of Appetite, Metabolism and Weight (Z5)
May 9 – 13, 2017 | Copenhagen, Denmark
Scientific Organizers: Lora K. Heisler and Scott M. Sternson

Gastrointestinal Control of Metabolism (Z6)
May 9 – 13, 2017 | Copenhagen, Denmark
Scientific Organizers: Randy J. Seeley, Matthias H. Tschöp and Fiona M. Gribble

Integrating Metabolism and Immunity (E4)
May 29 – June 2, 2017 | Dublin, Ireland
Scientific Organizers: Hongbo Chi, Erika L. Pearce, Richard A. Flavell and Luke A.J. O’Neill

Neurobiology

Transcriptional and Epigenetic Control in Stem Cells (J1)
January 8 – 12, 2017 | Olympic Valley, California, USA
Scientific Organizers: Konrad Hochedlinger, Kathrin Plath and Marius Wernig

Neurogenesis during Development and in the Adult Brain (J2)
January 8 – 12, 2017 | Olympic Valley, California, USA
Scientific Organizers: Alysson R. Muotri, Kinichi Nakashima and Xinyu Zhao

Rare and Undiagnosed Diseases: Discovery and Models of Precision Therapy (C2)
March 5 – 8, 2017 | Boston, Massachusetts, USA
Scientific Organizers: William A. Gahl and Christoph Klein

mRNA Processing and Human Disease (C3)
March 5 – 8, 2017 | Taos, New Mexico, USA
Scientific Organizers: James L. Manley, Siddhartha Mukherjee and Gideon Dreyfuss

Synapses and Circuits: Formation, Function, and Dysfunction (X1)
March 5 – 8, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Tony Koleske, Yimin Zou, Kristin Scott and A. Kimberley McAllister

Connectomics (X2)
March 5 – 8, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Olaf Sporns, Danielle Bassett and Jeremy Freeman

Neuronal Control of Appetite, Metabolism and Weight (Z5)
May 9 – 13, 2017 | Copenhagen, Denmark
Scientific Organizers: Lora K. Heisler and Scott M. Sternson

Neuroinflammation: Concepts, Characteristics, Consequences (E5)
June 19 – 23, 2017 | Keystone, Colorado, USA
Scientific Organizers: Richard M. Ransohoff, Christopher K. Glass and V. Hugh Perry

Plant Biology

Phytobiomes: From Microbes to Plant Ecosystems (S2)
November 8 – 12, 2016 | Santa Fe, New Mexico, USA
Scientific Organizers: Jan E. Leach, Kellye A. Eversole, Jonathan A. Eisen and Gwyn Beattie

Structural Biology

Frontiers of NMR in Life Sciences (C5)
March 12 – 16, 2017 | Keystone, Colorado, USA
Scientific Organizers: Kurt Wüthrich, Michael Sattler and Stephen W. Fesik

Technologies

Cell Plasticity within the Tumor Microenvironment (A1)
January 8 – 12, 2017 | Big Sky, Montana, USA
Scientific Organizers: Sergei Grivennikov, Florian R. Greten and Mikala Egeblad

Precision Genome Engineering (A2)
January 8 – 12, 2017 | Breckenridge, Colorado, USA
Scientific Organizers: J. Keith Joung, Emmanuelle Charpentier and Olivier Danos

Transcriptional and Epigenetic Control in Stem Cells (J1)
January 8 – 12, 2017 | Olympic Valley, California, USA
Scientific Organizers: Konrad Hochedlinger, Kathrin Plath and Marius Wernig

Protein-RNA Interactions: Scale, Mechanisms, Structure and Function of Coding and Noncoding RNPs (J6)
February 5 – 9, 2017 | Banff, Alberta, Canada
Scientific Organizers: Gene W. Yeo, Jernej Ule, Karla Neugebauer and Melissa J. Moore

Lipidomics and Bioactive Lipids in Metabolism and Disease (B6)
February 26 – March 2, 2017 | Tahoe City, California, USA
Scientific Organizers: Alfred H. Merrill, Walter Allen Shaw, Sarah Spiegel and Michael J.O.Wakelam

Connectomics (X2)
March 5 – 8, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Olaf Sporns, Danielle Bassett and Jeremy Freeman

Engineered Cells and Tissues as Platforms for Discovery and Therapy (K1)
March 9 – 12, 2017 | Boston, Massachusetts, USA
Scientific Organizers: Laura E. Niklason, Milica Radisic and Nenad Bursac

Frontiers of NMR in Life Sciences (C5)
March 12 – 16, 2017 | Keystone, Colorado, USA
Scientific Organizers: Kurt Wüthrich, Michael Sattler and Stephen W. Fesik

October 2016

Translational Vaccinology for Global Health (S1)
October 25 – 29, 2016 | London, United Kingdom
Scientific Organizers: Christopher L. Karp, Gagandeep Kang and Rino Rappuoli

November 2016

Phytobiomes: From Microbes to Plant Ecosystems (S2)
November 8 – 12, 2016 | Santa Fe, New Mexico, USA
Scientific Organizers: Jan E. Leach, Kellye A. Eversole, Jonathan A. Eisen and Gwyn Beattie

December 2016

Hemorrhagic Fever Viruses (S3)
December 4 – 8, 2016 | Santa Fe, New Mexico, USA
Scientific Organizers: William E. Dowling and Thomas W. Geisbert

Cellular Stress Responses and Infectious Agents (S4)
December 4 – 8, 2016 | Santa Fe, New Mexico, USA
Scientific Organizers: Margo A. Brinton, Sandra K. Weller and Beth Levine

January 2017

Cell Plasticity within the Tumor Microenvironment (A1)
January 8 – 12, 2017 | Big Sky, Montana, USA
Scientific Organizers: Sergei Grivennikov, Florian R. Greten and Mikala Egeblad

Precision Genome Engineering (A2)
January 8 – 12, 2017 | Breckenridge, Colorado, USA
Scientific Organizers: J. Keith Joung, Emmanuelle Charpentier and Olivier Danos

Transcriptional and Epigenetic Control in Stem Cells (J1)
January 8 – 12, 2017 | Olympic Valley, California, USA
Scientific Organizers: Konrad Hochedlinger, Kathrin Plath and Marius Wernig

Neurogenesis during Development and in the Adult Brain (J2)
January 8 – 12, 2017 | Olympic Valley, California, USA
Scientific Organizers: Alysson R. Muotri, Kinichi Nakashima and Xinyu Zhao

TGF-ß in Immunity, Inflammation and Cancer (A3)
January 9 – 13, 2017 | Taos, New Mexico, USA
Scientific Organizers: Wanjun Chen, Joanne E. Konkel and Richard A. Flavell

Mitochondria Communication (A4)
January 14 – 18, 2017 | Taos, New Mexico, USA
Scientific Organizers: Jared Rutter, Cole M. Haynes and Marcia C. Haigis

New Developments in Our Basic Understanding of Tuberculosis (A5)
January 14 – 18, 2017 | Vancouver, British Columbia, Canada
Scientific Organizers: Samuel M. Behar and Valerie Mizrahi

PI3K Pathways in Immunology, Growth Disorders and Cancer (A6)
January 19 – 23, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Leon O. Murphy, Klaus Okkenhaug and Sabina C. Cosulich

Biobetters and Next-Generation Biologics: Innovative Strategies for Optimally Effective Therapies (A7)
January 22 – 26, 2017 | Snowbird, Utah, USA
Scientific Organizers: Cherié L. Butts, Amy S. Rosenberg, Amy D. Klion and Sachdev S. Sidhu

Diabetes (J3)
January 22 – 26, 2017 | Keystone, Colorado, USA
Scientific Organizers: Jiandie Lin, Clay F. Semenkovich and Rohit N. Kulkarni

Obesity and Adipose Tissue Biology (J4)
January 22 – 26, 2017 | Keystone, Colorado, USA
Scientific Organizers: Marc L. Reitman, Ruth E. Gimeno and Jan Nedergaard

Omics Strategies to Study the Proteome (A8)
January 29 – February 2, 2017 | Breckenridge, Colorado, USA
Scientific Organizers: Alan Saghatelian, Chuan He and Ileana M. Cristea

Epigenetics and Human Disease: Progress from Mechanisms to Therapeutics (A9)
January 29 – February 2, 2017 | Seattle, Washington, USA
Scientific Organizers: Johnathan R. Whetstine, Jessica K. Tyler and Rab K. Prinjha

Hematopoiesis (B1)
January 31 – February 4, 2017 | Banff, Alberta, Canada
Scientific Organizers: Catriona H.M. Jamieson, Andreas Trumpp and Paul S. Frenette

February 2017

Noncoding RNAs: From Disease to Targeted Therapeutics (J5)
February 5 – 9, 2017 | Banff, Alberta, Canada
Scientific Organizers: Kevin V. Morris, Archa Fox and Paloma Hoban Giangrande

Protein-RNA Interactions: Scale, Mechanisms, Structure and Function of Coding and Noncoding RNPs (J6)
February 5 – 9, 2017 | Banff, Alberta, Canada
Scientific Organizers: Gene W. Yeo, Jernej Ule, Karla Neugebauer and Melissa J. Moore

Inflammation-Driven Cancer: Mechanisms to Therapy (J7)
February 5 – 9, 2017 | Keystone, Colorado, USA
Scientific Organizers: Fiona M. Powrie, Michael Karin and Alberto Mantovani

Microbiome in Health and Disease (J8)
February 5 – 9, 2017 | Keystone, Colorado, USA
Scientific Organizers: Julie A. Segre, Ramnik Xavier and William Michael Dunne

Autophagy Network Integration in Health and Disease (B2)
February 12 – 16, 2017 | Copper Mountain, Colorado, USA
Scientific Organizers: Ivan Dikic, Katja Simon and J. Wade Harper

Asthma: From Pathway Biology to Precision Therapeutics (B3)
February 12 – 16, 2017 | Keystone, Colorado, USA
Scientific Organizers: Clare M. Lloyd, John V. Fahy and Sally Wenzel-Morganroth

Viral Immunity: Mechanisms and Consequences (B4)
February 19 – 23, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Akiko Iwasaki, Daniel B. Stetson and E. John Wherry

Malaria: From Innovation to Eradication (B5)
February 19 – 23, 2017 | Kampala, Uganda
Scientific Organizers: Marcel Tanner, Sarah K. Volkman, Marcus V.G. Lacerda and Salim Abdulla

Lipidomics and Bioactive Lipids in Metabolism and Disease (B6)
February 26 – March 2, 2017 | Tahoe City, California, USA
Scientific Organizers: Alfred H. Merrill, Walter Allen Shaw, Sarah Spiegel and Michael J.O.Wakelam

March 2017

Bile Acid Receptors as Signal Integrators in Liver and Metabolism (C1)
March 3 – 7, 2017 | Monterey, California, USA
Scientific Organizers: Luciano Adorini, Kristina Schoonjans and Scott L. Friedman

Rare and Undiagnosed Diseases: Discovery and Models of Precision Therapy (C2)
March 5 – 8, 2017 | Boston, Massachusetts, USA
Scientific Organizers: William A. Gahl and Christoph Klein

mRNA Processing and Human Disease (C3)
March 5 – 8, 2017 | Taos, New Mexico, USA
Scientific Organizers: James L. Manley, Siddhartha Mukherjee and Gideon Dreyfuss

Kinases: Next-Generation Insights and Approaches (C4)
March 5 – 9, 2017 | Breckenridge, Colorado, USA
Scientific Organizers: Reid M. Huber, John Kuriyan and Ruth H. Palmer

Synapses and Circuits: Formation, Function, and Dysfunction (X1)
March 5 – 8, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Tony Koleske, Yimin Zou, Kristin Scott and A. Kimberley McAllister

Connectomics (X2)
March 5 – 8, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Olaf Sporns, Danielle Bassett and Jeremy Freeman

Tumor Metabolism: Mechanisms and Targets (X3)
March 5 – 9, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: Brendan D. Manning, Kathryn E. Wellen and Reuben J. Shaw

Adaptations to Hypoxia in Physiology and Disease (X4)
March 5 – 9, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: M. Celeste Simon, Amato J. Giaccia and Randall S. Johnson

Engineered Cells and Tissues as Platforms for Discovery and Therapy (K1)
March 9 – 12, 2017 | Boston, Massachusetts, USA
Scientific Organizers: Laura E. Niklason, Milica Radisic and Nenad Bursac

Frontiers of NMR in Life Sciences (C5)
March 12 – 16, 2017 | Keystone, Colorado, USA
Scientific Organizers: Kurt Wüthrich, Michael Sattler and Stephen W. Fesik

Sex and Gender Factors Affecting Metabolic Homeostasis, Diabetes and Obesity (C6)
March 19 – 22, 2017 | Tahoe City, California, USA
Scientific Organizers: Franck Mauvais-Jarvis, Deborah Clegg and Arthur P. Arnold

Cancer Immunology and Immunotherapy: Taking a Place in Mainstream Oncology (C7)
March 19 – 23, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: Robert D. Schreiber, James P. Allison, Philip D. Greenberg and Glenn Dranoff

Pattern Recognition Signaling: From Innate Immunity to Inflammatory Disease (X5)
March 19 – 23, 2017 | Banff, Alberta, Canada
Scientific Organizers: Thirumala-Devi Kanneganti, Vishva M. Dixit and Mohamed Lamkanfi

Type I Interferon: Friend and Foe Alike (X6)
March 19 – 23, 2017 | Banff, Alberta, Canada
Scientific Organizers: Alan Sher, Virginia Pascual, Adolfo García-Sastre and Anne O’Garra

Injury, Inflammation and Fibrosis (C8)
March 26 – 30, 2017 | Snowbird, Utah, USA
Scientific Organizers: Tatiana Kisseleva, Michael Karin and Andrew M. Tager

HIV Vaccines (C9)
March 26 – 30, 2017 | Steamboat Springs, Colorado, USA
Scientific Organizers: Andrew B. Ward, Penny L. Moore and Robin Shattock

Immune Regulation in Autoimmunity and Cancer (D1)
March 26 – 30, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: David A. Hafler, Vijay K. Kuchroo and Jane L. Grogan

Molecular Mechanisms of Heart Development (X7)
March 26 – 30, 2017 | Keystone, Colorado, USA
Scientific Organizers: Benoit G. Bruneau, Brian L. Black and Margaret E. Buckingham

RNA-Based Approaches in Cardiovascular Disease (X8)
March 26 – 30, 2017 | Keystone, Colorado, USA
Scientific Organizers: Thomas Thum and Roger J. Hajjar

April 2017

Genomic Instability and DNA Repair (Z1)
April 2 – 6, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Julia Promisel Cooper, Marco F. Foiani and Geneviève Almouzni

DNA Replication and Recombination (Z2)
April 2 – 6, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: John F.X. Diffley, Anja Groth and Scott Keeney

B Cells and T Follicular Helper Cells – Controlling Long-Lived Immunity (D2)
April 23 – 27, 2017 | Whistler, British Columbia, Canada
Scientific Organizers: Stuart G. Tangye, Ignacio Sanz and Hai Qi

Mononuclear Phagocytes in Health, Immune Defense and Disease (D3)
April 30 – May 4, 2017 | Austin, Texas, USA
Scientific Organizers: Steffen Jung and Miriam Merad

May 2017

Modeling Viral Infections and Immunity (E1)
May 1 – 4, 2017 | Estes Park, Colorado, USA
Scientific Organizers: Alan S. Perelson, Rob J. De Boer and Phillip D. Hodgkin

Angiogenesis and Vascular Disease (Z3)
May 8 – 12, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: M. Luisa Iruela-Arispe, Timothy T. Hla and Courtney Griffin

Mitochondria, Metabolism and Heart (Z4)
May 8 – 12, 2017 | Santa Fe, New Mexico, USA
Scientific Organizers: Junichi Sadoshima, Toren Finkel and Åsa B. Gustafsson

Neuronal Control of Appetite, Metabolism and Weight (Z5)
May 9 – 13, 2017 | Copenhagen, Denmark
Scientific Organizers: Lora K. Heisler and Scott M. Sternson

Gastrointestinal Control of Metabolism (Z6)
May 9 – 13, 2017 | Copenhagen, Denmark
Scientific Organizers: Randy J. Seeley, Matthias H. Tschöp and Fiona M. Gribble

Aging and Mechanisms of Aging-Related Disease (E2)
May 15 – 19, 2017 | Yokohama, Japan
Scientific Organizers: Kazuo Tsubota, Shin-ichiro Imai, Matt Kaeberlein and Joan Mannick

Single Cell Omics (E3)
May 26 – 30, 2017 | Stockholm, Sweden
Scientific Organizers: Sarah Teichmann, Evan W. Newell and William J. Greenleaf

Integrating Metabolism and Immunity (E4)
May 29 – June 2, 2017 | Dublin, Ireland
Scientific Organizers: Hongbo Chi, Erika L. Pearce, Richard A. Flavell and Luke A.J. O’Neill

Cell Death and Inflammation (K2)
May 29 – June 2, 2017 | Dublin, Ireland
Scientific Organizers: Seamus J. Martin and John Silke

June 2017

Neuroinflammation: Concepts, Characteristics, Consequences (E5)
June 19 – 23, 2017 | Keystone, Colorado, USA
Scientific Organizers: Richard M. Ransohoff, Christopher K. Glass and V. Hugh Perry

SOURCE

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Previously undiscerned value of hs-troponin

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN

LPBI

 

Troponin Rise Predicts CHD, HF, Mortality in Healthy People: ARIC Analysis

Veronica Hackethal, MD

Increases in levels of cardiac troponin T by high-sensitivity assay (hs-cTnT) over time are associated with later risk of death, coronary heart disease (CHD), and especially heart failure in apparently healthy middle-aged people, according to a report published June 8, 2016 in JAMA Cardiology[1].

The novel findings, based on a cohort of >8000 participants from the Atherosclerosis Risk in Communities (ARIC) study followed up to 16 years, are the first to show “an association between temporal hs-cTnT change and incident CHD events” in asymptomatic middle-aged adults,” write the authors, led by Dr John W McEvoy (Johns Hopkins University School of Medicine, Baltimore, MD).

Individuals with the greatest troponin increases over time had the highest risk for poor cardiac outcomes. The strongest association was for risk of heart failure, which reached almost 800% for those with the sharpest hs-cTnT rises.

Intriguingly, those in whom troponin levels fell at least 50% had a reduced mortality risk and may have had a slightly decreased risk of later HF or CHD.

“Serial testing over time with high-sensitivity cardiac troponins provided additional prognostic information over and above the usual clinical risk factors, [natriuretic peptide] levels, and a single troponin measurement. Two measurements appear better than one when it comes to informing risk for future coronary heart disease, heart failure, and death,” McEvoy told heartwire from Medscape.

He cautioned, though, that the conclusion is based on observational data and would need to be confirmed in clinical trials. Moreover, high-sensitivity cardiac troponin assays are widely used in Europe but are not approved in the US.

An important next step after this study, according to an accompanying editorial from Dr James Januzzi (Massachusetts General Hospital, Boston, MA), would be to evaluate whether the combination of hs-troponin and natriuretic peptides improves predictive value in this population[2].

“To the extent prevention is ultimately the holy grail for defeating the global pandemic of CHD, stroke, and HF, the main reason to do a biomarker study such as this would be to set the stage for a biomarker-guided strategy to improve the medical care for those patients at highest risk, as has been recently done with [natriuretic peptides],” he wrote.

The ARIC prospective cohort study entered and followed 8838 participants (mean age 56, 59% female, 21.4% black) in North Carolina, Mississippi, Minneapolis, and Maryland from January 1990 to December 2011. At baseline, participants had no clinical signs of CHD or heart failure.

Levels of hs-cTnT, obtained 6 years apart, were categorized as undetectable (<0.005 ng/mL), detectable (≥0.005 ng/mL to <0.014 ng/mL), and elevated (>0.014 ng/mL).

Troponin increases from <0.005 ng/mL to 0.005 ng/mL or higher independently predicted development of CHD (HR 1.41; 95% CI 1.16–1.63), HF (HR 1.96; 95% CI 1.62–2.37), and death (HR 1.50; 95% CI 1.31–1.72), compared with undetectable levels at both measurements.

Hazard ratios were adjusted for age, sex, race, body-mass index, C-reactive protein, smoking status, alcohol-intake history, systolic blood pressure, current antihypertensive therapy, diabetes, serum lipid and cholesterol levels, lipid-modifying therapy, estimated glomerular filtration rate, and left ventricular hypertrophy.

Subjects with >50% increase in hs-cTnT had a significantly increased risk of CHD (HR 1.28; 95% CI 1.09–1.52), HF (HR 1.60; 95% CI 1.35–1.91), and death (HR 1.39; 95% CI 1.22–1.59).

Risks for those end points fell somewhat for those with a >50% decrease in hs-cTnT (CHD: HR 0.47; 95% CI 0.22–1.03; HF: HR 0.49 95% CI 0.23–1.01; death: HR 0.57 95% CI 0.33–0.99).

Among participants with an adjudicated HF hospitalization, the group writes, associations of hs-cTnT changes with outcomes were of similar magnitude for those with HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF).

Few biomarkers have been linked to increased risk for HFpEF, and few effective therapies exist for it. That may be due to problems identifying and enrolling patients with HFpEF in clinical trials, Dr McEvoy pointed out.

“We think the increased troponin over time reflects progressive myocardial injury or progressive myocardial damage,” Dr McEvoy said. “This is a window into future risk, particularly with respect to heart failure but other outcomes as well. It may suggest high-sensitivity troponins as a marker of myocardial health and help guide interventions targeting the myocardium.”

Moreover, he said, “We think that high-sensitivity troponin may also be a useful biomarker along with [natriuretic peptides] for emerging trials of HFpEF therapy.”

But whether hs-troponin has the potential for use as a screening tool is a question for future studies, according to McEvoy.

In his editorial, Januzzi pointed out several implications of the study, including the possibility for lowering cardiac risk in those with measurable hs-troponin, and that HF may be the most obvious outcome to target. Also, optimizing treatment and using cardioprotective therapies may reduce risk linked to increases in hs-troponin. Finally, long-term, large clinical trials on this issue will require a multidisciplinary team effort from various sectors.

“What is needed now are efforts toward developing strategies to upwardly bend the survival curves of those with a biomarker signature of risk, leveraging the knowledge gained from studies such as the report by McEvoy et al to improve public health,” he concluded.

 

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