Everything depends on having a partner you can trust

Transcription

Everything depends on having a partner you can trust
PUSHING THE LIMITS IN CLINICAL RESEARCH
Everything depends
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The limitations of conventional techniques are accelerating the adoption of
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If you’re ready to break through, look no further than the industry leader.
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Isn’t it time to break through the limits?
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© 2012 AB SCIEX. For Research Use Only. Not for use in diagnostic procedures. The trademarks mentioned herein are the property of AB SCIEX Pte. Ltd. or their respective owners.
AACC Booth #4824
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MOLECULAR DIAGNOSTICS
2014 Special Issue
call for papers
Clinical
Chemistry
Advancing Women’s Health: The
Impact of Biomarkers and Genomics
Submit Now
Clinical Chemistry is pleased to announce a special upcoming theme issue on Women’s Health edited
by Drs. Ann M. Gronowski, JoAnn E. Manson, Elaine R. Mardis, Samia Mora, and Catherine Y. Spong titled
“Advancing Women’s Health: The Impact of Biomarkers and Genomics.” Clinical Chemistry, published by the
American Association for Clinical Chemistry, is the most highly cited forum for peer-reviewed, original research
in the fields of clinical chemistry and laboratory medicine.
The purpose of this issue is to highlight recent advances in biochemical and genetic markers used for the
diagnosis, therapy, and preventive care of women during all stages of life. This issue will include diverse themes
such as cancer, cardiovascular disease, osteoporosis, metabolic disease, normal and abnormal pregnancy, infertility,
and infectious disease.
Clinical Chemistry invites authors to submit original articles related to women’s health to be considered for
publication in this special issue.
Potential topics of interest include:
s Discovery and validation of novel biomarkers for the diagnosis, prognosis, and monitoring therapy of
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diseases that affect women including: cancer, cardiometabolic and/or cerebrovascular disease, bone
disease, and autoimmune disorders
The genomics of ovarian, uterine, cervical, and breast cancer
The effect of gender on the risk factors and outcomes related to diabetes, obesity, and cardiovascular
disease
Changes in the microbiome and biomarkers related to pregnancy
Novel molecular diagnostic tools for pre-implantation genetic analysis
Non-invasive screening for fetal aneuploidies and other pregnancy outcomes
Novel biomarkers for the diagnosis of pregnancy-related disorders such as pre-eclampsia, ectopic pregnancy,
preterm delivery, and gestational diabetes
Biomarkers for the diagnosis of infertility, menopause, and premature ovarian failure
The impact of infectious disease on the global health of women
Be a part of this exciting issue. Submit now!
Submissions must be received through our online submission system at http://submit.clinchem.org.
We welcome submissions after July 1, 2013, but cannot guarantee the inclusion of late submissions for the Special
Issue. Your cover letter should express your interest in submitting your paper for consideration for the Women’s
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July 28–August 1, 2013
George R. Brown Convention Center
Houston, Texas
46/%":+6-:tQNoQN
DECONVOLUTING THE METABOLIC SYNDROME AT A MOLECULAR LEVEL
C. Ronald Kahn, MD
Type 2 diabetes (T2D) and metabolic syndrome are each the result of a
complex interaction between genes and environment. Studies in humans
have identified multiple genetic loci which contribute to these disorders,
but most have very small impact on disease expression. Mouse models
provide a powerful tool to investigate gene-environment interactions in
disease susceptibility. For example, among inbred mice, the C57BL/6J
mouse is susceptible to diet-induced T2D and metabolic syndrome,
whereas the 129 mouse is resistant to these phenotypes, despite the
fact that it eats more and moves less than the B6 mouse. Using these
and other mouse models, we have now identified genes which contribute to disease susceptibility. We have also explored the role of
environmental factors, including the gut microbiome. These studies
allow us for the first time to unravel how diet, genetic background, as
well as environment, contribute to creating common metabolic diseases
like obesity and T2D.
Come Prepared: Bezy O, Tran TT, Pihlajamäki J, Suzuki R, Emanuelli B,
Winnay J, et al. PKCð regulates hepatic insulin sensitivity and hepatosteatosis in mice and humans. J Clin Invest 2011;121:2504-17.
.0/%":+6-:tBNoBN
CHALLENGING THE DOGMA: A NEW VIEW OF THE GENOMIC PROGRAMMING OF HUMAN DEVELOPMENT John Mattick, PhD
Noncoding DNA accounts for 98.8% of the human genome. Many of these sequences are being shown to have important functions in differentiation
and development, as well as in cancer and other complex diseases. This session will examine the role of this noncoding or junk DNA in human
development.
56&4%":+6-:tBNoBN
THE VITAMIN D DEBATE: IS ENTHUSIASM OUTPACING THE EVIDENCE?
Vitamin D has been implicated in the prevention of cancer, cardiovascular disease (CVD), diabetes, infections, depression, asthma, autoimmune
diseases, and many other disorders. The available research derives primarily from laboratory research and observational epidemiologic studies,
but large-scale randomized trials of vitamin D are very limited. Small randomized trials to date have provided mixed and inconclusive results. Although many experts are now recommending vitamin D intakes at levels far above the IOM’s dietary recommended allowance (RDA), this remains
controversial. Two experts involved with vitamin D research will debate the evidence for and against public health recommendations for vitamin D
intakes above the RDA for the general population.
Advocating for Increased Intake – Bruce W. Hollis, PhD
Bruce W. Hollis, PhD, Professor and Director of Pediatric Nutritional Sciences at Medical University of South Carolina, will review and present
evidence for higher vitamin D intakes required to sustain adequate nutritional vitamin D status for all aspects of human development including
pregnancy and lactation. Human lactation and nourishment of the human neonate provides the most clear-cut evidence of why recent IOM
recommendations fall far short of what is actually required for adequate vitamin D intakes.
Come Prepared: Hollis BW and Wagner CL. Vitamin D and pregnancy: skeletal dffects, nonskeletal effects, and birth outcomes. Calcif Tissue
Intl 2013; 92:128-39.
S UND A Y, JUL Y 2 8 – T H U R S DA Y , A U G U S T 1 , 2 013
Opposing Increased Intake – JoAnn E. Manson, MD, DrPH
JoAnn E. Manson, MD, DrPH, endocrinologist, Professor at Harvard Medical School, and Principal Investigator of the large-scale VITamin D and
OmegA-3 TriaL (VITAL), will review the scientific evidence for the role of vitamin D in the prevention of cancer, CVD, and other chronic diseases.
She will address design issues relevant to current research, including the potential for confounding in observational studies, and will emphasize
the critical need for large-scale randomized trials before recommending high-dose vitamin D supplementation (well above the RDA) for the
general population.
Come Prepared: Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, et al. The 2011 report on dietary reference intakes for
calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab 2011; 96:53–8.
8&%/&4%":+6-:tBNoBN
PATIENT-BASED THERAPEUTICS DISCOVERY
Stuart L. Schreiber, PhD
Human biology, insights gained from patients, and small-molecule science offer a powerful way to propel the understanding and treatment of
human diseases. The ability to measure heritable and somatic genetic variation in humans with and without disease offers a particularly promising
avenue towards new small-molecule therapeutics. For this approach to be
successful, we will need to relate human genetic variation to small-molecule
sensitivity and drug efficacy as comprehensively as possible.
Therapeutic targets that emerge from human biology and patients have
been validated to some degree prior to clinical testing by genetic “experiments of nature.” But the therapeutic targets that emerge are often
unfamiliar to traditional small-molecule drug discovery efforts. Thus,
advances in chemistry and chemical biology are also required to test
hypotheses emerging from human biology in humans with small molecules.
Come Prepared: The Cancer Target Discovery and Development Network,
Schreiber SL, Shamji AF, Clemons PA, Hon C, Koehler AN, et al. Towards
patient-based cancer therapeutics. Nature Biotech 2010; 28:904-906.
5)634%":"6(645tQNoQN
DINING IN WITH TRILLIONS OF FASCINATING FRIENDS
Jeffrey Gordon, MD
Our genetic landscape is a summation of the genes embedded in our human genome and in the genomes of our microbial symbionts (the microbiome). Similarly, our metabolic features (metabotypes) are an amalgamation of human and microbial contributions. Therefore, understanding
of the range of human genetic and metabolic diversity means that we must characterize
our microbiomes, which contain >100-fold more genes than our human genome, as
well as the factors that influence the properties of our microbial communities. The
results should provide an additional perspective about contemporary human biology
as we seek to understand how our changing lifestyles, cultural norms, socioeconomic
status, and biosphere are influencing our microbial ecology and health status. I will
discuss the results of our group’s ongoing studies of the interrelationships between
diet and the structure and dynamic operations of the human gut microbiome. We
believe that understanding these interrelationships is important for advancing our
appreciation of the nutritional value and health effects of food ingredients, for creating
new nutritional guidelines for humans at various stages of their lifespan, and for
developing new ways to deliberately manipulate the properties of the gut microbiome
to prevent or treat various diseases, including those manifested by immune dysfunction.
Come Prepared: Smith MI, Yatsunenko T, Manary MJ, Trehan I, Mkakosya R, Cheng J, et al. Gut microbiomes of Malawian twin pairs
discordant for kwashiorkor. Science 2013;339:548-54.
Gordon, JI. Honor thy gut symbionts redux. Science 2012; 336:1251-3.
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