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Saturday, October 15
8:00
AM
–10:00
AM
Concurrent Invited Session IV (61-66)
SESSION 64 – Nutrigenomics: Genotype by
Environment Interaction and Disease Risk
Room 511, Level 5, Convention Center
Moderators:
Jose M. Ordovas, USDA at Tufts Univ.,
USA; Chao-Qiang Lai, USDA at Tufts Univ., USA
Genome-wide association studies (GWAS) are a
powerful tool to identify genetic risk factors of human
disease. Only a small fraction of disease risk, however,
is identified in a given GWAS, and even fewer genetic
variants are replicated in multiple populations.
Because genotype by environment (GxE) interactions
are crucial in contributing to disease risk, an urgent
need exists to examine GxE interactions in GWAS.
Nutrigenomics undertakes the study of interactions
between genotype and nutrition modulating clinical
outcomes or their risk factors. Defining GxE
interactions across the spectrum from single SNP or
gene studies to large-scale, GWAS will clarify the role
of these interactions in disease risk, provide an
understanding of how such interactions contribute to
disease risk, and allow more accurate predictions of
disease risk.
8:00
AM
Introduction.
J. M. Ordovas. USDA at Tufts
Univ., USA.
8:05
AM
Understanding GxE interaction and
cardiovascular disease risk.
C-Q. Lai. USDA at Tufts
Univ., USA.
8:25
AM
Interaction between whole grain foods
and genetic variants on diabetes risk.
J. A.
Nettleton. Univ. of Texas Sch. of Publ. Hlth., Houston,
USA.
8:45
AM
Pharmacogenetics: Understanding an
individual’s response to fenofibrate intervention by
genome-wide association study.
D. K. Arnett. Univ.
of Alabama at Birmingham, USA.
9:05
AM
Epigenomics: Understanding individual
differences in response to nutrition and aging?
J.
C. Mathers. Newcastle Univ., U.K.
9:25
AM
Effects of genetic variants and nutritional
factors on metabolic disease among Chinese
populations.
X. Lin. Shanghai Inst. for Biol. Sci.,
Chinese Acad. of Sci., China.
9:45
AM
Questions and answers.
J. M. Ordovas.
USDA at Tufts Univ., USA.
Cameras and all other recording devices are
strictly prohibited
in all session rooms. Thank you for your cooperation
Saturday, October 15
8:00
AM
–10:00
AM
Concurrent Invited Session IV (61-66)
SESSION 65 – Status and Prospects of Genetic
Therapy for Major Mendelian Diseases
Room 517A, Level 5, Convention Center
Moderators:
Gert-Jan B. van Ommen, Leiden Univ.
Med. Ctr., Netherlands; Brunhilde Wirth, Univ. Hosp.
Cologne, Germany
Two decades after the discovery of several genes fo
major Mendelian disorders, the first approaches of
mechanism-based therapy have successfully entere
the clinical phase. These include Duchenne muscula
dystrophy (DMD), spinal muscular atrophy (SMA),
Fragile X mental retardation (FraX) and Leber
congenital amaurosis (LCA). The approaches cover
great diversity, including splice modulation by
antisense oligonucleotides, chromatin alteration by
histone deacetylase inhibitors, compound library
screening for small molecules with specific effects,
and local injection of viral vectors. The speakers will
present one example of each approach: exon skippi
for DMD, HDAc inhibition in SMA, compound
screening for GABAergic inhibition in FraX, and
subretinal viral injection for LCA. As the approaches
modulate key mechanisms in cell biology, it is
plausible that future applications, following refineme
in their target diseases—with their advantage of well
defined readouts—may well extend to other conditi
including complex disease.
8:00
AM
Antisense-based exon skipping as a
therapy for DMD and other disorders.
G-J. B. van
Ommen. Leiden Univ. Med. Ctr., Netherlands.
8:25
AM
The use of
HDAc
inhibitors to upregula
SMN2
in SMA.
B. Wirth. Univ. Hosp. of Cologne,
Germany.
8:50
AM
From gene to bedside: Translating
lessons from Fragile X syndrome.
S. Warren. Emo
Univ., USA.
9:15
AM
Recombinant
AAV
gene therapy of Leb
congenital amaurosis.
S. G. Jacobson. Univ. of
Pennsylvania, USA.
9:40
AM
Questions and answers.
G-J. B. van
Ommen. Leiden Univ. Med. Ctr., Netherlands.