text: Australia Council launches Arts Funding Guide 2013 Print Email Email to a friend Your email Your name Friend's email Friend's name Verification (type the code in the image) Generate New Image Close Related Articles Aritst directs UN climate change conference towards the Reef An Australian artist will put the Great Barrier Reef in the spotlight in the UN's Artists 4 Paris Climate Change. National Ratings week beginning Sunday 4 October 2015 Slaughter by Nine as other results are abjectly horrible. Football. David Sefton announces Adelaide Festival swansong His fourth and final Adelaide Festival of Arts program features theatrical epics, post-rock legends, and… a stadium spectacular? Choir: cheaper than hospital and just as essential Researchers are measuring the value of arts engagement against psychiatric care and counting the benefits. (Premium content) Premium content Leo Ribeiro Thursday 13 December, 2012 In 2013, the Australia Council will deliver more than $170 million in funding for arts organisations and individual artists across Australia. This content is only available to members of ArtsHub Subscribe Now for instant access! A subscription to ArtsHub will enable you to: Access the most comprehensive jobs board for the arts sector, with hundreds of positions posted weekly Learn how and where to get grants, with the most extensive grant finder in the arts industry Monitor Australian art sales and trends with our Auction Tracker Post, manage and monitor your social media campaigns using our extensive social media toolkit Optimise your website for search engines using our auditing service Promote yourself and your career to the largest arts community in Australia by uploading your professional profile Gain an understanding of salaries within the Australian arts industry, by accessing our Salary Survey Access thousands of subscriber-only features, articles and guides Take advantage of exclusive ticket giveaways, offers and competitions Save hundreds of Dollars every year on cinema tickets, magazines, books, travel, shopping and more with the Member Rewards scheme ... and much, much more. Subscribe Now and be part of the Australian arts community Member login Email address Password Forgot password? About the author Leo Ribeiro is an ArtsHub writer.


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Dale Pierce wrote: Bobby Pico sometimes went as Bobby "Pancho" Pico when teaming with Cisco Grimaldo a la Pancho & Cisco from the old Cisco Kid tv show. he is not to be confused with Francisco "Pancho" Pico (Julio Arguello) who also wrestled along the Mexican border and the southwestern USA in the 1960s, as these are two separate people ..
Roberto Pico
Front Facelock
Don Arnold
Brute Bemis
Tarzan Baxter
Jesse "The Body" Ventura squares off against Ivan "The Polish Power" Putski on August 25,1984 in Madison Square Garden, NY!
This week's ClickWrestle Match of the Week is Leva Bates vs. Athena from July 11, 2015.
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SAINT Blog Tour, Sept. 25 - Oct. 4, 2013
Catholic PRWire
We're pleased to announce the launch of a blog tour for SAINT by Lino Rulli.
If Rulli has his way, he will be canonized on Divine Mercy Sunday, which, allegedly, is when Blessed Pope John Paul II and Pope John XXIII will be canonized in Rome. (The official announcement will be next week- Sept. 30.) Rulli provides evidence for his cause (and yours) in SAINT.
Each day during the SAINT blog tour- Sept. 25 through Oct. 4- one of 10 participating blogs will post unique content relating to the book.
As readers follow along on this virtual book tour, they will have a chance to read exclusive excerpts from SAINT, and watch Skype interviews with Rulli. They'll get honest reviews from Catholic bloggers, and have a chance to win a copy of the book at different stops along the tour.
Thank you to all the incredible bloggers who will be hosting stops on the tour. Please support them by visiting their sites.
You can purchase SAINT through Servant Books or Amazon.com. Also tune in to The Catholic Guy radio show on Sept. 30 for a special announcement!
Tour Schedule
Sept. 25: Catholic Fire Blog
Sept. 26: Snoring Scholar
Sept. 27: Catholic Book Blogger
Sept. 28: Catholic Hotdish
Sept. 29: Catholicism Anew
Sept. 30: The Curt Jester
Oct. 1: The Practicing Catholic
Oct. 2: A Catholic View
Oct. 3: CatholicMom.com
Oct. 4: Marc Cardaronella
About the book
Rulli's first book, SINNER, was full of stories- honest, humorous, bold, poignant- illustrating why he deserved that title. This new book takes another approach, another angle: why Lino is on his way to sainthood. Often hilarious, but always with a point, SAINT focuses on God's grace and shows how even a sinner like Lino can look forward to being a saint. As Lino puts it: "Instead of stories of small triumphs and many failures, this is a book to encourage you in your own triumphs, to realize you might not be as big a sinner as you think, and that with God's help, you might just become a saint."
Picking up where SINNER left off, SAINT points the way to our end goals: holiness and sainthood, and does so in a way that entertains as well as inspires.
Rulli had a special devotion to his favorite saint, Blessed Pope John Paul, which he chronicles throughout this book. Rulli discusses what it was like to have a front-row seat at the funeral of Blessed Pope John Paul II; the rosary Blessed Pope John Paul II gave him; visiting his tomb; and traveling to Poland, the birthplace of Blessed Pope John Paul II, to experience the historical places that molded the life of the memorable saint. Therefore, the official announcement on September 30 of Blessed John Paul II will be very special for Lino. Don't forget to tune in to The Catholic Guy radio show on that date for a special announcement!
About the author
Lino Rulli, with a bachelor's degree in communications and a master's degree in theology, has a style and personality unique in the world of religious media. Rulli is a three-time Emmy Award winner and hilarious host of the popular radio show, The Catholic Guy, on SiriusXM Radio- the Catholic Channel. He has lived in Italy, the Bahamas, and Minnesota, and currently lives in New York City.
Media inquiries should contact Kevin Wandra at: email@example.com. For any other inquiries regarding this blog tour or social media, contact Kelly Kracht at: email@example.com.
Carmel Communications
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Kelly Kracht - Media Relations Coordinator,
Saint, Lino Rulli, Sinner, Pope John Paul II, Catholic Blogger, Catholic
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(Chandler) Who We Are and What We?re Looking For? We are the Sales and Partner Operations Department and we serve as the cross-functional support of the Sales and Partner organization. Our mission is to increase operational efficiencies, maximize customer/employee delight, and9/14/2015 Chandler, AZ Save This Job
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Huntsville, ALFull-time Company Description GATR Technologies is a fast growing satellite communications company in Huntsville, Alabama, that designs, develops, and manufactures unique inflatable satellite antenna systems. For more information about GATR, visit our website at8/29/2015 Huntsville, AL Save This Job
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Location: Boston, MA Department: Technical Operations Type: Full Time Min. Experience: Entry Level WiserTogether is seeking a motivated, thoughtful, and curious individual to join the Technology Operations department as a Technical Support Analyst. This is an entry level9/10/2015 Boston, MA Save This Job
Description ePromos Promotional Products, Inc., a five time winner of ASI Best Places to Work, is one of the fastest growing promotional product companies in the US. We recommend and provide custom branded merchandise and apparel to businesses and organizations of all sizes8/22/2015 New York, NY Save This Job
ID 2014-2167 Job Location US-CA-City of Industry Posted Date 10/9/2014 Category Product Management More information about this job: Purpose Of The Job: Product Line Analyst: Research customer behaviors and industry conditions to determine new avenues to market technical8/17/2015 City of Industry, CA Save This Job


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This luscious bikini, with its delectable scalloped shape and lovely lace edging has a sort of perfect rowdy elegance. It's saturated silk meets feminine elegance, it's hubba-hubba meets smooth shape, it's French boudoir meets English garden. From daytime to date night, this one makes us want to shout out loud.
Wear With
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Clara Whispering Thong$65.00
Wide, body hugging sides, delectable scalloped edging, slinky silk, and a classic thong silhouette make this whisper of a thong absolutely lovely. Worth shouting about.
Stella McCartney
Clara Whispering Suspender Belt$95.00
This lovely silk and luscious lace suspender belt is a true classic. Traditional garter belt shape is rendered in fine fabrics and is begging to be shown off.
- Low-Rise
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Fit Notes
- True to Size
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May We Recommend?
This classic bikini's heat molded hem are totally, invisibly seamless, and the slinky smooth finish and impossibly airy fabrication are pretty much perfect and totally pretty.
This balconette from Stella's smooth line of everyday lovelies has all of the brilliant features of her standard basics while also being totally gorgeous on the body. Winning.
From the subtly Templar-tribal print of the cup overlay to the boldly gorgeous noir lace panels atop the cups, this one is an exercise in contradictions. We love that.


text:
|Reviews for Five Times Spock Scared Chekov
| tanseynz chapter 6 . 8/27
This makes a lot of sense. In essence, you REALLY want Spock to be on your side, even though it will never be as a friend as humans understand friend. His is different, but still valued.
A truly good piece of writing, and you got the various balances of action and thought just right.
| tigerlily124 chapter 6 . 3/24
Nicely done. Very much appreciated .
| Thiing1 chapter 6 . 11/26/2014
I loved this so much through it all! You have a great writing style, and you nailed the characters personalities! All in all, this was a great read. :)
| Lunar Crystallos chapter 6 . 7/31/2014
I loved this! Especially that last line... Great story, I'm so glad I came across it.
| Guest chapter 6 . 7/23/2014
I really like this story especially the ending , made me giggle, but there were a few spelling mistakes nothing major.
| Satin Ragdoll chapter 3 . 8/17/2013
I actually liked this! "He is strong!" Loud, too. :)
| WhatTheValhalla chapter 6 . 6/28/2013
Brilliant! I'm that one chapter I laughed and cried and it was just so beautifully sad and perfect. I'm going to go read everything else that you've written!
| WhatTheValhalla chapter 3 . 6/28/2013
Brilliant! (As always) I don't know why you wouldn't be happy with that chapter, it was really good, you should be very proud of it!
| WhatTheValhalla chapter 2 . 6/27/2013
Really good, I was almost crying, and Chekovs perspective was really well written
| WhatTheValhalla chapter 1 . 6/27/2013
Wow, for your first time writing that was pretty amazing! Icy Vulcan eyebrows of dooooooom, had me cracking up so much, how do you think of funny things like that. Oh and I love Chekov's tangents where he randomly goes from topic to topic in his mind, it can be hard to do that properly without forgetting the point completely, but you did it perfectly.
Also I'm so happy to find a Chekov-centric fic that doesn't have any pairings. Sometimes I want to read about an adorable russian without being reminded how forever-alone I am, so thanks
Great story, and keep writing (or some other inspirational thing :)
| Unleashed111 chapter 6 . 6/3/2013
| Pretentious Procrastinator chapter 6 . 5/25/2013
Ahhh, this is abosolutely wonderful and so masterfully written. Star Trek fanfic needs more of Spock showing how awesome he is, and you never have too much Chekov! Fantastic story, and I loved it.
| JustBlossom chapter 6 . 5/22/2013
This story is really good! I enjoyed reading it :) Chekov and Spock are my two fav characters, so it was perfect :D
| Cookie.Monster66 chapter 6 . 4/17/2013
Amazing story, perfect blend of comedy and angst; it works perfectly. You've captured all of the characters amazingly. Please write more!
| DragonsRme chapter 6 . 2/5/2013
Oh wow that was amazing and the last chapter with the demons and whatnot was phenomenal. I cried so hard through out it. Well done a fantastic story


text:
Sanbanto Premium Pork RestaurantMarch 24, 2012Burgers • Petaling Jaya, Malaysia
Staff r nice n hv good knowledge on their menu. Food is good as usual. Ps. Table in far end is kinda cool..
Staff r nice n hv good knowledge on their menu. Food is good as usual. Ps. Table in far end is kinda cool..
The only tomyam i can hv while I'm sick....tasty but not too spicy.. ♥ it!
2 drumsticks+ 1 breast+ 1/2 salted egg+ nasi putih wiv curry gravy: total rm19.50
Jelly ice cream forever - TAK ADA!!! Disappointed! The staff is rude!
Saturday open until 12:30.
Cheaper price compare to guardian n wstsons
Try to get discount on drugs with white tag.. ╭(′▽‵)╭(′▽‵)╭(′▽‵)╯ GO!
Public bank.Watson's. Sen Heng. Yum Yum 2. Loong Zhai. Elianto. Soul Sweet. De Band. Anakku. Big Apple-donut. Car wash 8am-5pm. Kdh-supplements+ organic food & skincare. Maxis centre. Tonight.
Good shopping experience ^O^ lady owner was very friendly. The S/A is polite + helpful. Bought few item thr for my princess.
Funny smell in restaurant... i can't eat thr... excuse my sensitive nose..
Just ask the staff and they'll assist u.


text:
- Age / Gender:
- n/a, Male
- Location:
- Location not disclosed
- Joined:
- 8/31/10
- All Stats >
User Statshot
- Community Stats
Level 4 Blank Slate
Normal Whistle
Ranked as Civilian
Contact Info / Websites
Recent Game Medals
Enquirer 10 Points Play for 30 minutes Medal Stats.
Target Hater 10 Points Destroy 500 targets Medal Stats.
BE NOBODY 100 Points Yay, you completed the whole demo! You dissident! Medal Stats.
An Act of Activation 50 Points Complete the "Activating iEye" levels Medal Stats.
Slidewalking 25 Points Complete the "Slidewalk" levels Medal Stats.
Self Surveillance 10 Points Complete the "Moving iEye" levels Medal Stats.
BE SOMEBODY 5 Points Run away, and begin your escape. Medal Stats.
Ending 2 5 Points Achieve Ending 2. Medal Stats.
Ending 1 5 Points Achieve Ending 1. Medal Stats.
Ending 3 5 Points Achieve Ending 3. Medal Stats.
Total Medals Earned: 827 (From 115 different games.)
Favorite Audio
|-Final Battle-
|Video Game Song
|A Stroll on the Internet
|Video Game Song
|Broken Monastery
|Video Game Loop
|Go Go 8-Bit Rangers!
|Video Game Song
Favorite Movies
Robot Masters Rated 4.3502 Stars Megaman faces off against the first 6 robot masters! Comedy - Parody Warriors of the Portal Rated 4.4598 Stars NG characters have been locked in a maze, and they must kill each other to survive Action Stamp on the Ground Rated 4.4285 Stars DDR dance party, everyone! I SAID, *EVERY*ONE. Music Video -The Guardian- Rated 4.4104 Stars A boy wanders through the woods and discovers his true potential. Music Video
Favorite Games
Overlod Rated 3.8154 Stars You are evil incarnate, the vagrant death, the Dark Lord. Simulation - Other Hardventure Into The Duat Rated 3.5444 Stars Take control of a dead man's heart and battle your way to the end of the Duat! Action - Platformer - Hop and Bop Phoenotopia Rated 4.4932 Stars Journey with Gale on a quest to thwart evil and save her village! Adventure - RPG Infectonator : Survivors Rated 3.9501 Stars Squad-Based Randomized Permadeath Tactical Survival Simulator Strategy - Other


text:
Page 1
Original Contribution
Prediction of Coronary Heart Disease Risk using a Genetic Risk Score: The
Atherosclerosis Risk in Communities Study
Alanna C. Morrison1, Lance A. Bare2, Lloyd E. Chambless3, Stephen G. Ellis4, Mary Malloy5,
John P. Kane5, James S. Pankow6, James J. Devlin2, James T. Willerson7, and Eric Boerwinkle1,7
1Human Genetics Center and Division of Epidemiology, University of Texas Health Science Center at Houston, Houston, TX.
2Celera, Alameda, CA.
3Collaborative Studies Coordinating Center, University of North Carolina, Chapel Hill, NC.
4Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, OH.
5Cardiovascular Research Institute, University of California, San Francisco, CA.
6Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN.
7Texas Heart Institute, Houston, TX.
Received for publication May 4, 2006; accepted for publication January 16, 2007.
Recent studies have evaluated whether incorporating nontraditional risk factors improves coronary heart dis-
ease (CHD) prediction models. This 1986–2001 US study aggregated the contribution of multiple single nucleotide
polymorphisms into a genetic risk score (GRS) and assessed whether the GRS plus traditional risk factors predict
CHD better than traditional risk factors alone. The Atherosclerosis Risk in Communities (ARIC) cohort was followed
for a median of 13 years for CHD events (n ¼ 1,452). Individuals were genotyped for 116 single nucleotide
polymorphisms associated with CHD in multiple case-control studies. Single nucleotide polymorphisms nominally
predicting incident CHD in the ARIC study were included in the GRS. The GRS was significantly associated
with incident CHD in Blacks (hazard rate ratio ¼ 1.20, 95% confidence interval: 1.11, 1.29) and Whites (hazard
rate ratio ¼ 1.10, 95% confidence interval: 1.06, 1.14) as well as in each tertile defined by the traditional cardio-
vascular risk score (p ? 0.02). When receiver operating characteristic curves based on traditional risk factors were
recalculated after the GRS was added, the increase in the area under the receiver operating characteristic curve
was statistically significant for Blacks and suggestive of improved CHD prediction for Whites. This study demon-
strates the concept of aggregating information from multiple single nucleotide polymorphisms into a risk score and
indicates that it can improve prediction of incident CHD in the ARIC study.
cardiovascular diseases; genetics; polymorphism, genetic; risk factors
Abbreviations: ACRS, ARIC Cardiovascular Risk Score; ARIC, Atherosclerosis Risk in Communities; AUC, area under the
curve; CHD, coronary heart disease; GRS, genetic risk score; SNP, single nucleotide polymorphism.
Coronary heart disease (CHD) is the leading cause of
mortality in the United States (1), and numerous studies
have focused on identifying risk factors contributing to
CHD. The Framingham Study developed a risk score that
includes major risk factors, such as age, blood pressure,
cigarette smoking, total cholesterol, high density lipoprotein
cholesterol, and diabetes status (2). A similar score was
developed that demonstrates the ability of traditional risk
factors to predict CHD in the Atherosclerosis Risk in Com-
munities (ARIC) study (3).
Recently, studies have evaluated whether emerging risk
factors, such as C-reactive protein, improve prediction of
Correspondence to Dr. Eric Boerwinkle, Human Genetics Center, University of Texas Health Science Center at Houston, 1200 Herman Pressler,
Suite 453E, Houston, TX 77030 (e-mail: email@example.com).
American Journal of Epidemiology
Copyright ª 2007 by the Johns Hopkins Bloomberg School of Public Health
All rights reserved; printed in U.S.A.
DOI: 10.1093/aje/kwm060
American Journal of Epidemiology Advance Access published April 18, 2007
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CHD beyond traditional risk factors (3–5). Genetic poly-
morphisms contributing to CHD incidence are another type
of emerging risk factor under investigation in studies gen-
erally focused on a priori selected candidate genes (6, 7).
Advances in genomic technologies have made it possible to
genotype and evaluate many single nucleotide polymor-
phisms (SNPs) throughout the human genome to identify
novel CHD susceptibility genes (8). The reported contribu-
tion of any single gene variant to CHD risk has been small,
underscoring the polygenic nature of the disease. This paper
describes aggregation of the contribution of multiple SNPs
into a single genetic risk score (GRS). The GRS comprises
SNPs selected from both candidate genes and genes identi-
Identification of the definitive set of SNPs for inclusion in
a GRS is evolving and was not the primary aim of this study.
Rather, the SNPsdescribed hereare usedtoillustratethe con-
cept of a GRS and to investigate whether addition of a GRS
of the GRS is needed in other population-based samples.
The ARIC study
The ARIC study is a prospective investigation of athero-
sclerosis and its clinical sequelae involving 15,792 US in-
dividuals aged 45–64 years at recruitment (1986–1989). A
detailed description of the ARIC study design and methods
is published elsewhere (9).
Incident CHD
Incident CHD was determined by contacting participants
annually and by surveying discharge lists from local hospi-
tals and death certificates for potential cardiovascular events
(10). Details on quality assurance for ascertainment and
classification of CHD events have been published elsewhere
(10). CHD cases (n ¼ 1,452) were defined as participants
with either definite or probable myocardial infarction, a si-
lent myocardial infarction between examinations (indicated
by electrocardiogram), a definite CHD death, or a coronary
revascularization. Participants were excluded from analyses
if they had a positiveor unknown history of prevalent stroke,
transient ischemic attack/stroke symptoms, or CHD at the
initial visit; an ethnic background other than Blacks from
Jackson, Mississippi, or Whites; restrictions on use of their
DNA; or missing data for any of the traditional cardiovas-
cular risk factors. The remaining 13,907 participants were
followed for incident CHD for a median of 13 years between
the baseline examination and December 31, 2001.
Examination and laboratory measures
Cardiovascular risk factors considered in this study were
measured at baseline and included age, systolic blood pres-
sure, use of antihypertensive medication, total cholesterol,
high density lipoprotein cholesterol, gender, diabetes, and
smoking status. These risk factors comprise the ARIC Car-
diovascular Risk Score (ACRS) established by Chambless
et al. (3) and are shown in table 1 for male and female cases
and controls in each racial group. Seated blood pressure was
measured three times with a random-zero sphygmomanom-
eter, and the last two measurements were averaged. Inter-
viewers administered a questionnaire to assess use of
antihypertensive medication. Plasma total cholesterol was
measured by an enzymatic method (11). High density lipo-
protein cholesterol was measured after dextran-magnesium
precipitation of non–high density lipoproteins (12). Diabe-
tes was defined by a fasting glucose level of ?126 mg/dl,
a nonfasting glucose level of ?200 mg/dl, or a self-reported
Risk in Communities study, United States, 1986–2001
Characteristics* of the cardiovascular risk score for cases and controls, by gender and racial group, in the Atherosclerosis
Cases Controls
White females
(n ¼ 346)
55.8 (5.4)
White males
(n ¼ 793)
55.7 (5.4)
Black females
(n ¼ 147)
55.0 (5.7)
Black males
(n ¼ 166)
55.0 (5.8)
White females
(n ¼ 5,285)
53.8 (5.7)
White males
(n ¼ 3,887)
54.3 (5.7)
Black females
(n ¼ 2,100)
53.1 (5.7)
Black males
(n ¼ 1,183)
53.4 (5.9) Age (years)
Systolic blood
124.9 (19.2)124.1 (17.3)141.2 (27.1)132.0 (20.2) 116.4 (17.4)119.2 (15.4)126.7 (20.1) 129.5 (21.1)
Total cholesterol
236.4 (45.1) 220.3 (38.8)232.3 (55.9)220.3 (47.6)216.7 (41.4) 208.0 (37.9)215.3 (44.3)209.8 (43.6)
High density
49.0 (13.5)39.8 (10.9) 51.1 (14.3)46.5 (13.2) 58.3 (17.2)43.8 (12.6)58.6 (17.4)51.5 (17.4)
36.1 24.168.048.217.316.241.429.3
Smoker18.104.22.1683.423.523.723.2 36.7
* All values are expressed as mean (standard deviation) or percent.
2 Morrison et al.
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diagnosis of diabetes or use of diabetic medication. Ciga-
rette smoking status was classified as current or not current.
Genotype determination
Two sources of SNPs were screened for their ability to
predict incident CHD in the ARIC study. Multiple, large-
scale genomic association studies of CHD identified 92
SNPs in 87 genes, and a literature review of CHD associa-
tion studies resulted in the selection and genotyping of 24
SNPs in 21 a priori candidate genes (Web table 1; this in-
formation is described in a supplementary table referred to
as ''Web table 1'' in the text and posted on the Journal's
website (http://aje.oupjournals.org/).) Genotyping was car-
ried out by allele-specific real-time polymerase chain reac-
tion following polymerase
amplification of genomic DNA and an oligonucleotide liga-
tion assay similar to a procedure previously described (13).
Primersweredesignedand validatedin-house,and the primer
and probe sequences for the amplification reactions and any
additional information about the genotyping methods are
available from the authors upon request. Previous analyses
of allele-specific real-time polymerase chain reaction assays
showed that the accuracy of our genotyping is greater than 99
percent, as determined by internal comparisons of differen-
tially designed assays for the same marker and comparisons
for the same marker across different studies (14).
The 92 SNPs from the genomic association studies dem-
onstrated a consistent association with CHD, either myocar-
dial infarction or severe coronary artery disease, in one of
three case-controlstudies. Subjects were self-described non-
Hispanic Whites who were recruited as previously detailed
by Shiffman et al. (15), had completed a questionnaire ap-
proved by the institutional review board, and gave informed
consent to participate in genetic studies. The severe coro-
nary artery disease study comprised 781 cases and 603 con-
trols drawn from 5,800 angiography patients enrolled by the
Cleveland Clinic Foundation. The severity of coronary ar-
tery disease was scored by summing the percentage of ste-
nosis (determined by coronary angiography, lesions of <50
percent stenosis were scored as 0 percent) in 10 segments:
the left main, and the proximal, medial, and distal segments
of each of the left anterior descending, left circumflex, and
right coronary arteries. Cases had the highest stenosis
scores: at least 150 for males and 75 for females. Controls
had stenosis scores of zero (unpublished data). In two
association studies of myocardial infarction, cases with
a history of myocardial infarction were compared with con-
trols with no history of myocardial infarction. These myo-
cardial infarction studies comprised 340 cases and 346
controls enrolled at the University of California, San Fran-
cisco (15) and 445 cases and 943 controls enrolled at the
Cleveland Clinic Foundation (D. Shiffman, Celera, personal
communication, 2006). Most of the approximately 14,000
SNPs investigated in thesegenomic association studies were
missense SNPs, and others were in predicted splice sites or
transcription factor binding sites. These approximately
14,000 assays comprise the 11,053 SNPs investigated by
Shiffman et al. plus approximately 400 subsequently devel-
oped assays. Hence, the 92 SNPs genotyped in the ARIC
chain reaction–based
study have already undergone an extensive testing and rep-
lication process.
Statistical analyses
Agreement of genotype frequencies with Hardy-Weinberg
equilibrium expectations was tested by using a v2goodness-
of-fit test for the controls.
Traditional cardiovascular risk factors were evaluated in
a Cox proportional hazards model of time to incident CHD
(3). For incident CHD cases, the follow-up time interval was
defined as the time between the initial clinical visit and the
date of the first CHD event. For noncases, follow-up con-
tinued until December 31, 2001; the date of death; or the
date of last contact if lost to follow-up. Each model was
evaluated separately among Whites and Blacks. An ACRS
was calculated for each subject by multiplying each model
coefficient by the associated risk-variable value and then
summing the products.
For each race, the 92 gene discovery SNPs and the 24
candidate gene SNPs were modeled as the additive effect of
the risk-raising allele and were individually evaluated by
Cox proportional hazards models adjusted for age and gen-
der. The risk-raising allele is the allele that resulted in a haz-
ard rate ratio greater than 1.0 for Whites. Within each race,
SNPs associated with p values greater than 0.10 were pruned
from further consideration for inclusion in the GRS. This
pruning criterion was chosen so that SNPs conferring only
modest levels of CHD risk could be aggregated into the
GRS. SNPs associated with p values less than or equal to
0.10 entered the race-specific GRS with a coding value of 1
for the risk homozygote, 0 for the heterozygote, and ?1 for
the nonrisk homozygote. The GRS for each individual was
created by summing these values for each SNP in the GRS.
For each race, the GRS was included in a Cox propor-
tional hazards model containing the traditional risk factors
comprising the ACRS. A new combined risk score was cal-
culated for each individual (ACRS þ GRS) by multiplying
each model coefficient by the associated risk variable and
then summing the products. The area under the receiver
operating characteristic curve equals the probability that
a randomly drawn subject who had an incident event within
a specifiedtimewould have ahigherrisk score than asubject
who did not have an event in that time period. An area under
the curve (AUC(ˆt )) for t equal to 13 years was calculated
for both the ACRS and the ACRS þ GRS (16). The AUC(ˆ t )
is a consistent predictor of the area under the sensitivity(t)
versus 1 – specificity(t) curve for prediction of t years of
risk. A comparison of the AUC(ˆ t) between the ACRS alone
and the ACRS þ GRS was performed via bootstrapping and
evaluating the overlap of the 95 percent confidence interval
of the point estimates (i.e., the median difference in AUC(ˆt )
among bootstrap samples).
An internal validation method using a bootstrap sampling
procedure (16) was used to evaluate potential upward bias in
the estimated hazard ratio of the GRS in the ARIC study.
The seven-step procedure was implemented as follows:
1. Create a bootstrap sample by randomly sampling N
participants with replacement from the original sample,
Genetic Risk Score Predicts CHD3
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where N is the total number of participants in the
original sample.
2. Select a new panel of GRS SNPs from the bootstrap
sample by using the same criteria used to select the
panel of SNPs from the original sample.
3. In the bootstrap sample, estimate the regression co-
efficient for the GRS by using a Cox proportional
hazards model adjusted for age and sex.
4. In the original sample, use the new panel of SNPs to
create a GRS for each subject and estimate the re-
gression coefficient (adjusted for age and sex) for the
5. Subtract the regression coefficients calculated in step 4
from those in step 3 to obtain an estimate of the bias in
the regression coefficient.
6. After performing 2,000 iterations of steps 2–5, calculate
the mean of the estimated bias in the regression
7. Subtract the mean bias in the regression coefficient as
calculated in step 6 from the regression coefficient
determined in the primary analysis to obtain an estimate
for a bias-corrected hazard ratio.
Of the 92 discovery SNPs and 24 candidate SNPs geno-
typed in the ARIC cohort, 110 and 112 were in accordance
with Hardy-Weinberg expectations in Whites and Blacks,
respectively. Of these SNPs, 11 in Whites and 11 in Blacks
were selected for inclusion in the GRS based on their nom-
inal association with incident CHD in a Cox proportional
hazards model (p ? 0.10). The GRS for each race included
10 SNPs from the 92 gene discovery SNPs and one SNP
from the 24 a priori candidate gene SNPs. These SNPs, the
genes in which they reside, allele frequencies, and results of
the Cox proportional hazards modeling are detailed in table
2. This same information for all 116 SNPs is presented in
Web table 1. The two ADAMTS1 SNPs, rs428785 and
rs402007, are separated by 725 base pairs, and the geno-
types were 99.7 percent concordant, demonstrating strong
linkage disequilibrium. Therefore, only rs402007 was cho-
sen to enter the GRS, resulting in a GRS for Whites com-
posed of 10 SNPs. Only rs20455 in KIF6 was common
between races for the SNPs selected for inclusion in the
As expected, each of the traditional cardiovascular risk
factor components of the ACRS was statistically significant
when evaluated in a Cox proportional hazards model. Ad-
ditionally, the components of the ACRS were significantly
different between males and females except for the propor-
tion of Whites using antihypertensive medication and smok-
ing (data not shown). The GRS for Whites, based on the 10
SNPs described in table 2, was calculated for 8,361 individ-
uals and ranged from ?7 to 6. The GRS for Blacks, based on
11 SNPs (table 2), was calculated for 2,624 individuals and
ranged from ?9 to 5. The GRS was normally distributed for
each race (figure 1). The range of individual risk scores
indicates that no individual of either race had all risk-raising
alleles or all risk-lowering alleles. This finding is consistent
with the hypothesis that, as a complex disease, CHD inci-
dence is the result of a balance of the contribution of mul-
tiple genes with small effects.
The association of the GRS with CHD in each race was
tested in a Cox proportional hazards model containing the
traditional risk factors comprising the ACRS. For both
Whites and Blacks, the GRS was a significant predictor of
incident CHD after accounting for the effects of the tradi-
tional risk factors (p < 0.01). The hazard ratios were 1.10
per unit (95 percent confidence interval: 1.06, 1.14) for the
GRS for Whites and 1.20 per unit (95 percent confidence
interval: 1.11, 1.29) for the GRS for Blacks. Thus, for
a White homozygous for six at-risk alleles or a Black ho-
mozygous for five at-risk alleles, the hazard rate ratio would
be 1.77 or 2.49, respectively. The GRS was also a significant
predictor of incident CHD after accounting for the effects of
the traditional risk factors (p < 0.02) in gender-specific
analyses within each race (data not shown). Use of an in-
ternal validation method based on a bootstrap sampling pro-
cedure indicated that in the 2,000 bootstrap samples, the
SNPs in the original GRS panels for Whites and Blacks
were the most frequently chosen for these new panels.
The bootstrap estimate of a bias-corrected hazard ratio
was 1.05 for the GRS for Whites and 1.09 for Blacks.
Next, the area under the receiver operating characteris-
tic curves for the ACRS þ GRS model, which included
both genetic and traditional risk factors, was compared
with the AUC for the ACRS model, which included only
the traditional risk factors. For each race, including the
GRS in the model used to calculate risk scores increased
the AUC over that observed when the receiver operating
characteristic curve was based on only traditional risk
factors (figure 2). For Whites, the AUC was 0.766 for
the ACRS þ GRS model and 0.764 for the ACRS model.
The increase in the AUC for Whites was 0.002 (95 percent
confidence interval: 0.000, 0.006). For Blacks, the AUC
was 0.769 for the ACRS þ GRS model and 0.758 for the
ACRS model. The increase in the AUC for Blacks was
0.011 (95 percent confidence interval: 0.002, 0.024). Thus,
for Whites, the 95 percent confidence interval of the in-
crease barely included zero (i.e., the null hypothesis), in-
dicating that the increase in the AUC caused by including
the GRS is marginally statistically significant at the 0.05
level. For Blacks, the 95 percent confidence interval of
the increase did not include zero, suggesting that the in-
crease in AUC caused by including the GRS is statistically
To further investigate the ability of the GRS to predict
incident CHD in the context of different levels of traditional
risk for CHD, the association of the GRS with risk of CHD
was evaluated within each tertile (e.g., 33.33 percentile) of
the ACRS by a Cox proportional hazards model (table 3).
Within each tertile of the ACRS, the GRS was a statistically
significant predictor of incident CHD in both races (p ?
0.02). Additionally, the interaction between the GRS and
the ACRS was not statistically significant for Whites (p ¼
0.62) or Blacks (p ¼ 0.12), further supporting the idea that
the GRS is predictive of CHD risk across the spectrum of
traditional risk factors.
4 Morrison et al.
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This study introduces the concept of a GRS that aggre-
gates information from multiple genetic variants into a sin-
gle score and indicates that a GRS can improve the ability to
predict incident CHD beyond that afforded by traditional
nongenetic risk factors. For both Blacks and Whites, the
GRS was statistically significantly associated with CHD in-
cidence in the ARIC cohort after adjustment for traditional
risk factors as well as within all tertiles of the ACRS. Sta-
tistically significant risk prediction was further confirmed
for Blacks, where inclusion of the GRS significantly in-
creased the area under the receiver operating characteristic
curves beyond that provided by the conventional risk fac-
tors. For Whites, the increase in the AUC was marginally
statistically significant. Improvement in the prediction of
incident CHD by inclusion of the GRS in the model is on
the magnitude observed for traditional risk factors, such as
total cholesterol levels. Removing total cholesterol from the
ACRS for Whites compared with the ACRS model resulted
in a difference in the AUCs equal to 0.014 (95 percent
confidence interval: 0.009, 0.020).
Several assumptions were made in calculating and inves-
tigating the GRS. First, gene discovery for CHD is an active
in Communities study, United States, 1986–2001
Genetic risk score SNPs,* their genes, and their association with incident coronary heart disease, the Atherosclerosis Risk
Gene symbolGene nameSNP ID*
VAMP8 Vesicle-associated membrane
protein 8
rs1010 2p11.2C (0.42)T (0.58)1.10 1.00, 1.190.04
PALLD Palladin, cytoskeletal-associated
rs7439293 4q32.3A (0.62)G (0.38)1.111.02, 1.21 0.02
KIF6 Kinesin family member 6rs204556p21.2G (0.36)A (0.64)1.09 1.00, 1.190.05
MKI67 Antigen identified by monoclonal
antibody Ki-67
rs1101607610q26.2G (0.17)C (0.83)1.10 0.98, 1.240.09
MYH15 Myosin, heavy polypeptide 15rs39009403q13.13C (0.30)T (0.70)1.18 1.08, 1.29
LOC646377 Similar to pyrin and the Hin
domain family, member 1 alpha
1 isoform
rs22139481q23.1A (0.16)G (0.84)1.12 1.00, 1.250.05
HPS1 Hermansky-Pudlak syndrome 1rs229643610q24.2T (0.92)C (0.08)1.18 1.00, 1.390.05
SNX19 Sorting nexin 19rs229856611q24.3C (0.75)A (0.25)1.12 1.01, 1.240.03
ADAMTS1 ADAM* metallopeptidase with
thrombospondin type 1 motif, 1
rs42878521q21.3G (0.78)C (0.22)1.131.02, 1.26 0.02
ADAMTS1ADAM metallopeptidase with
thrombospondin type 1 motif, 1
rs40200721q21.3 G (0.78)C (0.22)1.15 1.03, 1.280.01
b3 adrenergic receptorrs49948p12C (0.08)T (0.92)1.26 1.12, 1.43
DMXL2 Dmx-like 2 rs1210220315q21.2G (0.45)A (0.55)1.18 1.01, 1.390.04
ZNF132 Zinc finger protein 132rs112295519q13.43C (0.90)T (0.10) 1.45 1.04, 2.030.03
KIF6 Kinesin family member 6rs204556p21.2G (0.79)A (0.21)1.23 0.99, 1.520.06
F2 Coagulation factor II (thrombin)rs1799963 11p11.2A (0.01)G (0.99)3.64 1.50, 8.82
OR2A25 Olfactory receptor, family 2,
subfamily A, member 25
rs29611357q35G (0.32)C (0.68)1.22 1.03, 1.440.02
KRT5 Keratin 5rs89962 12q13.13T (0.07)G (0.93)1.290.97, 1.720.08
CTNNA3Catenin (cadherin-associated
protein), alpha 3
rs1082289110q21.3G (0.31)A (0.69)1.22 1.02, 1.450.03
HAP1Huntingtin-associated protein 1rs4796603 17q21.2A (0.47)T (0.53)1.211.02, 1.43 0.03
GIPR Gastric inhibitory polypeptide
rs1800437 19q13.32G (0.89)C (0.11) 1.38 1.02, 1.870.04
FSTL4 Follistatin-like 4rs37498175q31.1A (0.08)G (0.92)1.280.97, 1.700.08
* SNPs, single nucleotide polymorphisms; ID, identification; HRR, hazard rate ratio; CI, confidence interval; ADAM, a disintegrin and
y SNPs from the list of a priori candidate genes.
Thrombospondin 2rs80896q27G (0.21)T (0.79) 1.26 1.04, 1.510.02
Genetic Risk Score Predicts CHD5
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OKOLONA – The focus of Monday's Martin Luther King Day celebration was service to the community and nation. "Greatness comes from a willingness to serve," said Rev. Dr. Clementine Mays, keynote speaker at this year's celebration. "Sometimes you have to stand up and do it by yourself and sometimes you have to be willing to […]
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