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- Global Voices - http://globalvoicesonline.org -

Station's Rights to Sochi Games Leave Caribbean Viewers in the Dark

Written by Jason Nathu On 8 February 2014 @ 2:02 am | 4 Comments

In Arts & Culture, Barbados, Bermuda, British Virgin Islands, Caribbean, Cayman Islands, Citizen Media, Dominica, Economics & Business, English, Grenada, Jamaica, Law, Media & Journalism, Sport, Trinidad & Tobago, US Virgin Islands, Weblog

Six Caribbean teams are competing [1] in this year's winter Olympics in Sochi, Russia [2]: Bermuda [3]the Cayman Islands [4], Dominica [5], Jamaica [6], the British Virgin Islands [7] and the US Virgin Islands [8]. Naturally, sports fans throughout the region want to watch – but there's a problem. SportsMax [9], a premium subscription-based television station, has been awarded exclusive rights to the 2014 Sochi games in the Caribbean [10]. “Inside The Games [11]” reported on the details:

The deal, announced between the International Olympic Committee (IOC) and  International Media Content Ltd (IMC), the parent company of SportsMax, is applicable for 21 nations and territories ranging from Anguilla to Trinidad and Tobago.

It consists of exclusive English language broadcast rights on all media platforms, with live coverage to be provided on both SportsMax and SportsMax2 for the duration of the Games when they get underway in Sochi.

Columbus Communications [12], owners of the Flow [13]cable network which operates in several Caribbean territories, took to its social media outlets to address the issue [14]:

Flow Fans, please be advised that SportsMax holds the exclusive broadcast rights to the ‘2014 Winter Olympics’ in the Caribbean for the period February 7th to 23rd 2014. Olympic programming will be broadcast mainly on Sportsmax 1 with some content on Sportsmax 2. Consequently, we are legally required to blackout the coverage of the games on all channels including but not limited to NBC & CBC who will be carrying portions of the SOCHI games. During the blackout periods the affected channels will carry a notice to our customers advising of the blackout requirement and directing you to SportsMax.

We understand the inconvenience that this issue poses and are aware and acknowledge that blocked content is disruptive for our viewers, however we MUST comply. Once the broadcast rights to air a program is (sic) purchased we are obligated to block out that program (when requested) as both a legal and regulatory (TATT) obligation. Failing to comply could lead to legal actions against Columbus Communications Trinidad Limited. This arrangement is not unique to Trinidad, all video service providers worldwide will be required to take similar action based on the Network which has purchased the rights in that country.

Irate Jamaicans posted on Flow Jamaica's Facebook page about having to pay to watch their team parading in the opening ceremony and competing in the games. Diego Armando Thomas had this to say [15]

So because i don't have the #SportsMax package on #Flow I am not allowed to watch the #Olympics? This is BULL. You block the channels am paying for? Really!!!

Another viewer, David Valentine, urged Jamaicans to take action by writing [16] to the Jamaican Broadcast Commission [17]:

This is a sheg up situation, taking advantage of the people who no have no options. The blasted Olympics should not be held ransom, by forcing people to pay for some purely subscriber based channel. Imagine if Showtime did have the exclusive rights to the Olympics? Something wrong with this blow wow picture man. Them really corrupted. PEOPLE WRITE TO THE BROADCAST COMMISION!!

Others expressed their disgust on Twitter:

One viewer who subscribed to the SportsMax service was dissatisfied with the coverage of the opening ceremony:

Competitor cable provider Lime [24]has been offering viewers in some of the countries in which it operates, a free trial of SportsMax for the duration of the games:

The issue of broadcast rights for local television stations versus those of the cable company was discussed in this post [27]:

Television programmes generate advertising revenue for broadcasters such as TV6 and CNC3. While customers pay cable providers for premium channels, it should be noted that  the programmes which occupy the schedules on these channels are governed by separate contracts.

While SportsMax is indigenous to the region, it is a pay-per-view service, and some netizens have complained about the failure of free-to-air broadcasters to obtain rights to the games. Yvon Tripper commented on an article in the Bermuda Royal Gazette [28]:

IOC simply gives rights to the highest bidder. Nothing is stopping a Bermuda-based broadcaster from asking the IOC for Bermuda-only rights, and then just using the American and Canadian feeds. If no one in Bermuda pays for broadcast rights for the island's Olympic coverage rights, then there's no point in complaining when someone else does. The IOC would be happy to exclude Bermuda from the Caribbean region if it mean that they got more money — it's all about the Redbirds, baby.

While Trinidad and Tobago is not competing in the games, none of the terrestrial broadcasters have purchased rights to the games, forcing interested viewers to subscribe to SportsMax for live coverage. Annoyed cable subscribers vented their feelings on Twitter:

The Sochi Games [34] run until February 23, 2014.

Article printed from Global Voices: http://globalvoicesonline.org

URL to article: http://globalvoicesonline.org/2014/02/08/stations-rights-to-sochi-games-leaves-caribbean-viewers-in-the-dark/

URLs in this post:

[1] Six Caribbean teams are competing: http://www.sochi2014.com/en/teams

[2] this year's winter Olympics in Sochi, Russia: http://www.sochi2014.com/

[3] Bermuda: http://www.sochi2014.com/en/team-bermuda

[4] the Cayman Islands: http://www.sochi2014.com/en/team-cayman-islands

[5] Dominica: http://www.sochi2014.com/en/team-dominica

[6] Jamaica: http://www.sochi2014.com/en/team-jamaica

[7] the British Virgin Islands: http://www.sochi2014.com/en/team-virgin-isl-b

[8] the US Virgin Islands: http://www.sochi2014.com/en/team-virgin-isl-us

[9] SportsMax: http://www.sportsmax.tv/

[10] has been awarded exclusive rights to the 2014 Sochi games in the Caribbean: http://www.insidethegames.biz/olympics/winter-olympics/2014/1017997-sportsmax-awarded-exclusive-broadcasting-rights-in-caribbean-to-screen-sochi-2014

[11] Inside The Games: http://www.insidethegames.biz/

[12] Columbus Communications: http://www.columbuscommunications.com/

[13] Flow : http://discoverflow.co/

[14] took to its social media outlets to address the issue: https://www.facebook.com/flowtrinidad/posts/824996440860271?stream_ref=10

[15] Diego Armando Thomas had this to say: https://www.facebook.com/FlowJamaica/posts/10151984246038613

[16] David Valentine, urged Jamaicans to take action by writing: https://www.facebook.com/FlowJamaica/posts/10151984191123613

[17] Jamaican Broadcast Commission: http://www.broadcastingcommission.org/

[18] #WinterOlympics: https://twitter.com/search?q=%23WinterOlympics&src=hash

[19] @GoWithFlowJa: https://twitter.com/GoWithFlowJa

[20] #SMH: https://twitter.com/search?q=%23SMH&src=hash

[21] February 7, 2014: https://twitter.com/K_Wil_/statuses/431871867511918592

[22] #SportsMax: https://twitter.com/search?q=%23SportsMax&src=hash

[23] February 7, 2014: https://twitter.com/WhoDatLexy876/statuses/431857710305669120

[24] Lime : http://www.lime.com/en/

[25] pic.twitter.com/h0A1Z7bsWA: http://t.co/h0A1Z7bsWA

[26] February 7, 2014: https://twitter.com/bloodarmstrong/statuses/431910839701213184

[27] this post: http://nathulaw.com/blocked-on-cable/

[28] Yvon Tripper commented on an article in the Bermuda Royal Gazette: http://www.royalgazette.com/article/20140124/SPORT/140129837#

[29] @SportsMax_Carib: https://twitter.com/SportsMax_Carib

[30] @DayVan_TeaMal: https://twitter.com/DayVan_TeaMal

[31] @Flowtt: https://twitter.com/Flowtt

[32] February 6, 2014: https://twitter.com/tech_tt/statuses/431436138730254336

[33] February 7, 2014: https://twitter.com/Markanthonysilv/statuses/431821145613295616

[34] The Sochi Games: http://www.sochi2014.com/en

[35] thumbnail image used in this post: http://www.flickr.com/photos/dv0rsky/4152343471/in/photostream/

[36] an Attribution-NonCommercial-ShareAlike 2.0 Generic Creative Commons license: http://creativecommons.org/licenses/by-nc-sa/2.0/

[37] Giga Paitchadze's flickr photostream: http://www.flickr.com/photos/dv0rsky/

This site is licensed as Creative Commons Attribution 3.0. Please read our attribution policy: http://globalvoicesonline.org/about/global-voices-attribution-policy


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Friday, May 14, 2010

Beck: Cranking up the Crazy...

...and breaking off the dial.

Via Colbert Report:

Colbert pretty well sums it up here. Previous post's on Beck's modern twist of yellow journalism here. My first post on Glenn Beck was over his Comrade Update skit, which if you missed it a year ago, you can see the signs were all there:

Youtube clip of the fox news response as soon as Obama got done signing the schip bill:

They're not even trying anymore. Criminey.

This guy is out of his freaking mind.

Clinton Rushing said...

He's just a showman ffs.

geewits said...

Ick. Just thinking about Fox "News" actually made me shudder and gave me chill bumps on my arms. I'm serious.

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Gluten Free Food Reviews

Honest reviews of gluten free products for a tastier life

We have a winner for the July give-away!

Posted on | July 19, 2009 | No Comments

(I used random. org to determine this month’s winner.)
Congratulations to our July winner of the Betty Crocker prize pack! Our winner is . . .
LANA with the comment:

lana Jul 9

I left a reply yesterday but it seems to have disappeared! I like Pamela’s brownie mix, makes for an awesome brownie sundae!

You have until July 30th to email me your shipping address via the email glutenfreefoodreviews (at) gmail [dot] com. If I do not hear from you, a new winner will be announced.

Bummed you didn’t win? Check back on August 1st for a fantastic give-away that you will enjoy all year long ( that’s a hint hehe)

In the meantime, feel free to peruse my other gluten free bownie mix reviews and gluten free cake reviews!

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Featured Products

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Article: Gluten Free Market Trends

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Senza Glutine In The News

Published in the November 2014 Celiac Support Magazine!

Senza Glutine In The News!


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November 28, 2007

Filed under: — Chap @ 11:18 am

A coupla blogging Campbells might like this vignette.

November 25, 2007

Spot The Trendlines

Filed under: — Chap @ 9:42 pm

Via Hot Air’s news feed, indication that China may have been militarily effective in Darfur.

Filed under: — Chap @ 8:13 pm

I couldn’t write a short story with a tool like this in it because people would think he was too stereotyped.

Update: Whacked by Victor Davis Hanson.

Filed under: — Chap @ 12:41 pm

Now this is period artwork goodness, available for your home walls.
(Curated by Barry)

Filed under: — Chap @ 6:59 am

Seems to me if you’re writing a newspaper article, and want to get something across, then doing it the way the LAT attempted here ain’t it.

Lecturing the Pope on Catholic practices, doctrine, or dogma is insane enough, but for the editorial board of the LA Times to presume to tell Benedict it would be “wiser” to listen to “other Catholics” than “hard-liners” to avoid “mischief” is certifiable.

AP Pounds The Table

Filed under: — Chap @ 6:37 am

The local leftish radio station has been saying that guys like Scott Beauchamp and Bilal Hussein and Green Helmet Guy et al get attention because of the right. I think they forget that the military folks as an interest group (unfortunately so) respond because the issues are closer to them. That’s also why the PR defense for this kind of kerfuffle works in NYC but not in Fort Obscuro.

Innocent until proven guilty is a criminal case touchstone. Unfortunately for the AP’s Bilal Hussein, he was picked up in war, and not by cops. The recent announcement that the Iraq government will try charges against Hussein has AP blustering loudly without explaining what Hussein was doing with those guys he was photographing so closely. Funnily enough, the AP honcho who wrote an op-ed for the Washington Post not only got the op-ed printed, but apparently was newsworthy enough for CNN to write about the op-ed!

Bruised Orange has a five dollah challenge for one of the AP responses.

Especially worrisome is the note buried in the link the Orange refers to from the Associated Press’ lawyer for Bilal Hussein, where the lawyer says interviews were done with a brother of Hussein who works as a satellite tech for a news agency. Who else in the Hussein family is tangled up in this mess? Maybe the brother currently evading American and Iraqi military as a wanted AIF fighter?

And as Insta alludes, do we have a family of guys like this we’re talking about?

So I guess Hussein will have a day in court. Prepare for a bumpy ride.

Update: Confederate Yankee points out the thing that got many people wondering about Hussein–why would a reporter be in custody for a month and not say who he is? Also, Shackleford has a barrel with dead fish and a hole from a shotgun slug.

Filed under: — Chap @ 5:36 am

And to fill in some background is some ouch ouch ouch from Small Wars Journal about retired LGEN Sanchez.

Filed under: — Chap @ 5:33 am

This is a very interesting analysis of Iraq’s changing situation that matches descriptions of how the world works that I got from Iraqis and a few other places. My gut tends to agree with the “it’s still touch and go but we’ve got a shot” comments.

Filed under: — Chap @ 5:23 am
(via b3ta)

Snark Of The Day

Filed under: — Chap @ 5:11 am

How’d this show up in the Columbia Current?

I think of it when I walk down 116th & Broadway, and see all that ivy concealing all that rot.

Now that I think of it, a European I met at one of them fancy universities highly recommended Walt and Mearsheimer’s latest book…arrrgh.

Splodeydope Tells His Tale…And He Didn’t Like It Much

Filed under: — Chap @ 4:51 am

Also via John Burgess, an article that is best read while thinking of the newspaper’s target audience–it makes more sense that way.

Al-Shaie says he does not know the fate of his friend, who brought him to Iraq. He believes he may have died fighting. â€œThe conditions in Iraq are very difficult… We were brainwashed and were used by these people,â€ he said.

â€œMost Saudis in Iraq have gone because of fatwas permitting them to fight. However, we all know that the Kingdomâ€™s Higher Scholar Committee has not approved these decrees. Many young Saudis that went to Iraq have been influenced by what they see on websites and hear in cassettes,â€ he said.

â€œThe Iraqis are not happy with foreigners fighting in Iraq. They think weâ€™re interfering in their internal business,â€ he said. â€œI advise young Saudis not to go to Iraq.â€

Huh. How about that.

Filed under: — Chap @ 4:25 am

Geez. No sooner do I get a job that keeps me too busy to read than I find a new required reading list.

November 24, 2007

Filed under: — Chap @ 5:09 pm

Gerard Vanderleun has the ultimate Christmas gift for you. However, it’s not on this list.

November 22, 2007

Why I Scare People When They Ask Me What I Think The Future Is Like

Filed under: — Chap @ 8:19 am

Well, in the “happy future space”: making brains work on other stuff directly, Van Eck phreaking brain waves, memory, not to mention this week’s stem cell hooh hah, nanotech, etc….

Filed under: — Chap @ 8:18 am

John Stossel reflects on the capitalist nature of Thanksgiving. (Stossel’s in favor of both.)

Now That’s Good Parenting

Filed under: — Chap @ 8:18 am

Congratulations to Carl Brown, Sr. and his wife for raising a kid who can save a life in third grade.

Filed under: — Chap @ 8:17 am

I think I found the cover art for the Lost Led Zeppelin Album.

Filed under: — Chap @ 8:17 am

Dave Kopel’s excellent summary of the Knights Templar issue that popped up the other week is a useful reminder in terms of geopolitics.

To oversummarize: I have always rejected the “you Americans are arrogant and should do what we want instead” complaint, knowing there’s always a grain of truth in it somewhere; the Knights Templar shows the danger of falling off the tiger of primacy in power. That’s the challenge of being strong–the choices seem to be stay strong, disappear, get stomped by those you once protected, or somehow become beloved while weakening.

November 17, 2007

Dear Diary And All That

Filed under: — Chap @ 5:57 am

Hi there.

Long time no see.

Twenty uncompleted posts in the queue, all started over a month ago. Or maybe two months; the days have been running together. Haven’t been on line, save for a mail check at a break or the occasional quick scan, for about that long. I’ve got this set of notes here on the desk with the outline for a proposal I’ve yet to complete; should have done it a long time ago, it isn’t happening until at least Thanksgiving if I catch up on sleep. Typing hurts, whine moan complain. (I injured my wrist–no idea how, but the time online at the previous job and a nasty habit of carrying on volleyball spikes and a move and a new kid might have something to do with it. I think I have four different attention-grabbing gadgets for my arm at the moment from which to choose, most of which are broken in one way or another.) Not difficulty like it did for Chuck Ziegenfuss, mind you, and that’s a story worth considering right now, but a guy can whine.

On the other hand, the family’s doing okay, the kids remember who I am, and the bills are getting paid. The job’s getting done.

You know. The important things.

I guess this is a transition period of sorts for the old blog neighborhood I used to know. Many blogs lately went dark. Rantingprofs is gone–I know where she went, but she’s not coming back for a while. Nobody has a public idea where Smash went off to; he just up and left. Baldilocks shut down, but still lurks a few places and might appear occasionally at Milblogs. Gut Rumblings’ proprietor is no more. Geez, lots are gone–Prakash, 2Slick, Vadergrrl, Hubris, the group bloggers at Stryker’s, you name it.

Lex scared y’all the other week before he realized he was bitten by the writing bug too much to just go cold turkey. (Heh, I says; he threatens to leave for a weekend and gets a hunnert something farewell eulogies. Popular guy.) Sailors are used to close friends disappearing; the ship is the people inside it, after all, and when you leave the ship you can never ever go back the way it was. The advantage of the job is that you make close friends quickly; the disadvantage is that you keep saying goodbye to them. I am not leaving, but neither am I going to be of much use to anybody here on line checking hourly. I’ll pop in when I can–and if the other gig’s editor tells me she likes the columns I’ll do a few more. If I get asked by someone worth following to write something appropriate, then I’ll wait to get to a break period and crank something out, and when the time appears I’ll drop a note at Milblogs.

A few short notes of what I’m seeing here in the situation my old boss called “a fine and pleasant misery”:

  • If I were in a midlife crisis, this would be a good way to do it: new family, new career field, hanging out with people younger than some of my T-shirts. I’m unconnected from the friendships and information pipeline I’ve been associated with since 2001 and instead am inundated with a completely different subject. It’s a bit unnerving being so dissociated with the info flows of the rest of the military, but that’s okay. I’ve got work to do. I am back on the merry-go-round and grabbing for a brass ring again. One gets few chances like that in life.
  • And the youngsters? They may be young, and uninformed of some of the details of why we fight. But they get it. They get it just fine and have a clear sight picture of what’s downrange and why they’re there.
  • Guy I’m serving with here was in Iraq. He was there back before Petraeus &co., back when things were more rough. I had to print out current reports from our embedded samizdat reporters (Yon, Roggio, et cet) in the area he was in to show him the enormity of the change he had helped effect. It’s 180.
  • Quote (sort of) from someone else that explains the war change in a nutshell: “We were getting mortared every night; this was while General Casey was still there. One night, after getting shot at we heard this sound I’d never heard before. We all looked around, a little worried, and the artillery guy with us had this huge grin. “That’s outgoing ordnance, folks!”
  • Many, many interesting stories here. I’m awash in first termers but also guys who are on their way back out to the field; fascinating stuff.
  • Dedicated folks, some not even American, helping me get smarter on my new chosen field.
  • Guys, younger than my T-shirts, listening to a fellow teach us who casually mentions what it was like in a Saddamite prison. Not pretty, frankly.
  • Learning about the nukes and SEALs who rocked out of this place. It’s a different skill set, I guess, doing this job. I saw a 50% failure rate in another part of this circus and will act to avoid becoming that kind of statistic. Luckily I hit the ground running as fast as possible, but this job is for very young men and women and substituting effort for skill doesn’t work here like it did in nuke school back in the day.
  • Unrelated to the dear diary moment, but worth mentioning: I took heat from an unhinged stalker type who took umbrage at my agreeing with the New Republic’s Peter Beinart that we needed every American political party to understand and maintain cultural and intellectual institutions that perpetuate an understanding of the use of national force. Turns out that Senator Clinton must understand this, as she hired Michael O’Hanlon; so does Senator Lieberman, whose speech was pretty devastating.
  • The new Defense Department instruction is going to be a challenge to meet for Navy folks, who don’t do in country training or have a fully stood up community. My buddies working this have their work cut out for them in the Puzzle Palace.
  • I am very glad that I picked the Navy and haven’t been in boot camp for decades. I had forgotten how much quality-of-life suck is inherent to being such a junior pup in the world, and it only gets worse in some of the other services. It’s bad enough that more seem to be entering the service with more credit card debt than when I last looked at E-1-E3 financial health. I remember concrete drying watch (some clown put his initials in wet concrete on base in the ’80s and therefore our unit, not containing said miscreant, had four guys posted at each concrete square, literally assigned to watch concrete dry). Most depressing comment, from smart sergeant to married guy with a kid on the way, was to sign up for WIC right quick. I know there is income mobility in service life and salaries go up in a year or two for the average junior enlisted; I know it isn’t a great idea to be an E-1 with six kids and maxed out credit cards; but perhaps the salary of a guy about to get shot at, working 12 hr days plus en route to same, and married with one kid shouldn’t require a good leader of soldiers recommending resorting to WIC.
  • So. Back to work for me. I’ll write when I can and lurk when I get on line.

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GMAT Story 770

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GMAT Story 770 [#permalink] New post 16 Sep 2005, 09:14
Thank you all for the wonderful posts. They helped me along, especially towards the end of my studying. I received 770 on GMAT, although I hadn't expected anything higer than 720. I just wanted to share my experience.

First, the test itself was really difficult. There were 2 quant questions I have never even seen. I ended up guessing both. My advice is:arrive early, and if you are not a US citizen in America, have your green card or passport with you. There was an asian girl who got sent home right in front of me because all she had was a driver's license. The people at the test center are increadibly rude! They wouldn't give me scratch paper until the exam started. So, with the clock ticking on the essay, I still had to go get the scratch paper! Second, the scratch paper they give you might not be enough, and they won't provide more. So, during each break I made them exchange my scratch paper for a new set. I still ran out in quant, but it didn't really hurt. I was on question 36 then.

I actually was sure that I'd get 600 or less on the exam. It really kicked my a. By the time I got to question 10 on verbal, I could barely concentrate and had to pause constantly. I cannot stress this enough: buy something like a Kaplan CD with CATs and do those religiously! There is no better way to build endurance.

Now, here's how I prepped. I started slow about half a year ago with an old Arco book (2000 edition). These books rarely change. So, you can easily pick up a 94-96 book in the library and the questions will be the same as in a 2003 edition. It took me 3 months do finish the whole book.

I then began studying every day before and after work. I made a schedule and followed it. I tried to focus on one thing every day, and did not disregard anything, even the things I considered my strengths. This is what I ended up using:

Kaplan CD - it's great for practice and test taking tips. The theory is weak. I had to go back to Arco a lot for additional information on math. The tests are really hard. I got 620 on average, with 580 as the low score.

Barrons - this is one useless book. I only did a few tests. Math is decent, but verbal sections are antiquated. Only use it if you don't have anything better and need additional practice.

Powerprep - the free software is available from There are 2 full CATs and a bunch of small topical tests. I highly recommend this one. I took one CAT first (710). Then took all the quizzes, then the second CAT (770). This program is a must! First, it accurately represents GMAT, second, after Kaplan's scores, it will build your confidence.

Online - there are a lot of decent sites with practice tests, reviews and sample CATs. I went through all of them at work.

ETS Official Guide to GMAT. Now this one is interesting. You can't buy it in a bookstore. You can locate a used copy or a 2003 edition online, but by the time I read all the raving reviews on this site, I had one and a half week to go. This book proved to be a solid practice, but in retrospect not nearly as useful as I thought it would be. About half of all the questions in the book are from Powerprep. What I did the last week was take-on one chapter per evening. Friday night was the problem solving night. 250 questions took me about 5 hours.

Essays - as soon as I realized the essays in Kaplan and other materials are BS and there is a list of real essay topics at, I switched to writing as many of those real essays as I could. Also, make sure you read a couple of solid books dedicated to essay writing on GMAT. Every B&N has a couple. Read as many sample essays as you can. I would've completely failed AWA had I not read the sample essays. All in all, I probably wrote 20-30 essays of each type.

Finally, take notes of things you have trouble remembering. Review those notes every day, especially the last week before the exam. The most important advice: don't overstudy! Take breaks once in a while. I was forced to take 4 days off in the middle of training. That really helped. I also took 3 days off right before the test. I took the test at 1 pm on a Tuesday, and did not go to work that day. Sleep in, relax, and focus.

Good luck and thank you for reading!
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 [#permalink] New post 16 Sep 2005, 19:58
Kiev, that's an awesome score
Way to go man

I Blog at:-

  [#permalink] 16 Sep 2005, 19:58
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TOEFL 95 in a week

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Author Message
Current Student
Joined: 15 Nov 2009
Posts: 124
Concentration: Finance
GMAT 1: 680 Q48 V35
GMAT 2: 700 Q48 V37
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TOEFL 95 in a week [#permalink] New post 15 Dec 2012, 12:45
Just received my score and I am a bit frustrated. Not for the score, but to have an "almost there".

I did not have much time, either. I was not focused on studying it, because I thought: "I need to have a decent GMAT first. Before that, my dreams of MBA are unrealistic". Then I managed to score a 680 after 5 attempts from 480 to 560.
But as many of you may know, the R2 deadlines are about to come, and I don't have much time left. Then, I scheduled a TOEFL test for the following week.
It was a crazy week: getting back from vacations, several layoff in my work, writing essays,... phew!

Nonetheless, I scored:
Reading: 22
Listening: 22
Speaking: 24
Writing: 27

Total: 95

I did expect "low" scores in reading, listening and speaking. In reading, I read a too boring passage and could not manage to understand it well. In listening I had too many sections, probably because I did experimental questions. I know that because I was the last to leave the testing center, and I had read only 3 passages in the previous section.
I got tired and out of fuel, and because of that, I almost missed an entire listening talk.

In speaking, for me the most difficult part, I got a bit confused about how to answer to the questions. It's awkward to talk to a computer... lol!

To my surprise, I had a decent score in writing.

Well, I took another test yesterday and I am expecting the results... I'll keep you guys posted.
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Re: TOEFL 95 in a week [#permalink] New post 18 Dec 2012, 03:29
ok..gud luck!

not bad score.!!

gud luck for next one!

Bole So Nehal.. Sat Siri Akal.. Waheguru ji help me to get 700+ score !

Re: TOEFL 95 in a week   [#permalink] 18 Dec 2012, 03:29
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Welcome to Shell Beach

Hold onto your sanity, because Dark City is the Greatest Movie EVER!

Click on the Bluray cover or the title above to download our review of the film, featuring guest hosts

Daryl Surat of AnimeWorldOrder and Mike Toole of Anime News Network.

Review in a Nutshell: Few works of cinematic speculative fiction deserve the word ‘visionary’ to describe their aesthetic. Dark City is one such film, although Paul deducts a few points for the bombastic nature of the movie’s conclusion.

This movie contains:

Click the pic for MIND LASERS.

17 Responses

  1. Daryl Surat on a non-action movie podcast, you just blew my mind!

    Anyway, I don’t have much to say except that I love this movie. However, I’m surprised no one metioned the creepy-ass kid alien/tuner, that kid creeps me out.

    P.S This movie used to be on Netflix streaming (in Canada ayway) so it may come back for you cheapos out there

    P.S. II Rufus Sewell was very good in the Pillars of the Earth miniseries. Buy it and support the Canadian/German film industry (that makes movies about English history)

  2. Spoilers:
    What I find interesting about the film is that there is a possibility that the city dwellers do not know anything about Earth. How can they get to Earth if they do not know anything about it?

    Furthermore, the protagonist effectively becomes God at the end of the film. Will he tell the whole truth the city dwellers, or will he continue to let them live in their allegory of the cave/ Matrix predicament

    I also see some similarities with the anime, The Big O, which is also good.

  3. I like Mike’s mention of Disney’s 3 Musketeers movie, I love that flick! Me and my Dad used to watch it all the time.

  4. Don’t think I’ve seen the Director’s Cut of DARK CITY – OTOH, I remember liking the saw quite a bit…even if it was directed by the guy responsible for Brandon Lee’s death….

  5. To Daryl’s point about Director’s Cut versus Theater Cut: To reference “The Matrix” again, imagine if Morpheus’s infodump speech from the middle of the movie had instead been put as a voiceover right at the beginning.

  6. I think it’s a little harsh to say Alex Proyas was responsible for Brandon Lee’s death. If you really wanted to make him feel bad, all you need to say is: “Everything you made after Dark City, and by some accounts, before.”

  7. Jung-Ho – I don’t think it is, actually. Proyas is the one who sent the Armorer home (or let the Producer do it) to save a few bucks in the budget when he knew he had a scene using live weapons scheduled. As somebody who’s worked on low low budget movies, we were usually really careful to make sure the Armorer and Fight Choreographer stayed on-set if there was any chance we’d get to a gun or fight scene.

    I’m amazed he didn’t get tried for Negligent Homicide under the circumstances. I’m sure Proyas feels guilty as Hell about it now – but that isn’t bringing Brandon Lee back, is it…?

  8. Interesting. I didn’t know that. That’s my knee-jerk to jump to the defense of Mr. Proyas, who once said that he makes movies so infequently because he’s waiting for just the right script. (No kidding)

  9. Speaking of Rocky Horror, De Palma’s Phantom of the Paradise would make a great Greatest Movie Ever film.

  10. PHANTOM…. would probably make a better Greatest Movie Ever than ROCKY HORROR, which has been done pretty much to death – especially by nonfans. I was a huge ROCKY HORROR fan in college and it still holds a warm spot in my heart, but I’ve read too many articles and blog posts, and heard too many podcasts, done by people who don’t get why it’s such a huge cult hit and think it’s really stupid.

    PHANTOM…. is a brilliant, subversive and not very well known music business satire/horror fantasy done with real verve by Brian DePalma. I think Paul and co-host could get into a smart discussion of it because there wouldn’t be the cultural phenomenon that they’re not a part of to set their teeth on edge….

  11. Just listening to the podcast right now, and I hear that my wife has never seen Dark City AND I DIDN’T KNOW THIS?!? Paul, my marriage is falling apart :(

  12. And…. having listened to this entire podcast, despite your having Surat as one of your co-host? I really think you shouldn’t do ROCKY HORROR, Paul – it’s not your kind of movie, and I don’t think your disinterest would yield any fresh insights.

  13. Thomas – it’s an easy fix, b/c the BluRay’s $9.02 on Amazon.

    Paul – Rufus Sewell starred in the US version of the television series THE 11TH HOUR, played the title character in the BBC mystery series ZEN, and was the insane Hapsburg prince in THE ILLUSIONIST. He’s been around….

  14. “Daryl Surat on a non-action movie podcast, you just blew my mind!” — I was last on here reviewing The FP which is not an action movie, thanks for the vote of confidence

    “having listened to this entire podcast, despite your having Surat as one of your co-host” — jeez, I say one time that I don’t care about the entire fantasy genre and I’m branded anathema

  15. AND insulted my wife in the process, so your dittoheads would pile on in lockstep, Surat!

    I’ve demanded an apology for that which you’re too arrogant to give – Tammy’s of the opinion that you’re Just Not Worth The Trouble, but to me it’s the principle of the thing….

  16. timeliebe: Hold on a second! All I remember insulting was the cover art to a book I never heard of in which the person illustrated appeared to look more like a Best Buy employee than a fantasy hero, to which you said “we have no say over the cover art to the book” at which point it was revealed “oh okay, you guys wrote this book.” This is my mind means that I’m not insulting either of you, but whoever the artist was. Like my role model Norman Osborn, I’m not going to apologize for thinking that cover was goofy because I believed that sincerely.

    However, anything else other than that I don’t remember, so I’ll apologize for whatever those were. If this is “not good enough” or “too arrogant” or “not worth the trouble,” you’re going to have to spell things out for precisely what you’re looking for because I only need vocally speak when recording podcasts on account that I only physically see other people a few times a year, for a few hours each time. All of my other interactions are conducted just like this: text between boxes.

  17. @Surat – thank you for that.

    As for the cover art – well, yes, that’s been a long-standing bone of contention between Tammy and some of her publishers, who end up chasing current trends rather than being true to what the story itself is about. Few writers have the power to actually dictate what cover art looks like – “giving an author input on covers” means they send the author a rough, and when s/he points out that it’s not true to the story or the characters don’t look a thing like that the editor says “Oh, but our Market Research tells us these covers will make your book sell huge!” – and then they blame the author when the books with those covers tank.

    One of the best things about eBook self-publication is that an author has a lot more control over his/her cover art – of course, the author also has to secure that art somehow, which can be a pain. I shudder to think of what cover art a publisher like Simon & Schuster or HarperCollins would have given Paul for his collections PORN GNOMES or SAQSQUATCH RIDES A HARLEY….

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text:
22 Carly Wade
22 Carly Wade
Height: 5-10
Year: Freshman
Hometown: Placentia, CA
High School: Mater Dei HS
Position: P

Wade appeared in 38 games and made 20 starts for the Matadors in 2011 ... finished the year 7-15 with a 4.97 ERA, seven complete games, one shutout and three saves ... added 66 strikeouts and 101 walks in 136.2 innings of work ... numbers improved to 4-3 with a 2.70 ERA, three complete games, one shutout and a save in Big West season ... earned first career victory in win over Nevada by tossing 4.2 innings of one-run relief work ... nailed down first career save in CSUN's win over Portland State on Feb. 12 by recording the final two outs in a one-run game ... also posted victories over North Dakota and Ohio State ... tossed a complete game in Matadors' victory over Long Beach State on April 8 ... picked up both wins in a CSUN doubleheader sweep over UC Riverside on May 7 ... tossed first career shutout in Matadors' victory over Cal State Fullerton in game two of a doubleheader on May 13 ... picked up a save in Matadors' victory over Cal State Fullerton on May 14 ... the three saves already ties her for 10th in school history for a career and ranks seventh in school history for a single season.

Mater Dei High School

Wade played four years of Softball for the Monarchs ... earned all-league honors and helped team to two league championships ... graduated in 2010.

Born on August 20, 1992 ... daughter of Ann and John Wade ... has one brother, Ryan ... favorites include the Chicago Bears, Brian Urlacher and "Toy Story" ... most famous person she's ever met is Mike Ditka ... best advice she has been given is "everything happens for a reason" ... undecided on a major.

Text-Only Website


text:
FAQ Updates

Friday, 1st July 2005 by

Just a quick heads up to let you know that I’ve updated the FAQ page. You can now learn how to find the moved ‘satellite’ link, use the “z” variable to set a specific zoom level, and also how to search for a specific latitude and longitude.

Any suggestions or corrections, please leave in the comments thread of this post, thanks!


text:
Send your tips to gostips@gmail.com.

September 15, 2006

Remove Google's Top Ads

Here's a cool Google experiment found via Search Engine Roundtable. You know the ads that appear on top of the search results for competitive queries? Well, Google decided that they should remove them if users don't click on the ads.

So here's what you should do to move those ads in the right column: search for something that triggers the blue ads (for example loan) and refresh the page until they disappear. That's it.

"The rationale is that the user does not want to see the ads anyway and it lessens the chance of a poor prospect clicking on an ad. If you clear your cookies, the results will go back to normal."

This blog is not affiliated with Google.


text:
DIET, DNA METHYLATION AND OTHER EPIGENETIC EVENTS, AND CANCER PREVENTION RELEASE DATE: September 27, 2002 RFA: CA-03-016 National Cancer Institute (NCI) ( The Office of Dietary Supplements (ODS) ( LETTER OF INTENT RECEIPT DATE: February 18, 2003 APPLICATION RECEIPT DATE: March 18, 2003 THIS RFA CONTAINS THE FOLLOWING INFORMATION o Purpose of this RFA o Research Objectives o Mechanism of Support o Funds Available o Eligible Institutions o Individuals Eligible to Become Principal Investigators o Where to Send Inquiries o Letter of Intent o Submitting an Application o Peer Review Process o Review Criteria o Receipt and Review Schedule o Award Criteria o Required Federal Citations PURPOSE The NCI and the ODS invite applications for new R01 and R21 grants which are focused on research leading to the elucidation of mechanism(s) by which dietary factors influence epigenetic processes as well as increasing the understanding of these processes in cancer prevention. The approach is to encourage collaboration between nutrition and epigenetic /DNA methylation experts to study bioactive food components with cancer preventative properties, and to examine key epigenetic events in cancer processes (i.e., carcinogen metabolism, cell division, differentiation, apoptosis) so that investigators can begin to establish linkages between epigenetics, methylation pattern, and tumor incidence/behavior. It is anticipated that the information gained will provide guidance for the development of dietary intervention strategies for cancer prevention. In addition to the present announcement, the NCI and the ODS announce a related initiative about diet, DNA methylation and other epigenetic events, and cancer prevention utilizing an additional funding mechanism: Competing Supplements for existing NCI awardees ( which can extend the goals of active grants to include studies related to the impact of diet and nutrition on epigenetic events. Contact individuals listed under "INQUIRIES" of this RFA for further information. RESEARCH OBJECTIVES Background Cancer is a manifestation of both abnormal genetic and epigenetic events. The importance of epigenetic events is that it represents a mechanism by which gene function is selectively activated or inactivated. Actually DNA methylation is the covalent addition of a methyl group to the 5 position of cytosine within CpG dinucleotides and is a fundamental process that not only modulates gene expression, but is also key to regulating chromosomal stability. A variety of regulatory proteins including DNA methyltransferases, methyl-CpG binding proteins, histone- modifying enzymes, chromatin remodeling factors, and their multimolecular complexes are involved in the overall epigenetic process. Since epigenetic events are susceptible to change they represent excellent targets to explain how environmental factors, including diet, may modify cancer risk and tumor behavior. Abnormal DNA methylation patterns are a hallmark of most cancers, including those of high proportion in the United States i.e., colon, lung, prostate, and breast cancer. Preclinical and clinical studies provide intriguing evidence that part of the anticancer properties attributed to several bioactive food components, encompassing both essential and non-essential nutrients, may relate to DNA methylation patterns. There are four ways in which nutrients may be interrelated with DNA methylation. The first is that nutrients may influence the supply of methyl groups for the formation of S-adenosylmethionine (SAM). The second mechanism is that nutrients may modify utilization of methyl groups by processes including shifts in DNA methyltransferase activity. A third plausible mechanism may relate to DNA demethylation activity. Finally, the DNA methylation patterns may influence the response to a nutrient. These interactions are described in greater detail below. Global DNA Methylation Patterns Global hypomethylation, accompanied by region-specific hypermethylation, is a common characteristic among tumor cells. Global genomic hypomethylation has been linked to the induction of chromosomal instability. Hypermethylation is associated with the inactivation of virtually all pathways involved with the cancer process, including DNA repair (e.g., hMLH1, BRCA1, MGMT), cell cycle regulation (e.g., p16(INK4a), PTEN), inflammatory/stress response (e.g., COX- 2) and apoptosis (e.g., DAPK, APAF-1). Thus, evidence exists that variations in the degree or site of DNA methylation can lead to abnormal DNA repair and influence multiple cancer related genes and thereby influence the incidence and behavior of tumors. Stress including that resulting from dietary methionine/choline, folate, zinc, and selenium inadequacy, as well as excessive alcohol intake can lead to global DNA hypomethylation. Interestingly, the continuous feeding of a diet deficient in choline and methionine is recognized to lead to global DNA hypomethylation and cause hepatocellular carcinomas in rats in the absence of any exogenous carcinogen. Paradoxically, either deficient or excess dietary arsenic has also been shown to lead to global hypomethylation in rat liver. Treatment with excess retinoic acid can also lead to hypomethylation as recently shown in rat liver. Clinically, global DNA hypomethylation has been observed in lymphocytic DNA from individuals consuming inadequate folate. While limitations in the supply of methyl groups appear to be a common mechanism, available data suggest that other factors determining DNA methylation, including DNA methyltransferase (Dnmt), may be influenced by bioactive food components. Availability and Utilization of Methyl Groups SAM and S-adenosylhomocysteine (SAH), as components of methyl metabolism, are the substrate and product of essential cellular methyltransferase reactions. SAM is derived from an ATP-dependent transfer of adenosine to methionine via methionine adenosyltransferase and serves as the proximal methyl donor for most methylation reactions. Cellular methyl acceptors include phospholipids, proteins, histones, neurotransmitters, RNA and DNA. The formation of SAM requires a continuous supply of folate, methionine, choline, vitamin B12, vitamin B6, vitamin B2 and energy from the extracellular milieu. Polymorphisms in the methyl metabolism genes methionine synthase, methylenetetrahydrofolate reductase (MTHFR), and cystathione beta-synthetase affect concentrations of SAM and likely modify the susceptibility to cancer. Investigators are currently exploring the interaction between these polymorphisms, diet and DNA methylation. For example, subjects homozygous for the C677T polymorphism in the MTHFR gene exhibited a significantly lower level of methylated DNA but only under conditions of low folate status. The Dnmts are a family of enzymes that catalyze the transfer of methyl groups from SAM to cytosine residues in DNA. This produces 5-methylcytosine and SAH. Higher DNA methyltransferase activity has been observed in tumor cells compared to normal cells. Chronic dietary methyl deficiency also increases DNA methyltransferase activity, which may be an attempt to compensate for diminished SAM supply. Nutrient supply, therefore, appears to play a key role in regulating DNA methyltransferase activity. Selenium is a dietary trace element that is recognized as having potential anticancer properties. Interest in selenium as a prostate cancer preventative nutrient is showcased by the recent initiation of the SELECT trial by NCI ( While selenium is known to modify several aspects of the cancer process, the one that is most critical for bringing about a phenotypic change remains to be established. Interestingly, increased selenium concentrations have been found to inhibit Dnmt1 activity in vitro and decrease Dnmt1 protein expression in vitro. Consistent with these data, selenium deficiency leads to increased Dnmt1 protein expression in vitro. The effects of selenium on Dnmt activity suggest that dietary factors influencing methyl utilization may also modify DNA methylation patterns. Although the enzymes for direct methylation of DNA are well characterized, the demethylation process has been assumed to be a passive process. A mammalian gene that codes for a protein that can catalyze demethylation recently has been described, however other attempts have yielded variable results. Demethylation activity has been hypothesized to be higher in non-neoplastic compared to neoplastic cells. Loss of demethylation activity may account for some of the differences in methylation patterns between neoplastic and normal tissue. The role, if any, of bioactive food components in regulating the demethylation process remains to be established. Gene-Specific DNA Methylation Patterns Fluctuations in the degree of CpG island methylation are key to regulating functional promoters by modifying the binding of transcription factors and methyl-DNA binding proteins. Aberrant methylation of CpG islands on the promoter region may contribute to the progressive inactivation of growth- inhibitory genes resulting in the clonal selection of cells with growth advantage during cancer development. While methyl-deficiency leads to global DNA hypomethylation, it also simultaneously leads to gene-specific hypomethylation and hypermethylation. Preclinical studies reveal that consumption of a methyl deficient diet leads to hypomethylation of specific CpG sites within several genes including c-myc, c-fos and c-H-ras. This hypomethylation was accompanied by elevated levels of mRNA for these same genes. Folate depletion was shown to produce gene- specific, rather than global DNA hypomethylation in human nasopharyngeal carcinoma KB cells. Interestingly, these investigators also reported that folate depletion led to hypermethylation of a 5" sequence of the H-cadherin gene, which accompanied diminished mRNA expression. These data suggest that global DNA hypomethylation may incompletely predict the response to an individual dietary component. More probing studies are needed to characterize gene-specific changes brought about by bioactive food components. Epigenetic events occurring in utero can lead to persistent changes in gene expression and can be modified by the diet. For example, the diet provided to female mice of two strains during pregnancy modified the offsprings" hair coat color (increased agouti vs yellow) and DNA methylation patterns. Expression of the yellow hair color in these mice is recognized to be controlled by hypomethylation of the agouti long terminal repeat (LTR), which was hypermethylated by dietary supplementation of the maternal diet with zinc, methionine, betaine, choline, folate and vitamin B12. Expression of this yellow coat color is linked with increased risk of obesity, diabetes, and cancer. While long-term health implications remain to be determined, these studies demonstrate that feeding a methyl-supplemented diet increased levels of DNA methylation in the agouti LTR and increased the proportion of agouti to yellow mice. It should be noted that this effect occurred with control diets that are considered adequate for meeting nutritional needs. These data point to the likelihood that in utero nutrient exposures can lead to genomic imprinting in the offspring and potentially modify cancer risk. Invariably, increased fruit and vegetable consumption is associated with reduction in cancer risk. Evidence from a variety of sources suggests that flavonoids, including genistein may have merit as an effective deterrent of cancer. Dietary genistein has been shown to lead to changes in DNA methylation patterns in prostate tissue of C57BL/6J mice. After sequencing, it was determined that genistein consumption led to hypermethylation at 4 specific CpG islands, including a dexamethasone-induced product gene (D44443). Neonatal exposure to the phytoestrogens coumestrol and equol has been found to lead to specific gene hypermethylation in the c-H-ras proto-oncogene in pancreatic DNA. Data indicating that consumption of high fiber diets is accompanied by a reduction in estrogen receptor methylation in colon tissue from healthy subjects has also been noted. Hypermethylation of the promoter CpG islands is recognized to contribute to the loss of function of several tumor related genes, including estrogen receptor (ER). Overall, several studies illustrate that bioactive food components other than essential nutrients can influence DNA methylation processes. Cell Responsiveness to DNA Methylation Defects The ability of bioactive food components to reduce proliferation in normal cells has been reported to be less than in neoplastic cells. For example, selenium preferentially induces growth inhibition and apoptosis in prostate cancer cells, but not in normal prostate cells. Recently, the flavonoid apigenin has also shown selective growth inhibition in prostate cancer cells without affecting normal cells. It is unclear if these differences in sensitivity relate to epigenetic and DNA methylation processes. The gene encoding the pi class glutathione S-transferase (GSTP1) is known to be silenced by CpG island methylation in prostate cancer cells. It has been suggested that compensation for loss of GSTP1 activity is possible with inducers of general glutathione S-transferase activity and one such inducer is the isothiocyanate compound sulforophane found in cruciferous vegetables. That dietary factors might circumvent changes induced by aberrant DNA methylation patterns in cancer requires investigation. The short-chain fatty acid butyrate induces cell cycle arrest, differentiation and apoptosis in colon cancer cells, but often induces opposite effects in normal colonic epithelial cells. A stable transgenic cell line containing a lacZ reporter gene coupled with a hormone-inducible promoter was examined for reversal of methylation-mediated gene silencing. In the methylated form, the promoter is unable to induce lacZ expression and is insensitive to reactivation by the histone deacetylase inhibitors trichostatin A and suberoylanilide hydroxamic acid. In contrast, the short-chain fatty acids (including proprionic, butyric and valeric acid) were capable of overcoming methylation-mediated repression and restored lacZ expression to levels approaching that from an unmethylated promoter. Retinoic acid provides an example that some nutrients may also restore methylation patterns and gene expression. RA demethylated the retinoic acid receptor beta2 promoter in acute promyeocytic leukemia cells. This led to cellular differentiation and accumulation of retinoic acid receptor beta2 mRNA in these cells. It is unknown whether other bioactive food components also lead to DNA demethylation. Sensitizing tumor cells to the bioactive food component can also be accomplished by using demethylating agents, such as 5-aza-2"-deoxycytidine (5- aza-dC). This compound has been used as a therapeutic agent for certain cancers, although treatment-associated side effects preclude its general usefulness. Treatment of several cell lines with MLL (mixed-lineage leukemia or myeloid/lymphoid leukemia) translocations with 5-aza-dC increases the ability of all-trans retinoic acid or 1,25-dihydroxyvitamin D3 to cause differentiation. This study suggests that methylation patterns can influence the response to bioactive food components. These are intriguing results, but we need more. Other Epigenetic Events Emerging evidence indicates that various chromatin states such as histone modifications (acetylation and methylation) and nucleosome positioning (modulated by ATP-dependent chromatin remodeling machines) determine DNA methylation patterning. Additionally, various regulatory factors interacting with the DNA methyltransferases may direct them to specific DNA sequences, regulate their enzymatic activity, and allow their use as transcriptional repressors. Continued studies of the connections between DNA methylation and chromatin structure and the DNA methyltransferase-associated proteins, will likely reveal that many epigenetic modifications of the genome are directly connected. DNA hypermethylation is not likely to be an isolated layer of epigenetic control, but is likely to be linked to other pieces of the puzzle such as methyl-binding proteins, DNA methyltransferases and histone deacetylase. Our understanding of the degree of specificity of these epigenetic layers in the control of gene function remains incomplete. Histone modifications have recently generated excitement in epigenetic research, culminating in the `histone code" hypothesis. The idea is that the modified histone tails provide binding sites for chromatin-associated proteins, which in turn induce alterations in chromatin structure and other downstream events. In particular, for silent chromatin domains, histone H3 lysine 9 methylation by the Su(var)3-9 family of histone methyltransferases has been shown to play a key part in the formation of transcriptionally repressed chromatin by providing a high-affinity binding site for the chromodomain of the heterochromatic HP1 proteins. Recent evidence suggests that histone methylation has considerable epigenetic regulatory impact and is likely influenced by dietary methyl group sufficiency. Moreover, the recent finding that some histone methyltransferases function as tumor suppressors provides another rationale for continued exploration of the diet and epigenetic relationship in cancer prevention research. Acetylation of core histone tails is a conserved mechanism modulating gene expression. It is able to relax higher order chromatin, to promote factor binding to DNA and to recruit unique biological complexes that mediate downstream functions. A switch from inactive to active chromatin is often accompanied by histone hyperacetylation of critical sites in gene regulatory regions. The antagonistic activities of histone acetyltransferases and histone deacetylases control the nuclear steady-state balance of this covalent modification. In addition to any effect on methylation patterns, the short- chain fatty acid butyrate has been shown to induce histone hyperacetylation in vitro and inhibit histone deacetylase in vitro. Recent evidence demonstrates that butyrate promotes hyperacetylation of the upstream region of the RET gene (a proto-oncogene which encodes a tyrosine kinase receptor predominantly expressed in the developing embryo) and increases transcription of the gene. More probing studies are needed to characterize additional gene-specific acetylation changes brought about by bioactive food components. Calorie restriction is one of the best-documented and most potent experimental manipulations for decreasing tumor development in rodents and increasing longevity in diverse organisms. The mechanisms underlying the antitumorigenic effects of caloric restriction have not yet been elucidated. Nevertheless, there is great interest in translating the anticarcinogenic effects of caloric restriction into prevention strategies. Recent observations suggest that a protein important for heterochromatin formation, Sir2, is central for caloric- restriction induced longevity in animals. Any role for Sir2 in cancer prevention requires elucidation. Objectives and Scope This RFA seeks to promote innovative, preclinical and clinical research to determine how diet and dietary factors impact DNA methylation and other epigenetic processes involved with cancer prevention. Although much evidence exists that dietary components are linked to cancer prevention, the specific nutrients and sites of action remain elusive. Diet, in fact, has been implicated in many of the pathways of cancer, including apoptosis, cell cycle control, differentiation, inflammation, angiogenesis, DNA repair and carcinogen metabolism. These are also processes that are likely regulated by DNA methylation, and possibly other epigenetic events, which impact gene function. The objective of this RFA is to begin to address the following issues: how bioactive food components regulate DNA methylation or other epigenetic events for cancer prevention, if bioactive food components can alter DNA methylation or other aberrant epigenetic events and restore gene function, and if these components can circumvent or compensate for genes and pathways that are altered by epigenetic events. An important aim of this RFA is to encourage collaboration between nutrition and epigenetic/ DNA methylation experts to study bioactive food components with cancer preventative properties and to examine key epigenetic events in cancer processes (i.e., carcinogen metabolism, cell division, differentiation, apoptosis) in order to begin to establish linkages between epigenetics, methylation pattern, and tumor incidence/behavior. Thus, each application should demonstrate experience in nutrition and cancer prevention as well as DNA methylation or epigenetics. Studies should also link phenotypic changes to epigenetic alterations induced by specific essential and non-essential nutrients. The resulting information will be critical for optimizing effective dietary intervention strategies for cancer prevention. Investigators may choose from the full range of clinical and preclinical approaches. The focus should be on how individual dietary components influence DNA methylation and other epigenetic events and how this correlates with phenotypic change. Very little information currently exists about gene-specific changes in DNA methylation as influenced by bioactive food components, furthermore, very little information exists to adequately evaluate the specificity of individual nutrients, the impact of intakes/exposures, and any acclimation with time and/or tissue specificity. This RFA encourages the submission of novel approaches to unravel relationships between DNA methylation and other epigenetic events, diet, and cancer prevention. A variety of technologies to assess DNA methylation sequences may be utilized. These can be broadly classified into techniques that measure the overall content or distribution patterns of 5-methylcytosine (i.e., methylated CpG island amplification, methylation-sensitive restriction fingerprinting, differential methylation hybridization, and Restriction Landmark Genomic Scanning) and those that examine known gene sequences (i.e., methylation- sensitive single nucleotide primer extension, and combined bisulfite restriction analysis). The use of genetically engineered animal models including transgenic or gene knockouts are appropriate. The efficient utilization of molecular resources such as gene databases and bioinformatics may also be used to expedite identification of gene-specific methylation targets. The following are viewed as relevant examples for the development of the R01 and R21 applications: o Gene-specific changes in DNA methylation caused by excesses and limitations in bioactive food components. o Relationship between dietary induced global DNA hypomethylation and gene- specific hypermethylation. o Relationship between diet induced changes in DNA methylation and histone acetylation/methylation and control of gene function o Temporality in DNA methylation patterns as influenced by bioactive food components. o Bioactive food component regulation of DNA methylation/epigenetic processes, i.e., methylenetetrahydrofolate reductase, methionine synthase, DNA methyltransferases, demethylases (or various demethylation processes), methylcytosine-binding proteins, histone methyltransferases, histone aceyltransferases and deacetylases. o Linkages between DNA methylation or other epigenetic pattern and the anticancer properties of bioactive food components. MECHANISM OF SUPPORT This RFA will use the National Institutes of Health (NIH) research project grant (R01) and exploratory/developmental grants (R21) as award mechanisms. As an applicant you will be solely responsible for planning, directing, and executing the proposed project. Future unsolicited, competing-continuation applications based on this project will compete with all investigator- initiated applications and will be reviewed according to the customary peer review procedures. The anticipated award date is December 2003. This RFA uses just-in-time concepts. It also uses the modular as well as the non-modular budgeting formats (see Specifically, if you are submitting an application with direct costs in each year of $250,000 or less, use the modular format. Otherwise follow the instructions for non- modular research grant applications. FUNDS AVAILABLE NCI intends to commit approximately $2.5 million in FY 2004 to fund 7 to 10 grants in response to this RFA. The ODS intends to commit up to $800,000 in FY 2004 to fund 3 to 4 grants in response to this RFA. An R01 applicant may request a project period of up to 4 years. An R21 applicant may request a project period of up to 2 years and a budget for direct costs of up to $100,000 per year. Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary. Although the financial plans of NCI and the ODS provide support for this program, awards pursuant to this RFA are contingent upon the availability of funds and the receipt of a sufficient number of meritorious applications. At this time, it is not known if this RFA will be reissued. ELIGIBLE INSTITUTIONS You may submit (an) application(s) if your institution has any of the following characteristics: o For-profit or non-profit organizations o Public or private institutions, such as universities, colleges, hospitals, and laboratories o Units of State and local governments o Eligible agencies of the Federal government o Domestic or foreign o Faith-based or community based organizations INDIVIDUALS ELIGIBLE TO BECOME PRINCIPAL INVESTIGATORS Any individual with the skills, knowledge, and resources necessary to carry out the proposed research is invited to work with their institution to develop an application for support. Individuals from underrepresented racial and ethnic groups as well as individuals with disabilities are always encouraged to apply for NIH programs. WHERE TO SEND INQUIRIES We encourage inquiries concerning this RFA and welcome the opportunity to answer questions from potential applicants. Inquiries may fall into three areas: scientific/research, peer review, and financial or grants management issues: o Direct your questions about scientific/research issues related to diet and cancer prevention to: Dr. Sharon A. Ross Division of Cancer Prevention National Cancer Institute 6130 Executive Blvd., Room 3157 Bethesda, MD 20892 Telephone: (301) 594-7547 FAX: (301) 480-3925 Email: o Direct your questions about scientific/research issues related to dietary supplements to: Rebecca B. Costello, Ph.D. Office of Dietary Supplements Office of Disease Prevention, Office of the Director National Institutes of Health 6100 Executive Blvd., Room 3B01, MSC 7517 Bethesda, Maryland 20892-7517 Phone: 301-435-2920 Fax: 301-480-1845 Email: o Direct your questions about peer review issues to: Referral Officer National Cancer Institute Division of Extramural Activities 6116 Executive Boulevard, Room 8041, MSC 8329 Bethesda, MD 20892-8329 Telephone: (301) 496-3428 FAX: (301) 402-0275 Email: o Direct your questions about financial or grants management matters to: Jane Paull Grants Administration Branch National Cancer Institute 6120 Executive Blvd., EPS-243 Bethesda, MD 20892 Telephone: (301) 496-2182 FAX: (301) 496-8601 Email: LETTER OF INTENT Prospective applicants are asked to submit a letter of intent that includes the following information: o Descriptive title of the proposed research o Name, address, and telephone number of the Principal Investigator o Names of other key personnel o Participating institutions o Number and title of this RFA Although a letter of intent is not required, is not binding, and does not enter into the review of a subsequent application, the information that it contains allows NCI staff to estimate the potential review workload and plan the review. The letter of intent is to be sent by the date listed at the beginning of this document. The letter of intent should be sent to: Dr. Sharon A. Ross Division of Cancer Prevention National Cancer Institute 6130 Executive Blvd., Room 3157 Bethesda, MD 20892 Telephone: (301) 594-7547 FAX: (301) 480-3925 Email: SUBMITTING AN APPLICATION Applications must be prepared using the PHS 398 research grant application instructions and forms (rev. 5/2001). The PHS 398 is available at in an interactive format. For further assistance contact GrantsInfo, Telephone (301) 435-0714, Email: SPECIFIC INSTRUCTIONS FOR MODULAR GRANT APPLICATIONS: Applications requesting up to $250,000 per year in direct costs must be submitted in a modular grant format. The modular grant format simplifies the preparation of the budget in these applications by limiting the level of budgetary detail. Applicants request direct costs in $25,000 modules. Section C of the research grant application instructions for the PHS 398 (rev. 5/2001) at includes step-by-step guidance for preparing modular grants. Additional information on modular grants is available at USING THE RFA LABEL: The RFA label available in the PHS 398 (rev. 5/2001) application form must be affixed to the bottom of the face page of the application. Type the RFA number on the label. Failure to use this label could result in delayed processing of the application such that it may not reach the review committee in time for review. In addition, the RFA title and number must be typed on line 2 of the face page of the application form and the YES box must be marked. The RFA label is also available at: All application instructions outlined in the PHS 398 application kit are to be followed, with the following requirements for R21 applications: 1. R21 applications will use the "MODULAR GRANT" and "JUST-IN-TIME" concepts, with direct costs requested in $25,000 modules, up to the total direct costs limit of $100,000 per year. 2. Although preliminary data are not required for an R21 application, they may be included. 3. Sections a-d of the Research Plan of the R21 application may not exceed 25 pages, including tables and figures. 4. R21 appendix materials should be limited, as is consistent with the exploratory nature of the R21 mechanism, and should not be used to circumvent the page limit for the research plan. Copies of appendix material will only be provided to the primary reviewers of the application and will not be reproduced for wider distribution. The following materials may be included in the appendix: o Up to five publications, including manuscripts (submitted or accepted for publication), abstracts, patents, or other printed materials directly relevant to the project. These may be stapled as sets. Surveys, questionnaires, data collection instruments, and clinical protocols. These may be stapled as sets. Original glossy photographs or color images of gels, micrographs, etc., provided that a photocopy (may be reduced in size) is also included within the 25 page limit of items a-d of the research plan. SENDING AN APPLICATION TO THE NIH: Submit a signed, typewritten original of the application, including the Checklist, and three signed, photocopies, in one package to: Center for Scientific Review National Institutes of Health 6701 Rockledge Drive, Room 1040, MSC 7710 Bethesda, MD 20892-7710 Bethesda, MD 20817 (for express/courier service) At the time of submission, two additional copies of the application must be sent to: Referral Officer Division of Extramural Activities National Cancer Institute 6116 Executive Blvd., Room 8041, MSC-8329 Rockville, MD 20852 (express courier) Bethesda MD 20892-8329 APPLICATIONS HAND-DELIVERED BY INDIVIDUALS TO THE NATIONAL CANCER INSTITUTE WILL NO LONGER BE ACCEPTED. This policy does not apply to courier deliveries (i.e. FEDEX, UPS, DHL, etc.) ( This policy is similar to and consistent with the policy for applications addressed to Centers for Scientific Review as published in the NIH Guide Notice APPLICATION PROCESSING: Applications must be received by the application receipt date listed in the heading of this RFA. If an application is received after that date, it will be returned to the applicant without review. The Center for Scientific Review (CSR) will not accept any application in response to this RFA that is essentially the same as one currently pending initial review, unless the applicant withdraws the pending application. The CSR will not accept any application that is essentially the same as one already reviewed. This does not preclude the submission of substantial revisions of applications already reviewed, but such applications must include an Introduction addressing the previous critique. PEER REVIEW PROCESS Upon receipt, applications will be reviewed for completeness by the CSR and for responsiveness by the NCI and ODS program staff. Incomplete applications will be returned to the applicant without further consideration. And, if the application is not responsive to the RFA, CSR staff may contact the applicant to determine whether to return the application to the applicant or submit it for review in competition with unsolicited applications at the next appropriate NIH review cycle. Applications that are complete and responsive to the RFA will be evaluated for scientific and technical merit by an appropriate peer review group convened by the Division of Extramural Activities (DEA) at NCI in accordance with the review criteria stated below. As part of the initial merit review, all applications will: o Receive a written critique o Undergo a process in which only those applications deemed to have the highest scientific merit, generally the top half of the applications under review, will be discussed and assigned a priority score o Those that receive a priority score will undergo a second level review by the National Cancer Advisory Board. REVIEW CRITERIA The goals of NIH-supported research are to advance our understanding of biological systems, improve the control of disease, and enhance health. In the written comments, reviewers will be asked to discuss the following aspects of your application in order to judge the likelihood that the proposed research will have a substantial impact on the pursuit of these goals: o Significance o Approach o Innovation o Investigator o Environment The scientific review group will address and consider each of these criteria in assigning your application"s overall score, weighting them as appropriate for each application. Your application does not need to be strong in all categories to be judged likely to have major scientific impact and thus deserve a high priority score. For example, you may propose to carry out important work that by its nature is not innovative but is essential to move a field forward. (1) SIGNIFICANCE: Does this study address an important question about the role of (a) bioactive food components in DNA methylation or other epigenetic event involved with cell vulnerability to cancer or cellular responsiveness to cancer prevention? Do studies focus on how dietary components influence DNA methylation or other epigenetic event and how this correlates with phenotypic change. Will these research projects advance the field of nutrition and cancer prevention from observational to more probing studies? (2) APPROACH: Are the conceptual framework, design, methods, and analyses adequately developed, well integrated, and appropriate to the aims of the project? Does the applicant acknowledge potential problem areas and consider alternative tactics? (3) INNOVATION: Does the project employ novel concepts, approaches or methods? Are the aims original and innovative? Does the project challenge existing paradigms or develop new methodologies or technologies? (4) INVESTIGATOR: Is the investigator appropriately trained and well suited to carry out this work? Is experience in nutrition and cancer prevention as well as DNA methylation or epigenetics demonstrated in the application? Is the work proposed appropriate to the experience level of the principal investigator and other researchers (if any)? (5) ENVIRONMENT: Does the scientific environment in which the work will be done contribute to the probability of success? Do the proposed experiments take advantage of unique features of the scientific environment or employ useful collaborative arrangements (i.e., between nutrition and epigenetic /DNA methylation experts)? Is there evidence of institutional support? ADDITIONAL REVIEW CRITERIA: In addition to the above criteria, your application will also be reviewed with respect to the following: o PROTECTIONS: The adequacy of the proposed protection for humans, animals, or the environment, to the extent they may be adversely affected by the project proposed in the application. o INCLUSION: The adequacy of plans to include subjects from both genders, all racial and ethnic groups (and subgroups), and children as appropriate for the scientific goals of the research. Plans for the recruitment and retention of subjects will also be evaluated. (See Inclusion Criteria included in the section on Federal Citations, below) o DATA SHARING: The adequacy of the proposed plan to share data. o BUDGET: The reasonableness of the proposed budget and the requested period of support in relation to the proposed research. RECEIPT AND REVIEW SCHEDULE Letter of Intent Receipt Date: February 18, 2003 Application Receipt Date: March 18, 2003 Peer Review Date: June-July, 2003 Council Review: September 2003 Earliest Anticipated Start Date: December 2003 AWARD CRITERIA Award criteria that will be used to make award decisions include: o Scientific merit (as determined by peer review) o Availability of funds o Programmatic priorities. REQUIRED FEDERAL CITATIONS MONITORING PLAN AND DATA SAFETY AND MONITORING BOARD: Research components involving Phase I and II clinical trials must include provisions for assessment of patient eligibility and status, rigorous data management, quality assurance, and auditing procedures. In addition, it is NIH policy that all clinical trials require data and safety monitoring, with the method and degree of monitoring being commensurate with the risks (NIH Policy for Data Safety and Monitoring, NIH Guide for Grants and Contracts, June 12, 1998: Clinical trials supported or performed by NCI require special considerations. The method and degree of monitoring should be commensurate with the degree of risk involved in participation and the size and complexity of the clinical trial. Monitoring exists on a continuum from monitoring by the principal investigator/project manager or NCI program staff or a Data and Safety Monitoring Board (DSMB). These monitoring activities are distinct from the requirement for study review and approval by an Institutional review Board (IRB). For details about the Policy for the NCI for Data and Safety Monitoring of Clinical trials see: For Phase I and II clinical trials, investigators must submit a general description of the data and safety monitoring plan as part of the research application. See NIH Guide Notice on "Further Guidance on a Data and Safety Monitoring for Phase I and II Trials" for additional information: Information concerning essential elements of data safety monitoring plans for clinical trials funded by the NCI is available: INCLUSION OF WOMEN AND MINORITIES IN CLINICAL RESEARCH: It is the policy of the NIH that women and members of minority groups and their sub-populations must be included in all NIH-supported clinical research projects unless a clear and compelling justification is provided indicating that inclusion is inappropriate with respect to the health of the subjects or the purpose of the research. This policy results from the NIH Revitalization Act of 1993 (Section 492B of Public Law 103-43). All investigators proposing clinical research should read the AMENDMENT "NIH Guidelines for Inclusion of Women and Minorities as Subjects in Clinical Research - Amended, October, 2001," published in the NIH Guide for Grants and Contracts on October 9, 2001 (, a complete copy of the updated Guidelines are available at The amended policy incorporates: the use of an NIH definition of clinical research, updated racial and ethnic categories in compliance with the new OMB standards, clarification of language governing NIH-defined Phase III clinical trials consistent with the new PHS Form 398, and updated roles and responsibilities of NIH staff and the extramural community. The policy continues to require for all NIH-defined Phase III clinical trials that: a) all applications or proposals and/or protocols must provide a description of plans to conduct analyses, as appropriate, to address differences by sex/gender and/or racial/ethnic groups, including subgroups if applicable, and b) investigators must report annual accrual and progress in conducting analyses, as appropriate, by sex/gender and/or racial/ethnic group differences. INCLUSION OF CHILDREN AS PARTICIPANTS IN RESEARCH INVOLVING HUMAN SUBJECTS: The NIH maintains a policy that children (i.e., individuals under the age of 21) must be included in all human subjects research, conducted or supported by the NIH, unless there are scientific and ethical reasons not to include them. This policy applies to all initial (Type 1) applications submitted for receipt dates after October 1, 1998. All investigators proposing research involving human subjects should read the "NIH Policy and Guidelines" on the inclusion of children as participants in research involving human subjects that is available at REQUIRED EDUCATION ON THE PROTECTION OF HUMAN SUBJECT PARTICIPANTS: NIH policy requires education on the protection of human subject participants for all investigators submitting NIH proposals for research involving human subjects. You will find this policy announcement in the NIH Guide for Grants and Contracts Announcement, dated June 5, 2000, at A continuing education program in the protection of human participants in research in now available online at: HUMAN EMBRYONIC STEM CELLS (hESC): Criteria for federal funding of research on hESCs can be found at and at Guidance for investigators and institutional review boards regarding research involving human embryonic stem cells, germ cells, and stem cell-derived test articles can be found at Only research using hESC lines that are registered in the NIH Human Embryonic Stem Cell Registry will be eligible for Federal funding (see It is the responsibility of the applicant to provide the official NIH identifier(s)for the hESC line(s) to be used in the proposed research. Applications that do not provide this information will be returned without review. PUBLIC ACCESS TO RESEARCH DATA THROUGH THE FREEDOM OF INFORMATION ACT: The Office of Management and Budget (OMB) Circular A-110 has been revised to provide public access to research data through the Freedom of Information Act (FOIA) under some circumstances. Data that are (1) first produced in a project that is supported in whole or in part with Federal funds and (2) cited publicly and officially by a Federal agency in support of an action that has the force and effect of law (i.e., a regulation) may be accessed through FOIA. It is important for applicants to understand the basic scope of this amendment. NIH has provided guidance at Applicants may wish to place data collected under this RFA in a public archive, which can provide protections for the data and manage the distribution for an indefinite period of time. If so, the application should include a description of the archiving plan in the study design and include information about this in the budget justification section of the application. In addition, applicants should think about how to structure informed consent statements and other human subjects procedures given the potential for wider use of data collected under this award. URLs IN NIH GRANT APPLICATIONS OR APPENDICES: All applications and proposals for NIH funding must be self-contained within specified page limitations. Unless otherwise specified in an NIH solicitation, Internet addresses (URLs) should not be used to provide information necessary to the review because reviewers are under no obligation to view the Internet sites. Furthermore, we caution reviewers that their anonymity may be compromised when they directly access an Internet site. HEALTHY PEOPLE 2010: The Public Health Service (PHS) is committed to achieving the health promotion and disease prevention objectives of "Healthy People 2010," a PHS-led national activity for setting priority areas. This RFA is related to one or more of the priority areas. Potential applicants may obtain a copy of "Healthy People 2010" at AUTHORITY AND REGULATIONS: This program is described in the Catalog of Federal Domestic Assistance No. 93.3393 (Cancer Cause and Prevention Research) and is not subject to the intergovernmental review requirements of Executive Order 12372 or Health Systems Agency review. Awards are made under authorization of Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and administered under NIH grants policies described at and under Federal Regulations 42 CFR 52 and 45 CFR Parts 74 and 92. The PHS strongly encourages all grant recipients to provide a smoke-free workplace and discourage the use of all tobacco products. In addition, Public Law 103-227, the Pro-Children Act of 1994, prohibits smoking in certain facilities (or in some cases, any portion of a facility) in which regular or routine education, library, day care, health care, or early childhood development services are provided to children. This is consistent with the PHS mission to protect and advance the physical and mental health of the American people. The Office of Dietary Supplements (ODS) was mandated by Congress in 1994 and established within the Office of the Director, National Institutes of Health (NIH). The Dietary Supplement Health and Education Act (DSHEA) [Public Law 103-417, Section 3.a] amended the Federal Food, Drug, and Cosmetic Act "to establish standards with respect to dietary supplements." This law authorized the establishment of the ODS.

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