text:
CppJieba::Application* gApp;

NAN_METHOD(load) {
  NanScope();

  if(args.Length() != 5) {
    NanReturnValue (NanIntern::Factory<v8::Boolean>::New(false));
  }

  String::Utf8Value dictPath(args[0]->ToString());
  String::Utf8Value modelPath(args[1]->ToString());
  String::Utf8Value userDictPath(args[2]->ToString());
  String::Utf8Value idfPath(args[3]->ToString());
  String::Utf8Value stopWordsPath(args[4]->ToString());

  gApp = new CppJieba::Application(*dictPath,
                                  *modelPath,
                                  *userDictPath,
                                  *idfPath,
                                  *stopWordsPath);

  NanReturnValue (NanIntern::Factory<v8::Boolean>::New(true));
}

NAN_METHOD(cut) {
  NanScope();
  if (args.Length() == 0) {
    NanReturnValue (NanIntern::Factory<v8::Boolean>::New(false));
  }
  string sentence = *(String::Utf8Value(args[0]->ToString()));
  vector<string> words;

  if (args.Length() == 2) {
    string method = *(String::Utf8Value(args[1]->ToString()));
    if ("MP" == method) {
      gApp->cut(sentence, words, CppJieba::METHOD_MP);
    } else if ("HMM" == method) {
      gApp->cut(sentence, words, CppJieba::METHOD_HMM);
    } else if ("MIX" == method) {
      gApp->cut(sentence, words, CppJieba::METHOD_MIX);
    } else if ("FULL" == method) {
      gApp->cut(sentence, words, CppJieba::METHOD_FULL);
    } else if ("QUERY" == method) {
      gApp->cut(sentence, words, CppJieba::METHOD_QUERY);
    } else {
      gApp->cut(sentence, words, CppJieba::METHOD_MIX);
    }
  } else {
    gApp->cut(sentence, words, CppJieba::METHOD_MIX);
  }

  Local<Array> outArray;
  WrapVector(words, outArray);

  NanReturnValue(outArray);
}

NAN_METHOD(tag) {
  NanScope();
  if (args.Length() == 0) {
    NanReturnValue (NanIntern::Factory<v8::Boolean>::New(false));
  }

  vector<pair<string, string> > words;
  string sentence = *(String::Utf8Value(args[0]->ToString()));
  gApp->tag(sentence, words);

  Local<Array> outArray;
  WrapPairVector(words, outArray);

  NanReturnValue(outArray);
}

NAN_METHOD(extract) {
  NanScope();

  if (args.Length() != 2) {
    NanReturnValue (NanIntern::Factory<v8::Boolean>::New(false));
  }

  string sentence = *(String::Utf8Value(args[0]->ToString()));
  size_t topN = args[1]->Int32Value();
  vector<pair<string, double> > words;

  gApp->extract(sentence, words, topN);

  Local<Array> outArray;
  WrapPairVector(words, outArray);

  NanReturnValue(outArray);
}


text:
Q: error code ELIFECYCLE while running npm run build I have built react app based on fuse react theme it is running fine in the dev environment by npm start
but I'm getting error while making production build, running npm run build to make a production build but getting ELIFECYCLE error, I have tried all the options like.
npm ERR! code ELIFECYCLE
npm ERR! errno 1
npm ERR! fuse-react-app@6.1.4 build: `cross-env
GENERATE_SOURCEMAP=false craco build`
npm ERR! Exit status 1
npm ERR!
npm ERR! Failed at the fuse-react-app@6.1.4 build script.
npm ERR! This is probably not a problem with npm. There is likely
additional logging output above.

*

*Remove package-lock.json

*Delete node_modules

*Ran npm install

*Ran npm start and app is working fine I can access the app on the browser

*Ran npm run build getting ELIFECYCLE error

Here is my package.json file
{
"name": "fuse-react-app",
"version": "6.1.4",
"private": true,
"dependencies": {
    "@date-io/core": "1.3.13",
    "@date-io/date-fns": "1.3.13",
    "@date-io/moment": "1.3.13",
    "@fullcalendar/core": "5.7.0",
    "@fullcalendar/daygrid": "5.7.0",
    "@fullcalendar/interaction": "5.7.0",
    "@fullcalendar/react": "5.7.0",
    "@fullcalendar/timegrid": "5.7.0",
    "@hookform/resolvers": "2.5.1",
    "@material-ui/core": "4.11.4",
    "@material-ui/data-grid": "latest",
    "@material-ui/icons": "4.11.2",
    "@material-ui/lab": "4.0.0-alpha.58",
    "@material-ui/pickers": "3.3.10",
    "@mui/material": "^5.2.4",
    "@mui/x-data-grid-pro": "^4.0.0",
    "@reduxjs/toolkit": "1.5.1",
    "apexcharts": "3.26.3",
    "auth0-lock": "11.30.0",
    "autosuggest-highlight": "3.1.1",
    "axios": "0.21.1",
    "axios-mock-adapter": "1.19.0",
    "chart.js": "2.9.4",
    "clsx": "1.1.1",
    "cross-fetch": "3.1.4",
    "date-fns": "2.21.3",
    "draft-js": "0.11.7",
    "draftjs-to-html": "0.9.1",
    "firebase": "8.6.2",
    "formsy-react": "2.2.5",
    "framer-motion": "4.1.17",
    "google-map-react": "2.1.9",
    "history": "4.10.1",
    "i18next": "20.3.0",
    "jsonwebtoken": "8.5.1",
    "jss": "10.6.0",
    "jss-plugin-extend": "10.6.0",
    "jss-rtl": "0.3.0",
    "jwt-decode": "2.2.0",
    "keycode": "2.2.0",
    "lodash": "4.17.21",
    "marked": "0.8.2",
    "material-table": "^1.69.3",
    "material-ui-dropzone": "^3.5.0",
    "material-ui-popup-state": "1.8.3",
    "millify": "^4.0.0",
    "mobile-detect": "1.4.5",
    "moment": "^2.29.1",
    "notistack": "1.0.9",
    "path-to-regexp": "3.2.0",
    "perfect-scrollbar": "1.5.1",
    "prismjs": "1.23.0",
    "prop-types": "15.7.2",
    "qs": "6.10.1",
    "raw-loader": "4.0.2",
    "react": "17.0.2",
    "react-apexcharts": "1.3.9",
    "react-autosuggest": "10.1.0",
    "react-beautiful-dnd": "13.1.0",
    "react-chartjs-2": "2.11.2",
    "react-compound-timer": "^1.2.0",
    "react-dom": "17.0.2",
    "react-draft-wysiwyg": "1.14.7",
    "react-draggable": "4.4.3",
    "react-frame-component": "4.1.3",
    "react-hook-form": "7.7.1",
    "react-i18next": "11.9.0",
    "react-iframe": "^1.8.0",
    "react-json-editor-ajrm": "^2.5.13",
    "react-json-view": "^1.21.3",
    "react-masonry-css": "1.0.16",
    "react-number-format": "4.5.5",
    "react-popper": "1.3.11",
    "react-redux": "7.2.4",
    "react-router": "5.2.0",
    "react-router-config": "5.1.1",
    "react-router-dom": "5.2.0",
    "react-scripts": "^4.0.3",
    "react-select": "3.2.0",
    "react-show-more-text": "^1.5.0",
    "react-sparklines": "^1.7.0",
    "react-spring": "9.1.2",
    "react-swipeable": "6.1.2",
    "react-swipeable-views": "0.13.9",
    "react-swipeable-views-utils": "0.13.9",
    "react-table": "7.7.0",
    "react-terminal-component": "^1.5.0",
    "react-text-mask": "5.4.3",
    "react-virtualized": "9.22.3",
    "react-window": "1.8.6",
    "redux": "4.1.0",
    "redux-logger": "4.0.0",
    "styled-components": "5.3.0",
    "typeface-poppins": "1.1.13",
    "velocity-animate": "1.5.2",
    "velocity-react": "1.4.3",
    "web-vitals": "^0.2.4",
    "yup": "0.32.9"
},
"peerDependencies": {
    "autoprefixer": "9.8.6",
    "postcss": "7.0.35",
    "react": "17.0.2",
    "react-dom": "17.0.2"
},
"resolutions": {
    "react": "17.0.2",
    "react-dom": "17.0.2",
    "babel-loader": "8.1.0"
},
"devDependencies": {
    "@babel/core": "7.12.17",
    "@babel/node": "7.12.17",
    "@babel/plugin-transform-react-jsx": "7.12.17",
    "@babel/preset-env": "7.12.17",
    "@craco/craco": "^6.1.2",
    "@tailwindcss/postcss7-compat": "2.1.2",
    "@typescript-eslint/eslint-plugin": "^4.25.0",
    "@typescript-eslint/parser": "^4.25.0",
    "@yarnpkg/pnpify": "2.4.0",
    "autoprefixer": "9.8.6",
    "babel-eslint": "10.1.0",
    "cross-env": "7.0.3",
    "eslint": "7.27.0",
    "eslint-config-airbnb": "^18.2.1",
    "eslint-config-prettier": "^8.3.0",
    "eslint-config-react-app": "^6.0.0",
    "eslint-import-resolver-node": "^0.3.4",
    "eslint-plugin-flowtype": "^5.7.2",
    "eslint-plugin-import": "^2.23.3",
    "eslint-plugin-jsx-a11y": "^6.4.1",
    "eslint-plugin-prettier": "^3.4.0",
    "eslint-plugin-react": "^7.23.2",
    "eslint-plugin-react-hooks": "^4.2.0",
    "js-beautify": "1.13.13",
    "postcss": "7.0.35",
    "prettier": "^2.3.0",
    "promise": "8.1.0",
    "source-map-explorer": "2.5.2",
    "tailwindcss": "npm:@tailwindcss/postcss7-compat@2.1.2",
    "tailwindcss-dir": "4.0.0"
},
"scripts": {
    "start": "craco start",
    "build": "cross-env GENERATE_SOURCEMAP=false craco build",
    "test": "craco test --env=node",
    "eject": "craco eject",
    "build-docs": "find ./src/app/main/documentation/material-ui-components \\( -name '*.ts' -o -name '*.tsx' \\) -type f -delete && babel-node --presets @babel/preset-env src/app/main/documentation/material-ui-components/build.js",
    "analyze": "craco build && source-map-explorer 'build/static/js/*.js' --html analyze-result.html",
    "pnpify-sdk": "yarn pnpify --sdk",
    "lint": "eslint"
},
"browserslist": {
    "production": [
        ">0.2%",
        "not dead",
        "not op_mini all"
    ],
    "development": [
        "last 1 chrome version",
        "last 1 firefox version",
        "last 3 safari version"
    ]
}}

Node version = 14.2.0
npm version = 6.14.4
Any solution how can I resolve the above error and make a production build.

A: I think the main reason is the using cross-env package. Otherwise other scripts would cause same error, too.
FOr testing purpose, remove cross-env GENERATE_SOURCEMAP=false and pass false manually instead of process.env.GENERATE_SOURCEMAP. so your build script should be
 "build": "craco build",

*

*if it does not work, clean the cache
 npm cache clean –force

delete .npm
 rm -rf ~/.npm

then delete lock.json and node_modules, and reinstall
  npm install

redpajama_set_name: RedPajamaStackExchange


Pixel Socks - curated by.
Calf-high knit cotton socks in off-white, with CURATED BY. woven at each side in a pixel like font.
Crafted in Barcelona by a local socks manufacturer established in 1972, using high-quality sustainable materials to lower the environmental impact of the manufacturing process.
Made out of 95% cotton and 5% elastane. One unique size (EU 38-43/US 9-12).


TOKYO, Sept 17 (Reuters) - Eiji Toyoda, who helped steer Toyota Motor Corp's global rise and pioneered the automaker's vaunted production system, died on Tuesday, the Japanese automaker said. He was 100.
Toyoda, cousin of the automaker's founder, died of heart failure in Toyota City, the company said in a statement.
A taciturn engineer, Toyoda served as president between 1967 and 1982. He was chairman until 1994 and remained an honorary advisor at Toyota up until the time of his death.
Over his career, Toyoda presided over Toyota's rise in the U.S. market from the launch of the Corolla in the late 1960s to the decision to begin making cars in the United States in the late 1980s.
Toyoda was also instrumental in developing what became the automaker's much-imitated method of producing cars with as little waste as possible and continual quality improvements, a system that became known as the "Toyota Way".
In 1950, company founder Kiichiro Toyoda sent Eiji, a graduate of the University of Tokyo, to Ford Motor Co's massive Rouge Plant to learn about car making from the company that had pioneered mass production.
In a story that is still shared at Toyota training sessions, Toyoda returned to Japan impressed with U.S. materials and machinery but convinced that he could make improvements to Ford's world-famous production system.
"Japan's automobile industry facilities and engineers are good but our machine tools are inferior. If we can solve this problem, we can manufacture good and economic vehicles that are equal to America's," Toyoda wrote after his month and a half of training at Ford's major factories.
At the time of his death, Toyoda was being treated at a hospital the company had first founded as a clinic for its factory workers in 1938.


text:
Transfer Advising Guides
Visit SAC Visit
About SAC
Experience SAC
News & Events News 2018 March On the Record: SAC Journalism Association Celebrates Silver Anniversary
On the Record: SAC Journalism Association Celebrates Silver Anniversary
Russell Guerrero
In the early 1990s, the San Antonio College Journalism program set out to accomplish what had never been done: they wanted to bring a student chapter of the Society of Professional Journalists (SPJ) to a community college.
SPJ is the oldest professional journalism organization in the country and the most prestigious. Members include reporters and photographers for newspapers, magazines, radio and the internet. Along with professional chapters, the association also includes college chapters, which must meet stringent guidelines and practices.
The idea had been around for many years at SAC, but the mission to establish a student chapter gained momentum when faculty and students received strong support from the San Antonio Light and the San Antonio Express-News, the two major daily newspapers in the city at the time.
The National SPJ association gave SAC probationary status and two years later, in 1993, granted the journalism program an official student chapter.
"We hit the ground running," remembered Tricia Buchhorn, senior communications lab technician and part-time photography adviser. Buchhorn, who was a SAC student and the first official president of the SPJ chapter, said the students celebrated the announcement by planning a series of events during National Newspaper Week.
Twenty-five years later, the SAC SPJ chapter still plays an integral role for students going into journalism. Zachary-Taylor Wright, the current president of the SPJ chapter, said being part of the national association means students must uphold high journalism standards - no different than any working journalist.
In addition, the chapter also holds community forums to inform the public on the ethical practices in journalism. "I think we are trying to be more transparent now with what are ethics are so we can be trusted," he said.
Marianne Odom, SAC journalism-photography coordinator and a former adviser for the SPJ chapter, said there are other student benefits as well, including opportunities to network with professionals in the field. The organization also offers scholarships to students who transfer to journalism programs at other colleges.
"SPJ helps groom the next generation of journalists," she said.
To celebrate their silver anniversary, the SAC chapter hosted a conference for SPJ Region 8, which covers Texas and Oklahoma.
The conference, organized by SAC students, covered issues at the forefront of the industry, including the role of social media in covering traumatic events and copyright law.
But it also included sessions that showed where the future of journalism is headed - some of the speakers talked about the importance of being an entrepreneur and creating career opportunities were none exist.
After 25 years, the SAC SPJ chapter is still vibrant and essential to future journalists.
-SAC-
Nicole M. Bautista is vice president of the SAC SPJ chapter and multimedia editor of the SAC Ranger . She has created a video to celebrate the 25th anniversary of the the student SPJ chapter. You can see it on You Tube by going to https://youtu.be/pC7NoVGxIPk
Photo courtesy of the SAC Ranger.
Articulating Success
SAC Listed Among Best 20 Community Colleges in Texas
SAC Alumni Highlight - Adrianna Swindle
A Sweet Song of Success
SAC OTS Department Wins National Honor
SAC Rings in LULAC Parent/Child Scholarship
1819 N. Main Ave.
210-21-ALAMO
Concourse Syllabi
Jobs at SAC
© Copyright 2019 San Antonio College

redpajama_set_name: RedPajamaCommonCrawl


On Monday we had our first call with our advisors Sebastian and Evelyn. After introductions and some organisational details, we got to discussing robot strategies.
We explained our ideas to them, and showed them our blog.


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text:
#17: Imitation in Death (Abridged / Compact Disc): $10.99
Homicide detective Eve Dallas must untangle a twisted family history while a hostage's life hangs in the balance—in Abandoned in Death by New York Times bestselling author J. D. Robb.
The woman's body was found in the early morning, on a bench in a New York City playground. She was clean, her hair neatly arranged, her makeup carefully applied. But other things were very wrong—like the tattoo and piercings, clearly new. The clothes, decades out of date. The fatal wound hidden beneath a ribbon around her neck. And the note: Bad Mommy, written in crayon as if by a child.
Eve Dallas turns to the department's top profiler, who confirms what seems obvious to Eve: They're dealing with a killer whose childhood involved some sort of trauma—a situation Eve is all too familiar with herself. Yet the clues suggest a perpetrator who'd be roughly sixty years old, and there are no records of old crimes with a similar MO. What was the trigger that apparently reopened such an old wound and sent someone over the edge?
When Eve discovers that other young women—who physically resemble the first victim—have vanished, the clock starts ticking louder. But to solve this case she will need to find her way into a hidden place of dim light and concrete, into the distant past, and into the cold depths of a shattered mind.
J. D. Robb is the pseudonym for #1 New York Times bestselling author Nora Roberts. She is the author of over 230 novels, including the futuristic suspense In Death series. There are more than 500 million copies of her books in print.
"In the latest chilling and thrilling addition to her bestselling Eve Dallas series, Robb is perfectly on-brand with another cleverly constructed story that effectively blends daring suspense and dynamic plotting, all the while keeping the sexy chemistry between Eve and her husband, Roarke, as hot as ever." - Booklist
Publication Date: February 8th, 2022
Fiction / Mystery & Detective / Police Procedural
Fiction / Romance / Suspense
Fiction / Mystery & Detective / Women Sleuths
Kobo eBook (February 8th, 2022): $9.99
Mass Market (July 26th, 2022): $9.99
CD-Audio (August 9th, 2022): $19.99
CD-Audio (February 8th, 2022): $39.99


The 33091st positive integer is an odd prime number that follows the number 33090 and comes before 33092. Thirty-three thousand ninety-one is 5 digits long.
Q: Is 33091 a prime number?
Q: What is the negative number for 33091?
Q: What is half of 33091?
Q: What is a third of 33091?
Q: What is a quarter of 33091?
Q: What is the square root of 33091?
Q: What is 33091 times Pi?
Q: What is 33091 divided by Pi?
Q: What is the scientific notation for 33091?
Q: What are the divisors for 33091?
Q: What is the factorization of 33091?
Q: What is the sum of divisors of 33091, including itself?
Q: What is the sum of divisors of 33091, excluding itself?
The spelling of 33091 in different languages.
Q: What is the roman numeral for 33091?
Q: What is the digital capacity for 33091?
The number 33091 represented in different base number systems.
List the frequency of characters that make up the number 33091.
List of hash code values for 33091.


It often makes a very big difference in a portrait to ask the subject to tilt their head up or down. Here we have Nicole going from a chin-up pose to a chin-down pose, and if you want to see more, check out the way down and way up pages.
Bottom Line: Chin up or down makes a very big difference in a portrait.
Chin way up — clearly too far. Nicole is looking down her nose at us. Haughty.
This is a military-looking, at-attention look. Might work in some situations.
Chin is just a little bit higher than normal. Adds optimism.
Pretty much straight-ahead look, not as optimistic as the one to the left.
Chin slightly down, and now Nicole looks even less optimistic, almost sad.
Chin down more than normal, and the look is getting quite sad indeed.
Along with sadness, this pose brings a pious look to the shot.
Chin way down; looks like the judge has just pronounced her guilty.


text:
Home Bus and Coach CTTC members grateful but disappointed with Government Stimulus Package
CTTC members grateful but disappointed with Government Stimulus Package
While the Coach Tourism & Transport Council (CTTC), welcomed the Government's allocation of financial support to coach tour sector, the national body says it "falls short" on expectations. Coach tour operators need a more substantial stimulus to stay afloat and keep them in business until the market comes back to any level of normality.
The CTTC described the Government's decision to grant a €10 million Business Continuity Fund for Coach Tourism Operators in the July Stimulus Plan as welcome but "falls short" of what is required to help coach tour operators to stay afloat. Over the past number of months, the organisation had continuously expressed the need to directly support the sector which is facing financial peril. The coach tour sector is responsible for transporting two million tourists around Ireland every year.
CTTC members are leading providers of private scheduled services, international tours, school transport and private hire. In total there are 1,721 coach operators in Ireland, carrying over 75 million passengers per year, supporting 11,457 jobs and contributing €400 million to the economy.
Chairman of the CTTC, John Halpenny, commented on the development: "It is welcome news that Government saw the merit in delivering direct support for coach tour operators in the July Stimulus Plan. However, the amount announced represents only a fraction of what is required to help businesses survive. Many operators suffered a colossal drop-off in bookings and cancellations which means they are haemorrhaging millions in overheads every month and this is threatening the very survival of the sector."
"While the support will help operators in a small way, unquestionably there will be business and job casualties which will have a knock-on impact on scheduled services and school transport provision. It also presents real challenges to the tourism sector because the reduction in the numbers of operators will mean less visitors when fears surrounding the pandemic alleviate."
John Halpenny concluded by saying: "We now urge Government to move to the next stage of this process and ensure the timely delivery of the €10 million to our sector so operators can be supported without delay."
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L K Tack Shop Western Boutique & Gifts is located at the address 26359 S La Grange Rd in Monee, Illinois 60449. They can be contacted via phone at (815) 469-5882 for pricing, hours and directions.
For maps and directions to L K Tack Shop Western Boutique & Gifts view the map to the right. For reviews of L K Tack Shop Western Boutique & Gifts see below.


Probably the sickest 7 inch in my crates as of late. Especially in the hard hitting boogie department.
Although it would seem, just because the spelling is the exact same, that this is the same San Francisco boogie funk band SNAPP, with the two P's. But, it is not. At least as far as I could dissect.
This is one 45 that is dying to be heard and it's thunderous groove is very hypnotic. I'm glad to have nabbed one, and ever happier to share with you.


text:
Exelon Headquarters
The new headquarters of Exelon's Constellation business unit – a Fortune 150 company – features a 24-hour trading floor which represents the energy hub and heart of the new 350-foot tall building. The trading floor consists of 65,000 square feet of space with soaring ceilings and a 45,000 square foot mezzanine overlooking the sea of traders.
The opening of the tower moved 1,500 Exelon and Constellation employees from two downtown office buildings near the Power Plant to the new facility beyond Harbor East's offices and luxe hotels, expanding Baltimore's economic center further east along the harbor away from the aging core. The new building features 443,000 square feet of office space, 103 apartment units, 40,000 square feet of street-level retail and 750 parking spaces.
Project Awards/Certifications
2017 Baltimore Business Journal Best in Real Estate Inc. Award Winner: Best in Show
2017 ENR Mid-Atlantic Best Project Award in the Office/Retail/Mixed-Use Category LEED Gold Certified (2017)
LEED Building Design & Construction (LEED BD+C: Core and Shell v3-LEED 2009)
Major Tenants — Beatty Development Group
Contract Value — $182 Million
222 Central Park Ave., Suite 1000, Virginia Beach, VA 23462
UPDATE AS OF June 1, 2020: At Armada Hoffler, our goal remains the safety and well-being of our employees, their families and all of our stakeholder groups. In response to the ongoing COVID-19 pandemic, our offices have pivoted to a phased-in approach consisting of remote work and in office work. We are working every day to remain consistent with guidelines and protocol issued by the state authorities. Implementation of contingency plans for unseen circumstances such as this, allow our employees to conduct business as usual, regardless of office location. We are committed to providing the same support to our partners and tenants as well as continued communication for our investors. We have always been dedicated to the communities around us and devoted to do our part to keep them safe. We will continue to monitor the situation as it progresses and provide updates as needed.


Graham Budd has been critical of associations between Ediacaran fauna and Cambrian animals, and has also debunked alleged Precambrian animal ancestors such as Vernanimalcula (Stephen Meyer, Darwin's Doubt, pp. 85, 90-91). Budd also was in attendance at the Darwin-doubting Altenberg 16 conference in 2008 (p. 292), confessing that the fossil record tells little about the origin of biological forms. This Cambrian expert from Uppsala University has a new paper in Geology describing new exquisitely-preserved fossils of the Burgess Shale type, but earlier. Along with lead writer Ben Slater, Graham Budd's team unveils photographs of tiny but exquisite parts of arthropods, worms and other animals that burst into appearance in the Cambrian Explosion. What's amazing is that these fossils were collected not in Canada or China, but in the northern reaches of Greenland.
The location, called Sirius Passet in Peary Land in the far north of Greenland, has been known as an early Cambrian fossil site, but it lies close to a geological fold belt. Having been heated to 200° C or more by metamorphism, most of the fossils at Sirius Passet have suffered thermal alteration and are difficult to interpret. Not far to the south, however, the team found sites in the same formation that escaped most of the alteration. News from Uppsala University describes how they found a "treasure trove of highly detailed fossils" of the Burgess Shale type.
The 'Cambrian explosion' of animal diversity beginning ~541 million years ago is a defining episode in the history of life. This was a time when the seas first teemed with animal life, and the first recognisably 'modern' ecosystems began to take shape.
Current accounts of this explosion in animal diversity rely heavily on records from fossilised shells and other hard parts, since these structures are the most likely to survive as fossils. However, since most marine animals are 'soft-bodied' this represents only a small fraction of the total diversity.
Also important is that these fossils date earlier than the Burgess Shale by 10 million years (518 million instead of 508 million), and yet are recognizable as the same animals. This indicates that the Cambrian animals had a global distribution at the time they were fossilized. The same animals are found many thousands of miles apart on three continents.
Instead of the large, articulated fossils from China and Canada, those at the Greenland sites are made up of tiny fragments. So rich were the deposits, they often found 100 specimens in a 50-gram sample.
A team of palaeontologists from Uppsala (Ben Slater, Sebastian Willman, Graham Budd and John Peel) used a low-manipulation acid extraction procedure to dissolve some of these less intensively cooked mudrocks. To their astonishment, this simple preparation technique revealed a wealth of previously unknown microscopic animal fossils preserved in spectacular detail.
Most of the fossils were less than a millimetre long and had to be studied under the microscope. Fossils at the nearby Sirius Passet site typically preserve much larger animals, so the new finds fill an important gap in our knowledge of the small-scale animals that probably made up the majority of these ecosystems. Among the discoveries were the tiny spines and teeth of priapulid worms — small hook shaped structures that allowed these worms to efficiently burrow through the sediments and capture prey. Other finds included the tough outer cuticles and defensive spines of various arthropods, and perhaps most surprisingly, microscopic fragments of the oldest known pterobranch hemichordates — an obscure group of tube-dwelling filter feeders that are distant relatives of the vertebrates. This group became very diverse after the Cambrian Period and are among some of the most commonly found fossils in rocks from younger deposits, but were entirely unknown from the early Cambrian. This new source of fossils will also help palaeontologists to better understand the famously difficult to interpret fossils at the nearby Sirius Passet site, where the flattened animal fossils are usually complete, but missing crucial microscopic details.
Our report of early Cambrian pterobranch fragments confirms this hypothesis [of early origin], and their potential affinities to Graptolithina also suggest that the divergence and radiation of the pterobranch clades containing cephalodiscids and graptolites had a somewhat deeper, early Cambrian origin.
"The sheer abundance of these miniature animal fossils means that we have only begun to scratch the surface of this overlooked resource, but it is already clear that this discovery will help to reshape our view of the non-shelly animals that crawled and swam among the early Cambrian seas more than half a billion years ago," says Sebastian Willman, researcher at the Department of Earth Sciences, Uppsala University.
In 2013, U.C. Berkeley paleontologist Charles Marshall published a critique of Darwin's Doubt in the journal Science that Stephen Meyer considered the first critical review to actually address the main argument in the book: the inability of standard evolutionary mechanisms to explain the origin of morphological novelty in the Cambrian period. Meyer wrote a four-chapter response to Marshall in the follow-up book, Debating Darwin's Doubt (2015).
Late last year, Marshall wrote an article in Science (November 29, 2017) called "A tip of the hat to evolutionary change," in which he reviewed another paper in the same issue that claims to reveal "an unexpectedly simple pattern of driver action in peak evolutionary success." That paper by Žliobaitė et al concludes from the fossil record of herbivorous mammals that species rise toward success and decline toward extinction in a "hat shape" graph (thus his title). In passing, Marshall admits that "one of the challenges of studying evolution … is the hierarchical structure of the evolutionary process." What drives innovation: abiotic (environmental) processes or biotic processes, like competition? How do they work together? How simple is the rise to "evolutionary success"?
Though only peripherally related to evolutionary processes in the Cambrian explosion, Marshall's article shows what he thinks these days about the origin of biological novelty. Old-fashioned Darwinian competition is a driver of extinction, he agrees, but what drives innovation?
The results of Žliobaitė and colleagues' work also provide insight into the drivers of evolutionary innovation. The authors' data for North America and Europe show that, although both biotic and abiotic factors contribute roughly equally to genus origination rates, neither contribution is statistically significant. As the authors note, this provides evidence that evolutionary innovation is not driven by biotic or abiotic external changes. Instead, the data support the idea that evolutionary innovation is influenced by intrinsic factors — the less-predictable origin of the 'right' variants at the right time, able to exploit either existing or new resources.
This statement indicates that nothing much has changed in his thinking. It appears Marshall still has no better tool for innovation than lucky mutations that just happen to arrive at the right time to be exploited. How this solution can possibly address the "hierarchical structure of the evolutionary process" leading to body plans with hierarchical levels of morphological innovation seems lost in academic jargon and generalizations.
The Greenland fossils are observational facts. Graham Budd's team in that cold, remote, northern wasteland could look at those cold, hard facts under a microscope, seeing complexity that shouldn't be there by any unguided natural process. If Charles Marshall had a better mechanism for innovation than sheer dumb luck, he has had years to announce it. Until and unless he does, Meyer's thesis remains unchallenged: only intelligent design can account for the functional hierarchical organization revealed by the Cambrian animals.
Photo: Location in Greenland where fossils were found, by John S. Peel, via Uppsala University.


Just to inform you that Alliance is organizing a new project for dancers.
This project aims to be a platform for contemporary dancers (and traditional!) in Bangalore.
If you are a dancer yourself, or interested in movement, and that you want to share it with others: COME!
Maja will develop a contemporary dance technique based on building up the posture and integrating breath with the movement. Different modern and contemporary dance techniques will be used for better integration into the body mechanics and quality of movement. Classes will consist of combined stand-up exercises and the floor work which leads towards the improvisation sections and guided, yet free exploration of practiced material. We will create instant compositions that will be set and presented as a fixed material.
Eligibility: Professional dancers, amateurs with good experience in movement, artists interested in movement.
Maja Drobac has BaDance diploma from The Theatreschool in Amsterdam. She has been trained in Laban technique at School for Contemporary dance of Ana Maletić in Zagreb, Croatia, in Cunningham, Limon, Graham, Release and other contemporary dance techniques at AHK in Amsterdam, and Dunham and Horton techniques in Zagreb (Cro) and Toronto (CA).
She has done her internship with Magpie Music Dance Company, improvisation based company from Amsterdam, and she has done many workshops with different dance and theatre artists.
In partnership with Kalari Academy of Performing Arts.
The registration fee for this workshop is Rs. 300/- per session.To register please contact Marjory Dupres at 9535026419 or Veena Basavarajaiah at 08050821839.
In this session, we will tune as much into our bodies, as to what and who we meet in form of others and shifting spaces. We will explore how we can inspire each other to move into the moment, and how we are affected by changing environments. Our tool?... IMPROVISATION!!!.. and how we compose the now.
Christopher Lechner works as a performer with an emphasis on Labs and experiments with the body and light. He trained classically in Stuttgart and was a solo performer with the Hamburg, Zuerich and Stuttgart Ballets. Since working independently, his approach to work combines Visual arts with New Dance techniques, Physical Awareness, Training,Theatre, Voice and Movement, Deep Tissue -Structural work, Yoga and Martial Arts. In 2000, he was invited by Attakkalari and started working in India every year.


Some big news for fans of video game movies. Ubisoft announced that it is in the middle of making a movie based on Watch Dogs. It was also announced that the PS4 will get Watch Dogs 2 DLC first.
Ubisoft is confident that the Assassin's Creed movie will do well that it feels Watch Dogs will make a good fit in the film industry. Little is known about the movie yet, but presenter Aisha Tyler wanted Michael B. Jordan to be the lead actor.
As for Watch Dogs 2, it was revealed that the PS4 version of the game will get DLC 30 months before Xbox One and PC owners. Ubisoft did a deal with Sony in order to make this happen. If you love Watch Dogs, you might want to buy it on PS4.
Hopefully the movie can do well. Video game movies have been a mixed bag in 2016. Warcraft is doing well in China, but nowhere else. Not to mention critics hated it, but the fans have been a little more kinder to it. Watch Dogs 2 is out in November while no release window has been revealed for the movie.


text:
Valeriu Pleşca (born 8 November 1958) is a Moldovan lawyer and politician. He served as Minister of Defense of Moldova between 29 December 2004 and 11 June 2007.

Notes

External links
 VIP Magazin, VALERIU PLEŞCA. Un civil la apărare
 The official Site of the Ministry of Defense

1958 births
Living people
Moldovan Ministers of Defense
Moldovan economists
Moldovan lawyers

redpajama_set_name: RedPajamaWikipedia


text:
Q: Unable to access ID property from a datastore entity Using Google App Engine SDK and Python, I'm facing an issue : I'm unable to access the ID property of a given entity properties. The only properties I can access are those defined in my class Model, plus the key property (see answer below) :
class Question(db.Model):
    text = db.StringProperty()
    answers = db.StringListProperty()
    user = db.UserProperty()
    datetime = db.DateTimeProperty()

I can access text, answers, user, datetime and key properties just fine. However, I can't access the ID property.
For example, after fetching all entities (using Question.all()) :
# OK Within a template, this will return a string :
{{ question.text }}
# OK, this will return the entity key :
{{ question.key }}

# KO this will return nothing :
{{ question.id }}

Any ideas ? Thanks !

A: I just found a possible (inelegant, IMO) solution. After querying and fetching entities, loop through all of them and manually add the id parameter :
query = Question.all()
questions = query.fetch(10)

# Add ID property :
for question in questions:
    question.id = str(question.key().id())

I don't think it's efficient CPU wise, but it works as a quick/dirty fix.

A: According to the documentation, there is no id() instance method defined for Model subclasses.
Try {{ question.key }} instead.
Also note that the key is not created until the entity is saved to the datastore.

Edit:  more info based on OP's edit:
Since we're really after the numeric ID, we could do something like this in our template:
{{ question.key.id }}
Another note:  you should never expect numeric IDs to increase in value corresponding with the order of entity creation.  In practice, this is usually—but not always—the case.


text:
Q: Punctuation of sentence ending with the word "period" for emphasis I really enjoyed The Dark Knight Rises and want to send a grammatically correct tweet about it. Unfortunately correct punctuation of the following eludes me:

In other news The Dark Knight Rises was better than The Dark Knight.
  Not just a good super hero or action movie just a great movie, period.

What is the correct punctuation before the word "period?" Am I correct in using a comma or should an ellipsis or emdash be used instead?

A: I think you've punctuated it correctly, period.
NOAD agrees with us:

Macmillan lists this usage as a third meaning of the word, with the qualifier SPOKEN:

A:
In other news The Dark Knight Rises was better than The Dark Knight. Not just a good super hero movie or a good action movie, but a great movie, period.

It's still not grammatically correct as a whole, but it's good for every day language.

A: When ending a thought with the word period for emphasis, you can precede it with a comma followed by the word period and then a period to end the sentence, OR you could end the first sentence without emphasis and a period, and then start a new one-word sentence with the word period capitalized and then a period for punctuation.
Examples:

I think you've punctuated it correctly, period.
  I think you've punctuated it correctly. Period.
You are not going out tonight, period.
  You are not going out tonight. Period.
He is the sole owner of the trademark, period.
  He is the sole owner of the trademark. Period.

A: In other news, The Dark Knight Rises was better than The Dark Knight. Not just a good super-hero movie, or a good action movie—a good movie, period.


text:
Other Article Types
PLOS Medicine publishes research and commentary of general interest with clear implications for patient care, public policy or clinical research agendas.
Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
Dariush Mozaffarian ,
* E-mail: dmozaffa@hsph.harvard.edu
Affiliations Division of Cardiovascular Medicine and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America, Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, United States of America
Renata Micha,
Affiliation Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America
Sarah Wallace
Dariush Mozaffarian,
https://doi.org/10.1371/journal.pmed.1000252
Dariush Mozaffarian Renata Micha Sarah Wallace
Reduced saturated fat (SFA) consumption is recommended to reduce coronary heart disease (CHD), but there is an absence of strong supporting evidence from randomized controlled trials (RCTs) of clinical CHD events and few guidelines focus on any specific replacement nutrient. Additionally, some public health groups recommend lowering or limiting polyunsaturated fat (PUFA) consumption, a major potential replacement for SFA.
Methods and Findings
We systematically investigated and quantified the effects of increased PUFA consumption, as a replacement for SFA, on CHD endpoints in RCTs. RCTs were identified by systematic searches of multiple online databases through June 2009, grey literature sources, hand-searching related articles and citations, and direct contacts with experts to identify potentially unpublished trials. Studies were included if they randomized participants to increased PUFA for at least 1 year without major concomitant interventions, had an appropriate control group, and reported incidence of CHD (myocardial infarction and/or cardiac death). Inclusions/exclusions were adjudicated and data were extracted independently and in duplicate by two investigators and included population characteristics, control and intervention diets, follow-up duration, types of events, risk ratios, and SEs. Pooled effects were calculated using inverse-variance-weighted random effects meta-analysis. From 346 identified abstracts, eight trials met inclusion criteria, totaling 13,614 participants with 1,042 CHD events. Average weighted PUFA consumption was 14.9% energy (range 8.0%–20.7%) in intervention groups versus 5.0% energy (range 4.0%–6.4%) in controls. The overall pooled risk reduction was 19% (RR = 0.81, 95% confidence interval [CI] 0.70–0.95, p = 0.008), corresponding to 10% reduced CHD risk (RR = 0.90, 95% CI = 0.83–0.97) for each 5% energy of increased PUFA, without evidence for statistical heterogeneity (Q-statistic p = 0.13; I2 = 37%). Meta-regression identified study duration as an independent determinant of risk reduction (p = 0.017), with studies of longer duration showing greater benefits.
These findings provide evidence that consuming PUFA in place of SFA reduces CHD events in RCTs. This suggests that rather than trying to lower PUFA consumption, a shift toward greater population PUFA consumption in place of SFA would significantly reduce rates of CHD.
Please see later in the article for the Editors' Summary
Citation: Mozaffarian D, Micha R, Wallace S (2010) Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLoS Med 7(3): e1000252. https://doi.org/10.1371/journal.pmed.1000252
Academic Editor: Martijn B. Katan, Vrije Universiteit Amsterdam, Netherlands
Received: October 27, 2009; Accepted: February 18, 2010; Published: March 23, 2010
Copyright: © 2010 Mozaffarian et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: Supported by the National Heart, Lung, and Blood Institute, NIH (R01-HL-085710-01) and a Searle Scholar Award from the Searle Funds at the Chicago Community Trust. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Competing interests: DM: Research grants to study the effects of dietary factors on cardiovascular diseases from the US National Institutes of Health; the Searle Scholar Award from the Searle Funds at The Chicago Community Trust; the Genes and Environment Initiative at the Harvard School of Public Health; the Gates Foundation/World Health Organization Global Burden of Diseases, Injuries, and Risk Factors Study; and GlaxoSmithKline, Sigma Tau, and Pronova for an investigator-initiated trial of fish oil to prevent post-surgical arrhythmia. Honoraria and travel expenses for speaking at scientific conferences and reviewing on topics related to diet and cardiovascular disease, including from the U.S. Food and Drug Administration, International Life Sciences Institute, Aramark, Unilever, SPRIM, Nutrition Impact, World Health Organization, UpToDate, and several universities and scientific organizations. No ownership, patents, stocks, advisory board membership, nor speaking board membership. RM, SW: No disclosures.
Abbreviations: %E, percent energy; CHD, coronary heart disease; CI, confidence interval; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein-cholesterol; MUFA, monounsaturated fat; PUFA, polyunsaturated fat; RCT, randomized controlled trial; RR, risk ratio; SE, standard error; SFA, saturated fat; TC, total cholesterol
Editors' Summary
Coronary heart disease (CHD) is the leading cause of death among adults in developed countries. It is caused by disease of the coronary arteries, the blood vessels that supply the heart with oxygen and nutrients. With age, inflammatory deposits (atherosclerotic plaques) coat the walls of these arteries and restrict the heart's blood supply, causing angina (chest pains that are usually relieved by rest), shortness of breath, and, if these plaques rupture or break, heart attacks (myocardial infarctions), which can reduce the heart's function or even be fatal. The key risk factors for CHD are smoking, physical inactivity, and poor diet. Blood cholesterol levels are altered by consuming dietary fats. There are three main types of dietary fats—"saturated" fatty acids (SFA) and unsaturated fatty acids; the latter can be "mono" unsaturated (MUFA) or "poly" unsaturated (PUFA). Eating SFA-rich foods (for example, meat, butter, and cheese) increases the amount of LDL-C in the blood but also increases HDL-C (the "good" cholesterol) and decreases triglycerides. Eating foods that are rich in unsaturated fatty acids (for example, vegetable oils and fatty fish) decreases the amount of LDL-C and triglycerides in the blood and also raises HDL-C.
Because of the connection between eating SFA and high blood LDL-C levels, reduced SFA consumption is recommended as a way to avoid CHD. However, the evidence from individual randomized controlled trials that have studied CHD events (such as heart attacks and CHD-related deaths) have been mixed and could not support this recommendation. Furthermore, dietary recommendations to reduce SFA have generally not specified any replacement, i.e., whether SFA should be replaced with carbohydrate, protein, or unsaturated fats. Because of their beneficial effects on blood LDL-C and HDL-C levels, PUFA could be one important replacement for SFA, but, surprisingly, some experts argue that eating PUFA could actually increase CHD risk. Consequently, some guidelines recommend that PUFA consumption should be limited or even reduced. In this systematic review (a study that uses predefined criteria to identify all the research on a specific topic) and meta-analysis (a statistical method for combining the results of several studies) of randomized controlled trials, the researchers assess the impact of increased PUFA consumption as replacement for SFA on CHD events.
What Did the Researchers Do and Find?
The researchers' search of the published literature, "grey" literature (doctoral dissertations, technical reports, and other documents not printed in books and journals), and contacts with relevant experts identified eight trials in which participants were randomized to increase their PUFA intake for at least a year and in which CHD events were reported. 1,042 CHD events were recorded among the 13,614 participants enrolled in these trials. In their meta-analysis, the researchers found that on average the consumption of PUFA accounted for 14.9% of total energy intake in the intervention groups compared with only 5% of total energy intake in the control groups. Participants in the intervention groups had a 19% reduced risk of CHD events compared to participants in the control groups. Put another way, each 5% increase in the proportion of energy obtained from PUFA reduced the risk of CHD events by 10%. Finally, the researchers found that the benefits associated with PUFA consumption increased with longer duration of the trials.
These findings suggest that the replacement of some dietary SFA with PUFA reduces CHD events. Because the trials included in this study looked only at replacing SFA with PUFA, it is not possible from this evidence alone to distinguish between the benefits of reducing SFA and the benefits of increasing PUFA. Furthermore, the small number of trials identified in this study all had design faults, so the risk reductions reported here may be inaccurate. However, other lines of evidence (for example, observational studies that have examined associations between the fat intake of populations and their risk of CHD) also suggest that consumption of PUFA in place of SFA reduces CHD risk. Thus, in the light of these findings, future recommendations to reduce SFA in the diet should stress the importance of replacing SFA with PUFA rather than with other forms of energy, and the current advice to limit PUFA intake should be revised.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000252.
The American Heart Association provides information about all aspects of coronary heart disease for patients, caregivers, and professionals, including advice on dietary fats (in several languages)
The UK National Health Service Choices Web site provides information about coronary heart disease
Eatwell, a resource provided by the UK Food Standards Agency, gives advice on all aspects of healthy eating, including fat consumption
MedlinePlus provides links to further resources on coronary heart disease and on cholesterol (in English and Spanish)
Reduction in saturated fatty acid (SFA) consumption is traditionally a major focus of dietary recommendations to reduce coronary heart disease (CHD) risk. However, effects of such a strategy on clinical CHD events are surprisingly poorly established in both randomized controlled trials (RCTs) [1]–[8] and prospective cohort studies [9]. Prior meta-analyses of RCTs have either studied the effects of very heterogeneous dietary fat interventions on very heterogeneous combinations of cardiovascular outcomes [10], or studied effects of dietary fat interventions on intermediate risk markers, such as blood lipids [11]. Furthermore, although dietary guidelines often recommend reduction in SFA consumption, such guidelines often do not highlight any specific nutrient as preferable for replacing SFA in the diet [12]–[14], implying that any macronutrient replacement (unsaturated fats, carbohydrate, or protein) will produce similar effects.
Consumption of polyunsaturated fatty acids (PUFA) lowers the total∶high-density lipoprotein cholesterol (TC∶HDL-C) ratio, perhaps the best single lipid predictor of CHD risk [15], to a greater extent than carbohydrate or any other major class of fatty acids [11]. PUFA consumption may also improve insulin resistance [16],[17] and reduce systemic inflammation [18]–[20]. These effects on risk factors suggest that PUFA may be an ideal replacement for SFA in the population. However, surprisingly, some scientists and organizations argue that consumption of n-6 PUFA, by far the predominant dietary PUFA, will actually increase CHD risk and have recommended reduced consumption [21]–[23], and the Institute of Medicine recommends only a relatively modest range of 5%–10% energy (%E) consumption from PUFA [24], limiting its plausibility as a meaningful replacement for SFA. Several controlled intervention trials have evaluated whether increasing PUFA consumption, as replacement for SFA, impacts risk of CHD events but results of these trials have been inconsistent, with the majority of studies demonstrating no significant benefits [1]–[8]. Thus, the demonstration of whether replacing SFA with PUFA affects CHD outcomes and, if so, the direction and magnitude of this effect are surprisingly understudied matters of scientific and public health importance. To investigate and quantify this effect, we performed a systematic review and meta-analysis of randomized controlled clinical trials that assessed the impact of increased PUFA consumption, as replacement for SFA, on CHD endpoints.
We followed the Quality of Reporting of Meta-analyses (QUOROM – now PRISMA (http://www.prisma-statement.org/)) [25] guidelines throughout the design, implementation, analysis, and reporting of this meta-analysis (see Text S1 for PRISMA Statement).
We searched for all RCTs that randomized adults to increased total or n-6 PUFA consumption for at least 1 year without other major concomitant interventions (e.g., blood pressure or smoking control, other multiple dietary interventions, etc.), had an appropriate control group without this dietary intervention, and reported (or had obtainable from the authors) sufficient data to calculate risk estimates with standard errors for effects on occurrence of "hard" CHD events (myocardial infarction, CHD death, and/or sudden death). Studies were excluded if they were observational or otherwise nonrandomized; tested mainly n-3 (rather than total or n-6) PUFA interventions or evaluated only intermediate (e.g., lipid levels) or "soft" (e.g., angina) CHD endpoints; or were commentaries, reviews, or duplicate publications from the same study. We did not restrict to primary or secondary prevention trials, but included this as a prespecified factor for assessment of heterogeneity. We included both feeding trials and trials that utilized dietary advice; for both designs, the average change in PUFA consumption was assessed. Searches were performed of literature published through June 2009 using MEDLINE, Embase, AGRIS, AMED, HMIC, PsycINFO, Cochrane library, Web of Knowledge, CABI, CINAHL, conference abstracts (Zetoc), Faculty of 1,000, grey literature sources (SIGLE), related articles, and hand-searching of reference lists. Authors and experts were also directly contacted to identify potentially unpublished trials and, when necessary, request missing data or clarify methods or results.
A full list of search terms for all databases is available (see Text S2 for Protocol). For example, for MEDLINE, search terms were ("Fatty Acids, Omega-6"[Mesh] OR "unsaturated fatty acid"[tiab] OR "unsaturated fatty acids"[tiab] OR "unsaturated fat"[tiab] OR "unsaturated fats"[tiab] OR "polyunsaturated fatty acid"[tiab] OR "polyunsaturated fatty acids"[tiab] OR "polyunsaturated fat"[tiab] OR "polyunsaturated fats"[tiab] OR "omega-6"[tiab] OR "linoleic"[tiab] OR "octadecadienoic acid"[tiab] OR "safflower oil"[tiab] OR "sesame oil"[tiab] OR "soybean oil"[tiab] OR "soyabean oil"[tiab] OR "corn oil"[tiab]) AND ("cardiovascular diseases"[Mesh] OR "cardiovascular disease"[tiab] OR "cardiovascular diseases"[tiab] OR "heart disease"[tiab] OR "heart diseases"[tiab] OR "myocardial infarction"[tiab] OR "myocardial infarctions"[tiab] OR "heart attack"[tiab] OR "heart attacks"[tiab] OR "sudden death"[tiab] OR "sudden deaths"[tiab] OR "coronary syndrome"[tiab]) and NOT ("Fatty Acids, Omega-3"[Mesh] OR "omega-3"[tw] OR "n-3"[tw] OR "stroke"[tiab] OR "strokes"[tiab] OR "cerebrovascular accident"[tiab] OR "cerebrovascular accidents"[tiab] OR "Case Reports"[Publication Type]); limited to humans, adults, and clinical trials or RCTs; through June 2009 without other date or language limitations. For other databases, search terms followed similar concepts with variations based on the database structure.
Selection of Articles
Of 346 identified articles, 290 were excluded based upon review of the title and abstract (Figure 1). Full texts of the remaining 54 manuscripts were independently assessed in duplicate by two investigators to determine inclusion/exclusion. Forty-six studies were excluded because they did not meet inclusion and exclusion criteria (Table S1). The independent duplicate inclusion/exclusion adjudications were 96% concordant on initial comparison. The rare differences were resolved by group consultation among all investigators, with unanimous consensus.
Figure 1. Results of the systematic search strategy and study selection process.
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For each of the final identified trials, data were extracted independently and in duplicate by two investigators, including years the study was performed and reported, population characteristics, control and intervention diets, duration of follow-up, numbers and types of first CHD events during follow-up, risk ratios (RRs), and standard errors (SEs) of these estimates. When the latter were not available, they were directly calculated using binomial tests of proportions, given that most studies reported RRs rather than incidence rates; stronger findings were seen if SEs were directly calculated using person-time at risk for two reports using incidence rates (unpublished data). Differences in data extracted or quality assessment scores between investigators were very unusual and were resolved by consensus. Several different criteria have been proposed for judging quality of randomized trials in meta-analyses, although the validity and utility of different quality scores has been debated [26]. We assessed study quality using the validated Jadad scale [27], which includes criteria relating to randomization, blinding, and withdrawals and dropouts that are together summed to generate an overall quality score between 0 and 5. Following prior precedent [27], quality scores of 0–2 indicated lower-quality trials, and quality scores of 3–5 indicated higher-quality trials.
The overall pooled effect was calculated using random effects meta-analysis, which accounts for heterogeneity in treatment effects among studies, using the methods of Dersimonian and Laird [28] with inverse-variance (SE) weighting. Heterogeneity between studies was evaluated using the Dersimonian and Laird Q-statistic, the I2 statistic, and meta-regression [28],[29]. Potential for publication bias was assessed by visually inspecting a funnel plot of the treatment effect versus SE [30] and statistically using the Begg adjusted-rank correlation test [31]. Prespecified potential sources of heterogeneity were explored using stratified inverse-variance weighted random effects meta-analysis and inverse-variance weighted metaregression, including trial duration (< or ≥ median for all trials), study population (primary versus secondary prevention), and overall quality score (0–2 versus 3–5). We also performed post-hoc secondary analyses for CHD mortality alone and total mortality, as well as based on selected study characteristics, such as enrollment design (excluding trials with open enrollment), extent of blinding, and type of dietary intervention (provision of meals versus dietary advice). Analyses were performed using STATA 10.1 (College Station, TX), with two-tailed alpha <0.05.
The identified RCTs included a total of 1,042 CHD events among 13,614 participants (Table 1) [1]–[8],[32]–[34]. Average PUFA consumption ranged from 4.0%E to 6.4%E (weighted mean 5.0%E) in the control groups and from 8.0%E to 20.7%E (weighted mean 14.9%E) in the intervention groups. Diet was assessed in the majority of trials by either direct analysis of provided foods or by multiple-day weighed diet records. Four trials evaluated secondary prevention populations, three trials evaluated primary prevention populations, and one trial evaluated a mixed population of individuals with and without established CHD. Many of the trials had design limitations, such as single-blinding, inclusion of electrocardiographically defined clinical endpoints, or open enrollment. All trials utilized blinded endpoint assessment. Quality scores were in the modest range and relatively homogeneous: all trials had quality scores of either 2 or 3. Combining all trials, the pooled risk reduction for CHD events was 19% (RR = 0.81, 95% CI 0.70–0.95, p = 0.008) (Figure 2). Statistical evidence for substantial between-study heterogeneity was not present (Q-statistic p = 0.13; I2 = 37%). In evaluating potential for publication bias, the trial by Watts et al. [8] was clearly a potential outlier both in terms of sample size and risk reduction. Excluding this trial, there was little change in the overall pooled result: RR = 0.82, 95% CI 0.70–0.95; p heterogeneity = 0.11, I2 = 42%. Visual inspection of the resulting funnel plot indicated some potential for publication bias (Figure S1), with a borderline Begg's test (continuity corrected p = 0.07), although such determinations are limited when the number of studies is relatively small.
Figure 2. Meta-analysis of RCTs evaluating effects of increasing PUFA consumption in place of SFA and occurrence of CHD events.
Table 1. RCTs testing the effect on CHD events of increasing PUFA consumption in place of SFA.
https://doi.org/10.1371/journal.pmed.1000252.t001
Weighted by the inverse-variance of each trial, the mean increase in PUFA consumption in the intervention group, compared to the control group, was 9.9%E, corresponding to a risk reduction for each 5%E greater PUFA consumption of 10% (RR = 0.90, 95% CI 0.83–0.97). Weighted by the inverse-variance of each trial, the mean decrease in blood total cholesterol (TC) levels in the intervention group, compared to the control group, was 0.76 mmol/l (29 mg/dl), corresponding to an observed risk reduction of 24% for each 1 mmol/l reduction in TC (RR = 0.76, 95% CI = 0.62–0.93).
The median duration of all trials was 4.25 years. Among the four trials with duration <4.25 years, the pooled RR was 0.91 (95% CI 0.76–1.10). Among the four trials with duration ≥4.25 years, the pooled RR was 0.73 (95% CI 0.61–0.87). In the four trials that evaluated exclusively or predominantly primary prevention populations, the pooled RR was 0.76 (95% CI 0.55–1.04). In the four trials that evaluated secondary prevention populations, the pooled RR was 0.84 (95% CI 0.72–0.98). For the six trials with a quality score of 2, the pooled RR was 0.78 (95% CI 0.66–0.91); for the two trials with a quality score of 3, the pooled RR was 0.91 (95% CI 0.63–1.31). Evaluating each of these potential sources of variation together in a metaregression model, study duration (p = 0.016), but not primary versus secondary prevention (p = 0.71) nor quality score (p = 0.78), was identified as a significant independent determinant of the extent of risk reduction. For each additional year of study duration, PUFA consumption lowered the relative risk of CHD events by an additional 9.2% in the intervention group (95% CI 1.7%–16.8%), compared with the control group. In secondary analyses restricted to CHD mortality alone (855 events, including 312 events from the full mortality report of one trial [34]), the pooled RR was 0.80 (95% CI 0.65–0.98). Evaluating total mortality due to all causes (2,472 events), the pooled RR was 0.98 (95% CI 0.89–1.08).
The overall pooled result for CHD events was not substantially altered in post-hoc secondary analyses based on specific study design characteristics. For example, excluding the three reports (two trials) with open enrollment, the overall pooled RR was 0.83 (95% CI 0.72–0.95, p = 0.006). Excluding the Finnish mental hospital trial (two reports) that used a cluster-randomization design, the overall pooled RR was 0.87 (95% CI 0.76–1.00, p = 0.05). Only two trials were double-blind; restricting to these two studies, the pooled RR was 0.91 (95% CI 0.63–1.31), with wide confidence intervals indicative of limited statistical power. Restricting to the four reports that provided meals (i.e., that were feeding trials), the pooled RR was 0.76 (95% CI 0.55–1.04, p = 0.08). Restricting to the four trials that provided mainly dietary advice, the pooled RR was 0.84 (95% CI 0.72–0.98, p = 0.03). None of these subgroup analyses were significantly different from the main pooled result, as demonstrated by the 95% CIs in each subgroup analysis including the value of the main pooled RR estimate of 0.81.
In this meta-analysis of RCTs, increasing PUFA consumption as a replacement for SFA reduced the occurrence of CHD events by 19%; each 5%E greater PUFA consumption reduced CHD risk by 10%. Whereas nearly all these trials were insufficiently powered to detect a significant effect individually, the pooled results demonstrate a significant benefit of replacing PUFA for SFA on clinical CHD events. Thus, this is only the second dietary intervention, together with consumption of long-chain omega-3 fatty acids (fish oil) [7],[35]–[37], that has now been clearly demonstrated to reduce cardiovascular events in RCTs.
In short-term feeding trials, each 5%E of PUFA replacing SFA lowers low-density lipoprotein cholesterol (LDL-C) by 10 mg/dl, without an appreciable reduction in HDL-C, producing a lowering of the TC∶HDL-C ratio by 0.16; this can be compared to no significant change in the TC∶HDL-C ratio when SFA is replaced by carbohydrate [11]. In observational studies of adults aged 40–59 y, each 1 unit lower TC∶HDL-C is associated with 44% lower risk of CHD [15]. Based on these two sets of data, a 5%E increase in PUFA replacing SFA would be predicted, based on TC∶HDL-C effects alone, to reduce occurrence of CHD by 9% (Figure 3). Thus, the 10% risk reduction for a 5%E increase in PUFA replacing SFA demonstrated in the present meta-analysis of RCTs of clinical CHD outcomes is remarkably consistent with effects that would be predicted based on extension of the demonstrated lipid changes in short-term intervention trials to epidemiologic associations between TC∶HDL-C and CHD risk. A slightly greater risk reduction in studies of CHD events, compared with predicted effects based on lipid changes alone (Figure 3), is consistent with potential additional benefits of PUFA on other nonlipid pathways of risk such as insulin resistance [16],[17] and systemic inflammation [18]–[20]. Indeed, the impact of these additional benefits may be underestimated—the inevitable noncompliance in long-term dietary trials would attenuate true benefits, suggesting that the 10% risk reduction for a 5%E increase in PUFA in the present analysis may underestimate the full effects. Additionally, our analysis of heterogeneity indicates that longer-term trials showed greater benefits, suggesting that benefits of increasing PUFA consumption accrue over time.
Figure 3. Effects on CHD risk of consuming PUFA, carbohydrate, or MUFA in place of SFA.
Predicted effects are based on changes in the TC∶HDL-C ratio in short-term trials (e.g., each 5%E of PUFA replacing SFA lowers TC∶HDL-C ratio by 0.16) [11] coupled with observed associations between the TC∶HDL-C ratio and CHD outcomes in middle-aged adults (each 1 unit lower TC∶HDL-C is associated with 44% lower risk of CHD) [15]. Evidence for effects of dietary changes on actual CHD events comes from the present meta-analysis of eight RCTs for PUFA replacing SFA and from the Women's Health Initiative RCT for carbohydrate replacing SFA (n = 48,835, ∼3%E reduction in SFA over 8 years) [39]. Evidence for observed relationships of usual dietary habits with CHD events comes from a pooled analysis of 11 prospective cohort studies [38].
When all trials were pooled, CHD risk was reduced by 24% for each 1 mmol/l reduction in TC (95% CI 7%–38%). This finding is consistent with results of observational studies of usual TC levels and CHD risk. In a pooled analysis from 61 prospective cohort studies including nearly 900,000 adults, each 1 mmol/l lower TC was associated with 28% lower risk of CHD death in adults aged 60–69 (RR = 0.72, 95% CI 0.69–0.74) and 42% lower risk of CHD death in adults aged 50–59 (RR = 0.58, 95% CI 0.56–0.61) [15], the ranges of ages included in the present trials. A comparison of our findings to those of long-term prospective observational studies of PUFA consumption is also informative. The most robust evidence to date comes from a recent report of pooled individual-level data from 11 cohort studies in America, Europe, and Israel, including 344,696 adults and 5,249 CHD events [38]. Each 5%E of greater PUFA consumption, as a replacement for SFA, was associated with 13% lower risk of CHD (RR = 0.87, 95% CI 0.77–0.97) (Figure 3). Our finding in RCTs of 10% lower risk of CHD for each 5%E of greater PUFA consumption, as a replacement for SFA, strongly supports both the causality and magnitude of these observational findings.
Because each of the RCTs in this meta-analysis tested the effects of consuming PUFA in place of SFA, the present findings cannot distinguish between potentially distinct benefits of increasing PUFA versus decreasing SFA. Thus, the present evidence alone is insufficient to conclude that increasing PUFA in place of any other nutrient will reduce CHD events. Notably, this evidence is similarly insufficient to conclude that decreasing SFA in place of any other nutrient will reduce CHD events. However, our findings indicate that a strategy of replacing SFA with PUFA is likely to reduce the occurrence of CHD.
Other lines of evidence—in particular, findings from RCTs of lipid risk factors and prospective cohort studies of CHD events—can provide insights into whether benefits may be more strongly related to reduced SFA, increased PUFA, or both. Based on either the predicted effects on TC∶HDL-C, the results of a large RCT [39], or a pooled analysis of 11 prospective cohort studies [38], replacement of SFA with carbohydrate does not lower CHD risk (Figure 3). Evidence for CHD effects of replacing SFA with monounsaturated fatty acids (MUFA) is mixed (Figure 3); randomized trials have not tested the effects of replacing SFA with MUFA. Thus, the evidence is most consistent and robust for CHD benefits when SFA is replaced with PUFA, rather than with MUFA or carbohydrate, suggesting that lower risk may be more strongly related to increased PUFA rather than decreased SFA consumption. Recent ecological studies across nations over time also support this contention, with changes in population CHD mortality being most strongly related to increased consumption of vegetable oils that contained PUFA, particularly the n-3 PUFA alpha-linolenic acid, rather than decreases in animal fats or increases in overall vegetable consumption [40]. Further studies are needed to evaluate the role of MUFA or protein as a replacement for other macronutrients on risk of CHD.
The eight trials in this meta-analysis were performed and reported with a relatively regular distribution over nearly three decades between 1968 and 1992. This broad time span could increase generalizability, and there is likely little reason to believe that the biologic effects of PUFA have changed in recent years. The use of random-effects meta-analysis allowed the pooling and estimation of overall variance of different trials that may also each be estimating a different "true" effect. All of these RCTs had blinded endpoint ascertainment that would limit the magnitude of potential differential (biased) assignment of types of events or causes of death.
Many of the identified randomized trials in our meta-analysis had important design limitations (Table 1). For example, some trials provided all or most meals, increasing compliance but perhaps limiting generalizability to effects of dietary recommendations alone; whereas other trials relied only on dietary advice, increasing generalizability to dietary recommendations but likely underestimating efficacy due to noncompliance. Several of these trials were not double-blind, raising the possibility of differential classification of endpoints by the investigators that could overestimate benefits of the intervention. One trial used a cluster-randomization cross-over design that intervened on sites rather than individuals; and two trials used open enrollment that allowed participants to both drop-in and drop-out during the trial. The methods for estimating and reporting PUFA and SFA consumption in each trial varied, which could cause errors in our estimation of the quantitative benefit per %E replacement. One of the trials also provided, in addition to the main advice to consume soybean oil, sardines to the intervention group [3], so that observed benefits may be at least partly related to marine omega-3 PUFA rather than total PUFA consumption. Several of the trials specified use of vegetable oils containing, in addition to omega-6 PUFA, small amounts of the omega-3 PUFA alpha-linolenic acid [2]–[5],[8], although additional benefits of this plant-derived omega-3, compared with seafood-derived omega-3, are not yet clearly established [41].
Given these limitations of each individual trial, the quantitative pooled risk estimate should be interpreted with some caution. Nevertheless, this is the best current worldwide evidence from RCTs for effects on CHD events of replacing SFA with PUFA, and, as discussed above, the pooled risk estimate from this meta-analysis (10% lower risk per 5%E greater PUFA) is well within the range of estimated benefits from randomized controlled feeding trials of changes in lipid levels (9% lower risk per 5%E greater PUFA) and prospective observational studies of clinical CHD events (13% lower risk per 5%E greater PUFA). The consistency of the findings across these different lines of evidence provides substantial confidence in both the qualitative benefits and also a fairly narrow range of quantitative uncertainty.
As in any meta-analysis, publication bias is a potential limitation. It seems unlikely that large dietary clinical trials would have been performed and not reported without any knowledge of the community of experts, and if smaller trials were performed and unpublished, their addition would be unlikely to substantially alter the pooled risk estimate given the numbers of subjects and events currently included. Additionally, our direct contact with experts minimized the possibility of missing unpublished studies. The findings of this meta-analysis cannot be extrapolated to effects of replacing SFA with carbohydrate or MUFA (Figure 3), which were not evaluated in the present trials. Results should also not be extrapolated to effects of increasing PUFA as replacement for carbohydrate, although based on changes in TC∶HDL-C in feeding studies [11], and observed relationships with clinical events in cohort studies [38],[42], one would predict CHD benefit from such replacement. Future trials should investigate these other dietary interventions, in particular increasing PUFA consumption as a replacement for carbohydrate and also MUFA.
This current meta-analysis of RCTs of clinical CHD events, together with consistent findings from both prospective cohort studies of clinical CHD events and RCTs of intermediate risk factors, provides strong concordant evidence that consumption of PUFA, in place of SFA, lowers CHD risk. Our findings have several immediate implications. First, our results, together with data from other research paradigms discussed above, indicate that evidence-based population- and individual-level recommendations to reduce SFA consumption should specify the importance of replacement with PUFA. Second, because many of these trials used vegetable oils containing small amounts of plant-derived n-3 PUFA in addition to omega-6 PUFA, our findings as well as those of ecologic studies [40] would support focus on n-3 PUFA-containing vegetable oils, such as soybean or canola, to increase population PUFA intake. For example, daily consumption of 20 g soybean oil or 30 g canola oil, as an isocaloric replacement for other macronutrients, would increase PUFA consumption by ∼5%E on a 2000 kcal/d diet [43]. Third, our findings demonstrate reductions in CHD events, and no evidence for increased risk, in long-term trials utilizing PUFA consumption at very high levels (mean = 14.9%E, range 8.0%E –20.7%E). This suggests that current recommendations for an upper limit of PUFA consumption at 10%E [12]–[14] need to be revisited, particularly as PUFA appears to be the primary evidence-based replacement for SFA. Finally, whereas on a population-level even a small shift from SFA to PUFA consumption would produce meaningful reductions in CHD risk, the relatively modest magnitude of plausible benefit (∼10% lower risk for 5%E replacement) indicates a need for substantial policy focus on other dietary risk factors for CHD [44], in particular high consumption of salt and low consumption of seafood, whole grains, fruits, and vegetables.
Figure S1.
Funnel plot of the log-relative risks (beta) versus their standard error (s.e. of beta).
https://doi.org/10.1371/journal.pmed.1000252.s001
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Text S1.
PRISMA statement.
(0.08 MB DOC)
Table S1.
List of excluded studies.
ICMJE criteria for authorship read and met: DM RM SW. Agree with the manuscript's results and conclusions: DM RM SW. Designed the experiments/the study: DM RM SW. Analyzed the data: DM. Collected data/did experiments for the study: DM RM SW. Wrote the first draft of the paper: DM. Contributed to the writing of the paper: DM RM SW.
1. Dayton S, Pearce ML, Goldman H, Harnish A, Plotkin D, et al. (1968) Controlled trial of a diet high in unsaturated fat for prevention of atherosclerotic complications. Lancet 2: 1060–1062.
2. Medical Research Council (1968) Controlled trial of soya-bean oil in myocardial infarction. Lancet 2: 693–699.
3. Leren P (1970) The Oslo diet-heart study. Eleven-year report. Circulation 42: 935–942.
4. Turpeinen O, Karvonen MJ, Pekkarinen M, Miettinen M, Elosuo R, et al. (1979) Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study. Int J Epidemiol 8: 99–118.
5. Miettinen M, Turpeinen O, Karvonen MJ, Pekkarinen M, Paavilainen E, et al. (1983) Dietary prevention of coronary heart disease in women: the Finnish mental hospital study. Int J Epidemiol 12: 17–25.
6. Frantz ID Jr, Dawson EA, Ashman PL, Gatewood LC, Bartsch GE, et al. (1989) Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey. Arteriosclerosis 9: 129–135.
7. Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, et al. (1989) Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet 2: 757–761.
8. Watts GF, Lewis B, Brunt JN, Lewis ES, Coltart DJ, et al. (1992) Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas' Atherosclerosis Regression Study (STARS). Lancet 339: 563–569.
9. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM (2010) Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. [Epub ahead of print, January 13].
10. Hooper L, Summerbell CD, Higgins JP, Thompson RL, Capps NE, et al. (2001) Dietary fat intake and prevention of cardiovascular disease: systematic review. Bmj 322: 757–763.
11. Mensink RP, Zock PL, Kester AD, Katan MB (2003) Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 77: 1146–1155.
12. U.S. Department of Health and Human Services. U.S. Department of Agriculture (2005) Dietary Guidelines For Americans 2005.
13. Dietary Guidelines Advisory Committee (2005) 2005 Dietary Guidelines Advisory Committee Report. U.S. Department of Health and Human Services. U.S. Department of Agriculture.
14. World Health Organization, FAO (2003) Diet, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO expert consultation (Report 916). Geneva: World Health Organization.
15. Lewington S, Whitlock G, Clarke R, Sherliker P, Emberson J, et al. (2007) Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. Lancet 370: 1829–1839.
16. Summers LK, Fielding BA, Bradshaw HA, Ilic V, Beysen C, et al. (2002) Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity. Diabetologia 45: 369–377.
17. Salmeron J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, et al. (2001) Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr 73: 1019–1026.
18. Pischon T, Hankinson SE, Hotamisligil GS, Rifai N, Willett WC, et al. (2003) Habitual dietary intake of n-3 and n-6 fatty acids in relation to inflammatory markers among US men and women. Circulation 108: 155–160.
19. De Caterina R, Liao JK, Libby P (2000) Fatty acid modulation of endothelial activation. Am J Clin Nutr 71: 213S–223S.
20. Ferrucci L, Cherubini A, Bandinelli S, Bartali B, Corsi A, et al. (2006) Relationship of plasma polyunsaturated fatty acids to circulating inflammatory markers. J Clin Endocrinol Metab 91: 439–446.
21. Hamazaki T, Okuyama H (2003) The Japan Society for Lipid Nutrition recommends to reduce the intake of linoleic acid. A review and critique of the scientific evidence. World Rev Nutr Diet 92: 109–132.
22. Sears B (2003) The Omega Rx Zone: The Miracle of the New High-Dose Fish Oil. New York, NY: HarperCollins.
23. Simopoulos AP (2008) The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med (Maywood) 233: 674–688.
24. Institute of Medicine (2002) Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients). Washington, D.C: The National Academies Press.
25. Moher D, Cook DJ, Eastwood S, Olkin I, Rennie D, et al. (1999) Improving the quality of reports of meta-analyses of randomised controlled trials: the QUOROM statement. Quality of Reporting of Meta-analyses. Lancet 354: 1896–1900.
26. Moher D, Jadad AR, Tugwell P (1996) Assessing the quality of randomized controlled trials. Current issues and future directions. Int J Technol Assess Health Care 12: 195–208.
27. Moher D, Pham B, Jones A, Cook DJ, Jadad AR, et al. (1998) Does quality of reports of randomised trials affect estimates of intervention efficacy reported in meta-analyses? Lancet 352: 609–613.
28. DerSimonian R, Laird N (1986) Meta-analysis in clinical trials. Control Clin Trials 7: 177–188.
29. Takkouche B, Cadarso-Suarez C, Spiegelman D (1999) Evaluation of old and new tests of heterogeneity in epidemiologic meta-analysis. Am J Epidemiol 150: 206–215.
30. Egger M, Davey Smith G, Schneider M, Minder C (1997) Bias in meta-analysis detected by a simple, graphical test. BMJ 315: 629–634.
31. Begg CB, Mazumdar M (1994) Operating characteristics of a rank correlation test for publication bias. Biometrics 50: 1088–1101.
32. Rose GA, Thomson WB, Williams RT (1965) Corn Oil in Treatment of Ischaemic Heart Disease. Br Med J 1: 1531–1533.
33. Dayton S, Pearce ML (1969) Diet high in unsaturated fat. A controlled clinical trial. Minn Med 52: 1237–1242.
34. Miettinen M, Turpeinen O, Karvonen MJ, Elosuo R, Paavilainen E (1972) Effect of cholesterol-lowering diet on mortality from coronary heart-disease and other causes. A twelve-year clinical trial in men and women. Lancet 2: 835–838.
35. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico (1999) Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Lancet 354: 447–455.
36. Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, et al. (2007) Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet 369: 1090–1098.
37. GISSI-Heart Failure Investigators (2008) Effect of n-3 polyunsaturated fatty acids in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. Lancet Aug 29. [Epub ahead of print].
38. Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Balter K, et al. (2009) Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 89: 1425–1432.
39. Howard BV, Van Horn L, Hsia J, Manson JE, Stefanick ML, et al. (2006) Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 295: 655–666.
40. Zatonski W, Campos H, Willett W (2008) Rapid declines in coronary heart disease mortality in Eastern Europe are associated with increased consumption of oils rich in alpha-linolenic acid. Eur J Epidemiol 23: 3–10.
41. Mozaffarian D (2005) Does alpha-linolenic acid intake reduce the risk of coronary heart disease? A review of the evidence. Altern Ther Health Med 11: 24–30; quiz 31, 79.
42. Oh K, Hu FB, Manson JE, Stampfer MJ, Willett WC (2005) Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the nurses' health study. Am J Epidemiol 161: 672–679.
43. Mozaffarian D, Clarke R (2009) Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils. Eur J Clin Nutr 63: Suppl 2S22–33.
44. Danaei G, Ding EL, Mozaffarian D, Taylor B, Rehm J, et al. (2009) The preventable causes of death in the United States: comparative risk assessment of dietary, lifestyle, and metabolic risk factors. PLoS Med 6: Epub 2009 Apr 2028.
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Is the Subject Area "Coronary heart disease" applicable to this article?
Is the Subject Area "Fats" applicable to this article?
Is the Subject Area "Myocardial infarction" applicable to this article?
Is the Subject Area "Vegetable oils" applicable to this article?


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