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The Leading Edge
- Copyright © 2001 Society of Exploration Geophysicists
Editor's note: The other two parts of this study—titled "Dipping salt bodies, asymmetry of amplitude response and salt peaks" and "Salt ridges and furrows, shooting orientation of acquisition"—will be published in the July and August issues of TLE.
The complex structure and high velocity contrast of salt in the Gulf of Mexico create a difficult seismic imaging problem. 3-D prestack depth migration (PreSDM) of seismic data has allowed imaging of reflectors under the salt sheets and of detached bodies of irregular shape. But 3-D PreSDM cannot fill in shadow zones below salt where little energy is reflected. Additionally, amplitude variations caused by salt structures focusing or dispersing seismic energy are usually poorly handled by 3-D PreSDM. Ray-trace modeling can clarify subsalt imaging problems, and the modeling results should be incorporated into exploration and development plans.
The modeling process involves building a computer model that includes salt shapes and velocity variations, simulating an entire 3-D seismic survey with ray-trace modeling, and sorting the data into CRP gathers. Care must be taken in building and ray tracing the model to produce amplitude results that can be compared to seismic amplitudes on subsalt reflectors.
Because of space limitations, this study will appear as a three-part article. This initial paper contains an introduction to ray-trace modeling, ray-trace methods, and examples of simple 2-D salt models. In the second part, more complex models in 2-D and 3-D will be investigated to determine effects of more complicated structures. In the final part, results of ray-traced 3-D models will indicate the effects of shooting direction relative to the structural orientation. In all cases, comparisons are made to similar salt shapes in real seismic data taken from 3-D prestack depth migration surveys in the Gulf of Mexico. This study provides insights into possible imaging anomalies based on …


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Analyst: Intel, TSMC expand foundry ties
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SAN JOSE, Calif. -- More speculation is flying about a planned news conference Monday (March 2), where Intel Corp. and Taiwan Semiconductor Manufacturing Co. Ltd. (TSMC) are set to make a strategic announcement.
''According to our checks, Taiwan Semi will initially provide Intel contract manufacturing using its 200-mm capacity,'' according to a report from FBR. ''Additionally, we do not rule out Taiwan Semi manufacturing complex system-on-a-chip (SoC) products such as Atom (with wireless communication application) that require such advanced technology nodes as 45-nm.''
Intel and TSMC are no strangers to each other. TSMC has made chipsets and other products for Intel on a foundry basis.
''Although Taiwan Semi has in the past manufactured NOR Flash for Intel (with Intel accounting for less than 5 percent of Taiwan Semi's total revenue), we expect the new partnership to span to a wide range of logic products used in the communication products with a significant volume thus dramatically increasing Intel's mix of revenues at Taiwan Semi,'' according to the report.
''We note that Intel recently announced the closure of five 200-mm fabs, located in the Philippines, Malaysia, Oregon, and Santa Clara, California,'' the report said. ''Looking ahead, we expect Intel to focus solely on 300-mm capacity at 45-/32-nm technology nodes.''

subset: commoncrawl


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This was always going to be a difficult trip, but the tough part ultimately ended up being the promise the Toronto Maple Leafs frittered away.
After a strong game in Anaheim and a surprising win in Los Angeles, the potential was there to come back with six or more points and in even more stable position in the standings.
Instead, they lost two in a row to teams chasing them, and neither game was pretty.
On Sunday, a brutal start put them down 3-0 right away in Washington doomed the rest of the game despite the Capitals looking very shaky in the win.
Two nights later, a Detroit Red Wings team that was missing nine forwards to injury and playing a huge portion of its AHL roster – Drew Miller led all forwards in ice time – hung on for a 3-2 win after some terrible decisions by Leafs defencemen.
The damage in the end was a 2-3-0 trip that also included an embarrassing loss in San Jose.
Here are a few things we learned about the Maple Leafs the past week and a half:
1. As Kessel goes, so go the Leafs
You may think that goes without saying, but the numbers are truly startling.
Phil Kessel had a great start to the trip with a goal and three points against the Ducks but was then shutout thereafter, despite a strong night against the Red Wings in putting up seven shots in Tuesday's loss.
Kessel has now gone pointless in six of his last eight games, something that was in some ways expected given how incredibly hot he and his linemates had been prior to that point.
What's concerning, however, is Toronto's record when he is blanked is 6-19-2.
The Leafs entire top line is also not strong enough defensively to compensate for when they're not producing, as evidenced by some of the shot counts with them on the ice on the trip.
2. Don't blame the goalies
So much focus was on the goaltenders on the trip, primarily because Jonathan Bernier went down with an injury midgame in Los Angeles and James Reimer had to step in.
Don't let the scores fool you though: The goalies weren't why the Leafs lost three of the five games.Toronto's tandem may have allowed 16 goals, but in a familiar refrain, that was a result of the barrage they were facing. Combined, they posted a .919 save percentage that is well above average and that should be enough to win on most nights in the NHL.
3. Toronto's D remains a huge problem
All the goals against really come back to an old problem for this team: too many Grade A chances against.
Overall, the Leafs allowed 197 shots in the five games, or just shy of 40 a night. In Washington and Detroit, many of them came on 2-on-1s, breakaways or with a man wide open alone in the slot.
The Leafs are now 26th in the NHL in goals against with an even three allowed per game, which is way up from the 2.67 allowed per game a year ago – despite better goaltending.
This is a team that continues to struggle to start well (they've been outscored 62-46 in first periods) and has trouble holding late leads, two things that point to preparation and the system put in place by the coaching staff.
4. Cody Franson has faded
But Cody Franson is struggling – and not just with his defensive play.
A key member of a first power play unit that has gone ice cold – the Leafs have only three man advantage goals and a 9.4 per cent success rate in the last 13 games – Franson has looked tentative with the puck of late and isn't factoring in on scoring plays nearly as often.
He has only 12 points in his last 34 games, including just four on the man advantage in that span, and the Leafs have been badly outshot and outscored with him on the ice.
Like everyone on the blueline since the Leafs have gone to seven D, Franson's ice time is down lately, but likely not enough. With limited mobility and sagging production, he appears best suited for only third pairing duty.
5. David Clarkson is a lost cause
No points in the last 10 games, few shots on goal, a dwindling number of minutes and generally not all that noticeable in games save for when the play stops to allow him to fight.
Tied with Joffrey Lupul with the team's second highest cap hit for a forward, he has nonetheless been outscored by 13 teammates and has the same number of points as Troy Bodie, Dave Bolland (who last played Nov. 1) and Peter Holland.
Enough said.
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Clark announced Friday that he will retire at the end of the year.
The 54-year-old Clark was first elected in 2008. In 2011 he ran against Republican Sen. Luther Olsen in a recall election but lost.
Clark is one of 39 Democrats in the Assembly. Republicans have 60 members.
Clark's district covers an area just north of Madison and includes Sauk, Columbia, Marquette, Dane, Adams and Iowa counties.


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1982's Star Trek II: The Wrath of Khan is arguably the best Star Trek film ever made (I personally prefer 1992's Star Trek VI: The Undiscovered Country). Gamers who play Star Trek Online will be able to wear Khan's uniform; all they need to do is log in to STO via Cryptics Arc client.
The downside of this uniform is that it is classified as "Off-Duty," meaning only your captain can wear it, and you cannot have an entire crew of Khan-looking augments. Kind of a bummer.
Star Trek Online's Season 8.5 is scheduled to be released tomorrow, January 30th, 2014. Fourth Anniversary festivities are scheduled to follow.


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You have a unique medical history. Therefore, it is essential to talk with your doctor about your personal risk factors and/or experience with carpal tunnel syndrome. By talking openly and regularly with your doctor, you can take an active role in your care.
General Tips for Gathering Information
Here are some tips that will make it easier for you to talk to your doctor:
Specific Questions to Ask Your Doctor
About Symptoms
About Your Risk of Developing Carpal Tunnel Syndrome
About Treatment Options
About Lifestyle Changes
About Your Outlook
National Institutes of Health website. Available at:
Occupational Safety and Health Administration website. Available at:
Last reviewed September 2012 by John C. Keel, MD
Copyright © 2010 EBSCO Publishing All rights reserved.
Still have questions? Contact firstname.lastname@example.com. We are happy to assist you!


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I've had a fair amount of Middle Eastern pizza (also spelled pitza) since moving to NYC. Sometimes it truly is a thing unto itself, with lamb, onion, garlic, and spices piled liberally atop a crisp and puffy pita dough. Other times it's been just sort of Middle Eastern-ish toppings on a dough that doesn't seem to be much different from any other regular slice-joint dough. I prefer the former.
In all my reading on pizza and flatbreads, I've never seen anyone claim definitively where flatbread originated. Flatbreads seem to have sprung up in various Mediterranean cultures around the same time — so it's interesting to note that the words pita and pizza are pretty damn close.
I've often considered doing dispatches about the Middle Eastern stuff on Slice, but I'm not sure if y'all would be into it. What do you think? Are you a fan of Middle Eastern pizza?


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From eLinux.org
Revision as of 22:39, 20 May 2010 by Xinkeqiong (Talk | contribs) (→Our Project)
Hi, My name is Keqiong "Claire" Xin. I'm now pursuing the Master Degree of Computer Engineering in Rose-Hulman. This is my user page for course ECE597 Embedded Linux.
Our Project
Our project in this course is ECE597: Auto HUD.


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A stand off between police and the suspected Toulouse shooter happened early Wednesday.
Three hundred police officers surrounded an apartment in the south of France. Police reported that shots rang out from inside of the apartment where it wounded two officers at 3:30am.
The man apparently threw a handgun out the window, but police were sure there were more guns inside.
Interior Minister Claude Gueant hoped that the man would give himself up after the standoff reached the sixth hour.
"The suspect told me — and I hope he told me the truth — that he will surrender in the afternoon," Gueant said.
Later the suspect stopped responding to police, Gueant told reporters.
According to a source, the suspect is Mohammed Merah. Gueant also said that Merah had weapons stashed in a car near the apartment.
The suspect, 24, is accused of a series of shootings in the last 10 days which killed seven people including three children.
The suspect has been confirmed as a French national of Algerian origin who spent time in Afghanistan and Pakistan.
"He claims to be a jihadist and says he belongs to al Qaeda. He wanted to avenge the Palestinian children and take revenge on the French army because of its foreign interventions," Gueant told reporters at the scene.
However, Gueant did not confirm how they got this information.
The shootings targeted minorities which put France on scarlet alert. It is the highest level in the country.
The police tracked the suspect down by using internet technology. The suspect used his brother's IP address to respond to an ad that the first victim posted.
Imad Ibn Ziaten was a paratropper and was the first victim. Police discovered that Ziaten posted an ad online to sell his scooter.
The suspect, using the brother's IP address, set an appointment with Ziaten to inspect the bike. He agreed to meet the suspect in Toulouse where he was shot and killed on March 11, according to Gueant.
Four days later, a man wearing dark clothing and a motorcycle helmet shot and killed two soldiers in the southwestern French city of Montauban. A third soldier was injured.
A man with a similar helmet driving a scooter approached a Jewish school Monday. The shooter pulled up by the school and shot a teacher and three children, two of which was his sons. The third child was the daughter of the school's director.
According to police, the same guns were used in all three attacks.
As the manhunt was launched after the shootings, police zeroed in on the apartment. It was located close to the Jewish school.
As for the bodies of the four victims, they will be buried in Jerusalem.


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An arrest has been made in the case of the I-96 shootings. A man from Wixom by the name of Raulie Wayne Casteel has been taken into custody. According to the Daily Tribune, "Casteel was charged with six counts of a combination of felonious assault, carrying with unlawful intent, felony firearms, and discharge of a […]
Tag Archives: Wixom
I'm sure it's just a coincidence, but the man thought to be the I-96 shooter appears to identify as a Tea Party activist
By Mark | November 8, 2012
Posted in Michigan, Politics, Uncategorized | Also tagged angry white men, anti-government, gun violence, guns, I-96, Kerry Bentivolio, Libertarianism, mental illness, Obama is a Socialist, paranoia, patriot movement, Raulie Wayne Casteel, Ron Paul, shooting, tea party, violence on the extreme right | 17 Comments
U.S. Military Weapons Inscribed with Secret 'Jesus' Bible Codes Thanks to Michigan Company
By Mark | January 19, 2010
You know, it really doesn't help us make the case internationally that we're not waging a holy war against Islam when our own military suppliers, without our knowledge, are doing things like adding coded Bible text to the sights affixed to every rifle going to Iraq and Afghanistan in the hards of a U.S. Marine. […]
Posted in Corporate Crime, Religious Extremism | Also tagged armaments, arms, Crusade, devout Christian arms manufacturer, Glyn Bindon, Holy War, Jesus Christ, Michael "Mikey" Weinstein, Military Religious Freedom Foundation, rifle sights, spiritually transformed firearms of Jesus Christ, Tom Munson, Trijicon, when Michigan companies fuck up | 28 Comments


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The foothills town of Golden is full of historical lore: Coors Brewery, Foss Drug, Jolly Rancher, Lookout Mountain and the Colorado School of Mines are just a few of its landmarks, come and (some) gone. Town officials have done a great job of preserving the physical remains of all that history in a collection of more than 15,000 artifacts, ranging from the eighteen-foot-long Foss Drug sign (now all thats left of the downtown fountain and drugstore) to such minutiae as dental tools used in the 1920s by Golden dentist Doc Crawford. Those items and a mother lode of other old stuff eighty or so items including a galvanized bathtub used by one of Goldens first African-Americans, a nineteenth-century melodeon and a Wells Fargo stagecoach treasure box are featured in the Golden History Museums new Show & Tell exhibition.
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View the steamer trunks and Civil War uniforms of Goldens founding families and other, less reputable figures when the show opens with a reception from 6 to 8 p.m. tonight, with standards by George Gershwin, Cole Porter and the like performed by Golden favorites Dave Rucker, Ed Stephen and Dave Powers. Or just visit the museum, 923 Tenth Street, from 10 a.m. to 4 p.m. Tuesdays through Saturdays, when admission is $4 (or $6 with combined admission to the Astor House Museum); for more information, call 303-278-3557 or go to http://goldenhistorymuseums.org.
Starts: March 25. Daily, 2010


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Sterling Silver Snowflake Pendant Necklace With Black and White Diamond Accents. 18"
★ ★ ★ ★ ★ ★ ★ ★ ★ ★
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Due to the incredible value on your Clearance selection, no additional discounts apply.
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Necklace Drop close DROP: A dangling or stationary detail which "drops" from a bale, strand or earring backing. Length:
7/8 inch
Necklace Drop Width:
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Sterling close STERLING SILVER: Also known as "Standard Silver," sterling silver is silver alloyed with other metals to increase the hardness and durability. Generally, sterling is 92.5% silver and 7.5% other metals. Some sterling silver jewelry is plated with 14kt-18kt gold and referred to as "vermeil," or "gold over sterling." Silver
Polished close POLISHED: A buffed-out finish used to produce a mirror-like shine.
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Chain Size:
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Diamond close Diamond: The hardest and most brilliant of all gemstones, a diamond can make the heart race with its pure and fiery spark. An ancient symbol of love, a diamond is the preferred gemstone for tokens of affection, such as rings, earrings, necklaces and bracelets. Diamond is the birthstone for April. (Quantity: 1, Shape & Cutting Style: Round Brilliant close BRILLIANT: A gemstone cut to enhance brilliance without sacrificing much carat weight. Typically has 58 facets. , Color Grade: H-I close Color Grade H-I: Near-colorless , Clarity: I2-I3, Weight: 0.02 carats)
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Game Designer Is Hometown Hero to Burglarized Game Store
About a week ago, burglars completely wiped out the stock of I Got Game, an independent game store in Ogdensburg, N.Y., a town of about 10,000 on the St. Lawrence River. The store hadn't even been open a month. Nothing was insured. The owner was in a daze.


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Electric vehicle technology won't sound the death knell for the locally made large cars and could even extend the life of local family favourites, says Mitsubishi.
The Japanese-owned, Adelaide based company no longer builds large cars for the Australian market after its 380 model was discontinued in 2008. But it has thrown a lifeline to its former local rivals, the Holden Commodore and Ford Falcon, by suggesting size won't matter once manufacturers begin to electrify their model ranges.
Mitsubishi Australia's vice president of corporate affairs, Paul Stevenson, says Australians will still be able to indulge their love of large cars and SUVs in the future - provided a source of clean electricity can be tapped.
"At present everyone has got it in their heads that we have to drive towards smaller cars for the environment," he says. "That means for Australians in particular, we're asking them to make lifestyle changes. We like bigger cars, we like SUVs.
"The thing about hybrid and EV technology is that it doesn't matter what size car you have, you can have an electric or a plug-in hybrid Outlander, or a Pajero. While you're driving it around in electric mode, recharging it from renewable resources, it's completely clean.
"So SUV owners, hopefully in five or six or seven years, won't be the sort of environmental vandals that some people like to make them out as."
Mitsubishi will look to bring its first plug-in hybrid vehicle – believed to based on the PX-MiEV soft-roader – into Australia in 2012.
Stevenson says Mitsubishi is keen to eventually offer the choice of a plug-in hybrid powertrain across its entire model range.
"Our longer-term strategy over this decade is to get to a point where you walk into a dealership – 'what do you want? Outlander. OK, do you want diesel, petrol or plug-in hybrid?' So it'll be just a drivetrain option that you'll have on virtually any model," Stevenson says.
Already hybrid leader Toyota has confirmed it will have hybrid versions of every model in its range by 2020, while also moving on electric vehicles.
Mitsubishi is currently installing a fast-charging point at its Adelaide plant for its all-electric fleet of i-MiEV cars. Mitsubishi Australia chief executive Masahiko Takahashi says the station will be the fastest in the southern hemisphere, capable of charging an i-MiEV to 80 per cent of its battery capacity within 30 minutes.
The company plans to roll out more fast-charge points in other capital cities, and will continue to work with governments and infrastructure providers on regular charging points.
However, Stevenson says the current lack of widespread recharging stations should not stop customers keen to buy an electric car when Mitsubishi makes the i-MiEV available to private customers next year.
"I'm not convinced that recharge infrastructure is such a big issue, especially in Australia," he says.
"As battery performance improves, the need for infrastructure reduces. I know the head of Volkswagen engineering in Germany said he expects to have an 800km range out of batteries by the end of this decade.
"At the same time in Australia we've got some huge advantages because the majority of people live in detached houses. You drive home, you plug it in overnight like a mobile phone, it charges up and you're ready to go the next day.
"We don't really have the need for an external restructuring infrastructure like they do in a lot of European, Asian and American cities where they live in apartments and don't have access to an off-street charger.
"How many petrol stations would we need if we all had a petrol bowser in our driveway? Which is essentially what we've got, we've all got fuel-up capability sitting in your driveway."


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Reports: Oregon to promote Helfrich
The University of Oregon will promote offensive coordinator Mark Helfrich to replace Chip Kelly as head coach, according to multiple reports.
The move is expected to be announced Sunday, according to CBS Sports.
Helfrich has served as the Ducks' offensive coordinator since 2009, and was expected to be promoted when Kelly initially considered leaving for the NFL shortly after the Ducks won the Fiesta Bowl against Kansas State on Jan. 3. Kelly appeared set to return to Oregon, however, before informing the school Wednesday that he had indeed decided to take the Philadelphia Eagles' head coaching job.
The school then posted a job opening for "Head Football Coach," and Stanford offensive coordinator Pep Hamilton interviewed for more than four hours this week. He has since been named the offensive coordinator for the Indianapolis coach.
With Hamilton taking over, wide receivers coach Scott Frost will be promoted to offensive coordinator, according to a report by The Register-Guard.
Oregon finished second in the national with an average of 49.6 points per game in 2012 while averaging 537.4 yards of offense.


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The Georgia Bulldogs added another commitment for 2008 this afternoon this time from defensive end Jeremy Longo from Ft. Lauderdale, Florida (Cardinal Gibbons High School). Longo had received offe...
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(At Night I Think Of You)
Chicago, IL 60607
In (At Night, I Think Of You), Aay Preston-Myint presents a series of artworks that live double lives and investigate the place of yearning in between. The show contains objects existing both as themselves but also as parodies or replicas of those things a gay pride flag that is also a sculpture of a gay pride flag (which is also a statement of utopian desire), sculpture of a cake that is also a cake sculpture (which is also a meditation on companionship), wallpaper that is also a drawing of wallpaper (which is also a drawing of a mirror that, of course, fails to reflect, but suggests a space for self reflection). This back and forth between representation and embodiment suggests Preston-Myint's desire for these works to stake a claim in the middle ground between "identity art" and formal abstraction; that is, the artist is aware of what they are, but he is also open to the investigation of their basic materials and essences. They are uncanny and familiar entries in the documentation of a personal/political moment, or collection of moments, in (a) queer life.
+ + +
Aay PrestonMyint is an artist, printmaker, and educator based in Chicago, IL, and has exhibited nationally in San Francisco, Minneapolis, Cincinnati, Memphis, and New York. He loves pie, but is less partial to cake, and similarly enjoys the beach, but not the ocean. He spends most of the day thinking about things like Futurity, Slime, Pageantry, Exploring the Possibility of Radicalizing Contemporary Queer Night Life, Body Hair, Doubt, the Problematics of Aestheticizing Community, Labor vs. Value vs. Reward, and "Projects" vs. "Objects". In addition to his own work in interdisciplinary media, he does collaborative programming with No Coast and Chances Dances, and edits an online and print journal called Monsters and Dust. He might send you a mixtape sometime if you ask nice.


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Got Questions? Join My Assisted Living Group!
I often receive emails from you readers asking for help finding furnishings, be it something specific like Bella's bedding from New Moon or general like a fun affordable rug with brown tones to match your new living room. Sometimes, you write in asking for help dealing with a stubborn problem you're having with your home, like sprucing up mirrored closet doors. To make dealing with all these queries more of a collaborative effort, I started a new CasaSugar Community group, called Assisted Living.
Assisted Living is the place for you to post all of your questions and issues, and both myself and your fellow community members can all chime in with answers and suggestions. In some cases, I may even post your question as an Ask Casa on CasaSugar! It always helps if you post photos, whether it's a screenshot of the latest episode of Gossip Girl revealing the lamp you're trying to track down, or a photo of the living room you're decorating and need a rug for.
So join Assisted Living and begin posting your questions and photos!
Photo by Joanna Moorehouse


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They arrived this morning. 300+ Gold Star Layers.
New Babies
A mob of fluff!
wow that's a lot of chicks
Wow, hope you have a nice warm place to house them. That's a lot of babes. What are Gold Star? For meat, eggs, or??
Brown eggs. About 270 eggs per hen per year.
WOW! I don't think I could think of three hundred names! ;)
I think you've told us before, but at what age do Gold Stars start to lay?
I think they are like my golden comets that I had and they start early,I want to say four or five months
About right. We are looking at late June, about the time Farmers Market gets going good. I am selling about 180 dozen a month this winter. Doing a CSA. Extras go to the local food shelf.
Wow that is a lot of babies! Very cute!
Wow, that's amazing!!! Do you buy your food in bulk? I feel like my Layena for 7 chickens is so expensive, that I can't imagine for 300. I'm curious how/where you buy the feed for a chicken farm rather than a hobbyist.
A co-op feed mill. Chick starter is $13.50 for 50 lbs. Layer feed is around 19� a pound.
Guess I'm doing better than I thought. Starter here is $10.09 for 50#s, as is 20% Layer.
Everything here is around $13.00 for a 50 pound bag, starter or layer. With the 7 chickens I go through one 50 pound bag about every 10 days, I think. It seems expensive.
Those are some greedy chickens! Of course mine free range, but mine eat about 1/3 that much.
The 200+ hens eat about a bag a day. Produce $36 a day in eggs, so not bad.
Yeah, I haven't been able to let mine free range as much......I know that affects food intake. We have a hungry owl around here. 2 fatalities in the fall. I do wish they would eat less. I'm going to try an make a larger fenced area for them this summer that has a wire "roof" so they can go out more but stay safe from the owl and/or hawks around here. Switching to pelleted food from crumble helped some, with less waste. They just seem to eat a lot. wondering if their age affects food intake? Prime egg laying age.....almost 1 year old, so I wonder if they also eat more at this age? Kind of like teenagers???
It would make sense that high production be accompanied by high feed intake.
I used to lose an occasional hen to owls. I have always had to let mine out early in the morning when owls are still a threat, so I started throwing some corn chops into the coop area when I opened the doors hoping they will stay under cover until the owls have quit for the day. So far it seems to be working.
I found that I seemed to have more losses when I let them out early. Now they have to wait until _I_ think they're safe(er). I also ran a fence between the main coops and the "woods". It won't stop anything determined, but does prevent what I think of as a running attack. Usually dogs that just come in and start killing. Of course, my most vulnerable chickens insist on foraging in the cow field, and into said woods. I'm considering a donkey....
We have a chicken group here, and someone said that he runs string across his chicken "run" and it prevents the hawks from diving down and getting his chickens. I know this wouldn't work everywhere, like when you let them out. But in runs it could work.
I myself can't let my chickens out, due to my own dogs. I have two dogs, and one loves the chickens. She sits there and stares at them, or runs around the coops. The other one is purely interested in the wild life, like rodents, squirrels.... he is never at the coops. Funny hun?
Very nice, CountryGardens. I'm assuming they are all future pullets?
They should be laying eggs by July 1. Just in time for the busy Farmers Market season. They will be added to our flock of 200 hens that are in production now.
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Adam Rushforth may leave home without his wallet, but he always remembers his phone. He told tech.lds.org that even though he is blind, having access to the scriptures through the Gospel Library mobile app is wonderful. "One of my favorite features is the diction option while searching the database," Rushforth said. "I love how easy it is to tell the phone a phrase and have the Gospel Library app give me several options where that phrase or those words are found. It searches through its entire library and organizes the results in a way that makes it fast and easy for me to find the desired reference." The Gospel Library mobile app is just one of the many new or lesser-known LDS resources available to users of all ages and abilities. As The Church of Jesus Christ of Latter-day Saints continues to grow and technology advances, so does the information to learn, teach and promote the work of the Lord.
With an LDS Account, members can have a more personalized experience and interactive study of the gospel.
Many church websites, especially LDS.org, allow you to sign in with your LDS account. When you sign in, the website can deliver more personalized information to you.
"Without an LDS Account, you're missing a huge part of the online church experience," said Tom Johnson, a technical writer for the Church. Some sites using LDS Account include New.FamilySearch.org, Calendar, Directory, Maps, YW Personal Progress and Duty to God.
To sign up for an LDS Account, go to ldsaccount.lds.org and click "Register for an LDS Account." The full sign-up process requires you to know your membership record number (MRN). You can find your MRN on your Individual Ordinance Summary (available from your ward clerk), or on your temple recommend. If you don't know your MRN, you can still register for an LDS Account, but your access will be limited until you add it.
With instant access to mobile applications, members are finding the church apps to be a fun and convenient way to view church resources. Tech-savvy teens are no exception.
In the October 2011 Semiannual General Conference, Elder David A. Bednar spoke to the youth when he said, "Your fingers have been trained to text and tweet to accelerate and advance the work of the Lord - not just to communicate quickly with your friends."
With a touch of the finger users can hear the Gospel Library app, which according to tech.lds.org, allows users to "listen to audio narrations for English scriptures, general conference addresses, magazines and some lesson material." Other apps include Bible Videos, Mormon Channel, LDS Tools, Scripture Mastery, LDS Youth, LDS Music and the Ensign. Learn more at mobile.lds.org.
When you're preparing a talk or lesson, or just studying the gospel, My Study Notebook can help you gather and organize your sources in a convenient way. To see My Study Notebook in action, sign in to LDS.org and start reading content. Look for a black toolbar in the footer. You can click buttons on this toolbar to bookmark articles or write journal entries. You can also highlight passages with your cursor. When you highlight a passage, a pop-up window appears that allows you to add notes and tags.
All your bookmarks, highlights and notes are saved in a personal, private space on LDS.org that you can access by going to Tools > My Study Notebook, or by clicking Open Notebook in the footer toolbar.
Recently, My Study Notebook was integrated into the Gospel Library app for Apple. You can now access My Study Notebook directly within the Gospel Library interface, rather than just from LDS.org. Highlights and notes you add to verses on the mobile device sync with the content in My Study Notebook on LDS.org, and vice versa.
"Learn, Share, Create" is the invitation from the LDS Media Library. The site notes that the object of the library is to "help members access different types of media, such as videos, audio and images
come unto Christ through the use of wholesome media."
According to an interview with Church News and Events, digital media producer Bret Barton said, "The idea is to allow members to visit the site to find media to use in lessons, in their homes and for missionary work." Members can use the resources in "Learn to study about the Savior." "Share" will allow users to email links to friends, share videos in a blog and use media for teaching in the home and at church. Members can also contribute their talents in the Create section of lds.org/media-library.
In December 2007, Elder M. Russell Ballard invited BYU-Hawaii students to "join the conversation by participating on the Internet to share the gospel..."
The goal of Create.lds.org does just that. Scott Olson, project manager of member engagement, said Create allows members to get "involved in sharing their media talents."
Marianne Jennings, associate producer of member engagement, added that the two-fold mission of Create is to help members share their creations and to help members share the gospel by sharing their talents.
Currently members can share their talents through photos, video, music and radio. There will be more options in the near future, including design and writing, and a new video contest was recently announced. Additional information is at Deseret News and Church News and Events.
Now everyone has the opportunity to serve, right from the convenience of a computer.
"Vineyard.lds.org provides service activities online that can be completed in minutes," noted Jayson Seegmiller, Vineyard product manager. "As a result, the church is able to share more resources worldwide."
According to the website, "Church departments break projects into small bits and submit them to Vineyard. Volunteers complete the activities online and then church departments review completed work and distribute worldwide." Some activities include contributing photos, adding image search words, translating documents, family history indexing and donations to church causes.
By giving a couple of minutes or a couple of hours of time, all can be "anxiously engaged in a good cause.
As part of the LDS Media Library, Book of Mormon Stories has been updated to include sound effects and an original soundtrack together with new parallax animation. As noted in an article by the Church News, this technique "was used to cut out two-dimensional figures and move them independently around the screen. This pseudo-3D technique allows background images to move by the camera slower than foreground images, creating an illusion of depth in 2D images."
In an interview with Church News and Events, Brent Meisinger, product manager in the Scriptures Coordination Division of the Church Curriculum Department, said, "These scriptural stories help to plant the seed of testimony in the hearts of children and others who view these videos by teaching gospel truths they will remember for the rest of their lives." The stories are available in 12 languages, on the LDS.org website and other video channels.
In an effort to provide church-approved lesson ideas to teachers and parents, the new Children's Lesson Helps website is now available.
"We felt there was quite a large demand for Primary leaders and teachers to use church-approved resources to supplement their lessons. This site provides them that opportunity," said Chad Phares, senior editor of The Friend magazine.
The website lessonhelps.lds.org includes three sections. "Resources for Primary Lessons" includes links to stories, activities and media that correspond to each lesson. "Resources by Gospel Topic" will be updated to include an alphabetical list of gospel topics. The third section, "Weekly Thoughts and Tips," includes ideas on how to share the gospel with children.
As quoted from the website: "You are doing much more than teaching a lesson - you are teaching children to know and love the Savior, and helping them to be lifelong followers of Jesus Christ."
Additional information is also available on the Church News website and Church News and Events.
Much effort has been put into creating a site that has content specific for youths. Mike Madsen, product manager of the youth.lds.org website, shared the outlook for the site.
"The youth website has three main goals: to help youth understand, live and share the basic doctrines of the Gospel of Jesus Christ; to inspire youth to live the Gospel by seeing examples of other youth around the world living gospel principles; and to give families, youth and leaders access to programs and materials that will assist youth in their personal conversion, such as Personal Progress, Duty to God, scriptures, music and videos." Madsen also said the site will continue to be improved to meet the changing needs of youths and families.
Through topics such as Youth and Family History, For the Strength of Youth and messages From Church Leaders on subjects including dating, media and entertainment, and Sabbath observance, the youth of the church will be encouraged to "Arise and Shine Forth."
The First presidency of The Church of Jesus Christ of Latter-day Saints introduced The Life of Jesus Christ Bible Videos during the 2011 Christmas devotional. President Henry B. Eyring said at that event, "The objective in that effort has been to remain true to the scriptural text. Like the scriptures which these short films on biblevideos.lds.org follow faithfully, they may seem to you quiet. Your faith and the Holy Ghost will create the emotion these world-changing events deserve."
Over 100 videos are planned and will be available online free of charge. The videos, based on the King James Version of the Bible, are also available as a free mobile app and in many other popular channels (YouTube, iTunes, ROKU, etc).
Do you ever wonder where in the world the brethren are? Now you can follow their travels as they go "Unto All the World." Exclusive content is posted on the Prophets and Apostles Speak Today website.
"Today, as in ancient times, prophets and apostles minister throughout the world." As available, articles and videos from their visits are posted to the site. Messages from current and past leaders are also available with new information added each week.


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Bottom three guys...
-Jason Castro
-Colton Berry
-David Hernandez
Well my initial predictions weren't completely off but Jason Castro definitely will NOT be in bottom three. I was just thinking that one of the Jason's would go bottom three, iwith my pre-performance guesses..
I know I have to change my predictions but it's tough.
I'm gonna change it to....
To be honest Jason Y., Colton, David H., and Luke easily could end up in the bottom.
I think David Cook and Robbie could easily slip through the cracks as well.
I just don't think Danny will be going home. He was pretty bad but at least he was memorable.


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What do we do?
Our FMI Computational Biology Group is located at the Friedrich Miescher Institute in Basel. We study gene regulation through the analysis and modeling of genome-wide datasets. We collaborate closely with experimental researchers on various biological topics including cancer progression and cellular differentiation. Using statistical approaches, we aim to gain a better understanding on how the different layers of epigenetic, transcriptional and post-transcriptional regulation interact and contribute to the control of gene expression. The great majority of our projects measure various aspects of gene expression including DNA methylation, single cell transcription, protein-binding to DNA, and translation using high-throughput sequencing.
Highlights 2016
In most cells, the DNA is packaged around histone proteins. However, mammalian sperm cells have a highly compacted genome, and during maturation they evict the large majority of their histone proteins from the DNA. Whether the histones that are left carry epigenetic marks and could therefore serve as a carrier for epigenetic information across generations remains an open question. In a re-analysis of published datasets, we were able to clarify former contradicting reports on the subject, which associated retained histones with repeat elements, although open questions still remain in this intriguing research field.
For more information see "Royo et al., Dev Cell, 2016"
Main publications 2016
- Habacher C, Guo Y, Venz R, Kumari P, Neagu A, Gaidatzis D, Harvald EB, Færgeman NJ, Gut H, Ciosk R. Ribonuclease-Mediated Control of Body Fat. Dev Cell. 2016; 39(3):359-369.
- Miki TS, Carl SH, Stadler MB, Großhans H. XRN2 Autoregulation and Control of Polycistronic Gene Expresssion in Caenorhabditis elegans. PLoS Genet. 2016; 12(9):e1006313.
- Eymery A, Liu Z, Ozonov EA, Stadler MB, Peters AH. The methyltransferase Setdb1 is essential for meiosis and mitosis in mouse oocytes and early embryos. Development. 2016; 143(15):2767-79.
- Royo H, Stadler MB, Peters AH. Alternative Computational Analysis Shows No Evidence for Nucleosome Enrichment at Repetitive Sequences in Mammalian Spermatozoa. Developmental Cell. 2016; 37(1):98-104.


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Although cystic fibrosis (CF) is a monogenic disease, its clinical manifestations are influenced in a complex manner. Severity of lung disease, the main cause of mortality among CF patients, is likely modulated by several genes. The mannose-binding lectin 2 (MBL2) gene encodes an innate immune response protein and has been implicated as a pulmonary modifier in CF. However, reports have been conflicting, and interactions with other modifiers have not been investigated. We therefore evaluated the association of MBL2 with CF pulmonary phenotype in a cohort of 1,019 Canadian pediatric CF patients. MBL2 genotypes were combined into low-, intermediate-, and high-expression groups based on MBL2 levels in plasma. Analysis of age at first infection with Pseudomonas aeruginosa demonstrated that MBL2 deficiency was significantly associated with earlier onset of infection. This MBL2 effect was amplified in patients with high-producing genotypes of transforming growth factor beta 1 (TGFB1). Similarly, MBL2 deficiency was associated with more rapid decline of pulmonary function, most significantly in those carrying the high-producing TGFB1 genotype. These findings provide evidence of gene-gene interaction in the pathogenesis of CF lung disease, whereby high TGF-β1 production enhances the modulatory effect of MBL2 on the age of first bacterial infection and the rate of decline of pulmonary function.
Cystic fibrosis (CF) is an autosomal-recessive disease typically manifesting with progressive obstructive lung disease, insufficiency of the exocrine pancreas, and elevated electrolyte concentration in sweat glands (OMIM 219700). Although CF is a monogenic disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, genotype-phenotype correlation studies of some manifestations suggest more complex inheritance, involving other genetic and environmental factors (1, 2). In particular, the severity of pulmonary disease, which is the major cause of morbidity and mortality in CF, is poorly correlated with CFTR genotype. Patients carrying the same CFTR mutations show extremely variable lung phenotypes at all ages. It is postulated that the severity and progression of pulmonary disease in CF is modulated by secondary genetic factors called CF modifiers (1, 3).
The hallmark of CF pulmonary disease is chronic infection with characteristic pathogens such as Pseudomonas aeruginosa, Staphylococcus aureus, and Burkholderia cepacia, which leads to chronic inflammatory damage to lung tissue and progressive loss of pulmonary function. Genetic factors that influence susceptibility to infection are therefore of major interest. One of the first genes implicated as a pulmonary modifier in CF was the mannose-binding lectin 2 (MBL2) gene (4). MBL2 produces a protein of the collectin family, a key factor in the innate immune response (5, 6). MBL2 selectively binds D-mannose and N-acetyl-D-glucosamine (GlcNAc) on bacterial surfaces and triggers MBL2-associated serine proteases (MASPs), activation of the complement pathway, and eventual phagocytosis of opsonized bacteria (7). MBL2 also regulates the secretion of cytokines: intermediate levels of MBL2 (1–5 μg/ml) trigger secretion of proinflammatory cytokines (IL-6, TNF-α, and monocyte chemoattractant protein 1), while high levels of MBL2 (>6 μg/ml) are known to repress secretion of proinflammatory cytokines and upregulate the antiinflammatory cytokine IL-10 (8, 9). On the one hand, high levels of cytokines are beneficial because they initiate pathways necessary for clearing bacterial infection, but on the other hand, they can stimulate inflammatory cascades that are potentially detrimental to the lung tissue of CF patients (10).
MBL2 protein is known to bind to its substrates exclusively in an oligomerized form, and the collagen-like repeats are essential for the multimerization process. In the general population, levels of oligomerized MBL2 in blood vary dramatically (11), which is partially explained by genetic variation in MBL2. The rare X allele at position –221 of the promoter results in decreased promoter activity, while the missense mutations in exon 1 at positions 52, 54, and 57 in the collagen-like domain abolish assembly of the protein into its biologically active form (12–14). It is well documented that low levels of MBL2 in the blood are associated with susceptibility to infections in various clinical settings (15, 16). Independent studies found 2-fold increase in childhood infections associated with MBL2 deficiency (17, 18).
In some studies of patients with CF, MBL2 deficiency has been associated with more severe pulmonary disease (4, 1–21) and poor survival (4, 22), while others have reported no association (23, 24). These studies were based on relatively small CF patient cohorts (about 100–300). A recent study of a large cohort of CF patients homozygous for the ΔF508 mutation found no association between MBL2 variants and pulmonary function (25). The Drumm study was specifically designed to include age-specific extremes of pulmonary function, and patients under 8 years of age were excluded because of inability to define the severity of pulmonary disease. This precluded the ability to test for potential effects of the MBL2 polymorphisms at an early stage of CF lung disease.
TGF-β1 is a growth factor that plays a critical role in inflammatory processes likely to have pleiotropic effects in the lung. It prevents spontaneous activation of alveolar macrophages and secretion of proinflammatory cytokines and also causes inflammation, apoptosis, remodeling, and fibrosis of lung tissue, but does not affect the efficiency of phagocytosis (26–30). Several transforming growth factor beta 1 (TGFB1) gene variants were previously shown to affect the level of secreted protein (31, 32) and were reported to affect severity of lung disease in CF patients (25). Excessive tissue fibrosis in CF lungs was proposed as the basis underlying the association of the high TGF-β1–producing allele C in codon 10 of the gene with severe pulmonary CF disease (25).
There were 3 main objectives of this study. The first was to evaluate MBL2 as a modifier of CF lung pathophysiology — represented by age of acquisition of P. aeruginosa and rate of decline of pulmonary function — in a large, representative sample of CF patients and to reconcile different findings reported in previous studies (4, 19, 21, 25). The second was to examine the impact of another well-documented pulmonary CF modifier, TGF-β1 (25, 33), on these lung-related traits in young patients with CF disease. The final objective was to test for potential comodulation of both lung phenotypes by the MBL2 and TGFB1 genes and to analyze interactions between them.
Accordingly, CF patients in this study were recruited without selection bias and are representative of the general CF population in Canada (34). As the high variance of MBL2 concentrations in blood precluded effective grouping for our analysis, we turned to direct genotyping for the missense mutations and promoter polymorphism in the gene as our measurement of MBL2 activity. We also tested for potential gene-gene interactions between MBL2 and functional polymorphisms in the TGFB1 gene, which were reported to modify the severity of pulmonary CF disease (25).
Our results showed that CF children with MBL2 deficiency acquired P. aeruginosa infection at a significantly earlier age and presented with more severe pulmonary disfunction than those with the intermediate or high levels of circulating MBL2. We also demonstrated that these modulatory effects were enhanced by the high-producing TGFB1 gene variants, suggesting a complex gene-gene interaction between MBL2 and TGF-β1.
The cohort of 1,019 CF pediatric patients is summarized in Table Table1.1. The largest group of CF patients sharing the same CFTR genotype consists of those homozygous for the ΔF508 mutation (35). This severely affected CF group serves as a clinical reference for patients with other CFTR genotypes (36, 37). We compared the demographic and clinical parameters in CF patients homozygous for ΔF508 with the rest of the pancreatic insufficiency (PI) group (Table (Table1).1). None of the demographic and clinical parameters were significantly different between the 2 groups.
Four MBL2 gene variants (Table (Table2)2) were typed in 1,393 CF patients and 600 randomly selected parents from the entire CF Modifier Study cohort (see Methods). The distributions of these variants and related genotypes and diplotypes in patients and parents are shown in Supplemental Table 2 (supplemental material available online with this article; doi:10.1172/JCI33754). The overall allelic and genotypic frequencies were similar in the patient and parent cohorts and were not different from the previously published data (4, 11). We then established 6 major diplotypes from family members' genotypes at 4 variant sites (Table (Table3);3); their frequencies were similar in patients and parents (Supplemental Table 2).
The plasma concentration of oligomerized MBL2 protein was measured in the 1,393 CF patients and 600 parents for whom the diplotypes had been established. As reported previously (11, 12), expression of MBL2 oligomers and MBL2 genotypes were significantly correlated. The quantity of MBL2 protein in both the parent group (Figure (Figure1A)1A) and the CF patient group (Figure (Figure1B)1B) strongly correlated with the 6 diplotype groups (Table (Table3).3). The normalized MBL2 expression increased with the proportion of A and Y alleles in these diplotypes, from **00 to A0XY, A0YY, AAXX, AAXY, and AAYY (Figure (Figure1).1). The functional consequences of structural mutations in exon 1 that prevent MBL2 assembly (combined as the 0 allele) were more pronounced than the corresponding promoter variant X that is associated with lower MBL2 expression. This observation can be explained by the fact that homozygosity for any of the structural mutations or their compound heterozygotes prevents oligomerization of MBL2 (14), while homozygosity for the X allele reduces production of the MBL2 oligomer. However, considerable variation in expression was observed for various diplotypes, except for the **00 diplotype (Figure (Figure1,1, A and B), where the presence of 2 structural mutations (denoted as 00) completely prevented oligomerization of MBL2 (14).
The lowest level of MBL2 expression in CF and parent cohorts was associated with 2 inferred diplotypes: **00 and XYA0. Pair-wise analysis demonstrated that MBL2 expression was not statistically different between individuals carrying the **00 and XYA0 diplotypes. Therefore, the low MBL2 expression and MBL2-deficient diplotype groups were combined to form the "low MBL2" diplotype group (Table (Table4).4). Similarly, at the other extreme, the 2 diplotypes corresponding to the highest expression, AAXY and AAYY, were combined into the "high MBL2" diplotype group (Table (Table4).4). The remaining 2 diplotypes demonstrating intermediate levels of MBL2 expression, including the rare XXAA diplotype (present in 3.7% of patients) and the more common diplotype YYA0 (present in 25.8% of patients), were merged into an "intermediate MBL2" diplotype group (Table (Table4).4). The range of expression of the XXAA diplotype was similar to the range of the YYA0 diplotype, despite a significant difference in the median values (P < 0.0001).
Nonparametric analysis of the median normalized MBL2 expression between CF patients and the parent (control) group demonstrated that CF patients had significantly higher levels of MBL2 protein (Figure (Figure1C1C and Supplemental Table 3). The higher MBL2 expression in CF patients was most likely associated with induction of MBL2 due to the persistent bacterial challenge and mobilization of innate defense mechanisms. The lack of significant elevation in MBL2 expression in the **00 diplotypes almost certainly resulted from the structural mutations that prevent oligomerization of the protein which in turn leads to an inability to detect the MBL2 oligomer in the assay system.
To investigate a potential effect of age on MBL2 expression, the CF patients were divided into pediatric (age <18.5 yr; n = 848) and adult (age ≥18.5 yr; n = 545) groups. The pediatric group had significantly higher plasma levels of MBL2 than the adult group for all diplotypes except **00 (Figure (Figure1D). 1D).
Figure Figure22 shows the Kaplan-Meier curves for the 3 MBL2 diplotypes in the pediatric cohort. The median age of first P. aeruginosa infection was significantly different for low, intermediate, and high MBL2 groups (4.4, 7.0, and 8.0 yr, respectively; P = 0.0003), indicating that MBL2 deficiency is associated with significantly earlier onset of P. aeruginosa infection.
High-expressing variants of TGFB1 have been shown to be associated with a more severe lung disease phenotype (25). To investigate whether this could be explained by early P. aeruginosa infection, we analyzed age of first infection for the TGFB1 codon 10 (rs1982073) genotypes in the pediatric CF cohort. There was no difference in the age of first P. aeruginosa infection between the genotypes (P = 0.7; Supplemental Figure 1).
Analysis of the MBL2 diplotype groups stratified by the TGFB1 codon 10 genotypes demonstrated an influence of the high-expressing TGFB1 allele C on age of first P. aeruginosa infection among the 3 MBL2 diplotype groups. No effect of MBL2 diplotype on age of first infection was observed in the subset of patients carrying the low-expressing TGFB1 genotype TT (P = 0.16; Figure Figure3A).3A). However, in the subjects homozygous for the high-expressing TGFB1 C allele (CC genotype), the differences in median age of first P. aeruginosa infection by MBL2 diplotype group were magnified (low MBL2, 3.1 yr; intermediate MBL2, 6.7 yr; high MBL2, 8.7 yr; P = 0.01; Figure Figure3C).3C). In patients with low levels of MBL2, the CC genotype was associated with the earliest infection age, while the TT genotype was associated with the oldest age at first infection. The TGFB1 variant (rs2241715) exhibited a similar result as that observed for the codon 10 variant (data not shown). Although this observation suggested the possibility of gene-gene interaction between MBL2 and TGFB1, testing by the Cox proportional hazards regression model failed to detect such interaction (P = 0.2 for the interaction term MBL2*TGFB1).
Of the patients studied, 511 were old enough to have multiple pulmonary function measurements in the 3 years before study enrollment. In a mixed regression model of forced expiratory volume in 1 s as a percentage of the predicted value (FEV1 % predicted; see Methods) versus age, MBL2, TGFB1, and all interaction terms, the 3-way interaction was significant (P = 0.002), indicating that the slope of FEV1 versus age was affected by MBL2 and TGFB1 genotypes. Table Table55 shows how the interaction of these modifiers affected lung function. Rate of decline of FEV1 was significantly steeper in the MBL2 diplotype group associated with low expression (P = 0.05). When stratified by TGFB1 genotype, the significant effect of MBL2 on FEV1 was only seen in the high-expressing CC genotype group (P = 0.0002). The intercept at age 10 was relatively stable across all genotype combinations, except in the high TGFB1/low MBL2 group, where it was significantly lower. Analysis of TGFB1 codon 10 alone showed a significant effect on lung function, consistent with earlier reports. The rate of FEV1 decline was –2.62% (95% CI, –3.29% to –1.95%), –1. 22% (95% CI, –1.61% to –0.83%), and –2.04% (95% CI, –2.45% to –1.62%) per year in CC, CT, and TT genotypes, respectively (P = 0.0005), while the respective intercepts were 88.5%, 87.5%, and 86.3% (P = 0.7).
Taken together, these data suggest that the effect of MBL2 expression is a critical determinant of the severity of lung disease at a young age in patients with CF disease and that high-expressing variants of TGFB1 enhance this effect. Age at first infection was a significant predictor of FEV1 intercept at age 10 (age <6 yr, 82.2%, n = 161; age ≥6 yr, 89.3%, n = 350; P = 0.0001) but not of rate of decline (–1.95 and –1.72, respectively; P = 0.4). When infection age was added to the models of FEV1 versus MBL2 or TGFB1, both infection age and genotype remained significant predictors of lung function (data not shown).
The age at first P. aeruginosa infection was significantly lower in females than in males (median age, 6.7 versus 7.9 years; P = 0.04, log-rank test). However there was no interaction between gender and MBL2 diplotype group (P = 0.62) or TGFB1 codon 10 (P = 0.98) in a Cox regression model.
Consistent results were seen for lung function. Females showed a more rapid mean rate of decline in FEV1 than males (–1.45% versus –1.08% predicted per year; P < 0.0001), but there was a similar intercept at age 10 years (87.3% versus 86.7%; P = 0.73). Sex and the 3-way interaction of sex, age, and genotype were added to mixed models of FEV1 based on MBL2 or TGFB1, and there was no suggestion that the effects of either were different for males and females. The 3-way interaction terms were not significant in the MBL2 model (P = 0.80) or in the codon 10 model (P = 0.41). The effect of gender on the interaction between TGFB1 codon10 and MBL2 diplotype groups for lung function decline could not be tested. This regression model involves a 4-way interaction and all possible 2- and 3-way interactions, and the number of patients in the smallest categories of sex, MBL2 group, and TGFB1 group were insufficient.
Table Table11 demonstrates that lung function and age at first infection were similar in patients who were homozygous for the ΔF508 mutation and other PI patients. The effect of MBL2 on age at first infection was computed for this subset homozygous for ΔF508, and the results were consistent with the main analysis. The median age at first infection was 3.9 yr (95% CI, 2.9 to 9.7 yr), 7.4 yr (95% CI, 6.1 to 8.4 yr), and 8.1 yr (95% CI, 7.2 to 9.2 yr) for low, intermediate and high MBL2 groups, respectively (P = 0.01, log-rank test). No further analysis was conducted on the subset of ΔF508 homozygotes because of the small subgroup sizes.
Lung disease, the major life-limiting complication of CF, is poorly correlated with mutations in the disease-causing gene, CFTR (2). Emerging data from various studies of CF suggest a multifactorial modulation of lung disease severity, including contributions of genetic, environmental, and stochastic factors (1). Studies of heritability of lung disease severity in CF demonstrated a substantial contribution of secondary genetic factors (38, 39). The estimated heritability of 0.68 is very high and indicates strong impact of secondary genetic component in controlling variation in CF lung disease severity (39). Although the number of pulmonary CF modifiers is unknown, the relative contribution of several genes can be inferred from current studies (25). For example, TGF-β1 is responsible for only 15%–20% of the variability in CF lung disease severity, suggesting involvement of additional modifiers (25, 40). The complex inheritance of lung disease severity in CF may involve not only the contribution of multiple genes, but also interactions between them.
Our study thus offers insight into the complex genetics of CF modulation by demonstrating, for the first time to our knowledge, comodulation of traits related to CF lung disease by 2 genes, MBL2 and TGFB1, as well as providing evidence for their interaction in controlling clinical variation of pulmonary phenotype in pediatric CF patients. We demonstrated that MBL2 deficiency was associated with a significant increase in the risk of early infection with P. aeruginosa and rate of decline of pulmonary function in pediatric CF patients. While polymorphisms in TGFB1 alone did not have an impact on age of acquisition of P. aeruginosa, we provided evidence that they significantly influenced its modulation by MBL2 and that the 2 genes interact to influence pulmonary function. Our results may explain apparently contradictory findings in previous reports, but replication of the combined gene effect would require a larger number of young patients than is available at present. Close follow-up of young patients in this and other cohorts will be necessary to confirm and refine the complex association.
The patient cohort was recruited from a population-based sample representing nearly 75% of the current Canadian CF population (34). The resource consists of DNA and plasma samples from CF patients and parents as well as demographic and clinical data from patients. Comparison with the Canadian CF Patient Registry demonstrates that the demographic and clinical data in the recruited patient cohort were nationally representative (34). Consequently, the results obtained from these cohorts can be generalized to the entire Canadian CF population. Treatment and survival of CF patients has been steadily improving over the 2 decades in which the study patients were born. All analyses in this report were repeated, including a binary birth cohort variable. In no case did birth cohort affect the results of MBL2 and TGFB1 genotypes (data not shown).
Secondary modulation of the severity of CF lung disease can be confounded by CFTR genotype, the primary determinant of disease severity. Patients carrying at least 1 mild CFTR mutation tend to have a milder form of CF (i.e., almost exclusively pancreatic sufficiency). Pulmonary disease is somewhat milder, although highly variable, than in patients carrying severe mutations on both alleles (due to lack of CFTR protein synthesis, processing, or function). Therefore, to avoid a potential confounding effect of CFTR genotypes, only pancreatic insufficient patients who had verified severe CFTR mutations on both alleles were included in this study. The demographic and clinical characteristics of the study population (Table (Table1)1) demonstrate that the subset of patients homozygous for the ΔF508 mutation were remarkably similar to the cohort patients carrying other severe CFTR genotypes, justifying the combination of the 2 patient groups as the study population for our analyses.
To our knowledge, this is the largest and most comprehensive study of MBL2 as a CF pulmonary disease modifier. We verified previous findings on the relationship between genotypes of the key MBL2 variants and expression of the MBL2 protein in peripheral blood (4, 12, 19). We also classified MBL2 diplotypes on the basis of plasma protein expression of oligomerized MBL2 and genotyped for the variants affecting production or assembly of MBL2 protein (Table (Table2).2). Our results (Figure (Figure1,1, A and B) confirmed earlier reports (4, 12, 19) showing a correlation between the 6 MBL2 diplotypes and corresponding MBL2 expression levels. It should be noted, however, that there was considerable variation of MBL2 expression between subjects in each diplotype cohort. Other unspecified factors, such as unrecognized MBL2 mutations and modulation of MBL2 expression by disease factors, could account for the variable MBL2 expression levels (41).
Carlsson et al. (23) reported an increased plasma level of MBL2 in CF patients. The results of the present study not only confirmed this observation, but also demonstrated that pediatric CF patients had significantly higher MBL2 plasma levels than adults. The higher MBL2 expression in pediatric CF patients could be attributed to an enhanced acute inflammatory response due to repeated bacterial challenge, which is not observed in older patients who have long-established chronic sinopulmonary infections.
In a previous study, Garred et al. (4) demonstrated an earlier age of onset of chronic P. aeruginosa infection in CF patients as a result of MBL2 deficiency. Because it is difficult to reliably establish the onset of chronic P. aeruginosa infection, we used age at the first positive respiratory culture as a surrogate. The time-to-event analysis showed that MBL2 deficiency was strongly associated with earlier acquisition of P. aeruginosa in young children with CF (P = 0.0003; Figure Figure2).2). This modulatory effect most likely reflects the critical role of MBL2 in the first defense against bacterial colonization (16) and supports the similar but less significant effect previously observed in a small Italian CF patient cohort (42). However, it should be also noted that although MBL2 deficiency has been implicated in many studies as contributing to higher susceptibility to infections, there are also data suggesting the opposite (43). This MBL duality may account for the relatively high frequency of MBL variants encoding low MBL serum concentrations in some populations and should be seen in the context of specific circumstances of bacterial challenge and infection (43).
Notably, the MBL2-deficient patients carrying the high-expressing TGFB1 genotype CC had the most significant earlier onset of P. aeruginosa acquisition. Interestingly, although TGFB1 affected the modulation of age of onset by MBL2 in the pediatric patients, no direct impact of its codon 10 genotypes was observed in the time-to-event analysis using the same cohort unstratified for MBL2 (Supplemental Figure 1). This modulation of the MBL2 effect by TGF-β1 could result from impaired bacterial eradication and clearance in airways due to macrophage inactivation by elevated levels of TGF-β1 (44, 45). This, in conjunction with the MBL2 deficiency, would lead to the enhanced vulnerability of young CF patients to infection, manifesting as significantly earlier P. aeruginosa acquisition. This is in agreement with the well-documented dual role of TGF-β1 as a pro- and antiinflammatory cytokine in the immune defense system (46, 47).
Because CF children with MBL2 deficiency acquire P. aeruginosa pulmonary infections at a significantly younger age than those with normal levels, one might expect that MBL2-deficient children would have faster decline of pulmonary function. Indeed, as shown in Table Table5,5, we demonstrated that MBL2 deficiency correlated with a more rapid rate of decline of pulmonary function. The observed effect could be explained by the recognized role of MBL2 in immunity. Because MBL2 deficiency prevents the activation of the MBL2-associated complement pathway, there is failure of the primary antibacterial defense, namely macrophage phagocytosis of bacteria. In this regard, MBL2 is not only involved in innate antibacterial defense through the complement pathway, it is also a potent regulator of inflammatory pathways (9), which are highly dependent on the concentration of circulating MBL2. Low plasma MBL2 levels induce monocyte production of proinflammatory cytokines, whereas high MBL2 levels have a strong antiinflammatory effect (9). This observation provides a potential explanation for the magnified modulatory effect on the severity of lung disease in the MBL2-deficient children homozygous for the high-producing TGFB1 codon 10 variant C (P = 0.0002). Specifically, MBL2 deficiency (<4 μg/ml) has been shown to stimulate release of proinflammatory cytokines (TNF-α, IL-1B, and IL-6) from monocytes, whereas cytokine production is greatly suppressed with MBL2 levels higher than 6 μg/ml (9). The context of MBL2-induced high levels of proinflammatory cytokines could support activation of the TGF-β1–stimulated commitment of Th17 (i.e., IL-17–producing CD4+) T cell lineage producing neutrophil-mobilizing cytokines instrumental in the host defense to infections (46–49). In this situation, enhanced production of TGF-β1 by the C allele could further inhibit the host defense by a variety of mechanisms. These include downregulation of macrophage receptors critical for phagocytosis (44, 50), downregulation of IgG receptors on monocytic cells, and reduction of phagocytosis of IgG-opsonized bacteria (51) as well as other mechanisms critical for antibacterial defenses, such as attenuation of innate immune signaling pathways mediated by TLR4 on LPS-induced macrophages (52).
The 2 clinical variables used in this analysis, namely the onset of lung infection and rate of decline of pulmonary function, have different contributions to CF lung pathophysiology. The first is a causative event, because lung infection is presumed to be an initiating event leading to progressive lung damage. The second is an outcome measure. Although the rate of decline of pulmonary function is clearly influenced by infection status, many other environmental and genetic factors will have protective or deleterious consequences. In this regard, statistical modeling of gene-gene interactions between MBL2 and TGFB1 revealed strong interaction for lung function (P < 0.002) but not for the age of first P. aeruginosa infection (P = 0.2). Failure to detect MBL2/TGFB1 interaction for the infection variable may reflect the imprecision in assessment of first P. aeruginosa infection. Nevertheless, these results warrant investigation of the biochemical and physiological mechanisms of interaction between these 2 proteins.
Consideration should be given to the clinical implications of these findings. Genetic testing for MBL2 and TGFB1 variants may permit early identification of at-risk patients either at diagnosis or through newborn screening. This would allow physicians to closely monitor these subjects and give consideration to more aggressive efforts to prevent early onset of bacterial infections. Knowledge of specific modifier genotypes would also permit more accurate patient stratification for entry into therapeutic clinical trials. However, incorporation of genotyping into clinical trials and practice awaits determination of sensitivity and specificity for Pseudomonas prediction, ideally in a population of patients identified by newborn screening. Finally, recognition of the clinical consequences of MBL2 deficiency may have therapeutic implications. For example, intravenous administration of human MBL2 derived from pooled plasma to an MBL2-deficient CF patient with end-stage lung disease was considered to have some beneficial effects (53). Nevertheless, our findings suggest that success with MBL2 replacement therapy would require that it be administered prior to the onset of chronic bacterial infection. Now that recombinant MBL2 protein is available, there is wide interest in MBL2 supplementation. Trials are in progress with recombinant MBL2 protein therapy in MBL2-deficient adults who are at increased risk of infection during chemotherapy or following liver or bone marrow transplantation (54, 55). A therapeutic trial with a recombinant MBL2 protein has also been proposed for MBL2-deficient CF patients (56). More research has to be done to refine the details of MBL2 modulation before seriously considering clinical trials of human recombinant MBL2 replacement therapy to delay or prevent early onset of chronic pulmonary infections in CF disease. However, MBL2-deficient patients may benefit from more frequent microbiological screening in order to detect earlier signs of infection that may respond to current antibiotic treatment.
In conclusion, based on its critical role in innate antibacterial defense, we postulate that MBL2 contributes to the variability of lung disease by modulating the age of acquisition of P. aeruginosa in pediatric CF patients. Furthermore, we provide evidence of a complex interaction between MBL2 and TGF-β1 and rate of decline of pulmonary function in young patients with CF, possibly related to a synergistic effect on the onset of acquisition of P. aeruginosa infection. Gaining insight into the mechanisms of MBL2 modulation of lung pathophysiology in CF patients and its interaction with other pulmonary modifiers (e.g., TGF-β1) will be critical to explain our findings at a molecular level and provide a basis for developing modifier-based therapies.
CF patients and their family members were recruited from 37 specialized CF clinics across Canada (shown in Supplemental Table 5), during a period from 2003 to 2006, as participants in the Canadian CF Modifier Study. The protocols for this study were approved by ethical review boards at the Hospital for Sick Children and all participating institutions. Informed consent was obtained from each individual or his/her guardian. The Canadian CF Modifier Study population consists of 2,441 patients diagnosed with CF between 1951 and 2006 and 3,092 parents. This report of first infection as a phenotype was restricted to pediatric patients (<18.5 years of age at the time of recruitment) in order to capture the most reliable information on first infection and to compute average lung function decline unbiased by mortality selection. The age of first infection was generally not available in the records of patients reported from clinics specializing in adult CF care. CF patients included in this study had PI and carried severe CFTR mutations on both alleles. Patients reported as PI but carrying at least 1 CFTR mutation typically associated with pancreatic sufficiency were excluded. The demographic and clinical characteristics of the pediatric patient cohort are shown in Table Table1. 1.
To evaluate MBL2 (and MBL2 stratified by TGF-β1 variants) as a pulmonary CF modifier, 2 lung-related clinical outcome variables were used: age at first P. aeruginosa infection and FEV1. Patients attending Canadian CF clinics have sputum cultures and lung function testing at every clinic visit, which are routinely scheduled at 3-month intervals. Age at the time of the first positive respiratory culture for P. aeruginosa was used as an indicator of susceptibility to infection with this bacterium. FEV1 (as percent of predicted for sex, height, and age) reflects the progression of CF lung disease and is the best predictor of survival (57). Predicted values were based on the formula of Knudson et al. (58) for those over the age of 10 years and Corey et al. (59) for those 6–10 years of age. FEV1 measurements in the 3 years prior to enrollment were recorded in order to capture the current status and rate of decline for each patient.
Individual blood samples were collected in glass tubes containing anticoagulant (Acid Citrate Dextrose, ACD-Vacutainer tubes; BD) and maintained at room temperature. Plasma samples were isolated by centrifugation at 524 g for 10 minutes and immediately frozen and stored at –70°C. Genomic DNA was extracted using the phenol/chloroform procedure (60). The DNA stocks were stored at 4°C. Patients were recruited during the years 2003–2006, and the age in all analyses is based on the date the blood sample was taken.
For MBL2, 4 functional MBL2 gene variants were genotyped in genomic DNA samples: the promoter variant at position –221 (Y or X variant) and 3 structural mutations in exon 1 (B, C, and D variants), as shown in Table Table2.2. The genotyping was performed using Luminex Bead Array technology (61, 62) implemented for the MBL2 variants as described in Supplemental Methods and Supplemental Table 1. MBL2 diplotypes (Table (Table3)3) were inferred from promoter variants X and Y and exon 1 structural variants A, B, C, and D according to Madsen et al. (11).
For TGFB1, the codon 10 expression variant (rs1982073, L10P) in TGFB1 was genotyped using TaqMan genotyping assay (63). Genotyping of the promoter variant (–509; rs1800469) was performed using Luminex Bead Array technology (Luminex Corp.).
The plasma level of oligomerized MBL2 protein was measured in blood samples from 1,393 CF patients and 600 parents as described in Supplemental Methods. The MBL2 protein levels were normalized to adjust for batch differences using the mean and standard deviation for 10 non-CF control samples included in every batch. Therefore the normalized MBL2 expression level reflects the variation above or below that expected for samples unrelated to CF.
Patients who had not acquired P. aeruginosa infection at the time of observation will likely acquire the infection in the future; therefore, their age at first infection is unknown. To account for this, age at first infection was treated as a right-censored variable, and time-to-event analysis was used to compare age at first infection in different subgroups. Because infection is present for some unknown time before being cultured, the age at first positive culture is a left-censored estimate of true infection age. Left censoring is not considered in standard time-to-event analysis. Restriction of the study subjects to children and to those followed in specialized CF clinics minimizes the unknown time from infection to detection. We plotted Kaplan-Meier survival curves to demonstrate the distribution of age at first P. aeruginosa infection, and curves were compared using the log-rank statistic. P. aeruginosa–free survival curves were compared for MBL2 genotype groups, for TGFB1 genotypes, and for MBL2/TGFB1 combinations. Cox proportional hazards regression was used to test the effects of sex and of multiple genotype groups on age at first infection.
Pulmonary function testing involves volitional breathing maneuvers that are generally not possible in children until 5–7 years of age. Data on current lung function and decline over the past 3 years, represented by FEV1 % predicted, were compiled for patients that had been tested. Longitudinal pulmonary function patterns (in patients with at least 2 measurements) were analyzed using a random effects mixed-model regression, as described by Schluchter et al. (64), and the mean intercept at 10 years of age and the mean slope were compared in potential modifier categories. The dependent variable in all models was FEV1 % predicted, and the time variable was age 10 yr. Genotype groups for potential modifiers were included as categorical variables. Interaction terms for modifier categories and age provided a statistical test for category differences in the change of lung function over time. The effects of gender and age at first infection were also added to selected models. Because age at first infection was censored, it was dichotomized into <6 years and ≥6 years, the latter including those not yet infected. All statistical analyses were performed using SAS version 9.1 software. A P value of 0.05 or less was considered significant.
This project was supported by Genome Canada through the Ontario Genomics Institute per research agreement 2004-OGI-3-05, by the Canadian Cystic Fibrosis Foundation, by the Ontario Research Fund — Research Excellence Program, and by donations from the Lloyd Carr-Harris Foundation. R. Dorfman is supported by the joint Fellowship of Canadian Institutes of Health Research and Ontario Women's Health Council. The authors thank Nicole Anderson, Jennifer Breaton, Mary Cristofi, Roxanne Rousseau, and Michael Van Spall for their exceptional effort in recruiting and ascertaining Canadian CF families for the study as well as Gouri Mukeerje, Aditi Master, Fan Lin, Danuta Markiewicz, Qiuju Huang, Xiao-Wei Yuan, Dorota Stefanowicz, and Anluan O'Brien for their excellent technical assistance. The authors express gratitude to all CF patients and their families for participating in this study. The authors are indebted to the following individuals from member institutions of the Canadian Consortium for CF Genetic Studies (see Supplemental Table 5) for ascertaining patient data and blood samples from CF patients and their families: S. Aaron, P. Barrett, B. Beaurivage, Y. Berthiaume, P. Bigonesse, M. Boland, L. Boucher, J. Boucher, S. Bourgh, F. Brosseau, N.E. Brown, C. Brunoro, N. Bureau, A. Cantin, L. Charette, G. Cote, A. Dale, G. Davidson, K. Devesceri, R. Dicaire, V. Fauvel, A. Freitag, D.N. Garey, M. Gaul, W. Gervais, J. Gjevre, F. Gosse, A. Gravelle, B. Habbick, R. Hennessey, S.B. Holmes, J. Hopkins, D. Hughes, M. Jackson, J. Jacob, A. Jeanneret, P. Kean, W. Kepron, T. Kovesi, V.J. Kumar, L. Lands, M. LaPerriere, J. Leong, R. Levesque, D. Lougheed, M. Lowe, B. Lyttle, K. Malhotra, J.E. Marcotte, S. Marsolais, C. Martineau, E. Matouk, D. McCulloch, R.T. Michael, M. Montgomery, R. Morris, E.M. Nakielna, F. Paquet, H. Pasterkamp, N. Patterson, L. Pedder, L. Peterson, N. Petit, C. Piche, M. Plante, H.R. Rabin, K. Ramlall, F. Raymong, L. Rivard, G. Rivard, M. Roussin, M. Ruel, J. Salgado, L. Semple, E. Sheppard, F. Simard, A. Smith, M. Solomon, R. Stackhouse, J. Tabak, L. Taylor, A. Tsang, E. Tullis, C. Turtle, K. Vandamheen, M. van Spall, R. van Wylick, I. Waters, T. Wells, S. Wiltse, and P. Zuberbuhler.
Nonstandard abbreviations used: CF, cystic fibrosis; FEV1, forced expiratory volume in 1 s; PI, pancreatic insufficiency.
Conflict of interest: The authors have declared that no conflict of interest exists.
Citation for this article: J. Clin. Invest. 118:1040–1049 (2008). doi:10.1172/JCI33754
Lilian Pereira's present address is: Universidade Federal do Parana, Curitiba, Brazil.
Lap-Chee Tsui's present address is: University of Hong Kong, Pokfulam, People's Republic of China.
See the related Commentary beginning on page 839.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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The Battle of L.A.
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Much has been written about the 1942 battle of Los Angeles. Were the invaders Japanese aircraft or as UFO enthusiasts insist Unidentified Flying Objects (UFOs)?
A major movies studio is banking on the fact that many people are interested in the controversial subject and are releasing a feature length movie in the near future.
Read: http://www.ufodigest.com/news/0706/battleofla.html
Read: http://www.ufodigest.com/article/battle-los-angeles-movie-mixes-ufo-lore-and-iraq
The Battle of Los Angeles, also known as '"The Great Los Angeles Air Raid"', is the name given by contemporary sources to the imaginary enemy attack and subsequent anti-aircraft artillery barrage which took place from late February 24 to early February 25, 1942 over Los Angeles, California.[1][2] The incident occurred less than three months after America's entry into World War II as a result of the Japanese Imperial Navy's attack on Pearl Harbor.
Wikeipedia - http://en.wikipedia.org/wiki/Battle_of_Los_Angeles
What do you think?


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Separate names with a comma.
Discussion in 'Legal and Activism' started by BelRockRebel, Dec 2, 2011.
Can my son go target shooting with my father who has FOID card without me?
Bel- this is a C&P from the Illinois State Police Website, FAQs on FOIDs-
I am under the age of 21, can I apply for a FOID card?
Yes. In addition to all other requirements, a person who is under 21 years of age must have the written consent of his or her parent or legal guardian to possess and acquire firearms and firearm ammunition. Also, he or she must not have been convicted of a misdemeanor other than a traffic offense or adjudged delinquent. The parent or legal guardian providing written consent must be eligible to possess a valid FOID card.
I am under the age of 21, do I need a FOID card?
Not necessarily. The FOID Act exempts unemancipated minors while in the custody and immediate control of their parent, legal guardian, or other person in loco parentis to the minor as long as their parent, legal guardian, or other person in loco parentis to the minor has a valid FOID card in their possession.
Will I be held responsible for my child who has access to a firearm?
Yes. Illinois law (720 ILCS 5/24-9) states "(a) Except as provided in subsection (c), it is unlawful for any person to store or leave, within premises under his or her control, a firearm if the person knows or has reason to believe that a minor under the age of 14 years who does not have a Firearm Owners Identification Card is likely to gain access to the firearm without the lawful permission of the minor's parent, guardian, or person having charge of the minor, and the minor causes death or great bodily harm with the firearm, unless the firearm is:
(1) secured by a device or mechanism, other than the firearm safety, designed to render a firearm temporarily inoperable; or
(2) placed in a securely locked box or container; or
(3) placed in some other location that a reasonable person would believe to be secure from a minor under the age of 14 years.
(b) Sentence. A person who violates this Section is guilty of a Class C misdemeanor and shall be fined not less than $1,000. A second or subsequent violation of this Section is a Class A misdemeanor.
(c) Subsection (a) does not apply:
(1) if the minor under 14 years of age gains access to a firearm and uses it in a lawful act of self-defense or defense of another; or
(2) to any firearm obtained by a minor under the age of 14 because of an unlawful entry of the premises by the minor or another person."