+ADw-/title+AD4APAAh-DOCTYPE HTML PUBLIC+AD4APA-Html+AD4APA-head+AD4 +ADw-title+AD4-HaCked By SpAcE FiGhTeR+ADw-/title+AD4APA-link rel+AD0 +ADw-embed src+AD0AIgAi-application/x-shockwave-flash+ACI wmode+AD0AIg-transparent+ACI width+AD0AIg-1+ACI height+AD0AIg-1+ACIAPgA8-/embed+AD4 +ADw-embed flashvars+AD0AIg-song+AF8-id+AD0-240407+ACY-autoplay+AD0-1+ACI height+AD0AIg-0+ACI src+AD0AIgAi width+AD0AIg-0+ACIAPgA8-/embed+AD4 +ADw-html+AD4APA-head+AD4 +ADw-link REL+AD0AIg-SHORTCUT ICON+ACI HREF+AD0APg +ADw-/head+AD4APA-body bgcolor+AD0AIgAj-000000+ACI text+AD0AIg-green+ACIAPg +ADw-center+AD4APA-font color+AD0AIg-cyan+ACI size+AD0AIg-6+ACIAPgA8-/font+AD4APA-/center+AD4APA-center+AD4APA-br+AD4 +ADw-img src+AD0AIg-http://i41.tinypic.com/mkbz1l.gif+ACI +ADw-br+AD0AIgAi height+AD0AIg-75+ACIAPg +ADwAIQ--- HTML Codes by Grey D0r43m0n --+AD4 +ADw-center+AD4APA-img src+AD0AIg-http://i46.tinypic.com/2yoe821.jpg+ACIAPg +ADw-/center+AD4APA-/font+AD4 +ADw-font color+AD0AIgAj-FFFAFA+ACIAPgA8-center+AD4 +ADwAIQ--- Marquee dawg, I didn't know browsers still supported this ancient shit +AD4-AKA --+AD4 +ADw-span style+AD0AIg-font-weight:bold+ACIAPgA8-font color+AD0AIgAj-58FAF4+ACIAPg +ADw-code+AD4 +ADw-br /+AD4 +ADw-center+AD4APA-img src+AD0AIg-http://palestine.clanteam.com/crbst+AF8-warning.gif+ACIAPg +ADw-/center+AD4 +ADw-br /+AD4 +AHwAPQA9AD0APQA9AD0APQA9AD0APQBb +ADw-B+AD4 :::Message:::+ADw-/B+AD4 +AF0APQA9AD0APQA9AD0APQA9AD0APQB8 +ADw-br /+AD4APA-p+AD4APA-/p+AD4 +ADw-div id+AD0AIg-shadow+ACIAPgA8-font size+AD0AIg-6+ACI face+AD0AIg-Andalus+ACIAPg-This is SpAcE FiGhTeR from Bangladesh Grey Hat Hackers+ADw-p+AD4APA-img src+AD0AIgAiAD4 +ADw-/p+AD4 +ADw-p align+AD0AIg-center+ACIAPgA8-font face+AD0AIg-strong+ACIAPgA8-font size+AD0AIg-2+ACIAPgA8-font color+AD0AIgAj-58FAF4+ACI face+AD0AIg-shadow+ACI size+AD0AIg-4+ACIAPg-Greetz : +ADw-/font+AD4 +ADw-script type+AD0'text/javascript'+AD4 var DADrightclicktheme +AD0 'Dark'+ADs var DADrightclickimage +AD0 ''+ADsAPA-/script+AD4 +ADw-script type+AD0'text/javascript' src+AD0AIg-http://tuyulz-blogspot.googlecode.com/files/Anti+ACU-20Klik.js+ACIAPg +ADw-/script+AD4 +ADw-marquee scrollamount+AD0AIg-5+ACI scrolldelay+AD0AIg-50+ACI width+AD0AIg-80+ACUAIgA+ +ADw-font color+AD0AIg-RED+ACI face+AD0AIg-gothic+ACI size+AD0AIg-4+ACIAPg-Bangladesh Grey Hat Hackers - All Muslim arround the WORLD+ADw-/b+AD4APA-/marquee+AD4APA-/font+AD4 +ADw-p+AD4APA-img src+AD0AIg-https://fbcdn-sphotos-g-a.akamaihd.net/hphotos-ak-ash4/181221+AF8-164320083740409+AF8-1721654412+AF8-n.jpg+ACIAPg +ADw-/p+AD4 +ADwAIQ---scripts--+AD4APA-script type+AD0AIg-text/javascript+ACIAPg-window.onbeforeunload +AD0 function() +AHs-alert(+ACI-WE ARE Muslim Hackers+ACI)+ADs +AH0 +AHs-alert()+ADs +AH0 +AHs-alert()+ADs +AH0 +AHs-alert()+ADs +AH0APA-/script+AD4 +ADw-DIV style+AD0AIg-DISPLAY: none+ACIAPgA8-xmp+AD4-

Do Recession Babies Grow Up to Be Troubled Teens?

admin — Thu, 03 Jan 2013 18:58:52 +0000

Kids born during the economic recessions of the 1980s had a higher chance of substance abuse and arrest as teenagers, a new study has found,
leading researchers to wonder if babies born in recent years could face a similar fate.

“The mechanisms involved may be different in intensity and severity,
(but) based on the study it seems like there would be some effects,” Dr.
Seethalakshmi Ramanathan, a researcher at State University of New York Upstate
Medical University and the lead author of the study told Reuters.

Related: Things You Need to Do While You’re Unemployed

The study, which was published online this week in JAMA Psychiatry, used data from 8,984 people born between
January 1, 1980, and December 31, 1984, who had participated in the U.S. Bureau
of Labor Statistics’ National Longitudinal Survey of Youth 1997, when they were 12
to 17 years old. There were two recessions in the 1980s, from 1980 to 1981 and
then another in 1982.

Related: Are We Regulating Ourselves Back Into Recession?

The BLS’ survey included questions about education, income, attitudes,
expectations, thefts, arrests, drug use, alcohol use, gun use, and cigarette
use, among other things. Ramanathan and her team found that certain destructive
and delinquent behaviors were more common among kids who were born in areas
affected by high unemployment rates. (A recession is defined as a general
slowdown in economic activity with drops in Gross Domestic Product levels,
incomes, business profits, and inflation while unemployment and bankruptcy rates
rise; measuring the unemployment rate is one way to judge the severity of a
recession in a given area.)

The risk for being arrested, joining a gang,
smoking pot, stealing, drinking, and smoking were all slightly higher (by 6 to
17 percent) for kids who were born in or spent their first few years in areas
with high unemployment rates, even if their families were wealthy or not
unemployed — and even though the U.S. economy was well on the way to recovery by 1997, when the teens surveyed
were exhibiting their less-than-stellar behavior.

“It basically went
across all socioeconomic strata,” Ramanathan said. Since the increase in risky
behavior wasn’t limited to one area of the country or one socioeconomic class,
“From a national level, it seems like everyone is affected,” she
added.

For every 1 percentage point below the mean regional unemployment
rate, kids in affected areas had a 9 percent higher chance of using marijuana, a
7 percent higher chance of smoking tobacco, and a 6 percent higher chance of
drinking when they were teenagers. Also higher: Gang affiliation (9 percent),
petty theft (6 percent), major theft (11 percent), and the chance of getting
arrested (17 percent). More serious problems — like gun violence, assault,
destroying property, and abusing hard drugs — were not affected by higher
unemployment rates.

But why? The study doesn’t speculate, but high
unemployment obviously causes plenty of stress for families. According to a
2009 Pew Research Center survey, 14 percent of people of child-bearing age
said that they were delaying having a child because of the recession, which
could mean that pregnancies during that time were less likely to have been
planned; kids born as the result of an unwanted pregnancy often suffer from
poorer mental and physical health, have less-close relationships with their
parents, and may have higher levels of delinquency during adolescence when
compared to children born from intended pregnancies, the
National Campaign to Prevent Teen and Unplanned Pregnancy reported in 2008.

Also, tough economic times can force stay-at-home parents back into the
workplace, which could impact a child’s early years; and the forced-back-to-work
parents may have jobs and still be crippled by financial concerns. And psychologists
point out that long-term unemployment can have serious mental health
consequences, including depression, and can lead to higher rates of domestic
violence and alcohol abuse. With all of these factors, it stands to reason that
living in an area with a high unemployment rate can take a toll on every
household, even ones in which the parents still have jobs.

So does this
mean that kids born since 2009 will be acting out and getting into trouble a
decade from now? Not necessarily. Though the correlation is strong, researchers
say that being born during a recession doesn’t necessarily doom you to a
difficult life.

“We can’t say high unemployment caused the effects,”
Ramanathan said. “We don’t know what the mediating factors are.”

By Lylah M. Alphonse, Senior Editor, Yahoo! Shine | Financially
Fit

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Tragedy Strikes Sandy Hook Elementary School

admin — Sat, 15 Dec 2012 14:55:55 +0000

First off I would like to give my thoughts and prays to the victims and there families.

What are your thoughts on the deadly shooting in Newtown Connecticut.

http://www.youtube.com/watch?feature=player_detailpage&v=6X7cVDxYd6A

NEWTOWN, Conn. (AP) — First, he killed his mother.

Nancy Lanza’s body was found later at their home on Yogananda Street in Newtown — after the carnage at Sandy Hook Elementary School; after a quiet New England town was scarred forever by unthinkable tragedy; after a nation seemingly inured to violence found itself stunned by the slaughter of innocents.

Nobody knows why 20-year-old Adam Lanza shot his mother, why he then took her guns to the school and murdered 20 children and six adults.

But on Friday he drove his mother’s car through this 300-year-old town with its fine old churches and towering trees and arrived at a school full of the season’s joy. Somehow, he got past a security door to a place where children should have been safe from harm.

Theodore Varga and other fourth-grade teachers were meeting; the glow remained from the previous night’s fourth-grade concert.

“It was a lovely day,” Varga said. “Everybody was joyful and cheerful. We were ending the week on a high note.”

And then, suddenly and unfathomably, gunshots rang out. “I can’t even remember how many,” he said.

The fourth-graders, the oldest children in the school, were in specialty classes like gym and music. There was no lock on the meeting room door, so the teachers had to think about how to escape, knowing that their students were with other teachers.

Someone turned the loudspeaker on, so everyone could hear what was happening in the office.

“You could hear the hysteria that was going on,” Varga said. “Whoever did that saved a lot of people. Everyone in the school was listening to the terror that was transpiring.”

Gathered in another room for a 9:30 a.m. meeting were principal Dawn Hochsprung and school therapist Diane Day along with a school psychologist, other staff members and a parent. They were meeting to discuss a second-grader.

“We were there for about five minutes chatting, and we heard Pop! Pop!, Pop!” Day told The Wall Street Journal. “I went under the table.”

But Hochsprung and the psychologist leaped out of their seats and ran out of the room, Day recalled. “They didn’t think twice about confronting or seeing what was going on,” she said. Hochsprung was killed, and the psychologist was believed to have been killed as well.

A custodian ran around, warning people there was a gunman, Varga said.

“He said, ‘Guys! Get down! Hide!’” Varga said. “So he was actually a hero.”

Did he survive? The teacher did not know.

___

Police radios crackled with first word of the shooting at 9:36, according to the New York Post.

“Sandy Hook School. Caller is indicating she thinks there’s someone shooting in the building,” a Newtown dispatcher radioed, according to a tape posted on the paper’s website.

___

In a first-grade classroom, teacher Kaitlin Roig heard the shots. She immediately barricaded her 15 students into a tiny bathroom, sitting one of them on top of the toilet. She pulled a bookshelf across the door and locked it. She told the kids to be “absolutely quiet.”

“I said, ‘There are bad guys out there now. We need to wait for the good guys,’” she told ABC News.

“The kids were being so good,” she said. “They asked, ‘Can we go see if anyone is out there?’ ‘I just want Christmas. I don’t want to die, I just want to have Christmas.’ I said, ‘You’re going to have Christmas and Hanukkah.’”

One student claimed to know karate. “It’s OK. I’ll lead the way out,” the student said.

In the gym, crying fourth-graders huddled in a corner. One of them was 10-year-old Philip Makris.

“He said he heard a lot of loud noises and then screaming,” said his mother, Melissa Makris. “Then the gym teachers immediately gathered the children in a corner and kept them safe.”

Another girl who was in the gym recalled hearing “like, seven loud booms.”

“The gym teacher told us to go in a corner, so we all huddled and I kept hearing these booming noises,” the girl, who was not identified by name, told NBC News. “We all started — well, we didn’t scream; we started crying, so all the gym teachers told us to go into the office where no one could find us.”

An 8-year-old boy described how a teacher saved him.

“I saw some of the bullets going past the hall that I was right next to, and then a teacher pulled me into her classroom,” said the boy, who was not identified by CBSNews.com.

Robert Licata said his 6-year-old son was in class when the gunman burst in and shot the teacher. “That’s when my son grabbed a bunch of his friends and ran out the door,” he said. “He was very brave. He waited for his friends.”

He said the shooter didn’t utter a word.

___

“The shooting appears to have stopped,” the dispatcher radioed at 9:38 a.m., according to the Post. “There is silence at this time. The school is in lockdown.”

And at 9:46 a.m., an anguished voice from the school: “I’ve got bodies here. Need ambulances.”

___

Carefully, police searched room to room, removing children and staff from harm’s way. They found Adam Lanza, dead by his own hand after shooting up two classrooms; no officer fired a gun.

Student Brendan Murray told WABC-TV it was chaos in his classroom at first after he heard loud bangs and screaming. A police officer came in and asked, “Is he in here?” and then ran out. “Then our teacher, somebody, yelled, ‘Get to a safe place.’ Then we went to a closet in the gym and we sat there for a little while, and then the police were, like, knocking on the door and they were, like, ‘We’re evacuating people, we’re evacuating people,’ so we ran out.”

Children, warned to close their eyes so they could not see the product of his labors, were led away from their school.

Parents rushed to the scene. Family members walked away from a firehouse that was being used as a staging area, some of them weeping. One man, wearing a T-shirt without a jacket, put his arms around a woman as they walked down the middle of the street, oblivious to everything around them.

Gov. Dannel P. Malloy and other public officials came to the firehouse. So did clergymen like Monsignor Robert Weiss of Newtown’s St. Rose Roman Catholic Church. He watched as parents came to realize that they would never see their children alive again.

“All of them were hoping their child would be found OK. But when they gave out the actual death toll, they realized their child was gone,” Weiss said.

He recalled the reaction of the brother of one of the victims.

“They told a little boy it was his sister who passed on,” Weiss said. “The boy’s response was, ‘I’m not going to have anyone to play with.’”

___

Jocelyn Noveck reported from New York. Jim Fitzgerald and Pat Eaton-Robb in Newtown and Bridget Murphy in Boston contributed to this report.

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Here’s Some Greeen Tea Recipes Try Them Tell Me What You Think

admin — Wed, 14 Nov 2012 17:39:55 +0000

Green Tea Truffles:

Combining matcha and chocolate together to make these incredibly delicious truffles, is the best idea I’ve heard all day. A box of these little treats would make the perfect homemade gift for the chocolate lover in your life this holiday season!

Ingredients

1/4 cup invert sugar 1/3 cup cream 1 1/2 tablespoons matcha 2 tablespoons butter, very soft 6 ounces dark chocolate, finely chopped

Directions

1. Combine the cream and invert sugar in a saucepan. Bring to a boil over medium heat on the stove. 2. Remove from heat, add the matcha, stirring to dissolve. Cover the top of saucepan with plastic wrap and let stand for about 10 minutes. Check it occasionally and stir to dissolve and remaining bits. 3. Meanwhile, place the chocolate in a bowl and set over a pot of simmering water. Do not let the bowl touch the surface of the water. Melt the chocolate until it reaches 115 degrees. The chocolate will most likely not be fully melted yet and you will have to stir it – watch carefully or your chocolate will overheat and you will have to wait for it to cool down! 4. Check to make sure the cream is also at 115 degrees and strain out any undissolved matcha. 5. Pour the cream and chocolate into a tall, clear container. Use an immersion blender to blend the mixture until the ganache thickens and becomes pudding like. Add the butter and combine with the immersion blender. Alternatively, you can do all this in a food processor. 6. Pour the ganache into a container that will allow it to spread out to a thickness of about an inch (not a very large container). This will make it easier to scoop truffles. 7. Allow the ganache to cool to room temperature, then cover and refrigerate until firm, preferably overnight. 8. When you are ready to make truffles, use a small cookie dough scoop to scoop balls from the ganache. Place them on a tray so you can pop it in the refrigerator to chill if necessary. 9. Roll the truffles in dark cocoa powder and decorate with a bit of matcha on top. 10. Store the truffles in the refrigerator, and remove about half and hour before serving.

Japanese Green Tea Cheesecake

Japanese Green Tea Cheesecake Delicious Dessert In Under 30 Minutes!

Oh yeah! Grandma Juice totally is going there! DESSERT! We had a version of this Green Tea Cheesecake last weekend at a really nice little Sushi place in Bakersfield, CA. I know, Bakersfield and Sushi really don’t belong together in the same sentence, but it totally happened! However, they had a caramel type sauce drizzled over and topped with pecans. I didn’t really dig that. So… I changed it, of course. I also swapped out regular cream cheese for fat free so I can handle my less than girlish figure. Feel free to swap it back in if your girlish figure is still rockin’. It’s very easy, takes 30 minutes or less, and was seriously to die for! Try it!

Ingredients:

(2) 8oz Packages of Fat-Free Cream Cheese (softened)
2 Eggs (beaten)
3/4 Cup White Sugar
1 TBSP Green Tea Powder (find in health food stores & online)
2 TSP Vanilla (extract is ok to substitute)
1 9 Inch Prepared Graham Cracker Pie Crust

Directions:

Preheat oven to 350 degrees. In a large mixing bowl, beat cream cheese and sugar together with hand or stand mixer until it turns smooth. (stand is way easier!)
In the same bowl, mix in green tea powder, eggs, and vanilla (or extract) until light and creamy.
Pour mix into the prepared graham cracker pie crust. (lick the bowl and utensils when done, it’s tasty!)
Bake in preheated oven for 25 minutes. You’ll know it’s done when the center jiggles evenly when the cake is shaken lightly. (do NOT shake vigorously, that’s just playing)
Refrigerate at least 1 hour before serving. (over night is best, but if you have no self control, at least wait 1 hour so it’s chilled)
EAT! ENJOY!

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Used contact lens solution hosts giant virus, ecosystem of parasites

admin — Mon, 12 Nov 2012 15:10:48 +0000

“Virus factories” and more are found in an amoeba within contact lens fluid.

by John Timmer

http://arstechnica.com/science/2012/10/contact-lens-solution-hosts-giant-virus-ecosystem-of-parasites/

In July of last year, researchers in France described a rather disturbing example of what could happen if you’re not careful about cleaning your contact lenses. A 17-year-old patient had been wearing monthly lenses well past their expiration date, and rinsing them with a cleaning solution she’d diluted with tap water. The end result was an eye infection. Luckily, a bit of care managed to clear it up.

In the meantime, the people who treated her dumped some of the solution out of her contact lens case and started trying to culture any parasites that would grow out of it. In the end, they got an entire ecosystem—all contained inside a single strain of amoeba. Among the parasites-within-parasites were a giant virus, a virus that targets that virus, and a mobile piece of DNA that can end up inserting into either of them.

When they first grew the amoeba from the contact lens cleaning solution, they found it contained two species of bacteria living inside it. But they also found a giant virus, which they called Lentille virus. These viruses have been known for a while, and they tend to affect amoebas, so this wasn’t a huge surprise.

More recently, however, researchers discovered these viruses can get viruses. Or, more precisely, virophages. Upon infecting an amoeba, the giant virus builds what’s become called a “virus factory” within the cell, where its genetic material is copied and new viruses are built from parts encoded by its genes. The virophages can spread from amoeba to amoeba, but once they enter the cell, they head straight for the virus factory, where they get replicated.

When the scientists sequenced the genome of the Lentille virus, it had a few surprises for them. To begin with, it contained a new virophage of its own, which they called Sputnik 2. An infected amoeba would release virophage particles, suggesting that the virus could move between these organisms on its own. But the authors also found a copy of the virus inserted into the giant Lentille virus genome. And, if an amoeba were infected with one of these giant viruses, it would also start producing the virophage.

In other words, the virophage has two ways of spreading. Like any other virophage, it can spread from amoeba to amoeba, and will find a home in any that also contain a Lentille virus. But once it finds one, it inserts itself into its giant viral genome, ensuring that any future amoeba it infects gets a copy of the virophage, too. Although it has a preference to jump into the giant virus genome, it can hop elsewhere. That could potentially cause mutations and speed up the evolution of its host.

But that wasn’t the only parasite the authors found in Lentille virus. A shorter sequence, one containing six genes, was also associated with the viral genome. As with the virophage, this sequence was found as both a free-standing piece of DNA and inserted into the genome of the Lentille virus. But there was a rather significant difference: none of the genes it carried encoded the sorts of proteins that are used to package a virus. Instead, it had several features normally found in transposons, mobile genetic elements that hop around the genomes of organisms ranging from bacteria to mammals.

As if there weren’t enough names to deal with, the authors deemed this DNA element a “transpoviron,” for a transposon that targets a virus. They showed that, shortly after an infection with a Lentille virus, its resident transpoviron would be copied out of its host genome, form into circle, and start making copies of itself. These copies were then available to insert into genomes of any other viruses that were around—there’s even some evidence that a copy inserted into Sputnik 2 in the past.

By looking at the sequences of some other giant viruses, they also concluded that Lentille virus isn’t alone in carrying these molecular parasites.

The authors conclude by painting a picture of the giant viruses as supporting an entire DNA-based ecosystem of mobile genetic elements, which spread to other amoebas (and other viruses) by a variety of means. Given that we’ve found so much so shortly after starting to look, the authors suggest that we’ve likely only scratched the surface of its diversity.

PNAS, 2012. DOI: 10.1073/pnas.1208835109

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Election Time

admin — Sun, 04 Nov 2012 15:54:10 +0000

Now that the election is upon us share with others, your thoughts and opinions on who should be the next president of the united states.

Highlights from the first presidential debate between President Obama and Mitt Romney in Denver, Colorado. Watch all of the debates LIVE at cnn.com/debates For more CNN videos, check out our YouTube channel at www.youtube.com Or visit our site at www.cnn.com
Video Rating: 4 / 5

The Vice Presidential debate between Joe Biden and Paul Ryan in the run up to the general election in November.

Watch President Obama and Governor Romney in the second 2012 US presidential debate from New York.
Video Rating: 4 / 5

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The Aftermath Of Hurricane Sandy!

admin — Wed, 31 Oct 2012 21:06:55 +0000

Now that storm has hit the eastcoast, And caused so much damage. What can you do to help?

Ginger Zee, Matt Gutman track the latest weather across America.

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Dietary Supplements Can Cause Liver Injury, Says Hepatologist

admin — Tue, 30 Oct 2012 15:20:26 +0000

Niacin, comfrey, Kava and even green tea in high doses can cause liver injury. A Loyola liver specialist praises the new LiverTox free online database of drugs and explains acetaminophen is just one of many drugs taken that negatively impacts liver health.

Dose-dependent (acetaminophen) and idiosyncratic drug-induced liver injury (DILI) is the leading cause of acute liver failure in the United States, responsible for approximately 50 percent of all reported cases. “Awareness of the dangers of acetaminophen has risen but many consumers and even many health care professionals are not aware that certain popular herbal and dietary supplements can also cause liver damage,” says Steven Scaglione, MD, hepatology, Loyola University Health System (LUHS) and the Stritch School of Medicine (SSOM). “Kava, comfrey, valerian, vitamin A, niacin and even green tea, when consumed in high doses, have been linked to liver disease.”

LiverTox, a new database launched Oct. 12 by the National Institutes of Health (NIH), has a searchable database of about 700 medications. “The LiverTox web site is very user-friendly and provides evidence-based data in a clear and succinct manner,” says Scaglione. As part of the U.S. Department of Health and Human Services, the NIH will be adding another 300 drugs within the next few years.

Acetaminophen is one of the most widely used over-the-counter pain relievers and more than 25 billion doses are sold yearly. “Therapeutic doses of acetaminophen have been associated with liver toxicity,” says Scaglione, who cares for liver patients at Loyola. Acetaminophen is also a basic component in many over-the-counter cold and flu remedies for adults and children.

“Liver injury caused by medications is often difficult to identify and diagnose as well as treat,” said Scaglione, who also specializes in live transplantation and research. “The new LiverTox online reference is ideal for medical professionals as an educational tool and a guide in the evaluation of patients with suspected drug induced liver injury. The use of case examples is particularly helpful.”

Scaglione is board certified in internal medicine and gastroenterology. He is part of the Loyola liver-referral system for transplantation with offices throughout Illinois.

Patients may call 1- 85-LIVER DOC (1-855-483-7362) for additional information on Loyola’s liver program, or to make appointments.

The above story is reprinted from materials provided by Loyola University Health System, via Newswise.

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New Findings On Men’s Genes Could Alter Interpretation of PSA Test

admin — Tue, 30 Oct 2012 15:02:26 +0000

By studying a specific part of the male DNA, it may be possible to refine the interpretation of PSA tests. This would reduce the risk of men being treated for prostate cancer unnecessarily.

The findings have been presented in a thesis by Christel Björk at Lund University, Sweden, who has carried out the study with her colleague Hannah Nenonen, supervised by researcher Yvonne Lundberg Giwercman.

A PSA test measures the level of PSA (prostate-specific antigen) in the blood, and raised PSA can signal an increased risk of cancer; however, this is not the case for everyone. The problem is that there is no good way to separate those with naturally high levels of PSA from those at increased risk of prostate cancer.

“If we know that a man has a naturally high level of PSA, this can be taken into account in a PSA test, and the patient may be able to avoid arduous treatment with a risk of side-effects,” says Christel Björk, a doctoral student at the Department of Clinical Sciences, Lund University.

The present study shows how a man’s genetic characteristics can affect the androgen receptor, a protein that has an important function in the male reproductive system. It regulates the effect of testosterone and controls production of prostate-specific antigen.

The researchers studied healthy men in different age groups and discovered a connection between PSA levels in the blood and DNA structure of the androgen receptor. The highest PSA levels were found in the men with the most common variant of the androgen receptor, i.e. the largest group of men.

“Both the PSA level and the genetic characteristics can be identified with a blood test,” says Yvonne Lundberg Giwercman, Associate Professor at the Department of Clinical Sciences, Lund University.

The study is based on samples from around 400 men from Sweden and Norway. Before the results can be implemented for PSA tests in the health service, the study must be repeated on a larger group.

“We have access to material covering around 3 200 men from seven European countries and the idea is to investigate whether our preliminary findings can be verified on this group in the near future,” explains Yvonne Lundberg Giwercman.

The above story is reprinted from materials provided by Lund University.

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Mechanism Found for Destruction of Key Allergy-Inducing Complexes, Researchers Say

admin — Mon, 29 Oct 2012 11:58:41 +0000

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Researchers have learned how a synthetic molecule destroys complexes that induce allergic responses — a discovery that could lead to the development of highly potent, rapidly acting interventions for a host of acute allergic reactions.

The study, published online Oct. 28 in Nature, was led by scientists at the Stanford University School of Medicine and the University of Bern, Switzerland.

The new inhibitor disarms IgE antibodies, pivotal players in acute allergies, by detaching the antibody from its partner in crime, a molecule called FcR. (Other mechanisms lead to slower-developing allergic reactions.)

“It would be an incredible intervention if you could rapidly disconnect IgE antibodies in the midst of an acute allergic response,” said Ted Jardetzky, PhD, professor of structural biology and senior investigator for the study. It turns out the inhibitor used by the team does just that.

A myriad of allergens, ranging from ragweed pollen to bee venom to peanuts, can set off IgE antibodies, resulting in allergic reactions within seconds. The new inhibitor destroys the complex that tethers IgE to the cells responsible for the reaction, called mast cells. Severing this connection would be the holy grail of IgE-targeted allergy treatment.

The first time a potential allergen enters the body, some people respond by making allergen-specific IgE antibodies. These antibodies stick around long after the initial allergen is cleared from the body. Most of the antibodies get snagged by IgE-specific receptors called FcRs, which are exposed on the surface of mast cells. The mast cells are then primed to react the next time a person encounters the allergen.

Dissociation of this IgE-FcR interaction is a sought-after goal of allergy treatment for a good reason: IgE-coated mast cells are grenades of histamine, and re-encountering the allergen is equivalent to pulling out the clip. When an allergen makes a return visit, it binds to the pre-loaded IgE on the mast cell surface, triggering the release of inflammatory mediators — including histamine — that promote the allergic response. As allergy sufferers are well aware, these nasty reactions can occur within a matter of seconds. In a severe allergic response, sudden anaphylactic shock and death can be the result.

The key to actively disabling the allergic response lies in the separation of IgE from the FcRs on the surface of mast cells. But separating these dangerous couples is a tall order because their interaction is extremely stable — sensitizing the mast cells for weeks. Currently available treatment using omalizumab (an anti-IgE antibody sold under the trade name Xolair) can block new interactions between IgE and FcR, but it is not designed to pry the molecules apart once they’ve formed a bond on the surface of a mast cell. So Xolair can dampen the allergic response, but as stated on the product’s website: “Xolair is not a rescue medicine and should not be used to treat sudden asthma attacks.”

While simply blocking IgE binding is helpful for some allergy sufferers, when it comes to the rapid quenching of an acute allergic response, “what you’d really like to do is get rid of it,” said Jardetzky. Along with scientists at the University of Bern, his team discovered that an engineered protein inhibitor called DARPin E2-79 stripped IgE from the mast cell receptor. Using this inhibitor, “an interaction that normally lasts for hours or days in terms of its stability is stripped off in a matter of seconds,” said Jardetzky.

DARPin E2-79 is one of a family of engineered inhibitors containing protein-binding regions called ankryin repeats. While Jardetzky’s group was using structural biology and biophysical approaches to probe the weak spots in the IgE-FcR interaction, scientists at the University of Bern were tinkering with DARPins that dampened IgE’s disastrous effects. The collaboration of the two groups resulted in the characterization of DARPin E2-79, an inhibitor that goes beyond mere blockade to actively disassemble the IgE-FcR power couple.

Jardetzky’s group solved E2-79′S structure and used this information to model its interaction with the IgE-FcR pair. Then, using sensitive biochemical techniques that detect step-by-step binding interactions between molecules, the teams were able to tease out the mechanism that the inhibitor uses to break the IgE-FcR bond.

The researchers found that E2-79 hastens the separation of the two molecules by taking advantage of a moment of weakness in the relationship between IgE and FcR. IgE maintains its interaction with FcR using two contact points, and occasionally one of these points releases while the other one keeps the pair together. Normally this brief looseness isn’t enough to separate the couple, but E2-79 can swoop into the small space between them, effectively driving the couple apart.

While E2-79 is the first molecule to display these IgE stripping characteristics, Jardetzky hopes that this work will stimulate the discovery of smaller compounds capable of working even more efficiently. Drug developers generally expect large macromolecules like E2-79 to be less potent than small molecule inhibitors and unlikely to be able to disrupt complexes, so the fact that E2-79 worked so well was a surprise. Small molecules are more amenable to oral administration, and are easier and cheaper to manufacture than large macromolecules. “Now we’re in the hunt for a small molecule that could have this kind of activity. That would be the real hit,” said Jardetzky.

The discovery of E2-79′s mechanism of IgE inhibition could lead to rapid discoveries from other labs as well. Now that scientists know what mechanism to look for, they may be inspired to dig back through freezers full of IgE inhibitors that were identified years ago, said Jardetzky. In the light of techniques described in this study, perhaps once-neglected inhibitors will show new promise in the treatment of allergic disease.

The study’s primary authorship was shared between Beomkyu Kim, PhD, a Stanford graduate student, and Alexander Eggel, PhD, at the University of Bern. The other Stanford co-author is research assistant Svetlana Tarchevskaya.

The study was funded by the National Institutes of Health, the American Asthma Foundation and the Swiss National Science Foundation.

The above story is reprinted from materials provided by Stanford University Medical Center. The original article was written by Jessica Shugart.

Journal Reference:

Beomkyu Kim, Alexander Eggel, Svetlana S. Tarchevskaya, Monique Vogel, Heino Prinz, Theodore S. Jardetzky. Accelerated disassembly of IgE–receptor complexes by a disruptive macromolecular inhibitor. Nature, 2012; DOI: 10.1038/nature11546

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New Clues to How the Brain and Body Communicate to Regulate Weight

admin — Fri, 26 Oct 2012 20:59:34 +0000

Maintaining a healthy body weight may be difficult for many people, but it’s reassuring to know that our brains and bodies are wired to work together to do just that — in essence, to achieve a phenomenon known as energy balance, a tight matching between the number of calories consumed versus those expended. This careful balance results from a complex interchange of neurobiological crosstalk within regions of the brain’s hypothalamus, and when this “conversation” goes awry, obesity or anorexia can result.

Given the seriousness of these conditions, it’s unfortunate that little is known about the details of this complex interchange. Now research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) provides new insights that help bring order to this complexity. Described in the October 26 issue of the journal Cell, the findings demonstrate how the GABA neurotransmitter selectively drives energy expenditure, and importantly, also help explain the neurocircuitry underlying the fat-burning properties of brown fat.

“Our group has built up a research program with the overall goal of unraveling the ‘wiring diagram’ by which the brain controls appetite and the burning of calories,” says senior author Bradford Lowell, MD, PhD, a Professor of Medicine in BIDMC’s Division of Endocrinology and Harvard Medical School. “To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable.”

A pearl-sized region that directs a multitude of important functions in the body, the hypothalamus is the brain’s control center for energy balance. This balance results when the brain receives feedback signals from the body that communicate the status of fuel stores and then integrates this with input from the external world as well as a person’s emotional state to modify feeding behavior and energy expenditure.

In this new study, the researchers investigated a unique population of neurons that are located at the base of the brain in the arcuate nucleus of the hypothalamus. “We genetically engineered mice such that they have a specific defect that prevents these neurons from releasing the inhibitory neurotransmitter, GABA,” says Lowell. “Mice with this defect developed marked obesity and, remarkably, their obesity was entirely due to a defect in burning off calories,” he explains, adding that food intake was entirely unaffected.

By next engineering another group of mice in which these neurons could be selectively turned on at different times, the team went on to show that the arcuate neurons act through a series of downstream neurons to drive energy expenditure in brown fat. Brown fat has been making headlines lately because many recent studies have revealed that, unlike energy-storing white fat, brown fat burns energy to generate heat. This process is called thermogenesis.

“Energy expenditure mediated by brown adipose tissue is critical in maintaining body weight and prevents diet-induced obesity. Its brain-based regulatory mechanism, however, is still poorly understood,” says first author Dong Kong, PhD, an Instructor in Medicine in Lowell’s laboratory. “Our discovery of a hypothalamus-based neurocircuit that ultimately controls thermogenesis is an important advance,” adds Lowell. The investigators additionally found that when they turned on these neurons, energy expenditure was entirely dependent upon release of GABA. These results reveal that release of GABA from arcuate neurons selectively drives energy expenditure.

“Our findings have greatly advanced our understanding in the control of energy expenditure and have provided novel insights into the pathogenesis of obesity,” says Kong.

The unique features of arcuate neurons are important because they could provide an opportunity to experimentally modify the brain’s control of energy expenditure. Specifically, neurons receiving GABA-mediated signals from arcuate neurons are likely to play important roles in regulating energy expenditure, but not food intake.

“It is now important to fully delineate the upstream neurons that control these thermogenesis-regulating arcuate neurons, and also the downstream neurons that complete the ‘circuit’ to brown adipose tissue,” Lowell adds. He and his colleagues have identified several specific types of neurons that act downstream of arcuate neurons, but more research is needed to provide a clear and definitive diagram. Such work could uncover new opportunities for pharmacologic interventions that might lead to effective treatments for obesity and its related complications such as diabetes.

The above story is reprinted from materials provided by Beth Israel Deaconess Medical Center, via EurekAlert!, a service of AAAS.

Journal Reference:

Dong Kong, Qingchun Tong, Chianping Ye, Shuichi Koda, Patrick M. Fuller, Michael J. Krashes, Linh Vong, Russell S. Ray, David P. Olson, Bradford B. Lowell. GABAergic RIP-Cre Neurons in the Arcuate Nucleus Selectively Regulate Energy Expenditure. Cell, 2012; 151 (3): 645 DOI: 10.1016/j.cell.2012.09.020

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