Chris Brown has dropped a brand new video for his song "Fine China" off his upcoming album "X." The singer stopped by TODAY on Monday to promote the premiere of his new music, which can be seen here:
The video offers a semi-futuristic take on the classic good-girl-hooks-up-with-bad-boy story line. It even starts with a disapproving dad (hey, that's the?Dharma Initiative guy?from "Lost"!) chastising his daughter before she's whisked away by the "outsider, thug" Brown in an orange Lamborghini.
"I'll go anywhere with you," the girl tells Brown as the music starts and they drive through a Tron-like urban setting before arriving at a back-alley club. As the music kicks into high gear and Brown demonstrates his dance moves, this is where you remember all of those Michael Jackson comparisons.
"I'm not dangerous. When you're mine, I'll be generous. You're irreplaceable, a collectible. Just like fine china."?
The R&B star started the morning by joining a flash mob of dancers on the TODAY Plaza. He later sat down with Matt Lauer to discuss his maturity as a musician and the changes he's made as a man since being convicted of assaulting girlfriend Rihanna in 2009.
As for the music, Brown said his approach to making "X" was to put a lot of writers and producers in the same place and have a "camp" aimed at generating chemistry between everybody. A tactic that he says leads to more creative energy.
Lauer asked Brown what has changed musically in the years since he released his first music at age 16. "My music is maturing so I have a lot more to talk about, whether it be personal relationships, trials and tribulations, just me as a young 23-year-old man."
Mechanism of mutant histone protein in childhood brain cancer revealedPublic release date: 1-Apr-2013 [ | E-mail | Share ]
Contact: Joseph Bonner joseph.bonner@rockefeller.edu 212-327-8998 Rockefeller University
Most cancer treatments are blunt. In an attempt to eradicate tumors, oncologists often turn to radiation or chemotherapy, which can damage healthy tissue along with the cancerous growths. New research from C. David Allis' laboratory at Rockefeller University may bring scientists closer to designing cancer therapeutics that can target tumors with pinpoint accuracy.
Their findings, published last week in Science Express, follow a recent series of discoveries by several international genome sequencing consortiums that directly links a mutated histone protein to a rare brain stem cancer in children called DIPG. Collectively, these studies represented the first time scientists had linked a histone mutation to a disease, and piqued the interest of Peter Lewis, a research associate in Allis' Laboratory of Chromatin Biology and Epigenetics, who spearheaded these new studies.
Together with DNA, histones comprise the gene packaging material called chromatin. The mutation occurs on histone H3, and involves the remarkably specific substitution of one amino acid, lysine, for another, methionine, at a key position on the histone's tail, "silencing" the associated gene. Normally, gene silencing arises when an enzyme called a methyltransferase, containing a structural region called the SET domain, attaches a methyl chemical group to the lysine at position 27 in the H3 tail. This highly specific chemical reaction, called methylation, is disrupted by the replacement of the lysine with methionine, which could result in gene mis-regulation.
Lewis and his colleagues looked at human DIPG tumors that contained the lysine-to-methionine substitution and determined that mutated histone H3 comprised anywhere from 3.6 percent to 17.6 percent of total H3 in DIPG samples. They also found a global reduction in the levels of methylation of normal H3 histones when small amounts of the mutant H3 were added to normal human cells.
"I have often said, 'Every amino acid in histones matters,'" says Allis, who is the Joy and Jack Fishman Professor. "These studies underscore just how true that may be."
The researchers went on to demonstrate that the reduction in methylation of normal H3 histones results from interference with activity of a methyltransferase called PRC2 by the mutant histone. Methylation of normal H3 by PRC2 leads to repression of genes involved in cellular growth pathways. Without methylation, genes involved in these pathways likely become activated, promoting the growth of tumors in DIPG. Allis and Lewis received funding from the National Institutes of Health and the Starr Cancer Consortium. Key collaborators in this work included Oren Becher at Duke University Medical Center and Tom Muir at Princeton University and their colleagues.
"Our finding provides us with a useful tool for probing biological processes," says Lewis. "This also tells us how to inhibit enzymes, which could lead to the development of pharmaceuticals that mimic the action of these mutants."
"We now have a model for the promotion of brain stem cancers through aberrant epigenetic silencing through the inhibition of PRC2 by a mutant histone," says Allis. "We have uncovered a potentially useful mechanism to exclusively inhibit individual SET-domain methyltransferases, and conceivably other chromatin-modifying enzymes, implicated in a variety of malignancies."
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Mechanism of mutant histone protein in childhood brain cancer revealedPublic release date: 1-Apr-2013 [ | E-mail | Share ]
Contact: Joseph Bonner joseph.bonner@rockefeller.edu 212-327-8998 Rockefeller University
Most cancer treatments are blunt. In an attempt to eradicate tumors, oncologists often turn to radiation or chemotherapy, which can damage healthy tissue along with the cancerous growths. New research from C. David Allis' laboratory at Rockefeller University may bring scientists closer to designing cancer therapeutics that can target tumors with pinpoint accuracy.
Their findings, published last week in Science Express, follow a recent series of discoveries by several international genome sequencing consortiums that directly links a mutated histone protein to a rare brain stem cancer in children called DIPG. Collectively, these studies represented the first time scientists had linked a histone mutation to a disease, and piqued the interest of Peter Lewis, a research associate in Allis' Laboratory of Chromatin Biology and Epigenetics, who spearheaded these new studies.
Together with DNA, histones comprise the gene packaging material called chromatin. The mutation occurs on histone H3, and involves the remarkably specific substitution of one amino acid, lysine, for another, methionine, at a key position on the histone's tail, "silencing" the associated gene. Normally, gene silencing arises when an enzyme called a methyltransferase, containing a structural region called the SET domain, attaches a methyl chemical group to the lysine at position 27 in the H3 tail. This highly specific chemical reaction, called methylation, is disrupted by the replacement of the lysine with methionine, which could result in gene mis-regulation.
Lewis and his colleagues looked at human DIPG tumors that contained the lysine-to-methionine substitution and determined that mutated histone H3 comprised anywhere from 3.6 percent to 17.6 percent of total H3 in DIPG samples. They also found a global reduction in the levels of methylation of normal H3 histones when small amounts of the mutant H3 were added to normal human cells.
"I have often said, 'Every amino acid in histones matters,'" says Allis, who is the Joy and Jack Fishman Professor. "These studies underscore just how true that may be."
The researchers went on to demonstrate that the reduction in methylation of normal H3 histones results from interference with activity of a methyltransferase called PRC2 by the mutant histone. Methylation of normal H3 by PRC2 leads to repression of genes involved in cellular growth pathways. Without methylation, genes involved in these pathways likely become activated, promoting the growth of tumors in DIPG. Allis and Lewis received funding from the National Institutes of Health and the Starr Cancer Consortium. Key collaborators in this work included Oren Becher at Duke University Medical Center and Tom Muir at Princeton University and their colleagues.
"Our finding provides us with a useful tool for probing biological processes," says Lewis. "This also tells us how to inhibit enzymes, which could lead to the development of pharmaceuticals that mimic the action of these mutants."
"We now have a model for the promotion of brain stem cancers through aberrant epigenetic silencing through the inhibition of PRC2 by a mutant histone," says Allis. "We have uncovered a potentially useful mechanism to exclusively inhibit individual SET-domain methyltransferases, and conceivably other chromatin-modifying enzymes, implicated in a variety of malignancies."
###
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
If you apply heading styles to section or chapter titles in your document, then turn on the Navigation Pane (View tab,? Show group, Navigation Pane check box checked). You will be able to jump to different sections without beating up your Page Down and Page Up keys! To easily assign heading styles, use the Ctrl+Alt+1, Ctrl+Alt+2 and Ctrl+Alt+3 shortcuts to assign Heading 1, Heading 2 and Heading 3 styles respectively.
Have to refer back to certain sections of your document that aren?t necessarily notated by a heading style? Use a Bookmark!? Click into the area you?d like to mark. On the Insert tab, in the Links group, choose the Bookmark button. Type in a name for your bookmark, like ?needs org chart diagram,? then when you?re ready to start adding illustrations to your document, you use the Ctrl+G shortcut to ?go to? your bookmarks.
Thinking about doing a Find/Replace all, but not sure if it will give the desired results? Using the Browse the results? tab in the Navigation Pane will show you the results, in context everywhere they appear, giving you an opportunity to predict the outcome of a global change. Have an older version of Office? Just use the Find dialog box (Ctrl+F) and choose the Reading Highlight button to highlight the search results all over your document.
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Listen, when you work hard (and play hard) the way we do, your hands are going to get dirty from time to time. In fact, if we've got one piece of advice for frequent trade show attendees, it would be: wash your hands. A lot. Of course, a clean water source isn't always waiting for you between booths -- when that happens, there's no beating a well-placed bottle of hand sanitizer. But while the likes of Purell and its ilk have traditionally done the trick, we've always longed for a solution that could combine our sanitization obsessions with our passion for casual gaming. That wait, mercifully, is now over, thanks to a groundbreaking partnership between the fowl flingers at Rovio and those Ph.D.s in oral care products (the Firefly Hello Kitty toothbrush, anyone?): Dr. Fresh.
Part of the industry-leading Infectiguard Kids line, Angry Birds Hand Sanitizer offers a slim and slick profile, perfect for tiny hands. The twist-off lid is located at the bottom of the bottle, pointing in a downward orientation when positioned as intended. The whole thing is supported by a carabiner laced through a loop in the top of the skinny bottle, so the sanitizer can be suspended from a backpack, messenger bag or other carrying case for easy access to its cleansing contents. And at 1.8 fluid ounces, the whole thing comes in well under the TSA's carry-on liquid restrictions.
MOSCOW (Reuters) - The last Soviet leader Mikhail Gorbachev said on Saturday Russia will face unrest unless society is made more democratic despite President Vladimir Putin's success in cracking down on dissent.
Gorbachev, whose perestroika (restructuring) and glasnost (openness) reforms in the 1980s failed to avert the collapse of the Soviet Union, has sympathized with protests, mainly by the rising urban middle class, against alleged ballot fraud and political corruption.
"The authorities have managed to beat down the wave of protest for a while, but the problems have not disappeared. If everything remains as before, they will escalate," Gorbachev was quoted by the RIA news agency as saying in a lecture.
"This means that we face a new attempt by Russian society to move to real democracy and it will be of historic significance."
The warning by Gorbachev, active in public life at the age of 82 and co-publisher of the independent Novaya Gazeta newspaper, came as Putin, who won a third presidential term a year ago, seeks to consolidate power.
Rather than engaging in dialogue with opponents, Putin has sought to marginalize them, while ratcheting up foreign policy rhetoric to create an atmosphere of a nation under siege.
In the past week, officials searched offices of foreign non-governmental organizations, Putin ordered snap military exercises in the Black Sea and he created a 'hero of labor' honor reminiscent of a Soviet command economy.
Russia's economic growth has more than halved since before the 2008 financial crisis and is now close to stagnating, reflecting its reliance on oil export revenues.
Experts call for long-term structural reforms to reducing the state's role in the economy, addressing pressures caused by an ageing population, and cutting red tape and corruption.
Gorbachev said Russia risked stagnation.
"We have come to the point when we have cut off perestroika. Politics is increasingly turning into imitation. We need a new system of the governance of the country," said Gorbachev.
(Reporting by Maya Dyakina; Editing by Jason Webb)
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Public release date: 1-Apr-2013
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