Apr. 24, 2013 ? A team of researchers led by Artem R. Oganov, a professor of theoretical crystallography in the Department of Geosciences, has made a startling prediction that challenges existing chemical models and current understanding of planetary interiors -- magnesium oxide, a major material in the formation of planets, can exist in several different compositions. The team's findings, "Novel stable compounds in the Mg-O system under high pressure," are published in the online edition of Physical Chemistry Chemical Physics. The existence of these compounds -- which are radically different from traditionally known or expected materials -- could have important implications.
"For decades it was believed that MgO is the only thermodynamically stable magnesium oxide, and it was widely believed to be one of the main materials of the interiors of the Earth and other planets," said Qiang Zhu, the lead author of this paper and a postdoctoral student in the Oganov laboratory.
"We have predicted that two new compounds, MgO2 and Mg3O2, become stable at pressures above one and five million atmospheres, respectively. This not only overturns standard chemical intuition but also implies that planets may be made of totally unexpected materials. We have predicted conditions (pressure, temperature, oxygen fugacity) necessary for stability of these new materials, and some planets, though probably not the Earth, may offer such conditions," added Oganov.
In addition to their general chemical interest, MgO2 and Mg3O2 might be important planet-forming minerals in deep interiors of some planets. Planets with these compounds would most likely be the size of Earth or larger.
The team explained how its paper predicted the structures in detail by analyzing the electronic structure and chemical bonding for these compounds. For example, Mg3O2 is forbidden within "textbook chemistry," where the Mg ions can only have charges "+2," O ions are "-2, and the only allowed compound is MgO. In the "oxygen-deficient" semiconductor Mg3O2, there are strong electronic concentrations in the "empty space" of the structure that play the role of negatively charged ions and stabilize this material. Curiously, magnesium becomes a d-element (i.e. a transition metal) under pressure, and this almost alchemical transformation is responsible for the existence of the "forbidden" compound Mg3O2.
The findings were made using unique methods of structure prediction, developed in the Oganov laboratory. "These methods have led to the discovery of many new phenomena and are used by a number of companies for systematically discovering novel materials on the computer -- a much cheaper route, compared to traditional experimental methods," said Zhu.
"It is known that MgO makes up about 10 percent of the volume of our planet, and on other planets this fraction can be larger. The road is now open for a systematic discovery of new unexpected planet-forming materials," concluded Oganov.
This work is funded by the National Science Foundation and DARPA.
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Journal Reference:
Qiang Zhu, Artem R. Oganov, Andriy O. Lyakhov. Novel stable compounds in the Mg?O system under high pressure. Physical Chemistry Chemical Physics, 2013; DOI: 10.1039/C3CP50678A
Note: If no author is given, the source is cited instead.
Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
HENDERSON, Nev. (AP) ? A Las Vegas man is behind bars after police say he became so enraged at being turned away from speaking with a pastor that he plowed his car through an entrance and down the hall of a large Henderson church.
Kevin Wilson was being held Thursday on $8,000 bail at the Henderson city jail pending a court appearance Monday on felony burglary and destruction of property charges.
Henderson police say the 51-year-old Wilson got out of his Kia Spectra, smashed furniture and knocked holes in the walls at Central Christian Church before police arrested him about 5 a.m. Wednesday.
Police spokesman Keith Paul says a city building inspector later determined the church building remained structurally sound.
It wasn't immediately clear if Wilson had an attorney.
"Why don't you leave him alone?" supporters of President Obama tweet me. "Give the man a break and stop being disrespectful."
"You're all just a bunch of suck-up lefties," opponents of President Obama tweet at me, referring, I presume, to the White House Press Corps. "Why don't you try asking a real question for a change?"
SEE MORE: Could the 2013 NFL draft be one of the weakest ever?
You can't please everyone. And someone is always going to be mad at the White House Press Corps. But it's all in eye of the beholder. And, as I'll explain, there have been times when both sides have been right.
Conservatives often like to say that White House reporters (who often work for big, conservative companies like News Corp., Time Warner, and Disney) are liberals who just pass along whatever they are spoonfed by Team Obama. In this view, it's all a big love fest between journalists and the president down the hall.
They ask why the "liberal media" ignored the Sept. 11 Benghazi attack that killed four Americans, including Ambassador Chris Stevens. Somehow these critics missed the 800+ articles that The Washington Post and New York Times alone have run on the story.
Also: If White House reporters are lapdogs, why does President Obama hold so few news conferences? If we are lapdogs, why doesn't Obama talk more to newspapers and TV networks accused of being "friendlies," like the Times or the Post or MSNBC??And if reporters are so eager to passively be spoonfed everything Obama says, why does he feel it necessary build his own massive network to get his point of view out?
If anything, Obama is press averse to an historic degree. "The way the president's availability to the press has shrunk in the last two years is a disgrace," ABC News White House reporter Ann Compton recently told Politico. Ann should know. She's been at the White House since Gerald Ford was president. "This is different from every president I covered. This White House goes to extreme lengths to keep the press away," she adds.
Today's White House Press Corp. is hardly a lapdog. But in the past, Beltway reporters have been cowed by presidents.?
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Franklin D. Roosevelt, who was paralyzed by polio, served 12 years as president, yet the FDR library in Hyde Park, N.Y., only has three photos of him in a wheelchair. "There was a gentlemen's understanding with the press," says the library's website, that photographs displaying FDR's disability were not published." Think that would happen today?
Similarly, as the Monica Lewinsky scandal showed, reporters today simply won't turn a blind eye to a philandering president. In the 1960s, the press corps did exactly that with John F. Kennedy. While in office, it's believed he slept with a woman who also slept with two Mafia bosses; it's also believed that another mistress was an East German spy. Think a White House reporter would ignore a bombshell like that today?
Of course, it's also true that journalists were obedient little lapdogs on matters far more serious than even Benghazi. After that other September 11 attack (you know, back in 2001), the White House leaned on the press corps big time. Attorney General John Ashcroft said questioning the Bush administration "only aids terrorists" and "gives ammunition to America's enemies," while Press Secretary Ari Fleischer warned that "all Americans... need to watch what they say, watch what they do."
In the run-up to the Iraq war from September 2002 to February 2003,?414 Iraq stories aired on the evening broadcasts of ABC, CBS and NBC News, according to media analyst Andrew Tyndall. More than 9 in 10 of them relied on Bush administration sourcing. Reporters did just 34 stories (8 percent) that required independent questioning of non-administration sources. And talk about not wanting to offend the White House: MSNBC fired its top-rated host, the super liberal Phil Donahue, because, as an internal memo said, Donahue's anti-administration views presented "a difficult public face for NBC in a time of war."
It gets worse still. In a news conference two weeks before the Iraq invasion, President Bush mentioned al Qaeda and the terrorist attacks of September 11 multiple times. No one challenged the connection Bush appeared to be making between al Qaeda and Iraq ? even though intelligence sources by then were publicly questioning the connection.
SEE MORE: What we don't know about Boston
That, ladies and gentlemen, is a lapdog press.
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PRAGUE (AP) ? The Czech Republic plans to donate 4 million koruna (some $200,000) to help the Texas town of West recover from a devastating fertilizer plant explosion.
The government decided to the provide aid in solidarity because a significant number of people in the town of 2,700 have Czech roots. The blast damaged numerous homes in the town.
The Foreign Ministry says Czech Ambassador to the U.S. Petr Gandalovic visited West last week and talked to Texas Gov. Rick Perry, West Mayor Tommy Muska and other officials about how to help.
A ministry statement Wednesday said the money will go toward repairing property in the town.
Thousands of Czechs, mostly from the eastern part known of Moravia, settled in Texas more than 100 years ago.
A housing complex, destroyed by a deadly fertilizer plant explosion, is pictured in the town of West, near Waco, Texas, April 21, 2013. Authorities said the death toll from the explosion on April 17, ... more? A housing complex, destroyed by a deadly fertilizer plant explosion, is pictured in the town of West, near Waco, Texas, April 21, 2013. Authorities said the death toll from the explosion on April 17, 2013 remained at 14 in West, a community of some 2,700 people, with 200 people injured. REUTERS/Michael Ainsworth/Pool (UNITED STATES - Tags: DISASTER ENVIRONMENT AGRICULTURE) less? ?
Projections continue to suggest negative results for Apple, but what is preventing Apple from dominating the market like it used to?
By Steph Solis / April 23, 2013
A man looks at his Apple iPad in front an Apple logo outside an Apple store in downtown Shanghai. Apple's luster is diminishing as it continues to lose market share to its competitors and face criticism from investors and suppliers.
Aly Song/Reuters/File
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As Apple continues to face growing competition, the company's allure is starting to fade in the eyes of investors and suppliers, according to new report from?Reuters. Meanwhile, the once dominant tech giant is losing market share as Samsung and other rivals continue to grow.?
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The concerns of shareholders apparently range from worries about smaller shipments to criticisms that the company has lost its innovative edge since iconic co-founder Steve Jobs died a year and a half ago.
Asian suppliers have told Reuters that they are trying to become less dependent on Apple as they encountered delays on deadlines from the company.
For the first time since December 2011, Apple?s stock closed last week below $400.
Apple will hold its financial conference call on quarterly results Tuesday afternoon. While Apple is still expected to show growth ? estimates of quarterly revenue currently circle $42.77 billion ? the projection is that Apple may be moving downward, Dan Moren of MacWorld reports.
"Apple is in some ways a sort of victim of its own success, especially when the term innovation starts being thrown around," says?Charles Golvin, a principal analyst at Forrester Research. In other words, Apple, which?has introduced multiple revolutionary products in the past, is under fire for not bringing an entirely different product to the market recently ? or at least fast enough.
What seems to be preventing Apple from owning the market is its pricing for smart phones, Golvin says. Apple could benefit from having a range of smart phone prices, similar to the range of options that were available for the iPod.?
Another possible issue is Apple?s pattern of releasing new products every year, some of which had relatively minor adjustments. Golvin notes that it seems to be harder for Apple to continue that trend with Samsung and other competitors releasing products more often.
John Koetsier of VentureBeat expressed similar concerns with Apple?s dominance in the market in December. He emphasizes the need for a change in Apple?s market strategy, including more aggressive pricing, if the company expects to stay on top.?
He notes that while Apple has helped innovate the computer and electronics industry, they need to "fill available niches in the new ecosystem" to compete with rivals like Google and Samsung.?
The company is at risk of falling back into the lull it saw in the late 20th century, according to Mr. Koetsier. "The problem for Apple, if the current sales and market trends continue, is that iOS will get less and less important, relatively speaking," Koetsier said. "And those massive profits will start to wither away, start to follow the leaders ? the new leaders ? and we?ll be back to the 90s."?
For more tech news, follow Steph on Twitter: @stephmsolis
Mayor Billy Kenoi and the Hawai?i County Department of Parks and Recreation are proud to welcome the public back to a thoroughly renovated and improved Wai?kea Recreation Center.
Under renovations a few months ago.
A public blessing and re-dedication ceremony will be held from 5:30 p.m. to 7 p.m. Friday, April 26, at the Hilo facility. Refreshments will be served, and several martial arts and other groups that use the Wai?kea Recreation Center will perform free athletic demonstrations.
Located at 1634 Kamehameha Avenue, the Wai?kea Recreation Center has undergone a five month, $1.7 million makeover that has made it more comfortable, accessible and safer for the numerous groups and individuals who use it.
New roof insulation, ceiling fans and lighting have been installed in the main gym area. Extensive termite and water damage have been repaired, new roofing systems installed, hazardous building materials removed, existing bathrooms and showers renovated, the entire facility repainted, and various other improvements performed to meet federal accessibility standards.
General contractor Stan?s Contracting Inc. also installed an underground drainage system in the parking lot, graded and repaved the parking area and three driveway entrances, and connected the facility to the County?s wastewater treatment system.
Many others helped to make an improved Wai?kea Recreation Center and save taxpayer money. Several martial arts organizations volunteered their time to complete various finishing touches in preparation for this weekend?s reopening, while personnel from the Department of Parks and Recreation?s Maintenance Division performed numerous repair tasks that complemented the contractor?s efforts.
The Department of Parks and Recreation wishes to thank the Shudokan Judo Club for improving the judo mat area, the Hilo Seishikan Aikido Club for repainting the kitchen, the Hilo Shin Shin Toitsu Aikido Club for beautifying the planter boxes, and the Kongo Zen Shorinji Ryu Son Ryu Karate Club for repainting the wooden floor of the martial arts practice area.
The department also wishes to recognize the following organizations for their monetary contributions and/or volunteer efforts toward improving the facility: Hilo Reshinkan Kendo Club; Hilo Tae Kwon Do Association; Wai?kea Judo Club; Hawai?i International Karate League; Hilo Kobukan Kendo Club; Hayaite Shotokan Karate; Atkins Martial Arts; Mo Min Kuen; Danish Fitness; Morning Fitness; Evening Fitness; and Insane Workout.
A sincere mahalo is extended to all Wai?kea Recreation Center users and the general public for their patience and understanding while this important recreational center was being enhanced, repaired, and made more accessible.
For more information, please contact Jason Armstrong, Public Information Officer, at 345-9105, or jarmstrong@co.hawaii.hi.us.
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Filed under: aloha, Announcements, Big Island, Community, Entertainment, Hawaii, Hawaii County Public Notices, Hilo, Kids, Sports Tagged: | Hawaii County Parks and Recreation, Mayor Billy Kenoi, Waiakea Recreation Center
Link between inherited endocrine tumor syndrome and much-studied cell pathwayPublic release date: 24-Apr-2013 [ | E-mail | Share ]
Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine
PHILADELPHIA A mutation in a protein called menin causes a hereditary cancer syndrome called MEN1 (multiple endocrine neoplasia type 1). Individuals with MEN1 are at a substantially increased risk of developing neuroendocrine tumors, including cancer of the pancreatic islet cells that secrete insulin.
Yet knowing these connections and doing something to improve fighting the syndrome are two different things. Researchers still did not exactly understand how menin mutations lead to MEN1 syndrome, and more importantly, what molecular pathways might be dysregulated by menin mutations and thus can be targeted to improve therapy against this type of cancer. Now, researchers at the Perelman School of Medicine at the University of Pennsylvania have found that pathway, which may lead to a new treatment for patients with MEN1 and sporadic endocrine tumors.
A research team led by Xianxin Hua, MD, PhD, associate professor of Cancer Biology at the Abramson Family Cancer Research Institute, report in Cancer Research that menin suppresses signaling in the much-studied Hedgehog pathway in endocrine organs. Menin mutations lead to increased Hedgehog signaling and cell proliferation. They found that inhibiting proteins in the Hedgehog network using drugs reduces growth of tumors in an animal model of human MEN1 syndrome.
Unlike many cancer-associated proteins, menin is neither an enzyme nor a signaling receptor. Instead, the team discovered that menin works by physically interacting with a second protein, PRMT5. The menin-PRMT5 complex binds to the promoter of the Gas1 gene, where PRMT5 (an enzyme that adds methyl groups to histone proteins) functions as an epigenetic inhibitor, tamping down gene transcription. The GAS1 protein promotes Hedgehog signaling, and thus by inhibiting Gas1 expression, menin and PRMT5 effectively dial down the pathway's tendency towards cell proliferation.
"This study uncovered a new layer of regulation of pro-proliferative genes by menin via the Hedgehog signaling pathway," Hua says. "These pro-replication genes are regulated through GAS1 and PRMT5."
Discovering the link between menin and Hedgehog was serendipitous, says Hua. Using microarray analysis, his team found that loss of menin results in increased expression of the Gas1 gene. Separately, other groups reported that GAS1 mediates Hedgehog signaling. That knowledge gave Hua's team the missing piece of information required to identify menin's normal cellular function. "We found menin linked to Hedgehog signaling by suppressing expression of GAS1, leading to the suppression of Hedgehog signaling in endocrine tissue."
Significantly, Hua's team found that menin mutant proteins associated with MEN1 cancer in patients were impaired in their ability to interact with PRMT5, and thus, in adding the methyl chemical group to the Gas1 promoter gene. What's more, treating a mouse model of human MEN1 syndrome with a Hedgehog pathway inhibitor called Erivedge (FDA-approved in 2012 for metastatic or locally advanced basal cell carcinoma) reduced proliferation of tumor cells and blood insulin levels. That, says Hua, suggests a potential new treatment for patients with MEN1 syndrome, and also likely for sporadic endocrine tumors, some 40 percent of which also contain menin mutations
"Because we show in this mouse tumor model that we can significantly suppress proliferation of tumor cells in pancreatic islets and that we can reduce the higher insulin levels with a drug, which was just clinically approved to be safe, that naturally raises the question of whether, in patients who have mutation in this gene or enhanced Hedgehog signaling, this drug can improve patient symptoms to reduce tumor progression or insulinemia," Hua asks.
First author and postdoctoral fellow in the Hua lab Buddha Gurung, PhD, adds "the possibilities of translating these findings into a viable therapeutic option is extremely exciting."
###
Co-authors include Zijie Feng, Daniel V. Iwamoto, and Austin Thiel of the Abramson Family Cancer Research Institute; Guanghui Jin of Xiamen University, Fujian, China; Chen-Min Fan of the Carnegie Institution for Science, Baltimore, MD; and Jessica M.Y. Ng and Tom Curran of the Children's Hospital of Philadelphia.
The research was supported by Caring for Carcinoid Foundation and the National Cancer Institute (R01-CA-113962, 548 R01-DK085121; R01 DK084963).
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.
The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2012, Penn Medicine provided $827 million to benefit our community.
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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.
Link between inherited endocrine tumor syndrome and much-studied cell pathwayPublic release date: 24-Apr-2013 [ | E-mail | Share ]
Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine
PHILADELPHIA A mutation in a protein called menin causes a hereditary cancer syndrome called MEN1 (multiple endocrine neoplasia type 1). Individuals with MEN1 are at a substantially increased risk of developing neuroendocrine tumors, including cancer of the pancreatic islet cells that secrete insulin.
Yet knowing these connections and doing something to improve fighting the syndrome are two different things. Researchers still did not exactly understand how menin mutations lead to MEN1 syndrome, and more importantly, what molecular pathways might be dysregulated by menin mutations and thus can be targeted to improve therapy against this type of cancer. Now, researchers at the Perelman School of Medicine at the University of Pennsylvania have found that pathway, which may lead to a new treatment for patients with MEN1 and sporadic endocrine tumors.
A research team led by Xianxin Hua, MD, PhD, associate professor of Cancer Biology at the Abramson Family Cancer Research Institute, report in Cancer Research that menin suppresses signaling in the much-studied Hedgehog pathway in endocrine organs. Menin mutations lead to increased Hedgehog signaling and cell proliferation. They found that inhibiting proteins in the Hedgehog network using drugs reduces growth of tumors in an animal model of human MEN1 syndrome.
Unlike many cancer-associated proteins, menin is neither an enzyme nor a signaling receptor. Instead, the team discovered that menin works by physically interacting with a second protein, PRMT5. The menin-PRMT5 complex binds to the promoter of the Gas1 gene, where PRMT5 (an enzyme that adds methyl groups to histone proteins) functions as an epigenetic inhibitor, tamping down gene transcription. The GAS1 protein promotes Hedgehog signaling, and thus by inhibiting Gas1 expression, menin and PRMT5 effectively dial down the pathway's tendency towards cell proliferation.
"This study uncovered a new layer of regulation of pro-proliferative genes by menin via the Hedgehog signaling pathway," Hua says. "These pro-replication genes are regulated through GAS1 and PRMT5."
Discovering the link between menin and Hedgehog was serendipitous, says Hua. Using microarray analysis, his team found that loss of menin results in increased expression of the Gas1 gene. Separately, other groups reported that GAS1 mediates Hedgehog signaling. That knowledge gave Hua's team the missing piece of information required to identify menin's normal cellular function. "We found menin linked to Hedgehog signaling by suppressing expression of GAS1, leading to the suppression of Hedgehog signaling in endocrine tissue."
Significantly, Hua's team found that menin mutant proteins associated with MEN1 cancer in patients were impaired in their ability to interact with PRMT5, and thus, in adding the methyl chemical group to the Gas1 promoter gene. What's more, treating a mouse model of human MEN1 syndrome with a Hedgehog pathway inhibitor called Erivedge (FDA-approved in 2012 for metastatic or locally advanced basal cell carcinoma) reduced proliferation of tumor cells and blood insulin levels. That, says Hua, suggests a potential new treatment for patients with MEN1 syndrome, and also likely for sporadic endocrine tumors, some 40 percent of which also contain menin mutations
"Because we show in this mouse tumor model that we can significantly suppress proliferation of tumor cells in pancreatic islets and that we can reduce the higher insulin levels with a drug, which was just clinically approved to be safe, that naturally raises the question of whether, in patients who have mutation in this gene or enhanced Hedgehog signaling, this drug can improve patient symptoms to reduce tumor progression or insulinemia," Hua asks.
First author and postdoctoral fellow in the Hua lab Buddha Gurung, PhD, adds "the possibilities of translating these findings into a viable therapeutic option is extremely exciting."
###
Co-authors include Zijie Feng, Daniel V. Iwamoto, and Austin Thiel of the Abramson Family Cancer Research Institute; Guanghui Jin of Xiamen University, Fujian, China; Chen-Min Fan of the Carnegie Institution for Science, Baltimore, MD; and Jessica M.Y. Ng and Tom Curran of the Children's Hospital of Philadelphia.
The research was supported by Caring for Carcinoid Foundation and the National Cancer Institute (R01-CA-113962, 548 R01-DK085121; R01 DK084963).
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.
The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2012, Penn Medicine provided $827 million to benefit our community.
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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.
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Public release date: 24-Apr-2013
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