SAN FRANCISCO (AP) ? Microsoft is trying to fix what it got wrong with its radical makeover of Windows. It's making the operating system easier to navigate and enabling users to set up the software so it starts in a more familiar format designed for personal computers.
The revisions to Windows 8 will be released later this year. The free update, called Windows 8.1, represents Microsoft's concessions to long-time customers taken aback by the dramatic changes to an operating system that had become a staple in households and offices around the world during the past 20 years.
Microsoft Corp. announced its plans for Windows 8.1 earlier this month. The first details about what will be included in the update are being offered in a Thursday post on Microsoft's website at http://tinyurl.com/ogjfknb .
The Redmond, Wash., company gave The Associated Press a glimpse of Windows 8.1 Wednesday. It will provide a more extensive tour of Windows 8.1 and several new applications built into the upgrade at a conference for programmers in San Francisco, scheduled to begin June 26.
With the release of Windows 8 seven months ago, Microsoft introduced a startup screen displaying applications in a mosaic of interactive tiles instead of static icons.
The shift agitated many users who wanted the option to launch the operating system in a mode that resembled the old setup.
That choice will be provided in Windows 8.1, although Microsoft isn't bringing back the start menu. That menu that could be found in the left-hand corner of a computer screen by clicking a Windows logo on all other versions of the operating system since 1995. The lack of a start button ranks among the biggest gripes about Windows 8.
Microsoft is hoping to quiet the critics by allowing users start the operating system in a desktop design with an omnipresent Windows logo anchored in the lower left corner of the display screen. Users will also be able to ensure their favorite applications, including Word and Excel, appear in a horizontal task bar next to the Windows logo.
The switch should ease the "cognitive dissonance" caused by Windows 8, said Antoine Leblond, who helps oversee the operating system's program management.
Microsoft views Windows 8.1 as more than just a fix-it job. From its perspective, the tuneup underscores Microsoft's evolution into a more nimble company capable of moving quickly to respond to customer feedback while also rolling out more innovations for a myriad of Windows devices ? smartphones, tablets or PCs.
"Windows 8 has been out long enough for us to take stock of where things are going and what we need to do to move it forward," Leblond said.
It's crucial that Microsoft sets things right with Windows 8.1 because the outlook for the PC market keeps getting gloomier. IDC now expects PC shipments to fall by nearly 8 percent this year, worse than its previous forecast of a 1 percent dip. IDC also anticipates tablets will outsell laptop computers for the first time this year.
The growing popularity of tablets is now being driven largely by less expensive devices with 7- and 8-inch display screens. Microsoft built Windows 8 to primarily to run on tablets with 10-inch to 12-inch screens, an oversight that Leblond said the company is addressing by ensuring Windows 8.1 works well on smaller devices.
If Windows 8.1 doesn't stimulate more sales of PCs and tablets running on the operating system, it could escalate the pressure on Microsoft CEO Steve Ballmer. Although the company's revenue and earnings have steadily risen since Ballmer became CEO 13 years ago, Microsoft's stock performance has lagged other technology companies. Investors, though, appear to becoming more optimistic about Ballmer's strategy. Microsoft's stock has risen by about 25 percent since Windows 8's release last October, outpacing the 17 percent gain in the Standard & Poor's 500 index during the same period.
Microsoft's stock added 12 cents to $35 in Thursday's early afternoon trading.
Windows 8.1 will lean heavily on Microsoft's Bing search technology to simplify things.
As with Windows 8, the search bar can be found by pulling out a menu from the right side of a display screen. Rather than requiring a user to select a category, such as "files" or "apps," Windows 8.1 will make it possible to find just about anything available on the computer's hard drive or on the Web by just typing in a few words. For instance, a search for "Marilyn Monroe" might display biographical information about the late movie star pulled from the Web, a selection of photos and video and even songs she sang. Anyone who wants to hear a particular song stored on the computer or play a specific game such as "Angry Birds" will just need to type a title into the search box to gain access within seconds.
The redesigned search tool is meant to provide Windows 8.1 users with "pure power and instant entertainment," said Jensen Harris, Microsoft's director of user experience for the operating system.
Applications also can be found by sorting them by letter or category.
Other new features in Windows 8.1 include a built-in connection with Microsoft's online storage system, SkyDrive, to back up photos, music and program files; Internet Explorer 11, the next generation of Microsoft's Web browser; a lock-up screen that will display a slide show of a user's favorite pictures; resized interactive tiles; and a photo editor.
In an effort to avoid further confusion about the operating system, Windows 8.1 also will plant a tile clearly labeled "helps and tips" in the center of the startup screen.
Microsoft made the dramatic overhaul to Windows in an attempt to expand the operating system's franchise beyond personal computers that rely on keyboards and mice to smartphones and tablet computers controlled by a touch or swipe of the finger.
But Windows 8 has been widely panned as a disappointment, even though Microsoft says it has licensed more than 100 million copies so far.
One major research firm, International Data Corp., blamed the redesigned operating system for worsening a decline in PC sales by confusing prospective buyers. Meanwhile, Windows 8 hasn't proven it's compelling enough to put a major dent in the popularity of Apple Inc.'s pioneering iPad or other tablets running on Google Inc.'s Android software.
Microsoft, though, remains convinced that Windows 8 just needs a little fine tuning.
"We feel good about the basic bets that we have made," Leblond said.
May 30, 2013 ? The disappearance of large, fruit-eating birds from tropical forests in Brazil has caused the region's forest palms to produce smaller, less successful seeds over the past century, researchers say. The findings provide evidence that human activity can trigger fast-paced evolutionary changes in natural populations.
Mauro Galetti from the Universidade Estadual Paulista in S?o Paulo, Brazil, along with an international team of colleagues, used patches of rainforest that had been fragmented by coffee and sugar cane development during the 1800's to set up their natural experiment. They collected more than 9,000 seeds from 22 different Euterpe edulis palm populations and used a combination of statistics, genetics and evolutionary models to determine that the absence of large, seed-dispersing birds in the area was the main reason for the observed decrease in the palm's seed size.
The study appears in the 31 May issue of the journal Science.
"Unfortunately, the effect we document in our work is probably not an isolated case," said Galetti. "The pervasive, fast-paced extirpation of large vertebrates in their natural habitats is very likely causing unprecedented changes in the evolutionary trajectories of many tropical species."
In general, researchers estimate that human activity, such as deforestation, drives species to extinction about 100 times faster than natural evolutionary processes. However, very few studies have successfully documented such rapid evolutionary changes in ecosystems that have been modified by human activity.
Galetti and the other researchers found that palms produced significantly smaller seeds in patches of forest that had been fragmented by coffee and sugar cane plantations and were no longer capable of supporting large-gaped birds, or those whose beaks are more than 12 millimeters wide, such as toucans and large cotingas. In undisturbed patches of forest, on the other hand, large-gaped birds still make their homes and palms continue to produce large seeds, successfully dispersed by the birds, they say.
"Small seeds are more vulnerable to desiccation and cannot withstand projected climate change," explained Galetti. But, small-gaped birds, such as thrushes, that populate the fragmented patches of forest are unable to swallow and disperse large seeds. As a result of this impaired dispersal, palm regeneration became less successful in the area, with less-vigorous seedlings germinating from smaller seeds.
The researchers considered the influence of a wide range of environmental factors, such as climate, soil fertility and forest cover, but none could account for the change in palm seed size over the years in the fragmented forests. They performed genetic analyses to determine that the shrinkage of seeds among forest palms in the region could have taken place within 100 years of an initial disturbance.
This timescale suggests that the conversion of tropical forests for agriculture, which began back in the 1800's and displaced many large bird populations in the region, triggered a rapid evolution of forest palms that resulted in smaller, less successful seeds.
Long periods of drought and increasingly warmer climate (as predicted by climate model projections for South America) could be particularly harmful to tropical tree populations that depend on animals to disperse their seeds. About 80 percent of the entire Atlantic rainforest biome remains in small fragments, according to the researchers, and the successful restoration of these habitats critically depends on the preservation of mutualistic interactions between animals and plants.
"Habitat loss and species extinction is causing drastic changes in the composition and structure of ecosystems, because critical ecological interactions are being lost," said Galetti. "This involves the loss of key ecosystem functions that can determine evolutionary changes much faster than we anticipated. Our work highlights the importance of identifying these key functions to quickly diagnose the functional collapse of ecosystems."
The report by Galetti et al. was supported by the Funda??o de Amparo do Estado de S?o Paulo, Conselho Nacional de Desenvolvimento Cient?fico and Programa Iberoamericano de Ciencia y Tecnolog?a para el Desarollo.
BRUSSELS (AP) ? Fears grew of a foreign-fed arms race in Syria on Tuesday as European Union countries decided they could provide weapons to the rebels and Russia disclosed that it has signed a contract to provide Syria with sophisticated anti-aircraft missiles.
Either development would significantly raise the firepower in the two-year civil war has already killed more than 70,000 people and sent hundreds of thousands fleeing the country, just as the key countries prepare for a major peace conference in Geneva that had been described as the best chance yet to end the bloodshed.
Russian officials criticized the EU decision Monday night to allow their arms embargo against Syria to expire, freeing its member countries to provide weapons for the outgunned rebels. Russia, which has been a strong supporter of the Syrian government, said the British- and French-driven decision undermined peace efforts.
Deputy Foreign Minister Sergei Ryabkov said Tuesday that Russia has signed a contract with the government of Syrian President Bashar Assad to provide it with state-of-the-art S-300 air defense missiles, which he said were important to prevent foreign intervention in the country. Ryabkov would not say whether Russia has shipped any of the missiles to Syria yet.
Ryabkov said Russia understands the concerns about providing such weapons to Syria, but believes that may "help restrain some hot-heads considering a scenario to give an international dimension to this conflict."
EU diplomats have said Britain and France are considering providing equipment to the rebels, and Syrian neighbors Turkey and Lebanon risk being drawn into the conflict.
Ryabkov called the EU move to end its arms embargo "a manifestation of double standards" that will hurt the prospects for the Geneva talks, which are expected to happen in June.
In Damascus, a Syrian lawmaker on Tuesday also criticized the EU decision, saying that efforts to arm the rebels will discourage the opposition from seeking a peaceful solution to the conflict. The comments by Essam Khalil, a member of the parliament for the ruling Baath Party, were the first by a Syrian official.
U.S. Sen. John McCain, meanwhile, made an unannounced visit to rebel forces in Syria, putting more pressure on Assad to seek a negotiated settlement.
During an interview tonight at the D11 conference, Apple CEO Tim Cook made a few references to what we can expect at his company's WWDC 2013 event in a few weeks. As expected, he mentioned we'll see the future of iOS and OS X revealed there, and directly referenced the recent management shakeup. Craig Federighi is running both teams, and Cook mentioned designer Jony Ive has been "really key" to this version of iOS. He left it up to interviewer Kara Swisher to decide if the changes made are as dramatic as have been reported, stating only that collaboration has been enhanced, with an "amped up" intersection of hardware, software and services.
Another name dropped is that of Eddy Cue, who is busy heading up work on services since Scott Forstall's departure. We'll have to wait until WWDC to find out the fruits of the various executives' labor but Cook did leave us with this to chew on: "The whole concept was to tighten the groups even more, so we could spend more time finding magic in intersections. Seven months later, give or take, I think it has been an incredibly great change."
NORTH LIBERTY-- Reports of discrimination against Cub Scout and Boy Scout groups around the country are beginning to surface.
This comes less than a week after the Boy Scouts of America lifted its longtime ban on allowing gay kids to be members.
An anonymous viewer sent us an email accusing North Liberty Church of Christ of wanting to minimize its interaction with a local Cub Scout group.??
The church says that's just not true.
North Liberty Church of Christ opens its doors to more than 40 members of the Cub Scout Pack 241.???
It says the scouts use a room called the student center each month for meetings, and the church allows the pack to use its land for campouts and other activities.???
A senior pastor for the church says that's not going to change.
Tim Stewart says, "We're a church. We're here to show the compassion of Christ and reach out to people no matter where they come from in life." ???
An anonymous complaint to our newsroom said the church is reducing the amount of time scouts can use the facility.???
The person who sent the email didn't respond to our requests for an interview, but the pastor says the church wants to continue to serve the community and that includes the Cub Scouts regardless of the lifted ban.????
He adds that his church is not homophobic and says even if one of the Cub Scouts was gay, it wouldn't be a problem.?
Stewart says, "Having a young boy come in here and tell us that whether they are or they feel this way, they think this way, it's not going to change our conduct towards that young boy." ???
The pastor wasn't sure why someone would send this email but wants everyone to know scouts will continue to be welcome.????
One woman who is a member of the church is glad to hear North Liberty's stance on this issue.???
She supports lifting the ban and allowing openly gay kids to be scouts.
Jessica Carpenter says, "I don't think it's right to ban anybody for being gay. I personally have gay people in my family. I've got gay friends, and I don't look at them any different." ?????
The pastor says every year, they always go over building usage and re-evaluate the groups they serve, but he says they do that with every group.
People opposed to lifting the ban argue that allowing gay members goes against the traditional morals of the Boy Scouts.?
Others against the change say they view it as possibly endangering children.
Openly gay adults are still banned from being leaders of a troop or pack.
The Scout Executive for the LaSalle Council, which oversees a number of scouts in our area, says he is not aware of any other complaints from other local troops or packs following the lifted ban.
In this Saturday, April 20, 2013 photo, Notre Dame junior quarterback Everett Golson leaves the field following the annual Blue-Gold spring football game at Notre Dame Stadium in South Bend, Ind. After having led the Fighting Irish to an unbeaten regular season and a national championship appearance, Golson was confirmed to have no longer been enrolled at the University of Notre Dame as of Saturday, May 25, 2013. (AP Photo/The Elkhart Truth, Ryan Dorgan)
In this Saturday, April 20, 2013 photo, Notre Dame junior quarterback Everett Golson leaves the field following the annual Blue-Gold spring football game at Notre Dame Stadium in South Bend, Ind. After having led the Fighting Irish to an unbeaten regular season and a national championship appearance, Golson was confirmed to have no longer been enrolled at the University of Notre Dame as of Saturday, May 25, 2013. (AP Photo/The Elkhart Truth, Ryan Dorgan)
FILE - In this April 16, 2011, file photo, Notre Dame quarterback Everett Golson sprints out of the pocket during the first half of a spring NCAA college football game in South Bend, Ind. A Notre Dame spokesman says Golson is no longer enrolled at the school. (AP Photo/Joe Raymond, File)
SOUTH BEND, Ind. (AP) ? Everett Golson is out for at least the fall semester at Notre Dame, saying he has been suspended by the university for what he called poor academic judgment.
"I take full responsibility for my poor choices and will do all that is asked of me to regain the trust of my family, friends, teammates, coaches and the entire Notre Dame community," he wrote in a letter released Sunday by the university.
Golson was officially no longer enrolled at Notre Dame as of Friday, university spokesman Dennis Brown said Saturday night.
Golson helped the Irish go 12-0 during the regular season last year, regain the No. 1 ranking for the first time in nearly two decades and get to the national title game against Alabama in January. Coach Brian Kelly was counting on him to play an even bigger role in 2013 after his play steadily improved throughout last season.
Golson did not specify what he did to get suspended, and wrote that he understands his integrity could be in question.
"But I want to reassure my supporters that through this experience I will return a better student athlete as well as a better individual," he said.
He said he chose to attend Notre Dame because of its mission to develop him both on and off the field.
"My parents and the community I grew up in have instilled values in me that have and will continue to allow me to be successful in the future. There have been many lessons learned as I worked to become the starting quarterback at Notre Dame and each was a result of Coach Kelly's belief in me as an athlete and a person," he wrote.
He also thanked the university for the opportunity it already has given him and the opportunity to retain his eligibility in January.
"At this point, I understand how my integrity could be in question but I want to reassure my supporters that through this experience I will return a better student athlete as well as a better individual," Golson said. "Lastly, I want to thank the University of Notre Dame for the opportunity already granted and also the opportunity going forth to regain my eligibility in the winter of 2014."
Golson did not respond to telephone or text messages left by The Associated Press.
Athletic Director Jack Swarbrick declined to elaborate on Golson's situation earlier in the day. Brown said the university would have nothing to add to Golson's statement.
Golson's abrupt exit leaves the Irish unsettled at a position they were hoping would be a strength in 2013. The most likely replacement is Tommy Rees, the 2011 starter who played key roles in four victories last season when Golson either struggled or was injured.
Golson completed 58.8 percent of his passes last year for 2,405 yards with 12 touchdown passes and six interceptions. He also ran for 298 yards and team-high six touchdowns.
Notre Dame also has Andrew Hendrix, a senior with no starts, and freshman Malik Zaire at quarterback.
So now quarterback is question mark for the Irish and Golson's future with Notre Dame is uncertain.
One thing is clear: The good feelings in South Bend produced by the best Notre Dame football season in more than two decades have been muted by everything that has come after 12-0.
It started with an embarrassing 42-14 loss against Alabama in the BCS title game, when the Crimson Tide scored on their first three possessions and jumped to a 35-0 lead.
That was quickly followed by news Kelly had interviewed for the vacant Philadelphia Eagles job the day after the BCS game.
Then the bizarre.
Part Manti Te'o's inspirational story turned out to be the result of an elaborate hoax. The dead girlfriend that supposedly inspired throughout his Heisman Trophy run did not exist. He had been duped and embarrassed.
Since then, it's been a series of smaller setbacks.
In March, Kelly announced Gunner Kiel, one of the top-rated quarterbacks coming out of high school a year ago, was leaving before even trying to challenge Golson for the starter's job during spring practice. Kiel transferred to Cincinnati.
NCAA rules would permit Kiel to return, but texted "I'm a Bearcat" to The (Cincinnati) Enquirer.
Then came reports that standout defensive lineman Eddie Vanderdoes from Auburn, Calif., a five-star recruit who signed a letter of intent in February with Notre Dame, was having second thoughts about playing for the Irish.
Though none of those problems will affect the Irish this season like not having Golson.
Since World War II, Germany has preferred to stay out of international leadership roles. But the eurocrisis has put the country at Europe's head ? with all the criticism that entails.
By Sara Miller Llana,?Staff writer / May 16, 2013
German Chancellor Angela Merkel attends a discussion panel on 'making Europe strong' during the Europe forum conference in Berlin Thursday. Germany has consciously avoided a leadership role in Europe since the end of World War II, but the eurocrisis has put it in the limelight ? with all the criticism that brings.
Gero Breloer/AP
Enlarge
Americans took a leading role in the world in the post-World War II era. And today they are used to being unpopular, yet called upon when needed.
Skip to next paragraph Sara Miller Llana
Europe Bureau Chief
Sara Miller Llana?moved to Paris in April 2013 to become the Monitor's Europe Bureau?Chief. Previously she was the?paper's?Latin America Bureau Chief, based in Mexico City, from 2006 to 2013.
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Germans in the postwar era, on the other hand, have preferred to blend into the background.
But amid Europe's sovereign debt crisis, as Germany's healthy economy has put it at the head of the 27-member European Union, that's been proving impossible. And now Germans are dealing with the criticism that accompanies being a regional ? if unwilling ? hegemon.
While a recent Pew poll shows Germany to be considered by many countries to be the most trustworthy nation in Europe, it has also accrued new enemies far and wide, with Greeks burning German flags or picketing with signs of German Chancellor Angela Merkel dressed in Nazi uniform. There have even been?claims from France that Germans are out to rule the Continent.
?We have made a lot of commitment to help those people,? says Markus, a musical theater stage producer, in Berlin?s Alexanderplatz, a public square and major transportation hub in Germany?s capital Berlin. ?It?s really unfair.?
It?s also untrue ? at least the part about Germany wanting continental dominion, say German and European observers. Instead, the avoidance of tough positions in foreign policy, so Germany is not led into a moral dilemma, is ingrained in the postwar mentality, they say.
?There is no appetite for domination. Germany has been pushed into this position by default,? says Jan Techau, director of Carnegie Europe in Brussels for the Carnegie Endowment for International Peace. ?There is no ambition to shape the continent in the image of Germany.?
?Germans want to be liked by the rest of the world,? says Michael Wohlgemuth, director of Open Europe Berlin. ?Germany feels uneasy in its new powerful role. We don?t want to be leaders of Europe.?
Outside the US embassy in Berlin, Erkan Arikan says that Germany is being unfairly maligned in Europe. But he says he can also laugh it off, as a German of Turkish descent in a multicultural Germany that has nothing to do with the 1930s.
He says that he can see some parallels between the hegemonic positions of Germany and the US today, but there is a limit. ?The US is still the world police for everyone; Germany doesn?t want to be the focus,? he says. ?But maybe it?s becoming the economic police of Europe.?
It?s a role that many Germans might feel uncomfortable playing, especially with the bad will that can breed.
If Americans don?t like the term ?ugly American,? Germans like it even less.
Ulrike Gu?rot of the European Council of Foreign Relations says when she travels around the country and talks to everyday Germans, they are starting to ask, ?Are we responsible for this youth unemployment in Spain? There is an uneasiness they they are just starting to feel,? she says. ?They don?t want to be the ?ugly German.??
A date has been set to unveil President Dr Mohamed Waheed?s running mate for September?s presidential election, Dhivehi Rayyithunge Party?(DRP) MP Dr Abdulla Mausoom has said,?with details to be ?disclosed at a later stage.?
Following an inaugural rally of President Waheed?s coalition on Friday night (May 24), local media reported that DRP Leader Ahmed Thasmeen Ali was likely to become Dr Waheed?s running mate.
A senior member of the coalition told local news website CNM that Thasmeen?s appointment was ?almost finalised? and other coalition parties had no objections.
Earlier this month, the?government-aligned DRP announced it would be joining?the?religious conservative Adhaalath Party?and the?Dhivehi Qaumee Party (DQP)?in a coalition?backing President Waheed.
Both the DQP and GIP are small political parties currently facing potential dissolution for lacking the minimum requirement of 10,000 members as stipulated in the recently passed Political Parties Act.
Dr Waheed?s Gaumee Ithihaad Party?(GIP)?currently has 3,930 registered members while the DRP has 21,411 members, according to the?Elections Commission (EC). The DRP is also the third largest party in parliament while the GIP has no representation in either the legislature or local councils.
Speaking at the inaugural rally on Friday night, DRP Leader Thasmeen praised President Waheed for taking office at a ?very tense? time for the country ? referring to the controversial transfer of power on February 7, 2012.
Thasmeen was quoted by local newspaper Haveeru as praising the president?s coalition, which he said had the professionals and academics capable of ?saving the nation?.
Contacted for comment, DRP Parliamentary Group Leader Dr Mausoom requested Minivan News contact the coalition?s media team.
The media team in turn forwarded all media requests to spokesperson Abbas Adil Riza.?Abbas, also spokesperson for President Waheed?s GIP, was not responding to call at time of press.
Meanwhile, Minister of Gender, Family and Human Rights Azima Shukoor called for more parties to back President Waheed?s coalition to ensure former President Mohamed Nasheed did not return to office, according to local media reports.
Shukoor, former Attorney General under both Dr Waheed and former President Maumoon Abdul Gayoom, and a founding member of the Progressive Party of Maldives (PPM), was noticeably present at Friday night?s coalition rally, where she declared her support for President Waheed?s bid for the presidency.
Shukoor requested that other government-aligned parties who had not joined the coalition so so far opt to side with President Waheed in order to secure a first round win.
?Today, I think that the best thing to do would be to support the broad coalition and ensure its success in the election. We can?t let Nasheed become president. What we can do is be united, work together, and make sure that the broad coalition wins the election,? she was quoted as saying by Sun Online.
Shukoor was not responding to calls from Minivan News at time of press.
In his speech at the inaugural rally, President Dr Mohamed Waheed meanwhile contended that only the coalition could foster national unity and overcome divisions in society.
?Only this coalition can create fraternity and unity among the people. Only this coalition can create unity out of different opinions,? he was quoted as saying.
Referring to the murder of moderate religious scholar and MP Dr Afrasheem Ali, President Waheed vowed that ?no stone will be left unturned? to bring the perpetrators to justice.
Dr Afrasheem?s murder was ?an atrocity that only happens in extreme political societies like Afghanistan and Pakistan,? he said.
?The man who slew him has confessed in front of judges. But the people who were said to have paid him to do it are still free. The fact that they are the cronies of the presidential candidate of the party that claims to be the largest in the country is something that all citizens should be concerned about,? he said.
Broad coalition
The government-aligned Jumhoree Party (JP) meanwhile?announced?last week that no decision has been made on whether to join a coalition backing President Dr Mohamed Waheed in September?s election, as it prepares to officially choose it presidential candidate and leader.
Fellow government-aligned PPM ? the country?s second largest party ? back in March elected MP Abdulla Yameen?to stand as its presidential candidate and has continued to reject calls to join a coalition against the opposition Maldivian Democratic Party (MDP) ahead of elections.
PPM Leader Gayoom previously told local media that Dr Waheed?s coalition presented no threat to the election bid of its own candidate MP Yameen.
Former Home Minister Dr Mohamed Jameel Ahmed, who was sacked from the post after becoming Yameen?s running mate, strongly criticised President Waheed?s coalition at a campaign rally on the island of Villingili in Gaaf Alif atoll last night (May 25).
Coalition parties were more concerned about their share in the government ? in terms of cabinet posts and positions in state-owned enterprises ? than serving the public, Dr Jameel reportedly said.
Meanwhile, MDP presidential candidate Mohamed Nasheed contended during an interview?with state broadcaster Television Maldives (TVM) on May 16 that President Waheed and the DRP had been forced to form a coalition out of necessity.
Nasheed questioned the coalition?s claims that it presented a ?third way? for voters as opposed to the policies of the MDP and PPM and reiterated his belief that?power-sharing coalitions were not compatible with a presidential system of government.
?I do not see a citizen who wants ?another way.? What is the path to deliver this way [to development]? We do not hear [political parties] talking about that,? he said. ?We are presenting one path to that [development]. We believe MDP?s policies will bring prosperity to the people. I do not see this third way you referred to as ?a way.? I see it as two men with no other way. That is not a political philosophy,? he said at the time.
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WASHINGTON (AP) ? Jordan Zimmermann became the National League's first eight-game winner, and the Washington Nationals followed a calamitous road trip with a winning start to a homestand, beating the Philadelphia Phillies 5-2 on Friday night.
Zimmermann (8-2) allowed two runs and six hits with no walks over seven innings ? actually raising his ERA to 1.71 ? on an unseasonably chilly and windy night in the nation's capital. There was at least a bit of heat from the Nationals' bats, which have been going through such a cold spell that manager Davey Johnson said before the game he wouldn't shave again until his lineup started hitting.
As it turned out, the Nationals scored their most runs in a week, and they got four or more in the same inning for the first time almost a month. Steve Lombardozzi, playing second while Danny Espinosa recovers from a broken wrist, had three hits, including a two-out, two-run double that capped the rally in the four-run fifth.
Phillies starter Kyle Kendrick (4-3) had his shortest outing of the season, allowing five runs and eight hits over five innings. He walked four for the second consecutive start, including three consecutive bases on balls that allowed the Nationals to score a run in the second with a sacrifice fly and no hits.
The Phillies missed a chance to pull even in two ways. A win would have put them at .500 for the first time since April 14, and it also would have tied them with the Nationals, who had lost four of five and have been mired in mediocrity while dealing with the expectations of Johnson's preseason proclamation of "World Series or bust."
The Nationals just completed a 10-game West Coast road trip that included a four-game losing streak, the team's sixth shutout loss of the season, Bryce Harper's head-first collision with a wall and a broken hand for Ryan Mattheus after he punched his locker following a rough outing. Washington entered the game hitting .225, second worst in the majors, and the scraggly-looking Johnson arrived at the ballpark saying: "I decided I wouldn't shave until we started hitting."
Both teams are missing some star power. The Phillies don't have Roy Halladay (shoulder surgery) and Chase Utley (oblique strain), while the Nationals are making do without Jayson Werth (hamstring) and Espinosa, who learned Friday that he's been playing with a slight fracture in his right wrist and will need a few days of rest, if not more.
Domonic Brown's RBI single in the second and Erik Kratz' sacrifice fly in the fifth gave the Phillies a 2-1 lead, but the Nationals put together five hits in the bottom of the inning to go ahead 5-2. Adam LaRoche hit an RBI triple off the center field wall and Kurt Suzuki had an RBI single before Lombardozzi's drove in two more.
Tyler Clippard pitched the eighth for the Nationals, and Rafael Soriano sailed through the ninth for his 14th save.
Notes: Washington's last four-run inning came April 25 against the Cincinnati Reds. ... Headgear on both players when flying when Tyler Moore crashed into Kratz while trying to score on Lombardozzi's single in the fourth inning. Kratz held on to the ball, and Moore was out. ... Philadelphia recalled INF-OF Michael Martinez and RHP Michael Stutes to replace Utley (disabled list) and RHP Phillippe Aumont (optioned to Triple-A Lehigh Valley). ... Phillies RHP Mike Adams (right back strain) felt fine after a second rehab bullpen session Friday and is expected to be reactivated Sunday. ... Washington LHP Ross Detwiler will throw a full bullpen session Saturday and remains on pace to return to the rotation Tuesday after skipping one start because of back spasms.
___
Follow Joseph White on Twitter: http://twitter.com/JGWhiteAP
NEW DELHI (AP) -- A senior American official on Friday praised India for reducing oil imports from Iran and said the U.S. government will decide soon on New Delhi's request to renew a waiver from sanctions on Tehran.
U.S. Under Secretary for Political Affairs Wendy Sherman said that India's reduction of oil imports was supporting U.S. and European Union sanctions against Iran, which are aimed at deterring the country from developing nuclear weapons.
India slashed imports of Iranian crude by nearly 27 percent in the financial year that ended March 31, according to the Press Trust of India news agency.
However, India is reliant on imported crude and is reluctant to completely stop imports from Iran. India's waiver from the sanctions runs out next month.
"I think that India has really made a tremendous progress in reducing the level of its importation of Iranian oil," Sherman told reporters. "All of the data is certainly in a positive direction."
She also said India had stood with the international community in telling Iran that that it should not acquire nuclear weapons. Iran insists its nuclear program is for peaceful purposes
Sherman was in New Delhi to prepare for U.S. Secretary of State John Kerry's visit to India next month.
She said that Indian Prime Minister Manmohan Singh was expected to visit Washington in the near future.
Energy-starved India imports around 75 percent of its oil to power its economic growth.
India's junior minister for petroleum, Panabakka Lakshmi, told Parliament in March that Saudi Arabia was India's main supplier of crude oil, followed by Iraq, Venezuela, Kuwait, the United Arab Emirates and Nigeria. Iran was seventh, down from its earlier position as India's third-largest supplier of crude oil in 2011.
Scientists have uncovered a survival mechanism that occurs in breast cells that have just turned premalignant-cells on the cusp between normalcy and cancers-which may lead to new methods of stopping tumors.
In their Molecular Cell study, the Salk Institute researchers report that a protein known as transforming growth factor beta (TGF-?), considered a tumor suppressor in early cancer development, can actually promote cancer once a cell drifts into a pre-cancerous state.
The discovery-a surprise to the investigators-raises the tantalizing possibility that, with novel treatment, some cancers might be prevented before they even develop.
"Our work suggests it might be possible to halt cancer development in premalignant cells-those that are just a few divisions away from being normal," says the study's lead author, Fernando Lopez-Diaz, a researcher in the Regulatory Biology Laboratory at Salk.
Agents designed to inhibit TGF-? are already being tested against cancers that have already spread, says Beverly M. Emerson, a Salk professor, head of the lab and the study's senior author. "This study offers both significant insights into early cancer development and a new direction to explore in cancer treatment," she says. "It would be fantastic if a single agent could shut down both advanced cancer and cancer that is primed to develop."
Oncologists might also be able to use their discovery to predict whether premalignant cells in a patient are destined to become full-fledged cancer, Emerson adds. "Not all premalignant cells morph into cancer," she says. "Many self-destruct due to cellular protective mechanisms. But some will become tumors and, at this point, there is no way to predict which of these cells are a risk."
The two faces of TGF-?
TGF-? molecules are secreted proteins found in most human tissues. They play a number of different biological roles, including controlling cell proliferation and inflammation and assisting in wound healing.
The prevailing dogma in cancer research is that TGF-? signaling keep cells from morphing into cancer, says Lopez-Diaz. Scientists also recognized that cancer cells that "want" to spread learn how to use TGF-? wound-healing function to break from a tumor, he says.
Another protein, P53 is a known tumor suppressor. During the stress response that occurs as a cell becomes cancerous, and in response to chemotherapy, p53 attempts to repair DNA damage that has occurred, and, if not successful, p53 orders the cell to die. "The p53 pathway must be sabotaged for cells to become cancerous," Lopez-Diaz says. "This happens when its gene becomes mutated, if the p53 protein is exaggeratedly degraded or, less appreciated, if p53 biosynthesis is impeded."
The researchers conducted this study to learn exactly how p53 and TGF-? interact in cancer development. "For the past decade, everyone has believed that these two pathways work together in normal and premalignant cells to stop cancer, even though there was not much data to support this assumption," he says.
The team examined premalignant as well as cancer cells from breast and lung tumors and matched normal and premalignant breast cells from healthy women provided by scientists at the University of California San Francisco.
But no matter how many different ways they did their experiments, the Salk researchers found that TGF-? can interfere with cells' damage responses in premalignant or cancer cells.
In fact, they found that TGF-? halts both the transcription of the p53 gene-the process by which cellular machinery reads the DNA code for a gene-and the subsequent process by which the corresponding p53 protein is produced, known as translation.
This could explain why, in about half of the breast tumors, including premalignant lesions, that the team studied at both UC San Francisco and at Sanford Burnham Medical Research Institute, when TGF-?1 signaling was highly activated, the levels of p53 were reduced, and vice versa-if the TGF-?1 pathway was reduced, there were high levels of p53. " A similar trend was seen with PUMA, a protein which induces cell death," Fernando Lopez-Diaz adds. "There was rather abundant PUMA protein when little TGF-?1 activation existed and vice versa."
"The bad face of TGF-? emerged within just a few cell divisions away from normality, allowing cells to avoid death," he says.
Filling in the cancer puzzle
This newfound immortality explains many oncologic mysteries, Lopez-Diaz says. "One is that it sheds light on how premalignant and early cancer cells are able to withstand the assault of chemotherapy and other treatments," he says.
It may explain why 77 percent of breast cancers have a normal p53 gene, and it further suggests a way that cancer cells can use both to metastasize and survive the journey to organs where they set up a new home.
"Because it helps cells avoid death, TGF-? can reduce the negative impact that the metastatic process has in the cancer cells," Lopez-Diaz says.
He adds that there is much work yet to do. "We want to understand the signals that turn TGF-? into a bad guy," he says. "If we know that, we might be able to inhibit those signals, and force damaged cells to die, as they should. That may offer us another treatment possibility, along with TGF-? inhibitors now being tested."
###
Salk Institute: http://www.salk.edu
Thanks to Salk Institute for this article.
This press release was posted to serve as a topic for discussion. Please comment below. We try our best to only post press releases that are associated with peer reviewed scientific literature. Critical discussions of the research are appreciated. If you need help finding a link to the original article, please contact us on twitter or via e-mail.
When oxygen is short, EGFR prevents maturation of cancer-fighting miRNAsPublic release date: 23-May-2013 [ | E-mail | Share ]
Contact: Scott Merville smerville@mdanderson.org 713-792-0661 University of Texas M. D. Anderson Cancer Center
With tumor suppressors frozen in adolescence, resistant cancer cells cheat death
HOUSTON - Even while being dragged to its destruction inside a cell, a cancer-promoting growth factor receptor fires away, sending signals that thwart the development of tumor-suppressing microRNAs (miRNAs) before it's dissolved, researchers reported in an early online publication at Nature.
Under conditions of oxygen starvation often encountered by tumors, the epidermal growth factor receptor (EGFR) gums up the cell's miRNA-processing machinery, an international team led by scientists at The University of Texas MD Anderson Cancer Center discovered.
"So when hypoxia stresses a cell, signaling by EGFR prevents immature miRNAs from growing up to fight cancer," said senior author Mien-Chie Hung, Ph.D., professor and chair of MD Anderson's Department of Molecular and Cellular Oncology and holder of the Ruth Legett Jones Distinguished Chair.
The group's findings point to a potential new prognostic marker for breast cancer, Hung noted, but also provide the first evidence of a growth factor signaling pathway regulating miRNA maturation.
"Inside of a cell, you have signal induction, in this case through EGFR, and you also have a protein complex that processes precursors into mature miRNA to perform a function. They didn't appear to talk to each other, it's as if one speaks English and the other Chinese," Hung said. "This is the first paper to show how they communicate."
The scientists established the relationship in cell line experiments, confirmed it in a mouse model and human breast cancer samples, then found that it reduced breast cancer patient survival in a review of 125 cases.
A new cancer-promoting role identified for EGFR
EGFR penetrates the cell membrane to receive signals from growth factors outside of the cell. After a growth factor binds to it, EGFR conveys the signal into the cell by attaching phosphate groups to other proteins, often acting as a molecular "on switch."
In many cancers, EGFR is overexpressed or dysfunctional, constantly sending signals to cells to divide. Hung and colleagues found that EGFR also fuels cancer progression by stifling tumor-suppressing miRNAs.
As a tumor grows, large portions of its interior can become starved for oxygen (hypoxia) for lack of adequate blood vessels. This stress suffocates many tumor cells, but the few that endure become highly malignant, resist treatment and are most likely to spread, Hung said.
Anti-angiogenesis drugs designed to kill tumors by blocking their ability to spin webs of supportive blood vessels often succeed at first, Hung said, but then fail against the more malignant cells that survive hypoxia.
When hypoxia hits, EGFR gets active and gets eaten
Low-oxygen conditions cause EGFR overexpression. EGFR also is pulled into the cell interior, captured in cavities called vesicles and eventually fed into lysosomes, a membrane-enclosed organelle loaded with enzymes to dissolve proteins.
It was known that EGFR continues to signal even while caught in the vesicles, which actually prolongs its activation. Hung and colleagues found that EGFR signals to a key protein in miRNA processing called argonaute 2, or AGO2.
AGO2 connects with two other proteins called Dicer and TRBP to form a complex that processes microRNA precursors into mature miRNAs, which regulate gene expression after messenger RNA has been expressed but before it's translated into a protein.
Oncoprotein-regulating miRNAs don't grow up
The scientists found that EGFR attaches phosphate groups to AGO2, which in turn weakens AGO2's ability to connect with Dicer to produce mature microRNAs. EGFR's effect is stronger during oxygen starvation than under normal conditions.
The team identified a number of specific miRNAs affected by EGFR, most of which have been reported to have tumor suppressor characteristics. The miRNAs regulated by phosphorylated AGO2, including miR-31, miR-192 and miR-193a-5p, also shared a long-loop structure in their precursors that miRNAs unaffected by AGO2 phosphorylation lack.
Hypoxic environments around tumors promote metastasis by helping cells evade programmed cell death. Hung and colleagues showed that EGFR-mediated AGO2 phosphorylation blocks cell death and enhances invasiveness under hypoxia.
Experiments in a mouse model of breast cancer confirmed that expression of EGFR and the presence of phosphorylated AGO2 increase during tumor progression under oxygen-starved conditions.
EGFR-AGO2 connection found in human breast tumors; reduces survival
The hypoxia-EGFR-AGO2 connection was strong in tumor samples from 128 breast cancer patients, but it was low or absent in normal breast tissue. In 125 breast cancer cases analyzed by the team, half of 62 patients with high levels of phosphorylated AGO2 survived to 48 months and beyond. Median survival had not been reached for the 63 patients in the low-level group, but 78 percent had survived to 48 months.
"One can imagine other receptors for platelet-derived growth factor and insulin-like growth factor also regulating miRNAs, perhaps by regulating Dicer or TBRP," Hung said. "This is a turning-point paper; it will induce lots of new questions for scientists to pursue."
###
Co-authors with Hung are lead author Jia Shen, Weiya Xia, M.D., Yekaterina Khotskaya, Ph.D., Longfei Huo, Ph.D., Seung-Oe Lim, Ph.D., Yi Du, Ph.D., Yan Wang, Ph.D., Jennifer Hsu, Ph.D., and Yung Carmen Lam, Ph.D., all of MD Anderson's Department of Molecular and Cellular Oncology; Wei-Chao Chang, Ph.D., of China Medical University, Taichung, Taiwan, and Chung-Hsuan Chen, Ph.D., of Genomics Research Center of Academica Sinica, Taipei; Yun Wu, M.D., Ph.D., of MD Anderson's Department of Pathology; Brian James, Ph.D., Xiuping Liu, M.D., and Chang-Gong Liu, Ph.D., of MD Anderson's Department of Experimental Therapeutics; and Kotaro Nakanishi, Ph.D., and Dinshaw Patel, Ph.D., of Memorial Sloan-Kettering Cancer Center.
Shen is a graduate student at The University of Texas Graduate School of Biomedical Sciences at Houston, a joint program of MD Anderson and The University of Texas Health Science Center at Houston.
This research was funded by grants from the U.S. National Institutes of Health (CA109311 and CA099031), MD Anderson's Cancer Center Support Grant from the National Cancer Institute (CA16672), the U.S. National Breast Cancer Foundation, MD Anderson's Center for Biological Pathways, Susan G. Komen for the Cure, the Sister Institution Fund of China Medical University and Hospital and MD Anderson, the Taiwan Cancer Research Center of Excellence, a Private University grant from Taiwan and the Taiwan Program for Stem Cell and Regenerative Medicine Frontier Research.
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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.
When oxygen is short, EGFR prevents maturation of cancer-fighting miRNAsPublic release date: 23-May-2013 [ | E-mail | Share ]
Contact: Scott Merville smerville@mdanderson.org 713-792-0661 University of Texas M. D. Anderson Cancer Center
With tumor suppressors frozen in adolescence, resistant cancer cells cheat death
HOUSTON - Even while being dragged to its destruction inside a cell, a cancer-promoting growth factor receptor fires away, sending signals that thwart the development of tumor-suppressing microRNAs (miRNAs) before it's dissolved, researchers reported in an early online publication at Nature.
Under conditions of oxygen starvation often encountered by tumors, the epidermal growth factor receptor (EGFR) gums up the cell's miRNA-processing machinery, an international team led by scientists at The University of Texas MD Anderson Cancer Center discovered.
"So when hypoxia stresses a cell, signaling by EGFR prevents immature miRNAs from growing up to fight cancer," said senior author Mien-Chie Hung, Ph.D., professor and chair of MD Anderson's Department of Molecular and Cellular Oncology and holder of the Ruth Legett Jones Distinguished Chair.
The group's findings point to a potential new prognostic marker for breast cancer, Hung noted, but also provide the first evidence of a growth factor signaling pathway regulating miRNA maturation.
"Inside of a cell, you have signal induction, in this case through EGFR, and you also have a protein complex that processes precursors into mature miRNA to perform a function. They didn't appear to talk to each other, it's as if one speaks English and the other Chinese," Hung said. "This is the first paper to show how they communicate."
The scientists established the relationship in cell line experiments, confirmed it in a mouse model and human breast cancer samples, then found that it reduced breast cancer patient survival in a review of 125 cases.
A new cancer-promoting role identified for EGFR
EGFR penetrates the cell membrane to receive signals from growth factors outside of the cell. After a growth factor binds to it, EGFR conveys the signal into the cell by attaching phosphate groups to other proteins, often acting as a molecular "on switch."
In many cancers, EGFR is overexpressed or dysfunctional, constantly sending signals to cells to divide. Hung and colleagues found that EGFR also fuels cancer progression by stifling tumor-suppressing miRNAs.
As a tumor grows, large portions of its interior can become starved for oxygen (hypoxia) for lack of adequate blood vessels. This stress suffocates many tumor cells, but the few that endure become highly malignant, resist treatment and are most likely to spread, Hung said.
Anti-angiogenesis drugs designed to kill tumors by blocking their ability to spin webs of supportive blood vessels often succeed at first, Hung said, but then fail against the more malignant cells that survive hypoxia.
When hypoxia hits, EGFR gets active and gets eaten
Low-oxygen conditions cause EGFR overexpression. EGFR also is pulled into the cell interior, captured in cavities called vesicles and eventually fed into lysosomes, a membrane-enclosed organelle loaded with enzymes to dissolve proteins.
It was known that EGFR continues to signal even while caught in the vesicles, which actually prolongs its activation. Hung and colleagues found that EGFR signals to a key protein in miRNA processing called argonaute 2, or AGO2.
AGO2 connects with two other proteins called Dicer and TRBP to form a complex that processes microRNA precursors into mature miRNAs, which regulate gene expression after messenger RNA has been expressed but before it's translated into a protein.
Oncoprotein-regulating miRNAs don't grow up
The scientists found that EGFR attaches phosphate groups to AGO2, which in turn weakens AGO2's ability to connect with Dicer to produce mature microRNAs. EGFR's effect is stronger during oxygen starvation than under normal conditions.
The team identified a number of specific miRNAs affected by EGFR, most of which have been reported to have tumor suppressor characteristics. The miRNAs regulated by phosphorylated AGO2, including miR-31, miR-192 and miR-193a-5p, also shared a long-loop structure in their precursors that miRNAs unaffected by AGO2 phosphorylation lack.
Hypoxic environments around tumors promote metastasis by helping cells evade programmed cell death. Hung and colleagues showed that EGFR-mediated AGO2 phosphorylation blocks cell death and enhances invasiveness under hypoxia.
Experiments in a mouse model of breast cancer confirmed that expression of EGFR and the presence of phosphorylated AGO2 increase during tumor progression under oxygen-starved conditions.
EGFR-AGO2 connection found in human breast tumors; reduces survival
The hypoxia-EGFR-AGO2 connection was strong in tumor samples from 128 breast cancer patients, but it was low or absent in normal breast tissue. In 125 breast cancer cases analyzed by the team, half of 62 patients with high levels of phosphorylated AGO2 survived to 48 months and beyond. Median survival had not been reached for the 63 patients in the low-level group, but 78 percent had survived to 48 months.
"One can imagine other receptors for platelet-derived growth factor and insulin-like growth factor also regulating miRNAs, perhaps by regulating Dicer or TBRP," Hung said. "This is a turning-point paper; it will induce lots of new questions for scientists to pursue."
###
Co-authors with Hung are lead author Jia Shen, Weiya Xia, M.D., Yekaterina Khotskaya, Ph.D., Longfei Huo, Ph.D., Seung-Oe Lim, Ph.D., Yi Du, Ph.D., Yan Wang, Ph.D., Jennifer Hsu, Ph.D., and Yung Carmen Lam, Ph.D., all of MD Anderson's Department of Molecular and Cellular Oncology; Wei-Chao Chang, Ph.D., of China Medical University, Taichung, Taiwan, and Chung-Hsuan Chen, Ph.D., of Genomics Research Center of Academica Sinica, Taipei; Yun Wu, M.D., Ph.D., of MD Anderson's Department of Pathology; Brian James, Ph.D., Xiuping Liu, M.D., and Chang-Gong Liu, Ph.D., of MD Anderson's Department of Experimental Therapeutics; and Kotaro Nakanishi, Ph.D., and Dinshaw Patel, Ph.D., of Memorial Sloan-Kettering Cancer Center.
Shen is a graduate student at The University of Texas Graduate School of Biomedical Sciences at Houston, a joint program of MD Anderson and The University of Texas Health Science Center at Houston.
This research was funded by grants from the U.S. National Institutes of Health (CA109311 and CA099031), MD Anderson's Cancer Center Support Grant from the National Cancer Institute (CA16672), the U.S. National Breast Cancer Foundation, MD Anderson's Center for Biological Pathways, Susan G. Komen for the Cure, the Sister Institution Fund of China Medical University and Hospital and MD Anderson, the Taiwan Cancer Research Center of Excellence, a Private University grant from Taiwan and the Taiwan Program for Stem Cell and Regenerative Medicine Frontier Research.
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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.
REYKJAVIK (Reuters) - Iceland must find stability by aiming for the same economic goals as those set for European Union states, even though it is skeptical about joining the EU and will keep its own currency, the new prime minister said.
Iceland is still recovering from the collapse of its top three banks in late 2008 and although growth has returned, many Icelanders are disappointed at what they see as a slow recovery.
Sigmundur David Gunnlaugsson's center-right Progressive party made big gains in elections last month where voters handed the incumbent Social Democrats the worst defeat of any ruling party since independence from Denmark in 1944.
"It is clear that Iceland will use the Icelandic krona (crown) for the foreseeable future, for the next years at least," Gunnlaugsson told Reuters Television late on Thursday after formally taking office.
This week he announced that the government would suspend Iceland's talks on entering the EU, pending a referendum on whether they should continue.
Still, the 38-year-old party leader, who has studied in Copenhagen and at Oxford University in Britain, saw benefits from the economic goals EU countries are supposed to meet, including limits on budget deficits, public debt and inflation.
"All politicians, all political parties, the unions, the employers, the central bank, should all join hands in fulfilling those criteria," he added.
"Not necessarily because we want to join the EU, but because it makes economic sense, as it is what needs to happen in all cases, whether we want to continue with the krona, or make some changes," he added.
The Progressive Party and Independence Party won April's election despite being blamed for pursuing policies that laid the groundwork for the banks' expansion abroad, and then their collapse in the 2008 credit crunch.
Capital controls to protect the crown are still in force, preventing free flows of funds and hampering investment.
Some in Iceland have suggested the crown should be dumped, or linked to a more stable currency.
Gunlaugsson said he would aim to simplify the tax system and make it more conducive to growth with what he called "positive incentives", without giving further details.
The new government has also said that it would aim to reduce high levels of household debt, and Gunlaugsson said that this was of vital importance for the economy.
Large-river specialist fishes ? from giant species like paddlefish and blue catfish, to tiny crystal darters and silver chub ? are in danger, but researchers say there is greater hope to save them if major tributaries identified in a University of Wisconsin-Madison study become a focus of conservation efforts.
The study says 60 out of 68 U.S. species, or 88 percent of fish species found exclusively in large-river ecosystems like the Mississippi, Missouri and Ohio rivers, are of state, federal or international conservation concern. The report is in the April issue of the journalFrontiers in Ecology and the Environment.
On the other hand, says lead author Brenda Pracheil, a postdoctoral researcher in the UW's Center for Limnology, the study offers some good news, too.
Traditionally, the conservation emphasis has been on restoring original habitat. This task proves impossible for ecosystems like the main trunk of the Mississippi River ? the nation's shipping, power production, and flood control backbone. While the locks, dams and levees that make the Mississippi a mighty economic force have destroyed fish habitat by blocking off migration pathways and changing annual flood cycles species need to spawn, removing them is not a realistic conservation option.
But, says Pracheil, we're underestimating the importance of tributaries. Her study found that, for large-river specialist fish, it's not all or nothing. Some rivers are just big enough to be a haven.
For any river in the Mississippi Basin with a flow rate of less than 166 cubic meters of water per second, virtually no large-river specialist fishes are present. But in any river that even slightly exceeds that rate, 80 percent or more of the large-river species call it home.
That means Mississippi tributaries about the size of the Wisconsin River and larger are providing crucial habitat for large-river fishes. When coupled with current efforts in the large rivers themselves, these rivers may present important opportunities for saving species.
"Talk to any large-river fish biologist, and they will tell you how important tributaries are to big river fish," says Pracheil. "But, until now, we've not really understood which rivers are most important. Our study tackles that and shows which tributaries in the Mississippi River Basin show the most promise for conservation of large-river fishes."
Current policies governing large river restoration projects are funded largely through the U.S. Army Corps of Engineers, which requires that funds be spent on mainstems ? or the big rivers themselves. Pracheil's study suggests spending some of that money on tributary restoration projects might do more conservation good for fish, while also letting agencies get more bang for their habitat restoration buck.
"Tributaries may be one of our last chances to preserve large-river fish habitat," Pracheil says. "Even though the dam building era is all but over in this country, it's just starting on rivers like the Mekong and Amazon ? places that are hotspots for freshwater fish diversity. While tributaries cannot offer a one-to-one replacement of main river habitats, our work suggests that [they] provide important refuges for large-river fishes and that both main rivers and their tributaries should be considered in conservation plans."
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University of Wisconsin-Madison: http://www.wisc.edu
Thanks to University of Wisconsin-Madison for this article.
This press release was posted to serve as a topic for discussion. Please comment below. We try our best to only post press releases that are associated with peer reviewed scientific literature. Critical discussions of the research are appreciated. If you need help finding a link to the original article, please contact us on twitter or via e-mail.
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