"iTunes is a stepping stone along the way." -- Jim Griffin, OneHouse LLC
On April 28th, the iTunes Store basked in a milestone 10th birthday. Two years before its 2003 launch (as the iTunes Music Store), Apple introduced the iTunes client as a desktop music management program and implemented it as the device manager for the first iPod later in 2001. In those two years, Apple laid the groundwork for what can reasonably be called the iTunes era of music.
Apple did not invent digital music, even though for many iTunes embodies 21st century music buying. However, during the past 10 years, it has become the US' top music retailer, with customers currently downloading 15,000 songs per minute from the app's library of 26 million songs, according to an Apple spokesperson. Since its launch, it has evolved into the hub of a powerhouse media / tech ecosystem that turned Apple into the world's most valuable company in 2012.
As a symbolic milestone, the iTunes anniversary encourages reflection on the past, a survey of the present and predictions of the future. Digital music continues to evolve, for businesses, consumers and musicians.
SAVAR, Bangladesh (AP) -- A fire broke out late Sunday in the wreckage of the garment factory that collapsed last week in Bangladesh, with smoke pouring from the piles of shattered concrete and some of the rescue efforts forced to stop.
The fire came four days after the collapse, as rescuers were trying to free a woman they found trapped in the rubble. The flames broke out when sparks were generated by those rescuers trying to cut through a steel rod to reach the woman, said a volunteer rescuer, Syed Al-Amin Roman. At least three rescue workers were injured in the fire, he said.
Rescuers have retreated from the part of the wreckage where the fire erupted, but were still trying to reach any possible survivors in other parts of the destroyed eight-story building.
Firefighters were frantically hosing down the flames.
"Hopefully we will be able to control it," said Brig. Gen. Mohammed Siddiqul Alam Shikder, who is overseeing rescue operations.
It wasn't immediately clear what happened to the trapped woman.
The fire came hours after the owner of the illegally-constructed building was captured Sunday at a border crossing with India.
Mohammed Sohel Rana was arrested in Benapole in western Bangladesh, just as he was about to flee into India's West Bengal state, said Jahangir Kabir Nanak, junior minister for local government. Rana was brought back by helicopter to the capital Dhaka where he faced charges of negligence.
Rana's capture brought cheers and applause when it was announced on a loudspeaker at the site of the collapsed building in the Dhaka suburb of Savar.
At least 377 people are confirmed to have died in the Wednesday collapse. Three of the building's floors were built illegally. The death toll is expected to rise but it is already the deadliest tragedy to hit Bangladesh's garment industry, which is worth $20 billion annually and is a mainstay of the economy. The collapse and previous disasters in garment factories have focused attention on the poor working conditions of workers who toil for as little as $38 a month to produce clothing for top international brands.
Bangladesh's garment industry was the third largest in the world in 2011, after China and Italy, having grown rapidly in the past decade. The country's minimum wage is the equivalent of about $38 a month.
Twitter is great if you're famous. But Jawbone's founding CEO Alexander Asseily thinks everyone deserves a powerful voice online, so today he's launching State, a structured opinion-sharing network where people don't need to follow you see your posts. You can get an early State invite now and start contributing to an opinion graph where what matters is what you believe, not who follows you.
ALGIERS (Reuters) - Algerian President Abdelaziz Bouteflika has been transferred to France for further medical tests after suffering a minor stroke on Saturday, Algeria's official news agency said.
The APS agency said late on Saturday that Bouteflika, 76, was in Paris at the recommendation of his doctors.
He was hospitalized after a minor stroke, according to an earlier state press agency report that quoted the prime minister as saying his condition was "not serious."
The health of Bouteflika is a central factor in the stability of the oil-exporting country of 37 million people that is emerging from a long conflict against Islamist insurgents.
APS said Bouteflika had an "ischemic transitory attack," or mini-stroke, at 12:30 p.m. (1130 GMT) on Saturday.
"A few hours ago, the president felt unwell and he has been hospitalized but his condition is not serious at all," Prime Minister Abdelmalek Sellal was quoted as saying.
Elected in 1999, Bouteflika is a member of a generation of leaders who have ruled Algeria since winning independence from France in a 1954-62 war.
They also defeated Islamist insurgents in the 1990s and saw off the challenge of Arab Spring protests two years ago, with Bouteflika's government defusing unrest through pay rises and free loans for young people.
Bouteflika has served three terms as president and is thought unlikely to seek a fourth at an election due in 2014. Leaked U.S. diplomatic cables said in 2011 that Bouteflika had been suffering from cancer, but that it was in remission.
It is unknown who might take over Africa's biggest country by land area, an OPEC oil producer that supplies a fifth of Europe's gas imports and cooperates with the West in combating Islamist militancy.
More than 70 percent of Algerians are under 30. About 21 percent of young people are unemployed, the International Monetary Fund says, and many are impatient with the gerontocracy ruling a country where jobs, wages and housing are urgent concerns.
(Reporting by Lamine Chikhi; Editing by Peter Cooney)
Clarifying the effect of stem cell therapy on cancerPublic release date: 28-Apr-2013 [ | E-mail | Share ]
Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central
Injection of human stem cells into mice with tumors slowed down tumor growth, finds research published in BioMed Central's open access journal Stem Cell Research & Therapy. Human mesenchymal stem cells (MSC), isolated from bone marrow, caused changes in blood vessels supplying the tumor, and it is this modification of blood supply which seems to impact tumor growth.
The use of stem cells in treating cancer has been controversial, with some studies finding that stem cells force tumors to enter programmed cell death. However other studies find that stem cells actually promote tumor growth by inducing infiltration of new blood vessels. In attempting to sort out this puzzle researchers from INSERM groups at Universit Joseph Fourier in collaboration with CHU de Grenoble investigated the impact of MSC on already established subcutaneous or lung metastasis in mice.
For both the subcutaneous and lung tumors, injection of MSC reduced cell division, consequently slowing the rate of tumor growth. Part of the mode of action of stem cells therefore appears to be due to with angiogenesis, but the mechanism behind this is still unclear.
Claire Rome who led this study explained, "We found that MSC altered vasculature inside the tumor - although new blood vessels were generated, overall they were longer and fewer than in untreated tumors. This could be restricting the oxygen and nutrients to the tumor, limiting cell division." She continued, "Our study confirms others which propose that stem cells, in particular MSC, might be one way forwards in treating cancer."
Commenting on this study Celia Gomes, from the University of Coimbra, said, "One of the interesting questions this study raises is when MSC promote tumor growth and when they restrict it. The answer seems to be timing this study looks at already established tumors, while others, which find that MSC increase growth, tend to be investigating new tumors. This is a first step in the path to identifying exactly which patients might benefit from stem cell therapy and who will not."
The dual effect of MSCs on tumour growth and tumour angiogenesis
Michelle Kramidas, Florence de Fraipont, Anastassia Karageorgis, Anack Moisan, Virginie Persoons, Marie-Jeanne Richard, Jean-Luc Coll and Claire Rome
Stem Cell Research & Therapy 2013, 4:41
Commentary
The dual role of mesenchymal stem cells in tumor progression
Clia MF Gomes
Stem Cell Research & Therapy 2013, 4:42
Please name the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central's open access policy.
2. Stem Cell Research & Therapy is the major forum for translational research into stem cell therapies. An international peer-reviewed journal, it publishes high quality open access research articles with a special emphasis on basic, translational and clinical research into stem cell therapeutics and regenerative therapies, including animal models and clinical trials. The journal also provides reviews, viewpoints, commentaries and reports.
3. BioMed Central is an STM (Science, Technology and Medicine) publisher which has pioneered the open access publishing model. All peer-reviewed research articles published by BioMed Central are made immediately and freely accessible online, and are licensed to allow redistribution and reuse. BioMed Central is part of Springer Science+Business Media, a leading global publisher in the STM sector. @BioMedCentral
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Clarifying the effect of stem cell therapy on cancerPublic release date: 28-Apr-2013 [ | E-mail | Share ]
Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central
Injection of human stem cells into mice with tumors slowed down tumor growth, finds research published in BioMed Central's open access journal Stem Cell Research & Therapy. Human mesenchymal stem cells (MSC), isolated from bone marrow, caused changes in blood vessels supplying the tumor, and it is this modification of blood supply which seems to impact tumor growth.
The use of stem cells in treating cancer has been controversial, with some studies finding that stem cells force tumors to enter programmed cell death. However other studies find that stem cells actually promote tumor growth by inducing infiltration of new blood vessels. In attempting to sort out this puzzle researchers from INSERM groups at Universit Joseph Fourier in collaboration with CHU de Grenoble investigated the impact of MSC on already established subcutaneous or lung metastasis in mice.
For both the subcutaneous and lung tumors, injection of MSC reduced cell division, consequently slowing the rate of tumor growth. Part of the mode of action of stem cells therefore appears to be due to with angiogenesis, but the mechanism behind this is still unclear.
Claire Rome who led this study explained, "We found that MSC altered vasculature inside the tumor - although new blood vessels were generated, overall they were longer and fewer than in untreated tumors. This could be restricting the oxygen and nutrients to the tumor, limiting cell division." She continued, "Our study confirms others which propose that stem cells, in particular MSC, might be one way forwards in treating cancer."
Commenting on this study Celia Gomes, from the University of Coimbra, said, "One of the interesting questions this study raises is when MSC promote tumor growth and when they restrict it. The answer seems to be timing this study looks at already established tumors, while others, which find that MSC increase growth, tend to be investigating new tumors. This is a first step in the path to identifying exactly which patients might benefit from stem cell therapy and who will not."
The dual effect of MSCs on tumour growth and tumour angiogenesis
Michelle Kramidas, Florence de Fraipont, Anastassia Karageorgis, Anack Moisan, Virginie Persoons, Marie-Jeanne Richard, Jean-Luc Coll and Claire Rome
Stem Cell Research & Therapy 2013, 4:41
Commentary
The dual role of mesenchymal stem cells in tumor progression
Clia MF Gomes
Stem Cell Research & Therapy 2013, 4:42
Please name the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central's open access policy.
2. Stem Cell Research & Therapy is the major forum for translational research into stem cell therapies. An international peer-reviewed journal, it publishes high quality open access research articles with a special emphasis on basic, translational and clinical research into stem cell therapeutics and regenerative therapies, including animal models and clinical trials. The journal also provides reviews, viewpoints, commentaries and reports.
3. BioMed Central is an STM (Science, Technology and Medicine) publisher which has pioneered the open access publishing model. All peer-reviewed research articles published by BioMed Central are made immediately and freely accessible online, and are licensed to allow redistribution and reuse. BioMed Central is part of Springer Science+Business Media, a leading global publisher in the STM sector. @BioMedCentral
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
We visited LG's HQ earlier this month and heard that the curved OLED HDTV prototypes it showed at CES are due for release, and now it's official. A Korean press release indicates we can expect the 55EA9800 to launch in the next month, with shipments starting in June. According to the specs, its 4.3mm depth results in a weight of just 17kg, probably thinks to a carbon-fiber reinforced frame. Like an IMAX theater screen, the edges are curved towards the viewer to provide a more immersive feeling. Given the fact that we're still waiting for LG's flat OLED TVs to see a wider release we doubt it will arrive on US shelves any time soon, but until then you can check out our in-person pics from CES below, and a video after the break.
We've been doing a lot of teasing about #TM13 on Twitter, Google+, YouTube, and more, but for anyone who's been on this walk for us for a while, it should be fairly obvious where's we've been and where we're going. Back when we were still Smartphone Experts, we did the Round Robin for 3 years in a row. When Microsoft and BlackBerry got left behind for a while, it made that impossible to continue in a meaningful way. Now that Windows Phone and BlackBerry 10 have launched, everyone is firing on all cylinders again, and that makes things interesting.
We're Mobile Nations now, however, and that means the old Round Robin has to give way to give way to something equally newer, better, and bolder.
Enter #TM13.
I don't want to oversell it. It's going to be a blast, and it's going to benefit all of the Mobile Nations communities in a lot of subtle yet cool ways for a long time to come, but we're not HALO dropping Phil with a pair of glasses on, or shooting Kevin out of a canon in Times Square to see how many characters he can type on a QWERTY before splat-down, or anything stunty like that. Now I did get hung off the roof of a 50 floor building, but the intent here isn't shock and awe. It's what Mobile Nations always does -- entertain, inform, and engage our awesome community.
Speaking of which, Georgia, Martin, and I managed to knock this little video out at the Grand Central Apple Store. They have a rule that you can't use a tripod or monopod, so Martin had to shoot hand-held and we had to stabilize in Final Cut Pro X, which led to some background warp. I like to think it's just rocking out to the iMore theme though. (And by the way, if you haven't subscribed to the iMore YouTube channel yet, do that ASAP -- we've got some great stuff coming your way over the next few weeks...)
I'll be in NYC for another week, but Peter starts full time tomorrow, so look for much more from both of us, and the whole team, as the week goes on.
After that, it's full speed ahead to WWDC 2013 and what I hope is the first look at iOS 7 and OS X 10.9. It's been a long, long, LONG, time since an Apple exec stepped out on the Keynote stage. Any guesses what they have in store for us?
As I get closer to closer to buying my first home, I?m getting pretty excited. It?s not just the extra freedom and satisfaction that I?m excited about though. I?m also excited about how this plays into eventual retirement plans.
Many people just think of stocks, bonds and mutual fund investments when saving for retirement is mentioned. Really there is so much more than just market related investments. Physical assets such as your home should definitely be considered.
For people like me who live in an expensive city this is especially true. The home we are buying now will go a long way to fulfilling our retirement savings needs. Eventually we can sell off this condo, downgrade to something cheaper and use the cash for day to day needs. With any luck, the housing market keeps growing here and we even net a nice profit from that sale.
There is the possibility that the housing market collapses in the meantime though. So we cannot count on definitely getting the full amount back down the road. With that in mind we?ll still need to save as much money as possible on top of the value of our home. Most likely the condo will keep its value, but it?s best to play it safe.
The route we will likely take is to one day upgrade to a bigger home. At that time we can sell our current condo and have a major chunk of the next home paid off. Either way we?d be building up equity that can later be liquidated.
Some of you are probably wondering why we don?t just plan to rent the condo out. Unfortunately this condo does have rental restrictions which drastically limits how many units in the building can be rentals. So that?s not really something we can rely upon. If not it would be great to be able to rent out our home to add some nearly passive income.
Part of our plan is to gradually do some renovations to our condo. Not only will this make it a nicer place to live, but it will raise the value of our home and make it easier to sell when the time is right. Who wouldn?t want to make an investment that will also make you more proud of your home and ultimately happier? And yes I know that some renovations don?t add a comparative value back to the home. We?ll just have to keep that in mind when deciding on renovations to tackle.
The great part of including your home value in your retirement planning is that it can lead to extra motivation to put aside more money. While putting money into stocks and other investments, it can be tough to be satisfied with progress towards a large end goal. As a result you might not save as much money. When paying off a mortgage, reducing that total is a much more attainable goal that can be achieved a lot quicker than your final retirement goal. For psychological reasons it is just easier to get motivated to pay off debt than it is to save for a long term goal.
What about you? Is your home a major part of your retirement plan? Or do some of you choose to exclude it as somewhere that you will still live when you are older?
Apr. 25, 2013 ? Liver fibrosis results from an excessive accumulation of tough, fibrous scar tissue and occurs in most types of chronic liver diseases. In industrialized countries, the main causes of liver injury leading to fibrosis include chronic hepatitis virus infection, excess alcohol consumption and, increasingly, nonalcoholic steatohepatitis (NASH).
Now, in a new study published in the journal Cell, scientists at the Salk Institute for Biological Studies have discovered that a synthetic form of vitamin D, calcipotriol (a drug already approved by the FDA for the treatment of psoriasis), deactivates the switch governing the fibrotic response in mouse liver cells, suggesting a potential new therapy for fibrotic diseases in humans.
"Because there are currently no effective drugs for liver fibrosis, we believe our findings would open a new door for treatment," says senior author Ronald M. Evans, a professor in Salk's Gene Expression Laboratory and lead researcher in the Institute's new Helmsley Center for Genomic Medicine.
The Salk study focused on a star-shaped "stellate" cell in the liver that serves as a beacon for damage. When called into action, stellate cells produce fibrotic proteins in an attempt to heal an injury. Under chronic stress, however, localized fibrosis expands, eventually leading to cirrhosis, increased risk of liver cancer, and the need for a liver transplant in advanced cases.
The Evans lab discovered a genetic switch through which vitamin D-related ligands such as calcitriol, a hormonally active form of the vitamin, can put the brakes on fibrosis. "Preclinical results suggest the 'vitamin D brake' is highly efficacious and led us to believe that the time is right to consider a trial in the context of chronic liver disease," says Evans, a Howard Hughes Medical Institute Investigator and holder of the March of Dimes Chair in Molecular and Developmental Biology.
Previous studies have shown a physiologic role for vitamin D in liver function, but "it was our discovery of high levels of vitamin D receptor (VDR) in the stellate cell that led us to consider it as a possible off switch for liver fibrosis," says lead author Ning Ding, a research associate in the Gene Expression Laboratory.
"Current therapeutic approaches, which treat the symptoms of liver disease, don't stop liver fibrosis from progressing," says Michael Downes, a senior staff scientist in the Gene Expression Laboratory and co-corresponding author on the paper. "In liver diseases where the underlying cause cannot be cured, progression to cirrhosis is currently inevitable in some people. What we have discovered is that by acting on the genome, VDR can simultaneously defend against multiple fibrotic activators. This is important because many different pro-fibrotic signaling pathways converge on the genome to affect their fibrotic response."
The Salk discovery that calcipotriol counters the fibrotic response in stellate cells illuminates a potentially safer, more effective strategy capable of neutralizing multiple convergent fibrotic triggers.
The Salk scientists say that clinical trials of the vitamin D analog for the treatment of liver fibrosis are being planned. The synthetic vitamin D analog is better than natural vitamin D, they say, for a couple of reasons. First, natural vitamin D, which is found in small amounts in a few foods and produced in the body by exposure to sunlight, degrades quickly, while synthetic versions of vitamin D are less susceptible to breakdown. Second, too much natural vitamin D can cause hypercalcemia, or elevated calcium in the blood, which can lead to nausea and vomiting, frequent urination, muscle weakness and joint aches and pain. The synthetic vitamin D analog, on the other hand, produces a strong response without adding calcium to the blood.
In addition, the researchers say this new model for treating liver fibrosis may also be helpful in treating other diseases with a fibrotic component, including those of the lung, kidney and pancreas.
Other researchers on the study were Ruth T. Yu, Mara H. Sherman, Mathias Leblanc, Mingxiao He, Annette R. Atkins and Grant D. Barish, from the Salk Institute; Nanthakumar Subramaniam, Caroline Wilson, Renuka Rao, Sally Coulter and Christopher Liddle, of the University of Sydney (Australia); and Sue L. Lau , Christopher Scott and Jenny E. Gunton, of the Garvan Insitute for Medical Research (Australia).
The work was supported by grants from the National Institutes of Health, the Howard Hughes Medical Institute, the National Health and Medical Research Council of Australia, the Genentech Foundation, the Leona M. and Harry B. Helmsley Charitable Trust, the Samuel Waxman Cancer Research Foundation, Stand Up to Cancer and Ipsen/Biomeasure.
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Owning a Wii U can feel like an exercise in patience: games and apps can take up to 30 seconds to load, and downloaded software needs to be manually installed. Thankfully, Nintendo heard its fans lamentations, and has issued the first of two major updates designed to mitigate the problem. In addition to dramatically speeding up software load times, the update revises how the Wii U handles downloads and installs. Rather than manually having to install software, the system will automatically update, download and unwrap patches in the background, even if the console is powered down. The system update also puts the finishing touches on the Wii U Virtual Console, which is promised to launch officially in the coming days. Nintendo's old VC can be accessed a little quicker now, too, as the update now allows users to jump directly into the sandboxed Wii ecosystem by holding the B button during start up. All in all, a pretty solid update to a system that needs a little fixing. Check out the full list of changes after the break.
BERLIN (AP) ? They were feasts of sublime asparagus ? laced with fear. And for more than half a century, Margot Woelk kept her secret hidden from the world, even from her husband. Then, a few months after her 95th birthday, she revealed the truth about her wartime role: Adolf Hitler's food taster.
Woelk, then in her mid-twenties, spent two and a half years as one of 15 young women who sampled Hitler's food to make sure it wasn't poisoned before it was served to the Nazi leader in his "Wolf's Lair," the heavily guarded command center in what is now Poland, where he spent much of his time in the final years of World War II.
"He was a vegetarian. He never ate any meat during the entire time I was there," Woelk said of the Nazi leader. "And Hitler was so paranoid that the British would poison him ? that's why he had 15 girls taste the food before he ate it himself."
With many Germans contending with food shortages and a bland diet as the war dragged on, sampling Hitler's food had its advantages.
"The food was delicious, only the best vegetables, asparagus, bell peppers, everything you can imagine. And always with a side of rice or pasta," she recalled. "But this constant fear ? we knew of all those poisoning rumors and could never enjoy the food. Every day we feared it was going to be our last meal."
The petite widow's story is a tale of the horror, pain and dislocation endured by people of all sides who survived World War II.
Only now in the sunset of her life has she been willing to relate her experiences, which she had buried because of shame and the fear of prosecution for having worked with the Nazis, although she insists she was never a party member. She told her story as she flipped through a photo album with pictures of her as a young woman, in the same Berlin apartment where she was born in 1917.
Woelk first revealed her secret to a local Berlin reporter a few months ago. Since then interest in her life story has been overwhelming. School teachers wrote and asked her for photos and autographs to bring history alive for their students. Several researchers from a museum visited to ask for details about her life as Hitler's taster.
Woelk says her association with Hitler began after she fled Berlin to escape Allied air attacks. With her husband gone and serving in the German army, she moved in with relatives about 435 miles (700 kilometers) to the east in Rastenburg, then part of Germany; now it is Ketrzyn, in what became Poland after the war.
There she was drafted into civilian service and assigned for the next two and a half years as a food taster and kitchen bookkeeper at the Wolf's Lair complex, located a few miles (kilometers) outside the town. Hitler was secretive, even in the relative safety of his headquarters, that she never saw him in person ? only his German shepherd Blondie and his SS guards, who chatted with the women.
Hitler's security fears were not unfounded. On July 20, 1944, a trusted colonel detonated a bomb in the Wolf's Lair in an attempt to kill Hitler. He survived, but nearly 5,000 people were executed following the assassination attempt, including the bomber.
"We were sitting on wooden benches when we heard and felt an incredible big bang," she said of the 1944 bombing. "We fell off the benches, and I heard someone shouting 'Hitler is dead!' But he wasn't. "
Following the blast, tension rose around the headquarters. Woelk said the Nazis ordered her to leave her relatives' home and move into an abandoned school closer to the compound.
With the Soviet army on the offensive and the war going badly for Germany, one of her SS friends advised her to leave the Wolf's Lair.
She said she returned by train to Berlin and went into hiding.
Woelk said the other women on the food tasting team decided to remain in Rastenburg since their families were all there and it was their home.
"Later, I found out that the Russians shot all of the 14 other girls," she said. It was after Soviet troops overran the headquarters in January 1945.
When she returned to Berlin, she found a city facing complete destruction. Round-the-clock bombing by U.S. and British planes was grinding the city center to rubble. ??
On April 20, 1945, Soviet artillery began shelling the outskirts of Berlin and ground forces pushed through toward the heart of the capital against strong resistance by die-hard SS and Hitler Youth fighters.
After about two weeks of heavy fighting, the city surrendered on May 2 ? after Hitler, who had abandoned the Wolf's Lair about five months before, had committed suicide. His successor surrendered a week later, ending the war in Europe.
For many Berlin civilians ? their homes destroyed, family members missing or dead and food almost gone ? the horror did not end with capitulation.
"The Russians then came to Berlin and got me, too," Woelk said. "They took me to a doctor's apartment and raped me for 14 consecutive days. That's why I could never have children. They destroyed everything."
Like millions of Germans and other Europeans, Woelk began rebuilding her life and trying to forget as best she could her bitter memories and the shame of her association with a criminal regime that had destroyed much of Europe.
She worked in a variety of jobs, mostly as a secretary or administrative assistant. Her husband returned from the war but died 23 years ago, she said.
With the frailty of advanced age and the lack of an elevator in her building, she has not left her apartment for the past eight years. Nurses visit several times a day, and a niece stops by frequently, she said.
Now at the end of her life, she feels the need to purge the memories by talking about her story.
"For decades, I tried to shake off those memories," she said. "But they always came back to haunt me at night." ??
Firefly protein lights up degenerating muscles, aiding muscular-dystrophy research
Thursday, April 25, 2013
Stanford University School of Medicine scientists have created a mouse model of muscular dystrophy in which degenerating muscle tissue gives off visible light.
The observed luminescence occurs only in damaged muscle tissue and in direct proportion to cumulative damage sustained in that tissue, permitting precise monitoring of the disease's progress in the mice, the researchers say.
While this technique cannot be used in humans, it paves the way to quicker, cheaper and more accurate assessment of the efficacy of therapeutic drugs. The new mouse strain is already being employed to test stem cell and gene therapy approaches for muscular dystrophies, as well as drug candidates now in clinical trials, said Thomas Rando, MD, PhD, professor of neurology and neurological sciences and director of Stanford's Glenn Laboratories for the Biology of Aging.
Rando is the senior author of a study, to be published online April 24 in the Journal of Clinical Investigation, describing his lab's creation of the experimental mouse strain in which an inserted gene coding for luciferase, the protein that causes fireflies' tails to glow, is activated only in an important class of rare stem cells that, collectively, serve as a reserve army of potential new muscle tissue. Under normal circumstances, these muscle stem cells, or "satellite cells," sit quietly adjacent to muscle fibers. But muscular injury or degeneration prompts satellite cells to start dividing and then to integrate themselves into damaged fibers, repairing the muscle tissue.
Muscular dystrophy is a genetically transmitted, progressive condition whose hallmark is the degeneration of muscle tissue. There are many different forms, whose severity, time of onset and preference for one set of muscles versus another depends on which gene is defective. But as a general rule, the disease begins to develop well before symptoms show up.
As the muscle fibers of someone with muscular dystrophy die off, nearby satellite cells ? which are normally dormant in the tissue ? begin replicating in an attempt to replace the lost muscle tissue. "But in the end, satellite cells' attempt to restore tissue is overwhelmed," said Rando, who is the founding director of Stanford's Muscular Dystrophy Association Clinic.
No truly effective treatments for muscular dystrophy exist. "Drug therapies now available for muscular dystrophy can reduce symptoms a bit, but do nothing to prevent or slow disease progression," said Rando. Testing a drug's ability to slow or arrest muscular dystrophy in one of the existing mouse models means sacrificing a few of them every couple of weeks and conducting labor-intensive, time-consuming microscopic and biochemical examinations of muscle-tissue samples taken from them, he said.
So Rando decided to design a better mouse. Dozens of mouse models of different varieties of muscular dystrophy, designed to best reflect different forms of the disease, already exist. Rando's team chose to start with a strain whose human analog is called limb-girdle muscular dystrophy. This steadily progressive form of the disease, whose clinical manifestations typically are most pronounced in limb muscles close to the torso (the thigh versus calf, or upper arm versus forearm), begins during the second or third decade of life, after the muscle-building burst of childhood is largely complete.
From that "starter" mouse strain, Rando's team developed another strain of mice that were prone to the same disease process but whose muscle cells contained the luciferase gene. When these mice are 2 months old, Rando and his associates use a sophisticated laboratory technique to activate the luciferase gene in the mice's satellite cells.
Once a luciferase gene is activated in a satellite cell, it stays "on" permanently in that cell and in all of its progeny, including mature muscle cells, causing them to glow whenever the mice are given a compound that gives off light in the presence of luciferase. So, as the muscular dystrophy progressed in the new mouse strain, the damage it inflicted on muscle fibers and the ensuing recruitment of neighboring satellite cells resulted in the affected muscle tissue's being increasingly luminescent. This luminescence, which could be observed through the mice's skin, was strong enough to be monitored and attributed to a precise anatomical location by a highly sensitive camera.
Invasive microscopic and biochemical methods are first able to detect disease symptoms in mice with the limb-girdle-analog strain when they are about 6 months old. In contrast, using this new method, the Stanford team could literally "see" the first signs of the disease's manifestation as early as 3 months.
Rando and his colleagues confirmed the validity of their luminescence assay with parallel examinations of the mice by standard microscopy and biochemical analysis. They also confirmed, in potentially luminescent but otherwise normal mice not suffering from progressive muscle deterioration, that healthy muscle tissue is ordinarily quiescent. In these mice, the Stanford scientists observed negligible luminescent output reflecting the less than 1 percent of all cells in muscle tissue that are satellite cells.
"In these luminescent mice, we could pick up the disease's pathological changes well before they could be seen otherwise," said Rando. "The readout was so sensitive we could observe those changes within a two-week period. Not only that, but we got our measurements instantaneously, without killing the mice."
The new assay's speed, accuracy and relative noninvasiveness will advance the pace of preclinical work, Rando said. "A lot of head-to-head comparisons of muscular-dystrophy therapies, including drugs already in clinical trials as well as stem cell therapies and gene therapies on the near horizon, can now be made that couldn't have been tried before, because they would have been too expensive and time-consuming to make them worth the effort."
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Stanford University Medical Center: http://med-www.stanford.edu/MedCenter/MedSchool
Thanks to Stanford University Medical Center for this article.
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Shareholders at MetroPCS made the final vote to approve the carrier marriage
After FCC approval, a planned shareholder vote, and a revised deal by T-Mobile, MetroPCS shareholders have finally voted to approve the reverse merger between the two companies. In this 'reverse merger,' the smaller company, MetroPCS, will be buying the larger T-Mobile.
René Obermann, the CEO of Deutsche Telekom (T-Mobile's parent company), says this is an important step in the company's plans going forward, as "it enables us to be more aggressive in the USA." With T-Mobile's recent and continuing network improvements, revamped monthly plans, and its ability to offer phones like the Galaxy S4 and iPhone, the company is working hard to improve their competitive position in the United States.
With the recent approval by MetroPCS, the deal to merge the two carriers is set to close on May 1, 2013. MetroPCS shareholders will receive $1.5 billion in advance, and get 26 percent of the shares of the newly merged company. The changes that subscribers on both ends of this deal will see are still yet to be determined. Expect more as this milestone deal develops.
Twitter is great if you're famous. But Jawbone's founding CEO Alexander Asseily thinks everyone deserves a powerful voice online, so today he's launching State, a structured opinion-sharing network where people don't need to follow you see your posts. You can get an early State invite now and start contributing to an opinion graph where what matters is what you believe, not who follows you.![[ Back to EurekAlert! ]](http://www.eurekalert.org/images/back2e.gif){kind=small}
Public release date: 28-Apr-2013
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