So it's the zombie apocalypse, and your neighborhood is being overrun. Quick, grab your... sporting goods? Before the zombies attack you with... golf balls? Then run for the nearest... stadium?
No, this Norwegian commercial doesn't make any sense. But like so many recent zombie movies, the production values are so high that it basically doesn't have to. (World War Z, this means you.)
Despite its gratuitous comical nonsense, viewers in Norway complained after the commercial for sporting goods store XXL aired during family-oriented programming, calling it irrelevant, disgusting and stupid, according to a Huffington Post translation of a Norwegian news website.
The commercial will now air after 9 p.m., when it will target teenagers and other zombies.
According to the video's Vimeo description, the commercial was produced by Storm Studios. It was shot in Miami in October 2012.
DHAKA/CHICAGO (Reuters) - Bangladesh said a fire that killed 111 textile workers was sabotage, as protesters took to the streets for a second day on Tuesday and garment factories across the world's second-biggest clothes exporter stopped work to mourn.
Meanwhile two other incidents this week, neither of which caused injuries, had local manufacturing leaders scrambling to assess whether their industry was under attack.
Saturday's fire has put a spotlight on global retailers that source clothes from Bangladesh, where the cost of labour is low - as little as $37 a month for some workers - and rights groups have called on firms to sign up to a fire safety program.
U.S. retailer Sears Holdings Corp said its clothing was not meant to be made in that textile factory, and was investigating reports that one of its brands had been found in the charred debris. Other brands, such as Esprit Holdings Ltd, continued to deny any connection and distanced themselves from the disaster.
The country's worst-ever industrial blaze consumed a multi-story building of a Taren Fashions factory. More than 150 workers were injured.
The interior minister, Mohiuddin Khan Alamgir, said that, according to a preliminary inquiry, the fire was the result of arson. He promised to bring the culprits to justice.
"We have come to the conclusion that it was an act of sabotage. We are finding out as of now who exactly the saboteurs are and all culprits will be brought to book," Alamgir said.
Earlier, Prime Minister Sheikh Hasina said she suspected the fire was an act of sabotage, but she did not identify any suspect or say why she thought the cause might have been arson.
Dhaka district police chief Habibur Rahman told Reuters his men were investigating complaints from some survivors that factory managers stopped workers from running out of the building when a fire alarm went off.
In addition to Saturday's blaze, two other incidents outside Dhaka -- a fire at a factory Monday morning and an explosion and fire at a facility Tuesday evening -- had the country's manufacturing leaders scared something bigger was at play.
"If you ask me as to what happened at the factory, today I'm a little confused because having such incidents all around naturally raises questions in the mind," said Annisul Huq, former president of the Bangladesh Garment Manufacturers and Exporters Association, in an interview.
"The government today says they are smelling sabotage. We don't yet know what they mean by that, we will know in a few days. I don't know what information they have but we don't like this link," he said, adding that association members would meet Wednesday to discuss the recent events.
RECORD OF POOR CONDITIONS
Wal-Mart Stores Inc, the world's largest retailer, said one of its suppliers subcontracted work to the burned factory without authorization and would no longer be used. The company declined additional comment Tuesday on the details of its factory audit program.
Sears also suggested something illicit may have taken place.
"Any merchandise found at that factory should NOT have been manufactured there and we are currently investigating further," the company said in a statement.
The International Labor Rights Forum, in a statement on Sunday, said evidence discovered in the factory suggested Sears' True Desire line may have been manufactured there, as well as other prominent brands.
As of Tuesday afternoon, a petition on Change.org calling on major retailers to join an industry fire safety program for suppliers had more than 22,000 supporters, having roughly doubled in just a few hours.
Representatives of the Tazreen Fashions factory, including the owner, were not available for comment.
Bangladesh has about 4,500 garment factories and is the world's biggest exporter of clothing after China, with garments making up 80 percent of its $24 billion annual exports.
Working conditions at Bangladeshi factories are notoriously poor, with little enforcement of safety laws. Overcrowding and locked fire doors are common.
"There are sometimes very basic issues ? having an emergency exit, not being locked in and being able to take bathroom breaks," said Erica Smiley, campaigns director for Jobs with Justice, which works with workers' rights groups in Bangladesh.
"We've known for a long time about conditions in these plants in Bangladesh ... The organizations we work with in Bangladesh had a track of these factories including the (Tazreen) factory," she said.
More than 300 factories near the capital were shut for almost a week earlier this year as workers demanded higher wages and better conditions. At least 500 people have died in garment factory accidents in Bangladesh since 2006, according to fire brigade officials.
More than 1,000 workers, some carrying black flags, demonstrated Tuesday in the Ashulia industrial belt on the outskirts of the capital where the factory is located. They blocked traffic moving on a highway and vowed to avenge the deaths of their colleagues, witnesses said.
"Never shall we give up demands for punishment for those responsible for the tragedy," one worker said.
(Reporting by Ruma Paul and Anis Ahmed in Dhaka and Jessica Wohl and Nivedita Bhattacharjee in Chicago; Additional reporting by Anne Marie Roantree in Hong Kong and Dhanya Skariachan in New York; Writing by Ben Berkowitz; Editing by Robert Birsel, Gunna Dickson, Tim Dobbyn and Andrew Hay)
TEHRAN, Iran (AP) ? Iran will step up its uranium enrichment program by sharply increasing the number of centrifuges used to make nuclear fuel, a senior official said Wednesday, in direct defiance of Western demands.
The statement by Iran's nuclear chief, Fereidoun Abbasi, is likely to escalate tensions. The West suspects Iran's nuclear program could be headed toward weapons production and has imposed punishing sanctions to try to persuade Tehran to stop enrichment.
Iran has denied the charges, saying its program is peaceful and geared toward generating electricity and producing radioisotopes to treat cancer patients.
Uranium enriched to a low level is used to produce nuclear fuel for reactors, but high level enrichment would make it suitable for use in atomic warheads.
Abbasi said Iran is making nuclear advances in the face of the severe economic measures imposed by the U.N. and the West.
"Despite sanctions, we will most likely see a substantial increase in the number of centrifuge machines this year. We will continue enrichment with intensity," Abbasi was quoted by state TV as saying Wednesday. The Iranian calendar year ends on March 20.
Abbasi did not say if Iran's stepped up work would be at the five percent fuel level or the higher 20 percent quality, which has worried the West because it can be purified to weapons grade more quickly. There have been indications that Iran may push its enrichment even higher than the 20 percent acknowledged to U.N. nuclear watchdogs.
His remarks came days after the U.N. agency said Iran is about to double its output of higher enriched uranium at its fortified Fordo underground facility. That could move Iran closer to weapons capability.
A Nov. 8 report by the International Atomic Energy Agency said Iran has installed about 2,800 centrifuges at Fordo and is poised to double the number of operating centrifuges, from the current 700 to nearly 1,400.
Iran says it needs 20 percent enriched uranium to make fuel for a medical research reactor in Tehran that produces isotopes for about 1 million patients annually.
Abbasi also said Iran will soon conduct a test run of its heavy water reactor in Arak in central Iran, despite demands from the U.N. to stop the work. The test will use virtual fuel, not actual radioactive material, he said.
He said construction of the 40-megawatt research reactor is progressing on schedule, but he noted that experts are handling the project with greater care in anticipation of possible sabotage attempts.
"The Arak reactor is progressing without any problem according to the schedule. Only because of security considerations, we are moving with caution, since enemy intends to harm this reactor," he was quoted by state TV as saying. "All the equipment needed to operate this reactor has been purchased."
The West is concerned that the heavy water reactor could produce enough plutonium for a nuclear weapon each year, if the spent fuel is reprocessed. That would be another pathway for bomb-grade material, but Iran is not known to possess a plutonium reprocessing facility
Iran has experienced explosions and malfunctions at its nuclear and industrial sites, partly due to faulty equipment secretly procured on the global market.
Also, Iran says it is the target of a campaign that has included the abduction and assassination of scientists, the sale of faulty equipment and the planting of a destructive computer worm known as Stuxnet, which briefly brought Iran's uranium enrichment activity to a halt in 2010.
MRAUK-U, Myanmar (AP) ? It was dusk in a corner of Myanmar recently shaken by some of the bloodiest sectarian violence in a generation, and a dozen Canadian tourists climbed to the top of a grassy hill, cameras ready to capture the sweeping view.
Moss-covered pagodas rose from foggy hilltops all along the horizon, their bell-shaped silhouettes dark against the blue sky. Birds flitted through lush treetops. A small throng of children played on a dirt road nearby.
From here, it was hard to tell anything was wrong.
Just six miles (10 kilometers) to the south, though, security forces have blocked roads to a village that was reportedly overrun last month by a frenzied mob of Rakhine Buddhists armed with swords and spears who beheaded Muslim civilians and slaughtered women and children.
Across western Myanmar's Rakhine state, the United Nations is distributing emergency supplies of food and shelter to terrified refugees who have fled burning homes. A nighttime curfew is in force in several townships, including Mrauk-U.
But none of that has kept a small but steady trickle of determined tourists from traveling here to ogle at the monuments of this region's glorious past.
"We heard the news before coming," Caroline Barbeau, a French-speaking social worker from Montreal, said of violence that has shaken the region since June, displacing 110,000 people from their homes.
But "we've had no problems," she said. "The people are very nice, very kind."
Asked what had touched her most, Barbeau turned pensive. "Their smiles."
Mrauk-U itself has been spared the bloodshed between Buddhist and Muslims that has scarred other parts of Rakhine state. It is calm, and for foreign tourists, safe. But the Muslims who once worked and traded here just a few months ago no longer dare set foot in the town, part of a worrying new pattern of segregation that has split the two communities.
What draws tourists to this remote place are its storied relics ? hundreds of them, scattered across the hilltops. Mrauk-U is the spiritual heartland of the Rakhine, the former capital of a now-defunct Buddhist kingdom that reached its height in the 16th century. The dynasty conquered a swath of mountainous territory along what is now Myanmar's western coast, waging major battles against rival empires ? including Muslims from Bengal.
Their descendants ? the Buddhist Rakhine and the Muslim Rohingya ? have been fighting and killing each other across this region in recent months.
The conflict centers around the question of nationality, scarce land, and some say, racism. The Rakhine consider the darker-skinned Muslims among them to be foreign intruders from Bangladesh, even though many have lived here for generations. The government denies the Rohingya citizenship, considering them "Bengalis." But Bangladesh does too, effectively rendering them stateless.
After three Muslim Rohingya men allegedly raped and murdered a Buddhist Rakhine woman in late May, violence rocked the state for a week in June, then again in October. In what may have been the bloodiest episode so far, a thousands-strong mob of Buddhists with spears, arrows and homemade guns overran the village Yan Thei, just south of Mrauk-U, razing most of it to the ground, according to Human Rights Watch.
Although the violence has subsided, tensions have not, and there are fears the worst is yet to come.
Which raises the question: Should any tourists be traveling here at all?
During Myanmar's half-century of military rule, which ended last year, only the most intrepid travelers made their way to places like Mrauk-U, and even then there was debate over whether traveling to the Southeast Asian country would bolster the oppressive junta.
But after the army ceded direct power last year to an elected but still military-dominated government, the new president embarked on a wave of widely praised democratic reforms, and the number of tourists skyrocketed.
The serene pace and historic legacy of places like this are a big part of the draw.
Even the route to Mrauk-U is worth the trip ? a slow, meandering boat journey up the Kaladan River past a timeless horizon of shimmering rice fields. Thatched bamboo huts rise from the water's edge on stilts. Oxen graze. Golden pagodas rise from green hills.
Philippe Grivel, a retired Frenchman traveling solo in Rakhine state, said he was afraid not of the potential for violence, but of the possibility of missing one of Myanmar's grandest historical sites.
After the fighting began, the government banned local travel agencies from taking foreign tourists to the region. But nothing has stopped individual travelers from making the journey, and special permits have been granted to some larger tour groups.
When Grivel emailed a hotel in Mrauk-U to inquire if it was possible to visit, they told him that if the authorities didn't turn him back at the airport in Sittwe, the state capital, he was free to come.
Explorateur, the Canadian tour agency that arranged Barbeau's travel and advertises three-week trips to Myanmar called "Light and Harmony," assured its clients the trip would be safe.
And it was.
"This is still a virgin country without many tourists," said another of the Canadian tourists, a francophone from Montreal who gave only her family name, Allard, because of security concerns. "It's magnificent."
The sightseers ? 12 tourists and one guide ? spent several days bicycling through Mrauk-U's quaint, crumbling streets. They visited the town market. They saw nothing disturbing.
Allard, though, was surprised to learn that one of Mrauk-U's monasteries is home to more than 700 Buddhist refugees, nine of whom had just walked there after hearing rumors that Muslims armed with Molotov cocktails were readying for an assault.
The tour group did not visit the monastery. But they did express concern over the violence. Allard called the recent bloodshed "horrible."
On the eve of their final day, the group toured Mrauk-U's most famous temple, a stone labyrinth called Shittaung. Also known as the "Temple of Victory," it was built in 1535 to commemorate King Min Bin's conquest over the 12 provinces of Muslim-dominated Bengal.
As a Burmese guide explained the temple's history, the group snapped photos of the ubiquitous stone Buddhas lined up inside its dim, maze-like hallways. Some strained their necks to gaze up at the elaborate royal artwork painted on the ceilings above.
Kyaw Zaw Tun, who works at the temple and lost a brother in the October clashes, said it would normally be full of local Buddhist pilgrims at this time of year.
But its halls are almost empty, its guest book filled with, on average, one or two foreign visitors a day.
Asked if Muslims had ever visited before the violence began, he shook his head with disgust.
Never.
"If they came in here now," he said, pausing to tighten his right hand as if it were a knife about to slice meat, "chop, chop, chop."
As he spoke, the Canadians walked out of one of the temple's stone doors, one by one. They then climbed to the top of a nearby hill beside Shittaung, pulled out bottles of mineral water, and watched the sun sink beneath the hills.
Seeking?a low-cost way to launch their experiments into space, a team of scientists has designed a space-ready, 3-D printed CubeSat.
CubeSats are standardized, tiny satellites, often only 3.9 inches on each side and weighing just under 3 pounds. They are so small that they have room for only a few sensors, and burn up in the Earth's atmosphere after just a few months. Kits cost under $10,000, which is considered cheap for the space industry. But Jacopo Piattoni of the University of Bologna and his team aim to drive the satellites' price down even further, while making the devices easier to customize.
In 3-D printing, a computer-directed nozzle "prints" a three-dimensional object in plastic. Often, engineers use this method to design a prototype for a product that will then be built out of metal or another, sturdier medium. But Piattoni?s team hopes their plastic CubeSat could survive launch and low-Earth orbit.
Using 3-D printers, researchers can automate the CubeSat production process. ?We don?t need a technician,? Piattoni said, adding that this also makes the process faster.
[NASA Turns to 3-D Printing for Self-Building Spacecraft]
The CubeSat?s sensors and computer chips, of course, weren't printed in the lab, and the team had to add a small, metal heat sink to disperse the electronic components' heat. The method holds promise, though. When the researchers tested the chassis in near-space conditions, "it did really well," Piattoni said.
Piattoni chose ABS plastic, the same type of plastic used in Lego bricks, to construct his CubeSat because of that material's resilience to extreme temperatures, vibrations, radiation and more. A satellite will absorb a lot of solar radiation during its spaceflight, and its temperature will swing from -4 degrees F (-20 degrees C) to 176 degrees F (80 degrees C) each orbit. "It's not so easy for plastics in that environment," Piattoni said.
In fact, ABS plastic was famously indicted in a massive seat-belt buckle recall in the mid-90s because UV radiation weakened buckles made from the material. But such radiation, even at elevated levels, won't pose a problem for the CubeSat, due to its short lifetime.
With one successful satellite constructed, the team can now use the 3-D printer to crank out another copy each night. They can also test new designs or build support for other sensors or modules, just by clicking a few buttons on a computer.
The final product passed its tests with flying colors. Now, like most other CubeSats, it will hitch a ride into space as secondary cargo on a rocket already headed to its preferred orbit. Piattoni's team is working with QB50, which will put 50 CubeSats into orbit at once on a Russian Shtil-2.1 scheduled to launch in 2014.
The satellite was designed and tested by Piattoni and researchers in the University of Rome's Department of Astronautical, Electrical and Energy Engineering and the Department of Mechanical and Aerospace Engineering.
Copyright 2012 TechNewsDaily, a TechMediaNetwork company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
JCI early table of contents for Nov. 26, 2012Public release date: 26-Nov-2012 [ | E-mail | Share ]
Contact: Jillian Hurst press_releases@the-jci.org Journal of Clinical Investigation
Bariatric surgery procedures have similar therapeutic benefits in obese adults
Obesity is associated with insulin resistance and type 2 diabetes, both of which can be significantly improved by weight loss. Gastric bypass and adjustable gastric banding are two bariatric surgery techniques that are frequently used to effect weight loss in obese patients, but it is unclear if the two procedures produce different outcomes. In this issue of the Journal of Clinical Investigation, researchers led by Samuel Klein at the University of Washington School of Medicine in St. Louis compared the effects of 20% weight loss induced by either gastric bypass or adjustable gastric banding on metabolic response. They found that patients had different metabolic responses after eating, but both procedures equally improved insulin sensitivity and glucose tolerance. The researchers concluded that weight loss itself is primarily responsible for the therapeutic effects of gastric bypass and adjustable gastric banding in non-diabetic obese adults.
TITLE:
Gastric bypass and banding equally improve insulin sensitivity and ?-cell function
AUTHOR CONTACT:
Samuel Klein
Washington University School of Medicine, St Louis, MO, USA
Phone: 314-362-8708; E-mail: sklein@dom.wustl.edu
View this article at: http://www.jci.org/articles/view/64895?key=31c84cf8f52f834d9914
Identifying the cause of anesthesia-induced seizures
Antifibrinolytic drugs are frequently used to prevent blood loss during surgery, but sometimes cause convulsive seizures. In this issue of the Journal of Clinical Investigation, researchers led by Beverly Orser at the University of Toronto investigated the molecular mechanisms that underlie this side effect. By studying antifibrinolytics in mice, Orser and colleagues found that the drugs inhibited the activity of glycine receptors in the brain, leading to seizures. Seizures could be prevented by co-treatment with the general anesthetic isoflurane. This study explains the causes of and proposes treatment for antifibrinolytic-induced seizures. In a companion commentary, Debra Schwinn of the University of Washington reviews the connection between seizures and antifibrinolytic drugs.
TITLE:
Tranexamic acid concentrations associated with human seizures inhibit glycine receptors
AUTHOR CONTACT:
Irene Lecker
Faculty of Medicine, University of Toronto, Toronto, ON, CAN
Phone: 416-978-1518; E-mail: irene.lecker@utoronto.ca
View this article at: http://www.jci.org/articles/view/63375?key=806b0eca4232a067ca57
ACCOMPANYING COMMENTARY
TITLE:
Understanding the TXA seizure connection
AUTHOR CONTACT:
Debra Schwinn
University of Washington, Seattle, WA, USA
Phone: 206-543-2673; Fax: 206-543-2958; E-mail: debra-schwinn@uiowa.edu
View this article at: http://www.jci.org/articles/view/66724?key=bd9895d06f784ef4366f
Parallel structure: Surprising similarities between kidney cells and neurons
The primary function of the kidneys is to filter the blood to remove waste and retain blood cells and proteins. Podocytes are specialized kidney cells that form a filtering structure known as a slit diaphragm. Disruption of the podocytes results in the enlargement of the slit diaphragm, causing nephrotic syndrome, and, eventually, renal failure. In this issue of the Journal of Clinical Investigation, researchers led by Shuta Ishibe and Pietro De Camilli at Yale University identified a protein network in podocytes that is responsible for maintaining the structural integrity of the slit diaphragms. By engineering mice that lack components of this protein network, Ishibe, Camilli, and colleagues found that they could block the formation of the slit diaphragms in the kidney. Interestingly, they found that this protein network is highly similar to the networks that mediate the development of neuronal synapses. In a companion commentary, Rosemary Sampogna and Qais Al-Awqati of Columbia University discuss how these findings alter our understanding of how slit diaphragms function in the ever-changing environment of the kidney.
TITLE:
Role of dynamin, synaptojanin and endophilin in podocyte foot processes
AUTHOR CONTACT:
Shuta Ishibe
Yale University School of Medicine, New Haven, CT, USA
Phone: 203-737-4170; E-mail: shuta.ishibe@yale.edu
View this article at: http://www.jci.org/articles/view/65289?key=b558c1e93de5879b6116
ACCOMPANYING COMMENTARY
TITLE:
Taking a bite: endocytosis in the maintenance of the slit diaphragm
AUTHOR CONTACT:
Qais Al-Awqati
Dept. Of Medicine & Physiology, New York, NY, USA
Phone: 212-305-3512; Fax: 212-305-3475; E-mail: qa1@columbia.edu
View this article at: http://www.jci.org/articles/view/65785?key=28148c95a955cf51dfc9
Mutations in ?Klotho underlie a genetic form of rickets
FGF23, a growth factor that regulates the metabolism of calcium and phosphate, binds and activates a circulating receptor known as ?Klotho (cKL). In a study published in the Journal of Clinical Investigation, researchers led by Kenneth White at Indiana University describe a patient with a chromosomal translocation that results in increased levels of ?Klotho. The patient presented with rickets, low blood phosphate and calcium levels, and increased FGF23. To determine how ?Klotho effects these changes, White and colleagues over-expressed cKL in mice and found that increased cKL resulted in enhanced FGF23 levels, decreased serum calcium and phosphate levels, low bone mineral content, and bone fractures. These data establish cKL as an important regulator of FGF23 production and phosphate metabolism and may have implications for the treatment of rickets. In a companion commentary, Harald Jppner of Massachusetts General Hospital and Myles Wolf of the University of Miami discuss the role of FGF23 and ?Klotho in mineral metabolism.
TITLE:
Circulating ?Klotho influences phosphate handling by controlling FGF23 production
AUTHOR CONTACT:
Kenneth E White
Indiana University School of Medicine, Indianapolis, IN, USA
View this article at: http://www.jci.org/articles/view/64986?key=7d8ae8802deff9a3caa3
ACCOMPANYING COMMENTARY
TITLE:
?Klotho: FGF23 coreceptor and FGF23-regulating hormone
AUTHOR CONTACT:
Harald Jppner
Massachusetts Gen Hosp, Boston, MA, USA
Phone: 617-726-3966; Fax: 617-726-7543; E-mail: jueppner@helix.mgh.harvard.edu
View this article at: http://www.jci.org/articles/view/67055?key=97377cc82306b227bcad
USP44 helps cells double check chromosome segregation to prevent cancer
Tumor cells frequently have an irregular number of chromosomes, a condition known as aneuploidy. During cell division, checkpoint proteins stop the process of division to ensure that each daughter cell receives the appropriate number of chromosomes; defects in these checkpoints can cause aneuploidy. In this issue of the Journal of Clinical Investigation, researchers led by Paul Galardy at the Mayo Clinic in Rochester, MN, investigated the role of the checkpoint protein USP44. Using a mouse that lacks Usp44, they found that loss of USP44 prevents chromosomes from splitting evenly between daughter cells. Usp44-deficient mice were prone to spontaneous tumors, particularly in the lungs. Interestingly, low USP44 expression was correlated with poor prognosis in human lung cancer. In a companion commentary, Andrew Holland and Don Cleveland of the University of California, San Diego, discuss how theses findings impact our understanding of aneuploidy in cancer.
TITLE:
USP44 regulates centrosome positioning to prevent aneuploidy and suppress tumorigenesis
AUTHOR CONTACT:
Paul Galardy
Mayo Clinic, Rochester, MN, USA
Phone: 507-284-2695; E-mail: galardy.paul@mayo.edu
View this article at: http://www.jci.org/articles/view/63084?key=3be5fa433c36a4a45295
ACCOMPANYING COMMENTARY
TITLE:
The deubiquitinase USP44 is a tumor suppressor that protects against chromosome missegregation
AUTHOR CONTACT:
Andrew Holland
Ludwig Inst. Cancer Research & UCSD, La Jolla, CA, USA
Phone: 858-534-7899; E-mail: a1holland@ucsd.edu
View this article at: http://www.jci.org/articles/view/66420?key=50440b6db78075ffec3c
A sticky situation: researchers identify mucus-producing pathway in human airway cells
Inflammatory airway diseases such as asthma, COPD, and cystic fibrosis are associated with increased mucus production, but the molecular mechanisms that are responsible for mucus production in these diseases have not been determined. In this issue of the Journal of Clinical Investigation, researchers led by Michael Holtzman at Washington University of St. Louis defined a cell signaling pathway that enhances mucus production in the cells that line the human airway. The pathway, which involves the protein MAPK13, was also activated in human COPD patients. By inhibiting the activity of MAPK13, Holtzman and colleagues were able to reduce mucus production in human airway epithelial cells, suggesting that therapeutics targeting this pathway might be useful for the treatment of mucus production in humans.
TITLE:
IL-13-induced airway mucus production is blocked by MAPK13 inhibition
AUTHOR CONTACT:
Michael Holtzman
Washington University School of Medicine, St. Louis, MO, USA
Phone: 314-362-8970; Fax: 314-362-9002; E-mail: holtzmanm@wustl.edu
View this article at: http://www.jci.org/articles/view/64896?key=33af0229095ae19f52d5
Too much of a good thing: extra VEGF signaling slows tumor growth
Angiogenesis is the formation of new blood vessels. Establishment of a blood supply promotes tumor growth by providing access to oxygen and nutrients. Blood vessel development is largely mediated by a growth factor known as VEGF, which is targeted by anti-angiogenic therapies. In this issue of the Journal of Clinical Investigation, researchers led by Hong Chen at the University of Oklahoma identified two new proteins, epsin1 and epsin2, as important regulators of VEGF-stimulated angiogenesis. VEGF mediates angiogenesis by binding to a cell surface protein that instigates cellular changes that are required for blood vessel formation. Epsins are known to remove proteins from the cell surface, preventing their activation. Normally, the number of VEGF binding proteins (VEGFR) on the cell surface is tightly controlled, but Chen and colleagues found that mice lacking epsin1/2 had a greater number of VEGFR on the cell surface that led to extra VEGF signaling, abnormal tumor vasculature, and slower tumor growth. In a companion commentary, Nancy Klauber-DeMore of the University of North Carolina at Chapel Hill discusses how these findings could contribute to the development of epsin-based therapeutic targeting of tumor angiogenesis.
AUTHOR CONTACT:
Hong Chen
Oklahoma Medical Research Foundation, Oklahoma City, OK, USA
Phone: 405-271-2750; E-mail: hong-chen@omrf.org
View this article at: http://www.jci.org/articles/view/64537?key=8b9e9a01382464f1fc75
ACCOMPANYING COMMENTARY
TITLE:
Are epsins a therapeutic target for tumor angiogenesis?
AUTHOR CONTACT:
Nancy Demore
University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Phone: 919-216-9754; E-mail: nancy_demore@med.unc.edu
View this article at: http://www.jci.org/articles/view/66171?key=7e2e14d5e5eda41ede24
Mouse model explains how calcium channel mutation causes hypokalemic periodic paralysis
Hypokalemic periodic paralysis (HypoPP) is a skeletal muscle disorder that is characterized by episodes of severe muscle weakness and low serum potassium levels. It is caused be a genetic mutation in protein channels that pump calcium or sodium ions across the cell membrane, but it is unclear exactly how the calcium channel mutations cause muscle weakness. In this issue of the Journal of Clinical Investigation, researchers led by Stephen Cannon at the University of Texas Southwestern Medical Center created a mouse with the HypoPP-associated calcium channel mutation that had symptoms that were similar to human HypoPP. They found that the mutant calcium channel caused changes in the cellular membrane potential that altered the ability of the muscle fibers to contract. This study explains how an inherited mutation causes HypoPP in humans. In a companion commentary, Alfred George of Vanderbilt University discusses how inherited mutations in channels contribute to human disease.
TITLE:
A calcium channel mutant mouse model of hypokalemic periodic paralysis
AUTHOR CONTACT:
Stephen C. Cannon
Southwestern Medical School, Dallas, TX, USA
Phone: 214-648-2564; Fax: 214-648-6306; E-mail: steve.cannon@utsouthwestern.edu
View this article at: http://www.jci.org/articles/view/66091?key=0f8ffec321a1fe4d328b
ACCOMPANYING COMMENTARY
TITLE:
Leaky channels make weak muscles
AUTHOR CONTACT:
Alfred L George, Jr.
Vanderbilt University, Nashville, TN, USA
Phone: 615-936-2660; Fax: 615-936-2661; E-mail: al.george@vanderbilt.edu
View this article at: http://www.jci.org/articles/view/66535?key=6b5240ca1c7bbbfe9a54
A tale of two heme transporters
Erythropoiesis, or the production of red blood cells, is a tightly regulated process that is sensitive to the balance of the proteins that form hemoglobin, heme and globin. The protein FLVCR1a is responsible for removing excess heme from cells and is essential for erythropoiesis. In this issue of the Journal of Clinical Investigation, researchers led by Emanuela Tolosano at the University of Torino in Italy identified another form of FLVCR1, FLVCR1b, that is responsible for exporting heme from the mitochondria of the cell, the location of heme production. By manipulating the expression of the FLVCR1 proteins in mice, Tolosano and colleagues found that FLVCR1b was required for erythropoiesis. FLVCR1a was not required for erythropoiesis, but was necessary to prevent excess bleeding, swelling, and skeletal abnormalities in the developing mouse embryo. These results indicate that mutations in the Flvcr1 gene may underlie diseases characterized by abnormal heme levels, such as Sideroblastic anemia. In a companion commentary, Mark Fleming of Children's Hospital Boston discusses the role of heme transport in human physiology and disease.
TITLE:
The mitochondrial heme exporter FLVCR1b mediates erythroid differentiation
AUTHOR CONTACT:
Emanuela Tolosano
University of Torino, Torino, UNK, ITA
Phone: 39-011-670-6423; Fax: 39-011-670-6432; E-mail: emanuela.tolosano@unito.it
View this article at: http://www.jci.org/articles/view/62422?key=da4e860633582101d3cb
ACCOMPANYING COMMENTARY
TITLE:
Mitochondrial heme: an exit strategy at last
AUTHOR CONTACT:
Mark Fleming
Children's Hospital Boston, Boston, MA, USA
Phone: 617-919-2664; E-mail: mark.fleming@childrens.harvard.edu
View this article at: http://www.jci.org/articles/view/66607?key=70b59624a5b601a3a137
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JCI early table of contents for Nov. 26, 2012Public release date: 26-Nov-2012 [ | E-mail | Share ]
Contact: Jillian Hurst press_releases@the-jci.org Journal of Clinical Investigation
Bariatric surgery procedures have similar therapeutic benefits in obese adults
Obesity is associated with insulin resistance and type 2 diabetes, both of which can be significantly improved by weight loss. Gastric bypass and adjustable gastric banding are two bariatric surgery techniques that are frequently used to effect weight loss in obese patients, but it is unclear if the two procedures produce different outcomes. In this issue of the Journal of Clinical Investigation, researchers led by Samuel Klein at the University of Washington School of Medicine in St. Louis compared the effects of 20% weight loss induced by either gastric bypass or adjustable gastric banding on metabolic response. They found that patients had different metabolic responses after eating, but both procedures equally improved insulin sensitivity and glucose tolerance. The researchers concluded that weight loss itself is primarily responsible for the therapeutic effects of gastric bypass and adjustable gastric banding in non-diabetic obese adults.
TITLE:
Gastric bypass and banding equally improve insulin sensitivity and ?-cell function
AUTHOR CONTACT:
Samuel Klein
Washington University School of Medicine, St Louis, MO, USA
Phone: 314-362-8708; E-mail: sklein@dom.wustl.edu
View this article at: http://www.jci.org/articles/view/64895?key=31c84cf8f52f834d9914
Identifying the cause of anesthesia-induced seizures
Antifibrinolytic drugs are frequently used to prevent blood loss during surgery, but sometimes cause convulsive seizures. In this issue of the Journal of Clinical Investigation, researchers led by Beverly Orser at the University of Toronto investigated the molecular mechanisms that underlie this side effect. By studying antifibrinolytics in mice, Orser and colleagues found that the drugs inhibited the activity of glycine receptors in the brain, leading to seizures. Seizures could be prevented by co-treatment with the general anesthetic isoflurane. This study explains the causes of and proposes treatment for antifibrinolytic-induced seizures. In a companion commentary, Debra Schwinn of the University of Washington reviews the connection between seizures and antifibrinolytic drugs.
TITLE:
Tranexamic acid concentrations associated with human seizures inhibit glycine receptors
AUTHOR CONTACT:
Irene Lecker
Faculty of Medicine, University of Toronto, Toronto, ON, CAN
Phone: 416-978-1518; E-mail: irene.lecker@utoronto.ca
View this article at: http://www.jci.org/articles/view/63375?key=806b0eca4232a067ca57
ACCOMPANYING COMMENTARY
TITLE:
Understanding the TXA seizure connection
AUTHOR CONTACT:
Debra Schwinn
University of Washington, Seattle, WA, USA
Phone: 206-543-2673; Fax: 206-543-2958; E-mail: debra-schwinn@uiowa.edu
View this article at: http://www.jci.org/articles/view/66724?key=bd9895d06f784ef4366f
Parallel structure: Surprising similarities between kidney cells and neurons
The primary function of the kidneys is to filter the blood to remove waste and retain blood cells and proteins. Podocytes are specialized kidney cells that form a filtering structure known as a slit diaphragm. Disruption of the podocytes results in the enlargement of the slit diaphragm, causing nephrotic syndrome, and, eventually, renal failure. In this issue of the Journal of Clinical Investigation, researchers led by Shuta Ishibe and Pietro De Camilli at Yale University identified a protein network in podocytes that is responsible for maintaining the structural integrity of the slit diaphragms. By engineering mice that lack components of this protein network, Ishibe, Camilli, and colleagues found that they could block the formation of the slit diaphragms in the kidney. Interestingly, they found that this protein network is highly similar to the networks that mediate the development of neuronal synapses. In a companion commentary, Rosemary Sampogna and Qais Al-Awqati of Columbia University discuss how these findings alter our understanding of how slit diaphragms function in the ever-changing environment of the kidney.
TITLE:
Role of dynamin, synaptojanin and endophilin in podocyte foot processes
AUTHOR CONTACT:
Shuta Ishibe
Yale University School of Medicine, New Haven, CT, USA
Phone: 203-737-4170; E-mail: shuta.ishibe@yale.edu
View this article at: http://www.jci.org/articles/view/65289?key=b558c1e93de5879b6116
ACCOMPANYING COMMENTARY
TITLE:
Taking a bite: endocytosis in the maintenance of the slit diaphragm
AUTHOR CONTACT:
Qais Al-Awqati
Dept. Of Medicine & Physiology, New York, NY, USA
Phone: 212-305-3512; Fax: 212-305-3475; E-mail: qa1@columbia.edu
View this article at: http://www.jci.org/articles/view/65785?key=28148c95a955cf51dfc9
Mutations in ?Klotho underlie a genetic form of rickets
FGF23, a growth factor that regulates the metabolism of calcium and phosphate, binds and activates a circulating receptor known as ?Klotho (cKL). In a study published in the Journal of Clinical Investigation, researchers led by Kenneth White at Indiana University describe a patient with a chromosomal translocation that results in increased levels of ?Klotho. The patient presented with rickets, low blood phosphate and calcium levels, and increased FGF23. To determine how ?Klotho effects these changes, White and colleagues over-expressed cKL in mice and found that increased cKL resulted in enhanced FGF23 levels, decreased serum calcium and phosphate levels, low bone mineral content, and bone fractures. These data establish cKL as an important regulator of FGF23 production and phosphate metabolism and may have implications for the treatment of rickets. In a companion commentary, Harald Jppner of Massachusetts General Hospital and Myles Wolf of the University of Miami discuss the role of FGF23 and ?Klotho in mineral metabolism.
TITLE:
Circulating ?Klotho influences phosphate handling by controlling FGF23 production
AUTHOR CONTACT:
Kenneth E White
Indiana University School of Medicine, Indianapolis, IN, USA
View this article at: http://www.jci.org/articles/view/64986?key=7d8ae8802deff9a3caa3
ACCOMPANYING COMMENTARY
TITLE:
?Klotho: FGF23 coreceptor and FGF23-regulating hormone
AUTHOR CONTACT:
Harald Jppner
Massachusetts Gen Hosp, Boston, MA, USA
Phone: 617-726-3966; Fax: 617-726-7543; E-mail: jueppner@helix.mgh.harvard.edu
View this article at: http://www.jci.org/articles/view/67055?key=97377cc82306b227bcad
USP44 helps cells double check chromosome segregation to prevent cancer
Tumor cells frequently have an irregular number of chromosomes, a condition known as aneuploidy. During cell division, checkpoint proteins stop the process of division to ensure that each daughter cell receives the appropriate number of chromosomes; defects in these checkpoints can cause aneuploidy. In this issue of the Journal of Clinical Investigation, researchers led by Paul Galardy at the Mayo Clinic in Rochester, MN, investigated the role of the checkpoint protein USP44. Using a mouse that lacks Usp44, they found that loss of USP44 prevents chromosomes from splitting evenly between daughter cells. Usp44-deficient mice were prone to spontaneous tumors, particularly in the lungs. Interestingly, low USP44 expression was correlated with poor prognosis in human lung cancer. In a companion commentary, Andrew Holland and Don Cleveland of the University of California, San Diego, discuss how theses findings impact our understanding of aneuploidy in cancer.
TITLE:
USP44 regulates centrosome positioning to prevent aneuploidy and suppress tumorigenesis
AUTHOR CONTACT:
Paul Galardy
Mayo Clinic, Rochester, MN, USA
Phone: 507-284-2695; E-mail: galardy.paul@mayo.edu
View this article at: http://www.jci.org/articles/view/63084?key=3be5fa433c36a4a45295
ACCOMPANYING COMMENTARY
TITLE:
The deubiquitinase USP44 is a tumor suppressor that protects against chromosome missegregation
AUTHOR CONTACT:
Andrew Holland
Ludwig Inst. Cancer Research & UCSD, La Jolla, CA, USA
Phone: 858-534-7899; E-mail: a1holland@ucsd.edu
View this article at: http://www.jci.org/articles/view/66420?key=50440b6db78075ffec3c
A sticky situation: researchers identify mucus-producing pathway in human airway cells
Inflammatory airway diseases such as asthma, COPD, and cystic fibrosis are associated with increased mucus production, but the molecular mechanisms that are responsible for mucus production in these diseases have not been determined. In this issue of the Journal of Clinical Investigation, researchers led by Michael Holtzman at Washington University of St. Louis defined a cell signaling pathway that enhances mucus production in the cells that line the human airway. The pathway, which involves the protein MAPK13, was also activated in human COPD patients. By inhibiting the activity of MAPK13, Holtzman and colleagues were able to reduce mucus production in human airway epithelial cells, suggesting that therapeutics targeting this pathway might be useful for the treatment of mucus production in humans.
TITLE:
IL-13-induced airway mucus production is blocked by MAPK13 inhibition
AUTHOR CONTACT:
Michael Holtzman
Washington University School of Medicine, St. Louis, MO, USA
Phone: 314-362-8970; Fax: 314-362-9002; E-mail: holtzmanm@wustl.edu
View this article at: http://www.jci.org/articles/view/64896?key=33af0229095ae19f52d5
Too much of a good thing: extra VEGF signaling slows tumor growth
Angiogenesis is the formation of new blood vessels. Establishment of a blood supply promotes tumor growth by providing access to oxygen and nutrients. Blood vessel development is largely mediated by a growth factor known as VEGF, which is targeted by anti-angiogenic therapies. In this issue of the Journal of Clinical Investigation, researchers led by Hong Chen at the University of Oklahoma identified two new proteins, epsin1 and epsin2, as important regulators of VEGF-stimulated angiogenesis. VEGF mediates angiogenesis by binding to a cell surface protein that instigates cellular changes that are required for blood vessel formation. Epsins are known to remove proteins from the cell surface, preventing their activation. Normally, the number of VEGF binding proteins (VEGFR) on the cell surface is tightly controlled, but Chen and colleagues found that mice lacking epsin1/2 had a greater number of VEGFR on the cell surface that led to extra VEGF signaling, abnormal tumor vasculature, and slower tumor growth. In a companion commentary, Nancy Klauber-DeMore of the University of North Carolina at Chapel Hill discusses how these findings could contribute to the development of epsin-based therapeutic targeting of tumor angiogenesis.
AUTHOR CONTACT:
Hong Chen
Oklahoma Medical Research Foundation, Oklahoma City, OK, USA
Phone: 405-271-2750; E-mail: hong-chen@omrf.org
View this article at: http://www.jci.org/articles/view/64537?key=8b9e9a01382464f1fc75
ACCOMPANYING COMMENTARY
TITLE:
Are epsins a therapeutic target for tumor angiogenesis?
AUTHOR CONTACT:
Nancy Demore
University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Phone: 919-216-9754; E-mail: nancy_demore@med.unc.edu
View this article at: http://www.jci.org/articles/view/66171?key=7e2e14d5e5eda41ede24
Mouse model explains how calcium channel mutation causes hypokalemic periodic paralysis
Hypokalemic periodic paralysis (HypoPP) is a skeletal muscle disorder that is characterized by episodes of severe muscle weakness and low serum potassium levels. It is caused be a genetic mutation in protein channels that pump calcium or sodium ions across the cell membrane, but it is unclear exactly how the calcium channel mutations cause muscle weakness. In this issue of the Journal of Clinical Investigation, researchers led by Stephen Cannon at the University of Texas Southwestern Medical Center created a mouse with the HypoPP-associated calcium channel mutation that had symptoms that were similar to human HypoPP. They found that the mutant calcium channel caused changes in the cellular membrane potential that altered the ability of the muscle fibers to contract. This study explains how an inherited mutation causes HypoPP in humans. In a companion commentary, Alfred George of Vanderbilt University discusses how inherited mutations in channels contribute to human disease.
TITLE:
A calcium channel mutant mouse model of hypokalemic periodic paralysis
AUTHOR CONTACT:
Stephen C. Cannon
Southwestern Medical School, Dallas, TX, USA
Phone: 214-648-2564; Fax: 214-648-6306; E-mail: steve.cannon@utsouthwestern.edu
View this article at: http://www.jci.org/articles/view/66091?key=0f8ffec321a1fe4d328b
ACCOMPANYING COMMENTARY
TITLE:
Leaky channels make weak muscles
AUTHOR CONTACT:
Alfred L George, Jr.
Vanderbilt University, Nashville, TN, USA
Phone: 615-936-2660; Fax: 615-936-2661; E-mail: al.george@vanderbilt.edu
View this article at: http://www.jci.org/articles/view/66535?key=6b5240ca1c7bbbfe9a54
A tale of two heme transporters
Erythropoiesis, or the production of red blood cells, is a tightly regulated process that is sensitive to the balance of the proteins that form hemoglobin, heme and globin. The protein FLVCR1a is responsible for removing excess heme from cells and is essential for erythropoiesis. In this issue of the Journal of Clinical Investigation, researchers led by Emanuela Tolosano at the University of Torino in Italy identified another form of FLVCR1, FLVCR1b, that is responsible for exporting heme from the mitochondria of the cell, the location of heme production. By manipulating the expression of the FLVCR1 proteins in mice, Tolosano and colleagues found that FLVCR1b was required for erythropoiesis. FLVCR1a was not required for erythropoiesis, but was necessary to prevent excess bleeding, swelling, and skeletal abnormalities in the developing mouse embryo. These results indicate that mutations in the Flvcr1 gene may underlie diseases characterized by abnormal heme levels, such as Sideroblastic anemia. In a companion commentary, Mark Fleming of Children's Hospital Boston discusses the role of heme transport in human physiology and disease.
TITLE:
The mitochondrial heme exporter FLVCR1b mediates erythroid differentiation
AUTHOR CONTACT:
Emanuela Tolosano
University of Torino, Torino, UNK, ITA
Phone: 39-011-670-6423; Fax: 39-011-670-6432; E-mail: emanuela.tolosano@unito.it
View this article at: http://www.jci.org/articles/view/62422?key=da4e860633582101d3cb
ACCOMPANYING COMMENTARY
TITLE:
Mitochondrial heme: an exit strategy at last
AUTHOR CONTACT:
Mark Fleming
Children's Hospital Boston, Boston, MA, USA
Phone: 617-919-2664; E-mail: mark.fleming@childrens.harvard.edu
View this article at: http://www.jci.org/articles/view/66607?key=70b59624a5b601a3a137
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