DENVER ? A powerful winter storm swept across Colorado on Friday as it headed east, bringing blizzard warnings to eastern Colorado and western Kansas, and winter storm warnings for southeast Wyoming and western Nebraska.
The storm stretched as far south as New Mexico, where Department of Transportation reported difficult driving conditions on several state highways because of the winter weather, leaving highways snow packed and icy.
The Colorado Avalanche Information Center issued a warning through Friday east of the Continental Divide, saying 2 feet of snow or more could overwhelm a weak snow pack, with natural and human-triggered avalanches likely Friday.
The storm forced the cancellation of more than 200 arriving and departing flights at the Denver airport that had been scheduled through Friday night.
Southwest Airlines canceled all its flights through 4 p.m. Friday at Denver International Airport because of the storm. The airline said it wanted to mitigate the impact of the storm on its operations elsewhere across the country.
The Colorado Department of Transportation closed portions of Interstate 70 and Interstate 25, the two main arteries crisscrossing the state. The National Weather Service said snow was falling at 2 inches an hour on the Eastern Plains, producing some blizzard conditions.
Colorado State Patrol spokesman Josh Lewis said non-essential staffers were told to come in at 10 a.m. and Gov. John Hickenlooper told state workers in the Denver metro area to stay home until 10 a.m. unless their jobs involved health and safety.
Transportation spokeswoman Becky Navarro said Friday eastbound I-70 was closed from Aurora, Colo., to Limon, Colo., and a ramp was closed on Interstate 25 in Denver because of numerous accidents.
"There are a lot of areas on the Front Range where there is very poor visibility," she said.
One of the largest snow totals Friday morning was 2 feet in Pinecliff west of Denver, and snow totals were mounting rapidly along the Front Range and eastern Colorado.
Jim Kalina of the National Weather Service said another foot of snow was expected in some areas along the Front Range before the storm moves out on Saturday.
The weather service said the snow will be moderate at times on Friday in Wyoming and Nebraska. However, winds could gust up to 35 mph and produce blowing snow from the southern Laramie Range to Sidney, Neb.
Cities in the Front Range urban corridor from Colorado Springs, Colo., in the south to Fort Collins, Colo., and Greeley, Colo., in the north were under a winter storm warning.
The storm warnings prompted shoppers to stock up on food and liquor, while Colorado lawmakers canceled legislative work on Friday.
Stores in Denver reported brisk business Thursday night.
"The cheese wall is hammered, bread's kind of hammered, milk's kind of low," said Aaron McFadden, a manager at a King Soopers store.
Ted Vaca at Argonaut Liquor said customers were snapping up all kinds of drink.
"It was more like a Friday than a Thursday," he said.
A Learjet ran off a runway at the Pueblo, Colo., airport as the storm moved in, but investigators hadn't determined if the weather was a factor. None of the 10 people aboard was injured, the Federal Aviation Administration said.
Many school districts announced they would be closed on Friday, including the two largest, in Jefferson County and Denver.
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Associated Press Writer Dan Elliott also contributed to this report.
Pedestrians pass Viacom headquarters, Wednesday, Feb. 1, 2012 in New York. Viacom posted a 65 percent drop in net income for the latest quarter, as it took a charge related to the ?Rock Band? series of video games. (AP Photo/Mark Lennihan)
Pedestrians pass Viacom headquarters, Wednesday, Feb. 1, 2012 in New York. Viacom posted a 65 percent drop in net income for the latest quarter, as it took a charge related to the ?Rock Band? series of video games. (AP Photo/Mark Lennihan)
NEW YORK (AP) ? Viacom Inc., the owner of Paramount Pictures, MTV and Comedy Central, on Thursday posted a 65 percent drop in net income for the latest quarter, as it took a charge related to the "Rock Band" series of video games.
Revenue was below analyst estimates, sending its stock down.
Viacom earned $212 million, or 38 cents per share, in the October-December quarter, down from $610 million, or $1 per share, a year ago.
The New York-based company took a charge of $379 million to cover an arbitration award won by the original shareholders of Harmonix Music Systems Inc., which created "Rock Band."
The game let players take "Guitar Hero" one step further by connecting a drum-kit and a microphone to a game console, along with a guitar, and play and sing along to songs. It was hit when it came out in 2007, but its popularity faded quickly, along with that of "Guitar Hero."
Viacom had acquired Harmonix in 2006, but sold it back to its founders in 2010. The founders then sued, claiming that they were owed extra payments for the performance of "Rock Band" during its spell of popularity. They won an arbitration award of $383 million in December. Viacom is contesting it, but has set aside the money to cover the award, reflected in the charge to earnings.
Excluding the "Rock Band" charge, earnings were $1.06 per share in its fiscal first quarter, a penny above the average analyst estimate as polled by FactSet.
Operating income fell 2 percent as expenses outpaced revenue, which rose 3 percent to $3.95 billion from $3.83 billion. Analysts expected $3.99 billion, mainly because they were expecting advertising to hold up better.
Viacom's Class B shares fell $1.90, or 4.1 percent, to $45.06 in morning trading.
Paramount posted a small operating loss, reversing a small profit a year ago, mainly because it booked a one-time gain then from the sale of some movie distribution rights to Marvel Studios, part of The Walt Disney Co. Revenue rose slightly on strong box-office results from "Paranormal Activity 3" and "Mission Impossible ? Ghost Protocol."
At the TV networks, Viacom's larger and more profitable division, results were buoyed by an increase in fees from cable companies and online streaming services like Netflix. Advertising, the largest single source of revenue, declined 3 percent.
CEO Phillippe Dauman said ad sales would have grown except for a ratings dip at Nickelodeon, as measured by Nielsen. The apparent loss of viewers showed up in mid-September. Viacom said in November that it thought the dip was due to some sort of measurement error, and Dauman stuck to that explanation on Thursday.
One explanation that has been floated by analysts is that the availability of older Nickelodeon shows on Netflix is digging into viewership. Dauman said he didn't think that was the case. The company gets viewer data from Netflix and didn't see a sudden spike in September, he told analysts on conference call after the release of the results.
Fitness is not only a matter of physical health, but of mental and emotional health. Exercising your mind by learning new things and exercising your body with aerobics, is very important for optimal health. Read this article for tips on how to remain completely fit, inside and out, for a healthier lifestyle.
A great fitness tip to build up your forearm muscles is to start doing wrist curls. Wrist curls are great because they don?t require much effort or very heavy weights. All you do to perform a wrist curl is to curl your wrists while holding a dumbbells.
When working out your calves, make sure to perform both standing and sitting calf raises. This is important because your caves consist of two different muscles, and hitting them from the bent and straight leg positions ensures that you are getting a total workout. Try and do one right after the other for maximum gains.
Get fit by jumping! If you jump 30 times a day, it will strengthen your bones and improve both health and fitness. Don?t try jumping prior to warming up. Warm up until you break a little sweat, and then jump up and down 30 times. You don?t need to jump on and off anything as it?s the impact that strengthens your bones. Just make sure you are doing it on a soft surface such as a padded exercise mat.
Try not to work out your lower and upper extremities on the same day. This can cause injuries or muscle strains. Instead work on your upper body one day, and your lower body the next day. For instance, if you work on your legs today, work on your arms tomorrow.
Although it may seem painful, it is important to to begin exercising a muscle injury as soon as you can. By not doing so, you are allowing other muscles to tighten up. You do not have to do any intense exercises. Go slowly and make sure to apply ice to the injured area when finished.
Weight training is vital in a well-rounded fitness program. While not every program needs to concentrate on building muscle mass like a pro weightlifter, some attention to weight training is necessary for every fitness regimen. Weight training tones the muscles and makes them work efficiently. This has a positive impact on overall health and fitness at even the most modest levels of weight training.
When beginning your exercise routine, always warm-up. It is important to warm-up for at least ten minutes at a low intensity. This will get your muscles ready by promoting blood flow, raising muscle temperature for greater elasticity and will help to lubricate the joints. Try jogging, walking or calisthenics.
Sometimes it is hard to stick to a healthy diet, especially when everyone around you is eating away. If you have this problem, you should try to bring healthy snacks with wherever you go. This will make it impossible for you to eat those bad things, making your job a lot easier.
Fitness doesn?t have to include daily trips to the gym or eating salad for every meal. If you make a few changes every day, you can be on your way to having the fittest body and mind of your life! Remember the tips in this article to become a healthier version of yourself.
It matters not how much you think you are informed about Medical Alert Devices, read this wonderful site to be amazed at very important information.
LOS ANGELES (Reuters) ? Don Cornelius, creator of iconic dance program "Soul Train" that helped introduce Americans to black culture on TV, died on Wednesday after shooting himself in the head, officials in Los Angeles said.
Police discovered the body of Cornelius, 75, at his house after responding to reports of shots fired in the wealthy, hillside area of Los Angeles called Sherman Oaks where he lived. The community is home to many celebrities and entertainment executives.
"The death was reported as a suicide, a self-inflicted gunshot wound to the head," said Los Angeles coroner's Assistant Chief Ed Winter.
Cornelius was taken to a nearby hospital where he was pronounced dead, Police Department spokesman Kevin Maiberger said. He declined to give details because detectives were still at the scene investigating.
Cornelius launched "Soul Train" in the early 1970s as a local dance show from Chicago. It relocated to Los Angeles the following year and became part of pop culture history by boosting the careers of young artists such as the Jackson Five, and older artists such as James Brown who were trying to tap into a younger audience.
As the smooth-talking host with a deep voice, Cornelius gave to hip youths of the '70s what "American Bandstand" creator Dick Clark offered to viewers in the early days of rock 'n' roll.
As the popularity of "Soul Train" grew, the show crossed over into mainstream TV and R&B artists broadened their fan base. "Soul Train" aired until 2006, making it the longest running U.S. series in first-run syndication.
Civil rights activist Reverend Al Sharpton, a long time friend, expressed shock and grief over the news of the death.
"He brought soul music and dance to the world in a way that it had never been shown and he was a cultural game changer on a global level," Sharpton said in a statement.
Composer-producer Quincy Jones said he was "deeply saddened" at the sudden passing of his friend, colleague and business partner.
"Before MTV there was 'Soul Train,' that will be the great legacy of Don Cornelius," Jones said. "His contributions to television, music and our culture as a whole will never be matched."
(Reporting By Lauren Keiper and Jill Serjeant; writing by Dan Burns and Bob Tourtellotte; Editing by Paul Thomasch and Vicki Allen)
JCI online early table of contents: Feb. 1, 2012Public release date: 1-Feb-2012 [ | E-mail | Share ]
Contact: Karen Honey press_releases@the-jci.org 734-546-5242 Journal of Clinical Investigation
EDITOR'S PICK: A thought-provoking new therapeutic target for brain cancer?
Glioblastoma multiforme (GBM) is the most common of all malignant brain tumors that originate in the brain. Patients with GBM have a poor prognosis because it is a highly aggressive form of cancer that is commonly resistant to current therapies. New therapeutic approaches are therefore much needed. Joanna Phillips, Zena Werb, and colleagues, at the University of California, San Francisco, have now identified a potential new therapeutic target for the treatment of GBM.
A substantial proportion of GBMs show evidence of abnormal activation of signaling pathways triggered by a cell surface protein known as PDGFR-alpha, and this is thought to drive the tumor. PDGFR-alpha triggers activation of signaling pathways when it binds the growth factor PDGF. Phillips, Werb, and colleagues found that the protein SULF2, which is known to regulate the availability of growth factors such as PDGF, was expressed in primary human GBM tumors and cell lines. Moreover, GBMs characterized by abnormal activation of signaling pathways downstream of PDGFR-alpha showed the strongest SULF2 expression. Importantly, knocking down expression of SULF2 in human GBM cell lines decreased the growth of these cells upon transplantation into mice. Phillips, Werb, and colleagues therefore suggest that SULF2 is a candidate therapeutic target for the treatment of GBM and that assessing its levels could identify tumors dependent on growth factors such as PDGF. The latter is important as PDGFR-alpha and other molecules to which growth factors bind are themselves good therapeutic targets.
TITLE: Heparan sulfate sulfatase SULF2 regulates PDGFR-alpha signaling and growth in human and mouse malignant glioma
AUTHOR CONTACT:
Joanna J. Phillips
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.514.4929; Fax: 415.514.9792; E-mail: joanna.phillips@ucsf.edu.
Zena Werb,
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.476.4622; Fax: 415.476.4565; E-mail: zena.werb@ucsf.edu.
View this article at: http://www.jci.org/articles/view/58215?key=7d9ee1ebe13cc1c6c025
ONCOLOGY: Answers to age-old questions surrounding fat cell cancer
Myxoid round cell liposarcoma (MRCLS) is a cancerous tumor that typically arises in deep fat tissues of the limbs or abdomen. It was shown almost 20 years ago to be characterized by a chromosomal change that generates a fusion protein known as TLS:CHOP. Despite this, neither the cell from which MRCLS arise nor the mechanism(s) by which TLS:CHOP induces tumor formation have been definitively determined. A team of researchers led by Igor Matushansky, at Columbia University, New York, has now provided some answers to these questions; in doing so, they identified a potential new combination therapy for the treatment of MRCLS.
A compound isolated from the sea squirt Ecteinascidia turbinate, ET-743, is a highly effective therapy for patients with MRCLS, but how it works has not been determined. Using a new mouse model of MRCLS that they developed, Matushansky and colleagues found that expression of TLS:CHOP in endogenous mesenchymal stem cells led to the in vivo development of MRCLS and that ET-743 worked by decreasing expression of TLS:CHOP. Moreover, combining ET-743 treatment with administration of agonists of the protein PPAR-gamma improved survival of the mice. Matushansky and colleagues therefore suggest that ET-743 plus PPAR-gamma agonist could provide a rational combination for treating MRCLS.
TITLE: PPAR-gamma agonists enhance ET-743induced adipogenic differentiation in a transgenic mouse model of myxoid round cell liposarcoma
AUTHOR CONTACT:
Igor Matushansky
Columbia University, New York, New York, USA.
Phone: 212.851.4556; Fax: 212.851.4784; E-mail: im17@columbia.edu.
View this article at: http://www.jci.org/articles/view/60015?key=ace2cdfd6a47aee95dac
TUMOR IMMUNOLOGY: Access denied: dense matrix blocks immune cell path to cancer cells
An individual's immune system does respond to a tumor. However, in individuals diagnosed with cancer, the antitumor response was obviously inadequate to clear the tumor. It is hoped that understanding how tumors escape the antitumor immune response will identify candidate therapeutic approaches, with the rationale being that if the escape mechanism can be blunted then an individual's immune system will be able to destroy the tumor. In this context, a team of researchers led by Emmanuel Donnadieu, at Institut Cochin, France, has determined that in human lung tumors, immune cells known as T cells are rarely found in the clusters of cancer cells. Rather, they accumulate in the stromal region of the tumors (that is, the tissue that surrounds and supports the cancer cells). Moreover, Donnadieu and colleagues found that the T cells could not enter the cancer cell regions because a dense matrix that the T cells could not penetrate surrounded these regions. Treating human lung tumor slices with matrix-degrading compounds increased the ability of T cells to enter the cancer cell clusters. Donnadieu and colleagues hope that future studies will increase understanding of the mechanisms by which the dense matrix is generated and thereby identify potential new therapeutic approaches.
TITLE: Matrix architecture defines the preferential localization and migration of T cells into the stroma of human lung tumors
View this article at: http://www.jci.org/articles/view/45817?key=3f332821bf27bc9a78d3
VIROLOGY: Finally, experimental transformation of a primary cell into a tumor cell by the cancer-causing virus KSHV
Kaposi sarcoma herpesvirus (KSHV) is the causative agent of several cancers that arise most commonly in individuals with HIV/AIDS. Developing therapeutic approaches to treat individuals with these cancers is hampered by a lack of understanding of the mechanisms by which KSHV transforms normal cells into cancerous cells. This is poorly understood in part because researchers have been unable to experimentally infect a primary cell with KSHV and turn it into a cancer cell. However, Shou-Jiang Gao and colleagues, at the University of Texas Health Science Center at San Antonio, San Antonio, have now done just that.
Gao and colleagues found that KSHV efficiently infects primary rat embryonic metanephric mesenchymal precursor cells and transforms them into cells that form tumors when injected into mice. They hope to use this model to study the molecular mechanisms by which KSHV transforms normal cells into cancerous cells, although they caution that additional analysis would be required to determine whether mechanisms uncovered using transformed rat cells are relevant to human cancers caused by KSHV.
TITLE: Direct and efficient cellular transformation of primary rat mesenchymal precursor cells by KSHV
AUTHOR CONTACT:
Shou-Jiang Gao
University of Southern California, Keck School of Medicine, Los Angeles, California, USA.
Phone: 323.442.8028; Fax: 323.442.1721; E-mail: shoujiag@usc.edu.
View this article at: http://www.jci.org/articles/view/58530?key=b593e40b17636db485f1
ONCOLOGY: Taking on features of cancer cells
The protein p27Kip1 has a role in suppressing tumor development and progression. It does so by inhibiting the activity of protein complexes that promote cell proliferation (cyclincyclin-dependent kinase complexes). In contrast, mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote tumor development in mice. Now, a team of researchers led by Arnaud Besson, at INSERM UMR1037, France, has identified a mechanism by which mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote cells to take on features of cancer cells. Future studies will determine whether normal p27Kip1 protein can regulate the same mechanism if mislocalized, as it often is in human tumors.
TITLE: p27Kip1 controls cytokinesis via the regulation of citron kinase activation
AUTHOR CONTACT:
Arnaud Besson
INSERM UMR1037, Cancer Research Center of Toulouse, Toulouse, France.
Phone: 33.561556435; Fax: 33.561558109; E-mail: arnaud.besson@inserm.fr.
View this article at: http://www.jci.org/articles/view/60376?key=2721832273bd35b1e9f0
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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.
JCI online early table of contents: Feb. 1, 2012Public release date: 1-Feb-2012 [ | E-mail | Share ]
Contact: Karen Honey press_releases@the-jci.org 734-546-5242 Journal of Clinical Investigation
EDITOR'S PICK: A thought-provoking new therapeutic target for brain cancer?
Glioblastoma multiforme (GBM) is the most common of all malignant brain tumors that originate in the brain. Patients with GBM have a poor prognosis because it is a highly aggressive form of cancer that is commonly resistant to current therapies. New therapeutic approaches are therefore much needed. Joanna Phillips, Zena Werb, and colleagues, at the University of California, San Francisco, have now identified a potential new therapeutic target for the treatment of GBM.
A substantial proportion of GBMs show evidence of abnormal activation of signaling pathways triggered by a cell surface protein known as PDGFR-alpha, and this is thought to drive the tumor. PDGFR-alpha triggers activation of signaling pathways when it binds the growth factor PDGF. Phillips, Werb, and colleagues found that the protein SULF2, which is known to regulate the availability of growth factors such as PDGF, was expressed in primary human GBM tumors and cell lines. Moreover, GBMs characterized by abnormal activation of signaling pathways downstream of PDGFR-alpha showed the strongest SULF2 expression. Importantly, knocking down expression of SULF2 in human GBM cell lines decreased the growth of these cells upon transplantation into mice. Phillips, Werb, and colleagues therefore suggest that SULF2 is a candidate therapeutic target for the treatment of GBM and that assessing its levels could identify tumors dependent on growth factors such as PDGF. The latter is important as PDGFR-alpha and other molecules to which growth factors bind are themselves good therapeutic targets.
TITLE: Heparan sulfate sulfatase SULF2 regulates PDGFR-alpha signaling and growth in human and mouse malignant glioma
AUTHOR CONTACT:
Joanna J. Phillips
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.514.4929; Fax: 415.514.9792; E-mail: joanna.phillips@ucsf.edu.
Zena Werb,
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.476.4622; Fax: 415.476.4565; E-mail: zena.werb@ucsf.edu.
View this article at: http://www.jci.org/articles/view/58215?key=7d9ee1ebe13cc1c6c025
ONCOLOGY: Answers to age-old questions surrounding fat cell cancer
Myxoid round cell liposarcoma (MRCLS) is a cancerous tumor that typically arises in deep fat tissues of the limbs or abdomen. It was shown almost 20 years ago to be characterized by a chromosomal change that generates a fusion protein known as TLS:CHOP. Despite this, neither the cell from which MRCLS arise nor the mechanism(s) by which TLS:CHOP induces tumor formation have been definitively determined. A team of researchers led by Igor Matushansky, at Columbia University, New York, has now provided some answers to these questions; in doing so, they identified a potential new combination therapy for the treatment of MRCLS.
A compound isolated from the sea squirt Ecteinascidia turbinate, ET-743, is a highly effective therapy for patients with MRCLS, but how it works has not been determined. Using a new mouse model of MRCLS that they developed, Matushansky and colleagues found that expression of TLS:CHOP in endogenous mesenchymal stem cells led to the in vivo development of MRCLS and that ET-743 worked by decreasing expression of TLS:CHOP. Moreover, combining ET-743 treatment with administration of agonists of the protein PPAR-gamma improved survival of the mice. Matushansky and colleagues therefore suggest that ET-743 plus PPAR-gamma agonist could provide a rational combination for treating MRCLS.
TITLE: PPAR-gamma agonists enhance ET-743induced adipogenic differentiation in a transgenic mouse model of myxoid round cell liposarcoma
AUTHOR CONTACT:
Igor Matushansky
Columbia University, New York, New York, USA.
Phone: 212.851.4556; Fax: 212.851.4784; E-mail: im17@columbia.edu.
View this article at: http://www.jci.org/articles/view/60015?key=ace2cdfd6a47aee95dac
TUMOR IMMUNOLOGY: Access denied: dense matrix blocks immune cell path to cancer cells
An individual's immune system does respond to a tumor. However, in individuals diagnosed with cancer, the antitumor response was obviously inadequate to clear the tumor. It is hoped that understanding how tumors escape the antitumor immune response will identify candidate therapeutic approaches, with the rationale being that if the escape mechanism can be blunted then an individual's immune system will be able to destroy the tumor. In this context, a team of researchers led by Emmanuel Donnadieu, at Institut Cochin, France, has determined that in human lung tumors, immune cells known as T cells are rarely found in the clusters of cancer cells. Rather, they accumulate in the stromal region of the tumors (that is, the tissue that surrounds and supports the cancer cells). Moreover, Donnadieu and colleagues found that the T cells could not enter the cancer cell regions because a dense matrix that the T cells could not penetrate surrounded these regions. Treating human lung tumor slices with matrix-degrading compounds increased the ability of T cells to enter the cancer cell clusters. Donnadieu and colleagues hope that future studies will increase understanding of the mechanisms by which the dense matrix is generated and thereby identify potential new therapeutic approaches.
TITLE: Matrix architecture defines the preferential localization and migration of T cells into the stroma of human lung tumors
View this article at: http://www.jci.org/articles/view/45817?key=3f332821bf27bc9a78d3
VIROLOGY: Finally, experimental transformation of a primary cell into a tumor cell by the cancer-causing virus KSHV
Kaposi sarcoma herpesvirus (KSHV) is the causative agent of several cancers that arise most commonly in individuals with HIV/AIDS. Developing therapeutic approaches to treat individuals with these cancers is hampered by a lack of understanding of the mechanisms by which KSHV transforms normal cells into cancerous cells. This is poorly understood in part because researchers have been unable to experimentally infect a primary cell with KSHV and turn it into a cancer cell. However, Shou-Jiang Gao and colleagues, at the University of Texas Health Science Center at San Antonio, San Antonio, have now done just that.
Gao and colleagues found that KSHV efficiently infects primary rat embryonic metanephric mesenchymal precursor cells and transforms them into cells that form tumors when injected into mice. They hope to use this model to study the molecular mechanisms by which KSHV transforms normal cells into cancerous cells, although they caution that additional analysis would be required to determine whether mechanisms uncovered using transformed rat cells are relevant to human cancers caused by KSHV.
TITLE: Direct and efficient cellular transformation of primary rat mesenchymal precursor cells by KSHV
AUTHOR CONTACT:
Shou-Jiang Gao
University of Southern California, Keck School of Medicine, Los Angeles, California, USA.
Phone: 323.442.8028; Fax: 323.442.1721; E-mail: shoujiag@usc.edu.
View this article at: http://www.jci.org/articles/view/58530?key=b593e40b17636db485f1
ONCOLOGY: Taking on features of cancer cells
The protein p27Kip1 has a role in suppressing tumor development and progression. It does so by inhibiting the activity of protein complexes that promote cell proliferation (cyclincyclin-dependent kinase complexes). In contrast, mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote tumor development in mice. Now, a team of researchers led by Arnaud Besson, at INSERM UMR1037, France, has identified a mechanism by which mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote cells to take on features of cancer cells. Future studies will determine whether normal p27Kip1 protein can regulate the same mechanism if mislocalized, as it often is in human tumors.
TITLE: p27Kip1 controls cytokinesis via the regulation of citron kinase activation
AUTHOR CONTACT:
Arnaud Besson
INSERM UMR1037, Cancer Research Center of Toulouse, Toulouse, France.
Phone: 33.561556435; Fax: 33.561558109; E-mail: arnaud.besson@inserm.fr.
View this article at: http://www.jci.org/articles/view/60376?key=2721832273bd35b1e9f0
###
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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.
Building plans are in everyone?s minds again as the spring season approaches.
On big home improvement projects, homeowners must take information from contractors wisely. It is not uncommon for unscrupulous contractors to mislead homeowners who are not involved in the process or are easily intimidated. When a contractor mentions a problem or issue, a homeowner should verify it or get a second opinion before paying the contractor additional money or allowing construction to run longer than initially scheduled. Specifically ask them if they employ a qualified architect to produce building plans.
Be certain that you protect all surfaces by covering them, no matter what project you are doing. If you protect them from paint or scratches, you are saving yourself work in the long run. Some specific areas to keep in mind are freshly painted walls, light fixtures, carpeting and sensitive hard floors.
Ensure that there are no low-lying areas, and make sure doubly sure there are none near your home?s foundation. Soil should be added to these areas to stop pooled water from eating away at your yard. Water that collects and seeps through the ground near your foundation can cause cracks that can be very expensive to fix.
Before deciding on a project, determine what improvements would be most valuable based on your location. In a balmy coastal region, installing air conditioning would carry more importance than adding a fireplace. An outdoor swimming pool will add a lot of value to a home in southern California, Arizona or Florida. A pool is not useful during most months in states that are known for cold weather.
Interested in doing a little updating? When you want to personalize your space you can use things you already own to inspire you. Frames should match the decor style you have.
When you are working outside in the heat, sometimes time slips away. Just as it is important to think about your safety when you work, it is also important to remember to stay hydrated on a sweltering day. Be sure to take a break from the manual labor to drink some water and enjoy the work you have accomplished.
Upgrading your appliances goes a long way in improving the overall quality and value of your home. Whatever your situation, home improvement encompasses upgrading your appliances.
Use high-quality insulation around your plumbing system to prevent your water from freezing during this coming winter. Any hardware store will have a selection of foam insulation and other products to help you easily cover your pipes and protect them from the cold. Together, this will keep your water-flow safe and secure. Safe plumbing is vital in the months of winter, because lacking it can result in your pipes cracking or bursting open from the temperatures.
Make sure you have all required safety gear that you need for heavier projects. You want to have gear, like a helmet and back harness. These are but some of the essential items you should have just in case any falling objects come your way.
Keeping safety in mind is important for any home improvement work you do. When you take safety precautions, you can be relatively certain that you will not be hurt and your home will not be harmed. Make sure that you have read all instructions and tutorials before you start any renovation project.
Turning off the water is important when you are working to improve your kitchen or bathroom. Before you start working, locate the shutoff when you working around your house?s water supply or pipes. By doing this, you are making sure that you do not get a flood.
Improve water efficiency while improving your home. Try to put in a toilet with low-flow, a good water heater and a water saving shower head. In addition to being earth-friendly, these projects will increase the value of your home and lower your water bill.
You can make a small niche or alcove really pop by using colorful paint or wallpaper to cover the back surface of the inlaid area. If it?s an especially small niche, you can just use a sample container of paint, so there?s no need to buy a whole gallon.
Seal off the crack that mice are entering into, try steel wool. Mice are unable to chew through steel wool; therefore, it will prevent them from entering.
By starting with various small do-it-yourself projects, the homeowner can build up their confidence to the point they will be ready to tackle the more challenging project. This is a very good thing. Learning a little about home improvement goes a long way. It helps a person build the confidence to take on even more complex projects and increases the resale value of the home. Do not forget that some building plans need planning permission and other do not so it is better to check with the local council first.
To get the real lowdown about how to get your building plans completed quickly and at the right price click here now!
LONDON ? Four British men fueled by the words of a U.S.-born Muslim cleric pleaded guilty on Wednesday to involvement in an al-Qaida inspired plot to spread terror and cause economic damage by bombing the London Stock Exchange at Christmastime.
The men were among nine defendants facing trial in London over an alleged plot to attack the exchange and several other high-profile targets in December 2010. All had initially pleaded not guilty to all the charges against them.
But on Wednesday four of the defendants pleaded guilty at Woolwich Crown Court to involvement in the Stock Exchange plan, and the five other British Muslims to lesser charges.
Mohammed Chowdhury, 21; Shah Rahman, 28; Gurukanth Desai, 30; and Abdul Miah, 25, all admitted preparing for acts of terrorism by planning to plant an improvised explosive device in the toilets of the London Stock Exchange.
Prosecution lawyer Andrew Edis accepted that the men had not planned to kill anyone.
"Their intention was to cause terror and economic harm and disruption," he said. "But their chosen method meant there was a risk people would be maimed or killed."
Chowdhury, from London, was described by prosecutors as the "lynchpin" of the plot. His lawyer, Christopher Blaxland, said Chowdhury admitted planning to plant the bomb, "with the obvious attendant risk but without any intention to cause death or even injury but with the intention to terrorize, damage property and to cause economic damage."
The other five defendants admitted attending planning meetings, fundraising for terrorism or possessing copies of the al-Qaida magazine, Inspire.
Prosecutors said they had not made any bombs or set dates for the attacks.
They said the men were not members of al-Qaida but had been inspired by the terror network and the sermons of its Yemen-based American-born cleric Anwar al-Awlaki, who was killed last year in a U.S. drone strike.
Edis said the nine defendants "were implementing the published strategy of AQAP" ? al-Qaida in the Arabian Peninsula.
The suspects, then aged between 20 and 30, were arrested in London, Cardiff and Stoke-on-Trent in central England, in what police called the biggest anti-terror raid for two years.
Prosecutors said they plotted to send mail bombs to various targets in the run-up to Christmas 2010 and had discussed launching a "Mumbai-style" atrocity ? referring to the bomb blasts that killed 166 people in India's financial center in 2008.
The nine defendants were accused of agreeing on targets, discussing materials and methods, and researching files "containing practical instruction for a terrorist attack."
The men held planning meetings, researched bomb-making and scouted out locations including Parliament, Westminster Abbey and the London Eye Ferris wheel ? not knowing that they were under police surveillance and their homes and cars had been bugged.
A handwritten target list found at one of the defendant's homes listed the names and addresses of London Mayor Boris Johnson, two rabbis, the American Embassy and the Stock Exchange.
The defendants will be sentenced next week, but the judge has already told Chowdhury he will receive 18 1/2 years and Rahman 17 years. They are likely to serve half that time before being eligible for parole.
When police swooped on the suspects in three cities in the early morning of Dec. 20, 2010, they said it was the most significant anti-terror raid for two years.
London has been targeted several times by violent Islamists affiliated with or inspired by al-Qaida.
In July 2005, four suicide bombers killed 52 commuters on three London subway trains and a bus. A year later, U.S. and British intelligence officials thwarted one of the largest plots yet ? a plan to explode bombs on nearly a dozen trans-Atlantic airliners.
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Public release date: 1-Feb-2012
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