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Tuesday, October 23, 2012
Monday, October 22, 2012
New study charts the living habits of Europe's tweens
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Public release date: 22-Oct-2012[ | E-mail |
Share ] Contact: Gabriele Eiben
gabriele.eiben@medfak.gu.se
46-317-866-846
University of Gothenburg
Greater independence, less parent control, approaching puberty and changing demands in school. For a tween life can be both exciting and demanding and presumably decisive for their future health. This is the starting point for a study designed to chart the living habits of children between the ages of 8 and 14 in Sweden and Europe, and where the University of Gothenburg, Sweden is one of the participants.
Boy and girls who are no longer children but who are not yet teenagers, so-called tweens, face many challenges. Greater independence and exposure to behaviours which lie outside the control of the family, approaching puberty and changing demands in school can make this an exciting but nonetheless demanding period both for the children themselves and for their families.
During this transitional period there is a risk that children may develop bad habits which can lead to poorer health later on in life. At the same time, increased individuality and autonomy may lead tweens to adopt healthy living habits more readily.
With this as a point of departure, fifteen groups of researchers from twelve countries have gathered to study those factors which cause European tweens to adopt healthy as opposed to unhealthy living habits.
The total of 16,000 children who are taking part in the project previously participated in the IDEFICS project which received considerable attention, a project in which researchers studied the diet and lifestyle associated with obesity among younger children.
In this new project, which is called I.Family, the researchers aim to follow up on children's eating habits and physical activity but also to chart how factors such as tastes, genetic markers, children's immediate environment and the influence of family and school may affect children's behaviour.
Children's living habits are influenced by group pressure, information obtained in school as well as marketing via TV, mobile phones, music and the Internet. Some companies turn their attention precisely to tweens as a group because they are starting to get their own money to spend, according to Gabriele Eiben, researcher at the Sahlgrenska Academy, University of Gothenburg, Sweden and manager of the Swedish part of the project:
By gathering information on the current state of health among these children and comparing it with the comprehensive mapping that was done earlier, we will have unique opportunities to study which factors cause children to adopt a healthy as opposed to an unhealthy lifestyle.
The project's overriding goal is to develop advice and recommendations that decision makers may use in order to help families develop good healthy lifestyles.
###
Contact:
Gabriele Eiben, researcher at the Sahlgrenska Academy, University of Gothenburg and project manager I.Family Sweden
+4631-786 6846
gabriele.eiben@medfak.gu.se
Lauren Lissner, researcher at the Sahlgrenska Academy, University of Gothenburg
031-7866847
lauren.lissner@medfak.gu.se
INFO about I.Family
The research project I.Family is financed by the European Commission and will run for a period of 5 years beginning in March 2012. Participating in the project are children from Spain, Italy, Cyprus, Hungary, Estonia, Germany, Belgium and Sweden.
[ | 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.
Public release date: 22-Oct-2012[ | E-mail |
Share ] Contact: Gabriele Eiben
gabriele.eiben@medfak.gu.se
46-317-866-846
University of Gothenburg
Greater independence, less parent control, approaching puberty and changing demands in school. For a tween life can be both exciting and demanding and presumably decisive for their future health. This is the starting point for a study designed to chart the living habits of children between the ages of 8 and 14 in Sweden and Europe, and where the University of Gothenburg, Sweden is one of the participants.
Boy and girls who are no longer children but who are not yet teenagers, so-called tweens, face many challenges. Greater independence and exposure to behaviours which lie outside the control of the family, approaching puberty and changing demands in school can make this an exciting but nonetheless demanding period both for the children themselves and for their families.
During this transitional period there is a risk that children may develop bad habits which can lead to poorer health later on in life. At the same time, increased individuality and autonomy may lead tweens to adopt healthy living habits more readily.
With this as a point of departure, fifteen groups of researchers from twelve countries have gathered to study those factors which cause European tweens to adopt healthy as opposed to unhealthy living habits.
The total of 16,000 children who are taking part in the project previously participated in the IDEFICS project which received considerable attention, a project in which researchers studied the diet and lifestyle associated with obesity among younger children.
In this new project, which is called I.Family, the researchers aim to follow up on children's eating habits and physical activity but also to chart how factors such as tastes, genetic markers, children's immediate environment and the influence of family and school may affect children's behaviour.
Children's living habits are influenced by group pressure, information obtained in school as well as marketing via TV, mobile phones, music and the Internet. Some companies turn their attention precisely to tweens as a group because they are starting to get their own money to spend, according to Gabriele Eiben, researcher at the Sahlgrenska Academy, University of Gothenburg, Sweden and manager of the Swedish part of the project:
By gathering information on the current state of health among these children and comparing it with the comprehensive mapping that was done earlier, we will have unique opportunities to study which factors cause children to adopt a healthy as opposed to an unhealthy lifestyle.
The project's overriding goal is to develop advice and recommendations that decision makers may use in order to help families develop good healthy lifestyles.
###
Contact:
Gabriele Eiben, researcher at the Sahlgrenska Academy, University of Gothenburg and project manager I.Family Sweden
+4631-786 6846
gabriele.eiben@medfak.gu.se
Lauren Lissner, researcher at the Sahlgrenska Academy, University of Gothenburg
031-7866847
lauren.lissner@medfak.gu.se
INFO about I.Family
The research project I.Family is financed by the European Commission and will run for a period of 5 years beginning in March 2012. Participating in the project are children from Spain, Italy, Cyprus, Hungary, Estonia, Germany, Belgium and Sweden.
[ | 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.
Source: http://www.eurekalert.org/pub_releases/2012-10/uog-nsc102212.php
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Natural process activating brain's immune cells could point way to repairing damaged brain tissue
Public release date: 21-Oct-2012[ | E-mail |
Share ] Contact: Bruce Goldman
goldmanb@stanford.edu
650-725-2106
Stanford University Medical Center
STANFORD, Calif. The brain's key "breeder" cells, it turns out, do more than that. They secrete substances that boost the numbers and strength of critical brain-based immune cells believed to play a vital role in brain health. This finding adds a new dimension to our understanding of how resident stem cells and stem cell transplants may improve brain function.
Many researchers believe that these cells may be able to regenerate damaged brain tissue by integrating into circuits that have been eroded by neurodegenerative disease or destroyed by injury. But new findings by scientists at the Stanford University School of Medicine suggest that another process, which has not been fully appreciated, could be a part of the equation as well. The findings appear in a study that will be published online Oct. 21 in Nature Neuroscience.
"Transplanting neural stem cells into experimental animals' brains shows signs of being able to speed recovery from stroke and possibly neurodegenerative disease as well," said Tony Wyss-Coray, PhD, professor of neurology and neurological sciences in the medical school and senior research scientist at the Veterans Affairs Palo Alto Health Care System. "Why this technique works is far from clear, though, because actually neural stem cells don't engraft well."
Neural stem cells can endure essentially unchanged for decades in two places in the mammalian brain, replicating just enough to meet the routine needs of those regions. In most parts of the brain, they aren't found at all.
While of critical importance to maintaining healthy brain function, true neural stem cells are rare. Far more common are their immediate progeny, which are called neural progenitor cells, or NPCs. These robust, rapidly dividing cells are poised to travel down a committed path of differentiation to yield new brain cells of several different types including neurons.
It's known that treating humans with radiation or drugs that prevent NPC replication causes memory deficits ("chemo brain") and, in children, IQ losses of up to 20 points. Conversely, studies are being initiated to see whether infusing neural stem cells into brains affected by Alzheimer's disease can enhance patients' memory function.
One category of brain cells, microglia, descends not from neural stem cells but from an immune lineage and retains several features of immune cells. "Microglia are the brain's own resident immune cells," Wyss-Coray said. Unlike most other mature brain cells, microglia can proliferate throughout adulthood, especially in response to brain injury. They can, moreover, migrate toward injury sites, secrete various "chemical signaling" substances, and gobble up bits of debris, microbial invaders or entire dead or dying neurons.
Microglia normally are distributed throughout the brain rather small, quiescent cells sprouting long, skinny projections that meekly but efficiently survey large areas that, taken together, cover the entire brain. But if this surveillance reveals signs of a disturbance, such as injury or infection, the microglia whirl into action. They begin proliferating and their puny bodies puff up, metamorphosing from mild-mannered Clark Kent-like reporters to buffed Supermen who fly to the scene of trouble, where they secrete substances that can throttle bad actors or call in reinforcements. Within these activated cells, internal garbage disposals called lysosomes form in large numbers and start whirring, ready to make mincemeat out of pathogens or cellular debris.
In addition to their part patrol-officer, part cleanup-crew status, microglia can also secrete substances that help neurons thrive. They also contribute to the ongoing pruning of unneeded connections between neurons that occurs throughout our lives.
But like immune cells elsewhere, said Wyss-Coray, microglia can be a force for evil if they engage in too much or inappropriate activity. They might, for instance, start to remove healthy cells (as occurs in Parkinson's) or stop cleaning up garbage strewn about the brain (for example, Alzheimer's plaque).
In a series of experiments, Wyss-Coray and his colleagues have shown that NPCs secrete substances that activate microglia. First, the researchers observed that microglia were uncharacteristically abundant and activated in the two regions in the mammalian brain where NPCs reside and new neurons are formed. Wondering whether the NPCs might be causing this increased microglial activity, the investigators incubated mouse microglia in a culture medium in which NPCs had previously been steeped. Two days later, they saw that the microglia had multiplied more, expressed different amounts of various signal molecules and featured more lysosomes. "The microglia were ready for action," said Wyss-Coray.
So they injected NPCs into an area of mice's brains where these cells are normally not found. In the same area in the opposing brain hemisphere, they injected a control solution. Again they found significant differences in microglial proliferation and activity, and more microglia in the NPC-injected side had assumed a "Superman" as opposed to a "Clark Kent" body shape. When they repeated this experiment using only the NPCs' "discarded bath water" rather than NPCs themselves, they got similar results.
Clearly NPCs were secreting something, or some things, that were spurring microglia to action.
Using sophisticated lab techniques, the team monitored purified NPCs plus several other cell types found in the brain and assessed nearly 60 different substances known to have powerful cell-to-cell signaling properties. Several such substances, it turned out, were secreted in much larger amounts by NPCs than by the other cell types: most notably, vascular endothelial growth factor, or VEGF a well-known molecule produced by many cell types throughout the body. VEGF stimulates the formation of blood vessels and exerts a beneficial effect on neurons. Conversely, drugs that block VEGF (such as Avastin) are frequently used to combat cancer because tumors require an immense blood supply in order to grow quickly.
VEGF is also known to boost microglial proliferation. Because it is produced in such volumes by NPCs, Wyss-Coray's team wanted to see if VEGF alone could mimic any of the changes wrought by NPCs or their culture-medium-borne detritus. So they injected VEGF into mice's right brain hemisphere, and saline solution into the left again with the same outcomes. Taking the opposite tack, the team injected NPC-saturated medium devoid of the cells, as they had done earlier. But this time they first used various laboratory techniques to deplete the fluid of the VEGF secreted by its former inhabitants. Doing this almost completely reversed its microglia-activating effects.
"All of this strongly suggests that VEGF produced by NPCs is playing a strong role in influencing microglial behavior," said Wyss-Coray. "This is important, because in all neurodegenerative diseases we know of we see microglia out of control." The new finding may open the door to reprogramming misbehaving microglia to play better with other cells.
###
The study's first author was graduate student Kira Mosher. Other contributors were graduate student Gregor Bieri; postdoctoral scholars Robert Andres, MD, Takeshi Fukuhara PhD, Maiko Hasegawa-Moriyama MD, PhD, and Yingbo He, PhD; and Raphael Guzman, MD, a former associate professor of neurosurgery now at the University of Basel, Switzerland. The work was funded by the U.S. Department of Veterans Affairs, the California Institute for Regenerative Medicine and the National Institute on Aging.
Information about the medical school's Department of Neurology and Neurological Sciences, which also supported the work, is available at http://neurology.stanford.edu/.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
PRINT MEDIA CONTACT: Bruce Goldman at (650) 725-2106 (goldmanb@stanford.edu)
BROADCAST MEDIA CONTACT: M.A. Malone at (650) 723-6912 (mamalone@stanford.edu)
[ | 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.
Public release date: 21-Oct-2012[ | E-mail |
Share ] Contact: Bruce Goldman
goldmanb@stanford.edu
650-725-2106
Stanford University Medical Center
STANFORD, Calif. The brain's key "breeder" cells, it turns out, do more than that. They secrete substances that boost the numbers and strength of critical brain-based immune cells believed to play a vital role in brain health. This finding adds a new dimension to our understanding of how resident stem cells and stem cell transplants may improve brain function.
Many researchers believe that these cells may be able to regenerate damaged brain tissue by integrating into circuits that have been eroded by neurodegenerative disease or destroyed by injury. But new findings by scientists at the Stanford University School of Medicine suggest that another process, which has not been fully appreciated, could be a part of the equation as well. The findings appear in a study that will be published online Oct. 21 in Nature Neuroscience.
"Transplanting neural stem cells into experimental animals' brains shows signs of being able to speed recovery from stroke and possibly neurodegenerative disease as well," said Tony Wyss-Coray, PhD, professor of neurology and neurological sciences in the medical school and senior research scientist at the Veterans Affairs Palo Alto Health Care System. "Why this technique works is far from clear, though, because actually neural stem cells don't engraft well."
Neural stem cells can endure essentially unchanged for decades in two places in the mammalian brain, replicating just enough to meet the routine needs of those regions. In most parts of the brain, they aren't found at all.
While of critical importance to maintaining healthy brain function, true neural stem cells are rare. Far more common are their immediate progeny, which are called neural progenitor cells, or NPCs. These robust, rapidly dividing cells are poised to travel down a committed path of differentiation to yield new brain cells of several different types including neurons.
It's known that treating humans with radiation or drugs that prevent NPC replication causes memory deficits ("chemo brain") and, in children, IQ losses of up to 20 points. Conversely, studies are being initiated to see whether infusing neural stem cells into brains affected by Alzheimer's disease can enhance patients' memory function.
One category of brain cells, microglia, descends not from neural stem cells but from an immune lineage and retains several features of immune cells. "Microglia are the brain's own resident immune cells," Wyss-Coray said. Unlike most other mature brain cells, microglia can proliferate throughout adulthood, especially in response to brain injury. They can, moreover, migrate toward injury sites, secrete various "chemical signaling" substances, and gobble up bits of debris, microbial invaders or entire dead or dying neurons.
Microglia normally are distributed throughout the brain rather small, quiescent cells sprouting long, skinny projections that meekly but efficiently survey large areas that, taken together, cover the entire brain. But if this surveillance reveals signs of a disturbance, such as injury or infection, the microglia whirl into action. They begin proliferating and their puny bodies puff up, metamorphosing from mild-mannered Clark Kent-like reporters to buffed Supermen who fly to the scene of trouble, where they secrete substances that can throttle bad actors or call in reinforcements. Within these activated cells, internal garbage disposals called lysosomes form in large numbers and start whirring, ready to make mincemeat out of pathogens or cellular debris.
In addition to their part patrol-officer, part cleanup-crew status, microglia can also secrete substances that help neurons thrive. They also contribute to the ongoing pruning of unneeded connections between neurons that occurs throughout our lives.
But like immune cells elsewhere, said Wyss-Coray, microglia can be a force for evil if they engage in too much or inappropriate activity. They might, for instance, start to remove healthy cells (as occurs in Parkinson's) or stop cleaning up garbage strewn about the brain (for example, Alzheimer's plaque).
In a series of experiments, Wyss-Coray and his colleagues have shown that NPCs secrete substances that activate microglia. First, the researchers observed that microglia were uncharacteristically abundant and activated in the two regions in the mammalian brain where NPCs reside and new neurons are formed. Wondering whether the NPCs might be causing this increased microglial activity, the investigators incubated mouse microglia in a culture medium in which NPCs had previously been steeped. Two days later, they saw that the microglia had multiplied more, expressed different amounts of various signal molecules and featured more lysosomes. "The microglia were ready for action," said Wyss-Coray.
So they injected NPCs into an area of mice's brains where these cells are normally not found. In the same area in the opposing brain hemisphere, they injected a control solution. Again they found significant differences in microglial proliferation and activity, and more microglia in the NPC-injected side had assumed a "Superman" as opposed to a "Clark Kent" body shape. When they repeated this experiment using only the NPCs' "discarded bath water" rather than NPCs themselves, they got similar results.
Clearly NPCs were secreting something, or some things, that were spurring microglia to action.
Using sophisticated lab techniques, the team monitored purified NPCs plus several other cell types found in the brain and assessed nearly 60 different substances known to have powerful cell-to-cell signaling properties. Several such substances, it turned out, were secreted in much larger amounts by NPCs than by the other cell types: most notably, vascular endothelial growth factor, or VEGF a well-known molecule produced by many cell types throughout the body. VEGF stimulates the formation of blood vessels and exerts a beneficial effect on neurons. Conversely, drugs that block VEGF (such as Avastin) are frequently used to combat cancer because tumors require an immense blood supply in order to grow quickly.
VEGF is also known to boost microglial proliferation. Because it is produced in such volumes by NPCs, Wyss-Coray's team wanted to see if VEGF alone could mimic any of the changes wrought by NPCs or their culture-medium-borne detritus. So they injected VEGF into mice's right brain hemisphere, and saline solution into the left again with the same outcomes. Taking the opposite tack, the team injected NPC-saturated medium devoid of the cells, as they had done earlier. But this time they first used various laboratory techniques to deplete the fluid of the VEGF secreted by its former inhabitants. Doing this almost completely reversed its microglia-activating effects.
"All of this strongly suggests that VEGF produced by NPCs is playing a strong role in influencing microglial behavior," said Wyss-Coray. "This is important, because in all neurodegenerative diseases we know of we see microglia out of control." The new finding may open the door to reprogramming misbehaving microglia to play better with other cells.
###
The study's first author was graduate student Kira Mosher. Other contributors were graduate student Gregor Bieri; postdoctoral scholars Robert Andres, MD, Takeshi Fukuhara PhD, Maiko Hasegawa-Moriyama MD, PhD, and Yingbo He, PhD; and Raphael Guzman, MD, a former associate professor of neurosurgery now at the University of Basel, Switzerland. The work was funded by the U.S. Department of Veterans Affairs, the California Institute for Regenerative Medicine and the National Institute on Aging.
Information about the medical school's Department of Neurology and Neurological Sciences, which also supported the work, is available at http://neurology.stanford.edu/.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
PRINT MEDIA CONTACT: Bruce Goldman at (650) 725-2106 (goldmanb@stanford.edu)
BROADCAST MEDIA CONTACT: M.A. Malone at (650) 723-6912 (mamalone@stanford.edu)
[ | 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.
Source: http://www.eurekalert.org/pub_releases/2012-10/sumc-npa101912.php
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Does your family play board games? - My Husband Ate All My Ice ...
'Round these parts, we love board games. But it's really hard to find ones that all of us can play, without the adults feeling bored by a kid game, or the younger kids feeling left out because they can't figure out a game that is geared towards older kids.?
When I saw that Morphology Junior was suggested for ages 8+, I was a little skeptical about how much the younger kids would be able to participate, considering they are 2 and 3.5 years old. So, as always, I sat down and read the instructions first, so that I could continue to act like the all-knowing mother when we sat down to play the game.?It comes with these pieces, and the game board, and 480 word cards:
Since the game comes with the instruction manual, I'm not going to give you a whole step-by-step, but basically, this is how it works:
You play on teams, and when it's your turn you become the 'morphologist'. You draw a card, and decide if you are going to use the easy or hard word on it, and whether or not you are going to use the clue on the card. Then, you have to use some of the game pieces to create an illustration of that word, so that your team can guess it before the time runs out. Sometimes, there are twists thrown in, like these:
Then, if your team guesses the word, you get to move your little frog further on the board. Our 9 and ?8 year old didn't have any problem with being able to play the game, although we sometimes had a little trouble guessing their interpretations. We just let our 3 year old be on whatever time he decided to be on at that moment, and try and help guess the words, and he was perfectly fine with that. Him and our 2 year old also sat and played with the pieces that we weren't using at the time.
Does your family play board games? What are some of your favorites? Morphology is one of the sponsors of the Better Than Black Friday Bash. Throughout October and November, I'm going to be doing reviews on some of this season's most awesome toy brands. Then, right before Black Friday, I'm having a huge giveaway event where you can win some things from the sponsors! Because nothing is better than Black Friday... except for getting things for free!I received compensation for this post, in the form of merchandise. All opinions expressed here are 100% mine, and not affected by any outside source.
Source: http://www.myhusbandateallmyicecream.com/2012/10/does-your-family-play-board-games.html
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Tuesday, October 16, 2012
America's Problems Solved With "Genghis Khan Economics"
CCN News?? October 14, 2012
Latest Brief Editor's Interview / in-house staff
Interviewer:? Mr. Cassone' it has been said that Genghis Khan has secretly been one of your top, all-time heroes! That being said, how would you feel that this hero might approach the "American Dilemma" of today?
Cassone':?? He would likely begin with rounding up the top 300 individuals most responsible for the "financial meltdown" of 2008, along with every Zionist in government and as many throughout the society as could be found out, including on Wall Street. I believe he would then proceed on to arrest every Rothschild, Morgan and every other top international banking family member and culprits of the "New World Order" scheme!
He would also, bring 75% of all overseas' jobs pegged to US companies back to the mainland!
Interviewer:? I see; so and what do you think he might do then, in the aftermath?
Cassone':??? Simple. He would seize all their total assets and have them swiftly executed in their front yard!
Interviewer:? Wowie! And then, what type of effect do you feel this might have?
Cassone':?? Gold would crash, the dollar would soar, the budget would be balanced, jobs and prosperity would flourish everywhere and do I dare say, things would be quite heavenly for "we the people"; the 99%!
Source: http://hamsayeh.net/world/2394-americas-problems-solved-with-qgenghis-khan-economicsq.html
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Monday, October 15, 2012
Countdown to Halloween Day 15 - Go Batty Card Game | AEIOU ...
One thing that's really been lacking on the market until recently is Halloween themed games. You'd think it would be a no brainer, right? Sure there have been a few games with Nightmare Before Christmas versions. And even Disney's Haunted Mansion versions of Clue and The Game of Life. There's even a Halloween themed Monopoly knock off called Boo-Opoly, which I have yet to get.
It's only in the past few years that I started to see Halloween themed games, mostly at Target. For the most part, they're classic games like Bingo, Twister, and Ring Toss with Halloween graphics. They're cute but usually don't appeal to my Halloween collecting need because they're not Halloween-y enough.
When I visited Micheal's craft store last week, I found this cute kids card game for $2.
As you can see, it's called Go Batty! and it plays just like Go Fish. Instead of a normal deck of cards with numbered suits, there are 13 sets of four cartoony creatures. For the price, the cards are made from surprisingly good stock. However, the big problem with them for me is the box.
The box is mounted to the backing card and I don't think there's any way of removing it without destroying the box short of cutting the card away with scissors. Also because of the way the interior tabs are placed in the box, it's impossible to close the top flap with the cards in there unless you remove the two foreign language rules cards. Even when I manage to get it closed, it's just as difficult to open because in order to get your fingertip on the flap you have to bend the backing card.
Despite all my whining about the box, you can't do much better for only two bucks, especially if you're not a stickler for keeping the packaging intact.
Be sure to visit the other bloggers that have their porch lights on by clicking below.?
They're waiting for you!?
Source: http://aeiouwhy.blogspot.com/2012/10/countdown-to-halloween-day-15-go-batty.html
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NASA sees Tropical Cyclone Anais headed near La Reunion Island
Public release date: 15-Oct-2012[ | E-mail |
Share ] Contact: Rob Gutro
robert.j.gutro@nasa.gov
443-858-1779
NASA/Goddard Space Flight Center
Tropical Cyclone Anais, the first tropical cyclone of the Southern Indian Ocean's tropical cyclone season, has strengthened over the weekend of Oct. 13 and 14 and by Oct. 15, the storm was packing sustained winds near 100 knots (115 mph/185 kph).
The Moderate Resolution Imaging Spectroradiometer (MODIS) instrument aboard NASA's Aqua satellite captured a visible image of Tropical Cyclone Anais off Madagascar on Oct. 15 at 0940 UTC (5:40 a.m. EDT) and revealed an eye. Multi-spectral satellite imagery showed that convection has continued to decrease around Anais' ragged eye, indicating that the storm may be weakening.
On Oct. 15 at 1500 UTC (11 a.m. EDT) Anais was 650 nautical miles (748 miles/1,024 km) northeast of La Reunion, and has been moving to the southwest at 8 knots (9.2 mph/14.8 kph).
Over the next several days, Anais is forecast to move past La Reunion Island, while the center of the storm stays to the north and west of the island. As the storm moves further southward, it will move into waters below the 80 degree Fahrenheit (26.6 Celsius) threshold needed to maintain the system. In addition to the cooler waters wind shear is forecast to increase, so Anais is expected to weaken over the next several days.
###
[ | 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.
Public release date: 15-Oct-2012[ | E-mail |
Share ] Contact: Rob Gutro
robert.j.gutro@nasa.gov
443-858-1779
NASA/Goddard Space Flight Center
Tropical Cyclone Anais, the first tropical cyclone of the Southern Indian Ocean's tropical cyclone season, has strengthened over the weekend of Oct. 13 and 14 and by Oct. 15, the storm was packing sustained winds near 100 knots (115 mph/185 kph).
The Moderate Resolution Imaging Spectroradiometer (MODIS) instrument aboard NASA's Aqua satellite captured a visible image of Tropical Cyclone Anais off Madagascar on Oct. 15 at 0940 UTC (5:40 a.m. EDT) and revealed an eye. Multi-spectral satellite imagery showed that convection has continued to decrease around Anais' ragged eye, indicating that the storm may be weakening.
On Oct. 15 at 1500 UTC (11 a.m. EDT) Anais was 650 nautical miles (748 miles/1,024 km) northeast of La Reunion, and has been moving to the southwest at 8 knots (9.2 mph/14.8 kph).
Over the next several days, Anais is forecast to move past La Reunion Island, while the center of the storm stays to the north and west of the island. As the storm moves further southward, it will move into waters below the 80 degree Fahrenheit (26.6 Celsius) threshold needed to maintain the system. In addition to the cooler waters wind shear is forecast to increase, so Anais is expected to weaken over the next several days.
###
[ | 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.
Source: http://www.eurekalert.org/pub_releases/2012-10/nsfc-nst101512.php
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