Black Friday is the Super Bowl of retail, but some of the nation's largest big-box stores can't wait until the day after Thanksgiving to open their doors to shoppers eager to grab great deals the same day as their turkey dinners.
Traditional Black Friday door-busting deals now start tonight, on what's been dubbed Gray Thursday. Major retail stores such as Kmart, Toys R Us, Walmart and Sears will open their doors beginning at 8 p.m. Target will join the party an hour later.
"It's traditionally been the day after Thanksgiving when the stores go into the black, where they make all their money. But that's not true anymore," retail expert Michelle Madhock said.
With Black Friday sales starting Thursday, that means lines started forming Wednesday, or in some extreme cases a week before as bargain hunters tried to get a turkey leg up on their competition.
READ: The Best Black Friday Freebies 2012
Luciana Pendleton pitched a tent outside a Deptford Township, N.J., Best Buy Monday fully equipped with all she needed to spend the next few days away from home so she could be first in line when the doors open.
"I am just happy I beat my competition. They pulled up here around 3 p.m., and we were already here so I was happy," she said Monday.
READ: How to Beat Black Friday Stress
Last year, some sale seekers became a little too excited and turned holiday shopping into a contact sport. In one ugly incident, a woman was accused of unleashing pepper spray on other shoppers in a dash for electronics at Walmart in Los Angeles.
This year, stores are beefing up security, and Best Buy even participated in training drills to handle the large crowds. More than 147 million people plan to shop this weekend, according to the National Retail Federation.
The hottest deals that are up for grabs this year include a 46-inch Samsung LED flat screen TV at Walmart with $200 off the original price. If that's not good enough, Sears has knocked $500 off the price of a 50-inch Toshiba flat screen. Target is offering the Nook Simple Touch at half price.
Black Friday officially kicks off at midnight for Best Buy, Sports Authority and Macy's.
A strong strategy for search engine optimization is key for any business website. Most of your customers use the Internet. In order to obtain as many potential customers as possible, it is therefore important to have a high search ranking. This will help your business become successful.
Make use of the SEO, or search engine optimization, services that are offered by many companies. This is when your site is marketed in a way that will bring it up to the top of search engine results. Tons of companies offer great deals on these sorts of services.
A good way to boost your search engine ranking with little effort is to buy an already established domain name. If your domain name is over two years old, the search engines give it more weight. Review lists of recently deleted domains looking for ones that could possibly suit your new site?s purpose.
Gear your efforts toward getting a few of the most popular search engines to rank your site highly. Taking certain steps will help you on all sorts of search engines. , Ask. Many of the large sites publish SEO guidelines for you to follow.
The best way to improve your website is by keeping your content fresh and unique at all times. If your content is outdated, readers will tend to skip over your site.
The domain name that you choose should be easy for your customers to recall, and closely related to the type of merchandise that you offer. This is very helpful to people who have found your content on YouTube. They are memorable and easy to say.
When you blog through your own site, it increases your search engine visibility. You will then get more visitors coming to your site.
Even if all of your content is about the same topic, keep each title or heading interesting, attention-grabbing and unique. Each word in your title reduces its importance, so make sure your titles are concise. The title?s first words matter most when trying to hook readers.
A site map which has your keywords included should be created. The purpose of the site map is to index the pages on your site, making it easier for search engine spiders, and viewers alike, to find important information. The presence of a site map also influences your search engine rankings, since ease of navigation is something search engines take into account.
Ask questions before hiring an SEO company. Research their skills and experience, what SEO methods they use and what their charges are. You should also view some of their prior work, and talk to formal customers. A reputable company will have no problem doing this.
Focus on mastering one SEO strategy at a time. There just isn?t enough time in the day for you to learn every technique, so select one which you think will be the most valuable to you and make the most of its capabilities.
Include transcripts for your site?s videos and audio in order to help your rankings. This can make it easier for search engines to find your content in searches.
Read some blogs that are relevant to your site, and comment on them in order to get links back to your website. Throughout these blogs, you can leave your link if the blog owner allows it. Do not post your link on irrelevant blogs, or it will clog the value of their site, giving you a bad reputation. If you know your subject well, it will be easy for you to leave acceptable comments, along with your link, on many blogs.
Increasing your ranking on search engines will allow your regular customers to access your site. There are a lot of web-based business that do not know this.
It is extremely important that all of your site?s images have a corresponding alt tag. Use these tags to replace pictures if a site visitor disables his or her image display. Search engine spiders can?t read images, only alt tags, which means they?ll be seeing those keywords. And this can improve your search ranking.
Doing search engine optimization to help draw traffic to your website is actually something that can be done with minimal muss and fuss. All you need is a little versatility and attention to detail. If you employ the tips you have read here, you will get a higher rank.
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Robert Lieberman, the maker of the critically acclaimed documentary, They Call It Myanmar ? Lifting the Curtain, tells a story that exposes some of the cynical reality behind President Obama?s historic visit to politically imprisoned Myanmar today. Shortly after Aung San Suu Kyi, the Nobel Prize-winning democracy activist, was released from two decades of house arrest in November of 2010, Lieberman was invited to show his film at a Yangon festival that Suu Kyi was organizing called ?The Art of Freedom.? Thoughtfully, he informed the U.S. Embassy of his plans. Their reaction? Near-panic.
Please contact me and I can assist you in finding a QUALIFIED short sale agent in your area. ==================== From California???
Quite frankly, It reads that your home owners' assiciation is heavily in the red. There won't be available financing for anyone to buy there if that's the case which means a shortsale won't help you.
The assessment will probably scare off ?most anyone else.
Research breakthrough selectively represses the immune systemPublic release date: 18-Nov-2012 [ | E-mail | Share ]
Contact: Margot Kern nibibpress@mail.nih.gov 301-496-3500 NIH/National Institute of Biomedical Imaging & Bioengineering
NIH-funded scientists develop new treatment to combat autoimmune disease in mouse model
Reporters, please see "For news media only" box at the end of the release for embargoed sound bites of researchers.
In a mouse model of multiple sclerosis (MS), researchers funded by the National Institutes of Health have developed innovative technology to selectively inhibit the part of the immune system responsible for attacking myelinthe insulating material that encases nerve fibers and facilitates electrical communication between brain cells.
Autoimmune disorders occur when T-cellsa type of white blood cell within the immune systemmistake the body's own tissues for a foreign substance and attack them. Current treatment for autoimmune disorders involves the use of immunosuppressant drugs which tamp down the overall activity of the immune system. However, these medications leave patients susceptible to infections and increase their risk of cancer as the immune system's normal ability to identify and destroy aberrant cells within the body is compromised.
Supported by the National Institute of Biomedical Imaging and Bioengineering (NIBIB) at NIH, Drs. Stephen Miller and Lonnie Shea at Northwestern University, Evanston, teamed up with researchers at the University of Sydney, and the Myelin Repair Foundation in Saratoga, Calif. to come up with a novel way of repressing only the part of the immune system that causes autoimmune disorders while leaving the rest of the system intact.
The new research takes advantage of a natural safeguard employed by the body to prevent autoreactive T-cellswhich recognize and have the potential to attack the body's healthy tissuesfrom becoming active. They report their results in the Nov. 18 online edition of Nature Biotechnology.
"We're trying to do something that interfaces with the natural processes in the body," said Shea. "The body has natural mechanisms for shutting down an immune response that is inappropriate, and we're really just looking to tap into that."
One of these natural mechanisms involves the ongoing clearance of apoptotic, or dying, cells from the body. When a cell dies, it releases chemicals that attract specific cells of the immune system called macrophages. These macrophages gobble up the dying cell and deliver it to the spleen where it presents self-antigenstiny portions of proteins from the dying cellto a pool of T-cells. In order to prevent autoreactive T-cells from being activated, macrophages initiate the repression of any T-cells capable of binding to the self-antigens.
Dr. Miller was the first to demonstrate that by coupling a specific self-antigen such as myelin to apoptotic cells, one could tap into this natural mechanism to suppress T-cells that would normally attack the myelin. The lab spent decades demonstrating that they could generate antigen-specific immune suppression in various animal models of autoimmune diseases. Recently, they initiated a preliminary clinical trial with collaborators in Germany to test the safety of injecting the antigen-bound apoptotic cells into patients with MS. While the trial successfully demonstrated that the injections were safe, it also highlighted a key problem with using cells as a vehicle for antigen delivery:
"Cellular therapy is extremely expensive as it needs to be carried out in a large medical center that has the capability to isolate patient's white blood cells under sterile conditions and to re-infuse those antigen-coupled cells back into the patients," said Miller. "It's a costly, difficult, and time-consuming procedure."
Thus began a collaboration with Dr. Shea, a bioengineer at Northwestern University, to discuss the possibility of developing a surrogate for the apoptotic cells. After trying out various formulations, his lab successfully linked the desired antigens to microscopic, biodegradable particles which they predicted would be taken up by circulating macrophages similar to apoptotic cells.
Much to their amazement, when tested by the Miller lab, the antigen-bound particles were just as good, if not better, at inducing T-cell tolerance in animal models of autoimmune disorders.
Using their myelin-bound particles, the researchers were able to both prevent the initiation of MS in their mouse model as well as inhibit its progression when injected immediately following the first sign of clinical symptoms.
The research team is now hoping to begin phase I clinical trials using this new technology. The material that makes up the particles has already been approved by the U.S. Food and Drug Administration and is currently used in resorbable sutures as well as in clinical trials to deliver anti-cancer agents. Miller believes that the proven safety record of these particles along with their ability to be easily produced using good manufacturing practices will make it easier to translate their discovery into clinical use.
"I think we've come up with a very potent way to induce tolerance that can be easily translated into clinical practice. We're doing everything we can now to take this forward," said Miller.
In addition to its potential use for the treatment of MS, the researchers have shown in the lab that their therapy can induce tolerance for other autoimmune diseases such as type I diabetes and specific food allergies. They also speculate that transplant patients could benefit from the treatment which has the potential to retract the body's natural immune response against a transplanted organ. Dr. Christine Kelley, NIBIB director of the Division of Science and Technology, points to the unique collaboration between scientists and engineers that made this advance a reality.
"This discovery is testimony to the importance of multidisciplinary research efforts in healthcare," said Kelley. "The combined expertise of these immunology and bioengineering researchers has resulted in a valuable new perspective on treating autoimmune disorders."
###
In addition to a grant from NIBIB (R01-EB013198-02), the research was also supported by NIH's National Institute of Neurological Disorders and Stroke (NS026543), the Myelin Repair Foundation, and the Juvenile Diabetes Research Foundation (17-2011-343).
NIBIB's mission is to support multidisciplinary research and research training at the crossroads of engineering and the biological and physical sciences. NIBIB supports emerging technology research and development within its internal laboratories and through grants, collaborations, and training. More information is available at the NIBIB website: http://www.nibib.nih.gov/.
NINDS is the nation's leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease a burden borne by every age group, by every segment of society, by people all over the world.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
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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.
Research breakthrough selectively represses the immune systemPublic release date: 18-Nov-2012 [ | E-mail | Share ]
Contact: Margot Kern nibibpress@mail.nih.gov 301-496-3500 NIH/National Institute of Biomedical Imaging & Bioengineering
NIH-funded scientists develop new treatment to combat autoimmune disease in mouse model
Reporters, please see "For news media only" box at the end of the release for embargoed sound bites of researchers.
In a mouse model of multiple sclerosis (MS), researchers funded by the National Institutes of Health have developed innovative technology to selectively inhibit the part of the immune system responsible for attacking myelinthe insulating material that encases nerve fibers and facilitates electrical communication between brain cells.
Autoimmune disorders occur when T-cellsa type of white blood cell within the immune systemmistake the body's own tissues for a foreign substance and attack them. Current treatment for autoimmune disorders involves the use of immunosuppressant drugs which tamp down the overall activity of the immune system. However, these medications leave patients susceptible to infections and increase their risk of cancer as the immune system's normal ability to identify and destroy aberrant cells within the body is compromised.
Supported by the National Institute of Biomedical Imaging and Bioengineering (NIBIB) at NIH, Drs. Stephen Miller and Lonnie Shea at Northwestern University, Evanston, teamed up with researchers at the University of Sydney, and the Myelin Repair Foundation in Saratoga, Calif. to come up with a novel way of repressing only the part of the immune system that causes autoimmune disorders while leaving the rest of the system intact.
The new research takes advantage of a natural safeguard employed by the body to prevent autoreactive T-cellswhich recognize and have the potential to attack the body's healthy tissuesfrom becoming active. They report their results in the Nov. 18 online edition of Nature Biotechnology.
"We're trying to do something that interfaces with the natural processes in the body," said Shea. "The body has natural mechanisms for shutting down an immune response that is inappropriate, and we're really just looking to tap into that."
One of these natural mechanisms involves the ongoing clearance of apoptotic, or dying, cells from the body. When a cell dies, it releases chemicals that attract specific cells of the immune system called macrophages. These macrophages gobble up the dying cell and deliver it to the spleen where it presents self-antigenstiny portions of proteins from the dying cellto a pool of T-cells. In order to prevent autoreactive T-cells from being activated, macrophages initiate the repression of any T-cells capable of binding to the self-antigens.
Dr. Miller was the first to demonstrate that by coupling a specific self-antigen such as myelin to apoptotic cells, one could tap into this natural mechanism to suppress T-cells that would normally attack the myelin. The lab spent decades demonstrating that they could generate antigen-specific immune suppression in various animal models of autoimmune diseases. Recently, they initiated a preliminary clinical trial with collaborators in Germany to test the safety of injecting the antigen-bound apoptotic cells into patients with MS. While the trial successfully demonstrated that the injections were safe, it also highlighted a key problem with using cells as a vehicle for antigen delivery:
"Cellular therapy is extremely expensive as it needs to be carried out in a large medical center that has the capability to isolate patient's white blood cells under sterile conditions and to re-infuse those antigen-coupled cells back into the patients," said Miller. "It's a costly, difficult, and time-consuming procedure."
Thus began a collaboration with Dr. Shea, a bioengineer at Northwestern University, to discuss the possibility of developing a surrogate for the apoptotic cells. After trying out various formulations, his lab successfully linked the desired antigens to microscopic, biodegradable particles which they predicted would be taken up by circulating macrophages similar to apoptotic cells.
Much to their amazement, when tested by the Miller lab, the antigen-bound particles were just as good, if not better, at inducing T-cell tolerance in animal models of autoimmune disorders.
Using their myelin-bound particles, the researchers were able to both prevent the initiation of MS in their mouse model as well as inhibit its progression when injected immediately following the first sign of clinical symptoms.
The research team is now hoping to begin phase I clinical trials using this new technology. The material that makes up the particles has already been approved by the U.S. Food and Drug Administration and is currently used in resorbable sutures as well as in clinical trials to deliver anti-cancer agents. Miller believes that the proven safety record of these particles along with their ability to be easily produced using good manufacturing practices will make it easier to translate their discovery into clinical use.
"I think we've come up with a very potent way to induce tolerance that can be easily translated into clinical practice. We're doing everything we can now to take this forward," said Miller.
In addition to its potential use for the treatment of MS, the researchers have shown in the lab that their therapy can induce tolerance for other autoimmune diseases such as type I diabetes and specific food allergies. They also speculate that transplant patients could benefit from the treatment which has the potential to retract the body's natural immune response against a transplanted organ. Dr. Christine Kelley, NIBIB director of the Division of Science and Technology, points to the unique collaboration between scientists and engineers that made this advance a reality.
"This discovery is testimony to the importance of multidisciplinary research efforts in healthcare," said Kelley. "The combined expertise of these immunology and bioengineering researchers has resulted in a valuable new perspective on treating autoimmune disorders."
###
In addition to a grant from NIBIB (R01-EB013198-02), the research was also supported by NIH's National Institute of Neurological Disorders and Stroke (NS026543), the Myelin Repair Foundation, and the Juvenile Diabetes Research Foundation (17-2011-343).
NIBIB's mission is to support multidisciplinary research and research training at the crossroads of engineering and the biological and physical sciences. NIBIB supports emerging technology research and development within its internal laboratories and through grants, collaborations, and training. More information is available at the NIBIB website: http://www.nibib.nih.gov/.
NINDS is the nation's leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease a burden borne by every age group, by every segment of society, by people all over the world.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
[ | 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.
For the moment, your arsenal of touchscreen gestures is effectively limited by the number of fingers you can use. a ten-finger gesture isn't going to be particularly helpful for most of us. New tech that can tell the difference between fingertips, knuckles, and fingernails however, could throw some more variables into the mix. More »
??When a Florida shock jock threatened to "deep fat fry" a Quran earlier this year, Gen. John Allen and CIA Director David Petraeusreached out to Tampa socialite Jill Kelley to help tamp down what they saw as a potential threat to the safety of U.S. troops, according to emails released by the city of Tampa.
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Public release date: 18-Nov-2012
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