Wednesday, April 17, 2013

Search and Disarm: The Cop Bot That Takes Down Bombs

Explosive ordinance disposal (EOD) is one of the deadliest jobs in the military and it's no less dangerous here at home. But since Lieutenant-Colonel 'Peter' Miller designed the Wheelbarrow in 1972 against IRA IEDs in Northern Ireland, remote EOD robots have played an enormous part in explosive disarmarment. So when police find a suspicious package, they don't send in Officer Traven, they send in Officer tEODor. More »
    


Source: http://feeds.gawker.com/~r/gizmodo/full/~3/U7obSMqM9_I/search-and-disarm-the-cop-bot-that-takes-down-bombs

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Cantankerous Historian of Science Questions Whether Science Can Achieve "Truth"

One of the best things about teaching at Stevens Institute of Technology, which I joined in 2005, is shooting the shit with distinguished historian of science James E. McClellan III. Jim has authored, co-authored or edited half a dozen books, including Science and Technology in World History: An Introduction, which he wrote with our late Stevens colleague Harold Dorn. The book, which won an award from the World History Association, serves as my textbook when I teach ?History of Science and Technology.? Every time I read the book I learn something new, which perhaps means that I never read it carefully enough. Just kidding. I?ve learned more about the history of science from Jim than I like to admit.

Jim knows much about many things, but he is especially knowledgeable about the history of French science. That is the topic of his monumental new book The Colonial Machine: French Science and Overseas Expansion in the Old Regime, co-written with Francois Regourd. Based on exhaustive research into original archival sources (which gave Jim an excuse to spend lots of time in Paris), the book yields disturbing lessons about the historical linkages of modern science to state power, colonialism and slavery. I recently asked Jim some questions about his book, the history of science and related topics:

Horgan: To what extent can we learn about the emergence of modern science by focusing on pre-revolutionary France?

McClellan: You wouldn?t think that Old-Regime France has much to do with anything except Old-Regime France, yet important stuff happens in the history of science in the period. Conceptually, intellectually, the long eighteenth century bridges the Scientific Revolution and more modern science in the 19th century and down to today. Organizationally, institutionally and in terms of emerging norms in science, pre-revolutionary France is remarkable and incomparable. The history of modern science runs through it.

Horgan: Are there any aspects of pre-revolutionary French science that especially fascinated you?

McClellan: How can anyone seriously be interested in this topic? Of course, I have found much that is fascinating and compelling, but for most people I might as well be talking about Ming dynasty horse farms.

Horgan: Ming dynasty horse farms sound fascinating, actually. So to what extent did early French science help to promote colonialism and slavery?

McClellan: Read our book! Science and medicine were virtually ?means of production? facilitating the success of European expansion, colonialism and slavery. Conversely, Western science and the enterprise of science were enriched and expanded by dint of expanding outward with European and American economic and political imperialism.

Horgan: Is there such a thing as ?pure? science? Science for its own sake? Or does science always serve the interests of some group?

McClellan: Well, there?s ?pure? science in the sense of disinterested natural philosophy and the pursuit of inquiry into nature that is not looking for immediate, applied ends. What science knows and can say of the world abstractly today is a great human accomplishment. By the same token, only na?ve realists like you, John, don?t subscribe to the notion of the social construction of knowledge made by human groups that have their own interests, practices and sociologies. No?

Horgan: I?m the one asking the questions here. Rumor has it that you studied under historian of science Thomas Kuhn at Princeton. Did he turn you into one of those postmodernists who think science never really achieves truth?

McClellan: I took two seminars with Kuhn and saw a fair bit of him over the years I was in graduate school. My dissertation director was the eminent historian of science, Charles Gillispie. Kuhn was a realist (of sorts), but realism and postmodernism are not incompatible. Kuhn and postmodernism are self-evidently correct that science cannot make true and lasting discoveries about nature because we are all stuck within our paradigms (taken loosely), language games, cognitive structures, etc. Is anyone actually seriously going to stand up and tell me something true that is not at the same time a human creation? Let him or her start by telling me what gravity is.

Horgan: Yeah, yeah. Save it for our next faculty lunch. Can history ever become a scientific field, perhaps by incorporating more mathematical modeling or concepts from neuroscience and evolutionary biology?

McClellan: We need to make the (elementary) distinction between ?history? as what happened in the past versus ?history? as the scholarly, intellectual discipline that seeks to inquire into the past and explain change in the past by pursuing debates and research. The latter is already quite multifaceted, with many of its elements and methods scientific, as in a social science. It can even be theory guided, but if you mean that history should or could be like physics, then I think not. But then most sciences aren?t like physics, either.

Horgan: Sometimes physics isn?t like physics, like when it?s peddling string theory. Final question: Do you think modern scientists and engineers can benefit from knowing more history of science?

McClellan: Not really. Stephen Brush?s old 1974 article, ?Should the History of Science be Rated X?,? argued that knowing the history of science is positively harmful to the pursuit of research in science.

Horgan: Just found Brush?s paper online. Provocative! Next time I teach History of Science and Technology, I?m going to force my students to read it and blame you. Thanks, Jim.

Photo: http://crcv.revues.org.

Source: http://rss.sciam.com/click.phdo?i=b55546f6c6a5de3412ce9e5c8842a840

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Brain development is guided by junk DNA that isn't really junk

Apr. 15, 2013 ? Specific DNA once dismissed as junk plays an important role in brain development and might be involved in several devastating neurological diseases, UC San Francisco scientists have found.

Their discovery in mice is likely to further fuel a recent scramble by researchers to identify roles for long-neglected bits of DNA within the genomes of mice and humans alike.

While researchers have been busy exploring the roles of proteins encoded by the genes identified in various genome projects, most DNA is not in genes. This so-called junk DNA has largely been pushed aside and neglected in the wake of genomic gene discoveries, the UCSF scientists said.

In their own research, the UCSF team studies molecules called long noncoding RNA (lncRNA, often pronounced as "link" RNA), which are made from DNA templates in the same way as RNA from genes.

"The function of these mysterious RNA molecules in the brain is only beginning to be discovered," said Daniel Lim, assistant professor of neurological surgery, a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF, and the senior author of the study, published online April 11 in the journal Cell Stem Cell.

Alexander Ramos, a student enrolled in the MD/PhD program at UCSF and first author of the study, conducted extensive computational analysis to establish guilt by association, linking lncRNAs within cells to the activation of genes.

Ramos looked specifically at patterns associated with particular developmental pathways or with the progression of certain diseases. He found an association between a set of 88 long noncoding RNAs and Huntington's disease, a deadly neurodegenerative disorder. He also found weaker associations between specific groups of long noncoding RNAs and Alzheimer's disease, convulsive seizures, major depressive disorder and various cancers.

"Alex was the team member who developed this new research direction, did most of the experiments, and connected results to the lab's ongoing work," Lim said. The study was mostly funded through Lim's grant - a National Institutes of Health (NIH) Director's New Innovator Award, a competitive award for innovative projects that have the potential for unusually high impact.

Unlike messenger RNA, which is transcribed from the DNA in genes and guides the production of proteins, lncRNA molecules do not carry the blueprints for proteins. Because of this fact, they were long thought to not influence a cell's fate or actions.

Nonetheless, lncRNAs also are transcribed from DNA in the same way as messenger RNA, and they, too, consist of unique sequences of nucleic acid building blocks.

Evidence indicates that lncRNAs can tether structural proteins to the DNA-containing chromosomes, and in so doing indirectly affect gene activation and cellular physiology without altering the genetic code. In other words, within the cell, lncRNA molecules act "epigenetically" -- beyond genes -- not through changes in DNA.

The brain cells that the scientists focused on the most give rise to various cell types of the central nervous system. They are found in a region of the brain called the subventricular zone, which directly overlies the striatum. This is the part of the brain where neurons are destroyed in Huntington's disease, a condition triggered by a single genetic defect.

Ramos combined several advanced techniques for sequencing and analyzing DNA and RNA to identify where certain chemical changes happen to the chromosomes, and to identify lncRNAs on specific cell types found within the central nervous system. The research revealed roughly 2,000 such molecules that had not previously been described, out of about 9,000 thought to exist in mammals ranging from mice to humans.

In fact, the researchers generated far too much data to explore on their own. The UCSF scientists created a website through which their data can be used by others who want to study the role of lncRNAs in development and disease.

"There's enough here for several labs to work on," said Ramos, who has training grants from the California Institute for Regenerative Medicine (CIRM) and the NIH.

"It should be of interest to scientists who study long noncoding RNA, the generation of new nerve cells in the adult brain, neural stem cells and brain development, and embryonic stem cells," he said.

Other co-authors who worked on the study include UCSF postdoctoral fellows Aaron Diaz, PhD, Abhinav Nellore, PhD, Michael Oldham, PhD, Jun Song, PhD, Ki-Youb Park, PhD, and Gabriel Gonzales-Roybal, PhD; and MD/PhD student Ryan Delgado. Additional funders of the study included the Sontag Foundation and the Sandler Foundation.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

###

Follow UCSF UCSF.edu | Facebook.com/ucsf | Twitter.com/ucsf | YouTube.com/ucsf

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Story Source:

The above story is reprinted from materials provided by University of California, San Francisco (UCSF).

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Alexander D. Ramos, Aaron Diaz, Abhinav Nellore, Ryan N. Delgado, Ki-Youb Park, Gabriel Gonzales-Roybal, Michael C. Oldham, Jun S. Song, Daniel A. Lim. Integration of Genome-wide Approaches Identifies lncRNAs of Adult Neural Stem Cells and Their Progeny In Vivo. Cell Stem Cell, 2013 DOI: 10.1016/j.stem.2013.03.003

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_science/~3/Lj8DVrDLFOg/130415172010.htm

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Tuesday, April 16, 2013

Color of OLEDs can now at last be predicted thanks to new modeling technique

Apr. 15, 2013 ? OLEDs can be made more efficiently and at lower cost by a better understanding of the electronic processed.

OLEDs -- thin, light-emitting surfaces -- are regarded as the light sources of the future. White OLEDs consist of stacked, ultra-thin layers, each emitting its own light color, all together resulting in white light. Up to now it has been impossible to predict the exact light color produced by a white OLED; manufacturers had to rely on trial and error. Researchers at Eindhoven University of Technology, Philips Research, Dresden University of Technology and other institutes have now developed a method that allows the color of light produced by a specific OLED design to be calculated with high precision. They did this by modeling the complex processes in OLEDs on a molecular scale. This technique will allow manufacturers to greatly improve their OLED design processes and reduce the cost. At the same time the energy efficiency and lifetime of OLEDs can be increased.

The results were published online on Sunday 14 April 2013 in the journal Nature Materials.

Revolution

It looks as though OLEDs -- organic light emitting diodes -- will cause a revolution in the world of lighting. OLEDs are light-emitting surfaces, which means they are visually more attractive than point light sources such as conventional or LED lamps. They can also be flexible and transparent, which opens up all kinds of new opportunities. Plus -- and unlike normal LEDs -- OLEDs are made of very low-cost materials, of which only very thin layers are needed. As a result, the prices of OLEDs are expected to be low once mass production starts. This clip gives an impression of what's possible with OLEDs.

To predict what kind of light an OLED design will produce, the researchers made computer models of the electronic processes in the OLED at the deepest level. These showed for example the injection of electrical charge, the creation and distribution of the 'excitons' -- pairs of positively charged electrons and holes in a bound state -- and the creation from these of individual photons, the light that is emitted. "At first we thought it would never be possible," says researcher Peter Bobbert of Eindhoven University of Technology. The main difficulty was that each change in the electrical charge also influences all the other charges, which makes the simulation extremely complex. But they succeeded by using Monte Carlo simulations with nanosecond steps. The results proved to correspond very well to measurements carried out at Philips on real OLEDs made at Dresden University of Technology.

Factor of three

One of the results is that the researchers can now predict where light is produced and lost in the ultra-thin layers. That makes it possible to optimize OLEDs so they produce the same amount of light using much less electric power. The researchers expect that the efficiency can still be increased by a factor of three. Manufacturers can also use this new knowledge to design OLEDs with specific colors. They can calculate in advance exactly how thick the different layers need to be, and how much pigment has to be added to the layers. The much shorter and less costly design process will allow the overall development costs to be reduced, leading to lower prices of the final products. "This has already been possible for a long time in the field of micro-electronics, with the ability to precisely predict the behavior of integrated circuits," says Bobbert. "Now we can do the same thing with OLEDs."

The research was made possible by financial support from the European Union (FP7 project AEVIOM), the Dutch Polymer Institute, NanoNextNL and NanoNed.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:


Story Source:

The above story is reprinted from materials provided by Eindhoven University of Technology.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Note: If no author is given, the source is cited instead.

Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_technology/~3/74lBlOeeEGA/130415094847.htm

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Brain development is guided by junk DNA that isn't really junk

Brain development is guided by junk DNA that isn't really junk [ Back to EurekAlert! ] Public release date: 15-Apr-2013
[ | E-mail | Share Share ]

Contact: Jeffrey Norris
jeff.norris@ucsf.edu
415-502-6397
University of California - San Francisco

Specific DNA once dismissed as junk plays an important role in brain development and might be involved in several devastating neurological diseases, UC San Francisco scientists have found.

Their discovery in mice is likely to further fuel a recent scramble by researchers to identify roles for long-neglected bits of DNA within the genomes of mice and humans alike.

While researchers have been busy exploring the roles of proteins encoded by the genes identified in various genome projects, most DNA is not in genes. This so-called junk DNA has largely been pushed aside and neglected in the wake of genomic gene discoveries, the UCSF scientists said.

In their own research, the UCSF team studies molecules called long noncoding RNA (lncRNA, often pronounced as "link" RNA), which are made from DNA templates in the same way as RNA from genes.

"The function of these mysterious RNA molecules in the brain is only beginning to be discovered," said Daniel Lim, assistant professor of neurological surgery, a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF, and the senior author of the study, published online April 11 in the journal Cell Stem Cell.

Alexander Ramos, a student enrolled in the MD/PhD program at UCSF and first author of the study, conducted extensive computational analysis to establish guilt by association, linking lncRNAs within cells to the activation of genes.

Ramos looked specifically at patterns associated with particular developmental pathways or with the progression of certain diseases. He found an association between a set of 88 long noncoding RNAs and Huntington's disease, a deadly neurodegenerative disorder. He also found weaker associations between specific groups of long noncoding RNAs and Alzheimer's disease, convulsive seizures, major depressive disorder and various cancers.

"Alex was the team member who developed this new research direction, did most of the experiments, and connected results to the lab's ongoing work," Lim said. The study was mostly funded through Lim's grant a National Institutes of Health (NIH) Director's New Innovator Award, a competitive award for innovative projects that have the potential for unusually high impact.

Unlike messenger RNA, which is transcribed from the DNA in genes and guides the production of proteins, lncRNA molecules do not carry the blueprints for proteins. Because of this fact, they were long thought to not influence a cell's fate or actions.

Nonetheless, lncRNAs also are transcribed from DNA in the same way as messenger RNA, and they, too, consist of unique sequences of nucleic acid building blocks.

Evidence indicates that lncRNAs can tether structural proteins to the DNA-containing chromosomes, and in so doing indirectly affect gene activation and cellular physiology without altering the genetic code. In other words, within the cell, lncRNA molecules act "epigenetically" beyond genes not through changes in DNA.

The brain cells that the scientists focused on the most give rise to various cell types of the central nervous system. They are found in a region of the brain called the subventricular zone, which directly overlies the striatum. This is the part of the brain where neurons are destroyed in Huntington's disease, a condition triggered by a single genetic defect.

Ramos combined several advanced techniques for sequencing and analyzing DNA and RNA to identify where certain chemical changes happen to the chromosomes, and to identify lncRNAs on specific cell types found within the central nervous system. The research revealed roughly 2,000 such molecules that had not previously been described, out of about 9,000 thought to exist in mammals ranging from mice to humans.

In fact, the researchers generated far too much data to explore on their own. The UCSF scientists created a website through which their data can be used by others who want to study the role of lncRNAs in development and disease.

"There's enough here for several labs to work on," said Ramos, who has training grants from the California Institute for Regenerative Medicine (CIRM) and the NIH.

"It should be of interest to scientists who study long noncoding RNA, the generation of new nerve cells in the adult brain, neural stem cells and brain development, and embryonic stem cells," he said.

###

Other co-authors who worked on the study include UCSF postdoctoral fellows Aaron Diaz, PhD, Abhinav Nellore, PhD, Michael Oldham, PhD, Jun Song, PhD, Ki-Youb Park, PhD, and Gabriel Gonzales-Roybal, PhD; and MD/PhD student Ryan Delgado. Additional funders of the study included the Sontag Foundation and the Sandler Foundation.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

Follow UCSF
UCSF.edu | Facebook.com/ucsf | Twitter.com/ucsf | YouTube.com/ucsf


[ Back to EurekAlert! ] [ | E-mail | Share 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.


Brain development is guided by junk DNA that isn't really junk [ Back to EurekAlert! ] Public release date: 15-Apr-2013
[ | E-mail | Share Share ]

Contact: Jeffrey Norris
jeff.norris@ucsf.edu
415-502-6397
University of California - San Francisco

Specific DNA once dismissed as junk plays an important role in brain development and might be involved in several devastating neurological diseases, UC San Francisco scientists have found.

Their discovery in mice is likely to further fuel a recent scramble by researchers to identify roles for long-neglected bits of DNA within the genomes of mice and humans alike.

While researchers have been busy exploring the roles of proteins encoded by the genes identified in various genome projects, most DNA is not in genes. This so-called junk DNA has largely been pushed aside and neglected in the wake of genomic gene discoveries, the UCSF scientists said.

In their own research, the UCSF team studies molecules called long noncoding RNA (lncRNA, often pronounced as "link" RNA), which are made from DNA templates in the same way as RNA from genes.

"The function of these mysterious RNA molecules in the brain is only beginning to be discovered," said Daniel Lim, assistant professor of neurological surgery, a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF, and the senior author of the study, published online April 11 in the journal Cell Stem Cell.

Alexander Ramos, a student enrolled in the MD/PhD program at UCSF and first author of the study, conducted extensive computational analysis to establish guilt by association, linking lncRNAs within cells to the activation of genes.

Ramos looked specifically at patterns associated with particular developmental pathways or with the progression of certain diseases. He found an association between a set of 88 long noncoding RNAs and Huntington's disease, a deadly neurodegenerative disorder. He also found weaker associations between specific groups of long noncoding RNAs and Alzheimer's disease, convulsive seizures, major depressive disorder and various cancers.

"Alex was the team member who developed this new research direction, did most of the experiments, and connected results to the lab's ongoing work," Lim said. The study was mostly funded through Lim's grant a National Institutes of Health (NIH) Director's New Innovator Award, a competitive award for innovative projects that have the potential for unusually high impact.

Unlike messenger RNA, which is transcribed from the DNA in genes and guides the production of proteins, lncRNA molecules do not carry the blueprints for proteins. Because of this fact, they were long thought to not influence a cell's fate or actions.

Nonetheless, lncRNAs also are transcribed from DNA in the same way as messenger RNA, and they, too, consist of unique sequences of nucleic acid building blocks.

Evidence indicates that lncRNAs can tether structural proteins to the DNA-containing chromosomes, and in so doing indirectly affect gene activation and cellular physiology without altering the genetic code. In other words, within the cell, lncRNA molecules act "epigenetically" beyond genes not through changes in DNA.

The brain cells that the scientists focused on the most give rise to various cell types of the central nervous system. They are found in a region of the brain called the subventricular zone, which directly overlies the striatum. This is the part of the brain where neurons are destroyed in Huntington's disease, a condition triggered by a single genetic defect.

Ramos combined several advanced techniques for sequencing and analyzing DNA and RNA to identify where certain chemical changes happen to the chromosomes, and to identify lncRNAs on specific cell types found within the central nervous system. The research revealed roughly 2,000 such molecules that had not previously been described, out of about 9,000 thought to exist in mammals ranging from mice to humans.

In fact, the researchers generated far too much data to explore on their own. The UCSF scientists created a website through which their data can be used by others who want to study the role of lncRNAs in development and disease.

"There's enough here for several labs to work on," said Ramos, who has training grants from the California Institute for Regenerative Medicine (CIRM) and the NIH.

"It should be of interest to scientists who study long noncoding RNA, the generation of new nerve cells in the adult brain, neural stem cells and brain development, and embryonic stem cells," he said.

###

Other co-authors who worked on the study include UCSF postdoctoral fellows Aaron Diaz, PhD, Abhinav Nellore, PhD, Michael Oldham, PhD, Jun Song, PhD, Ki-Youb Park, PhD, and Gabriel Gonzales-Roybal, PhD; and MD/PhD student Ryan Delgado. Additional funders of the study included the Sontag Foundation and the Sandler Foundation.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

Follow UCSF
UCSF.edu | Facebook.com/ucsf | Twitter.com/ucsf | YouTube.com/ucsf


[ Back to EurekAlert! ] [ | E-mail | Share 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/2013-04/uoc--bdi041513.php

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Monday, April 15, 2013

Woman arrested for approaching Hugh Jackman with electric razor: police

NEW YORK (Reuters) - Officers arrested a woman for stalking after she wielded an electric razor while approaching Australian actor Hugh Jackman at a New York City gym, police said on Sunday.

Katherine Thurston, 47, went into the gym where Jackman was working out early on Saturday morning, and after a brief encounter with the 44-year-old actor, she fled and was arrested a few blocks away, a New York police spokeswoman said.

Thurston shouted that she loved the actor before throwing the electric razor, which was filled with hair clippings, at Jackman, who was not injured, local radio station and CBS affiliate 1010 WINS reported. Police officials said they could not confirm those details about the incident.

Jackman told officers that Thurston has been following him and his family for some time, police said.

"I suppose for me the primary concern is my family, obviously," Jackman, who plays Wolverine in the "X-Men" superhero film series, told the station. "But, you know, here's a woman who obviously needs help, so I just hope she gets the help she needs."

Thurston, who police said was charged with fourth-degree stalking was awaiting her arraignment on Sunday and could not be reached for comment.

(Reporting by Jonathan Allen; Editing by Alex Dobuzinskis and Bill Trott)

Source: http://news.yahoo.com/woman-arrested-approaching-hugh-jackman-electric-razor-police-193853533.html

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Tax Day Freebies 2013 and other freebies - Recipes, Cooking, and ...

April 13, 2013 04:18 PM EDT

views: 140 | 1 person recommends this | comments: 1

tax day freebies 2013

Tax Day Freebies

?

File Your Taxes FREE! And, of course, if you still need to file your taxes, check these out:

Big List of Tax Day Freebies & Discounts

  • AMC Theaters
    FREE Small Popcorn with Printable Coupon on April 15
  • Arby?s
    Free Value Curly Fries on Tax Day 4/15
  • Bonefish Grill
    Bang Bang Shrimp for $5 from 4PM -close on April 15th
  • Boston Market
    BOGO Free Ribs ~ get a $1 coupon and enter for the chance to win free food in link
  • Bruegger?s Bagels
    Special Tax Break ? a $10.40 Big Bagel Bundle (Bakers Dozens & 2 Tubs of Cream Cheese) at participating bakeries, today through Monday, April 15th!! List originally published http://bit.ly/Zo0BsB. Get your coupon on Bruegger?s Bagels facebook page.
  • California Tortilla
    FREE Chips & Queso, (which is ?cheese?) when you say ?1040? on Tax Day
  • Cinnabon
    FREE Cinnabon Bites on April 15
  • Chik Fil A
    Make a purchase on 4/15, and then bring your receipt back on 5/13 to get a full refund. http://bit.ly/Zo0BsB (Participating locations only, call ahead)
  • Chili?s
    Free Appetizer or Dessert w/entree purchase. Valid 4/16-4/18.

?

1 person recommends this post

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Source: http://food-cooking.gather.com/viewArticle.action?articleId=281474981869404

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