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Import Help for Adobe FormsCentral ReplacementAsked by aclayman93 on January 26, 2015 at 01:22 PM
I am having trouble importing the form below. Also, can my form be embedded like the current form? Thanks in advance!
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Are you sick of hearing me talk about Q&A Tuesday yet? No? Well, good! All summer long I answer questions from social media LIVE on Facebook. Usually I answer a money, budgeting, or frugal living question. But a few weeks ago I did the ol' classic "ask me anything" live Q&A, and realize I forgot
Don't miss anything!
Freezer Hacks! + Things you (most likely) didn't know you could freeze…
You may or may not know that I have a crazy addiction to freezing things. Like, it's bad. I won't even tell you how many freezers I have, because you will judge me. …he'em…cough…SEVEN!…cough… What can I say?? We have the space, my husband loves me anyway, and it just makes my life SO MUCH
The Bachelor…Beck Style.
Spoiler alert: This post doesn't have anything to do with saving money. But it's my party and I can cry if I want to. …Aaaaaaaaaaand ultimately I just got back from Puerto Rico and I'm super behind and haven't had time to finish the 8000 posts I'm working on so this will just have to
10 Morning Hacks for Moms (PLUS – FREE Printable Morning Chore Chart!)
Want some life changing morning hacks in your life? Yes. Yes you do. Why? Raise your hand if you have perfectly smooth mornings every day! (Crickets…) Mornings can be CRAZY, especially around our house. Luckily through lots of trial and error, we finally have a solid morning routine that really works! In today's Millennial Moms video I'm
Makeup Tutorial…from a 4 year old :)
Today's Millennial Moms video is just for kicks and giggles…because it's just about the cutest thing you've ever seen. My 4 year old, Priya, is OBSESSED with doing makeup. She asked me almost every day if she can do my makeup. I finally let her have free reign, and decided to film it of course.
My 6 Best Natural Makeup Tips! + My Fave Beauty Tools
We all know I love makeup, and wear a full face of it just about every day (as I show in my tutorials). BUT…the purpose of makeup is to enhance beauty, not mask it with layers of goop. Today on Millennial Moms I'm sharing my top 6 best NATURAL makeup tips! They are simple things
GENDER REVEAL! Page Baby #5 is a…
You all have waited SO patiently for this GENDER REVEAL, I won't make you wait any longer! I hope you enjoy this video I did for Millennial Moms (where I do new videos every Wednesday) showing the gender of Page Baby #5, due early May! Unfortunately Priya had to miss it because she has morning
Millennial Moms – my new WEEKLY video series!
Did you know I'm part of a new weekly YouTube video series for moms? It's true! Mindy from CuteGirlsHairstyles (basically the Queen of YouTube) started a NEW channel recently called Millennial Moms. She recruited me to be the Wednesday contributor, where I share comedic mom advice about beauty, fashion, makeup, shopping, parenting, and just about everything else! The
Shopping Online: What To Look For in Clothing and Accessories
One of the main questions I get asked is about FRUGAL FASHION! Freebs want to know how to look good on a serious budget. It's no secret that much of my wardrobe I have bought online (aside from yard sales). With 4 little kids I just don't have time to go to stores any more!

subset: commoncrawl


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| This 1983: Doomsday page is obsolete.
Events in this article are no longer part of the 1983: Doomsday timeline, but the page has been saved for reference purposes. You can comment on this page's talkpage.
The Federated States of Carolina is a small US remnant. Its capital is Charleston. It controls much of the coast of South Carolina.


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Welcome to Our Schaumburg Dentistry Practice!
Dr. Amelia Aristodemo-Paul and the team at Happy Smiles Family Dentistry welcome you to our Schaumburg dentistry practice. We've been a part of the Schaumburg community for over 20 years, and we are committed to providing our patients with the affordable dental care and personalized service they've come to expect from us. If you're looking for a Hoffman Estates dentist, our neighborhood dental office is close to you too!
We've designed our practice with your comfort and convenience in mind, from the TVs and blankets in our treatment rooms to the digital technology that allows us to offer the most state-of-the-art care possible. Our experienced dentists offer a wide range of advanced general, restorative and cosmetic dentistry services, including Six Month Smiles® cosmetic braces, an accelerated form of adult orthodontics. We're a truly do-it-all practice, so you won't have to drive all over town to receive the dental treatment you need.
In addition to providing exceptional care and painless dentistry, we also understand the difference a friendly and compassionate team can make in your dental experience. When you visit us, our Schaumburg dentists will get to know you on a personal level and thoroughly discuss your unique needs and goals for your smile. Our entire team genuinely cares about your oral health, and our mission is to help you enjoy a lifetime of healthy, beautiful smiles.
We Look Forward to Hearing from You...
(847) 524-0488
We want to be the Schaumburg dentists your family turns to for quality, personalized care. We hope our website proves to be a useful tool to learn more about our dentists, practice and dental services. Please take a look around the site and contact us with any questions or to schedule an appointment. Talk to you soon!
Conveniently Located in Schaumburg, Illinois
To get step-by-step directions from your location to our office, click on the Google logo in the map above to go to Google Maps.


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Featuring Model Prices and Specifications, plus Reviews,News and Videos.
WE'VE COMBED through the mountain of entries, sorted the wheat from the chaff and found the best submission to our Nokia N96/Need For Speed giveaw...
Interested in a new car? Simply tell us the vehicle you are interested in and we can take care of the rest.
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This is one of our favorite Pick a Part Locations, you see I once lived in Idaho and loved shopping there 🙂
Pick A Part Jalopy Jungle came to be in 1957 and now is considered the biggest salvage yards in Idaho, The massive junk yard has 3 locations. They have most of their clients who provide them with their inventory of vehicles through the Treasure Valley, this parts come to be of high grade and quality that represents their business model.
The supply used auto parts to everyone in between, from collision repair experts to auto traders, insurance companies and repair shops and of course the general public, all of this at an exceptional price that is just a fraction of the price you will pay at the retail store or dealer.
Pick A Part Jalopy purchases all of their vehicles from auctions, towing companies, insurance companies, and the general public. This vehicles come to Pick A Part's yard to be hand picked, drained from toxic liquids, set on stands at the yard and be ready for anyone to pull parts from them. The vehicles that enter the yard have a ID number to track them through the disassemble process and to let you know if the vehicle is in the yard or if it has been crushed. The yard doesn't keep an inventory of parts but they have an interexchange system to help you find another vehicle that may have the part you need.
Pick A Part Jalopy Jungle aids in the effort to minimize pollution to our area. Pull-A-Part employees drain all fluids including oil, antifreeze, brake fluid, washer solvent, power steering fluid, and fuel. Making sure that they are in a safe containment until they are picked up by a registered waste hauler for recycling. Also all batteries, and catalytic converters are removed for recycling.
If you have a vehicle that you want to get rid of, the vehicles doesn't have to be in running conditions, just give Pick A Part a call and they will give you an offer over the phone, they will come to pick up the vehicle free of charge and pay you cash on the spot.
[schema type="organization" orgtype="LocalBusiness" url="http://www.pickajunkyard.com/junkyard/pickapart-jalopy-jungle/boise/" name="Pick-A-Part Jalopy Jungle" description="Pick A Part Jalopy Jungle came to be in 1957 and now is considered the biggest salvage yards in Idaho, The massive junk yard has 3 locations" street="5501 State St" city="Boise" state="Idaho" postalcode="83703" country="US" [email protected] phone="(208) 853-7266" ]
Incoming search terms:
- Junkyard Locator Zip Code
- jalopy jungle inventory
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Place Categories: Junk Yards Near Me and Junkyards Near Me


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Let us know when your receive great advice so we can thank our lawyers and point others with similar questions in the right direction.Got it!
Who holds the will and living trust documents after they are created? Is it kept in the home or in a safety deposit box?
The best place to deposit the original will is with the attorney who drafted it. That way there is no automatic presumption of revocation if it isnt found among the testator's documents. Do not keep it in the safe deposit box because it might contain important instructions which need to be followed before the safe deposit box can even be opened.
This answer does not constitute legal advice and no attorney client relationship has been formed. Before choosing a course of action, it is always advisable to seek the advice of an attorney in your area.Ask a similar question
I believe that the client should have their original documents in their possession and that all successor fiduciaries should know where to find the documents, in the event of an emergency. The attorney can keep a copy, and should. But I do not believe the attorney should keep the originals.
There is room for disagreement on that point, and Attorney Aminov's point about revocation laws is well taken. Those laws only apply if the documents cannot be found, however. I have had cases where family members have gone in and removed documents. As long as copies are available, this does not defeat the intent of the grantor(s).
A safe deposit box is not ideal, because you may not be able to get access, in an emergency situation. But there are ways of making this work, if desired. I usually recommend that the clients keep their documents in a fire-resistant box, at home. The successor trustee should know where to find them. Copies of the DPOA and any medical directives should be on file with the bank and any doctor or hospital where the client would go to, respectively.
James Frederick
*** LEGAL DISCLAIMER I am licensed to practice law in the State of Michigan and have offices in Wayne and Ingham Counties. My practice is focused in the areas of estate planning and probate administration. I am ethically required to state that the above answer does not create an attorney/client relationship. These responses should be considered general legal education and are intended to provide general information about the question asked. Frequently, the question does not include important facts that, if known, could significantly change the answer. Information provided on this site should not be used as a substitute for competent legal advice from a licensed attorney that practices in your state. The law changes frequently and varies from state to state. If I refer to your state's laws, you should not rely on what I say; I just did a quick Internet search and found something that looked relevant that I hoped you would find helpful. You should verify and confirm any information provided with an attorney licensed in your state.Ask a similar question
Both Mr. Aminov and Mr. Frederick give you good advice. You'll notice, of course, that their advice differs from one another -- which is fair, because every attorney brings his own approach to legal issues.
Let me try to give you an answer that is both correct and shows my respect for both of these fine attorneys. Where you keep a will and other estate-related documents doesn't really matter so long as it is in a safe place, provided, of course, that it will be secure in case of a storm or fire. Bank safe deposit boxes are not the best place to keep such documents. Neither is a kitchen drawer.
Whether to allow an attorney to hold on to the originals of these documents is a personal choice. If you do that, be sure to keep a copy at home, and attach a note indicating the name, address, and telephone number of the attorney, and the date that the documents were left with the attorney.
When I hold on to a client's will, it is only with the client's direct consent, and with the client's knowledge that it is being kept in my old, turn-of-the-century fireproof safe.
Good luck to you.
Michael S. Haber is a New York attorney. As such, his responses to posted inquiries, such as the one above, are limited to his understanding of law in the jurisdiction in which he practices and not to any other jurisdiction. In addition, no response to any posted inquiry should be deemed to constitute legal advice, nor to constitute the existence of an attorney/client or other contractual or fiduciary relationship, inasmuch as rendering legal advice involves the ability of the attorney to ask appropriate questions of the person seeking such advice and to thus gather appropriate information. In addition, an attorney/client relationship is formed only by specific agreement. The purpose of this answer is to provide the questioner with general information, not to outline specific legal rights and remedies.Ask a similar question
I agree with Mr. Haber's answer. There are a few reasons I would suggest leaving it with the lawyer, and retaining a copy. If a person passes at home and it is sealed, no one will be able to get to the will until the police unseal the plaace of death. The surest way that your last will(as opposed to a prior) is probated is to leave it with the lawyer. This way, if a relative finds the original will and is not happy with its terms, you can imagine that it may not be locatable. There are many other scenarios under which I would suggest leaving it with the lawyer. However, request a copy. Anytime I send a copy of an executed will to a client, I stamp it with an old fashioned ink stamp on every page: "Original Maintained at Siegel & Siegel, P.C. ......" with my address and phone number. You could never imagine where the copy ends up and who winds up calling me to probate it! Also, like Mr. Haber said, most lawyers have a fire proof vault.Ask a similar question
Except when the copy is misplaced or buried and none of the family members know who the lawyer was. (Or the copy is removed and no one knows there is a Will.) Unless the lawyer is scanning the death notices every day, the lawyer may never find out the client died. There is no fool-proof system. I get calls all of the time, and messages on my listserves asking if anyone knows who the lawyer was that prepared documents for Client "X". Some clients prefer to file the original with the probate court for safe-keeping. That can work, as well. But there are disadvantages, even there. And what if the lawyer dies or becomes incapacitated? It would be a nightmare for whoever is left "holding the vault" to try to locate and contact hundreds of clients to let them know their original documents need to be moved.
This is why I agree with Mr. Haber's answer. Just like car mechanics or doctors, lawyers will all have different procedures and believe in them. No one procedure is right or wrong. It is only an opinon.
I agree. This is one of the many areas where reasonable minds can certainly differ. There are pluses and minuses with each approach.
Wills and estates Estates Wills Trusts Successor trustee Living trust
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Hottest Articles on BWWVisual ArtsWorld.com from 8/24/2014 - 8/31/2014
Below are BWWVisual ArtsWorld.com's most popular articles from 8/24/2014 - 8/31/2014. Catch up below on anything that you might have missed from the past week!
Hottest Articles on BWWVisual ArtsWorld.com from 8/17/2014 - 8/24/2014
by BWW - August 24, 2014
Hottest Articles on BWWVisual ArtsWorld.com from 8/17/2014 - 8/24/2014. (more...)
AxS Festival 2014 to Mix Art and Science in Pasadena, 9/19-10/5
by BWW News Desk - August 28, 2014
Pasadena Arts Council (PAC) is proud to announce AxS Festival 2014 | Curiosity, in diverse venues throughout the greater Pasadena area from Friday, September 19, 2014, through Sunday, October 5, 2014. (more...)
Soho Contemporary Art to Present Rich Simmons' LONDON CALLING, Opening 9/20
by BWW News Desk - August 25, 2014
Soho Contemporary Art introduces artist Rich Simmons in his first solo exhibition in the United States, "London Calling." There will be a private VIP invitation only reception on Thursday evening, September 18, from 7 p.m. to 9 p.m. and a public grand opening on Saturday, September 20, from 1 p.m. to 4 p.m. Rich Simmons will be in attendance for both events. (more...)
Texas A&M University Press to Release KENNEWICK MAN: THE SCIENTIFIC INVESTIGATION OF AN ANCIENT AMERICAN SKELETON
by BWW News Desk - August 25, 2014
Nearly 20 years since Kennewick Man was serendipitously discovered along the banks of the Columbia River in Washington State, the scientific saga of his life and legacy is being released. A new book entitled Kennewick Man: The Scientific Investigation of an Ancient American Skeleton, co-edited by forensic anthropologists Douglas Owsley at the Smithsonian Institution and Richard Jantz at the University of Tennessee, will be published this September by Texas A&M University Press. It provides the most thorough analysis of any Paleoamerican skeleton to date. (more...)
BWW Reviews: MODERNISM IN THE PACIFIC NORTHWEST Offers a New Angle on 20th Century Art
by Patrick Kennedy - August 26, 2014
By drawing on painters and sculptors from outside the modernist mainstream, the Seattle Art Museum delivers an exhibition that is visually ravishing and historically enlightening. (more...)
The Art Institute of New York City's Students and Grads Will Present at Mercedes-Benz Fashion Week, 9/9
by BWW News Desk - August 29, 2014
NEW YORK, Aug. 28, 2014 /PRNewswire/ Fashion designers have a dreamto see their collections on the runway. For 13 Fashion Design students and graduates of The Art Institute of New York City, that dream will become reality at Mercedes-Benz Fashion Week. They'll debut their Spring/Summer 2015 collections in front of an international audience of fashion professionals and journalists, and make their entrance into New York City's vibrant fashion scene. The show will take place on Sept. 9, at 8 p.m. (ET) at Lincoln Center in New York City. (more...)
Weber State University Announces Faculty Exhibition, 9/5
by BWW News Desk - August 28, 2014
OGDEN, Utah, Aug. 28, 2014 /PRNewswire/ The Telitha E. Lindquist College of Arts & Humanities at Weber State University (www.weber.edu/cah) today announced the opening of the Department of Visual Art & Design Biennial Faculty Exhibition on September 5, 2014 at 7 p.m. Weber State University President Charles Wight will be offering remarks during the opening night reception. The exhibition is free and open to the public and will be on display in the Mary Elizabeth Dee Shaw Gallery from September 5 November 15. (more...)
BWW Previews: DENNIS LARKINS at Sacred Gallery in NYC, 'Road Trip to the Fourth Dimension'
by Marina Kennedy - August 25, 2014
'Road Trip to the Fourth Dimension' by Dennis Larkins will be on exhibit at Sacred Gallery at 424 Broadway in New York City from 9/4/14 through 10/31/14. (more...)
National Geographic Photographer James Blair to Present Work at THT
by BWW News Desk - August 28, 2014
James Blair worked as a staff photographer for the National Geographic Magazine for thirty years. He has had more than 45 stories published in the magazine, and more than 2000 of his photos have appeared within its covers. (more...)
The Smithsonian Celebrates Hispanic Heritage Month, 9/15-10/15
by BWW News Desk - August 29, 2014
The Smithsonian invites the public to celebrate Hispanic Heritage Month (Sept. 15 to Oct. 15) through a series of vibrant performances, lectures, family activities and exhibitions at various museums around the Institution. All programs are free unless otherwise indicated. A full calendar of events and information about tickets is available here. (more...)


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What is JotForm?
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We believe that if one user has a question, there could be more users who may have the same question. This is why many of our support forum threads are public and available to be searched and viewed. If you'd like help immediately, feel free to search for a similar question, or submit your question or concern.
Trying to output a report that will automatically updateAsked by WUOT on November 27, 2013 at 02:23 PM
1) I'd like to embed a URL on our web site with the results of a survey. Every time someone hits the "submit" button on the form, I'd like it to update that URL with the new information.
2) I like the looks of the Results when they are outputted to a Google doc. Is there any way to get that same look if I'm not using Google docs (I don't want the people who look at the results to have to log into their Google accts)
Thank you!
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Love Michael Kors - I have liked his designs even before I really got into fashion. Although I don't like his excessive use of furs, as nice as they might look, I still really enjoyed this collection. I thought it was funny how many of the models, both male and female, were wearing leg warmers over their shoes/boots. This was something that I tried last May for fun, so it is a little bit interesting for me to see it on the runway. To be fair, I never tried it over strappy platforms. As well this line wasn't exactly incredibly innovative, I believe I saw over a dozen circle scarves, and I can't tell you how tired I am of those! Every single person on my campus, it seems, has one, and gone are the days when I felt unique wearing mine in Montreal. I did like the deep v-necks, sheer fabrics, tailored trouser, and combination of grays and tans in a single outfit. So for that, I applaud Kors.
I must be in a good mood today or something - but I really liked this collection too. Not going to lie, the graphic prints were a little bit busy for my taste, but if done correctly, could result in an amazing look. I have no doubt that we will soon see many celebrities wearing that mini doll dress around the streets of New York and LA (yellow), and probably at least one of the Olsen twins. If I had the money I would buy the shoes they used in this show in one second - so incredible!
WOW. Ok so this is one of those times when it is really important, if you are in love with fashion, to go see the whole collection! To save space I only post four of the looks for each designer, but there is so much variety that you are doing yourself, AND your opinion of the line, an injustice by only looking at the shots I post. Anna Sui outdid herself in this line, in my opinion, as far as maximalism goes. This notion dates back to a post I did in August, specifically the idea that models can sometimes be nothing more than really pretty clothes' hangers. I wouldn't necessarily advise anyone to wear these pieces all together like the show was styled - but hey, if that's what you like! The colours were very exuberant and eye catching, and the designs on some of these pieces were just stunning! For example, the red tight with an orange asian design on the knee - wow! So cool. I also liked the use of the low heeled mary-janes. Having said that, I don't think I, personally, would ever wear any of these clothes, but they sure are nice to look at! (Save the fur rimmed boots - ick)
Now this is what I'm talking about! The whole collection this season by 3.1 Phillip Lim was just spectacular, and I loved almost every piece; there were, however, a few purple sparkly numbers that I'm not so sure about. Lim used many of the great spring colours: the beiges, and nudes, yet at the same time he artfully integrated the fall/winter charcoals into his pieces. This styling is similar to that of Derek Lam who I also enjoyed very much this week. Some of my favourite looks, though perhaps not all included above, were the flared 70s trouser, the middle-high waisted shorts that resemble costumes from the tv show the Tudors (amazing!), billowy white blouses, butterfly jackets, and front suspenders. Excellent!
What recession? I had to include Oscar de la Renta, simply because he is incredibly divine..usually. This season though, I didn't find myself in awe. Perhaps, like with Anna Sui, it was simply because I would never personally wear any of these clothes. I just thought it was a bit over done, and an overly exaggerated statement of 'hah, I'm luxurious'. I do really find that bright tangerine dress beautiful though. Moreover, although the floor length ball room gown isn't something that ad idem would normally post a picture of, I felt a duty to - it being Oscar de la Renta and all.
-- 1,000 individual American visitors today! Thank you to our wonderful neighbouring readers! 71 different countries, the latest including Slovenia, Luxembourg and the Ukraine. Also, Natalie has been on somewhat of a hiatus lately, but she will be back soon.
|runway shots from style.com
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- The Sounds of Learning
- Rethinking Alzheimer's Disease
- Learning to Walk Again
- Return of the jazz Singer
- New Dean Named
- How to Build a Bigger Brain
- Protecting Med Students from Influences of Pharma
- Chain of Life
- Transplatation Milestones
- More Obesity Blues
- Dr. Daniel Geschwind
- Do No Harm
- The Surgeon Scientist
- Comfort Measures
- Dr. Slamon's Perspective
- Award/Honors
- Rock On!
- A Toast from Classes Past
- Cheers to the Classes of '55-'60, '70, '80, '90 and '00
- Come One, Come All
- Give Back
- Welcome Back, Donald
- Supper Time
- The Dean's Visit
- Visionaries
- Gifts
- Events
- Chairs of Distinction
- Memories of Marwa
The Dean's Visit
DURING THE FALL MAA Board of Directors meeting, Gerald S. Levey, M.D., vice chancellor for UCLA Medical Sciences and dean of the David Geffen School of Medicine at UCLA, gave his annual address. He expressed his pride for the medical school's new Learning Center, the growing number of medical student scholarships, and the school's relationship with Charles R. Drew University of Medicine and Science and the University of California, Riverside, and the extraordinary success of the new Ronald Reagan UCLA Medical Center.
"Over the last 15 years, we have expanded and enhanced our donor base, increased the number of scholarships, added more than 100 endowed chairs, increased National Institutes of Health grant funding almost threefold, strengthened relationships with our colleagues across campus, completed construction of Ronald Reagan UCLA Medical Center and five new research buildings and experienced the exhilaration of Mr. David Geffen endowing and naming the school of medicine," he said. Dr. Levey reported that the school and hospital system are in great shape and that his successor will inherit an "A-team" to manage the large, complicated and dynamic academic medical center.
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03 November 2016 | News | By BioSpectrum Bureau
Japanese firm invests $11.4 mn in TB and malaria research
Singapore: With a view to curb the menace of malaria and tuberculosis(TB), Japan's investment firm, Global Health Innovative Technology Fund (GHIT Fund) has issued funding totaling $11.4 million for six research projects that aim to fight malaria and tuberculosis.
As per the company announcements, nearly $1.8 million will be spent of developing anti-malaria drugs. The research is an on-going project carried out by a partnership between Swiss-based Medicines for Malaria Venture (MMV), a product development partnership in the field of antimalarial drug research, and major Japanese pharmaceutical company Daiichi Sankyo. GHIT Fund has been financing this project since the fund's establishment three years ago, the company said.
Daiichi sankyo said that the research aims to identify and develop new drugs that could cure malaria-infected patients of both Plasmodium falciparum and Plasmodium vivax with a single dose.
Apart from this, GHIT Fund has made two new investments into tuberculosis research. The first was to a research group comprising scientists from Japan, Malaysia, Mexico, and Chile, for the development of an early-stage TB vaccine that would be given intranasally, making it easier to administer and less costly than the standard injectable vaccine.
GHIT Fund has also provided $200,000 in funding for researchers at the Japan-based RIKEN Center for Life Science Technologies and the United Nations' International Center for Genetic Engineering and Biotechnology, who are studying how tuberculosis survives and replicates in humans-particularly in those who, while infected with latent tuberculosis, stay immune their entire lives.
GHIT also said that nearly $7.5 million of the funds will be allocated for malaria research conducted by Japan's largest pharmaceutical company Takeda Pharmaceuticals. The company is working on a candidate for malaria- DSM421 which is currently under clinical trials.
Around $600,000 was allocated to Japan's Mitsubishi Tanabe Pharma Corporation and MMV as part of GHIT Fund's Hit-to-Lead platform, which optimizes the hit chemical compounds that were identified in the screening platform, the company said.


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In Greek mythology Chione (English translation: "snow white") was the daughter of Daedalion. She was very beautiful, and had countless suitors, including the gods Apollo and Hermes. Apollo waited for nightfall and then approached her in the guise of an old woman. Hermes put her to sleep and raped her. She became pregnant with twins, one (Autolycus) the son of Hermes, and the other (Philammon), the son of Apollo. Chione became so vain she compared her beauty favorably to that of Artemis, whereupon the goddess shot and killed her with an arrow. Daedalion grieved so much at his daughter's death that he flung himself down from a peak of Mount Parnassus and was transformed by Apollo into a hawk.
- Ovid, Metamorphoses 11. 339 ff
- M. Grant & J. Hazel. Who's Who in Classical Mythology. David McKay & Co Inc, 1979.
|This page uses content from the English Wikipedia. The original article was at Chione (daughter of Daedalion). The list of authors can be seen in the page history.


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Author | exchange4media News Service | Saturday, Oct 23,2004 8:03 AM
It took the shape of a meeting ground for the who's who of the Indian advertising as most of the ad gurus converged at the Subhas Ghosal Foundation Lecture presented by Rajasthan Patrika on Monday. Author and management consultant Gurcharan Das spoke on the changing trends at a lecture on 'Good and Bad Corporate Behaviour'. Das has held senior positions at P&G, Richardson Hindustan Ltd etc.
On the rising peer pressure and competition in the market, Das said: "The principle of 'karma' is very much applicable in the corporate world." He said that most company officials are competing amongst each other and for real success need to sacrifice their egos.
Rajasthan Patrika was the main sponsor for the programme. UDV India, the Advertising Club, Mumbai, Advertising Agencies Association of India and International Advertising Association also supported the event.
Subhas Ghosal Foundation holds such lectures each year, paying tribute to the brightest advertising personality of India. The foundation promotes values of excellence, aesthetics, business integrity, effective communication and mutual self-respect. The lecture sought to promote self-governance in the industry and urged to uphold values and ethics.
Programming HeadRadio Mango


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Dilip and the breakfast ladies are really nice!
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Great place. I'll stay there in futher ocasions for sure.
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text: I LOOK forward to wakeing up now and not reaching for slow death. I look forward to going to sleep at night without reaching for slow death. I find other BETTER things to replace it.OTHER things that needed to be down Well now my house is spotless LOL from top to bottom and it smells so so fresh in here.MY friends that smoke know not to smoke in my house LOL. I REFUSE TO DO DAY ONE AGAIN. PEACE,LOVE AND RESPECT TO ALL ENJOY YOUR DAY.MY POST ON HERE REALLY HELPS ME.


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Shruti Mishra
my new picture so cute
and this is my old original picture. so boring
as you may see this picture shows teamwork by helping each other from bullies.
they might look a bit alike but there are some changes.
this is my best picture yet and it shows standing up for your-self in a team.
this is my original picture, cool.
real funny and shows alot of teamwork and maybe if this goes well, then looks like these little cute kitties might get a fishy dinner.
and this my original picture


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The chapters throughout this volume illustrate the many contributions of mitochondria to the maintenance of normal cell and tissue function, experienced as the health of the individual. Mitochondria are essential for maintaining aspects of physiology as fundamental as cellular energy balance, the modulation of calcium signalling, in defining cellular redox balance, and they house significant biosynthetic pathways. Mitochondrial numbers and volume within cells are regulated and have an impact on their functional roles, while, especially in the CNS (central nervous system), mitochondrial trafficking is critical to ensure the cellular distribution and strategic localization of mitochondria, presumably driven by local energy demand. Maintenance of a healthy mitochondrial population involves a complex system of quality control, involving degrading misfolded proteins, while damaged mitochondria are renewed by fusion or removed by autophagy. It seems evident that mechanisms that impair any of these processes will impair mitochondrial function and cell signalling pathways, leading to disordered cell function which manifests as disease. As gatekeepers of cell life and cell death, mitochondria regulate both apoptotic and necrotic cell death, and so at its most extreme, disturbances involving these pathways may trigger untimely cell death. Conversely, the lack of appropriate cell death can lead to inappropriate tissue growth and development of tumours, which are also characterized by altered mitochondrial metabolism. The centrality of mitochondrial dysfunction to a surprisingly wide range of major human diseases is slowly becoming recognized, bringing with it the prospect of novel therapeutic approaches to treat a multitude of unpleasant and pervasive diseases.
Mitochondria are the primary providers of ATP in most mammalian cells, they regulate both necrotic and apoptotic cell death pathways, they are intimately involved with the co-ordination of cellular Ca2+ signalling and they both generate and are targets of free radical species that modulate many aspects of cell physiology (see Figure 1). It therefore inevitably follows that disordered mitochondrial function will lead to altered cellular physiology and that this will manifest in disease. In this chapter, we will try to identify some of the major cellular mechanisms which contribute to the pathophysiology of mitochondrial-related disease and to explore the functional consequences of such changes for cells and tissues so that we can better understand the roles of mitochondrial dysfunction as a determinant of the phenotypic manifestations of disease.
At its extreme, we tend to focus on roles of mitochondria in cell death as the major role of mitochondria in disease, and this is without doubt hugely important. However, in this chapter, we will also take a far broader view of the roles of mitochondrial (dys)function in disease. This will include the down-regulation of mitochondrial OXPHOS (oxidative phosphorylation) which accompanies the shift towards a more glycolytic phenotype of neoplastic cells defined as the Warburg shift, indicating that mitochondria play critical roles in many cancers, not only through the suppression of apoptotic cell death, but also through the modulation of mitochondrial metabolism. We will consider changes in mitochondrial trafficking that lead to neuropathic disorders, changes in mitochondrial fission and fusion that seem so important for mitochondrial 'quality control', changes in mitochondrial mass through changes in turnover, i.e. either mitochondria-specific macroautophagy (mitophagy) or altered biogenesis. We will also consider further mechanisms by which altered mitochondrial function may contribute to disease, which seem to be recapitulated repeatedly in many apparently diverse diseases. One repeated theme in mitochondrial pathogenesis is the mitochondrial generation of reactive free radical species such as superoxide or peroxide [often termed ROS (reactive oxygen species)] which may, in turn, impact on Ca2+ signalling, on cell death signalling pathways and indeed on mitochondrial turnover. In many instances, multiple mechanisms may create a cascade of effects that all contribute to disease. Changes in mitochondrial Ca2+ handling may alter the dynamics of cellular Ca2+ signals that are themselves critical in defining cell function and so will lead to impaired tissue function if disturbed, while changes in intramitochondrial [Ca2+] may sensitize mitochondria to injury. It should be clear then that the potential roles of mitochondria in disease, and the array of mechanisms through which altered mitochondrial function may contribute to pathogenesis, are many and varied, and that to understand all of these, we need to understand the fundamental phenomena involved: the mechanisms of biogenesis, trafficking, autophagy, free radical generation and calcium handling, and mitochondria-mediated cell death, most of which are covered elsewhere in this volume.
In order to approach this very broad topic, it is perhaps simplest to consider mitochondrial function in terms of inherited (primary) and acquired (secondary) defects. The first includes disorders in which alterations in proteins encoded by either the mitochondrial or nuclear genome impact on mitochondrial function and so lead to disease. The second category includes disorders in which changes in cell physiology, changes in mitochondrial biogenesis or autophagy, changes in extramitochondrial signals, such as impaired provision of substrate or oxygen, exposure to cytokines, changes in intracellular Ca2+, oxidative stress or exposure to xenobiotics cause mitochondrial dysfunction and so contribute to the progression or outcome of disease. However, many diseases show a multifactorial aetiology and it is difficult to distinguish between the primary and secondary origin of the accompanying mitochondrial dysfunction. We have therefore organized the chapter according to pathomechanisms where they are known and to disease manifestations in those examples which seem more multifactorial.
Defects in mtDNA (mitochondrial DNA) and disease
Mitochondria house their own very much reduced gene pool as mtDNA, packaged into nucleoids [1]. This DNA encodes just 13 key proteins of OXPHOS, along with rRNAs (ribosomal RNAs; 12S and 16S rRNA) and 22 tRNAs (transfer RNAs) required for the synthesis of these proteins [2–4]. Inevitably it follows that mutations will arise, and those which are not lethal will give rise to disease. mtDNA is transmitted through a non-Mendelian maternal pathway and so mitochondrial genetic disease is characteristically inherited through the maternal family line [5]. The genetics are even more complicated, as the majority of mtDNA genetic diseases are heteroplasmic: subjects carry both normal and mutant mtDNA [6,7]. It is assumed that the burden of that mutant load, its partitioning between tissues and the interaction between the nuclear and mitochondrial genomes will define the actual pathological phenotype [8]. However, except for some cases, the exact relationship between genotype and phenotype remains obscure. For example, there is no explanation why one mutation of a complex I subunit gives rise to a disease that causes primarily only optic atrophy developing in adolescence or early adult life {LHON (Leber's Hereditary Optic neuropathy); for a review see [9]}, while another mutation in the same complex may give rise to a severe myopathy, neuropathy and lactic acidosis in early childhood (e.g. see [10]). Pathogenic mechanisms in these diseases also remain poorly understood; most of the diseases affect mostly the CNS (central nervous system) and muscle and this is usually explained by the high dependence of these tissues on OXPHOS, but it is not at all clear that the manifestations of disease are direct consequences of impaired OXPHOS (i.e. in impaired provision of ATP) or whether there are more subtle alterations, for example in free radical or calcium signalling (see below). These issues will be covered in more detail in other chapters in this volume and we simply flag these here for completeness. Recently, several mutations have been detected in numerous cancer tissues, most probably reflecting the anti-apoptotic effect of the mild impairment of OXPHOS (see below).
Defects in nuclear-encoded mitochondrial-related proteins and disease
While mtDNA-encoded proteins are important and mutations at many sites of mtDNA have been identified in association with disease, the vast majority of mitochondrial proteins are encoded in nuclear DNA [11–13]. Indeed, the tissue- or cell-specific differences in mitochondrial structure and function that are long familiar to histologists and electron microscopists must largely reflect differences in the palette of nuclear-encoded, mitochondrial-targeted proteins expressed by specific cell types. Once again, it seems inevitable that diseases associated with mutations of impaired function of these proteins will be identified. The number of nuclear-encoded mitochondrial-directed proteins associated with human disease is rapidly growing (e.g. see http://mitomed.bio.uci.edu/bin/view/Mitomap/WebHome and [14,15]). Most of these genes encode enzymes of mitochondrial respiratory chain complexes, structural proteins required for the assembly of these complexes, mitochondrial transporters and a number of proteins involved in various aspects of quality control of the organelle, as well as its individual protein components. These include structural proteins and large mechanochemical enzymes (GTPases) that control mitochondrial fission and fusion [16,17], chaperones responsible for correct folding of soluble and membrane proteins, and proteases clearing non-functional, damaged proteins, all involved in various ways in maintaining the integrity of the mitochondrial population (for a recent review, see [18]). It is notable that by far the majority of clinical presentations of the various diseases associated with mutations of these proteins involve disorders of the CNS, emphasizing the importance of mitochondrial function in this tissue, although we still understand little of the mechanisms by which changes in these specific functions cause the specific and varied disease phenotypes, nor indeed why these can differ so radically with different mitochondrial mutations.
Mitochondrial 'quality control' and disease: proteases, fission, fusion and turnover
Of the mitochondrial proteins that are involved in mitochondrial quality control, mutations in several have now been associated unambiguously with human disease, in all cases primarily affecting the CNS. These include a number of proteins associated with hereditary (and even some sporadic) forms of PD (Parkinson's disease), hereditary optic atrophy and motor neuron degeneration. Mitochondrial integrity is maintained partly through the activity of chaperones and intramitochondrial proteases that either support protein folding or that remove misfolded proteins [19–22]. These include the Lon protease, which seems to selectively remove oxidatively damaged proteins [23]. Accumulation of oxidatively damaged mitochondrial proteins with age has been attributed, in part, to declining activity of Lon with age, and deletion of Lon from mitochondria increases oxidative cell death, decreases mitochondrial mass and promotes a more glycolytic metabolic phenotype [24]. Another major protein involved in regulation of mitochondrial protein folding is the protease known as paraplegin. Mutations of paraplegin give rise to the motor neuron degenerative disease, hereditary spastic paraplegia [25,26]. This disease is characterized by the degeneration of cortical motor neurons, which begins in their very long axons, suggesting that mitochondrial function at axonal terminals may be critically damaged by accumulation of misfolded proteins [27]. Interestingly, mutations in a mitochondrial matrix chaperone Hsp60 (heat-shock protein 60), also required to maintain correct folding of mitochondrial proteins, also cause an autosomal dominant form of hereditary spastic paraplegia [28], consistent with the suggestion that mitochondrial quality control is critical for maintenance of axons. What remains mysterious, a word we have perhaps already used too often but which remains true, is why global defects in these proteins should give such a very specific phenotypic defect: why do defects in such fundamentally important processes not cause cardiac or liver defects, or even defects in other parts of the CNS? In contrast, another fundamental mitochondrial chaperone, grp75 (also known as mthsp70), which mediates folding as part of the protein import machinery [29] and has been shown to play a role in mitochondrial oxidative damage [30] and cellular senescence [31], is associated with a much broader variety of diseases, ranging from inflammatory and immune disease to cancer [32], in addition to neurodegenerative disease [33].
The dynamic nature of the mitochondrial network also seems to play an important role in mitochondrial quality control. Damaged mitochondria can be either 'repaired' or removed by fusion with neighbouring intact mitochondria [34,35] or by autophagy, which removes the damaged organelles while avoiding the potential catastrophe of the release of pro-apoptotic proteins [36,37]. The difference between these two fates seems to depend on the degree of damage, as severely damaged and fragmented mitochondria will not undergo fusion, but may instead be destroyed. Mitochondria constantly undergo cycles of fusion and fission, a process which is mediated by several highly conserved proteins [34,38,39]. At least four dynamin-related GTPases mediate fission and fusion, a process which determines the shape and extent of the mitochondrial network. Fusion is driven by the mitofusins MFN1 and MFN2 which localize to the OMM (outer mitochondrial membrane) and interact with transport structures such as microtubules. The IMM (inner mitochondrial membrane) protein OPA1 (optic atrophy 1), controls mitochondrial fusion, while fission is triggered by DRP1 (dynamin-related protein 1). Fusion seems to promote intermingling of the matrix contents of intact and dysfunctional mitochondria [40]. Thus replacement of damaged mtDNA may contribute to the integrity of the cellular mitochondrial population. In fusion-deficient fibroblasts lacking OPA1 or the mitofusins, mitochondria showed both a loss of mtDNA nucleoids and impaired mitochondrial respiration, suggesting an accumulation of damaged mitochondria [5,41]. Mutations in the mitochondrial fusion gene Mfn2 cause the human neurodegenerative disease Charcot–Marie–Tooth, a sensory neuropathy [42]. Deletion of Mfn2 from the cerebellum caused impaired dendritic outgrowth, spine formation and cell survival of Purkinje cells, in which mitochondrial distribution, ultrastructure and electron transport chain activity were all abnormal. Thus exchange of mitochondrial contents plays an important role in mitochondrial function and distribution in neurons.
Fragmented and damaged mitochondria can be removed by a mitochondrial-specific form of autophagy; the term mitophagy was recently coined [36]. Studies in yeast have identified ∼30 proteins (Atg) involved in autophagy, many of which are conserved in higher eukaroytes [43]. Deletion of yeast ATG genes causes phenotypes which reflect altered mitochondrial function, including growth defects on non-fermentable growth medium, suggesting a requirement for autophagy in mitochondrial maintenance [44]. Two mitochondrial-specific proteins, termed Uth1 and Aup1, are not part of the general autophagic machinery and have been linked specifically to mitophagy: Uth1 localizes to the mitochondrial outer membrane and Aup1, a phosphatase, to the intermembrane space [45,46].
Accumulating evidence suggests that autophagy is initiated by increased mitochondrial ROS generation [47,48]. This seems to be mediated by the redox regulation of a protein known as Atg4, an essential cysteine protease in the autophagic pathway [49]. Formation of autophagosomes requires the Atg4-mediated cleavage of Atg8 and its conjugation to phosphatidylethanolamine, a lipid constituent of autophagosomal membranes [43]. Antioxidant treatment suppresses lipidation of Atg8 and autophagosome formation, suggesting that lipid conjugation is a direct consequence of ROS production. Increased chronic ROS generation by damaged mitochondria has also been shown to promote autophagy and so reduce the mitochondrial volume fraction in cells in which the protein IF1 has been knocked down [47]. In this model, autophagosome formation and mitochondrial volume were restored by antioxidant treatment. Interestingly, endophilin B1 (also known as Bif-1), first described as a factor in the mitochondrial outer membrane necessary for the maintenance of the organelle structure [50], was later shown to be part of the protein complex forming the early autophagosome [51]. Down-regulation or missense mutations of this protein have been associated with tumour formation [52], again underlying the importance of mitochondrial turnover for cell growth and proliferation.
Mitochondria and neurodegenerative disease
Mitochondrial dysfunction has been implicated in almost all of the major neurodegenerative and neuroinflammatory diseases, including AD (Alzheimer's disease), PD, Huntington's disease, Friedreich's ataxia, motor neuron disease [ALS (amyotrophic lateral sclerosis)] and multiple sclerosis. There are others that have been mentioned already, Charcot–Marie–Tooth and other neuropathies including diabetic sensory and autonomic neuropathy, hereditary spastic paraplegia and others, which are all clearly and directly associated with impaired mitochondrial function. Friedreich's ataxia is caused by a mutation of frataxin, a mitochondrial protein required for normal iron homoeostasis in mitochondria; iron is critical as a component of several parts of the respiratory chain. Yet again, the mystery is why this defect should be specific for the spinal sensory and motor tracts which degenerate, why these axons become demyelinated, and why other tissues do not show major defects (for a review see [53]). Evidence for mitochondrial contribution to pathophysiology of PD is fairly strong, and we will elaborate on this below. In AD and ALS the story is far more complex and, while there seem to be disorders of mitochondrial function associated with both diseases, it is hard to disentangle which of the observed changes are primary and which secondary in the progression of disease. Even if the changes are secondary, it does not mean that they are not potentially interesting as if they contribute to disease progression, they still may represent valuable therapeutic targets (see [54–56]), especially given the lack of satisfactory treatment strategies for these dreadful diseases.
PD is a common age-associated disease, characterized by degeneration of dopaminergic neurons in the substantia nigra which leads to a very characteristic movement disorder. Most patients with PD have sporadic disease of unknown cause, but in a small proportion of patients the disease is familial. In these families, and to some extent in sporadic disease, the disorder has been linked to a number of mutations of proteins which are mostly associated with mitochondrial function in ways that are not yet entirely clear. Mitochondrial dysfunction appears to play a prevalent role in the pathogenesis of the disease [57,58]. Defects of mitochondrial complex I have been specifically and repeatedly associated with PD. Chronic treatment of mice with rotenone, an inhibitor of complex I, where systemic treatment might be expected to cause very general and nasty toxic effects, remarkably leads to a parkinsonian syndrome (one wonders why not a cardiomyopathy for example?). Gene defects in a number of proteins have been shown to associate with PD, including α-synuclein, Parkin, DJ-1, PINK1 (PTEN-induced putative kinase 1, also known as PARK6) and LRRK2 (leucin-rich repeat kinase 2) and HTRA2/OMI [59]. All of these proteins are in some way associated with mitochondria and apparently form part of a cascade of related interacting proteins. Heterozygous missense mutations in HTRA2/OMI have been found in sporadic cases of PD. HtrA2, homologous with bacterial Deg proteases, localizes to the mitochondrial intermembrane space where it is thought to protect against mitochondrial stress. HtrA2 may act to degrade misfolded polypeptides in the mitochondrial intermembrane space or, in analogy to bacterial DegS, be part of an adaptive stress signalling cascade, and HtrA2-deficient mice show neurodegeneration and Parkinson-like phenotypes [60,61].
HtrA2 associates with the mitochondrial-localized protein PINK1, a serine/threonine kinase, mutations of which have also been found associated with PD [62]. PINK1 is required for phosphorylation of HtrA2, which increases its proteolytic activity in vitro. PINK1-mediated phosphorylation has been demonstrated for TRAP1 [TNF (tumour necrosis factor) receptor-associated protein 1], a putative molecular chaperone with significant homology with the HSP90AA1 family [62a]. Overexpression of PINK1 protects cells from apoptosis induced by oxidative stress, while PINK1-knockout cells are more vulnerable to apoptosis inducers [63], suggesting that PINK1 and TRAP1 are part of an anti-apoptotic signalling cascade. We found recently that mitochondrial Ca2+ handling was defective in cells in which PINK1 is knocked down (Figure 1). Thus, following a calcium load, mitochondria were not able to restore intramitochondrial Ca2+ concentration ([Ca2+]m). This was attributed to a defect in the mitochondrial sodium/calcium exchanger which is required for the rapid restoration of [Ca2+]m. As a result, mitochondria quickly became calcium overloaded and cells showed a much reduced threshold for mPTP (mitochondrial permeability transition pore; see below and Figure 1) opening [64], demonstrating what may be a common paradigm – the interaction of a genetic defect with environmental or cell signalling events as a basis for pathophysiology (see below). PINK1 mutations have also been associated with altered mitochondrial fission and fusion when knocked out in Drosophila, while the associated PD-related protein PARKIN has also been related to the targeting of mitochondria for autophagy [65]. It remains a tantalizingly complex field and it is difficult to understand now exactly how these various strands will eventually fit together, but the whole complex tale places mitochondria centre stage in the pathogenesis of a common and serious neurodegenerative disorder that causes havoc in far too many lives.
Mitochondrial dysfunction in aging
The role of accumulating mitochondrial defects as a cause of aging remains highly controversial. There is a widespread belief that mitochondrial-generated oxidative stress and accumulated gene defects may itself cause aging. A recent TV documentary likened accumulated oxidative stress in aging to the oxidation involved in a rusting motor car. It is not at all clear how valid such analogies really are. Through an ingenious strategy, two groups have generated mice in which a mutant PolG (polymerase γ) introduces mutations in mtDNA at an increased rate so that animals expressing this protein accumulate mitochondrial mutations at a high frequency. These animals appear to age prematurely, developing age-related diseases early, losing their hair and greying prematurely [66,67]. This feat of genetic engineering has been met with a mixture of enthusiasm and scepticism. For example both Miller [68] and Khrapko et al. [69] have pointed out that the rate of mutations in these animals exceeds anything seen in aging in real life by orders of magnitude, and that there are other associated pathologies that appear in these animals that might make them sick, with very low red cell counts, intestinal damage etc. It is always hard to be sure when an animal ages or dies prematurely how good a model this is to relate to normal aging as it is always likely that non-specific pathological changes may shorten life.
Extending life span is perhaps more challenging, and this was achieved in the knockout mouse for the adaptor protein p66shc [70]. These animals showed a 30% increase in lifespan and their cells showed a resistance to oxidative stress. Remarkably, the implication is that we all express a protein which normally reduces our life span and drives aging. It also encourages the idea that aging is associated with accumulating oxidative damage.
Mitochondrial damage by changes in cell signalling and local environment
Mitochondria are subject to changes in their local environment, through changes in intracellular calcium signalling, changes in free radicals generated either by mitochondria themselves or by other mechanisms [XO (xanthine oxidase) and NADPH oxidase], and they are exposed to and are sensitive to changes in NO (nitric oxide) as it changes with cell signalling events. These are all part of the normal life of a mitochondrion inside the cell and, under normal physiological circumstances, may act as important signalling mechanisms driving altered mitochondrial function in response to altered cell physiology. The best characterized mechanism here involves changes in intracellular calcium. Once controversial, it is now clear that mitochondria will accumulate Ca2+ in response to a rise in cytosolic Ca2+ during routine cell signalling events: the Ca2+ signals that drive contraction of muscle (be it heart, skeletal or smooth) and the Ca2+ signals involved in secretion or those involved in neuronal signalling all cause a rise in intramitochondrial Ca2+ mediated by the mitochondrial calcium uniporter. Calcium is then returned to the cytosol by a sodium/calcium exchanger (mtNCX). It is now a widely held view that these changes in matrix calcium concentration are largely responsible for the up-regulation of OXPHOS that increases mitochondrial ATP generation in response to the increased demand that will inevitably accompany these physiological events. Ca2+ in the matrix activates rate-limiting enzymes of the tricarboxylic acid cycle, seems to increase ATP synthase activity (although the mechanism remains unclear [71]), and increased cytosolic Ca2+ also increases mitochondrial transporter activity [72,73]. NO will compete with oxygen at complex IV and so may inhibit mitochondrial respiration, especially at the low ambient pO2 that is probably present deep within most tissues [74]. The functional roles of this mechanism during normal NO signalling remains controversial, as does the specific role of intramitochondrial NO generation [75,76]. There is also some evidence that ROS generated by the electron transport chain may be important in some physiological signalling pathways (e.g. see [77]).
The mitochondrial permeability transition and disease
All of these mechanisms may become 'unstuck' during pathological conditions, where the combination of an excessive Ca2+ load, excessive free radical generation sufficient to induce a state of oxidative stress (a much abused term, which specifically implies an excessive oxidation that exceeds the antioxidant capacity of the cell or tissue), or excessive or inappropriate NO generation. The mitochondria under these circumstances seem to act as coincidence detectors, so that a combination of Ca2+ overload and oxidative stress will trigger mitochondrial dysfunction which may be fatal. The mitochondrial mechanism driving cell death under these circumstances is ascribed to opening of the mPTP (see Figure 1). The molecular identity of this pore has been a source of great confusion. Until recently, we thought we knew that this consisted of the ANT (adenine nucleotide translocase; in the inner membrane), VDAC (voltage-dependent anion channel; in the outer membrane) and CypD (cyclophilin D; in the matrix) which binds CsA (cyclosporin A) [78–80]. The roles of ANT and VDAC have been thrown into question by the failure of knockout experiments to prevent mPTP opening [81,82], whereas the role of CypD has been convincingly confirmed using the same approach [83–85]. It seems likely that the ANT is involved somehow in the modulation of pore opening rather than forming part of the pore, although it was established many years ago that the ANT can change conformational state to act as a pore in the presence of raised Ca2+ [86], repeatedly shown also for other inner membrane transporters [87].
At present then, the molecular identity of the pore remains uncertain. Spanning at least the IMM, pore opening causes a complete collapse of mitochondrial membrane potential (Δψm) and the loss of some matrix components, certainly a loss of Ca2+ and, indeed, it seems likely that NADH will also leak from the matrix, silencing respiration. The pore has such a large conductance that neither an increase in respiratory rate nor reversal of the ATPase can counter this leak. It seems that the pore can show brief transient openings which are harmless for the cell [88], but once pore opening is sustained, mitochondria cannot synthesize ATP and will even consume ATP as the ATPase runs 'backwards', and so cell death seems inevitable mostly through collapse of ATP. In cells that have a high glycolytic capacity and which can therefore maintain cellular ATP reserves, mitochondrial swelling and the translocation of pro-apoptotic factors may initiate the apoptotic cascade, although apoptosis induced by classical inducers (such as staurosporine) appears to be primarily independent of CypD and mPTP opening [83].
mPTP opening is inhibited by ATP and promoted by Pi and is most likely to occur under conditions of ATP depletion coupled with Ca2+ overload. These are precisely the conditions that prevail at a time of reperfusion following a period of ischaemia in the heart; at reperfusion, Δψm is restored at a time when ATP is depleted and Pi and Ca2+ are both high. What is perhaps most exciting about the pore is its clear involvement as a decisive event which defines the point of no return in the progression to necrotic cell death and also its modulation by pharmacological agents, classically CsA, while some newer agents are now beginning to appear as mPTP suppressors (see e.g. [89,90]). This raises the potential for therapeutic intervention for major diseases and represents perhaps the greatest translational triumph so far for mitochondrial-related disease. Predicted by Crompton and co-workers [91], protection of the heart by CsA specifically at the time of reperfusion was later demonstrated by Halestrap and others and now this approach is being applied in clinical trials (for a review see [92]). The same scenario of raised intramitochondrial Ca2+ and oxidative stress seems to be repeatedly recapitulated as a pathogenic mechanism. In the CNS a role for the mPTP has also been proposed in ischaemia and in the related glutamate excitotoxicity [93]. Ischaemic injury in the CNS is reduced in the CypD-knockout mouse [83], but evidence for mPTP opening to glutamate toxicity is not so strong and neurons cultured from CypD-knockout mice are not significantly protected from glutamate-induced cell death [94]. In the pancreas there is increasing evidence for a role of the mPTP in acute pancreatitis [95]. A most surprising role for the mPTP has been proposed for two human diseases involving a deficiency of collagen VI (known as Ullrich's Congenital Muscular Dystrophy and Bethlem myopathy) [96]. It is not clear in any way how or why a mutation in an extracellular matrix protein should alter myocyte mitochondrial function, and the findings remain somewhat controversial [97,98]. Genetic ablation of CypD or pharmacological suppression of the mPTP seems to be effective in preventing muscle loss in animal models of the disease and clinical trials are in process in children with this horrible disease [89,99,100].
Role of the mitochondrial ATPase as an ATP consumer: pathological consequences
One issue that has specifically interested us in recent years has been the potential role of mitochondria as drivers of ATP consumption. This paradoxical role is based on the fundamental properties of the ATP synthase. The enzyme is in effect a membrane-bound proton-translocating ATPase which normally runs as an ATP synthase driven by the proton gradient established by respiration. However, it will operate in either direction, depending on the balance of free energies available from the phosphorylation potential and from the protonmotive force. Normally it will run in the synthetic mode, as the intramitochondrial phosphorylation potential is kept low (by the export of ATP via ANT) and the protonmotive force is high. If mitochondrial respiration is compromised, most simply by anoxia/ischaemia, but also by mutations, by secondary oxidant damage, by inhibition of cytochrome c oxidase by NO etc., and the protonmotive driving force fails, the enzyme will operate in reverse, consuming glycolytic ATP and pumping protons. Inhibition of respiration is accompanied by up-regulation of glycolysis, and the proton pumping may sustain or even increase the potential [101,102]. We have seen this mechanism in operation repeatedly in pathological models, in ischaemia in rat cardiomyocytes, Δψm is maintained by the ATPase which is a sufficiently powerful mechanism to deplete cellular ATP and precipitate cell death [103–105]. The reversal of the ATPase and a role in maintaining Δψm is apparent in neurons with knockout of PINK1 (a protein associated with PD; see above), and in transmitochondrial cybrid cells carrying a mutation associated with a MELAS (mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes)-like syndrome [10]. While Δψm is maintained by this mechanism rather than by respiration, especially in the presence of oxygen, it seems likely that ROS generation will be increased, and as the sustained potential will still promote Ca2+ influx it is more likely that mitochondria may become Ca2+ overloaded in the face of pathology and cellular deregulation of Ca2+ homoeostasis. What is most interesting here is that a compound BMS-199264, which selectively inhibits ATPase without inhibiting synthase activity, reduces infarct size in Langendorff perfused rat hearts, suggesting potential therapeutic avenues for dealing with this mechanism [105]. Equally interesting is the fact that the ATPase activity is regulated by a protein, known as IF1 (the gene is ATPIF1), which inhibits this reverse activity. At present almost nothing is known about the relative expression level of this protein in different tissues, or about the regulation of expression, but this again will interfere with the ATPase activity and its contribution to pathophysiology needs further exploration (see [106] for a recent review).
Mitochondria in tumour formation and proliferation
Studies on altered cellular metabolism and mitochondrial function in tumour formation and cancer cell proliferation have recently gained an unexpected momentum, following the recognition of mitochondrial involvement in the development of at least two fundamental hallmarks of cancer: limitless proliferation and evasion of apoptosis [107,108]. Given the role of mitochondria in adapting cellular energetics in response to internal (genetically determined) and external (nutrient supply, metabolic stress) demands, it is perhaps evident that the organelle will also dictate differences between the metabolism of resting and proliferating cells. Glucose uptake is enhanced in many cancers (exploited by diagnostic imaging techniques; [109]), which primarily use glycolysis for energy production in contrast with the greater dependence of their non-transformed tissue counterparts on OXPHOS, even under conditions in which the oxygen supply is adequate to support the more efficient production of ATP by the mitochondria (Warburg effect; [110]). There is now substantial evidence indicating that enhanced glycolysis coupled with increased NADPH formation through the pentose phosphate shunt, and enhanced exit of citrate from the tricarboxylic acid cycle, together produce sufficient amounts of ATP and supply the necessary carbon source for lipid and protein biosynthesis for proliferating cells (for reviews see [111,112]). In addition, enhanced lactate production and extrusion which acidify the extracellular space promote tumour growth and invasion [113].
In his pioneering work Warburg also proposed that changes in the intermediary metabolism of proliferating tumour cells are triggered by primary changes in mitochondrial function, and this is still one of the much debated, and recently intensely studied, questions in the field of cancer metabolism [114,115]. Two lines of evidence support this view. First, both oncogenic and tumour suppressor pathways directly impinge on pyruvate entry into the tricarboxylic acid cycle and OXPHOS, either reducing or enhancing mitochondrial ATP production respectively [116–119]. Moreover, mutations of the mitochondrial genome are frequently observed in tumour tissues [120] and were shown to drive metastasis formation [121]. These changes appear to promote cell proliferation either by promoting the Warburg effect or by enhancing cellular ROS production. However, it should be noted that (i) reduced OXPHOS may be secondary to hypoxia in the tumour environment, mediated by an evolutionarily conserved adaptive pathway, principally implemented by the oxygen-sensing HIF-1 (hypoxia-induced factor 1) [122,123], and (ii) mitochondrial cellular transformation can also be accompanied even by increased OXPHOS (see e.g. [124]). Thus further studies will be necessary to dissect primary and secondary mitochondria-related metabolic pathways in tumour cells with the promise of developing radically new approaches in cancer therapy [125,126].
The relationship between cell death and mitochondrial function is a similarly complex issue that we are just beginning to understand. Mitochondrial dysfunction is usually associated with cell death; for example, when accompanied by cellular Ca2+ deregulation in situations such as glutamate-induced neurotoxicity (see above). Under these conditions, mitochondrial biogenesis can play a protective role, e.g. induced by PGC-1α (peroxisome-proliferator-activated receptor γ co-activator 1α) in neurodegenerative disease [127–129]. However, in cancer cells, the situation seems quite different and, instead, a reciprocal relationship between mitochondrial function and apoptosis has been found in several instances (for a review see [130]). Thus cancer cells, in which OXPHOS is impaired (see above), are more resistant to apoptosis induced either by stress (hypoxia, oxidative stress or nutrient depletion) or by chemotherapeutic agents (see e.g. [131]). This phenomenon could be explained by (i) the double-edged function of certain pro-apoptotic proteins [e.g. cytochrome c, and AIF (apoptosis-inducing factor)], which are required both for maintaining OXPHOS and triggering apoptosis, following their release from mitochondria [132]; or by (ii) the ATP-dependence of the apoptotic machinery [133]. Although none of these mechanisms has been compellingly demonstrated, the further investigation of these pathways holds an enormous potential for the development of alternative strategies in cancer therapy [134].
Mitochondria in diabetes
We have recently published a detailed account of the fundamental role of mitochondria in β-cell death in both Type 1 and Type 2 diabetes mellitus (T1DM and T2DM respectively; [135]). Intriguingly, similarly to cancer, mitochondria appear to represent a pathologically important hub of metabolic deregulation and cell death pathways also in diabetes. Indeed, combined mitochondrial apoptotic and necrotic cell death pathways, induced by cytokines, virus recognition and cellular stress pathways, are responsible for β-cell death in T1DM [136,137]. Furthermore, while mitochondrial dysfunction triggers a similar apoptotic/necrotic β-cell death in T2DM accompanying overnutrition-induced stress [138], it is also responsible for the functional derangement of GSIS (glucose-stimulated insulin secretion), reflecting the central role of mitochondria between glucose provision and insulin secretion [139,140].
Caspase-dependent β-cell apoptosis in T1DM is mediated by the combination of either IL-1β (interleukin-1β) or TNFα with IFN-γ (interferon-γ) [141], but can also be observed due to the induction of cellular stress responses, reflecting altered ER (endoplasmic reticulum) Ca2+ homoeostasis [142] and increased NO synthesis [143], examples of secondary (acquired) mitochondrial dysfunction. This can lead to depletion of the cellular ATP pool, accumulation of AMP, and cell death induction by overactivation of the AMPK (AMP-activated kinase pathway) [144]. Alternatively, apoptosis/necrosis can be induced by the depletion of the cellular NAD+/NADH pool mediated by PARP [poly(ADP-ribose) polymerase] activation and accompanied by AIF translocation from the mitochondrial intermembrane space to the nucleus [145,146]. Similarly, ER stress and NO signalling have also been found responsible for mitochondria-mediated β-cell death in T2DM, but evidence is accumulating that even primary mitochondrial dysfunction can link altered metabolism to the development of at least the Type 2 variety of diabetes [147]. Although the exact nature of the primary mitochondrial alterations has not yet been clarified, mechanisms similar to those that operate in increased OXPHOS-dependent cell death of cancer cells might be relevant in this case. Chronic exposure of pancreatic islets to elevated levels of nutrients induces β-cell dysfunction and ultimately triggers β-cell death, usually requiring both increased glucose and lipid exposure resulting in increased pyruvate supply to the mitochondria [148]. Moreover, this effect appears to be combined with an imbalance between the anaplerotic (pyruvate carboxylase-mediated) and oxidative (pyruvate dehydrogenase-mediated) metabolic routes [149]. Again, how these processes are linked to increased apoptotic sensitivity of the β-cell is poorly understood, but further studies on these fundamental mechanisms will most likely reveal alternative therapeutic targets of the disease.
Mitochondria are fundamental to cell life and to maintain normal physiological function. It is therefore hardly surprising that defects in mitochondrial function that are not lethal will cause disease, and this chapter indicates perhaps the breadth of that involvement and the array of major diseases in which mitochondrial dysfunction is implicated. As we begin to unravel the mechanisms underlying mitochondrial dysfunction in disease and new potential therapeutic targets are revealed, so the prospect of developing new therapeutic strategies becomes closer to a reality.
• As mitochondria are fundamental to cell life, maintain normal physiological function and control pathways to cell death, defects in mitochondrial function cause cellular dysfunction or death underlying a wide range of diseases.
• Mitochondria-related diseases can be triggered by inherited (primary) and acquired (secondary) defects in organelle function.
• Mutations of both nuclear and mitochondrial DNA encoded proteins are the cause of primary mitochondrial diseases, following Mendelian or maternal inheritance patterns respectively.
• Secondary mitochondrial diseases may result from impaired mitochondrial quality control. These include disorders of intramitochondrial protein folding, degradation, mitochondrial fusion and fission, and selective mitochondrial autophagy.
• Both primary and secondary mitochondrial dysfunction manifest as altered intermediary metabolism of carbohydrates, lipids and proteins, redox imbalance and the tendency to undergo mitochondrion-mediated cell death (outer membrane permeabilization/apoptosis or permeability transition/necrosis). Together these lead to a failure of the cell to cope with environmental and intrinsic stressors.
• Mitochondrial dysfunction underlies a wide variety of diseases including muscle and neurodegenerative disease, cardiovascular diseases, diabetes and cancer, providing an important potential therapeutic target for many current major diseases.
G.S. is supported by the Parkinson's Disease Society (Project Grant number G-0905), and work in the laboratory of M.R.D. is supported by grants from the Wellcome Trust and Medical Research Council.
- © The Authors Journal compilation © 2010 Biochemical Society
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text:
The History Of Bingo And Some Tips
Yelling "Bingo" at a church social or in a VFW hall gives most people a wave of excitement as we find that we've won a game of this age old sport that dates clear back to the 16th century. But when did it come to the U.S. and why is this game so popular?
How did Bingo got started in the U.S?
Bingo actually derives its roots from a game invented by Edwin S. Lowe, a New York toy salesman who invented a similar game called Beano. When Lowe introduced the game of Beano to his friends, the story goes that one player got so thrilled, she yelled "Bingo," and that's exactly what was called since that time.
Bingo became popular within the U.S. throughout the 20th century, and was quickly
adopted by churches and other clubs because it did wonders for fund raising. Players would purchase a Bingo card or two and win a prize or money if they matched a row of numbers called out by the Bingo caller.
U.S. Rules of Bingo
Bingo is a fun game just to play and can be played by people of all ages. Bingo isn't hard to play. Each card contains 25 little boxes in five rows of five and at the top of the card is the word BINGO, with a letter for each of the top five boxes. Under the letters are random numbers and there is a free space box in the center of the card. It's said that there are more than 9,000 possible combinations of numbers, so no two cards are identical.
Then, throughout the game, a caller spins a wheel full of little Bingo balls with numbers written on them. He then reads off the number and if your card has it, then you mark it off. The instant you have the proper pattern of numbers marked off that win the game, you are expected to yell out, "BINGO!" and you are declared the winner if your card has got the proper numbers marked.
Playing Bingo Tips
Playing Bingo can be very fast paced and here are several useful tips and hints on how to do a better job playing this fun game:
Sit Near the Bingo Caller – Sitting nearby where the numbers are being called can help so that you can hear him straight away and never miss a single chance at matching a number and completing a winning Bingo pattern.
You can disregard the numbers written on the left side of a square – This saves time, for example, if the caller yells B12, then you should look for twos first then check to see if the other number is there afterwards.
Look closely at your card for any patterns – In the heat of the moment you may not see a winning Bingo, so be sure to watch carefully for the right pattern that could win the game.
Pre-mark spaces you don't need – If the winning pattern is a special kind, then you can pre-mark all the spaces you are sure that won't be used in a different color than the ones that can win.
Don't play way too many cards at the same time – One other essential hint would be to not get greedy and try to play a lot of cards at the same time. This may only make it so you could miss a winning number and lose the game.T
All in all, Bingo is a very fun game that will not simply be played as a fund raiser, but may be played at your house as a great way to socialize with your friends.
Gamble Aware (www.gambleaware.co.uk) is managed by the Responsibility in Gambling Trust, an independent charity which funds treatment, research and education about responsible gambling. The website has been developed by a Task Force made up of representatives from the Gambling Commission, DCMS, academia and industry.


text:
Life as a pregnant father is a little scary and a lot wonderful. On one hand, what's going on seems totally out of your control. On the other hand, there is such joy in knowing that you helped make a baby! And, as a man, people expect you to be strong and macho, but there's so much to worry about and so many feeling that you'd like to share. There's just so many emotions to go through - not too stereotypically manly, I guess.

When I found out that my wife was pregnant, I went ballistic. Even though we'd been trying for two years to have a baby, and even after all the miscarriages, I was mad. Real rational, huh? I just wanted to give up after all we'd been through so far. It took a few days for it to sink into my oh-so-very thick skull that this was a good thing. Then I was happy. Well, mostly happy.

Then, I had to worry about things like, "Gee, is it okay to have sex with my wife, or is it going to hurt the baby? If I wasn't careful, would that child be born with a dent in the top of it's head?" Well, fortunately, common sense, and plenty of reading assured me that this was not going to happen. Which brings me to my next point.

Men: Do your homework! Read pregnancy books, and attend childbirth classes with your wife. My personal recommendation for a good book for the men to read would be The Birth Partner by Penny Simkin. It's pretty neutral about how you should have your baby (natural or not; in a hospital, birth center, or at home) and will certainly give you an better idea about "what to expect" than a certain other book.

Childbirth classes really helped me a lot. It helped me be more in tune to what's going on. And, they gave me more of a clue about what was to be expected of me at the birth. All my wife really wanted to share with me is how much she wanted to puke all of the time, but when we got to class and could focus more on the pregnancy, I did get a better feel for the whole process. It really feels good to be a part of your child's life, even before it arrives.

I don't know about other men, but I spent entirely too much time worrying about everything. Robin was ready to kill me every time she ate. She knew I was thinking about how much protein, vitamins, minerals, and fat she was getting. I couldn't help wondering if she was getting enough fat and protein to grow the baby's brain. Okay, so I worried too much. That's part of being the daddy.

We just want the best for our babies! They're a reflection of who we are. So, even though we might drive the moms a little crazy sometimes by being the "food police," it's only because we care. The moms can live with that, because the daddies' hearts are in the right place.

When it comes to the actual birth, just be prepared and educated. Of course, you should be prepared for just about anything. There's no telling what might happen. But, remember that it is important for you to be strong. You can be most helpful by being supportive. Make sure that you and the mom discuss, in great detail, how you want the birth to go. If she tells you beforehand that she doesn't want an epidural, even if she's in pain and screaming, "Give me drugs now!", then you will know not to grab the anesthesiologist at the first sign of discomfort. Even better, write down the intentions you two have in a birth plan. If it's in writing, and your doctor approves, you'll be much more likely to get your way in the hospital or birth center.

Oh, and when my pregnant wife looked at me with a hateful look and screamed, "You did this to me, it's all your fault!" just remember what she really means is, "I love you and I'm so happy to be having your baby!"


text:
Data entry data processing simple data entry jobs
Customer Service Rep/Office Assistant Type: Full-Time Reports to: Owner Experience: 1+ year Closing: ASAP Who are we? Our company owns a variety of e-commerce properties including brick-and-mortar. We run multiple online ecommerce stores in the sporting, hunting, camping industry. We are fast growing and a well-established company of over 30 years. The Job. Looking for an ...
Financial market data analysis and processing
Are you someone who likes doing research and wants to earn some extra money by doing data processing? Then this is the project for you! We are looking for people to help us gather some data to support our fast growing company! The project will be temporary and paid for a certain number of addresses. What will you be doing? - Researching stores
My project requires skills like Natural Language processing and Case based [url removed, login to view] for more details.
looking for researcher on image processing. must have publication record and passion to work on timely manner.
we want a such project in c# using emgu API which takes a microscopic images from the saved data set an on the base of their shapes etc it will decide weathers its a healthy cell or nor
I need you to develop some software for me. I would like this software to be developed for Mac using Python. Intelligent project for data scientists in healthcare systems
I have a written an Information Memorandum which i need to make look more professional - with appropriate spacing, heading and subheading sizing, column widths etc. I am hoping to have the work done over the next 12 hours
Image processing expert is required for analysis of shape and size of any material.
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1) I need to install SDR sharp into matlab or beable to run rtl-sdr in matlab. 2) I need to be able to fm demodulate the live software defined radio frequency signal, and be able to record the demodulated frequencies audio. 3) I need to beable to load audio files into matlab, and beable to fm demodulate them. Then record or save the demodulated audio into a separate file.
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data manage data entry data analyse and more
A. Implement 10 (separate) MATLAB functions to calculate the following measures of central tendency for greyscale test image Lena. You must not use pre-built libraries, but are encouraged to use vectorized code (rather than loops), where possible. In addition to reporting the results for Lena, you will test your functions for alist of values for which the statistic has been calculated manuall...
...improvements of design and selected components. - Consultant shall provide feedback assessment and how to improve design for manufacture. Expertise Required: – Signal Processing – Circuit Design – Knowledge of Delta-Sigma ADCs Inputs: – Schematic (High-Resolution + Eagle) – Board Layout (High-Resolution + Eagle) – BOM Deliverables: &nd...
60$ matlab image processing project..pattern recognition or neural network
[url removed, login to view] Here is the site where you can find SDK for VeriFinger. Where you can find a software VeriFinger when you will run this software it required a Finger print. after successful image load it will show a processed image. Need to built a software which can be save all finger print images into processed images.
...for a very well organized, professional, virtual assistant to assist in processing customer orders, data entry, customer service and support, and sales related tasks. MUST speak EXCELLENT english, have a FAST internet connection for remote connections to complete data processing tasks, and make/receive calls to the U.S. This is a FULL TIME position.
We need to process Echeck on offline payment gateway on our magento store. Thanks
Are you someone who likes doing research and wants to earn some extra money by doing data processing? Then this is the project for you! We are looking for people to help us gather some data to support our fast growing company! The project will be temporary and paid for a certain number of addresses. What will you be doing? - Researching stores


text:
Jared Allen
October 25, 2010 by staff
Jared Allen, The least possible scenarios related to Green Bay today's game the Packers, Minnesota Vikings, and, fans dressed in green and gold to turn the pages of a new book by Jared Allen, probably ranks somewhere between sprint Jermichael Finley in the players tunnel after the onset of curing Reggie White-style and Deanna Favre sent a personalized copy of "The Cure for chronic life of Jenn Sterger.
But despite his dismissal of Aaron Rodgers antics as an excellent defensive end the Packers' most hated rival, Allen also shares much in common with orange flames from the masses who have been known to fill the cup of Lambo.
That's why – if you can, just for a moment – forget the countless times he played conclusion calf-rope bag last year, Allen believes you can not only find your new boldly titled "Defender murderer Cookbook helpful. You are – gulp – maybe even enough love.
"Oh, I know they love me there," said Allen, laughing, when asked that his stay would be Packers fans. "But forget football. If you like hunting, if you like a game, pick up the kitchen."
Big game hunter who has killed from Canada to New Zealand and even went to hunt wild pigs in Texas is nothing but a knife, Allen is not one to retreat from the problem. That is why the self-proclaimed "redneck" and "adrenaline junkie" is not ashamed to share his philosophy in a cookbook that is part biography, part manifesto and part summary of the recipe.
"I've always been a big supporter of that kill you," said Allen. "I thought it might at first be just a cookbook, but then I started thinking that we should write some stories with the recipes and really make a good read. I want people to get something from it, especially some of the humor.
"After going through the other cookbooks, you tend to see the same thing. You know, marinate the meat of wild animals, this kind of thing. So I told the co-chef (Aaron May), we the church to some of these recipes and give to all this is a completely different style. "
Along with May – the chef's favorite restaurant, Lodge of Allen, his offseason home in Scottsdale, Arizona – two joined forces in a series of culinary mixtures, including meatloaf buffalo, wild boar ragout with Fettuccine, Spice Wild Turkey Frittata, cocoa crusted venison sauce and brown sauce Pheasant Nuggets Allen Field, the main house he describes as "a version of chicken Maknugdzhets man."
The recipes are mixed with stories of parents Allen (he calls his father and grandfather, "the two men is more pronounced in the planet") and his appreciation for the art of cooking. It also includes the classic Allen-isms like, "Mallett helps when hunting animals because they think you're one of them" and "Anyone who thinks the kitchen is not manly, it's probably offensive lineman."
Allen also said not a great cook, just a master griller. At home, his wife does most of the kitchen, but Allen admits he would like to learn more about the techniques of cold or complex mixtures of spices, including "taking a semester at Le Cordon Bleu."
Of course, Allen has already caused confusion by claiming that he participated in a fiction "Culinary Academy" during the presentations on-screen player for NBC "Sunday Night Football." Incidentally, he received a degree in sackology Idaho. His love for food just a consequence of his greatest passion, not football – to be outdoors.
"People probably think:" Oh, play football. I know you are going hunting, "but this is just the opposite," said Allen. "I find comfort in the forest. This is my time to sit and think and just look around."
As for spreading the Gospel murderer quarterback Green Bay Packers Allen assured fans that also serve as hunters to get some of his book – even if the cover photo is for darts. You can even throw in a stocking stuffer at Rogers, if he happens to have a clean shot today.
"Yes, definitely I have a copy with me in the field," said Allen. "No, I'm not sure Aaron Rodgers is a hunter. I do not think that hunting is his style. Maybe we will cross over it."
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