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Wednesday, March 5th, 2014
just a li'l taste of a new Nik Furious jam I'm working on…
r a w f u n k y s h * t.
just a li'l taste of a new Nik Furious jam I'm working on…
r a w f u n k y s h * t.
On last Friday's episode of Animatic Attack (the AudioShocker's animation podcast), I snuck in a special opening theme — my new Nik Furious song, Jackpot.
The song is a Valentine's Day gift I made for Justique. This year was our seventh Valentine's Day together, so riffing on the lucky number theme I decided to name the song Jackpot because when I met Justique I hit the jackpot!!!
The music starts at about 3:20 into the episode. It's a mellow instrumental funk jam with a slow go-go style drum beat, fat fretless bass, squealy synths, and acoustic guitar. I hope you dig it!
(FYI, be forewarned… AudioShocker conversation is always NSFW!)
Thanks to everyone who backed the crazy Love & Monsters comics and music anthology on Kickstarter.
It was a real nail-biter but we passed our funding goal with less than 24 hours to go and even reached a couple of stretch goals before things wrapped up last night.
I truly appreciate your support. I've had a lot of fun working on my Nik Furious cuts for Love & Monsters and I can't wait for you to hear all of the finished songs.
In case you missed 'em, you can listen to three of the six Nik Furious songs that you'll receive as a backer of this project:
– Wet-On-Wet
– Rare Tear demo
– Don't Stop demo
Props to Cynthia Lee, who organized and ran the campaign. There was a while there where I thought we might not make it, but she was confident in her plan and made sure that we finished in fine form.
I've got plans for a special solo Kickstarter campaign (both comics and music again) in 2014, so get ready for a li'l more crowdfunded fun from me next year!
Listen to the demo version of my Nik Furious song "Don't Stop" recorded for the upcoming Love & Monsters comics and music anthology:
This song takes its inspiration from a story by Shawn Atkins.
The anthology is currently funding on Kickstarter and there's only one week left to become a part of our project!
When you back us, you'll get this demo version plus the final full band version of Don't Stop AND more Nik Furious original instrumental songs like Rare Tear.
Listen to the demo version of my Nik Furious song "Rare Tear" recorded for the upcoming Love & Monsters comics and music anthology:
This song takes its inspiration from a story by Virginia Shields.
The anthology is currently funding on Kickstarter. When you back our project, you not only get this demo version but the final full band version as well AND more Nik Furious original instrumental songs!
We want you to be a part of this exciting anthology so click the link, check it out, and become a backer of Love & Monsters if you like what you see and hear.
I'm creating original songs for the Love & Monsters anthology on Kickstarter.
It's a comics and music anthology featuring four incredible cartoonists and three kickass musicians (including yours truly!). I'm proud to be a part of this collection because it blends mediums and genres in a really fun, thoughtful way.
I think you're gonna dig it too!!! And I need your support to make it happen. Pop over to the Kickstarter campaign and pick a pledge level that makes you and your wallet happy.
Here's me talking about why I love making instrumental theme music and why I'm stoked to be a part of this project:
I'm creating music for stories by Shawn Atkins and Virginia Shields, two of my favorite people AND favorite cartoonists!
Shawn's story is a crazy sci-fi music adventure featuring an underwater battle of the bands with robots, monsters, and more.
One of the songs I've crafted for Shawn's project is called Wet-On-Wet and you can listen to it now.
Virginia's story is about a romance between unlikely forest creatures.
I've already completed a crazy synthed-out jam for her story that I think you'll love, especially if you dig my other tunes like RAW or Destruct-O-Groove.
I need your help to make Love & Monsters into the biggest and best anthology that it can be. A few bucks goes a long way towards making it happen, and that's why I need your support on Kickstarter! Thx 😀
13 original instrumental songs. Electronic, surf, funk, rock, and more.
Each song on 7 Star Sky Flash Kick has a special story behind it. I'll be sharing those stories with you and adding them to the tracklist below as I go. I changed my mind! Though the stories are awesome, I'd rather spend my time making new songs than writing blog posts about ones I've already made 😉
7 Star Sky Flash Kick tracklist:
01. Adamantium 2:28 (mp3) (artwork) (history)
02. Da Bounce 3:20 (mp3) (artwork) (history)
03. Destruct-O-Groove 8:51 (mp3) (artwork) (history)
04. Dora Milaje 1:42 (mp3) (artwork) (history)
05. Egg Shaker 3:01 (mp3) (artwork) (history)
06. Intra Venus 1:48 (mp3) (artwork) (history)
07. Nazo 7:09 (mp3) (artwork) (history)
08. Never 1:54 (mp3) (artwork) (history)
09. Philly Right 2:57 (mp3) (artwork) (history)
10. Smells Like Cupcakes 5:34 (mp3) (artwork)(history)
11. Sultry Storm 2:04 (mp3) (artwork) (history)
12. Synthezoid Rock 4:15 (mp3) (artwork) (history)
13. Zero 2:32 (mp3) (artwork) (history)
• Download the 7 Star Sky Flash Kick ZIP file (47:30, 75 MB)
• Listen to 7 Star Sky Flash Kick on SoundClound
• Watch the 7 Star Sky Flash Kick album sampler video:
The songs on this album were written and recorded between 2003-2013. A few of them have been released with older mixes and different names. Many of them are theme songs to podcasts produced by myself and my friends including Comic Book Pitt, 3 Chicks Review Comics, and various shows on AudioShocker.com.
The album cover is a collaboration between myself and my incredible girlfriend, Justique Woolridge. She created a painting inspired by the title. I scanned in both the front of it and the paint-smudged back…
…and then I layered both of them on top of each other in Photoshop and altered the colors to produce the final album design.
The album is named after one of Chun-Li's moves from Marvel vs. Capcom. Here's what the 7 Star Sky Flash Kick looks like in the video game:
Finally but most importantly, a lot of people have supported me, inspired me, and helped me create these songs. Thanks to Justique, Ed Marino, Jennifer Marino-Gabrielli, Josh Kobylarz, Dan Greenwald, Kelly Thompson, Ross Campbell, Scott Niekum, Kaylie McDougal, Neal Shyam, Brian John Mitchell, and Shawn Atkins.
I often forget the process of building a beat once it's complete. Even though most of my songs and remixes take hours to create, once a song is finished my memories of the process float off into the aether.
But that's not the case with Wakanda. I remember the arduous cutting that it took to make the sample of D'Angelo's solo piano demo of Africa line up with my digital drums and synth bass.
It was the winter of 2004-2005. I was living in Brooklyn and sitting around my room sweating in my underwear because all of the building's pipes ran through my apartment. The heat was annoying but it was a good problem to have because it gets fucking cold in NYC!
The version of Africa used in this remix wasn't officially released at the time. It'd leaked and made its way onto Limewire, the popular pirating software of the day.
Though I was working on tons of beats at the time, Wakanda stands out because it required a degree of precision that I'd never used before. D'Angelo's performance here is loose and raw, not set to a perfect rhythm. That fluidity made it impossible to neatly line up some digital drums and quickly turn out the beat.
Basically, while creating Wakanda I taught myself how to make micro-edits to audio and alter the speed of a song without destroying the music or making it sound choppy. Once you figure out how to do this sort of thing, it's just a matter of practice. But until that time, it seems like some kind of unimaginable magic (especially in the pre-YouTube days where tutorials rarely found their way online).
My name for this remix has a pretty simple story behind it. In Marvel Comics, Wakanda is the fictional African nation ruled by the Black Panther. It's one of my favorite pieces of Marvel lore and a worthy moniker for this beat, which I think carries a lot of emotion and elegance.
This track was also used for a dirty NSFW rap song by the Unlicensed Attorneys at Law. Don't click the link to that song unless you think you can handle it! Otherwise, just forget about it. Trust me.


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Prospective Students
Prospective Students
The Middle Eastern Studies Program (MESP) is an interdisciplinary area
studies program, comprising faculty members drawn from the social
sciences, humanities, and natural sciences within the School of Arts and
Sciences. It offers a major and a minor in Middle Eastern Studies, as
well as courses on the history, politics, cultures and religions of the
Middle East. The MESP also organizes and sponsors a range of social,
cultural, and educational events related to the Middle East, in
conjunction with the Center for Middle Eastern Studies (CMES), ensuring
an informative and immersive environment at Rutgers to study the region.
Students majoring or minoring in the program will benefit from a wide
array of Middle Eastern Studies resources at Rutgers. There are 91 core
courses which fulfill non-language credit for the major and minor, which
are regularly offered by MESP itself, the Department of African, Middle
Eastern and South Asian Languages and Literatures (AMESALL), Art
History, History, Jewish Studies, Political Science, Philosophy, and
Religion. In addition, MESP also cooperates closely with AMESALL, the
Department of Jewish Studies, and the Armenian Studies Program to offer
instruction up to the advanced level in a number of languages of the region,
such as Arabic, Armenian, Hebrew, Persian, and Turkish. In total,
Rutgers-New Brunswick regularly offers a total of 152 courses of
interest to students of the Middle East, including 32 language courses.

subset: commoncrawl


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Dispatches From LeConte Hall 323
In a few minutes, I'll go upstairs to the third floor of LeConte Hall and start another term of my HIST3150 - Religion in American History course. I'm teaching two sections of it this time around, one in the morning, one in the afternoon, and, for the most part, it's a redesigned course.
Earlier, I wrote here about my reflections on the course's purpose and pedagogy and, with the blessings of this blog's big kahuna, we've decided to invite y'all along for the ride.
So, over the next fifteen weeks, in the moments I have away from the dissertation, I'll send in regular dispatches from LeConte Hall 323. By opening the door to my classroom, I hope to offer an inside look at how my students and I are working through my "uncoverage" survey of American religious history. Student privacy, of course, will be maintained, but I'll try to be as honest as possible about what I see as the course's successes and failures. I don't intend these dispatches to be an exercise in narcissism or catharsis, but rather an informal and informative way to discuss publicly the ins-and-outs of teaching religious history in university classrooms today. As such, I welcome your thoughts and reflections on my thoughts and reflections.
FYI, the course's website is here.
Darren's Uncoverage Course in American Religious History -- Part 1 of Many!
Categories: deg's posts, pedagogy, syllabi, teaching philosophy, teaching resources
Posted by Paul Harvey
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text: This article is a stub. You can help Animal Database by expanding it. For a list of families, see families. A Family (plural: families) is a taxanomic rank in Linnaean classification, the rank above it is Order and the rank below it is Genus. Retrieved from "http://animals.wikia.com/wiki/Family?oldid=3649" Ad blocker interference detected! Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers Wikia is not accessible if you've made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected. Categories: Article stubs Classification Add category Cancel Save


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Story updated at 9:50 a.m. with market information.
NEW YORK (TheStreet) -- Credit Suisse lowered its price target for Mondelez (MDLZ) to $35 from $37 following the company's fourth-quarter results and lowered guidance.
Shares of Mondelez gaine 1.3% to $33.65 in morning trading Thursday.
The analyst firm maintained its "neutral" rating for the company, but also lowered its estimates through 2015.
The firm wrote, "Following MDLZ's rather messy 4Q results, we are lowering our target price to $35 to reflect an 18x P/E multiple against our 2015 estimate of $1.88 (down from $1.92). We are lowering our 2014 EPS estimate to $1.68 (down from $1.71), which represents the middle of management's EPS guidance for 2014 (including 7c FX headwind)."
Separately, TheStreet Ratings team rates MONDELEZ INTERNATIONAL INC as a Buy with a ratings score of B-. TheStreet Ratings Team has this to say about their recommendation:
"We rate MONDELEZ INTERNATIONAL INC (MDLZ) a BUY. This is driven by a few notable strengths, which we believe should have a greater impact than any weaknesses, and should give investors a better performance opportunity than most stocks we cover. The company's strengths can be seen in multiple areas, such as its revenue growth, increase in net income, largely solid financial position with reasonable debt levels by most measures, increase in stock price during the past year and impressive record of earnings per share growth. We feel these strengths outweigh the fact that the company shows weak operating cash flow."
Highlights from the analysis by TheStreet Ratings Team goes as follows:


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"Atos Origin selected by Sabeco to develop its Intranet"
Zaragoza - May 12th, 2004
Atos Origin, a leading international information technology services company, announced today that it has been selected by the food distribution company Sabeco to develop and implement its corporate Intranet.
This initiative is part of Sabeco's strategic plan to introduce new technologies into key business processes. Its objective is to establish a common access point to the information system for all users, both local and remote; thus fully integrating its offices into the corporate system.
Atos Origin has developed the solution using the Oracle Portal tool on the Oracle 9i platform. The portal will bring together the communication, news, centre search modules and related links. It will also provide access to marketing, human resources, and document management applications (which include all the company's documents with multiple search criteria). It will also establish a profile system and access rights to stored information and implement workflow procedures to control new document and information approval processes. Solutions for any new needs will be incorporated in the portal as they arise, thus providing fast and consistent feedback for all of Sabeco's internal departments.
This project will provide Sabeco with multiple benefits, including a unified work environment, the integration of documents used by the different lines of business and departments, the update of information in a distributed manner, or immediate availability of newly created documents. The search and control of the documents approval processes will also be streamlined, saving time and providing greater flexibility.
# # #
About Atos Origin
Atos Origin is an international information technology (IT) services company. Its business is turning client vision into results through the application of consulting, systems integration and managed operations. The company's annual revenues are more than EUR 5 billion and it employs 47,000 people in 50 countries. Atos Origin is the Worldwide Information Technology Partner for the Olympic Games and its clients include ABN AMRO, Akzo Nobel, Alstom, BNP Paribas, BP, Ericsson, EDF, Euronext, Fiat, France Telecom, ICI, ING, KPN, Lucent, Philips, Renault, Royal Bank of Scotland, Saudi Aramco, Schlumberger, Shell, Telecom Italia, UBS, UK Department for Work and Pensions, Unilever, Vivendi Universal and Vodafone.
Atos Origin is quoted on the Paris Euronext Premier Marché and trades as Atos Origin, AtosEuronext, Atos Worldline, Atos KPMG Consulting and Atos Odyssée.
About Sabeco
Sabeco S.A. is part of the Auchan Group, leader in food distribution, with 122 establishments, and more than 6,000 employees in 9 autonomous Communities in Spain.
Press Contacts
Antonio Ferreiro
Tel: +34 91 214 89 15
Anne-Marie Capilla
Tel: 33 1 55 91 26 62


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Listen to free music
Blip.fm is internet radio made social. It's easy to search for, play, and discover free music recommended by real people. Join today to create your own free station.
Matericia Staten Island was one of the worst hit by #Sandy #StatenIslandStrong #RebuildSI http://www.buzzfeed.com/mjs538/the-spirit-of-staten-island
Bruce Springsteen – Death To My Hometown| play
Nov 6, 2012 at 2:26 pm via YouTube | AMAZON | ITUNES


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Kurt Cobain
Biography Project for Mrs. Hemry's 8th grade Language Arts class
Kurt Cobain was born on February 20, 1967 in Aberdeen, Washington and died April 5, 1994
Significant Events in History that Affected Kurt's Life
The Grunge Movement
Kurt's Childhood
When Kurt was 8, his parents marriage began to fall apart. His mom and dad divorced in 1975. In 1978, Kurt began to pick on his stepbrother and as a response, Kurt's dad began to beat him. Kurt was always being passes around to one family member to another. Around that time, Kurt began to cut classes and skip school entirely. Six weeks before graduation, Kurt dropped out of school.
People who Influenced Kurt's Life
His mother, Wendy Cobain, came from a very musical family.
Kurt's uncle was in a rock band
Unique Facts
- Diagnosed as Hyperactive.
Didn't like his fame.
Died at age 27, as did Jim Morrison, Jimi Hendrix, and Sid Vicious.
Married Courtney Love on February 24, 1992.
He was in trouble with the law a lot.
Was in Nirvana
Perfected Grunge
Won 10 awards and 25 nominations
Won Best Alternative Music Performance
Heart-Shaped Box won Best Alternative Video and Best art Direction
The Theme of Kurt's Life Was...
To never give up and try as hard as you can to get what you want. Even though things seem tough now, they will always get better.
Works Cited
Gracie, Andrew. Kurt Cobain. Philadelphia, PA: Chelsea House, 1998. Print.


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I collect old English film posters. I have framed the posters of the film Godfather and a few other films, and put it up on the walls of my house.
I am very proud of my DVD collection and love to flaunt it to my family and friends. I also enjoy travelling. I often pack my bags and head to a new place for some adventure and good food.


text:
You are here
Relocation Tips
How can I lighten the load of relocating?
No matter how excited you are about your new home—or new geographic location—relocating can be burdensome. Check this list of common sense and insightful suggestions for ways to make moving to your new life easier.
1. Give yourself plenty of time to arrange for movers.
You not only want to shop for a good price, you also want to make sure it's a bona fide business, not a scam. Check references. And call the Better Business Bureau to get a report on the moving company you use. Even if the company name sounds familiar, be diligent and pay a visit to their headquarters. Sometimes a bogus company will use a name reminiscent of a well advertised mover to give clients a false sense of security. If the company doesn't welcome a visit to their facility, call someone else.
2. Make a "to do" list and post it where the whole family can make additions and check off accomplished tasks.
Give assignments to the whole family—teens on up—to lighten the load on yourself. It will also make everyone feel they're doing their part.
3. Clean up and throw out as you pack.
Don't move a lot of stuff that's going to end up at a thrift shop anyway. And if you're having your things professionally packed, make labels ahead of time that will help movers identify where things go on the other end. Jane's clothes. Jimmy's athletic gear. John's office papers. Etc.
4. Keep important papers with you.
Don't ship them. Things like passports, birth certificates, bank statements, licenses should all travel with the family, not with everything else.
5. Do not ship fine jewelry, stocks and bonds, bank notes and the like.
Keep them on your person.
6. Alert utility companies at the new and old house of your termination/start date.
7. Submit a change of address form to the post office.
Be sure to advise banks, insurers and publications of your new address, remembering that it can take a month or two for them to catch up with data entry.
8. Install phones
It's best to have phones installed sooner rather than later. You want to be sure to have service on hand when you arrive, even though you may have cell coverage as well.
9. If you're moving to a new jurisdiction, be sure to register your car and get inspections taken care of right away.
Not doing so can mean costly tickets and a rude introduction to your new community.
10. Prep your pets.
Be sure that your pets are in good health, clean, flea- free and have any prescribed medications they may require before you travel. You won't want to have to find and visit a new vet in your first few days at your new home.. Many pets can become unnerved by all the hubbub of a move, so be patient with them. They're going to miss their old home, too.
11. Give it back.
Return your library books, your friend's sweater, your neighbors rake, your sister's Tupperware.
12. Get it back.
Try to remember the things you've loaned out or left at service businesses and get them back. Things like dry cleaning, shoe repairs, appliance repairs, safe deposit items, the earrings you loaned your sister. Be politic in your requests though. No need to sour a relationship over something you've lived without all this time.
13. Take your medicine.
Be sure you have plenty of prescribed medications (packed with your personal items), important medical records, vaccination verifications for the kids, and, if possible, recommendations for doctors in your new location.
14. Just in case…pack a small suitcase with "must have" items you'll want handy when you arrive.
Include things like batteries, tooth paste and brushes, shampoo, combs, kids toys, pet food, canned soups and easy-prepare food stuffs, a pan, paper plates and cups, simple tools, a knife, candles, light bulbs, a transistor radio, a telephone, a knife, a first aid kit.


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What is JotForm?
JotForm is a free online form builder which helps you create online forms without writing a single line of code. No sign-up required.
At JotForm, we want to make sure that you're getting the online form builder help that you need. Our friendly customer support team is available 24/7.
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.
I've created 2 virtually identical forms and integrated them to support uploads of results to Google Drive, but I'm getting different results.Asked by sjsusalzburg on October 23, 2015 at 08:46 PM
One form uploads properly - results from each entry include 2 files in a single folder.
The other form uploads a single folder, but there are no files in the folder. However, I can access the files by clicking the download button on the folder and then manually drop copies of each file on the folder. This works, but involves extra steps and time.
Given how well Jotform works, this seems crazy. I've tried deactivating the latter integration settings and starting over, but to no avail.
Any suggestions. Anyone I can call to discuss?
Bill Reckmeyer
JotForm Support
Hello Bill,
Unfortunately, we do not have phone support available but we'll do our best to assist you here on support forum.
So far I am unable to reproduce the problem. Mine goes through on both form. May we know if you have already re-integrated the cloned form? Doing this will create another integrated folder, so files should go on different folder for both forms.
May I suggest to re-integrate both form to Google Drive if necessary then run a test on both form, this should help. Most problems with integration can be resolved by re-integrating the form.
Feel free to update us the result. Thanks!


text:
Aaron R. Kristopeit, PGA
Main Address:
4001 NE Grand Blvd
Oklahoma City, OK 73111-5400
(405) 424-1421
Oklahoma City, OK 73111-5400
Oklahoma City, OK 73111-5400
Graduate of Mississippi State University's Professional Golf Management Program. Past places of employment include The Woodlands Resort & Country Club, Hillwood Country Club (Nashville, TN), Sea Island Golf Club, Quail Creek Golf & Country Club (Oklahoma City), and Oklahoma City Golf & Country Club. Currently the Head Golf Professional at Lincoln Park Golf Course in Oklahoma City. Worked with and for some of the best golf professionals in the country, including three instructors within Golf Digest's Top 50 in America, as well as multiple Golf Professional of the Year award winners within their PGA section.
Services Offered:
- Instruction
- Trade-In Network
- Club Fitting
- Play Golf of America Participant
National Awards
- 2010 PGA President's Council on Growing the Game
- 2009 PGA President's Council on Growing the Game
- 2008 PGA President's Council on Growing the Game
- 2007 PGA President's Council on Growing the Game
PGA of America Championships
Quail Hollow Club
Charlotte, North Carolina
Le Golf National
Guyancourt, France
Olympia Fields Country Club
Olympia Fields, Illinois
Trump National Golf Club
Washington, D.C.


text:
prabhas theme song....GIVE ME THE WAY(rebel) MP3
prabhas theme song....GIVE ME THE WAY(rebel)
The Rebel Fleet Theme MP3
This is a cut from The song at the end of the Empire Strike Back. And for my good friend Tony :) Enjoy~
Star Wars Throne Room Theme Song MP3
Rebel Alliance / Alianza Rebelde (Old flag / bandera antigua) MP3
Rebel Alliance National Anthem (fictional, Star Wars) "The Throne Room" (John Williams) Himno Nacional de la Alianza Rebelde (ficción, Star Wars)
Rebels Theme (Flux Pavilion's The Ghost Remix/From "Star Wars: Rebels"/Audio Only) MP3
Catch new episodes of Star Wars Rebels beginning Monday October 13th at 9/8c on Disney XD! Download and stream "Rebel's Theme" below Download: ...
Final Fantasy II - Rebel Army Theme (Orchestrated) MP3
I cut it off the "Distant Worlds" FF 1-3 medley song. It stands well on its own. The whole medley can be found here: ...
Stars Wars (Rebel Alliance Theme) - Banana Acapella Version MP3
I like bananas and Star Wars and so should you. On iTunes! - http://smarturl.it/DavidChoi Facebook! - http://facebook.com/DavidChoi Tweet Me!
Star Wars Rebels Soundtack: Title Theme MP3
Star Wars Rebels Original TV Soundtrack. Music composed and conducted by Kevin Kiner. Original Star Wars themes and Score by John Williams. All rights ...
Star Wars Rogue Squadron III Soundtrack - Rebel Strike Title Theme MP3
The Spiderman 3 of the Rogue Squadron Trilogy, slightly enjoyable yet ultimately far inferior to its predecessors.
Scott Dunn conducts the Main Theme from the Rebel without a Cause Suite MP3
March 2nd, 2009 at 8 pm, Skirball Center for the Performing Arts NYU SYMPHONY Scott Dunn, conductor MUSIC AND MOVIES: THE LEONARD ROSENMAN ...
The Rebel Johnny Yuma Theme Song II Classic MP3
Subscribe to this channel, new vintage commercials are added daily!The Rebel Johnny Yuma Theme Song II Classic.
WWE: Wade Barrett New Theme 2013 "Rebel Son" (Longer Version) [CDQ + Download Link] MP3
Download Link: mp3: http://www.sendspace.com/file/p372b2 m4a: http://www.sendspace.com/file/sravge Buy on iTunes: ...
rebel telugu movie theme song ''Give Me The Way'' MP3
FF2 - Rebel Army Theme (PSP Version) MP3
The theme of the Rebel Army theme from ff2.
The Rebel Johnny Yuma Intro and Ending theme ( Original ) MP3
The Rebel Johnny Yuma Original Intro.
A New World - Final Fantasy II - Rebel Army Theme MP3
Full Album Name: A New World: Intimate Music from Final Fantasy Composed by: Nobuo Uematsu, Masashi Hamauzu, Kumi Tanioka, Hitoshi Sakimoto ...
Final fantasy II OST - Rebel army theme 11 minute loop MP3
One day I was searching for a bigger version of this song... I failed .__. So.. I made one myself :D Hope you like it, If you like the song you can download it with ...
Theme Song to The Rebel MP3
Song from the CD: "Television's Greatest Hits Volume II." *See video for copyright and ownership info." More to come! Thanks for watching! Bye!
FF2 Symphonic Suite Rebel Army's Theme MP3
ファイナルファンタジーⅡ - 反乱軍のテーマ # FF2 - Rebel Army Theme MP3


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Spicy Chicken Vindaloo
Be the first to review
READY IN: 45mins
Recipe by By The Lake
Spicy chicken vindaloo is a delicious Indian curry recipe that tastes amazing with naan, raita, or steamed basmati rice. It is spicy so make sure you have some yogurt or something on hand to take the heat away if you're not used to spicy foods.
See Discussion:
Ingredients Nutrition
- 3 cups chopped red onions
- 1 1⁄2 cups chopped seeded tomatoes
- 2 1⁄2 tablespoons distilled white vinegar
- 2 large garlic cloves, chopped
- 1 teaspoon minced peeled fresh ginger
- 1 teaspoon tomato paste
- 1 teaspoon garam masala
- 1 teaspoon ground turmeric
- 1⁄2 teaspoon paprika
- 1⁄2 teaspoon ground cumin
- 1⁄2 teaspoon ground coriander
- 1⁄4 teaspoon cayenne pepper
- 2 tablespoons canola oil
- 6 skinless boneless chicken thighs, cubed
- 1 1⁄2 lbs new potatoes, peeled, cut into cubes
- 1 1⁄2 cups low-salt chicken broth or 1 1⁄2 cups water
Directions See How It's Made
- Mix your first 11 ingredients and 1/4 teaspoon cayenne pepper in processor until a smooth paste forms. Heat your canola oil in a mid sized non-stick pot over medium-high heat. Add your paste from your processor and cook until just shy of brown, stirring for about 4 minutes. Add your cubed chicken and cubed red potatoes; simmer about 6 minutes.
- Add you chicken broth and raise it to a boil. Reduce your heat to medium-low; cover and let cook until potatoes are softened, stir every so often, this should take about about 15 - 20 minutes.
- Uncover your pan and saute until your cubed chicken is completely cooked, about 5-7 minutes. Serve over basmati rice, raita or naan, and enjoy your spicy chicken vindaloo.


text: According to Raul Miller: > I think that eventually we'll have to have a page detailing where we > haven't been able to reconcile our views: Basically, for each > example, a link to the license, and a statement defining where we > differ. I suspect you're right. The OSD is an explicit enumeration of requirements, while reedom is an amorphous, ever-changing concept -- and no two people see it quite the same way. -- Chip Salzenberg - a.k.a. - <firstname.lastname@example.com> "When do you work?" "Whenever I'm not busy."


text: Anyone try these yet (actually don't know if they're available yet.) New compact design can go up against a wall. No unions necessary because the whole inner section is removable with a couple screws. http://www.zurn.com/operations/wilkins/pdfs/specsheets/BF-375(sm).pdf Took a sample apart at the distributor... looks like good engineering to me. R.P.P.s are required within 3 feet of the water meter here for a dedicated landscape meter (office complexes, medical buildings, shopping ceneters, condos, etc.) Most guys will use them on single family residences too, just because if you're on a slope it's usually easier and less expensive than running the mainline to the top of a hill... D.C.V.s aren't readily available and generally not used. But oddly enough, I come across a lot of DIY installations with A/S valves below grade or even in boxes below grade. I'm replacing 12 valves on a job next week were the gardener installed a dozen A/S valves at the bottom of a slope to run a whole backyard. This on a $3.5 M residential property. Funny thing is, he didn't realize there was already an R.P.P. protecting the system (hidden behind a hedge).. main problem is the dumping thru the A/S valves of all the water left in the laterals after every run... I think I'll take photos and post 'em. Gnats and mosquitoes seem to love it.


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Charlize Theron, American, Wide Awake on Letterman
Charlize Theron, American, Wide Awake on Letterman
It's black, it's white, it's Charlize Theron's blazer collection outside Letterman yesterday. The Sleepwalking star stopped by to visit Dave last night, looking gorgeous as usual. Charlize talked about recently becoming an American citizen — congrats! — and her recent time up in Boston getting her Hasty Pudding Woman of the Year award while "completely wasted." Fun times. Of course, she also touched upon that movie of hers and what it was like to film in 57 below zero. Brrrrrrr.
To see more of Charlize just
0previous images
-17more images


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Musical Indulgence #6:
Christmas Week Edition
Between 1977 and 1980, Elvis Costello recorded four sessions for Radio 1 eminence John Peel.
Each session consisted of four songs.
On all four he was accompanied by The Attractions.
All four sessions constitute today's offering.
This was posted by Tom Sutpen
|your thoughts:
The series is: Musical Indulgences
3 comments:
With this post of Elvis in his prime, this is now officially my new favorite blog. The Dylan WBAI show was a nice companion to the recent New Yorker profile of Bob Fass, too.
I discovered you through a link to that Pauline Kael talk from '63, and you keep pulling more rabbits out of the hat.
Thanks much....
- December 27, 2006 10:04 PM
- Tom Sutpen said...
You are welcome! Keep visiting these shores and we'll try to make it worth your while (along with everyone else).
- December 28, 2006 1:25 AM
- Blind said...
I didn't even know audio was available on this site, I have only visited a few times to muse over the imagery. Thanks for the Elvis!
- December 28, 2006 3:46 PM
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My friend and I had a wonderful time at this beautiful and friendly riad. Fantastic location to walk through the souks, with great restaurants close by. The staff are excellent, and on hand to help with anything we needed. Owner John is a real character, and we enjoyed our chats with him over breakfast! Rooms and beds extremely comfortable, with great bathroom and showers. The roof terrace is also a highlight - great place to relax in the sun. We will definitely come back and would highly recommend to all!
- Official Description (provided by the hotel):
- Riad Elizabeth is an elegant and chic riad located in the heart of the ancient medina of Marrakech. An oasis of style and a calm refuge from the feverish pace and excitement of the souk.British-owned Riad Elizabeth offers modern comfort and facilities whilst maintaining an air of exotic Moroccan charm and romance.The riad offers six en-suite bedrooms, each tastefully and individually furnished to a high standard. For your comfort, all rooms are equipped with controllable air conditioning/heating as well as crisp Egyptian cotton sheets, complimentary toiletries and an iPod dock. Just a short walk from the Medersa Ben Youssef and Musée de Marrakech, Riad Elizabeth provides everything needed to make your stay in Marrakech enjoyable and relaxing. ... more less
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- Also Known As:
- Riad Elizabeth Marrakech
- Riad Elizabeth Hotel Marrakech


text:
Vinyl Mastercut Records & More
Usually Master Records are only used as the expensive "mother cut" in the production of regular, pressed, records. We at SUPERSENSE are proud to cut these highest quality sound treasures for you here in Vienna at our Living Room studio one by one. Without any digital interference, compression or compromise in real time with all our expertise and passion. Please have a look at our services and our EDITION 77, selected artists recorded direct-to-disc at SUPERSENSE
Visit our Living Room Recording Studio and see how we hand cut Master Records →


text:
Buttons / Tiny Snowmen / Light Ice Blue Silver Snow Handmade Button Notions
Tiny snowman buttons, handcrafted by Phydeaux! Lightweight and perfect for your delicate hand knits, Phydeaux buttons are handmade by me in my forest studio in the Northern California mountains.
These sweet little snowmen are handmade in a one of a kind unique pale icy blue, marble with silver, snowy white, and pale aqua, with washes of iridescence. Perfect for the holidays!
Each button takes days to create, from initial mixing of polymer clay with paints and resin and fine glitter and other inclusions, to curing to antiquing to hand sanding with eight increasingly fine levels of sandpaper and finishing with three to four levels of buffing and two final levels of polishing to create a glassy, glossy shine.
Your buttons will arrive in a pretty bright pink organza bag tucked into a sweet little kraft paper pillow box, topped off with a bow. Ready to give as a special gift - even if to yourself.
▶ Two tiny snowman shaped buttons: blue, silver, white, pale aqua marbled with a glaze of pearly iridescence
▶ 1" (2.5 cm) high
▶ Polymer clay, acrylic paint
▶ Water resistant, not waterproof: clean with damp cloth and immediately buff dry
▶ Not safe for children
© 2016 Phydeaux Designs & Fiber


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(320) 274-8211
Lundeen Brothers, Inc.
86 years in business870 Elm St E
Annandale, MN 55302-1152
Fax Numbers
- (320) 274-8217
Additional Phone Numbers
- (320) 274-8569
- (800) 457-8969
Additional Email Addresses
- email@example.com
Find a Location
BBB File Opened: 12/05/2000
Business Started: 04/30/1931
Business Started Locally: 04/30/1931
Business Incorporated: 04/30/1931 in MN
Type of EntityCorporation
Business Management
- Vincent Lundeen, CEO
- Doug Kelm, General Manager
- Kermit Lundeen, Vice President
Business Category
- Auto Dealers - New Cars
- Auto Dealers - Used Cars
- Auto Parts & Supplies - New
- Auto Customizing
- Auto Detailing
- Auto Renting & Leasing
- Auto Repair & Service
- Brake Service
- Wheel Alignment, Frame & Axle Service - Auto
- Auto Services
- Auto Services - Oil & Lube
Service AreaTWIN CITIES METRO - 11 COUNTY
According to the information provided by Lundeen Brothers, Inc. this company offers new and used automobiles, specializing in Fords, appraiser, parts and service.
BBB Reason for Ratings
Licensing information is provided in the BBB Business Profiles to inform the public about industries that may require professional licensing, bonding, or registration. Better Business Bureau encourages you to check with the appropriate agency to be certain any requirements are currently being met.
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BBB promotes truth in advertising by contacting advertisers whose claims conflict with the BBB Code of Advertising. These claims come to our attention from our internal review of advertising, consumer complaints and competitor challenges. BBB asks advertisers to substantiate their claims, change ads to make offers more clear to consumers, and remove misleading or deceptive statements.
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BBB reports on a company that is out of business for three years from the date the company closes its doors or ceases to do business.
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BBB reports on a business's bankruptcy as long as the business remains in bankruptcy.
Mail Returned
BBB reports when mail sent to the business was returned by the Postal Service.


text:
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Rainy day in Titusville Florida I am now here 100 % fulltime in fact I own a home here and I am currently doing renovations big DYI guy I am listening to pandora radio and just working away. Give me a reason to take a break ........
Ready to make new friends that may lead to more hope to here from you . Let's meet for lunch .........kidding ?
Take care
If you are interested please do not just " like " me I am flattered but
I am not an upgraded member and I cannot see who you are . Please send me a little note I will respond I promise........thank you
Now on to the good stuff ........wink wink 😉
It is just me the hottest less than average looking guy you will ever meet ? Let's let that marinate for a bit till the smile washes over your face.......... (Well I think I have a good sense of humor) I am originally from Boston and I recently moved to Phoenix for a job transfer but months later I was merged out after 14 years ..... I have switched careers and settled in Florida to be closer to my widowed elderly Mom and to start a new career still in the logistics field ( I am/was a professional driver ) yes the big 18 wheel kind I have to put in 1 full year driving all 48 states which I have now completed so I can then apply for a local job where I can be home much more often to hopefully build a good life with maybe ........YOU !!! ;-) .........looking for a lady who wants to be good friends,part of a team and hopefully more.
I am just trying to make it in the world and maybe find that one special girl who wants to take the journey with me .........very loyal , very honest !!!........almost to a fault. Kind of a hopeless romantic with a slightly kinky side 😈. I am fun ..........please be honest .......I am very open minded. I can deal with ANYTHING and I mean ANYTHING if you tell me upfront, just be honest ! That is how trust is built right ?
Trying to keep hope alive that the right lady is out there.
Learning to stop and smell the roses once and awhile.
Trying to be a good person to all it is all about Karma baby !
Give me 1 week with anything and I can become good at it .
Movie=The Godfather
TV shows =24, Curb , X-Files,
Music = All types ....Chill R+B music ( Maxwell, etc etc)
just to name a few, remember I am pretty open minded
Warm weather
Family of any type......it's alittle more involved we'll talk
BONUS can't live without item = giving long warm oil massages ..........always learning but you'll love the effort ☺


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We have recently reported that Pdx1-Cre-mediated whole pancreas inactivation of IGF-I gene [in pancreatic-specific IGF-I gene-deficient (PID) mice] results in increased β-cell mass and significant protection against both type 1 and type 2 diabetes. Because the phenotype is unlikely a direct consequence of IGF-I deficiency, the present study was designed to explore possible activation of proislet factors in PID mice by using a whole genome DNA microarray. As a result, multiple members of the Reg family genes (Reg2, -3α, and -3β, previously not known to promote islet cell growth) were significantly upregulated in the pancreas. This finding was subsequently confirmed by Northern blot and/or real-time PCR, which exhibited 2- to 8-fold increases in the levels of these mRNAs. Interestingly, these Reg family genes were also activated after streptozotocin-induced β-cell damage and diabetes (wild-type T1D mice) when islet cells were undergoing regeneration. Immunohistochemistry revealed increased Reg proteins in exocrine as well as endocrine pancreas and suggested their potential role in β-cell neogenesis in PID or T1D mice. Previously, other Reg proteins (Reg1 and islet neogenesis-associated protein) have been shown to promote islet cell replication and neogenesis. These uncharacterized Reg proteins may play a similar but more potent role, not only in normal islet cell growth in PID mice, but also in islet cell regeneration after T1D.
- pancreatic islets
- DNA microarray
- gene-targeted mice
- insulin-like growth factor I
insulin-like growth factor I (IGF-I) is produced from hepatocytes and many other cells and tissues, including the pancreas (9, 14, 23). Acting through its receptor IGF-IR, which is expressed ubiquitously, IGF-I promotes cell proliferation and growth and inhibits cell apoptosis. In normal growth of the bone, muscle, reproductive systems, and the whole mammalian organisms, IGF-I plays an irreplaceable, essential role (25, 33). In cultured cells, IGF-I causes pancreatic islet β-cell mitogenesis in a glucose-dependent manner via activation of phosphatidylinositol 3-kinase (PI3K), ERK1/2, and 70-kDa protein S6 kinase (p70S6K) (15, 24). Although IGF-I and IGF-IR are normally expressed in both endocrine and exocrine pancreas (8, 9), their in vivo role in islet cell growth has been questioned by the results of most gene-targeted studies. For example, combined inactivation of insulin receptor and IGF-IR genes in early embryos results in a 50% decrease in the size of the exocrine pancreas without affecting the development of endocrine cells (19). Combined ablation of IGF-I and IGF-II genes results in an identical phenotype (19). Moreover, islet β-cell-specific inactivation of IGF-IR gene causes no change in β-cell mass despite hyperinsulinemia, glucose intolerance, and a decrease in glucose-stimulated insulin release, suggesting that IGF signaling is not essential for normal growth and development of the pancreatic islets (20, 52). Our own research of liver-specific IGF-I gene deficiency (in liver-specific IGF-I gene-deficient mice) suggests that IGF-I exerts an inhibitory effect on islet cell growth, albeit indirectly through controlling the release of growth hormone from the pituitary (53, 55). More surprisingly, inactivation of pancreatic expression of IGF-I gene [in pancreatic-specific IGF-I gene-deficient (PID) mice] increases islet β-cell mass and renders mice resistant to the β-cell damage that occurred in both T1D and T2D models (26). These effects are unlikely to be caused directly by the deficiency of IGF-I, an undisputed growth factor. In an effort to reveal potential mediators of islet cell hypertrophy and/or hyperplasia in PID mice, we performed a DNA microarray analysis of pancreatic RNA prepared from control mice, PID mice, and both after streptozotocin-induced β-cell damage. As a result, multiple members of the Reg family genes were upregulated and seemed to promote islet cell growth, protection, and/or regeneration. Reg family proteins have been known for years; e.g., Reg1 [pancreatic thread protein (PTP), pancreatic stone protein (PSP)] stimulates islet cell proliferation/regeneration (45, 47); islet neogenesis-associated protein [INGAP; INGAP-related peptide (rp) Reg3δ] promotes β-cell neogenesis from pancreatic ductal cells (35, 38). Consequently, five new members of the family (Reg2, -3α, -3β, -3γ, and -4) have been discovered (1, 22, 27, 56); three of them (Reg2, -3α, and -3β) exhibited elevated expression in our PID mice. Increased Reg2 and Reg3β levels have been reported in human and rodent T1D (4, 13). Transgenic Reg3β stimulates hypatocyte growth (41). Although not yet directly known for promoting islet β-cell growth and regeneration, the mRNA levels of these previously uncharacterized Reg proteins exhibit significant increases under the two conditions of islet overgrowth and regeneration, much more than Reg1 and INGAP, the two known growth factors. In this report, we present subtype-specific quantification of mRNAs and some evidence on the localization of the Reg proteins.
Animal procedures.
On a hybrid C57BL/6 × DBA background, mice homozygous for IGF-I/loxP carrying the Pdx1-Cre transgene (L/L+; PID mice) were crossed with L/L− mice (lacking the transgene; control mice), and the resulting offspring, females only, were used in experiments. This was based on our previous report that, although both male and female PID mice showed similar extents of islet enlargement, female PID mice exhibited more complete resistance to streptozotocin-induced diabetes. The protection in male mice was only partial (26). Genotypes were determined using a double-PCR strategy, as described before (26). The animals were maintained in 12:12-h dark-light cycles at room temperature with free access to food and water. At the desired age, the mice were anesthetized with a cocktail of ketamine-xylazine-acepromazine and killed by cervical dislocation. For streptozotocin-induced islet cell damage and diabetes, PID mice and control littermates, 3 mo old, were injected daily for 5 days with streptozotocin (80 mg/kg qd ip; Calbiochem), prepared fresh as a 0.8% solution in 0.1 M sodium citrate, pH 4.5 (26). This dose of streptozotocin causes a significant loss of β-cells and 90% reduction in serum insulin levels. When the control mice became diabetic by 15 days, they were killed for the purpose of performing pancreatic RNA analysis and histology. All animal handling procedures were approved by the McGill University Animal Care Committee.
RNA isolation and Northern blots.
Total RNA was isolated by acid guanidinium isothiocyanate-phenol-chloroform extraction (5). To minimize RNA degradation, control, PID, control-T1D, and PID-T1D mice were anesthetized, and their pancreases were dissected and homogenized immediately. After centrifugation, the aqueous phase was mixed with 1 vol of isopropanol and passed through RiboPure glass fiber filter cartridges (Ambion no. 1924) for purification. The RNA quality was confirmed using Agilent's Bioanalyzer. For Northern blot analysis, 10 μg of total RNA was subjected to electrophoresis and transferred to positively charged nylon membranes (Roche Applied Science, Penzberg, Germany). Antisense RNA probes were transcribed from mouse Reg1, Reg2, Reg3α, and Reg3β cDNAs (27, 48) and from the pTRI-β-actin-mouse vector (Ambion, Austin, TX), by use of a digoxigenin RNA labeling mix (Roche). The membranes were hybridized to probes overnight at 68°C in DIG Easy Hyb solution (Roche) and washed according to the manufacturer's instructions. To detect the chemiluminescence signals, the membranes were incubated with alkaline phosphatase-conjugated antibody against digoxigenin (Roche) for 30 min. The substrate CSPD (Roche) was applied for 10 min before the membranes were exposed to BioMax light films (Kodak) for 10 min. The intensity of the hybridization signals on the autoradiogram was analyzed using a FluorChem 8900 imaging system (Alpha Innotech).
Oligonucleotide microarray analysis.
Two samples of pancreatic RNA from each of the four groups of mice (control, PID, control-T1D, and PID-T1D) were used for microarray analysis, each pooled from three individual animals to minimize variability. From each sample, 5 μg of total RNA were used for the microarray experiment. Affymetrix GeneChip one-cycle target labeling and control reagents kit was used according to the GeneChip Analysis Technical Manual, Rev. 5 (Affymetrix, 2004). The target cRNAs derived from each sample were hybridized to the Affymetrix GeneChip Mouse Genome 430 2.0 array. The chips were stained and washed using the GeneChip Fluidics Station 450 and visualized on an Affymetrix GeneChip Scanner 3000. The image files were processed using the GeneChip Operating Software, which calculates "signal" values and provides "detection" calls that are "present," "marginal," or "absent" for each probe set. Only genes with a detection call present in both control and PID duplicates were subsequently used for comparison. The result was processed using the Robust Multichip Average system, which involves a probe-specific background correction, a probe-level multichip quantile normalization, and a robust probe set summary of the log-normalized probe-level data (16).
Real-time and RT-PCR.
One microgram of pancreatic RNA from each mouse was transcribed into first-strand cDNA using M-MLV Reverse Transcriptase and oligo(dT)12–18 primers (Invitrogen). Real-time PCR was performed using ABI 7500 System (Applied Biosystems) with ABI certified Reg3β [pancreatitis-associated protein (PAP)], Reg2, β-actin TaqMan primers and Universal PCR Master Mix, following the manufacturer's instructions. Five individual samples were amplified from each group in duplicates. The results of each sample were normalized using β-actin. Fold change was determined on the basis of comparative cycle threshold values for all duplicates and converted into signal log ratio. RT-PCR was performed using Reg3α (forward sequence: GTC ACC TTT GTC CTG ACA AAC C; reverse sequence: TTA CTC CAC TCC CAT CCA CC; length: 420; melting temperature (Tm): 58°C) (27) and INGAP-rp (Reg3δ; forward sequence: CTC ACA AGA CCC TTC ATA GC; reverse sequence: AAT CTC TCC ACT TCT GAT AAC C; length: 474; Tm: 56°C) primers (40). Expression levels were corrected by β-actin (forward sequence: ACA GAC TAC CTC ATG AAG ATC C; reverse sequence: TAA CAG TCC GCC TAG AAG C; length: 584, Tm: 58°C). To avoid overamplification and ensure linear responses, we have limited the cycle numbers to 25.
The pancreata from 3.5-mo-old control, PID, control-T1D, and PID-T1D mice were fixed, embedded in paraffin, and cut into 5-μm sections. The use of diaminobenzidine substrate, a mouse monoclonal antibody against recombinant rat Reg1 protein, of 144 amino acids without the signal sequence (Dr. Okamoto) (44) resulted in a brown immunoreactive signal with a hematoxylin counterstain (blue) of the cell nuclei. To ensure specific staining to Reg proteins, control slides were stained without the primary antibody, which revealed no specific signals. Because of high homologies within the Reg family proteins, especially a 76% sequence identity between Reg1 and Reg2, this antibody would likely cross-react with other Reg proteins. Because it has not been fully tested for subtype specificity, we have termed its staining as Reg1 immunoreactivity (Reg1-IR) in this report. Images of all pancreatic sections were captured with a Retiga 1300 digital camera (Q Imaging, Burnaby, BC, Canada) at magnifications of ×400 (oil) using Northern Eclipse software version 6.0 (Empix Imaging, Mississauga, ON, Canada).
Triple-labeled immunofluorescence for Reg, insulin, and amylase.
To further determine which type of pancreatic cells produce Reg proteins under various conditions, we have performed a colocalization study using immunofluorescence. Paraffin sections of pancreatic tissues from four groups of mice were dewaxed, rehydrated, and blocked with 5% normal donkey serum (NDS; Jackson Immuno Research, West Grove, PA). They were first incubated with rabbit anti-amylase (1:100 in 1% NDS; Sigma) at 4°C overnight followed by rhodamine red-X-conjugated donkey anti-rabbit IgG (1:100; Jackson) for 2 h at room temperature. After the signal was confirmed under a microscope, the sections were blocked again with NDS and incubated with guinea pig anti-insulin (1:100 in 1% NDS; Biomeda) at 4°C overnight followed by incubation with 7-amino-4-methylcoumarin-3-acetic acid (AMCA)-conjugated donkey anti-guinea pig IgG for 2 h at room temperature. After signal confirmation, the sections were again blocked with NDS and incubated with mouse anti-Reg1 (1:500 in 1% NDS; H. Okamoto) at 4°C overnight followed by FITC-conjugated donkey anti-mouse IgG for 2 h at room temperature (26). Sections were washed with PBS after each step, mounted, and stored at 4°C at the end. The images were analyzed using an Axioshop 2 plus microscope (Carl Zeiss), a Retiga 1300 digital camera, and Northern Eclipse software (Empix Imaging).
Statistical analysis.
Data are expressed as means ± SE. Student's t-test and one-way analysis of variance followed by posttest comparisons were performed using InStat software version 3 (GraphPad Software, San Diego, CA).
Increased expression of Reg family genes in the pancreas of PID mice: DNA microarray analysis.
We performed a DNA microarray analysis of pancreatic RNA prepared from control mice, PID mice, and both after streptozotocin-induced β-cell damage. Of the 39,000 transcripts included in the mouse MOE430-2 gene chip, the expression of about 8,000 were detectable. Among the four groups of mice, e.g., control, PID, control after being made T1D, and PID after being made T1D, 430 transcripts exhibited specific alterations greater than 1.5-fold, as illustrated in Fig. 1. The results are partially highlighted in Table 1, with genes grouped into three clusters: Reg family, islet and endocrine, and immunity-related genes. Compared with control littermates, PID mice exhibited altered levels of expression in 72 transcripts, highlighted in column 1 in Fig. 1. Among them, the mean levels of Reg family genes Reg2, Reg3α, and Reg3β (PAP) were increased 2.55-, 2.03-, and 3.02-fold, respectively. The expression levels of the other 3 Reg family genes, Reg3γ, INGAP-rp (Reg3δ), and Reg4 were not altered. Reg1 was not included in the probe collection. As a confirmation of gene knockout and test of validity, the IGF-I gene expression was decreased. Additionally, the expression of many genes related to immune responses, such as immunoglobulin joining chain and heavy-chain 6, was inhibited in PID mice.
Increased expression of Reg family genes in the pancreas of PID mice: Northern blots, real-time PCR, and RT-PCR.
Generated from small sample numbers, the microarray results need to be reconfirmed with large samples and a more accurate quantification. We performed Northern blots, real-time PCR, and/or conventional RT-PCR to different molecular targets, shown in Fig. 2. With the use of Northern blots and digoxigenin-labeled riboprobes transcribed from full-length cDNA templates, Reg1 mRNA level was slightly elevated in PID mice vs. control littermates. Those of Reg2, -3α, and -3β were increased significantly, 2.5-, 2.0-, and 2.7-fold, respectively. Similar results in Reg2 and Reg3β were obtained using real-time PCR and in Reg3α using RT-PCR. Lastly, INGAP-rp (Reg3δ) mRNA level was unaffected in PID mice, determined using RT-PCR alone. Thus, revealed by microarray analysis and confirmed using Northern and other techniques, the mRNA levels of Reg2, -3α, and -3β in the pancreas were more than doubled in PID mice. These changes seemed to be age dependent, because they were not seen in younger mice aged 1 mo (data not shown). Changes in Reg1 and INGAP-rp (Reg3δ) were insignificant. Two other Reg genes, Reg3γ and Reg4, were not tested.
Increased expression of Reg family genes in control mice after streptozotocin-induced diabetes: DNA microarray analysis.
The level of Reg1 is increased during islet cell regeneration after pancreatectomy or streptozotocin-induced T1D (3, 45). As part of the DNA microarray analysis, we have compared control untreated mice and 15 days after streptozotocin-induced diabetes (when the β-cells were mostly destroyed and islet regeneration was activated). The status of β-cell damage and hyperglycemia has been described in our previous report (26). Among the detectable transcripts, the expression of 264 transcripts in T1D group exhibited alterations greater than 1.5-fold vs. untreated control mice, as shown in Fig. 1. Among them, the levels of Reg family genes Reg2, -3α, -3β, and -3γ were increased 5.94-, 4.35-, 12.12-, and 3.21-fold, respectively (Table 1, data column 2). INGAP-rp (Reg3δ) level was only slightly elevated and Reg4 level was unaffected, whereas Reg1 probe was not included. As a confirmation and test of validity, the expression of β-cell-specific genes such as insulin I and II and islet amyloid polypeptide was ablated together with β-cells. Changes in immune-related genes were more limited and the directions reversed than in PID mice (result 1), including 2.36- and 2.31-fold increases, respectively, in the transcripts of chemokine ligand 13 and interferon-γ-induced GTPase.
Increased expression of Reg family genes in control mice after streptozotocin-induced diabetes: Northern blots, real-time PCR, and RT-PCR.
The microarray result was reconfirmed using various techniques available, as shown in Fig. 2. With the use of Northern blot hybridization, the level of pancreatic Reg1 mRNA (not included in the microarray chip) was increased 1.5-fold. Those of Reg2, -3α, and -3β were increased more significantly, 3.4-, 2.7-, and 3.6-fold, respectively. Similar results were obtained using real-time PCR for Reg2 and -3β and conventional RT-PCR for Reg3α. Lastly, INGAP-rp (Reg3δ) mRNA level was increased only 1.5-fold in T1D mice with the use of RT-PCR. Thus, in the pancreas of control mice after being made diabetic, there were 2- to 8-fold significant elevations in the levels of Reg2, -3α, and -3β mRNAs. Changes in Reg1 and INPAP-rp (Reg3δ) were significant but less dramatic. Two other Reg genes, Reg3γ and Reg4, were not tested.
Levels of Reg family mRNAs were not increased further in PID mice after being made diabetic.
As described above and illustrated in Fig. 2, the levels of Reg2, -3α, and -3β mRNAs were significantly elevated in PID mice (second group) vs. control littermates (first group) and were increased even further in control mice after being made diabetic (third group). To explore a compounded effect of PID and T1D, in Northern blot analysis we had included a fourth group, e.g., PID mice after being made diabetic (PID-T1D). As we have reported previously (26), PID mice only exhibit marginal hyperglycemia and islet damage after streptozotocin treatment. The levels of Reg family mRNAs in PID-T1D group exhibited levels of increases similar to the PID alone (second group) but less than the T1D (third group). Consistent with the fact that PID mice are protected from streptozotocin and have only a very mild form of diabetes, the PID-T1D mice did not exhibit uniformed increases in Reg family gene expression after streptozotocin treatment in contrast to control T1D mice (in Fig. 1, column 3, and Table 1). Another comparison we have made is in Table 1, data column 4: PID-T1D vs. control T1D mice. Fifteen days after an identical treatment with streptozotocin, PID-T1D mice exhibited slightly smaller increases in the expression of Reg family genes but preserved (increased) expression of β-cell specific genes, again consistent with the mild diabetes.
Cell-specific alterations in Reg immunoreactivities.
The results described above represent specific changes in mRNA level only, and the RNA was isolated from the whole pancreas. To reveal changes at the protein level, especially with cell-specific resolution, we have performed immunohistochemistry using a specific antibody against Reg proteins (anti-Reg1) provided by Dr. H. Okamoto. As shown in Fig. 3, top left, in normal control mice Reg1-IR was detectable at scattered exocrine cells (brown pigmentation indicated by blue arrows) as reported, but not within the endocrine islets (black arrows) (27, 56). In PID mice (Fig. 3, top right) brown Reg1-IR was clearly visible in some islets in addition to exocrine cells. In control-T1D mice (Fig. 3, bottom left) with significant atrophy after the onset of diabetes, many islet cells were positively stained for Reg1-IR. A drastic increase in the staining was also observed in patches of exocrine cells, some being adjacent to the islets. In the fourth group of PID-T1D mice (Fig. 3, bottom right), Reg1-IR in exocrine cells was obviously higher than in control and PID mice (Fig. 3, top left and top right), although less than in control-T1D mice (Fig. 3, bottom left). Their islets were mostly protected from streptozotocin-induced damage and exhibited low levels of Reg1-IR (Fig. 3, bottom right). Presently, the specificity of available antibodies against various subtypes of Reg proteins has been unsatisfactory for this purpose (data not shown).
Evidence for islet neogenesis and regeneration involving Reg proteins.
Increased β-cell mass in PID mice indicates islet hypertrophy, hyperplasia, and/or increased islet neogenesis (26). In control T1D mice, islet neogenesis is expected for the mice to recover from diabetes (3). In adult rodents, pancreatic acinar or ductal cells are putative progenitors of new islets (3, 38). To provide evidence that Reg family proteins are involved in islet neogenesis in both scenarios, we performed a triple-labeled immunofluorescence on pancreatic sections. As shown in Fig. 4, as positive control for the three-color scheme in control pancreas (top), an insulin-stained islet (blue) and the surrounding amylase-labeled acinar cells (red) were clearly segregated. Reg1-IR (green) normally produced in exocrine cells was invisible in this field. In PID mice (Fig. 4, middle), we have detected several clusters of cells that were positively labeled by all three antibodies. It seems that they were newly formed islets, from amylase-producing acinar cells (red), induced by Reg proteins (green) that started to synthesize insulin (blue), albeit at a low level. This phenomenon was not observed in control mice. The "new" islets resemble those in hamsters and mice in response to INGAP treatment (see Figs. 1B and 7A in Ref. 38) and exocrine cell transdifferentiation in rats (21). In T1D mice (Fig. 4, bottom), we detected scattered "new β-cells" that were presumably formed from Reg1-IR-producing acinar cells (white arrows) and serve as β-cell precursors. Although still dispersed as single cells among exocrine tissues, these cells produced noticeable amounts of Reg1-IR and insulin concurrently, whereas the mice were undergoing acute diabetes 15 days after streptozotocin. The only other member of the Reg family that is known to stimulate β-cell neogenesis is INGAP (38). On the basis of previous reports, our result provides further evidence that the expression of the Reg genes is associated with islet neogenesis (3, 38), which may potentially contribute to increased β-cell mass in PID mice.
This study was designed in order to understand the unexpected phenotype of PID mice; i.e., as an undisputed growth factor, IGF-I gene deficiency causes increased islet cell mass rather than growth defect. The islet cells are further protected from damage caused in both T1D and T2D models (26). These beneficial outcomes are likely caused by indirect activation of proislet factors rather than a direct IGF-I deficiency. Indeed, using a high throughput microarray analysis, we have hereby rediscovered Reg family proteins: 1) The mRNA levels of Reg2, -3α, and -3β in the pancreas were significantly increased in PID mice, which were associated with islet enlargement and protection against damage; 2) those mRNA levels were again increased in control mice after being made diabetic, when islet cells were expected to undergo active regeneration, and minor elevations were also detected on Reg1 and INGAP-rp (Reg3δ) mRNA levels in diabetic pancreas; and 3) interestingly, the most significant changes occurred in new members of the Reg family that are not yet known to play a significant role in islet cells, rather than Reg1 and INGAP, which stimulate islet cell replication and/or regeneration. Our results suggest that these uncharacterized Reg proteins are involved in promoting islet cell growth, protection, and/or regeneration.
Reg family proteins have been known for years. In rats, a 90% pancreatectomy causes a drastic increase in islet β-cell regeneration, which was thought to be driven by novel growth factors (54). In 1988, Terazono et al. (45) isolated a novel cDNA from these regenerating islets and named it Reg, or regeneration-associated gene; it is now called Reg1 (PTP, PSP). Ever since then, Reg-related genes have been shown to constitute a multigene family in humans and rodents. Independently, by using a partial pancreatic duct obstruction (cellophane wrapping), Rosenberg et al. (37) have shown islet neogenesis from ductal epithelium, which functioned to reverse a diabetic state. A soluble tissue fraction, ilotropin, was later proven effective, too (39). A major constituent of the extract was characterized, its cDNA was cloned, and it was named islet neogenesis-associated protein (INGAP) (35). With homology with Reg3 proteins, INGAP is expressed in acinar but not in islet cells of mice and hamsters (35). On the basis of its genomic organization and protein structure, the hamster INGAP has the greatest homology to mouse INGAP-rp (also named Reg3δ; 72% amino acid identity) (43). Four other members of the Reg family (Reg3α, -3β, -3γ, and -4) have been discovered since then. All 7 subtypes of Reg proteins are encoded by independent genes, but in a highly similar configuration (1, 18, 27, 56).
Reg1 is involved in cell cycle progression and normal islet growth and could potentially be used to prevent T1D (31, 32). Disruption of Reg1 gene through homologous recombination causes significant reductions in islet cell mass and the rate of DNA synthesis in isolated islet cells (47). Conversely, islet-specific Reg1 transgenic mice exhibit increased DNA synthesis in islet cells. When crossed onto a nonobese diabetic (NOD) background, Reg1 transgene causes a significant delay in the development of the diabetes (47). In another study (12), injection of Reg1 into NOD mice also postpones the onset of diabetes. In isolated rat islets, Reg1 significantly increased [3H]thymidine incorporation into the cell nuclei (50). As for its intracellular mechanism, Reg1 has been reported to cause phosphorylation of ATF-2 via a PI3K-depedent pathway (42). As a specific transcription factor, ATF-2 activates cyclin D1 promoter and increases cyclin D1 protein level in islet cells. As a Ser/Thr kinase, cyclin D1 promotes cell cycle progression by inactivating retinoblastoma protein (51). To support its role in neogenesis, Reg1 has been found in acinoductular cells that are also positive for cytokeratin 19, trypsin, and chromogranin A and supposedly a source of islet neogenesis (46). Most recently, Reg1 and Reg2 proteins are indicated in the early response of the pancreas to obesity-induced T2D in mice. At 2 wk after a high-fat diet, well before onset of obesity and insulin resistance, there are two- to threefold increases in Reg1 and Reg2 protein levels and a 15-fold elevation in Reg2 mRNA levels (34). Hamster INGAP is mitogenic for pancreatic duct- but not β-cell-derived cells. Because ductal cell proliferation seems to be a prerequisite for islet neogenesis, it is postulated that this protein could be involved in islet neogenesis (35). Indeed, a pentadecapeptide fragment of INGAP increases β-cell mass and reverses diabetes in mice (38). Although a receptor is still elusive, INGAP-induced transformation from duct cells to islets is dependent on PI3K-mediated activations of Akt1 and ERK1/2, which in turn cause activation of islet-specific transcription factors including neurogenin-3 and Pdx1 (17). Thus Reg1 and INGAP are known growth factors to the islet cells.
Although Reg family genes were activated under two different conditions in this study, the implications in PID mice and control mice after being made diabetic are quite different. 1) PID mice have 2.3-fold increased β-cell mass, and the islets are resistant to both T1D and T2D. Increased islet density and islet cell size indicate increased neogenesis and hypertrophy in PID mice (26). Concurrent increases in Reg2 and Reg3β levels strongly suggest that Reg proteins are involved. Increased islet neogenesis was strongly suggested by our triple-labeled experiment (Fig. 4, middle row), where insulin-producing clusters (new islets) were captured producing Reg1-IR proteins and amylase as well. This type of neogenesis, i.e., transdifferentiation from exocrine to endocrine, has been proposed recently (21). Although it might be one possibility, our evidence does not necessarily contradict to the notion that acinar cells undergo an intermediate, ductal-like dedifferentiation before becoming new β-cells (49). 2) In control mice, 15 days after streptozotocin treatment, most islet β-cells have been destroyed (26). To restore β-cell mass and recover from T1D, β-cells would be increased through active neogenesis, which is much more prominent than replication. Even greater increases in the levels of Reg2 and Reg3β, under this condition and in both islets and exocrine cells, again suggest that Reg proteins are involved in islet neogenesis. Except for Reg1, similar change in T1D has never been reported for other Reg proteins (30). Furthermore, this observation is consistent with two recent reports of T1D models. Reg3β (PAP) is overexpressed in islet cells of human T1D (13); the level of mouse Reg2 gene expression (but not of Reg1 and Reg3β) is significantly increased in the pancreas of diabetes-prone NOD and in cyclophosphamide (causing T1D)-treated mice (4). It is important to note that, although Reg2 is closely related to Reg1 and Reg3β resembles INGAP (Reg3δ), they are definitely distinct proteins coded by independent genes and potentially more potent islet growth factors. Reg2 has a unique 7-aa insertion (QVAEEDF) near its NH2 terminus, although an overall 76% sequence identity to Reg1 (48), and has only 40% identity to INGAP or the 15-aa hamster INGAP peptide (38). Reg3β has a 5-aa insertion (PNGGG) near its COOH terminus and only 40% identity to Reg1 (1), along with a 52% identity to INGAP and a 67% identity to the 15-aa INGAP peptide (1, 38). Their significant upregulation in our systems is in contrast to the minor or no increases in the levels of Reg1 and INGAP.
Insufficient islet β-cell mass is a key element in the development of autoimmunity-induced T1D and in T2D associated with insulin resistance. Various growth factors such as epidermal and hepatocyte growth factors, PTH-related protein, prolactin, placental lactogen, and glucagon-like peptide-1 stimulate islet cell growth (7, 11, 28, 36). β-cell mass can also be supplemented by islet transplantation, where growth factors have been found to promote the survival of transplanted cells in rodents (2, 6, 36). Many intracellular signaling molecules [such as p8, Cdk4, T-antigen, Akt1/PKB, insulin receptor substrate (IRS)-1, IRS-2, Bcl-2 and Bcl-x(L)] and islet-specific transcriptional factors (such as PAX-6, nkx 6.1, neurogenin-3, and Pdx1) also affect islet cell replication, islet cell differentiation (and thus islet neogenesis), and cell apoptosis (11). Unfortunately, after decades of research, very few of these factors have been proven potent and specific enough for clinical applications. Novel growth factors, including members of Reg family, are still highly desirable in combating diabetes. Toward this goal, the receptors for Reg proteins and signal mechanisms are still unclear, and questions remain in their intracellular processing, potential secretion, and regulation; except for nutrients, cytokines, and glucocorticoids, what else regulates their endogenous production? The most intriguing question from our demonstration of increased levels of Reg2, -3α, and -3β mRNAs in PID mice of increased islet growth and protection is whether they are the underlying mechanism and have more potent effects than Reg1 or INGAP. To provide direct evidence, we are working on their overexpression or knocking down in islet cells or transgenic mice.
Results from present study would imply that IGF-I produced from the pancreas normally inhibits Reg protein production, a prediction that so far has not been supported by experimental evidence. In isolated rat islets, Reg1 mRNA level is significantly increased after a 2-day incubation with insulin, growth hormone, and platelet-derived growth factor but unaffected by IGF-I treatment (10). In a preliminary experiment, a general and robust overexpression of IGF-I gene in metallothionein (MT)-IGF mice (29) caused no significant change in pancreatic Reg1 or Reg2 mRNA levels but 5- to 25-fold drastic elevations in the levels of Reg3α and Reg3β (Y. Lu et al., unpublished observations). Although this result cannot be directly reconciled with our data obtained from the PID mice, it clearly suggested that the expression of some Reg family genes is affected by IGF-I and provides an interesting clue for future investigation. Finally, the changes in immunity-related genes reflected from the DNA microarray (Table 1) are interesting. Whether they can be confirmed using more quantitative methods such as Northern blotting and what it might mean for islet growth and protection need to be addressed in future studies.
In summary, we have demonstrated increased Reg gene expression in the pancreases of PID mice and control mice after being made diabetic, and changes occurred mostly to new members of the Reg family including Reg2, -3α, and -3β that are not known to promote islet cell growth. These results were further supported at the protein level by immunohistochemistry and suggested that these uncharacterized Reg proteins are activated in PID mice and participate in islet neogeneis, growth, and/or protection. At the same time, they may also play a role in islet regeneration after β-cell damage in a similar fashion as hamster INGAP.
This work was supported by a Career Development Award (2–2000-507) from the Juvenile Diabetes Research Foundation (JDRF) International, New York, NY, a J. R. & C. M. Fraser Memorial Award, and the Shanghai Education Commission (China) to J. -L. Liu. Y. Lu received studentship support from the Research Institute of McGill University Health Centre. P. L. Herrera was supported by the JDRF International and the Swiss National Science Foundation.
We are grateful for contributions made by Amy Norris, Katie Roberston, and Drs. Dengshun Miao and Yingben Xue of McGill University. Dr. Derek LeRoith of the National Institutes of Health provided the IGF-I/loxP mice.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2006 by American Physiological Society


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Q: What's the deal with alkalinity-enhancing products?
–Alexandra Spunt, Los Angeles
A: The usual selling point associated with products such as alkaline water is that they help prevent disease by balancing your body's pH—but your body doesn't need help adjusting its acid-alkaline balance.
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Under normal circumstances, the pH of your blood and most bodily fluids is near 7.4—close to neutral—and very small changes in either direction do not affect your health or well-being. The internal balance of your body is naturally under extremely tight biological control by your blood, lungs, and kidneys. This means that unless you are critically ill with a lung or kidney condition, your body's pH will naturally remain in balance no matter what you eat or drink.
It is true, however, that the mainstream Western diet, high in animal protein and processed foods, imposes a significant acid load on the body. A healthy body continues to maintain acid/alkaline balance, but over time this pattern of eating can stress the system, which some experts believe leads to a minute degree of acidification that may cause leaching of calcium from bones, thereby increasing the risk of osteoporosis. Research is ongoing, but it is clear—even before the results are in—that the best way to counter this potential risk is to eat more alkaline foods such as vegetables, fruits, and whole grains. An easy way to do this is to follow my anti-inflammatory diet, which includes as much fresh food as possible and minimal processed foods.
Drinking mineral water may also play a beneficial role in your health, but additional investigation is required before I would recommend it. For now, my bottom line is this: I advise against using water ionizers or drinking alkaline water; the health claims made in support of these products are hype at best. (If it's just jazzed up water you're looking for, try these flat belly sassy water recipes.)
ANDREW WEIL, MD, is founder and director of the Arizona Center for Integrative Medicine and clinical professor of medicine at the University of Arizona. For more information, go to DrWeil.com.
Send your questions for Dr. Weil to [email protected].Copyright © 2017 Rodale Inc.
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What to do when a girl says we need to slow things down and don't want to ruin what we already have. We were spending a lot of time together and everything felt so right, going with the flow. There are feelings on my side and think she has some to yet there are barriers also which I get.
Most Helpful Girl
Speaking from her pov, go slow. When she says she wants things to slow down, it means she is uncomfortable. It could be that she has other priorities that she wants to set straight before getting serious, or it could simply be that she is uncomfortable with some kinds of physical contact. Try to judge things by her body language and if all else fails, sit down and ask her what it is that's making her want to slow down. It depends on your relationship, how long you've known each other, etc. Stick to fun dates, stress free dates such as bowling or movies, and allow her to take a little control as she's ready. Good luck!00|00|0


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Filip's Blog
While creating a page that used server side includes, I ran into some very strange behavior. Right before each SSI, a blank line would appear on the page. It didn't have anything to do with margins or padding. It was just like an empty line appeared right out of nowhere, messing up the layout. First, I thought it was some problem with IIS and SSI, but I couldn't find anything there.
After a few hours of frustration and trying the weirdest solutions I could think of, I started playing around with saving the include files with different file names. Well, when I got to the *.txt, I noticed that Visual Studio gives me a new option under "Save As"... its "Advanced Save Options". When I looked at the encoding of the file, it was set to "Unicode (UTF-8 with signature) - Codepage 65000". I then switched to "Unicode (UTF-8 without signature) - Codepage 65001", and the blank lines disappeared.
It appears that Visual Studio picks an encoding when saving pages that doesn't really produce desirable effects when using server side includes. However, you can go to File -> Advanced Save Options and select a different encoding. I'm not sure how to set the one w/o signature as the default yet, but hopefully soon I'll figure that out :)
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Web Development
I've ran into issues using the WebService object in Flash. The thing is incredibly buggy. In certain cases, it works just fine, but in other cases, it flat out does not work. In my last case, the web service loaded perfectly fine (onLoad was called), but the PendingCall would not return anything. The onFault method was never called after I invoked my web service call, but the web service never returned either. Examining the outgoing messages from Flash (using HTTP headers in Firefox) revealed that Flash was never even attempting to call the web service. Flash did correctly acquire the crossdomain.xml file (which allowed access from all domains), and it did load the WSDL. But, for whatever reason, it did not call the web method like it was supposed to.
Well, after a few hours or attempging to make this work, I gave up with the WebService object. Instead, I went to the LoadVars object, something I'm more confident in than the WebService class, simply due to the fact that it has been around much longer and has had more attention from the Adobe / Macromedia team.
Using the WebService object, my code looked like the following:
The above was replaced with the code below, and it works perfectly fine:
<add name="HttpGet"/>
<add name="HttpPost"/>
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Hello everyone.
as stated i need some advice. i have fallen in love for a girl i know who i consider my best friend for about 8 years now.. 3-4 years ago she got into a relationship and i never told her how i felt because of how shy i was at that point in these last 3-4 years i realised she meant everything for me, now last week she broke up with her boyfriend which was a good friend of mine it was kinda a harsh break up and it came out of no where for her. now i don't know how to asses this situation or when i should tell her since i'm kinda bad at this stuff. she usually comes to me and some of her other friends for advice but i'm incredibly conflicted about what i can tell her and what i cannot because i have the feeling i might just slip what i wanna say eventually when she is atm still in the phase where she is heart broken by her Ex.
So pretty much my question is how long should i wait before i should or should not confess my feelings for her because if i don't and won't go after her i have the feeling i will live with regret for the rest of my life like i have done these past 4 years.
Thank you in advance to everyone who reply's.
I am conflicted about what to do right now can any one give me advice?
Hello everyone.
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What Girls Said 1
Well like you stated she has just recently been in a harsh break up with her ex. Maybe when she comes to ask you advice about something guy related (maybe that is her moving on, it will give you a hint). Maybe by then, tell her that you like her. But don't tell her now.00|00|0
That is the thing she always asks me about advice wether this had been with her now broken relationship or just something about school so i would not know if that is her moving on or not if she keeps doing the same as she has done before. because she has said over the coarse of our friendship i'm probably the only one where she is 100% herself. and yea i know i should not tell her now.
Not school things, when she comes to ask you about boy things. The trust is there. I hope she just hasn't friend zoned you already, that's all.
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Location: Detroit
Device: Nook Glowlight, iPad, iPhone
I find the Nook is not too good as synchronizing between devices. Unlike the Kindle, for example, which opens to the furthest position in the book that was last open, the Nook opens the book to the last position in the book that was opened on any device. So if you, say, open the Nook app on the iPad and it goes to page 153, then when you open the same book on the Nook STR it will try to go page 153, even though you may have read as far as 194.
I just try to leave the wifi off on my STR all the time so that won't happen. If I'm reading on my iPad or iPod touch I will find where I was in the book by myself.
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