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Related movies/dramas
Source : star.moneytoday.co.kr...
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Korean cowboy "The Good, the Bad, the Weird" charms at Cannes
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petfood.com > Cat Supplies > Toys > Interactive Toys > Item # 498546
promotional discount applied. Cart total will reflect savings.
Buy 2 or more, each at $7.19 Buy 3 or more, each at $7.03 Buy 6 or more, each at $6.79
Quantity discount will reflect in cart.
Sometimes, manufacturers require that products be advertised only at their suggested prices. When we choose to sell these items for less, we display the sale price only in the cart. To see the price, click Add to Cart.
One-time delivery
Save 15% with Auto Ship (Details) Deliver Every: 2 Weeks 3 Weeks 4 Weeks 5 Weeks 6 Weeks 7 Weeks 8 Weeks 1 Month 2 Months 3 Months 6 Months
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subset: commoncrawl


text:
04/03/2012, 04:21 AM | #62 (permalink) |
Posts: 154
dear ,
1.all i get in SMS is that my is phone (Veer US model ) is not supported for 3g when i send that 3g activation SMS to carrier(DOCOMO / AIRCEL / AIRTEL) ... 2.and i dont think any of the customer support Rep from any carrier in INDIA has any clue about this phone or other webOS phones... So for me its really intriguing that u r getting 3g in VEER ...may b i should doctori the device and then try again...that is my only hope ...also in my Veer i cant open all my emails of the same a/c in separate card form whereas in PRE2 i have no problem ..just tap n hold for 2 secs the email will pop up as separate card..so i think i need to doctor the device...to give it one more shot for 3g
pixi plus (webOS 2.1)>pre2>HP Veer>touchpad |
04/03/2012, 09:14 AM | #63 (permalink) |
My model number is P160UNA or something like that. I believe you have European Veer.
When I was chatting with Vodafone Customer Care, Executive told me that, he can see in his system that my Veer supports 3G and that 3G would run on it. Although he also didn't have clue about Veer as mobile phone. I can surf the net with 3G speeds. |
06/08/2012, 02:28 AM | #64 (permalink) | |
Posts: 22
I am using Vodafone 3g in India now. |
12/11/2012, 09:44 PM | #65 (permalink) |
Posts: 110
Hi, all Indians on this forum!
I just wanted to say that I am also a fellow Indian on the forum. As you can see from my Signature, I am a longtime Palm fan. And now I have got my hands on a Touchpad also. Like all other WebOs users in India I am also suffering from India-centric problems like not being able to buy apps etc. But still, I am enjoying WebOs devices.
Palm III> Visor> Visorphone> Treo 180> 270> 600> 650> 680> Centro> HTC Tilt> BB-8310> Pixi-Plus> Pre 3 Touchpad 16GB Last edited by jmdesai; 12/11/2012 at 09:46 PM. Reason: spellings / typo correction |
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text:
A Bearskin's Crimea (Paperback)
Lieutenant Colonel Henry Percy VC and his Brother Officers
Memoirs & Military Biography Crimean War
Imprint: Pen & Sword Military
Pages: 272
Published: 15th November 2007
+£4 UK Delivery or free UK delivery if order is over £30
(click here for international delivery rates)
Other formats available | Price |
A Bearskin's Crimea Kindle (8.4 MB) Add to Basket | £4.99 |
A Bearskin's Crimea ePub (6.1 MB) Add to Basket | £4.99 |
Using much previously untapped source material A Bearskin's Crimea is a blow-by-blow account of the Grenadier Guards' experiences in the Crimean War. The principal character, The Honourable Henry Percy, a member of the distiguished and powerful Northumberland family (known as 'The Kings of the North'), was present at all the major battles of that appalling conflict: The Alma, Balaklava, Inkerman and the Seige of Sebastopol. Percy was no ordinary soldier: not only was he a shrewd observer with a skilled pen but a thoroughly capable and courageous officer. This is borne out by his winning the Victoria Cross and his rapid promotion.
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text:
Debian Information for VU#572183
ISC BIND 4 contains buffer overflow in nslookupComplain()
- Vendor Information Help Date Notified: 03 Jan 2001
- Statement Date:
- Date Updated: 05 Apr 2001
Unknown. If you are the vendor named above, please contact us to update your status.
Vendor Statement
No statement is currently available from the vendor regarding this vulnerability.
Vendor Information
The vendor has not provided us with any further information regarding this vulnerability.
Vendor References
Debian has made an announcement regarding this vulnerability; for further information, please see:
If you have feedback, comments, or additional information about this vulnerability, please send us email.


text:
This is hardly news, but it bears repeating every so often: Houston's punk, indie and noise communities, accustomed to being ignored or spurned outright by the more staid elements of the local music scene, have long cultivated an underground network of venues — mostly private residences and warehouses — that regularly fill up with people who found out about the shows on KTRU, online or just saw a flyer at Sound Exchange (see also the weeks-old Saturday Secret Shows series at the Shady Tavern in the Heights, and next week's six-band We Are the Hollow Men warehouse art opening/blowout at 1620 Keene St.).
Saturday, venerable DIY venue Southmore House, currently bunking up with East End/OST all-purpose creative space Bill Hicks Resurrection Laboratories, hosts a hefty cross-section of Texas punk for Punx-Mas Fest 3: Metal-tinged Arlington thrashers Unit 21, Corpus Christi's beer-soaked snarlers Drastic Actions, the scattergun guitars of Richmond's Rats in the Attic, Austin's vein-popping Exile and their ragged-throat, vintage-SoCal neighbors The 13th Victim, and San Antone Johnny Cash worshippers Hellbound Herse. Houston classic-hardcore bleaters Absence of Change, psychobilly poltergeists Ghost Storys, spirit-of-'77 true believers Deathbed Repentance and boisterous ska-baiting crew Molotov Compromise play the not-so-gracious hosts. Really now, what would the holidays be without a little BYOB one-two-three-four underneath the mistletoe?


text:
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Born in Mexico City my father is from NY my mother from Scotland. Im a freelance shooter currently based out of Mexico City. adam wiseman 's current location:Mexico Df , Mexico Play slideshow → |


text:
The epicenter of Cajun and Creole country, Lafayette attracts a steady flow of tourism traffic looking to sample its trademark cuisine and experience the unique cultural influence based on its French heritage. But Lafayette's spicy flavor doesn't only come from its food and traditions. It is home to four different colleges and always brimming with youthful energy willing to share its nonstop festive atmosphere. If you're looking for an opportunity to express your creativity and establish a solid professional career in this type of atmosphere, look no further than the Aveda Institute Lafayette.
Programs Offered: Cosmetology, Esthiology
Where to Find Us
2922 Johnston Street
Lafayette, LA 70503
Service Hours:
Wednesday - Saturday 9:30am - 5:30pm
Retail Hours:
Monday - Saturday 9am - 6pm
We look forward to meeting you.
Thank You.


text:
1 recommendation
quote:can't even find the device on Ubee's website (Cursory glance).
Or you can have it bridged so none of the "junk" is present. Lots of people on here do that and don't have an issue.
to log into them try user/user if can get the 10. IP try admin & then cableroot
"Bridging" in this form simply means turning off TWC's router functionality and using your own. At that point your router would handle all the firewall issues, so unless it was turned off, you would still have that protection.The NAT funtionality on the all in ones (Not just TWC's) is poor at best. If you only have a few devices it works fine, but if you start loading up a bunch of devices, I've heard reports of the all in one routers locking up or rebooting or other strange things because the router can't handle that load, whereas third party routers have no problems. That way all of your protection/routing is handled on your side and you can make changes easier, rather than calling in to have stuff changed (if they'll even support some of it).


text:
The efficacy of a single maintained contact drop piece manipulation technique in the treatment of sacroiliac syndrome
dc.contributor.author | Botha, Quentin Martin | |
dc.date.accessioned | 2008-09-04T06:56:30Z | |
dc.date.available | 2008-09-04T06:56:30Z | |
dc.date.issued | 2005 | |
dc.identifier.other | DIT112706 | |
dc.identifier.uri | http://hdl.handle.net/10321/337 | |
dc.description | Thesis (M.Tech.: Chiropractic)- Dept of Chiropractic, Durban Institute of Technology, 2005. xiii, 129 leaves :|bill. (some col.) ;|c30 cm | en_US |
dc.description.abstract | Research indicates the sacroiliac joint (prevalence of sacroiliac syndrome ranges from 19.3% and 47.9% (Toussaint et al., 1999)) as being the primary source of low-back pain in 22.5% of patients with back pain (Bernard et al., 1987:2107-2130). Treatment options that are available for the treatment of low-back pain include allopathic (Hellman and Stone, 2000), and manual therapies such as hydrotherapy and traction (Cull and Will, 1995). It has been found that allopathic interventions have been less effective than spinal manipulative therapy, even with spinal manipulative therapy having various modes of application (e.g. side posture and drop piece manipulations) (Gatterman et al., 2001). Drop table thrusting techniques were found to be effective for patients with neuromuskuloskeletal problems such as facet syndrome (Haldeman et al., 1993), however, it is still not known which specific drop piece technique is the most appropriate for sacroiliac syndrome. Thus it is important to ascertain the clinical effectiveness of the technique as certain conditions prevent the patient from being positioned in the conventional side posture for treatment of sacroiliac syndrome (White, 2003; Pooke, 2003; Hyde, 2003; Pretorius, 2003; Haldeman, 2003; Cramer, 2003; Engelbrecht, 2003). Therefore this study aims at determining the efficacy of a maintained contact drop piece manipulation technique. | en_US |
dc.language.iso | en | en_US |
dc.subject | Chiropractic | en_US |
dc.subject | Sacroiliac joint | en_US |
dc.subject | Backache | en_US |
dc.subject | Manipulation (Therapeutics) | en_US |
dc.title | The efficacy of a single maintained contact drop piece manipulation technique in the treatment of sacroiliac syndrome | en_US |
dc.type | Thesis | en_US |


text:
These Stunning Paintings Are Made From Coal Mine Sludge
The toxic, acidic runoff from mines operating in the 1970s is still a problem. An Ohio engineer and an artist have joined together to clean up the sludge and create beautiful paintings in the process.
In the foothills of southeastern Ohio, where ghost towns are all that's left of what was once a bustling coal mining economy, small streams run in vibrant hues of orange and bright yellow, or sometimes a milky white. Put your hands into the waters near these "black diamond cities," and you can cup the pigment in your palms.
Before 1977, there were no laws that required companies to clean up the wastewater full of iron, bauxite, sulfuric acid, and other trace metals that flowed freely from mines into surrounding waterways. The acidic runoff, which polluted streams and killed off wildlife that couldn't adjust to the lowered pH levels, continued after those coal mining operations left. "A million gallons per day of highly acidic high iron content pours into a creek nearby—and the creek is bright orange," says environmental engineer and Ohio University professor Guy Riefler. That's why, for the past five years, Riefler has been tinkering with an economically viable way to clean up the rivers and turn acid mine drainage sludge into something beautiful: paint.
"My main objective is to clean up the streams around here," Riefler explains. "I figured if we could collect the sludge we make, it could offset the cost of operating [a] water treatment plant [near the abandoned mines]. Based on the numbers we got, I'm sure we could at least break even or make a profit by neutralizing the sulfuric acid, and that's what really kills the fish."
After lugging five gallons of sludge per trip from the nearby Truetown creek back to the lab (something that happened several times a month with graduate and undergraduate students over the last half-decade), Riefler is now in the final stage of refining his method. The line of pigment he's currently working on is about 97% iron, and ranges "from orange to yellow to brown to deep red to black." Riefler has also worked with local artist and art professor John Sabraw to come up with the right formulations, which Sabraw incorporates in huge canvas paintings that depict endangered islands and estuaries across the globe.
Sabraw says he first found out about Riefler's project through one of his graduate students two years ago. Sabraw taught collaborative art classes based around the idea of sustainability, but shifted gears when one of his first assignments—an idea to save the world in two weeks—failed miserably. "They realized the crushing impossibility of doing this," Sabraw says. Instead, "We did something they cared about, but could take immediate action to help. And if they didn't implement it they'd fail."
Sabraw adds that his students, who "have the world's most sensitive bullshit meter," encouraged him to think about his own practice in a different way. "I'm an artist and I buy stuff to make stuff," he says. "And I have to be responsible for what I buy and what I produce."
After working with Riefler, Sabraw has gone on to produce several paintings with the acid mine drainage pigment both on aluminum panels and canvas. He also runs a website that helps artists "offset" the environmental toll of their paints and shipping. (Once, Sabraw purchased enough carbon credits to offset the Mona Lisa, after rigorously researching the greenhouse gases generated from Leonardo DaVinci's materials and the painting's travel history.)
Sabraw's latest project, the canvas paintings, will be open to the public on August 22 at Ohio Wesleyan University. Riefler, meanwhile, is working to gain the interest of paint and pigment companies that could partner with his plentiful, unnaturally occurring product. "If I could get that stream cleaned up I'd be really satisfied," Riefler says. The Truetown seep, which filters into a larger waterway called the Sunday Creek, passes on about a million gallons of water a day—and polluted with 350 mg of iron per liter, works out to about 4,000 pounds of iron dumped into the river daily.
"It's like you went to the creek and dumped two cars into the creek a day," Riefler adds. The prospect of cleaning it up through selling off the sludge, he says, is "what keeps me going."


text:
Badger & Blade Awards The Gentlemens Refinery After Shave Balm Best After Shave of 2014
December 2014Shaving enthusiast website Badger & Blade has announced that The Standard After Shave Balm is the "Best in Class" After Shave winner for 2014. This "special weapons and tactics aftershave balm" is "a home run."
Read More >>
"In Gastis We Trust" - Montecristo Magazine
November 2nd, 2009"...Asking themselves who was the best, they looked to their products and landed on the Gentlemens Refinery, a professional line
developed by master barber Perry Gastis. The products are 100 per cent natural} organic in every possible ingredient} and top quality...."
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The Gentlemens Refinery In Dolce Vita Magazine
December 18th, 2008"With a fourth-generation master barber at the helm, you know you're getting superiority..."
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The Gentlemens Refinery on Fox 5 News Las Vegas
July 31st, 2008"A local company is putting an all natural spin on men's grooming..."
Watch Video >>
The Gentlemens Refinery in Beauty Launchpad
July 15th, 2008"Perfect for the polished man: The Gentlemens Refinery Nickel Shave Set."
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The Gentlemens Refinery on Badger & Blade
April 22nd, 2008"Simply the best. The Gentlemens Refinery makes the finest after shave balm in the world, bar-none."
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The Gentlemens Refinery on Uncrate.com
June 4th, 2007"The Gentlemens Refinery After Shave Balm was created to quickly heal and seal your skin without an intense shock like your cheap chemical-filled after shave gives you"
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The Gentlemens Refinery on Evening Times Online
June 4th, 2007"Robert Gillespie's The Perfect Shave has become the sole distributor of US brand The Gentlemens Refinery in the UK and Ireland... Perry knows a thing or two about what customers expect from their shaving products."
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The Gentlemens Refinery on Men.Style.com
March 26th, 2007The Gentlemens Refinery on Shaveblog.com
November 16th, 2006"By blending the best of the old ways (barbershop shaving techniques and
disciplines) with the best of the new (all-natural ingredients), he's developed a new line of men's shaving products which isn't simply just another minor variation on what's already been done".
- Article written by Corey Greenberg, of Shaveblog.com
Read More >>


text:
The Cartographers Guild is a forum created by and for map makers and aficionados, a place where every aspect of cartography can be admired, examined, learned, and discussed. Our membership consists of professional designers and artists, hobbyists, and amateursall are welcome to join and participate in the quest for cartographic skill and knowledge.
Although we specialize in maps of fictional realms, as commonly used in both novels and games (both tabletop and role-playing), many Guild members are also proficient in historical and contemporary maps. Likewise, we specialize in computer-assisted cartography (such as with GIMP, Adobe apps, Campaign Cartographer, Dundjinni, etc.), although many members here also have interest in maps drafted by hand.
If this is your first visit, be sure to check out the FAQ. You will have to register before you can post or view full size images in the forums.
Rite Publishing has posted part II of its interview the amazing cartographer Jonathan Roberts (Halls of the Mountain King, Fantastic Maps) about The Breaking of Fostor Nagar patronage project (PFRPG)
Steve "Qwilion" Russell Rite Publishing "A hundred thousand lemmings can't be wrong!"
Forum Rules


text:
Emerging innovation networks and the print-on-paper sociotechnical regime
Piterou, Athena and Steward, Fred (2011) Emerging innovation networks and the print-on-paper sociotechnical regime. Procedia-Social and Behavioral Sciences, 10. pp. 104-122. ISSN 1877-0428 (doi:10.1016/j.sbspro.2011.01.014)
Full text not available from this repository.Abstract
The sociotechnical regime of the print-on-paper prevails as the main medium of textual communication despite concerns on its environmental implications. Radical innovation in the form of application of generic technologies is required to address these sustainability concerns. Electronic book technologies are seen as those applications of IT providing an alternative form of textual display. According to sociotechnical transitions theory the electronic book is positioned as a niche in relation to the print-on-paper regime. SNA is applied in order to describe the niche as a sociotechnical network. It emerges that network substructures indicate potential sociotechnical trajectories regarding the development of the electronic book niche.
Item Type: | Article |
Additional Information: | [1] This paper is a later version of the paper given at Sustainable Consumption and Production: Framework for Action 2nd Conference of the Sustainable Consumption Research Exchange (SCORE!) Network Monday 10 and Tuesday 11 March 2008, Halles des Tanneurs, Brussels, Belgium - see record 5691. [2] This paper is one of a selection of papers from the 4th and 5th UKSNA conferences (July 2008 and July 2009), both held at the University of Greenwich, which have been published as a special volume in Procedia-Social and Behavioural Sciences edited by Bruce Cronin |
Uncontrolled Keywords: | electronic book, actor-network theory, sociotechnical trajectories Electronic book, actor-network theory, sociotechnical trajectories |
Subjects: | H Social Sciences > HF Commerce H Social Sciences > HM Sociology |
School / Department / Research Groups: | School of Business School of Business > Department of Systems Management & Strategy |
Related URLs: | |
Last Modified: | 28 May 2014 14:43 |
URI: | http://gala.gre.ac.uk/id/eprint/5689 |
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text:
Online edition of India's National Newspaper Sunday, August 12, 2001 |
Front Page |
National |
Southern States |
Other States |
International |
Opinion |
Business |
Sport |
Entertainment |
Miscellaneous |
Features |
Classifieds |
Employment |
Index |
Home |
Southern States
| Previous
| Next
Antony sees bid to oust him
By Our Special Correspondent
THIRUVANANTHAPURAM, AUG. 11. The Chief Minister, Mr. A.K. Antony,
has said that some forces are trying to oust his Government by
creating unnecessary controversies.
Addressing a press conference here today on his return from
Delhi, the Chief Minister said Cabinet notes were leaked by the
Opposition. ``It was improper for the Kerala Congress(Joseph)
leader, Mr. T.S. John, to have leaked the papers. It was not
gentlemanly. Nor was it a very wise action,'' he said.
Mr. Antony parried questions on whether leaders in the ruling
front were also trying to bring his government down.
The Chief Minister said the allegation that the Government did
not grant new engineering colleges to the NSS or the SNDP was a
fabricated story. They had not applied and had not figured in the
list approved by the AICTE. Some people were trying to settle
personal grudge by raising criticisms like that, he said in an
oblique reference to the Kerala Congress(B) leader, Mr. R.
Balakrishna Pillai.
Mr. Antony said he was more confident now that Kerala could be
made a leading State in the South. ``Give me six months. The
performance of the Government, including its financial position,
will improve. After six months, I am willing to undergo a trial
by you (over omissions and commissions of the Government). I have
no magic wand with me. So, my request to the people is to wait
for six months,'' he said.
The Chief Minister said the Vigilance inquiry into the leak of
Cabinet notes was not decided by him, but by the Council of
Ministers. He was not pre-judging the outcome of the inquiry.
There was also no concern about the outcome. Leakage of
information about Cabinet decisions was not a new thing. The
inquiry was ordered just to find out who had leaked it. Once a
Vigilance inquiry is ordered, it was not his practice to
frequently enquire about its progress or dictate how the
Vigilance should proceed with the inquiry.
The Vigilance officials had not sought permission to question
the Ministers. He did not want to jump the gun by commenting on
the issue of possibility of the Vigilance questioning the
Ministers. When he spoke of a `thief in the ship', he meant that
the one who leaked the notes should be in the Secretariat. (Mr.
Antony's remark had been interpreted to mean a Minister of his
He said that he did not wish to enter into the legal aspects of
the controversy as he had long ceased to be a lawyer. If I argue
a legal case now, I would not be successful. Mr. T.S. John had
played a political drama. Its legal implications, including the
questions of contempt of court, would have to be examined in
detail before he could comment on it. The Government needed time
to decide on the minority status of the new colleges. It had
allowed them to start functioning without deciding on the status
for the sake of the students. If the matter was delayed, more
than 2,100 students could not have missed their admissions.
Asked about the senior Congress leader, Mr. K. Karunakaran's
comment that the Government should not have ordered a Vigilance
inquiry into the leak, Mr. Antony said Mr. Karunakaran was free
to hold his view. He was not for an infighting in the Congress
over this or other issues.
He said an official team would visit Manila shortly for
discussions with the Asian Development Bank on a bail-out loan
from the Bank. The Government would be fully transparent about
its decisions in the matter. It would see to that the employees
get their bonus and festival allowance during Onam, if necessary,
by availing of loans.
Send this article to Friends by E-Mail |
Section : Southern States Previous : Veerabhadrappa resigns as minister Next : Further easing of treasury curbs on Monday | |
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Copyrights © 2001 The Hindu Republication or redissemination of the contents of this screen are expressly prohibited without the written consent of The Hindu |


text:
The same might be happening to the current slate of music games. NPD reports (via Gamasutra) that revenue for the Guitar Hero franchise have dropped 34% year over year. Even worse, the Rock Band franchise has dropped 67%. (Although, it should be noted that the Rock Band series has not had a major console release this year.)
Jesse Divnich of EEDAR argues that "the music and rhythm genre is being monetized more closely in terms of a pop-culture fad," which explains the increasing number of releases we see from the Guitar Hero franchise. He argues that the window of opportunity for making money is limited and that both Activision and MTV Games are "[striking] when the iron is hot." The upcoming The Beatles: Rock Band and Guitar Hero 5 may make a big splash this holiday season, but it might not be long until gamers put away the plastic instruments and look for the next big thing.
Source - Analysis: Guitar Hero / Rock Band retail sales down by half
Source - The Divnich Debrief: Roadblocks in the Music Genre


text:
8 Ways to Wash Away Your Laundry Costs
How to Get Organized With Dollar Store Finds
5 Career Industries With the Largest Wage Gap
10 Things to Never Buy at Target
11 Ways to Keep Identity Thieves from Ruining Your Vacation
Simple Strategies to Boost Your Budget
Do You Have One of The World's Most Powerful Passports?
New Diabetes Discovery Shocks Doctors
Easy Ways to Bring in Extra Money
15-Year-Old Gets Surgery to Win Back Ex-Boyfriend?
5 Best Vest Styles for the Office
Is Your Credit Card Debt Average? And What's Average?
20 Dazzling Songs for Walking Down The Aisle
Laundry Tips to Make Clothes Last
Save, Don't Splurge on These Items
Lane Bryant Finally Redefines Sexy
4 Boss Moves to Get Salary You Deserve
10 Engagement Photos That Will Make You Completely Jealous
10 Annoying Habits That Drive Gym-Goers Crazy
12 Ways to Look Thinner in a Swimsuit
Beautiful Ideas For a Pacific Northwest Wedding
Fight The Bloat: How to Get Rid of Water Weight
Watch Ellen Shut Down Bethenny Frankel's Ignorant Comments
Heavenly Pink and Gold Wedding Ideas
Why We Want The Lesbian Taylor Swift Rumors To Be True
A Byron Bay Farm Wedding
32 Ridiculously Cute Queer Women Couples
Money Saving Ways to Salvage Overripe Fruit
9 Next-Level Mason Jar Recipes
Have You Discovered The Joy of Motherhood?


text:
In US v. Ruiz-Gaxiola, No. 08-10378, an illegal reentry prosecution, the court reversed the district court's order authorizing the government to administer antipsychotic medication forcibly, where 1) the district court erred in finding that the Sell factors were met without affording the question the "thorough consideration and justification" and "especially careful scrutiny" required; 2) the district court clearly erred in finding that the government proved by clear and convincing evidence that the proposed regime of involuntary medication is substantially likely to restore defendant to competency, as required under the second Sell factor; and 3) the district court clearly erred in finding that the government proved by clear and convincing evidence that the proposed treatment was medically appropriate, as required under the fourth Sell factor.
In US v. Ramos, No. 09-50059, which involved defendant's appeal from the district court's denial of his motion to dismiss an indictment for unlawful reentry after a prior deportation in violation of 8 U.S.C. section 1326, which he collaterally attacked in his motion to dismiss, the court affirmed where, although the prior, stipulated removal proceedings denied defendant due process of law and violated the applicable regulation, he suffered no prejudice as a result.
Related Resources
- Full Text of US v. Ruiz-Gaxiola, No. 08-10378
- Full Text of US v. Ramos, No. 09-50059


text:
An investigation of somatic embryogenesis in tea (Camellia sinensis(L.)O.Kuntze)
Akula, Anisha (2000) An investigation of somatic embryogenesis in tea (Camellia sinensis(L.)O.Kuntze). .
Find a copy in the QUT Library.
Impact and interest:
Citation countsare sourced monthly from Scopus and Web of Science® citation databases.
These databases contain citations from different subsets of available publications and different time periods and thus the citation count from each is usually different. Some works are not in either database and no count is displayed. Scopus includes citations from articles published in 1996 onwards, and Web of Science® generally from 1980 onwards.
Citations counts from the Google Scholar™ indexing service can be viewed at the linked Google Scholar™ search.
ID Code: | 37062 |
Item Type: | QUT Thesis (PhD) |
Additional Information: | Presented to the Centre for Molecular Biotechnology, School of Life Science, Queensland University of Technology. |
Keywords: | Plant tissue culture, Tea Somatic embryogenesis, betaine, clonal propagation, dessication, germination, immature embryo, maturation, mature seed, micropropagation, nodal cuttings, osmoticum, osmotic stress, repetitive embryogenesis, tissue culture, temporary immersion system, tea, thesis, doctoral |
Institution: | Queensland University of Technology |
Copyright Owner: | Copyright Anisha Akula |
Deposited On: | 22 Sep 2010 23:06 |
Last Modified: | 09 Feb 2011 23:55 |
Export: EndNote | Dublin Core | BibTeX
Repository Staff Only: item control page


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UPDATE: Congratulations to Arraybracket Limited – Fill 'Er Up for winning the random draw! Thank you for everyone who entered the competition. A great selection of apps have been released as a result.
The following 29 linked apps made it into the draw, there are currently 6 other applications that have failed certification and 5 that are pending certification.
Following on from The Great Kiwi Windows Azure Competition I got a taste for the 10 hour app. I started looking across other areas where I have been procrastinating. This lead me to Windows Phone 7, despite having a phone and also having a developer account for the marketplace I hadn't built and released my own app! I invested 10 hrs over the last couple of weeks and have now released my first app.
What I want from you: I did a quick check on the number of apps released by NZ developers and discovered that we currently have 95 123 applications in the marketplace. I've been saying for months that I want to break the magic 100 mark and I figured it was time for me to put some flesh in the game.
The Challenge: Finish, build and release your app in 7 days and be in to win a new HTC 7 Trophy Phone!
1. Contact me through this blog and if you convince me that you are based in New Zealand (e.g. give me a phone number for me to call you on) I'll give you a token to get a free one year membership in the Windows Phone 7 marketplace. Do this first as it takes a number of business days to confirm your identity and access your account.
3. Build and/or finish that WP7 app that you've been working on or meaning to create!
4. Release it to the marketplace!
5. I will collect all the apps released into the marketplace by NZ developers (excluding Microsoft employees and their families) from today Monday 16th May until Monday the 6th June 2011 (the extra time is so you can get your account setup and activated and also enable you to fail certification a couple of times but still be able to enter the draw).
6. From the applications I get I will draw the phone winner at random and announce the winner here on the 7th June 2011. Good Luck!
If you are the sort of person that is short of ideas here are a few:
My Idea: Group buy and daily deal sites are invading New Zealand in mass with every man and his dog is launching one. I figured it would be worthwhile building a simple REST service on an Azure Extra Small instance to act as an aggregator then build a WP7 mobile app to display all the deals together in one place.
The Process: The project took me under 10 hours from idea to delivery.
I got the Buzz:
After releasing the app (within my 10 hour self imposed timeframe) I was motivated to enhance the app and release another version that supports more cites in New Zealand and takes advantage of the panorama control. Enter On Sale in New Zealand, this app took 2 hours yesterday to build from my existing services and is currently being tested for marketplace release.
Getting Over the Line: I have noticed other kiwi WP7 apps getting close to shipping hopefully the chance of winning a new phone will push some developers to publish their apps. I'm looking at you @rushdigital.
Im keen! I have a developers account already setup. Once I deploy, what is my next step?
No next step once it's in marketplace it is in the draw.
I'll list the apps as they arrive in this blog post.
Look out for 2 apps from my end! HomeLink and Events New Zealand! Now I just need to get a hold off a WP7 to see how it looks in hand.


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North Carolina vs. Duke
March 17, 2011
Scoring | |
Billy Bitter | (3, 1) |
Thomas Wood | (2, 1) |
Nicky Galasso | (1, 1) |
Marcus Holman | (2, 0) |
Ryan Flanagan | (0, 1) |
Pat Foster | (1, 0) |
Saves | |
Chris Madalon | 8 (0.364) |
Current Record | |
North Carolina | 5-2 |
go to North Carolina page |
Scoring | |
Jordan Wolf | (4, 0) |
Zach Howell | (1, 2) |
Christian Walsh | (2, 1) |
Josh Dionne | (2, 0) |
Justin Turri | (2, 0) |
Tom Rynn | (0, 1) |
Robert Rotanz | (1, 0) |
Josh Offit | (1, 0) |
David Lawson | (1, 0) |
Jake Tripucka | (0, 1) |
Saves | |
Dan Wigrizer | 11 (0.550) |
Current Record | |
Duke | 5-2 |
go to Duke page |
The Game Story: | |||||
CHAPEL HILL, N.C.-Eight different Blue Devils tallied goals to lead the seventh-ranked Duke men's lacrosse team to a 13-9 victory over No. 8 North Carolina tonight at Fetzer Field. Freshman Jordan Wolf led all Blue Devils with four goals to post his third hat trick in the past four games. Duke (5-2, 2-0 ACC) has beaten North Carolina in 13 of the previous 14 meetings and pushes its win streak to four overall on the season. The Blue Devils capture the win in the Battle of the Blues Presented by Continental Tire competition between the two rivals. Duke closes the gap to one point as North Carolina holds a narrow 9-8 lead. Six different Blue Devils scored on the team's opening eight goals of the game and 10 players overall notched at least one point. Four players tallied multiple goals. Freshman Christian Walsh registered a career-high three points, while senior Justin Turri and freshman Josh Dionne both had two goals apiece. The Blue Devils defense was equally as impressive as they held a team to under 10 goals for the fifth time this season. Duke held the Tar Heels without a goal for 21:02 over the course of the first and second quarter as it built a 5-1 edge midway through the second frame. In goal, sophomore Dan Wigrizer made 11 saves, his fourth straight game with double digit stops. The two squads got off to a fast start as they traded goals in the first 1:26 of the contest. The next 20 minutes was all Duke as the Blue Devils held North Carolina (5-2, 0-1 ACC) scoreless. Duke added goals from Wolf and sophomore Josh Offit for a 3-1 lead after the first period. Sophomore David Lawson got into the mix in the second quarter to push the Duke advantage to 4-1 and Wolf notched his second of the game to make it 5-1 at the 8:08 mark of the second frame. After being held scoreless for 21:02, the Tar Heels stopped the scoring drought with a pair of goals in 1:26 to make it a 5-3 game. However, Duke responded right away and dropped in the next three scores, two of which came from the stick of Josh Dionne, to head into the locker room with an 8-3 lead. North Carolina, trailing by five to start the third quarter, scored the frame's first two goals to make it a three-goal game at the 6:57 mark of the stanza. Howell put Duke back on track with an unassisted marker at 4:18 and the two teams traded scores in the final four minutes to keep the Blue Devils in front by five after 45 minutes of lacrosse. The Blue Devils headed into the fourth quarter with a lead for the fourth time on the season and never faltered as they outscored the Tar Heels 4-3 to come away with the five-goal victory. Two of North Carolina's goals came in the final two minutes of the game. Billy Bitter led all Tar Heels with three goals and an assist, while Thomas Wood netted two scores and a helper. North Carolina held a 40-31 advantage in shots, but had just 20 on frame. Duke fired 22 of its 31 shots on the cage. The Blue Devils dominated the ground ball game, winning the battle 36-23. CJ Costabile picked up five ground balls to lead the way for Duke and Wigrizer added four. The faceoff game was controlled by the Tar Heels with R.G. Keenan winning 18-of 27 restarts. North Carolina goaltender Chris Madalon had eight saves overall. |


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Code covered by the BSD License
by Sven Koerner Sven Koerner (view profile) 22 files 427 downloads 4.49583
14 Feb 2011
Example Code of MultipleXYSeries using JFreeChart within Matlab
| Watch this File
The code behind is just a demo of what is possible with JFreeChart using it in Matlab. I played a little with codesnippets I found on the web and the API-Documentation. (http://www.jfree.org/jfreechart/api/javadoc/index.html). When you want to explore the whole functionality, I think it is better to buy the JFreeChart Developer Guide (http://www.jfree.org/jfreechart/devguide.html).
This function shows a multiple domain and range axis plot as an example of JFreeChart (http://www.jfree.org/). The Idea to this code is based on the UndocumentedMatlab-Blog of Yair Altman, who shows a sample Code of JFreeChart for creating a PieChart (http://undocumentedmatlab.com/blog/jfreechart-graphs-and-gauges/#comments)
Within the plot you can zoom by pressing the left mouse button and moving the pointer. Also you have some properties by right-clicking on the chart.
Before this demo works, you need to download JFreeChart and make matlab get to know with it. There are 2 ways you can do this: 1. Add the jcommon and jfreechart jar to the dynamic matlab JavaClassPath (uncommented lines in the first cell an change path to your local installation path) 2. Add the jcommon and jfreechart jar to the static matlab JavaClassPath (see Matlab Help, modify classpath.txt on matlabroot\toolbox\local)
Finally you must donwload jcontrol from Malcom Lidierth (http://www.mathworks.com/matlabcentral/fileexchange/15580-using-java-swing-components-in-matlab).
Using Java Swing Components In Matlab inspired this file.
Contact us


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http://www.w3.org/Bugs/Public/show_bug.cgi?id=1174 Summary: font-family parsing error (with escapes) Product: CSSValidator Version: CSS Validator Platform: All OS/Version: All Status: NEW Severity: major Priority: P2 Component: CSS 2.0 AssignedTo: email@example.com ReportedBy: firstname.lastname@example.com QAContact: firstname.lastname@example.com Trying to validate a { font-family: Times \!important 5, serif;} yields a { font-family: Times !important } which is wrong. The result according to CSS2 (and CSS21) must be (equivalent): a { font-family: "Times !important 5", serif } Similarly, a { font-family: Times \! important 5, serif;} yields the wrong result. Regards, Christian.Received on Monday, 21 March 2005 13:32:43 UTC
This archive was generated by hypermail 2.3.1 : Wednesday, 7 January 2015 15:17:20 UTC


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Search from over 10 Million Auto Parts
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1998-2001 Audi A4 Quattro ABS Speed Sensor - Rear - Bosch W0133-1809376
Product DescriptionWithout an effective, properly functioning ABS speed sensor, your 1998-2001 Audi A4 Quattro may have faulty, unpredictable brakes. A high quality Bosch ABS speed sensor for your 1998-2001 Audi can help ensure that faulty brakes are not a problem for you when driving on the road. When you see or hear the signs of a faulty ABS speed sensor, such as vibrations or noises coming from your vehicle's brakes when the pedal is pushed down, then you may want to invest in a new Bosch ABS speed sensor. It could be the difference life and death in some circumstances. This Bosch ABS speed sensor is for the right rear of your 1998-2001 Audi A4 Quattro, and is a bolt-on style. |
More ABS Speed Sensor Brands for 1998-2001 Audi A4 Quattro
Very satisfied with the part and the timeliness of receiving the part. Great price.


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Road Work for the week of July 14, 2014
• Replacement of the Pelandale Avenue interchange at Highway 99 will require shoulder closures at various times this week. Details are at www.sr99pelandale.org.• Expansion of the Virginia Corridor trail will require temporary closure of Bowen Avenue just east of Beard School.
• Traffic will be reduced to one lane in each direction for intersection improvements at Roselle and Merle avenues .
• Briggsmore Avenue from Sisk Road to 500 feet west of McHenry Avenue will have alternating lane closures for pavement work.
• Tree trimming will require closures in the right lane on northbound and southbound McHenry from Needham Street to Claratina Avenue .• Delays are expected for construction of a right-turn lane from eastbound Bangs Avenue to southbound Prescott Road .
• Sections of Carver Road will be closed to through traffic from Orangeburg Avenue to Roseburg Avenue from 8 a.m. to 4:30 p.m. for pipeline construction. Some lane closures are planned on Orangeburg Avenue between Grape Avenue and Del Vale Avenue.
• Water main work will take place mainly at night on Sisk Road, starting about 500 feet north of Kiernan Avenue, then west on Kiernan to the opposite side of Highway 99, ending at Elm Street and Broadway Avenue.
• Sewer work will continue near Elm and Rosemore avenues.
Join the Discussion
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Summary: STABILITY OF SOLITARY-WAVE SOLUTIONS TO LONG-WAVE EQUATIONS WITH GENERAL DISPERSION John Albert Felipe Linares 1. Introduction In this report we consider nonlinear dispersive systems of the form ut + D(f(u) - Mu)x = 0, (1) where u(x, t) = (u1(x, t), . . . , un(x, t)) is a map from R × R to Rn , D is a constant diagonal matrix with positive entries, f : Rn Rn is nonlinear, and the dispersion operator M acts as a Fourier multiplier operator in the x variable. More precisely, for each fixed t, Mu is a vector-valued function defined by Mu(k, t) = m(k)u(k, t), k R, where circumflexes denote Fourier transforms with respect to x, g(k) = R e-ikx g(x) dx.
Source: Albert, John - Department of Mathematics, University of Oklahoma
Collections: Mathematics


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Former general moved to prison with Al-Qaeda members
Source: TanjugLONDON -- Former Bosnian Serb Army (VRS) General Radislav Krstić has been transferred to another prison in Britain, said reports.
Krstić, who was beaten up and narrowly survived the torture by three Muslim inmates in Wakefield Prison in early May is now detained along with a number of people suspected of terrorism, including Osama Bin Laden's right-hand man, the Daily Star newspaper said.
Krstić's lawyer, Tomislav Višnjić, told Tanjug that his defendant was transferred to another prison in Britain, but refused to disclose the name of the institution for safety reasons.
In a statement for Tanjug, Višnjić said that he has been informed that The Hague-based war crimes tribunal was closely following the situation concerning Krstić, after the reports by the British press about his transfer.
Višnjić failed to be more specific about the steps the Hague could take.
According to the newspaper, General Krstić, 62, was permanently transferred to Long Lartin Prison, also known as "terror headquarters", since Abu Qatada, who is believed to be Al-Qaeda's right-hand man in Europe, is serving his sentence there.
Krstić is held in a secure area at the category A jail, according to this report.
Krstić was sentenced by the Hague Tribunal to 35 years in prison for involvement in the 1995 Srebrenica genocide.


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Your favorite Apple, iPhone, iPad, iOS, Jailbreak, and Cydia site.
Thread: Little problem mapping command key
09-27-2009, 02:33 PM #1Little problem mapping command key
So I have a PC, running VMware with OS X as a guest computer, and I am having trouble mapping the command key with my PC keyboard. Any help with this? I need a way to map my PC keyboard to utilize the command key while in VMWare, or on my Mac, essentially. Thanks.
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[Date Index] [Thread Index] [Author Index]
Re: Problem with loading SuperWidgetPackage
Thanks both of you.. (esp. David, yes, i reach the mail, but was busy in between) your instructions helps me to solve my little problem.. That was my mistake .. i didn't realise needs for GUIKit for running SWP.. becouse i don't know what GUIKit is at all:) and didn't find explicitly requirement for it.. so i quickly jumped over introduction on David's website :) David Bailey wrote: >The problem with the help system ... >.. seems to generate an error under 5.0 > (although, at least in my experiments, its contents were still >visible using 5.0). Yes, in spite of error, i was able to reach the help contents. Ok, lets summarise again to help others: SWP http://www.dbaileyconsultancy.co.uk/superwidgetpackage/superwidgetpackage.html works fine on Mathematica5.1 and needs GUIKit version 1.0.2 http://www.wolfram.com/solutions/guikit/ ( GUIKit version 1.0.1, which came with Mathematica5.1, needs uprgrade to run SWP) thanks again ____________ iscekujuci dizajn: http://mapmf.pmfst.hr/~matko1/


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text:
Best of November 2011Hello everyone! :iconskyandnatureclub: proudly features the best submissions of November!We will feature the best pictures of every month, so make sure you submit your best works to increase your chance to be featured Not yet a member? Have a look at our Blog and feel free to join!And now enjoy our monthly feature! ----Flowers, Plants & Macro "The Golden Age" by SummerLadyx :thumb266593155:droplets... by efeline Under the Oaks by wosicz Last of Autumn by InnocentDriveAutumn's Fire by goRillA-iNK Berries by Kokopa :thumb270225757:grand theft autumn... by Juhubaer Dream scene I by CrazyMurdock1 Drunk on luve by BlanchiiLandscapesGhostly by Angie-Pictures Red creek 2 by Neshom The One And Only Magical Moment by kauf-michTable by the Tree by EmersonStem Autumn by mutos The Sunset Rocks by MorkelErasmusMorning light by awropa Sonoran glow by PeterJCoskun Winter Dream by A-Motive:
My dog... Updates!Update:Hey Guys,Over the last week, Rocket has been recovering well! She has sphincter ontrol about 90% back, an she is walking and sliding around. She is still basically bunny hopping at times, and doesn't have the strength to stay up for liong, but she is on the road to recovery!Thank you all for your kind wishes. It means so much to both of us!ZevNote: Faving this journal will be seen as a sign of support Hey GuysSo, I have for the last 4 years had a wonderful Yellow Lab Mixed with Terrier and Pitbull. She is a gorgeous dog, and one that I love dearly. We got her as a rescue when she was just a few months old, and quickly we found her name... "Rocket". She can jump straight up and down almost 6 feet, able to grab toys from way above our heads. However, this sadly may have been her downfall as well.In the last week or so, she started displaying symptoms that were not healthy. First she was unable to hold her feces, and we assumed at first that it was a dietary i
dA Font Formatting GuideTo READ this with a Fancy Layout WITH source code, see http://viclou.deviantart.com/journal/DeviantART-lt-font-gt-Formatting-Guide-261232088IntroductionDid YOU Know that you can use the  tag in boxes, journals, descriptions, and in litterature?Well, yes you can! No Premium Membership REQUIRED!To prove my point, below!Test.Test.Test.Test.Test.LOL!The TagDid you enjoy the awesome presentation of the "Test." text above? Well, here's the source code:Test.Test.Test.Test.Test.<font face="Helskini, Klavika, FF Me
Spreading the dA Love: Vol. 6Welcome to the 6th volume of Spreading the DA Love:iconGoldendAplz::iconGoldendAplz:As the title suggests, this news article series aim to promote wonderful aspects of the deviantART community, from showcasing beautiful works of art, to informing you of great groups, and to interviewing inspirational deviants. I feel so happy being part of such a wonderful community and I hope to make it better, even if it's only a little bit, by making these articles. My goal is to bring to light everything that impassions me and, hopefully, inspire you!=======================================================Showcasing Gorgeous Artwork=======================================================Here I will showcase art that has simply left me speechless from all genres, from digital/traditional, artisan, emoticons, fractals, etc. :thumb2604302


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USA, OH, Aurora
Joined Jan 2006
30,076 Posts
FG's Scale Forums Expand!
As Flyinggiants.com continues down its interwebz journey, the website (now in its 7th year) has witnessed many things change. From the radio equipment we use, the companies who supply us to the motors and motor sizes available to us. As I sit here and monitor the journey we are all taking together, I have watched many of us slowly start to eyeball scale airplanes. Don't get me wrong, 3D is here to stay, develop and expand and FG will always be the site to expose, promote and adore all things 3D! But I think it's time that we shine a little light on the other side of this awesome hobby. Scale Airplanes!
If you haven't noticed, we have added a few new forums to FG in the past week or so, and we would like to point them out. Together as a community we can start to build a great "Scale" resource to use and share. If you click the "forums" button and scroll down, you will see a new main header: "Scale Airplanes and Techniques". This main forum has five sub headings: -Scale Civilian Planes -Scale Warbirds -Scale Build Project Logs -Scale Techniques and Tricks -Scale Event Photo/Video Coverage These forums should cover all the different aspects of the scale world. FG will attend a few of the major scale events and cover them like they have never been covered before. Instead of scale pilots/builders waiting six months to see their 10,000 hour scratch-built warbird in a magazine, FG will have 25+ detailed photos and some videos up usually the same day! We are going to bring the exciting and friendly vibe that FG is to the Scale world. It's about time. So all you closet Scale/Warbird guys, get to posting and join the ranks of Crazy Karl and his 50% Pitts Pyton M12 Scratch Build or Damon "dag214" and his insane 257" B-36D Scratch Build. Or if you are building a civilian or warbird ARF and you're going to "scale" it out, please share your tricks and tips. I really think we can add a whole new level of fun to our web community. Heck, maybe this year we add "lowest, fastest, inverted warbird pass" to the Huckfest Tour! Guys, please enjoy the new scale forums, adding some new flavor will be a lot of fun! |
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Report Vol. 2 - 2013 - Circular Economy Reports - Ellen MacArthur Foundation - 1 views
"Analysis shows that the adoption of the circular economy could be worth as much as USD 700 billion in consumer goods material savings alone, and also highlights added benefits in terms of land productivity and potential job creation. The report features specific examples in product categories that represent 80% of the total consumer goods market by value, namely food, beverages, textiles, and packaging. "


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Vesicular monoamine transporter
This article's lead section may not adequately summarize key points of its contents. (May 2013) |
The vesicular monoamine transporter (VMAT) is a transport protein integrated into the membrane of synaptic vesicles of presynaptic neurons. It acts to transport monoamine neurotransmitters – such as dopamine, serotonin, norepinephrine, epinephrine, and histamine – into the vesicles, which release the neurotransmitters into synapses as chemical messages to postsynaptic neurons. VMATs utilize a proton gradient generated by V-ATPases in vesicle membranes to power monoamine import.
Pharmaceutical drugs that target VMATs have possible applications for many conditions, leading to a plethora of biological research. These applications include drug addiction, psychiatric disorders, Parkinson's disease, and other neurological disorders. Many drugs that target VMAT act as inhibitors and alter the kinetics of the protein. Much research regarding the effects of altered VMATs on biological systems is still ongoing.
The two VMAT isoforms are:
Monoamines transported by VMATs are mainly noradrenaline, adrenaline, dopamine, serotonin, histamine, and trace amines.[1] Exogenous substrates include guanethidine and MPP+.[2]
VMAT research began in 1958 with the discovery of secretory vesicles by Nils-Åke Hillarp. VMATs have been studied for nearly four decades. In the 1970s, scientists such as Arvid Carlsson recognized the need to understand how transport systems and ion gradients work in different organisms in order to explore new treatment options such as Reserpine. Researchers discovered inhibitors that blocked the uptake of neurotransmitters into vesicles, suggesting the existence of VMATs.[3] A decade later molecular genetic tools have improved methods for protein identification. Scientists have used these tools to analyze DNA and amino acid sequences, discovering that transporters in bacteria and humans were very similar. This finding illustrated the importance and universality of transporters.[4] The transporters were first structurally identified by cloning VMATs in rats.[3] VMAT was first isolated and purified in bovine chromaffin granules, in both native and denatured forms.[5]
There are two types of VMATs expressed in humans: VMAT1 and VMAT2.[4] VMAT1 is expressed mainly in large dense-core vesicles (LDCVs) of the peripheral nervous system. VMAT1 may be found in neuroendocrine cells, particularly chromaffin and enterochromaffin granules which are largely found in the medulla of the adrenal glands. It is also expressed in sympathetic neurons and blood platelets.[6]
VMAT2 favors expression in a variety of monoaminergic cells of the CNS such as the brain, sympathetic nervous system, mast cells, and cells containing histamine in the gut.[citation needed] It is also prevalent in β-cells of the pancreas.[7] VMAT2 is also co-expressed in chromaffin cells.[7] Expression of the two transporters in internal organs seems to differ between species: only VMAT1 is expressed in the rat adrenal medulla cells whereas VMAT2 is the major transporter in the bovine adrenal medulla cells.[8]
Structure and Function[edit]
Both isoforms of VMAT, VMAT1 and VMAT2, are acidic glycoproteins with a molecular weight of approximately 70 kDa.[4][9] Both isoforms are transmembrane proteins with 12 transmembrane domains (TMD's).[4]
VMAT functions in loading the neurotransmitters dopamine, serotonin, histamine, norepinephrine, and epinephrine into transport vesicles.[10] Collectively these neurotransmitters are referred to as monoamines. VMAT uses the same transport mechanism for all types of monoamines.[5] VMATs transport monoamines from the cytosol into high-concentration storage vesicles.[4] Transport vesicles are released into the space between neurons, called the synaptic cleft, where they convey a chemical message to the next neuron. VMATs also function in sorting, storing, and releasing neurotransmitters, and are believed to participate in protecting these neurotransmitters from autoxidation.[4] VMATs are also known to continue biochemical modification after loading of certain neurotransmitters.[4]
Vesicle packing requires a large energy source to store large numbers of neurotransmitters into a small vesicular space at high concentrations. VMAT transport relies upon the pH and electrochemical gradient generated by a vesicular H+-ATPase for this energy source.[4][11] The current model of VMAT function proposes that efflux of two protons against the H+ gradient is coupled with influx of one monoamine.[4][11] The first H+ efflux generates a transporter conformation associated with a high-affinity amine-binding site in the cytosolic phase; the second H+ efflux is coupled with a second large conformational change that leads to amine transport from the cytosolic side into the vesicle, reducing amine-binding affinity.[4]
Studies indicate that the amino acid residue His419, located on the domain between TMD X and XI of rat VMAT1, plays a role in energy coupling to the amine transport by assisting the first proton-dependent conformational change.[4][12] It has been proposed that Reserpine (RES) inhibits VMAT by interacting with this conformation.
VMAT gene sequence analysis demonstrates that 4 aspartic acid residues in the middle region of TMD I, VI, X, and XI and one Lysine residue in TMDII have highly conserved gene sequences, suggesting these residues play a critical role in transporter structure and function.[4][13] Specifically, the residues Lys 139 and Asp 427 are thought to compose an ion pair that promotes high-affinity interaction with VMAT substrates and inhibitors.[4][13] The Asp431 residue located in TMD XI is believed to be critical for amine transport, but does not interact with RES binding; this residue is thought to complete the substrate transport cycle.[4][14]
VMATs have a relatively low Vmax, with an estimated rate of 5–20/sec depending on the substrate.[15] Vesicle filling may limit monoamine release from neurons with high rates of firing.
Specific amine-binding affinity varies by VMAT isoform; studies indicate that catecholamines dopamine, norepinephrine, and epinephrine have three-fold higher affinity for VMAT2 binding than for VMAT1 binding and uptake.[4][11][16] The Imidazoleamine Histamine has a thirty-fold higher affinity for VMAT2 compared to VMAT1[4] and is thought to bind to a different site from that of other monoamines.[11] Unlike catecholamines and histamine, the indoleamine serotonin (5HT) binds to VMAT1 and VMAT2 with a similar affinity for both transporter isoforms.[4][16]
VMAT1 has a lower turnover number and a lower affinity for most monoamine substrates than VMAT2. This may be because of VMAT2's location in the central nervous system, which demands fast recovery from neurotransmitter release in order to prepare for the subsequent release. The uptake efficiencies of each VMAT substrate can be ranked in order of efficiency as follows: serotonin, dopamine, epinephrine, and norepinephrine.[4]
Methamphetamines decrease Vmax, while cocaine increases Vmax reversibly in rat brain.[4]
The effects of VMAT inhibition have been studied in-depth in animal models. Mutant homozygous VMAT(-/-) mice move little, feed poorly, and die within a few days of birth.
More specifically, inhibition of VMAT2 may cause an increase in cytosolic catecholamine levels. This can result in an increase in efflux of catecholamines through the plasma membrane, depleting catecholamine concentrations and causing increased oxidative stress and oxidative damage to the neuron.
Heterozygous VMAT mutants display hypersensitivity to amphetamine, cocaine and MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), the latter being a substance causally linked to Parkinson's Disease in rodents.[6] This suggests a protective role of VMATs against oxidative stress through removal of such substances from the cytosol.[6]
VMAT inhibitors include:
- Reserpine(RES), bietaserpine, and ketanserin(KET) (potent inhibitors of VMAT2 mediated serotonin transport)
- Tetrabenazine(TBZ) (specific to VMAT2)
- Phenylethylamine
- Amphetamine
- N-methyl-4-phenylpyridinium (MPP+)(very potent inhibitors of VMAT2 mediated serotonin transport)
- Fenfluramine (specific to VMAT1 )
- Non-hydrolysable GTP-analogue guanylyllimidodiphosphate GMP-P(NH)P (VMAT2 only)
Binding Site Structures[edit]
Ligand-binding affinities and structures[edit]
Two known binding sites for VMAT inhibitors include the Reserpine (RES) binding site and the Tetrabenazine (TBZ) binding site. Some evidence suggests these two sites may overlap or may actually exist as two separate conformations of the same binding site.[4][11] VMAT inhibitors tend to fall into two classes; those that interact with the RES binding site and those that interact with the TBZ binding site.[11]
Reserpine (RES), Methoxytetrabenazine (MTBZ), and the drug Amiodarone bind to the RES binding site conformation. Tetrabenazine (TBZ, also called Nitoman and Xenazine), Dihydrotetrabenazine (DTBZOH), Ketanserin (KET), and the drug Lobeline bind to the TBZ binding site/conformation. Amphetamine, methamphetamine and GZ-7931 are also known to interact with VMAT2.[4][17][18][19]
Inhibitor affinity varies among VMAT isoforms. RES and KET have higher inhibitory affinity for VMAT2–mediated 5HT transport than for that of VMAT1; TBZ seems to inhibit VMAT2 exclusively.[4]
The residues aspartate-33 and serines-180, 181, and 182 are believed to be involved in substrate recognition; these residues interact with the protonated amino group and hydroxyl group on the catechol or indole rings.[11]
Cocaine and methylphenidate (MPD, also known as Ritalin and Concerta) are believed to interact with VMAT2 in such a way that causes a shift in VMAT2 protein "from a plasmalemmal membrane-associated fraction to a vesicle-enriched, nonmembrane-associated fraction."[20]
Reserpine binding site[edit]
Consistent with catecholamine-binding affinity, Reserpine (RES) has a threefold higher affinity for VMAT2 than for VMAT1.[11][16] The RES binding sight is known to be hydrophobic, and this is thought to contribute to ligand binding affinity.[4] Methamphetamine binds to the reserpine site on VMATs.[21]
The current working model proposes that RES and the substrate bind to a single site in a pH-gradient modulated conformational structure of the transporter. This conformation occurs after the transport of one proton across the membrane and into the vesicle; proton transport drives the substrate recognition site from the lumen to the cytoplasmic surface of the vesicle for RES and substrate binding.[4][11][22] Methoxytetrabenazine (MTBZ) may bind to the RES binding site, based on studies indicating that RES significantly inhibited MTBZ-binding.[4] The drug Amiodarone is also believed to inhibit monoamine vesicular uptake by binding to the RES binding site.[4]
Tetrabenazine binding site[edit]
Tetrabenazine (TBZ) and Dihydrotetrabenazine (DTBZOH) are believed to bind to a different binding site from the RES/substrate binding site, or to a different conformation of the RES/substrate binding site.[4][11][23] This site is believed to be located at the N-terminus, based on studies done in bovine VMAT2.[11] Tyrosine-434 and aspartate-461 are identified as being responsible for the high-affinity interaction of TBZ, serotonin, and histamine in VMAT2.[11] Unlike methamphetamine, amphetamine binds to the TBZ site on hVMAT2.[21]
Unlike Reserpine inhibition, TBZ inhibition is affected only by very high concentrations of monoamines; however, single injections of Reserpine can inhibit TBZ binding.[11] Ketanserin (KET)[4][22] and the drug Lobeline[4][11] also bind to the TBZ binding site conformation.
Glycosolation sites: N- and C-linked terminals[edit]
Three to four glycosolation sites exist in the vesicular matrix on a loop between TMDI and TMDII.[4] In biology, the vesicle matrix refers to the material or tissue between cells in which more specialized structures are embedded. Two of the glycosylation sites, the N-linked glycosylation terminal and C-linked terminal, are located in the cytosolic portion of the vesicle.[4][24]
The highest amount of genetic variance between VMAT1 and VMAT2 exists near the N- and C- terminals in the cytosolic phase, and in the glycosylated loop between transmembrane domains I and II.[4]
C-Terminus and VMAT Trafficking Cycle[edit]
Several motifs involved in the VMAT trafficking cycle are believed to be encoded in the C-terminus. A dileucine motif in the C-terminus is required for VMAT2 endocytosis.[7] Studies suggest the acidic residues in the dileucine motif sort VMAT2 away from constitutive secretory vesicles and into the regulated secretory pathway.[7] The hydrophobic residues in the dileucine motif are thought to further couple with the acidic residues as a single unit to help sort VMAT2 to large dense course vesicles.[7] Acidic glutamate residues located upstream of the dileucine motif are known to be important for localization of VMAT2 to large dense core vesicles; these residues are also conserved in VMAT1.[7]
Genetic Expression and Transporter Regulation[edit]
Although both VMAT1 and VMAT2 are encoded by two different genes, the individual genetic sequences demonstrate high homology.Polymorphisms in VMAT2 that effect regulation and quantitative expression may pose genetic risk factors for Parkinson's disease. Moreover, a specific VMAT1 gene (SLC18A2) has several associated polymorphisms which have a locus 8p21.3 that has been strongly connected to schizophrenia susceptibility.
Over-expression of VMAT2 results in increased secretion of neurotransmitter upon cell stimulation. Data suggests that deletion of the VMAT2 genes does not effect the size of small clear-core vesicles.
VMATs may be regulated by changes in transcription, post-transcriptional modifications such as phosphorylation and mRNA splicing of exons, and vesicular transport inactivation facilitated by heterotrimeric G-proteins. It is thought that chromaffin granules possess these heterotrimeric G-proteins which have shown to be regulatory to small clear-core vesicles.[6][7]
Specific heterotrimeric G-protein type regulation is tissue-dependent for VMAT2; it is not known whether this is the case for VMAT1. Heterotrimeric G-protein Gαo2 decreases VMAT1 activity in pancreatic and adrenal medulla cells, and activates heterotrimeric G-proteins inhibit VMAT2 activity in the brain, regardless of whether localised on small clear-core or large-dense-core vesicles. Activated heterotrimeric G-protein Gαq downregulates VMAT2 mediated serotonin transport in blood platelets, but this is not the case in the brain where Gαq inhibits VMAT2 activity completely.[6] Although the exact signalling pathway for G-protein mediated regulation of VMATs is not known,[6] it has recently been described that implicated G-proteins act directly on the VMATs themselves.[25]
Clinical significance[edit]
VMAT2 has been shown to contribute to many clinical neurological disorders including drug addiction, mood disorders and stress,[26] as well as Parkinson's Disease[27] and Alzheimer's Disease.[28][29]
Parkinson's Disease[edit]
Studies indicate VMAT2 mRNA is present in all cell groups damaged by Parkinson's Disease (PD);[30] these findings have identified VMAT2 as a target for Parkinson's prevention. VMAT2 presence does not independently protect neurons from Parkinsonian damage; however, a decrease in VMAT2 expression has been shown to correlate with susceptibility to Parkinson's Disease[30] and this may be due to a ratio between the Dopamine transporter and VMAT2.[30]
Based on the understanding the increased cytosolic Dopamine levels lead to dopaminergic cell death in PD, it has been proposed that regulatory polymorphisms in VMAT2 affect VMAT2 quantitative expression and may serve as a genetic risk factor for PD. Specifically, the SLC18A2 promoter region for the VMAT2 gene has been identified as an area where several polymorphisms form discrete haplotypes.[4][31]
Mood Disorders[edit]
Studies using a genetic rodent model to understand clinical depression in humans suggest that VMAT2 genetic or functional alterations may play a role in depression.[32] Reduced VMAT2 levels were identified in specific subregions of the striatum involved in clinical depression, including the nucleus accumbens shell but not the core, the ventral tegmental area, and the substantia nigra pars compacta. The reduced VMAT2 protein levels were not accompanied by similar levels of VMAT2 mRNA alterations. Based on these findings it has been proposed that VMAT2 activity is not altered at the level of genetic expression, but may rather be altered at the functional level in ways that may correlate with clinical depression.[4]
Drug Addiction[edit]
Many Psychostimulant drugs are known to interact with VMAT, including Amphetamine analogs such as Methamphetamine (METH), Cocaine, and Ecstasy (MDMA). See the Pharmacology section of this article for more information on these drugs' interactions.
As addressed above, VMAT inhibitors tend to fall into two classes; those that interact with the RES binding site and those that interact with the TBZ binding site.[11]
Reserpine, methoxytetrabenazine, and the drug amiodarone bind to the RES binding site conformation.
Tetrabenazine (branded Nitoman and Xenazine), dihydrotetrabenazine, ketanserin, and the drug lobeline bind to the TBZ binding site/conformation.
Substituted amphetamines, including but not limited to methamphetamine, as well as cocaine, are known to interact with VMAT2. Studies indicate that both amphetamines and cocaine act to increase non-exocytotic release of dopamine in specific regions of the brain by interacting directly with VMAT2 function.[4][20][17]
VMAT is a main target of methamphetamine. Studies indicate that substituted amphetamines including methamphetamine interact with VMAT2 at the TBZ/DTBZOH binding site/conformation.[4][20] By acting as a competitive antagonist, methamphetamine blocks the presynaptic cell's ability to use VMAT for vesicular packaging.
Methamphetamine alters the subcellular location of VMAT2 which affects the distribution of dopamine in the cell. Treatment with methamphetamine relocates VMAT2 from a vesicle-enriched fraction to a location that is not continuous with synaptosomal preparations.[8]
Repeated amphetamine exposure may increase VMAT2 mRNA in certain brain regions with little or no decline upon withdrawal from the drug.[8]
A study performed by Sonsalla et al. demonstrates that methamphetamine treatment decreases DHTBZ binding and vesicular Dopamine uptake.[20][4] Another study demonstrated that multiple high doses of methamphetamine removed DTBZ binding sites from the vesicles.[11]
In addition to an interaction with the TBZ/DTBZOH binding site, some propose that substituted amphetamines like methamphetamine decrease dopamine uptake because of the weak base properties of substituted amphetamines.[20] This "Weak Base Hypothesis" proposes that amphetamine analogs enters the cell through transport and lipophilic diffusion then likewise diffuses through the vesicular membrane where it accumulates in synaptic vesicles and offsets the proton electrochemical gradient in the vesicle that drives monoamine transport through VMAT.[20] In this way, amphetamine administration would prevent vesicular DA uptake through VMAT, and explain the finding that amphetamine administration correlates with decreased dopamine release from vesicles and a neurotoxic increase in intracellular dopamine.[4][20]
Unlike methamphetamine, the psychostimulant cocaine interacts with VMAT2 in such a way that mobilizes VMAT2-expressing vesicles, causing a shift in VMAT2 protein from a plasmalemmal (synaptosomal) membrane fraction to a vesicle-enriched fraction that is not associated with the synaptosomal membrane and not retained in synaptosomal preparations.[4][11][20] The drug methylphenidate (branded Ritalin and Concerta) is believed to interact with VMAT2 in a similar fashion.[20]
In addition to mobilizing VMAT2-expressing vesicles, cocaine has been shown to increase Vmax of VMAT2 for dopamine, and to increase the number of DTBZ binding sites.[11] Cocaine has also been shown to mobilize a synapsin-dependent reserve pool of dopamine-containing synaptic vesicles, thereby interacting with the vesicular trafficking cycle to increase dopamine release.[11]
Short-term exposure to cocaine increases VMAT2 density in the prefrontal cortex and striatum of mammalian brains. This is theorised to be a defensive mechanism against the depletive effects cocaine has on cytosolic dopamine through increasing monoamine storage capacity.[8] Chronic cocaine use has been implicated with a reduction in VMAT2 immunoreactivity as well as a decrease in DTBZOH binding in humans.
Research suggests a decline in VMAT2 protein through prolonged cocaine use could play an important role in the development of cocaine induced mood-disorders.[8]
The psychostimulant MDMA (popularized as ecstasy or XTC) is known to affect serotonergic neurons, but has been shown to inhibit synaptosomal and vesicular uptake of serotonin and dopamine[4] to roughly the same extent in vitro.[11] En vivo studies indicate short-term MDMA exposure causes short-term reduction in VMAT2 activity, which is reversed after 24h.[11]
Current Research[edit]
Clinical Research[edit]
Genetic research models have shown that polymorphisms in SLC18A1 and SLC18A2, the genes that encode for VMAT1 and 2 proteins respectively, may confer risk for some neuropsychiatric disorders;.[4][33][34] however, no specific diseases have yet been identified as directly resulting from a genetic mutation in an SLC18 gene, the gene that codes for VMAT proteins.[34]
Much of the current research related to VMAT explores the genetic underpinnings of neuropsychiatric disorders as they may be affected by SLC18A family mutations.
The dopaminergic neuron is known to play a central role in drug addiction and abuse and the potential role of the dopamine transporter (DAT) has been well-explored as a target for amphetamine and cocaine. Current research looks toward VMAT2 as a target for such psychostimulants. This is discussed in the Pharmacology section of this article. A combination of imaging, neurochemical, biochemical, cell biological, genetic, and immunohistochemical evidence has been compiled to provide the most current comprehensive understanding of the role the VMAT2 plays in AMPH and cocaine abuse and addiction through aminergic neurotransmission.[34][35]
As VMATs are membrane proteins, structural information is limited and researchers have yet to completely understand the structure of both isoforms. Further studies are needed in order to determine the structure and therefore complete function of these proteins. There is preliminary evidence that the gene for VMAT1 may be linked to susceptibility to schizophrenia, bipolar disorder, and various anxiety disorders.[4] Further studies are needed in order to confirm these findings and to gain a better understanding of the role of VMATs in the central nervous system.
Multiple single-nucleotide polymorphisms (SNPs) have been identified in the coding region of VMATs. The effects of some of these SNPs have been alteration of VMAT function, structure and regulation.[36] Further investigation of these SNPs is required in order to distinguish whether they may be attributable to certain diseases with suspected SNP-mutation origins.
α-synuclein, a cytosolic protein found mainly in pre-synaptic nerve terminals has been found to have regulatory interactions with the trafficking of VMATs. Moreover, mutations involving α-synuclein have been linked to familial Parkinson's Disease.[36] Further research is needed to clarify the extent to which these proteins modulate the trafficking of VMATs and whether they may be exploited in order to gather more information as to the exact mechanism of how disorders such as Parkinson's occur, and therefore, how they may potentially be treated.
Studies have shown that at the synaptic membrane, enzymes responsible for the synthesis of dopamine, tyrosine hydroxylase (TH) and amino acid aromatic decarboxylase (AADC) are physically and functionally coupled with VMAT2.[37] It was initially thought that the synthesis of these substances and the subsequent packaging of them into vesicles were two entirely separate processes. Such a finding could impact the approach to treatment methods for dopamine-related disorders such as schizophrenia and Parkinson's Disease.
Animal Research[edit]
Current research related to VMAT uses VMAT2 knockout mice to explore the behavioral genetics of this transporter in an animal model. VMAT2 knockouts are known to be lethal as homozygotes, but heterozygote knockouts are not lethal and are used in many studies as a durable animal model.[34] For more complete discussions on VMAT2 animal research, see discussions in the following review articles: (Lawal & Krantz, 2013),[8][34]
From knockout and knockdown mice researchers have discovered that it is good to have over-expression or under-expression of the VMAT genes in some circumstances.[34] Mice are also used in drug studies, particularity studies involving the effect cocaine and methamphetamine have on VMATs.[34] Studies involving animals have prompted scientists to work on developing drugs that inhibit or enhance the function of VMATs. Drugs that inhibit VMATs may have use in addiction but further studies are needed.[34] Enhancing the function of VMATs may also have therapeutic value.[34]
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VMAT2 is the CNS vesicular transporter for not only the biogenic amines DA, NE, EPI, 5-HT, and HIS, but likely also for the trace amines TYR, PEA, and thyronamine (THYR) ... [Trace aminergic] neurons in mammalian CNS would be identifiable as neurons expressing VMAT2 for storage, and the biosynthetic enzyme aromatic amino acid decarboxylase (AADC).
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- ^ Schwartz K, Yadid G, Weizman A, Rehavi M (2003). "Decreased limbic vesicular monoamine transporter 2 in a genetic rat model of depression". Brain Res 965: 174–179. doi:10.1016/s0006-8993(02)04167-7.
- ^ Glatt CE, Wahner AD, White DJ, Ruiz-Linares A, Ritz B (2006). "Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women". Hum Mol Genet 15: 299–305. doi:10.1093/hmg/ddi445.
- ^ a b c d e f g h i Lawal HO, Krantz DE. (2013). "SLC18: Vesicular neurotransmitter transporters for monoamines and acetylcholine," Molecular Aspects of Medicine; 34(2-3) 360-372. Doi: 10.1016/j.mam.2012.07.005
- ^ Eiden E, Weihe (2011). "VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse." Ann. NY Acad". Sci 1216: 86–89. doi:10.1111/j.1749-6632.2010.05906.x.
- ^ a b Sager, J.J. & Torres, G.E., 2011. Proteins interacting with monoamine transporters: Current state and future challenges. Biochemistry, [online] Available at: <http://pubs.acs.org/doi/ipdf/10.1021/bi200405c>[Accessed 20 April 2013]
- ^ Sager, J.J. & Torres, G.E., 2011. Proteins interacting with monoamine transporters: Current state and future challenges. Biochemistry, [online] Available at: <http://pubs.acs.org/doi/ipdf/10.1021/bi200405c>[Accessed 20 April 2013]
External links[edit]
- Vesicular Monoamine Transport Proteins at the US National Library of Medicine Medical Subject Headings (MeSH)
Further reading[edit]
- Kilbourn MR (1997). "In vivo radiotracers for vesicular neurotransmitter transporters". Nucl. Med. Biol. 24 (7): 615–9. doi:10.1016/S0969-8051(97)00101-7. PMID 9352531.
- Lawal HO, Krantz DE (2013). "SLC18: Vesicular neurotransmitter transporters for monoamines and acetylcholine". Molecular Aspects of Medicine 34 (2-3): 360–372. doi:10.1016/j.mam.2012.07.005.
- Weihe E, Eiden LE (2000). "Chemical neuroanatomy of the vesicular amine transporters". FASEB J. 14 (15): 2435–49. doi:10.1096/fj.00-0202rev. PMID 11099461.
- Wimalasena, K. (2011). "Vesicular Monoamine Transporters: Structure-Function, Pharmacology, and Medicinal Chemistry". Medicinal Research Reviews 31 (4): 483–519. doi:10.1002/med.20187. PMC 3019297. PMID 20135628.


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The notorious Gang of Eight decided to waste no time after the elections.
The bipartisan group of senators, which is meeting in an unofficial capacity to try and reach agreements on how to head off the fiscal cliff, scheduled a conference call on Wednesday to regroup post election.
The gang has not been sanctioned by leadership for either party to try to negotiate a deal, but members hope that if they can reach a bipartisan compromise they can help the fractured parties come together.
The gang is not expected to meet again in person until after Congress resumes for a lame-duck session.
The gang consists of Democratic Sens. Kent Conrad of North Dakota, Dick Durbin of Illinois, and Mark Warner of Virginia; and Republican Sens. Saxby Chambliss of Georgia, Tom Coburn of Oklahoma, and Mike Crapo of Idaho, as well as additions Michael Bennet, D-Colo., and Mike Johanns, R-Neb.
Gang of Eight Regroups Post-Election