text:
Kitty: I do hope your Seamus gets to feeling perkier soon...poor kitty
cat! Now are the other two positive for this disease or are you still
waiting on their test results? Sounds like this bartonellosis is quite
the serious thing...best of luck to you and your furry pals with it! And
yes, our pup is getting to be quite a good size...had her at the vet for
the current round of puppy vaccinations and she weighed in at 48.5
pounds at 16 weeks...started out at 19 pounds at 9 weeks so she has
doubled her weight in 7 weeks time. But this is what we wanted...a big
dog who is noticeable around the neighborhood for her size and she's got
quite a loud bark...she is quite attentive to the goings on around her
and already is good at letting us know when someone is coming around. A
few more months of growing and training and she'll be ready to take over
doing my worrying for me when I'm at home with just me and the
kids...And I need to teach her the difference between a garden spot s
he needs to stay out of and an acceptable place for her to be tramping
about in...any body got any suggestions for that one I'd appreciate
hearing about it! Thanks!
Melody, IA (Z 5/4)
"The most beautiful thing we can experience is the mysterious."
--Albert Einstein
--- On Sat 04/12, Kitty Morrissy < email@example.com > wrote:
From: Kitty Morrissy [mailto: firstname.lastname@example.com]
To: email@example.com
Date: Sat, 12 Apr 2003 22:50:57 -0500
Subject: Re: [CHAT] Re: < now Thelma
The vet says Seamus should be more active after treatment
for
bartonellosis, because he'll feel so much better. Hopefully,
he'll work
off some of the weight. It's much harder to restrict one
cat's diet when
you feed 5.
Melody, sounds like a sizeable puppy
there. I had a Malamute puppy years
ago. Weighed about 20 when we got
him. Weeks later wehn he should have
been 45#, he'd barely gained
any. Found out his body stopped making
enzymes. So we used ground up
lamb's pancreas to digest his food before he
ate it and he was
quickly back up to speed on weight. At 6mo. he was 90#.
And he
always liked to sleep on my pillow...which got kind of
difficult.

Kitty

> [Original Message]
> From: Pamela J.
Evans <email@example.com>
> To: <firstname.lastname@example.com>
>
Date: 4/12/2003 9:03:30 PM
> Subject: Re: [CHAT] Re: < now
Thelma
>
> Well Melody - he'll figure it out if they whack him
one, assuming your
cats have their h
ooks of course.
> Sugar does, but I know some people de-claw
theirs.
> And even on 1/2 to 2/3 cup of food a day, I can't seem to
get Sugar to
lose weight. Sigh. Just like her mama.
>
>
>
---------- Original Message ----------------------------------
>
From: "Melody" <email@example.com>
> Reply-To:
email@example.com
> Date: Fri, 11 Apr 2003 05:43:06 -0400
(EDT)
>
> >Good luck there, Kitty...I've never had much luck in my
past with
> >getting my fat cats to lose weight once they'd already
gained it. With
> >our current two cat companions, we've worked hard
at keeping their
> >weights down to within normal range. Course,
right now, they are
> >probably being fed a little too often, because
with the new puppy in the
> >house who eats anything in sight,
including the cats' food, we are
> >filling their bowl more often
just to make sure they are getting
> >something to eat everyday. This
pup is gaining nearly 2.5 pounds
a week,
> >on average...last week she weighed in at a little over 35
pounds and
> >she's only 16 weeks (4 months) old!!!!! Of course, the
cats are getting
> >considerably more exercise, too, with her in the
house...she seems to
> >think that all that hissing and growling they
do at her means they
> >actually like her and just want to play!
LOL!!!
> >
> >
> >
> >Melody, IA (Z 5/4)
> >
> >"The
most beautiful thing we can experience is the mysterious."
>
>--Albert Einstein
> >
> > --- On Tue 04/08, Kitty Morrissy <
email@example.com > wrote:
> >From: Kitty Morrissy [mailto:
email@example.com]
> >To: email@example.com
> >Date: Tue, 8
Apr 2003 21:12:11 -0500
> >Subject: Re: [CHAT] Re: < now Thelma
>
>
> >Well, it is his winter weight. Hopefully he'll peel off a few
#
> >before
summer.

Kitty

> [Original
Message]
>
> >From: Island Jim <email@example.com>
> To:
br>>
> >Date: 4/8/2003 6:15:20 PM
> Subject: Re: [CHAT] Re: <
now
> >Thelma
>
> 20 pounds? man, that diet must be
working.
>
> At
> >02:09 PM 4/8/03 -0500, you wrote:
>
>Zem,
> >ONE pound!?! How
> >darling! Seamus went in for his Bart
test and....I
> >hesitate to say
> >this becuase Jim is going to
jump all over it.....but
> >he's now 20
> >pounds. It's a bear
just picking this guy up. I think we're
> >ALL
> >going to go on a
diet just to give him moral support. Now I just
>
> >>have to
figure out how to keep him from "dining out". Very happy to
>
>hear
> >that Thelma is doing so well...but how could she not, with
a
> >mommy like
> >you?
> >
> >
> >Just cats for you from
now on?
> >sometimes that can be the smart choice.
> >
>
>Kitty
> >
>
> >>-------Origi
> >
> >nal
Message-------
> >From: firstname.lastname@example.com
> >Sent: 04/08/03
03:35
> >PM
> >To: email@example.com> >Subject: Re: [CHAT] Re: < now
> >moving north, now hot
weather
> >
> > >
> > > In a message
> >dated 04/08/2003
12:03:10 PM Central Daylight Time,
>
> >>firstname.lastname@example.com
writes:
> >
> >
> > > Well take into
> >account that I've
had rheumatoid arthritis since I was
15
> >
> >>
> >
>
>Good grief, you too? Well, I didn't get juvenile RA until
> >I was
30, but
> >then
> >I've always known I was a "late bloomer."
>
><LOL> Anyway, mine went into
> >remission when I got a divorce!
>
>Should have paid attention to that
> >because
> >the next time
I
> >tried being married I got cancer! Another divorce seems
>
>to
>
> >>have cured that as well... From here on it's just cats
for me.
> >Speaking
of
> >
> >which, took Thelma to the vet
today. She
> >weighs one pound and is in
> >excellent health.
>
>
> >zem
>
> >>
> >
> >If
> >
> >you have weeds,
Join Excite! - http://www.excite.com
The most personalized portal on the Web!
To sign-off this list, send email to email@example.com with the
message text UNSUBSCRIBE GARDENCHAT


text:
TCM Archive Materials VIEW ALL ARCHIVES (0)
Recent DVDs
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|Also Known As:
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|San Saba, Texas, USA
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Students from opposite sides of the tracks fight for their love.
Please support TCMDB by adding to this information.Click here to contribute

subset: commoncrawl


text:
It was so much fun; we're doing it again! Join UW-Green Bay alumni, along with eight UW System campuses, for fun and relaxation at the Kalahari Resort and Waterpark Friday through Sunday, Jan. 6 through 8. This is a great deal and one event you don't want to miss.
Friday night will include an all UW pizza party. Be sure to wear your UWGB gear and show your Phoenix pride. Prizes will be given to those who show the most school spirit.
Saturday, swim the day away in the water park or just have good ole fun at the amusement park.
This is a "bring your family and friends" event. To make reservations, please call 877-253-5466 and ask for the UW-Green Bay Alumni Association room block with a rate of $159 per night. Reservations must be made by Tuesday, Dec. 6, 2016. Reserve today.
Room rate includes:
- Guest room, up to 4 people (suites available at discounted rates)
- Friday Evening Pizza Social – 6:30 – 8:00 in the Indoor Theme Park (additional $14.99 per person gets you all-weekend access to the Indoor Theme Park)
- All-weekend access to the Indoor waterpark – 125,000 square feet of wet & wild indoor fun!
- Saturday, 9 a.m. to 2 p.m. access to the UWGB indoor cabana with flat screen TV, chaise lounges, snacks, and activities & contests for kids.
- Ask for block "UW-Green Bay Alumni Association"
- Two Room Suite is $269.00 per night
We hope you can join us for this fantastic weekend of fun!


text:
Read More About
Recommended For You
Villa Enterprises Management Ltd. Inc., a global multi-concept restaurant franchisor, announced the opening of two Villa Italian Kitchen locations this month at the Outlet Shoppes at Atlanta in Woodstock, Georgia, and the Las Vegas Premium Outlets in Las Vegas.
"We're committed to growing our brand's presence in outlet shopping centers, which gives us a great opportunity to introduce our authentic Italian flavors to millions of shoppers," says Adam Torine, senior vice president of business development at Villa Enterprises Management. "Our growth continues with the outlet centers in Atlanta and Las Vegas, and we're thrilled to have a place to call home in each community."
The Outlet Shoppes at Atlanta opened its doors in July and has quickly become a staple in the community, attracting shoppers and countless travelers from throughout the state. Located near downtown Las Vegas, the Las Vegas Premium Outlets in Las Vegas draws shoppers and tourists from around the world.
Villa Enterprises' family of brands has more than 330 quick-serve concepts in shopping centers, airports, college campuses and casinos worldwide. To date, the global restaurant franchisor operates in 38 U.S. states, Washington, D.C., Puerto Rico, and seven additional countries.
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tweets replied on Permalink
I recently visited the outlet mall in Woodstock GA on Mar 1 2014. I wanted to eat at the villa italian kitchen since there was no line, needless to say we figured out why! the 2 girls working said they was the only ones there and they was not going to make strombolis, we can have cold pizza or nothing! As the minutes went on people coming and going, I notice the one girl making pizzas without using gloves. Neither of the girls had name tags on, and just plain RUDE!


text:
Conflict of Interest:
Policy and Procedure
Angelo State University's policy and procedure applies to all faculty and staff who serve as the principal investigator, project director, or other senior/key personnel responsible for the development and conduct of a sponsored project.
What do I have to report?
In short, you must report any significant financial interests that might reasonably appear to be affected by your institutional responsibilities. Specific details regarding the types of interest and dollar thresholds are outlined in ASU's Operating Policy 56.08.
How often do I have to report?
Upon submitting a proposal for an externally sponsored grant, cooperative agreement, or contract and once a year thereafter. Additionally, if you gain a significant financial interest during the course of the year, you must report the new interest within 30 days of acquiring it.
How often do I have to attend training?
For individuals working on projects funded by the Public Health Service (PHS) or the Cancer Prevention and Research Institute of Texas (CPRIT), training must be completed once every four years or whenever the policy is revised, whichever comes first. Online training is available through ASU's subscription to the CITI Program. Individuals needing to complete training should e-mail the Office of Sponsored Projects for more details on accessing the online course.


text:
Minority Rights, Majority Rule
Partisanship and the Development of Congress
By (author) Sarah A. Binder
Format: Hardback
Normal Price: $180.00
Your Price: $162.00 AUD, inc. GST
Shipping: $7.95 per order
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Availability: Available to Backorder, No Due Date for Supply
Minority Rights, Majority Rule by Sarah A. Binder
Book DescriptionMinority Rights, Majority Rule seeks to explain a phenomenon evident to most observers of the US Congress. In the House of Representatives, majority parties rule and minorities are seldom able to influence national policy making. In the Senate, minorities quite often call the shots, empowered by the filibuster to frustrate the majority. Why did the two chambers develop such distinctive legislative styles? Conventional wisdom suggests that differences in the size and workload of the House and Senate led the two chambers to develop very different rules of procedure. Sarah Binder offers an alternative, partisan theory to explain the creation and suppression of minority rights, showing that contests between partisan coalitions have throughout congressional history altered the distribution of procedural rights. Most importantly, new majorities inherit procedural choices made in the past. This institutional dynamic has fuelled the power of partisan majorities in the House but stopped them in their tracks in the Senate.
Buy Minority Rights, Majority Rule book by Sarah A. Binder from Australia's Online Bookstore, Boomerang Books.
Book DetailsISBN: 9780521582391
(228mm x 152mm x 19mm)
Pages: 256
Imprint: Cambridge University Press
Publisher: Cambridge University Press
Publish Date: 13-Jun-1997
Country of Publication: United Kingdom
Other Editions...
Books By Author Sarah A. Binder
Advice and Dissent, Paperback (August 2009)
For better or worse, federal judges in the United States today are asked to resolve some of the nation's most important and contentious public policy issues.
Oxford Handbook of Political Institutions, Paperback (June 2008)
The Oxford Handbooks of Political Science are the essential guide to the state of political science today. With engaging contributions from 39 major international scholars, The Oxford Handbook of Political Institutions provides the key point of reference for anyone working on political institutions and beyond.
Institutions of American Democracy: The Legislative Branch, Hardback (April 2006)
A collection of essays by the nation's leading Congressional scholars examine the history, identity, roles, and future of the Legislative Branch.
Stalemate, Paperback (February 2003)» View all books by Sarah A. Binder
Gridlock is not a modern legislative condition. Although the term is said to have entered the American political lexicon after the 1980 elections, Alexander Hamilton complained about it more than two hundred years ago.
» Have you read this book? We'd like to know what you think about it - write a review about Minority Rights, Majority Rule book by Sarah A. Binder and you'll earn 50c in Boomerang Bucks loyalty dollars (you must be a member - it's free to sign up!)
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text:
- Home
- Prospective Students
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- Interdepartmental Modules
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Programme contacts
- Undergraduate Admissions Officer
- Mrs Jo Wolff
- firstname.lastname@example.com
- +44 (0)20 7679 3096
Fees and funding
Tuition fees
The fees indicated are for undergraduate entry in the 2017/18 academic year and are for the first year of the programme at UCL only.
- UK & EU fee
- £9,250 (2017/18)
- Overseas fee
- £17,710 (2017/18)
Various funding options are available, including student loans, scholarships and bursaries. UK students whose household income falls below a certain level may also be eligible for a non-repayable bursary or for certain scholarships. Please see the Fees and funding pages for more details.
We offer the A A Parker and Alcana Galiano prizes annually to the most outstanding undergraduates studying Spanish and Latin American Studies.
Departmental scholarships
The Scholarships and Funding website lists scholarships and funding schemes available to UCL students. These may be open to all students, or restricted to specific nationalities, regions or academic department.
This four-year programme combines the study of Spanish language and its varieties with modules in the film, languages, literature, history and cultures of Spain and Latin America, from the early modern period to the present day. Year three is spent abroad in a Spanish-speaking country.
Degree benefits
- UCL is an important centre for Hispanic and Latin American Studies, with a wealth of expertise in areas from Cervantes to Borges.
- You will receive high-quality language instruction combined with innovative, research-led teaching of a wide range of Spanish and Latin American literature, culture and film topics.
- Your third year will be spent in a Spanish-speaking country - an experience which contributes vastly to your linguistic competence and cultural understanding. The department currently has links with universities in Argentina, Chile, Mexico and Spain.
- You will benefit from the resources of the UCL Library, Senate House Library of the University of London, the Instituto Cervantes, Canning House and the Institute for the Study of the Americas.
Research Excellence Framework (REF) 2014
The Research Excellence Framework, or REF, is the system for assessing the quality of research in UK higher education institutions. The 2014 REF was carried out by the UK's higher education funding bodies, and the results used to allocate research funding from 2015/16.
The following REF score was awarded to the department: School of European Languages, Culture and Society.
- 74% rated 4* (world-leading) or 3* (internationally excellent)
Learn more about the scope of UCL's research, and browse case studies, on our Research Impact website.
Students must take a total of 4 course units each year.
Year One
Compulsory Modules (3.0 course units)
- SPAN1001 Spanish Language 1 (1.0cu)
- SPAN1*/PORT1* modules (2.0cu)
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Two ELCS1* first-year level modules (1.0cu)
Year Two
Compulsory Modules (1.0 course units)
- SPAN2001 Spanish Language 2 (1.0cu)
Optional Modules (3.0 course units)
A total of 2.5cu from SPAN2*/SPAN7*/PORT2* optional modules plus one 0.5cu ELCS6* intermediate-level module.
A total of 2.0cu from SPAN2*/SPAN7*/PORT2* optional modules plus two 0.5cu ELCS6* intermediate-level modules.
Year Three (Year Abroad)
Final Year
Compulsory Modules (1.0 course units)
- SPAN4001 Spanish Language 3 (1.0cu)
Optional Modules (3.0 course units)
A total of 2.5cu from SPAN4*/SPAN7*/PORT4* optional modules plus one 0.5cu ELCS4* advanced-level module.
A total of 2.0cu from SPAN4*/SPAN7*/PORT4* optional modules plus two 0.5cu ELCS4* advanced-level modules.
Interdepartmental Modules
Entry requirements
A Levels
- Grades
- Subjects
- Spanish grade A required.
- GCSEs
- English Language at grade B, plus Mathematics at grade C. For UK-based students, a grade C or equivalent in a foreign language (other than Ancient Greek, Biblical Hebrew or Latin) is required. UCL provides opportunities to meet the foreign language requirement following enrolment, further details at: www.ucl.ac.uk/ug-reqs
IB Diploma
- Points
- 36
- Subjects
- A score of 17 points in three higher level subjects including Spanish at grade 6, with no score lower than 5.
UK applicants qualifications
For entry requirements with other UK qualifications accepted by UCL, choose your qualification from the list below:
Equivalent qualification
Not acceptable for entrance to this programme
Pass in Access to HE Diploma, with a minimum of 18 credits awarded with Distinction in the Level 3 units, the remainder of the Level 3 units awarded with Merit.
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A,A,B at Advanced Highers (or A,A at Advanced Higher and B,B,B at Higher), including Spanish at grade A
Successful completion of the WBQ Advanced Skills Challenge Certificate plus 2 GCE A-Levels at grades AAB. Spanish is required.
International applications
In addition to A level and International Baccalaureate, UCL considers a wide range of international qualifications for entry to its undergraduate degree programmes.
Undergraduate Preparatory Certificates
The Undergraduate Preparatory Certificates (UPCs) are intensive one-year foundation courses for international students of high academic potential who are aiming to gain access to undergraduate degree programmes at UCL and other top UK universities.
Typical UPC students will be high achievers in a 12-year school system which does not meet the standard required for direct entry to UCL.
For more information see: www.ucl.ac.uk/upc.
English language requirements
If your education has not been conducted in the English language, you will be expected to demonstrate evidence of an adequate level of English proficiency. Information about the evidence required, acceptable qualifications and test providers can be found on our English language requirements page.
The English language level for this programme is: Advanced
A variety of English language programmes are offered at the UCL Centre for Languages & International Education.
In addition to your language competence your studies will develop skills in close and critical reading, the analysis and communication of complex material, and the ability to organise your own time - all of value in your future employment.
Fluency in the Spanish language opens up exciting career paths around the world as politics and commerce become increasingly global.
Career alternatives include areas such as finance, journalism, law, education, commerce, arts administration, the civil service, the media, or translation and interpreting. Of course, the pursuit of further study is also an option open to you.
First career destinations of recent graduates (2012-2014) of Spanish and Latin American Studies programmes at UCL include:
- Teaching Assistant, London
- Assistant TV Producer, Disney World Company
- Technology Consultant, Asenqen
- Press Officer, Maido
- Live Subtitler, Independent Media Support (2010)
*Data taken from the 'Destinations of Leavers from Higher Education' survey undertaken by HESA looking at the destinations of UK and EU students in the 2012-2014 graduating cohorts six months after graduation.
UCL is committed to helping you get the best start after graduation. Read more about how UCL Careers and UCL Innovation and Enterprise can help you find employment or learn about entrepreneurship.
Application and next steps
Your application
We will be looking for a demonstrable interest in literary, historical and cultural studies, and will be curious to learn about your motivation for applying for this programme. Evidence of extracurricular interest in the culture of Spanish-speaking countries, such as reading books, newspapers and magazines, watching films, or travel to one of these countries, will be looked on favourably.
How to apply
Application for admission should be made through UCAS (the Universities and Colleges Admissions Service). Applicants currently at school or college will be provided with advice on the process; however, applicants who have left school or who are based outside the United Kingdom may obtain information directly from UCAS.
Application deadline: 15 January 2017
If your application demonstrates that your academic ability and motivation makes you well-suited to our degree and you receive an offer, then we shall invite you to a post-offer Open Day, where you can experience the sort of teaching which we offer and life in SELCS.
Our admissions process aims to assess your linguistic abilities and attainment as well as cultural awareness, motivation for study and intellectual potential.We may interview candidates by telephone in order to establish a level of language ability.
Applicants must have A level or equivalent knowledge of Spanish.
For further information on UCL's selection process see: Selection of students


text:
Yeah, a Hosta Ladies' slumber party sounds like a blast!!
Kate Ardissono wrote:
> isn't it exciting.... My poor family just watches as I just drool over my
> catalogs. Let's see If I take a second.. oops I mean third job maybe I can
> afford them all... hum... Too bad you don't live closer Lu we could curl up
> and have a sleep over and talk hosta all night <giggle> then talk about all
> those hostalets and hostavites <giggles some more>
> Oh well maybe next year,
> Kate
> | I got Ran's catalog! I got Ran's catalog!
> |
> | <giggles>
> |
> | Lu (Atlanta, Zone 7B)
> ---------------------------------------------------------------------
> To sign-off this list, send email to firstname.lastname@example.com with the
> message text UNSUBSCRIBE HOSTA-OPEN
To sign-off this list, send email to email@example.com with the
message text UNSUBSCRIBE HOSTA-OPEN


text: We went out of our way to check this please out. DO Not waste your time. The bread is not good and what bakery has no breakfast parties?! We waited 45 minutes for two regular cups of coffee. The people who work there are the most inefficient folks I have come across in a service business.


text:
Steph Ackerman
Contact me
On Blogger since May 2007
Profile views - 5129
My blogs
- The Rubber Buggy
- The Rubber Buggy Challenge. Come join us for a fun Challenge second Wednesday of each month.
- {my sweet earth}
- Live Laugh Scrap with Steph Ackerman
- Just For Fun Rubber Stamps
- The Stamp Doctor
- Tiny Tool Time
- Paverpol USA
Blogs I follow
|East Meadow, New York, United States
|Welcome to my blog. I've been married to Gary for 34 years. We have a 20 year old Criminal Justice college student and 6 year old pup. I've been creating in some form since I was a child. It started with crochet, sewing, macramé and beading. Turning down a scholarship to the Fashion Institute of Technology, I became a business major managing several major corporations during my career; however, I always kept my crafty endeavors. I love to teach classes and can be found teaching in my craft room as well as my local stores.
|Scrapping, Mix'd Media, Home Decor
|Favorite Movies
|Ghost, Pretty Woman
|Favorite Music
|Billy Joel, Celene Dion
|Favorite Books
|Harry Potter


text:
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text:
Regional North America United States Texas Metro Areas Dallas-Fort Worth Recreation and Sports
Subcategories 50
Related categories 1
Sites 16
Armed Forces Bowl
College football bowl game; press releases and information on events, tickets and accommodations.
ASI Gymnastics
Provides instruction for boys and girls including beginner and experienced gymnast. Includes map to Metroplex locations and contact information.
Dallas Underwater Hockey
Information on gatherings, the sport's rules, tournaments and pictures.
Dallas Water Polo Club
Masters and youth programs.
Dallas/Fort Worth Field Hockey Club
Social club formed by field hockey players from the Dallas Fort Worth metropolitan area.
DFW Working Dogs
Schutzhund training club working with all breeds and using several training methods. Photos, calendar of events, articles, and video clips.
Dedicated to Ford and Mustang enthusiasts in the North Texas Area. Includes tech articles, messageboards, events, and local news.
Fort Worth Star-Telegram: Sports
Fort Worth Star-Telegram online sports coverage.
Goalie Station
Listing of area ice hockey players willing to serve as substitute or permanent goaltenders.
Lone Star Cyclists
Group of road bicycling enthusiasts. News, membership details, calendar and information on the Tour d'Italia race in Italy, Texas.
North Texas Cricket Association
Information on teams, schedules, players, matches, rules, tournaments, scores, and articles.
North Texas High School Rodeo Association
Overview, results, changes, forms, schedule, calendar, arena rental details and past champions.
North Texas River Runners
Club for canoers, kayakers and rafters. Includes information on monthly meetings in Bedford, membership, and trips.
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The official site with information on youth soccer, amateur soccer, sanctioned tournaments, Olympic development, referee clinics, and coaching education.
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Information and links to sports teams and activities in the Dallas-Fort Worth area.
Tri-County Amateur Radio Club of North Texas WC5C
Serving Parker, Tarrant and Wise counties since 1994, including Aledo, Azle, Boyd, Decatur, Fort Worth, La Junta, Lake Worth, Lakeside, Reno, Saginaw, Springtown, and Weatherford.
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7 nights with an arrival from
Not far from Lyon, between the Saône and the Ain you will find the Village de Vacances Champ d'Été only walking distance from the friendly Pont-de-Vaux. At this well-maintained holiday park a balance has been successfully maintained between beautiful, natural surroundings and a comfortable holiday resort.
Children will have great fun on the water slides and the large outdoor pool or in the indoor pool during the off-peak season.
The holiday park has many sporting activities to enjoy if you want to keep yourself moving whilst on holiday. For example, you can go pony riding, take part in volleyball, tennis, badminton and football. After all these activities you can then sit back and relax in the sauna. There is also a well stocked lake for fishing 500 m away from the campsite.
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Truth For The World Podcast
The Truth For The World Podcast is released every other week, and features Lee Davis (Director) and Benjamin Bruce (Internet & Mobile Services Coordinator) talking about various aspects of mission work. If you are a Christian and have interest in mission work, check it out, and be sure to send us any questions you may have!
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When you subscribe to the Truth For The World podcast, each episode will automatically be delivered to you, and you can listen to it at your convenience. You can take it with you to the park, listen at home, or share it with others. Below are some applications and sites that you can use to listen. If you have any questions, please let us know!


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Horror Crash Audi Le Mans 2011
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CRAZY!!! Street Racing Gone Wrong!
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Racing and Rally Crash Compilation Week 25 June 2015
Please visit our friends at http://www.racingshirt.net/?tracking=55648ce3e262c to support us and see a cool collection of motorsport shirts! Thanks to: Motulski https://www.youtube.com/user/motulski komiknm https://www.youtube.com/user/komiknm Motorsportvideos Luky M. https://www.youtube.com/channel/UC0FWm2AlaiRyzeNIqnbXJIQ mikedehoogh black flag race photos https://www.youtube.com/user/mikedehoogh fukku666 https://www.youtube.com/user/fukku666 laci7508 https://www.youtube.com/user/laci7508 Sport Video https://www.youtube.com/channel/UCPh7XWWeQ6tP86kj788WeKg Sandris Zonbergs https://www.youtube.com/user/Zonbergs lepetitvosgiens88 https://www.youtube.com/user/lepetitvosgiens88 Skid Rallye https://www.youtube.com/channel/UCDImj5AJoiz-khSumVuja7w This video is for educational purposes only. This compilation brings all the best of crashes all over the world during the week of 15/06 to 21/06. Catch up all the crashes, smashes, thrills and spills from the past week in this video. Every week RacingFail channel compiles what worse has happened in the world of motorsport in the past week. Subscribe for more! PLEASE: If you see your clip, just leave a comment with a note and we'll add credits straight away to this video AND the clip. You won't regret it! If you still don't want to see your clip in our video just leave a message and we'll remove it as soon as possible. We use very small portions of Videos, therefore these Clips are under the Copyright Law 107 of Fair Use. Wouldn't it be nice to have a single video with nearly every crash in motorsport of the previous week? Now it's possible with a lot of work and research from RacingFail Channel, and it can even be easier if you cooperate with us. We believe you will only gain if doing so. We will help you to Boost up your viewless video (that we were able to find) and hopefully give some subscribers as well. If you want to partner with us and save us some time just leave a private message with a crash link, and you'll see your clip in our next video full of credits and links.
2011 Ricky Carmichael HARD CRASH NASCAR CWTS at the Lucas Oil 200 in Dover DE.
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text: We're sorry, Lowestoft Beach Cosmetic Bag is no longer available Why not try one of these instead? Personalised Bridesmaid Make Up Bag by The Alphabet Gift Shop £16.99$29.15€20.36$21.77 Personalised Name Make Up Bag by Jonny's Sister £16$27.45€19.17$20.50 Personalised Bridesmaid Make Up Bag by Twenty-Seven £12.50$21.45€14.98$16.01 free UK delivery Birthday Make Up Bag by Lovethelinks £12.95$22.22€15.52$16.59 free UK delivery Pinch to zoom Lowestoft Beach Cosmetic Bag by Michelle Mason £15$25.74€17.97$19.22 This item is no longer available free gift wrap Favourite Favourite View your favourites we're sorry we're sorry, This item is no longer available buy a gift voucher related categories fashion > women's accessories > bags & purses > make-up bags health & beauty > make-up & wash bags > wash & toiletry bags by Michelle Mason Location: London, GB read seller's profile see seller's complete range more items from this seller Seaside Wallpaper by Michelle Mason £150$257.43€179.77$192.21 Stella Felt Rug by Michelle Mason £350$600.67€419.47$448.49 Secret London Cushions by Michelle Mason £50$85.81€59.92$64.07 'Home Sweet Home' Organic Tea Towel by Michelle Mason £10$17.16€11.98$12.81 Park Hill Wallpaper by Michelle Mason £150$257.43€179.77$192.21 Wedding Special Personalised Wedding Print by Michelle Mason £35$60.06€41.94$44.84 view all you may also like PRODUCT DETAILS DELIVERY RETURNS Made in Britain free gift wrap ask seller a question save for later A seaside inspired cosmetic bag, designed to add a drop of sunshine to any bathroom. Makes a perfect gift. This seaside themed make-up bag showcases a hand drawn Beach design inspired by Michelle's partnership with the National Railway Museum. Michelle has worked closely with NRM to produce designs inspired by British Railway travel posters from the mid 1950s to create colourful vintage beach scenes with sunny seaside graphics. Colour print on cotton canvas coated with a fully waterproof oilcloth finish. Lined with a white waterproof interior. Printed, coated and made in the UK. made from: Full colour print on cotton canvas coated with a fully waterproof oilcloth finish. Lined with a white waterproof interior. dimensions: Flat make-up bag: 24 x 16 cm The medium and large sizes are no longer in stock product code: 223147 This product is dispatched to you by Michelle Mason. You have 28 days, from receipt of cancellable goods, to notify the seller if you wish to cancel your order or exchange an item. Please note: goods that are personalised, bespoke or made-to-order to your specific requirements, perishable products and personal items sold with a hygiene seal (cosmetics, underwear) in instances where the seal is broken are non-refundable, unless faulty. Read more about our returns policy.Should you choose to return or exchange your order you will need to deliver the item(s) to the UK, where this seller is based. Michelle Mason's return policy Please see notonthehighstreet.com's returns policy.


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Virtual online worlds hold enormous potential outside of gaming to build social connectivity and services, according to Jackie Morie, project director at the University of Southern California's Institute for Creative Technologies. The avatars in virtual worlds are the key, Morie says, providing "a fundamentally positive aspect to this kind of connectedness we have not yet leveraged to the extent we can." The new worlds have potential business and psychological uses.
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Hallmark Tin Ornament Stocked With Joy - Christmas Stocking
This precious ornament is pressed tin and dated 1992. It is an Artists' Favorites and was designed by Linda Sickman. On the box Linda states: "The doll on the stocking is identical to a doll I had as a child. My sister gave it to me, and I've kept it all these years. I filled the stocking with playthings that people might have enjoyed as children. And there's also a surprise gift--the package wrapped in brown paper!"
Artists' Favorites designs reflect the personal interests and memories of the artists who create them.
This ornament is new in its box and has only been removed to take pictures. There is a little tiny bit of shelf wear to the box. Please reference the 199 Edition of Hallmark Keepsake Ornaments page 163.
Great Holiday Gift Idea!
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There is increasing evidence that human atherosclerosis is associated with damage to the DNA of both circulating cells, and cells of the vessel wall. Reactive oxygen species are the most likely agents inducing DNA damage in atherosclerosis. DNA damage produces a variety of responses, including cell senescence, apoptosis and DNA repair. This review summarises the evidence for DNA damage in atherosclerosis, the cellular responses to damage and the mechanisms of signalling DNA damage.
1. Introduction
Atherosclerotic plaques consist of an accumulation of vascular smooth muscle cells (VSMCs) (for full list of abbreviations, see Table 1) and inflammatory cells, together with lipid and extracellular matrix proteins–advanced plaques also show calcification. Although the plaque develops as a chronic inflammatory reaction, there is increasing evidence that DNA damage to cells within the lesion plays an important role in both atherogenesis and the behaviour of established lesions. DNA damage ranges from 'macro' damage, including deletions or additions of whole chromosomes or parts of chromosomes, to 'micro' damage, which includes DNA strand breaks, mutations of single bases, modified bases (including oxidation) or DNA adducts. This review outlines the evidence for DNA damage in atherosclerosis, the inducers of damage, the response to damage and repair pathways, the consequences of damage and potential therapies to prevent/reduce damage.
|8-Oxo-guanine, an oxidative modification of guanine in DNA
|Multiprotein complex consisting of Rad9–Rad1–Hus1
|Ataxia–telangiectasia mutated (protein)
|ATM and Rad3-related (protein)
|Checkpoint kinase 1
|Checkpoint kinase 2
|Double-stranded (DNA) breaks
|Phosphorylated form of the histone protein H2AX
|3-Hydroxy-3-methylglutaryl coenzyme A
|Murine double minute 2 gene
|Multiprotein complex consisting of MRE11–RAD50–NBS1
|Protein mutated in Nijmegen breakage syndrome
|Phosphatidylinositol 3-kinase
|Reactive oxygen species
|Stress-induced premature senescence
|Single-stranded (DNA) breaks
|Vascular smooth muscle cell
|8-Oxo-guanine, an oxidative modification of guanine in DNA
|Multiprotein complex consisting of Rad9–Rad1–Hus1
|Ataxia–telangiectasia mutated (protein)
|ATM and Rad3-related (protein)
|Checkpoint kinase 1
|Checkpoint kinase 2
|Double-stranded (DNA) breaks
|Phosphorylated form of the histone protein H2AX
|3-Hydroxy-3-methylglutaryl coenzyme A
|Murine double minute 2 gene
|Multiprotein complex consisting of MRE11–RAD50–NBS1
|Protein mutated in Nijmegen breakage syndrome
|Phosphatidylinositol 3-kinase
|Reactive oxygen species
|Stress-induced premature senescence
|Single-stranded (DNA) breaks
|Vascular smooth muscle cell
Evidence for DNA damage in atherosclerosis
DNA damage is present both in the circulation of patients with atherosclerosis and the plaques themselves. For example, patients with coronary artery disease have a higher micronucleus index (a marker of genetic instability) than healthy controls, which correlates with disease severity [1,2]. There is also a significantly higher incidence and extent of a common mitochondrial DNA deletion (mtDNA4977) [3]. Premature atherosclerosis is a feature of defects in DNA repair pathways, such as Werner syndrome, a disease characterised by predisposition to cancer and early onset of symptoms related to normal aging including osteoporosis, ocular cataracts, graying and loss of hair, diabetes mellitus, and atherosclerosis. Werner protein guards the genetic stability of cells, playing an integral role in base excision repair and at telomere ends [4].
There is also evidence of 'macro' DNA damage within atherosclerotic plaques. Cytogenetic analysis of primary cell cultures from human plaques identified loss of the Y chromosome and del13q14, XXY karyotype, and trisomy 7, 10 and 18 [5], whilst unstable carotid plaques demonstrated trisomy and tetrasomy of chromosome 7, and monosomy of chromosome 11 [6]. Although it was not clear from these studies which cells had chromosomal defects, VSMCs demonstrate microsatellite instability (mutations in microsatellite regions that may affect gene expression) [7,8] and loss of heterozygosity [8], suggesting that genomic destabilization/mutation may play a pivotal role in atherosclerosis. Indeed, monoclonality of VSMCs within lesions suggests that atherosclerosis may be characterised by a sub-population of VSMCs that undergo selective replication [9]. DNA damage can also occur in the mitochondria. Indeed, mitochondrial DNA damage correlates with the extent of atherosclerosis in human specimens and aortas from apolipoprotein E(− / −) mice [10].
This 'macro' DNA damage is also associated with biomarkers of carcinogen exposure–such as DNA adducts or modifications to specific bases in atherosclerotic plaques. 'Bulky' aromatic DNA-adducts in VSMCs (most likely related to environmental exposure to genotoxic chemicals) are a predictor of atherosclerosis extent in humans even after adjustment for age, smoking, obesity, heart weight and genetic susceptibility markers [11]. DNA strand breaks, oxidised pyrimidines and altered purines are also significantly higher in patients with coronary artery disease than controls [12], and human plaques show markers of oxidative damage, including DNA strand breaks, expression of 8-oxo-G (an oxidative modification of guanine residues in DNA) and activation of DNA repair enzymes [13]. Strong nuclear and cytoplasmic immunoreactivity for 8-oxo-G is detected in plaque VSMCs, macrophages and endothelial cells, but not in VSMCs of adjacent normal media or normal arteries [13]. DNA damage is also a direct correlate of extent of atherosclerosis in experimental animals. For example, cholesterol feeding of rabbits induces oxidative damage in plaques, manifested by 8-oxo-G staining [14], DNA strand breaks, and apoptosis.
Causes of DNA damage–risk factors for atherosclerosis
DNA can be damaged in numerous ways. Spontaneous damage due to replication errors, deamination, or depurination has to be repaired in addition to damage derived from oxidation and environmental chemicals. Many of the risk factors associated with atherogenesis, such as smoking and diabetes mellitus, may directly induce DNA damage. For example, smoking can cause oxidative DNA damage, inhibit DNA repair, and induce the production of advanced glycation end products, which themselves cause DNA mutation (reviewed in [15]). Similarly, advanced glycation end products have been implicated in the oxidation of low-density lipoprotein [16] and elevated levels of 8-oxo-G. Although direct damage from specific risk factors or environmental agents may contribute to DNA damage in atherosclerosis, the most likely triggers of damage are reactive oxygen species.
Cause of DNA damage in atherosclerosis–reactive oxygen species
It has been estimated that approximately 2 × 104 DNA damaging events occur in every cell/day [17]; a major portion of these occur via reactive oxygen species (ROS) [18]. ROS include the superoxide anion (*O2−), hydrogen peroxide, hydroxyl radical, peroxynitrite and lipid peroxides (Fig. 1), with their reactivity and half-life varying according to species. ROS are constantly produced within the cell, in particular via mitochondrial oxidative metabolism and pathological processes such as inflammation [18]. In vascular cells, the primary source of ROS may be xanthine oxidase and NAD(P)H oxidases (Noxs) [19,20]. Other sources of ROS include cytochrome P450 isoenzymes, lipoxygenase, cyclooxygenase, hemoxygenase, and glucose oxidase. Myeloperoxidase is also produced by invading macrophages (reviewed in [21]). ROS are also secondary messengers in specific signalling pathways, generated by specific plasma membrane oxidases in response to growth factors and cytokines.
DNA lesions caused by ROS include double- and single-stranded breaks (DSBs and SSBs), DNA–DNA and DNA–protein cross links and base modifications, including thymine glycol, 8-hydroxyguanine and 8-oxo-guanine. Certain types of damage can be traced back to specific insults. Whilst superoxide and hydrogen peroxide are normally not reactive to DNA, both can be converted to the extremely reactive hydroxyl radical via the Fenton reaction. The hydroxyl radical can induce a vast array of damage to both nuclear and mitochondrial DNA [22]. Hydroxyl radicals may induce base or nucleotide loss, adducts, and single- and double-strand breaks. In particular, hydroxyl radicals can interact with pyrimidine double bonds causing glycolytic damage (e.g. thymine glycol, uracil glycol) that can cause mis-pairing, transcriptional interrupts and, if left un-repaired, induce cell cycle arrest. Similarly, interaction of OH radicals with purines will generate formamidopyrimidines and other purine oxidative products that are usually recognised by the DNA repair mechanism. Thymidine oxidation, or the addition of methyl and alkyl groups, is frequently attributed to ROS of all types. Interestingly, 8-oxo-G, which frequently causes oxidative damage to deoxyguanines, is not recognised by the DNA repair system and is thus highly deleterious to cells. Un-repaired 8-oxo-G will mis-pair with dA, leading to an increase in G to T transition mutations.
The cell has a number of mechanisms of protection against oxidative damage (reviewed in [23]), including direct interaction with antioxidants such as α-tocopherol, ascorbic acid and glutathione (scavengers). Glutathione exists in both its oxidised form (GSSG) and reduced (GSH) forms, and can function alone or in association with enzyme activities. In addition, antioxidant enzymes are present such as superoxide dismutases (which convert the superoxide radical to hydrogen peroxide and water), and glutathione S transferases that conjugate reduced GSH to hydrophobic organic compounds such as lipid peroxides. In general, the balance between ROS levels and the activity of these defence mechanisms determines the degree of oxidative stress encountered by the cell.
Evidence for oxidant stress in atherosclerosis
Increased levels of ROS are found in all layers of the atherosclerotic arterial wall, and particularly in the plaque itself [24]. Although ROS are associated with upregulation of several vascular NAD(PH) oxidase subunits and increased enzyme activity [25], confirmation of the role of ROS in atherosclerosis comes from studies with genetic disruption of the p47phox subunit of NAD(P)H oxidase, which causes dramatic inhibition of atherogenesis in ApoE− / − mice [26]. Increased levels of xanthine oxidase and reduced ecSOD are found in coronary arteries and plasma of patients with coronary artery disease [27]. Similarly, low levels of glutathione peroxidase activity are an independent risk factor for cardiovascular events in patients with coronary artery disease [28].
Oxidative damage to the mitochondrial genome with resultant mitochondrial dysfunction is also an important consequence of increased intracellular ROS. Hydrogen peroxide and peroxynitrite induce mitochondrial DNA damage and dysfunction in endothelial cells and VSMCs, with endothelial cells being particularly sensitive [29]. As mentioned above, mitochondrial DNA damage correlates with the extent of atherosclerosis in human specimens and aortas from ApoE(− / −) mice, whilst disruption of manganese superoxide dismutase, a mitochondrial antioxidant enzyme, show increased mitochondrial DNA damage and accelerated atherogenesis at arterial branch points [10].
The DNA damage response pathway
The plethora of DNA damage lesions in cells is rapidly detected by a complex web of signalling pathways called the DNA damage response pathway. This pathway involves three groups of evolutionarily conserved proteins, which act in concert to translate the DNA damage signal into a specific cellular response (Figs. 2 and 3). These are:
Sensors: recognise the lesions themselves or chromatin alterations that follow DNA damage. Examples include the MRN and 9–1–1 complexes.Fig. 3Fig. 3Fig. 2Fig. 2
Transducers: initiate a signal transduction cascade that propagate and amplify the signal. Examples include ATM and ATR.
Effectors: execute the specific cellular response. Examples include ChK1 and ChK2.
Double-stranded DNA breaks (DSBs) may cause chromosomal aberrations and disrupt genetic integrity, leading to carcinogenesis. DNA replication errors are the major cause of DSBs in dividing cells, although they may also arise from ionising radiation and genotoxic agents. The two mechanisms for DSB repair are homologous recombination between sister chromatids and the rapid, error prone non-homologous end joining [30]. The MRN complex plays a key role in the cellular response to DSBs [31] as well as other aspects of DNA metabolism such as telomere maintenance [32]. The MRE11 protein has an amino terminal phosphoesterase domain and two DNA binding sites. The phosphoesterase domain not only contains the NBS1 binding site, but also functions as both a single and double stranded DNA endonuclease as well as a 3′-5′ double strand exonuclease [33]. RAD50 contains a bipartite ATP binding cassette joined by two coiled-coil domains, with a Cys-X–X-Cys motif located in the middle of the coiled-coil domain, which serves as a dimerization domain [34]. NBS1 is essential for the nuclear transportation of the MRN complex and binding of phospho-H2AX, and is responsible for MRN recruitment to sites of DSBs [35].
The key role of the MRN complex in the DSB response has been emphasized by genetic studies. Hypomorphic mutations in MRE11 lead to ataxia–telangiectasia-like disease, which like ataxia–telangiectasia (A–T–see below), includes progressive cerebellar degeneration, hypersensitivity to ionising radiation and radioresistant DNA synthesis [36]. Hypomorphic mutations in NBS1 lead to the Nijmegen breakage syndrome (NBS), which is characterised by microcephaly, mental deficiency, immunodeficiency, hypersensitivity to irradiation, chromosomal instability and cancer predisposition. A variant of this disease is caused by RAD50 mutations.
The similarities noted amongst ataxia–telangiectasia, ataxia–telangiectasia-like disease, and NBS suggest a functional link between MRN and ATM. This link is complex and is explained by a two-step model in which NBS1 is firstly recruited to sites of DSB by binding to MRE11 in an ATM-dependent manner. ATM activation and phosphorylation of its downstream targets such as γ-H2AX are thought to assist in the recruitment and retention of further MRN molecules by NBS1–γ-H2AX interaction [37].
Rad9–Rad1–Hus1 (9–1–1)
The 9–1–1 complex is present in the nucleus of both damaged and undamaged cells. The complex resembles the proliferating nuclear antigen, a doughnut shaped homotrimeric complex, which forms a sliding clamp at sites of DNA replication and serves as a sliding platform for the accumulation of the replicative machinery [38]. The 9–1–1 complex is loaded around the DNA by the Rad17-replication factor C in response to genotoxic stresses such as ionising radiation, UV light and replication inhibitors [39]. The 9–1–1 complex is involved in the ATR/ChK1 signalling axis [40] and is loaded onto DNA following single strand DNA damage. The Rad9 tail, which contains a consensus phosphatidylinositol 3-kinase (PIKK) site, is then phosphorylated by ATR and in turn facilitates the phosphorylation and activation of ChK1 [41].
The two main transducers of DNA damage in mammals are ATM (ataxia–telangiectasia gene product) and ATR (ATM and Rad3-related) [42]. Both are members of the phosphatidylinositol 3-kinase-like family of serine/threonine protein kinases (PIKK) [42]. ATM functions particularly after DSBs, ATR after SSBs and separate N-glycosylases function in base excision repair.
ATM deficiency leads to ataxia–telangiectasia (A–T), an autosomal recessive syndrome with early childhood onset of progressive cerebellar ataxia, occulocutaneous telangiectasia, primary immunodeficiency (decreased IgA, IgE, and IgG2), retarded somatic growth, premature ageing, and predisposition to lymphoreticular malignancy [43]. In addition, these patients exhibit chromosomal aberrations, cell cycle checkpoint defects and increased rates of telomere shortening [44,45]. Patients with two mutant alleles develop new cases of cancer at approximately 100 times the age-specific population rate and have a median age of death of approximately 20years.
Over 400 different ATM mutations have so far been identified of which more than 85% are null mutations resulting in no detectable ATM protein [46,47]. A–T heterozygotes comprise approximately 1.4–2% of the general population [48]. ATM carriers have an increased risk of cancer, but also of ischaemic heart disease [49,50], dying on average 7–8years earlier. Importantly, the effect of ATM carrier status on cardiovascular mortality is similar to that of smoking or male gender. Although this suggests that ATM carriage may account for a significant proportion of the genetic inheritance of coronary artery disease, the mechanism by which ATM heterozygosity promotes coronary artery disease is unknown.
ATM is located within the nucleus of most cells as dimers or higher order multimers with the kinase domain of each molecule being blocked by the other [51]. In response to DSBs, each ATM molecule phosphorylates the other on ser1981 leading to monomerisation and activation of ATM [51]. The active ATM molecules are then recruited to DSB sites, an event which is facilitated by the MRN complex, serving as a platform for further enzymatic reactions [52] as well as initiating phosphorylation events leading to regulation of specific cell cycle checkpoints [53]. The main target for ATM in this pathway is the tumour suppressor gene p53, which is phosphorylated on ser15[54–56], enhancing its transcriptional activity [57]. ATM also phosphorylates and activates ChK2, which in turn phosphorylates p53 on ser20[58], and interferes with the p53–MDM2 interaction. Finally, ATM directly phosphorylates MDM2 on ser395 thereby inhibiting the nuclear export of the p53–MDM2 complex and the subsequent degradation of p53 [59]. The ATM mediated modulation of p53 is an illustrative example of the numerous mechanisms by which ATM can regulate a single protein within the same pathway.
In addition to its critical role in cell cycle checkpoints, and maintenance of telomere length and integrity [60], A–T cells show abnormal responses to oxidant stress and increased oxidative stress is evident in A–T. For example, A–T fibroblasts are more sensitive to oxidant stress-induced DNA damage than normal cells [61], and have constitutive activation of DNA damage repair pathways that are reversed in part by antioxidants [62]. Oxidant stress can induce ATM kinase activity, which in normal cells is associated with cell cycle arrest in G1 and G2/M; indeed, ATM is required for growth arrest after oxidative stress [63]. In addition, tissues from ATM knockout mice show increased oxidative stress, including elevated levels of 3-nitrotyrosine [64], lipid peroxidation [64], and accumulation of superoxide and hydrogen peroxide [65]. Whilst the most striking effects are seen in the brain, patients with A–T show reduced total plasma antioxidant capacity, suggesting that they may sustain constant systemic oxidative stress [66].
ATM-mediated pathways are not completely abolished in A–T cells, but are rather dampened and turned on slowly. This indicates the presence of parallel kinases, which act in concert with ATM. One such system is ATR, which can phosphorylate ATM substrates albeit with much slower kinetics [67]. ATR responds to UV-light, stalled replication forks and hypoxia [53]. The recruitment of ATR to DNA lesions is facilitated by the ATR interacting protein. This is accompanied by phosphorylation of some ATM substrates such as p53 [68] as well as ATR-specific targets such as ChK1 and RAD17 [69]. Mice lacking ATR die in the early stages of embryogenesis and ATR deficiency is not compatible with cellular viability in culture [70]. This is because the ATR–ChK1 axis is fundamental in S phase, preventing the progression of damaged DNA and hence preventing mitotic catastrophe. Mutations causing partial loss of ATR activity in humans have been associated with the autosomal recessive disorder Seckel syndrome, which shares features in common with A–T [71].
The ChK1 protein consists of a kinase domain and an SQ domain, containing multiple phosphorylation sites. ChK1 is present in an active form during the S and G2 phases of the cell cycle even in the absence of DNA damage [72], but is activated in response to DNA damage and stalled replication forks by ATR, which phosphorylates ChK1 at ser317[72]. Mice lacking ChK1 die early in embryogenesis [73] and embryonic stem cells lacking ChK1 are not viable in culture [74]. In human cells, ChK1 is essential in Cdc25A metabolism as well as the checkpoint response to ionising radiation and DNA damaging agents [75].
The ChK2 protein contains multiple ATM recognition sites and both dimerization and kinase domains. ChK2 is expressed throughout the cell cycle and is inactive in the absence of DNA damage [76]. Following DNA damage and ATM activation, ChK2 is phosphorylated at thr68 and forms a homodimer [77]. Mice deficient in ChK2 are viable, fertile and exhibit increased resistance to ionising radiation [74]. In humans, mutations in ChK2 are associated with a spectrum of malignancies including the Li Fraumeni syndrome [78], breast and colon cancer [79].
The ATM/ChK2 and ATR/ChK1 pathways are no longer considered as parallel branches of the DNA damage response pathway, but rather a system where there is a high degree of cross talk and connectivity. For instance, ATM can activate ChK1 in response to ionising radiation, and ChK2 can be activated independently of ATM [80].
Effects of DNA damage in atherosclerosis
DNA damage to cells of the vessel wall may have a number of effects. However, the most likely consequences are cell senescence, cell death and DNA repair.
Cell senescence
Extensive characterisation of lesion development has shown that cell proliferation is low in early atherosclerosis (Fatty streak, Stary Type I lesion), peaks in the intermediate lesions (Stary II–IV), and declines in advanced fibroproliferative, complicated plaques (Stary type V lesions) [81,82]. In vitro studies have confirmed that plaque VSMCs show reduced cell proliferation rates, increased population doubling times, and earlier failure to proliferate (senescence) than medial VSMCs [83].
Cell senescence may be triggered by two broadly different mechanisms. Replicative senescence may be induced by reduction of telomere length, changes in structure such as telomeric fusion or dicentrics, or loss of telomere-bound factors. Telomeres may trigger growth arrest via DNA damage responses at critical telomere lengths or structure. Cells subjected to sub-lethal stress due to DNA damage (UV and γ-irradiation, oxidative stress and treatment with histone deacetylase inhibitors) also undergo 'stress-induced premature senescence' (SIPS). SIPS resembles replicative senescence, cells demonstrating a similar morphology and pattern of cell cycle regulators.
ROS can induce both telomere-based senescence and SIPS. ROS induce DNA strand breaks, and base and nucleotide modifications, particularly in sequences with high guanosine content [84], such as telomeres. Indeed, telomeres are one of the DNA structures most sensitive to oxidative damage [85] and ROS can accelerate telomere loss in vitro [86]. Increased telomere loss/division can also occur in individual cells due to a telomere-specific deficiency in base excision repair, leading to preferential accumulation of ROS-induced single-stranded DNA breaks [85] preventing replication of distal telomeres when cells divide. Thus, it is possible that oxidative DNA damage to telomeres induces a DNA repair response that induces senescence. Not only do ROS induce senescence, but also senescent cells produce high levels of ROS, and contain higher levels of oxidatively damaged DNA [87]. In vitro, VSMCs from aged mice have decreased proliferation, yet generated higher levels of ROS in comparison with cells from younger mice, associated with decreased endogenous antioxidant activity, increased lipid peroxidation, and mitochondrial DNA damage [88].
Cell death
In cells where the DNA damage is too much to repair, or in cells that are driven to proliferate, DNA damage induces apoptosis. Apoptosis is evident in endothelial cells, macrophages and VSMCs in atherosclerotic plaques. Endothelial cell death is implicated in both atherogenesis and plaque erosion [89], whereas VSMC death may promote thinning of the fibrous cap and plaque rupture. Indeed, increased levels of VSMC apoptosis are seen in mature plaques when compared to control vessels [90], and in unstable versus stable plaques or patients [91,92]. Cell death can be induced by ROS and oxidised lipids in vascular cells, whereas p53 expression in an experimental neointima can induce apoptosis and promote plaque rupture [93].
DNA repair
Although there is evidence of activation of DNA repair pathways in human atherosclerosis, cells displaying DNA damage are much more frequent than cells displaying markers of apoptosis, implying that repair occurs to prevent death [13]. In human plaques markers of DNA damage are associated with activation of base excision repair or nonspecific repair pathways [13]. In cholesterol-fed rabbits plaques also manifest DNA damage associated with upregulation of DNA repair enzymes [14]. In these studies, DNA strand breaks normalized after 4weeks of dietary lipid lowering, but a significant reduction of 8-oxo-G immunoreactivity was only observed after a prolonged period of lipid lowering, emphasizing the longevity of DNA damage in atherosclerosis. In addition, repair pathways started to decline progressively when cholesterol-fed animals were placed on a normal diet [14]. These studies demonstrate that DNA damage and activation of repair pathways occur in atherosclerosis, and are also reversible, at least in the early stages of atherosclerosis.
Prevention/treatment of DNA damage in atherosclerosis
The presence and biological consequences of DNA damage in atherosclerosis mean that both prevention and reversal of damage are therapeutic aims. In vitro, antioxidants can ameliorate ROS-induced DNA damage, although antioxidant trials in humans have been disappointing. In contrast, cholesterol lowering by diet is associated with a reduction in DNA damage and markers of DNA repair, at least in animal models. Drugs that have been proven to alter plaque progression and patient events have also been shown to alter vascular oxidative stress. In particular, HMGCoA reductase inhibitors ('Statins') reduce NAD(P)H oxidase activation [94,95] and superoxide production in vitro, in part by inhibiting the membrane translocation (and thus activity) of the small GTP-binding protein Rac-1 [96,97], a regulatory component of vascular NAD(P)H oxidase. Statins can also reduce superoxide production, and mRNA expression of specific nox subunits in vivo [96,98]. This effect may underlie the observation that atorvastatin reduces the degree of DNA damage of peripheral lymphocytes as well levels of oxidant stress in hyperlipidaemic patients [99].
DNA damage is increasingly recognised as being present in all cells within the atherosclerotic plaque. DNA damage may promote atherogenesis, and in advanced lesions induce phenotypic changes such as cell senescence and cell death that promote unstable plaques. Knowledge of both the triggers of DNA damage and the pathways underlying the DNA damage responses should lead to both prevention and treatment of DNA damage in atherosclerosis.
MM, JM and MB are supported by British Heart Foundation Grants FS/05/008 and RG/04/001.


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10 Techies in the Shadows - Bryan Cantrill, creator of DTrace, Sun Microsystems
DTrace is a dynamic tracing framework for Solaris, FreeBSD and Mac OS X, and is likely headed for Linux and other operating systems in the future. It allows people to look inside running software and work out problems while the program executes. What this means is that DTrace allows enterprise software to be far better tuned and debugged because both system administrators and developers can inspect the running code. DTrace could be a game changer for enterprise software, once it gets onto more platforms.
Some of the people on this list are little-known co-founders playing second banana to more famous names. Others have broken new ground or developed much-heralded technologies without winning much fame for themselves. You should know them, and, more importantly, you should know what they do. By Michael Hickins


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Goldstar Member's Event Journal
Friday January 17, 2014 / 11:00amNew York Philharmonic: Mozart, Zemlinsky, Stravinsky
1 ticket
Orchestra 1
How was your experience?
The Zemlinsky piece was so gorgeous and rarely done. Conductor was sometimes too loud - like Gergiev - but otherwise good. Assistant concertmaster Sheryl Staples is totally second rate and the piece would have been better with Glenn Dicterow, who is retiring soon.


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BlogHer 2010: What to Wear
Because I cannot leave well enough alone, let's talk about what to wear to BlogHer '10. That will be fun, don't you think?
Yes. Yes it will.
You're waiting for me to make some big pronouncement now, aren't you, like DON'T WEAR JEANS or PACK SOME HEELS or FOR THE LOVE OF ALL THAT IS HOLY BUY A PROPER COCKTAIL DRESS. But I'm not going to do it. Instead, I'm going to give you three simple things to think about while you're instead of standing in your closet freaking out about what to wear.
scarf: J. Crew tee: Old Navy
1. Identify your goals. Ooh, that sounds lofty, doesn't it? What I mean is this: be clear about why you're going to BlogHer. Are you thinking of this as a girls' getaway weekend? Are you hoping to make professional connections? Or are you doing a little of both? Be honest with yourself about what you're hoping to get out of the conference and pack accordingly.
2. Know your comfort zone. Every year I hear the same things: I don't ever dress up! I don't own a cocktail dress! And -- my favorite -- I'm a mom! I only wear capri pants and t-shirts! (That last one kills me. Truly.) Wear what's comfortable for BlogHer -- if you're a flats girl (holla!) don't feel compelled to bring heels. If you're not a dress person, then don't bring one. If your entire closet is tees and capris, pack 'em. Just leave the stained tees and ill-fitting capris at home. Please.
3. Remember: New York City, baby! Maybe it's just me, but I'm geeking out about spending five days in New York City, largely because I know I can get away with wearing things there that I cannot pull off at home, both because I'll be in the Fashion Capital of America and because my kids will be half a continent away and not wiping their hands on my dress. Take advantage of the opportunity and do something out of the ordinary. Why not?
I'm happy to offer packing basics or tell you specifically what I'm taking, but the bottom line is this: stop worrying. If you really feel like you have nothing to wear for BlogHer, think about why that is. Are you afraid that your current wardrobe won't measure up to some imaginary fashion standard? Or are you honestly working with a closet that consists entirely of yoga pants and logo tees? Either way, think less about what everyone else will be wearing and more about what you can put on each day that will make you feel like your best self.
And then do that every day, not just for the two and half days of BlogHer. The end.
This week the talened BlogHer CEs who cover Style will be providing tips and encouragement to help you pack your suitcase. Tomorrow, Kelly Wickham has some shoe advice, and on Wednesday blackbird tells you where to shop while you're in NYC. And next week, I'll have a full packing list from my suitcase -- you know, once I get all the vacation laundry done and figure out precisely what I'm wearing. Odds are good that it will be mostly flats and dresses.
Susan Wagner writes about pragmatic fashion at The Working Closet and chic suburban living at Friday Playdate, where this post originally appeared.
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This is an awesome camera and it has great reviews. I know my boys certainly love to take pictures with my camera and I would definitely feel safer if they were using this one!
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Hotels in Winsum
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There are not so many hotel rooms in Winsum, just 1, still everyone can find an offer to suit his choice. The most common offers in this city are hotels, they count 1 out of 1, and their prevalent location is central district. According to our practice, it is the most profitable to book a hotel in the south of Winsum, as it is the location of the hotels with optimal cost and quality offers along with the cheap hotels. Taking into account the small size of the city, there is no need to dwell hotel reservation on the location: the road to the city center would take less then half an hour, so one can book a hotel in any district of Winsum. The most populated with hotels district of Winsum is the north, 100% of cheap hotel rooms are concentrated here. Winsum is a truly multifaceted city, here everyone can find a hotel of his choice: a business person, a young couple or a family with little children. Take a look at our selection of the cheap hotel rooms in Winsum to make a well-informed choice for your reservation!
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Crans-Montana Youth Hostel Bella Lui
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Day 203: Lucerne - Lauterbrunnen
... duration - about two hours - was something you have to see to believe. The train was winding its way through the Swiss Alps with little villages littered throughout for locals and tourists to hop and off at their leisure. There were a few little towns along the way, particularly Sarnen, Giswil, Meiringen and Brienz that looked incredible. Some of the lakes that were at the bottom of the alps had the clearest water I have ever seen. There ...
Time after time
So I return to Lauterbrunnen.
Last time I was here it was freezing and snowing but it was beautiful. The beauty hasn't changed and up the top there still is snow. Down in the valley though was rather hot. I am from Australia so I can deal with the heat wave In Switzerland at the moment.
We had breakfast and then went to go to the cafe to get coffee. Amber was excited about the coffee because they made a good one and they had soy milk. Coffee in ...
The final road to the Alps
... all gets backed-up and comes to a stand those fast cars simply have to sit there stationary while me on my bike plod on passed between the slow moving cars. At one point I must have passed well over 2000 stationery cars.
Finally I approach the Swiss border and police are cars and doing a random search. I was just glad when they waved me through as I really did not want to unload all my boxes here at the side of the road.
After a ...
... way to get there except to return to Kleine Scheidegg. Luckily this was the short hike of the day since the two train stations were only a little over a mile apart. We found a trail, however, it was not marked along the way and we had to go through three closed fences to get there. Thankfully it was the correct trail and fences were to keep the cattle that we walked by contained.
We had a nice lunch in Kleine ...
Toon Town... not what you'd think
... heights so that she could go up to the Schilthorn. We met her on the way back down to Murren on the cable car and she joined us on our hike down to Gimmelwald and our picnic. We ran into her again on the train to Interlaken this morning. She said she has a group of friends that we remind her of. We laughed about how her posse and we could meet up in the future for another adventure.
Also, one of the owners of ...


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|Custom Storm
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I am a cosplayer and an aspiring costume designer, among other things. I'm still young, and I have a long way to go! That's where the fun is. Support my work if you like it.
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Transition Center Gives Women, Children Fresh Start
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Oscar Nominees For Best Picture Include 'Captain Phillips,' 'Gravity'
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WATCH: After Health Scare, Fiona The Baby Hippo Goes For A Dip
As Negotiators Talk Peace In Geneva, Bombings Kill At Least 32 In Syrian City
FCC Chairman Goes After His Predecessor's Internet Privacy Rules
Bounding Baby Bongo Born
Los Angeles Officials To ICE: Stop Identifying Yourselves As Police
The Problem With That Video Of Tigers Squaring Off With A Drone
VX: The Nerve Agent Used To Kill Kim Jong Nam Is Rare And Deadly
71 Degrees In February: Temperatures In Boston And Buffalo Rewrite Record Book
Car Bomb Kills More Than 50 People Near Syrian Town Captured From ISIS
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A short film series examining the severe underrepresentation of African-Americans in the sciences.
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Get more out of your classical music experience and check out Vic Di Geronimo's blog.
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AFX has been offering a diverse and evolving array of energy-efficient and affordable lighting solutions for commercial and residential spaces for over 75 years. The brand delivers innovative ideas and expertise, adding value to your lighting concept. At AFX, it's the values, brought forward from their past, that create the foundation for the future. Partnerships that stand the test of time are at the core of AFX's success.
Rated 4 out of 5 by Adam G. from Nice product machine work on the metal housing is good ...but there are some flaws in the frosted glass shades
Date published: 2011-10-03
Aria Sconce is rated out of 5 by 1.


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- Christian Anderson's Profile
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Grapevine Police Officer Ryan Sayre has been recognized by the National Association of Police Organizations (NAPO) for the 21st annual TOP COPS Awards.
He was honored at an awards ceremony in Washington, D.C., on May 12.
Sayre was one of three officers from Texas and the only one from Tarrant County to be honored.
Some facts about Sayre:• Grapevine High School graduate, 2002.
• Grapevine Police Department Explorer Post, 1999-2004.
• Irving Police Department detention officer, 2004-2006.
• NCTCOG Regional Police Academy.
• Grapevine Police Department hired, 2006.
• DWI officer, 2009-2011.
• Currently assigned to the Uniform Operations Division.
• Last 16 months activity resulted in 29 drug possession arrests, nine DWI arrests, 11 drug paraphernalia arrests and numerous other routine arrests.
The purpose of the TOP COPS Awards, which was created in 1994, is to educate the public about the nation's heroes and to pay tribute to law enforcement officers in federal, state, county and local agencies from across the country for actions above and beyond the call of duty during the preceding year.
TOP COPS are nominated by fellow officers. An independent awards selection committee comprised of national law enforcement representatives select candidates from hundreds of nominations.
"The TOP COPS Awards provide an opportunity for all of us to recognize the brave men and women in America's law enforcement community who selflessly put their lives on the line day in and day out," NAPO President Thomas J. Nee said in a news release. "Law enforcement officers care deeply about the citizens and communities they serve, and this honor is one way of letting them know their contributions are not taken for granted."
Many celebrities from NBC's hit programs "Law and Order" and "Law and Order: Criminal Intent," and CBS's "Cold Case," "NCIS" and "CSI: Crime Scene Investigation" served as award presenters.
All proceeds from the TOP COPS Awards benefit the Police Research and Education Project (PREP), NAPO's 501(c)(3) sister organization, which promotes the well-being of officers and their families and educates and informs the public about the role of law enforcement in a democratic society.
NAPO is a coalition of more than 1,000 police units and associations representing 241,000 rank-and-file law enforcement officers from across the United States. For more than 30 years, NAPO has been instrumental in the passage of laws protecting citizens and police officers.


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Mary Scott, 67, of Sweet Springs, died Saturday, Jan. 14, 2012.
Funeral Services will be at 12 p.m. Friday, Jan. 20, at Sweet Springs Assembly of God Church in Sweet Springs. Visitation will be from 11:00 a.m. to 12:00 p.m. Friday at the church. Burial will be in Fairview Cemetery in Marshall. Condolences can be sent to htmayfuneralhome.com. In lieu of flowers, donations for the family can be sent to Alexander-May Funeral Home in Sedalia.
Born Aug. 26, 1944, in Jennings, Fla., she was the daughter of the late Rev. John H. Rich and Vernell Rich, who survives. In 1945, she moved to Malta Bend and later moved to Sweet Springs. She graduated high school in 1962. She was a member of Yokum Chapel A.M.E Church in Malta Bend for many years serving on the Women's Missionary Society and as church secretary. She was currently a member of Sweet Springs Assembly of God Church. She was a member of Sweet Springs Optimist Club and was one of its founders, serving on the board and helping earn distinguished club of the year during one of her presidencies. She worked for Tyson Foods in Concordia for 15 years.
In addition to her mother, she is survived by one son, Larry Scott of Sedalia; one daughter, Tiffany Scott of Sweet Springs; three grandchildren; one sister, Anna Kemp of Columbia; three brothers, George Rich of Sweet Springs, Lonnie Rich Sr. of Jefferson City and John Rich Jr. of Sweet Springs.