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The November election for governor of Connecticut will be a rematch of 2010's razor-close contest.
Thomas C. Foley, a Greenwich businessman and a former ambassador to Ireland, handily defeated the State Senate minority leader, John P. McKinney, on Tuesday to win the Republican nomination, according to unofficial results.
Mr. Foley, who captured about 56 percent of the vote to Mr. McKinney's 44 percent, will take on Dannel P. Malloy, the incumbent Democratic governor, who beat him by about 6,500 votes four years ago.
"Change is on the way; change is coming to Connecticut," Mr. Foley said, addressing supporters in Waterbury late Tuesday. "Dan Malloy has had his chance, and change is coming."
"I'm a businessperson," Mr. Foley said, after ticking off some problems in the state such as high taxes, poorly maintained bridges and underperforming schools. "I know how to fix these problems. I've been doing them for 35 years and will represent everyday citizens, not insiders, not special interests."
Mr. McKinney, 50, called Mr. Foley, 62, to congratulate him. By 9:45 p.m., Mr. McKinney was addressing his supporters in Fairfield and urging them to support Mr. Foley in his quest to retake the governorship and make Mr. Malloy a "one-term governor."
The Republican gubernatorial primary was the most closely watched of the 30 primaries on Tuesday in Connecticut, where turnout was said to be light.
Mr. Foley, who won his party's endorsement at its convention in May, is considered more conservative than Mr. McKinney, a veteran state legislator from Fairfield who is seen as more centrist on issues like gun control.
Mr. Foley will now have to appeal beyond his political base to beat Mr. Malloy. There are 700,000 registered Democrats in Connecticut, 400,000 Republicans and 800,000 unaffiliated voters.
Nancy DiNardo, the chairman of the state's Democratic Party, said late Tuesday she was not worried.
"I think we have seen over and over again how Foley does not give consistent answers," she said, "and the press has called him out a number of times on some of his comments and Dan Malloy is going to run on the record he has: 55,000 new private sector jobs created. He's given money back to education."
Mr. McKinney's term in the State Senate ends in December, and he had announced that he would not be seeking re-election.
In his concession speech Tuesday night, he thanked his supporters for "making this the best campaign of my life."
While Republicans were going to the polls to choose which of two candidates would represent them on the November ballot, another gubernatorial hopeful, Jonathan Pelto, was defending his quest to secure a line on the November ballot as a third-party candidate against critics like Representative Rosa DeLauro of Connecticut who are urging him to pull out. She and other Democrats claim that Mr. Pelto, farther to the left than other candidates on most issues, will siphon votes from Governor Malloy and help hand the election to the Republicans.
Mr. Pelto, a former five-term member of Connecticut's House of Representatives, first elected in 1984 when he was a senior at the University of Connecticut, submitted petitions to the Secretary of State's office this month, which are being verified by local registrars as well as Hartford.
He will need 7,500 qualifying signatures from Connecticut residents who are on the voter rolls to meet the test, and is not thought to have a huge cushion if too many of his names are eliminated.
One signature on his petitions was that of Ralph Nader, one of Connecticut's most prominent activists and a former presidential contender who was criticized as a "spoiler" by some for taking votes from Al Gore in his race against George W. Bush in 2000.


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Great news folks, Big Country are only on tour RIGHT NOW and they are looking forward to playing across the UK.
The tour opens up tonight in Preston, then the guys head all over the place, down through the midlands, Bristol, Exeter, onto Falmouth and Swansea then back up the South coast stopping off in Brighton and Southend-on-Sea prior to hitting the midlands prior to ending up 'oop North' in Grimsby and Doncaster.....quite a trek between now and the 9th November (I hope they aren't all crammed into one Transit van).
22/10/2013 - 53 Degrees – Preston
23/10/2013 - Central Station – Wrexham
25/10/2013 - Picturedrome – Holmfirth
26/10/2013 - The Vault – Rugby
27/10/2013 - The Fleece – Bristol
29/10/2013 - Phoenix – Exeter
30/10/2013 - Princess Pavillion – Falmouth
01/11/2013 - Sin City – Swansea
02/11/2013 - The Haunt – Brighton
03/11/2013 - Chinnerys – Southend-on-Sea
05/11/2013 - Railway – Ipswich
06/11/2013 - River Rooms – Stourbridge
07/11/2013 - Rescue Rooms – Nottingham
08/11/2013 - The Leopard – Doncaster
09/11/2013 - Yardbirds – Grimsby
You can keep upto date with the band's whereabouts and happenings by clicking HERE
Big Country were formed in 1981 in Dunfermline (Fife), comprising of original members Stuart Adamson (Vocals/Guitar), Bruce Watson (Guitar), Tony Butler (Bass) and Mark Brzezicki (Drums).
The height of the band's popularity was in the 1980s, although it retained a cult following for many years after. The band's music was most recognisable for the sounds it infused with Scottish folk and martial music styles, as well as for playing and engineering their guitar driven sound to evoke the inspirational spirit of bagpipes, fiddles and other traditional folk instruments.
Following the sad passing of Stuart Adamson in December 2001, a memorial to Adamson was held at Dunfermline's Carnegie Hall in January 2002, followed by a tribute concert at the Barrowlands (Glasgow) in May. It brought together the remaining members of both Big Country and The Skids; Adamson's teenage children, Callum and Kirsten; as well as Steve Harley, Runrig, Simon Townshend, Midge Ure and Bill Nelson.
In 2007, to celebrate 25 years of Big Country, founding members Bruce Watson, Tony Butler (now lead vocalist for the first time), and Mark Brzezicki reunited to embark on a tour of the UK with dates in Scotland and England and a gig in Cologne (Germany).
The surviving original members toured again in late December 2010 and January 2011 with Mike Peters of The Alarm and Jamie Watson (Bruce's son), added to the lineup.
In January 2013, the band announced on their website that they had completed recording a new 12-track studio album entitled The Journey, this was released on April 30, 2013.
So, there we have it, a potted history of the band, 9 albums since they started their journey, they are still out there, gigging all over the place and making people smile.
For a special treat, here's Big Country performing 'Chance' LIVE on Top of the Pops way back in 1983 (okay, it wasn't live but you'd never guess !!)

subset: commoncrawl


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I'm sure I'm not alone in feeling utterly demoralised by the frequent news stories on the continued degradation of the natural world. From the shocking levels of plastic pollution in our seas to the now obvious signs of climate change, and industrial scale destruction of habitats, it's hard to avoid feeling hopeless about the planet's current and future state. While it is clear that addressing these issues will require major policy changes on the part of governments and a shift in culture from big business I do believe that individuals can also make a difference by becoming more engaged and changing their own habits.
53.200779 -2.891149


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Toppan supplies exterior parts for a variety of mobile equipment such as smartphones and personal computers by fusing various elemental technologies including printing, coating and deposition on processed goods such as plastic and metallic material.
We also provide precision processed and exterior decorated components for various devices.
By combining fundamental processing technologies such as plastic molding, and metal, film, and glass processing with a variety of decorating techniques such as printing, painting and vapor deposition, Toppan provides various precision processed and exterior decorated components that satisfy customer needs.


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Where do sight words come from I ask myself? Well I used to. Now I know! In our house they come from a quarry! The fat controller tells Thomas that 'and' and 'the' need collecting from the quarry urgently and should be brought to the station. Thomas, being a really useful engine, collects them (with Oscar's help of course). I kid you not that's how the first 20 were learnt!
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Making the most of your outdoor environment involves many choices and decisions.
The team at ARTVIEW Landscapes are dedicated to enhancing your environment and we provide a complete landscape design service.
From concept to completion, we work closely with you to bring your ideas to life – and always with a 'view' to creating a work of 'art'.
View a sandstone landscape design and construction project by Brian Baker of Artview Landscapes.
ARTVIEW Landscapes design services include:
- Concept designs;
- Consultation with engineers and landscape architects when the project works require engineers approval or plans need to be lodged for DA approval;
- Developing work from clients existing plans.
We will take the time to look at your outdoor environment and discuss all the options. The team at ARTVIEW Landscapes have the experience to help you make the most suitable choices for your garden.
We place great value on exact communication between you, ARTVIEW Landscapes and any specialist contracted into the project.
By really listening to your requests, the work is clearly directed to ensure your complete satisfaction.
Read what our clients have to say.
Important considerations for landscaping and designing your garden are available on our tips page.


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Wednesday, November 5, 2008
Pedal Power Update - October 2008
5 comments:
- story girl said...
This is way way off topic - but do you know when in where in the Brazos Valley we can get good, local apples?? It's fall and it feels like we should be eating lots of apples, but I don't even know where to look!
- November 5, 2008 at 5:50 PM
- Heather @ SGF said...
story girl - Unfortunately, apples don't grow here in the BV. The closest you can get is north Texas. Here's a link to some orchards in TX:
I've been eating a lot of citrus lately (from South Texas), but you might call the Farm Patch and see if they have any fruit from inside the BV. Let me know what you find out :)
- November 5, 2008 at 6:35 PM
- Beany said...
I didn't know pecans grew in Texas. I had some really amazing pecan waffles in Decatur, TX a few days back and learned that pecans are now in season.
The other thing that really shocked me was how many bicyclists Texas has. I thought you were some sort of anomally but then we keep running into lots of bicycle commuters. Its so encouraging and wonderful to see this. The more bikers the better.
Good job on the bicycling!
- November 6, 2008 at 8:44 AM
- sunflowerchilde said...
Great job with the bike! And I'm jealous you have a Prius (I have a Matrix, which works better for us b/c we need a station-wagon-type car). I live in Davis, which is an incredibly bikeable city, so I've always felt comfortable on the roads, but it takes a lot more nerve to ride around Sacramento, where I work. I honestly do feel that riding on the street is safer than riding on the sidewalk, though.
I have a really nice road bike that I use to commute for work, but I need a more useful bike for running errands. I bought an older road bike and put a newspaper-delivery-style basket on it, but it keeps having mechanical problems and the basket is really heavy. I want to sell it and start over, but I don't know what to do. Any suggestions?
- November 6, 2008 at 11:28 AM
- Heather @ SGF said...
beany - oh, yeah! We have lots of pecan. They should hit our farmers market in the next couple weeks too, although I saw a news report that this year's harvest has suffered. We'll only get about 1/2 the normal this year.
All the bikers must be in North Texas. We have some here, but not all that many. Most are students of the university or the poor trying to get to work. We have very few who actually choose to bike, but there are a few.
sunflowerchilde - I agree that once you get comfortable enough, you are safer biking in the street than on the sidewalk. You are FAR less visible to a car on the sidewalk. As far as selling your old bike, have you tried Craigslist or perhaps you have a university near by that has a for sale list on google? We have one here for our university called tamuforsale. It's a great place to post items. Hope this helps!
- November 6, 2008 at 1:29 PM


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To the Shippensburg Area School Board:
The purpose of this letter is to introduce the Shippensburg Area School Board (SASD) to the mission of Shippensburg Community Parks and Recreation Authority (SCPRA), to clarify SCPRA's relationship with our partners, and to address issues related to Veteran's Stadium.
SCPRA was created for the purpose of providing positive, meaningful, and quality recreation facilities and programs that will encourage and promote a healthy and growing community.
SCPRA was organized in June 2015. Currently, Shippensburg Borough and Southampton Township, Franklin County are our two partners. This means that SCPRA manages all of the parks and other recreational resources of both municipalities. The Board of SCPRA consists of five members. Two members were appointed by the Borough and two members by the Township. The fifth member was selected by the four appointed members.
SCPRA has entered into lease agreements with the partners for a duration of 25 years. This includes any real property dedicated to recreational purposes, including buildings, sports fields, trails, pavilions, and playgrounds. If SCPRA decides to make changes/improvements to any leased real property, there are procedures to be followed. A significant alteration or improvement costing $15,000 or more or a demolition of any structure with an appraised value of $5,000 or more requires SCPRA to obtain approval from the partner.
The partners have agreed to a five year funding commitment. Additional short-term funding is provided through the Department of Conservation and Natural Resources (DCNR).
SCPRA has obtained a Circuit Rider grant from DCNR. This grant includes significant guidance from representatives of DCNR. During the orientation provided to SCPRA Board members from DCNR representatives, the benefits of a Park and Recreation Board were outlined. Some of the benefits are:
provides for citizen representation and ongoing public input and support
is composed of conscientious volunteers who want to make a difference
relieves elected officials of day-to-day operations and concerns
encourages proactivity and forces forward thinking
Another point that was stressed by DCNR was to develop working relationships with community organizations and school districts. This letter is SCPRA's attempt to initiate that relationship.
SCPRA's mission is to serve the community. It is SCPRA's mission to provide recreational activities to the community in accordance with the needs of the community. We are in the process of writing a comprehensive plan which will provide us with a guideline to follow to accomplish that mission. Presently, SCPRA maintains Veteran's Stadium with that purpose in mind. This is done at break even costs. SCPRA is completely neutral concerning the final decision about whether to build a new stadium or to continue using Veteran's Stadium.
If the decision is made to continue to use Veteran's Stadium indefinitely, SCPRA is very interested in developing a working relationship with SASD and the various Booster Clubs to develop a plan for needed capital improvements to the stadium, including a strategy for fund raising to make such improvements. SCPRA has access to grants to improve the existing facilities.
As Veteran's Stadium is presently maintained almost exclusively for the use of home athletic events, should SASD choose to build a new stadium, SCPRA will then reevaluate whether maintaining a stadium at Memorial Park is in the best interest of the community. SCPRA will then consider other uses for the Stadium. SCPRA will maintain the stadium for safety but we will have no choice but to pursue a different path. This will determine the direction of our comprehensive plan.
In summary, SCPRA is very much interested in forming a working relationship with SASD. This relationship would allow us to share facilities, ideas, and work together to benefit the entire community. Representatives of SCPRA would be happy to attend a SASD Board meeting to answer any questions that SASD Board members may have. The SCPRA Board also invites SASD Board members to attend any SCPRA meeting. SCPRA meets on the first Thursday of every month at the Southampton Township Building on Orrstown Road at 6 pm. We hope to hear from you soon.
Shippensburg Community Parks and Recreation Authority
Gerilee Davis, Chairperson
Ed Barrett, Vice President
Maria Misner, Secretary
Derek Bostick, Treasurer
Nathan Goates, Right to Know Officer


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Not terrible dramas, just kitchen ones mostly, though the whole thing can be a little exhausting. I like the calm of Christmas Eve best, everything wrapped and ready and a few wines with the family. I mean, I had a lovely time of it of course, once my health picked up and I could go for drinks and buy books for friends and wrap gifts in ribbons. But things never feel as 'just right' as I plan for. I made the Momofuku 'crack pie' for Christmas day, but failed miserably. After spending two days (biscuit prep for the base on Christmas Eve, filling on Christmas Day) and having it set poorly, the butter conversions obviously wrong, I had a bit of a cry. Or quite a cry. I'd double-checked everything, but knew as I was folding it through that it wasn't quite right.
It was my contribution to our family dinner but by 3 PM, all signs pointing towards a wreck of a pie, I had to pull myself together and used the leftover eggwhites for an emergency pavlova. Which turned out very nicely, two perfectly crisp bases which I sandwiched with thick cream and a bucket-load of fresh strawberries and blueberries. But I was nonetheless disappointed and emotional. Not to mention confused and mildly angry. As my cousin Lucy kindly pointed out, at least I'm the kind of person who can make an emergency pavlova, which I guess is something.
No qualms with the gift my father gave me though. We do a draw each year, and it's always a good year when he's buying for you, or in this case, making. We have a limit which he thoroughly disregards, making me two 18C gold fine bangles. They're delicate and just the right amount of clink as I walk or turn on the tap or, as of late, drink a glass of wine. I absolutely love them. Spoilt rotten, no question.


text: Beautiful brunette babe Coco Velvett enjoys playing with big hard cock. She gives to this cock a great handjob and doing it with great pleasure, as can be seen on her sweet face. And while this horny babe jerks off this hard white cock she starts to lick his balls.


text: Fruit of Labor June 2016 Newsletter June 2016 Fruit of Labor World Cultural Center Newsletter produced by: Black Workers For Justice's Hip Hop 4 Justice edited by: Mari Caldwell-Robinson Contact Information: Address: 4200 Lake Ridge Rd, Raleigh NC 27604 (919) 231-2660 – Anytime (919) 876-7187 – Day email: firstname.lastname@example.com website: www.fruitoflabor.org Verizon strike picket lines proliferate: With at least ten Verizon strike picket lines from Germantown to College Park and DC today, there's sure to be a line near you to show your solidarity with the nearly 40,000 striking CWA and IBEW members. A number of local unions and organizations – including Jobs with Justice, Jews United for Justice, SEIU 32BJ, and the transit workers -- have adopted area picket locations; check our updated calendar listings here for the latest details. The main event this week is tomorrow's Verizon National Day of Action, with major picket lines planned for DC, Montgomery County and Annapolis; we'll have complete details in tomorrow's Union City.photo: L Street picket line Tuesday; photo by Chris Garlock/Union City Prince was a champion for working people: The world lost a musical icon when Prince died, and working people lost a champion. The AFL-CIO Now blog recently reported on Prince's career-spanning fights on behalf of working people. For more than 40 years, Prince was a union member, a long-standing member of both the Twin Cities Musicians Local 30-73 of the American Federation of Musicians (AFM) and SAG-AFTRA. Beginning with "Ronnie Talk to Russia" in 1981 on through hits like "Sign o' the Times" and later works like "We March" and "Baltimore," Prince's music often reflected the dreams, struggles, fears and hopes of working people. And he wasn't limited to words; his Baltimore concert in the wake of Freddie Gray's death raised funds to help the city recover. Few of America's artists have so well captured the plight of working Americans as Prince, putting him in the line of artists like Woody Guthrie and Bruce Springsteen as working-class heroes. "Prince was not only a talented and innovative musician, but also a true champion of musicians' rights," said AFM president Ray Hair. Legal SEIU Law Student Program, SEIU (Posted: 4/28/2016) "Trans Pacific Partnership Agreement Meeting with US House of Rep. GK Butterfield" On May 9th, we finally met with U.S. House of Representative G.K. Butterfield (Wilson, NC/1st District ) at his Durham district office at the NC Mutual Insurance Bldg. He is the chair of the Congressional Black Caucus/CBC. We been trying to set this up with him since Nov.2015 to share our opposition to Pres. Obama's and Secretary of State Hillary Clinton's secretly negotiated "Trans Pacific Partnership Agreement" also known as TPPA or TPP. Our phone calls , e-mails, letters and persistence pays off. Eighteen people representing Black Workers for Justice ( Linda Suggs/Jim Grant), NC Public Service Workers Union-UE Local150 ( Angaza Sababu Laughinghouse), Common Cause, Communication Workers of America, Durham People's Alliance, Eastern NC Labor Council, Food & Water Watch, NC Council of Churches, NC Democratic Party Executive Committee, NC Environmental Justice Network, Southern Workers Assembly,NC Raise Up for 15, NC State AFL-CIO, Pitt County Coalition Against Racism, Triangle TPP Working Group, and Witness for Peace Southeast. Our delegation showed Representative Butterfield that opposition to the TPP is broad and diverse. We were very pleased with Representative Butterfield's demeanor.....( he recognized Jim Grant {arrested w/GKB}, Angaza Sababu {1980's NC ML King State Holiday Day petition campaign/MWBE/Collective Bargaining & Workers Rights efforts, George White Day events}, Linda {she is everywhere representing labor and BWFJ ! ], Marybe {NC AFL-CIO}, and CWA {as political financial contributors) and had a warm response to our large Anti-TPPA delegation. We showed up with 13 more representatives than protocol of 5 allowed, but he assured us he knew many of us and would "make it work" and heard our concerns in the reception area of his office. Each representative was introduced and briefly explained why our various constituency was opposed to the TPP. He stated that our presentations were well organized. Then, MaryBe McMillan from NC State AFL-CIO asked if Representative Butterfield would publicly oppose the TPP. Rep. Butterfield stated that if he had to vote today, he would vote no on the TPP. He noted that the vote is unlikely to come up before the election in November, so to assure us of his position, he stated that he is 99.9% against the TPP. He explained that he was "taught a long time ago that a congressional representative should never come out 100% for or against an issue, because things can change so quickly on Capitol Hill". For example, a vote on the TPP could be included in a bill that affects the essential functions of the federal government, like a budget bill. He assured us that if his position changes, he would let us know. We are pleased with this initial result. However, we have to remember that this meeting was not the end goal ! The ultimate goal is getting a vote against the TPP from Representative Butterfield. We must continue this conversation and invite more voices from NC District 1 to engage in this oppositional TPPA struggle for workers rights at home & abroad, safe/clean environment/Mother Earth and living wage jobs for all. Report & photos submitted by Linda Suggs, Jim Grant and Angaza Sababu Laughinghouse Black Power: The Women's Movement A coalition of young Black women raise their fists in a gesture of Black power and defiance as they block all traffic on a major Chicago roadway! Both the intersection of resistance and culture and the clear-cut demands hark back to the best of the sixties motion for self-determination. I'm uplifted & encouraged as we continue to battle in the "trenches". Check it out! http://www.truth-out.org/news/item/35962-inspired-by-beyonce-black-organizers-get-in-formation-to-disrupt-nfl-draft> Culture is a main arena of identity and struggle Clintons took payments from Trans-Pacific Partnership backers last year | 18 May 2016 | Former President Bill Clinton raked in millions of dollars from special interest groups in the weeks just before and after his wife announced her presidential campaign, including $325,000 from a group that pushed for the Trans-Pacific Partnership. Hillary Clinton came out against the trade deal in October under pressure from her rival, Bernie Sanders, and his progressive supporters. Sanders denounced the agreement early in his campaign, arguing the deal benefits major corporations at the expense of American jobs. But the National Association of Manufacturers, which paid Bill Clinton a hefty fee just one month before Hillary Clinton launched her candidacy in April, lobbiedfor the Trans-Pacific Partnership, according to the Center for Responsive Politics. New poll shows Trump beating Clinton in general election | 22 May 2016 | Donald Trump's presidential campaign has been given a boost by a new poll showing the presumptive Republican nominee winning November's general election against likely Democratic nominee Hillary Clinton. An ABC News/ Washington Postpoll published on Sunday shows Trump with a two percent advantage over Clinton with registered voters in a hypothetical general election matchup. According to Langer Research, Trump's "enhanced competitiveness reflects consolidation in his support since his primary opponents dropped out." NRA Endorses Donald Trump at National Convention | 20 May 2016 | The National Rifle Association endorsed Donald Trump at its national convention here on Friday, a late show of support from the nation's biggest pro-gun-rights group for the presumptive GOP nominee. The endorsement comes despite persistent skepticism from conservatives over Trump's sincerity on the Second Amendment, after the candidate shifted from backing an assault weapons ban in 2000 to voicing outspoken opposition to any weapons bans and support for an expansion of gun rights since launching his presidential bid. WORKERS ARE IN CRISIS! Two-thirds of Americans would have difficulty coming up with the money to cover a $1,000 emergency, according to an exclusive poll released Thursday, a signal that despite years of recovery from the Great Recession, Americans' financial conditions remain precarious as ever. These financial difficulties span all income levels, according to the poll conducted by The Associated Press-NORC Center for Public Affairs Research. Seventy-five percent of people in households making less than 50,000 a year would have difficulty coming up with 1,000 to cover an unexpected bill. San Francisco police chief resigns under pressure after officer shooting | 19 May 2016 | San Francisco's embattled police chief, Greg Suhr, resigned under pressure from the city's mayor on Thursday, just hours after an officer fatally shot a black woman, as the mayor indicated he had lost confidence in the chief. The police department and Suhr have faced mounting criticism and protests for months in the wake of several high-profile police killings and a racist text scandal. "Our Heroe/mentor transitioned... Brother Jim Haughton Presenté!" Meet our beloved Brother Jim Haughton of " Harlem Fightback" as a teenager when I lived on 178th St. and St. Nicholas Ave. in the Bridge Apartments/Manhattan NYC. Finding good paying jobs was hard for Black youth then in the 1960's and spurned our interest and involvement in the rising tide of protest and resistance ! Our beloved leader Brother Jim, a socialist/anti-capitalist veteran activist and organizer, helped Black workers develop the political understanding, strategy,tactics and protest that altered the racist economic power relationships between us , the construction industry and several "white only" construction skilled trade unions. These historic and powerful protests were workplace actions lead by Black workers and our community.They later evolved and created the "affirmative action programs" that you and others enjoy today ! Brother Haughton, a former Student Non Violent Coordinating Committee (SNCC) white activist and neighbor Don Hamer, and our Black Workers movement got me a union construction job with great pay and benefits through engaging in these militant protests ( chaining up the construction site fences with live young bodies of Black workers and powerful chains).I These protests at the late 1960s-1970 Harlem State Office Building construction site at a 125th Street and Adam Clayton Powell Blvd ( now known as Malcolm X Plaza) had a great impact on our communities, national unions and the broader society. The racist International Brotherhood of Electricians ( IBEW) Local 3 and the white Construction / Development Co. were also sued by African-American working class youth, Harlem Fightback as well as the Workers Defense League in a historic class action discrimination legal action. We won and I became an "apprentice electrician" in IBEW Local 3. No doubt, many youth like myself were engaged and politically educated in this struggle, and we became strong activists in this struggle against the racist construction trades in NYC and other struggles for power around the U.S..Jim Haughton taught and made us study his self authored brief pamphlet "The Centrality of the Black Worker: in the Black Liberation Movement & Labor Movements ". We were encouraged to join in political youth organizations, continue our formal and political education, and use it to serve our people and class struggle for fundamental change and power, During the mid 1960's period, Malcolm X had lectured at Columbia University and left his mark on forward thinking students, especially its few Black students. By 1968, my older Brother Adilifu ( Charles Levonne) attended Columbia in the midst of these students' historic rebellions and subsequent protests. While I was at Stuyvesant High School, my brother had invited me to stay with him in his campus dorm room. This was yet another important lesson about the urgent need to challenge racism, white supremacy and classism. I applied to attend Columbia with my brother's encouragement and was accepted.This was an exciting time, like the struggle today, in our peoples ' struggle ! Please take time to borrow/copy Haughton's papers from our home library or the FRUIT OF LABOR WORLD CULTURAL CENTER"S ARCHIVE This and other readings/studies and actual early organizing efforts working with youth and elders nurtured my revolutionary spirit and growing into a socialist. Later, when I turned nineteen or twenty years old, I was hired as a recruiter and organizer for the "Workers Defense League" and later A. Phillip Randolph's & Bayard Rustin's RECRUITMENT & TRAINING PROGRAM, INC taking on the .challenging work of continuing this important organizing work. Please take the time to read up on the piece below and the web sites within. It will give you insight into your Dad and our peoples' struggles. Angaza Sababu Laughinghouse NewsletteradminMay 29, 2016 Facebook0 Twitter LinkedIn0 StumbleUpon Reddit Tumblr 0 Likes


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The bubbly Just Married star will make her return to the big screen in the film after taking two years off to nurse her sick mum.
She says, "My mom had cancer and she's doing incredible now."
Stallone will direct and star in the film, which will also feature martial arts star Jet Li, Eric Roberts, Brit Jason Statham and Terry Crews, who has replaced rapper 50 Cent in the movie, which revolves around a group of mercenaries who set out to overthrow a South American dictator.


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Whether one talks about a hundred industries for each region or merely ten new industries annually, there is work to be done to realize that objective, and ideas may differ as to how to go about it, partners to be found, financing to be assured, etc. Geita is privileged in many ways as it makes plans for industries, but it also faces drawbacks that a number of other regions would appear better off.
A recent write up in our sister newspaper showed the parameters that top regional and district officials in the zone are mapping out, for instance the collaboration they are picking up with the Open University of Tanzania (OUT ) which has operating centres in various regions. This element is one aspect of how regions can go about mapping their own process towards industrialization, as the country is vast, with uneven distribution of resources, in which case the methods, industrial mix, will be different in each case. The question is whether any position agreed on such initiatives is workable, or wider policy is essential.
Planning has different meanings for different sociopolitical systems, and in Tanzania at present there is something clearly experimental as to what ought to be done. There is a first phase legacy of centrally planned industries where the government took initiative and sourced the financing, which a good number of academics and even parliamentarians still think is the best approach. Then there is the market-led way that has been in the vogue for the past 30 years but doesn't appear to have achieved plenty, and the crisis of unemployment compelled the fifth phase to rethink it. So it isn't just a matter of market forces alone.
Two problems stand out for industrial take off as well as regional initiatives to that effect, namely how far they can initiate own strategies and expect that they will be sustainable. The best way to ensure that they are sustainable is not to expect financial assistance from public sources, and to the best extent possible, anchor such initiatives in competition with other goods, especially imports. Despite that initiatives can be taken by regional and district authorities, they can only mobilize and harness private sector resources.
The bigger issue is growing the market, as many initiatives especially in the agricultural sector (direct crop produce and soon, agro-processing) continually faces a problem of reliable markets, on account of limited purchasing power. This is the big policy snag, that hasn't been sufficiently worked out yet, namely that each industrialist will do better for the country's economy by being allowed or directed to purchase land from farmers or buy existing industries so as to start, and be assured long lease. Such cash adds to purchasing power and prepares the economy to absorb the new products, while merely allocating land is acceptable for export processing zones. Investors come here to seek rising markets, not to export.


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Days of Treatment
FIGURE 6.3 Antimesothelioma effects of a-tocopheryl succinate. (A) Immunocompro-mised mice were injected intraperitoneally (i.p.) with human mesothelioma cells and peritoneal mesotheliomas allowed to established. On week 4 after the animals were injected with the cells, treatment was initiated consisting of i.p. administration of 200 |ll of 200 ||M a-TOS (in DMSO) every third day for more than 20 weeks. Survival was used as a marker for the effect of a-TOS. (Adapted from Reference 16.) (B) Immunocompromised mice were injected subcutaneously with human mesothelioma cells and tumors allowed to reach 100 mm3 before treatment onset. The mice were then injected i.p. with 200 |ll of 200 mM a-TOS (in DMSO) every second day for up to 2 weeks. Tumor size was estimated and volume calculated. (Adapted from Reference 96.)
Recently, Kline's group demonstrated anticancer activity of a novel VE analog against breast cancer and lung metastases alone or in combination with celo-coxib.4344 These data demonstrate the therapeutic promise of a-TOS and are likely to result in clinical application of the agent and design of novel anticancer agents.
A major reason for the anticancer efficacy of VE analogs is their high apo-ptogenic activity. We observed that while a-TOS significantly suppressed experimental colon cancer, a-TOH showed only marginal, nonsignificant effect.37 Analysis of the tumor sections revealed that both agents inhibited proliferation, but only a-TOS induced apoptosis.45,46 Apoptosis as a major mechanism for antitumor activity of VE analogs has also been proposed for its antimelanoma effect39 and may be expected also in mesotheliomas.41 Although multiple modes of action may be expected for VE analogs, induction of apoptosis is the major determinant of their anticancer efficacy.
6.3.3 Selectivity of VE Analogs Increases Their Clinical Application
A paradigm rendering VE analogs clinically applicable is their selectivity for neoplastic cells,1 as shown in many cultured cells.28 45 47-49 The reasons for the selectivity are not fully understood. Some types of normal cells have the propensity to hydrolyze a-TOS into its redox-active counterpart.1 Selective hydrolysis of a-TOS may, at least in some cases, explain the selective toxicity of the agent, since the proapoptotic species a-TOS would then accumulate in nonmalignant cells at levels below the toxicity threshold.
Hydrolysis of a-TOS cannot always explain its selectivity. For example, a-TOS is highly toxic to mesothelioma cells but not to nonmalignant mesothelial cells.4150 However, in this case, the resistant cells do not hydrolyze a-TOS. It is possible that the selectivity is given here by the resistance of the nonmalignant cells to oxidative stress. It has been published that a-TOS provokes generation of ROS in cancer cells.51-53 We observed that mesothelioma cells generated ROS as a fast response to a-TOS while nonmalignant mesothelial cells showed very little ROS accumulation (J. Neuzil, unpublished data). It is possible that anti-oxidant enzymes are more expressed in nonmalignant cells, whereby affording protection from ROS-induced apoptosis. In support of this, it has been published that cells depleted of their mtDNA are resistant to apoptosis,51 53 54 and a recent paper showed that a reason for this was adaptive upregulation of the mitochondrial superoxide dismutase.55 It remains to be shown whether this is a mechanism of resistance of nonmalignant cells to apoptosis induced by a-TOS, although there is a report indicating the importance of lack of efficient antioxidant systems to render cancer cells susceptible to the VE analog.56 A recent report documented a direct correlation between susceptibility of cancer cells to a-TOS and their propensity to respond to this agent by generation of ROS.57 In support for low ROS accumulation as a mode of resistance to a-TOS, we have observed relatively low accumulation of ROS in a-TOS-resistant differentiated neuroblastoma cells when compared to the a-TOS-susceptible parental cells (J. Neuzil, unpublished data).
There is yet another plausible explanation for selectivity of VE analogs for malignant cells. This is based on the physicochemical nature of these compounds that are weak acids and that are deprotonated at physiological pH but largely protonated at the acidic pH of the tumor interstitium. This allows selective faster diffusion of the drug across the plasma membrane of malignant cells. Thus, there are several alternative or parallel mechanisms underlying the selectivity of VE analogs for cancer cells. Because this is one of the most important features of VE analogs, it is important to understand these mechanisms and, consequently, design and synthesize novel agents with higher proapoptotic activity while retaining selectivity.
We have recently studied the effect of a-TOS on neuroblastoma cells and their differentiated counterparts mimicking nonmalignant neurons. While the former were highly susceptible to the VE analog, the latter were relatively resis-tant.58 We found two lines of defense against a-TOS in the differentiated cells. First, the cells, unlike the parental neuroblastomas, did not accumulate ROS. Second, their levels of antiapoptotic Bcl-2 family proteins were elevated, in particular that of Mcl-1. These data clearly suggest that mitochondria are important not only in induction of apoptosis, but also in the selectivity of importance VE analogs for malignant cells.
6.3.4 VE Analogs Overcome Resistance of Mutant Cancer Cells to Apoptosis, Induce the Mitochondrial Apoptotic Pathway, and Cooperate with Immunological Apoptogens
Many cancer cells avoid established therapy by constantly mutating the relevant genes. This is a complicating factor, compromising many successful treatments. Therefore, it is imperative to design novel agents that would overcome these complications. Many anticancer drugs act via induction of apoptosis of malignant cells by causing damage to their genomic DNA, which results in activation of p53 and inhibition of proliferation accompanied by apoptosis. VE analogs show promise for treatment of cancers where such genes are mutated, most likely because they use the mitochondrial apoptogenic route.
It was reported by Coffey's laboratory that Trolox, a water-soluble analog of VE, inhibited proliferation and induced apoptosis in human colon cancer cells by increasing the expression of the cell cycle protein p21 Cip1/Waf1 in a p53-inde-pendent manner.59 This paper also showed that the agent could efficiently inhibit growth of tumors in athymic mice derived from p53- but not p21Cip1/Waf1 -deficient colon cancer cells. It was later observed that a-TOS caused efficient apoptosis in both p53- and p21Cip1/Waf1 -deficient colon cancer cells.38 These findings place VE analogs among potential anticancer drugs capable of being used instead of or as adjuvants to other drugs whose application may be compromised by mutations in the above genes.
Antiapoptotic/pro-survival consequences of other mutations can also be overcome by VE analogs. For example, overexpression of the receptor tyrosine kinase erbB2/HER2 complicates breast cancer treatment.60 The reason is that the auto-activated erbB2 activates Akt, a protein kinase phosphorylating multiple substrates, including IkB kinase (IKK), caspase-9, and Bad, resulting in elevated expression of pro-survival genes and inhibition of proapoptotic proteins.6162 It has been suggested that VE analogs overcome the erbB2-Akt antiapoptotic signaling. Akazawa et al.63 showed that a-tocopheryloxybutyric acid suppressed auto-phosphorylation of erbB2, shutting down the whole signaling pathway, although the mechanism is not clear. We have observed that a-TOS caused comparable apoptosis in both erbB2-low and erbB2-high breast cancer cells by a two-tier mechanism64 that includes cytosolic mobilization of cytochrome c, activating the downstream caspases, as well as that of Smac/Diablo, a protein antagonizing the caspase-inhibitory activity of the inhibition of apoptosis proteins (IAPs) that are elevated due to Akt-dependent activation of nuclear factor-KB (NF-kB).65 66 a-TOS thus induces apoptosis in cells over-expressing erbB2 on at least three levels (Figure 6.4). We are currently investigating the anticancer activity of VE analogs using transgenic mice overexpressing erbB2 in the mammary epithelial cells, resulting in spontaneous formation of breast carcinomas.67
The major apoptogenic pathway induced by VE analogs is linked to mito-chondrial destabilization. This is compatible with mitochondria as a novel target for anticancer drugs.6869 Mitochondrial proapoptotic signaling has been documented in several papers, and involves activation of the sphingomyelinase pathways, generation of ROS, and mitochondrial translocation of Bax.51 52 70-73 Conceivably, the ratio between the mitochondrial pro- and antiapoptotic proteins may determine the overall susceptibility of the cells to VE analogs.
Perhaps more importantly, the mode of proapoptotic signaling of VE analogs makes them candidates for adjuvant therapy, that is, synergizing with apoptogens using a different mode of action. a-TOS has been investigated for sensitization of cancer cell to apoptosis induced by the Fas ligand (FasL) and the TNF-related apoptosis-inducing ligand (TRAIL). Kline's group has shown that the VE analog sensitized cancer cells to FasL by mobilizing the latent cytosolic Fas to the plasma membrane,7475 as also observed for gastric cancer cells.76 77 This may suggest a role of a-TOS in cancer surveillance by boosting the immune anticancer/proap-optotic mechanism.
We have explored the possibility that VE analogs synergize/cooperate with TRAIL. In colon cancer cells, a-TOS synergized with TRAIL in apoptosis induction, by utilizing different, convergent pathways. Cooperation between aTOS and TRAIL was observed in experimental colon cancer.38 In mesothelioma cells, a-TOS synergized with TRAIL by upregulating the TRAIL death receptor-4 (DR4) and DR5.50 This report as well as our recent finding that a-TOS extends survival of mice with experimental mesothelioma41 is important because
FIGURE 6.4 Possible mechanism of apoptosis induction by a-TOS in erbB2/HER2 over-expressing cells. a-TOS causes cytosolic mobilization of cytochrome c (Cyt c) and Smac/Diablo. Cyt c forms a ternary complex with Apaf-1 and pro-caspase-9, resulting in activation of the initiator caspase-9 that, in turn, leads to activation of the effector caspases. Smac/Diablo amplifies this process by suppressing the IAP family proteins that are elevated due to Akt-dependent activation of NF-kB. This suggests that a-TOS induces apoptosis in cells overexpressing erbB2 on at least three levels: inhibition of erbB2 activation, induction of the mitochondrial-linked apoptotic pathway, and relocalization of Smac/Diablo, thereby suppressing the caspase-inhibitory IAP activity. Mechanistically, aTOS induces mitochondrial generation of ROS as well as mitochondrial translocation of Bax. Additional effects of a-TOS include: inhibition of erbB2 and NF-kB activation and suppression of Akt-dependent phosphorylation of Bad (rendering it inactive due to association with the protein 14-3-3) and pro-caspase-9 (suppressing its activity normally leading to activation of effector caspases). These effects of a-TOS not only induce apop-tosis in erbB2-overexpressing cells, but also sensitize them to other apoptogens, as shown here for TRAIL.
mesotheliomas are refractory to treatment, largely due to resistance to apoptosis by established drugs.78 Another mode by which a-TOS can sensitize cancer cells to TRAIL killing is its interference with activation of NF-kB, as shown for Jurkat cells.79 A possible mechanism of inhibition of the pro-survival transcription factor may be caspase-dependent cleavage of its subunit p65 due to activation of the apoptosis machinery.8081
6.3.5 Vitamin E Analogs as Antitumor Agents: Beyond Mitochondria
Although the mitochondrial pathway is central to the apoptogenic action of VE analogs, there are other pathways that may play an important role in the effects of the agents. Kline's group reported regulation of the AP-1 and mitogen-activated protein kinase/extracellular-regulated protein kinase pathways as additional signaling routes for apoptosis induced by a-TOS.82-86 Some but not all papers suggested that a-TOS induces apoptosis by interfering with the tumor necrosis factor-P (TGF-P) signaling, compromising the expression of pro-survival factors.87-89 These findings may be related to the effect of the VE analog on transition of cell through the cell cycle. Several reports showed that the agent caused arrest in G1 or G2. Turley et al.90 presented evidence that a-TOS inhibited proliferation of breast cancer cells by interfering with the cyclin A-E2F restriction point machinery. Yeh's group reported that a-TOS inhibited proliferation of cancer cells by modulation of the cell cycle transition91 as well as cell invasiveness due to inhibition of the activity of matrix metalloproteinase-9.92 These effects may be more specific for prostate cancer cells, as a-TOS has been reported to inhibit the function of the prostate-specific antigen.93
Our results also show inhibitory effects of a-TOS on cell cycle transition, with G1 and/or G2 arrest, depending on the cell type.94-96 The mode of cell cycle inhibition may be related to the effect of a-TOS on its modulators. The G1 arrest of the osteosarcoma cells may be linked to inhibition of the activity of the cyclin A/cyclin-dependent kinase-2 complex, while the levels of the transcription factor E2F1 were enhanced and were followed by phosphorylation of p53.94
Mesothelioma cells undergo a G2 arrest when exposed to low levels of a-TOS.95 96 This is related to disruption of the FGF-FGFR autocrine proliferation signaling loop by selective downregulation of both FRF2 and its receptor FGFR1 in the mesothelioma but not the nonmalignant mesothelial cells.95,96 a-TOS exerts its effect on the transcriptional level, downregulating FGFR1 by inhibiting the activity of E2F1,95 while FGF2 is downregulated via modulating the transcriptional activity of the early-response growth factor-1.96 The selectivity appears related to the low level of ROS generation by the nonmalignant mesothelial cells while their malignant counterparts respond to a-TOS by early generation of high levels of ROS.96
There are reports suggesting the possibility that VE analogs inhibit angio-genesis, which indicates an effect of the agents on tumorigenesis and the meta-static potential. We have observed a reduction in the number of blood vessels in experimental colon cancer xenografts in mice treated with a-TOS (J. Neuzil, unpublished data). Preliminary results also indicate an effect of a-TOS on pro-angiogenic cytokines in endothelial cells, suggesting a proliferation-suppressive activity of the VE analog. This can be reconciled with findings that a-TOS caused downregulation of VEGF.36 Another possibility follows from studies indicating that proliferating endothelial cells are highly susceptible to a-TOS while the confluent arrested cells are resistant.80 This highly intriguing paradigm is supported by comparable results from Hogg's group using a different inducer of apoptosis.97 Thus, a-TOS may specifically target angiogenic endothelial cells while being nonapoptotic toward normal endothelium. Resistance of endothelial cells suspended in G0 can be explained by high levels of expression of the checkpoint proteins p21 WafllC^' and p27Kip1 that prevent reentry of the cells into the cell cycle98,99 and that inhibit caspase activity.100
By virtue of inhibiting angiogenesis, VE analogs would be efficient against cancers irrespective of the frequent mutations in various genes. This area is also worth exploring for novel VE analogs. A recent paper showed a potential anti-angiogenic effect of y-TOH by inhibiting the activity of cyclooxygenase-2,101 thereby suppressing formation of pro-angiogenic eicosanoids.102 It is expected that y-TOS combines an antiangiogenic effect with apoptogenic activity (see Table 6.1).
6.3.6 Pharmacokinetics of VE Analogs — A Potential Secondary Beneficial Bioactivity
A most intriguing aspect of the potential use of VE analogs as anticancer agents follows from their pharmacokinetics. These agents are esters of VE and, therefore, hydrolyzed upon intestinal intake after ingestion.103 To overcome the intestinal hydrolysis step, agents such as a-TOS need to be administered intraperi-toneally. After reaching the circulation, they associate with lipoproteins104 105 that carry them to the neoplastic microvasculature. Once in the tumor blood vessels, a-TOS migrates to the malignant tissue where it induces apoptosis, thereby suppressing growth of the tumor. Because the blood components and the peripheral tissue are a dynamic system, there is constant exchange of hydrophobic molecules. a-TOS is thus gradually moved from the tumor and cleared, bound to remnant lipoproteins, via the liver. Here, a-TOS is hydrolyzed by nonspecific esterases. It is then partially disposed of within the bile, partially resecreted into circulation depending on the level of the saturable a-tocopherol-binding protein (a-TTP).105-108
The paradigm described above is shown in Figure 6.5. It is clear that, based on this scheme, supported by theoretical considerations and experimental data,109110 esters of VE are hydrolyzed in the liver into the redox-active VE that is, in part, returned into circulation. From this, it can be deduced that a-TOS and similar compounds possess at least two bioactivities. In the pro-vitamin form, aTOS suppresses cancer. After conversion to its vitamin form, it acts as a redox-active compound and as an anti-inflammatory agent.111115 Thus, we believe that the novel VE analogs represent agents with thus far unrecognized dual beneficial bioactivity relevant to a variety of highly deleterious pathologies, including cancer and inflammatory diseases.
VE accumulates in circulating lipoproteins, thus enhancing the anti-oxidant/anti-inflammatory defences a-TOS —► (circuí
Lipoprotein-associated VES exerts its anti neoplastic effect within tumor microcirculation
FIGURE 6.5 Proposed molecular mechanism for the "double-edge" activity of a-toco-pheryl succinate. Following entry into the bloodstream, the pro-vitamin a-TOS vitamin E succinate (VES) associates with circulating lipoproteins (LP) that carry the agent to the microvasculature of the neoplastic tissue. Here, VES exerts its antiproliferative/proapop-totic activity toward malignant cells that translates into inhibition of tumor growth. Since there is a constant exchange of hydrophobic molecules between the peripheral tissues and the circulation, a-TOS is gradually removed by virtue of remnant lipoproteins that are endocytosed by hepatocytes that possess high levels of nonspecific esterases (NE). Here, the remnants are dissembled and nascent VLDL formed. a-TOH (VE), both the original and that formed by hydrolysis of VES, is partially shuttled to nascent VLDL bound to the saturable tocopherol-transfer protein (TTP), partially excreted in the bile. Nascent VLDL enriched with VE is then resecreted into circulation, endowing the system with additional VE that promotes the antioxidant and anti-inflammatory defenses.
The above discussion reveals the exceptional promise of VE analogs as therapeutic agents. There are several features that make these compounds unique: (1) VE analogs induce apoptosis selectively in malignant cells and inhibit tumor growth in experimental models; (2) they overcome resistance to established anticancer drugs due to bypassing mutations in or deletions of critical genes; (3) they synergize with anticancer agents and/or sensitize resistant cells toward them; (4) they cause apoptosis in proliferating endothelial cells, suggesting their anti-angiogenic activity; and (5) they are metabolized into the redox-active VE with secondary beneficial bioactivity.
At this stage, we need more data to understand the exact mechanisms by which these compounds exert their proapoptotic/anticancer activity and, in particular, what makes them selective for malignant cells. Importantly, too, we need to obtain more data from preclinical studies using several experimental models. Thus far, the majority of these data comes from work with athymic mice. Transgenic mice predisposed to develop tumors need to be used because in such animals the role of the immune system, essential for tumor surveillance, is not impaired. It is hoped that, with better understanding of the molecular mechanism underlying the activity of VE analogs, they will be approved for clinical testing. Should they prove successful, the very cheap a-TOS or its derivatives may become drugs of choice against multiple malignancies with a secondary beneficial activity.
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- Yu W, Sanders BG, Kline K. RRR-a-tocopheryl succinate-induced apoptosis of human breast cancer cells involves Bax translocation to mitochondria. Cancer Res 2003; 63:2483-2491.
Yu W, Israel K, Liao QY, Aldaz M, Sanders BG, Kline K. Vitamin E succinate (VES) induces Fas sensitivity in human breast cancer cells: Role for Mr 43,000 Fas in VES-triggered apoptosis. Cancer Res 1999; 59:953-961. Israel K, Yu W, Sanders BG, Kline K. Vitamin E succinate induces apoptosis in human prostate cancer cells: Role of Fas in vitamin E succinate-triggered apop-tosis. Nutr Cancer 2000; 36:90-100.
Wu K, Li Y, Zhao Y, Shan YJ, Xia W, Yu WP, Zhao L. Roles of Fas signaling pathway in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells. World J Gastroenterol 2002; 8:982-986.
Wu K, Zhao L, Li Y, Shan YJ, Wu LJ. Effects of vitamin E succinate on the expression of Fas and PCNA proteins in human gastric carcinoma cells and its clinical significance. World J Gastroenterol 2004; 10:945-949.
Tomek S, Emri S, Krejcy K, Manegold C. Chemotherapy for malignant pleural mesothelioma: past results and recent developments. Br J Cancer 2003;
Dalen H, Neuzil J. a-Tocopheryl succinate sensitises T lymphoma cells to TRAIL killing by suppressing NF-kB activation. Br J Cancer 2003; 88:153-158. Neuzil J, Schröder A, von Hundelshausen P, Zernecke A, Weber T, Gellert N, Weber C. Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage. Biochemistry 2001; 40:4686-4692. Levkau B, Scatena M, Giachelli CM, Ross R, Raines EW. Apoptosis overrides survival signals through a caspase-mediated dominant-negative NF-kB loop. Nat Cell Biol 1999; 1:227-233.
Qian M, Kralova J, Yu W, Bose HR, Dvorak M, Sanders BG, Kline K. c-Jun involvement in vitamin E succinate induced apoptosis of reticuloendotheliosis virus transformed avian lymphoid cells. Oncogene 1997; 15:223-230. Zhao B, Yu W, Qian M, Simmons-Menchaca M, Brown P, Birrer MJ, Sanders BG, Kline K. Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells. Mol Carcinogen 1997; 19:180-190.
Yu W, Simmons-Menchaca M, You H, Brown P, Birrer MJ, Sanders BG, Kline K. RRR-a-tocopheryl succinate induction of prolonged activation of c-jun amino-terminal kinase and c-jun during induction of apoptosis in human MDA-MB-435 breast cancer cells. Mol Carcinogen 1998; 22:247-257.
Yu W, Liao QY, Hantash FM, Sanders BG, Kline K. Activation of extracellular signal-regulated kinase and c-Jun-NH2-terminal kinase but not p38 mitogen-acti-vated protein kinases is required for RRR-a-tocopheryl succinate-induced apoptosis of human breast cancer cells. Cancer Res 2001; 61:6569-6576. Wu K, Zhao Y, Li GC, Yu WP. c-Jun N-terminal kinase is required for vitamin E succinate-induced apoptosis in human gastric cancer cells. World J Gastroenterol 2004; 10:1110-1114.
You H, Yu W, Munoz-Medellin D, Brown PH, Sanders BG, Kline K. Role of extracellular signal-regulated kinase pathway in RRR-a-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Mol Carcinogen 2002; 33:228-236.
Turley JM, Funakoshi S, Ruscetti FW, Kasper J, Murphy WJ, Longo DL, Birch-enall-Roberts MC. Growth inhibition and apoptosis of RL human B lymphoma cells by vitamin E succinate and retinoic acid: role for transforming growth factor-ß. Cell Growth Differ 1995; 6:655-663.
- Yu W, Sanders BG, Kline K. RRR-a-tocopheryl succinate induction of DNA synthesis arrest of human MDA-MB-435 cells involves TGF-ß-independent activation of p21Waf1/CiP1. Nutr Cancer 2002; 43:227-236.
- Turley JM, Ruscetti FW, Kim SJ, Fu T, Gou FV, Birchenall-Roberts MC. Vitamin E succinate inhibits proliferation of BT-20 human breast cancer cells: increased binding of cyclin A negatively regulates E2F transactivation activity. Cancer Res 1997; 57:2668-2675.
- Ni J, Chen M, Zhang Y, Li R, Huang J, Yeh S. Vitamin E succinate inhibits human prostate cancer cell growth via modulating cell cycle regulatory machinery. Bio-chem Biophys Res Commun 2003; 300:357-363.
- Zhang M, Altuwaijri S, Yeh S. RRR-a-tocopheryl succinate inhibits human prostate cancer cell invasiveness. Oncogene 2004; 23:3080-3088.
- Zhang Y, Ni J, Messing EM, Chang E, Yang CR, Yeh S. Vitamin E succinate inhibits the function of androgen receptor and the expression of prostate-specific antigen in prostate cancer cells. Proc Natl Acad Sci USA 2002; 99:7408-7413.
- AllevaR, Benassi MS, Neuzil J, Tomasetti M, Gellert N, Borghi B, Procopio A, Picci P. a-Tocopheryl succinate controls cell growth and apoptosis of osteosarcoma cells by modulation of E2F1 independent of p53. Biochem Biophys Res Commun 2005; 331:1515-1521.
- Stapelberg M, Tomasetti M, Gellert, N, Alleva R, Procopio A, Neuzil J. a-Toco-pheryl succinate inhibits proliferation of mesothelioma cells by differential down-regulation of fibroblast growth factor receptors. Biochem Biophys Res Commun 2004; 318:636-641.
- Stapelberg M, Gellert N, Swettenham E, Tomasetti M, Witting KP, Procopio A, Neuzil J. a-Tocopheryl succinate inhibits malignant mesothelioma by disruption of the fibroblast growth factor autocrine signaling loop. J Biol Chem, in press.
- Don AS, Kisker O, Dilda P, Donoghue N, Zhao X, Decollogne S, Creighton B, Flynn E, Folkman J, Hogg PJ. A peptide trivalent arsenical inhibits tumor angio-genesis by perturbing mitochondrial function in angiogenic endothelial cells. Cancer Cell 2003; 3:497-509.
- Artwohl M, Roden M, Waldhausl W, Freudenthaler A, Baumgartner-Parzer SM. Free fatty acids trigger apoptosis and inhibit cell cycle progression in human vascular endothelial cells. FASEB J 2004; 18:146-148.
- Chen D, Walsh K, Wang J. Regulation of cdk2 activity in endothelial cells that are inhibited from growth by cell contact. Arterioscler Thromb Vasc Biol 2000; 20:629-635.
- Coqueret O. New roles for p21 and p27 cell-cycle inhibitors: a function for each cell compartment? Trends Cell Biol 2003; 13:65-70.
- Jiang Q, Elson-Schwab I, Courtemanche C, Ames BN. y-Tocopherol and its major metabolite, in contrast to alpha-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells. Proc Natl Acad Sci USA 2000; 97:11494-11499.
- Jiang Q, Ames BN. y-tocopherol, but not a-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats. FASEB J 2003; 17:816-822.
- Borel P, Pasquier B, Armand M, Tyssandier V, Grolier P, Alexandre-Gouabau MC, Andre M, Senft M, Peyrot J, Jaussan V, Lairon D, Azais-Braesco V. Processing of vitamin A and E in the human gastrointestinal tract. Am J Physiol 2001; 280:G95-G103.
Pussinen PJ, Lindner H, Glatter O, Reicher H, Kostner GM, Wintersperger A, Malle E, Sattler W. Lipoprotein-associated a-tocopheryl-succinate inhibits cell growth and induces apoptosis in human MCF-7 and HBL-100 breast cancer cells. Biochim Biophys Acta 2000; 1485:129-144.
Hrzenjak A, Reicher H, Wintersperger A, Steinecker-Frohnwieser B, Sedlmayr P, Schmidt H, Nakamura T, Malle E, Sattler W. Inhibition of lung carcinoma cell growth by high density lipoprotein-associated alpha-tocopheryl-succinate. Cell Mol Life Sci 2004; 61:1520-1531.
Kayden HJ, Traber MG. Absorption, lipoprotein transport, and regulation of plasma concentrations of vitamin E in humans. J Lipid Res 1993; 34:343-358. Traber MG, Ramakrishnan R, Kayden HJ. Human plasma vitamin E kinetics demonstrate rapid recycling of plasma RRR-a-tocopherol. Proc Natl Acad Sci USA 1994; 91:10005-10008.
Kaempf-Rotzoll DE, Traber MG, Arai H. Vitamin E and transfer proteins. Curr Opin Lipidol 2003; 14:249-254.
Neuzil J. a-Tocopheryl succinate epitomizes a compound with a shift in biological activity due to pro-vitamin-to-vitamin conversion. Biochem Biophys Res Commun 2002; 293:1309-1313.
Neuzil J, Massa H. Hepatic processing determines dual activity of vitamin E succinate. Biochem Biophys Res Commun 2005; 327:1024-1027. Brigelius-Flohe R, Kelly FJ, Salonen JT, Neuzil J, Zingg JM, Azzi A. The European perspective on vitamin E: current knowledge and future research. Am J Clin Nutr 2002; 76:703-716.
Neuzil J, Thomas SR, Stocker R. Requirement for, promotion, or inhibition by a-tocopherol of radical-induced initiation of plasma lipoprotein lipid peroxidation. Free Radical Biol Med 1997; 22:57-71.
Neuzil J, Kontush A, Weber C. Vitamin E in atherosclerosis: Linking the chemical, biological and clinical aspects of the disease. Atherosclerosis 2001; 157:257-283. Li-Weber M, Weigand MA, Giaisi M, Suss D, Treiber MK, Baumann S, Ritsou E, Breitkreutz R, Krammer PH. Vitamin E inhibits CD95 ligand expression and protects T cells from activation-induced cell death. J Clin Invest 2002; 110:681-690.
Li-Weber M, Giaisi M, Treiber MK, Krammer PH. Vitamin E inhibits IL-4 gene expression in peripheral blood T cells. Eur J Immunol 2002; 32:2401-2408. Kristal AR, Stanford JL, Cohen JH, Wicklund K, Patterson RE. Vitamin and mineral supplement use is associated with reduced risk of prostate cancer. Cancer Epidemiol Biomarkers Prev 1999; 8:887-892.
Jacobs EJ, Connell CJ, Patel AV, Chao A, Rodriguez C, Seymour J, McCullough ML, Calle EE, Thun MJ. Vitamin C and vitamin E supplement use and colorectal cancer mortality in a large American cancer society cohort. Cancer Epidemiol Biomarkers Prev 2000; 10:17-23.
Murtaugh MA, Ma KN, Benson J, Curtin K, Caan B, Slattery ML. Antioxidants, carotenoids, and risk of rectal cancer. Am J Epidemiol 2004; 159:32-41. Bidoli E, Bosetti C, La Vecchia C, Levi F, Parpinel M, Talamini R, Negri E, Maso LD, Franceschi S. Micronutrients and laryngeal cancer risk in Italy and Switzerland: a case-control study. Cancer Causes Control 2003; 14:477-484.
- Weiser H, Vecchi M, Schlachter M. Stereoisomers of a-tocopheryl acetate. IV. USP units and a-tocopherol equivalents of all-rac-, 2-ambo- and RRR-a-toco-pherol evaluated by simultaneous determination of resorption-gestation, myopathy and liver storage capacity in rats. Int J Vitamin Nutr Res 1986; 56:45-56.
- Leth T, Sondergaard H. Biological activity of vitamin E compounds and natural materials by the resorption-gestation test, and chemical determination of vitamin E activity in foods and feeds. J Nutr 1977; 107:2236-2243.
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Column: Muslims Lose Out In Campaign Rhetoric
I can imagine the shock that Obama opponents felt when they realized that many Americans are no longer afraid of putting a biracial man-and, in accordance to the enduring one-drop rule, a black man-into the White House. Desperate times call for desperate measures, and so I envision their brainstorming went something like this:
"What is the only thing scarier than a black man in office?"
To which someone responded, "A black man with an angry black wife."
That didn't work either.
So someone came to the conclusion that in a post 9/11 America-one with fear and prejudice resuscitated, at a time when the words Arab, Muslim and terrorist have become readily interchangeable-if the thought of a black man in the White House picking up that "3 a.m. phone call" isn't enough to send Americans into a shiver, then certainly a scary Arab-Muslim-terrorist is.
After recent criticism about going too negative, Sen. John McCain's campaign tried to switch gears and quiet disrespectful comments from supporters. At a recent McCain rally, supporters expressed their fear of an Obama presidency.
One woman said to McCain, "I can't trust Obama, I have read about him and he's not, he's not... he's an Arab."
McCain shook his head in disapproval and responded, "No ma'am. He's a decent family man, a citizen that I just happen to have disagreements with on fundamental issues, and that's what this campaign is all about. He's not, thank you."
Although McCain admirably denounced his supporter's racist remark and corrected false information, I take issue with the way in which "decent family man" and "citizen" were posed as being antithetical to being an Arab.... as if Arabs can never be decent family men or citizens.
Rumors of Obama's religious background have flooded the election and, despite one very outspoken reverend, Obama's opponents have made consistent efforts to not so subtly link him with Arabs, which mean Muslims, which mean terrorists.
The reference to Obama as Barack Hussein Obama by McCain supporters looks to tie the presidential candidate to the villainy of Saddam Hussein, a strategy that has proven ineffective. A last-minute attempt to connect Obama with William Ayers, which inevitably involved a lazy attempt to connect Ayers with radical Islamic terrorism, proved even less successful.
Back in February at a McCain event, when the Barack Hussein Obama reference was made, McCain quickly condemned it. But the stakes have changed, and in this month alone the reference has been made on several occasions. Obama opponents have continually tried to use Obama's multicultural background to characterize him as a Muslim and, in so doing, as an anti-Semite.
On the flip side, in response to accusations that Obama is Muslim, the Obama camp's defense has been to relentlessly dismiss such rumors by reminding Americans not to fear, as he is no unfriendly foreigner but rather a God-fearing Christian just like "the rest of us."
My disappointment with both sides lies in the fact that neither has halted the finger-pointing to call attention to the fact that the rumors concerning Obama's religion and ethnicity are inherently bigoted. Questions regarding Obama's cultural and ethnic background are rooted in xenophobia and hold the very same religious discrimination that both sides so vocally condemn of anti-Semites.
The FBI reported an overall 8 percent increase in hate crimes in 2006, but acknowledged that some groups, including Muslims, experienced an even greater increase. According to the reports there was a 22 percent increase in attacks on Muslims, which came to 156 hate crimes in 2006. Although political leaders havecondemned the hate crimes themselves, they have been either too willing to capitalize on post-9/11 fears for political gain or too quick to dismiss these fears. Despite politicians' claims to be on the side of the American people, I don't see either side standing up for their fellow citizens.
The statement that has been made loud and clear is: If you are Muslim or an Arab, don't even think about running for president. Matter of fact, don't even bother considering yourself an American.
At some point I so badly wanted Obama to halt all conversation and beg the question that I think needs to be asked: "So what if I was a Muslim?" Surely that would have been the death of his campaign, and that scares me.


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Ben King (Cannondale) won stage two of the 2016 Amgen Tour of California on Monday having survived from the day's escape group.
King and Evan Huffman (Rally Cycling) battled it out for the stage victory having both been part of the day's four-man break.
Alexander Kristoff (Katusha) brought the bunch home for third place, with stage one winner Peter Sagan (Tinkoff) in fourth.
Thanks to the time bonuses picked up during the stage and the winner's time bonus, King replaced Sagan as overall race leader. Huffman is second at eight seconds, with Sagan third at 14 seconds.
King was the main animator of the day's break, and he was joined by Huffman, Sindre Skjøstad Lunke (Giant-Alpecin) and William Barta (Axeon Hagens Berman).
On the second categorised climb of the day to Upper Big Tujunga, the break had stretched out their lead to over six minutes.
>>> Tour of California 2016: Latest news, reports and info
As the break navigated the final pair of category two climbs over Little Tujunga, Lunke was dropped. Barta had a mechanical issue but managed to catch back up with King and Huffman. With 24km to go, the gap was two and a half minutes.
Mark Cavendish (Dimension Data) and Bradley Wiggins (Team Wiggins) were among those dropped on the climbs.
Barta lost contact with King and Huffman on a draggy climb with 8.5km to go. At this point Direct Energie and BMC had the most riders at the front of the peloton, trying to make the catch.
Huffman and King continued to work well together and the gap was pushed out to a minute with two kilometres to go, with no chance of the peloton catching up with them.
It was left for the two leaders to fight it out for the victory. Despite tired legs from a day out front on hilly terrain, both put in a good sprint, with King just edging out Huffman.
Tuesday's stage three holds the first chance for the general classification contenders to really show their hand, with a significant ascent to the finish in Santa Barbara County.
The 2016 Amgen Tour of California concludes on Sunday, May 22.
>> Tour of California 2016: Stage by stage
Amgen Tour of California 2016, stage two: South Pasadena to Santa Clarita, 148km
1. Ben King (USA) Cannondale in 3-52-09
2. Evan Huffman (USA) Rally Cycling at same time
3. Alexander Kristoff (Nor) Katusha at 8 secs
4. Peter Sagan (Svk) Tinkoff
5. Niccolo Bonifazio (Ita) Trek-Segafredo
6. Danny van Poppel (Ned) Team Sky
7. Patrick Bevan (NZl) Cannondale
8. Nathan Haas (Aus) Dimension Data
9. Bryan Coquard (Fra) Direct Energie
10. Marco Canola (Ita) UnitedHealthcare at same time
24. Tao Geoghegan Hart (GBr) Axeon Hagens Berman at same time
130. Bradley Wiggins (GBr) Team Wiggins at 15-30
135. Mark Cavendish (GBr) Dimension Data at 15-30
General classification after stage two
1. Ben King (USA) Cannondale
2. Evan Huffman (USA) Rally Cycling at 8 secs
3. Peter Sagan (Svk) Tinkoff at 14 secs
4. Alexander Kristoff (Nor) Katusha at 20 secs
5. Daniel Eaton (USA) UnitedHealthcare at 21 secs
6. William Barta (USA) Axeon Hagens Berman at 21 secs
7. Sindre Skjøstad Lunke (Nor) Giant-Alpecin at 23 secs
8. Niccolo Bonifazio (Ita) Trek-Segafredo at 24 secs
9. Bryan Coquard (Fra) Direct Energie at 24 secs
10. Danny van Poppel (Ned) Team Sky at 24 secs
19. Tao Geoghegan Hart (GBr) Axeon Hagens Berman at 24 secs
128. Mark Cavendish (GBr) Dimension Data at 15-46
135. Bradley Wiggins (GBr) Team Wiggins at 15-46


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Essay american revolution
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