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What would the government have to do to convince you to get married when you otherwise wouldn't? More than pay you $80 a month, I'll bet, the amount Wisconsin's much-ballyhooed "Bridefare" pilot program offered unwed teen welfare mothers beginning in the early nineties, which is perhaps why then-Governor Tommy Thompson, now Health and Human Services Secretary, was uninterested in having it properly evaluated and why you don't hear much about Bridefare today. OK, how about $100 a month? That's what West Virginia is currently offering to add to a couple's welfare benefits if they wed. But even though the state has simultaneously cut by 25 percent the checks of recipients living with adults to whom they are not married (including, in some cases, their own grown children, if you can believe that!), results have been modest: Only around 1,600 couples have applied for the bonus and presumably some of these would have married anyway. With the state's welfare budget expected to show a $90 million shortfall by 2003, the marriage bonus is likely to be quietly abolished.
Although welfare reform was sold to the public as promoting work, the Personal Responsibility and Work Opportunity Reconciliation Act of l996 actually opens with the declaration that "marriage is the foundation of a successful society." According to Charles Murray, Robert Rector and other right-wing ideologues, welfare enabled poor women to rely on the state instead of husbands; forcing them off the dole and into the rigors of low-wage employment would push them into marriage, restore "the family" and lift children out of poverty. That was always a silly idea. For one thing, as any single woman could have told them, it wrongly assumed that whether a woman married was only up to her; for another, it has been well documented that the men available to poor women are also poor and often (like the women) have other problems as well: In one study, 30 percent of poor single fathers were unemployed in the week before the survey and almost 40 percent had been incarcerated; drugs, drink, violence, poor health and bad attitudes were not uncommon. Would Murray want his daughter to marry a guy with even one of those strikes against him? Not surprisingly, there has been no upsurge of marriage among former welfare recipients since 1996. Of all births, the proportion that are to unwed mothers has stayed roughly where it was, at 33 percent.
Since the stick of work and the carrot of cash have both proved ineffective in herding women to the altar, family values conservatives are calling for more lectures. Marriage promotion will be a hot item when welfare reform comes up for reauthorization later this year. At the federal level conservatives are calling for 10 percent of all TANF money to be set aside for promoting marriage; Utah, Arizona and Oklahoma have already raided TANF to fund such ventures as a "healthy marriage" handbook for couples seeking a marriage license. And it's not just Republicans: Senator Joe Lieberman and Representative Ben Cardin, the ranking Democrat on the House Ways and Means Committee, are also interested in funding "family formation." In place of cash bonuses to individuals, which at least put money in the pockets of poor people, look for massive funding of faith-based marriage preparation courses (and never you mind that pesky separation of church and state), for fatherhood intervention programs, classes to instruct poor single moms in the benefits of marriage (as if they didn't know!), for self-help groups like Marriage Savers, abstinence education for kids and grownups alike and, of course, ingenious pilot projects by the dozen. There's even been a proposal to endow pro-marriage professorships at state universities--and don't forget millions of dollars for evaluation, follow-up, filing and forgetting.
There's nothing wrong with programs that aim to raise people's marital IQ--I love that journalistic evergreen about the engaged couple who take a quiz in order to qualify for a church wedding and call it off when they discover he wants seven kids and she wants to live in a tree. But remember when it was conservatives who argued against social engineering and micromanaging people's private lives and "throwing money at the problem"?
Domestic violence experts have warned that poor women may find themselves pushed into marrying their abusers and staying with them--in a disturbing bit of Senate testimony, Mike McManus of Marriage Savers said domestic violence could usually be overcome with faith-based help. Is that the message women in danger should be getting? But there are even larger issues: Marriage is a deeply personal, intimate matter, involving our most private, barely articulated selves. Why should the government try to maneuver reluctant women into dubious choices just because they are poor? Even as a meal ticket wedlock is no panacea--that marriage is a cure for poverty is only true if you marry someone who isn't poor, who will share his income with you and your children, who won't divorce you later and leave you worse off than ever. The relation between poverty and marriage is virtually the opposite of what pro-marriage ideologues claim: It isn't that getting married gives feckless poor people middle-class values and stability, it's that stable middle-class people are the ones who can "afford" to be married. However marriage functioned a half-century ago, today it is a class marker. Instead of marketing marriage as a poverty program, how much better to invest in poor women--and poor men--as human beings in their own right: with education, training for high-paying jobs, housing, mental health services, really good childcare for their kids. Every TANF dollar spent on marital propaganda means a dollar less for programs that really help people.
The very fact that welfare reformers are reduced to bribing, cajoling and guilt-tripping people into marriage should tell us something. Or have they just not hit on the right incentive? As a divorced single mother, I've given some thought to what it would take for me to marry against my own inclination in order to make America great again. Here's my offer: If the government brings Otis Redding back to life and books him to sing at my wedding, I will marry the Devil himself. And if the Devil is unavailable, my ex-husband says he's ready.
If you believe President Bush, Kenneth Lay--one of his top financial backers and his "good friend"--was merely an equal-opportunity corrupter of our political system, buying off Democrats and Rep
The new education law is a victory for Bush--and for his corporate allies.
Sure, he's a cartoon character, but it still takes courage to speak out.
Drug companies influence research; they also affect what gets published.
"Former Yankee virtues, common sense, scepticism if not suspicion of authority, a belief in the mastery of the future, have been driven underground.
Read Senator Joe Lieberman's letter to ACTA.
Read comments from other new members of Tattletales for an Open Society.
Read Eric Scigliano's Naming-and un-naming-Names.
UPDATE, January 14
On August 21 in Lake Charles, Louisiana, a struggling oil-refinery town on the Texas border, Wilbert Rideau walked to the center of the modern courtroom, hobbled by shackles. The man Life magazine called "the most rehabilitated man in America" lifted up his furrowed brow and looked at the judge. And stillness came over the crowd of mostly elderly blacks, as Rideau pleaded not guilty to a murder committed forty years ago.
Interest in the case lies not in Rideau's innocence or guilt. On numerous occasions he has accepted responsibility for murdering a woman after robbing a bank in 1961. Rideau, 59, received the death penalty, but by an accident of history, lived to become a famous journalist. As editor of a prison magazine called The Angolite, he has won almost every journalistic award and become a national expert on prison life; he's been "Person of the Week" on World News Tonight with Peter Jennings and a pundit on Nightline--all from behind prison bars in Angola, Louisiana. In 1994 Rideau's lawyers, in a last-ditch effort to free him, filed a habeas corpus petition in federal court. In December 2000 the Fifth Circuit Court of Appeals in New Orleans found that the original prosecutor of the case had excluded blacks from the grand jury in blatant violation of the Constitution, and ruled that the state must retry Rideau or release him.
This year Rideau is set to stand trial in the same Louisiana town where he was first convicted forty years ago. Many thought that Lake Charles and Calcasieu Parish would look the other way rather than reprosecute an age-old case with lost evidence and a manifestly rehabilitated defendant. Rideau's lawyers have said he would settle by pleading guilty to manslaughter and walk away with more time served than all but four convicted murderers in Louisiana history. But the state won't offer any deal.
The reason can be found in Lake Charles, a town where redemption may not be possible when a black man kills a white woman. Powerful people in the parish have blocked Rideau's release, whereas other inmates sentenced for similar crimes have received parole. During Rideau's time in Louisiana State Penitentiary in Angola, nearly 700 convicted murderers have been freed. Four pardon boards have recommended Rideau for release--but two governors have denied clemency. "Why Not Wilbert Rideau?" was the title of a 20/20 segment exploring why he has not been able to get parole. "I think he is a con artist," said District Attorney Rick Bryant. "He's a master manipulator of the media and people who have supported him."
The vehemence stems in part from the fact that Rideau is a prosecutor's nightmare. This is the fourth time the parish has tried him. Each time Rideau is convicted, he appeals and exposes shameful structural flaws in how the justice system here really works. And he's doing it again. This past November 29 the Louisiana Supreme Court struck down the parish's process for selecting judges in capital cases, which the court faulted for allowing judge-picking, a practice used by prosecutors to obtain judges favorable to the state. The prosecution had filed its new case against Rideau when the only ball left in the bingolike hopper was the one for Michael Canaday, a white judge who had never before tried a felony. After watching Judge Canaday in court, Marjorie Ross, 68, a retired department store salesperson, said, "I look back forty years ago and things haven't changed. It's because of this." She pointed to her dark-skinned face.
But the new judge, selected "at random" with all seven balls in the hopper, happens to be one Wilford Carter, who is black and was elected from a black district with many voters fixated on this case. It's a boon that has become Rideau's signature--the grace of luck appears just when it seems to have run out. "The fact that I excelled beyond anybody's wildest expectations not only vindicated official decisions but increased the hostility of my enemies," Rideau said in a series of telephone interviews. "Everything I became, everything I have achieved, has been in spite of this unholy force from Lake Charles dedicated to destroying me and denying me the ability to be anything more than the criminal they wanted me to be."
His crime has been hard for the town to forget. According to the original prosecutor, Frank Salter, on February 16, 1961, Wilbert Rideau, then 19, knocked on the door of the Gulf National Bank at closing time. Bank manager Jay Hickman unlocked the door. He knew Rideau as the errand runner at Halperin's, the sewing shop next door, who would fetch sodas for bank employees, until the relationship became too friendly for the whites. "We stopped [asking him for sodas] because he started talking," said victim Dora McCain in her trial testimony, "calling us by our first names. So we just--we just got a refrigerator for the bank." That day, Rideau produced a gun and demanded that Hickman empty the money drawer. Rideau put $14,000 in a gray suitcase (leaving $30,000 on the floor and in coffers) and forced Hickman and two women bank tellers into a car. They drove to a country road in a wooded area, where Rideau lined up his three hostages and began firing. One bullet landed in Jay Hickman's arm. Hickman rolled off into a bayou out of sight. The two women fell to the ground with gunshot wounds. Julia Ferguson, 49, cried out, "Think of my poor old daddy," who lived with her. "Don't worry, it will be quick and cool," Rideau allegedly said before slitting her throat and stabbing her in the heart. Ferguson died at the scene. Rideau approached the other teller, Dora McCain, a pretty twentysomething with a well-known family, who lay face down. He kicked her in the side three times to see if she was dead. When she didn't cry out, Rideau took the car and left. Two state troopers stopped Rideau in his car as he was leaving town. They found the suitcase with the money in the back seat. (Rideau's counsel declined to comment on the facts before trial.)
That year, the first of three all-white, all-male juries convicted Rideau and sentenced him to death. Rideau appealed on grounds that a TV station, KPLC-TV, had secretly filmed the sheriff posing questions to Rideau, who had no access to a lawyer, and aired his mumbled answers as a confession. The US Supreme Court slammed the parish's "kangaroo court proceedings" and found that the broadcast had unfairly prejudiced the jury pool. The Court reversed the conviction and said Rideau could not be tried anywhere within the reach of KPLC. In 1964 at a second trial, in Baton Rouge, the jury deliberated for fifteen minutes before deciding to give him the electric chair. Rideau appealed again, and a federal court overturned his conviction on grounds that the state court had rejected jurors with doubts about the death penalty, in effect stacking the jury with death penalty proponents--a violation of due process. In 1970 at a third trial, in Baton Rouge, the jury took eight minutes to give Rideau the death penalty. His appeals were unsuccessful, and he returned to death row--just in time to benefit from Furman v. Georgia, the 1972 Supreme Court decision that temporarily found the death penalty unconstitutional. As a result, every death-row inmate in America, including Rideau, had his death sentence commuted to life imprisonment.
Rideau won't comment on the crime because he is facing a new trial. But he agreed to talk about the person he was at the time and how he has changed. Though he usually speaks quickly, in perfect sentences, his cadence is deliberate in describing the man he was when he entered prison. "I wouldn't recognize him today," he said. "I was typical in a lot of ways. I was another dumb black, immature, angry. Not even aware that there is a world bigger than me." He says he had a fairly normal childhood, moving to Lake Charles when he was 6. "My home life wasn't the best," Rideau says. "But that doesn't say much because a lot of people's family lives weren't." His problems, he says, began during adolescence. "People used to pass by and they would throw Coke bottles and spit and holler at you," he says. "You could be walking by with your girl and they would call at you talking about you--'Hey nigger, blah blah blah, whatever.'" Rideau knew it wasn't directed at him alone. But he took it as "the end of the world." "I saw whites as enemies responsible for everything wrong with my world. Whites created this bizarre segregated world where racism ruled," he says. In his segregated school, he dismissed the hand-me-down books from white schools, which held forth ideas of "rights" and "how life was so wonderful." Though he had a straight-A average, he quit school in the eighth grade because he saw no use for an education. "I wanted to be a spaceman like Flash Gordon," he says. At 13, he began a series of low-paying jobs and spent most of his time in pool halls and gin joints. "I didn't even know the name of the governor of the state," he said. "I was totally out of it."
Eventually, he became an errand runner in the fabric shop, his last job before being sent to Angola. In prison, he noticed the strange ethics of prison life, starting with white guards who smuggled him novels and science texts. "I read a library on death row," he says. And in a Baton Rouge jail, where he stayed for part of his appeals, Rideau lived in the segregated white section as punishment for leading a "strike" in protest against prison conditions--flooding the commodes and burning mattresses. When Rideau led white prisoners in a strike as well, the prison put him in solitary confinement. And to Rideau's shock, whites began secretly sending him food and kind words. "Whites started taking care of me," he said.
Within the first year of his life sentence, Rideau asked to join the then-all-white newspaper, the Angolite, only to have administrative officials turn him down. "I read in the paper that they couldn't find a black who could write," he says. The rejection stung. Over the past decade, he had penned a book-length analysis of criminality and corresponded with a young editor at a New York publishing house, who tutored him in the art of writing. Rideau rounded up an all-black staff and started The Lifer, which chronicled stories like that of a group of elderly women who brought a truckload of toilet paper to the prison and were turned away. Eventually, the administration put him out of business. "They threw me in the dungeon saying I was advocating insurrection," he says. White prisoners petitioned a black senator to demand Rideau's release from solitary confinement. "Along the way, the whites that I initially saw as enemies befriended me and fought for me, not blacks," he says. "That experience caused hell with the way I saw things."
In 1975, the warden made Rideau editor of the Angolite as part of compliance with a federal court order mandating integration of the segregated Angola prison. A year later a new warden, C. Paul Phelps, arrived and offered to strike a deal. Phelps promised that the Angolite would operate under the same standards that applied to journalists in the free world--he could print whatever he could prove--so long as Rideau would teach him about life at Angola. Over the years, the two men had many philosophical and political discussions. And they ate together in the dining hall. "He told me that like begets like," Rideau says. Phelps permitted Rideau to become a public speaker, a reward for well-behaved prisoners to travel and explain the dangers of prison life to youth at risk. And with his new freedom, Rideau jettisoned a longtime plan to escape. "The thing that is most respected in prison is character, loyalty, keeping your word," says Rideau. "These are things that are highly valued in the real world, but they are really, really valued in ours." This and the passage of time have changed him. "Part of it is just growing up," he says. And growing up has meant a realization that he may die in prison. Since 1997 Rideau has been president of the Angola Human Relations Club, which cares for elderly inmates by providing such essentials as toiletries, warm caps and gloves, and which buries the dead.
After Rideau became editor of the Angolite, the paper changed from a mimeographed newsletter into a glossy magazine exposing systemic problems and an emotional inner life. One story revealed that the Department of Corrections had doled out money for AIDS programs that were never implemented. Another issue featured pictures of inmates after electrocution--a portrait so horrifying that Louisiana changed its method to lethal injection. The magazine has won seven nominations for a National Magazine Award, and Rideau has won the Robert F. Kennedy Journalism Award, the George Polk Award and an Academy Award nomination for The Farm, a documentary film about Angola that he co-directed. He co-edited a book, Life Sentences (Random House). He addressed the convention of the American Society of Newspaper Editors in 1989 and 1990. And he's a correspondent for National Public Radio's Fresh Air program. While Lake Charles watched, the man many faulted with ushering in an era of crime became a nationally respected writer and commentator. "There's no way you're going to give life back where it's been taken," Rideau opined on Nightline in 1990. "But you--you just try to make up.... When it's all over and done with, Wilbert Rideau will have tried."
One blistering August afternoon in Lake Charles, I locked my keys in my rental car and called "Pop-A-Lock" for help. As owner Jim Rawley jimmied the lock, he recalled the night Rideau committed the crime. Rawley was in high school then. His friends wanted to kill Rideau and mobbed the courthouse. "There was a group of vigilantes among us," he says. "I can't remember the specifics. But I remember the atmosphere. Macho kind of stuff, except that we were scared too." Years later, Rawley became a Calcasieu Parish deputy and knew Rideau, who was awaiting trial in the Lake Charles jail, as "a troublemaker." Once, he says, a friend and fellow officer "beat the hell out of [Rideau]" for being "belligerent and uncooperative." When asked if he thought Rideau had changed, he said, "By all appearances he has rehabilitated himself, for lack of a better word. He seems to be a different man than he used to be. But that doesn't negate what he did.... It doesn't change the fact that he was convicted three times. He has never claimed that he didn't commit the crimes. He is fortunate he didn't receive the death penalty." He also said Rideau is a burden to the courts and should stop appealing his case. "If he's a different person he needs to go through the pardon board," he argued. But everyone knows that governors have blocked his release. Rawley shrugs, "It's already been decided, then."
Rawley's reaction was typical of whites I met. Rideau's good actions matter little next to the fact that he escaped the death penalty, as if death had somehow been cheated. And one has to wonder if there isn't some jealousy of his fame in the world outside Lake Charles. Elliott Currie, a professor of criminology at the University of California, Berkeley, calls the unceasing and vindictive punishment of those who have committed bad acts, without regard for the genuineness of their remorse or rehabilitation, "punitive individualism." Law-abiding people don't want prisoners to have anything they can't have--thus the 1994 elimination of Pell Grants (federal educational scholarships) for prisoners and the conflicts over whether taxpayers should pay for weightlifting equipment for prisoners. Rideau represents the extreme of this line of thinking: Most of us are never going to get to be on Nightline. Why does this murderer get to do it? Many white observers view the legal mistakes in his case as technicalities, and his appeals a waste of taxpayer money. After the arraignment, a blue-blazered security guard grabbed my hand very tightly and muttered, "If I killed your grandmother could you rehabilitate her?"
And the more well-known a defendant, the more the public focuses on preventing release. In this sense, Rideau is not unlike famous white prisoners who can't get a break despite impeccable prison records--like Kathy Boudin, the former Weather Underground radical, denied parole last August for a 1981 murder conviction; or Karla Faye Tucker, a convicted murderer executed in 1998, even after the victim's brother begged Texas Governor George W. Bush to pardon her. Their violent offenses do not elicit leniency. "It's not that people are afraid he is going to do it to her again," says Currie. "They are saying, 'Anybody who does this can't be free again; in our moral universe that can't happen.'" This attitude pervades public policy. Federal laws passed in 1994 provide matching funds to states to keep violent criminals in prison longer by denying parole.
But perhaps the biggest strike against Rideau is his race: No black man convicted of murdering a white person in Lake Charles has ever been released from prison, according to The Rideau Project, a research effort at Loyola University in New Orleans (see www.wilbertrideau.com). Whether or not people were alive at the time of the crime, feelings seem to be as strong as they were forty years ago. A 33-year-old white saleswoman at an electronics store, who asked not to be identified, said, "He should die the same death like everyone else," adding that she had to put her kids in private schools because of the "kids who cause trouble." She then mouthed the word "blacks." Her co-worker, a 30-year-old white man, used lynching imagery to say he agreed: "They should have swung him a long time ago." But then he asked, "What did he do?"
This is what gives District Attorney Rick Bryant his mandate. He's up for re-election in November, which means trying Rideau during campaign fundraising season. In two conversations, one at his desk and a second in a downtown bar, he said that even if Rideau were rehabilitated (and he wouldn't admit this), he would reprosecute. "He did the crime, didn't he?" Bryant refuses to recognize his own prosecutorial discretion, implying that he actually doesn't have the power to decide not to prosecute. This may be true, but only in the sense that his political survival in this majority-white town depends on a conviction. "They are trying to make me into a glorified pardon board. I am not a pardon board. I am a DA. Like I should be God of this case! Like I don't care! Or that I should decide he's a good guy in prison! That is not my job. The only reason I would not retry him is if there is no evidence, he's innocent or the victims want his release," he says. I suggest that his job is to seek justice, not just to convict, and that a retrial can only divide the town. "They line up and tell me to keep him in prison," Bryant says.
Of course, there are those--mostly black and some influential whites--lining up on the other side, too. Cliff Newman, an attorney and Democratic state senator from 1980 to 1988, once lobbied the governor to keep Rideau in prison at the behest of Dora McCain, the only victim who is still alive today. In the following years, Newman met Rideau in Angola at the prison rodeo and followed his story in the media. Today Newman has changed his mind: "From a political point of view it is not popular to ever say a murderer should be released. But I am not in politics anymore. And I am not going to be. Everyone is capable of rehabilitation."
Even conservative whites are hard pressed to argue that Rideau is not a different man today. Bill Shearman, owner of the town's conservative weekly newspaper, said, "Well, yeah, I think Rideau is rehabilitated," explaining that his view isn't representative. "Only a scant minority realized he has changed." Jim Beam, 68, a columnist of the American Press, the conservative daily that has opposed Rideau's freedom, admitted, "If you asked me if he's rehabilitated I would say yes." And Peggi Gresham, retired assistant warden and Angolite supervisor for twelve years, said, "I am not a bleeding-heart liberal. I don't think that everybody should get out. But when a person is as successful as some individuals are they can get out and have a good life. Wilbert is one of those people."
Young black professionals I met generally thought Rideau should be released because he has changed but see his plight as a remnant of past prejudice that doesn't really concern them. Rideau's real support in Lake Charles has come from the local NAACP and black press who believe that Rideau didn't commit the crime alone and is part of a larger conspiracy. "Blacks don't rob banks and they don't commit suicide," says Lawrence Morrow, publisher and editor of the black magazine Gumbeaux. Rideau had a good job, they argue, at a time when it was difficult for blacks to find jobs, and he took only $14,000, leaving $30,000 in the bank. Joshua Castille, 73, a retired black law enforcement officer, had drinks with Rideau the night before the crime and saw no peculiar behavior. He believes Rideau acted in concert with bank manager Hickman. Even back then, he said, a bank would never open its doors after closing hours. For a black person? "For anyone," he says. "They just wouldn't do it." The contrasting perceptions of the Rideau case among blacks and whites is emblematic of the different ways the two groups view crime, as well as issues like the death penalty. "Blacks are more likely to understand that people like Rideau are less likely to have committed the crime because they are monsters than because of circumstances that put them in that situation-- 'there but for their fortune go I,'" says Currie. "And they know that the criminal justice system has been pushed toward punishing blacks more than whites for as long as the justice system has existed."
Rideau's trial could go either way. On the one hand, Lake Charles elects its judges and Judge Carter is accountable to a black constituency that cares about this case enormously, which could mean openness to arguments about prosecutorial vindictiveness. On the other hand, when Carter's son, then 16, was charged with second-degree murder, he received a plea deal from Bryant reducing the charge to manslaughter--which, critics say, could predispose the judge to be friendly to the prosecution. And while, after so many years of appeals, the evidence is mostly lost, Dora McCain's lawyer, Frank Salter, the original prosecutor, said she would testify, which could mean a conviction based on her testimony alone (McCain did not respond to interview requests). Rideau's lawyer is the formidable George Kendall of the NAACP Legal Defense & Educational Fund, but it isn't yet clear how Judge Carter feels about counsel who swoops in from New York.
Rideau says if he does get out, he wants to leave Louisiana and write two books. "And neither one of them is about me," he says, explaining that he hopes to redefine criminality. "But I am telling you they are going to give me the Pulitzer Prize for this." It's hardly what Lake Charles wants to hear. When does he believe punishment should stop? "Whatever it should be, it should be," he says. "But it should be equal."
Last spring Richard Pollak asked in these pages, "Is GE Mightier Than the Hudson?" (May 28, 2001). Given the Environmental Protection Agency's December 4 decision to dredge the PCB-contaminated river, it is tempting to ring in the new year with a resounding No. Despite the company's multimillion-dollar blitz of lawyering, lobbying and PR, the Bush Administration, in the person of its EPA Administrator, Christine Todd Whitman, has come down squarely on the side of those in New York's historic Hudson River Valley who have been agitating for years to make GE clean up the lethal mess it created by dumping more than a million pounds of polychlorinated biphenyls in the river from the 1940s into the 1970s. This pollution has turned 200 miles of the Hudson, from just above Albany south to New York Harbor, into the biggest Superfund site in the nation; EPA law requires that GE pay the cost of removing the toxic chemicals, which the agency estimates at $460 million. More than once, the company has told its stockholders it can well afford this sum, as a multinational with a market value of some $500 billion surely can.
Still, it may be premature to pop the champagne corks. This past fall, fearing that Whitman might follow the lead of her Clinton Administration predecessor, Carol Browner, and endorse the cleanup, GE filed a federal suit attacking as unconstitutional a Superfund provision that allows the EPA, if the company refuses to dredge, to do the job itself and bill GE for three times the final cost plus penalties of $27,500 a day. GE has plenty of time (and cash) to pursue this and other maneuvers against dredging, which is needed to remove some 150,000 pounds of PCBs still in the Hudson. The EPA estimates it will take at least three years to work out the project's engineering and other details--e.g., what kind of equipment is needed, how much stirred-up sediment is acceptable and what landfills can safely handle the contaminated mud. Many residents along the banks of the river are divided--sometimes angrily--on these and several other issues. During the EPA's 127-day comment period in 2001 it received about thirty-eight boxes of letters and 35,000 e-mails, many spurred by GE's scare campaign--on billboards, in newspaper ads and on TV infomercials--warning that dredging will destroy the river.
The EPA has pledged that the public will have even more of a voice in the project's design decisions over the coming months--a welcome process but one that GE is likely to exploit with more propaganda. At its enviro-friendly-sounding website (hudsonwatch.com), for example, the company continues to insist, on no hard evidence, that the citizens of the Hudson River Valley oppose dredging "overwhelmingly." Some residents do resist dredging and the inevitable inconvenience it will bring to their communities, and not all have arrived at their view because of GE's PR tactics. But after almost two decades of review by the EPA, the burden of scientific evidence shows that the remaining PCBs, which cause cancer in laboratory animals and probably in humans, continue to poison the river a quarter-century after their use was banned and GE stopped dumping them.
The EPA's December 4 order could be the precedent that requires the company to clean up forty other sites where it has dumped PCBs. This would cost several billion dollars, a hit not so easy to reassure shareholders about. Even with GE master-builder Jack Welch retired and busy flogging his bestselling How-I-Did-It book, don't look for the company to roll over anytime soon.


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I would like to publish a book regarding a research and subsequent discovery. The book will be about numerical sequences and matrices. These 'simple' numbers I have then found to be the 'template' for all ancient civilizations, from the dimensions of the Great Pyramid to the layout of the Sri Yantra, to references to Stonehenge etc but also referred to in the Bible, the Vedas etc.
Subsequently I have linked this mathematical structure or laws to find a perfect match so to speak with empirical published data on the Genetic Code. From there it shows why we have only 20 amino acids out of the 64 bases (this is evidence not proof). Also it 'explains' why we have the 'octet rule' in chemistry.
Part of this discovery is also the finding that even the Prime Numbers become 'organized' and they are not just randomly distributed in the infinite series of numbers and from the same table I can show how the 360 degrees of a circle may just not be a 'human construct' as it is believed today but...
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Perturbations in the composition and assembly of extracellular matrices (ECMs) contribute to progression of numerous diseases, including cancers. Anchoring of laminins at the cell surface enables assembly and signaling of many ECMs, but the possible contributions of altered laminin anchoring to cancer progression remain undetermined. In this study, we investigated the prominence and origins of defective laminin anchoring in cancer cells and its association with cancer subtypes and clinical outcomes. We found loss of laminin anchoring to be widespread in cancer cells. Perturbation of laminin anchoring originated from several distinct defects which all led to dysfunctional glycosylation of the ECM receptor dystroglycan. In aggressive breast and brain cancers, defective laminin anchoring was often due to suppressed expression of the glycosyltransferase LARGE. Reduced expression of LARGE characterized a broad array of human tumors where it was associated with aggressive cancer subtypes and poor clinical outcomes. Notably, this defect robustly predicted poor survival in patients with brain cancers. Restoring LARGE expression repaired anchoring of exogenous and endogenous laminin and modulated cell proliferation and tumor growth. Together, our findings suggest that defects in laminin anchoring occur commonly in cancer cells, are characteristic of aggressive cancer subtypes, and are important drivers of disease progression.
The heterogeneity of cancers is evident by a growing list of genetic and epigenetic changes that perturb cell regulatory networks. Among these changes are regulatory defects that alter the interaction of cells with their microenvironment, leading to a loss of normal tissue architecture, invasion of surrounding tissues, and metastasis (1). Extracellular matrices (ECMs) are prominent and influential components of the cellular microenvironment in both normal and cancerous tissues, and changes in the expression, deposition, cross-linking, and degradation of ECM components have been clearly implicated in the progression of cancers (2–6).
Normal cell-ECM communications are modulated not only by the presence of ECM ligands and receptors, but also by the higher order assembly of ECM components into multimeric complexes. Many widely expressed ECM molecules, including fibronectins, collagens, fibrillins, and laminins are assembled into polymers. These assembly processes modulate the architecture of the matrices, and their biophysical and signaling properties, with direct consequences on cell function and tissue organization (7, 8). Therefore, changes in the ordered assembly of ECM molecules have the potential to strongly modulate cancer cell behavior.
Assembly of laminin isoforms into polymeric arrays across cell surfaces is believed to initiate the higher order organization of basement membranes (BMs), with resulting impact on BM integrity and signaling functions (7, 9). This assembly takes place via interactions of the laminin side arms, and is receptor-facilitated wherein anchoring of the laminin's C-terminal domains to the cell surface initiates polymerization (10). Multiple laminin receptors have been implicated in this process of receptor-facilitated assembly including the integrins, dystroglycan and sulfatides (10–14). Cues from laminins modulate several cellular homeostatic functions in normal cells which are often found deregulated in carcinomas, including cell proliferation, adhesion, migration, differentiation, cell polarity, responsiveness to soluble factors and angiogenesis (15–18). In functionally normal epithelial cells, loss of laminin anchoring alone leads to loss of cell polarity signals and tissue-specific gene expression (13). Laminins have also been proposed to regulate resistance of cancer cells to therapeutic agents and apoptotic stimuli (19, 20). The effect of laminins on these many cell functions underscores the potential influence of deregulated laminin anchoring and assembly on cancer progression, from the growth and invasion of cancers to therapeutic responsiveness.
In this study, we investigate the prevalence of defective laminin anchoring, and the underlying causes, in cancer cells of distinct subtypes and tissue origins. We report that defective laminin anchoring is a prominent phenotype of cancer cells, caused by multiple distinct mechanisms. The most common of these defects is identified as reduced expression of the glycosyltransferase like-acetylglucosaminyltransferase (LARGE). Loss of LARGE expression is found to be a surrogate marker for the loss of laminin anchoring, and leads to enhanced cell proliferation and tumor growth. Reduced expression of LARGE is evident in diverse human cancers and associated with more aggressive tumor subtypes and decreased patient survival. These results reveal that inability to anchor laminin is a prevalent malignant phenotype, is associated with poor clinical outcomes, and is a potential target for the modulation of aggressive cancer cell behavior.
Standard molecular biology methods were used (as detailed in supplementary information). Briefly, LARGE and β3-N-acetylglucosaminyltransferase-1 (β3GnT1), were cloned into the retroviral vector pBMN-IRES-PURO or adenoviral pShuttle vector (provided by Dr G. Inesi, CPMCRI, San Francisco) for generation of pAdeasy-LARGE which was transfected into HEK 293 cells. Viral particles were plaque-purified, amplified and further purified by CsCl density-gradient. Retroviral infections were achieved as previously described (13).
All cancer cell lines used in this study were obtained from the American Type Culture Collection or from collections developed in the laboratories of Drs. Steve Ethier and Adi Gazdar, and have been carefully controlled for quality and identity as previously described (21). Primary normal human breast cells were obtained as a generous gift from Dr. Martha Strampfer (LBNL, Berkeley, California). The generation of immortalized floxed DG mouse mammary epithelial cells (Floxed-DG), knockout of DG (DG−/−) and re-expression of DG (DG+) or vector control has been previously described (13). The same method was used to generate the immortalized floxed-β1 integrin and β1 integrin knockout (β1−/−) mouse mammary epithelial cells.
Laminin labeling, laminin assembly, immunofluorescence and biochemical assays were performed as previously described (13) and detailed in supplementary information. For surface labeling, samples were directly stained with primary antibody in growth media at 4 °C for 90 min prior to fixation and permeabilization.
MTT Cell Proliferation Assay was used according to manufacturer's protocol (ATCC). Percent increase in cells proliferation was calculated by the formula (dx-d1/d1) X 100. Data obtained from MTT assay was confirmed by counting cells seeded on 6 well plates.
Cell cycle assessment was performed by flow cytometry. Briefly, cells were labeled with 10 μM Bromodeoxyuridine (BrdU), fixed in 70% ethanol and stained with an anti-BrdU antibody, FITC-conjugated secondary, counterstained with propidium iodide (PI) and analyzed by FACScan. Treatments with laminin fragments E1 and E4 were done 24 hrs prior to labeling with BrdU at 40 μg/ml and 20 μg/ml, respectively.
One million cells were injected into mammary fat pad of 6–8 weeks old female Balb/c nu/nu mice (Harlan). Tumor size was evaluated every other day and tumor volume was calculated using the formula Length X Width2/2 and graphed (7 mice per group).
LARGE expression in primary tumor versus normal tissue was compared using data deposited on Oncomine™; website (www.oncomine.com). Normalized mean gene expression levels for LARGE (Affymetrix 215543_s_at) in 36 human glioblastoma samples were obtained from a previous study (42). Kaplan-Meier survival plots for 343 glioma samples were obtained from data deposited in the Repository of Molecular Brain Neoplasia Data (Rembrandt), National Cancer Institute (2005), accessed July 21, 2011 (http://rembrandt.nci.nih.gov).
Whole transcriptome shotgun sequencing (RNA-seq) was performed on the Illumina GAII system using standard protocols as previously described (27) and analysis was performed with the ALEXA-seq software package (22). An average of 74.8 million (76bp paired-end) reads passed quality control per sample. Subtype specific expression was determined by Wilcoxon signed-rank test. Genes were considered differentially expressed if they displayed fold-change greater than 2 and had a p-value less than 0.05 after multiple testing corrections by Benjamini-Hochberg method. The MD Anderson (GSE25066A) dataset of breast cancers was screened to verify subtype-specific expression of LARGE in tumors based on subtypes assigned by Hatzis and colleagues (23). Analysis of the TCGA dataset appears in the Supplementary Materials.
We assessed the capacity of cancer cells to anchor and assemble laminins at the cell surface, focusing first on breast cancer cells as a model system. To accomplish this we used a well established assay wherein cells incubated with exogenous laminin-111 are examined for accumulation of laminin on the cell surface (12, 13, 24, 25). In functionally normal mammary epithelial cell lines and primary cultures, fluorescently labeled laminin-111 (fl-Ln) accrued at the surface of living cells within minutes, beginning at discreet foci, and continued to accumulate over several hours (Figure 1A) (13, 24). However, while some breast cancer cells displayed normal anchoring and assembly of fl-Ln, others showed no detectable fl-Ln at the cell surface, even after 24 hours incubation (Figure 1A). The same defect was observed when assaying for assembly of endogenous laminin at the cell surface by immunofluorescence (Figure 1B). We then asked whether the variable capacity of cells to anchor laminin is reliant on inherent cell properties or on secreted factors transferable from neighboring cells, such as proteolytic enzymes or inhibitory peptides. Treatment of cells with the broad spectrum metalloproteinase inhibitor GM6001 did not restore laminin assembly at the cell surface (data not shown). Furthermore, in co-culture experiments in which MDA-MB-231 (MDA231) cells were mixed with T47D cells, fl-Ln anchoring was again observed uniquely on the T47D cells (Figure 1C). These data suggest that the ability to anchor laminin is cell autonomous and heterogeneous among cancer cells, likely arising from differences in laminin receptor functions.
We determined the prevalence and origins of defective laminin anchoring among cancer cells by testing a large panel of human breast cancer cell lines for their ability to anchor fl-Ln. This particular panel of cancer cell lines has been developed as a model system displaying a molecular heterogeneity resembling that observed in human breast cancers (21). A key advantage of testing this panel of cancer cells is the large collection of gene expression and genomic data that has been assembled for these cell lines, which permits rapid in silico exploration of the molecular mechanisms underlying cellular phenotypes (21, 26). Less than 30% of the 29 cell lines tested exhibited clear fl-Ln binding, as revealed by the accumulated fluorescence signal at the cell surface (Figure 2A). In the other lines, the fluorescent signal was either entirely absent (15 out of 29) or it was detected in only a small subpopulation of cells (Figure 2A). The majority of cell lines displaying defects of laminin anchoring fell within the basal-like subtypes (summarized in the Table S1). Taken together, these data indicated that defects of laminin anchoring are prevalent in human breast cancer cells.
Numerous laminin-binding receptors have been identified as potential mediators of laminin anchoring, including DG, integrins, and sulfatides (11–14, 25). We sought to identify changes in gene expression that could explain the loss of laminin assembly among these cell lines by interrogating the comprehensive gene expression data generated from this cell line panel by massively parallel RNA-sequencing (RNA seq) (27). None of the known laminin receptor genes exhibited a loss of gene expression that correlated with loss of laminin anchoring, including DG and the integrin subunits β1, β4,α1, α2, α3, α6 α7, α8, and α9 (Figures S1). Likewise, genes encoding enzymes essential for sulfatide synthesis exhibited generally low or undetectable expression among both luminal and basal-like carcinoma cells (Figure S1). Therefore, the defect of breast cancer cells to anchor laminin was not associated with variable expression of known laminin receptors.
Deletion of the DG gene from mammary epithelial cells and embryonic stem cells abolishes laminin-111 anchoring, and DG may perform this function in cooperation with β1 integrins (13, 24, 25). We directly tested the requirement for β1 integrin heterodimers in laminin-111 anchoring by eliminating their expression through deletion of the shared β1 integrin subunit by Cre-lox recombination in mammary epithelial cells established from β1 integrin fl/fl mice (Figure S2A). Ln anchoring in the β1 −/− cells was comparable to control cells, demonstrating that β1 integrin function is not essential for laminin-111 anchoring (Figure S2B). In contrast; deletion of DG completely abrogated laminin anchoring in normal mammary epithelial cells (Figure S2B).
The interaction of DG with laminins is reliant on O-linked carbohydrate modifications of the α-DG mucin domain, making altered glycosylation of DG a potential modulator of laminin anchoring (28). Defects of DG glycosylation cause loss of DG function in some muscular dystrophies (28), and similar defects have been observed in cancer cell lines (29–32). We assessed the glycosylation state of DG within the breast cancer cell line panel by performing western blot analysis using a well-characterized monoclonal antibody (IIH6) that binds to critical carbohydrate residues on α-DG that are required for binding to laminin. The vast majority of these cell lines (more than 70%) did not display any IIH6 immunoreactivity (Figure S3A). In contrast, the immunoblot analysis of β-DG subunit confirmed strong expression of the DG protein (Figure S3A). In addition, direct assessment of α-DG expression in some cells indicated that loss of IIH6 immunoreactivity was accompanied by a reduction in the mass of the α-DG subunit; consistent with α-DG hypoglycosylation (Figure S3B). There is a strong correlation between the IIH6 immunoreactivity and ability to anchor fl-Ln across the collection of human breast cancer cell lines tested (Table S1). All 15 cell lines deficient in laminin anchoring lacked IIH6 immunoreactivity. In aggregate, these results reveal that abnormal glycosylation of α-DG correlates strongly with the inability of human breast cancer cells to anchor laminin-111, and suggest that hypoglycosylation of DG is causative.
Genetic studies of congenital muscular dystrophies in humans have identified six genes that modulate DG glycosylation: POMT1, POMT2, POMGnT1, LARGE, FKTN and FKRP (28, 33). More recently, β3GNT1 has been implicated in DG glycosylation(30). RNA-seq expression data for the cell lines revealed minimal variation in mRNA expression of these genes (Figure S4A), with the sole exception of LARGE (Figure 2B and Figure S4B). LARGE expression levels were highly variable across the breast cancer cell lines and significantly higher in luminal lines compared to basal types (p=6.696e-05) (Figure 2C).
Cell lines exhibiting decreased expression of LARGE (indicated by white bars in Figure 2B) were unable to anchor laminin-111 and did not display IIH6 immunoreactivity. These data indicated that loss of laminin anchoring in these cells is caused by reduced expression of LARGE and dysfunctional glycosylation of DG. This hypothesis was directly tested in these cells by re-expression of LARGE. Restoring expression of LARGE by viral transduction repaired fl-Ln anchoring at the cell surface in all 10 cell lines that lack endogenous LARGE expression (Figure 3A). Consistently, in parallel with repairing laminin-binding, LARGE expression also restored IIH6 immunoreactivity (Figure 3B).
Cell lines CAMAI, MCF7, HCC1954 and BT549 showed defects in laminin anchoring and DG glycosylation that were not attributed to lack of LARGE expression. Significantly, over-expression of LARGE restored anchoring of fl-Ln and endogenous laminin in most lines, but not in HCC1954, demonstrating additional heterogeneity within this subset of cells (Figure S5A and S5B). Likewise, over-expression of LARGE restored glycosylation of DG in all cell lines but HCC1954 (Figure S5C). In contrast, over-expression of β3GNT1 did not restore fl-Ln anchoring or DG glycosylation in any of the cell lines tested (Figure S5D and E).
We searched for alternative causes for loss of laminin anchoring in the CAMAI, MCF7, HCC1954 and BT549 lines by sequencing mRNA from genes implicated in DG glycosylation. Analysis of cDNA sequence did not reveal additional mutations, deletions or alternate splicing (Figures S4C). Thus, while these results do not specify the origin or number of additional defects, they do reveal that at least two defects other than reduced expression of LARGE can account for loss of laminin anchoring and DG glycosylation in cancer cells, a set that can be repaired by LARGE over-expression, and a set that cannot.
We observed that expression of LARGE resulted in slower proliferation in some cell lines. In particular, CAMAI cells exhibited markedly reduced cell proliferation upon stable expression of LARGE. Quantitative assessments indicated that LARGE-expressing cells were significantly less proliferative than cells expressing vector control and this difference was enhanced with time in culture (Figure 4A). Assessment of cell cycle progression indicated that expression of LARGE produced significant differences in phases of cell cycle, most noticeably by reducing the fraction of cells in S phase (Figure 4B). The presence of the assembly-blocking laminin fragments E1 and E4 significantly increased the percentage of LARGE-expressing cells in S phase relative to cells expressing the vector control (Figure 4C). These results indicate that loss of LARGE expression promotes cell proliferation by disabling laminin anchoring.
Next, we assessed the consequence of LARGE expression on the tumorigenic capacity of cancer cells in vivo using orthotopic xenograft models generated by MDA231 cells expressing vector control or LARGE. Both cell types generated palpable tumors in 100% of injected mice. However, tumors generated by cells expressing LARGE were significantly smaller and exhibited a decrease in cell proliferation (Figure 5A and B). In sum, reduced expression of LARGE enhanced cell proliferation and tumor growth in vivo.
Analyses of breast cancer cell lines indicted that loss of LARGE expression is a surrogate measure for loss of laminin anchoring function and is more commonly observed in basal-like breast cancer cells. We examined the clinical relevance of these observations by analyzing two publically available datasets, each comprised of data from more than 500 patients, for LARGE expression in human breast cancers. In both datasets, reduced expression of LARGE mRNA was significantly associated with basal-like breast tumors (p=9.9533e-19 and p=2.29e-18, respectively) (Figure 5C and S6), a subtype which displays shortest overall and relapse free survival (34). These results corroborated the breast cancer cell line studies which showed reduced LARGE expression in the basal-like breast cancer cells. We then compared LARGE expression between normal and cancerous human tissues using the public datasets in Oncomine (Oncomine™ Compendia Bioscience, accessed July 2011) (Table S2). These analyses showed significantly decreased LARGE expression in infiltrating and superficial bladder carcinomas (35); various forms of colon adenocarcinomas (36); kidney clear cell adenocarcinoma (37); prostate adenocarcinomas (38) skin basal cell carcinoma (39) and a particularly strong decrease in brain cancers (40). Only squamous cell carcinomas showed significant overexpression of LARGE in primary cancers (41).
The highly significant reduction of LARGE expression in brain malignancies suggested that defects of laminin anchoring and assembly are functionally important in brain cancer cells, as they are in breast cancer cell lines. We tested this using cultured human glioblastoma cell lines. First, we confirmed that normal astrocytes displayed laminin anchoring and assembly, and that this capacity was lost in astrocytes obtained from mice lacking LARGE gene function (42) (Figure S7). In contrast, glioblastoma cell lines (LN-18, LN-229, U87 and U251) had deficiencies in laminin anchoring and DG glycosylation (Figure 6A and B) and, except for LN-229 cells, had reduced expression of LARGE (Figure 6C). Expression of exogenous LARGE in these cells restored laminin anchoring and DG glycosylation as observed in breast cancer cells - again with the exception of LN-229 (Figure 6A and B). Cell proliferation was also reduced, and surface accumulation of endogenous laminin increased, in LN-18 cells upon expression of LARGE (Figure 6D and E).
We investigated LARGE expression in a cohort of glioblastomas (GBMs) classified by aggressiveness and by expression profiling as proneural (PN), proliferative (Prolif), and mesenchymal (Mes) (43). Expression of LARGE was significantly lower in the two most aggressive subclasses, Mes and Prolif (Figure 7A). Patient outcome is markedly worse for Prolif and Mes compared to PN (median survival= 174.5 weeks for PN, 60.5 weeks for Prolif, and 65 weeks for Mes) (42). We next assessed the prognostic value of LARGE expression in independent cohorts of astrocytomas using the REMBANDT database (See Methods). As shown in Figure 7B, reduced expression of LARGE was strongly correlated with poor patient survival (p=7.9e-7).
Our study shows that loss of laminin anchoring is a prominent phenotype of cancer cells of distinct pathophysiological and tissue origins. We reveal a clear association of this defect with aggressive cancer subtypes in breast cancers and glioblastomas, and demonstrate changes in cell proliferation and tumor growth as a result of this defect. Correspondingly, loss of laminin anchoring is also associated with poor clinical outcomes. Surprisingly, this defect is attributed to altered glycosylation of the laminin receptor DG, and not the expression of any known laminin receptors, including the integrins. Our assessment of a large panel of cancer cells provides a broad characterization of the molecular defects underlying the loss of laminin anchoring, pointing to at least three mechanistically distinct defects. This work introduces novel factors to the study of cancer progression, novel markers of cancer heterogeneity, and potentially novel therapeutic targets, with relevance to a very broad array of human cancers.
Several lines of evidence indicate that laminin anchoring acts as a tumor suppressor. We demonstrate that exogenous expression of LARGE in cancer cells slows cell proliferation by enabling assembly of laminins on the surface of cancer cells. Xenograft assays showed that restoration of LARGE expression moderates tumor growth in vivo. Work by Beltran et al. showed that suppression of LARGE expression enhances the invasiveness of one breast cancer cell line (31). Interactions of cells with ECM constituents, in particular laminins, contribute to tumor suppressive properties and play a dominant role in the normal morphogenesis and function of epithelia (17, 18). Importantly, the laminin anchoring activity of DG is a determinant of epithelial cell polarization (13), a characteristic of epithelial tissues which is lost in tumor cells and which exerts potent tumor suppressor properties (17, 46). Ultimately, in vivo assessment of tumor suppressive properties of laminin anchoring is necessary, including the analysis of transgenic models manipulating LARGE expression or function, but such models have not yet been developed. Mice completely lacking LARGE expression have been identified and serve as models of congenital muscular dystrophy, however loss of LARGE expression in these models results in muscle disease and death at ~16 weeks of age, precluding studies of cancer progression in this context (42).
Agents that elevate LARGE expression may prove therapeutic in a large number of cancers, however, the cause of LARGE suppression is not yet known and such agents have not yet been identified. The LARGE locus was first discovered as a tumor-specific deletion (47). However, examination of SNP and CGH data for the breast cancer cell lines did not reveal any evidence of deletions in the LARGE gene (data not shown). DNA methylation has previously been implicated in the loss of LARGE expression in one breast cancer cell line (MDA-MB-231 cells) (31). Broad measures of DNA methylation have been obtained for the panel of breast cancer cells, and included 2 probes within the LARGE promoter (48). Among the cell lines in this study exhibiting loss of LARGE expression, hypermethylation of the LARGE promoter was detected in only 2 lines (MDA-MB-231, and HCC1143 cells) (data not shown). Therefore, the frequent loss of LARGE expression in cancers is not uniquely a consequence of methylation changes at the LARGE promoter.
The findings reported here have numerous implications for the understanding and treatment of cancers. The decrease in cell proliferation and tumor growth associated with restoration of laminin anchoring suggests novel therapeutic opportunities focused on enhancement of LARGE expression or other mechanisms to restore laminin anchoring. Because these defects are more prevalent in aggressive cancer subtypes, novel therapeutic approaches targeting these pathways can address cancers that are currently most difficult to treat and have the fewest treatment options. The responsiveness of cancers cells to therapeutic manipulations is influenced by cell-ECM interactions (19, 20, 49), therefore, loss of laminin anchoring can potentially modulate response to therapies. Our results on cancer heterogeneity and subtype association suggest that assays for laminin assembly or LARGE expression might serve as prognostic biomarkers for diverse cancers, although useful antibodies for LARGE are currently lacking. Lastly, our study highlights the potential importance of ECM assembly processes in cancer heterogeneity and cancer cell behavior. A closer look at the assembly processes of other ECM molecules in cancer cells may expose more novel factors contributing to disease heterogeneity and progression.
We thank Heidi Feiler and Mark Lenburg for helpful discussion, Sean McAllister, Ryuichi Murase and Pouya Mohajer for help with xenograft assays, Peter Yurchenco for the generous gift of laminin fragments, Mark LaBarge and Martha Stampfer for primary human cultures, and Rajendra Pilakatta for help in adenovirus generation.
Grant Support
This work was supported by grants from the National Institutes of Health (CA109579) to J.L.M. and (CA058207) to J.W.G., the Department of Defense Breast Cancer Research Program (W81XWH-07-1-0416) to J.L.M., a Stand Up to Cancer-American Association for Cancer Research Dream Team Translational Cancer Research Grant SU2C-AACR-DT0409 to J.W.G., a Komen for the Cure Postdoctoral fellowship to A.A., a Belgian American Educational Foundation Postdoctoral fellowship to A.D., and a Canadian Institutes of Health Research Postdoctoral fellowship to O.L.G.
This work was supported by grants from the National Institutes of Health (CA109579) to J.L.M. and (CA058207) to J.W.G., the Department of Defense Breast Cancer Research Program (W81XWH-07-1-0416) to J.L.M., a Stand Up to Cancer-American Association for Cancer Research Dream Team Translational Cancer Research Grant SU2C-AACR-DT0409 to J.W.G.
No conflicts of interest exist among the authors.
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Special Issue Paper
Effective and accurate approaches for wind turbine gearbox condition monitoring
Article first published online: 7 FEB 2013
DOI: 10.1002/we.1595
Copyright © 2013 John Wiley & Sons, Ltd.
Wind Energy
Special Issue: Condition Monitoring
Volume 17, Issue 5, pages 715–728, May 2014
Additional Information
How to Cite
Luo, H., Hatch, C., Kalb, M., Hanna, J., Weiss, A. and Sheng, S. (2014), Effective and accurate approaches for wind turbine gearbox condition monitoring. Wind Energ., 17: 715–728. doi: 10.1002/we.1595
Publication History
- Issue published online: 2 APR 2014
- Article first published online: 7 FEB 2013
- Manuscript Accepted: 17 DEC 2012
- Manuscript Revised: 15 OCT 2012
- Manuscript Received: 11 JUL 2012
- Abstract
- Article
- References
- Cited By
- condition monitoring;
- wind turbine;
- synthesized synchronous sampling;
- acceleration enveloping;
- bearing damage;
- gear damage;
- drivetrain
This paper presents effective and accurate approaches in vibration-based wind turbine drivetrain component condition monitoring. Detailed spectral analysis and acceleration enveloping techniques were used to effectively extract the gear and bearing damage features. Synchronous analysis was used to accurately detect specific damage features during constantly varying operational conditions. A typical wind turbine gearbox amplifies shaft speed two orders of magnitude from the rotor to the generator. To account for all necessary vibration signatures, synchronous sampling must be carried out for multiple revolutions and at a relatively high rate. The synchronous sampling used in this paper was carried out in the digital domain after both the keyphasor and the vibration signals were digitized at high sampling rate and high sampling resolution analog-to-digital conversion. Sometimes, the shaft speed is provided in a speed time history format, as in the case of the National Renewable Energy Laboratory (NREL) Round Robin project. To carry out synchronous sampling using the speed time history, a unique synthesized synchronous sampling technique was adopted. The approach presented in this paper was realized using MATLAB (MathWorks, Natick, MA) codes and then validated with a wind turbine field case. It was also applied to the NREL wind turbine drivetrain condition monitoring Round Robin project. The identified damage results using the techniques discussed were compared with post-test inspection results with good correlation. Copyright © 2013 John Wiley & Sons, Ltd.


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to everyone who donated boots!
Schools & Organizations who Received Boots in 2014
St. Ann's School
Roxborough Park
Queen Victoria School
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Prince of Wales Elementary School
T-Shirts available for sale at our main event on May 2nd
May 2nd, 2015
National Puddle Day is in memory of Matthew
Chatelain. It is a day to honour those children whose
lives are cut short and this year support a local charity, Bereaved Families of Ontario-Hamilton/Burlington, the only local resource whose primary mandate is to provide grief support to families who have experienced the death of a child of any age.
Read Matthew's Story Here
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Letter to Kinderseeds Families
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***Please make all cheques payable to 'Bereaved Families Of Ontario-Hamilton/Burlington'***
Participating Schools 2014
Farmers' Dell Preschool Co-op
Imagineer's Childcare Centre
Daycare on Delaware
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St. Matthew's Catholic Elementary
St. Vincent de Paul Catholic Elementary
Bellmoore Elementary
St. Marguerite d'Youville Elementary
Mount Albion Elementary
Bell-Stone Elementary
Mt. Hope Public School
Linden Park Elementary
McKinnon Park Secondary School
Norwood Park Elementary School
Westmount Secondary School
Our Lady of Mt. Carmel Catholic Elementary
Hagersville Elementary
Village Treehouse Childcare
Adelaide Hoodless Public School
Franklin Junior Public School
Dundas Elementary
Copyright 2015


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I grew up seeing how my Father shows his affection to Mamang by giving her flowers, cards , giving her gifts and making her feel very special. 866 more words
Tags » Celebrating Valentine's Day
This Valentines Day... Let there be Love
This is the time of year when all writers, bloggers and television presenters will begin every sentence with 'this is the time of year… "When describing what time of year it is before either launching in a hearty attempt to promote the idea of celebrating the day or go at a complete tangent by going Joan Rivers style on the day ripping it apart sadistically and robbing It of any form of positivity and dignity left of it. 1,284 more words
Valentine's Day Is NOT CUTE. Here's Why.
Valentines day is a delusion.
Trust me, it's not that I find the idea of people falling in love offensive. (Um….well….to be honest, sometimes I do.) 565 more words


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The Journal Sentinel sports staff brings fans the latest news and inside information on the Brewers
Mark Rogers on hill for Brewers on Sunday
Phoenix - Right-hander Mark Rogers, who says he feels better this spring than ever, will get his first exhibition start Sunday for the Brewers against Cleveland at Maryvale Baseball Park. »Read Full Blog Post
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Not a game that Rogers will tell his grandkids about someday.Hope he just had the nerves and nothing else wrong.
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After Taylor Swift revived a public debate over payments to artists by streaming-music services, Prince is the next high-profile musician to pull his catalog off some Web venues.
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