Pres. Obama’s End Game on the fiscal cliff negotiations
This post is part of the “Future of Business” series, which examines how cutting-edge technologies are rapidly reshaping our world, from how businesses run to how we live. “The Future of Business” is sponsored by SAP.
If you’ve heard it once, you’ve heard it a million times: Get a flu shot. But how come that works? There are countless strains of flu, so unlike vaccines for childhood illnesses, you have to get a flu shot every year. Once is not enough.
It works because of a massive collaboration of doctors, hospitals, and labs that report mega amounts of data to the Centers for Disease Control (CDC). The CDC fields some 700,000 reports of patents with flu-like symptoms per week. During flu season, doctors will send more than 5,000 lab tests to the CDC for further analysis.
Using that data, the CDC has created complex flu-tracking systems to determine things like: what strains of flu should go in the annual flu vaccine (which is changed twice a year); is this year’s flu outbreak the kind of flu that will respond well to anti-viral drugs; how deadly the flu is.
The flu season is in full swing right now, according to data analyzed by Lynnette Brammer, a flu epidemiologist at the Centers for Disease Control and the woman that helped Google create its flu tracking system.
She told Business Insider:
- The flu started earlier this year and is now quickly on the rise.
- The flu shot has been proven to protect well against this year’s strains. (So if you haven’t gotten one, you might want to rethink that.)
- This year’s flu strains respond well to anti-viral meds, so those who get really sick can be helped by seeing their doctor.
If you want to see how bad certified flu cases are in your state, the CDC reports that data weekly on a website called FluView. Meanwhile Google used FluView data to help them build their own flu-tracking website, Google Flu Trends. Flu Trends tracks the spread of the illness based on people searching on flu symptoms. It offers a more instantaneous view of where people are getting sick, but it doesn’t verify if those people really have the flu or just bad head colds.
The ultimate goal is not to end flu forever, but to keep people from becoming severely ill or dying from the flu.
Here’s a lightly edited transcript of the interview.
Flu map, click for interactive map
Business Insider: How are you saving the world from the flu using technology?
Lynnette Brammer: The data I use is the data contained in FluView. None of it comes from Google. There are basically eight different sources of data that go into FluView every week. It includes about 3,000 primary care providers across the country who report every week how many patients they saw that had Influenza-like illness. That gives us information on the proportion of people going to the doctor with flu-like illness.
BI: How many entries a week do you get?
LB: More than 700,000 patient encounters per week. But then you pair that up with other data sources, like our ViralLogic Lab data. That’s the U.S. World Health Organization collaborating lab system. It’s about 85 labs.
[Doctors] can take samples from a subset of their patients, send them off to their state public health lab who will do testing for flu. All the results from the state public health lab come to the ViralLogic Lab.
The majority of labs are reporting to us electronically. When the test results are final, it goes to a folder on their system and then it transfers it over here to the CDC. It’s very timely. It’s a fabulous reporting system. We then report out on a weekly basis. We could analyze that and report daily, but weekly is really fine.
BI: What types of things do you learn with all of this data?
LB: We learn where flu is and in what relative proportion [to the general population], what age groups are getting flu. We do what’s called “antigenic characterization” [of flu strains that made people sick] to see how close they look to the strains used in the vaccine. We do anti-viral resistance testing to make sure the strains are still sensitive to the drugs for flu and we do genetic sequencing on some of them.
We get rates of hospitalizations from lab-confirmed flu to see how much severe disease there is. We have another system that tracks pneumonia and influenza deaths so we can see on the whole population if flu activity is causing more deaths than you would expect for this time of year.
We try and cover the spectrum of where people would come into the healthcare system from flu. We can’t cover people not going to the doctor.
Things like Google Flu trends is where you get that type of data.
BI: How long have you been collecting this much data on the flu?
A lot started with the 2009 pandemic [popularly called Swine Flu], with so many labs reporting. But we have Virtual Logic data from as far back as 1976.
BI: What can you tell us about this year’s flu so far?
LB: Right now, the majority of the viruses are Influenza A, H2 and H3 viruses but there’s a fair amount of influenza B out there. The viruses look like the vaccine strains by and large, so the vaccine ought to work pretty well.
We’re not seeing any anti-viral resistance. There’s more flu going on in the south and southeast than in other parts, but in most of the country, it’s going up pretty quickly.
BI: How does this year compare to other years so far?
LB: So far this year it’s a little earlier. Whether or not it will peak early, I don’t know. It could be one of those years where it finishes by the end of January. Or it could keep increasing steadily for a while and drag on for months.
BI: Is the ultimate goal to end flu?
LB: Influenza strains are changing all the time. And there are animal reservoirs that spread it. Pigs can get flu, birds can get flu. A lot of animals can get flu; dogs, horses, seals, whales … so you are never going to eliminate flu. But we don’t collect data just to know. We collect so we can know enough to pick the strains to go in the vaccine each year. And if we have anti-viral resistance or not and can urge doctors to use more anti-viral.
Our hope is to make better vaccines to reduce the impact of flu and to reduce hospital visits and deaths due to flu.
Blacks voted at a higher rate this year than other minority groups and for the first time in history may also have voted at a higher rate than whites, according to a Pew Research Center analysis of census data, election day exit poll data and vote totals from selected cities and counties.
Unlike other minority groups whose increasing electoral muscle has been driven mainly by population growth, blacks’ rising share of the vote in the past four presidential elections has been the result of rising turnout rates.
These participation milestones are notable not just in light of the long history of black disenfranchisement, but also in light of recently-enacted state voter identification laws that some critics contended would suppress turnout disproportionately among blacks and other minority groups.
In fact, according to census data and the election day exit polls, blacks made up 12 percent of the eligible electorate this year but accounted for an estimated 13 percent of all votes cast—a repeat of the 2008 presidential election, when blacks “over-performed” at the polls by the same ratio. In all previous presidential elections for which there are reliable data, blacks had accounted for a smaller share of votes than eligible voters.
The candidacy in 2008 and 2012 of Barack Obama, the nation’s first black president, is no doubt one of the main reasons for these new patterns. But there are other explanations as well, including the increased racial and ethnic diversity of the electorate, and a declining turnout rate among whites.
In 2012, more Hispanics and Asian-Americans voted than ever before, but the turnout rates among these groups (votes cast as a share of eligible voters), while rising, continues to lag that of the general public by a substantial margin. Their growing electoral muscle is mainly due to their rapid population growth.
As for whites, not only has their share of the eligible electorate been falling for decades, but their turnout rate appears to have declined in 2012 for the second presidential election in row.
Did the turnout rate of blacks exceed that of whites this year for the first time ever? For now, there’s circumstantial evidence but no conclusive proof. And there’ll be no clear verdict until next spring, when the U.S. Census Bureau publishes findings from its biannual post-election survey on voter turnout.
Even so, there’s a good bit that’s already known. Overall, about 129 million votes were cast for president in 2012, down slightly from 131 million in 2008. When one factors in a 9 million increase in the age and citizen eligible electorate due to normal population growth between those two elections, the turnout rate among all eligible voters fell by more than 3 percentage points—to about 60% in 2012 from more than 63% in 2008.
The most authoritative measure of turnout by racial and ethnic groups comes from the census survey known as Voting and Registration Supplement, which is conducted in late November after every federal election among a nationally representative sample of about 100,000 adults.
While the 2012 finding won’t be made public for several months, a backward look at recent trends from this data set is instructive. In 2008, according to the post-election census survey, the gap between white and black turnout was the smallest on record. Some 66.1% of all age and citizen eligible whites voted that year, compared with 65.2% of blacks, 49.9% of Hispanics and 47% of Asian Americans. The survey found that the white turnout rate had declined by 1.1 percentage points between 2004 and 2008, while the rates for the other groups all rose—by 4.9 percentage points among blacks, 2.7 among Hispanics and 2.4 among Asians.
The post-election survey also showed that in 2008, young blacks (18 to 29 year olds) voted at a higher rate than young whites (58% versus 52%) – a difference that was almost certainly related to the historic nature of the Obama candidacy, but that might foreshadow patterns in political engagement among the Millennial generation that could persist throughout adulthood.
The political importance of turnout rates by race was brought into sharp focus by last month’s election, in which Obama won 80% of the non-white vote (including 93% of blacks, 73% of Asian Americans and 71% of Hispanics) and just 39% of the white vote. That constellation of votes by race gave Obama a popular vote victory margin this year of 4.7 million and an Electoral College victory of 332-206.
For comparative purposes, consider the 1988 presidential race between GOP nominee George H.W. Bush and Democrat Michael Dukakis. Bush received the identical share of the white vote that GOP nominee Mitt Romney won this year – 59%. But 24 years ago, that share was good enough to give Bush a popular vote margin of 7 million and an Electoral College landslide of 426-111.
The stark difference in those two outcomes is a reflection of the country’s rapidly changing demographic makeup, driven mainly by the population growth among Hispanic and Asian American immigrants and their children.
Blacks, by contrast, have not seen their share of the population grow during this period. But their electoral clout has increased because their participation rates have risen steadily in the three presidential elections from 2000 to 2008.
As for 2012, the best available data for now on turnout by racial and ethnic groups are from the National Election Pool, an election day exit survey of more than 26,000 voters conducted by a consortium of major media organizations.
These surveys are best known for enabling an analysis of which groups voted for which candidate. They can also be used to estimate the share of all voters by race and ethnicity (as well as by other demographic characteristics). However, these estimates should be treated with caution. In 2008, as the accompanying tables show, the estimates derived from the election day exit poll were not the same as the estimates derived from the post-election survey by the U.S. Census Bureau. There is no guarantee this will not be the case again in 2012.
Even with that caveat in mind, the exit poll is instructive. As the tables show, in 2012 blacks and whites both appear to have cast a slightly higher shares of votes (72% and 13%, respectively) than their share of eligible voters (71% and 12%), while Hispanics and Asians cast a lower share of votes (10% and 3%) than their share of eligible voters (11% and 4%).
That still leaves unanswered whether the black turnout rate in 2012 surpassed the white turnout rate. If so, it would be a notable denouement to the charged debate this year between state GOP leaders who pressed for tougher laws to deter voter fraud and black and other minority group leaders who accused them of trying to suppress the minority vote. This fall, black pastors, community leaders and elected officials across the country used these new identification laws as a spur to energize turnout.
In an effort to further explore whether black turnout exceeded white turnout in 2012, Pew Research asked voter turnout expert Rhodes Cook to analyze the number of votes cast in 2008 and 2012 in a sampling of heavily black and heavily white cities and counties across the country. Cook gathered the official counts from state election officials and relied on his extensive knowledge of the nation’s demographic and political characteristics, down to the county level, to select the sample.
His findings are presented in Appendix A. They show a mix of turnout increases and decreases, with no clear pattern. In short, blacks may have achieved an historic turnout milestone at the polls last month – even in the face of what many black leaders said was an effort to suppress their vote. But for now, there’s no conclusive proof.
Click the link to see the rest of the article: http://www.pewsocialtrends.org/2012/12/26/the-growing-electoral-clout-of-blacks-is-driven-by-turnout-not-demographics/
University of Oxford December 2012
Cannabis makes pain more bearable rather than actually reducing it, a study from the University of Oxford suggests.
Using brain imaging, researchers found that the psychoactive ingredient in cannabis reduced activity in a part of the brain linked to emotional aspects of pain.But the effect on the pain experienced varied greatly, they said.The researchers’ findings are published in the journal Pain.
The Oxford researchers recruited 12 healthy men to take part in their small study.Participants were given either a 15mg tablet of THC (delta-9-tetrahydrocannabinol) – the ingredient that is responsible for the high – or a placebo. The volunteers then had a cream rubbed into the skin of one leg to induce pain, which was either a dummy cream or a cream that contained chilli – which caused a burning and painful sensation.Each participant had four MRI scans which revealed how their brain activity changed when their perception of the pain reduced.
Dr Michael Lee, lead study author from Oxford University’s Centre for Functional Magnetic Resonance Imaging of the Brain, said: “We found that with THC, on average people didn’t report any change in the burn, but the pain bothered them less. “MRI brain imaging showed reduced activity in key areas of the brain that explained the pain relief which the study participants experienced. Dr Lee suggested that the findings could help predict who would benefit from taking cannabis for pain relief – because not everyone does. “We may in future be able to predict who will respond to cannabis, but we would need to do studies in patients with chronic pain over longer time periods.”He added: “Cannabis does not seem to act like a conventional pain medicine. Some people respond really well, others not at all, or even poorly. “Brain imaging shows little reduction in the brain regions that code for the sensation of pain, which is what we tend to see with drugs like opiates.”Instead cannabis appears to mainly affect the emotional reaction to pain in a highly variable way.”
Mick Serpell, a senior lecturer in pain medicine at Glasgow University, said the study confirmed what was already known.”It highlights the fact that cannabis may be a means of disengagement for the patient, rather than a pain reliever – but we can see that happen with opioids too.”The study was funded by the UK Medical Research Council and the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre.
On June 23, 2005, American medicine managed to take a small step forward and a giant step backward at precisely the same time, with government approval of the first medication to be earmarked for a specific racial group. It was BiDil, a drug designed to treat heart failure in blacks.
Enthusiasts hailed BiDil’s approval by the Food and Drug Administration as a landmark event in the nascent field of pharmacogenomics, which aims to create drugs tailored to fit an individual’s genetic makeup as precisely as a bespoke suit drapes its owner’s shoulders. Critics just winced and clocked one more misstep in medicine’s long history of race-related disasters.
You would think that the elucidation of the human genome would have cleared up most of the hoary untruths surrounding race and health. But as Jonathan Kahn makes clear in his worthy if convoluted review of the events surrounding the birth of BiDil, the genome has in many respects only made things worse.
It has been clear for decades that race has minimal relevance to the body’s inner workings. Research has repeatedly shown that the biologic variations among individuals of the same race are reliably great enough for race to retain little utility as a biologic predictor. You might as well sort people by height. Or, in the words of an editorial writer for Nature Biotechnology in 2005, “Pooling people in race silos is akin to zoologists grouping raccoons, tigers and okapis on the basis that they are all stripy.”
But old misconceptions die hard, particularly for entrepreneurs eagerly awaiting cash bonanzas from the genomic revolution.
Race may be irrelevant; it may be, as Dr. Francis Collins, the director of the National Institutes of Health, put it, “a weak and imperfect proxy” for genetic differences. But it is also a familiar concept — and asking people what race they are is substantially cheaper than genotyping them.
So in a peculiar paradox, race has come to serve in some circles as a crude surrogate for genetic analysis until actual genomic medicine comes along — a temporary bridge from now to later, known to be flawed but still a quasi-legitimate stand-in for the real thing.
Against this background unfolds the story of BiDil, a drama of greed and good intentions.
Several observations prompted the drug’s development. Among them was the common assertion from the last century that blacks with heart failure were more likely to die than whites. (Mr. Kahn does an impressive job of researching and debunking this statistic.) Then there was the belief that blacks often reacted badly to some of the newer drugs used for treating heart failure, and the results of a study dating from the 1980s suggesting that many black patients did well with two old standby drugs.
Those two drugs were (and are) on sale as generics, costing pennies a pill. But just suppose they were combined into a single pill that could be then specifically marketed to patients who just happened to be thought in particular need of effective medication? Now there was a pharmacologic and marketing plan that would extend a lucrative new patent for decades.
And so it came to pass that a collection of eager investors and some of the nation’s foremost cardiologists smiled on the results of an industry-sponsored trial performed on self-identified black subjects with heart failure: The two cheap drugs combined into the not-so-cheap BiDil reduced mortality by 40 percent compared with placebo. This figure was impressive enough to end the trial early and speed BiDil to market.
How did whites do on BiDil? Nobody bothered to check.
Mr. Kahn deserves credit for teasing out all the daunting complexities behind these events, including the details of genetic analysis, the perils of racial determinations and the minutiae of patent law. Unfortunately, though, he suffocates his powerful subject in a dry, repetitive, ponderous read.
A law professor with a doctorate in history and longstanding interest in race issues, Mr. Kahn trudges a partisan path through the drama in which he himself was a player. (He testified before an F.D.A. advisory committee that BiDil should be approved without racial qualifications.)
He heads bravely into many statistical thickets, but omits relevant clinical data; he repeatedly refers to the trial that led to BiDil’s approval, for instance, but I could find its numerical findings nowhere in the book and had to look them up. In a story that fairly drips with potential human interest, he offers the reader not one sip.
The issues raised on every page are so important and so thought-provoking that it would be irresponsible to warn interested readers away. Still, it would be almost as irresponsible to misrepresent the difficulty of the journey.
As it happens, BiDil itself has had a remarkably inglorious career. Despite its much-trumpeted release, patients did not request the medication, and practicing doctors did not prescribe it.
NitroMed, the company that developed it, sponsored no further studies and failed in 2009.
The drug still lingers on the market; Mr. Kahn writes that BiDil may be resurrected in sustained-release form — that other time-honored technique for wringing a few more years from a drug’s patent.
For a parable of early 21st-century medicine, as it treads water between past and future and never hesitates to reach for a buck, it doesn’t get much better than BiDil.
And there were in the same country shepherds abiding in the field, keeping watch over their flock by night. And, lo, the angel of the Lord came upon them, and the glory of the Lord shone round about them: and they were sore afraid. And the angel said unto them, Fear not: for, behold, I bring you good tidings of great joy, which shall be to all people. For unto you is born this day in the city of David a Saviour, which is Christ the Lord. And this [shall be] a sign unto you; Ye shall find the babe wrapped in swaddling clothes, lying in a manger. And suddenly there was with the angel a multitude of the heavenly host praising God, and saying, Glory to God in the highest, and on earth peace, good will toward men.
That’s what Christmas is all about, Charlie Brown.
During the making of the animated Christmas classic A Charlie Brown Christmas, Peanuts creator Charles Schulz had a meeting with Lee Mendelson, the show’s producer, and Bill Melendez, its lead animator. The discussion concerned Schulz’s insistence about including a New Testament scripture reading of the Christmas story from the Bible. The scripture reading was to be spoken by Peanuts character Linus Van Pelt in response to Charlie Brown’s lament, “Isn’t there anyone who knows what Christmas is all about?” Mendelson and Melendez both voiced their concern about the reading, with Melendez telling Schulz, “It’s very dangerous for us to start talking about religion now.” Schulz answered him by saying, “Bill, if we don’t, who will?” In the end, the scripture reading was retained, and the CBS special was the second-most watched show of the week when it debuted on December 9, 1965.
By GLENN THRUSH | 12/23/12 7:05 AM EST
President Barack Obama’s stiffening resolve during the fight over the fiscal cliff can be traced directly to the lessons he drew from his hard-won triumph of the 2012 campaign.
He whipped Republicans a second time, parried the best attacks they could muster, and is now demanding that they respect the victory, if not the man who won it. That doesn’t mean Obama won’t eventually compromise, especially with the specter of a renewed recession lingering just over the horizon, but his body language is a lot more combative than the kinder, gentler Obama negotiating style of yore.
The roots of his new toughness are rooted in the nature of his convincing November win over Mitt Romney. Obama was carried to the finish line by supporters after his epic flop at the Denver debate. That seeded in him a greater sense of confidence and deepened his resolve not to be rolled by a recalcitrant GOP, as he was during the bitter 2011 fight over the debt ceiling, according to interviews with staffers and friends for “The End of the Line,” an eBook published in collaboration between POLITICO and Random House.
After his 2008 win, he talked a lot about bipartisanship. This time he’s determined to squeeze it out of Republicans. He believes he owes that to the people who voted for him.
“There’s no doubt that he found this one to be sweeter than the last one,” said one of Obama’s top aides. “It was weighing on him how much was at stake, how much of his entire legacy was on the line. His legacy had not been determined by the previous four years; that wouldn’t matter to history. It was all about the outcome on Election Day.”
With that outcome now in the history books, the people around the president now see him as a Democratic Reagan, a resilient and popular figure who can unify the country — if only the dead-enders will give him a chance.
When the book’s authors asked David Plouffe, Obama’s most influential political adviser, whether the campaign’s organizational success could be replicated with other Democrats, he sprang forward in his chair. “The organization doesn’t exist without belief in the candidate … they turned out for Barack Obama,” he said. “It was all because of him.”
But the buzz from Election Day has proven to be remarkably brief. The White House has been thrust from its post-victory reverie into a Groundhog Day partisan battle that makes any talk of a new “mandate” seem laughable. Romney was a comprehensible threat Obama had gamed out for nearly two years. A fractious, collapsing GOP House majority leaves him in a much more dangerous and uncertain position, at least in the short term.
So far, he’s staked out a tough position, refusing to get too specific on spending and entitlement cuts, and threatening GOP leaders — whose popularity is tanking — with the bully pulpit of his inauguration and State of the Union speech. But many Hill Democrats, accustomed to seeing Obama give in, remain only cautiously optimistic.
“So far, so good. [But] we’ll see how this shakes out,” said a top Senate Democrat, who is queasy about the administration’s overtures to the GOP on entitlement reform.
For the first time ever, three pharmaceutical companies are poised to test whether new drugs can work against a wide range of cancers independently of where they originated — breast, prostate, liver, lung. The drugs go after an aberration involving a cancer gene fundamental to tumor growth. Many scientists see this as the beginning of a new genetic age in cancer research.
Great uncertainties remain, but such drugs could mean new treatments for rare, neglected cancers, as well as common ones. Merck, Roche and Sanofi are racing to develop their own versions of a drug they hope will restore a mechanism that normally makes badly damaged cells self-destruct and could potentially be used against half of all cancers.
No pharmaceutical company has ever conducted a major clinical trial of a drug in patients who have many different kinds of cancer, researchers and federal regulators say. “This is a taste of the future in cancer drug development,” said Dr. Otis Webb Brawley, the chief medical and scientific officer of the American Cancer Society. “I expect the organ from which the cancer came from will be less important in the future and the molecular target more important,” he added.
And this has major implications for cancer philanthropy, experts say. Advocacy groups should shift from fund-raising for particular cancers to pushing for research aimed at many kinds of cancer at once, Dr. Brawley said. John Walter, the chief executive officer of the Leukemia and Lymphoma Society, concurred, saying that by pooling forces “our strength can be leveraged.”
At the heart of this search for new cancer drugs are patients like Joe Bellino, who was a post office clerk until his cancer made him too sick to work. Seven years ago, he went into the hospital for hernia surgery, only to learn he had liposarcoma, a rare cancer of fat cells. A large tumor was wrapped around a cord that connects the testicle to the abdomen. “I was shocked,” he said in an interview this summer.
Companies have long ignored liposarcoma, seeing no market for drugs to treat a cancer that strikes so few. But it is ideal for testing Sanofi’s drug because the tumors nearly always have the exact genetic problem the drug was meant to attack — a fusion of two large proteins. If the drug works, it should bring these raging cancers to a halt. Then Sanofi would test the drug on a broad range of cancers with a similar genetic alteration. But if the drug fails against liposarcoma, Sanofi will reluctantly admit defeat.
“For us, this is a go/no-go situation,” said Laurent Debussche, a Sanofi scientist who leads the company’s research on the drug.
The genetic alteration the drug targets has tantalized researchers for decades. Normal healthy cells have a mechanism that tells them to die if their DNA is too badly damaged to repair. Cancer cells have grotesquely damaged DNA, so ordinarily they would self-destruct. A protein known as p53 that Dr. Gary Gilliland of Merck calls the cell’s angel of death normally sets things in motion. But cancer cells disable p53, either directly, with a mutation, or indirectly, by attaching the p53 protein to another cellular protein that blocks it. The dream of cancer researchers has long been to reanimate p53 in cancer cells so they will die on their own.
The p53 story began in earnest about 20 years ago. Excitement ran so high that, in 1993, Science magazine anointed it Molecule of the Year and put it on the cover. An editorial held out the possibility of “a cure of a terrible killer in the not too distant future.”
Companies began chasing a drug to restore p53 in cells where it was disabled by mutations. But while scientists know how to block genes, they have not figured out how to add or restore them. Researchers tried gene therapy, adding good copies of the p53 gene to cancer cells. That did not work.
Then, instead of going after mutated p53 genes, they went after half of cancers that used the alternative route to disable p53, blocking it by attaching it to a protein known as MDM2. When the two proteins stick together, the p53 protein no longer functions. Maybe, researchers thought, they could find a molecule to wedge itself between the two proteins and pry them apart.
The problem was that both proteins are huge and cling tightly to each other. Drug molecules are typically tiny. How could they find one that could separate these two bruisers, like a referee at a boxing match?
In 1996, researchers at Roche noticed a small pocket between the behemoths where a tiny molecule might slip in and pry them apart. It took six years, but Roche found such a molecule and named it Nutlin because the lab was in Nutley, N.J.
But Nutlins did not work as drugs because they were not absorbed into the body.
Roche, Merck and Sanofi persevered, testing thousands of molecules.
At Sanofi, the stubborn scientist leading the way, Dr. Debussche, maintained an obsession with p53 for two decades. Finally, in 2009, his team, together with Shaomeng Wang at the University of Michigan and a biotech company, Ascenta Therapeutics, found a promising compound.
The company tested the drug by pumping it each day into the stomachs of mice with sarcoma.
Michael Steele: NRA Press Conference ‘Very Haunting And Very Disturbing’
N.R.A. Press Conference: Group Calls for Armed Guards in Schools