1, THERE WILL BE NO CLASS THIS WEEK BUT STUDENTS
WILL MEET INDIVIDUALLY FOR CONFERENCES.
Patterson Hall, Room 429, at scheduled time. Please
bring all work to the meeting (unless I have it already)
HOMEWORK: DUE April 3, 2007
1, READING
Ch.10 pages, (170 - 204) In EAA, Ch.4 in TSIS
ALSO --for Documenting Sources (CITATION)
there are good examples in EAC, pg 424- 442
2, Post your weekly blog entry.
3, Comment on NY times article below. Answer the
questions - a, What is the author's claim? Do you agree
with this claim? Use quotes to support your comment.
http://www.nytimes.com/2007/03/25/opinion/25gilbert.html?_r=1&oref=slogin
March 25, 2007
Op-Ed Contributor
Compassionate Commercialism
By DANIEL GILBERT
Cambridge, Mass.
IN an advertising campaign that began last week, Nissan left 20,000 sets of keys in bars, stadiums, concert halls and other public venues. Each key ring has a tag that says: “If found, please do not return. My next generation Nissan Altima has Intelligent Key with push-button ignition, and I no longer need these.”
This campaign is clever, but not particularly original.
It was 1997, and the man who was crouched on the sidewalk at 68th and Broadway in New York City was one of the most pathetic souls I’d ever seen. His limbs were twisted in what appeared to be arthritic agony and tears were streaming down his face. “Please,” he whimpered. “Please, somebody help me.”
Most passers-by did what they were named for, but my wife and I stopped. The man looked up. “Please,” he sobbed. “I just want to go home.” My hand needed no guidance from my brain as it reached into my wallet and extracted $10. “Thank you,” he said as I handed him the money. “Thank you so much.” My wife and I mumbled some embarrassed words and walked on.
We hadn’t gone a block when she tugged my sleeve. “Maybe we should have gotten him into a cab,” she said. “He could barely stand up. He might need help. We should go back to see.” My wife is the patron saint of lost kittens and there is no arguing, so we went back to see. And what we saw was our horribly crippled friend walking briskly and happily up 68th Street, opening the door to a late-model car, getting in and driving away after what was apparently a short day of theatrical work.
I know two things now that I didn’t know then.
First, I now know that my hand did what human hands were designed to do. Research suggests that we are hard-wired with a strong and intuitive moral impulse — an urge to help others that is every bit as basic as the selfish urges that get all the press. Infants as young as 18 months will spontaneously comfort those who appear distressed and help those who are having difficulty retrieving or balancing objects. Chimpanzees will do the same, though not so reliably, which has led scientists to speculate about the precise point in our evolutionary history at which we became the “hypercooperative” species that out-nices the rest.
The second thing I know now that I didn’t know then is that this was the most damaging crime I had ever experienced. Like most residents of large cities, I’d been a victim before — of burglary once, of vandalism several times. But this was different. The burglars and vandals had taken advantage of my forgetfulness (“Why didn’t I double lock the door?”) and taught me to be better.
But the actor on 68th Street had taken advantage of my helpfulness and taught me to be worse. The hand that had automatically reached for my wallet had been slapped, and once slapped was twice shy. I’ve never again given money to a stranger without scrutinizing him for the signs that distinguish suffering from its imitation. And because I don’t know what those signs are, I typically just walk by.
Now corporate America has taken a lesson from the guild of shameless grifters. Nissan’s plan to leave those 20,000 sets of keys in public venues is every bit as crafty as the fraudulent performance that a decade ago left me with holes in both my pocketbook and soul. There is no selfish reason to bend down and pick up a key ring, but Nissan knows that we will bend without thinking because the impulse to help is bred into our marrow. Our best instinct will be awakened by a key ring and then punished by a commercial. Like rubes throughout the ages, we will be lured by a false cry of distress and quickly cured of our innocence and compassion.
We are used to commercial tricks that play on our fears. The official-looking letter marked “Verification Audit” is actually a magazine subscription renewal form; the credit card company’s ominous call to “discuss your account” is actually an attempt to sell new services.
Should we now get used to commercial tricks that play on our humanity? How would we feel about a device planted in trash bins that screams “I’m stuck!” until the lid is opened, at which point it continues, “Stuck in a dead end job, that is — and if you are too, then let us show you how to make millions in real estate with no money down”? Is it O.K. to send a thousand doleful puppies into the streets with tags that say: “Thanks for checking. And speaking of checking, our bank charges no monthly fees”?
What happens to us when greed masquerades as need, when cries for help become casting calls for chumps, when our most noble actions make us patsies? “You put an idea out there and seed it,” said the president of the advertising agency that came up with Nissan’s key ring ploy. “And people carry it for you.” Indeed they do. The idea being seeded and carried in this case is that the world cries wolf, that our moral impulse betrays us and that smart people should keep on walking.
Daniel Gilbert, a professor of psychology at Harvard, is the author of “Stumbling on Happiness.”
Sunday, March 25, 2007
Wednesday, March 21, 2007
HOMEWORK: Due March 22, 2007
1, Please bring a draft of your Research Paper: Part II to class as we'll be doing peer editing.
2, Weekly entry on your blog
2, Weekly entry on your blog
Tuesday, March 13, 2007
HOMEWORK: Due March 20, 2007
1, Final Draft: Rhetorical Analysis
2, Research Paper, Part II (Draft only for peer review)
3,Comment on 2 classmate's blogs (if you haven't yet done so)
Note: (DO NOT COME TO CLASS March 20 unless YOU HAVE THE WORK COMPLETED. Class will not meet Thursday, March 15! Use this time to do research)
4, Read and comment on the NY Times article below (on this blog)
http://nytimes.com/marketing/winatrip/?mkt=tsmmphoto
http://www.nytimes.com/2007/03/11/opinion/11kristof.html?n=Top%2fOpinion%2fEditorials%20and%20Op%2dEd%2fOp%2dEd%2fColumnists%2fNicholas%20D%20Kristof
March 11, 2007
Op-Ed Columnist
Win a Trip, and See a Different World
By NICHOLAS D. KRISTOF
Cast your eyes above and meet Hidaya Abatemam, whom I met last month in a remote area of southern Ethiopia. She is 6 years old and weighs 17 pounds.
Hidaya was starved nearly to death and may well have suffered permanent mental impairment, helping to trap her — and her own children, if she lives that long — in another generation of poverty.
Yet maybe the more interesting question is not why Hidaya is starving but why the world continues to allow 30,000 children like her to die each day of poverty.
Ultimately what is killing girls like her isn’t precisely malnutrition or malaria, but indifference. And that, in turn, arises from our insularity, our inexperience in traveling and living in poor countries, so that we have difficulty empathizing with people like Hidaya.
I often hear comments from readers like: “It’s tragic over there, but we’ve got our own problems that we have to solve first.” Nobody who has held the hand of a starving African child could be that dismissive.
That lack of firsthand experience abroad also helps explain why we are so awful at foreign policy: we just don’t “get” how our actions will be perceived abroad, so time and again — in Vietnam, China, Iran, Iraq, Lebanon, Afghanistan and Latin America — we end up clumsily empowering our enemies.
Part of the problem is that American universities do an execrable job preparing students for global citizenship. A majority of the world’s population lives on less than $2 a day, but the vast majority of American students graduate without ever gaining any insight into how that global majority lives.
According to a Roper/National Geographic poll, 38 percent%
2, Research Paper, Part II (Draft only for peer review)
3,Comment on 2 classmate's blogs (if you haven't yet done so)
Note: (DO NOT COME TO CLASS March 20 unless YOU HAVE THE WORK COMPLETED. Class will not meet Thursday, March 15! Use this time to do research)
4, Read and comment on the NY Times article below (on this blog)
http://nytimes.com/marketing/winatrip/?mkt=tsmmphoto
http://www.nytimes.com/2007/03/11/opinion/11kristof.html?n=Top%2fOpinion%2fEditorials%20and%20Op%2dEd%2fOp%2dEd%2fColumnists%2fNicholas%20D%20Kristof
March 11, 2007
Op-Ed Columnist
Win a Trip, and See a Different World
By NICHOLAS D. KRISTOF
Cast your eyes above and meet Hidaya Abatemam, whom I met last month in a remote area of southern Ethiopia. She is 6 years old and weighs 17 pounds.
Hidaya was starved nearly to death and may well have suffered permanent mental impairment, helping to trap her — and her own children, if she lives that long — in another generation of poverty.
Yet maybe the more interesting question is not why Hidaya is starving but why the world continues to allow 30,000 children like her to die each day of poverty.
Ultimately what is killing girls like her isn’t precisely malnutrition or malaria, but indifference. And that, in turn, arises from our insularity, our inexperience in traveling and living in poor countries, so that we have difficulty empathizing with people like Hidaya.
I often hear comments from readers like: “It’s tragic over there, but we’ve got our own problems that we have to solve first.” Nobody who has held the hand of a starving African child could be that dismissive.
That lack of firsthand experience abroad also helps explain why we are so awful at foreign policy: we just don’t “get” how our actions will be perceived abroad, so time and again — in Vietnam, China, Iran, Iraq, Lebanon, Afghanistan and Latin America — we end up clumsily empowering our enemies.
Part of the problem is that American universities do an execrable job preparing students for global citizenship. A majority of the world’s population lives on less than $2 a day, but the vast majority of American students graduate without ever gaining any insight into how that global majority lives.
According to a Roper/National Geographic poll, 38 percent%
Monday, March 12, 2007
HOMEWORK: Due March 13, 2007
1, Rhetorical analysis
2, Comment on 2 class mates' blogs
3, Review ch.2, They Say, I Say
2, Comment on 2 class mates' blogs
3, Review ch.2, They Say, I Say
Thursday, March 1, 2007
2 New Drugs Offer Options in H.I.V. Fight
February 28, 2007
2 New Drugs Offer Options in H.I.V. Fight
By LAWRENCE K. ALTMAN and ANDREW POLLACK
LOS ANGELES, Feb. 27 — Two new AIDS drugs, each of which works in a novel way, have proved safe and highly successful in large studies, a development that doctors said here on Tuesday would significantly expand treatment options for patients.
The two drugs, which could be approved for marketing later this year, would add two new classes of drugs to the four that are available to battle H.I.V., the AIDS virus. That would be especially important to tens of thousands of patients in the United States whose treatment is failing because their virus has become resistant to drugs already in use.
“This is really a remarkable development in the field,” Dr. John W. Mellors of the University of Pittsburgh said at a news conference here at the 14th Annual Conference on Retroviruses and Opportunistic Infections.
Dr. Mellors, who was not involved in the studies but has been a consultant to the manufacturers of the drugs, said he “wouldn’t be going out on a limb” to say the new results were as exciting as those from the mid-1990s, when researchers first discovered that cocktails of drugs could significantly prolong lives.
Dr. Scott Hammer, chief of infectious diseases at Columbia University Medical Center, who also was not involved in the studies but has been a consultant to the manufacturers, agreed that the new drugs “will provide extended years of meaningful survival to patients.”
One drug, maraviroc, was developed by Pfizer, which has already applied for approval to sell it. The Food and Drug Administration has scheduled an advisory committee meeting on April 24 to discuss the application.
The other drug, raltegravir, was developed by Merck, which has said it will apply in the second quarter for approval.
Experts said the new drugs would be used in combination with older drugs. Both drugs stem from scientific findings made a decade or more ago that have peeled back the intricate molecular process used by H.I.V. to infect human immune system cells and to replicate themselves.
While there are now more than 20 approved drugs to treat H.I.V. and AIDS, there are only four different mechanisms by which the drugs work. In many patients, the virus develops resistance to one or more drugs, usually because patients do not take their drugs on time as prescribed.
And if the virus develops resistance to one drug in a class, it often becomes resistant to others in that class and sometimes in other classes. So AIDS experts have said there is an urgent need for drugs that work by new mechanisms.
The two new drugs would represent the first new classes since 2003, when an injectable drug called Fuzeon was approved. They would be the first new classes of oral H.I.V. drugs in a decade.
Merck’s drug works by inhibiting the action of integrase, an enzyme produced by the virus that incorporates the virus’s genetic material into the DNA of a patient’s immune cell. Once incorporated, the viral DNA commandeers the cell to make more copies of the virus.
In two Merck studies involving a total of 700 patients, virus levels dropped to below 50 copies per milliliter of blood, an amount considered undetectable, in about 60 percent of patients who received raltegravir. That compared with about 35 percent of those who received a placebo.
The patients in the two Phase 3 trials, typically the last stage of testing before approval, were resistant to at least one drug in each of three classes of antiretroviral drugs. All the patients also received a combination of older drugs that their doctors deemed to be the most appropriate. The results reported here were after 16 weeks, in a study that is continuing so it is possible that longer-term side effects might yet arise.
Other integrase inhibitors, like one from Gilead Sciences, are also under development. Gilead’s drug is 18 months to 2 years behind Merck’s.
Pfizer’s drug works by blocking a protein on human immune system cells that H.I.V. uses as a portal to enter and infect the cell. It would be the first drug that targets the human body rather than the virus.
The portal, known as CCR5, was discovered in 1996 by several groups of scientists, and there has been a race to develop drugs to block it.
In two Phase 3 studies sponsored by Pfizer involving 1,049 patients, more than 40 percent of patients who received maraviroc had undetectable levels of virus after 24 weeks of a 48-week study. That was about twice the rate of those who received placebo. As in the Merck trials, patients were resistant to three classes of drugs and were receiving an optimized combination of older drugs.
Some experts said they were a bit cautious about maraviroc, in part because it blocks a human protein instead of a viral one, with possible unknown long-term effects. One CCR5 inhibitor that was being developed by GlaxoSmithKline was dropped because it caused liver toxicity, and a second being developed by Schering-Plough appeared to possibly raise the risk of blood cancers.
But in Pfizer’s study there was no increased incidence of cancers. In one study there was a higher rate of death among those who took the drug, but Pfizer said the deaths were not associated with the drug.
Experts are also encouraged that about 1 percent of Caucasians have a particular mutation in both copies of their CCR5 gene that knocks out its function. These people are resistant to H.I.V. infection and apparently live otherwise normal lives.
Yet another issue is that some viruses use a different entry portal called CXCR4. Before getting maraviroc, patients will have to be tested to see which portal their virus uses, which would make the drug an early example of “personalized medicine” tailored to the patient.
The test, which will probably take two weeks for results, was developed by Monogram Biosciences of South San Francisco, Calif. It is expected to cost as much as $1,000, or more.
About 85 percent of newly infected patients have a virus that uses CCR5 while only about half of highly drug-resistant viruses use that portal. There has been some concern that blocking CCR5 would encourage the development of viruses that use the alternative portal — and those viruses seem to be associated with worse outcomes.
But that has not proven so far to be a big problem, according to Edward A. Berger of the National Institute of Allergy and Infectious Diseases, who played a key role in the discovery of the two portals.
Government, academic and industry experts said there was no reliable estimate of the number of people who would need one of the new drugs. But the number is declining as more and better AIDS drugs become available.
“The numbers are not what they used to be six years ago,” said Norbert Bischofberger, executive vice president for research and development at Gilead, which makes some widely used AIDS drugs.
Both Merck and Pfizer say they are conducting studies testing their drugs for use as initial treatments. They would not say how much their drugs would cost.
2 New Drugs Offer Options in H.I.V. Fight
By LAWRENCE K. ALTMAN and ANDREW POLLACK
LOS ANGELES, Feb. 27 — Two new AIDS drugs, each of which works in a novel way, have proved safe and highly successful in large studies, a development that doctors said here on Tuesday would significantly expand treatment options for patients.
The two drugs, which could be approved for marketing later this year, would add two new classes of drugs to the four that are available to battle H.I.V., the AIDS virus. That would be especially important to tens of thousands of patients in the United States whose treatment is failing because their virus has become resistant to drugs already in use.
“This is really a remarkable development in the field,” Dr. John W. Mellors of the University of Pittsburgh said at a news conference here at the 14th Annual Conference on Retroviruses and Opportunistic Infections.
Dr. Mellors, who was not involved in the studies but has been a consultant to the manufacturers of the drugs, said he “wouldn’t be going out on a limb” to say the new results were as exciting as those from the mid-1990s, when researchers first discovered that cocktails of drugs could significantly prolong lives.
Dr. Scott Hammer, chief of infectious diseases at Columbia University Medical Center, who also was not involved in the studies but has been a consultant to the manufacturers, agreed that the new drugs “will provide extended years of meaningful survival to patients.”
One drug, maraviroc, was developed by Pfizer, which has already applied for approval to sell it. The Food and Drug Administration has scheduled an advisory committee meeting on April 24 to discuss the application.
The other drug, raltegravir, was developed by Merck, which has said it will apply in the second quarter for approval.
Experts said the new drugs would be used in combination with older drugs. Both drugs stem from scientific findings made a decade or more ago that have peeled back the intricate molecular process used by H.I.V. to infect human immune system cells and to replicate themselves.
While there are now more than 20 approved drugs to treat H.I.V. and AIDS, there are only four different mechanisms by which the drugs work. In many patients, the virus develops resistance to one or more drugs, usually because patients do not take their drugs on time as prescribed.
And if the virus develops resistance to one drug in a class, it often becomes resistant to others in that class and sometimes in other classes. So AIDS experts have said there is an urgent need for drugs that work by new mechanisms.
The two new drugs would represent the first new classes since 2003, when an injectable drug called Fuzeon was approved. They would be the first new classes of oral H.I.V. drugs in a decade.
Merck’s drug works by inhibiting the action of integrase, an enzyme produced by the virus that incorporates the virus’s genetic material into the DNA of a patient’s immune cell. Once incorporated, the viral DNA commandeers the cell to make more copies of the virus.
In two Merck studies involving a total of 700 patients, virus levels dropped to below 50 copies per milliliter of blood, an amount considered undetectable, in about 60 percent of patients who received raltegravir. That compared with about 35 percent of those who received a placebo.
The patients in the two Phase 3 trials, typically the last stage of testing before approval, were resistant to at least one drug in each of three classes of antiretroviral drugs. All the patients also received a combination of older drugs that their doctors deemed to be the most appropriate. The results reported here were after 16 weeks, in a study that is continuing so it is possible that longer-term side effects might yet arise.
Other integrase inhibitors, like one from Gilead Sciences, are also under development. Gilead’s drug is 18 months to 2 years behind Merck’s.
Pfizer’s drug works by blocking a protein on human immune system cells that H.I.V. uses as a portal to enter and infect the cell. It would be the first drug that targets the human body rather than the virus.
The portal, known as CCR5, was discovered in 1996 by several groups of scientists, and there has been a race to develop drugs to block it.
In two Phase 3 studies sponsored by Pfizer involving 1,049 patients, more than 40 percent of patients who received maraviroc had undetectable levels of virus after 24 weeks of a 48-week study. That was about twice the rate of those who received placebo. As in the Merck trials, patients were resistant to three classes of drugs and were receiving an optimized combination of older drugs.
Some experts said they were a bit cautious about maraviroc, in part because it blocks a human protein instead of a viral one, with possible unknown long-term effects. One CCR5 inhibitor that was being developed by GlaxoSmithKline was dropped because it caused liver toxicity, and a second being developed by Schering-Plough appeared to possibly raise the risk of blood cancers.
But in Pfizer’s study there was no increased incidence of cancers. In one study there was a higher rate of death among those who took the drug, but Pfizer said the deaths were not associated with the drug.
Experts are also encouraged that about 1 percent of Caucasians have a particular mutation in both copies of their CCR5 gene that knocks out its function. These people are resistant to H.I.V. infection and apparently live otherwise normal lives.
Yet another issue is that some viruses use a different entry portal called CXCR4. Before getting maraviroc, patients will have to be tested to see which portal their virus uses, which would make the drug an early example of “personalized medicine” tailored to the patient.
The test, which will probably take two weeks for results, was developed by Monogram Biosciences of South San Francisco, Calif. It is expected to cost as much as $1,000, or more.
About 85 percent of newly infected patients have a virus that uses CCR5 while only about half of highly drug-resistant viruses use that portal. There has been some concern that blocking CCR5 would encourage the development of viruses that use the alternative portal — and those viruses seem to be associated with worse outcomes.
But that has not proven so far to be a big problem, according to Edward A. Berger of the National Institute of Allergy and Infectious Diseases, who played a key role in the discovery of the two portals.
Government, academic and industry experts said there was no reliable estimate of the number of people who would need one of the new drugs. But the number is declining as more and better AIDS drugs become available.
“The numbers are not what they used to be six years ago,” said Norbert Bischofberger, executive vice president for research and development at Gilead, which makes some widely used AIDS drugs.
Both Merck and Pfizer say they are conducting studies testing their drugs for use as initial treatments. They would not say how much their drugs would cost.
---------------------------------------
I am going to include funny advertisements each week to make my posts a little more interesting. So, if you don't read what I have to say, atleast you can check in and see some funny commercials and stuff!
Have a great week everyone...
Subscribe to:
Posts (Atom)