Synopsis
Chef has a new woman enter his life, and he no longer has much time to spend with the boys. He then decides to marry her and get a new job, leaving the school cafeteria to be run by other employees of South Park Elementary. The boys soon discover that the soon-to-be Mrs. Chef is actually an evil Succubus that intends to devour Chef's soul once they get married and set out to stop her.
Full Recap
Cartman visits the optometrist, a man who makes fun of Cartman's weight problem, by calling him "Piggy". The optometrist dilates Cartman's pupils and Cartman shows up at school with his eyes wide open. The boys discover that Chef has been replaced by a new character called Mr. Derf, who does his best to entertain them in line. After school the boys go to Chef's home where they find out that Chef had quit his job. Chef has quit his job because he met a woman whose changed his life and helped him to see the error of his ways. The boys decide they need to do something to save Chef. The optometrist prescribes stupid looking glasses for Cartman and then staples to his head to make sure he doesn't take them off. The boys (with a bespectacled Cartman) visit Chef at his new job at an accounting firm. The boys appeal to Chef, but he tells them this is just something they are going to have to learn to deal with. He promises to meet the boys after work to play some ball. The following morning after he didn't show up to play ball, the boys return to his house. Chef tells the boys that he and Veronica are planning to get married.
Mr. Garrison tells the children about The Facts of Life, the TV show, not the real ones. The boys ask Mr. Garrison advice about their problem with Chef. He tells them about the "succubus syndrome", a woman sent from hell to suck the life out of a man. The boys plan to tell the Chef about the succubus, but Cartman is diverted for another trip to the optometrist. At Chef's home, the boys meet Chef's parents. Chef's parents tell them about all the times they saw the Loch Ness monster, who is always asking them for about "tree fiddy" ($3.50). Cartman gets his laser eye surgery, which goes bad, so he must wear bandages over his eyes. Veronica, the succubus, comes to Cartman's home to help the boys understand why she is going to marry Chef. Before she leaves she reveals her true self to the boys and tells them there isn't anything they can do about it.
At the rehearsal dinner, Chef's father tells the story about the time the Loch Ness monster impersonated his son. The boys arrive to tell Chef the bad news, Veronica is a succubus. Chef tells the boys to accept the marriage, or get out his life. Stan isn't going to give up. The boys seek a way to destroy the succubus. They learn that if they sing the song of the succubus "There's Got to be a Morning After" backwards they can destroy her. They've got three hours to learn the song. At the church, the boys start to execute their plan, but the tape jams. In the process the succubus reveals itself and kills Kenny. They get the taped restarted and finish singing the song backwards, causing the succubus to disappear. In the aftermath, Chef wonders what he ever saw in her.
Back at school, things are back to normal; Chef is back in job and singing. At the optometrist Cartman brings in Kenny's head, hoping to get an eye transplant.
Kenny dies when he is attacked after the succubus reveals itself at the church.
Tuesday, June 30, 2009
Wednesday, May 20, 2009
Boston University 6.bu.3401 Louis J. Sheehan, Esquire
When deadly bird flu strikes, six degrees of separation could be the distance from here to hell. Even if a vaccine is found to be effective, it may be impossible to produce enough shots for everybody quickly enough, so authorities would have to decide how to use the doses they have in the most effective way. Researchers are now proposing a new strategy for targeting shots that could, at least in theory, stop a pandemic from spreading along the network of social interactions.
Vaccinating selected people is essentially equivalent to cutting out nodes of the social network. As far as the pandemic is concerned, it’s as if those people no longer exist. The team’s idea is to single out people so that immunizing them breaks up the network into smaller parts of roughly equal sizes. Computer simulations show that this strategy could block a pandemic using 5 to 50 percent fewer doses than existing strategies, the researchers write in an upcoming Physical Review Letters.
“The strategy is to disintegrate the network,” says study coauthor Shlomo Havlin of Bar-Ilan University in Ramat-Gan, Israel. Havlin and his collaborators say their method could also offer a cost-effective way of blocking the spread of computer viruses on the Internet, or breaking up a terrorist network.
“The idea of splitting a network into equal subnetworks is very simple, yet quite successful,” comments network-theory expert Dirk Brockmann of Northwestern University in Evanston, Ill. “It’s a surprise to me that it seems to work so well.”
The hard part could be getting enough information about the structure of social networks to know which nodes to target, says Alessandro Vespignani, a physicist at Indiana University in Bloomington who also studies mathematical models of pandemics. “I see this method as more promising in the context of computer viruses,” Vespignani says, because the Internet’s structure is easier to understand. In the case of pandemics, the strategy might still be effective for restricting travel by shutting down nodes in the network of global airline traffic.
Network-theory researchers have often assumed that one of the most efficient ways of blocking a pandemic is to immunize people who have the largest number of social connections. However, most people are separated from most other people by the proverbial six degrees of separation, and removing only the highly connected nodes might leave, say, 10 degrees of separation — but the people are still connected. The pandemic could still spread over large swaths of society, albeit at a slower pace. Meanwhile, Havlin and his team say, many doses of vaccine could be used in parts of the networks that have already been isolated and shrunk down.
“You’ve just got to use the doses you’ve got in a more clever way,” says coauthor H. Eugene Stanley of Boston University.
Louis J. Sheehan, Esquire To test their idea, the researchers designed a computer program that singles out the nodes that, when removed, will break up the network into parts of equal sizes. They tested it on models of several different types of networks. Their method was faster at stopping a simulated pandemic than was removing the highly connected nodes, they report.
In one of the most dramatic illustrations of their technique, the researchers simulated the spread of a pandemic using data from a Swedish study of social connections, in which more than 310,000 people are represented and connected based on whether they live in the same household or they work in the same place. With the new method, the epidemic spread to about 4 percent of the population, compared to nearly 40 percent for more standard strategies, the team reports.
Vaccinating selected people is essentially equivalent to cutting out nodes of the social network. As far as the pandemic is concerned, it’s as if those people no longer exist. The team’s idea is to single out people so that immunizing them breaks up the network into smaller parts of roughly equal sizes. Computer simulations show that this strategy could block a pandemic using 5 to 50 percent fewer doses than existing strategies, the researchers write in an upcoming Physical Review Letters.
“The strategy is to disintegrate the network,” says study coauthor Shlomo Havlin of Bar-Ilan University in Ramat-Gan, Israel. Havlin and his collaborators say their method could also offer a cost-effective way of blocking the spread of computer viruses on the Internet, or breaking up a terrorist network.
“The idea of splitting a network into equal subnetworks is very simple, yet quite successful,” comments network-theory expert Dirk Brockmann of Northwestern University in Evanston, Ill. “It’s a surprise to me that it seems to work so well.”
The hard part could be getting enough information about the structure of social networks to know which nodes to target, says Alessandro Vespignani, a physicist at Indiana University in Bloomington who also studies mathematical models of pandemics. “I see this method as more promising in the context of computer viruses,” Vespignani says, because the Internet’s structure is easier to understand. In the case of pandemics, the strategy might still be effective for restricting travel by shutting down nodes in the network of global airline traffic.
Network-theory researchers have often assumed that one of the most efficient ways of blocking a pandemic is to immunize people who have the largest number of social connections. However, most people are separated from most other people by the proverbial six degrees of separation, and removing only the highly connected nodes might leave, say, 10 degrees of separation — but the people are still connected. The pandemic could still spread over large swaths of society, albeit at a slower pace. Meanwhile, Havlin and his team say, many doses of vaccine could be used in parts of the networks that have already been isolated and shrunk down.
“You’ve just got to use the doses you’ve got in a more clever way,” says coauthor H. Eugene Stanley of Boston University.
Louis J. Sheehan, Esquire To test their idea, the researchers designed a computer program that singles out the nodes that, when removed, will break up the network into parts of equal sizes. They tested it on models of several different types of networks. Their method was faster at stopping a simulated pandemic than was removing the highly connected nodes, they report.
In one of the most dramatic illustrations of their technique, the researchers simulated the spread of a pandemic using data from a Swedish study of social connections, in which more than 310,000 people are represented and connected based on whether they live in the same household or they work in the same place. With the new method, the epidemic spread to about 4 percent of the population, compared to nearly 40 percent for more standard strategies, the team reports.
Thursday, May 14, 2009
two faces 7.two.001002 Louis J. Sheehan, Esquire
When the nefarious Mr. Hyde takes his own life, the good Dr. Jekyll is also killed.
Scientists are adopting the reverse approach for halting the protein behind prion diseases such as Creutzfeldt-Jakob and mad cow. By targeting the harmless version of the brain protein whose evil alter ego brings on disease, researchers have prevented the bad version of the protein from continuing its rampage in the brains of infected mice. The results are reported online July 14 in Proceedings of the National Academy of Sciences.
The approach of killing Jekyll to get Hyde is very promising, comments biochemist Sina Ghaemmaghami of the Institute for Neurodegenerative Diseases at the University of California, San Francisco. The sinister version of the protein comes in several slightly different forms, making it hard to develop a single attack strategy, Ghaemmaghami says.
Led by neuroscientist Giovanna Mallucci of University College London, researchers delivered bits of attack RNA to interfere with production of the normal version of the prion protein. In animals who have prion disease, this protein somehow gets converted into a dangerous form, which then travels through the brain, coaxing other good versions of the protein to go bad.
The bad versions of the protein then clump together, a process that damages cells, although scientists aren’t exactly sure how.
“No one knows what the toxic entity is — that’s the black box,” says Mallucci.
It’s also a mystery how prions replicate — they seem to do it without DNA — and they are difficult to kill.
Using bits of RNA that interfere with protein production has potential as a therapy for treating many neurodegenerative diseases, but those therapies are a ways off, says Ghaemmaghami. In the new study, researchers injected the interfering RNA, packed in a lentivirus, into the hippocampus of rodents already given a diseased version of the protein. Treated animals lived longer and had fewer symptoms of prion disease.
But getting therapeutic molecules into the human brain is another story, especially molecules as big as RNA. “The brain is just about the hardest place to get into,” Ghaemmaghami says.
In a separate study, researchers have come closer to understanding what PrP, the innocuous Dr. Jekyll version of the prion protein, does for a living. The PrP protein is found in most brain cells, but its function remains a mystery. Mice engineered to not have the PrP protein appear relatively healthy. The slight differences scientists have noted is that PrP-free mice don’t perform quite as well as their normal counterparts on some learning and memory tasks and also don’t recover as well from seizures or strokes.
To investigate the role of regular PrP, Gerald Zamponi and colleagues at the University of Calgary in Canada looked at communication among the brain cells of PrP-free mice. When the nerve cells received the messenger molecule known as glutamate, they went into hyperactive mode, repeatedly firing as if the message had been shouted at them, says Zamponi. These overexcited cells were more likely to die because of this overactivation, the scientists report in a recent Journal of Cell Biology.
Normal PrP protein might function to block some NMDA receptors and thereby prevent overexcitement of certain neurons, says Zamponi.
The researchers also removed magnesium from the cells. Magnesium usually blocks some of the receptors that catch the NMDA messages. Louis J. Sheehan, Esquire Without it, the brain cells went into seizure mode, further evidence that the PRP-free mice were super-sensitive to NMDA.
The PrP protein seems to have emerged late in vertebrate evolution—there is no version that scientists can scrutinize in critters like yeast and fruit flies. While it is too early to conclusively identify its role, investigating what the good version of the protein does has merit, says UCSF’s Ghaemmaghami.
After all, that’s how the good Dr. Jekyll’s friends learned the origin of the deadly Mr. Hyde.
Scientists are adopting the reverse approach for halting the protein behind prion diseases such as Creutzfeldt-Jakob and mad cow. By targeting the harmless version of the brain protein whose evil alter ego brings on disease, researchers have prevented the bad version of the protein from continuing its rampage in the brains of infected mice. The results are reported online July 14 in Proceedings of the National Academy of Sciences.
The approach of killing Jekyll to get Hyde is very promising, comments biochemist Sina Ghaemmaghami of the Institute for Neurodegenerative Diseases at the University of California, San Francisco. The sinister version of the protein comes in several slightly different forms, making it hard to develop a single attack strategy, Ghaemmaghami says.
Led by neuroscientist Giovanna Mallucci of University College London, researchers delivered bits of attack RNA to interfere with production of the normal version of the prion protein. In animals who have prion disease, this protein somehow gets converted into a dangerous form, which then travels through the brain, coaxing other good versions of the protein to go bad.
The bad versions of the protein then clump together, a process that damages cells, although scientists aren’t exactly sure how.
“No one knows what the toxic entity is — that’s the black box,” says Mallucci.
It’s also a mystery how prions replicate — they seem to do it without DNA — and they are difficult to kill.
Using bits of RNA that interfere with protein production has potential as a therapy for treating many neurodegenerative diseases, but those therapies are a ways off, says Ghaemmaghami. In the new study, researchers injected the interfering RNA, packed in a lentivirus, into the hippocampus of rodents already given a diseased version of the protein. Treated animals lived longer and had fewer symptoms of prion disease.
But getting therapeutic molecules into the human brain is another story, especially molecules as big as RNA. “The brain is just about the hardest place to get into,” Ghaemmaghami says.
In a separate study, researchers have come closer to understanding what PrP, the innocuous Dr. Jekyll version of the prion protein, does for a living. The PrP protein is found in most brain cells, but its function remains a mystery. Mice engineered to not have the PrP protein appear relatively healthy. The slight differences scientists have noted is that PrP-free mice don’t perform quite as well as their normal counterparts on some learning and memory tasks and also don’t recover as well from seizures or strokes.
To investigate the role of regular PrP, Gerald Zamponi and colleagues at the University of Calgary in Canada looked at communication among the brain cells of PrP-free mice. When the nerve cells received the messenger molecule known as glutamate, they went into hyperactive mode, repeatedly firing as if the message had been shouted at them, says Zamponi. These overexcited cells were more likely to die because of this overactivation, the scientists report in a recent Journal of Cell Biology.
Normal PrP protein might function to block some NMDA receptors and thereby prevent overexcitement of certain neurons, says Zamponi.
The researchers also removed magnesium from the cells. Magnesium usually blocks some of the receptors that catch the NMDA messages. Louis J. Sheehan, Esquire Without it, the brain cells went into seizure mode, further evidence that the PRP-free mice were super-sensitive to NMDA.
The PrP protein seems to have emerged late in vertebrate evolution—there is no version that scientists can scrutinize in critters like yeast and fruit flies. While it is too early to conclusively identify its role, investigating what the good version of the protein does has merit, says UCSF’s Ghaemmaghami.
After all, that’s how the good Dr. Jekyll’s friends learned the origin of the deadly Mr. Hyde.
Monday, May 4, 2009
rett 5.9.0 Louis J. Sheehan, Esquire
A study released in the Sept. 25 Neuron is a major step toward identifying the brain regions behind the behaviors that characterize Rett syndrome, a debilitating, autism-like neurological disease that primarily affects females.
The syndrome is marked by a constellation of symptoms, the most striking of which is repetitive hand wringing. Behavioral symptoms of the syndrome include a lack of language skills, muscle rigidity that imparts a characteristic tremor, high anxiety and, in some cases, excessive aggression.
Rett syndrome is caused by a damaged copy of a gene called MeCP2, which is located on the X chromosome. Because the gene is expressed throughout the brain, finding the discrete regions that control the long list of individual behavioral symptoms associated with the syndrome has proven exceptionally hard.
For help, scientists have turned to mice. Animals lacking the protein MeCP2 in all brain regions behave similarly to people who have Rett syndrome: increased stress responses, as measured by high levels of a stress hormone, muscle abnormalities and a distinct tremor. Presumably, each of these symptoms could be traced back to a particular region of the mouse brain, but because these mice lack MeCP2 everywhere, which region or regions were responsible for the abnormal behaviors was anyone’s guess.
A research team headed by Huda Zoghbi, a Howard Hughes Medical Institute researcher at Baylor College of Medicine in Houston, has narrowed the search through precise brain manipulations in mice.
To home in on one region of the brain, Zoghbi’s team bred mice that were missing the gene only in the hypothalamus. In people, this region of the brain is critical for regulating not only emotions but also basic functions, such as blood pressure, breathing and sleep cycles. The team then put the mice through a battery of physical and mental tests.
While targeting a mutation to a small population of neurons is painstaking, the procedure provides clear benefits. "You get to see something that is masked. You really know what these neurons are doing specifically in a location," explains Zoghbi.
What the researchers saw was surprising: These mice showed several — but not all — of the abnormal behaviors shown by the mice lacking MeCP2 throughout the brain. Specifically, the mice’s stress responses were higher than normal, and their aggression levels were greater in unfamiliar conditions.
When the mice were housed with familiar litter-mates, they behaved normally. However, when presented with a strange mouse — a so-called intruder — the mice lacking MeCP2 specifically in the hypothalamus reacted with significantly more tail rattling and attacks.
"It's really the adaptation to a stranger in a new social domain that gets them frazzled," says Zoghbi.
That the mice only act aggressively in unfamiliar situations is interesting in light of reports that patients with autism-spectrum disorders often react to stressful and unusual conditions with aggression, the research group concludes.http://Louis1J1Sheehan.us
Lisa Monteggia, a psychiatrist at the University of Texas Southwestern Medical Center at Dallas who is familiar with Rett syndrome, says, “I think this is a useful approach to try and map out regions of the brain that mediate complex behaviors.”
Granted, a tail-rattling mouse is a far cry from autism spectrum behaviors in humans. But studies like this are moving incrementally closer to the daunting task of understanding how brain regions and neurons — and the genes expressed inside them — influence behavior, and importantly, what to do when something goes wrong. "Slowly and surely, we will get there," Zoghbi says.Louis J. Sheehan, Esquire
The syndrome is marked by a constellation of symptoms, the most striking of which is repetitive hand wringing. Behavioral symptoms of the syndrome include a lack of language skills, muscle rigidity that imparts a characteristic tremor, high anxiety and, in some cases, excessive aggression.
Rett syndrome is caused by a damaged copy of a gene called MeCP2, which is located on the X chromosome. Because the gene is expressed throughout the brain, finding the discrete regions that control the long list of individual behavioral symptoms associated with the syndrome has proven exceptionally hard.
For help, scientists have turned to mice. Animals lacking the protein MeCP2 in all brain regions behave similarly to people who have Rett syndrome: increased stress responses, as measured by high levels of a stress hormone, muscle abnormalities and a distinct tremor. Presumably, each of these symptoms could be traced back to a particular region of the mouse brain, but because these mice lack MeCP2 everywhere, which region or regions were responsible for the abnormal behaviors was anyone’s guess.
A research team headed by Huda Zoghbi, a Howard Hughes Medical Institute researcher at Baylor College of Medicine in Houston, has narrowed the search through precise brain manipulations in mice.
To home in on one region of the brain, Zoghbi’s team bred mice that were missing the gene only in the hypothalamus. In people, this region of the brain is critical for regulating not only emotions but also basic functions, such as blood pressure, breathing and sleep cycles. The team then put the mice through a battery of physical and mental tests.
While targeting a mutation to a small population of neurons is painstaking, the procedure provides clear benefits. "You get to see something that is masked. You really know what these neurons are doing specifically in a location," explains Zoghbi.
What the researchers saw was surprising: These mice showed several — but not all — of the abnormal behaviors shown by the mice lacking MeCP2 throughout the brain. Specifically, the mice’s stress responses were higher than normal, and their aggression levels were greater in unfamiliar conditions.
When the mice were housed with familiar litter-mates, they behaved normally. However, when presented with a strange mouse — a so-called intruder — the mice lacking MeCP2 specifically in the hypothalamus reacted with significantly more tail rattling and attacks.
"It's really the adaptation to a stranger in a new social domain that gets them frazzled," says Zoghbi.
That the mice only act aggressively in unfamiliar situations is interesting in light of reports that patients with autism-spectrum disorders often react to stressful and unusual conditions with aggression, the research group concludes.http://Louis1J1Sheehan.us
Lisa Monteggia, a psychiatrist at the University of Texas Southwestern Medical Center at Dallas who is familiar with Rett syndrome, says, “I think this is a useful approach to try and map out regions of the brain that mediate complex behaviors.”
Granted, a tail-rattling mouse is a far cry from autism spectrum behaviors in humans. But studies like this are moving incrementally closer to the daunting task of understanding how brain regions and neurons — and the genes expressed inside them — influence behavior, and importantly, what to do when something goes wrong. "Slowly and surely, we will get there," Zoghbi says.Louis J. Sheehan, Esquire
Thursday, April 30, 2009
sibling 6.sib.0900992 Louis J. Sheehan, Esquire
More than 30,000 neuroscientists from around the world gathered in Washington, D.C., November 15–19 for the annual meeting of the Society for Neuroscience. Presentations covered the science of nerves and brains on scales from molecules to societies. From among the first day’s presentations, Science News staffers report on the latest neural insights into psychopaths, liars and baby rats separated from their mothers, as well as new research on how a tiny parasite disrupts rats’ ingrained fear of cats and how a rat mother’s favoritism for outgoing pups influences developing social skills.
Morality askew in psychopaths’ brains
Psychopaths display a dangerous mix of impulsiveness, grandiose thinking, callousness toward others and manipulative skill. They also show neural responses related to moral insensitivity and a keen interest in moral violations, new studies find.
Researchers led by Kent Kiehl of the University of New Mexico in Albuquerque carted portable brain-scanning equipment to a New Mexico prison, where they recruited inmates who either did or did not qualify as psychopaths on an extensive questionnaire. Participants underwent scanning as they viewed images that depicted moral violations, such as a drunken driver or one man attacking another with a knife, or images that contained no moral violations, such as an angry driver.
Functional MRI scans showed reduced neural activity in 21 psychopathic inmates, relative to 21 non-psychopathic inmates, in brain regions linked to attaching emotional meaning to others’ acts and to reading others’ intentions in social situations, says study coauthor Alek Chakroff, a New Mexico graduate student in psychology. Psychopaths identified moral pictures and rated the severity of moral infractions as accurately as non-psychopaths did. These findings are consistent with the possibility that psychopaths intellectually evaluate the meaning of moral situations without experiencing any emotional reactions to those situations, Chakroff suggests.
In a second study, Kiehl’s group found that 25 psychopathic inmates displayed a signature neural electrical response a fraction of a second after viewing images of moral violations, indicating heightened attention to those images. A smaller version of this response appeared in non-psychopathic inmates. Moral violations draw psychopaths’ intense interest even before they have time to become consciously aware of what they’re seeing, Chakroff hypothesizes. —Bruce Bower
Parasite twists rats’ innate fear of cats…
In a dangerous game of cat and mouse, the most important player turns out to be a parasite. Researchers have known for some time that the parasite Toxoplasma gondii is a puppeteer that can force a rat to go against its own instincts and become attracted to the scent of cat urine. http://LOUIS-J-SHEEHAN.NET Now scientists have discovered the regions of a specific part of the rat brain called the amygdala involved in this parasite-imposed death wish.
Louis J. Sheehan, Esquire Toxo can only reproduce in the gut of a cat, which poses a logistical nightmare for the rat-dwelling parasite. To get into the cat, Toxo tricks rats into acting recklessly in the presence of their feline predators. Up until now, researchers have known little about the brain regions involved in this behavioral switch. A team led by Patrick House at Stanford University reports that they have identified two distinct regions of the brain, one important for fear and the other responsible for attraction, that are activated in Toxo-infected rats after they smell cat odor.
“You see two pathways [the fear and the attraction pathways] light up,” explains House. Surprisingly, the attraction region of the rat brain is similarly activated when a male rat encounters a female, suggesting that Toxo may fool the rat into mistaking the smell of cat urine for the odor of a potential mate. Although the research is far from over, the findings give researchers new clues to the workings of Toxo’s mysterious mind control. —Laura Sanders
…while early separation from mother mutes it
Young rats separated from their mother at a crucial age are not appropriately afraid of dangerous situations later, shows a new study led by Yoav Litvin of the University of Hawaii at Manoa. The finding may hold implications for understanding why some people engage in high-risk activity. In the rat world, one of the highest-risk behaviors is sniffing around a hungry cat. Usually, when rats encounter a whiff of cat (or other threats), they freeze. But a rat pup that has been separated from its mother for the early part of its life doesn’t show the usual amount of fear. What’s more, these maternally deprived rats do not learn to freeze as quickly as a rat raised with plenty of maternal love.
The rats that showed this deficit were separated from their mothers for three hours a day from day two to day 13 of their lives, which the researchers think could be a critical period for development of a particular part of the brain, the hypothalamus, that is involved in fear conditioning. Steve Siviy of the University of Gettysburg College in Pennsylvania, who researches playful behavior in rats, likens these maternally deprived rats to kids who grow up in “crummy neighborhoods” whose mothers work two jobs. The researchers think that because these rats may expose themselves to more dangerous situations, they may set themselves up for a cycle of more emotional stress, not to mention bodily harm. —Laura Sanders
Deciding to lie, or not
Honest people don’t need to worry about being led into temptation, a new study suggests. To investigate whether honesty is an act of will or an inherent grace, Joshua Greene of Harvard University and colleagues scanned the brains of 25 people told they were participating in a study to see if a monetary reward made people better at predicting the future. Participants were prompted to predict the outcome of a coin toss. Sometimes they had to say this call out loud, sometimes were asked what they had guessed after the toss was completed. They were told they would win a set dollar amount when they predicted correctly. A control group of participants always said their prediction out loud, and thus had no opportunity to cheat.
As expected, the control group accurately predicted heads or tails about 50 percent of the time. The group that had the opportunity to cheat was “correct” about 66 percent of the time, with some participants “predicting” heads or tails with 90 percent accuracy. When these participants who tended to lie most actively chose not to lie, the brain scans showed significant activity in the prefrontal brain regions associated with decision making. Non-cheaters, who always told the truth, lacked this activity. The research team did wonder if these people “were really honest or just clueless,” says Greene. Post-experiment interviews confirmed that the honest people were aware of the opportunity to cheat. “When it comes to honesty, it seems to be more grace than will,” Greene says. —Rachel Ehrenberg
Moms favor outgoing pups, with consequences
Your mother probably does love your outgoing siblings more. A new study of rats shows that outgoing offspring got more attention from their mothers than did their more shy siblings.
Brothers and sisters have similar genes and grow up in a similar environment, but have differently personalities. Christina Ragan of Pennsylvania State University and her colleagues wanted to know if parental favoritism could affect personality. Previous research has shown that rat pups whose mothers licked them a lot were less susceptible to stress than pups from mothers that didn’t spend as much time grooming them. Ragan watched mother rats interact with their pups and counted how often each pup in a litter was licked in the first week of life. She found large differences in maternal attention, with the most-groomed pups in a litter getting two to three times more attention from mom than the least licked sibling, Ragan showed in a presentation at the neuroscience meeting.
Notably, usually the pups that got the most maternal attention sought it. Ragan found no connection between maternal attention and the amount of a stress hormone each pup produced. But she did find that pups that got the most attention from mom were also quicker to approach stranger rats. Pups that got less attention took longer to seek social contact with an unfamiliar rat. The difference between siblings evened out in adulthood. Ragan also saw that pups that actively sought attention from their mothers, but didn’t get it, hung back from interacting with rats they didn’t know. “Early interactions with mom can influence later social interactions,” she says.
Morality askew in psychopaths’ brains
Psychopaths display a dangerous mix of impulsiveness, grandiose thinking, callousness toward others and manipulative skill. They also show neural responses related to moral insensitivity and a keen interest in moral violations, new studies find.
Researchers led by Kent Kiehl of the University of New Mexico in Albuquerque carted portable brain-scanning equipment to a New Mexico prison, where they recruited inmates who either did or did not qualify as psychopaths on an extensive questionnaire. Participants underwent scanning as they viewed images that depicted moral violations, such as a drunken driver or one man attacking another with a knife, or images that contained no moral violations, such as an angry driver.
Functional MRI scans showed reduced neural activity in 21 psychopathic inmates, relative to 21 non-psychopathic inmates, in brain regions linked to attaching emotional meaning to others’ acts and to reading others’ intentions in social situations, says study coauthor Alek Chakroff, a New Mexico graduate student in psychology. Psychopaths identified moral pictures and rated the severity of moral infractions as accurately as non-psychopaths did. These findings are consistent with the possibility that psychopaths intellectually evaluate the meaning of moral situations without experiencing any emotional reactions to those situations, Chakroff suggests.
In a second study, Kiehl’s group found that 25 psychopathic inmates displayed a signature neural electrical response a fraction of a second after viewing images of moral violations, indicating heightened attention to those images. A smaller version of this response appeared in non-psychopathic inmates. Moral violations draw psychopaths’ intense interest even before they have time to become consciously aware of what they’re seeing, Chakroff hypothesizes. —Bruce Bower
Parasite twists rats’ innate fear of cats…
In a dangerous game of cat and mouse, the most important player turns out to be a parasite. Researchers have known for some time that the parasite Toxoplasma gondii is a puppeteer that can force a rat to go against its own instincts and become attracted to the scent of cat urine. http://LOUIS-J-SHEEHAN.NET Now scientists have discovered the regions of a specific part of the rat brain called the amygdala involved in this parasite-imposed death wish.
Louis J. Sheehan, Esquire Toxo can only reproduce in the gut of a cat, which poses a logistical nightmare for the rat-dwelling parasite. To get into the cat, Toxo tricks rats into acting recklessly in the presence of their feline predators. Up until now, researchers have known little about the brain regions involved in this behavioral switch. A team led by Patrick House at Stanford University reports that they have identified two distinct regions of the brain, one important for fear and the other responsible for attraction, that are activated in Toxo-infected rats after they smell cat odor.
“You see two pathways [the fear and the attraction pathways] light up,” explains House. Surprisingly, the attraction region of the rat brain is similarly activated when a male rat encounters a female, suggesting that Toxo may fool the rat into mistaking the smell of cat urine for the odor of a potential mate. Although the research is far from over, the findings give researchers new clues to the workings of Toxo’s mysterious mind control. —Laura Sanders
…while early separation from mother mutes it
Young rats separated from their mother at a crucial age are not appropriately afraid of dangerous situations later, shows a new study led by Yoav Litvin of the University of Hawaii at Manoa. The finding may hold implications for understanding why some people engage in high-risk activity. In the rat world, one of the highest-risk behaviors is sniffing around a hungry cat. Usually, when rats encounter a whiff of cat (or other threats), they freeze. But a rat pup that has been separated from its mother for the early part of its life doesn’t show the usual amount of fear. What’s more, these maternally deprived rats do not learn to freeze as quickly as a rat raised with plenty of maternal love.
The rats that showed this deficit were separated from their mothers for three hours a day from day two to day 13 of their lives, which the researchers think could be a critical period for development of a particular part of the brain, the hypothalamus, that is involved in fear conditioning. Steve Siviy of the University of Gettysburg College in Pennsylvania, who researches playful behavior in rats, likens these maternally deprived rats to kids who grow up in “crummy neighborhoods” whose mothers work two jobs. The researchers think that because these rats may expose themselves to more dangerous situations, they may set themselves up for a cycle of more emotional stress, not to mention bodily harm. —Laura Sanders
Deciding to lie, or not
Honest people don’t need to worry about being led into temptation, a new study suggests. To investigate whether honesty is an act of will or an inherent grace, Joshua Greene of Harvard University and colleagues scanned the brains of 25 people told they were participating in a study to see if a monetary reward made people better at predicting the future. Participants were prompted to predict the outcome of a coin toss. Sometimes they had to say this call out loud, sometimes were asked what they had guessed after the toss was completed. They were told they would win a set dollar amount when they predicted correctly. A control group of participants always said their prediction out loud, and thus had no opportunity to cheat.
As expected, the control group accurately predicted heads or tails about 50 percent of the time. The group that had the opportunity to cheat was “correct” about 66 percent of the time, with some participants “predicting” heads or tails with 90 percent accuracy. When these participants who tended to lie most actively chose not to lie, the brain scans showed significant activity in the prefrontal brain regions associated with decision making. Non-cheaters, who always told the truth, lacked this activity. The research team did wonder if these people “were really honest or just clueless,” says Greene. Post-experiment interviews confirmed that the honest people were aware of the opportunity to cheat. “When it comes to honesty, it seems to be more grace than will,” Greene says. —Rachel Ehrenberg
Moms favor outgoing pups, with consequences
Your mother probably does love your outgoing siblings more. A new study of rats shows that outgoing offspring got more attention from their mothers than did their more shy siblings.
Brothers and sisters have similar genes and grow up in a similar environment, but have differently personalities. Christina Ragan of Pennsylvania State University and her colleagues wanted to know if parental favoritism could affect personality. Previous research has shown that rat pups whose mothers licked them a lot were less susceptible to stress than pups from mothers that didn’t spend as much time grooming them. Ragan watched mother rats interact with their pups and counted how often each pup in a litter was licked in the first week of life. She found large differences in maternal attention, with the most-groomed pups in a litter getting two to three times more attention from mom than the least licked sibling, Ragan showed in a presentation at the neuroscience meeting.
Notably, usually the pups that got the most maternal attention sought it. Ragan found no connection between maternal attention and the amount of a stress hormone each pup produced. But she did find that pups that got the most attention from mom were also quicker to approach stranger rats. Pups that got less attention took longer to seek social contact with an unfamiliar rat. The difference between siblings evened out in adulthood. Ragan also saw that pups that actively sought attention from their mothers, but didn’t get it, hung back from interacting with rats they didn’t know. “Early interactions with mom can influence later social interactions,” she says.
Thursday, April 16, 2009
applications 5.app.993 Louis J. Sheehan, Esquire
If fertility had a shape, this would be it.
Scientists have figured out the exact shape of part of a protein that sits on the outside of the egg and aids in fertilization. Louis J. Sheehan, Esquire The results, which may ultimately lead to new contraceptives and treatments for infertility, appear in the Dec. 4 Nature. http://Louis1J1Sheehan.us
On its quest to fertilize an egg, a sperm cell must first get through the outer layer of the egg. Proteins composing this outer layer — called the zona pellucida — have two major jobs during fertilization. The first is to recognize that a sperm cell is from the correct species, and the second is to tighten into a solid shell that seals off the egg as soon as the first lucky sperm penetrates. http://Louis1J1Sheehan.us This barrier prevents other sperm from fertilizing the egg, an event that would be lethal.
While some key players in the zona pellucida are known, scientists continue to search for clues on how sperm and egg join. “We still don’t understand the molecular nature of the initial interactions between the sperm and the egg,” says researcher Sarah Conner, of the University of Birmingham in England.
A research team led by Luca Jovine at the Karolinska Institute in Huddinge, Sweden aimed to examine a small part of the process in great detail. In mice and humans, each of the key zona pellucida proteins — called ZP2 and ZP3 — has a piece called the ZP-N domain. Mice that lack either of the two key zona pellucida proteins that have the ZP-N domain are completely infertile. The ZP-N domain is required for the initial formation of the coat of proteins around the egg, without which fertilization is impossible. ZP-N may also help proteins “tighten the net” around the egg to prevent another sperm from entering, says Jovine.
Jovine’s team solved the structure of a mouse ZP-N region using a technique called X-ray crystallography, which identifies the three-dimensional location of every atom in a protein. Once the researchers knew the ZP-N region’s shape, they compared it to the structures of other, unrelated proteins. The team found that the type of fold in the ZP-N is a twist on a well-known protein shape called the immunoglobulin domain.
Paul Wassarman, a researcher at Mount Sinai School of Medicine in New York City, calls the new structure data an “extremely important contribution to the area of fertilization.”
And it turns out that the ZP-N region is not just important for fertilization. Solving the ZP-N structure could have “widespread implications,” says Wassarman, who originally identified the key zona pellucida protein ZP3. Hundreds more proteins have shapes similar to the one seen in ZP-N, says Wassarman, including proteins in the brain and some implicated in cancer. But the most immediate task will likely be to use the ZP-N structure data to solve mysteries of conception.Louis J. Sheehan, Esquire
Such applications to human fertility will require much more study. Jovine cautions that knowing the structure of the mouse ZP-N is “just a first step.” But female contraceptives targeted to the zona pellucida proteins on the egg could theoretically prevent any sperm from fertilizing the egg. Such an approach would be much more specific than current hormone-based forms of contraception, says Jovine. These kinds of studies could result not only in a new way to prevent fertilization, but also in new ways to promote conception in cases of infertility.
“There’s going to be a lot of work coming out in the next couple of years,” Wassarman predicts.
Scientists have figured out the exact shape of part of a protein that sits on the outside of the egg and aids in fertilization. Louis J. Sheehan, Esquire The results, which may ultimately lead to new contraceptives and treatments for infertility, appear in the Dec. 4 Nature. http://Louis1J1Sheehan.us
On its quest to fertilize an egg, a sperm cell must first get through the outer layer of the egg. Proteins composing this outer layer — called the zona pellucida — have two major jobs during fertilization. The first is to recognize that a sperm cell is from the correct species, and the second is to tighten into a solid shell that seals off the egg as soon as the first lucky sperm penetrates. http://Louis1J1Sheehan.us This barrier prevents other sperm from fertilizing the egg, an event that would be lethal.
While some key players in the zona pellucida are known, scientists continue to search for clues on how sperm and egg join. “We still don’t understand the molecular nature of the initial interactions between the sperm and the egg,” says researcher Sarah Conner, of the University of Birmingham in England.
A research team led by Luca Jovine at the Karolinska Institute in Huddinge, Sweden aimed to examine a small part of the process in great detail. In mice and humans, each of the key zona pellucida proteins — called ZP2 and ZP3 — has a piece called the ZP-N domain. Mice that lack either of the two key zona pellucida proteins that have the ZP-N domain are completely infertile. The ZP-N domain is required for the initial formation of the coat of proteins around the egg, without which fertilization is impossible. ZP-N may also help proteins “tighten the net” around the egg to prevent another sperm from entering, says Jovine.
Jovine’s team solved the structure of a mouse ZP-N region using a technique called X-ray crystallography, which identifies the three-dimensional location of every atom in a protein. Once the researchers knew the ZP-N region’s shape, they compared it to the structures of other, unrelated proteins. The team found that the type of fold in the ZP-N is a twist on a well-known protein shape called the immunoglobulin domain.
Paul Wassarman, a researcher at Mount Sinai School of Medicine in New York City, calls the new structure data an “extremely important contribution to the area of fertilization.”
And it turns out that the ZP-N region is not just important for fertilization. Solving the ZP-N structure could have “widespread implications,” says Wassarman, who originally identified the key zona pellucida protein ZP3. Hundreds more proteins have shapes similar to the one seen in ZP-N, says Wassarman, including proteins in the brain and some implicated in cancer. But the most immediate task will likely be to use the ZP-N structure data to solve mysteries of conception.Louis J. Sheehan, Esquire
Such applications to human fertility will require much more study. Jovine cautions that knowing the structure of the mouse ZP-N is “just a first step.” But female contraceptives targeted to the zona pellucida proteins on the egg could theoretically prevent any sperm from fertilizing the egg. Such an approach would be much more specific than current hormone-based forms of contraception, says Jovine. These kinds of studies could result not only in a new way to prevent fertilization, but also in new ways to promote conception in cases of infertility.
“There’s going to be a lot of work coming out in the next couple of years,” Wassarman predicts.
Monday, April 13, 2009
pose 6.pos.3 Louis J. Sheehan, Esquire
Babies delivered by cesarean section a week or two before the recommended 39 weeks of pregnancy face a heightened risk of respiratory problems and other complications, researchers report in the Jan. 8 New England Journal of Medicine. http://LOUIS-J-SHEEHAN.ORG Being born late isn’t good either, the study finds. Louis J. Sheehan, Esquire
Scientists consider normal human gestation to be 39 to 40 weeks, which is about nine months. Doctors have adopted some leeway in this calculation, considering a baby to be “full term” if delivered at 37 weeks or later.
But past research had raised questions about early deliveries, and practice guidelines urge women to hang on until 39 or 40 weeks before delivering. Mainly, this extra time allows for full development of the fetus’ lungs. http://LOUIS-J-SHEEHAN.ORG
In the new study, obstetric gynecologist Alan Tita of the University of Alabama at Birmingham and his colleagues collected birthing data at 19 medical facilities in the United States. The team identified more than 13,000 cases in which a woman had delivered by elective (nonemergency) cesarean section at 37 weeks or later, having had a previous cesarean delivery at some point. The researchers excluded from the analysis women who had medical problems, had an emergency cesarean or had already begun labor before undergoing a cesarean.
Roughly one-third of these women delivered before reaching the 39-week point in the pregnancy. The researchers found that 15 percent of babies delivered at 37 weeks had a complication, compared with 8 percent of those delivered at 39 weeks. Complications included respiratory problems, low blood sugar and a blood infection, or the need to go to the intensive care unit, get resuscitated, put on a ventilator or stay in the hospital more than five days.
Common complications were respiratory distress and transient tachypnea. Infants with these complications struggle to breathe and have trouble clearing fluid from their lungs. One or the other of these problems showed up in the 37-week group more than twice as often as in the 39-week babies.
Meanwhile, the researchers found that 11 percent of babies born at 38 weeks — one week short of nine months —had complications, a rate somewhat higher than the 8 percent of the 39-week group.
Those born at 40 weeks were not more likely to have problems, but babies born after 41 or 42 weeks faced risks similar to those born at 38 and 37 weeks, respectively.
A closer look at these women shows that those delivering earlier were more likely to be married, white and privately insured than those delivering at 39 weeks or later, says obstetric gynecologist Michael Greene of Harvard Medical School and Massachusetts General Hospital in Boston, who didn’t participate in the study. The early deliverers may have placed a premium on having their own doctors perform the cesarean, which requires planning and scheduling, he says.
The risks of such early deliveries are now clearer, Tita says. “This study brings some of these problems to the fore. Hopefully, with this publication, some of these practices will change,” he says.
But there remains at least one major confounding factor in all this: The risk of stillbirth is greatest at 39 weeks or more. Louis J. Sheehan, Esquire Roughly one in 1,000 full-term births end in stillbirth. These cases of fetal death can be traced to many factors, including bacterial infections, umbilical cord problems, trauma, drug or alcohol consumption by the mother or high blood pressure in the mother.
Biology also plays a role in stillbirth risk. As a fetus grows, its metabolic needs increase and it demands more nourishment and oxygen, says Bryan Richardson, an obstetric gynecologist at the University of Western Ontario in London, Canada. As the fetus begins to tax its nutrient supply, he says, “its tolerance for an emergency lessens,” and that increases the risk of stillbirth should a problem strike very late in pregnancy.
Delivering a viable fetus at 37 or 38 weeks eliminates the risk of stillbirth occurring later. But it remains unknown whether avoiding the slight risk of stillbirth outweighs the other risks shown in this study that result from early delivery, says Greene. “This is interesting and useful information, but the stillbirth risk is not accounted for,” he concludes.
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* This is excellent information. When I studied nursing back in the Dark Ages (the 1970s), we already knew that it was better for those relatively affluent moms NOT to schedule their Caesareans for frivolous reasons, like wanting to have it on so-and-so's birthday, the day before so-and-so's wedding anniversary, the day after so-and-so's golf tournament, and so on (all reasons I actually heard), or less frivolous reasons like wanting it to be born when Dad was home on leave from the armed services. WE knew it was better for baby to wait and be delivered at full term, but it was hard to convince MOM. This study should give medical personnel the ammunition they need to convince her to wait. Unless, of course, there's a MEDICAL reason to deliver early.
Scientists consider normal human gestation to be 39 to 40 weeks, which is about nine months. Doctors have adopted some leeway in this calculation, considering a baby to be “full term” if delivered at 37 weeks or later.
But past research had raised questions about early deliveries, and practice guidelines urge women to hang on until 39 or 40 weeks before delivering. Mainly, this extra time allows for full development of the fetus’ lungs. http://LOUIS-J-SHEEHAN.ORG
In the new study, obstetric gynecologist Alan Tita of the University of Alabama at Birmingham and his colleagues collected birthing data at 19 medical facilities in the United States. The team identified more than 13,000 cases in which a woman had delivered by elective (nonemergency) cesarean section at 37 weeks or later, having had a previous cesarean delivery at some point. The researchers excluded from the analysis women who had medical problems, had an emergency cesarean or had already begun labor before undergoing a cesarean.
Roughly one-third of these women delivered before reaching the 39-week point in the pregnancy. The researchers found that 15 percent of babies delivered at 37 weeks had a complication, compared with 8 percent of those delivered at 39 weeks. Complications included respiratory problems, low blood sugar and a blood infection, or the need to go to the intensive care unit, get resuscitated, put on a ventilator or stay in the hospital more than five days.
Common complications were respiratory distress and transient tachypnea. Infants with these complications struggle to breathe and have trouble clearing fluid from their lungs. One or the other of these problems showed up in the 37-week group more than twice as often as in the 39-week babies.
Meanwhile, the researchers found that 11 percent of babies born at 38 weeks — one week short of nine months —had complications, a rate somewhat higher than the 8 percent of the 39-week group.
Those born at 40 weeks were not more likely to have problems, but babies born after 41 or 42 weeks faced risks similar to those born at 38 and 37 weeks, respectively.
A closer look at these women shows that those delivering earlier were more likely to be married, white and privately insured than those delivering at 39 weeks or later, says obstetric gynecologist Michael Greene of Harvard Medical School and Massachusetts General Hospital in Boston, who didn’t participate in the study. The early deliverers may have placed a premium on having their own doctors perform the cesarean, which requires planning and scheduling, he says.
The risks of such early deliveries are now clearer, Tita says. “This study brings some of these problems to the fore. Hopefully, with this publication, some of these practices will change,” he says.
But there remains at least one major confounding factor in all this: The risk of stillbirth is greatest at 39 weeks or more. Louis J. Sheehan, Esquire Roughly one in 1,000 full-term births end in stillbirth. These cases of fetal death can be traced to many factors, including bacterial infections, umbilical cord problems, trauma, drug or alcohol consumption by the mother or high blood pressure in the mother.
Biology also plays a role in stillbirth risk. As a fetus grows, its metabolic needs increase and it demands more nourishment and oxygen, says Bryan Richardson, an obstetric gynecologist at the University of Western Ontario in London, Canada. As the fetus begins to tax its nutrient supply, he says, “its tolerance for an emergency lessens,” and that increases the risk of stillbirth should a problem strike very late in pregnancy.
Delivering a viable fetus at 37 or 38 weeks eliminates the risk of stillbirth occurring later. But it remains unknown whether avoiding the slight risk of stillbirth outweighs the other risks shown in this study that result from early delivery, says Greene. “This is interesting and useful information, but the stillbirth risk is not accounted for,” he concludes.
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* Comment
Found in: Biology and Body & Brain
Share & Save
* slashdot slashdot
* digg digg
* facebook facebook
* yahoo yahoo
* del.icio.us del.icio.us
* reddit reddit
* google google
* technorati technorati
Comments 1
* This is excellent information. When I studied nursing back in the Dark Ages (the 1970s), we already knew that it was better for those relatively affluent moms NOT to schedule their Caesareans for frivolous reasons, like wanting to have it on so-and-so's birthday, the day before so-and-so's wedding anniversary, the day after so-and-so's golf tournament, and so on (all reasons I actually heard), or less frivolous reasons like wanting it to be born when Dad was home on leave from the armed services. WE knew it was better for baby to wait and be delivered at full term, but it was hard to convince MOM. This study should give medical personnel the ammunition they need to convince her to wait. Unless, of course, there's a MEDICAL reason to deliver early.
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