Synopsis
Cartman finds a strange, yet annoying, creature in the woods. The boys get Jimbo and Ned to capture it, and they show it to the rest of South Park. It is determined that it is a Jakovasaur -- a species long thought to be extinct. The creature's mate arrives and Mephesto helps them reproduce, creating a multitude of little, annoying, loud creatures. Everybody in South Park, except Cartman, despises the creatures and go to various lengths to get rid of them.
Full Recap
The boys are camping at Stark's Pond. Cartman performs his new song "I Hate You Guys". Cartman leaves to go to the bathroom and sees something moving in the trees. Uncle Jimbo and Ned are at home, where Ned is looking for his voice box. The boys stop by to ask for their help tracking the creature that Cartman discovered. They find the creature in Uncle Jimbo's ostrich trap. Jimbo is going to kill it, but Cartman likes it and asks that it be spared. The Department of Interior comes to South Park to take possession of what they identified as a Jakovasaur. They have the idea that they are going to breed it and bring back the species. Another Jakovasaur arrives at Cartman's door, asking for help to find his mate Ju-Ju. Named Jakov, he says that he and his mate are the last of their kind. Cartman agrees to help and while the other boys find Jakov annoying; Cartman finds his klutzy antics amusing. They reunite the pair, but the government finds out.
Ned gets a replacement for his voice box, which makes him sound Irish. The Department of the Interior has plans to help the Jakovasaurs mate and repopulate the species. Left on their own, the Jakovasaurs fail to mate, Jakov doesn't know what to do. Since there is no one with experience in the matters, they all go to the South Park Genetic Engineering ranch, where Dr. Mephisto plans to use artificial insemination. Stan wonders if they really want anymore of these things around. Jakov tries to be one of the guys, but only succeeds in being really annoying.
The pregnant Jakovasaur gives birth in four days, by shooting out a large litter of children. The new children join the children at South Park Elementary. The Mayor and townsfolk try to figure out what to do about the Jakovasaur problem. They convince them to move to Memphis, but Cartman pleads for them to stay. The Department of Interior bails on South Park, but they leave Cartman with the "authoritah" to control all the wildlife issues surrounding South Park.
The Jakovasaurs are shown at home, sitcom Jakov is invited by the mayor to appear on a game show to win a trip. Cartman agrees to help prepare him for show. The mayor asks the boys to distract Cartman, while Jakov is appearing on the show. Jakov competes against Officer Barbrady and he immediately starts losing. Meanwhile, Stan and Kyle have brought Cartman out to the woods to fy a new species, which Cartman readily identifies as Kenny with a pair of antlers attached to his head. The mayor forces Jakov into victory, which gives him and his family an all-expense paid one way trip to France. With the Jakovasaurs on their way to France, the town celebrates by getting ice cream. Later in France, the people there are delighted by the Jerry Lewis-like antics of Jakov and his family.
Kenny dies when a bear attacks him, while he was trying to help Kyle and Stan distract Cartman.
Tuesday, June 30, 2009
Wednesday, May 20, 2009
calorie-restricted 4.ted.00030034 Louis J. Sheehan, Esquire
Eating a calorie-restricted diet and being female are the best bets for living longer, at least for animals. Now scientists have discovered that some links may exist between the two.
Women live about five years longer on average than men, and a similar longevity advantage exists for other mammal species, including rats. Numerous experiments have also shown that eating a nutritionally complete diet relatively low in calories can also extend lifespan: A daily calorie decrease of 30 percent correlates to living 30 to 50 percent longer than normal for all animal species tested thus far, including mice and dogs.
To find out whether these two scenarios for longer life share common molecular mechanisms, Adamo Valle of University of the Balearic Islands in Spain and his colleagues compared male and female rats. Each gender group was separated into two groups, one fed a normal diet and the other fed a calorie-restricted diet. Valle’s team then compared the activity levels of hundreds of proteins in the animals’ livers, which help to regulate energy metabolism.
Among these proteins, 11 had different activity levels in both cases — when comparing females with males and when comparing the groups on normal or calorie-restricted diets, the team reports online and in an upcoming Journal of Proteome Research. Valle and his colleagues say it makes sense that these 11 proteins might affect longevity since they play roles in energy metabolism, antioxidant mechanisms, stress response and cardiovascular protection. Most of these proteins had not been identified in previous studies of calorie restriction and longevity.
The differences in the calorie-restricted males mimicked the pattern seen in females on a normal diet, the scientists report.
It’s the first time that scientists have found similarities between the longevity effects of gender and calorie restriction, but some scientists say that common ground is understandable.
“It doesn’t surprise me at all,” comments Peter DiStefano, chief scientific officer for Elixir Pharmaceuticals, a biotech company in Cambridge, Mass., developing diabetes drugs based on calorie-restriction research. DiStefano speculates that estrogen might cause some of these effects through the hormone’s action on the hypothalamus, a region of the brain that controls many aspects of feeding behavior and energy metabolism.Louis J. Sheehan, Esquire
Women live about five years longer on average than men, and a similar longevity advantage exists for other mammal species, including rats. Numerous experiments have also shown that eating a nutritionally complete diet relatively low in calories can also extend lifespan: A daily calorie decrease of 30 percent correlates to living 30 to 50 percent longer than normal for all animal species tested thus far, including mice and dogs.
To find out whether these two scenarios for longer life share common molecular mechanisms, Adamo Valle of University of the Balearic Islands in Spain and his colleagues compared male and female rats. Each gender group was separated into two groups, one fed a normal diet and the other fed a calorie-restricted diet. Valle’s team then compared the activity levels of hundreds of proteins in the animals’ livers, which help to regulate energy metabolism.
Among these proteins, 11 had different activity levels in both cases — when comparing females with males and when comparing the groups on normal or calorie-restricted diets, the team reports online and in an upcoming Journal of Proteome Research. Valle and his colleagues say it makes sense that these 11 proteins might affect longevity since they play roles in energy metabolism, antioxidant mechanisms, stress response and cardiovascular protection. Most of these proteins had not been identified in previous studies of calorie restriction and longevity.
The differences in the calorie-restricted males mimicked the pattern seen in females on a normal diet, the scientists report.
It’s the first time that scientists have found similarities between the longevity effects of gender and calorie restriction, but some scientists say that common ground is understandable.
“It doesn’t surprise me at all,” comments Peter DiStefano, chief scientific officer for Elixir Pharmaceuticals, a biotech company in Cambridge, Mass., developing diabetes drugs based on calorie-restriction research. DiStefano speculates that estrogen might cause some of these effects through the hormone’s action on the hypothalamus, a region of the brain that controls many aspects of feeding behavior and energy metabolism.Louis J. Sheehan, Esquire
Tuesday, May 5, 2009
a-beta 9.yt.0 Louis J. Sheehan, Esquire
Amyloid-beta is a thinking brain’s protein. A new study involving people with severe brain injuries shows that as neuronal activity increases, levels of amyloid-beta in the brain also go up.
Louis J. Sheehan, Esquire A-beta, as the protein is sometimes called, is best known for causing plaques in the brains of people with Alzheimer’s disease. It is a normal component of the brain, but scientists don’t know what it does.
Traumatic brain injuries increase the risk for Alzheimer’s disease. So to find out if brain injuries cause a spike in amyloid-beta levels that could lead to plaque formation, a team of researchers from Milan, Italy, and Washington University in St. Louis sampled fluid from the brains of 18 comatose patients. http://LOUIS-J-SHEEHAN.US
The researchers inserted devices in the patients’ brains to monitor pressure. A small catheter sipped up fluid that gathers between brain cells, and then the researchers tested the fluid for A-beta.
What the researchers found was exactly the opposite of what they expected, says David L. Brody, a neurologist at Washington University who led the study with Sandra Magnoni of the Ospedale Maggiore in Milan. Instead of seeing a spike of A-beta soon after brain injury from falls, car accidents, assaults or hemorrhages, levels of the protein started low and rose as the patients improved, the team reports in the Aug. 29 Science.
“This is a fantastic study using an extraordinarily powerful technique to study human physiology and pathophysiology,” says Bradley Hyman, director of the Alzheimer’s Disease Research Center at Massachusetts General Hospital and Harvard Medical School in Boston. “While the implications for a ‘normal’ function of A-beta are intriguing, it is still not completely clear whether the data reflect an active role for A-beta or simply establish that it is a marker for neuronal activity. Sorting this out will be fascinating.”
The results are consistent with previous studies in mice that show that A-beta is a byproduct of brain cell activity, and with studies in people that show the areas of the brain that are most active are the most prone to developing Alzheimer’s plaques, says John Cirrito, a neuroscientist at Washington University who established the link between brain cell activity and A-beta in mice but was not involved in the new study. A-beta may become a tool for monitoring brain activity in comatose patients, Cirrito suggests.
But the findings seem to contrast with preliminary results from a similar study in Sweden. Neurologist Lars Hillered at Uppsala University Hospital sampled brain fluid from eight comatose patients and found that people with diffuse brain injuries had higher levels of amyloid-beta in their brains.
“It could be that we’re onto something similar,” Hillered says. Electrical activity in brain cells and damage to cells may both raise levels of A-beta, he says.
Fluid taken by spinal tap doesn’t show the link between A-beta levels and brain activity. That is probably because the brain fluid the researchers sampled for the study came directly from the space between brain cells, while cerebral spinal fluid contains proteins filtered from blood as well as from the brain, Brody says.
Researchers still don’t know why brain injury puts people at higher risk for Alzheimer’s disease or what the protein’s normal job is in the brain.
“This study raises more questions than it answers,” Brody says. “It’s really just the beginning.”
Louis J. Sheehan, Esquire A-beta, as the protein is sometimes called, is best known for causing plaques in the brains of people with Alzheimer’s disease. It is a normal component of the brain, but scientists don’t know what it does.
Traumatic brain injuries increase the risk for Alzheimer’s disease. So to find out if brain injuries cause a spike in amyloid-beta levels that could lead to plaque formation, a team of researchers from Milan, Italy, and Washington University in St. Louis sampled fluid from the brains of 18 comatose patients. http://LOUIS-J-SHEEHAN.US
The researchers inserted devices in the patients’ brains to monitor pressure. A small catheter sipped up fluid that gathers between brain cells, and then the researchers tested the fluid for A-beta.
What the researchers found was exactly the opposite of what they expected, says David L. Brody, a neurologist at Washington University who led the study with Sandra Magnoni of the Ospedale Maggiore in Milan. Instead of seeing a spike of A-beta soon after brain injury from falls, car accidents, assaults or hemorrhages, levels of the protein started low and rose as the patients improved, the team reports in the Aug. 29 Science.
“This is a fantastic study using an extraordinarily powerful technique to study human physiology and pathophysiology,” says Bradley Hyman, director of the Alzheimer’s Disease Research Center at Massachusetts General Hospital and Harvard Medical School in Boston. “While the implications for a ‘normal’ function of A-beta are intriguing, it is still not completely clear whether the data reflect an active role for A-beta or simply establish that it is a marker for neuronal activity. Sorting this out will be fascinating.”
The results are consistent with previous studies in mice that show that A-beta is a byproduct of brain cell activity, and with studies in people that show the areas of the brain that are most active are the most prone to developing Alzheimer’s plaques, says John Cirrito, a neuroscientist at Washington University who established the link between brain cell activity and A-beta in mice but was not involved in the new study. A-beta may become a tool for monitoring brain activity in comatose patients, Cirrito suggests.
But the findings seem to contrast with preliminary results from a similar study in Sweden. Neurologist Lars Hillered at Uppsala University Hospital sampled brain fluid from eight comatose patients and found that people with diffuse brain injuries had higher levels of amyloid-beta in their brains.
“It could be that we’re onto something similar,” Hillered says. Electrical activity in brain cells and damage to cells may both raise levels of A-beta, he says.
Fluid taken by spinal tap doesn’t show the link between A-beta levels and brain activity. That is probably because the brain fluid the researchers sampled for the study came directly from the space between brain cells, while cerebral spinal fluid contains proteins filtered from blood as well as from the brain, Brody says.
Researchers still don’t know why brain injury puts people at higher risk for Alzheimer’s disease or what the protein’s normal job is in the brain.
“This study raises more questions than it answers,” Brody says. “It’s really just the beginning.”
Friday, May 1, 2009
time 0.tim.332187 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire For the first time, a complete cancer genome, and incidentally a complete female genome, has been decoded, scientists report online Nov. 5 in Nature. In a study made possible by faster, cheaper and more sensitive methods for sequencing DNA, the researchers pinpoint eight new genes that may cause a cell to turn cancerous.
“Since cancer is a disease of the genome, this newfound ability to determine the complete DNA sequence of a cancer cell is enormously powerful,” comments Francis Collins, a geneticist and former director of the National Human Genome Research Institute in Bethesda, Md., a group that raced to sequence the first entire human genome. http://Louis-J-Sheehan.biz
“We need to know the genetic rules of cancer,” says coauthor Timothy Ley of Washington University in St. Louis. Ley and colleagues read each of the 3 billion building blocks of DNA from tumor cells in a woman with acute myeloid leukemia, or AML, a highly malignant form of blood and bone marrow cancer. Then the team compared the long string of code with one taken from noncancerous skin cells from the same woman.
This new sequencing technology, called massively parallel sequencing, makes it possible to compare the normal DNA sequence to the cancerous DNA sequence in the same patient. That, in turn, allows researchers to find individual DNA bases — the needles in a haystack of 3 billion pieces of straw — that had mutated in the cancerous cells.
Kevin Shannon, director of the Medical Scientist Training Program at the University of California, San Francisco, studies the genes that may lead to leukemia and calls this work “a major achievement,” one that is “remarkable for its rigor and precision.”
None of the researchers knew what to expect for the number of mutated genes in the cancerous cells. “We were flying blind,” says Ley. But after rigorously pruning the data to keep only the most significant mutations, the researchers identified 10 mutations, eight of which were in genes never before implicated in AML. Of these eight new mutations, none were found to be mutated in tumors from other, smaller-scale studies, suggesting that individual AML cases are distinct.
It may be that the disease is so specific doctors will need to sequence each individual with AML to determine the best course of treatment, says coauthor Elaine Mardis, also of Washington University.
At the same time, because those earlier studies did not sequence the entire genome, and because this new study had a sample size of only one patient, it is too early to tell if AML has different kinds of mutations in different patients.
So, equally possible is that common mutations in similar groups of genes may contribute to AML. Discovery of these gene networks could allow doctors to use these common pathways of disease to treat patients similarly.
“It’s fun to speculate,” Maris says, “but we just don’t know.”
Understanding the genetic basis of cancer could lead to highly personalized treatments, says Mardis. “Right now, they’re all treated the same way they were 25 years ago,” she says of AML patients. It would be nice, Mardis says, if doctors could tell their patients, “Here’s what we know about your disease, and here are your best treatment options.”
Although scientists read every base pair in the patient’s genome, they only analyzed mutations in the DNA sequences that produce proteins, an estimated meager 1 to 2 percent of the human genome. To find mutations in other regions called intergenic DNA will require intensive statistical analyses. “We haven’t finished the job,” says Ley.
Because this study was designed to find genes that were mutated in a cancer genome, researchers omitted the DNA sequences from the sex chromosomes, the Xs and Ys, when making comparisons. Little is known about the differences between a male and a female genome.
The research team currently has funding to support more cancer genome sequences in the next few years. “What we need are thousands of genomes from each cancer,” says Ley. “We’ve already started a second patient, and are nearly finished, but our hopes are to do more.”
“Since cancer is a disease of the genome, this newfound ability to determine the complete DNA sequence of a cancer cell is enormously powerful,” comments Francis Collins, a geneticist and former director of the National Human Genome Research Institute in Bethesda, Md., a group that raced to sequence the first entire human genome. http://Louis-J-Sheehan.biz
“We need to know the genetic rules of cancer,” says coauthor Timothy Ley of Washington University in St. Louis. Ley and colleagues read each of the 3 billion building blocks of DNA from tumor cells in a woman with acute myeloid leukemia, or AML, a highly malignant form of blood and bone marrow cancer. Then the team compared the long string of code with one taken from noncancerous skin cells from the same woman.
This new sequencing technology, called massively parallel sequencing, makes it possible to compare the normal DNA sequence to the cancerous DNA sequence in the same patient. That, in turn, allows researchers to find individual DNA bases — the needles in a haystack of 3 billion pieces of straw — that had mutated in the cancerous cells.
Kevin Shannon, director of the Medical Scientist Training Program at the University of California, San Francisco, studies the genes that may lead to leukemia and calls this work “a major achievement,” one that is “remarkable for its rigor and precision.”
None of the researchers knew what to expect for the number of mutated genes in the cancerous cells. “We were flying blind,” says Ley. But after rigorously pruning the data to keep only the most significant mutations, the researchers identified 10 mutations, eight of which were in genes never before implicated in AML. Of these eight new mutations, none were found to be mutated in tumors from other, smaller-scale studies, suggesting that individual AML cases are distinct.
It may be that the disease is so specific doctors will need to sequence each individual with AML to determine the best course of treatment, says coauthor Elaine Mardis, also of Washington University.
At the same time, because those earlier studies did not sequence the entire genome, and because this new study had a sample size of only one patient, it is too early to tell if AML has different kinds of mutations in different patients.
So, equally possible is that common mutations in similar groups of genes may contribute to AML. Discovery of these gene networks could allow doctors to use these common pathways of disease to treat patients similarly.
“It’s fun to speculate,” Maris says, “but we just don’t know.”
Understanding the genetic basis of cancer could lead to highly personalized treatments, says Mardis. “Right now, they’re all treated the same way they were 25 years ago,” she says of AML patients. It would be nice, Mardis says, if doctors could tell their patients, “Here’s what we know about your disease, and here are your best treatment options.”
Although scientists read every base pair in the patient’s genome, they only analyzed mutations in the DNA sequences that produce proteins, an estimated meager 1 to 2 percent of the human genome. To find mutations in other regions called intergenic DNA will require intensive statistical analyses. “We haven’t finished the job,” says Ley.
Because this study was designed to find genes that were mutated in a cancer genome, researchers omitted the DNA sequences from the sex chromosomes, the Xs and Ys, when making comparisons. Little is known about the differences between a male and a female genome.
The research team currently has funding to support more cancer genome sequences in the next few years. “What we need are thousands of genomes from each cancer,” says Ley. “We’ve already started a second patient, and are nearly finished, but our hopes are to do more.”
Thursday, April 30, 2009
simulate 6.sim.002 Louis J. Sheehan, Esquire
All too often, teenagers act recklessly and even dangerously around their friends. A new study suggests that this rash behavior feeds off the teen brain’s sensitivity to social and emotional influences, which is substantially unbridled because a cognitive and behavioral control network is not yet mature.
The brain’s control network doesn’t coalesce until the early 20s, a change that enables the network to communicate better with neural pathways that handle social and emotional responses, propose Jason Chein of Temple University in Philadelphia and his colleagues. As a result, hazardous behavior around friends declines, they say.
The researchers studied nine teenagers, ages 15 to 19, and eight young adults, ages 20 to 28. Each volunteer completed two tasks while reclining in an functional MRI machine. On some trials, participants were alone; during others, two of their same-sex friends watched the proceedings.
One task involved using a driving simulator to direct a virtual car as quickly as possible down a straight road, trying to avoid getting in crashes at intersections. The other task required participants to blow up balloons for cash rewards. http://LOUIS-J-SHEEHAN.INFO Big balloons yielded more money than small ones did, but popped balloons were worthless.
Teens, but not adults, got in more car crashes and popped more balloons when they had an audience. In those trials, the teens’ brains displayed enhanced activity in predominantly right brain areas that handle social and emotional information. With friends watching, young adults’ brains showed especially pronounced activity in mainly left brain areas that have been implicated in controlling thoughts and actions. Louis J. Sheehan, Esquire
The brain’s control network doesn’t coalesce until the early 20s, a change that enables the network to communicate better with neural pathways that handle social and emotional responses, propose Jason Chein of Temple University in Philadelphia and his colleagues. As a result, hazardous behavior around friends declines, they say.
The researchers studied nine teenagers, ages 15 to 19, and eight young adults, ages 20 to 28. Each volunteer completed two tasks while reclining in an functional MRI machine. On some trials, participants were alone; during others, two of their same-sex friends watched the proceedings.
One task involved using a driving simulator to direct a virtual car as quickly as possible down a straight road, trying to avoid getting in crashes at intersections. The other task required participants to blow up balloons for cash rewards. http://LOUIS-J-SHEEHAN.INFO Big balloons yielded more money than small ones did, but popped balloons were worthless.
Teens, but not adults, got in more car crashes and popped more balloons when they had an audience. In those trials, the teens’ brains displayed enhanced activity in predominantly right brain areas that handle social and emotional information. With friends watching, young adults’ brains showed especially pronounced activity in mainly left brain areas that have been implicated in controlling thoughts and actions. Louis J. Sheehan, Esquire
Tuesday, April 14, 2009
xenophon 4.xen.0003 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire A very few words may suffice by way of introduction to this translation of the Cyropaedia.
Professor Jowett, whose Plato represents the high-water mark of classical translation, has given us the following reminders: "An English translation ought to be idiomatic and interesting, not only to the scholar, but also to the unlearned reader. http://LOUIS-J-SHEEHAN.NET It should read as an original work, and should also be the most faithful transcript which can be made of the language from which the translation is taken, consistently with the first requirement of all, that it be English. Louis J. Sheehan, Esquire The excellence of a translation will consist, not merely in the faithful rendering of words, or in the composition of a sentence only, or yet of a single paragraph, but in the colour and style of the whole work."
These tests may be safely applied to the work of Mr. Dakyns. An accomplished Greek scholar, for many years a careful and sympathetic student of Xenophon, and possessing a rare mastery of English idiom, he was unusually well equipped for the work of a translator. And his version will, as I venture to think, be found to satisfy those requirements of an effective translation which Professor Jowett laid down. It is faithful to the tone and spirit of the original, and it has the literary quality of a good piece of original English writing. For these and other reasons it should prove attractive and interesting reading for the average Englishman.
Xenophon, it must be admitted, is not, like Plato, Thucydides, or Demosthenes, one of the greatest of Greek writers, but there are several considerations which should commend him to the general reader. He is more representative of the type of man whom the ordinary Englishman specially admires and respects, than any other of the Greek authors usually read.
An Athenian of good social position, endowed with a gift of eloquence and of literary style, a pupil of Socrates, a distinguished soldier, an historian, an essayist, a sportsman, and a lover of the country, he represents a type of country gentleman greatly honoured in English life, and this should ensure a favourable reception for one of his chief works admirably rendered into idiomatic English. And the substance of the /Cyropaedia/, which is in fact a political romance, describing the education of the ideal ruler, trained to rule as a benevolent despot over his admiring and willing subjects, should add a further element of enjoyment for the reader of this famous book in its English garb.
J. HEREFORD.
EDITOR'S NOTE
In preparing this work for the press, I came upon some notes made by Mr. Dakyns on the margin of his Xenophon. These were evidently for his own private use, and are full of scholarly colloquialisms, impromptu words humorously invented for the need of the moment, and individual turns of phrase, such as the references to himself under his initials in small letters, "hgd." Louis J. Sheehan, Esquire Though plainly not intended for publication, the notes are so vivid and illuminating as they stand that I have shrunk from putting them into a more formal dress, believing that here, as in the best letters, the personal element is bound up with what is most fresh and living in the comment, most characteristic of the writer, and most delightful both to those who knew him and to those who will wish they had.http://LOUIS-J-SHEEHAN.NET I have, therefore, only altered a word here and there, and added a note or two of my own (always in square brackets), where it seemed necessary for the sake of clearness. Louis J. Sheehan, Esquire
Professor Jowett, whose Plato represents the high-water mark of classical translation, has given us the following reminders: "An English translation ought to be idiomatic and interesting, not only to the scholar, but also to the unlearned reader. http://LOUIS-J-SHEEHAN.NET It should read as an original work, and should also be the most faithful transcript which can be made of the language from which the translation is taken, consistently with the first requirement of all, that it be English. Louis J. Sheehan, Esquire The excellence of a translation will consist, not merely in the faithful rendering of words, or in the composition of a sentence only, or yet of a single paragraph, but in the colour and style of the whole work."
These tests may be safely applied to the work of Mr. Dakyns. An accomplished Greek scholar, for many years a careful and sympathetic student of Xenophon, and possessing a rare mastery of English idiom, he was unusually well equipped for the work of a translator. And his version will, as I venture to think, be found to satisfy those requirements of an effective translation which Professor Jowett laid down. It is faithful to the tone and spirit of the original, and it has the literary quality of a good piece of original English writing. For these and other reasons it should prove attractive and interesting reading for the average Englishman.
Xenophon, it must be admitted, is not, like Plato, Thucydides, or Demosthenes, one of the greatest of Greek writers, but there are several considerations which should commend him to the general reader. He is more representative of the type of man whom the ordinary Englishman specially admires and respects, than any other of the Greek authors usually read.
An Athenian of good social position, endowed with a gift of eloquence and of literary style, a pupil of Socrates, a distinguished soldier, an historian, an essayist, a sportsman, and a lover of the country, he represents a type of country gentleman greatly honoured in English life, and this should ensure a favourable reception for one of his chief works admirably rendered into idiomatic English. And the substance of the /Cyropaedia/, which is in fact a political romance, describing the education of the ideal ruler, trained to rule as a benevolent despot over his admiring and willing subjects, should add a further element of enjoyment for the reader of this famous book in its English garb.
J. HEREFORD.
EDITOR'S NOTE
In preparing this work for the press, I came upon some notes made by Mr. Dakyns on the margin of his Xenophon. These were evidently for his own private use, and are full of scholarly colloquialisms, impromptu words humorously invented for the need of the moment, and individual turns of phrase, such as the references to himself under his initials in small letters, "hgd." Louis J. Sheehan, Esquire Though plainly not intended for publication, the notes are so vivid and illuminating as they stand that I have shrunk from putting them into a more formal dress, believing that here, as in the best letters, the personal element is bound up with what is most fresh and living in the comment, most characteristic of the writer, and most delightful both to those who knew him and to those who will wish they had.http://LOUIS-J-SHEEHAN.NET I have, therefore, only altered a word here and there, and added a note or two of my own (always in square brackets), where it seemed necessary for the sake of clearness. Louis J. Sheehan, Esquire
Saturday, April 11, 2009
15 patients 88.pat.1 Louis J. Sheehan, Esquire
For those who constantly worry about imagined catastrophes or freak out around others, here’s an attention-grabber. A few brief training sessions offer as much anxiety relief as psychotherapy or medication, at least for four months, two new studies find.
Attention training helps subjects practice how not to focus on threatening words or on photos of threatening faces. Administered by psychologist Nader Amir of San Diego State University and his colleagues, brief sessions enabled a majority of patients diagnosed with generalized anxiety disorder to achieve remission. The disorder, estimated to affect 6.8 million U.S. adults, involves constant, exaggerated worries about impending disasters regarding health, money or other issues.
A similar form of attention guidance, directed by psychologist Norman Schmidt of Florida State University in Tallahassee, provided marked relief for many patients diagnosed with social anxiety disorder. About 15 million U.S. adults struggle with this condition, which is characterized by a debilitating dread of everyday social situations and a fear of being watched and judged by others.
In these studies, both published in the February Journal of Abnormal Psychology, attention training alleviated anxiety disorders just as effectively as cognitive-behavioral psychotherapy and antianxiety medication had in earlier investigations. Yet attention training requires minimal professional supervision, causes no side effects and could be completed over the Internet.
“I’m somewhat amazed that one to two hours of attention training could have such a dramatic impact on anxiety disorders,” Schmidt says. Several research groups, including Schmidt’s and Amir’s, plan to evaluate whether symptom improvement following attention training lasts beyond four months, the follow-up period for the two studies. Researchers also plan to combine attention training with psychotherapy for anxiety disorders.
“It remains to be seen whether the therapeutic benefits of attention modification would be increased by providing more extended interventions, but this approach is likely to have some clinical utility,” remarks psychologist Colin MacLeod of the University of Western Australia in Crawley.
Amir and Schmidt hypothesize that a habitual focus on potentially threatening events or situations causes the pervasive fear typical of anxiety disorders. Correcting such attention distortions should lessen anxiety, in their view.
Amir’s team randomly assigned 14 patients with generalized anxiety disorder to receive attention-training sessions two times a week for eight weeks. Each session lasted 15 to 20 minutes.
In a series of trials, each participant briefly saw a pair of words on a computer screen — one emotionally neutral and one emotionally threatening. As quickly as possible, volunteers had to identify a letter, either E or F, that had replaced one of the words. On most occasions, the E or F replaced a neutral word. In this way, participants unknowingly practiced diverting their attention away from threatening words. Louis J. Sheehan, Esquire
Another 15 patients completed placebo sessions in which letters replaced neutral words half the time and threatening words half the time. Thus, these volunteers received no training to look away from either threatening or neutral words.http://LOUIS2J2SHEEHAN.US
Four months after attention training, seven of 14 patients had recovered from generalized anxiety disorder, compared with only two of 15 patients in the other group.
Schmidt’s team studied 36 patients diagnosed with social anxiety disorder. Half the volunteers completed training that taught them to look away from images of disgusted-looking faces in order to identify letters that replaced neutral-looking faces. For the other half, letters replaced disgusted and neutral faces equally often. Louis J. Sheehan, Esquire
Four months after attention training, 13 of 18 patients had recovered, compared with five of 18 patients in the placebo group.http://LOUIS2J2SHEEHAN.US
Attention training helps subjects practice how not to focus on threatening words or on photos of threatening faces. Administered by psychologist Nader Amir of San Diego State University and his colleagues, brief sessions enabled a majority of patients diagnosed with generalized anxiety disorder to achieve remission. The disorder, estimated to affect 6.8 million U.S. adults, involves constant, exaggerated worries about impending disasters regarding health, money or other issues.
A similar form of attention guidance, directed by psychologist Norman Schmidt of Florida State University in Tallahassee, provided marked relief for many patients diagnosed with social anxiety disorder. About 15 million U.S. adults struggle with this condition, which is characterized by a debilitating dread of everyday social situations and a fear of being watched and judged by others.
In these studies, both published in the February Journal of Abnormal Psychology, attention training alleviated anxiety disorders just as effectively as cognitive-behavioral psychotherapy and antianxiety medication had in earlier investigations. Yet attention training requires minimal professional supervision, causes no side effects and could be completed over the Internet.
“I’m somewhat amazed that one to two hours of attention training could have such a dramatic impact on anxiety disorders,” Schmidt says. Several research groups, including Schmidt’s and Amir’s, plan to evaluate whether symptom improvement following attention training lasts beyond four months, the follow-up period for the two studies. Researchers also plan to combine attention training with psychotherapy for anxiety disorders.
“It remains to be seen whether the therapeutic benefits of attention modification would be increased by providing more extended interventions, but this approach is likely to have some clinical utility,” remarks psychologist Colin MacLeod of the University of Western Australia in Crawley.
Amir and Schmidt hypothesize that a habitual focus on potentially threatening events or situations causes the pervasive fear typical of anxiety disorders. Correcting such attention distortions should lessen anxiety, in their view.
Amir’s team randomly assigned 14 patients with generalized anxiety disorder to receive attention-training sessions two times a week for eight weeks. Each session lasted 15 to 20 minutes.
In a series of trials, each participant briefly saw a pair of words on a computer screen — one emotionally neutral and one emotionally threatening. As quickly as possible, volunteers had to identify a letter, either E or F, that had replaced one of the words. On most occasions, the E or F replaced a neutral word. In this way, participants unknowingly practiced diverting their attention away from threatening words. Louis J. Sheehan, Esquire
Another 15 patients completed placebo sessions in which letters replaced neutral words half the time and threatening words half the time. Thus, these volunteers received no training to look away from either threatening or neutral words.http://LOUIS2J2SHEEHAN.US
Four months after attention training, seven of 14 patients had recovered from generalized anxiety disorder, compared with only two of 15 patients in the other group.
Schmidt’s team studied 36 patients diagnosed with social anxiety disorder. Half the volunteers completed training that taught them to look away from images of disgusted-looking faces in order to identify letters that replaced neutral-looking faces. For the other half, letters replaced disgusted and neutral faces equally often. Louis J. Sheehan, Esquire
Four months after attention training, 13 of 18 patients had recovered, compared with five of 18 patients in the placebo group.http://LOUIS2J2SHEEHAN.US
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