New Scientist Life's top 10 greatest inventions - Features: "THE BRAIN
BRAINS are often seen as a crowning achievement of evolution - bestowing the ultimate human traits such as language, intelligence and consciousness. But before all that, the evolution of brains did something just as striking: it lifted life beyond vegetation. Brains provided, for the first time, a way for organisms to deal with environmental change on a timescale shorter than generations.
A nervous system allows two extremely useful things to happen: movement and memory. If you're a plant and your food source disappears, that's just tough. But if you have a nervous system that can control muscles, then you can actually move around and seek out food, sex and shelter.
With brains come senses, to detect whether the world is good or bad, and a memory. Together, these let the animal monitor in real time whether things are getting better or worse. This in turn allows a simple system of prediction and reward. Even animals with really simple brains - insects, slugs or flatworms - can use their experiences to predict what might be the best thing to do or eat next, and have a system of reward that reinforces good choices.
The more complex functions of the human brain - social interaction, decision-making and empathy, for example - seem to have evolved from these basic systems controlling food intake. The sensations that control what we decide to eat became the intuitive decisions we call gut instincts. The most highly developed parts of the human frontal cortex that deal with decisions and social interactions are right next to the parts that control taste and smell and movements of the mouth, tongue and gut. There is a reason we kiss potential mates - it's the most primitive way we know to check something out.
Saturday, April 09, 2005
Thursday, April 07, 2005
taoist-arts.com: News: Tai Chi Helps Parkinson's Patients
taoist-arts.com: News: Tai Chi Helps Parkinson's Patients: "Tai Chi, an ancient Chinese form of martial art that is practiced by about 300 million people worldwide, incorporates circular, concentrated movements that are proving helpful for Parkinson's disease patients. In Tai Chi, when one part of the body moves, all parts move, and the exercises improve flexibility, energy and balance.
'The patients get such wonderful benefits from it,' said Lyvonne Carriero, Parkinson's program coordinator at Shands. 'They say after one class they can see a difference in their balance.'
At a recent class, Jones and Saul were joined by their wives, Mae and Elayne, respectively, and about a dozen other participants. Instructor Genera Holladay led the group through a series of postures that were challenging but designed around the limitations of Parkinson's patients. Tai Chi techniques vary by style, and Holladay, who also is a pharmacist and acupuncturist, was using modified medical forms of the Yang style.
'This class differs from most Tai Chi classes,' said Holladay, who learned the ancient art while living in Japan and Korea in the early 1960s. In martial arts, the movements are geared outward for defense and striking. For this class, she emphasizes inner energy instead.
'If we are in a challenged health position, using these same techniques can strengthen the body for health,' Holladay said. 'Instead of letting the energy out, we use it to strengthen the organs, bones and muscles.' "
'The patients get such wonderful benefits from it,' said Lyvonne Carriero, Parkinson's program coordinator at Shands. 'They say after one class they can see a difference in their balance.'
At a recent class, Jones and Saul were joined by their wives, Mae and Elayne, respectively, and about a dozen other participants. Instructor Genera Holladay led the group through a series of postures that were challenging but designed around the limitations of Parkinson's patients. Tai Chi techniques vary by style, and Holladay, who also is a pharmacist and acupuncturist, was using modified medical forms of the Yang style.
'This class differs from most Tai Chi classes,' said Holladay, who learned the ancient art while living in Japan and Korea in the early 1960s. In martial arts, the movements are geared outward for defense and striking. For this class, she emphasizes inner energy instead.
'If we are in a challenged health position, using these same techniques can strengthen the body for health,' Holladay said. 'Instead of letting the energy out, we use it to strengthen the organs, bones and muscles.' "
Wednesday, April 06, 2005
New Scientist Breaking News - TV may turn four-year-olds into bullies
so we know how depression can make us sick... So what about the TV pumping our minds full of crap? How uncivilized do we ahve to get before we will change this???
New Scientist Breaking News - TV may turn four-year-olds into bullies Young children who watch a lot of television are more likely to become bullies, a new study reveals. The authors suggest the increasingly violent nature of children’s cartoons may be to blame.
Previous studies have linked television to aggressive behaviour in older children and adolescents. But a team led by Frederick Zimmerman, an economist at the University of Washington in Seattle, US, has now traced the phenomenon to four-year-olds.
The researchers used existing data from a national US survey to study the amount of television watched by 1266 four-year-olds. Then they compared that amount with follow-up reports - by the children's mothers - on whether the children bullied or were "cruel or mean to others" when they were between six and 11 years old.
New Scientist Breaking News - TV may turn four-year-olds into bullies Young children who watch a lot of television are more likely to become bullies, a new study reveals. The authors suggest the increasingly violent nature of children’s cartoons may be to blame.
Previous studies have linked television to aggressive behaviour in older children and adolescents. But a team led by Frederick Zimmerman, an economist at the University of Washington in Seattle, US, has now traced the phenomenon to four-year-olds.
The researchers used existing data from a national US survey to study the amount of television watched by 1266 four-year-olds. Then they compared that amount with follow-up reports - by the children's mothers - on whether the children bullied or were "cruel or mean to others" when they were between six and 11 years old.
Thursday, February 24, 2005
Optimism associated with lowered risk of dying from heart disease
Optimism associated with lowered risk of dying from heart disease:
Optimism associated with lowered risk of dying from heart disease
CHICAGO – Patients who described themselves as highly optimistic had lower risks of all-cause death, and lower rates of cardiovascular death than those with high levels of pessimism, according to an article in the November issue of The Archives of General Psychiatry, one of the JAMA/Archives journals.
According to the article, major depression is a known risk factor for cardiovascular death. However, the relationship between optimism and death has not received as much attention.
"'In conclusion, we found that the trait of optimism was an important long-term determinant of all-cause and cardiovascular mortality in elderly subjects independent of sociodemographic characteristics and cardiovascular risk factors,' the authors write. 'A predisposition toward optimism seemed to provide a survival benefit in elderly subjects with relatively short life expectancies otherwise.'
'Our results, combined with the finding that hopelessness was associated with an increased incidence or progression of disease, suggest that dispositional optimism affects the progression of cardiovascular disease,' the researchers state. 'Although optimism reduces the risk of cardiovascular death through mechanisms largely unaffected by baseline values of physical activity, obesity, smoking, hypertension, and lipid profile, pessimistic subjects may be more prone to changes across time in risk factors that affect the progression of cardiovascular disease (e.g., the development of smoking habits, obesity, or hypertension) than optimistic subjects. Dispositional optimism may also be associated with better coping strategies that are adhered to throughout life.'
Dispositional Optimism and All-Cause and Cardiovascular Mortality in a Prospective Cohort of Elderly Dutch Men and Women.Archives of General Psychiatry. 61(11):1126-1135, November 2004. Giltay, Erik J. MD, PhD; Geleijnse, Johanna M. PhD; Zitman, Frans G. MD, PhD; Hoekstra, Tiny PhD; Schouten, Evert G. MD, PhD
"
Optimism associated with lowered risk of dying from heart disease
CHICAGO – Patients who described themselves as highly optimistic had lower risks of all-cause death, and lower rates of cardiovascular death than those with high levels of pessimism, according to an article in the November issue of The Archives of General Psychiatry, one of the JAMA/Archives journals.
According to the article, major depression is a known risk factor for cardiovascular death. However, the relationship between optimism and death has not received as much attention.
"'In conclusion, we found that the trait of optimism was an important long-term determinant of all-cause and cardiovascular mortality in elderly subjects independent of sociodemographic characteristics and cardiovascular risk factors,' the authors write. 'A predisposition toward optimism seemed to provide a survival benefit in elderly subjects with relatively short life expectancies otherwise.'
'Our results, combined with the finding that hopelessness was associated with an increased incidence or progression of disease, suggest that dispositional optimism affects the progression of cardiovascular disease,' the researchers state. 'Although optimism reduces the risk of cardiovascular death through mechanisms largely unaffected by baseline values of physical activity, obesity, smoking, hypertension, and lipid profile, pessimistic subjects may be more prone to changes across time in risk factors that affect the progression of cardiovascular disease (e.g., the development of smoking habits, obesity, or hypertension) than optimistic subjects. Dispositional optimism may also be associated with better coping strategies that are adhered to throughout life.'
Dispositional Optimism and All-Cause and Cardiovascular Mortality in a Prospective Cohort of Elderly Dutch Men and Women.Archives of General Psychiatry. 61(11):1126-1135, November 2004. Giltay, Erik J. MD, PhD; Geleijnse, Johanna M. PhD; Zitman, Frans G. MD, PhD; Hoekstra, Tiny PhD; Schouten, Evert G. MD, PhD
"
Wednesday, February 02, 2005
Wired News: Neurons Derived From Stem Cells
yes we can dreate all sorts with this, but is it the mix of chemicals and the timing, or the conscious choice that makes it???
Wired News: Neurons Derived From Stem Cells: "The conclusion, reported in the science journal Nature Biotechnology, is important for two reasons. First, stem-cell scientists have struggled to accomplish what researcher Su-Chun Zhang and his colleagues have just accomplished. It took Zhang's team two years of tedious trial-and-error experiments to direct stem cells to turn into motor neurons.
Perhaps more important, Zhang's recipe shows researchers that timing is everything when adding their chemical cocktails to stem-cell stews. Stem cells are vulnerable to successful human manipulation for only the briefest of moments -- and at different intervals depending on the results each researcher craves.
'This shows that you can't dump whatever growth factors you want in there,' Zhang said. 'It's not that simple. It's very specific. You have to have the right cocktail in the right amount at the right time.'
But with Zhang and others showing that the biological clock ticks differently in different animals and in each type of cell, it appears translating animal data to human terms is more about timing than biology.
"That is also somewhat reassuring," said Isacson, who has created dopamine-producing brain cells from stem cells. Parkinson disease patients lose dopamine cells, which help regulate body movement.
Embryonic stem cells are created in the first days after conception and ultimately turn into the 220 or so types of cells that make up the human body. Scientists believe they can someday control what stem cells become and when, using that power to replace damaged and dead cells that cause a wide range of suffering, from diabetes to Parkinson's.
But harnessing that power has proved elusive in all but a few cell types such as heart and two other types of brain cells.
'This is an important contribution because stem cell biology is difficult," Isacson said. "It helps decode the locks.'"
Wired News: Neurons Derived From Stem Cells: "The conclusion, reported in the science journal Nature Biotechnology, is important for two reasons. First, stem-cell scientists have struggled to accomplish what researcher Su-Chun Zhang and his colleagues have just accomplished. It took Zhang's team two years of tedious trial-and-error experiments to direct stem cells to turn into motor neurons.
Perhaps more important, Zhang's recipe shows researchers that timing is everything when adding their chemical cocktails to stem-cell stews. Stem cells are vulnerable to successful human manipulation for only the briefest of moments -- and at different intervals depending on the results each researcher craves.
'This shows that you can't dump whatever growth factors you want in there,' Zhang said. 'It's not that simple. It's very specific. You have to have the right cocktail in the right amount at the right time.'
But with Zhang and others showing that the biological clock ticks differently in different animals and in each type of cell, it appears translating animal data to human terms is more about timing than biology.
"That is also somewhat reassuring," said Isacson, who has created dopamine-producing brain cells from stem cells. Parkinson disease patients lose dopamine cells, which help regulate body movement.
Embryonic stem cells are created in the first days after conception and ultimately turn into the 220 or so types of cells that make up the human body. Scientists believe they can someday control what stem cells become and when, using that power to replace damaged and dead cells that cause a wide range of suffering, from diabetes to Parkinson's.
But harnessing that power has proved elusive in all but a few cell types such as heart and two other types of brain cells.
'This is an important contribution because stem cell biology is difficult," Isacson said. "It helps decode the locks.'"
Saturday, January 15, 2005
The Endocrine Regulation of Aging by Insulin-like Signals
Science -- Tatar et al. 299 (5611): 1346: "Pituitary Endocrine Deficiency in Mammals Of the half-dozen genetic models that retard murine aging, four involve deficiency of pituitary endocrine action. The mutations Prop1df (42) and Pit1dw impede pituitary production of growth hormone (GH), thyroid stimulating hormone (TSH), and prolactin; reduce growth rate and adult body size; and increase adult life-span by 40 to 60% (43, 44). Small adults with similar improvement in longevity are also produced by a knockout of growth hormone receptor (GHR-KO) (45). Expressed throughout life, these mutations produce many secondary alterations in endocrine systems. Without GH, the synthesis of circulating IGF-1 is suppressed, as is plasma insulin as a result of enhanced sensitivity in the liver combined with altered pancreatic islet development (46). Thyroid function is reduced in Prop1df and Pit1dw mutants deficient for TSH (45); GHR-KO mice are mildly hypothyroid, presumably as a result of impaired development (47). The challenge is to identify which of these hormones regulate aging and at which stage of life.
In invertebrates, reduced insulin/IGF signaling increases longevity, but it remains unclear whether or how reduction in GH and IGF-1 directly affects aging in rodents (Fig. 1C). In addition to its impact on IGF-1, GH influences somatic metabolism--for instance, by inducing adipocyte lipolysis. IGF-1 itself may affect aging in both beneficial and detrimental ways. In rodents as in humans, levels of GH and IGF-1 decline with adult age. Short-term GH supplementation in aged adults restores some aspects of body composition and cognition (48, 49). Thus, the withdrawal of GH and IGF-1 has been suggested to be a cause of senescence rather than a condition that retards aging. On the other hand, because it stimulates metabolism and cell growth, GH may hasten tissue pathology. Indeed, chronic treatment of GH-deficient dwarf rats with GH increased tumor incidence in response to a carcinogen (50). High IGF-1 titers in young wild-type animals may produce a trade-off between current benefits to reproduction and later costs in senescence (51).
Powerful evidence for the direct role of IGF-1 signaling in the control of mammalian aging was provided by mice mutant for the IFG-1 receptor Igf1r (52): Igf1r+/ females, but not males, live 33% longer than wild-type controls. These mutants exhibit minimal reduction in growth with no alterations in the age of sexual maturation, fertility, metabolism, food intake, or temperature. Life extension is associated with increased tolerance of oxidative stress and reduced phosphorylation of Shc, a gene previously implicated in the control of longevity and stress resistance in mice (53). Mouse longevity is also increased 18% by fat-specific disruption of the insulin receptor gene (54). These mice have normal caloric intake yet retain leanness and glucose tolerance with age. Multiple intriguing changes in adipocytes underlie these effects, including elevated plasma leptin relative to adipose tissue mass, reduced lipolysis, and polarization of adipocytes into populations with altered expression of fatty acid synthase (55). Thus, insulin at adipose tissue may affect aging through impacts on neural-targeted hormones as well as through regulation of intermediary metabolism."
Science, Vol 299, Issue 5611, 1346-1351 , 28 February 2003
In invertebrates, reduced insulin/IGF signaling increases longevity, but it remains unclear whether or how reduction in GH and IGF-1 directly affects aging in rodents (Fig. 1C). In addition to its impact on IGF-1, GH influences somatic metabolism--for instance, by inducing adipocyte lipolysis. IGF-1 itself may affect aging in both beneficial and detrimental ways. In rodents as in humans, levels of GH and IGF-1 decline with adult age. Short-term GH supplementation in aged adults restores some aspects of body composition and cognition (48, 49). Thus, the withdrawal of GH and IGF-1 has been suggested to be a cause of senescence rather than a condition that retards aging. On the other hand, because it stimulates metabolism and cell growth, GH may hasten tissue pathology. Indeed, chronic treatment of GH-deficient dwarf rats with GH increased tumor incidence in response to a carcinogen (50). High IGF-1 titers in young wild-type animals may produce a trade-off between current benefits to reproduction and later costs in senescence (51).
Powerful evidence for the direct role of IGF-1 signaling in the control of mammalian aging was provided by mice mutant for the IFG-1 receptor Igf1r (52): Igf1r+/ females, but not males, live 33% longer than wild-type controls. These mutants exhibit minimal reduction in growth with no alterations in the age of sexual maturation, fertility, metabolism, food intake, or temperature. Life extension is associated with increased tolerance of oxidative stress and reduced phosphorylation of Shc, a gene previously implicated in the control of longevity and stress resistance in mice (53). Mouse longevity is also increased 18% by fat-specific disruption of the insulin receptor gene (54). These mice have normal caloric intake yet retain leanness and glucose tolerance with age. Multiple intriguing changes in adipocytes underlie these effects, including elevated plasma leptin relative to adipose tissue mass, reduced lipolysis, and polarization of adipocytes into populations with altered expression of fatty acid synthase (55). Thus, insulin at adipose tissue may affect aging through impacts on neural-targeted hormones as well as through regulation of intermediary metabolism."
Science, Vol 299, Issue 5611, 1346-1351 , 28 February 2003
Monday, January 10, 2005
Sir2: scrambling for answers: researchers have yet to solidify links for the proposed longevity lynchpin.
The Scientist, Dec 6, 2004 v18 i23 p20(2)
(Research) Maria W. Anderson.
Full Text: COPYRIGHT 2004 Scientist Inc.
Low-calorie diets extend lifespan in almost every model tested, but scientists can't yet agree on what controls this phenomenon. biologist Leonard Guarente at Massachusetts Institute of Technology, contend that Sir2 is dependent on nicotinamide adenine di-nucleotide (NAD) and that CR activates Sir2 by reducing glucose metabolism, which increases the ratio of NAD to its reduced version, NADH. (2) Others, such as Harvard Medical School pathologist David Sinclair, hold that nicotinamide, not NAD, is the control switch for Sir2, and that the deaminase PncI converts nicotinamide to nicotinic acid, which in turn increases Sir2 activity.
"I think it's a push and a pull system," explains Sinclair. Work by Guarente and Shin-Ichiro Imai, a molecular biologist at Washington University, St. Louis, showed that increases in NAD activate yeast Sirz in vivo, while Sinclair's studies indicated that removing nicotinamide, a Sir2 inhibitor, can pull the reaction forward. "So we've got them pushing and us pulling, and [these mechanisms] probably work in concert with each other," says Sinclair.
In September, a group of researchers from Stan Fields' lab at the University of Washington (UW), Seattle, published a paper offering evidence that CR may work through a pathway not involving Sir2. In yeast lacking Sir2, CR did not extend lifespan
Matt Piper, a biologist at University College London, says he sees a role for Sir2 in lifespan extension by CR but notes that an organism's diet influences its physiology in multiple ways that might affect its lifespan. "Because diet is so complex, you have many different signaling pathways in the organism determining many different physiological processes, which result in lifespan extension or shortening," says Piper. "To put it all down to one gene in one pathway is a very big call." He explains that both the insulin-signaling pathway, which responds to sugar, and the TOR-signaling pathway, which is affected by dietary protein, probably play a role in CR-mediated longevity. Having at least two different signaling pathways for lifespan extension in flies and worms, Piper adds, "would suggest that there's probably a number of different feed-ins to get lifespan extension."
References
(1.) L.P. Guarente, "Forestalling the great beyond with the help of SIR2," The Scientist, 18:34-5, April 26, 2004.
(2.) S.J. Lin et al., "Calorie restriction extends yeast life span by lowering the level of NADH," Genes Dev, 18:12-6, 2004.
(3.) R.M. Anderson et al., "Nicotinamide and PNCl govern lifespan extension by calorie restriction in Saccharomyces cerevisiae," Nature, 423:181-5,2003.
(4.) M. Kaeberlein et al., "Sir2-independent life span extension by calorie restriction in yeast," PLoS Biology, 2:1381-87, September 2004.
(5.) H. Tissenbaum, L. Guarente, "Increased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans," Nature, 410:227-30, 200l.
(6.) K. Houthoofd et al., "Life extension via dietary restriction is independent of the Ins/IGF-1 signaling pathway in Caenorhabditis elegans," Exp Gemntol, 38:947-54, 2003.
(7.) B. Lakowski, S. Hekimi, "The genetics of caloric restriction in Caenorhabditis elegans," Proc Nat/Acad Sci, 95:13091-6, 1998.
(8.) B. Rogina, S.L. Helfand, "Sir2 mediates longevity in the fly through a pathway related to calorie restriction," Proc Natl Acad Sci, 101:15998-16003, Nov. 9, 2004.
(9.) D. Secko, "'Longevity' gene, diet linked," The Scientist Daily News, June 18, 2004, available online at www.biomedcentral.com/news/2005540618/01.
Maria W. Anderson (manderson@the-scientist.com)
(Research) Maria W. Anderson.
Full Text: COPYRIGHT 2004 Scientist Inc.
Low-calorie diets extend lifespan in almost every model tested, but scientists can't yet agree on what controls this phenomenon. biologist Leonard Guarente at Massachusetts Institute of Technology, contend that Sir2 is dependent on nicotinamide adenine di-nucleotide (NAD) and that CR activates Sir2 by reducing glucose metabolism, which increases the ratio of NAD to its reduced version, NADH. (2) Others, such as Harvard Medical School pathologist David Sinclair, hold that nicotinamide, not NAD, is the control switch for Sir2, and that the deaminase PncI converts nicotinamide to nicotinic acid, which in turn increases Sir2 activity.
"I think it's a push and a pull system," explains Sinclair. Work by Guarente and Shin-Ichiro Imai, a molecular biologist at Washington University, St. Louis, showed that increases in NAD activate yeast Sirz in vivo, while Sinclair's studies indicated that removing nicotinamide, a Sir2 inhibitor, can pull the reaction forward. "So we've got them pushing and us pulling, and [these mechanisms] probably work in concert with each other," says Sinclair.
In September, a group of researchers from Stan Fields' lab at the University of Washington (UW), Seattle, published a paper offering evidence that CR may work through a pathway not involving Sir2. In yeast lacking Sir2, CR did not extend lifespan
Matt Piper, a biologist at University College London, says he sees a role for Sir2 in lifespan extension by CR but notes that an organism's diet influences its physiology in multiple ways that might affect its lifespan. "Because diet is so complex, you have many different signaling pathways in the organism determining many different physiological processes, which result in lifespan extension or shortening," says Piper. "To put it all down to one gene in one pathway is a very big call." He explains that both the insulin-signaling pathway, which responds to sugar, and the TOR-signaling pathway, which is affected by dietary protein, probably play a role in CR-mediated longevity. Having at least two different signaling pathways for lifespan extension in flies and worms, Piper adds, "would suggest that there's probably a number of different feed-ins to get lifespan extension."
References
(1.) L.P. Guarente, "Forestalling the great beyond with the help of SIR2," The Scientist, 18:34-5, April 26, 2004.
(2.) S.J. Lin et al., "Calorie restriction extends yeast life span by lowering the level of NADH," Genes Dev, 18:12-6, 2004.
(3.) R.M. Anderson et al., "Nicotinamide and PNCl govern lifespan extension by calorie restriction in Saccharomyces cerevisiae," Nature, 423:181-5,2003.
(4.) M. Kaeberlein et al., "Sir2-independent life span extension by calorie restriction in yeast," PLoS Biology, 2:1381-87, September 2004.
(5.) H. Tissenbaum, L. Guarente, "Increased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans," Nature, 410:227-30, 200l.
(6.) K. Houthoofd et al., "Life extension via dietary restriction is independent of the Ins/IGF-1 signaling pathway in Caenorhabditis elegans," Exp Gemntol, 38:947-54, 2003.
(7.) B. Lakowski, S. Hekimi, "The genetics of caloric restriction in Caenorhabditis elegans," Proc Nat/Acad Sci, 95:13091-6, 1998.
(8.) B. Rogina, S.L. Helfand, "Sir2 mediates longevity in the fly through a pathway related to calorie restriction," Proc Natl Acad Sci, 101:15998-16003, Nov. 9, 2004.
(9.) D. Secko, "'Longevity' gene, diet linked," The Scientist Daily News, June 18, 2004, available online at www.biomedcentral.com/news/2005540618/01.
Maria W. Anderson (manderson@the-scientist.com)
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