Diners in the Far East are quite partial to a variety of sweet, pink-skinned tomatoes. Now, a researcher has revealed the secret behind this pink vegetable.
Asaph Aharoni of the Weizmann Institute's Plant Sciences department in Israel says that a mutated gene, SIMYB12, is responsible for producing these pink tomatoes.
This gene acts as a 'master switch' that regulates the activities of a whole network of other genes, controlling the amounts of yellow pigments as well as a host of other substances in the tomato.
Aharoni's research focuses on plants' thin, protective outer layers, called cuticles, which are mainly composed of fatty, wax-like substances.
In the familiar red tomato, this layer also contains large amounts of antioxidants called flavonoids forming the tomatoes' first line of defence.
Some of these flavonoids also give the tomato cuticles a bright yellow cast - the colour component that is missing in the translucent pink skins of the mutants.
Using a lab system that's unique in Israel, and one of only a few in the world, Aharoni and his team are able to rapidly and efficiently identify hundreds of active plant substances called metabolites.
A multidisciplinary approach developed over the past decade, known as metabolomics, enables them to create a comprehensive profile of all these substances in mutant plants and compare it with that of normal ones.
The research showed that the differences between pink and red tomatoes go much deeper than skin colour, says a Weizmann release.
The pink tomato also has less lycopene, a red pigment known to be a strong antioxidant that's been shown to be associated with reduced risk of cancer, heart disease and diabetes.
These findings were published in the Friday issue of Science.
Showing posts with label LATEST NEWS OF SCIENCE. Show all posts
Showing posts with label LATEST NEWS OF SCIENCE. Show all posts
Friday, January 22, 2010
Saturday, January 2, 2010
Indian Ocean climate event occurring more frequently due to global warming
In a new research, a team of scientists has determined that the Indian Ocean Dipole (IOD), an oscillation of sea surface temperatures in the Indian Ocean, is occurring more frequently because of global warming.
The research was done by Nobuko Nakamura and his team from the University of Tokyo, along with Timothy R. McClanahan from Wildlife Conservation Society, and Swadhin K. Behera from the Frontier Research Center for Global Change, Yokohama, Japan.
Recently, the IOD has become a major influence on the weather variations in the Indian Ocean region.
During positive IOD events, abnormally warm sea surface temperatures in the western Indian Ocean are accompanied by severe droughts over the Indonesian region and heavy rainfall over east Africa.
To learn more about IOD patterns, the team of scientists studied a 115-year coral record from Kenya.
They analyzed coral oxygen isotope ratios, which trace rainfall anomalies, to reconstruct IOD variability.
The results add to evidence that the IOD has been occurring more frequently in recent decades.
They found that before 1924, the IOD occurred approximately every 10 years, but since 1960, IOD events have been occurring approximately 18 months to 3 years apart.
The researchers suggested that global warming effects on the western Indian Ocean have driven the observed shift in IOD variability and note that the IOD has replaced the El Nino-Southern Oscillation as the major driver of climate patterns over the Indian Ocean region.
The research was done by Nobuko Nakamura and his team from the University of Tokyo, along with Timothy R. McClanahan from Wildlife Conservation Society, and Swadhin K. Behera from the Frontier Research Center for Global Change, Yokohama, Japan.
Recently, the IOD has become a major influence on the weather variations in the Indian Ocean region.
During positive IOD events, abnormally warm sea surface temperatures in the western Indian Ocean are accompanied by severe droughts over the Indonesian region and heavy rainfall over east Africa.
To learn more about IOD patterns, the team of scientists studied a 115-year coral record from Kenya.
They analyzed coral oxygen isotope ratios, which trace rainfall anomalies, to reconstruct IOD variability.
The results add to evidence that the IOD has been occurring more frequently in recent decades.
They found that before 1924, the IOD occurred approximately every 10 years, but since 1960, IOD events have been occurring approximately 18 months to 3 years apart.
The researchers suggested that global warming effects on the western Indian Ocean have driven the observed shift in IOD variability and note that the IOD has replaced the El Nino-Southern Oscillation as the major driver of climate patterns over the Indian Ocean region.
No rise in atmospheric CO2 fraction in past 150 years
In a new study, a scientist has found that the airborne fraction of carbon dioxide (CO2) has not increased either during the past 150 years.
The scientist in question is Wolfgang Knorr, from the Department of Earth Sciences, University of Bristol, UK.
Most of the CO2 emitted by human activity does not remain in the atmosphere, but is instead absorbed by the oceans and terrestrial ecosystems.
In fact, only about 45 percent of emitted carbon dioxide stays in the atmosphere.
However, some studies have suggested that the ability of oceans and plants to absorb carbon dioxide recently may have begun to decline and that the airborne fraction of anthropogenic CO2 emissions is therefore beginning to increase.
Many climate models also assume that the airborne fraction will increase.
Because understanding of the airborne fraction of carbon dioxide is important for predicting future climate change, it is essential to have accurate knowledge of whether that fraction is changing or will change as emissions increase.
To assess whether the airborne fraction is indeed increasing, Knorr reanalyzed available atmospheric CO2 and emissions data since 1850 and considers the uncertainties in the data.
In contradiction to some recent studies, he found that the airborne fraction of CO2 has not increased either during the past 150 years or during the most recent five decades.
The scientist in question is Wolfgang Knorr, from the Department of Earth Sciences, University of Bristol, UK.
Most of the CO2 emitted by human activity does not remain in the atmosphere, but is instead absorbed by the oceans and terrestrial ecosystems.
In fact, only about 45 percent of emitted carbon dioxide stays in the atmosphere.
However, some studies have suggested that the ability of oceans and plants to absorb carbon dioxide recently may have begun to decline and that the airborne fraction of anthropogenic CO2 emissions is therefore beginning to increase.
Many climate models also assume that the airborne fraction will increase.
Because understanding of the airborne fraction of carbon dioxide is important for predicting future climate change, it is essential to have accurate knowledge of whether that fraction is changing or will change as emissions increase.
To assess whether the airborne fraction is indeed increasing, Knorr reanalyzed available atmospheric CO2 and emissions data since 1850 and considers the uncertainties in the data.
In contradiction to some recent studies, he found that the airborne fraction of CO2 has not increased either during the past 150 years or during the most recent five decades.
Monday, December 28, 2009
Brain can distinguish real sugar from fake
While products with calorie-free artificial sugar claim to be as sweet as actual sugar, researchers have claimed that our brains can distinguish real from fake.
Saccharin, the first of the industrially manufactured artificial sweeteners, was discovered late in the 19th century and soon became popular.
Since then, a parade of sweeteners has come on stream, including cyclamate, aspartame, the sucrose-like (and very sweet) sucralose, and several others, including one called Rebiana, derived from a South American herb.
A handful of studies, starting in the 1980s, suggested that regular use of artificial sweeteners might even make people eat more, rather than less, by stimulating their appetites without satisfying them.
And recently, Guido Frank, a psychiatrist at the University of Colorado in Denver who has a particular interest in eating disorders, compared how the brain responds to sucralose and sucrose.
Thus, he fed the sweetener and the sugar to 12 women, adjusting the concentrations so that the sweetness of the two matched.
"They consciously could not distinguish them," New Scientist quoted Frank as saying.
But, when he looked at their brain responses with functional magnetic resonance imaging (fMRI), he saw clear differences.
Sucrose produced stronger activation in the "reward" areas of the brain that light up in response to pleasurable activities such as eating and drinking.
Sucralose didn't activate these areas as strongly, but it synchronised the activity in a whole constellation of taste-associated brain areas - and it did this more strongly than sucrose did.
Frank suggested that sucralose activates brain areas that register pleasant taste, but not strongly enough to cause satiation.
"That might drive you to eat something sweet or something calorific later on," he said.
Similar results emerged from brain-scanning experiments by Paul Smeets, a neuroscientist at Utrecht University Medical Center in the Netherlands, in which he fed volunteers two versions of an orangeade drink.
All these results suggest the brain has some way of detecting calories while food is still in the mouth.
Saccharin, the first of the industrially manufactured artificial sweeteners, was discovered late in the 19th century and soon became popular.
Since then, a parade of sweeteners has come on stream, including cyclamate, aspartame, the sucrose-like (and very sweet) sucralose, and several others, including one called Rebiana, derived from a South American herb.
A handful of studies, starting in the 1980s, suggested that regular use of artificial sweeteners might even make people eat more, rather than less, by stimulating their appetites without satisfying them.
And recently, Guido Frank, a psychiatrist at the University of Colorado in Denver who has a particular interest in eating disorders, compared how the brain responds to sucralose and sucrose.
Thus, he fed the sweetener and the sugar to 12 women, adjusting the concentrations so that the sweetness of the two matched.
"They consciously could not distinguish them," New Scientist quoted Frank as saying.
But, when he looked at their brain responses with functional magnetic resonance imaging (fMRI), he saw clear differences.
Sucrose produced stronger activation in the "reward" areas of the brain that light up in response to pleasurable activities such as eating and drinking.
Sucralose didn't activate these areas as strongly, but it synchronised the activity in a whole constellation of taste-associated brain areas - and it did this more strongly than sucrose did.
Frank suggested that sucralose activates brain areas that register pleasant taste, but not strongly enough to cause satiation.
"That might drive you to eat something sweet or something calorific later on," he said.
Similar results emerged from brain-scanning experiments by Paul Smeets, a neuroscientist at Utrecht University Medical Center in the Netherlands, in which he fed volunteers two versions of an orangeade drink.
All these results suggest the brain has some way of detecting calories while food is still in the mouth.
Bonding between mother, baby reduces childhood neglect
Strengthening the bond between mother and baby is one way of reducing childhood neglect, says a new study.
University of Queensland (UQ) researcher Lane Strathearn's study identifies how increased pressures placed on mothers by society have reduced the perceived importance of raising children.
'I feel that the basic needs of children have fallen lower and lower on the priority list of families and society, with physical or emotional neglect often the unfortunate result,' Strathearn warned.
'This study emphasises the need to address the basic, universal needs of children, and stresses the importance of this early mother-infant relationship.
'Strengthening this crucial relationship may help to prevent some of the long term consequences of neglect that we are seeing more commonly today, such as delinquency, crime, developmental delay and psychiatric disorders.'
'Our subsequent study showed that the hormone, oxytocin, which is involved in breastfeeding, is also related to secure attachment in mothers and to brain 'reward' activation when they view pictures of their baby,' Strathearn said.
A father of seven, Strathearn grew up in Redcliffe, studied medicine at UQ and completed paediatric training at the Brisbane Mater Children's Hospital, before heading to the US in 2001.
Spanning nine years and drawing upon large longitudinal studies based in Brisbane and brain imaging data collected in Houston, Strathearn's research aimed to develop a better understanding of the pervasive problem of child neglect.
Watching mothers and babies 'connect' was one of the most enjoyable parts of the research, Strathearn said, according to a university release
University of Queensland (UQ) researcher Lane Strathearn's study identifies how increased pressures placed on mothers by society have reduced the perceived importance of raising children.
'I feel that the basic needs of children have fallen lower and lower on the priority list of families and society, with physical or emotional neglect often the unfortunate result,' Strathearn warned.
'This study emphasises the need to address the basic, universal needs of children, and stresses the importance of this early mother-infant relationship.
'Strengthening this crucial relationship may help to prevent some of the long term consequences of neglect that we are seeing more commonly today, such as delinquency, crime, developmental delay and psychiatric disorders.'
'Our subsequent study showed that the hormone, oxytocin, which is involved in breastfeeding, is also related to secure attachment in mothers and to brain 'reward' activation when they view pictures of their baby,' Strathearn said.
A father of seven, Strathearn grew up in Redcliffe, studied medicine at UQ and completed paediatric training at the Brisbane Mater Children's Hospital, before heading to the US in 2001.
Spanning nine years and drawing upon large longitudinal studies based in Brisbane and brain imaging data collected in Houston, Strathearn's research aimed to develop a better understanding of the pervasive problem of child neglect.
Watching mothers and babies 'connect' was one of the most enjoyable parts of the research, Strathearn said, according to a university release
Saturday, December 26, 2009
New discovery may help develop drugs that kill cancer cells
Scientists claim to have identified a family of "limpet-like" proteins that appears to play a vital role in repairing DNA damage which triggers cancer.
They hope that the finding may lead to new drugs, which could help kill cancer cells, and promote production of healthy replacements.
The Small Ubiquitin-like Modifier (SUMO) proteins appear to have a remarkable ability to zero in on the damaged areas.
They bind to normal proteins and direct them in to repair genetic glitches.
With this method, the proteins were even able to repair double strand DNA breaks - the most severe type of DNA damage.
And after the work is complete, the proteins detach themselves and move on.
The researchers focussed their study on BRCA1 gene, which, if damaged, is associated with a very high risk of breast cancer.
SUMO was shown to attach to the damaged gene, and switch it back on - helping prevent breast cancer forming.
"This new insight is the first step towards developing drugs which may protect normal cells from the side effects of chemotherapy, or improve the effectiveness of current breast cancer treatments," BBC News quoted Researcher Dr Jo Morris, from King's College London, as saying.
"DNA damage, particularly double strand DNA breaks, are a fundamental cause of cancer and we know that people who have mutations in the BRCA1 gene have a higher risk of developing some kinds of cancer," said Dr Lesley Walker, of Cancer Research UK, which part-funded the study
"Discovering that these limpet-like proteins play such an important role in repair may provide new opportunities to stop cancer from growing.
"This is an extremely complex and intricate biological process so it may be many years before we can use this knowledge to safely intervene and help treat cancer patients
They hope that the finding may lead to new drugs, which could help kill cancer cells, and promote production of healthy replacements.
The Small Ubiquitin-like Modifier (SUMO) proteins appear to have a remarkable ability to zero in on the damaged areas.
They bind to normal proteins and direct them in to repair genetic glitches.
With this method, the proteins were even able to repair double strand DNA breaks - the most severe type of DNA damage.
And after the work is complete, the proteins detach themselves and move on.
The researchers focussed their study on BRCA1 gene, which, if damaged, is associated with a very high risk of breast cancer.
SUMO was shown to attach to the damaged gene, and switch it back on - helping prevent breast cancer forming.
"This new insight is the first step towards developing drugs which may protect normal cells from the side effects of chemotherapy, or improve the effectiveness of current breast cancer treatments," BBC News quoted Researcher Dr Jo Morris, from King's College London, as saying.
"DNA damage, particularly double strand DNA breaks, are a fundamental cause of cancer and we know that people who have mutations in the BRCA1 gene have a higher risk of developing some kinds of cancer," said Dr Lesley Walker, of Cancer Research UK, which part-funded the study
"Discovering that these limpet-like proteins play such an important role in repair may provide new opportunities to stop cancer from growing.
"This is an extremely complex and intricate biological process so it may be many years before we can use this knowledge to safely intervene and help treat cancer patients
Friday, December 25, 2009
Scientists complete sequencing Tibetan antelope genome
Chinese scientists said Friday they have completed sequencing the genome of the Tibetan antelope which will hopefully explain the pathogenesis of chronic plateau sickness.
Tibetan antelopes, which live on China's Qinghai-Tibet Plateau, have been given the highest level of protection under the UN Convention on International Trade in Endangered Species since 1979, and listed among the most endangered species by the Chinese government since 1988.
They are considered to be ideal species for evolution studies, as they had lived on 'the Roof of the World' for millions of years against the backdrop of various environmental extremes, such as extreme cold and low oxygen levels.
'By sequencing the Tibetan antelope genome, we have laid the scientific foundation to decode the pathogenesis of chronic plateau sickness,' said Yang Huanming, an academician of the Chinese Academy of Sciences and a participant of the project.
'The studies can also contribute to improving the health of the plateau inhabitants, especially those of Tibetan ethnic group that has lived on the plateau generations after generations,' he said.
The project was jointly launched by the Qinghai University and the Beijing Genomics Institute's Shenzhen branch in April this year.
In addition to Tibetan antelopes, scientists are working to sequence the genomes of penguins and polar bears as part of the project.
'Sequencing the Tibetan antelope genome also lays the genetic foundation for us to carry out plateau life sciences studies, but it is only the first step,' said Gerili, vice president of the Qinghai University and director of the International Society for Mountain Medicine.
'We will further identify the functors on the genome, decode all the genetic information, and explore the genetic basis of Tibetan antelopes' ability to evolve and to adapt to harsh environment,' he said.
It is the world's first genome sequencing project for endangered species which live on the plateaus, he added.
Chinese scientists have contributed to the genome sequencing of rice, silkworm, hen, pig and giant panda. In October 2007, they finished sequencing the first Han Chinese genome.
Saturday, December 12, 2009
Scientists identify human body's natural defenses against cancer
Researchers in Canada have identified a novel molecular mechanism that prevents cancer.
Researchers from the Universite de Montreal and the Universite de Sherbrooke have found that the SOCS1 molecule prevents the cancer-causing activity of cytokines, hormones that are culprits in cancer-prone chronic inflammation diseases such as Crohns, in smokers and people exposed to asbestos.
"Excessive cytokine activity promotes cancer," said Dr. Gerardo Ferbeyre, senior author and a Universite de Montreal biochemistry professor.
"Discovery of these mechanisms will enable scientists to design a cancer-prevention strategy for people with chronic inflammatory diseases and lead to better understanding of the human body's natural defenses against cancer," Ferbeyre added.
The researchers say they were surprised to find that SOCS1 is linked to p53, the master regulator of natural anticancer defenses.
"Our team showed that SOCS1 is a direct regulator of the p53 gene and that in its absence the p53 pathway is significantly disabled," said Ferbeyre, noting the p53 gene is frequently lost in human cancer patients as it is SOCS1.
The new research suggests that the effects of SOCS1 loss in patients might also disable the p53 tumour suppression pathway.
The researchers also showed that the reintroduction of SOCS1 into tumour cells locked them into a permanent dormant state known as cell senescence preventing them from multiplying wildly as is typical of cancer cells.
"With this study, we provide new hope of finding a treatment to activate natural anticancer defenses in people at risk of suffering from cancer prompted by chronic inflammation," Ferbeyre said.
The research has been published in the prestigious journal Molecular Cell. (ANI)
Researchers from the Universite de Montreal and the Universite de Sherbrooke have found that the SOCS1 molecule prevents the cancer-causing activity of cytokines, hormones that are culprits in cancer-prone chronic inflammation diseases such as Crohns, in smokers and people exposed to asbestos.
"Excessive cytokine activity promotes cancer," said Dr. Gerardo Ferbeyre, senior author and a Universite de Montreal biochemistry professor.
"Discovery of these mechanisms will enable scientists to design a cancer-prevention strategy for people with chronic inflammatory diseases and lead to better understanding of the human body's natural defenses against cancer," Ferbeyre added.
The researchers say they were surprised to find that SOCS1 is linked to p53, the master regulator of natural anticancer defenses.
"Our team showed that SOCS1 is a direct regulator of the p53 gene and that in its absence the p53 pathway is significantly disabled," said Ferbeyre, noting the p53 gene is frequently lost in human cancer patients as it is SOCS1.
The new research suggests that the effects of SOCS1 loss in patients might also disable the p53 tumour suppression pathway.
The researchers also showed that the reintroduction of SOCS1 into tumour cells locked them into a permanent dormant state known as cell senescence preventing them from multiplying wildly as is typical of cancer cells.
"With this study, we provide new hope of finding a treatment to activate natural anticancer defenses in people at risk of suffering from cancer prompted by chronic inflammation," Ferbeyre said.
The research has been published in the prestigious journal Molecular Cell. (ANI)
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