People With Bigger Ears May Have Longer Lifespan
According to report, recently, Japanese experts found that, people with bigger ears or from the family having the longevous usually have longer lifespan and rarely get colds.
After investigation, the physician from School of Medicine of Keio University found that, centenarians' faces share a common feature of big ears, either with a big ear as a whole or with a big earlobe.
He said: "The ear is composed of cartilage which also covers the surface of joint and helps to reduce the frictions between the bones. Lack of cartilage will cause arthrosis deformans." That is to say, the big ears may mean higher synthesized frequency of cartilage tissues and less change of having arthrosis deformans, thus will lead to longevity.
Centenarians Reveal Genetic Key to Longevity
Spanish and Japanese men and women who live beyond the age of 100 have revealed that the key to longevity, at least in southern Europe, lies in their genes; specifically in a variant on chromosome 9p21.3, according to a recent study.
In addition to living more than 100 years, centenarians are people who live at least 15 years longer than the average individual in the West. The findings, published in the journal Age, establish that it's not entirely due to their lifestyle or diet that they are blessed with a long life, but that it is an inherited privilege.
This polymorphism - which is a particular sequence variation in the DNA among individuals from a particular population - located on chromosome 9p21.3 is responsible. It also has been previously proven to be associated with the risk of cardiovascular disease.
"This variant may be associated with extreme longevity, particularly among the Spanish population," lead author Alejandro LucÃa, researcher at the European University, told SINC. "The study also revealed that the risk allele reduces the possibilities of reaching one hundred years of age."
Researchers analyzed the frequencies of this polymorphism among centenarians and healthy adults, separating them into groups based on geographical regions and ethnic groups.
Participants included 152 Spaniards aged between 110 and 111 years and 742 Japanese people aged between 100 and 115 years.
The frequency of the risk C variant - carrying the greatest risk for cardiovascular disease - in Spanish centenarians was 47 percent. That's lower than in the healthy control sample group (53 percent) and in individuals with cardiovascular diseases (51 percent).
But among the Japanese participants, the results were more uniform. The risk gene variant had a similar frequency in centenarians (46 percent) and in healthy controls (47 percent), but it was less frequent than in controls performed with cardiovascular disease (57 percent).
Although the biological mechanisms are not yet known, chromosome 9p21.3 plays a role based on these results, and coincides with past research on the Mediterranean population north of Italy, "therefore the effect of this gene seems to exist in southern Europe at least," LucÃa concluded.
Study finds unexpected link between cell suicide and longevity
What is the secret to aging more slowly and living longer? Not antioxidants, apparently.
Many people believe that free radicals, the sometimes-toxic molecules produced by our bodies as we process oxygen, are the culprit behind aging. Yet a number of studies in recent years have produced evidence that the opposite may be true.
Now, researchers at McGill University have taken this finding a step further by showing how free radicals promote longevity in an experimental model organism, the roundworm C. elegans. Surprisingly, the team discovered that free radicals - also known as oxidants - act on a molecular mechanism that, in other circumstances, tells a cell to kill itself.
Programmed cell death, or apoptosis, is a process by which damaged cells commit suicide in a variety of situations: to avoid becoming cancerous, to avoid inducing auto-immune disease, or to kill off viruses that have invaded the cell. The main molecular mechanism by which this happens is well conserved in all animals, but was first discovered in C. elegans - a discovery that resulted in a Nobel Prize.
The McGill researchers found that this same mechanism, when stimulated in the right way by free radicals, actually reinforces the cell's defenses and increases its lifespan. Their findings are reported in a study published online May 8 in the journal Cell.
"People believe that free radicals are damaging and cause aging, but the so-called 'free radical theory of aging' is incorrect," says Siegfried Hekimi, a professor in McGill's Department of Biology and senior author of the study. "We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat - not cause - aging. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life."
The findings have important implications. "Showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signaling molecules", Hekimi says. "It also means that apoptosis signaling can be used to stimulate mechanisms that slow down aging".
"Since the mechanism of apoptosis has been extensively studied in people, because of its medical importance in immunity and in cancer, a lot of pharmacological tools already exist to manipulate apoptotic signaling. But that doesn't mean it will be easy."
Stimulating pro-longevity apoptotic signaling could be particularly important in neurodegenerative diseases, says Hekimi. In the brain the apoptotic signaling might be particularly tilted toward increasing the stress resistance of damaged cells rather than killing them, explains Hekimi. That's because it is harder to replace dead neurons than other kinds of cells, partly because of the complexity of the connections between neurons.
sources：[http://en.twwtn.com/Bignews/66434.html]
After investigation, the physician from School of Medicine of Keio University found that, centenarians' faces share a common feature of big ears, either with a big ear as a whole or with a big earlobe.
He said: "The ear is composed of cartilage which also covers the surface of joint and helps to reduce the frictions between the bones. Lack of cartilage will cause arthrosis deformans." That is to say, the big ears may mean higher synthesized frequency of cartilage tissues and less change of having arthrosis deformans, thus will lead to longevity.
Centenarians Reveal Genetic Key to Longevity
Spanish and Japanese men and women who live beyond the age of 100 have revealed that the key to longevity, at least in southern Europe, lies in their genes; specifically in a variant on chromosome 9p21.3, according to a recent study.
In addition to living more than 100 years, centenarians are people who live at least 15 years longer than the average individual in the West. The findings, published in the journal Age, establish that it's not entirely due to their lifestyle or diet that they are blessed with a long life, but that it is an inherited privilege.
This polymorphism - which is a particular sequence variation in the DNA among individuals from a particular population - located on chromosome 9p21.3 is responsible. It also has been previously proven to be associated with the risk of cardiovascular disease.
"This variant may be associated with extreme longevity, particularly among the Spanish population," lead author Alejandro LucÃa, researcher at the European University, told SINC. "The study also revealed that the risk allele reduces the possibilities of reaching one hundred years of age."
Researchers analyzed the frequencies of this polymorphism among centenarians and healthy adults, separating them into groups based on geographical regions and ethnic groups.
Participants included 152 Spaniards aged between 110 and 111 years and 742 Japanese people aged between 100 and 115 years.
The frequency of the risk C variant - carrying the greatest risk for cardiovascular disease - in Spanish centenarians was 47 percent. That's lower than in the healthy control sample group (53 percent) and in individuals with cardiovascular diseases (51 percent).
But among the Japanese participants, the results were more uniform. The risk gene variant had a similar frequency in centenarians (46 percent) and in healthy controls (47 percent), but it was less frequent than in controls performed with cardiovascular disease (57 percent).
Although the biological mechanisms are not yet known, chromosome 9p21.3 plays a role based on these results, and coincides with past research on the Mediterranean population north of Italy, "therefore the effect of this gene seems to exist in southern Europe at least," LucÃa concluded.
Study finds unexpected link between cell suicide and longevity
What is the secret to aging more slowly and living longer? Not antioxidants, apparently.
Many people believe that free radicals, the sometimes-toxic molecules produced by our bodies as we process oxygen, are the culprit behind aging. Yet a number of studies in recent years have produced evidence that the opposite may be true.
Now, researchers at McGill University have taken this finding a step further by showing how free radicals promote longevity in an experimental model organism, the roundworm C. elegans. Surprisingly, the team discovered that free radicals - also known as oxidants - act on a molecular mechanism that, in other circumstances, tells a cell to kill itself.
Programmed cell death, or apoptosis, is a process by which damaged cells commit suicide in a variety of situations: to avoid becoming cancerous, to avoid inducing auto-immune disease, or to kill off viruses that have invaded the cell. The main molecular mechanism by which this happens is well conserved in all animals, but was first discovered in C. elegans - a discovery that resulted in a Nobel Prize.
The McGill researchers found that this same mechanism, when stimulated in the right way by free radicals, actually reinforces the cell's defenses and increases its lifespan. Their findings are reported in a study published online May 8 in the journal Cell.
"People believe that free radicals are damaging and cause aging, but the so-called 'free radical theory of aging' is incorrect," says Siegfried Hekimi, a professor in McGill's Department of Biology and senior author of the study. "We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat - not cause - aging. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life."
The findings have important implications. "Showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signaling molecules", Hekimi says. "It also means that apoptosis signaling can be used to stimulate mechanisms that slow down aging".
"Since the mechanism of apoptosis has been extensively studied in people, because of its medical importance in immunity and in cancer, a lot of pharmacological tools already exist to manipulate apoptotic signaling. But that doesn't mean it will be easy."
Stimulating pro-longevity apoptotic signaling could be particularly important in neurodegenerative diseases, says Hekimi. In the brain the apoptotic signaling might be particularly tilted toward increasing the stress resistance of damaged cells rather than killing them, explains Hekimi. That's because it is harder to replace dead neurons than other kinds of cells, partly because of the complexity of the connections between neurons.
sources：[http://en.twwtn.com/Bignews/66434.html]