UC Science Today

This week on Science Today. The oldest documented person lived to 122. Was it luck, or was it genetics? Researchers at UC Berkeley recently found two genes in mice and worms that may explain why some humans can live past one hundred.

"These genes are the number one correlation of extreme longevity."

And while UC Berkeley scientists study aging at the molecular level, researchers at the Lawrence Livermore National Laboratory and UC Davis are looking to prevent the wear and tear our bodies experience over a lifetime. For instance, when a person suffers a traumatic joint injury, it often leads to damaged cartilage and this results in the development of osteoarthritis.

"We try to understand what happens at the joint level, what are all the factors that contribute to post traumatic osteoarthritis."

We’ll also check in with a UC San Francisco study exploring resilience in the classroom, and how mentoring programs may be tailored to encourage these qualities in young students.

"Motivation, grit, mindset – these are all concepts that are very popular in education right now, on how to raise a successful child."

To listen to these and other episodes about University of California research, subscribe to UC Science Today on iTunes or follow us on Facebook. Thanks for listening, I’m Larissa Branin.

Subscribe to Science Today on iTunes: http://apple.co/1TQBewD

Follow us on Facebook: https://www.facebook.com/ucsciencetoday/

This is Science Today. Low calorie diets in the early lives of some animals have long been associated with metabolic changes that increase lifespan. In experiments on mice and worms known as C.elegans, biologist Andrew Dillin of the University of California, Berkeley and his team uncovered two critical genes responsible for these striking changes. Dillin’s laboratory also discovered that these metabolic shifts are caused by genetic switches, or enzymes that can control these genes and be manipulated by the researchers as well.

"These genes are the number one correlation of extreme longevity. So the ones that are long-lived have these two genes very highly upregulated, and the animals that are short-lived have these two genes downregulated."

Basically, the long-lived organisms express these genes more than the short-lived ones. These observations may also reflect aging in humans.

"The next step is, can we begin to look at super centenarians, people that are living well into their hundreds. Do they have alterations in these genes that people that are only living to be 80 or 70 don’t have?"

For Science Today, I’m Larissa Branin.

This is Science Today. Low calorie diets in the early lives of some animals have long been associated with metabolic changes that increase lifespan. In experiments on mice and worms known as C.elegans, biologist Andrew Dillin of the University of California, Berkeley and his team uncovered two critical genes responsible for these striking changes. Dillin’s laboratory also discovered that these metabolic shifts are caused by genetic switches, or enzymes that can control these genes and be manipulated by the researchers as well.

"These genes are the number one correlation of extreme longevity. So the ones that are long-lived have these two genes very highly upregulated, and the animals that are short-lived have these two genes downregulated."

Basically, the long-lived organisms express these genes more than the short-lived ones. These observations may also reflect aging in humans.

"The next step is, can we begin to look at super centenarians, people that are living well into their hundreds. Do they have alterations in these genes that people that are only living to be 80 or 70 don’t have?"

For Science Today, I’m Larissa Branin.

This week on Science Today. The oldest documented person lived to 122. Was it luck, or was it genetics? Researchers at UC Berkeley recently found two genes in mice and worms that may explain why some humans can live past one hundred.

"These genes are the number one correlation of extreme longevity."

And while UC Berkeley scientists study aging at the molecular level, researchers at the Lawrence Livermore National Laboratory and UC Davis are looking to prevent the wear and tear our bodies experience over a lifetime. For instance, when a person suffers a traumatic joint injury, it often leads to damaged cartilage and this results in the development of osteoarthritis.

"We try to understand what happens at the joint level, what are all the factors that contribute to post traumatic osteoarthritis."

We’ll also check in with a UC San Francisco study exploring resilience in the classroom, and how mentoring programs may be tailored to encourage these qualities in young students.

"Motivation, grit, mindset – these are all concepts that are very popular in education right now, on how to raise a successful child."

To listen to these and other episodes about University of California research, subscribe to UC Science Today on iTunes or follow us on Facebook. Thanks for listening, I’m Larissa Branin.

Subscribe to Science Today on iTunes: http://apple.co/1TQBewD

Follow us on Facebook: https://www.facebook.com/ucsciencetoday/

More than half of people who suffer traumatic injury to their knee by tearing ligaments in their joint will eventually develop osteoarthritis within ten to fifteen years post-injury. This has huge quality of life issues, as well as the economic burden of medical costs. So researchers are trying to see if they can prevent cartilage degeneration immediately post-injury as a potential therapy. Biomedical scientist Gabriela Loots of the Lawrence Livermore National Laboratory says there are strains of mice that are not as susceptible to cartilage degeneration.

"So, we’re trying to understand what is it about the resistant strains that prevents them from having this cartilage degradation because if we can understand why they don’t degrade, maybe we can understand what molecules we can target to prevent degradation."

Loots is working on this study in collaboration with scientists at the University of California, Davis.

"We try to understand what happens at the joint level, what are all the factors that contribute to post traumatic osteoarthritis."

More than half of people who suffer traumatic injury to their knee by tearing ligaments in their joint will eventually develop osteoarthritis within ten to fifteen years post-injury. This has huge quality of life issues, as well as the economic burden of medical costs. So researchers are trying to see if they can prevent cartilage degeneration immediately post-injury as a potential therapy. Biomedical scientist Gabriela Loots of the Lawrence Livermore National Laboratory says there are strains of mice that are not as susceptible to cartilage degeneration.

"So, we’re trying to understand what is it about the resistant strains that prevents them from having this cartilage degradation because if we can understand why they don’t degrade, maybe we can understand what molecules we can target to prevent degradation."

Loots is working on this study in collaboration with scientists at the University of California, Davis.

"We try to understand what happens at the joint level, what are all the factors that contribute to post traumatic osteoarthritis."

From a dolphin’s mouth to the Atacama desert in Chile, microbes can turn up where scientists least expect them. Using DNA sequencing technology, a team of researchers recently published a new version of biology’s tree of life to include many of these elusive microbes. Microbiologist Karthik Anantharaman of the University of California, Berkeley says that these organisms just didn’t fit many of biology’s definitions.

"There’s a particular group of bacteria that we are calling the CPRs, or the candidate phyla radiation. And the common thread through all of these organisms is that they’re extremely tiny. So if we opened up any microbiology textbook today, they would tell you that the average size of a bacteria is about one micron. But these organisms are smaller than .1 microns. So they’re ten times smaller in diameter and a thousand times smaller in volume. And over the last 15 years, we have deciphered that biology can be very unpredictable."

From a dolphin’s mouth to the Atacama desert in Chile, microbes can turn up where scientists least expect them. Using DNA sequencing technology, a team of researchers recently published a new version of biology’s tree of life to include many of these elusive microbes. Microbiologist Karthik Anantharaman of the University of California, Berkeley says that these organisms just didn’t fit many of biology’s definitions.

"There’s a particular group of bacteria that we are calling the CPRs, or the candidate phyla radiation. And the common thread through all of these organisms is that they’re extremely tiny. So if we opened up any microbiology textbook today, they would tell you that the average size of a bacteria is about one micron. But these organisms are smaller than .1 microns. So they’re ten times smaller in diameter and a thousand times smaller in volume. And over the last 15 years, we have deciphered that biology can be very unpredictable."

With the ongoing epidemic, Zika virus remains an ominous diagnosis for pregnant mothers. Since little was known about this disease prior to the outbreak, scientists are working quickly to close the research gap. Neurologist Arnold Kriegstein of the University of California, San Francisco recently identified a molecular bridge that could allow Zika to enter a baby’s brain from the bloodstream. Before, Zika’s use of this channel was mainly hypothetical.

"But now, we do have access to the virus from Brazil, and we are actually doing these experiments. We’re taking these live cells and we’re exposing them to the virus."

Kriegstein and his team will look at a variety of cell types, including developing neurons known as radial glial cells.

"We’re also looking not just at the radial glial cells, which we expect will be infected, but other cell types, some of which we don’t expect to be infected. If we can understand the mechanism of how the virus is invading the brain, how it’s causing microcephaly that may provide some therapeutic targets that you could use to block the infection at some level."

With the ongoing epidemic, Zika virus remains an ominous diagnosis for pregnant mothers. Since little was known about this disease prior to the outbreak, scientists are working quickly to close the research gap. Neurologist Arnold Kriegstein of the University of California, San Francisco recently identified a molecular bridge that could allow Zika to enter a baby’s brain from the bloodstream. Before, Zika’s use of this channel was mainly hypothetical.

"But now, we do have access to the virus from Brazil, and we are actually doing these experiments. We’re taking these live cells and we’re exposing them to the virus."

Kriegstein and his team will look at a variety of cell types, including developing neurons known as radial glial cells.

"We’re also looking not just at the radial glial cells, which we expect will be infected, but other cell types, some of which we don’t expect to be infected. If we can understand the mechanism of how the virus is invading the brain, how it’s causing microcephaly that may provide some therapeutic targets that you could use to block the infection at some level."