UC Science Today

Parents, the next time your child picks up a can of soda, tell them they're at risk of shortening their telomeres. These are the protective caps at the ends of our chromosomes and they affect how quickly our cells age. And when our telomeres are shortened, this puts us at risk of age-related maladies like heart disease, diabetes, and some types of cancer. Dr. Cindy Leung of the University of California, San Francisco, says that while their study surveyed healthy adults, it's also possible that soda consumption is associated with telomere shortening in kids.

"We know that childhood is a really critical window for our telomeres to develop. If we're marketing sugary beverages to children and they're drinking them at such high levels, it could really put them on this accelerated aging trajectory before they even hit adolescence."

The good news - Leung says that telomere shortening is reversible.

"Drinking less sugary beverages would be one way to either halt or slow down their telomere shortening process. We should promote other health behaviors that would help to lengthen our telomeres."

Parents, the next time your child picks up a can of soda, tell them they're at risk of shortening their telomeres. These are the protective caps at the ends of our chromosomes and they affect how quickly our cells age. And when our telomeres are shortened, this puts us at risk of age-related maladies like heart disease, diabetes, and some types of cancer. Dr. Cindy Leung of the University of California, San Francisco, says that while their study surveyed healthy adults, it's also possible that soda consumption is associated with telomere shortening in kids.

"We know that childhood is a really critical window for our telomeres to develop. If we're marketing sugary beverages to children and they're drinking them at such high levels, it could really put them on this accelerated aging trajectory before they even hit adolescence."

The good news - Leung says that telomere shortening is reversible.

"Drinking less sugary beverages would be one way to either halt or slow down their telomere shortening process. We should promote other health behaviors that would help to lengthen our telomeres."

Currently, the best known cure for liver cirrhosis is an organ transplant. But in a mouse model, University of California, San Francisco researchers have found a way to transform the diseased cells that drive this progressive scarring into healthy cells. Postdoctoral scholar Milad Rezvani says a big question is whether this technique will prove to be clinically relevant and safe to treat damaged livers in humans.

"Liver cirrhosis is still a huge public health burden. Right now we have shown that we can turn this one cirrhosis causing cell type into normal liver cells that function. So the obvious question after a successful mouse in vivo study is, can we do this in human patients?"

The technique used a virus to shuttle the desirable genes into diseased cells, and also proved successful on plates of cirrhosis-causing human cells. Rezvani’s team is now working to refine this virus so it only targets the liver and avoids infecting other cells in the body.

Currently, the best known cure for liver cirrhosis is an organ transplant. But in a mouse model, University of California, San Francisco researchers have found a way to transform the diseased cells that drive this progressive scarring into healthy cells. Postdoctoral scholar Milad Rezvani says a big question is whether this technique will prove to be clinically relevant and safe to treat damaged livers in humans.

"Liver cirrhosis is still a huge public health burden. Right now we have shown that we can turn this one cirrhosis causing cell type into normal liver cells that function. So the obvious question after a successful mouse in vivo study is, can we do this in human patients?"

The technique used a virus to shuttle the desirable genes into diseased cells, and also proved successful on plates of cirrhosis-causing human cells. Rezvani’s team is now working to refine this virus so it only targets the liver and avoids infecting other cells in the body.

This week on Science Today. Is there anything one can’t make with 3D printing technology? How about living blood vessels? We visit Monica Moya at the Lawrence Livermore National Laboratory to find out more about how she created 3D bioprints of a vasculature system using natural ‘bioinks'.

"So one of our inks is made out of the same stuff that you find in a blood clot. And we intentionally do this because we are in a sense, are co-engineering with the cells."

Given this this ability to print vasculature, the feasibility of 3D printable organs doesn’t seem so farfetched anymore. On a somewhat related note, we next take a look at organoids, or miniature lab models that mimic the physiology of real organs.

These systems are helping researchers in their quest to learn as much as possible about Zika virus. Finding a good lab model has been challenging, so UC San Francisco's Arnold Kriegstein and his colleagues are stepping in to examine the options.

"We were looking at what other model systems could be used to study how the Zika virus infects cells".

And we sort of went out on a limb for this last one. Nadav Ahituv of UCSF tells us about how novel genes associated with limb development in bats may help us understand how our own arms and legs grow.

"So when our limbs grow, we basically have webbing between them, and then that webbing sort of dies, but in the bat forelimbs, that webbing remains and makes part of the wing."

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

More information:

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

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

Stories mentioned in this roundup:

https://soundcloud.com/sciencetoday/vasculature_bioprint

https://soundcloud.com/sciencetoday/organoid_lab

https://soundcloud.com/sciencetoday/limbs_bats

This week on Science Today. Is there anything one can’t make with 3D printing technology? How about living blood vessels? We visit Monica Moya at the Lawrence Livermore National Laboratory to find out more about how she created 3D bioprints of a vasculature system using natural ‘bioinks'.

"So one of our inks is made out of the same stuff that you find in a blood clot. And we intentionally do this because we are in a sense, are co-engineering with the cells."

Given this this ability to print vasculature, the feasibility of 3D printable organs doesn’t seem so farfetched anymore. On a somewhat related note, we next take a look at organoids, or miniature lab models that mimic the physiology of real organs.

These systems are helping researchers in their quest to learn as much as possible about Zika virus. Finding a good lab model has been challenging, so UC San Francisco's Arnold Kriegstein and his colleagues are stepping in to examine the options.

"We were looking at what other model systems could be used to study how the Zika virus infects cells".

And we sort of went out on a limb for this last one. Nadav Ahituv of UCSF tells us about how novel genes associated with limb development in bats may help us understand how our own arms and legs grow.

"So when our limbs grow, we basically have webbing between them, and then that webbing sort of dies, but in the bat forelimbs, that webbing remains and makes part of the wing."

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

More information:

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

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

Stories mentioned in this roundup:

https://soundcloud.com/sciencetoday/vasculature_bioprint

https://soundcloud.com/sciencetoday/organoid_lab

https://soundcloud.com/sciencetoday/limbs_bats

A recent collaboration between the University of California, San Francisco and international researchers has revealed some surprising genes linked to limb development in bats. Associate professor Nadav Ahituv studies human limb malformations and says these are novel genes that were not previously associated with limb development at all.

"For example, one gene that we see is expressed specifically in elongating digits three to five in the developing bat, but in mice, they’re not expressed in that location. And so it looks like bats adopted that gene to work in that location, and making it an important gene for wing development. We found genes that are involved in apoptosis and cell death. So when our limbs grow, we basically have webbing between them, and then that webbing sort of dies, but in the bat forelimbs, that webbing remains and makes part of the wing."

Ahituv says their work offers insight into the unique growth of arms and legs in other mammals such as ourselves.

A recent collaboration between the University of California, San Francisco and international researchers has revealed some surprising genes linked to limb development in bats. Associate professor Nadav Ahituv studies human limb malformations and says these are novel genes that were not previously associated with limb development at all.

"For example, one gene that we see is expressed specifically in elongating digits three to five in the developing bat, but in mice, they’re not expressed in that location. And so it looks like bats adopted that gene to work in that location, and making it an important gene for wing development. We found genes that are involved in apoptosis and cell death. So when our limbs grow, we basically have webbing between them, and then that webbing sort of dies, but in the bat forelimbs, that webbing remains and makes part of the wing."

Ahituv says their work offers insight into the unique growth of arms and legs in other mammals such as ourselves.

A new study from the University of California, San Francisco may help physicians treat inflammation in diabetic patients without causing complete suppression of the immune system. Endocrinologist Suneil Koliwad recently discovered the mechanism behind the inflammation that occurs when particular immune cells known as macrophages are exposed to excess saturated fats.

"We might have uncovered an inroad into a way that we could alleviate the form of inflammation that goes on in the fat tissue where lipids may serve as a trigger, but still allow the macrophages in the tissue to remain responsive to triggers of inflammation that might represent infection or injury. To stimuli that we would want to maintain responsiveness against."

Immune suppression drugs may often keep over-the-top immune reactions in check, but they can also put the person at risk of other conditions. Koliwad says the next step is to hone in even more on this pathway to see how it may help scientists develop better diabetes drugs.

Photo by Steve Gschmeissner.

A new study from the University of California, San Francisco may help physicians treat inflammation in diabetic patients without causing complete suppression of the immune system. Endocrinologist Suneil Koliwad recently discovered the mechanism behind the inflammation that occurs when particular immune cells known as macrophages are exposed to excess saturated fats.

"We might have uncovered an inroad into a way that we could alleviate the form of inflammation that goes on in the fat tissue where lipids may serve as a trigger, but still allow the macrophages in the tissue to remain responsive to triggers of inflammation that might represent infection or injury. To stimuli that we would want to maintain responsiveness against."

Immune suppression drugs may often keep over-the-top immune reactions in check, but they can also put the person at risk of other conditions. Koliwad says the next step is to hone in even more on this pathway to see how it may help scientists develop better diabetes drugs.

Photo by Steve Gschmeissner.