Jason Silva, Neil deGrasse Tyson and Melissa Sterry on Startalk Radio

Jason Silva, Neil deGrasse Tyson and Melissa Sterry on Startalk Radio

Astrophysicist Neil deGrasse Tyson, comic co-host Eugene Mirman and guest futurists Jason Silva and Melissa Sterry answer questions that lie at the intersection of technology, human biology and urban planning. Will bio-ware and nanotechnology allow humans to reprogram our biology? Can smart-materials, adaptive structures and sensor nets help city planners and policy makers create smart cities that adapt to environmental change the way forests do? Are we really approaching a “technological singularity” of emerging super-intelligence beyond which events cannot be predicted — and has humanity actually experienced one before?

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Our bodies, the tumor feeders

Our bodies, the tumor feeders

Our blood vessels, like the veins shown here, carry nutrients or waste to and from important body parts. They can also carry nutrients to tumors that can grow in the body.

Our blood vessels, like the veins shown here, carry nutrients or waste to and from important body parts. They can also carry nutrients to tumors that can grow in the body.

Tumors are kind of like mold. Molds find a nice dark spot to grow—maybe in the corner of the pantry or in the cabinet under the sink. It grows somewhere where it can find the resources it needs, like water and the right temperature. As a tumor grows, it needs resources as well—iron, oxygen, and sugar.

Those are the same nutrients that the human body uses to feed the heart, the lungs, and the brain. So if our bodies need these special nutrients, how do tumors get them? Well, if someone has a tumor, that tumor is fed from that person’s very own blood vessels.

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As a tumor grows, the body will build blood vessels that go right to the tumor tissue, putting nutrients within the reach of the tumor. This is similar to how we might accidentally drop food behind the counter and feed any mold that might be growing there. In the PLOSable article, “Generation of Functional Blood Vessels from a Single c-kit+ Adult Vascular Endothelial Stem Cell,” a group of scientists identified which genes and cells make new blood vessels. If scientists can understand how our bodies are tricked into building blood vessels that deliver nutrient-rich blood to tumors, they may be able to use this information to stop our bodies from building those vessels. That way, they might be able to stop tumors from growing.

Vessels are the Way to My Heart

Blood is pushed through our bodies to our tissues and organs with the help of the heart.

Blood is pushed through our bodies to our tissues and organs with the help of the heart.

Blood vessels are the tubes that carry blood through your body. Because this is such an important job, these vessels have to be healthy. Your body also has to be able to make more blood vessels as you grow, so your tissues and organs can get the nutrients they need. So how does your body make thin, flat cells that make blood vessels?

The Stem is Where It’s At

Different cells in your body are assigned different jobs. You have skin cells that help protect you from injury, hair cells that make your hair grow, brain cells that help you think and react, and more. But some cells are assigned to the job of making other cells. These are like parent cells, since they make new cells, but we call them stem cells. When your body needs more cells, it can activate a certain type of stem cell so they will make specific cells that your body needs.

Here we can see a different layers of one type of blood vesel.

Here we can see a different layers of one type of blood vesel.

So Many Cells, So Little Time

To figure out how your body makes blood vessel cells, called endothelial cells, scientists studied their parent cells. These cells can be found along the walls of blood vessels, where they sit and wait to make endothelial cells. The parent cells are called vascular endothelial stem cells. Anytime the body needs more blood vessels, the vascular endothelial stem cells can divide to make more endothelial cells.

But the thin, flat endothelial cells that are made are quickly used by the body because blood vessels need to be repaired anytime you get a cut or injury, and anytime you grow. This is why the stem cells making endothelial cells are so important. These stem cells can also be dangerous if they start building blood vessels to the wrong places.

Genes Tell the Body What to Do

Hold on… if the stem cells keep making new endothelial cells, won’t the body have too many cells? Actually, no. Your body only makes new cells when your genes tell it to.  Your genes are kind of like your parents – your parents tell you when to clean your room and genes tell your body when to build new cells. C-kit genes tell the vascular endothelial stem cells to make more endothelial cells to build more blood vessels, but only when the body needs more.  This makes sure the body doesn’t make too many cells.

To find this group of genes, the scientists took samples from vascular endothelial stem cells in mice. They then extracted the DNA contained in these cells. Cells don’t hold a lot of DNA, so scientists have to copy the DNA until there is enough for them to use. To do this, they take the double-stranded DNA, split it in half, and put the pieces in a vial with building blocks called nucleotides.

Researchers used two kinds of mice--regular mice that make lots of endothelial cells, and mutant mice, that make very few endothelial cells.

Researchers used two kinds of mice–regular mice that make lots of endothelial cells, and mutant mice, that make very few endothelial cells.

These nucleotides attach to each half in a specific way, re-creating the strand that was removed. The scientists do this again and again, until they have thousands of DNA strands.

The scientists then looked at the order of nucleotides in the DNA to map out all the different genes. But mice have thousands of genes—how did the scientists figure out which ones are involved in making cells for blood vessels?

They compared the genes of mice that made a lot of vascular endothelial stem cells to the genes of mutant mice that didn’t make very many vascular endothelial stem cells. By comparing the genes of these two mice types, they figured out what genes controlled the formation of blood vessels. Those genes are called C-kit genes.

Usually c-kit genes tell the blood vessels to grow only when they’re needed. But if cells are exposed to harmful materials, the genes they carry can be damaged and may no longer work correctly. This damage often causes c-kit genes to keep making blood vessels even when the body doesn’t need any more. If scientists can find a way to turn these genes off or fix them, they can stop the unneeded growth of endothelial cells. The body would not build blood vessels to feed tumors and the tumors would die.

This image has four parts. The first two (A and B) are graphs showing that mice with mutant c-kit genes (the mice on the left) make lower numbers of endothelial cells. The green on the graphs represents the endothelial cells. The mice with mutant c-kit genes only have 1% endothelial cells, while the other mice have 35%. This shows that c-kit genes are the genes that control the production of endothelial cells. The second two parts (C and D) are graphs showing that in the mice with mutant c-kit genes (the mice on the left), tumors grow far less quickly than in mice with normal c-kit genes. In C, the images on the left show that mice with abnormal genes make fewer blood vessels and fewer endothelial cells than the mice on the right, that have regular c-kit genes. In D, the graph shows the size of a tumor as it grows over time. The green line represents the mice with normal c-kit genes, that have faster-growing tumors, while the red line represents mice with mutant c-kit genes.

This image has four parts. The first two (A and B) are graphs showing that mice with mutant c-kit genes (the mice on the left) make lower numbers of endothelial cells.
The green on the graphs represents the endothelial cells. The mice with mutant c-kit genes only have 1% endothelial cells, while the other mice have 35%. This shows that c-kit genes are the genes that control the production of endothelial cells.
The second two parts (C and D) are graphs showing that in the mice with mutant c-kit genes (the mice on the left), tumors grow far less quickly than in mice with normal c-kit genes.
In C, the images on the left show that mice with abnormal genes make fewer blood vessels and fewer endothelial cells than the mice on the right, that have regular c-kit genes.
In D, the graph shows the size of a tumor as it grows over time. The green line represents the mice with normal c-kit genes, that have faster-growing tumors, while the red line represents mice with mutant c-kit genes.

From Stem Cells to Cancer

Just like food crumbs can feed mold, extra blood vessels in your body can feed tumors. But if we can figure out a way to stop our bodies from creating the vessels tumors use to get resources, maybe we can stop some tumors from growing. Now that scientists have figured out which genes are responsible for building blood vessels, they can focus on ways to change the activation of this gene. This puts us one step closer to stopping tumor growth.

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Article by Alexis Abboud oryginally posted on askabiologist.asu.edu

Why dogs are such diverse?

Why dogs are such diverse?

Pulis have a very distinct coat.

Pulis have a very distinct coat.

Do you have a dog? A Golden Retriever, Poodle, Great Dane or maybe a tiny Chihuahua? That’s just listing a few – there are over 170 recognized dog breeds! Scientists are finding out that what makes dogs look different from one another (their doggie DNA) is less complicated than many other species, like you and me. In the PLoS Biology article,A Simple Genetic Architecture Underlies Morphological Variation in Dogs, scientists are examining what causes dogs to look the way they do.

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Doggie Diversity

There are 170 official dog breeds recognized by The American Kennel Club, and that’s not even counting the unregistered breeds and mutts. With all these different types of dogs, how did Great Danes and tiny Chihuahuas come to look so different?

The answer is in the doggie DNA.

Many scientists are just as curious as you about what makes dogs look the way they do, or in other words, how the genes in dog DNA are expressed as a phenotype. Just like us, dogs inherit genetic information from their doggie dad and mom. That genetic information determines how they look. Scientists have identified how many different genes get passed down through the generations to affect how dogs look.

One group of scientists set out to answer this question with the CanMap Project. They created a huge genetic map of canine DNA. The scientists gathered this DNA from 80 different dog breeds as well as wolves, jackals, and even feral African village dogs. We wouldn’t want to cuddle with some of those breeds.

Dogs are diverse. They come in all different colors, shapes and sizes.

Dogs are diverse. They come in all different colors, shapes and sizes.

Mapping Doggie DNA

The scientists mapped over 120,000 spots on each dog’s DNA. They did this to see how the dog’s nucleobases fit together. Nucleobases are the puzzle pieces that make up genes. By looking at the nucleobases, scientists can determine where differences arise in the doggie DNA. When the DNA of one dog breed has more bases in common with the DNA of another dog breed, it means they are more closely related. Just like you and your family have more bases in common than you and a stranger.

Nucleobases like adenine, thymine, cytosine, and guanine are the building blocks of DNA.

Nucleobases like adenine, thymine, cytosine, and guanine are the building blocks of DNA.

Humans have had a large influence on dog DNA too since dogs were domesticated and bred by humans to look the way they do. For instance, humans bred Chihuahuas with other Chihuahuas for a very long time. This means that Chihuahuas have many identical nucleobases on their DNA, and all those puzzle pieces fit together to look like a Chihuahua.

Short segments of genes from a distant dog relative, the gray wolf, were found in every sample of the dogs’ genetic information. However, the nucleotides that make dogs look different were only found in a few areas of the DNA. These reflect the areas that have changed in the centuries since people started breeding dogs for different traits, creating many different breeds of dog in the process.

In humans, our diversity and nucleotide puzzle pieces work differently. Instead of human diversity arising from a few different areas on the gene, the way we look is regulated by hundreds of different weak genes that interact to make us unique! Dogs may have less areas of diversity compared to humans because of what scientists call a gene bottleneck.

What’s a Gene Bottleneck?

Imagine black and red ants trying to get into your house through a very small neck of a bottle. There may be many ants outside, but only so many can enter the house because they have to go one-by-one in a single file line.

If only red ants get through before the bottleneck closes, those ants may go on to have only red ant babies in the future. Even though there used to be more diversity in ant color, only red ants got through and it changed how the entire population looked. This is similar to how a gene bottleneck works.

Imagine that you could line up all the different dog genes in a single-file line and march them through a bottleneck. Only a certain number get through, and those determine how a dog looks. It’s on a larger scale, but it’s like only letting the red ants through. We humans are the ones that are responsible for closing off the bottleneck, and we choose which dog traits we like best. So a dachshund (or wiener dog) is chosen because of his short and long body, while a Great Dane is chosen for his huge body.

Genes from this Great Dane and Chihuahua mix are similar, even though they look very different. Wikimedia - Ellen Levy Finch

Genes from this Great Dane and Chihuahua mix are similar, even though they look very different. Wikimedia – Ellen Levy Finch

Diversity is lost in this process, or in other words, lots of those nucleotide puzzle pieces get eliminated. For centuries people have been creating gene bottlenecks by selectively breeding different dogs for different traits. That explains why so few areas on the genome are responsible for how dogs look.

So What Did We Learn?

So are Great Danes and Chihuahuas pretty much the same? Yes and no. Just by looking at these dogs, you can tell that they are very different, but that’s because of humans breeding them to look like that. Scientists found that only a small number of genes actually account for different phenotypes. So only a few very powerful gene locations lead to doggie diversity, even though dog breeds look so different!

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Article by Emilio Galan oryginally posted on askabiologist.asu.edu

What’s Happening to Honey Bees?

What’s Happening to Honey Bees?

You’ve probably heard about the sudden and mysterious drop in honey bee populations throughout the U.S.A. and Europe. Beekeepers used to report average losses in their worker bees of about 5-10% a year, but starting around 2006, that rate jumped to about 30%. Today, many large beekeeping operations are reporting that up to 40 or 50 percent of their swarms have mysteriously disappeared. This massive die-off of honey bee populations has been dubbed colony collapse disorder, and it is a big, big deal.

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