Last quarter moon and Jupiter December 3

Tomorrow morning – December 3, 2015 – you can see the moon and the king planet Jupiter quite close together on the great dome of sky. Watch for these two worlds no matter where you live on Earth. They’re up in the wee hours, higher in the sky before dawn. Just look for the brilliant starlike object close to the moon in the predawn sky on December 3, and sure enough, that’ll be the giant planet Jupiter.

The moon on December 3 will be at or near its last quarter phase. The last quarter moon will come to pass on December 3 at 7:40 Universal Time. Although the last quarter moon happens at the same instant worldwide, the clock reads differently according to time zone. At U.S. time zones, the last quarter moon falls on December 3 at 2:40 a.m. EST, 1:40 a.m. CST, 12:40 a.m. MST – and on December 2 at 11:40 p.m. PST. What does it all mean? It only means that – depending on where you live worldwide – the moon might or might not be above the horizon at the instant that it reaches the crest of its last quarter phase.

Meanwhile, all of us will see an approximate last quarter moon, in the shape of half a pie, on the morning of December 3.

By the way, the moon and Jupiter will be even closer together on the sky’s dome on the morning on December 4. See the chart below.

Get up early to see the waning moon, Regulus and Jupiter. For illustrative purposes, the moon appears larger on this chart than in the real sky. The green line depicts the ecliptic – Earth’s orbital plane projected outward onto the constellations of the Zodiac.

Jupiter is very bright, but another planet up before dawn outshines it. In fact, two celestial bodies – the moon and Venus – outshine Jupiter in the morning sky before sunrise.

But there’s not much chance of mistaking Venus for Jupiter, or vice versa, on the mornings of December 3 and 4.

On these dates, Jupiter shines closer to the moon on the sky’s dome than Venus does. See the sky chart below.

EarthSky astronomy kits are perfect for beginners. Order today from the EarthSky store

For illustrative purposes the moon appears larger than it does in the actual sky. The green line depicts the ecliptic – the sun’s apparent pathway in front of the backdrop stars.

Later on in the first week of December, 2015, the waning crescent moon will swing by the red planet Mars and then Venus.

What’s more, people in central and eastern Africa can watch the moon occult – cover over – Mars in the December 6 predawn/dawn sky; and people in northwestern North America (Alaska, Yukon, British Columbia, Northwest Territories) can witness the moon occulting Venus in their December 7 predawn/dawn sky.

Bottom line: In the predawn hours on December 3, 2015, the moon will be at or near its last quarter phase and shining close to the planet Jupiter on the sky’s dome.

Almost gone! EarthSky lunar calendars make great gifts. Order now.

Donate: Your support means the world to us

from EarthSky http://ift.tt/1Nnnclp

Tomorrow morning – December 3, 2015 – you can see the moon and the king planet Jupiter quite close together on the great dome of sky. Watch for these two worlds no matter where you live on Earth. They’re up in the wee hours, higher in the sky before dawn. Just look for the brilliant starlike object close to the moon in the predawn sky on December 3, and sure enough, that’ll be the giant planet Jupiter.

The moon on December 3 will be at or near its last quarter phase. The last quarter moon will come to pass on December 3 at 7:40 Universal Time. Although the last quarter moon happens at the same instant worldwide, the clock reads differently according to time zone. At U.S. time zones, the last quarter moon falls on December 3 at 2:40 a.m. EST, 1:40 a.m. CST, 12:40 a.m. MST – and on December 2 at 11:40 p.m. PST. What does it all mean? It only means that – depending on where you live worldwide – the moon might or might not be above the horizon at the instant that it reaches the crest of its last quarter phase.

Meanwhile, all of us will see an approximate last quarter moon, in the shape of half a pie, on the morning of December 3.

By the way, the moon and Jupiter will be even closer together on the sky’s dome on the morning on December 4. See the chart below.

Get up early to see the waning moon, Regulus and Jupiter. For illustrative purposes, the moon appears larger on this chart than in the real sky. The green line depicts the ecliptic – Earth’s orbital plane projected outward onto the constellations of the Zodiac.

Jupiter is very bright, but another planet up before dawn outshines it. In fact, two celestial bodies – the moon and Venus – outshine Jupiter in the morning sky before sunrise.

But there’s not much chance of mistaking Venus for Jupiter, or vice versa, on the mornings of December 3 and 4.

On these dates, Jupiter shines closer to the moon on the sky’s dome than Venus does. See the sky chart below.

EarthSky astronomy kits are perfect for beginners. Order today from the EarthSky store

For illustrative purposes the moon appears larger than it does in the actual sky. The green line depicts the ecliptic – the sun’s apparent pathway in front of the backdrop stars.

Later on in the first week of December, 2015, the waning crescent moon will swing by the red planet Mars and then Venus.

What’s more, people in central and eastern Africa can watch the moon occult – cover over – Mars in the December 6 predawn/dawn sky; and people in northwestern North America (Alaska, Yukon, British Columbia, Northwest Territories) can witness the moon occulting Venus in their December 7 predawn/dawn sky.

Bottom line: In the predawn hours on December 3, 2015, the moon will be at or near its last quarter phase and shining close to the planet Jupiter on the sky’s dome.

Almost gone! EarthSky lunar calendars make great gifts. Order now.

Donate: Your support means the world to us

from EarthSky http://ift.tt/1Nnnclp

45 años cumpliendo nuestra misión

Por Gina McCarthy
Apenas dos semanas después de que se estableció la EPA en 1970, nuestro primer administrador, Bill Ruckelshaus, emitió una declaración calificando el nacimiento de nuestra agencia como el comienzo de “la recuperación de la pureza del aire, del agua, y del medio ambiente viviente” de Estados Unidos.
Tan solo la semana pasada, casi exactamente 45 años más tarde, el presidente Obama galardonó a Ruckelshaus con la Medalla Presidencial de la Libertad por su labor infatigable para establecer nuestra agencia, proteger la salud pública, y combatir los retos globales como el cambio climático.
Al otorgar el galardón, el presidente Obama declaró, “Bill estableció un poderoso precedente de que la protección de nuestro medio ambiente es algo que todos debemos unirnos para realizar juntos como un país”.
Cada día, cuando voy a trabajar y camino por los pasillos de la EPA me siento orgullosa de que nuestra agencia continúa trabajando y desarrollando el legado de Bill.
Luego esta semana, me uniré a la delegación de Estados Unidos ante la Cumbre sobre el Cambio Climático de la ONU en París, donde nuestra agencia desempeñará un papel central en las negociaciones que podrían marcar un punto crítico histórico para proteger nuestro planeta para las generaciones venideras. Confío en que Estados Unidos podrá realizar la labor.
El bien merecido honor de Ruckelshaus es un recordatorio del progreso increíble que hemos realizado como agencia en tan solo cuatro décadas y media. Nos hemos convertido en un modelo de clase mundial de la protección ambiental conforme a la ley.
Hemos avanzado tanto juntos. Hace cincuenta años atrás, llenábamos los tanques de nuestros autos con gas tóxico a base de plomo; la gente fumaba en los aviones; y los residentes en ciudades como Los Angeles casi no podían verse al otro lado de la calle.
Hoy, la labor de la EPA ha cambiado todo eso y mucho más. Hemos reducido la contaminación del aire por 70 por ciento. Hemos eliminado la gasolina con plomo. Hemos removido el ácido de la lluvia. Hemos ayudado a disipar el aire del tabaquismo pasivo; y hemos limpiados las playas y vías acuáticas, y todo esto se ha logrado mientras nuestra economía se ha triplicado.
Durante todo ese tiempo, la EPA ha personificado el concepto del gobierno participativo. Hemos colaborado con los estados, comunidades, socios industriales, y el público. Hemos escuchado las necesidades de la gente que está directamente en las comunidades, y hemos trabajado de manera transparente, mano a mano con ciudadanos y sus familias para proteger su salud, sus comunidades, y su habilidad para ganarse una vida decente. Eso es algo del cual nos debemos sentir orgullosos.
A cada paso del camino, seguimos la ciencia y el derecho para abordar retos inmensamente difíciles. Y el trabajo continúa todos los días.
Le doy las gracias y felicito a todos los que han desempeño un rol en desarrollar el legado de la EPA.
Trabajemos juntos para cumplir nuestra misión por otros 45 años más.

from The EPA Blog http://ift.tt/1SwJPUA

Por Gina McCarthy
Apenas dos semanas después de que se estableció la EPA en 1970, nuestro primer administrador, Bill Ruckelshaus, emitió una declaración calificando el nacimiento de nuestra agencia como el comienzo de “la recuperación de la pureza del aire, del agua, y del medio ambiente viviente” de Estados Unidos.
Tan solo la semana pasada, casi exactamente 45 años más tarde, el presidente Obama galardonó a Ruckelshaus con la Medalla Presidencial de la Libertad por su labor infatigable para establecer nuestra agencia, proteger la salud pública, y combatir los retos globales como el cambio climático.
Al otorgar el galardón, el presidente Obama declaró, “Bill estableció un poderoso precedente de que la protección de nuestro medio ambiente es algo que todos debemos unirnos para realizar juntos como un país”.
Cada día, cuando voy a trabajar y camino por los pasillos de la EPA me siento orgullosa de que nuestra agencia continúa trabajando y desarrollando el legado de Bill.
Luego esta semana, me uniré a la delegación de Estados Unidos ante la Cumbre sobre el Cambio Climático de la ONU en París, donde nuestra agencia desempeñará un papel central en las negociaciones que podrían marcar un punto crítico histórico para proteger nuestro planeta para las generaciones venideras. Confío en que Estados Unidos podrá realizar la labor.
El bien merecido honor de Ruckelshaus es un recordatorio del progreso increíble que hemos realizado como agencia en tan solo cuatro décadas y media. Nos hemos convertido en un modelo de clase mundial de la protección ambiental conforme a la ley.
Hemos avanzado tanto juntos. Hace cincuenta años atrás, llenábamos los tanques de nuestros autos con gas tóxico a base de plomo; la gente fumaba en los aviones; y los residentes en ciudades como Los Angeles casi no podían verse al otro lado de la calle.
Hoy, la labor de la EPA ha cambiado todo eso y mucho más. Hemos reducido la contaminación del aire por 70 por ciento. Hemos eliminado la gasolina con plomo. Hemos removido el ácido de la lluvia. Hemos ayudado a disipar el aire del tabaquismo pasivo; y hemos limpiados las playas y vías acuáticas, y todo esto se ha logrado mientras nuestra economía se ha triplicado.
Durante todo ese tiempo, la EPA ha personificado el concepto del gobierno participativo. Hemos colaborado con los estados, comunidades, socios industriales, y el público. Hemos escuchado las necesidades de la gente que está directamente en las comunidades, y hemos trabajado de manera transparente, mano a mano con ciudadanos y sus familias para proteger su salud, sus comunidades, y su habilidad para ganarse una vida decente. Eso es algo del cual nos debemos sentir orgullosos.
A cada paso del camino, seguimos la ciencia y el derecho para abordar retos inmensamente difíciles. Y el trabajo continúa todos los días.
Le doy las gracias y felicito a todos los que han desempeño un rol en desarrollar el legado de la EPA.
Trabajemos juntos para cumplir nuestra misión por otros 45 años más.

from The EPA Blog http://ift.tt/1SwJPUA

Your dog’s spit holds clues for human mental health

There goes some precious DNA…. Photo credit: Graeme Bird/Flickr

By Elinor Karlsson, University of Massachusetts Medical School

Dogs were the first animals people domesticated, long before the earliest human civilizations appeared. Today, tens of thousands of years later, dogs have an unusually close relationship with us. They share our homes and steal our hearts – and have even evolved to love us back. Sadly, they also suffer from many of the same difficult-to-treat psychiatric and neurological diseases we do.

Beskow, in fine spirits. Photo credit: Elinor Karlsson

I learned this firsthand about six years ago, when my sister Adria adopted Beskow, a beautiful, boisterous, black and white mutt. Beskow became my constant companion on my morning runs along the Charles River. Her joy in running was obvious to everyone we passed, and she kept me going mile after mile.

When not running, though, Beskow suffered from constant anxiety that left her stressed and unhappy – on edge around other dogs and prone to aggressive behavior. Beskow had trouble even playing outdoors, since she was compelled to attend to every sound and movement. Working one-on-one with skilled behaviorists and trainers helped immensely, but poor Beskow still never seemed able to relax. Eventually, Adria combined the intensive training with medication, which finally seemed to give Beskow some relief.

Beskow’s personality – her intelligence, her focus and her anxiety – was shaped not only by her own life experiences, but by thousands of years of evolution. Have you ever known a dog who would retrieve the same ball over and over again, for hours on end? Or just wouldn’t stay out of the water? Or wasn’t interested in balls, or water, but just wanted to follow her nose? These dogs are the result of hundreds of generations of artificial selection by human beings. By favoring useful behaviors when breeding dogs, we made the genetic changes responsible more common in their gene pool.

When a particular genetic change rapidly rises in prevalence in a population, it leaves a “signature of selection” that we can detect by sequencing the DNA of many individuals from the population. Essentially, around a selected gene, we find a region of the genome where one particular pattern of DNA – the variant linked to the favored version of the gene – is far more common than any of the alternative patterns. The stronger the selection, the bigger this region, and the easier it is to detect this signature of selection.

In dogs, genes shaping behaviors purposely bred by humans are marked with large signatures of selection. It’s a bit like evolution is shining a spotlight on parts of the dog genome and saying, “Look here for interesting stuff!” To figure out exactly how a particular gene influences a dog’s behavior or health, though, we need lots more information.

To try to unravel these connections, my colleagues and I are launching a new citizen science research project we’re calling Darwin’s Dogs. Together with animal behavior experts, we’ve put together a series of short surveys about everything from diet (does your dog eat grass?) to behavior (is your dog a foot sitter?) to personality (is your dog aloof or friendly?).

Any dog can participate in Darwin’s Dogs, including purebred dogs, mixed breed dogs, and mutts of no particular breed – our study’s participants will be very genetically diverse. We’re combining new DNA sequencing technology, which can give us much more genetic information from each dog, with powerful new analysis methods that can control for diverse ancestry. By including all dogs, we hope to be able to do much larger studies, and home in quickly on the important genes and genetic variants.

A beagle considers making the saliva donation. Photo credit: Stephen Schaffner

Once an owner has filled out the survey, there’s a second, crucial step. We send an easy-to-use kit to collect a small dog saliva sample we can use for DNA analysis. There’s no cost, and we’ll share any information we find.

Our plan is to combine the genetic data from many dogs and look for changes in DNA that correlate with particular behaviors. It won’t be easy to match up DNA with an obsession with tennis balls, for instance. Behavior is a complex trait that relies on many genes. Simple Mendelian traits, like Beskow’s black and white coat, are controlled by a single gene which determines the observable characteristic. This kind of inherited trait is comparatively easy to map. Complex traits, on the other hand, may be shaped by tens or even hundreds of different genetic changes, each of which on its own only slightly alters the individual carrying it.

Adding to the complexity, environment often plays a big role. For example, Beskow may not have been as anxious if she’d lived with Adria from puppyhood, even though her genetics would be unchanged.

Darwin’s Dogs team member Jesse McClure extracts DNA from a sample. Photo credit: Elinor Karlsson

To succeed, we need a lot of dogs to sign up. Initially, we’re aiming to enroll 5,000 dogs. If successful, we’ll keep growing. With bigger sample sizes, we’ll be able to tackle even more complex biological puzzles.

This is a huge effort, but could offer huge rewards. By figuring out how a genetic change leads to a change in behavior, we can decipher neural pathways involved in psychiatric and neurological diseases shared between people and dogs. We already know these include not just anxiety, but also PTSD, OCD, autism spectrum disorders, phobias, narcolepsia, epilepsy, dementia and Alzheimer’s disease.

Understanding the biology underlying a disease is the first step in developing more effective treatments – of both the canine and human variety. For example, genetic studies of narcolepsy in Doberman pinschers found the gene mutation causing the disease – but only in this one dog population. Researching the gene’s function, though, led to critical new insights into the molecular biology of sleep, and, eventually, to new treatment options for people suffering from this debilitating disease.

Darwin’s Dogs is investigating normal canine behaviors as well as diseases. We hypothesize that finding the small genetic changes that led to complex behaviors, like retrieving, or even personality characteristics, like playfulness, will help us figure out how brains work. We need this mechanistic understanding to design new, safe and more effective therapies for psychiatric diseases.

Beskow with one of her loving family members. Photo credit: Adria Karlsson

And Beskow? Six years later, she is as wonderful as ever. While still anxious some of the time, the medication and training have paid off, and she enjoys her daily walks, training and playtime. She still gets very nervous around other dogs, but is a gentle, playful companion for my sister’s three young children.

We are now sequencing her genome. In the next few months, we should have our first glimpse into Beskow’s ancestry. We know she is a natural herder, so we’re curious to find out how much her genome matches up to herding breeds, and which genes are in that part of the genome.

Of course, we can’t figure out much from just one dog – if you are a dog owner, please enroll your dog today!

Elinor Karlsson, Assistant Professor of Bioinformatics and Integrative Biology, University of Massachusetts Medical School

This article was originally published on The Conversation. Read the original article.

Enjoying EarthSky? Sign up for our free daily newsletter today!

from EarthSky http://ift.tt/1TvezGi

There goes some precious DNA…. Photo credit: Graeme Bird/Flickr

By Elinor Karlsson, University of Massachusetts Medical School

Dogs were the first animals people domesticated, long before the earliest human civilizations appeared. Today, tens of thousands of years later, dogs have an unusually close relationship with us. They share our homes and steal our hearts – and have even evolved to love us back. Sadly, they also suffer from many of the same difficult-to-treat psychiatric and neurological diseases we do.

Beskow, in fine spirits. Photo credit: Elinor Karlsson

I learned this firsthand about six years ago, when my sister Adria adopted Beskow, a beautiful, boisterous, black and white mutt. Beskow became my constant companion on my morning runs along the Charles River. Her joy in running was obvious to everyone we passed, and she kept me going mile after mile.

When not running, though, Beskow suffered from constant anxiety that left her stressed and unhappy – on edge around other dogs and prone to aggressive behavior. Beskow had trouble even playing outdoors, since she was compelled to attend to every sound and movement. Working one-on-one with skilled behaviorists and trainers helped immensely, but poor Beskow still never seemed able to relax. Eventually, Adria combined the intensive training with medication, which finally seemed to give Beskow some relief.

Beskow’s personality – her intelligence, her focus and her anxiety – was shaped not only by her own life experiences, but by thousands of years of evolution. Have you ever known a dog who would retrieve the same ball over and over again, for hours on end? Or just wouldn’t stay out of the water? Or wasn’t interested in balls, or water, but just wanted to follow her nose? These dogs are the result of hundreds of generations of artificial selection by human beings. By favoring useful behaviors when breeding dogs, we made the genetic changes responsible more common in their gene pool.

When a particular genetic change rapidly rises in prevalence in a population, it leaves a “signature of selection” that we can detect by sequencing the DNA of many individuals from the population. Essentially, around a selected gene, we find a region of the genome where one particular pattern of DNA – the variant linked to the favored version of the gene – is far more common than any of the alternative patterns. The stronger the selection, the bigger this region, and the easier it is to detect this signature of selection.

In dogs, genes shaping behaviors purposely bred by humans are marked with large signatures of selection. It’s a bit like evolution is shining a spotlight on parts of the dog genome and saying, “Look here for interesting stuff!” To figure out exactly how a particular gene influences a dog’s behavior or health, though, we need lots more information.

To try to unravel these connections, my colleagues and I are launching a new citizen science research project we’re calling Darwin’s Dogs. Together with animal behavior experts, we’ve put together a series of short surveys about everything from diet (does your dog eat grass?) to behavior (is your dog a foot sitter?) to personality (is your dog aloof or friendly?).

Any dog can participate in Darwin’s Dogs, including purebred dogs, mixed breed dogs, and mutts of no particular breed – our study’s participants will be very genetically diverse. We’re combining new DNA sequencing technology, which can give us much more genetic information from each dog, with powerful new analysis methods that can control for diverse ancestry. By including all dogs, we hope to be able to do much larger studies, and home in quickly on the important genes and genetic variants.

A beagle considers making the saliva donation. Photo credit: Stephen Schaffner

Once an owner has filled out the survey, there’s a second, crucial step. We send an easy-to-use kit to collect a small dog saliva sample we can use for DNA analysis. There’s no cost, and we’ll share any information we find.

Our plan is to combine the genetic data from many dogs and look for changes in DNA that correlate with particular behaviors. It won’t be easy to match up DNA with an obsession with tennis balls, for instance. Behavior is a complex trait that relies on many genes. Simple Mendelian traits, like Beskow’s black and white coat, are controlled by a single gene which determines the observable characteristic. This kind of inherited trait is comparatively easy to map. Complex traits, on the other hand, may be shaped by tens or even hundreds of different genetic changes, each of which on its own only slightly alters the individual carrying it.

Adding to the complexity, environment often plays a big role. For example, Beskow may not have been as anxious if she’d lived with Adria from puppyhood, even though her genetics would be unchanged.

Darwin’s Dogs team member Jesse McClure extracts DNA from a sample. Photo credit: Elinor Karlsson

To succeed, we need a lot of dogs to sign up. Initially, we’re aiming to enroll 5,000 dogs. If successful, we’ll keep growing. With bigger sample sizes, we’ll be able to tackle even more complex biological puzzles.

This is a huge effort, but could offer huge rewards. By figuring out how a genetic change leads to a change in behavior, we can decipher neural pathways involved in psychiatric and neurological diseases shared between people and dogs. We already know these include not just anxiety, but also PTSD, OCD, autism spectrum disorders, phobias, narcolepsia, epilepsy, dementia and Alzheimer’s disease.

Understanding the biology underlying a disease is the first step in developing more effective treatments – of both the canine and human variety. For example, genetic studies of narcolepsy in Doberman pinschers found the gene mutation causing the disease – but only in this one dog population. Researching the gene’s function, though, led to critical new insights into the molecular biology of sleep, and, eventually, to new treatment options for people suffering from this debilitating disease.

Darwin’s Dogs is investigating normal canine behaviors as well as diseases. We hypothesize that finding the small genetic changes that led to complex behaviors, like retrieving, or even personality characteristics, like playfulness, will help us figure out how brains work. We need this mechanistic understanding to design new, safe and more effective therapies for psychiatric diseases.

Beskow with one of her loving family members. Photo credit: Adria Karlsson

And Beskow? Six years later, she is as wonderful as ever. While still anxious some of the time, the medication and training have paid off, and she enjoys her daily walks, training and playtime. She still gets very nervous around other dogs, but is a gentle, playful companion for my sister’s three young children.

We are now sequencing her genome. In the next few months, we should have our first glimpse into Beskow’s ancestry. We know she is a natural herder, so we’re curious to find out how much her genome matches up to herding breeds, and which genes are in that part of the genome.

Of course, we can’t figure out much from just one dog – if you are a dog owner, please enroll your dog today!

Elinor Karlsson, Assistant Professor of Bioinformatics and Integrative Biology, University of Massachusetts Medical School

This article was originally published on The Conversation. Read the original article.

Enjoying EarthSky? Sign up for our free daily newsletter today!

from EarthSky http://ift.tt/1TvezGi

Lungs of the Sea

As a diver and marine biologist for EPA, I spend a fair amount of time underwater. My area of expertise is in the study and conservation of seagrass. These underwater meadows can cover vast swaths of the seafloor and they serve as important nurseries for many fish and shellfish species.

Recently, I had the great fortune of taking a family trip to France and spending some time along the southern coast. It was my first visit to the Mediterranean Sea and I was looking forward to exploring the underwater realm. We stopped in the small town of Cassis, which reminded us of Gloucester, Mass. Cassis has its own fisherman’s statue. It does not have a greasy pole to climb like Gloucester, but it does have its own unique tradition. Local fishermen mount planks on the back of two dories. Boys of about 10 years old are lifted up onto the planks wearing pads on their chests and are given lances. The boats then drive directly at each other and the boys joust until one or both fall into the water.

The local culture was interesting, but Cassis is also known for “les calanques.” Calanques are inlets surrounded on three sides by steep cliffs; they also are known as mini-fjords. Within these inlets, seagrass flourishes in the clean, calm protected waters. The French refer to seagrass as “les poumons de le mer,” which translates to the lungs of the sea. Like all plants, seagrasses produce oxygen through photosynthesis. On sunny days, it is common to see bubbles of oxygen being released from the leaves of seagrass into the water.

In Cassis, protecting seagrass is taken very seriously with a variety of rules. Boaters are not allowed to anchor or place a mooring in seagrass meadows. Boaters are required to stay in the marked navigation channels and when in shallow water reduce their speed so no wakes are produced. In our three days in Cassis, we watched many boats come and go, and not one of them broke the rules.

I approached one of the local fishermen and with my limited French asked him about the local seagrass meadows. He spoke little English. I spied a shoot of seagrass floating near his boat. He scooped it up and held it close to his heart and said “les poumons de le mer.”

We didn’t speak the same language, but our common love of the ocean easily transcended the language barrier.

More information on EPA Seagrass research: http://ift.tt/1Qet4y9

Connect with EPA New England on Facebook: http://ift.tt/1jyuRkT

Connect with EPA Divers on Facebook: http://ift.tt/1Qet4yb

About the author: Phil Colarusso is a marine biologist in the Coastal and Ocean Protection Section of EPA’s New England office, and is an avid diver.

from The EPA Blog http://ift.tt/1jyuRB7

As a diver and marine biologist for EPA, I spend a fair amount of time underwater. My area of expertise is in the study and conservation of seagrass. These underwater meadows can cover vast swaths of the seafloor and they serve as important nurseries for many fish and shellfish species.

Recently, I had the great fortune of taking a family trip to France and spending some time along the southern coast. It was my first visit to the Mediterranean Sea and I was looking forward to exploring the underwater realm. We stopped in the small town of Cassis, which reminded us of Gloucester, Mass. Cassis has its own fisherman’s statue. It does not have a greasy pole to climb like Gloucester, but it does have its own unique tradition. Local fishermen mount planks on the back of two dories. Boys of about 10 years old are lifted up onto the planks wearing pads on their chests and are given lances. The boats then drive directly at each other and the boys joust until one or both fall into the water.

The local culture was interesting, but Cassis is also known for “les calanques.” Calanques are inlets surrounded on three sides by steep cliffs; they also are known as mini-fjords. Within these inlets, seagrass flourishes in the clean, calm protected waters. The French refer to seagrass as “les poumons de le mer,” which translates to the lungs of the sea. Like all plants, seagrasses produce oxygen through photosynthesis. On sunny days, it is common to see bubbles of oxygen being released from the leaves of seagrass into the water.

In Cassis, protecting seagrass is taken very seriously with a variety of rules. Boaters are not allowed to anchor or place a mooring in seagrass meadows. Boaters are required to stay in the marked navigation channels and when in shallow water reduce their speed so no wakes are produced. In our three days in Cassis, we watched many boats come and go, and not one of them broke the rules.

I approached one of the local fishermen and with my limited French asked him about the local seagrass meadows. He spoke little English. I spied a shoot of seagrass floating near his boat. He scooped it up and held it close to his heart and said “les poumons de le mer.”

We didn’t speak the same language, but our common love of the ocean easily transcended the language barrier.

More information on EPA Seagrass research: http://ift.tt/1Qet4y9

Connect with EPA New England on Facebook: http://ift.tt/1jyuRkT

Connect with EPA Divers on Facebook: http://ift.tt/1Qet4yb

About the author: Phil Colarusso is a marine biologist in the Coastal and Ocean Protection Section of EPA’s New England office, and is an avid diver.

from The EPA Blog http://ift.tt/1jyuRB7

On the Mend — Natick Investigates Self-Healing Protective Clothing

Microcapsules – shown here sprayed on Army fabric – are being developed to enable chemical-biological protective clothing to mend itself when punctured or torn. The Natick Soldier Research, Development and Engineering Center, the University of Massachusetts Lowell and Triton Systems, Inc., are collaborating on the technical development of self-healing fabric technologies. Photo by Jesse Hamilton, University of Massachusetts Lowell

By Jane Benson, NSRDEC Public Affairs

Army researcher Quoc Truong wants to fill in the gaps in soldier protective clothing — literally.

Truong is a physical scientist at the U.S. Army Natick Soldier Research, Development and Engineering Center, or NSRDEC. He is collaborating with other researchers at NSRDEC, the University of Massachusetts Lowell, and Triton Systems, Inc., on the technical development of self-healing coatings that contain micro-capsules of healing fluid, which will be used to mend chemical-biological, or CB, protective clothing. 

“When soldiers are wearing a chem-bio protective garment, they are basically isolating themselves from their environment and any harmful agents, such as nerve gases, viruses and bacteria,” said Truong. “Soldiers are very active and can encounter thorny bushes or other things that could result in pin-hole-sized damage to their chem-bio garment while carrying out their missions. The damage may not be visible to the human eye, but it is there.”

The self-healing technologies will enable cuts, tears and punctures in fabrics to quickly repair themselves. This means that the protective qualities of the garments will be far less apt to become compromised by tears and punctures. The technology will be incorporated into both the Joint Service Lightweight Integrated Suit Technology, or JSLIST, garment, and the Joint Protective Aircrew Ensemble, or JPACE, garment.

“The self-healing coatings can be a spray-on coating or a continuous coating — depending on the type of protective clothing they are applied on,” said Truong. “The idea is just like when a scratch breaks open the skin. Our body has the ability to heal and mend, make a scab and heal. The same idea applies to the self-mending fabric; when the fabric containing these self-healing materials gets cut, it comes back together and heals. It forms something very much like a scab on the skin except it is on the fabric.”

Researchers, at the Natick Soldier Research, Development and Engineering Center, the University of Massachusetts Lowell, and Triton Systems, Inc., are collaborating on the technical development of self-healing technologies that will be used to mend chemical-biological protective clothing. Photo by David Kamm, NSRDEC

The technology combines innovative approaches to gap-closure with healing micro-capsules that are activated when torn to repair cuts and punctures. The self-healing layer contains reactive agents to deactivate dangerous threats, including deadly chemicals, and also acts to reform the physical barrier to bacteria and viruses. When integrated into a CB protective garment, the self-healing technologies help ensure that the CB protection is uninterrupted.

The JPACE’s protective mechanism is based on a selectively permeable membrane; therefore, the microcapsules are embedded into the selectively permeable membrane and/or in a supporting reactive selectively permeable membrane layer, which will act as a self-healing supporting barrier material. When the membrane breaks, these microcapsules open and mend the tear in about 60 seconds, filling the gap with the aid of the gap-closure technology. 

“This helps preserve the capabilities of the fabric,” said Truong. “The idea is to support chemical-biological protective clothing. The self-healing textile would have the ability to neutralize the chemical agents. The selectively permeable membrane structure acts like a barrier to agents, but allows warm/hot body sweat, i.e., moisture vapor, to be transported from the body to the environment outside of the protective clothing.”

The JSLIST chemical protective overgarment is based on a non-woven material that carries activated carbon spheres. Thus, it is air permeable and doesn’t lend easily to the use of microcapsules. So, the JSLIST suit configuration has to be sprayed with microcapsules and a foaming agent. 

Truong is dedicated to continuously improving safety for the soldier.

“Ideas to help the soldier come to me all the time,” said Truong. “It makes me feel good to know that some of these ideas can be transformed into protection for the soldier.”

The technology also has commercial applications.

“For instance, this technology could be used to develop self-mending tents to ensure protection against the elements since holes would be repaired quickly,” Truong said. “It could also be used for commercial workers who handle chemicals, work in the rain, or work in extreme cold. Their protective clothing would be self-mending to keep them safe, dry and protected from the elements.”

Follow us on Twitter for military science and technology updates!

Disclaimer: Re-published content may have been edited for length and clarity. The appearance of hyperlinks does not constitute endorsement by the Department of Defense. For other than authorized activities, such as, military exchanges and Morale, Welfare and Recreation sites, the Department of Defense does not exercise any editorial control over the information you may find at these locations. Such links are provided consistent with the stated purpose of this DoD website.

from Armed with Science http://ift.tt/1O3HlZY

Microcapsules – shown here sprayed on Army fabric – are being developed to enable chemical-biological protective clothing to mend itself when punctured or torn. The Natick Soldier Research, Development and Engineering Center, the University of Massachusetts Lowell and Triton Systems, Inc., are collaborating on the technical development of self-healing fabric technologies. Photo by Jesse Hamilton, University of Massachusetts Lowell

By Jane Benson, NSRDEC Public Affairs

Army researcher Quoc Truong wants to fill in the gaps in soldier protective clothing — literally.

Truong is a physical scientist at the U.S. Army Natick Soldier Research, Development and Engineering Center, or NSRDEC. He is collaborating with other researchers at NSRDEC, the University of Massachusetts Lowell, and Triton Systems, Inc., on the technical development of self-healing coatings that contain micro-capsules of healing fluid, which will be used to mend chemical-biological, or CB, protective clothing. 

“When soldiers are wearing a chem-bio protective garment, they are basically isolating themselves from their environment and any harmful agents, such as nerve gases, viruses and bacteria,” said Truong. “Soldiers are very active and can encounter thorny bushes or other things that could result in pin-hole-sized damage to their chem-bio garment while carrying out their missions. The damage may not be visible to the human eye, but it is there.”

The self-healing technologies will enable cuts, tears and punctures in fabrics to quickly repair themselves. This means that the protective qualities of the garments will be far less apt to become compromised by tears and punctures. The technology will be incorporated into both the Joint Service Lightweight Integrated Suit Technology, or JSLIST, garment, and the Joint Protective Aircrew Ensemble, or JPACE, garment.

“The self-healing coatings can be a spray-on coating or a continuous coating — depending on the type of protective clothing they are applied on,” said Truong. “The idea is just like when a scratch breaks open the skin. Our body has the ability to heal and mend, make a scab and heal. The same idea applies to the self-mending fabric; when the fabric containing these self-healing materials gets cut, it comes back together and heals. It forms something very much like a scab on the skin except it is on the fabric.”

Researchers, at the Natick Soldier Research, Development and Engineering Center, the University of Massachusetts Lowell, and Triton Systems, Inc., are collaborating on the technical development of self-healing technologies that will be used to mend chemical-biological protective clothing. Photo by David Kamm, NSRDEC

The technology combines innovative approaches to gap-closure with healing micro-capsules that are activated when torn to repair cuts and punctures. The self-healing layer contains reactive agents to deactivate dangerous threats, including deadly chemicals, and also acts to reform the physical barrier to bacteria and viruses. When integrated into a CB protective garment, the self-healing technologies help ensure that the CB protection is uninterrupted.

The JPACE’s protective mechanism is based on a selectively permeable membrane; therefore, the microcapsules are embedded into the selectively permeable membrane and/or in a supporting reactive selectively permeable membrane layer, which will act as a self-healing supporting barrier material. When the membrane breaks, these microcapsules open and mend the tear in about 60 seconds, filling the gap with the aid of the gap-closure technology. 

“This helps preserve the capabilities of the fabric,” said Truong. “The idea is to support chemical-biological protective clothing. The self-healing textile would have the ability to neutralize the chemical agents. The selectively permeable membrane structure acts like a barrier to agents, but allows warm/hot body sweat, i.e., moisture vapor, to be transported from the body to the environment outside of the protective clothing.”

The JSLIST chemical protective overgarment is based on a non-woven material that carries activated carbon spheres. Thus, it is air permeable and doesn’t lend easily to the use of microcapsules. So, the JSLIST suit configuration has to be sprayed with microcapsules and a foaming agent. 

Truong is dedicated to continuously improving safety for the soldier.

“Ideas to help the soldier come to me all the time,” said Truong. “It makes me feel good to know that some of these ideas can be transformed into protection for the soldier.”

The technology also has commercial applications.

“For instance, this technology could be used to develop self-mending tents to ensure protection against the elements since holes would be repaired quickly,” Truong said. “It could also be used for commercial workers who handle chemicals, work in the rain, or work in extreme cold. Their protective clothing would be self-mending to keep them safe, dry and protected from the elements.”

Follow us on Twitter for military science and technology updates!

Disclaimer: Re-published content may have been edited for length and clarity. The appearance of hyperlinks does not constitute endorsement by the Department of Defense. For other than authorized activities, such as, military exchanges and Morale, Welfare and Recreation sites, the Department of Defense does not exercise any editorial control over the information you may find at these locations. Such links are provided consistent with the stated purpose of this DoD website.

from Armed with Science http://ift.tt/1O3HlZY

45 Years of fulfilling our Mission

By Gina McCarthy

Just two weeks after the EPA was established in 1970, our first-ever Administrator, Bill Ruckelshaus, issued a statement calling the birth of our agency the start of America’s “reclaiming the purity of its air, its water, and its living environment.”

Just last week, 45 years later – nearly to the day – President Obama honored Ruckelshaus with the Presidential Medal of Freedom for his tireless work to get our agency up and running, protect public health, and combat global challenges like climate change.

In bestowing the award, President Obama said, “Bill set a powerful precedent that protecting our environment is something we must come together and do as a country.”

Each day, when I come to work and walk the halls at EPA, I feel proud that our agency is continuing to build on Bill’s legacy.

Later this week, I will join the US delegation to the UN Conference on Climate Change in Paris, where our agency will play a central role in negotiations that could mark a historic turning point to protect our planet for generations to come. I’m confident that the US can get the job done.

Ruckelshaus’ well-deserved honor is a reminder of the amazing progress we’ve made as an agency in just four and a half decades. We have evolved into a world-class model of environmental protection under the law.

We’ve come so far together. Fifty years ago, we pumped toxic leaded-gas into our cars; people smoked on airplanes; and residents of cities like Los Angeles could barely see each other across the street.

Today, EPA’s work has changed all of that – and more. We’ve cut air pollution by 70 percent; we’ve phased out leaded-gasoline; we’ve removed the acid from rain, we’ve helped clear the air of second-hand smoke; and we’ve cleaned up beaches and waterways, all while our economy has tripled.

Throughout it all, EPA has embodied the concept of participatory government. We’ve engaged states, communities, industry partners, and the public. We’ve listened to the needs of people on the ground, and we’ve worked transparently, hand in hand with citizens and families to protect their health, their communities, and their ability to earn a decent living. That’s something to be proud of.

At every step of the way, we’ve followed the science and the law to tackle immensely difficult challenges. And that work is continuing every day.

I thank and congratulate everyone who has played a part in building EPA’s legacy.

Here’s to working together to fulfill our mission for another 45 years!

from The EPA Blog http://ift.tt/1N3GyZj

By Gina McCarthy

Just two weeks after the EPA was established in 1970, our first-ever Administrator, Bill Ruckelshaus, issued a statement calling the birth of our agency the start of America’s “reclaiming the purity of its air, its water, and its living environment.”

Just last week, 45 years later – nearly to the day – President Obama honored Ruckelshaus with the Presidential Medal of Freedom for his tireless work to get our agency up and running, protect public health, and combat global challenges like climate change.

In bestowing the award, President Obama said, “Bill set a powerful precedent that protecting our environment is something we must come together and do as a country.”

Each day, when I come to work and walk the halls at EPA, I feel proud that our agency is continuing to build on Bill’s legacy.

Later this week, I will join the US delegation to the UN Conference on Climate Change in Paris, where our agency will play a central role in negotiations that could mark a historic turning point to protect our planet for generations to come. I’m confident that the US can get the job done.

Ruckelshaus’ well-deserved honor is a reminder of the amazing progress we’ve made as an agency in just four and a half decades. We have evolved into a world-class model of environmental protection under the law.

We’ve come so far together. Fifty years ago, we pumped toxic leaded-gas into our cars; people smoked on airplanes; and residents of cities like Los Angeles could barely see each other across the street.

Today, EPA’s work has changed all of that – and more. We’ve cut air pollution by 70 percent; we’ve phased out leaded-gasoline; we’ve removed the acid from rain, we’ve helped clear the air of second-hand smoke; and we’ve cleaned up beaches and waterways, all while our economy has tripled.

Throughout it all, EPA has embodied the concept of participatory government. We’ve engaged states, communities, industry partners, and the public. We’ve listened to the needs of people on the ground, and we’ve worked transparently, hand in hand with citizens and families to protect their health, their communities, and their ability to earn a decent living. That’s something to be proud of.

At every step of the way, we’ve followed the science and the law to tackle immensely difficult challenges. And that work is continuing every day.

I thank and congratulate everyone who has played a part in building EPA’s legacy.

Here’s to working together to fulfill our mission for another 45 years!

from The EPA Blog http://ift.tt/1N3GyZj

Grand Challenge one: can we develop a jab to prevent cancer?

This entry is part 2 of 2 in the series Grand Challenge

In October we launched the Cancer Research UK Grand Challenge – a £100m scheme to tackle seven of the biggest challenges in understanding and treating cancer.  

And in a series of posts over the next two months we’ll be exploring each of the seven Grand Challenge questions set by a panel of the world’s leading cancer experts, starting with question one: Can we develop vaccines to prevent cancers that aren’t caused by viruses?

Many of us will be familiar with the idea of vaccines – one of the greatest advances in medicine – which trigger our immune systems to recognise and attack infectious diseases. Vaccines remain the only medical advance to have ever fully eradicated a disease, ridding the world of the smallpox virus.

But the big question is: could a vaccine do the same for cancer? Obviously, cancers aren’t infections – unlike bacteria and viruses, they develop from our own cells, posing a big challenge for our immune system in recognising them as harmful.

Nevertheless, harnessing the power of the immune system to fight cancer has been a goal for scientists for over a century. But it’s only recently that we’ve begun to understand exactly how immune cells (mistakenly) view cancer as a friend to leave in peace, rather than an enemy to destroy. And then harness this knowledge to develop new cancer treatments.

But this has also raised the question of whether we might be able to use vaccines to prevent – as well as treat – the disease.

Immune surveillance

Vaccines work by training the immune system to recognise small, harmless pieces of a disease, so that it can eradicate anything that looks like it in the future. Once convinced that a particular molecule belongs to the enemy, the immune system is forever primed to treat it as hostile.

Vaccines have already been developed against certain forms of cancer that are caused by viruses, such the human papillomavirus (HPV) – which causes cervical, oral and anal cancers. And eradicating cancers caused by the Epstein Barr Virus (EBV) – such as certain forms of lymphoma – is the second of our Grand Challenge questions (more on this next week). So the idea of creating a vaccine to prevent or treat cancers linked to viruses certainly works in theory.

But only three in every 100 cancers in the UK each year are linked to infections. And in these cases the immune system’s target is distinct – it’s definitely ‘foreign’.

Without that ‘foreign invader’, alerting the immune system becomes a lot more complicated.

So the first challenge set by our panel is to take this a step further, and find a way to directly target cells in our bodies in the earliest stages of becoming a cancer. Helping the immune system destroy these abnormal cells before they develop into cancer could not only save lives, but spare thousands from even becoming a cancer patient in the first place.

It sounds incredible – so how might this work in practice?

What do we mean by a cancer jab?

It’s up to the applicants to come up with the best way to tackle this problem, but the rewards could be incredible – Professor Tyler Jacks

Professor Tyler Jacks, director of the Koch Institute for integrative cancer research at MIT in the US, and one of the members of our Grand Challenge scientific panel, is incredibly excited by the prospect of this question.

“To be clear, the point is not to have a one-size-fits-all vaccine preventing all cancers,” he explains.

“Every cancer is different. But I would be happy, I would be thrilled actually, if this question stimulated research that found a set of molecules, probably not just one, which we could develop into a vaccine for people at a higher risk of certain cancers.”

Professor Christian Ottensmeier, a Cancer Research UK expert in immunology at the University of Southampton, shares his enthusiasm. “It’s entirely possible that as a result of this Grand Challenge people will start to look at the puzzle of preventative vaccination in a different way,” he says.

“So I’m really excited about this opportunity, because I think this will make the research community look at this particular question in a way it hasn’t so far.”

But creating a vaccine to prevent cancer is easier said than done, and Professor Jacks sees several important steps that must be overcome, each with its own unique challenges and hurdles. But the biggest, he says, is the first – finding targets for the vaccine that are hallmarks of developing cancer cells.

Spotting cancer before it happens

Finding suitable vaccine targets requires researchers to pinpoint molecules that the immune system can recognise as ‘foreign’. These are known as ‘antigens’.

“We know that cancers develop due to changes in the DNA,” says Jacks. “Some of these genetic mistakes will result in molecules that look completely different to how they should in a normal healthy cell. If we can find which of these mutations are common in certain types of cancer, we might be able to use these in a vaccine against that cancer type.”

Alongside these faulty ‘self’ molecules, researchers have also found that certain forms of cancer produce normal molecules when they shouldn’t, or in far greater amounts than healthy cells. These are known as ‘tumour-associated antigens’. For example, a molecule that’s only made during early childhood and not at all in a healthy adult might be switched back on and produced inside cancer cells to help them grow.

And as well as these faulty or inappropriately produced molecules, there could be an entirely new method for finding the best targets.

According to Ottensmeier it’s difficult to know what the explosion in data generation will lead to.

“Even three to five years ago it was unimaginable that you would even consider making a patient -specific vaccine,” he says.

“But now that’s already a reality with a number of bespoke, experimental ‘vaccines’ in development as treatments.”

Finding the target is just the first step

Once a suitable collection of vaccine targets are found, there would then be a huge amount of work to make sure the vaccine actually worked, and was safe.

Neither of these will be easy. And since the goal is to create something that protects over a lifetime, it won’t be quick either. It could take decades to ensure that a vaccine preventing cancer in the general population truly works.

But rather than going for this ultimate goal, Ottensmeier thinks that a better strategy – and one that might be achievable within the timeframe of our Grand Challenge – could be to identify and begin developing vaccines that could be used among small groups of high risk patients – for example, women with a family history of breast cancer.

“Women with known faults in their DNA are already offered preventative measures,” he says.

For some this may involve a double mastectomy, like the high-profile actress and filmmaker, Angelina Jolie had in 2013.

“But what if we could offer these women a vaccine against breast cancer rather than surgery?” asks Ottensmeier. It’s a tantalising prospect.

The patient perspective

The Grand Challenge that most excites me has to be research into a vaccine to help prevent cancer. Easy words to write – but I’ve probably only a small idea of what a huge undertaking this is. When I was diagnosed with lung cancer with a prognosis of 3 months, I was left wishing I could pop along to my GPs for a cancer jab and it would all be over (we didn’t even have the flu jab then). But that wasn’t to be, and it’s a small miracle that I am still here. Reading through the seven questions put forward I was unsure which one I would like to see a group of scientists take on. But as I looked up from my laptop, stuck on the rim of a shelf, was a yellow sticky note reminding me that I was due for my flu jab that afternoon. Believe me, my selection is not one of divine intervention, rather the simplicity of its use if it was to work.

– Terry, patient panel member for the Grand Challenge

High hopes

Our understanding of the immune system has come on in leaps and bounds in the last decade, and the resulting progress in immune-based treatments has made things possible that were previously considered completely untenable.

So, in a period of such rapid progress, Professor Jacks argues: “Why not reach for the stars a little bit here”.

“A Grand Challenge should be challenging, and shouldn’t be obvious. It’s up to the applicants to come up with the best way to tackle this problem, but the rewards could be incredible if successful.”

And being on the cusp of discovery is exactly how this type of research should be carried out. “Honestly, we just don’t know if we can do this,” he says.

“But failure in research is commonplace. We make progress despite a great deal of failure.

“If you don’t try, you’ll never succeed, and just because it might not work is no reason not to try.”

Alan

• If you’re a researcher and want to build a team to take on this challenge, visit our website to find out how you can apply.

from Cancer Research UK - Science blog http://ift.tt/1Qeb4E2

This entry is part 2 of 2 in the series Grand Challenge

In October we launched the Cancer Research UK Grand Challenge – a £100m scheme to tackle seven of the biggest challenges in understanding and treating cancer.  

And in a series of posts over the next two months we’ll be exploring each of the seven Grand Challenge questions set by a panel of the world’s leading cancer experts, starting with question one: Can we develop vaccines to prevent cancers that aren’t caused by viruses?

Many of us will be familiar with the idea of vaccines – one of the greatest advances in medicine – which trigger our immune systems to recognise and attack infectious diseases. Vaccines remain the only medical advance to have ever fully eradicated a disease, ridding the world of the smallpox virus.

But the big question is: could a vaccine do the same for cancer? Obviously, cancers aren’t infections – unlike bacteria and viruses, they develop from our own cells, posing a big challenge for our immune system in recognising them as harmful.

Nevertheless, harnessing the power of the immune system to fight cancer has been a goal for scientists for over a century. But it’s only recently that we’ve begun to understand exactly how immune cells (mistakenly) view cancer as a friend to leave in peace, rather than an enemy to destroy. And then harness this knowledge to develop new cancer treatments.

But this has also raised the question of whether we might be able to use vaccines to prevent – as well as treat – the disease.

Immune surveillance

Vaccines work by training the immune system to recognise small, harmless pieces of a disease, so that it can eradicate anything that looks like it in the future. Once convinced that a particular molecule belongs to the enemy, the immune system is forever primed to treat it as hostile.

Vaccines have already been developed against certain forms of cancer that are caused by viruses, such the human papillomavirus (HPV) – which causes cervical, oral and anal cancers. And eradicating cancers caused by the Epstein Barr Virus (EBV) – such as certain forms of lymphoma – is the second of our Grand Challenge questions (more on this next week). So the idea of creating a vaccine to prevent or treat cancers linked to viruses certainly works in theory.

But only three in every 100 cancers in the UK each year are linked to infections. And in these cases the immune system’s target is distinct – it’s definitely ‘foreign’.

Without that ‘foreign invader’, alerting the immune system becomes a lot more complicated.

So the first challenge set by our panel is to take this a step further, and find a way to directly target cells in our bodies in the earliest stages of becoming a cancer. Helping the immune system destroy these abnormal cells before they develop into cancer could not only save lives, but spare thousands from even becoming a cancer patient in the first place.

It sounds incredible – so how might this work in practice?

What do we mean by a cancer jab?

It’s up to the applicants to come up with the best way to tackle this problem, but the rewards could be incredible – Professor Tyler Jacks

Professor Tyler Jacks, director of the Koch Institute for integrative cancer research at MIT in the US, and one of the members of our Grand Challenge scientific panel, is incredibly excited by the prospect of this question.

“To be clear, the point is not to have a one-size-fits-all vaccine preventing all cancers,” he explains.

“Every cancer is different. But I would be happy, I would be thrilled actually, if this question stimulated research that found a set of molecules, probably not just one, which we could develop into a vaccine for people at a higher risk of certain cancers.”

Professor Christian Ottensmeier, a Cancer Research UK expert in immunology at the University of Southampton, shares his enthusiasm. “It’s entirely possible that as a result of this Grand Challenge people will start to look at the puzzle of preventative vaccination in a different way,” he says.

“So I’m really excited about this opportunity, because I think this will make the research community look at this particular question in a way it hasn’t so far.”

But creating a vaccine to prevent cancer is easier said than done, and Professor Jacks sees several important steps that must be overcome, each with its own unique challenges and hurdles. But the biggest, he says, is the first – finding targets for the vaccine that are hallmarks of developing cancer cells.

Spotting cancer before it happens

Finding suitable vaccine targets requires researchers to pinpoint molecules that the immune system can recognise as ‘foreign’. These are known as ‘antigens’.

“We know that cancers develop due to changes in the DNA,” says Jacks. “Some of these genetic mistakes will result in molecules that look completely different to how they should in a normal healthy cell. If we can find which of these mutations are common in certain types of cancer, we might be able to use these in a vaccine against that cancer type.”

Alongside these faulty ‘self’ molecules, researchers have also found that certain forms of cancer produce normal molecules when they shouldn’t, or in far greater amounts than healthy cells. These are known as ‘tumour-associated antigens’. For example, a molecule that’s only made during early childhood and not at all in a healthy adult might be switched back on and produced inside cancer cells to help them grow.

And as well as these faulty or inappropriately produced molecules, there could be an entirely new method for finding the best targets.

According to Ottensmeier it’s difficult to know what the explosion in data generation will lead to.

“Even three to five years ago it was unimaginable that you would even consider making a patient -specific vaccine,” he says.

“But now that’s already a reality with a number of bespoke, experimental ‘vaccines’ in development as treatments.”

Finding the target is just the first step

Once a suitable collection of vaccine targets are found, there would then be a huge amount of work to make sure the vaccine actually worked, and was safe.

Neither of these will be easy. And since the goal is to create something that protects over a lifetime, it won’t be quick either. It could take decades to ensure that a vaccine preventing cancer in the general population truly works.

But rather than going for this ultimate goal, Ottensmeier thinks that a better strategy – and one that might be achievable within the timeframe of our Grand Challenge – could be to identify and begin developing vaccines that could be used among small groups of high risk patients – for example, women with a family history of breast cancer.

“Women with known faults in their DNA are already offered preventative measures,” he says.

For some this may involve a double mastectomy, like the high-profile actress and filmmaker, Angelina Jolie had in 2013.

“But what if we could offer these women a vaccine against breast cancer rather than surgery?” asks Ottensmeier. It’s a tantalising prospect.

The patient perspective

The Grand Challenge that most excites me has to be research into a vaccine to help prevent cancer. Easy words to write – but I’ve probably only a small idea of what a huge undertaking this is. When I was diagnosed with lung cancer with a prognosis of 3 months, I was left wishing I could pop along to my GPs for a cancer jab and it would all be over (we didn’t even have the flu jab then). But that wasn’t to be, and it’s a small miracle that I am still here. Reading through the seven questions put forward I was unsure which one I would like to see a group of scientists take on. But as I looked up from my laptop, stuck on the rim of a shelf, was a yellow sticky note reminding me that I was due for my flu jab that afternoon. Believe me, my selection is not one of divine intervention, rather the simplicity of its use if it was to work.

– Terry, patient panel member for the Grand Challenge

High hopes

Our understanding of the immune system has come on in leaps and bounds in the last decade, and the resulting progress in immune-based treatments has made things possible that were previously considered completely untenable.

So, in a period of such rapid progress, Professor Jacks argues: “Why not reach for the stars a little bit here”.

“A Grand Challenge should be challenging, and shouldn’t be obvious. It’s up to the applicants to come up with the best way to tackle this problem, but the rewards could be incredible if successful.”

And being on the cusp of discovery is exactly how this type of research should be carried out. “Honestly, we just don’t know if we can do this,” he says.

“But failure in research is commonplace. We make progress despite a great deal of failure.

“If you don’t try, you’ll never succeed, and just because it might not work is no reason not to try.”

Alan

• If you’re a researcher and want to build a team to take on this challenge, visit our website to find out how you can apply.

from Cancer Research UK - Science blog http://ift.tt/1Qeb4E2