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My specialty is neuroscience and physiology, but I love all sciences, athletics, healthy food and fun people.

I love interaction and scientific dicussion. Never be afraid to ask me questions. I may not have the answer, but I'll be damned if I haven't learned how to do a good, quick Google Scholar search to find out.

In addition I like to look at non-science related cute animal pictures, art and funny comics too :)

Hope you enjoy my blog but please, feel free to leave suggestions for improvement!
biocanvas:

Neuromuscular junctions in fruit flies
Our nerves send chemical signals to muscle fibers in order to stimulate muscle contraction, resulting in movement and locomotion. For this to happen, the ends of nerve fibers must be in very close proximity to the muscle—and we mean very close: The average space of a neuromuscular junction is just 30 nanometers, which is over 2,600-times smaller than the width of a human hair. In this neuromuscular junction of a fruit fly, nerve terminals (in red) can be seen intermingling with structural components (in green and blue). Diseases like Duchenne muscular dystrophy destabilize the structural integrity of neuromuscular junctions, greatly impairing muscle movement and strength.
Image by Vanessa Auld, University of British Columbia, Canada.

biocanvas:

Neuromuscular junctions in fruit flies

Our nerves send chemical signals to muscle fibers in order to stimulate muscle contraction, resulting in movement and locomotion. For this to happen, the ends of nerve fibers must be in very close proximity to the muscle—and we mean very close: The average space of a neuromuscular junction is just 30 nanometers, which is over 2,600-times smaller than the width of a human hair. In this neuromuscular junction of a fruit fly, nerve terminals (in red) can be seen intermingling with structural components (in green and blue). Diseases like Duchenne muscular dystrophy destabilize the structural integrity of neuromuscular junctions, greatly impairing muscle movement and strength.

Image by Vanessa Auld, University of British Columbia, Canada.





The Wine-Throated Hummingbird. More info: http://is.gd/vXEUlx© José Yee
The Wine-Throated Hummingbird. 

More info: http://is.gd/vXEUlx
© José Yee

usmlenotes:

Have some fun with Medicine!

usmlenotes:

Have some fun with Medicine!


neurosciencestuff:

Scientists Discover Area of Brain Responsible for Exercise Motivation
Scientists at Seattle Children’s Research Institute have discovered an area of the brain that could control a person’s motivation to exercise and participate in other rewarding activities – potentially leading to improved treatments for depression.
Dr. Eric Turner, a principal investigator in Seattle Children’s Research Institute’s Center for Integrative Brain Research, together with lead author Dr. Yun-Wei (Toni) Hsu, have discovered that a tiny region of the brain – the dorsal medial habenula – controls the desire to exercise in mice. The structure of the habenula is similar in humans and rodents and these basic functions in mood regulation and motivation are likely to be the same across species.  
Exercise is one of the most effective non-pharmacological therapies for depression. Determining that such a specific area of the brain may be responsible for motivation to exercise could help researchers develop more targeted, effective treatments for depression. 
“Changes in physical activity and the inability to enjoy rewarding or pleasurable experiences are two hallmarks of major depression,” Turner said. “But the brain pathways responsible for exercise motivation have not been well understood. Now, we can seek ways to manipulate activity within this specific area of the brain without impacting the rest of the brain’s activity.” 
Dr. Turner’s study, titled “Role of the Dorsal Medial Habenula in the Regulation of Voluntary Activity, Motor Function, Hedonic State, and Primary Reinforcement,” was published today by the Journal of Neuroscience and funded by the National Institute of Mental Health and National Institute on Drug Abuse. The study used mouse models that were genetically engineered to block signals from the dorsal medial habenula. In the first part of the study, Dr. Turner’s team collaborated with Dr. Horacio de la Iglesia, a professor in University of Washington’s Department of Biology, to show that compared to typical mice, who love to run in their exercise wheels, the genetically engineered mice were lethargic and ran far less. Turner’s genetically engineered mice also lost their preference for sweetened drinking water. 
“Without a functioning dorsal medial habenula, the mice became couch potatoes,” Turner said. “They were physically capable of running but appeared unmotivated to do it.” 
In a second group of mice, Dr. Turner’s team activated the dorsal medial habenula using optogenetics – a precise laser technology developed in collaboration with the Allen Institute for Brain Science. The mice could “choose” to activate this area of the brain by turning one of two response wheels with their paws. The mice strongly preferred turning the wheel that stimulated the dorsal medial habenula, demonstrating that this area of the brain is tied to rewarding behavior.  
Past studies have attributed many different functions to the habenula, but technology was not advanced enough to determine roles of the various subsections of this area of the brain, including the dorsal medial habenula. 
“Traditional methods of stimulation could not isolate this part of the brain,” Turner said. “But cutting-edge technology at Seattle Children’s Research Institute makes discoveries like this possible.” 
As a professor in the University of Washington Department of Psychiatry and Behavioral Sciences, Dr. Turner treats depression and hopes this research will make a difference in the lives of future patients. 
“Working in mental health can be frustrating,” Turner said. “We have not made a lot of progress in developing new treatments. I hope the more we can learn about how the brain functions the more we can help people with all kinds of mental illness.”

neurosciencestuff:

Scientists Discover Area of Brain Responsible for Exercise Motivation

Scientists at Seattle Children’s Research Institute have discovered an area of the brain that could control a person’s motivation to exercise and participate in other rewarding activities – potentially leading to improved treatments for depression.

Dr. Eric Turner, a principal investigator in Seattle Children’s Research Institute’s Center for Integrative Brain Research, together with lead author Dr. Yun-Wei (Toni) Hsu, have discovered that a tiny region of the brain – the dorsal medial habenula – controls the desire to exercise in mice. The structure of the habenula is similar in humans and rodents and these basic functions in mood regulation and motivation are likely to be the same across species.  

Exercise is one of the most effective non-pharmacological therapies for depression. Determining that such a specific area of the brain may be responsible for motivation to exercise could help researchers develop more targeted, effective treatments for depression. 

“Changes in physical activity and the inability to enjoy rewarding or pleasurable experiences are two hallmarks of major depression,” Turner said. “But the brain pathways responsible for exercise motivation have not been well understood. Now, we can seek ways to manipulate activity within this specific area of the brain without impacting the rest of the brain’s activity.” 

Dr. Turner’s study, titled “Role of the Dorsal Medial Habenula in the Regulation of Voluntary Activity, Motor Function, Hedonic State, and Primary Reinforcement,” was published today by the Journal of Neuroscience and funded by the National Institute of Mental Health and National Institute on Drug Abuse. The study used mouse models that were genetically engineered to block signals from the dorsal medial habenula. In the first part of the study, Dr. Turner’s team collaborated with Dr. Horacio de la Iglesia, a professor in University of Washington’s Department of Biology, to show that compared to typical mice, who love to run in their exercise wheels, the genetically engineered mice were lethargic and ran far less. Turner’s genetically engineered mice also lost their preference for sweetened drinking water. 

“Without a functioning dorsal medial habenula, the mice became couch potatoes,” Turner said. “They were physically capable of running but appeared unmotivated to do it.” 

In a second group of mice, Dr. Turner’s team activated the dorsal medial habenula using optogenetics – a precise laser technology developed in collaboration with the Allen Institute for Brain Science. The mice could “choose” to activate this area of the brain by turning one of two response wheels with their paws. The mice strongly preferred turning the wheel that stimulated the dorsal medial habenula, demonstrating that this area of the brain is tied to rewarding behavior.  

Past studies have attributed many different functions to the habenula, but technology was not advanced enough to determine roles of the various subsections of this area of the brain, including the dorsal medial habenula. 

“Traditional methods of stimulation could not isolate this part of the brain,” Turner said. “But cutting-edge technology at Seattle Children’s Research Institute makes discoveries like this possible.” 

As a professor in the University of Washington Department of Psychiatry and Behavioral Sciences, Dr. Turner treats depression and hopes this research will make a difference in the lives of future patients. 

“Working in mental health can be frustrating,” Turner said. “We have not made a lot of progress in developing new treatments. I hope the more we can learn about how the brain functions the more we can help people with all kinds of mental illness.”


alexofeddis:

thescienceoffandom:

Here are some basics on herd immunity, and here is some more technical research if you’re interested in the details! 

If you’ve ever heard my rants about vaccination, you know it’s a major topic with me. Because hey, I’m one of these immunosuppressed people this comic talks about, so it’s a bit of a sensitive subject. (“Oh, I’m sorry, you don’t like getting vaccinated? I don’t like having three month long respiratory infections because you gave me the freaking flu, but I guess you don’t care about that”)

Essentially, Ellen and her wonderful character Katherine have just said it better than I ever could—and using Shaun of the Dead references, too!!! It’s all about herd immunity—getting vaccinated isn’t just about your own health, it’s about the health—and non-zombification—of the entire human race.

SO REBLOG THIS!! LIKE THIS!!! SPREAD IT LIKE WILDFIRE!!!!!


libutron:

Spotted unicornfish  (Short-nosed unicornfish)
Yes, unicornfish exist! and there are about 20 species of them, belonging to the genus Naso, in the Acanthuridae Family.
This one, for example, is Naso brevirostris (Perciformes - Acanthuridae), distinctive by its long, broad-based tapering horn before eye (a bump on forehead of juveniles). This species is olive-brown to grey; has many small dark spots on the head and lower body, and many thin dark bars on the upper body; the tail is whitish with dark blotch at base.
Naso brevirostris is widespread and cosmopolitan, occupying a wide range of habitats. It is found in the Pacific and Indian oceans.
Other common names: Palefin Unicornfish, Shortsnout Unicornfish, Brown Unicornfish, Shortnosed Kala, Shortnose Unicornfish, Longnose Unicornfish, Corne, Nasique, Nason à Rostre Court, Nason Pointillé.
References: [1] - [2] - [3]
Photo credit: ©Sue Merrifield
Locality: Maldives

libutron:

Spotted unicornfish  (Short-nosed unicornfish)

Yes, unicornfish exist! and there are about 20 species of them, belonging to the genus Naso, in the Acanthuridae Family.

This one, for example, is Naso brevirostris (Perciformes - Acanthuridae), distinctive by its long, broad-based tapering horn before eye (a bump on forehead of juveniles). This species is olive-brown to grey; has many small dark spots on the head and lower body, and many thin dark bars on the upper body; the tail is whitish with dark blotch at base.

Naso brevirostris is widespread and cosmopolitan, occupying a wide range of habitats. It is found in the Pacific and Indian oceans.

Other common names: Palefin Unicornfish, Shortsnout Unicornfish, Brown Unicornfish, Shortnosed Kala, Shortnose Unicornfish, Longnose Unicornfish, Corne, Nasique, Nason à Rostre Court, Nason Pointillé.

References: [1] - [2] - [3]

Photo credit: ©Sue Merrifield

Locality: Maldives


montereybayaquarium:

Plankton of the world, beware!

While most nudibranchs, or sea slugs, crawl and graze, the melibe sweeps its hood through the water like a net, capturing unsuspecting tiny drifters. A fringe of tentacles interlock and trap prey as the hood collapses to help the slug digest its meal.

Melibes may be expert plankton snatchers, but how do these soft-bodied invertebrates escape being a meal? Researchers have followed their noses to the melibe’s uniquely fruity smell—noxious secretions which may ward off nibbling fish. They can also “swim” away from predators by wiggling from side to side. 

Living on giant kelp fronds or sea grass, melibes live higher up in the water column than most seafloor-bound nudibranchs. They’ve adapted well to the vertical life—as you can see in the background, their white ribbon eggs hang and sway with currents.

Learn more


neurosciencestuff:

Researchers find new target for chronic pain treatment
Researchers at the UNC School of Medicine have found a new target for treating chronic pain: an enzyme called PIP5K1C. In a paper published today in the journal Neuron, a team of researchers led by Mark Zylka, PhD, Associate Professor of Cell Biology and Physiology, shows that PIP5K1C controls the activity of cellular receptors that signal pain.
By reducing the level of the enzyme, researchers showed that the levels of a crucial lipid called PIP2 in pain-sensing neurons is also lessened, thus decreasing pain.
They also found a compound that could dampen the activity of PIP5K1C. This compound, currently named UNC3230, could lead to a new kind of pain reliever for the more than 100 million people who suffer from chronic pain in the United States alone.
In particular, the researchers showed that the compound might be able to significantly reduce inflammatory pain, such as arthritis, as well as neuropathic pain – damage to nerve fibers. The latter is common in conditions such as shingles, back pain, or when bodily extremities become numb due to side effects of chemotherapy or diseases such as diabetes.
The creation of such bodily pain might seem simple, but at the cellular level it’s quite complex. When we’re injured, a diverse mixture of chemicals is released, and these chemicals cause pain by acting on an equally diverse group of receptors on the surface of pain-sensing neurons.
“A big problem in our field is that it is impractical to block each of these receptors with a mixture of drugs,” said Zylka, the senior author of the Neuron article and member of the UNC Neuroscience Center. “So we looked for commonalities – things that each of these receptors need in order to send a signal.” Zylka’s team found that the lipid PIP2 (phosphatidylinositol 4,5-bisphosphate) was one of these commonalities.
“So the question became: how do we alter PIP2 levels in the neurons that sense pain?” Zylka said. “If we could lower the level of PIP2, we could get these receptors to signal less effectively. Then, in theory, we could reduce pain.”
Many different kinases can generate PIP2 in the body.  Brittany Wright, a graduate student in Zylka’s lab, found that the PIP5K1C kinase was expressed at the highest level in sensory neurons compared to other related kinases. Then the researchers used a mouse model to show that PIP5K1C was responsible for generating at least half of all PIP2 in these neurons.
“That told us that a 50 percent reduction in the levels of PIP5K1C was sufficient to reduce PIP2 levels in the tissue we were interested in – where pain-sensing neurons are located” Zylka said. “That’s what we wanted to do – block signaling at this first relay in the pain pathway.”
Once Zylka and colleagues realized that they could reduce PIP2 in sensory neurons by targeting PIP5K1C, they teamed up with Stephen Frye, PhD, the Director of the Center for Integrative Chemical Biology and Drug Discovery at the UNC Eshelman School of Pharmacy.
They screened about 5,000 small molecules to identify compounds that might block PIP5K1C. There were a number of hits, but UNC3230 was the strongest. It turned out that Zylka, Frye, and their team members had come upon a drug candidate. They realized that the chemical structure of UNC3230 could be manipulated to potentially turn it into an even better inhibitor of PIP5K1C. Experiments to do so are now underway at UNC.

neurosciencestuff:

Researchers find new target for chronic pain treatment

Researchers at the UNC School of Medicine have found a new target for treating chronic pain: an enzyme called PIP5K1C. In a paper published today in the journal Neuron, a team of researchers led by Mark Zylka, PhD, Associate Professor of Cell Biology and Physiology, shows that PIP5K1C controls the activity of cellular receptors that signal pain.

By reducing the level of the enzyme, researchers showed that the levels of a crucial lipid called PIPin pain-sensing neurons is also lessened, thus decreasing pain.

They also found a compound that could dampen the activity of PIP5K1C. This compound, currently named UNC3230, could lead to a new kind of pain reliever for the more than 100 million people who suffer from chronic pain in the United States alone.

In particular, the researchers showed that the compound might be able to significantly reduce inflammatory pain, such as arthritis, as well as neuropathic pain – damage to nerve fibers. The latter is common in conditions such as shingles, back pain, or when bodily extremities become numb due to side effects of chemotherapy or diseases such as diabetes.

The creation of such bodily pain might seem simple, but at the cellular level it’s quite complex. When we’re injured, a diverse mixture of chemicals is released, and these chemicals cause pain by acting on an equally diverse group of receptors on the surface of pain-sensing neurons.

“A big problem in our field is that it is impractical to block each of these receptors with a mixture of drugs,” said Zylka, the senior author of the Neuron article and member of the UNC Neuroscience Center. “So we looked for commonalities – things that each of these receptors need in order to send a signal.” Zylka’s team found that the lipid PIP2 (phosphatidylinositol 4,5-bisphosphate) was one of these commonalities.

“So the question became: how do we alter PIP2 levels in the neurons that sense pain?” Zylka said. “If we could lower the level of PIP2, we could get these receptors to signal less effectively. Then, in theory, we could reduce pain.”

Many different kinases can generate PIP2 in the body.  Brittany Wright, a graduate student in Zylka’s lab, found that the PIP5K1C kinase was expressed at the highest level in sensory neurons compared to other related kinases. Then the researchers used a mouse model to show that PIP5K1C was responsible for generating at least half of all PIP2 in these neurons.

“That told us that a 50 percent reduction in the levels of PIP5K1C was sufficient to reduce PIP2 levels in the tissue we were interested in – where pain-sensing neurons are located” Zylka said. “That’s what we wanted to do – block signaling at this first relay in the pain pathway.”

Once Zylka and colleagues realized that they could reduce PIP2 in sensory neurons by targeting PIP5K1C, they teamed up with Stephen Frye, PhD, the Director of the Center for Integrative Chemical Biology and Drug Discovery at the UNC Eshelman School of Pharmacy.

They screened about 5,000 small molecules to identify compounds that might block PIP5K1C. There were a number of hits, but UNC3230 was the strongest. It turned out that Zylka, Frye, and their team members had come upon a drug candidate. They realized that the chemical structure of UNC3230 could be manipulated to potentially turn it into an even better inhibitor of PIP5K1C. Experiments to do so are now underway at UNC.


sixpenceee:

Here is something phenomenal, I have to share with you all: 
A mother cichlid keeps her babies in her mouth to protect them. Sometimes she let’s them out as shown above. Her mouth serves as a nest and nursery. 
It may seem like a good system, but it’s not exactly.
Let me introduce these guys: 

These catfish are notorious parasites. The catfish try and pick up a few of cichlid eggs. The mother defends her station, while the catfish drop a few of their own eggs. They know the cichlid mother will pick them up and think of it as her own egg.

So the cichlid become a surrogate mother for the offspring of their enemy. The catfish take off soon, not knowing what’s becomes of their young. The cichlid mother does her job, letting her brood grow in her mouth. 

Like in a horror movie, the catfish eggs hatch first. The baby catfish gobbles up every single one of the cichlid babies.

The cichlid mother releases, not her own babies, but the killer catfish baby that ate of all her own children.

The cichlid mom doesn’t realize the switch and treats the catfish baby as if it were her own.

A morbid, ironic twist. Here’s the video for this
Another interesting science post: How the Mokin Children Are Able to See Crystal Clear Underwater

sixpenceee:

Here is something phenomenal, I have to share with you all: 

A mother cichlid keeps her babies in her mouth to protect them. Sometimes she let’s them out as shown above. Her mouth serves as a nest and nursery. 

It may seem like a good system, but it’s not exactly.

Let me introduce these guys: 

These catfish are notorious parasites. The catfish try and pick up a few of cichlid eggs. The mother defends her station, while the catfish drop a few of their own eggs. They know the cichlid mother will pick them up and think of it as her own egg.

So the cichlid become a surrogate mother for the offspring of their enemy. The catfish take off soon, not knowing what’s becomes of their young. The cichlid mother does her job, letting her brood grow in her mouth. 

Like in a horror movie, the catfish eggs hatch first. The baby catfish gobbles up every single one of the cichlid babies.

The cichlid mother releases, not her own babies, but the killer catfish baby that ate of all her own children.

The cichlid mom doesn’t realize the switch and treats the catfish baby as if it were her own.

A morbid, ironic twist. Here’s the video for this

Another interesting science post: How the Mokin Children Are Able to See Crystal Clear Underwater


From The Scientist



"Image of the Day: Bongo-netted Baby"



This tiny larva—either an octopus or a squid in the making—was captured in a remotely operated underwater vehicle’s bongo-shaped suction net.”(Credit: NOAA, Matt Wilson and Jay Clark) bit.ly/1l0Fmxq

Anyone know which it is?

From The Scientist

"Image of the Day: Bongo-netted Baby"
This tiny larva—either an octopus or a squid in the making—was captured in a remotely operated underwater vehicle’s bongo-shaped suction net.”
(Credit: NOAA, Matt Wilson and Jay Clark) 
bit.ly/1l0Fmxq
Anyone know which it is?


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