Edifying in curious letters

A pursuit of all things intellectual, moral, and spiritual (with an occasional touch of humor)


Ask me anything  
Reblogged from fastcompany
You should take a look at this,” he told her. “I can move my toes on command.” “Her jaw about hit the floor at that point.

How A New Technology Is Helping Paralyzed Patients Regain Use Of Their Legs

image

Watch: Co.Exist

(via fastcompany)

(via emergentfutures)

Reblogged from mothernaturenetwork
mothernaturenetwork:

Making strides with a running gait analysisMNN’s family blogger attempts to outrun chronic injuries with a 3-D assessment of her running form.

mothernaturenetwork:

Making strides with a running gait analysis
MNN’s family blogger attempts to outrun chronic injuries with a 3-D assessment of her running form.

Reblogged from fastcodesign
It’s a bit like flashcards on steroids.

How Spritz Redesigned Reading, Letting You Scan 1,000 Words A Minute

image

When we read, our eyes move across a page or a screen to digest the words. All of that eye movement slows us down, but a new technology called Spritz claims to have figured out a way to turn us into speed-readers. By flashing words onto a single point on a screen, much like watching TV, Spritz says it will double your reading speed.

More> Co.Design

(via fastcodesign)

(via fastcompany)

Reblogged from ucsdhealthsciences
ucsdhealthsciences:

A hairy death
Apoptosis or programmed cell death is an essential part of life. For example, it’s critical to human development. Where would we be if every fetal cell survived? Some cells must die to form, say, our fingers and toes; others must perish to shape our functional brains.
Cells frequently commit suicide for the good of the whole. They may become apoptotic in response to viruses or gene mutations in order to prevent further damage. Menstruation relies upon programmed cell death.
Apoptosis may be necessary, but it’s not necessarily pretty. Above is a scanning electron micrograph of several cultured HeLa cancer cells. The cell at the center is undergoing apoptosis. During the process, the cell’s cytoskeleton breaks up, causing the outer membrane to bulge and decouple. The resulting wart-like structures are called blebs, which eventually break off and are consumed by phagocytic cells for recycling.
The hairy extensions are filopodia, extremely tiny extensions of cytoplasm used by cells for sensing, migration and cell-cell interactions.

ucsdhealthsciences:

A hairy death

Apoptosis or programmed cell death is an essential part of life. For example, it’s critical to human development. Where would we be if every fetal cell survived? Some cells must die to form, say, our fingers and toes; others must perish to shape our functional brains.

Cells frequently commit suicide for the good of the whole. They may become apoptotic in response to viruses or gene mutations in order to prevent further damage. Menstruation relies upon programmed cell death.

Apoptosis may be necessary, but it’s not necessarily pretty. Above is a scanning electron micrograph of several cultured HeLa cancer cells. The cell at the center is undergoing apoptosis. During the process, the cell’s cytoskeleton breaks up, causing the outer membrane to bulge and decouple. The resulting wart-like structures are called blebs, which eventually break off and are consumed by phagocytic cells for recycling.

The hairy extensions are filopodia, extremely tiny extensions of cytoplasm used by cells for sensing, migration and cell-cell interactions.

Reblogged from neurosciencestuff
neurosciencestuff:

Filling me softly
Surgical implants are widely used in modern medicine but their effectiveness is often compromised by how our bodies react to them. Now, scientists at the University of Cambridge have discovered that implant stiffness is a major cause of this so-called foreign body reaction. 
This is the first time that stiffness of implant materials has been shown to be involved in foreign body reactions. The findings – published in the journal Biomaterials – could lead to major improvements in surgical implants and the quality of life of patients whose lives depend on them.
Foreign bodies often trigger a process that begins with inflammation and ends with the foreign body being encapsulated with scar tissue. When this happens after an accident or injury, the process is usually vital to healing, but when the same occurs around, for example, electrodes implanted in the brain to alleviate tremor in Parkinson’s disease, it may be problematic.
Despite decades of research, the process remains poorly understood as neither the materials from which these implants are made, nor their electrical properties, can explain what triggers inflammation.
Instead of looking for classical biological causes, a group of Cambridge physicists, engineers, chemists, clinical scientists and biologists decided to take a different tack and examine the impact of an implant’s stiffness on the inflammatory process.
According to Dr Kristian Franze, one of the authors of the study: “Electrodes that are implanted in the brain, for example, should be chemically inert, and these foreign body reactions occur whether or not these electrodes are switched on, so it’s not the electrical signalling.
“We thought that an obvious difference between electrodes and brain tissue is stiffness. Brain tissue is as soft as cream cheese, it is one of the softest tissues in the body, and electrodes are orders of magnitude stiffer.”
To test their hypothesis that mechanical signals trigger inflammation, the team cultured brain cells on two different substrates. The substrates were chemically identical but one was as soft as brain tissue and the other two orders of magnitude stiffer, akin to the stiffness of muscle tissue.
When they examined the cells, they found major differences in their shape. “The cells grown on the stiffer substrate were very flat, whereas those grown on the soft substrate looked much more like cells you find in the brain,” he explained.
To confirm the findings they did genetic and other tests, which revealed that many of the inflammatory genes and proteins known to be involved in foreign body reactions had been upregulated on stiff surfaces.
The team then implanted a tiny foreign body into rats’ brains. The implant was made of a single material but one side was as soft as brain tissue and the other as stiff as muscle. They found much greater foreign body reaction around the stiff part of the implant.
“This strongly indicates that stiffness of a material may trigger foreign body reactions. It does not mean there aren’t other triggers, but stiffness definitely contributes and this is something new that hasn’t been known before,” he said.
The findings could have major implications for the design of implants used in the brain and other parts of the body.
“While it may eventually be possible to make implants out of new, much softer materials, our results suggest that in the short term, simply coating existing implants with materials that match the stiffness of the tissue they are being implanted into will help reduce foreign body reactions,” said Dr Franze.

neurosciencestuff:

Filling me softly

Surgical implants are widely used in modern medicine but their effectiveness is often compromised by how our bodies react to them. Now, scientists at the University of Cambridge have discovered that implant stiffness is a major cause of this so-called foreign body reaction.

This is the first time that stiffness of implant materials has been shown to be involved in foreign body reactions. The findings – published in the journal Biomaterials – could lead to major improvements in surgical implants and the quality of life of patients whose lives depend on them.

Foreign bodies often trigger a process that begins with inflammation and ends with the foreign body being encapsulated with scar tissue. When this happens after an accident or injury, the process is usually vital to healing, but when the same occurs around, for example, electrodes implanted in the brain to alleviate tremor in Parkinson’s disease, it may be problematic.

Despite decades of research, the process remains poorly understood as neither the materials from which these implants are made, nor their electrical properties, can explain what triggers inflammation.

Instead of looking for classical biological causes, a group of Cambridge physicists, engineers, chemists, clinical scientists and biologists decided to take a different tack and examine the impact of an implant’s stiffness on the inflammatory process.

According to Dr Kristian Franze, one of the authors of the study: “Electrodes that are implanted in the brain, for example, should be chemically inert, and these foreign body reactions occur whether or not these electrodes are switched on, so it’s not the electrical signalling.

“We thought that an obvious difference between electrodes and brain tissue is stiffness. Brain tissue is as soft as cream cheese, it is one of the softest tissues in the body, and electrodes are orders of magnitude stiffer.”

To test their hypothesis that mechanical signals trigger inflammation, the team cultured brain cells on two different substrates. The substrates were chemically identical but one was as soft as brain tissue and the other two orders of magnitude stiffer, akin to the stiffness of muscle tissue.

When they examined the cells, they found major differences in their shape. “The cells grown on the stiffer substrate were very flat, whereas those grown on the soft substrate looked much more like cells you find in the brain,” he explained.

To confirm the findings they did genetic and other tests, which revealed that many of the inflammatory genes and proteins known to be involved in foreign body reactions had been upregulated on stiff surfaces.

The team then implanted a tiny foreign body into rats’ brains. The implant was made of a single material but one side was as soft as brain tissue and the other as stiff as muscle. They found much greater foreign body reaction around the stiff part of the implant.

“This strongly indicates that stiffness of a material may trigger foreign body reactions. It does not mean there aren’t other triggers, but stiffness definitely contributes and this is something new that hasn’t been known before,” he said.

The findings could have major implications for the design of implants used in the brain and other parts of the body.

“While it may eventually be possible to make implants out of new, much softer materials, our results suggest that in the short term, simply coating existing implants with materials that match the stiffness of the tissue they are being implanted into will help reduce foreign body reactions,” said Dr Franze.

Reblogged from scienceisbeauty

scienceisbeauty:

Talent vs. Training (VIDEO)

When it comes to being great at something, which matters more - relentlessly training your whole life, or the genes you are born with?

Reblogged from neurosciencestuff
Reblogged from neurosciencestuff
neurosciencestuff:

How Inactivity Changes the Brain
A number of studies have shown that exercise can remodel the brain by prompting the creation of new brain cells and inducing other changes. Now it appears that inactivity, too, can remodel the brain, according to a notable new report.
The study, which was conducted in rats but likely has implications for people too, the researchers say, found that being sedentary changes the shape of certain neurons in ways that significantly affect not just the brain but the heart as well. The findings may help to explain, in part, why a sedentary lifestyle is so bad for us.
Until about 20 years ago, most scientists believed that the brain’s structure was fixed by adulthood, that you couldn’t create new brain cells, alter the shape of those that existed or in any other way change your mind physically after adolescence.
But in the years since, neurological studies have established that the brain retains plasticity, or the capacity to be reshaped, throughout our lifetimes. Exercise appears to be particularly adept at remodeling the brain, studies showed.
But little has been known about whether inactivity likewise alters the structure of the brain and, if so, what the consequences might be.
So for a study recently published in The Journal of Comparative Neurology, scientists at Wayne State University School of Medicine and other institutions gathered a dozen rats. They settled half of them in cages with running wheels and let the animals run at will. Rats like running, and these animals were soon covering about three miles a day on their wheels.
The other rats were housed in cages without wheels and remained sedentary.
Read more

neurosciencestuff:

How Inactivity Changes the Brain

A number of studies have shown that exercise can remodel the brain by prompting the creation of new brain cells and inducing other changes. Now it appears that inactivity, too, can remodel the brain, according to a notable new report.

The study, which was conducted in rats but likely has implications for people too, the researchers say, found that being sedentary changes the shape of certain neurons in ways that significantly affect not just the brain but the heart as well. The findings may help to explain, in part, why a sedentary lifestyle is so bad for us.

Until about 20 years ago, most scientists believed that the brain’s structure was fixed by adulthood, that you couldn’t create new brain cells, alter the shape of those that existed or in any other way change your mind physically after adolescence.

But in the years since, neurological studies have established that the brain retains plasticity, or the capacity to be reshaped, throughout our lifetimes. Exercise appears to be particularly adept at remodeling the brain, studies showed.

But little has been known about whether inactivity likewise alters the structure of the brain and, if so, what the consequences might be.

So for a study recently published in The Journal of Comparative Neurology, scientists at Wayne State University School of Medicine and other institutions gathered a dozen rats. They settled half of them in cages with running wheels and let the animals run at will. Rats like running, and these animals were soon covering about three miles a day on their wheels.

The other rats were housed in cages without wheels and remained sedentary.

Read more

Reblogged from neurosciencestuff
Reblogged from neurosciencestuff
neurosciencestuff:

Age no obstacle to nerve cell regeneration
In aging worms at least, it is insulin, not Father Time, that inhibits a motor neuron’s ability to repair itself — a finding that suggests declines in nervous system health may not be inevitable.
All organisms show a declining ability to regenerate damaged nervous systems with age, but the study appearing in the Feb. 5 issue of the journal Neuron suggests this deficit is not due to the ravages of time.
“The nervous system regulates its own response to age, separately from what happens in the rest of the body,” said Marc Hammarlund, assistant professor of genetics and senior author of the new study. “By manipulating the insulin pathway, we can make animals that live longer but have nervous systems that age normally, or conversely, we can make animals that die at a normal age but have a young nervous system.”
Alexandra Byrne, postdoctoral associate in genetics and lead author of the study, identified two genetic pathways that regulate insulin activity and are responsible for age-related declines in a worm’s ability to regenerate neuronal axons, or connective branches. The team pinpointed two other pathways that also regulate a neuron’s ability to regenerate, but that have no connection to the age of the worm.
The worm C. elegans is a well-established model to study the genetics of aging, and manipulation of the family of genes that regulate insulin activity has been shown to dramatically increase lifespan of the organism. The new study reveals that insulin signaling is also directly affecting the nervous system.
“We hope to understand how different pathways coordinately regulate neuronal aging, and more specifically, how to entice an aged neuron to regenerate after injury,” Byrne said.
“The hope is to increase healthspan, not just lifespan,” Hammarlund said.

neurosciencestuff:

Age no obstacle to nerve cell regeneration

In aging worms at least, it is insulin, not Father Time, that inhibits a motor neuron’s ability to repair itself — a finding that suggests declines in nervous system health may not be inevitable.

All organisms show a declining ability to regenerate damaged nervous systems with age, but the study appearing in the Feb. 5 issue of the journal Neuron suggests this deficit is not due to the ravages of time.

“The nervous system regulates its own response to age, separately from what happens in the rest of the body,” said Marc Hammarlund, assistant professor of genetics and senior author of the new study. “By manipulating the insulin pathway, we can make animals that live longer but have nervous systems that age normally, or conversely, we can make animals that die at a normal age but have a young nervous system.”

Alexandra Byrne, postdoctoral associate in genetics and lead author of the study, identified two genetic pathways that regulate insulin activity and are responsible for age-related declines in a worm’s ability to regenerate neuronal axons, or connective branches. The team pinpointed two other pathways that also regulate a neuron’s ability to regenerate, but that have no connection to the age of the worm.

The worm C. elegans is a well-established model to study the genetics of aging, and manipulation of the family of genes that regulate insulin activity has been shown to dramatically increase lifespan of the organism. The new study reveals that insulin signaling is also directly affecting the nervous system.

“We hope to understand how different pathways coordinately regulate neuronal aging, and more specifically, how to entice an aged neuron to regenerate after injury,” Byrne said.

“The hope is to increase healthspan, not just lifespan,” Hammarlund said.