science-junkie:

Diagnosis by Light: Shrinking Chemical Labs Onto Optical Fibers
Lab-on-fiber sensors could monitor the environment and hunt for disease inside your body
Imagine an entire laboratory that fits inside a case the size of a tablet computer. The lab would include an instrument for reading out results and an array of attachable microsize probes for detecting molecules in a fluid sample, such as blood or saliva. Each probe could be used to diagnose one of many different diseases and health conditions and could be replaced for just a few cents.
This scenario is by no means a pipe dream. The key to achieving it will be optical glass fibers—more or less the same as the ones that already span the globe, ferrying voluminous streams of data and voice traffic at unmatchable speeds. Their tiny diameter, dirt-cheap cost, and huge information-carrying capacity make these fibers ideal platforms for inexpensive, high-quality chemical sensors.
We call this technology a lab on fiber. Beyond being an affordable alternative to a traditional laboratory, it could take on tasks not possible now. For instance, it could be snaked inside industrial machines to ensure product quality and test for leaks. It could monitor waterways and waste systems, survey the oceans, or warn against chemical warfare. One day, maybe as soon as a decade from now, it could be injected into humans to look for disease or study the metabolism of drugs inside the body.
Read the full article (via spectrum.ieee.org)

This technology is really remarkable it’s the innovation in the medical field  that will ultimately change the way doctors diagnose patients. However, how this technology is implemented in the future may also take a toll on the health care system as we know it. People won’t go to a Radiologist any more if this technology can identify Glioblastoma multiforme without expert analysis. Technology becomes more affordable as time goes on. Can this new form of scanning mean the end of many professional specializations? Only time will tell. High-res

science-junkie:

Diagnosis by Light: Shrinking Chemical Labs Onto Optical Fibers

Lab-on-fiber sensors could monitor the environment and hunt for disease inside your body

Imagine an entire laboratory that fits inside a case the size of a tablet computer. The lab would include an instrument for reading out results and an array of attachable microsize probes for detecting molecules in a fluid sample, such as blood or saliva. Each probe could be used to diagnose one of many different diseases and health conditions and could be replaced for just a few cents.

This scenario is by no means a pipe dream. The key to achieving it will be optical glass fibers—more or less the same as the ones that already span the globe, ferrying voluminous streams of data and voice traffic at unmatchable speeds. Their tiny diameter, dirt-cheap cost, and huge information-carrying capacity make these fibers ideal platforms for inexpensive, high-quality chemical sensors.

We call this technology a lab on fiber. Beyond being an affordable alternative to a traditional laboratory, it could take on tasks not possible now. For instance, it could be snaked inside industrial machines to ensure product quality and test for leaks. It could monitor waterways and waste systems, survey the oceans, or warn against chemical warfare. One day, maybe as soon as a decade from now, it could be injected into humans to look for disease or study the metabolism of drugs inside the body.

Read the full article (via spectrum.ieee.org)

This technology is really remarkable it’s the innovation in the medical field  that will ultimately change the way doctors diagnose patients. However, how this technology is implemented in the future may also take a toll on the health care system as we know it. People won’t go to a Radiologist any more if this technology can identify Glioblastoma multiforme without expert analysis. Technology becomes more affordable as time goes on. Can this new form of scanning mean the end of many professional specializations? Only time will tell.

New drug makes brain cancer cells explode

Sounds like people may have a chance to live longer lives thanks to this new drug. Unbelievable, medical science is really making a difference in the lives of people diagnosed with Glioblastoma multiforme.

discoverynews:

Monster Rare Yellow Hypergiant Star Discovered

A gargantuan star, measuring 1,300 times the size of our sun, has been uncovered 12,000 light-years from Earth — it is one of the ten biggest stars known to exist in our galaxy. The yellow hypergiant even dwarfs the famous stellar heavyweight Betelgeuse by 50 percent. While its hulking mass may be impressive, astronomers have also realized that HR 5171 is a double star with a smaller stellar sibling physically touching the surface of the larger star as they orbit one another. Read more

neurosciencestuff:

Substance in Humans is Effective Fighting Stroke Damage
A molecular substance that occurs naturally in humans and rats was found to “substantially reduce” brain damage after an acute stroke and contribute to a better recovery, according to a newly released animal study by researchers at Henry Ford Hospital.
The study, published online before print in Stroke, the journal of the American Heart Association, was the first ever to show that the peptide AcSDKP provides neurological protection when administered one to four hours after the onset of an ischemic stroke.
This type of stroke occurs when an artery to the brain is blocked by a blood clot, cutting off oxygen and killing brain tissue with crippling or fatal results.
“Stroke is a leading cause of death and disability worldwide,” said Li Zhang, M.D., a researcher at Henry Ford and lead author of the study. “Our data showed that treatment of acute stroke with AcSDKP alone or in combination with tPA substantially reduced neurovascular damage and improved neurological outcome.”
Commonly called a “clot-buster,” tPA, or tissue plasminogen activator, is the only FDA-approved treatment for acute stroke.

However, tPA must be given shortly after the onset of stroke to provide the best results. It also has the potential to cause a brain hemorrhage.

The Henry Ford study found that this narrow “therapeutic window” is extended for up to four hours after stroke and the therapeutic benefit of tPA is amplified when tPA is combined with AcSDKP. Further, the researchers discovered that AcSDKP alone is an effective treatment if given up to one hour after the brain attack.

The researchers tested the actions of both substances on laboratory rats in which acute stroke had been induced. It was already known that the peptide AcSDKP provides anti-inflammatory effects and helps protect the heart when used to treat a variety of cardiovascular diseases. The Henry Ford scientists reasoned that the peptide may have similar neurological benefits.

Significantly, they found that AcSDKP can readily cross the so-called “blood brain barrier” that blocks other neuroprotective substances.

A battery of behavioral tests was given to the lab rats both before and after stroke was induced to measure the effects of AcSDKP administered alone one hour after onset and combined with tPA four hours after stroke.

Besides finding that both methods “robustly” decreased neurological damage associated with stroke, they did so without increasing the incidence of brain hemorrhage or the formation of additional blood clots.

“With the increased use of clot-busting therapy in patients with acute stroke, both the safety and effectiveness of the combined treatment shown in our study should encourage the development of clinical trials of AcSDKP with tPA,” Dr. Zhang says. High-res

neurosciencestuff:

Substance in Humans is Effective Fighting Stroke Damage

A molecular substance that occurs naturally in humans and rats was found to “substantially reduce” brain damage after an acute stroke and contribute to a better recovery, according to a newly released animal study by researchers at Henry Ford Hospital.

The study, published online before print in Stroke, the journal of the American Heart Association, was the first ever to show that the peptide AcSDKP provides neurological protection when administered one to four hours after the onset of an ischemic stroke.

This type of stroke occurs when an artery to the brain is blocked by a blood clot, cutting off oxygen and killing brain tissue with crippling or fatal results.

“Stroke is a leading cause of death and disability worldwide,” said Li Zhang, M.D., a researcher at Henry Ford and lead author of the study. “Our data showed that treatment of acute stroke with AcSDKP alone or in combination with tPA substantially reduced neurovascular damage and improved neurological outcome.”

Commonly called a “clot-buster,” tPA, or tissue plasminogen activator, is the only FDA-approved treatment for acute stroke.

However, tPA must be given shortly after the onset of stroke to provide the best results. It also has the potential to cause a brain hemorrhage.

The Henry Ford study found that this narrow “therapeutic window” is extended for up to four hours after stroke and the therapeutic benefit of tPA is amplified when tPA is combined with AcSDKP. Further, the researchers discovered that AcSDKP alone is an effective treatment if given up to one hour after the brain attack.

The researchers tested the actions of both substances on laboratory rats in which acute stroke had been induced. It was already known that the peptide AcSDKP provides anti-inflammatory effects and helps protect the heart when used to treat a variety of cardiovascular diseases. The Henry Ford scientists reasoned that the peptide may have similar neurological benefits.

Significantly, they found that AcSDKP can readily cross the so-called “blood brain barrier” that blocks other neuroprotective substances.

A battery of behavioral tests was given to the lab rats both before and after stroke was induced to measure the effects of AcSDKP administered alone one hour after onset and combined with tPA four hours after stroke.

Besides finding that both methods “robustly” decreased neurological damage associated with stroke, they did so without increasing the incidence of brain hemorrhage or the formation of additional blood clots.

“With the increased use of clot-busting therapy in patients with acute stroke, both the safety and effectiveness of the combined treatment shown in our study should encourage the development of clinical trials of AcSDKP with tPA,” Dr. Zhang says.

canadian-space-agency:

The Right Stuff
Both astronauts and Olympians are chosen by rigorous selection processes as they compete for much-vaunted positions in their respective fields. Regardless of natural abilities, they both work, sweat, and shed blood and tears to excel. Their hard work realized, they inspire us all to push past barriers to reach our potential.
Congratulations to all the athletes of the Canadian Olympic Team who represented our country so well! Today, the whole nation is united in pride. Go Canada Go! #WeAreWinter
Photo credit: Ed Kaiser/Postmedia High-res

canadian-space-agency:

The Right Stuff

Both astronauts and Olympians are chosen by rigorous selection processes as they compete for much-vaunted positions in their respective fields. Regardless of natural abilities, they both work, sweat, and shed blood and tears to excel. Their hard work realized, they inspire us all to push past barriers to reach our potential.

Congratulations to all the athletes of the Canadian Olympic Team who represented our country so well! Today, the whole nation is united in pride. Go Canada Go! #WeAreWinter

Photo credit: Ed Kaiser/Postmedia

(Source: facebook.com)

neurosciencestuff:




Researchers Pinpoint Brain Region Essential for Social Memory

Columbia University Medical Center (CUMC) researchers have determined that a small region of the hippocampus known as CA2 is essential for social memory, the ability of an animal to recognize another of the same species. A better grasp of the function of CA2 could prove useful in understanding and treating disorders characterized by altered social behaviors, such as autism, schizophrenia, and bipolar disorder. The findings, made in mice, were published on Feb. 23, 2014, in the online edition of Nature.
Scientists have long understood that the hippocampus—a pair of seahorse-shaped structures in the brain’s temporal lobes—plays a critical role in our ability to remember the who, what, where, and when of our daily lives. Recent studies have shown that different subregions of the hippocampus have different functions. For instance, the dentate gyrus is critical for distinguishing between similar environments, while CA3 enables us to recall a memory from partial cues (e.g., Proust’s famous madeleine). The CA1 region is critical for all forms of memory.
“However, the role of CA2, a relatively small region of the hippocampus sandwiched between CA3 and CA1, has remained largely unknown,” said senior author Steven A. Siegelbaum, PhD, professor of neuroscience and pharmacology, chair of the Department of Neuroscience, a member of the Mortimer B. Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, and a Howard Hughes Medical Institute Investigator. A few studies have suggested that CA2 might be involved in social memory, as this region has a high level of expression of a receptor for vasopressin, a hormone linked to sexual motivation, bonding, and other social behaviors.
To learn more about this part of the hippocampus, the researchers created a transgenic mouse in which CA2 neurons could be selectively inhibited in adult animals. Once the neurons were inhibited, the mice were given a series of behavioral tests. “The mice looked quite normal until we looked at social memory,” said first author Frederick L. Hitti, an MD-PhD student in Dr. Siegelbaum’s laboratory, who developed the transgenic mouse. “Normally, mice are naturally curious about a mouse they’ve never met; they spend more time investigating an unfamiliar mouse than a familiar one. In our experiment, however, mice with an inactivated CA2 region showed no preference for a novel mouse versus a previously encountered mouse, indicating a lack of social memory.”
In two separate novel-object recognition tests, the CA2-deficient mice showed a normal preference for an object they had not previously encountered, showing that the mice did not have a global lack of interest in novelty. In another experiment, the researchers tested whether the animals’ inability to form social memories might have to do with deficits in olfaction (sense of smell), which is crucial for normal social interaction. However, the mice showed no loss in ability to discriminate social or non-social odors.
In humans, the importance of the hippocampus for social memory was famously illustrated by the case of Henry Molaison, who had much of his hippocampus removed by surgeons in 1953 in an attempt to cure severe epilepsy. Molaison (often referred to as HM in the scientific literature) was subsequently unable to form new memories of people. Scientists have observed that lesions limited to the hippocampus also impair social memory in both rodents and humans.
“Because several neuropsychiatric disorders are associated with altered social behaviors, our findings raise the possibility that CA2 dysfunction may contribute to these behavioral changes,” said Dr. Siegelbaum. This possibility is supported by findings of a decreased number of CA2 inhibitory neurons in individuals with schizophrenia and bipolar disorder and altered vasopressin signaling in autism. Thus, CA2 may provide a new target for therapeutic approaches to the treatment of social disorders.



High-res

neurosciencestuff:

Researchers Pinpoint Brain Region Essential for Social Memory

Columbia University Medical Center (CUMC) researchers have determined that a small region of the hippocampus known as CA2 is essential for social memory, the ability of an animal to recognize another of the same species. A better grasp of the function of CA2 could prove useful in understanding and treating disorders characterized by altered social behaviors, such as autism, schizophrenia, and bipolar disorder. The findings, made in mice, were published on Feb. 23, 2014, in the online edition of Nature.

Scientists have long understood that the hippocampus—a pair of seahorse-shaped structures in the brain’s temporal lobes—plays a critical role in our ability to remember the who, what, where, and when of our daily lives. Recent studies have shown that different subregions of the hippocampus have different functions. For instance, the dentate gyrus is critical for distinguishing between similar environments, while CA3 enables us to recall a memory from partial cues (e.g., Proust’s famous madeleine). The CA1 region is critical for all forms of memory.

“However, the role of CA2, a relatively small region of the hippocampus sandwiched between CA3 and CA1, has remained largely unknown,” said senior author Steven A. Siegelbaum, PhD, professor of neuroscience and pharmacology, chair of the Department of Neuroscience, a member of the Mortimer B. Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, and a Howard Hughes Medical Institute Investigator. A few studies have suggested that CA2 might be involved in social memory, as this region has a high level of expression of a receptor for vasopressin, a hormone linked to sexual motivation, bonding, and other social behaviors.

To learn more about this part of the hippocampus, the researchers created a transgenic mouse in which CA2 neurons could be selectively inhibited in adult animals. Once the neurons were inhibited, the mice were given a series of behavioral tests. “The mice looked quite normal until we looked at social memory,” said first author Frederick L. Hitti, an MD-PhD student in Dr. Siegelbaum’s laboratory, who developed the transgenic mouse. “Normally, mice are naturally curious about a mouse they’ve never met; they spend more time investigating an unfamiliar mouse than a familiar one. In our experiment, however, mice with an inactivated CA2 region showed no preference for a novel mouse versus a previously encountered mouse, indicating a lack of social memory.”

In two separate novel-object recognition tests, the CA2-deficient mice showed a normal preference for an object they had not previously encountered, showing that the mice did not have a global lack of interest in novelty. In another experiment, the researchers tested whether the animals’ inability to form social memories might have to do with deficits in olfaction (sense of smell), which is crucial for normal social interaction. However, the mice showed no loss in ability to discriminate social or non-social odors.

In humans, the importance of the hippocampus for social memory was famously illustrated by the case of Henry Molaison, who had much of his hippocampus removed by surgeons in 1953 in an attempt to cure severe epilepsy. Molaison (often referred to as HM in the scientific literature) was subsequently unable to form new memories of people. Scientists have observed that lesions limited to the hippocampus also impair social memory in both rodents and humans.

“Because several neuropsychiatric disorders are associated with altered social behaviors, our findings raise the possibility that CA2 dysfunction may contribute to these behavioral changes,” said Dr. Siegelbaum. This possibility is supported by findings of a decreased number of CA2 inhibitory neurons in individuals with schizophrenia and bipolar disorder and altered vasopressin signaling in autism. Thus, CA2 may provide a new target for therapeutic approaches to the treatment of social disorders.