s-c-i-guy:

Rewritten in Blood
A modified gene-editing technique corrects mutations in human hematopoietic stem cells.
Targeted gene editing is an experimental therapeutic approach that avoids the risk of insertional mutagenesis associated with the more traditional gene-therapy method of adding a functional gene copy to cells. In gene editing, special nuclease enzymes, such as zinc finger nucleases (ZFNs), are directed to cut the mutant gene of interest, and a replacement piece of DNA—containing the desired sequence—is then integrated by means of the cell’s own homology-directed repair pathway.
While the approach has been used to correct mutations in a variety of cell lines, attempts to edit genes in human primary hematopoietic stem cells (HSCs)—important targets for treating a number of inherited blood disorders—have proved unsuccessful.
“The real hurdle was to achieve gene editing in cells relevant for [clinical] translation,” says Luigi Naldini of the San Raffaele Scientific Institute in Milan. The challenge is that homology-directed repair requires cells to be cycling, and, for the most part, HSCs are quiescent. Stimulating HSCs to divide induces differentiation, however, so the team “fine-tuned the conditions” to both expand HSCs and maintain their undifferentiated state, Naldini explains. These tweaks have now allowed his team to use ZFNs to rewrite a disease-causing mutation in HSCs from a patient with X-linked severe combined immunodeficiency (X-SCID).
The group successfully repaired between 3 percent and 11 percent of the patient’s HSCs. While that may not sound like many cells, “it’s pretty exciting,” says Harry Malech of the National Institute of Allergy and Infectious Diseases who was not involved in the study, because “it’s encouraging that you can do it at all.”
Improving the efficiency may be necessary to fix certain blood-based disorders, says Malech, but he adds that “for diseases like X-linked SCID … the goal can be quite low” because the corrected stem cells will likely be able to expand once inside the patient.
source

s-c-i-guy:

Rewritten in Blood

A modified gene-editing technique corrects mutations in human hematopoietic stem cells.

Targeted gene editing is an experimental therapeutic approach that avoids the risk of insertional mutagenesis associated with the more traditional gene-therapy method of adding a functional gene copy to cells. In gene editing, special nuclease enzymes, such as zinc finger nucleases (ZFNs), are directed to cut the mutant gene of interest, and a replacement piece of DNA—containing the desired sequence—is then integrated by means of the cell’s own homology-directed repair pathway.

While the approach has been used to correct mutations in a variety of cell lines, attempts to edit genes in human primary hematopoietic stem cells (HSCs)—important targets for treating a number of inherited blood disorders—have proved unsuccessful.

“The real hurdle was to achieve gene editing in cells relevant for [clinical] translation,” says Luigi Naldini of the San Raffaele Scientific Institute in Milan. The challenge is that homology-directed repair requires cells to be cycling, and, for the most part, HSCs are quiescent. Stimulating HSCs to divide induces differentiation, however, so the team “fine-tuned the conditions” to both expand HSCs and maintain their undifferentiated state, Naldini explains. These tweaks have now allowed his team to use ZFNs to rewrite a disease-causing mutation in HSCs from a patient with X-linked severe combined immunodeficiency (X-SCID).

The group successfully repaired between 3 percent and 11 percent of the patient’s HSCs. While that may not sound like many cells, “it’s pretty exciting,” says Harry Malech of the National Institute of Allergy and Infectious Diseases who was not involved in the study, because “it’s encouraging that you can do it at all.”

Improving the efficiency may be necessary to fix certain blood-based disorders, says Malech, but he adds that “for diseases like X-linked SCID … the goal can be quite low” because the corrected stem cells will likely be able to expand once inside the patient.

source

(via alpha-canismajoris)

malformalady:

The sternal cartilage of a juvenile cat. The top photo shows the structure just after soaking in ammonia, the bottom photo reflects the degeneration just a few hours after soaking. In immature animals the bones and cartilage are not fully developed and when cleaned, will shrivel up like this cartilage.
Photo credit: brandonssk

malformalady:

The sternal cartilage of a juvenile cat. The top photo shows the structure just after soaking in ammonia, the bottom photo reflects the degeneration just a few hours after soaking. In immature animals the bones and cartilage are not fully developed and when cleaned, will shrivel up like this cartilage.

Photo credit: brandonssk

spaceplasma:

The Large Hadron Collider (LHC) is the world’s largest and most powerful particle collider, built by the European Organization for Nuclear Research (CERN). The LHC is designed to answer some of the most profound questions about the universe: What is the origin of mass? Why are we made of matter and not antimatter? What is dark matter made of? It could also provide important new clues about conditions in the very early universe, when the four forces of nature were rolled into one giant superforce.
For more information click: here
Credit: Michael Hirst
spaceplasma:

The Large Hadron Collider (LHC) is the world’s largest and most powerful particle collider, built by the European Organization for Nuclear Research (CERN). The LHC is designed to answer some of the most profound questions about the universe: What is the origin of mass? Why are we made of matter and not antimatter? What is dark matter made of? It could also provide important new clues about conditions in the very early universe, when the four forces of nature were rolled into one giant superforce.
For more information click: here
Credit: Michael Hirst
spaceplasma:

The Large Hadron Collider (LHC) is the world’s largest and most powerful particle collider, built by the European Organization for Nuclear Research (CERN). The LHC is designed to answer some of the most profound questions about the universe: What is the origin of mass? Why are we made of matter and not antimatter? What is dark matter made of? It could also provide important new clues about conditions in the very early universe, when the four forces of nature were rolled into one giant superforce.
For more information click: here
Credit: Michael Hirst
spaceplasma:

The Large Hadron Collider (LHC) is the world’s largest and most powerful particle collider, built by the European Organization for Nuclear Research (CERN). The LHC is designed to answer some of the most profound questions about the universe: What is the origin of mass? Why are we made of matter and not antimatter? What is dark matter made of? It could also provide important new clues about conditions in the very early universe, when the four forces of nature were rolled into one giant superforce.
For more information click: here
Credit: Michael Hirst
allthingshyper:

gehayi:

hiddlesbatchlove:

forever-falling-forward:

platredeparis:

bnycolew:

mannysiege:

Progress

What

Imma just let this sit here

MOTHA FUCKIN SCIENCE

sources:
Engagdget
DailyTech
CBS

They turned RNA into an anti-virus program. That is amazing.

Let me restate this in case it didn’t sink in the first time
Researchers physically DELETED ALL TRACES of the HIV virus from a human cell.
ALL OF IT.
IF YOU ARE NOT EXCITED ABOUT THAT I DON’T THINK YOU KNOW WHAT HIV IS

allthingshyper:

gehayi:

hiddlesbatchlove:

forever-falling-forward:

platredeparis:

bnycolew:

mannysiege:

Progress

What

Imma just let this sit here

MOTHA FUCKIN SCIENCE

sources:

Engagdget

DailyTech

CBS

They turned RNA into an anti-virus program. That is amazing.

Let me restate this in case it didn’t sink in the first time

Researchers physically DELETED ALL TRACES of the HIV virus from a human cell.

ALL OF IT.

IF YOU ARE NOT EXCITED ABOUT THAT I DON’T THINK YOU KNOW WHAT HIV IS

(Source: mannysiege, via lelosa)

sixpenceee:

When does this self-awareness set in? 
A particular study has shed some light. 
In this study, pregnant mothers read aloud a 3 minute story, in the last 6 weeks on their pregnancy. 
Within 2 days of birth, these babies were tested if they recognized the story or not. Researchers measured the rate of sucking a nipple, while the mothers read aloud the story. It turns out when the same story was read to them, the rate went up, but when it was a different story the rate went down.
They preferred the familiar story, hinting that 3rd trimester fetuses can acquire some audible information in the womb. 
Some say that a baby is completely unconscious until birth, this study proves that they are aware of auditory details even in the womb. 
The question of when thoughts start rising in the brain, is still up to debate, although scientists have found that 5 month old babies have working memory, and have certain spikes in their brain waves when seeing a moving object. 
Their brain reactions were similar to that of an adult suggesting they may be capable of thought. 
SOURCE: Evolution of Consciousness by Euan M. Macphail and this article
TWINS WHO MAY SHARE CONSCIOUSNESS

sixpenceee:

When does this self-awareness set in? 

A particular study has shed some light. 

In this study, pregnant mothers read aloud a 3 minute story, in the last 6 weeks on their pregnancy. 

Within 2 days of birth, these babies were tested if they recognized the story or not. Researchers measured the rate of sucking a nipple, while the mothers read aloud the story. It turns out when the same story was read to them, the rate went up, but when it was a different story the rate went down.

They preferred the familiar story, hinting that 3rd trimester fetuses can acquire some audible information in the womb. 

Some say that a baby is completely unconscious until birth, this study proves that they are aware of auditory details even in the womb. 

The question of when thoughts start rising in the brain, is still up to debate, although scientists have found that 5 month old babies have working memory, and have certain spikes in their brain waves when seeing a moving object. 

Their brain reactions were similar to that of an adult suggesting they may be capable of thought. 

SOURCE: Evolution of Consciousness by Euan M. Macphail and this article

TWINS WHO MAY SHARE CONSCIOUSNESS

(via sixpenceee)

malformalady:

A  baby in India born with a 12cm ‘tail’ has had it removed at just five days old. The as yet unnamed child was born with a heteropagus conjoined twin, where his sibling was anatomically incomplete and had formed as a tail on his back. He underwent a four-hour operation to remove the 350g growth.  Dr Rohit Joshi, chairman of the hospital where surgery took place, said: ‘Heteropagus conjoined twins are asymmetrically conjoined twins. [They] differ in several ways from symmetrical conjoined twins, as they have no major connection of vessels, bowels or bones.‘It is more commonly reported in India and Africa.’

malformalady:

A baby in India born with a 12cm ‘tail’ has had it removed at just five days old. The as yet unnamed child was born with a heteropagus conjoined twin, where his sibling was anatomically incomplete and had formed as a tail on his back. He underwent a four-hour operation to remove the 350g growth.  Dr Rohit Joshi, chairman of the hospital where surgery took place, said: ‘Heteropagus conjoined twins are asymmetrically conjoined twins. [They] differ in several ways from symmetrical conjoined twins, as they have no major connection of vessels, bowels or bones.‘It is more commonly reported in India and Africa.’

(via zygoma)

sixpenceee:

Have you ever wondered why an ice pack relieves pain? Why should cold make the pain go away? 
It works because a cold object activates fast fibers in your spinal cord, while pain travels up to your brain in slow fibers. So when you press a cold pack against a sore muscle your fast fibers beat out the slow ones. You feel cold not pain. 
Source: The Body Has A Mind Of Its Own by Sandra & Matthew Blackeslee

sixpenceee:

Have you ever wondered why an ice pack relieves pain? Why should cold make the pain go away? 

It works because a cold object activates fast fibers in your spinal cord, while pain travels up to your brain in slow fibers. So when you press a cold pack against a sore muscle your fast fibers beat out the slow ones. You feel cold not pain. 

Source: The Body Has A Mind Of Its Own by Sandra & Matthew Blackeslee

(via sixpenceee)

malformalady:

Diphylleia grayi also known as the skeleton flower’ has petals that turn transparent with the rain. Diphylleia grayi is native to moist wooded mountainsides in colder regions of China and Japan, where you’ll find the large fuzzy green, umbrella-like, bold foliage topped by small clusters of white, may apple-like flowers in late spring.

malformalady:

Diphylleia grayi also known as the skeleton flower’ has petals that turn transparent with the rain. Diphylleia grayi is native to moist wooded mountainsides in colder regions of China and Japan, where you’ll find the large fuzzy green, umbrella-like, bold foliage topped by small clusters of white, may apple-like flowers in late spring.

neuromorphogenesis:

Schizophrenia not a single disease but multiple genetically distinct disorders
About 80 percent of the risk for schizophrenia is known to be inherited, but scientists have struggled to identify specific genes for the condition. Now, in a novel approach analyzing genetic influences on more than 4,000 people with schizophrenia, the research team has identified distinct gene clusters that contribute to eight different classes of schizophrenia.
“Genes don’t operate by themselves,” said C. Robert Cloninger, MD, PhD, one of the study’s senior investigators. “They function in concert much like an orchestra, and to understand how they’re working, you have to know not just who the members of the orchestra are but how they interact.” Cloninger, the Wallace Renard Professor of Psychiatry and Genetics, and his colleagues matched precise DNA variations in people with and without schizophrenia to symptoms in individual patients. In all, the researchers analyzed nearly 700,000 sites within the genome where a single unit of DNA is changed, often referred to as a single nucleotide polymorphism (SNP). They looked at SNPs in 4,200 people with schizophrenia and 3,800 healthy controls, learning how individual genetic variations interacted with each other to produce the illness. 
In some patients with hallucinations or delusions, for example, the researchers matched distinct genetic features to patients’ symptoms, demonstrating that specific genetic variations interacted to create a 95 percent certainty of schizophrenia. In another group, they found that disorganized speech and behavior were specifically associated with a set of DNA variations that carried a 100 percent risk of schizophrenia.“What we’ve done here, after a decade of frustration in the field of psychiatric genetics, is identify the way genes interact with each other, how the ‘orchestra’ is either harmonious and leads to health, or disorganized in ways that lead to distinct classes of schizophrenia,” Cloninger said. 
Although individual genes have only weak and inconsistent associations with schizophrenia, groups of interacting gene clusters create an extremely high and consistent risk of illness, on the order of 70 to 100 percent. That makes it almost impossible for people with those genetic variations to avoid the condition. In all, the researchers identified 42 clusters of genetic variations that dramatically increased the risk of schizophrenia.
 “In the past, scientists had been looking for associations between individual genes and schizophrenia,” explained Dragan Svrakic, PhD, MD, a co-investigator and a professor of psychiatry at Washington University. “When one study would identify an association, no one else could replicate it. What was missing was the idea that these genes don’t act independently. They work in concert to disrupt the brain’s structure and function, and that results in the illness.”
Svrakic said it was only when the research team was able to organize the genetic variations and the patients’ symptoms into groups that they could see that particular clusters of DNA variations acted together to cause specific types of symptoms.
Then they divided patients according to the type and severity of their symptoms, such as different types of hallucinations or delusions, and other symptoms, such as lack of initiative, problems organizing thoughts or a lack of connection between emotions and thoughts. The results indicated that those symptom profiles describe eight qualitatively distinct disorders based on underlying genetic conditions. 
The investigators also replicated their findings in two additional DNA databases of people with schizophrenia, an indicator that identifying the gene variations that are working together is a valid avenue to explore for improving diagnosis and treatment. 
By identifying groups of genetic variations and matching them to symptoms in individual patients, it soon may be possible to target treatments to specific pathways that cause problems, according to co-investigator Igor Zwir, PhD, research associate in psychiatry at Washington University and associate professor in the Department of Computer Science and Artificial Intelligence at the University of Granada, Spain.
And Cloninger added it may be possible to use the same approach to better understand how genes work together to cause other common but complex disorders.
“People have been looking at genes to get a better handle on heart disease, hypertension and diabetes, and it’s been a real disappointment,” he said. “Most of the variability in the severity of disease has not been explained, but we were able to find that different sets of genetic variations were leading to distinct clinical syndromes. So I think this really could change the way people approach understanding the causes of complex diseases.”
neuromorphogenesis:

Schizophrenia not a single disease but multiple genetically distinct disorders
About 80 percent of the risk for schizophrenia is known to be inherited, but scientists have struggled to identify specific genes for the condition. Now, in a novel approach analyzing genetic influences on more than 4,000 people with schizophrenia, the research team has identified distinct gene clusters that contribute to eight different classes of schizophrenia.
“Genes don’t operate by themselves,” said C. Robert Cloninger, MD, PhD, one of the study’s senior investigators. “They function in concert much like an orchestra, and to understand how they’re working, you have to know not just who the members of the orchestra are but how they interact.” Cloninger, the Wallace Renard Professor of Psychiatry and Genetics, and his colleagues matched precise DNA variations in people with and without schizophrenia to symptoms in individual patients. In all, the researchers analyzed nearly 700,000 sites within the genome where a single unit of DNA is changed, often referred to as a single nucleotide polymorphism (SNP). They looked at SNPs in 4,200 people with schizophrenia and 3,800 healthy controls, learning how individual genetic variations interacted with each other to produce the illness. 
In some patients with hallucinations or delusions, for example, the researchers matched distinct genetic features to patients’ symptoms, demonstrating that specific genetic variations interacted to create a 95 percent certainty of schizophrenia. In another group, they found that disorganized speech and behavior were specifically associated with a set of DNA variations that carried a 100 percent risk of schizophrenia.“What we’ve done here, after a decade of frustration in the field of psychiatric genetics, is identify the way genes interact with each other, how the ‘orchestra’ is either harmonious and leads to health, or disorganized in ways that lead to distinct classes of schizophrenia,” Cloninger said. 
Although individual genes have only weak and inconsistent associations with schizophrenia, groups of interacting gene clusters create an extremely high and consistent risk of illness, on the order of 70 to 100 percent. That makes it almost impossible for people with those genetic variations to avoid the condition. In all, the researchers identified 42 clusters of genetic variations that dramatically increased the risk of schizophrenia.
 “In the past, scientists had been looking for associations between individual genes and schizophrenia,” explained Dragan Svrakic, PhD, MD, a co-investigator and a professor of psychiatry at Washington University. “When one study would identify an association, no one else could replicate it. What was missing was the idea that these genes don’t act independently. They work in concert to disrupt the brain’s structure and function, and that results in the illness.”
Svrakic said it was only when the research team was able to organize the genetic variations and the patients’ symptoms into groups that they could see that particular clusters of DNA variations acted together to cause specific types of symptoms.
Then they divided patients according to the type and severity of their symptoms, such as different types of hallucinations or delusions, and other symptoms, such as lack of initiative, problems organizing thoughts or a lack of connection between emotions and thoughts. The results indicated that those symptom profiles describe eight qualitatively distinct disorders based on underlying genetic conditions. 
The investigators also replicated their findings in two additional DNA databases of people with schizophrenia, an indicator that identifying the gene variations that are working together is a valid avenue to explore for improving diagnosis and treatment. 
By identifying groups of genetic variations and matching them to symptoms in individual patients, it soon may be possible to target treatments to specific pathways that cause problems, according to co-investigator Igor Zwir, PhD, research associate in psychiatry at Washington University and associate professor in the Department of Computer Science and Artificial Intelligence at the University of Granada, Spain.
And Cloninger added it may be possible to use the same approach to better understand how genes work together to cause other common but complex disorders.
“People have been looking at genes to get a better handle on heart disease, hypertension and diabetes, and it’s been a real disappointment,” he said. “Most of the variability in the severity of disease has not been explained, but we were able to find that different sets of genetic variations were leading to distinct clinical syndromes. So I think this really could change the way people approach understanding the causes of complex diseases.”
neuromorphogenesis:

Can your blood type affect your memory?
People with blood type AB may be more likely to develop memory loss in later years than people with other blood types, according to a study published in the September 10, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. 
AB is the least common blood type, found in about 4 percent of the U.S. population. The study found that people with AB blood were 82 percent more likely to develop the thinking and memory problems that can lead to dementia than people with other blood types. Previous studies have shown that people with type O blood have a lower risk of heart disease and stroke, factors that can increase the risk of memory loss and dementia.
The study was part of a larger study (the REasons for Geographic And Racial Differences in Stroke, or REGARDS Study) of more than 30,000 people followed for an average of 3.4 years. In those who had no memory or thinking problems at the beginning, the study identified 495 participants who developed thinking and memory problems, or cognitive impairment, during the study. They were compared to 587 people with no cognitive problems.
People with AB blood type made up 6 percent of the group who developed cognitive impairment, which is higher than the 4 percent found in the population.
"Our study looks at blood type and risk of cognitive impairment, but several studies have shown that factors such as high blood pressure, high cholesterol and diabetes increase the risk of cognitive impairment and dementia," said study author Mary Cushman, MD, MSc, of the University of Vermont College of Medicine in Burlington. "Blood type is also related to other vascular conditions like stroke, so the findings highlight the connections between vascular issues and brain health. More research is needed to confirm these results."
Researchers also looked at blood levels of factor VIII, a protein that helps blood to clot. High levels of factor VIII are related to higher risk of cognitive impairment and dementia. People in this study with higher levels of factor VIII were 24 percent more likely to develop thinking and memory problems than people with lower levels of the protein. People with AB blood had a higher average level of factor VIII than people with other blood types. neuromorphogenesis:

Can your blood type affect your memory?
People with blood type AB may be more likely to develop memory loss in later years than people with other blood types, according to a study published in the September 10, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. 
AB is the least common blood type, found in about 4 percent of the U.S. population. The study found that people with AB blood were 82 percent more likely to develop the thinking and memory problems that can lead to dementia than people with other blood types. Previous studies have shown that people with type O blood have a lower risk of heart disease and stroke, factors that can increase the risk of memory loss and dementia.
The study was part of a larger study (the REasons for Geographic And Racial Differences in Stroke, or REGARDS Study) of more than 30,000 people followed for an average of 3.4 years. In those who had no memory or thinking problems at the beginning, the study identified 495 participants who developed thinking and memory problems, or cognitive impairment, during the study. They were compared to 587 people with no cognitive problems.
People with AB blood type made up 6 percent of the group who developed cognitive impairment, which is higher than the 4 percent found in the population.
"Our study looks at blood type and risk of cognitive impairment, but several studies have shown that factors such as high blood pressure, high cholesterol and diabetes increase the risk of cognitive impairment and dementia," said study author Mary Cushman, MD, MSc, of the University of Vermont College of Medicine in Burlington. "Blood type is also related to other vascular conditions like stroke, so the findings highlight the connections between vascular issues and brain health. More research is needed to confirm these results."
Researchers also looked at blood levels of factor VIII, a protein that helps blood to clot. High levels of factor VIII are related to higher risk of cognitive impairment and dementia. People in this study with higher levels of factor VIII were 24 percent more likely to develop thinking and memory problems than people with lower levels of the protein. People with AB blood had a higher average level of factor VIII than people with other blood types.