Neuroscience

Articles and news from the latest research reports.

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Why Music Moves Us
Universal emotions like anger, sadness and happiness are expressed nearly the same in both music and movement across cultures, according to new research.
The researchers found that when Dartmouth undergraduates and members of a remote Cambodian hill tribe were asked to use sliding bars to adjust traits such as the speed, pitch, or regularity of music, they used the same types of characteristics to express primal emotions. What’s more, the same types of patterns were used to express the same emotions in animations of movement in both cultures.
"The kinds of dynamics you find in movement, you find also in music and they’re used in the same way to provide the same kind of meaning," said study co-author Thalia Wheatley, a neuroscientist at Dartmouth University.
The findings suggest music’s intense power may lie in the fact it is processed by ancient brain circuitry used to read emotion in our movement.
"The study suggests why music is so fundamental and engaging for us," said Jonathan Schooler, a professor of brain and psychological sciences at the University of California at Santa Barbara, who was not involved in the study. "It takes advantage of some very, very basic and, in some sense, primitive systems that understand how motion relates to emotion."
Universal emotions
Why people love music has been an enduring mystery. Scientists have found that animals like different music than humans and that brain regions stimulated by food, sex and love also light up when we listen to music. Musicians even read emotions better than nonmusicians.
Past studies showed that the same brain areas were activated when people read emotion in both music and movement. That made Wheatley wonder how the two were connected.
To find out, Wheatley and her colleagues asked 50 Dartmouth undergraduates to manipulate five slider bars to change characteristics of an animated bouncy ball to make it look happy, sad, angry, peaceful or scared.
"We just say ‘Make Mr. Ball look angry or make Mr. Ball look happy,’" she told LiveScience.
To create different emotions in “Mr. Ball,” the students could use the slider bars to affect how often the ball bounced, how often it made big bounces, whether it went up or down more often and how smoothly it moved.
Another 50 students could use similar slider bars to adjust the pitch trajectory, tempo, consonance (repetition), musical jumps and jitteriness of music to capture those same emotions.
The students tended to put the slider bars in roughly the same positions whether they were creating angry music or angry moving balls.
To see if these trends held across cultures, Wheatley’s team traveled to the remote highlands of Cambodia and asked about 85 members of the Kreung tribe to perform the same task. Kreung music sounds radically different from Western music, with gongs and an instrument called a mem that sounds a bit like an insect buzzing, Wheatley said. None of the tribes’ people had any exposure to Western music or media, she added.
Interestingly, the Kreung tended to put the slider bars in roughly the same positions as Americans did to capture different emotions, and the position of the sliders was very similar for both music and emotions.
The findings suggest that music taps into the brain networks and regions that we use to understand emotion in people’s movements. That may explain why music has such power to move us — it’s activating deep-seated brain regions that are used to process emotion, Wheatley said.
"Emotion is the same thing no matter whether it’s coming in through our eyes or ears," she said.

Why Music Moves Us

Universal emotions like anger, sadness and happiness are expressed nearly the same in both music and movement across cultures, according to new research.

The researchers found that when Dartmouth undergraduates and members of a remote Cambodian hill tribe were asked to use sliding bars to adjust traits such as the speed, pitch, or regularity of music, they used the same types of characteristics to express primal emotions. What’s more, the same types of patterns were used to express the same emotions in animations of movement in both cultures.

"The kinds of dynamics you find in movement, you find also in music and they’re used in the same way to provide the same kind of meaning," said study co-author Thalia Wheatley, a neuroscientist at Dartmouth University.

The findings suggest music’s intense power may lie in the fact it is processed by ancient brain circuitry used to read emotion in our movement.

"The study suggests why music is so fundamental and engaging for us," said Jonathan Schooler, a professor of brain and psychological sciences at the University of California at Santa Barbara, who was not involved in the study. "It takes advantage of some very, very basic and, in some sense, primitive systems that understand how motion relates to emotion."

Universal emotions

Why people love music has been an enduring mystery. Scientists have found that animals like different music than humans and that brain regions stimulated by food, sex and love also light up when we listen to music. Musicians even read emotions better than nonmusicians.

Past studies showed that the same brain areas were activated when people read emotion in both music and movement. That made Wheatley wonder how the two were connected.

To find out, Wheatley and her colleagues asked 50 Dartmouth undergraduates to manipulate five slider bars to change characteristics of an animated bouncy ball to make it look happy, sad, angry, peaceful or scared.

"We just say ‘Make Mr. Ball look angry or make Mr. Ball look happy,’" she told LiveScience.

To create different emotions in “Mr. Ball,” the students could use the slider bars to affect how often the ball bounced, how often it made big bounces, whether it went up or down more often and how smoothly it moved.

Another 50 students could use similar slider bars to adjust the pitch trajectory, tempo, consonance (repetition), musical jumps and jitteriness of music to capture those same emotions.

The students tended to put the slider bars in roughly the same positions whether they were creating angry music or angry moving balls.

To see if these trends held across cultures, Wheatley’s team traveled to the remote highlands of Cambodia and asked about 85 members of the Kreung tribe to perform the same task. Kreung music sounds radically different from Western music, with gongs and an instrument called a mem that sounds a bit like an insect buzzing, Wheatley said. None of the tribes’ people had any exposure to Western music or media, she added.

Interestingly, the Kreung tended to put the slider bars in roughly the same positions as Americans did to capture different emotions, and the position of the sliders was very similar for both music and emotions.

The findings suggest that music taps into the brain networks and regions that we use to understand emotion in people’s movements. That may explain why music has such power to move us — it’s activating deep-seated brain regions that are used to process emotion, Wheatley said.

"Emotion is the same thing no matter whether it’s coming in through our eyes or ears," she said.

Filed under music universal emotional expressions movement emotions cross-cultural neuroscience science

75 notes

Hypertension traced to source in brain
When the heart works too hard, the brain may be to blame, says new Cornell research that is changing how scientists look at high blood pressure (hypertension). The study, published in the Journal of Clinical Investigation in November, traces hypertension to a newfound cellular source in the brain and shows that treatments targeting this area can reverse the disease.
In what peer reviewers are calling “a new paradigm” for tackling the worldwide hypertension epidemic, this insight into its roots could give hope to the billion people it currently afflicts. Hypertension occurs when the force of blood against vessel walls grows strong enough to potentially cause such problems as heart attack, stroke and heart or kidney disease. The heart pumps harder, and often the hormone angiotensin-II (AngII) gets the pressure cooking by triggering nerve cells that constrict blood vessels.
"We knew the central nervous system orchestrates this process, and now we’ve found the conductor," said Robin Davisson, the Andrew Dickson White Professor of Molecular Physiology with a joint appointment at Cornell’s College of Veterinary Medicine and Weill Cornell Medical College.
Two-thirds of Americans have hypertension, which is the leading cause of North America’s No. 1 killer: heart disease, according to the Centers for Disease Control and Prevention.
Davisson’s lab traced neurochemical signals back to endoplasmic reticulum (ER), the protein factory and stress-management control center in every cell. If something goes wrong in a cell, the ER activates processes to adapt to the stress. Long-term ER stress can cause chronic disease, and several stressors that ER responds to have been connected to hypertension. Davisson’s lab found that high levels of AngII put stress on the ER, which responds by triggering the cascade of neural and hormonal signals that start hypertension.
But not just any cell’s ER can conduct this complex orchestra. Those that can trigger the signal cascade are clustered near the bottom of the brain in a gatelike structure called the subfornical organ (SFO). Unlike most of the brain, the SFO hangs outside a protective barrier that keeps most circulating particles from entering the brain. The SFO can interact with particles like AngII that are too big to cross through and can also communicate with the brain’s inner chambers.
This is good news for developing therapies—because the SFO sits outside the barrier, it can be reached through such normal treatment routes as pills or injections rather than riskier brain procedures. Davisson’s lab showed that treatments that inhibit ER stress in the SFO can completely stop AngII-based hypertension and lower blood pressure to normal levels.
"Our work provides the first evidence that higher levels of AngII cause ER stress in the SFO, that this causes hypertension, and that we can do something about it," said Davisson. "This finding may also suggest a role for ER stress in hypertension types that don’t involve AngII, like some spontaneous or genetic forms."
Inspired by the paradigm shift that this study has sparked, the editors of the Journal of Clinical Investigation published a commentary concluding that this discovery “opens new avenues for investigation and may lead to new therapeutic approaches for this disease.”

Hypertension traced to source in brain

When the heart works too hard, the brain may be to blame, says new Cornell research that is changing how scientists look at high blood pressure (hypertension). The study, published in the Journal of Clinical Investigation in November, traces hypertension to a newfound cellular source in the brain and shows that treatments targeting this area can reverse the disease.

In what peer reviewers are calling “a new paradigm” for tackling the worldwide hypertension epidemic, this insight into its roots could give hope to the billion people it currently afflicts. Hypertension occurs when the force of blood against vessel walls grows strong enough to potentially cause such problems as heart attack, stroke and heart or kidney disease. The heart pumps harder, and often the hormone angiotensin-II (AngII) gets the pressure cooking by triggering nerve cells that constrict blood vessels.

"We knew the central nervous system orchestrates this process, and now we’ve found the conductor," said Robin Davisson, the Andrew Dickson White Professor of Molecular Physiology with a joint appointment at Cornell’s College of Veterinary Medicine and Weill Cornell Medical College.

Two-thirds of Americans have hypertension, which is the leading cause of North America’s No. 1 killer: heart disease, according to the Centers for Disease Control and Prevention.

Davisson’s lab traced neurochemical signals back to endoplasmic reticulum (ER), the protein factory and stress-management control center in every cell. If something goes wrong in a cell, the ER activates processes to adapt to the stress. Long-term ER stress can cause chronic disease, and several stressors that ER responds to have been connected to hypertension. Davisson’s lab found that high levels of AngII put stress on the ER, which responds by triggering the cascade of neural and hormonal signals that start hypertension.

But not just any cell’s ER can conduct this complex orchestra. Those that can trigger the signal cascade are clustered near the bottom of the brain in a gatelike structure called the subfornical organ (SFO). Unlike most of the brain, the SFO hangs outside a protective barrier that keeps most circulating particles from entering the brain. The SFO can interact with particles like AngII that are too big to cross through and can also communicate with the brain’s inner chambers.

This is good news for developing therapies—because the SFO sits outside the barrier, it can be reached through such normal treatment routes as pills or injections rather than riskier brain procedures. Davisson’s lab showed that treatments that inhibit ER stress in the SFO can completely stop AngII-based hypertension and lower blood pressure to normal levels.

"Our work provides the first evidence that higher levels of AngII cause ER stress in the SFO, that this causes hypertension, and that we can do something about it," said Davisson. "This finding may also suggest a role for ER stress in hypertension types that don’t involve AngII, like some spontaneous or genetic forms."

Inspired by the paradigm shift that this study has sparked, the editors of the Journal of Clinical Investigation published a commentary concluding that this discovery “opens new avenues for investigation and may lead to new therapeutic approaches for this disease.”

Filed under brain hypertension nerve cells CNS heart science

69 notes

Brain imaging identifies bipolar risk
Researchers from the Black Dog Institute and University of NSW have used brain imaging technology to show that young people with a known genetic risk of bipolar but no clinical signs of the condition have clear and quantifiable differences in brain activity when compared to controls.
“We found that the young people who had a parent or sibling with bipolar disorder had reduced brain responses to emotive faces, particularly a fearful face. This is an extremely promising breakthrough,” says study leader Professor Philip Mitchell.
Affecting around 1 in 75 Australians, bipolar disorder involves extreme and often unpredictable fluctuations in mood. The mood swings and associated behaviours such as disinhibited behaviour, aggression and severe depression, have a significant impact on day-to-day life, careers and relationships. Bipolar has the highest suicide rate of all psychiatric disorders.
“We know that bipolar is primarily a biological illness with a strong genetic influence but triggers are yet to be understood. Being able to identify young people at risk will enable implementation of early intervention programs, giving them the best chance for a long and happy life,” says Prof Mitchell.
Researchers used functional MRI to visualise brain activity when participants were shown pictures of happy, fearful or calm (neutral) human faces. Results showed that those with a genetic risk of bipolar displayed significantly reduced brain activity in a specific part of the brain known to regulate emotional responses.
“Our results show that bipolar disorder may be linked to a dysfunction in emotional regulation and this is something we will continue to explore,” Professor Mitchell said.
“And we now have an extremely promising method of identifying children and young people at risk of bipolar disorder.”
 “We expect that early identification will significantly improve outcomes for people that go on to develop bipolar disorder, and possibly even prevent onset in some people.”
Results are published this week in Biological Psychiatry and come from the NHMRC-funded ‘Kids and Sibs study’, the biggest research study in the world focusing on genetic and environmental aspects of bipolar disorder. Based at the Black Dog Institute, the trial is still recruiting.

Brain imaging identifies bipolar risk

Researchers from the Black Dog Institute and University of NSW have used brain imaging technology to show that young people with a known genetic risk of bipolar but no clinical signs of the condition have clear and quantifiable differences in brain activity when compared to controls.

“We found that the young people who had a parent or sibling with bipolar disorder had reduced brain responses to emotive faces, particularly a fearful face. This is an extremely promising breakthrough,” says study leader Professor Philip Mitchell.

Affecting around 1 in 75 Australians, bipolar disorder involves extreme and often unpredictable fluctuations in mood. The mood swings and associated behaviours such as disinhibited behaviour, aggression and severe depression, have a significant impact on day-to-day life, careers and relationships. Bipolar has the highest suicide rate of all psychiatric disorders.

“We know that bipolar is primarily a biological illness with a strong genetic influence but triggers are yet to be understood. Being able to identify young people at risk will enable implementation of early intervention programs, giving them the best chance for a long and happy life,” says Prof Mitchell.

Researchers used functional MRI to visualise brain activity when participants were shown pictures of happy, fearful or calm (neutral) human faces. Results showed that those with a genetic risk of bipolar displayed significantly reduced brain activity in a specific part of the brain known to regulate emotional responses.

“Our results show that bipolar disorder may be linked to a dysfunction in emotional regulation and this is something we will continue to explore,” Professor Mitchell said.

“And we now have an extremely promising method of identifying children and young people at risk of bipolar disorder.”

 “We expect that early identification will significantly improve outcomes for people that go on to develop bipolar disorder, and possibly even prevent onset in some people.”

Results are published this week in Biological Psychiatry and come from the NHMRC-funded ‘Kids and Sibs study’, the biggest research study in the world focusing on genetic and environmental aspects of bipolar disorder. Based at the Black Dog Institute, the trial is still recruiting.

Filed under brain brain imaging bipolar disorder brain activity emotional response neuroscience science

159 notes

Hybrid tunnel may help guide severed nerves back to health
Building a tunnel made up of both hard and soft materials to guide the reconnection of severed nerve endings may be the first step toward helping patients who have suffered extensive nerve trauma regain feeling and movement, according to a team of biomedical engineers.
"Nerve injury in both central nervous system and peripheral nervous system is a major health problem," said Mohammad Reza Abidian, assistant professor of biomedical engineering, Penn State. "According to the National Spinal Cord Injury Statistical Center, there are approximately 290,000 individuals in the US who suffer from spinal cord injuries with about 12,000 new injuries occurring each year."
Spontaneous nerve regeneration is limited to small lesions within the injured peripheral nerve system and is actively suppressed within central nervous system. When a nerve in the peripheral nervous system is cut slightly, nerve endings can regenerate and reconnect. However, if the distance between the two endings is too far, the growth can go off course and fail to connect.
The researchers, who published their results in the current issue of Advanced Healthcare Materials, developed a novel hybrid conduit that consisted of a soft material, called a hydrogel, as an external wall along with an internal wall made of an electrically-active conducting polymer to serve as a tunnel that guides the regrowth and reconnection of the severed nerve endings.
Abidian said that the method could offer advantages over current surgeries that are used to reconnect severed nerves.
"Autografts are currently the gold standard for bridging nerve gaps," said Abidian. "This is an operation that takes the nerve from another portion of the body — for instance — from a tendon, and then it is grafted onto the injured nerve."
However, the operation can be painful and there are often mismatches in size between the severed nerve endings and the new grafted portion of the nerve, Abidian said.

Hybrid tunnel may help guide severed nerves back to health

Building a tunnel made up of both hard and soft materials to guide the reconnection of severed nerve endings may be the first step toward helping patients who have suffered extensive nerve trauma regain feeling and movement, according to a team of biomedical engineers.

"Nerve injury in both central nervous system and peripheral nervous system is a major health problem," said Mohammad Reza Abidian, assistant professor of biomedical engineering, Penn State. "According to the National Spinal Cord Injury Statistical Center, there are approximately 290,000 individuals in the US who suffer from spinal cord injuries with about 12,000 new injuries occurring each year."

Spontaneous nerve regeneration is limited to small lesions within the injured peripheral nerve system and is actively suppressed within central nervous system. When a nerve in the peripheral nervous system is cut slightly, nerve endings can regenerate and reconnect. However, if the distance between the two endings is too far, the growth can go off course and fail to connect.

The researchers, who published their results in the current issue of Advanced Healthcare Materials, developed a novel hybrid conduit that consisted of a soft material, called a hydrogel, as an external wall along with an internal wall made of an electrically-active conducting polymer to serve as a tunnel that guides the regrowth and reconnection of the severed nerve endings.

Abidian said that the method could offer advantages over current surgeries that are used to reconnect severed nerves.

"Autografts are currently the gold standard for bridging nerve gaps," said Abidian. "This is an operation that takes the nerve from another portion of the body — for instance — from a tendon, and then it is grafted onto the injured nerve."

However, the operation can be painful and there are often mismatches in size between the severed nerve endings and the new grafted portion of the nerve, Abidian said.

Filed under nerve transplant nerve injury spinal cord injury regeneration hybrid conduit PEDOT medicine science

57 notes

New immune therapy successfully treats brain tumors in mice
Using an artificial protein that stimulates the body’s natural immune system to fight cancer, a research team at Duke Medicine has engineered a lethal weapon that kills brain tumors in mice while sparing other tissue. If it can be shown to work in humans, it would overcome a major obstacle that has hampered the effectiveness of immune-based therapies.
The protein is manufactured with two arms – one that exclusively binds to tumor cells and another that snags the body’s fighter T-cells, spurring an attack on the tumor. In six out of eight mice with brain tumors, the treatment resulted in cures, according to findings published Dec. 17, 2012, in the Proceedings of the National Academy of Sciences.
"This work represents a revival of a somewhat old concept that targeting cancer with tumor-specific antigens may well be the most effective way to treat cancer without toxicity," said senior author John H. Sampson, M.D., PhD, a neurosurgeon at The Preston Robert Tisch Brain Tumor Center at Duke. "But there have been problems with that approach, especially for brain tumors. Our therapeutic agent is exciting, because it acts like Velcro to bind T-cells to tumor cells and induces them to kill without any negative effects on surrounding normal tissues."
Sampson and colleagues focused on the immune approach in brain tumors, which are notoriously difficult to treat. Despite surgery, radiation and chemotherapy, glioblastomas are universally fatal, with a median survival of 15 months.
Immunotherapies, in which the body’s B-cells and T-cells are triggered to attack tumors, have shown promise in treating brain and other cancers, but have been problematic in clinical use. Treatments have been difficult to administer at therapeutic doses, or have spurred side effects in which the immune system also attacks healthy tissue and organs.
Working to overcome those pitfalls, the Duke-led researchers designed a kind of connector - an artificial protein called a bispecific T-cell engager, or BiTE – that tethers the tumor to its killer. Their newly engineered protein includes fractions of two separate antibodies, one that recruits and engages the body’s fighter T-cells and one that expressly homes in on an antigen known as EGFRvIII, which only occurs in cancers.
Once connected via the new bispecific antibody, the T-cells recognize the tumor as an invader, and mount an attack. Normal tissue, which does not carry the tumor antigen, is left unscathed.

New immune therapy successfully treats brain tumors in mice

Using an artificial protein that stimulates the body’s natural immune system to fight cancer, a research team at Duke Medicine has engineered a lethal weapon that kills brain tumors in mice while sparing other tissue. If it can be shown to work in humans, it would overcome a major obstacle that has hampered the effectiveness of immune-based therapies.

The protein is manufactured with two arms – one that exclusively binds to tumor cells and another that snags the body’s fighter T-cells, spurring an attack on the tumor. In six out of eight mice with brain tumors, the treatment resulted in cures, according to findings published Dec. 17, 2012, in the Proceedings of the National Academy of Sciences.

"This work represents a revival of a somewhat old concept that targeting cancer with tumor-specific antigens may well be the most effective way to treat cancer without toxicity," said senior author John H. Sampson, M.D., PhD, a neurosurgeon at The Preston Robert Tisch Brain Tumor Center at Duke. "But there have been problems with that approach, especially for brain tumors. Our therapeutic agent is exciting, because it acts like Velcro to bind T-cells to tumor cells and induces them to kill without any negative effects on surrounding normal tissues."

Sampson and colleagues focused on the immune approach in brain tumors, which are notoriously difficult to treat. Despite surgery, radiation and chemotherapy, glioblastomas are universally fatal, with a median survival of 15 months.

Immunotherapies, in which the body’s B-cells and T-cells are triggered to attack tumors, have shown promise in treating brain and other cancers, but have been problematic in clinical use. Treatments have been difficult to administer at therapeutic doses, or have spurred side effects in which the immune system also attacks healthy tissue and organs.

Working to overcome those pitfalls, the Duke-led researchers designed a kind of connector - an artificial protein called a bispecific T-cell engager, or BiTE – that tethers the tumor to its killer. Their newly engineered protein includes fractions of two separate antibodies, one that recruits and engages the body’s fighter T-cells and one that expressly homes in on an antigen known as EGFRvIII, which only occurs in cancers.

Once connected via the new bispecific antibody, the T-cells recognize the tumor as an invader, and mount an attack. Normal tissue, which does not carry the tumor antigen, is left unscathed.

Filed under brain tumors protein cancer immunotherapies immune system medicine science

103 notes

Neurons die in Alzheimer’s because of faulty cell cycle control before plaques and tangles appear

The two infamous proteins, amyloid-beta (Aβ) and tau, that characterize advanced Alzheimer’s disease (AD), start healthy neurons on the road to cell death long before the appearance of the deadly plaques and tangles by working together to reactivate the supposedly blocked cell cycle in brain cells, according to research presented on Dec. 17 at the American Society for Cell Biology’s Annual Meeting in San Francisco.

Working in a mouse model of AD, George Bloom, PhD, of the University of Virginia (UVA) reports that neurons in AD start dying because they break the first law of human neuronal safety ⎯ stay out of the cell cycle.

Most normal adult neurons are permanently postmitotic; that is, they have finished dividing and are locked out of the cell cycle. In contrast, AD neurons frequently re-enter the cell cycle but fail to complete mitosis, and ultimately die. By considering this novel perspective on AD as a problem of the cell cycle, Dr. Bloom and colleagues at UVA and at the University of Alabama, Birmingham, have discovered what they call an “ironic pathway” to neuronal cell death. The process requires the coordinated action of both Aβ and tau, which are the building blocks of plaques and tangles, respectively. Dr. Bloom’s results show just how toxic the two proteins can be even when free in solution and not aggregated into plaques and tangles.

Using mouse neurons grown in culture, the UVA researchers found that Aβ oligomers, which are small aggregates of just a few Aβ molecules each, induce the neurons to re-enter the cell cycle. Interestingly, the neurons must make and accumulate tau in order for this cell cycle re-entry to occur. The mechanism for this misplaced re-entry into the cell cycle requires that Aβ oligomers activate multiple protein kinase enzymes, each of which must then attach a phosphate to a specific site on the tau protein.

Following up on the cell culture results, Dr. Bloom and colleagues confirmed that Aβ-induced, tau-dependent cell cycle re-entry occurs in the brains of mice that were genetically engineered to mimic brains with human AD. The mouse brains were found to accumulate massive numbers of neurons that had transitioned from a permanent cell cycle stop, known as G0 (G zero), to G1, the first stage of the cell cycle, by the time they were 6 months old. Remarkably, otherwise identical mice that lacked functional tau genes showed no sign of cell cycle re-entry, confirming the cell culture results.

Neuronal cell cycle re-entry, a key step in the development of AD, can therefore be caused by signaling from Aβ through tau. Thus, Aβ and tau co-conspire to trigger seminal events in AD pathogenesis independently of their incorporation into plaques and tangles. Most important, Dr. Bloom believes that the activated protein kinases and phosphorylated forms of tau identified in this study represent potential targets for early diagnosis and treatment of AD.

(Source: eurekalert.org)

Filed under alzheimer’s disease proteins amyloid-beta tau brain cells neuron science

1,036 notes

New form of cell division found
Researchers at the University of Wisconsin Carbone Cancer Center have discovered a new form of cell division in human cells.
They believe it serves as a natural back-up mechanism during faulty cell division, preventing some cells from going down a path that can lead to cancer.
"If we could promote this new form of cell division, which we call klerokinesis, we may be able to prevent some cancers from developing," says lead researcher Dr. Mark Burkard, an assistant professor of hematology-oncology in the department of medicine at the UW School of Medicine and Public Health.
Burkard presented the finding on Monday, Dec. 17 at the annual meeting of the American Society for Cell Biology in San Francisco.
(View a short video of the process here)

New form of cell division found

Researchers at the University of Wisconsin Carbone Cancer Center have discovered a new form of cell division in human cells.

They believe it serves as a natural back-up mechanism during faulty cell division, preventing some cells from going down a path that can lead to cancer.

"If we could promote this new form of cell division, which we call klerokinesis, we may be able to prevent some cancers from developing," says lead researcher Dr. Mark Burkard, an assistant professor of hematology-oncology in the department of medicine at the UW School of Medicine and Public Health.

Burkard presented the finding on Monday, Dec. 17 at the annual meeting of the American Society for Cell Biology in San Francisco.

(View a short video of the process here)

Filed under cancer cell division klerokinesis cytokinesis biology science

254 notes

ucsdhealthsciences:



A hierarchical ontology of genes, cellular components and processes derived from large genomic datasets.
Toward a New Model of the CellEverything You Always Wanted to Know About GenesTurning vast amounts of genomic data into meaningful information about the cell is the great challenge of bioinformatics, with major implications for human biology and medicine. Researchers at the University of California, San Diego School of Medicine and colleagues have proposed a new method that creates a computational model of the cell from large networks of gene and protein interactions, discovering how genes and proteins connect to form higher-level cellular machinery.The findings are published in the December 16 advance online publication of Nature Biotechnology.“Our method creates ontology, or a specification of all the major players in the cell and the relationships between them,” said first author Janusz Dutkowski, PhD, postdoctoral researcher in the UC San Diego Department of Medicine. It uses knowledge about how genes and proteins interact with each other and automatically organizes this information to form a comprehensive catalog of gene functions, cellular components, and processes.“What’s new about our ontology is that it is created automatically from large datasets. In this way, we see not only what is already known, but also potentially new biological components and processes – the bases for new hypotheses,” said Dutkowski.Originally devised by philosophers attempting to explain the nature of existence, ontologies are now broadly used to encapsulate everything known about a subject in a hierarchy of terms and relationships. Intelligent information systems, such as iPhone’s Siri, are built on ontologies to enable reasoning about the real world. Ontologies are also used by scientists to structure knowledge about subjects like taxonomy, anatomy and development, bioactive compounds, disease and clinical diagnosis.A Gene Ontology (GO) exists as well, constructed over the last decade through a joint effort of hundreds of scientists. It is considered the gold standard for understanding cell structure and gene function, containing 34,765 terms and 64,635 hierarchical relations annotating genes from more than 80 species.“GO is very influential in biology and bioinformatics, but it is also incomplete and hard to update based on new data,” said senior author Trey Ideker, PhD, chief of the Division of Genetics in the School of Medicine and professor of bioengineering in UC San Diego’s Jacobs School of Engineering. “This is expert knowledge based upon the work of many people over many, many years,” said Ideker, who is also principal investigator of the National Resource for Network Biology, based at UC San Diego. “A fundamental problem is consistency. People do things in different ways, and that impacts what findings are incorporated into GO and how they relate to other findings. The approach we have proposed is a more objective way to determine what’s known and uncover what’s new.”
Read more

ucsdhealthsciences:

A hierarchical ontology of genes, cellular components and processes derived from large genomic datasets.

Toward a New Model of the Cell
Everything You Always Wanted to Know About Genes

Turning vast amounts of genomic data into meaningful information about the cell is the great challenge of bioinformatics, with major implications for human biology and medicine. Researchers at the University of California, San Diego School of Medicine and colleagues have proposed a new method that creates a computational model of the cell from large networks of gene and protein interactions, discovering how genes and proteins connect to form higher-level cellular machinery.

The findings are published in the December 16 advance online publication of Nature Biotechnology.

“Our method creates ontology, or a specification of all the major players in the cell and the relationships between them,” said first author Janusz Dutkowski, PhD, postdoctoral researcher in the UC San Diego Department of Medicine. It uses knowledge about how genes and proteins interact with each other and automatically organizes this information to form a comprehensive catalog of gene functions, cellular components, and processes.

“What’s new about our ontology is that it is created automatically from large datasets. In this way, we see not only what is already known, but also potentially new biological components and processes – the bases for new hypotheses,” said Dutkowski.

Originally devised by philosophers attempting to explain the nature of existence, ontologies are now broadly used to encapsulate everything known about a subject in a hierarchy of terms and relationships. Intelligent information systems, such as iPhone’s Siri, are built on ontologies to enable reasoning about the real world. Ontologies are also used by scientists to structure knowledge about subjects like taxonomy, anatomy and development, bioactive compounds, disease and clinical diagnosis.

A Gene Ontology (GO) exists as well, constructed over the last decade through a joint effort of hundreds of scientists. It is considered the gold standard for understanding cell structure and gene function, containing 34,765 terms and 64,635 hierarchical relations annotating genes from more than 80 species.

“GO is very influential in biology and bioinformatics, but it is also incomplete and hard to update based on new data,” said senior author Trey Ideker, PhD, chief of the Division of Genetics in the School of Medicine and professor of bioengineering in UC San Diego’s Jacobs School of Engineering.

“This is expert knowledge based upon the work of many people over many, many years,” said Ideker, who is also principal investigator of the National Resource for Network Biology, based at UC San Diego. “A fundamental problem is consistency. People do things in different ways, and that impacts what findings are incorporated into GO and how they relate to other findings. The approach we have proposed is a more objective way to determine what’s known and uncover what’s new.”

Read more

81 notes

They came from the sea: the gene behind limb evolution

image

In the late Devonian period, roughly 365 million years ago, fish-like creatures started venturing from shallow waters onto land.

Among the various adaptations associated with the switch to land life was the conversion of fins into limbs. This transition allowed animals to both navigate aquatic habitats and walk on land.

We already know that fins and limbs share the same genetic program for their induction and early development. But due to their divergent morphological traits (form and structure), it was unknown how a fin could evolve into a limb.

But now, a paper published in the journal Developmental Cell by Renata Freitas and colleagues from the University of Andalusia (Seville, Spain), suggests the key to fin-to-limb transition lies in the regulation of the homeotic (responsible for the formation of body parts) gene hoxd13.

(Source: theconversation.edu.au)

Read more …

Filed under evolution limb development genetics hoxd13 autopod zebrafish science

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European Project Aims To Create 1,500 New Stem Cell Lines
A joint public-private collaboration between the European Union and Europe’s pharmaceutical industry, called the StemBANCC project, will spend nearly 50 million euros to create 1,500 pluripotent stem cell lines. But the initiative’s goal isn’t to find a stem cell-based cure for diabetes or Alzheimer’s disease. They hope instead that their stem cell lines will prove to be faster and more effective drug screens in the search for drugs to fight these and other conditions.
A frustrating problem in medical research is the inadequacy of animal models. All too often a treatment works great in laboratory rats or mice but then its efficacy fails to repeat in human trials. But researchers are beginning to capitalize on the potential of stem cells – not as cures, but as means to finding cures.
Scientists are becoming more adept at turning skin cells into pluripotent stem cells, which can then be converted to other cell types such as neurons or heart cells. And because these are human cells they are superior to animal models for drug screening or toxicity testing. Human cell lines have been used for many years, but before pluripotent stem cells creating cell lines involved immortalizing the cells and thus drastically changing their physiology.
The goal of StemBANCC is to use these human-induced pluripotent stem cells as a drug discovery platform to treat the following 8 common diseases: Alzheimer’s disease, Parkinson’s disease, autism, schizophrenia, bipolar disorder, migraine, pain and diabetes. Studying these conditions typically involves creating an animal model, such as a rat that exhibits some behavioral hallmarks of autism after being given valproic acid. The cells from StemBANCC would improve upon animal models by providing, not only cells from humans but cells from patients with the actual disorders being studied. Skin cells gotten from a schizophrenia patient and converted (via pluripotency) to neurons, for instance, would give scientists a powerful tool with which to screen drugs.
Led by Oxford University, StemBANCC will involve 10 pharmaceutical companies and 23 academic institutions across 11 different countries. Part of the Innovative Medicines Initiative that pairs the European Union and the pharmaceutical industry. The EU is contributing 26 million euros ($33.5 million). Another 21 million euros ($27 million) are coming from the pharmaceutical industry. StemBANCC’s “kick-off” meeting took place in 2012 in Basel, Switzerland.
Zameel Cader, neurologist at the University of Oxford and a leader on the project, told Nature, “We’re specifically trying to develop a panel of lines across a range of diseases that are important to address. There isn’t another institution that’s doing this at the same scale across the same range of diseases.”
The hype surrounding stem cells typically extolls their virtues as a miraculous ‘cure all’ replacing damaged or diseased cells with new, healthy ones. And while stem cells have given blind people back part of their sight and have shown to restore some hearing in animals or even help paralyzed ones walk again in the lab, mainstream cures derived from stem cells are still rare. In the meantime, places like StemBANCC can pursue the less sexy, perhaps, but more reachable near term benefits of stem cells.

European Project Aims To Create 1,500 New Stem Cell Lines

A joint public-private collaboration between the European Union and Europe’s pharmaceutical industry, called the StemBANCC project, will spend nearly 50 million euros to create 1,500 pluripotent stem cell lines. But the initiative’s goal isn’t to find a stem cell-based cure for diabetes or Alzheimer’s disease. They hope instead that their stem cell lines will prove to be faster and more effective drug screens in the search for drugs to fight these and other conditions.

A frustrating problem in medical research is the inadequacy of animal models. All too often a treatment works great in laboratory rats or mice but then its efficacy fails to repeat in human trials. But researchers are beginning to capitalize on the potential of stem cells – not as cures, but as means to finding cures.

Scientists are becoming more adept at turning skin cells into pluripotent stem cells, which can then be converted to other cell types such as neurons or heart cells. And because these are human cells they are superior to animal models for drug screening or toxicity testing. Human cell lines have been used for many years, but before pluripotent stem cells creating cell lines involved immortalizing the cells and thus drastically changing their physiology.

The goal of StemBANCC is to use these human-induced pluripotent stem cells as a drug discovery platform to treat the following 8 common diseases: Alzheimer’s disease, Parkinson’s disease, autism, schizophrenia, bipolar disorder, migraine, pain and diabetes. Studying these conditions typically involves creating an animal model, such as a rat that exhibits some behavioral hallmarks of autism after being given valproic acid. The cells from StemBANCC would improve upon animal models by providing, not only cells from humans but cells from patients with the actual disorders being studied. Skin cells gotten from a schizophrenia patient and converted (via pluripotency) to neurons, for instance, would give scientists a powerful tool with which to screen drugs.

Led by Oxford University, StemBANCC will involve 10 pharmaceutical companies and 23 academic institutions across 11 different countries. Part of the Innovative Medicines Initiative that pairs the European Union and the pharmaceutical industry. The EU is contributing 26 million euros ($33.5 million). Another 21 million euros ($27 million) are coming from the pharmaceutical industry. StemBANCC’s “kick-off” meeting took place in 2012 in Basel, Switzerland.

Zameel Cader, neurologist at the University of Oxford and a leader on the project, told Nature, “We’re specifically trying to develop a panel of lines across a range of diseases that are important to address. There isn’t another institution that’s doing this at the same scale across the same range of diseases.”

The hype surrounding stem cells typically extolls their virtues as a miraculous ‘cure all’ replacing damaged or diseased cells with new, healthy ones. And while stem cells have given blind people back part of their sight and have shown to restore some hearing in animals or even help paralyzed ones walk again in the lab, mainstream cures derived from stem cells are still rare. In the meantime, places like StemBANCC can pursue the less sexy, perhaps, but more reachable near term benefits of stem cells.

Filed under stem cells StemBANCC project drug screening drug development neurodegenerative diseases medicine science

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