Birthday Matters for Wiring-Up the Brain’s Vision Centers
Researchers at the University of California, San Diego School of Medicine have evidence suggesting that neurons in the developing brains of mice are guided by a simple but elegant birth order rule that allows them to find and form their proper connections.
The study is published online July 31 in Cell Reports.
“Nothing about brain wiring is haphazard,” said senior author Andrew Huberman, PhD, assistant professor in the Department of Neurosciences, Division of Biological Sciences and Department of Ophthalmology, UC San Diego.
A mature, healthy brain has billions of precisely interconnected neurons. Yet the brain starts with just one neuron that divides and divides – up to 250,000 new neurons per minute at times during early development. The question for biologists has been how do these neurons decide which other neurons to connect to, a process neuroscientists call target selection.
The answer has both fundamental scientific value and clinical relevance. Some researchers believe that autism and other disorders linked to brain development may be caused, in part, by a failure of neurons to properly reposition their axons as needed when mistakes in target selection occur.
To better understand how a young brain gets wired, researchers focused on the development of retinal ganglion cells (RGCs) in mice. These cells connect the eyes and brain. Specifically, the main cell bodies of RGCs reside in the retina but their axons – slender projections along which electrical impulses travel – extend into the centers of the brain that process visual information and give rise to what we commonly think of as “sight,” as well as other light-influenced physiological processes, such as the effect of light on mood.
For the study, scientists tagged RGCs and watched where they directed their axons during development. The experiments revealed that specific types of RGCs target specific areas of the brain, allowing mice to do things such as sense direction of motion, move their eyes and detect changes in daily light cycles. It was also observed that some types of RGCs (such as those that detect brightness and control pupil constriction) are created early in development while others (such as those controlling eye movements) are created later.
The study’s main finding is that early RGCs (those created early in the sequence of brain division) make a lot of connections to other neurons and a lot of mistakes, which they then correct by repositioning or removing their axons. By contrast, later RGCs were observed to be highly accurate in their target selection skills and made almost no errors.
“The neurons are paying attention to when they were born and reading out which choices they should make based on their birthdate,” said Jessica Osterhout, a doctoral student in biology and the study’s lead author. “It seems to all boil down to birthdate.”
The idea that timing is important for cell differentiation is a classic principle of developmental biology, but this study is among the first to show that the timing of neuronal generation is linked to how neurons achieve specific brain wiring.
In addition to clarifying normal brain development, researchers plan to examine the role of time-dependent wiring mishaps in models of human disorders, such as autism and schizophrenia, as well as diseases specific to the visual system, such as congenital blindness.
“We want to know if in diseases such as autism neurons are made out of order and as a result get confused about which connections to make,” Huberman said.

Birthday Matters for Wiring-Up the Brain’s Vision Centers

Researchers at the University of California, San Diego School of Medicine have evidence suggesting that neurons in the developing brains of mice are guided by a simple but elegant birth order rule that allows them to find and form their proper connections.

The study is published online July 31 in Cell Reports.

“Nothing about brain wiring is haphazard,” said senior author Andrew Huberman, PhD, assistant professor in the Department of Neurosciences, Division of Biological Sciences and Department of Ophthalmology, UC San Diego.

A mature, healthy brain has billions of precisely interconnected neurons. Yet the brain starts with just one neuron that divides and divides – up to 250,000 new neurons per minute at times during early development. The question for biologists has been how do these neurons decide which other neurons to connect to, a process neuroscientists call target selection.

The answer has both fundamental scientific value and clinical relevance. Some researchers believe that autism and other disorders linked to brain development may be caused, in part, by a failure of neurons to properly reposition their axons as needed when mistakes in target selection occur.

To better understand how a young brain gets wired, researchers focused on the development of retinal ganglion cells (RGCs) in mice. These cells connect the eyes and brain. Specifically, the main cell bodies of RGCs reside in the retina but their axons – slender projections along which electrical impulses travel – extend into the centers of the brain that process visual information and give rise to what we commonly think of as “sight,” as well as other light-influenced physiological processes, such as the effect of light on mood.

For the study, scientists tagged RGCs and watched where they directed their axons during development. The experiments revealed that specific types of RGCs target specific areas of the brain, allowing mice to do things such as sense direction of motion, move their eyes and detect changes in daily light cycles. It was also observed that some types of RGCs (such as those that detect brightness and control pupil constriction) are created early in development while others (such as those controlling eye movements) are created later.

The study’s main finding is that early RGCs (those created early in the sequence of brain division) make a lot of connections to other neurons and a lot of mistakes, which they then correct by repositioning or removing their axons. By contrast, later RGCs were observed to be highly accurate in their target selection skills and made almost no errors.

“The neurons are paying attention to when they were born and reading out which choices they should make based on their birthdate,” said Jessica Osterhout, a doctoral student in biology and the study’s lead author. “It seems to all boil down to birthdate.”

The idea that timing is important for cell differentiation is a classic principle of developmental biology, but this study is among the first to show that the timing of neuronal generation is linked to how neurons achieve specific brain wiring.

In addition to clarifying normal brain development, researchers plan to examine the role of time-dependent wiring mishaps in models of human disorders, such as autism and schizophrenia, as well as diseases specific to the visual system, such as congenital blindness.

“We want to know if in diseases such as autism neurons are made out of order and as a result get confused about which connections to make,” Huberman said.

You Might Hear A Cricket Chirp
Ormia ochracea is a tiny, parasitical fly and the bane of crickets. The fly listens for cricket chirps, homes in and deposits larvae on the back of the cricket’s back. The larvae then proceed to burrow into the cricket and eat it alive.
While this scenario is nothing for crickets to sing about, it’s absolute inspiration for researchers trying to develop the next generation of directional hearing aids, who describe a new, fly-inspired prototype in the journal Applied Physics Letters.
What’s particularly notable about the fly’s hearing abilities is that they derive from ears that are, well, extremely small. Human ability to detect the source and direction of sounds derives significantly from our large heads and widely separated ears. The latter receive the same sound at slightly different times. Our brains analyze that time difference and use it to locate the sound source.
The heads of flies, though, are just a millimeter or so wide, about the thickness of an average fingernail. (Incidentally, the fly above is resting on a fingernail so you can get a good sense of scale.) Flies overcome their size limitations by creatively tweaking the internal hearing structure. Between the two ears of a fly is a sort of see-saw that moves up and down, amplifying the incredibly small time differences of incoming sounds. It allows the fly to find chirping crickets quite well.
Researchers at the University of Texas have used the fly’s ear structure as a model to create minute pressure-sensitive devices out of silicon that they hope can eventually be used in new directional hearing aids that are smaller, more comfortable and longer-lasting.

You Might Hear A Cricket Chirp

Ormia ochracea is a tiny, parasitical fly and the bane of crickets. The fly listens for cricket chirps, homes in and deposits larvae on the back of the cricket’s back. The larvae then proceed to burrow into the cricket and eat it alive.

While this scenario is nothing for crickets to sing about, it’s absolute inspiration for researchers trying to develop the next generation of directional hearing aids, who describe a new, fly-inspired prototype in the journal Applied Physics Letters.

What’s particularly notable about the fly’s hearing abilities is that they derive from ears that are, well, extremely small. Human ability to detect the source and direction of sounds derives significantly from our large heads and widely separated ears. The latter receive the same sound at slightly different times. Our brains analyze that time difference and use it to locate the sound source.

The heads of flies, though, are just a millimeter or so wide, about the thickness of an average fingernail. (Incidentally, the fly above is resting on a fingernail so you can get a good sense of scale.) Flies overcome their size limitations by creatively tweaking the internal hearing structure. Between the two ears of a fly is a sort of see-saw that moves up and down, amplifying the incredibly small time differences of incoming sounds. It allows the fly to find chirping crickets quite well.

Researchers at the University of Texas have used the fly’s ear structure as a model to create minute pressure-sensitive devices out of silicon that they hope can eventually be used in new directional hearing aids that are smaller, more comfortable and longer-lasting.

Liver Scarring Mechanism Identified In Mice
The human liver may be our most undervalued organ.
Not only does it have lizard-like regenerative powers, its eight connected lobes work round the clock to detoxify us of our vices – be they a slab of fatty steak or a flagon of beer.
When we aren’t being bad, and even when we are, the liver also helps us digest our food, store energy and vitamins (it can hold several years’ worth of B-12), and clear our blood of residues from taking medications. It even plays a role in maintaining our hormonal balance and keeping our bones strong.
It does all of this if that meaty three-pound organ under the right side of our ribcage is working properly. If the liver becomes diseased, many vital bodily processes can go awry.
Regardless of the type of assault or insult, the liver almost always shows signs of abuse by forming fibrous scar tissue, which can further impair the liver’s ability to function, with profound health consequences.
Reporting in the current issue of Proceedings of the National Academy of Sciences, researchers at the University of California, San Diego School of Medicine have described a fundamental mechanism underlying the progression of cholestatic liver fibrosis, which is caused by the impairment of bile formation or bile flow not by lifestyle choices, like heavy drinking.
“Our study puts into perspective many previously contradictory studies, and provides a general approach to understanding the distinct mechanisms which lead to liver scaring and fibrosis,” said senior author Tatiana Kisseleva, MD, PhD and an assistant professor in the Department of Surgery. Fibrosis refers to progressive liver scarring, occurring in most types of chronic liver disease.
In the study, researchers identified a type of cell in the livers of mice (portal fibroblasts) that respond to bile-related liver injuries. When these cells become activated and proliferate, they secrete fibrous scar tissue.
Though the study was conducted in mice, preventing the activation of these cells in human livers could help prevent liver scarring in people with cholestatic liver disease.
Toward this effort, the scientists have now identified novel markers of activated portal fibroblasts that could be used to evaluate the source of liver injury in patients.

Liver Scarring Mechanism Identified In Mice

The human liver may be our most undervalued organ.

Not only does it have lizard-like regenerative powers, its eight connected lobes work round the clock to detoxify us of our vices – be they a slab of fatty steak or a flagon of beer.

When we aren’t being bad, and even when we are, the liver also helps us digest our food, store energy and vitamins (it can hold several years’ worth of B-12), and clear our blood of residues from taking medications. It even plays a role in maintaining our hormonal balance and keeping our bones strong.

It does all of this if that meaty three-pound organ under the right side of our ribcage is working properly. If the liver becomes diseased, many vital bodily processes can go awry.

Regardless of the type of assault or insult, the liver almost always shows signs of abuse by forming fibrous scar tissue, which can further impair the liver’s ability to function, with profound health consequences.

Reporting in the current issue of Proceedings of the National Academy of Sciences, researchers at the University of California, San Diego School of Medicine have described a fundamental mechanism underlying the progression of cholestatic liver fibrosis, which is caused by the impairment of bile formation or bile flow not by lifestyle choices, like heavy drinking.

“Our study puts into perspective many previously contradictory studies, and provides a general approach to understanding the distinct mechanisms which lead to liver scaring and fibrosis,” said senior author Tatiana Kisseleva, MD, PhD and an assistant professor in the Department of Surgery. Fibrosis refers to progressive liver scarring, occurring in most types of chronic liver disease.

In the study, researchers identified a type of cell in the livers of mice (portal fibroblasts) that respond to bile-related liver injuries. When these cells become activated and proliferate, they secrete fibrous scar tissue.

Though the study was conducted in mice, preventing the activation of these cells in human livers could help prevent liver scarring in people with cholestatic liver disease.

Toward this effort, the scientists have now identified novel markers of activated portal fibroblasts that could be used to evaluate the source of liver injury in patients.

Strathdee’s calling
Steffanie Strathdee became involved in HIV/AIDS research at the University of Toronto after one of her professors failed to show up for class. “He had died of AIDS,” Strathdee said. “Later I lost my PhD supervisor and my best friend to the disease as well, so for me, coming to work in the HIV/AIDS field was a calling, something I had to do.”
The journal Lancet offers a nice profile of Strathdee’s work in its current online edition. Strathdee is associate dean of Global Health Sciences and chief of the Division of Global Public Health in the Department of Medicine at UC San Diego. An infectious disease epidemiologist, she has focused her research over the past two decades on HIV prevention in underserved, marginalized populations in developed and developing countries, including injection drug users, men having sex with men and sex workers.
The U.S.-Mexico border is a particular focus. Strathdee is one of the leaders of the Health Frontiers in Tijuana project, in which a student-run free clinic provides health services to marginalized populations, in collaboration with the UC San Diego School of Medicine and Tijuana’s Autonomous University of Baja California School of Medicine.
Not coincidentally, Strathdee was also recently featured as one of 40 women offering thoughts and wisdom in a San Diego exhibition called Notes to Our Sons & Daughters.
Photograph courtesy of Pablo Mason/Notes to Our Sons & Daughters project. 2014. Alexis Dixon.

Strathdee’s calling

Steffanie Strathdee became involved in HIV/AIDS research at the University of Toronto after one of her professors failed to show up for class. “He had died of AIDS,” Strathdee said. “Later I lost my PhD supervisor and my best friend to the disease as well, so for me, coming to work in the HIV/AIDS field was a calling, something I had to do.”

The journal Lancet offers a nice profile of Strathdee’s work in its current online edition. Strathdee is associate dean of Global Health Sciences and chief of the Division of Global Public Health in the Department of Medicine at UC San Diego. An infectious disease epidemiologist, she has focused her research over the past two decades on HIV prevention in underserved, marginalized populations in developed and developing countries, including injection drug users, men having sex with men and sex workers.

The U.S.-Mexico border is a particular focus. Strathdee is one of the leaders of the Health Frontiers in Tijuana project, in which a student-run free clinic provides health services to marginalized populations, in collaboration with the UC San Diego School of Medicine and Tijuana’s Autonomous University of Baja California School of Medicine.

Not coincidentally, Strathdee was also recently featured as one of 40 women offering thoughts and wisdom in a San Diego exhibition called Notes to Our Sons & Daughters.

Photograph courtesy of Pablo Mason/Notes to Our Sons & Daughters project. 2014. Alexis Dixon.

Study gives promise to new treatment for appendix cancer
Appendix cancer is rare, with approximately 600 to 1,000 new patients diagnosed each year and an estimated 10,000 currently living with the disease. Because it is rare, few studies have been devoted to this cancer and standard treatment for appendix cancers relies upon the same chemotherapy drugs used for colorectal cancer. A new study by researchers at the University of California, San Diego School of Medicine has found that genetic mutations in appendix and colon cancers are, in fact, quite different, suggesting that new and different approaches to appendix cancer treatment should be explored.
The study was published in a recent issue of Genome Medicine.
Cancers are characterized by different gene mutations. Historically, genetic mutations in appendix cancer have been poorly characterized due to its low incidence. The cancer often remains undiagnosed until it is discovered during or after abdominal surgery or when an abnormal mass is detected  during a CT scan for an unrelated condition.
The primary treatment of localized appendix cancer is surgical but treatment for patients with inoperable appendix cancer has been limited to therapies developed for colorectal cancer. Although the chemotherapy drugs used for colorectal cancer dramatically improve patient outcomes, they have not proven to be as successful in patients with appendix cancer.
“We have been treating appendix cancer like colorectal cancer because it was thought to be the most similar tumor type, but this study identifies the signature differences between these two cancers,” said Andrew Lowy, MD, FACS, a senior author of the study and professor of Surgery at UC San Diego School of Medicine. “These findings suggest opportunities to develop novel therapies that specifically target appendix cancer.”  
The study initially evaluated 10 cases, nine with low-grade appendix cancers and one with high-grade cancer. The results from this group were then validated with 19 additional cases.
The results also identified a gene mutation in appendix cancer that is commonly found in a form of pancreatic cancer, which typically spreads rapidly and is seldom detected in its early stages.
“The study’s results are promising for patients. We now have a more in-depth knowledge of the biological make up of appendix cancers, which allow for a more customized approach,” said Lowy, who also serves as chief of the Division of Surgical Oncology at UC San Diego Health System. “The goal is to now conduct more studies that will test specific treatments targeted to these unique genetic mutations.”
To learn more about cancer treatments at UC San Diego Health System, visit cancer.ucsd.edu         Image: A histopathological photomicrograph depicting cancerous cells in the appendix.

Study gives promise to new treatment for appendix cancer

Appendix cancer is rare, with approximately 600 to 1,000 new patients diagnosed each year and an estimated 10,000 currently living with the disease. Because it is rare, few studies have been devoted to this cancer and standard treatment for appendix cancers relies upon the same chemotherapy drugs used for colorectal cancer. A new study by researchers at the University of California, San Diego School of Medicine has found that genetic mutations in appendix and colon cancers are, in fact, quite different, suggesting that new and different approaches to appendix cancer treatment should be explored.

The study was published in a recent issue of Genome Medicine.

Cancers are characterized by different gene mutations. Historically, genetic mutations in appendix cancer have been poorly characterized due to its low incidence. The cancer often remains undiagnosed until it is discovered during or after abdominal surgery or when an abnormal mass is detected  during a CT scan for an unrelated condition.

The primary treatment of localized appendix cancer is surgical but treatment for patients with inoperable appendix cancer has been limited to therapies developed for colorectal cancer. Although the chemotherapy drugs used for colorectal cancer dramatically improve patient outcomes, they have not proven to be as successful in patients with appendix cancer.

“We have been treating appendix cancer like colorectal cancer because it was thought to be the most similar tumor type, but this study identifies the signature differences between these two cancers,” said Andrew Lowy, MD, FACS, a senior author of the study and professor of Surgery at UC San Diego School of Medicine. “These findings suggest opportunities to develop novel therapies that specifically target appendix cancer.”  

The study initially evaluated 10 cases, nine with low-grade appendix cancers and one with high-grade cancer. The results from this group were then validated with 19 additional cases.

The results also identified a gene mutation in appendix cancer that is commonly found in a form of pancreatic cancer, which typically spreads rapidly and is seldom detected in its early stages.

“The study’s results are promising for patients. We now have a more in-depth knowledge of the biological make up of appendix cancers, which allow for a more customized approach,” said Lowy, who also serves as chief of the Division of Surgical Oncology at UC San Diego Health System. “The goal is to now conduct more studies that will test specific treatments targeted to these unique genetic mutations.”

To learn more about cancer treatments at UC San Diego Health System, visit cancer.ucsd.edu        

Image: A histopathological photomicrograph depicting cancerous cells in the appendix.

Novel Technologies Advance Brain Surgery to Benefit Patients
Minimally invasive brain surgery at UC San Diego Health System

In a milestone procedure, neurosurgeons at UC San Diego Health System have integrated advanced 3D imaging, computer simulation and next-generation surgical tools to perform a highly complex brain surgery through a small incision to remove deep-seated tumors. This is the first time this complex choreography of technologies has been brought together in an operating room in California.

“Tumors located at the base of the skull are particularly challenging to treat due to the location of delicate anatomic structures and critical blood vessels,” said neurosurgeon Clark C. Chen, MD, PhD, UC San Diego Health System. “The conventional approach to excising these tumors involves long skin incisions and removal of a large piece of skull. This new minimally invasive approach is far less radical. It decreases the risk of the surgery and shortens the patient’s hospital stay.” 

“A critical part of this surgery involves identifying the neural fibers in the brain, the connections that allow the brain to perform its essential functions. The orientation of these fibers determines the trajectory to the tumor,” said Chen, vice-chairman of Academic Affairs for the Division of Neurosurgery at UC San Diego School of Medicine. “We visualized these fibers with restriction spectrum imaging, a proprietary technology developed at UC San Diego. Color-coded visualization of the tracts allows us to plot the safest path to the tumor.”

After surgery planning, a 2-inch incision was made near the patient’s hairline, followed by a quarter-sized hole in the skull. The surgery was carried out through a thin tube-like retractor that created a narrow path to the tumor.  Aided by a robotic arm and high-resolution cameras, the team was able to safely remove two tumors within millimeter precision.

“What we are seeing is a new wave of advances in minimally invasive surgery for patients with brain cancer,” said Bob Carter, MD, PhD, professor and chief of Neurosurgery, UC San Diego School of Medicine. “These minimally invasive approaches permit smaller incisions and a shorter recovery. In this case, the patient was able to go home the day after the successful removal of multiple brain tumors.”

A Moveable Yeast: modeling shows proteins never sit still
Our body’s proteins – encoded by DNA to do the hard work of building and operating our bodies – are forever on the move. Literally, according to new findings reported by Trey Ideker, PhD, chief of the Division of Genetics in the UC San Diego School of Medicine, and colleagues in a recent issue of the Proceedings of the National Academy of Sciences.
Hemoglobin protein molecules, for example, continuously transit through our blood vessels while other proteins you’ve never heard of bustle about inside cells as they grow, develop, respond to stimuli and succumb to disease.
To better understand the role of proteins in biological systems, Ideker and colleagues developed a computer model that can predict a protein’s intracellular wanderings in response to a variety of stress conditions.
To date, the model has been used to predict the effects of 18 different DNA-damaging stress conditions on the sub-cellular locations and molecular functions of more than 5,800 proteins produced by yeasts. They found, for example, that yeast proteins could move from mitochondria to the cell nucleus and from the endoplasmic reticulum to Golgi apparatus.
Though the model debut involved yeasts, researchers said the coding can be adapted to study changes in protein locations for any biological system in which gene expression sequences have been identified, including stem cell differentiation and drug response in humans.
Image courtesy of Material Mavens

A Moveable Yeast: modeling shows proteins never sit still

Our body’s proteins – encoded by DNA to do the hard work of building and operating our bodies – are forever on the move. Literally, according to new findings reported by Trey Ideker, PhD, chief of the Division of Genetics in the UC San Diego School of Medicine, and colleagues in a recent issue of the Proceedings of the National Academy of Sciences.

Hemoglobin protein molecules, for example, continuously transit through our blood vessels while other proteins you’ve never heard of bustle about inside cells as they grow, develop, respond to stimuli and succumb to disease.

To better understand the role of proteins in biological systems, Ideker and colleagues developed a computer model that can predict a protein’s intracellular wanderings in response to a variety of stress conditions.

To date, the model has been used to predict the effects of 18 different DNA-damaging stress conditions on the sub-cellular locations and molecular functions of more than 5,800 proteins produced by yeasts. They found, for example, that yeast proteins could move from mitochondria to the cell nucleus and from the endoplasmic reticulum to Golgi apparatus.

Though the model debut involved yeasts, researchers said the coding can be adapted to study changes in protein locations for any biological system in which gene expression sequences have been identified, including stem cell differentiation and drug response in humans.

Image courtesy of Material Mavens

Food for thought
Admittedly there’s no known scientific or therapeutic value to the brain image above. It’s not likely to satisfy our hunger for knowledge in, say, the way a tractograph or fMRI might. Instead, it’s just likely to make you hungry – for more.
Feast your eyes on Sara Asnaghi’s similar cerebral takes of the edible brain here.

Food for thought

Admittedly there’s no known scientific or therapeutic value to the brain image above. It’s not likely to satisfy our hunger for knowledge in, say, the way a tractograph or fMRI might. Instead, it’s just likely to make you hungry – for more.

Feast your eyes on Sara Asnaghi’s similar cerebral takes of the edible brain here.

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