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.

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.

Fighting dead zones of cancer
Almost all high-risk, poor-prognosis cancers have very low levels of oxygen in the primary tumor’s interior. A marker for this oxygen-depleted state is the presence of a protein known as H1FI alpha. 
In healthy cells, HIF1 alpha is degraded into harmless nothingness in the cytoplasm. In low-oxygen cancer cells however, the normal breakdown goes awry and HiFl alpha is able to enter the nucleus, where it may activate genes that further promote aberrant cell growth.
A new study conducted by researchers at the University of California, San Diego School of Medicine shows that an emerging class of anticancer treatments known as PI-3K inhibitors help to degrade the HIF1 alpha protein and thus may offer a potential therapy for treating deadly hypoxic tumors. The study was published in a recent issue of the Journal of Biological Chemistry.
“Our main finding is that, in the absence of PI-3K signaling, MDM2 proteins cannot go inside the nucleus,” said lead author Shweta Joshi, PhD, postdoctoral researcher. “In the cytoplasm, the MDM2 proteins degrade HIF1 alpha. This is good news because it means that some new cancer therapies may help patients in more ways that was initially realized.”
"These HIF1 proteins are major players in driving the cancer state," said co-author Donald Durden, MD, PhD, professor and vice chair for Research in the Department of Pediatrics and research director, Division of Hematology/Oncology at the UC San Diego Moores Cancer Center. “They control degradation of surrounding tissues, induce a change in metabolism and induce the formation of blood vessels. That is why our observation is so important, because it reveals an entirely new way of HIF1 regulation.”
Pictured: A false-color, scanning electron micrograph of two cultured HeLa cancer cells, courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research at San Diego.

Fighting dead zones of cancer

Almost all high-risk, poor-prognosis cancers have very low levels of oxygen in the primary tumor’s interior. A marker for this oxygen-depleted state is the presence of a protein known as H1FI alpha.

In healthy cells, HIF1 alpha is degraded into harmless nothingness in the cytoplasm. In low-oxygen cancer cells however, the normal breakdown goes awry and HiFl alpha is able to enter the nucleus, where it may activate genes that further promote aberrant cell growth.

A new study conducted by researchers at the University of California, San Diego School of Medicine shows that an emerging class of anticancer treatments known as PI-3K inhibitors help to degrade the HIF1 alpha protein and thus may offer a potential therapy for treating deadly hypoxic tumors. The study was published in a recent issue of the Journal of Biological Chemistry.

“Our main finding is that, in the absence of PI-3K signaling, MDM2 proteins cannot go inside the nucleus,” said lead author Shweta Joshi, PhD, postdoctoral researcher. “In the cytoplasm, the MDM2 proteins degrade HIF1 alpha. This is good news because it means that some new cancer therapies may help patients in more ways that was initially realized.”

"These HIF1 proteins are major players in driving the cancer state," said co-author Donald Durden, MD, PhD, professor and vice chair for Research in the Department of Pediatrics and research director, Division of Hematology/Oncology at the UC San Diego Moores Cancer Center. “They control degradation of surrounding tissues, induce a change in metabolism and induce the formation of blood vessels. That is why our observation is so important, because it reveals an entirely new way of HIF1 regulation.”

Pictured: A false-color, scanning electron micrograph of two cultured HeLa cancer cells, courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research at San Diego.

Uh oh!
A diagnosis of prostate cancer can be an “uh oh” moment. After skin cancer, it’s the most common cancer in American men, with more than 238,000 new cases diagnosed each year and almost 30,000 deaths.
However, the confocal micrograph above, produced by Xiaochen Lu and C. Chase Bolt at the University of Illinois at Urbana-Champaign, is not an uh-oh moment. Rather, it may be an “ah-hah!”
It depicts the actual prostate and ureter of an embryonic mouse – a winning image from the 2013 Olympus BioScapes competition.
Mouse models of prostate cancer are widely used, in part because the disease is often very slow progressing in humans and typically not detected in men until their 60s or older.

Uh oh!

A diagnosis of prostate cancer can be an “uh oh” moment. After skin cancer, it’s the most common cancer in American men, with more than 238,000 new cases diagnosed each year and almost 30,000 deaths.

However, the confocal micrograph above, produced by Xiaochen Lu and C. Chase Bolt at the University of Illinois at Urbana-Champaign, is not an uh-oh moment. Rather, it may be an “ah-hah!”

It depicts the actual prostate and ureter of an embryonic mouse – a winning image from the 2013 Olympus BioScapes competition.

Mouse models of prostate cancer are widely used, in part because the disease is often very slow progressing in humans and typically not detected in men until their 60s or older.

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