Delivering Imani’s baby was truly a team effort.
Here’s our anesthesiologist Dr. Mark Greenberg getting some cuddle time with the baby gorilla.

Delivering Imani’s baby was truly a team effort.

Here’s our anesthesiologist Dr. Mark Greenberg getting some cuddle time with the baby gorilla.

A star is born!
At 6:30 pm on Thursday, March 13, Imani, an 18 year-old Gorilla at the San Diego Zoo Safari Park, gave birth to a baby girl via emergency C-Section. Neonatologist Dawn Reeves of UC San Diego Health System was on hand to aid the team with this very special delivery.
Pictured above are Dr. Reeves and Caitlin Forrest, one of our NICU nurses, with Imani’s baby very soon after her birth. This little baby melted the hearts of all who cared for her and, despite a few early complications, Imani has successfully reunited with her baby and introduced her to the troop.A happy ending, indeed!

A star is born!

At 6:30 pm on Thursday, March 13, Imani, an 18 year-old Gorilla at the San Diego Zoo Safari Park, gave birth to a baby girl via emergency C-Section. Neonatologist Dawn Reeves of UC San Diego Health System was on hand to aid the team with this very special delivery.

Pictured above are Dr. Reeves and Caitlin Forrest, one of our NICU nurses, with Imani’s baby very soon after her birth.

This little baby melted the hearts of all who cared for her and, despite a few early complications, Imani has successfully reunited with her baby and introduced her to the troop.

A happy ending, indeed!

Good Vibrations: Using Light-Heated Water to Deliver DrugsResearchers use near-infrared light to warm water-infused polymeric particles
Researchers from the University of California, San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences, in collaboration with materials scientists, engineers and neurobiologists, have discovered a new mechanism for using light to activate drug-delivering nanoparticles and other targeted therapeutic substances inside the body.
This discovery represents a major innovation, said Adah Almutairi, PhD, associate professor and director of the joint UC San Diego-KACST Center of Excellence in Nanomedicine. Up to now, she said, only a handful of strategies using light-triggered release from nanoparticles have been reported.
The mechanism, described in the April 1, 2014 online issue of ACS Nano, employs near-infrared (NIR) light from a low-power laser to heat pockets of water trapped within non-photo-responsive polymeric nanoparticles infused with drugs. The water pockets absorb the light energy as heat, which softens the encapsulating polymer and allows the drug to be released into the surrounding tissue. The process can be repeated multiple times, with precise control of the amount and dispersal of the drug.
“A key advantage of this mechanism is that it should be compatible with almost any polymer, even those that are commercially available,” said Mathieu Viger, a post-doctoral fellow in Almutairi’s laboratory and co-lead author of the study. “We’ve observed trapping of water within particles composed of all the biodegradable polymers we’ve so far tested.”
The method, noted Viger, could thus be easily adopted by many biological laboratories.
The combined use of hydrated polymers and near-infrared light appears to resolve a host of technological and health barriers that have hindered previous, similar approaches. Earlier efforts to use NIR-triggered release have not been widely exploited because they required special designer polymers, expensive high-powered lasers and/or the co-encapsulation of inorganic particles whose safety in the body remains questionable.
The new method described by Almutairi and colleagues in the departments of Mechanical and Aerospace Engineering, Neuroscience, and Chemistry and Biochemistry at UC San Diego uses NIR at a vibrational wavelength cued to excite water molecules, which absorb the optical energy and convert it to heat. NIR is capable of penetrating biological tissues to greater depths than visible or ultraviolet light.
Co-lead author Wangzhong Sheng, a graduate student in Department of Mechanical and Aerospace Engineering, explained the selectivity of heating by comparing the trapped water within particles to a glass of water and the surrounding water within the solution or tissue to a bathtub. The smaller amount of water is heated much more rapidly because of the enormous volume difference.
An obvious use of the method, said Almutairi, is light-triggered drug delivery, but with more research, she anticipates the new method could provide a variety of industrial, medical and scientific applications, including “any technological application requiring that chemistry be controlled in time and in space, such as in catalysis or self-repairing materials or light-activated sunscreens or pesticide dosing.”

Good Vibrations: Using Light-Heated Water to Deliver Drugs
Researchers use near-infrared light to warm water-infused polymeric particles

Researchers from the University of California, San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences, in collaboration with materials scientists, engineers and neurobiologists, have discovered a new mechanism for using light to activate drug-delivering nanoparticles and other targeted therapeutic substances inside the body.

This discovery represents a major innovation, said Adah Almutairi, PhD, associate professor and director of the joint UC San Diego-KACST Center of Excellence in Nanomedicine. Up to now, she said, only a handful of strategies using light-triggered release from nanoparticles have been reported.

The mechanism, described in the April 1, 2014 online issue of ACS Nano, employs near-infrared (NIR) light from a low-power laser to heat pockets of water trapped within non-photo-responsive polymeric nanoparticles infused with drugs. The water pockets absorb the light energy as heat, which softens the encapsulating polymer and allows the drug to be released into the surrounding tissue. The process can be repeated multiple times, with precise control of the amount and dispersal of the drug.

“A key advantage of this mechanism is that it should be compatible with almost any polymer, even those that are commercially available,” said Mathieu Viger, a post-doctoral fellow in Almutairi’s laboratory and co-lead author of the study. “We’ve observed trapping of water within particles composed of all the biodegradable polymers we’ve so far tested.”

The method, noted Viger, could thus be easily adopted by many biological laboratories.

The combined use of hydrated polymers and near-infrared light appears to resolve a host of technological and health barriers that have hindered previous, similar approaches. Earlier efforts to use NIR-triggered release have not been widely exploited because they required special designer polymers, expensive high-powered lasers and/or the co-encapsulation of inorganic particles whose safety in the body remains questionable.

The new method described by Almutairi and colleagues in the departments of Mechanical and Aerospace Engineering, Neuroscience, and Chemistry and Biochemistry at UC San Diego uses NIR at a vibrational wavelength cued to excite water molecules, which absorb the optical energy and convert it to heat. NIR is capable of penetrating biological tissues to greater depths than visible or ultraviolet light.

Co-lead author Wangzhong Sheng, a graduate student in Department of Mechanical and Aerospace Engineering, explained the selectivity of heating by comparing the trapped water within particles to a glass of water and the surrounding water within the solution or tissue to a bathtub. The smaller amount of water is heated much more rapidly because of the enormous volume difference.

An obvious use of the method, said Almutairi, is light-triggered drug delivery, but with more research, she anticipates the new method could provide a variety of industrial, medical and scientific applications, including “any technological application requiring that chemistry be controlled in time and in space, such as in catalysis or self-repairing materials or light-activated sunscreens or pesticide dosing.”

Yeast of our problems
Scientists at NYU Langone Medical Center’s Institute for Systems Genetics reported last week that  they had synthesized one of the 16 chromosomes in Saccharomyces cerevisiae.
“We have a yeast that looks, smells and behaves like a regular yeast, but this yeast is endowed with properties normal yeast don’t have,” lead study scientist Jef Boeke told The Los Angeles Times.
The larger goal, however, is to create a yeast cell that contains an entirely human-designed genome that could be manipulated to do new and better things in the service of mankind.
S. cerevisiae is already something of an industrial workhorse. It’s widely used in baking, brewing, winemaking and the manufacture of everything from vaccines to biofuels. And it’s a reliable scientific model, long employed by researchers to parse the mysteries of genetics.
Above, a colored X-ray micrograph by Carolyn Larabell of UC San Francisco and Lawrence Berkeley National Laboratory shows a fast-frozen yeast cell in the process of dividing into two copies, called budding. 

Yeast of our problems

Scientists at NYU Langone Medical Center’s Institute for Systems Genetics reported last week that  they had synthesized one of the 16 chromosomes in Saccharomyces cerevisiae.

“We have a yeast that looks, smells and behaves like a regular yeast, but this yeast is endowed with properties normal yeast don’t have,” lead study scientist Jef Boeke told The Los Angeles Times.

The larger goal, however, is to create a yeast cell that contains an entirely human-designed genome that could be manipulated to do new and better things in the service of mankind.

S. cerevisiae is already something of an industrial workhorse. It’s widely used in baking, brewing, winemaking and the manufacture of everything from vaccines to biofuels. And it’s a reliable scientific model, long employed by researchers to parse the mysteries of genetics.

Above, a colored X-ray micrograph by Carolyn Larabell of UC San Francisco and Lawrence Berkeley National Laboratory shows a fast-frozen yeast cell in the process of dividing into two copies, called budding

Gulf War Illness Not in Veterans’ Heads, But in Their Mitochondria
Researchers at the UC San Diego School of Medicine have demonstrated for the first time that veterans of the 1990-91 Persian Gulf War who suffer from “Gulf War illness” have impaired function of mitochondria – the energy powerhouses of cells.
The findings, published in the March 27, 2014 issue of PLOS ONE, could help lead to new treatments benefitting affected individuals – and to new ways of protecting servicepersons (and civilians) from similar problems in the future, said principal investigator Beatrice A. Golomb MD, PhD, professor of medicine.
Golomb, with associate Hayley Koslik and Gavin Hamilton, PhD, a research scientist and magnetic resonance physicist, used the imaging technology to compare Gulf War veterans with diagnosed Gulf War illness to healthy controls. Cases were matched by age, sex and ethnicity.
The technique used – 31-phosphorus magnetic resonance spectroscopy or 31P-MRS – reveals amounts of phosphorus-containing compounds in cells. Such compounds are important for cell energy production, in particular phosphocreatine or PCr, which declines in muscle cells during exercise. PCr recovery takes longer when mitochondrial function is impaired, and delayed recovery is recognized as a robust marker of mitochondrial dysfunction.
Affected Gulf War veterans displayed significantly delayed PCr recovery after an exercise challenge. In fact, said Golomb, there was almost no overlap in the recovery times of Gulf War illness veterans compared to controls: All but one control participant had a recovery time-constant clustered under 31 seconds. In contrast, all but one Gulf Illness veteran had a recovery time-constant exceeding 35 seconds, with times ranging as high as 70 seconds.
There were 14 participants in the study: seven Gulf War illness cases and seven matching controls. Golomb notes that the use of 1:1 matching markedly improves statistical “power,” allowing a smaller sample size. The separation between the two groups was “visibly striking, and the large average difference was statistically significant,” she said.
Golomb noted that impaired mitochondrial function accounts for numerous features of Gulf War illness, including symptoms that have been viewed as perplexing or paradoxical.
“The classic presentation for mitochondrial illness involves multiple symptoms spanning many domains, similar to what we see in Gulf War illness. These classically include fatigue, cognitive and other brain-related challenges, muscle problems and exercise intolerance, with neurological and gastrointestinal problems also common.”
There are other similarities between patients with mitochondrial dysfunction and those suffering from Gulf War illness: Additional symptoms appear in smaller subsets of patients; varying patterns of symptoms and severity among individuals; different latency periods across symptoms, or times when symptoms first appear; routine blood tests that appear normal.
“Some have sought to ascribe Gulf War illness to stress,” said Golomb, “but stress has proven not to be an independent predictor of the condition. On the other hand, Gulf veterans are known to have been widely exposed to acetylcholinesterase inhibitors, a chemical class found in organophosphate and carbamate pesticides, nerve gas and nerve gas pre-treatment pills given to troops.
“These inhibitors have known mitochondrial toxicity and generally show the strongest and most consistent relationship to predicting Gulf War illness. Mitochondrial problems account for which exposures relate to Gulf War illness, which symptoms predominate, how Gulf War illness symptoms manifest themselves, what objective tests have been altered, and why routine blood tests have not been useful.”
Pictured: mitochondria, false colored.

Gulf War Illness Not in Veterans’ Heads, But in Their Mitochondria

Researchers at the UC San Diego School of Medicine have demonstrated for the first time that veterans of the 1990-91 Persian Gulf War who suffer from “Gulf War illness” have impaired function of mitochondria – the energy powerhouses of cells.

The findings, published in the March 27, 2014 issue of PLOS ONE, could help lead to new treatments benefitting affected individuals – and to new ways of protecting servicepersons (and civilians) from similar problems in the future, said principal investigator Beatrice A. Golomb MD, PhD, professor of medicine.

Golomb, with associate Hayley Koslik and Gavin Hamilton, PhD, a research scientist and magnetic resonance physicist, used the imaging technology to compare Gulf War veterans with diagnosed Gulf War illness to healthy controls. Cases were matched by age, sex and ethnicity.

The technique used – 31-phosphorus magnetic resonance spectroscopy or 31P-MRS – reveals amounts of phosphorus-containing compounds in cells. Such compounds are important for cell energy production, in particular phosphocreatine or PCr, which declines in muscle cells during exercise. PCr recovery takes longer when mitochondrial function is impaired, and delayed recovery is recognized as a robust marker of mitochondrial dysfunction.

Affected Gulf War veterans displayed significantly delayed PCr recovery after an exercise challenge. In fact, said Golomb, there was almost no overlap in the recovery times of Gulf War illness veterans compared to controls: All but one control participant had a recovery time-constant clustered under 31 seconds. In contrast, all but one Gulf Illness veteran had a recovery time-constant exceeding 35 seconds, with times ranging as high as 70 seconds.

There were 14 participants in the study: seven Gulf War illness cases and seven matching controls. Golomb notes that the use of 1:1 matching markedly improves statistical “power,” allowing a smaller sample size. The separation between the two groups was “visibly striking, and the large average difference was statistically significant,” she said.

Golomb noted that impaired mitochondrial function accounts for numerous features of Gulf War illness, including symptoms that have been viewed as perplexing or paradoxical.

“The classic presentation for mitochondrial illness involves multiple symptoms spanning many domains, similar to what we see in Gulf War illness. These classically include fatigue, cognitive and other brain-related challenges, muscle problems and exercise intolerance, with neurological and gastrointestinal problems also common.”

There are other similarities between patients with mitochondrial dysfunction and those suffering from Gulf War illness: Additional symptoms appear in smaller subsets of patients; varying patterns of symptoms and severity among individuals; different latency periods across symptoms, or times when symptoms first appear; routine blood tests that appear normal.

“Some have sought to ascribe Gulf War illness to stress,” said Golomb, “but stress has proven not to be an independent predictor of the condition. On the other hand, Gulf veterans are known to have been widely exposed to acetylcholinesterase inhibitors, a chemical class found in organophosphate and carbamate pesticides, nerve gas and nerve gas pre-treatment pills given to troops.

“These inhibitors have known mitochondrial toxicity and generally show the strongest and most consistent relationship to predicting Gulf War illness. Mitochondrial problems account for which exposures relate to Gulf War illness, which symptoms predominate, how Gulf War illness symptoms manifest themselves, what objective tests have been altered, and why routine blood tests have not been useful.”

Pictured: mitochondria, false colored.

UC San Diego researchers have found clear and direct new evidence that autism begins during pregnancy, reporting that patches of disrupted brain development occur in the womb.

Patches of Cortical Layers Disrupted During Early Brain Development in Autism

Researchers at the University of California, San Diego School of Medicine and the Allen Institute for Brain Science have published a study that gives clear and direct new evidence that autism begins during pregnancy.

The study will be published in the March 27 online edition of the New England Journal of Medicine.  

The researchers – Eric Courchesne, PhD, professor of neurosciences and director of the Autism Center of Excellence at UC San Diego, Ed S. Lein, PhD, of the Allen Institute for Brain Science in Seattle, and first author Rich Stoner, PhD, of the UC San Diego Autism Center of Excellence – analyzed 25 genes in post-mortem brain tissue of children with and without autism. These included genes that serve as biomarkers for brain cell types in different layers of the cortex, genes implicated in autism and several control genes.

“Building a baby’s brain during pregnancy involves creating a cortex that contains six layers,” Courchesne said. “We discovered focal patches of disrupted development of these cortical layers in the majority of children with autism.” Stoner created the first three-dimensional model visualizing brain locations where patches of cortex had failed to develop the normal cell-layering pattern.

“The most surprising finding was the similar early developmental pathology across nearly all of the autistic brains, especially given the diversity of symptoms in patients with autism, as well as the extremely complex genetics behind the disorder,” explained Lein.

During early brain development, each cortical layer develops its own specific types of brain cells, each with specific patterns of brain connectivity that perform unique and important roles in processing information. As a brain cell develops into a specific type in a specific layer with   specific connections, it acquires a distinct genetic signature or “marker” that can be observed.

The study found that in the brains of children with autism, key genetic markers were absent in brain cells in multiple layers. “This defect,” Courchesne said, “indicates that the crucial early developmental step of creating six distinct layers with specific types of brain cells – something that begins in prenatal life – had been disrupted.”

Equally important, said the scientists, these early developmental defects were present in focal patches of cortex, suggesting the defect is not uniform throughout the cortex. The brain regions most affected by focal patches of absent gene markers were the frontal and the temporal cortex, possibly illuminating why different functional systems are impacted across individuals with the disorder.

The frontal cortex is associated with higher-order brain function, such as complex communication and comprehension of social cues. The temporal cortex is associated with language. The disruptions of frontal and temporal cortical layers seen in the study may underlie symptoms most often displayed in autistic spectrum disorders. The visual cortex – an area of the brain associated with perception that tends to be spared in autism – displayed no abnormalities. 

“The fact that we were able to find these patches is remarkable, given that the cortex is roughly the size of the surface of a basketball, and we only examined pieces of tissue the size of a pencil eraser,” said Lein. “This suggests that these abnormalities are quite pervasive across the surface of the cortex.”

Data collected for the Allen Brain Atlas, as well as the BrainSpan Atlas of the Developing Human Brain was developed by a consortium of partners and funded by the National Institute of Mental Health. It allowed scientists to identify specific genes in the developing human brain that could be used as biomarkers for the different layer cell types.

Researching the origins of autism is challenging because it typically relies upon studying adult brains and attempting to extrapolate backwards. “In this case,” Lein noted, “we were able to study autistic and control cases at a young age, giving us a unique insight into how autism presents in the developing brain.”

“The finding that these defects occur in patches rather than across the entirety of cortex gives hope as well as insight about the nature of autism,” added Courchesne.

According to the scientists, such patchy defects, as opposed to uniform cortical pathology, may help explain why many toddlers with autism show clinical improvement with early treatment and over time. The findings support the idea that in children with autism the brain can sometimes rewire connections to circumvent early focal defects, raising hope that understanding these patches may eventually open new avenues to explore how that improvement occurs.

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