UC Science Today

Autism is five times more common in boys than girls, and a recent study at the University of California, San Francisco suggests a possible explanation for what’s called the Female Protective Effect. Using zebrafish carrying a gene known to lead to autism in humans, researcher Matthew State found that estrogens, an important hormone in females, reversed autism-like behavior.

"From our genetic studies, we’ve identified that genetic changes that lead to autism in girls, as a general proposition, are more numerous and carry larger effects than they do in boys. And what that suggests is that you need more of a disturbance in girls, in order to get the same outcome as you do in boys. If you knew what the protective factor was, you would understand not only something about the biology of autism, but you would also understand something about the biology of resilience to autism risk."

State hopes these insights will eventually lead to ways to treat or prevent autism.

Autism is five times more common in boys than girls, and a recent study at the University of California, San Francisco suggests a possible explanation for what’s called the Female Protective Effect. Using zebrafish carrying a gene known to lead to autism in humans, researcher Matthew State found that estrogens, an important hormone in females, reversed autism-like behavior.

"From our genetic studies, we’ve identified that genetic changes that lead to autism in girls, as a general proposition, are more numerous and carry larger effects than they do in boys. And what that suggests is that you need more of a disturbance in girls, in order to get the same outcome as you do in boys. If you knew what the protective factor was, you would understand not only something about the biology of autism, but you would also understand something about the biology of resilience to autism risk."

State hopes these insights will eventually lead to ways to treat or prevent autism.

Researchers have never identified a biological process linking sleep and depression – until now. Study leader Louis Ptacek and his team at the University of California, San Francisco found a gene mutation in a family suffering from both a chronic sleep disorder and seasonal depression. The team engineered mice and fly models with the genetic mutation to see how changes in light exposure, or the length of daylight, affected behavior.

"And since we had generated the animal models of the human mutation and showed that they have a circadian phenotype, we tested whether they had a depression-like phenotype."

It turns out that extreme changes in light exposure, such as that caused by very short days, elicited depression-like behavior in mice. Although animal models cannot be directly extended to humans, Ptacek says the study suggests a mechanism behind these disorders in people.

"Part of our mission moving forward is to really push the notion that we can improve health through better sleep."

Researchers have never identified a biological process linking sleep and depression – until now. Study leader Louis Ptacek and his team at the University of California, San Francisco found a gene mutation in a family suffering from both a chronic sleep disorder and seasonal depression. The team engineered mice and fly models with the genetic mutation to see how changes in light exposure, or the length of daylight, affected behavior.

"And since we had generated the animal models of the human mutation and showed that they have a circadian phenotype, we tested whether they had a depression-like phenotype."

It turns out that extreme changes in light exposure, such as that caused by very short days, elicited depression-like behavior in mice. Although animal models cannot be directly extended to humans, Ptacek says the study suggests a mechanism behind these disorders in people.

"Part of our mission moving forward is to really push the notion that we can improve health through better sleep."

Researchers have never identified a biological process linking sleep and depression – until now. Study leader Louis Ptacek and his team at the University of California, San Francisco found a gene mutation in a family suffering from both a chronic sleep disorder and seasonal depression. The team engineered mice and fly models with the genetic mutation to see how changes in light exposure, or the length of daylight, affected behavior.

"And since we had generated the animal models of the human mutation and showed that they have a circadian phenotype, we tested whether they had a depression-like phenotype."

It turns out that extreme changes in light exposure, such as that caused by very short days, elicited depression-like behavior in mice. Although animal models cannot be directly extended to humans, Ptacek says the study suggests a mechanism behind these disorders in people.

"Part of our mission moving forward is to really push the notion that we can improve health through better sleep."

The University of California launched the UC Cures for Alzheimer’s Disease Initiative to accelerate the development of promising Alzheimer’s disease research by scientists throughout the university system. UC President Janet Napolitano says the university is already playing a critical role in the field by conducting basic research and clinical trials.

"We want to focus our research efforts in part because we can see the future that there is progress to be made here, and we have the laboratories, the scientists, the post-docs, the students, the resources available to put mass on target for this disease, which is terrible for anyone who has a loved one or has experience being in contact with someone suffering from Alzheimer’s, but also because of the aging of the U.S. population, we know it’s only going to grow in prevalence."

The goal of the initiative is to move research for potential treatments into early proof-of-concept clinical trials.

The University of California launched the UC Cures for Alzheimer’s Disease Initiative to accelerate the development of promising Alzheimer’s disease research by scientists throughout the university system. UC President Janet Napolitano says the university is already playing a critical role in the field by conducting basic research and clinical trials.

"We want to focus our research efforts in part because we can see the future that there is progress to be made here, and we have the laboratories, the scientists, the post-docs, the students, the resources available to put mass on target for this disease, which is terrible for anyone who has a loved one or has experience being in contact with someone suffering from Alzheimer’s, but also because of the aging of the U.S. population, we know it’s only going to grow in prevalence."

The goal of the initiative is to move research for potential treatments into early proof-of-concept clinical trials.

The University of California launched the UC Cures for Alzheimer’s Disease Initiative to accelerate the development of promising Alzheimer’s disease research by scientists throughout the university system. UC President Janet Napolitano says the university is already playing a critical role in the field by conducting basic research and clinical trials.

"We want to focus our research efforts in part because we can see the future that there is progress to be made here, and we have the laboratories, the scientists, the post-docs, the students, the resources available to put mass on target for this disease, which is terrible for anyone who has a loved one or has experience being in contact with someone suffering from Alzheimer’s, but also because of the aging of the U.S. population, we know it’s only going to grow in prevalence."

The goal of the initiative is to move research for potential treatments into early proof-of-concept clinical trials.

Developing clean, renewable energy sources is a global challenge. But through advances in semiconductor nanowire technology, University of California, Berkeley chemist Peidong Yang has a potential game-changer in the field of artificial photosynthesis. Yang and his colleagues are developing a way to capture carbon dioxide from the air and turn it into a sustainable transportation fuel. Yang says the whole system looks like a semiconductor chip.

"They look like a forest of nanowires. And underneath these forests basically, we culture these bacteria. So the bacteria basically is directly attached to the semiconductor surface."

This artificial forest of nanowires could reduce carbon dioxide from the air in part by generating enough energy from sunlight.

Basically it provides the capability to capture as much as possible, the solar spectrum, because that’s the energy input to these carbon dioxide reduction reactions. Second, it provides interface with these bacteria so that the bacteria can take the energy and the electron from the whole process and do the next step, which is the CO2 reduction.

Developing clean, renewable energy sources is a global challenge. But through advances in semiconductor nanowire technology, University of California, Berkeley chemist Peidong Yang has a potential game-changer in the field of artificial photosynthesis. Yang and his colleagues are developing a way to capture carbon dioxide from the air and turn it into a sustainable transportation fuel. Yang says the whole system looks like a semiconductor chip.

"They look like a forest of nanowires. And underneath these forests basically, we culture these bacteria. So the bacteria basically is directly attached to the semiconductor surface."

This artificial forest of nanowires could reduce carbon dioxide from the air in part by generating enough energy from sunlight.

Basically it provides the capability to capture as much as possible, the solar spectrum, because that’s the energy input to these carbon dioxide reduction reactions. Second, it provides interface with these bacteria so that the bacteria can take the energy and the electron from the whole process and do the next step, which is the CO2 reduction.