Category Archives: University of California, Berkeley

We say these relationships are our most difficult

Participants surveyed for a new study were more apt to report that the most difficult people in their lives were female family members such as wives, mothers, and sisters, researchers report.

“With female relatives, it can be a two-sided thing. They may be the people you most depend on, but also the people who nag you the most.”

Close female kin may be disproportionately named as difficult because they’re more likely to be actively and emotionally involved in people’s lives, researchers say.

“The message here is that, with female relatives, it can be a two-sided thing. They may be the people you most depend on, but also the people who nag you the most,” says senior author Claude Fischer, a sociology professor at the University of California, Berkeley. “It’s a testament to their deeper engagement in social ties.”

Family, not friends

Overall, the findings show that, on average, about 15 percent of the relationships that survey takers talked about were categorized as difficult, and that their conflicts were most often with close kin such as parents, siblings, and spouses.

Friends were least likely to be difficult, representing about 6 or 7 percent of the annoying members of social circles for both younger and older adults.

“Social ties can be as much a source of stress as a source of joy…”

“The results suggest that difficult people are likely to be found in contexts where people have less freedom to pick and choose their associates,” says Shira Offer, a professor of sociology at Bar-Ilan University and lead author of the study, which appears in American Sociological Review.

Researchers analyzed relationship data from more than 1,100 younger and older adults in the San Francisco Bay Area, more than half of whom are female, using the University of California Social Networks Study (UCNets), of which Fischer is the principle investigator.

Launched in 2015, the multiyear UCNets survey uses face-to-face and online interviews to assess how people’s social connections affect their health and happiness.

“It’s commonly agreed that maintaining strong social ties is healthy,” Fischer says. “But social ties can be as much a source of stress as a source of joy, and so it’s important to understand how different relationships affect our health and well-being.”

Who do we find most difficult?

Offer and Fischer studied more than 12,000 relationships that included casual friendships, work relations, and close family bonds.

The researchers asked participants to name the people with whom they engaged in different social activities and, of those, identify the ones they found difficult or burdensome.

The relationship categories were divided into “difficult only,” meaning ties that participants mentioned solely as difficult, and “difficult engaged in exchange ties,” meaning relationships that are considered difficult but that also include confiding in, and giving and/or receiving emotional and practical support.

Younger people aged 21 to 30 named more “difficult engaged” people in their lives (16 percent) than the older cohort. They most frequently described sisters (30 percent), wives (27 percent), and mothers (24 percent) as being burdensome, and to a lesser degree fathers, brothers, boyfriends, and roommates.

Older people in their 50s, 60s, and 70s identified about 8 percent of the people in their social networks as “difficult engaged.” Topping their list were mothers (29 percent), female romantic partners (28 percent), and fathers and housemates tied at 24 percent.

Tension with mom and siblings predicts midlife depression

As for relationships with coworkers and other acquaintances, younger people named a little over 11 percent of those connections as difficult only. For older people, that number was slightly higher, amounting to 15.5 percent of acquaintances and 11.7 percent of coworkers. Overall, workplaces were hotbeds of trouble, but not of the “difficult engaged” kind.

So, why don’t we get rid of the difficult people in our lives? Fischer has an answer.

“Whether it’s an alcoholic father whom you want to cut ties with, an annoying friend with whom you have a long history, or an overbearing boss, relationships are complicated and in many cases unavoidable.”

Source: UC Berkeley

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‘Pillows’ reveal when oceans got spurt of oxygen

The transition to a world with an oxygenated deep ocean occurred between 540 and 420 million years ago, new research suggests.

Researchers attribute the change to an increase in atmospheric O2 to levels comparable to the 21 percent oxygen in the atmosphere today.

This inferred rise comes hundreds of millions of years after the origination of animals, which occurred between 700 and 800 million years ago.

pillow basalt
By measuring the oxidation of iron in pillow basalts from undersea volcanic eruptions, scientists have more precisely dated the oxygenation of the deep ocean, inferring from that when oxygen levels in the atmosphere rose to current high levels. (Credit: UC Berkeley)

“The oxygenation of the deep ocean and our interpretation of this as the result of a rise in atmospheric O2 was a pretty late event in the context of Earth history,” says Daniel Stolper, an assistant professor of Earth and planetary science at the University of California, Berkeley.

“This is significant because it provides new evidence that the origination of early animals, which required O2 for their metabolisms, may have gone on in a world with an atmosphere that had relatively low oxygen levels compared to today.”

Tracing oxygen’s history

Oxygen has played a key role in the history of Earth, not only because of its importance for organisms that breathe it, but because of its tendency to react, often violently, with other compounds to make iron rust, plants burn, and natural gas explode.

Tracking the concentration of oxygen in the ocean and atmosphere over Earth’s 4.5-billion-year history isn’t easy. For the first 2 billion years, most scientists believe very little oxygen was present in the atmosphere or the oceans.

About 2.5-2.3 billion years ago, however, atmospheric oxygen levels first increased. The geologic effects of this are evident: rocks on land exposed to the atmosphere suddenly began turning red as the iron in them reacted with oxygen to form iron oxides similar to how iron metal rusts.

Earth scientists have calculated that around this time, atmospheric oxygen levels exceeded about a hundred thousandth of today’s level (0.001 percent) for the first time, but still remained too low to oxygenate the deep ocean, which stayed largely anoxic.

By 400 million years ago, fossil charcoal deposits first appear, an indication that atmospheric O2 levels were high enough to support wildfires, which require about 50 to 70 percent of modern oxygen levels, and oxygenate the deep ocean. How atmospheric oxygen levels varied between 2,500 and 400 million years ago is less certain and remains a subject of debate.

“Filling in the history of atmospheric oxygen levels from about 2.5 billion to 400 million years ago has been of great interest given O2‘s central role in numerous geochemical and biological processes. For example, one explanation for why animals show up when they do is because that is about when oxygen levels first approached the high atmospheric concentrations seen today,” Stolper says.

“This explanation requires that the two are causally linked such that the change to near-modern atmospheric O2 levels was an environmental driver for the evolution of our oxygen-requiring predecessors,” he says.

In contrast, some researchers think the two events are largely unrelated. Critical to helping to resolve this debate is pinpointing when atmospheric oxygen levels rose to near modern levels. But past estimates of when this oxygenation occurred range from 800 to 400 million years ago, straddling the period during which animals originated.

‘Submarine’ volcanic eruptions

The researchers hoped to pinpoint a key milestone in Earth’s history: when oxygen levels became high enough—about 10 to 50 percent of today’s level—to oxygenate the deep ocean. Their approach is based on looking at the oxidation state of iron in igneous rocks formed undersea (referred to as “submarine”) volcanic eruptions, which produce “pillows” and massive flows of basalt as the molten rock extrudes from ocean ridges.

How 1 key nutrient limited life in ancient oceans

Critically, after eruption, seawater circulates through the rocks. Today, these circulating fluids contain oxygen and oxidize the iron in basalts. But in a world with deep-oceans devoid of O2, they expected little change in the oxidation state of iron in the basalts after eruption.

“Our idea was to study the history of the oxidation state of iron in these basalts and see if we could pinpoint when the iron began to show signs of oxidation and thus when the deep ocean first started to contain appreciable amounts of dissolved O2,” Stolper says.

To do this, they compiled more than 1,000 published measurements of the oxidation state of iron from ancient submarine basalts.

The researchers found that the basaltic iron only becomes significantly oxidized relative to magmatic values between about 540 and 420 million years ago, hundreds of millions of years after the origination of animals. They attribute this change to the rise in atmospheric O2 levels to near modern levels. This finding is consistent with some but not all histories of atmospheric and oceanic O2 concentrations.

“This work indicates that an increase in atmospheric O2 to levels sufficient to oxygenate the deep ocean and create a world similar to that seen today was not necessary for the emergence of animals,” Stolper says.

“Additionally, the submarine basalt record provides a new, quantitative window into the geochemical state of the deep ocean hundreds of millions to billions of years ago,” he says.

Will animals need ‘oxygen tanks’ as oceans warm?

The researchers report their findings in the journal Nature.

Source: UC Berkeley

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CRISPR knocks out ALS gene mutation in mice

For the first time, scientists have used CRISPR-Cas9 gene editing to disable a defective gene that causes amyotrophic lateral sclerosis, or Lou Gehrig’s disease, in mice.

The therapy delayed the onset of the muscle wasting that characterizes the disease, which results in progressive weakness and eventually proves fatal when the muscles that control breathing fail, and extended the lifespan of the mice by 25 percent.

Rescuing motor neurons

Researchers genetically engineered the mice to express a mutated human gene that, in humans, causes about 20 percent of all inherited forms of the disease and about 2 percent of all cases of ALS worldwide.

Though the genetic cause is not known for all cases of ALS, all are accompanied by the premature death of motor neurons in the brain stem and spinal cord. The neurons allow the brain to control muscles, so loss of this connection means loss of muscle control.

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Diagram of an adeno-associated virus, a benign virus Schaffer uses to ferry Cas9 genes into brain and spinal cord cells. Schaffer ‘evolves’ these viruses to target specific types of cells and to avoid immune cells that try to destroy them. (Credit: UC Berkeley)

“Being able to rescue motor neurons and motor neuron control over muscle function, especially the diaphragm, is critically important to being able to not only save patients, but also maintain their quality of life,” says senior author David Schaffer, a professor of chemical and biomolecular engineering and director of the University of California, Berkeley’s Stem Cell Center.

The devastating disease usually strikes people between the ages of 40 and 70. An estimated 20,000 Americans are afflicted, and there are no treatments to slow the muscle degeneration.

The research team used a virus that Schaffer’s team engineered to seek out only motor neurons in the spinal cord and deliver a gene encoding the Cas9 protein into the nucleus. There, the gene was translated into the Cas9 protein, a molecular scissors that cut and disabled the mutant gene responsible for ALS.

Cautious optimism

In this case, researchers programmed Cas9 to knock out only the mutated gene SOD1 (superoxide dismutase 1). The onset or start of the disease was delayed by almost five weeks, and mice treated by the gene therapy lived about a month longer than the typical four-month lifespan of mice with ALS. Healthy mice can live a couple of years.

The researchers found that, at death, the only surviving motor neuron cells in the mice were those that had been “infected” with the virus and contained Cas9 protein, says Thomas Gaj, a postdoctoral fellow who led the study, now at the University of Illinois at Urbana-Champaign.

“The treatment did not make the ALS mice normal and it is not yet a cure,” Schaffer cautions. “But based upon what I think is a really strong proof of concept, CRISPR-Cas9 could be a therapeutic molecule for ALS. When we do additional optimization of the delivery to get CRISPR-Cas9 into an even higher percentage of cells, we think we are going to see even better increases in lifespan.”

A cross-section of mouse spinal cord tissue
A cross-section of mouse spinal cord tissue showing cells in which the CRISPR-Cas9 gene has been expressed (green). The Cas9 gene has been successfully inserted into motor neurons (yellow), rescuing them from death, but not the support cells called astrocytes (red). The research team is now developing improved viral vectors to insert the Cas9 gene into astrocytes so that their death does not also kill surviving motor neurons. (Credit: David Schaffer/UC Berkeley)

One of several challenges is to eliminate the SOD1 mutation in other brain and spinal cord cells that support motor neurons. Schaffer’s team is designing a version of the virus—a highly modified adeno-associated virus, or AAV—that will deliver the Cas9 gene to two types of glial cells, astrocytes and oligodendrocytes, that appear to take out neighboring motor neurons, effectively a “bystander effect.”

“I tend to be really cautious, but in this case I would be quite optimistic that if we are able to eliminate SOD1 within not just the neurons but also the astrocytes and supporting glia, I think we are going to see really long extensions of lifespan,” he says.

Schaffer also is working on a self-destruct switch for the Cas9 protein, so that once it knocks out the SOD1 gene, the Cas9 can be eliminated from the cell so as not to accidentally modify other genes or trigger an immune reaction.

Vehicle plus cargo

Schaffer has been working with the AAV virus for nearly 20 years, evolving it to target specific cells, like motor neurons, without infecting other types of cells. AAV is found in many if not all humans and primates, and appears to be benign.

Using CRISPR against cancer shows success in mice

“We have engineered new AAV vehicles that are capable of high-efficiency delivery to a number of cell and tissue targets in the body, and when CRISPR-Cas9 came along, we viewed it as a wonderful opportunity to put together this incredibly powerful cargo with the ability to carry that cargo to a number of cells and disease targets in vivo,” he says.

The Food and Drug Administration is likely to approve a modified AAV as a delivery vehicle for a gene therapy against a rare disease called Leber congenital amaurosis type 2 soon, and other therapies delivered by AAV are in the pipeline, Schaffer says.

These therapies are currently based on natural versions of AAV, however, which are not optimized for high-efficiency delivery to most therapeutically important cell targets, so clinicians must either use massive doses or apply the AAV using an invasive surgery.

Schaffer has developed technology to engineer viruses for targeted delivery to many cells and tissues following simple routes of administration, for example directly into tissue such as the eye and brain. This led him to cofound a company in 2014, 4D Molecular Therapeutics, to optimize AAV to target any tissue and carry a variety of gene therapies into cells.

“Researchers in the field really know we need better vectors that can target cells through a simple, logical route of administration, and can do so in a very, very efficient way,” he says. “Ours do.”

How CRISPR could fight genetic hearing loss

The researchers report their findings in the journal Science Advances.

Support for the research came from the National Institutes of Health. Additional coauthors of the paper from UC Berkeley are Thomas Gaj, David Ojala, Freja Ekman, Leah Byrne, and Prajit Limsirichai.

Source: UC Berkeley

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This keeps older adults from ‘saving’ memories during sleep

For older adults, slow and speedy brain waves must sync up at exactly the right moment during sleep to move new memories into long-term storage, according to a new study.

While these brain rhythms, occurring hundreds of times a night, move in perfect lockstep in young adults, findings published in the journal Neuron show that, in old age, slow waves during non-rapid eye movement (NREM) sleep fail to make timely contact with speedy electrical bursts known as “spindles.”

“…there is a silver lining: Sleep is now a new target for potential therapeutic intervention.”

“The mistiming prevents older people from being able to effectively hit the save button on new memories, leading to overnight forgetting rather than remembering,” says study senior author Matthew Walker,  professor of neuroscience and psychology and director of the Center for Human Sleep Science at the University of California, Berkeley.

“As the brain ages, it cannot precisely coordinate these two deep-sleep brain waves,” Walker adds. “Like a tennis player who is off their game, they’re swiping and missing.”

In tennis lingo, the slow brainwaves or oscillations represent the ball toss while the spindles symbolize the swing of the racket as it aims to make contact with the ball and serve an ace.

“Timing is everything. Only when the slow waves and spindles come together in a very narrow opportunity time window (approximately one-tenth of a second), can the brain effectively place new memories into its long-term storage,” says study lead author Randolph Helfrich, a postdoctoral fellow in neuroscience.

Moreover, researchers found that the aging brain’s failure to coordinate deep-sleep brainwaves is most likely due to degradation or atrophy of the medial frontal cortex, a key region of the brain’s frontal lobe that generates the deep, restorative slumber that we enjoy in our youth.

“The worse the atrophy in this brain region of older adults, the more uncoordinated and poorly timed are their deep-sleep brainwaves,” Walker says. “But there is a silver lining: Sleep is now a new target for potential therapeutic intervention.”

Brain clutter makes older adults doubt memories

To amplify slow waves and get them into optimal sync with spindles, researchers plan to apply electrical brain stimulation to the frontal lobe in future experiments.

“By electrically boosting these nighttime brainwaves, we hope to restore some degree of healthy deep sleep in the elderly and those with dementia, and in doing so, salvage aspects of their learning and memory,” Walker says.

For the study, researchers compared the overnight memory of 20 healthy adults in their 20s to that of 32 healthy older adults, mostly in their 70s. Before going to bed for a full night’s sleep, participants learned and were then tested on 120 word sets.

As they slept, researchers recorded their electrical brain-wave activity using scalp electroencephalography (EEG). The next morning, study participants were tested again on the word pairs, this time while undergoing functional and structural magnetic resonance imaging (fMRI) scans.

The EEG results showed that in older people, the spindles consistently peaked early in the memory-consolidation cycle and missed syncing up with the slow waves.

Moreover, brain imaging showed grey matter atrophy in the medial frontal cortex of older adults, which suggests that deterioration within the frontal lobe prevents deep slow waves from perfectly syncing up with spindles.

Insomnia drugs may up fall risk for older adults

In addition to Walker and Helfrich, Robert Knight and William Jagust of UC Berkeley and Bryce Mander, now of UC Irvine, are coauthors of the study.

Source: UC Berkeley

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This molecule may stop glaucoma’s progress

Naturally occurring molecules known as lipid mediators could potentially halt the progress of glaucoma, new research suggests.

“We know of no drug that can do this.”

The world’s second-leading cause of blindness, glaucoma is a neurodegenerative disease in which fluid buildup in the frontal eye causes irreversible damage to the optic nerve and vision loss. At present, there is no cure for glaucoma, which is estimated to affect 80 million people worldwide.

“Not only could this discovery lead to drugs to treat glaucoma, but the same mechanism, and options for prevention, may be applicable to other neurodegenerative diseases,” says study senior author Karsten Gronert, professor of optometry and chair of vision science at University of California, Berkeley.

Preventing damage

Using rodent models, Gronert and fellow researchers found that inflammation-regulating lipid mediators known as lipoxins, secreted from star-shaped cells known as astrocytes, stopped the degeneration of retinal ganglion cells in rats and mice with glaucoma. Ganglion cells are the neurons of the retina and optic nerve that receive information from photoreceptors.

“We’ve taken something everyone assumed was anti-inflammatory, and found that these same small molecules play a key role in neuroprotection, which is really exciting,” says study co-senior author John Flanagan, dean and professor of optometry.

“This little-known lipid mediator has shown the potential to reverse cell death…”

Specifically, researchers found that astrocytes, which help maintain brain function and form the nerve fiber layer of the retina and optic nerve, release therapeutic biological agents known as lipoxins A4 and B4, but only when the astrocytes are at rest and maintaining nerve function.

“It is commonly assumed that astrocytes activated by injuries release stress signals that kill off ganglion cells in the retina, causing optic nerve damage,” says Flanagan. “However, our research discovered that astrocytes that are triggered by injury actually turn off novel neuroprotective signals that prevent optic nerve damage.”

Researchers discovered secretions of lipoxins A4 and B4 in resting astrocytes in culture in the retina and optic nerve head. To test their potential as a treatment, they administered the lipoxins to rodents eight weeks after the onset of glaucoma-like damage and neurodegeneration.

At 16 weeks, they gauged electrical activity in the rodents’ ganglion cells, among other measures, and found that lipoxin B4 in particular stopped the cells’ degeneration.

“This little-known lipid mediator has shown the potential to reverse cell death,” Gronert says. “We know of no drug that can do this.”

‘Great potential’

For decades, pharmaceutical companies have searched for neuroprotective drugs to treat glaucoma and other disorders marked by the death of nerve cells such as Alzheimer’s, Parkinson’s, and ALS. Glaucoma is by far the most prevalent of these neurodegenerative diseases.

Glaucoma biomarker may predict speed of vision loss

“At the same time, lipoxins have been explored as promising drug targets for treating inflammatory diseases, but nobody has been looking at them as being neuroprotective,” Gronert says.

At present, the treatment option for glaucoma is to lower ocular pressure, but there are no effective treatments for preventing or stopping the neurodegeneration of glaucoma, which is irreversible and eventually leads to blindness, Flanagan says

The study authors are excited at the prospect of further investigations into the therapeutic benefits and mechanisms of lipoxins A4 and B4 and their potential to stop or reverse neural damage. They have jointly filed a patent application for use of lipoxins A4 and B4 to treat glaucoma and neurodegenerative diseases. Their eventual goal is to test the lipoxins as drugs in humans.

“These naturally occurring small lipids have great potential as therapies because they may play a fundamental role in preventing other neurodegenerative diseases. And that’s hugely significant, ” Flanagan says.

New way of imaging eyes could spot glaucoma sooner

Additional researchers contributing to the study are from UC Berkeley and the University of Toronto.

The researchers detail their findings in the Journal of Clinical Investigation.

Source: Purdue University

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Watch: How museum moths end up on pins

Natural history museums are full of specimens, including mounted examples of butterflies, moths, beetles, and other insects.

In the video above, Peter Oboyski, collections manager at the UC Berkeley Museum of Entomology, shows how the process works.

In addition, here’s a look behind the scenes at the “museum of bugs” and into their “oh my” collection:

Source: Marica Petry for UC Berkeley

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Cactus genomes reveal complex family tree

When scientists sequenced the complete genomes of four columnar cacti, they were surprised to find that their family relationships are not as straightforward as their shapes suggest.

The cactus family tree and the giant cacti in particular—the giant saguaro, organ pipe, senita, and cardón, also called the Mexican giant cactus—have been very difficult to trace.

Found only in the Americas, cacti have adapted to a broad range of environments. The current count is 1,438 species, but scientists disagree by a factor of 10 about how many genera of cacti the species represent.

That’s in part because the same traits—succulence and a columnar form, for example—seem to have evolved separately in different lineages: what’s known as parallel evolution.

Ancient genes

For a new study in the Proceedings of the National Academy of Sciences, researchers created individual family trees of each gene shared across all species.

The findings show that their histories were scrambled as a result of long generation times—saguaro cacti can live 150 years or more—making the relationships among the species even with complete genomic information difficult to understand.

They did determine, however, that some similarities, like the succulent flesh that makes some cacti a good emergency source of water, resulted from ancient genes that were retained by some cacti but lost by others.

What looked like parallel evolution, with some species gaining new genes and new functions, was actually just the random loss of genes in all the other species.

Losing ground

The findings could have implications for the fate of these cacti, which are losing habitat because of human development in arid areas of the Americas.

“Many species are endangered, and the fact that we don’t understand their relationships makes this fraught,” says Noah Whiteman, associate professor of integrative biology at the University of California, Berkeley, and a faculty member with the Center for Computational Biology and an affiliate of the University and Jepson Herbaria and the Museum of Vertebrate Zoology.

The work also addresses a recently recognized complication in interpreting the evolution of all plants and animals.

Without much rain, roots dive deep to find water

“Only with whole-genome sequencing were we able to see this pattern of incomplete lineage sorting, called hemiplasy, which looks superficially like convergent or parallel evolution, or homoplasy,” he says.

“It’s an important advance because one could mistake such patterns as evidence for parallel evolution at the molecular level, which is a hot topic in evolutionary biology right now.”

Other coauthors are from the University of Arizona and the Universidad Nacional Autónoma de México.

Source: UC Berkeley

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How mosquitoes get away before you can slap them

Strong, rapid wing beats with hardly any push off let mosquitoes make a fast getaway.

The technique is in stark contrast to other insects, like flies, that push off first and then start beating their wings frantically, often tumbling uncontrollably in the process. That strong push off also lets us know they’re there before they have a chance to escape.

“Mosquitoes take off mostly with their wings and push off with their legs very, very lightly, or maybe not at all,” says Sofia Chang, a graduate student at the University of California, Berkeley who wrangled and fed malarial mosquitoes in order to study their takeoffs.

Mosquitoes are able to make these stealthy takeoffs with an empty belly or one filled with a blood meal, which nearly doubles their weight.

“If they were to push off a lot more with their legs, they wouldn’t have to produce as much lift with their wings. But if they lift just with their wings, you won’t feel them coming off your skin.”

Mosquitoes are able to make these stealthy takeoffs both with an empty belly and one filled with a blood meal, which nearly doubles their weight.

Working in the laboratory of Florian Muijres at Wageningen University in the Netherlands, Chang cycled through 600 mosquitoes as the team perfected its setup to film mosquito takeoffs with three high-speed cameras shooting at 125,000 frames per second.

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Photomontage of a blood-fed mosquito taking off. (Credit: Florian Muijres)

Chang initially fed them blood from her own arm before Wageningen University entomologist Jeoren Spitzen contributed the expertise and equipment to feed them artificially.

The team used the mosquito species Anopheles coluzzii—which can carry malaria but was kept sterile during the experiment—in hopes of finding clues to flight maneuvers that could be used against them.

“These studies may also give tips about how to build very, very small robots. That is a field where miniaturization is a Holy Grail,” Chang says.

600 beats per second

Chang and colleagues, including UC Berkeley integrative biology professors Robert Dudley and Mimi Koehl, were primarily interested in how insects alter their takeoffs when carrying extra weight, like a blood meal.

The high-speed cameras captured stark silhouettes of the mosquitoes and their beating wings, which Muijres was able to turn into three-dimensional renderings of the wingbeats to help calculate lift and other aerodynamic forces. Of the many mosquitoes filmed, 63 videos were analyzed in the study: 32 of blood-laden mosquitoes, 31 unfed.

The researchers were surprised to find that the mosquitoes began beating their wings about 30 milliseconds before liftoff using an extraordinarily high—and annoyingly whining—wing-beat frequency of about 600 beats per second. Other similarly sized insects beat their wings about 200 times per second.

The insects took advantage of their exceptionally long legs to extend them gently and push down slowly over the 30 milliseconds before takeoff, lifting free with barely a rebound. The wings’ contribution to the takeoff was at least 60 percent of the force—and possibly all of what is needed to lift a well-fed mosquito off the skin.

“Instead of going fast, they take their time, but they accelerate the entire time so that they reach a final velocity pretty much the same as fruit flies,” Chang says. “That is something that might be unique to mosquitoes, and maybe even unique to blood feeders.”

Mosquitoes vs. fruit flies

Fruit flies exerted almost four times the force exerted by mosquitoes during takeoff. Coauthor Bart Biemans compared the anatomy of the mosquitoes’ and fruit flies’ leg muscles and found that mosquitoes are missing the quick-kick muscles that fruit flies have, presumably “because [mosquitoes] need to produce a lower force at pushoff,” Muijres says.

The videos show that female mosquitoes carrying blood meals generate the extra lift they need to take off with such heavy loads by sweeping their wings across a greater distance during each wingbeat than do mosquitoes that are not carrying loads,” Koehl says.

The team next plans to look at mosquito landings, which are equally stealthy, and compare them to takeoffs and landings of other blood-sucking insects and non-blood-sucking mosquitoes, to determine if they exert a similarly light touch.

Mosquitoes only mate once and 4 other facts

The National Science Foundation and the Wageningen Institute of Animal Sciences funded the work that appears in the Journal of Experimental Biology.

Source: UC Berkeley

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First trimester fevers may cause birth defects

Fever during the first trimester of pregnancy may boost the risk of heart defects and facial deformities such as cleft lip or palate.

Researchers have known about the risks for decades, but how it happens has been unclear. Is a virus or other infection source—or fever alone—the underlying problem?

Now, a new study in Science Signaling points to the fever itself, not its root source, that can interfere with the development of the heart and jaw during the first three to eight weeks of pregnancy.

“Our study identified a specific molecular pathway that links maternal fever directly to some of those defects.”

The findings, demonstrated in animal embryos, provide new leads as scientists continue investigating heart defects, which affect 1 percent of live births in the US, and cleft lip or palate, affecting about 4,000 infants per year.

“Congenital heart and cranial facial defects are very common in live births, but most of the time they have unknown causes,” says co-senior author Chunlei Liu, an associate professor of neuroscience and electrical engineering and computer sciences at the University of California, Berkeley. “Our study identified a specific molecular pathway that links maternal fever directly to some of those defects.”

The animal models suggest a portion of congenital birth defects in humans might be prevented if fevers are treated through means including the judicious use of acetaminophen during the first trimester, says co-senior author Eric Benner, a neonatologist and assistant professor of pediatrics at Duke University.

Take some Tylenol?

“My hope is that right now, as women are planning to become pregnant and their doctors advise them to start taking prenatal vitamins and folic acid, their doctor also informs them if they get a fever, they should not hesitate to call and consider taking a fever reducer, specifically acetaminophen (Tylenol), which has been studied extensively and determined to be safe during the first trimester.

“While doctors advise most women to avoid any drug during pregnancy, there may be benefits to taking acetaminophen to reduce fever. Women should discuss all risks and benefits with their doctors.”

Benner cautions that nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and aspirin also reduce fevers, but women shouldn’t use aspirin, naproxen, or ibuprofen during pregnancy. There is also ongoing debate over whether sustained use of acetaminophen is safe during pregnancy to manage ongoing conditions such as arthritis, he says.

“However, its judicious use for an acute problem such as fever is considered safe. These findings suggest we can reduce the risk of birth defects that otherwise could lead to serious health complications requiring surgery.”

Neural crest cells

To observe how fever impacts a developing fetus, researchers studied zebrafish and chicken embryos and found that neural crest cells—cells that are critical building blocks for the heart, face, and jaw—contain temperature-sensitive properties.

“We found that these neural crest cells contain temperature-sensitive ion channels that typically are found in your sensory neurons,” Benner says. “They’re the channels that, when you stick your hand in a hot cup of water, tell your body the temperature has changed.”

Researchers engineered a noninvasive magnet-based technology to create fever-like conditions in two specific temperature-sensitive ion channels called TRPV1 and TRPV4 in the neural crest cells involved in developing the heart and face.

When those neural crest cells were subjected to conditions mimicking a transient fever, the embryos developed craniofacial irregularities and heart defects, including double outlet right ventricle, Tetralogy of Fallot, and other outflow obstructions.

Women “shouldn’t just tough it out if they develop a fever.”

“With electrical magnetic waves coupled with engineered ion channel proteins, we are able to impact specific biological cells remotely without affecting other biochemical environments,” Liu says. “The technique can be applied to study many different cell types and their roles at various developmental stages.”

The type of defect depends on whether the fever occurs during heart development or head and face development in the embryo. What researchers still don’t know is whether or how the severity or duration of a fever impacts development.

“We have known since the early 1980s that fevers are associated with birth defects, but how that was happening has been a complete mystery,” Benner says. It is challenging to gather data from mothers on the circumstances, severity, or duration of a fever from many months before.

“I hope moving forward, we can educate more women about fever as a risk factor for birth defects and let them know they shouldn’t just tough it out if they develop a fever,” Benner says. “They should ask their doctor before getting pregnant whether they may benefit from taking a fever-reducer such as acetaminophen in the event they develop a fever.”

The Jean and George Brumley Jr. Neonatal Perinatal Research Institute, the Zeist Foundation, the Hartwell Foundation, the Mandel Foundation, the Duke Health Scholars Award, the American Heart Association, and the National Institutes of Health supported the work.

Benner and Liu have filed a patent application relating to the use of FeRIC technology for cell modulation and treatments.

Source: Duke University, UC Berkeley

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Parole violations send felons through prison’s ‘revolving door’

New research on the US prison system suggests parole violations—such as failing a drug test or associating with felons—play a central role in people returning to prison and the high prison population in the United States.

“One implication is that mass imprisonment is giving us less crime prevention than we might have assumed…”

The study finds that felons who served time behind bars were more likely to return to prison within five years of their release, compared to equivalent offenders who were sentenced to probation.

Moreover, it found that most of their later returns to prison were due to parole violations rather than new crimes.

“This study shows that the revolving door is primarily a product of post-prison community supervision rather than the commission of new felony crimes, as so many people become trapped in the criminal justice system’s accelerating cycle of surveillance and punishment,” says study lead author David Harding, an associate professor of sociology at the University of California, Berkeley.

The results suggest that alternatives to imprisonment for parole violators, such as treatment programs or community service, might slow down prison’s revolving door, he says.

The findings shed new light on contributors to the soaring US prison population which, according to a Pew Charitable Trusts report, saw a 700-percent increase between 1970 and 2005.

The full cost of incarceration in the United States has been estimated at over $1 trillion when factoring in prisoners’ diminished wages and job prospects, the socio-economic burden to families and communities, as well as government operational costs, according to a study from Washington University in St. Louis.

For this new study, researchers analyzed the criminal records of more than 100,000 people sentenced for violent and nonviolent felonies in Michigan between 2003 and 2006, tracking them through September 2013.

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The researchers’ statistical methods enabled them to determine the extent to which being sentenced to prison rather than probation increased the chances of a future felony conviction or prison term.

The results also showed a small decrease in crime during the time that the offenders were behind bars, and that after their release, they committed slightly fewer crimes than felons who had been sentenced to probation.

“One implication is that mass imprisonment is giving us less crime prevention than we might have assumed,” Harding says.

Parole violations include failing to complete certain programs, breaking curfew, failing a drug or alcohol test, associating with other felons, moving home, or leaving the state without permission.

While not felony crimes per se, these breaches are subject to prison terms and, as this latest study shows, may play an integral role in the growth of prison populations, researchers says.

Additional coauthors of the study are from the University of Michigan and the State University of New York at Albany.

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The study appears in the Proceedings of the National Academy of Sciences.

Source: UC Berkeley

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