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sunaleisocial · 1 year ago

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Mouth-based touchpad enables people living with paralysis to interact with computers

New Post has been published on https://sunalei.org/news/mouth-based-touchpad-enables-people-living-with-paralysis-to-interact-with-computers/

Mouth-based touchpad enables people living with paralysis to interact with computers

When Tomás Vega SM ’19 was 5 years old, he began to stutter. The experience gave him an appreciation for the adversity that can come with a disability. It also showed him the power of technology.

“A keyboard and a mouse were outlets,” Vega says. “They allowed me to be fluent in the things I did. I was able to transcend my limitations in a way, so I became obsessed with human augmentation and with the concept of cyborgs. I also gained empathy. I think we all have empathy, but we apply it according to our own experiences.”

Vega has been using technology to augment human capabilities ever since. He began programming when he was 12. In high school, he helped people manage disabilities including hand impairments and multiple sclerosis. In college, first at the University of California at Berkeley and then at MIT, Vega built technologies that helped people with disabilities live more independently.

Today Vega is the co-founder and CEO of Augmental, a startup deploying technology that lets people with movement impairments seamlessly interact with their personal computational devices.

Augmental’s first product is the MouthPad, which allows users to control their computer, smartphone, or tablet through tongue and head movements. The MouthPad’s pressure-sensitive touch pad sits on the roof of the mouth, and, working with a pair of motion sensors, translates tongue and head gestures into cursor scrolling and clicks in real time via Bluetooth.

“We have a big chunk of the brain that is devoted to controlling the position of the tongue,” Vega explains. “The tongue comprises eight muscles, and most of the muscle fibers are slow-twitch, which means they don’t fatigue as quickly. So, I thought why don’t we leverage all of that?”

People with spinal cord injuries are already using the MouthPad every day to interact with their favorite devices independently. One of Augmental’s users, who is living with quadriplegia and studying math and computer science in college, says the device has helped her write math formulas and study in the library — use cases where other assistive speech-based devices weren’t appropriate.

“She can now take notes in class, she can play games with her friends, she can watch movies or read books,” Vega says. “She is more independent. Her mom told us that getting the MouthPad was the most significant moment since her injury.”

That’s the ultimate goal of Augmental: to improve the accessibility of technologies that have become an integral part of our lives.

“We hope that a person with a severe impairment can be as competent using a phone or tablet as somebody using their hands,” Vega says.

Making computers more accessible

In 2012, as a first-year student at UC Berkeley, Vega met his eventual Augmental co-founder, Corten Singer. That year, he told Singer he was determined to join the Media Lab as a graduate student, something he achieved four years later when he joined the Media Lab’s Fluid Interfaces research group run by Pattie Maes, MIT’s Germeshausen Professor of Media Arts and Sciences.

“I only applied to one program for grad school, and that was the Media Lab,” Vega says. “I thought it was the only place where I could do what I wanted to do, which is augmenting human ability.”

At the Media Lab, Vega took classes in microfabrication, signal processing, and electronics. He also developed wearable devices to help people access information online, improve their sleep, and regulate their emotions.

“At the Media Lab, I was able to apply my engineering and neuroscience background to build stuff, which is what I love doing the most,” Vega says. “I describe the Media Lab as Disneyland for makers. I was able to just play, and to explore without fear.”

Vega had gravitated toward the idea of a brain-machine interface, but an internship at Neuralink made him seek out a different solution.

“A brain implant has the highest potential for helping people in the future, but I saw a number of limitations that pushed me from working on it right now,” Vega says. “One is the long timeline for development. I’ve made so many friends over the past years that needed a solution yesterday.”

At MIT, he decided to build a solution with all the potential of a brain implant but without the limitations.

In his last semester at MIT, Vega built what he describes as “a lollipop with a bunch of sensors” to test the mouth as a medium for computer interaction. It worked beautifully.

“At that point, I called Corten, my co-founder, and said, ‘I think this has the potential to change so many lives,’” Vega says. “It could also change the way humans interact with computers in the future.”

Vega used MIT resources including the Venture Mentoring Service, the MIT I-Corps program, and received crucial early funding from MIT’s E14 Fund. Augmental was officially born when Vega graduated from MIT at the end of 2019.

Augmental generates each MouthPad design using a 3D model based on a scan of the user’s mouth. The team then 3-D prints the retainer using dental-grade materials and adds the electronic components.

With the MouthPad, users can scroll up, down, left, and right by sliding their tongue. They can also right click by doing a sipping gesture and left click by pressing on their palate. For people with less control of their tongue, bites, clenches, and other gestures can be used, and people with more neck control can use head-tracking to move the cursor on their screen.

“Our hope is to create an interface that is multimodal, so you can choose what works for you,” Vega says. “We want to be accommodating to every condition.”

Scaling the MouthPad

Many of Augmental’s current users have spinal cord injuries, with some users unable to move their hands and others unable to move their heads. Gamers and programmers have also used the device. The company’s most frequent users interact with the MouthPad every day for up to nine hours.

“It’s amazing because it means that it has really seamlessly integrated into their lives, and they are finding lots of value in our solution,” Vega says.

Augmental is hoping to gain U.S. Food and Drug Administration clearance over the next year to help users do things like control wheelchairs and robotic arms. FDA clearance will also unlock insurance reimbursements for users, which will make the product more accessible.

Augmental is already working on the next version of its system, which will respond to whispers and even more subtle movements of internal speech organs.

“That’s crucial to our early customer segment because a lot of them have lost or have impaired lung function,” Vega says.

Vega is also encouraged by progress in AI agents and the hardware that goes with them. No matter how the digital world evolves, Vega believes Augmental can be a tool that can benefit everyone.

“What we hope to provide one day is an always-available, robust, and private interface to intelligence,” Vega says. “We think that this is the most expressive, wearable, hands-free operating system that humans have created.”

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jcmarchi · 1 year ago

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Mouth-based touchpad enables people living with paralysis to interact with computers

New Post has been published on https://thedigitalinsider.com/mouth-based-touchpad-enables-people-living-with-paralysis-to-interact-with-computers/

Mouth-based touchpad enables people living with paralysis to interact with computers

When Tomás Vega SM ’19 was 5 years old, he began to stutter. The experience gave him an appreciation for the adversity that can come with a disability. It also showed him the power of technology.

Today Vega is the co-founder and CEO of Augmental, a startup deploying technology that lets people with movement impairments seamlessly interact with their personal computational devices.

That’s the ultimate goal of Augmental: to improve the accessibility of technologies that have become an integral part of our lives.

“We hope that a person with a severe impairment can be as competent using a phone or tablet as somebody using their hands,” Vega says.

Making computers more accessible

Vega had gravitated toward the idea of a brain-machine interface, but an internship at Neuralink made him seek out a different solution.

At MIT, he decided to build a solution with all the potential of a brain implant but without the limitations.

In his last semester at MIT, Vega built what he describes as “a lollipop with a bunch of sensors” to test the mouth as a medium for computer interaction. It worked beautifully.

Augmental generates each MouthPad design using a 3D model based on a scan of the user’s mouth. The team then 3-D prints the retainer using dental-grade materials and adds the electronic components.

“Our hope is to create an interface that is multimodal, so you can choose what works for you,” Vega says. “We want to be accommodating to every condition.”

Scaling the MouthPad

“It’s amazing because it means that it has really seamlessly integrated into their lives, and they are finding lots of value in our solution,” Vega says.

Augmental is already working on the next version of its system, which will respond to whispers and even more subtle movements of internal speech organs.

“That’s crucial to our early customer segment because a lot of them have lost or have impaired lung function,” Vega says.

Vega is also encouraged by progress in AI agents and the hardware that goes with them. No matter how the digital world evolves, Vega believes Augmental can be a tool that can benefit everyone.

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evoldir · 4 years ago

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Fwd: Postdoc: UCalifornia_Berkeley.PupfishSpeciationGenetics

Begin forwarded message: > From: [email protected] > Subject: Postdoc: UCalifornia_Berkeley.PupfishSpeciationGenetics > Date: 19 May 2021 at 06:14:08 BST > To: [email protected] > > > > > Postdoctoral position on the genetics, development, and origins of adaptive > radiation in Caribbean pupfishes > > The Martin Fish Speciation Lab at the University of California Berkeley > Museum of Vertebrate Zoology seeks a postdoc for functional genetic and > quantitative genetic studies of adaptive craniofacial traits in a sympatric > radiation of trophic specialist pupfishes. Pupfishes present a rare > opportunity to investigate the origins of a spectacular adaptive radiation > and the evolution of novel niches (e.g. scale-eating) localized to a single > Bahamian island despite thousands of similar Caribbean lake environments. > > A multi-year position is available (initial 12 month appointment with the > possibility of renewal for at least one more year). This research is funded > by both NIH and NSF grants. Start date is flexible, but ideally around > August 2021. Salary starts at $54,540/year. > > We are seeking postdoctoral applicants with interests/expertise in any of > the following areas: *functional genetics (CRISPR experience preferred), > quantitative genetics, craniofacial development, or speciation genomics*. > > We have identified several candidate causal variants in craniofacial > regulatory networks that warrant further functional investigation. See our > recent PNAS paper for additional context: > https://ift.tt/2RxOUHf > > The postdoc will have the opportunity to participate in short fieldwork > excursions to the Bahamas starting in 2022, but previous field experience > is not necessary and participation is not required. > > Required qualifications: > > Ph.D. or equivalent degree in biology, evolution, genetics, or related > field. Publication of work based on dissertation. Programming experience in > R or python. BIPOC applicants are especially encouraged to apply. > > UC Berkeley contains a world-class community of integrative biologists > studying adaptive radiation and speciation spanning the Department of > Integrative Biology, the Museum of Vertebrate Zoology, the Department of > Environmental Science, Policy, and Management, the Department of Molecular > and Cell Biology, the Center for Theoretical Evolutionary Genomics, and > more. UC Berkeley offers competitive salaries, excellent benefits, and is > an equal opportunity employer. The city of Berkeley and the surrounding San > Francisco Bay Area is known for its progressive values, vibrant social and > cultural scene, and beautiful surrounding environment. > > The University of California is an Equal Opportunity/Affirmative > > Action Employer. All qualified applicants will receive consideration > > for employment without regard to race, color, religion, sex, sexual > > orientation, gender identity, national origin, disability, > > age, or protected veteran status. > > Interested candidates should send an email detailing their interest in the > position and relevant experience along with their CV, PDFs of two recent > publications, and contact information for three references to Chris Martin > at [email protected] > > This position is open until filled, but please apply within the next two > weeks for full consideration. Please feel free to contact me at the above > email address with any questions. > > Christopher Martin > Assistant Professor, Department of Integrative Biology > Assistant Curator of Ichthyology, Museum of Vertebrate Zoology > University of California, Berkeley > https://ift.tt/3wm080v > > @fishspeciation > > > [email protected] > via IFTTT

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sciencebulletin · 6 years ago

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Scientists recreate in flies the mutations that let monarch butterfly eat toxic milkweed with impunity

The fruit flies in Noah Whiteman's lab may be hazardous to your health. Whiteman and his University of California, Berkeley, colleagues have turned perfectly palatable fruit flies—palatable, at least, to frogs and birds—into potentially poisonous prey that may cause anything that eats them to puke. In large enough quantities, the flies likely would make a human puke, too, much like the emetic effect of ipecac syrup. That's because the team genetically engineered the flies, using CRISPR-Cas9 gene editing, to be able to eat milkweed without dying and to sequester its toxins, just as America's most beloved butterfly, the monarch, does to deter predators. This is the first time anyone has recreated in a multicellular organism a set of evolutionary mutations leading to a totally new adaptation to the environment—in this case, a new diet and new way of deterring predators. Like monarch caterpillars, the CRISPRed fruit fly maggots thrive on milkweed, which contains toxins that kill most other animals, humans included. The maggots store the toxins in their bodies and retain them through metamorphosis, after they turn into adult flies, which means the adult "monarch flies" could also make animals upchuck. The team achieved this feat by making three CRISPR edits in a single gene: modifications identical to the genetic mutations that allow monarch butterflies to dine on milkweed and sequester its poison. These mutations in the monarch have allowed it to eat common poisonous plants other insects could not and are key to the butterfly's thriving presence throughout North and Central America. Flies with the triple genetic mutation proved to be 1,000 times less sensitive to milkweed toxin than the wild fruit fly, Drosophila melanogaster. Whiteman and his colleagues will describe their experiment in the Oct. 2 issue of the journal Nature. Monarch flies The UC Berkeley researchers created these monarch flies to establish, beyond a shadow of a doubt, which genetic changes in the genome of monarch butterflies were necessary to allow them to eat milkweed with impunity. They found, surprisingly, that only three single-nucleotide substitutions in one gene are sufficient to give fruit flies the same toxin resistance as monarchs. "All we did was change three sites, and we made these superflies," said Whiteman, an associate professor of integrative biology. "But to me, the most amazing thing is that we were able to test evolutionary hypotheses in a way that has never been possible outside of cell lines. It would have been difficult to discover this without having the ability to create mutations with CRISPR." Whiteman's team also showed that 20 other insect groups able to eat milkweed and related toxic plants—including moths, beetles, wasps, flies, aphids, a weevil and a true bug, most of which sport the color orange to warn away predators—independently evolved mutations in one, two or three of the same amino acid positions to overcome, to varying degrees, the toxic effects of these plant poisons. In fact, his team reconstructed the one, two or three mutations that led to each of the four butterfly and moth lineages, each mutation conferring some resistance to the toxin. All three mutations were necessary to make the monarch butterfly the king of milkweed. Resistance to milkweed toxin comes at a cost, however. Monarch flies are not as quick to recover from upsets, such as being shaken—a test known as "bang" sensitivity. "This shows there is a cost to mutations, in terms of recovery of the nervous system and probably other things we don't know about," Whiteman said. "But the benefit of being able to escape a predator is so high ... if it's death or toxins, toxins will win, even if there is a cost." Plant vs. insect Whiteman is interested in the evolutionary battle between plants and parasites and was intrigued by the evolutionary adaptations that allowed the monarch to beat the milkweed's toxic defense. He also wanted to know whether other insects that are resistant—though all less resistant than the monarch—use similar tricks to disable the toxin. "Since plants and animals first invaded land 400 million years ago, this coevolutionary arms race is thought to have given rise to a lot of the plant and animal diversity that we see, because most animals are insects, and most insects are herbivorous: they eat plants," he said. Milkweeds and a variety of other plants, including foxglove, the source of digitoxin and digoxin, contain related toxins—called cardiac glycosides—that can kill an elephant and any creature with a beating heart. Foxglove's effect on the heart is the reason that an extract of the plant, in the genus Digitalis, has been used for centuries to treat heart conditions, and why digoxin and digitoxin are used today to treat congestive heart failure. These plants' bitterness alone is enough to deter most animals, but a small minority of insects, including the monarch (Danaus plexippus) and its relative, the queen butterfly (Danaus gilippus), have learned to love milkweed and use it to repel predators. Whiteman noted that the monarch is a tropical lineage that invaded North America after the last ice age, in part enabled by the three mutations that allowed it to eat a poisonous plant other animals could not, giving it a survival edge and a natural defense against predators. "The monarch resists the toxin the best of all the insects, and it has the biggest population size of any of them; it's all over the world," he said. The new paper reveals that the mutations had to occur in the right sequence, or else the flies would never have survived the three separate mutational events. Thwarting the sodium pump The poisons in these plants, most of them a type of cardenolide, interfere with the sodium/potassium pump (Na+/K+-ATPase) that most of the body's cells use to move sodium ions out and potassium ions in. The pump creates an ion imbalance that the cell uses to its favor. Nerve cells, for example, transmit signals along their elongated cell bodies, or axons, by opening sodium and potassium gates in a wave that moves down the axon, allowing ions to flow in and out to equilibrate the imbalance. After the wave passes, the sodium pump re-establishes the ionic imbalance. Digitoxin, from foxglove, and ouabain, the main toxin in milkweed, block the pump and prevent the cell from establishing the sodium/potassium gradient. This throws the ion concentration in the cell out of whack, causing all sorts of problems. In animals with hearts, like birds and humans, heart cells begin to beat so strongly that the heart fails; the result is death by cardiac arrest. Scientists have known for decades how these toxins interact with the sodium pump: they bind the part of the pump protein that sticks out through the cell membrane, clogging the channel. They've even identified two specific amino acid changes or mutations in the protein pump that monarchs and the other insects evolved to prevent the toxin from binding. But Whiteman and his colleagues weren't satisfied with this just so explanation: that insects coincidentally developed the same two identical mutations in the sodium pump 14 separate times, end of story. With the advent of CRISPR-Cas9 gene editing in 2012, coinvented by UC Berkeley's Jennifer Doudna, Whiteman and colleagues Anurag Agrawal of Cornell University and Susanne Dobler of the University of Hamburg in Germany applied to the Templeton Foundation for a grant to recreate these mutations in fruit flies and to see if they could make the flies immune to the toxic effects of cardenolides. Seven years, many failed attempts and one new grant from the National Institutes of Health later, along with the dedicated CRISPR work of GenetiVision of Houston, Texas, they finally achieved their goal. In the process, they discovered a third critical, compensatory mutation in the sodium pump that had to occur before the last and most potent resistance mutation would stick. Without this compensatory mutation, the maggots died. Their detective work required inserting single, double and triple mutations into the fruit fly's own sodium pump gene, in various orders, to assess which ones were necessary. Insects having only one of the two known amino acid changes in the sodium pump gene were best at resisting the plant poisons, but they also had serious side effects—nervous system problems—consistent with the fact that sodium pump mutations in humans are often associated with seizures. However, the third, compensatory mutation somehow reduces the negative effects of the other two mutations. "One substitution that evolved confers weak resistance, but it is always present and allows for substitutions that are going to confer the most resistance," said postdoctoral fellow Marianna Karageorgi, a geneticist and evolutionary biologist. "This substitution in the insect unlocks the resistance substitutions, reducing the neurological costs of resistance. Because this trait has evolved so many times, we have also shown that this is not random." The fact that one compensatory mutation is required before insects with the most resistant mutation could survive placed a constraint on how insects could evolve toxin resistance, explaining why all 21 lineages converged on the same solution, Whiteman said. In other situations, such as where the protein involved is not so critical to survival, animals might find different solutions. "This helps answer the question, 'Why does convergence evolve sometimes, but not other times?'" Whiteman said. "Maybe the constraints vary. That's a simple answer, but if you think about it, these three mutations turned a Drosophila protein into a monarch one, with respect to cardenolide resistance. That's kind of remarkable." Provided by: University of California - Berkeley More information: Marianthi Karageorgi et al. Genome editing retraces the evolution of toxin resistance in the monarch butterfly. Nature (2019). DOI: 10.1038/s41586-019-1610-8 Image: A Drosophila melanogaster "monarch fly" with mutations introduced by CRISPR-Cas9 genome editing (V111, S119 and H122) to the sodium potassium pump, on a wing of a monarch butterfly (Danaus plexippus). Credit: copyright Julianne Pelaez Read the full article

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fitnesshealthyoga-blog · 6 years ago

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New Post has been published on https://fitnesshealthyoga.com/crispr-babies-lives-could-be-cut-short/

CRISPR Babies' Lives Could Be Cut Short

When Jiankui He shocked the world last year by editing the genomes of twin girls, he offered the rationale that the CCR5-∆32 mutation would protect the babies from HIV infection. Not only was this reason widely denounced by the scientific community, but new research from the University of California (UC), Berkeley, suggests that the mutation may actually shorten the lives of the twins.

The researchers used genotyping and death register information from 409,693 individuals in the UK Biobank to investigate fitness effects of the CCR5-∆32 mutation. They found that people who had two mutated copies of the gene had a significantly higher death rate between ages 41 and 78 than those with one or no copies. The authors “estimate a 21% increase in the all-cause mortality rate in individuals who are homozygous for the ∆32 allele.”

The work is published in a paper in Nature Medicine titled “CCR5-∆32 is deleterious in the homozygous state in humans.”

“Beyond the many ethical issues involved with the CRISPR babies, the fact is that, right now, with current knowledge, it is still very dangerous to try to introduce mutations without knowing the full effect of what those mutations do,” said Rasmus Nielsen, PhD, a professor of integrative biology at UC Berkeley. “In this case, it is probably not a mutation that most people would want to have. You are actually, on average, worse off having it.”

Previous studies have associated two mutated copies of the gene, CCR5, with a fourfold increase in the death rate after influenza infection, and the higher overall mortality rate may reflect this greater susceptibility to death from the flu. But the researchers say there could be any number of explanations, since the protein that CCR5 codes for, and which no longer works in those having the mutation in both copies of the gene, is involved in many body functions.

“Because one gene could affect multiple traits, and because, depending on the environment, the effects of a mutation could be quite different, I think there can be many uncertainties and unknown effects in any germline editing,” noted first author Xinzhu “April” Wei, PhD, a postdoctoral researcher in the Neilsen lab.

The gene CCR5 codes for a protein that, among other things, sits on the surface of immune cells and helps some strains of HIV, including the most common ones, to enter and infect them. Naturally-occurring mutations that disable the protein are rare in Asians, but a mutation found in about 11% of Northern Europeans protects them against HIV infection.

The genetic mutation, ∆32 (Delta 32), refers to a missing 32-base-pair segment in the CCR5 gene. This mutation interferes with the localization on the cell surface of the protein for which CCR5 codes, thwarting HIV binding and infection. He was unable to duplicate the natural mutation, but appears to have generated a similar deletion that would also inactivate the protein. One of the twin babies reportedly had one copy of CCR5 modified by CRISPR-Cas9 gene editing, while the other baby had both copies edited.

But inactivating a protein found in all humans and most animals is likely to have negative effects, Nielsen said, especially when homozygous. “Here is a functional protein that we know has an effect in the organism, and it is well-conserved among many different species, so it is likely that a mutation that destroys the protein is, on average, not good for you,” Nielsen said. “Otherwise, evolutionary mechanisms would have destroyed that protein a long time ago.”

After He’s experiment became public, Nielsen and Wei, who study current genetic variation to understand the origin of human, animal and plant traits, decided to investigate the effect of the CCR5-∆32 mutation using data from UK Biobank. The database houses genomic information on a half million U.K. citizens that is linked to their medical records.

Two independent measures indicated a higher mortality rate for those with two mutated genes. Fewer people than expected with two mutations enrolled in the database, indicating that they had died at a higher rate than the general population. And fewer than expected survived from ages 40 to 78.

“Both the proportions before enrollment and the survivorship after enrollment tell the same story, which is that you have lower survivability or higher mortality if you have two copies of the mutation,” Nielsen said. “There is simply a deficiency of individuals with two copies.”

Because the ∆32 mutation is relatively common in Northern Europeans, it must have been favored by natural selection at some point, Nielsen said, though probably not to protect against HIV, since the virus has circulated among humans only since the 1980s.

Wei said that some evidence links the mutation to increased survival after stroke and protection against smallpox and flaviviruses, a group that includes the dengue, Zika, and West Nile viruses. Despite these possible benefits, the potential unintended effects of creating genetic mutations, in both adult somatic cells and in embryonic, germline cells, argue for caution, the researchers said.

“I think there are a lot of things that are unknown at the current stage about genes’ functions,” Wei said. “The CRISPR technology is far too dangerous to use right now for germline editing.”

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fumpkins · 6 years ago

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The search for the kryptonite that can stop CRISPR

In September 2016, Jennifer Doudna called a new colleague named Kyle Watters to her office. By then, the University of California, Berkeley, biochemist was famous as the coinventor of CRISPR. The invention of the fast and versatile tool to edit genes had vaulted her to global notoriety and to considerable wealth. She was the founder of several startup companies and had collected millions in science-prize money.

Ominously, though, as Doudna has recounted, she was haunted by a dream in which Adolf Hitler appeared, holding a pen and paper, requesting a copy of the CRISPR recipe. What horrible purpose could Hitler have? Doudna, in her retellings of her dream, didn’t say.

Now Doudna’s question was, would Watters like to work on a way to stop it? Stop CRISPR.

CRISPR is found inside bacteria. It’s a billion-year-old defense against marauding viruses that spots their DNA and uses a scissors-like protein to chop it up. Doudna played a key role in transforming the find into a revolutionary gene-editing tool that’s been taken up worldwide, propelling a wave of new research and potential cures.

But if scientists learn to deliver gene editors inside people’s bodies, what’s to stop a madman, terrorist, or state from employing CRISPR to cause harm? People imagine personalized attacks that would strike only at certain ethnic groups or super soldiers edited to feel no pain. Doudna was well familiar with the dilemma. In her book A Crack in Creation, she wrote that she feared gene editing could come to the world’s attention, as atomic power did, in a mushroom cloud. “Could I and other concerned scientists save CRISPR from itself … before a cataclysm occurred?”

Now she would have a chance. Earlier in 2016, the US intelligence agencies had designated gene editing as a potential weapon of mass destruction. That September, the Defense Advanced Research Projects Agency (DARPA) had jumped in, putting out a call for new ways to control or reverse the effects of gene-editing technology. The program, called Safe Genes, would end up with a budget of more than $65 million, making it one of the largest sources of cash for CRISPR research, aside from biotech startups developing new genetic treatments.

One problem, as DARPA saw it, was the lack of any easy-to-use countermeasure, undo button, or antidote for CRISPR. And the more powerful gene editing becomes, the more we might need one—in case of a lab accident, or worse. As UC Berkeley put it in a 2017 press release after Doudna, with Watters’s help, claimed part of the big DARPA contract, the university intended to build tools to counter bioterrorism threats including “weapons employing CRISPR itself.”

CRISPR weapons? We’ll leave it to your imagination exactly what one could look like. What is safe to say, though, is that DARPA has asked Doudna and others to start looking into prophylactic treatments or even pills you could take to stop gene editing, just the way you can swallow antibiotics if you’ve gotten an anthrax letter in the mail. Scientists under Doudna’s project say they are set to begin initial tests on mice to see if the rodents can be made immune to CRISPR editors.

“Can we shut off CRISPR?” asks Joseph S. Schoeniger, who leads one arm of the defense effort at Sandia National Laboratories, in Livermore, California. “That is what we are looking at. The basic concept is that this technology is coming along, [so] wouldn’t it be nice to have an ‘off’ switch.”

Jennifer Doudna

Alexander Heinl/picture-alliance/dpa/AP Images

Anti-CRISPR

By the time Doudna drafted her proposal to DARPA, other scientists already had one big clue for how to stop CRISPR. In the ancient struggle between bacteria and the viruses called phage that infect them, phage had developed their own antidotes to CRISPR. In fact, their genomes, it’s been found, harbor the ability to produce what is essentially CRISPR kryptonite—small proteins exquisitely tuned by evolution to disable the gene-editing tool. Scientists call these molecules “anti-CRISPRs.”

The first anti-CRISPRs were discovered in 2013 by a student at the University of Toronto named Joseph Bondy-Denomy. “It was serendipity. We stumbled onto the fact that some phages seemed to be resistant to CRISPR. When we put the phage into a cell, the bacteria couldn’t protect itself,” says Bondy-Denomy, now a professor at the University of California, San Francisco. He quickly zeroed in on one of the virus’s 50 or so genes as the reason. “We thought, wow, maybe this is turning off CRISPR.”

The number of labs studying such defenses is smaller than the number working with CRISPR. But anti-CRISPR is becoming a booming field in its own right. More than 40 anti-CRISPR proteins have already been found, many by Doudna’s lab. Other teams are having early success locating conventional chemicals that can inhibit CRISPR as well. Today, Amit Choudhary of Harvard Medical School, in Boston, also with funding from DARPA, reported he had found two drugs that prevent gene-editing when mixed with human cells. “The hallmark of any powerful technology is control,” says Choudhary. “It’s that simple.”

Researchers like Bondy-Denomy believe anti-CRISPRs could have a role in improving future gene-editing treatments, by giving researchers more precise control. For instance, a team in Germany recently showed if they combined CRISPR and anti-CRISPR, they could create an editor that will change DNA only in liver cells, not neurons or muscle.

Another application being studied is whether anti-CRISPR could create a safeguard against “gene drives.” The Bill & Melinda Gates Foundation is backing the development of a CRISPR tool that will spread though wild mosquitoes, causing their populations to crash, with the idea of preventing malaria. Others want to develop such gene drives in mice, so they can eradicate the rodents from islands without using poison.

But what if these experiments go haywire and lead to an extinction? Researchers think they can create organisms with anti-CRISPR programmed into their genomes so they’re immune. In an initial proof of principle, scientists in Kansas last year engineered yeast cells with anti-CRISPR to resist a gene drive. “If some North Korean lab comes at you with a gene drive to wipe out an economically important crop, you could have a transgenic crop that [is resistant]. That is the drawing board scenario,” says Erik Sontheimer of the University of Massachusetts Medical School.

A biosurprise

The advent of the CRISPR tool starting in mid-2012 surprised scientists. Essentially overnight, ham-fisted ways of genetic engineering were replaced by a cheap, versatile, and programmable means of changing DNA inside any living thing. Forecasters whose job was to anticipate new dangers “totally missed” CRISPR, says Renee Wegrzyn, the biodefense scientist who runs DARPA’s program. The humbling failure to see the future quickly morphed into a “critical urgent issue for national security.”

That’s because researchers, doctors, and startups backed by venture capitalists began a race to learn how to deploy CRISPR inside plants, animals, and humans, using viruses, injections, nanoparticles, or electrical shocks. And the better they got at it, the more realistic some sort of novel biothreat could become.

By 2015, Doudna had also started to question how CRISPR was being used in more-routine laboratory research settings. Some of the experiments looked dangerous—what if a graduate student was hurt? “We are pushing these technologies out into the world, and we are not accompanying them with the safety measures that should be in place,” Wegrzyn told a gathering of the Long Now Foundation, in 2017, in San Francisco. “I really started to feel this sense of urgency that someone needed to do something about this.”

In her talk, Wegrzyn said the danger of CRISPR was obvious from how scientists were already using gene-editing to make mice sick by snipping important genes. “I don’t think you need to be a biosecurity expert to recognize that there is a need for scrutiny when you look at a tool that can both cure and cause disease,” she told the California gathering. “If we need to shut down a gene editor immediately, we just don’t know how to do this.”

There’s still no agreement about how dangerous CRISPR could be in the wrong hands. “Red team” exercises sponsored by the Central Intelligence Agency over the summer of 2016, where a group of analysts called the Jasons were asked to dream up their worst ideas, didn’t settle the question. Later, the National Academies of Sciences, Engineering and Medicine, at the request of the Department of Defense, produced an entire ranking of possible threats from synthetic biology, putting CRISPR weapons toward the middle of the pack. The military said it saw no imminent danger to soldiers.

Doudna agrees that CRISPR’s dangers should not be overblown. “I get these questions a lot about CRISPR systems and nefarious uses, and my feeling is that I am no more or less worried about CRISPR than other things. Someone could synthesize the smallpox virus,” she says. Similarly, while her research may lead to an eventual gene-editing antidote, her lab’s work with anti-CRISPRs is mainly addressing fundamental biological questions. “I am still at step one,” she says. “How do these work?”

Others, though, worry the risks are already apparent and that antidotes can’t come soon enough. For instance, some scientists have sought to prevent public discussion of specific CRISPR studies, or even delete mention of them from the internet, presumably to allow scientists more time to develop countermeasures. “The general prevailing attitude is not to give people nightmare fuel while we are actively looking for answers. There’s always a concern about an early freak-out,” says Doudna’s former collaborator Watters, who in 2018 authored a review of gene editing’s implications for biosecurity.

A video showing CRISPR editing DNA in real time

Osamu Nureki, Nature Communications

CRISPR defense

This year, as part of Doudna’s DARPA project, teams of scientists plan to begin their first experiments—in mice—to determine if it’s possible to protect them from CRISPR. One lab involved in the work is at Sandia National Laboratories, which will employ mice primed for editing because they are engineered to be born with CRISPR’s molecular scissors, a protein called Cas9, in every cell.

Schoeniger, who leads the Sandia effort, says soon his lab will instruct the mice to edit themselves but will also give them a shot of anti-CRISPR molecules, to see if the process is blocked. “Anti-CRISPR works well in nature, and we are trying to see if it works well in animals,” he says.

Schoeniger believes there is a “significant risk of accidental exposure” to CRISPR agents. As a large industry leaps up around the editing tool, CRISPR is being formulated into gene therapies, injections, ointments, and food, which raises the chance of a laboratory accident. Even a secret bioweapons program is more likely to release a designer germ by accident than it is to launch an attack. “As people use this in bigger and bigger amounts, there is an increased chance of people coming into contact, of getting stabbed or sprayed,” he says. “And if I get a mutagen sprayed in my eyes, it would be nice to stop it.”

Work on an antidote might also be helpful just as public relations. It could, at the very least, “tamp down the mental accessibility to a malign personality,” Schoeniger says. “If you can turn it off, maybe they won’t bother. From a psychological point of view, it’s nice to have an ‘off’ button. It’s nice for positioning that technology in society.”

Schoeniger isn’t under an illusion that an antidote to CRISPR will make threats go away. In fact, the security problem is growing, as laboratories improve the tool and invent related ones, each with different implications for biodefenders. Scientists can feel baffled by the tremendous speed at which gene editing, and synthetic biology more broadly, is speeding up, and how information is spreading online.

“We look at the overall risk front of the technology, how it keeps evolving, and how hard [it is] to stay on top of it, and how fast people are throwing out scenarios, and it’s hard to rationally address that risk,” Schoeniger says. In the meantime, he says, learning how to block CRISPR, in its classic, simplest form, seems like a good place to start. “It seems obvious we would like to modulate the technology, so let’s do that while trying to sort out the priorities,” says Schoeniger. “To a certain extent, it’s a mess; new technology is exploding so fast.”

New post published on: https://www.livescience.tech/2019/05/05/the-search-for-the-kryptonite-that-can-stop-crispr/

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morganbelarus · 7 years ago

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It’s incredibly hard to get by as a contractor in America. It shouldn’t have to be.

Retirement, paid sick days, a steady schedule — in theory, these should be a given for all working people. In practice, not so much.

Right now, a little over 10% of the American workforce is part of the “gig economy,” according to the UC Berkeley Labor Center, which means that most or all of their main income comes from work they do as independent contractors or through temp, on-call, and contract work.

They aren't guaranteed direct deposits, they don't get paid-time off, and they often have to grapple with stagnating wages and self-employment taxes. Plus, there is no employer contribution when it comes to saving for retirement and health care coverage.

This means that health care can also get expensive quickly. Full-time employment versus contract employment is the difference between putting an average of $89 a month toward the health care benefits provided by your company and paying an average of $396 a month for coverage on your own.

All photos via iStock.

Making matters worse, many low-earning contractors or gig economy workers are among the 55% of Americans that live paycheck to paycheck. This means that they don’t earn enough to build a safety net in case of an unexpected emergency. According to a report by the Federal Reserve, nearly half of Americans struggle to scrape together even $400 when something unexpected comes up — like car trouble.

The solutions available during these times of emergency, such as borrowing from friends and family or payday lending, can be inaccessible or predatory, which means that these workers are often forced to make an impossible choice between feeding their family or fixing the car.

There's a clear need for a safety net for these workers — that's why one organization, The Workers Lab, is working tirelessly to provide it.

Supported by The Rockefeller Foundation, The Workers Lab funds experiments and innovations that build power for working people.

“What we learn is that working people are living the unjust reality of being poor while working harder and producing more than ever,” says Carmen Rojas, CEO of The Workers Lab.

One way to help these contractors is by providing them with access to portable benefits. These are benefits that would stay with contractors even as they move among jobs. Portable benefits could include paid sick leave, disability insurance, and an emergency fund, for starters.

“These workers deserve more than merely making ends meet. They deserve to live lives of opportunity, mobility, and dignity,” says Rojas.

The Workers Lab also believes we need to reimagine and rebuild the social safety net for all workers, regardless of where and how they work. All workers need the security of knowing that their immediate needs are being met and that they have health care, a steady paycheck, and a way to retire when it comes time for that.

“We owe it to all working people to ensure that they are not wasting the best years of their lives barely scraping by,” says Rojas.

61% of American workers struggle to come up with $1,000 in a financial emergency. To help them thrive instead of scrape by, The Workers Lab’s immediate goal is to get low-earning contractors and low wage workers the money they need when they are hit with an unexpected expense.

That's why they are working to establish a fund that would give contractors access to meaningful cash infusions for such situations — which can be a huge relief.

Failing to adapt to workers’ immediate needs could be detrimental to the future, which is why organizations like The Workers Lab are working so hard to find timely solutions.

Because of your support we had an incredibly successful 2017! Including TRIPLING our funding. Read more about all of our...

Posted by The Workers Lab on Saturday, December 30, 2017

Imagine a workforce where all you have to think about is your work. You wouldn't have to worry about whether or not you’ll be able to pay for your annual physical or your upcoming knee surgery. You can rest easy knowing that if an emergency hits, you won’t have to make an impossible choice or turn to a payday lender just to feed your family.

This might sound like an impossible dream now, but with increased awareness of the problems faced by contract workers and with organizations like The Workers Lab working tirelessly to find solutions to help workers without safety nets, it's closer to reality than ever before.

For more than 100 years, The Rockefeller Foundation’s mission has been to promote the well-being of humanity throughout the world. Together with partners and grantees, The Rockefeller Foundation strives to catalyze and scale transformative innovations, create unlikely partnerships that span sectors, and take risks others cannot — or will not.

Join The Rockefeller Foundation Community

Original Article : HERE ; This post was curated & posted using : RealSpecific

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It’s incredibly hard to get by as a contractor in America. It shouldn’t have to be. was originally posted by 16 MP Just news

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scienceblogtumbler · 5 years ago

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‘AeroNabs’ Promise Powerful, Inhalable Protection Against COVID-19

As the world awaits vaccines to bring the COVID-19 pandemic under control, UC San Francisco scientists have devised a novel approach to halting the spread of SARS-CoV-2, the virus that causes the disease.

Led by UCSF graduate student Michael Schoof, a team of researchers engineered a completely synthetic, production-ready molecule that straitjackets the crucial SARS-CoV-2 machinery that allows the virus to infect our cells. As reported in a new paper, now available on the preprint server bioRxiv, experiments using live virus show that the molecule is among the most potent SARS-CoV-2 antivirals yet discovered.

In an aerosol formulation they tested, dubbed “AeroNabs” by the researchers, these molecules could be self-administered with a nasal spray or inhaler. Used once a day, AeroNabs could provide powerful, reliable protection against SARS-CoV-2 until a vaccine becomes available. The research team is in active discussions with commercial partners to ramp up manufacturing and clinical testing of AeroNabs. If these tests are successful, the scientists aim to make AeroNabs widely available as an inexpensive medication to prevent and treat COVID-19.

“Far more effective than wearable forms of personal protective equipment, we think of AeroNabs as a molecular form of PPE that could serve as an important stopgap until vaccines provide a more permanent solution to COVID-19,” said AeroNabs co-inventor Peter Walter, PhD, professor of biochemistry and biophysics at UCSF and a Howard Hughes Medical Institute Investigator. For those who cannot access or don’t respond to SARS-CoV-2 vaccines, Walter added, AeroNabs could be a more permanent line of defense against COVID-19.

“We assembled an incredible group of talented biochemists, cell biologists, virologists and structural biologists to get the project from start to finish in only a few months,” said Schoof, a member of the Walter lab and an AeroNabs co-inventor.

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Llama-Inspired Design

Though engineered entirely in the lab, AeroNabs were inspired by nanobodies, antibody-like immune proteins that naturally occur in llamas, camels and related animals. Since their discovery in a Belgian lab in the late 1980s, the distinctive properties of nanobodies have intrigued scientists worldwide.

Aashish Manglik (left), MD, PhD, and Peter Walter, PhD

“Though they function much like the antibodies found in the human immune system, nanobodies offer a number of unique advantages for effective therapeutics against SARS-CoV-2,” explained co-inventor Aashish Manglik, MD, PhD, an assistant professor of pharmaceutical chemistry who frequently employs nanobodies as a tool in his research on the structure and function of proteins that send and receive signals across the cell’s membrane.

For example, nanobodies are an order of magnitude smaller than human antibodies, which makes them easier to manipulate and modify in the lab. Their small size and relatively simple structure also makes them significantly more stable than the antibodies of other mammals. Plus, unlike human antibodies, nanobodies can be easily and inexpensively mass-produced: scientists insert the genes that contain the molecular blueprints to build nanobodies into E. coli or yeast, and transform these microbes into high-output nanobody factories. The same method has been used safely for decades to mass-produce insulin.

But as Manglik noted, “nanobodies were just the starting point for us. Though appealing on their own, we thought we could improve upon them through protein engineering. This eventually led to the development of AeroNabs.”

Spike Is the Key to Infection

SARS-CoV-2 relies on its so-called spike proteins to infect cells. These spikes stud the surface of the virus and impart a crown-like appearance when viewed through an electron microscope – hence the name “coronavirus” for the viral family that includes SARS-CoV-2. Spikes, however, are more than a mere decoration – they are the essential key that allows the virus to enter our cells.

Like a retractable tool, spikes can switch from a closed, inactive state to an open, active state. When any of a virus particle’s approximately 25 spikes become active, that spike’s three “receptor-binding domains,” or RBDs, become exposed and are primed to attach to ACE2 (pronounced “ace two”), a receptor found on human cells that line the lung and airway.

SARS-CoV-2 is part of the coronavirus family, named for the spikes that stud the surface of the virus and impart a crown-like appearance when viewed through an electron microscope. Image by NIH

UCSF researchers believed that if they could find nanobodies that impede spike-ACE2 interactions, they could prevent the virus from infecting cells. Photo by Noah Berger

Through a lock-and-key-like interaction between an ACE2 receptor and a spike RBD, the virus gains entry into the cell, where it then transforms its new host into a coronavirus manufacturer. The researchers believed that if they could find nanobodies that impede spike-ACE2 interactions, they could prevent the virus from infecting cells.

Nanobodies Disable Spikes and Prevent Infection

To find effective candidates, the scientists parsed a library of over 2 billion synthetic nanobodies jointly developed in the labs of Manglik and Harvard Medical School’s Andrew Kruse, PhD. After successive rounds of testing, during which they imposed increasingly stringent criteria to eliminate weak or ineffective candidates, the scientists ended up with 21 nanobodies that prevented a modified form of spike from interacting with ACE2.

UCSF graduate student Bryan Faust examines a 3D representation of a COVID-19 spike particle, created using a cryo-electron microscope. Photo by Noah Berger

Further experiments, including the use of cryo-electron microscopy to visualize the nanobody-spike interface, showed that the most potent nanobodies blocked spike-ACE2 interactions by strongly attaching themselves directly to the spike RBDs. These nanobodies function a bit like a sheath that covers the RBD “key” and prevents it from being inserted into an ACE2 “lock.”

With these findings in hand, the researchers still needed to demonstrate that these nanobodies could prevent the real virus from infecting cells. Veronica Rezelj, PhD, a virologist in the lab of Marco Vignuzzi, PhD, at Institut Pasteur in Paris, tested the three most promising nanobodies against live SARS-CoV-2, and found the nanobodies to be extraordinarily potent, preventing infection even at extremely low doses.

The most potent of these nanobodies, however, not only acts as a sheath over RBDs, but also like a molecular mousetrap, clamping down on spike in its closed, inactive state, which adds an additional layer of protection against the spike–ACE2 interactions that lead to infection.

From Nanobodies to AeroNabs

The scientists then engineered this double-action nanobody in a number of ways to make it into an even more potent antiviral. In one set of experiments, they mutated every one of the amino-acid building blocks of the nanobody that contacts spike to discover two specific changes that yielded a 500-fold increase in potency.

Due to the inherent stability of nanobodies, there was no loss of antiviral potency in the aerosolized form, suggesting that AeroNabs are a potent SARS-CoV-2 antiviral that could be practical to administer via a shelf-stable inhaler or nasal spray. Photo by Noah Berger

In a separate set of experiments, they engineered a molecular chain that could link three nanobodies together. As noted, each spike protein has three RBDs, any of which can attach to ACE2 to grant the virus entry into the cell. The linked triple nanobody devised by the researchers ensured that if one nanobody attaches itself to an RBD, the other two would attach to the remaining RBDs. They found that this triple nanobody is 200,000 times more potent than a single nanobody alone.

And when they drew on the results of both modifications, linking three of the powerful mutated nanobodies together, the results were “off the charts,” said Walter. “It was so effective that it exceeded our ability to measure its potency.”

Would Be Easy to Administer as an Aerosol

This ultrapotent three-part nanobody construct formed the foundation for AeroNabs.

In a final set of experiments, the researchers put the three-part nanobodies through a series of stress tests, subjecting them to high temperatures, turning them into a shelf-stable powder, and making an aerosol. Each of these processes is highly damaging to most proteins, but the scientists confirmed that, thanks to the inherent stability of nanobodies, there was no loss of antiviral potency in the aerosolized form, suggesting that AeroNabs are a potent SARS-CoV-2 antiviral that could be practical to administer via a shelf-stable inhaler or nasal spray.

“We’re not alone in thinking that AeroNabs are a remarkable technology,” said Manglik. “Our team is in ongoing discussions with potential commercial partners who are interested in manufacturing and distributing AeroNabs, and we hope to commence human trials soon. If AeroNabs prove as effective as we anticipate, they may help reshape the course of the pandemic worldwide.”

Authors: Additional authors include Bryan Faust, Reuben A. Saunders, Smriti Sangwan, Nick Hoppe, Morgane Boone, Christian Bache Billesbølle, Marcell Zimanyi, Ishan Deshpande, Jiahao Liang, Aditya A. Anand, Niv Dobzinski, Beth Shoshana Zha, Benjamin Barsi-Rhyne, Vladislav Belyy, Silke Nock and Yuwei Liu of UCSF; Camille R. Simoneau, Kristoffer Leon, Nevan J. Krogan, Danielle L. Swaney and Melanie Ott of the UCSF Quantitative Biosciences Institute (QBI) and the J. David Gladstone Institutes; Andrew W. Barile-Hill of Cytiva Life Sciences; Sayan Gupta and Corie Y. Ralston of Lawrence Berkeley National Laboratory; Kris M White and Adolfo García-Sastre of the Icahn School of Medicine at Mount Sinai; and the QBI Coronavirus Research Group Structural Biology Consortium. Schoof, Faust, Saunders, Sangwan and Rezelj are co-first authors of the manuscript.

Funding: This work was supported by the UCSF COVID-19 Response Fund, a grant from Allen & Company, and supporters of the UCSF Program for Breakthrough Biomedical Research (PBBR), which was established with support from the Sandler Foundation. Other support included National Institutes of Health (NIH) grants DP5OD023048, S10OD020054, S10OD021741, 1R01GM126218; Laboratoire d’Excellence grant ANR-10-LABX-62-IBEID; the URGENCE COVID-19 Institut Pasteur fundraising campaign; the Office of Science and Office of Biological and Environmental Research of the U.S. Department of Energy under contract DE-AC02-05CH11231; a Helen Hay Whitney postdoctoral fellowship; the Alfred Benzon Foundation; a gift from the Roddenberry Foundation; the Howard Hughes Medical Institute; the Pew Charitable Trusts; the Esther A. & Joseph Klingenstein Fund; and the Searle Scholars Program.

Disclosures: Schoof, Faust, Saunders, Hoppe, Walter and Manglik are inventors on a provisional patent describing the anti-Spike nanobodies described in the manuscript.

The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. UCSF Health, which serves as UCSF’s primary academic medical center, includes top-ranked specialty hospitals and other clinical programs, and has affiliations throughout the Bay Area.

source https://scienceblog.com/517955/aeronabs-promise-powerful-inhalable-protection-against-covid-19/

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disabilityjusticeandyou · 6 months ago

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About this subject guide

A subject guide is a collection of annotated citations that can be used as a starting point for research on a specific topic. In this subject guide, you'll find sources to help introduce you to the language used by disability studies – the academic study of the position of disabled people in society – and some introductory sources on disability justice, as well as resources for already disabled people. I hope this guide will serve both the disabled and nondisabled community and facilitate more engagement with disability justice!

So, what is disability justice?

Disability justice and disability inclusion are facets of the disability rights movement that gained momentum in the 1990’s and 2000’s and sought equal rights for disabled people in the US and internationally. Disability inclusion argues that simply fighting for access rights for disabled people is not enough; instead, disabled people need to be actively and intentionally included in daily life by going above and beyond the minimum required level of accessibility. Disability justice goes further by demanding the broader disability rights movement fight for justice for all disabled people, highlighting the imperative to learn and incorporate the liberatory practices of other historically marginalized peoples.

Table of Contents

Reference Books:

"Demystifying Disability: What to Know, What to Say, and How to be an Ally"

"Handbook of Disability: Critical Thought and Social Change in a Globalizing World"

"Introducing Disability Studies"

"Routledge Handbook of Disability Studies"

Books:

"Care Work: Dreaming Disability Justice"

"Disability Visibility: First-Person Stories from the Twenty-First Century"

Databases:

Disability in the Modern World

Disability Studies Quarterly

Web Resources:

Disability & Philanthropy Forum

Project LETS

UC Berkeley Disability Lab

World Institute on Disability

#disability #disability justice #disability inclusion #disability rights #disability studies #disability community #disability pride #subject guide #disability justice subject guide #disability studies subject guide #disability resources #resources for disabled people

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nxfury · 5 years ago

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The Power To Serve: Setting Up FreeBSD

Most would agree that IT and Computer geeks have an intense passion for Open Source Software and quality code. Due to this, Linux is a staple in the tech community... But is it the only option? Enter FreeBSD, an Operating System whose roots trace all the way back to the original UNIX. Buckle up, and prepare for an introduction to FreeBSD and setting it up yourself.

Wait, Slow Down. What's FreeBSD?

Back in the 1970s and 1980s, AT&T Bell Labs invented UNIX and would go on to sell commercial copies of said Operating System to various colleges. The awesome thing was that AT&T shipped source code bundled right in! One of these places was the University of California at Berkeley, who aptly wrote more tools for UNIX such as vi and the original Berkeley Fast Filesystem (what most Linux/UNIX Filesystems are based on nowadays). Eventually UC Berkeley went on to redistribute their own variant of UNIX called BSD, setting up a hotline at 1-800-ITS-UNIX. This ROYALLY pissed off AT&T and they sued for copyright infringement. For reference, around this time Linus Torvalds was beginning the Linux Kernel development.

Needless to say, UC Berkeley won the case almost totally- so much so that AT&T only kept copyright to 3-4 files of the entire UNIX system. This enabled the release of i386BSD, which spawned the FreeBSD, NetBSD and OpenBSD projects. Their licenses are all very close to the original license of the code which is extremely permissive and allows the user to do almost anything except take credit for the work, sue the developer and remove the license.

Cool! Let's Install It!

Awesome! At this time of writing, the latest stable version of FreeBSD is 12.1. If you browse to the FreeBSD Site, you'll notice a big "Download Now" button. For this series of blog posts, we'll install 12.1 because stability matters for a daily-driver laptop. Pick the correct CPU architecture and you'll be taken to a web open directory. There are multiple images available for download, generally DVD1 and memstick images have all installation files embedded into the image so no network connection is needed to install the system.

Now that the image is downloaded, pick an installation medium. For usb, you would insert a thumb drive and type sudo dd if=/path/to/FREEBSDIMAGE of=/dev/sdX status=progress, where the "if" argument is the location of your downloaded FreeBSD installer image and the "of" argument is the name of your drive under Linux.

After this is done, let's yank out our computer and boot into the installer! On most laptops, there is a key combination to enter the BIOS, like spamming F12 or delete on boot. Once you've done this, allow USB booting, disable secure boot, and configure your flash drive to boot first. With the flash drive plugged in, you should be greeted by a FreeBSD bootloader, waiting a moment will take you to a graphical menu that looks like this:

The FreeBSD Installer

Select your responses with the arrow keys, and press enter to continue.

In prompts like this one, you'll need to use the space bar to alter selections.

The menu is very simple and easy to go through... Once you arrive at what disk format to use, the most common option FreeBSD users select is entire-disk ZFS.

Remember to select your disks in the ZFS Pool! The original option is stripe/0 disks, but you still need to go into it's submenu and select a disk even if you don't want to use the mirroring abilities of ZFS. There is an option to enable encryption, enabling it will provide a prompt later for your disk encryption password. If you're content with the settings, continue on.

After this, you'll be greeted by a menu of what packages you'd like to install, selectable by spacebar and arrow keys. Pressing enter will allow you to continue to the installation. Once complete, the interface will drop to a shell for you to set the root user password. Once that's done, the installer will take you back to the UI and offer to create a user account (DO THIS!), where you drop back to the shell to create it. Lastly, there will be system hardening options that you can optionally check. If you're concerned with privacy, it is recommended to enable all of them. Finally, it will provide an option to exit the installer and reboot.

Welcome To FreeBSD!

On fresh installation, FreeBSD is extremely plain and doesn't even have a desktop. Our first priority is to connect to the internet, so we can update our system. Running the ifconfig command will list all devices that are recognized by FreeBSD. If your network card isn't recognized, you will want to search to see if it's supported. If so, there's probably a kernel module that hasn't been loaded for it. To remedy this, a simple kldload xxx (where xxx is the name of the kernel module corresponding to your device driver) will enable your hardware. If this works, you can make this change permanent by editing /etc/rc.conf. FreeBSD makes use of wpa_supplicant and ifconfig to connect- more comprehensive guides on getting connected can be found here:

Wireless Networking in FreeBSD Networking in FreeBSD

Once connected, updating the system and fetching a few apps to get started with configuration is critical. There's three ways a user can install software on FreeBSD: compiling from source by hand, compiling from source through the ports collection (automatically), or using the pkg package manager which feels very much like apt.

Set up the FreeBSD ports tree by running portsnap fetch extract. If you ever wish to use it, cd into /usr/ports and find the proper directory of the application you wish to install. Then type make clean install.

As for pkg, let's update, upgrade and install vim:

pkg update pkg upgrade pkg install vim

Once all the software required for a desktop or whatever use case is necessary, setup is just like any *nix-based system.

So What Makes FreeBSD Different???

FreeBSD has a bunch of unique development tools, such as dtrace, for programming and understanding how the Operating System works and programming good, solid code. On top of that, it comes with pf instead of iptables, which is the de-facto standard on many enterprise networking devices such as Cisco or Palo Alto (they actually ship with FreeBSD installed). The entire Operating System source code can be found in /usr/src, and you can recompile the entire OS with a one-line terminal command. FreeBSD and similar systems are known for having the best TCP/IP networking stack in the world, so much so that even Microsoft still uses FreeBSD code for driving the internet on Windows to this very day.

Be sure to stick around for the next post, where we'll compile a custom kernel on FreeBSD!

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kathleenseiber · 6 years ago

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Biomarker may clear up how depression saps motivation

Researchers have identified biomarkers—genes and specific brain circuits in mice—associated with a common symptom of depression: lack of motivation.

The finding could guide research to find new ways to diagnose and potentially treat individuals suffering from lack of motivation and bring closer the day of precision medicine for psychiatric disorders like depression.

Depression is the most prevalent mental health disorder in the world, affecting around 9% of the American population each year, and is among the top causes of disability in the workplace.

Depression symptoms can differ significantly between patients who have the same depression diagnosis, and the lack of a connection between symptoms and treatments is a main reason that about half of all people with depression fail to respond to medication or other therapies, and that side effects of these medications are common.

“If we had a biomarker for specific symptoms of depression, we simply could do a blood test or image the brain and then identify the appropriate medication for that patient,” says Stephan Lammel, an assistant professor of molecular and cell biology at the University of California, Berkeley, and senior author of a paper on the discovery in Neuron. “That would be the ideal case, but we are far away from that situation right now.”

Lack of motivation and chronic stress

Now, for the first time, Lammel and his team have identified genes in a brain region—the lateral habenula—that are strongly turned on, or upregulated, in mice that show reduced motivation as a result of chronic stress. This brain region in mice is not associated with other depression symptoms, including anxiety and anhedonia, the inability to feel pleasure.

“We think that our study not only has the potential to transform how basic scientists study depression in animals, but the combination of anatomical, physiological, and molecular biomarkers described could lay the foundation for guiding the development of the next generation of antidepressants that are tailored to specific depression symptoms,” says Lammel, who worked with first author Ignas Cerniauskas, a graduate student.

The researchers work on mouse models of depression that have been a mainstay of basic research on this disorder for the past 60 years. Putting mice under constant stress produces at least three common symptoms of human depression—anxiety, lack of motivation, and loss of pleasure—that scientists study to try to understand in humans.

Until now, however, researchers have sought answers by disregarding the variability of symptoms and instead categorizing all mice as either stressed (“depressed”) or non-stressed (“not depressed”). Cerniauskas and Lammel wanted to try to find changes in the brain that were associated with each specific symptom.

“Unfortunately, depression treatment is currently often based on guesswork. No one treatment works for everyone, and no one has objective data on how to differentiate the enormous variability of depression symptoms and subtypes,” Lammel says. “If we understand specifically how the brain changes in those animals with one certain type of symptom, there may be a way we can specifically reverse these symptoms.”

Zeroing in

In response to a recent small clinical study in which doctors electrically stimulated the lateral habenula and found symptom improvement in depressed patients who were resistant to other therapies, Lammel and Cerniauskas decided to investigate that area of the brain. The lateral habenula has received increasing attention in the last few years, in part because it is connected to the dopamine and serotonin systems in the brain, both of which are known to be involved in depression. The most common drugs doctors currently use to treat depression are serotonin reuptake inhibitors (SRIs) such as Zoloft and Prozac.

“After chronic stress, there is an increase in the neural activity of the lateral habenula cells—they fire more, they become overactive—and we found that this overactivity was present only in mice that showed very strong deficits in motivated behavior, but not in animals that showed anxiety or animals that showed anhedonia,” Lammel says.

His team subsequently identified the specific synapses, cells, and circuits in the lateral habenula that chronic stress alters in these particular mice, and in collaboration with Csaba Földy and colleagues at the University of Zurich, they found genes that are overexpressed as well.

Lammel and Cerniauskas are currently working with the Földy lab to use CRISPR-Cas9 to interfere with or completely knock out these genes to determine which ones are critical to the overactivity of the lateral habenula cells causing lack of motivation. This could potentially lead to drugs to interfere with those pathways, reduce activity of the cells in the lateral habenula, and increase motivation.

They also plan to look for biomarkers of other symptoms of depression, including anxiety and anhedonia.

“Our strategy, one we think all basic researchers should adopt, is to move away from considering depression as a single or homogeneous disease. Many physicians already view depression this way, which shows that it is critical to have collaboration between basic and clinical researchers,” says Lammel.

Additional coauthors are from UC Berkeley, the University of Zurich, and UC San Diego. Funding for the work came from the National Institute on Mental Health, the Hellman Foundation, the Whitehall Foundation, the Shurl and Kay Curci Foundation, the Rita Allen Foundation, the Wayne and Gladys Valley Foundation, and a UC Regents’ Junior Faculty Fellowship.

Source: UC Berkeley

The post Biomarker may clear up how depression saps motivation appeared first on Futurity.

Biomarker may clear up how depression saps motivation published first on https://triviaqaweb.weebly.com/

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inbonobo · 6 years ago

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Research conducted at the University of Toronto by Stéphane Côté and colleagues confirms that the rich are less generous than the poor, but their findings suggest it’s more complicated than simply wealth making people stingy.

Rather, it’s the distance created by wealth differentials that seems to break the natural flow of human kindness. Côté found that “higher-income individuals are only less generous if they reside in a highly unequal area or when inequality is experimentally portrayed as relatively high.” Rich people were as generous as anyone else when inequality was low. The rich are less generous when inequality is extreme, a finding that challenges the idea that higher-income individuals are just more selfish. If the person who needs help doesn’t seem that different from us, we’ll probably help them out. But if they seem too far away (culturally, economically) we’re less likely to lend a hand.

The social distance separating rich and poor, like so many of the other distances that separate us from each other, only entered human experience after the advent of agriculture and the hierarchical civilizations that followed, which is why it’s so psychologically difficult to twist your soul into a shape that allows you to ignore starving children standing close enough to smell your plate of curry. You’ve got to silence the inner voice calling for justice and for fairness. But we silence this ancient, insistent voice at great cost to our own psychological well-being.

A wealthy friend of mine recently told me, “You get successful by saying ‘yes,’ but you need to say ‘no’ a lot to stay successful.” If you’re perceived to be wealthier than those around you, you’ll have to say “no” a lot. You’ll be constantly approached with requests, offers, pitches, and pleas—whether you’re in a Starbucks in Silicon Valley or the back streets of Calcutta. Refusing sincere requests for help doesn’t come naturally to our species. Neuroscientists Jorge Moll, Jordan Grafman, and Frank Krueger of the National Institute of Neurological Disorders and Stroke (NINDS) have used fMRI machines to demonstrate that altruism is deeply embedded in human nature. Their work suggests that the deep satisfaction most people derive from altruistic behavior is not due to a benevolent cultural overlay, but from the evolved architecture of the human brain.

Psychologists Dacher Keltner and Paul Piff monitored intersections with four-way stop signs and found that people in expensive cars were four times more likely to cut in front of other drivers, compared to folks in more modest vehicles. When the researchers posed as pedestrians waiting to cross a street, all the drivers in cheap cars respected their right of way, while those in expensive cars drove right on by 46.2 percent of the time, even when they’d made eye contact with the pedestrians waiting to cross. Other studies by the same team showed that wealthier subjects were more likely to cheat at an array of tasks and games. For example, Keltner reported that wealthier subjects were far more likely to claim they’d won a computer game—even though the game was rigged so that winning was impossible. Wealthy subjects were more likely to lie in negotiations and excuse unethical behavior at work, like lying to clients in order to make more money. When Keltner and Piff left a jar of candy in the entrance to their lab with a sign saying whatever was left over would be given to kids at a nearby school, they found that wealthier people stole more candy from the babies.

Researchers at the New York State Psychiatric Institute surveyed 43,000 people and found that the rich were far more likely to walk out of a store with merchandise they hadn’t paid for than were poorer people. Findings like this (and the behavior of drivers at intersections) could reflect the fact that wealthy people worry less about potential legal repercussions. If you know you can afford bail and a good lawyer, running a red light now and then or swiping a Snickers bar may seem less risky. But the selfishness goes deeper than such considerations. A coalition of nonprofit organizations called the Independent Sector found that, on average, people with incomes below $25,000 per year typically gave away a little over 4 percent of their income, while those earning more than $150,000 donated only 2.7 percent (despite tax benefits the rich can get from charitable giving that are unavailable to someone making much less).

There is reason to believe that blindness to the suffering of others is a psychological adaptation to the discomfort caused by extreme wealth disparities. Michael W. Kraus and colleagues found that people of higher socio-economic status were actually less able to read emotions in other people’s faces. It wasn’t that they cared less what those faces were communicating; they were simply blind to the cues. And Keely Muscatell, a neuroscientist at UCLA, found that wealthy people’s brains showed far less activity than the brains of poor people when they looked at photos of children with cancer.

Books such as Snakes in Suits: When Psychopaths Go to Work and The Psychopath Test argue that many traits characteristic of psychopaths are celebrated in business: ruthlessness, a convenient absence of social conscience, a single-minded focus on “success.” But while psychopaths may be ideally suited to some of the most lucrative professions, I’m arguing something different here. It’s not just that heartless people are more likely to become rich. I’m saying that being rich tends to corrode whatever heart you’ve got left. I’m suggesting, in other words, that it’s likely the wealthy subjects who participated in Muscatell’s study learnedto be less unsettled by the photos of sick kids by the experience of being rich—much as I learned to ignore starving children in Rajastan so I could comfortably continue my vacation.

In an essay called “Extreme Wealth is Bad for Everyone—Especially the Wealthy,” Michael Lewis observed, “It is beginning to seem that the problem isn’t that the kind of people who wind up on the pleasant side of inequality suffer from some moral disability that gives them a market edge. The problem is caused by the inequality itself: It triggers a chemical reaction in the privileged few. It tilts their brains. It causes them to be less likely to care about anyone but themselves or to experience the moral sentiments needed to be a decent citizen.”

Ultimately, diminished empathy is self-destructive. It leads to social isolation, which is strongly associated with sharply increased health risks, including stroke, heart disease, depression, and dementia.

In one of my favorite studies, Keltner and Piff decided to tweak a game of Monopoly. The psychologists rigged the game so that one player had huge advantages over the other from the start. They ran the study with over a hundred pairs of subjects, all of whom were brought into the lab where a coin was flipped to determine who’d be “rich” and “poor” in the game. The randomly chosen “rich” player started out with twice as much money, collected twice as much every time they went around the board, and got to roll two dice instead of one. None of these advantages was hidden from the players. Both were well aware of how unfair the situation was. But still, the “winning” players showed the tell-tale symptoms of Rich Asshole Syndrome. They were far more likely to display dominant behaviors like smacking the board with their piece, loudly celebrating their superior skill, even eating more pretzels from a bowl positioned nearby.

After 15 minutes, the experimenters asked the subjects to discuss their experience of playing the game. When the rich players talked about why they’d won, they focused on their brilliant strategies rather than the fact that the whole game was rigged to make it nearly impossible for them to lose. “What we’ve been finding across dozens of studies and thousands of participants across this country,” said Piff, “is that as a person’s levels of wealth increase, their feelings of compassion and empathy go down, and their feelings of entitlement, of deservingness, and their ideology of self-interest increases.”

Of course, there are exceptions to these tendencies. Plenty of wealthy people have the wisdom to navigate the difficult currents their good fortune generates without succumbing to RAS—but such people are rare, and they tend to come from humble origins. Perhaps an understanding of the debilitating effects of wealth explains why some who have built large fortunes are vowing not to pass their wealth to their children. Several billionaires, including Chuck Feeney, Bill Gates, and Warren Buffett have pledged to give away all or most of their money before they die. Buffet has famously said that he intends to leave his kids “enough to do anything, but not enough to do nothing.” The same impulse is expressed among those lower on the millionaire totem pole. According to an article on CNBC.com, Craig Wolfe, the owner of CelebriDucks, the largest custom collectible rubber duck manufacturer, intends to leave the millions he’s made to charity, which is amazing—but nowhere near as amazing as the fact that someone made millions of dollars selling collectible rubber ducks.

Do you know someone who suffers from RAS? There may be help for them. UC Berkeley researcher Robb Willer and his team conducted studies in which participants were given cash and instructed to play games of various complexity that would benefit “the public good.”

Participants who showed the greatest generosity benefited from more respect and cooperation from their peers and had more social influence. “The findings suggest that anyone who acts only in his or her narrow self-interest will be shunned, disrespected, even hated,” Willer said. “But those who behave generously with others are held in high esteem by their peers and thus rise in status.” Keltner and Piff have seen the same thing: “We’ve been finding in our own laboratory research that small psychological interventions, small changes to people’s values, small nudges in certain directions, can restore levels of egalitarianism and empathy,” said Piff. “For instance, reminding people of the benefits of cooperation, or the advantages of community, cause wealthier individuals to be just as egalitarian as poor people.” In one study, they showed subjects a short video—just 46 seconds long—about childhood poverty. They then checked the subjects’ willingness to help a stranger presented to them in the lab who appeared to be in distress. An hour after watching the video, rich people were as willing to lend a hand as were poor subjects. Piff believes these results suggest that “these differences are not innate or categorical, but are malleable to slight changes in people’s values, and little nudges of compassion and bumps of empathy.”

(via Why Are Rich People So Mean? | WIRED)

#rich #income inequality #compassion #empathy #sociology #society #inequality #generosity #poverty

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evoldir · 4 years ago

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Fwd: Postdoc: UCalifornia_Berkeley.PupfishSpeciationGenetics

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inhandnetworks-blog · 6 years ago

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Atomic-Scale Structure of Ribosome industrial wireless Could Lead to Better Antibiotics

www.inhandnetworks.com

Researchers at the Lawrence Berkeley National Laboratory have imaged the atom-by-atom structure of the ribosome attached to a molecule that controls its motion for the first time, providing a step forward for the development of better antibiotics.

The above image may look like a tangle of squiggly lines, but you’re actually looking at a molecular machine called a ribosome. Its job is to translate DNA sequences into proteins, the workhorse compounds that sustain you and all living things.

The image is also a milestone. It’s the first time the atom-by-atom structure of the ribosome has been seen as it’s attached to a molecule that controls its motion. That’s big news if you’re a structural biologist.

But there’s another way to look at this image, one that anyone who’s suffered a bacterial infection can appreciate. The image is also a roadmap to better antibiotics. That’s because this particular ribosome is from a bacterium. And somewhere in its twists and turns could be a weakness that a new antibiotic can target.

“We’re in an arms race with the resistance mechanisms of bacteria,” says Jamie Cate, a staff scientist in Berkeley Lab&rsq Vending Telemetry uo;s Physical Biosciences Division and a professor of biochemistry, biophysics and structural biology at UC Berkeley.

“The better we understand how bacterial ribosomes work, the better we can come up with new ways to interfere with them,” he adds.

Cate developed the structure with UC Berkeley’s Arto Pulk. Their work is described in the June 28 issue of the journal Science.

Their image is the latest advance in the push for more effective antibiotics. The goal is new drugs that kill the bacteria that make us sick, stay one step ahead of their resistance mechanisms, and leave our beneficial bacteria alone.

One way to do this is to get to know the bacterial ribosome inside and out. Many of today’s antibiotics target ribosomes. A better understanding of how ribosomes function will shed light on how these antibiotics work. This could also lead to even “smarter” molecules that quickly target and disable a pathogen’s ribosomes without affecting friendly bacteria.

Cate and Pulk used protein crystallography beamlines at Berkeley Lab’s Advanced Light Source to create diffraction patterns that show how the ribosome’s molecules fit together. They then used computational modeling to combine these patterns into incredibly high-resolution images that describe the locations of the individual atoms.

The result is the colorful structure at the top of this article. Those blue and purple halves are ribosomes. They’re from E. coli bacteria, but they work in similar ways throughout nature. Ribosomes move along messenger RNA and interpret its Vending Computer genetic code into directions on how to stitch amino acids into proteins.

But sometimes ribosomes want to move backward, which isn’t good when you’re in the protein-making business. That’s where that yellow-red-green squiggle wedged between the two ribosome halves comes in. It’s elongation factor G. It acts like a ratchet and prevents the ribosome from slipping backward. It also pushes the ribosome forward when it’s sluggish.

Scientists knew that elongation factor G performs these jobs, but they didn’t know how. Now, with an atomic-scale structure in hand, they can study the chemical and molecular forces involved in this ratcheting process. Cate and Pulk found that the ratchet controls the ribosome’s motion by stiffening and relaxing over and over. This is the kind of insight that could lead to new ways to monkey-wrench the ribosome.

“To create better antibiotics, we need to learn how bacterial ribosomes work at the smallest scales, and this is a big step in that direction,” says Cate.

The National Institutes of Health and the National Cancer Institute supported the research. The U.S. Department of Energy provides support for the Advanced Light Source, where this research was conducted.

Publication: Arto Pulk, et al., “Control of Ribosomal Subunit Industrial 3g router Rotation by Elongation Factor G,” Science 28 June 2013: Vol. 340 no. 6140; DOI: 10.1126/science.1235970

Image: Lawrence Berkeley National Laboratory

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epacer · 7 years ago

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EDUCATION

CALmatters

California Voters Will Weigh 100-Plus School Funding Measures in November

Californians in November will weigh billions of dollars’ worth of ballot measures for low-income housing, children’s hospitals and more. But one of the biggest asks will be mostly invisible to most voters—nearly 100 local proposals to sell bonds for school construction projects that, if passed, could total more than $12 billion in local borrowing in coming years.

About 90 school districts across the state have construction bond measures on the Nov. 6 ballot, asking local voters to approve borrowing for projects from security upgrades in the wake of the Parkland, Fla., mass shooting to air conditioning to the removal of lead from school drinking water. Another 13 districts are asking voters for harder-to-pass parcel taxes, which require a two-thirds majority for approval, and which total about $43 million.

The requests are fewer than in the 2016 general election, when more than 180 school bond measures were on local ballots, but still a hefty reflection of the ongoing need to repair and renovate aging public schools in California. Though the state spends more of its general fund on K-12 education than any other line item—$11,639 per student this year—that money is just for the classroom, and can’t be used for capital projects.

Meanwhile, a UC Berkeley study in 2012 put the statewide backlog of needed repairs and renovations at $117 billion over the next decade.

As a result, local bond measures have proliferated, particularly since 2000, when voters lowered the threshold for approval of school bonds to 55 percent, rather than the two-thirds supermajority that had been the requirement. Repaid from property tax increases in the local district, local school bond measures typically pass at high rates.

Voters approved all but five of the 35 school bond measures in the June 5 primary, according to data from the California State Treasurer’s Office. Since 2012, 86 percent of bond measures introduced by school districts have passed in California. Those bonds have totaled more than $45 billion, state data show.

This year’s measures run the gamut, though most concentrate on the basics—heating, cooling, leaky roofs.

One of the biggest is the San Diego Unified School District‘s $3.5 billion Measure YY, which would improve school security, upgrade classrooms, remove lead from drinking water and also fund charter schools. San Diego is California’s second-largest district after Los Angeles.

Salida Union School District, north of Modesto, is asking for a $2.5 million bond partly to construct secure school entrances, exits and fencing as part of its school safety plan, as well as classroom renovations and repairs to leaky plumbing.

The Lowell Joint School District in Los Angeles County is asking its voters to approve a $48 million bond that would partly repair termite damage, dry rot and deteriorating roofs in its six schools.

Palo Alto Unified School District is proposing a $460 million bond to upgrade aging classrooms, libraries and science labs and make improvements in school security and accessibility for students with disabilities.

And Bonsall Unified School District in San Diego County plans to build a new high school and replace its schools’ track and field facilities with a proposed $38 million bond.

Despite new requirements that districts specify how they will spend bond proceeds, most of the measures are worded in ways that maximize the flexibility of the money and the appeal to the public, reflecting the cottage industry of consultants school bonds have spawned.

At least 50 school district bond measures have ballot wording—some of them share exact phrasing—that explicitly states the bond funding would go toward improving schools’ safety and security systems.

Richard Michael, a Southern California bond watchdog whose California School Bonds Clearinghouse comprehensively tracks school bond measures, said one of his criticisms of school bond measures is that their ballot statements do not specify exactly how much money districts plan to devote to each of their proposed causes.

Michael said school safety has become “a hot-button” issue for voters following recent, tragic school shooting incidents and believes the reason so many districts cite safety and security in their bond proposals is that it helps appeal to voters.

“That to me is just a predatory tactic by people who want to get something passed,” Michael said. “Many of these schools have had safety (and security projects) on their previous bond measures.”

State law requires school districts that have passed bond measures to form local, volunteer oversight groups to monitor how they spend bond dollars through public meetings.

While voters approved $9 billion to fund a statewide school bond finance program in 2016—the first statewide bond to be approved in a decade—local measures remain a major source of funding for capital and facilities expenses such as school construction and renovation and technology.

The statewide bond program gives additional incentive for schools to try passing local bonds because of how the money is doled out: The state matches funds with school districts on a first come, first served basis and matches for new school facilities and renovations and repairs.

Critics of that system say it favors wealthier school districts that have the bonding capacity to raise more money and specialized staff to navigate the cumbersome application process. Districts that have applied, meanwhile, complain that the state has released only a fraction those matching funds. *Reposted article from the Times of SD by Ricardo Cano of October 6, 2018

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