Google Funds a Design School That Works Like a Tech Incubator

Ponder this for a second: How different would HBO’s Silicon Valley be if the main character Richard had been a designer instead of a programmer?

The choice to feature a bumbling, awkward coder is illustrative of the greater Silicon Valley ecosystem, but it ignores a growing trend: Designers are playing an increasingly important role in leading startups and businesses.

Granted, the number of designers-turned-founders is still comparatively small, but a new incubator/school called 30 Weeks, is hoping to change that. The program is a collaboration between Google, The Cooper Union, education company Hyper Island and top-notch design schools including School of Visual Arts, Parsons and Pratt.

Starting this September, 20 designers will enroll in a 30-week program, working out of a co-working space in Brooklyn’s DUMBO neighborhood in hopes of turning their ideas into full-fledged, scalable businesses. Sound cool? Good, because they’re still accepting applications until June 20.

Tesla Just Gave All Its Patents Away to Competitors

Elon Musk. Photo: Ariel Zambelich/WIRED

Much like Tony Stark, Elon Musk likes to do the impossible. Electric cars, spaceships and now … patents?

Tesla CEO Elon Musk announced today that his company will not “initiate patent lawsuits against anyone who, in good faith, wants to use our technology.” In plain English, that means that if other car companies want to produce electric cars, they can use Tesla’s technology to do it, and, in turn, advance Musk’s sustainability vision.

“The mission of the company is to accelerate the widespread adoption of electric cars,” explained Tesla spokesperson Simon Sproule in an interview before the patent announcement was made. “If Tesla acts as the catalyst for other manufacturers … that will have been achieved.”

Later, in a conference call, Musk reiterated the point, saying that “putting in long hours for a corporation is hard, putting in long hours for a cause is easy.”

Of course, Tesla wants to make and sell electric cars (it exists to make a profit, theoretically), but in order to do that on a large scale, the company needs to move past the niche markets that the Model S currently plays in. They need the public to stop thinking of them as electric cars and to start thinking of them simply as cars.

“They need to see Americans … at least be open to switching to an electric vehicle lifestyle,” Kelly Blue Book analyst Karl Brauer said. By themselves, “they’re never going to convert the average American into an electric car fan, even with great press and great publicity.” A $90,000 electric car for celebrities and the Silicon Valley elite isn’t going to save the world. Tesla needs to, and is thinking much bigger.

The Tesla Model S at the company’s factory in Northern California. Photo: Ariel Zambelich/WIRED

At the moment, the Model S is the only electric car that acts as a true replacement for a more traditional gasoline-powered automobile, with its 200+ mile range and network of rapid charging stations that stretches from coast-to-coast across 96 stations in the US, with dozens more coming in North America, Europe and Asia. Not enough people are interested in electric cars with 70-100 miles of range, as Nissan and others are discovering. But, if other car companies adopt some of Tesla’s technology to develop long-range electric cars, that’s nothing but good for the company.

Tesla’s longer-term goal is to sell a $30,000 car with 200-miles of range. At that point, a potential owner worries less about whether they can get to Grandma’s house in an emergency, and starts to assess it as a normal piece of transportation. Tesla’s cars remain a curiosity. In order to transition from a technological plaything that nerds get excited about into something that busy regular people want to buy, Tesla needs to prove that driving an electric car is a normal thing to do.

Finally, if other automakers begin using Tesla’s technology, it increases the value of the company and its inventions as well as validating what the company is doing. Tesla has hundreds of patents, but if the company goes bust because not enough people buying electric cars, they’re all meaningless. Tesla needs widespread adoption of electric cars and the easiest way to do that is to get other automakers to sell them too. More electric cars in the world means Tesla’s cars aren’t so weird, and they become an easier sell to a skeptical public.

Releasing its patents is certainly a controversial move, though TSLA shareholders seem fairly indifferent — shares are trading only slightly lower following the announcement.

At the end of the day, the biggest risk for Musk isn’t that BMW or Toyota will steal his technology. It’s that the big automakers might not be interested in electric cars enough to bother building them at all.

Increasing the Fragmentation of Natural Landscapes May Help Spread Disease

Powdery mildew-afflicted ribwort plantain leaves. Image: Susanna Kekkonen/Science

The modern natural world is an increasingly fragmented one, with islands of ecological integrity isolated in vast sprawls of human development.

An environment arranged in such a fashion may inadvertently fuel the spread of disease, according to a new study of the interaction of plants and a fungus pathogen. Conversely, large and continuous natural areas may dampen the spread. While the observations can’t be directly extrapolated from a single system to nature at large, they hint at a potentially troubling dynamic.

“If we have these little islands of susceptible hosts in a landscape, harboring high levels of infection that transmit to everything around them, the potential is there for spillover” to agriculture and perhaps humans, said biologist Anna-Liisa Laine of the University of Helsinki.

The study, published June 12 in Science , describes 12 years of the battle between Plantago lanceolata, a herb commonly known as ribwort plantain, and leaf-blighting powdery mildew in forests on the Åland Islands in the Baltic Sea.

The researchers, led by Laine and fellow University of Helsinki biologists Jussi Jousimo and Ayco Tack, found that vulnerability to the disease changed depending on the area of ribwort populations. Plants in isolated populations were more likely to become infected, and those in larger, connected patches were more likely to resist infection.

It’s a counterintuitive dynamic: At least on the surface, conventional ecological theory predicts that disease should spread much more readily through larger patches. Instead, those regular exposures seemed to heighten plant defenses, serving almost as evolutionary inoculations.

In large patches, disease-resistant plants were more likely to reproduce and spread, and—crucially—there was a larger gene pool from which disease-resistant mutations might arise. Small-patch plants, less-exposed and with a smaller gene pool to draw from, remained susceptible to infection when it finally did occur.

'We've known for some time that habitat fragmentation exacerbates many diseases, but this study reveals a whole new mechanism.'

“I would have predicted exactly the opposite result—that hosts in fragmented populations would be protected from this fungus,” said disease ecologist Richard Ostfeld of the Cary Institute for Ecosystem Studies, who was not involved in the research.

“We’ve known for some time that habitat fragmentation exacerbates many diseases, but this study reveals a whole new mechanism,” Ostfeld added.

Among the exacerbations to which Ostfeld refers are enhanced virulence of the lethal Hendra virus in isolated populations of Australian flying foxes, and also outbreaks of yellow fever in fragmented forests in southern Brazil.

Common to these incidents is a newfound appreciation for disease dynamics, with healthy ecologies linked to evolutionary patterns that naturally reduce the dangers of epidemic outbreaks.

Disease ecologist Meghan Duffy of the University of Michigan did, however, caution against extrapolating too much from the new study. More research involving other hosts and diseases is needed to see whether similar patterns are found elsewhere, she said.

“Whether habitat fragmentation is likely to contribute to increased infectious disease in a wide range of systems is an open question,” she said, but the findings underscore how links between the environment, human impacts and disease “might be more complicated than we might initially guess.”

Laine, whose group is now studying infection dynamics of viruses in ribwort, said that one significant, broad-spectrum message is the importance of genetic diversity. “It’s enough in itself to dilute disease transmission,” she said. “We see less infection when there is a diversity in resistance traits.”

Aside from possible spillovers from habitat pockets into human areas, as with the Hendra virus, there may also be conservation implications to the new findings. Some scientists have wondered whether connecting protected areas may increase the spread of disease; instead, said Laine, connection provides protection.

ACLU Sues After Illinois Mayor Has Cops Raid Guy Parodying Him on Twitter

Peoria Mayor Jim Ardis. Image: Ron Johnson/AP

Countless parody Twitter accounts have been created over the years — British Petroleum, Mark Zuckerberg, the NSA, the Queen of England and even God.

In each case, the target of the account either did nothing in response or simply requested that the owner of the account clearly label it a fake.

Not the mayor of Peoria, Illinois, however.

Mayor Jim Ardis directed his city manager to use the police to hunt down the author of a parody account about him and threatened Twitter with litigation unless it suspended the account, which it did. Now a man who was raided and arrested for creating the account is suing the mayor, a former police chief, and others for violating his constitutional rights.

Jonathan Daniel, 29, created the Twitter account @peoriamayor in March and used it primarily to amuse his friends by retweeting their comments as the mayor. Daniel sent out satiric tweets that contradicted the mayor’s clean-cut image by conveying the mayor as having a preoccupation with sex, drugs, and alcohol. Though he also sent out tweets from the account, he labeled it a parody account three days after he created it, and the account was only active 10 days before it closed.

“The joke of the account was to have my fictional mayor saying things that no one would possibly think that Mayor Jim Ardis would say,” Daniel said in a statement. “If the Mayor was concerned, all he had to do was tell the public that his was not his account and not his words, rather than involving the police.”

The matter didn’t end there, however. Peoria police obtained two warrants, under false pretenses the ACLU alleges, to obtain the subscriber IP address used with the Twitter account and to get Daniel’s home address from his internet service provider.

They also obtained a search warrant and on April 15 raided Daniel’s home while the defendant was at work and seized several computers, phones and other electronic devices while Daniel’s roommates were present. Police also arrived to Daniel’s place of employment where they searched him before arresting him for falsely impersonating a public official and taking him to the police station for interrogation. Daniel was only released after demanding to speak with a lawyer, but police refused to return his mobile phone or other property to him.

Illinois law defines false personation of a public official as someone “knowingly and falsely represent[ing] himself or herself to be . . . [a] public officer or a public employee or an official or employee of the federal government.”

But according to the ACLU, the provision only criminalizes false representations made in person. “Illinois courts require as an element of the offense that there be an intent to deceive the public that the impersonator is acting in the official capacity of a public official,” the organization notes in its complaint. But Daniel’s account “was not reasonably believable as conveying the voice or message of the actual mayor,” the group wrote, and Daniel had “no intention of deceiving people into believing the account was actually operated by a representative of the mayor or the mayor himself, and no reasonable person could conclude such an intent from the content of the tweets or the Twitter account’s profile page.”

Daniel was never charged with any crime because the state’s attorney determined that his conduct did not violate the false personation statute. The American Civil Liberties Union of Illinois filed a lawsuit on his behalf today (.pdf) alleging that the mayor, city manager Patrick Urich, former police chief Steven Settingsgaard, and other officials violated his First and Fourth Amendment rights.

“Political parody is a great tradition in the United States – from Thomas Nast to Jon Stewart,” Harvey Grossman, legal director for the ACLU of Illinois said in a statement. “The only way to hold these government officials accountable is to have a federal court rule that their actions violated the fundamental constitutional rights of our client.”

No one at the mayor’s office was available to respond to questions. A clerk in the office said the mayor would be releasing a statement later today.

Key step toward a safer strep vaccine

An international team of scientists, led by researchers at the University of California, San Diego School of Medicine, have identified the genes encoding a molecule that famously defines Group A Streptococcus (strep), a pathogenic bacterial species responsible for more than 700 million infections worldwide each year.

The findings, published online in the June 11 issue of Cell Host & Microbe, shed new light on how strep bacteria resists the human immune system and provides a new strategy for developing a safe and broadly effective vaccine against strep throat, necrotizing fasciitis (flesh-eating disease) and rheumatic heart disease.

"Most people experience one or more painful strep throat infections as a child or young adult," said senior author Victor Nizet, MD, professor of pediatrics and pharmacy. "Developing a broadly effective and safe strep vaccine could prevent this suffering and reduce lost time and productivity at school and work, estimated to cost $2 billion annually."

Efforts to develop such a vaccine have been significantly hindered by complexities in how the human immune system reacts to the bacterial pathogen. Specifically, some patients with strep infections produce antibodies that cross-react with their own heart valve tissue, leading to rheumatic fever and heart damage. Though rare in the United States, rheumatic fever remains common in some developing countries and causes significant disability and death.

The Cell Host & Microbe study suggests a way to circumvent the damaging autoimmune response triggered by strep. Specifically, the researchers noted that the cell wall of strep is composed primarily of a single molecule known as the group A carbohydrate (or GAC) which, in turn, is built from repeating units of the bacterial sugar rhamnose and the human-like sugar N-acetylglucosamine (GlcNAc).

Previous research has indicated that GlcNAc sugars present in GAC may be responsible for triggering production of heart-damaging antibodies in some patients. Nizet said the latest findings corroborate this model, and suggest that eliminating the pathogen's ability to add GlcNAc sugars to GAC could be the basis for a safe vaccine.

"In this study, we discovered the strep genes responsible for the biosynthesis and assembly of GAC, the very molecule that defines the pathogen in clinical diagnosis," said first author Nina van Sorge, PharmD, PhD, a former postdoctoral fellow at UC San Diego who now leads her own laboratory at Utrecht University Medical Center in the Netherlands. "This discovery allowed us to generate mutant bacterial strains and study the contribution of GAC to strep disease."

The researchers found that a mutant strep strain lacking the human-like GlcNAc sugar on the GAC molecule exhibited normal bacterial growth and expressed key proteins known to be associated with strep virulence, but was easily killed when exposed to human white blood cells or serum. The mutant strep bacteria also lost the ability to produce severe disease in animal infection models

"Our studies showed that the GlcNAc sugar of GAC is a critical virulence factor allowing strep to spread in the blood and tissues," van Sorge said. "This is likely important for the rare, but deadly, complications of strep infection such as pneumonia, necrotizing fasciitis and toxic shock syndrome."

The researchers also identified a way to remove the problematic GlcNAc sugar so that a mutant form of the bacteria with only rhamnose-containing GAC could be purified and tested as a vaccine antigen.

"We showed that antibodies produced against mutant GAC antigen helped human white blood cells kill the pathogen and protected mice from lethal strep infection," said Jason Cole, PhD, a visiting project scientist from the University of Queensland, Australia, and co-lead author of the paper. "Because GAC is present in all strep strains, this may represent a safer antigen for inclusion in a universal strep vaccine."

Researchers plan to assess the new modified antigen against other candidates in advanced strep throat vaccine tests in nonhuman primates beginning later this year in Atlanta, Georgia, funded by the National Health and Medical Research Council of Australia.

"It is satisfying to find that a fundamental observation regarding the genetics and biochemistry of the pathogen can have implications not only for strep disease pathogenesis, but also for vaccine design," Nizet said.

Gum disease bacteria selectively disarm immune system, study finds

The human body is comprised of roughly 10 times more bacterial cells than human cells. In healthy people, these bacteria are typically harmless and often helpful, keeping disease-causing microbes at bay. But, when disturbances knock these bacterial populations out of balance, illnesses can arise. Periodontitis, a severe form of gum disease, is one example.

In a new study, University of Pennsylvania researchers show that bacteria responsible for many cases of periodontitis cause this imbalance, known as dysbiosis, with a sophisticated, two-prong manipulation of the human immune system.

Their findings, reported in the journal Cell Host & Microbe, lay out the mechanism, revealing that the periodontal bacterium Porphyromonas gingivalis acts on two molecular pathways to simultaneously block immune cells' killing ability while preserving the cells' ability to cause inflammation. The selective strategy protects "bystander" gum bacteria from immune system clearance, promoting dysbiosis and leading to the bone loss and inflammation that characterizes periodontitis. At the same time, breakdown products produced by inflammation provide essential nutrients that "feed" the dysbiotic microbial community. The result is a vicious cycle in which inflammation and dysbiosis reinforce one another, exacerbating periodontitis.

George Hajishengallis, a professor in the Penn School of Dental Medicine's Department of Microbiology, was the senior author on the paper, collaborating with co-senior author John Lambris, the Dr. Ralph and Sallie Weaver Professor of Research Medicine in the Department of Pathology and Laboratory Medicine in Penn's Perelman School of Medicine. Collaborators included Tomoki Maekawa and Toshiharu Abe of Penn Dental Medicine.

Work by Hajishengallis's group and collaborators had previously identified P. gingivalis as a "keystone pathogen." Drawing an analogy from the field of ecology, in which a species such as a grizzly bear is thought of as a keystone species because of the influence it has over a number of other species in the community, the idea suggests that, although P. gingivalis may be relatively few in number in the mouth, their presence exerts an outsized pull on the overall microbial ecosystem. Indeed, the team has shown that, although P. gingivalis is responsible for instigating the process that leads to periodontitis, it can't cause the disease by itself.

"Scientists are beginning to suspect that keystone pathogens might be playing a role in irritable bowel disease, colon cancer and other inflammatory diseases," Hajishengallis said. "They're bugs that can't mediate the disease on their own; they need other, normally non-pathogenic bacteria to cause the inflammation."

In this study, they wanted to more fully understand the molecules involved in the process by which P. gingivalis caused disease.

"We asked the question, how could bacteria evade killing without shutting off inflammation, which they need to obtain their food," Hajishengallis said.

The researchers focused on neutrophils, which shoulder the bulk of responsibility of responding to periodontal insults. Based on the findings of previous studies, they examined the role of two protein receptors: C5aR and Toll-like receptor-2, or TLR2.

Inoculating mice with P. gingivalis, they found that animals that lacked either of these receptors as well as animals that were treated with drugs that blocked these receptors had lower levels of bacteria than untreated, normal mice. Blocking either of these receptors on human neutrophils in culture also significantly enhanced the cells' ability to kill the bacteria. Microscopy revealed that P. gingivalis causes TLR2 and C5aR to physically come together.

"These findings suggest that there is some crosstalk between TLR2 and C5aR," Hajishengallis said. "Without either one, the bacteria weren't as effective at colonizing the gums."

Further experiments in mice and in cultured human neutrophils helped the researchers identify additional elements of how P. gingivalis operates to subvert the immune system. They found that the TLR2-C5aR crosstalk leads to degradation of the protein MyD88, which normally helps clear infection. And in a separate pathway from MyD88, they discovered that P. gingivalis activates the enzyme PI3K through C5aR-TLR2 crosstalk, promoting inflammation and inhibiting neutrophils' ability to phagocytose, or "eat," invading bacteria.

Inhibiting the activity of either PI3K or a molecule that acted upstream of PI3K called Mal restored the neutrophils' ability to clear P. gingivalis from the gums.

"P. gingivalis uses this connection between C5aR and TLR2 to disarm and dissociate the MyD88 pathway, which normally protects the host from infection, from the proinflammatory and immune-evasive pathway mediated by Mal and PI3K," Hajishengallis said.

Not only does the team's discovery open up new targets for periodontitis treatment, it also suggests a bacterial strategy that could be at play in other diseases involving dysbiosis.

New sensor to detect harmful bacteria on food industry surfaces

A new device designed to sample and detect foodborne bacteria is being trialled by scientists at the University of Southampton.

The Biolisme project is using research from the University to develop a sensor capable of collecting and detecting Listeria monocytogenes on food industry surfaces, thereby preventing contaminated products from entering the market.

Listeria monocytogenes is a pathogen that causes listeriosis, an infection with symptoms of fever, vomiting and diarrhoea, that can spread to other parts of the body and lead to more serious complications, like meningitis.

Transmitted by ready-to-eat foods, such as milk, cheese, vegetables, raw and smoked fish, meat and cold cuts, Listeria monocytogenes has the highest hospitalisation (92 per cent) and death (18 per cent) rate among all foodborne pathogens. Listeriosis mainly affects pregnant women, new-born children, the elderly and people with weakened immune systems.

Current techniques to detect the bacteria take days of testing in labs, but the new device aims to collect and detect the pathogen on location within three to four hours. This early and rapid detection can avoid the cross contamination of ready-to-eat food products.

Traditional methods of testing, where sample cells are cultivated in labs, are also flawed. 'Stressed' cells will not grow in cultures (and will therefore produce negative results) despite the bacteria being present, live and potentially harmful.

Alternative techniques, based on molecular methods, will detect all cell types, but don't differentiate between live and harmless dead cells, which can remain after disinfection.

The new device is designed to sample single cells and biofilms -- groups of microorganisms where cells stick together on surfaces. Compressed air and water is used to remove the cells before they are introduced to an antibody. If Listeria monocytogenes is present, cells react with the antibody to produce a florescent signal, which is detected by a special camera.

Doctor Salomé Gião and Professor Bill Keevil from Southampton's Centre for Biological Science Unit have been studying Listeria monocytogenes biofilms under different conditions and will be testing the new prototype. "We researched biofilms under different stresses to find the optimum pressure to remove cells from different surfaces, without disrupting the cells themselves," says Dr Gião. "We also found that biofilms can form on surfaces even if they are covered in tap water.

"The scientific research we have carried out at the University of Southampton has been used by our Biolisme project partners to develop a device which will have major implications for the food industry. By making the process simpler we hope that testing will be conducted more frequently, thereby reducing the chance of infected food having to be recalled or making its way to the consumer."

The prototype sensor has been finalized in France and field trials are now underway to test the device before it is demonstrated in food factories.

José Belenguer Ballester, from project partner ainia centro tecnológico, added: "Biolisme has raised the expectations of food business operators because the devices being developed will allow rapid assessment of the cleanliness of manufacturing plants."

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The above story is based on materials provided by University of Southampton . Note: Materials may be edited for content and length.