Scientists plan to release altered mosquitoes designed to sabotage the species' ability to reproduce. Is this safe? Here's everything you need to know:

Who's doing this?The federal Environmental Protection Agency has approved a plan by a British biotech company called Oxitec to release about 1 billion genetically modified (GM) mosquitoes in the Florida Keys and, next year, Texas. The mosquitoes (code-named OX5034) will only be male the gender that does not bite humans and will carry a new gene that will be passed on to their female offspring and cause them to die while they're still larvae. Repeated releases of such "Trojan horse" mosquitoes should kill, in theory, 90 percent of the local population of the Aedes aegypti mosquito, which is capable of transmitting the Zika and West Nile viruses, as well as dengue and yellow fever. Oxitec claims it's safe and notes that the species is invasive to south Florida, anyway. But the plan has drawn protest from residents and some in the scientific community. "People here in Florida do not consent to the genetically engineered mosquitoes or to being human experiments," said Barry Wray of the Florida Keys Environmental Coalition. Henry Greely, a Stanford law professor and bioethicist, said the Oxitec plan reflects the almost limitless possibilities and dangers of genetic technology. "We can remake the biosphere to be what we want, from woolly mammoths to nonbiting mosquitoes," he said. "How should we feel about that? Do we want to live in nature, or in Disneyland?"

How does this technology work?Scientists first genetically modified an animal a mouse in 1974. But the process remained cumbersome and slow until the development of the CRISPR technique and other "gene-editing" technology this decade. Now scientists can target exactly which genes they want to modify using RNA, break the DNA apart at the gene's location using an enzyme, and then insert a new gene. Last year, University of Georgia researchers created the first genetically modified reptile, a brown anole, and an Indiana company, AquaBounty, expects to begin harvesting tons of salmon genetically modified to grow faster at an indoor facility later this year. Critics say this is all moving too fast, without adequate study of risks and unintended consequences. Jaydee Hanson, policy director for the International Center for Technology Assessment and Center for Food Safety, calls Oxitec's project a "Jurassic Park experiment, except without the island."

Where do the plans stand?In May, the EPA greenlighted Oxitec's plans for both Florida and Texas, issuing the company an experimental use permit. Florida state authorities followed suit with their own approval. Texas authorities and the Florida Keys Mosquito Control commission still need to sign off, and may face lawsuits. More than 31,000 people filed objections with the EPA and only 56 expressed support with some accusing the agency of relying solely on data supplied by Oxitec to issue permits. "What could possibly go wrong?" asked Hanson. "We don't know, because they unlawfully refused to seriously analyze environmental risks."

What could go wrong?Some geneticists, including Dr. Ricarda Steinbrecher of EcoNexus, a public-interest research organization, have raised alarms that Oxitec's altered mosquitoes haven't been adequately studied. The researcher said "the underlying mechanism(s) leading to cell death" in the larvae aren't "fully understood" and thus can't yield "precise and predictable results." An independent group of researchers also claimed that some of the larvae produced from an earlier Oxitec field study in Brazil survived to sexual maturity and were able to reproduce introducing the mosquitoes' modified DNA into the local population. (So far, there is no evidence that the resulting hybrid is more robust or dangerous to humans.) Critics also warn that the potential removal of even an invasive species from the food chain and ecosystem could have profound unintentional consequences; many kinds of birds and bats, for example, eat mosquitoes. "I'm not sure I care if mosquitoes suffer, if they can suffer," Greely said. "But mammals or birds, I do care."

What's the upside?Some see world-changing possibilities. Florida witnessed its first mosquito-to-human transmission of the Zika virus (which causes serious birth defects) in 2016, and West Nile is a perennial problem. As these diseases spread northward in a warming world, the elimination of a species that transmits them could prevent many illnesses and save lives. Meanwhile, a team of scientists led by the renowned botanist Joanne Chory is using CRISPR to create plants capable of storing extra carbon dioxide. Theoretically, if applied on a large scale, such plants could suck more greenhouse gases from the atmosphere and arrest the forces of climate change. "I feel like I have the weight of the world on my shoulders," Chory has said. In Australia, researchers are devising a genetically modified coral capable of withstanding rising sea temperatures. "The worst thing that we could do is ignore genetic engineering because it's frightening for some people," said coral geneticist Line Bay, "and then get 10 or 15 years down the road and realize it's the only option."

Oxitec's modified mothsSouth Florida and Texas aren't the only places that Oxitec is testing its genetically modified insects. Earlier this year, Cornell University scientists announced the results of a project they had conducted with the company involving its genetically modified diamondback moths, or Plutella xylostella. The pest reportedly wreaks between $4 billion and $5 billion a year of damage to crops like broccoli, canola, cauliflower, and cabbage. Scientists and farmers are eager to find ways of limiting the damage as well as reducing the $19 billion worth of chemical pesticides sprayed on crops each year. The modified male moths come with a self-limiting gene that causes their female progeny to die. The Cornell team declared the test a success, saying that the modified moths should "effectively suppress populations of pest P. xylostella in the field." The company is also at work developing a modified, self-limiting version of the fall armyworm, which is responsible for terrible crop losses across sub-Saharan Africa and parts of Asia. An Oxitec scientist who co-authored the Cornell report hailed the "immense potential" of protecting plants without resorting to potentially toxic pesticides.

This article was first published in the latest issue of The Week magazine. If you want to read more like it, you can try six risk-free issues of the magazine here.

Continued here:

Why are scientists creating genetically modified mosquitoes? - The Week

A long-running attempt to resurrect the American chestnut tree from the blight that virtually exterminated it an attempt that can be seen in a Plymouth germplasm conservation orchard among other places is now running on two tracks, one with traditional cross-breeding and one with genetic modification.

Well be harvesting nuts in late September. Hopefully were going to have hundreds if not thousands, said Thomas Klak, a professor at the University of New England in Maine who is about to send modified chestnut tree genes into the wild. The weird weather has not helped us. Flower development on chestnut trees has been relatively slow this year.

At UNE, Klak has built a lab that uses high-intensity light and fertilizers to bring trees to sexual maturity in six months as compared to a few years, speeding up cross-breeding efforts.

Recently his lab has used this process to grow trees developed at the State University of New York that contain a gene common in grasses which neutralizes the fungal toxin, rendering the blight harmless. This month he will perform the first cross-pollination between these genetically modified trees and American chestnut trees in the wild, having obtained permission from the U.S. Department of Agriculture.

If all goes as expected, Klak said, Half of the offspring wont die from the fungal blight and there will be renewed hope of returning the American chestnut to our forests.

Weve got a long way to go. There are four billion trees to bring back, he said.

From Georgia to Maine

The chestnut was one of the giants of Eastern forests, so prevalent that foresters joked a squirrel could travel from Georgia to Maine without leaving the chestnut canopy. It was valued both for its wood and for its bounty of nuts that were a major source of wildlife food.

Around 1904, however, a bark fungus was carried here on Chinese chestnut trees and within a few decades it had exterminated the native species. The only American chestnut trees around now are sprouts from stumps that occasionally live long enough to produce flowers and nuts for a year or two before dying.

For decades the American Chestnut Federation has been hunting down these natural remnants to mix their pollen with the flowers of Chinese chestnut trees, which resist the blight but dont have the beauty and heft of the American species. These cross-bred trees have been grown in orchards around the country and bred back and forth with other American chestnuts or Chinese chestnuts or with each other.

The orchard in Plymouth has only pure American chestnuts that were cross-bred with each other, preserving the germplasm of the native species so it can be added to any resistant strain that gets created.

This has gone on for more than six generations in hopes that genes for resistance will be transferred via germplasm, or the heritable DNA, to a tree that looks and grows like the American chestnut.

Earlier this month I saw this process in action when Curt Laffin of Hudson came to my town to pollinate a chestnut tree that my wife had spotted. It probably wont last much longer because it has a big ugly canker, a sure sign of the blight, but for the moment its a handsome, 30-foot tree full of green leaves and long, hanging flowers.

Laffin, a wildlife biologist and American Chestnut Foundation member who Ive interviewed several times over the years, brought male flowers from two surviving chestnut trees in Merrimack and spent a half-hour shaking them next to female flowers on our tree. Part of the work was done with an extendable pole that he designed. Then he cut off some male flowers that hell take back to Merrimack to do the same there.

We collect as much DNA from wild trees as we can, he said.

Hell put small bags over the flowers so they wont be pollinated by anything else, then later will collect the nuts. Theyll be planted and the resulting trees added to the cross-breeding mix at orchards throughout the Vermont-New Hampshire chapter of the American Chestnut Foundation, increasing the genetic diversity of this long-running effort.

It takes a couple of years to grow a mature tree and more years to see if the tree can resist the blight thats present in the environment before deciding which individuals to use for the next generation, so this has been a slow, laborious process.

And its beginning to look like a process that wont succeed.

Genetic modification

Originally they thought that it took three or four genes from Chinese chestnut to provide resistance. Now we know dozens of genes are needed, Laffin said. The possibility of transferring that many genes via the random mixing of cross-breeding is beginning to seem very unlikely.

Enter genetic modification, which can pick and choose among the genes that get transferred.

Scientists at SUNYs College of Environmental Science and Forestry were able to insert a gene that lets a plant create an enzyme called oxalate oxidase, written as OxO. The enzyme neutralizes the acid produced by the fungus, which is what destroys the chestnut trees cells and kills it.

Klak said OxO is a good candidate for genetic transfer because it exists naturally in many different plants, from azaleas to bananas the one used at SUNY-ESF came from wheat. Klak said theres hardly a person in the U.S. who hasnt eaten something which contains the gene already.

Just as importantly, Klak said OxO wont push the chestnut tree blight into evolving resistant strains because it doesnt alter the fungal life cycle, but merely neutralizes a side effect.

The blight can function and live well. It doesnt kill the blight, just makes the chestnut tree tolerate it, said Klak.

The resulting tree is normal in all other ways, he said: Dozens of studies have been done to document that transferring it creates a tree that is just like the wild chestnut except it wont die from blight.

GMO concern

That isnt any solace to opponents, who are opposed to the project because of concerns about the unintended consequences of genetic modification, particularly when it transfers a gene from a species that would not naturally cross-breed with the host.

Once a gene becomes released in the wild it is almost impossible to contain it. Thats especially true if the gene jumps to other species, which has happened with some genes inserted into domestic crops, where it might cause a different and unwelcome response.

There is also a concern from opponents that the chestnut program will be used as a sort of biotech Trojan horse. If creating a GMO chestnut helps bring back a beloved and valuable species, it might become a poster boy for other GMO trees and then genetic modification of other wild species, they fear.

As might be expected, Klak thinks these concerns are misplaced.

This doesnt open up a Pandoras box, he said. It doesnt affect other attempts to bring genetically engineered plants into deregulation. They have to go through the same process go through a very rigorous scientific process to ensure there are no dangers of releasing the transgenic species.

As for Laffin and the American Chestnut Federation, they will continue with the decades-old program of crossing Chinese and American chestnuts in hopes that nature will create the solution.

The New Hampshire-Vermont chapter of the ACF is one of 16 around the country. Each is supposed to provide 35 trees that can be fertilized with pollen from the transgenic tree, which is a clone my towns tree and the Merrimack tree will be part of that. The idea is to create a diverse population with traits developed from growing in different parts of the Eastern seaboard, each carrying the OxO gene.

This is a pretty vigorous tree, he commented as he loaded his pickup. Well have to see how it goes.

Read this article:

Breeding isn't resurrecting the chestnut tree; genetic engineering might - Concord Monitor

A medical student studying under a controversial professor finds herself entangled in a world offorbidden science. A tale as old as time. But what if theres another, more personal reason shes embraced synthetic biology and genetic enhancements? Its not just because she thinksbiohackingis cool. Shes there to bring someone down.

Netflix has released the first trailer forBiohackers, a German sci-fi series directed by Christian Ditter(Girlboss), coming on the heels of the third and final season ofDark. It stars Luna Wedler as Mia Akerlund, a medical student studying under Professor Tanja Lorenz (Jessica Schwartz). Thanks to her roommates (and a cute colleague), Mia finds herself embroiled in the world of biohacking, which is the catch-all term for citizen or do-it-yourself biology.

But its not all silent discos and bioluminescent mice. Mias determined tofigure out the truth behind Tanjas experiments, which destroyed her family years ago and could, even now, be placing biohack technology in the wrong hands.

Its interesting that this series takes place in Germany, as the country is known for its opposition to the practice of biohacking. The government has had a long-standing law that prohibits genetic engineering experiments outside of state-licensed facilities. In 2017, the German governmentgot aggressiveagainst biohackers, warning them that anyone caught doing genetic experiments outside of a lab could face a huge fine or up to three years in prison. That said, there has been some slow progress. Last year, two officers from the German Armed Forcesannouncedtheir own line of biohacking supplements, which were inspired by their time studying at a California university.

According toBiohackinfo, some folks in the DIY science community are worried that the countrys general anti-biohacking stance means the series could wind up promoting the same viewpoint (likeGattaca, a movie they donotcare for). That doesnt mean basement biohacking isnt immune to criticism. There are somelegitimate issueswith the practice, namely when folks do things like inject themselveswith their own semento try and cure their back pain.

The six-episode first season ofBiohackersdebuts on Netflix August 20.

View post:

A Woman Goes All Count of Monte Cristo on Genetics in the Biohackers Trailer - Gizmodo UK

The novel CRISPR-Cas enzyme, isolated from bacteriophages, can target a wider range of genetic sequences, say the researchers.

Scientists reveal a newly discovered CRISPR enzyme, CRISPR-Cas, can target a wider range of genetic sequences than either Cas9 or Cas12, and its comparatively small size could make cellular delivery easier.

In their study published in Science, Patrick Pausch, Jennifer Doudna and colleagues from University of California Berkeley, US, tested the functionality of the new Cas enzyme in both human and plant cells. They concluded that the enzyme, isolated from bacteriophages, provides a powerful new tool in the CRISPR genome editing toolbox.

While commonly known as a tool for genetic engineering, in their natural habitat CRISPR-Cas systems provide single-celled organisms with adaptive immunity against viruses and plasmids. CRISPR RNAs (crRNA) in the host recognise DNA from previously encountered viruses upon reinfection and direct CRISPR-associated or Cas enzymes to destroy the viruses.

While CRISPR-Cas systems almost exclusively exist and operate in the genomes of bacteria and archaea, they have also recently been discovered in the viruses that attack bacteria, called bacteriophages. However, these systems notably lack the Cas proteins commonly found in other CRISPR-Cas systems, instead they harbour the genetically unique and unusually small Cas enzyme.

In their paper, the team demonstrated how the phage-derived CRISPR-Cas system functions: according to the researchers, Cas uses a single active site for both CRISPR RNA (crRNA) production and processing; and crRNA-guided DNA cutting to target foreign nucleic acids. This enzyme is the most compact CRISPR-Cas system identified so far, remarked the scientists.

Visit link:

Novel CRISPR enzyme could expand the range of targets for gene therapy - Drug Target Review

UNIVERSITY PARK, Pa. Ateam of Penn State and University of Washington researchersrecentlydeveloped anewalgorithmtohelp prevent the failure of engineered genetic systems,ororganisms engineered to have new capabilities.

Engineered genetic systems are the source of biotechnology's revolution, said Howard Salis, Penn State associate professor of biological engineeringand chemical engineering andcorresponding author of the study. Engineered organisms produce a cornucopia of biorenewable products, including biodegradable plastic bottles, therapeutic proteins and nutritional supplements. Probiotic bacteria have been engineered to live in your gut and cure metabolic disease. TheImpossible Burgerwas made possible by engineering organisms to produceheme.

The Salis Lab at Penn State created thousands of highly non-repetitive genetic parts for engineering organisms with much greater genetic stability, using a newly developed algorithm that uses graph theory to solve a challenging computational problem.

In synthetic biology, engineers select genetic parts and assemble them into engineered genetic systems. However, problems arise when engineers reuse genetic parts in multiple locations or choose genetic parts with similar DNA sequences, which include genes and their controlling sequences.

Engineers often build systems by repeatedly using the same components, whether it's a multi-truss bridge or a multi-core CPU, Salis said. However, when synthetic biologists apply the same strategy to add new capabilities to organisms, millions of dollars of R&D [research and development] effort can be lost overnight. The key challenge is that reusing genetic parts will introduce long repetitive sequences of DNA into an organism,which often causes the organism to spontaneously break this DNA, removing the newly added capabilities.

Repetitive DNA is modified by a biological process called homologous recombination, where two regions of DNA with similar nucleotide sequences will swap locations or be deleted. When these sequences are modified, it disrupts the cells ability to produce RNA and protein molecules. This process severely limits synthetic biologists ability to engineer cells that produce several types of RNA and protein molecules at the same time, which is necessary for many biotechnology applications.

Our research has solved this challenge by developing a novel algorithm, the Non-Repetitive Parts Calculator, and using it to rapidly create thousands of highly non-repetitive genetic parts with desired functionalities, Salis said. We now have enough characterized non-repetitive genetic parts to completely rebuild the genomes of simple organisms.

As part of the study published in Nature Biotechnology, the research team designed, constructed and characterized 4,350 highly non-repetitive bacterial promoters and 1,722 highly non-repetitive yeast promoters. Promoters are genetic parts that express genes, using transcription to produce corresponding RNA molecules.

These promoters enable the co-expression of many genes at desired expression levels, all at the same time without inadvertently introducing repetitive DNA, Salis said. It increases the availability of characterized non-repetitive genetic parts from dozens to thousands.

According to Salis, the team's unique solution can prevent significant R&D losses when engineering organisms.

Large Fortune 500 companies have spent many millions of dollars on engineering metabolic pathways in organisms to produce a desired product, he said. And then their engineered organism self-deletes the introduced DNA when grown overnight in a bioreactor,shutting down all production, a costly failure. Our non-repetitive genetic parts will prevent spontaneous failures like these from occurring.

Along with Salis, other researchers involved in the study from Penn State include Ayaan Hossain, doctoral graduate student in bioinformatics and genomics; and Sean Halper, Daniel Centar and Alexander Reis, graduate students in chemical engineering. Researchers from the University of Washington include Eirberto Lopez, research scientist/engineer; Devin Strickland, senior research scientist; and Eric Klavins, professor and chair of the Electrical and Computer Engineering Department.

The study was supported by funding from the Air Force Office of Scientific Research, the Defense Advanced Research Projects Agency, the United States Department of Energy, and a Graduate Research Innovation award to Hossain from Penn States Huck Institutes of the Life Sciences.

View post:

Researchers offer solution for one of synthetic biology's biggest problems - Penn State News

Theres a certain kind of person who upon hearing or reading any praise of markets or capitalism, immediately demands clarification or expansion. Dont forget the government!

For instance: Mention Google or Amazon as great examples of American free enterprise, and they will immediately counter with What about ARPANet?, referring the Pentagon-backed predecessor to the modern internet. No ARPANet, no Amazon, no Google, no digital economy. Of course, no market-driven commercialization, no savvy entrepreneurs, no Amazon Prime, no amazingly efficient search engine.

Which brings us to Nikki Haley, former US ambassador to the United Nations and former governor of South Carolina. (Maybe also a 2024 Republican presidential candidate.) Yesterday, Haley tweeted:

When you consider that the antiviral drug Remdesivir was developed by biopharmaceutical company Gilead Sciences and that private companies are playing a critical role in developing a vaccine [see below], crediting capitalism doesnt seem like much of a stretch to me.

Now as that chart shows, government is playing an important role by supplying market and funding certainty. And of course, government spends massively on medical research every year maybe not enough! I mean, we all know this. We all know federal research spending is important.

And yet Twitter went crazy nuts about Haleys tweet because she didnt also credit government. (Some of this group even blames, bizarrely, capitalism for the pandemic.) What about NIH? As if she thinks we are living in some minimalist government utopia where government doesnt spend quite a bit on science research.

On the other hand, many capitalism critics seem to think the private sector really contributes nothing, that drug companies merely exploit government research and US taxpayers for filthy profit. Rep. Alexandria Ocasio-Cortez, for instance, has said that by funding federal research agencies such as the National Institutes of Health, the public is acting as an early investor, putting tons of money in the development of drugs that then become privatized. The American people get no return on the investment that they have made. Here is part of my 2019 podcast chat with biotechnology entrepreneur Safi Bahcall (also author of Loonshots: How to Nurture the Crazy Ideas That Win Wars, Cure Diseases, and Transform Industries):

There are three things that people who talk about this get wrong so often. Number one, that federal dollars pay for new drugs. No. Federal dollars pay for ideas. Heres the difference. I have an idea in the shower for a movie. Heres my vision: Robots take over the world. Thats an idea. Heres the product: the movie Terminator. The distance between an idea and basic research and a finished drug is roughly the distance between me having that idea in the shower and James Cameron making the movie Terminator. Its a huge, huge distance. So no, federal research does not pay for drugs. Federal research pays for ideas, and there are lots and lots of ideas for biology and drugs just like there are lots of ideas for movies. And very, very few actually get turned into something useful.

Number two, that federal research turning into something commercial is a bad thing. As you just said in that sentence, thats exactly the point of federal research. Federal research funds market failures, game-theory issues where it doesnt make sense for any one company to invest but it does make sense for the entire society. Lets say the invention of GPS or the internet or fusion power or nuclear power or genetic engineering. The goal of that is to create something commercial. Otherwise, what are we doing it for? Just for fun?

Number three, that the government doesnt get any economic return. Of course it does. Once its created, whether its the biotechnology industry or the satellites that deliver GPS and its empowered every smartphone in the world or the internet which has enabled these trillion-dollar companies. What do those companies do every year? They pay taxes, a lot of taxes. And what do those individuals who work at those companies do every year? They pay taxes. So, of course they get an economic return.

And, finally, to ignore the indispensable role of the private sector in frontier-pushing innovation and tech progress is a massive mistake. As I have written:

The old Soviet Union, recall, had plenty of natural resources and an educated population. In his famous analysis of why the Soviets centrally planned economy failed, economist Joseph Berliner wrote, It is only a slight exaggeration to assert that if the Soviet Union had succeeded in matching the technological attainment of the leading capitalist countries, there would have been no Gorbachev, no perestroika, and no retreat from socialism. But the Soviet economy lacked the Darwinian struggle for market share and profits that otherwise would have compelled industry to seek and adopt new innovation, either technological or operational. There was, Berliner explains, no invisible foot of competition where firms faced the threat of failure from new rivals if they did not innovate.

And if you think China is powerful counter-evidence, think again.

See the article here:

Nikki Haley, capitalism, and fighting the coronavirus pandemic - American Enterprise Institute

Stranded on a tiny Italian island, a cancer researcher grew increasingly alarmed to hear that one, and then three more visitors had fallen ill with Covid-19.

Paola Muti braced for a rapid spread of the coronavirus to the 800 closely-knit islanders, many of whom she knows well. Her mother was born on Giglio Island and she often stays at the family home with its charming view of the sea through the parlor's windows.

But days passed and none of Giglio's islanders developed any Covid-19 symptoms even though the conditions seemed favorable for the disease to spread like wildfire.

The Gigliesi, as the residents are known, socialise in the steep alleys near the port or on the granite steps that serve as narrow streets in the hilltop Castle neighbourhood, with densely packed homes built against the remnants of a fortress erected centuries ago to protect against pirates.

Follow latest updates on the Covid-19 pandemic here

Dr. Armando Schiaffino, the island's sole physician for around 40 years, shared Muti's worry that there would be a local outbreak.

Every time an ordinary childhood illness, like scarlet fever, measles or chicken pox strikes, within a very few days practically all get infected on Giglio, he said in an interview in his office near the port.

Muti, a breast cancer researcher at the University of Milan where she is an epidemiology professor, decided to try to find out why it wasn't happening this time.

Were residents perhaps infected but didn't show symptoms? Was it something genetic? Something else? Or just plain luck?

Dr. Schiaffino came to me and told me, 'Hey, look, Paola, this is incredible. In this full pandemic, with all the cases that came to the island, nobody is sick.' So I said to myself: 'Right, here we can do a study, no? I am here,' Muti said.

By then, Muti was trapped on the island by Italy's strict lockdown rules. What was especially puzzling to her was that many of the islanders had had close contact with the visitors.

Giglio's first known Covid-19 case was a man in his 60s who arrived on February 18 a couple of days before Italy's first native case" would be diagnosed in the north.

The man came to Giglio for a relative's funeral, and had been coughing all the way though the service, Muti said.

The virus is mainly spread through droplets when someone coughs, sneezes or talks. The man headed back on the ferry the same day to the mainland and died three weeks later in a hospital.

On March 5, four days before the national lockdown was declared, three more visitors came from the mainland and would test positive on the island. One of them was a German man from northern Italy, the initial epicenter of Europe's outbreak.

He socialised for several days with longtime friends in Giglio, including in public eateries. After a week, due to a bad cough, he was tested on the island and the result was positive. He self-isolated in a house on Giglio.

There were other known cases, including an islander who had lived in Australia for two years before slipping back onto Giglio in mid-March during lockdown to see his parents.

Three days after arriving on Giglio, he developed a mild fever and tested positive, Muti said. He self-isolated at his parents' home.

No other case has surfaced on Giglio, including since lockdown was lifted in early June, and tourists from throughout Italy have been arriving.

Giglio is part of Tuscany, and its health office quickly sent over kits to test for antibodies to see if others may have had Covid-19.

In late April, just before the first lockdown travel restrictions would be eased, the islanders had their blood tested, lining up outside the island's school and doctor's office.

Of the 800 or so year-round residents, 723 volunteered to be tested.

We all wanted to do it, to be tranquil about any possible infection, but also to help science,'' said Simone Madaro, who had been working at the cemetery while the infected man had gathered with fellow mourners.

The Reverend Lorenzo Pasquotti, the priest who conducted the service for around 50 mourners, and who himself was tested recalled: After the funeral, there were greetings, hugging and kissing, as is the custom.

Then came the procession to the cemetery, where there were more hugs and kisses.

Of the islanders tested, only one was found to have antibodies, an elderly Gigliese man who had sailed on the same ferry to the island with the German visitor, Muti said.

Intrigued about why the virus didn't seem to interact" with the island's native population, Muti hadn't reached any conclusions by the time she was preparing to leave the island this month. She plans to write up up her study for eventual publication.

It's possible, Muti guessed, that islanders weren't exposed to enough Covid-19 to get infected.

That possibility was also voiced by Massimo Andreoni, head of infectious diseases at Rome's Tor Vergata hospital. He noted some patients are simply less capable of spreading the disease for reasons that are still unclear.

Chance might have played a role, said Daniel Altmann, a professor of immunology at Imperial College London.

It could be something more or less trivial nobody got infected because through good luck there was little contact,'' he said in an email exchange.

Or, Altmann also noted that it could be something important and exotic, such as a genetic variant common among the island's population.

With many of the Gigliesi intermarrying through generations, Muti would like to do a genetic study someday if she could obtain funding.

Giglio lies in pristine waters in a protected regional marine sanctuary, and the islanders voice relief that they live in a natural environment they like to think is good for health, whatever Muti's study might determine.

As an island, as the environment goes, we're OK, no? said Domenico Pignatelli, as the elderly man kept company with friends in chairs placed on a stony street atop Giglio.

See more here:

Luck? Genetics? Italian island spared from Covid-19 outbreak - Deccan Herald

By Gretchen ReynoldsExercise may help change exercisers brains in surprising ways, according to a new study of physical activity and brain health. The study, which included both mice and people, found that exercise prompts the liver to pump out a little-known protein, and that chemically upping the levels of that protein in out-of-shape, elderly animals rejuvenates their brains and memories. The findings raise provocative questions about whether the brain benefits of exercise might someday be available in a capsule or syringe form essentially exercise in a pill.

We already have considerable evidence, of course, that physical activity protects brains and minds from some of the declines that otherwise accompany aging. In past rodent studies, animals that ran on wheels or treadmills produced more new neurons and learned and remembered better than sedentary mice or rats. Similarly, older people who took up walking for the sake of science added tissue volume in portions of their brains associated with memory. Even among younger people, those who were more fit than their peers tended to perform better on cognitive tests.

But many questions remain unanswered about how, at a cellular level, exercise remodels the brain and alters its function. Most researchers suspect that the process involves the release of a cascade of substances inside the brain and elsewhere in the body during and after exercise. These substances interact and ignite other biochemical reactions that ultimately change how the brain looks and works. But what the substances are, where they originate and how they meet and mingle has remained unclear.

So, for the new study, which was published this month in Science, researchers at the University of California, San Francisco, decided to look inside the minds and bloodstreams of mice. In past research from the same lab, the scientists had infused blood from young mice into older ones and seen improvements in the aging animals thinking. It was like transferring a memory of youth through blood, says Saul Villeda, a professor at UCSF, who conducted the study with his colleagues Alana Horowitz, Xuelai Fan and others.

Those benefits were a result of the donor animals young age, though, not their exercise habits. The scientists suspected that exercise would spark additional changes in the bloodstream that might be transferable, whatever an animals years.

Intrigued, the scientists next set out to find what differed in the exercisers blood. Using sophisticated mass spectrometry and other techniques, they separated out and enumerated various proteins in the running animals blood that were not seen in similar profusion in blood from inactive mice.

Exercise may help change exercisers brains in surprising ways.

So, the researchers now employed genetic engineering to amplify the release of GPLD1 from the livers of old, inactive mice. Afterward, those animals performed almost like young mice on tests of learning and memory, and their brains teemed with far more newborn neurons than in other old mice. In effect, they gained the brain benefits of exercise without the effort of actually exercising.

To ensure that this reaction was not purely rodent-based, the scientists also checked blood drawn from elderly people. The older men and women who habitually walked for exercise showed higher levels of GPLD1 in their bloodstreams than those who did not.

The combined upshot of these findings seems to be that exercise improves brain health in part by prompting the liver to pump out extra amounts of GPLD1, Villeda says, although it is not yet clear how the protein then changes the brain. Subsequent experiments by the scientists showed that the protein probably does not breach the blood-brain barrier and act directly on the brain, Villeda says. Instead, it is likely to incite alterations in other tissues and cells elsewhere in the body. These tissues, in turn, produce yet more proteins that have effects on other tissues that eventually lead to direct changes to the neurotransmitters, genes and cells in the brain itself that undergird cognitive improvements.

Villeda believes that if further experiments show that GPLD1, in isolation, helps to initiate this molecular chain reaction, then it is at least conceivable that infusions of the substance might offer the brain benefits of exercise to people who are too frail or disabled for regular physical activity.

This experiment principally involved mice, though, not people, and does not tell us anything about the systemic effects of extra GPLD1, which in high amounts might be undesirable. More fundamentally, the findings highlight the pervasive, intricate, whole-body effects of exercise, with the liver, in this case, somehow changing minds and brains after workouts. At the moment, it is impossible to know if the same synchronized, interwoven processes all would occur in response to a GPLD1 exercise pill and, if not, whether it could be considered an exercise pill at all.

Villeda is quick to agree that pharmaceutical GPLD1, even if effective for brain health, would not recapitulate the benefits of exercise. There would be none of the usual fat burning, muscle building or cardiovascular improvements, he points out. But he hopes that, if future experiments in his lab with animals and people show consistent results, the substance might eventually help people who find moving difficult to think better.

Being diagnosed with any health problem is taxing, but correctly understanding it is the key to dealing with a progressive, neurological condition. One such neurological condition is Parkinsons disease, first described by James Parkinsons 200 years ago. It is characterised by tremours, overall slowing, rigidity, falls, speech troubles, constipation and more.

With research ongoing to find a permanent cure, there are many things one can routinely do to keep its multifaceted symptoms under control.

On World Parkinsons Day, Dr Azad M Irani, Consultant Department of Neurology at Jaslok Hospital and Research Centre, shares some points that will help you fight the disease.

Educating Oneself About Their IllnessUnderstanding the disease is a key to successful management. Once diagnosed with Parkinsons, request your doctor for reliable sources of information. Avoid reading unreliable information online as it may often be untrue and stressful. Advice received during small talks with relatives and friends must also be counter-checked as it may often be untrue and add to unnecessary stress.

Treatment Compliance And Timely Follow-UpsOne must take medicines on time. Dont miss follow-up appointments. Dont adjust your own medication. These can be harmful.

Physical ActivityAn essential part of successful treatment is daily exercise and physiotherapy, as this can delay progression of symptoms significantly if done regularly. Adequate sleep, preventing constipation are very important to minimise symptoms. The significance of weight loss for those overweight-obese should be emphasised. Continuing household chores, taking walks, and yoga help delay progression of symptoms significantly.

Healthy LifestyleKeeping oneself fit with a nutritious diet, sleeping on time, and daily meditation to relax calm a worried mind.

More here:

Scientists find the secret ingredient to improve brain power; exercise in a pill may soon be a reality - Economic Times