杭州桑拿网

The earliest asteroids were probably made of mud, not rock.

Radioactive heat in the early solar system could have melted globs of dust and ice before they had a chance to turn to rock, a new simulation published July 14 in Science Advances shows. The results could solve several puzzles about the composition of meteorites found on Earth and may explain why asteroids are different from comets.

Most knowledge about the first solid bodies in the solar system comes from meteorites called carbonaceous chondrites, thought to be chunks of the first asteroids. Their chemical compositions are almost identical to the sun’s — if you took all the hydrogen and helium out of the sun, you’d get the mineral ratios found in these bits of rock.
That similarity suggests the first asteroids formed directly from the disk of gas and dust that preceded the planets. The composition also suggests that these rocks formed in the presence of water and at relatively low temperatures, around 150° Celsius.

It’s hard to explain all those features at once. If the original asteroids were bigger than about 20 kilometers across — and there’s no reason to think they weren’t — decaying radioactive elements inside them would have made the rock hotter than that. Some planetary scientists have suggested that the asteroids were porous, and water flowing through a primitive plumbing system cooled them. But the water should have stripped some elements from the rock, ruining their sunlike chemistry.

“It was a paradox,” says planetary scientist Philip Bland of Curtin University of Technology in Perth, Australia.
Bland was modeling how those original globs of ice and dust could have compressed into solid rock, when it hit him: What if they weren’t rock at all?
“At that moment, nothing has happened to force those grains together to turn it into a rock,” he says. That was just something everyone had assumed.

Bland reasoned that heat from radioactive decay would melt the ice, and the resulting body would be an enormous dollop of mud. The mud would suspend sediment particles, so they wouldn’t be stripped of their sunlike elements. And it would allow the early asteroids to be any size and remain cool.

Bland and Bryan Travis of the Planetary Science Institute, who is based in Los Alamos, N.M., ran computer models of how the mud balls would evolve. Convection currents, like those that move molten rock within the Earth’s mantle, would develop, helping to transfer heat into space, the models showed. After several million years, the ball would harden completely, yielding the asteroids seen today.

“It nails the paradox,” Bland says.

Mud balls could even explain the difference between asteroids and comets, he says. Comets, which are more icy than rocky and tend to live farther from the sun, may simply have formed later in the solar system’s history, when there was less radioactive heat available to melt them.

The model also showed that some asteroids would be muddy all the way through, while others would develop cores of larger grains, with a great mud ocean on top of them.

The latter result could describe not just asteroids but bodies like the dwarf planet Ceres, the largest object in the asteroid belt. Observations from NASA’s Dawn spacecraft showed that Ceres has a rocky core and may once have had an ocean that has since evaporated, says UCLA planetary scientist Edward Young. “That process may have been something like what they’re describing.”

Planetary scientist Brandon Johnson of Brown University in Providence, R.I., thinks the model will inspire more research. “I’m interested in it myself, actually,” he says. “It makes a lot of sense and paints a clear picture of what might have been happening.”

But Young is concerned that the model’s flexibility means it won’t make specific enough predictions for future work to test it. “It has so many knobs, you can get it to do whatever you want,” he says. “I’m trying to think of what the killer observation would be.”

Some people might think that online privacy is a, well, private matter. If you don’t want your information getting out online, don’t put it on social media. Simple, right?

But keeping your information private isn’t just about your own choices. It’s about your friends’ choices, too. Results from a study of a now-defunct social media site show that the inhabitants of the digital age may need to stop and think about just how much they control their personal information, and where the boundaries of their privacy are.

When someone joins a social network, the first order of business is, of course, to find friends. To aid the process, many apps offer to import contact lists from someone’s phone or e-mail or Facebook, to find matches with people already in the network.

Sharing those contact lists seems innocuous, notes David Garcia, a computational social scientist at the Complexity Science Hub Vienna in Austria. “People giving contact lists, they’re not doing anything wrong,” he says. “You are their friend. You gave them the e-mail address and phone number.” Most of the time, you probably want to stay in touch with the person, possibly even via the social media site.

But the social network then has that information — whether or not the owner of it wanted it shared.

Social platforms’ ability to collect and curate this extra information into what are called shadow profiles first came to light with a Facebook bug in 2013. The bug inadvertently shared the e-mail addresses and phone numbers of some 6 million users with all of their friends, even when the information wasn’t public.

Facebook immediately addressed the bug. But afterward, some users noticed that the phone numbers on their Facebook profiles had still been filled in — even though they had not given Facebook their digits. Instead, Facebook had collected the numbers from the contact lists innocently provided by their friends, and filled in the missing information for them. A shadow profile had become reality.
It’s no surprise that a social platform could take names, e-mail addresses and phone numbers and match them up with other people on the same platform. But Garcia wondered if these shadow profiles could be extended to people not on the social platform at all.

He turned to a now-defunct social network called Friendster. A precursor to sites like MySpace and Facebook, Friendster launched in 2002. In 2008, the social site boasted more than 115 million users. But by 2009 people began to jump ship for other sites, and in 2015 Friendster closed for good. Millions of abandoned public profiles vanished into the ether.

Or did they? The Internet Archive — a nonprofit library — has an archive of more than 200 billion web pages, including Friendster. Garcia was able to use that repository to get data on 100 million public accounts from the social media site. Garcia dug through the records in a process he calls Internet Archaeology, after a satirical video from The Onion in which an internet archaeologist announces that he has, ironically, discovered Friendster. “The time scale of online media is very fast, but it’s still studying things in society that don’t exist anymore,” he explains.

Garcia hunted for patterns in the data. Most people don’t have a random assortment of friends. Married people tend to be friends with other married people, for example. But people also have connections that complicate the ability to predict who’s connected to who. People who identified as gay men were more likely to be friends with other gay men, but also likely to be friends with women. Straight women were more likely to be friends with men.

Using this information, Garcia was able to show that he could predict characteristics such as the marital status and sexual orientation of users’ friends who were not on the social media network. And the more people in the social network who shared their own personal information, the more information the network received about their contacts, and the better the prediction about people not on the network got.

“You are not in full control of your privacy,” he concludes. If your friend is on a social platform, so are you. And you don’t have a choice in the matter. Garcia published his findings August 4 in Science Advances.

This does not mean that social platforms are creating shadow profiles of your social media–averse friends, Garcia notes. But with the information people give to social networks and with the platforms’ computing abilities, they certainly could. To prevent the data being used this way, Garcia only used the most basic, public information. He didn’t predict anything about specific people. He only checked to see if it was possible. Garcia also kept the power of his predictions low and very general. And he was careful to not construct an algorithm that could actually build a shadow profile, to make sure that others cannot misuse the findings.

But the results do show that information from your friends on a social network could accurately predict your marital status, location, sexual orientation or political affiliation — information that you may not want anyone to know, let alone in a social network you’re not even on.

“It’s a good illustration of an issue we have in society, which is that we no longer have control over what people can infer about us,” says Elena Zheleva, a computer scientist at the University of Illinois in Chicago. “If I decide not to participate in a certain social network, that doesn’t mean that people won’t be able to find things about me on that network.”

This means we might need to think differently about what privacy means. “We’re used to thinking of having a private space,” Garcia says. “We think we’ve got a room with keys and we let some people in.” But a better image, he argues, might be to imagine ourselves covered in the wet paint of our personal information. If we touch someone else, we leave a handprint. “The more you touch other people, the more you leave on them,” he explains. Touch enough people, and anyone who looks at those people and their paint-covered sleeves will be able to pick out your personal shade of teal.

And because we are no longer in full control of our privacy, Garcia notes, it also means that protecting privacy isn’t something any one person can do. “In some sense it resembles climate change,” he says. “It’s not something you can solve on your own. It’s everyone’s problem or it’s no one’s problem.”

Earthworms are great for soil, right? Well, not always. In places where there have been no earthworms for thousands of years, foreign worms can wreak havoc on soils. And that can cause a cascade of problems throughout an area’s food web. Now comes evidence that invader worms in the Upper Great Lakes may be stressing the region’s sugar maples.

There are native earthworms in North America, but not in regions that had been covered in glaciers during the Ice Age. Once the ice melted, living things returned. Earthworms don’t move that quickly, though, and even after 10,000 years, they’ve only made small inroads into the north on their own.

But people have inadvertently intervened. Sometimes they’ve dumped their leftover bait in worm-free zones. Or they’ve accidentally brought worms or eggs in the soil stuck to cars or trucks. And the worms took up residence as far north as Alberta’s boreal forests.

Earthworms “are not really supposed to be in some of these areas,” says Tara Bal, a forest health scientist at Michigan Technological University in Houghton. “In a garden, they’re good,” she notes. They help to mix soil. But that isn’t a good thing in a northern forest where soil is naturally stratified and nutrients tend to be found only in the uppermost layer near the leaf litter. “That’s what the trees have been used to,” Bal says. Those trees include sugar maples, which have shallow roots to get those nutrients. But worms mix up the soils and take away that nutrient-rich layer.
Bal didn’t start out studying worms in northern regions. She and her colleagues were brought in to address a problem that sugar maple growers were experiencing. Some of the trees appeared to be stressed out. They were experiencing what’s called dieback, when whole branches die, fall off and regrow. This is worrisome because if enough of the tree dies off, “it’s a slow spiral from there,” Bal says — the whole tree eventually dies.
To investigate, the researchers collected data on trees and anything that could be affecting them, from soil type to slope to insects. They looked at trees in 120 plots in Michigan, Wisconsin and Minnesota. And they compared trees that were on growers’ land with those on public land, thinking that how the trees were managed might have some effect.
When the researchers analyzed the data, “the same thing that kept coming up over and over again was the forest floor condition,” Bal says. “That is directly related to the presence of earthworms.” They didn’t go out to look for the worms, but they could see signs of them in the amount of carbon in the soil and in changes in the ground cover. Wildflowers, for instance, were replaced by grasses and sedges, the researchers report July 26 in Biological Invasions.

Bal and her team can’t say what this means for maple syrup production. It might not mean anything at all. But “worms are ecosystem engineers,” she notes. “They’re changing the food chain.” Everything from insects to birds to salamanders could be affected by the arrival of worms.

Even if the sugar maples take a hit, though, there could be an upside, Bal says. These trees are often grown with few other types of trees around. Such a grove is naturally less resilient to climate change and extreme weather. So replacing some of those sugar maples with other trees could result in a healthier, more resilient forest in the future, Bal says.

While volunteering at the University of New Mexico’s Children’s Hospital in Albuquerque, Quinton Smith quickly realized that he could never be a physician.

Then an undergrad at the university, Smith was too sad seeing sick kids all the time. But, he thought, “maybe I can help them with science.”

Smith had picked his major, chemical engineering, because he saw it as “a cooler way to go premed.” Though he ultimately landed in the lab instead of at the bedside, he has remained passionate about finding ways to cure what ails people.

Today, his lab at the University of California, Irvine uses tools often employed in fabricating tiny electronics to craft miniature, lab-grown organs that mimic their real-life counterparts. “Most of the time, when we study cells, we study them in a petri dish,” Smith says. “But that’s not their native form.” Prodding cells to assemble into these 3-D structures, called organoids, can give researchers a new way to study diseases and test potential treatments.

By combining Silicon Valley tech and stem cell biology, scientists are now “making tissues that look and react and function like human tissues,” Smith says. “And that hasn’t been done before.”

The power of stem cells
Smith’s work began in two dimensions. During his undergraduate studies, he spent two summers in the lab of biomedical engineer Sharon Gerecht, then at Johns Hopkins University. His project aimed to develop a device that could control oxygen and fluid flow inside minuscule chambers on silicon wafers, with the goal of mimicking the environment in which a blood vessel forms. It was there that Smith came to respect human induced pluripotent stem cells.

These stem cells are formed from body cells that are reprogrammed to an early, embryonic stage that can give rise to any cell type. “It just blew my mind that you can take these cells and turn them into anything,” Smith says.

Smith ultimately returned to Gerecht’s lab for his Ph.D., exploring how physical and chemical cues can push these stem cells toward becoming blood vessels. Using a technique called micropatterning — where researchers stamp proteins on glass slides to help cells attach — he spurred cells to organize into the beginnings of artificial blood vessels. Depending on the pattern, the cells formed 2-D stars, circles or triangles, showing how cells come together to form such tubular structures.
While a postdoc at MIT, he transitioned to 3-D, with a focus on liver organoids.

Like branching blood vessels, a network of bile ducts carry bile acid throughout the liver. This fluid helps the body digest and absorb fat. But artificial liver tissue doesn’t always re-create ducts that branch the way they do in the body. Cells growing in the lab “need a little bit of help,” Smith says.
To get around the problems, Smith and his team pour a stiff gel around minuscule acupuncture needles to create channels. After the gel solidifies, the researchers seed stem cells inside and douse the cells in chemical cues to coax them to form ducts. “We can create on-demand bile ducts using an engineering approach,” he says.

This approach to making liver organoids is possible because Smith speaks the language of biology and the language of engineering, says biomedical engineer Sangeeta Bhatia, a Howard Hughes Medical Institute investigator at MIT and Smith’s postdoc mentor. He can call on his cell biology knowledge and leverage engineering techniques to study how specific cell types are organized to work together in the body.

For example, Smith’s lab now uses 3-D printing to ensure liver tissues grown in the lab, including blood vessels and bile ducts, organize in the right way. Such engineering techniques could help researchers study and pinpoint the root causes behind some liver diseases, such as fatty liver disease, Smith says. Comparing organoids grown from cells from healthy people with those grown from cells from patients with liver disease — including Hispanic people, who are disproportionately affected — may point to a mechanism.

Looking beyond the liver
But Smith isn’t restricting himself to the liver. He and his trainees are branching out to explore other tissues and diseases as well.

One of those pursuits is preeclampsia, a disease that affects pregnant women, and disproportionately African American women. Women with preeclampsia develop dangerously high blood pressure because the placenta is inflamed and constricting the mother’s blood vessels. Smith plans to examine lab-grown placentas to determine how environmental factors such as physical forces and chemical cues from the organ impact attached maternal blood vessels.

“We’re really excited about this work,” Smith says. It’s only recently that scientists have tricked stem cells to enter an earlier stage of development that can form placentas. These lab-grown placentas even produce human chorionic gonadotropin, the hormone responsible for positive pregnancy tests.

Yet another win for the power of stem cells.

New gene-editing tools can correct typos that account for about half of disease-causing genetic spelling errors.

Researchers have revamped the CRISPR/Cas9 gene editor so that it converts the DNA base adenine to guanine, biological chemist David Liu and colleagues report October 25 in Nature. In a separate study, published October 25 in Science, other researchers led by CRISPR pioneer Feng Zhang re-engineered a gene editor called CRISPR/Cas13 to correct the same typos in RNA instead of DNA.
Together with other versions of CRISPR/Cas9, the new editors offer scientists an expanded set of precision tools for correcting diseases.

CRISPR/Cas9 is a molecular scissors that snips DNA. Scientists can guide the scissors to the place they want to cut in an organism’s genetic instruction book with a guide RNA that matches DNA at the target site. The tool has been used to make mutations or correct them in animals and in human cells, including human embryos (SN: 10/14/17, p. 8).

A variety of innovations allow CRISPR/Cas9 to change genetic instructions without cutting DNA (SN: 9/3/16, p. 22). Earlier versions of these “base editors,” which target typos related to the other half of disease-causing genetic spelling errors, have already been used to alter genes in plants, fish, mice and even human embryos.
Such noncutting gene editors are possibly safer than traditional DNA-cutting versions, says Gene Yeo, an RNA biologist at the University of California, San Diego. “We know there are drawbacks to cutting DNA,” he said. Mistakes often arise when cellular machinery attempts to repair DNA breaks. And although accurate, CRISPR sometimes cuts DNA at places similar to the target, raising the possibility of introducing new mutations elsewhere. Such “permanent irreversible edits at the wrong place in the DNA could be bad,” Yeo says. “These two papers have different ways to solve that problem.”
The new editors allow researchers to rewrite all four bases that store information in DNA and RNA. Those four bases are adenine (A) which pairs with thymine (T) (or uracil (U) in RNA), and guanine (G) pairs with cytosine (C). Mutations that change C-G base pairs to T-A pairs happen 100 to 500 times every day in human cells. Most of those mutations are probably benign, but some may alter a protein’s structure and function, or interfere with gene activity, leading to disease. About half of the 32,000 mutations associated with human genetic diseases are this type of C-G to T-A change, says Liu, a Howard Hughes Medical Institute investigator at Harvard University. Until now, there was little anyone could do about it, he says.

In RNA, DNA’s chemical cousin, some naturally occurring enzymes can reverse this common mutation. Such enzymes chemically convert adenine to inosine (I), which the cell interprets as G. Such RNA editing happens frequently in octopuses and other cephalopods and sometimes in humans (SN: 4/29/17, p. 6).

Zhang, of the Broad Institute of MIT and Harvard, and colleagues made an RNA-editing enzyme called ADAR2 into a programmable gene-editing tool. The team started with CRISPR/Cas13, molecular scissors that normally cut RNA. Dulling the blades let the tool grasp instead of slice. Zhang and colleagues then bolted the A-to-I converting portion of ADAR2 onto CRISPR/Cas13. Dubbed REPAIR, the conglomerate tool edited from 13 percent to about 27 percent of RNAs of two genes in human cells grown in dishes. The researchers did not detect any undesired changes.

Editing RNA is good for temporary fixes, such as shutting down inflammation-promoting proteins. But to fix many mutations, it requires permanent DNA repairs, says Liu.

In 2016, Liu’s team made a base editor that converts C to T. Chinese researchers reported in Protein & Cell on September 23 that they used the old base editor in human embryos to repair a mutation that causes the blood disorder beta-thalassemia. But that editor couldn’t make the opposite change, switching A to G.

Unlike with RNA, no enzymes naturally make the A-to-I conversion in DNA. So Nicole Gaudelli in Liu’s lab forced E. coli bacteria to evolve one. Then the researchers bolted the E. coli DNA converter, TadA, to a “dead” version of Cas9, disabled so it couldn’t cut both strands of DNA. The result was a base editor, called ABE, that could switch A-T base pairs into G-C pairs in about 50 percent of human cells tested.

This base editor works more like a pencil than scissors, Liu says. In lab dishes, Liu’s team corrected a mutation in human cells from a patient with an iron-storage blood disorder called hereditary hemochromatosis. The team also re-created beneficial mutations that allow blood cells to keep making fetal hemoglobin. Those mutations are known to protect against sickle cell anemia.

Another group reported in the October Protein & Cell that base editing appears to be safer than traditional cut-and-paste CRISPR/Cas9 editing. Liu’s results seem to support that. His team found that about 14 percent of the time cut-and-paste CRISPR/Cas9 made changes at nine of 12 possible “off-target” sites. The new A-to-G base editor altered just four of the 12 off-target sites and only 1.3 percent of the time.

That’s not to say cut-and-paste editing isn’t useful, Liu says. “Sometimes, if your task is to cut something, you’re not going to do that with a pencil. You need scissors.”