南京新龙凤

To zip through the bloodstream and spread infection throughout the body, the bacteria that cause Lyme disease take a cue from the white blood cells trying to attack them. Both use specialized bonds to stick to the cells lining blood vessels and move along at their own pace, biologist Tara Moriarty and colleagues report September 6 in Cell Reports.

“It’s really an amazing case of convergent evolution,” says Wendy Thomas, a biologist at the University of Washington in Seattle who wasn’t part of the study. “There’s little structural similarity between the molecules involved in these behaviors, and yet their behavior is the same.”
Traveling through the bloodstream is more like a whitewater rafting adventure than a lazy Sunday afternoon float. It can be a highly efficient way for bacteria to spread from an infection site to set up shop elsewhere in the body, but the microbes need some way to control where they go instead of just being swept away. So to move at their own speed while withstanding the forces of blood flow, bacteria creep along the side walls by steadily making and breaking bonds with other cells, says Moriarty, of the University of Toronto.

Borrelia burgdorferi is a corkscrew-shaped bacterium that causes Lyme disease. It works its way into the human body via a bite from an infected tick but then spreads through the whole body, causing joint pain and neurological problems. Biologists have known that B. burgdorferi can move in and out of the bloodstream, says Mark Wooten, a microbiologist at the University of Toledo in Ohio who wasn’t involved in the work. But this study gives a detailed explanation of exactly how it might do so.
Moriarty and her colleagues lined flow chambers with human endothelial cells to mimic the bloodstream environment. Then her team used high-powered microscopes to watch what happened to bacteria moving through the chamber along with blood cells. A computer program helped the scientists track exactly how individual bacteria navigated the mock bloodstream.
The researchers found that B. burgdorferi making a protein called BBK32 form specialized links called “catch bonds” with the endothelial cells — a technique that white blood cells also use. Catch bonds get stronger when under mechanical stress, helping the bacteria to hold on under pressure. Bungee cord–like structures called tethers work alongside the catch bonds to even out the load placed on the bonds.

But B. burgdorferi need to move to infect, and if they let go of the blood vessel walls completely, they’ll be washed away. So like someone moving hand-over-hand across monkey bars, B. burgdorferi shift their load from bond to bond. As they break one bond, they transfer their load to a new bond, moving steadily forward while remaining continually attached. White blood cells use a similar trick to move across endothelial cells.

B. burgdorferi can also use whiplike appendages called flagella to control their movement through the bloodstream. In B. burgdorferi and other related bacteria, the flagella wrap around the bacteria to help the microbes propel themselves forward like drill bits. The force generated by the B. burgdorferi flagella is greater than the forces trying to rip the bacteria off the blood vessel walls, Moriarty and her colleagues found.

“What that basically means is that bacteria are strong enough to overcome the force that they experience under blood flow, which means they should be theoretically strong enough to get to a spot where they can exit the bloodstream,” says Moriarty. That might allow Lyme bacteria to control when and where they exit the bloodstream to infect other organs.

Color vision may actually work like a colorized version of a black-and-white movie, a new study suggests.

Cone cells, which sense red, green or blue light, detect white more often than colors, researchers report September 14 in Science Advances. The textbook-rewriting discovery could change scientists’ thinking about how color vision works.

For decades, researchers have known that three types of cone cells in the retina are responsible for color vision. Those cone cells were thought to send “red,” “green” and “blue” signals to the brain. The brain supposedly combines the colors, much the way a color printer does, to create a rainbow-hued picture of the world (including black and white). But the new findings indicate that “the retina is doing more of the work, and it’s doing it in a more simpleminded way,” says Jay Neitz, a color vision scientist at the University of Washington in Seattle who was not involved in the study.
Red and green cone cells each come in two types: One type signals “white”; another signals color, vision researcher Ramkumar Sabesan and colleagues at the University of California, Berkeley, discovered. The large number of cells that detect white (and black — the absence of white) create a high-resolution black-and-white picture of a person’s surroundings, picking out edges and fine details. Red- and green-signaling cells fill in low-resolution color information. The process works much like filling in a coloring book or adding color to a black-and-white film, says Sabesan, who is now at the University of Washington.

Sabesan and colleagues discerned this color vision strategy by stimulating about 273 individual cone cells in the eyes of two men from the lab. The technological accomplishment of stimulating single cone cells in the retina is akin to getting people to walk on the moon, says Neitz. “It is a super technological achievement. It is an amazing thing.”

Sabesan’s team first used a microscope that could peer into living human eyes to map hundreds of light-detecting cone cells in the two volunteers. In order to get a clear picture of the cells through the distortion of the lens and cornea, the researchers borrowed techniques that astronomers use to compensate for disturbances in the atmosphere.
With the blur from imperfections in the eye corrected, the researchers had to precisely target individual cells to hit with the laser. Because the eye is constantly jiggling, the researchers had to determine the pattern of the eye movements to predict where cone cells would be several milliseconds in the future. Over about two years, the researchers repeatedly stimulated 273 red or green cones one by one. After a flash of laser light was delivered to the cone, the men would indicate on a keyboard what color they had seen.

Of the red cones the researchers stimulated, 119 made the men see white, while only 48 flashed red. Similarly, only 21 of the green cones tested actually signaled green, while 77 registered white. Each individual cone probably signals only white or color, the researchers say. “It’s a rather inefficient arrangement,” says Donald MacLeod, a vision scientist at the University of California, San Diego. All the cone cells are capable of detecting color, but few actually seem to do so.
Cells surrounded by cones that detect a different color were more likely to send white signals, the researchers found. That finding is unexpected and runs counter to a popular idea that cones ringed by cells detecting other colors would be better at color detection, MacLeod says.

These findings could be good news for people with color blindness. The results suggest that gene therapy that adds red or green cones could work even in adults, Neitz says. Although his group gave a monkey full color vision (SN: 10/10/09, p.14), many researchers thought human brains would never be able to incorporate additional color information even though the eye could detect it. The new findings indicate the brain needs to learn only that there is one more color needed to fill in to a basically black-and-white picture, a task it should accomplish easily, Neitz says.

VANCOUVER — Zika virus’s tricks for interfering with human brain cell development may also be the virus’s undoing.

Zika infection interferes with DNA replication and repair machinery and also prevents production of some proteins needed for proper brain growth, geneticist Feiran Zhang of Emory University in Atlanta reported October 19 at the annual meeting of the American Society of Human Genetics.

Levels of a protein called p53, which helps control cell growth and death, shot up by 80 percent in human brain cells infected with the Asian Zika virus strain responsible for the Zika epidemic in the Americas, Zhang said. The lab dish results are also reported in the Oct. 14 Nucleic Acids Research. Increased levels of the protein stop developing brain cells from growing and may cause the cells to commit suicide.
A drug that inactivates p53 stopped brain cells from dying, Zhang said. Such p53 inhibitors could help protect developing brains in babies infected with Zika. But researchers would need to be careful giving such drugs because too little p53 can lead to cancer.

Zika also makes small RNA molecules that interfere with production of proteins needed for DNA replication, cell growth and brain development, Zhang said. In particular, a small viral RNA called vsRNA-21 reduced the amount of microcephalin 1 protein made in human brain cells in lab dishes. The researchers confirmed the results in mouse experiments. That protein is needed for brain growth; not enough leads to the small heads seen in babies with microcephaly. Inhibitors of the viral RNAs might also be used in therapies, Zhang suggested.

Muons, electrons’ heftier cousins, rain down through the Earth’s atmosphere in numbers higher than physicists expect. The discrepancy could simply point to a gap in physicists’ understanding of the nitty-gritty physics of particle interactions, or perhaps something unexpected is going on, such as the creation of a new state of matter.

When cosmic rays — spacefaring protons or atomic nuclei — smash into the atmosphere at ultrahigh energies, they launch a cascade of many other types of particles, including muons. New observations made at the Pierre Auger Observatory detect about 30 percent more muons than simulations predict, scientists report October 31 in Physical Review Letters.
The Auger observatory, located in Argentina, uses telescopes to observe faint light from particle showers in the atmosphere, and detects particles that reach the ground using tanks of water. By comparing simulated particle showers to real data, and allowing for possible miscalibration of their detectors, the scientists concluded that the predicted numbers of muons don’t match up with reality. Hints of the muon excess have been popping up since the ’90s, says physicist Thomas Gaisser of the University of Delaware. But the new measurement is “a better job, which confirms the excess compared to what’s predicted by the models.”

The ultrahigh energy cosmic rays that the researchers analyzed probe physics at energies 10 times those reached at the world’s most powerful particle accelerator, the Large Hadron Collider, potentially allowing scientists to detect new phenomena. But, says Spencer Klein of the Lawrence Berkeley National Laboratory in California, “it’s premature to say that this is something really interesting.” He suggests that the discrepancy could simply be due to an incomplete grasp of the physics of how protons and neutrons inside a nucleus behave when nuclei collide. The complexities of that behavior could result in particles that eventually decay into more muons than scientists naïvely expected, thus explaining the glut.

But, says Auger physicist Glennys Farrar of New York University, scientists have unsuccessfully tried to explain the muon surplus using standard physics for many years. “That’s in a way the most convincing reason to think that there may be new physics.” An explanation Farrar favors is a phenomenon in which a new state of matter appears at high energies. In such a state, large numbers of gluons — particles that transmit the strong nuclear force — may behave collectively, like photons in sync in a laser. If enough energy is pumped in by the cosmic rays, the gluons could “start to develop a life of their own,” Farrar says. The gluons might then gang up into hypothetical particles called glueballs, which could decay into particles that produce more muons.

The decades-long dwindling of glaciers is “categorical evidence of climate change,” a new study affirms.

The link between global warming and glacial retreat had previously garnered only a “likely,” or at least 66 percent probability, rating from the Intergovernmental Panel on Climate Change. Comparing the long-term decline of 37 glaciers, researchers estimate that all but one are “very likely” – or with at least 90 percent probability – the result of climate change.

Natural variability and complex dynamics make sussing out climate change’s role in glacial retreat difficult. Earth system scientist Gerard Roe of the University of Washington in Seattle and colleagues calculated the natural ups and downs of well-documented glaciers from around the world. The researchers then noted how far the glaciers have drifted from that natural variability and compared that trend with changes in the nearby climate.

For 21 out of the 37 glaciers, the researchers say it is “virtually certain” that climate change caused the glaciers’ retreat, the researchers report December 12 in Nature Geoscience. Glaciers hold about 75 percent of Earth’s freshwater and their decline serves as a canary in the coal mine for climate change.

The sound of someone slurping coffee or crunching an apple can be mildly annoying — but it leaves some people seething. These people aren’t imagining their distress, new research suggests. Anger and anxiety in response to everyday sounds of eating, drinking and breathing come from increased activity in parts of the brain that process and regulate emotions, scientists report February 2 in Current Biology.

People with this condition, called misophonia, are often dismissed as just overly sensitive, says Jennifer Jo Brout, a clinical psychologist not involved with the study. “This really confirms that it’s neurologically based,” says Brout, founder of the Sensory Processing and Emotion Regulation Program at Duke University Medical Center.
Researchers played sounds to 20 people with misophonia and 22 people without. Some sounds were neutral, such as rain falling. Others, like a wailing baby, were annoying to both groups of people but didn’t cause a misophonic response. A third set were sounds known to cause distress in people with misophonia — chewing and breathing noises.

MRI brain scans showed that both groups of people reacted similarly to the neutral and annoying sounds. But misophonics responded far more dramatically to the chewing and breathing. They showed more activity in their anterior insular cortex, a brain structure involved in emotional processing. Scientists found structural differences, too — more connections from the anterior insular cortex to structures like the amygdala and the hippocampus, which also help with processing emotions.
People with misophonia also showed increased heart rate and skin conductivity. That’s the same sort of flight-or-fight response that gets triggered when facing a wild animal or a public speaking engagement.
Sounds most people ignore in their day-to-day listening create a very strong emotional response in misophonics, says study coauthor Sukhbinder Kumar, a cognitive neuroscientist at Newcastle University in Newcastle upon Tyne, England. Their brains are ascribing extra importance to certain sounds. But it’s still unclear why only specific sounds cause a reaction.

A pair of bacterial genes may enable genetic engineering strategies for curbing populations of virus-transmitting mosquitoes.

Bacteria that make the insects effectively sterile have been used to reduce mosquito populations. Now, two research teams have identified genes in those bacteria that may be responsible for the sterility, the groups report online February 27 in Nature and Nature Microbiology.

“I think it’s a great advance,” says Scott O’Neill, a biologist with the Institute of Vector-Borne Disease at Monash University in Melbourne, Australia. People have been trying for years to understand how the bacteria manipulate insects, he says.
Wolbachia bacteria “sterilize” male mosquitoes through a mechanism called cytoplasmic incompatibility, which affects sperm and eggs. When an infected male breeds with an uninfected female, his modified sperm kill the eggs after fertilization. When he mates with a likewise infected female, however, her eggs remove the sperm modification and develop normally.

Researchers from Vanderbilt University in Nashville pinpointed a pair of genes, called cifA and cifB, connected to the sterility mechanism of Wolbachia. The genes are located not in the DNA of the bacterium itself, but in a virus embedded in its chromosome.

When the researchers took two genes from the Wolbachia strain found in fruit flies and inserted the pair into uninfected male Drosophila melanogaster, the flies could no longer reproduce with healthy females, says Seth Bordenstein, a coauthor of the study published in Nature. But modified uninfected male flies could successfully reproduce with Wolbachia-infected females, perfectly mimicking how the sterility mechanism functions naturally.

The ability of infected females to “rescue” the modified sperm reminded researchers at the Yale School of Medicine of an antidote’s reaction to a toxin.

They theorized that the gene pair consisted of a toxin gene, cidB, and an antidote gene, cidA. The researchers inserted the toxin gene into yeast, activated it, and saw that the yeast was killed. But when both genes were present and active, the yeast survived, says Mark Hochstrasser, a coauthor of the study in Nature Microbiology.
Hochstrasser’s team also created transgenic flies, but used the strain of Wolbachia that infects common Culex pipiens mosquitoes.

Inserting the two genes into males could be used to control populations of Aedes aegypti mosquitoes, which can carry diseases such as Zika and dengue.

The sterility effect from Wolbachia doesn’t always kill 100 percent of the eggs, says Bordenstein. Adding additional pairs of the genes to the bacteria could make the sterilization more potent, creating a “super Wolbachia.”

You could also avoid infecting the mosquitoes altogether, says Bordenstein. By inserting the two genes into uninfected males and releasing them into populations of wild mosquitoes, you could “essentially crash the population,” he says.

Hochstrasser notes that the second method is safer in case Wolbachia have any long-term negative effects.

O’Neill, who directs a research program called Eliminate Dengue that releases Wolbachia-infected mosquitoes, cautions against mosquito population control through genetic engineering because of public concerns about the technology. “We think it’s better that we focus on a natural alternative,” he says.

Dad bod is a big deal for albatrosses. Bigger male wandering albatrosses live longer and are more likely to breed successfully compared with lighter birds, while mass has no observable effect on female breeding or survival, researchers report May 3 in Proceedings of the Royal Society B.

Climate change could shift the degree to which some seabirds pack on the pounds. It’s unclear how those shifts will play out in species like wandering albatrosses (Diomedea exulans), in which males are much bigger than females.

To investigate, Tina Cornioley of the University of Zurich and her colleagues examined how body mass affects certain aspects of an albatross’s life — survival, odds of mating, having chicks, chick size and chick survival. From 1988 to 2013, the team tracked 662 adult albatrosses on Possession Island in the southern Indian Ocean. Albatross parents take turns sitting on their eggs, but dads actually invest more energy in rearing chicks after they hatch.

In addition to the survival and breeding advantages, the team also found that heavier dads were more likely to have heavier sons, but not daughters, and those sons had better survival odds. Although the team can’t rule out the possibility of a genetic element, the fact that body mass fluctuates throughout a bird’s life and the absence of the trend in mothers and daughters makes genetics a less likely explanation, says Cornioley. Instead, the researchers think that heftier dads invest more in sons than daughters.

Dogged genetic detective work has led scientists to a hybrid red blood cell protein that offers some protection against malaria.

Reporting online May 18 in Science, researchers describe a genetic variant that apparently is responsible for the fusion of two proteins that protrude from the membranes of red blood cells. In its hybrid form, the protein somehow makes it more difficult for the malaria parasite to invade the blood cells.

Successful invasion by the parasite can cause flulike illness, and in severe cases, death. In 2015, 212 million cases of malaria occurred worldwide, according to the World Health Organization, and 429,000 people died, mostly young children.
People carrying the protective genetic variant are 30 to 50 percent less likely to develop severe malaria than those without, the researchers report. The genetic change was found largely in people from Kenya, Malawi and Tanzania, suggesting that it occurred relatively recently in East Africa.

Discovering any genetic changes that protect against malaria is of great interest, says hematologist and malaria specialist Dave Roberts of the University of Oxford, who was not involved with the study. Understanding such changes, he says, “may help us understand the pathological pathways by which the parasite causes so much disease.”

Previous research had hinted that genetic changes to a particular stretch of DNA on chromosome 4 offered some protection against malaria. But the research team, an international collaboration that included researchers and clinicians from across Africa, had to do substantial legwork spanning 10 years to unmask the changes. Databases that gather the genetic instruction books, or genomes, of individuals are biased toward European populations, while African samples are underrepresented. And human genetic diversity is particularly high in sub-Saharan Africa, so genomes with rare genetic changes can be easily missed.

To overcome these hurdles, the researchers analyzed the genomes of more than 12,000 people, sampling widely in Africa. They surveyed 765 individuals from 10 ethnic groups in Gambia, Burkina Faso, Cameroon and Tanzania, as well as more than 2,000 genomes from the 1000 Genomes Project, a public catalog of genetic data. The team also examined genomes of nearly 10,000 people from Gambia, Kenya and Malawi, about half of whom had been hospitalized with severe malaria.

The team discovered that the stretch of DNA in question has undergone major changes; chunks of genes have been deleted, other chunks duplicated or even triplicated. One result stood out in the DNA of the people who were less at risk for malaria: Two genes that provide instructions for two proteins called glycophorin A and glycophorin B were snipped, fused together and duplicated. These proteins are known red blood cell proteins that the malaria parasite Plasmodium falciparum can use to gain access to the cells.
This genetic mash-up seems to lead to a protein mash-up: The arm sticking inside the red blood cell is made up of protein A, while the arm sticking out of the cell is made up of protein B. This hybrid protein turns out to have been first described in 1984. Called the Dantu antigen, it’s found on red blood cells of only a small percentage of people outside of Africa and is part of a rare blood group called MNS.
It isn’t clear why the hybrid protein makes it harder for the malaria parasite to breach a blood cell. “It might just make the cell more squishy so it feels different to the parasite,” says study coauthor Chris Spencer, a statistical geneticist at Oxford.

The new research suggests that there may be other stretches of DNA in the human genome that may reveal the diversity of responses to the parasite. Those spots are worth looking for, even if the search is difficult, says Spencer.

Typically, genome analysis studies primarily look for single changes — one altered unit of DNA — not wholesale copying or halving of genes. And because researchers break apart and then reassemble the 3-billion-letter-long genetic instruction book in order to analyze it, sections that have duplicated genes are harder to put in the right order and thus harder to study, which was the case with the region containing the red blood cell protein DNA.

“The genome is a big place and it’s natural to look at the things that are easiest,” Spencer says. “But it could be that the most interesting parts of the genome we just haven’t looked at yet.”

West German power companies have decided to go ahead with two nuclear power station projects…. Compared with the U.S. and Britain, Germany has been relatively backward in the application of nuclear energy…. The slow German start is only partly the result of restrictions placed upon German nuclear research after the war. — Science News, September 16, 1967

Update
Both East and West Germany embraced nuclear power until antinuclear protests in the 1970s gathered steam. In 1998, the unified German government began a nuclear phaseout, which Chancellor Angela Merkel halted in 2009. The 2011 Fukushima nuclear disaster in Japan caused a rapid reversal. Germany closed eight of its nuclear plants immediately, and announced that all nuclear power in the country would go dark by 2022 (SN Online: 6/1/11). A pivot to renewable energy — wind, solar, hydropower and biomass — produced 188 billion kilowatt-hours of electricity in 2016, nearly 32 percent of German electricity usage.