NASA maps inner Milky Way, sees cosmic 'candy cane'

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A feature resembling a candy cane appears at the center of this colorful composite image of our Milky Way galaxy's central zone. But this is no cosmic confection. It spans 190 light-years and is one of a set of long, thin strands of ionized gas called filaments that emit radio waves.

This image includes newly published observations using an instrument designed and built at NASA's Goddard Space Flight Center in Greenbelt, Maryland. Called the Goddard-IRAM Superconducting 2-Millimeter Observer (GISMO), the instrument was used in concert with a 30-meter radio telescope located on Pico Veleta, Spain, operated by the Institute for Radio Astronomy in the Millimeter Range headquartered in Grenoble, France.

"GISMO observes microwaves with a wavelength of 2 millimeters, allowing us to explore the galaxy in the transition zone between infrared light and longer radio wavelengths," said Johannes Staguhn, an astronomer at Johns Hopkins University in Baltimore who leads the GISMO team at Goddard. "Each of these portions of the spectrum is dominated by different types of emission, and GISMO shows us how they link together."

GISMO detected the most prominent radio filament in the galactic center, known as the Radio Arc, which forms the straight part of the cosmic candy cane. This is the shortest wavelength at which these curious structures have been observed. Scientists say the filaments delineate the edges of a large bubble produced by some energetic event at the galactic center, located within the bright region known as Sagittarius A about 27,000 light-years away from us. Additional red arcs in the image reveal other filaments.

"It was a real surprise to see the Radio Arc in the GISMO data," said Richard Arendt, a team member at the University of Maryland, Baltimore County and Goddard. "Its emission comes from high-speed electrons spiraling in a magnetic field, a process called synchrotron emission. Another feature GISMO sees, called the Sickle, is associated with star formation and may be the source of these high-speed electrons."

Two papers describing the composite image, one led by Arendt and one led by Staguhn, were published on Nov. 1 in the Astrophysical Journal.

The image shows the inner part of our galaxy, which hosts the largest and densest collection of giant molecular clouds in the Milky Way. These vast, cool clouds contain enough dense gas and dust to form tens of millions of stars like the Sun. The view spans a part of the sky about 1.6 degrees across -- equivalent to roughly three times the apparent size of the Moon -- or about 750 light-years wide.

To make the image, the team acquired GISMO data, shown in green, in April and November 2012. They then used archival observations from the European Space Agency's Herschel satellite to model the far-infrared glow of cold dust, which they then subtracted from the GISMO data. Next, they added, in blue, existing 850-micrometer infrared data from the SCUBA-2 instrument on the James Clerk Maxwell Telescope near the summit of Maunakea, Hawaii. Finally, they added, in red, archival longer-wavelength 19.5-centimeter radio observations from the National Science Foundation's Karl G. Jansky Very Large Array, located near Socorro, New Mexico. The higher-resolution infrared and radio data were then processed to match the lower-resolution GISMO observations.

The resulting image essentially color codes different emission mechanisms.

Blue and cyan features reveal cold dust in molecular clouds where star formation is still in its infancy. Yellow features, such as the Arches filaments making up the candy cane's handle and the Sagittarius B1 molecular cloud, reveal the presence of ionized gas and show well-developed star factories; this light comes from electrons that are slowed but not captured by gas ions, a process also known as free-free emission. Red and orange regions show areas where synchrotron emission occurs, such as in the prominent Radio Arc and Sagittarius A, the bright source at the galaxy's center that hosts its supermassive black hole.

Mitochondria are the 'canary in the coal mine' for cellular stress

Illustration of mitochondria

Mitochondria, tiny structures present in most cells, are known for their energy-generating machinery. Now, Salk researchers have discovered a new function of mitochondria: they set off molecular alarms when cells are exposed to stress or chemicals that can damage DNA, such as chemotherapy. The results, published online in Nature Metabolism on December 9, 2019, could lead to new cancer treatments that prevent tumors from becoming resistant to chemotherapy.

"Mitochondria are acting as a first line of defense in sensing DNA stress. The mitochondria tell the rest of the cell, 'Hey, I'm under attack, you better protect yourself,'" says Gerald Shadel, a professor in Salk's Molecular and Cell Biology Laboratory and the Audrey Geisel Chair in Biomedical Science.

Most of the DNA that a cell needs to function is found inside the cell's nucleus, packaged in chromosomes and inherited from both parents. But mitochondria each contain their own small circles of DNA (called mitochondrial DNA or mtDNA), passed only from a mother to her offspring. And most cells contain hundreds -- or even thousands -- of mitochondria.

Shadel's lab group previously showed that cells respond to improperly packaged mtDNA similarly to how they would react to an invading virus -- by releasing it from mitochondria and launching an immune response that beefs up the cell's defenses.

In the new study, Shadel and his colleagues set out to look in more detail at what molecular pathways are activated by the release of damaged mtDNA into the cell's interior. They homed in on a subset of genes known as interferon-stimulated genes, or ISGs, that are typically activated by the presence of viruses. But in this case, the team realized, the genes were a particular subset of ISGs turned on by viruses. And this same subset of ISGs is often found to be activated in cancer cells that have developed resistance to chemotherapy with DNA-damaging agents like doxyrubicin.

To destroy cancer, doxyrubicin targets the nuclear DNA. But the new study found that the drug also causes the damage and release of mtDNA, which in turn activates ISGs. This subset of ISGs, the group discovered, helps protect nuclear DNA from damage -- and, thus, causes increased resistance to the chemotherapy drug. When Shadel and his colleagues induced mitochondrial stress in melanoma cancer cells, the cells became more resistant to doxyrubicin when grown in culture dishes and even in mice, as higher levels of the ISGs were protecting the cell's DNA.

"Perhaps the fact that mitochondrial DNA is present in so many copies in each cell, and has fewer of its own DNA repair pathways, makes it a very effective sensor of DNA stress," says Shadel.

Most of the time, he points out, it's probably a good thing that the mtDNA is more prone to damage -- it acts like a canary in a coal mine to protect healthy cells. But in cancer cells, it means that doxyrubicin -- by damaging mtDNA first and setting off molecular alarm bells -- can be less effective at damaging the nuclear DNA of cancer cells.

"It says to me that if you can prevent damage to mitochondrial DNA or its release during cancer treatment, you might prevent this form of chemotherapy resistance," Shadel says.

Blue light may not be as disruptive to our sleep patterns as originally thought

Person using mobile phone

Contrary to common belief, blue light may not be as disruptive to our sleep patterns as originally thought -- according to University of Manchester scientists.

According to the team, using dim, cooler, lights in the evening and bright warmer lights in the day may be more beneficial to our health.

Twilight is both dimmer and bluer than daylight, they say, and the body clock uses both of those features to determine the appropriate times to be asleep and awake.

Current technologies designed to limit our evening exposure to blue light, for example by changing the screen colour on mobile devices, may therefore send us mixed messages, they argue.

This is because the small changes in brightness they produce are accompanied by colours that more resemble day.

The research, which was carried out on mice, used specially designed lighting that allowed the team to adjust colour without changing brightness.

That showed blue colours produced weaker effects on the mouse body clock than equally bright yellow colours.

The findings, say the team, have important implications for the design of lighting and visual displays intended to ensure healthy patterns of sleep and alertness.

The study is published in Current Biology and funded by the Biotechnology and Biological Sciences Research Council.

The body clock uses a specialised light sensitive protein in the eye to measure brightness, called melanopsin, which is better at detecting shorter wavelength photons.

This is why, say the team, researchers originally suggested blue light might have a stronger effect.

However, our perception of colour comes from the retinal cone cells and the new research shows that the blue colour signals they supply reduce the impact on light on the clock.

Dr Tim Brown, from The University of Manchester, said: "We show the common view that blue light has the strongest effect on the clock is misguided; in fact, the blue colours that are associated with twilight have a weaker effect than white or yellow light of equivalent brightness.

"There is lots of interest in altering the impact of light on the clock by adjusting the brightness signals detected by melanopsin but current approaches usually do this by changing the ratio of short and long wavelength light; this provides a small difference in brightness at the expense of perceptible changes in colour."

He added: "We argue that this is not the best approach, since the changes in colour may oppose any benefits obtained from reducing the brightness signals detected by melanopsin.

"Our findings suggest that using dim, cooler, lights in the evening and bright warmer lights in the day may be more beneficial.

"Research has already provided evidence that aligning our body clocks with our social and work schedules can be good for our health. Using colour appropriately could be a way to help us better achieve that."

A new gene therapy strategy, courtesy of nature

Scientists have developed a new gene-therapy technique by transforming human cells into mass producers of tiny nano-sized particles full of genetic material that has the potential to reverse disease processes.

Though the research was intended as a proof of concept, the experimental therapy slowed tumor growth and prolonged survival in mice with gliomas, which constitute about 80 percent of malignant brain tumors in humans.

The technique takes advantage of exosomes, fluid-filled sacs that cells release as a way to communicate with other cells.

While exosomes are gaining ground as biologically friendly carriers of therapeutic materials -- because there are a lot of them and they don't prompt an immune response -- the trick with gene therapy is finding a way to fit those comparatively large genetic instructions inside their tiny bodies on a scale that will have a therapeutic effect.

This new method relies on patented technology that prompts donated human cells such as adult stem cells to spit out millions of exosomes that, after being collected and purified, function as nanocarriers containing a drug. When they are injected into the bloodstream, they know exactly where in the body to find their target -- even if it's in the brain.

"Think of them like Christmas gifts: The gift is inside a wrapped container that is postage paid and ready to go," said senior study author L. James Lee, professor emeritus of chemical and biomolecular engineering at The Ohio State University.

And they are gifts that keep on giving, Lee noted: "This is a Mother Nature-induced therapeutic nanoparticle."

Forgetfulness might depend on time of day

Pocket watch

Can't remember something? Try waiting until later in the day. Researchers identified a gene in mice that seems to influence memory recall at different times of day and tracked how it causes mice to be more forgetful just before they normally wake up.

"We may have identified the first gene in mice specific to memory retrieval," said Professor Satoshi Kida from the University of Tokyo Department of Applied Biological Chemistry.

Every time you forget something, it could be because you didn't truly learn it -- like the name of the person you were just introduced to a minute ago; or it could be because you are not able to recall the information from where it is stored in your brain -- like the lyrics of your favorite song slipping your mind.

Many memory researchers study how new memories are made. The biology of forgetting is more complicated to study because of the difficulties of distinguishing between not knowing and not recalling.

"We designed a memory test that can differentiate between not learning versus knowing but not being able to remember," said Kida.

Researchers tested the memories of young adult male and female mice. In the "learning," or training, phase of the memory tests, researchers allowed mice to explore a new object for a few minutes.

Later, in the "recall" phase of the test, researchers observed how long the mice touched the object when it was reintroduced. Mice spend less time touching objects that they remember seeing previously. Researchers tested the mice's recall by reintroducing the same object at different times of day.

They did the same experiments with healthy mice and mice without BMAL1, a protein that regulates the expression of many other genes. BMAL1 normally fluctuates between low levels just before waking up and high levels before going to sleep.

Mice trained just before they normally woke up and tested just after they normally went to sleep did recognize the object.

Mice trained at the same time -- just before they normally woke up -- but tested 24 hours later did not recognize the object.

Healthy mice and mice without BMAL1 had the same pattern of results, but the mice without BMAL1 were even more forgetful just before they normally woke up. Researchers saw the same results when they tested mice on recognizing an object or recognizing another mouse.

Something about the time of day just before they normally wake up, when BMAL1 levels are normally low, causes mice to not recall something they definitely learned and know.

According to Kida, the memory research community has previously suspected that the body's internal, or circadian, clock that is responsible for regulating sleep-wake cycles also affects learning and memory formation.

"Now we have evidence that the circadian clocks are regulating memory recall," said Kida.