A newly discovered object from another star system that’s passing through ours is shaped like a giant pink fire extinguisher.

 

That’s the word this week from astronomers who have been observing this first-ever confirmed interstellar visitor.

 

“I’m surprised by the elongated shape — nobody expected that,” said astronomer David Jewitt of the University of California, Los Angeles, who led the observation team that reported on the characteristics.

 

Scientists are certain this asteroid or comet originated outside our solar system. First spotted last month by the Pan-STARRS telescope in Hawaii, it will stick around for another few years before departing our sun’s neighborhood.

 

Jewitt and his international team observed the object for five nights in late October using the Nordic Optical Telescope in the Canary Islands and the Kitt Peak National Observatory near Tucson, Arizona.

 

At approximately 100 feet by 100 feet by 600 feet (30 meters buy 30 meters by 180 meters), the object has proportions roughly similar to a fire extinguisher — though not nearly as red, Jewitt said Thursday. The slightly red hue — specifically pale pink — and varying brightness are remarkably similar to asteroids in our own solar system, he noted.

 

Astronomer Jayadev Rajagopal said in an email that it was exciting to point the Arizona telescope at such a tiny object “which, for all we know, has been traveling through the vast emptiness of space for millions of years.”

 

“And then by luck passes close enough for me to be able to see it that night!”

 

The object is so faint and so fast  it’s zooming through the solar system at 40,000 mph (64,000 kph) — it’s unlikely amateur astronomers will see it.

 

In a paper to the Astrophysical Journal Letters, the scientists report that our solar system could be packed with 10,000 such interstellar travelers at any given time. It takes 10 years to cross our solar system, providing plenty of future viewing opportunities, the scientists said.

 

Trillions of objects from other star systems could have passed our way over the eons, according to Jewitt.

 

It suggests our solar system ejected its own share of asteroids and comets as the large outer planets — Jupiter, Saturn, Neptune — formed.

 

Why did it take so long to nail the first interstellar wanderer?

 

“Space is big and our eyes are weak,” Jewitt explained via email.

 

Anticipating more such discoveries, the International Astronomical Union already has approved a new designation for cosmic interlopers. They get an “I” for interstellar in their string of letters and numbers. The group also has approved a name for this object: Oumuamua (OH’-moo-ah-moo-ah) which in Hawaiian means a messenger from afar arriving first.
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Passenger pigeons were once so plentiful they could darken the daytime sky when they flew over North America, but oddly, their abundance may have played a role in their extinction, researchers said Thursday.

Though it may seem counter-intuitive, the pigeons (Ectopistes migratorius), evolved quickly and in the process, lost certain traits that might have been useful for surviving in smaller groups, said the study in the journal Science.

The findings have implications for other creatures threatened by swift changes in the world around them.

“Our results suggest that even species with large and stable population sizes can be at risk of extinction after a sudden environmental change,” said the study led by Beth Shapiro, a professor at the University of California, Santa Cruz.

Numbering three to five billion before they began to decline in the 1800s due to a surge in hunting, these social birds were once “the most abundant bird in North America, and possibly the world,” said the report.

And although large populations of animals tend to be genetically quite diverse, researchers were stunned by their analysis of four extinct pigeon genomes, which were compared to two modern carrier pigeons.

They found that passenger pigeon diversity was “surprisingly low,” said the study.

Researchers also found areas of very high diversity in the genomes, which told researchers the birds had been around for 20,000 years or more — another surprise.

The last passenger pigeon died in a U.S. zoo in 1914.

Until now, the prevailing theory was the birds went extinct due to a booming commercial hunting industry that forced their populations to become demographically isolated, leading to lots of inbreeding, lower genetic diversity and weaker health.

But the latest findings suggest the reason was more complex. The birds evolved quickly and may have adapted to large social groups, hunting and breeding together.

Flying in gargantuan masses, their sheer size protected them against predators.

But in smaller groups, the theory goes, these defenses fell short, leading the birds’ relatively quick die-off in the matter of a few decades.

“Passenger pigeons may have evolved traits that were adaptive when their population was large but that made it more difficult for them to survive after their population was diminished by the commercial harvest,” said the report.
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Battle lines are being drawn as the first gene therapy for an inherited condition nears the U.S. market, offering hope for people with a rare form of blindness and creating a cost dilemma for health care providers.

Spark Therapeutics, whose Luxturna treatment has been recommended for U.S. approval, told investors last week there was a case for valuing it at more than $1 million per patient, although it has yet to set an actual price.

However, the U.S. Institute for Clinical and Economic Review (ICER) said this week “at a placeholder price of $1,000,000, the high cost makes this unlikely to be a cost-effective intervention at commonly used cost-effectiveness thresholds.”

The ICER analysis did concede Luxturna was likely to be more cost-effective for younger patients.

The expected U.S. approval of Luxturna by Jan. 12 is seen as kick-starting the sector, following disappointing sales of the first two gene therapies in Europe.

More treatments based on fixing faulty genes using viruses to carry DNA into cells are coming from companies like Bluebird Bio, BioMarin and Sangamo.

Spark’s Chief Financial Officer Stephen Webster said Thursday that gene therapy was upending conventional thinking by offering a one-time cure, rather than years of repeat prescriptions, but health systems were struggling to keep pace.

“Gene therapy creates an unusual conundrum because we are fitting a round peg in a square hole … it’s tough,” he told a Jefferies health care conference in London.

Spark would like to say “if it works, pay us, and if it stops working, stop paying us,” Webster told the meeting.

But for Luxturna, which cost some $400 million to develop, such an offer was impractical, given the mechanics of the U.S. system and a reluctance by big health plans to move away from upfront payments for rare disease drugs.

Longer-term, pay-for-performance models could be adopted for hemophilia, where the benefits of one-time treatment can be weighed against the huge cost of regular infusions of blood-clotting factors, Webster said.

A one-off treatment would slash the need for such expensive care. But there are also indirect costs and quality of life benefits — especially in a condition like blindness — that manufacturers argue should be recognized.

Nightstar Therapeutics CEO David Fellows, whose company is also developing gene therapies for eye disorders, said calculating gene therapy’s true value was not easy.

“Trying to capture all this into some sort of price algorithm is very challenging. But we are trying to quantify the emotional impact, the care-giver impact, the effect on careers and so on,” he told the conference.
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Soldiers in Myanmar have gang raped Rohingya women in continued violence against the Muslim minority in Rakhine state, according to a Human Rights Watch report.

Human Rights Watch cited first-hand interviews with 52 Rohingya women and girls who fled to Bangladesh and reported being raped by security forces in Myanmar, also known as Burma.

“Rape has been a prominent and devastating feature of the Burmese military’s campaign of ethnic cleansing against the Rohingya,” said Skye Wheeler, women’s rights emergencies researcher at Human Rights Watch and author of the report. “The Burmese military’s barbaric acts of violence have left countless women and girls brutally harmed and traumatized.”

All but one of the interviewees was gang raped, HRW said.

 

WATCH: HRW Report: Myanmar Security Forces Using Sexual Violence as Scare Tactic

Hundreds of cases

HRW also spoke with multiple humanitarian organizations in Bangladesh who have reported “hundreds” of rape cases. Numbers of rape victims are likely much higher, as social stigma keeps many women silent.

“I have had to deal with disgust, others looking away from me,” Isharahat Islam, who was raped by soldiers in her village Hathi Para in October 2016, told HRW.

The numbers also cannot account for those who were killed after they were raped.

Fifteen-year-old Hala Sadak from a village in the Maungdaw Township told HRW that soldiers had dragged her from her home, stripped her naked, and pushed her against a tree where she estimates as many as 10 men raped her from behind.

“They left me where I was … when my brother and sister came to get me, I was lying there on the ground, they thought I was dead,” she said.

Emotional, physical injuries

In addition to depression and post-traumatic stress disorder, women reported untreated injuries including vaginal tears, bleeding, and infections, the report said.

More than 600,000 Rohingya Muslims have left Myanmar’s Rakhine State since Aug. 25, after insurgents attacked security forces and prompted a brutal military crackdown that has been described as ethnic cleansing.

Myanmar’s government has repeatedly rejected claims that atrocities, including rape and extrajudicial killings, are occurring in northern Rakhine, the epicenter of the violence that the United Nations has called “textbook ethnic cleansing.”

Denials from Myanmar

In September, the Rakhine state border security minister denied reports of rape by security forces in the state, according to HRW.

“Where is the proof? Look at those women who are making these claims — would anyone want to rape them?” he was quoted as saying in Thursday’s report.

Myanmar does not recognize the Rohingya and denies them citizenship, referring to them as “Bengali” to imply origins in Bangladesh.

Though Aung San Suu Kyi has been criticized for sidestepping allegations of abuses, many Western governments have been reluctant to ostracize her during a fragile transition to democracy.
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Giant rats are probably not the first thing that come to mind to tackle tuberculosis but scientists hope their sniffing skills will speed up efforts to detect the deadly disease in major cities across the world.

Tuberculosis, which is curable and preventable, is one of the world’s deadliest infectious diseases, according to the World Health Organization (WHO), killing 1.7 million people in 2016 and infecting 10.4 million others.

African Giant Pouched Rats, trained by Belgian charity APOPO, are known for sniffing out landmines in countries from Angola to Cambodia and for detecting TB cases in East Africa.

Over the next few years, APOPO plans to fight tuberculosis at the source by launching TB-detection rat facilities in major cities of 30 high-risk countries including Vietnam, India and Nigeria.

“One of the best ways to fight TB at source is in major cities that draw a lot of people from the rural areas,” James Pursey, APOPO spokesman, told the Thomson Reuters Foundation.

“It is a vicious circle. You can be reinfected. To fight TB, you have to hit it hard,” he said by phone from Zimbabwe.

Many people get infected in big, densely populated cities and spread the disease to rural areas, according to Pursey.

The rats learn to recognize the presence of TB in samples of mucus that is coughed up from the patient’s lower airways.

In Tanzania, people in communities where TB is most common, including in prisons, often fail to show up for screening because of a lack of money or awareness, placing a huge burden on health authorities, health experts said.

“TB is a disease of poverty,” said Pursey. “If nothing changes it can only get worse.”

The APOPO has seen the TB detection rate increase by 40 percent in clinics it has worked with in Tanzania and Mozambique, according to Pursey, who said that using rats to screen did not negate the need for proper diagnostic testing.

While a technician may take four days to detect a case of TB, a trained rat can screen 100 samples in 20 minutes, and a rat screening costs as little as 20 US cents, APOPO said.
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Climate change threats, from worsening drought and flooding to sea level rise, could increase the risks of hunger and child malnutrition around the world by 20 percent by 2050, food security researchers warned Wednesday.

But looking carefully at the very different risks facing each country, region and type of food producer — from highland rice farmers in Cambodia to cattle herders in South Sudan — could help reduce that threat of growing hunger, they said.

In North Africa, for instance, both herders and farmers face fast-growing risks from more frequent, longer and more intense heatwaves and declining water availability, while population growth and greater urbanization could also hit food security, according to a report by the World Food Program (WFP) released Wednesday at the U.N. climate talks in Bonn.

In South Asia, by comparison, dense populations of farmers face threats from worsening floods, cyclones and droughts, as well as long-term threats to the stability of monsoons and water flow in glacier-fed rivers.

“Different groups are affected by different types of risks, at different intensities and at different times,” said Gernot Laganda, the director of climate and disaster risk reduction programs at WFP.

Building greater resilience to the threats will require “layers” of responses, he said.

Catastrophic threats of large-scale losses of crops or animals — the type that might come along every 5 to 10 years, for instance, and force those hit to migrate — might be dealt with in part with insurance plans, Laganda said.

But more regular seasonal threats — of smaller-scale flooding, for instance — cannot be insured, he said, as the problems come too frequently.

In those cases, building savings groups among women farmers, for instance, to ensure cash is on hand to deal with the crop failures, could be a better way to deal with risks.

The report aims to give country governments, and food security organizations, a clearer and more specific look at the threats they face, and better tools to deal with them. It looks in detail at particularly threatened regions, including parts of Africa and Asia, and at 15 specific countries, from Afghanistan to Mali.

One surprise from the work, Laganda said, is that it was not always the poorest countries that were most vulnerable to hunger threats.

“Sometimes we assume middle-income countries have a much easier time … which is not necessarily the case,” he said.

South Asia, in particular, has big numbers of hungry people, he said and overall “the largest vulnerabilities to loss and damage in food systems occur in Asia.”

In Africa, drought is the biggest threat to hunger levels, but conflicts also play a big role, he said.

Laganda said such differences need a careful look if countries and food security agencies are to better manage coming climate threats and achieve the international goal of ending hunger by 2030, one of a set of so-called Sustainable Development Goals.

“We are not going to achieve zero hunger by 2030 if we do not factor climate-related shocks and stresses into our equation,” he warned. “Climate needs to factor into food security discussions … at a country level in a much bigger form than it does now.”

And aid agencies like WFP “as much as governments” need to focus more on risk management, he said.

Mikael Eriksson, who works on climate, energy and environmental issues for Sweden’s government, said the growing complexity of humanitarian disasters requires innovation and rethinking old ways of doing things.

“Prevention is so much more efficient than disaster management,” he said.

 
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Scientists for the first time have tried editing a gene inside the body in a bold attempt to permanently change a person’s DNA to try to cure a disease.

 

The experiment was done Monday in California on 44-year-old Brian Madeux. Through an IV, he received billions of copies of a corrective gene and a genetic tool to cut his DNA in a precise spot.

 

“It’s kind of humbling” to be the first to test this, said Madeux, who has a metabolic disease called Hunter syndrome. “I’m willing to take that risk. Hopefully it will help me and other people.”

 

Signs of whether it’s working may come in a month; tests will show for sure in three months.

 

If it’s successful, it could give a major boost to the fledgling field of gene therapy. Scientists have edited people’s genes before, altering cells in the lab that are then returned to patients. There also are gene therapies that don’t involve editing DNA.

 

But these methods can only be used for a few types of diseases. Some give results that may not last. Some others supply a new gene like a spare part, but can’t control where it inserts in the DNA, possibly causing a new problem like cancer.

 

This time, the gene tinkering is happening in a precise way inside the body. It’s like sending a mini surgeon along to place the new gene in exactly the right location.

 

“We cut your DNA, open it up, insert a gene, stitch it back up. Invisible mending,” said Dr. Sandy Macrae, president of Sangamo Therapeutics, the California company testing this for two metabolic diseases and hemophilia. “It becomes part of your DNA and is there for the rest of your life.”

 

That also means there’s no going back, no way to erase any mistakes the editing might cause.

 

“You’re really toying with Mother Nature” and the risks can’t be fully known, but the studies should move forward because these are incurable diseases, said one independent expert, Dr. Eric Topol of the Scripps Translational Science Institute in San Diego.

 

Protections are in place to help ensure safety, and animal tests were very encouraging, said Dr. Howard Kaufman, a Boston scientist on the National Institutes of Health panel that approved the studies.

 

He said gene editing’s promise is too great to ignore. “So far there’s been no evidence that this is going to be dangerous,” he said. “Now is not the time to get scared.”

 

Woe from head to toe 

Fewer than 10,000 people worldwide have these metabolic diseases, partly because many die very young. Those with Madeux’s condition, Hunter syndrome , lack a gene that makes an enzyme that breaks down certain carbohydrates. These build up in cells and cause havoc throughout the body.

 

Patients may have frequent colds and ear infections, distorted facial features, hearing loss, heart problems, breathing trouble, skin and eye problems, bone and joint flaws, bowel issues and brain and thinking problems.

 

“Many are in wheelchairs… dependent on their parents until they die,” said Dr. Chester Whitley, a University of Minnesota genetics expert who plans to enroll patients in the studies.

 

Weekly IV doses of the missing enzyme can ease some symptoms, but cost $100,000 to $400,000 a year and don’t prevent brain damage.

 

Madeux, who now lives near Phoenix, is engaged to a nurse, Marcie Humphrey, who he met 15 years ago in a study that tested this enzyme therapy at UCSF Benioff Children’s Hospital Oakland, where the gene editing experiment took place.

 

He has had 26 operations for hernias, bunions, bones pinching his spinal column, and ear, eye and gall bladder problems.

 

“It seems like I had a surgery every other year of my life” and many procedures in between, he said. Last year he nearly died from a bronchitis and pneumonia attack. The disease had warped his airway, and “I was drowning in my secretions, I couldn’t cough it out.”

 

Madeux has a chef’s degree and was part owner of two restaurants in Utah, cooking for U.S. ski teams and celebrities, but now can’t work in a kitchen or ride horses as he used to.

 

Gene editing won’t fix damage he’s already suffered, but he hopes it will stop the need for weekly enzyme treatments.

 

Initial studies will involve up to 30 adults to test safety, but the ultimate goal is to treat children very young, before much damage occurs.

 

How it works

 

A gene-editing tool called CRISPR has gotten a lot of recent attention, but this study used a different one called zinc finger nucleases. They’re like molecular scissors that seek and cut a specific piece of DNA.

 

The therapy has three parts: The new gene and two zinc finger proteins. DNA instructions for each part are placed in a virus that’s been altered to not cause infection but to ferry them into cells. Billions of copies of these are given through a vein.

 

They travel to the liver, where cells use the instructions to make the zinc fingers and prepare the corrective gene. The fingers cut the DNA, allowing the new gene to slip in. The new gene then directs the cell to make the enzyme the patient lacked.

 

Only 1 percent of liver cells would have to be corrected to successfully treat the disease, said Madeux’s physician and study leader, Dr. Paul Harmatz at the Oakland hospital.

 

“How bulletproof is the technology? We’re just learning,” but safety tests have been very good, said Dr. Carl June, a University of Pennsylvania scientist who has done other gene therapy work but was not involved in this study.

 

What could go wrong

 

Safety issues plagued some earlier gene therapies. One worry is that the virus might provoke an immune system attack. In 1999, 18-year-old Jesse Gelsinger died in a gene therapy study from that problem, but the new studies use a different virus that’s proved much safer in other experiments.

 

Another worry is that inserting a new gene might have unforeseen effects on other genes. That happened years ago, when researchers used gene therapy to cure some cases of the immune system disorder called “bubble boy” disease. Several patients later developed leukemia because the new gene inserted into a place in the native DNA where it unintentionally activated a cancer gene.

 

“When you stick a chunk of DNA in randomly, sometimes it works well, sometimes it does nothing and sometimes it causes harm,” said Hank Greely, a Stanford University bioethicist. “The advantage with gene editing is you can put the gene in where you want it.”

 

Finally, some fear that the virus could get into other places like the heart, or eggs and sperm where it could affect future generations. Doctors say built-in genetic safeguards prevent the therapy from working anywhere but the liver, like a seed that only germinates in certain conditions.

 

This experiment is not connected to other, more controversial work being debated to try to edit genes in human embryos to prevent diseases before birth — changes that would be passed down from generation to generation.

 

Making history

 

Madeux’s treatment was to have happened a week earlier, but a small glitch prevented it.

 

He and his fiancee returned to Arizona, but nearly didn’t make it back to Oakland in time for the second attempt because their Sunday flight was canceled and no others were available until Monday, after the treatment was to take place.

 

Scrambling, they finally got a flight to Monterey, California, and a car service took them just over 100 miles north to Oakland.

 

On Monday he had the three-hour infusion, surrounded by half a dozen doctors, nurses and others wearing head-to-toe protective garb to lower the risk of giving him any germs. His doctor, Harmatz, spent the night at the hospital to help ensure his patient stayed well.

 

“I’m nervous and excited,” Madeux said as he prepared to leave the hospital. “I’ve been waiting for this my whole life, something that can potentially cure me.”
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