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 Ian Harvey

A Trillion Tonnes of Antarctica Fell into the Sea


Antarctica, Earth’s coldest continent, is known for its remoteness, its unique fauna, and its frigid surface of ice. Around Antarctica’s periphery, dozens of ice shelves (that is, masses of glacier-fed floating ice that are attached to land) project outward into the Southern Ocean. The two largest ice shelves, the Ross Ice Shelfand the Ronne Ice Shelf, span a combined area of nearly 350,000 square km (about 135,000 square miles)—an area roughly equivalent to Venezuela—but Antarctica’s Larsen Ice Shelf, the continent’s fourth largest, has received the bulk of the attention over the last 25 years because it is slowly coming apart. The latest episode in this saga occurred between July 10 and July 12, 2017, when a one-trillion-metric-ton chunk of ice—possibly critical to holding back a large section of the remaining shelf—calved (that is, broke away).

The Larsen Ice Shelf is located on the eastern side of the Antarctic Peninsula and juts out into the Weddell Sea. It originally covered an area of 86,000 square km (33,000 square miles), but its footprint has declined dramatically, possibly as a result of warming air temperatures over the Antarctic Peninsula during the second half of the 20th century. In January 1995 the northern portion (known as Larsen A) disintegrated, and a giant iceberg calved from the middle section (Larsen B). Larsen B steadily retreated until February–March 2002, when it too collapsed and disintegrated. The southern portion (Larsen C) made up two-thirds of the ice shelf’s original extent, covering an area of about 50,000 square km (19,300 square miles) alone. Its thickness ranges from 200 to 600 meters (about 660 to 1,970 feet). Sometime between July 10 and July 12, 2017, a 5,800-square-km- (~2,240-square-mile-) section—some 12% of the Larsen C—broke away. Signs of Larsen C’s impending fracture date back to 2012, when satellite monitoring detected a steadily growing crack near the Joerg Peninsula at the southern end of the shelf. NASA and ESA satellites tracked the rift as it grew to more than 200 km (124 miles) in length and the huge iceberg separated from the continent.

Although some 88% of Larsen C remains, many scientists worry that it will fall apart like Larsen A and Larsen B, because the loss of such a huge area of the shelf’s ice front may make the remainder of the ice shelf less stable. The shelf’s mass, along with the fact that it is pinned behind shallow undersea outcrops of rock below, creates a natural dam that significantly slows the flow of the ice into the Weddell Sea. Scientists note that the section that calved was not held back by rock, so they are less worried that the loss of the calved section will result in the shelf’s wholesale disintegration in the near term. Some scientists even concede that the calved area could regrow to form a new ice dam that reinforces the shelf. However, the results of ice-calving and glacier-flow models predict that the shelf will continue to break apart over the course of years and decades.

Calving is a natural process driven, in part, by seasonal changes in temperature and the pressures associated with the build-up of compressional stress on the ice. Some studies argue that spring and summer foehns (warm dry gusty winds that periodically descend the leeward slopes of mountain ranges) have also contributed to the weakening of the ice. As investigations into ice shelf dynamics continue, such large iceberg calving events are often regarded as symptoms of climate changeassociated with global warming. While global warming may turn out to play a part in ice shelf calving events, scientists disagree on the role, if any, the phenomenon has played in recent developments on Larsen C.

Disintegration of Larsen Ice ShelfThe map shows the section of Larsen C that calved in July 2017.Encyclopædia Britannica, Inc.

Tracking Down the Origins of Cystic Fibrosis in Ancient Europe

Human Lungs CF
The airways inside the human lung. (Magic mine/

Imagine the thrill of discovery when more than 10 years of research on the origin of a common genetic disease, cystic fibrosis (CF), results in tracing it to a group of distinct but mysterious Europeans who lived about 5,000 years ago.

CF is the most common, potentially lethal, inherited disease among Caucasians—about one in 40 carry the so-called F508del mutation. Typically only beneficial mutations, which provide a survival advantage, spread widely through a population.

CF hinders the release of digestive enzymes from the pancreas, which triggers malnutrition, causes lung disease that is eventually fatal and produces high levels of salt in sweat that can be life-threatening.

CF Symptom Diagram
Depending on the mutation a patient carries, they may experience some or all symptoms of cystic fibrosis. ( staff (2014), CC BY-SA)

In recent years, scientists have revealed many aspects of this deadly lung disease which have led to routine early diagnosis in screened babies, better treatments and longer lives. On the other hand, the scientific community hasn’t been able to figure out when, where and why the mutation became so common. Collaborating with an extraordinary team of European scientists such as David Barton in Ireland and Milan Macek in the Czech Republic, in particular a group of brilliant geneticists in Brest, France led by Emmanuelle Génin and Claude Férec, we believe that we now know where and when the original mutation arose and in which ancient tribe of people.

We share these findings in an article in the European Journal of Human Genetics which represents the culmination of 20 years’ work involving nine countries.

What is cystic fibrosis?

My quest to determine how CF arose and why it’s so common began soon after scientists discovered the CFTR gene causing the disease in 1989. The most common mutation of that gene that causes the disease was called F508del. Two copies of the mutation—one inherited from the mother and the other from the father—caused the lethal disease. But, inheriting just a single copy caused no symptoms, and made the person a “carrier.”

I had been employed at the University of Wisconsin since 1977 as a physician-scientist focusing on the early diagnosis of CF through newborn screening. Before the gene discovery, we identified babies at high risk for CF using a blood test that measured levels of protein called immunoreactive trypsinogen (IRT). High levels of IRT suggested the baby had CF. When I learned of the gene discovery, I was convinced that it would be a game-changer for both screening test development and epidemiological research.

That’s because with the gene we could offer parents a more informative test. We could tell them not just whether their child had CF, but also whether they carried two copies of a CFTR mutation, which caused disease, or just one copy which made them a carrier.

CF Mutation
Parents carrying one good copy of the CF gene (R) and one bad copy of the mutated CF gene (r) are called carriers. When both parents transmit a bad copy of the CF gene to their offspring, the child will suffer from cystic fibrosis. Children who inherit just one bad copy will be carriers like their parents and can transmit the gene to their children. (Cburnett, CC BY-SA)

One might ask what is the connection between studying CF newborn screening and learning about the disease origin. The answer lies in how our research team in Wisconsin transformed a biochemical screening test using the IRT marker to a two-tiered method called IRT/DNA.

Because about 90 percent of CF patients in the U.S. and Europe have at least one F508del mutation, we began analyzing newborn blood for its presence whenever the IRT level was high. But when this two-step IRT/DNA screening is done, not only are patients with the disease diagnosed but also tenfold more infants who are genetic carriers of the disease are identified.

As preconception-, prenatal- and neonatal screening for CF have proliferated during the past two decades, the many thousands of individuals who discovered they were F508del carriers and their concerned parents often raised questions about the origin and significance of carrying this mutation themselves or in their children. Would they suffer with one copy? Was there a health benefit? It has been frustrating for a pediatrician specializing in CF to have no answer for them.

The challenge of finding origin of the CF mutation

I wanted to zero in on when this genetic mutation first starting appearing. Pinpointing this period would allow us to understand how it could have evolved to provide a benefit—at least initially—to those people in Europe who had it. To expand my research, I decided to take a sabbatical and train in epidemiology while taking courses in 1993 at the London School of Hygiene and Tropical Medicine.

The timing was perfect because the field of ancient DNA research was starting to blossom. New breakthrough techniques like the Polymerase Chain Reaction made it possible to study the DNA of mummies and other human archaeological specimens from prehistoric burials. For example, early studies were performed on the DNA from the 5,000-year-old Tyrolean Iceman, which later became known as Ötzi.

Ancient Burial
A typical prehistoric burial in a crouched fetal position. (Philip Farrell, CC BY-SA)

I decided that we might be able to discover the origin of CF by analyzing the DNA in the teeth of Iron Age people buried between 700-100 B.C. in cemeteries throughout Europe.

Using this strategy, I teamed up with archaeologists and anthropologists such as Maria Teschler-Nicolaat the Natural History Museum in Vienna, who provided access to 32 skeletons buried around 350 B.C. near Vienna. Geneticists in France collected DNA from the ancient molars and analyzed the DNA. To our surprise, we discovered the presence of the F508del mutation in DNA from three of 32 skeletons.

This discovery of F508del in Central European Iron Age burials radiocarbon-dated to 350 B.C. suggested to us that the original CF mutation may have arisen earlier. But obtaining Bronze Age and Neolithic specimens for such direct studies proved difficult because fewer burials are available, skeletons are not as well-preserved and each cemetery merely represents a tribe or village. So rather than depend on ancient DNA, we shifted our strategy to examine the genes of modern humans to figure out when this mutation first arose.

Why would a harmful mutation spread?

To find the origin of CF in modern patients, we knew we needed to learn more about the signature mutation—F508del—in people who are carriers or have the disease.

This tiny mutation causes loss of one amino acid out of the 1,480 amino acid chain and changes the shape of a protein on the surface of the cell that moves chloride in and out of the cell. When this protein is mutated, people carrying two copies of it—one from the mother and one from the father—are plagued with thick sticky mucus in their lungs, pancreas and other organs. The mucus in their lungs allows bacteria to thrive, destroying the tissue and eventually causing the lungs to fail. In the pancreas, the thick secretions prevent the gland from delivering the enzymes the body needs to digest food.

So why would such a harmful mutation continue to be transmitted from generation to generation?

Iron and Bronze Age Teeth and Bones
The Natural History Museum in Vienna, Austria, houses a large collection of Iron Age and Bronze Age skeletons which are curated by Dr. Maria Teschler-Nicola. These collections were the source of teeth and bones for investigation of ancient DNA and studies on ‘The Ancient Origin of Cystic Fibrosis.’ (Philip Farrell, CC BY-ND)

A mutation as harmful as F508del would never have survived among people with two copies of the mutated CFTR gene because they likely died soon after birth. On the other hand, those with one mutation may have a survival advantage, as predicted in Darwin’s “survival of the fittest” theory.

Perhaps the best example of a mutation favoring survival under stressful environmental conditions can be found in Africa, where fatal malaria has been endemic for centuries. The parasite that causes malaria infects the red blood cells in which the major constituent is the oxygen-carrying protein hemoglobin. Individuals who carry the normal hemoglobin gene are vulnerable to this mosquito-borne disease. But those who are carriers of the mutated “hemoglobin S” gene, with only one copy, are protected from severe malaria. However two copies of the hemoglobin S gene causes sickle cell disease, which can be fatal.

Here there is a clear advantage to carrying one mutant gene—in fact, about one in 10 Africans carries a single copy. Thus, for many centuries an environmental factor has favored the survival of individuals carrying a single copy of the sickle hemoglobin mutation.

Sickle Cell Gene
Individuals who carry two copies of the sickle cell gene suffer from sickle cell anemia, in which the blood cells become rigid sickle shapes and get stuck in the blood vessels, causing pain. Normal red blood cells are flexible discs that slide easily through vessels. (Designua/

Similarly we wondered whether there was a health benefit to carrying a single copy of this specific CF mutation during exposures to environmentally stressful conditions. Perhaps, we reasoned, that’s why the F508del mutation was common among Caucasian Europeans and Europe-derived populations.

Clues from modern DNA

To figure out the advantage of transmitting a single mutated F508del gene from generation to generation, we first had to determine when and where the mutation arose so that we could uncover the benefit this mutation conferred.

We obtained DNA samples from 190 CF patients bearing F508del and their parents residing in geographically distinct European populations from Ireland to Greece plus a Germany-derived population in the U.S. We then identified a collection of genetic markers—essentially sequences of DNA—within the CF gene and flanking locations on the chromosome. By identifying when these mutations emerged in the populations we studied, we were able to estimate the age of the most recent common ancestor.

Next, by rigorous computer analyses, we estimated the age of the CF mutation in each population residing in the various countries.

Sickle Cell and Malaria
Two copies of the sickle cell gene cause the disease. But carrying one copy reduces the risk of malaria. The gene is widespread among people who live in regions of the world (red) where malaria is endemic. ( ellepigrafica)

We then determined that the age of the oldest common ancestor is between 4,600 and 4,725 years and arose in southwestern Europe, probably in settlements along the Atlantic Ocean and perhaps in the region of France or Portugal. We believe that the mutation spread quickly from there to Britain and Ireland, and then later to central and southeastern European populations such as Greece, where F508del was introduced only about 1,000 years ago.

Who spread the CF mutation throughout Europe?

Thus, our newly published data suggest that the F508del mutation arose in the early Bronze Age and spread from west to southeast Europe during ancient migrations.

Moreover, taking the archaeological record into account, our results allow us to introduce a novel concept by suggesting that a population known as the Bell Beaker folk were the probable migrating population responsible for the early dissemination of F508del in prehistoric Europe. They appeared at the transition from the Late Neolithic period, around 4000 B.C., to the Early Bronze Age during the third millennium B.C. somewhere in Western Europe. They were distinguished by their ceramic beakers, pioneering copper and bronze metallurgy north of the Alps and great mobility. All studies, in fact, show that they were into heavy migration, traveling all over Western Europe.

Bell Beaker Sites
Distribution of Bell Beaker sites throughout Europe. (DieKraft via Wikimedia Commons)

Over approximately 1,000 years, a network of small families and/or elite tribes spread their culture from west to east into regions that correspond closely to the present-day European Union, where the highest incidence of CF is found. Their migrations are linked to the advent of Western and Central European metallurgy, as they manufactured and traded metal goods, especially weapons, while traveling over long distances. It is also speculated that their travels were motivated by establishing marriage networks. Most relevant to our study is evidence that they migrated in a direction and over a time period that fit well with our results. Recent genomic data suggest that both migration and cultural transmission played a major role in diffusion of the “Beaker Complex” and led to a “profound demographic transformation” of Britain and elsewhere after 2400 B.C.

Determining when F508del was first introduced in Europe and discovering where it arose should provide new insights about the high prevalence of carriers—and whether the mutation confers an evolutionary advantage. For instance, Bronze Age Europeans, while migrating extensively, were apparently spared from exposure to endemic infectious diseases or epidemics; thus, protection from an infectious disease, as in the sickle cell mutation, through this genetic mutation seems unlikely.

As more information on Bronze Age people and their practices during migrations become available through archaeological and genomics research, more clues about environmental factors that favored people who had this gene variant should emerge. Then, we may be able to answer questions from patients and parents about why they have a CFTR mutation in their family and what advantage this endows.

Bell Beaker Artifacts
Examples of tools and ceramics created by the Bell Beaker people. (Benutzer:Thomas Ihle via German Wikipedia, CC BY-SA) 

This article was originally published on The Conversation. The ConversationMatthew E. Baker, Professor of Geography and Environmental Systems, University of Maryland, Baltimore County

Japan’s Hayabusa 2 spacecraft reaches cosmic ‘diamond’

RyuguImage copyright JAXA ET AL.
Image caption Scientists will map Ryugu with a view to choosing the best location to sample

A Japanese spacecraft has arrived at its target – an asteroid shaped like a diamond or, according to some, a spinning top.

Hayabusa 2 has been travelling toward the space rock Ryugu since launching from the Tanegashima spaceport in 2014.

It is on a quest to study the object close-up and deliver rocks and soil from Ryugu to Earth.

It will use explosives to propel a projectile into Ryugu, digging out a fresh sample from beneath the surface.

Dr Makoto Yoshikawa, Hayabusa 2’s mission manager, talked about the plan now that the spacecraft had arrived at its destination.


A copper projectile, or “impactor” will separate from the spacecraft, floating down to the surface of the asteroid. Once Hayabusa 2 is safely out of the way, an explosive charge will detonate, driving the projectile into the surface.

“We have an impactor which will create a small crater on the surface of Ryugu. Maybe in spring next year, we will try to make a crater… then our spacecraft will try to reach into the crater to get the subsurface material.”

“But this is a very big challenge.”

Hayabusa 2Image copyright JAXA / AKIHIRO IKESHITA
Image caption Hayabusa 2 will use a projectile to excavate fresh material from beneath Ryugu’s surface

Why is this story important?

Scientists study asteroids to gain insights into the origins and evolution of our cosmic neighbourhood, the Solar System.

Asteroids are essentially leftover building materials from the formation of the Solar System 4.6 billion years ago.

It’s also thought they may contain chemical compounds that could have been important for kick-starting life on Earth.

They contain water, organic (carbon-rich) compounds and precious metals. The last of those has tempted several companies to look into the feasibility of asteroid mining.

‘Dumpling’ space rock comes into view

DangoImage copyright GETTY IMAGES
Image caption From far away, the asteroid seemed to resemble a Japanese dango dumpling…
Spinning topImage copyright GETTY IMAGES
Image caption…but now we have close-up images, scientists are comparing its shape to that of a spinning top

Dr Yoshikawa, who is an associate professor at Japan’s Institute of Space and Astronautical Science (ISAS), said Ryugu’s shape was unexpected.

He said asteroids with this general shape tended to be fast-rotating, completing one revolution every three or four hours. But Ryugu’s spin period is relatively long – about 7.5 hours.

“Many scientists in our project think that in the past the spin period was very short – it rotated very quickly – and the spin period has slowed down. We don’t know why it slowed down, but this is a very interesting topic,” he told BBC News.

Hayabusa 2 will spend about a year and a half surveying the 900m-wide space rock, which is about 290 million km (180 million miles) from Earth.

During this time, it will aim to deploy several landing craft to the surface, including small rovers and a German-built instrument package called Mascot (Mobile Asteroid Surface Scout).

MASCOTImage copyright DLR
Image caption Hayabusa 2 is carrying a German-built lander called MASCOT

Ryugu is a so-called C-type asteroid, a kind that is thought to be relatively primitive. This means it may be rich in organic and hydrated minerals (those combined with water). Studying what Ryugu is made from could provide insights into the molecular mix that contributed to the origin of life on Earth.

The surface of the asteroid is likely to have been weathered – altered by aeons of exposure to the harsh environment of space. That’s why Hayabusa 2’s scientists want to dig down for as fresh a sample as possible.

The onboard Lidar (light detection and ranging) instrument is used partly as a navigation sensor for rendezvous, approach, and touchdown. It illuminates the target with pulsed laser light to measure variable distances between the two objects. On Tuesday, scientists successfully used the Lidar to measure the distance from Hayabusa to the asteroid for the first time.

The mission will depart from Ryugu in December 2019 with the intention of returning to Earth with the asteroid samples in 2020.

The first Hayabusa spacecraft was launched in 2003 and reached the asteroid Itokawa in 2005.

Despite being hit by a series of mishaps, it returned to Earth in 2010 with a small amount of material from the asteroid.

An American asteroid sample return mission, Osiris-Rex, will rendezvous with the object 101955 Bennu in August.

Chasing the Sun: The woman forgotten by science

Annie MaunderImage copyright RAS/DORRIE GILES
Image caption Annie Maunder: A pioneer of solar astronomy






The ‘lady computers’




The Royal Observatory, GreenwichImage copyright NATIONAL MARITIME MUSEUM, LONDON
Image caption The Royal Observatory, Greenwich, in 1933




‘Grit and devotion’




Image caption Annie Maunder on an eclipse expedition in Labrador, Newfoundland
Walter MaunderImage copyright MAUNDER FAMILY














Studying the Sun

Annie Russell married her colleague Edward Walter Maunder in 1895.



Family photos show preparations for observing an eclipseImage copyright MAUNDER FAMILY
Image caption Family photos show preparations for observing an eclipse








The Heavens and Their Story



Annie Maunder medal Image copyright RAS
Image caption The RAS has set up the Annie Maunder medal





Much of their work still holds true today.

Annie’s legacy



Annie Maunder died in 1947, long after her husband.








15 Tiny Things That Could Seriously Improve Your Life In Just A Month

1. If a task if going to take you less than a minute to complete, do it as soon as you think of it.

The One-Minute Rule is simple, but it works! Getting out of the habit of putting things off is the easiest way to get shit done.

2. Read for a set amount of time every single day.

Even if it’s 10 or 20 minutes, you’ll either finish or make good progress on a book by the end of the month.

@empowerpuffgurl / Via

3. Actually start flossing your teeth at least once a day.

It will be worth it when you don’t have to lie at your next dentist appointment.

4. Try and go to bed at the same time each night, and wake up at a similar time each morning.

Your body loves habits, especially good sleep habits. Set a go-to-bed alarm, as well as a wake-up alarm, and try and stick to both most days.

5. Make your bed each and every morning.

Coming home to a bedroom with a made bed is a pure delight. Once you’re in the habit of making your bed, you won’t be able to believe you ever left the house without doing it.

@inbedstore / Via

6. Add one new healthy food or ingredient into your diet.

Adding something healthy feels way better than taking something out of your diet, so choose a new vegetable, grain, or spice and work it into your meal rotation.

7. Find a workout you can do comfortably in your own home, and do it regularly.

Even if it’s just a short routine of push-ups, sit-ups, lunges, and squats, you’ll always have something to do on days you can’t be bothered getting to the gym or a class.

8. Instead of putting things down, put them away.

Leaving things where they don’t belong is how homes get messy. Avoid an hour of tidying up by taking a few seconds to put things away as you finish with them.

@mojkkaa / Via

9. Each night, plan what you’re going to wear the next day.

If you find mornings a struggle, try preparing your outfit for the next day, the night before.

10. Practice a new skill or hobby for 10 minutes every day.

Whether it’s watercolor painting, embroidery, violin, or learning a new language, dedicating10 minutes a day to it guarantees you’ll have improved by the end of the month.

@threadhoney / Via

11. Save every $5 bill that makes its way into your wallet.

A lot of people swear by this simple money-saving trick. Stash away every $5 note you come across, and enjoy your savings at a later date.

12. Write down three things you’re grateful for each night before bed.

Keeping a gratitude list or journal is a lovely practice that helps highlight all the good things you have going on in your life.

@bujocute / Via

13. Try meditating, starting with just three minutes a day.

The first session on the Calm app is just three minutes long. Start there, and see how you feel after a month of daily meditation.

14. Keep track of how much water you’re drinking, and set daily hydration goals.

Most of us aren’t drinking enough water, so keeping a tally of how many glasses you’re having a day is a good way to see if you need to improve your habit.

@rockonrubyxx / Via

15. Call someone when you’re having a bad day, whether that person is a friend, family member, or health professional.

Find your person, then get into the habit of calling them to chat more regularly.

@sarachengrocks / Via
Gyan Yankovich

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