Sir Isaac Newton was a mathematician and physicist during the late 17th and early 18th centuries. He developed the principles of modern physics, especially about motion and gravity, and was considered instrumental in the Scientific Revolution of the 17th century, according to Biography.
Newton is a very multifaceted figure. He was undeniably a brilliant scientific mind, and a very pious man. He was also prone to fits of rage, insecurity, and social withdrawal, where he would do no work and isolate himself from everyone.
He had a longtime interest in the study of alchemy, and was searching for the recipe to create the Philosopher’s Stone, which was reputed to turn base metals into gold, and have the power to confer eternal life.
Unlike with his interests in math and physics, his alchemical research was a very private pursuit, and was not driven by money so much as it was inspired by a desire for power over nature, according to Nova.
All of these things taken together build a picture of a man who struggled with mental illness, probably bipolar disorder, according to Futurism.
When he was around 19 or 20, Newton maintained a diary in which he cataloged a list of his sins. Examining his list, it’s clear that he had problems with anger from a young age.
He identifies, among his sins, “peevishness” with his mother, his sister, and at “Master Clarks, for a piece of bread and butter”. He lists “falling out with the servants”, as well.
You could say that bad temper and grouchiness are par for the course for a boy of his years, and that would certainly be true, but he also specifies, as number 13, “threatening my father and mother Smith to burn them, and the house over them”.
He also cites multiple examples of physical aggression, punching his sister, beating people, and putting a pin in someone’s hat, so that it will scratch them. He comes across as anxious, egotistical, and dominating.
Newton was not a people person. He didn’t make friends. In his personal life, he only had close emotional relation relationships with two people, his niece Catherine Barton, who became his housekeeper in London, and a mathematician named Fatio de Duillier, who was only 25 when he and Newton met.
Their relationship was very emotionally intense, and neither man ever married, which makes some of Newton’s biographers speculate that the men were romantically involved, although there is no proof.
In his professional life, he was very touchy and insecure about his work, and would fly into fits of rage over its criticism, resulting in his withdrawing and refusing to continue his work. These episodes of withdrawal could last for months. He shied away from fame, and requested that his papers be published anonymously.
He had sincere religious beliefs, and was a nominal Anglican, but seemed to have a Puritan view of morality and religious observance, as can be seen from his list of sins.
Multiple items reflect his notions of what he owed to God, and his remorse at not always living up to that standard. He had a keen interest in mysticism that was tied firmly to his study of alchemy.
He believed that he had been chosen by God. In fact, the pseudonym he took to communicate with fellow alchemists was Jehovah Sanctus Unus, which translates to “Holy God”, according to the New York Post.
Despite all of these issues, Sir Isaac Newton was brilliant, and prolific in his work. His intellectual curiosity was not hampered by what was clearly a difficult personality, and despite his struggles and mood swings he still made a large and incredibly significant contribution to the world of science.
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.
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.
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.
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.
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?
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.
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.
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.
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.
This article was originally published on The Conversation.Matthew E. Baker, Professor of Geography and Environmental Systems, University of Maryland, Baltimore County
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.
“At first, we will study very carefully the surface features. Then we will select where to touch down. Touchdown means we get the surface material,” he told me.
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.”
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.
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).
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.
On the far side of the Moon lies the Maunder crater, named after two British astronomers – Annie and Walter Maunder.
Annie worked alongside her husband at the end of the 19th Century, recording the dark spots that pepper the Sun.
The name Maunder is still known in scientific circles, yet Annie has somehow slipped from history.
“I think the name Maunder is there and we have all rather forgotten that that’s two people,” says Dr Sue Bowler, editor of the Royal Astronomical Society magazine, Astronomy and Geophysics.
“She was acknowledged on papers, she published in her own name as well as with her husband, she wrote books, she was clearly doing a lot of work but she also clearly kept to the conventions of the day, I think.”
The ‘lady computers’
Annie Scott Dill Russell was born in 1868 in Strabane, the daughter of a Reverend.
Clearly of fierce intelligence, she won a scholarship to Girton College, Cambridge, and became one of the first female scientists to work at the Royal Observatory, Greenwich.
In the courtyard of the observatory, looking over the park, curator Dr Louise Devoy, tells me what little they know about her work.
“She was one of what we now call the ‘lady computers’ employed in the early 1890s by the then Astronomer Royal, William Christie,” she explains.
“I believe she came from Northern Ireland and she worked here for several years on very low pay just like many of the computers here, both male and female.
“In terms of what she actually did here, we have very little concrete record or photographs.'”
‘Grit and devotion’
Female scientists were hindered because of their gender until the 1920s and 30s, despite superb skills and experience, says Dr Devoy.
At Greenwich, employing women with a university education in mathematics was an audacious experiment.
Women were only considered because the Astronomer Royal needed skilled assistants but could afford only lowly computers – historically, schoolboys on a wage of £4 per month.
Maunder was offered a post as a lady computer, which meant a huge drop in pay for someone who had been working, briefly, as a school teacher.
Letters show that she appealed for more money but was turned down.
The lady computers would carry out routine calculations to turn raw observations into usable data. They were also trained to use telescopes.
At times, this meant walking through Greenwich Park at night without a chaperone, an activity that was frowned on at the time.
“In an age when many middle-class women were still chaperoned, the grit and devotion of these young women astronomers, clad in their clumsy long gowns as they worked at their telescopes or in the laboratories, were surely remarkable,” wrote the science historian and astronomer Mary T Brück.
In 1892, the names of Annie Russell and fellow Greenwich astronomer Alice Everett were put forward to become fellows of the Royal Astronomical Society.
However, they failed to gain enough of the popular vote in a secret ballot and were rejected.
The RAS had long argued that since the pronoun “he” was used in the charter, women could not be admitted alongside men.
Instead, Annie Russell and Alice Everett, who had studied together at Cambridge, joined the amateur British Astronomical Association (BAA).
Alice Everett grew tired of the low pay and left Greenwich, eventually developing an interest in the new field of television. Annie Russell stayed on.
“She was clearly very tough and wanted to follow her science,” says Dr Bowler.
“She sat the [difficult] mathematical Tripos at a time when women couldn’t actually be awarded a degree and there were even protests at Cambridge against the whole idea of giving women degrees.
“So she was clearly tough enough to do that and to do it well and to succeed then in getting employment as a scientist, which was fairly rare anyway – astronomy was still very much a gentleman’s pursuit.”
Studying the Sun
Annie Russell married her colleague Edward Walter Maunder in 1895.
Under civil service rules, as a married woman, she was forced to give up her paid position, bringing the age of lady computers to an end.
“She did come back as a volunteer during the First World War and then she was taken on as a paid employee later in the 1920s,” says Dr Devoy.
Annie worked alongside Walter taking photographs of the Sun, laying the groundwork for a modern understanding of solar activity.
“They would take photographs of the Sun every clear day just to note where the sunspots were and to sketch where they were,” says Dr Bowler. “But she also, as a trained mathematician, put quite a bit of effort into analysis. She wasn’t just writing things down; she wasn’t just Walter’s assistant.”
Annie Maunder went on many scientific expeditions to observe eclipses around the turn of the century, often as the only woman. She travelled to Lapland, India, Algiers, Mauritius and Labrador.
She even designed her own camera to take spectacular pictures of the Sun, including the first photograph ever of streamers from the Sun’s outer layer, or corona.
“She particularly caught an extremely long ray – a streak of the corona – coming out from the Sun, while it was eclipsed, that nobody had ever seen before – a feature of the corona that people just didn’t know about,” says Dr Bowler.
“I’ve seen photos of her adjusting the instruments. She’s taking her photographs. She’s not at all a passenger.
“It may have been only socially acceptable for her to go because she’s travelling with her husband but she was on official scientific expeditions and her photographs were acknowledged as among the best.”
The Heavens and Their Story
The conventions of the time meant that Annie’s photographs were published under her husband’s name and she could not speak at scientific meetings.
However, she was eventually made a fellow of the Royal Society in 1916, 24 years after first being proposed.
She was involved with promoting astronomy to a general audience as vice president of the BAA and edited the in-house journal.
In 1908, the Maunders published the book, The Heavens and Their Story, which was aimed at popular science.
The book was released under both their names, but her husband acknowledged in the preface that it was almost all her work.
The Maunders are also well known for the butterfly diagram, which shows how the number of sunspots varies with time, and the Maunder Minimum, a period in the 17th Century when sunspots all but disappeared.
Much of their work still holds true today.
This year, Annie’s name is being remembered through the inaugural Annie Maunder Medal, to recognise public engagement in science.
“She is an ideal person for that medal to be named after,” says Dr Bowler. “That’s largely what she was doing, certainly later in her career.”
Annie Maunder died in 1947, long after her husband.
On a leafy street near Clapham Common I find the Victorian terraced house where she spent her final years.
From the outside there is nothing to speak of the pioneering scientist.
Yet, despite perhaps not getting the recognition she deserved in her lifetime, she clearly left her mark on science.
“From her letters which are in the Royal Astronomical Society archives she was a very strong-minded, very decided personality,” says Sue Bowler.
“She didn’t mince her words. She’s really quite amusingly rude in some of her letters and very precise.
“I really admire her – she’s one of the people I would definitely have at my dream dinner party – I think she would be extraordinarily interesting.
“And her thoughts, her opinions about the paper based on her observations are very modern and form the basis for solar physics through a lot of the years following.”