NASA Saw Something Come Out Of A Black Hole For The First Time Ever

NASA Saw Something Come Out Of A Black Hole For The First Time Ever

The World’s First Bionic Kidney Is All Set To Replace Dialysis in Just Two Years

The World’s First Bionic Kidney Is All Set To Replace Dialysis in Just Two Years

Why Creative People Sometimes Make No Sense.

Why Creative People Sometimes Make No Sense – Matthew Schuler

Insulin Goes Viral?

New study shows some viruses produce insulin-like hormones that have potential to cause disease

Every cell in your body responds to the hormone insulin, and if that process starts to fail, you get diabetes.

In an unexpected finding, Harvard Medical School scientists at Joslin Diabetes Center have identified four viruses that can produce insulin-like hormones that are active on human cells. The discovery brings new possibilities for revealing biological mechanisms that may cause diabetes or cancer.

“Our research may help open up a new field that we might call microbial endocrinology,” said Emrah Altindis, HMS instructor in medicine at Joslin Diabetes Center and lead author on a paper in the journal PNAS  on the work.

“We show that these viral, insulin-like peptides can act on human and rodent cells. With the very large number of microbial peptides to which we are exposed, there is a novel window for host-microbe interactions. We hope that studying these processes will help us to better understand the role of microbes in human disease,” Altindis said.

“Indeed, the discovery of the viral insulin-like hormones raises the question of what their role might be in diabetes, as well as in autoimmune disease, cancer and other metabolic conditions,” said C. Ronald Kahn, the HMS Mary K. Iacocca Professor of Medicine and Joslin’s chief academic officer.

The key idea for the investigation came when Altindis, whose previous research focused on creating vaccines against bacteria, attended a Joslin seminar that discussed potential causes of the autoimmune reaction that drives type 1 diabetes.

From left, Altindis and Kahn.  Image: Courtesy Joslin Diabetes CenterFrom left, Altindis and Kahn. Image: Courtesy Joslin Diabetes Center

He began to hypothesize whether bacteria or viruses could create insulin-like peptides (small versions of proteins) that could help to trigger the disease.

By analyzing large public research databases that hold viral genomic sequences, he and his colleagues at Joslin found that various viruses can produce peptides that are similar in whole or in part to 16 human hormones and regulatory proteins.

“What really caught our attention were four viruses that had insulin-like sequences,” said Kahn, who was senior author on the paper.

Infecting Fish

These viruses were from a family of viruses known to infect fish. To find out if they could be active in mammals, the Joslin team collaborated with Richard DiMarchi, professor of chemistry at Indiana University, Bloomington, whose lab chemically synthesized these viral insulin-like peptides (VILPs).

Experimenting in mouse and human cells, the scientists studied whether the VILPs could act like hormones. Their experiments proved that the VILPs could indeed bind to human insulin receptors and receptors for a closely related hormone called IGF-1 (insulin-like growth factor 1).

These are the critical proteins on the cells that tell them to take up glucose and to grow. Additionally, the peptides could stimulate all of the signaling pathways inside the cells that were stimulated by human insulin and IGF-1.

Mice injected with the viral peptides exhibited lower levels of blood glucose, another sign of insulin action. Moreover, analysis of databases of viruses found in the human intestine showed evidence that humans are exposed to these viruses.

“These viruses are definitely known to infect fish and amphibians, but they are not known to infect humans,” Kahn pointed out. “However, it’s possible that humans get exposed to these viruses through just eating fish. Nobody has checked directly whether under some conditions the viruses could either infect cells or be at least partly absorbed through the gut intestine.”

The scientists now will broaden their search for other viruses that produce human-like hormones.

“This finding is the tip of an iceberg,” Kahn said. “There are thought to be more than 300,000 viruses that can infect or be carried in mammals, and only 7,500 or so of these, or about 2.5 percent, have been sequenced. Thus, we certainly expect to find many more viral hormones, including more viral insulins, in the future.”

“This research also opens up a new aspect to study in type 1 diabetes and autoimmunity,” he said.

“It may be that these or similar microbial insulin-like molecules could be an environmental trigger to start the autoimmune reaction in type 1 diabetes. On the other hand, you could also imagine that this might desensitize the immune response and could be protective,” Kahn said.

Viral Peptides

A similar question is open for metabolic diseases such as type 2 diabetes and obesity, in which the body fails to respond properly to insulin.

“You could envision that these viral peptides could either protect from or contribute to insulin resistance,” Kahn said.

These or similar viruses might also be a factor in certain human cancers.

“If these viruses are inside the gut, could the VILPs they produce stimulate growth of gut cells so that you get polyps or tumors of the gut?” Kahn asks. “Or if they’re absorbed or become infectious, could they infect any organ in the body?”

Analyzing such viral peptides may eventually help drug companies to design new forms of synthesized human insulins.

“We might be able to learn something, for example, about making insulins that don’t need refrigeration and can be stored for long periods of time, or insulins that are absorbed more quickly or degrade more slowly,” he said.

Given Altindis’s earlier research on infectious disease rather than in endocrinology, “our discovery gives an example of how work in one field can stimulate thought in another field,” Kahn added. “It really underlines the importance of cross-fertilization in the scientific discovery process, which is so valuable but so underappreciated.”

Curbing Gun Violence

HMS internal medicine physician discusses gun reform and health care

AR-15 rifles.

Having undergone her training as a medical student on the South Side of Chicago, Chana Sacks thought she understood the ramifications of gun violence.

Then, in December 2012, during Sacks’ residency at Massachusetts General Hospital, a harrowing personal experience reframed her understanding of gun violence in the most painful of ways. Her cousin’s 7-year-old son, Daniel, was gunned down at Sandy Hook Elementary School in Connecticut. For Sacks, now a Harvard Medical School instructor, gun violence became an aching personal reality.

Sacks powerfully captured this scarring—and transformative—experience in a 2015 commentary for The New England Journal of Medicine.

Now, an internal medicine physician at Mass General, Sacks has formed the MGH Gun Violence Prevention Coalition. She co-leads the effort with Peter Masiakos, HMS associate professor of surgery and director of the pediatric trauma service at Mass General, and Paul Currier, HMS assistant professor of medicine and a pulmonary and critical specialist at Mass General, along with Kim Sheppard Smith, a registered nurse.

For this group, the Feb. 14 shooting in Parkland, Florida, that left 17 dead is the latest tragic reminder that their work is more urgently needed than ever.

Sacks sat down with Harvard Medicine News to discuss the state of gun violence research, policy and more.

HMN: Nearly 33,000 people die of firearm injuries in the United States each year and more than 67,000 are injured by gun violence. What does this mean to you as a physician and a scientist?

Sacks: These numbers are staggering and tragic because these deaths and injuries are preventable. While the stats are stark, they actually underestimate the magnitude of the problem, because this is not just about body counts. There were 3,000 students at the school in Parkland and, while thankfully most were not physically injured, those students and faculty and staff and parents and family friends are all facing long-lasting emotional sequelae. It’s important to remember that while mass shootings like this tragedy in Parkland capture the country’s attention, gun violence is a daily reality across the country for many people and many families whose pain never makes the news.

“These numbers are staggering and tragic because these deaths and injuries are preventable.” — Chana Sacks

My colleagues across every discipline—from emergency medicine, trauma surgery, rehabilitation, psychiatry, social work and other specialties—witness the devastation of gun violence firsthand. We all see the devastation of entire families when one person comes in shot.

As a clinician, I thought I understood this issue. I thought I knew what it meant. Then, when Daniel was killed, gun violence became a haunting personal reality.

HMN: Going back to cold clinical numbers, can we put them in a public health context?

Sacks: Thirty-three thousand people die each year from gun violence—that’s the same number of people dying from liver disease, and about the same number of people dying from sepsis. As clinicians, we are taught how to deal with these other causes of death that threaten our patients. I have sat through lectures on those topics, pored over well-conducted research studies funded by the National Institutes of Health. Not a single lecture, no emphasis in the curriculum, hardly any federal research funding for gun violence, which is taking just as many lives. We’re not taught how to approach it.

HMN: If you had a wish list of things to do to curb gun violence, what would the list include?

Sacks: One of the critical things we have to do to address gun violence is to reframe it as the public health and medical issue that it is. Then, we will have the power to approach it in a way that can lead to real solutions. Addressing firearm-related injuries will take a constellation of strategies. Reducing deaths from gun suicides demands a very different approach from one making sure a 5-year-old doesn’t get his hands on a gun and accidentally shoot his sister. We need to develop an understanding of the different pathways that lead to different types of gun violence. We would never expect one treatment to cure every type of heart disease. Whether it’s cardiovascular illness or gun violence, once we understand them we can devise targeted treatments.

At the same time, there are things we already know.  The common link in these tragedies is easy access to firearms. We know that access to firearms is an independent risk factor for suicide and homicide. We know that stronger firearm policies in general and stronger laws regulating permits and background checks are associated with decreased firearm homicides. We know that states with the most firearm legislation have the lowest rates of gun suicide and homicide. We know that in most mass shootings, the shooter gave warning signs that either weren’t recognized or weren’t acted upon. We know that too many guns in this country are not safely stored.

We know from the firsthand accounts of emergency room physicians, trauma surgeons and radiologists who treat gunshot victims that certain semi-automatic rifles spew lethality like no other, causing often irreparable organ damage, the kind once seen only on the battlefield.

We have important, actionable knowledge already, but still, many questions remain unanswered because of the lack of federal research funding. Speaking of a wish list, repealing the federal legislation first passed in 1996 that effectively shut down funding for gun violence research is a first order of business.  When data are absent, people get to choose their own anecdotes and treat them as fact. We cannot develop sound policy from gestalt alone. We have to test interventions and evaluate what works in a measurable way.

HMN: Much has been made of the mental health component in the gun debate. Can you address this?

Sacks: Tackling the mental health aspect of gun violence is, without doubt, critical, but it’s one component in a complex dynamic. There is a risk that people with mental illness get scapegoated in the national conversation. The fact is that people with mental illness are more likely to be victims of crime rather than perpetrators. Painting gun violence as a mental health problem alone is reductive and is exploited by some people who are very good at distracting from the real evidence-based ways of moving forward.

HMN: The human toll of gun violence appears immeasurable. Let’s talk about dollars and cents.

Sacks: The medical costs and loss of productivity alone are estimated to cost tens of billions of dollars a year. When costs of psychological trauma, litigation, the economic impact of lower property values and the closing of businesses in areas of cities that are seen as dangerous are factored in, some estimates reach $100 billion a year or more. The ripple effects spread quickly.

HMN: What is the role of clinicians in informing the public conversation on gun violence?

 Sacks: Our first obligation is to our patients in the clinic, in the hospital, in the emergency room. We must ask about gun safety and firearms in the home. Beyond the walls of the hospital, we have an obligation to speak out about what we witness on a daily basis. We must demand policy change because gun injuries and gun deaths are, at their core, medical. Gun violence affects every discipline in medicine in a really far-reaching way: emergency medicine doctors and nurses, trauma surgeons, primary care doctors dealing with the longer term sequelae, rehabilitation specialists, infectious disease doctors who take care of patients with spinal cord injuries and neurogenic bladder who get recurrent infections, mental health specialists, social workers and so on.

HMN: If gun violence is at its core a public health issue with cultural and political dimensions, how do we disentangle one from the others?

Sacks: I don’t know that they are easily disentangled. But an organized movement demanding substantive change is growing. There are many different groups saying the same thing—enough is enough. The Parkland students are really making a difference, leading with their powerful voices.

Responsible gun owners, of whom there are millions, have a big role to play in this conversation, and many of them are part of the effort for sensible gun reform. This goes to show it’s not “us” versus “them,” although this framing may be politically expedient for some.

But ultimately, we do have to bring the political and cultural discussion back to the core question of how to reduce morbidity and mortality from firearms and how to keep our communities safe. We are talking 33,000 deaths a year from gun violence—what could be more medical than that?

Trimethoprim Is Associated with Excess Risk for Acute Kidney Injury in Elders

In this cohort study, higher odds of hyperkalemia and kidney injury with TMP weren’t dependent on drug interactions.


Trimethoprim/sulfamethoxazole (TMP/SMX) use is associated with excess risk for hyperkalemia and related adverse events in patients who take angiotensin-converting–enzyme inhibitors, angiotensin-receptor blockers (NEJM JW Gen Med Sep 1 2010 and JAMA Intern Med 2010; 170:1045; NEJM JW Gen Med Dec 15 2014 and BMJ 2014; 349:6196), or spironolactone (NEJM JW Gen Med Nov 1 2011 and BMJ 2011; 343:5228). However, whether TMP confers risk for hyperkalemia when it is used without SMX and in the absence of renin-angiotensin system blockers is unknown. In the U.K., TMP often is prescribed without SMX, giving researchers an opportunity to clarify this issue in a cohort of 180,000 patients (age, ≥65) who experienced at least one urinary tract infection (UTI) and received antibiotics.

After adjustment for numerous potential confounders (including use of renin-angiotensin system blockers and potassium-sparing diuretics), odds of acute kidney injury during the 14 days following antibiotic initiation were 72% higher with TMP and 48% higher with ciprofloxacin than with amoxicillin. Odds of hyperkalemia occurrence during the 14 days following antibiotic initiation were 127% higher with TMP than with amoxicillin. TMP, compared with amoxicillin, was not associated with increased odds of death. Trimethoprim was associated with 1 to 2 additional cases of hyperkalemia and 2 admissions for acute kidney injury per 1000 treated patients; for people taking renin-angiotensin system blockers and spironolactone, 18 additional cases of hyperkalemia and 11 additional admissions for acute kidney injury occurred.


TMP use alone was associated with excess risk for hyperkalemia and acute kidney injury, but not death, compared with amoxicillin use for primary care treatment of UTIs among elders. This hyperkalemia finding is unsurprising, as TMP reduces potassium excretion in the distal renal tubule. Although TMP can raise serum creatinine concentration (by reducing tubular secretion of creatinine), which could result in overestimation of “true” kidney injury, the authors provide several reasons to believe that kidney injury in their study was real — a novel observation for TMP. Antibiotics other than those that contain TMP should be used in patients at risk for hyperkalemia and acute kidney injury.

Tenofovir to Prevent Perinatal Transmission of Hepatitis B

A 36-year-old pregnant woman, originally from Southeast Asia, presents to her family medicine physician for prenatal care in the first trimester. She has had no history of medical problems. On family history, she reports that her mother recently died of liver cancer due to hepatitis B virus (HBV). The patient’s prenatal screening indicates that she is hepatitis B e antigen (HBeAg)-positive, with normal liver function tests. The physician explains to the patient that the blood test showed that she is a chronic carrier of hepatitis B, which she likely got as a baby from her mother. The patient asks, “Are there any new treatments to prevent me from passing hepatitis B to my baby?”

Mother-to-child transmission of HBV is a leading cause of chronic HBV infection and liver cancer worldwide, particularly in Asia. Prior to the availability of perinatal interventions to prevent HBV transmission, mothers with chronic HBV infection had an approximate 1 in 3 chance of passing HBV to their baby during pregnancy, delivery, or infancy; and more than 65%-90% of infected children developed chronic HBV infection.

Over the past few decades, perinatal transmission of HBV has been reduced dramatically by two key interventions: Universal HBV immunization for infants starting at birth, with at least 3 doses by 6 months of age, and administration of hepatitis B immunoglobulin (HBIg) at birth to infants born to HBV-infected mothers. However, for mothers who are HBeAg-positive with high HBV loads (>200,000 IU/mL), perinatal HBV transmission still occurs in up to one third of cases. Researchers have postulated that perinatal administration of antiviral medication could inhibit HBV replication and reduce the risk of perinatal HBV transmission.

This week, NEJM published a multicenter, double-blind, randomized clinical trial conducted in Thailand to test the effectiveness of antiviral medication to prevent perinatal HBV transmission. A total of 331 HBeAg-positive pregnant women with normal liver function tests (ALT ≤60 IU/L) were randomized to receive tenofovir or placebo from 28 weeks of gestation to 2 months postpartum. All infants received HBIg at birth and HBV vaccine at birth and at ages 1, 2, 4, and 6 months. The primary outcome was HBV surface-antigen (HBsAg) positivity, confirmed by HBV-DNA in the infants at 6 months of age.

The results showed that maternal HBV viral load declined substantially in the tenofovir group, with no change in the placebo group; and at delivery, 12% of women in the tenofovir group had elevated HBV DNA levels versus 90% in the placebo group. Among the live-born babies, 0 of the 147 babies in the tenofovir group were HBsAg positive (0%; 95% CI, 0-2), compared to 3 of 147 in the placebo group (2%; 95% CI, 0-6), a nonsignificant difference (P=0.12). Adverse events in mothers and babies did not differ significantly between groups.

The authors concluded that in the setting of low HBV transmission rates, treating pregnant women with tenofovir in addition to administration of infant HBV vaccine and HBIg did not significantly reduce mother-to-child transmission of HBV. However, the small sample size may have limited the study’s ability to demonstrate statistical significance. This study joins a handful of similar studies — some considered low-quality — with conflicting results about whether antiviral treatment significantly reduces perinatal HBV transmission. As a result, expert recommendations have differed (e.g., the 2015 WHO hepatitis guidelines for management of chronic HBV did not recommend antiviral treatment, but the 2016 American Association for the Study of Liver Diseases guidelines did recommend antiviral treatment for pregnant women who were HBsAg positive with high HBV DNA levels). Dr. Lindsey Baden, an infectious diseases specialist and Deputy Editor at NEJM commented, “The benefits of preventing maternal-to-child transmission of HBV are life-long, and we must continue to improve our ability to do this. These data are encouraging, but it will require a substantially larger study to definitively demonstrate additional benefits to current practices.”

Returning to the physician and the pregnant patient, the physician should express sympathy about the patient’s mother’s death and reassure her that they will work closely together in consultation with a liver specialist to try to keep her healthy. The physician should also reassure the patient that the current treatments for babies born to women carrying hepatitis B, which were not available when she was born, can usually prevent hepatitis B from passing from mothers to babies. Because there a low risk of passing hepatitis B to the baby, the physician and patient should discuss whether the patient wishes to take tenofovir.

Elephants Are Strangely Resistant to Cancer – And We May Finally Know Why

The genetic clues could help humans, too.

A research team peering into the relatively underexplored “junk” DNA of mammals has found more clues as to elephants’ extraordinary ability to evade cancer – and determined that the genes responsible for mitigating damage in elephant cells can also be found in humans.

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Most of the world’s mammals are prone to cancer, but elephants are strangely resistant. They’re not completely immune, but compared to humans, they get it surprisingly rarely – especially considering that they have 100 times the number of cells that humans do.

Cancer occurs when a cell randomly mutates during division, so the fact that only around 1 in 20 elephants develops cancer, compared to 1 in 5 humans, is extremely curious.

Researchers had been trying to figure out why this was the case for decades, but it was only a few years ago that a team of researchers narrowed this incredible trait down to an overabundance of a gene called p53, which suppresses tumours. African elephants have 40 copies of p53. Humans have just one.

But now a team of researchers at the University of Utah has found more clues as to how it occurs, and it’s not just down to p53.

They studied what had been known for several decades since the 1960s as “junk DNA” – DNA that does not code for proteins. That doesn’t make it useless, however – recent studies have found that it performs other functions, such as being able to control when and where genes are expressed.

“People used to call the noncoding regions ‘junk DNA’, but I see it as a jungle that has not been explored,” said neurobiologist Christopher Gregg from the University of Utah.

“We are exploring the noncoding regions to try to discover new parts of the genome that might control different diseases.”

The team searched the parts of the elephant genome that are common to all vertebrates, but specifically evolved more rapidly in elephants. They were scanning these regions for elements that help resist mutation – and therefore cancer.

They identified three genes in the elephants’ DNA – FANCL, VRK2 and BCL11A – after exposing the DNA to gamma radiation and observing how it responded to damage. These genes in particular are involved in DNA repair that guards against mutations – and they’re strongly associated with elephant accelerations.

Because vertebrates have so much DNA in common – having evolved from a common ancestor – many other mammals have these genes, too. The human versions don’t protect us from cancer in the same way that they seem to do in elephants, but just knowing what these genes are can help us narrow down their evolution in elephants, and determine if we can effect a similar change in our own genes.

Other animals the team studied were the hibernating bat, to study limb abnormalities; orca and dolphin, to study eye and corneal development, as well as adaptation to high pressure environments to study blood clotting disorders; naked mole rat, to study eye development and glaucoma; and thirteen-lined ground squirrel, to study albinism and leopard syndrome.

Future research will be needed to determine whether these accelerated regions in other mammals could be applied therapeutically to help control diseases in humans.

“We are staring at uncharted territory,” Gregg said. “This method gives us a new way to explore the genome and potentially uncover new approaches to identify, diagnose and treat disease.”

A Strange Quantum Effect Could Give Rise to a Completely New Kind of Star

A near cousin to black holes.

We might have to add a brand new category of star to the textbooks: an advanced mathematical model has revealed a certain ultracompact star configuration could in fact exist, when scientists had previously thought it impossible.

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This model mixes the repulsive effect of quantum vacuum polarisation – the idea that a vacuum isn’t actually empty but is filled with quantum energy and particles – with the attractive principles of general relativity.

The calculations are the work of Raúl Carballo-Rubio from the International School for Advanced Studies in Italy, and describe a hypothesis where a massive star doesn’t follow the usual instructions laid down by astrophysics.

“The novelty in this analysis is that, for the first time, all these ingredients have been assembled together in a fully consistent model,” says Carballo-Rubio.

“Moreover, it has been shown that there exist new stellar configurations, and that these can be described in a surprisingly simple manner.”

Due to the push and pull of gigantic forces, massive stars collapse under their own weight when they run out of fuel to burn. They then either explode as supernovae and become neutron stars, or collapse completely into a black hole, depending on their mass.

There’s a particular mass threshold at which the dying star goes one way or another.

 But what if extra quantum mechanical forces were at play? That’s the question Carballo-Rubio is asking, and he suggests the rules of quantum mechanics would create a different set of thresholds or equilibriums at the end of a massive star’s life.

Thanks to quantum vacuum polarisation, we’d be left with something that would look like a black hole while behaving differently, according to the new model. These new types of stars have been dubbed “semiclassical relativistic stars” because they the result of both classical and quantum physics.

One of the differences would be that the star would be horizonless – like another theoretical star made possible by quantum physics, the gravastar. There wouldn’t be the same ‘point of no return’ for light and matter as there is around a black hole.

The next step is to see if we can actually spot any of them – or rather spot any of the ripples they create through the rest of space. One possibility is that these strange types of stars wouldn’t exist for very long at all.

“It is not clear yet whether these configurations can be dynamically realised in astrophysical scenarios, or how long would they last if this is the case,” says Carballo-Rubio.

Interest in this field of astrophysics has been boosted by the progress scientists have been making in detecting gravitational waves, and it’s because of that work that it might be possible to find these variations on black holes.

The observatories and instruments coming online in the next few years will give scientists the chance to put this intriguing hypothesis to the test.

“If there are very dense and ultracompact stars in the Universe, similar to black holes but with no horizons, it should be possible to detect them in the next decades,” says Carballo-Rubio.

Scientists Just Discovered a Strange New Type of Ice Inside Deep-Earth Diamonds

We’ve never seen ice-VII in nature before.

Thanks to the discovery of water trapped inside diamonds from deep underground, geologists are thinking our planet could have much more water inside than we ever knew.

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Not only would this require a slight recalculation of the total amount of water our planet happens to hold, it would change how we model everything from the way heat moves through the crust to models predicting the frequency of earthquakes.

Researchers made the find by analysing the way X-rays diffracted through diamonds collected from southern Africa, China, Zaire, and Sierra Leone.

The water molecules found in these diamonds were squeezed into a solid form of ice, but they represent briny pools of liquid water that would be trapped in rocks far, far down – below a section of the mantle called the transition zone.

While there have been previous estimates on how much water could be contained by the hot, pressurised rocks at those depths, the only way to be confident in any of the guesses is to acquire a sample.

Since we’re talking more than 600 kilometres (roughly 400 miles) underground, you can forget digging down to grab a handful of magma.

Luckily there’s a solution in nature’s own tiny glass elevator – the diamond.

Only recently flecks of a mineral called calcium silicate perovskite (CaSiO3) were discovered inside a diamond. Despite the mineral’s predicted prevalence in our planet’s geology, it had never been seen – because it forms so far underground.

Similarly, the water molecules from below the transition zone were held under pressure inside flaws in the diamond crystal’s matrix of carbon atoms.

Squeezing water molecules together forces them to arrange themselves into different structures, effectively turning them into forms of ice – and it’s not like the simple stuff you can find in your freezer.

Different pressures can push the water molecules into a range of configurations, and this particular structure is called ice-VII. While it has been produced in the laboratory using containers pressurised to tens of thousands of atmospheres, this is the first time ice-VII has been shown to exist in the natural world, officially making it a bona fide mineral.

Based on the team’s analysis of the diamonds, the water molecules must have become trapped as liquid when crystals formed around 610 to 800 kilometres (400 to 500 miles) beneath the surface.

Only as they ascended did the changing pressure push them into a form that allowed them to stick in place as ice-VII.

The good news is the inclusions provide the first hard evidence that unbound water exists at such depths, most likely as a salty fluid.

Unfortunately it doesn’t say how much water there is inside such pockets, or how common these aqueous zones would be.

Knowing more about them would help inform our understanding of how soluble radioactive particles flow beneath the crust, which in turn would affect how we calculate the transfer of heat from the core to the surface.

Nailing down the distribution of water could also alter predictions on how sections of the crust sink beneath one another.

The mineral constitution of tectonic plates makes a significant difference to their density and the temperature at which they melt, factors that could help improve earthquake models.

Having confirmation that flowing water does indeed exist at these depths is a good start, and makes you wonder what other secrets might be lurking inside the world’s favourite gem.