Marcos Fernandez Tous, University of North Dakota

Off the coast of Baja California in December 2022, sun sparkled over the rippling sea as waves sloshed around the USS Portland dock ship. Navy officials on the deck scrutinized the sky in search of a sign. The glow appeared suddenly.

A tiny spot at first, it gradually grew to a round circle falling at a great speed from the fringes of space. It was NASA’s Orion capsule, which would soon end the 25-day Artemis I mission around and beyond the Moon with a fiery splashdown into the ocean.

Orion’s reentry followed a sharply angled trajectory, during which the capsule fell at an incredible speed before deploying three red and white parachutes. As the mission finished its trip of over 270,000 miles (435,000 kilometers), it looked to those on the deck of the USS Portland like the capsule had made it home in a single piece.

As the recovery crew lifted Orion to the carrier’s deck, shock waves ruffled across the capsule’s surface. That’s when crew members started to spot big cracks on Orion’s lower surface, where the capsule’s exterior bonds to its heat shield.

But why wouldn’t a shield that has endured temperatures of about 5,000 degrees Fahrenheit (2,760 degrees Celsius) sustain damage? Seems only natural, right?

This mission, Artemis I, was uncrewed. But NASA’s ultimate objective is to send humans to the Moon in 2026. So, NASA needed to make sure that any damage to the capsule– even its heat shield, which is meant to take some damage – wouldn’t risk the lives of a future crew.

On Dec. 11, 2022 – the time of the Artemis I reentry – this shield took severe damage, which delayed the next two Artemis missions. While engineers are now working to prevent the same issues from happening again, the new launch date targets April 2026, and it is coming up fast.

As a professor of aerospace technology, I enjoy researching how objects interact with the atmosphere. Artemis I offers one particularly interesting case – and an argument for why having a functional heat shield is critical to a space exploration mission.

Taking the heat

To understand what exactly happened to Orion, let’s rewind the story. As the capsule reentered Earth’s atmosphere, it started skimming its higher layers, which acts a bit like a trampoline and absorbs part of the approaching spacecraft’s kinetic energy. This maneuver was carefully designed to gradually decrease Orion’s velocity and reduce the heat stress on the inner layers of the shield.

After the first dive, Orion bounced back into space in a calculated maneuver, losing some of its energy before diving again. This second dive would take it to lower layers with denser air as it neared the ocean, decreasing its velocity even more.

While falling, the drag from the force of the air particles against the capsule helped reduced its velocity from about 27,000 miles per hour (43,000 kilometers per hour) down to about 20 mph (32 kph). But this slowdown came at a cost – the friction of the air was so great that temperatures on the bottom surface of the capsule facing the airflow reached 5,000 degrees Fahrenheit (2,760 degrees Celsius).

At these scorching temperatures, the air molecules started splitting and a hot blend of charged particles, called plasma, formed. This plasma radiated energy, which you could see as red and yellow inflamed air surrounding the front of the vehicle, wrapping around it backward in the shape of a candle.

No material on Earth can stand this hellish environment without being seriously damaged. So, the engineers behind these capsules designed a layer of material called a heat shield to be sacrificed through melting and evaporation, thus saving the compartment that would eventually house astronauts.

By protecting anyone who might one day be inside the capsule, the heat shield is a critical component.

In the form of a shell, it is this shield that encapsulates the wide end of the spacecraft, facing the incoming airflow – the hottest part of the vehicle. It is made of a material that is designed to evaporate and absorb the energy produced by the friction of the air against the vehicle.

The case of Orion

But what really happened with Orion’s heat shield during that 2022 descent?

In the case of Orion, the heat shield material is a composite of a resin called Novolac – a relative to the Bakelite which some firearms are made of – absorbed in a honeycomb structure of fiberglass threads.

As the surface is exposed to the heat and airflow, the resin melts and recedes, exposing the fiberglass. The fiberglass reacts with the surrounding hot air, producing a black structure called char. This char then acts as a second heat barrier.

NASA used the same heat shield design for Orion as the Apollo capsule. But during the Apollo missions, the char structure didn’t break like it did on Orion.

After nearly two years spent analyzing samples of the charred material, NASA concluded that the Orion project team had overestimated the heat flow as the craft skimmed the atmosphere upon reentry.

As Orion approached the upper layers of the atmosphere, the shield started melting and produced gases that may have escaped through pores in the material. Then, when the capsule gained altitude again, the outer layers of the resin froze, trapping the heat from the first dive inside. This heat vaporized the resin.

When the capsule dipped into the atmosphere the second time, the gas expanded before finding a way out as it heated again – kind of like how a frozen lake thaws upward from the bottom – and its escape produced cracks in the capsule’s surface where the char structure got damaged. These were the cracks the recovery crew saw on the capsule after it splashed down.

In a Dec. 5, 2024, press conference, NASA officials announced that the Artemis II mission will be designed with a modified reentry trajectory to prevent heat from accumulating.

For Artemis III, which is planned to launch in 2027, NASA intends to use new manufacturing methods for the shield, making it more permeable. The outside of the capsule will still get very hot during reentry, and the heat shield will still evaporate. But these new methods will help keep the astronauts cozy in the capsule all the way through splashdown.

Chonglin Zhang, assistant professor of mechanical engineering at the University of North Dakota, assisted in researching this article.

Marcos Fernandez Tous, Assistant Professor of Space Studies, University of North Dakota

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Brody H. Foy, University of Washington

If you’ve ever had a doctor order a blood test for you, chances are that they ran a complete blood count, or CBC. One of the most common blood tests in the world, CBC tests are run billions of times each year to diagnose conditions and monitor patients’ health.

But despite the test’s ubiquity, the way clinicians interpret and use it in the clinic is often less precise than ideal. Currently, blood test readings are based on one-size-fits-all reference intervals that don’t account for individual differences.

I am a mathematician at the University of Washington School of Medicine, and my team studies ways to use computational tools to improve clinical blood testing. To develop better ways to capture individual patient definitions of “normal” lab values, my colleagues and I in the Higgins Lab at Harvard Medical School examined 20 years of blood count tests from tens of thousands of patients from both the East and West coasts.

In our newly published research, we used machine learning to identify healthy blood count ranges for individual patients and predict their risk of future disease.

Clinical tests and complete blood counts

Many people commonly think of clinical tests as purely diagnostic. For example, a COVID-19 or a pregnancy test comes back as either positive or negative, telling you whether you have a particular condition. However, most tests don’t work this way. Instead, they measure a biological trait that your body continuously regulates up and down to stay within certain bounds.

Your complete blood count is also a continuum. The CBC test creates a detailed profile of your blood cells – such as how many red blood cells, platelets and white blood cells are in your blood. These markers are used every day in nearly all areas of medicine.

For example, hemoglobin is an iron-containing protein that allows your red blood cells to carry oxygen. If your hemoglobin levels are low, it might mean you are iron deficient.

Platelets are cells that help form blood clots and stop bleeding. If your platelet count is low, it may mean you have some internal bleeding and your body is using platelets to help form blood clots to plug the wound.

White blood cells are part of your immune system. If your white cell count is high, it might mean you have an infection and your body is producing more of these cells to fight it off.

Normal ranges and reference intervals

But this all raises the question: What actually counts as too high or too low on a blood test?

Traditionally, clinicians determine what are called reference intervals by measuring a blood test in a range of healthy people. They usually take the middle 95% of these healthy values and call that “normal,” with anything above or below being too low or high. These normal ranges are used nearly everywhere in medicine.

But reference intervals face a big challenge: What’s normal for you may not be normal for someone else.

Nearly all blood count markers are heritable, meaning your genetics and environment determine much of what the healthy value for each marker would be for you.

At the population level, for example, a normal platelet count is approximately between 150 and 400 billion cells per liter of blood. But your body may want to maintain a platelet count of 200 – a value called your set point. This means your normal range might only be 150 to 250.

Differences between a patient’s true normal range and the population-based reference interval can create problems for doctors. They may be less likely to diagnose a disease if your set point is far from a cutoff. Conversely, they may run unnecessary tests if your set point is too close to a cutoff.

Defining what’s normal for you

Luckily, many patients get blood counts each year as part of routine checkups. Using machine learning models, my team and I were able to estimate blood count set points for over 50,000 patients based on their history of visits to the clinic. This allowed us to study how the body regulates these set points and to test whether we can build better ways of personalizing lab test readings.

Over multiple decades, we found that individual normal ranges were about three times smaller than at the population level. For example, while the “normal” range for the white blood cell count is around 4.0 to 11.0 billion cells per liter of blood, we found that most people’s individual ranges were much narrower, more like 4.5 to 7, or 7.5 to 10. When we used these set points to interpret new test results, they helped improve diagnosis of diseases such as iron deficiency, chronic kidney disease and hypothyroidism. We could note when someone’s result was outside their smaller personal range, potentially indicating an issue, even if the result was within the normal range for the population overall.

The set points themselves were strong indicators for future risk of developing a disease. For example, patients with high white blood cell set points were more likely to develop Type 2 diabetes in the future. They were also nearly twice as likely to die of any cause compared with similar patients with low white cell counts. Other blood count markers were also strong predictors of future disease and mortality risk.

In the future, doctors could potentially use set points to improve disease screening and how they interpret new test results. This is an exciting avenue for personalized medicine: to use your own medical history to define what exactly healthy means for you.

Brody H. Foy, Assistant Professor of Laboratory Medicine and Pathology, University of Washington

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Andrea Kaston Tange, Macalester College

Modern medicine has enabled citizens of wealthy, industrialized nations to forget that children once routinely died in shocking numbers. Teaching 19th-century English literature, I regularly encounter gutting depictions of losing a child, and I am reminded that not knowing the emotional cost of widespread child mortality is a luxury.

In the first half of the 19th century, between 40% and 50% of children in the U.S. didn’t live past the age of 5. While overall child mortality was somewhat lower in the U.K., the rate remained near 50% through the early 20th century for children living in the poorest slums.

Threats from disease were extensive. Tuberculosis killed an estimated 1 in 7 people in the U.S. and Europe, and it was the leading cause of death in the U.S. in the early decades of the 19th century. Smallpox killed 80% of the children it infected. The high fatality rate of diphtheria and the apparent randomness of its onset caused panic in the press when the disease emerged in the U.K. in the late 1850s.

Multiple technologies now prevent epidemic spread of these and other once-common childhood illnesses, including polio, tetanus, whooping cough, measles, scarlet fever and cholera.

Closed sewers protect drinking water from fecal contamination. Pasteurization kills tuberculosis, diphtheria, typhoid and other disease-causing organisms in milk. Federal regulations stopped purveyors from adulterating foods with the chalk, lead, alum, plaster and even arsenic once used to improve the color, texture or density of inferior products. Vaccines created herd immunity to slow disease spread, and antibiotics offer cures to many bacterial illnesses.

As a result of these sanitary, regulatory and medical advances, child mortality rates have sat below 1% in the U.S. and U.K. since the 1930s.

Victorian novels chronicle the terrible grief of losing children. Depicting the cruelty of diseases largely unfamiliar today, they also warn against being lulled into thinking that child deaths can never be inevitable again.

Routine death meant relentless grief

Novels tapped into communal fears as they mourned fictional children.

Little Nell, the angelic figure at the center of Charles Dickens’ wildly popular “The Old Curiosity Shop,” fades away from an unnamed illness over the last few installments of this serialized novel. When the ship carrying the printed pages with the final part of the story pulled into New York, people apparently shouted from the docks, asking if she had survived. The public investment in, and grief over, her death reflects a shared experience of helplessness: No amount of love can save a child’s life.

Eleven-year-old Anne Shirley of “Green Gables” fame became a hero for pulling 3-year-old Minnie May through a dramatic battle with diphtheria. Readers knew this as a horrendous illness in which a membrane blocks the throat so effectively that a child will gasp to death.

Children were familiar with disease risks. While typhus runs rampant in “Jane Eyre,” killing nearly half the girls at their charity school, 13-year-old Helen Burns is struggling against tuberculosis. Ten-year-old Jane is filled with horror at the possible loss of the only person who has ever truly cared for her.

An entire chapter deals frankly and emotionally with all this dying. Jane cannot bear separation from quarantined Helen and seeks her out one night, filled with “the dread of seeing a corpse.” In the chill of a Victorian bedroom, she slips under Helen’s blankets and tries to stifle her own sobs as Helen is overtaken with coughing. A teacher discovers them the next morning: “my face against Helen Burns’s shoulder, my arms round her neck. I was asleep, and Helen was – dead.”

The disconcerting image of a child nestled in sleep against another child’s corpse may seem unrealistic. But it is very like the mid-19th-century memento photographs taken of deceased children surrounded by their living siblings. The specter of death, such scenes remind us, lay at the center of Victorian childhood.

Fiction was not worse than fact

Victorian periodicals and personal writings remind us that death being common did not make it less tragic.

Darwin agonized at losing “the joy of the Household,” when his 10-year-old daughter Annie succumbed to tuberculosis in 1851.

The weekly magazine “Household Words” reported the 1853 death of a 3-year-old from typhoid fever in a London slum contaminated by an open cesspool. But better housing was no guarantee against waterborne infection. President Abraham Lincoln was “convulsed” and “unnerved,” his wife “inconsolable,” watching their son Willie, 11, die of typhoid in the White House.

In 1856, Archibald Tait, then headmaster of Rugby and later Archbishop of Canterbury, lost five of his seven children in just over a month to scarlet fever. At the time, according to historians of medicine, this was the most common pediatric infectious disease in the U.S. and Europe, killing 10,000 children per year in England and Wales alone.

Scarlet fever is now generally curable with a 10-day course of antibiotics. However, researchers warn that recent outbreaks demonstrate we cannot relax our vigilance against contagion.

Forgetting at our peril

Victorian fictions linger on child deathbeds. Modern readers, unused to earnest evocations of communal grief, may mock such sentimental scenes because it is easier to laugh at perceived exaggeration than to frankly confront the specter of a dying child.

“She was dead. Dear, gentle, patient, noble Nell was dead,” Dickens wrote in 1841, at a time when a quarter of all the children he knew might die before adulthood. For a reader whose own child could easily trade places with Little Nell, becoming “mute and motionless forever,” the sentence is an outpouring of parental anguish.

These Victorian stories commemorate a profound, culturally shared grief. To dismiss them as old-fashioned is to assume they are outdated because of the passage of time. But the collective pain of a high child mortality rate was eradicated not by time, but by effort. Rigorous sanitation reform, food and water safety standards, and widespread use of disease-fighting tools like vaccines, quarantine, hygiene and antibiotics are choices.

And the successes born of these choices can unravel if people begin choosing differently about health precautions.

While tipping points differ by illness, epidemiologists agree that even small drops in vaccine rates can compromise herd immunity. Infectious disease experts and public health officials are already warning of the dangerous uptick of diseases whose horrors 20th century advances helped wealthy societies forget.

People who want to dismantle a century of resolute public health measures, like vaccination, invite those horrors to return.

Andrea Kaston Tange, Professor of English, Macalester College

This article is republished from The Conversation under a Creative Commons license. Read the original article.