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.

Libby Richards, Purdue University

You’ve probably heard “Don’t go outside in the winter with your hair wet or without a coat; you’ll catch a cold.”

That’s not exactly true. As with many things, the reality is more complicated. Here’s the distinction: Being cold isn’t why you get a cold. But it is true that cold weather makes it easier to catch respiratory viruses such as the cold and flu.

Research also shows that lower temperatures are associated with higher COVID-19 rates.

As a professor of nursing with a background in public health, I’m often asked about infectious disease spread, including the relationship between cold and catching a cold. So here’s a look at what actually happens.

Many viruses, including rhinovirus – the usual culprit for the common cold – influenza, and SARS-CoV-2, the virus that causes COVID-19, remain infectious longer and replicate faster in colder temperatures and at lower humidity levels. This, coupled with the fact that people spend more time indoors and in close contact with others during cold weather, are common reasons that germs are more likely to spread.

The flu and respiratory syncytial virus, or RSV, tend to have a defined fall and winter seasonality. However, because of the emergence of new COVID-19 variants and immunity from previous infections and vaccinations decreasing over time, COVID-19 is not the typical cold-weather respiratory virus. As a case in point, COVID-19 infection rates have surged every summer since 2020.

Virus transmission is easier when it’s cold

More specifically, cold weather can change the outer membrane of the influenza virus, making it more solid and rubbery. Scientists believe that the rubbery coating makes person-to-person transmission of the virus easier.

It’s not just cold winter air that causes a problem. Air that is dry in addition to cold has been linked to flu outbreaks. That’s because dry winter air further helps the influenza virus to remain infectious longer. Dry air, which is common in the winter, causes the water found in respiratory droplets to evaporate more quickly. This results in smaller particles, which are capable of lasting longer and traveling farther after you cough or sneeze.

How your immune system responds during cold weather also matters a great deal. Inhaling cold air may adversely affect the immune response in your respiratory tract, which makes it easier for viruses to take hold. That’s why wearing a scarf over your nose and mouth may help prevent a cold because it warms the air that you inhale.

Also, most people get less sunlight in the winter. That is a problem because the sun is a major source of vitamin D, which is essential for immune system health. Physical activity, another factor, also tends to drop during the winter. People are three times more likely to delay exercise in snowy or icy conditions.

Instead, people spend more time indoors. That usually means more close contact with others, which leads to disease spread. Respiratory viruses generally spread within a 6-foot radius of an infected person.

In addition, cold temperatures and low humidity dry out your eyes and the mucous membranes in your nose and throat. Because viruses that cause colds, flu and COVID-19 are typically inhaled, the virus can attach more easily to these impaired, dried-out passages.

What you can do

The bottom line is that being wet and cold doesn’t make you sick. That being said, there are strategies to help prevent illness all year long:

• Wash your hands often.

• Avoid touching your face, something people do between nine and 23 times an hour.

• Stay hydrated. Eight glasses a day of water is a good goal, but that could be more or less depending on lifestyle and the size of the person.

• Eat a well-balanced diet. Dark green, leafy vegetables are rich in immune system-supporting vitamins, while eggs, fortified milk, salmon and tuna have vitamin D.

• Stay physically active, even during the winter.

• Get adequate sleep.

• Clean hard, high-touch surfaces in your home often.

• If your nose or throat gets dry in the winter, consider using a humidifier.

• Get your annual flu and COVID-19 vaccine.

Following these tips can ensure you have a healthy winter season.

This is an updated version of an article originally published on Dec. 15, 2020.

Libby Richards, Professor of Nursing, Purdue University

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.