super El Niño, is creeping up the Pacific coast of Central and North America and will soon reach California's shores, where it could raise sea levels by up to 1 foot (30 centimeters) for months, researchers warn.

Kelvin waves are a well-known, planetary-scale ocean phenomenon, but this particular forecast has experts worried because it will likely amplify the damage from severe storms, storm surges, flooding and coastal erosion that the record-shattering El Niño is expected to bring this winter.

In general, a Kelvin wave is a swell wave that spans thousands of miles and balances Earth's rotation, David Webb, a physical oceanographer at the National Oceanography Centre in the U.K., told Live Science in an email. But the waves generated during El Niño years are not normal Kelvin waves, because they cause oscillations of a boundary within the ocean as well as a height increase at the surface. In particular, these waves trigger the border between warmer, less-dense surface water and colder, denser bottom layers to move up and down within about 330 feet (100 m). For this reason, these El Niño-driven waves are called internal Kelvin waves.

Internal Kelvin waves are triggered by changes in surface winds around the equator in the far-western Pacific Ocean. Specifically, westerly wind bursts weaken the background trade winds that blow from South America toward Asia, thereby allowing warm water and elevated sea states that occur in the far-western Pacific to slowly "slosh" eastward.

In this case, "the generation process will have involved changes in the winds at different locations and at different times, so it may not be a particularly clean single wave — possibly a bit messy," Webb said.

Once an internal Kelvin wave kicks off, researchers can track its advance along the equator and predict when it will hit the South American coastline. The wave can't go farther east than that, so it spreads into two branches — known as coastal trapped waves — that continue north and south for thousands of miles at a speed of around 6 mph (10 km/h). This means California is not uniquely exposed to the current wave; all of the countries and regions that border the eastern Pacific Ocean are vulnerable, Webb said.

In California and elsewhere, the influence of the internal Kelvin wave will be in addition to the tides, regardless of whether El Niño sparks storm activity there. "What is most likely to be seen is a period, or maybe a few weeks, when the normal [pattern] of tides and tidal currents is distorted, with both high and low tides being higher than normal," Webb said, adding that tides could rise by "tens of centimeters," or about a foot.

The problem is that higher tides magnify the impacts of storms, which are more likely in some parts of the U.S. during an El Niño, Kate Huckelbridge, executive director of the California Coastal Commission, wrote in a Sept. 11 memo. The memo was sent to warn coastal California homeowners and residents to prepare for extreme conditions, such as flooding.

"A key observation from past El Niño events is that the most damaging storms are often those that coincide with the highest tides," Huckelbridge wrote. "Storms that peak during high tides are far more likely to cause damage than if the same storm peaked during low tide."

Storms alone can raise coastal sea levels by more than 3 feet (1 m), Webb noted, and sea levels have already increased by at least 8 inches (20 cm) due to climate change. Last week, California Gov. Gavin Newsom declared a state of emergency in response to experts' weather predictions so the state could mobilize equipment and resources before storms strike, The Guardian reported Monday (Sept. 28).

Several internal Kelvin waves can occur within a single El Niño event, with the largest waves typically recorded in the winter. However, Webb said he doubts there will be more than one full wave this time.

'> Powerful 'Kelvin wave' triggered by super El Niño threatens to raise sea levels off the California coast for months

Astronomers have discovered a few exoplanets with retrograde orbits before; these orbits often happen when the gravitational attraction of other massive objects in their star systems scrambles the planets' orbits. However, this newly discovered planetary system doesn't seem to have any massive objects that could have changed the retrograde planet's orbit, researchers reported in a study published Sept. 21 in the journal Astronomy and Astrophysics.

"We looked for the kind of massive companion that could have forced the planet into such an extreme orbit," study co-author Yann Carteret, an astronomer at the University of Geneva, said in a statement. "We may need to think differently about how this system acquired its unusual architecture."

A planetary mystery

For their new study, the researchers analyzed 23 hours of observations from two exoplanet-hunting instruments installed on a 12-foot-wide (3.6 meters) telescope at La Silla Observatory in Chile. They saw the retrograde planet cross in front of its star 10 times. Each time it passed in front of the star, the starlight reaching Earth dimmed a little. Measuring the extent and duration of that dimming revealed the planet's size and information about its orbit.

What made this detection particularly difficult was the type of star: an M dwarf. These stars are small, relatively cool and so dim that even the closest M dwarf stars to Earth can't be seen with the naked eye. About three-quarters of the stars in the Milky Way are M dwarfs, so studying them is particularly important for understanding our galaxy's exoplanets.

The star system in question is made of two, or possibly three, planets smaller than Neptune, each of which takes less than 16 days to orbit the star. GJ 3090 b is the innermost planet, completing an orbit about once every 2.9 days. Its orbit is one of the most misaligned ones scientists have detected so far, at a whopping 136 degrees out of alignment with the star's spin, making the planet nearly upside down ‪—‬ similar to Venus in our solar system.

Because GJ 3090 b is the planet closest to the star, it's unlikely that its orbit was disturbed by a massive planet or a hidden binary star; the other planets in the system are not upside down. And because they're farther from the star, a large gravitational disruption would probably affect them more, not less.

Instead, the researchers suggested that the unusual planet may have simply been born upside down. If a lot of gas and dust from outside the star system got sucked into the system, it might have replaced the protoplanetary disk with a second, newer disk at a different angle to the original, which could have formed the retrograde planet. The amount of material making up the inner planets (formed from the dusty, gaseous disk) is less than the amount that would pull on the star's spin enough to make the star change its rotational direction, keeping the system in a balanced misalignment, the researchers explained.

"The idea that a planetary system could be rebuilt from a second, differently oriented disk is particularly exciting," Vincent Bourrier, an astronomer at the University of Geneva and co-author of the study, said in the statement. "It suggests that the environment around a young star can play a much bigger role in determining the architecture of its planets than we might have expected."

'> Astronomers discover 'backward' planet orbiting its star in the wrong direction

The findings, published Sept. 18 in the journal Science Advances, point to potential pathways for managing chronic diseases, such as diabetes, heart disease and cancer, the scientists say.

The team of researchers analyzed data from the Chinese Immune Multi-omics Atlas (CIMA), which includes data from 400 adults who gave blood samples and answered an in-depth questionnaire about their lifestyles.

To capture the biggest possible effects of exercise, the team included only data from participants who did the most or least exercise. One group worked out at least three times a week, racking up more than 150 minutes of moderate exercise or 75 minutes of high-intensity exercise in that timeframe. The sedentary group said they did not work out at all.

The researchers then analyzed their volunteers' blood samples for physiological markers, such as blood sugar and fat levels. They found that the participants who exercised more had signs of boosted sugar and fat metabolism, stronger muscle metabolism, and higher levels of antioxidant molecules, which combat cell-damaging processes.

Many of these systems and their links to exercise were already known, said Dr. Michael Siebers, a researcher at the University of Duisburg-Essen who wasn't involved with the study. The study's real step forward was its subsequent cellular analysis, he said.

"It's a really good paper, which is showing, for the first time, what is really happening when you're doing sports on the intercellular level," he said.

How exercise changes the immune system

This analysis used a multiomics approach, meaning it combined data from multiple biological sources. These included metabolites (the byproducts of metabolism), fats, proteins and RNA (a cousin of DNA that helps build proteins).

The team also studied a feature of DNA called chromatin accessibility. Our genes are wound onto DNA helices, creating structures that resemble tightly packaged spools of film. Higher chromatin accessibility means that the spool is less tightly wound, so the individual images on that film can be seen more easily. Ultimately, those genes are more easily switched on. In cells, this mechanism is essential for enabling genes to be transcribed and translated into the proteins that help the body function properly.

Together, these analyses enabled the research team to closely examine how cells in people who exercise regularly functioned differently from people with sedentary lifestyles. This deep dive showed multiple changes in immune cells.

The activity of exercisers' immune foot soldiers — including cytotoxic T cells and natural killer cells — was boosted compared with those of participants with sedentary lifestyles. Additionally, naive immune cells, which act as nonspecialized reservists that can be recruited to the immune infantry, had greater chromatin accessibility in genes needed to fight off threats. That meant they were more ready to enlist.

The team also noted changes in cells that are in charge of alerting the rest of the immune system to threats, called immune monocytes and B cells. In people who regularly exercised, these cells had increased expression of alarm-sounding genes.

The findings suggest that regular physical activity may make the immune system better prepared to fight potential threats, the researchers wrote in their study. It's already known that not exercising is a risk factor for chronic health conditions, including type 2 diabetes, and that working out reduces these risks. The study gives "a molecular perspective on [exercise's] systemic health benefits," the researchers wrote.

That said, there were limitations to the study. Siebers pointed out that, beyond the number of minutes participants worked out, the study didn't record what type of exercise they did and had little information about the participants' physical makeup.

The researchers also couldn't show that the regular exercise caused the immune improvements. It's possible that the reduced activation in sedentary participants' immune systems made them less able to exercise.

Despite the limitations, these types of deep dives into the cellular basis of exercise are important for furthering our understanding of why working out feels good, Siebers said. "This is really deep stuff."

This article is for informational purposes only and is not meant to offer medical advice.

'> Regular exercise reshapes the immune system at a cellular level, study suggests

Over time, increased rigidity in her right leg began affecting her balance and caused frequent falls. Doctors prescribed her ibuprofen and physical therapy, but the stiffness and pain continued.

During the patient's first hospital visit, blood tests had revealed that her white blood cell count was normal, suggesting that she was not fighting an infection. She was not producing antibodies that might have suggested she had rheumatoid arthritis, an autoimmune disease that causes joint stiffness. Nor did she have antibodies associated with other several conditions that can cause pain, numbness or stiffness in the extremities, such as HIV, Lyme disease or the autoimmune condition Sjögren's disease.

Nevertheless, over the next month, her symptoms steadily worsened until she couldn't get out of bed; she was also unable to sit up or turn to either side.

At her second hospital visit, the patient's arm had normal movement during an exam, but her leg stiffness prevented doctors from testing the range of motion in her lower extremities. When the doctors tried to flex the woman's knee, it caused contraction in her quadriceps — the large muscle in the front of the thigh — and "was painful for the patient," the doctors wrote in a report of the case.

The diagnosis: Based on her earlier test results and her past and current symptoms, the doctors suspected that the woman had developed an extremely rare autoimmune neurological disorder: stiff person syndrome (SPS).

Autoimmune disorders are characterized by the immune system attacking healthy tissues in the body. In the case of SPS, this rogue immune response targets nerve cells that control muscle contraction. Destruction of these cells disrupts signals to the muscles, causing painful muscle spasms and contractions that affect a person's balance and restrict their movement.

A clue from the woman's blood tests hinted at this condition. Doctors found high levels of antibodies that block the enzyme glutamic acid decarboxylase (GAD). Elevated levels of these antibodies are seen in up to 80% of people with SPS. The anti-GAD antibodies prevent the enzyme from producing a chemical messenger called GABA, which acts like a brake on nerve cell activity. Without enough GABA, the nerve cells that control how muscles move can go into overdrive, which can cause spasms and prevent muscles from relaxing as they normally would.

The treatment: There is no cure for SPS, but medication can help slow the disease's progression and manage symptoms. This patient received intravenous immune globulin, an antibody treatment that regulates the immune system and is often used to treat autoimmune disorders. She also received rituximab, another type of antibody that targets specific immune cells to pare down their activity.

In addition, her doctors prescribed the steroid prednisone, the anticonvulsant gabapentin and the sedative diazepam, along with a regimen of physical therapy to help relax the woman's spasming muscles.

Within a few days, the woman's condition had significantly improved. "Prior to discharge, the patient could turn in her bed unassisted, could flex her left hip and knee fully, could flex [her] right hip fully and right knee with assistance to 110 degrees, and could stand with assistance," the report authors noted.

At a three-month checkup after being discharged, the patient could stand unassisted and walk using a rolling walker. The doctors started reducing her steroid dose, but she continued taking diazepam and gabapentin as prescribed, along with a monthly dose of immune globulin and a maintenance dose of rituximab every six months.

What makes the case unique: Just 1 to 2 in 1 million people are thought to be affected by SPS each year, although by some recent estimates, that number is higher. Its rarity and the slow development of symptoms make the condition challenging for health professionals to recognize and treat. What's more, the mechanisms and progression of the disease are "incompletely understood," the case report authors noted.

Often, SPS is misidentified as other conditions, including psychiatric disorders, Parkinson's disease, multiple sclerosis, or a neurological disorder called dystonia, which causes muscle spasms.

On average, the diagnosis of SPS takes about seven years from the start of symptoms, according to the Stiff Person Syndrome Research Foundation. It is most commonly diagnosed in people ages 40 to 50, but SPS can also appear in older adults and in children. It affects about twice as many women as it does men, according to the National Institute of Neurological Disorders and Stroke.

One well-known person with SPS is singer Celine Dion. She publicly shared her diagnosis in 2022, after her illness led her to cancel multiple shows in 2021. Dion told People magazine that she was experiencing "severe and persistent muscle spasms" and that the pain caused by her condition eventually became so intense that she was sometimes unable to walk.

This article is for informational purposes only and is not meant to offer medical advice.

Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!

'> Woman's 5-year struggle with balance and walking was caused by a 'one-in-a-million' disorder Saturn therefore rises in the east around sunset, 100% illuminated, before reaching its highest point around midnight and finally sinking toward the western horizon around sunrise.

This year's opposition occurs Sunday (Oct. 4), making the few weeks on each side an excellent time to start looking. At 784 million miles (1.26 billion kilometers) away, Saturn will be relatively close to Earth, causing its disk to appear about as large as it gets through a telescope and making its pale-yellow light shine more brightly than at other times of the year. You won't need any equipment to find it; under a clear sky, Saturn will be easily visible to the naked eye as a bright, steady point of light, between the constellations Pisces and Cetus.

Once you've located Saturn, the best way to view it is in a backyard telescope so you can see the planet's rings in sharp relief. Try it yourself — observing Saturn's rings for the first time is one of the most memorable sights available to amateur astronomers. Larger apertures and higher magnifications may also reveal some of Saturn's moons, including Titan, the planet's largest satellite, but even a relatively modest backyard telescope can reveal Saturn's rings.

The rings themselves are particularly interesting this year. Saturn's axial tilt means our viewing angle of the planet's rings changes throughout its roughly 29-year journey around the sun. After the rings appeared almost edge-on from Earth in 2025, they're gradually opening up again, giving observers an increasingly clear view.

You don't need to restrict your observing to the night of opposition; Saturn will remain a prominent evening target throughout October. However, the nights of Sept. 30 to Oct. 4 offer an ideal combination of brightness, visibility and all-night observing. There are also plenty of other great stargazing sights to look for this fall.

If you've been waiting for an excuse to point a telescope at Saturn, this is your moment. The next time Saturn will be at opposition will be Oct. 18, 2027.

'> Now is the best time to see Saturn all year — yes, even with the naked eye