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SpinLaunch wants to send 250 broadband 'microsatellites' to orbit with a single launch

SpinLaunch wants to send 250 broadband 'microsatellites' to orbit with a single launch

Yahoo04-04-2025

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SpinLaunch has unveiled its plans for a new broadband satellite constellation known as Meridian Space.
The Meridian Space constellation will consist of small "microsatellites" that can be sent to low-Earth orbit with as many as 250 spacecraft on a single launch vehicle, according to SpinLaunch. The company received $12M in funding from Kongsberg NanoAvionics to help develop and commercialize the satellites, with a planned launch date of 2026 for its first on-orbit demonstrator.
It's unclear if SpinLaunch will be launching the demonstrator itself with its revolutionary rocket-flinging centrifuge or if it will hitch a ride on another rocket.
The Meridian Space constellation will provide "significantly higher broadband capacity in a satellite constellation compared with what is available on the market today," said Eirik Lie, president of Kongsberg Defense & Aerospace, in a statement.
David Wrenn, CEO of SpinLaunch, added that NanoAvionics' small, modular satellite platforms offer "a reliable foundation to scale our constellation quickly and confidently."
Along with the statement announcing the partnership, SpinLaunch shared an image of a stack of Meridian Space satellites atop a launch vehicle. The flat satellites appear to stack on top of on another, hinting at how the company plans to fit 250 of the spacecraft on a single rocket.
If SpinLaunch can successfully loft 250 satellites at once, it would set a new record for spacecraft launched by a single flight. That record currently stands at 143, set by SpaceX's Transporter-1 mission in 2021.
SpinLaunch aims to disrupt the launch services market with its wild new concept for reaching orbit. The company is developing a 108-foot-long (33-meter) spinning arm that accelerates launch vehicles to high speeds inside a centrifuge before flinging them into the sky.
Once at altitude, the flung rockets then ignite their engines. The concept greatly reduces the amount of fuel and hardware needed to reach orbit.
NASA signed an agreement with the company in 2022 for a technology demonstration that saw third-party experiments from the agency, Airbus and Cornell University lofted to suborbital space with the centrifuge.

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Regeneron, Sanofi Stock Falls After Uneven Smoker's Lung Drug Data
Regeneron, Sanofi Stock Falls After Uneven Smoker's Lung Drug Data

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Regeneron, Sanofi Stock Falls After Uneven Smoker's Lung Drug Data

Regeneron Pharmaceuticals, Inc. (NASDAQ:REGN) and Sanofi SA (NASDAQ:SNY) on Friday announced results from two Phase 3 trials of itepekimab in chronic obstructive pulmonary disease (COPD) patients. Phase 3 AERIFY-1 trial evaluating itepekimab in adults who were former smokers with inadequately controlled COPD met the primary endpoint of significantly reducing moderate or severe acute exacerbations by 27% compared to placebo at week 52, a clinically meaningful benefit. A second Phase 3 trial, AERIFY-2, did not meet the same primary endpoint. Despite showing some benefit earlier in the trial (at week 24), itepekimab did not achieve a statistically significant reduction in moderate or severe exacerbations at week 52 in the second the trials, patients were randomized to receive itepekimab every two weeks (AERIFY-1: n=375; AERIFY-2: n=326), every four weeks (AERIFY-1: n=377; AERIFY-2: n=303), or placebo (AERIFY-1: n=375; AERIFY-2: n=324), which was added to inhaled triple or double standard-of-care therapy. The primary endpoint for AERIFY-1 and AERIFY-2 was the reduction in the annualized rate of acute moderate or severe COPD exacerbations with itepekimab treatment. The total number of exacerbations was lower than prospectively anticipated, decreasing the power of both trials. Enrollment largely occurred during the global COVID-19 pandemic, which could have contributed to the lower overall exacerbation rates. The safety profile of itepekimab was consistent across dosing regimens, and adverse events (AEs) were generally comparable between treatment and placebo groups. Regeneron and Sanofi will review the data and discuss it with regulatory authorities to evaluate the next steps. Itepekimab is also being evaluated in other respiratory conditions, including chronic rhinosinusitis without nasal polyps, chronic rhinosinusitis with nasal polyps, and non-cystic fibrosis bronchiectasis. In November 2024, Regeneron and Sanofi's Dupixent gained FDA approval for COPD, marking its sixth U.S. indication since its first use for atopic dermatitis seven years ago. This expansion positions Dupixent as the first targeted therapy for COPD, a significant leap in treating this progressive lung condition that impedes breathing due to obstructed airflow. Last Thursday, the U.S. Food and Drug Administration (FDA) approved GSK Plc's (NYSE:GSK) Nucala (mepolizumab) as an add-on maintenance treatment for adult patients with inadequately controlled COPD and an eosinophilic phenotype. Last June, the FDA approved Verona Pharma plc's (NASDAQ:VRNA) Ohtuvayre (ensifentrine) for the maintenance treatment of chronic obstructive pulmonary disease (COPD) in adult patients. Ohtuvayre is the first inhaled product with a novel mechanism of action available for the maintenance treatment of COPD in more than 20 years. In May, Sanofi announced it will invest at least $20 billion in the U.S. through 2030. Research and development, plus U.S. manufacturing, will receive the bulk of the spending. The company also expects higher job creation within the communities where Sanofi and its partners are located, which will help enhance the U.S. supply chain. Earlier in May, Regeneron secured the winning bid in the bankruptcy auction for key assets of 23andMe Holding Co. in a $256 million deal to boost its genetics-based drug discovery efforts. Price Action: REGN stock is down 9.98% at $545, and SNY stock is down 4.57% at $49.96 during the premarket session at last check Friday. Read Next:Photo by Marianne Campolongo via Shutterstock Up Next: Transform your trading with Benzinga Edge's one-of-a-kind market trade ideas and tools. Click now to access unique insights that can set you ahead in today's competitive market. Get the latest stock analysis from Benzinga? REGENERON PHARMACEUTICALS (REGN): Free Stock Analysis Report SANOFI (SNY): Free Stock Analysis Report This article Regeneron, Sanofi Stock Falls After Uneven Smoker's Lung Drug Data originally appeared on © 2025 Benzinga does not provide investment advice. All rights reserved. Sign in to access your portfolio

Single gene may help explain the plague's persistence throughout human history
Single gene may help explain the plague's persistence throughout human history

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Single gene may help explain the plague's persistence throughout human history

When you buy through links on our articles, Future and its syndication partners may earn a commission. Scientists have discovered how adaptations in a single gene helped the plague survive for hundreds of years. Responsible for the deadliest pandemic in history, the bacterium that causes the plague, Yersinia pestis, has existed in varying strains from ancient times until today. Now, scientists have unearthed a genetic clue as to how the infamous disease has persisted for millennia, with devastating outbreaks smoldering across centuries. They published their findings Thursday (May 29) in the journal Science. "This is one of the first research studies to directly examine changes in an ancient pathogen, one we still see today, in an attempt to understand what drives the virulence [disease severity], persistence and/or eventual extinction of pandemics," study co-senior author Hendrik Poinar, director of the Ancient DNA Centre at McMaster University in Ontario, Canada, said in a statement. Y. pestis has been infecting humans since before recorded history began. The most common form of the disease is known as "bubonic" and most often enters the body through bites from infected fleas, although people can less commonly catch it directly from infected animals, including rats and cats. Once inside the body, the bacterium travels to the lymph nodes and replicates. As it multiplies, it triggers the formation of painful, pus-filled "buboes," for which the bubonic plague is named. The plague bacterium can also cause a blood infection, called septicemic plague, and lung infection called pneumonic plague. Related: Oregon's 1st bubonic plague case in 8 years tied to patient's pet cat The three major plague pandemics are among the deadliest outbreaks in human history. The first pandemic, the Justinian Plague (which occurred roughly between A.D. 542 and 750), slashed the population in parts of the Mediterranean to by an estimated 40% by the end of the sixth century. The second, and most infamous, outbreak of the disease was the 14th-century Black Death that ravaged Europe and the Middle East. The single deadliest pandemic in recorded history, the Black Death killed approximately 25 million people in Europe alone — between 33% and 50% of its population. A third, lesser-known global plague pandemic began in 1855 in China's Yunnan province and killed more than 12 million people in India and China alone. This pandemic was considered active until 1960, after which plague deaths dropped to lower levels. Plague epidemics continue to this day, with the Democratic Republic of the Congo, Madagascar and Peru being the most endemic countries, according to the World Health Organization. Besides the staggering death counts associated with the pathogen, what's perhaps most remarkable about Y. pestis is the longevity of its strains. Strains of the Justinian Plague bacterium took 300 years to go extinct after outbreaks were first recorded, and one of the two lineages from the Black Death re-emerged in waves for 500 years before its disappearance, while the other became the ancestor of all present-day strains. To investigate the genetic toolkit Y. pestis uses to persist for so long, researchers conducted an analysis of a plague gene known as pla across hundreds of samples collected from ancient and modern victims of the disease. The pla gene codes for an enzyme that helps Y. pestis move through the body undetected by the host's immune system. Previous studies have suggested that pla is a key factor that modulates both the lethality of a given plague strain and its ability to spark outbreaks in humans. However, one plague strain can carry a different number of pla genes than the next, and it wasn't clear how this copy number might impact their biology, the researchers noted. To investigate, they collected multiple modern strains of Y. pestis from Vietnam that had varying numbers of copies of pla inside their genomes; carrying more copies of the gene means that the bacteria can crank out more copies of the enzyme. After injecting these different plague strains into mice, they found that the strains with fewer copies of pla led to longer infections but reduced the disease's mortality rate by up to 20%. RELATED STORIES —Diagnostic dilemma: A scientist caught plague from bacteria thought to be 'noninfectious' —Could bacteria or viruses lurking in ancient Egyptian mummies unleash a plague today? —'Black death' survivors had plague-resistant genes that may boost their descendants' risk of autoimmune disease Across the ancient plague genomes they analyzed — 20 of which dated to the first plague pandemic and 94 of which were from the second — the researchers noted a pattern where the plague strains lost copies of pla over time, namely in later stages of each pandemic. Among the modern genomes, they found three strains that hint that the same pattern is unfolding today. They theorized this adaptation likely made infections less virulent, or harmful to the host's body, over time. This suggests that the evolutionary change helped the disease to keep its hosts — be they rat or human — alive for longer, thereby enabling it to spread more widely. This adaptation may have been especially necessary after populations of the plague's primary hosts, rats, were killed off en masse during outbreaks. "The reduction of pla may reflect the changing size and density of rodent and human populations," Poinar said. "It's important to remember that plague was an epidemic of [flea-ridden] rats, which were the drivers of epidemics and pandemics. Humans were accidental victims." The scientists say that further research into both ancient and contemporary plague strains could reveal more pla depletions and help them to better understand how such changes to the germ's genome have shaped its virulence through history. Nowadays, Y. pestis infections can be cured with antibiotics, though some strains have shown troubling signs of antibiotic resistance. To head off the threat of a superbug plague outbreak, scientists in the U.K. have already started developing a bubonic plague vaccine to add to stockpiles. This article is for informational purposes only and is not meant to offer medical advice.

Heat waves may accelerate the aging process
Heat waves may accelerate the aging process

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Heat waves may accelerate the aging process

When you buy through links on our articles, Future and its syndication partners may earn a commission. Every day, Kalpana Suryawanshi, 48, looks into the mirror and whispers, "I look older than my age." Eight years ago, she was diagnosed with Type 2 diabetes. Since then, her health has deteriorated, which she attributes to increased exposure to heat while working in the fields, planting crops, harvesting produce, and carrying heavy loads of cattle fodder. During this time, she frequently experienced dizziness and weakness as temperatures exceeded 40 degrees Celsius (104 F) in her village of Nandani in Maharashtra state, India. Heat is known to affect cognitive function, cardiovascular health, and kidney function, and a growing body of research suggests that exposure to rising temperatures also accelerates the body's aging process. A 2023 German study published in Environment International was the first to find that higher air temperatures are associated with faster aging at the cellular level. It found that prolonged exposure to elevated temperatures can make the body age faster than its chronological age, a phenomenon known as epigenetic age acceleration. Scientists measure this process using epigenetic clocks, which analyze chemical markers called DNA methylation that turn genes on and off. The study found that in areas where the average annual temperature is 1°C higher, people tend to show signs of accelerated aging at the cellular level. When scientists talk about epigenetic age, they measure how old a body is at the cellular level, which can differ from the actual age in years. This is based on changes to DNA called epigenetic markers, the chemical tags that turn genes on or off. Environment, lifestyle, and stress influence these markers. As one ages, the pattern of these chemical tags changes, and scientists use this information to create an epigenetic clock, a tool that estimates biological age. The genes affected by these changes control many vital functions, like repairing cells and tissues and protecting against toxins. When the wrong genes are switched on or off, it can make it harder for the body to repair itself, fight disease, or recover from stress. Over time, these hidden changes can lead to outward signs of aging, such as weaker bones or slower healing. Epigenetic age gives a glimpse into how well the body is holding up on the inside. 2024 was the hottest year on record, with 6.8 billion people worldwide experiencing extreme heat for at least 31 days. One unusual effect of this rising heat is observed firsthand by India's community health care workers, who report that more people appear older than their actual age. Scientists are now also finding the biological mechanisms that contribute to premature aging. Wenli Ni, a postdoctoral research fellow at Harvard T.H. Chan School of Public Health and the lead author of the German study, said heat exposure can induce alterations in DNA methylation, which is a biological process that can influence gene expression and cellular function. She explained that this mechanism can trigger harmful biological processes and accelerate aging. "Heat exposure may also lead to oxidative stress, resulting in DNA damage that could alter DNA methylation patterns and impact aging," she added. Oxidative damage occurs when unstable molecules called free radicals attack cells. They can harm DNA, cell membranes, and proteins, contributing to aging, cancer, and cardiovascular health issues. These results were repeated in Taiwan, where scientists examined over 2,000 people and found high ambient temperature and heat index exposure were linked to increased aging, with stronger associations in prolonged exposure. The study revealed that a 1°C increase in the 180-day average temperature was linked to a rise of 0.04 to 0.08 years in biological age acceleration, as measured by three different epigenetic aging clocks that estimate biological age. Related: Human aging accelerates dramatically at age 44 and 60 While this increase in age acceleration might seem small at first, it's important to consider how these effects can build up over time. Even slight increases in biological aging, when sustained year after year, can add up to several years of accelerated aging. This can mean an earlier occurrence of age-related illnesses. Moreover, when these small shifts affect large populations, they can contribute to a tremendous rise in disease burden and health care costs. A recent study published in Science Advances examined the relationship between heat and aging in more than 3,500 adults aged 56 and above in the U.S. The study found that long-term heat exposure, lasting from one to six years, was associated with epigenetic aging. Persistent exposure to high temperatures can result in frequent sleep disturbances, raising stress and anxiety levels. Over time, this physiological degradation accumulates and may accelerate health decline with age. The German study found that women and individuals with obesity or Type 2 diabetes exhibited stronger associations between air temperature and aging. Women generally sweat less and have different body responses to heat, which can make it harder for them to cool down and sometimes cause their body temperature to rise faster, Ni explained. She also said that studies suggest women have a higher threshold for activating the sweating mechanism at high temperatures, indicating their bodies take longer to start sweating. Diabetes also makes people more susceptible to high temperatures. People with diabetes often have reduced blood flow to their skin, which can interfere with the body's ability to release heat and stay cool in hot weather. Additionally, body fat can act as insulation, making it harder for heat to move from the body's core to the skin, reducing its ability to release heat and stay cool. Epigenetic age acceleration can contribute to cardiovascular diseases, cancer, diabetes, and mortality, putting more pressure on public health care systems. In 2016, Rajma Jamadar, now 47 years old, from Maharashtra's Haroli village, woke up in the middle of the night with irregular heartbeats. The next day, the doctor said that her blood pressure spiked and prescribed lifelong medication. Within months, her symptoms worsened as her cardiovascular health declined. "Upon further diagnosis, the doctor then told me my heart isn't pumping blood efficiently," she said. She prepares meals for 175 children at a public school in her village, but rising temperatures make her job increasingly difficult as the heat from cooking takes a toll on her. "Every day, I feel sick," she said. Remarkably, climate change may sometimes accelerate epigenetic aging in children even before birth. A study published last year in Nature examined 104 drought-exposed children and 109 same-sex sibling controls in northern Kenya. It found a positive association between in-utero drought exposure and aging, emphasizing that the stressors from drought may decrease overall life expectancy. According to study author Bilinda Straight, changes can happen through three key pathways in the body. The first is the immune system, the body's first line of defense that protects one from infections and diseases. The second involves metabolic processes that provide the body with energy. The third is responsible for maintaining and repairing cells in response to stress. "Whether the threat we face is physical or emotional, we still perceive it as a danger to our homeostasis, a health-preserving balance between all our physiological systems," she explained. This suggests that the emotional stress experienced by the women in the study, along with caloric restriction and dehydration, activated systems that help the body manage stress but can harm health if overactivated for extended periods. Women in the study were seen to be engaged in outdoor labor while they were also experiencing hunger and dehydration. "Those physiological stressors were accompanied by worry about the next meal, for themselves, their children, and loved ones," she added. Moreover, social factors like gender inequality exposed women to coercion, overwork, and violence. While farmers risk loss from drought, those in livestock agriculture suffer the emotional and financial toll of watching their animals die. Combined with heat stress, dehydration, and hunger, this creates immense hardship. Eventually, this maternal stress during pregnancy contributes to changes in DNA methylation in their children, Straight said. RELATED STORIES —Biological aging may not be driven by what we thought —Climate change is spoiling food faster, making hundreds of millions of people sick around the world —Climate wars are approaching — and they will redefine global conflict She suggests adequate nutrition and close monitoring of children's cardiovascular and metabolic health. Researchers advocate for long-term studies to better understand the impacts of the environment on epigenetic age acceleration. "Slowing down epigenetic age acceleration is going to be tied to increasing food security and identifying alternatives to women engaging in high-risk occupational labor," she added. Effective policies are needed to achieve food and livelihood security while reducing social and economic inequalities. However, for many women, economic insecurity and the lack of social safety nets make it nearly impossible to prioritize health. Suryawanshi's struggle highlights this problem. So far, she has spent over 600,000 Indian rupees ($7,046) on medical treatment. "I can't afford any more expenses, so I've stopped taking some medicines," she said. She visited eight hospitals in two years to search for an effective treatment. "It's a miracle that I survived. Despite being only 48, I have no strength left, but I still have to work." This article was originally published by Yale Climate Connections.

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