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  • Targeting the adrenomedullin pathway may be a potential therapy for liver failure

    Targeting the adrenomedullin pathway may be a potential therapy for liver failure

    Background and aims

    Liver failure syndromes are characterized by a dysregulated immune response leading to immune paralysis. Adrenomedullin (ADM) is a potent vasodilator and immunoregulator. This study aimed to explore the role of ADM in liver failure, hypothesizing that there is a detrimental imbalance between ADM and adrenomedullin binding protein (AMBP)1 that promotes a switch of monocytes/macrophages towards a pro-restorative phenotype and function.

    Methods

    Consecutive patients with acute liver failure (ALF), acute-on-chronic liver failure (ACLF), and decompensated cirrhosis, as well as healthy controls (HC) were included between April 2020 and June 2024. Peripheral blood mononuclear cells/monocytes were isolated and used for RNA sequencing and cell culture. ADM and AMBP1 were measured by enzyme-linked immunosorbent assay.

    Results

    Fifty-four patients with ALF, 25 with ACLF, 9 with decompensated cirrhosis, and 16 with HC were included. ADM expression in isolated monocytes was increased in ALF (log fold change = 5.88, p = 0.000216413) and ACLF (log fold change = 4.62, p = 0.00057122) compared to HC. Plasma ADM concentration was higher in ALF (1,684 ± 1,156 pg/mL) vs ACLF (836.1 ± 765.2 pg/mL) and HC (164.8 ± 62.73 pg/mL). AMBP1 was significantly reduced in ALF (59.27 ± 44 µg/mL) vs ACLF (126.3 ± 72.23 µg/mL) and HC (252.8 ± 159.7 µg/mL) (p < 0.0001, ALF vs HC). Treatment with LPS increased ADM concentration in peripheral blood mononuclear cell supernatant (ALF n = 6; 561.4 ± 1,038 pg/mL vs 259.2 ± 213.7 pg/mL, ACLF n = 4; 3,202 ± 491.2 vs 1,757 ± 1,689 pg/mL). The percentage of CD14+ cells expressing Mer tyrosine kinase was reduced after culture with LPS (2.077 ± 0.87%); however, co-culture with ADM 100 nM restored the phenotype (3.852 ± 1.063%).

    Conclusions

    ADM is increased in acute liver failure syndromes (ALF and ACLF), and AMBP1 is, on the contrary, reduced, mirroring the severity of the disease expressed by the SOFA score. ADM affects monocyte function, increasing MerTK after LPS stimulation and promoting a pro-restorative, anti-inflammatory phenotype. Further studies are needed to fully understand how to modulate this pathway as a possible therapeutic target and restore monocyte function.

    Source:

    Journal reference:

    Trovato, F. M., et al. (2025). Adrenomedullin as an Immunomodulator of CD14+MerTK+ Circulating Monocytes in Liver Failure Syndromes. Journal of Clinical and Translational Hepatology. doi.org/10.14218/jcth.2025.00074.

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  • A new fossil plesiomorphic flat bug (Aradidae) suggests widespread flower visiting in Heteroptera during the Mesozoic

    A new fossil plesiomorphic flat bug (Aradidae) suggests widespread flower visiting in Heteroptera during the Mesozoic

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  • Swiatek downs Paolini to claim first Cincinnati Open title

    Swiatek downs Paolini to claim first Cincinnati Open title


    CINCINNATI:

    Iga Swiatek captured her first Cincinnati Open title on Monday by beating Jasmine Paolini 7-5 6-4, with the Pole third seed sending a powerful message ahead of the U.S. Open.

    The six-times Grand Slam winner did not drop a set on her way to the title and was clinical in the final, converting all six of her break points to clinch her 11th WTA 1000 crown and first since last year’s Italian Open.

    She is now the second all-time winner in the WTA 1000 format history, trailing only Serena Williams (23). “I want to thank my team. I don’t know why I won tournaments that were like the last ones in terms of where I thought I would be playing well,” Swiatek said.

    “Thank you for forcing me to become a better player and learning how to play on these faster surfaces. I’m shocked and super happy.”

    Paolini made the brighter start, surging to a 3-0 lead and pushing Swiatek to the brink of a double break. Yet the Pole responded with a five-game run and, after squandering her first chance to serve out the opening set, closed it on her second attempt.

    Swiatek carried her momentum into the second set, saving two break points at 4-3 before holding firm to move within one game of the title. She sealed victory at the first opportunity with a big serve, extending her perfect record against the Italian to 6–0.

    The win ensures Wimbledon champion Swiatek will climb back to world number two, securing the second seed for the final major of the year at Flushing Meadows, where singles action begins on Sunday.

    Swiatek is also set to team up with Norway’s Casper Ruud in the new U.S. Open mixed doubles event.

    Earlier in the day, Spain’s Carlos Alcaraz claimed the men’s title after top seed Jannik Sinner retired in the first set.

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  • Early puberty and childbirth tied to accelerated aging and higher disease risk

    Early puberty and childbirth tied to accelerated aging and higher disease risk

    Reproductive timing matters when it comes to aging and age-related disease. In a study now online at eLife¸ Buck researchers determine that girls who go through puberty (the onset of menstruation) before the age of 11 or women who give birth before the age of 21 have double the risk of developing type 2 diabetes, heart failure and obesity and quadruple the risk of developing severe metabolic disorders. The study also reveals that later puberty and childbirth are genetically associated with longer lifespan, lower frailty, slower epigenetic aging and reduced risk of age-related diseases, including type 2 diabetes and Alzheimer’s.

    Buck professor Pankaj Kapahi, PhD, senior author of the study says the public health implications of the research are significant. “Even though women are routinely asked about their menstrual and childbirth history when they receive medical care, this information has rarely factored into the care they receive outside of OB/GYN,” he says. “These risk factors, whether positive or negative, clearly have significant influence on a variety of age-related diseases and should be considered in the larger context of overall health.”

    The research was based on one of the most comprehensive analyses to date, using regression analysis on nearly 200,000 women in the UK Biobank to confirm genetic associations. “We identified 126 genetic markers that mediate the effects of early puberty and childbirth on aging,” said postdoctoral fellow Yifan Xiang, MD, who led the research. “Many of these markers are involved in well-known longevity pathways, such as IGF-1, growth hormone, AMPK and mTOR signaling, key regulators of metabolism and aging.” 

    Genetic associations for antagonistic pleiotropy in humans

    Evolution is based on natural selection acting on traits early in life to encourage reproduction and survival of the species. The antagonistic pleiotropy theory of aging suggests that traits beneficial in the young can have negative effects later in life.

    Our study provides some of the strongest human evidence for this theory. We show that genetic factors favoring early reproduction come with the significant cost later in life including accelerated aging and disease. It makes sense that the very factors that help enhance survival of the offspring may lead to detrimental consequences for the mother.”


    Pankaj Kapahi, PhD, senior author of the study

    The role of BMI in aging and disease risk

    Kapahi says the study highlights the role of Body Mass Index (BMI) as a critical mediator of this process, finding that early reproductive events contribute to a higher BMI, which in turn increases the risk of metabolic disease. “One can envisage that enhancing the ability to absorb nutrients would benefit the offspring but if nutrients are plentiful then it can enhance the risk of obesity and diabetes.” 

    Implications for public health and basic science

    Kapahi says understanding the long-term impact of reproductive timing allows for the development of personalized healthcare strategies that could help mitigate the risks associated with early puberty and early childbirth, adding that lifestyle modifications, metabolic screenings and tailored dietary recommendations could improve long-term health in women. He says taking reproductive timing into account is currently relevant based on research that shows the age at which girls in the US begin menstruating has dropped by about three months per decade since the 1970s. No specific causes for the phenomena have been identified, but research suggests obesity may play a role.

    While updated research guidelines call for the use of both sexes in preclinical research in mice, Kapahi says this current study still challenges traditional experimental design, noting that most disease models use virgin female mice, which may not accurately represent real-world aging patterns.

    “If evolution has shaped us to prioritize early reproduction at the cost of aging, how can we leverage this knowledge to extend healthspan in modern society? Kapahi asks. “While we cannot change our genetic inheritance, understanding these genetic tradeoffs empowers us to make informed choices about health, lifestyle and medical care.” The study also identifies several genetic pathways that can be manipulated to optimize health for mothers as well as her offspring Kapahi says.

    Source:

    Buck Institute for Research on Aging

    Journal reference:

    Xiang, Y., et al. (2025). Early menarche and childbirth accelerate aging-related outcomes and age-related diseases: Evidence for antagonistic pleiotropy in humans. eLife. doi.org/10.7554/elife.102447.4.

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  • US spy chief Gabbard says UK agreed to drop 'backdoor' mandate for Apple – Reuters

    1. US spy chief Gabbard says UK agreed to drop ‘backdoor’ mandate for Apple  Reuters
    2. UK has ‘agreed to drop’ demand for access to Apple user data, says US  Financial Times
    3. US spy chief Gabbard says UK agreed to drop ‘backdoor’ mandate for Apple  Free Malaysia Today
    4. Inside Apple’s legal black box  Financial Times

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  • Intel gets $2 billion lifeline in the form of SoftBank equity investment – Reuters

    1. Intel gets $2 billion lifeline in the form of SoftBank equity investment  Reuters
    2. Intel shares jump as Softbank to buy $2bn stake in chip giant  BBC
    3. SoftBank Group and Intel (INTC.O) Sign $2 Billion Investment Agreement  Bitget
    4. SoftBank to invest $2 billion in Intel to become a top-10 shareholder  Reuters
    5. Intel Secures $2B Investment from SoftBank to Accelerate AI and Technology Leadership  The Fast Mode

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  • Intel’s stock rallies after $2 billion investment by Japan’s SoftBank

    Intel’s stock rallies after $2 billion investment by Japan’s SoftBank

    By Mike Murphy

    Intel headquarters in Santa Clara, Calif.

    Intel Corp. shares jumped in after-hours trading Monday after the chipmaker announced a $2 billion investment by Japan’s SoftBank Group Corp.

    Earlier in the day, Bloomberg News had reported the Trump administration was in talks to take a 10% stake in Intel, essentially equal to the amount of funding the company received from the Chips and Science Act under the Biden administration. That sent the stock down 3.7% in regular trading.

    But shares turned around in the extended session after the SoftBank announcement, rallying 5.4%.

    In a statement late Monday, Intel (INTC) said the deal with SoftBank (JP:9984) comes as both companies “deepen their commitment to investing in advanced technology and semiconductor innovation” in the U.S.

    “Semiconductors are the foundation of every industry,” SoftBank Chief Executive and Chairman Masayoshi Son said in a statement. “For more than 50 years, Intel has been a trusted leader in innovation. This strategic investment reflects our belief that advanced semiconductor manufacturing and supply will further expand in the United States, with Intel playing a critical role.”

    SoftBank shares fell 1.8% in Tokyo trading.

    Intel has been undergoing a painful restructuring as it tries to catch up in the AI chip game, after being surpassed by rivals such Taiwan Semiconductor Manufacturing Corp. (TSM). Intel reported another quarterly loss last month, and President Donald Trump recently called for CEO Lip-Bu Tan’s resignation, though Trump toned down his rhetoric following a meeting with Tan last week.

    Read more: Trump’s clash with Intel’s CEO isn’t just politics – it’s a crucial test for U.S. chip making

    In a statement Monday, Tan said he was “pleased” with SoftBank’s investment, “and I appreciate the confidence [Son] has placed in Intel.”

    SoftBank will pay $23 per share of Intel common stock.

    Intel shares closed Monday at $23.66 a share, and are up about 18% year to date, compared to the S&P 500’s SPX nearly 10% gain.

    Also read: Opinion: Intel has 18 months to determine its future – or Qualcomm and Arm will

    -Mike Murphy

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  • Nepal eliminates rubella, highly contagious viral disease: WHO

    Nepal eliminates rubella, highly contagious viral disease: WHO