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  • Managing Severe Asthma in the Real World

    Managing Severe Asthma in the Real World

    Nicola A. Hanania, MD, MS

    Credit: American Lung Association

    Over the past decade, the treatment paradigm for severe asthma has been reshaped by the approval of targeted biologics and a deeper understanding of inflammatory pathways driving disease. What began with agents like omalizumab has rapidly expanded with the approvals of mepolizumab, benralizumab, and dupilumab—and most recently, tezepelumab in 2021, which became the first biologic approved for severe asthma regardless of baseline eosinophil count. These therapies have set a new standard of care for type 2–high asthma and are prompting earlier identification of eligible patients, more nuanced treatment algorithms, and greater emphasis on biomarker-driven decisions.1 More recently, the 2024 approval of dupilumab for eosinophilic chronic obstructive pulmonary disease (COPD) has opened new doors for targeted therapy in a population that long lagged behind asthma in biologic innovation.2

    With each new approval, the expectations for disease control and long-term outcomes continue to evolve, ushering in a new era where earlier diagnosis, individualized therapy selection, and consistent biomarker assessment are becoming essential components of care. Clinicians are now tasked not just with managing symptoms, but with navigating a growing array of therapeutic options, understanding nuanced eligibility criteria, and integrating these treatments into increasingly complex clinical workflows. The potential for long-term steroid-sparing, exacerbation reduction, and quality-of-life improvements is greater than ever—but so too is the need for clear guidance on optimizing these innovations in practice.

    At a recent clinical forum convened by HCPLive in Houston, Texas, a group of pulmonologists, led by Nicola A. Hanania, MD, MS, Associate Professor of Medicine at Baylor College of Medicine Airways Clinical Research Center, gathered to examine how these developments are playing out in practice.

    Their discussion focused on the practicalities of initiating and sequencing biologics, the value and limitations of biomarkers like eosinophils and FeNO, and the need for more structured approaches to early referral and diagnosis. They discussed how the last 2 decades of asthma research have shifted clinical paradigms toward targeted, phenotype-driven biologic therapies.

    “The biggest thing that I think is missed in all these discussions are that the steroid inhalers are still the key and making sure they’re taking it correctly. And taking regularly Because the compliance on the steroid inhaler is still the biggest problem. They get better, they stop using it,” one panelist pointed out.

    Type 2 inflammation remains a central focus, with discussion on how eosinophils, FeNO, and IgE levels guide patient selection and biologic choice, although real-world use is hampered by access, education, and insurance hurdles. These barriers highlight how real-world implementation is now the critical frontier in maximizing biologic impact. They also emphasized the critical role of multidisciplinary collaboration in delivering personalized asthma care.

    “The big issue is, should we phenotype everybody with asthma? Probably not. But the ones that we see as specialists are the ones that are problematic. I think primary care, we are trying to build bridges with primary care for them at least to look at the blood eosinophils, to think about deferring patients with high risk of exacerbation,” Hanania said.

    Panel participants shared insights on challenges in diagnosis, treatment adherence, inhaler technique, and navigating insurance for biologics, underscoring the complexity of treating severe asthma in both public and private settings. They outlined how shared decision-making, comorbidity considerations, and patient convenience shape treatment plans.

    Looking at the long-term impact of biologics on the asthma field, they reiterated that real-world evidence supports sustained biologic efficacy, while questions do remain about tapering, biomarker monitoring, and the possibility of treatment discontinuation in clinical remission. The group also touched on emerging needs in COPD and non-type 2 asthma, as well as the potential for dual-target or multi-mechanism therapies in the future.

    “I think every single biologic out there has to be experimented with. I’d really love to see if we can expand the use of what’s out there that people can do and make it even a little more accessible for patients,” one panelist concluded.

    REFERENCES
    1. FDA Approves Tezspire™ (Tezepelumab-ekko) in the U.S. for Severe Asthma. News release. Amgen. December 17, 2021. https://www.amgen.com/newsroom/press-releases/2021/12/fda-approves-tezspire-tezepelumabekko-in-the-us-for-severe-asthma
    2. Dupixent® (dupilumab) Approved in the U.S. as the First-ever Biologic Medicine for Patients with COPD. Regeneron Pharmaceuticals, Inc. September 27, 2024. https://www.globenewswire.com/news-release/2024/09/27/2954552/0/en/Dupixent-dupilumab-Approved-in-the-U-S-as-the-First-ever-Biologic-Medicine-for-Patients-with-COPD.html.

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  • Michael C. Hall on Batista Confrontation

    Michael C. Hall on Batista Confrontation

    [This story contains major spoilers for the series premiere of Dexter: Resurrection.]

    Dexter Morgan died once before, born again as a lumberjack and eventually an upstate New York man about town. What’s one more resurrection between friends?

    After getting fatally shot in the heart in the 2022 finale of Dexter: New Blood, Michael C. Hall‘s outlandishly lucky serial killer-killing serial killer once again stalks the land, thanks to the latest entry in the franchise, Dexter: Resurrection.

    The series premiere (the first two episodes began streaming on Friday) reveals how Dexter survived a point-blank gunshot wound to the chest, leveled his way by son Harrison (Jack Alcott), thanks to the violence occurring in the midst of radically cold temperatures. Just a few degrees warmer and Dexter would be as dead as all the villains he’s killed in the past. Instead Resurrection finds him alive, if not exactly well, as he suffers through an existential end-of-life crisis littered with ghosts from his past only to come out the other side of it as a man on the run in New York City. (John Lithgow’s Trinity Killer, Jimmy Smits’ Miguel Prado, Erik King’s Sgt. Doakes make cameos; James Remar’s father Harry is also there, along with the graves of departed sister Debra, wife Rita and former colleague Maria LaGuerta.)

    Before hitting the road toward the Big Apple, however, Dexter faces down his even bigger past in the form of an old friend shaping up to be a new foe: Angel Batista, the fedora-hatted Miami cop played across the decades by David Zayas. After having returned to the franchise in New Blood, Angel reemerges here with newfound awareness about Dexter, all-but completely clued in on his old colleague’s status as the infamous Bay Harbor Butcher. Angel and Dexter’s wariness of one another comes to a head in the premiere during a scene in the hospital, when Angel lays his cards out on the table, without making a full on declaration of war. 

    “That scene is one of my favorite scenes I’ve ever gotten to play in the show,” Hall tells The Hollywood Reporter about the long-awaited showdown between Dexter and Angel. “It’s a scene you could only enjoy if you’ve been doing something for as long as we’ve been doing it. We have real memories between us [as actors].

    Hall found the scene to be a complicated one for Dexter, who is being confronted by the former Miami Metro Homicide chief he has long respected. “It’s really bittersweet for him to reconnect with someone who was once his friend and colleague, when it was a much simpler relationship,” says Hall. “It’s incredibly rich to face Batista with the knowledge of what Batista now has every reason to suspect, or even knows. It makes for some delicious dynamics. Ultimately, Dexter’s a self-preservationist, but he does have a genuine fondness for Angel, and Angel for him, in spite of everything.”

    Michael C. Hall as Dexter Morgan with David Zayas as Angel Batista in the premiere.

    Zach Dilgard/Paramount+

    For Zayas, the view of the scene is a bit different: “This is a different Angel, with all the information he has now, particularly Dexter just being alive. It’s a new case he has to deal with outside of his environment, in a new place, in New York, where he has no authority as a police officer. He’s having to deal with the cold coming from Miami. There’s so many little issues for him to navigate, while he’s trying to get some justice for all of what he’s missed over those many years.”

    Rather than face that justice, Dexter evades it, hitting the road for New York for one reason and one reason only: Harrison. Dexter finds out his son is still alive and not all that far away, living in Manhattan working at a hotel. What’s more, he’s killing at that hotel, and Dexter hears about it, leading him to charge into action to atone for his biggest sin of all: letting his son down.

    “Dexter’s invested in the fact of his humanity in a way that feels more substantial and committed than ever before,” says Hall, adding, “But there’s also a new set of characters Dexter interacts with that feels fantastical in a good way.”

    Those new characters are a who’s-who of serial killers, played by Uma Thurman, Peter Dinklage, Neil Patrick Harris, Krysten Ritter, Eric Stonestreet and David Dastmalchian.

    “The spectrum between those two things feels even broader and more vibrant. We’re proud of it,” says Hall of the show’s confrontation between Dexter’s humanity and serial killer identity. “The show belongs to us while we’re making it. We’re finished making it, and now it belongs to the fans. I’m excited to give it to them.”

    But is he excited to bring justice to Dexter’s doorstep? When the dust settles on Resurrection, it’s hard to imagine how both Dexter and Angel can walk away intact — or even alive, in Batista’s case. If it came down to ensuring Angel’s survival, is Hall open to the idea of finally putting Dexter behind bars?

    “It’s certainly within the realm of possibility,” he muses. “If he were to be apprehended, he would probably find himself in a prison population that was pretty ripe for his code. It’s a compelling idea.”

    ***

    Dexter: Resurrection’s first two episodes are now streaming on Paramount+ for Paramount+ with Showtime subscribers, before an on-air debut Sunday at 8:00 p.m. Remaining episodes drop weekly. 

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  • Omnicom – A Look Back at Cannes – Omnicom Group

    1. Omnicom – A Look Back at Cannes  Omnicom Group
    2. Cannes Leadership Conversations 2025: ‘The Next Billion’ Leadership Brunch  Little Black Book | LBBOnline
    3. How Brand Leaders Are Helping Shape the Future of Marketing, AI, and DOOH  Cynopsis
    4. Judging at Cannes Lions: Silly sells, challenging convention and more  Campaign Asia
    5. Insights from Cannes – How CMOs define the future of work and what’s to come  PharmaLive

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  • A mess of its own making: Google nerfs second Pixel phone battery this year

    A mess of its own making: Google nerfs second Pixel phone battery this year

    Not all batteries age the same way. Some problems will appear quickly, but others won’t be noticeable until after many charge/discharge cycles. A few years back, Samsung released the Galaxy Note 7 with a slightly larger battery than the previous model. Within weeks, the phones started to catch fire, and even after swapping in a different battery pack, the issue persisted. It was a huge mess that led to a recall and steep financial losses.

    Samsung’s battery missteps may have prompted manufacturers to take possible battery defects more seriously. So when Google detected problems with aging Pixel 4a batteries, it didn’t take any chances. It decided to degrade the experience on the remaining Pixel 4a units out there, even if the lower capacity and slower charging upset users. When Pixel 6a units started to catch fire again, Google decided to simply limit battery performance.

    The mandatory Android 16 July update will limit battery charging speed and capacity on affected phones.

    Credit:
    Ryan Whitwam

    The mandatory Android 16 July update will limit battery charging speed and capacity on affected phones.


    Credit:

    Ryan Whitwam

    Pixel 4a units contained one of two different batteries, and only the one manufactured by a company called Lishen was downgraded. For the Pixel 6a, Google has decreed that the battery limits will be imposed when the cells hit 400 charge cycles. Beyond that, the risk of fire becomes too great—there have been reports of Pixel 6a phones bursting into flames.

    Clearly, Google had to do something, but the remedies it settled on feel unnecessarily hostile to customers. It had a chance to do better the second time, but the solution for the Pixel 6a is more of the same.

    A problem of Google’s making

    Like other smartphone manufacturers, Google moved away from offering removable batteries in the 2010s to make phones slimmer and more durable. Smartphone makers largely dismissed the concerns of repair advocates who pointed out that lithium-ion batteries degrade over time, and making them difficult to remove wasn’t the best idea. However, this was a time when people only kept smartphones for a year or two before upgrading, but we have since entered an era in which people use phones for much longer. The way phones are marketed has changed to reflect that—Google has enacted longer support windows, topping out at seven years for its latest phones.

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  • Pakistan reaffirms regional engagement, condemns rights violations in IIOJK: FO Spox

    Pakistan reaffirms regional engagement, condemns rights violations in IIOJK: FO Spox

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    ISLAMABAD, Jul 11 (APP):Foreign Office Spokesperson Ambassador Shafqat Ali Khan Friday in his weekly media briefing shed light on Pakistan’s diplomatic engagements, regional security concerns, and reiterated its condemnation of human rights violations in Indian Illegally Occupied Jammu and Kashmir (IIOJK).

    The Spokesperson, highlighted the country’s active multilateral diplomacy, evolving bilateral relations, and firm positions on key foreign policy issues.

    He mentioned that the Deputy Prime Minister and Foreign Minister Senator Mohammad Ishaq Dar was currently leading the Pakistani delegation at the 32nd ASEAN Regional Forum (ARF) Ministerial Meeting in Kuala Lumpur, Malaysia. The forum was discussing political and security issues impacting the Asia-Pacific region with the goal of fostering peace and cooperation through dialogue, he said.

    On the sidelines of the ARF meeting, he said Senator Dar held bilateral meetings with leaders from Malaysia, Canada, Australia, Laos, Sri Lanka, Russia, the European Union, Switzerland, and the United Kingdom. These interactions focused on strengthening economic ties, trade, education, and cultural exchanges, as well as addressing regional and global challenges.

    The Foreign Office Spokesperson also highlighted the visit of Turkish Foreign Minister Hakan Fidan and Minister of National Defence Yasar Güler to Islamabad. Co-chairs of the Joint Commissions under the High-Level Strategic Cooperation Council (HLSCC), the Turkish officials discussed expanding bilateral cooperation in trade, energy, and investment. The inaugural meeting of the Joint Commission reviewed the progress of twelve standing committees under the HLSCC, he added.

    In parallel, he said a Pakistani delegation led by Special Assistants to the Prime Minister, Ambassador Syed Tariq Fatemi and Haroon Akhtar Khan, met with Russian Deputy Prime Minister Alexei Overchuk in Moscow. Discussions covered wide-ranging cooperation including trade, energy, agriculture, and investment. Pakistan reiterated its desire to deepen ties with Russia, recognizing its stabilizing role in global affairs.

    He added that a key development was the inaugural round of Additional Secretary-level talks between Pakistan and Afghanistan held in Islamabad on July 7. The talks, he said focused on trade, refugee repatriation, regional connectivity, and security cooperation. “Pakistan underscored its concerns over terrorist sanctuaries in Afghanistan and urged Kabul to take concrete actions against groups threatening Pakistan’s security,” he said.

    He also shed light on the 9th round of Bilateral Political Consultations between Pakistan and Poland took place in Warsaw on July 4. Delegations reviewed cooperation across various sectors including energy, defence, mobility, and higher education. Both countries agreed to enhance engagement through high-level visits and multilateral cooperation, with the next round to be held in Islamabad in 2026, he said.

    The spokesperson announced that July 13 will mark the 94th Youm-e-Shuhada-e-Kashmir (Kashmir Martyrs Day), commemorating the 1931 massacre of 22 Kashmiris in Srinagar. He denounced ongoing human rights abuses in IIOJK, including recent restrictions on Ashura preparations and the humiliating treatment of a Kashmiri youth by Indian forces.

    “Indian armed forces are operating with impunity, with license to kill,” Ambassador Shafqat Ali Khan said, reiterating Pakistan’s call for an end to extrajudicial killings and for the international community to take notice of the situation.

    Commenting on Indian National Security Advisor Ajit Doval’s claim of attacking 13 Pakistani airbases, the FO Spokesperson termed the remarks “distortions and misrepresentations” and a “violation of international law.” He reminded that Pakistan had downed multiple Indian aircraft and rejected India’s attempts to glorify aggression.

    On Afghanistan, the Spokesperson acknowledged ongoing concerns about terrorist sanctuaries and stressed that Pakistan continues to engage with Kabul in good faith, hoping for more responsible action from the Afghan side.

    In response to questions about declassified U.S. documents on Pakistan’s role during the Soviet-Afghan war, the spokesperson noted, “What is in the past is in the past,” emphasizing Pakistan’s current efforts to chart a peaceful and cooperative future for the region.

    Addressing climate change, the Spokesperson said Pakistan remains one of the most vulnerable nations despite its negligible contribution to global emissions. He reiterated Islamabad’s leading role in advocating for climate finance and justice for developing countries.

    Responding to questions on remarks made by PPP Chairman Bilawal Bhutto Zardari regarding the potential extradition of individuals of concern, the Spokesperson clarified: “He did not name anyone. The government’s position remains consistent and unchanged.” He directed inquiries to the PPP’s official spokesperson for further clarification.

    The Spokesperson deferred a direct response on the status of U.S. aid under former President Donald Trump but indicated that dialogue with Washington on all matters, including aid and cooperation, is ongoing.

    Asked about hypothetical global conflict scenarios involving China, the Spokesperson declined to speculate but reaffirmed the strength of Pakistan-China relations, describing China as “our iron brother” and a strategic partner.

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  • Association Between Fractional Exhaled Nitric Oxide (FeNO) and Cogniti

    Association Between Fractional Exhaled Nitric Oxide (FeNO) and Cogniti

    Introduction

    Obstructive sleep apnea (OSA) is a widespread sleep disorder that involves repeated partial or complete blockage of the upper airway during sleep, causing intermittent oxygen deprivation and sleep disruption.1 The prevalence of OSA is particularly on the rise in developed nations.2 OSA is associated with numerous neurological cognitive deficits, such as deficits in memory, executive function and concentration,3,4 which can significantly enhance the probability neurodegenerative diseases.5,6

    Although the exact mechanisms of cognitive dysfunction in OSA remain unclear, chronic intermittent hypoxia, oxidative stress, and systemic inflammation are thought to play critical roles.7 Airway inflammation in OSA may result from mechanical trauma due to recurrent upper airway obstruction, as well as the impact of intermittent hypoxia.8 Additionally, there is evidence of systemic inflammation in OSA.9 Persistent airway inflammation in OSA might be involved in the disorder’s complex pathophysiology, indicating the necessity for a comprehensive examination of this relationship.

    Fractional exhaled nitric oxide (FeNO) provides a rapid and non-invasive method for evaluating airway inflammation,10–12which has been extensively studied in asthma, chronic obstructive pulmonary disease, OSA, and COVID-19.13–15 NO is produced by endothelial and epithelial cells, as well as macrophages, providing insights into respiratory tract inflammation.16 FeNO has been recognized as a noninvasive biomarker of airway inflammation.17

    Increased levels of exhaled NO may predict moderate-to-severe OSA.18 Transcriptomic analysis revealed that peripheral inflammation triggers neuroinflammation within the central nervous system, leading to cognitive decline.19 However, the mechanisms linking exhaled NO to cognition in OSA remain to be elucidated.

    Therefore, the primary aim of this research is to explore the characteristics of exhaled NO in individuals with OSA and to examine its association with cognitive function.

    Methods

    Participants

    This prospective study was conducted at the Affiliated Nantong Hospital 3 of Nantong University from December 2023 to December 2024. Initially, individuals who underwent polysomnography (PSG) for snoring were recruited for the study.

    According to the clinical practice guideline for diagnostic testing of adult OSA,20 the apnea-hypopnea index (AHI) was used as the diagnostic indicator. Ultimately, 102 individuals were included. Participants with AHI≥15/h were classified as moderate/severe OSA (n = 62); while those with AHI<15/h were classified as snoring/mild OSA (n = 40)4,21 (Figure 1).

    Figure 1 Flow chart illustrating the process of selecting patients for this study.

    Inclusion criteria: (1) participants must be aged between 18 and 65 years; (2) participants with at least 9 years of education; (3) participants who have not received OSA treatment. Exclusion criteria: (1) participants with asthma, chronic obstructive pulmonary disease, cancer, cardiopulmonary failure, stroke, hepatic dysfunction, renal dysfunction, anxiety, Parkinson’s disease, or Alzheimer’s disease; (2) sleep disorders such as insomnia or central sleep apnea; (3) current use of psychotropic medications and corticosteroids; (4) total sleep duration< 5 hours during PSG; (5) smoking in the past three months or active upper airway infection.

    The research was performed in compliance with the Declaration of Helsinki, and all procedures were conducted after obtaining written informed consent from the participants. Ethical approval for the study was granted by the Ethics Committee of the Affiliated Nantong Hospital 3 of Nantong University (EK2023115).

    Measurement

    Fundamental Information

    Comprehensive demographic and previous health history information were gathered from all patients. This included age, sex, educational level, body mass index (BMI), neck circumference (NC), history of alcohol consumption and smoking habits, history of hypertension and diabetes, and the presence of symptoms such as nocturnal snoring, nocturnal awakenings, excessive daytime sleepiness, dreaming, memory impairment, morning tiredness, headaches, and dry mouth.

    Epworth Sleepiness Scale (ESS)

    We utilized the validated Chinese version of the ESS.22,23 Scores range between 0 and 24, a score of 10 or higher indicating significant sleepiness. The ESS assessments for the patients were administered by experts at the sleep center.

    The validated Chinese version of the ESS was used in this study with proper authorization from the Mapi Research Trust (license ID: 116777).

    Cognitive Function Assessment

    Cognitive assessments were performed 1 hour before PSG to avoid the influence of sleep deprivation on performance. Tests included the Digit Ordering Test (DOT) for working memory, the Logical Memory Test (LMT) for logical memory, and the Rey-Osterrieth Complex Figure Test (RCFT) for visual memory.24,25 The RCFT involved three phases:Firstly, participants were asked to copy the geometric shape to assess their copying ability (P1). Secondly, without prior notice, participants were asked to immediately redraw the figure from memory on a blank sheet, assessing their immediate visual memory (P2). Thirdly, participants were required to redraw the figure again after 30 minutes to evaluate their delayed visual memory (P3).26,27 All cognitive tests were conducted approximately one hour before PSG to avoid fatigue or confounding effects from sleep monitoring. Assessors were blinded to participants’PSG and FeNO results to reduce bias.

    Polysomnography

    Overnight PSG recordings were conducted in a sound-insulated room. Recording began at 9:00 pm and ended at 6:00 am, ensuring at least 7 hours of data. Signals were acquired by the Nox A1 system (ResMed, Australia). The PSG data included eight electroencephalogram channels (F3, F4, C3, C4, O1, O2, M1, M2), electrocardiogram, electromyograms of both anterior tibialis muscles, bilateral electrooculograms, finger pulse oximetry for oxygen saturation, a nasal pressure monitor, a thermistor for airflow, and thoracic/abdominal movements via inductance plethysmography. All data were scored according to the American Academy of Sleep Medicine.28 Recorded parameters included sleep stages (N1, N2, N3, REM), AHI, oxygen desaturation index (ODI), total sleep time (TST), sleep efficiency (SE), lowest arterial oxygen saturation (LSpO2), percentage of sleep time with arterial oxygen saturation below 90% (TS90%), and sleep latency.

    FeNO Measurements

    FeNO measurements adhered to the American Thoracic Society’s guidelines29 and were consistently performed immediately after PSG by a skilled technician. The measurements were taken using a nitric oxide analyzer (Wuxi Shangwo, China) and results were recorded in parts per billion (ppb). FeNO levels were assessed at two flow rates: 50 mL/s (FeNO50) and 200 mL/s (FeNO200), with measurement errors below 10%. Participants refrained from smoking, eating, vigorous exercise, and pulmonary function testing for at least 1 hour, and avoided consuming nitrogen-rich food for at least 3 hours before the test. Participants took a deep breath, then exhaled steadily at 50 mL/s for at least 6 seconds or at 200 mL/s for at least 4 seconds. Each flow rate was measured 2–3 times, and the mean value of each was recorded. The alveolar NO concentration (CaNO) was estimated using a two-flow rate linear regression model based on FeNO measurements at 50 and 200 mL/s.30 FeNO50 reflects NO from the central airways, FeNO200 from the distal airways, and JawNO from the nasal cavity. These measures represented different airway regions and provided complementary information.

    Although FeNO was measured post-PSG while cognition was assessed pre-PSG, this design reflects standard clinical practice and minimizes sleep deprivation’s potential effects on cognition. The temporal gap was less than 12 hours.

    Statistical Analysis

    Statistical analyses were conducted with SPSS (version 25.0; SPSS Inc, Chicago, IL, USA), GraphPad Prism (version 9.0; GraphPad Software, San Diego, CA, USA) and the beanplot package (version 1.2).31 Continuous variables were presented as mean ± standard deviation (M ± SD), and group differences were evaluated using the independent samples t-test. Categorical variables were analyzed using the chi-square (χ²) test. Spearman’s rank correlation analysis was used to assess the relationship between cognitive function and clinical or FeNO-related variables. A mixed-design repeated measures ANOVA was used to evaluate cognitive function over time. Group (moderate/severe OSA vs snoring/mild OSA) served as the between-subjects factor, and cognitive domains (copying, immediate, and delayed visual memory) as the within-subjects factor. The Greenhouse-Geisser correction was applied when necessary, and multiple comparisons were adjusted using the Bonferroni correction. Hierarchical regression analysis further explored the relationship between cognitive function and exhaled NO levels. Hierarchical regression analysis was conducted to explore the relationship between cognitive function and exhaled NO levels. Potential confounders—including age, sex, educational level, BMI, and ESS score—were selected based on prior literature and clinical relevance, and were included in the regression models to minimize bias and enhance interpretability. Although no formal a priori power analysis was conducted, the sample size was comparable to previous studies in this field. P < 0.05 was considered statistically significant.

    Results

    Demographic, Clinical, and Sleep Characteristics of All Patients Stratified by AHI

    In Table 1, the demographic, clinical, and sleep characteristics are outlined. There were no notable differences between the moderate/severe OSA group and the snoring/mild OSA group in terms of age, gender, years of education, smoking history, drinking history, history of hypertension or diabetes, dreaming, morning fatigue, morning headache, TST, SE, proportion of non-rapid eye movement (NREM) 2 sleep, or proportion of REM sleep (P > 0.05). However, BMI, NC, witnessed apnea, drowsiness, dry mouth, memory deterioration, ESS score, proportion of NREM1 sleep, ODI, TS90%, longest apnea duration, and arousal index (ArI), and LSpO2 were significantly higher in the moderate/severe OSA group than in the snoring/mild OSA group (P < 0.05).

    Table 1 Comparison of Demographic and Clinical Traits Between the Snoring/Mild and Moderate/Severe OSA Group

    The Cognitive Function and Exhaled NO Parameters in OSA Patients

    The results of the cognitive function and exhaled NO parameters between the snoring/mild OSA group and the moderate/severe OSA group are presented in Table 2. There were no notable differences between the two groups regarding DOT, LMT delay, copying ability scores (P1), or CaNO (all P > 0.05). However, the LMT immediate, immediate visual memory (P2) and delayed visual memory (P3) were significantly higher in the snoring/mild OSA group compared to the moderate/severe OSA group (P < 0.05). Additionally, FeNO50 and FeNO200 were significantly higher in the moderate/severe group than in the snoring/mild OSA group (P < 0.05). Additionally, FeNO50 and FeNO200 were significantly higher in the moderate/severe group than in the snoring/mild OSA group (P < 0.001). FeNO200 was included to assist in CaNO estimation, not as a standalone marker. While CaNO levels slightly exceeded normal values (6 ppb), no significant group difference was observed.(Table 2 and Figure 2).

    Table 2 Cognitive Function and Exhaled NO Parameters for the Snoring/Mild OSA and Moderate/Severe OSA

    Figure 2 The Cognitive Function and Exhaled NO Parameters in OSA patients. (A) Bean plot for the comparison of fractional exhaled NO values between the snoring/mild OSA group and the moderate/severe OSA group. (B) Bean plot for the comparison of RCFT scores (P1, P2, P3) between the snoring/mild OSA group and the moderate/severe OSA group. The green distributions present results for the snoring or mild OSA group, and the Orange distributions present results for the moderate or severe OSA group. Horizontal black lines denote the averages of each experiment-specific distribution, while dashed lines indicate the overall averages.

    Correlation of Exhaled NO with Cognitive Function

    Firstly, results showed a significant negative correlation between immediate visual memory and FeNO50 (r = −0.286, P = 0.039), AHI (r = −0.088, P = 0.036), and witnessed apnea (r = −0.211, P = 0.034). Furthermore, delayed visual memory (P3) showed a negative relationship with FeNO50 (r = −0.302, P = 0.037) and AHI (r = −0.103, P = 0.031) (Figure 3). FeNO200 and CaNO were not significantly correlated with cognitive test scores (P > 0.05).

    Figure 3 Correlation of Exhaled NO with Cognitive Function. (A) Correlation between RCFT scores at various time points and FeNO50. (B) Correlation between RCFT scores at various time points and AHI.

    Secondly, The RCFT scores at three different time points (P1, P2, P3) for patients in both the snoring/mild OSA group and the moderate/severe OSA group followed a normal distribution. In the moderate/severe OSA group, P2 and P3 were significantly lower than those in the snoring/mild group (P < 0.05), indicating statistically significant differences. A one-way repeated measures ANOVA revealed that the immediate visual memory and delayed visual memory in the moderate/severe OSA group differed significantly from those in snoring/mild group (P < 0.05). Moreover, multiple comparisons using the LSD method demonstrated significant differences in RCFT scores across all time points.

    The main effect of time was significant, F = 271.171, P < 0.001, indicating that P1, P2, and P3 scores changed significantly over time. Furthermore, the group-by-time interaction was significant, with F = 3.065, P < 0.05, suggesting that the RCFT scores in the moderate/severe OSA group decreased more rapidly over time. The between-subjects main effect revealed a significant difference, F = 6.041, P < 0.05, indicating that the reduction in P1, P2, and P3 scores differed significantly between the two groups according to Table 3.

    Table 3 RCFT Scores Comparison Between the Moderate/Severe OSA and Snoring/Mild OSA Group at Different Time Points

    Impact of Exhaled Nitric Oxide on Cognitive Function

    To investigate the effect of FeNO on cognitive function, a hierarchical regression analysis was conducted with immediate memory as the dependent variable. We employed a two-step modeling approach. Model 1: We first included the following covariates: age, gender, longest apnea duration, ArI, witnessed apnea, BMI, ODI, TS90%, LSpO2, and AHI, constituting Model 1. The results indicated that ArI and AHI were positively associated with immediate visual memory (P < 0.05). Model 2: Building upon Model 1, FeNO50 and FeNO200 were added as predictors. The findings showed that FeNO50 had a significant negative impact on immediate visual memory (P < 0.05), while FeNO200 did not show a significant association (P > 0.05) (Table 4).

    Table 4 Hierarchical Regression Analysis of Exhaled Nitric Oxide Levels on Cognitive Function

    We also included delayed visual memory as a dependent variable in the hierarchical regression analysis; however, no significant effect of exhaled NO on delayed visual memory was observed. These findings suggest that higher FeNO50 are associated with poorer immediate visual memory in OSA, independent of other factors.

    Discussion

    Earlier research, including our own, has demonstrated that cognitive function is impaired in patients with OSA.4,32 In this study, we quantified proximal and distal airway inflammation by chemiluminescence analysis and assessed dynamic cognitive trajectories via multi-phase RCFT. Our findings revealed that elevated FeNO50 independently predicted impaired visual memory. Furthermore, a significant group × time interaction indicated that RCFT scores declined more rapidly over time in the moderate/severe OSA patients than those in the snoring/mild OSA group. These results underscore the specificity of airway inflammation in driving OSA-related cognitive impairment.

    This study provides significant insights into the relationship between FeNO and cognitive function in OSA patients. Notably, we are the first to report that FeNO50, a marker of proximal airway inflammation, independently predicts immediate visual memory deficits in OSA. In contrast, FeNO200, reflecting distal airway inflammation, showed no significant correlation with cognition. This distinction highlights that proximal airway inflammation may have a more direct cognitive impact than distal inflammation.

    Furthermore, our findings reveal that individuals suffering from moderate/severe OSA exhibit a more rapid decline in RCFT scores over time. The significant group-by-time interaction highlights the progressive nature of cognitive decline in OSA, which is often overlooked in traditional single time point studies. Through multi-time point assessments, we delineated the dynamic trajectory of cognitive deterioration, offering a comprehensive understanding of cognitive impairment in OSA.

    Studies have focused on the link between exhaled NO and cognitive function. The RCFT is widely used to assess visual memory, including both copying and recall tasks,25,33 and is applied to evaluate cognitive function in OSA patients. Ribeiro34 demonstrated that in OSA patients following weight loss treatment, the RCFT effectively captures changes in cognitive function, particularly improvements in executive function, memory, and information processing speed. Our study extends these findings by using the RCFT to assess dynamic cognitive trajectories. We observed that immediate and delayed visual memory were negatively correlated with AHI and FeNO50, suggesting that FeNO50 may be associated with cognitive impairment in OSA.

    A meta-analysis found elevated post-sleep FeNO levels in OSA, a pattern absent in controls. Furthermore, long-term continuous positive airway pressure (CPAP) therapy markedly reduces FeNO.17 In obese OSA patients, this post-sleep FeNO increase is particularly pronounced, likely due to obesity-related oxidative stress and comorbidities.17 Elevated NO has been recognized as a risk factor for Alzheimer’s disease.35 These findings support FeNO as a marker related to cognitive deficits in OSA. Accordingly, we hypothesized that elevated FeNO50 indicates inflammation in OSA patients, contributing to cognitive decline.

    Despite progress, inconsistencies remain regarding the relationship between FeNO and cognitive function. Some studies have reported higher bronchial NO and lower alveolar NO in OSA, with CPAP enhancing alveolar NO.36 Conversely, others have found elevated alveolar NO without bronchial NO level differences,37 likely due to variations in study design and sample size. Furthermore, a study on vehicle pollution found cognitive impairment in the high-pollution group despite no difference in FeNO.38 Our analysis of FeNO50, FeNO200, and CaNO, clarifies their distinct roles.

    The negative correlation between FeNO50 and immediate visual memory can be explained by proximal airway inflammation triggering systemic inflammation. Gramiccioni39 reported that exhaled NO increases with age and correlates with systemic oxidative stress and neurocognitive dysfunction, supporting eNO as a biomarker for cognitive impairment in OSA. In contrast, the absence of an association between FeNO200 and cognitive function suggests that distal airway inflammation has a limited systemic impact and fewer neurotoxic effects.

    FeNO and CaNO primarily reflect inducible nitric oxide synthase (iNOS) activity in the airway, indicating inflammation. In contrast, neuronal nitric oxide synthase (nNOS), expressed in the brain, regulates synaptic plasticity and memory. Dysregulated nNOS impair cognition through disrupted neurotransmission and neurotoxicity. Although FeNO50 is a peripheral marker, it may reflect systemic inflammation that affects central nNOS activity. This suggests interaction between iNOS and nNOS, warranting further investigation, ideally combining FeNO with neuroimaging or cerebrospinal fluid biomarkers.

    NO is essential for vascular regulation and neurotransmission.40 However, in inflammation, excessive NO can worsen neurodegeneration by promoting neuronal apoptosis and oxidative stress.41,42 Elevated NO levels have been linked to cognitive decline,35 and patients with OSA are prone to repeated hypoxia-reoxygenation cycles, which trigger oxidative stress and systemic inflammation, further impacting neurocognitive function.43 FeNO50, a marker of proximal airway inflammation, may exacerbate this process by increasing oxidative stress, impairing neuronal integrity and synaptic plasticity, particularly in memory-related regions like the hippocampus.44

    The observed interaction between OSA severity and cognitive trajectory supports this hypothesis. Studies indicate that high concentrations of NO can lead to the formation of reactive nitrogen species.45 This aligns with neuroimaging studies demonstrating that severe OSA is associated with structural brain changes, including reduced gray matter volume in the prefrontal cortex and hippocampus, regions critical for memory and executive function.46 Our findings linking FeNO50 to impaired memory reinforce the notion that airway inflammation contributes to neurocognitive dysfunction. Studies on RCFT indicate that memory is closely tied to hippocampal integrity, whereas familiarity-based recognition is associated with the medial temporal cortex.47,48

    Although cognitive tests were conducted before PSG and FeNO was measured after PSG, this sequence was chosen to minimize fatigue-related interference with cognitive assessments. Since FeNO may reflect acute airway inflammation influenced by nocturnal hypoxia and arousals, post-PSG measurement helps capture relevant physiological changes. We acknowledge this time gap as a methodological limitation.

    This study has several limitations. First, its cross-sectional design restricts causal inferences between FeNO and cognitive decline. Second, although the sample size was acceptable for exploratory analysis, it was relatively small, which may limit the generalizability of the findings. Although our regression models adjusted for key covariates including age, sex, education, BMI, and ESS score, we acknowledge that not all significantly different clinical or sleep-related variables (eg, ODI, TS90%) were included. This decision was made to avoid overfitting and maintain model stability given the sample size. Future studies with larger cohorts may incorporate a broader range of variables to further clarify the independent contribution of FeNO to cognitive impairment in OSA. Third, while we measured FeNO, we did not assess other inflammatory markers, which could offer a more comprehensive understanding of the inflammatory processes underlying cognitive decline in OSA. Finally, investigating the effects of OSA treatment on exhaled NO and cognitive function could provide further insights into the reversibility of cognitive impairment in OSA.

    Conclusions

    This study enhances understanding of the association between exhaled NO and cognitive impairment in patients with OSA. Our results indicate that FeNO50, a marker of proximal airway inflammation, is independently associated with poorer immediate visual memory. Additionally, patients with moderate to severe OSA exhibited a faster decline in cognitive function over time. These findings suggest that FeNO50 may serve as a potential non-invasive indicator of cognitive dysfunction in OSA; however, as a cross-sectional study, causality cannot be inferred. The time gap between cognitive testing (pre-PSG) and FeNO measurement (post-PSG) may affect the temporal interpretation of this association. In addition, although key covariates were adjusted for, the possibility of residual confounding remains. Further studies are needed to confirm its diagnostic and prognostic value of FeNO in this population.

    Data Sharing Statement

    To access the data supporting this study’s findings, one must make a reasonable request to Qilin Zhu and obtain permission from the Third Hospital of Nantong University, Jiangsu, China.

    Ethics Approval and Consent to Participate

    This study adhered to the guidelines set by the Declaration of Helsinki, and approved by the Ethics Committee of the Third Hospital of Nantong University (protocol code K2023115). Informed consent was obtained from all subjects involved in the study.

    Acknowledgments

    We acknowledge all the patients involved in this study.

    Author Contributions

    Qilin Zhu (QZ): Conceptualization; Data curation; Formal analysis; Writing–original draft. Lili Huang (LH): Methodology; Investigation; Writing–review & editing. Licheng Zhu (LZ): Formal analysis; Visualization. Xiaobai Zhang (XZ): Investigation; Resources. Honghua Ji (HJ): Data curation. Donghua Niu (DN): Data curation. Wangfei Ji (WJ): Data curation. Qingqing Ma (QM): Data curation. Rong Chen (RC): Data curation. Haiyan Shi (HS): Data curation. Yihua Wang (YW): Supervision; Writing–review & editing. Lina Xu (LX): Funding acquisition; Project administration; Supervision.

    All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

    Funding

    This work was supported by Jiangsu Science and Technology Think Tank Program (JSKX24017) and Scientific Research Project of Nantong Health Committee (JCZ20080).

    Disclosure

    The authors declare that they have no conflicts of interests.

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  • Earth will spin unusually quickly in July and August

    Earth will spin unusually quickly in July and August

    Earth does not always spin at the exact same speed. In fact, in recent years, Earth has been spinning a bit more quickly. Scientists are unsure why. Image via NASA.
    • Not all days are created equal. Some days are actually a millisecond shorter than other days.
    • Since 2020, Earth has notched up unprecedentedly short days midway through the year. It happens again in 2025 around July 9, July 10, July 22 and August 5.
    • So why has Earth accelerated? Many factors affect Earth’s spin. But as of now, no one knows for sure.

    TimeandDate published this original post on June 16, 2025. Edits by EarthSky.

    Earth does not quite spin at a constant rate

    Our planet is an almost-but-not-quite-perfect timekeeper. On average, from the point of view of the sun, Earth completes one full rotation on its axis in exactly 86,400 seconds, give or take a millisecond or so.

    So, 86,400 seconds is another way of saying 24 hours. A millisecond (ms) is 0.001 seconds. That’s considerably less than a blink of an eye, which lasts around 100 milliseconds.

    The only way to measure these tiny day-to-day variations in Earth’s spin speed is with atomic clocks. The first practical atomic clocks began their timekeeping in the 1950s. The number of milliseconds above or below 86,400 seconds is what we call the length of day.

    Earth speeds up

    Until 2020, the shortest length of day that atomic clocks ever recorded was -1.05 ms. This means Earth completed one rotation with respect to the sun in 1.05 milliseconds less than 86,400 seconds.

    Since then, however, Earth has managed to shatter this old record every year by around half a millisecond. The shortest day of all was -1.66 ms on July 5, 2024. Earth should get close to this again in 2025 around July 9, July 10, July 22 and August 5. The newest estimates from July 10 confirm these as the shortest days of 2025. Also, the latest figures suggest the shortest day of the year overall may in fact turn out to be July 10. But this still needs to be confirmed.

    Chart showing days of 2025 with predicted negative milliseconds for each.
    New estimates released on July 10 confirm the shortest days of 2025 should fall around July 9, July 10, July 22 and August 5. The latest figures suggest the shortest day of the year overall may in fact turn out to be July 10. But this is still to be confirmed. Image via TimeandDate.
    Chart showing years past with the shortest length of day.
    This table shows the shortest length of day in every year for the past five years. Image via TimeandDate.

    Why multiple possible dates?

    The orbit of the moon affects the short-term variations in the length of day. Our planet spins more quickly when the moon’s position is far to the north or south of Earth’s equator.

    The moon will be around its maximum distance from Earth’s equator on these dates. Input the date into TimeandDate’s Moon Light World Map. This will show you the moon’s position – indicated by the moon symbol – at the time and date you choose.

    Why is all this happening?

    Why has Earth accelerated, and when will it slow down again? These are difficult questions. Long-term variations in Earth’s spin speed are affected by a long list of factors that includes the complex motion of Earth’s core, oceans and atmosphere. Leonid Zotov, a leading authority on Earth rotation at Moscow State University, said:

    Nobody expected this. The cause of this acceleration is not explained.

    Most scientists believe it is something inside the Earth. Ocean and atmospheric models don’t explain this huge acceleration.

    Early last year, there were indications Earth might be slowing down, and Dr. Zotov predicted that Earth would decelerate. Zotov said at the time:

    But the future will show if that’s right.

    That prediction turned out to be premature. Yet Dr. Zotov is striking a similar note in 2025:

    I think we have reached the minimum. Sooner or later, Earth will decelerate.

    Bottom line: The shortest days on Earth for 2025 will be in July and August. But why is Earth spinning faster? It’s a bit of a mystery.

    Via TimeandDate

    Read more: Why don’t we feel Earth’s spin?

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  • Billionaire private astronaut Jared Isaacman donating $15 million for Space Camp programs

    Billionaire private astronaut Jared Isaacman donating $15 million for Space Camp programs

    Jared Isaacman is donating a big chunk of change to help inspire the astronauts and space scientists of tomorrow.

    The billionaire tech entrepreneur and private astronaut, who until recently was on track to become NASA administrator, announced today (July 11) that he’s gifting $15 million to the U.S. Space & Rocket Center in Alabama for its Space Camp programs.

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  • Circular Debt of Pakistan: Understanding the Crisis

    Circular Debt of Pakistan: Understanding the Crisis

    Circular debt is a major financial problem in Pakistan’s energy sector, created by a mismatch between the cost of generating electricity and the revenue collected from consumers. It involves a complex chain of payments between different stakeholders, including power generation companies (IPPs), suppliers, distributors (Discos), gas utilities, and the government.

    As of now, Pakistan’s energy sector faces a massive deficit, with circular debt accumulating to around Rs2.3 trillion. This growing debt has significant economic implications, leading to inefficient power supply, higher electricity costs, and fiscal stress on the government.

    What is Circular Debt?

    Circular debt refers to the financial shortfall in Pakistan’s energy sector, where various entities involved in electricity generation, supply, and distribution owe large amounts of money to each other. The problem is rooted in poor management, delayed payments, and inefficiencies in revenue collection.

    The key players involved in this circular chain include the federal government, independent power producers (IPPs), government-owned power supply companies (Gencos and Discos), energy suppliers, and the financial institutions that finance the sector. These players often fail to pay one another on time, causing the debt to spiral out of control.

    How Circular Debt Has Grown

    Circular debt in Pakistan’s energy sector has grown significantly over the years due to several factors:

    Low Recoveries & Theft: Power companies struggle to recover payments from consumers, and widespread theft further exacerbates financial losses.

    Unreimbursed Tariff Subsidies: The government has failed to fully compensate power companies for the tariff subsidies, increasing the debt burden.

    Misaligned Billing Cycles: Billing inefficiencies and long delays in the collection process lead to a backlog of unpaid dues.

    Capacity Payments: IPPs are required to make large capacity payments, regardless of whether electricity is generated or consumed. This contributes to the increasing debt as power plants get paid without generating enough electricity to cover costs.

    As a result, the total circular debt has reached staggering amounts, leading to an unbalanced energy market where costs are passed down to consumers and institutions that are unable to meet their obligations.

    Key Components of Circular Debt

    The circular debt issue in Pakistan is divided into three main components:

    Payables of PSC (Power Supply Chain): These are the costs incurred by the power supply chain, including losses from electricity theft, unpaid bills, and support for life-line consumers.

    Payables of ESC (Energy Supply Chain): The ESC is burdened by unpaid fuel bills, especially for gas and other essential energy resources.

    Payables of GOP (Government of Pakistan): The government owes significant amounts due to subsidies for power generation and distribution, as well as unpaid payments to energy companies.

    Government’s Response and Proposed Solutions

    To address the growing circular debt, the Government of Pakistan has begun implementing several measures to resolve the issue. These steps focus on managing the debt more effectively, streamlining payments, and negotiating better terms with stakeholders.

    Debt Settlement Efforts: The finance ministry has started discussions with IPPs and other stakeholders to settle the existing circular debt. Negotiations include restructuring payment terms and adjusting tariffs to lower the debt.

    Debt Service Surcharge (DSS): A new DSS of Rs3.23 per kWh has been introduced, which will be added to electricity bills. This surcharge will help generate funds to pay off the outstanding debt to banks and other financial institutions.

    Interest Rate Adjustments: The KIBOR (Karachi Interbank Offered Rate) has been adjusted to ease the debt burden, which will reduce the overall financial pressure on the sector.

    Improving Cash Flow Management: The government has stressed the importance of transparent and real-time tracking of financial flows to better manage the circular debt and ensure timely payments.

    Why Circular Debt Has Spiraled

    The circular debt crisis in Pakistan’s energy sector has spiraled out of control for several reasons:

    Low Payment Recoveries: One of the main causes of the growing debt is the inability of power companies to recover payments from consumers. This is exacerbated by inefficiencies in billing and distribution.

    Theft and Mismanagement: Power theft is rampant across the country, leading to significant financial losses. Poor management and a lack of accountability have only worsened the situation.

    Structural Inefficiencies: The energy sector suffers from misaligned tariff structures, inadequate infrastructure, and weak planning, which causes delays in generating sufficient revenue to cover costs.

    Governance Failures: A lack of effective governance and sector regulation has led to inflation in power tariffs and inefficiencies that have compounded the financial crisis.

    Solutions and Future Roadmap

    Moving forward, the Pakistani government must focus on comprehensive reforms to tackle circular debt in the energy sector:

    Improving Billing and Collection Systems: The government needs to reform the billing process to ensure timely payments and minimize losses due to inefficient systems.

    Better Financial Management: Effective cash flow management, including real-time tracking of payments, will help reduce inefficiencies and increase accountability.

    Addressing Structural Inefficiencies: Tariffs must be reviewed and aligned with actual costs to ensure the sector remains financially viable in the long term.

    Governance Reforms: Stronger governance and accountability measures will help improve sector management, reduce financial mismanagement, and ensure that funds are used effectively.

    The circular debt problem in Pakistan’s energy sector is a complex challenge that requires a multi-pronged solution. While the government has made strides in addressing the issue, long-term success depends on structural reforms, improved financial management, and better governance. By implementing these measures, Pakistan can begin to reduce its circular debt, improve energy supply, and create a more sustainable energy market for the future.

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  • Former swimming coach to be extradited to Ireland

    Former swimming coach to be extradited to Ireland

    BBC George Gibney has thinning hair, glasses, a blue shirt, and a green fleece and is walking across a car park. He looks down at the groundBBC

    George Gibney left Ireland more than 30 years ago

    Former Irish national swimming coach George Gibney, who is wanted in the Republic of Ireland to face historical sexual abuse charges, is to be extradited there, a court in the United States has ruled.

    A US district magistrate made the order at a hearing in Orlando, Florida, on Friday.

    The Irish government has sought Mr Gibney’s return to face 78 counts of indecent assault and one count of attempted rape against four girls aged between eight and 14 at the time of the alleged offences.

    Mr Gibney had consented to his extradition and asked the court to expedite his departure to Ireland.

    He left Ireland more than 30 years ago and has not been back since.

    Mr Gibney was arrested in Florida by US Marshals at the start of this month.

    He has been remanded in the custody of the US Marshals at Orange County Jail, pending arrangements being made to transport him to Ireland.

    Mr Gibney sat in a wheelchair in the courtroom and was dressed in a uniform issued by Orange County Jail, Irish national broadcaster RTE said..

    The judge asked Mr Gibney a series of questions about the affidavit he signed giving up his right to contest his detention and his right to contest the extradition request.

    Mr Gibney replied “yes” to the questions.

    It was previously reported that gardaí (Irish police) reopened an investigation into Mr Gibney after a number of people made allegations against him on the BBC podcast Where is George Gibney? five years ago.

    The criminal investigation was commenced in 2020 by a specialist team within the Garda National Protective Services Bureau.

    A file was sent to the Director for Public Prosecutions (DPP) three years later.

    The DPP examined the file and recommended that Mr Gibney was charged.

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