Category: 8. Health

  • Dapagliflozin Fails to Lower Cardiovascular Risk in Patients with HF

    Dapagliflozin Fails to Lower Cardiovascular Risk in Patients with HF

    David Berg, MD, MPH | Image Credit: Brigham and Women’s Hospital

    Dapagliflozin, an SGLT2 inhibitor, did not significantly reduce short-term risk of cardiovascular death or worsening heart failure (HF) in patients admitted with HF, according to results from the DAPA ACT HF-TIMI 68 trial.1

    Presented as late-breaking research at the European Society of Cardiology Congress 2025 in Madrid, the trial involved the administration of dapagliflozin to patients currently hospitalized for HF. Despite the lack of significant cardiovascular death risk reduction, the trial did exhibit positive effects when data were combined.1

    HF is the leading cardiovascular reason for hospital admission worldwide, with rates increasing dramatically over the last 10 years. Patients hospitalized for HF also have a high risk of death and other adverse outcomes in the early post-discharge period. Previous clinical trials have suggested that initiating and optimizing disease-modifying chronic heart failure therapies, including beta-blockers and mineralocorticoid receptor antagonists, in the early post-discharge period may improve both short- and long-term outcomes.2

    “However, there are limited data on initiating sodium-glucose cotransporter-2 inhibitors in patients hospitalized for HF,” David Berg, MD, MPH, investigator in the TIMI Study Group at Brigham and Women’s Hospital and principal investigator of DAPA ACT, said in a statement. “We designed the trial to test the hypothesis that in-hospital initiation of the SGLT2i, dapagliflozin, as compared with placebo, could safely and effectively decrease the early risk of cardiovascular death or worsening HF among patients hospitalized for HF.”1

    The trial was a double-blind, placebo-controlled, randomized trial conducted at 210 sites in the USA, Canada, Poland, Hungary, and the Czech Republic. For inclusion, patients had to be ≥18 years of age and be hospitalized with a primary diagnosis of HF, including signs and symptoms of fluid overload, as well as elevated natriuretic peptide levels during index hospitalization.1

    A total of 2401 patients were included in the study and randomly assigned in a 1:1 ratio to dapagliflozin 10 mg daily or placebo at least 24 hours and no later than 14 days after hospital admission and as early as possible following initial stabilization. The median age was 69 years, and 33.9% of patients were women. Investigators noted a primary efficacy outcome composite of cardiovascular death or worsening HF over the first 2 months.1

    Ultimately, the primary outcome occurred in 10.9% of patients assigned to dapagliflozin and 12.7% of patients in the placebo group (hazard ratio [HR], 0.86; 95% CI, 0.68-1.08; P = .20). Cardiovascular death occurred in 2.5% of patients with dapagliflozin and 3.1% with placebo (HR, 0.78; 95% CI, 0.48-1.27), and a worsening HF event occurred in 9.4% and 10.3% of patients, respectively (HR, 0.91; 95% CI, 0.71-1.18).1

    All-cause mortality occurred in 3% of patients receiving dapagliflozin and 4.5% receiving placebo (HR, 0.66; 95% CI, 0.43-1). Rates of symptomatic hypotension were 3.6% and 2.2%, respectively, and rates of worsening kidney function were 5.9% and 4.7%, respectively.1

    A prespecified meta-analysis was conducted, including 2 other SGLT2i trials – specifically, empagliflozin and sotagliflozin – to assess in-hospital initiation in a total of 3527 patients hospitalized for HF. SGLT2is reduced early risks of cardiovascular death or worsening HF (HR, 0.71; 95% CI, 0.54-0.93; P = .012) and all-cause mortality (HR, 0.57; 95% CI, 0.41-0.8; P = .001).1

    “In-hospital initiation of dapagliflozin did not significantly reduce the risk of cardiovascular death or worsening HF over the first 2 months in DAPA ACT HF-TIMI 68,” Berg said. “However, the totality of trial data suggests that in-hospital initiation of an SGLT2i reduces the early risk of cardiovascular death or worsening HF and all-cause mortality.”1

    References
    1. 1: European Society of Cardiology. Evidence appears supportive for the initiation of SGLT2 inhibitors in patients hospitalized for heart failure. August 30, 2025. Accessed September 4, 2025. https://www.escardio.org/The-ESC/Press-Office/Press-releases/Evidence-appears-supportive-for-the-initiation-of-SGLT2-inhibitors-in-patients-hospitalised-for-heart-failure
    2. 2: Berg DD, Patel SM, Haller PM, et al. Dapagliflozin in Patients Hospitalized for Heart Failure: Primary Results of the DAPA ACT HF-TIMI 68 Randomized Clinical Trial and Meta-Analysis of Sodium-Glucose Cotransporter-2 Inhibitors in Patients Hospitalized for Heart Failure. Circulation. Published online August 29, 2025. doi:10.1161/CIRCULATIONAHA.125.076575

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  • Researchers note spike in kidney deaths related to blood pressure

    Researchers note spike in kidney deaths related to blood pressure

    Deaths from blood-pressure-driven kidney disease have increased dramatically during the past quarter-century, according to a new study.

    Deaths from high blood pressure-related kidney disease increased by nearly half in the U.S. over the past 25 years, researchers reported Thursday at an American Heart Association meeting in Baltimore.

    The highest death rates were among Black Americans, followed by Hispanic people, results show.

    “Despite national efforts to reduce health inequalities, Black individuals still had over three times the death rate compared to other groups of people,” researcher Dr. Joiven Nyongbella said in a news release. He’s an internal medicine resident at Wayne State University/Henry Ford Rochester Hospital in Detroit.

    High blood pressure is a known risk factor for kidney damage, according to the AHA. It can damage the blood vessels in and around the kidneys, contributing to scarring of the organs.

    For the new study, researchers looked at death certificate data from 1999 to 2023 maintained by the U.S. Centers for Disease Control and Prevention.

    Results showed a 48% increase in deaths from kidney disease related to high blood pressure.

    Men and Black or Hispanic adults had rates that were even higher than average, researchers found.

    “High blood pressure isn’t just about strokes or heart attacks — it’s also a major cause of kidney disease and death, especially in Black and Hispanic communities,” Nyongbella said.

    Overall, the death rate rose from 3.3 deaths per 100,000 people in 1999 to 4.9 per 100,000 in 2023.

    Researchers also found that:

    Men had a higher death rate than women, 4.5 versus 3.7 deaths per 100,000.

    Black adults had the highest death rate at nearly 10.4 per 1000,000.

    Hispanic adults had a 15% higher death rate compared to non-Hispanic people, 4.5 versus just under 4 per 100,000.

    “The message is simple: Check your blood pressure, treat it early and don’t ignore it, because it can quietly lead to life-threatening kidney problems,” Nyongbella said.

    Findings presented at medical meetings should be considered preliminary until published in a peer-reviewed journal.

    More information

    The American Heart Association has more on high blood pressure and your kidneys.

    Copyright © 2025 HealthDay. All rights reserved.

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  • MD Anderson Research Highlights for September 5, 2025

    MD Anderson Research Highlights for September 5, 2025

    HOUSTON, SEPTEMBER 5, 2025 ― The University of Texas MD Anderson Cancer Center’s Research Highlights showcases the latest breakthroughs in cancer care, research and prevention. These advances are made possible through seamless collaboration between MD Anderson’s world-leading clinicians and scientists, bringing discoveries from the lab to the clinic and back. 

    Targeted radiation helps patients with kidney cancer delay systemic therapy 
    Read summary | Read in Lancet Oncology

    Some patients with clear cell renal cell carcinoma (ccRCC) – the most common type of kidney cancer in adults – experience oligometastatic disease, where the cancer has spread to only a few sites. Patients with oligometastatic ccRCC often are treated with whole-body systemic treatments like immunotherapy and targeted therapy, which are effective but can come with unwanted side effects. A Phase II clinical trial led by Chad Tang, M.D., and Pavlos Msaouel, M.D., Ph.D., explored the use of metastasis-directed targeted radiation therapy to avoid or delay systemic treatments. In a cohort of 121 patients, survival remained high, with 94% of patients alive at two years and 87% at three years. Overall, patients went a median of 34 months without needing systemic treatment. Researchers also used a novel circulating tumor DNA (ctDNA) test to look for traces of cancer. Patients with no detectable disease stayed off systemic treatments twice as long as those with detectable traces, which suggests that this marker may help select patients for this treatment strategy in the future. These data originally were presented at the American Association for Cancer Research (AACR) Annual Meeting 2025 in April.

    Final trial data from ELI-002 cancer immunotherapy vaccine reinforce promising results
    Read summary | Read in Nature Medicine 

    In initial results from the AMPLIFY-201 trial, co-led by Shubham Pant, M.D., an immunotherapy vaccine targeting the lymph nodes showed potential in delaying relapse of KRAS-mutated pancreatic and colorectal cancers for patients who had previously undergone surgery. Long-term final follow-up data of this vaccine, ELI-002 2P, now shows that 17 of 25 patients (68%) had robust T cell responses, which were associated with increased survival. At 24 months, the median recurrence-free survival had not yet been reached for the higher response group – including all of the patients at the highest two dose levels – with 75% of them still relapse-free, compared to three months for patients who were not high responders. These data prompted the initiation of a Phase II trial that is currently ongoing and includes a new formulation of the vaccine (ELI-002 7P) targeting additional KRAS mutations. 

    Triple combination therapy shows promise for treatment-resistant microsatellite stable BRAF V600E-mutant metastatic colorectal cancer
    Read summary | Read in Cancer Cell

    The BRAF V600E gene mutation makes colorectal cancers (CRCs) more aggressive, leading to poorer survival rates. While some CRCs with high microsatellite instability respond well to immunotherapy, most BRAF V600E-mutant metastatic CRCs are microsatellite stable (MSS) and do not benefit from these treatments. The combination of encorafenib and cetuximab is Food and Drug Administration (FDA)-approved but has limited duration of response in these patients, which led Van Morris, M.D., and colleagues at MD Anderson to examine the safety and efficacy of adding the anti-PD-1 antibody nivolumab to this combination in patients with MSS BRAF V600E-mutant metastatic CRC. This Phase I/II trial enrolled 26 patients and showed an overall response rate of 50%, with a median progression-free survival of over seven months. RNA analysis from liquid biopsies identified distinct patterns of response among patients who did or did not benefit from the triple combination. The positive outcomes of this study led to the launch of SWOG S2107, a nationwide Phase II trial in the same patient population, also led by Morris. 

    Novel sequencing technology links DNA and RNA to provide molecular insights into breast cancer progression
    Read summary | Read in Cell

    Breast cancer often starts in the epithelial cells lining the milk ducts and lobules, but there are many subtypes that make it challenging to identify the cancer’s starting point within normal tissue. Researchers led by Nicholas Navin, Ph.D., developed a new single-cell DNA and RNA sequencing technology – called wellDR-seq – to identify ancestral breast cancer cells. By studying the impact of chromosome gains or losses on gene expression, the researchers were able to uncover the molecular aspects of why some breast cancers are more aggressive or invasive.  The researchers profiled 33,646 single cells from 12 estrogen-receptor (ER)-positive breast cancers, quantifying the amount of certain genes that are actively expressed in tumor cells, as well as the number of copies of specific genes or chromosome segments and their genetic changes over time. These results provide insights into cancer initiation and invasion. While this technique was applied to cancer research, it can also be used to understand the molecular biology of other diseases.

    Large-scale CRISPR screening in stomach organoids reveals gene-drug interactions
    Read summary | Read in Nature Communications 

    Scientists often use organoids – laboratory-grown human cell culture systems that closely mimic body organs – to gain deeper insights into cancer biology and understand how tumors respond to drugs. Researchers led by Yuan-Hung Lo, Ph.D., used organoids along with several CRISPR  gene editing tools to study how cisplatin chemotherapy interacts with different genes in the human stomach. The screens revealed an unexpected link between cisplatin sensitivity and fucosylation, a process that adds sugar molecules to cells. The researchers identified the TAF6L gene as a key regulator of cell recovery from cisplatin-induced cytotoxicity. These results show that CRISPR genetic screens in organoids are a powerful way to identify drug-gene interactions that might explain why some people respond better to certain treatments. 

    First-in-class pan-KRAS inhibitor shows strong antitumor activity in preclinical models
    Read summary | Read in Science Translational Medicine

    KRAS is the most commonly mutated gene in cancer, but targeting the mutant protein is notoriously difficult because current therapies work only for certain KRAS mutations. This led researchers Kathleen McAndrews, Ph.D., Anirban Maitra, M.B.B.S., Raghu Kalluri, M.D., Ph.D., and Timothy Heffernan, Ph.D., to examine the efficacy of a first-in-class inhibitor called BI-2493. This pan-KRAS inhibitor can target the mutant protein in multiple cancer types, regardless of the specific mutation present. BI-2493 was developed as part of the strategic collaboration between Boehringer Ingelheim and MD Anderson. In several models of pancreatic cancer, BI-2493 effectively suppressed tumor growth in vitro and prolonged survival in vivo, with further analysis showing confirmed RAS pathway inhibition. BI-2493 also remodeled the tumor microenvironment of immune-compromised models, increasing intratumoral immune cells and decreasing myeloid cells, allowing for better immunotherapy response. These findings highlight the therapeutic potential of combining BI-2493 with other treatments to inhibit a variety of KRAS mutations and improve patient outcomes. 

    High-dose chemotherapy improves outcomes for multiply relapsed and refractory germ-cell tumors
    Read summary | Read in Clinical Cancer Research

    Testicular cancer is the most common malignancy in young men ages 15 to 35. Most patients respond well to cisplatin-based chemotherapy, with cure rates for metastatic disease as high as 70-80%, but some patients have tumors that relapse. High-dose chemotherapy (HDC) can be effective for some patients after an initial relapse, but outcomes are poor for those with multiple relapses or refractory tumors. In a Phase II trial, researchers led by Yago Nieto, M.D., Ph.D., examined the safety and efficacy of a new HDC specifically targeting DNA damage repair in combination with the targeted therapy bevacizumab. The trial enrolled 65 patients with multiply relapsed and heavily pretreated testicular and other germ-cell tumors. The five-year relapse-free and overall survival rates were 54% and 55.5%, respectively, exceeding expectations. However, the addition of bevacizumab did not improve outcomes. These results were subsequently validated in a prospective cohort of 100 patients with similar poor prognosis, highlighting the promising impact of targeting DNA damage repair pathways to improve outcomes for these patients. 

    Fluorescent tracer helps identify precancerous lesions in pancreatic cancer models
    Read summary | Read in Clinical Cancer Research

    During surgical treatment for pancreatic cancer, pre-malignant pancreatic lesions – which can develop into pancreatic cancer – often go unnoticed and can later cause recurrence. Researchers led by Charles Manning, Ph.D., investigated whether a new fluorescent imaging agent, V-1520, could better identify these areas for removal. V-1520 works by locating and binding to a specific protein biomarker that is overexpressed in high-risk tumor-associated macrophages within the pancreatic tumor microenvironment. Once bound, it emits near-infrared light that can be detected by imaging equipment, allowing surgeons to visualize high-risk areas during surgery. Notably, preclinical models showed a strong uptake of V-1520 in cancer-associated inflammation, but not in pancreatitis – a common but benign condition. Since V-1520 does not target tumors directly and instead binds to overexpressed proteins in the tumor microenvironment, this early detection strategy could also be effective in other cancer types. 

    Researchers identify predictive biomarkers for oral cancer metastasis
    Read summary | Read in PLOS Genetics

    Most oral cancers start in squamous cells lining the mouth and tongue, and frequently metastasize to the lymph nodes. To identify potential biomarkers that predict this metastasis, researchers led by Koichi Takahashi, M.D., Ph.D., and Ken Furudate, D.M.D., Ph.D., performed a comprehensive spatial analysis of the tumor microenvironment surrounding oral cancer cells that metastasized to the lymph nodes. They found increased levels of a specific type of activated supportive cell, called myofibroblastic cancer-associated fibroblasts (myCAFs), located within the invasive tumor front. The researchers showed that cancer cells don’t act alone, and are, instead, aided by these myCAF “accomplices.” The researchers also characterized several key players in the metastasis pathway, extracting a spatial molecular fingerprint to create a 23-gene signature that can predict lymph node metastasis and poor prognosis in patients with oral cancer.

    Honors and Awards

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  • Dr. Pechuho inaugurates national cervical cancer vaccination campaign

    Dr. Pechuho inaugurates national cervical cancer vaccination campaign

    – Advertisement –

    NAWABSHAH, Sep 05 (APP):Provincial Minister for Health and Population Welfare, Dr. Azra Fazal Pechuho, inaugurated the national cervical cancer vaccination campaign here on Friday.

    Deputy Commissioner Shaheed Benazirabad, Abdul Samad Nizamani was also present on the occasion.

    Speaking at the ceremony, Dr. Pechuho said that the Health Department is taking all possible steps to provide quality medical facilities to the public. She added that the cervical cancer prevention campaign will begin on September 15 across Shaheed Benazirabad district. Minister urged parents to fully cooperate with the health department and ensure their daughters receive the vaccine during this national drive.

    District Health Officer Dr. Asadullah Dahri informed that the national cervical cancer vaccination campaign will run from September 15 to 29.

    DHO said that during this period, around 166,000 girls aged 9 to 14 years will be vaccinated. He said that for the campaign, 126 vaccination teams and 86 supervisors have been deployed.

    He further noted that the provision of motorcycles and the mobile vaccination van by the provincial minister would greatly assist vaccinators in achieving the set target.

    On the occasion, Minister Pechuho distributed 50 motorcycles among district vaccinators and handed over a mobile vaccination van to the District Health Officer (DHO) for field vaccination.

    The event was also attended by Chairman District Council Ali Akbar Jamali, Dr. Allah Bux Rajpar, Dr. Riaz Shah, Dr. Amina Brohi, Dr. Aslam Pervez Dahri, District Education Officer Muhammad Saleem Bhatti, Sohrab Mari, and other officials of the Health Department.

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  • The World Is On the Verge of Wiping Out Polio — So Why Did Germany Cut Funding Now?

    The World Is On the Verge of Wiping Out Polio — So Why Did Germany Cut Funding Now?

    The world is close to wiping out polio, and that in itself is close to miraculous. Of the thousands of diseases that afflict humans, only one, smallpox, has ever been eradicated before.

    But despite tremendous progress, polio isn’t going down without a fight. Budget cuts, vaccination gaps, and difficulties reaching hard-to-access communities keep pushing the finish line further back. As cases creep upward, virus strains have re-emerged in countries that were long ago declared polio free — including Germany.

    What makes that even more worrying? Germany is one of the latest countries to cut down its international aid budget, planning to trim €17 million from polio vaccination efforts alone in 2025 and 2026. These financial shortfalls could end up accelerating polio’s spread, ushering in a future where resurgences become the norm.

    We spoke with the World Health Organization (WHO) to find out exactly how Germany’s budget cuts could spell future trouble for all of global health.

    But First — What Exactly Is Polio? 

    Poliomyelitis, or polio, is a highly infectious virus that spreads mainly through contaminated water and food, mostly striking children under five. It usually settles in the gut but can eventually attack the central nervous system. Its symptoms are brutal, ranging from fever, headaches, and vomiting, to irreversible paralysis in about 1 of every 200 infections. In the worst cases it can even paralyze breathing muscles, causing suffocation. In fact, a horrific outbreak of polio in Copenhagen in 1952 prompted doctors to create the first ‘iron lung’ — a precursor to today’s hospital intensive care units (ICUs). 

    Before vaccines entered the picture in the 1960s, there were more than 600,000 cases recorded worldwide each year. There’s still no cure — but it can be prevented, which is partially why global health advocates set their sights on the goal of eradicating it entirely.

    As Dr. Shahin Huseynov, Regional Advisor at the WHO Regional Office for Europe, explained, “The chance of success in eradicating polio is unique.” While the virus is incredibly contagious, unlike coronaviruses or monkeypox, it can’t infect animals — eliminating a loop of cross-contamination and putting victory within reach.

    How the World United to Fight Back

    In 1988, the Global Polio Eradication Initiative (GPEI) launched as a partnership between major global health heavy-hitters like WHO, UNICEF, the US Center for Disease Control, the Gates Foundation, Rotary International, Gavi, and others. With two powerful vaccines introduced — the cheap, accessible oral polio vaccine (OPV) delivered by drops, and the highly effective injectable inactivated polio vaccine (IPV) — global immunization campaigns began, driving infections down by 99%.

    In the 1980s, wild poliovirus paralyzed about 1,000 children daily. But by 2021, cases had dwindled to single digits. “To date, 20 million cases of paralysis have been prevented — one of humanity’s greatest achievements in global health. The eradication of the second disease in history after smallpox seems within reach,” said Dr. Huseynov.

    In wealthy nations with strong healthcare systems and widespread vaccination resources, fears of polio have largely become a relic of history. Germany, for instance, saw its last case of wild polio decades ago in 1990.

    So How Has Polio Stuck Around? 

    Total eradication requires closing every elusive immunization gap worldwide at once — a daunting task. At-risk communities face a litany of obstacles including faltering funding, conflict, weak infrastructure, misinformation, and slipping vaccination rates, leaving openings for the virus to proliferate.

    Still, GPEI has scored some major triumphs. India was declared polio-free in 2014, as well as the entire African continent in 2020. And as Dr. Huseynov emphasized: “The polio program is more than just a vaccination program. It strengthens local health systems and achieves success even in crisis areas.”

    “GPEI health workers have provided the infrastructure for COVID-19 vaccination campaigns, fought Ebola outbreaks, taken malaria prevention measures, and continuously improved disease surveillance. Even in the recent conflict in the Gaza Strip, a humanitarian pause allowed children to be vaccinated — a measure that was only possible thanks to the existing infrastructure of the polio program.”

    Yet challenges remain. Wild polio is still endemic in Afghanistan and Pakistan, where political instability, misinformation, and rural inaccessibility fuel setbacks. COVID-19 also paid polio a huge favor by disrupting global childhood immunization campaigns. “If the international community fails now, the virus will return. Models predict 200,000 children will be paralyzed each year if this happens, including in Europe,” added Dr. Huseynov.

    If that happens, decades of effort and billions of dollars will have been effectively wasted. 

    How Polio Bounces Back 

    Another chilling complication? Variant, or vaccine-derived poliovirus (VDPV). Though rare, this emerges when weakened strains from the OPV are able to spread and end up mutating and strengthening, threatening unvaccinated communities and immunocompromised individuals. In 2024, variants of poliovirus were found in 38 countries worldwide, including Palestine and Yemen. Since 2022, VDPV has been found everywhere from Jerusalem, London, Finland, Spain, Poland, and New York City — where an unvaccinated young man subsequently developed polio, leaving him paralyzed.

    And as Dr. Huseynov warned, Germany has also found VDPV in wastewater across major cities since late 2024, including Munich, Berlin, Bonn, Cologne, Hamburg, Dresden, Düsseldorf, Stuttgart, and Mainz. “This is an alarming signal. It highlights the fact that even in Germany and other high-income countries of Europe, there is a risk of infection for people who are not adequately protected against the virus. Combating the disease at its source is therefore crucial also for the protection of public health in Germany.”

    The Cost of Cutting Budgets

    Currently, polio eradication campaigns are like a game of whack-a-mole — but to finish the job, every outbreak everywhere must be stopped, all at once. That requires steady international coordination, along with harmonious synchronization of vaccine supply, access, political will, public demand, and crucially, funding to back it all up.

    GPEI relies primarily on governments and NGOs for its financial support. Dr. Huseynov explained, “Significant reductions to the GPEI’s budget mean certain activities, like disease surveillance and critical immunity building, may not be able to continue everywhere… Not least, the withdrawal of the US from key areas of global health financing once again highlights that multilateral solutions are more important than ever.”

    Germany is GPEI’s historic third-largest donor. Since its founding, it has donated €854 million — proportionally, this means Germany has helped GPEI immunize 123 million children and avert 824,000 cases of paralysis since 1988. At the 2022 World Health Summit in Berlin, it pledged €72 million over 2022–2026. But now it’s looking to cut €17 million over the next two years — nearly half its commitment for that time frame. “These cuts not only send the wrong signal to other countries, but also jeopardize the successes achieved by GPEI.” Based on previous calculations, this cut could result in 2.6 million fewer vaccinated children around 17,700 children at risk of lifelong paralysis. 

    Dr. Huseynov also explained that Germany’s funding isn’t earmarked for any specific region or program, making its contribution extra impactful as it gives GPEI flexibility to direct resources where they’re needed most. With less to work with, campaigns could face delays and difficult trade-offs. And left unchecked, viruses will inevitably spill across borders, creating the perfect conditions for a global health crisis to spiral. 

    New Donors on the Horizon?

    GPEI’s endgame strategy requires $6.9 billion through 2029. While some wealthy nations are stepping back, others are stepping up: Pakistan is funding more of its own efforts through subsidized loans, Saudi Arabia pledged $500 million earlier this year, and the UAE funded a large-scale campaign after last year’s outbreak in Gaza.

    But fragile states facing outbreaks today like Afghanistan, Somalia, and Yemen still lack the resources to do the same. Without sustained commitments from long-standing donors like Germany, eradication will keep slipping out of reach — giving the virus time to evolve and spread as the world stumbles at the finish line.

    Near-Victory Isn’t Enough

    Eradicating polio for all is still possible — but viruses thrive amid negligence. Global health depends not just on scientific breakthroughs, but also simple human choices. Whether world leaders use the tools we have at hand, or fail to, determines health outcomes for all.

    Many in Germany and across the Global North have never experienced polio, making it easy to dismiss its gravity. But the stakes are generational. As Dr. Huseynov emphasized, “With prioritization of health security, Germany has a unique chance to regain a leadership role in the fight against polio and in safeguarding the health of Europe.”

    The finish line is in sight. Now is the time to double down, not pull back. Memories may be short — but the consequences of failing to act could last lifetimes.


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  • An animal sedative keeps turning up in opioid deaths – what you need to know about medetomidine

    An animal sedative keeps turning up in opioid deaths – what you need to know about medetomidine

    A dangerous new drug adulterant is spreading through America’s illicit opioid supply, and it’s making overdoses significantly harder to reverse. Medetomidine, a veterinary sedative normally used to sedate pets, is increasingly being mixed with heroin and fentanyl, creating a cocktail that experts warn could be far deadlier than previous street drug combinations.

    Known as “flysky” on the streets, this animal tranquilliser has already been linked to at least two overdose deaths in Pennsylvania and represents a troubling evolution in the continuing opioid crisis. Unlike traditional opioid overdoses, those involving medetomidine can’t be effectively treated with naloxone, the medication paramedics use to reverse overdoses.

    The emergence of medetomidine mirrors the earlier spread of xylazine, another veterinary sedative that earned the nickname “zombie drug” for its ability to cause severe, treatment-resistant skin wounds. The earliest confirmed detection of medetomidine as a street drug adulterant occurred in Maryland, where it was found in a synthetic opioid mixture probably containing fentanyl.

    From there, the drug spread rapidly. Traces appeared across multiple US states and into Canada, and by early 2024, medetomidine was linked to overdose clusters in Philadelphia and other locations, following the same geographical pattern that xylazine had taken years earlier.

    Unfortunately, opioid-overdose reversal drugs don’t work against veterinary tranquillisers.
    rblfmr/Shutterstock.com

    What makes medetomidine particularly concerning is its extraordinary potency. Medetomidine is an alpha-2 adrenergic receptor agonist – a type of drug that affects the nervous system. While approved only for veterinary use in the UK to sedate animals and provide pain relief for pets, experts estimate it may be 200 to 300 times more potent than xylazine when used as a drug adulterant.

    This extreme potency means that even tiny amounts can have devastating effects. Users experiencing medetomidine-laced drug overdoses typically display extreme drowsiness, muscle twitching, dangerously low heart rate and blood pressure, and laboured breathing.

    Chicago cases from 2024 revealed additional concerning symptoms: extremely high blood pressure, severe confusion and critically low blood oxygen levels – often dropping below 90%, a threshold that can cause organ damage.

    Perhaps most alarming is medetomidine’s resistance to naloxone, the opioid overdose-reversal drug that has saved countless lives. While naloxone can counteract heroin and fentanyl by blocking opioid receptors in the brain, medetomidine affects the body through entirely different pathways. This means there is no approved antidote for medetomidine poisoning, leaving healthcare professionals with limited options when treating overdoses involving this adulterant.

    The withdrawal process is equally tricky. Philadelphia health officials report that people withdrawing from medetomidine-laced drugs experience dangerous spikes in blood pressure and heart rate – symptoms severe enough to trigger a heart attack in some cases. Users also endure uncontrollable nausea and vomiting, intense anxiety, restlessness and violent shaking.

    Understanding why dealers add these veterinary drugs to street opioids requires examining the economics of the illicit drug trade. According to a 2022 DEA report, a kilogram of xylazine powder can be bought from Chinese suppliers for as little as U$6.00 (£4.44). This rock-bottom pricing allows drug traffickers to increase their profit margins significantly while making weak or diluted opioid batches feel more potent to users.

    These sedatives also serve as effective cutting agents (substances used to add bulk and weight to drugs without requiring expensive active ingredients). For dealers, it’s a win-win. They can stretch their supply while creating a product that feels stronger and lasts longer than pure opioids alone.

    Managing new drug adulterants like medetomidine presents unique difficulties for both medical professionals and law enforcement. The drugs make intoxication and withdrawal symptoms more severe and complicated, while also making it harder to identify which specific substance is causing particular symptoms in a patient.

    Medetomidine compounds these problems because it’s rapidly metabolised by the body, making it difficult to track the timing and duration of its effects. Additionally, these veterinary sedatives are not included in routine drug screenings or toxicology tests, meaning their presence often goes undetected by medical professionals and law enforcement, despite their potentially lethal effects.

    UK response

    While no cases of acute medetomidine toxicity have been published in the UK, the country has already experienced problems with xylazine, a similar veterinary sedative.

    British health authorities have detected xylazine in 35 cases through toxicology tests and drug seizures. Of 16 people found to have xylazine in their systems, 11 cases proved fatal – deaths that occurred primarily during May 2022 and August 2023.

    In response to the growing threat, the government has taken decisive action. Over 20 dangerous substances have been banned as part of efforts to combat synthetic drugs and improve public safety.

    Xylazine is now controlled as a class C substance, carrying penalties of up to two years in prison for possession and up to 14 years for production and supply.

    The government is also working to better equip police, healthcare workers and Border Force agents to tackle this evolving threat through improved training and detection capabilities.

    The case of medetomidine highlights a disturbing reality about modern drug policy: the illicit drug supply continues to change in unpredictable and dangerous ways. Neither medetomidine nor xylazine was developed for human consumption, and there are no human studies examining their drug interactions, lethal doses or safe reversal protocols.

    As these veterinary sedatives become more common in street drugs, the challenge for healthcare professionals continues to grow. Traditional overdose response protocols, built around reversing opioid effects with naloxone, become inadequate when faced with multi-drug combinations that affect the body through completely different mechanisms.




    Read more:
    ‘There has never been a more dangerous time to take drugs’: the rising global threat of nitazenes and synthetic opioids


    For users, families and communities already devastated by the opioid crisis, the emergence of medetomidine represents yet another layer of risk in an already dangerous landscape.

    As the drug supply becomes increasingly unpredictable, the need for comprehensive approaches to drug policy – encompassing everything from harm reduction to treatment access to law enforcement – becomes ever more urgent.

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  • WHO adds weight-loss, diabetes drugs to essential medicines list | World Health Organization News

    WHO adds weight-loss, diabetes drugs to essential medicines list | World Health Organization News

    UN agency urges production of affordable generics for GLP-1 drugs to treat obesity and diabetes in developing countries.

    The World Health Organization (WHO) has added a new set of drugs for obesity and diabetes to its essential medicines list, alongside treatments for cancer and cystic fibrosis.

    Cheap generic versions of the glucagon-like peptide-1 (GLP-1) drugs should also be made available for people in developing countries, the United Nations agency said in a statement on Friday.

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    The list, consisting of 523 medicines for adults and 374 for children, is a catalogue of the drugs the WHO believes should be available in all functioning health systems.

    “The new editions of essential medicines lists mark a significant step toward expanding access to new medicines with proven clinical benefits and with high potential for global public health impact,” said Yukiko Nakatani, WHO’s assistant director-general for Health Systems, Access and Data.

    The expert committee added the active ingredients in Novo Nordisk’s Ozempic and Eli Lilly’s Mounjaro to the list, to treat type 2 diabetes in conjunction with established cardiovascular disease, chronic kidney disease or obesity.

    The medicines were initially developed for diabetes, and have become wildly popular as weight-loss drugs, too, under different brand names. But the WHO stopped short of adding them to treat obesity alone, as it also did in 2023.

    The committee said this decision provided clear guidance on which patients would most benefit from the therapies.

    “High prices of medicines like semaglutide and tirzepatide are limiting access to these medicines,” the WHO statement added, saying that encouraging generic drugmakers to produce the product would also help when patents begin to expire on the drugs next year.

    Other additions

    According to the WHO, more than 800 million people around the world were living with diabetes in 2022, while more than one billion people are affected by obesity.

    Earlier this year, the organisation announced plans to recommend the use of medications for obesity, which is separate from their inclusion on the essential medicines list.

    WHO data shows that, in 2021, more than 3.7 million people died from conditions linked to being overweight or obese – a number that exceeds the combined deaths from malaria, tuberculosis and HIV.

    The list also includes Vertex Pharmaceuticals’ combination therapy for cystic fibrosis, Trikafta or Kaftrio. Activists have criticised its high price and lack of accessibility for years.

    WHO’s list also includes Merck’s top-selling cancer immunotherapy drug, Keytruda, for the treatment of cervical cancers, colorectal cancers, and non-small cell lung cancers that have spread, or metastasised. The agency also recommended strategies to increase access to this drug.

    The WHO further added rapid-acting insulin analogues, also made by Novo Nordisk and Eli Lilly, among others, to the list for treating type 1, type 2 and gestational diabetes.


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  • Viral: Chinese café that sells coffee at -86 degrees Celsius has netizens in shock

    Viral: Chinese café that sells coffee at -86 degrees Celsius has netizens in shock

    Image credits: Instagram/shufofood

    Hot and cold coffee have been fan favourites for decades. But have you ever heard of freezing cold coffee? Not yet? Well, it’s time.Recently, a Chinese digital creator and food vlogger Shufosho shared a video on Instagram, sharing with viewers a glimpse at an extraordinary coffee drink. “I got this coffee in China, served in a -86 degree glass. It was created as a way to make iced lattes without ice,” he said in the clip.

    How is the freezing cold coffee made?

    How is the freezing cold coffee made?

    Image credits: Instagram/ shufofood

    The staff takes a frozen cup from a -86 degree Celsius freezer, pours milk into the frosty cup and then tops it up with rich, aromatic coffee. Since the cup consists of frost, it doesn’t need extra ice.“Because melting ice dilutes the flavour, the owner recommended drinking it in big gulps without stirring, immediately after it’s made. This way, the hot espresso and super-cold milk create a contrasting taste – kind of like ice cream on a warm apple pie,” revealed the vlogger.The name of the café was Luna Café at 24 Fanghua Street, Chengdu, China. The video about their unique coffee service has received 120K likes and numerous comments from curious netizens.

    Netizens react to the freezing coffee

    People on the internet have been amazed by the extraordinary recipe shown in the reel. Many took to the comments to share their reactions, wanting to try the coffee.“Someone in the USA recreate this so I can have it for 100 dollars yay,” wrote one.Others were wondering about the science associated with the recipe, writing, “I’m surprised that pouring boiling hot water into these does not crack them” and “Wouldn’t the jar explode?”“Wouldn’t your fingers getting freezed touching the cold cup?” pondered another.“Don’t forget to peel off ur lips afterwards 😂,” quipped another.


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  • Fine Particulate Matter Exposure Tied to Lewy Body Dementia

    Fine Particulate Matter Exposure Tied to Lewy Body Dementia

    A team of researchers at Johns Hopkins Medicine say they have revealed a possible molecular connection between air pollution and an increased risk of developing Lewy body dementia.

    The findings add to a growing body of evidence indicating how environmental factors may trigger harmful protein changes in the brain that lead to neurodegeneration.

    Lewy body diseases are a group of neurodegenerative disorders marked by the abnormal buildup of a protein, alpha-synuclein, in the brain. These clumps, known as Lewy bodies, are a hallmark of the conditions Parkinson’s disease and Lewy body dementia.

    The study, published in Science September 4, builds on a decade of research linking exposure to fine particulate air pollution (PM2.5) — tiny particles from industrial activity, residential burning, wildfires and vehicle exhaust — to a higher risk of developing these diseases, says lead investigator Xiaobo Mao, Ph.D., associate professor of neurology at the Johns Hopkins University School of Medicine and a member of the Johns Hopkins Institute for Cell Engineering.

    In their new work, Mao’s team discovered that exposing mice to PM2.5 triggered the formation of abnormal alpha-synuclein clumps. These toxic protein clusters shared key structural and disease-related features with those found in the brains of patients with Lewy body dementia.

    “We have identified a novel strain of Lewy bodies formed after exposure to air pollution,” Mao says. “By defining this strain, we hope to establish a specific target for future drugs aimed at slowing the progression of neurodegenerative diseases marked by Lewy bodies.”

    The research began with an analysis of hospital data from 56.5 million U.S. patients admitted between 2000 and 2014 with neurodegenerative diseases. The team focused on patients hospitalized for the first time with Lewy body-related conditions and used data from their ZIP codes to estimate their long-term exposure to PM2.5. The scientists found that each interquartile range increase in PM2.5 concentration in these ZIP code areas resulted in a 17% higher risk of Parkinson’s disease dementia and a 12% higher risk of dementia with Lewy bodies.

    “The statistical association we uncovered is even stronger than what previous studies found when lumping all Alzheimer’s and related dementias together — highlighting Lewy body formation as a potentially pivotal pathway that warrants deeper biological investigation,” says Xiao Wu, Ph.D., a co-first and co-corresponding author of the study and assistant professor of biostatistics at Columbia University Mailman School of Public Health. “We hope to inspire researchers to conduct both epidemiologic and molecular studies that focus on dementia subtypes linked to Lewy bodies.”

    Exploring the biological reason for this association between exposure to PM2.5 and Lewy body dementia, Mao’s team of researchers exposed both normal mice and genetically modified mice lacking the alpha-synuclein protein to PM2.5 pollution every other day for a period of 10 months.

    “In normal mice, we saw brain atrophy, cell death and cognitive decline — symptoms similar to those in Lewy body dementia,” says study collaborator Ted Dawson, M.D., Ph.D., the Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases and director of the Institute for Cell Engineering. “But in mice lacking alpha-synuclein, the brain didn’t exhibit any significant changes.”

    The researchers then studied mice with a human gene mutation (hA53T) linked to early-onset Parkinson’s disease. After five months of PM2.5 exposure, these mice developed widespread pockets of alpha-synuclein and experienced cognitive decline. Observed through biophysical and biochemical analysis, these protein clumps were structurally distinct from those that form during natural aging.

    The researchers also set out to determine whether air pollution effects varied by location. They found that mice exposed to separate samples of PM2.5 from China, Europe and the United States led to similar brain changes and development of alpha-synuclein pockets.

    “This suggests that the harmful effects of PM2.5 may be broadly consistent across different regions,” says Haiqing Liu, Ph.D., first author of the study and postdoctoral fellow at Johns Hopkins University School of Medicine.

    The researchers say changes in gene expression in the brains of PM2.5-exposed mice were strikingly similar to those found in human patients with Lewy body dementia.

    “This suggests that pollution may not only trigger the build-up of toxic proteins but also drive disease-related gene expression changes in the human brain,” says Shizhong Han, Ph.D., lead investigator at the Lieber Institute and for Brain Development and an associate professor of psychiatry and behavioral sciences at the school of medicine.

    “We believe we’ve identified a core molecular link between PM2.5 exposure and the propagation of Lewy body dementia,” Mao says.

    While genetic factors play a significant role in neurodegenerative disease, the researchers say people can potentially control their exposure to pollution.

    “Our next goal is to figure out which specific components in air pollution are driving these effects,” says Xiaodi Zhang, Ph.D., a first author of the study and postdoctoral fellow at the school of medicine. “Understanding that could help guide public health efforts to reduce harmful exposures and lower the risk of disease.”

    Reference: Zhang X, Liu H, Wu X, et al. Lewy body dementia promotion by air pollutants. Science. 2025;389(6764):eadu4132. doi: 10.1126/science.adu4132

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