Just when you thought cold-season sniffles were par for the course — think again. This year, health experts are sounding the alarm about a mutated flu strain…
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Global CKD Burden Nearly Doubles Since 1990, Reaching 788 Million Adults Worldwide
Chronic kidney disease (CKD) has emerged as one of the fastest-growing noncommunicable diseases worldwide, according to new estimates from the Global Burden of Disease Study 2023.1The analysis, published in
The Lancet , reports that 788 million…Continue Reading
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‘I’ll stick up for you’: key moments from the cordial Trump-Mamdani meeting | Donald Trump
1. Trump and Mamdani <3 New York
The president likes a winner and he loves New York – and both were clear on Friday, when he extolled Mamdani for running an “incredible race” against some “very tough people”.
“We have one thing in…
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Will Trump’s no-show eclipse South Africa’s moment?
Mayeni JonesAfrica correspondent, Johannesburg
Gallo Images via Getty ImagesSouth Africa held a “social summit” ahead of the main event, in a bid to involve civil society voices in the G20’s decisions When it assumed the presidency of the G20 last…
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PM for unified industrial policy framework
ISLAMABAD:Prime Minister Shehbaz Sharif on Friday directed the relevant…
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New Proteomic Analysis Maps Cytokine Signatures Driving IPF
A new proteomic analysis is shedding a fresh light on the cytokine networks fueling idiopathic
pulmonary fibrosis (IPF), identifying a set of differentially expressed signaling proteins and potential drug targets that may help reshape future therapeutic strategies for one of the most challenging interstitial lung diseases (ILDs) to treat.The integrative proteomic study provides one of the most comprehensive views to date of cytokine abnormalities in IPF. By defining core signaling hubs, immune-cell associations, and potential therapeutic targets, the research offers new molecular signposts for drug development—an urgent need for a disease that remains fatal for most patients despite current treatments.
“While pirfenidone and nintedanib (the only antifibrotic drugs currently approved for treating IPF) can slow lung function decline, their efficacy in halting pulmonary fibrosis progression and enhancing patients’ quality of life remains limited,” wrote the researchers. “Additionally, there are concerns regarding drug resistance and adverse effects. Therefore, safe and effective pharmacological agents are urgently needed.”
The new findings, generated from cytokine profiling of lung tissue and supported by bioinformatics, single-cell sequencing, and drug–gene interaction mapping, offer a high-resolution look into the molecular dysregulation underlying fibrosis.
IPF is defined by relentless scarring of lung tissue, eventual respiratory failure, and a median survival
between 3 and 5 years .2 Although decades of research have highlighted roles for transforming growth factor-β (TGF-β) and other profibrotic mediators, no study until now has systematically examined hundreds of cytokines directly within human lung tissue. In the current work, detailed in Canadian Respiratory Journal, researchers collected explanted lungs from 5 individuals undergoing transplantation for IPF and compared them with donor control lungs. Using high-throughput protein microarrays capable of detecting 440 cytokines, the team constructed one of the most detailed IPF cytokine maps to date.The analysis identified 32 differentially expressed proteins (DEPs) between IPF and control lungs, with 11 upregulated and 21 downregulated. Many of these proteins have been previously associated with IPF development, including chemokines, matrix-remodeling enzymes, and receptors involved in immune signaling. The expression patterns were sufficiently distinct to separate IPF and control samples through principal component analysis, emphasizing that cytokine dysregulation is a defining molecular feature of the disease.
Functional enrichment analysis revealed that these DEPs were highly concentrated in pathways associated with cell chemotaxis, growth factor binding, PI3K–Akt signaling, MAPK signaling, and cytokine–receptor interactions—all known contributors to fibroblast activation, epithelial injury, and extracellular matrix accumulation. Additional gene-set enrichment analysis performed across all 440 measured cytokines highlighted enrichment of biological processes tied to peptide hormone signaling, nitrogen compound response, and insulin-response pathways, suggesting oversights in current models of IPF pathophysiology.
To understand how these DEPs organize into functional networks, the researchers generated a protein–protein interaction map using STRING and identified 5 hub proteins with high centrality scores: FGF2, HGF, HBEGF, ERBB3, and ANGPT2. These molecules act as central communication nodes in cytokine signaling and growth-factor pathways, and their dysregulation may represent core drivers of IPF progression. One hub protein, HGF, showed the strongest functional similarity to other hub proteins, implying it may be especially critical in the broader cytokine network.
The study also used transcription-factor prediction algorithms to map which upstream regulators may drive the expression of these hub proteins. Thirty-one transcription factors—including SP1, STAT3, HIF1A, and LMO2—emerged as potential regulatory controllers, underscoring the deep integration of cytokine signaling with inflammation, hypoxia, and wound-repair pathways.
Since IPF is strongly linked to immune dysregulation, the team analyzed immune-cell infiltration using the CIBERSORT algorithm. Among 22 immune-cell types examined, resting natural killer (NK) cells were significantly more abundant in IPF lung tissue and were inversely correlated with HBEGF expression. This relationship suggests an underexplored interface between NK-cell activity and cytokine-driven injury repair.
Recognizing the urgent need for new treatment strategies, investigators used the DGIdb database to explore whether the five hub proteins are targetable by existing drugs. The analysis surfaced 67 potential agents, 13 of which have prior evidence of antifibrotic or immunomodulatory effects. These include widely studied compounds such as sirolimus, imatinib, resveratrol, and atorvastatin, as well as chemotherapy agents used in patients with lung cancer and comorbid fibrosis. While these findings do not establish clinical efficacy, they highlight promising entry points for drug repurposing.
Hub-protein expression was further validated in 3 independent GEO datasets and through immunohistochemistry on IPF lung tissue. Finally, single-cell RNA sequencing revealed the specific cellular sources of these cytokines—fibroblasts, myofibroblasts, macrophages, epithelial cells, and specialized vascular endothelial populations—confirming that cytokine dysregulation in IPF arises from multiple interacting cell types, not a single dominant driver.
References
- Shen C, Wang W, Li G, et al. Cytokine expression profiling in idiopathic pulmonary fibrosis: insights from integrative proteomic analysis. Can Respir J. Published online November 7, 2025. doi:10.1155/carj/2272156
- Raghu G, Remy-Jardin M, Richeldi L, Thomson CC, Inoue Y, Johkoh T, et al. Idiopathic pulmonary fibrosis (an update) and progressive pulmonary fibrosis in adults: an official ATS/ERS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med 2022;205:e18–e47.
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Move over fillers – people are getting facial injections derived from fish sperm
Ruth CleggHealth and Wellbeing reporter
BBCIn my many years as a journalist, I never thought I would be asking someone how it feels to have trout sperm injected into their face.
And yet, here I am.
Abby Warnes is lying on a large, black padded chair at a small aesthetics clinic in south Manchester.
She winces as a small cannula is delicately inserted into her cheek.
“Ouch. Ouch,” she exclaims.
I should make it clear that 29-year-old Abby is not actually receiving a pure dose of trout sperm.
The lower part of her face is being injected with tiny fragments of DNA, known as polynucleotides, which have been extracted from either trout or salmon sperm.
Why? Well, interestingly, our DNA is pretty similar to that of a fish.
So the hope is Abby’s body will not only welcome these tiny strands of fish DNA, her skin cells will be spurred into action, producing more collagen and elastin, two proteins which are vital for maintaining the structural integrity of our skin.
For Abby, the aim is to freshen her skin, keep it healthy, and hopefully, treat the acne she’s lived with for many years by reducing scarring and redness.
“I just want to target those problem areas,” she explains.
Abby is having injections in her lower face to help rejuvenate her skin and tackle “problem areas” Polynucleotides are being touted as the next big skincare “miracle” and are rapidly gaining popularity after a number of celebrities have spoken candidly about their “salmon sperm facials”.
Earlier this year, Charli XCX told her nine million Instagram followers that she felt “fillers are kind of over now”, and explained she had moved onto polynucleotides, which are “kinda like deep vitamins”.
Kim and Khloe Kardashian are also reportedly avid fans. And when asked about her skincare routine on a recent episode of Jimmy Kimmel Live, Jennifer Aniston responded: “Don’t I have beautiful salmon skin?”
EPA-EFE/REX/ShutterstockCharli XCX says she uses polynucleotides which are “kinda like” injectable vitamins for the skin So, despite their fishy beginnings, are polynucleotides transforming skincare?
“We are having a Benjamin Button moment,” Suzanne Mansfield, who works for aesthetics company Dermafocus, tells me.
That’s a reference to the 2008 film The Curious Case of Benjamin Button, where Brad Pitt plays a man who ages backwards. By the time he’s in his later years, he has the skin of a baby’s bottom.
While such an effect is highly unlikely and would probably be a tad disconcerting, Ms Mansfield says polynucleotides are forging the way when it comes to regenerative skincare.
A small but growing body of research and clinical trials suggest that injecting polynucleotides can rejuvenate skin, not only making it healthier but potentially reducing fine lines, wrinkles and scars.
“All we are doing, by using it in the aesthetics industry,” she says, “is enhancing something the body already does. That’s why these are so special.”
But they also come with a pretty hefty price tag.
A single session of polynucleotide injections can cost anywhere from £200 to £500 – and it’s recommended you have three of these over several weeks.
After that clinics tend to advise you need to top up every six to nine months to maintain the look.
Back at the clinic, Abby’s treatment is almost finished.
“Just one area left,” Helena Dunk, the aesthetic nurse practitioner who owns the clinic, Skin HD, reassures her.
She says polynucleotides have massively increased in popularity over the past 18 months.
“Half my clients really notice a huge difference – their skin feels more hydrated, healthier, younger – while the other half don’t see such a big change. But their skin does tend to feel tighter and fresher.”
Abby has already had the area under her eyes injected as part of a three-course treatment at the clinic – and she’s really pleased with the results.
She received lots of tiny injections of polynucleotides, which was a “pretty painful procedure”, but says it’s helped reduce the dark circles under her eyes.
Charlotte BickleyCharlotte says she has been left with black rings under her eyes after being injected with polynucleotides before her wedding While a growing number of studies consider it a safe and effective treatment, it is still relatively new and some experts warn the hype may be outpacing the science.
Consultant dermatologist Dr John Pagliaro, based in Brisbane, Australia, says that while we know that nucleotides play an important role in our bodies – they are the building blocks of our DNA for a start – he questions whether “injecting salmon DNA, cut into little pieces” into our faces is going to work as well as our own nucleotides.
“We do not have good, strong data,” he says. “As a medical specialist, I would want to see at least a few more years of big, credible studies showing safety and efficacy before I started using them in my practice. We’re just not there yet.”
Charlotte Bickley describes her foray into the world of polynucleotides as “salmon-gate”.
The 31-year-old from New York had the treatment last year as part of her “wedding glow up”, shortly before she was due to get married.
But Charlotte ended up with a skin infection, inflammation and darker rings under her eyes than before she had the treatment.
“I got the complete opposite of what I wanted,” she says. “I trusted that doctor, but he’s left me scarred.”
Charlotte believes she was injected too deeply under her eyes, causing a negative reaction. There can be side effects – such as redness, swelling and bruising but these tend to be temporary.
In some cases, people can have an allergic reaction, or, if polynucleotides are not injected properly, there are longer term risks, such as skin pigmentation and infections.
Polynucleotides are widely used across the UK. They are registered as medical devices with the Medicines Health and Regulatory Authority (MHRA) but they are not regulated like medicines.
They have not been approved by the UK’s equivalent in the US, the Food and Drug Administration (FDA).
“I just keep thinking, ‘Why did I go through with it?’” Charlotte says. “When something goes wrong on my face I hyperfixate on it.”
She’s paid thousands in medical bills to try to rectify the situation, but 10 months on, there’s still some scarring below her eyes.
“I would never have salmon DNA injected into my face again,” Charlotte says, “ever.”
Ashton Collins, director of Save Face, an organisation which campaigns for better regulation of the cosmetic industry and who runs a government-approved register of clinics in the UK, says polynucleotides are generally considered a safe treatment when administered by a medically-trained professional and the brand of polynucleotides used is from a reputable company.
“But, we are now seeing products coming onto the market that haven’t been tested properly, that’s the worry,” she says.
Dr Sophie Shotter, president of the British College of Aesthetic Medicine, agrees.
“Due to the lack of regulation, anyone can use products that have not been robustly tested. It is a real issue.”
In her opinion, are polynucleotides effective though?
“I have them on my shelf, in my toolbox. I definitely offer them to clients, who want a natural look and want to potentially invest long-term,” Dr Shotter says.
“Polynucleotides as a treatment is not the panacea. There are plenty of other treatments out there that can do similar, and have more data behind them.”
There is no one treatment that will work for everyone, she adds.
“We all respond differently to different things, and that is not always predictable.”
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Worm experiments expose hidden health risks of deep space travel
When scientists first sent microscopic worms into orbit in 2018, they hoped to answer a question that has shaped every discussion about long missions. What really happens to your body when gravity no longer pulls at your muscles and bones?
You…
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When loss strikes twice: Health shocks and household financial distress
Financial distress affects roughly one in five adults in OECD countries (OECD 2024). It constrains access to credit, impairs labour market outcomes, and makes the economy less resilient to macroeconomic shocks (Dobbie et al. 2020, Bos et al. 2018, Maturana and Nickerson 2020, Kaur et al. 2025, Mustre-del-Río et al. 2025).
While prior studies have examined the role of individual characteristics and abilities in shaping financial distress (Parise and Peijnenburg 2019, Keys et al. 2023), less is known about how health shocks – especially fatal ones – trigger financial instability.
To address this gap, we examine the financial consequences of a spouse’s illness or death, using data from Sweden (Majlesi et al. 2025). We use population-wide administrative data, linking detailed health and mortality records with information on all unpaid financial claims handled by the Swedish Enforcement Authority. This captures both households with and without access to formal credit markets. Because Sweden’s universal healthcare limits out-of-pocket medical costs and strategic default is rare, these records provide an unusually precise measure of genuine financial distress.
When tragedy triggers financial strain
We compare households that experience a severe health shock to otherwise similar households that experience the same event a few years later. This quasi-experimental design isolates the causal effect of the health shock on financial well-being.
The results are striking. The death of a spouse raises the likelihood of default on financial claims by about 20%, with effects persisting for several years (Figure 1). Spouses exposed to a fatal health shock are nearly 1 percentage point more likely to receive a debt claim within four years – a 56% increase from baseline – showing that more individuals continue to fall into financial distress over time.
Defaults are not driven by forgetfulness or grief: small debts are repaid promptly, while large debts (over roughly $1,000) often enter debt collection. These findings point to liquidity constraints rather than inattention as the key mechanism.
Even among financially stable households with no prior defaults, the incidence of unpaid bills rises sharply after a spouse’s death. The shock effectively pushes many previously solvent households into financial trouble.
Figure 1 Dynamic effects of a fatal health shock on the probability of receiving a claim from the Swedish Enforcement Authority
Note: This figure shows the estimated effect of a fatal health shock on the probability of receiving a claim from the Swedish Enforcement Authority. Estimates are obtained using the difference-in-differences method of Callaway and Sant’Anna (2021). The figure reports coefficient estimates with 95% confidence intervals, along with the average treatment effect on the treated (ATT) and the effect in percentage terms relative to the mean one year before the event. Standard errors are clustered at the household level.
Housing wealth as self-insurance
Income losses following a spouse’s death are substantial: households’ disposable income falls by about 50%. But the ability to draw on housing wealth determines who can cope. Homeowners generally avoid defaults by liquidating their homes, whereas renters face a higher risk of entering debt collection (Figure 2).
Figure 2 Dynamic effect of a fatal health shock on the probability of entering collection for a large debt
Note: This figure displays the dynamic treatment effects of a fatal health shock on the likelihood of facing collection for a large debt, estimated separately for renters and homeowners. Estimates are obtained using the difference-in-differences method of Callaway and Sant’Anna (2021). The figure reports coefficient estimates with 95% confidence intervals, along with the average treatment effect on the treated (ATT) and the effect in percentage terms relative to the mean one year before the event. Standard errors are clustered at the household level.
Although the loss of a spouse can also take a toll on mental health, this does not explain the financial divide. Both homeowners and renters experience similar increases in prescriptions for antidepressants and diagnoses of mental disorders after the event. These differences are not observed when comparing households with different incomes, suggesting that wealth, rather than income alone, provides a financial buffer.
Intergenerational echoes
The financial repercussions extend beyond the immediate household. Adult children of survivors also experience higher financial stress, particularly when the surviving parent suffered a large income loss and lacked home equity (Figure 3). For this group, the probability of entering debt collection rises by about 10%, and reliance on social benefits increases markedly. All children reduce labour earnings following these shocks, but those with vulnerable parents are less able to cope.
These intergenerational effects suggest that when parents cannot self-insure, financial distress cascades down family lines, either because children step in to support parents or because parental assistance dries up.
Figure 3 The effect of a fatal health shock on adult children, by income loss and homeownership status of the surviving spouse
Note: This figure presents estimates of the effect of a fatal health shock on adult children, by the homeownership status and income loss of the surviving parent. Panels A–D correspond to children of renters or homeowners, further distinguished by whether the deceased parent was the primary earner (smaller income loss) or the secondary earner (larger income loss). Effects on debt collection, social benefits, and labour income are estimated with 95% confidence intervals using the Callaway–Sant’Anna (2021) difference-in-differences method, controlling for 10-year age bins of the children. The reported coefficients are expressed as percentage impacts relative to the mean outcome one year prior to the event. Standard errors are clustered at the parent level.
Beyond death: Non-fatal health shocks
Severe but non-fatal health shocks, such as heart attacks, strokes, or injuries, also raise the risk of default, though by a smaller margin (around 9%). The mechanism differs: income losses are smaller and more temporary, and both homeowners and renters face increased risk of debt collection, unlike after fatal shocks where housing wealth provides protection.
These findings are consistent with the idea that housing is a ‘consumption commitment’, which is costly to adjust when shocks are temporary (Chetty and Szeidl 2007).
Policy implications
Our findings have two key implications.
- Housing equity acts as self-insurance, mainly for permanent shocks. Households use housing wealth to cushion permanent income losses, such as after a spouse’s death, but home equity is less protective for temporary shocks, consistent with housing as a consumption commitment. For homeowners, formal insurance is therefore more welfare-improving for short-term risks, when selling a home is too costly.
- Survivor benefits should target the asset-poor. Increasing survivor pensions for renters could prevent long-term and intergenerational hardship by helping them better withstand permanent income losses.
Concluding thoughts
Health shocks expose the limits of even generous welfare systems. When one partner dies or falls ill, many families ‘lose twice’ – first emotionally, then financially. Our results underscore the need to evaluate household insurance in terms of both income and wealth access.
As ageing populations strain public insurance systems, understanding how families self-insure – through housing, savings, and intergenerational transfers – will be central to strengthening financial resilience to life’s most severe shocks.
References
Bos, M, E Breza, and A Liberman (2018), “The labor market effects of credit market information”, The Review of Financial Studies 31(6): 2005–37.
Callaway, B, and P H Sant’Anna (2021), “Difference-in-differences with multiple time periods”, Journal of Econometrics 225(2): 200–230.
Chetty, R, and A Szeidl (2007), “Consumption commitments and risk preferences”, The Quarterly Journal of Economics 122(2): 831–77.
Dobbie, W, P Goldsmith-Pinkham, N Mahoney, and J Song (2020), “Bad credit, no problem? Credit and labor market consequences of bad credit reports”, The Journal of Finance 75(5): 2377–419.
Kaur, S, S Mullainathan, S Oh, and F Schilbach (2025), “Do financial concerns make workers less productive?”, Quarterly Journal of Economics 140(1): 635–89.
Majlesi, K, E Molin, and P Roth (2025), “Severe health shocks and financial well-being”.
Keys, B J, N Mahoney, and H Yang (2023), “What determines consumer financial distress? Place-and person-based factors”, The Review of Financial Studies 36(1): 42–69.
Maturana, G, and J Nickerson (2020), “Real effects of workers’ financial distress: Evidence from teacher spillovers”, Journal of Financial Economics 136: 137–51.
Mustre-del-Río, J, J M Sánchez, R Mather, and K Athreya (2025), “The effects of macroeconomic shocks: Household financial distress matters”, The Review of Financial Studies 38(2): 564–604.
OECD (2024), How’s life? 2024: Well-being and resilience in times of crisis, OECD Publishing.
Parise, G, and K Peijnenburg (2019), “Noncognitive abilities and financial distress: Evidence from a representative household panel”, The Review of Financial Studies 32(10): 3884–919.
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Google denies ‘misleading’ reports of Gmail using your emails to train AI
Google is pushing back on viral social media posts and articles like this one by Malwarebytes, claiming Google has changed its policy to use your Gmail messages and attachments to train AI models, and the only way to opt out is by disabling…
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