Category: Dermatology

Categories : DermatologyTags :

New Research Sheds Light on Why Atopic Dermatitis So Often Begins in Childhood

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A team of researchers at the Icahn School of Medicine at Mount Sinai, Weill Cornell Medicine, and other institutions have uncovered a key biological explanation for why atopic dermatitis (eczema) so often starts in childhood. The study, in young mice, found that some types of immune cells in early-life skin are more reactive than those in adults, a difference that may help explain why children are more vulnerable to inflammation and allergic skin disease. 

The findings, reported in Nature, suggest that early childhood represents a critical window for immune-driven skin disease and may shed light on why atopic dermatitis is often the first condition in a broader pattern of allergic disease.

Atopic dermatitis (AD) affects nearly one in four children and often appears early in life. It can also precede other allergic conditions, including asthma and food allergies. Until now, scientists have not fully understood why the disease is so strongly linked to early childhood. 

“We found that allergy risk is shaped very early in life, when the skin’s immune system is biologically programmed to overreact to allergens, with important consequences for understanding how immune-mediated diseases emerge and should be treated,” says senior study author Shruti Naik, PhD, Associate Professor of Immunology and Immunotherapy, and Dermatology at the Icahn School of Medicine. “By pinpointing the cells and hormonal signals that control this window of vulnerability, we open the door to strategies that could prevent allergic disease before it spreads from the skin to the lungs, gut, and beyond.”  

The researchers discovered that a specific immune cell type, the dendritic cell, in young skin behaves differently than in adults. These cells do not overreact to everything – but when it comes to allergens, they respond faster and more strongly, setting the stage for inflammation and AD early in life. In adult skin, the same cells are far less reactive.  

To understand why allergies often start in early childhood, researchers exposed infant mice to everyday allergens such as dust mites and mould. Unlike adult mice, the infants developed strong skin inflammation, revealing a brief early-life period when the skin’s immune system is especially sensitive.  

The scientists traced this response to dendritic cells, which are unusually active shortly after birth and triggers allergic inflammation. When this pathway was blocked, the young mice did not develop skin allergies.  

The team also found that infants lack normal levels of stress hormones that later help keep immune reactions in check, allowing these allergic responses to take hold. Importantly, signs of the same immune activity were found in skin samples from children with early-onset AD, but not in adults, suggesting this early-life window may also be important in humans. 

“This work was only possible through a true clinic-to-lab collaboration – where insights from paediatric patients shaped the questions we asked in the lab,” says study co-author Emma Guttman-Yassky, MD, PhD, professor at the Icahn School of Medicine. “By studying allergic disease where it actually begins, in early life, and by modelling clinically relevant allergens and disease features, lead author Yue Xing, PhD, uncovered immune biology that simply doesn’t appear in adult models. By revealing what’s unique about the early-life immune system, this work explains why eczema so often begins in infancy.” 

Next, the investigators plan to explore ways to block this early-life immune pathway to stop allergic disease before it spreads from the skin to other organs.  

“Beyond eczema, this study reinforces a critical point for medicine,” says Dr Naik. “Children are not simply small adults when it comes to immunity. Their immune system follows a unique set of rules, and recognising that difference is essential for understanding – and ultimately preventing – allergic, immune-driven diseases that begin in childhood.” 

Source: Mount Sinai

Categories : Ageing DermatologyTags :

Why Grey Hair Happens – and How Science May Soon Turn Back the Clock

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From genetics to stress myths, researchers reveal what really drives greying and the breakthroughs pointing to natural colour restoration

Photo by Ravi Patel on Unsplash

Grey hair is more than a cosmetic concern – it drives a booming industry, influences how people are perceived, and can affect confidence. Globally, the hair colour market was valued at nearly USD 28 billion in 2025, with over half of purchases linked specifically to concealing greys. In South Africa, spending on hair colourants is projected to grow from roughly USD 172 million in 2021 to over USD 228 million by 2028, highlighting the demand for solutions that go beyond temporary cover-ups.

By age 50, roughly 50-70% of adults have visible grey hair, while premature greying can appear in some as early as the 20s. The psychological weight is clear: studies indicate grey hair can make people appear 20-30% older, influencing workplace perception, social interactions, and self-esteem. Studies show faces with grey hair are consistently perceived as more subdued than the same faces without greys, confirming that hair colour alone can shape social impressions.

“Many popular beliefs about greying hair are misleading,” says Dr Kashmal Kalan, Medical Director at Alvi Armani. “Stress does not turn hair grey overnight, plucking one strand won’t trigger several more, and no supplement or home remedy has been proven to restore pigment reliably. The reality is far more biological – genetics and pigment cell behaviour are the keys we are finally beginning to understand.”

At the heart of greying are melanocyte stem cells (McSCs) within hair follicles. In youth, these cells migrate and maintain melanin production, the pigment responsible for hair colour. With age, many become inactive or “trapped,” interrupting pigment delivery and causing grey strands. In mouse models, freeing these cells restored pigment production in roughly half of cases – a major step toward therapies that could reawaken natural colour without dyes.

Emerging research aims to tackle the root cause rather than just the appearance of grey hair. Scientists are exploring topical agents that target dormant pigment cells, metabolic modulators that influence follicle behaviour, and activation therapies designed to revive pigment production. These innovations could allow hair to regain its natural shade – not just cover it – while supporting overall follicle health.

“We are witnessing science that was once purely theoretical become reality,” says Dr Sunaina Paima, aesthetic and hair-restoration physician at Alvi Armani Johannesburg. “For patients, this could mean seeing grey strands regain their original shade naturally – a moment the hair science world has long dreamed of. The potential impact on confidence and self-esteem is enormous, because this isn’t just about covering colour, it’s about restoring it at a biological level.”

While most pigment-restoring therapies remain in development, advances in genetics, dermatology, and biotechnology are converging at unprecedented speed. “For decades, grey hair was seen as an irreversible hallmark of ageing,” adds Dr Kalan. “Today, that assumption is being seriously challenged. We’re on the brink of options that rejuvenate hair from the inside out, not just cosmetically.”

These breakthroughs signal a new era in hair science: ageing hair may no longer be inevitable or purely cosmetic, but a biological process that can be understood, guided, and ultimately restored.

Categories : DermatologyTags :

Copper Peptides: These Powerful Molecules are Worth the Skincare Hype

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Picture by Macrovector on Freepik

Ahmed Elbediwy, Kingston University and Nadine Wehida, Kingston University

Peptides have become one of the skincare industry’s most popular ingredients. It’s no wonder why, with evidence showing these powerful molecules hold the secret to healthier, firmer and more radiant skin.

But out of the many peptides that exist, one in particular has been gaining attention lately in the beauty industry: copper peptides.

It’s not surprising that copper peptides are garnering so much attention. This peptide is special because of its ability to multitask – with research showing that not only does it help make the skin firmer and more supple, it also protects the skin from damage.

The human body naturally produces many types of peptides. Each supports vital body functions, acting like tiny building blocks of life. Many help form the foundation of essential proteins – such as collagen and elastin, which help keep skin healthy and youthful.

The three main types of peptides in cosmetics are: carrier peptides, signal peptides and neurotransmitter-inhibiting peptides.

Carrier peptides aid in wound repair by physically transporting important minerals into the cells to initiate repair.

Signal peptides can prevent ageing by stimulating the activation of the skin’s fibroblasts – specialised skin cells that produce substances such as collagen, a protein which helps maintain the skin’s elasticity.

Neurotransmitter-inhibiting peptides act like botulinum toxin, relaxing facial muscles by blocking the signals that make them contract. This may reduce wrinkles.

Copper peptides are actually a type of carrier peptide. They’re produced naturally by your body. But as we age, the concentration of copper peptides in our bodies drops. Applying synthetic, lab-made versions – found in creams, serums and masks – can help replenish these molecules and help your skin.

Copper peptides were first discovered in 1973. Research found that these molecules aided wound healing, which is why the first commercialised carrier peptide in 1985 was designed to deliver copper into wounded tissue.

After gaining research attention for this role, further studies examined what other functions copper peptides had on the skin. Researchers found that they had anti-ageing, anti-inflammatory and renewing properties and also supported hair growth.

Copper peptides act as little helpers that tell your skin cells to repair and rebuild themselves. They do this by boosting collagen and elastin, key proteins that keep your skin feeling smooth and firm.

Copper peptides have been also found to reduce inflammation and calm skin redness, too. But perhaps most crucially, they have been found to act as antioxidants, fighting damage caused by pollution and the sun’s ultraviolet rays.

On top of that, copper peptides improve wound healing. This is why they’re often used after cosmetic treatments – such as face and neck lifts and micro-needling – that can damage the skin. Copper infused wound dressings are also used to help chronic wounds heal faster.

Overall, skin cell studies have shown that copper peptides increase collagen production, improve skin thickness and skin elasticity. Clinical trials and lab tests confirm these benefits, making copper peptides one of the most researched anti-ageing ingredients.

For best results, you might want to try applying it twice a day – first in the morning so it can act as a potent antioxidant, then in the evening so it can replenish collagen overnight.

Copper peptides can also penetrate the skin more effectively when delivered with microneedles, which makes them even more useful in advanced skincare products.

Copper peptides v other peptides

Other peptides do work well on the skin – such as palmitoyl-based peptides and acetyl hexapeptide-8 peptide – both of which fight wrinkles. But these both work differently to copper peptides.

Palmitoyl peptides signal the skin to make more collagen, while acetyl hexapeptide-8 relaxes facial muscles to reduce expression lines, acting like a less expensive version of botulinum toxin.

Copper peptides stand out among these other peptides because they can do the work of multiple peptides in one. Copper peptides boost collagen, improve skin healing and fight oxidative stress. This appears to make them better at preventing the signs of ageing.

Some skin cell studies show they work even better when combined with other well known skincare ingredients, such as hyaluronic acid (which boosts hydration).

However, some combinations of peptides can cause copper peptides to be unstable – making them fall apart. This could increase skin sensitivity, especially when combined with peptides, such as vitamin A and C.

Copper peptides themselves can also cause, in a few people, some skin irritation and mild allergic reactions. If you find you experience these symptoms after using copper peptides, stop use immediately.

Copper peptides are more than just a trend – they’re backed by science. They help keep skin healthy and speed up healing. They might even play a role in future cancer treatments.

Research has shown copper peptides turn on genes that tell damaged cancer cells to shut themselves down and stop replicating. They’ve also been shown to fix other genes that control cell growth and repair.

If you’re curious about skincare, copper peptides may be worth incorporating into your daily routine. Just remember that good, healthy skin also needs other measures – such as sunscreen, hydration and a healthy lifestyle.

Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Categories : Cancer DermatologyTags :

Research Finds Protein Behind Radiotherapy-induced Skin Damage

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The protein Dickkopf 3 plays a key role in the development of radiation-induced fibroses – and could be a promising target for novel therapies

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Radiotherapy is one of the main treatment forms for cancer. Among its most common side effects is skin damage, right up to chronic inflammations and fibroses. At present, such long-term damage can only be treated symptomatically and leads to thickened, painful, or sensitive skin for months to years after the radiation treatment. A team led by LMU immunologist Professor Peter Nelson (LMU University Hospital) and Roger Sandhoff and Peter E. Huber from the German Cancer Research Center (DKFZ) has identified a protein called Dickkopf 3 (DKK3) as a main cause of long-term skin damage after radiotherapy – a decisive step for the development of novel, more targeted therapy options.

The results were published in Signal Transduction and Targeted Therapy.

By investigating mouse models and human cells and tissue samples, the researchers demonstrated that DKK3 is activated after radiotherapy in a certain group of skin cells that are responsible for skin renewal. This activity triggers a chain reaction which promotes inflammations and the formation of scar-like tissue and leads to chronic skin damage. The key findings were driven by the work of LMU students, Li Li and Khuram Shehzad. Their efforts were essential in identifying DKK3 as the critical molecular mediator and in establishing the mechanistic framework presented in the paper. “We also observed similar processes in the kidney,” says Nelson. “This indicates that the activation of DKK3 is a fundamental mechanism that promotes fibrosis in various tissues.”

According to the researchers, these findings underscore that DKK3 represents a promising new treatment target. “Drugs that block DKK3 could one day help prevent or reduce long-term skin damage after radiotherapy and thus improve the quality of life of cancer patients and survivors,” says Nelson. The researchers are currently investigating, moreover, whether this approach could also contribute to the prevention of scar formation in other organs.

Source: Ludwig Maximilian University of Munich

Categories : Dermatology Injury & TraumaTags :

The Face Scars Less than the Body – New Study Explains Why

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The face is privileged when it comes to scarring after injury. A Stanford Medicine study in mice not only discovers why but also finds a drug that helps skin from other sites regenerate.

Tweaking a pattern of wound healing established millions of years ago may enable scar-free injury repair after surgery or trauma, Stanford Medicine researchers have found. If results from their study, which was conducted in mice, translate to humans, it may be possible to avoid or even treat the formation of scars anywhere on or within the body.

Scarring is more than a cosmetic problem. Scars can interfere with normal tissue function and cause chronic pain, disease and even death. It’s estimated that about 45% of deaths in the United States are due to some type of fibrosis – usually of vital organs like the lungs, liver or heart.

Scars on the skin’s surface, while rarely fatal, are stiffer and weaker than normal skin and they lack sweat glands or hair follicles, making it difficult to compensate for temperature changes.

Surgeons have known for decades that facial wounds heal with less scarring than injuries on other parts of the body. This phenomenon makes evolutionary sense: Rapid healing of body wounds prevents death from blood loss, infection or impaired mobility, but healing of the face requires that the skin maintain its ability to function well.

“The face is the prime real estate of the body,” said professor of surgery Michael Longaker, MD. “We need to see and hear and breathe and eat. In contrast, injuries on the body must heal quickly. The resulting scar may not look or function like normal tissue, but you will likely still survive to procreate.”

Exactly how this discrepancy happens has remained a mystery, although there were some clues.

“The face and scalp are developmentally unique,” said professor of surgery Derrick Wan, MD. “Tissue from the neck up is derived from a type of cell in the early embryo called a neural crest cell. In this study we identified specific healing pathways in scar-forming cells called fibroblasts that originate from the neural crest and found that they drive a more regenerative type of healing.”

Activating this pathway in even a subset of fibroblasts around small wounds on the abdomen or backs of mice caused them to heal with much less scarring – similar to untreated facial or scalp wounds.

Longaker, the Deane P. and Louise Mitchell Professor in the School of Medicine, and Wan, the Johnson & Johnson Distinguished Professor in Surgery II, are the senior authors of the study, which was published January 22 in Cell. Plastic surgery resident Michelle Griffin, MD, PhD, and clinical and postdoctoral scholar Dayan Li, MD, PhD, are the lead authors of the research.

“Many of the authors on this paper are fellow physician scientists,” said Li, who is board certified in dermatology. “This project was inspired by what we’ve observed in our patients – facial wounds in general heal with less scarring. We wanted to understand, mechanistically, why this is.”

Proteins determine scarring

Li and his colleagues used laboratory mice to investigate differences in wound healing at various sites on the animals’ bodies. They anesthetised the mice before creating small skin wounds on the face, scalp, back and abdomen. The wounds were stabilised by suturing small plastic rings around them to prevent differences in mechanical forces as the animals moved. Mice were given pain relief during the healing process.

After 14 days, the wounds on the face and scalp expressed lower levels of proteins known to be involved in scar formation as compared with those on the abdomen or back of the animals. The sizes of the scars were also smaller.

The researchers then transplanted skin from the face, scalp, back and abdomen of mice onto the backs of control mice. After the transplants had engrafted, they repeated the experiment on the transplanted skin. As before, wounds in the skin transplanted from the faces of the donor mice expressed lower levels of scarring-associated proteins.

Additionally, Li and his colleagues isolated fibroblasts from skin samples from the four body sites in the donor mice and injected them into the backs of control mice. They observed reduced levels of scarring-associated proteins on the recipient animals’ backs injected with fibroblasts from the donor animals’ faces as compared with fibroblasts from the scalp, back or abdomen.

Now that we understand this pathway and the implications of the differences among fibroblasts that arise from different types of stem cells, we may be able to improve wound healing after surgeries or trauma.”

–Derrick Wan

“We found you don’t need to change or manipulate all fibroblasts within the tissue to have a positive outcome,” Li said. “When we injected fibroblasts that we had genetically altered to more closely resemble facial fibroblasts, we saw that the back incisions healed very much like facial incisions, with reduced scarring, even when the transplanted fibroblasts made up only 10% to 15% of the total number of surrounding fibroblasts. Changing just a few cells can trigger a cascade of events that can cause big changes in healing.”

A less-fibrotic wound healing

Digging deeper, the researchers identified changes in gene expression between facial fibroblasts and those from other parts of the body and followed these clues to identify a signaling pathway involving a protein called ROBO2 that maintains facial fibroblasts in a less-fibrotic state. They also saw something interesting in the genomes of fibroblasts making ROBO2.

“In general, the DNA of the ROBO2-positive cells is less transcriptionally active, or less available for binding by proteins required for gene expression,” Li said. “These fibroblasts more closely resemble their progenitors, the neural crest cells, and they might be more able to become the many cell types required for skin regeneration.”

In contrast, the DNA in fibroblasts from other sites of the body allows free access to genes like collagen that are involved in the creation of scar tissue.

“It seems that, in order to scar, the cells must be able to express these pro-fibrotic genes,” Longaker said. “And this is the default pathway for much of the body.”

ROBO2 doesn’t act alone. It triggers a signalling pathway that results in the inhibition of another protein called EP300 that facilitates gene expression. EP300 plays an important role in some cancers, and clinical trials of a small drug molecule that can inhibit its activity are underway. Li and his colleagues found that using this pre-existing small molecule to block EP300 activity in fibroblasts prone to scarring caused back wounds to heal like facial wounds.

“Now that we understand this pathway and the implications of the differences among fibroblasts that arise from different types of stem cells, we may be able to improve wound healing after surgeries or trauma,” Wan said.

The findings are likely to extend to internal scarring as well, Longaker said. “There’s not a million ways to form a scar,” he said. “This and previous other findings in my lab suggest there are common mechanisms and culprits regardless of the tissue type, and they strongly suggest there is a unifying way to treat or prevent scarring.”

By Krista Conger

Source: Stanford University Medical Center

Categories : DermatologyTags :

Hair Transplants 101: The Journey to Successful Hair Restoration

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Your guide to safe, effective, and natural hair restoration in 2026

Hair restoration is one of the fastest-growing aesthetic procedures worldwide. The International Society of Hair Restoration Surgery (ISHRS) reports hundreds of thousands of procedures performed globally each year, with demand climbing steadily. As more people seek confidence-boosting solutions to start the new year, South African specialists warn that choosing the wrong clinic can turn a life-changing decision into lasting damage.

Dr Kashmal Kalan, Medical Director at Alvi Armani South Africa, explains: “January brings a sense of renewal. Many people reassess their goals, and hair restoration has become one of the most transformative ways to invest in yourself. It’s no longer just about fitness or weight loss – hair and skin now play a central role in personal confidence.”

A successful hair restoration journey begins long before the procedure and continues well beyond it. At Alvi Armani, every patient undergoes a thorough, personalised consultation. The team evaluates hair loss patterns, donor density, scalp condition, hair type, and personal goals. Advanced AI-assisted microscopic analysis helps ensure patients are suitable and that the procedure is planned for optimal, natural results.

On procedure day, patients enter a calm, controlled environment. Hairline design is finalised, Follicular Unit Extraction (FUE) is performed with precision, and grafts are implanted to follow the natural flow of hair. Recovery is gradual, with initial shedding giving way to new growth. Density and texture refine over 12-18 months, and ongoing check-ins ensure progress stays on track.

Hairline design is the most artistic aspect of the process. Age, facial symmetry, ethnicity, and donor capacity all influence the final outcome. “We aim for perfection within imperfection. The goal is a hairline that complements the face naturally. No one should be able to tell a transplant took place.”

Strategic density planning is equally critical. Every follicle in the donor area is finite, and poor planning can create gaps or thin patches. This can leave permanent aesthetic imbalance. Reputable clinics plan for decades, not just the first few months. Patients should also understand that growth is gradual, and progressive hair loss may require more than one procedure to achieve the desired result.

Alvi Armani ensures every procedure is doctor-led and supported with ongoing care, including stabilisation medications, regenerative therapies, and annual check-ups. Dr Kalan cautions against so-called “dark clinics” offering prices too good to be true, often operating in unhygienic or mobile facilities. “These clinics treat hair restoration as a commodity rather than medicine. They overharvest donor areas, produce unnatural results, and leave patients needing urgent repairs. Repair procedures now make up roughly a quarter of our cases.”

Beyond procedural excellence, Alvi Armani educates patients on lifestyle choices that support lasting results, from nutrition and scalp care to ongoing therapies. While the process requires patience, the rewards – confidence, natural appearance, and the security of a clinic that plans carefully for the future – make it worthwhile.

For anyone considering hair restoration in 2026, the advice is clear: invest in quality from the start. With the right clinic, personalised planning, and medical oversight, patients can achieve safe, natural results that endure for years to come.

Categories : Cancer DermatologyTags :

Lower Doses of Immunotherapy for Skin Cancer Give Better Results

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According to a new study, lower doses of approved immunotherapy for malignant melanoma can give better results against tumours, while reducing side effects. This is reported by researchers at Karolinska Institutet in the Journal of the National Cancer Institute.

“The results are highly interesting in oncology, as we show that a lower dose of an immunotherapy drug, in addition to causing significantly fewer side effects, actually gives better results against tumours and longer survival,” says last author Hildur Helgadottir, a researcher at the Department of Oncology-Pathology at Karolinska Institutet, who led the study.

The traditional dose of nivolumab and ipilimumab is the one that is approved and established. Due to the extensive side effects, Sweden has increasingly begun to use a treatment regimen with a lower dose of ipilimumab, which is both gentler and cheaper. Ipilimumab is the most expensive part of this immunotherapy and causes the most side effects.

“In Sweden, we have greater freedom to choose doses for patients, while in many other countries, due to reimbursement policies, they are restricted by the doses approved by the drug authorities,” says Hildur Helgadottir.

Lower dose is more effective

The study included nearly 400 patients with advanced, inoperable malignant melanoma, the most serious form of skin cancer. The study shows that the regimen with the lower dose of ipilimumab is more effective, with a higher proportion of patients responding to treatment, 49%, compared to the traditional dose, 37%.

Progression-free survival, the time the patient lives without the disease worsening, was a median of nine months for the lower dose, compared to three months for the traditional dose. Overall survival was also longer, 42 months compared to 14 months.

Serious side effects were seen in 31% of patients in the low-dose group, compared to 51% in the traditional group.

“The new immunotherapies are very valuable and effective, but at the same time they can cause serious side effects that are sometimes life-threatening or chronic. Our results suggest that this lower dosage may enable more patients to continue the treatment for a longer time, which is likely to contribute to the improved results and longer survival,” says Hildur Helgadottir.

There were some differences between the two treatment groups, but even after adjusting for several factors such as age and tumour stage, the better outcome for the lower dose of ipilimumab remained. The study is a retrospective observational study and therefore it is not possible to definitively establish a causal relationship.

Source: Karolinska Institutet

Categories : Dermatology PaediatricsTags :

Do Babies Really Need Sunscreen? The Risks of Overuse and Underuse

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When it comes to protecting babies from the sun, many parents wonder if sunscreen is safe and necessary. The truth is, experts advise against using sunscreen on infants under six months old as their skin is thinner and more sensitive, leading to greater absorption of chemicals and a higher risk of irritation and rashes.

Babies under six months have a higher surface-area-to-body-weight ratio, which increases their exposure to sunscreen chemicals. Some chemical ingredients, like oxybenzone, may cause allergic reactions or disrupt hormones. Sunscreen can also impede a baby’s ability to sweat and regulate their body temperature. 

Instead, the best protection for young babies is to keep them out of direct sunlight, dress them in lightweight, long-sleeved clothing, and use hats and shade as natural barriers. 

For babies over six months, a gentle, broad-spectrum baby sunscreen with at least SPF 30 can be safely applied. However, using sunscreen should complement, not replace, other sun safety measures, which are vital – especially in our sunny South African climate! 

Karen Van Rensburg, spokesperson for Sanosan, explains, “Parents often struggle with knowing how much sunscreen to use on their babies. It’s important to understand that while sunscreen is a helpful tool, relying solely on it, especially for very young infants, can be risky. Using physical barriers like shade and protective clothing alongside sunscreen provides the safest approach to sun care for babies.”

To keep babies safe, parents should:

  • Avoid sun exposure during peak hours (10 a.m. to 4 p.m.)
  • Use shade and protective clothing as the first defence.
  • For babies over six months, reapply a suitable sunscreen on a regular basis to maintain protection, especially after going in the water, after drying off or after sweating. 
  • Your baby should not stay in the sun too long even with sunscreen because every sunburn damages the skin and is a serious risk to their health. 

This balanced approach highlights that cautious sunscreen use combined with physical protection methods is key to keeping baby skin healthy and safe from sun damage.

Sanosan Baby Sun Cream SPF 50+ is a top-tier sunscreen designed specifically for delicate baby skin including broad range of UVA+UVB protection SPF 50+. With its pleasant texture, this cream absorbs quickly for easy application and delivers 24 hours of nourishing care, making it suitable for babies, children, and adults alike. With its gentle formula, this sun cream helps maintain skin hydration while protecting against sun damage, allowing for worry-free outdoor playtime. Plus, its microplastic-free, and safe for our oceans!

Categories : DermatologyTags :

Phase 3 Success for Rocatinlimab in Moderate-to-severe Eczema

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Two global trials show durable improvements in skin clearance, itch, and quality of life by targeting OX40 immune receptor

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An international team of investigators led by Emma Guttman-Yassky, MD, PhD, Waldman Professor and System Chair of the Kimberly and Eric J. Waldman Department of Dermatology at the Icahn School of Medicine at Mount Sinai, has reported results from the first phase 3 clinical trials of rocatinlimab, a novel treatment for moderate-to-severe atopic dermatitis (eczema). The landmark findings from the ROCKET-IGNITE and ROCKET-HORIZON studies were published in The Lancet. 

Eczema affects hundreds of millions of people worldwide and is notoriously difficult to treat due to its complex and chronic inflammatory pathways. Current biologics focus on blocking “allergy” cytokines but fail to address the memory T cells that sustain disease activity. Rocatinlimab is the first antibody to selectively block the OX40 receptor on effector and memory T cells, rebalancing the immune system and altering the long-term course of disease. 

Across the two global, double-blind, placebo-controlled randomised phase 3 clinical trials, nearly 1,500 patients were followed for 24 weeks, and rocatinlimab showed robust and lasting benefits. Patients receiving the treatment were three times more likely to achieve significant improvement in eczema severity, as measured by EASI and vIGA-AD scores, compared to those on placebo. Improvements continued beyond week 24, suggesting that the benefits strengthen over time. The therapy also led to meaningful reductions in itch, pain, and sleep disturbances, enhancing overall quality of life. Importantly, rocatinlimab was well tolerated, with adverse events comparable to placebo, and demonstrated high selectivity by reducing only the OX40R+ CD4+ T cells responsible for eczema’s persistence, without off-target effects. 

“These findings represent a major advance for patients living with eczema, who often face years of uncontrolled symptoms and few effective options,” said physician scientist, Dr. Guttman-Yassky, lead author of the study. “By targeting memory T cells through OX40, rocatinlimab not only clears the skin and relieves itch, but continues to improve patients’ lives over time with a strong safety profile. This is the first phase 3 proof that rebalancing these immune cells can transform how we treat atopic dermatitis.” 

The results establish OX40 as a validated treatment target in eczema and position rocatinlimab as a potential first-in-class therapy. Patients from the phase 3 trials are now being followed in the ROCKET-ASCEND extension study, which will track outcomes for up to two years. Additional research will explore its role in paediatric patients, in combination with other therapies, and in direct comparisons to existing systemic treatments. 

Source: The Mount Sinai Hospital

Categories : Cancer DermatologyTags :

Controlling Inflammation from Sunburn May Prevent Skin Cancer

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In a new study published in Nature Communications, researchers at the University of Chicago have discovered how prolonged exposure to ultraviolet (UV) radiation can trigger inflammation in skin cells through degradation of a key protein called YTHDF2. This protein acts as a gatekeeper in preventing normal skin cells from becoming cancerous. The finding reveals that YTHDF2 plays a crucial role in regulating RNA metabolism to keep cells in a healthy state and opens the door to developing potential new approaches to skin cancer prevention and treatment.

Uncontrolled inflammation triggers skin cancer

Each year, nearly 5.4 million people in the United States are diagnosed with skin cancer, with more than 90% of cases attributed to excessive UV exposure. UV rays can damage DNA and cause oxidative stress and inflammation in skin cells — leading to redness, pain and blistering, commonly known as sunburn.

“We’re interested in understanding how inflammation caused by UV exposure contributes to the development of skin cancer,” said Yu-Ying He, PhD, Professor of Medicine in the Section of Dermatology at the University of Chicago.

RNA or ribonucleic acid is an essential molecule that helps convert genetic information into proteins. A special class known as non-coding RNAs regulates gene expression without producing proteins. These molecules typically function in either the nucleus, where a cell’s DNA is stored or the cytoplasm, where most cellular activity occurs.

Low levels of YTHDF2 turn normal skin cells cancerous

He’s laboratory studies how environmental stressors, such as UV radiation or arsenic in drinking water, affect molecular pathways and damage cellular systems, leading to cancer. Through screening various enzymes, the researchers found that UV exposure causes a marked decrease in levels of YTHDF2, a “reader” protein that specifically binds to RNA sequences marked with a chemical tag known as N6-methyladenosine (m6A).

“When we removed YTHDF2 from skin cells, we saw that UV-triggered inflammation was much worse,” He said. “This suggests that the YTHDF2 protein plays a key role in suppressing inflammatory responses.”

Although inflammation is essential for fighting off infections, it also plays a major role in causing life-threatening diseases, including cancer. However, the molecular mechanisms that regulate this response, especially after UV damage, are not well understood.

YTHDF2 in regulation of non-coding RNA interactions

Using multi-omics analysis and additional cellular assays, the research team found that YTHDF2 binds to a specific non-coding RNA known as U6, which is modified by m6A and classified as a small nuclear RNA (snRNA). Under UV stress, cancer cells showed increased levels of U6 snRNA, and these modified RNAs were found to interact with toll-like receptor 3 (TLR3), an immune sensor known to activate inflammatory pathways linked to cancer.

Surprisingly, these interactions occurred within endosomes, where cellular compartments are typically involved in recycling materials, not where U6 snRNA is usually located.

“We spent a lot of time figuring out how these non-coding RNAs get to the endosome, since that’s not where they usually reside,” He explained. “For the first time, we showed that a protein called SDT2 transports U6 into the endosome, and YTHDF2 travels with it.”

Once both YTHDF2 and m6A-modified U6 RNA arrive at the endosome, YTHDF2 blocks the RNA from activating TLR3. However, when YTHDF2 is absent – such as after UV damage, the RNA freely binds to TLR3, triggering harmful inflammation.

“Our study uncovers a new layer of biological regulation, a surveillance system through YTHDF2 that helps protect the body from excessive inflammation and inflammatory damage,” He said.

The findings could open the door to new strategies for preventing or treating UV-induced skin cancer by targeting the RNA-protein interactions that regulate inflammation.

Source: University of Chicago Medicine

The study, “YTHDF2 regulates self non-coding RNA metabolism to control inflammation and tumorigenesis,” was supported by grants from the National Institutes of Health, the University of Chicago Medicine Comprehensive Cancer Center, the ChicAgo Center for Health and EnvironmenT (CACHET), and the University of Chicago Friends of Dermatology Endowment Fund.