"During a flare-up, it’s almost impossible to explain how you feel—you can barely breathe,” said 77-year-old Pointing from Banbury, England, in a recent news release.

For people like Pointing, a new clinical trial offers hope. Benralizumab, an existing injectable drug, may significantly reduce the severity of asthma and COPD attacks and could make it far less daunting, report researchers. The study is published in The Lancet Respiratory Medicine. While the drug has already been approved for treating asthma patients, it could also replace steroid medication as the go-to treatment for flare-ups.

What did The Study find?

As per the findings in the study, the monoclonal antibody outperformed steroids in reducing symptoms like coughing, wheezing, breathlessness, and phlegm production.

Trial results also showed that after three months, individuals taking benralizumab were four times less likely to experience an asthma or COPD attack compared to those on the steroid prednisolone.

The lead researcher Dr Mona Bafadhel, who is also the chair of respiratory Medicine at King's College London said, "This could be transformative for people with asthma and COPD. Treatment for these exacerbations hasn’t evolved in 50 years, despite causing 3.8 million deaths globally each year. Benralizumab, a safe and effective drug already used for severe asthma, showed greater effectiveness when given at the point of an exacerbation compared to steroid tablets, which are currently the only option available."

Pointing who was one of the participant of the trial, praised the drug and said that it was "fantastic" and that he did not experience the usual side effects he gets with the steroid tablets. "“Steroids used to ruin my sleep, especially the first night. But with benralizumab, I slept well and could go about my life without issues.”

How does Benralizumab work?

It targets eosinophils, a type of white blood cell that drives lung inflammation during flare-ups. Eosinophilic exacerbations account for about 30% of COPD attacks and nearly half of asthma attacks. These episodes also involve a surge in eosinophiles in the lungs, and cause severe wheezing, coughing, and chest tightness.

The trial placed patients into three groups: one received benralizumab during flare-ups, another was given prednisolone tablets, and a third received both. The benralizumab group not only had fewer symptoms, but it also took longer to develop a serious episode that necessitated medical attention or hospitalization.

The researchers also discovered that the injections increased the individuals' overall quality of life.

Although the medicine is now provided by healthcare professionals, researchers anticipate it will be safe to administer at home or in a doctor's office in the future.

“Our study demonstrates enormous potential for asthma and COPD treatment,” said Dr. Sanjay Ramakrishnan, clinical senior lecturer at the University of Western Australia and one of the researchers. “COPD is the third leading cause of death worldwide, yet treatment remains outdated. We need life-saving options to prevent these patients from running out of time.”

With 3.8 million deaths annually attributed to asthma and COPD, researchers hope benralizumab can soon provide a modern, effective solution for managing these life-threatening conditions.

For generations, congenital deafness has been a lifetime of silence or partial hearing regained by way of invasive procedures such as cochlear implants. As revolutionary as those devices have been, however, they have their limitations—especially for people who are born with genetic types of hearing loss that destroy the natural processes of sound conduction but a new scientific advance is now making something once considered impossible a possibility- actually restoring natural hearing through gene therapy.

First-of-a-kind, researchers have been able to restore hearing in youngsters, teens, and even young adults who were born with a certain form of congenital deafness. The therapy, which aims at an errant gene called OTOF, is a landmark in the management of genetic hearing disorders.

What Is OTOF-Related Deafness?

The culprit gene, OTOF, encodes a protein known as otoferlin, which is vital for the conduction of sound signals from the inner ear to the brain. When the gene is mutated, the otoferlin protein is either absent or defective, and the person experiences severe hearing loss since birth. The inner ear itself is normal—only the signaling system is defective.

That's precisely why OTOF-associated deafness is such a strong candidate for gene therapy. If you can restore or replace the defective gene, the body already has the physical equipment in place to naturally process sound.

The research team, based in five hospitals and spearheaded by genetic hearing loss experts, employed a virus that has been altered as a delivery vehicle. This virus was altered to transport a healthy version of the OTOF gene and inject it directly into the hair cells of the inner ear—the sound-detecting sensory cells.

This is how it works: the genetically altered virus binds to a hair cell surface, enters the cell, and delivers the repaired gene into the nucleus. The cell then starts manufacturing working otoferlin protein, effectively rewiring the ear-to-brain communication line. It's not science fiction—this is precision molecular medicine in action.

The most impressive feature of this research is its wide range of participant ages, ten people between 1 and 24. All ten of them had OTOF-related congenital deafness. It was the first research study to consider whether gene therapy might cure hearing in children and young adults—not only in babies or toddlers.

The treatment consisted of a single injection of the virus carrying the gene into the inner ear of the patient. Patients were tested for 12 months with both objective hearing measures (such as auditory brainstem responses) and behavioral tests (like button-pushing in response to hearing specific tones). Results were immediate and dramatic. During the initial month, patients showed:

• A 62% increase in brainstem hearing response tests
• A 78% increase in behavioral hearing tests
• In a few instances, near-normal speech perception

A seven-year-old patient reportedly started reacting to sounds only three days post-treatment—a moment that surprised the medical staff and the family alike.

Even more promising, the side effects were minimal and easy to manage, the most frequent being a brief fall in white blood cell level. No severe adverse events were noted, affirming the safety of this gene therapy strategy.

How Does Gene Therapy Works?

Interestingly, the research found that 5- to 8-year-old children gained the most—more than toddlers. This contradicts earlier beliefs that earlier is always better in cases of congenital conditions. It implies that the brain's preparedness to receive new auditory information could be as crucial as the ear's structural integrity.

Why exactly this age window is optimal is still unclear, but it's an important question for future scientists to answer as they continue to fine-tune the timing of treatments.

This is not merely another clinical milestone, it's a shift in paradigm. By addressing the root genetic cause of deafness, this therapy holds the potential for a one-time fix that restores hearing naturally without the implant or the lifetime devices.

And although this trial involved the relatively uncommon OTOF mutation, the implications are far-reaching. Researchers are currently investigating gene therapies for other, more prevalent forms of inherited deafness with complicated patterns of genetics. Promising early results have been seen in animal studies, and human trials may follow in the next few years.

Additional information will be required to ascertain for how long the restored hearing lasts. Will the effects last the rest of one's life, or will there be the need for booster shots? Long-term follow-up studies are already in process.

Meanwhile, this achievement is a beacon of hope for families who suffer from genetic deafness—and a strong reminder that the future of medicine is not about compensating for our genes but rather about correcting them.

For the first time, gene therapy has shown that it can restore hearing in individuals born with silence—not only control their condition, but change it. The more this research grows and technology develops, the world is moving closer to a time when congenital deafness could one day not only be treated, but cured and for families with genetic hearing loss, that's not only science—it's life-altering.

Scientists may have discovered a critical clue that helps explain why polycystic ovary syndrome (PCOS)—a hormonal condition affecting up to 13% of women of reproductive age—tends to run in families. New research presented at the 41st Annual Meeting of the European Society of Human Reproduction and Embryology in Paris suggests that PCOS may be passed down not just through classic genetics, but through what’s known as epigenetic memory.

In simple terms, epigenetics is chemical change that affects how genes are switched on or off without actually changing the DNA sequence itself. These changes can be caused by environment, stress, and diet and more importantly, they can occasionally be passed on. This throws open the gate for a whole new perspective of PCOS as not only a genetic disorder but an epigenetic disorder, possibly heritable from mother to daughter through early cellular processes.

PCOS is characterized by an extensive array of symptoms that can significantly affect quality of life. They encompass irregular or heavy menstrual periods, ovarian cysts, weight gain, acne, hirsutism, thinning hair, and infertility. The disorder also elevates the risk of developing metabolic complications like hypertension, type 2 diabetes, and endometrial cancer.

Despite decades of studies, the underlying cause of PCOS has not been determined. Nonetheless, it is firmly established that the condition usually has an inherited pattern. PCOS is estimated to affect 20% to 40% of patients who have one affected mother or sister, and findings from twin studies—such as the Dutch Twin-Family Study—indicate a very strong genetic basis.

The research, led by Dr. Qianshu Zhu of Chongqing Medical University in China, explored the epigenetic signatures in egg cells and embryos from women who were receiving in vitro fertilization (IVF). Of the 230 women researched, 133 had PCOS while 95 did not.

The scientists tested both unfertilized egg cells and early embryos for epigenetic markers—chemical labels that perch on DNA and control gene expression. What they discovered was dramatic: egg cells and embryos from PCOS women had pervasive disturbances in important genes, especially those related to metabolism and early embryo growth.

Also, they found abnormalities in an epigenetic marker called H3K27me3, which is important for gene expression. These abnormalities were present in the egg cells and were inherited by the embryo—indicating that epigenetic signals might be inheritable, even prior to the onset of implantation.

This indicates that an epigenetic message is being transmitted from mother to embryo prior to implantation even starting," said Dr. Zhu. A woman's gene expression related to PCOS, in other words, might be pre-programmed into the development of the embryo from day one.

What Is Epigenetic Inheritance Exactly?

Whereas genetic mutations entail alterations in the DNA sequence itself, epigenetic inheritance refers to the passing on of gene expression patterns from one generation to the next. Such changes are initiated by lifestyle elements, but once they take root, they could be "remembered" by cells—and transmitted to offspring.

If these results hold up to further study, it may be that PCOS is inherited, at least in part, by epigenetic memory, which would explain its familial occurrence even in the absence of identifiable genetic mutations.

Dr. Sydney Chang, a fertility specialist and medical director of CCRM Fertility of Austin, said that the new discovery provides an explanation for why identical twins (who have 100% DNA in common) are much more likely to both develop PCOS compared to fraternal twins. "This indicates that much of the risk of developing PCOS is inherited by genes," she said—but possibly not so-called "traditional" genes.

Implications for IVF and Reproductive Health

The possible uses of this work are both thrilling and morally complicated. Dr. Zhu's lab implies IVF technology may eventually involve screening or intervening on the epigenetic level to prevent PCOS—perhaps by fine-tuning the gene expression of embryos prior to implantation—a frontier currently years from use in clinics, but in theory possible.

Also, this study may have an impact on how fertility clinics select embryos and further our knowledge of the direct influence of maternal health on early embryonic development.

But Zhu was quick to caution: these are laboratory-created embryos, not kids. His lab now is carrying out mouse studies to observe how these epigenetic alterations impact real offspring.

Why Early Detection Of PCOS Is Important for Women Health?

One of the most exciting implications of this research is that it has the potential to induce early diagnosis and treatment. Eventually, the findings may enable clinicians to identify risk of PCOS earlier in life—even prior to the onset of symptoms.

What is interesting about this research is that it validates a true genetic link among PCOS in families, It sheds light for early diagnosis and preventive interventions to keep PCOS from being passed through families.

In the future, this could translate into lifestyle or medical interventions that alter epigenetic expression before the condition fully develops, opening new doors in both prevention and personalized care.

Although the research provides an important new perspective on PCOS, it also brings as many questions as answers. How do those epigenetic changes cross-talk with environmental influences such as diet, stress, or hormonal exposure? Can they be undone later in life? Are they specific to PCOS, or can they have a role in other hormonal conditions as well?

Dr. Zhu's continued research in animal models will help work through these unknowns, but longitudinal studies and human clinical trials will be essential to translating the laboratory findings into actual practice.

PCOS has long baffled scientists and plagued patients with imprecise diagnoses, capricious symptoms, and too often, delayed treatment. But as new research points toward an epigenetic memory with risk that gets passed across generations, the disease may soon be explained not just as a hormonal imbalance—but as a biological inheritance that contemporary medicine can detect more effectively and one day, conceivably, interrupt.

Will This Genetic Breakthrough Prevent PCOS?

Yes, this gene find may open the door to possible prevention, but with significant qualifications. The research unveiled at the European Society of Human Reproduction and Embryology indicates that polycystic ovary syndrome (PCOS) might be affected not only by genes that are passed down, but by epigenetic memory—chemical modifications to DNA that influence the activation or deactivation of genes. Scientists discovered these epigenetic indicators in the egg cells and early embryos of women with PCOS, suggesting that the risk could be transmitted even before implantation.

Though that does not mean that we can stop PCOS today, knowledge of these processes provides the hope of targeted intervention during fertility treatments like IVF someday. But these results are early and from lab-produced embryos. Additional studies—particularly in animal models and ultimately in the clinic—will be needed before these findings can be used to prevent PCOS in people. Nevertheless, the research is an encouraging step toward ending the cycle of PCOS from one generation to the next.

In what could be a transformative moment in the fight against HIV, the World Health Organization (WHO) has officially recommended the use of injectable lenacapavir—a long-acting antiretroviral medication—in the prevention of HIV. The news comes barely weeks after the U.S. Food and Drug Administration (FDA) approved lenacapavir as a twice-yearly injection for PrEP (pre-exposure prophylaxis).

Timing is everything, in 2024 alone, an estimated 1.3 million new HIV cases were reported globally, disproportionately falling on populations already suffering from stigma and barriers to healthcare. From Kigali to California, this new strategy has the potential to change the delivery of HIV prevention—and to whom.

The medication lenacapavir acts on the HIV capsid, or virus protein shell, inhibiting its capacity to make copies of itself and infect new cells. Its uniqueness lies in the fact that it has a long half-life and is effective at low doses. A single injection administered subcutaneously establishes a reservoir of drug that gradually delivers medication into circulation for 26 weeks.

This enables dosing every two years, a huge benefit for individuals who might not be able to manage daily oral PrEP because of lifestyle, access, or stigma. As WHO Director-General Dr. Tedros Adhanom Ghebreyesus said, "While an HIV vaccine remains elusive, lenacapavir is the next best thing."

The historic guidelines, released at the International AIDS Society Conference in Kigali, Rwanda, encourage governments and health systems to implement this new tool, especially in high-incidence settings and among priority groups such as sex workers, men who have sex with men, transgender people, people who inject drugs, and adolescents.

The Evolution of HIV Prevention

Since the discovery of HIV in the 1980s, prevention has been held on three pillars: biomedical progress, barrier methods, and behavioral change. The early decades were dedicated to encouraging condom usage, lowering high-risk behavior, and public awareness. These strategies slowed but did not curb the virus.

In 2010, a new era opened up. Clinical trials revealed that antiretroviral drugs not only treated HIV but could also prevent it. This led to widespread adoption of PrEP, typically in the form of daily oral pills. Meanwhile, the concept of U=U (Undetectable = Untransmittable) proved that treatment with good adherence blocked transmission altogether.

By 2019, PrEP had been given an "A" rating by the U.S. Preventive Services Task Force, resulting in its coverage without out-of-pocket expense. Despite all these developments, the HIV epidemic has continued, with more than 30,000 new infections reported every year in the U.S. alone.

Why Daily PrEP Isn't Enough?

PrEP taken daily is effective, but it has conditions. It needs to be used every day consistently, tested regularly for HIV and STIs, and have a reliable healthcare system in place. For most, these are difficult requirements to fulfill.

Individuals most vulnerable to these challenges, such as people of color, LGBTQ+ persons, low-income individuals, and those in the southern United States, frequently experience substantial barriers to daily PrEP maintenance. These barriers often involve lack of insurance, transportation, stigma, and health system distrust.

Injectable lenacapavir bypasses several of these obstacles. Just two shots annually, it provides an inconspicuous, low-fuss choice that might significantly boost takeup among under-served communities.

The breakthrough arrived with the PURPOSE 1 trial, which took place in South Africa and Uganda. More than 5,300 young women and adolescent girls, among the most at-risk populations in the world, were recruited.

The results were astonishing: zero new infections in participants who received lenacapavir, compared with 39 and 16 infections in two oral PrEP control groups. The background incidence rate was 2.41 per 100 person-years. In the world of HIV prevention, this is as close to a vaccine-level efficacy as we’ve ever seen.

How Funding Crisis Threatens Momentum?

As the excitement takes hold, a new challenge is on the horizon. UNAIDS warns that a huge funding gap threatens to undermine global HIV gains. The U.S. President's Emergency Plan for AIDS Relief (PEPFAR), which had committed $4.3 billion to 50 nations in 2025, suddenly suspended funding earlier this year.

Already, the effect can be seen. In Nigeria, access to PrEP fell from 40,000 recipients to fewer than 7,000 within months. Kenya documented dramatic drops in women receiving preventive treatment after giving birth. "This is not a funding gap—it's a ticking time bomb," UNAIDS Executive Director Winnie Byanyima said. "Health workers are being sent home. Services are disappearing overnight."

The WHO is banking on lenacapavir's ease and extended dosing interval to reverse some of this backlash by lowering costs per patient and alleviating pressures on overwhelmed systems. But to be realized, its promise will have to be matched by global cooperation and domestic investment.

With WHO backing, FDA approval, and compelling trial data, lenacapavir is poised to become a pillar of modern HIV prevention. Countries must now prioritize fast-tracking its regulatory approval, training providers, and ensuring equitable access.

It's not about a new drug. It's about giving individuals more control of their sexual health, providing options that work in real lives, and ending the gap between what we know we can do and what people end up getting.

The global HIV epidemic is far from over. But with tools like lenacapavir, we are getting closer to turning the tide—and protecting the next generation from a virus that has shaped public health for over four decades.