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Wednesday, August 26, 2026 9:18 AM

Monash University

PCOS Renamed as PMOS in Landmark Move to Improve Global Diagnosis and Women’s Healthcare

In a major step toward better awareness and treatment, the condition long known as Polycystic Ovary Syndrome (PCOS) has officially been renamed Polyendocrine Metabolic Ovarian Syndrome (PMOS). The disorder affects more than 170 million women globally, or roughly 1 in 8 women, and experts say the new name more accurately reflects its complex nature. The renaming initiative was the result of a 14-year international collaboration involving over 50 medical and patient advocacy organizations, including the Endocrine Society. The announcement and findings were published in The Lancet. Health experts explained that the old term “PCOS” often created confusion by focusing on ovarian cysts, despite evidence showing that abnormal cysts are not a defining feature of the condition. This misunderstanding frequently led to delayed diagnoses, incomplete treatment, and a narrow view of a disorder that also impacts hormones, metabolism, mental health, skin, weight management, and reproductive health. Professor Helena Teede of Monash University, who led the global process, said the new terminology is designed to improve recognition and long-term care for millions of women. She noted that although medical guidelines have improved over time, changing the name was essential to better reflect the science and lived experiences of patients. The consultation process included more than 22,000 survey responses, workshops with healthcare professionals, and direct input from women living with the condition across multiple countries. Experts also emphasized the importance of selecting a name that works across cultures and avoids unnecessary stigma, especially in regions where reproductive terminology can carry social sensitivity. A three-year transition period has now begun, with global education campaigns underway. PMOS is expected to be fully adopted in the 2028 International Guideline update. Patient advocates welcomed the change, calling it a historic moment that could lead to earlier diagnosis, fairer healthcare access, and stronger research investment for future generations. Source: Endocrine Society  

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Targeting TB Bacteria’s Fatty Outer Coat May Boost Drug Effectiveness: IIT Bombay–Monash Study

Researchers from IIT Bombay and Monash University have discovered that the fatty outer coat of Mycobacterium tuberculosis—the bacteria that causes TB—plays a crucial role in helping it evade antibiotics. By altering this lipid-rich membrane, TB bacteria can survive drug treatment, especially when they enter a dormant state. Despite over a century of research, tuberculosis remains a major global threat. In 2023, 10.8 million people fell ill and 1.25 million died from the disease, with India recording more than 2.6 million cases in 2024. One of the biggest hurdles in treatment is the bacteria’s ability to slip into dormancy shortly after infection. In this phase, the bacteria remain alive but inactive, causing no symptoms and unable to spread. However, if a person’s immunity drops—due to HIV, illness or immunosuppressive medication—the bacteria can reactivate. Since standard TB drugs mainly target bacteria that are actively growing, dormant cells are far less affected and often survive long treatment cycles. The new study led by Prof Shobhna Kapoor of IIT Bombay and Prof Marie-Isabel Aguilar of Monash University examined how TB bacteria survive this drug assault. The researchers found that the dormant bacteria’s outer membrane undergoes changes that make it harder for antibiotics to penetrate. Drug concentrations needed to inhibit these dormant cells were up to ten times higher than those needed for active ones. Advanced mass spectrometry allowed the team to map more than 270 lipid molecules in the bacterial membranes, revealing significant differences between active and dormant bacterial states. According to the researchers, weakening this lipid barrier could make existing drugs far more effective. Instead of relying solely on new antibiotics, combining current treatments with molecules that disrupt the outer membrane could help kill persistent bacteria without promoting genetic resistance. Prof Kapoor noted that such an approach could shorten therapy durations and restore drug sensitivity, giving TB bacteria little room to adapt permanently. Source: PTI

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