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Microplastics found in brain, ovaries, and placenta: Experts warn of silent threat to vital organs
Microplastics found in brain, ovaries, and placenta: Experts warn of silent threat to vital organs

Time of India

time01-07-2025

  • Health
  • Time of India

Microplastics found in brain, ovaries, and placenta: Experts warn of silent threat to vital organs

1 2 Nagpur: As 'Plastic Free July' begins, experts are raising an alarm over emerging evidence that microplastics — tiny fragments smaller than 5 millimetres — are infiltrating the human body and lodging themselves in vital organs, potentially altering human health in ways science is only beginning to grasp. Recent studies detected microplastics not only in blood and lung tissue but disturbingly in the brain, ovaries, placenta, and even testicular tissue. Scientists fear these microscopic invaders could spark a cascade of health consequences, from neurological disorders to reproductive challenges and cancer. "It's terrifying to think that the plastic we use every day may be silently making its way into our brain and reproductive organs," said Malvvika Fulwani, clinical dietician, adding, "Beyond reducing plastic waste for the planet, 'Plastic Free July' is now a call to protect our own bodies." In March 2024, researchers from the Medical University of Vienna revealed that micro and nano plastic (MNP) can cross the blood–brain barrier (BBB) — a protective shield that normally keeps harmful substances out of the brain. This raises fears of neuroinflammation, impaired memory, and degenerative brain conditions. "The brain is uniquely vulnerable because any inflammatory reaction or cellular damage can be irreversible," warned Dr Ninad Shrikhade, a neurologist. "Neuro inflammation linked to microplastics might one day be implicated in diseases like Alzheimer's or Parkinson's. It's a serious public health concern," he added. Equally concerning is the detection of micro plastics in the ovarian tissue. A 2023 study published in the 'Environmental Health Perspectives' found microplastics embedded in the ovaries of women undergoing surgery, suggesting possible disruption of egg maturation, hormone production, and fertility. "Microplastics may carry endocrine-disrupting chemicals like phthalates and bisphenols," explained Dr Sanjay Deshpande, senior sexologist. "These chemicals mimic hormones, leading to early puberty in girls, reduced sperm counts in men, thyroid dysfunction, and even increased risks of hormone-sensitive cancers such as breast and prostate cancer." According to the Developmental Origins of Health and Disease (DOHaD) framework, exposure to microplastics during pregnancy — particularly endocrine disruptors — could affect a child's metabolism, immunity, and brain function later in life. Beyond hormonal disruption, microplastics may be implicated in cancer development. Scientists suspect they can carry carcinogens, cause DNA damage, and provoke chronic inflammation — all known pathways to cancer. "Cancer is a multi-hit process," said Dr Riya Ballikas, hemato oncologist, adding, "Microplastics might not be the single cause, but they could be one more dangerous hit our cells don't need." Experts have urged people to limit single-use plastic, especially in food packaging, cosmetics, and baby products. Choosing glass, steel, or paper alternatives, reducing packaged foods, and supporting plastic-free initiatives are small but crucial steps. "This 'Plastic Free July', remember it's not just about oceans and turtles," Fulwani said. "It's about what's ending up in our own organs — and in the next generation." WHAT TO DO IN PLASTIC FREE JULY * Carry a cloth bag instead of accepting plastic bags * Switch to steel or glass bottles for water * Buy loose grains, pulses, and spices rather than plastic-packed products * Say no to plastic straws and cutlery when eating out * Choose bar soaps and shampoos instead of products in plastic bottles * Store leftovers in steel or glass containers instead of disposable plastic boxes Get the latest lifestyle updates on Times of India, along with Doctor's Day 2025 , messages and quotes!

New Potential Treatment Strategy for Brain Metastases and Leptomeningeal Disease: HER3-DXd Shows Promising Results in the Phase II TUXEDO-3 Study for Patients With Limited Therapeutic Options
New Potential Treatment Strategy for Brain Metastases and Leptomeningeal Disease: HER3-DXd Shows Promising Results in the Phase II TUXEDO-3 Study for Patients With Limited Therapeutic Options

Business Wire

time04-06-2025

  • Business
  • Business Wire

New Potential Treatment Strategy for Brain Metastases and Leptomeningeal Disease: HER3-DXd Shows Promising Results in the Phase II TUXEDO-3 Study for Patients With Limited Therapeutic Options

CHICAGO--(BUSINESS WIRE)--Leading international medical research company, MEDSIR announced today the positive results of the TUXEDO-3 trial at the American Society of Clinical Oncology (ASCO) Annual Meeting 2025. This phase II study funded by Daiichi Sankyo and Merck, known as MSD outside of the United States and Canada, evaluates the efficacy and safety of patritumab deruxtecan (HER3-DXd) in patients with active brain metastases and leptomeningeal disease, serious complications associated with advanced stages of the cancer. "This study represents a significant advancement in our understanding of how to treat brain metastases and leptomeningeal disease" - Dr. Matthias Preusser. Share The study was carried out to evaluate HER3-DXd in patients with metastatic breast cancer (mBC) and advanced non-small cell lung cancer (aNSCLC) with active brain metastases, and patients with leptomeningeal disease from solid tumors. This is an antibody-drug conjugate to target HER3, a protein receptor found on the surface of cancer cells in brain metastases. HER3-DXd is an investigational agent consisting of a fully human anti-HER3 IgG1 monoclonal antibody attached to a number of topoisomerase I inhibitor payloads (an exatecan derivative, DXd) via tetrapeptide-based cleavable linkers. The DXd ADC Technology payload causes tumor DNA damage, killing cancer cells within and surrounding the tumor microenvironment The study showed promising results, which were presented today in an oral session. Results from the leptomeningeal cohort have been simultaneously published in the renowned journal Nature Medicine due to its potential benefit in patients with a high unmet medical need. In patients with breast cancer and brain metastases, intracranial responses were observed across all breast cancer subtypes, including luminal, HER2-positive, and triple-negative. A NEW HOPE FOR DIFFICULT-TO-TREAT METASTASES 'This study represents a significant advancement in our understanding of how to treat brain metastases and leptomeningeal disease, and we are hopeful that our findings will pave the way for new, effective therapies for these patients,' stated Dr. Matthias Preusser, MD, Medical Oncologist and Head of the Clinical Division of Oncology, Medical University of Vienna and Principal Investigator of TUXEDO-3. Dr. Rupert Bartsch, MD, PhD, Consultant Hematology and Medical Oncology, Medical University of Vienna, added: 'Brain metastases and leptomeningeal disease represent severe complications in cancer, leading to increased morbidity and mortality, and HER3-DXd could be a promising therapeutic alternative for these patients.' MEDSIR's trial DEMETHER, an international, phase II trial exploring the maintenance of trastuzumab and pertuzumab following trastuzumab deruxtecan as induction treatment for HER2-positive recurrent metastatic breast cancer patients, was mentioned during today's Discussion of LBA1008. DEMETHER's strategy is to optimize the sequence to increase patients' progression free survival (PFS) while improving their quality of life. The relevance of this mention highlighted the ability of MEDSIR for anticipating patients' needs and designing strategical trials to keep on pushing the barriers of clinical research. MEDSIR active presence at the ASCO Annual Meeting 2025 reinforces its leadership in excellence-driven oncology research and highlights its focus on addressing unmet needs in cancer treatment, with the aim of not leaving any patient left behind.

Tea and dark chocolate could help you live longer, Queens study shows
Tea and dark chocolate could help you live longer, Queens study shows

Irish Examiner

time02-06-2025

  • Health
  • Irish Examiner

Tea and dark chocolate could help you live longer, Queens study shows

Tea, berries and dark chocolate could lead to a longer life span, new research has indicated. The study found those who consume a diverse range of foods rich in flavonoids, such as tea, berries, dark chocolate, and apples, could lower their risk of developing serious health conditions and have the potential to live longer. The study was led by a team of researchers from Queen's University Belfast, Edith Cowan University Perth, and the Medical University of Vienna and Universitat Wien. The findings reveal increasing the diversity of flavonoids within your diet could help prevent the development of health conditions such as type 2 diabetes, cardiovascular disease, cancer and neurological disease. Flavonoids are found in plant foods like tea, blueberries, strawberries, oranges, apples, grapes, and even red wine and dark chocolate. Published on Tuesday in Nature Food, the research tracked more than 120,000 participants aged from 40 to 70 years old for over a decade. It is the first study of its kind to suggest there is a benefit to consuming a wide range of flavonoids beyond that of simply consuming a high quantity. Study co-lead, Professor Aedín Cassidy from the Co-Centre for Sustainable Food Systems and Institute for Global Food Security at Queen's said: 'We have known for some time that higher intakes of dietary flavonoids, powerful bioactives naturally present in many foods and drinks, can reduce the risk of developing heart disease, type 2 diabetes, and neurological conditions like Parkinson's. 'We also know from lab data and clinical studies that different flavonoids work in different ways, some improve blood pressure, others help with cholesterol levels and decrease inflammation. This study is significant as the results indicate that consuming a higher quantity and wider diversity has the potential to lead to a greater reduction in ill health than just a single source.' Edith Cowan University research fellow, first author and co-lead of the study, Dr Benjamin Parmenter, made the initial discovery that a flavonoid-diverse diet is good for health. He explained: 'Flavonoid intakes of around 500mg a day was associated with a 16% lower risk of all-cause mortality, as well as a 10% lower risk of CVD [cardiovascular disease], type 2 diabetes, and respiratory disease. That's roughly the amount of flavonoids that you would consume in two cups of tea. 'However, those who consumed the widest diversity of flavonoids, had an even lower risk of these diseases, even when consuming the same total amount.' Read More Families criticise delays to inquiry into epilepsy drug valproate

What did Beethoven really look like? Scientists think they finally know — and he was a bit of a grouch
What did Beethoven really look like? Scientists think they finally know — and he was a bit of a grouch

Yahoo

time29-05-2025

  • Entertainment
  • Yahoo

What did Beethoven really look like? Scientists think they finally know — and he was a bit of a grouch

Turns out Beethoven didn't just sound intense — he looked it, too. Nearly 200 years after Ludwig van Beethoven's death, scientists say they've finally pieced together what the famously moody maestro actually looked like — and let's just say he wouldn't exactly be mistaken for a people person, originally reported by the Daily Mail. 'I found the face somewhat intimidating,' admitted Cicero Moraes, a Brazilian graphics expert who used 19th-century skull photos, facial modeling, and AI to reconstruct the furrowed countenance of classical music's original bad boy. The first-of-its-kind digital render shows the German composer just as he's often been depicted in oil paintings: scowling and brooding. 'He was indeed irritable, untidy, clumsy, rude, and misanthropic,' British conductor Mark Wigglesworth said in a blog post — though he added, 'Beethoven could be witty, caring, mischievous, generous, and kind.' So what turned the artist formerly known as Ludwig into such a legendary grouch? Experts say it may have been as much biology as biography. In 2023, a groundbreaking DNA study published in Current Biology cracked open the medical mystery of Beethoven's tumultuous life — and painful death at age 56. Researchers sequenced his genome using five strands of his preserved hair and determined he likely died from liver failure caused by chronic alcohol consumption, combined with hepatitis B and a genetic predisposition for liver disease. Reportedly, the beloved composer began suffering bouts of jaundice in 1821, a symptom of liver disease, and had progressive hearing loss that left him completely deaf by his mid-40s. 'Most people who do genetic testing for fun, including myself, will find that there is nothing wrong with them,' lead researcher Tristan Begg said. 'But in this study we had fascinating results in every branch we looked at, from disease risk to the family tree.' Indeed, Beethoven's tangled roots may have been more than musical — the study also suggested a child may have been born from an affair in his family line. As if that weren't enough, bones believed to be fragments of Beethoven's skull — long stashed in a tin marked 'Beethoven' by the descendant of a Viennese doctor — were recently donated to the Medical University of Vienna by California businessman Paul Kaufmann. 'It is extremely emotional to me to return the fragments where they belong, back to where Beethoven is buried,' Kaufmann told CNN in 2023. Moraes reconstructed Beethoven's famously intense visage — aided by old skull images and tissue-thickness data — and reinforced by a death mask made while the composer still had a pulse. 'I academically explored his genius, revealing what made him an icon of Western music,' Moraes said of his 2025 study. 'I analyzed his revolutionary creativity, resilience in composing despite deafness, intense focus, problem-solving ability, and tireless productivity, despite a challenging personality.'

Drug Slows Progression of Primary Sclerosing Cholangitis
Drug Slows Progression of Primary Sclerosing Cholangitis

Medscape

time12-05-2025

  • Health
  • Medscape

Drug Slows Progression of Primary Sclerosing Cholangitis

AMSTERDAM — Norucholic acid (NCA), an investigational therapy, demonstrated significant superiority over placebo in halting disease progression in patients with primary sclerosing cholangitis (PSC), meeting the primary efficacy endpoint in a phase 3 trial presented on May 10 at the European Association for the Study of the Liver (EASL) Congress 2025. NCA was four times more effective in partially normalizing the liver enzyme alkaline phosphatase (ALP) (odds ratio [OR], 4.16), without worsening of the histologic Ludwig stage of PSC. Results held true with and without concomitant ursodeoxycholic acid (UDCA). Michael Trauner, MD The interim 96-week efficacy and safety results were presented by Michael Trauner, MD, professor of gastroenterology and hepatology at the Medical University of Vienna, Austria, who first developed the compound two decades ago. 'In this study, NCA hit the primary and key secondary endpoint in this clinical trial that included liver histology and biochemical features,' said Trauner. 'There were higher response rates for NCA than placebo both with and without concomitant UDCA, as well as improvement and less worsening of histological disease stages with NCA compared with placebo.' First Data to Offer Hope for Reducing PSC Progression PSC is a rare, progressive cholangiopathy characterized by inflammation and fibrosis of the bile ducts, with no current medical therapy proven to alter its course. NCA works by inducing bicarbonate-rich hypercholeresis and promoting cholangiocyte protection, with additional anti-inflammatory and immunomodulatory effects. The multicenter, international, randomized, placebo-controlled, double-blind phase 3 study builds on earlier phase 2 findings in which NCA improved cholestasis markers in a dose-dependent manner and was well tolerated. Patients (n = 301) were randomized in a 2:1 ratio to receive either NCA 1500 mg once daily (n = 205) or placebo (n = 96), stratified by concomitant UDCA use. Biopsies were done 4-8 weeks prior to randomization and again at week 96 and will be repeated at week 192. The study remains ongoing, with 2 additional years of blinded treatment planned. The combined primary endpoint was defined as partial normalization of ALP to less than 1.5 times the upper limit of normal and no worsening of Ludwig histologic stage. Secondary endpoints included modified Nakanuma staging, liver stiffness measurement (FibroScan), enhanced liver fibrosis and Amsterdam-Oxford scores, patient-reported pruritus and fatigue, and overall quality of life. 'The population was typical of PSC, with men in their 40s making up 74% of participants, and around 70% had inflammatory bowel disease,' reported Trauner. Baseline ALP was approximately 300 U/L, and liver stiffness and enhanced liver fibrosis scores were around 10. Most patients presented with Ludwig stage 2 or 3 disease. Statistically Significant Benefit Compared With Placebo By week 96, 27.3% of patients in the NCA group and 37.5% in the placebo group had discontinued the trial. In the intention-to-treat analysis, the combined primary endpoint was achieved by 15.1% of patients in the NCA group vs 4.2% in the placebo group, a difference of 10.96% (95% CI, 4.6%-17.3%) and an OR of 4.16 (95% CI, 1.42-12.22; P = .0048). Patients without a second biopsy were considered nonresponders. In the per-protocol analysis, which included only participants who completed both biopsies, the benefit remained significant: 18.2% for NCA vs 6.6% for placebo, with a difference of 11.7% (95% CI, 3.0%-20.3%) and an OR of 3.36 (95% CI, 1.12-10.11; P = .0155). The key secondary endpoint of ALP less than 1.5 times the upper limit of normal and no worsening according to modified Nakanuma staging was also met. NCA again outperformed placebo: 15.1% vs 5.2%, a difference of 9.9% (95% CI, 3.3%-16.5%). Consistent Efficacy, With or Without UDCA Trauner noted that NCA demonstrated greater efficacy than placebo in both subgroups, with and without concomitant UDCA. The treatment difference with UDCA was 7.5% (95% CI, 0.4%-14.7%), whereas without UDCA, the difference increased to 23.4% (95% CI, 11.3%-35.5%). 'Those not receiving UDCA had a much higher response rate at 23% with NCA,' he said. Histologic and Biochemical Improvements; Safety Good Histologic improvement by at least one Ludwig stage occurred in 25.2% of patients in the NCA group compared with 10.5% in the placebo group ( P = .0217). Notably, progression to cirrhosis (Ludwig stage 4) occurred less frequently in the NCA group (5.9% vs 10.7%). Significant improvements were also seen in liver enzymes, including ALP, alanine aminotransferase, and gamma-glutamyltransferase, with greater reductions in the NCA group at week 96. The Amsterdam-Oxford prognostic score increased significantly more in the placebo group, indicating greater disease progression. NCA was generally well tolerated, with a safety profile comparable to that of placebo. Treatment-emergent adverse events occurred in 97.6% of the NCA group and 92.7% of the placebo group. The most common adverse events included diarrhea, SARS-CoV-2 infection, and nasopharyngitis. Expert: 'Desperate Need for Treatment' Ahmed Elsharkawy, MD, consultant hepatologist at University Hospitals Birmingham NHS Foundation Trust, United Kingdom, who co-moderated the session, underscored the importance of these findings. 'There is a desperate need for patients with PSC to have access to treatments that slow down the progression of their condition, as we currently do not have any available drugs to treat them,' he explained. Reflecting on the study's impact, he added, 'This study provides the first-ever data that offers some hope that norucholic acid can help reduce progression of the disease for some but unfortunately not yet all patients with the condition. This is hopefully the first step towards developing a cure for this devastating condition that disproportionately affects young individuals.'

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