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The world’s rivers are facing an alarming threat: millions of kilometers of waterways are being contaminated with antibiotics from human use. According to a recent study led by McGill University researchers, this pollution has the potential to promote drug resistance and harm aquatic life on a massive scale.

Published in PNAS Nexus, the groundbreaking research is the first to estimate the global scope of river contamination caused by human antibiotic consumption. The team calculated that approximately 8,500 tonnes of antibiotics – about one-third of what people consume annually – end up in river systems worldwide each year, even after passing through wastewater treatment plants.

While individual antibiotic residues might be present at very low concentrations in most rivers, making them difficult to detect, the chronic and cumulative environmental exposure can still pose a risk to human health and aquatic ecosystems. This is particularly concerning for amoxicillin, the world’s most commonly used antibiotic, which was found to be most likely present at risky levels in Southeast Asia.

The region’s rising use of antibiotics combined with limited wastewater treatment has amplified the problem. The study emphasizes that it’s not about discouraging the use of antibiotics – we rely on them for global health treatments. Instead, the findings indicate unintended effects on aquatic environments and antibiotic resistance, which calls for mitigation and management strategies to minimize their implications.

The research used a global model validated by field data from nearly 900 river locations, excluding antibiotics from livestock or pharmaceutical factories, both significant contributors to environmental contamination. The study’s authors suggest that monitoring programs are essential to detect antibiotic or chemical contamination in waterways, especially in areas predicted to be at risk.

In conclusion, the study highlights the critical issue of antibiotic pollution in rivers arising from human consumption alone. While it would likely worsen with contributions from veterinary or industry sources, immediate action is needed to address this pressing concern and protect our planet’s precious aquatic resources.

The Min protein system is a complex process that helps bacteria divide evenly and correctly. For decades, scientists have studied this system, but understanding how it works efficiently has been a challenge. Recently, researchers at the University of California San Diego (UCSD) made a groundbreaking discovery that sheds new light on the efficiency of cell division.

The UCSD team developed a way to control Min protein expression levels independently in E. coli cells. This allowed them to observe how different concentrations of Min proteins affect the oscillations between the poles of the cell. The results were surprising: despite varying concentrations, the oscillations remained stable across a wide range, with E. coli producing just the right amount of Min proteins.

This breakthrough is significant because it shows that the Min protein system can efficiently guide division to the correct location without relying on precise control over protein levels. This finding has far-reaching implications for our understanding of cellular organization and function.

The study was published in Nature Physics, a leading scientific journal, and was funded by the National Institutes of Health (NIH). The research team consisted of experts from both physics and chemistry/biochemistry departments at UCSD, highlighting the importance of interdisciplinary collaboration in advancing our knowledge of cellular biology.

The world’s deadliest infectious disease, tuberculosis (TB), claims over 1 million lives annually. Despite advancements in diagnosis and treatment, TB remains a significant challenge, particularly in developing nations where access to chest X-rays and molecular diagnostics is limited. Current diagnostic methods often have high false negative rates and require extensive sample preparation, delaying diagnosis.

MIT chemists have developed a breakthrough approach using an organic molecule that reacts with specific sulfur-containing sugars found only in three bacterial species, including Mycobacterium tuberculosis (Mtb), the microbe responsible for TB. By labeling a glycan called ManLAM using this small-molecule tag, researchers can now visualize where it is located within the bacterial cell wall and study what happens to it throughout the first few days of tuberculosis infection.

The research team led by Laura Kiessling, Novartis Professor of Chemistry at MIT, aims to use this approach to develop a diagnostic that could detect TB-associated glycans in culture or urine samples. This would provide a cheaper and faster alternative to existing diagnostics, making it more accessible to developing nations where TB rates are high.

Using their small-molecule sensor instead of antibodies, the researchers hope to create a more sensitive test that can detect ManLAM in the urine even when only small quantities are present. This has significant implications for TB diagnosis and treatment, particularly for patients with very active cases or those who are immunosuppressed due to HIV or other conditions.

The research was funded by the National Institute of Allergy and Infectious Disease, the National Institutes of Health, the National Science Foundation, and the Croucher Fellowship. The findings have the potential to revolutionize TB diagnosis and improve patient outcomes worldwide.