Current research suggests that we only remove 1% of the plastic waste in our oceans. Thankfully, researchers in the UK have developed a technique to find the rest!
Researchers at the University of Warwick, UK, have developed a new and cheap method to find even the smallest bits of plastic that are floating around in oceans. The research published in Environmental Science & Technology outlines how the fluorescent dye specifically binds to plastic particles, making it possible to see them under a microscope and easily distinguishable from natural materials. The researchers found that tiny pieces of plastic are present at much higher levels than previously thought, which challenges current beliefs regarding the fate of plastic waste.
We produce almost 300 million tons of plastic each year, and more than 8 million tons of this is thought to end up in our oceans. Large pieces of plastic break down over time through weathering, producing tiny particles called ‘microplastics’. These microplastics often go undetected and can be very dangerous for the wildlife living there.
Seawater samples from Plymouth, on the South West coast of England, were taken and used to test the researchers’ dye. The plastic-binding dye could effectively quantify very small fragments of microplastics, less than 1mm, under a fluorescent microscope. The researchers found that these microplastics were present at higher levels than previously thought, as the new technique could detect significantly more than traditional methods.
They also discovered that the majority of microplastic was polypropylene, which is commonly used for food packaging. Carbios, a pioneer in the bioplasturgy field, is tackling this problem head-on by developing infinitely recyclable bioplastics. This overcomes issues with the current process of recycling plastic, which requires high temperatures and a lot of energy. In contrast, Carbios’ system uses enzymes to break down plastics into their original monomers, which can be re-used.
Carbios recently teamed up with cosmetics giant, L’Oréal, which has agreed to use the biotech’s technology for its new packaging. More and more firms are keen to make themselves ‘green’. Coca Cola and Danone are working with Dutch biotech Avantium to develop sustainable bottles and yoghurt pots, while Audi is collaborating with the French Global Bioenergies for the production of renewable gasoline. Even Lego is investigating the possibility of making its toy blocks out of bioplastics.
Big firms getting involved in renewable materials and energy sets a great example for smaller companies. With companies making an effort to reduce the amount of waste that ends up in our oceans – and throughout the rest of the environment – the challenge of finding a way to remove what’s already there remains within reach.
Images – Lycia Walter / shutterstock.com; University of Warwick; Plastic Oceans
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No need to call the fire brigade! The University of Dresden’s cancer sensor spots a mutation to p53, the most important cancer gene, and kills the cell.
Researchers at the University of Dresden, Germany, have developed a molecular sensor that detects a mutation in tumor protein p53 – implicated in 50% of cancers – and kills the cell. The research, published in Nature Communications, found that the sensor can detect mutations in p53 and kill the cell before it undergoes the cancer transformation process. Although the technology is at a very early stage, it could offer additional levels of protection against the development of cancer-causing mutations.
Cancer remains one of the biggest causes of mortality, with 8.8 million deaths recorded in 2015. Cancers evolve through natural selection, as mutations accumulate in oncogenes and tumor-suppressor genes over time. Strikingly, British researchers have recently shown that it can take as few as 10 mutations to cause cancer. For this reason, having a system in place to spot potential damaging mutations and prevent their spread to daughter cells could be a great way to get ahead of cancer.
The molecular “smoke detector” monitors p53, making sure that the gene is functioning as it should – binding DNA to stimulate the expression of p21, which controls cell division. The group designed a genetic element that makes the cell reliant on normal p53 function, which, if interrupted, initiates cell death. The researchers believe that this should suppress tumor formation at a very early stage.
With the technology firmly in the preclinical stages, a lot of work remains to be done. However, Frank Buchholz, Project Leader at University Hospital Carl Gustav Carus, is hopeful the technology could have a big impact: “The p53 sensor enables an active precocious intervention for the first time. Our results show that cells with p53 mutations can be selectively detected and eliminated at an early stage. Hence, the transformation process is prevented.”
p53 has been known about for a while now, with researchers and biotechs around the world devising plans to bring it back under control. Aprea Therapeutics is developing a drug to restore normal p53 function, which is being tested in a Phase II trial, while Orca Therapeutics has developed p53-expressing oncolytic viruses that rapidly eradicate tumors. Elsewhere, AstraZeneca and the Babraham Institute have improved our understanding of another cancer-causing gene, PTEN, which is highly implicated in breast and prostate cancers.
Looking forward, it will be interesting to see how clinicians decide who receives the p53 sensor if it can be developed for the market and whether the technology can be adapted for other genes like PTEN.
Images – Kateryna Kon / shutterstock.com; Meletios Verras / shutterstock.com
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Autolus has revealed a new strategy to treat T-cell lymphoma without harming healthy, protective T cells. The therapy is expected to start human tests soon.
T-cell lymphoma is a form of cancer that affects the cells responsible for protecting our body against infections. Unlike it’s done with cancer types that affect other blood cells, it’s not possible to just wipe all T-cells, which would leave the patient at the mercy of viruses and bacteria.
Autolus, a young biotech spun from University College London (UCL), wants to end this situation with a therapy that selectively removes cancerous T-cells while leaving enough healthy T-cells required for protection. In a study published today in Nature, researchers from Autolus and UCL detail their strategy and prove it works in mice.
The basis of Autolus approach is based on two subtypes of receptors that T-cells naturally produce, called TRBC1 and TRBC2. While healthy T-cells randomly express one of either, those affected by lymphoma always express only one of either in each patient. In the study, the researchers created CAR-T cells engineered to recognize and kill T-cells expressing TRBC1 in mice, which killed tumoral cells while sparing the portion of healthy T cells that expressed TRBC2.
This strategy is the basis of AUTO4, a CAR-T cell therapy being developed by Autolus. The company, which recently closed a big €68M Series C fundraising to boost its technology, expects the treatment to enter a first clinical trial in humans in the coming months. AUTO4 will be the fourth cancer therapy from Autolus to enter the clinic, and the first for T-cell lymphoma.
CAR-T cell therapies have been hailed as a “miracle cure” for cancer. However, the first ones, which were approved just this year, are directed at blood cancers affecting B-cells instead of T-cells. If successful, Autolus could bring the first effective therapy for T-cell lymphoma, for which current treatment options are not good enough. So much so that the US National Comprehensive Cancer Network (NCCN) recommends clinical trials as the preferred option after a first treatment for patients diagnosed with this form cancer.
Images via Christoph Burgstedt /Shutterstock; Autolus
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