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San Diego-based biotechnology company Samumed has recently announced that it will be moving to phase 3 clinical trials of its drug lorecivivint (SM04690) for the treatment of knee osteoarthritis.

What is osteoarthritis?

Osteoarthritis is the most common form of arthritis in the knee and a leading cause of adult disability, particularly among older people. This degenerative, “wear-and-tear” arthritis is characterized by the destruction of the articular cartilage and structural changes to the bone, which leads to pain, inflammation, and loss of joint function and mobility. It occurs most often in people who are at least 50 years old, but it may occur in younger people as well.

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Even in this “age of the genome,” much about genes remains shrouded in mystery. This is especially true for “cryptic mutations”—mutated genes that are hidden, and have unexpected effects on traits that are only revealed when combined with other mutations. Learning from one infamous cryptic mutation in particular, researchers from CSHL share important lessons for breeding or gene editing in crops.

This story starts with the Campbell Soup Company and a field of tomatoes in the mid 20th century. One particular tomato plant had an unexpected beneficial trait: the fruits separated from the vine right where the green cap and stem touch the rest of the fruit. It turned out that this spontaneous natural mutant was ideal for large-scale production.

Other tomato varieties would break away at a joint-like nub in their fruit stems, leaving the pointed green caps on the fruits. With stems still present, these capped tomatoes would get easily bruised in the machine-picking process or end up puncturing one another in transit. However, the lucky Campbell Soup mutant didn’t have these problems. It was jointless, and perfect for a growing, automated industry. Unsurprisingly, breeders called the that drives this beneficial trait jointless-2 (j2).

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Many in-development cures for type 1 diabetes have understandably focused on tackling the autoimmune aspect of the disease before figuring out a way to replace the destroyed beta cells. But what if focusing on the beta cells first could prevent their destruction altogether?

Researchers at Joslin have found that increasing the proliferation and turnover of before signs of type 1 diabetes could halt the development of the disease. In animal models, researchers in the lab of Rohit N. Kulkarni MD Ph.D., HMS Professor of Medicine and Co-Section Head of Islet and Regenerative Biology in the Joslin Diabetes Center, pushed the growth of beta while the animals were still young—meaning organs of the immune system were still developing, and still susceptible to manipulation. The results were published today in Nature Metabolism.

“We are clearly the first to show that if you push the proliferation to continuously generate new insulin producing beta-cells before the immune cell invasion starts then, for some reason we are still trying to figure out, stop attacking the beta cell,” says Dr. Kulkarni.

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A machine learning algorithm can detect signs of anxiety and depression in the speech patterns of young children, potentially providing a fast and easy way of diagnosing conditions that are difficult to spot and often overlooked in young people, according to new research published in the Journal of Biomedical and Health Informatics.

Around one in five suffer from anxiety and depression, collectively known as “internalizing disorders.” But because children under the age of eight can’t reliably articulate their emotional suffering, adults need to be able to infer their mental state, and recognise potential mental health problems. Waiting lists for appointments with psychologists, insurance issues, and failure to recognise the symptoms by parents all contribute to children missing out on vital treatment.

“We need quick, objective tests to catch kids when they are suffering,” says Ellen McGinnis, a at the University of Vermont Medical Center’s Vermont Center for Children, Youth and Families and lead author of the study. “The majority of kids under eight are undiagnosed.”

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To kill bacteria in the blood, our immune system relies on nanomachines that can open deadly holes in their targets. UCL scientists have now filmed these nanomachines in action, discovering a key bottleneck in the process which helps to protect our own cells.

The research, published in Nature Communications, provides us with a better understanding of how the kills bacteria and why our own cells remain intact. This may guide the development of new therapies that harness the immune system against bacterial infections, and strategies that repurpose the immune system to act against other rogue cells in the body.

In earlier research, the scientists imaged the hallmarks of attack in live bacteria, showing that the immune system response results in ‘bullet holes’ spread across the cell envelopes of bacteria. The holes are incredibly small with a diameter of just 10 nanometres.

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