The study on the reproducibility of behavioral experiments with insects has now been published, providing evidence that some results cannot be fully reproduced. This “reproducibility crisis” affects different disciplines, including biomedical research and behavioral studies on mammals. However, there have been no comparable systematic studies on insects – until now.

A team of researchers from the Universities of Münster, Bielefeld, and Jena (Germany) conducted a multi-laboratory approach to test the reproducibility of ecological insect studies. They performed three different behavioral experiments using different insect species: the turnip sawfly, meadow grasshopper, and red flour beetle.

Each experiment was carried out in laboratories in Münster, Bielefeld, and Jena, and the results were compared. The studies examined the effects of starvation on behavior in larvae of the turnip sawfly, the relationship between body color and preferred substrate color in grasshoppers, and the choice of habitat in red flour beetles.

To the research team’s knowledge, this study is the first to systematically demonstrate that behavioral studies on insects can also be affected by poor reproducibility. This was surprising, as insect studies generally use large sample sizes and could provide more robust results. However, reproducibility was higher compared to other systematic replication studies not carried out on insects.

The results are of particular interest to scientists in behavioral biology and ecology but also for all disciplines where behavioral experiments are conducted with animals. The research team concludes that deliberately introducing systematic variations could improve reproducibility in studies with living organisms.

Researchers from St. Jude Children’s Research Hospital and the Medical College of Wisconsin have made a groundbreaking discovery that sheds light on how cells travel through the body. By developing a data science framework, they were able to analyze chemokines and their associated G protein-coupled receptors (GPCRs), which are proteins that govern cell movement.

The scientists found that specific positions within structured and disordered regions of both proteins determine how chemokines and GPCRs bind each other. This understanding enabled them to artificially change chemokine-GPCR binding preferences and alter the resulting cell migration. Their findings have significant implications for disease treatment, such as enhancing cellular therapies’ ability to reach tumor sites, and increasing clarity about healthy processes like heart and blood vessel development.

Cell migration is a crucial process that influences many aspects of our bodies, including how immune cells travel to infection sites, brain development, and wound repair. However, the vast similarities between members of each protein family have presented a challenge in understanding how correct pairs form and control cell movement. The researchers’ data-driven approach identified the exact parts of each protein governing their molecular interactions.

“We found that cells have an elegant system that uses structure and disorder together to control cell migration,” said senior co-corresponding author M. Madan Babu, PhD. “With this understanding, we can now rationally introduce small changes in a chemokine’s structure to ultimately alter cell migration in desired ways.”

The scientists compared all human chemokine-binding GPCRs and all chemokines, then compared similar chemokines and GPCRs from other species. They also looked at each protein individually at a population level, finding places that stayed the same across groups and those that differed.

“Through our data analysis, we discovered that the information for how chemokines and GPCRs select for each other is stored in small, discrete packages of highly unstructured, disordered regions,” said first and co-corresponding author Andrew Kleist, MD. “The mix of those small packages from both the chemokine and receptor results in the unique interaction, similar to website data encryption keys, which governs cell migration.”

This discovery has significant implications for disease treatment and therapy development. The researchers’ framework can guide exploration into new medicines and improvements for existing cellular therapies.

“Now that we’ve shown a proof of concept, our approach will guide exploration into new medicines and improvements for existing cellular therapies,” Kleist said. “For example, it may be possible to create molecules that better lead immune cells to cancers or help recruit more blood stem cells for bone marrow transplants.”

The framework is freely available online at: https://github.com/andrewbkleist/chemokine_gpcr_encoding.

When people think about the body, we often think every cell stays in place. However, that’s a simplistic view. Depending on the tissue, cells are moving all the time, and our new understanding of those systems opens novel avenues for therapeutic development.

This discovery has the potential to revolutionize our understanding of cell movement and its role in various biological processes. By unlocking the code of cell movement, researchers can develop more effective treatments and therapies that target specific aspects of cellular behavior.

For years, doctors have been puzzled by the mysterious case of post-treatment Lyme disease syndrome (PTLD), where patients who have received treatment for Lyme disease still experience severe fatigue, cognitive challenges, body pain, and arthritis. A recent study found that 14% of patients who were diagnosed and treated early with antibiotic therapy would still develop PTLD.

Now, Northwestern University scientists believe they have cracked the code to understanding the causes behind this condition. According to Brandon L. Jutras, a bacteriologist leading the research, the body may be responding to remnants of the Borrelia burgdorferi cell wall, which breaks down during treatment yet lingers in the liver.

The key lies in peptidoglycan, a structural feature of virtually all bacterial cells and a common target of antibiotics. Jutras’ team found that while peptidoglycan from other bacteria is rapidly shed after treatment, Lyme disease’s peptidoglycan persists for weeks to months. In humans, pieces of this peptidoglycan were omnipresent in the fluid of patients with Lyme arthritis, even after treatment.

The research suggests that the maladaptive response to these lingering molecules may be behind PTLD. Jutras explained that some patients have a more robust immune response, which could result in a worse disease outcome, while others’ immune systems largely ignore the molecule. This individualized response is likely influenced by genetic factors.

The findings open up new avenues for research and treatment options. Jutras hopes to develop more accurate tests for PTLD patients and refine treatment options when antibiotics have failed. He also proposes neutralizing the inflammatory molecule using monoclonal antibodies to target peptidoglycan for destruction.

With this breakthrough, scientists are one step closer to understanding and effectively treating PTLD, providing relief to millions of people worldwide affected by this debilitating condition.