Lifeboat Foundation

Melanoma, the most dangerous type of skin cancer, remains in the top five cancers diagnosed in both men and women. Scientists understand that most melanoma cells express antigens, proteins that prompt the body to initiate an immune response. We consider these antigens “unique” because other non-melanoma cells do not usually express them. Thus, melanoma antigens present a viable target for cancer treatment.

However, melanoma vaccines made to target antigens remain limited in clinical efficacy. One potential opportunity for cancer vaccines involves the antigens targeted by a particular vaccine. While original vaccines targeted one or two antigens, studies have shown that vaccines that recognize up to 12 antigens elicit a more robust immune response.

Still, vaccine development has continued to evolve to improve clinical efficacy. One area of focus concerns the type of immune cells elicited by the vaccine. CD8+ T cells, the immune cells that kill cancer cells, represent the most critical type of immune cell needed for an effective anti-tumor immune response. However, during an immune response, CD4+ T cells, also known as “helper” T cells, stimulate CD8+ T cells. In other words, CD4+ T cells “help” CD8+ T cells become activated and eliminate cancer cells.

The 2023 Nobel Prize in Chemistry was focused on quantum dots – objects so tiny, they’re controlled by the strange and complex rules of quantum physics. Many quantum dots used in electronics are made from toxic substances, but their nontoxic counterparts are now being developed and explored for uses in medicine and in the environment. One team of researchers is focusing on carbon-and sulfur-based quantum dots, using them to create safer invisible inks and to help decontaminate water supplies.

The researchers will present their results today at the spring meeting of the American Chemical Society (ACS).

Quantum dots are synthetic nanometer-scale semiconductor crystals that emit light. They are used in applications such as electronics displays and solar cells. “Many conventional quantum dots are toxic, because they’re derived from heavy metals,” explains Md Palashuddin Sk, an assistant professor of chemistry at Aligarh Muslim University in India. “So, we’re working on nonmetallic quantum dots because they’re environmentally friendly and can be used in biological applications.”

One of the largest threats to human health is obesity, but now researchers from the University of Aberdeen Rowett Institute have made an important discovery in how the brain controls food intake.

Obesity and being overweight have become the “new normal” in modern times and can lead to a multitude of health problems. We know that excess weight is primarily caused by eating more calories than the body needs; however, new research published in Current Biology has found a specific cluster of cells in the brain that control body weight.

How the brain controls hunger has not been fully defined. The researchers discovered a cluster of brain cells that can be harnessed to reduce food intake and body weight. One way they do this is by turning down cells that stimulate hunger.

Israeli scientists have made yet another cancer treatment breakthrough, this time using nanosized polymers. Researchers from Ben Gurion University say they developed a way to selectively deliver chemotherapeutic drugs to blood vessels that feed tumors and metastases.

The polymer eliminates colorectal cancer liver metastases and prolongs mice survival, after a single dose-therapy, they said. The findings were published in Nano Today, a leading journal in the field of nanotechnology.

A nanosized polymer is a polymer that has been engineered to have dimensions in the nanometer range. By comparison, a human hair is about 80,000–100,000 nanometers wide. These tiny particles offer unique properties that make them desirable for a wide range of applications.

There are trillions of microorganisms living in our gastrointestinal tract. So why doesn’t the immune system launch a massive response against all of those foreign microbes? Scientists have now provided new details about the process. The findings have been reported in Nature.

The gut microbiome has to maintain a careful balance, and promote the growth of healthy and beneficial organisms while tamping down the growth of potential pathogens. While scientists have not defined exactly what a healthy microbiome is made of, and it may differ from one person to another, we do know that when the balance in the microbial community of the gut is disrupted, health problems can arise.

Scientists studying learning in mice have inadvertently encountered ‘zombie neurons’ in the brain – not flesh-eating, virus-spreading monsters, but cells that stop interacting normally even though they’re functionally alive. What’s more, they shed new light on learning processes in the brain.

A team from Portugal discovered the cells as part of an investigation into how a part of the brain called the cerebellum learns from the environment around us.

The cerebellum processes sensory information related to motor movements. It helps us walk down a crowded street, or pick up a drink without spilling it, and it’s also important for learning: so if we bump into something, we know how to refine our movement to avoid it next time. Exactly how that learning happens was the subject of this new study.

🦠🔬🩹

Study explores how wound microbiota affect skin repair and infection risk by altering host immune responses, underscoring the complexity of microbial interactions in wound healing.

Using only DNA and glass, researchers made a material four times stronger and five times lighter than steel. It was inspired by Iron Man.

Your immune system should ideally recognize and attack infectious invaders and cancerous cells. But the system requires safety mechanisms, or brakes, to keep it from damaging healthy cells. To do this, T cells—the immune system’s most powerful attackers—rely on immune “checkpoints” to turn immune activation down when they receive the right signal. While these interactions have been well studied, a research team supported in part by NIH has made an unexpected discovery into how a key immune checkpoint works, with potentially important implications for therapies designed to boost or dampen immune activity to treat cancer and autoimmune diseases.¹

The checkpoint in question is a protein called programmed cell death-1 (PD-1). Here’s how it works: PD-1 is a receptor on the surface of T cells, where it latches onto certain proteins, known as PD-L1 and PD-L2, on the surface of other cells in the body. When this interaction occurs, a signal is sent to the T cells that stops them from attacking these other cells.

Cancer cells often take advantage of this braking system, producing copious amounts of PD-L1 on their surface, allowing them to hide from T cells. An effective class of immunotherapy drugs used to treat many cancers works by blocking the interaction between PD-1 and PD-L1, to effectively release the brakes on the immune system to allow the T cells to unleash an assault on cancer cells. Researchers have also developed potential treatments for autoimmune diseases that take the opposite tact: stimulating PD-1 interaction to keep T cells inactive. These PD-1 “agonists” have shown promise in clinical trials as treatments for certain autoimmune diseases.