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Immunotherapy is a fast-growing field designed to stimulate the immune system and target different diseases, including cancer. Some immunotherapies include immune cell activation therapies such as checkpoint inhibitors that block the interaction of cell markers which in turn allows the cell to kill the bound tumor cell. One example of a checkpoint inhibitor is anti-programmed cell death-1 (Anti-PD-1). Programmed cell death-1 (PD-1) is expressed on immune cells, specifically T cells. On responsibility of T cells include killing infected cells, such as cancer. The PD-1 marker is bound to PD-L1 on the infected cell and blocks the T cell’s ability to kill the tumor. Checkpoint inhibitors are effective in some subsets of cancer patients, but in more aggressive cancers such as liver cancer, immunotherapy is limited. Interestingly, a recent study in Nature Medicine by Dr. Miriam Merad and colleagues from the Ichan School of Medicine at Mount Sinai recently reported a new strategy to improve immunotherapy in liver cancer.

Merad and colleagues have uncovered a “trio of immune cells” within the tumor that helps improve immunotherapy. Researchers discovered this cohort of cells specifically in hepatocellular carcinoma (HCC), an aggressive and deadly liver cancer. It was demonstrated that specific populations in the tumor would be needed to activate T cells with immunotherapy, specifically anti-PD-1. Increased activation of T cells in HCC is critical because it demonstrates that an aggressive tumor has become sensitized to the immune system.

Researchers studied this phenomenon in patients to determine why some immune cells present in the tumor allow improved immunotherapy response, while others do not. The research team analyzed patient samples before and after checkpoint inhibitor treatment. Analysis was performed through computational methods, which allowed Merad and others to determine the immune cells necessary that help patients improve with immunotherapy. Through this computational cell analysis researchers are able to improve patient outcomes by determining if the “trio of cells” is present in the tumor.

The Y chromosome is the smallest chromosome, and holds the least amount of genes, but scientists are still learning about all of its biological functions. Research has shown that many men start to lose Y chromosomes in blood cells as they get older, and this phenomenon has been linked to some disorders including heart disease and now, cancer. Some studies have suggested that the loss of the Y chromosome may help explain why men tend to die at slightly younger ages compared to women, or why there are sex differences in some types of cancer… Two new studies reported in Nature have explored the link between cancer and the loss of the Y chromosome.

One study used a mouse model to show that a specific gene on the Y chromosome known as KDM5D increases the chance that some types of colorectal cancer will metastasize. The other research report showed that when some cells lose the Y chromosome, bladder tumors are better at evading the immune system, and the risk of aggressive bladder cancer increases.

“There is no way of knowing Cassius’ actual age as he was born in the wild and the age is just an estimate,” Toody Scott, a crocodile keeper who looks after Cassius at Marineland Crocodile Park on Green Island, told Live Science in an email. The nearly 18-foot-long (5.5 meters) saltwater giant’s birthday “was essentially made up a few years ago” and this time of year is actually “the wrong time of year for a crocodile to be born in northern Australia,” Scott added.

In 1984, researchers captured the crocodile on a cattle ranch southwest of Darwin, Australia, after the ranch owners complained they were losing livestock. Even then, when Cassius was estimated to be between 30 and 80 years old, he was the biggest crocodile ever caught alive in Australia.

“He was 16 feet, 10 inches [5.13 m] with at least another 6 inches [15 centimeters] of tail missing and a bit of a snout missing,” Grahame Webb, a crocodile researcher who participated in the capture, told ABC News. “He was a big old gnarly crocodile then. Crocs of that size are not normal.”

Insects, with their remarkable ability to undergo complete metamorphosis, have long fascinated scientists seeking to understand the underlying genetic mechanisms governing this transformative process.

Now, a recent study conducted by the Institute for Evolutionary Biology (IBE, CSIC-UPF) and the IRB Barcelona has shed light on the crucial role of three genes – Chinmo, Br-C and E93 – in orchestrating the stages of insect development. Published in eLife, this research provides valuable insights into the evolutionary origins of metamorphosis and sheds new light on the role of these genes in growth, development and cancer regulation [1].

Longevity. Technology: Chinmo might sound like a Pokémon character, but the truth is much more interesting. Conserved throughout the evolution of insects, scientists think it, and the more conventionally-named Br-C and E93, could play a key role in the evolution of metamorphosis, acting as the hands of the biological clock in insects. A maggot is radically different from the fly into which it changes – could understanding and leveraging the biology involved one day allow us to change cultured skin cells into replacement organs or to stop tumors in their early stages of formation? No, Dr Seth Brundle, you can buzz off.

This study demonstrates that AI can be incredibly effective in helping us identify new drug candidates – particularly at early stages of drug discovery and for diseases with complex biology or few known molecular targets.


A machine learning model has been trained to recognise the key features of chemicals with senolytic activity. It recently found three chemicals able to remove senescent cells without damaging healthy cells.

Molecular structure of oleandrin. Credit: Mplanine, CC BY-SA 4.0, via Wikimedia Commons.

Senescent cells, often referred to as “zombie cells”, are cells that have stopped dividing but remain metabolically active. These cells increase with age and secrete harmful substances that can lead to chronic inflammation and affect the function of nearby cells. This contributes to aging and various age-related diseases like heart disease, diabetes, Alzheimer’s, and certain cancers. Their elimination or reprogramming is a key focus of aging-related research.

According to a news release from the Vienna University of Technology (TU Wien), oxygen-ion batteries don’t have the same aging issue that lithium batteries face, which means they can maintain effectiveness for an incredibly long period.

They can also be manufactured using incombustible materials and don’t require the same rare elements as lithium batteries, which means they won’t have nearly as substantial of an environmental footprint and won’t spontaneously explode if mishandled.

“In many batteries, you have the problem that at some point the charge carriers can no longer move,” said Alexander Schmid of TU Wien’s Institute for Chemical Technologies. “Then they can no longer be used to generate electricity, the capacity of the battery decreases. After many charging cycles, that can become a serious problem.”

Researchers have used a machine learning model to identify three compounds that could combat aging. They say their approach could be an effective way of identifying new drugs, especially for complex diseases.

Cell division is necessary for our body to grow and for tissues to renew themselves. Cellular senescence describes the phenomenon where cells permanently stop dividing but remain in the body, causing tissue damage and aging across body organs and systems.

Ordinarily, senescent cells are cleared from the body by our immune system. But, as we age, our immune system is less effective at clearing out these cells and their number increases. An increase in senescent cells has been associated with diseases such as cancer, Alzheimer’s disease and the hallmarks of aging such as worsening eyesight and reduced mobility. Given the potentially deleterious effects on the body, there has been a push to develop effective senolytics, compounds that clear out senescent cells.