Toggle light / dark theme

Abstract: Offering a topical strategy in skin cancer

https://doi.org/10.1172/JCI189044 Brian C. Capell & team identify the epigenetic regulator LSD1 as critical for epidermal development and find its inhibition suppresses tumors in two cutaneous squamous cell carcinoma mouse models by promoting immunosurveillance.

The image shows immunofluorescence from mice lacking LSD1 in the skin, revealing profound activation of cutaneous retinoid signaling (as measured by CRABP2 levels in green); keratin 14 (red); nuclei (blue).


1Department of Dermatology and.

2Penn Epigenetics Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.

3Division of Allergy and Immunology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.

A better flu shot may be coming: How epitope targeting could widen protection

Doctors recommend getting your flu shot annually, since the specific influenza strain it targets varies from year to year. But what if the shot could be more effective while protecting against more strains? Researchers from the University of Missouri School of Medicine are one step closer to making this happen. When the immune system sees a new strain of a familiar virus, it typically focuses on the parts it “remembers” most, even if those regions have changed. “Epitope-spanning antigenic variation reprograms immunodominance and broadens immunity in sequential influenza vaccination” was recently published in Nature Communications.

“In our vaccine model, we targeted specific but distinct regions of the protein on the surface of the influenza virus. These regions are called epitopes,” said study author Henry Wan. “The model included different versions of epitopes in hopes of redirecting how the immune system responds. We found that the vaccine approach helped the immune system target more variants of the virus, leading to broader protection.”

Wan says the epitopes help the immune system see the flu virus differently, and it learns to respond with more coordination between the different types of immune cells. Some of the epitopes are also not as likely to change, which could make flu vaccines more reliable or even help create a universal flu vaccine.

Abstract: Implications for protecting against cognitive impairment following HeadInjury👇

Here, Michael T. Heneka & team find the inflammasome adaptor ASC drives long-lasting brain inflammation and cognitive problems after mild head injury in a closed-head injury model.

The figure shows skeletonized activated microglia (Iba1+ cells) following closed head injury, with mice lacking ASC show showing preservation of morphological features, particularly at later time points.


3Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Belvaux, Luxembourg.

4German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

5Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, PR China.

How do cancer cells ‘learn’ to resist treatment?

Researchers at NYU Langone Health propose a model that could explain how cancer cells adapt to environmental stress, an approach that may lead to new therapies. Published online April 15 as the cover story of the journal Nature, the perspective article centers on a family of proteins called AP-1, which are quickly activated in cells in response to stressful situations—like being exposed to chemotherapy.

While AP-1 proteins have been studied for many decades, the authors propose they are part of a previously overlooked molecular mechanism in which cells survive by learning to rewire their circuitry. This process depends not on permanent changes to a cell’s DNA code, but rather on the cell’s ability to turn genes on or off, and then “remember” the changes that improve its survival chances.

The work suggests that cancer cells use this plasticity to explore gene expression patterns until they find a combination that helps them survive. Once a successful survival state is discovered, it can be locked in and passed down to future cell generations, leading to drug-resistant tumors.

Eosinophil extracellular traps: heterogeneity of their stimuli, components, and functions

Like neutrophil extracellular traps, eosinophil extracellular trap formation also involves two distinct processes: suicidal EETosis and vital eosinophil extracellular trap release.

Eosinophil extracellular trap contains chromatin and/or mitochondrial DNA, granular proteins, nuclear histone variants, cytosolic mediators, cytoskeletal proteins, organelle proteins, and cell membrane proteins.

There are at least four major classes of stimuli that contribute to eosinophil extracellular trap formation via NADPH induced reactive oxygen species generation and/or peptidylarginine deiminase4-dependent histone citrullination pathways.

Cell necrosis, autophagy, and apoptosis, disease status and severity, and eosinophil subtypes all affect eosinophil extracellular trap formation.

The diversities of DNA sources and granule protein types in eosinophil extracellular trap all determine eosinophil extracellular trap’s functional heterogeneity, depending on stimulation environments and disease status. sciencenewshighlights ScienceMission https://sciencemission.com/Eosinophil-extracellular-traps


Eosinophils participate in immune regulation through their granule proteins and cytokines. Recent studies demonstrate eosinophil functional versatility through the mechanism of eosinophil extracellular traps (EETs). EET formation occurs via suicidal eosinophil extracellular trap cell death (EETosis) and vital EET release. EETs contain chromatin-or mitochondrial-derived DNA, granule proteins, nuclear proteins, and cytosolic components that vary depending on the type and intensity of stimuli. Synthetic compounds, pathogenic microorganisms, endogenous molecules, and co-stimulatory factors stimulate EET formation via diverse signaling pathways through receptors that rely on or operate independently of NADPH oxidase-mediated reactive oxygen species production and peptidylarginine deiminase-4-dependent histone modification.

Val Kilmer Resurrected by AI: ‘As Deep as the Grave’ Trailer Brings Late Actor Back to the Big Screen (EXCLUSIVE)

The filmmakers behind “As Deep as the Grave” have debuted the trailer for the upcoming historical drama, giving viewers a first look at the AI technology that was used to create Val Kilmer’s performance.

Kilmer, who died in 2025 after battling throat cancer, was cast as Father Fintan, a Catholic priest and Native American spiritualist, but was too sick to shoot his role. With the cooperation of Kilmer’s estate and his daughter Mercedes, the “As Deep as the Grave” team used generative AI to include the actor in the finished film.

Jellyfish-Inspired Ultrafast and Versatile Magnetic Soft Robots for Biomedical Applications

JUST PUBLISHED: jellyfish-inspired ultrafast and versatile magnetic soft robots for biomedical applications

Click here to read the latest free, Open Access article from Cyborg and Bionic Systems.

Marine sponge bacterium enzyme reveals a two-part route to make terpenoids

The molecular structure of an enzyme from a marine bacterium with potential industrial uses has been determined by RIKEN researchers. The insights they have gained could help make a range of useful compounds through genetic modification. The research is published in the journal Chemical Science.

The class of natural compounds known as terpenoids is nothing if not versatile, being used in a wide assortment of products, from perfumes and insect repellents to pesticides and drugs. More than 100,000 terpenoids have been identified so far. They are produced by an impressive range of organisms spanning animals, plants, fungi, bacteria, and viruses.

Recently, marine organisms such as corals, sponges, and marine bacteria have been found to produce terpenoids with complex structures that show promise for fighting infectious diseases.

Self-propulsion or slow diffusion: How bacteria, cells, and colloids respond to stimuli

What physical processes govern the movement of microscopic structures capable of interacting with their environment? The answer lies in two mechanisms: self-propulsion, to escape unfavorable locations; and slow diffusion, to move toward more advantageous ones. This is the finding of scientists Jacopo Romano and Andrea Gambassi from SISSA-Scuola Internazionale Superiore di Studi Avanzati in their new study published in Physical Review Letters.

In their work, the researchers combined computer simulations with mathematical calculations, taking inspiration from nature. It is well known that feedback-driven motion underlies the behavior of various microorganisms, which analyze incoming and outgoing signals and adapt their direction of movement accordingly. The study reproduces the physical behavior of natural and synthetic agents in two distinct scenarios: when a specific destination must be avoided based on signals, and when it must instead be reached.

The researchers found that in the first case, a process of “superdiffusion” occurs, with accelerated motion, while in the second case a subdiffusive process takes place, with much slower movement. These findings provide important insights for the design of smart particles capable of moving at the microscale, with potential applications in medicine, particularly for more efficient drug delivery.

/* */