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Nanofiber patch for psoriasis treatment has dual release functionality

The researchers used electrospinning to produce the patch—a method where high voltage is applied to a polymer solution to produce synthetic nanofibers. The fibers are then used to make a fiber mat that may be attached to the skin like a plaster.

The researchers are still working on the patch. More research, and are needed before the method is ready for use.

According to Andrea Heinz, though, it has great potential that extends beyond psoriasis treatment, “A patch containing active ingredients may be an alternative to creams and ointments in the treatment of other inflammatory skin diseases, for instance atopic eczema. It may also be useful in connection with wound healing.”

Bioluminescent proteins made from scratch enable non-invasive, multi-functional biological imaging

Bioluminescence is the natural chemical process of light creation in some living creatures that makes fireflies flicker and some jellyfish glow. Scientists have long been interested in borrowing the secrets of these animals’ light-producing genes to create similar effects in vertebrates, for a variety of biomedical applications.

DNA repair defects in cancer and therapeutic opportunities

DNA repair and DNA damage signaling pathways are critical for the maintenance of genomic stability.


In this review, Hopkins et al. review the major classes of DNA repair and damage signaling defects in cancer, the genomic instability that they give rise to, and therapeutic strategies to exploit the resulting vulnerabilities. They also discuss the impacts of DNA repair defects on both targeted therapy and immunotherapy, and highlight emerging principles for targeting DNA repair defects in cancer therapy.

Synthetic cells successfully emulate natural cellular communication

A research team from the University of Basel has succeeded in synthesizing simple, environmentally sensitive cells complete with artificial organelles. For the first time, the researchers have also been able to emulate natural cell-cell communication using these protocells—based on the model of photoreceptors in the eye. This opens up new possibilities for basic research and applications in medicine.

Turtles have genomes unlike any other animal

For example, enhancers (DNA segments that promote gene expression) and gene promoters (regions that initiate transcription) can interact more readily in open, accessible regions of chromatin.

On the other hand, DNA in tightly packed chromatin regions remains less active. Through analyzing these contact points, researchers have developed models to map chromatin configurations across various species, such as humans, mice, birds, and more recently, turtles.

In a recent paper published in the journal Genome Research, Valenzuela’s team described the chromatin arrangement in the genomes of two turtle species, the spiny softshell and northern giant musk turtles, uncovering a structure previously unobserved in other organisms.

Unusual Stem Cell Discovery Challenges Longstanding Cellular Reprogramming Theories

Researchers found that neural crest stem cells are uniquely capable of reprogramming, challenging current reprogramming theories and opening possibilities for stem cell-based treatments.

A research team from the University of Toronto has identified that neural crest stem cells, a group of cells found in the skin and other parts of the body, are the origin of reprogrammed neurons previously found by other scientists.

Their findings refute the popular theory in cellular reprogramming that any developed cell can be induced to switch its identity to a completely unrelated cell type through the infusion of transcription factors. The team proposes an alternative theory: there is one rare stem cell type that is unique in its ability to be reprogrammed into different types of cells.

Chemists Create ‘Impossible’ Bond in Molecule, Defying 100-Year-Old Rule

Carbon is a gregarious little atom, bending over backwards to link with a wide variety of elements in what is collectively referred to as organic chemistry. Life itself wouldn’t be possible without carbon’s knack for making connections.

Yet even this friendly fellow has its limits. Take Bredt’s rule for instance, which says stable two-laned connections known as covalent double bonds won’t form adjacent to any V-shaped bridges that happen to form across ‘bicyclic’ molecules.

Now a team of chemists from the University of California, Los Angeles has uncovered a solution that violates Bredt’s century-old rule. This encourages future drug research to explore the use of molecules that we thought could not exist.

Google DeepMind open-sources AlphaFold 3, ushering in a new era for drug discovery and molecular biology

Google DeepMind has unexpectedly released the source code and model weights of AlphaFold 3 for academic use, marking a significant advance that could accelerate scientific discovery and drug development. The surprise announcement comes just weeks after the system’s creators, Demis Hassabis and John Jumper, were awarded the 2024 Nobel Prize in Chemistry for their work on protein structure prediction.

AlphaFold 3 represents a quantum leap beyond its predecessors. While AlphaFold 2 could predict protein structures, version 3 can model the complex interactions between proteins, DNA, RNA, and small molecules — the fundamental processes of life. This matters because understanding these molecular interactions drives modern drug discovery and disease treatment. Traditional methods of studying these interactions often require months of laboratory work and millions in research funding — with no guarantee of success.

The system’s ability to predict how proteins interact with DNA, RNA, and small molecules transforms it from a specialized tool into a comprehensive solution for studying molecular biology. This broader capability opens new paths for understanding cellular processes, from gene regulation to drug metabolism, at a scale previously out of reach.

Aging drives a program of DNA methylation decay in plant organs

How organisms age is a question with broad implications for human health. In mammals, DNA methylation is a biomarker for biological age, which may predict age more accurately than date of birth. However, limitations in mammalian models make it difficult to identify mechanisms underpinning age-related DNA methylation changes. Here, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing heterochromatin DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing lifespan, and that shoot apical meristems are protected from this aging process. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging, and that mutants of this mechanism display a complete absence of epigenetic decay. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging.

The authors have declared no competing interest.