Nasal drops fight brain tumors noninvasively

Researchers at WashU Medicine have developed a noninvasive medicine delivered through the nose that successfully eliminated deadly brain tumors in mice. The medicine is based on a spherical nucleic acid, a nanomaterial (labeled red) that travels along a nerve (green) from the nose to the brain, where it triggers an immune response to eliminate the tumor.
Image Credit: Courtesy of Alexander Stegh

Researchers at Washington University School of Medicine in St. Louis, along with collaborators at Northwestern University, have developed a noninvasive approach to treat one of the most aggressive and deadly brain cancers. Their technology uses precisely engineered structures assembled from nano-size materials to deliver potent tumor-fighting medicine to the brain through nasal drops. The novel delivery method is less invasive than similar treatments in development and was shown in mice to effectively treat glioblastoma by boosting the brain’s immune response.

Glioblastoma tumors form from brain cells called astrocytes and are the most common kind of brain cancer, affecting roughly three in 100,000 people in the U.S. Glioblastoma generally progresses very quickly and is almost always fatal. There are no curative treatments for the disease, in part because delivering medicines to the brain remains extremely challenging.

What Is: Mitochondrion

Evolutionary Singularities and the Eukaryotic Dawn

The mitochondrion represents a biological singularity, a discrete evolutionary event that fundamentally partitioned life on Earth into two distinct energetic stratums: the prokaryotic and the eukaryotic. While colloquially reduced to the moniker of "cellular powerhouse," the mitochondrion is, in functional reality, a highly integrated endosymbiont that serves as the master regulator of eukaryotic physiology. It is the nexus of cellular respiration, the arbiter of programmed cell death, a buffer for intracellular calcium, and a hub for biosynthetic pathways ranging from heme synthesis to steroidogenesis. To comprehend the complexity of multicellular life, one must first dissect the intricate molecular sociology of this organelle.   

The origin of the mitochondrion is the subject of intense phylogenomic reconstruction. The prevailing consensus, the endosymbiotic theory, posits that the mitochondrion descends from a free-living bacterial ancestor—specifically a lineage within the Alphaproteobacteria—that entered into a symbiotic relationship with a host archaeal cell approximately 1.5 to 2 billion years ago. This was not a trivial acquisition but a transformative merger. The energetic capacity afforded by the internalization of a bioenergetic specialist allowed the host cell to escape the surface-area-to-volume constraints that limit prokaryotic genome size, facilitating the expansion of the nuclear genome and the development of complex intracellular compartmentalization. 

New type of DNA damage found in our cells’ powerhouses

Linlin Zhao (left) and Yu Hsuan Chen
Photo Credit: Courtesy of University of California, Riverside

A previously unknown type of DNA damage in the mitochondria, the tiny power plants inside our cells, could shed light on how our bodies sense and respond to stress. The findings of the UC Riverside-led study are published in the Proceedings of the National Academy of Sciences and have potential implications for a range of mitochondrial dysfunction-associated diseases, including cancer and diabetes. 

Mitochondria have their own genetic material, known as mitochondrial DNA (mtDNA), which is essential for producing the energy that powers our bodies and sending signals within and outside cells. While it has long been known that mtDNA is prone to damage, scientists didn't fully understand the biological processes. The new research identifies a culprit: glutathionylated DNA (GSH-DNA) adducts.

An adduct is bulky chemical tag formed when a chemical, such as a carcinogen, attaches directly to DNA. If the damage isn’t repaired, it can lead to DNA mutations and increase the risk of disease.

Scientists observe metabolic activity of individual lipid droplets in real time

LipiPB Red shows longer fluorescence lifetimes in stable lipid droplets (red) and shorter lifetimes as they undergo degradation (blue). This probe revealed that lipid droplets sequentially degrade, where lipolysis precedes lipophagy.
Image Credit: Issey Takahashi, Nagoya University

A research team has developed a fluorescent probe that allows scientists to visualize how individual lipid droplets break down inside living cells in real time. The probe changes its fluorescence properties depending on the chemical composition of each droplet, which allows researchers to observe not only their location within cells, but also their metabolic activity during lipid breakdown. The findings, published in the Journal of the American Chemical Society, may contribute to the development of new strategies to treat metabolic diseases such as obesity and diabetes, as well as cancers associated with abnormal lipid metabolism. 

“Lipid droplets are cellular organelles that not only store excess lipids but also play critical roles in lipid metabolism. However, understanding how individual droplets function has been challenging,” Professor Shigehiro Yamaguchi, from the Institute of Transformative Bio-Molecules (ITbM) at Nagoya University, explained. 

A cellular protein, FGD3, boosts breast cancer chemotherapy, immunotherapy

The research team included, front row, from left: graduate student Junyao Zhu, biochemistry professor David Shapiro, and senior researcher Chengiian Mao; back row, from left: graduate students Abigail Spaulding, Xinyi Dai and Qianjin Jiang.
Photo Credit: Fred Zwicky

A naturally occurring protein that tends to be expressed at higher levels in breast cancer cells boosts the effectiveness of some anticancer agents, including doxorubicin, one of the most widely used chemotherapies, and a preclinical drug known as ErSO, researchers report. The protein, FGD3, contributes to the rupture of cancer cells disrupted by these drugs, boosting their effectiveness and enhancing anticancer immunotherapies.

The new findings were the happy result of experiments involving ErSO, an experimental drug that killed 95-100% of estrogen-receptor-positive breast cancer cells in a mouse model of the disease. ErSO upregulates a cellular pathway that normally protects cancer cells from stress, said University of Illinois Urbana-Champaign biochemistry professor David Shapiro, who led the new work with Illinois graduate student Junyao Zhu. But when that protective pathway is ramped up, the system goes awry.

How chromosomes separate accurately

Representation how separase recognizes the cohesin subunit SCC1 before chromosome segregation occurs.
Illustration Credit: © Margot Riggi

Cell division is a process of remarkable precision: during each cycle, the genetic material must be evenly distributed between the two daughter cells. To achieve this, duplicated chromosomes, known as sister chromatids, are temporarily linked by cohesin – a ring-shaped protein complex that holds them together until separation. Researchers at the University of Geneva (UNIGE), in collaboration with the National Cancer Institute (NCI) and the University of California, San Francisco (UCSF), have uncovered the mechanism by which separase – the molecular ‘‘scissors’’ responsible for this cleavage – recognizes and cuts cohesin. Their findings, published in Science Advances, shed new light on chromosome segregation errors that can lead to certain forms of cancer. 

Biochemistry: In-Depth Description

Image Credit: Scientific Frontline

Biochemistry is a branch of biology and chemistry that explores the chemical processes within and relating to living organisms. Its primary goal is to understand the chemical basis of life by studying the structure, function, and interactions of biological macromolecules.

This field seeks to answer fundamental questions about how collections of inanimate molecules interact to constitute, maintain, and perpetuate living organisms.

Nonsurgical treatment shows promise for targeted seizure control

Jerzy Szablowski
Photo Credit: Jeff Fitlow/Rice University

Rice University bioengineers have demonstrated a nonsurgical way to quiet a seizure-relevant brain circuit in an animal model. The team used low-intensity focused ultrasound to briefly open the blood-brain barrier (BBB) in the hippocampus, delivered an engineered gene therapy only to that region and later flipped an on-demand “dimmer switch” with an oral drug. The research shows that a one-time, targeted procedure can modulate a specific brain region without impacting off-target areas of the brain.

“Many neurological diseases are driven by hyperactive cells at a particular location in the brain,” said study lead Jerzy Szablowski, assistant professor of bioengineering and a member of the Rice Neuroengineering Initiative. “Our approach aims the therapy where it is needed and lets you control it when you need it, without surgery and without a permanent implant.”

Scientists Removed Amino Acids From the Diet of Lab Mice — and They Lost Weight

Legumes are a diverse group of plants from the Fabaceae family, including beans, peas, lentils, and peanuts, that grow in pods. They are a highly nutritious food, rich in protein, fiber, vitamins, and minerals, and are often considered a plant-based alternative to animal protein. Legumes also have the unique ability to fix nitrogen from the atmosphere, which benefits soil health.
Photo Credit: Shelley Pauls

It’s not pleasant to shiver from the cold, but for some, it has the appeal of making the body burn more energy as heat than when staying in a warmer environment. According to several studies, exposure to cold is a reliable way to boost energy expenditure in mice and humans. This process of burning energy through heat loss is called thermogenesis.

While scientists and pharmaceutical companies are exploring ways to trick the body into thinking it’s cold—so that it activates thermogenesis and burns energy without the need for ice baths or winter walks in a T-shirt—obesity researchers Philip Ruppert and Jan-Wilhelm Kornfeld from the Department of Biochemistry and Molecular Biology (BMB) set out to investigate another route:

A form of thermogenesis triggered by eating specialized diets rather than temperature.

Researchers decipher mechanism that prevents the loss of brown adipose tissue activity during ageing

From left to right, Tania Quesada-López, Francesc Villarroya, Albert Blasco-Roset, Marta Giralt, Alberto Mestres-Arenas, Joan Villarroya, Aleix Gavaldà-Navarro and Rubén Cereijo.
Photo Credit: Courtesy of University of Barcelona

As the body ages, brown adipose tissue activity decreases, fewer calories are burned, and this can contribute to obesity and certain chronic cardiovascular diseases that worsen with age. A study led by the University of Barcelona has identified a key molecular mechanism in the loss of brown fat activity during ageing. The study opens up new perspectives for designing strategies to boost the activity of this tissue and prevent chronic metabolic and cardiovascular diseases as the population ages.

The paper, published in the journal Science Advances, is led by Professor Joan Villarroya, from the Faculty of Biology and the Institute of Biomedicine of the UB (IBUB) — based at the Barcelona Science Park-UB  — and the CIBER Area for Physiopathology of Obesity and Nutrition  (CIBEROBN). Teams from the Albert Einstein College of Medicine in New York (United States) are also collaborating.

UQ scientists uncover secrets of yellow fever

Dr Summa Bibby
Photo Credit: The University of Queensland

University of Queensland researchers have captured the first high-resolution images of the yellow fever virus (YFV), a potentially deadly viral disease transmitted by mosquitoes that affects the liver.

They’ve revealed structural differences between the vaccine strain (YFV-17D) and the virulent, disease-causing strains of the virus.

Dr Summa Bibby from UQ’s School of Chemistry and Molecular Bioscience said despite decades of research on yellow fever, this was the first time a complete 3D structure of a fully mature yellow fever virus particle had been recorded at near-atomic resolution.

“By utilising the well-established Binjari virus platform developed here at UQ, we combined yellow fever’s structural genes with the backbone of the harmless Binjari virus and produced virus particles that could be safely examined with a cryo-electron microscope,” Dr Bibby said.

Scientists Produce Powerhouse Pigment Behind Octopus Camouflage

An octopus camouflages itself with the seafloor. UC San Diego scientists have discovered a new way to produce large amounts of xanthommatin, a natural pigment used in animal camouflage, in a bacterium for the first time.
Photo Credit: Charlotte Seid

Scientists at UC San Diego have moved one step closer to unlocking a superpower held by some of nature’s greatest “masters of disguise.”

Octopuses, squids, cuttlefish and other animals in the cephalopod family are well known for their ability to camouflage, changing the color of their skin to blend in with the environment. This remarkable display of mimicry is made possible by complex biological processes involving xanthommatin, a natural pigment.

Because of its color-shifting capabilities, xanthommatin has long intrigued scientists and even the military, but has proven difficult to produce and research in the lab — until now.

New switch for programmed cell death identified

During the analysis work: Prof. Franz Hagn (left) and Dr. Umut Günsel
Photo Credit: Astrid Eckert / TUM 

In the fight against disease, programmed cell death – also known as apoptosis – is a key protective function of the body. It breaks down cells that are damaged or have undergone dangerous changes. However, cancer cells often manage to override this mechanism. A research team at the Technical University of Munich (TUM) has now succeeded in identifying a new molecular switch in this process and elucidating how it works.

The activation and deactivation of apoptosis is a promising field of research in basic biomedical research. The team led by Prof. Franz Hagn from the Chair of Structural Membrane Biochemistry at the TUM School of Natural Sciences has now discovered a new switch: "Many research teams worldwide are working on the exciting topic of apoptosis and its targeted control. The big advantage is that we are dealing with a highly efficient, evolutionarily developed regulatory mechanism. So, we don't have to invent something completely new, but can use the appropriate structural methods to learn from nature's optimized processes."

Researchers decipher a mechanism that determines the complexity of the glucocorticoid receptor

Above, from left to right, Pilar Montanyà-Vallugera, José Luis Torbado-Gardeazábal, Inés Montoya-Novoa and Montse Abella-Monleón. Below, from left to right, Alba Jiménez-Panizo, Pablo Fuentes-Prior, Eva Estébanez-Perpiñá and Andrea Alegre-Martí.
Photo Credit: Courtesy of University of Barcelona

Drugs to treat inflammatory and autoimmune diseases — such as asthma, psoriasis, rheumatoid arthritis or Chrousos syndrome — act mainly through the glucocorticoid receptor (GR). This essential protein regulates vital processes in various tissues, so understanding its structure and function at the molecular level is essential for designing more effective and safer drugs. Now, a study published in the journal Nucleic Acids Research (NAR) has revealed the mechanism of multimerization — the association of different molecules to form complex structures — of the glucocorticoid receptor, a process critical to its physiological function.

Deciphering how the GR forms oligomers — through the binding of several subunits — opens a crucial avenue for developing more selective drugs. These new drugs could modulate this association and thus minimize serious adverse effects, such as immunosuppression or bone loss.

Nanopore signals, machine learning unlocks new molecular analysis tool

Illustration of voltage-matrix nanopore profiling. The artistic rendering depicts proteins (colored shapes) being analyzed by solid-state nanopores under varying voltage conditions. By combining nanopore signals with machine learning, researchers can discriminate protein mixtures and detect changes in molecular populations.
Image Credit: ©2025 Sotaro Uemura, The University of Tokyo

Understanding molecular diversity is fundamental to biomedical research and diagnostics, but existing analytical tools struggle to distinguish subtle variations in the structure or composition among biomolecules, such as proteins. Researchers at the University of Tokyo have developed a new analytical approach, which helps overcome this problem. The new method, called voltage-matrix nanopore profiling, combines multivoltage solid-state nanopore recordings with machine learning for accurate classification of proteins in complex mixtures, based on the proteins’ intrinsic electrical signatures.

The study, published in Chemical Science, demonstrates how this new framework can identify and classify “molecular individuality” without the need for labels or modifications. The research holds promise of providing a foundation that could lead to more advanced and wider applications of molecular analysis in various areas, including disease diagnosis.

In a surprising discovery, scientists find tiny loops in the genomes of dividing cells

MIT experiments have revealed the existence of “microcompartments,” shown in yellow, within the 3D structure of the genome. These compartments are formed by tiny loops that may play a role in gene regulation.
Illustration Credit: Ed Banigan, edited by MIT News
(CC BY-NC-ND 4.0)

Before cells can divide, they first need to replicate all of their chromosomes, so that each of the daughter cells can receive a full set of genetic material. Until now, scientists had believed that as division occurs, the genome loses the distinctive 3D internal structure that it typically forms.

Once division is complete, it was thought, the genome gradually regains that complex, globular structure, which plays an essential role in controlling which genes are turned on in a given cell.

However, a new study from MIT shows that in fact, this picture is not fully accurate. Using a higher-resolution genome mapping technique, the research team discovered that small 3D loops connecting regulatory elements and genes persist in the genome during cell division, or mitosis.

“This study really helps to clarify how we should think about mitosis. In the past, mitosis was thought of as a blank slate, with no transcription and no structure related to gene activity. And we now know that that’s not quite the case,” says Anders Sejr Hansen, an associate professor of biological engineering at MIT. “What we see is that there’s always structure. It never goes away.”

The Many FACES of Lipid Research

Subcellular lipid distributions (magenta) in mitochondria (green) revealed using FACES and super-resolution structure illuminated microscopy.
Image Credit: William Moore

Lipids are fatty molecules that play critical roles in cell function, including membrane structure, energy storage and nutrient absorption. Most lipids are made in a cell organelle called the endoplasmic reticulum, but specific lipid types are shuttled around to different parts of the cell depending on their purpose. Each organelle serves a specific role in a cell and has its own unique mixture of lipids called a lipidome.

Scientists have long wanted to get a closer look at the movement of lipids around a cell, but because organelles are so close together – often only tens of nanometers apart – it’s tough to visualize with traditional light microscopy, which only has resolutions up to 250 nanometers.

Now researchers at the University of California San Diego have unveiled a new technology with the power to see cells in unprecedented detail. The tool, called fluorogen-activating coincidence encounter sensing (FACES), was developed in Associate Professor of Biochemistry & Molecular Biophysics Itay Budin’s lab. This work appears in Nature Chemical Biology.

Why women's brains face higher risk: scientists pinpoint X-chromosome gene behind MS and Alzheimer's

Image Credit: Scientific Frontline / AI generated

New research by UCLA Health has identified a sex-chromosome linked gene that drives inflammation in the female brain, offering insight into why women are disproportionately affected by conditions such as Alzheimer’s disease and multiple sclerosis as well as offering a potential target for intervention. 

The study published in the journal Science Translational Medicine, used a mouse model of multiple sclerosis to identify a gene on the X chromosome that drives inflammation in brain immune cells, known as microglia. Because females have two X chromosomes, as opposed to only one in males, they get a “double dose” of inflammation, which plays a major role in aging, Alzheimer’s disease and multiple sclerosis.  

When the gene, known as Kdm6a, and its associated protein were deactivated, the multiple sclerosis-like disease and neuropathology were both ameliorated with high significance in female mice.  

Cholesterol-lowering drugs could reduce the risk of dementia

Low cholesterol can reduce the risk of dementia, a new University of Bristol-led study with more than a million participants has shown.

The research, led by Dr Liv Tybjærg Nordestgaard while at the University of Bristol and the Department of Clinical Biochemistry at Copenhagen University Hospital – Herlev and Gentofte, found that people with certain genetic variants that naturally lower cholesterol have a lower risk of developing dementia.

The study, which is based on data from over a million people in Denmark, England, and Finland, has been published in the journal Alzheimer's & Dementia: The Journal of the Alzheimer's Association. 

Some people are born with genetic variants that naturally affect the same proteins targeted by cholesterol-lowering drugs, such as statins and ezetimibe. To test the effect of cholesterol-lowering medication on the risk of dementia, the researchers used a method called Mendelian Randomization — this genetic analysis technique allowed them to mimic the effects of these drugs to investigate how they influence the risk of dementia, while minimizing the influence of confounding factors like weight, diet, and other lifestyle habits.

Programmable proteins use logic to improve targeted drug delivery

Therapies that are sensitive to multiple biomarkers could allow medicines to reach only the areas of the body where they are needed. The diagram above shows three theoretical biomarkers that are present in specific, sometimes overlapping areas of the body. A therapy designed to find the unique area of overlap between the three will act on only that area.
Image Credit: DeForest et al./Nature Chemical Biology

Targeted drug delivery is a powerful and promising area of medicine. Therapies that pinpoint the exact areas of the body where they’re needed — and nowhere they’re not — can reduce the medicine dosage and avoid potentially harmful “off target” effects elsewhere in the body. A targeted immunotherapy, for example, might seek out cancerous tissues and activate immune cells to fight the disease only in those tissues.

The tricky part is making a therapy truly “smart,” where the medicine can move freely through the body and decide which areas to target.