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Category: biotech/medical

Superconductivity switched on in material once thought only magnetic

Superconductivity—the ability of a material to conduct electricity without any energy loss to heat—enables highly efficient, ultra-fast electronics essential for advanced technologies such as magnetic resonance imaging (MRI) machines, particle accelerators and, potentially, quantum computers. New research has now revealed that iron telluride (FeTe), a compound composed of the chemical elements iron and tellurium and long thought to be an ordinary magnetic metal, is in fact a superconductor. The researchers found that hidden excess iron atoms induce the material’s magnetism, and removing these atoms allows electricity to flow with zero resistance.

Two papers describing the research, both led by Penn State Professor of Physics Cui-Zu Chang, were published back-to-back today (April 1) in the journal Nature. The first paper focuses on how to “switch on” superconductivity in FeTe, while the second paper reveals a new kind of “quantum dance,” where superconductivity interacts with the material’s atomic structure when a different top layer is added, allowing researchers to tune its behavior.

“Unlike the well-known iron-based superconductor iron selenide (FeSe), FeTe has long been considered a magnetic metal without superconductivity, despite having an almost identical crystal structure,” Chang said. “It has remained a mystery why FeTe doesn’t share this important property.”

Precision work prior to cell division: How enzymes optimize DNA structure

Before a cell can divide, it has to precisely duplicate its entire genetic information. However, the DNA in the cell exists as part of a DNA-protein complex known as chromatin. For this purpose, the DNA is wrapped around a core of histone proteins and tightly packed into so-called nucleosomes.

So that the genetic material can be reliably copied, the chromatin has to be temporarily reorganized in certain places and adopt a very specific architecture.

A team led by molecular biologists Professor Axel Imhof and Professor Christoph Kurat at the Biomedical Center (BMC) has now deciphered how the precise packaging of DNA is controlled at the beginning of cell division. The work is published in the journal Nature Communications.

Accuracy test for protein language models shines light into AI ‘black box’

AI language models, used to generate human-like text to power chatbots and create content, are also revolutionizing biology by treating complex biological data like a language. Language models are increasingly used, for example, to find patterns in DNA and proteins, to make predictions and speed research into biological complexity. A critical gap, however, is the lack of a method to estimate the reliability of these predictions.

Computational biologists at Emory University have bridged this gap, developing a simple way to test the accuracy of a language model’s understanding of proteins. Nature Methods has published their system, which scores the reliability of a model’s predictions by comparing how it embeds (numerically codifies) synthetic random proteins versus proteins found in nature.

“To the best of our knowledge, our framework is the first generalized method to quantify protein sequence embedding reliability,” says Yana Bromberg, senior author of the paper and Emory professor of biology and computer science.

Semaglutide ameliorates osteoarthritis progression through a weight loss-independent metabolic restoration mechanism

Weight loss-independent mechanism to ameliorate osteoarthritis by semaglutide.

Occurrence and progression of osteoarthritis (OA) is linked to metabolic disorders but molecular mechanism is not clear.

The researchers in this study demonstrate chondroprotective effects of a glucagon-like peptide-1 receptor (GLP-1R) agonist, semaglutide, in obesity-related osteoarthritis.

Mechanistically, these effects are independent of body weight loss and involve metabolic reprogramming of chondrocyte via the GLP-1R-AMPKPFKFB3 signaling axis. sciencenewshighlights ScienceMission https://sciencemission.com/Semaglutide-ameliorates-osteoarthritis

Qin et al. demonstrated the chondroprotective effects of semaglutide in obesity-related osteoarthritis. Mechanistically, these effects are independent of body weight loss and involve metabolic reprogramming of chondrocyte via the GLP-1R-AMPK-PFKFB3 signaling axis.

Advancing the Manufacture of Patient Accessible Cell and Gene Therapies at Place-of-Care

A partnership involving a medical school, a non-profit organization, and a biotech company have formed a partnership for the development and manufacture of an accessible and commercially viable hematopoietic stem cell (HSC) manufacturing platform for diseases like sickle cell disease (SCD). The alliance combines Trenchant BioSystems’ technology for automating patient-specific cell and gene therapy (CGT) processes, the University of Massachusetts Chan Medical School’s expertise on blood stem cell processes, and Caring Cross’s expertise in increasing patient access.

The collaboration will focus on developing a gene-modified stem cell manufacturing process with Trenchant’s AutoCell automated CGT manufacturing platform that is designed to be scalable and operate at place-of-care in an ISO class 7 environment to increase efficiencies and decrease costs.

A key reason Trenchant BioSystems’ automated CGT manufacturing platform was selected is its use of a microbubble separation approach as an alternative to immunomagnetic bead-based separation for stem cell gene therapies, point out officials at Caring Cross and Chan Medical School. In addition, AutoCell has a small footprint and significantly fewer facility requirements, important factors for lowering the cost of these therapies, adds Jon Ellis, CEO, Trenchant BioSystems.

Therapeutic, nasally delivered DNA vaccine fuses two genes to help fight tuberculosis

In a paper published in the Journal of Clinical Investigation, a research team at Johns Hopkins Medicine and the Johns Hopkins Bloomberg School of Public Health reports developing a therapeutic intranasal (nose-delivered) DNA vaccine against tuberculosis (TB) that fuses two genes with the goal of directing the immune system to fight drug-tolerant bacterial “persisters” that can survive prolonged antibiotic therapy and contribute to disease relapse.

A scourge for at least the past 6,000 years, TB is estimated by the World Health Organization (WHO) to be a latent, symptom-free infection in about one-quarter of the world’s population, approximately 2 billion people. In 2024 alone, WHO reported that more than 10 million people worldwide developed active TB disease, with 1.2 million deaths recorded. This makes TB the leading cause of death from a single infectious disease.

In recent years, WHO has called for therapeutic vaccines that can be used alongside drug therapies to shorten TB treatment regimens and improve outcomes, particularly because long multidrug courses are difficult to complete, and drug-resistant TB strains continue to emerge. The vaccine described in the new Johns Hopkins study shows promise for meeting that need.

Scientists find a new therapeutic target present on up to half of all tumors

For five decades, scientists have known about a notorious cancer-causing enzyme called SRC. But they always assumed it only appeared on the inside of cells, where it sent signals that fueled tumor growth and stayed hidden from the immune system. But now researchers at UC San Francisco have discovered that the SRC enzyme also appears like a flag on the surface of bladder, colorectal, breast, pancreatic and probably many other tumor cells.

As cancer cells furiously divide, they produce a lot of garbage. In healthy cells, the trash gets broken down. But in tumors, the recycling system gets overwhelmed, and the cells expel some of their trash. This pushes the SRC onto the surface of the cell, where it is visible to potential therapies, like antibodies.

Researchers targeted SRC with antibodies that carried radioactive payloads or summoned immune cells. This killed the cancer cells, shrinking tumors in mice. The new target could apply to up to half of all tumors.

Pck1 Deficiency Drives Mitochondrial Dysfunction and Cellular Senescence in Adipocytes

Adipose tissue is one of the most vulnerable tissues during aging, and its dysfunction plays a pivotal role in age-associated physiological impairments (Ou et al. 2022). As the primary energy storage and endocrine organ, adipose tissue serves as a central hub for maintaining energy and metabolic homeostasis (Zwick et al. 2018). Age-related accumulation of the dysfunctional adipose tissue, particularly visceral fat, induces chronic inflammation and insulin resistance, leading to metabolic disorders (Reyes-Farias et al. 2021 ; Zhang, Jiang, et al. 2024). Clearance of senescent cells in white adipose tissue (WAT) has been shown to significantly mitigate aging-related metabolic dysfunction in murine models, highlighting a pivotal role of WAT in organismal aging (Palmer et al. 2019 ; de Oliveira et al. 2025).

Senescent cells undergo metabolic reprogramming, resulting in abnormal accumulation of detrimental metabolites that further reinforce inflammatory and senescence pathways (Maqdasy et al. 2022 ; Dou et al. 2023 ; Zhang, Higgins, et al. 2024). These cells are identified by a combination of molecular features, including elevated senescence-associated β-galactosidase (SA-β-gal) activity, increased expression of cyclin-dependent kinase inhibitors p21 and p16, persistent DNA damage response, and secretion of the senescence-associated secretory phenotype (SASP) (Di Micco et al. 2021). Mitochondrial dysfunction is a critical driver of cellular senescence (Gonzalez-Freire et al. 2015), marked by impaired mitochondrial quality control, heightened oxidative stress, accumulation of mitochondrial DNA damage, and disruption of cytosolic nicotinamide adenine dinucleotide (NAD+ and NADH) balance (de Mello et al. 2018 ; Das et al. 2021). Emerging studies indicate that impaired TCA cycle metabolism reduces mitochondrial membrane potential, exacerbates mitochondrial damage, and contributes to cellular senescence (Kurhaluk 2024 ; Cappel et al. 2019). However, the precise mechanisms linking mitochondrial dysfunction to the onset and progression of cellular senescence and age-related inflammation remain incompletely understood.

Phosphoenolpyruvate carboxykinase 1 (Pck1) is well recognized as a rate-limiting enzyme in hepatic and renal gluconeogenesis; however, in adipose tissue, it predominantly facilitates glyceroneogenesis, playing a pivotal role in modulating mitochondrial-cytosolic carbon flux via TCA cycle cataplerosis. Our prior research demonstrates that Pck1 modulates replicative lifespan in yeast (Yuan et al. 2020), suggesting its potential role in aging processes. In this study, we showed that Pck1 was essential for mitochondrial function and adipose tissue aging. Pck1 deficiency induced premature adipocyte senescence, exacerbated age-related metabolic abnormalities and inflammation in WAT. Mechanistically, Pck1 deficiency impaired TCA cycle catabolism, leading to fumarate accumulation, which further promoted cellular senescence. These findings identify Pck1 as a key metabolic effector that links mitochondrial metabolism in adipocytes to adipocyte aging and inflammation, with potential implications for targeting age-related diseases.

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