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CarbonationEmpowered Offshore Deep Cement Mixing Enables Undredged Land

A new study in Communications Engineering reports a construction strategy that could change how offshore reclaimed land is stabilized—using carbonation to strengthen deep cement mixing from microscopic reactions to full in-situ performance.

Conventional deep cement mixing relies on mechanically blending cement and soil, but its long-term durability in waterlogged, newly dredged environments remains a challenge. The researchers propose mixing: a process that uses carbon dioxide to drive mineral formation within the cemented soil matrix, improving both strength and stability.

At the micro-scale, carbonation converts reactive components in the cement into carbonate minerals. This reaction can refine the pore structure, reduce permeability, and bind loose particles more effectively than ordinary curing alone. In practical terms, the cement-soil composite becomes less vulnerable to water ingress and chemical attack.

3D-printable material can heal the body, build better robots and recover critical minerals

A new type of 3D-printable material developed by researchers at The University of Texas at Austin mimics human tissue’s ability to sort and filter, allowing certain molecules to pass through while keeping others out. This broad functionality means the material can be used in a variety of applications across medicine, water and robotics.

Current methods for building small tissue-like materials don’t scale to sizes that can make applications possible, the researchers say. The team overcame these issues of speed and scalability by jamming billions of tiny water droplets tightly together using simple mixing and centrifuge techniques to form large, tissue-like materials in just a few minutes. Each droplet is separated by a thin membrane, allowing the membranes to link up, similar to cell organization in human tissue.

“Tissues can separate and transport ions and molecules; that’s how our kidneys or intestines work, taking only what they need and leaving the rest behind,” said Manish Kumar, professor in the Cockrell School of Engineering’s Fariborz Maseeh Department of Civil, Architectural and Environmental Engineering and the McKetta Department of Chemical Engineering. This work was recently published in Nature Materials.

How Meta’s AI Models Are Powering the First Wave of Genesis Mission Projects

Lawrence Berkeley National Laboratory — one of the US Department of Energy’s premier research laboratories, known for Nobel Prize-winning work in physics, chemistry, and materials science — operates some of the most advanced scientific facilities on the planet. Among them is the Advanced Light Source (ALS), a football field-sized facility that produces intensely bright beams of X-ray light, allowing researchers to study materials from the atomic and molecular scale all the way to plants. The ALS’s instruments, known as beamlines, generate enormous quantities of data — and as recent facility upgrades have dramatically increased their resolution and speed, the volume of data has exploded beyond what scientists can keep up with.

Tiny BAP1 mutations can disrupt internal signals that suppress tumor growth

Scientists at the Institute of Biochemical Sciences at National Taiwan University have uncovered how tiny genetic changes can disable one of the body’s most important tumor-suppressing proteins. Their study, published in Nature Communications, reveals how cancer-associated mutations interfere with the function of BRCA1-associated protein 1 (BAP1), a protein that helps maintain normal cell growth and is frequently mutated in cancers such as mesothelioma, uveal melanoma and kidney cancer.

Although many cancer mutations in BAP1 have been identified over the years, it has remained unclear exactly how they impair the protein. To answer this question, the research team examined nearly 50 cancer-associated mutations using advanced nuclear magnetic resonance (NMR) spectroscopy, computer simulations and biochemical experiments.

‘Pro version’ of cisplatin keeps its cancer-killing power while reducing side effects

Cisplatin is one of the most successful cancer medicines ever developed. Doctors use it to treat many cancers, including lung, ovarian, breast, testicular and head and neck cancers. However, cisplatin has a serious problem. It does not attack only cancer cells. It can also reach healthy organs and damage them. In particular, cisplatin can harm the kidneys and peripheral nerves. Patients receiving cisplatin often experience pain, tingling, numbness or weakness in their hands and feet. These side effects can become so severe that doctors must reduce the dose or stop treatment completely.

This led our research team to ask a simple question: Can we keep cisplatin’s cancer-fighting power while reducing its harmful side effects?

To explore this idea, we developed a new molecule called cisproplatin, or CPP. We can think of it as a smarter, “pro version” of cisplatin designed to remain stable while traveling through the body and become active under tumor-like conditions. The research is published in the Journal of Medicinal Chemistry.

Aspirin reverses diet-driven depression-like behavior in mice

Depression is among the most common psychiatric disorders, estimated to affect between 280 million and 332 million people worldwide. This disorder is characterized by persistent sadness and hopelessness, low energy, a loss of interest in everyday activities and sometimes changes in appetite or sleep.

Several factors can contribute to the onset of depression, including genetics, chronic stress, traumatic or challenging life events and biochemical imbalances in the brain. Recent studies suggest that people’s diets can also sometimes influence their mental health and may play a role in the emergence of depressive symptoms.

Some research findings suggest that the long-term consumption of foods rich in fat is linked to an increased risk of depression. The biological processes underpinning this relationship, however, have not yet been clearly elucidated.

Synergistic senolyticregenerative therapy significantly extends healthspan and lifespan Translational Medicine

Current barriers to achieving radical life extension include the inability to use syngeneic, youthful mesenchymal stem cells (MSCs) and the anti-regenerative effects of senescence-associated secretory phenotype (SASP) factors. We aim to overcome this by a combination approach in which senescent cell burden is reduced utilizing SenoVax™ a dendritic cell based senolytic immunotherapy combined with syngeneic pluripotent stem cell derived MSC.

We induced hepatic injury and accelerated aging using two established murine models: carbon tetrachloride (CCl₄) mediated liver injury and doxorubicin induced systemic senescence. Animals were treated with control, SenoVax, pMSCs or the combination. Outcomes included biochemical and histologic indices of liver injury, circulating and tissue biomarkers of senescence (IL-11, YKL-40, IL-6, IL-23 R) and regeneration (Klotho, FGF-2, neo-VEGF, GDF-11).

Both CCl₄ and doxorubicin induced a robust senescent phenotype characterized by increased pro-inflammatory and pro-fibrotic mediators and downregulation of regenerative biomarkers. Combined senolytic and pMSC therapy outperformed mono therapies and produced clear synergistic benefits, including significant biochemical improvement of liver failure parameters, reversal of accelerated aging features, and restoration of regenerative signaling pathways. Senolytic monotherapy yielded partial improvements, while pMSCs alone showed limited activity in the presence of a high senescent-cell burden.

A fully integrated smart ring for daily biochemical monitoring

Commercial smart rings lack biochemical sensing. Here, the authors present a fully integrated ring that measures multiple chemical biomarkers from osmotically extracted sweat without iontophoresis, validated for daily analysis in both healthy and type 1 diabetic individuals.

Gold-catalyzed chemical reaction advances next-generation anticancer prodrugs

Anticancer prodrugs have attracted significant attention from the medical and scientific communities in recent years because of their potential to improve treatment precision while reducing side effects. These drugs are engineered to remain inactive until they are activated at specific sites or under particular physiological conditions within the body, at which point they release their therapeutic effect.

This targeted approach helps minimize damage to healthy tissues that often occurs when conventional chemotherapy agents attack cancer cells, addressing the longstanding challenge of collateral toxicity in cancer treatment.

However, achieving precise drug activation within the body’s highly complex biological environment remains a considerable challenge. Existing chemical strategies and activation technologies continue to face a number of technical limitations and obstacles, highlighting the need for further innovation in this field.

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