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Scientists “recharge” damaged nerves to ease chronic pain

Now, researchers at Duke University School of Medicine say restoring healthy mitochondria could offer a completely new way to treat that pain.

In a study published in Nature, the team used both human tissue and mouse models to test whether replenishing mitochondria could help damaged nerve cells recover. The treatment significantly reduced pain linked to diabetic neuropathy and chemotherapy-related nerve damage. In some cases, the relief lasted for up to 48 hours.

Rather than simply blocking pain signals, the researchers believe the approach may address one of the underlying causes of chronic nerve pain by restoring the energy supply nerve cells need to function properly.

Experimental plague vaccine strategy protects mice with missing key immune defenses

The plague has killed more people than World War II. The bacterium Yersinia pestis (Yp), which causes plague, has triggered three major pandemics throughout history, leaving behind a casualty toll of more than 200 million people. Although the plague no longer causes pandemics on the scale seen in history, it still occurs in many parts of the world today. Vaccination remains our best defense against the disease, but approved options remain scarce.

In a new study, scientists tested two live-attenuated plague vaccines, LMA and LMP—weakened forms of the plague bacterium that cannot cause disease—both alone and in combination with the virus-based vaccine Ad5-YFV.

They genetically engineered the mice to completely lack a signaling protein called interferon-gamma, which plays a crucial role in activating immune cells. Despite lacking a key immune protein, the vaccines protected 80% to 100% of mice exposed to highly lethal doses of the pneumonic plague-causing Yp CO92 strain, while triggering strong antibody and immune responses in all vaccinated animals.

Natural clotting ‘switch’ may one day reduce reliance on blood thinners to prevent heart attacks and strokes

Cardiovascular conditions such as strokes or heart attacks are among the most common causes of death in Germany. Today, treatment and prevention are primarily based on so-called platelet aggregation inhibitors and anticoagulants—types of medication commonly referred to as blood thinners. They inhibit or prevent blood coagulation, which in turn prevents the formation of blood clots and life-threatening medical emergencies such as strokes or heart attacks. However, by intervening directly in the hemostasis process, they increase the risk of dangerous bleeding.

In a study published in the journal Science Advances, researchers led by Dr. Marcel Benkhoff (Department of Cardiology, Pneumology and Angiology at the UKD) have mapped a novel therapy approach that utilizes the body’s own mechanisms. The study focused on two substances produced by the body: sphingosine-1-phosphate (S1P) and thrombomodulin ™.

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.

Could permanent magnets protect astronauts from solar storms?

Shielding astronauts from the deadly radiation they face is a central challenge for any designer of a deep-space crewed mission. Even relatively low levels of exposure over long periods can lead to everything from central nervous system damage to cancer. But current solutions, such as passive water shells or active superconducting magnets, have their own limitations. To get around those, a new paper, available in preprint on arXiv by Valerio Parisi and a team of researchers from Italy and Germany, looks at the feasibility of using a permanent magnet (and its associated permanent magnetic field) to potentially block some of that radiation without the costs of competing technologies.

First, let’s look at the specific types of radiation that make it so dangerous. One is galactic cosmic rays (GCR), which are continuous, extremely good at getting through things, and seem to come from everywhere. Another is a ferocious burst of protons known as a solar particle event (SPE)—essentially a solar storm directed at a spacecraft. Each has the potential to devastate the biological payload of any deep-space craft—including living humans.

The most common way to protect against these radiation sources is simply putting a bunch of stuff between them and the fragile biological systems. This technique relies on low atomic number materials, such as aluminum, polyethylene or, in many cases, water (which is needed for many other biological functions on a deep-space craft). The problem with this technique is weight. The tyranny of the rocket equation means getting enough material into orbit to protect the crew from an SPE is extraordinarily expensive—and could amount to bringing tens of tonnes out of Earth’s gravity well.

Can This New Enzyme Reverse Aging?

This is rather technical.


Researchers at Revel Pharmaceuticals and Calico Life Sciences have engineered CMLase, an enzyme that removes carboxymethyl-lysine (CML) — a glycation product long considered permanent damage on our longest-lived proteins. In this video I explain the details behind this discovery and what it means for the aging field.

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through PayPal — https://paypal.me/sheekeyscience?coun… through Patreon — / thesheekeyscienceshow TIMESTAMPS 0:00 – Intro: what CML is and why it seemed irreversible 2:25 – How they made the enzyme 6:20 – Human tissue data 7:40 – My thoughts and limitations Paper: Trabosh et al., Nature Communications, 2026 — https://doi.org/10.1038/s41467-026-75… note that The Sheekey Science Show is distinct from Eleanor Sheekey’s teaching and research roles. The information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Sheekey Science Show and guests assume no liability for the application of the information discussed. Icons in intro; “https://www.freepik.com/free-photos-v…“Background vector created by freepik — www.freepik.com.
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TIMESTAMPS

‘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.

JCI: Shiley Eye Institute, Department of Ophthalmology, University of California, San Diego, San Diego, California, USA

Shiley Eye Institute, Department of Ophthalmology, University of California, San Diego, San Diego, California, USA.

2Department of Ophthalmology, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.

3Lowy Medical Research Institute, La Jolla, California, USA.

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.

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