Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog – Page 5

Get the latest international news and world events from around the world.

Log in for authorized contributors

Ultrafast 3D imaging captures fleeting motion at 150,000 frames per second

A research team from the Institut national de la recherche scientifique (INRS), led by professor Jinyang Liang, is pushing the limits of ultrafast imaging with a new technology capable of capturing three-dimensional images at speeds of up to 150,000 frames per second. Published in the journal Nature Communications, this study establishes a new world record in profilometry.

The breakthrough could transform the way scientists observe and measure extremely fast, hard-to-reproduce phenomena. The technology, called C-BLIP (chromatically band-limited illumination profilometry), makes it possible to visualize collisions, aerodynamic motion and ultrasonic vibrations in three dimensions. It could find applications in fields ranging from mechanics and aerodynamics to microfluidics, high-rate material testing and additive manufacturing.

Using C-BLIP, the researchers successfully captured and measured a variety of transient phenomena, including the collision between a projectile and a turbofan blade, the aerodynamics of a falling maple samara and the vibrations of a loudspeaker membrane.

Inner Workings: A massive star dies without a bang, revealing the sensitive nature of supernovae

In 2008, a huge red star in another galaxy reached the end of its life. A star as heavy as this one, born with 25 times the mass of the Sun, was supposed to go out in a fiery flash of light known as a supernova, millions or billions of times brighter than our Sun. But this one refused to play the role of drama queen. Instead, it brightened just a little, then vanished, possibly leaving behind a black hole.

No one had ever seen one of these huge red stars wink out of existence with so little fuss before. It was a sign that the lives and deaths of these stars are more complex than our simplest theories had claimed. “As amazing and important and fun and exciting as this is, it’s not a surprise,” says Stan Woosley at the University of California, Santa Cruz. In fact, the discovery may help explain why the massive stars in computer models often fail to blow up.

We’ve got biology wrong, and that’s why the Human Genome Project failed

The Human Genome Project promised genetic-based cures for all the major diseases of mankind, from cancer, to Alzheimer, to schizophrenia. A quarter of a century later, and these sweeping cures haven’t materialized. Biologist Denis Noble and his co-authors Raymond Noble and Reine Bourret argue that this failure reveals a flawed foundation in modern biology: treating genes as the system’s controllers rather than its tools. For 60 years this central dogma has mislead biology. Once we overthrow it, we can transform our understanding of how species evolve.

Figure 1: diagram of the Central Dogma

Biology during the twentieth century was firmly based on Watson and Crick’s famous work on the structure of DNA. They discovered (with important data input from Wilkins and Franklin) that DNA forms double helical threads, each thread being a complementary sequence to the other. The nucleotide bases C and G join together, while A and T also do so. So, a sequence like AACGTTCC in one thread is matched by the complement TTGCAAGG. They realized that this has an important implication. When the threads are unwound, each thread can attract its complementary sequence automatically, so creating two new threads. It is easy to imagine their excitement since the quantum mechanics pioneer, Erwin Schrödinger, had proposed self-replication “like a crystal” in his book What is Life? a decade or so earlier. Crick incorporated all of this into his Central Dogma of Molecular Biology.

Physicists Say They’ve Sidestepped a Nearly 100-Year-Old Quantum Limit Using Hindsight

The Heisenberg uncertainty principle, introduced by German physicist Werner Heisenberg in 1927, puts forward the concept of a certain fuzziness in physics. It says that if one characteristic of a quantum particle can be predicted with precision, a paired characteristic becomes less certain.

Position and momentum are the most often-mentioned of these pairs, known as non-commuting variables. Being able to ascertain where a quantum particle is makes it harder to judge its movement, and vice versa.

That fuzziness makes it more difficult to take accurate measurements of weaker signals in physics – in everything from the LIGO gravitational wave detector to the atomic clocks that underpin systems like GPS.

Recovering from a therapeutic stall in higher-risk myelodysplastic syndromes: re-examining biology, backbones and study designs

Therapeutic progress in higher-risk myelodysplastic syndromes (HR-MDS) has stalled. Despite repeated attempts to improve outcomes through incremental refinements to classification systems and hypomethylating agent (HMA)-based backbones, no phase III study since AZA-001 has replicated even the modest survival benefit observed with azacitidine. We propose that this stagnation results from a fundamental mismatch between the biological realities of HR-MDS and the assumptions underpinning contemporary drug development. HR-MDS encompasses biologically diverse ecosystems characterized by distinct clonal architectures, evolutionary trajectories and marrow microenvironmental dysfunction, despite overlapping phenotypic and genotypic features. Treating this heterogeneity as a single entity anchored to a HMA backbone, risks obscuring therapeutic signals and misinterpreting responses. Here, we examine the potential biological, microenvironmental, and methodological drivers of therapeutic insufficiency in HR-MDS, to advocate for biologically coherent adaptive platform trials using biomarker-enriched selection of patients, and propose shifting away from default HMA backbones. Only by redesigning strategy around biology, rather than prioritizing ease of recruitment, or historical precedent, can we restore momentum and lift in HR-MDS drug development.

In higher-risk myelodysplastic syndromes (HR-MDS), promising agents from early-phase clinical studies have repeatedly failed to improve survival in phase III trials of previously untreated patients.1–4 Much like an aircraft entering a slow-speed stall, continued progression along the same trajectory, through minor adjustments to existing frameworks or trial designs, risks deepening descent. Recovery will require abandoning ingrained reflexes and embracing counterintuitive inputs, including a biological and phenotypic re-examination of disease boundaries, rethinking trial design, and aligning trial endpoints with outcomes meaningful to patients. Recent reviews have elegantly summarized lessons from contemporary trials in treatment-naïve HR-MDS, highlighting opportunities to refine study design and endpoints.1–4

Here, we extend this discussion by focusing on relatively under-explored biological constraints related to disease dynamics, microenvironmental dysfunction, and treatment backbones, beginning with the challenge of defining what constitutes ‘HR-MDS’. In practice, this umbrella term is pragmatic but imprecise, encompassing patients defined by increased blast burden, adverse genetic features, or combinations of these factors, in whom variable degrees of marrow failure represent a shared phenotypic feature.5,6 Reliance on prognostic frameworks, such as the Revised International Prognostic Scoring System (IPSS-R)7 or Molecular International Prognostic Scoring System for Myelodysplastic Syndromes (IPSS-M),8 designed to estimate risk rather than to inform therapeutic strategy, has shaped clinical trial enrollment in HR-MDS and contributed to the uniform therapy of biologically heterogeneous diseases.

Cytotoxic CD8+ T cells in cancer and cancer immunotherapy

The natural immune response relies on the interaction of adaptive and innate immunity systems and the synergy between them. The essential aspects of this response in terms of anticancer immunity are the surveillance, detection and destruction of neoplastic cells. However, despite meticulous immune surveillance, cancer might eventually gain a foothold, and most immune cells will polarise into pro-tumorigenic or anti-tumorigenic cells, depending on a multitude of activating and inhibitory signals derived from cancer cells and their microenvironment. The outcome of this balance is a strong predictor of clinical outcome, with the infiltration of immune cells into, or their exclusion from, a tumour also being critical to the efficacy of immunotherapy.

Cytotoxic CD8+ T cells of the adaptive immune system are the most powerful effectors in the anticancer immune response and constitute the backbone of cancer immunotherapy. Immune-checkpoint inhibitors aim to block suppressive immune receptors and revitalise dysfunctional T cells, including CD8+ T cells, and adoptive cell transfer uses CD8+ T cells with genetically modified receptors (chimaeric antigen receptors [CARs]). Both approaches have had enormous impacts on the outcomes of various cancers; indeed, the field of immuno-oncology has revolutionised the treatment of cancer in terms of efficacy and personalised treatment options, as monotherapy or combinatorial regimens, and will continue to do so in the years to come. Nevertheless, any positive responses might not last, and the side effects could force treatment discontinuation, indicating the need to continuously improve treatment strategies. New pathways and immune checkpoints are being investigated, and new generations of CAR T-cell products are currently being evaluated in clinical trials. This review summarises advances in research into cytotoxic CD8+ T cells, the most prominent effector cell type in cancer and cancer immunotherapy.