Real Madrid have revealed their squad for the clash with Osasuna on LaLiga matchday one, ahead of their opener at the Bernabéu (Tuesday, 9:00 pm CEST).
REAL MADRID SQUAD:
Goalkeepers: Courtois, Lunin and Sergio Mestre.
Defenders: Carvajal, Militão, Alaba, Trent, Asencio, Á. Carreras, Fran García and Huijsen.
Midfielders: Valverde, Tchouameni, Arda Güler, Ceballos and Thiago.
Forwards: Vini Jr., Mbappé, Rodrygo, Gonzalo, Brahim and Mastantuono.
Biomarkers are measurable signs of what’s happening inside the body and are essential for running successful Huntington’s disease (HD) trials. Right now, neurofilament light (NfL) is the star of the HD biomarker world, but we need more players on the team. A new study from Cyprus scanned every type and amount of protein molecules found in blood samples, to see how these changed over time in people with HD. They found two potential biomarker candidates, CAP1 and CAPZB, which seem to be linked to very early changes in HD. With follow up studies, these findings could add powerful new tools for tracking disease progression and measuring the impact of future treatments.
Imagine running a race without a finish line. That’s what testing an HD treatment would be like without biomarkers. You could hand someone a promising new drug, but without a way to measure what’s happening in the brain, you wouldn’t know if it’s helping, hurting, or doing nothing at all.
That’s why biomarkers are so important. In HD, one of the best so far is neurofilament light (NfL), a protein released when neurons are damaged. NfL seems to be reliable, it’s being used in many ongoing trials, seems to track with some of the earliest changes that HD causes, and it’s taught us a lot about how possible HD treatments might impact brain health. But no single biomarker can capture the whole progressive story of HD, or how things might change with different treatments. We need a team of biomarkers that can cover different angles, especially ones that show up before the earliest of symptoms start.
Enter this new research study, which is a wide-angle look at the blood for signs of HD, even in its earliest days.
Think of your body as a giant city. Your genes are the blueprints for all the buildings, roads, and systems. Proteins are the workers – the electricians, the bus drivers, the teachers, the police officers. They’re the ones making things actually happen.
The proteome is the full roster of those workers at any given moment. And just like in a real city, the lineup changes depending on what’s going on, like if there’s a festival, a storm, or a traffic jam, the people you would want on your crew would change. Proteomics is the science of counting and studying all those workers to see who’s showing up, who’s missing, and who’s acting differently than usual.
In this study, the “city” in question was the blood of people with and without HD.
The researchers studied 36 people with the gene for HD, split into three groups:
They also included 36 healthy controls, all from Cyprus. Using blood serum (the clear liquid part of blood), they analyzed thousands of proteins to see which ones changed at each stage of HD.
The advantage of blood serum is that it’s far easier to collect than spinal fluid, no lumbar punctures required, making it a practical (and much desired!) source for future biomarker testing.
The first finding from this research seemed to show up before symptoms appeared, suggesting there may be changes in proteins linked to the cell’s cytoskeleton. The cytoskeleton is the internal scaffolding that gives cells their shape and allows them to move and connect.
This work suggests the city’s buildings may be losing their supporting beams before any cracks appear in the walls. Identifying changes that happen early in HD, before symptoms are readily apparent, will help researchers identify key molecular events in HD progression.
As the disease advanced, two other themes emerged. First, the complement system, a frontline part of the immune response, seemed to be stuck in an overactive state, which in the brain could mean inflammation and loss of brain cell connections. Second, lipid and cholesterol regulation appeared to go off balance, which matters because cholesterol is vital for healthy brain cell communication.
While all of these are interesting findings, none of this is particularly new for HD researchers. There have been several studies looking at cytoskeleton differences in brain cells, changes to the complement system, and cholesterol dysregulation in HD before. But those studies have largely focused on the molecular changes HD causes within those biological functions, and not using those changes to identify biomarkers.
Biomarkers are measurable signs of what’s happening inside the body and are essential for running successful Huntington’s disease (HD) trials. Right now, neurofilament light (NfL) is the star of the HD biomarker world, but we need more players on the team.
From the long list of changing proteins identified in this study, two stood out for the researchers:
If validated in larger, more diverse groups, CAP1 and CAPZB could join NfL in the HD biomarker toolkit. Together, they could help flag HD-related changes years before symptoms start, which will be critical for advancing trials aimed at treating HD before the more obvious symptoms of the disease begin. They could help track how fast the disease is progressing, which could help people with planning life events. And they could help show whether a treatment is making a difference, which is why biomarkers are so critical for HD research.
This is especially important in prevention trials, where the goal is to treat people before the disease has visibly started. Without early biomarkers, we’d have no way to see if those treatments are working.
This study was done on a very specific population of people – those from the small island of Cyprus. Because this is a limited population of people, there could be “founder effects” at play, which means that the population of people with HD on Cyprus could have started from one person or just a few individuals that, over time, produced the family(ies) on Cyprus with HD.
In theory, that limited initial person/people could have had unique genetic signatures that made the biomarkers identified in this study specific for them and their progeny. Because of that, a more diverse set of people needs to be studied before we could say if these are solid biomarkers to chase for HD.
Another thing to keep in mind here is that only 36 people were assessed in this study. That’s a small number of people when it comes to a biological study. Combined with the fact that the diversity is limited, and that small pool of participants could really mask results or skew findings.
While the points above are important caveats that suggest we should interpret these findings with a healthy pinch of salt until larger studies are done, the importance of these types of studies for advancing HD research cannot be overstated.
Having biomarkers that track with disease progression, particularly in people that are at the earliest stages of HD, is essential for advancing disease modifying drugs. This is especially important as we move toward trials aimed at treating people with HD earlier on in their HD journey, perhaps even before notable symptoms arise.
Another important note from this work is that it was done using blood serum, showing that researchers are committed to discovering biomarkers that track with early disease progression that can be measured in a minimally invasive way. We know everyone would appreciate not having to get a spinal tap at every appointment! So while we’re not quite there yet, it is certainly something scientists are working toward.
Lastly, the results from this study were made possible by “omics” studies – giant, detailed inventories of all the parts in a living thing, whether that’s all the genes, all the proteins, all the fats, or all the other molecules that keep it alive. These types of research studies that look at how everything changes, then narrow in on those things that change the most have transformed our understanding of HD over the past decade. It was omics studies that initially defined genetic modifiers from the GeM-HD Consortium study, contributing to the discovery of somatic instability. And omics studies will undoubtedly help usher in the forthcoming treatments we’re all eagerly awaiting.
Having biomarkers that track with disease progression, particularly in people that are at the earliest stages of HD, is essential for advancing disease modifying drugs. This is especially important as we move toward trials aimed at treating people with HD earlier on in their HD journey, perhaps even before notable symptoms arise.
First and foremost, before CAP1 and CAPZB can move from research to clinic, it’s critical that scientists test them in bigger, global HD cohorts. They also need to follow people over time to see how levels might shift as HD progresses in those larger populations. They should also check whether they’re unique to HD or also change in other brain diseases.
So, while there’s a long road ahead for CAP1 and CAPZB, work advancing new biomarkers for HD is critical, and it’s ongoing. It’s especially important as we move toward clinical trials aimed at treating HD earlier, perhaps even before symptoms arise. And the added benefit of blood biomarkers is incredibly exciting. Imagine having a simple blood test that could tell researchers, with confidence, that a new drug is slowing HD in its tracks. That’s the kind of advancements that these biomarker studies could bring.
Original research article, “Stage-Specific Serum Proteomic Signatures Reveal Early Biomarkers and Molecular Pathways in Huntington’s Disease Progression” (open access).
Trichomes are hair-like projections found on the surface of many plants, offering protection against environmental stressors and insects, while also influencing commercial appeal. In cucumbers, multicellular trichomes—fruit spines—are especially prominent and variable, yet the genetic mechanisms driving their formation remain elusive. Studies in model plants like Arabidopsis have shed light on trichome biology, highlighting the roles of cytoskeleton dynamics, transcriptional regulation, and hormone signaling. However, cucumbers possess distinct spine morphologies and cellular architectures that demand crop-specific exploration. Due to these complexities, there is a critical need to investigate how cucumber plants coordinate internal cellular processes to sculpt their outermost structures.
A research team at Shanghai Jiao Tong University has identified the cucumber gene CsTs as a pivotal regulator of fruit spine development and texture. The study (DOI: 10.1093/hr/uhae235), published August 14, 2024, in Horticulture Research, demonstrates how this single gene controls spine formation by modulating cell division, wall composition, and intracellular transport. Employing gene-editing, microscopy, and protein interaction analyses, the researchers unveiled a sophisticated genetic network behind cucumber surface architecture. The findings illuminate key processes in plant development and lay a foundation for enhancing crop quality through targeted genetic strategies.
To confirm CsTs’s role, scientists generated knockout cucumber lines using CRISPR/Cas9, resulting in trichomes that were flattened and malformed—mirroring the naturally occurring “tender spine” mutant. Microscopy revealed a lack of structural differentiation between the stalk and base of the fruit spines, leading to loose attachment to the fruit surface. Biochemical analysis showed these mutants had reduced cellulose and lignin but elevated levels of pectin and hemicellulose, weakening cell wall rigidity.
Transcriptomic profiling across developmental stages revealed that CsTs influences gene networks related to auxin transport, cytoskeletal arrangement, and secondary metabolism. Protein interaction studies identified direct partners such as SNARE proteins and ROP GTPases—key players in vesicle trafficking and cell polarity. These interactions were lost in the mutant due to protein mislocalization. Interestingly, overexpressing CsTs in an Arabidopsis homolog mutant partially restored normal trichome morphology, suggesting functional conservation across species. Additional genetic analysis indicated that CsTs operates in the same pathway as CsMict, a gene involved in cuticle formation, although the two proteins do not interact directly. Together, the findings position CsTs as a critical node in a network that shapes cucumber spine morphology through tightly coordinated cellular and molecular processes.
“Our study reveals that CsTs is not only essential for cucumber spine development but also plays a broader role in organizing cellular architecture,” said Dr. Junsong Pan, the study’s lead investigator. “By pinpointing how this gene influences cytoskeletal structure and hormone transport, we’ve uncovered a key mechanism in plant surface biology. This opens new possibilities for improving crop resilience and appearance through genetic approaches.” He added that future research would explore how CsTs coordinates signaling cascades through phosphorylation and how it may interact with broader metabolic pathways in plants.
The identification of CsTs offers valuable opportunities for breeding cucumbers with customized spine textures, enhancing both marketability and pest resistance. By manipulating this gene, breeders could potentially develop varieties that are tougher, more aesthetically uniform, or better protected from insects such as aphids, which tend to favor softer mutants. Moreover, insights into how CsTs regulates cytoskeleton and cuticle biosynthesis could extend to other crops where trichomes affect flavor, texture, or defense. As scientists further explore the genetic pathways linked to CsTs, the work could lead to innovative strategies in sustainable agriculture and precision horticulture.
Source: NewsWise
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We all know that our body gives off smells, but did you know these odours can also reveal a lot about your health? Scientists say certain diseases can actually change the way our body smell, sometimes years before symptoms appear.
A famous example is of Joy Mile, a woman from Scotland who discovered that her husband smelled different years before he was diagnosed with Parkison’s disease.
Later, she realized other Parkison’s patients had the same musky smell. Doctors tested her ability, and she correctly identified patients just by sniffing their T-shirts. In one case, she even predicted the illness before doctors confirmed it.
This showed that diseases can release special chemicals through our skin, sweat, or breath. Experts call them volatile organic compounds (VOCs). These are tiny molecules produced when our body breaks down food for energy. If something wrong inside the body, these molecules change and so does our smell.
For example:
Dogs, with their powerful noses, can detect cancer, diabetes, Parkinson’s and even malaria. Scientists are now trying to build machines that can do the same job, simple tests that could catch illnesses early without painful or costly procedures.
Researchers in the UK are already developing a skin swab test to spot Parkinson’s disease in its early stages. Others are studying how odours can help diagnose cancers, brain injuries, and infections.
This could be life changing, instead of waiting years for symptoms to appear, doctors might one day identify diseases through a quick smell-based test.
Around 1.1 billion years ago, the oldest and most tectonically stable part of North America—called Laurentia—was rapidly heading south toward the equator. Laurentia eventually slammed into Earth’s other landmasses during the Grenville orogeny to form the supercontinent Rodinia.
Laurentia’s path during that period is known, thanks to paleomagnetism. By tracing the orientation and magnetism of rocks in the lithosphere, scientists can approximate the relative position and movement of Laurentia leading up to Rodinia’s formation.
The rocks along Lake Superior in northern Wisconsin and Michigan are especially important for tracing Laurentia’s movement. These rocks—dominated by red sandstones, siltstones, and minor conglomerates—were deposited during extensive sedimentation caused by the North American Midcontinent Rift and are rife with iron oxides like hematite. Hematite can acquire magnetization when it is deposited, which records where the rock was in relation to Earth’s poles at the time.
Unfortunately, the existing paleomagnetic record is marred by a gap between 1,075 million and 900 million years ago, limiting our understanding of how, when, and where Rodinia formed.
To fill this data gap, Fuentes et al. collected new samples from the Freda Formation near Lake Superior, which formed in floodplain environments an estimated 1,045 million years ago. The authors combined these data with stratigraphic age modeling to estimate a new, sedimentary paleopole, or the position of the geomagnetic pole at a particular time in the past.
Previous studies indicate that for 30 million years, sometime between 1,110 million and 1,080 million years ago, Laurentia moved from about 60°N to 5°N at a rate of 30 centimeters (12 inches) per year—faster than the Indian plate’s collision with Eurasia pushing up the Himalayas. This study showed that over the following 30 million years, Laurentia’s progress slowed to 2.4 centimeters (1 inch) per year as it crossed the equator.
The paleocontinent’s slowdown during Freda Formation deposition coincides with the onset of the Grenville orogeny. The results confirm that a stagnant single-lid regime—in which the lithosphere behaves as a single, continuous plate rather than multiple independent plates—was not in effect during this interval. (Journal of Geophysical Research: Solid Earth, https://doi.org/10.1029/2025JB031794, 2025)
—Aaron Sidder, Science Writer
Anker’s 3-in-1 MagSafe charging station is on sale for a record low price of $63 — that works out to savings of 30 percent.The Qi2-certified charger wirelessly charges your compatible iPhone, Apple Watch, and AirPods on one compact and convenient dock. Qi2 boasts 15W of power, so you can take advantage of fast charging on compatible devices.
This means the station can charge an iPhone 16 Pro Max to 20 percent in just 20 minutes and an Apple Watch Series 10 from zero to 100 percent in just over an hour. The magnetic stand for your iPhone is adjustable with 45 degrees of vertical rotation and 360 degrees of horizontal rotation, so you can always find the perfect angle for your phone while charging.
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Samsung is catching up to Apple (AAPL, Financials) in the U.S. smartphone market. Its share went from 23% to 31% in the second quarter of 2025, while Apple’s share went from 56% to 49%. A key cause is foldables. The new Samsung Z Fold 7 and Z Flip are getting a lot of attention because they combine new ideas with old ones. They are selling well and going viral on social media, where people are posting videos of them passing durability tests.
Samsung has a wide selection of products that cost between $650 and more than $2,400, so they can reach customers at every price point. Apple’s current iPhone assortment is still constrained in both design and flexibility. People say that Apple will soon release a thinner iPhone and a foldable one in 2026. However, Apple’s glacial changes to its design and AI features have given Samsung the chance to take the lead.
Foldables are ready for the mainstream now since there aren’t any big trade-offs, there is a lot of demand, and AI is becoming more and more integrated. Samsung has an edge not just in hardware but also in timing. Apple may triumph in the long run, but for now, Samsung is in the lead.
This article first appeared on GuruFocus.