LV‐GLS 18% predicts mortality, recurrent stroke, and poor mRS-based functional outcome after acute ischemic stroke. @Minkwan_Kim84
LV‐GLS Globally, stroke is the second‐leading cause of death and the third most common cause of combined death and disability.1 Over the past decade, stroke‐related death has been steadily declining; however, health care expenditures associated with stroke have continued to increase.1, 2 Recurrence of ischemic stroke adversely affects patient prognosis and increases the mortality rate.3 Previous studies have identified several clinical factors contributing to the occurrence and recurrence of ischemic stroke, including stroke subtype, age, hypertension, atrial fibrillation (AF), heart failure (HF), and diabetes.2, 4
HF is also a risk factor for stroke and is associated with stroke recurrence and death.5, 6 Left ventricular (LV) global longitudinal strain (LV‐GLS), a measure of myocardial deformation along the long axis of the left ventricle, is assessed using the speckle‐tracking method. It is a sensitive measure of myocardial fiber shortening and has become a reliable parameter for evaluating subtle systolic dysfunction.7 In patients with acute HF, LV‐GLS is frequently reduced regardless of the LV ejection fraction (LVEF), the traditional measure of LV systolic function. LV‐GLS has also been shown to be a superior prognostic marker for death than LVEF.8 Furthermore, in severe mitral regurgitation and severe aortic stenosis, LV‐GLS has proven useful as a predictor of postoperative outcomes and a tool for identifying patients who may benefit from early surgical intervention.9, 10 Recent research has demonstrated that LV‐GLS can effectively predict incident strokes in patients who are stroke naïve.11 However, to date, no study has evaluated the prognostic implications of LV‐GLS in patients with acute ischemic stroke (AIS) about subsequent cardiovascular outcomes. In this study, we aimed to investigate the prognostic utility of LV‐GLS, a novel marker of subclinical LV dysfunction, in patients with AIS.
Robots small enough to travel autonomously through the human body to repair damaged sites may seem the stuff of science fiction dreams. But this vision of surgery on a microscale is a step closer to reality, with news that researchers from the University of Pennsylvania and the University of Michigan have built a robot smaller than a millimeter that has an onboard computer and sensors.
Scientists have been trying for decades to develop microscopic robots, not only for medical applications but also for environmental monitoring and manufacturing. However, they have faced formidable challenges. Existing microbots typically require large, external control systems, such as powerful magnets and lasers, and cannot make autonomous decisions in unfamiliar environments.
Knots are everywhere—from tangled headphones to DNA strands packed inside viruses—but how an isolated filament can knot itself without collisions or external agitation has remained a longstanding puzzle in soft-matter physics.
Now, a team of researchers at Rice University, Georgetown University and the University of Trento in Italy has uncovered a surprising physical mechanism that explains how a single filament, even one too short or too stiff to easily wrap around itself, can form a knot while sinking through a fluid under strong gravitational forces.
The discovery, published in Physical Review Letters, provides new insight into the physics of polymer dynamics, with implications ranging from understanding how DNA behaves under confinement to designing next-generation soft materials and nanostructures.
A new study from a research team at the Center for Wireless Communications Network and Systems (CWC-NS) at the University of Oulu has introduced an approach using near-infrared (NIR) light beyond light therapy to facilitate simultaneous wireless power transfer and communication to electronic implantable medical devices (IMDs). Previously, the research team demonstrated that NIR light for wireless communication is feasible, and now the team made progress by involving wireless charging capabilities using the same light.
Featured in Optics Continuum, the research outlines an approach that promises to enhance the performance and durability of IMDs while providing more secure, safer, more private, and radio interference-free communication. The published paper, authored by Syifaul Fuada, Mariella Särestöniemi, and Marcos Katz at the CWC-NS, has demonstrated research merit as it was designated an Editor’s Pick, highlighting articles of excellent scientific quality and representing the work occurring in a specific field.
The paper is a small part of Syifaul Fuada’s doctoral research. “This is the initial step that could open other ideas to advance the proposed approach,” Fuada says.
Scientists at the University of Oxford demonstrate an approach to interpreting how materials interact with polarized light, which could help advance biomedical imaging and material design.
Their work, reported in Advanced Photonics Nexus, focuses on improving how researchers analyze a key optical property known as the retarder.
In optics, a retarder is a material or device that changes the way light waves are oriented as they pass through. Light waves have an orientation called polarization, and a retarder shifts the phase between different components of that light—essentially delaying one part of the wave compared to another.
Senescent “zombie” cells are linked to aging and multiple diseases, but spotting them in living tissue has been notoriously difficult. Researchers at Mayo Clinic have now taken an inventive leap by using aptamers—tiny, shape-shifting DNA molecules—to selectively tag these elusive cells. The project began as an offbeat conversation between two graduate students and quickly evolved into a collaborative, cross-lab effort that uncovered aptamers capable of binding to unique surface proteins on senescent cells.
Here, Pengda Liu & team show SPOP inhibitors act as molecular glue degraders, stabilizing and activating STING to enhance immunotherapy in melanoma mouse models:
The figure shows the SPOP inhibitor 6lc reduces CBX4 and BMI1 foci, while ectopic CBX4 restores BMI1 foci and H2AX interactions.
4Department of Pharmacology.
5Division of Oncology, Department of Medicine, and.
6UNC Metabolomics and Proteomics Core, Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
“I just can’t make it tonight. You have fun without me.” Across much of the animal kingdom, when infection strikes, social contact shuts down. A new study details how the immune and central nervous systems implement this sickness behavior.
It makes perfect sense that when we’re battling an infection, we lose our desire to be around others. That protects them from getting sick and lets us get much needed rest. What hasn’t been as clear is how this behavior change happens.
In the research published in Cell, scientists used multiple methods to demonstrate causally that when the immune system cytokine interleukin-1 beta (IL-1β) reaches the IL-1 receptor 1 (IL-1R1) on neurons in a brain region called the dorsal raphe nucleus, that activates connections with the intermediate lateral septum to shut down social behavior.
“Our findings show that social isolation following immune challenge is self-imposed and driven by an active neural process, rather than a secondary consequence of physiological symptoms of sickness, such as lethargy,” said study co-senior author.