Once a $4 billion apparel juggernaut, Allbirds will rebrand as NewBird AI, a “GPU-as-a-Service” company. Hey, if you can’t beat ’em, join ’em.
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CT and MRI LI-RADS Treatment Response Assessment 2024: Core Concepts for Clinical Practice
Post-treatment HCC imaging just got clearer. The updated 2024 LI-RADS TR algorithm refines criteria for radiation vs non-radiation therapies and adds MRI features to better detect viable tumor, key for accurate response assessment and management.
Multiple locoregional therapies are available for HCC, with imaging findings specific to each modality. The updated 2024 CT and MRI LI-RADS TR assessment criteria provided distinct algorithms for use after nonradiation or radiation-based therapies, simplified the definition of viable disease, and incorporated MRI ancillary features to enhance detection of tumor viability. These updated criteria can improve diagnostic accuracy, resulting in more effective clinical management of HCC.
Confirmed precursor to commonest form of esophageal cancer offers opportunities to catch the disease early
Scientists have found the strongest evidence to date that a condition known as Barrett’s esophagus is the starting point for all cases of esophageal adenocarcinoma—the most common type of esophageal cancer in the developed world—even when telltale signs of this pre-cancerous stage are no longer visible. The findings, published in Nature Medicine, could help improve screening for and early detection of esophageal cancer, the sixth-most deadly cancer, helping improve outcomes for the disease.
Cancer of the esophagus, including its most common form, esophageal adenocarcinoma (OAC), is on the rise in Western countries. It is difficult to treat because it is often caught at an advanced stage, when treatment options are limited. Scientists and doctors have known for some time that the development of esophageal cancer is linked with Barrett’s esophagus, which shows up in endoscopy as a pink patch on the surface of the esophagus. Barrett’s esophagus affects around one out of every 100 to 200 people in the United Kingdom.
Between three and 13 people out of 100 with Barrett’s esophagus will go on to develop esophageal adenocarcinoma in their lifetime. However, around half of OAC patients have no detectable Barrett’s esophagus when their cancer is found, raising doubts about whether it is always the precursor.
Abstract: Offering a topical strategy in skin cancer
https://doi.org/10.1172/JCI189044 Brian C. Capell & team identify the epigenetic regulator LSD1 as critical for epidermal development and find its inhibition suppresses tumors in two cutaneous squamous cell carcinoma mouse models by promoting immunosurveillance.
The image shows immunofluorescence from mice lacking LSD1 in the skin, revealing profound activation of cutaneous retinoid signaling (as measured by CRABP2 levels in green); keratin 14 (red); nuclei (blue).
1Department of Dermatology and.
2Penn Epigenetics Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
3Division of Allergy and Immunology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
10 Terrifying Theories About What Exists Outside The Universe
All right, let’s go. Number 10, the infinite bubble bath.
In 1980, physicist Alan Guth proposed a theory that solved several major problems in cosmology at once. His idea, called cosmic inflation, suggested that in the first fraction of a second after the Big Bang, the universe expanded faster than the speed of light, doubling in size repeatedly until it became the cosmos we observe today.
A better flu shot may be coming: How epitope targeting could widen protection
Doctors recommend getting your flu shot annually, since the specific influenza strain it targets varies from year to year. But what if the shot could be more effective while protecting against more strains? Researchers from the University of Missouri School of Medicine are one step closer to making this happen. When the immune system sees a new strain of a familiar virus, it typically focuses on the parts it “remembers” most, even if those regions have changed. “Epitope-spanning antigenic variation reprograms immunodominance and broadens immunity in sequential influenza vaccination” was recently published in Nature Communications.
“In our vaccine model, we targeted specific but distinct regions of the protein on the surface of the influenza virus. These regions are called epitopes,” said study author Henry Wan. “The model included different versions of epitopes in hopes of redirecting how the immune system responds. We found that the vaccine approach helped the immune system target more variants of the virus, leading to broader protection.”
Wan says the epitopes help the immune system see the flu virus differently, and it learns to respond with more coordination between the different types of immune cells. Some of the epitopes are also not as likely to change, which could make flu vaccines more reliable or even help create a universal flu vaccine.
Abstract: Implications for protecting against cognitive impairment following HeadInjury👇
Here, Michael T. Heneka & team find the inflammasome adaptor ASC drives long-lasting brain inflammation and cognitive problems after mild head injury in a closed-head injury model.
The figure shows skeletonized activated microglia (Iba1+ cells) following closed head injury, with mice lacking ASC show showing preservation of morphological features, particularly at later time points.
3Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Belvaux, Luxembourg.
4German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
5Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, PR China.
How do cancer cells ‘learn’ to resist treatment?
Researchers at NYU Langone Health propose a model that could explain how cancer cells adapt to environmental stress, an approach that may lead to new therapies. Published online April 15 as the cover story of the journal Nature, the perspective article centers on a family of proteins called AP-1, which are quickly activated in cells in response to stressful situations—like being exposed to chemotherapy.
While AP-1 proteins have been studied for many decades, the authors propose they are part of a previously overlooked molecular mechanism in which cells survive by learning to rewire their circuitry. This process depends not on permanent changes to a cell’s DNA code, but rather on the cell’s ability to turn genes on or off, and then “remember” the changes that improve its survival chances.
The work suggests that cancer cells use this plasticity to explore gene expression patterns until they find a combination that helps them survive. Once a successful survival state is discovered, it can be locked in and passed down to future cell generations, leading to drug-resistant tumors.
Eosinophil extracellular traps: heterogeneity of their stimuli, components, and functions
Like neutrophil extracellular traps, eosinophil extracellular trap formation also involves two distinct processes: suicidal EETosis and vital eosinophil extracellular trap release.
Eosinophil extracellular trap contains chromatin and/or mitochondrial DNA, granular proteins, nuclear histone variants, cytosolic mediators, cytoskeletal proteins, organelle proteins, and cell membrane proteins.
There are at least four major classes of stimuli that contribute to eosinophil extracellular trap formation via NADPH induced reactive oxygen species generation and/or peptidylarginine deiminase4-dependent histone citrullination pathways.
Cell necrosis, autophagy, and apoptosis, disease status and severity, and eosinophil subtypes all affect eosinophil extracellular trap formation.
The diversities of DNA sources and granule protein types in eosinophil extracellular trap all determine eosinophil extracellular trap’s functional heterogeneity, depending on stimulation environments and disease status. sciencenewshighlights ScienceMission https://sciencemission.com/Eosinophil-extracellular-traps
Eosinophils participate in immune regulation through their granule proteins and cytokines. Recent studies demonstrate eosinophil functional versatility through the mechanism of eosinophil extracellular traps (EETs). EET formation occurs via suicidal eosinophil extracellular trap cell death (EETosis) and vital EET release. EETs contain chromatin-or mitochondrial-derived DNA, granule proteins, nuclear proteins, and cytosolic components that vary depending on the type and intensity of stimuli. Synthetic compounds, pathogenic microorganisms, endogenous molecules, and co-stimulatory factors stimulate EET formation via diverse signaling pathways through receptors that rely on or operate independently of NADPH oxidase-mediated reactive oxygen species production and peptidylarginine deiminase-4-dependent histone modification.