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Mexico signs decree requiring digital platforms to protect minors

Mexican President Claudia Sheinbaum signed a federal decree on 14 October 2026 requiring digital platforms to strengthen protections for children and adolescents online. The measure is mandatory and gives platforms 30 calendar days to adapt their services to the new requirements.

The decree applies to digital platforms that allow users to interact, communicate, create, distribute or share content. It prohibits platforms from allowing children and adolescents to access, be exposed to or be recommended content promoting hate speech, violent extremism, sexual abuse or exploitation, suicide, self-harm, eating disorders, school violence, harassment, cyberbullying, unlawful conduct and explicit sexual material.

Platforms must build child protection into the design of their services. This includes identifying and removing accounts or content that promote violence, providing age-appropriate content classification, parental supervision and reporting tools, and applying stronger privacy and safety settings for younger users. The decree also requires platforms to maintain mechanisms for cooperation with authorities where serious risks to children are identified.

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Sleep deprivation causes memory deficits by negatively impacting neuronal connectivity in hippocampal area CA1

Brief periods of sleep loss have long-lasting consequences such as impaired memory consolidation. Structural changes in synaptic connectivity have been proposed as a substrate of memory storage. Here, we examine the impact of brief periods of sleep deprivation on dendritic structure. In mice, we find that five hours of sleep deprivation decreases dendritic spine numbers selectively in hippocampal area CA1 and increased activity of the filamentous actin severing protein cofilin. Recovery sleep normalizes these structural alterations. Suppression of cofilin function prevents spine loss, deficits in hippocampal synaptic plasticity, and impairments in long-term memory caused by sleep deprivation. The elevated cofilin activity is caused by cAMP-degrading phosphodiesterase-4A5 (PDE4A5), which hampers cAMP-PKA-LIMK signaling. Attenuating PDE4A5 function prevents changes in cAMP-PKA-LIMK-cofilin signaling and cognitive deficits associated with sleep deprivation. Our work demonstrates the necessity of an intact cAMP-PDE4-PKA-LIMK-cofilin activation-signaling pathway for sleep deprivation-induced memory disruption and reduction in hippocampal spine density.

DOI: http://dx.doi.org/10.7554/eLife.13424.001.

Adropin Reduces Early Brain Injury and Delayed Cerebral Ischemia After Severe Subarachnoid Hemorrhage in a Mouse Model

Cell‐free hemoglobin and heme in the subarachnoid space disrupt endothelial cell function. This occurs by generating reactive oxygen species and decreasing nitric oxide (NO) production.6 In summary, these events lead to significant endothelial dysfunction resulting in DCI most strongly correlates with the 3‐month outcome.7

The only current proven treatment for post‐SAH DCI is prophylactic nimodipine driven by data from a single large clinical trial.8 However, a Cochrane worst‐case‐scenario meta‐analysis showed no statistically significant difference between nimodipine and placebo, casting doubt on its benefit.9 Even with nimodipine, up to 30% of patients will suffer cerebral infarction.10 This leaves a significant gap in the treatment of post‐SAH DCI.

Adropin is a potential therapeutic to bridge the current gap in treatments for post‐SAH DCI. It is a 4.5 kDa peptide encoded by the energy homeostasis‐associated (ENHO) gene, discovered in 2008 by Kumar et al. as a regulator of lipid metabolism and insulin sensitivity, that is highly expressed in the liver and brain tissue of mice.11 Adropin has a direct effect on endothelial cell function by increasing VEGFR2 (vascular endothelial growth factor receptor 2) expression12 and by regulating of NO bioavailability through stimulation of eNOS (endothelial NO synthase) phosphorylation at Ser1177.13 Our laboratory has demonstrated that adropin is protective against both early and delayed brain injury following a single injection of the SAH model in mice.14 However, its efficacy when administered at a clinically relevant time point, with a severe double‐injection SAH model, has not yet been evaluated. The median time from SAH symptoms to treatment is 169 minutes, making a therapeutic with efficacy at a delayed time point critical.15 In this study, we seek to investigate the therapeutic effects of adropin in severe double‐injection SAH (compared with mild single blood injection), including its efficacy in a mouse model within a clinically relevant time window.

Minimally Invasive Murine Model of Transcarotid Wire‐Induced Mitral Stenosis

Mitral stenosis remains a critical driver of atrial fibrillation and pulmonary hypertension.1 However, there is a lack of animal models that faithfully reproduce this human pathology.2 Here, we describe a novel transcarotid wire‐induced mitral stenosis (TWIMS) mouse model developed in accordance with institutional guidelines with approval by the Institutional Animal Care and Use Committee of University of Missouri (Approval #40285). The data, analytic methods, and study materials supporting the findings of this study are available from the corresponding author upon reasonable request.

TWIMS uses a closed‐chest, retrograde transcarotid approach guided by B‐mode echocardiography (Figure 1A and 1B). Four‐month‐old mice were used to balance technical feasibility, procedural reproducibility, and postoperative survival. A tip‐curved guide wire (G02426 RX, Cook Medical Inc.; shaped as depicted in Figure 1A) was introduced into the right common carotid artery via blunt dissection. The guidewire was advanced to aortic root; upon encountering tactile resistance, the operator used a standardized “rotate‐and‐advance” maneuver coordinated with systole to safely cross the aortic valve. Once within the left ventricle, the external shaft of the wire was deflected laterally, using a levering action to direct the intracardiac tip toward the mitral annulus. Following visual confirmation of leaflet contact, controlled injury was delivered via 100 translational and rotational passes to ensure endothelial disruption on the mitral leaflets.

Conținut negăsit

Q: What happens to AI without a harness?

A: AI without a harness means:

🌟 No Real-World Action — The model can’t independently browse, run code, open files, or call external apps/APIs.

🌟 No Persistent Memory — It can’t retain long-term session history or track multi-step workflows across sessions without external memory provided by the harness.

🌟 Weaker Multi-Step Performance — Single-turn tasks may still work well, but complex, long-horizon, or tool-dependent tasks degrade sharply.

🌟 Unchecked Errors — Without verification loops, routing logic, and guardrails, the model can repeat mistakes, hallucinate, or fail to parse complex outputs.

🌟 Isolated Reasoning — It can still generate text or predict tokens, but it can’t function as a practical, goal-oriented agent inside a software project or business workflow.

Continue reading “Conținut negăsit” | >

FAA Approves Test Flights for Real-Life $300,000 Electric Flying Car

You might think that one time travel adventure might be enough for a lifetime, but in the final scene of Back to the Future, Marty (Michael J. Fox) hops into the passenger seat of Doc Brown’s (Christopher Lloyd) DeLorean and sets out for parts, and times, unknown. We didn’t know what that adventure would be yet (to find out, we had to wait for Back to the Future II) but we knew it was going to be wild because Doc Brown flipped down his suitability retro-future style sunglasses, flipped a switch, and the DeLorean took to the air with a suitably cool quip. “Roads? Where we’re going, we don’t need roads.”

When we came back for the sequel Marty, Doc Brown, and Jennifer (Elisabeth Shue) arrived in the distant future of 2015, where kids ride hoverboards, adults drive flying cars, and they’re still making Jaws movies. Sadly, 2015 came and went and there aren’t any flying cars in sight. At least not any that look and feel like the flying cars of our imagination. However, all of that is primed to change, thanks to the folks at Alef Aeronautics.