Javi Tejeda

Heavenly Father, Bless this new week ahead of me. I step into this week with fire in my spirit and purpose in my stride. Every moment, every breath, every decision—I’m moving with divine precision. Strengthen my hands for the work, steady my heart for the climb, and sharpen my focus for the vision. This is my week to build, to break through, and to walk boldly into what’s already mine. In Jesus’ name, Amen🙏🏾♥️🪽✨

Praise The Lord 🙏🏼❤️🕊️✨ Thank you Jesus for your Merci. Your Grace, your Love.

@dvorahfr @grok ya es posible extender a 50 segundos?

50 seconds entirely created using Grok Imagine's tools. Grok can create scenes that could be featured in a film.

@Dr_Singularity @grok what this article says ? Explain to me like if I’m 10 years old

paper nature.com/articles/s4158…

wow, amazing anti aging news/paper. This is Huge. Here's why. Reseachers in new review published in Nature reframe ageing as a system wide failure of epigenetic control, not just random damage, but a coordinated breakdown of the system that keeps your cells knowing what they are. In other words: ageing isn’t just wear and tear, but loss of biological information and control. The authors introduce a systems level framework showing that ageing happens when "epigenetic fidelity" collapses, the ability of cells to maintain precise gene expression over time. And they identify 4 interconnected failure modes: 1. Nuclear architecture breaks down. The physical structure of DNA organization deteriorates. Chromatin domains lose their integrity. 2. Epigenetic memory gets scrambled. Systems that maintain gene “on/off” states (like PRC2) stop working properly. 3. Nucleosome instability increases. Histone changes (like H3.3 accumulation) disrupt DNA packaging. 4. Transcription gets reprogrammed. Gene expression patterns drift away from their original identity. And these don’t happen in isolation, they feed into each other, creating cascading failure across the cell. Why this is a HUGE deal It’s a unifying theory. It explains why ageing affects so many systems at once. It connects previously separate ageing mechanisms into one network. It shows ageing is systemic and programmable, not purely random. It turns ageing into something that looks…engineerable. Instead of targeting individual damage, this framework suggests we can target the epigenetic system itself. Potentially reverse multiple ageing features at once. Because these systems are interconnected, fixing the control layer could fix everything downstream. This paper is basically saying: Ageing = loss of biological information integrity And that’s massive, almost insane because: Information loss is reversible in principle. It aligns with ideas like cellular reprogramming. It suggests ageing could be treated like a software problem, not just hardware damage.

@MetabolicUncle @grok dame un resumen de lo que explican aquí

AUTOPHAGY WITHOUT FASTING Your cells run a recycling program. Most people think fasting activates it. They skip breakfast, wait 16 hours, track their eating window, and assume the machinery starts automatically. Research published in Nature Cell Biology says otherwise. Fasting sends a signal. That signal triggers the release of specific compounds inside your cells. Those compounds execute the actual program. Without adequate levels of those compounds, the signal arrives and nothing happens. The recycling plant stays closed. One compound is called spermidine. Your body produces it naturally, but production declines with age. By your 40s, cellular spermidine levels drop by roughly half. By your 60s, they're lower still. The fasting signal keeps firing. The machinery doesn't respond. This explains why some people fast for years and see minimal results. The signal works fine. The execution mechanism is depleted. Autophagy is cellular recycling. Your cells accumulate damaged proteins, dysfunctional mitochondria, and oxidized lipids during normal metabolism. When autophagy functions properly, specialized structures called autophagosomes form around this cellular debris, fuse with lysosomes, and break everything down into reusable components. Amino acids get recycled into new proteins. Damaged mitochondria get cleared before they can trigger inflammation. Oxidized fats get processed before they accumulate. When autophagy slows or stops, cells fill with junk. Damaged mitochondria leak inflammatory signals. Misfolded proteins aggregate. Energy production drops. Inflammation rises. The aging process accelerates. Two master switches control whether autophagy happens. The first is mTOR, mechanistic target of rapamycin. When mTOR is active, your cells are in growth mode. Protein synthesis runs high. Cell division proceeds. Autophagy stays suppressed. You need mTOR active when you're young, growing, recovering from injury, or building muscle. You don't need it active 24 hours a day for decades. The second switch is AMPK, AMP-activated protein kinase. AMPK activates when cellular energy drops. When AMPK senses low energy, it suppresses mTOR and activates autophagy. Fasting activates AMPK naturally by depleting glucose and lowering insulin. But fasting isn't the only trigger. Most autophagy research focuses on these two switches. Suppress mTOR or activate AMPK, and autophagy begins. Hundreds of studies confirm this. Thousands of protocols are built around it. But August 2024 changed the framework. The Nature study showed that mTOR suppression and AMPK activation are necessary but insufficient. Even with both switches in the correct position, autophagy doesn't fully execute without adequate spermidine. Spermidine works through a completely different mechanism. It operates at the gene expression level, not the metabolic signaling level. Spermidine inhibits an enzyme called EP300. EP300 normally keeps autophagy genes in a suppressed state through acetylation. When spermidine inhibits EP300, three critical autophagy genes are released from suppression simultaneously: ATG7, ATG5, and ATG11. These genes encode the structural proteins that build autophagosomes. Spermidine also activates a translation factor called eIF5A through hypusination. Hypusinated eIF5A dramatically increases synthesis of TFEB, transcription factor EB. TFEB moves into the cell nucleus and switches on the lysosomal biogenesis program. This builds entirely new lysosomes, the organelles that fuse with autophagosomes to complete the recycling process. Most importantly, spermidine activates autophagy independent of mTOR status. This means it works even when you've just eaten, even when insulin is elevated, even when mTOR is fully active. Every other autophagy trigger requires metabolic preconditions. Spermidine bypasses them entirely. The practical implication is straightforward. If you fast without adequate spermidine, the metabolic signals fire but the genetic machinery doesn't fully respond. If you consume spermidine without fasting, autophagy activates anyway. Spermidine declines with age for a simple reason. Your gut bacteria produce it from the amino acid ornithine. Aging reduces both the diversity and metabolic activity of your gut microbiome. Bacterial spermidine production drops. Dietary intake becomes essential. The highest dietary source is aged hard cheese. Parmesan contains roughly 200 milligrams of spermidine per kilogram. Gruyere contains similar levels. The aging process concentrates spermidine as bacteria metabolize amino acids during fermentation. Longer aging produces higher spermidine content. Studies on longevity consistently show spermidine extends lifespan across multiple species. Yeast, roundworms, fruit flies, and mice all live longer with spermidine supplementation. The mechanism appears to be autophagy activation. When researchers block autophagy genes, spermidine's longevity effects disappear entirely. Human epidemiological data supports this. A 2018 study tracked dietary spermidine intake in over 800 participants for 20 years. Higher spermidine intake correlated with significantly reduced all-cause mortality. The effect remained after adjusting for other dietary factors. People eating the most spermidine-rich foods lived longer. But spermidine works best as part of a system, not in isolation. Seven other compounds activate autophagy through complementary mechanisms. Together, they create a multi-directional activation protocol that addresses every known bottleneck in the autophagy pathway. Each compound works through a different mechanism. Each targets a different bottleneck in the autophagy pathway. Together, they create a system that activates cellular recycling from multiple directions simultaneously. No single food replaces fasting entirely, but the combination addresses every known limitation in the autophagy activation sequence. All the compounds and their practical application organized into a daily protocol that maximizes autophagy activation while maintaining metabolic flexibility, appears in Part 2.

@Anaro74 Me alegra saber que estás bien @Anaro74 ☺️✨Yo también, gracias a Dios. Cielos! apenas me di cuenta que se me fue “esta” con acento en la à. Entiendo que por mi error decidiste mejor no decir nada. Te preguntaba, como esta jugada de Raúl ? youtube.com/shorts/ezZGgLi…

@MiraclesShower Bien gracias ¿Y usted?

El pase que le pone Quiñones... esas no se fallan. Si hubiera sido Raúl, se lo hubieran tragado, pero como es la Hormiga, no dicen nada.

@Carlosgarciabre @Anaro74 Quien le puso este pase a Raúl Jiménez @grok ?

@Anaro74 Pues con Raul Jimenez, el cero goles en mundiales, contra Costa Rica tampoco dijeron NADA... Y Costa Rica lejos de ser Portugal jajajajajaja

🔴📈✨

Red light + green tea powerfully reduces skin aging in clinical trial. This is one month of progress utilizing: ◇ Green tea filled cotton pads applied to the face ◇ 670 nm red light For 20 mins per day. Both tools work on the key paths found in skin aging - collagen/elastin preservation + synthesis, reduction of ROS.

Glory be to the Father, to the Son and to the Holy Spirit… Can you finish this sentence?

Your VO2 Max is the #1 predictor of all-cause mortality. But your VO2 Max is limited by one thing: the health of your mitochondria. If you aren't training your cellular 'engines,' you’re leaving decades of life on the table. Here are 12 ways to optimize your mitochondria to live longer:

Another great Robots in healthcare usecase. Aletta is a robot that fully automates blood draws. The patient sits down; the robot uses ultrasound to find a vein, helps position the arm, collects the sample, and applies a bandage—fully automated

@BigolWave Es esto cierto @grok ?

Aspirin uncouples mitochondria increasing the speed of the metabolism and increasing the amount of heat your body produces. Aspirin shifts your body towards glucose metabolism which over time can feasibly cure diseases like cancer and diabetes.. which are caused by impaired glucose metabolism. Not only that but shifting the body towards glucose metabolism obviously makes the body more efficient at burning glucose.. which provides a performance boost during exercise because when the body needs energy fast it uses glucose. Your body using glucose more efficiently also provides a performance boost by increasing the amount of CO2 your body produces which increases vasodilation, increases the amount of oxygen your blood carries, and is also anti inflammatory decreasing muscle soreness in a few ways.. by fighting general inflammation and also by reducing lactate buildup allowing your muscles to work harder for longer. Aspirin reduces inflammation in a plethora of ways including blocking prostaglandin formation. Aspirin blocks cortisol and adrenaline. Aspirin blocks serotonin. Prolactin. Helps with pain. Like I mentioned before it also helps with blood flow and in large doses has been shown to be as effective for erectile dysfunction as viagra. This is not an exhaustive list of the benefits of aspirin. Far from it. It’s just a few but it just goes to show how many benefits it has because this post barely scratches the surface

Poderoso Versículo Bíblico: “No se preocupen por qué responder o qué decir. Dios les dará las palabras apropiadas en el momento preciso. Pues no serán ustedes los que hablen, sino que el Espíritu de su Padre hablará por medio de ustedes” - Mateo 10:19-20

@Juampachabal03 😂

“La que falló el chavo, la firma Raúl” Raúl Jiménez:

@SergioADippW Si

¿Sí o no? 👀🔥🇲🇽 ¡Las Chivas de Milito le hubieran ganado hoy a Portugal!

@matawilos @Carlos_Ponz Creo que @Carlos_Ponz no vio este juego 😂

@Carlos_Ponz Jajajaja apoco si Tampoco mamen

La Hormiga es solución para Chivas …pero no para la Selección, aún no. La que falló el chavo de cabeza la firma Raúl. Hasta Berterame. La gente lo quiere mucho, pero creo que le va a costar el Mundial. 🇲🇽0-0🇵🇹

@matawilos @Carlos_Ponz 😂😂😂

@Carlos_Ponz Cada quien lo ve de distinta manera. Yo vi que aportó más el en 5 mins que los otros en todo el partido.