This mesmerizing timelapse captures the nonstop motion inside an... animal cell. Moving red/orange streaks are the growing ends of microtubules, tiny “highways” that move proteins & other molecules within the cell. 📸: Andy Moore, HHMI’s Janelia Research Campusshow more

Inside every cell, there is a transport system that... determines how materials move, signals propagate, and structure is maintained. This video captures that system in motion. The glowing streaks mark the growing ends of microtubules (protein polymers that constantly assemble and disassemble through a process called dynamic instability). Rather than forming permanent tracks, microtubules are rebuilt continuously, allowing cells to reorganize their internal layout in real time. This behavior is essential for life. Cells rely on microtubule dynamics to divide accurately, migrate during development and repair, and maintain long-distance transport in neurons that may span over a meter in length. When this system is altered, the consequences are significant. Certain cancer therapies work by locking microtubules in place, preventing cell division. In contrast, failures in microtubule transport are linked to neurodegenerative conditions (like Alzheimer's) where intracellular delivery breaks down. What appears as abstract motion under a microscope is actually one of the core systems that keeps cells functional, adaptable, and alive. Video Credit: Andy Mooreshow more

The most detailed 3D reconstruction of a cell ever... created. Blows my mind every time. But what exactly are we looking at here? The average human cell contains: ~ 15-20 total distinct organelle types, totalling between ~1-10 million working together per cell. All these nano-machines in the cell are made up of proteins. ~ 8,000-10,000 distinct types of unique proteins, adding up to between 40 million - 10 trillion total proteins making up all those cellular systems. ~ 10,000 - 15,000 distinct types of RNA shuttling information around the cell, totalling up to ~10 million RNA molecules moving around the cell simultaneously. ~ Billions of Lipid molecules packed together into the cell membrane, which is also packed tightly with millions more protein-based nano-machines. And let's not forget billions of lines of DNA information to build and run it all. That's TRILLIONS of of individual molecular pieces working together to make a single cell function. That means there is more complexity in a single cell than humanity's largest cities. And people still believe this wasn't Divinely Designed. This is God's Glory on Display. But to make the point. A cell couldn't have evolved from some nebulous simpler "protocell" because even the simplest cells still require massive complexity. The "simplest" cell ever created was engineered by scientists knocking out pieces of a functional cell until it stopped functioning. Here is what they found is the absolute necessary minimal requirements of a cell to function: - Over ~531,000 lines of coded DNA information - 473 total genes to create hundreds of unique protein products (they later added 19 genes back in because the cell was so weak) - Hundreds of thousands of total proteins all working together - Extensive regulatory networks guiding all these interactions If the cell doesn't have all these systems in place, from the start... it doesn't live. Cell rely on an intricate network of complex systems, which are themselves built from complex interconnected pieces woven together into an incomprehensibly complex web of functionilty. Only intelligence has ever been observed creation vast interconnected systems like this. Life was clearly Created. It couldn't happen any other way.show more

A single E. coli cell, placed on a dish,... will become 70 billion cells in just 12 hours. That’s exponential growth. But a new preprint shows that it's possible to engineer E. coli to grow linearly instead, where only one daughter cell continues dividing and the other stops. First, some context. In nature, there is a bacterium called Mycobacterium smegmatis (initially discovered in 1884 in ulcers scraped from syphilis patients.) M. smegmatis is weird because it divides asymmetrically. These cells grow only from one end, and all their cell wall biosynthesis machinery is located on that one end. So when the cell divides, one daughter gets this machinery and the other gets nothing. The daughter that gets the machinery can keep dividing immediately, but the other daughter has to remake all that machinery from scratch, so its growth is delayed. E. coli doesn’t grow like this. When it divides, it pinches in the middle and splits everything evenly. Enzymes, metabolites, and proteins get partitioned more or less randomly between the two daughters. For the new preprint, though, researchers engineered E. coli to behave more like M. smegmatis. Here is how they did it: First, they deleted a gene called cyaA, which encodes an enzyme (adenylate cyclase) that makes a molecule called cAMP. cAMP is SUPER IMPORTANT! It is a nutrient sensor that instructs E. coli to switch on genes that help it digest non-glucose carbon sources when glucose is scarce. Without cAMP, E. coli cells growing on alternative carbon sources will starve; they won’t know how to eat the food. Next, they added back a “split” version of the cyaA gene into the cells. In other words, they split the gene in two so that each half of the enzyme is made separately. Cells can only make cAMP, and thus eat non-glucose carbon sources, if these two halves come together. To facilitate that “coming together,” the researchers also fused the split cyaA proteins to sticky proteins that clump together, and to a fluorescent protein (to make it easy to track these molecules in the cell.) So now some interesting things start to happen if you grow E. coli on a growth medium lacking glucose. As the cell grows, its cyaA “halves” start clumping together into a giant ball. Inside the aggregate, the two enzyme halves come together and make cAMP. And when the cell gets big enough and divides, the clump of cyaA RANDOMLY goes to either daughter cell #1 or #2. The daughter that gets the aggregate (called PA+ in this paper) can keep dividing. The daughter that doesn’t (PA–) cannot. It still grows a few times — about four divisions — because it inherits some leftover cAMP from its mother. But after that, the metabolite is diluted away, and the cell stops growing. PA+ cells went through about 23 divisions on average before their aggregate decayed. And the population of cells, as a whole, grew linearly. This paper is cool because there are many applications where exponential growth is too unpredictable and, perhaps, unsafe. If you want to engineer bacteria to deliver drugs, clean up waste, or live in the gut, you don’t want them to double uncontrollably. This paper shows you can make them expand in a controlled, linear way. Alas, mutations could break this whole engineered system. A mutation that restores cyaA, for example, would give cells a new way to make cAMP. Mutations that make the aggregates split between daughters would break the asymmetry, too. But still, I really enjoy proof-of-concept engineering papers like this.show more

True, even a two DOF system can exhibit chaotic... behavior, and a single cell is an at least an ~10^7 DOF system (i.e., protein molecules per cell). I still fail to properly convey to others the insane complexity I see in our microscopes, and why successes like AlphaFold only work because of the huge number of unnatural constraints placed on the training data. Case in point (below): lysosome dynamics over 12 min across a 200 x 70 um region in the head of a developing zebrafish embryo, color-coded by depth -- just one of 20k proteins at work. Our Cell Observatory Initiative is more important than ever, but while we have petabytes of the most mind-blowing data ever, we are still hamstrung by insufficient AI talent and compute -- two resources in great demand everywhere. If anyone can help us over this hurdle, we'd be eternally grateful.show more

Some microbes carry a protein, called SNIPE, that "chops... up" phage DNA as it's being injected into the cell. This is a new mechanism for phage defense! CRISPR–Cas and restriction enzymes also evolved to fight against phages, but they work by recognizing sequences. SNIPE works, instead, by sensing "touch." SNIPE is a protein with about 500 amino acids. After it's made by the ribosome, it latches onto ManYZ, two proteins which sit on the cell's inner membrane. (ManYZ is an importer; it brings mannose and other sugars into the cell.) Once attached to ManYZ, SNIPE sits and waits for an invading phage. Some phages, including lambda, actually infect cells by pushing their DNA through this ManYZ channel. Lambda uses its "tail" to reach inside the protein channel, basically, and inject its DNA. When this physical touch happens, though, SNIPE is waiting. As soon as the phage DNA starts entering the cell, and passes through ManYZ and SNIPE, it gets immediately destroyed. This means that SNIPE is the first phage defense system discovered, so far, that uses spatial positioning at the injection site to destroy invaders. But there are caveats, of course. If you untether SNIPE from ManYZ, such that it can freely diffuse through the cell, it will chew up the bacterium's genome. It is not a highly discerning nuclease! Also, SNIPE is not found in most bacteria. A prior pangenome study, which sequenced lots of different microbes, found that roughly a third of well-studied bacterial lineages had at least one member with a SNIPE-like protein. (For this paper, they just ported one of those homologs into an E. coli laboratory strain.) And finally, because SNIPE's mechanism is tightly tied to ManYZ, it cannot be used to defend against phages that enter the cell through different routes. T4 phages, for example, inject their DNA straight through the cell membrane and into the cytoplasm, without interacting with ManYZ. This is a nice basic science paper. Applications TBD. (Just remember that scientists figured out that bacteria had a phage defense system, called CRISPR-Cas, many years before it was repurposed into a gene-editing tool.) P.S. The video below shows how cells with the SNIPE gene (middle row) kill invading phages, and thus continue growing and dividing. Empty vector (top row) refers to bacteria carrying a plasmid with no SNIPE gene; this is a control group. And SNIPE E414A refers to cells which received a mutated SNIPE gene, where the glutamate at position 414 has been changed to an alanine, thus destroying the protein's nuclease activity. These cells also die when they get infected with a phage.show more

There are many of them but one of the... most incredible adaptations I've seen is that of an animal that "dies and resurrects," every year. Behold the wood frogs. They're found in North America. In the northern regions where it gets really cold in the winter, these frogs can freeze up to 60-65% of their body. Their heart stops, breathing ceases, and ice forms in body cavities. If this happens to humans or most animals, that's the end. But for wood frogs, they produce glucose and cryoprotectants that prevent cell damage. In spring, they thaw and resume normal functions. Talk about coming back from the dead.show more

💪 Muscle cells merging in real time You’re watching... one of [in my opinion] the coolest things your body does without you ever noticing (muscle precursor cells literally fusing into one long, powerful fiber). 🔵 Alignment: individual myoblasts migrate and line up like they’re preparing for formation 🟢 Recognition: cells “sense” compatible neighbors through surface proteins 🟡 Contact: membranes begin to thin and synchronize their signaling 🟠 Fusion: boundaries dissolve and nuclei gather inside a shared cytoplasm 🔴 Strengthening: the new multinucleated fiber becomes the machinery that lets you lift, run, and repair The glowing green nuclei are each a tiny command center contributed by a merging cell. The red signal traces the membranes as they stretch, touch, and finally blend into a unified structure. This is how muscles grow and regenerate - i.e. this is "strength" engineerednat the cellular level Credit: Yue Lu, Elizabeth Chen Labshow more

The bacterial flagellum looks like a simple tail, or... whip. But it’s actually a rotating motor, and perhaps the most sophisticated protein complex nature has ever evolved. In e. coli, these motors are capable of astonishing speeds; about 15,000 rpm. (The world record, according to one study, is for a Vibrio cell that was “clocked at 100,000 rpm by laser microscopy.) The flagellum propels the cell forward at speeds of 20-30 microns per second, or roughly 15 body lengths per second. If scaled up to the size of a cheetah, E. coli would *nearly* be the fastest land organism. The darting movements of a microbe were first observed in 1676 by Antony van Leeuwenhoek, a Dutch cloth merchant. Antony was delighted by the motion of his “animalcules,” writing: “I must say, for my part, that no more pleasant sight has ever yet come before my eye than these many thousands of living creatures, seen all alive in a little drop of water, moving among one another, each several creature having its own proper motion.” But Leeuwenhoek did not see flagella. He assumed, rather, that these animalcules must be “furnished with paws” instead. Christian Ehrenberg would not properly describe flagella until 1836. But amazingly, all the way up until the 1970s, nobody actually knew how the flagellum spun! In 1973, there were two competing models people argued over: the helical-wave (bending) model and the rotating (corkscrew) model. The first model suggested that the flagellum whipped back and forth, side-to-side, to propel the cell like paddle. The corkscrew model suggested that the whole flagellum instead spins around like a screw. In 1974, the corkscrew model finally won out. For two separate studies, scientists affixed flagella to glass slides using antibodies, and watched as the cells spun around and around like corkscrews. And finally, in just the last year, high-resolution structures of the flagellum have revealed a LOT more about its intricate assembly. The tail is made from ~20,000 self-assembling copies of a single protein, called flagellin. A “driveshaft,” or rod, spins the tail and is itself made of 26 protein subunits. Each “motor” in E. coli consists of 11 stators, each of which is made from 7 proteins.(Other types of cells have even more stators, and swim with much higher torques.) The flagellum spins when protons flow into the cell through tiny channels in these stators; akin to water running through a turbine. Each proton makes a small part of the stator change shape and push against the rotor, nudging it forward one step. With dozens of stators working at once, these nudges quickly spin the propeller. I'm writing an essay for Asimov Press about this now, and am really enjoying learning about the flagellum and its history. It's an extraordinarily complicated structure, though, and has been a challenge to understand!show more

🚨 NASA JUST FOUND THE RAW INGREDIENTS OF DNA... INSIDE A ROCK OLDER THAN EARTH ITSELF. Samples returned from the asteroid Bennu contain complex organic molecules including precursors to DNA and RNA, plus many of the amino acids used by all life on Earth. These molecules formed in the early solar system and survived for billions of years inside the asteroid. Earth didn’t have to invent the chemistry of life from nothing. It was delivered ready-made from space. Why this matters: • Bennu is a primitive asteroid that has remained largely unchanged since the birth of the solar system (~4.5 billion years ago) • The samples contain the molecular building blocks of DNA, RNA, and proteins the core components of life as we know it • These organics were preserved through the violent early days of the solar system and could have been delivered to Earth by asteroids and comets • This is some of the strongest direct evidence yet that life’s chemistry has cosmic origins The deeper implication: This doesn’t mean aliens or microbes came from space. It means the raw materials for life were already floating around the solar system long before Earth cooled enough to support life. Our planet likely received these ingredients from above rather than creating them all from scratch. If these building blocks were common in the early solar system, then the starting chemistry for life may have been widespread dramatically raising the chances that similar processes could have happened elsewhere. How does it change your perspective to know that the molecular ingredients for DNA were already present in space billions of years before the first living cell appeared on Earth? Follow for more discoveries about the origins of life and what we’re learning from asteroid samples.show more

Contact in the desert was the biggest ever this... year and so was the sky watch. We witnessed dozens of orbs. With 5 minutes left before the hotel turned the lights on, I told more than a 1000k people present why pointing my laser in a certain direction that the phenomenon may give us a grand Finale and it may be an orb with wings. Within seconds a glowing orb with wings appeared and flew past the crowd. No it’s not a bird if you If you want to learn something about the phenomenon and 20 years of research with scientists and not speculation , join us on one of our adventures you will never be the same. We have this on several cameras from full spectrum to cell phones to Two types of night vision. Also scientists from NASA and Lockheed the NSA and The CIA were standing next to me during the filming of this orb and has witnessed this many times.show more

The $640,000 Ferrari Luce EV has a unique way... of creating sound inside/outside when accelerating. Unlike other systems (Mercedes, Hyundai, Porsche) that just use synthetic audio files, Ferrari took a different approach. On the rear axle next to the inverter, they installed a high-precision accelerometer that captures the actual mechanical vibrations and noises from the electric motors, gears, inverters, and drivetrain components. Those signals are then filtered, equalized, and amplified through the car’s external and internal speakers. Ferrari compares it directly to how an electric guitar operates. You can hear it in the video below when Lewis & Charles are driving. I think this may be the only part of the Luce I find interesting tbh lol.show more

I see the Left-wing/Ukrainian bots got their talking points.... They went from “the labs don’t exist”, to “okay the labs exist but they were doing defensive research”. “Defensive research” is a lie. In the process of defensive research, you create a bioweapon. I’ll explain. Defensive zoonotic research, is when scientists intentionally make animal viruses transmissible in humans, so they can study the virus and proactively develop vaccines, just in case these animal viruses naturally mutate and jump to humans. This way, we have the vaccines already on hand if something were to happen. In theory, it sounds like a good idea, but in the process of creating these vaccines, you must first modify a deadly zoonotic disease, and give it the ability to jump to humans. That’s a biological weapon. If it gets out of the lab, it can now infect the world, and in the case of C19, a man-made bat coronavirus, it did infect the world, and killed millions of people. Why was it so contagious? Because scientists artificially gave it the ability to be transmissible in humans, thus the term “gain of function”. What is the function these zoonotic diseases are gaining? The ability to jump to, and kill, humans. So when anyone says “it’s just defensive research”, they have no idea what they are talking about, and are either running cover or repeating talking points. Defensive research/gain of function, is just a way to circumvent the Geneva Convention and develop biological weapons under the guise of “defense”. Russian MIL alleged that elements within the US, specifically the Democrat Party, in coordination with nefarious NGO’s and Big Pharma, have been using “defensive research” in an offensive capacity, to manufacture global biological crises, to impose global control.show more

🚨 Scientists discover wisdom teeth contain stem cells capable... of repairing the heart, brain, and bones. Wisdom teeth contain dental pulp, a soft connective tissue threaded with blood vessels and nerves. Inside that pulp lives a dense population of mesenchymal stem cells, a class of undifferentiated cells that researchers classify as among the most therapeutically valuable biological material a human body produces. These are not ordinary cells maintaining routine tissue. They are blueprint cells, capable of receiving chemical signals from damaged environments and reshaping themselves into whatever the body needs most, neurons, cardiomyocytes, osteoblasts, even hepatic cells under the right conditions. The brain operates under a brutal rule: most of its neurons do not regenerate after damage. A stroke, a traumatic injury, a neurodegenerative disease removes cells the brain cannot replace through normal biological processes. Researchers have spent decades attempting to solve this through synthetic means, engineered cell therapies, growth factor injections, gene editing approaches that cost extraordinary resources and produce inconsistent results. What dental pulp stem cells demonstrated in laboratory conditions is that they can migrate toward neural damage sites, integrate with existing tissue architecture, and begin producing neurons and glial support cells. The mechanism involves neurotrophic factor secretion, essentially the cells releasing signaling proteins that stimulate the surrounding neural environment to repair itself from within. Cardiac muscle operates under a similarly unforgiving rule. After a heart attack, the dead muscle tissue becomes fibrotic scar material. The heart compensates by making surviving muscle work harder, a process that gradually leads to enlargement, weakening, and eventual failure. Dental pulp stem cells introduced into cardiac tissue in multiple studies produced measurable reductions in scar formation and demonstrated the ability to differentiate into functional cardiomyocytes, beating in synchrony with native heart cells. Some studies recorded improved ejection fraction in animal models, the core measurement of how effectively the heart pumps blood. Bone regeneration represents the most clinically advanced application already moving toward human trials. Dental pulp stem cells express high levels of osteogenic markers and respond rapidly to bone morphogenetic proteins, the chemical messengers that trigger skeletal repair. Their application in craniofacial reconstruction, spinal fusion, and long bone defect repair is being studied across multiple institutions simultaneously. What separates these cells from other stem cell sources is the combination of accessibility and biological youth. Bone marrow aspiration requires sedation and produces significant post procedure pain. Umbilical cord blood requires planning around birth. Wisdom teeth emerge between 17 and 25, during peak cellular vitality, and come out during a procedure most people already schedule. The extraction window is permanent. Once the teeth are gone and the pulp degrades, that specific population of young, highly potent cells is irretrievable from that individual. Cryogenic preservation protocols now exist that maintain dental pulp stem cell viability for over two decades. Several countries have commercial dental stem cell banks operating with the same institutional model as cord blood banking, long term frozen storage, indexed against future therapeutic need. The science supporting the value of preservation is no longer speculative. What lags behind is public awareness and clinical infrastructure in markets where this remains obscure. The wider pattern is worth recognizing. Medicine has repeatedly discovered that profound biological tools were present in tissues it previously categorized as vestigial, unnecessary, or inconvenient. The appendix was considered evolutionary junk for over a century before researchers identified its role in gut microbiome preservation. Wisdom teeth carried the same dismissal, a developmental relic from ancestors who needed extra molars for coarse diets, relevant only in their capacity to cause orthodontic problems. The pulp inside them was never junk. It was a repair system the body built during youth and stored in one of the most protected anatomical locations, surrounded by enamel, the hardest substance the human body produces. Evolution rarely wastes that kind of architecture.show more

New Corridor of the UAE's RSF Dirty War in... Sudan Previously, the route used by Colombian mercenaries extended from Bosaso to Nyala. Recent developments point to a further deepening of the regional dimension of the war in Sudan. According to new evidence, with Ethiopia now reportedly becoming directly involved in the equation, the route once again begins in Bosaso, continues to Addis Ababa, and then proceeds to Assosa Airport near the Ethiopia–Sudan border. Within this framework, it is alleged that soldiers are being trained at an RSF camp in Ethiopia said to be financed by the UAE, and that drones prepared there are being deployed inside Sudanese territory. All of these flights are reportedly being carried out illegally by Ethiopian Airlines. This picture suggests that the war in Sudan is being shaped not only by internal actors but also by the indirect involvement of regional powers. In particular, the use of border areas as logistical and military transit corridors signals a growing risk of further internationalization of the conflict.show more

A serious incident has been reported from Siddhartha Medical... College in T. Beguru village of Nelamangala taluk, where a lecturer allegedly proposed to a female student inside a classroom, leading to a tense situation and subsequent violence on campus. The accused lecturer has been identified as Abdul. According to initial information, he reportedly approached the student during class hours and offered her a chocolate while proposing to her. The unexpected act was strongly opposed by the student, who allegedly reacted by hitting him with a slipper. Following this, the situation escalated quickly. Other students on campus gathered and confronted the lecturer. Reports suggest that a group of students chased Abdul across the campus and physically assaulted him near a parked vehicle. The assault reportedly continued within the college premises, where the lecturer was beaten by students. As the situation intensified, Abdul managed to escape from the spot while being attacked. The incident has also led to allegations of misconduct against the lecturer, with claims of inappropriate behaviour towards the student. The episode took place under the jurisdiction of the Nelamangala Rural Police Station. Authorities are expected to look into both the alleged harassment and the assault that followed. The college, which is associated with Karnataka Home Minister Dr. G. Parameshwara, witnessed a chaotic scene as the incident unfolded, drawing attention to safety and conduct within educational institutions. Further investigation is likely to determine the full sequence of events and any legal action that may follow.show more

🚨 SCIENTISTS ARE USING AI TO MAP A HIDDEN... “CLEANING SYSTEM” INSIDE THE HUMAN BRAIN AND IT COULD CHANGE HOW WE UNDERSTAND SLEEP, AGING, AND NEURODEGENERATIVE DISEASE. It’s called the glymphatic system a vast network of fluid channels that flushes toxic waste from the brain while you sleep. For years it was almost impossible to observe in detail. Now AI-powered imaging is revealing it like a living galaxy of microscopic rivers and pathways inside neural tissue. Why this matters: Your brain produces toxic proteins constantly. The glymphatic system is one of its primary waste-clearance mechanisms clearing the very proteins linked to Alzheimer’s, Parkinson’s, and other neurodegenerative diseases. But here’s the unsettling part: This cleaning system becomes dramatically less efficient with age, poor sleep, stress, and brain injury. Sleep may not just “rest” your mind it may literally wash your brain. The deeper implication is staggering: The brain isn’t just a computer. It’s a dynamic, living network that constantly rebuilds and cleanses itself in real time. The more we map it, the more it looks like an entire universe of connected energy flows inside our skulls. What if some neurological diseases begin when the brain can no longer properly “wash” itself at night? Follow for more frontier neuroscience and future technology.show more

We are getting absurdly close to the point where... “learning Blender” means learning how to direct an AI. A shot like this looks soft and playful on the surface, but under it is the usual 3D pain: modeling, layout, materials, lighting, atmosphere, animation, and endless tiny fixes until the frame stops looking dead. That is why Kimi K3 matters. With Blender MCP, you can describe a scene like a robotic goat walking through a dreamy field and let the model help build the environment, place the camera, shape the materials, script the motion, and iterate inside the real Blender project. The real shift is not text-to-image. It is text-to-workflow. Kimi K3 does not just give you a pretty output and disappear. It can help move the actual scene from rough setup to something that looks art-directed. Soon the hardest part of 3D will not be the software. It will be whether your imagination is good enough to deserve tools like this.show more

⚾️ It is no secret that elbow injuries, specifically... UCL injuries, have been on a rise in recent years ➡️ The reason for this is so multi-factorial that it is impossible to pinpoint any 1 reason for an injury 💪 With the constant improvement in the development of pitchers, both skill side and S&C, we are seeing an increase in velocity across all levels of baseball 🎟This is obviously a Great thing for Punching Tickets but also leads to more forces being passed through the medial elbow 🔥There are really 3 proactive actions we actions we can take to counteract this: 1) Address pitching mechanics if there are deficiencies 2) Appropriately manage chronic/acute AND Total workloads 3) Increase the capacity and stress the elbow can handle 🔥 We will specifically dive in to the 3rd component of this in this thread. In short, the answer is simple, GET STRONG FOREARMS 3 WAYS VALGUS FORCE IS DISPERSED ✅ Radiocapitellar Joint Compression When a valgus stress is applied to the elbow, it is attempting to open up or gap the medial (inside) portion of the elbow. This is also the Orthopedic Test for a UCL injury. While this force is trying to gap the medial portion of the elbow, it is also compressing the lateral side. When the radius and lateral humerus compress, this acts as a stopping point for the elbow going into that valgus motion ✅ Forearm Musculature In addition to the UCL on the medial side of the elbow, there is also a group of forearm muscles that span that area and attach to the same portion of the elbow, the medial epicondyle. These muscles include: Pronator Teres, Flexor Carpi Ulnaris, Flexor Carpi Radialis, Flexor Digitorum Superfiscialis, and the Palmaris Longus. With that specific attachment to the medial epicondyle and their respective distal attachments, these do a great job of accepting the valgus force and protecting the UCL. There is some research that states FCU does the best job of the muscles listed, but we believe the best action is to strengthen all of them. The best ways to attack this is with movements including: finger flexion, wrist flexion, Ulnar deviation (moving pinky towards medial elbow), and Pronation of the forearm ✅ Ulnar Collateral Ligament (UCL) What doesn’t get absorbed by the first two structures is placed on the UCL. Previous research has shown that a UCL with no other structures involved is able to withstand ~35 nm of force before failure The Problem is: Every Pitch produces far more than 35nm of Valgus Stress. This shows us just how important the other 2 mechanisms are! * Exercises in the videos should be a complement to your entire S&C Program and is not designed to replace itshow more