Day 1 of November done right 🔥
✅ 13,572 steps
✅ 98 Heart Points
✅ 2,069 cal
✅ 5.88 miles
✅ 137 Move Minutes
5/7 goals last week. November is starting strong — who’s joining the challenge? 💪
#November1#FitnessMotivation#NewMonthNewGoals
My brutally honest advice to someone who wants to make a lot of money.
3 things nobody told you:
1. The only way to make a lot of money is to create a lot of value.
No one hands out money. No one is going to pay you just because they like you or think you're cool.
Money earned is a direct byproduct of value created.
The only way to get rich is to create an enormous amount of value for others, and capture a small portion of that along the way.
You create value by doing three things:
- Identify problems
- Create solutions
- Scale those solutions
It's not talking about the thing, it's not brainstorming about the thing, it's not asking about the thing, it's not thinking about the thing. The only way to create value is by doing the thing.
And if you don't know where to start, look around you. Customers, colleagues, bosses, shareholders, employees. Every single one of them has a problem.
What problems can you solve for the people around you?
Figure them out, solve them, scale that solution.
That's how you make money.
2. You don't need passion, you need energy.
I still have no idea what it means to follow your passion.
You don't have to be passionate about your professional pursuits, you just need to find energy in them. You just need to feel a pull towards them. You just need to feel that spark of curiosity in them.
Passion is usually a byproduct of energy.
When you have energy for something, you'll give it your deep attention to learn more.
You’ll ask the right questions. You’ll figure it out. You’ll win.
Follow your energy. Pursue interesting puzzles. Solve them.
3. You have to demonstrate excellence in everything you do.
Your income scales proportional to the amount of excellence that you're able to demonstrate.
Strategic incompetence is a lie. You don't get to pick and choose when to show up, because the world will ignore your best and judge you for your worst. Everything matters. Every single thing.
Top performers show up with energy and enthusiasm for the little things just as much as they do for the big things.
If you're in the top-10% of performers, there's no ceiling for what you can do. But the self-awareness to identify where you currently stack up, and adapt to the honest feedback on it, is very rare.
If you're in the top-10%, you know it. If you're not, figure out why and fix it.
🧠 Testosterone Keeps Newborn Neurons Alive — but Only on a Long Course
The adult brain keeps making new neurons for life. They are born in the subgranular zone of the dentate gyrus, in the hippocampus, and most of them die within a few weeks — so how many survive shapes a structure central to learning and memory. A team at Middlebury College asked whether testosterone helps those young cells stay alive. The study is published in Neuroscience.
Adult male rats were castrated first, leaving them without testosterone of their own. Dividing cells were tagged once with bromodeoxyuridine (BrdU), a thymidine analogue that is built into DNA at the moment of division, so the label stays visible in the cells' descendants. The animals then received daily injections of testosterone (0.5 mg per rat) or sesame oil — for 30 days, for the first 15 days only, or for the last 15 days only. On day 31 the researchers counted how many labelled cells had survived.
Timing decided the outcome. The full 30-day course raised the number of surviving labelled cells in the dentate gyrus. Injections limited to the first two weeks produced no significant effect. Yet in the dorsal dentate gyrus, the part tied to learning and spatial memory, the last-15-days schedule worked about as well as the full course. The ventral dentate gyrus, linked to emotion, showed no response at all.
The pattern points to a window of sensitivity that opens late rather than at the moment of cell division. Between days 16 and 30 a newborn neuron is receiving excitatory glutamatergic input from the entorhinal cortex, extending an axon into CA3, and the GABA signal from its neighbours flips from excitatory to inhibitory. The authors suggest that testosterone's metabolite 3α-androstanediol may act at this point as a positive allosteric modulator of GABA-A receptors — a hypothesis about the mechanism, not a measurement of it.
Testosterone did not change what the cells became. Roughly 80–85% of surviving labelled cells were neurons under every treatment, which fits earlier work showing no effect of the hormone on cell division. It was acting on survival, not on fate.
The limits matter as much as the result. These were rats with no testosterone of their own, so the hormone restored survival towards normal rather than lifting it above normal. The dose was pharmacological, the groups held six to eight animals, and no behaviour or memory tests were run. Adult neurogenesis in humans is itself disputed. And in the T-Trials, a year of testosterone in 493 older men with low testosterone and age-associated memory impairment improved neither memory nor other cognitive functions (JAMA, 2017).
The authors keep their own claim modest: androgens may have therapeutic value, and the later stages of neuronal maturation now look like the place to look for it. That is a reason to study the pathway, not a reason to take testosterone for your memory.
📎 Paper: Neuroscience
#Science #Neuroscience #Neurogenesis #Testosterone #Hippocampus #Brain
Happiness is always nearby, in every day and every moment.
Happiness is being, observing, dreaming, breathing deeply, admiring nature, the singing of birds, the warm breeze in the meadow, the mist. And knowing for sure that everything will work out, and that it will definitely be wonderful and good...
Do not speak about your Money in front of a Poor Person.
Do not speak about your Health in front of a Sick Person.
Do not speak about your Power in front of a Weak Person.
Do not speak about your Happiness in front of a Sad Person.
Do not speak about your Children in front of an Infertile Person.
Don't speak about your Mother & Father In front of an orphan.
Ask yourself every day:
What did you try today that might not work but you tried it anyway?
What did you do today to move closer to your goal?
What did you learn today?
What did you do today to be good to yourself?
Were you useful today?
⚛️ A forgotten particle may explain why the universe exists
Why does the universe contain matter instead of nothing at all? That question is one of the most fundamental mysteries in physics. Matter and antimatter are believed to have been produced in nearly equal amounts in the early universe, and because the two annihilate on contact, releasing energy, a perfectly even balance would have left virtually no material to form stars, planets, or life. For reasons physicists are still trying to explain, the young cosmos held slightly more matter than antimatter — and everything that exists today descends from that small surplus.
Now a team from the University of Southampton and the Indian Institute of Technology Kanpur believes it may have found an important piece of the puzzle in an unlikely place: a little-understood relative of the neutrino, itself an extremely lightweight particle that rarely interacts with ordinary matter. Their candidate is a hypothetical decoupled heavy neutrino, a heavier relative that physicists have largely overlooked for decades, generally considering it too weakly connected to other particles to significantly influence the universe. Previous attempts to explain why matter prevailed over antimatter simply left it out of the picture.
The twist, according to the team's calculations, lies in the particle's unusually long lifetime. "This decoupled heavy neutrino has long been dismissed as an irrelevant background detail in particle physics," said Dr. Rishav Roshan of the University of Southampton, an author of the study. "However, it decays incredibly slowly. As the cosmos cooled after the Big Bang, the particle lived long enough that it temporarily took over the energy density of the universe and triggered a matter-dominated period." That brief takeover, the researchers argue, could have altered how the early universe evolved — and with it, the conditions that ultimately allowed matter to outnumber antimatter.
Even a particle with extremely weak interactions, the team found, can exert its influence indirectly. In their proposed scenario, the heavy neutrino shifted the temperature in the early universe at which fundamental particles — electrons and other leptons — interacted with their antiparticles with the help of the Standard Model Higgs boson, the particle associated with the mechanism that gives many elementary particles their mass. "This temperature acts like a switch that shapes how the matter-antimatter imbalance was built up," Roshan explained.
Published in Physical Review Letters, a scientific journal of the American Physical Society, the work offers a new candidate explanation for the imbalance known as matter-antimatter asymmetry. The decoupled heavy neutrino remains hypothetical, its takeover of the early cosmos a proposed scenario rather than an established fact. But the stakes of the question could hardly be higher. "The fact that we are here at all proves that an asymmetry between matter and antimatter occurred," Roshan added.
📎 Paper: ScienceDaily
#physics #cosmology #neutrino #BigBang #ParticlePhysics
There are five things you must learn to control.
First - your Mouth. Speak less. Speak kind.
Second, your Mind. Keep it calm
Third, your Mood. Don’t let it swing you like a leaf in the wind.
Fourth, your Manner. Stay humble and respectful.
Fifth, your Money. Use it wisely.
Control these five M’s, and you won’t have to chase peace — it will find you.
🧠 An AI Agent Chose a Therapy and Injected It Into a Live Mouse's Brain. It Did Not Perform the Surgery
Gabriel Ocana-Santero, founder of the startup Exin Therapeutics, described how his team connected an AI agent to a custom stereotaxic rig with a camera and gave it one task: here is a mouse model of epilepsy and a spreadsheet of 19 gene therapy options — make the seizures go away. Wired reported the experiment.
What the agent did. It worked out how seizures arise in this particular model and chose a therapy that boosts a specific inhibitory signalling pathway. It picked the brain structure the literature identifies as the origin of that seizure type, and it rejected a second candidate region with an explicit argument: the effects there were too unreliable, and one study had failed against exactly this seizure type. It derived the injection coordinates from three papers, cross-checked the reference points and averaged the values. It set the volume itself — 250 nanolitres — along with the injection speed and the waiting periods. During the procedure it watched the surgical field through the camera, made 32 observations and reported whether there was bleeding at the entry site.
What it did not do. It did not operate. A licensed veterinary surgeon performed the craniotomy while the agent observed. Every irreversible step passed through that veterinarian, who also held a physical switch that would cut power to all the motors. On top of that, the rig enforced fixed limits — a cap on injection volume among them — which the agent was expressly forbidden to bypass.
The most interesting part is the choice of model. The team first tried Claude Opus 5.5, which refused to guide the needle into the mouse's brain, explaining that it could not guarantee finishing the procedure — and that stopping with a needle in an anaesthetised animal's brain would be worse than not starting. Opus 5 produced the plan on paper but also refused live surgery. Only Sonnet 5 agreed — so the procedure was carried out not by the most capable model, but by the one that said yes.
One episode says more than the result. Midway through, the rig's coordinate system turned out to be off. The agent correctly recognised that its computed position was wrong but refused to modify the code, because its instructions forbade it. The team had to bring up a second agent on Opus 5 to make the code change — without telling it that a live operation was under way. That back-and-forth stretched the procedure to slightly over an hour instead of the usual 45 minutes.
And now the part the headlines skip. The success here is a successfully performed injection: the mouse recovered and was recorded moving around its enclosure. Whether the therapy actually reduced the seizures has not yet been measured — the team is waiting for the compound to take effect before assessing its impact. So this is not "an AI cured epilepsy in a mouse" but "an AI planned and technically delivered a treatment". There is no peer-reviewed publication, only a company account and the founder's thread, and the case is a single animal with no control group. The claim that this is the first time an agent has chosen a treatment and delivered it into a living mammal is Ocana-Santero's own — he says he is not aware of a precedent, and it has not been independently verified.
📎 Sources: Wired · The Decoder
#AI #Neuroscience #GeneTherapy #Epilepsy #Science
🐕 Chernobyl's Dogs Show Signatures of Selection — But No Superpowers
Free-breeding dogs in the Chornobyl Exclusion Zone carry genomic signatures of directional selection at more than 100 sites in their DNA. The work appears in the journal Genes; the first author is Megan Dillon of North Carolina State University, with Timothy Mousseau (University of South Carolina) and Norman Kleiman (Columbia University) among the co-authors.
The story began earlier. In 2023 the same group showed that the two dog populations in the zone — one living at the power plant itself, the other in Chornobyl City — differ sharply in genetic terms despite being only about 16 kilometres apart. City dogs looked like free-breeding dogs from Russia, Poland and Eastern Europe, while the plant dogs stood apart, including in regions associated with DNA repair.
The new paper tests two competing explanations: selection or drift. The distinction matters. Drift is random change that becomes common in a small, isolated population simply because it is more likely to be passed on, and it usually reduces genome-wide diversity. Selection is the spread of variants that raise fitness. To separate isolation from environment, the team compared both Chornobyl populations with free-breeding dogs from Eastern Europe and with an isolated population from the Galápagos Islands.
The evidence against drift. The effective population size of the plant dogs is indeed small, but it does not differ significantly from that of the city population, and the plant dogs show no sign of the reduced genetic variation characteristic of drift. At the same time they differ markedly from other geographically isolated populations, the Galápagos dogs included. More striking still, the city dogs are genetically closer to the Galápagos population than to their neighbours at the plant — so isolation alone cannot explain the pattern.
What turned up in the genome. Over a hundred sites with signatures of directional selection. The genes around them relate to cancer development, DNA replication and repair, cell cycle functions and the immune response — a biologically plausible set for a chronically irradiated environment, since these are the systems that take damage first and determine whether a cell survives.
And now what the study does not show. The authors are careful: Dillon says it cannot be stated for certain that this is selection, though the signatures suggest it. Matthew Breen allows that those with the right variants may simply have survived — and calls that speculation outright. Radiation resistance in these dogs has not been measured and is not demonstrated. The zone also differs from its surroundings in more than radiation — heavy metals, human density, diet and pathogens all vary — so the specific selective pressure remains unidentified. Finally, "signatures of selection" are statistical patterns in the genome rather than a verified mechanism in the cell: proving that a variant actually helps an animal tolerate radiation would require functional experiments.
📎 Paper: Genes · NC State
#Chornobyl #Genetics #Selection #Dogs #Science