“It’s not only Akara. We also have tomato sellers, Boli, and those selling pepper, vegetables in the market. We’ll continue to empower them.”
~ Nigeria First Lady Oluremi Tinubu responds to criticism as she gives JUST ₦100m to 2,000 market women
Wasted my whole afternoon so you don't have to 😂
Tested the App TradingView mode across @BingXOfficial , Binance, Bybit, OKX, and MEXC side by side.
I Wanted to see which one actually lets you DO stuff on the chart.
The short answer? Only @BingXOfficial Ultra TradingView lets you fully trade while reading the chart. The rest are basically just fancy chart viewers, look but don't touch lol.
#BingXUltraTV #Bingx
The games we remember are rarely the ones that paid the most. They're the ones that made us want to come back.
The biggest challenge in Web3 gaming isn't attracting players. It's giving them a reason to stay after the excitement of launch fades.
I've come to appreciate that lasting gaming communities aren't built around constant rewards alone. They're built around progress that feels meaningful, social interactions that create memories, and worlds that continue evolving long after the first login.
That's why I pay attention to ecosystems that focus on long-term engagement instead of short-lived attention. When players can shape their experience, own what they earn, and contribute to a living world, participation starts to feel like something worth investing time in rather than simply chasing incentives.
That's one of the reasons @ChainersGame stands out to me. The project continues to build an experience where creativity, ownership, and community naturally come together, allowing players to become active participants in the game's evolution instead of passive users.
For me, the future of Web3 gaming belongs to projects that make people excited to return tomorrow, not because they have to, but because there's always another story to create, another connection to make, and another milestone to reach.
Explore more on: https://t.co/3QLBiGKIaN
Aging isn't just the passage of time. It's a molecular process — and that means, at least in principle, it can be interrupted.
A growing body of research is testing exactly that idea. The approach is called reprogramming-induced rejuvenation, and it builds on a Nobel Prize-winning discovery from 2006: four specific proteins, known as the Yamanaka factors, can erase a cell's identity entirely and return it to an embryonic-like state.
Full reprogramming destroys what the cell is. But researchers have been exploring whether a carefully timed, partial version of that process can roll back biological age without erasing cellular identity.
The early results from animal studies are striking.
In mice engineered with inducible Yamanaka factors, short cycles of activation — switching the factors on briefly, then off — extended median lifespan in accelerated-aging models by 33%. Chromatin marks associated with younger cells returned. Mitochondrial health improved.
A separate study applying the same cyclic approach to normal mice found that tissue-level molecular profiles across multiple organ systems shifted measurably toward younger states.
The most dramatic result came from a gene therapy study delivering three of the four factors to very old mice, deliberately omitting c-Myc to reduce cancer risk. Remaining lifespan extended by 109% compared to untreated animals of the same age. Frailty scores improved.
In targeted applications to the eye, partial reprogramming partially restored visual function in aged and glaucomatous mice — without producing tumours even after more than a year of continuous expression.
Chemical alternatives are also advancing. Rather than introducing genetic factors, small-molecule cocktails can partially mimic the reprogramming signal. A seven-compound chemical approach in mouse cells showed measurable rejuvenation across multiple biological systems, with epigenetic clocks registering a genuine decrease in cellular biological age.
Critically, where genetic reprogramming suppresses p53 — the major tumour suppressor — the chemical version upregulates it. That difference matters enormously for safety.
And safety is where the field is honest about its limits. Full reprogramming carries teratoma risk. Prolonged factor expression has caused organ failure in mice. Only around 25% of cells successfully undergo partial reprogramming in culture. The epigenetic clocks used to measure success may be capturing adaptive changes alongside genuinely damaging ones, making it difficult to know with precision what's actually being reversed.
None of that invalidates the direction. It defines the work still ahead.
What's being built here, piece by piece, is an understanding of whether biological age is a fixed trajectory or an adjustable variable. The evidence increasingly suggests the latter — and the implications of that, if it holds, reach into nearly every corner of medicine.
We're not there yet. But the cells are getting younger in the lab. That's where it starts.
#Longevity #Transhumanism