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If a trip to Venice is your ideal holiday, then you’re going to love the future.

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Most of us, however, will be quite sobered by Kim Stanley Robinson’s upcoming novel, New York 2140, a near-future projection of a world reshaped by climate change. Sea level has risen by 50 feet, flooding the Big Apple and countless coastal cities around the planet. Thousands of species have gone extinct.

The same economic and political forces driving the world ever closer to that reality are still in charge, setting life on a perpetual spin cycle of boom and bust, with the rich always getting richer.

More evidence to support that excess fat ages the body and is linked with inflammation and senescent cells.


Excess visceral fat tissue is very bad for long-term health. Being obese is by some measures as harmful as a smoking habit when it comes to remaining life expectancy. Even modest amounts of excess weight have a measurable negative impact on the future trajectory of health and longevity. There is an enormous mountain of data to support these points, ranging from large human studies to simple but compelling experiments in which the surgical removal of fat from mice leads to extended life spans. Unfortunately we evolved in an environment of scarcity and so find it a challenge to stay slim in an environment of plenty; this is a high class problem to have in exchange for an end to unavoidable famine and malnutrition, but a problem nonetheless.

One of the contributing causes of degenerative aging is the growing presence of senescent cells in tissues. While investigating the effects of changes in the amount of fat tissue in mice, researchers here find evidence to suggest that some portion of the damage done by fat tissue occurs because it hosts many more senescent cells than would otherwise be present in the body. These cells produce a mix of inflammatory signals, and may well be a sizable cause of the well-known link between visceral fat and increased inflammation. Chronic inflammation alone drives a faster progression of most of the common fatal age-related conditions, and that is without considering all of the other damage done due to the signaling produced by senescent cells.

In 1965, Intel co-founder Gordon Moore published a remarkably prescient paper which observed that the number of transistors on an integrated circuit was doubling every two years and predicted that this pace would lead to computers becoming embedded in homes, cars and communication systems.

That simple idea, known today as Moore’s Law, has helped power the digital revolution. As computing performance has become exponentially cheaper and more robust, we have been able to do a lot more with it. Even a basic smartphone today is more powerful than the supercomputers of past generations.

Yet the law has been fraying for years and experts predict that it will soon reach its limits. However, I spoke to Bernie Meyerson, IBM’s Chief Innovation Officer, and he feels strongly that the end of Moore’s Law doesn’t mean the end of progress. Not by a long shot. What we’ll see though is a shift in emphasis from the microchip to the system as a whole.

https://youtube.com/watch?v=DnYUNQVcVnI

IBM has unveiled its annual “5 in 5” – a list of ground-breaking innovations that will change the way people work, live, and interact during the next five years.

In 1609, Galileo invented the telescope and saw our cosmos in an entirely new way. He proved the theory that the Earth and other planets in our Solar System revolve around the Sun, which until then was impossible to observe. IBM Research continues this work through the pursuit of new scientific instruments – whether physical devices or advanced software tools – designed to make what’s invisible in our world visible, from the macroscopic level down to the nanoscale.

There are a couple of reasons that scar tissue looks different than regular skin – it lacks hair follicles, and it has no fat cells. Recently, though, scientists from the University of Pennsylvania and the University of California, Irvine succeeded in addressing both factors. They’re now able to get wounds to heal with regenerated skin, instead of with scar tissue.

Myofibroblasts are the most common type of cell found in healing wounds, and they’re associated with scar formation. Led by U Penn’s Dr. George Cotsarelis, the research team was able to get those cells to transform into ones known as adipocytes – these are the fat cells that are present in normal skin, but absent in scars.

Scientists in the Cotsarelis Lab already knew which growth factors were necessary for hair follicles to form in the skin. This knowledge previously allowed them to induce follicles to grow at wound sites on mice, although that would supposedly only be solving half of the problem.