Lifeboat Foundation

In Brief

• Peter Diamandis, founder and chairman of the XPRIZE Foundation, thinks the human species is headed for an evolutionary transformation.
• The evolution of life has slowly unfolded over 3.5 billion years; but its pace has rapidly increased in recent years. Diamandis believes this heralds the next, exciting stages of human evolution.

In the next 30 years, humanity is in for a transformation the likes of which we’ve never seen before—and XPRIZE Foundation founder and chairman Peter Diamandis believes that this will give birth to a new species. Diamandis admits that this might sound too far out there for most people. He is convinced, however, that we are evolving towards what he calls “meta-intelligence,” and today’s exponential rate of growth is one clear indication.

In an essay for Singularity Hub, Diamandis outlines the transformative stages in the multi-billion year pageant of evolution, and takes note of what the recent increasing “temperature” of evolution—a consequence of human activity—may mean for the future. The story, in a nutshell, is this—early prokaryotic life appears about 3.5 billion years ago (bya), representing perhaps a symbiosis of separate metabolic and replicative mechanisms of “life;” at 2.5 bya, eukaryotes emerge as composite organisms incorporating biological “technology” (other living things) within themselves; at 1.5 bya, multicellular metazoans appear as eukaryotes are yoked together in cooperative colonies; and at 400 million years ago, vertebrate fish species emerge onto land to begin life’s adventure beyond the seas.

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A .gif image. Evolution Chart Bacteria to humans in only 3.5 Billion years.

Happy Holidays; happy end of the year, happy launch of next year, happy snow days, happy hot chocolate day, etc. Nonetheless, my gift to you this year is a Nanoscale Snowman.

Would a jewel-encrusted snowman make the perfect Christmas present? At only 5 nanometres in size, the price might be lower than you think. And it’s functional too, catalysing the splitting of water to make green hydrogen for fuel cells.

The nanoparticle, as imaged with the aberration-corrected scanning transmission electron microscopes, features eyes, nose and mouth of precious-metal platinum clusters embedded in a titanium dioxide face. Each platinum cluster typically contains 30 platinum atoms; within the whole nanoparticle there are approximately 1680 titanium atoms and 180 platinum atoms.

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Herbs treating Tuberculosis.

A centuries-old herbal medicine, discovered by Chinese scientists and used to effectively treat malaria, may help treat tuberculosis and slow the evolution of drug resistance.

A new study shows the ancient remedy artemisinin stopped the ability of TB-causing bacteria, known as Mycobacterium tuberculosis, to become dormant. This stage of the disease often makes the use of antibiotics ineffective.

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Machines lace almost all social, political cultural and economic issues currently being discussed. Why, you ask? Clearly, because we live in a world that has all its modern economies and demographic trends pivoting around machines and factories at all scales.

We have reached the stage in the evolution of our civilization where we cannot fathom a day without the presence of machines or automated processes. Machines are not only used in sectors of manufacturing or agriculture but also in basic applications like healthcare, electronics and other areas of research. Although, machines of varying types had entered the industrial landscape long ago, technologies like nanotechnology, the Internet of Things, Big Data have altered the scenario in an unprecedented manner.

The fusion of nanotechnology with conventional mechanical concepts gives rise to the perception of ‘molecular machines’. Foreseen to be a stepping stone into nano-sized industrial revolution, these microscopic machines are molecules designed with movable parts that behave in a way that our regular machines operate in. A nano-scale motor that spins in a given direction in presence of directed heat and light would be an example of a molecular machine.

In Brief:

Researchers at MIT have developed an easy-to-use “biological programming language” that allows genetic engineers (or just about anyone) to design biological circuits and “hack” the genomes of living cells.

The evolution of human technology has proceeded in lockstep with the biological evolution of our species. For millions of years we were content with our primitive Oldowan choppers and Acheulean bifaces; in the Neolithic, we started playing with more sophisticated tools, and the Bronze and Iron ages followed in quick succession.

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The death throes of nearby stars might have influenced evolution on Earth.

2013 saw the release of one of the most important papers in aging research and one that saw renewed interest and support for the concept of SENS.

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects.

More news on senolytics.

Efforts to build rejuvenation therapies that work by selectively destroying senescent cells are very much in the news of late. One class of senolytic drug candidates works by inducing apoptosis, a form of programmed cell death, via reduced levels of Bcl-2 family proteins, such as Bcl-2 itself, Bcl-xL, and Bcl-W, all of which normally act to suppress apoptosis. Senescent cells are inclined towards apoptosis already, so a modest nudge in that direction can destroy a fair proportion of these unwanted cells without causing harm to healthy cells. These apoptosis-related proteins have numerous other roles as well, however, since evolution is very much in favor of reusing the tools to hand. For example, Bcl-xL is also involved in mitochondrial damage protection, the immune response, cellular respiration and DNA repair: quite the portfolio, and all items that are connected to aging in one way or another. I noted an open access paper today that muddies the water considerably on the topic of Bcl-xL, as it shows that more Bcl-xL rather than less (a) reduces incidence of cellular senescence in tissue cultures, (b) extends life in nematode worms, and © is found in human centenarians, but not younger individuals.

Ordinary somatic cells, the vast majority of the cells in the body, become senescent when they reach the Hayflick limit at the end of their replicative life span, or in response to damage, or a toxic local environment, or as a part of the wound healing process. Senescent cells cease dividing, and most either self-destruct or are destroyed by the immune system soon afterwards. This behavior has evolved because it suppresses cancer incidence, at least initially, by removing those cells most at risk. Unfortunately not all are destroyed, and those that linger cause harm to surrounding tissues via a potent mix of inflammatory signals known as the senescence-associated secretory phenotype (SASP). Given enough senescence cells, as few as 1% or less of all the cells in an organ, significant dysfunction and inflammation is the result, contributing to the development and progression of age-related disease.

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