Lifeboat Foundation

Men and women differ in obvious and less obvious ways—for example, in the prevalence of certain diseases or reactions to drugs. How are these connected to one’s sex? Weizmann Institute of Science researchers recently uncovered thousands of human genes that are expressed—copied out to make proteins—differently in the two sexes. Their findings showed that harmful mutations in these particular genes tend to accumulate in the population in relatively high frequencies, and the study explains why. The detailed map of these genes, reported in BMC Biology, provides evidence that males and females undergo a sort of separate, but interconnected evolution.

Several years ago, Prof. Shmuel Pietrokovski and Dr. Moran Gershoni of the Weizmann Institute’s Molecular Genetics Department asked why the prevalence of certain human diseases is common. Specifically, about 15% of couples trying to conceive are defined as infertile, which suggested that mutations that impair fertility are relatively widespread. This seems paradoxical: Common sense says that these mutations, which directly affect the survival of the species by reducing the number of offspring, should have been quickly weeded out by natural selection. Pietrokovski and Gershoni showed that mutations in genes specific to sperm formation persist precisely because the genes are expressed only in men. A mutation that is problematic for only half the population, no matter how detrimental, is freely passed on to the next generation by the other half.

In the present study, the researchers expanded their analyses to include genes that, though not necessary for fertility, are still expressed differently in the two sexes. To identify these genes, the scientists turned to the GTEx project—a very large study of human gene expression recorded for numerous organs and tissues in the bodies of close to 550 adult donors. That project enabled, for the first time, the comprehensive mapping of the human sex-differential genetic architecture.

Continue reading “Researchers identify 6,500 genes that are expressed differently in men and women” »

An event on #transhumanism at a Christian university in Southern California in June. Looks interesting:

Humanism is “our most sympathetic understanding and treatment of human nature.”

TRANShumanism is “the drive to fundamentally revolutionise what it means to be human by way of technological advancements.”

Continue reading “Crosswise Summer Experience” »

Octopuses are so clever that they can ignore their genetic programming, in turn slowing down their DNA evolution.

This is a fair enough article, though I believe I’m more Libertarian than it paints me. I think a lot of people forget or simply don’t know my book The Transhumanist Wager (how I started my futurist career back in 2009) is known by many as transhumanist libertarian manifesto. Also, ideas from my past political campaign do not always correspond to my current gubernatorial run:

Like many libertarians, I was initially excited when Zoltan Istvan announced his candidacy for Governor of California.

Istvan is the founder of the Transhumanist Party and author of “The Transhumanist Wager,” which is considered a manifesto on transhumanist philosophy. The basic premise of transhumanism is that the next step in human evolution will be to improve our bodies and expand our lifespan with radical technology, eventually leading towards immortality. While he still needs to obtain the nomination, having someone announce their intents this early gave me hope that maybe the party would have a shot at making an impact in the California mid-terms.

Continue reading “Is Zoltan Istvan a Libertarian?” »

The series, which is scheduled to launch in 2070, will provide the people of Earth and beyond a glimpse into the extreme applications that science brought us over the past 7 decades.

We’ve discovered that evolution strategies (ES), an optimization technique that’s been known for decades, rivals the performance of standard reinforcement learning (RL) techniques on modern RL benchmarks (e.g. Atari/MuJoCo), while overcoming many of RL’s inconveniences.

In particular, ES is simpler to implement (there is no need for backpropagation), it is easier to scale in a distributed setting, it does not suffer in settings with sparse rewards, and has fewer hyperparameters. This outcome is surprising because ES resembles simple hill-climbing in a high-dimensional space based only on finite differences along a few random directions at each step.

Really good article by Dr. Kristin Kostick at Bayor College of Medicine. I’m excited to see #transhumanism spreading!

Dr. Kristin Kostick discusses LVADs, transhumanism, and how the integration of our bodies with technology can lead to longer, healthier lives.

Humans on Earth might not be allowed to meet Martians.

Interesting read especially as we look at various areas including synbio and super humans.

The results are significant for gene therapy procedures and for our understanding of cell transformation. A team of researchers from the biology department at TU Darmstadt has discovered that the processes for repairing DNA damage are far more complex than previously assumed. The ends of breaks in the double helix are not just joined, they are first changed in a meticulously choreographed process so that the original genetic information can be restored. The results have now been published in the research journal Molecular Cell.

DNA, the carrier of our genetic information, is exposed to continual damage. In the most serious damage of all, the DNA double-strand break, both strands of the double helix are broken and the helix is divided in two. If breaks like this are not efficiently repaired by the cell, important genetic information is lost. This is often accompanied by the death of the cell, or leads to permanent genetic changes and cell transformation. Over the course of evolution, ways to repair this DNA damage have developed, in which many enzymes work together to restore the genetic information with the maximum possible precision.

As it stands today, there are two main ways of repairing DNA double-strand breaks, which differ greatly in terms of their precision and complexity. The apparently simpler method, so-called non-homologous end joining, joins together the break ends as quickly as possible, without placing particular importance on accurately restoring the damaged genetic information. The second method of repair, homologous recombination, on the other hand, uses the exactly identical information present on a sister copy to repair the damaged DNA with great precision. However, such sister copies are only present in dividing cells, as the genetic information has to be duplicated before the cells divide. But most cells in the human body do not undergo division, which therefore assigns them to the apparently more inaccurate method of end joining.