Lifeboat Foundation

But U.S. is not the only country engaged in human enhancement and transhumanism, as Russia and China are also in hot pursuit with exoskeletons, vaccines and brain implants. As this competition gains traction, one wonders what the future of their militaries may look like as human beings are steadily integrated with machines to become armies of iron man.

From the blog of Christina Lin at The Times of Israel.

The evolving understanding of cancer genetics is allowing for clinicians to look at how to move rare cancer treatments, and identifications, forward.

A striking new study has found young cancer survivors show high expression of a gene known to be an effective marker of aging. The researchers suggest this genetic biomarker could be used to identify cancer survivors most at risk of later-life frailty due to their treatment.

As we age, concentrations of a gene called p16INK4a gradually increase in our cells, making it a potentially useful molecular marker for aging. One of the gene’s roles is to slow cell division and reduce the proliferation of stem cells.

In a new study researchers set out to investigate p16INK4a levels in pediatric and young adult cancer survivors. The hypothesis was that increased p16INK4a levels could be an effective sign of frailty among young cancer survivors.

This is an excerpt of a conversation between Dr. Daniel Stickler and Brian Rose.
Dr. Stickler is the Medical Director for the Neurohacker Collective, a consultant for Google on epigenetics and AI in healthcare, and a lecturer at Stanford University.
Brian Rose is the founder of London Real, a curator of people worth watching. Its mission is to promote personal transformation through inspiration, self-discovery and empowerment.
CUENTA CON SUBTÍTULOS EN ESPAÑOL
To watch the entire conversation clic here: https://youtu.be/ynbaJ2038K0

Using nothing but light and bioink, scientists were able to directly print a human ear-like structure under the skin of mice. The team used a healthy ear as a template and 3D printed a mirror image of that ear—tissue layer by tissue layer—directly onto the back of a mouse.

All without a single surgical cut.

If you’re thinking that’s super creepy, yeah…I’m with you. As a proof-of-concept, however, the team shows that it’s possible to build or rebuild tissue layers, even those as intricate as an ear, without requiring surgical implant. This means that it could one day be possible to fix an ear or other surface tissue defects—either genetic or from injuries—directly at the injury site by basically waving a sophisticated light wand.

Could speed up healing.

Wound healing in mammalian skin often results in fibrotic scars, and the mechanisms by which original nonfibrotic tissue architecture can be restored are not well understood. Here, Wei et al. have shown that pharmacological activation of the nociceptor TRPA1, which is found on cutaneous sensory neurons, can limit scar formation and promote tissue regeneration. They confirmed the efficacy of TRPA1 activation in three different skin wounding mouse models, and they also observed that localized activation could generate a response at distal wound sites. TRPA1 activation induced IL-23 production by dermal dendritic cells, which activated IL-17–producing γδ T cells and promoted tissue regeneration. These findings provide insight into neuroimmune signaling pathways in the skin that are critical to mammalian tissue regeneration.

Adult mammalian wounds, with rare exception, heal with fibrotic scars that severely disrupt tissue architecture and function. Regenerative medicine seeks methods to avoid scar formation and restore the original tissue structures. We show in three adult mouse models that pharmacologic activation of the nociceptor TRPA1 on cutaneous sensory neurons reduces scar formation and can also promote tissue regeneration. Local activation of TRPA1 induces tissue regeneration on distant untreated areas of injury, demonstrating a systemic effect. Activated TRPA1 stimulates local production of interleukin-23 (IL-23) by dermal dendritic cells, leading to activation of circulating dermal IL-17–producing γδ T cells. Genetic ablation of TRPA1, IL-23, dermal dendritic cells, or γδ T cells prevents TRPA1-mediated tissue regeneration.

A plan to release over 750 million genetically modified mosquitoes into the Florida Keys in 2021 and 2022 received final approval from local authorities, against the objection of many local residents and a coalition of environmental advocacy groups. The proposal had already won state and federal approval.

“With all the urgent crises facing our nation and the State of Florida — the Covid-19 pandemic, racial injustice, climate change — the administration has used tax dollars and government resources for a Jurassic Park experiment,” said Jaydee Hanson, policy director for the International Center for Technology Assessment and Center for Food Safety, in a statement released Wednesday.

“Now the Monroe County Mosquito Control District has given the final permission needed. What could possibly go wrong? We don’t know, because EPA unlawfully refused to seriously analyze environmental risks, now without further review of the risks, the experiment can proceed,” she added.

Glycerol, used in the past as antifreeze for cars, is produced by a range of organisms from yeasts to vertebrates, some of which use it as an osmoprotectant—a molecule that prevents dangerous water loss in salty environments—while others use it as an antifreeze. Here, scientists from the University of Nevada and Miami University in Ohio show that two species of the single-celled green algae Chlamydomonas from Antarctica, called UWO241 and ICE-MDV, produce high levels of glycerol to protect them from osmotic water loss, and possibly also from freezing injury. Presently, only one other organism, an Arctic fish, is known to use glycerol for both purposes. Both species synthesize glycerol with enzymes encoded by multiple copies of a recently discovered ancient gene family. These results, published today in the open-access journal Frontiers in Plant Science, illustrate the importance of adaptations that allow life to not only survive but to thrive in extreme habitats.

The researchers collected both Chlamydomonas species from depths of 13 to 17 m, a region with a steep salinity gradient, in Lake Bonney, a permanently ice-covered lake in the McMurdo Dry Valleys of Victoria Land, Antarctica. Previously, they showed that both species are remarkably adapted to their extreme habitat, with a photosynthetic apparatus adapted to cold, saline, and light-poor conditions, novel proteins, more fluid cell membranes that function at low temperatures, and ice-binding proteins that protect against freeze-thaw injury.

“Our overall goal is to understand how microorganisms survive in extreme environments. The Chlamydomonas species of Lake Bonney are well-suited for such studies because they are exposed to many extremes, including low light, low temperature, oxidative stress, and high salinity. The present results are the first to show that glycerol production by microorganisms, which is well-known in warm, salty environments, is also important in polar regions,” says corresponding author Dr. James Raymond, Adjunct Research Professor at the School of Life Sciences, University of Nevada, Las Vegas, USA.

In this Review, Suhre, McCarthy and Schwenk describe how combining genetics with plasma proteomics is providing notable insights into human disease. As changes in the circulating proteome are often an intermediate molecular readout between a genetic variant and its organismal effect, proteomics can enable a deeper understanding of disease mechanisms, clinical biomarkers and therapeutic opportunities.