Think transhumanism is a relatively new social and intellectual phenomenon? Guess again.
Many of the ideas characteristic of the movement have already been bantered about for literally hundreds of years—whether it be such things as radical life extension or the construction of machine minds. The Enlightenment period in particular was a fruitful time for these ideas to take flight, mostly on account of the new sciences, the rise of rationalism and secular humanism, and the waning influence of religion. Two thinkers that best exemplified Enlightenment-era proto-transhumanism were Denis Diderot and Marquis de Condorcet, and their early contributions are worth revisiting.
The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions.
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What determines how long people live, and how much of their lifespan is influenced by genetics?
For many years, scientists believed the genetic contribution to human lifespan was relatively modest compared with other biological traits. Earlier estimates placed the heritability of lifespan at around 20 to 25 percent, and some more recent large studies suggested it might be even lower, in some cases below 10 percent.
A new study from the Weizmann Institute of Science now challenges that view. The research, published in the journal Science, reports that genetic differences may account for roughly half of the variation in human lifespan. This estimate is more than double many previous calculations. The work was led by Ben Shenhar in the laboratory of Prof. Uri Alon of the Weizmann Institute’s Molecular Cell Biology Department.
Now online! A multi-omic single-cell atlas of the aging mouse brain reveals cell-type-specific transposon methylation changes, strengthening of 3D genome boundaries, and regionally heterogeneous aging signatures. These findings offer a resource to understand the molecular mechanisms of brain aging and guide future research on neurodegeneration.
From O’Neill cylinders to spiral habitats, discover how humanity might build colossal, interconnected cities high above Earth.
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/ discord Credits: Orbital Arcologies — Mega Cities in Space Written, Produced & Narrated by: Isaac Arthur Graphics: Bryan Versteeg, Jeremy Jozwik, Katie Byrne, Udo Schroeter Select imagery/video supplied by Getty Images Music Courtesy of Epidemic Sound http://epidemicsound.com/creator Chapters 0:00 Intro — The Conductor’s Tale 4:43 Why Megacities in Space? 6:02 The Four Foundational Assumptions of Space Habitat Design 10:11 Flawed Assumptions & Specialized Habitats 11:28 The Urban Web – Tethered Transit and Megacity Growth 17:14 Nebula 18:24 Spiral Habitats – A Rolled-Up City in Space 20:19 Density and Design – Population Scaling 23:17 Green Limits – CO₂, Heat, and Living Space 26:08 The Future of Orbital Urbanization – Terran Swarms and Beyond.
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Credits:
Orbital Arcologies — Mega Cities in Space.
Written, Produced & Narrated by: Isaac Arthur.
Graphics: Bryan Versteeg, Jeremy Jozwik, Katie Byrne, Udo Schroeter.
Select imagery/video supplied by Getty Images.
Music Courtesy of Epidemic Sound http://epidemicsound.com/creator.
Chapters.
0:00 Intro — The Conductor’s Tale.
4:43 Why Megacities in Space?
6:02 The Four Foundational Assumptions of Space Habitat Design.
10:11 Flawed Assumptions & Specialized Habitats.
11:28 The Urban Web – Tethered Transit and Megacity Growth.
17:14 Nebula.
18:24 Spiral Habitats – A Rolled-Up City in Space.
20:19 Density and Design – Population Scaling.
23:17 Green Limits – CO₂, Heat, and Living Space.
26:08 The Future of Orbital Urbanization – Terran Swarms and Beyond.
The sight of a delectable plate of lasagna or the aroma of a holiday ham are sure to get hungry bellies rumbling in anticipation of a feast to come. But although we’ve all experienced the sensation of “eating” with our eyes and noses before food meets mouth, much less is known about the information superhighway, known as the vagus nerve, that sends signals in the opposite direction — from your gut straight to your brain.
These signals relay more than just what you’ve eaten and when you are full. A new study in mice from researchers at Stanford Medicine and the Palo Alto, California-based Arc Institute has identified a critical link between the bacteria that live in your gut and the cognitive decline that often occurs with aging.
“Although memory loss is common with age, it affects people differently and at different ages,” said Christoph Thaiss, PhD, assistant professor of pathology. “We wanted to understand why some very old people remain cognitively sharp while other people see significant declines beginning in their 50s or 60s. What we learned is that the timeline of memory decline is not hardwired; it’s actively modulated in the body, and the gastrointestinal tract is a critical regulator of this process.”
Aging causes changes in gut bacteria in mice, which hampers communication between the intestines and the brain. Restoring this connection helped old mice form memories as well as young animals.
Audra M. Rogers, Martin J. Egan et al. @UArkansas demonstrate that heat stress triggers nucleolar remodeling in filamentous fungi, enabling segregation of damaged material and selective inheritance of a new nucleolar compartment. This reveals a chaperone-mediated quality control mechanism that preserves nuclear function in highly polarized, multinucleate cells.
Model for nucleolar remodeling, partitioning, and quality control following heat shock. Schematic illustration of nucleolar remodeling in M. oryzae during recovery from heat stress. Heat shock damages the existing nucleolus. (2–3) A new nucleolar bud emerges from the old (preexisting) nucleolus and expands through de novo synthesis. Partial nuclear envelope breakdown permits entry of the molecular chaperones such as Hsp104 and Hsp70. The old nucleolar compartment accumulates SUMO-modified material and selectively recruits Hsp70 and Hsp104, mediating the partitioning of old and new nucleolar material. The newly formed nucleolus disassembles at mitotic onset and is preferentially inherited by daughter nuclei, while the old nucleolus is extruded and diminishes.
Figure 5.
