A new review explores how episodic memories are formed, stored, and reshaped over time, revealing why our recollections of past events often change.
As prominent artificial intelligence (AI) researchers eye limits to the current phase of the technology, a different approach is gaining attention: using living human brain cells as computational hardware.
These “biocomputers” are still in their early days. They can play simple games such as Pong, and perform basic speech recognition.
But the excitement is fuelled by three converging trends.
Follow Closer To Truth on Instagram for daily videos, updates, and announcements: https://www.instagram.com/closertotruth/
AI consciousness, its possibility or probability, has burst into public debate, eliciting all kinds of issues from AI ethics and rights to AI going rogue and harming humanity. We explore diverse views; we argue that AI consciousness depends on theories of consciousness.
Make a tax-deductible donation of any amount to help support Closer To Truth continue making content like this: https://shorturl.at/OnyRq.
Philip Goff is a British author, panpsychist philosopher, and professor at Durham University whose research focuses on philosophy of mind and consciousness. Specifically, it focuses on how consciousness can be part of the scientific worldview.
Closer To Truth, hosted by Robert Lawrence Kuhn and directed by Peter Getzels, presents the world’s greatest thinkers exploring humanity’s deepest questions. Discover fundamental issues of existence. Engage new and diverse ways of thinking. Appreciate intense debates. Share your own opinions. Seek your own answers.
Non-conjugative plasmids limit their mobility to persist in nature.
Sabnis et al. explain why non-conjugative plasmids move at a low rate in nature. While increased mobility can easily evolve by incorporating phage DNA into plasmids, this is disadvantageous because it reduces diversity in populations. This ultimately leaves bacterial populations more vulnerable to being killed, for example by antibiotics.
In line with the original observation by Selye of an involution of the thymus and other lymphoid organs in response to stress (205) and the subsequent demonstration of the immunosuppressive effects of glucocorticoids (101), glucocorticoids have traditionally been seen as the hormonal mediators of the immunosuppressive effects of stressors. We will not delve into the details of the vast literature on the effects of stress on immunity, as this topic has been reviewed on several occasions and it is not directly relevant to the present review (3, 9, 160, 169, 204, 220).
Glucocorticoids act on their cellular targets by binding to glucocorticoid receptors (GRs). GRs normally reside in the cytosol in the form of a protein complex that brings together heat-shock proteins and FK506 binding protein 52. Upon binding to their ligand, GRs dissociate from this complex to form monomers or dimers and translocate to the nucleus The anti-inflammatory effects of glucocorticoids are mediated by transcriptional repression following nuclear translocation and tethering of monomeric GRs to the glucocorticoid-response elements of transcription factors such as NF-κB, activator protein (AP)-1, and IFN-regulating factor-3 (234). This results in the downregulation of genes coding for inflammatory mediators, enzymes, and adhesion molecules. Although the hypothesis is still controversial, GR dimerization and transactivation are thought to play an important role in the anti-inflammatory activity of glucocorticoids. This phenomenon is illustrated by data obtained in GR(dim/dim) mutant mice that show reduced GR dimerization and increased sensitivity to TNF-induced inflammation, and to experimental models of sepsis induced by LPS or cecal ligation and puncture (123, 235).
Glucocorticoids can be proinflammatory under certain conditions. This effect can be secondary to the selection of corticoid-resistant inflammatory cells, such as pathogenic Th17 cells that overexpress IL-23 receptor and multidrug-resistance protein and that are found in inflamed gut tissue from patients with Crohn’s disease (186). The proinflammatory effect of glucocorticoids may also result from inhibition of the production and release of anti-inflammatory factors, or conversely from enhanced production and release of proinflammatory mediators. In the first case, dexamethasone administered 24 h before LPS was found to enhance the placenta’s proinflammatory cytokine response to LPS as a consequence of the inhibition of lipoxin A4 synthesis (255). In the second case, it is the dose of glucocorticoids that makes the difference: as mentioned above, physiological glucocorticoid levels can be proinflammatory in some circumstances, whereas high or pharmacological levels are anti-inflammatory. For instance, low doses of glucocorticoids increase the production of macrophage migration inhibitory factor, and this effect is sufficient to override glucocorticoid-mediated inhibition of cytokine production and release by LPS-stimulated monocytes (39).
Students use AI to write papers, professors use AI to grade them, degrees become meaningless, and tech companies make fortunes. Welcome to the death of higher education.
An international collaboration led by Cornell researchers used a combination of psilocybin and the rabies virus to map how—and where—the psychedelic compound rewires the connections in the brain.
Specifically, they showed psilocybin weakens the cortico-cortical feedback loops that can lock people into negative thinking. Psilocybin also strengthens pathways to subcortical regions that turn sensory perceptions into action, essentially enhancing sensory-motor responses.
The findings were published Dec. 5 in Cell. The lead author is postdoctoral researcher Quan Jiang.