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In this video, we explore 20 emerging technologies changing our future, including super-intelligent AI companions, radical life extension through biotechnology and gene editing, and programmable matter. We also cover advancements in flying cars, the quantum internet, autonomous AI agents, and other groundbreaking innovations transforming the future.

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00:07 Super Intelligent AI Companions.
04:27 Radical Life Extension.
08:40 Programmable Matter.
11:33 Flying Cars.
16:29 Quantum Internet.
20:34 Autonomous AI Agents.
25:21 Hypersonic Aircraft And Missiles.
29:19 Invisibility Suits.
33:45 Human Brain Simulations.
37:02 Synthetic Biology.
40:54 AI-Enabled Warfare.
44:58 Solar Sail Technology.
49:42 Bionic Eyes.
53:20 Swarm Robotics.
56:40 Room-Temperature Superconductors.
01:01:42 Optical Computing.
01:05:59 Graphene Technology.
01:11:01 Artificial Trees.
01:15:07 Web 3.0
01:18:03 Vertical Farming.

💡 Future Business Tech explores AI, emerging technologies, and future technologies.

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In early 2023, following an international conference that included dialogue with China, the United States released a “Political Declaration on Responsible Military Use of Artificial Intelligence and Autonomy,” urging states to adopt sensible policies that include ensuring ultimate human control over nuclear weapons. Yet the notion of “human control” itself is hazier than it might seem. If humans authorized a future AI system to “stop an incoming nuclear attack,” how much discretion should it have over how to do so? The challenge is that an AI general enough to successfully thwart such an attack could also be used for offensive purposes.

We need to recognize the fact that AI technologies are inherently dual-use. This is true even of systems already deployed. For instance, the very same drone that delivers medication to a hospital that is inaccessible by road during a rainy season could later carry an explosive to that same hospital. Keep in mind that military operations have for more than a decade been using drones so precise that they can send a missile through a particular window that is literally on the other side of the earth from its operators.

We also have to think through whether we would really want our side to observe a lethal autonomous weapons (LAW) ban if hostile military forces are not doing so. What if an enemy nation sent an AI-controlled contingent of advanced war machines to threaten your security? Wouldn’t you want your side to have an even more intelligent capability to defeat them and keep you safe? This is the primary reason that the “Campaign to Stop Killer Robots” has failed to gain major traction. As of 2024, all major military powers have declined to endorse the campaign, with the notable exception of China, which did so in 2018 but later clarified that it supported a ban on only use, not development—although even this is likely more for strategic and political reasons than moral ones, as autonomous weapons used by the United States and its allies could disadvantage Beijing militarily.

A research team led by Osaka University discovered that the new organic molecule thienyl diketone shows high-efficiency phosphorescence. It achieved phosphorescence that is more than ten times faster than traditional materials, allowing the team to elucidate this mechanism.

The paper is published in the journal Chemical Science.

Phosphorescence is a valuable optical function used in applications such as organic EL displays (OLEDs) and cancer diagnostics. Until now, achieving high-efficiency phosphorescence without using rare metals such as iridium and platinum has been a significant challenge. Phosphorescence, which occurs when a molecule transitions from a high-energy state to a low-energy state, often competes with non-radiative processes where the molecule loses energy as heat.

In 2006, just a few years after the fruit fly genome had been sequenced, geneticists at the University of California, Davis, made a startling discovery: Several new genes had cropped up, seemingly out of nowhere.

These “de novo genes” weren’t simply new variants of existing ones; they had sprung forth from the supposedly inert spaces in between the coding sections of DNA—regions long dismissed as the junkyards of the double helix. Since the days of Darwin, such sprightly biological change agents had never before been seen.

A young graduate student at the time, Li Zhao was so intrigued that upon graduating in 2011, she set out to join the lab of David Begun, where the discovery was first made. She soon revealed that these little genetic big bangs happen all the time­­—over the past decade, she and her team have identified more than 500 de novo genes in the Drosophila lineage alone.

Over the recent decades, comprehensive genome-wide association studies (GWAS) have indicated the potential influence of genetic factors on one’s alcohol consumption volume and identified over 100 related variants6,7. However, a predominant proportion of the identified variants are localized within noncoding regions, and their effect sizes tend to be small, making interpretation and identification of the causal gene challenging8. In addition, previous GWAS mainly utilized imputed genotype data, which only cover limited regions of the genome, and thus may have missed many potential genes. Furthermore, GWAS studies focused mainly on common variants, and few studies have investigated rare variants associated with alcohol consumption, which yield greater potential to interpret biological function and elucidate mechanisms9. Although there are studies that have attempted to leverage exome chip data to identify rare variants contributing to alcohol consumption, the sample size was small and limited regions of the whole exome were examined10.

The introduction of whole exome sequencing (WES) provides a great chance to overcome the limitations of previous genetic studies on alcohol consumption with a substantially larger amount of rare and ultra-rare protein-coding variants11,12,13. Collapsing of loss-of-function (LOF) variants helps estimate the effect direction of associated genes13,14. When combined with large-scale population cohorts with multi-modal phenotypic data, WES would greatly facilitate our understanding of the genetic underpinnings of alcohol consumption as well as its implication on physical and mental health6. However, to our knowledge, there have been few large-scale WES studies on alcohol consumption, let alone elucidating the potential implications of the identified genes10,15. Meanwhile, as indicated by a previous genome-wide association study, significant genetic associations existed between alcohol consumption and several body health phenotypes7. The application of phenome-wide analysis for alcohol-related genes can help extend and deepen our current comprehension of the association between alcohol consumption and human health.

Hence, aiming to refine the genetic architecture of alcohol consumption, we conduct an exome-wide association study (ExWAS) for alcohol consumption among 304,119 individuals from the UK Biobank (UKB). We also examine the rare-variant associations with genes reported by previous GWAS6,7,16,17. Finally, we provide biological insights into the identified genes via bioinformatics analyses and phenome-wide association analysis (PheWAS).

Genome editing stands as one of the most transformative scientific breakthroughs of our time. It allows us to dive into the very code of life and make precise modifications. Imagine being able to rewrite the genetic instructions that determine almost everything about an organism—how it looks, behaves, interacts with its environment, and its unique characteristics. This is the power of genome editing.

We use genome editing tools to tweak the genetic sequences of microbes, animals, and plants. Our goal? To develop desired traits and eliminate unwanted ones. This technology’s impact has been felt across biotechnology, human therapeutics, and agriculture, bringing rapid advancements and solutions.

The most widely used proteins in genome editing are Cas9 and Cas12a. These proteins are like the scissors of the genetic world, allowing us to cut and edit DNA. However, they are quite bulky, consisting of 1,000–1,350 amino acids. Advanced editing technologies like base editing and prime editing require the fusion of additional proteins with Cas9 and Cas12a, making them even bulkier. This bulkiness poses a challenge to delivering these proteins efficiently into cells, where the resides.

Scientists at Weill Cornell Medicine discovered a previously unknown link between two key pathways that regulate the immune system in mammals — a finding that impacts our understanding of chronic inflammatory bowel diseases (IBD). This family of disorders severely impacts the health and quality of life of more than 2 million people in the United States.

The immune system has many pathways to protect the body from infection, but sometimes an overactive immune response results in autoimmune diseases including IBD, psoriasis, rheumatoid arthritis and multiple sclerosis. Interleukin-23 (IL-23) is one such immune factor that fights infections but is also implicated in many of these inflammatory diseases. However, it was unknown why IL-23 is sometimes beneficial, and other times becomes a driver of chronic disease.

In the study, published June 12 in Nature, the team found that IL-23 acts on group 3 innate lymphoid cells (ILC3s), a family of immune cells that are a first line of defense in mucosal tissues such as the intestines and lungs. In response, ILC3s increase activity of CTLA-4, a key regulatory factor that prevents the immune system from attacking the body and beneficial gut microbiota. This interaction critically balances the pro-inflammatory effects IL-23 to maintain gut health, but is impaired in IBD.

Is Medical Director of the Adult Extracorporeal Membrane Oxygenation (ECMO) Program at Methodist Hospital, San Antonio, Texas. He is also the Medical Director of the Cardiovascular Intensive Care Unit at Methodist Healthcare System and the Texas IPS Critical Care Service Line (https://texasips.com/jeffrey-dellavol…). He also serves as chair of the Joint Society of Critical Care Medicine/Extracorporeal Life Support Organization Task Force and has created a platform for ECMO training and ECMO transport (https://ecmotransports.com/about/).

ECMO is a form of extracorporeal life support, providing prolonged cardiac and respiratory support to persons whose heart and lungs are unable to provide an adequate amount of oxygen, gas exchange or blood supply (perfusion) to sustain life.

Dr. DellaVolpe served as a Flight Surgeon with the 27th Special Operations Wing where he deployed twice in support of Operation Enduring Freedom – Trans Sahara. After completing his fellowship, he was assigned to the San Antonio Military Medical Center where he served as a critical care physician and a member of the 59th Medical Wing Critical Care Air Transport Team and Acute Lung Rescue Team.

Dr. DellaVolpe is originally from Newport, RI. After receiving his bachelor’s degree at Dartmouth College, he went on to attend medical school at Tulane University School of Medicine. He then completed his residency in Internal Medicine at Tulane Medical Center and his fellowship in Critical Care Medicine at the University of Pittsburgh Medical Center.

Dr. DellaVolpe wrote The ECMO Book, published Elsevier Health Sciences, in 2023 (https://www.us.elsevierhealth.com/the…).

#JeffreyDellaVolpe #MedicalDirector #ExtracorporealMembraneOxygenation #ECMO #MethodistHospital #SanAntonio #Texas #Cardiovascular #IntensiveCare #CriticalCare #LifeSupport #ProgressPotentialAndPossibilities #IraPastor #Podcast #Podcaster #ViralPodcast #STEM #Innovation #Technology #Science #Research

Common treatments for Parkinson’s disease can address short-term symptoms, but can also cause extensive problems for patients in the long run. Namely, treatments can cause dyskinesia, a form of uncontrollable movements and postures.

In a recent study published in The Journal of Neuroscience, researchers at the University of Alabama at Birmingham took a different approach to and treated it like a “bad motor memory.” They found that blocking a protein called Activin A could halt dyskinesia symptoms and effectively erase the brain’s “bad memory” response to certain Parkinson’s treatments.

“Instead of looking for a completely alternative treatment, we wanted to see if there was a way to prevent dyskinesia from developing in the first place,” said David Figge, M.D., Ph.D., lead study author and assistant professor in the UAB Department of Pathology. “If dyskinesia does not occur, then patients could potentially stay on their Parkinson’s treatment for longer.”