Genius series: Nikola Tesla, the original tech superstar
Big Think has launched a line of apparel and goods that celebrate the life and work of four geniuses. First up, Nikola Tesla.
- Big Think has just launched its Genius Series of tees, sweatshirts, posters and more! Buy here.
- First up, we're paying tribute to the original tech superstar, Nikola Tesla.
- Select Rush or Super Rush Delivery to get your order before Christmas Day!
I do not think there is any thrill that can go through the human heart like that felt by the inventor as he sees some creation of the brain unfolding to success. ... Such emotions make a man forget food, sleep, friends, love, everything.
– Nikola Tesla
Nikola Tesla was a pioneer scientist during the turn of the 20th century, best known for developing the technology our modern alternating current (AC) electricity supply system is based on. He was a prolific inventor and the ultimate mad scientist, holding 300 patents, speaking eight languages, and he was said to have a near-eidetic memory. Despite his era-shifting contributions to humanity and his bold visions for the future (he predicted the smartphone -- in 1926!), he died broke and alone in the New Yorker Hotel in 1943.
In the 1990s, Tesla was rescued from decades of obscurity by a wave of popular interest. Today, he is known as "the man who invented the 20th century," and his legacy has experienced a major resurgence—the name Tesla, as you might have heard, is way in vogue right now.
Check out the Nikola Tesla range of apparel and goods in Big Think's Genius Series.
Select Rush or Super Rush Delivery to get your order before Christmas Day!
This could change how researchers approach vaccine development.
- The reason children suffer less from the novel coronavirus has remained mysterious.
- Researchers identified a cytokine, IL-17A, which appears to protect children from the ravages of COVID-19.
- This cytokine response could change how researchers approach vaccine development.
A member of staff wearing personal protective equipment (PPE) takes a child's temperature at the Harris Academy's Shortland's school on June 04, 2020 in London, England.
Photo by Dan Kitwood/Getty Images<p>Experts don't want to place kids at the back of the line, regardless of how strong their immune systems appear. Complications are. At least one company recognizes this: Moderna <a href="https://www.businessinsider.com/coronavirus-vaccine-for-kids-moderna-plans-pediatric-trial-2020-9" target="_blank">hopes to begin testing</a> vaccines in pediatric volunteers by year's end.</p><p>Innate immune response is especially high during childhood (compared to adaptive immunity). This makes evolutionary sense: nature wants an animal to survive until they're ready to procreate. Turns out the children in the study possessed high levels of cytokines that boost their immune response. The biggest impact is made by IL-17A, which appears to protect the youngest cohort from the ravages of the coronavirus. </p><p>While both age groups produced antibodies to fight off the infamous spike protein, adults that produce neutralizing antibodies actually suffer a <em>worse</em> fate. Herold says this "over-vigorous adaptive immune response" might promote inflammation, triggering acute respiratory distress syndrome. </p><p>This matters for vaccine development. As Herold says, </p><p style="margin-left: 20px;">"Our adult COVID-19 patients who fared poorly had high levels of neutralizing antibodies, suggesting that convalescent plasma—which is rich in neutralizing antibodies—may not help adults who have already developed signs of ARDS. By contrast, therapies that boost innate immune responses early in the course of the disease may be especially beneficial."</p><p>Herold says current vaccine trials are focused on boosting neutralizing-antibody levels. With this new information, researchers may want to work on vaccines that boost the innate immune response instead. </p><p>With <a href="https://www.nytimes.com/interactive/2020/science/coronavirus-vaccine-tracker.html" target="_blank">at least 55 vaccine trials</a> underway, every piece of data matters. </p><p>--</p><p><em>Stay in touch with Derek on <a href="http://www.twitter.com/derekberes" target="_blank">Twitter</a>, <a href="https://www.facebook.com/DerekBeresdotcom" target="_blank">Facebook</a> and <a href="https://derekberes.substack.com/" target="_blank" rel="noopener noreferrer">Substack</a>. His next book is</em> "<em>Hero's Dose: The Case For Psychedelics in Ritual and Therapy."</em></p>
Researchers from the University of Toronto publish a new map of cancer cells' genetic defenses against treatment.
A moving target<img type="lazy-image" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNDQzNjQ2Ny9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTY1MDM3OTA0N30.z4u2eaulqRu8cslqqny8t9G7iaHr_DarbDJSFKLdDwI/img.jpg?width=980" id="21b22" class="rm-shortcode" data-rm-shortcode-id="f464c399c8024d03eaa35e24606fcdd0" data-rm-shortcode-name="rebelmouse-image" />
Credit: Marcelo Leal/Unsplash<p><span>Speaking to </span><a href="https://www.utoronto.ca/news/u-t-researchers-identify-genes-enable-cancer-evade-immune-system" target="_blank" rel="noopener noreferrer"><span data-redactor-tag="span" data-verified="redactor"><em data-redactor-tag="em">U of T News</em></span></a><span>, lead author of the study molecular geneticist </span><a href="http://www.moleculargenetics.utoronto.ca/faculty/2014/9/30/jason-moffat" target="_blank" rel="noopener noreferrer"><span data-redactor-tag="span" data-verified="redactor">Jason Moffat</span></a><span> of the university's </span><a href="https://ccbr.utoronto.ca/donnelly-centre-cellular-and-biomolecular-research" target="_blank" rel="noopener noreferrer"><span data-redactor-tag="span" data-verified="redactor">Donnelly Centre for Cellular and Biomolecular Research</span></a><span> says, "Over the last decade, different forms of immunotherapy have emerged as really potent cancer treatments, but the reality is that they only generate durable responses in a fraction of patients and not for all tumor types."</span></p><p>There can be a significant degree of heterogeneity between cancer cells from human to human, and even within the same person, making the development of therapies maddeningly difficult. Attempting to address potential cancer-cell vulnerabilities across these variations is a life-or-death game of whack-a-mole.</p><p>"It's an ongoing battle between the immune system and cancer, where the immune system is trying to find and kill the cancer whereas the cancer's job is to evade that killing," says Moffat.</p>
Mapping the mechanisms<img type="lazy-image" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNDQzNjQ3Ni9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTYyMjQ1OTM0MX0.HNtivrlU9VBYxcG9JaWKvPJ5RrBsgqd8Fw6ohfSpfh0/img.jpg?width=980" id="0faa6" class="rm-shortcode" data-rm-shortcode-id="7687cdc5abe93503764c1c0401b65fd4" data-rm-shortcode-name="rebelmouse-image" />
Credit: National Cancer Institute/Unsplash<p>Moffat and his colleagues decided to investigate and identify genes within cancer cells that help them defeat treatment. Co-lead author Keith Lawson of Moffat's lab explains, "It's important to not just find genes that can regulate immune evasion in one model of cancer, but what you really want are to find those genes that you can manipulate in cancer cells across many models because those are going to make the best therapeutic targets."</p><p>To accomplish this, the researchers, working with scientists at <a href="https://www.agios.com" target="_blank">Agios Pharmaceuticals</a> in Cambridge, Massachusetts, first exposed cells from breast, colon, kidney and skin cancer tumors to T cells in lab dishes. This established a baseline of their responses to treatment. Next, using CRISPR, the scientists went through the cells, exhaustively turning off one gene at a time to determine its role in immunotherapy resistance by comparing the cells' response to the T cells compared to their original baseline response.</p><p>The team identified 182 "core cancer intrinsic immune evasion genes" that affected the cells' response to T cells. The fact that some of the identified genes were already known to be involved in resistance provided the researchers with some confidence that they were on the right track.</p><p>Still, many of the genes they ID'ed had not been previously implicated. Says Lawson, "That was really exciting to see because it means that our dataset was very rich in new biological information."</p>
It's complicated<p>Unfortunately, Moffat's research also makes clear that defeating cancer-cell resistance is not as simple as removing certain genes. It's true that when the team switched off some of the genes they'd identified, the cancer cells became more vulnerable to T cells, but on the other hand, removal of some other genes made the cancer cells <em>more</em> resistant.</p><p>There also appear to be relationships between multiple genes that complicate matters. The researchers offer an example to <em>U of T News</em>.</p><p>The team explored the manipulation of the genes that allow cancer cells to engage in <a href="https://en.wikipedia.org/wiki/Autophagy" target="_blank">autophagy</a>, the process by which cells clear out no-longer useful materials to facilitate speedy recovery from damage. Surprisingly, when the researchers deleted certain genes responsible for cancer cells' autophagy, they found the cells' resistance to T cells <em>increased</em>. Apparently, removing one autophagy gene strengthened another mutated autophagy gene.</p><p>"We found this complete inversion of gene dependency," according to Moffat. "We did not anticipate this at all. What it shows us is that genetic context — what mutations are present — very much dictates whether the introduction of the second mutation will cause no effect, resistance or sensitivity to therapy."</p><p>There remains a long road ahead when it comes to unraveling cancer cells' resistance to immunotherapy. However, this new study presents a new map that can help scientists navigate what lies ahead.</p>
The number of people with dementia is expected to triple by 2060.
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