Lifeboat Foundation: Safeguarding Humanity
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Blog – Page 6280

Dr. Ryuki Hyodo. Credit: JAXA

At ISAS, researchers watched the progress with particularly keen attention. In just a few years from now, we are about to attempt the same feat of visiting the Martian sphere. But for us, the destination is not the red planet but its two small moons. The Martian Moons eXploration (MMX) mission is scheduled to launch in the fiscal year of 2024. Largely ignoring the looming presence of Mars, the spacecraft will focus its suite of observing instruments on the moons, Phobos and Deimos. The mission plans to land on Phobos and collect samples to bring back to Earth in 2029. It is these barren moons that scientists believe contain evidence of the early days of the Solar System, and how habitability may have flourished and died on the planet below.

Dr. Ryuki Hyodo is researcher in the division of Solar System Sciences at ISAS, working on simulations of how the moons formed. Hyodo holds one of the institute’s independent ITYF (International Top Young Fellowship) positions; a program designed to support and promote talented researchers from around the world in the early stage of their careers. He explains that the first mystery surrounding Phobos and Deimos is how they came to be there at all. In fact, there are two main competing theories for how the moons formed.

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From ecosystem development to talent, much effort is still required for practical implementation of edge AI.

By Pushkar Apte and Tom Salmon

Rapid advances in artificial intelligence (AI) have made this technology important for many industries, including finance, energy, healthcare, and microelectronics. AI is driving a multi-trillion-dollar global market while helping to solve some tough societal problems such as tracking the current pandemic and predicting the severity of climate-driven events like hurricanes and wildfires.

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FedEx Corp. and self-driving vehicle startup Aurora Innovation Inc. are launching a pilot program for autonomous-truck shipments between Dallas and Houston, with the companies announcing Wednesday what they called a first-of-its-kind partnership involving the two companies and a truck maker.

“This is an exciting, industry-first collaboration that will work toward enhancing the logistics industry through safer, more efficient transportation of goods,” said Rebecca Yeung, vice president of advanced technology and innovation at FedEx FDX,-9.12% 0 in a news release.

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Cancer heterogeneity impacts therapeutic response, driving efforts to discover over-arching rules that supersede variability. Here, we define pan-cancer binary classes based on distinct expression of YAP and YAP-responsive adhesion regulators. Combining informatics with in vivo and in vitro gain-and loss-of-function studies across multiple murine and human tumor types, we show that opposite pro-or anti-cancer YAP activity functionally defines binary YAPon or YAPoff cancer classes that express or silence YAP, respectively. YAPoff solid cancers are neural/neuroendocrine and frequently RB1−/−, such as retinoblastoma, small cell lung cancer, and neuroendocrine prostate cancer. YAP silencing is intrinsic to the cell of origin, or acquired with lineage switching and drug resistance. The binary cancer groups exhibit distinct YAP-dependent adhesive behavior and pharmaceutical vulnerabilities, underscoring clinical relevance. Mechanistically, distinct YAP/TEAD enhancers in YAPoff or YAPon cancers deploy anti-cancer integrin or pro-cancer proliferative programs, respectively. YAP is thus pivotal across cancer, but in opposite ways, with therapeutic implications.

Pearson et al. demonstrate that YAP/TAZ, well-known oncogenes, are tumor suppressors in a large group of cancers. Pan-cancer analyses reveal that opposite YAP/TAZ expression, adhesive behavior, and oncogenic versus tumor suppressor YAP/TAZ activity functionally stratify binary cancer classes, which interchange to drive drug resistance. Contrasting YAPoff/YAPon classes exhibit unique vulnerabilities, facilitating therapeutic selection.

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Past and present nuclear activities (energy, research, weapon tests) have increased the urgency to understand the behavior of radioactive materials in the environment. Nuclear wastes containing actinides (e.g. plutonium, americium, curium, neptunium…) are particularly problematic as they remain radioactive and toxic for thousands of years.

Lawrence Livermore National Laboratory (LLNL) scientists and collaborators proposed a new mechanism by which nuclear waste could spread in the environment.

The new findings, that involve researchers at Penn State and Harvard Medical School, have implications for nuclear waste management and environmental chemistry. The research is published in the Journal of the American Chemical Society.

“This study relates to the fate of nuclear materials in nature, and we stumbled upon a previously unknown mechanism by which certain could spread in the environment,” said LLNL scientist and lead author Gauthier Deblonde. “We show that there are molecules in nature that were not considered before, notably proteins like ‘lanmodulin’ that could have a strong impact on radioelements that are problematic for management, such as americium, curium, etc.”

Continue reading “Nuclear waste interaction in the environment may be more complicated than once thought” | >

These club cell-secreted factors are able to nullify immune suppressor cells that otherwise help tumors escape an effective antitumor response,” said co-senior author Dr. Vivek Mittal, director of research at the Neuberger Berman Lung Cancer Center and the Ford-Isom Research Professor of Cardiothoracic Surgery at Weill Cornell Medicine. “We’re excited by the possibility of developing these club cell factors into a cancer treatment.

Malignant tumors can enhance their ability to survive and spread by suppressing antitumor immune cells in their vicinity, but a study led by researchers at Weill Cornell Medicine and NewYork-Presbyterian has uncovered a new way to counter this immunosuppressive effect.

In the study, published Sept. 20 in Nature Cancer, the researchers identified a set of anti-immunosuppressive factors that can be secreted by called cells that line airways in the lungs. They showed in a mouse model of lung cancer that these club cell factors inhibit highly potent immunosuppressive cells called myeloid-derived suppressor cells (MDSCs), which tumors often recruit to help them evade antitumor immune responses.

The inhibition of the MDSCs led to an increase in the number of antitumor T cells at the tumor site, and greatly improved the effectiveness of FDA approved PD1 immunotherapy.

Continue reading “Scientists find a new way to reverse immune suppression in tumors” | >