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From: Savant4/16/2017 5:32:48 PM
   of 1171
 

Dutch flying car to take off in 2018...a mere $400k

msn.com

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To: Savant who wrote (1136)4/21/2017 10:14:02 PM
From: Savant
   of 1171
 
vtol electric jet wow/... https://lilium.com/

















f/b Dimitri

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From: Savant4/22/2017 8:19:13 AM
   of 1171
 

An ambitious project, to say the least....Elon Musk's Neuralink...
Elon Musk’s Neuralink wants to turn cloud-based AI into an extension of our brains

https://techcrunch.com/2017/04/20/elon-musks-neuralink-wants-to-turn-cloud-based-ai-into-an-extension-of-our-brains/


Elon Musk has been working on a Neuralink, a human-computer brain interface company, in whatever spare moments he has between running Tesla and also running SpaceX. Neuralink’s ultimate aim may actually be the most ambitious of all three of his companies, surprisingly, and a new exploration of the foundational ideas behind Neuralink on Wait But Why goes deep within what Musk hopes to achieve by creating better, higher-bandwidth connections between our brains and computers.

Musk has confirmed that he will indeed occupy the CEO role at Neuralink, which means he’ll be the CEO of three separate companies. But Neuralink’s goals definitely sound the most science fictional of all three of his ventures, which is saying something considering Musk’s SpaceX is all about making humans an intergalactic colonial species.

Basically, Musk seems to want to achieve a communications leap equivalent in impact to when humans came up with language – this proved an incredibly efficient way to convey thoughts socially at the time, but what Neuralink aims to do is increase that efficiency by multiple factors of magnitude. Person-to-person, Musk’s vision would enable direct “uncompressed” communication of concepts between people, instead of having to effectively “compress” your original thought by translating it into language, and then having the other party “decompress” the package you send them linguistically, which is always a lossy process.

Neuralink’s tech would also be able to help humans keep pace with the rapid advances in AI, and would achieve this by basically integrating AI with human consciousness. Neuralink’s tech would enable human use of AI as just an additional faculty – like our sense of selves or other higher in-brain thought faculties. Making it possible to connect with such high bandwidth directly into the brain would allow us to integrate cloud-based AI computing within our selves in a way that’s indistinguishable from our core selves, Musk proposes, much like how most people would now find it difficult to separate their statements and expressions in language from the parts of the brain that generate them.

This tech is still far away from any kind of broad commercial application – maybe farther than a SpaceX trip to Mars. Musk says that it’s probably going to be at least “eight to 10 years” before tech the company produces can be used by someone without a disability. Neuralink is aiming to create therapeutic applications of its tech first, which will likely help as it seeks the necessary regulatory approvals for human trials.

Musk taking on a third CEO role is bound to raise eyebrows among his company’s investors, but Neuralink’s mission is in keeping with the aim of his other two companies: All three focus on solving problems that present what Musk would term existential threats – Neuralink’s agenda of countering AI not least among them.

Featured Image: Sebastian Kaulitzki/ Shutterstock


f/b Fubho

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From: Savant4/24/2017 10:43:39 AM
   of 1171
 

Giant Tinker Toy //world's largest double hulled ship...built in pieces...unloads in a few hours
Hellespont Fairfax... incredible how the pieces all fit together. video of construction thru launch
$100 mln project


youtube.com

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From: Savant5/3/2017 8:30:50 AM
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What will we do w/all the extra people by Y10K, if they cure most/all of the diseases...Mayo>>
Researchers develop new tumor-shrinking nanoparticle to fight cancer, prevent recurrence

Posted: May 01, 2017

(Nanowerk News) A Mayo Clinic research team has developed a new type of cancer-fighting nanoparticle aimed at shrinking breast cancer tumors, while also preventing recurrence of the disease. In the study, published today in Nature Nanotechnology ( "Multivalent bi-specific nanobioconjugate engager for targeted cancer immunotherapy"), mice that received an injection with the nanoparticle showed a 70 to 80 percent reduction in tumor size. Most significantly, mice treated with these nanoparticles showed resistance to future tumor recurrence, even when exposed to cancer cells a month later.
The results show that the newly designed nanoparticle produced potent anti-tumor immune responses to HER2-positive breast cancers. Breast cancers with higher levels of HER2 protein are known to grow aggressively and spread more quickly than those without the mutation.
"In this proof-of-concept study, we were astounded to find that the animals treated with these nanoparticles showed a lasting anti-cancer effect," says Betty Y.S. Kim, M.D., Ph.D., principal investigator, and a neurosurgeon and neuroscientist who specializes in brain tumors at Mayo Clinic's Florida campus. "Unlike existing cancer immunotherapies that target only a portion of the immune system, our custom-designed nanomaterials actively engage the entire immune system to kill cancer cells, prompting the body to create its own memory system to minimize tumor recurrence. These nanomedicines can be expanded to target different types of cancer and other human diseases, including neurovascular and neurodegenerative disorders."
Dr. Betty Kim
Dr. Kim's team developed the nanoparticle, which she has named "Multivalent Bi-specific Nano-Bioconjugate Engager," a patented technology with Mayo Clinic Ventures, a commercialization arm of Mayo Clinic. It's coated with antibodies that target the HER2 receptor, a common molecule found on 40 percent of breast cancers. It's also coated with molecules that engage two distinct facets of the body's immune system. The nanoparticle hones in on the tumor by recognizing HER2 and then helps the immune cells identify the tumor cells to attack them.
The molecules attached to the nanoparticle rev up the body's nonspecific, clean-up cells (known as macrophages and phagocytes) in the immune system that engulf and destroy any foreign material. The design of the nanoparticle prompts these cells to appear in abundance and clear up abnormal cancer cells. These clean-up cells then relay information about the cancer cells to highly specialized T-cells in the immune system that help eradicate remaining cancer cells, while maintaining a memory of these cells to prevent cancer recurrence. It's the establishment of disease-fighting memory in the cells that makes the nanoparticle similar to a cancer vaccine. Ultimately, the body's own cells become capable of recognizing and destroying recurrent tumors.
Since the late 1990s, the field of nanomedicine has focused on developing nanoparticles as simple drug delivery vehicles that can propel chemotherapy drugs to tumors. One pitfall is that the body tends to purge the particles before they reach their destination.
"Our study represents a novel concept of designing nanomedicine that can actively interact with the immune cells in our body and modulate their functions to treat human diseases," says Dr. Kim. "It builds on recent developments in cancer immunotherapy, which have been successful in treating some types of tumors; however, most immunotherapy developed so far does not harness the power of the entire immune system. We've developed a new platform that reaches tumor cells and also recruits abundant clean-up cells for a fully potent immune response."

Video explanation>> https://www.youtube.com/watch?time_continue=6&v=Ly8rlaF4pTc




Future studies in the lab will explore the ability of the nanoparticle to prevent long-term recurrence of tumors, including metastases at sites distant from the primary tumor. What's more, the nanoparticle is designed to be modular, meaning it can carry molecules to fight other types of disease. "This approach hopefully will open new doors in the design of new nanomedicine-based immunotherapies," she says.

Source: Mayo Clinic

Researchers develop new tumor-shrinking nanoparticle to fight cancer, prevent recurrence

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From: Savant5/4/2017 8:59:05 AM
   of 1171
 

Salk Institute...Better living through chemistry.. increasing endurance & insulin effectiveness

https://www.sciencedaily.com/releases/2017/05/170502142024.htm








'Exercise-in-a-pill' boosts athletic endurance by 70 percent
www.sciencedaily.com
Sedentary mice given the drug ran longer without training.




Salk scientists move one step closer to developing 'exercise-in-a-pill.' Partial view of a mouse calf muscle stained for different types of muscle fibers: oxidative slow-twitch (blue), oxidative fast-twitch (green), glycolytic fast-twitch (red).
Credit: Salk Institute/Waitt Center








Salk scientists move one step closer to developing 'exercise-in-a-pill.' Partial view of a mouse calf muscle stained for different types of muscle fibers: oxidative slow-twitch (blue), oxidative fast-twitch (green), glycolytic fast-twitch (red).
Credit: Salk Institute/Waitt Center
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Every week, there seems to be another story about the health benefits of running. That's great -- but what if you can't run? For the elderly, obese or otherwise mobility-limited, the rewards of aerobic exercise have long been out of reach.





Salk Institute scientists, building on earlier work that identified a gene pathway triggered by running, have discovered how to fully activate that pathway in sedentary mice with a chemical compound, mimicking the beneficial effects of exercise, including increased fat burning and stamina. The study, which appears in Cell Metabolism on May 2, 2017, not only deepens our understanding of aerobic endurance, but also offers people with heart conditions, pulmonary disease, type 2 diabetes or other health limitations the hope of achieving those benefits pharmacologically.

"It's well known that people can improve their aerobic endurance through training," says senior author Ronald Evans, Howard Hughes Medical Institute investigator and holder of Salk's March of Dimes Chair in Molecular and Developmental Biology. "The question for us was: how does endurance work? And if we really understand the science, can we replace training with a drug?"

Developing endurance means being able to sustain an aerobic activity for longer periods of time. As people become more fit, their muscles shift from burning carbohydrates (glucose) to burning fat. So researchers assumed that endurance is a function of the body's increasing ability to burn fat, though details of the process have been murky. Previous work by the Evans lab into a gene called PPAR delta (PPARD) offered intriguing clues: mice genetically engineered to have permanently activated PPARD became long-distance runners who were resistant to weight gain and highly responsive to insulin -- all qualities associated with physical fitness. The team found that a chemical compound called GW1516 (GW) similarly activated PPARD, replicating the weight control and insulin responsiveness in normal mice that had been seen in the engineered ones. However, GW did not affect endurance (how long the mice could run) unless coupled with daily exercise, which defeated the purpose of using it to replace exercise.





In the current study, the Salk team gave normal mice a higher dose of GW, for a longer period of time (8 weeks instead of 4). Both the mice that received the compound and mice that did not were typically sedentary, but all were subjected to treadmill tests to see how long they could run until exhausted.

Mice in the control group could run about 160 minutes before exhaustion. Mice on the drug, however, could run about 270 minutes -- about 70 percent longer. For both groups, exhaustion set in when blood sugar (glucose) dropped to around 70 mg/dl, suggesting that low glucose levels (hypoglycemia) are responsible for fatigue.

To understand what was happening at the molecular level, the team compared gene expression in a major muscle of mice. They found 975 genes whose expression changed in response to the drug, either becoming suppressed or increased. Genes whose expression increased were ones that regulate breaking down and burning fat. Surprisingly, genes that were suppressed were related to breaking down carbohydrates for energy. This means that the PPARD pathway prevents sugar from being an energy source in muscle during exercise, possibly to preserve sugar for the brain. Activating fat-burning takes longer than burning sugar, which is why the body generally uses glucose unless it has a compelling reason not to -- like maintaining brain function during periods of high energy expenditure. Although muscles can burn either sugar or fat, the brain prefers sugar, which explains why runners who "hit the wall" experience both physical and mental fatigue when they use up their supply of glucose.





"This study suggests that burning fat is less a driver of endurance than a compensatory mechanism to conserve glucose," says Michael Downes, a Salk senior scientist and co-senior author of the paper. "PPARD is suppressing all the points that are involved in sugar metabolism in the muscle so glucose can be redirected to the brain, thereby preserving brain function."

Interestingly, the muscles of mice that took the exercise drug did not exhibit the kinds of physiological changes that typically accompany aerobic fitness: additional mitochondria, more blood vessels and a shift toward the type of muscle fibers that burn fat rather than sugar. This shows that these changes are not exclusively driving aerobic endurance; it can also be accomplished by chemically activating a genetic pathway. In addition to having increased endurance, mice who were given the drug were also resistant to weight gain and more responsive to insulin than the mice who were not on the drug.

"Exercise activates PPARD, but we're showing that you can do the same thing without mechanical training. It means you can improve endurance to the equivalent level as someone in training, without all of the physical effort," says Weiwei Fan, a Salk research associate and the paper's first author.

Although the lab's studies have been in mice, pharmaceutical companies are interested in using the research to develop clinical trials for humans. The team can envision a number of therapeutic applications for a prescription drug based on GW, from increasing fat burning in people suffering from obesity or type 2 diabetes to improving patients' fitness before and after surgery.






Story Source:

Materials provided by Salk Institute. Note: Content may be edited for style and length.



Journal Reference:

  • Weiwei Fan, Wanda Waizenegger, Chun Shi Lin, Vincenzo Sorrentino, Ming-Xiao He, Christopher E. Wall, Hao Li, Christopher Liddle, Ruth T. Yu, Annette R. Atkins, Johan Auwerx, Michael Downes, Ronald M. Evans. PPARd Promotes Running Endurance by Preserving Glucose. Cell Metabolism, 2017; 25 (5): 1186 DOI: 10.1016/j.cmet.2017.04.006


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  • Salk Institute. "'Exercise-in-a-pill' boosts athletic endurance by 70 percent." ScienceDaily. ScienceDaily, 2 May 2017. <www.sciencedaily.com/releases/2017/05/170502142024.htm

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    From: Savant5/8/2017 6:51:54 PM
       of 1171
     
    http://www.msn.com/en-us/health/healthtrending/scientists-discover-why-hair-turns-gray-and-goes-bald/ar-BBASSWM?li=BBmkt5R&ocid=spartanntp










    Scientists Discover Why Hair Turns Gray and Goes Bald
    www.msn.com
    Scientists have pinpointed the cells that cause hair to turn gray and to go bald in mice, but more research is needed to understand how the process works in humans.



    Scientists have pinpointed the cells that cause hair to turn gray and to go bald in mice, according to a new study published in the journal Genes & Development.




    Researchers from the University of Texas Southwestern Medical Center accidentally stumbled upon this explanation for baldness and graying hairs-at least in mouse models-while studying a rare genetic disease that causes tumors to grow on nerves, according to a press release from the center.



    They found that a protein called KROX20 switches on skin cells that become a hair shaft, which then causes cells to produce another protein called stem cell factor. In mice, these two proteins turned out to be important for baldness and graying.




    When researchers deleted the cells that produce KROX20, mice stopped growing hair and eventually went bald; when they deleted the SCF gene, the animals' hair turned white.




    "Although this project was started in an effort to understand how certain kinds of tumors form, we ended up learning why hair turns gray and discovering the identity of the cell that directly gives rise to hair," said lead researcher Dr. Lu Le, associate professor of dermatology at the University of Texas Southwestern Medical Center, in a statement.

    More research is needed to understand if the process works similarly in humans, and Le and his colleagues plan to start studying it in people. "With this knowledge, we hope in the future to create a topical compound or to safely deliver the necessary gene to hair follicles to correct these cosmetic problems," he said.

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    From: Savant5/19/2017 9:26:01 PM
       of 1171
     

    Google/Android O/Project Treble/VR/TV upcoming features
    cnet.com

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    From: Savant5/22/2017 5:03:55 PM
       of 1171
     

    Princeton physicist give answer as to Why We Are Here?
    msn.com

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    From: Savant5/22/2017 6:50:13 PM
       of 1171
     

    Communicate w/Dolphins using computer AI by 2021

    thesun.co.uk

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