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Showing posts from November, 2018

Opinion: Scientifically-backed software is shifting patient care from the hospital to the home.

Originally shared by WIRED

Opinion: Scientifically-backed software is shifting patient care from the hospital to the home. https://wrd.cm/2QY06HM
https://wrd.cm/2QY06HM

Ask Ethan: Are Quantum Fields Real?

Originally shared by David Fuchs
https://www.forbes.com/sites/startswithabang/2018/11/17/ask-ethan-are-quantum-fields-real/#e2dc30e777a7

New research adds another branch to the evolutionary tree of life

Originally shared by David Fuchs
https://futurism.com/tree-life-evolution-hemimastigotes/

The Human-Machine Collaboration

Originally shared by Gideon Rosenblatt

The Human-Machine Collaboration

Humans Assisting Machines:
Humans need to perform three crucial roles. They must train machines to perform certain tasks; explain the outcomes of those tasks, especially when the results are counterintuitive or controversial; and sustain the responsible use of machines (by, for example, preventing robots from harming humans).

Machines Assisting Humans:
Smart machines are helping humans expand their abilities in three ways. They can amplify our cognitive strengths; interact with customers and employees to free us for higher-level tasks; and embody human skills to extend our physical capabilities.

Through our work with hundreds of companies, we have identified five characteristics of business processes that companies typically want to improve: flexibility, speed, scale, decision making, and personalization.

The lesson is clear: Organizations that use machines merely to displace workers through automation will miss the full potential of AI. Such a strategy is misguided from the get-go. Tomorrow’s leaders will instead be those that embrace collaborative intelligence, transforming their operations, their markets, their industries, and—no less important—their workforces.
https://hbr.org/2018/07/collaborative-intelligence-humans-and-ai-are-joining-forces

Some of the world's most creepiest robots, ranked!

Originally shared by Jason Mayes

Some of the world's most creepiest robots, ranked! Some are quite amusing and some are quite impressive. Still a long way to go though before anything like the movies though :-p

https://robots.ieee.org/robots/?t=rankings-creepiest-robots
https://robots.ieee.org/robots/?t=rankings-creepiest-robots

Fossil hunters are launching an Antarctic expedition to learn how fish developed into land animals.

Originally shared by WIRED

Fossil hunters are launching an Antarctic expedition to learn how fish developed into land animals. https://wrd.cm/2DTPSFs
https://wrd.cm/2DTPSFs

Does time exist? Very interesting video to think about. Worth 5 minutes of your time - if that is even a thing! ;-)

Originally shared by Jason Mayes

Does time exist? Very interesting video to think about. Worth 5 minutes of your time - if that is even a thing! ;-)
https://youtu.be/R3tbVHlsKhs
https://youtu.be/R3tbVHlsKhs

A major cause of type 2 diabetes is obesity, in which fat cells expand rapidly, in both size and number, and their...

Originally shared by Manuela Casasoli

A major cause of type 2 diabetes is obesity, in which fat cells expand rapidly, in both size and number, and their oxygen demand outstrips supply. This low-oxygen state, known as hypoxia, leads to upregulation of the anti-hypoxic protein HIF-1α, which in turn causes tissue inflammation and prevents fat cells (adipocytes) from responding normally to insulin. Hypoxia in expanding fat is often thought of mainly as a problem of supply, caused by the inability of blood vessels that deliver oxygen to grow as fast as the surrounding tissue. Writing in Nature Metabolism, Seo et al. highlight a pathway by which excessive oxygen consumption in adipocytes can also contribute to hypoxia in expanding fat tissue. This pathway involves the enhanced activity of the enzyme adenine nucleotide translocase 2 (ANT2) in energy-generating organelles called mitochondria.

Seo et al. (2018) Knockdown of ANT2 reduces adipocyte hypoxia and improves insulin resistance in obesity: https://www.nature.com/articles/s42255-018-0003-x
https://www.nature.com/articles/d41586-018-07248-6

Morphing brain DNA hints at a whole new way to treat Alzheimer’s

Originally shared by Ward Plunet

Morphing brain DNA hints at a whole new way to treat Alzheimer’s

Brain cells are reshuffling their own DNA. The finding may explain how Alzheimer’s disease develops and pave the way for new treatments using existing HIV drugs. Most drugs for treating Alzheimer’s disease are designed to clear out clumps of beta-amyloid protein that build up in the brain of people with the condition. But they have had disappointing outcomes in clinical trials so far. While studying the gene responsible for making beta-amyloid – called APP – Jerold Chun at Sanford Burnham Prebys Medical Discovery Institute in California and his colleagues discovered something strange. The gene appeared to be able to reshuffle its DNA, allowing it to take thousands of different forms. The team found about 10 times more variants of the APP gene in brain cells from people with Alzheimer’s disease than without. These different forms were able to produce a range of toxic proteins in addition to beta-amyloid. The finding may explain why Alzheimer’s drugs that specifically target beta-amyloid have had limited success, says Chun. “They may be missing thousands of other toxic products that are a bit different or maybe very different,” he says.


https://www.newscientist.com/article/2186180-morphing-brain-dna-hints-at-a-whole-new-way-to-treat-alzheimers/?utm_campaign=RSS%7CNSNS&utm_source=NSNS&utm_medium=RSS&campaign_id=RSS%7CNSNS-

Besides pouncing, purring, and pestering their owners for treats, cats spend much of their waking time licking...

Originally shared by Manuela Casasoli

Besides pouncing, purring, and pestering their owners for treats, cats spend much of their waking time licking themselves. Now, scientists have shed light on how sharp, tiny cones on cats’ tongues give their coats and skin a deep clean, instead of merely spreading their spit around.
[...]
The scientists have used the findings to create a “tongue-inspired grooming [TIGR] brush” that mimics a cat’s tongue with 3D-printed papillae embedded in a flexible silicone pad. Compared with a regular, stiff-bristled hairbrush, the researchers say the TIGR brush tugged less as it passed through human hair, and was easier to clean.

Schembri (2018) How do cats stay so clean? Video reveals secrets of the feline tongue: https://scim.ag/2ORLtnF

Noel and Hu (2018) Cats use hollow papillae to wick saliva into fur: http://www.pnas.org/content/early/2018/11/14/1809544115
https://youtu.be/Nu3a6rn2HZM

Stunning fall colours in this maple variant. Not to mention the stunning blue sky framing nature's handiwork.


Originally shared by Peter Vogel

Stunning fall colours in this maple variant. Not to mention the stunning blue sky framing nature's handiwork.

Title


Originally shared by Damian

#swarmrobotics #robotics #health

#swarmrobotics #robotics #health

Originally shared by Manuela Casasoli

Although the mere thought of a swarm of microrobots burrowing into an eyeball is enough to make some people squirm, scientists believe tiny, controllable delivery vehicles could be the future of eye medicine. Now, researchers have developed a tiny, rotini-shaped spiral that could one day be deployed in the thousands for targeted drug delivery.

Schembri (2018) Watch tiny robots swim through an eyeball to deliver medicine: https://www.sciencemag.org/news/2018/11/watch-tiny-robots-swim-through-eyeball-deliver-medicine

Wu et al. (2018) A swarm of slippery micropropellers penetrates the vitreous body of the eye: http://advances.sciencemag.org/content/4/11/eaat4388
https://youtu.be/zygGq0tV0hg

Title


Originally shared by Giuseppe Bertino

Built from the bottom up, synthetic cells and other creations are starting to come together and could soon test the...

Originally shared by Manuela Casasoli

Built from the bottom up, synthetic cells and other creations are starting to come together and could soon test the boundaries of life.
There were just eight ingredients: two proteins, three buffering agents, two types of fat molecule and some chemical energy. But that was enough to create a flotilla of bouncing, pulsating blobs — rudimentary cell-like structures with some of the machinery necessary to divide on their own.
To biophysicist Petra Schwille, the dancing creations in her lab represent an important step towards building a synthetic cell from the bottom up, something she has been working towards for the past ten years, most recently at the Max Planck Institute of Biochemistry in Martinsried, Germany.
https://www.nature.com/articles/d41586-018-07289-x

Again about the "Bottom-up biology", published on the last issue of Nature.

Originally shared by Manuela Casasoli

Again about the "Bottom-up biology", published on the last issue of Nature.
Researchers are tearing up the biology rule books by trying to construct cells from scratch. A special issue explores the lessons being learnt about life.
Cells are often called the building blocks of life — but that metaphor fails to capture their complexity. How do the multitudes of different molecules within a lipid envelope come together to carry out the functions required to sustain organisms? The standard approach in biology has been to work from the top down to study how cell components interact in their natural environment. But technical advances now allow researchers to take a different tack: using engineering principles to reconstruct biological processes from the bottom up. This special issue explores the potential and possible limits of bottom-up cell biology.

Latorre et al. (2018) Active superelasticity in three-dimensional epithelia of controlled shape: https://www.nature.com/articles/s41586-018-0671-4

Fletcher (2018) Which biological systems should be engineered?: https://www.nature.com/articles/d41586-018-07291-3

Nature Editorial (2018) Focus on the benefits of building life’s systems from scratch: https://www.nature.com/articles/d41586-018-07285-1
https://www.nature.com/articles/d41586-018-07290-4

Seems the same as Google Drive but with new subscription options and family sharing.

Seems the same as Google Drive but with new subscription options and family sharing. Overall an improvement, but still no Linux sync, so it can't be my sole cloud storage. Pity.. Google is missing so much not supporting #Linux..

#cloudstorage #googleone #linux #googledrive #googlephotos#gmail #google
https://www.androidauthority.com/google-one-vs-the-competition-917551/

What a pain.

What a pain.. I've installed Dropbox in a NTFS partition exactly for compatibility issues, both Windows and Ubuntu could sync it on the same folder. Now not only that won't be possible anymore, but my Ubuntu won't be able to sync on a NTFS partition at all.. I'm in the middle of a bit project!! Argh!! Any ideas? I'm considering getting an external driver for it, but that also isn't very reliable..

#dropbox #linux #ubuntu #ntfs #ext4
https://itsfoss.com/dropbox-linux-ext4-only/

Why the number 137 is one of the greatest mysteries in physics...

Originally shared by Rob Jongschaap

Why the number 137 is one of the greatest mysteries in physics https://bigthink.com/surprising-science/why-the-number-137-is-one-of-the-greatest-mysteries-in-physics
https://bigthink.com/surprising-science/why-the-number-137-is-one-of-the-greatest-mysteries-in-physics

The discovery of a mechanism that leads to cancer-therapy resistance highlights the many ways that tumour cells can...

Originally shared by Manuela Casasoli

The discovery of a mechanism that leads to cancer-therapy resistance highlights the many ways that tumour cells can adapt to survive — and reveals the limitations of categorizing patients by their gene mutations.
The development of resistance to cancer therapy is a major predictor of patient mortality. Therefore, understanding resistance mechanisms is key to improving therapeutic outcomes. Writing in Nature, He et al. report their discovery of a resistance mechanism in ovarian-cancer cells that contain a mutant version of the BRCA1 gene.

He et al. (2018) DYNLL1 binds to MRE11 to limit DNA end resection in BRCA1-deficient cells: https://www.nature.com/articles/s41586-018-0670-5
https://www.nature.com/articles/d41586-018-07188-1