Science science

Methane Seeps Out as Arctic Permafrost Starts to Resemble Swiss Cheese

Methane Seeps Out as Arctic Permafrost Starts to Resemble Swiss Cheese
Methane Seeps Out as Arctic Permafrost Starts to Resemble Swiss Cheese

Transition from fossil fuels to clean energy. Stop cutting down forests to grow beef, and plant a whole bunch of trees.

Simple, right?

Is there anything we can do to reverse this or bring it to a stop within a decade or two? I feel most of the world greatly underestimates the power of feedback loops.

edit: typo

It's about mitigating damage. Sure we could shrug and say "it can't be helped" but then things will be even worse for future generations

Even if we did all this in an instantaneous switch, the planet wouldnt start cooling off or something like that, it would just hold it's current temperature (best case scenario) and since that permafrost has already started to melt, and methane is being released, it wouldnt matter.

Poaching pushes pangolin closer to extinction

Poaching pushes pangolin closer to extinction
Poaching pushes pangolin closer to extinction

Pangolins are nocturnal mammals that typically eat ants and termites. They're the only known mammals that have keratin (the protein family that is the key structure material of the human skin) scales.

Damn, I don't want these beautiful creatures to go extinct :(

What are these creatures?

They kinda look like a Sandslash from Pokémon if that helps.

I'm Roger Lemon, a just-retired Professor of Neurophysiology at the Institute of Neurology, UCL. I do research on understanding the cerebral control of hand and finger movements in humans and in non-human primate models and I’m here today to talk about it. AMA!

I'm Roger Lemon, a just-retired Professor of Neurophysiology at the Institute of Neurology, UCL. I do research on understanding the cerebral control of hand and finger movements in humans and in non-human primate models and I’m here today to talk about it. AMA!

Hi Reddit,

My name is Roger Lemon, I am a just-retired Professor of Neurophysiology at the Institute of Neurology, UCL, where I worked for 22 years, after university posts in Sheffield, Melbourne, Rotterdam and Cambridge. I am a Fellow and past Council Member of the Academy of Medical Sciences.

My main research interest is the control of skilled hand movements by the brain and is prompted by the need to understand why hand and finger movements are particularly affected by damage to the cortex, and its major descending pathways, for instance as a result of stroke, spinal injury and motor neuron disease. My experiments involve the use of purpose-bred non-human primates, since these provide the best available model for the human sensorimotor system controlling the hand.

My research is complemented by parallel studies in normal human volunteers and in patients: interactions between discoveries gained from work in monkeys and understanding the effects of neurological disorders on hand function in patients has been an important part of my career, especially when working at the Institute of Neurology, a world centre for the treatment of neurological disorders. I have helped to develop better ways of studying the human motor system, to understand the process of recovery after injury and to investigate therapies that might enhance recovery.

I am firmly of the opinion that we still need some research in monkeys to understand the complex functions of the human brain. This is fundamental research aimed at understanding normal brain function in, for example, learning, memory, emotion and, my own research area, motor skill. I believe that this work should only be carried out with careful regulation that ensures responsible, high-quality research and requires the highest possible welfare standards, driven by application of the 3Rs.

I am also keen to explain that without supporting this basic type of research, we will not get the translational benefits that results from a small but important fraction of the work that leads on to impact on the clinical conditions such as those listed above.

So I am a strong advocate for better engagement between scientists and the public about how we use animals in science, which has been vital for much of my own research.

This is my first AMA, I’m here to talk about the neuroscience of skilled movement, the miracle of the human hand, and how it is disrupted by disease, about animal research, particularly research in non-human primates, and well Ask Me Anything!

This AMA has been organised by Understanding Animal Research.

EDIT: I've now finished. Thanks for all the interest and fascinating questions. I only hope I went some way to answering some of them.

Hkw has human hand writing affected the brain over the course of the last few thousand years?

I've read about non-human primates being able to learn some sign language, is it possible that they could ever learn to write?

Fascinating, I think your performance is probably close to the limit. My understanding is that the limit is set not by the brain but by the response of the muscles in the hand and forearm where the maximum frequency is limited by the time it takes to develop a mechanical contraction in response to the neural control signal. This is probably in the order of 40-50 milliseconds i.e. around 20 hertz. I think this is the speed that violinists can exhibit during a vibrato sequence.

Dr Lemon, I kinda feel intimidated by all the other questions since mine is more rudimentary, but I'm gonna ask anyways. I'm playing guitar since 10 years now, and one of my goals is to play 16th triplets at 180bpm; that'd be 18 single movements of my left Hand in a second, but even after trying for a year now, I can't seem to nail a Solo that fast. Would you say (in general) that there is a maximum speed your fingers can move?

I have not directly contributed to understanding of cerebral palsy. Although I have worked with paediatricians caring for these children and I think my work has helped to explain the primacy of the motor cortex for human hand control and why this structure is so vulnerable to damage early in life. I am not aware that cerebral palsy regularly presents as a condition in nonhuman primates, but there are certainly scattered reports of monkeys with poorly-developed cortex. In terms of anthropomorphising: yes of course. I think I have always avoided the infliction of unnecessary pain to the animals in my care. If such a procedure was needed, I think I would generally try and find another way of using a less painful test or avoiding it altogether. I am very much aware that all biomedical research inflicts some harms on the animals used and it is our duty as scientists to try to minimise those harms and at all times to make sure that the benefits of the research justify the harms inflicted.

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PLOS Science Wednesday: Hi reddit, I’m Neus and the results of my PLOS Pathogens study show that one influenza virus may protect against later infections caused by other viruses of different subtypes in mallard ducks – Ask Me Anything!

PLOS Science Wednesday: Hi reddit, I’m Neus and the results of my PLOS Pathogens study show that one influenza virus may protect against later infections caused by other viruses of different subtypes in mallard ducks – Ask Me Anything!Hi Reddit,

My name is Neus Latorre-Margalef and I am currently a postdoctoral fellow at Lund University, Sweden. My research focuses on host-pathogen interactions and processes of diversification in pathogen populations. My study systems are low-pathogenic influenza A virus circulating in wild birds and I recently started working also with Borrelia causing Lyme disease.

Together with Prof. David Stallknecht and colleagues at the University of Georgia, we recently published a study in PLOS Pathogens entitled Competition between influenza A virus subtypes through heterosubtypic immunity modulates re-infection and antibody dynamics in the mallard duck.

We investigated how mallard ducks respond to influenza infection and how influenza viruses of different so-called “subtypes” interact with each other after re-infection. We found that one virus can partially protect against later infections caused by other viruses of different subtypes— infections were much shorter and fewer viruses were shed. The results clearly demonstrate that the degree of protection depends on the genetic similarities between the influenza subtypes. Thus a primary infection can influence later infections in life and suggests that primary infections could induce protection against “novel” highly pathogenic strains like H5N8. This indicates that there is competition between influenza subtypes that has great importance for the evolution of diversity within influenza infecting wild birds.

I will be answering your questions at 1pm ET. Ask Me Anything!
PLOS Science Wednesday: Hi reddit, I’m Neus and the results of my PLOS Pathogens study show that one influenza virus may protect against later infections caused by other viruses of different subtypes in mallard ducks – Ask Me Anything!

Hi Reddit,

My name is Neus Latorre-Margalef and I am currently a postdoctoral fellow at Lund University, Sweden. My research focuses on host-pathogen interactions and processes of diversification in pathogen populations. My study systems are low-pathogenic influenza A virus circulating in wild birds and I recently started working also with Borrelia causing Lyme disease.

Together with Prof. David Stallknecht and colleagues at the University of Georgia, we recently published a study in PLOS Pathogens entitled Competition between influenza A virus subtypes through heterosubtypic immunity modulates re-infec....

We investigated how mallard ducks respond to influenza infection and how influenza viruses of different so-called “subtypes” interact with each other after re-infection. We found that one virus can partially protect against later infections caused by other viruses of different subtypes— infections were much shorter and fewer viruses were shed. The results clearly demonstrate that the degree of protection depends on the genetic similarities between the influenza subtypes. Thus a primary infection can influence later infections in life and suggests that primary infections could induce protection against “novel” highly pathogenic strains like H5N8. This indicates that there is competition between influenza subtypes that has great importance for the evolution of diversity within influenza infecting wild birds.

I will be answering your questions at 1pm ET. Ask Me Anything!

Hey Neus, fairly specific application of your area of knowledge (flu virus effects in ducks); how did you end up using ducks as your model species?

This AMA is being permanently archived by The Winnower, a publishing platform that offers traditional scholarly publishing tools to traditional and non-traditional scholarly outputs—because scholarly communication doesn’t just happen in journals.

To cite this AMA please use: https://doi.org/10.15200/winn.150046.68648

You can learn more and start contributing at authorea.com

Can your conclusions carryover to other species such as humans?

Why did you choose ducks as the host for influenza and not another type of animal?

Strangely enough, the animals that humans share susceptibility with for strains of the flu are pigs and ducks. IIRC, a strain which manifests itself in the duck's upper respiratory system will manifest itself in our lower respiratory system. This leads to a lower transmission rate, but a higher morbidity due to alveolar damage and risk of pneumonia

Bacteria in a one-year-old's poop can predict how he or she will perform on cognitive tests by age two. This is the first study to link gut microbes to cognitive development in humans.

Bacteria in a one-year-old's poop can predict how he or she will perform on cognitive tests by age two. This is the first study to link gut microbes to cognitive development in humans.
Bacteria in a one-year-old's poop can predict how he or she will perform on cognitive tests by ag...

All I can find is they had 89 samples and they clustered them into 3 groups using the microbial communities as predictors for classification.

I can believe that the MC can be used to predict but I still want to see the confusion matrix.

found the paper. They didn't predict anything. They built regression models to fit the data which help to explain what's going on, but so far I see no indication that they did any out of sample predicting and I don't even see anything more than the 1 mention of the model. Also from the figures right now I think they just calculated the correlation between a feature and their measured response. Their R2 values aren't good enough to convince me they're really explaining what's going on.

tl;dr - So far to me it looks like a descriptive analysis masquerading as a predictive one.

link to paper - took too long to find: http://www.sciencedirect.com/science/article/pii/S0006322317317201#fig2

The article says that less diverse bacteria in the gut leads to higher cognitive performance, is it possible that they have wealthier parents who are more likely to take them to the Dr when sick and get antibiotics that are the cause of the reduced diversity and the higher cognitive function is just genetics and the other benefits that wealthy parents can provide?

Maybe this is just a proxy measure for breastfeeding which carries important fats for the brain (e.g. DHA).

Human breast milk has a special type of sugar in it that deliberately discourages some species of bacteria and encourages others. Thus, ↓ microbiome diversity might be a consequence of ↑ human milk oligosaccharide exposure. This might form an exception to our usual expectation that greater diversity is better since a reduced HMO exposure would mean being less exposed to a beneficial agent that is simultaneously inhibitory and also acting as a growth medium for specific species of bacteria.

The intestinal collection of bacteria (microbiome) in exclusively breastfed children is dominated (up to ~80%) by bifidobacteria. Bif are lactic acid bacteria which acidify the colon, which makes components of breastmilk (lactoferrin and lysozyme) more effective at preventing the colonisation and growth of Gram-negative bacteria.

The sugars (oligosaccharides) act as both, anti-infectives against pathogens by acting as decoys of the cell surface sugars, and as growth/colonisation promoting factors for beneficial bacteria. There are over 200 unique sugar structures in human breastmilk which can't yet be replicated in the lab to add to infant formula.

Breastmilk also contains a source of sialic acid (either free or attached) which are also beneficial for neurological development in children.

Other things leading to increased bacterial diversity is the means of delivery (c-section or natural), formula feeding, and the early administration of antibiotics.

Source: PhD on the effects of breastmilk sugars on bacterial colonisation of the infant GI tract.

Edited for spelling.

Science AMA Series: I’m Dr. Adrian Owen, a neuroscientist whose research focuses on brain imaging, cognitive function and consciousness. We’re finding new ways to decode the complex workings of the brain. AMA.

Science AMA Series: I’m Dr. Adrian Owen, a neuroscientist whose research focuses on brain imaging, cognitive function and consciousness. We’re finding new ways to decode the complex workings of the brain. AMA.

I’m Dr. Adrian Owen, a professor of neuroscience, here to answer your questions about our breakthroughs in brain science.

I’ve been fascinated with the human brain for more than 25 years: how it works, why it works, what happens when it doesn’t work so well. At the Owen Lab at Western University in Canada, my team studies human cognition using brain imaging, sleep labs, EEGs and functional MRIs. We’ve learned that one in five people in a vegetative state are actually conscious and aware (I recently wrote a book on it – www.intothegrayzone.com, if you’re interested).

We’ve also examined whether brain-training games actually make you smarter (pro tip: they don’t).

Now my team is working on a cool new project to understand what happens to specific parts of people’s brains when they get too little sleep. We’re testing tens of thousands of people around the world to learn why we need sleep, how much we need, and the long- and short-term effects sleep loss has on our brains. A lot of scientists and influencers, such as Arianna Huffington and her company Thrive Global, have already raised awareness about the dangers of sleep loss and the need for research like this. Since we can’t bring everyone to our labs, we’re bringing the lab to people’s homes through online tests we’ve designed at www.worldslargestsleepstudy.com or www.cambridgebrainsciences.com. We hope to be able to share our findings in science journals in about six months.

So … if you want to know about sleep-testing, brain-game training or how we communicate with people in the gray zone between life and death … AMA!

I will be here at 1:00pm EDT (10:00am PDT / 5:00pm UTC), with researchers from my lab, Western University and the folks who host the www.worldslargestsleepstudy.com platform—ask me anything!

Update: We're here now! Ask us anything! Proof that I am real: http://imgur.com/a/NvPMK

Update 2: I appreciate all the questions! I tried my best to answer as many as I could. This was really fun. See you next time. Now, time for some pineapple pizza! http://imgur.com/a/Yy88r

Do you believe that research focused on psychedelics and psychoactive substances (that induce altered states of consciousness) can provide meaningful insights for our understanding of consciousness and other concepts in neuroscience?

If brain games don't make us smarter, are there other cognitive benefits besides intelligence that they do lend? Are there similar activities that you believe you would find to yield the types of results that "brain games" promise?

As a follow-up, what types of methods do you use to study any improvement of cognitive performance following an activity?

This AMA is being permanently archived by The Winnower, a publishing platform that offers traditional scholarly publishing tools to traditional and non-traditional scholarly outputs—because scholarly communication doesn’t just happen in journals.

To cite this AMA please use: https://doi.org/10.15200/winn.150038.82260

You can learn more and start contributing at authorea.com

Has brain/gut interactions started to gain more time in your research ?

Science AMA Series: We’re Professor Kristine DeLong and documentary journalist Ben Raines, our discovery of a preserved underwater forest in the Gulf of Mexico that’s been submerged since an Ice Age 60,000 years ago when sea levels were 400 feet lower than they are today. Ask Us Anything!

Science AMA Series: We’re Professor Kristine DeLong and documentary journalist Ben Raines, our discovery of a preserved underwater forest in the Gulf of Mexico that’s been submerged since an Ice Age 60,000 years ago when sea levels were 400 feet lower than they are today. Ask Us Anything!

PROFESSOR: Kristine DeLong, paleoclimatologist at Louisiana State University

DOCUMENTARY JOURNALIST: Ben Raines, AL.com environmental reporter https://twitter.com/benhraines

The Underwater Forest details the discovery and exploration of an ancient cypress forest found sixty feet underwater in the Gulf of Mexico, due south of Gulf Shores, Alabama. The forest dates to an ice age more than 60,000 years ago, when sea levels were about 400 feet lower than they are today. The forest appears to be a wholly unique relic of our planet’s past, the only known site where a coastal ice age forest this old has been preserved in place. It is considered a treasure trove of information, providing new insights into everything from climate in the region to annual rainfall, insect populations, and the types of plants that inhabited the Gulf Coast before humans arrived in the new world. Scientific analysis of the site is ongoing.

The documentary follows the work of the team investigating the site, both underwater and in the laboratory. The film was written and directed by AL.com’s Ben Raines, who also filmed the underwater sequences and organized the first scientific missions to the site.

The scientists believe the forest was buried beneath the Gulf sediments for eons, until giant waves driven by Hurricane Ivan in 2004 uncovered it. Raines and AL.com collected the first samples from the site, and participated in every scientific mission to the site, beginning in 2012. Dropping 10 fathoms down, below the green waves of the Gulf and back in time to this prehistoric world amounts to a sort of time traveler’s journey. Nothing like the forest, in terms of age or scale, has ever been found. The oxygen-free underwater environment has hermetically sealed the trees in a sort of natural time capsule.

Watch the documentary here: http://www.thisisalabama.org/underwaterforest/

About Kristine: I study past climate and am interested in the changes that occurred in the last 2,000 years as well as the past 125,000 years during the last ice age. I am a scuba diver and my research is mostly in the tropics and subtropics (I prefer warm water diving).

I just spent an amazing three days introducing Louisiana wetlands to 10 incredible minority undergraduates, many of whom have never seen an ocean or a wetland. We saw how Tropical Storm Cindy changed a barrier island, dodge thunderstorms in boat, kayaked in the salt grass marsh lands, had a shrimp boil with my colleagues from the United Houma native american tribe (Merci beaucoup Seafood Kingdom!), and toured the Atchafalaya baldcypress swamp with The Nature Conservancy - Louisiana.

I earned a Bachelor of Science degree in Mechanical Engineering and worked in the corporate world for 12 years before going back to school to get my Ph.D.

The Underwater Forest is a project I have been involved in for five years now and it has truly been a unique experience in many ways. I found Ben online and we started to talk about the forest and he took me out to see it. I contacted colleagues to tell them about the trees and we dated the first wood samples; we were very surprise to learn how old they were. This is truly a unique site due to its location and age. I now lead a team of six scientists, four graduate students, one undergraduate, and other colleagues in researching the underwater ancient forest. I am seeking new collaborations and I want to bring in other experts to the project so we can learn as much as we can from this unique time capsule of an ice age landscape. Our team has learned a lot about the site but we still have many more questions to answer.

About Ben: I first learned of the Underwater Forest from a dive shop owner in Alabama. He discovered the forest about a year after Hurricane Ivan, when a fisherman came into the dive shop and said, “I’ve found this spot that’s just loaded with fish but there’s barely anything in terms of structure that shows up on my depth finder. Why don’t you go out there and take a look.” The fisherman turned over the coordinates to his spot, and the dive shop owner made a trip and found the bottom littered with cypress stumps and logs scattered around.

Luckily, the dive shop guy decided to keep the location a secret. He did so because of his experience seeing small natural coral outcroppings destroyed by divers collecting live rock for the aquarium trade. Knowing I was an environmental journalist, he decided to tell me about the forest. After a couple years of bugging him, he agreed to take me to the site on the condition that I never reveal the coordinates to anyone. He agreed to let me write a story. Kristine called me the day the story came out, explained her expertise as a scuba diving paleoclimatologist, and asked if I could get her samples of the wood so she could have them carbon dated.

When those first samples turned out to be radio-carbon dead, meaning too old to be dated that way, she asked if she could come with us to the site and collect more samples. You see her first visit to the forest in the film. She assembled a team of scientists including dendrochronologists, geologists and paleontologists. Much of their research is revealed in the film and in several papers Kristine has published. Some of the most interesting finds are newly revealed, since filming was completed.

In particular, the pollen assemblage seen in the sediment cores that LSU collected. The story at this link provides a sort of layman’s primer on everything I’ve gleaned about the forest from my earliest visits to Kristine’s research. It also has a lot of pictures of the site and a link to the Underwater Forest film. A quick read might be useful to help formulate your questions.

What are the conditions for a forest to be preserved like this? I'm assuming it has something to do with quick and sustained flooding, because normal sea level rise would take too long.

Kristine here - Yes, baldcypress trees naturally are resistant to water damage and termites, that is one of the reasons they were heavily logged in the 1800s for building materials and today there are few large old trees. However, even cypress should decompose on 10,000 years time scales, unless they are preserved in low oxygen sediments that inhibit bacteria from decomposing the wood. The sediments around the wood are dark in color and full of organics (roots, small pieces of wood, seeds, and pollen) are all remarking well-preserved. This suggests low-oxygen environment in the sediments that can be found in back swamps areas where water mixing and flow is low or standing water occurs for long periods of time leaving the water anoxic. If you ever been in a back swamp, the sulfur smell is one that tells you there are low oxygen conditions.

From what I could gather from the documentary. It's a cypress forest. Those are trees growing in the water and have adapted to that environment. Which means that even when dead, they don't disintegrate as fast as an oak tree e.g. would do.

What helped over the millenia was a lot of mud that was on the trees, preventing oxygen from getting through.

How do you go about inspecting the area, I am sure you have to be as careful as possible but what types of methods are you all using to prevent harm to the sight?

An evolutionary biologist at the University of Houston has published new calculations that indicate no more than 25% of the human genome is functional.

An evolutionary biologist at the University of Houston has published new calculations that indica...

copying my comment from another post of the same research to this sub:

Wait... what am I missing here:

The mean fitness of the population can be defined by two variables, the mean deleterious mutation rate per functional nucleotide site per generation ( μdel ) and the number of functional nucleotide sites (n) in the genome (Kimura 1961; Nei 2013).

w=(1−μdel)n

kay, this is the probability that an individual offspring has zero mutations in any of the functional nucleotide sites. I will grant that this metric is related to fitness, but by what function?

Let us now consider the connection between mutational load and replacement level fertility ( F ). If the mortality rate before reproduction age is 0 and mean fertility is 1, then the population will remain constant in size from generation to generation. In real populations, however, the mortality rate before reproduction is greater than 0 and, hence, mean fertility needs to be larger than 1 to maintain a constant population size. In the general case, for a population to maintain constant size, its replacement level fertility should be

F=1 / w

Uhhhhhhhhh, what? All of a sudden the probability of mortality before reproduction is identically equal to the probability that an individual offspring has more than zero mutations in functional nucleotide sites? I'm pretty sure we know that's not how it works, for a typical definition of "functional". This would imply that there is no genetic drift of functional genomic data. This would imply that there's no speciation, because there can be no change in function. Right?

Ok, so the only way any of this makes sense to me is if the "functional fraction" isn't really the fraction of the genome that has any function, but the fraction that is vitally functional. They're literally equating "functional genome" length with the number of single site deadly mutational targets in the genome.

This strikes me as a nonsensical way to define functionality. Just look at protein tertiary structure. We know that there's structural redundancy in proteins. Many structures are stabilized by multiple bonds between adjacent alpha helices, or by a cloud of buried hydrophobic residues, all of which contribute to the structural stability of the molecule (across temperature, say). We would never call the group of hydrophobic residues that stabilize a globular protien "nonfunctional," although substitution of any given one wouldn't necessarily be deadly.

I don't know, maybe this calculated functional fraction relates in a useful way to the information density or informational redundancy of the genome. But if that's the case then the phrasing is obfuscatory and misleading. The title makes it sound like 75% of the coding regions of the genome don't do anything.

EDIT: I've gotten good criticisims of my criticism. One important mis-understanding that folks have brought to my attention is that the definition of "fitness" here includes the rate of offspring production by an individual's offspring, so the mutation doesn't need to be deadly: the total long term selective pressure on a mutation is folded into the "w" metric. I've also had my argument that the scenario captured by the model doesn't allow for drift or speciation refuted. So I think that the only reason my comment is the top comment here is not because it's necessarily a great refutation (it isn't) but because it was posted early, and lots of readers share the same sentiment (that this analysis is excessively simplistic).

I still am left with the impression that the simplifications used to make the analysis have caused so much complexity to be folded into the working definition of "functional genome" (even beyond the careful definition that the authors give) that it's just not super useful to talk about the fraction of the genome which is functional by this metric.

what exactly does 'functional' mean? does this mean i can remove 75% of my genome and still be completely normal?

His idea of using deleterious mutations to determine function is flawed at the offset when you consider the possibility of multiple areas producing the same product.

Let's say that there is a piece of miRNA that is vital to the regulation of a certain protein and is produced at 3 spots in the genome. A mutation in one location would cause that site to stop producing the miRNA, but the other two sites would continue to be productive and no negative effects would be observed.

As to why we should think there would be multiple sites of the genome doing the same thing? That all comes down to the existence of transposons: genetic elements that are able to copy themselves and inject themselves into other parts of the genome. Transposons are found all over the genome and dominate the areas previously thought of as 'junk'.

Edit: Putting this at the top because it's super important. The term 'functional' is generally used in two different ways. It is either used to a describe causal role (this thing performs this funcition within this system) or a selected effect (this feature contributes to the rate of fertility as influenced by selective pressures). Most people tend think in terms of the first definition. Selected effects are a subset of causal roles. This author used the latter definition. One is not necessarily better or worse than the other. Depends on what you're trying to do. So their title is technically correct, but it's disingenuous to compare the results of this analysis to the results of other analyses using the other definition (like ENCODE). It's this choice that bothers me the most. Yes, Graur argues for the selective effect definition, but I still think they're really two different ideas that are both useful. Not one or the other. End edit.

Nope. You'd almost certainly be dead. While his analysis does provide some information about what percent of the genome affects fertility rates, it definitely does not measure potential functionality (in terms of causal role) across the entire genome. It's unfortunate that they are trying to pitch it that way on the website. Had they just said "This percent of genes are essential for fertility rate," then I would be happy with their contribution. But they didn't.

There are tons of mutations that aren't selected on (or are selected so weakly we can't measure it) but do lead to functional changes. Without them, there would be no changes in hair or eye color. It also ignores all the loss of function mutations that cause diseases but don't affect reproduction. We know about those mutations and diseases because living people have them. For example, certain versions of color blindness are the result of loss of function mutations. These mutations clearly have functional outcomes, but his analysis is blind to them.

Furthermore, the physical organization of the genome is important to its function. Removing 75% of the genome would almost certainly disrupt processes like mitosis, meiosis, and transcriptional regulation that in part depend on physical location. Even if the authors are actually correct, and we only need 25% of the total sequence for everything, simply removing the other 75% may render the remaining genome non-functional absent a complete re-engineering of chromosomal organization and structure. I could go on, but you get the point.

Remember, when you see a claim this bold and potentially game-changing and the paper isn't published in Nature/Science/Cell (or some other very high tier journal), your bull shit radar should start pinging. Particularly when the result disagrees with one of the largest, best funded projects (ENCODE) run by some of the smartest people in the game. Who do you think has a better grasp on things, a rando guy (EDIT: I was being a dick, this author is fully legit. I was trying to argue consensus vs individual opinion, but did it in a dickish way.) publishing in a journal with an impact actor of 4, or a massive group of some of the best minds available publishing large scale projects in top tier journals? Ultimately, I think they're just talking about two different things, and we're getting caught in the middle.

Dislike for unfamiliar groups of people may be learned. By the age of one, infants already prefer speakers of their native tongue, but do not necessarily view speakers of an unfamiliar language negatively

Dislike for unfamiliar groups of people may be learned. By the age of one, infants already prefer speakers of their native tongue, but do not necessarily view speakers of an unfamiliar language negatively
Dislike for unfamiliar groups of people may be learned. By the age of one, infants already prefer...

I don't like the fundamental premises of the article. The kids reacted to the strangers with observant neutrality, which is of course how people should generally react to strangers. The notion that we should instantly have the warm and fuzzies for strangers is bizarre.

The researchers are not saying these infants had learned to be racist, quite the opposite.

Although the infants showed a positive attitude towards speakers of their native tongue, they only behaved neutrally towards people speaking unfamiliar languages; their reactions were not negative.

This suggests negative reactions towards 'unfamiliar groups' develop later and are perhaps learned.

TL;DR Not only are people not reading the article, they're not even reading the whole title!

The researchers didn't just observe how the children reacted to one group of strangers and then arrive at their conclusions, they compared the children's reactions to strangers who spoke their language and strangers who did not.

This statement of yours:

which is of course how people should generally react to strangers.

Is moot though because they compared to strangers who spoke the child's language.

And I didn't see any reference to racial bigotry, just dislike of unfamiliar groups, which isn't actually the same thing.

First Battery-Free Cellphone Harvests Power from Ambient Radio Signals, Light

First Battery-Free Cellphone Harvests Power from Ambient Radio Signals, Light

So currently it is a short range walkie talkie?

Exactly. It’s more like a passive RFID card than a real mobile. I don’t understand why all the newspapers are picking it up too. They might as well call it a battery-free laptop while they are at it since it has a microcontroller on it.

Of course it could be interesting for truly wireless and battery-free sensors around the house but afaik those already exist.

I don’t understand why all the newspapers are picking it up

Because most ppl writing about this:

1) don't understand any of that and are not aware of their huge lack of knowledge

2) care more about clickbait than facts

Is this not how a crystal AM radio works? We've had this for 100 years. You can use an unpowered high impedance earbud attached to a passive bandpass filter to listen to AM radio. ex: http://www.ke3ij.com/xtal.htm

Presumably you can run it the other way to transmit extremely low power signals by using the acoustic power in your voice applied to the piezoelectric crystal to power the antenna. Unfortunately the other person listening would probably have to be in the same room to have any hope of receiving the signal... We need more power to boost the signal and for any digital processing.

Try one of these subthreads