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Neuroscientists assume that these mental powers somehow emerge from the electrical signaling of neurons — the circuitry of the brain. But no one has come close to explaining how that occurs. Continue reading the main story Continue reading the main story That, Dr. Nagel proposes, might require another revolution: showing that mind, along with matter and energy, is “a fundamental principle of nature” — and that we live in a universe primed “to generate beings capable of comprehending it.” Rather than being a blind series of random mutations and adaptations, evolution would have a direction, maybe even a purpose.

“Above all,” he wrote, “I would like to extend the boundaries of what is not regarded as unthinkable, in light of how little we really understand about the world.”

Dr. Tegmark, in his new book, “Our Mathematical Universe: My Quest for the Ultimate Nature of Reality,” turns the idea on its head: The reason mathematics serves as such a forceful tool is that the universe is a mathematical structure. Going beyond Pythagoras and Plato, he sets out to show how matter, energy, space and time might emerge from n

the mathematician Edward Frenkel noted that only a small part of the vast ocean of mathematics appears to describe the real world. The rest seems to b

“This is a biggie,” said Eric Kandel, the neuroscientist and Nobel Laureate. “Who thinks of the bone as being an endocrine organ? You think of the adrenal gland, you think of the pituitary, you don’t think of bone.”

he most recent finding concerns the skeleton and the brain.

Karsenty showed that bone plays a direct role in memory and mood. Mice whose skeletons did not produce osteocalcin as a result of genetic manipulation were anxious, depressed, and almost completely unable to master a test of spatial memory. When Karsenty infused them with the missing hormone, however, their moods improved and their performance on the memory test became nearly normal. He also found that, in pregnant mice, osteocalcin from the mother’s bones crossed the placenta and helped shape the development of the fetus’s brain. In other words, bones talk to neurons even before birth.

As we age, our bone mass decreases. Memory loss, anxiety, and depression also become more common. These may be separate, unfortunate facts about getting old, but they could also be related.

Even more fantastically: Would it ever be possible to protect memory or treat age-related cognitive decline with a skeletal hormone? These are the kinds of questions that can spur either false hopes or imaginative leaps.

“I don’t know of any hormone that functions in mice but not to some extent in humans,” Thomas Clemens, of Johns Hopkins, told me in 2011

ne tantalizing hint comes from men who are unable to respond to the hormone as a result of a genetic mutation

Karsenty also believes that we know enough now to recognize that the body is far more networked and interconnected than most people think. “No organ is an island,” he likes to say.

working on more broadly applying [the therapy] to other forms of genetic hearing loss,” he said. But in contrast to VGLUT3 mutant mice, which are missing the protein entirely, humans with missense mutations expressed a defective transporter, making it unclear whether Lustig’s strategy could translate to human VGLUT3-linked deafness.

Taste and smell are two of the senses that have received less attention from gene therapy researchers—but that’s changing

The neurons [in VGLUT3 mutant mice] are waiting for the neurotransmitter to activate them”—but no signal comes, and the mice are profoundly deaf,

Treating the mice intra-nasally with gene therapy vectors carrying the wildtype Ift88 gene, researchers saw significant regrowth of nasal cilia, whereas control mice given empty vectors showed no regrowth. Treated mice almost doubled in weight compared to controls.

So far, no scientists have designed a gene therapy to target taste buds, but at least one team is tackling an important factor in taste: saliva. If a person’s saliva production drops below 50 percent of normal, “you get tooth decay and trouble swallowing,”

Scientists are also developing gene therapies for disorders involving touch—or at least pain-sensing—neurons, with one drug candidate

Wolfe envisions that someday pain treatment could be as simple as visiting the doctor every few months for a quick skin prick “wherever it hurts”—choosing between a variety of genes to get the best effect.

His theory draws upon many of the most prominent views of how humans emerged. These range from our evolution of the ability to run long distances to our development of the earliest weapons, which involved the improvement of hand-eye coordination. Dramatic climate change in Africa over the course of a few tens of thousands of years also may have forced Australopithecus and Homo to adapt rapidly. And over roughly the same span, humans became cooperative hunters and serious meat eaters, vastly enriching our diet and favoring the development of more-robust brains. By themselves, Wilson says, none of these theories is satisfying. Taken together, though, all of these factors pushed our immediate prehuman ancestors toward what he called a huge pre-adaptive step: the formation of the earliest communities around fixed camps.

“When humans started having a camp—and we know that Homo erectus had campsites—then we know they were heading somewhere,” he told me. “They were a group progressively provisioned, sending out some individuals to hunt and some individuals to stay back and guard the valuable campsite. They were no longer just wandering through territory, emitting calls. They were on long-term campsites, maybe changing from time to time, but they had come together. They began to read intentions in each other’s behavior, what each other are doing. They started to learn social connections more solidly.”

“The humans become consistent with all the others,” he said, and the evolutionary steps were likely similar—beginning with the formation of groups within a freely mixing population, followed by the accumulation of pre-adaptations that make eusociality more likely, such as the invention of campsites. Finally comes the rise to prevalence of eusocial alleles—one of two or more alternative forms of a gene that arise by mutation, and are found at the same place on a chromosome—which promote novel behaviors (like communal child care) or suppress old, asocial traits. Now it is up to geneticists, he adds, to “determine how many genes are involved in crossing the eusociality threshold, and to go find those genes.”

Wilson posits that two rival forces drive human behavior: group selection and what he calls “individual selection”—competition at the level of the individual to pass along one’s genes—with both operating simultaneously. “Group selection,” he said, “brings about virtue, and—this is an oversimplification, but—individual selection, which is competing with it, creates sin. That, in a nutshell, is an explanation of the human condition.

“Within groups, the selfish are more likely to succeed,” Wilson told me in a telephone conversation. “But in competition between groups, groups of altruists are more likely to succeed. In addition, it is clear that groups of humans proselytize other groups and accept them as allies, and that that tendency is much favored by group selection.” Taking in newcomers and forming alliances had become a fundamental human trait, he added, because “it is a good way to win.”

If Wilson is right, the human impulse toward racism and tribalism could come to be seen as a reflection of our genetic nature as much as anything else—but so could the human capacity for altruism, and for coalition- and alliance-building. These latter possibilities may help explain Wilson’s abiding optimism—about the environment and many other matters. If these traits are indeed deeply written into our genetic codes, we might hope that we can find ways to emphasize and reinforce them, to build problem-solving coalitions that can endure, and to identify with progressively larger and more-inclusive groups over time.

Large-scale surveys of the genome have led a number of researchers to expect that the human genome will turn out to be even more full of activity than previously thought.

“It was pretty much a case of hubris to imagine that we could dispense with any part of the genome — as if we knew enough to say it wasn’t functional.”

If every piece of the genome were essential, then many of those mutations would lead to significant birth defects, with the defects only multiplying over the course of generations; in less than a century, the species would become extinct.

“Much of what has been called ‘junk DNA’ in the human genome is actually a massive control panel with millions of switches regulating the activity of our genes.”

It’s no coincidence, researchers like Gregory argue, that bona fide creationists have used recent changes in the thinking about junk DNA to try to turn back the clock to the days before Darwin. (The recent studies on noncoding DNA “clearly demonstrate we are ‘fearfully and wonderfully made’ by our Creator God,” declared the Institute for Creation Research.)

Over millions of years, the human genome has spontaneously gotten bigger, swelling with useless copies of genes and new transposable elements.

our immune system should hunt out and destroy mutated cells before they ever develop into cancer. Occasionally, however, these cells manage to sneak under the radar, reproducing until they grow into a full-blown tumour.

For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide — the so-called bliss molecule and our own natural marijuana — in our brains.

Rousseau wrote about “amour-propre,” a kind of self-love based on the opinions of others. He considered it unnatural and unhealthy, and believed that arbitrary social comparison led to people wasting their lives trying to look and sound attractive to others.

Narcissus falls in love not with himself, but with his reflection. In the modern version, Narcissus would fall in love with his own Instagram feed, and starve himself to death while compulsively counting his followers.

If our egos are obese with amour-propre, social media can indeed serve up the empty emotional carbs we crave. Instagram and the like doesn’t create a narcissist, but studies suggest it acts as an accelerant — a near ideal platform to facilitate what psychologists call “grandiose exhibitionism.”

No doubt you have seen this in others, and maybe even a little of it in yourself as you posted a flattering selfie — and then checked back 20 times for “likes.”

A healthy self-love that leads to true happiness is what Rousseau called “amour de soi.” It builds up one’s intrinsic well-being, as opposed to feeding shallow cravings to be admired.

First, take the Narcissistic Personality Inventory test.

Here is an individual self-improvement strategy that combines a healthy self-love (for Valentine’s Day) with a small sacrifice (possibly for Lent).

Cultivating amour de soi requires being fully alive at this moment, as opposed to being virtually alive while wondering what others think. The soulful connection with another person, the enjoyment of a beautiful hike alone (not shared on Facebook) or a prayer of thanks over your sleeping child (absent a #blessed tweet) could be considered expressions of amour de soi.

Second, get rid of the emotional junk food that is feeding any unhealthy self-obsession. Make a list of opinions to disregard — especially those of flatterers and critics — and review the list each day. Resolve not to waste a moment trying to impress others,

Third, go on a social media fast. Post to communicate, praise and learn — never to self-promote.

As for clinically significant narcissism—along with greed, invidious prejudice, and habitual lying—it is simply another one of our anti-social behaviors that mutated from our basic genetic drives…in this case the drive to survive. The opposite of narcissism is empathy, a brain-wiring that evolved much later and in parallel with our increased reliance on social interaction as a means to improve the chances of sending our genes down the line (the drive to reproduce). There is thus a certain irony in the fact that the misnamed “social” media are encouraging a decline in empathy. Your thoughts?

Sure you're not confusing narcissism with vanity? If you've ever had the misfortune of having someone with narcissistic personality disorder in your life, you would know it's about more than selfies and seeking constant approval. They are truly sick individuals that destroy the lives of those they claim to love.I would say people's addictions to social media "likes" and posting selfies is vanity

Perhaps we need to distinguish between Narcissistic Personality Disorder (NPD) and the adjective "narcissistic." We all know lots of people with way too much self-regard. NPD on the other hand ruins lives and certainly families. People who have NPD are way beyond self centered. They see the world as black and white and all people they interact with become reflections. People with NPD go to extreme lengths to control those around them and will lie, cheat and steal to do that. They are never wrong the other person is always wrong. I have worked for Narcissists and lived with one. Let's not throw around this term without defining it, please.

The researchers note that only a few modifier genes of disease mutations such as Ankrd16 have been identified and a modifier-based mechanism for understanding the underlying pathology of neurodegenerative diseases may be a promising route to understand disease development.

One way alcohol may lead to cancer is because the body metabolizes it into acetaldehyde, which causes changes and mutations in DNA, Dr. Gapstur said. The formation of acetaldehyde starts when alcohol comes in contact with bacteria in the mouth, which may explain the link between alcohol and cancers of the throat, voice box and esophagus

A major concern with any type of gene therapy is that the inserted genetic material could have dangerous side effects, like turning off an essential gene or turning on one that could lead to cancer.

Globally, the numbers can be even worse, and the stakes often higher. “Say a person comes into the hospital in Sierra Leone with a fever and flulike symptoms,” DeRisi says. “After a few days, or a week, they die. What caused that illness? Most of the time, we never find out. Because if the cause isn’t something that we can culture and test for” — like hepatitis, or strep throat — “it basically just stays a mystery.”

It would be better, DeRisi says, to watch for rare cases of mystery illnesses in people, which often exist well before a pathogen gains traction and is able to spread.

Based on a retrospective analysis of blood samples, scientists now know that H.I.V. emerged nearly a dozen times over a century, starting in the 1920s, before it went global.

Zika was a relatively harmless illness before a single mutation, in 2013, gave the virus the ability to enter and damage brain cells.

The beauty of this approach” — running blood samples from people hospitalized all over the world through his system, known as IDseq — “is that it works even for things that we’ve never seen before, or things that we might think we’ve seen but which are actually something new.”

In this scenario, an undiscovered or completely new virus won’t trigger a match but will instead be flagged. (Even in those cases, the mystery pathogen will usually belong to a known virus family: coronaviruses, for instance, or filoviruses that cause hemorrhagic fevers like Ebola and Marburg.)

And because different types of bacteria require specific conditions in order to grow, you also need some idea of what you’re looking for in order to find it.

The same is true of genomic sequencing, which relies on “primers” designed to match different combinations of nucleotides (the building blocks of DNA and RNA).

Even looking at a slide under a microscope requires staining, which makes organisms easier to see — but the stains used to identify bacteria and parasites, for instance, aren’t the same.

The practice that DeRisi helped pioneer to skirt this problem is known as metagenomic sequencing

Unlike ordinary genomic sequencing, which tries to spell out the purified DNA of a single, known organism, metagenomic sequencing can be applied to a messy sample of just about anything — blood, mud, seawater, snot — which will often contain dozens or hundreds of different organisms, all unknown, and each with its own DNA. In order to read all the fragmented genetic material, metagenomic sequencing uses sophisticated software to stitch the pieces together by matching overlapping segments.

The assembled genomes are then compared against a vast database of all known genomic sequences — maintained by the government-run National Center for Biotechnology Information — making it possible for researchers to identify everything in the mix

Traditionally, the way that scientists have identified organisms in a sample is to culture them: Isolate a particular bacterium (or virus or parasite or fungus); grow it in a petri dish; and then examine the result under a microscope, or use genomic sequencing, to understand just what it is. But because less than 2 percent of bacteria — and even fewer viruses — can be grown in a lab, the process often reveals only a tiny fraction of what’s actually there. It’s a bit like planting 100 different kinds of seeds that you found in an old jar. One or two of those will germinate and produce a plant, but there’s no way to know what the rest might have grown into.

Such studies have revealed just how vast the microbial world is, and how little we know about it

“The selling point for researchers is: ‘Look, this technology lets you investigate what’s happening in your clinic, whether it’s kids with meningitis or something else,’” DeRisi said. “We’re not telling you what to do with it. But it’s also true that if we have enough people using this, spread out all around the world, then it does become a global network for detecting emerging pandemics

One study found more than 1,000 different kinds of viruses in a tiny amount of human stool; another found a million in a couple of pounds of marine sediment. And most were organisms that nobody had seen before.

After the Biohub opened in 2016, one of DeRisi’s goals was to turn metagenomics from a rarefied technology used by a handful of elite universities into something that researchers around the world could benefit from

metagenomics requires enormous amounts of computing power, putting it out of reach of all but the most well-funded research labs. The tool DeRisi created, IDseq, made it possible for researchers anywhere in the world to process samples through the use of a small, off-the-shelf sequencer, much like the one DeRisi had shown me in his lab, and then upload the results to the cloud for analysis.

he’s the first to make the process so accessible, even in countries where lab supplies and training are scarce. DeRisi and his team tested the chemicals used to prepare DNA for sequencing and determined that using as little as half the recommended amount often worked fine. They also 3-D print some of the labs’ tools and replacement parts, and offer ongoing training and tech support

The metagenomic analysis itself — normally the most expensive part of the process — is provided free.

But DeRisi’s main innovation has been in streamlining and simplifying the extraordinarily complex computational side of metagenomics

IDseq is also fast, capable of doing analyses in hours that would take other systems weeks.

“What IDseq really did was to marry wet-lab work — accumulating samples, processing them, running them through a sequencer — with the bioinformatic analysis,”

“Without that, what happens in a lot of places is that the researcher will be like, ‘OK, I collected the samples!’ But because they can’t analyze them, the samples end up in the freezer. The information just gets stuck there.”

Meningitis itself isn’t a disease, just a description meaning that the tissues around the brain and spinal cord have become inflamed. In the United States, bacterial infections can cause meningitis, as can enteroviruses, mumps and herpes simplex. But a high proportion of cases have, as doctors say, no known etiology: No one knows why the patient’s brain and spinal tissues are swelling.

When Saha and her team ran the mystery meningitis samples through IDseq, though, the result was surprising. Rather than revealing a bacterial cause, as expected, a third of the samples showed signs of the chikungunya virus — specifically, a neuroinvasive strain that was thought to be extremely rare. “At first we thought, It cannot be true!” Saha recalls. “But the moment Joe and I realized it was chikungunya, I went back and looked at the other 200 samples that we had collected around the same time. And we found the virus in some of those samples as well.”

Until recently, chikungunya was a comparatively rare disease, present mostly in parts of Central and East Africa. “Then it just exploded through the Caribbean and Africa and across Southeast Asia into India and Bangladesh,” DeRisi told me. In 2011, there were zero cases of chikungunya reported in Latin America. By 2014, there were a million.

Chikungunya is a mosquito-borne virus, but when DeRisi and Saha looked at the results from IDseq, they also saw something else: a primate tetraparvovirus. Primate tetraparvoviruses are almost unknown in humans, and have been found only in certain regions. Even now, DeRisi is careful to note, it’s not clear what effect the virus has on people. “Maybe it’s dangerous, maybe it isn’t,” DeRisi says. “But I’ll tell you what: It’s now on my radar.

it reveals a landscape of potentially dangerous viruses that we would otherwise never find out about. “What we’ve been missing is that there’s an entire universe of pathogens out there that are causing disease in humans,” Imam notes, “ones that we often don’t even know exist.”

“The plan was, Let’s let researchers around the world propose studies, and we’ll choose 10 of them to start,” DeRisi recalls. “We thought we’d get, like, a couple dozen proposals, and instead we got 350.”

Metagenomic sequencing is especially good at what scientists call “environmental sampling”: identifying, say, every type of bacteria present in the gut microbiome, or in a teaspoon of seawater.

“When you draw blood from someone who has a fever in Ghana, you really don’t know very much about what would normally be in their blood without fever — let alone about other kinds of contaminants in the environment. So how do you interpret the relevance of all the things you’re seeing?”

Such criticisms have led some to say that metagenomics simply isn’t suited to the infrastructure of developing countries. Along with the problem of contamination, many labs struggle to get the chemical reagents needed for sequencing, either because of the cost or because of shipping and customs holdups

we’re less likely to be caught off-guard. “With Ebola, there’s always an issue: Where’s the virus hiding before it breaks out?” DeRisi explains. “But also, once we start sampling people who are hospitalized more widely — meaning not just people in Northern California or Boston, but in Uganda, and Sierra Leone, and Indonesia — the chance of disastrous surprises will go down. We’ll start seeing what’s hidden.”

In contrast to a previous study6, they observed a robust lifespan extension in male mice fed a BCAA-restricted diet throughout life, equal to the benefits of dietary protein restriction.

Interestingly, female mice showed no lifespan extension from BCAA or dietary protein restriction, and if BCAA restriction was started during middle age, the benefits on males were greatly reduced. Thus, both studies collectively point to mTOR as a primary mediator of the benefits associated with BCAA restriction (Fig. 1).

A clear picture is emerging of how specific amino acids are sensed by sestrin to regulate mTOR signalling and autophagy and so preserve the function of intestinal stem cells during ageing.

Genetic background is crucial in the response to dietary restriction, with an identical low-calorie regimen increasing lifespan in some mouse strains but shortening it in others

There is also evidence that dietary restriction initiated later in life might have reduced benefits in rodents and, in some cases, result in premature death

Taken together, these observations suggest that although protein- and BCAA-restricted diets are a powerful research tool for exploring the fundamental mechanisms of ageing, it is premature to recommend adoption by the general population.

Makeshift morgues have been set up across the state, ICUs are full, oxygen is being rationed and ambulance teams have been told not to transport those unlikely to survive the night because hospitals are too full.

Disneyland, which has been closed since March, is now being turned into a massive vaccination centre

And like most places, Covid-19 has hit Los Angeles' poor the hardest.

For every case of Covid in Beverly Hills, there are six times more in Compton. While two people from Bel Air have died, more than 230 people have lost their lives in working-class East LA.

As the virus spreads, it's likely mutating more than we know, says Dr Neha Nanda."Maybe the bigger the place, the more variation," she says.

Animal communication systems, in contrast, typically have at most a few dozen distinct calls, and they are used only to communicate immediate issues such as food, danger, threat, or reconciliation. Many of the sorts of meanings conveyed by chimpanzee communication have counterparts in human 'body language'.

The basic difficulty with studying the evolution of language is that the evidence is so sparse. Spoken languages don't leave fossils, and fossil skulls only tell us the overall shape and size of hominid brains, not what the brains could do

All present-day languages, including those of hunter-gatherer cultures, have lots of words, can be used to talk about anything under the sun, and can express negation. As far back as we have written records of human language - 5000 years or so - things look basically the same.

According to current thinking, the changes crucial for language were not just in the size of the brain, but in its character: the kinds of tasks it is suited to do - as it were, the 'software' it comes furnished with.

So the properties of human language are unique in the natural world.

About the only definitive evidence we have is the shape of the vocal tract (the mouth, tongue, and throat): Until anatomically modern humans, about 100,000 years ago, the shape of hominid vocal tracts didn't permit the modern range of speech sounds. But that doesn't mean that language necessarily began the

Some researchers even propose that language began as sign language, then (gradually or suddenly) switched to the vocal modality, leaving modern gesture as a residue.

. In an early stage, sounds would have been used to name a wide range of objects and actions in the environment, and individuals would be able to invent new vocabulary items to talk about new things

In order to achieve a large vocabulary, an important advance would have been the ability to 'digitize' signals into sequences of discrete speech sounds - consonants and vowels - rather than unstructured calls.

These two changes alone would yield a communication system of single signals - better than the chimpanzee system but far from modern language. A next plausible step would be the ability to string together several such 'words' to create a message built out of the meanings of its parts.

This has led some researchers to propose that the system of 'protolanguage' is still present in modern human brains, hidden under the modern system except when the latter is impaired or not yet developed.

Again, it's very hard to tell. We do know that something important happened in the human line between 100,000 and 50,000 years ago: This is when we start to find cultural artifacts such as art and ritual objects, evidence of what we would call civilization.

One tantalizing source of evidence has emerged recently. A mutation in a gene called FOXP2 has been shown to lead to deficits in language as well as in control of the face and mouth. This gene is a slightly altered version of a gene found in apes, and it seems to have achieved its present form between 200,000 and 100,000 years ago.

Nevertheless, if we are ever going to learn more about how the human language ability evolved, the most promising evidence will probably come from the human genome, which preserves so much of our species' history. The challenge for the future will be to decode it.