By Stephanie Pappas

The Big Bang is commonly thought of as the start of it all: About 13.8 billion years ago, the observable universe went boom and expanded into being.

But what were things like before the Big Bang?

Short answer: We don’t know. Long answer: It could have been a lot of things, each mind-bending in its own way.

The first thing to understand is what the Big Bang actually was.

“The Big Bang is a moment in time, not a point in space,” said Sean Carroll, a theoretical physicist at the California Institute of Technology and author of “The Big Picture: On the Origins of Life, Meaning and the Universe Itself” (Dutton, 2016).

So, scrap the image of a tiny speck of dense matter suddenly exploding outward into a void. For one thing, the universe at the Big Bang may not have been particularly small, Carroll said. Sure, everything in the observable universe today — a sphere with a diameter of about 93 billion light-years containing at least 2 trillion galaxies — was crammed into a space less than a centimeter across. But there could be plenty outside of the observable universe that Earthlings can’t see because it’s physically impossible for the light to have traveled that far in 13.8 billion years.
Thus, it’s possible that the universe at the Big Bang was teeny-tiny or infinitely large, Carroll said, because there’s no way to look back in time at the stuff we can’t even see today. All we really know is that it was very, very dense and that it very quickly got less dense.

As a corollary, there really isn’t anything outside the universe, because the universe is, by definition, everything. So, at the Big Bang, everything was denser and hotter than it is now, but there was no more an “outside” of it than there is today. As tempting as it is to take a godlike view and imagine you could stand in a void and look at the scrunched-up baby universe right before the Big Bang, that would be impossible, Carroll said. The universe didn’t expand into space; space itself expanded.

“No matter where you are in the universe, if you trace yourself back 14 billion years, you come to this point where it was extremely hot, dense and rapidly expanding,” he said.

No one knows exactly what was happening in the universe until 1 second after the Big Bang, when the universe cooled off enough for protons and neutrons to collide and stick together. Many scientists do think that the universe went through a process of exponential expansion called inflation during that first second. This would have smoothed out the fabric of space-time and could explain why matter is so evenly distributed in the universe today.

Before the bang

It’s possible that before the Big Bang, the universe was an infinite stretch of an ultrahot, dense material, persisting in a steady state until, for some reason, the Big Bang occured. This extra-dense universe may have been governed by quantum mechanics, the physics of the extremely small scale, Carroll said. The Big Bang, then, would have represented the moment that classical physics took over as the major driver of the universe’s evolution.

For Stephen Hawking, this moment was all that mattered: Before the Big Bang, he said, events are unmeasurable, and thus undefined. Hawking called this the no-boundary proposal: Time and space, he said, are finite, but they don’t have any boundaries or starting or ending points, the same way that the planet Earth is finite but has no edge.

“Since events before the Big Bang have no observational consequences, one may as well cut them out of the theory and say that time began at the Big Bang,” he said in an interview on the National Geographic show “StarTalk” in 2018.

Or perhaps there was something else before the Big Bang that’s worth pondering. One idea is that the Big Bang isn’t the beginning of time, but rather that it was a moment of symmetry. In this idea, prior to the Big Bang, there was another universe, identical to this one but with entropy increasing toward the past instead of toward the future.

Increasing entropy, or increasing disorder in a system, is essentially the arrow of time, Carroll said, so in this mirror universe, time would run opposite to time in the modern universe and our universe would be in the past. Proponents of this theory also suggest that other properties of the universe would be flip-flopped in this mirror universe. For example, physicist David Sloan wrote in the University of Oxford Science Blog, asymmetries in molecules and ions (called chiralities) would be in opposite orientations to what they are in our universe.

A related theory holds that the Big Bang wasn’t the beginning of everything, but rather a moment in time when the universe switched from a period of contraction to a period of expansion. This “Big Bounce” notion suggests that there could be infinite Big Bangs as the universe expands, contracts and expands again. The problem with these ideas, Carroll said, is that there’s no explanation for why or how an expanding universe would contract and return to a low-entropy state.

Carroll and his colleague Jennifer Chen have their own pre-Big Bang vision. In 2004, the physicists suggested that perhaps the universe as we know it is the offspring of a parent universe from which a bit of space-time has ripped off.

It’s like a radioactive nucleus decaying, Carroll said: When a nucleus decays, it spits out an alpha or beta particle. The parent universe could do the same thing, except instead of particles, it spits out baby universes, perhaps infinitely. “It’s just a quantum fluctuation that lets it happen,” Carroll said. These baby universes are “literally parallel universes,” Carroll said, and don’t interact with or influence one another.

If that all sounds rather trippy, it is — because scientists don’t yet have a way to peer back to even the instant of the Big Bang, much less what came before it. There’s room to explore, though, Carroll said. The detection of gravitational waves from powerful galactic collisions in 2015 opens the possibility that these waves could be used to solve fundamental mysteries about the universes’ expansion in that first crucial second.

Theoretical physicists also have work to do, Carroll said, like making more-precise predictions about how quantum forces like quantum gravity might work.

“We don’t even know what we’re looking for,” Carroll said, “until we have a theory.”

https://www.livescience.com/65254-what-happened-before-big-big.html

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by Linda Geddes

You need only to look at families to see that height is inherited — and studies of identical twins and families have long confirmed that suspicion. About 80% of variation in height is down to genetics, they suggest. But since the human genome was sequenced nearly two decades ago, researchers have struggled to fully identify the genetic factors responsible.

Studies seeking the genes that govern height have identified hundreds of common gene variants linked to the trait. But the findings also posed a quandry: each variant had a tiny effect on height that together didn’t amount to the genetic contribution predicted by family studies. This phenomenon, which occurs for many other traits and diseases, was dubbed missing heritability, and had even prompted some researchers to speculate that there’s something fundamentally wrong with our understanding of genetics.

Now, a study suggests that most of the missing heritability for height and body mass index (BMI) can, as some researchers had suspected, be found in rarer gene variants that had lain undiscovered until now.

“It is a reassuring paper because it suggests that there isn’t something terribly wrong with genetics,” says Tim Spector, a genetic epidemiologist at King’s College London. “It’s just that sorting it out is more complex than we thought.” The research was posted1 to the bioRxiv preprint server on 25 March.

Scouring the genome

To seek out the genetic factors that underlie diseases and traits, geneticists turn to mega-searches known as genome-wide association studies (GWAS). These scour the genomes of, typically, tens of thousands of people — or, increasingly, more than a million — for single-letter changes, or SNPs, in genes that commonly appear in individuals with a particular disease or that could explain a common trait such as height.

But GWAS have limitations. Because sequencing the entire genomes of thousands of people is expensive, GWAS themselves scan only a strategically selected set of SNPs, perhaps 500,000, in each person’s genome. That’s only a snapshot of the roughly six billion nucleotides — the building blocks of DNA — strung together in our genome. In turn, these 500,000 common variants would have been found from sequencing the genomes of just a few hundred people, says Timothy Frayling, a human geneticist at the University of Exeter, UK.

A team led by Peter Visscher at the Queensland Brain Institute in Brisbane, Australia, decided to investigate whether rarer SNPs than those typically scanned in GWAS might explain the missing heritability for height and BMI. They turned to whole-genome sequencing — performing a complete readout of all 6 billion bases — of 21,620 people. (The authors declined to comment on the preprint, because it is under submission at a journal.)

They relied on the simple, but powerful, principle that all people are related to some extent — albeit distantly — and that DNA can be used to calculate degrees of relatedness. Then, information on the people’s height and BMI could be combined to identify both common and rare SNPs that might be contributing to these traits.

Say, for instance, that a pair of third cousins is closer in height than a pair of second cousins is in a different family: that’s an indication that the third cousins’ height is mostly down to genetics, and the extent of that correlation will tell you how much, Frayling explains. “They used all of the genetic information, which enables you to work out how much of the relatedness was due to rarer things as well as the common things.”

As a result, the researchers captured genetic differences that occur in only 1 in 500, or even 1 in 5,000, people.

And by using information on both common and rare variants, the researchers arrived at roughly the same estimates of heritability as those indicated by twin studies. For height, Visscher and colleagues estimate a heritability of 79%, and for BMI, 40%. This means that if you take a large group of people, 79% of the height differences would be due to genes rather than to environmental factors, such as nutrition.

Complex processes

The researchers also suggest how the previously undiscovered variants might be contributing to physical traits. Tentatively, they found that these rare variants were slightly enriched in protein-coding regions of the genome, and that they had an increased likelihood of being disruptive to these regions, notes Terence Capellini, an evolutionary biologist at Harvard University in Cambridge, Massachusetts. This indicates that the rare variants might partly influence height by affecting protein-coding regions instead of the rest of the genome — the vast majority of which does not include instructions for making proteins, but might influence their expression.

The rarity of the variants also suggests that natural selection could be weeding them out, perhaps because they are harmful in some way.

The complexity of heritability means that understanding the roots of many common diseases — necessary if researchers are to develop effective therapies against them — will take considerably more time and money, and it could involve sequencing hundreds of thousands or even millions of whole genomes to identify the rare variants that explain a substantial portion of the illnesses’ genetic components.

The study reveals only the total amount of rare variants contributing to these common traits — not which ones are important, says Spector. “The next stage is to go and work out which of these rare variants are important for traits or diseases that you want to get a drug for.”

Nature 568, 444-445 (2019)

doi: 10.1038/d41586-019-01157-y

https://www.nature.com/articles/d41586-019-01157-y?utm_source=Nature+Briefing&utm_campaign=26855a4182-briefing-dy-20190424&utm_medium=email&utm_term=0_c9dfd39373-26855a4182-44039353

Having a go on your PlayStation, going to the cinema with your friends, playing outdoors — that’s how the spare time of most 12-year-old children looks.

That’s not how it is for Jackson Oswalt though. Two years ago, the now 14-year-old achieved something even some of the most renowned scientists have been unable to: he carried out nuclear fusion, in his parent’s garage in Texarkana, Ark.

“One day I had a sudden epiphany,” wrote the teen on amateur physicist forum, Fusor. “I realized that I could be the absolute best at whatever video game, but in the end it still wouldn’t mean much. I realized that, in the grand scheme of things, video games had no role to play.”

It was at this point that he decided to dedicate himself to science and to pursue a new hobby — nuclear fusion.

While other children want a bicycle or a game console for their birthday or Christmas, Oswalt ordered the parts he needed for a nuclear reactor from eBay.

Instead of watching videos of gamers, Oswalt would watch physics videos — his parents agreed to give him financial support if he promised to first check through expert guidelines on a forum and to pay attention to their tips and advice.

They spent somewhere between $8,000 and $10,000 collecting the parts he needed to build his nuclear reactor, and also footed a bill for 50,000 volts and radioactive radiation.

Using Open Source Fusor Research Consortium— an online forum for amateur physicists — Oswalt relied on trial and error to ensure he was taking the appropriate measures to build a reactor and successfully carry out fusion reactions.

According to Fox News, just before his thirteenth birthday in early 2018, Oswalt finally succeeded in what he’d been working towards for such a long time — a nuclear fusion reactor.

“Being a parent of someone that was as driven as he was for 12 months was really impressive to see. I mean it was everyday grinding; every day learning something different; every day failing and watching him work through all those things,” said his father, Chris Oswalt.

Whether Oswalt is actually the youngest person ever to have succeeded in doing something like this now needs to be confirmed by experts.

In addition to a world record title, Oswalt may also be given a letter of recommendation from his school for a scholarship.

In the meantime, however, he still has some plans: he wants to build an even bigger nuclear reactor.

https://www.businessinsider.com/12-year-old-builds-nuclear-reactor-at-home-with-equipment-from-ebay-2019-4

By Saskya Vandoorne and Gianluca Mezzofiore

The bees that live on the roof of Notre Dame are alive and buzzing, having survived the devastating fire that ripped through the cathedral on Monday, the beekeeper Nicolas Geant confirmed to CNN.

“I got a call from Andre Finot, the spokesman for Notre Dame, who said there were bees flying in and out of the hives which means they are still alive!” Geant said. “Right after the fire I looked at the drone pictures and saw the hives weren’t burnt but there was no way of knowing if the bees had survived. Now I know there’s activity it’s a huge relief!”

Notre Dame has housed three beehives on the first floor on a roof over the sacristy, just beneath the rose window, since 2013. Each hive has about 60,000 bees.

Geant said the hives were not touched by the blaze because they are located about 30 meters below the main roof where the fire spread.

“They weren’t in the middle of the fire, had they been they wouldn’t have survived,” Geant said. “The hives are made of wood so they would have gone up in flames.”
“Wax melts at 63 degrees, if the hive had reached that temperature the wax would have melted and glued the bees together, they would have all perished.”

While it is likely that the hives were filled with smoke, that doesn’t impact them like it would with humans, Geant explained.
“Bees don’t have lungs like us,” he said. “And secondly, for centuries to work with the bees we have used bee smokers.”

A bee smoker is a box with bellows which creates a white, thick cold smoke in the hives, prompting the bees to calmly gorge on the honey while beekeepers do their work, Geant said.

Geant said he wouldn’t be able tell whether all of the bees are alive until he was able to inspect the site, but he’s confident because the hives didn’t burn, and because bees have been spotted flying in and out.

“I was incredibly sad about Notre Dame because it’s such a beautiful building, and as a catholic it means a lot to me. But to hear there is life when it comes to the bees, that’s just wonderful. I was overjoyed,” he added.

“Thank goodness the flames didn’t touch them. It’s a miracle!”

https://edition.cnn.com/2019/04/19/europe/notre-dame-bees-fire-intl-scli/index.html

Williams Syndrome, a rare neurodevelopmental disorder that affects about one in 10,000 babies born in the United States, produces a range of symptoms including cognitive impairments, cardiovascular problems, and extreme friendliness, or hypersociability.

In a study of mice, MIT neuroscientists have garnered new insight into the molecular mechanisms that underlie this hypersociability. They found that loss of one of the genes linked to Williams Syndrome leads to a thinning of the fatty layer that insulates neurons and helps them conduct electrical signals in the brain.

The researchers also showed that they could reverse the symptoms by boosting production of this coating, known as myelin. This is significant, because while Williams Syndrome is rare, many other neurodevelopmental disorders and neurological conditions have been linked to myelination deficits, says Guoping Feng, the James W. and Patricia Poitras Professor of Neuroscience and a member of MIT’s McGovern Institute for Brain Research.

“The importance is not only for Williams Syndrome,” says Feng, who is one of the senior authors of the study. “In other neurodevelopmental disorders, especially in some of the autism spectrum disorders, this could be potentially a new direction to look into, not only the pathology but also potential treatments.”

Zhigang He, a professor of neurology and ophthalmology at Harvard Medical School, is also a senior author of the paper, which appears in the April 22 issue of Nature Neuroscience. Former MIT postdoc Boaz Barak, currently a principal investigator at Tel Aviv University in Israel, is the lead author and a senior author of the paper.

Impaired myelination

Williams Syndrome, which is caused by the loss of one of the two copies of a segment of chromosome 7, can produce learning impairments, especially for tasks that require visual and motor skills, such as solving a jigsaw puzzle. Some people with the disorder also exhibit poor concentration and hyperactivity, and they are more likely to experience phobias.

In this study, the researchers decided to focus on one of the 25 genes in that segment, known as Gtf2i. Based on studies of patients with a smaller subset of the genes deleted, scientists have linked the Gtf2i gene to the hypersociability seen in Williams Syndrome.

Working with a mouse model, the researchers devised a way to knock out the gene specifically from excitatory neurons in the forebrain, which includes the cortex, the hippocampus, and the amygdala (a region important for processing emotions). They found that these mice did show increased levels of social behavior, measured by how much time they spent interacting with other mice. The mice also showed deficits in fine motor skills and increased nonsocial related anxiety, which are also symptoms of Williams Syndrome.

Next, the researchers sequenced the messenger RNA from the cortex of the mice to see which genes were affected by loss of Gtf2i. Gtf2i encodes a transcription factor, so it controls the expression of many other genes. The researchers found that about 70 percent of the genes with significantly reduced expression levels were involved in the process of myelination.

“Myelin is the insulation layer that wraps the axons that extend from the cell bodies of neurons,” Barak says. “When they don’t have the right properties, it will lead to faster or slower electrical signal transduction, which affects the synchronicity of brain activity.”

Further studies revealed that the mice had only about half the normal number of mature oligodendrocytes—the brain cells that produce myelin. However, the number of oligodendrocyte precursor cells was normal, so the researchers suspect that the maturation and differentiation processes of these cells are somehow impaired when Gtf2i is missing in the neurons.

This was surprising because Gtf2i was not knocked out in oligodendrocytes or their precursors. Thus, knocking out the gene in neurons may somehow influence the maturation process of oligodendrocytes, the researchers suggest. It is still unknown how this interaction might work.

“That’s a question we are interested in, but we don’t know whether it’s a secreted factor, or another kind of signal or activity,” Feng says.

In addition, the researchers found that the myelin surrounding axons of the forebrain was significantly thinner than in normal mice. Furthermore, electrical signals were smaller, and took more time to cross the brain in mice with Gtf2i missing.

Symptom reversal

It remains to be discovered precisely how this reduction in myelination leads to hypersociability. The researchers suspect that the lack of myelin affects brain circuits that normally inhibit social behaviors, making the mice more eager to interact with others.

“That’s probably the explanation, but exactly which circuits and how does it work, we still don’t know,” Feng says.

The researchers also found that they could reverse the symptoms by treating the mice with drugs that improve myelination. One of these drugs, an FDA-approved antihistamine called clemastine fumarate, is now in clinical trials to treat multiple sclerosis, which affects myelination of neurons in the brain and spinal cord. The researchers believe it would be worthwhile to test these drugs in Williams Syndrome patients because they found thinner myelin and reduced numbers of mature oligodendrocytes in brain samples from human subjects who had Williams Syndrome, compared to typical human brain samples.

“Mice are not humans, but the pathology is similar in this case, which means this could be translatable,” Feng says. “It could be that in these patients, if you improve their myelination early on, it could at least improve some of the conditions. That’s our hope.”

Such drugs would likely help mainly the social and fine-motor issues caused by Williams Syndrome, not the symptoms that are produced by deletion of other genes, the researchers say. They may also help treat other disorders, such as autism spectrum disorders, in which myelination is impaired in some cases, Feng says.

“We think this can be expanded into autism and other neurodevelopmental disorders. For these conditions, improved myelination may be a major factor in treatment,” he says. “We are now checking other animal models of neurodevelopmental disorders to see whether they have myelination defects, and whether improved myelination can improve some of the pathology of the defects.”

More information: Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drug, Nature Neuroscience (2019). DOI: 10.1038/s41593-019-0380-9 , https://www.nature.com/articles/s41593-019-0380-9

https://medicalxpress.com/news/2019-04-neuroscientists-reverse-behavioral-symptoms-williams.html

by Lindsey Valich

Explorers have dreamt for centuries of a Fountain of Youth, with healing waters that rejuvenate the old and extend life indefinitely.

Researchers at the University of Rochester, however, have uncovered more evidence that the key to longevity resides instead in a gene.

In a new paper published in the journal Cell, the researchers—including Vera Gorbunova and Andrei Seluanov, professors of biology; Dirk Bohmann, professor of biomedical genetics; and their team of students and postdoctoral researchers—found that the gene sirtuin 6 (SIRT6) is responsible for more efficient DNA repair in species with longer lifespans. The research illuminates new targets for anti-aging interventions and could help prevent age-related diseases.

Inevitable double-strand breaks

As humans and other mammals grow older, their DNA is increasingly prone to breaks, which can lead to gene rearrangements and mutations—hallmarks of cancer and aging. For that reason, researchers have long hypothesized that DNA repair plays an important role in determining an organism’s lifespan. While behaviors like smoking can exacerbate double-strand breaks (DSBs) in DNA, the breaks themselves are unavoidable. “They are always going to be there, even if you’re super healthy,” says Bohmann. “One of the main causes of DSBs is oxidative damage and, since we need oxygen to breathe, the breaks are inevitable.”

Organisms like mice have a smaller chance of accumulating double-strand breaks in their comparatively short lives, versus organisms with longer lifespans, Bohmann says. “But, if you want to live for 50 years or so, there’s more of a need to put a system into place to fix these breaks.”

The longevity gene

SIRT6 is often called the “longevity gene” because of its important role in organizing proteins and recruiting enzymes that repair broken DNA; additionally, mice without the gene age prematurely, while mice with extra copies live longer. The researchers hypothesized that if more efficient DNA repair is required for a longer lifespan, organisms with longer lifespans may have evolved more efficient DNA repair regulators. Is SIRT6 activity therefore enhanced in longer-lived species?

To test this theory, the researchers analyzed DNA repair in 18 rodent species with lifespans ranging from 3 years (mice) to 32 years (naked mole rats and beavers). They found that the rodents with longer lifespans also experience more efficient DNA repair because the products of their SIRT6 genes—the SIRT6 proteins—are more potent. That is, SIRT6 is not the same in every species. Instead, the gene has co-evolved with longevity, becoming more efficient so that species with a stronger SIRT6 live longer. “The SIRT6 protein seems to be the dominant determinant of lifespan,” Bohmann says. “We show that at the cell level, the DNA repair works better, and at the organism level, there is an extended lifespan.”

The researchers then analyzed the molecular differences between the weaker SIRT6 protein found in mice versus the stronger SIRT6 found in beavers. They identified five amino acids responsible for making the stronger SIRT6 protein “more active in repairing DNA and better at enzyme functions,” Gorbunova says. When the researchers inserted beaver and mouse SIRT6 into human cells, the beaver SIRT6 better reduced stress-induced DNA damage compared to when researchers inserted the mouse SIRT6. The beaver SIRT6 also better increased the lifespan of fruit flies versus fruit flies with mouse SIRT6.

Species with even more robust SIRT6?

Although it appears that human SIRT6 is already optimized to function, “we have other species that are even longer lived than humans,” Seluanov says. Next steps in the research involve analyzing whether species that have longer lifespans than humans—like the bowhead whale, which can live more than 200 years—have evolved even more robust SIRT6 genes.

The ultimate goal is to prevent age-related diseases in humans, Gorbunova says. “If diseases happen because of DNA that becomes disorganized with age, we can use research like this to target interventions that can delay cancer and other degenerative diseases.”

https://phys.org/news/2019-04-longevity-gene-responsible-efficient-dna.html

By Mindy Weisberger

Organizers of an annual conference that brings together people who believe that the Earth is flat are planning a cruise to the purported edge of the planet. They’re looking for the ice wall that holds back the oceans.

The journey will take place in 2020, the Flat Earth International Conference (FEIC) recently announced on its website. The goal? To test so-called flat-Earthers’ assertion that Earth is a flattened disk surrounded at its edge by a towering wall of ice.

Details about the event, including the dates, are forthcoming, according to the FEIC, which calls the cruise “the biggest, boldest adventure yet.” However, it’s worth noting that nautical maps and navigation technologies such as global positioning systems (GPS) work as they do because the Earth is … a globe.

Believers in a flat Earth argue that images showing a curved horizon are fake and that photos of a round Earth from space are part of a vast conspiracy perpetrated by NASA and other space agencies to hide Earth’s flatness. These and other flat-Earth assertions appear on the website of the Flat Earth Society (FES), allegedly the world’s oldest official flat Earth organization, dating to the early 1800s.

However, the ancient Greeks demonstrated that Earth was a sphere more than 2,000 years ago, and the gravity that keeps everything on the planet from flying off into space could exist only on a spherical world.

But in diagrams shared on the FES website, the planet appears as a pancake-like disk with the North Pole smack in the center and an edge “surrounded on all sides by an ice wall that holds the oceans back.” This ice wall — thought by some flat-Earthers to be Antarctica — is the destination of the promised FEIC cruise.

There’s just one catch: Navigational charts and systems that guide cruise ships and other vessels around Earth’s oceans are all based on the principle of a round Earth, Henk Keijer, a former cruise ship captain with 23 years of experience, told The Guardian.

GPS relies on a network of dozens of satellites orbiting thousands of miles above Earth; signals from the satellites beam down to the receiver inside of a GPS device, and at least three satellites are required to pinpoint a precise position because of Earth’s curvature, Keijer explained.

“Had the Earth been flat, a total of three satellites would have been enough to provide this information to everyone on Earth,” Keijer said. “But it is not enough, because the Earth is round.”

Whether or not the FEIC cruise will rely on GPS or deploy an entirely new flat-Earth-based navigation system for finding the end of the world, remains to be seen.

https://www.livescience.com/65053-flat-earther-cruise-antarctica-ice-wall.html?utm_source=ls-newsletter&utm_medium=email&utm_campaign=20190422-ls