Posts Tagged ‘science’

by Laura Elizabeth Mason

Elephants have developed a way to resist cancer, by resurrecting a ‘zombie’ gene known as leukemia inhibitory factor 6 (LIF6). Activated LIF6 responds to damaged DNA and efficiently kills cells that are destined to become cancer cells.

Cancer is a complex genetic disease that is caused by specific changes to the genes in one cell or group of cells. These genetic alterations cause the cell to divide uncontrollably. If all mammalian cells were equally susceptible to the genetic mutations that cause cancer, then theoretically the risk of developing cancer should be greater in larger animals – due to them having more cells and a longer life-span. However, previous studies have demonstrated that elephants have a lower-than-expected rate of cancer, compared to other mammals.

“Elephants get cancer far less than we’d expect based on their size, so we want to understand the genetic basis for this cancer resistance,” said senior author Vincent Lynch from the University of Chicago, in a recent press release.

“We found that elephants and their relatives have many non-functioning copies of the LIF gene, but that elephants themselves evolved a way to turn one of these copies, LIF6, back on.”

p53 wakes up LIF6

The TP53 gene is found in all animals, it codes for the protein p53, a tumor suppressor, that stops cells with damaged DNA from dividing. Unlike humans, who only have one copy of TP53, elephants have 20. An increased number of TP53 genes enhances the DNA-damage response, providing elephants with a distinct advantage – they are able to either repair the damaged cells or ‘kill off’ irreparable cells more efficiently.

In their latest study the researchers found that in response to DNA damage, LIF6 is transcriptionally upregulated by p53. LIF6 codes for a protein that rapidly translocates to the cell’s mitochondria. Once it reaches the mitochondrion it causes the outer mitochondrial membrane pore to open – leading to mitochondrial dysfunction, causing the cell to die.

The researchers plan to conduct additional studies to further define the molecular mechanisms by which LIF6 induces cell death.

The team hope their findings will aid efforts to therapeutically target cancer. “Maybe we can find ways of developing drugs that mimic the behaviors of the elephant’s LIF6 or of getting cancerous cells to turn on their existing zombie copies of the LIF gene,” concluded Lynch.

Reference
Vazquez et al. A zombie LIF gene in elephants is up-regulated by TP53 to induce apoptosis in response to DNA damage. Cell Reports. 2018. http://dx.doi.org/10.1016/j.celrep.2018.07.042

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By Yasemin Saplakoglu

The newest neuron has been named the “rosehip neuron,” thanks to its bushy appearance. The brain cell, with its unique gene expressions, distinctive shape and diverse connections with other neurons, has not been described before and, what’s more, it isn’t present in neuroscientists’ favorite subject: mice.

“It’s very bushy,” said Trygve Bakken, one of the lead authors of the paper and senior scientist at the Allen Institute for Brain Science in Seattle. Neurons have long branches called dendrites that receive signals from other neurons. In the rosehip cells, these dendrites are “very compact with lots of branch points, so it kind of looks a little bit like a rosehip,” Bakken told Live Science. (Rosehips are a type of fruit produced by rose plants.)

Also adding to the rosehip appearance are the large bulbs at the end of their axons that release neurotransmitters or chemical signals to other neurons, Bakken added.

The new finding is the result of a collaboration between Bakken and his team and researchers at the University of Szeged in Hungary. Both teams independently identified the distinctive-looking neurons and, when the teams learned they were looking at the same thing, they decided to work together, Bakken said.

The researchers at the Allen Institute documented the strange new neuron by examining the brain tissue of two deceased middle-age men. When the researchers looked at the genes of the rosehip neuron in this post-mortem tissue, they found that the neurons acted differently. “There are a number of genes that are turned on just in that cell and not in other[s],” Bakken said

Meanwhile, the team in Hungary further documented the rosehip neuron by studying the electrical activity and shapes of neurons in brain tissue that had been removed from people’s brains during surgery and kept alive in a solution.

A rare neuron

One reason rosehip neurons eluded neuroscientists for so long is likely because the cells are so rare in the brain, Bakken said. Another reason, he added, is because human brain tissue is difficult for scientists to obtain for study. Indeed, in the study, the researchers examined only one layer of the brain. It’s possible, however, that rosehip neurons could be found in other layers, too, Bakken said.

Specifically, the researchers found that the rosehip neurons make up about 10 percent of the first layer of the neocortex — the most recently evolved part of the cortex that’s involved in sight and hearing. They also found that rosehip neurons connect to neurons called pyramidal cells, a type of excitatory neuron that makes up two-thirds of all the neurons in the cortex, according to Cell.

The full extent of the rosehip neurons relationship to the pyramidal neurons is unclear, but the researchers did find that the rosehip neurons act as inhibitory neurons, or those that restrain the activity of other neurons. “They have the potential to sort of put the brakes on the excitability” of pyramidal neurons, Bakken said. But as to how this influences the brain’s behavior, “we don’t really know yet,” he added.

Absent in mice

All mammals have a cortex, and within it a neocortex, Bakken said. But there are about “a thousand times more cells in the human cortex compared to the mouse,” he said. In other words, it makes up a much bigger part of our brain than it does a mouse’s. So then, perhaps it’s not surprising that the team didn’t find any genetic hint of rosehip neurons in mice.

“Finding cell types that are uniquely human… helps our understanding of the physiological differences that under[lie] our higher cognitive abilities and may better inform upon treatment strategies for brain-related disorders,” said Blue B. Lake, an assistant project scientist in the bioengineering department at the University of California, San Diego who was not part of the study.

The absence of the rosehip neuron in mice brains might serve as a cautionary reminder that the results of some brain studies done on rats can’t be translated to humans, the researchers said.

“Mice have been a wonderful model organism for understanding how brains work in general and can help us understand how human brains work,” Bakken said. “But I think finding a part of that circuit that is not seen in a mouse that points to needing to study actual human tissue.”

There are enough parts of the brain conserved among mice, humans and other mammals that people can make “inferences about things we learn in the mouse and sort of, at least, hypothesize that something similar is likely to be happening in the human brain,” Bakken said. But, sometimes things present in human brains are “just not there” in mouse brains.


The brain anatomy is consistently shaped by socioeconomic status from childhood to early adulthood, a study has found.

The brain anatomy is consistently shaped by socioeconomic status from childhood to early adulthood, a study has found. The findings, published in the journal JNeurosci, draws attention to the importance of preschool life as a period when associations between SES and brain organisation may first develop.

Researchers from the National Institute of Mental Health in the US analysed brain scans of the same individuals collected over time between five and 25 years of age. Comparing this data to parental education and occupation and each participants’ intelligence quotient (IQ) allowed the researchers to demonstrate positive associations between socioeconomic status (SES) and the size and surface area of brain regions involved in cognitive functions such as learning, language, and emotions.

This is the first study to associate greater childhood SES with larger volumes of two subcortical regions — the thalamus and striatum — thereby extending previous SES research that has focused on its relationship to the cortex.

Finally, the researchers identify brain regions underlying the relationship between SES and IQ. A better understanding of these relationships could clarify the processes by which SES becomes associated with a range of life outcomes, and ultimately inform efforts to minimise SES-related variation in health and achievement, they said.

https://www.timesnownews.com/health/article/socioeconomic-status-shapes-developing-brains-study/336480


Before light reaches these rods and cones in the retina, it passes through some specialized cells that send signals to brain areas that affect whether you feel happy or sad.

by Jon Hamilton

Just in time for the winter solstice, scientists may have figured out how short days can lead to dark moods.

Two recent studies suggest the culprit is a brain circuit that connects special light-sensing cells in the retina with brain areas that affect whether you are happy or sad.

When these cells detect shorter days, they appear to use this pathway to send signals to the brain that can make a person feel glum or even depressed.

“It’s very likely that things like seasonal affective disorder involve this pathway,” says Jerome Sanes, a professor of neuroscience at Brown University.

Sanes was part of a team that found evidence of the brain circuit in people. The scientists presented their research in November at the Society for Neuroscience meeting. The work hasn’t been published in a peer-reviewed journal yet, but the researchers plan to submit it.

A few weeks earlier, a different team published a study suggesting a very similar circuit in mice.

Together, the studies offer a strong argument that seasonal mood changes, which affect about 1 in 5 people, have a biological cause. The research also adds to the evidence that support light therapy as an appropriate treatment.

“Now you have a circuit that you know your eye is influencing your brain to affect mood,” says Samer Hattar, an author of the mouse study and chief of the section on light and circadian rhythms at the National Institute of Mental Health. The finding is the result of a decades-long effort to understand the elusive link between light and mood. “It is the last piece of the puzzle,” Hattar says.

The research effort began in the early 2000s, when Hattar and David Berson, a professor of neuroscience at Brown University, were studying cells in the retina.

At the time, most scientists thought that when light struck the retina, only two kinds of cells responded: rods and cones. But Hattar and Berson thought there were other light-sensitive cells that hadn’t been identified.

“People used to laugh at us if we say there are other photoreceptors distinct from rods and cones in the retina,” Hattar says.

The skeptics stopped laughing when the team discovered a third kind of photoreceptor that contained a light-sensitive substance called melanopsin not found in rods and cones. (The full name of these cells, if you’re interested, is intrinsically photosensitive retinal ganglion cells, or ipRGCs.) These receptors responded to light but weren’t part of the visual system.

Instead, their most obvious function was keeping the brain’s internal clock in sync with changes in daylight. And many scientists assumed that this circadian function also explained seasonal depression.

“People thought that the only reason you get mood problems is because your clock is misaligned,” Hattar says.

Other potential explanations included speculation that reduced sunlight was triggering depression by changing levels of serotonin, which can affect mood, or melatonin, which plays a role in sleep patterns and mood. But the evidence for either of these possibilities has been weak.

Hattar and Berson were pretty sure there was a better reason. And, after years of searching, they found one.

In September, Hattar’s team published a study about mice suggesting a direct pathway between the third kind of photoreceptor in the retina and brain areas that affect mood.

When these cells were present, an artificially shortened cycle of light and dark caused a version of depression in a mouse. But when the team removed the cells with gene-editing tools, the mouse didn’t become depressed.

Sanes knew about the research, in part because he and Berson are neuroscientists at Brown. And he was so intrigued by the discovery of the new pathway between retina and brain in mice that he decided to see whether something similar was going on in human brains.

Sanes’ team put young adults in an MRI machine and measured their brain activity as they were exposed to different levels of light. This allowed the team to identify brain areas that seemed to be receiving signals from the photoreceptors Hattar and Berson had discovered.

Two of these areas were in the front of the brain. “It’s interesting because these areas seem to be the areas that have been shown in many studies to be involved in depression and other affective disorders,” Sanes says.

The areas also appeared to be part of the same circuit found in mice.

The finding needs to be confirmed. But Hattar is pretty confident that this circuit explains the link between light exposure and mood.

So now he’s trying to answer a new question: Why would evolution produce a brain that works this way?

“You will understand why you would need light to see,” he says, “but why do you need light to make you happy?”

Hattar hopes to find out. In the meantime, he has some advice for people who are feeling low: “Try to take your lunch outside. That will help you adjust your mood.”

https://www.npr.org/sections/health-shots/2018/12/21/678342879/scientists-find-a-brain-circuit-that-could-explain-seasonal-depression


A normal brain of a 70-year-old (left slice), compared with the brain of a 70-year-old with Alzheimer’s disease.Credit: Jessica Wilson/Science Photo Library

Neuroscientists have amassed more evidence for the hypothesis that sticky proteins that are a hallmark of neurodegenerative diseases can be transferred between people under particular conditions — and cause new damage in a recipient’s brain.

They stress that their research does not suggest that disorders such as Alzheimer’s disease are contagious, but it does raise concern that certain medical and surgical procedures pose a risk of transmitting such proteins between humans, which might lead to brain disease decades later.

“The risk may turn out to be minor — but it needs to be investigated urgently,” says John Collinge, a neurologist at University College London who led the research, which is published in Nature1 on 13 December.

The work follows up on a provocative study published by Collinge’s team in 20152. The researchers discovered extensive deposits of a protein called amyloid-beta during post-mortem studies of the brains of four people in the United Kingdom. They had been treated for short stature during childhood with growth-hormone preparations derived from the pituitary glands of thousands of donors after death.

The recipients had died in middle-age of a rare but deadly neurodegenerative condition called Creutzfeldt-Jakob disease (CJD), caused by the presence in some of the growth-hormone preparations of an infectious, misfolded protein — or prion — that causes CJD. But pathologists hadn’t expected to see the amyloid build up at such an early age. Collinge and his colleagues suggested that small amounts of amyloid-beta had also been transferred from the growth-hormone samples, and had caused, or ‘seeded’, the characteristic amyloid plaques.

Seeds of trouble
Amyloid plaques in blood vessels in the brain are a hallmark of a disease called cerebral amyloid angiopathy (CAA) and they cause local bleeding. In Alzheimer’s disease, however, amyloid plaques are usually accompanied by another protein called tau — and the researchers worry that this might also be transmitted in the same way. But this was not the case in the brains of the four affected CJD patients, which instead had the hallmarks of CAA.

The team has now more directly tested the hypothesis that these proteins could be transmitted between humans through contaminated biological preparations. Britain stopped the cadaver-derived growth hormone treatment in 1985 and replaced it with a treatment that uses synthetic growth hormone. But Collinge’s team was able to locate old batches of the growth-hormone preparation stored as powder for decades at room temperature in laboratories at Porton Down, a national public-health research complex in southern England.

When the researchers analysed the samples, their suspicions were confirmed: they found that some of the batches contained substantial levels of amyloid-beta and tau proteins.

Mouse tests
To test whether the amyloid-beta in these batches could cause the amyloid pathology, they injected samples directly into the brains of young mice genetically engineered to be susceptible to amyloid pathology. By mid-life, the mice had developed extensive amyloid plaques and CAA. Control mice that received either no treatment or treatment with synthetic growth hormone didn’t have amyloid build up.

The scientists are now checking in separate mouse experiments whether the same is true for the tau protein.

“It’s an important study, though the results are very expected,” says Mathias Jucker at the Hertie Institute for Clinical Brain Research in Tubingen, Germany. Jucker demonstrated in 2006 that amyloid-beta extracted from human brain could initiate CAA and plaques in the brains of mice3. Many other mouse studies have also since confirmed this.

Surgical implications
That the transmissibility of the amyloid-beta could be preserved after so many decades underlines the need for caution, says Jucker. The sticky amyloid clings tightly to materials used in surgical instruments, resisting standard decontamination methods4. But Jucker also notes that, because degenerative diseases take a long time to develop, the danger of any transfer may be most relevant in the case of childhood surgery where instruments have also been used on old people.

So far, epidemiologists have not been able to assess whether a history of surgery increases the risk of developing a neurodegenerative disease in later life — because medical databases tend not to include this type of data.

But epidemiologist Roy Anderson at Imperial College London says researchers are taking the possibility seriously. Major population cohort studies, such as the US Framingham Heart Study, are starting to collect information about participants’ past surgical procedures, along with other medical data.

The 2015 revelation prompted pathologists around the world to reexamine their own cases of people who had been treated with similar growth-hormone preparations — as well as people who had acquired CJD after brain surgery that had involved the use of contaminated donor brain membranes as repair patches. Many of the archived brain specimens, they discovered, were full of aberrant amyloid plaques5,6,7. One study showed that some batches of growth-hormone preparation used in France in the 1970s and 1980s were contaminated with amyloid-beta and tau — and that tau was also present in three of their 24 patients.8

Collinge says he applied unsuccessfully for a grant to develop decontamination techniques for surgical instruments after his 2015 paper came out. “We raised an important public-health question, and it is frustrating that it has not yet been addressed.” But he notes that an actual risk from neurosurgery has not yet been established.

https://www.nature.com/articles/d41586-018-07735-w?utm_source=fbk_nnc&utm_medium=social&utm_campaign=naturenews&sf204283628=1

Thank to Kebmodee for bringing this to the It’s Interesting community.

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Whiile human genetic mutations are involved in a small number of Parkinson’s disease (PD) cases, the vast majority of cases are of unknown environmental causes, prompting enormous interest in identifying environmental risk factors involved. The link between Helicobacter pylori (H. pylori) and gastric ulcers has been known for several decades, but new evidence suggests that this harmful bacterium may play a role in PD as well. A new review in the Journal of Parkinson’s Disease summarizes the current literature regarding the link between H. pylori and PD and explores the possible mechanisms behind the association.

In a comprehensive review of prior studies, investigators uncovered four key findings:

People with PD are 1.5-3-fold more likely to be infected with H. pylori than people without PD.
H. pylori-infected PD patients display worse motor functions than H. pylori-negative PD patients.
Eradication of H. pylori improved motor function in PD patients over PD patients whose H. pylori was not eradicated.
Eradication of H. pylori improved levodopa absorption in PD patients compared to PD patients whose H. pylori was not eradicated.
“This is an in-depth and comprehensive review that summarizes all the major papers in the medical literature on Parkinson’s disease and H. pylori, the common stomach bacterium that causes gastritis, ulcers and stomach cancer,” explained lead investigator David J. McGee, PhD, Associate Professor, Department of Microbiology and Immunology, LSU Health Sciences Center-Shreveport, Shreveport, LA, USA. “Our conclusion is that there is a strong enough link between the H. pylori and Parkinson’s disease that additional studies are warranted to determine the possible causal relationship.”

Investigators also analyzed existing studies to try and find possible testable pathways between the bacterial infection and Parkinson’s to lay the groundwork for future research. They found four main possible explanations for the association:

Bacterial toxins produced by H. pylori may damage neurons.

The infection triggers a massive inflammatory response that causes damage to the brain.

H. pylori may disrupt the normal gut microbial flora.

The bacteria might interfere with the absorption properties of levodopa, the medication commonly used to treat the symptoms of Parkinson’s disease.

The onset of PD is often preceded by gastrointestinal dysfunction, suggesting that the condition might originate in the gut and spread to the brain along the brain-gut axis. In the review, investigators note that this has been documented in rats.

Screening PD patients for the presence of H. pylori and subsequent treatment if positive with anti-H. pylori triple drug therapy, may contribute to improved levodopa absorption and ultimately improvement of PD symptoms, potentially leading to a longer life span in patients with PD.

“Evidence for a strong association among H. pylori chronic infection, peptic ulceration and exacerbation of PD symptoms is accumulating,” concluded Dr. McGee.

“However, the hypotheses that H. pylori infection is a predisposing factor, disease progression modifier, or even a direct cause of PD remain largely unexplored. This gut pathology may be multifactorial, involving H. pylori, intestinal microflora, inflammation, misfolding of alpha-synuclein in the gut and brain, cholesterol and other metabolites, and potential neurotoxins from bacteria or dietary sources. Eradication of H. pylori or return of the gut microflora to the proper balance in PD patients may ameliorate gut symptoms, L-dopa malabsorption, and motor dysfunction.”

https://scienmag.com/eradicating-helicobacter-pylori-infections-may-be-a-key-treatment-for-parkinsons-disease/

by Alison Abbott

It had been hiding in plain sight. The original letter — long thought lost — in which Galileo Galilei first set down his arguments against the church’s doctrine that the Sun orbits the Earth has been discovered in a misdated library catalogue in London. Its unearthing and analysis expose critical new details about the saga that led to the astronomer’s condemnation for heresy in 1633.

The seven-page letter, written to a friend on 21 December 1613 and signed “G.G.”, provides the strongest evidence yet that, at the start of his battle with the religious authorities, Galileo actively engaged in damage control and tried to spread a toned-down version of his claims.

Many copies of the letter were made, and two differing versions exist — one that was sent to the Inquisition in Rome and another with less inflammatory language. But because the original letter was assumed to be lost, it wasn’t clear whether incensed clergymen had doctored the letter to strengthen their case for heresy — something Galileo complained about to friends — or whether Galileo wrote the strong version, then decided to soften his own words.

Galileo did the editing, it seems. The newly unearthed letter is dotted with scorings-out and amendments — and handwriting analysis suggests that Galileo wrote it. He shared a copy of this softened version with a friend, claiming it was his original, and urged him to send it to the Vatican.

The letter has been in the Royal Society’s possession for at least 250 years, but escaped the notice of historians. It was rediscovered in the library there by Salvatore Ricciardo, a postdoctoral science historian at the University of Bergamo in Italy, who visited on 2 August for a different purpose, and then browsed the online catalogue.

“I thought, ‘I can’t believe that I have discovered the letter that virtually all Galileo scholars thought to be hopelessly lost,’” says Ricciardo. “It seemed even more incredible because the letter was not in an obscure library, but in the Royal Society library.”

Ricciardo, together with his supervisor Franco Giudice at the University of Bergamo and science historian Michele Camerota of the University of Cagliari, describe the letter’s details and implications in an article in press at the Royal Society journal Notes and Records. Some science historians declined to comment on the finding before they had scrutinized the article. But Allan Chapman, a science historian at the University of Oxford, UK, and president of the Society for the History of Astronomy, says “it’s so valuable — it will allow new insights into this critical period”.

Mixed messages
Galileo wrote the 1613 letter to Benedetto Castelli, a mathematician at the University of Pisa in Italy. In it, Galileo set out for the first time his arguments that scientific research should be free from theological doctrine (see ‘The Galileo affair’).

He argued that the scant references in the Bible to astronomical events should not be taken literally, because scribes had simplified these descriptions so that they could be understood by common people. Religious authorities who argued otherwise, he wrote, didn’t have the competence to judge. Most crucially, he reasoned that the heliocentric model of Earth orbiting the Sun, proposed by Polish astronomer Nicolaus Copernicus 70 years earlier, is not actually incompatible with the Bible.

Galileo, who by then was living in Florence, wrote thousands of letters, many of which are scientific treatises. Copies of the most significant were immediately made by different readers and widely circulated.

His letter to Castelli caused a storm.

Of the two versions known to survive, one is now held in the Vatican Secret Archives. This version was sent to the Inquisition in Rome on 7 February 1615, by a Dominican friar named Niccolò Lorini. Historians know that Castelli then returned Galileo’s 1613 letter to him, and that on 16 February 1615 Galileo wrote to his friend Piero Dini, a cleric in Rome, suggesting that the version Lorini had sent to the Inquisition might have been doctored. Galileo enclosed with that letter a less inflammatory version of the document, which he said was the correct one, and asked Dini to pass it on to Vatican theologians.

His letter to Dini complains of the “wickedness and ignorance” of his enemies, and lays out his concern that the Inquisition “may be in part deceived by this fraud which is going around under the cloak of zeal and charity”.

At least a dozen copies of the version Galileo sent to Dini are now held in different collections.

The existence of the two versions created confusion among scholars over which corresponded to Galileo’s original.

Beneath its scratchings-out and amendments, the signed copy discovered by Ricciardo shows Galileo’s original wording — and it is the same as in the Lorini copy. The changes are telling. In one case, Galileo referred to certain propositions in the Bible as “false if one goes by the literal meaning of the words”. He crossed through the word “false”, and replaced it with “look different from the truth”. In another section, he changed his reference to the Scriptures “concealing” its most basic dogmas, to the weaker “veiling”.

This suggests that Galileo moderated his own text, says Giudice. To be certain that the letter really was written in Galileo’s hand, the three researchers compared individual words in it with similar words in other works written by Galileo around the same time.

Chance discovery
Ricciardo uncovered the document when he was spending a month this summer touring British libraries to study any handwritten comments that readers might have left on Galileo’s printed works. When his one day at the Royal Society was finished, he idly flicked through the online catalogue looking for anything to do with Castelli, whose writings he had recently finished editing.

One entry jumped out at him — a letter that Galileo wrote to Castelli. According to the catalogue, it was dated 21 October 1613. When Ricciardo examined it, his heart leapt. It appeared to include Galileo’s own signature, “G.G.”; was actually dated 21 December 1613; and contained many crossings out. He immediately realized the letter’s potential importance and asked for permission to photograph all seven pages.

“Strange as it might seem, it has gone unnoticed for centuries, as if it were transparent,” says Giudice. The misdating might be one reason that the letter has been overlooked by Galileo scholars, says Giudice. The letter was included in an 1840 Royal Society catalogue — but was also misdated there, as 21 December 1618.Another reason might be that the Royal Society is not the go-to place in the United Kingdom for this type of historical document, whose more natural home would have been the British Library.

The historians are now trying to trace how long the letter has been in the Royal Society library, and how it arrived there. They know that it has been there since at least the mid-eighteenth century, and they have found hints in old catalogues that it might even have been there a century or more earlier. The researchers speculate that it might have arrived at the society thanks to close connections between the Royal Society and the Academy of Experiments in Florence, which was founded in 1657 by Galileo’s students but fizzled out within a decade or so.

For now, the researchers are stunned by their find. “Galileo’s letter to Castelli is one of the first secular manifestos about the freedom of science — it’s the first time in my life I have been involved in such a thrilling discovery,” says Giudice.

TIMELINE: THE GALILEO AFFAIR
1543 Polish astronomer Nicolaus Copernicus publishes his book On the Revolutions of the Heavenly Spheres, which proposes that the planets orbit the Sun.

1600 The Inquisition in Rome convicts Dominican friar and mathematician Giordano Bruno of heresy on multiple counts, including supporting and extending the Copernican model. Bruno is burnt at the stake.

1610 Galileo publishes his book The Starry Messenger (Sidereus nuncius), describing discoveries made with his newly built telescope that provide evidence for the Copernican model.

1613 Galileo writes a letter to his friend Benedetto Castelli, arguing against the doctrine of the Roman Catholic Church in matters of astronomy. Copies of this letter are circulated.

1615 Dominican friar Niccolò Lorini forwards a copy of the letter to the inquisition in Rome. Galileo asks a friend to forward what he claims to be a copy of his original letter to Rome; this version is less inflammatory than Lorini’s.

1616 Galileo is warned to abandon his support of the Copernican model. Books supporting the Copernican model are banned. On the Revolutions of the Heavenly Spheres is withdrawn from circulation pending correction to clarify that it is only a theory.

1632 Galileo publishes Dialogue Concerning the Two Chief World Systems, in which he lays out the various evidence for and against the Church’s Ptolemaic model of the Solar System, and the Copernican model. The Inquisition summons Galileo to Rome to stand trial.

1633 Galileo is convicted on “vehement suspicion of heresy” and the book is banned. He is issued with a prison sentence, later commuted to house arrest, under which lived the last nine years of his life.

Nature 561, 441-442 (2018)

https://www.nature.com/articles/d41586-018-06769-4