Category Archives: Human Genetics

Summary: The absence of the NCX3 gene amplifies pain signals within the spinal cord, a new mouse study reveals. Increasing levels of NCX3 in the spinal cord helped reduce symptoms associated with chronic pain.

Source: University of Oxford

Oxford researchers have discovered a gene that regulates pain sensitization by amplifying pain signals within the spinal cord, helping them to understand an important mechanism underlying chronic pain in humans and providing a new treatment target.

Chronic pain is a common issue affecting millions of people worldwide, but why some people are more prone to it and what factors lead tochronic painare not fully understood.

It is well known that repeated stimulation, such as with a sharp pin prick, can lead to a heightened sensitivity to pain. This process is called pain wind-up and contributes to clinical pain disorders.

In a two-part study, researchers from Oxfords Nuffield Department of Clinical Neurosciences first comparedgenetic variationin samples from more than 1,000 participants from Colombia, to look for clues as to whether there were any genetic variants more common in people who experienced greater pain wind-up. They noted a significant difference in variants of one specific gene (the protein Sodium Calcium exchanger type-3, NCX3).

The researchers then undertook a series of experiments in mice, to understand how NCX3 regulates pain wind-up and whether it may be a treatment target. NCX3 was expressed in the mousespinal cordneurons that process and transmitpain signalsto the brain.

NCX3 was needed by these neurons to export the excess calcium that builds up following activity. In the absence of NCX3 the spinal cord neurons showed more activity in response to injury signals from the periphery and pain wind-up was increased.

Conversely, increasing the levels of NCX3 within the spinal cord could reduce pain in the mouse.

David Bennett, professor of neurology and neurobiology of the Nuffield Department of Clinical Neuroscience, said: This is the first time that we have been able to study pain in humans and then to directly demonstrate the mechanism behind it in mice, which provides us with a really broad understanding of the factors involved and how we can begin developing new treatments for it.

Professor Bennett added: Chronic pain is a global problem, and can be immensely debilitating. We carried out the study in Colombia because of the mixed ancestry of the population there, including Native Indian, African and European populations, which gave us a broad range of genetic diversity to look at. This makes these findings so exciting because of their potential international applications.

The findings imply that any drugs which can increase activity of NCX3 would be predicted to reducepainsensitization in humans.

Author: Press OfficeSource: University of OxfordContact: Press Office University of OxfordImage: The image is in the public domain

Original Research: Open access.Sodium-calcium exchanger-3 regulates pain wind-up: From human psychophysics to spinal mechanisms by Teodora Trendafilova et al. Neuron

Abstract

Sodium-calcium exchanger-3 regulates pain wind-up: From human psychophysics to spinal mechanisms

Repeated application of noxious stimuli leads to a progressively increased pain perception; this temporal summation is enhanced in and predictive of clinical pain disorders. Its electrophysiological correlate is wind-up, in which dorsal horn spinal neurons increase their response to repeated nociceptor stimulation.

To understand the genetic basis of temporal summation, we undertook a GWAS of wind-up in healthy human volunteers and found significant association withSLC8A3encoding sodium-calcium exchanger type 3 (NCX3).NCX3was expressed in mouse dorsal horn neurons, and mice lackingNCX3showed normal, acute pain but hypersensitivity to the second phase of the formalin test and chronic constriction injury.

Dorsal horn neurons lackingNCX3showed increased intracellular calcium following repetitive stimulation, slowed calcium clearance, and increased wind-up. Moreover, virally mediated enhanced spinal expression ofNCX3reduced central sensitization.

Our study highlights Ca2+efflux as a pathway underlying temporal summation and persistent pain, which may be amenable to therapeutic targeting.

The rest is here:
Discovery of Gene Involved in Chronic Pain Creates New Treatment Target - Neuroscience News

Javier M. Floren, CEO & Co-founder ofDNAverse

As the metaverse concept continues to develop at pace, it is absolutely vital that human characteristics are embedded within. Our physical world has already evolved into a digital hybrid, with smartphones becoming digital extensions of ones self. We need the same process of hybridisation to take place within the metaverse. It is high time that scientific innovations are leveraged to enhance social interactions in the metaverse.

At this juncture, we are still in the early adopter/innovation phase. It has beenreportedthat throughout 2021, approximately28.6million wallets actively exchanged NFTs, representing a volume close to $25 billion. Platforms like Sandbox raising $93 million and Yuga Labs raising $450 million demonstrate the scale of interest in this burgeoning space, and point to long-term viability of Web3.0 and the metaverse.

The ongoing proliferation of Artificial Intelligence (AI) makes it increasingly difficult to identify who is on the other side of our interactions. The chatbots commonly deployed across a wide range of websites aim to make us believe that were talking to a real person. Weve all seen movies like The Matrix, I Robot or TV series like Black Mirror. They generally paint a negative picture of how humans and machines can co-exist. While bucketed under the catalogue of Science Fiction, if history tells us anything, Science Fiction can rapidly become Science Fact. If these visions come to fruition, how will we distinguish humans from machines when using avatars in a virtual world?

Science Fiction or Decentralized Science (DeSci)?

DNAVERSE is releasing a 3,200 NFT collection, the first one to be fully customized with real DNA. After a centralized drop, the process becomes decentralizedto initiate the BIOmetaverse as the goal is to let life replicate itself in all metaverses. Currently whitelisting for the Genesis drop, the process isopen and democratic and can be accessed by simply signing up with a form avalanche at DNAVERSE.io.

We are at a time in history where we can access technology that allows us to leave an indelible mark as human beings in digital ecosystems. We are already seeing NFT collections focused exclusively on the scientific field, DNA-based customization in the metaverse like DNAVERSE, genetic sequencing, decentralized health services and even the tokenization of blood samples.

When a real person cannot be distinguished from AI, being able to verify that you are a human using science and genetics will be paramount to future social interactions in the metaverse. Taking a small section of DNA and having scientists create a unique artistic representation of an individual as NFTs will be one of the ways to ensure human verification in this new paradimg. This practical application represents just one of the many possibilities that Web3 technology offers us. The benefits of introducing an individuals genetics into an NFT art piece also extend to personalizing digital assets with an individuals true essence, or transferring consciousness into web3.

Lets not confuse genetic verification with a form of KYC. The goal is not to create a biological database or fill out forms to show who we are or where we live, but to distinguish who is a real person and who has been programmed to interact with us.

The sustainability of the metaverse and future NFT projects hinges on demonstrable utility for individuals, who will constitute the community of participants. Sharing the benefits of each project in a sustainable way is essential so, for example, genetized NFTs can be used in human verification.

The key will be creating an ecosystem based on collaboration, ensuring the metaverse is open to all and offers us the opportunity to interact safely. Every technological advancement has the opportunity to be used by good and nefarious actors. Just consider how the emergence of social media keeps the world connected seamlessly, but can also be used to facilitate the rapid spread of fake news. Its impossible to make any new technology perfect, but by putting certain safeguards in place, and ensuring we have ways to identify ourselves and keep ourselves safe, humanity can be preserved in this new digital universe.

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Entering The DeSci era: Human Verification In The Metaverse Wi... - PressReleaseNetwork.com

South African researchers and surgeons are using artificial intelligence and robotics to enhance healthcare in the country, BBC News reports.

The improvements include a video-call robot that patients can use to speak to their families without needing to be present in the room and an app currently in development that can detect tuberculosis by listening to people cough.

The technologies are also improving surgical procedures at Tygerberg hospital in Cape Town by allowing surgeons to perform precise operations via the DaVinci robot.

The surgeon controls the robot from a console in the corner, surgeon and University of Stellenbosch lecturer Dr Tim Forgan told the BBC.

One can do really fine dissection and fine work under vision, so it really is a bit of a game-changer as far as the precision of surgery goes.

Forgan added that procedures conducted with the robot result in less blood loss and makes it possible for patients to get out of hospital sooner.

The DaVinci robot used at Tygerberg Hospital is one of two in the country.

Researchers from the University of Stellenbosch are also working on an app that can determine whether someone has tuberculosis by analysing their cough.

It uses an artificial intelligence-based, machine learning approach, where we have identified parts of the audio spectrum that are linked very strongly with the presence of tuberculosis, said Grant Theron, Stellenbosch Universitys principal investigator for the molecular biology and human genetics division.

We almost want to apply [artificial intelligence] to computing devices that are available everywhere. Most commonly, this is a cellphone.

The Tygerberg hospital also implemented the use of video-call robots in light of the Covid-19 pandemic.

The robots are controlled by hospital staff and patients can use them to communicate with loved ones without them needing to be in the room, or even at the hospital.

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The robots and AI technologies advancing South African health care - MyBroadband

This whole genealogical effort could lead to a new genre of bumper stickers, I think, like My forefathers were Philistines or like Goliath was in my family or I come from a long line of Hittite kings or heres a good one, My ancestors killed your ancestors.

In 2001, John MacArthur delivered that line to roaring laughter from his congregation. In a sermon dealing with slavery.

This and other cringe-worthy things MacArthur has preached about race and slavery came to the attention of social media users last week when Illinois pastor Sharon Autenriethtweeted, I have just read a long sermon in which John MacArthur promoted the Curse of Ham racial theory in 2001. He was in his early 60s at the time. Can we PLEASE stop talking about this guy like hes the assistant manager to the Trinity?

In the world of conservative evangelicalism, MacArthur is held in that kind of high esteem.

After he spent three years at the notoriously segregationistBob Jones Universityfrom 1957 to 1959, he returned to Los Angeles to follow in the footsteps of his father as a pastor. He completed an undergraduate degree at Los Angeles Pacific College and a master of divinity degree at what then was the brand-new Talbot Theological Seminary.

In 1969, at age 29, he became pastor ofGrace Community Church in Los Angeles, a post he has held ever since. He also leads The Masters UniversityandThe Masters Seminary,which boasts of having graduatedmore than 1,800 men.Hes the voice of the international radio ministryGrace to You, a bestselling author and editor of more than 150 books and was named byChristianity Today as one of the 25most influential pastorsof the past 50 years.

It is impossible to overstate the power MacArthur wields and the influence he has had on shaping the world of conservative evangelicalism today.

It is impossible to overstate the power MacArthur wields and the influence he has had on shaping the world of conservative evangelicalism today.

But while many conservative evangelicals look up to MacArthur for what they consider to be his boldness in preaching the Bible through the lens of conservative evangelical Reformed Baptist theology, Autenrieths tweet opened a larger conversation about this influential pastors views on race and slavery and the Bible.

Scott Coley, who serves on the philosophy faculty at Mount St. Marys University, retweetedAutenrieth andwent on to add: John MacArthur has been at the forefront of the anti-justice movement within white evangelicalism (which has spilled over into right wing politics at large). And here he is, using the Bible to craft a myth that legitimizes racial hierarchy. He and his colleagues deny that systemic racism is to blame for racial disparities in wealth, income and opportunity. So what explains such disparities? According to John MacArthur, its the curse of Canaan. Not incidentally, 10 out of 10 white supremacist theologians used *precisely* this logic to justify race-based, chattel slavery in the 19th century, as did segregationists in the 20th century. Whatever you do, stop listening to John MacArthur. He regularly manipulates Scripture to legitimize his own extra-biblical social agenda.

Sociologist Samuel Perry of the University of Oklahomatweeted, Wow. Just one of the most famous contemporary evangelical radio preachers and authors promoting the Curse of Ham like it was 1850.

In a series of sermons from Genesis preached during the summer of 2001, MacArthur laid out the case that many white supremacists have used throughout history to promote racism and defend slavery.

He began by sharing the story ofNoah getting nakedin his tent after the flood, discovering that his son Ham had seen him, and cursing Hams son Canaan to be a servant of servants to his brothers. MacArthur pointed out that Canaan would serve Shem, while Japheth would be enlarged.

MacArthur laid out the case that many white supremacists have used throughout history to promote racism and defend slavery.

He then moved into a discussion of Israels destruction of the Canaanites. And while many conservative evangelicals try to findother waysto describe the Canaanite conquest than to call it genocide, MacArthur is totally fine setting aside his own humanity and embracing it as genocide.

To any normal person, the thought of genocide, going in and massacring an entire population of people, was a frightening thing, he said. Natural human affections would cause some revulsion against such a command. It must have been a very, very severe challenge to their righteousness thinking to see themselves going into a land and committing genocide. Its massacring the Canaanites. Taking their land, taking their homes, and taking their lives.

The reason MacArthur gave to justify this genocide was that Canaan and his progeny was cursed. And so when Israel heard this read, they knew they had a cursed ancestry, and that they were acting on the basis of divine judgment which had already been determined, giving them historical justification for being the instrument of judgment on Canaan.

As Brock Bahler, a philosophy of religion professor at the University of Pittsburgh,points out, in the Middle Ages, a dominant map of the world in Europe was the T-O map that associated three known continents Africa, Europe & Asia w/ Noahs three sons. This doesnt become racialized until after [the] colonial era.

He claimed Shems descendants are Semites who became the Jews.

He claimed Shems descendants are Semites who became the Jews.

And what of the cursed descendants of Ham?MacArthur confidently proclaimed: If you study the territory of Ham, the territory of Canaan coming from Ham, it included Sodom and Gomorrah afterward, the families of the Canaanites were spread abroad. Wicked, wicked people. Corrupt and corrupting. Then the following week,MacArthur added, Ham settles the south: Africa and to Asia.

During a Q&A session from 2010, somebody asked MacArthur how we have so many races. And according to the text from the Grace to You website, MacArthur responded, It seems that Ham became a more servile people and may have moved south and wound up in Africa.

However, the audio version of MacArthurs response does not include that section. Either somebody from Grace to You added that section to the text of the page when MacArthur never said those words, or MacArthur did indeed say them and somebody edited those words out of the audio version. So it would seem that Grace to You either has something to add or hide regarding MacArthurs views about race.

Bahler goes on to describehow biblical literalists came up with all kinds of wild theories to get white supremacy to work w/ the Bible, with some claiming that Blackness was the curse of Cain, others calling it the curse of Ham, and others claiming skin color was determined by a divine act created at the Tower of Babel.

MacArthur decided to go with all of the above, while mixing in his own shot ofpseudoscience.

All human beings came from Adam through Noah, which means that all there is in the genetic code for all human races was in Adam and Eve, and all that there is of genetic coding that is in all the races that exist today was in the family of Noah, MacArthur assumed. That has all kinds of interesting implications because in the world you have so much diversity: you have very dark-skinned people, very light-skinned people. You have various features of certain kinds of people that are identifiable: Caucasoid, Negroid, Austrailoid, etcetera Mongoloid particular descriptions of physical features. And you have all these differences in skin color, and all these differences in facial look and body design. And the question is often asked, Where did this diversity come from? And the answer is the genetic code for all of that was in Adam and Eve. And the genetic code for all of the humanity in all of its diversity today was in the family of Noah. Everyone from pygmies and dwarves and aborigines to seven-foot-two Zulus and basketball players came from Noah and his wife. All physical features, all skin colors, all physical characteristics, all eye shapes, noses, eye colors, hair colors, etcetera all the necessary genetic coding was in Adam and Eve, and all of it was in those eight people.

And whatever the features were that God designed, in his sovereignty, in those genetic groups then became normalized in those groups. And so, various characteristics began to appear.

Unfortunately, MacArthur suggested, because humanity supposedly lived as one big family with no barriers to marriage, there was very little diversity in skin color. In order to get diversity in skin color, Youd have to pull people off and isolate them, and then they would begin to be dominated by the genetic features that are within that people group. The Tower of Babel did that. God separated the languages, scattered the people all over the planet, and they were isolated. And whatever the features were that God designed, in his sovereignty, in those genetic groups then became normalized in those groups. And so, various characteristics began to appear.

He added inanother Q&A session, Now, though, I believe the direct act of God, God distinguished between those people. At the Tower of Babel, God scattered all those nations, scattered all those people. And I believe in scattering them, he developed, by his own supernatural, providential will, distinctive characteristics of those people to identify them uniquely to their own areas and their own culture. In other words, God was trying to eliminate amalgamation and make them distinct. And I think there is some adaptation isnt there? Darker-skinned people living in areas where the sun was more severe. I dont think thats a process of evolution; I think that was a supernatural act on Gods part. So, the answer to your question is God made the races the way they are, and God put them in certain places of the world and adapted them to that in a distinction.

In an odd statementthat seemed to reflect Bob Jones Universitys historical ban on interracial marriage, MacArthur said the Assyrians became racially mixed, even though elsewhere he denied opposing interracial marriage.

MacArthur tried to say that because we all descended from Noah, we really are one family. There shouldnt be any racism. But the way he separated African descendants as cursed by God to serve European descendants might suggest otherwise.

In addition to his dehumanizing pseudoscience, MacArthur has also given rather offensive descriptions of people. Hespoke ofpygmies in Africa and primitive people that have painted their faces with some kind of plant these people that run around stabbing pigs in the jungle naked.

And lest were unclear about what MacArthur thinks about nakedness, he proclaims, Nakedness leads to wickedness. Nakedness leads to vice, every imaginable and unimaginable kind. Nudists, primitive people, exhibitionists, pornographers they all advocate nakedness as if it was a virtue.

It would be one thing if MacArthur simply interpreted the Bible as a slavery promoting document from two to three millennia ago. But he wants to use that interpretation to defend slavery today.

In 2001, MacArthur declared: The curse falls on Canaan. And the curse is that he would be a servant of servants, and he would wind up enslaved under the dominant rulership of others. And here we find that in Gods purposes, children of Ham through Canaan would be servants to the descendants of Japheth and Shem. He added that their descendants are doomed to perpetual slavery because they followed the moral turpitude of their ancestors, Ham and Canaan.

Here we find that in Gods purposes, children of Ham through Canaan would be servants to the descendants of Japheth and Shem.

In a 2012 YouTube video, MacArthur showed his true colors, stating: It is a little strange that we have such an aversion to slavery because historically there have been abuses. There have been abuses in marriage. We dont have an aversion to marriage particularly because there have been abuses. There are parents who abuse their children. We dont have an aversion to having children because some parents have been abusive. To throw out slavery as a concept simply because there have been abuses, I think, is to miss the point . There can also be benefits. For many people, poor people, perhaps people who werent educated, perhaps people who had no other opportunity, working for a gentle, caring, loving master was the best of all possible worlds. So we have to go back and take a more honest look at slavery and understand that God has, in a sense, legitimized it when its handled correctly. Slavery is not objectionable if you have the right master. Its the perfect scenario.

In one sermon, MacArthur described the descendants of Japheth whom he identified as Europeans as being in a peaceful partnership with Shem. Is it any wonder then why MacArthur would happen to promote dispensational theologies of the end times as well as popular Republican policies regarding Israel?

When President Donald Trump moved the U.S. embassy from Tel Aviv to Jerusalem in 2017,he declared at a rally, And we moved the capital of Israel to Jerusalem. Thats for the evangelicals. You know, its amazing with that the evangelicals are more excited by that than Jewish people.

In a Q&A about dispensationalism, MacArthur joked, People used to say of me that his hope is built on nothing less than Scofields notes and Moody Press. He went onto explain, Theres a difference between the church and Israel. Period. That demands a kingdom. And that makes you pre-millennial. The promises of a kingdom to Israel have to come to pass. And thats why you have to have a kingdom.

In other words, MacArthurs theology that white people are descendants of Japheth who are in a peaceful partnership with Israel as the descendants of Shem, combined with his theology that Israel must have a literal kingdom has led him to use the full force of his own media kingdom to promote political policies among evangelicals that would affect the decisions of President Trump.

Japheth is enlarged, as a peaceful partnership with Shem, and is served by Canaan whos a descendant of Ham.

And where are the descendants of Ham whom MacArthur identifies as Africans in all of this? According to MacArthur, Japheth is enlarged, as a peaceful partnership with Shem, and is served by Canaan whos a descendant of Ham.

For MacArthur, slavery appears to be more than simply a secondary issue Christians can disagree about. He believes slavery is central. In fact, he believes slavery is the gospel. So for MacArthur to reject slavery would be to reject the gospel.

InThe Gospel According to Jesus, MacArthur said, The gospel is an invitation to slavery.

He added inanother article, The Bible is abundantly clear slavery is the heart of what it means to be a true Christian. Slavery to Christ is not a minor or secondary feature of true discipleship. It is exactly how Jesus himself defined the personal relationship he must have with every true follower. In fact, the fundamental aspects of slavery are the very features of redemption. We are chosen, bought, owned, subject to his will and control, called to account, evaluated, and either chastened or rewarded by him. Those are all essential components of slavery.

Since Jesus said he came to set the oppressed free, one might assume MacArthur would desire to see slaves set free.

But instead,MacArthur says: Christianity does not free slaves. Christianity does not give equal social rights. Jesus did not propound equal rights and he did not upset the social order. Neither did Peter, neither did Paul, neither did John, neither did any New Testament writer.Rather, they all affirmed that with great fear of God and great respect you are to be submissive to your masters, whether theyre good and gentle or whether they are unreasonable. You are to submit.

Jesus did not propound equal rights and he did not upset the social order. Neither did Peter, neither did Paul, neither did John, neither did any New Testament writer.

InThe MacArthur New Testament Commentary, he continued: Although slavery was carefully regulated under Mosaic law, neither the Old nor New Testaments condemns slavery as such. Social strata are recognized and even designed by God for mans good. Some people will be served, and some will serve others. New Testament teaching does not focus on reforming and restructuring human systems.

And for those who might wish to reform such systems, MacArthur objects: Nowhere in Scripture is rebellion or revolution justified in order to gain freedom, opportunity or economic, social or political rights. The emphasis is rather on the responsibility of slaves to serve their human masters faithfully and fully.

Human rights seem to mean nothing to MacArthur.He says there is no place for asserting our rights. Its not our concern to have rights in this world. It is our concern to be obedient and submissive in this world. If youre a slave when youre saved, stay a slave. The system stands.

Of course, MacArthur admits slave masters can be abusive. But to those who suffer under physical abuse and starvation,he advises: Now heres a guy in the workplace and hes a slave.And in the Roman world he might be getting whipped unjustly.He might be getting deprived of his food unjustly.He might be working long hours beyond what is reasonable unjustly. He might be punished in a number of ways unjustly.But if for the sake of his consciousness of God he endures all of those sorrows, God is thankful.Did you get that?What pleases God?When you protest?When you strike?When you picket?When you walk out?No, what pleases God, what finds favor with him is when you bear up under the sorrows that come when you suffer unjustly.That pleases God.

What pleases God, what finds favor with him is when you bear up under the sorrows that come when you suffer unjustly.

Given the amount of sheer absurdities that pour from MacArthurs mouth, one might wonder if hes simply ignorant of history, genetics and edifying language. But MacArthur isnt ignorant. He knows full well what hes doing. He brags about studying anthropologists, linguists and scientists.

John MacArthur is pastorally careless. He is a pastor with decades of experience. He should have the pastoral wisdom to know you dont say the things hes said about race and slavery in a country thats given itself over so much to racism and slavery.

John MacArthur is a racist. His entire framing of world history and the gospel itself as Gods slavery design where Africans are to serve Europeans in perpetuity, while the Europeans are enlarged and in partnership with Israel, is a sacralization of racism and white supremacy.

John MacArthur is a dangerous man. Heclaims, The facts that are here are potent and greatly informative to those of us who want to understand the world the way God views it. To MacArthur, the curse of Ham wasnt merely part of a dispensation in the past or the way God used to work, but a revelation into how God presently views the world.

Notice his use of the word potent.

Thats what all of this is about. Its not about unleashing Gods truth one verse at a time. Its aboutMacArthurs power.

When MacArthur told Beth Moore to go home, he said of women who want to be pastors, They want power, not equality. This is the highest location they can ascend to that power in the evangelical church.

In that quote, MacArthur revealed his own cards. He identified how he sees his role as a pastor. To him, the office of being an evangelical pastor is an ascension to power. In MacArthurs world, he is the master to whom others must submit.

The reason MacArthur so easily sets aside the humanity of others is that he is disconnected from his own humanity. And his disconnection from self poses a very real threat to all of us through every power wielder his empire sends out.

John MacArthur has built an entire theology that glorifies slavery and defends genocide against a people group he claims must serve Europeans and Israel in perpetuity. His dispensationalist theology brings his views of slavery in the Bible through today all the way to the end of the world. And he has showed during the COVID crisis that he believes he is above the law. Its time his charade of a ministry be exposed and shut down. Its time for MacArthur to go home.

Rick Pidcockis a 2004 graduate of Bob Jones University, with a bachelor of arts degree in Bible. Hes a freelance writer based in South Carolina and a former Clemons Fellow with BNG. He recently completed a master of arts degree in worship from Northern Seminary. He is a stay-at-home father of five children and produces music under the artist name Provoke Wonder. Follow his blog atwww.rickpidcock.com.

Related articles:

The curse of Ham: Black Baptists question their place in the SBC | Opinion by Alan Bean

Are Black people cursed? | Opinion by Charles Holley

How John MacArthur loves the Bible but not his neighbor | Analysis by Rick Pidcock

Neither democracy nor religious freedom are biblical concepts, John MacArthur declares

John MacArthur rallies pastors to preach against government bans on conversion therapy Jan. 16

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What has John MacArthur actually said about race, slavery and the Curse of Ham? - Baptist News Global

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First, it was a doppelgnger of the late Lee Kuan Yew; now, a Gen Z lookalike of Deputy Prime Minister and Finance Minister Lawrence Wong has gone viral on social media.

A Singaporean TikTok user named Cyrus easily morphs into a photo of Mr Wong because of their striking resemblance.

It has been about two months since the teenager has been morphing (a TikTok shapeshift effect that transforms a persons face into their alleged celebrity or prominent person lookalike) into Mr Wong, in hopes of the minister finally noticing him.

Photo: TikTok screengrab/teocyrus

Needless to say, the bespectacled teen does look like Mr Wong; hence he has been dubbed the Lawrence Wong Gen Z version.

In one of Cyrus latest videos, netizens began poking fun that he was the long-lost son of Mr Wong.

@lawrencewongst brois this your son? asked TikTok user @junee.

Many also took the time to make requests, such as can reduce GST (Goods and Services Tax) and petrol price or sir, can increase budget for 2022?

So how much does Cyrus look like Mr Wong? Here are a few comparisons.

Photo: TikTok screengrab/teocyrus

Photo: TikTok screengrab/teocyrus

It appears that Mr Wong might have caught wind of Cyrus efforts because he uploaded a video on TikTok revealing how he looked like while he was in Secondary 4.

I understand some on TikTok have done #morphing videos of me. So heres one from my social media team, said Mr Wong.

Photo: TikTok screengrab/lawrencewongst

According to an article by Sunway, the chances of someone looking exactly like someone theyre not related to is about one in one trillion.

Theres definitely a mathematical chance for two doppelgngers to exist, but its highly unlikely, said University of Adelaide biologist Teghan Lucas who conducted a study on the doppelgnger occurrence.

The human face is extraordinarily unique. I mean think about it. The chance has to be quite low otherwise, you would be bumping into people who looked like you all the time, and you dont, added Sir Walter Bodmer, a professor of human genetics from the University of Oxford./TISG

Reply to @theresalwaysabeeliverinu Started as a joke but I dont think its a joke anymore #fy #fyp #shapeshift

dis it is

Lee Kuan Yew lookalike seen at coffeeshop, netizens say, Hes back!

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Gen Z version of Lawrence Wong spotted, netizens joke he's a long-lost son - The Independent

Despite big improvements in survival, cancer is still one of the worlds biggest killers. Leading Cancer Research UK-funded scientists explain why it presents such a challenge and look at how far weve come

Written by Natalie Grover for Guardian Labs

Part of a pancreatic tumour seen down a microscope, with tumour cells labelled in green, and different types of immune cell in pink, yellow, red, and turquoise. Image credit: Silvia Cusumano, Assya Legrini, Leah Officer-Jones, Dr Nigel Jamison and Prof John La Quesne

Recent decades have yielded extraordinary progress in cancer survival, but many cancers remain deadly, with half of people diagnosed dying within 10 years. So why hasnt science found a way to cure more people yet?

A major challenge is that scientists arent in fact targeting a single disease but a constellation of hundreds of diseases that are lumped together under the umbrella classification of cancer. This came about because all cancers start in the same way, with mutations in genes that control cell function.

Such mutations can fuel the unfettered replication of a single cell. If conditions are right, the cell grows and divides, escalating to millions of cells that may clump together to form a tumour in which no two tumour cells are identical in a single tumour.

I might have been pessimistic that we would ever be able to control these rapidly multiplying clumps of cells, says Prof Sir Mike Stratton, director of the Wellcome Sanger Institute and a genetics expert.

But time and again, the achievements of cancer research have mitigated that pessimism and converted it to optimism. It isnt that one drug will wipe the whole lot [of cancers] off the map, but bit by bit we are eroding the mortality rates of many cancers.

Stratton, leader of the Cancer Grand Challenges Mutographs team, which is working on a 20m project to look for unknown causes of cancer, adds: Were learning that research finding out what is actually going on in cancer cells is the route to new strategies for undermining the ability of cancer cells to behave in the way that they do.

While cancers may start in the same way, decades of research have shown that they evolve into very different diseases requiring a panoply of treatments. So far, scientists have classified more than 200 types of cancer, and found a myriad of genetic mutations underlying them.

Out of around 20,000 genes in the human genome, between 500 and 1,000 have been identified as contributing, when mutated, to a cell becoming cancerous. There is, however, a set of cancers for which the genes are still unclear, says Stratton, who is credited with identifying the breast cancer susceptibility gene BRCA2 among others.

Its tempting to think that the way forward is to target all the genes known to be implicated in cancer by launching 500-plus drug development programmes.

But not only is this a huge task, its by no means certain that the drugs developed would be the answer to curing the different cancers. This is because tumours develop considerable genetic diversity as they evolve, and often become resistant to treatments as more mutations occur in cells.

Targeted therapies have been approved for a range of cancers including breast, liver and lung cancers, and are helping more people to live longer. For now, though, the search for more precision treatments goes on. There is a set of cancer genes that are switched off by their own mutations, Stratton says. So how do we use those genes in order to develop new therapies?

Cancer cells growing in 2D, labelled with fluorescent markers showing the cells nuclei in blue, their cytoplasm in red, and areas of DNA damage in green. Image credit: Getty Image

Drug resistance is one of the biggest challenges in cancer thats why its so important to diagnose cancers early when treatment is more likely to be successful, says our chief clinician Prof Charles Swanton, group leader at the Francis Crick Institute, co-director of the charitys Lung Cancer Centre of Excellence and a consultant at University College London Hospitals (UCLH).

Early diagnosis isnt always possible, for a range of reasons. For example, there are very few techniques that can detect small, early tumours, and some cancers simply dont trigger symptoms early enough until they have already spread (or metastasised) and it is at this stage that the oncologists toolkit of drugs often falls short.

Each cancer has a different suite of signals which its responding to

Robert Insall, professor of mathematical and computational biology

To help uncover the tricks that tumours deploy to evolve, spread and develop drug resistance, we are supporting the TRACERx clinical study for which Swanton is chief investigator. By following the progress of hundreds of patients with the most common form of lung cancer from the point of diagnosis onwards, the study views cancer through an evolutionary lens, and uses a vast array of cutting-edge techniques to monitor participants disease.

According to Swanton, the lessons already learned from tracking these patients are applicable to many types of cancer. For instance, the study has shown that tumours with a high level of genetic diversity have the worst clinical outcomes, and that tumours use an assortment of ploys to elude the immune system, including losing the flags on their cell surface that enable them to be recognised as problematic.

Overall, says Swanton, the major barriers to successfully treating metastatic cancer are the genetic diversity within tumours, the evolutionary fitness of cancer cells that allows them to adapt, and of increasing focus the ways tumours modify their local microenvironment to support their survival.

The tumour microenvironment is composed of non-malignant cells that have been hijacked by cancer cells to support and nourish the tumour. This allows the cancer to smother the bodys immune defence.

Prof Fran Balkwill

Typically, half of the cells that make up a tumour are non-cancerous, and include fibroblasts (for structural support), fat cells and endothelial cells (which can form blood vessels that deliver oxygen and nutrients, and eliminate waste), says Prof Fran Balkwill, whose work at the Barts Cancer Institute in London centres on the links between cancer and inflammation.

Better understanding of this microenvironment and potentially reprogramming it could restrict nourishment of this cancerous rogue organ and reawaken the bodys immune cells to recognise and destroy it.

Already this ecosystem of hijacked normal cells within tumours is being targeted by cancer treatments, whether immunotherapy or chemotherapy, says Balkwill, noting that it is likely that treatments in the future will be combinations of drugs that target malignant cells and this microenvironment.

What makes cancer ultimately so dangerous, however, is the suite of signals that induce it to move beyond its primary site into the blood, lymphatic system or other tissues.

Robert Insall, professor of mathematical and computational biology.

Typically, chemical signals steer a cancer cell to move in a particular direction, but in many cases we dont know what they are, says Robert Insall, professor of mathematical and computational cell biology at the our Beatson Institute in Glasgow. So, if youre looking at this theme of why isnt cancer cured yet, its because each cancer has a different suite of signals which its responding to.

In the case of melanoma, a serious form of skin cancer, Insalls research suggests that the cancer cells themselves make their own spreading signals, creating the local instructions that direct them to spread.

Other kinds of skin cancer are not nearly as scary because they either dont, or rarely, spread. And one of the reasons is that they are not primed to drive themselves outwards in the same way, he says. My suspicion is that the most metastatic, the most deadly, cancers have this same property [as melanoma].

Reprogramming a tumours microenvironment could reawaken the bodys immune cells to destroy it

Professor Fran Balkwill

Insights such as Insalls continue to inform research into the biology of cancer, building on the decades of endeavour that have gone before. This burgeoning knowledge has transformed the way doctors diagnose and treat cancers in the UK, for instance, survival rates have doubled in the past 40 years for all cancers combined. On this journey to cure patients with cancer, says Swanton, I think were about half way there.

Part of an ovarian tumour viewed down a microscope, with cancer cells in blue and immune cells in brown Barts Cancer Institute

The second half of this odyssey demands further research. Research that will not just benefit the cancer patients of tomorrow, but is keeping hope alive for people affected by cancer now who may have limited or no treatment options if their cancer progresses.

Eileen Rapley, a participant in the TRACERx study who is being treated at UCLH, and who has also been receiving an immunotherapy drug that has so far kept her cancer at bay, says: When youre diagnosed with cancer and youre suddenly very dependent on other people, being able to contribute something makes it a little more palatable. You feel that at least this cancer is having a positive effect rather than a negative one.

But funding for this type of lifesaving research has come under considerable strain, in large part due to the pandemic, with CRUK needing to reduce its planned spending for 2022-23 from 400m to 300m.

Maintaining investment in cancer research and getting back to where we were in 2017, 2018 and 2019 is going to be absolutely crucial, says Swanton.

We are now getting to the point of being able to personalise medicines given to patients upon the genetic basis of their disease, he says. But we need new medicines to circumvent and overcome drug resistance in cancers that have spread, and new approaches to detect small, early stage tumours, and treat them before they become malignant thats where some of the major advances are going to come from over the next five decades.

This article was originally published on theguardian.com as part of the Cancer Research UK and Guardian Labs Cancer revolutionaries campaign.

To dig deeper into why we havent cured cancer, we heard from Dr Alanna Skuse, Dr Mariam Jamal-Hanjani and Sir Leszek Borysiewicz in the latest episode of our podcast That Cancer Conversation.

From Egyptian mummies and medieval wolves, to precision medicine and microscopic evolution, we take a look at the past to find out why curing cancer is more complex than we think, and what is needed next to get us closer to a future without cancer.

More on this topic

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Why havent we cured cancer? - Cancer Research UK News

ENDANGERED SPECIES ESSAY

Im still here. Dont let me go. ~Robert Krulwich

Once deemed extinct in Lord Howe Island (LHI), where they are endemic, today only 35 Lord Howe Island Stick insects (Dryococelus australis), are alive in the wild, but not in LHI.

The Lord Howe Island Stick Insect is also called the tree lobster, the name well use in this article. The tree lobster has a massive genome, larger than a human genome by 25%. And yet, this stick insect will only stretch six inches long large enough to fit on an adult humans palm. Its perhaps both the largest stick insect and the rarest invertebrate in the world.

The tree lobster thrived and is endemic to Lord Howe Island. In 1916 Australian Entomologist Arthur Lea counted 68 of them in the hollow of a single tree on the island. But by the 1920s, all tree lobsters disappeared, and by the 1960s they were declared extinct.

The black rats

Their disappearance was blamed on black rats (Rattus rattus) that swam from the British ship, SS Makambo, to LHI when it ran aground in 1918. The rats ate the tree lobsters like candy.

They also decimated five bird species and 12 other invertebrate species. Island inhabitants saw the rats running up and down tree trunks. They spoiled human food and compromised human hygiene.

LHI has some 350 permanent residents. The rodent population in 1918 rose to 300,000 rats and mice. The ratio was roughly 1,000 rodents per human.

This is a story just as much about the decimation of an entire rat population on an island, as it is about the extinction and rediscovery of the tree lobster.

Tree lobster rediscovered elsewhere

In 1964, a group of climbers navigated Balls Pyramid, a steep, rocky outcrop situated 27.2 km from Lord Howe Island. They found a few stick insect corpses that seemed to be recently dead. They took pictures but left the Pyramid before nightfall.

Balls pyramid is very different from Lord Howes Island. Its a steep and tall promontory that juts out vertically from the Tasman sea. Its hard to climb not just because of its straight-up form, but also because its inhabited by barnacles, poisonous centipedes, spiny sea urchins, and other tiny, local wildlife.

Scientists decided in 2001 to find the tree lobsters. Two of them were Australian scientists, David Priddel and Nicholas Carlile. Two others were their assistants. All four rode a boat through shark-infested waters. Upon landing, they climbed 500 feet up.

But all they found were crickets. Upon heading back down, they saw a melaleuca bush peeping out of a crack. Underneath it was fresh poop from evidently large insects.

Priddle and Carlile returned to the site after nightfall, armed with flashlights and cameras. They found 24 tree lobsters beneath the melaleuca bush, dining on tea. Aside from that, very little is known about tree lobsters in the wild.

However, they took two pairs of insects, both male, and female, to breed them in captivity. The goal was to establish an alternate population if those on Balls Pyramid went extinct.

As of now, only 35 adult Lobster Stick Insects live in the wild on Balls Pyramid. Because they only feed on tea, theyre endangered by the possible eradication of their food source by the invasive Morning Glory creeper, Ipomoea cairica. To thwart this, in 2003, the Morning Glory vine was partially removed from Balls Pyramid. A small portion was kept because it helps stabilize the soil of outcrops from steeper slopes.

Another threat is the possible poaching of the tree lobster and its eggs by private collectors, which is why access is restricted on the pyramid. Doing so also protects the habitat.

A third threat is natural disturbances like drought, storms, and landslides that could eradicate the entire tree lobster population in the wild, rendering them extinct within seconds.

These are the reasons why the International Union for the Conservation of Nature (IUCN) rates the tree lobster as Critically Endangered.

By 2017, 35 individuals were seen on Balls Pyramid. Surveys are infrequent because of the abovementioned vulnerabilities of the tree lobster.

Adam and Eve

The tree lobsters were brought to Zoos Victoria for captive breeding with the aim to eventually rewild them. One pair didnt survive, so the remaining pair were named Adam and Eve by Zoos Victoria. Initially, Eve became critically ill, but the zoo staff successfully enabled her recovery, and she laid 248 eggs. The tree lobsters were fed Moreton Bay figs and alfalfa. The juveniles were given blackberries.

The entire captive population that descended from Adam and Eve numbers more than 14,000 in captivity, in Melbourne Zoo alone. Others are being bred in Bristol Zoo, San Diego Zoo in California, and other zoos and museums around the world.

Today thousands of Lobster Stick Insects exist in zoos and museums around the world. They hope to eventually recolonize Lord Howe Island, the land thats their natural home.

Genome and differences measured

There are morphological differences between the Lord Howe Stick Insect before its extinction, and the same insect in Balls Pyramid today. These differences raised questions about whether the two were of the same species.

To settle the issue, Alexander S. Mikheyev et. al. assembled a complete mitochondrial genome from a tree lobster in Balls Pyramid and compared it to a mitochondrial genome from a stick insect museum specimen that lived on Lord Howes Island before their extinction.

Results showed less than 1% difference between both genomes, falling within range to be considered the same species. It was safe to say that the tree lobster was no longer extinct.

As for their physical differences, scientists mused it could be due to genetics or the environment. By raising them in captivity, they could observe this insect regularly, and they noticed that it evolved frequently. They believe it was for morphological convergence, meaning, each tree lobster would morph and still remain similar to one another. The morphing of insects is usually an adaptation to a shared environment.

Another possibility is that tree lobsters from Balls Pyramid and those from Lord Howe Island both had a shared origin, but the tree lobsters at Balls Pyramid were perhaps isolated for a very long time.

How they got to Balls Pyramid

Another question was how they reached the Pyramid. It is the remains of a former, far larger volcano. Now its a steep, vertical, rocky cliff that rises 560 meters above sea level.

True, the Pyramid is less than 30 km away from LHI, but this insect can neither fly nor swim, and no land bridge connects them. Scientists theorized that birds may have mistaken them for twigs, and flew them to Balls Pyramid where they built their nests.

Theres a precedent to this theory. Scientists in Japan studying another stick insect species noted that even if birds eat stick insects, the insects eggs can pass through the birds digestive tracts and hatch. Extrapolating from this, it may be that unborn offspring was airlifted to Balls Pyramid, and repopulated there.

Rat story

Theres the hope of rewilding the tree lobster on Lord Howe Island where they truly belong. In fact, the Lord Howe Island Board decided in 2019 to undertake the biggest Rodent Eradication Program (REP) in the world. Strategies included:

Eliminating mice and rats simultaneously, to derive the best long-term results from REP.

Distribution of rat baits by hand, and setting up bait stations in residential areas.

Setting up over 23,000 rat baits inside all buildings, and throughout the island.

Dropping 42 tons of poisoned cereal from helicopters on areas highly populated by rats.

Dropping by helicopter 22,000 lockable traps that held rat poison over uninhabited, hard-to-reach mountains and forests.

Arming worker teams with GPS trackers to log rat movements on their mobile phones.

Enlisting the expertise of dozens of scientists.

The task wasnt easy. There were some 200,000 rats on the island, running up tree trunks, destroying gardens, and disturbing the natural environment. In the end, they killed 300,000 rodents.

Paradise found

The REP was highly successful, and currently, the task is to make sure that there are absolutely no rats left on Lord Howe Island and to ensure that the rodents dont make a comeback.

In April 2021 an island resident reported that she saw two adult rats on a road. After they were hunted and killed, they discovered that one rodent was male, and the other one was a pregnant female.

Every few months, rat detection dogs inspect the island. The most recently seen rat was caught by a detection dog in August 2021. The goal now is to make sure the rats are gone for good and to ensure that they dont make a comeback via boats and other means to reach the island.

With the eradication of the rats, new fruit that has never before been seen by residents now grows, and people have photographed hundreds of unfamiliar insects and sent their photos to the Australian Museum. Also, four snail species previously presumed to be extinct have resurfaced.

Hank Bower, World Heritage manager of the Lorde Howe Island Board Environment, has lived on the island for 15 years. He told the Sydney Morning Herald, Everything is blooming, all the plants are flowering and we are seeing a carpet of seedlings.

Ecological importance

In general, stick insects are like gardeners. By feeding on leaves, they prune shrubs, in this way allowing new plants to grow. Their defecation builds up soil nutrients that will enrich succeeding new plants. This activity permits forest recycling.

They also play a vital role as the prey of certain meat-eating amphibians, birds, some mammals, and several reptiles. The latter, by only eating meat, are deprived of necessary nutrients from the sun that plants generate through photosynthesis.

By feeding on plant-eating insects like the tree lobster, these animals are able to absorb the valuable nutrients of the son through this and other insects.

When meat-eaters prey on the tree lobster, they absorb valuable energy and nutrition that is generated by the plants that these insects eat.

In sum, the tree lobster is equally valuable in its diet, and as prey. In the latter case, it links sun-generated energy derived from plants and transposes it to the animals that eat it. In this way, the tree lobster passes the suns energy up through the food chain.

It may sound heartless, but according to entomologist Matan Shelomi, insects have no pain receptors, so they cant feel pain, but irritation. If damaged, they have no emotions, implying that they cant suffer. So dying isnt torturous, for them, its inconvenient.

We hope Shelomi is right, but there are conflicting beliefs on this. Some studies show that insects have a wider range of emotions than we realize. Its also suggested that they can feel delight, depression, fear, and respond to pain.

The bottom line is that everybody dies, and in death, a role is played in the well-being of an ecosystem. And in this sense, tree lobsters are no different from all the rest of us.

See more here:
Lord Howe Stick Insects: Wrongly Deemed Extinct; With Genome 25% Larger Than a Human's - PRESSENZA International News Agency

Enterovirus isolation

Three isolates were obtained from the clinical samples of the patients involved in the small outbreak. One was obtained from the hepatic biopsy of patient 1, here referred to as Iso_pt1_L, while the others were obtained from the serums of patient 2 and patient 3, named Iso_pt2_S and Iso_pt3_S respectively (see Table 3).

The Enterovirus strains involved in this small outbreak were typed, basing on VP1 partial sequences and all resulted belonging to E-11. Moreover, the phylogenetic analysis performed comparing the VP1 sequences with a set of E-11 strains retrieved from GenBank shows that our strains strictly correlated and segregated in a unique and well separated clade which belongs to the D5 genotype of E-11 according to Li et al. [31], thus confirming the epidemiological link between the Enterovirus infections described here. (Additional file 3).

To further characterize the RNA genome, the EVs isolated in cell culture (Iso_pt1_L, Iso_pt2_S and Iso_pt3_S) and the virus from the liver biopsy of patient 1 (Pt1_L) were entirely sequenced. All nucleotide sequences were then aligned using Clustal W and the amino acid sequences of the polyproteins were compared. As expected, all viral strains revealed a high identity at nucleotide level (median=99.87%, ranging from 99.83 to 100%); two schematic tables of the nucleotides and amino acid differences respectively found, are provided in Additional file 4. Moreover, comparing the Liver Enterovirus strain (Pt1_L) with the corresponding Liver isolate (Iso_pt1_L), no amino acid differences were observed, while the sequence of Iso_pt2_S compared to Enterovirus strains of pt1, shows one amino acid substitution, C1677 L, located in the P3 region of the polyprotein. Specifically, it maps in the region encoding for the protein complex of 3BCD that is the precursor of the non-structural proteins 3B (Vpg primers for RNA transcription), 3C (protease) and 3D (viral polymerase). Similarly, we compared the amino acid sequence of Iso_pt3_S with those of pt1 (Iso_pt1_L and pt1_L) and we found the following four substitutions: D478G localized in the P1 portion of the polyprotein encoding for capsid proteins; T1898A, G2100V and E2101T, located in the portion encoding for the viral RNA polymerase 3D. Furthermore, comparing the amino acid sequence of the virus described here with 35 polyprotein sequences of other E-11 strains downloaded from Genbank, we found 25 amino acid substitutions (V101I, E115D, I310V, V572A, T651V, E895D, Q1031H, C1033S, L1938F, I1084V, T1122A, Q1185H, S1213E, S1365N, T1418S, S1429N, N1536S, P1539L, A1533S, V1558I, L1298I, T1868N, I2135V and D2140N). To date, no biological significance associated with any of these substitutions have been described.

Despite the typing of the VP1 gene assigned our virus to an E-11, the phylogenetic analysis of the full-genome sequence of ECHO11_INMI against a set of 123 sequences retrieved from the Picornavirus homepage, showed an unexpected pattern: ECHO11_INMI strain did not segregate with E-11 serotypes, but with a CV-B1 (Acc N: MG845887) (Fig.2). This finding led us to hypothesize that ECHO11_INMI could be a chimeric strain, maybe originating from a recombination event between an E-11 (Acc N: AY167103) and CV-B1 (Acc N: MG845887).

Unfortunately, we were not able to sequence the entire genome of the virus infecting Pt 0 (index case) due to the low quantity of virus in residual material, as the liver bioptic sample (Pt0_L) was fixed in paraffin which badly conserved the nucleic acid. However, we were able to obtain two amplicons of the sequence by RT-PCR that localized upstream and downstream from the recombination breakpoint respectively. Both amplicons were sequenced and show a high identity (median value=99.78% and 98.17% of upstream and downstream fragment, respectively) both with the sequences of the three isolates and the virus detected in the liver of patient 1 (Pt1_L), therefore suggesting that the recombination had already occurred in the virus infecting the source (Pt0).

The phylogenetic tree of the full genome sequences (data not shown) shows that ECHO11_INMI, segregates with the CV-B1 (MG845887.1). To better define the phylogenetic relationships, we analyzed separately the P1, containing the VP1 gene, and the P3 region as it locates close to 3 end of the genome and far from P1 (Fig.1). The phylogenetic tree of the P1 region (Fig.2) shows that our ECHO11_INMI sequence clusters together with all E-11 types while CV-B1 (MG845887.1) segregates with CV-B1 type in a separate clade. The P1 region contains the sequence coding for the capsid proteins, VP4, VP2, VP3 and VP1. In particular, it is well known that VP1 is the most antigenic protein and its sequence is used for the typing of Enterovirus genus as it has been shown to correlate very well with the classical serotype [32]. Indeed, phylogenetic studies on VP1 sequences of the genus have clearly shown that strains of the same serotype always cluster together [33].

Phylogenetic trees. Phylogenetic trees constructed on the basis of P1 region [nucleotide positions from 726 to 3253 referring to Human echovirus 11 prototype strain Kust/86 (Accession N GenBank: AY167105.1)] and of the P3 region [nucleotide positions from 6956 to 7256 referring to Human echovirus 11 prototype strain Kust/86 (Accession N GenBank: AY167105.1)]. The nodes defining the clade including ECHO11_INMI strain are indicated with a black dot (Bootstrap value in a, b, and c tree are: 99, 100 and 94 respectively). ECHO11_INMI strain are reported in red, Echo 11 types are reported in blu and CVB1 types are reported in green

Therefore, this result confirms that our sequence belongs to the E-11 type. The last tree (Fig.2), constructed on the basis of the P3 region of the genome, shows that the ECHO11_INMI segregates close to the CV-B1 (MG845887.1). This result is consistent with the hypothesis that recombination occurred in the P2 region of the genome, between P1 and P3.

To confirm the presence of a recombination breakpoint in our strains, we performed a recombination detection analysis, using RDP4 software (Fig.3). Specifically, the analysis recognized that ECHO11_INMI was a chimeric strain of E-11 (AY167103) and CV-B1 (MG845887); it also identified the breakpoint of recombination between nucleotide 4083 and 4201 of ECHO11_INMI sequence without gap, with 99% certainty (p values 5.259*1024, as reported by RDP4).

Recombination analysis results using RDP4. The plot shows the pairwise identity between ECHO11_INMI (accession no: KX527626) and the Human E-11 strain Hun/90 (accession no: AY167103.1) or CV-B1 (accession n. MG845887), represented in green and purple line respectively. While the yellow line shows the pairwise identity between E-11 strain Hun/90 and CV-B1. Each polymorphic site detected in the sequence dataset analyzed, was marked with a black bar. Then, the long black lines above the plot equivalent to the high number of nucleotide variation among sequences; the white spaces identify regions where the polymorphism are absent

The recombination site is located in the region encoding for P2 of the polyprotein that is the precursor of three non-structural proteins involved in the replication process: 2Apro, 2B and 2C.

To confirm that the virus in our samples is a new variant originating from a recombination event between an E-11 and a CV-B1, and to exclude the hypothesis of a co-infection with both viruses, we designed four sets of primers. Two of them were specific for E-11 serotype, targeting respectively the region upstream and downstream of the breakpoint (E11 2F-E11 2R, E11 3F-E11 3R); in the same way we designed two sets of primers specific for CV-B serotypes, targeting respectively the region upstream and downstream from the recombination site (CVB 2F-CVB 2R, CVB 3F-CVB 3R). Figure1 shows a schematic representation of the EVs genome and details of experimental design for RT-PCR amplification of both E-11 and a CV-B1.

Pt1_S and all isolates were tested with all sets of primers described and we obtained similar results(Additional File 5). The amplification resulted positive with the set E112F-E112R, that targets the region upstream of the recombination breakpoint, and with the set CVB 3F-CVB 3R, that targets the region downstream of the breakpoint, instead the other sets of primers, CVB 2F-CVB 2R and E11 3F-E11 3R, that map at 5 and 3 of the genome, respectively, gave negative results (Fig.4).

RT-PCR performed with specific sets of primers for E-11 and CV-B on Pt1_S and Iso_PT1_S

These findings are consistent with the recombination hypothesis and confirm the presence of only the recombinant variant in the examined samples; in addition the presence of the same pattern of amplification obtained by the analysis of the virus in serum sample and the one isolated from cell culture, revealed that the recombination was not generated by the isolation procedure.

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Detection of recombinant breakpoint in the genome of human enterovirus E11 strain associated with a fatal nosocomial outbreak - Virology Journal -...

It has been almost 44 years years since the first in vitro fertilisation (IVF) procedure was successfully performed in 1978 in Lancashire, England. Since then, more than 8 million babies have been born worldwide to assisted reproductive technologies, such as IVF.

But despite its increasing use, the success rate of IVF still remains relatively low, at around 30%. There may be a number of reasons for this. In our recent paper, we argue that this low rate is partially due to the many unfavourable genetic changes that we carry in our DNA.

Genetic changes happen when mutations in our genes replace, insert or delete sections of DNA. More of these mutations are occurring now in humans because were having babies at a later age. As we get older, more mutations are likely to accumulate meaning older parents are more likely to pass on genetic mutations to their children than younger parents. Mutations may also be caused by environmental factors (such as ultraviolet radiation in sunlight), or lifestyle choices (for example, smoking).

All of the genetic changes we inherit or develop throughout our lifetime constitute whats known as our genetic load. This genetic load can impact our ability to reproduce. And as our study suggests, this may also affect our ability to reproduce via methods such as IVF.

Genetic mutations make evolution possible. They provide the new material for natural selection that allows species to adapt and evolve. While most of these mutations have no effect, some are slightly harmful. Such harmful mutations may cause diabetes or breast cancer, for example or they may disrupt the healthy development of an embryo.

Human DNA carries more than 1,000 harmful mutations, most of which happened many generations ago. Yet, even though they are harmful, they have not (yet) been removed, because natural selection is a very slow process.

In addition to the large number of old mutations, new mutations also enter the population every generation. On average, every person acquires approximately 70 new mutations during their lifetime. But since some of these mutations are harmful, they need to be removed by natural selection, so that they arent passed on to future offspring. One of the most important times this happens is during natural conception.

When a child is conceived naturally, the body has many mechanisms in place to remove some of these harmful mutations.

For example, the female reproductive system is designed in such a way that only the fittest sperm cells can reach the egg for fertilisation. Although evidence is scarce, animal studies suggest that the sperm that reach the fertilisation site have a better DNA quality and potentially fewer mutations.

Mature eggs also undergo a sort of quality check during fertilisation. This too helps purge some of the genetic load. The implantation stage (where a fertilised embryo implants itself in the mothers womb) is also important, as many embryos with severe genetic abnormalities tend to be lost naturally during pregnancies.

However, IVF bypasses some of these natural mechanisms. During IVF, multiple eggs are harvested from the womans ovaries and fertilised with sperm in a laboratory. After they have been fertilised, the embryos are then returned to the womb. This reduces the opportunity for natural selection, which may therefore make IVF less efficient in reducing the genetic load. This could potentially increase the likelihood that harmful variants of genes may be passed onto the next generation.

So, the genetic load has two big implications for human reproduction. First, the genetic load of parents affects their ability to successfully reproduce. This is true both for natural conception, as well as for IVF. Second, by relaxing natural selection, IVF may let more mutations slip through the net. As such, it could slowly increase our genetic load in future generation. But there may be a solution.

Fertility rates have suffered an unprecedented decline in recent decades. In fact, sperm count has fallen by about 50 to 60% between 1973 and 2011. Its unclear why this is, but if this trend continues it could mean more people turn to IVF to conceive.

Yet we still know surprisingly little about human reproduction and the selective processes operating during natural conception. We must understand natural conception first if we want to improve assisted reproduction methods, including IVF. But recent technological advances in assisted reproductive technologies mean that we may soon be better able to counteract some of the genetic load in humans. For example selection at sperm level in the IVF process has been shown to improve the offspring fitness in animal models. In particular, selection of longer-lived sperm in zebrafish results in healthier offspring that live longer.

Advances in genomic technologies also have the potential to affect human evolution. Already, genomic data is effectively being used in clinical care, and the genomic bases of thousands of human diseases are now known. Furthermore, changes to our environment and our lifestyle are affecting the genetic load and human health. Most often, these changes have a negative effect, which makes these technological advances ever more important. As new advances are made, it will also be important to consider the potential consequences of using assisted reproductive technologies if these become the norm.

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IVF: heres how genetics may be affecting its success new insights - The Conversation Indonesia

Using DNA extracted from blood, tissue or skin samples, researchers looked for 566 mutations linked to disease, including 84 for cancer, 77 for heart conditions, and others affecting responses to medicines

Image: Reuters)

Whole genome sequencing could be offered to all adults on the NHS within five years to help millions cut their risk of conditions such as cancer and heart disease, experts have revealed.

Thousands of lives could be saved annually if the tests - which read a persons entire genetic code - were widely available, it was said.

In a study of 102 healthy patients at a GP surgery, one in four were found to carry actionable mutations.

These were changes to their genes which increased risk of certain diseases but could be mitigated through lifestyle changes, extra monitoring or other preventative measures.

Six in ten carried an inherited mutation in a recessive gene, meaning they were not affected by a condition but could pass it on to their children.

Detecting such mutations can guide healthcare decisions and enable more personalised treatment.

Study leader Professor Ros Eeles, an expert in oncogenetics at The Institute of Cancer Research in London, said the results could spark a revolution in healthcare, paving the way for testing to be rolled out to anyone who wants it in the next two to five years.

Image:

No countries are yet offering genome tests on this scale.

Prof Eeles added: Our findings suggest that integrating whole-genome sequencing into primary care could change the way most patients and their families are managed by their GPs.

Health Secretary Sajid Javid said genomics was changing the future of healthcare.

He added: This study shows the potential for genome sequencing in enabling patients with life-changing diseases to receive early diagnoses just by visiting their GPs in future.

The UK continues to lead the way in genomics expertise and this exciting collaboration between the Institute of Cancer Research, the NHS and the wider health sector has the potential to save lives by increasing the detection and prevention of diseases such as cancer and heart disease.

The study was the first to trial offering the tests at GP surgeries and recruited participants from The London Genetics Centre, at 90 Sloane Street.

A human genome contains around 20,000 genes made up of 3.2 billion letters of DNA.

Using DNA extracted from blood, tissue or skin samples, researchers looked for 566 mutations linked to disease, including 84 for cancer, 77 for heart conditions, and others affecting responses to medicines.

Some 26 patients had potentially actionable genetic variants, 61 had a recessive gene that could be passed on should their partner also carry it, and 38 had changes linked to medicine responses.

Dr Eeles, also a cancer consultant at The Royal Marsden NHS Foundation Trust, said the most common action taken as a result was more frequent screening for patients at risk of cancer.

One woman found to be at elevated risk of ovarian cancer chose to have her ovaries removed.

Another who frequently travelled discovered she was at high risk of deep vein thrombosis and now uses an injectable anticoagulant before flights to prevent blood clots.

Other possible benefits include the ability to select drugs that cause less side effects, or earlier prescribing of statins for people predisposed to have high-cholesterol.

People with mutations that could be passed onto their children can be offered IVF with embryo screening.

Around 70 per cent of those with actionable mutations would not have been identified through normal checks and family history.

Whole genome sequencing is available for certain conditions including some cancers and rare diseases.

Dr Eeles said her team was in discussions with NHS England and the tests could eventually become a routine part of GP registration.

She added: The power of new genetics really needs to be enhanced for healthcare and this is the first study along the way.

Its definitely coming. Theres a huge impetus in genome integration into healthcare in the UK.

Sequencing each patients genome cost 1,800 but researchers believe this can be cut to under 1,000 for the NHS.

Dr Eeles added: It sounds like a lot but to treat somebody with metastatic [cancer] you could be talking about 200,000 for two years of immunotherapy treatment.

Patients were not told about their risk of diseases with no known treatments, such as dementia. Specially trained staff helped them understand their results and deal with any concerns.

The findings will be presented at the American Society of Clinical Oncologys Annual Conference in Chicago.

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Genome sequencing could be offered to all adults on NHS in bid to defeat cancers - The Mirror