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Court Says Google Has A First Amendment Right To Delist Competitor’s ‘Spammy’ Content – Above the Law

Posted: February 19, 2017 at 10:55 am

Last summer, a Florida federal court reachedsome unusual conclusionsin a lawsuit filed by SEO company e-ventures, which felt Google had overstepped its bounds in delisting a lot of its links. Google defended itself, citing both Section 230 and the First Amendment. The court disagreed with both arguments.

As to Section 230, the court found that Googles delisting efforts werent in good faith. The reason cited was e-ventures claim that the delisting was in bad faith. So much for this seldom-used aspect of Section 230: the Good Samaritan clause which states no third-party company can be found liable for actions it takes to remove content it finds questionable. And so much for viewed in the light most favorable to the non-moving party. Apparently, Googles long history of spam-fighting efforts is nothing compared to an SEO wranglers pained assertions.

The court also said Google had no First Amendment right to handle its search rankings however it saw fit, which is more than a little problematic. While it admitted Googles search rankings were protected speech, its statements about how it handled search engines werent. And, for some reason, the court felt that Googles ads undermined its First Amendment protections because its desire to turn a profit somehow nullified its editorial judgment.

It was a strange decision and one that suggested this court might be considering getting into the business of telling service providers how to run their businesses. It also suggested this court believed the more successful the business was, the fewer rights and protections it had. These dubious conclusions prevented Google from having the case dismissed.

Fortunately, this wasnt the final decision. As Eric Goldman points out, last years denial only delayed the inevitable. After a few more rounds of arguments and legal paperwork, Google has prevailed. But theres not much to celebrate in this decision as the court has (again) decided toroute around Googles Section 230 Good Samaritan defense.

Regarding 230(c)(2), the court says spam can qualify as harassing or objectionable content (cite toe360insightwith a but-see to theSong Ficase). Still, the court says e-ventures brought forward enough circumstantial evidence about Googles motivations to send the case to a trial. By making it so Google cant even win on summary judgment, rulings like this just reinforce how Section 230(c)(2) is a useless safe harbor.

Had it ended there, Google would be still be facing e-ventures claims. But it didnt. The court takes another look at Googles First Amendment claims and finds that the search engine provider does actually have the right to remove spammy links. Beyond that, it finds Google even has the First Amendment right to remove competitors content. From theorder[PDF]:

[T]he First Amendment protects as speech the results produced by an Internet search engine. Zhang v. Baidu.com, Inc., 10 F. Supp. 3d 433, 435 (S.D.N.Y. 2014). A search engine is akin to a publisher, whose judgments about what to publish and what not to publish are absolutely protected by the First Amendment. See Miami Herald Publg Co. v. Tornillo, 418 U.S. 241, 258 (1974) (The choice of material to go into a newspaper . . .whether fair or unfairconstitute[s] the exercise of editorial control and judgment that the First Amendment protects.) The presumption that editorial judgments, no matter the motive, are protected expression is too high a bar for e-ventures to overcome.

And the court walks back its earlier conclusion the one that seemed to find profit-motivated editorial judgment to be unworthy of First Amendment protections.

Googles actions in formulating rankings for its search engine and in determining whether certain websites are contrary to Googles guidelines and thereby subject to removal are the same as decisions by a newspaper editor regarding which content to publish, which article belongs on the front page, and which article is unworthy of publication. The First Amendment protects these decisions, whether they are fair or unfair, or motivated by profit or altruism.

The case is now dismissed with prejudice which bars e-ventures from complaining about Googles delisting efforts in federal court. e-ventures has gone this far already in hopes of seeing its terms-violating content reinstated, so it will likely attempt to appeal this decision. But it really shouldnt. Its unlikely another set of judges will help it clear the First Amendment hurdle. Not only that, but this area of law should be well-settled by now, as Goldman points out:

Of course Google can de-index sites it thinks are spam. Its hard to believe were still litigating that issue in 2017; these issues were explored in suits likeSearchKingandKinderStartfrom over a decade ago.

The plaintiff was given a long leash by the court, which should have tossed last year. Even with the extra time and the court doings its Section 230 circumvention work for it, e-ventures still couldnt prevail.

Court Says Google Has A First Amendment Right To Delist Competitors Spammy Content

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Molecular hairpin structures make effective DNA replicators – Phys.Org

Posted: February 17, 2017 at 12:51 am

February 16, 2017 Credit: rost9 / fotolia.com

The evolution of cells and organisms is thought to have been preceded by a phase in which informational molecules like DNA could be replicated selectively. New work shows that hairpin structures make particularly effective DNA replicators.

In the metabolism of all living organisms there is a clear division of labor: Nucleic acids (DNA and RNA) carry the information for the synthesis of proteins, and proteins provide the structural and executive functions required by cells, such as the controlled and specific catalysis of chemical reactions by enzymes. However, in recent decades, it has become clear that this distinction is by no means absolute. In particular RNA is capable of ignoring the boundary outlined above and is known to play a catalytic role in many important processes. For example, certain RNA molecules can catalyze the replication of other nucleic acids, and this versatility could help to explain how life originated on Earth.

Nucleic acid molecules are made up of subunits called nucleotides, which differ in their so-called bases. The bases found in RNA are referred to as A, C, G and U (DNA uses T in place of U). These bases fall into two complementary pairs, whose members specifically interact, A with T (or U) and G with C. This complementarity is what accounts for the stability of the DNA double helix, and enables single strands of RNA to fold into complex shapes.

Life is thought to have emerged from a process of chemical evolution in which nucleic acid sequences could be selectively replicated. Thus, in prebiotic systems certain molecular “species” that carried information were reproduced at the expense of others. In biological systems, such selectivity is normally mediated by so-called primersstrands of nucleic acid that pair (as described above) with part of the molecule to be replicated, to form a short double helix. The primer provides a starting point for the extension of the double-stranded region to form a new daughter strand. Moreover, this process can be reconstructed in the test-tube.

The pros and cons of hairpin replicators

Georg Urtel and Thomas Rind, who are members of the research group led by Dieter Braun (Professor of Systems Biophysics at LMU), have used such a system to identify properties the might favor the selective replication of DNA molecules. For their experiments, they chose a single-stranded DNA sequence that adopts a so-called hairpin structure. In these molecules, the base sequences at either end are complementary to each other, as are short stretches of sequence within the rest of the molecule. This distribution of complementary sequences causes such a strand to fold into a hairpin-like conformation.

Thanks to the pairing rules outlined above, replication of a single strand of DNA produces a second strand whose sequence differs from that of the first. Each strand of a non-hairpin structure therefore needs its own primer for replication. But with hairpins, one primer suffices to prime synthesis of both the original and its complementary strand. “This means that hairpins are relatively simple replicators,” Georg Urtel points out. The downside is that the hairpin structure makes primer binding more difficult, and this in turn limits their replication rate. Molecular species that are devoid of hairpin structures don’t have this problem.

Cooperation beats competition

In subsequent experiments the researchers discovered that two simple hairpin species could cooperate to give rise to a much more efficient replicator, which requires two primers for its amplification. The two hairpin species selected each required a different primer, but their sequences were in part identical. The switch to cooperative replication occurs when replication of one of the hairpins stalls. “As a rule, replication processes in nature are never perfect,” says Dieter Braun. “Such a premature halt is not something that one needs to design into the system. It happens stochastically and we make use of it in our experiments.” The partially replicated hairpin can, however, bind to a molecule of the second species, and serves as a primer that can be further elongated. Moreover, the resulting product no longer forms a hairpin. In other words, it represents a new molecular species.

Saved from extinction

Such so-called ‘crossbreeds’ need two primers for their replication, but can nevertheless be replicated significantly faster than either of their hairpin progenitors For further experiments showed that, upon serial dilution of the population, the hairpin DNAs soon become extinct. However, the sequence information they contained survives in the crossbreeds and can be replicated further.

The converse experiment confirmed that information is indeed conserved: If crossbreeds are supplied with only one primer, the corresponding progenitor hairpin species can still be replicated by the kind of switching process mentioned above. But, in the absence of the second primer, the crossbreed dies out. “Thus, the crossbreeding process not only provides for the transition from ‘simple and slow’ replicators to more rapid replicators, it also makes it possible for the system to adapt to the prevailing conditions,” Urtel explains. “It also suggests how early replicators could have cooperated with each other under prebiotic conditions prior to the origin of living systems.”

Explore further: Genetic switch regulates transcription and replication in human mitochondria

More information: Georg C. Urtel et al. Reversible Switching of Cooperating Replicators, Physical Review Letters (2017). DOI: 10.1103/PhysRevLett.118.078102

(Phys.org)The majority of the human genome is located within the nucleus. However, there is a small but important portion of DNA located within the mitochondria. This mitochondrial DNA (mtDNA) has received much attention …

Researchers at Case Western Reserve University and the University of Michigan have produced the first image of an important human protein as it binds with ribonucleic acid (RNA), a discovery that could offer clues to how …

MIT scientists have found a new way that DNA can carry out its work that is about as surprising as discovering that a mold used to cast a metal tool can also serve as a tool itself, with two complementary shapes each showing …

DNA lesions are really common about one million individual molecular lesions per cell per day because its long strands usually have one missing base or are damaged. These lesions can stall the DNA replication process, …

The original recipe for gene soup may have been simplerain, a jumble of common molecules, warm sunshine, and nighttime cooling. Then add a pinch of thickener.

UV light damages DNA. But LMU researchers now show that it can also mediate non-enzymatic repair of one type of damage, albeit in a specific context. This effect may have played vital role in early evolution of living systems.

Research led by ANU on the use of magnets to steer light has opened the door to new communications systems which could be smaller, cheaper and more agile than fibre optics.

University of Toronto (U of T) researchers have demonstrated a way to increase the resolution of microscopes and telescopes beyond long-accepted limitations by tapping into previously neglected properties of light. The method …

The demand for faster computers is growing rapidly and the rise of big data demands novel solutions be explored to deliver quicker results.

Although scientists have been able to levitate specific types of material, a pair of UChicago undergraduate physics students helped take the science to a new level.

Experiments at ANSTO have provided supporting evidence of unexpected enhancement of water solubility of biomolecules in an aqueous solution of divalent transition-metal cations.

A detection device designed and built at Yale is narrowing the search for dark matter in the form of axions, a theorized subatomic particle that may make up as much as 80% of the matter in the universe.

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Telomeres nature’s anti-ageing scheme – Varsity Online

Posted: at 12:49 am

Zi Ran looks into the exciting biology surrounding telomeres and their potential impact

The thread of never-ending life has always been a part of the canvas of myths and religion subsequently morphed seamlessly into everyday culture. Every religion and culture has their own telling of the tale. The Abrahamic religions have heaven, the Norse gods ate Iunns apples, the Greek gods ate ambrosia and drank nectar, the Taoists sought the elixir of life, and the medieval alchemists sought the philosophers stone. Though these ancient symbols may have been metaphoric, with current technology eternal youth feels to be almost within our grasp. With organisations like Google Calico, A4M (American Academy of Anti-Aging Medicine), Human Longevity Inc and sponsors like Peter Thiel and Mark Zuckerberg, it seems as though humanity may finally taste that fountain of life.

To find immortality, one must understand mortality. Cells seemingly repair and divide without end, but they exhibit signs of ageing as well. The crux of the issue lies in the inherent structure of our genetic material, DNA. Human DNA is linear, so there must be two ends to the double helix. Every time DNA is replicated, information on the ends of the strands are lost. With increasing divisions, more and more information is lost to the point where the cell is no longer able to function cells senescence. Cells with this kind of DNA structure must have an extra layer of molecular protection which ensure many healthy divisions before their eventual death. These protective elements are called telomeres. Telomere research has been a hot topic within the anti-ageing community, as its length is directly correlated to longevity. These DNA aglets are extra pieces of DNA which cap on to the ends of the double helix strand and tightly wraps itself together to protect the genetic material both from chemical and mechanical damage. However, this method is not fool-proof. Telomeres also run out, and with time all cells eventually die.

The miracle of the fountain of life, if it exists at all, can only be found in the moment of conception. In embryos, the DNA is refreshed, and old used telomeres are extended. Embryonic cells are a rare type of cells which express telomerase, the only protein capable of extending the length of telomeres. These little molecular machines use RNA as a template to extend the depleted telomeres, elongating the lifespan of the cell. Telomerases are also expressed in some stem cells, which supply the body with red blood cells and repair large damages. As attractive as telomerases sound as a solution to age, their over-expression can also become a problem. Many tumours and cancer types use telomerase as a tool to extend their lifespan indefinitely, outliving their healthy counterparts and taking over the body. To fine-tune the activity of this protein such that humans achieve eternal life while escaping the potential over-proliferation of cells is something that has yet to be achieved.

The most important breakthrough of 2016?

Telomeres, all in all, may only be one piece of the longevity biochemical puzzle. Many other biological processes are affected by age, although the precise mechanisms remain shrouded in mystery. Mitochondria become less efficient, transport to and from the nucleus becomes much less regulated, proteins are misshapen more often, and the DNA racks up too many mutations to efficiently repair them. It looks as though humanity still has so much to learn in terms of mortality that the seemingly tiny gap to eternal life may actually be a journey of a thousand miles.

Once we understand the essentials of life, will eternity still be attractive? The underlying basis of all living things is maintenance of a dynamic equilibrium, meaning that balance is maintained through constant life and death. The confusion of age for life has been recorded since the time of the ancient Greeks. When Eos mistakenly asked on Tithonus behalf for immortality and not eternal youth, what she really obtained from Zeus was eternal torture. The ancient Homeric hymns only remember Tithonus as a withered old man with no strength to even sit up, certainly an anecdote to keep us grounded in our search

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Euthanasia’s march Down Under – Catholic Herald Online (blog)

Posted: February 15, 2017 at 9:46 pm

Stories of suffering are the currency use to validate assisted suicide (Getty)

A coalition of academics, journalists and celebrities is trying to convince Australians that legalisation is overdue. But were fighting back

The internationally renowned psychiatrist and Holocaust survivor Viktor Frankl experienced first hand the utter depravity of Auschwitz and Dachau. He knew the immense physical torment, psychological torture and spiritual desolation of those most inhuman of places. They were not called death camps for figurative effect.

Suicide was not unknown among those sent there to suffer grievously and die. Yet, strikingly, Frankl writes in his autobiographical study, Mans Search for Meaning, of the obligation fellow inmates accepted to frustrate such occurrences: A very strict camp ruling forbade any efforts to save a man who attempted suicide Therefore, it was all-important to prevent these attempts from occurring.

In naming the reason for this paramount calling, Frankl said: When a man finds that it is his destiny to suffer, he will have to accept his suffering as his task; his single and unique task His unique opportunity lies in the way in which he bears his burden.

As words such as compassion and dignity and care become (mis)appropriated by advocates for legalising euthanasia and assisted suicide (EAS), I have often thought of Frankls enduring insight that human life is essentially a quest for meaning. Advocates of legalised EAS seem unable to grasp the deep meaning to be discovered by a person in that uniquely human project of embracing what Frankl called the wider cycles of life and death, of suffering and of dying.

It is realistic to acknowledge that some individuals, in the midst of their own mortal suffering, will seek out euthanasia, and that others will be willing to assist in that desperate act. God only knows and only God can judge the existential torment that might overwhelm a person, and their loved ones, as they suffer in dying. But when societies start to legislate for this, when they actively chose killing over living as the better way, then much will be lost of our common human project. Legalising EAS is a society giving up on its own people.

Unlike in Britain, where debate happens on a national level, the question of legalising EAS in Australia is a state-based issue. This is because healthcare is the responsibility of the eight states and territories, and not the single Commonwealth. Consequentially, there is a rolling debate on euthanasia across the country, depending on which parliament is considering legislative action at any particular time. The parliament of South Australia, for example, has recently defeated (by a single vote) the 13th attempt at legalising EAS. The State of Tasmania has had several goes at pushing through legalisation. A cross-party bill will be considered in the parliament of New South Wales this year, and parliamentary advocates in Queensland and Western Australia are testing the waters. This creates difficulties in rallying resources and people to counter such developments.

The major battleground, however, is Victoria. It is in this state that, for the first time, a government-sponsored bill will be tabled in the second half of this year, following a parliamentary inquirys recommendation to legalise EAS.

Who is supporting this move? There is a socially liberal disposition among many academics and the media, which is being encouraged by a handful of celebrity campaigners and supported by some professional bodies of medical practitioners.

EAS is spoken of by these advocates as a step forward, overdue and an idea whose time has come. It is presented as the morally decent thing to do, demanding of those who resist change the justification of their unenlightened position. Those who do not support EAS are quickly dismissed as either religiously motivated or doctrinaire.

It is telling that this most basic question of our common humanity is couched by EAS advocates in bygone sectarian images and language. Yet that is the nature of the debate in Australia: euthanasia is but one flank of a wider front in a battle for radical cultural change.

It is in the stories we tell that our humanity will be revealed. Personal stories of suffering are the currency used to validate the wielding of a blunt and crude legislative instrument over the lives of the dying. In telling only of ordeal and despair, advocates of EAS seek to privilege the reduction of a persons entire life to the end part only. The task is no longer how to support someone in the living of their life, but how to effectively bring about their death. In the legalising of EAS, dying is no longer viewed as a uniquely human dimension of living, but rather as a process to be brought about as proficiently as possible.

Might we not find a more truthful storytelling of our humanity in Viktor Frankl? And finally, he wrote, I spoke [to my comrades] of our sacrifice, which had meaning in every case. It was in the nature of this sacrifice that it should appear to be pointless in the normal world But in reality our sacrifice did have a meaning The purpose of my words was to find a full meaning in our life, then and there, in that hut and in that practically hopeless situation.

To legalise EAS is to give up on telling the story of the full meaning of our lives. This story is not always easily told, but it is a true story in need of listening ears.

The Most Rev Dr Peter Comensoli is Bishop of Broken Bay and the Australian Bishops Delegate on Euthanasia

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Davenport talks free speech, diversity, AD search on first day – Knoxville News Sentinel

Posted: at 9:04 pm

VIDEOS: NEW UNIVERSITY OF TENNESSEE CHANCELLOR BEVERLY DAVENPORTBeverly Davenport, UTK chancellor, speaking on first day at work | 1:25

Beverly Davenport, UTK chancellor, speaking to media on first day at work in Knoxville. Michael Patrick/News Sentinel

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UT Chancellor Jimmy Cheek offers words of advice for his successor, Beverly Davenport, at a reception during his last week as chancellor on Wednesday, Feb. 8, 2017. Rachel Ohm/News Sentinel

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Beverly J. Davenport, interim president at the University of Cincinnati, speaking in an open forum with faculty and students at the Howard H. Baker Jr. Center on campus Monday, Nov. 7, 2016. Davenport is the second candidate to visit UTK. Michael Patrick/News Sentinel

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Beverly Davenport, UTK chancellor, speaking on first day at work

Jimmy Cheek offers words of advice for his successor

Chancellor candidate Beverly Davenport speaking at open forum at UTK

University of Tennessee Chancellor Beverly Davenport spent her first morning on the job Wednesday, Feb. 15, 2017, talking to students and media.(Photo: Michael Patrick/News Sentinel)Buy Photo

In her first interview on the University of Tennessee’s Knoxville campus, new Chancellor Beverly Davenport said she doesn’t think the state needs a law protecting free speech on college campuses and suggested she would work to reinstatefunding for UT’s Office for Diversity and Inclusion.

Davenport, who took office Wednesday as the first female chancellor at UT, also touched on the search for a new athletic director, outsourcing of facilities management jobs and Title IX issues in a wide-ranging discussion with members of the media Wednesday morning.

Davenport, 62, takes over from Chancellor Emeritus Jimmy Cheek, who is moving to a tenured faculty position in the College of Education, Health and Human Sciences. With a $585,000 base salary, Davenport will earn more than her predecessor.

She isinheriting a wide range of issues and said she has “a lot of listening to do” in her first few weeks on campus.

Among the most recent is a bill proposed by state lawmakers last week that aims toprotect free speech on campusafter a Breitbart News editor whose planned speech at the University of California, Berkeley, spurred violent protests that promptedcollege officials there to cancel the event.

Rep. Martin Daniel, R- Knoxville, a sponsor of the bill, said last week the legislation is “designed to implement oversight of administrators’ handling of free speech issues.”

Beverly Davenport, UTK chancellor, speaking to media on first day at work in Knoxville. Michael Patrick/News Sentinel

Davenport, who has a background in communications and comes to UT from the University of Cincinnati, where she most recently served as interim president, said she is a First Amendment advocateand proponent of free speech on campus, but doesn’t see the need for a bill.

“It’s a constitutional right. I don’t think we need a bill,” Davenport said.

She’s also expected to work with state lawmakers when it comes to funding for UT’s Office for Diversity and Inclusion.Last year the state diverted more than $400,000 away from the office after conflicts with lawmakers over Sex Weekevents and a post on the office’s website promoting the use of gender-neutral pronouns and advising against Christmas-themed holiday parties.

When asked by a reporter Wednesday whether that money, which was diverted to pay for scholarships for minority students, would be redirected, Davenport said “there will be funding.”

“I will only be on a campus where every student is supported and made to feel welcome and important and safe,” she said. “I wouldn’t be on a campus if I wasn’t committed to and wouldn’t find revenue to support the programs that serve all of our students.”

She also said communicatingwith state lawmakers is one area where universities, in general, need to improve.

“We say this when Im among administrators at national meetings, we say this all the time: ‘We havent constructed our narrative very well. We havent told our story well enough,'” Davenport said.”The burden is on us. The responsibility is on us to make that argument, to tell that story.”

On the search for a new athletic director, Davenport said the university is “moving really quickly” but no firm timeline is in place for filling the post. She would not comment when asked to disclose the names of specific candidates.

“I have no doubt she’ll make a great decision,” said Lady Vols coach Holly Warlick.”I think she’s going to take her time. Do I want an AD yesterday? Yeah. But I think she’s going to do her homework. She’s going to do her due diligence. I think she’s going to try to get the best fit here. I respect that. I want her to do that. We’ve got to get it right.”

In an interview last week, Davenport also talked about the importance of education on Title IX issues, especially given that UT in July settled a $2.48 million lawsuit accusing the university of fostering a “sexually hostile environment” and mishandling allegations of sexual assault on campus, especially allegations made against athletes.

She reiteratedWednesday that Title IX and campus sexual assaults arethe issue that “probably keeps me up at night more so than any other issue that I deal with.”

Davenport cited a meeting with Gov. Bill Haslam during her interview process as one thing that attracted her to Tennessee, but said she needs to research more his proposal to outsource facilities management on public college campuses. She said she would consider options for UT to opt out of the outsourcing proposal but “its certainly one of those topics I need to know more about.”

An avid Twitter user, Davenport also expressed her excitement to be on campus Wednesday morning on Twitter and said it’s one way Tennesseans both on and off campus can keep in touch with her – though it’s not the only way.

“I will be outin as many places as I can be every day,” Davenport said.”I want them to know me some other way than through a Tweet, too. I will be out there.I will be visible.”

University of Tennessee Chancellor Beverly Davenport spent her first morning on the job Wednesday, Feb. 15, 2017, talking to students and media.(Photo: Michael Patrick/News Sentinel)

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Diabetes in your DNA? Scientists zero in on the genetic signature of risk – U of M News Service

Posted: February 14, 2017 at 11:51 pm

The researchers’ findings suggest that DNA variations linked to Type 2 diabetes interfere with the ability of Regulatory Factor X to bind to a “runway” of DNA before the start of various genes, and therefore with its ability to do its job in the reading of those genes.ANN ARBORWhy do some people get type 2 diabetes, while others who live the same lifestyle never do?

For decades, scientists have tried to solve this mysteryand have found more than 80 tiny DNA differences that seem to raise the risk of the disease in some people, or protect others from the damagingly high levels of blood sugar that are its hallmark.

But no one “type 2 diabetes signature” has emerged from this search.

Now, a team of scientists has reported a discovery that might explain how multiple genetic flaws can lead to the same disease. They’ve identified something that some of those diabetes-linked genetic defects have in common: they seem to change the way certain cells in the pancreas “read” their genes.

The discovery could eventually help lead to more personalized treatments for diabetes. But for now, it’s the first demonstration that many type 2 diabetes-linked DNA changes have to do with the same DNA-reading molecule. Called Regulatory Factor X, or RFX, it’s a master regulator for a number of genes.

The team reporting the findings in a new paper in the Proceedings of the National Academy of Sciences comes from the University of Michigan, National Institutes of Health, Jackson Laboratory for Genomic Medicine, University of North Carolina and University of Southern California.

They report that many diabetes-linked DNA changes affect the ability of RFX to bind to specific locations in the genomes of pancreas cell clusters called islets. And that in turn changes the cells’ ability to carry out important functions.

Islets contain the cells that make hormones, including insulin and glucagon, which keep blood sugar balanced in healthy people. In people with diabetes, that regulation goes awryleading to a range of health problems that can develop over many years.

“We have found that many of the subtle DNA spelling differences that increase risk of type 2 diabetes appear to disrupt a common regulatory grammar in islet cells,” said Stephen Parker, assistant professor of computational medicine and bioinformatics, and of human genetics, at the U-M Medical School. “RFX is probably unable to read the misspelled words, and this disruption of regulatory grammar plays a significant role in the genetic risk of type 2 diabetes.”

Parker is one of four co-senior authors on the study, which also includes Michael Boehnke of the U-M School of Public Health’s Department of Biostatistics; Francis Collins, director of the National Institutes of Health; and Michael Stitzel of the Jackson Laboratory.

Prior to their current faculty positions Parker and Stitzel worked in Collins’ lab at the National Human Genome Research Institute. Parker’s graduate student, Arushi Varshney, is one of the study’s co-first authors with Laura Scott and Ryan Welch of the U-M School of Public Health’s Department of Biostatistics and Michael Erdos of the National Human Genome Research Institute.

They performed an extensive examination of DNA from islet samples isolated from 112 people. They characterized differences not just in DNA sequences, but also in the way DNA was packaged and modified by epigenetic factors, and the levels of gene expression products that indicated how often the genes had been read and transcribed.

This allowed them to track the “footprints” that RFX and other transcription factors leave on packaged DNA after they have done their job.

RFX and other factors don’t bind directly to the part of a gene that encodes a protein that does a cellular job. Rather, they bind to a stretch of DNA near the genea runway of sorts. But when genetic changes linked to type 2 diabetes are present, that runway gets disrupted, and RFX can’t bind as it should.

Each DNA change might alter this binding in a different way, leading to a slightly different effect on type 2 diabetes risk or blood sugar regulation. But the common factor for many of these changes was its effect on the area where RFX is predicted to bind, in the cells of pancreatic islets.

So, says Parker, this shows how the genomethe actual sequence of DNAcan influence the epigenome, or the factors that influence gene expression.

The researchers note that a deadly form of diabetes seen in a handful of babies born each year may be related to RFX mutations. That condition, called Mitchell-Riley syndrome, involves neonatal diabetes and malformed pancreas, and is known to be caused by a rare autosomal recessive mutation of one form of RFX.

In addition to co-senior and co-first authors listed above, the study’s authors include a range of researchers from several institutions. The study was funded by the National Institutes of Health.

Parker is a 2014 recipient of the American Diabetes Association’s Pathway to Stop Diabetes grant, a type of grant awarded annually by the American Diabetes Association to provide up to $1.625 million to each scientist over a five- to seven-year grant term to spur breakthroughs in clinical science, technology, diabetes care and potential cures. Since launching in 2013, Pathway has awarded more than $36 million to 23 leading scientists.

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Neural Network Learns to Select Potential Anticancer Drugs – Drug Discovery & Development

Posted: at 11:50 pm

Scientists from Mail.Ru Group, Insilico Medicine and MIPT have for the first time applied a generative neural network to create new pharmaceutical medicines with the desired characteristics. By using Generative Adversarial Networks (GANs) developed and trained to “invent” new molecular structures, there may soon be a dramatic reduction in the time and cost of searching for substances with potential medicinal properties. The researchers intend to use these technologies in the search for new medications within various areas from oncology to CVDs and even anti-infectives. The first results were submitted toOncotargetin June 2016 and spent several months in review. Since that time, the group has made many improvements to the system and engaged with some of the leading pharmaceutical companies.

Currently, the inorganic molecule base contains hundreds of millions of substances, and only a small fraction of them are used in medicinal drugs. The pharmacological methods of making drugs generally have a hereditary nature. For example, pharmacologists might continue to research aspirin that has already been in use for many years, perhaps adding something into the compound to reduce side effects or increase efficiency, yet the substance still remains the same. Earlier this year, the scientists at Insilico Medicine demonstrated that it is possible to substantially narrow the search using deep neural networks. But now they have focused on a much more challenging question: Is there a chance to create conceptually new molecules with medicinal properties using the novel flavor of deep neural networks trained on millions of molecular structures?

Generative Adversarial Autoencoder (AAE) architecture, an extension of Generative Adversarial Networks, was taken as the basis, and compounds with known medicinal properties and efficient concentrations were used to train the system. Information on these types of compounds was input into the network, which was then adjusted so that the same data was acquired in the output. The network itself was made up of three structural elements: an encoder, decoder and discriminator, each of which had its own specific role in “cooperating” with the other two. The encoder worked with the decoder to compress and then restore information on the parent compound, while the discriminator helped make the compressed presentation more suitable for subsequent recovery. Once the network learned a wide swath of known molecules, the encoder and discriminator “switched off”, and the network generated descriptions of the molecules on its own using the decoder.

Developing Generative Adversarial Networks that produce high-quality images based on textual inputs requires substantial expertise and lengthy training time on high-performance computing equipment. But with images and videos, humans can quickly perform quality control of the output. In biology, quality control cannot be performed by the human eye and a considerable number of validation experiments will be required to produce great molecules.

All the molecules are represented as “SMILEs”, or graphical annotations of chemical substances that allow their structure to be restored. The standard registration taught in schools does not fit for network processing, but SMILEs do not do the job very well either, as they have a random length from one symbol to 200. Neural network training requires an equal description length for the vector. The “fingerprint” of a molecule will solve this task, as it contains complete information on the molecule. There are a lot of methods out there for making these fingerprints, but the researchers used the simplest binary one available consisting of 166 digits. They converted SMILEs into fingerprints and taught the network with them, after which the fingerprints of known medicinal compounds were input into the network. The network’s job was to allocate inner neuron parameter weights so that the specified input created the specified output. This operation was then repeated many times, as this is how training with large quantities of data is performed. As a result, a “black box” capable of producing a specified output for the specified input was created, after which the developers removed the first layers, and the network generated the fingerprints by itself when the information was run through again. The scientists thus built “fingerprints” for all 72 million molecules, and then compared the network-generated fingerprints with the base. The molecules selected must potentially possess the specified qualities.

Andrei Kazennov, one of the authors of the study and an MIPT postgraduate who works at Insilico Medicine, comments, “We’ve created a neuronal network of the reproductive type, i.e. capable of producing objects similar to what it was trained on. We ultimately taught this network model to create new fingerprints based on specified properties.”

The anticancer drug database was used to check the network. First the network was trained on one half of the medicinal compounds, and then checked on the other part. The purpose was to predict the compounds already known but not included in the training set. A total of 69 predicted compounds have been identified, and hundreds of molecules developed using a more powerful extension of the method are on the way.

According to one of the authors of the research, Alex Zhavoronkov, the founder of Insilico Medicine and international adjunct professor at MIPT, “Unlike the many other popular methods in deep learning, Generative Adversarial Networks (GANs) were proposed only recently, in 2014, by Ian Goodfellow and Yoshua Bengio’s group and scientists are still exploring its power in generating meaningful images, videos, works of art and even music. The pace of progress is accelerating and soon we are likely to see tremendous advances stemming from combinations of GANs with other methods. But everything that my groups are working on relates to extending human longevity, durability and increasing performance. When humans go to Mars, they will need the tools to be more resilient to all kinds of stress and be able to generate targeted medicine on demand. We will be the ones supplying these tools.”

“GANs are very much the frontline of neuroscience. It is quite clear that they can be used for a much broader variety of tasks than the simple generation of images and music. We tried out this approach with bioinformatics and obtained great results,” concludes Artur Kadurin, Mail.Ru Group lead programmer of the search optimizing team and Insilico Medicine independent science advisor.

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Valentine’s day: what’s your secret technology crush? – Naked Security

Posted: at 11:13 am

Valentines day is traditionally a time when you can act on your secret crushes and let them know how you feel about them.

Anyone who cares about security and technology has an app or a platform or a programming language or something that might not be very cool or very glamorous but which they love, trust and rely on. So this year weve decided to ask Naked Security writers what their secret crushes are.

Mark Stockley, our web technologies guru, has had a long, slightly dysfunctional love-hate relationship withPerl. He says:

My secret tech crush is Perl.

Its not for looks, mind.In a bad light Perl looks like the contents of the unix tool chain after a heavy fall down some stairs.

Its not because Perl loves me and nobody else either. When I first met Perl (in its prime in the late 90s), it had caught everyones eye and was living it up at the heart of things on seemingly every server and every website.

And its not because Perl was nice to me, either.Back then, we didnt have well lit safe spaces like Stackoverflow to get to know a programming language that had caught our eye. We had to use usenet and meeting Perl meant risking the piranha-infested waters of comp.lang.misc.perl, a usenet group so fierce and elitist that suitors with questions were publicly eviscerated for sport.

Perl is complex difficult moody, even. On the rare occasions that things go well, working with Perl can be like painting with oils or dancing with Darcey Bussell. But when they arent (and they frequently arent) it can feel like wrestling socks on to an octopus.

In fact there are a hundred reasons to choose something else, but for me there is no doubt that its Perl. For all its faults it was my gateway drug, the red pill that led me to late night Slackware installs, unfathomable man pages and scratching my head for two weeks as I looked in the wrong place for Apaches it works! page.

Here at Naked Security, were upfront about our love for password managers and multifactor authentication. But Naked Security stalwart Lisa Vaasfell out of love with hers recently. She says:

I dont know if youd call this a secret crush. The feelings I have for my password manager are more along the lines of master-sub, with a dash of Stockholm syndrome. The strength of the bondage came clear recently when I lost my phone during a trip. Got off the Metro, but somehow, the phone did not.

After a good deal of hand-wringing and fruitless searching , I gave up and ordered a replacement phone courtesy of my insurance company. Thats when the fun really began.

The lost phone had my multifactor authentication (MFA) app on it, Google Authenticator, and without it, I couldnt get into any email accounts. The lost password hoops Google made me jump through were recursive and failed every time.

Using a friends laptop, I tried to reach my password manager vendor (LastPass) to help me out. I could get one toe into LastPass, given that Ive memorized that one password, but losing my Google Authenticator app on the phone meant that I couldnt verify my login with the second factor: the one-time use password Authenticator produces.

Turns out that LastPass has no phones. None. OK, so Ill write to customer support, I thought. Explain the situation, see what they can do to ascertain Im not a hacker trying to hijack my account. Automatic LastPass responses kept telling me Id get a faster response if I upgraded to premium, and I kept wailing that I am a premium user. Days later, I finally got a response: well send you the instructions to download a new Authenticator instance, they said. To your email address on file. which I couldnt get into.

Ill stop there. Suffice it to say that I was rather impressed with the locks and chains set up around my accounts by MFA and that crazy, frustrating password manager. One lesson I learned quite well, after about a week of writhing in those bonds: I need to set up a safe word. What does that extended metaphor translate into? Well, Im not going to give it away, but lets just say that its along the lines of writing down a password. and then locking that physical token safely (hopefully!) away, not putting it on a sticky note on my monitor!

Sometimes the old loves are the best, and Naked Security writer Maria Varmazis remains devoted to Notepad++. She tells us:

As someone who dabbles in code but primarily writes for a living, my indispensable but slightly-unsexy tool is a text editor. For my PCs, Im a Notepad++ fiend. For my Macs, Im devoted to SublimeText.(Linux text editing is a sore subject in my household. I cling to emacs, which I picked up in college, while my husband is a vi die-hard. Somehow were still married.)

The simplicity of these editors is what makes them so beautiful and so useful. When you just want to write without distraction or frill, theres nothing better than opening a simple text editor and getting to work. Text editors let me type without worrying about font and format, or being interrupted by grammatical suggestions and when youre on deadline, interruption-free writing is precisely what you need. Once Ive written what I need and start editing, the built-in line numbering and contextual highlighting many of these text editors come with (handy for folks who are deep in code all day) make my life a lot easier as well.

Perhaps my devotion to these humble text editors comes from habit: back in the 90s when so many of my peers and I were learning rudimentary HTML, we went to work with just Notepad. I still remember the humble Made with Notepad buttons some of us would put on our sites as our nerdy badge of honor. Notepad was still my editor of choice in the years following when working on professional website development, Dreamweaver and others be damned.

I know a text editor isnt the first thing people think of when they need to write, but if you find it hard to get started and the thought of firing up Word makes your blood run cold, open a text editor instead. They provide minimal distractions and render no judgments so you may write freely. And for that, they will always have my devotion.

Google may be dominant on the search scene, but not everyone is comfortable with the amount of data it scavenges about users. So Danny Bradbury, our man in British Columbia, tells us why hes quietly in love with DuckDuckGo:

Google is great at delivering the results you want, in an attractive style. Half the time, thanks to voice search and Google Assistant, you dont even have to type anything. But I dont like searching for things using a tool run by a company that makes money by selling my data, especially when my work causes me to search for a lot of strange things. Evidence suggests that while Google enables users to switch off the search history that it shows them, its still collecting a lot behind the scenes. DuckDuckGo isnt as polished as Google, but Im becoming increasingly paranoid about giving my data to large companies, especially given the political uncertainties facing us over the next few years. Perhaps Im not the only one, given that DuckDuckGo racked up 4bn searches last year.

Love is wide-ranging, and its not just software and applications that Naked Security writers are secretly in love with. Freelancer Bill Camarda has been faithful to a much-loved headset for many years. He tells us:

Im jaded. Ive been disappointed too often. My idea of lovable tech is something that just works, doesnt demand a lot, didnt cost a lot, and stays out of my way the rest of the time. Thatd be my old Logitech ClearChat Comfort USB Headset H390.

I mean, this is seriously mature technology. Introduced a decade ago this coming August, you can still buy one new at Amazon. Where youre informed that itll Elevate the Power of Windows Vista. Hey marketers, I love the thing, but please: nothing could do that.

Heres what it does do: whatever I plug it into Windows 7, 8.x, 10, Mac it goes right to work. No waiting for drivers to fail install. Never crashes the system. Good sound. Good mic thats easy to adjust (and moves neatly up out of the way when Im only listening.) Handy mute button. Well-made USB cable. Fairly if not perfectly comfy adjustable padded earphones, for todays endless Hangouts, Skype videocalls, et al. Not sexy: stable, reliable, there for me. If thats not love, what is?

Meanwhile, Naked Security freelancer John E Dunn, also has a hardware love: its the privacy- and security-focused Blackphone. He says:

From the femtosecond I first saw version 1 in 2014, Ive wanted one. If they ever get around to making Men in Black 4, this is the smartphone theyd use. But how to justify paying nearly 600 for an uneventful Android smartphone? One answer is that in an age obsessed with features and looks, the Blackphone strips away all that nonsense and just does the important thing privacy well.

Granted, a lot of people think that privacy is another feature but a lot of people are wrong. Security and privacy is the future of everything, the destiny of the world. Finding all of this in a slim black device that can trace its software lineage back to the genesis of popular encryption with Phil Zimmermanns PGP just adds to its desirability. Its old but new with it.

And what about me? Ive only been editing Naked Security for a few months, but Ive been writing about technology and security for many years, and so Ive had plenty of time to fall in love with any number of flighty suitors. But the technology I still love, even though its almost as old and uncool as Donny Osmond (who I saw performing in London earlier this month; I still love him, too) is Windows Phone.

Ive been using Windows devices since back when it was known as Windows CE, and Ive only reluctantly moved to Android after smashing the screen of my beloved Nokia Lumia 1520 and discovering it would cost 250 to fix (Im now rocking a Pixel XL).

I love Windows Phone for its elegant design language: instead of dozens of multicoloured icons splattered across several pages theres a homescreen of tiles displaying all the information you need at a glance. On my homescreen I could see how many emails were waiting for me, if Id missed any calls, which of my key contacts had tried to reach me, if I had any Twitter mentions or DMs, when my next train was, and so on.

I also love that it remains a pretty secure platform: theres been almost no malware spotted in the wild. And finally, while other manufacturers made Windows Phones, the Lumia range had (and to some, still has) the very best cameras a cellphone could sport: the 1020s camera, amazing in its day, is still one to beat.

Whats your secret technology crush? Wed love to hear about your first and current loves.

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Diabetes in your DNA? Scientists zero in on the genetic signature of … – Medical Xpress

Posted: at 10:47 am

February 13, 2017 A depiction of the double helical structure of DNA. Its four coding units (A, T, C, G) are color-coded in pink, orange, purple and yellow. Credit: NHGRI

Why do some people get Type 2 diabetes, while others who live the same lifestyle never do?

For decades, scientists have tried to solve this mystery – and have found more than 80 tiny DNA differences that seem to raise the risk of the disease in some people, or protect others from the damagingly high levels of blood sugar that are its hallmark.

But no one “Type 2 diabetes signature” has emerged from this search.

Now, a team of scientists has reported a discovery that might explain how multiple genetic flaws can lead to the same disease.

They’ve identified something that some of those diabetes-linked genetic defects have in common: they seem to change the way certain cells in the pancreas “read” their genes.

The discovery could eventually help lead to more personalized treatments for diabetes. But for now, it’s the first demonstration that many Type 2 diabetes-linked DNA changes have to do with the same DNA-reading molecule. Called Regulatory Factor X, or RFX, it’s a master regulator for a number of genes.

The team reporting the findings in a new paper in the Proceedings of the National Academy of Sciences comes from the University of Michigan, National Institutes of Health, Jackson Laboratory for Genomic Medicine, University of North Carolina, and the University of Southern California.

They report that many diabetes-linked DNA changes affect the ability of RFX to bind to specific locations in the genomes of pancreas cell clusters called islets. And that in turn changes the cells’ ability to carry out important functions.

Islets contain the cells that make hormones, including insulin and glucagon, which keep blood sugar balanced in healthy people. In people with diabetes, that regulation goes awry – leading to a range of health problems that can develop over many years.

“We have found that many of the subtle DNA spelling differences that increase risk of Type 2 diabetes appear to disrupt a common regulatory grammar in islet cells,” says Stephen C.J. Parker, Ph.D., an assistant professor of computational medicine and bioinformatics, and of human genetics, at the U-M Medical School. “RFX is probably unable to read the misspelled words, and this disruption of regulatory grammar plays a significant role in the genetic risk of Type 2 diabetes.”

Parker is one of four co-senior authors on the paper, which also includes Michael Boehnke, Ph.D., of the U-M School of Public Health’s Department of Biostatistics, Francis Collins, M.D., Ph.D., director of the National Institutes of Health, and Michael L. Stitzel, Ph.D. of the Jackson Laboratory.

Prior to their current faculty positions Parker and Stitzel worked in Collins’ lab at the National Human Genome Research Institute. Parker’s graduate student, Arushi Varshney, is one of the paper’s co-first authors with Laura Scott, Ph.D., and Ryan Welch, Ph.D., of the U-M School of Public Health’s Department of Biostatistics and Michael Erdos, Ph.D., of the National Human Genome Research Institute.

They performed an extensive examination of DNA from islet samples isolated from 112 people. They characterized differences not just in DNA sequences, but also in the way DNA was packaged and modified by epigenetic factors, and the levels of gene expression products that indicated how often the genes had been read and transcribed.

This allowed them to track the “footprints” that RFX and other transcription factors leave on packaged DNA after they have done their job.

RFX and other factors don’t bind directly to the part of a gene that encodes a protein that does a cellular job. Rather, they bind to a stretch of DNA near the gene – a runway of sorts.

But when genetic changes linked to Type 2 diabetes are present, that runway gets disrupted, and RFX can’t bind as it should.

Each DNA change might alter this binding in a different way, leading to a slightly different effect on Type 2 diabetes risk or blood sugar regulation. But the common factor for many of these changes was its effect on the area where RFX is predicted to bind, in the cells of pancreatic islets.

So, says Parker, this shows how the genome – the actual sequence of DNAcan influence the epigenome, or the factors that influence gene expression.

The researchers note that a deadly form of diabetes seen in a handful of babies born each year may be related to RFX mutations. That condition, called Mitchell-Riley syndrome, involves neonatal diabetes and malformed pancreas, and is known to be caused by a rare autosomal recessive mutation of one form of RFX.

Explore further: Unique mapping of methylome in insulin-producing islets

More information: Genetic regulatory signatures underlying islet gene expression and type 2 diabetes, PNAS, http://www.pnas.org/cgi/doi/10.1073/pnas.1621192114

Throughout our lives, our genes are affected by the way we live. Diet, exercise, age and diseases create imprints that are stored in something called methylome. Now, for the first time, researchers at the Lund University …

Variations in non-coding sections of the genome might be important contributors to type 2 diabetes risk, according to a new study.

Problems with insulin secretion experienced by people with Type 2 diabetes, parallel similar problems with insulin-secreting beta cells in many individuals with Down syndrome. A new study, published on May 19 in PLOS Genetics …

Personalized treatment for people with diabetes could be a step closer after researchers discovered how a single gene mutation fundamentally alters pancreatic development.

Doctors have long known that men with low testosterone are at greater risk for developing type 2 diabetes. For the first time, researchers have identified how testosterone helps men regulate blood sugar by triggering key …

Researchers at Wake Forest Baptist Medical Center’s Institute for Regenerative Medicine and colleagues have discovered a new protein that may play a critical role in how the human body regulates blood sugar levels. Reporting …

Why do some people get Type 2 diabetes, while others who live the same lifestyle never do?

It is now possible to reprogram cells from the liver into the precursor cells that give rise to the pancreas by altering the activity of a single gene. A team of researchers at the Max Delbrck Center for Molecular Medicine …

Keeping blood sugar levels within a safe range is key to managing both type 1 and type 2 diabetes. In a new finding that could lead to fewer complications for diabetes patients, Yale School of Medicine researchers have found …

Latino children who live in areas with higher levels of air pollution have a heightened risk of developing Type 2 diabetes, according to a new USC-led study.

Bladder dysfunction is a reality for about half of patients with diabetes and now scientists have evidence that an immune system receptor that’s more typically activated by bacteria is a major contributor.

Rat-grown mouse pancreases help reverse diabetes in mice, say researchers at Stanford, University of Tokyo

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China aims for share of precision medicine – Arkansas Online

Posted: February 13, 2017 at 8:47 am

When Nisa Leung was pregnant with her first child in 2012, her doctor in Hong Kong offered her a choice. She could take a prenatal test that would require inserting a needle into her uterus, or pay $130 more for an exam that would draw a little blood from her arm.

Leung opted for the simpler and less risky test, which analyzed bits of the baby’s DNA that had made its way into her bloodstream. Then Leung went on to do what she often does when she recognizes a good product: look around for companies to invest in.

The managing partner at Qiming Venture Partners decided to put money into Chinese genetic testing firm Berry Genomics, which eventually entered into a partnership with the Hong Kong-based inventor of the blood test. Over the next few months, Berry is expected to be absorbed into a Chinese developer in a $625 million reverse merger. And Leung’s venture capital firm would be the latest to benefit from a boom in so-called precision medicine, an emerging field that includes everything from genetic prenatal tests to customizing treatments for cancer patients.

China has made the precision medicine field a focus of its 13th five-year plan, and its companies have been embarking on ambitious efforts to collect a vast trove of genetic and health data, researching how to identify cancer markers in blood, and launching consumer technologies that aim to tap potentially life-saving information. The push offers insight into China’s growing ambitions in science and biotechnology, areas where it has traditionally lagged developed nations like the U.S.

“Investing in precision medicine is definitely the trend,” said Leung, who’s led investments in more than 60 Chinese health-care companies in the past decade. “As China eyes becoming a biotechnology powerhouse globally, this is an area we will venture into for sure and hopefully be at the forefront globally.”

New Chinese firms like iCarbonX and WuXi NextCode that offer consumers ways to learn more about their bodies through clues from their genetic make up are gaining popularity. Chinese entrepreneurs and scientists are also aiming to dominate the market for complex new procedures like liquid biopsy tests, which would allow for cancer testing through key indicators in the blood.

Such research efforts are still in early stages worldwide. But doctors see a future beyond basic commercial applications, aiming instead for drugs and treatment plans tailored to a person’s unique genetic code and environmental exposure, such as diet and infections.

Isaac Kohane, a bioinformatics professor at Harvard University, says when it comes to precision medicine, the science community has “Google maps envy.” Just as the search engine has transformed the notion of geography by adding restaurants, weather and other locators, more details on patients can give doctors a better picture on how to treat diseases.

For cancer patients, for example, precision medicine might allow oncologists to spot specific mutations in a tumor. For many people with rare ailments like muscle diseases or those that cause seizures, it allows for earlier diagnosis. Pregnant women, using the kind of tests that Leung used, could also learn more about the potential for a child to inherit a genetic disease.

The global interest in the field comes as the cost of sequencing DNA, or analyzing genetic information, is falling sharply. But a number of hurdles remain. Relying on just genes isn’t enough, and there must also be background information on a patient’s lifestyle and medication history.

Precision medicine applications also require heavy investment to store large amounts of information. A whole genome is more than 100 gigabytes, according to an e-mailed response to questions from Edward Farmer, WuXi NextCode’s vice president of communications and new ventures. “So you can imagine that analyzing thousands or hundreds of thousands of genomes is a true big data challenge.”

WuXi NextCode was formed after Shanghai-based contract research giant WuXi AppTec Inc. acquired genomic analysis firm NextCode Health, a spin-off from Reykjavik, Iceland-based Decode Genetics, which has databases on the island’s population. Wuxi NextCode continues to have an office in Iceland, where the population is relatively homogenous and therefore good for gene discovery.

“Genomics today is like the computer industry in the ’70s,” said Hannes Smarason, WuXi NextCode’s co-founder and chief operating officer. “We’ve made great progress but there’s still a long way to go.”

In China, Wuxi NextCode now offers consumers genetic tests that cost between about $360 and $1,160, providing more details on rare conditions a child might be suffering from or even the risk of passing on an inherited disease.

China is diverse, and with 1.4 billion people, the planet’s most populous nation. WuXi NextCode announced a partnership with Huawei Technologies Co., China’s largest telecommunications equipment maker, in May to enable different institutions and researchers to store their data.

The goal is to use that deep pool of information — which ranges from genome sequences to treatment regimens — to find more clues on tackling diseases. WuXi says that “this will in many instances enable the largest studies ever undertaken in many diseases.”

Another Chinese player, iCarbonX, which received a $200 million investment from Tencent Holdings Ltd. and other investors in April, is valued at more than $1 billion. It announced last month that it had invested $400 million in several health data companies to enable the use of algorithms to analyze reams of genomic, physiological and behavioral data to provide customized medical advice directly to consumers through an app.

The global precision medicine market was estimated to be worth $56 billion in revenue at the end of 2016, with China holding about 4 percent to 8 percent of the global market, according to a December report from Persistence Market Research.

Encouraging interventions for some patients too early, even before they have life-threatening diseases, comes with risks and ethical questions, Laura Nelson Carney, an analyst at Sanford C Bernstein, wrote in a Jan. 6 note. Still, precision medicine research has many benefits, and some in China see the country’s push as a significant opportunity “to scientifically leapfrog the West,” she said.

In the U.S., universities, the National Institutes of Health and American drugmakers are part of a broad march into precision medicine.

Amgen Inc. bought Icelandic biotechnology company DeCode Genetics for $415 million in 2012, to acquire its massive database on Iceland’s population. U.S.-based Genentech Inc. is collaborating with Silicon Valley startup 23andMe to study the genetic underpinnings of Parkinson’s disease.

“Humans are computable,” said Wang Jun, the chief executive officer of China’s iCarbonX. “So we need a computable model that we can use to intervene and change people’s status, that’s the whole point.”

SundayMonday Business on 02/13/2017

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