Archive for June, 2017

In Brief The CRISPR process will be used inside the human body for the first time on July 15th to combat HPV, which impacts millions of people worldwide. And this is just one of a huge amount of proposed CRISPR studies occurring soon. Uninvasive CRISPR

A new CRISPR trial, which hopes to eliminate thehuman papillomavirus (HPV), is set to be the first to attempt to use thetechnique inside the human body. In the non-invasive treatment, scientists will apply a gel that carries the necessary DNA coding for the CRISPR machinery to the cervixes of 60 women between the ages of 18 and 50. The team aims to disable the tumor growth mechanism in HPV cells.

The trial stands in contradistinction to the usual CRISPR method of extracting cells and re-injecting them into the affected area; although it will still use the Cas9 enzyme (which acts as a pair of molecular scissors) and guiding RNA that is typical of the process.

20 trials are set to begin in the rest of 2017 and early 2018. Most of the research will occur in China, and will focus on disabling cancers PD-1 gene that fools the human immune system into not attacking the cells. Different trials are focusing on different types of cancer including breast, bladder, esophageal, kidney, and prostate cancers.

The study, if it succeeds, will be promising for sufferers of HPV and act as a milestone in the CRISPR process. Although HPV is not necessarily cancerous, it cancause cervical cancer. In the U.S. alone, there are more than 3 million new infections every year.Although there is a vaccine for the virus, currently, once you have it you can never get rid of it.

More generally, the CRISPR process could be nothing short of a miracle: if it passes all medical tests it wouldnt just make medicine a whole new kettle of fish, it would reinvent the kettleand the fish, for almost any field. It is cheaper than other gene editing therapies, and could potentially save millions of lives by curing diseases we can only deal with therapeutically like cancer, diabetes and cystic-fibrosis. Crops could be altered more effectively using the process. Drugs and materials that were never possible before could be pioneered.

However, it is still extremely nascent technology, and many fear that there could also be a host of unexpected consequences. Recently, it has been found that it causes hundreds of unexpected mutations in DNA. While these concerns are valid, more research is necessary. Which is why the upcoming studies over the next few years are so vital to the future of our health.

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A World First CRISPR Trial Will Edit Genes Inside the Human Body - Futurism

All pipelines showed that F03 harbored 164 indels and 1,736 SNVs (63 and 885 of these, respectively, associated with known genes). F05 harbored 128 indels and 1,696 SNVs (51 and 865 of these, respectively, associated with known genes). . .The same 117 indels and 1,397 SNVs were detected in both of the CRISPR-treated mice, which indicated nonrandom targeting. . .The mutation rate detected in CRISPR- treated mice was substantially higher than that generated by spontaneous germline mutations (3 to 4 indels and 90 to 100 SNVs, de novo, per generation).

Oh dear. If that holds up, thats clearly going to be a major difficulty in bringing CRISPR-based therapeutics forward, at least with the current state of the art. Just as worrisome, if not more, is that fact that software predictions of the fifty most likely off-target sites of action did not match any of the variants that were actually seen. So it would appear that we have no idea of whats going on here. As the paper says, with great restraint, The unpredictable generation of these variants is of concern.

Now we get to the arguing, though, because the big question is whether these results are correct. They do not match up well with whats already in the literature on the subject, thats for sure. On Twitter, Nicolas Bray brought up one of the concerns. His question is a simple one, but it needs to be answered: The two treated mice were siblings, while the control was (apparently) more distantly related. How many of these variations, then, can be ascribed to what the mice started out with?

The control animal was from the same inbred strain, but still the number of variations seen in this paper is way off what others have reported. Sam Sternberg noted that the paper (and its supplementary information) is not very clear about the relationship between the mice, and also suspects that many of these mutations are from the founders and not the CRISPR treatment per se. Meanwhile, Gaetan Burgio pointed out that the experimental details say:

Briefly, an sgRNA-expressing plasmid had been co-injected, into FVB/NJ zygotes, with the single-stranded oligodeoxynucleotide (ssODN) donor template and Cas9 protein to generate mosaic F0 founders.

Plasmids themselves, he notes, are known to cause mutations, since they have much longer half-lives than RNA or protein, and he says his own labs work with direct injection of sgRNA and Cas9 protein showed far fewer mutations, in keeping with the rest of the literature. Another potential problem has been brought up by many observers: This study has an n of 2, with one control animal. Thats a pretty thin platform on which to build the CRISPR Is Doomed! monument.

So there are a number of reasons to wonder if these results are real. If they are, other questions arise about the newer Cas9 variant enzymes and various sgRNA designs, but Im not even going to think about those, to be honest, until this result has been replicated and given a thorough going over. The implications are too big to start running around in circles just yet. There will be time for that, if needed...

Update, in the interests of full disclosure: After publishing this post and looking at the moves in the stock prices of both EDIT and CRSP yesterday and today, I found my own doubts convincing enough to have bought some of both as a short-term trade. I have no idea what their long-term prospects are, but their sudden drops due to this news may not be justified. On the rare occasions that Ive taken a position in any sort of individual biopharma stock, Ive noted it on the blog, and will continue to do so. Now you all can watch me lose money in real time...

Disclosure: I am long EDIT and CRSP.

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Trouble With CRISPR? Maybe - But Maybe Not - Seeking Alpha

Michael J. Wade. Credit: James Brosher, IU Communications

Researchers are exploring the use of the revolutionary gene-editing tool CRISPR-Cas9 to fight human disease and agricultural blight. But a study from Indiana University has found several challenges to the method's use in saving lives and crops.

The research, reported today in the journal Science Advances, combines advanced genetic and statistical analyses to show how certain genetic and behavioral qualities in disease-carrying insects, like mosquitoes, make these species resistant to genetic manipulation.

This resistance could complicate attempts to use CRISPR-Cas9 in the fight against malaria -- a deadly mosquito-borne disease that threatens over 3 billion people worldwide -- or crop blights such as the western corn rootworm, an invasive species that costs the U.S. about $1 billion in lost crops each year.

The discovery of the CRISPR-Cas9 system -- or simply "CRISPR" -- in the early 2010s introduced an unprecedented level of accuracy in genetic editing. Scientists can use the method to design highly precise genetic "scissors" that snip out and replace specific parts of the genome with sequences of their choosing. Two English scientists were the first to show the method could spread infertility in disease-carrying mosquitoes in late 2015.

"We found that small genetic variation within species -- as well as many insects' tendency to inbreed -- can seriously impact the effectiveness of attempts to reduce their numbers using CRISPR technology," said Michael J. Wade, Distinguished Professor of Biology at IU Bloomington. "Although rare, these naturally occurring genetic variants resistant to CRISPR are enough to halt attempts at population control using genetic technology, quickly returning wild populations to their earlier, 'pre-CRISPR' numbers."

This means costly and time-consuming efforts to introduce genes that could control insect populations -- such as a trait that causes female mosquitoes to lay fewer eggs -- would disappear in a few months. This is because male mosquitoes -- used to transmit new genes since they don't bite -- only live about 10 days.

The protective effect of naturally occurring genetic variation is strong enough to overcome the use of "gene drives" based on CRISPR-based technology -- unless a gene drive is matched to the genetic background of a specific target population, Wade added. Gene drives refer to genes that spread at a rate of nearly 90 percent -- significantly higher than the normal 50 percent chance of inherence that occurs in sexually reproducing organisms.

Wade, an expert in "selfish genes" that function similarly to gene drives due to their "super-Darwinian" ability to rapidly spread throughout a population, teamed up with colleagues at IU -- including Gabriel E. Zentner, an expert in CRISPR-based genetic tools and assistant professor in the Department of Biology -- to explore the effectiveness of CRISPR-based population control in flour beetles, a species estimated to destroy 20 percent of the world's grain after harvest.

The team designed CRISPR-based interventions that targeted three segments in the genome of the flour beetle from four parts of the world: India, Spain, Peru and Indiana. They then analyzed the DNA of all four varieties of beetle and found naturally occurring variants in the targeted gene sequence, the presence of which would impact the effectiveness of the CRISPR-based technology.

The analysis revealed genetic variation in all four species at nearly every analyzed DNA segment, including a variance rate as high as 28 percent in the Peruvian beetles. Significantly, Wade's statistical analysis found that a genetic variation rate as low as 1 percent -- combined with a rate of inbreeding typical to mosquitos in the wild -- was enough to eliminate any CRISPR-based population-control methods in six generations.

The results suggest that a careful analysis of genetic variation in the target population must precede efforts to control disease-carrying insects using CRISPR technology. They also suggest that the unintended spread of modified genes across the globe is highly unlikely since typical levels of genetic variation place a natural roadblock on spread between regions or species.

"Based on this study, anyone trying to reduce insect populations through this method should conduct a thorough genetic analysis of the target gene region to assess variation rates," Wade said. "This will help predict the effectiveness of the method, as well as provide insight into ways to circumvent natural genetic variation through the use of Cas9 variants with an altered sequence specificity."

This article has been republished frommaterialsprovided by Indiana University. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference

Drury, D. W., Dapper, A. L., Siniard, D. J., Zentner, G. E., & Wade, M. J. (2017). CRISPR/Cas9 gene drives in genetically variable and nonrandomly mating wild populations. Science Advances, 3(5), e1601910.

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CRISPR Gene Drives May Not Be As Effective As Once Hoped - Technology Networks

Skip to content On November 4 2016, the Eiffel Tower was illuminated in green to celebrate the entry into the Paris Agreement. Credit: U.S. Department of State

This week, President Trump pulled the U.S. from the Paris Climate Agreement, which 195 countries had signed in 2015, pledging to reduce greenhouse emissions. Trump said that the agreement imposed draconian financial burdens on the U.S. and that he would negotiate for a deal that is fair. Maggie Koerth-Baker, senior science reporter at Fivethirtyeight.com, fills us in on the announcement. Plus, she talks about new CRISPR clinical trials, and NASAs Parker Probe Plus, a mission to explore the sun.

[What happens if the U.S. leaves the Paris climate deal?]

Maggie Koerth-Baker

Maggie Koerth-Baker is a senior science reporter with FiveThirtyEight.com.Shes based inMinneapolis, Minnesota.

Alexa Lim is a producer for Science Friday. Her favorite stories involve space, sound, and strange animal discoveries.

One way is fast and dramatic. The other is slower and leaves wiggle room.

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Science Friday is produced by the Science Friday Initiative, a 501(c)(3) nonprofit organization. Created by Bluecadet

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Trump Pulls US From Climate Agreement, CRISPR Human Trials, And A NASA Sun Orbiter - Science Friday

Bacteria genomes have repeating sequences of DNA with bits of other DNA sandwiched between them. These are the "clustered regularly interspaced short palindromic repeats" that give CRISPR its name. What scientists eventually discovered is that those sequences of unique DNA, in between the repeating bits, matched the DNA of viruses. Basically, it's a gallery of Bacteria's Most Wanted.

A set of enzymes called CRISPR-associated proteins, or Cas for short, looks for these bits of DNA as a way to identify danger when an intruder is detected. When a virus is spotted, the proteins act like assassins, snipping out those offending bits of DNA, rendering the virus harmless. More important, it turns out, you can basically train these Cas proteins to look for any sequence of DNA you want. Then they can replace it with another piece of genetic code.

This all sounds pretty complicated, but you can actually do it in your kitchen with a $160 kit from a company called The Odin. The particular kit I used includes everything you need to make baking or brewing yeast glow green under a black light.

To start, I prepared a whole bunch of agar plates -- petri dishes filled with a nutrient-rich gel for the yeast to grow on. Then I had to wake up my dried French Saison yeast with a little bit of water and "streak" the little guys out on the plates and put aside for about 24 hours to let them grow.

Once the yeast was healthy and I had full cultures, it was time to prep them for their transformation. I introduced them to a solution of chemicals and salts that weakened the cell walls so that our new DNA can enter more easily. Then it was time to introduce the plasmid (a small molecule of DNA) carrying the genes I want the yeast to adopt. The genetic code introduced in this case tells the yeast to produce green fluorescent protein, which is what causes it to glow. Basically, we're tricking the yeast into thinking the DNA we introduced is its own so that it makes the Cas proteins that will cut out the parts we want to replace.

Once it's all combined, the mixture gets incubated in a warm water bath for about an hour, before adding nutrients to the solution and putting the whole thing back in a warm-water bath for another four hours. This gives the yeast time to recover and replicate the DNA that will make it fluoresce. Then it's time to streak the modified yeast on some new agar plates and wait again for them to grow into thriving colonies.

A few days later, I had yeast that glowed green under a black light.

Now, a petri dish worth of yeast isn't nearly enough to brew a beer with. So I had to make a starter -- a weak proto-beer on which the yeast can feast and build its strength. Eventually, I had a 1 liter Erlenmeyer flask filled with fluorescent French Saison yeast.

Brewing beer itself is pretty straightforward but here's the TL;DR version of how it works: Grains, such as barley, are steeped in hot water to extract their sugars. This creates a liquid called wort, which is then boiled to sterilize it, break down and remove unwanted proteins, and extract flavors from additives like hops -- the little green cones that deliver all that lovely beer flavor and aroma.

Then the wort is cooled and the yeast is added, and it becomes a waiting game. The yeast eats away at the sugar, converting it to carbon dioxide and delicious, delicious alcohol.

The results of my grand experiment were successful ... ish.

The yeast certainly glowed and the first couple of samples pulled from the fermenter did as well. But, as the beer settled and the yeast dropped out of my brew, the glow became fainter and fainter. By the end, it was a pale glimmer rather than a blinding glare.

At the end of the day, my glowing beer was a strange novelty; it's merely meant to show off the power and simplicity of CRISPR. It's a technology that could one day lead to a cure for diseases like sickle cell or AIDS, or be used to breed drought-resistant plants. But that's still a ways off. Right now, CRISPR is in its infancy, so I'll just have to settle for yeast that can brew unique-looking (if not particularly unique-tasting) beer.

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I bio-engineered glowing beer and it hasn't killed me (yet) - Engadget - Engadget

BBC News

Hair loss: What is female-pattern baldness? BBC News Hayley Jennings, who set up the Yorkshire Hair Loss Clinic, said the majority of her clients were women - especially mothers - in their 30s and 40s with female pattern hair loss. "This effects one ... Dihydrotestosterone (DHT) is the main hormone ... and more »

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Hair loss: What is female-pattern baldness? - BBC News

Breast cancer is thought of as a womens disease, with less than 1 percent of breast cancers affecting men, according to breastcancer.org. Because of that, there is a lack of awareness about the disease in males, which leads to late diagnoses and lower chances of survival.

As part of Mens Health Month in June, learn the facts about male breast cancer and what can be done to treat it.

Everyone has breast tissue

Male bodies dont make as much of the hormone that stimulates breast growth as female bodies, but men still have breast tissue and can even develop medium or large breasts, according to breastcancer.org.

Usually these breasts are just mounds of fat, the website says. But sometimes men can develop real breast gland tissue because they take certain medicines or have abnormal hormone levels.

While testosterone in men and estrogen in women controls their sex characteristics, those hormones are found in both sexes.

Most people think of estrogen as an exclusively female hormone, but men also produce it though normally in small quantities, the Mayo Clinic says. However, male estrogen levels that are too high or are out of balance with testosterone levels can cause gynecomastia."

Gynecomastia happens when males have swollen breast tissue which, on its own, is not a serious problem but, because both the condition and breast cancer are related to more breast tissue, one could be a sign of the other.

Male breast cancer is usually advanced

Although breast cancer in men is uncommon, its usually diagnosed late, meaning the cancer is more advanced.

Overall survival is shorter in men, possibly because they tend to be older and have more comorbid conditions, according to research in medical journal the BMJ.

Having comorbid conditions means a person has more than one disease or condition at a time. Men may also have advanced stages of breast cancer because they ignore symptoms.

Men carry a higher mortality than women do, primarily because awareness among men is less and they are less likely to assume a lump is breast cancer, which can cause a delay in seeking treatment, the National Breast Cancer Foundation says.

Men can check for symptoms, at home

Men with a family history of breast cancer are at a higher risk of developing it, but all men should tell their doctor if they have any of these symptoms:

Before going to the doctor, men can perform a self-check, something they should do every month. That may sound like a lot, but it takes less than 30 seconds and is simple, involving looking for changes on or around the nipple and feeling in the area for lumps or discharge. Detailed instructions are available from multiple online resources.

Men can treat and beat breast cancer

If a biopsy confirms a man has cancer cells in his breast, medical tests will determine the stage. As with other cancers, a lower stage means the cancer has not progressed as far.

Treatment options could include surgery, chemotherapy, hormone therapy, radiation therapy and targeted therapy, according to the National Cancer Institute.

Men's and womens breast cancer survival rates are the same, so the stage is more important. For example, if men visit the doctor early, and the breast cancer is caught and treated at stage 0 or 1, there is a 100 percent survival rate, according to the American Cancer Society. That rate drops for every subsequent stage until stage 4, which has a 20 percent survival rate.

The best thing a man with a family history or symptoms of breast cancer can do is visit his doctor right away for diagnosis and treatment.

Sinclair Broadcasting is committed to the health and well-being of our viewers, which is why were introducing Sinclair Cares. Every month well bring you information about the Cause of the Month, including topical information, education, awareness and prevention.

Continued here:
Here Are The Facts About Male Breast Cancer - KUTV 2News

A federal judge in Minnesota dealt a devastating blow to parental rights last week. Senior U.S. District Judge Paul Magnuson dismissed a lawsuit brought by a mother who accused school officials, healthcare providers, and doctors of violating her parental rights by assisting her son with gender transition without the mothers consent.

Anmarie Calgaros case made international headlines last year when she sued her teenage son known only as EKJ for undergoing a sex change through hormonal therapy without her permission, as well as numerous state agencies for the role they played in helping him to transition from male to female. Calgaros lawsuit claimed that she was neither consulted nor informed about the transition, thereby stripping her of her constitutionally protected parental rights.

The U.S. Constitution says that parental rights are fundamental rights, that cant be terminated without due process, said Calgaros attorney, Erick Kaardal of the Thomas More Society.

At particular issue in Calgaros lawsuit was a Minnesota law that allows minors to undergo medical care and procedures without parental consent. According to Calgaros suit, Park Nicollet and Fairview Health Services began providing hormone therapy to her son in November without consulting Calgaro or even informing her about it. Calgaro also argued that St. Louis County violated her parental rights by providing government assistance in the form of medical payments to cover the costs of the childs transition.

Calgaro indicates she is fighting for parents to be included in their minors medical decisions.

"I'm also taking this action for the benefit of all parents and families, who may be facing the same violation of their rights so that they and others in the future may be spared from the same tragic events," she opined.

Sadly, some media outlets portrayed Calgaro less as a champion of parental rights and more as an anti-LGBTQ activist, even quoting critics who took issue with Calgaros and her attorneys repeated references to her son as male, which of course squares with reality, but not with her sons desire to be acknowledged as female.

For Calgaro, however, the case is not about her son's transgenderism, but with his ability to obtain medical treatment without her knowledge or consent, particularly potentially harmful treatment. At a press conference, Calgaro told reporters that "The transitioning thing isn't even the issue, the issue is that he's able to make these [medical] decisions."

In fact, scientists suggest that it is psychologically harmful for adolescents to undergo hormonal therapy in the name of transgenderism, as most children outgrow gender confusion.

"Children are a special case when addressing transgender issues. Only a minority of children who experience cross-gender identification will continue to do so into adolescence or adulthood, a study in The New Atlantis reads.

There is little scientific evidence for the therapeutic value of interventions that delay puberty or modify the secondary sex characteristics of adolescents, although some children may have improved psychological well-being if they are encouraged and supported in their cross-gender identification," it continues. "There is no evidence that all children who express gender-atypical thoughts or behavior should be encouraged to become transgender."

The study argues that enabling acceptance of transgenderism through medical intervention is particularly harmful. An area of particular concern involves medical interventions for gender-nonconforming youth. They are increasingly receiving therapies that affirm their felt genders, and even hormone treatments or surgical modifications at young ages, the authors observe.

Calgaros lawsuit also focused on the absence of an official legal process in the state for the emancipation of minors, and this absence served to create considerable confusion and inconsistencies in Calgaros case. Some of the agencies involved considered the teenage boy to be emancipated from his mother based on the grounds that he no longer lived with Calgaro and was not financially supported by her. EKJ reportedly moved out of his mothers home in 2015 to move in with his father so that he could attend a better school and has not returned since. He eventually moved in with friends until he finally began living on his own.

EKJ also filled out an emancipation form with the help of a homosexual advocacy group without Calgaros knowledge. In the lawsuit, Calgaro notes that the emancipation form was riddled with falsehoods. For example, the form claimed that Calgaro failed to report her teen son as a runaway and made no attempt to bring him home, thereby concluding that she wished to have no contact with him, all of which Calgaro denies.

The Minneapolis Star Tribune reports that an attorney with the Mid-Minnesota Legal Aid clinic then provided EJK with a letter that concluded the teen was legally emancipated under Minnesota law.

Meanwhile, Calgaros attorney noted at a news conference last year that Calgaro was never given notice that her child was seeking emancipation and the emancipation determination was reached without a hearing or court order.

"If there had been a court order of emancipation, then Anmarie would have received notice and an opportunity to be heard," said Kaardal.

Once it was determined that EKJ was emancipated, the school then refused to provide Calgaro her sons medical records, and the Department of Human Services refused to provide her information about her sons hormonal therapy, Life Site News reports.

Yet, while these particular agencies accepted EKJs emancipation determination, the St. Louis County District Court had rejected the teens application for a name change because of the lack of any adjudication relative to emancipation, underscoring the flimsy legal grounds on which the defendants case stood.

Calgaro turned to the federal court to intervene, and asked the court to stop the teens hormone treatment and award her financial damages.

But Judge Magnuson determined on Tuesday that Calgaros claims were meritless.

Magnuson admitted that the boy was not legally emancipated, and that Calgaro's parental right "remain[ed] intact." However, he decided that the defendants could not be held liable because they did not act under color of state law. Without evidence that the school and agencies violated a law or a policy or custom, Calgaro had no claim, he determined.

Magnuson revealed his flagrant disregard for parental rights by going so far as to question whether those include access to school records.

Furthermore, Kaardal asserts that Judge Magnusons decision has done little to clarify the states emancipation issue.

On the legislative front, people on the left and on the right believed that emancipation procedures in Minnesota should be put in statutes and codified, Kaardal said. But until then, its confusing and the courts decision hasnt cleared up that confusion.

NBC News notes the potential impact that a decision on the states emancipation process could have on abortion in Minnesota, since current statute mandates that a non-emancipated minor cannot access an abortion until 48 hours after parental notification has taken place.

Predictably, EJKs attorneys welcomed the judges decision, saying it shows the resilience of transgender youth and the importance of access to appropriate health care.

The law protects all young people, including transgender young people, and we are pleased that this outcome supports her access to essential health care and other critical service, said Asaf Orr, a staff attorney for the National Center for Lesbian Rights Transgender Youth Project in San Francisco.

According to theMinneapolis Star Tribune, Kaardal and Calgaro are considering an appeal.

Anmarie Calgaro is living a parents worst nightmare," Kaardalsaid. "Her minor child has been piloted by third parties through a life-changing, permanent body altering process by organizations that have no legal authority over him, and that have denied his own mother access.

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Judge Dismisses Mother's Lawsuit Over Her Son's Transition to a "Girl" - The New American

Illustration of the heart patch using artificial capillaries.

Editors note: This is a guest post by Frances Ligler, Lampe Distinguished Professor in the Joint Department of Biomedical Engineering (BME) at NC State and UNC-Chapel Hill. This is one of a series of posts from NC State researchers that address the value of science, technology, engineering and mathematics.

Judging from evidence provided by Star Wars and The Six Million Dollar Man, repairing body parts seems to require a screwdriver. However, teams of scientists and engineers are exploring other ways to repair our bodies and NC State faculty and students are collaborating across colleges to perform cutting-edge experiments to further regenerative medicine therapeutics.

Before joining NC State, Michael Daniele (an assistant professor of BME and electrical and computer engineering) and I invented a method of making long strings of artificial blood capillaries by creating soft walls in between fluids streaming through a small channel. Cells present in the streams were incorporated into the capillaries to mimic the 3-D architecture of your capillaries and veins.

At NC State, we joined forces with Ke Cheng, an expert in stem cells and cardiology from the College of Veterinary Medicine, to incorporate these artificial capillaries into a degradable patch containing cardiac stem cells. Postdoctoral fellow Teng Su placed the patches on damaged areas of rat hearts and showed both repair of the rat heart tissue and return of the pumping capacity of the heart (which does not happen under the untreated condition where scar tissue forms in the damaged heart).

In another exciting collaboration, Matt Fisher from BME, Rohan Shirwaiker (an associate professor of industrial and systems engineering) and Behnam Pourdeyhimi from the College of Textiles are teaming up to reconstruct damaged knees. They are recreating the underlying fibrous scaffolds that support the cartilage in a manner that better mimics the original knee and supports the growth of the normal cell type within the new scaffolds which should improve healing and support a return to normal function in the knee.

The variety of skills required for this project include designing an entirely new device for printing fibers, understanding how to arrange the fibers and change their composition to accommodate bone or cartilage-forming cells, and learning how the new tissue develops to accommodate physical motion.

The lure of replacement body parts is widespread. There are far more people waiting for replacement organs than can be accommodated by human donors. Learning to use an individuals own cells to trigger tissue regeneration has far more long-term potential to address the ever-growing needs of accident victims and an aging population.

The key to success lies with teams of dedicated scientists, engineers, medical professionals and financial supporters that are focused on using the lessons learned across many fields to solve this grand challenge.

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Can Tiny Plumbing Fix Broken Hearts? - NC State News

The Expedition 51 crew members are awaiting a new space shipment and getting ready for new science experiments. The crew is also preparing for the departure of a pair of International Space Station flight engineers.

The Falcon 9 rocket that will launch the SpaceX Dragon cargo craft to space is resting at its launch pad today at the Kennedy Space Center in Florida. Dragon will lift off Thursday at 5:55 p.m. EDT on a three-day trip to the stations Harmony module.

Inside the commercial space freighter is nearly 6,000 pounds of crew supplies, station hardware and science experiments. One of those experiments, Cardiac Stem Cells, will research how stem cells affect cardiac biology and tissue regeneration in space. The stations Microgravity Science Glovebox is being readied for the study which may provide insight into accelerated aging due to living in microgravity.

On Friday, cosmonaut Oleg Novitskiy will command the Soyuz MS-03 spacecraft to return him and European Space Agency astronaut Thomas Pesquet back to Earth after 196 days in space. The two crew members are packing their spacecraft with research samples, hardware and personal items for the near 3.5 hour ride home. The duo will undock from the Rassvet module at 6:47 a.m. EDT. They will then parachute to a landing in Kazakhstan at 10:10 a.m. (8:10 p.m. Kazakh time).

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Station Ramps Up for Cardiac Research Loaded on Dragon - Space Fellowship

Friday November 20 2009

Human embryonic stem cells

Stem cells could create new skin to help burn victims, BBC News reported. It said that French researchers have duplicated the biological steps that occur during skin formation in embryos. This could potentially provide an unlimited source of temporary skin replacements for burn victims while they wait for grafts from their own skin.

The study in mice behind this report used human embryonic stem cells to make keratinocytes (the most common cell types in the skin). These cultured cells were used to create skin equivalents, which grew successfully when they were grafted onto the backs of mice.

This well-conducted research has potentially developed a successful method of culturing tissue in the laboratory that resembles human skin. Only human trials of the technology will show whether such grafts will be accepted (i.e. not rejected by human patients) as permanent transplants or can provide a temporary skin replacement before grafting.

The research was carried out by Dr Hind Guenou and colleagues from the Institute for Stem Cell Therapy and Exploration of Monogenic disease, and BIOalternatives SAS in France along with colleagues in Madrid. The research was funded by the Institut National de la Sant et de la Recherche Mdicale, University Evry Val dEssonne, Association Franaise contre les Myopathies, Fondation Ren Touraine, and Genopole. The authors declare that they have no conflicts of interest and say that the funders had no role in the studys design, analysis or write-up.

The research was published in thepeer-reviewed medical journal the Lancet.

BBC News has covered this research in a balanced way, pointing out that thiswas animal research and that human studies will follow.

This well-conducted research involved laboratory and animal research which investigated whether epidermal stem cells could be cultured in the laboratory and used in skin grafts.

Burn patients are often treated using autologous skin grafts. These involve a section of healthy skin being removed from another part of the body to harvest the patients own skin cells for culture. A graft for the burn site is produced from this culture. There is a delay of about three weeks between the harvesting of the skin and the graft to allow the cells to grow. During this time, the patient is at risk of dehydration and infection.

Having a ready source of skin cells for temporary grafts while patients are waiting for their autologous grafts would improve the outcome of treatment. With this in mind, the researchers investigated whether keratinocytes (the major cell constituent of the outer layer of the skin, or epidermis) could be derived from human embryonic stem cells.

The researchers began by culturing embryonic stem cells in a specialised medium that encourages cell differentiation (the process whereby cells become specialised). Embryonic stem cells can renew themselves and also have the potential to develop into any type of specialised cell.

Cultures of human embryonic stem cells were then grown on a framework made of fibroblast cells and collagen (a fibrous protein that can form a mesh-like structure) made by fibroblasts. Fibroblasts are the cells that form the underlying structure of tissues and are involved in healing.

The stem cells were manipulated so that they developed into epidermal cells, and monitored throughout their specialisation process to make sure the cells were developing into skin cells. The researchers named the cells keratinocytes derived from human embryonic stem cells (K-hESCs).

After several rounds of subculturing and replication, the cells could be frozen and used in further experiments. Bioengineered skin equivalents were then created by growing the K-hESCs on an artificial matrix. These were then grafted onto the backs of five six-week-old immunodeficient female mice. After 10 to 12 weeks, samples were taken from the implants for analysis.

The researchers confirmed thatthe embryonic stem cells differentiated into keratinocytes, which could be grown in culture medium and which replicated well. These derived skin cells were structurally and functionally similar to normal skin cells in that they could be grown on an artificial matrix using classic techniques.

After 12 weeks of growth on immunodeficient mice, the grafted epidermis had developed into a structure that was consistent with mature human skin.

The researchers concluded that their findings build on previous research and show that K-hESCs can develop into a multi-layer epithelium. This epithelium resembles normal human skin both in cell cultures (in vitro) and following grafting onto live animals (in vivo).

They say that growing human skin from human embryonic stem cells could provide an unlimited resource for temporary skin replacement in patients with large burns who are waiting for autologous skin grafts.

If it can be demonstrated that it works in humans, this technology could improve outcomes for burns patients. The researchers report that the first human trial is currently underway.

At present, skin from deceased donors is used to treat burns patients while they wait for their own skin transplant, but there are often problems with rejection. The researchers highlight several potential benefits of an epidermis reconstructed using K-hESCs, including:

It is important to note that, at present, the researchers are only investigating this technology for providing temporary grafts. They say that whether it can be used for permanent grafts for patients who cant use their own cells needs further investigation. They say that for temporary use, the grafts would only be used for the three-week period while the patients permanent graft is grown.

This is a good study and the findings are exciting in this field, but only human research will tell whether it will have a wider application in the treatment of burns patients.

The rest is here:
Skin grafts from stem cells - NHS

In experiments in mice, UC San Francisco researchers have discovered that regulatory T cells (Tregs; pronounced tee-regs), a type of immune cell generally associated with controlling inflammation,directly trigger stem cells in the skin to promote healthy hair growth. Without these immune cells as partners, the researchers found, the stem cells cannot regenerate hair follicles, leading to baldness.

Our hair follicles are constantly recycling: when a hair falls out, a portion of the hair follicle has to grow back, saidMichael Rosenblum, M.D., an assistant professor of dermatology at UCSF and senior author on the new paper. This has been thought to be an entirely stem cell-dependent process, but it turns out Tregs are essential. If you knock out this one immune cell type, hair just doesnt grow.

The new study published online May 26 inCell suggests that defects in Tregs could be responsible for alopecia areata, a common autoimmune disorder that causes hair loss, and could potentially play a role in other forms of baldness, including male pattern baldness, Rosenblum said. Since the same stem cells are responsible for helping heal the skin after injury, the study raises the possibility that Tregs may play a key role in wound repair as well.

Normally Tregs act as peacekeepers and diplomats, informing the rest of the immune system of the difference between friend and foe. When Tregs dont function properly, we may develop allergies to harmless substances like peanut protein or cat dander, or suffer from autoimmune disorders in which the immune system turns on the bodys own tissues.

Like other immune cells, most Tregs reside in the bodys lymph nodes, but some live permanently in other tissues, where they seem to have evolved to assist with local metabolic functions as well as playing their normal anti-inflammatory role. In the skin, for example, Rosenblum and colleagues have previously shown that Tregs help establish immune tolerance to healthy skin microbes in newborn mice, and these cells also secrete molecules that help with wound healing into adulthood.

Rosenblum, who is both an immunologist and a dermatologist, wanted to better understand the role of these resident immune cells in skin health. To do this, he and his team developed a technique for temporarily removing Tregs from the skin. But when they shaved patches of hair from these mice to make observations of the affected skin, they made a surprising discovery. We quickly noticed that the shaved patches of hair never grew back, and we thought, Hmm, now thats interesting, Rosenblum said. We realized we had to delve into this further.

In the new research, led by UCSF postdoctoral fellow and first authorNiwa Ali,several lines of evidence suggested that Tregs play a role in triggering hair follicle regeneration.

First, imaging experiments revealed that Tregs have a close relationship with the stem cells that reside within hair follicles and allow them to regenerate: the number of active Tregs clustering around follicle stem cells typically swells by three-fold as follicles enter the growth phase of their regular cycle of rest and regeneration. Also, removing Tregs from the skin blocked hair regrowth only if this was done within the first three days after shaving a patch of skin, when follicle regeneration would normally be activated. Getting rid of Tregs later on, once the regeneration had already begun, had no effect on hair regrowth.

Tregs role in triggering hair growth did not appear related to their normal ability to tamp down tissue inflammation, the researchers found. Instead, they discovered that Tregs trigger stem cell activation directly through a common cell-cell communication system known as the Notch pathway. First, the team demonstrated that Tregs in the skin express unusually high levels of a Notch signaling protein called Jagged 1 (Jag1), compared to Tregs elsewhere in the body. They then showed that removing Tregs from the skin significantly reduced Notch signaling in follicle stem cells, and that replacing Tregs with microscopic beads covered in Jag1 protein restored Notch signaling in the stem cells and successfully activated follicle regeneration.

Its as if the skin stem cells and Tregs have co-evolved, so that the Tregs not only guard the stem cells against inflammation but also take part in their regenerative work, Rosenblum said. Now the stem cells rely on the Tregs completely to know when its time to start regenerating.

Rosenblum said the findings may have implications for alopecia areata, an autoimmune disease that interferes with hair follicle regeneration and causes patients to lose hair in patches from their scalp, eyebrows, and faces. Alopecia is among the most common human autoimmune diseases its as common as rheumatoid arthritis, and more common than type 1 diabetes but scientists have little idea what causes it.

After his team first observed hair loss in Treg-deficient mice, Rosenblum learned that the genes associated with alopecia in previous studies are almost all related to Tregs, and treatments that boost Treg function have been shown to be an effective treatment for the disease. Rosenblum speculates that better understanding Tregs critical role in hair growth could lead to improved treatments for hair loss more generally.

The study also adds to a growing sense that immune cells play much broader roles in tissue biology than had previously been appreciated, said Rosenblum, who plans to explore whether Tregs in the skin also play a role in wound healing, since the same follicle stem cells are involved in regenerating skin following injury.

We think of immune cells as coming into a tissue to fight infection, while stem cells are there to regenerate the tissue after its damaged, he said. But what we found here is that stem cells and immune cells have to work together to make regeneration possible.

Niwa Aliof UCSF was the lead author on the new study. Additional authors were Bahar Zirak,Robert Sanchez Rodriguez, Mariela L. Pauli,Hong-An Truong, Kevin Lai,Richard Ahn, Kaitlin Corbin, Margaret M. Lowe, PharmD,Tiffany C. Scharschmidt, M.D., Keyon Taravati, Madeleine R. Tan,Roberto R. Ricardo-Gonzalez, M.D., Audrey Nosbaum, M.D.,Wilson Liao, M.D., andAbul K. Abbas, MBBS, of UCSF; Frank O. Nestle, M.D., of Kings College London; Marta Bertoliniand Ralf Paus, M.D., of the University of Mnster in Germany; and George Cotsarelis, M.D., of the University of Pennsylvanias Perelman School of Medicine.

The work was primarily supported by the U.S. National Institutes of Health (K08-AR062064, DP2-AR068130, R21-AR066821), the Burroughs Wellcome Fund, a Scleroderma Research Foundation grant, the National Psoriasis Foundation and the Dermatology Foundation.

Here is the original post:
A new baldness treatment? | University of California - University of California

By Ian Haydon 3 minute Read

A new research paper is stirring up controversy among scientists interested in using DNA editing to treat disease.

In a two-page article published in the journal Nature Methods on May 30, a group of six scientists report an alarming number of so-called off-target mutations in mice that underwent an experimental gene repair therapy.

CRISPR, the hot new gene-editing technique thats taken biology by storm, is no stranger to headlines. What is unusual, however, is a scientific article so clearly describing a potentially fatal shortcoming of this promising technology.

The research community is digesting this newswith many experts suggesting flaws with the experiment, not the revolutionary technique.

The research team sought to repair a genetic mutation known to cause a form of blindness in mice. This could be accomplished, they showed, by changing just one DNA letter in the mouse genome.

They were able to successfully correct the targeted mutation in each of the two mice they treated. But they also observed an alarming number of additional DNA changesmore than 1,600 per mousein areas of the genome they did not intend to modify.

The authors attribute these unintended mutations to the experimental CRISPR-based gene-editing therapy they used.

Cas9, the CRISPR enzyme that snips DNA, in contact with its target. [Graph: via rcsb.org]A central promise of CRISPR-based gene editing is its ability to pinpoint particular genes. But if this technology produces dangerous side effects by creating unexpected and unwanted mutations across the genome, that could hamper or even derail many of its applications.Several previous research articles have reported off-target effects of CRISPR, but far fewer than this group found.

The publicly traded biotech companies seeking to commercialize CRISPR-based gene therapiesEditas Medicine, Intellia Therapeutics, and Crispr Therapeuticsall took immediate stock market hits based on the news.

Experts in the field quickly responded.

Either the enzyme is acting at near optimal efficiency or something fishy is going on here, tweeted Matthew Taliaferro, a postdoctoral fellow at MIT who studies gene expression and genetic disease.

The Cas9 enzyme in the CRISPR system is what actually cuts DNA, leading to genetic changes. Unusually high levels of enzyme activity could account for the observed off-target mutationsmore cutting equals more chances for the cell to mutate its DNA. Different labs use slightly different methods to try to ensure the right amount of cuts happen only where intended.

Gatan Burgio, whose laboratory at the Australian National University is working to understand the role that cellular context plays on CRISPR efficiency, believes the papers central claim that CRISPR caused such an alarming number of off-target mutations is not substantiated.

Burgio says there could be a range of reasons for seeing so many unexpected changes in the mice, including problems with accurately detecting DNA variation, the extremely small number of mice used, random events happening after Cas9 acted, or, he concedes, problems with CRISPR itself.

Burgio has been editing the DNA of mice using CRISPR since 2014 and has never seen a comparable level of off-target mutation. He says hes confident that additional research will refute these recent findings.

Although the news of this two-mouse experiment fired up the science-focused parts of the Twittersphere, the issue it raises is not new to the field.

Researchers have known for a few years now that off-target mutations are likely given certain CRISPR protocols. More precise variants of the Cas9 enzyme have been shown to improve targeting in human tissue in the lab.

Researchers have also focused on developing methods to more efficiently locate off-target mutations in the animals they study.

As scientists continue to hone the gene-editing technique, we recognize theres still a way to go before CRISPR will be ready for safe and effective gene therapy in humans.

Ian Haydon is a doctoral student in Biochemistry at the University of Washington. This story originally appeared at The Conversation.

See the original post here:

Unraveling The Controversy Over The CRISPR Mutations Study - Fast Company

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More here:

CRISPR stocks sank on news the gene editing tool can veer off target. But that's hardly news - STAT

CRISPR-Cas9 is the gene editing tool that promised to change the world.

In the short time since its discovery, it has snipped HIVout of human immune cells, sparked a biomedical race between the US and China to work towardbioengineered humans, and now scientists have used CRISPR-Cas9 to slow the spread of cancer.

Every living cell goes through a reproduction cycle, known as the 'cell cycle' a sequence of events that result in cell growth and division.

When this cycle gets out of hand, it becomes a serious and life-threatening problem.Once a cell becomes cancerous it will divide without stopping and quickly invade surrounding the tissue.

And trying to stop cancer is no easy feat. Scientists have used a range of approaches to try to stop it from forming and spreading.

A previous study has turned the body's own immune systemagainst cancer cells, and another team of researchers has created an artificial organthat can pump out cancer-fighting T-cells.

We've even worked out a way to cause particularly aggressiveforms of cancer to self-destruct.

In the latest study, scientists from the University of Rochester have interrupted the cell cycle by targeting a protein responsible for preparing the cell for division, called Tudor-SN.

Tudor-SN influences the cell cycle by controlling microRNA, which are the molecules that fine tune the expression of thousands of genes.

"We know that Tudor-SN is more abundant in cancer cells than healthy cells, and our study suggests that targeting this protein could inhibit fast-growing cancer cells," says lead researcher,Reyad A. Elbarbary.

When Tudor-SN was removed from human cells, using CRISPR-Cas9, the level of microRNAs increases.

With more microRNAs in the mix, it slows down the genes that encourage cell growth. With these genes hindered, the cell transitions slowly to the cell division phase of the cell cycle.

The researchers used this approach to slow the growth of kidney and cervical cancer cells.

"Because cancer cells have a faulty cell cycle, pursuing factors involved in the cell cycle is a promising avenue for cancer treatment," said Lynne E. Maquat, senior researcher on the paper.

The next step for the research is to work out how Tudor-SN functions in combination with other molecules and proteins. That way, scientists may be able to identify the most appropriate drugs to target it.

While the researchers admit that they have a long way to go before we see this technology being used in humans, any new approach that could provide a cure to the millions ofpeople living with cancer is always welcome.

The findings have been reported in Science.

See more here:

Scientists have used CRISPR to slow the spread of cancer cells ... - ScienceAlert

A new research paper is stirring up controversy among scientists interested in using DNA editing to treat disease.

In a two-page article published in the journal Nature Methods on May 30, a group of six scientists report an alarming number of so-called off-target mutations in mice that underwent an experimental gene repair therapy.

CRISPR, the hot new gene-editing technique thats taken biology by storm, is no stranger to headlines. What is unusual, however, is a scientific article so clearly describing a potentially fatal shortcoming of this promising technology.

The research community is digesting this news with many experts suggesting flaws with the experiment, not the revolutionary technique.

The research team sought to repair a genetic mutation known to cause a form of blindness in mice. This could be accomplished, they showed, by changing just one DNA letter in the mouse genome.

They were able to successfully correct the targeted mutation in each of the two mice they treated. But they also observed an alarming number of additional DNA changes more than 1,600 per mouse in areas of the genome they did not intend to modify.

The authors attribute these unintended mutations to the experimental CRISPR-based gene editing therapy they used.

A central promise of CRISPR-based gene editing is its ability to pinpoint particular genes. But if this technology produces dangerous side effects by creating unexpected and unwanted mutations across the genome, that could hamper or even derail many of its applications.

Several previous research articles have reported off-target effects of CRISPR, but far fewer than this group found.

The publicly traded biotech companies seeking to commercialize CRISPR-based gene therapies Editas Medicine, Intellia Therapeutics and Crispr Therapeutics all took immediate stock market hits based on the news.

Experts in the field quickly responded.

Either the enzyme is acting at near optimal efficiency or something fishy is going on here, tweeted Matthew Taliaferro, a postdoctoral fellow at MIT who studies gene expression and genetic disease.

The Cas9 enzyme in the CRISPR system is what actually cuts DNA, leading to genetic changes. Unusually high levels of enzyme activity could account for the observed off-target mutations more cutting equals more chances for the cell to mutate its DNA. Different labs use slightly different methods to try to ensure the right amount of cuts happen only where intended.

Unusual methods were used, https://twitter.com/LluisMontoliu/status/869705549453119489">tweeted Lluis Montoliu, who runs a lab at the Spanish National Centre for Biotechnology that specializes in editing mice genes using CRISPR. He believes the authors used suboptimal molecular components in their injected CRISPR therapies specifically a plasmid that causes cells to produce too much Cas9 enzyme likely leading to the off-target effects they observed.

Gatan Burgio, whose laboratory at the Australian National University is working to understand the role that cellular context plays on CRISPR efficiency, believes the papers central claim that CRISPR caused such an alarming number of off-target mutations is not substantiated.

Burgio says there could be a range of reasons for seeing so many unexpected changes in the mice, including problems with accurately detecting DNA variation, the extremely small number of mice used, random events happening after Cas9 acted or, he concedes, problems with CRISPR itself.

Burgio has been editing the DNA of mice using CRISPR since 2014 and has never seen a comparable level of off-target mutation. He says hes confident that additional research will refute these recent findings.

Although the news of this two-mouse experiment fired up the science-focused parts of the Twittersphere, the issue it raises is not new to the field.

Researchers have known for a few years now that off-target mutations are likely given certain CRISPR protocols. More precise variants of the Cas9 enzyme have been shown to improve targeting in human tissue the lab.

Researchers have also focused on developing methods to more efficiently locate off-target mutations in the animals they study.

As scientists continue to hone the gene-editing technique, we recognize theres still a way to go before CRISPR will be ready for safe and effective gene therapy in humans.

This article was originally published on The Conversation. Read the original article.

Ian Haydon does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond the academic appointment above.

See the original post here:

CRISPR controversy raises questions about gene-editing technique - Joplin Globe

Associate biology and microbiology professor Wanlong Li assesses the growth of two-week-old wheat seedlings. Credit: South Dakota State University

Larger, heavier wheat kernelsthats how associate professor Wanlong Li of the SDSU Department of Biology and Microbiology seeks to increase wheat production. Through a three-year, $930,000 U.S. Department of Agriculture grant, Li is collaborating with Bing Yang, an associate professor in genetics, development and cell biology at Iowa State, to increase wheat grain size and weight using a precise gene-editing tool known as CRISPR/Cas9.

South Dakota State is one of seven universities nationwide to receive funding to develop new wheat varieties as part of the National Institute of Food and Agricultures International Wheat Yield Partnership (IWYP) Program. The program supports the G20s Wheat Initiative, which seeks to enhance the genetics related to yield and develop varieties adapted to different regions and environmental conditions.

The goal of IWYP, which was formed in 2014, is to increase wheat yields by 50 percent in 20 years. Currently, the yearly yield gain is less than1 percent, but to meet the IWYP goal wheat yields must increase 1.7 percent per year. Its a quantum leap, he said. We need a lot of work to reach this.

Humans consume more than 500 million tons of wheat per year, according to Li. However, United States wheat production is decreasing, because farmers can make more money growing other crops. He hopes that increasing the yield potential will make wheat more profitable.

First, the researchers will identify genes that control grain size and weight in bread wheat using the rice genome as a model.

The CRISPR editing tool allows the researchers to knockout each negatively regulating gene and thus study its function, according to Li. CRISPR is both fast and precise, he added. It can produce very accurate mutations.

This technique will be used to create 30 constructs that target 20 genes that negatively impact wheat grain size and weight. From these, the University of California Davis Plant Transformation Facility, through a service contract, will produce 150 first-generation transgenic plants and the SDSU researchers will then identify which ones yield larger seeds. One graduate student and a research assistant will work on the project.

The end products are not genetically modified organisms, Li emphasized. When we transfer one of the CRISPR genes to wheat, its transgenic. That then produces a mutation in a different genomic region. When the plants are then self-pollinated or backcrossed, the transgene and the mutation are separated.

The researchers then screen the plants to select those that carry the desired mutations. This is null transgenic, Li said, noting USDA has approved this process in other organisms. Yang used this technique to develop bacterial blight-resistant rice.

As part of the project, the researchers will also transfer the mutations into durum wheat. Ultimately, these yield-increasing mutations, along with the markers to identify the traits, can be transferred to spring and winter wheat.

This article has been republished frommaterialsprovided by South Dakota State University. Note: material may have been edited for length and content. For further information, please contact the cited source.

Read the rest here:

Increasing Wheat Yields with CRISPR - Technology Networks

To Be a Machine: Adventures among Cyborgs, Utopians, Hackers, and the Futurists Solving the Modest Problem of Death Mark O'Connell Granta 242 pages ISBN: 978-1-78378-196-6 12.99

"We built ingenious devices and we destroyed things." These words are easy to imagine carved on the tombstone of the human race. In To Be a Machine, where these words appear after an alarming session with people working on artificial intelligence, they're just one of the many possible futures that Dublin journalist Mark O'Connell visits. None seem to appeal to him much.

A friend once observed that anyone who had ever watched a baby could see how limited AI really is. Here, O'Connell's new baby son helpfully provides him with a grounding biological balance as he ponders the work of people who, in one way or another, all want to transcend biology.

Many of the ideas O'Connell explores, and some of the people he interviews, will be familiar to those who who've read prior efforts, beginning with Ed Regis's Great Mambo Chicken and the Transhuman Condition. It's probably a mark of some kind of social change that Regis, writing 26 years ago, couldn't avoid -- or rather, embraced -- a certain, "Oh, my God, are these people nuts or what?" tone, while O'Connell, writing now, can be more soberly reflective. The Singularity, mind uploading, cryonics, whole-brain emulation, real-life 'cyborgs', and escaping the surly bonds of Earth to colonise distant planets and save the future of humanity may be no closer to reality than they were in 1991, but the ideas are more familiar: twenty-five years of Wired magazine and Silicon Valley hegemony have had their effect.

Today, when Nick Bostrom predicts (in his book Superintelligence) that an AI might turn all the Earth's resources to making paper clips he may still seem crazy -- but he's an Oxford University professor and director of the Future of Humanity Institute. Colonizing space to save the human race may be a fringe notion -- but it's also been embraced by the physicist Stephen Hawking.

To embrace biology, O'Connell is told during his study of cryonics, is to buy into "deathist ideology". I sympathize here: visiting the leading cryonics company, Alcor, and learning the details of cryopreservation can make death seem almost cuddly. Cryonicists themselves admit that revival is a very long shot -- but it's the only non-zero option.

The one overtly comic section of To Be a Machine, therefore, is the one that's most embodied: O'Connell watches as robots try to complete DARPA's 2015 challenge -- there's a collection of the best pratfalls at Popular Mechanics. The hardest things to automate are the things humans learn earliest: the 2015 state of the art, after millions of dollars and millions of hours of human engineering, couldn't climb stairs or open doors as well as a two-year-old. So in that area, at least, we can feel smug.

Given that the technology industry famously loves disruption, it should be no surprise that it attracts people who favour disrupting life itself. In the end, however, O'Connell favours blood and bone.

Read more book reviews

Read the rest here:
To Be a Machine, book review: Disrupting life itself - ZDNet