Medical Breakthrough – Gizmocrazed – Future Technology News https://www.gizmocrazed.com Artificial Intelligence, Medical Breakthroughs, Virtual Reality Fri, 14 Dec 2018 20:19:19 +0000 en-US hourly 1 https://www.gizmocrazed.com/wp-content/plugins/squirrly-seo/view/css/feed.css Scientists Find What Makes Our Bones Strong When We Exercise https://www.gizmocrazed.com/2018/12/scientists-find-what-makes-our-bones-strong-when-we-exercise/ Fri, 14 Dec 2018 03:40:30 +0000 https://www.gizmocrazed.com/2018/12/scientists-find-what-makes-our-bones-strong-when-we-exercise/ Scientists Find What Makes Our Bones Strong When We Exercise

(Credit: Flamingo Images/Shutterstock)

Exercise is good for us in a lot of ways. It helps cut the pounds, increases cardiovascular health, adds muscle mass and can boost our mood. What it also does, though, is help keep our bones strong.

Studies have shown that regular exercise, especially involving weights, ups bone mass and maintains the health of our skeletal system. For us spring chickens, having strong bones might not sound all that critical, as our skeleton seems to get by just fine no matter what we do. But in the elderly, osteoporosis, the gradual weakening of bones, is a real threat, and it’s estimated to be responsible for around two million fractures annually in the U.S. Finding a way to make bones strong without exercise, which can be difficult for older individuals, could help cut that number substantially.

Better Bones

A group lead by researchers from the Dana-Farber Cancer Institute may have found a way to begin creating such a treatment. Working in mice, the scientists have found a hormone linked to exercise that helps regulate the process of bone growth. The hormone is called irisin, and it’s linked to a protein known as sclerostin, another mediator of skeletal health.

Both irisin and sclerostin play a role in the regular turnover of bone cells. While most of our bone cells are quite long-lived, there’s still a regular background of death and regrowth among skeletal cells. Irisin and sclerostin both help signal our bodies to begin the process of breaking down old cells so new ones can form, and it’s something that’s kicked into a higher gear when we work out.

While it may seem confusing that something involved in killing bone cells also keeps our bones strong, it’s important to remember that this process is part of a natural cycle of death and renewal. As bone cells are removed, it seems to signal our bodies to create new ones as well, and the end result is stronger, healthier bones.

The researchers confirmed their results with tests in mice modified to lack irisin. As they report in Cell, these mice didn’t lose any bone mass when subjected to a model of osteoporosis, indicating that the researchers’ hunch was correct. Again, it’s counterintuitive, but the test proved that irisin is involved with the turnover of bone cells, which is a critical component of bone health. Paired with previous studies showing that mice treated with irisin have stronger bones, they say it’s evidence that the hormone is an important part of skeletal health.

Additionally, irisin has been linked in other studies to fat regulation and brain activity as well, meaning that the hormone could prove beneficial in other ways as well.

The researchers also found a receptor for irisin within bone cells, something that they say should help them to further explore exactly how the hormone works within our bodies. Better understanding how the irisin produced by exercise works to strengthen bones could help lead to treatments based on the hormone in the future.

If so, we’ll finally be able to reap the benefits of exercise without the sweat and exertion. At least, when it comes to our bones, that is.

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Starting School Later Helps Teens Get More Sleep https://www.gizmocrazed.com/2018/12/starting-school-later-helps-teens-get-more-sleep/ Thu, 13 Dec 2018 03:40:30 +0000 https://www.gizmocrazed.com/2018/12/starting-school-later-helps-teens-get-more-sleep/ Starting School Later Helps Teens Get More Sleep

(Credit: Jamesboy Nuchaikong/Shutterstock)

Ah, adolescence. A time of change, of navigating awkward social situations, figuring out who you are, maybe holding down that first job or focusing on extracurriculars — all while juggling the demands of school. And for most teens, managing all of this happens on too little sleep.

To help alleviate the lack of Z’s, experts in the U.S. have been pushing for school systems across the country to roll back the start times for middle and high school students. Now, a new paper in the journal Science Advances (titled, in part, “Sleepmore in Seattle”) could help throw some more weight behind that push.

A Later Start

Sleep researchers have known for decades that the circadian rhythm — the natural sleep/wake cycle — of teens is different from those of kids and adults. Normally, our bodies release certain hormones that play a big role in helping us wake up and feel drowsy at certain times. But for teenagers, this hormone release schedule gets pushed back, so they tend to stay up and wake up later.

Despite this biological difference, school start times for teens, especially those in high school, are usually earlier than for younger kids. Which makes it tough for teens to stay focused in school. “To ask a teen to be up and alert at 7:30 a.m. is like asking an adult to be active and alert at 5:30 a.m.,” says Horacio de la Iglesia, a biology professor at the University of Washington and one of the study’s authors, in a press release. But recently, many school districts have been toying with having their start times better align with adolescents’ internal clocks.

In the fall of 2016, Seattle Public Schools committed to the idea and changed the start time of all of its high schools from 7:50 a.m. to 8:45 a.m. Capitalizing on this switch, which took over a year of planning, researchers from UW and the Salk Institute for Biological Studies followed the sleep cycles of two group of students from two of the high schools for two weeks.

In group one were roughly 90 pupils from both schools; the research team tracked them before the start time switch. But the second group, again made up of around 90 students from both schools, weren’t monitored until after the change. Regardless of group, each teen wore a wristband that tracked light and activity levels every 15 seconds to help the scientists pinpoint when they were asleep.

Though many critics of later school start times argue teens will just stay up even later, that wasn’t the case here. Generally, the students still went to bed around the same time. The end result was that they got more shuteye on weeknights when classes started later, going from sleeping six hours and 50 minutes, on average, to seven hours and 24 minutes. It’s still not the recommended minimum of eight hours per night that health experts recommend, but it’s an improvement. A significant one, according to the researchers. It’s “a huge impact to see from a single intervention,” says de la Iglesia.

A Spark for Change

de la Iglesia and his team hope the results they’ve seen will push more school administrators to follow the lead of districts like Seattle that have been willing to give the adjusted schedule a go. “School start time has serious implications for how students learn and perform in their education,” he says in the press release. “Adolescents are on one schedule. The question is: What schedule will their schools be on?”

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A Woman's Uterus May Play a Role in Memory and Cognition https://www.gizmocrazed.com/2018/12/a-woman039s-uterus-may-play-a-role-in-memory-and-cognition/ Wed, 12 Dec 2018 03:40:29 +0000 https://www.gizmocrazed.com/2018/12/a-woman039s-uterus-may-play-a-role-in-memory-and-cognition/ A Woman's Uterus May Play a Role in Memory and Cognition

One-third of women in the U.S. have their uterus removed by age 60. A study in rats (not pictured) showed the procedure can reduce memory and cognition. (Credit: IrinaK/Shutterstock)

(Inside Science) — In medical textbooks, the nonpregnant uterus is often described as quiescent, dormant and useless. But now, researchers have found that the uterus may play a role in memory and cognition — a role hitherto unappreciated because researchers haven’t looked closely at the uterus’s role outside of pregnancy.

A third of women in the U.S. have their uteruses removed, a procedure called hysterectomy, by age 60, according to Heather Bimonte-Nelson, who directs Arizona State University’s behavioral neuroscience of memory and aging lab and is senior author of a new paper detailing the research.

The uterus is connected to the autonomic nervous system, which coordinates unconscious functions like breathing and digestion. While researchers have long studied the way the ovaries interact in the body and with the brain, the uterus has often been overlooked, according to the researchers, who studied the effects of hysterectomy in female rats.

“People talk a lot about the ovary-brain connection because we know now that estrogen and progesterone have such marked effects on things like memory. But we hope that scientists will start thinking about the uterus-ovary-brain system instead of just the ovary-brain system,” said Bimonte-Nelson.

The research team systematically tested the role of the uterus and ovaries in learning and memory in four groups each consisting of 14 or 15 rats. One group underwent a sham surgery in which no organs were removed. The remaining three groups underwent either removal of the uterus alone, removal of the ovaries alone, or removal of the uterus and the ovaries.

Holly Fitch, a professor of behavioral neuroscience at the University of Connecticut who was not involved in the research, praised the study design, saying that it used appropriate sample sizes and control groups.

The rats recovered for six weeks after their procedures, and then performed memory tests in a water maze that contained eight arms radiating out from a circular center — four arms contained hidden platforms and four arms were empty. The researchers placed the rats in the center of the maze, and once the rat found a platform it and the rat were removed. The rat then restarted the maze to search for the remaining platforms.

The test, Bimonte-Nelson said, is one that requires the rats to use their working memory. She compared it to the difference between a human remembering a phone number, which uses short-term memory, versus adding up the numbers in the phone number, which uses working memory.

Only the rats that had only their uteruses removed were unable to remember which arms of the maze never had a platform, while the other groups did remember.

The group that had both the uterus and the ovaries removed did not make as many errors as the group with only the uterus removed, indicating that the removal of the uterus alone had a unique and negative effect on working memory, or on how much information the rats could manage simultaneously, according to the researchers. The sham group and the group with only the ovaries removed performed similarly to the group with both the uterus and the ovaries removed.

The researchers were initially surprised by the results, prompting them to replicate the experiments. “When the second study results had the same effect and the same pattern was there, we knew that we had hit on something important,” Bimonte-Nelson said. “No matter how we looked at it, the data were telling us that removing the uterus was impacting cognition.”

The researchers developed the uterus and ovary removal surgeries to ensure that they were as similar to a human version of the surgery as possible, but still, results from a study looking at rats will not necessarily have the same results in humans. The researchers also noted that rat life spans are much shorter than humans’ and further research is necessary to understand if the cognitive effects of hysterectomy are long-lasting.

Furthermore, the researchers said that they don’t want the results to be alarming for women with hysterectomies, but rather a call to continue investigating the role of the uterus in cognition across the life span.

[This story was originally published on Inside Science.]

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Can We Blame Our Genes for Our Decisions? https://www.gizmocrazed.com/2018/12/can-we-blame-our-genes-for-our-decisions/ Tue, 11 Dec 2018 03:40:28 +0000 https://www.gizmocrazed.com/2018/12/can-we-blame-our-genes-for-our-decisions/ Can We Blame Our Genes for Our Decisions?

(Credit: Zita/Shutterstock)

Forget meditation, forget ayahuasca ceremonies and mindfulness practice. Today, knowing yourself is as easy as swabbing your cheek. Home genetics tests like those offered by 23andme are becoming readily affordable — just $69 for a test kit — and they offer an unprecedented look at our personal blueprint.

It’s even possible today to study the genetics of your potential offspring before they’re born. So-called pre-implantation genetic diagnosis analyzes DNA from an embryo, when it’s nothing more than a few cells. But even at that stage, it’s possible to divine the unique set of genes that will shape a person’s life.

The tests are currently used for parents at risk of passing on dangerous genetic conditions, but they could conceivably do much more. Studies have picked out groups of genes associated with intelligence, academic achievement, criminal activity and other life outcomes. It now seems possible to chart your children’s lives before they ever emerge into the world.

The implications are staggering. Knowing what kind of person a child is likely to become — a kind of scientific prejudice — could easily lead to discrimination. Kids with genes linked to low intelligence could be shunted into inferior schools, and adults with genes linked to criminal activity could be subjected to extra-judicial police scrutiny.

This kind of thinking can be termed “genetic determinism” — the idea that our genes conclusively shape our behavior — and it also wreaks havoc with our notions of morality and free will. If our genes are guiding our behavior, does that mean we’re not responsible? “It wasn’t my fault, officer, my genes made me do it”?

Rest assured, then: None of this is how the science actually works. But that we’ll still have to grapple with the consequences of reading our genetic code.

Keeping Score

To begin with, no genetics researcher would claim to know a person’s future based on a read through their genome.

“If you have two people in front of you with exactly the same genetic score, one might go on to commit a crime and the other one won’t,” says Jasmin Wertz, a postdoctoral fellow at Duke University, where she studies how genetics and the environment shape child development. “It doesn’t really give you the information you need to make predictions with any kind of certainty.”

Wertz would know. She conducted a study of how self-control, cognitive ability and difficulties in school — all affected by our genes — predicted criminal activity later in life. She and her co-authors gave each participant a genetic score based on whether their genes were correlated with positive outcomes in life. These genetic scores explained about one percent of the difference in whether people committed crimes or not, she found. That’s compared to three to five percent explained by “socio-economic deprivation,” meaning things like poverty or a difficult family situation. In other words, the genetic role is tiny.

classroom

(Credit: Monkey Business Images/Shutterstock)

“The majority of people, even with a lower than average genetic score, will never go on to commit a crime,” Wertz says. “It’s extremely hard to predict your criminal behavior based on just the information from a genetic score.”

The same technique has been used to look at other broadly defined societal outcomes, as well. Another study found that 16 percent of the difference in educational outcomes could be explained by a genetic score. That number’s higher, but it’s still small. And studies of identical twins, the gold standard for determining the influence genes have on given traits, have suggested that our DNA is probably responsible for around half of things linked to intelligence and behaviors like educational achievement and criminal activity. That’s far higher than one or 16 percent, but the conclusion is clear: Genetic determinism doesn’t seem to be scientifically possible.

Why not? There are just too many genes, and they interact with each other and with the environment in too many ways. We can’t simply look at a handful and divine the future.

“There’s not going to be one, or two or even a dozen genes that predict something like criminal behavior,” says J.C. Barnes, a researcher at the University of Cincinnati focused on the intersection of genetics and crime, and one of Wertz’s co-authors. “It’s going to be that there are hundreds or thousands of individual genetic variants, and those are only going to explain a small piece of why we see variation in criminal activity.”

The Genetic Defense

Even in cases where genes seem definitively linked to certain actions, things are not as straightforward as they seem.

Take certain mutations of the MAOA gene, found on the X chromosome, which studies have shown can predispose men to violence. What seems open and shut is actually anything but. MAOA is only correlated with violence in men who had bad childhoods — in others, the mutation didn’t have much effect at all. (Most genetics follows this pattern: A deficient copy of one gene is rarely tied to a single outcome)

That hasn’t deterred defense attorneys, though, who have pointed to the presence of a defective copy of the MAOA gene in attempts for clemency and reduced convictions. In 2010, Bradley Waldroup had a murder conviction dropped down to voluntary manslaughter, due in part to genetic evidence. His lawyers argued that a mutation in his copy of the MAOA gene predisposed him to aggression, and it was enough to sway the jury. The logic echoes the reasoning used in insanity pleas — something largely outside of the defendant’s control guided his actions.

Barnes doesn’t agree with that line of thinking. There’s not enough evidence linking MAOA to violent behavior for it to stand up in a court of law.

“There might be some effect there, but overall, the effect is quite small,” he says. “It can’t be just this gene, it can’t be ‘the one.’”

And even so, MAOA is by far an outlier — very few single genes can be tied to any discrete outcome.

In other words, even a gene that punches above its weight class likely doesn’t have enough of an effect on our actions that we can pin blame on it. Or, seen another way, it means that someone with the gene is not predestined to violence, another strike against genetic determinism.

Environmental Interplay

It may not reflect an accurate understanding of the science, but cases like Waldroup’s do seem to reflect how we view our genes today. 23andme ads invite us to “meet your genes,” and call out individual examples like ACTN3, a gene involved in determining muscle composition sometimes referred to as a “gene for speed.”

But studies have found only tentative connections between the genes and how our bodies respond to exercise, and indicate that the gene is also involved in a whole range of things affecting our muscles. Plus, many other genes related to muscle function also play a role in how fast or strong we might be.

Framing our genes in this deterministic way vastly oversimplifies the way they work, and grants genes powers they simply don’t have. Just like there’s no one “gene for speed,” there’s no “gene for crime.”

“It’s not like you have one mutation and now you’re a serial killer,” says Paige Harden, an associate professor of psychology at the University of Texas at Austin. Instead, thousands of genes each influence in a minuscule way the probability that a given person might develop a trait, like impulse control or poor literacy, that in turn is correlated with committing a crime. And that’s not even taking the environment into account.

The set of circumstances that surrounds us as we develop into adults also plays an integral role in who we turn out to be — it’s why identical twins can end up so different. Our experiences shape the influence our genes have on us. And our genes help determine what kinds of environments we seek out, which in turn shapes how our genes are expressed, and so on. The interactions are extraordinarily complex, and we’re nowhere near understanding the majority of them.

“Be very wary of claims to genetic exceptionalism, that genes are somehow special, that they play a causal role that nothing else does,” says Leslie Francis, a professor of law and philosophy at the University of Utah. If anything, research is showing that genes may play a lesser role than we think.

“The genetics research has really started to reveal just how powerful the environment really is,” Barnes says. “Even when we know the genetic background and we control for that, we still see a huge variation in behaviors.”

Embracing Our DNA

As cases like Waldroup’s, or ads from 23andme make clear, we as a society are still figuring out what to make of our genes. It’s difficult because there’s no one example that really explains the effects our genes have — the influences of DNA on our behavior and lives varies greatly from situation to situation.

That makes it really hard to turn our current understanding of genetics into ideas about morality and responsibility. Sure, not everyone is created equal, but that doesn’t mean genes somehow determine the outcomes of our lives. But if it’s done right, integrating genetics into our social systems could be a boon to our future children.

“I think it would be great to use the DNA to identify children at birth who have, for example, genetic risk of developing reading problems, and thus enabling early intervention, because we know that preventative interventions have a much greater probability of success early in life,” says Kaili Rimfeld, a geneticist at King’s College London.

In other fields, genetic foreknowledge could help avert — not punish — unwanted behavior. Ultimately, it will take realizing that while our genes do have a role to play in guiding our behavior, it is far from an absolute one. Comprehending exactly what our genes do — and don’t do — will be necessary to guide future policies.

“People are going to be born with the genes that they have, so if we want to create a society that looks like a society we want to live in, [we need to consider genetics] in terms of what are our responsibilities to each other,” Harden says. That way, “we can structure the environment such that this natural lottery doesn’t wreak havoc.”

Key to a more nuanced understanding of how we should work genes into or society, Harden suggests, is what may be a more fundamental problem when it comes to comprehending DNA. We seem to view our genes as something outside of ourselves, akin to a brain tumor that alters an existing personality. It’s a logic on display when defense attorneys use the “genetic defense,” or when we worry about whether our genes erase the concept of free will.

“We talk about genes like they’re this external force, and there’s some true self that’s separate from this external force,” says Harden, “but that distinction … really breaks down. What does it mean that I want something, when that “I” is the product of a brain, and that brain is the product of a genome?”

In other words, we are our genes. That’s not all we are, but our DNA is in literally every cell of our bodies. While genetics doesn’t rule over us, we cannot escape its influence. The best we can do is try to live with it.

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Scientists Achieve Breakthrough on Path to Pig-to-Human Heart Transplants https://www.gizmocrazed.com/2018/12/scientists-achieve-breakthrough-on-path-to-pig-to-human-heart-transplants/ Sun, 09 Dec 2018 03:40:27 +0000 https://www.gizmocrazed.com/2018/12/scientists-achieve-breakthrough-on-path-to-pig-to-human-heart-transplants/ Scientists Achieve Breakthrough on Path to Pig-to-Human Heart Transplants

Scientists say they have successfully kept a baboon alive with a pig’s heart for six months. (Credit: Dusan Petkovik/Shutterstock)

Although 54 percent of adults in the United States have registered as organ donors, just one in three people die in a way that allows for organ donation. That leaves more than 100,000 people in the United States waiting for a transplant. Many will die waiting.

Because demand for organs outpaces supply and probably always will, researchers have looked to xenotransplantation — placing animal organs into human bodies — as an alternative. However, getting to the point where xenotransplantation is safe enough for trials in humans has been a challenge because so many complications can occur. Now, a breakthrough by a group of researchers brings us one step closer to a day when organ shortages are a thing of the past.

A research team led by Bruno Reichart at the University of Munich in Germany has developed a technique allowing baboons to survive significantly longer than ever before with transplanted pig hearts. Figuring out how to safely xenotransplant hearts is an important area of study because of skyrocketing rates of heart problems, the researchers said.

“Heart failure in the United States is expected to reach more than eight million by 2030, and many of these people will die while waiting for a donor organ,” wrote Christoph Knosalla of the German Heart Center in a commentary published alongside the team’s research paper in Nature this week.

Despite 25 years of extensive study, the longest a baboon had survived after receiving a pig heart was 57 days. However, the researchers demonstrated it’s possible for a baboon to survive six months by modifying the typical heart transplantation protocol and using gene editing technology.

Beating Surgical Complications

Researchers refined the transplantation protocol over the course of three trials involving 16 baboons. Baboons received hearts from pigs that were genetically edited to reduce interspecies immune reactions and to prevent excessive blood clotting after surgery.

In the first trial, they learned that using an ice-cold storage solution, which is the typical method of organ storage prior to transplant procedures, can cause tissue damage once blood is recirculated through the heart. To prevent organ failure, they intermittently pumped an oxygenated, blood-based solution containing nutrients and hormones kept at 46 degrees Fahrenheit through the heart.

In the second trial, they aimed to solve the problem of heart overgrowth common in pig-to-baboon transplants. Although pig hearts are very similar to human and primate hearts, they are much bigger and are prone to complications arising from interspecies hormonal and blood pressure differences. Transplanted hearts that continue to grow to a size bigger than what the recipient’s body can support may damage nearby organs and cause death.

To prevent this from happening, researchers gave the baboons medication to reduce their blood pressure to levels found in pigs. Additionally, they gave the primates temsirolimus — a drug that prevents heart overgrowth. Finally, they modified the typical course of cortisone treatment to combat immunosuppression in transplant patients. Because cortisone can cause heart overgrowth, they tapered the treatments much earlier than usual.

Using a combination of these techniques in the third trial extended the post-transplantation survival of the baboons. Two lived healthily for three months — the entire length of the study — before they were euthanized. Another two lived for six months before they were euthanized. A fifth baboon involved in the trial developed complications and was euthanized after 51 days.

Although much more study is needed before researchers can begin xenotransplantation trials in humans, Reichart is optimistic it’s on the horizon.

“I think the technical expectations are solved, but we must produce more consistent results,” Reichart said. “We need additional experiments and achievements. On top of our funding by the German Research Foundation, we would need at least one private investor. Taken together, three years would be enough.”

In the short term, the researchers said the techniques used in the study could improve human-to-human transplant procedures. Additionally, the discovery that pumping oxygenated blood and nutrients through stored hearts could increase the availability of donor hearts by preserving those that aren’t able to withstand a lack of normal blood supply because of age or an underlying condition.

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Living in Space Makes Our Bodies More Susceptible to Infections https://www.gizmocrazed.com/2018/12/living-in-space-makes-our-bodies-more-susceptible-to-infections/ Sat, 08 Dec 2018 03:40:27 +0000 https://www.gizmocrazed.com/2018/12/living-in-space-makes-our-bodies-more-susceptible-to-infections/ Living in Space Makes Our Bodies More Susceptible to Infections

Mice have long been used for biomedical research here on Earth, but in the last few decades, they’ve been increasingly ferried to space to help scientists better understand how living in microgravity can affect biological organisms. (Credit: National Cancer Institute/Wikimedia Commons)

Even just 30 days in space can significantly reduce our immune system’s ability to fight infection, suggests a new analysis of mice that spent a month aboard an orbiting spacecraft.

The research, which was published December 6 in the journal Federation of American Societies for Experimental Biology, is a recent analysis of data from the Bion-M1 mission, which was a collaborative project carried out by NASA and the Russian Institute of Biomedical Problems in 2013.

Space Mice

As part of the study, an international team of researchers compared three distinct groups of mice. The first two groups spent 30 days orbiting the Earth at an altitude of 360 miles (575 kilometers), while the third group, which served as the control, remained on the planet under similar feeding and housing conditions. Of the two space-bound groups of mice, one was examined immediately following its return to Earth, whereas the other was evaluated a week later.

According to the study, which analyzed proteins found within the rodent’s femur bones, the researchers revealed that living in a microgravity environment for even 30 days is enough to dramatically impair the mice’s ability to produce vital immune system cells, and this effect persisted even after a week safely back on Earth.

Bion-M1

Although a series of equipment failures, including a malfunctioning feeding system, killed over half of the mice aboard the Bion-M1 biosatellite, enough specimens survived that researchers were still able to glean valuable insights related to how spaceflight affects the body. The opening of the Bion-M1 hatch after the flight landed is seen here. (Credit: IMBP)

Specifically, the space-bound mice experienced more than a 40 percent reduction in their number of B lymphocytes (or B cells). Since these lymphocytes are necessary for the production of antibodies, the researchers say the dearth of B cells may help explain why many organisms — including astronauts — tend to be more susceptibility to infection during stints in space.

“We hope these finding will encourage exploration of countermeasures to improve astronauts’ health and increase the safety of spaceflight,” said co-author Fabrice Bertile, a researcher at the Hubert Curien Multidisciplinary Institute’s Analytical Sciences Department in France, in a press release. “Such concerns are of major importance at a time when space agencies are envisioning manned missions to the moon, asteroids, and even Mars in the near future.”

Beyond Astronauts

But these new insights into how spaceflight affects the immune system are not only applicable to astronauts. A significant number of people on Earth are immobilized or lead sedentary lives, situations that also affect the immune system in ways similar to microgravity. Future research on how microgravity impacts the immune system may have serious implications for millions of Earth-bound residents.

Moving forward, the researchers suggest future studies should explore whether longer missions are more detrimental to the immune system than shorter ones, as well as investigate how the antibodies produced in a microgravity environment are qualitatively different from those produced on Earth.

[This article originally appeared on Astronomy.com]

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Scientists Discovered The Oldest Human Plague. It Took Down Neolithic Farmers And Changed Europe’s History https://www.gizmocrazed.com/2018/12/scientists-discovered-the-oldest-human-plague-it-took-down-neolithic-farmers-and-changed-europes-history/ Fri, 07 Dec 2018 03:40:28 +0000 https://www.gizmocrazed.com/2018/12/scientists-discovered-the-oldest-human-plague-it-took-down-neolithic-farmers-and-changed-europes-history/ Scientists Discovered The Oldest Human Plague. It Took Down Neolithic Farmers And Changed Europe’s History

Scientists found evidence of an ancient plague in the bones of a woman buried among 77 other people from her village in western Sweden. (Credit: Cell Press)

Buried among 77 other people from her village in western Sweden are the bones of a 20 year-old woman. Now an analysis of DNA extracted from her teeth reveals what likely killed her. An international team of researchers has discovered the woman, who died some 5,000 years ago, had the oldest known case of the plague.

The finding suggests the world’s first plague epidemic took out her community and vast swaths of the Neolithic farming population in Europe. If confirmed, the notorious pathogen might be what allowed for the massive human migrations that followed.

“These events had major consequences for the history of humanity,” said Nicolas Rascovan, a bioinformaticist at Aix Marseille Universite in France, who led the new research. The migrations of peoples from the steppe of what is now Russia and Ukraine into Europe in the Bronze Age overturned the European gene pool.

“This is actually when the genetic makeup of the modern European is created,” said Simon Rasmussen, an evolutionary and systems biologist at the University of Copenhagen in Denmark who led the new study with Rascovan.

The migrations also likely brought in significant cultural changes, including the forerunners of half the languages spoken around the world today.

Unprecedented Plague

Rascovan and Rasmussen teamed up with archaeologists to figure out why huge Neolithic farming villages of 10,000 to 20,000 people were suddenly abandoned and burned. The large population density and subsequent population collapse gave them a clue.

“The settlements are the classic, textbook examples of a how a new pathogen can emerge or evolve,” Rasmussen said. Thousands of people lived close together with poor sanitation in near proximity to livestock and other animals. So, the team went in search of disease-causing bugs in publicly available ancient human DNA datasets.

What they found was a surprise. Unambiguous evidence for the bacteria, Y. pestis, that causes plague. When the team compared the DNA sequences of the newfound plague to other known strains and a related bacterium, Y. pseudotuberculosis, they discovered it is the most evolutionary ancient version, they report today in the journal Cell.

The variety of plague the researchers discovered was not kind that causes the bubonic plague, the scourge thought to be responsible for the Black Death—an epidemic that took out 30 to 60 percent of Europe’s population in the mid-1300s—but its far more evil twin, pneumonic plague. In contrast to the bubonic plague, which spreads via flea-carrying rodents, the pneumonic plague infects the lungs and can spread from person to person through saliva droplets. It is the deadliest form of the plague.

The team suspects trade networks, newly established thanks to the advent of wheels and other technologies, spread it. If confirmed, “it will have great impact because it will show a single bacterium had such a massive effective on our history,” Rascovan said.

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A Compound that Makes Bees Into Queens Could also Aid Human Stem Cell Therapies https://www.gizmocrazed.com/2018/12/a-compound-that-makes-bees-into-queens-could-also-aid-human-stem-cell-therapies/ Thu, 06 Dec 2018 03:40:35 +0000 https://www.gizmocrazed.com/2018/12/a-compound-that-makes-bees-into-queens-could-also-aid-human-stem-cell-therapies/ A Compound that Makes Bees Into Queens Could also Aid Human Stem Cell Therapies

A queen bee cup with royal jelly in the wax comb of the honey bee (Apis mellifera). (Credit: Mirko Graul/Shutterstock)

Scientists have announced a breakthrough in stem cell research that could have major implications for medical treatments that involve regenerating human cells. And their discovery came from an unlikely source: royal jelly. It’s the same substance honey bees use to turn a common bee larvae into a queen.

Royal Jelly

A queen bee starts her life just like any other bee – a larva in the honey bee hive, taken care of by her siblings. But when it’s time for a new queen, this larva is pulled aside and fed copious amounts of royal jelly, a nutritious goop secreted by the hive’s nurse bees. This, rather than any genetic differences, is what makes her a queen.

This queen bee grows larger than the other bees in the hive, which means she ends up with substantially more cells in her body, despite being genetically similar to her sisters. Royal jelly is thought to increase her cell count by somehow triggering an increase in stem cells — cells that haven’t yet differentiated into specialized cells — early in her development.

Royal jelly is popular as a dietary supplement in many areas of the world. Though many of the claimed effects on human health are of dubious merit, a few have been supported by randomized controlled trials. The latter inspired researchers to examine what effects the jelly might have outside of a bee hive.

Now, a research team out of Stanford University has found that the active compound in royal jelly, royalactin, prevents stem cells from differentiating, or growing into mature versions of, say, muscle or skin cells. This means that as they continue to grow and multiply they create more stem cells, increasing their therapeutic potential.

If You Give a Mouse Royalactin

Kevin Wang, an assistant professor of dermatology, was the principal investigator on the study, which came out today in Nature Communications. He says that because of royalactin’s role in queen formation, and the rumors of regenerative human properties, it made sense to test it on stem cells. They used embryonic stem cells from a mouse for their experiments.

“This was a giant leap of faith,” says Wang.

They made royalactin in the lab rather than harvesting it from bee hives. “We would bankrupt our whole department if we used real royalactin,” says Wang. “To get that much royalactin we’d need gallons and gallons of royal jelly.”

In the end, the royalactin worked as hoped – it triggered a cellular response that made the stem cells self-renew. As the cells divided and multiplied, they all remained stem cells.

The Quest for Human Royalactin

The researchers suspected that the reason the mouse stem cells responded to royalactin was that there was an analogous compound — a protein with the same shape — naturally occurring in mice.

It’s a bit like finding a lock and key that shouldn’t match, but do. A bee-made key that fits into a mouse-made lock implies that out there somewhere is a mouse-made key identical in shape — even if it’s not identical in material — to the bee-made key. If there wasn’t, that mouse-made lock wouldn’t exist.

They found that mouse-made key – the mammalian analog to royalactin – by using an algorithm to search through every single protein secreted by humans, looking for one that matched the shape of royalactin.

They found one – and only one – protein that fit the bill. Nearly nothing was known about this protein except that it existed. And that it is expressed only briefly, very early on in human development.

Discovery of Regina

What do you name a newly discovered human queen bee compound?

“I wanted to name it ‘Beyoncé’ for ‘Queen Bey’ but the Nature Communications editor was strongly against it, which was too bad,” explains Wang. Instead, the team settled on “regina,” Latin for “queen.”

Wang’s dream is that the regina discovery will lead to advances in stem cell-based medical treatments. A patient recovering from a stroke, heart attack, Alzheimer’s, or a stomach ulcer might receive a stent, delivering regina directly to the area and allowing more stem cells to grow there, potentially speeding up recovery. Of course, this dream is far from reality, and much more research will be needed to figure out the true potential of the molecule.

For now, regina and royalactin can still be used as new stem cell renewal factors. These are the compounds added to stem cells in culture that keep them undifferentiated stem cells. Wang suspects these compounds are equal to, if not better than, the chemicals that are currently used for this task.

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Why Don't We Have an AIDS Vaccine? https://www.gizmocrazed.com/2018/12/why-don039t-we-have-an-aids-vaccine/ Wed, 05 Dec 2018 03:40:32 +0000 https://www.gizmocrazed.com/2018/12/why-don039t-we-have-an-aids-vaccine/ Why Don't We Have an AIDS Vaccine?

A demonstration for AIDS advances in July 2018 in The Netherlands, with Princess Margaret Van Orange pictured at the center. (Credit: Paolo Amorim/shutterstock)

I mentioned to a friend, a gay man nearing 60, that World AIDS Day, which has been observed on Dec. 1 since 1988, was almost upon us. He had no idea that World AIDS Day still exists.

This lack of knowledge is a testament to the great accomplishments that have occurred since World AIDS Day was created 30 years ago. It is also due to an accident in the timing of his birth that my friend escaped the devastation wreaked by AIDS among gay men in the U.S., before there was antiretroviral therapy.

Many people have forgotten AIDS, but there are consequences to forgetting. The fight against AIDS is at a tipping point. Increasingly, there are signs that we may be heading in the wrong direction.

The Elusive AIDS Vaccine

I am a social epidemiologist with more than 20 years of research experience in HIV and STD prevention. I am also the founder of The Basics with Dr. Mo, a sex health communications project that translates prevention science directly for people who need it most.

It is true that global HIV/AIDS success stories abound: Mother-to-child transmission can be reduced to below 5 percent, 75 percent of people living with HIV know their status and 59 percent receive antiretroviral therapy.

Most recently, Pre-Exposure Prophylaxis (PrEP) – the use of antiretrovial drugs to prevent HIV infection among those exposed – has proved to be a successful prevention approach.

Yet the prize – a vaccine that can prevent HIV infection – remains elusive, and makes impossible the use of the only known strategy to have ever eradicated an infectious disease: widespread vaccination. That disease was smallpox, in 1980.

Seeds of Unease

Despite the lack of a vaccine, in 2016 United Nations member states adopted a political declaration on ending the AIDS epidemic by 2030.

As part of the accountability framework, interim 2020 goals set a target of 500,000 new HIV infections for that year. A review of the most recent data estimated 1.8 million new HIV infections in 2017, exactly the same number as in 2016.

Prominent scientists have already begun to question the ability to eradicate AIDS by the 2030 deadline, and concede that the situation has stagnated. The attainment of eradication looks bleak, without the aid of either an effective vaccine or the immediate large-scale promotion and utilization of existing prevention tools (i.e., condoms, voluntary circumcision and potentially PrEP). Given that the vast majority of new HIV infections are sexually transmitted and that condoms have played a decisive role in the global control of HIV transmission, ongoing condom availability and use will be essential to future eradication.

Condoms – both male and female – remain a highly effective mechanism of HIV/AIDS prevention, as well as of other sexually transmitted infections that greatly enhance the risk of HIV transmission.

Condom use is also strongly advised by global public health institutions, including the World Health Organization and the U.S. Centers for Disease Control and Prevention, in conjunction will all other HIV prevention tools including PrEP, because of their lower levels of effectiveness in preventing transmission.

Condom availability is a different matter and varies greatly from country to country. Countries with the highest levels of HIV often rely heavily on donor support. According to the most recent data, in sub-Saharan Africa in 2013, only 10 condoms were availableannually for every man aged 15 to 64 (as compared with the recommended 50 to 60), and, on average, there was one female condom available for every eight women. Funding required to maintain – let alone scale up – HIV commitments, particularly those dedicated to prevention, are increasingly uncertain.

The hydra, sprouting new heads

Even though condoms are an extremely effective barrier method, it is usage that makes condoms efficacious in preventing HIV transmission. Reported condom use varies considerably around the world, and ranges from 80 percent use by men in Namibia and Cambodia to less than 40 percent usage by men and women in other countries, including some highly affected by HIV such as Sierra Leone and Mozambique.

Age plays a role, too. Among young people aged 15 to 24, condom use at last sex varies from more than 80 percent in some Latin American and European countries to less than 30 percent in some West African countries. In the U.S., condom use is at the lower end of the spectrum: Only one-third of the population uses condoms, a number that has not changed significantly over the past two decades.

The majority – 66 percent – of the world’s HIV/AIDS cases are in sub-Saharan Africa, where there has been much progress, particularly with the provision of antiretroviral therapy.

However, there are worrying signs in other parts of the world. There has been little change in new HIV infections in countries outside of sub-Saharan Africa between 1990 and 2017.

In fact, six of the 10 most populous countries in the world have experienced 10 percent to 45 percent increases in new HIV infections since 2010: Russia, China, Brazil, Pakistan, Mexico and Bangladesh. Even in countries such as the U.S., where new HIV infections have decreased by 8 percent overall, the rates of change are unevenly distributed. For example, young African-American men who have sex with men show no decrease in new infections; African-American gay and bisexual men represent the largest percentage of new HIV infections: more than one-quarter.

The increased provision of antiretroviral therapy to people living with AIDS has had a huge impact on extending life and in preventing new HIV infections. However, there remains 25 percent of the population who live with HIV, about 9 million people, who do not know their status.

While we have been necessarily focused on the head of the hydra in sub-Saharan Africa, other hydra heads are beginning to make their presence known, many in countries ill-prepared to deal with increases in the number of new HIV infections.

In the absence of a vaccine, behavior change in the form of condom use promotion, acceptance and adoption, at a scale that many gay men utilized during the peak of the AIDS epidemic in the industrialized world, will need to occur. There are many challenges: continued stigma and gender inequality, not to mention issues of availability, distribution and proactive, nonjudgmental promotion.

We must not forget. Progress on reducing the rate of new HIV infection has been done before. It can be done again, but only if we take forceful, funded action now.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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CRISPR Babies Raise an Uncomfortable Reality — Ethical Guidelines Don't Guarantee Ethical Research https://www.gizmocrazed.com/2018/12/crispr-babies-raise-an-uncomfortable-reality-ethical-guidelines-don039t-guarantee-ethical-research/ Tue, 04 Dec 2018 03:40:24 +0000 https://www.gizmocrazed.com/2018/12/crispr-babies-raise-an-uncomfortable-reality-ethical-guidelines-don039t-guarantee-ethical-research/ CRISPR Babies Raise an Uncomfortable Reality — Ethical Guidelines Don't Guarantee Ethical Research

He talks to Matthew Porteus of Stanford during a panel talk following his presentation. (Credit: Ernie Mastroianni/Discover)

Uncertainty continues to swirl around scientist He Jiankui’s gene editing experiment in China. Using CRISPR technology, He modified a gene related to immune function in human embryos and transferred the embryos to their mother’s womb, producing twin girls.

Many questions about the ethical acceptability of the experiment have focused on ethical oversight and informed consent. These are important issues; compliance with established standards of practice is crucial for public trust in science.

But public debate about the experiment should not make the mistake of equating ethical oversight with ethical acceptability. Research that follows the rules is not necessarily good by definition. As He pushed ahead with human gene editing, how much he skirted the rules may not be his primary ethical failing.

The ‘Right’ Way to Conduct Research

A statement signed by 122 Chinese scientists proclaimed He’s work “crazy” and in violation of ethical standards. Is that really the case?

Scientists undertake medical research to generate knowledge that may one day be used to improve human health. This work can help determine new strategies for prevention and early detection of disease, or develop new drugs and new technologies for treatment, for example. Without investigating them, no one knows which preventive measures, diagnostic tools, or treatments are most beneficial. They need to be rigorously tested.

Ethicists tend to focus most on studies that ask a lot of human subjects because these usually carry the most risks for volunteers. Picture a drug study with participants taking an experimental medication, keeping a daily diary of symptoms and side effects, meeting frequently with a physician and so on.

There’s a long history of abuse and misuse of human subjects in research, from medical workers withholding syphilis treatment from unsuspecting black men in Tuskegeee, Alabama so they could track the disease’s progress, to the deliberate infection of research participants with syphilis in Guatemala in the 1940s to more recently the role of conflicted investigators involved in psychiatric research at the University of Minnesota. In recognition of the potential for abuse, all research undertaken in the U.S. in institutions like universities that receive public research funds or by companies seeking FDA approval for a product is overseen by various ethical and regulatory committees.

tuskegee syphilis trial

A man has his blood drawn as part of the Tuskegee syphilis experiment. (Credit: PD-USGOV)

The ethical acceptability of research is contingent on an institutional review board’s judgment that the procedure has the potential for benefit that counterbalances risk of harm. Institutional review boards are typically internal to research institutions but are meant to be independent of investigators. The board also works to ensure the process of informed consent is robust, such that participants are appropriately educated about the relevant risks of participation, are free from coercion to participate and are aware of their ability to decline to participate without penalty.

Funders of research will also conduct scientific peer review of a protocol to ensure the quality of the research design. Poorly designed research is ethically problematic since it wastes financial, human and other resources that could be allocated to better justified research.

Journal editors play an important gatekeeper role, as well. Studies conducted without appropriate ethical oversight may not be reviewed for publication in journals that abide by the Recommendations for the Conduct, Reporting, Editing, and Publication of Scholarly work in Medical Journals adopted by the International Committee of Medical Journal Editors.

Concerns at any of these steps along the way can prevent health research from proceeding or from contributing to the scientific and medical literature.

Passing Ethical Review Doesn’t Mean It’s Ethical

When He presented his work at a session of the Second International Summit on Genome Editing in Hong Kong, many people raised questions about the informed consent process. Important as they are, the queries also seemed to be groping for a smoking gun — clear violation of existing standards — in order to declare what people already felt: that the research was unethical.

Having those standards and discovering a violation of them makes judgments of ethical responsibility feel straightforward and objective. A rule was broken, the research was unethical. Case closed. There are certainly questions about the adequacy of the processes He’s research went through. Were collaborators kept in the dark about its nature and aims? Was the experimental protocol and the informed consent process subjected to rigorous review by an independent oversight body? Was the consent process itself robust and not compromised by the interests of the researchers?

But by focusing heavily on these still-open questions, the scientific community risks implying that mere compliance with routines of oversight would have made it ethical. That approach fails to ask what is being overseen, what is being overlooked and whether that matters to how we judge the ethical acceptability of an experiment.

It’s important to ask not only whether there was ethical oversight, but what it consisted in. Just because there has been a process does not mean that it is thorough or sufficient.

This is particularly important in the case of germline editing, because it’s so unlike most conventional therapies. As the U.K. Nuffield Council has pointed out, it is incorrect to call it a therapy. If one were undertaking gene therapy in a baby, or even a fetus, to address a life-threatening genetic disease, it would be appropriate to accept a certain amount of risk, because the alternative is much worse: living with a life-threatening disease.

But in the case of embryo editing, there is not yet a child that is sick and needs to be healed. Because the genome editing molecules are delivered into the egg at the same time as the sperm, one brings the “patient” into being in the same moment as one undertakes the “therapy.” So, when the experiment is being contemplated, there is no child to heal.

Thus, the parents’ desires and interest are the focus. They are the patients/research subjects that the ethical oversight process is primarily built to address. This is a problem: There is something missing in a process that fails to prioritize the interests of the resulting child(ren). Yet since bringing them into being would involve risks that are significantly higher than normal reproduction, taking their interests into account may mean that the experiment simply should not be done.

In the case of the Chinese experiment, the situation is still more complex because the edit was made not to address a genetic disease that would otherwise affect the life of the resulting children, but to protect them against an entirely hypothetical risk, namely exposure to HIV.

These are highly unusual scenarios, and existing ethical oversight, even when done extremely well, is poorly equipped to deal with them. Even if He’s experiment had satisfied all the questions of the reviewing oversight body, that may have been insufficient simply because that oversight body may not be asking (or, indeed, allowed to ask) the right questions.

One risk of locating ethics primarily in research oversight is that in cases like this, the focus tends to be on whether the research was ethically compliant — that is, whether it followed the rules — not on whether it was ethically responsible. In a profoundly novel case like this, it’s worth questioning not only whether the rules were followed, but what they are, and are not, designed to protect against.

Today’s Outrage Suggests a Need to Revisit Rules

He’s experiments push into radically new territory.

His work should cause people to ask hard questions about this technology, its implications for human identity and for the integrity of foundational social relationships: parent to child, medicine to patient, state to citizen and society to its members. Under what circumstances if any might it be appropriate to tinker in the genomes of our children-to-be?

It should also cause us to ask hard questions about our “technologies” of research ethics – the machineries of evaluation that experiments must pass through. Like any test, they are necessarily incomplete. Yet functionally they are the standard, the primary repository of ethical judgment. And there is no already-settled higher standard against which we can evaluate these processes.

The difficult task of setting standards for the standards belongs to wider society. Processes of ethical oversight for genome editing research should ideally reflect society’s shared values and norms, not merely as they pertain to informed consent, but as they pertain to our sensibilities about the right ways to care for – and to bring into being – our children.

The crucial question is not what rules were broken, but what – and whose – judgments about what is right and appropriate should rule the human future. Deeming He “crazy” and a “rogue” does not answer the question of what went wrong. To answer that, we must all take a hard look at the potential limitations of current routines of ethical oversight. Are they asking the right questions – questions that those whose lives will be affected by these powerful new technologies would want researchers to ask? That is a question whose answer cannot come purely from within the hallowed halls of science but must be calibrated to the whole human community’s shared visions of the good.The Conversation

J. Benjamin Hurlbut, Associate Professor of Life Sciences, Arizona State University and Jason Scott Robert, Director of the Lincoln Center for Applied Ethics, Arizona State University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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