First Ever 3D Printed Thyroid Gland Announced by Russia’s 3D Bioprinting Solutions

March 29, 2015


The advancements seen within the field of 3D bioprinting are simply staggering. With numerous companies spending millions of dollars on advancing such technologies, we are in the early stages of what may be one of the most important medical revolutions of our time. With 3D printed human organs promising to one day eliminate the lengthy organ transplant waiting lists, perhaps saving hundreds of thousands of lives each year, these advances can not come soon enough.

Back in November we covered a story about a Skolkovo, Russia-based company called 3D Bioprinting Solutions. At the time, the company, which is headed up by Vladimir Mironov, made headlines, promising to have a 3D printed thyroid gland of a mouse by March of this year.

Here we are at the end of March, and the company has seemingly come through, holding a major press conference in Russia yesterday to announce their achievement. On March 12 the first ever thyroid gland for an animal — a mouse — was printed using the company’s patented bioprinting process. The goal here was to print a thyroid gland which could then be transplanted into a living mouse in order to further evaluate its capabilities.

The transplantation is expected to take place very soon, with researchers choosing to implant the organ into a mouse suffering from hypothyroidism, a condition which is caused by an excess of iodine in the body. Once implanted, they will evaluate the condition of the mouse and release the results of the study to the general public at the Second International Congress on Bioprinting in Singapore on July 9-10.

Researchers working for 3D Bioprinting Solutions chose the thyroid because of its simplicity. With that said, thyroid cancer is the 16th most commonly diagnosed form of cancer on the planet, with close to 300,000 new diagnoses in 2012 alone. Additionally, millions more suffer from other thyroid disorders, meaning that the ability to print a thyroid gland on demand could have major positive implications for an extraordinary number of individuals.

The printer used to construct the thyroid, works by using stem cells taken from the living orgasm via its fat cells. It then mixes these cells with a hydrogel, placing them down via an extruder, layer-by-layer. Once the cells take shape, the hydrogel dissolves, leaving the organ. The rejection of the organ should be minimal according to Mironov because it is created from the organism’s own stem cells. In essence, their body indirectly created the organ with the help of the 3D printer.


3D Bioprinting Solutions eventually wants to also 3D print other organs, especially the kidney. In fact, they claim that they are on pace to do so by 2018.

It will be interesting to see the results of the first animal trials in July, as well as if the company can remain on track to print out an actual kidney by 2018. Let’s hear your thoughts on this research in the 3D Printed Thyroid forum thread on  Check out the video below (in Russian) describing the process used to 3D print this thyroid gland.




Scientists Call for a Summit on Gene-Edited Babies

March 26, 2015

A group of senior American scientists and ethics experts is calling for debate on the gene-engineering of humans, warning that technology able to change the DNA of future generations is now “imminent.”

In policy recommendations published today in the journal Science, eighteen researchers, including two Nobel Prize winners, say scientists should accept a self-imposed moratorium on any attempt to create genetically altered children until the safety and medical reasons for such a step can be better understood.

The concern is over a rapidly advancing gene-editing technology, called CRISPR-Cas9, which is giving scientists the ability to easily alter the genome of living cells and animals (see “Genome Surgery”). The same technology could let scientists correct DNA letters in a human embryo or egg cell, for instance to create children free of certain disease-causing genes, or perhaps with improved genetics.

“What we are trying to do is to alert people to the fact that this is now easy,” says David Baltimore, a Nobel Prize winner and former president of Caltech, and an author of the letter. “We can’t use the cover we did previously, which is that it was so difficult that no one was going to do it.”

Many countries already ban “germ line” engineering—or changing genes in a way that would be heritable from one generation to the next—on ethical or safety grounds. Others, like the U.S., have strict regulations that would delay the creation of gene-edited children for years, if not decades. But some countries have weak rules, or none at all, and Baltimore said a reason scientists were speaking publicly now was to “keep people from doing anything crazy.”

The advent of CRISPR is raising social questions of a kind not confronted since the 1970s, when the ability to change DNA in microӧrganisms was first developed. In a now famous meeting in 1975, in Asilomar, California, researchers agreed to avoid certain kinds of experiments that were then deemed dangerous. Baltimore, who was one of the organizers of the Asilomar meeting, says the scientists behind the letter want to offer similar guidance for gene-engineered babies.

The prospect of genetically modified humans is surprisingly close at hand. A year ago, Chinese researchers created monkeys whose DNA was edited using CRISPR (see “10 Breakthrough Technologies 2014: Genome Editing”).

Since then, several teams of researchers in China, the U.S., and the U.K. have begun using CRISPR to change the DNA of human embryos, eggs, and sperm cells, with an eye toward applying the technology at in vitro fertility (IVF) clinics. That laboratory research was described by MIT Technology Review earlier this month (see “Engineering the Perfect Baby”).

Last week, in Nature, representatives of an industry group, the Alliance for Regenerative Medicine, recommended a wider moratorium that would also include a cessation of such laboratory studies, which it termed “dangerous and ethically unacceptable” (see “Industry Body Calls for Gene-Editing Moratorium”).

But that position was rejected by the authors of the current Science editorial. Instead, they said basic research on germ line engineering should move forward, including efforts to determine “what clinical applications, if any, might in the future be deemed permissible.”

Today’s statement was organized by Jennifer Doudna, a University of California, Berkeley, biologist who codiscovered the CRISPR technology. She confirmed that the group supports using it to edit the DNA of early-stage human embryos if it’s for scientific research.

That recommendation could come as a bombshell to critics of germ line engineering, as well as religious groups. Some believe an ethical “bright line” should separate humanity from the kind of gene-tinkering used on plants, microbes, and animals. If so, what is the point of testing the technology in human embryos?

But some authors of the Science editorial believe basic research must be given a free hand. “Science should not be impeded in its earliest stages by concerns that improvements in, and validations of, certain parts of the technology are opening the door to eugenics,” says Paul Berg, a professor emeritus at Stanford’s medical school, who also signed the letter. Berg said he supported research aimed at “perfecting the technology in preparation for the time when society could sanction germ line modification in medicine.”

A growing industry has already sprung up around gene editing, which is being applied to lab animals and farm species, and is being contemplated as a way to treat adults with diseases like muscular dystrophy or HIV infection. Such treatments of sick individuals are known as somatic gene therapy, and were not the subject of the current editorial, or the call for a moratorium.

Theoretically, germ line editing could correct genes that lead to lethal diseases before birth. For instance, if a person had Huntington’s disease, caused by a single faulty gene, CRISPR could be used to eliminate the mutation from that person’s children.

One biotechnology company, OvaScience of Cambridge, Massachusetts, has invested more than $2 million dollars investigating whether gene-editing could be used in IVF procedures. OvaScience did not respond to a request for comment.

While correcting inherited disease genes could prove medically useful, the authors of the Science editorial said much remained unknown. “Even this seemingly straightforward scenario raises serious concerns,” they said of editing disease genes back to their healthy form. That is because scientists are unable to predict all the consequences of changing DNA letters in a person, especially if multiple genes were corrected at once.

“You would be making changes in generations to come, in ways that are very hard to predict,” says Baltimore.

In their editorial, the researchers call for high-level technical forums to discuss CRISPR, as well as convening a “globally representative” group of government agencies, ethics experts, and scientists to recommend policies. In the meantime, they say, scientists must refrain from actually producing genetically engineered babies, even though the opportunity to do so now exists.

“Scientists should avoid even attempting, in lax jurisdictions, germline genome modification for clinical applications in humans,” they write



Tiny bio-robot is a germ suited-up with graphene quantum dots

March 26, 2015

As nanotechnology makes possible a world of machines too tiny to see, researchers are finding ways to combine living organisms with nonliving machinery to solve a variety of problems.

Like other first-generation bio-robots, the new nanobot engineered at the University of Illinois at Chicago is a far cry from Robocop. It’s a robotic germ.

UIC researchers created an electromechanical device — a humidity sensor — on a bacterial spore. They call it NERD, for Nano-Electro-Robotic Device. The report is online at Scientific Reports, a Nature open access journal.

“We’ve taken a spore from a bacteria, and put graphene quantum dots on its surface — and then attached two electrodes on either side of the spore,” said Vikas Berry, UIC associate professor of chemical engineering and principal investigator on the study.

“Then we change the humidity around the spore,” he said.

When the humidity drops, the spore shrinks as water is pushed out. As it shrinks, the quantum dots come closer together, increasing their conductivity, as measured by the electrodes.

“We get a very clean response — a very sharp change the moment we change humidity,” Berry said. The response was 10 times faster, he said, than a sensor made with the most advanced human-made water-absorbing polymers.

There was also better sensitivity in extreme low-pressure, low-humidity situations. “We can go all the way down to a vacuum and see a response,” said Berry, which is important in applications where humidity must be kept low, for example, to prevent corrosion or food spoilage. “It’s also important in space applications, where any change in humidity could signal a leak,” he said.

Currently available sensors increase in sensitivity as humidity rises, Berry said. NERD’s sensitivity is actually higher at low humidity.

“This is a fascinating device,” Berry said. “Here we have a biological entity. We’ve made the sensor on the surface of these spores, with the spore a very active complement to this device. The biological complement is actually working towards responding to stimuli and providing information.”

T. S. Sreeprasad and Phong Nguyen of UIC were lead co-authors on the study. Sreeprasad, a postdoctoral fellow, is now at Rice University in Houston. Ahmed Alshogeathri, Luke Hibbeler, Fabian Martinez and Nolan McNeiland, undergraduate students from Kansas State University, were also co-authors on the paper.

The study was supported by the Terry C. Johnson Center for Basic Cancer Research and partial support from the National Science Foundation (CMMI-1054877, CMMI-0939523 and CMMI-1030963) and the Office of Naval Research (N000141110767).

Story Source:

The above story is based on materials provided by University of Illinois at Chicago. The original article was written by Jeanne Galatzer-Levy. Note: Materials may be edited for content and length.

Journal Reference:

  1. T. S. Sreeprasad, Phong Nguyen, Ahmed Alshogeathri, Luke Hibbeler, Fabian Martinez, Nolan McNeil, Vikas Berry. Graphene Quantum Dots Interfaced with Single Bacterial Spore for Bio-Electromechanical Devices: A Graphene Cytobot. Scientific Reports, 2015; 5: 9138 DOI: 10.1038/srep09138

How to create 3D mini lungs

March 26, 2015

Scientists have coaxed stem cells to grow the first three-dimensional human mini lungs, or organoids, to help scientists learn more about lung diseases and test new drugs.

Previous research has focused on deriving lung tissue from flat (2D) cell systems or growing cells onto scaffolds made from donated organs.

“These mini lungs can mimic the responses of real tissues and will be a good model to study how organs form, change with disease, and how they might respond to new drugs,” says senior study author Jason R. Spence, Ph.D., assistant professor of internal medicine and cell and developmental biology at the University of Michigan Medical School.

In an open-access study published in the online journal eLife, the scientists decscribe how they succeeded in growing structures resembling both the large airways known as bronchi and small lung sacs called alveoli.

Since the mini lung structures were developed in a dish, they lack several components of the human lung, including blood vessels, which are a critical component of gas exchange during breathing. But the organoids may still serve as a discovery tool for researchers as they turn basic science ideas into clinical innovations. The idea is to use the 3D structures as a next step up from (or complement to) animal research.

Cell behavior has traditionally been studied in the lab in 2D situations where cells are grown in thin layers on cell-culture dishes.  But most cells in the body exist in a three-dimensional environment as part of complex tissues and organs. The advantage of growing 3-D structures of lung tissue, Spence says, is that their organization bears greater similarity to the human lung.

How to make a human lung organoid in a dish

To make these lung organoids, researchers at the U-M’s Spence Lab and colleagues from  the University of California, San Francisco; Cincinnati Children’s Hospital Medical Center;  Seattle Children’s Hospital, and University of Washington manipulated several of the signaling pathways that control the formation of organs:

  1. Stem cells were instructed to form a type of tissue called endoderm, found in early embryos and that gives rise to the lung, liver and several other internal organs.
  2. Scientists activated important development pathways that are known to make endoderm form three-dimensional tissue while inhibiting two other key development pathways at the same time.
  3. The endoderm became tissue that resembles the early lung found in embryos.
  4. This early lung-like tissue spontaneously formed three-dimensional spherical structures as it developed.
  5. To make these structures expand and develop into lung tissue, the team exposed the cells to additional proteins that are involved in lung development.
  6. The resulting lung organoids survived in the lab for more than 100 days.

“We expected different cells types to form, but their organization into structures resembling human airways was a very exciting result,” says lead study author Briana Dye, a graduate student in the U-M Department of Cell and Developmental Biology.

The research is supported by the National Heart, Lung and Blood Institute (NHLBI), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the March of Dimes and the U-M’s Center for Organogenesis and Biological Sciences Scholars Program (BSSP).

Abstract of In vitro generation of human pluripotent stem cell derived lung organoids

Recent breakthroughs in 3-dimensional (3D) organoid cultures for many organ systems have led to new physiologically complex in vitro models to study human development and disease. Here, we report the step-wise differentiation of human pluripotent stem cells (hPSCs) (embryonic and induced) into lung organoids. By manipulating developmental signaling pathways hPSCs generate ventral-anterior foregut spheroids, which are then expanded into human lung organoids (HLOs). HLOs consist of epithelial and mesenchymal compartments of the lung, organized with structural features similar to the native lung. HLOs possess upper airway-like epithelium with basal cells and immature ciliated cells surrounded by smooth muscle and myofibroblasts as well as an alveolar-like domain with appropriate cell types. Using RNA-sequencing, we show that HLOs are remarkably similar to human fetal lung based on global transcriptional profiles, suggesting that HLOs are an excellent model to study human lung development, maturation and disease.

Mind cloning: Imagining the brain at the 10 micron scale with subcellular resolution MRI

March 25, 2015


The brain’s connectivity matrix, or netlist if you will, is something that neuroscientists are still scratching their heads about. Some of them have already put their money where their mouth is and embarked on massive ‘connectome’ projects. The goal of these is to reconstruct a 3D model of the brain from impossibly thin slices, either pealed off or etched away with gallium ion beams, and then scanned with fancy multi-beam electron microscopes. A better way, if it can be done, is keep the brain intact and somehow scan it whole.

Researchers at the University of Florida have recently found a way to extend the resolution of noninvasive MRI down to the 10um range. This flies in the face of the unwritten Moore’s law of MRI, which throws up hard physical limits to what the technology is capable of. As the researchers have found, the first thing you have to do is change the name of your technique. Anything above a 100um^3 voxel resolution can still be called MRI. However, below that level, what you want to do is use the newer term MRM, which stands magnetic resonance microscopy.

As the researchers report in the journal Scientific Reports, the key is not just to use a super-strong magnet, but to also have equally strong and fast-switching gradients (the coils that provide for a graded field to superimpose location information) and the most sensitive RF detector coils possible.


RF coils can take any number of forms, but the design used here is a simple flat surface coil. Generally speaking, the depth of the image possible with surface coil maxes out at about one radius. The good news is that the sensitivity of the coil is inversely proportional to its size. Therefore, to image small brains, or parts of brain, small coils are better. The trick for would-be connectomists will be to get these coils right up next to where you want them, presumably either in the ventricles or the vasculature of the brain.

To demonstrate proof of principle, the researchers imaged a small fly brain scarcely half a micron wide. It may be tiny, but with over 10^5 neurons and 10^7 synapses this brain is certainly no slouch. Rather then sticking the head inside a complex solenoid or birdcage RF coil, as we would need to do in the hospital, the researchers were able to simply stick the fly brain right on top of the flat coil, essentially turning the scan geometry inside-out.

By combining several different ways to energize and read out the various coils, the researchers were able to create images on the scale of individual neurites. Instead of adding special contrast agents, or recording the so-called BOLD (Blood Oxygenation Level Dependent) signals sometimes used for functional mapping, the endogenous water in and around the cells was all that was needed for contrast. Normally known as diffusion MRI, this technique has been used to great effect in a more clinical setting for imaging the long axon tracts in the white matter of the brain.

The problem with diffusion MRI as it is practiced now is that the only thing you get are the big wires, bundles of wire really. You don’t get any actual connections, and you don’t get the directions. That is to say, you can’t unambiguously determine which direction the axon sends signals or to whom it connects. The beauty of a synapse-scale imaging technology is that since water is constrained in the small roundish synapses in much the same way that it is constrained in the longish axons, you can in theory fill in the fine-scale network topology from diffusion alone.

Imaging a live brain means that rather than just a one-shot picture of a static brain, you can potentially revisit it and record actual change. That’s all great for neuroscience, but what really sets the technique apart is that all the brain-uploaders, mind-cloners, and other would-be immortals no longer have to accept the illusory consolation prize of a vicarious immortality-by-proxy. In other words, you don’t have to turn your brain to mincemeat first in order to render a decent facsimile of its structure in a computer.

An important immediate benefit of this new tech is that it will better define the cellular basis of the actual MR signal itself. Right now the researchers are scanning brains for 40 hours  just to get the first indications of subcellular detail. They liken the situation to optical imaging in poor illumination, where one needs a very long exposure time to generate a visual signal. With improvements to the hardware, they hope to bring this time down to the point where it becomes more practical to image living, breathing brains in the lab.



Neuroscientists pinpoint cell type in the brain that controls body clock

March 25, 2015


UT Southwestern Medical Center neuroscientists have identified key cells in the brain that control 24-hour circadian rhythms (sleep and wake cycles) as well as functions such as hormone production, metabolism, and blood pressure.

The discovery may lead to future treatments for jet lag and other sleep disorders and even for neurological problems such as Alzheimer’s disease, as well as metabolism issues and psychiatric disorders such as depression.

It’s been known since 2001 that circadian rhythms are generated within a specific area of the brain called the suprachiasmatic nucleus (SCN), a tiny region located in the hypothalamus. But that region contains about 20,000 neurons that secrete more than 100 identified neurotransmitters, neuropeptides, cytokines, and growth factors, so researchers have not been able to pinpoint which neurons control circadian rhythms.

Neuromedin S: master controller of circadian rhythms

Now UT Southwestern neuroscientists report in the journal Neuron that they have found “a group of SCN neurons that express a neuropeptide called neuromedin S (NMS) is both necessary and sufficient for the control of circadian rhythms,” according to Dr. Joseph Takahashi*, Chairman of Neuroscience and Howard Hughes Medical Institute (HHMI) Investigator at UT Southwestern, who holds the Loyd B. Sands Distinguished Chair in Neuroscience.

NMS is a neuropeptide — a protein made of amino acids that neurons use to communicate. The researchers found in a mouse study that modulating the internal clock in just the NMS neurons altered the circadian period throughout the whole animal. The study also provided new insights into the mechanisms by which light synchronizes body clock rhythms.

“This study marks a significant advancement in our understanding of the body clock” said senior author Dr. Masashi Yanagisawa**, Adjunct Professor of Molecular Genetics, former HHMI Investigator at UT Southwestern, and current Director of the World Premier International Institute for Integrative Sleep Medicine at the University of Tsukuba in Japan.

The research was supported by the National Institute of Health and the Howard Hughes Medical Institute.

Overexposure to artificial light: don’t use TV, iPads and e-readers before sleeping

So what’s causing these neuropeptide changes? Scientists have found that modern life — a cycle of inadequate exposure to natural light during the day and overexposure to artificial light at night — can mess with the body’s natural sleep pattern.

The solution may be to change our lighting, says University of Connecticut Health cancer epidemiologist Richard Stevens, who has been studying the effects of artificial lighting on human health for three decades.

“It’s become clear that typical lighting is affecting our physiology,” Stevens says. “We’re learning that better lighting can reduce these physiological effects.

“By that we mean dimmer and longer wavelengths [yellow, orange, red] in the evening, and avoiding the bright blue of e-readers, tablets, and smart phones.”

Stevens and co-author Yong Zhu from Yale University explain this in an open-access paper published in the British journal Philosophical Transactions of the Royal Society B.

The paper summarizes what we know up to now on the effect of lighting on our health, Stevens says. While short-term effects can be seen in [disrupted] sleep patterns, “there’s growing evidence that the long-term implications of this have ties to obesity, diabetes, depression, breast cancer, and possibly other cancers.”

The major culprit is electronic devices, which emit enough blue light when used in the evening to suppress the sleep-inducing hormone melatonin and disrupt the body’s circadian rhythm.

(Blue light wakes us up in the morning, and reddish light, such as in a sunset, puts us to sleep.)

A recent study comparing people who used e-readers to those who read old-fashioned books in the evening showed a clear difference: those using e-readers showed delayed melatonin onset, Stevens said.

“It’s about how much light you’re getting in the evening,” Stevens says. “It doesn’t mean you have to turn all the lights off at eight o’clock every night, it just means if you have a choice between an e-reader and a book, the book is less disruptive to your body clock. At night, the better, more circadian-friendly light is dimmer and … redder, like an incandescent bulb.”

Stevens was on the scientific panel whose work led to the classification of shift work as a “probable carcinogen” by the International Agency on Cancer Research in 2007.

* Takahashi previously identified and cloned the first mammalian gene — called Clock—related to circadian rhythms. Since then, the Takahashi lab has determined that disruptions in the Clock and Bmal1 genes in mice can alter the release of insulin by the pancreas, resulting in diabetes, and they determined the 3-D structure of the CLOCK-BMAL1 protein complex, which are considered to be the batteries of the biological clock.

** Yanagisawa first identified the important role that endothelin plays on the cardiovascular system, and later, with his discovery of orexin, showed that sleep/wakefulness is controlled by a single neuropeptide. His lab has since identified numerous receptors involved in the regulation of appetite and blood pressure, as well as other neuropeptides that play an important role in the regulation of energy metabolism, stress responses, emotions, and other functions.

Abstract of Neuromedin S-Producing Neurons Act as Essential Pacemakers in the Suprachiasmatic Nucleus to Couple Clock Neurons and Dictate Circadian Rhythms

Circadian behavior in mammals is orchestrated by neurons within the suprachiasmatic nucleus (SCN), yet the neuronal population necessary for the generation of timekeeping remains unknown. We show that a subset of SCN neurons expressing the neuropeptide neuromedin S (NMS) plays an essential role in the generation of daily rhythms in behavior. We demonstrate that lengthening period within Nms neurons is sufficient to lengthen period of the SCN and behavioral circadian rhythms. Conversely, mice without a functional molecular clock within Nms neurons lack synchronous molecular oscillations and coherent behavioral daily rhythms. Interestingly, we found that mice lacking Nms and its closely related paralog, Nmu, do not lose in vivo circadian rhythms. However, blocking vesicular transmission from Nms neurons with intact cell-autonomous clocks disrupts the timing mechanisms of the SCN, revealing that Nms neurons define a subpopulation of pacemakers that control SCN network synchrony and in vivo circadian rhythms through intercellular synaptic transmission.

Abstract of Electric light, particularly at night, disrupts human circadian rhythmicity: Is that a problem?

Over the past 3 billion years, an endogenous circadian rhythmicity has developed in almost all life forms in which daily oscillations in physiology occur. This allows for anticipation of sunrise and sunset. This physiological rhythmicity is kept at precisely 24 h by the daily cycle of sunlight and dark. However, since the introduction of electric lighting, there has been inadequate light during the day inside buildings for a robust resetting of the human endogenous circadian rhythmicity, and too much light at night for a true dark to be detected; this results in circadian disruption and alters sleep/wake cycle, core body temperature, hormone regulation and release, and patterns of gene expression throughout the body. The question is the extent to which circadian disruption compromises human health, and can account for a portion of the modern pandemics of breast and prostate cancers, obesity, diabetes and depression. As societies modernize (i.e. electrify) these conditions increase in prevalence. There are a number of promising leads on putative mechanisms, and epidemiological findings supporting an aetiologic role for electric lighting in disease causation. These include melatonin suppression, circadian gene expression, and connection of circadian rhythmicity to metabolism in part affected by haem iron intake and distribution.



Massive breakthrough: Japanese scientists find a way to transmit energy wirelessly

March 15, 2015


Japanese scientists have made a breakthrough: researchers with Mitsubishi Heavy Industries have found a way to transmit energy wirelessly, a discovery that could completely change how energy is harvested in the future.

Scientists have long salivated at the idea of capturing solar energy in space, but had no way to do it until the researchers discovered they could use microwaves to deliver 10 kilowatts across a gap of 1,640 feet with pinpoint accuracy, according to a UPI report.

A small receiver captured the energy, which powered an LED light.

It wasn’t a big gap the energy traveled over, especially when you consider just how much space is between the surface of our planet and low-Earth orbit, and the energy transmitted wasn’t a lot — but it does show that it can be done.

Today, we depend on cables to conventionally transmit electricity from one place to another, but these new test results could mean big changes down the road for how energy is transmitted in the future, the company said in a press release.

MHI researchers are calling it “radio emission technology,” and it governs how a microwave beam is transmitted an aimed. The test occurred at Kobe Shipyard & Machinery Works. The Japanese Ministry of Economy, Trade, and Industry helped fund the project.

It won’t happen overnight, but the technology could eventually allow mankind to harvest the immense amount of solar energy raining down on Earth from space. It’s also a renewable, never-ending source of energy that wouldn’t depend on the weather, unlike typical solar power harvesters here on Earth.

The International Space Station has long been able to collect solar energy from the sun, but it hasn’t been able to send that power down to Earth. This new technology could allow that to happen.

Eventually, researchers hope to set up solar-collecting panels and antennas about 22,300 miles above the Earth, according to a Discovery News report, although the report acknowledges that we may be decades from practical application of the technology.

Still, it could have major impacts — perhaps even when it comes to global warming, as it could greatly reduce mankind’s dependency on fossil fuels, which are pumping huge amounts of carbon dioxide into the atmosphere.


New class of drugs dramatically increases healthy lifespan, mouse study suggests

March 15, 2015


A research team from The Scripps Research Institute (TSRI), Mayo Clinic and other institutions has identified a new class of drugs that in animal models dramatically slows the aging process — alleviating symptoms of frailty, improving cardiac function and extending a healthy lifespan.

The new research was published March 9 online ahead of print by the journal Aging Cell.

The scientists coined the term “senolytics” for the new class of drugs.

“We view this study as a big, first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders,” said TSRI Professor Paul Robbins, PhD, who with Associate Professor Laura Niedernhofer, MD, PhD, led the research efforts for the paper at Scripps Florida. “When senolytic agents, like the combination we identified, are used clinically, the results could be transformative.”

“The prototypes of these senolytic agents have more than proven their ability to alleviate multiple characteristics associated with aging,” said Mayo Clinic Professor James Kirkland, MD, PhD, senior author of the new study. “It may eventually become feasible to delay, prevent, alleviate or even reverse multiple chronic diseases and disabilities as a group, instead of just one at a time.”

Finding the Target

Senescent cells — cells that have stopped dividing — accumulate with age and accelerate the aging process. Since the “healthspan” (time free of disease) in mice is enhanced by killing off these cells, the scientists reasoned that finding treatments that accomplish this in humans could have tremendous potential.

The scientists were faced with the question, though, of how to identify and target senescent cells without damaging other cells.

The team suspected that senescent cells’ resistance to death by stress and damage could provide a clue. Indeed, using transcript analysis, the researchers found that, like cancer cells, senescent cells have increased expression of “pro-survival networks” that help them resist apoptosis or programmed cell death. This finding provided key criteria to search for potential drug candidates.

Using these criteria, the team homed in on two available compounds — the cancer drug dasatinib (sold under the trade name Sprycel®) and quercetin, a natural compound sold as a supplement that acts as an antihistamine and anti-inflammatory.

Further testing in cell culture showed these compounds do indeed selectively induce death of senescent cells. The two compounds had different strong points. Dasatinib eliminated senescent human fat cell progenitors, while quercetin was more effective against senescent human endothelial cells and mouse bone marrow stem cells. A combination of the two was most effective overall.

Remarkable Results

Next, the team looked at how these drugs affected health and aging in mice.

“In animal models, the compounds improved cardiovascular function and exercise endurance, reduced osteoporosis and frailty, and extended healthspan,” said Niedernhofer, whose animal models of accelerated aging were used extensively in the study. “Remarkably, in some cases, these drugs did so with only a single course of treatment.”

In old mice, cardiovascular function was improved within five days of a single dose of the drugs. A single dose of a combination of the drugs led to improved exercise capacity in animals weakened by radiation therapy used for cancer. The effect lasted for at least seven months following treatment with the drugs. Periodic drug administration of mice with accelerated aging extended the healthspan in the animals, delaying age-related symptoms, spine degeneration and osteoporosis.

The authors caution that more testing is needed before use in humans. They also note both drugs in the study have possible side effects, at least with long-term treatment.

The researchers, however, remain upbeat about their findings’ potential. “Senescence is involved in a number of diseases and pathologies so there could be any number of applications for these and similar compounds,” Robbins said. “Also, we anticipate that treatment with senolytic drugs to clear damaged cells would be infrequent, reducing the chance of side effects.”

Story Source:

The above story is based on materials provided by Scripps Research Institute. Note: Materials may be edited for content and length.

Journal Reference:

  1. Yi Zhu, Tamara Tchkonia, Tamar Pirtskhalava, Adam Gower, Husheng Ding, Nino Giorgadze, Allyson K. Palmer, Yuji Ikeno, Gene Borden, Marc Lenburg, Steven P. O’Hara, Nicholas F. LaRusso, Jordan D. Miller, Carolyn M. Roos, Grace C. Verzosa, Nathan K. LeBrasseur, Jonathan D. Wren, Joshua N. Farr, Sundeep Khosla, Michael B. Stout, Sara J. McGowan, Heike Fuhrmann-Stroissnigg, Aditi U. Gurkar, Jing Zhao, Debora Colangelo, Akaitz Dorronsoro, Yuan Yuan Ling, Amira S. Barghouthy, Diana C. Navarro, Tokio Sano, Paul D. Robbins, Laura J. Niedernhofer, James L. Kirkland. The Achilles’ Heel of Senescent Cells: From Transcriptome to Senolytic Drugs. Aging Cell, 2015; DOI: 10.1111/acel.12344

How to Live Forever

March 03, 2015

Could technology help to make our minds last forever? Consider the following parable, about a very wealthy man I’ll call Nicolas Flamel.

 As he became older, Flamel became fixated on the idea that he didn’t want to die. After considering the problem for a long time, he figured that what he needed to do was move the contents of his mind into a receptacle more stable than a human head. Flamel was an engineer who made his fortune in networks, and he felt confident that what we think of as our brains—and as ourselves—was really nothing more than a combination of electrical pathways. Surely these could be copied and stored somewhere safe. The task would be daunting but not impossible: there are eighty-five billion neurons in the average brain, and mapping them seemed to be a problem not unlike mapping the Internet. Flamel liked to tell his friends, “One day, you’ll start reading e-mails from me, and wonder where I went.”

Flamel dedicated his fortune to the brain-uploading project, and over the years came to realize that he’d be able to do what he wanted—with one rather important catch. Transferring the information contained in his physical brain would require the brain’s destruction. But, at the age of eighty-eight, after testing his technology on rats, he eventually decided to go forward. He would submit to his own procedure.

Flamel remained awake for his surgery, and as he lay on the hospital table his brain was picked apart, its information transferred to a computer one neural connection at a time. At first, he felt nothing, but eventually he experienced a sense of fading, as though he were falling asleep. And then something unexpected happened. The computer said to him, distinctly, “I am awake.” But Flamel observed that he was still lying on the table. And then he understood that, whatever might happen to the computer, he was about to die.

The story of Flamel is just a parable, but uploading the brain, or achieving “whole brain emulation,” has in recent years become something of a cause célèbre among certain scientists and entrepreneurs. “It’s theoretically possible to copy the brain onto a computer, and so provide a form of life after death,” Stephen Hawking said last year. Ray Kurzweil, the author of a series of books about what he calls the Singularity, has declared that we may be uploading our brains by the twenty-thirties. Currently, the best-known effort to develop brain uploads is something called the 2045 Initiative, founded by Dmitry Itskov, a Russian billionaire. His goal is to enable “the transfer of an individual’s personality to a more advanced non-biological carrier, and extending life, including to the point of immortality.”

Assume, along with Hawking and Kurzweil, that it is plausible for the information in our heads to be digitized and stored somewhere else. And assume, as scientists now tend to do, that our minds are actually stored in  our physical brains. (Descartes, on the other hand, thought that the mind resided in the pineal gland.) As the story of Nicolas Flamel suggests, it’s still not at all clear what uploading the brain would mean. What if what’s created, even if it has a copy of your brain, just isn’t you?

Some people don’t consider that a problem. After all, if a copy thinks it is you, perhaps that would be good enough. David Chalmers, a philosopher at the Australian National University, points out that we lose consciousness every night when we go to sleep. When we regain it, we think nothing of it. “Each waking is really like a new dawn that’s a bit like the commencement of a new person,” Chalmers has said. “That’s good enough…. And if that’s so, then reconstructive uploading will also be good enough.”

Maybe that is all that matters, particularly if you think that our sense of self is illusory. Many Buddhists take something close to this position: they regard our entire sense of self as a product of mistaking memories, thoughts, or emotions for something more than fleeting sensations. If the self has no meaning, its death has less significance; if the computer thinks it’s you, then maybe it really is. The philosopher Derek Parfit captures this idea when he says that “my death will break the more direct relations between my present experiences and future experiences, but it will not break various other relations. This is all there is to the fact that there will be no one living who will be me.”

I suspect, however, that most people seeking immortality rather strongly believe that they have a self, which is why they are willing to spend so much money to keep it alive. They wouldn’t be satisfied knowing that their brains keep on living without them, like a clone. This is the self-preserving, or selfish, version of everlasting life, in which we seek to be absolutely sure that immortality preserves a sense of ourselves, operating from a particular point of view.

The fact that we cannot agree on whether our sense of self would survive copying is a reminder that our general understanding of consciousness and self-awareness is incredibly weak and limited. Scientists can’t define it, and philosophers struggle, too. Giulio Tononi, a theorist based at the University of Wisconsin, defines consciousness simply as “what fades when we fall into dreamless sleep.” In recent years, he and other scientists, like Christof Koch, now at the Allen Institute for Brain Science*, have made progress in understanding when consciousness arises, namely from massive complexity and linkages between different parts of the brain. “To be conscious,” Koch has written, “you need to be a single, integrated entity with a large repertoire of highly differentiated states.” That is pretty abstract. And it still gives us little to no sense of what it would mean to transfer ourselves to some other vessel.

With just an uploaded brain and no body, would you even be conscious in a meaningful sense? Not according to Alva Noë, the author of a book called “Out of Our Heads: Why You Are Not Your Brain.” Noë argues that our sense of self does not arise simply from having a brain. It requires having a body and living in a world. “Meaningful thought arises only for the whole animal dynamically engaged with its environment,” he writes. What we call consciousness, according to Noë, is actually “an achievement of the whole animal in its environmental context.” By this measure, serious, conscious immortality would require not just an electronic brain but a fancy robot body to go with it, one with enough nerves to be capable of sensing what’s happening around it.

Personally, I tend to wonder if our powers of duplication have distorted our thinking in this area. We are capable of making copies of things that our ancestors might have thought of as ineffable, like Bach’s cantatas or images of the moment of birth. Perhaps this ability is what has given us the idea that we can copy other things that seem ethereal—like our minds. But, of course, achieving immortality will surely be much harder than backing up your hard drive.

Perhaps a better approach for future Nicolas Flamels—or Ray Kurzweils or Dmitry Itskovs—is not copying our brains but, rather, trying to migrate the self to a new physical host. Like a hermit crab seeking a new shell, immortality may not really be about copying ourselves but about creating a process in which we slowly leave behind our current, biological homes and move somewhere more durable, a point made by Steven Novella, a clinical neurologist and an assistant professor at Yale.

How might this work? In the past two decades, scientists have gained a better understanding of neuroplasticity, or the idea that the brain is continually rewiring itself. Stroke victims, for example, sometimes recover lost functions after their brains reallocate control of certain actions from a damaged area. The idea would be to encourage the brain’s activities to slowly begin migrating to a massively interconnected electronic brain. Over time, if things went well, our intelligence and identity might be coaxed into leaving behind the old brain and taking refuge in a more durable unit (which would be attached to the robot body mentioned earlier).

But it won’t necessarily work. After all, the real Nicholas Flamel was a French bookseller in the fourteenth century who practiced alchemy and was widely believed to have discovered the elixir of life and the philosopher’s stone. He died in 1418 and was buried in Paris.

*The post initially listed Christof Koch’s previous academic affiliation.