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How To 3D Print New Organs Using Stem Cells In Space

William Wagner, the director of the McGowan Institute for Regenerative Medicine at the University of Pittsburgh, a 250-strong team focused on organ and tissue failure, is at the center of possibly one of the most exciting projects in biomedical research today: can you use 3D printers to create new organs for people in space?

The ability to create new organs using stem cells is an exciting area of research that could help save lives, ending the scourge of donor shortages. Studying the concept further in microgravity could teach the team more about how these cells act, while enabling them to build more complex organs that could inform research on Earth. Early findings also suggest that these studies could reveal more about certain diseases. This vision came a bit closer to reality this week, when Wagner’s institute announced a multi-year research alliance with the International Space Station’s United States National Laboratory to explore the area further. The institute will develop facilities on Earth while working with the lab on flight opportunities to study experiments in the orbiting lab.

There’s been a lot of neat discovery science done on the space station,” Wagner says. “Let’s see what happens when we put stem cells in space. Oh, gosh, they stay more stem-like and they divide better! Okay, well, now what?”

Slowly but surely, organ printing is developing. At a 2016 conference, CELLINK detailed a future where organ shortages were a thing of the past. A team in May 2017 succesfully implanted artificial ovaries in mice. A Rutgers University group of researchers created a 3D-printable water gel that could one day help researchers print organs.

SpaceX’s CRS-18 resupply mission, which launched July 21 carrying Nickelodeon slime, also carried a Techshot biofabrication utility designed for exploring this area further: Wagner’s team is focused on using stem cells to fabricate new organs. These cells, which can further split into specialized cells, are also being used in the nascent area of lab-grown meat. Wagner explains that both areas involve similar problems of growing cells in a certain manner and rate. But while lab-based burgers could hit plates as early as 2021, printed livers and the like are nowhere near ready. “I can tell you from my perspective, organ printing’s got a long, long, long way to go,” Wagner says. “There’s a lot of barriers. At the same time, it’s exciting. There’s a lot of hope there if we can overcome any of these barriers.”


How To Make Solar Panels More Sustainable And Cheaper

An innovative way to pattern metals has been discovered by scientists in the Department of Chemistry at the University of Warwick in UK, which could make the next generation of  solar panels more sustainable and cheaperSilver and copper are the most widely used electrical conductors in modern electronics and solar cells. However, conventional methods of patterning these metals to make the desired pattern of conducting lines are based on selectively removing metal from a film by etching using harmful chemicals or printing from costly metal inks.

Scientists from the Department of Chemistry at the University of Warwick, have developed a way of patterning these metals that is likely to prove much more sustainable and cheaper for large scale production, because there is no metal waste or use of toxic chemicals, and the fabrication method is compatible with continuous roll-to-roll processing. Dr Ross Hatton and Dr Silvia Varagnolo have discovered that silver and copper do not condense onto extremely thin films of certain highly fluorinated organic compounds when the metal is deposited by simple thermal evaporation.

Thermal evaporation is already widely used on a large scale to make the thin metal film on the inside of crisp packets, and organofluorine compounds are already common place as the basis of non-stick cooking pans. The researchers have shown that the organofluorine layer need only be 10 billionths of a metre thick to be effective, and so only tiny amounts are needed. This unconventional approach also leaves the metal surface uncontaminated, which Hatton believes will be particularly important for the next generation sensors, which often require uncontaminated patterned films of these metals as platforms onto which sensing molecules can be attached.

To help address the challenges posed by climate change, there is a need for colour tuneable, flexible and light weight solar cells that can be produced at low cost, particularly for applications where conventional rigid silicon solar cells are unsuitable such as in electric cars and semi-transparent solar cells for buildings. Solar cells based on thin films of organic, perovskite or nano-crystal semiconductors all have potential to meet this need, although they all require a low cost, flexible transparent electrode. Hatton and his team have used their method to fabricate semi-transparent organic solar cells in which the top silver electrode is patterned with millions of tiny apertures per square centimetre, which cannot be achieved by any other scalable means directly on top of an organic electronic device.

This innovation enables us to realise the dream of truly flexible, transparent electrodes matched to needs of the emerging generation of thin film solar cells, as well as having numerous other potential applications ranging from sensors to low-emissivity glass” explains Dr Hatton from the Department of Chemistry at the University of Warwick.

The work is published in the journal Materials Horizons.


Long-term memory forming mechanism discovered

Your brain has its own box of memories. If you were to hold it in your hand, brush off the dust and open it up, you’d be able to pull out Polaroid snaps of your most treasured memories. Your graduation ceremony perhaps, your wedding day, your daughter’s first words – all things you wouldn’t want to forget. But how does your brain keep these memories in their crystal-clear clarity? The strength of a memory lies in its formation and upkeep. When we create a memory, thin connections, called axons, form between nerve cells in our brain. The point at which two axons connect is called a synapse, and it is the strength of the synapse that determines if the memory is kept or allowed to fade away.

Now, a study in mice carried out by Nobel Prize-winning researchers at Columbia University has shown that a protein called CPEB3 plays an important role in the formation of memories. The team discovered how this protein is stored and used in the brain and hope it could lead to new methods of slowing memory loss in humans.

The science of how synapses form and are strengthened over time is important for deciphering any disorder in which synapses – and the memories associated with them – degrade and die, such as Alzheimer’s disease,” said Dr Luana Fioriti. CPEB3 is created by the brain’s memory centre, the Hyppocampus. Once produced, it is stored in chamber-like structures called P bodies that protect it from other parts of the cell. It then travels to the synapse between nerve cells where required and is gradually released to help create a specific memory.

The findings suggest that the more CPEB3 released at a synapse, the stronger the connection and thus, the more concrete the resulting memory is. When the protein was removed, the mice could create new memories but were unable to keep them.


Nano Glass Bottles Attack Malignant Cells

Tiny silica bottles filled with medicine and a special temperature-sensitive material could be used for drug delivery to kill malignant cells only in certain parts of the body, according to a study published recently by researchers at the Georgia Institute of Technology. The research team devised a way to create silica-based hollow spheres around 200 nanometers in size, each with one small hole in the surface that could enable the spheres to encapsulate a wide range of payloads to be released later at certain temperatures only.

In the study, which was published on June 4 in the journal Angewandte Chemie International Edition, the researchers describe packing the spheres with a mixture of fatty acids, a near-infrared dye, and an anticancer drug. The fatty acids remain solid at human body temperature but melt a few degrees above. When an infrared laser is absorbed by the dye, the fatty acids will be quickly melted to release the therapeutic drug.

This new method could allow infusion therapies to target specific parts of the body and potentially negating certain side effects because the medicine is released only where there’s an elevated temperature,” said Younan Xia, professor and Brock Family Chair in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University. “The rest of the drug remains encapsulated by the solid fatty acids inside the bottles, which are biocompatible and biodegradable.”

The researchers also showed that the size of the hole could be changed, enabling nanocapsules that release their payloads at different rates. “This approach holds great promise for medical applications that require drugs to be released in a controlled fashion and has advantages over other methods of controlled drug release,” Xia said.


New Theory To Prevent Alzheimer’s

Alzheimer’s disease, the most common cause of dementia among the elderly, is characterized by plaques and tangles in the brain, with most efforts at finding a cure focused on these abnormal structures. But a University of California, Riverside, research team has identified alternate chemistry that could account for the various pathologies associated with the diseasePlaques and tangles have so far been the focus of attention in this progressive disease that currently afflicts more than 5.5 million people in the United States. Plaques, deposits of a protein fragment called beta-amyloid, look like clumps in the spaces between neurons. Tangles, twisted fibers of tau, another protein, look like bundles of fibers that build up inside cells.

The dominant theory based on beta-amyloid buildup has been around for decades, and dozens of clinical trials based on that theory have been attempted, but all have failed,” said Ryan R. Julian, a professor of chemistry who led the research team. “In addition to plaques, lysosomal storage is observed in brains of people who have Alzheimer’s disease. Neurons — fragile cells that do not undergo cell division — are susceptible to lysosomal problems, specifically, lysosomal storage, which we report is a likely cause of Alzheimer’s disease.”

An organelle within the cell, the lysosome serves as the cell’s trashcan. Old proteins and lipids get sent to the lysosome to be broken down to their building blocks, which are then shipped back out to the cell to be built into new proteins and lipids. To maintain functionality, the synthesis of proteins is balanced by the degradation of proteins.

The lysosome, however, has a weakness: If what enters does not get broken down into little pieces, then those pieces also can’t leave the lysosome. The cell decides the lysosome is not working and “stores it, meaning the cell pushes the lysosome to the side and proceeds to make a new one. If the new lysosome also fails, the process is repeated, resulting in lysosome storage.

The brains of people who have lysosomal storage disorder, another well-studied disease, and the brains of people who have Alzheimer’s disease are similar in terms of lysosomal storage,” Julian said. “But lysosomal storage disorder symptoms show up within a few weeks after birth and are often fatal within a couple of years. Alzheimer’s disease occurs much later in life. The time frames are, therefore, very different.”

Julian’s collaborative team of researchers in the Department of Chemistry and the Division of Biomedical Sciences at UC Riverside posits that long-lived proteins, including beta-amyloid and tau, can undergo spontaneous modifications that can make them undigestible by the lysosomes. “Long-lived proteins become more problematic as we age and could account for the lysosomal storage seen in Alzheimer’s, an age-related disease,” Julian said. “If we are correct, it would open up new avenues for treatment and prevention of this disease.”

Study results appear in ACS Central Science, a journal of the American Chemical Society.


VR Gives 3D Depiction Inside Blood Vessels

UW Medicine interventional radiologist Wayne Monsky first saw virtual reality’s vivid, 3D depiction of the inside of a phantom patient’s blood vessels, his jaw dropped in childlike wonder.

A virtual-reality depiction of a catheter navigating blood vessel. With a VR headset, this would be 3D (click on the image to enjoy video)

When you put the (VR) headset on … you have a giddy laugh that you can’t control – just sheer happiness and enthusiasm. (I’m) moving up to the mesenteric artery and I can’t believe what I’m seeing,” he recalled.

The experience reminds him of “Fantastic Voyage,” the ’60s-era sci-fi film about a submarine and crew that are miniaturized and injected into a scientist’s body to repair a blood clot.

As a child, and today, I’ve been amazed at the premise that one day you can swim around inside someone’s body. And really, that’s the sensation: You’re in it,” he said. Interventional radiologists use catheters, thin flexible tubes that are inserted into arteries and veins and steered to any organ in the body, guided by X-ray visuals. With this approach, they (and cardiologists, vascular surgeons, and neuro-interventionalists) treat an array of conditions: liver tumors, narrowed and bleeding arteries, uterine fibroids, and more.

Monsky and two collaborators have pioneered VR technology that puts the operator inside 3D blood vessels. By following an anatomically correct, dynamic, 3D map of a phantom patient’s vessels, Monsky navigates the catheter through junctions and angles. The catheter‘s tip is equipped with sensors that visually represent its exact location to the VR headset. It’s a sizable leap forward from the 2D, black-and-white X-ray perspective that has guided Monsky’s catheters through vessels for most of his career.

He recently presented study findings that underscore VR’s value: In tests of a phantom patient, VR guidance got him to the destination faster – about 40 seconds faster, on average, over 18 simulations – than was the case with X-ray guidance.


Brain Tumour Treatment Is Set To Be Revolutionised By A Cheap Drug

A trio of medical experts from Manchester have made a potentially revolutionary breakthrough for the treatment of brain tumours.   Innovate Pharmaceuticals – led by Dr James Stuart, Simon Cohen and Jan Cohen – was part of the development team for a new drug, known as IP1867B. The pioneering medication could transform the future treatment of brain tumours.  The major cause of treatment failure in patients is resistance to targeted therapies and pre-clinical trials of the new drug have demonstrated its ability to sensitise tumours to the latest generation of treatments. Trials have even demonstrated a capacity for the drug to prevent tumours from acquiring resistance at all, which would dramatically improve the success of treatment for this particular cancer.


Our work on multiple disease areas in the cancer field has shown that hitting a number of targets with IP1867B allows us to not only shrink tumours but unmask them allowing other therapies to attack them, said Dr James Stuart, medical director at Eccles based Innovate Pharmaceuticals. “This action of ‘turning cold tumours hot’ alongside the reversal of acquired resistance, boosting combination efficacy and a possible lowering of side effect burden makes IP1867B a true breakthrough in cancer treatment. The next step is to take IP1867B into ‘first in human’ trial. We actively driving this next stage of development and look forward to seeing the results,” he explained.

Alongside Innovate Pharmaceuticals, trials were led by the research team at the Brain Tumour Research Centre at University of Portsmouth, working with the University of Liverpool and the University of Algarve in Portugal.  The success rate for cancer therapies has been limited due to a combination of factors, such as the tumour’s ability to hide from and develop resistance to the treatment; excessive side effects; the treatment not being clinically effective; and the lack of penetration through the blood brain barrierIP1867B was shown to be effective at targeting all of these limiting factors.  The research team worked with existing cancer treatments and combination studies with traditional chemotherapy, targeted therapies and immunotherapies are now underway.


How To Turn Breast Cancer Cells Into Fat to Stop Them From Spreading

Researchers have been able to coax human breast cancer cells to turn into fat cells in a new proof-of-concept study in mice. To achieve this feat, the team exploited a weird pathway that metastasising cancer cells have; their results are just a first step, but it’s a truly promising approach. When you cut your finger, or when a foetus grows organs, the epithelium cells begin to look less like themselves, and more ‘fluid’ – changing into a type of stem cell called a mesenchyme and then reforming into whatever cells the body needs.

This process is called epithelial-mesenchymal transition (EMT) and it’s been known for a while that cancer can use both this one and the opposite pathway called MET (mesenchymal‐to‐epithelial transition), to spread throughout the body and metastasise. The researchers took mice implanted with an aggressive form of human breast cancer, and treated them with both a diabetic drug called rosiglitazone and a cancer treatment called trametinib. Thanks to these drugs, when cancer cells used one of the above-mentioned transition pathways, instead of spreading they changed from cancer into fat cells – a process called adipogenesis.

The image  shows this process, with the cancer cells tagged with a green fluorescent protein and normal red fat cell on the left. The cancer-turned-fat cells display as brown (on the right) because the red of the fat cells combines with the green of the protein cancer cell tag.

The models used in this study have allowed the evaluation of disseminating cancer cell adipogenesis in the immediate tumour surroundings,” the team wrote in their paper, published in January 2019. “The results indicate that in a patient-relevant setting combined therapy with rosiglitazone and trametinib specifically targets cancer cells with increased plasticity and induces their adipogenesis.

Although not every cancer cell changed into a fat cell, the ones that underwent adipogenesis didn’t change back. “The breast cancer cells that underwent an EMT not only differentiated into fat cells, but also completely stopped proliferating,” said senior author Gerhard Christofori, a biochemist at the University of Basel, in Switzerland. “As far as we can tell from long-term culture experiments, the cancer cells-turned-fat cells remain fat cells and do not revert back to breast cancer cells.

So how does this work? Well, as a drug trametinib both increases the transition process of cells – such as cancer cells turning into stem cells – and then increases the conversion of those stem cells into fat cellsRosiglitazone was less important, but in combination with trametinib, it also helped the stem cells convert into fat cells. “Adipogenic differentiation therapy with a combination of rosiglitazone and [trametinib] efficiently inhibits cancer cell invasion, dissemination, and metastasis formation in various preclinical mouse models of breast cancer,” wrote the team.


I-Phone Apps Could Identify Alzheimer’s

Drugmaker Eli Lilly said early results from a study suggest that Apple Inc devices, including the iPhone, in combination with digital apps could differentiate people with mild Alzheimer’s disease dementia and those without symptoms. The study, tested in 113 participants over the age of 60, was conducted by Apple along with Eli Lilly and Evidation Health. The Apple devices were used along with the Beddit sleep monitoring device and digital apps in the study.

The researchers looked at device usage data and app history of the study participants over 12 weeks. People with symptoms tended to have slower typing than health volunteers, and received fewer text messages in total.

The participants were also asked to answer two one-question surveys daily as well as perform simple activities every two weeks, such as dragging one shape to the other and tapping a circle as fast as possible on an app. The study also aimed to differentiate people with mild cognitive impairment, the pre-dementia stage of Alzheimer’s disease.



Biologists don’t understand the link between genes and behavior, so why should economists? Many outside critics of economics complain that it’s not a science. In response, most economists have steadily improved the quality of their empirical methods. But a few economists are taking a different tack by borrowing from natural science. Neuroeconomists, for example, have put experimental subjects in MRI machines to measure how their brains behave when they’re making economic decisions, in order to search for clues to the mechanisms behind everyday behavior. Recently, a few economists have sought to use genetics to augment their understanding of economic outcomes. This has become possible thanks to the advent of cheap genome sequencing and widely available databases of human genetic information. But there are a number of reasons this line of research is likely to do more harm than good, at least until biologists better understand the ways that genes affect human development.

One major foray into the field of geno-economics came from Quamrul Ashraf of Williams College and Oded Galor of Brown University. In a 2013 paper published in the American Economic Review — arguably the most prestigious journal in economics — Ashraf and Galor argue that genetic diversity exerts a big influence on economic developmentToo much diversity, they argue, and people don’t trust each other. Too little diversity, and original ideas are hard to come by. Thus, the optional amount of diversity is a happy medium — a population homogeneous enough to cooperate, but diverse enough to have originality. Looking at genetic data, they found that Europe and East Asia tend to have a medium range of genetic diversity, with Africa on the high end and the indigenous populations of the Americas and Oceania on the low end. Since Europe and East Asia contain the most industrialized nations, Ashraf and Galor concluded that the data supported their hypothesis. Another geno-economics paper was recently published in the Journal of Public Economics — also a top journal — by economists Daniel Barth, Nicholas Papageorge and Kevin Thom. Rather than tackling the broad sweep of international development as Ashraf and Galor did, Barth et al. tried to use genetics to explain differences in individual wealth, using the Health and Retirement Study, which measures wealth and various other financial information. For each individual, they obtained a polygenic score — a number that represents statistical differences in a large set of genes — that tends to be correlated with educational attainment. Restricting their analysis only to people of European descent, Barth et al. then showed that this genetic statistic is correlated with more success in investing, even after controlling for things like income and education. They concluded that genetic endowments help some people invest more successfully, leading them to build up wealth over time.