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The Research Group on Synthetic Biology for Biomedical Applications at Pompeu Fabra University in Barcelona, Spain, has designed a cellular device capable of computing by printing cells on paper. For the first time, they have developed a living device that could be used outside the laboratory without a specialist, and it could be produced on an industrial scale at low cost. The study is published in Nature Communications and was carried out by Sira Mogas-Díez, Eva Gonzalez-Flo and Javier Macía.

We currently have many electronic devices available to us such as computers and tablets whose computing power is highly efficient. But, despite their power, they are very limited devices for detecting biological markers, such as those that indicate the presence of a disease. For this reason, a few years ago ‘biological computers’ began to be developed—in other words, living cellular devices that can detect multiple markers and generate complex responses. In them, the researchers leverage biological receptors that allow detecting exogenous signals and, by means of synthetic biology, modify them to emit a response in accordance with the information they detect.

So far, cellular devices have been developed that must operate in the laboratory, for a limited time, under specific conditions, and must be handled by a specialist in molecular biology. Now, a team of researchers from Pompeu Fabra University has developed new technology to ‘print’ cellular devices on paper that can be used outside the laboratory.

The regeneration of damaged central nervous system (CNS) tissues is one of the biggest goals of regenerative medicine.

Most stroke victims don’t receive treatment fast enough to prevent brain damage. Scientists at The Ohio State University Wexner Medical Center, College of Engineering and College of Medicine have developed technology to “retrain” cells to help repair damaged brain tissue. It’s an advancement that may someday help patients regain speech, cognition and motor function, even when administered days after an ischemic stroke.

Engineering and medical researchers use a process created by Ohio State called tissue nanotransfection (TNT) to introduce genetic material into cells. This allows them to reprogram skin cells to become something different—in this case vascular cells—to help fix damaged brain tissue.

Continue reading “New technology ‘retrains’ cells to repair damaged brain tissue in mice after stroke” »

The development of gene therapy, in particular gene editing using the CRISPR-Cas9 method, has prompted a lively discussion around the world about how deeply you can interfere with the human genome. The creators of this method have turned to the world community, including lawyers, to undertake a public discussion of the implications that it can create (The National Academies of Sciences Engineering Medicine, 2015). The most important problem to be resolved in the future, in my opinion, will be the issue of establishing very clear legal principles of liability for damages resulting from the editing of genes in human embryos and reproductive cells. However, before this happens, it is necessary to show the possible legal problems that may arise and that will certainly appear in future legislative work in the world. Questions must be asked to which world legal experts will need to seek answers. The goal of this paper is to show the possible legal problems and ask questions related to the liability for damages resulting from the editing of genes in human embryos and reproductive cells that will be answered in the future.

Private law considerations will be based on Polish law, although it should be pointed out that the conclusions derived from them appear to be of universal nature for different legal systems. Despite the fact that legal considerations will refer to the regulation of Polish law, the subject of the analysis will also be the differences in the legal qualification of reproductive cells and embryos in other European legislations. It seems that nowhere in the world are there special regulations regarding the liability for damage related to the genetic editing of reproductive cells or embryos. Therefore, there is a need to present new challenges for classic private law institutions, such as legal abilities, torts, or liability for damages. Due to the lack of uniform European regulations and different conflicts of rights the subject of analysis will not be wrongful life and wrongful birth actions, but only claims of prenatal damage to a child.

The first major legal problem facing the international community is, of course, the question of the legal acceptability of the editing of genes of human reproductive cells and embryos (van Dijke et al., 2018). In this regard, it should be pointed out that despite the initial demand to ban such editing, over time, increasingly more scientists have pointed to the fact that it is not possible to maintain such a moratorium (Doudna and Sternberg, 2017). Jiankui’s presentation at the Second International Summit on Human Genome Editing on November 272018, showed that the introduction of a moratorium on genetic modifications of embryos in Europe, the condemnation of such research by a group of 120 of the greatest geneticists, even the Chinese regulations (Zhang and Lie, 2018) will not limit its conduct (Cyranoski and Ledford, 2018). Globalization of the medical market means that if any procedures are allowed on other continents, they will also become available to Europeans (Lunshof, 2016).

In his latest book, Walter Isaacson chronicles the discovery of CRISPR and delves into the ethics of gene editing.

Today on the Science Talk podcast, Noam Slonim speaks to Scientific American about an impressive feat of computer engineering: an AI-powered autonomous system that can engage in complex debate with humans over issues ranging from subsidizing preschool and the merit of space exploration to the pros and cons of genetic engineering.

In a new Nature paper, Slonim and colleagues show that across 80 debate topics, Project Debater’s computational argument technology has performed very decently—with a human audience being the judge of that. “However, it is still somewhat inferior on average to the results obtained by expert human debaters,” says Slonim.

Continue reading “AI Can Now Debate with Humans and Sometimes Convince Them, Too” »

Check out “How Watson Works here.”

Is it possible to live forever by using narrow AI that can perform faster and smarter than humans? Having a doctor give you the correct diagnosis and treatment plan only happens on average, 54% of the time, as the New England Journal of Medicine has pointed out. Having Watson instantly diagnose you with the correct diagnosis and treatment plan 95% of the time will become the new standard. Our crop of new personal medicine products such as continual internal diagnostics, synthetic immune systems, virtual assistants, and regenerative medicine will diagnose and stop sickness from ever occurring while constantly rebuilding and improving body and mind capabilities.

IBM has made a series of Watson computer systems so that any company can raise their industries products and services far beyond our human capability. IBM’s Watson was first featured to the public with its historic Jeopardy win over Ken Jennings and Brad Rutter the best human Jeopardy players. At the time, Watson contained 200 million pages of structured and unstructured content in a ninety server computing system with an analytical software IBM designed called DeepQA. Now, the financial markets, medicine, insurance companies, government, engineering, and customer service call centers are employing (buying) Watson is an artificial intelligence system, that can be specifically tailored to any digitized industry and quickly evolve their industries potential.

Most cancers are driven by continuous cell division, the cause of which is largely a mystery. Scientists at Vanderbilt University have discovered a genetic switch that seems to touch off that abnormal proliferation of cells—and they did it with the gene editing system CRISPR.

Using a genomewide CRISPR screen, the Vanderbilt team discovered that deleting a protein made by the gene TRAF3 causes cells to proliferate without stopping, even after they reach a certain density that would normally signal them to stop dividing. Because TRAF3 has not been linked to cancer before, the finding could offer key insights into the development of some cancers, the researchers reported in the journal eLife.

The team started with 40 million epithelial cells, using CRISPR to select cells that kept dividing uncontrollably. They were surprised to discover that a loss of TRAF3 activates signaling that in turn drives cell proliferation. TRAF3 normally activates immunity and had not been linked to uncontrolled cell growth before, they said.

As the world fights the SARS-CoV-2 virus causing the COVID-19 pandemic, another group of dangerous pathogens looms in the background. The threat of antibiotic-resistant bacteria has been growing for years and appears to be getting worse. If COVID-19 taught us one thing, it’s that governments should be prepared for more global public health crises, and that includes finding new ways to combat rogue bacteria that are becoming resistant to commonly used drugs.

In contrast to the current pandemic, viruses may be be the heroes of the next epidemic rather than the villains. Scientists have shown that viruses could be great weapons against bacteria that are resistant to antibiotics.

I am a biotechnology and policy expert focused on understanding how personal genetic and biological information can improve human health. Every person interacts intimately with a unique assortment of viruses and bacteria, and by deciphering these complex relationships we can better treat infectious diseases caused by antibiotic-resistant bacteria.

In the new study, researchers instead aimed to reduce the amount of Nav1.7 that cells make in the first place. Bioengineer Ana Moreno and her colleagues at the University of California, San Diego, modified the “molecular scissors” of the gene editor CRISPR. Changes to the cutting enzyme Cas9 caused it to bind to DNA that makes Nav1.7 without slicing it, effectively preventing the Nav1.7 protein from being made. The researchers enhanced this silencing effect by hitching Cas9 to a repressor, another protein that inhibits gene expression.

The researchers tested the Cas9 approach—and a similar approach using another gene-editing protein known as a zinc finger—in mice given the chemotherapy drug paclitaxel, which can cause chronic nerve pain in cancer patients. The team measured pain by poking the animals’ paws with a thin nylon filament. Paclitaxel prompted mice to withdraw from gentler pokes, indicating that a normally nonpainful stimulus had become painful. But 1 month after an injection of the gene-silencing treatment into their spinal fluid, rodents responded much like mice that had never gotten paclitaxel, whereas untreated rodents remained hypersensitive, the team reports today in.

The approach could also prevent pain when given before paw injections of either the inflammation-causing compound carrageenan or a molecule called BzATP that increases pain sensitivity. And treated mice behaved no differently from untreated ones when their opposite paw—not inflamed by carrageenan—was exposed to a hot surface. That’s an encouraging initial sign that the injection didn’t silence Nav1.7 so completely that it creates a dangerous numbness to all pain, Moreno says. Behavioral tests so far haven’t turned up evidence of potentially concerning side effects; the injections didn’t appear to alter the animals’ movement, cognition, or anxiety levels.