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Category: genetics – Page 524

CellAge: Dr. Aubrey de Grey Endorsement Video

Dr. Aubrey de Grey from the SENS Research Foundation was kind enough to talk in support of CellAge and their campaign on Lifespan.io

We are developing tools to help researchers accurately target and remove dysfunctional cells in the body that have entered a state called “senescence”, and thereby assist in restoring it to youthful functionality. Please subscribe, share, and fund our campaign today! ►Campaign Link: https://www.lifespan.io/campaigns/cellage-targeting-senescen…c-biology/ ►Subscribe: https://www.youtube.com/user/LifespanIO?sub_confirmation=1

Our society has never aged more rapidly – one of the most visible symptoms of the changing demographics is the exponential increase in the incidence of age-related diseases, including cancer, cardiovascular diseases and osteoarthritis. Not only does aging have a negative effect on the quality of life among the elderly but it also causes a significant financial strain on both private and public sectors. As the proportion of older people is increasing so is health care spending. According to a WHO analysis, the annual number of new cancer cases is projected to rise to 17 million by 2020, and reach 27 million by 2030. Similar trends are clearly visible in other age-related diseases such as cardiovascular disease. Few effective treatments addressing these challenges are currently available and most of them focus on a single disease rather than adopting a more holistic approach to aging.

Recently a new approach which has the potential of significantly alleviating these problems has been validated by a number of in vivo and in vitro studies. It has been demonstrated that senescent cells (cells which have ceased to replicate due to stress or replicative capacity exhaustion) are linked to many age-related diseases. Furthermore, removing senescent cells from mice has been recently shown to drastically increase mouse healthspan (a period of life free of serious diseases).

Here at CellAge we are working hard to help translate these findings into humans!

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CellAge AMA: Targeting Senescent Cells with Synthetic Biology for Human Longevity : Futurology

The CellAge AMA is open for questions, come along and ask about biotechnology, senolytics and so on.

Welcome to the CellAge AMA with Mantas Matjusaitis, PhD student in synthetic biology and founder of CellAge. I am here to talk about our work to improve the targeting of dysfunctional “senescent” cells in the body, and thereby aid in their eventual removal. This is important because removal of these cells has been shown to be a critical component in the effort to improve healthy human lifespan.

In short, CellAge is going to develop synthetic DNA promoters which are specific to senescent cells, as the promoters that are currently used for this purpose, such as the p16 gene promoter, suffer from various issues and limitations (not comprehensively targeting all senescent cells, collateral damage in targeting some cells that are not senescent, etc.). You can find more details in our technology video here, and on our Lifespan.io information page.

Seeing as our primary mission is to expand the interface between synthetic biology and aging research, as well as drive translational research forward, we will offer the senescence reporter assay we develop to academics for free. We predict that in the very near future this assay will be also used as a quality control step in the cell therapy manufacturing process to make cell therapies safer.

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Ginkgo Bioworks – Nanobots Are Finally Here

We recently wrote an article about how we need to redefine what “nanotechnology” means in the context of looking for “nanotech” companies to invest it. When you can use synthetic biology and gene editing to change the way that bacteria function by genetically modifying them, the result are microscopic biological machines. These tiny biological machines sound a whole lot like the nanobots that we were promised which would go around doing cool things without even being visible to the human eye. Earlier this year we profiled three companies that we claimed were working on building nanobot factories that create designer organisms on demand. Let’s take a closer look at one of these companies called Ginkgo Bioworks.

ginkgo-bioworks-logo

Founded in 2008, Massachusetts based startup Ginkgo Bioworks has taken in a total of $154 million in funding so far with their latest $100 million Series C round closing in summer of this year. The Company refers to themselves as “the organism company” and their value proposition has attracted investment from a whole slew of investors who realize the potential of developing new organisms that can replace technology with biology. In their own words, Ginkgo Bioworks is doing “programming without a debugger, manufacturing without CAD, and construction without cranes” which requires a whole lot of intellectual firepower and may be why they have 5 founders:

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An anti-CRISPR for gene editing

Researchers have discovered a way to program cells to inhibit CRISPR-Cas9 activity. “Anti-CRISPR” proteins had previously been isolated from viruses that infect bacteria, but now University of Toronto and University of Massachusetts Medical School scientists report three families of proteins that turn off CRISPR systems specifically used for gene editing. The work, which appears December 15 in Cell, offers a new strategy to prevent CRISPR-Cas9 technology from making unwanted changes.

“Making CRISPR controllable allows you to have more layers of control on the system and to turn it on or off under certain conditions, such as where it works within a cell or at what point in time,” says lead author Alan Davidson, a phage biologist and bacteriologist at the University of Toronto. “The three anti-CRISPR proteins we’ve isolated seem to bind to different parts of the Cas9, and there are surely more out there.”

CRISPR inhibitors are a natural byproduct of the evolutionary arms race between viruses and bacteria. Bacteria use CRISPR-Cas complexes to target and cut up genetic material from invading viruses. In response, viruses have developed proteins that, upon infection, can quickly bind to a host bacterium’s CRISPR-Cas systems, thus nullifying their effects.

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Advanced Radioactive Threat Detection System Completes First Large-Scale Citywide Test

The following press release was written and and published by the Defense Advanced Research Projects Agency (DARPA) and originally published on their website. Click here to see the original version of this post.

On a recent sunny fall day in the nation’s capital, several hundred volunteers—each toting a backpack containing smartphone-sized radiation detectors—walked for hours around the National Mall searching for clues in a “whodunit” scavenger hunt to locate a geneticist who’d been mysteriously abducted. The geneticist and his abduction were fictitious. But the challenge this scavenger hunt was designed to address is real: The need to detect even small quantities of radioactive material that terrorists might try to bring into an urban area with the intent of detonating a “dirty bomb,” or worse. By getting volunteers to walk all day looking for clues, the DARPA-sponsored exercise provided the largest test yet of DARPA’s SIGMA program, which is developing networked sensors that can provide dynamic, real-time radiation detection over large urban areas.

A key element of SIGMA, which began in 2014, has been to develop and test low-cost, high-efficiency, radiation sensors that detect gamma and neutron radiation. The detectors, which do not themselves emit radiation, are networked via smartphones to provide city, state, and federal officials real-time awareness of potential nuclear and radiological threats such as dirty bombs, which combine conventional explosives and radioactive material to increase their disruptive potential. Following a demonstration earlier this year with the Port Authority of New York and New Jersey involving more than 100 SIGMA sensors, the 1,000-detector deployment in Washington, D.C., marked the largest number of SIGMA mobile detectors ever tested at one time and was a demonstration of the program’s ability to fuse the data provided by all those sensors to create minute-to-minute situational awareness of nuclear threats.

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Logic of Signaling

Why Synbio computing is where we ultimately want to more and more progress towards especially once the basic infrastructure is updated with technology like QC.

Cells are often likened to computers, running an operating system that receives signals, processes their input, and responds, according to programming, with cellular output. Yet untangling computer-like pathways in cells is anything but simple, say Denise Montell, professor at the University of California, Santa Barbara, and Aviv Regev, a Howard Hughes Medical Institute investigator at the Massachusetts Institute of Technology and the Broad Institute. However, both are eager to try and will outline their latest efforts at the “Logic of Signaling” symposium at the 2016 ASCB Annual Meeting.

“My lab is understanding how cells maintain and build normal tissues. We’re studying cellular behaviors that underlie normal behavior and tumor metastasis, a great unsolved question in cancer,” Montell said. Her lab recently discovered that cells can bounce back from the brink of apoptotic cell death. “This wasn’t known before so now we’re looking at how cells do it, when do they do it, under what circumstances, and what does it mean,” Montell said.

To track these near-death experiences in cells the Montell lab generated a genetically coded sensor in Drosophila. The researchers expected the mechanism to be a stress response, but they found that it was normal during development. “It makes sense retrospectively,” Montell explained, pointing to neuronal development as an example. “You produce way more neurons that you need, and the neurons compete for trophic factors. If a group of cells are competing for trophic factors, then one cell starts to die, but if it gets more trophic factor, it could bounce back.”

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A New Aging Discovery Could Allow Humans to Extend Their Lifespan

In Brief

  • By observing the transparent cells of roundworms, researchers have uncovered a link between lifespan and the natural cellular process of RNA splicing.
  • This research could lead to new breakthroughs in anti-aging treatments that would allow humans to indefinitely keep ourselves healthy, stalling death for as long as possible.

Though aging seems like one of the most natural things, an affair common to all living creatures, the process is actually poorly understood by scientists. A new study detailed in Nature aims to shed light on the phenomenon as a research team led by the Harvard T.H. Chan School of Public Health has uncovered a relationship between lifespan and RNA splicing, a core function of cells that allows a single gene to produce a variety of proteins.

The researchers already knew that mutations in RNA splicing could lead to disease, but they wanted to find out if the act of splicing itself had an impact on the aging process. To find out, they designed experimental setups using the roundworm Caenorhabditis elegans, which show visible signs of aging during their short three-week lifespan.

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