Genome pioneers “Where Are They Now?”
Fifteen years after publication of the human genome’s first draft sequence, what has become of the hundreds of researchers who worked on the project?
Genome pioneers “Where Are They Now?”
Fifteen years after publication of the human genome’s first draft sequence, what has become of the hundreds of researchers who worked on the project?
Aging, inflammation, cancer, and cellular senescence are all intimately interconnected. Deciphering the nature of each thread is a tremendous task, but must be done if preventative and geriatric medicine ever hope to advance. A one dimensional analysis simply will not suffice. Without a strong understanding of the genetic, epigenetic, intercellular, and intracellular factors at work only an incomplete picture can be formed. However, even with an incomplete picture useful therapeutics can and are being developed. One face is cancer, a number of diseases characterized by uncontrolled cell division. The other is slue of degenerative disorders stemming from deterioration in regenerative capacity.
Geroprotectors are a diverse and growing family of compounds that assist in preventing and reversing the unwanted side-effects of aging. Senolytics, a subset of this broad group, accomplish this feat by encouraging the removal of decrepit cells. A few examples include dasatinib, quercetin, and ABT263. Although more research must be done, there are a precious handful of studies accessible to anyone with the inclination to scroll to the works cited section of this article. Those within the life extension community and a few enlightened souls outside of it already know this, but it bears repeating: in the developed world all major diseases are the direct result of the aging process. Accepting this rather simple premise, and you really ought to, should stoke your enthusiasm for the first generation of anti-aging elixirs. Before diving into the details of this promising new pharmaceuticals we must ask what is cellular senescence? What causes it? What purpose does it serve?
Depending on the context in which they are operating a single gene can have positive or negative effects on an organism’s phenotype. Often the gene is exerting both desirable and undesirable influences at the same time. This is called antagonistic pleiotropy. For example, high levels of testosterone can confer several reproductive advantages in youth, but in elderly men can increase their likelihood of developing prostate cancer. Cellular senescence is a protective measure; it is a response to damage that could potentially turn a healthy cell into a malignant one. Understandably, this becomes considerably more complex when one is examining multiple genes and multiple pathways. Identifying all of the players involved is difficult enough. Conboy’s famous parabiosis experiment shows that alterations in the microenviornment, in this case identified and unidentified factors in the blood of young mice, can have be very beneficial to their elders. Conversely, there is a solid body of evidence that shows senescent cells can have a bad influence their neighbors. How can something similar be achieved in humans without having to surgically attach a senior citizen to a college freshman?
Very messed up.
WASHINGTON, Feb. 1 (UPI) — Residents of Appalachia continue to have higher rates of cancer regardless of race and location.
Appalachia is a region of the Eastern United States defined by the presence of the Appalachian Mountains. It stretches from Mississippi to New York and includes 420 counties in 13 states and roughly 25 million people.
Continue reading “Cancer rates still higher in Appalachia, but gap is narrowing” »
YOU GOT A BOT PROBLEM — use DARPA’s BOT Killer”
DARPA shared their method of eliminating “bots.
Bots are a particularly pernicious presence on Twitter. While they can be used for good, (R.I.P., original @horse_ebooks), bots often power spam, scams and, most interestingly, very volatile clusters of political and cultural discussion on Twitter. Last year, DARPA confronted the problem and, according to MIT Tech Review, a new report shows just how researchers were able to identify and shutdown the malicious programs.
Continue reading “Here’s how DARPA trained researchers to kill bots” »
The lifting body vehicle will be launched on a United Launch Alliance (ULA) Atlas V rocket and will have the ability to return—along with cargo—by landing at any available airport. SNC’s Dream Chaser is made of non-toxic materials meaning it can touch down on commercial runways and be accessed immediately.
The chance to showcase a reusable spacecraft on government funded missions bodes well for a potential pivot to commercial use. SNC is at the leading edge of private space companies that one day might cater to a more diverse base of consumers like universities, medical companies and individuals.
To learn more about Dream Chaser’s history and development, we spoke to John Roth, Vice President of Business Development for SNC’s Space Systems.
Oxford researchers suggest the law might have to reassess what it considers person and property.
The Phoenix lets paraplegic people sit, stand, and walk. It costs just $40,000. Here’s how the designers pulled it off.
In 2005, Steven Sanchez was trying to do a flip off a BMX dirt ramp when he was paralyzed from the belly button down. 11 years later, with no miracle surgery to speak of, he stands like any other tourist in line at the Vatican.
“I had this awesome robotic suit on, and nobody cared,” he says. “They just waited for me to move up like everyone else moved up.” It was a moment of incredible, touristy normalcy, provided by a bit of practice—and the Phoenix exoskeleton.
A few weeks into sixth grade, Colman Chadam had to leave school because of his DNA.
The situation, odd as it may sound, played out like this. Colman has genetic markers for cystic fibrosis, and kids with the inherited lung disease can’t be near each other because they’re vulnerable to contagious infections. Two siblings with cystic fibrosis also attended Colman’s middle school in Palo Alto, California in 2012. So Colman was out, even though he didn’t actually have the disease, according to a lawsuit that his parents filed against the school district. The allegation? Genetic discrimination.
Yes, genetic discrimination. Get used to those two words together, because they’re likely to become a lot more common. With DNA tests now cheap and readily available, the number of people getting tests has gone way up—along with the potential for discrimination based on the results. When Colman’s school tried to transfer him based on his genetic status, the lawsuit alleges, the district violated the Americans With Disabilities Act and Colman’s First Amendment right to privacy. “This is the test case,” says the Chadam’s lawyer, Stephen Jaffe.
Less than a year after scientists in China became the first to genetically modify human embryos, a research team in Britain has been given the green light to perform similar work. It’s a huge moment in biotech history—one that could eventually lead to “designer babies.”
Last September, scientists at London’s Francis Crick Institute asked the U.K’s Human Fertilisation and Embryology Authority (HEFA) for permission to perform gene editing work on human embryos. Their request has now been granted, potentially paving the way for other similar work. Human germline editing is deemed controversial because any baby born through the technique has the potential to pass those genetically modified traits down to the next generation. Advocates of the practice say it could eliminate a host of genetic diseases, while at the same time introducing the possibility of human enhancement.
“The work carried out at the Crick will be for research purposes and will look at the first seven days of a fertilized egg’s development (from a single cell to around 250 cells),” noted the lab in a statement. “The knowledge acquired from the research will be important for understanding how a healthy human embryo develops.” Geneticist Kathy Niakan will be overseeing the work.