1 Million Dollar Race For Cure To End Aging

The $1 Million Race For The Cure To End Aging

The $1 Million Race For The Cure To End Aging

 

The hypothesis is so absurd it seems as though it popped right off the pages of a science-fiction novel. Some scientists in Palo Alto are offering a $1 million prize to anyone who can end aging. “Based on the rapid rate of biomedical breakthroughs, we believe the question is not if we can crack the aging code, but when will it happen,” says director of the Palo Alto Longevity Prize Keith Powers.

It’s a fantastical idea: curing the one thing we will all surely die of if nothing else gets us before that. I sat down with Aubrey de Grey, the chief science officer of the SENS Research Foundation and co-author of “Ending Aging,” to discuss this very topic a few days back. According to him, ending aging comes with the promise to not just stop the hands of time, but to actually reverse the clock. We could, according to him, actually choose the age we’d like to exist at for the rest of our (unnatural?) lives. But we are far off from possibly seeing this happen in our lifetime, says de Grey. “With sufficient funding we have a 50/50 chance to getting this all working within the next 25 years, but it could also happen in the next 100,” he says.

If you ask Ray Kurzweil, life extension expert, futurist and part-time adviser to Google’s somewhat stealth Calico project, we’re actually tip-toeing upon the cusp of living forever. “We’ll get to a point about 15 years from now where we’re adding more than a year every year to your life expectancy,” he told the New York Times in early 2013. He also wrote in the book he co-authored with Terry Grossman, M.D., that “Immortality is within our grasp.” That’s a bit optimistic to de Grey (the two are good friends), but he’s not surprised this prize is coming out of Silicon Valley. “Things are changing here first. We have a high density of visionaries who like to think high.”

And he believes much of what Kurzweil says is true with the right funding. “Give me large amounts of money to get the research to happen faster,” says de Grey. He then points out that Google’s Calico funds are virtually unlimited.

Whether it’s 15, 25 or even 100 years off, we need to spur a revolution in aging research, according to Joon Yun, one of the sponsors of the prize. “The aim of the prize is to catalyze that revolution,” says Yun. His personal assistant actually came up with the initial idea. She just happens to be an acquaintance of Wendy Schmidt, wife of Google’s Eric Schmidt. But it was the passing of Yun’s 68-year-old father-in-law and some conversations with his friends that got him thinking about how to take on aging as a whole.

The Palo Alto Prize is also working with a number of angel investors, venture capital firms, corporate venture arms, institutions and private foundations within Silicon Valley to create health-related incentive prize competitions in the future. This first $1 million prize comes from Yun’s own pockets.

The initial prize will be divided into two $500,000 awards. Half a million dollars will go to the first team to demonstrate that it can restore heart rate variability (HRV) to that of a young adult. The other half of the $1 million will be awarded to the first team that can extend lifespan by 50 percent. So far 11 teams from all over the world have signed up for the challenge.

Source:  techcrunch.com

Why homosexuality occurs

Study finds epigenetics, not genetics, underlies homosexuality:

Study finds epigenetics, not genetics, underlies homosexuality

Study finds epigenetics, not genetics, underlies homosexuality

 

KNOXVILLE – Epigenetics – how gene expression is regulated by temporary switches, called epi-marks – appears to be a critical and overlooked factor contributing to the long-standing puzzle of why homosexuality occurs. According to the study, published online today in The Quarterly Review of Biology, sex-specific epi-marks, which normally do not pass between generations and are thus “erased,” can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son. From an evolutionary standpoint, homosexuality is a trait that would not be expected to develop and persist in the face of Darwinian natural selection. Homosexuality is nevertheless common for men and women in most cultures. Previous studies have shown that homosexuality runs in families, leading most researchers to presume a genetic underpinning of sexual preference. However, no major gene for homosexuality has been found despite numerous studies searching for a genetic connection. In the current study, researchers from the Working Group on Intragenomic Conflict at the National Institute for Mathematical and Biological Synthesis (NIMBioS) integrated evolutionary theory with recent advances in the molecular regulation of gene expression and androgen-dependent sexual development to produce a biological and mathematical model that delineates the role of epigenetics in homosexuality. Epi-marks constitute an extra layer of information attached to our genes’ backbones that regulates their expression. While genes hold the instructions, epi-marks direct how those instructions are carried out – when, where and how much a gene is expressed during development. Epi-marks are usually produced anew each generation, but recent evidence demonstrates that they sometimes carryover between generations and thus can contribute to similarity among relatives, resembling the effect of shared genes. Sex-specific epi-marks produced in early fetal development protect each sex from the substantial natural variation in testosterone that occurs during later fetal development. Sex-specific epi-marks stop girl fetuses from being masculinized when they experience atypically high testosterone, and vice versa for boy fetuses. Different epi-marks protect different sex-specific traits from being masculinized or feminized – some affect the genitals, others sexual identity, and yet others affect sexual partner preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons, such as sexual preference, and similarly a partial masculinization of daughters. The study solves the evolutionary riddle of homosexuality, finding that “sexually antagonistic” epi-marks, which normally protect parents from natural variation in sex hormone levels during fetal development, sometimes carryover across generations and cause homosexuality in opposite-sex offspring. The mathematical modeling demonstrates that genes coding for these epi-marks can easily spread in the population because they always increase the fitness of the parent but only rarely escape erasure and reduce fitness in offspring.”Transmission of sexually antagonistic epi-marks between generations is the most plausible evolutionary mechanism of the phenomenon of human homosexuality,” said the study’s co-author Sergey Gavrilets, NIMBioS’ associate director for scientific activities and a professor at the University of Tennessee-Knoxville.

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The paper’s other authors are William Rice, a professor at the University of California, Santa Barbara, and Urban Friberg, a professor at Uppsala University in Sweden. The National Institute for Mathematical and Biological Synthesis (NIMBioS) brings together researchers from around the world to collaborate across disciplinary boundaries to investigate solutions to basic and applied problems in the life sciences. NIMBioS is sponsored by the National Science Foundation, the U.S. Department of Homeland Security, and the U.S. Department of Agriculture with additional support from The University of Tennessee, Knoxville. Homosexuality as a consequence of epigenetically canalized sexual development.

Anti-CD47 eliminates all cancer cells

One Drug to Shrink All Tumors:

 anti-CD47 in addition to chemotherapy

anti-CD47 in addition to chemotherapy

A single drug can shrink or cure human breast, ovary, colon, bladder, brain, liver, and prostate tumors that have been transplanted into mice, researchers have found. The treatment, an antibody that blocks a “do not eat” signal normally displayed on tumor cells, coaxes the immune system to destroy the cancer cells. A decade ago, biologist Irving Weissman of the Stanford University School of Medicine in Palo Alto, California, discovered that leukemia cells produce higher levels of a protein called CD47 than do healthy cells. CD47, he and other scientists found, is also displayed on healthy blood cells; it’s a marker that blocks the immune system from destroying them as they circulate. Cancers take advantage of this flag to trick the immune system into ignoring them. In the past few years, Weissman’s lab showed that blocking CD47 with an antibody cured some cases of lymphomas and leukemias in mice by stimulating the immune system to recognize the cancer cells as invaders. Now, he and colleagues have shown that the CD47-blocking antibody may have a far wider impact than just blood cancers. “What we’ve shown is that CD47 isn’t just important on leukemias and lymphomas,” says Weissman. “It’s on every single human primary tumor that we tested.” Moreover, Weissman’s lab found that cancer cells always had higher levels of CD47 than did healthy cells. How much CD47 a tumor made could predict the survival odds of a patient. To determine whether blocking CD47 was beneficial, the scientists exposed tumor cells to macrophages, a type of immune cell, and anti-CD47 molecules in petri dishes. Without the drug, the macrophages ignored the cancerous cells. But when the CD47 was present, the macrophages engulfed and destroyed cancer cells from all tumor types. Next, the team transplanted human tumors into the feet of mice, where tumors can be easily monitored. When they treated the rodents with anti-CD47, the tumors shrank and did not spread to the rest of the body. In mice given human bladder cancer tumors, for example, 10 of 10 untreated mice had cancer that spread to their lymph nodes. Only one of 10 mice treated with anti-CD47 had a lymph node with signs of cancer. Moreover, the implanted tumor often got smaller after treatment — colon cancers transplanted into the mice shrank to less than one-third of their original size, on average. And in five mice with breast cancer tumors, anti-CD47 eliminated all signs of the cancer cells, and the animals remained cancer-free 4 months after the treatment stopped. “We showed that even after the tumor has taken hold, the antibody can either cure the tumor or slow its growth and prevent metastasis,” says Weissman. Although macrophages also attacked blood cells expressing CD47 when mice were given the antibody, the researchers found that the decrease in blood cells was short-lived; the animals turned up production of new blood cells to replace those they lost from the treatment, the team reports online today in the Proceedings of the National Academy of Sciences. Cancer researcher Tyler Jacks of the Massachusetts Institute of Technology in Cambridge says that although the new study is promising, more research is needed to see whether the results hold true in humans. “The microenvironment of a real tumor is quite a bit more complicated than the microenvironment of a transplanted tumor,” he notes, “and it’s possible that a real tumor has additional immune suppressing effects.” Another important question, Jacks says, is how CD47 antibodies would complement existing treatments. “In what ways might they work together and in what ways might they be antagonistic?” Using anti-CD47 in addition to chemotherapy, for example, could be counterproductive if the stress from chemotherapy causes normal cells to produce more CD47 than usual. Weissman’s team has received a $20 million grant from the California Institute for Regenerative Medicine to move the findings from mouse studies to human safety tests. “We have enough data already,” says Weissman, “that I can say I’m confident that this will move to phase I human trials.”

 

Antibody prevents and cure’s flu

Single antibody found to both prevent and cure flu

Single antibody found to both prevent and cure flu

Single antibody found to both prevent and cure flu

A single antibody has been found to prevent the influenza virus from taking hold of host cells, as well as cure animals that are already infected, UT San Diego reported. Researchers from the Scripps Research Institute in La Jolla, Calif., examined thousands of proteins in order to identify the antibody.  After analyzing the influenza virus in its 3-D crystalline form, the scientists discovered the antibody attacks a structure of the virus that is used to take hold of healthy cells. Study author Ian Wilson, a professor of structural biology at Scripps, said this discovery of focused binding has “never been seen before.” “It gives us some good idea about designs for vaccines and therapies,” Wilson said. The study involved collecting bone marrow from patients exposed to different strains of the influenza virus.  According to UT San Diego, bone marrow essentially acts as a storage facility for all the antibodies a person’s body has ever produced, so the study’s researchers knew the antibody they were looking for would be there. Next, the researchers created a catalogue of billions of flu antibodies, allowing them to pinpoint Co5 – an antibody able to bind to influenza A viruses.  Added to petri dishes of healthy cells and influenza A, Co5 stopped the cells from getting infected.  Mice studies echoed the same results, with Co5 preventing influenza in mice.  Also, when mice were given Co5 after having contracted the flu, all were cured. “Clearly, the holy grail is a universal flu vaccine, and this is another important step toward that,” Wilson said