Designer baby warning as embryos are made using TWO women and one man by Oregon scientists

  • Procedure would swap the nucleus of a  mother’s egg containing mutated genes into a donor’s
  • The donor’s normal mitochondria replaces the  mother’s defective mitochondria containing mutated DNA
  • Donor’s genes would amount to 1 per cent of the embryo’s genes and not affect the  way a child looks
  • About 1 in every 5,000 children inherits a  disease caused by defective mitochondrial genes

By Associated Press

PUBLISHED:14:31 EST, 24  October 2012| UPDATED:15:53 EST, 24 October 2012

Scientists in Oregon have created embryos  with genes from one man and two women, using a controversial technique that  could one day be used to prevent babies from inheriting certain rare incurable  diseases.

The researchers at Oregon Health &  Sciences University said they are not using the embryos to produce children, and  it is not clear when or even if this technique will be put to use.

The ability has already stirred a debate over  its risks and ethics in Britain, where scientists did similar work a few years  ago.

Exchanging DNA: Swapping an embryo's mutated genes with a donor's, seen leaving right with a white mass of DNA, researchers said the technique would prevent babies from inheriting incurable disease, a red laser used in the procedure seenExchange: Swapping an embryo’s mutated genes with a  donor’s, seen leaving right with a white mass of DNA, researchers said the  technique would prevent babies from inheriting incurable disease, a red laser  used in the procedure seen

The British experiments, reported in 2008,  led to headlines about the possibility someday of babies with three  parents.

The DNA from the second woman amounts to less  than 1 per cent of the embryo’s genes, and it isn’t the sort that makes a child  look like Mom or Dad. The procedure is simply a way of replacing some defective  genes that sabotage the normal workings of cells.

The British government is asking for public  comment on the technology before it decides whether to allow its use in the  future. One concern it cites is whether such DNA alteration could be an early  step down a slippery slope toward ‘designer babies’ – ordering up, say, a  petite, blue-eyed girl or tall, dark-haired boy.

Questions have also arisen about the safety  of the technique, not only for the baby who results from the egg, but also for  the child’s descendants.

Method: Donated embryos, some seen here being frozen for storage, could be used with mothers wanting to give birth to babies without known mutated genes carried by the motherMethod: Donated embryos, some seen here being frozen for  storage, could be used with mothers wanting to give birth to babies without  known mutated genes carried by the mother

In June, an influential British bioethics  group concluded that the technology would be ethical to use if proven safe and  effective. An expert panel in Britain said in 2011 that there was no evidence  the technology was unsafe but urged further study.

Laurie Zoloth, a bioethicist at Northwestern  University in Evanston, Ill., said in an interview that safety problems might  not show up for several generations. She said she hopes the United States will  follow Britain’s lead in having a wide-ranging discussion of the  technology.

While the kind of diseases it seeks to fight  can be terrible, ‘this might not be the best way to address it,’ Zoloth  said.

Over the past few years, scientists have  reported that such experiments produced healthy monkeys and that tests in human  eggs showed encouraging results. The Oregon scientists reported on Wednesday  that they have produced about a dozen early human embryos and found the  technique is highly effective in replacing DNA.

Worry: Some worry the procedure could allow mothers to pick and choose their children's DNA, with the procedure undertaken at Oregon Health & Science University, pictured, after started then paused in LondonWorry: Some worry the procedure could allow mothers to  pick and choose their children’s DNA, with the procedure undertaken at Oregon  Health & Science University, pictured, after started then paused in  London

The genes they want to replace aren’t the  kind most people think of, which are found in the nucleus of cells and influence  traits such as eye color and height. Rather, these genes reside outside the  nucleus in energy-producing structures called mitochondria. These genes are  passed along only by mothers, not fathers.

About 1 in every 5,000 children inherits a  disease caused by defective mitochondrial genes. The defects can cause many rare  diseases with a host of symptoms, including strokes, epilepsy, dementia,  blindness, deafness, kidney failure and heart disease.

The new technique, if approved someday for  routine use, would allow a woman to give birth to a baby who inherits her  nucleus DNA but not her mitochondrial DNA.

Here’s how it would work:

Hopes: It's believed that this research, along with other efforts, will pave the way for future clinical trials in human subjects with about 1 in every 5,000 children inheriting a disease caused by defective mitochondrial genesHopes: It’s believed that this research, along with  other efforts, will pave the way for future clinical trials in human subjects  with about 1 in every 5,000 children inheriting a disease caused by defective  mitochondrial genes

Doctors would need unfertilized eggs from the  patient and a healthy donor. They would remove the nucleus DNA from the donor  eggs and replace it with nucleus DNA from the patient’s eggs. So, they would end  up with eggs that have the prospective mother’s nucleus DNA, but the donor’s  healthy mitochondrial DNA.

In a report published online Wednesday by the  journal Nature, Shoukhrat Mitalipov and others at OHSU report transplanting  nucleus DNA into 64 unfertilized eggs from healthy donors. After fertilization,  13 eggs showed normal development and went on to form early  embryos.

The researchers also reported that four  monkeys born in 2009 from eggs that had DNA transplants remain healthy, giving  some assurance on safety.

Mitalipov said in an interview that the  researchers hope to get federal approval to test the procedure in women, but  that current restrictions on using federal money on human embryo research stand  in the way of such studies.

The research was funded by the university and  the Leducq Foundation in Paris.

Dr. Douglass Turnbull of Newcastle University  in Britain, whose team has transplanted DNA between eggs using a different  technique, called the new research ‘very important and encouraging’ in showing  that such transplants could work.

But ‘clearly, safety is an issue’ with either  technique if it is applied to humans, he said

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Young blood really is the key to youth

HUMANS are constantly searching for an elixir of youth – could it be that an infusion of young blood holds the key?

18 October 2012 by Helen Thomson, New Orleans

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This seems to be true for mice, at least. According to research presented this week at the Society for Neuroscience conference in New Orleans, Louisiana, giving young blood to old mice can reverse some of the effects of age-related cognitive decline.

Last year, Saul Villeda, then at Stanford University in California, and colleagues showed they could boost the growth of new cells in the brains of old mice by giving them a blood infusion from young mice (Nature,

“We know that blood has this huge effect on brain cells, but we didn’t know if its effects extended beyond cell regeneration,” he says.

Now the team has tested for changes in cognition by linking the circulatory systems of young and old mice. Once the blood of each conjoined mouse had fully mixed with the other, the researchers analysed their brains.

Tissue from the hippocampus of old mice given young blood showed changes in the expression of 200 to 300 genes, particularly in those involved in synaptic plasticity, which underpins learning and memory. They also found changes in some proteins involved in nerve growth.

The infusion of young blood also boosted the number and strength of neuronal connections in an area of the brain where new cells do not grow. This didn’t happen when old mice received old blood.

To find out whether these changes improved cognition, the team gave 12 old mice eight intravenous shots of blood plasma either from a young or an old mouse, over the course of one month. They used plasma rather than whole blood to exclude any effect produced by blood cells.

The mice then took part in a standard memory task to locate a hidden platform in water. The old mice that had received young blood plasma remembered where to find the platform much quicker than the mice on the old plasma.

To find out which brain area was involved in this reversal of cognitive decline, the team performed fear conditioning tests. Mice that had been given young blood were better at remembering fear associated with tasks that activated the hippocampus, suggesting that young blood has a specific effect on this area of the brain.

But the mystery remains: what exactly is it about young blood that old blood doesn’t have? “We have not identified any individual factors responsible for the rejuvenating effects of young plasma yet,” says Tony Wyss-Coray, also at Stanford. His team is now trying to identify possible candidates such as lipids and hormones.

Villeda is hopeful the results might one day translate to humans since the components of blood that change with age in mice mirror those in humans.

While “it’s plausible that similar mechanisms operate in humans,” says Joseph Quinn at Oregon Health and Science University in Portland, there is no evidence yet to support this.

OHSU research suggests America may over-vaccinate



PORTLAND, Ore. –A new study published in the New England Journal of Medicine this week by Oregon Health & Science University researchers suggests that timelines for vaccinating and revaccinating Americans against disease should possibly be reevaluated and adjusted. The study shows that in many cases, the established duration of protective immunity for many vaccines is greatly underestimated. This means that people are getting booster shots when their immunity levels most likely do not require it. The results are published in the November 8 edition of the journal


“The goal of this study was to determine how long immunity could be maintained after infection or vaccination. We expected to see long-lived immunity following a viral infection and relatively short-lived immunity after vaccination, especially since this is the reasoning for requiring booster vaccinations. Surprisingly, we found that immunity following vaccination with tetanus and diphtheria was much more long-lived than anyone realized and that antibody responses following viral infections were essentially maintained for life,” explained Mark Slifka, Ph.D. Slifka serves as an associate scientist at the Vaccine and Gene Therapy Institute with joint appointments at the Oregon National Primate Research Center and the department of molecular microbiology and immunology in the OHSU School of Medicine.


The research also reconfirmed a previous finding by Slifka and his colleagues: that the duration of immunity after smallpox vaccination is much longer than previously thought. In that earlier study published in the journal Nature Medicine in 2003, these OHSU researchers observed surprisingly long-lived antiviral antibody responses but they were unable to measure the slow rate of decline. In this current study, they demonstrate that this type of immunity is maintained with a calculated half-life of 92 years – a number that is substantially longer than the estimate of only 3 to 5 years of immunity following vaccination that was previously proposed by experts at the Centers for Disease Control and Prevention.


“Another example is the tetanus vaccine,” said Slifka. “Doctors are told that vaccination is effective for a period of 10 years – but after that, people should be revaccinated. Based on our studies and the work of others, once a person has received their primary series of vaccinations they are likely to be protected for at least three decades. Indeed, other countries such as Sweden have changed their vaccination policies and doctors are advised to offer tetanus revaccination only once every 30 years.” Importantly, this has not resulted in any increase in the number of tetanus cases in Sweden and demonstrates first-hand that switching from the 10-year to 30-year policy is safe and effective. Taking this small step in vaccination scheduling could save hundreds of millions of dollars on health care here in the US.”

* Requested Repost


Chemotherapy causes a 30 Fold Increase in WNT16B which drives more cancer and resistance (2nd Confirmation)

Public release date: 5-Aug-2012 [

Contact: Kristen Woodward 206-667-5095 Fred Hutchinson Cancer Research Center

Researchers discover new mechanism behind resistance to cancer treatment

Finding could lead to development of better therapies

SEATTLE – Developing resistance to chemotherapy is a nearly universal, ultimately lethal consequence for cancer patients with solid tumors – such as those of the breast, prostate, lung and colon – that have metastasized, or spread, throughout the body. A team of scientists led by Fred Hutchinson Cancer Research Center has discovered a key factor that drives this drug resistance – information that ultimately may be used to improve the effectiveness of therapy and buy precious time for patients with advanced cancer. They describe their findings online Aug. 5 in advance of print publication in Nature Medicine.

“Cancer cells inside the body live in a very complex environment or neighborhood. Where the tumor cell resides and who its neighbors are influence its response and resistance to therapy,” said senior author Peter S. Nelson, M.D., a member of the Hutchinson Center’s Human Biology Division.

Nelson and colleagues found that a type of normal, noncancerous cell that lives in cancer’s neighborhood – the fibroblast – when exposed to chemotherapy sustains DNA damage that drives the production of a broad spectrum of growth factors that stimulate cancer growth. Under normal circumstances, fibroblasts help maintain the structural integrity of connective tissue, and they play a critical role in wound healing and collagen production.

Specifically, the researchers found that DNA-damaging cancer treatment coaxes fibroblasts to crank out a protein called WNT16B within the tumor neighborhood, or microenvironment, and that high levels of this protein enable cancer cells to grow, invade surrounding tissue and resist chemotherapy.

The researchers observed up to 30-fold increases in WNT production – a finding that was “completely unexpected,” Nelson said. The WNT family of genes and proteins plays an important role in normal development and also in the development of some cancers but, until now, was not known to play a significant role in treatment resistance.

This discovery suggests that finding a way to block this treatment response in the tumor microenvironment may improve the effectiveness of therapy.

“Cancer therapies are increasingly evolving to be very specific, targeting key molecular engines that drive the cancer rather than more generic vulnerabilities, such as damaging DNA. Our findings indicate that the tumor microenvironment also can influence the success or failure of these more precise therapies.” In other words, the same cancer cell, when exposed to different “neighborhoods,” may have very different responses to treatment.

The major clinical reason that chemotherapy ultimately fails in the face of advanced cancer, Nelson said, is because the doses necessary to thoroughly wipe out the cancer would also be lethal to the patient. “In the laboratory we can ‘cure’ most any cancer simply by giving very high doses of toxic therapies to cancer cells in a petri dish. However, in people, these high doses would not only kill the cancer cells but also normal cells and the host.” Therefore, treatments for common solid tumors are given in smaller doses and in cycles, or intervals, to allow the normal cells to recover. This approach may not eradicate all of the tumor cells, and those that survive can evolve to become resistant to subsequent rounds of anti-cancer therapy.

For the study the team of researchers – which also involved investigators at the University of Washington, Oregon Health and Science University, the Buck Institute for Research on Aging, the Lawrence Berkeley National Laboratory – examined cancer cells from prostate, breast and ovarian cancer patients who had been treated with chemotherapy.

“This study is an example of collaborative, translational research that capitalizes on years of federally funded investments into the development of tissue banks and clinical trials in which we were able to track long-term patient outcomes. Investing in this type of infrastructure is critical but may take many years to see payoff,” said Nelson, who serves as principal investigator of the Pacific Northwest Prostate Cancer SPORE, a federally funded, multi-institution research consortium led by the Hutchinson Center.