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Astronaut Edgar Mitchell Claims Alien Cover-up

Dr. Edgar Mitchell is a veteran of the Apollo 14 mission and he was the sixth man to walk on the Moon. Dr. Mitchell also insists that aliens have visited Earth and that governments are actively covering it up. "I happen to have been privileged enough to be in on the fact that we've been visited on this planet and the UFO phenomena is real," Dr Mitchell said. "It's been well covered up by all our governments for the last 60 years or so, but slowly it's leaked out and some of us have been privileged to have been briefed on some of it. "I've been in military and intelligence circles, who know that beneath the surface of what has been public knowledge, yes - we have been visited. Reading the papers recently, it's been happening quite a bit." Dr Mitchell, who has a Bachelor of Science degree in aeronautical engineering and a Doctor of Science degree in Aeronautics and Astronautics claimed Roswell was real and similar alien visits continue to be investigated. He told the astonished Kerrang! radio host Nick Margerrison: "This is really starting to open up. I think we're headed for real disclosure and some serious organisations are moving in that direction." NASA issued a quick denial. In a statement, a spokesman said: "NASA does not track UFOs. NASA is not involved in any sort of cover up about alien life on this planet or anywhere in the universe. "Dr Mitchell is a great American, but we do not share his opinions on this issue." If Dr. Mitchell is correct about a cover-up than this is exactly the type of denial one would expect NASA to make. You can listen to the interview with Dr. Mitchell where he discusses the UFO phenomena here. Permalink | Recent Headlines | News Feeds Read more…

Gene Defects Could Be New Cause Of Male Infertility

18.10.2007 13:44 Science - Source: ScienceDaily Headlines

Science Daily — Scientists at the University of North Carolina at Chapel Hill have identified a gene crucial to the final step of the formation of a functional sperm cell.

That final step -- called spermiogenesis -- entails the compaction of DNA into a tight ball within the head of the sperm so it can successfully penetrate an egg.

Mice engineered to lack the crucial gene, Jhdm2a, that triggers this process did not produce many mature sperm, and those they did produce had abnormally shaped heads and immotile tails.

"Defects in this gene could be the cause for some cases of male infertility," said study senior author Yi Zhang, Ph.D., Howard Hughes Medical Institute investigator and professor of biochemistry and biophysics in the UNC School of Medicine. Zhang is also a member of the UNC Lineberger Comprehensive Cancer Center.

"Because this gene has a very specific effect on the development of functional sperm, it holds great potential as a target for new infertility treatments that are unlikely to disrupt other functions within the body."

The study, published on-line in the journal Nature Oct. 17, 2007, provides evidence that Jhdm2a directly controls expression of several genes required for DNA packaging in sperm cells. For a sperm cell to mature fully, multiple molecular events have to occur, such as assembly of a sperm tail and packaging of sperm DNA.

In the sperm cell, yarn-like strands of DNA wrap around spools of protein called histones that package the DNA so it fits into the nucleus. Chemical tags such as methyl groups affixed to the histones govern how tightly the DNA can be packaged, affecting the accessibility for the gene to be switched on or off.

Previous studies have shown that when a gene is turned off, one of these histones, H3K9, carries a methyl tag. In a study published in Cell last year, Zhang's laboratory demonstrated that the enzyme Jhdm2a removes this methyl tag, allowing the gene to become switched on, or expressed.

"Although a number of histone demethylases have been identified, very little is known regarding their biological functions, particularly in the context of whole animals," said Yuki Okada, Ph.D., a postdoctoral fellow in Zhang's laboratory and lead author on the study.

The unique expression pattern of Jhdm2a suggests that this demethylase may play an important role in the late stages of sperm cell development. In this study, mice genetically engineered to lack this gene had smaller testes, a significantly lower sperm count, and were infertile.

In addition, the few sperm that were produced by these mutant mice displayed significant morphological defects, including abnormally shaped heads and immotile tails.

To assess the packaging state of the sperm DNA, the researchers used electron microscopy and a fluorescent dye called acridine orange, which fluoresces differently depending on the packaging state of a sperm. Both techniques revealed a defect in sperm DNA packaging in the mutant mice, suggesting that incomplete DNA packaging was the cause of infertility.

"There are several mouse models that exhibit the male infertility seen in human syndromes such as azoospermia (absence of sperm) or globozoospermia (sperm with round heads)," said Zhang, "However, most of the genes required for normal spermatogenesis in mice are intact in human patients, raising the possibility that we might consider the jhdm2a gene as a culprit in these human male infertility syndromes."

Zhang and his colleagues are now looking for mutations in this gene in infertility patients, and are also interested in identifying the partners or cofactors in the cell that help this gene do its job.

Study co-authors include Greg Scott, Manas K. Ray and Yuji Mishina from the National Institute of Environmental Health Sciences.

The research was funded by the Howard Hughes Medical Institute and the National Institutes of Health.

Note: This story has been adapted from material provided by University of North Carolina at Chapel Hill.