BlackHoleNews.net
Space, UFO and Science Digest

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…

Key Blood Protein Discovered

12.10.2007 08:21 Science - Source: ScienceDaily Headlines

Science Daily — Scientists working in the only lab at MIT doing hematology research have uncovered a protein that plays a key role in the recycling of iron from blood.

Dr. Jane-Jane Chen and post-doc Sijin Liu of the Harvard-MIT Division of Health Sciences and Technology. Their research team has identified a protein that is key in regulating iron recycling in blood, and could lead to therapeutic drugs for certain blood diseases. (Credit: Photo / Donna Coveney)

Their work, described in the October 11 Journal of Clinical Investigation, could lead to new therapies for certain inherited blood disorders such as beta-thalassemia, a condition that causes chronic anemia. The team is led by Jane-Jane Chen, a principal research scientist in the Harvard-MIT Division of Health Sciences and Technology (HST).

Two years ago Chen and colleagues showed that a protein, heme-regulated eukaryotic translational initiation factor 2 ±-subunit (eIF2-alpha) kinase, or HRI for short, keeps mice with beta-thalassemia alive. This protein minimizes an abnormal and toxic imbalance of globin chains, the protein base for the hemoglobin found in red blood cells. Hemoglobin carries oxygen to our organs and carts away carbon dioxide waste.

In the new work, the team has found that HRI also plays a key role in the body's iron recycling process. Chen observed that this process falters in mice lacking HRI. As a result, less iron was available for use in the creation of new red blood cells.

A closer look revealed that HRI influences two mechanisms in this recycling process. First, a lack of HRI reduces levels of another protein called hepcidin. Hepcidin, recently discovered to be the master regulator of the iron cycle, releases iron from stores in the body and makes it available to be processed into hemoglobin. Without hepcidin, the body retains iron, but never puts it to work.

The team also found that HRI, which is expressed predominantly in the precursors of red blood cells, is expressed in macrophages. Macrophages are cells that literally reach out and grab dying red blood cells and eat them, digesting them and releasing the iron from their hemoglobin back into the system.

A lack of HRI causes these macrophages to lose their appetite, gobbling down fewer red blood cells. Instead of being digested and recycled, the red blood cells die and end up excreted through the kidneys. The result is a net loss of iron from the body.

With this new understanding of HRI's dual role in iron recycling-that it both keeps iron in the body and puts it to work-Chen is conducting a search for small molecules that might modulate the HRI signaling pathway. In turn, these compounds could potentially help diseased precursors of red blood cells survive and boost the iron recycling process.

"Perhaps we will find a compound that could help patients with beta-thelassemia or other diseases where HRI plays a role," said Chen. Such conditions include a genetic disorder called erythropoietic protoporphyria (EPP), which causes photosensitivity and liver disease, as well as a condition called the anemia of inflammation in which the iron recycling process breaks down under the influence of stress, chronic disease, aging, or cancer.

In addition to Chen, the research team includes first author Sijin Liu, an HST postdoctoral fellow; Fudi Wang and Nancy Andrews of Harvard Medical School; Rajasekhar N.V.S. Suragani and Anping Han, both HST postdoctoral fellows, and Wanting Zhao, an HST technical assistant.

The work was funded by the National Institutes of Health and the Cooley's Anemia Foundation.

Note: This story has been adapted from material provided by Massachusetts Institute of Technology.