Occassionally, one of these technologies leaks out into public awareness. The one below was funded by the CIA and is definitely not pseudoscience. Our so-called experts on “pseudoscience” will be scanned at the airport at the molecular level like anyone else by a remote device.

New Homeland Security Laser Scanner Reads People At Molecular Level

July 11, 2012 11:01 AM, CBS

File photo of an airport security checkpoint. (Photo by Natalie Behring/Getty Images)

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News, Syndicated Local,Tech

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CIA, Congress, Genia Photonics, Homeland Security, In-Q-Tel, laser-based scanner, Picosecond Programmable Laser

WASHINGTON (CBSDC) – The Department of Homeland Security will soon be using a laser at airports that can detect everything about you from over 160-feet away.

Gizmodo reports a scanner that could read people at the molecular level has been invented. This laser-based scanner – which can be used 164-feet away — could read everything from a person’s adrenaline levels, to traces of gun powder on a person’s clothes, to illegal substances — and it can all be done without a physical search. It also could be used on multiple people at a time, eliminating random searches at airports.

The laser-based scanner is expected to be used in airports as soon as 2013, Gizmodo reports.

The scanner is called the Picosecond Programmable Laser. The device works by blasting its target with lasers which vibrate molecules that are then read by the machine that determine what substances a person has been exposed to. This could be Semtex explosives to the bacon and egg sandwich they had for breakfast that morning.

The inventor of this invasive technology is Genia Photonics. Active since 2009, they hold 30 patents on laser technology designed for scanning. In 2011, they formed a partnership with In-Q-Tel, a company chartered by the CIA and Congress to build “a bridge between the Agency and a new set of technology innovators.”

Genia Photonics wouldn’t be the only ones with similar technology as George Washington University developed something similar in 2008, according to Gizmodo. The Russians also developed something akin to the Picosecond Programmable laser. The creators of that scanner claim that “it is even able to detect traces of explosives left by fingerprints.”

But what makes Genia Photonics’ version so special is that the machine is more compact compared to the other devices and can still maintain its incredible range.

Although the technology could be used by “Big Brother,” Genia Photonics states that the device could be far more beneficial being used for medical purposes to check for cancer in real time, lipids detection, and patient monitoring.

During my recent visit to Dr. Grossman’s Wellness Center, I asked him what was the most significant advance in antiaging medicine since my last visit six years ago. He said TA-65. Flipping the switch to turn on the genes that extend telomere length is the first “Bridge 2” technology to become available. See Dr. Grossman’s book, “Fantastic Voyage: Live Long Enough to Live Forever.”

Nature News 28 Nov 2010

Telomerase reverses ageing process

Protecting chromosome tips doesn’t just prevent ageing. It can reverse it.Peter Lansdorp/Visuals Unlimited/Corbis

Premature ageing can be reversed by reactivating an enzyme that protects the tips of chromosomes, a study in mice suggests.

Mice engineered to lack the enzyme, called telomerase, become prematurely decrepit. But they bounced back to health when the enzyme was replaced. The finding, published online today inNature¹, hints that some disorders characterized by early ageing could be treated by boosting telomerase activity.

It also offers the possibility that normal human ageing could be slowed by reawakening the enzyme in cells where it has stopped working, says Ronald DePinho, a cancer geneticist at the Dana-Farber Cancer Institute and Harvard Medical School in Boston, Massachusetts, who led the new study. “This has implications for thinking about telomerase as a serious anti-ageing intervention.”

Other scientists, however, point out that mice lacking telomerase are a poor stand-in for the normal ageing process. Moreover, ramping up telomerase in humans could potentially encourage the growth of tumours.

Australian research scientists have developed a strategy for fighting Dengue fever, a viral disease spread by mosquitoes that affects more than 50 million people annually and causes fever and crippling joint and muscle pain—and in some cases even death.

Dengue kills FAR more people worldwide than influenza, yet it is rarely even mentioned by Western media.

A bacterium named Wolbachiapipientis naturally infects many insect species and has the ability to interfere with its host’s reproductive ability in such a way that entire populations become infected within just a few generationsⁱ. When Wolbachia infects mosquitoes, the mosquitoes’ ability to transmit Dengue virus is almost completely blocked.

Researchers are encouraged that these bacterially infected mosquitoes are safe to humans and, once set loose, are capable of spreading on their own and overtaking the wild mosquito populations that transmit disease to humans.

In two northern Australian towns, between 10,000 and 20,000 of these infected mozzies were released (“mozzie” is Australian for mosquito), and wild mosquito infection rates neared 100 percent—meaning, mosquitoes that can infect humans were almost completely replaced by the ones that can’t.

This approach is a change from the swarms of genetically engineered mosquitoes being bred by companies like Oxitec, a British biotechnology company that has released millions of mutant mosquitoes into the fields of unsuspecting Australians.

Oxitec has found a way to genetically manipulate Aedes aegypti, the mosquito species mainly responsible for transmitting Dengue and yellow fever viruses to humans. These “frankenskeeters” represent a new and terrifying twist in potential GMO (genetically modified organisms) dangers—another product of modern science outpacing common sense when big money is thrown into the equation.

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Responding to reader requests, I recently published a summary paper on my work on carcinogenesis on this site. The paper was based in part, on my Ph.D. thesis which was published (in short form) as:

The multihit model of carcinogenesis: etiologic implications for colon cancer.
Sutherland JV, Bailar JC 3rd.
J Chronic Dis. 1984;37(6):465-80.

Noting that this paper is the basis of current understanding of cancer induction, I mentioned that recent sequencing of the genome has simply given more weight to the basic hypotheses. A recently published paper replicates my previous work. In fact the coauthor was a reviewer of my earlier paper. The National Academy of Sciences provides access to full text of the article.

Multistage carcinogenesis and the incidence of colorectal cancer
E. Georg Luebeck* and Suresh H. Moolgavkar
Proceedings of the National Academy of Sciences 99:23:15095-15100, November 12, 2002

We use general multistage models to fit the age-specific incidence of colorectal cancers in the Surveillance, Epidemiology, and End Results registry, which covers 10% of the U.S. population, while simultaneously adjusting for birth cohort and calendar year effects. The incidence of colorectal cancers in the Surveillance, Epidemiology, and End Results registry is most consistent with a model positing two rare events followed by a high-frequency event in the conversion of a normal stem cell into an initiated cell that expands clonally to give rise to an adenomatous polyp. Only one more rare event appears to be necessary for malignant transformation. The two rare events involved in initiation are interpreted to represent the homozygous loss of adenomatous polyposis coli gene function. The subsequent transition of a preinitiated stem cell into an initiated cell capable of clonal expansion via symmetric division is predicted to occur with a frequency too high for a mutational event but may reflect a positional effect in colonic crypts. Our results suggest it is not necessary to invoke genomic instability to explain colorectal cancer incidence rates in human populations. Temporal trends in the incidence of colon cancer appear to be dominated by calendar year effects. The model also predicts that interventions, such as administration of nonsteroidal anti-inflammatory drugs, designed to decrease the growth rate of adenomatous polyps, are very efficient at lowering colon cancer risk substantially, even when begun later in life. By contrast, interventions that decrease the rate of mutations at the adenomatous polyposis coli locus are much less effective in reducing the risk of colon cancer.