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The counterfeiter's trap of the XNUMXst century

16.12.2004

American scientists have come up with a method by which you can identify which printer printed a counterfeit bill, passport or any other document.

Previously, when computers had not yet appeared, and typewriters were in use, detectives could easily find out which typewriter a particular document was printed on and get on the trail of a criminal. The fact is that the letters on the hammers of each typewriter were erased differently and an "individual handwriting" arose.

The advent of laser and inkjet printers, it would seem, forever buried this method of searching for intruders. In fact, what kind of individual handwriting can a powder that pours onto a sheet of paper have? It turns out it can.

This conclusion was made by scientists from Purdue University, led by Professor Edward Delp, who were involved in correcting the print quality on laser printers: the stripes that inevitably occur during printing are individual for each printer and the cartridge inserted into it.

“In order to know the signature of a printer and not a cartridge, you need to slightly change the subtle details of its operation, such as variations in the intensity of the laser beam or the duration of its pulse,” says Professor George Chiu. “We have been working for a long time on how to remove banding when printing images, and we know how to add artificial stripes that are invisible to the human eye, but visible to the equipment of special services."

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Risk genes told about the work of the immune system 13.08.2016

Scientists from the UK have studied how the genes responsible for the risk of contracting a disease work, and have discovered a new mechanism that triggers the processing of energy in our immune cells, activating the fight against infection.

Scientists have identified hundreds of single nucleotide polymorphisms - gene variations that increase or decrease the risk of developing various diseases - from cancer and diabetes to tuberculosis and mental disorders. However, for most of these genes, it is not known how their variants affect the disease. One such gene, C13orf31, is found on chromosome 13. Previously, scientists led by Professor Arthur Kaser of the Cambridge University Department of Medicine showed that a single nucleotide polymorphism in the C13orf31 gene is associated with a risk of contracting the leprosy bacterium and getting chronic inflammatory Crohn's disease and a form of juvenile rheumatoid arthritis.

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To edit the genes, the scientists used the CRISPR/Cas9 method, which acts like a biological copy-paste. They edited a single nucleotide in the C13orf31 gene in the mouse genome and showed that even small changes in genetic structures have a big effect: as a result, mice become more susceptible to sepsis. It was found that FAMIN affects the ability of cells to function normally by controlling the ability to kill bacteria and release mediator molecules that trigger an inflammatory response - a key tool in fighting infection and repairing damage to the body.

Thus, by studying the disease risk gene down to the level of a single nucleotide, scientists have discovered a completely new and important mechanism that affects the ability of the immune system to protect the body.

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