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One of these resistance genes -- Xa13 -- is included in the Nature article and was discovered by White's lab in For the plant, these genes are involved in normal development.
However, once the pathogen takes control of expression, it makes the plant susceptible. They collaborated with researchers from Iowa State University to investigate a second susceptibility gene and its role in the spread of disease.
White's laboratory has been working on such rice research for 15 years, but started collaborating with the Stanford researchers earlier this year.
Although the research is important in the field of plant genetics, it has broader applications as well.
Because researchers have a better understanding of how to control pathogen food supplies, they can use this research to reduce crop diseases and subsequent losses.
The plant research may also apply the findings to humans or animals because both use similar sugar transporter genes to transfer glucose, leading to new possibilities for medicine and diabetes research.
Department of Agriculture's National Research Initiative program through the Cooperative State Research, Education and Extension Service.
Source: Frank White Kansas State University. Molecular Prosthesis Against Gout. Researchers from the ETH Zurich's Department of Biosystems Science and Engineering D-BSSE have devised a new method for preventing and permanently eradicating the cause of gout.
It involves implanting a biological network that regulates the uric acid levels autonomously. As Paracelsus once stated, the dose makes the poison.
This not only goes for chemical substances introduced to the body, but also those produced by it. The uric acid in the blood especially needs to be in the proper dosage.
If the level is too high i. However, uric acid is an important part of the human detoxification system, acting as a so-called "scavenger" of free radicals, which cause neurological disorders, brain diseases and tumors.
A team of re-searchers headed by Professor Martin Fussenegger from ETH Zurich's D-BSSE in Basle has now succeeded in building a network of genes which permanently keep the uric acid concentration in check.
The preliminary trials in mice have been encouraging. The research results will be published on Sunday in the journal Nature Biotechnology. Self-regulating network In most mammals, the enzyme urate oxydase controls the uric acid level.
As humans evolved from the apes, however, they lost this enzyme, which is why we suffer more from an elevated uric acid concentration.
Researchers from ETH Zurich set about finding a way to rectify the defect and restore the subtle control of the uric acid level.
With this in mind, they put together a biological network of genes called UREX. The individual components of UREX were "programmed" differently by the researchers: a uric acid sensor constantly gauges and controls the concentration in the blood.
If the uric acid level reaches an alarming concen-tration, the sensor relays the information to a genetic circuit. This then makes sure that the third component of the network releases the correct amount of urate oxydase into the blood and that the uric acid level is restored to a healthy balance.
The three components of the network thus communicate with each other and work independently and automatically without any external assistance.
The uric acid level can therefore be controlled permanently using UREX. Genes left untouched The gene network is integrated in a single cell.
Around two million of these cells are enclosed in a seaweed gelatine capsule measuring 0. Pores in the capsule ensure that the cell receives an optimal supply of nutrients, the uric acid level can be gauged by the sensor and the enzyme can find its way into the blood.
However, the organism does not come into contact with the network's modified genes. Even if the method were used in humans, a direct intervention in the patient's genetic make-up would not be necessary.
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Diverse of thesecompounds are modern in clinical developmentMetalloproteinasesCartilage and bone destruction in rheumatoid arthritis andosteoarthritis is considered to be mediated before overproduction ofmetalloproteinases MMPs.
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