Daily non-political popular news in brief.

Scripps research study shows humans and plants share common regulatory pathway

In findings that some might find reminiscent of science fiction, scientists at the Scripps Research Institute have shown for the first time that humans and plants share a common pathogen recognition pathway as part of their innate immune systems. The data could help shed fresh light on how pathogen recognition proteins function and the role they play in certain chronic inflammatory diseases.

Read more »

Keywords: scripps, research, study, shows, humans, plants, share, regulatory, pathway, scripp, show, human, plant

« Previous | Next »

Similar news on "Scripps research study shows humans and plants share common regulatory pathway":

1. How to share a bat
   08-22-2007 · EurekAlert!
   New research shows how different species of plants evolve unique floral adaptations in order to transfer pollen on different regions of bats' bodies, thus allowing multiple plant species to share bats as pollinators. The study, titled "Character displacement among bat-pollinated flowers of the genus Burmeistera: analysis of the mechanism, process and pattern," was published in this week's journal Proceedings of the Royal Society B.
   Similar news · Read more »
   
2. Scripps research team discovers a chemical pathway that causes mice to overeat and gain weight
   02-12-2007 · EurekAlert!
   Researchers from the Scripps Research Institute who are studying how body temperature and energy metabolism are regulated have discovered a pathway that appears to play a critical role in the onset of obesity. Further study of the pathway could lead to better understanding of the physiological foundation of obesity in humans and even the discovery of new treatments for the condition.
   Similar news · Read more »
   
3. Insulin grown in plants relieves diabetes in mice; UCF study holds promise for humans
   07-30-2007 · EurekAlert!
   Professor Henry Daniell's research team genetically engineered tobacco plants with the insulin gene and then administered freeze-dried plant cells to five-week-old diabetic mice as a powder for eight weeks. By the end of the study, the diabetic mice had normal blood and urine sugar levels, and their cells were producing normal levels of insulin.
   Similar news · Read more »
   
4. Humans fostering forest-destroying disease
   08-15-2007 · EurekAlert!
   Paradoxically, the spread of Sudden Oak Death -- a potentially catastrophic tree killing disease that first invaded California in the 1990s -- is being encouraged by human landscape management practices that have increased the size and density of west coast oak forests, according to a forthcoming study. Research shows that other human activities may be involved as well.
   Similar news · Read more »
   
5. A longer-living, healthier mouse that could hold clues to human aging
   10-22-2007 · EurekAlert!
   A study by scientists at UCL shows that mice lacking the insulin receptor substrate-1 are more resistant to aging than normal mice. The research adds to a growing body of work showing the importance of insulin signaling pathways as an aging mechanism in mammals -- and potentially humans.
   Similar news · Read more »
   
6. Evolutionary biology research on plant shows significance of maternal effects
   11-15-2007 · EurekAlert!
   A University of Virginia study, published in the Nov. 16 issue of the journal Science, demonstrates that plants grown in the same setting as their maternal plant performed almost 3.5 times better than those raised in a different environment -- indicating that maternal plants give cues to their offspring that help them adapt to their environmental conditions.
   Similar news · Read more »
   
7. Advance in understanding of blood pressure gene could lead to new treatments
   02-04-2007 · EurekAlert!
   Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
   Similar news · Read more »
   
8. Radiation therapy combined with microsurgery shows promise for curing injured spinal cord
   07-24-2007 · EurekAlert!
   Research on rats with crushed spinal cords, similar to human injury, reveals that treatment soon after injury combining radiation therapy to destroy harmful cells and microsurgery to drain excess fluids significantly increases the body’s ability to repair the injured cord leading to permanent recovery from injury, according to the study published in the July 18 peer-reviewed journal PLoS ONE.
   Similar news · Read more »
   
9. Common virus may contribute to obesity in some people, new study shows
   08-20-2007 · EurekAlert!
   A common virus may cause obesity in some people, according to new evidence in a controlled laboratory study. Scientists showed that infection with human adenovirus-36, long recognized as a cause of respiratory and eye infections in humans, transforms adult stem cells obtained from fat tissue into fat cells. The study, which might lead to new treatments for obesity, will be reported in August at the American Chemical Society national meeting in Boston.
   Similar news · Read more »
   
10. Ancient retroviruses spurred evolution of gene regulatory networks in humans and other primates
    11-13-2007 · EurekAlert!
    Ancient retroviruses -- distant relatives of the human immunodeficiency virus -- helped a gene called p53 become an important "master gene regulator" in primates, according to a new study.
    Similar news · Read more »