Scientists have long seen evidence of social behavior among many species of animals, both on the earth and in the sea. Dolphins frolic together, lions live in packs, and hornets construct nests that can house a large number of the insects. And, right under our feet, it appears that nematodes -- also known as roundworms -- are having their own little gatherings in the soil. Until recently, it was unknown how the worms communicate to one another when it's time to come together. Now, however, researchers from the California Institute of Technology (Caltech) and the Boyce Thompson Institute at Cornell University have identified, for the first time, the chemical signals that promote aggregation.

"We now have an expanded view of a very fundamental type of communication, which is recognizing other members of the same species and getting together with them," says Jagan Srinivasan, a senior research fellow in biology at Caltech and lead author of the study detailing this process, which was published in the January issue of PLoS Biology.

The researchers looked at the lab-friendly Caenorhabditis elegans worm -- a relatively safe version of the phylum, whose parasitic cousins include hookworms, whipworms, and trichinas, which cause trichinosis -- to gather data.

According to Paul Sternberg, Thomas Hunt Morgan Professor of Biology at Caltech and a corresponding author on the paper, nearly 25 percent of the world's human population is infected with some type of parasitic nematode; animals and plants can fall prey to the nasty worms, too. Since nematode parasites live inside a host and attack it internally, knowing how the worms communicate via chemicals could be very important to the fields of biomedicine and agriculture.

"One of the ways to eradicate them would be to have some sort of a chemical that can attract them in order to kill them more efficiently," explains Srinivasan.

Sternberg and Srinivasan are not new to the idea of chemical signaling among C. elegans. In 2008, their research showed how the worms secrete chemicals as a sexual attractant. This time, they worked to find chemical cues that control the social behavior of aggregation. What they found is a complex "language," in which the worms combine different chemicals into compounds, building a molecular library of signals that regulate behavior. They did this by testing a previously identified family of chemicals in mutant worms -- made to not produce the chemicals on their own -- to measure the behavioral effects of the different chemical combinations.

"We're starting to get a hold on the chemical 'alphabet' that makes up these words, which have different meanings in different social contexts," says Srinivasan. "It's a modular code that tells us that within the physiology of the organism, there is a lot going on in terms of how the environment is interpreted and read out for social communication."

For example, one class of chemicals the researchers found encourages worm-to-worm company, while a different class of compounds being expressed at the same time keeps other worms away. This suggests that the worms release different amounts of each compound based on what each worm is trying to communicate. If the worm is starting a new colony, it probably just wants a certain number of worms around to find and share food -- too many and the colony may not thrive. However, if there is a big piece of fruit, the worm may call on a large group to help access the food source.

"The amazing thing here is that for one chemical, if it's modified even just a little bit, the meaning is changed," says Sternberg, who is also an investigator with the Howard Hughes Medical Institute. "That's what makes it more like a language. If I say a Chinese word, and my intonation is wrong, the word has a different meaning."

Next, the team will explore whether or not the same chemical compounds are made by other nematodes. They will also work to figure out how the worms' nervous system senses and sorts the different compounds.

"Understanding the worm's language is just a first step," says Srinivasan. "We hope that by learning more about how social recognition occurs in the worm nervous system, we can eventually provide insights into how the human brain encodes social information, too."

The above story is reprinted from materials provided by California Institute of Technology.

Wandering albatrosses have altered their foraging due to changes in wind fields in the southern hemisphere during the last decades. Since winds have increased in intensity and moved to the south, the flight speed of albatrosses increased and they spend less time foraging. As a consequence, breeding success has improved and birds have gained 1 kilogram. These are the results of the study of an international research team published in the latest issue of the Science journal. However, these positive consequences of climate change may last short if future wind fields follow predictions of climate change scenarios, researchers warn.

For this study, biologists had combined data on the duration of foraging trips and breeding success over the last 40 years, as well as foraging and body mass over the last 20 years of wandering albatross (Diomedea exulans) breeding in Crozet Islands. This archipelago lies approximately in the heart of the southern Indian Ocean (halfway between Madagascar and Antarctica). It belongs to the French Southern Territories and it is located in the windiest part of the Southern Ocean. The new findings are the result of an international research team from the French National Centre for Scientific Research (CNRS-CEBC) and the German Helmholtz-Centre for Environmental Research (UFZ).

Thanks to miniaturised tracking devices, researchers were able to track the foraging movement of albatrosses at a distance of 3500 kilometers from the colony. They found that albatross have altered their search patterns following changes in wind conditions over the past two decades. Females used increasingly more poleward and windy areas for foraging. As a consequence their travel speed increased while the total distance covered during foraging flights did not change. "This means that they spend less time at sea while incubating the egg and thus the breeding success increases" explains Dr. Henri Weimerskirch of the French National Centre for Scientific Research (CNRS-CEBC). Researchers were surprised that both females and males have increased their body mass in one kilogram, which corresponds approximately to one tenth of their total body weight. This could be not only a result of shorter incubation periods on the nest, but also an adaptation to windier conditions.

"The wandering albatross Crozet population has decreased as a result of adult mortality on longline fishing in subtropical waters, especially females since they favour warmer subtropical waters in the north compared to the more southerly distribution of males" says Dr. Maite Louzao Arsuaga, who has been modelling albatross movement from 2009 to 2011 at the UFZ. "Due to the changing wind conditions, females are now foraging in more southward areas where such fishing is not that widespread." However, the positive effects of changing environmental conditions of the last decades will not last in the future. Climate scenarios predict that westerly winds will move even further south by 2080 and wandering albatrosses might have to fly further to find optimal conditions for flying.

The total population of the wandering albatross is currently estimated at around 8,000 breeding pairs. All populations have shown a decrease at some stage over the last 25 years. This endangered species is threatened primarily by incidental catch in fisheries, especially longline fishing at sea, whereas the introduction of alien species (such as rats or cats) are a key conservation threat for the species on breeding colonies. Additionally, the accumulation of anthropogenic debris such as plastic and fishing hooks on albatrosses have negative effects on their populations. Thus, it is important to continue with monitoring programs of population trends and distribution at sea, as well as to undertake effective conservation measures. The foraging habitat of wandering albatrosses is managed by more than one Regional Fisheries Management Organisations, which makes it difficult to implement conservation measures for the species.

The wandering albatross has fascinated people for centuries. With a wingspan of over three meters and a half, it is the largest seabird in the world, surpassing just the Andean condor (Vultur fulvus). This elegant sailor, which spends most of its life flying, breeds on remote subantarctic islands over the Southern Ocean. They travel thousand of kilometers searching for fish and cephalopods like squids, often following ships and feeding on offal. The plumage of wandering albatrosses is variable, whitening with age. The maximum known age is 55 years old. Since the rearing of chicks takes a whole year, they breed only every second year

Apart from the study published in the latest Science issue, the research team has identified the key marine areas for the conservation of wandering albatrosses in the southern Indian Ocean published in 2011 in the Journal of Applied Ecology. This study provided the first map to support the future development of a network of priority protected areas in the southern part of the Indian Ocean, which are based on habitat predictions. "Because the species has no natural enemies and is at the top of the food web, it is particularly well suited as an indicator of the health of marine ecosystems," says Dr. Thorsten Wiegand from the UFZ, who supervised the work of Dr. Maite Louzao. "This could help not only a single species, but the underlying biodiversity associated with pelagic key habitats to protect Southern Ocean. Moreover, we have developed methods of habitat modelling broadly applicable and can be used to assess changes in species distribution within the current global change scenario."

The above story is reprinted from materials provided by Helmholtz Association of German Research Centres.

For the first time ever, stem cells from umbilical cords have been converted into other types of cells, which may eventually lead to new treatment options for spinal cord injuries and multiple sclerosis, among other nervous system diseases.

"This is the first time this has been done with non-embryonic stem cells," says James Hickman, a University of Central Florida bioengineer and leader of the research group, whose accomplishment is described in the Jan. 18 issue of the journal ACS Chemical Neuroscience.

"We're very excited about where this could lead because it overcomes many of the obstacles present with embryonic stem cells."

Stem cells from umbilical cords do not pose an ethical dilemma because the cells come from a source that would otherwise be discarded. Another major benefit is that umbilical cells generally have not been found to cause immune reactions, which would simplify their potential use in medical treatments.

The pharmaceutical company Geron, based in Menlo Park, Calif., developed a treatment for spinal cord repair based on embryonic stem cells, but it took the company 18 months to get approval from the FDA for human trials due in large part to the ethical and public concerns tied to human embryonic stem cell research. This and other problems recently led to the company shutting down its embryonic stem cell division, highlighting the need for other alternatives.

Sensitive Cells

The main challenge in working with stem cells is figuring out the chemical or other triggers that will convince them to convert into a desired cell type. When the new paper's lead author, Hedvika Davis, a postdoctoral researcher in Hickman's lab, set out to transform umbilical stem cells into oligodendrocytes -- critical structural cells that insulate nerves in the brain and spinal cord -- she looked for clues from past research.

Davis learned that other research groups had found components on oligodendrocytes that bind with the hormone norephinephrine, suggesting the cells normally interact with this chemical and that it might be one of the factors that stimulates their production. So, she decided this would be a good starting point.

In early tests, she found that norepinephrine, along with other stem cell growth promoters, caused the umbilical stem cells to convert, or differentiate, into oligodendrocytes. However, that conversion only went so far. The cells grew but then stopped short of reaching a level similar to what's found in the human nervous system.

Davis decided that, in addition to chemistry, the physical environment might be critical.

To more closely approximate the physical restrictions cells face in the body, Davis set up a more confined, three-dimensional environment, growing cells on top of a microscope slide, but with a glass slide above them. Only after making this change, and while still providing the norephinphrine and other chemicals, would the cells fully mature into oligodendrocytes.

"We realized that the stem cells are very sensitive to environmental conditions," Davis said.

Medical Potential

This growth of oligodendrocytes, while crucial, is only a first step to potential medical treatments. There are two main options the group hopes to pursue through further research. The first is that the cells could be injected into the body at the point of a spinal cord injury to promote repair.

Another intriguing possibility for the Hickman team's work relates to multiple sclerosis and similar conditions. "Multiple sclerosis is one of the holy grails for this kind of research," said Hickman, whose group is collaborating with Stephen Lambert at UCF's medical school, another of the paper's authors.

Oligodendrocytes produce myelin, which insulates nerve cells, making it possible for them to conduct the electrical signals that guide movement and other functions. Loss of myelin leads to multiple sclerosis and other related conditions such as diabetic neuropathy.

The injection of new, healthy oligodendrocytes might improve the condition of patients suffering from such diseases. The teams are also hoping to develop the techniques needed to grow oligodendrocytes in the lab to use as a model system both for better understanding the loss and restoration of myelin and for testing potential new treatments.

"We want to do both," Hickman said. "We want to use a model system to understand what's going on and also to look for possible therapies to repair some of the damage, and we think there is great potential in both directions."

Besides Hickman and Davis, the other authors on the paper were Xiufang Guo, Stephen Lambert, and Maria Stancescu, all from the University of Central Florida.

The above story is reprinted from materials provided by University of Central Florida.

A new UC Davis study shows how the brain reconfigures its connections to minimize distractions and take best advantage of our knowledge of situations.

"In order to behave efficiently, you want to process relevant sensory information as fast as possible, but relevance is determined by your current situation," said Joy Geng, assistant professor of psychology at the UC Davis Center for Mind and Brain.

For example, a flashing road sign alerts us to traffic merging ahead; or a startled animal might cue you to look out for a hidden predator.

When concentrating on a specific task, it's helpful to reconfigure brain networks so that task-relevant information is processed most efficiently and external distractions are reduced, Geng found.

Geng and co-author Nicholas DiQuattro, a graduate student in psychology, used functional magnetic resonance imaging to study brain activity in volunteers carrying out a simple test. They compared their results to mathematical models to infer connectivity between different areas of the brain. The study appeared in the Dec. 7 issue of the Journal of Neuroscience.

The subjects had to look for a letter "T" in a box and indicate which way it faced by pressing a button. They were also presented with a "distractor": another letter T in a box, but rotated 90 degrees.

The distractor was either similar in appearance to the target, or brightened to be more attention-getting.

Subjects did better in trials with an "attention-getting" distractor than a less obvious one, and lit up specific areas of the brain accordingly.

The new work shows that the brain doesn't always "ramp up" to deal with the situation at hand, Geng said. Instead, it changes how traffic moves through the existing hard-wired network -- rather like changing water flow through a network of pipes or information flow over a computer network -- in order to maximize efficiency.

The above story is reprinted from materials provided by University of California - Davis.

A large population-based study in Sweden indicates that there is no link between smoking during pregnancy and autism spectrum disorders (ASD) in children. The study, led by Dr. Brian Lee, an assistant professor at Drexel University and a team of international collaborators, will appear in a forthcoming issue of the Journal of Autism and Developmental Disorders and was published online in December.

Researchers have considered a variety of chemical exposures in the environment during pregnancy and early life as possible contributing factors in the development of autism spectrum disorders. Many have considered prenatal exposure to tobacco smoke a possible cause due to known associations with behavioral disorders and obstetric complications. Past studies of maternal smoking and autism have had mixed results.

"We found no evidence that maternal smoking during pregnancy increases the risk of autism spectrum disorders," said Lee, an epidemiologist at Drexel's School of Public Health, who led the research in collaboration with researchers from Sweden's Karolinska Institute and the University of Bristol (Bristol, UK). "Past studies that showed an association were most likely influenced by social and demographic factors such as income and occupation that have associations with both the likelihood of smoking and with the rate of autism spectrum disorders."

In the new study, Lee and colleagues analyzed data from Swedish national and regional registries for a set of 3,958 children with autism spectrum disorders, along with a control set of 38,983 children born during the same period who did not receive an ASD diagnosis. Overall, 19.8 percent of the ASD cases were exposed to maternal smoking during pregnancy, compared to 18.4 percent of control cases. These rates showed an association between maternal smoking and the odds of an autism spectrum disorder, in unadjusted analyses. However, the association disappeared when the analysis was adjusted for sociodemographic factors such as the parents' income level, education, and occupation.

The report helps to reassure mothers who smoked during pregnancy that their behavior wasn't likely responsible for their child's autism, Lee said, and "crosses off another suspect on the list of possible environmental risk factors for ASD." He cautioned, however, that smoking during pregnancy is still unhealthy for mothers and has other known risks for their children.

Lee received his Ph.D. and M.H.S. degrees in Epidemiology from The Johns Hopkins University, and graduated Cum laude with an A.B. in Biological Anthropology from Harvard College. His research interests include the epidemiology of neurological development, maintenance and decline, including prenatal environmental exposures and autism risk; gene-environment interaction; and epidemiological methods including causal inference methodology, data mining and machine learning algorithms.

Lee was recently awarded a 3-year grant from Autism Speaks to study whether early immune system abnormalities are associated with the risk of autism spectrum disorders.

The maternal smoking risk study was funded by a grant from the Stockholm County Council.

The above story is reprinted from materials provided by Drexel University.

Oxygen and glucose are the food of our brain. If they are absent, such as during a stroke, nerve cells die. An international research team at Charité -- Universitätsmedizin Berlin, Germany, and McMaster University, Canada, has discovered a novel mechanism to prevent this cell death. The results of the study have now been published in the journal Proceedings of the National Academy of Sciences of the USA.

Brief periods of oxygen deprivation can act like a training session for cells in the human body. As a result, they are better able to survive longer periods of oxygen deprivation -- they are "prepared," so to speak. In addition, it is known that oxygen deficiency also affects sugar metabolism. However, sugar metabolism and programmed death of a cell so far have been regarded as independent events.

A research team led by the two scientists Philipp Mergenthaler and Andreas Meisel, who work together at the NeuroCure Cluster of Excellence at the Charité, now explains the link between these two processes. The survival of the cell is regulated by a key enzyme of sugar metabolism, the so-called hexokinase II. This enzyme alters the sugar nutrient glucose in such a way that it can be processed by the cell. The researchers discovered that this enzyme is activated in the nerve cells of the brain after a lack of oxygen. This happens, for example in the case of a stroke, a circulatory disorder of the brain, resulting in insufficient oxygen and nutrient supplies in the brain. The enzyme then plays a protective role. "This self-protection of the nerve cell represents an important basis for further research, from which it may be possible to develop optimized stroke therapies," says Meisel.

However, the molecular mechanisms of the oxygen deficiency and altered cellular metabolism not only play a role for stroke, but are also very important for tumor development and the defense against infections by the immune system. Consequently, the enzyme is held responsible for alterations in sugar metabolism of malignant tumors. However, if there is glucose deficiency in the cell and normal oxygen supplies, it can also cause cell death. "Understanding the basic mechanism of how sugar metabolism regulates cell death might thus be used to protect against stroke, but could also be used to selectively cause cell death in malignant tumors," Mergenthaler explains. The mechanism how sugar metabolism regulates cell death thus fundamentally expands the basic medical knowledge of many diseases.

The above story is reprinted from materials provided by Charité - Universitätsmedizin Berlin.

Researchers at Columbia University Medical Center (CUMC) have identified the critical early cellular and molecular events that give rise to a type of esophageal cancer called esophageal adenocarcinoma, the fastest-rising solid tumor in the United States. The findings, recently published online in Cancer Cell, challenge conventional wisdom regarding the origin and development of this deadly cancer and its precursor lesion, Barrett's esophagus, and highlight possible targets for new clinical therapies.

Lacking a good animal model of esophageal adenocarcinoma (EAC), researchers have been hard pressed to explain exactly where and how this cancer arises. What is known is that EAC is usually triggered by gastroesophageal reflux disease (GERD), in which bile acid and other stomach contents leak backwards from the stomach to the esophagus, the muscular tube that moves food from the mouth to the stomach. Over time, acid reflux can irritate and inflame the esophagus, leading to Barrett's esophagus, an asymptomatic precancerous condition in which the tissue lining the esophagus is replaced by tissue similar to the lining of the intestine. A small number of people with Barrett's esophagus eventually go on to develop EAC.

Using a new genetically engineered mouse model of esophagitis, the CUMC researchers have clarified critical cellular and molecular changes that occur during the development of Barrett's esophagus and EAC. In human patients, acid reflux often leads to overexpression of a molecule called interleukin-1 beta, an important mediator of the inflammatory response, reported study leader Timothy C. Wang, MD, the Dorothy L. and Daniel H. Silberberg Professor of Medicine at CUMC. Thus, Wang and his colleagues created a transgenic mouse in which interleukin-1 beta was overexpressed in the esophagus.

Overexpression of interleukin-1 beta in the mouse esophagus resulted in chronic esophageal inflammation (esophagitis) and expansion of progenitor cells that were sustained by the notch signaling pathway. Notch is a fundamental signaling system used by neighboring cells to communicate with each other in order to assume their proper developmental role. "When we inhibited notch signaling, that blocked proliferation and survival of the pre-malignant cells, so that's a new possible clinical strategy to use in Barrett's patients at high risk for cancer development," noted Dr. Wang.

For decades, investigators thought that the physiological changes associated with Barrett's esophagus originate in the lower esophagus. "However, our study shows that Barrett's esophagus actually arises in the gastric cardia, a small region between the lower part of the esophagus and the upper, acid-secreting portion of the stomach," said Dr. Wang. "What happens is that the bile acid and inflammatory cytokines activate stem cells at this transition zone, and they begin migrating up toward the esophagus, where they take on this intestinal-like appearance."

The researchers also demonstrated that these changes occur primarily in columnar-like epithelial cells, rather than in goblet cells, as was previously thought.

"All told, the findings present a new model for the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma," said Dr. Wang.

Barrett's esophagus affects about 1 percent of adults in the United States. Men are affected by Barrett's esophagus twice as frequently as women, and Caucasian men are affected more frequently than men of other races. The average age at diagnosis is 50. At present, there is no way to determine which patients with the condition will develop EAC. EAC is increasing in incidence about 7 to 8 percent a year, making it the most rapidly rising solid tumor in the U.S.

Treatment with acid-reducing drugs can lessen symptoms of GERD and lower the chances of developing Barrett's esophagus and EAC. Low-grade EAC is highly treatable with endoscopic radiofrequency ablation, photodynamic therapy, or surgical resection. Patients with severe disease may require open surgery, in which most of the esophagus is removed. The overall five-year survival rate with advanced disease is about 25 percent.

Dr. Wang's paper is entitled, "Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett's-like metaplasia." The lead author is Michael Quante of CUMC and Technische Universität München, Munich, Germany. The other contributors are Govind Bhagat, Julian Abrams, Frederic Marache, Pamela Good, Michele D. Lee, Yoomi Lee, Richard Friedman, Samuel Asfaha, MD, PhD, Zinaida Dubeykovskaya, Carrie Shawber, and Charles Lightdale, all of CUMC; Umar Mahmood and Jose-Luiz Figueiredo, of Harvard Medical School and Massachusetts General Hospital, Boston; Jan Kitajewski of Technische Universität München; and Anil K Rustgi of the University of Pennsylvania, Philadelphia.

This research is supported by the National Cancer Institute of the National Institutes of Health grants (RO1DK060758, 1U54CA126513, and R01CA120979) to T.C. Wang; NIH U01 grant (5U01 CA143056) to A.K. Rustgi, T.C. Wang and U. Mahmood. A.K. Rustgi was further supported by NIH P01-CA098101 and P30-DK050306 grants. M. Quante was supported by a grant from the Mildred-Scheel-Stiftung, Deutsche Krebshilfe, Germany. J. Abrams is supported by a Career development Award from the NCI (K07CA132892) and by a Louis V. Gerstner, Jr. Scholars Award.

The above story is reprinted from materials provided by Columbia University Medical Center.

Scientists from the University of Helsinki, Finland, and from UCSF, US, have exposed a cell pathway that breast tumor cells use to destruct local tissue neighborhood. Cancer cells may use this pathway to free themselves from mammary epithelial tissue architecture, to spread to surrounding tissues. The cell pathway, the researchers found, is a biochemical chain of events leading to activation of a protein-cleaving enzyme on the surface of the tumor cells.

Cancer rarely kills unless it evolves the ability to spread beyond the tissue in which it developed, to grow into surrounding healthy tissues. An important roadblock for tumor spread is membranous scaffolding, basement membrane, which lines epithelial cell layers in tissues. Normal epithelial cells and even early-stage tumor cells remain tightly tethered to basement membrane, which segregates healthy and likewise cancerous epithelial cells from surrounding tissues. Breakdown of this barrier allows tumor cells to escape from the tethers of the epithelium, launching a tumor invasion to healthy tissues.

Finnish scientists from the University of Helsinki, together with UCSF researchers, have identified a molecular pathway in breast tumor cells leading to activation of a protein-cleaving enzyme hepsin on the surface of breast tumor cells. Tumor cells use hepsin to chop basement membrane proteins -- to break free from ties and matrix binding them to local neighborhood in their native epithelial tissue, the investigation suggests. The study will be published in the 16th January edition of the Proceedings of the National Academy of Sciences (PNAS).

"If we could delay or prevent a tumor from switching from one that grows in place to one that invades, then that would be a major milestone in cancer treatment," according to study co-author Zena Werb, PhD, a professor of anatomy at UCSF. Werb has for decades studied the ways in which the behavior of tumor cells is influenced by their surroundings, with a focus on breast tumors.

Working with genetically engineered mouse mammary glands and mammary epithelial fragments isolated from these glands (organoids), University of Helsinki scientist and Finnish Academy Research Fellow Juha Klefström, PhD, along with a University of Helsinki graduate student Johanna Partanen designed and led experiments that resulted in the discovery of a biochemical chain of events that is likely to be initiated by many breast tumor cells when they become invasive.

The research collaborators initially studied a tumor suppressor gene (a gene that prevents the growth of tumors) called Liver Kinase B1 (Lkb1). They found that shutdown of this gene disturbs development of parts of the mammary gland, including milk-secreting tissue structures. Especially, basement membrane, which normally surrounds tissue structures of the mammary gland was damaged and degraded.

A culprit for basement membrane damages was pinpointed: Lkb1 shutdown disconnected hepsin from normal regulation and the protein mistakenly started to blanket the surface of mammary epithelial cells, causing degradation of the basement membrane. Researchers found that inactivation of hepsin allowed the basement membrane to recover. These events may take place in many tumors, as the research found that Lkb1 is missing and hepsin is abnormally expressed in 1 out of 4 human breast cancer samples.

"These findings led us to ask an obvious question: does Hepsin mediated degradation of basement membrane make epithelial cells more cancer-prone?" says Johanna Partanen. She knocked out Lkb1 in the mouse mammary gland. Evidently, hepsin expression was abnormal and basement membrane shattered but even after a year, she did not observe any tumors forming in the glands.

"I was disappointed with the results. However, then I realized that even though broken basement membrane may give more freedom for cells to proliferate, the cells may just lay there, resting, and not start to over-proliferate unless they are pushed to cell division cycle.

Partanen re-engineered mice so that she combined cell cycle "driver" oncogene Myc with inactivated Lkb1 gene in the mammary glands and she soon noticed very fast growing mammary tumors in the mice. "We think that it is the combination of Myc empowered cell cycle and cell's ability to destroy basement membrane, which contributed to the vicious tumor formation" says Partanen.

Will these findings help us to fight cancer? -- Maybe, says Juha Klefström:

"Hepsin is of a type of protein known as a protease and proteases have been successfully targeted in drug development. We found that deactivation of hepsin in the mammary gland organoids prevents formation of a cancerous phenotype. This finding excites us as it leads us to think that inhibition of Hepsin by drug-like molecules could restrain breast cancer progression. However, we do not know yet if we can cure already formed tumors by blocking hepsin activity. We need to first improve our experimental systems to properly address this question."

According to Zena Werb, "In humans, breast cancers that have diminished amounts of Lkb1 show strong hepsin expression. Since hepsin sits on the cell membrane, it should be accessible to drugs. We believe that hepsin forms a novel target for treatment of a subset of breast cancer patients."

The above story is reprinted from materials provided by Helsingin yliopisto (University of Helsinki).

Researchers have devised a proposal for the first conclusive experimental test of a phenomenon known as 'Bell's nonlocality.' This test is designed to reveal correlations that are stronger than any classical correlations, and do so between high-energy particles that do not consist of ordinary matter and light. These results are relevant to the so-called 'CP violation' principle, which is used to explain the dominance of matter over antimatter.

These findings by Beatrix Hiesmayr, a theoretical physicist at the University of Vienna, and her colleagues, a team of quantum information theory specialists, particle physicists and nuclear physicists, have been published in The European Physical Journal C.

According to the famous Einstein-Podolsky-Rosen Gedanken-Experiment, two particles that are measured independently obey the principle of locality, implying that an external influence on the first particle, such as measurement, has no direct influence on the second -- in other words there is no "spooky action at distance," as Einstein would likely have described it.

In an experimental setup, however, measurement results for one particle revealed a correlated measurement result for the other particle. Initially, these correlations could only be explained by referring to hidden parameters. In 1964, John Bell found that so-called local realistic hidden parameter theories imply that the relations between these correlations could be experimentally tested through so-called Bell tests. Since then many experiments have proven that local, realistic hidden parameters cannot be used as an explanation for these correlations.

In this study, the authors have succeeded in devising a new Bell test, taking into account the decay property of high-energy particles systems, called kaon-antikaon systems. This procedure ensures that the test is conclusive -- a goal that has never before been achieved -- and simultaneously guarantees its experimental testability. Experimental testing requires equipment such as the KLOE detector at the accelerator facility DAPHNE in Italy.

Revealing "spooky action at distance" for kaon-antikaon pairs has fundamental implications for our understanding of such particles' correlations and could ultimately allow us to determine whether symmetries in particle physics and manifestations of particles correlations are linked.

The above story is reprinted from materials provided by Springer Science+Business Media.

Nitrogen is both an essential nutrient and a pollutant, a byproduct of fossil fuel combustion and a fertilizer that feeds billions, a benefit and a hazard, depending on form, location, and quantity. Agriculture, industry and transportation have spread nitrogen liberally around the planet, say sixteen scientists in the latest edition of ESA's Issues in Ecology series, "Excess Nitrogen in the U.S. Environment: Trends, Risks, and Solutions," with complex and interrelated consequences for ecological communities and our dependence upon the resources they provide, as well as human health.

Pulling from a broad pool of expertise in air quality, agronomy, ecology, epidemiology and groundwater geochemistry, the sixteen authors track nitrogen through its different chemical forms and biological incarnations as it progresses across economic, environmental and regulatory bounds. They argue for a systematic, rather than piecemeal, approach to managing the resource and its consequences. "We're really trying to identify solutions," said lead author Eric Davidson, a soil ecologist and executive director of the Woods Hole Research Center. "This is a paper about how much we do know, not about what we don't know. We know about nitrogen cycles, and sources, and we know problems can be addressed in economically viable ways."

Once a critical limiting element of agricultural production, excess nitrogen now overflows from fields and stockyards, typically in the forms of ammonia and nitrate, contaminating drinking water and air, and altering the chemistry and constituency of ecological communities. "Nitrogen is readily mobile, and very efficiently distributed through wind and water," said author James Galloway, a biogeochemist at the University of Virginia. Airborne nitrogen from agricultural fields, manure piles, automobile tailpipes, and smokestacks travels with the wind to settle over distant forests and coastal areas.

Though extra fertilizer sounds like a good thing, it does not benefit all species equally, leading, in more extreme cases, to sudden changes like algal blooms, which smother competing species and can create health hazards. Nitrogen also acidifies soil, leaching away other important nutrients. Interventions to control nitrogen oxide emissions from power plants and gasoline-fueled engines have made encouraging progress. Mitigating agricultural sources of excess nitrogen is more complicated.

"We know how to reduce nitrogen oxides from fossil fuel combustion to a very small amount. We know the science, we have the engineering, and we have the regulatory tools," said Galloway, setting emissions aside as a political, rather than a scientific, hurdle. "On the food side, that's where it gets interesting," he said. "How can you still produce the food the society demands, needs, yet use less nitrogen to produce it?"

The report tabulates strategies to help farmers maximize efficient use of fertilizer, rather than just maximize crop yield, including buffer strips and wetlands, manure management, and ideal patterns of fertilizer application. It also considers the cost of implementing them, and programs for buffering farmers against losses in bad years.

"There are a variety of impacts due to the human use of nitrogen," said Galloway. "The biggest is a positive one, in that it allows us to grow food for Americans and people in other countries, and we don't want to lose sight of that." Balancing inexpensive abundant food against the damage done by nitrogen escaping into the environment is a conversation the authors would like to hear more prominently in policy arenas.

"Yes, we have to feed people, but we also need clean drinking water, clean air, and fisheries in the Gulf of Mexico," said Davidson. "The science helps to show those tradeoffs, and where we most stand to gain from improved nutrient management in agriculture."

The above story is reprinted from materials provided by Ecological Society of America.