These journals are indexed with important bibliographic databases including EMBASE, CAB Abstracts, SCOPUS, Chemical Abstracts and many others.

 
Worm seeks worm: Chemical cues drive aggregation in nematodes
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 ...
 
Wandering albatross alters its foraging due to climate change
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 W...
 
Umbilical Cord Stem Cells Converted Into Brain Support Cells
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 com...
 
How the brain routes traffic for maximum alertness
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 ...
 
No link found between prenatal exposure to tobacco smoke and autism
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 associat...
 
Sugar for the Brain: Mechanism to Prevent Programmed Cell Death of Nerve Cells Deciphered
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 ...
 
Study reveals origins of esophageal cancer
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 inf...
 
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