Chemists at The Scripps Research Institute (TSRI) in La Jolla, California, have invented a powerful method for joining complex organic molecules. This method is extraordinarily robust and can be used to make pharmaceuticals, fabrics, dyes, plastics, and other materials previously inaccessible to chemists. “We are rewriting the rules for how one thinks about the reactivity of basic organic building blocks, and in doing so we’re allowing chemists to venture where none has gone before,” said Dr. Phil S. Baran, the Darlene Shiley Chair in Chemistry at TSRI, whose laboratory reported the finding on functionalized olefin cross-coupling in an online article in Nature published on December 17, 2014. With the new technique, scientists can join two compounds known as olefins to create a new bond between their carbon-atom backbones. Carbon-to-carbon coupling methods are central to chemistry, but until now have been plagued by certain limitations: they often fail if either of the starting compounds contains small, reactive regions known as “functional groups” attached to their main structure. They also frequently don’t work well in the presence of “heteroatoms”—non-carbon atoms such as nitrogen, oxygen and iodine—despite the importance of these types of atoms in chemical synthesis. The new method is what chemists call “mild,” meaning that it doesn’t require the use of extreme temperatures or pressures, nor harsh chemicals. As a result, portions of the building blocks used that are particularly fragile remain unaltered by the reaction. “Functional groups that would be destroyed by other cross-coupling methods are totally unscathed when using our method,” said Julian C. Lo, a graduate student who was a co-lead author of the report with Research Associate Dr. Jinghan Gui.
A team of biologists has identified a set of nerve cells in desert locusts that bring about ‘gang-like’ gregarious behavior when the insect are forced into a crowd. Dr. Swidbert Ott from the University of Leicester’s Department of Biology, working with Dr. Steve Rogers at the University of Sydney, Australia, has published a study, online on December 17, 2014 in an open-access article in The Royal Society Proceedings B, that reveals how newly identified nerve cells in locusts produce the neurochemical serotonin to initiate changes in their behavior and lifestyle. The findings demonstrate the importance of individual history for understanding how brain chemicals control behavior, which may apply more broadly to humans also. Locusts are normally shy, solitary animals that actively avoid the company of other locusts. But when they are forced into contact with other locusts, they undergo a radical change in behavior – they enter a “bolder” gregarious state in which they are attracted to the company of other locusts. This is the critical first step towards the formation of the notorious locust swarms. Dr. Ott said: “Locusts only have a small number of nerve cells that can synthesise serotonin. Now we have found that of these, a very select few respond specifically when a locust is first forced to be with other locusts. Within an hour, they produce more serotonin. It is these few cells that we think are responsible for the transformation of a loner into a gang member. In the long run, however, many of the other serotonin-cells also change, albeit towards making less serotonin.”
Ancient DNA extracted from the bones and teeth of giant lemurs that lived thousands of years ago in Madagascar may help explain why the giant lemurs became extinct. It also explains what factors make some surviving species more at risk today, says a study published online on December 16, 2014 in the Journal of Human Evolution. Most scientists agree that humans played a role in the giant lemurs' demise by hunting them for food and forcing them out of habitats. But an analysis of their DNA suggests that the largest lemurs were more prone to extinction than smaller-bodied species because of their smaller population sizes, according to a team of American and Malagasy researchers. By comparing the species that died out to those that survived, scientists hope to better predict which lemurs are most in need of protection in the future. The African island of Madagascar has long been known as a treasure trove of unusual creatures. More than 80 percent of the island's plants and animals are found nowhere else. But not long ago, fossil evidence showed there were even more species on the island than there are today. Before humans arrived on the island some 2,000 years ago, Madagascar was home to 10-foot-tall elephant birds, pygmy hippos, monstrous tortoises, a horned crocodile, and at least 17 species of lemurs that are no longer living -- some of which tipped the scales at 350 pounds, as large as a male gorilla. Using genetic material extracted from lemur bones and teeth dating back 550 to 5,600 years, an international team of researchers analyzed DNA from as many as 23 individuals from each of five extinct lemur species that died out after human arrival.
New research from The Johns Hopkins University suggests that the amount of mitochondrial DNA (mtDNA) found in peoples' blood directly relates to how frail they are medically. This DNA may prove to be a useful predictor of overall risk of frailty and death from any cause 10 to 15 years before symptoms appear. The investigators say their findings contribute to the scientific understanding of aging and may lead to a test that could help identify at-risk individuals whose physical fitness can be improved with drugs or lifestyle changes. A summary of the research was published online on December 4, 2014 in the Journal of Molecular Medicine. "We don't know enough yet to say whether the relationship is one of correlation or causation," says Dan Arking, Ph.D., associate professor of genetic medicine at Hopkins. "But either way, mitochondrial DNA could be a very useful biomarker in the field of aging." Mitochondria are structures within cells often referred to as "power houses" because they generate most of cells' energy. Unlike other cell structures, they contain their own DNA -- separate from that enclosed in the nucleus -- in the form of two to 10 small, circular chromosomes that code for 37 genes necessary for mitochondrial function. There are also genes important for mitochondrial function coded for by DNA in the cell nucleus. There are 10 to thousands of mitochondria per cell, depending on a cell's energy needs. Previous research from Dr. Arking's laboratory linked genetic differences in mtDNA to increased frailty and reduced muscle strength in older individuals. Medically speaking, frailty refers to a well-recognized collection of aging symptoms that include weakness, decreased energy, lower activity levels, and weight loss. To further test this link, Dr.
In a follow-up to her earlier studies of learning in infancy, developmental psychologist Dr. Lisa Scott (photo) and colleagues at the University of Massachusetts-Amherst (U Mass-Amherst) are reporting that talking to babies in their first year, in particular naming things in their world, can help them make connections between what they see and hear, and these learning benefits can be seen as much as five years later. "Learning in infancy between the ages of six to nine months lays a foundation for learning later in childhood," Dr. Scott says. "Infants learn labels for people and things at a very early age. Labeling helps them recognize people and objects individually and helps them decide how detailed their understanding of the object or face needs to be." Details of Scott's research, conducted with U Mass-Amherst psychological and brain science doctoral students Hillary Hadley and Charisse Pickron, were published online on November 29, 2014 in Developmental Science. Dr. Scott's own earlier experiments, as well as work by others, shows that before they are six months old, babies can easily tell faces apart within familiar (e.g., human faces) and unfamiliar (e.g, monkey faces) groups. But by nine months, they are no longer as good at distinguishing faces outside their own species compared to faces from their own species. This decline in recognizing unfamiliar individuals is called "perceptual narrowing" and is driven by the infants' experience interacting with some groups more than others and learning the names of individuals in some groups more than others during the six- to nine-month window, the neuroscience researchers say.
A team led by Brown University biologists, together with colleagues, has discovered the way in which a specific genetic mutation appears to lead to the lack of melanin production underlying a form of albinism. Newly published research provides the first demonstration of how a genetic mutation associated with a common form of albinism leads to the lack of melanin pigments that characterizes the condition. Approimately 1 in 40,000 people worldwide have type 2 oculocutaneous albinism, which has symptoms of unusually light hair and skin coloration, vision problems, and reduced protection from sunlight-related skin or eye cancers. Scientists have known for about 20 years that the condition is linked to mutations in the gene that produces the OCA2 protein, but they hadn’t yet understood how the mutations lead to a melanin deficit. In the new research, a team led by Brown University biologists Nicholas Bellono and Dr. Elena Oancea shows that the protein is necessary for the proper functioning of an ion channel on the melanosome organelle (image), the little structure in a cell where melanin is made and stored. The ion channel is like a gate that lets electrically charged chloride molecules flow into and out of the melanosome. When the melanosome lacks OCA2 or contains OCA2 with an albinism-associated mutation, the researchers found, the chloride flow doesn’t occur and the melanosome fails to produce melanin, possibly because its acidity remains too high. The discovery could inspire new ideas for treating albinism, said Dr. Oancea, assistant professor of medical science and senior author of the paper published online on December 16, 2014 in the open-access journal eLife. “From a therapeutic point of view, we now have a channel that’s a possible drug target,” she said.
University of Guelph researchers in Canada hope their new discovery will help combat a disease killing honeybee populations around the world. The researchers have found a toxin released by the pathogen that causes American foulbrood disease — Paenibacillus larvae (P. larvae) — and developed a lead-based inhibitor against it. The study was published online on December 4, 2014 in the Journal of Biological Chemistry. The finding provides much-needed insight into how the infection occurs, said Dr. Rod Merrill, a professor in Guelph’s Department of Molecular and Cellular Biology and a study co-author. It also could lead to natural and more effective approaches for fighting the most widespread and destructive of bee brood diseases. “We are the first to do this,” said Dr. Merrill, who conducted the study with graduate student Daniel Krska. Also involved were post-doctoral researchers Drs. Ravi Ravulapalli and Miguel Lugo, technician Tom Keeling, and Harvard Medical School’s Dr. Rob Fieldhouse. American foulbrood is found throughout Ontario and Canada, and affects both the honeybee industry and pollinator populations. Honeybees are among the world’s most important pollinators, and their numbers are already falling globally because of disease, pesticide use, climate change, and other factors. The disease spreads readily through spores transmitted within and between colonies by adult bee carriers, Dr. Merrill said. Developing larvae are infected by eating the spores. The larvae die but not before releasing millions of additional spores into the colony. As well, the hive’s weakened state attracts “robber bees” looking for honey, which then spread the disease to other colonies.
Dartmouth researchers have found a solution using visible light to reduce waste produced in chemically activated molecular switches, opening the way for industrial applications of nanotechnology ranging from anti-cancer drug delivery to LCD displays and molecular motors. The study was published online on September 15, 2014 in the Journal of the American Chemical Society. Chemically activated molecular switches are molecules that can shift controllably between two stable states and that can be reversibly switched -- like a light switch -- to turn different functions "on" and "off." For example, light-activated switches can fine-tune anti-cancer drugs, so they target only cancer cells and not healthy ones, thereby eliminating the side effects of chemotherapy. But such switches typically generate waste and side products that are problematic. One way of making these processes cleaner is by using light energy, similar to how photosynthesis operates in nature. In their experiments, the researchers show that a merocyanine-based photoacid derivative can effectively be used in a switching process that is fast, efficient, and forms no wastes. "We address a bottleneck that's been hampering the field for decades -- what to do with the accumulated salts and side products when activating such switches," says co-author Dr. Ivan Aprahamian, an associate professor of chemistry. "Acids, bases, and other compounds need to be constantly added to the mix to make sure the system can be switched, but within a few cycles there is so much waste that it interferes with the switching process. We found a neat solution by coupling an efficient photoacid to our chemically activated hydrazone switch. We showed the system can be efficiently modulated more than 100 times with no accumulation of waste or degradation.
A new study led by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) describes a novel marker that may help doctors choose the least toxic, most effective treatment for many older patients with acute myeloid leukemia (AML). AML occurs mainly in older patients and has a three-year survival rate of just 5 to 15 percent. The researchers investigated patterns of molecules called long noncoding RNAs (lncRNAs), a class of RNA molecules more than 200 nucleotide units long that are involved in regulating genes. The researchers examined the abundance, or expression, of lncRNAs in patients who were 60 years and older and who had cytogenetically normal (CN) AML. The study was published online on December 15, 2014 in PNAS..“We have identified a pattern of 48 lncRNAs that predicted both response to standard chemotherapy and overall survival in older CN-AML patients,” says first author Ramiro Garzon, M.D., associate professor of internal medicine at Ohio State. “Patients in the favorable group had a high probability of responding to standard chemotherapy, while those in the unfavorable group generally responded poorly to the treatment and had worse overall survival,” he says. These findings are important for several reasons, says principal investigator Clara D. Bloomfield (photo), M.D., Distinguished University Professor, Ohio State University Cancer Scholar and holder of the William Greenville Pace III Endowed Chair in Cancer Research.
To the casual observer, the colonies of social insects like bees and ants appear to be harmonious societies where individuals work together for the common good. But appearances can be deceiving. In fact, individuals within nests compete over crucial determinants of fitness such as reproductive dominance and production of male eggs. The intensity of competition often depends on the level of kinship between colony members. This is because selfish individuals lose indirect fitness when their behavior harms close relatives. A new study by Dr. Eva Schultner and colleagues from the Universities of Helsinki, St. Andrews, and Oxford reveals that in ants, such social conflict occurs even among the youngest colony members: the eggs and developing larvae. In behavioral experiments conducted at Tvärminne Zoological Station in Finland, ant larvae acted selfishly by cannibalizing eggs, but levels of cannibalism were lower when relatedness among brood was high. In addition, male larvae engaged in cannibalism more often than female larvae. Using evolutionary modeling, the researchers show that cannibalism is predicted to evolve when it carries a benefit to the cannibal (for example in the form of increased survival), and that the costs of consuming kin influence the intensity of cannibalism behavior. Differences in cannibalism benefits for male and female larvae on the other hand may be responsible for higher levels of cannibalism in males. By exploring the evolutionary causes and consequences of selfish larvae behavior, the study published in The American Naturalist sheds new light on the evolutionary constraints of competition in social insect colonies, and demonstrates how in complex societies, even the youngest individuals are potential players in social conflict.