Why some insects kill their mother? New study unlocks the puzzle for you!

For most social insects such as ants, wasps and bees, the workers which female, devote whole life to help the queen produce new offspring. But there were reports about workers kill their queen came out. Thus, why some insects kill their mothers has been a great puzzle for entomologists for a long time. Why do these workers help the queen in some situation but also kill them in other situation? That's paradoxical and confusing. In order to solve the puzzle, entomologist Kevin J. Loope, a postdoctoral researcher at the University of California, Riverside, set up observation colonies of yellow jacket wasps in his lab, used video camera to film them continuously and noted when matricide happened. Loope also collected wild colonies to increase the sample size and infer matricide from mature, queenless colonies. The worker wasps kill queens when they are in colonies with lots of full siblings, but not in colonies with a mix of full and half siblings. After research, the researchers found that workers can assess the relative proportions of full and half-siblings of their colony and respond adaptively when conflicts of interest turn up, such as rearing the sons of workers or the sons of the queen. This research shows the first thorough investigation of the behavior of queen-killing, which is an event, common but hard to observe. Loope now aims at finding out how yellow jacket wasps' interaction with other species. The report is published in Current Biology online. Go there to find more about the puzzle. Extended reading>>>http://www.cusabio.com/Clone/CT0239-1089564.html

Sing to calm down your baby instead of talking

A study involving thirty healthy infants aged between six and nine months was published in Infancy recently. It was conducted by the University of Montreal. During the research, the infants kept calm twice as long when they are listening to a song, as they did when listening to speech. There are a lot of studies about how singing and speech affect infants' attention, but more should be known, such as how they affect a baby's emotional self-control. "Emotional self-control is obviously not developed in infants, and we believe singing helps babies and children develop this capacity," said Professor Isabelle Peretz, of the university's Center for Research on Brain, Music and Language. In fact, humans are enraptured by music naturally. For adults and older children, they will behavior by foot-tapping, head-nodding, or drumming. But infants do not synchronize their external behavior with the music, or because they lack the requisite physical or mental ability. The findings show that the babies were actually caught by the music, suggesting that they have the ability of being entrained. The findings are quite important for mothers. Singing to their children can help the mothers avoid missing out on the emotion-regulatory properties of singing. Sing more to your infants from now on. You may like the content below>>>http://www.cusabio.com/Clone/dnaT-1089563.html

Great breakthrough: Scientists found new class of DNA repair enzyme

We all know that this year's Nobel Prize in chemistry was given to 3 scientists who focused on one piece of DNA repair puzzle apiece. Now a new-published study in the journal Nature showing the discovery of a new class of DNA repair enzyme. As early as the time when scientists first found the structure of DNA, they think it extremely chemically stable and the stability can allow DNA to pass the basic traits of parents along to offspring. However, biologists have learned that the double helix structure is a highly reactive molecule that is constantly being damaged in fact, and that cells must make endlessly efforts to repair and protect the genetic information that it contains. "More than 10,000 DNA damage events occur each day in every cell in the human body that must be repaired for DNA to function properly," said first author Elwood Mullins, a postdoctoral research associate in the Eichman lab. Tomas Lindahl, who received this year's Nobel Prize, found a new DNA repair enzyme, which is a DNA glycosylase. It is a family of enzymes. He recognized that these enzymes removed damaged DNA bases through a process called base-excision repair. The discovery is inspiring for scientists, and it also shows that more can be learnt about DNA repair. More repair pathways remains to be discovered. Read more:http://www.cusabio.com/Clone/ndhI-1089562.html

New shark fossils found in Texas break the fossil record

Before then, giant sharks had been recovered from rock dating back 130 million years - it is during the age of the dinosaurs.The largest shark that ever existed is much younger, occurring at about 15 million years ago. It is commonly called "Megalodon". However, the new fossils from Texas show that giant sharks go further back into the fossil record. After careful study, a team led by Dr. John Maisey of the American Museum of Natural History in New York finally could estimate the size of the entire sharks by comparing them with smaller and more complete fossils of related sharks. The results impressed the researchers. They estimated for the two Texas supersharks and targeted the size between 18 and 26 feet in length (5.5 to 8 meters). The largest of these specimens was twenty-five percent larger than today's largest predatory shark, which is the Great White. Although the fossil sharks from Texas are not nearly as large as Megalodon, which might have reached up to 67 feet in length (about 20 meters), they might have been the biggest sharks in the ocean by far. The fossil braincases are supposed to belong an extinct species of shark which is called Glikmanius occidentalis, or they may be a new and larger related species which is unknown by scientist till now. Closely related sharks are known from as far off as Scotland, suggesting that this group of sharks can disperse over great distance. The fossils are nearly 300 million years ago. Maisey and his team presented the results of the Texas 'supershark' at the annual meeting for the Society of Vertebrate Paleontology in Dallas, Texas. You may like this>>>http://www.cusabio.com/Polyclonal-Antibody/ST3GAL2-Antibody-11098180.html

New findings: some guppies have the ability of counting

A new research shows that the little guppies are smarter than we usually think. Some of them can count. The research was conducted by Associate Professor Culum Brown, from the Department of Biological Sciences at Macquarie University, and colleagues from the University of Padova. It is published in Frontiers in Behavioural Neuroscience, describing the surprising ability. After research, Professor Brown said that guppies that have very strongly lateralised brains are better at counting than those that have non-lateralised brains. For humans, the left hemisphere is often associated with language and maths, while the right hemisphere is more artistic. Scientists are always wondering why humans and other animals have lateralised brains, where the two halves of their brain execute different functions. There is a theory suggesting that having strongly lateralised brains allows each hemisphere to analyse information separately. The research shows that fish with strongly lateralised brains could distinguish between three versus four objects, while those with non-lateralised brains could only distinguish two versus three. Comparing sets of objects containing four items seems to be the upper limit of most animals — after this animals including humans switch to another system that relies on ratios when comparing sets. Further reading:http://www.cusabio.com/Recombinant-Protein/Recombinant-human-Medium-chain-specific-acyl-CoA-dehydrogenase-mitochondrial-11089628.html

Electrical eels deliver more electrical shocks by curling up

Electrical eels' ability of stunning preys then locating them through the similar power was found by Kenneth Catania, Stevenson Professor of Biological Sciences from Vanderbilt University. He has spent three years studying on this fish lived in South America and come to the conclusion. Almost two thirds of the eel's body is filled with specialized cells which is called electrocytes. They can store electricity acting as batteries. The cells discharge simultaneously which is at least 600 volts when an eel is around its prey. Catania found that the eels have a special skill to double the electrical shock that they can deliver to particularly large or difficult prey. The findings are reported in the journal Current Biology on Oct. 29. The eel had a second attack when it realized there is bigger fish and it is more difficult to beat the prey. Under these circumstances, the eel first bits the prey and curls its tail around the body of the prey until the tail lies directly across the body from the eel's head. Then the electrical pulses are greatly increased. The weapon used by electrical eels, that is the high-voltage system, is much complex than we thought. You may like the content below:http://www.cusabio.com/Recombinant-Protein/Recombinant-mouse-Oxysterol-binding-protein-related-protein-11-11089629.html

Electrical eels use electrolocation to locate prey

A study published in the journal Nature Communications describes the ability of electric eels to stun prey and locate them using their electrical powers. The study is reported by Kenneth Catania, a biological scientist from Vanderbilt University. The study shows how the electric eels use electrolocation to find the stunned prey. The jolt of electricity released by electric eel won't kill prey, which is contrary to what is believed by most people. The harm can only cause the prey's muscles to spasm uncontrollably, thus making it stunned and unable to escape. But this explanation is far from enough. You may know that the eel lives in the murky depths of the Amazon River, and it is hard to see far. How can the eels find a fish which just stunned? Catania conducted two sets of tests and drew a conclusion in the study that these eels are using the same electricity, that is electrolocation, which they used to stun preys. Read more:http://www.cusabio.com/Recombinant-Protein/Recombinant-Horse-Myelin-P2-protein--11089630.html

A whale found dead with stomach full of rubbish

Marine biologists from Taiwan conducted an autopsy on a dead while on October 24, 2015 and found the whale' stomach was full of plastic bags and fishing net. The rubbish found in the stomach is quite enough to fill up an excavator bucket. The whale was found stranding off the southern town of Tongshi on October 15. It is a mature sperm whale which is 15-metre long. Coastguards put them back to the ocean but found it dead around twenty kilometres away 3 days later. Scientists guess that the rubbish may be the greatest factor of the death. The whale might have suffered heart or lung disease and some other infections. However, the rubbish made by human beings, which can reduce appetite, thus causing malnutrition, may be the key point to the death. The whale's death highlights the increasing threat caused by ocean trash. Scientists are calling everyone to improve ocean environment. You can read more here:http://www.cusabio.com/ELISA-Kit/Human-alpha-II-spectrin-breakdown-product-SBDP145-ELISA-kit-1080879.html

Fish ask for help by releasing chemical substance

Research shows that when prey fish are caught by predators, they will release chemical cues, a distress call which will greatly enhance their chance for survival. The findings are published by researchers from Uppsala University, Sweden and James Cook University in Australia in Proceedings of the Royal Society B. The fish harbour a chemical substance under their skin and it will be released once injured. The chemical will affect the fish nearby and they will be fearful then escape immediately. However, the benefits to the sender have not been identified. Scientists have debated the evolutionary origin of chemical alarm cues in fish for many years. The chemical substance provides obvious benefits to surrounding fish, but the senders seem to have little benefits. The study shows that the chemical cue attracts more predators to the places. When caught by predators, the small damselfish have little chance to run away and not eating by the predators. But when other predators come, preys have more time to escape. The results of the research indicate that fish may benefit from the production and release of chemical alarm cues, and highlight the important role of chemical cues in predator-prey interactions on coral reefs. It indicates that coral reef fish have equipped with a various clever strategies to survive during long evolutionary time. You may like this>>>http://www.cusabio.com/ELISA-Kit/Rat-leukotriene-B5LT-B5-ELISA-kit-1081315.html

Study about chicken shows evolution can happen in a relatively short time

There is a popular assumption suggesting that evolution is only visible over long time scales. But recently a study about chickens overturns the assumption. A group of scientists led by Professor Greger Larson from Oxford University's Research Laboratory for Archaeology studied individual chickens that were part of a long-term pedigree and found two mutations that had occurred in the mitochondrial genomes of the birds in only 50 years. Before this, it is widely believed by scientists that the rate of change in the mitochondrial genome was never faster than about two percent per million years. The results showed that the rate of evolution in this pedigree is 15 times faster in fact. What's more, the group also found a single instance of mitochondrial DNA being passed down from a father by determining the genetic sequences along the pedigree. This unexpected discovery shows that paternal leakage is not that rare as it was believed before. The study is published in Biology Letters online. Read more:http://www.cusabio.com/ELISA-Kit/Human-Interleukin-18IL-18-ELISA-KIT-11090105.html

Motor proteins pause at the ends of microtubules and stimulate their growth

Researchers at Penn State suggest that motor proteins which pause at the ends of microtubules and produce pushing forces can also stimulate their growth. The function of the proteins is a critical component in understanding cell division and nerve branching and growth. Kinesins are found in multicellular organisms. They are a family of motor proteins. They act as little engines within the cells and transport molecular cargo along microtubules. The microtubules are hollow cylinders of the protein tubulin. They are dynamic and can grow and shrink when the cell change shape. The researchers are trying to understand more about the motor and what makes the sequences unique since they carry out so many vital functions in the cells. There are forty-five different kinesin motor proteins in human body in all. The researchers tracked the movements of each one and found that motor pauses at the end of the microtubules. Later it produces pushing forces to slide the microtubules apart and allow the motor to grow the microtubules. Their findings are reported in Nature Communications recently. They bound microtubules to a microscope slide and added free tubulin subunits together with modified kinesin-5 motor proteins. The results showed that the motor proteins added improve the rate and persistence of microtubule growth. In conclusion, if we can terminate cancer cell division, new approaches in treatment will come into being. Therefore, understanding more about how kinesin-5 influences microtubule dynamics and its importance in properly segregating genetic material in cell division is of great concern. Read more as you like:http://www.cusabio.com/Clone/RSc1635-1089576.html

Nanofiber hydrogel together with snake venom can stop bleeding quickly

SB50 which is a kind of hydrogel, incorporates batroxobin, venom produced by two species of South American pit viper. It can be injected as liquid and becomes a gel which can get a wound closed and promotes clotting in seconds. Rice University scientists think this nanofiber hydrogel infused with snake venom may be a good device to stop bleeding quickly. The researchers, including Rice chemist Jeffrey Hartgerink, lead author Vivek Kumar and their colleagues published their findings in the American Chemical Society journal ACS Biomaterials Science and Engineering. According to them, the hydrogel may be quite useful for surgeries, especially for patients who take anti-coagulant drugs to thin their blood. Isn't interesting that something deadly can be turned into something that may save people's life? Batroxobin has been taken as a coagulant, which can encourages blood to clot since 1936. It is used in many therapies to remove excess fibrin proteins from the blood to treat thrombosis and as a topical hemostat. It is also used to iagnostic tool to determine blood-clotting time in the presence of heparin (an anti-coagulant drug). That's important - There are many things which can trigger blood coagulation, but they usually stop work or work slowly and poorly when you're on heparin, therefore causing problems when bleeding. "Heparin blocks the function of thrombin, an enzyme that begins a cascade of reactions that lead to the clotting of blood," Hartgerink said. "Batroxobin is also an enzyme with similar function to thrombin, but its function is not blocked by heparin. This is important because surgical bleeding in patients taking heparin can be a serious problem. The use of batroxobin allows us to get around this problem because it can immediately start the clotting process, regardless of whether heparin is there or not." During tests, the new material stopped a wound from bleeding in six seconds and didn't reopen it. They also tested other conditions, such as the hydrogel without batroxobin, the batroxobin without the hydrogel, a current clinical hemostat known as GelFoam and an alternative self-assembling hemostat known as Puramatrix and found that none were as effective, especially in the presence of anti-coagulants. SB50 is thought to be great potential to stop surgical bleeding. It won't make batroxobin work alone. Read more:http://www.cusabio.com/Polyclonal-Antibody/MAGEA10-Antibody-FITC-conjugated-11098210.html

A new computational method developed to study protein dynamics

Researchers have developed the first computational method based on evolutionary principles to predict protein dynamics. These researchers are from the Structural Biology Computational Group of the Spanish National Cancer Research Centre (CNIO), led by Alfonso Valencia, together with a group led by Francesco Gervasio at the University College London (UK). Protein dynamics can explain the changes in the shape or dimensional structure that they experience in order to interact with other compounds or speed up chemical reactions. This study push the development of the computational study of protein dynamics, and it is helpful for the design of drugs and for the research about genetic disease. It is published in the journal Proceedings of the National Academy of Sciences (PNAS). As we know, proteins are crucial to the thousands of cellular functions which work in a living organism. It is chains of smaller molecules which are called amino acids that form the protein - a three-dimensional structure. By studying the co-evolution of amino acids, we can reconstruct the form or structure of these biological compounds in their natural surroundings. We can also predict physical contacts between amino acids with higher accuracy and in sufficient number by analyzing the sequences of a given family of proteins, to reconstruct the folding and structure of a protein accurately. Nevertheless, the structure won't remain changeless. It interacts with other biological compounds or with drugs, which is called protein dynamics. The study about it turns out to be extremely difficult no matter through experimental observations or computational tools. "We developed a model in which the amino acids that have a strong co-evolutionary relationship attracted each other, without further additional data," says Simone Marsili, researcher who has also participated in the project. "First, we simulate the folding process and then we can see how the simulations were able to predict the changes in shape of the proteins at different levels of complexity, including those required for kinases to function." By using the latest sequence analysis and 3D modeling technology, this new method combines experimental with genomic data. It also shows that genomic For more wonderful readings, click here:http://www.cusabio.com/Recombinant-Protein/Recombinant-Influenza-A-virus-strain-AEngland8781969-H3N2-Hemagglutinin-11089552.html

New unexpected findings of cell division published

In order to understand more about the mechanisms of cell division, researchers have conducted a series of research using eggs and embryos from frogs and starfish. They unexpectedly found new findings about how animal cells control the forces that shape themselves. The researchers published the paper in the online journal Nature Cell Biology. The study points out that during the process in which a cell divides its cytoplasm to create two daughter cells, which is called cytokinesis, a cell's cortex becomes an excitable medium. We all know that cytokinesis is highly dynamic, but an animal cell has no idea where it will happen before it really happens. The cell has literally ripped itself in two after the things happen. The contractile machinery is quite ephemeral, according to co-author George von Dassow, a University of Oregon biologist at the Oregon Institute of Marine Biology in Charleston. How the cell manages to ensure that the entire surface can participate is not obvious now. However, once specified, only one narrow equatorial band does the crucial act. After chromosomes separate deep in the cell cytoplasm, the surface of the cell immediately enters an excitable state, added von Dassow. During the state, waves of signaling molecules form. They tune in faint signals from deep in the cell to accurately and precisely delineate the working conditions for contractile proteins and other enzymes to assemble at the right place, in the right amount and at the right time during cell division, or during other cell-shape stage. The researchers show in the study that this "cell-cycle-entrained behavior" in the cortex is present in both vertebrates and invertebrates. The dynamic behavior will be clearer combining high-resolution live-cell imaging and mathematical modeling. Related reading:http://www.cusabio.com/Recombinant-Protein/Recombinant-Autographa-californica-nuclear-polyhedrosis-virus-AcMNPV-Viral-cathepsin-11089554.html

Boys are hopeful to be kept free from Duchenne Muscular Dystrophy

In America, muscular dystrophy affects nearly 250,000 people. It occurs when damaged muscle tissue is replaced with fatty, fibrous, bony tissue and loses function. After years' hard working, scientists have found a way to successfully treat Duchenne Muscular Dystrophy, short for DMD, the most common form of the disease which reatly affects boys. So far, a research group has treated dogs with DMD successfully. The researchers plan to set about human clinical trials in the following years. DMD is the most common muscle disease among boys, and no effective treatment exist at present. The new discovery can help to develop a wonderful therapy for this desease, according to Dongsheng Duan, the study leader and the Margaret Proctor Mulligan Professor in Medical Research at the MU School of Medicine. A gene mutation happens on patients with Duchenne muscular dystrophy, which disrupts the production of a protein known as dystrophin. Then a chain reaction that eventually leads to muscle cell degeneration and death will happen due to absence of dystrophin. Later the patients is hard to walk and breathe like an old man. Besides, dystrophin is one of the largest genes in human body. The group conducted a study, which shows a common virus can deliver the microgene to all muscles in the body of a diseased dog. When the dogs were 2 to 3 months old and starting to having sign of DMD, they were injected with the virus. They are now 6 to 7 months old and grow up normally. This virus is a common one and it produces no symptoms in the human body. This virus can yet be regarded as a safe way to spread the dystrophin gene all over our body. It is quite important to treat the disease early before it can do some damage. Click here to know more about life science:http://www.cusabio.com/Polyclonal-Antibody/UBE2C-Antibody-11098184.html

New bacteria is found in deep sea to neutralize industrial carbon dioxide

A health research team from University of Florida has found a type of bacteria plucked from the bottom of the ocean that can be used to work neutralizing large amounts of industrial carbon dioxide in the Earth's atmosphere. As we know that carbon dioxideis a major contributor to build atmospheric greenhouse gases. It can be captured and neutralized in a sequestration process. Most carbon dioxide in the atmosphere is from fossil fuel combustion, which is a kind of flue gas. But it requires a durable, heat-tolerant enzyme to convert the carbon dioxide into a harmless compound. That's what the UF Health researchers are working on. Thiomicrospira crunogena, the new-found bacterium, can produce carbonic anhydrase which can helps remove carbon dioxide in organisms. However, a great amount of carbonic anhydrase is needed to neutralize industrial quantities of carbon dioxide. The researchers found a way to produce the enzyme without repeatedly harvesting it from the sea floor. The production of this enzyme can be completed in a laboratory — using a genetically engineered version of the common E. coli bacteria. At present, the researchers have produced several milligrams of the carbonic anhydrase. More quantities of carbonic anhydrase are need to neutralize carbon dioxide on an industrial scale. Next, the researchers will conduct more research to produce a variant of the enzyme that is both heat-tolerant and fast-acting enough that it can be used in industrial settings. And they want to increase the enzyme's stability and longevity before the enzyme is put into widespread industrial use. Let's look forward to the final results. Read more:http://www.cusabio.com/Polyclonal-Antibody/UBE2C-Antibody-HRP-conjugated-11098185.html

Have you ever noticed cats' eating habits?

A new research shows that cats retain at least seven functional bitter taste receptors. This research was conducted by researchers from Monell Center. They compare cat to related species with differing dietary habits, and found that there is not a strong relationship between the number of bitter receptors and the extent to which a species consumed plants in its diet. This findings threaten the common assumption that bitter taste developed primarily to protect animals from ingesting poisonous plant compounds. Alternate physiological roles for bitter receptors may drive to mold bitter receptor number and function. For instance, recent findings from Monell Center show that bitter receptors are also involved in protecting us against internal toxins, including bacteria related to respiratory diseases. The researchers used previously published data to compare the number of bitter receptor types in cats to that of related species to provide a comparative perspective on the relationship between diet and bitter receptor function. Relative to the 12 receptors identified in cat, dog, ferret, giant panda, and polar bear all had a similar number of bitter receptors. Like cats, these species all belong to the order Carnivora. However, they differ considerably with regard to diet, ranging from strictly carnivorous to Therefore, unlike sweet receptors, there is not a strong relationship between the number of bitter receptors and the extent to which a Carnivora species consumed plants in its diet. However, it is possible that bitter taste could have a protective function related to feeding behavior. As we know, bitter taste could exist to minimize intake of toxic compounds from skin and other components of certain prey species, such as invertebrates, reptiles and amphibians. People always think that cats are picky eaters. Now we know that they have their reasons. They can taste different bitters. The findings may help to make better cat food with certain flavors and nutrients to meet the needs of the cat. The families with cats will be more happy. Read more here:http://www.cusabio.com/Polyclonal-Antibody/FGL2--Antibody-Biotin-conjugated-11098192.html

See the embodiment of innovation from prawns

I guess that you all have heard about the shocking news of super expensive prawns from Qingdao of China recently. The huge prawns bill sparks outrage online in China. Humans should pay for what they have eaten. But do you know what hungry prawns do to get their food? A new research about prewns is published yestoday in the journal PLOS ONE. According to the study, small and hungry prawns are more likely to be resourceful in the face of adversity than their less desperate counterparts. What's worthy to say, size and hunger have different effects, which depends on whether the prawns are acting alone or in a group. To be more specific, small individuals were more likely to innovate when they are alone.However, when they are in a group, size didn't matter and it was the hungry prawns that are more likely to be most resourceful. Innovation can allow individuals, no matter they are prawns or primates, to access new resources and deal with new urgent incidents. But we can know that the drivers of innovation are more complex than previously thought. Read more:http://www.cusabio.com/Recombinant-Protein/Recombinant-human-Target-of-rapamycin-complex-2-subunit-MAPKAP1-11089635.html

What's the link between male fistfights over females and human hand proportionsevolution?

You must be surprised that there is a link between male fistfights over females and human hand proportionsevolution. But what is it? A study conducted byUniversity of Utah have found new support for a theory that human hand proportions evolved not just for fine manipulation, but also to make a clenched fist that would buttress the hand to reduce the chance of injury or fracture during male fistfights over females. You can imagine that open-fist punches and open-handed slaps placed more strain on hand bones, which will increase the risk of injury during fights. The study is published online Oct. 21 in the Journal of Experimental Biology. This syudy is controversial for the moment. What do you think? Click here to know more:http://www.cusabio.com/Recombinant-Protein/Recombinant-Homo-sapiens-Human-Procollagen-C-endopeptidase-enhancer-2-11090019.html

Believe it or not: Poisonous frog species is more easily to become extinct!

Scientists have found that amphibians that use toxins to protect themselves against predators are more easily to face extinction than those frogs who use other types of defence. The result poses a challenge to a long-held evolutionary hypothesis. Animals get different defence mechanisms in the long evolutionary history. The defence mechanisms include chemical defences, such as poisons or irritants, camouflage, warning colouration and mimicry. Scientists have studied the way mechanisms deter predators to a great degree, but they still know little about how the mechanisms impact upon larger evolutionary processes such as speciation, such as the formation and extinction of species. The team examined how rates of extinction and speciation varied across different defensive traits in amphibians in the first large-scale empirical test in animals of its kind, and found animals that use chemical defence show higher rates of speciation, but also higher rates of extinction, compared to those without, resulting in a net reduction in species diversification. On the contrary, the use of warning colouration and mimicry was associated with higher rates of speciation, but unchanged rates of extinction. "There are a number of plausible reasons why the use of chemical defence might lead to higher extinction rates. For example, it could be that there is trade off which leaves prey vulnerable to other kinds of enemies, such as infectious diseases, but we don't yet understand what drives the relationship," lead author of the study, Dr Kevin Arbuckle who is from University's Institute of Integrative Biology. The study was published in the Proceedings of the National Academy of Sciences recently. The findings of this study can help to conserve the endangered species by allowing some predictability of extinction risk from knowledge of antipredator defences. Study of amphibians is a good example, Accoding to Dr Arbuckle. Read more:http://www.cusabio.com/ELISA-Kit/Rabbit-B-cell-lymphoma-extra-large-Bcl-xlELISA-kit-1035341.html

Study shows that the more tunnels means more food colony for ants

A study shows that the more connected the chambers an ant colony builds near the surface entrance, the faster the ants are able to collect nearby sources of food. The study of the underground "architecture" of harvester ant nests was conducted by UC San Diego. Here is the reason: Increased connectivity among chambers result in more social interactions among the ants within the nest. So when one group of ants within a colony which is comprised of individuals working toward a common goal, finds a particularly good source of food, it can more quickly communicate that finding to the rest of the colony. "The volume of the chambers has little influence on the speed of recruitment, suggesting that the spatial organization of a nest has a greater impact on collective behavior than the number of workers it can hold," said Noa Pinter-Wollman, a biologist at UC San Diego who conducted the study, which was published in this week's issue of the journal Biology Letters. She believes they can potentially inspire architectural designs that promote collaboration among humans. "One straightforward lesson that will probably not surprise many architects is that having more corridors connecting offices or rooms will facilitate easier movement of people among them, both promoting interactions and expediting evacuation in emergency," she said. "However, a less obvious potential addition to this lesson would be that increasing the connectivity of locations with an important function, such as break rooms, where people interact—similar to the entrance chamber of the ants—could increase interactions and collaborations." Other research was conducted by Noa Pinter-Wollman, who is a research scientist at UC San Diego's BioCircuits Institute. Her study was the first to find a link between a "naturally occurring nest architecture and the collective actions of the colony that resides in it." While more interconnected chambers near the entrance to the nest provides an advantage to food recruitment, she noted that there is also a downside to having too many chambers near the surface. Such an architecture could introduce structural instabilities that would cause the chambers to collapse during rains when the ground is softened, she noted. It will be interesting to see whether the harvester ants will build deeper chambers than before. More can be read here:http://www.cusabio.com/ELISA-Kit/Goat-Apolipoprotein-B-APOB-ELISA-kit-1042036.html

Caribbean wildlife is threatened by humans, followed by climate change

University of Florida researchers pulled nearly 100 fossils from a flooded cave in the Bahamas reveal a true story of persistence against all odds. They might date back to the time humans stepped foot on the islands. The discovery, published in the Proceedings of the National Academy of Sciences, indicates that many human activities pose a threat to the future of island biodiversity, with modern human-driven climate change not necessarily the most alarming. The new study discusses thirty-nine of the species no longer exsit on Great Abaco Island in the Bahamas. Among them, 17 species of birds likely fell victim to changes in climate and rising sea levels around the end of the Ice Age, about 10,000 years ago. Twenty-two other species of reptiles, birds and mammals persisted through those dramatic environmental changes only to vanish when humans first arrived on the island 1,000 years ago. According to the lead author Dave Steadman, ornithology curator at the Florida Museum of Natural History on the UF campus, understanding more about why some species were more flexible than others in the face of climate and human-driven changes could alter the way we think about conservation and restoration of species today, when scientists fear activities like habitat alteration and the introduction of invasive species could pose the greatest risk to island species. Further exploration of caves on Caribbean islands will begin in December at the budget of $375,000 by the National Science Foundation. Know more about life science:http://www.cusabio.com/ELISA-Kit/Rat-rotavirus-RV-antigen-Ag-ELISA-kit-11089488.html

How do living things deal with great changes?

Svientists have done a research about a small freshwater plant that has evolved to live in harsh seawater. It helps scientists to know how living things adapt to changes in their environment.
The results could help scientists better understand how species have been able to adapt to major shifts of circumstances in the past, such as transferring from water to land, or from light to dark environments.
To adapt new surroundings, organisms must develop ways to perform everyday functions, such as securing food and oxygen, and reproducing. The latest study is one of the first to track such a significant lifestyle transition in the lab, but not rely on fossil clues.
Researchers studied successive generations of a common freshwater algae, Chlamydomonas reinhardtii, in increasingly salty water. These plants have a key role in providing nutrients and removing carbon dioxide from the atmosphere, so understanding how they can evolve from freshwater to seawater is benefit for understanding of the history and diversity of life on Earth.
The scientists found that freshwater algae adapted to seawater in two stages. In the initial time, the plant was able to switch on genes that helped it tolerate low salt levels. Later, as salt levels increased, changes enabled those genes to stay switched on - indicative of a process known as epigenetics.
Later, random changes in the DNA itself during reproduction gave rise to individuals that could tolerate even higher levels of salt. As the algae multiplied, these genes became commonplace in the population, enabling the plant to thrive in seawater. The findings show the importance of genetic and epigenetic changes in adapting to new environments.
Josianne Lachapelle, who led the study, is from the University of Edinburgh's School of Biological Sciences, said: "Our approach enables a new way to understand how living things evolve new ways of life during major transitions. Our findings have significant potential for revealing more about the processes that underpin change during evolution."
The study was published in Evolution. It was carried out by the University of Edinburgh and McGill University in Canada, and supported by the Natural Sciences and Engineering Research Council in Canada.
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Scientists show you the inner ear cell development

Scientists now have created the first high-resolution gene expression map of the newborn mouse inner ear by use of a a sensitive new technology called single-cell RNA-seq on cells from mice. It helps scientists to know more about how epithelial cells in the inner ear develop and differentiate into specialized cells that serve critical functions for hearing and maintaining balance. The potential development of cell-based therapies for treating hearing loss and balance disorders will be pushed by the findings. It were scientists from the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health that conduted the research.
In another study, also published in the journal Nature Communications on October 15, researchers used a similar technique to identify a family of proteins which are important for the development of inner ear cells.
"Age-related hearing loss occurs gradually in most of us as we grow older. It is one of the most common conditions among older adults, affecting half of people over age 75. These new findings may lead to new regenerative treatments for this critical public health issue." said James F. Battey, Jr., M.D., Ph.D., director of the NIDCD.
Sensory epithelial cells in the inner ear include hair cells and supporting cells. The latter one provides the former one with crucial structural and functional support. Both kinds of them located in the cochlea--the snail-shaped structure in the inner ear. They work together to detect sound, so we can hear. On the contrary, hair cells and supporting cells in the utricle, which is a fluid-filled pouch near the cochlea, is critical to maintain our balance. They detect how we move our heads and how our heads are positioned. This information tells our brain whether we are standing or lying down or some other condition. The utricle, with other structures and organs in the body that provide our sense of balance, comprise the vestibular system together.
Medications, infections or disease, injury, or aging can damage hair cells and supporting cells, which results in hearing loss and balance problems. For humans, the cells cannot naturally repair themselves, thus effective treatments are limited.
What's worse, there are only a few thousand of these sensory cells , and they are deep in a bony channel, which makes them hard to study.
To know more about the inner ear cell development, a new technology was used by Matthew Kelley, Ph.D., chief of the Section on Developmental Neuroscience at the NIDCD, and his research team to do a related research. The technology is single-cell RNA-seq, which can extract comprehensive gene activity data from just one cell, while other methods need thousands of cells. Scientists can learn a lot about a cell's individual characteristics and function from knowing which genes are active.
They analyzed 301 cells taken from the cochlea and utricle of newborn mice and found unique patterns in hair cells and supporting cells. Evidence for subgroups of cells within each of these classes was also uncovered. The researchers speculate that the cells' distinct gene activity patterns may reflect specialized functions. The finding also helped the scientists to identify distinct developmental patterns of gene activity. Cells in the vestibular part of the inner ear develop at somewhat different rates, so each cell was at a slightly different point in its maturity when the researchers examined it. By analyzing the cells' gene activity profiles, the scientists were able to identify genes that are active at each stage of development, helping to understand about how the specialized hair cells are formed.
"Using this single-cell profiling technique provides a new option to identify the genetic activity of cells, particularly in systems with limited numbers of cells, like the inner ear," said Kelley, senior author of the study. "Identifying the gene expression maps for the development of inner ear cells is essential to understanding how they form, and may help us create ways to regenerate these cells."
Through the study, the scientists also found that a group of gene regulators called Regulatory Factor Xs (RFX) helps to drive genes that are preferentially active in hair cells. They also showed that RFX genes have an essential role in hearing.
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Is your brain as unique as your fingerprints?

Recently a new study published October in the journal Nature Neuroscience reveals that a person's brain activity is as unique as his or her fingerprints.
According to the study appeared in the journal Nature Neuroscience on October 12, these brains "connectivity profiles" allow researchers to identify individuals from fMRI images of brain activity of more than 100 people.
In most studies published before, fMRI data have been used to draw contrasts between patients and healthy controls, but these studies tend to obscure individual differences which may be important, according to Emily Finn, a Ph.D. student in neuroscience and co-first author of the paper.
Another co-first author Xilin Shen, under the direction of R. Todd Constable, professor of diagnostic radiology and neurosurgery at Yale, with Finn, they compiled fMRI data from 126 subjects who underwent six scan sessions in two days. The researchers kept their eyes on activities in 268 brain regions, especially the coordinated activity between pairs of regions. Highly coorfinated activities suggest that two regions are functionally connected. The strength of these connections across the whole brain helps the researchers to identify individuals from fMRI data alone, no matter the subject was at rest or engaged in a task. They can also predict how subjects would perform when in tasks.
They hope this ability one day might help doctors to predict or even treat neuropsychiatric diseases based on individual brain connectivity profiles.
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Do honey bees enjoy caffeinated nectar like humans do?

Many people enjoy having a cup of fresh coffee to start a new day in the morning. Do any animals also enjoy such a cup of joe? Recently researchers report in the Cell Press journal Current Biology on October 15 that when honey bees find caffeinated nectar, they will also be fascinated.
In fact, it appears that bees may select caffeinated nectar over an uncaffeinated but otherwise equal-quality alternative. As a result, the researchers say, plants may be lacing their nectar with caffeine as a way to pass off cheaper goods.
"We describe a novel way in which some plants, through the action of a secondary compound like caffeine that is present in nectar, may be tricking the honey bee by securing loyal and faithful foraging and recruitment behaviors, perhaps without providing the best quality forage," says Margaret Couvillon from the University of Sussex.
"The effect of caffeine is akin to drugging, where the honey bees are tricked into valuing the forage as a higher quality than it really is. The duped pollinators forage and recruit accordingly," says Roger Schürch, of the University of Sussex and the University of Bern.
They learned from the previous syudies that honey bees are better at learning and remembering particular scents when they are under the influence of caffeine, suggesting a role for reward pathways in the bees' brains. The nectar of many flowering plants contains caffeine in low concentrations. They all wondered how caffeine would affect the natural behaviors as seen in the field.
After research and investigation, they saw an effect of caffeine just about everywhere they looked in foraging and recruitment, and all in the direction to make the colony more faithful to the caffeinated source compared to an equal-quality, uncaffeinated source. According to the individual bees' behaviors, the researchers concluded that caffeinated nectar could reduce honey production in colonies if indeed plants reduce the sweetness of their nectar. The results show that the interests of plants and their pollinators don't always align.
The researchers hope to determine the effects of other compounds. They think that chemistry may be a popular way for plants to get the run upon the pollinators.
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Protein Panoramix summons cell's gene-silencing machinery without affecting the organism's own genes

It is known that organisms must defend themselves against parasitic genetic elements called transposons, from bacteria to humans, and the stake they undertake are high. These pieces of DNA jump around in the genome thus descripting genes. It can cause so much destruction that cells have dedicated surveillance mechanisms to keep them in check.
Defects in these innate defense systems usually result in sterility. In animals, the main defense against troublemaking transposons is the Piwi-interacting RNA pathway.
In new research, scientists led by Cold Spring Harbor Laboratory (CSHL) Professor Gregory Hannon, who is also a Professor and Senior Group Leader at the CRUK Cambridge Institute at the University of Cambridge, have identified a protein the Piwi system uses to guide a cell's gene-silencing machinery to the right spots in the genome, allowing it to keep transposons inactive without interfering with the organism's own genes.
Scientists led by Cold Spring Harbor Laboratory (CSHL) Professor Gregory Hannon, who is also a Professor and Senior Group Leader at the CRUK Cambridge Institute at the University of Cambridge just conducted a new research, identifying a protein the Piwi system uses to guide a cell's gene-silencing machinery to the right spots in the genome, which allows it to keep transposons inactive and not interfere with the organism's own genes. They playfully named the protein Panoramix, after a comic book character who endows others with great power.
The Piwi-interacting RNA pathway, which is active in germline cells - those that give rise to sperm and eggs—is a double-tiered defense system. The most direct line of defense finds and chews up RNA copies of transposons, while a second mechanism finds transposons within the genome and tags them with chemical signals that instruct the cell to keep them safely off. The two modes of control provide the tightest possible clamp on the system.
The study of Hannon and his colleagues are currently focusing on the system that chemically tags transposon DNA. It happens as the elements are preparing to move, when transposon DNA is copied from its place in the genome into RNA, a process known as transcription.
According to Hannon, the Piwi system's challenge is to locate these sequences which look a lot like an organism's own genes, and tag them to make them be recognized by the same machinery a cell uses to switch its own genes off as needed. They think Piwi-interacting RNAs are responsible for finding transposons as RNA copies emerge, but the next was unknown. They hope to figure out the link between this very transposon-specific pathway to the more general repressive machinery of the cell.
They listed a lot of molecules which are possible to play this role and tested them. The Piwi system is so fast that they have found it nearly impossible to follow its components as they silence their natural targets. Later they constructed an artificial Piwi target, then stuck different components of the Piwi system to it and saw what was going on next.
For the most part, cells treated the piece of DNA that encoded the target as one of their own genes. However, when Panoramix was tethered to the artificial RNA target, it was able to halt transcription of the foreign piece of DNA. It means that once transcription began, Panoramix recruited the cell's gene silencing machinery to shut off local transcription and mark the intrusive DNA so that it would remain off, even in future generations.
It's a quite specific phenomenon. Panoramix summons the cell's gene-silencing machinery without affecting the activity of any of the fruit fly's own genes.
The scientists believe that there may be a similar protein that plays the same role in humans and other animals.
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Are we really comfortable living in central heating environment?

A new paper published in the journal Proceedings of the Royal Society B indicates the dangers of living in an "eternal summer." The authors are from a team of researchers at the University of Aberdeen in the U.K. They think that we may be working against health related bodily systems which have evolved during hundreds of thousands of years to protect us from dangers in each unique season. Artificially changing the environment we live in, such as living in central heating environment, may be responsible for this.
Humans are sensitive to seasonal variations, as has been known for scientists—it is in our genes, about a quarter of them by recent estimates. We simulate summer conditions and go on to live in heated homes filled with light and heat when winter comes, doesn't it have any impacts on our bodies? It is still an unsolved mystery. The researchers evolved in this paper believe that there is an impact, which is not good.
According to the researchers, our bodies have been programmed to adapt regularly to seasonal changes. Important genes have evolved to the nudge the production of proteins, normally would be responsible for helping guard against ailments like the flu. If we stay in relatively high temperature, which seems to fool our body into thinking that they will be in summer all the time, it will make us more vulnerable. They also point out that modern people are protecting themselves artificially against global warming. When the temperature grows higher, we tend to keep the thermostat at the level we like. However, it could be dangerous, for we don't know what the real condition outside is when we are in the environment created as we like. It leads to disconnect between the reality and us.
The study provides many kinds of scenarios surrounding seasonal disruption, stressing out what the researchers believe are key areas of concern—all from a variety of viewpoints which include an overall environmental perspective, one focused on agricultural and others focused on anthropological, veterinary or biomedical standpoints—with each circling around the de-synchronization of our internal biology and the real environment outside of our virtual existences. Each topic can be an area of study and they can be put together to form the basis of a framework for trans-disciplinary research, which can finally unlock the secret of the impact of humans living in artificial environments, according to the researchers.
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Wars between deadly bacteria and the immune system: new drugs are coming up

The Group A Streptococcus (strep) infections are usually caused by a particularly nefarious strain - M1T1. One of the reasons for this name is the type of tentacle-like M protein projecting from the bacterium's surface. Despite that a lot of studies before proposed ways M1 might contribute to strep virulence, researchers at University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences have given another explanation that is more persuasive than those ones: M1's ability to hold off antimicrobial peptides—natural antibiotics that comprise one of the immune system's front lines of defense.
The new study was published October 14 by Cell Host & Microbe. It emphasizes the importance of antimicrobial peptides, thus suggesting a new therapeutic approach to helping the immune system get rid of this crafty pathogen.
"The famous strep M1 protein has been shown to have numerous virulence properties that aid in bacterial colonization, fool the immune system or provoke inflammation," said senior author Victor Nizet, MD, professor of pediatrics and pharmacy. "We found that a major contribution of M1 protein to severe invasive infections can be explained by its ability to inactivate antimicrobial peptides."
More than 700 million infections all over the world each year, most notably strep throat and "flesh-eating" skin infections are caused by Group A strep. The body unleashes small antimicrobial peptides reacting to strep and other bacterial infections. These short chains of amino acids are deadly to bacteria in many ways such as summoning reinforcements in the form of infection-fighting cells or poking holes in bacterial membranes.
After research, the team found that Group A strep lacking M1 protein were easily killed by cathelicidin, a critical antimicrobial peptide. But they were rescued when armed with added M1 protein.
Besides, a research conducted on a mouse model showed that M49, a less virulent strain of strep, caused larger skin lesions in mice lacking cathelicidin than in normal, cathelicidin-producing mice. It means that M49 is unable to stiff-arm antimicrobial peptides the way M1 can, which makes the immune response more effective and the M49 bacteria less virulent.
The study stresses out the need to fortify or optimize antimicrobial peptides to improve the odds of defending infection of immune system. To know more about the interaction between M1 and antimicrobial peptides may develop new potential way of treating Group A infections. It's considerable to find an effective drug to help immune system fight against the infections by itself.
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A new study shows that external environment and oxidation threats DNA most

Recently a study has found that forces from external environment and oxidation may be the greatest threats to an organism's ability to repair damage to its own DNA.
The results are published in the journal of the Proceedings of the National Academy of Sciences. The results are based on the first comprehensive, whole genome analysis of spontaneous mutation in the bacterium Escherichia coli.
"Our study investigated 11 DNA repair pathways previously identified as resulting in spontaneous mutations," said Foster, a professor in the IU Bloomington College of Arts and Sciences' Department of Biology. "The striking result was that only loss of the ability to prevent or repair oxidative DNA damage significantly impacted mutation rates. ... All other forms of DNA damage arising within the organism did not disturb the overall accuracy of DNA replication in normally growing cells.
"These results suggest that DNA repair pathways may exist primarily to defend against externally induced damage to the genome," she said. Foster's lab and her work concentrates on DNA mutagenesis and repair.
E. coli is a bacterium discovered in mammalian digestive tracts. It's more known as a source of food poisoning. It was chosen for the research because the biological pathways that control DNA repair have changed little as more complex organisms evolved, increasing the chances that the study's results are applicable to higher forms of life, including humans.
Foster's lab created the world's most comprehensive picture of genetic mutation in the species by tracing changes in E. coli's complete genome over the course of 200,000 generations.
The IU team concentrated on 11 processes identified in other studies as causing mutation when deactivated, to focus their investigation on the relative importance of the pathways that repair DNA damage to genetic mutation. The pathways were isolated using 11 different strains of E. coli, each defective for one of the specific pathways.
After investigation, the DNA repair pathways under investigation fell into three broad categories. They were the activities of error-prone DNA polymerases, repair of internally induced DNA damage, including oxidation, and repair of DNA damage due to external agents. Each pathway is more or less specific for a given type of DNA damage.
External agents such as radiation, chemical compounds and platinum-based compounds, are forces that affect DNA. And internal agents that damage DNA are produced by the body's own normal processes. Oxidation occurs in the body as a result of metabolic processes that use oxygen, creating molecules known as "free radicals" that steal electrons from other molecules in the body, causing damage. Many types of cancer and even aging have been linked to DNA oxidation
The IU scientists used whole genome sequencing to catalog the specific genetic changes that resulted from loss of each repair pathway.
Foster said that, surprisingly, the IU team found that none of the pathways resulted in mutations except the ones that deal with damage from oxidation. This means that the other types of damage—from either internal or external causes—are not a great threat to normally growing cells.
These pathways may be important, however, when cells are exposed to external agents or other forms of stress.
The more complete picture of genetic mutation—made possible by the IU team's previous documentation of the bacterium's evolution over 200,000 generations—is likely responsible for the difference in the study's results compared to previous research implicating all 11 DNA repair pathways in genetic mutation, Foster said.
"Previous studies on mutational processes have relied on reporter genes"—single genes that signal larger changes across the genome—"to detect mutations, and these may not be representative of the genome as a whole," she said. "While reporter genes can reveal important mutational processes that occur at particular spots in the DNA, when the whole genome is the target, these localized errors don't appear to contribute to overall mutation."
Foster's next step is investigate DNA repair functions in cells under stress, which may provide a more complete model for mutational processes in living human cells existing in different states and environments all over the body.
The experiments and research can help scientists understand more about DNA repair in our body and the importance of them.
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A team finds the first sensor mechanism of detecting electric fields

Many animals have the ability to sense and react to electric fields. Living human cells will move along an electric field for wound healing. But how do they sense the electric fields? A research team led by Min Zhao at the UC Davis Institute for Regenerative Cures now has found the first "sensor mechanism" that allows a living cell to detect an electric field. Their work is published in the journal Nature Communications on Oct. 9.
These researchers believed that there were several types of sensing mechanisms, and none of them were known. Now they provide experimental evidence to suggest a mechanism which has not been even hypothesized before. It is a two-molecule sensing mechanism.
Zhao and his colleagues have been studying these "electric senses" in cells from both larger animals and in the soil-dwelling amoeba Dictyostelium. By knocking out some genes in Dictyostelium, they previously identified some of the genes and proteins that allow the amoeba to move in a certain direction when exposed to an electric field.
In the new research a human cell line, they found that two elements, a protein called Kir4.2 which is made by gene KCNJ15, and molecules within the cell called polyamines, were needed for signaling to occur. Kir4.2 is a potassium channel. It forms a pore through the cell membrane that allows potassium ions to enter the cell. Such ion channels are often involved in transmitting signals into cells. Polyamines are molecules within the cell that carry a positive charge.
During the researche, they found that when the cells were in an electric field, the positively-charged polyamines tend to accumulate at the side of the cell near the negative electrode. The polyamines bind to the Kir4.2 potassium channel, and regulate its activity.
Zhao said that haven't got definitive evidence of how "switching" of the potassium channel by polyamines translates into directional movement by the cell. But the exploration of the sixth sense will never stop.
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Marine ecologists say that the climbing human CO2 emissions result in collapsing of food chain

The expected ocean acidification and warming may lead to a reduction in diversity and numbers of various key species that underpin marine ecosystems around the world, according to the paper published in the journal Proceedings of the National Academy of Sciences (PNAS) recently.
"This 'simplification' of our oceans will have profound consequences for our current way of life, particularly for coastal populations and those that rely on oceans for food and trade," says Associate Professor Ivan Nagelkerken, Australian Research Council (ARC) Future Fellow with the University's Environment Institute.
The researcher conducted a  'meta-analysis' of the data from 632 published experiments covering tropical to artic waters, and a range of ecosystems from coral reefs, through kelp forests to open oceans.
"We know relatively little about how climate change will affect the marine environment," says Associate Professor Nagelkerken and fellow University of Adelaide marine ecologist Professor Sean Connell. "Until now, there has been almost total reliance on qualitative reviews and perspectives of potential global change. Where quantitative assessments exist, they typically focus on single stressors, single ecosystems or single species.
"This analysis combines the results of all these experiments to study the combined effects of multiple stressors on whole communities, including species interactions and different measures of responses to climate change."
They found that there would be "limited scope" for acclimation to warmer waters and acidification. Little species can avoid the negative effects of increasing CO2 except microorganisms, which are expected to increase in number and diversity.
Seeing from the total food web, primary production from the smallest plankton is expected to increase in the warmer waters but this often doesn't translate into secondary production. It means decreased productivity under ocean acidification.
According to Associate Professor Nagelkerken, with higher metabolic rates in the warmer water which results in a greater demand for food, there is a mismatch with less food available for carnivores, which are bigger fish that fisheries industries are based around. They think there will be species collapse from the top of the food chain down.
Besides, acidification would decrease the dimethylsulfide gas production by ocean plankton which helps cloud formation and therefore in controlling the Earth's heat exchange.
From the global analysis we can see that human CO2 emissions are badly affecting global fisheries and ocean ecosystems. That's a terrible picture that we don't want to see. Shouldn't we do something positive next?
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How does DNA operate to drive cell activities?

A research group from Baylor College of Medicine revealed in unparalleled detail the three-dimensional structure of biologically active DNA. Their report is published in the journal Nature Communications online.
"The beautiful double-helical structure we all know and love is not the actual active form of DNA," said Dr. Lynn Zechiedrich, professor in the department of molecular virology and microbiology, and co-contributing author with Dr. Wah Chiu, professor in the Verna and Marrs McLean Department of Biochemistry and Molecular Biology.
Chiu and Zechiedrich, cooperating with Dr. Steven Ludtke and Dr. Michael Schmid, who is also at Baylor College of Medicine, and Dr. Sarah A. Harris of the University of Leeds in the United Kingdom, examined tiny DNA minicircles containing only 336 base pairs, using methods from chemistry, physics, math and computer modeling. Base pairs are the building blocks of genetic material.
Previous studies were on short fragments of linear DNA, but human DNA is constantly moving around in our body, and it coils and uncoils. Researchers can't coil linear DNA and study it, so they had to make circles so the ends would trap the different degrees of winding, according to Zechiedrich.
In the human body, each cell holds about a meter of DNA which is ten million times longer than the tiny circles the team made. In the research, the researchers wound or unwound a single turn when the DNA double helix comprising their circles and used very powerful microscopes to see how the winding changed what the circles looked like.
They did a test to ensure the tiny twisted up DNA circles that they made in the lab were biologically active. They used purified human topoisomerase II alpha. It's an essential enzyme that manipulates DNA and important target of anticancer drugs. The results indicate that the circles must look and act like the much longer DNA that topoisomerases encounter in human cells.
"Being able to observe individual DNA circles allows us to understand the different structures of biologically active DNA. Each of these different structures facilitates how DNA interacts with proteins, other DNA and RNA, and anticancer drugs, adapting to the cell processes required," said Dr. Jonathan Fogg, the other lead author of the publication, also of Baylor College of Medicine.
The researchers hoped to see the opening of base pairs when the DNA was underwound, but they were surprised to see the opening for the overwound DNA. They supposed this disruption of base pairs may cause flexible hinges, allowing the DNA to sharply bend, and it may help to explain how a meter of DNA can be pushed into a single human cell.
What the researchers will be aimed at is to add other components of the cell or anticancer drugs to figure out how the DNA shapes change. More researchers are joining in to get new findings.
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New technology developed to sequence genes: faster, better and cheaper

If DNA is called the blueprint of life, RNA is the construction contractor who interprets it. Therefore, it is quite important to sequence RNA for it shows you what is happening inside a cell.

Recently, researchers from UConn Institute of Systems Genomics have sequenced the RNA of the most complicated gene known in nature. What they use is a hand-held sequencer which is not as big as a cell phone.

Genomicists Brenton Graveley from the UConn Institute of Systems Genomics, postdoctoral fellow Mohan Bolisetty, and graduate student Gopinath Rajadinakaran together with UK-based Oxford Nanopore Technologies to show that the company's MinION nanopore sequencer can sequence genes faster, better, and at a much lower cost than the standard technology. Their findings were published in Genome Biology on Sept. 30.

If your genome was a library and every gene was a book, some genes would be straightforward reads, but some would be more like a "Choose Your Own Adventure" novel. Researchers tend to know which version of the gene is actually expressed in the body, but for complicated choose-your-own-adventure genes, it has been impossible. The researchers solved the problem in two parts.

The first was to find a better gene-sequencing technology. They used the old existing technology to sequence genes. This technique won't work for choose-your-own-adventure genes, because if you copy them the way the body does, using RNA, each copy can be slightly or very different from the next. Such different versions of the same gene are called isoforms. When the different isoforms get chopped up and sequenced, it becomes impossible to accurately compare the pieces and figure out which versions of the gene you started with.

Last year, the impossible things became possible. Oxford Nanopore, a company based in the UK, released its new nanopore sequencer, and offered one to Graveley's lab. The nanopore sequencer, called a MinION, works by feeding a single strand of DNA through a tiny pore. The pore can only hold five DNA bases - the 'letters' that spell out our genes - at a time. There are four DNA bases, G, A, T, and C, and 1,024 possible five-base combinations. Each combination creates a different electrical current in the nanopore. GGGGA makes a different current than AGGGG, which is different again than CGGGG. By feeding the DNA through the pore and recording the resulting signal, researchers can read the sequence of the DNA.

In the second part, the researchers chose the most complex one known, Down Syndrome cell adhesion molecule 1 (Dscam1), which controls the wiring of the brain in fruit flies. Dscam1 has the potential of making 38,016 possible isoforms, and every fruit fly has the potential to make every one of them, yet how many of these versions are actually made remains unknown.

Dscam1 looks like this: X-12-X-48-X-33-X-2-X, where X's denote sections that are always the same, and the numbers indicate sections that can vary (the number itself shows how many different options there are for that section).

The researchers had to convert Dscam1 RNA into DNA to study how many different isoforms of Dscam1 actually exist in a fly's brain. If DNA is the book or set of instructions, RNA is the transcriber that copies the book so that it can be translated into a protein. The DNA includes the instructions for all 38,016 isoforms of the Dscam1 gene, while each individual Dscam1 RNA contains the instructions for just one. No one had yet used a MinION to sequence copies of RNA, and though it was likely it could be done, demonstrating it and showing how well it worked would be a substantial advance in the field.

Rajadinakaran took a fruit fly brain, extracted the RNA and converted it into DNA, isolated the DNA copies of the Dscam1 RNAs, and then ran them through the MinION's nanopores. In this one experiment, they not only found 7,899 of the 38,016 possible isoforms of Dscam1 were expressed but also that many more, if not all versions are likely to be expressed.

The study shows that gene sequencing technology can now be accessed by more researchers than before, since the MinION is both relatively inexpensive and highly portable.

"This type of cutting-edge work puts UConn at the forefront of technology development and strengthens our portfolio of genomics research," says Marc Lalande, director of UConn's Institute for Systems Genomics. "Also, thanks to the investments in genomics through the University's Academic Plan, Brent Graveley can leverage his expertise so that faculty and students across our campuses will successfully compete for grant dollars and launch bioscience ventures."

The researchers are planning to sequence every bit of RNA from beginning to end inside a single cell. This can't be done by traditional gene sequencers. This new technology is supposed to transform the way we study RNA biology and the type information.

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New report shows relationship between ecotourism and wildlife

More and more tourists are willing to vacation in far-flung places around the places where they can use their money to make a positive impact on local people and local wildlife. However, researchers published a report in Trends in Ecology & Evolution on October 9th showed that the interactions between wild animals and friendly ecotourists eager to snap their pictures may unintentionally put animals at greater risk of being eaten.
It is obvious that ecotourism business is booming these years. "Recent data showed that protected areas around the globe receive 8 billion visitors per year; that's like each human on Earth visited a protected area once a year, and then some!" said Daniel Blumstein of the University of California, Los Angeles. "This massive amount of nature-based and ecotourism can be added to the long list of drivers of human-induced rapid environmental change."
The report shows the viewpoint that when animals interact with humans in benign ways, they may lower their guard. As they get used to staying with humans in comfortable environment, they may become bolder in other situations. It is difficult for them to recognize real predators.
Ecotourism is actually similar to domestication or urbanization. In all three cases, regular interactions between people and animals may lead to habituation. This is another kind of taming. A process that results from evolutionary changes but also from regular interactions with humans happens: domesticated silver foxes become more docile and less fearful. Domesticated fish are less responsive to simulated predatory attacks. Fox squirrels and birds that live in urbanized areas are bolder. It takes more to make them flee.
Besides, the presence of humans can also scare off natural predators, which creates a relatively safe environment for the smaller animals which could have become bolder. When humans are around, for example, vervet monkeys have fewer run-ins with predatory leopards.
The researchers hope more research on the interactions of humans with wildlife can be stimulated by this research. It will help people understand how different species and species in different situations respond to human visitation and under what conditions human act may put these species in danger situation.
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Scientists found new protein factors to control bacterial growth

It is well-known by those biochemists that crucial cell processes depend on a highly regulated cleanup system known as proteolysis, where specialized proteins called proteases degrade damaged or no-longer-needed proteins. These proteases must destroy their own targets but not damage other proteins. However, the process is still not very clear to the in many cases.
Recently, researchers in Peter Chien's group from the department of biochemistry and molecular biology at the University of Massachusetts Amherst report that they have found how an essential bacterial protease controls cell growth and division. You can read the details in the current issue of Cell.
The lead author of the report is Kamal Joshi, a doctoral candidate in the Chien lab. He conducted experiments in the model bacterium Caulobacter crescentus. In this species, the ability to grow and replicate DNA is regulated by ClpXP, a highly conserved protease that in many bacteria allows them to cope with stressful environments such as the human body. Understanding how ClpXP is controlled could open a path to antibiotics that inhibit harmful bacteria in new ways.
How proteolysis controls Caulobacter growth is still a secret in the field.
It is strange that ClpXP only destroys its target proteins at a specific time. They think there must be a factor they've ignored. There are some genetic evidence pointing to certain additional proteins, but no more details are discovered.
The lab purified all available proteins and designing experiments to query how they interacted and what functions were affected in their presence or absence. They found that the ClpXP protease could not by itself destroy the target proteins, and the additional regulatory proteins they had detected were controlling different parts of the process.
Later, they found these newly identified regulatory adaptors worked in a step-wise hierarchical way. The first adaptor was directly responsible for degrading a handful of proteins, but it could also recruit an additional adaptor that would deliver a different set of proteins and bind even more adaptors. Working with the Viollier lab from the University of Geneva, Switzerland, the researchers found scores of additional protease targets that were destroyed in this hierarchical way.
It is believed that this new fundamental knowledge may offer an entirely new target for developing new antibiotics with a high potential to avoid triggering drug resistance, because new compounds could be devised which would not simply target all bacterial growth, but only a specific pathway, such as virulence.
You don't force the benign bacteria to develop resistance in this approach because their growth isn't threatened. The hope is to target only those pathogenic organisms that are trying to overcome the stressful environment inside the human body.
Though the researchers haven't known if these adaptor factors are common among all bacteria, but they decide to figure out.
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Engineer stem cells to study leukemia better

In order to better understand the mechanisms behind a form of leukemia caused by changes in a key gene, scientists engineered stem cells for leukemia. The study was led by Mount Sinai researchers and published in the journal Cell Reports online.
Before then, it had been established that inherited changes in the DNA code for the gene PTPN11 cause Noonan syndrome, a genetic disease that comes with a high risk for the blood cancer called juvenile myelomonocytic leukemia (JMML). Scientists still didn't know the mechanisms behind the disease and what influences its severity.
What's worse, currently the only treatment for JMML - a bone marrow transplant to replace the hematopoietic stem cells that become blood cells - is effective only in 50% of patients. This pushes scientists to step more toward designing better treatments.
"By studying an inherited human cancer syndrome, our study clarified early events in the development of one kind of leukemia," said corresponding study author Bruce D. Gelb, MD, Gogel Family Chair and Director of The Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai. "More than just creating a model of a disease, we were able to prove that mechanisms seen in our model also happen in the bone marrow of people with this kind of leukemia. The work also provided new targets for the field to develop new drugs against in JMML."
In order to better understand diseases with a genetic component, scientists choose the approach of taking skin cells from patients with a disease and use enzymes to coax the cells back along the differentiation pathway to become induced pluripotent stem cells or iPSCs. Such cells can then be programmed to mature into cells including hematopoietic (blood) cells, which re-create a specific version of each person's genetic disease in a petri dish for study.
In the study, authors say that hematopoietic cells produced from induced stem cells with PTPN11 mutations known to cause JMML indeed act like cells seen in these patients. According to them, "gain of function" genetic changes that happen to increase this protein's expression were enough to cause leukemia-related changes in cells.
iPSCs used to model cancers are often created from cancer cells, a process with comes with a great many mutations (changes in the gene code) in genes that are part of the unstable, frequent cell division and multiplication seen in cancer. By starting with skin cells of JMML patients with inherited PTPN11 mutations, scientists could create JMML cells with only these mutations, screening out the "genetic noise" that can obscure disease mechanisms.
The results of the study show that the severity of this form of leukemia arises from the degree of changes in the gene PTPN11, altering the protein it codes for, SHP-2, and biologic pathways related to it. And these proteins promise to become a focus of future drug design efforts, According to Dr. Gelb.
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Researchers develop a platform to recognize specific target antibodies

A new study may completely change the slow, cumbersome and expensive process of detecting the antibodies that can help with the diagnosis of infectious and auto-immune diseases such as rheumatoid arthritis and HIV. An international research team have designed and synthetized a nanometer-scale DNA "machine" whose customized modifications enable it to recognize a specific target antibody. This new approach is said to support the development of rapid, low-cost antibody detection at the point-of-care, eliminating the treatment initiation delays and increasing healthcare costs associated with current techniques.
The binding of the antibody to the DNA machine causes a structural change which generates a light signal. The sensor does not need to be chemically activated and is rapid - in five minutes - enabling the targeted antibodies to be easily detected, even in complex clinical samples such as blood serum.
This DNA nanomachine is highly versatile that can be in fact custom-modified so that it can detect a huge range of antibodies, this makes our platform adaptable for many different diseases.
The modular platform provides significant advantages over existing methods for the detection of antibodies. It may prove to be useful in a range of different applications such as point-of-care diagnostics and bioimaging.
Besides, this platform has an advantage of low-cost. The materials needed for one assay cost about 15 cents, which makes the approach very competitive in comparison with other quantitative approaches.
These preliminary results make the researchers exciting. There are more to make this approach available to everyone.
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Observe living cells by use of a new DNA stain

Though bio-imaging is helpful to visualize the inner workings of a cell while it is still alive, the living cells put under the microscope risk being killed by the light and the fluorescent dyes used to highlight their structures. It is much like sunburnt - live cells are sensitive to intense light and the ultraviolet and blue lights used in live-cell imaging are the most dangerous. Now, EPFL scientists have developed a new DNA stain that can be used to safely image live mammalian cells for days even under demanding imaging conditions.
The work about this new DNA stain is published in Nature Communications.
Fluorescent stains that light up a cell's DNA allow people to track key biological processes such as cell division thus they are popular in live-cell imaging. But current DNA stains are themselves toxic or require types of light that can damage the cells. Ideally, a safe DNA fluorescent stain would be activated in the safer far-red spectrum of light.
What's more, a lot of DNA stains are not compatible with super-resolution microscopy, a modern imaging technique that can capture images of cells at higher resolution than that allowed by regular microscopes. So the bio-imaging community has been waiting for a DNA stain that shows low toxicity, works with far-red light and can be used in superresolution microscopy.
The lab of Kai Johnsson at EPFL has now developed a DNA stain that can satisfy all of the needs. The scientists combined two molecules together - One is a fluorescent molecule (silicon rhodamine or SiR) that works in the far-red spectrum and was previously developed in Johnsson's lab, and the other one is a well-known DNA stain Hoechst (the chemical name is bisbenzimide). Finally, the scientists named the DNA stain "SiR-Hoechst".
The new stain works by binding to a part of the DNA helix known as the "minor groove". Once bound, it turns on and emits a bright fluorescent red light. This is a tremendous advantage, as the stain produces very little noise - if it has not found its target, it stays "off". More importantly, SiR-Hoechst can bind to DNA without affecting its biological function in the cell. And because all cells possess DNA, the probe can be used across numerous species, types of cells, and tissues.
There is little risk of damage to cells because SiR-Hoechst works with far-red light. Besides, the light that it emits can be easily distinguished from any background fluorescence of living cells. These features give SiR-Hoechst a clear advantage over other DNA stains - it can safely maintain high-quality staining in live cells for over 24 hours, allowing biologists to identify individual cells in tissue or culture, or track delicate processes in real time.
This stain can be used in live-cell super-resolution imaging, helping to solve problems in DNA imaging in cells and biological tissues with exquisite resolution.
The SiR-Hoechst makes bioimaging safer. That is, it realizes the dream of observing details of nature without impacting them.
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