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Parenting from before conception: Babies' health doesn't 'start from scratch'

Parenting from before conception: Babies' health doesn't 'start from scratch' | Amazing Science | Scoop.it
There's now overwhelming evidence that a child's future health is influenced by more than just their parents' genetic material, and that children born of unhealthy parents will already be pre-programmed for greater risk of poor health, according to researchers. "The reality is, the child doesn't quite start from scratch -- they already carry over a legacy of factors from their parents' experiences that can shape development in the fetus and after birth. Depending on the situation, we can give our children a burden before they've even started life," experts say.


At fertilization, the gametes endow the embryo with a genomic blueprint, the integrity of which is affected by the age and environmental exposures of both parents. Recent studies reveal that parental history and experiences also exert effects through epigenomic information not contained in the DNA sequence, including variations in sperm and oocyte cytosine methylation and chromatin patterning, noncoding RNAs, and mitochondria. Transgenerational epigenetic effects interact with conditions at conception to program the developmental trajectory of the embryo and fetus, ultimately affecting the lifetime health of the child. These insights compel us to revise generally held notions to accommodate the prospect that biological parenting commences well before birth, even prior to conception.

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Critical Immune System Control Mechanism Discovered

Critical Immune System Control Mechanism Discovered | Amazing Science | Scoop.it

Researchers at the Salk Institute say they have discovered a key control mechanism on regulatory T cells (Tregs) that determine if they send a halt signal to killer T cells during a pathogenic attack on the immune system. The new research (“Function of a Foxp3 cis-Element in Protecting Regulatory T Cell Identity”), published in Cell, could help develop treatments for autoimmune disorders as well as some types of cancer, according to the scientists.


When faced with pathogens, the immune system summons a swarm of cells made up of Tregs and killer T cells. Basically, Tregs tell killer T cells to halt “their attack” when invaders are cleared. Without this signal killer T cells continue their activities and turn on the body, causing inflammation and autoimmune disorders such as allergies, asthma, rheumatoid arthritis, multiple sclerosis, and type 1 diabetes.


“We discovered a mechanism responsible for stabilizing the cells that maintain immune system balance,” said senior author Ye Zheng, Salk Ph.D., assistant professor and holder of the Hearst Foundation Developmental Chair. “The immune system plays a huge role in chronic inflammation and if we can better understand the immune system, we can start to understand and treat many diseases.”


Tregs are like the surveillance system of the immune response, noted Dr. Zheng, adding that this surveillance system is “key to healthy immune reactions, but it can be kicked into overdrive or turned entirely off.”  For about a decade, researchers knew that the key to Tregs' peacekeeping ability was the Foxp3 gene, but they weren't sure how exactly it worked. Scientists also knew that under certain conditions, Tregs can go rogue: They transform into killer T cells and join in the immune system battle. This change means that they lose the ability to send a “halt” signal and add to inflammation.


In the new paper, Dr. Zheng's lab reports that a particular genetic sequence in Foxp3 is solely responsible for the stability of a Treg. If they removed the sequence, dubbed CNS2, Tregs became unstable and often morphed into killer T cells—the type of cell they are supposed to be controlling—resulting in autoimmune disease in animal models.


“Conserved noncoding sequence 2 (CNS2), a CpG-rich Foxp3 intronic cis-element specifically demethylated in mature Tregs, helps maintain immune homeostasis and limit autoimmune disease development by protecting Treg identity in response to signals that shape mature Treg functions and drive their initial differentiation,” wrote the researchers. “In activated Tregs, CNS2 helps protect Foxp3 expression from destabilizing cytokine conditions by sensing TCR/NFAT activation, which facilitates the interaction between CNS2 and Foxp3 promoter. Thus, epigenetically marked cis-elements can protect cell identity by sensing key environmental cues central to both cell identity formation and functional plasticity without interfering with initial cell differentiation.”

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Escape from Telomere-Driven Crisis Is DNA Ligase III Dependent

Escape from Telomere-Driven Crisis Is DNA Ligase III Dependent | Amazing Science | Scoop.it

Short dysfunctional telomeres are capable of fusion, generating dicentric chromosomes and initiating breakage-fusion-bridge cycles. Cells that escape the ensuing cellular crisis exhibit large-scale genomic rearrangements that drive clonal evolution and malignant progression. We demonstrate that there is an absolute requirement for fully functional DNA ligase III (LIG3), but not DNA ligase IV (LIG4), to facilitate the escape from a telomere-driven crisis. LIG3- and LIG4-dependent alternative (A) and classical (C) nonhomologous end-joining (NHEJ) pathways were capable of mediating the fusion of short dysfunctional telomeres, both displaying characteristic patterns of microhomology and deletion. Cells that failed to escape crisis exhibited increased proportions of C-NHEJ-mediated interchromosomal fusions, whereas those that escaped displayed increased proportions of intrachromosomal fusions. We propose that the balance between inter- and intra-chromosomal telomere fusions dictates the ability of human cells to escape crisis and is influenced by the relative activities of A- and C-NHEJ at short dysfunctional telomeres.


http://www.cell.com/cell-reports/pdf/S2211-1247(14)00574-9.pdf

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Scientists turn a brown butterfly purple—in just six generations

Scientists turn a brown butterfly purple—in just six generations | Amazing Science | Scoop.it

For most forms of life, coloration is synonymous with the presence of a pigment that absorbs some wavelengths and reflects others. But butterflies and birds are different. Their wings and features have incredibly fine, microscopic features that can help channel light and create interference patterns that enhance some wavelengths while suppressing others.


Now, researchers have tested just how readily these complex optical systems can evolve. In just six generations of selection, they took a brown butterfly and shifted it to a rich, purple color. The species chosen for this work was Bicyclus anynana, an African species that also goes by the name of "squinting brown bush." As the name implies (and the image above shows), the majority of its pigmentation is brown, with a few prominent eye spots.


Several traits made this species a desirable choice for the work, not the least of which was practicality—it's easy to grow them in dense colonies in the lab. But pigmentation also mattered. "Squinting brown bush" coloration is a bit more complex than the human eye would lead us to believe, in that the butterfly's wings also readily reflect ultraviolet light. And two members of the genus have evolved purple pigmentation in the past, suggesting that a color change was within the realm of possibility.


The researchers started by checking the absorption spectrum of their existing lab strain of butterflies. This showed a peak of reflection at 300nm wavelengths, well within the UV range of the spectrum. But the peak was broad and varied from individual to individual, so the researchers selected the males and females that had the peak shifted closer to the visible spectrum, then mated them to produce the next generation. They repeated the process of mating and measuring reflection for five additional generations.


After six generations of selective breeding, the peak reflection had shifted well into the purple at 400nm. Six generations in this species take less than a year. The experiment actually involved eight generations total, though, because two generations saw low numbers of offspring and were simply allowed to mate randomly to build up the numbers again.


The researchers then put the butterfly wings under the microscope. The wings are a complicated, two-layer affair, with upper scales held on a network of pillars and interconnections, plus a lower scale attached to the body of the wing. Pigments are present in each, and both scale layers reflect and redirect light that reaches them.


The researchers found that both layers of scales evolved the ability to reflect more violet light, but the lower level of scales showed the most dramatic changes. Changes on the surface of these scales, notably a thinning of some ridges present on their surfaces, seem to account for much of the color difference (although there may also be some pigmentation changes). Scales also got significantly thicker in the animals with purple wings.

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Mathematical theory proposed by Alan Turing in 1952 can explain the formation of fingers

Mathematical theory proposed by Alan Turing in 1952 can explain the formation of fingers | Amazing Science | Scoop.it
Researchers have shown that BMP and WNT proteins are the so-called 'Turing molecules' for creating embryonic fingers. Findings explain why polydactyly -- the development of extra fingers or toes -- is relatively common in humans, affecting up to one in 500 births, and confirms a fundamental theory first proposed by the founding father of computer science, Alan Turing, back in 1952.


Alan Turing, the British mathematician (1912-1954), is famous for a number of breakthroughs, which altered the course of the 20th century. In 1936 he published a paper, which laid the foundation of computer science, providing the first formal concept of a computer algorithm. He next played a pivotal role in the Second World War, designing the machines which cracked the German military codes, enabling the Allies to defeat the Nazis in several crucial battles. And in the late 1940's he turned his attention to artificial intelligence and proposed a challenge, now called the Turing test, which is still important to the field today.


His contribution to mathematical biology is less famous, but was no less profound. He published just one paper (1952), but it triggered a whole new field of mathematical enquiry into pattern formation. He discovered that a system with just 2 molecules could, at least in theory, create spotty or stripy patterns if they diffused and chemically interacted in just the right way.


His mathematical equations showed that starting from uniform condition (ie. a homogeneous distribution -- no pattern) they could spontaneously self-organise their concentrations into a repetitive spatial pattern. This theory has come to be accepted as an explanation of fairly simple patterns such as zebra stripes and even the ridges on sand dunes, but in embryology it has been resisted for decades as an explanation of how structures such as fingers are formed.


Now a group of researchers from the Multicellular Systems Biology lab at the CRG, led by ICREA Research Professor James Sharpe, has provided the long sought-for data which confirms that the fingers and toes are patterned by a Turing mechanism. "It complements their recent paper (Science 338:1476, 2012), which provided evidence that Hox genes and FGF signaling modulated a hypothetical Turing system. However, at that point the Turing molecules themselves were still not identified, and so this remained as the critical unsolved piece of the puzzle. The new study completes the picture, by revealing which signaling molecules act as the Turing system" says James Sharpe, co-author of the study.


The approach taken was that of systems biology -- combining experimental work with computational modelling. In this way, the two equal-first authors of the paper were able to iterate between the empirical and the theoretical: the lab-work of Jelena Raspopovic providing experimental data for the model, and the computer simulations of Luciano Marcon making predictions to be tested back in the lab.


By screening for the expression of many different genes, they found that two signalling pathways stood out as having the required activity patterns: BMPs and WNTs. They gradually constructed the minimal possible mathematical model compatible with all the data, and found that the two signalling pathways were linked through a non-diffusible molecule -- the transcription factor Sox9. Finally, they were able to make computational predictions about the effects of inhibiting these 2 pathways -- either individually, or in combination -- which predicted how the pattern of fingers should change. Strikingly, when the same experiments were done on small pieces of limb bud tissue cultured in a petri dish the same alterations in embryonic finger pattern were observed, confirming the computational prediction.

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Immortal jellyfish: Does it really live forever?

Immortal jellyfish: Does it really live forever? | Amazing Science | Scoop.it
The Turritopsis nutricula jellyfish has displayed a remarkable ability to regenerate its cells in times of crisis.


While it is often joked that cats have nine lives, a certain species of jellyfish has been deemed “immortal” by scientists who have observed its ability to, when in crisis, revert its cells to their earliest form and grow anew. That means that these tiny creatures, 4 mm to 5 mm long, potentially have infinite lives.
 
The creature, known scientifically as Turritopsis nutricula, was discovered in the Mediterranean Sea in 1883, but its unique regeneration was not known until the mid-1990s. How does the process work? If a mature Turritopsis is threatened — injured or starving, for example — it attaches itself to a surface in warm ocean waters and converts into a blob. From that state, its cells undergo transdifferentiation, in which the cells essentially transform into different types of cells. Muscle cells can become sperm or eggs, or nerve cells can change into muscle cells, “revealing a transformation potential unparalleled in the animal kingdom,” according to the original study of the species published in 1996.


But Turritopsis can — and do — die. Their regeneration only occurs after sexual maturation, therefore they can succumb to predators or disease in the polyp stage. But because the jellyfish are the only known animal with this “immortality,” scientists are studying them closely, with the hopes of applying what they learn to issues such as human aging and illness.

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Invertebrate numbers nearly halve as human population doubles

Invertebrate numbers nearly halve as human population doubles | Amazing Science | Scoop.it

Invertebrate numbers have decreased by 45% on average over a 35 year period in which the human population doubled, reports a study on the impact of humans on declining animal numbers.


This decline matters because of the enormous benefits invertebrates such as insects, spiders, crustaceans, slugs and worms bring to our day-to-day lives, including pollination and pest control for crops, decomposition for nutrient cycling, water filtration and human health.


The study, published in Science and led by UCL, Stanford and UCSB, focused on the demise of invertebrates in particular, as large vertebrates have been extensively studied. They found similar widespread changes in both, with an on-going decline in invertebrates surprising scientists, as they had previously been viewed as nature’s survivors.


The decrease in invertebrate numbers is due to two main factors – habitat loss and climate disruption on a global scale. In the UK alone, scientists noted the areas inhabited by common insects such as beetles, butterflies, bees and wasps saw a 30-60% decline over the last 40 years.


Scientists believe there is a growing understanding of how ecosystems are changing but to tackle these issues, better predictions of the impact of changes are needed together with effective policies to reverse the losses currently seen. Using this approach, conservation of species can be prioritized with the benefit of protecting processes that serve human needs, and successful campaigns scaled-up to effect a positive change globally.

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Study of starling flight reveals message from turning bird sweeps through flock at constant speed

Study of starling flight reveals message from turning bird sweeps through flock at constant speed | Amazing Science | Scoop.it

A team of researchers with members from several countries working together in Rome, Italy, has come up with a new explanation of how it is that starlings are able to fly in a flock in a way that makes them appear as a single organism. In their paper published in the journal Nature Physics, the team describes how they used high-speed cameras to capture and study flight movement by individual bird members and what they found as a result.

Starling flight is as mesmerizing as it is mystifying—flocks of hundreds or thousands of birds sweep across the sky as if a single organism. The birds flying over Rome in particular have captured the imagination of bird enthusiasts, tourists, film makers and scientists alike. How do individual birds know when to turn and which way? Some have suggested it's a random thing, each bird simply flies making sure not to run into a neighbor. Others have suggested that some birds initiate a turn and others follow, creating a diffusion effect. In this new study, the researchers suggest that none of the earlier theories is correct—they've come up with something brand new.


To get a better look at the birds in flight, the researchers recorded flocks flying over Rome with high speed cameras and then took the results into their lab for examination. They found that turns are almost always initiated by just a few birds, but rather than other birds trying to figure out where to turn too, they instead simply copy how sharply their neighbor turns. This allows for the turn message to propagate through the flock at a very fast constant speed—approximately 20 to 40 meters per second, the team calculated. That constant message transfer speed means that each bird in a flock can respond in as little as half a second, without causing the flock to break apart.


Perhaps even more interesting is that when the researchers applied a spin factor for the turns by the birds, they found that applying it to the flock as a whole allowed for use of the same mathematical equations as physicists use to describe superfluid helium. The researchers believe that's not a coincidence, as there are many examples of physics and math principles that apply to the natural world.

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Biologist warn of early stages of Earth's sixth mass extinction event

Biologist warn of early stages of Earth's sixth mass extinction event | Amazing Science | Scoop.it
The planet's current biodiversity, the product of 3.5 billion years of evolutionary trial and error, is the highest in the history of life. But it may be reaching a tipping point. Scientists caution that the loss and decline of animals is contributing to what appears to be the early days of the planet's sixth mass biological extinction event. Since 1500, more than 320 terrestrial vertebrates have become extinct. Populations of the remaining species show a 25 percent average decline in abundance. The situation is similarly dire for invertebrate animal life.


And while previous extinctions have been driven by natural planetary transformations or catastrophic asteroid strikes, the current die-off can be associated to human activity, a situation that the lead author Rodolfo Dirzo, a professor of biology at Stanford, designates an era of "Anthropocene defaunation."


Across vertebrates, 16 to 33 percent of all species are estimated to be globally threatened or endangered. Large animals -- described as megafauna and including elephants, rhinoceroses, polar bears and countless other species worldwide -- face the highest rate of decline, a trend that matches previous extinction events.


Larger animals tend to have lower population growth rates and produce fewer offspring. They need larger habitat areas to maintain viable populations. Their size and meat mass make them easier and more attractive hunting targets for humans.


Although these species represent a relatively low percentage of the animals at risk, their loss would have trickle-down effects that could shake the stability of other species and, in some cases, even human health.


For instance, previous experiments conducted in Kenya have isolated patches of land from megafauna such as zebras, giraffes and elephants, and observed how an ecosystem reacts to the removal of its largest species. Rather quickly, these areas become overwhelmed with rodents. Grass and shrubs increase and the rate of soil compaction decreases. Seeds and shelter become more easily available, and the risk of predation drops.


Consequently, the number of rodents doubles -- and so does the abundance of the disease-carrying ectoparasites that they harbor.

"Where human density is high, you get high rates of defaunation, high incidence of rodents, and thus high levels of pathogens, which increases the risks of disease transmission," said Dirzo, who is also a senior fellow at the Stanford Woods Institute for the Environment. "Who would have thought that just defaunation would have all these dramatic consequences? But it can be a vicious circle."

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Museum workers pronounce dobsonfly found in China, largest aquatic insect

Museum workers pronounce dobsonfly found in China, largest aquatic insect | Amazing Science | Scoop.it

Workers with the Insect Museum of West China, who were recently given several very large dragon-fly looking insects, with long teeth, by locals in a part of Sichuan, have declared it, a giant dobsonfly the largest known aquatic insect in the world alive today. The find displaces the previous record holder, the South American helicopter damselfly, by just two centimeters.

The dobsonfly is common (there are over 220 species of them) in China, India, Africa, South America and some other parts of Asia, but until now, no specimens as large as those recently found in China have been known. The largest specimens in the found group had a wingspan of 21 centimeters, making it large enough to cover the entire face of a human adult. Locals don't have to worry too much about injury from the insects, however, as officials from the museum report that larger males' mandibles are so huge in proportion to their bodies that they are relatively weak—incapable of piercing human skin. They can kick up a stink, however, as they are able to spray an offensive odor when threatened.


Also, despite the fact that they look an awful lot like dragonflies, they are more closely related to fishflies. The long mandibles, though scary looking to humans, are actually used for mating—males use them to show off for females, and to hold them still during copulation. Interestingly, while their large wings (commonly twice their body length) make for great flying, they only make use of them for about a week—the rest of their time alive as adults is spent hiding under rocks or moving around on or under the water. That means that they are rarely seen as adults, which for most people is probably a good thing as the giants found in China would probably present a frightening sight. They are much better known during their long larval stage when they are used as bait by fishermen.

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Removing parasitic retroviruses from the genome is a critical step in evolving larger bodies and longer lifespans

Removing parasitic retroviruses from the genome is a critical step in evolving larger bodies and longer lifespans | Amazing Science | Scoop.it
Cancer has left its 'footprint' on our evolution, according to a study which examined how the relics of ancient viruses are preserved in the genomes of 38 mammal species. The team found that as animals increased in size they 'edited out' potentially cancer-causing relics from their genomes so that mice have almost ten times as many ERVs as humans. The findings offer a clue as to why larger animals have a lower incidence of cancer than expected compared to smaller ones, and could help in the search for new anti-viral therapies.


Viral relics are evidence of the ancient battles our genes have fought against infection. Occasionally the retroviruses that infect an animal get incorporated into that animal's genome and sometimes these relics get passed down from generation to generation -- termed 'endogenous retroviruses' (ERVs). Because ERVs may be copied to other parts of the genome they contribute to the risk of cancer-causing mutations.


Now a team from Oxford University, Plymouth University, and the University of Glasgow has identified 27,711 ERVs preserved in the genomes of 38 mammal species, including humans, over the last 10 million years. The team found that as animals increased in size they 'edited out' these potentially cancer-causing relics from their genomes so that mice have almost ten times as many ERVs as humans. The findings offer a clue as to why larger animals have a lower incidence of cancer than expected compared to smaller ones, and could help in the search for new anti-viral therapies.


We set out to find as many of these viral relics as we could in everything from shrews and humans to elephants and dolphins,' said Dr Aris Katzourakis of Oxford University's Department of Zoology, lead author of the report. 'Viral relics are preserved in every cell of an animal: Because larger animals have many more cells they should have more of these endogenous retroviruses (ERVs) -- and so be at greater risk of ERV-induced mutations -- but we've found this isn't the case. In fact larger animals have far fewer ERVs, so they must have found ways to remove them.'


A combination of mathematical modelling and genome research uncovered some striking differences between mammal genomes: mice (c.19 grams) have 3331 ERVs, humans (c.59 kilograms) have 348 ERVs, whilst dolphins (c.281 kilograms) have just 55 ERVs.


'This is the first time that anyone has shown that having a large number of ERVs in your genome must be harmful -- otherwise larger animals wouldn't have evolved ways of limiting their numbers,' said Dr Katzourakis. 'Logically we think this is linked to the increased risk of ERV-based cancer-causing mutations and how mammals have evolved to combat this risk. So when we look at the pattern of ERV distribution across mammals it's like looking at the 'footprint' cancer has left on our evolution.'


Dr Robert Belshaw of Plymouth University Peninsula Schools of Medicine and Dentistry, School of Biomedical and Healthcare Sciences, added: "Cancer is caused by errors occurring in cells as they divide, so bigger animals -- with more cells -- ought to suffer more from cancer. Put simply, the blue whale should not exist. However, larger animals are not more prone to cancer than smaller ones: this is known as Peto's Paradox (named after Sir Richard Peto, the scientist credited with first spotting this). A team of scientists at Oxford, Plymouth and Glasgow Universities had been studying endogenous retroviruses, viruses like HIV but which have become part of their host's genome and which in other animals can cause cancer. Surprisingly, they found that bigger mammals have fewer of these viruses in their genome. This suggests that similar mechanism might be involved in fighting both cancer and the spread of these viruses, and that these are better in bigger animals (like humans) than smaller ones (like laboratory mice)."

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Crystal structure of one of the most complex ternary complexes in cell division, important to cancer

Crystal structure of one of the most complex ternary complexes in cell division, important to cancer | Amazing Science | Scoop.it

Research carried out at the ICR has revealed the structure of one of the most important and complicated proteins in cell division – a fundamental process the development of cancer, published in Nature.


Images of the gigantic protein in unprecedented detail will transform scientists’ understanding of exactly how cells copy their chromosomes and divide, and could reveal binding sites for future cancer drugs.


A team from The Institute of Cancer Research, London, and the Medical Research Council Laboratory of Molecular Biology in Cambridge produced the first detailed images of the anaphase-promoting complex (APC/C).


The APC/C performs a wide range of vital tasks associated with mitosis, the process during which a cell copies its chromosomes and pulls them apart into two separate cells. Mitosis is used in cell division by all animals and plants.


Discovering its structure could ultimately lead to new treatments for cancer, which hijacks the normal process of cell division to make thousands of copies of harmful cancer cells.


In the study, which was funded by Cancer Research UK, the researchers reconstituted human APC/C and used a combination of electron microscopy and imaging software to visualize it at a resolution of less than a nanometer.


The resolution was so fine that it allowed the researchers to see the secondary structure – the set of basic building blocks which combine to form every protein. Alpha-helix rods and folded beta-sheet constructions were clearly visible within the 20 subunits of the APC/C, defining the overall architecture of the complex.


Previous studies led by the same research team had shown a globular structure for APC/C in much lower resolution, but the secondary structure had not previously been mapped. The new study could identify binding sites for potential cancer drugs.


Each of the APC/C’s subunits bond and mesh with other units at different points in the cell cycle, allowing it to control a range of mitotic processes including the initiation of DNA replication, the segregation of chromosomes along protein ‘rails’ called spindles, and the ultimate splitting of one cell into two, called cytokinesis. Disrupting each of these processes could selectively kill cancer cells or prevent them from dividing.

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Barnacle cement: Nature's strongest glue is a two-component adhesive

Barnacle cement: Nature's strongest glue is a two-component adhesive | Amazing Science | Scoop.it

Over a 150 years since it was first described by Darwin, scientists are finally uncovering the secrets behind the super strength of barnacle glue. 

Still far better than anything we have been able to develop synthetically, barnacle glue – or cement - sticks to any surface, under any conditions.

But exactly how this superglue of superglues works has remained a mystery – until now.


An international team of scientists led by Newcastle University, UK, and funded by the US Office of Naval Research, have shown for the first time that barnacle larvae release an oily droplet to clear the water from surfaces before sticking down using a phosphoprotein adhesive.


Publishing their findings this week in the prestigious academic journal Nature Communications, author Dr Nick Aldred says the findings could pave the way for the development of novel synthetic bioadhesives for use in medical implants and micro-electronics. The research will also be important in the production of new anti-fouling coatings for ships.


Thoracian barnacles rely heavily upon their ability to adhere to surfaces and are environmentally and economically important as biofouling pests. Their adhesives have unique attributes that define them as targets for bio-inspired adhesive development. With the aid of multi-photon and broadband coherent anti-Stokes Raman scattering microscopies, we report that the larval adhesive of barnacle cyprids is a bi-phasic system containing lipids and phosphoproteins, working synergistically to maximize adhesion to diverse surfaces under hostile conditions. Lipids, secreted first, possibly displace water from the surface interface creating a conducive environment for introduction of phosphoproteins while simultaneously modulating the spreading of the protein phase and protecting the nascent adhesive plaque from bacterial biodegradation. The two distinct phases are contained within two different granules in the cyprid cement glands, implying far greater complexity than previously recognized. Knowledge of the lipidic contribution will hopefully inspire development of novel synthetic bioadhesives and environmentally benign antifouling coatings.

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Patient-Zero: Ebola outbreak probably started with a 2-year-old child in Guinea

Patient-Zero: Ebola outbreak probably started with a 2-year-old child in Guinea | Amazing Science | Scoop.it

he worst outbreak of Ebola, which has killed 961 people and triggered an international public health emergency, may have started with a 2-year-old patient in a village in Guinea.


About eight months ago, the toddler, whom researchers believe may have been Patient Zero, suffered fever, black stool and vomiting. Just four days after showing the painful symptoms, the child died on December 6, 2013, according to a report published in The New England Journal of Medicine.


Scientists don't know exactly how the toddler contracted the virus. Ebola is spread from animals to humans through infected fluids or tissue, according to the World Health Organization.


"In Africa, infection has been documented through the handling of infected chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines," WHO says, though researchers think fruit bats are what they call the virus's "natural host."


After the child's death, the mother suffered bleeding symptoms and died on December 13, according to the report. Then, the toddler's 3-year-old sister died on December 29, with symptoms including fever, vomiting and black diarrhea. The illness subsequently affected the toddler's grandmother, who died on January 1, in the family's village of Meliandou in Guéckédou.


The area in southern Guinea is close to the Sierra Leone and Liberia borders. The illness spread outside their village after several people attended the grandmother's funeral. Funerals tend to bring people in close contact with the body. Ebola spreads from person to person through contact with organs and bodily fluids such as blood, saliva, urine and other secretions of infected people. It has no known cure.

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Single gene (Lhx1) found to control jet lag

Single gene (Lhx1) found to control jet lag | Amazing Science | Scoop.it

The discovery of the role of this gene, called Lhx1, provides scientists with a potential therapeutic target to help night-shift workers or jet lagged travelers adjust to time differences more quickly. The results, published in eLife, can point to treatment strategies for sleep problems caused by a variety of disorders.


“It’s possible that the severity of many dementias comes from sleep disturbances,” says Satchidananda Panda, a Salk associate professor who led the research team. “If we can restore normal sleep, we can address half of the problem.”


Every cell in the body has a “clock” – an abundance of proteins that dip or rise rhythmically over approximately 24 hours. The master clock responsible for establishing these cyclic circadian rhythms and keeping all the body’s cells in sync is the suprachiasmatic nucleus (SCN), a small, densely packed region of about 20,000 neurons housed in the brain’s hypothalamus.


More so than in other areas of the brain, the SCN’s neurons are in close and constant communication with one another. This close interaction, combined with exposure to light and darkness through vision circuits, keeps this master clock in sync and allows people to stay on essentially the same schedule every day. The tight coupling of these cells also helps make them collectively resistant to change. Exposure to light resets less than half of the SCN cells, resulting in long periods of jet lag.


In the new study, researchers disrupted the light-dark cycles in mice and compared changes in the expression of thousands of genes in the SCN with other mouse tissues. They identified 213 gene expression changes that were unique to the SCN and narrowed in on 13 of these that coded for molecules that turn on and off other genes. Of those, only one was suppressed in response to light: Lhx1.


“No one had ever imagined that Lhx1 might be so intricately involved in SCN function,” says Shubhroz Gill, a postdoctoral researcher and co-first author of the paper. Lhx1 is known for its role in neural development: it’s so important, that mice without the gene do not survive. But this is the first time it has been identified as a master regulator of light-dark cycle genes.

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DCC-Netrin1: Mystery of brain cell growth unraveled by scientists

DCC-Netrin1: Mystery of brain cell growth unraveled by scientists | Amazing Science | Scoop.it
Scientists have discovered how a single protein can exert both a push and a pull force to nudge a neuron in the desired direction, helping neurons navigate to their assigned places in the developing brain.


Jia-huai Wang, PhD, who led the work at Dana-Farber and Peking University in Beijing, is a corresponding author of a report published in the August 7 online edition of Neuron that explains how one guidance protein, netrin-1, can either attract or repel a brain cell to steer it along its course. Wang and co-authors at the European Molecular Biology Laboratory (EMBL) in Hamburg, Germany, used X-ray crystallography to reveal the three-dimensional atomic structure of netrin-1 as it bound to a docking molecule, called DCC (Deleted in Colorectal Carcinoma), on the axon of a neuron. The axon is the long, thin extension of a neuron that connects to other neurons or to muscle cells.


DCC in a receptor for netrin-1 and is currently believed by some to be a conditional tumour suppressor gene, meaning that it normally prevents cell growth when in the absence of netrin-1. DCC elimination is not believed to be a key genetic change in tumour formation, but one of many alterations that can promote existing tumour growth. DCC's possible role in migration of cancerous cells is in the process of being characterized. While recent results make it fairly likely that DCC is involved in the biology of several cancers, the extent of its involvement and the details of how it works are still being studied.


As connections between neurons are established -- in the developing brain and throughout life -- axons grow out from a neuron and extend through the brain until they reach the neuron they are connecting to. To choose its path, a growing axon senses and reacts to different molecules it encounters along the way. One of these molecules, netrin-1, posed an interesting puzzle: an axon can be both attracted to and repelled from this cue. The axon's behavior is determined by two types of receptors on its tip: DCC drives attraction, while UNC5 in combination with DCC drives repulsion.


"How netrin works at the molecular level has long been a puzzle in neuroscience field," said Wang, "We now provide structure evidences that reveal a novel mechanism of this important guidance cue molecule." The structure showed that netrin-1 binds not to one, but to two DCC molecules. And most surprisingly, it binds those two molecules in different ways.


"Normally a receptor and a signal are like lock-and-key, they have evolved to bind each other and are highly specific -- and that's what we see in one netrin site," said Meijers. "But the second binding site is a very unusual one, which is not specific for DCC."


Not all of the second binding site connects directly to a receptor. Instead, in a large portion of the binding interface, it requires small molecules that act as middle-men. These intermediary molecules seem to have a preference for UNC5, so if the axon has both UNC5 and DCC receptors, netrin-1 will bind to one copy of UNC5 via those molecules and the other copy of DCC at the DCC-specific site. This triggers a cascade of events inside the cell that ultimately drives the axon away from the source of netrin-1, author Yan Zhang's lab at Peking University found. The researchers surmised that, if an axon has only DCC receptors, each netrin-1 molecule binds two DCC molecules, which results in the axon being attracted to netrin-1. "By controlling whether or not UNC5 is present on its tip, an axon can switch from moving toward netrin to moving away from it, weaving through the brain to establish the right connection," said Zhang.

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TRAP-1 knock-out mice show signs of longer lives with fewer age-related diseases

TRAP-1 knock-out mice show signs of longer lives with fewer age-related diseases | Amazing Science | Scoop.it

While developing a new cancer drug, researchers at The Wistar Institute discovered that mice lacking a specific protein live longer lives with fewer age-related illnesses. The mice, which lack the TRAP-1 protein, demonstrated less age-related tissue degeneration, obesity, and spontaneous tumor formation when compared with normal mice. Their findings could change how scientists view the metabolic networks within cells.


In healthy cells, TRAP-1 is an important regulator of metabolism and has been shown to regulate energy production in mitochondria, organelles that generate chemically useful energy for the cell. In the mitochondria of cancer cells, TRAP-1 is universally overproduced.  


The Wistar team’s report, which appears in the journal Cell Reports (available online now), shows how “knockout” mice bred to lack the TRAP-1 protein compensate for this loss by switching to alternative cellular mechanisms for making energy.


“We see this astounding change in TRAP-1 knockout mice, where they show fewer signs of aging and are less likely to develop cancers,” said Dario C. Altieri. M.D., Robert and Penny Fox Distinguished Professor and director of The Wistar Institute’s National Cancer Institute-designated Cancer Center. “Our findings provide an unexpected explanation for how TRAP-1 and related proteins regulate metabolism within our cells.”


“We usually link the reprogramming of metabolic pathways with human diseases, such as cancer,” Altieri said. “What we didn’t expect to see were healthier mice with fewer tumors.”


Altieri and his colleagues created the TRAP-1 knockout mice as part of their ongoing investigation into their novel drug, Gamitrinib, which targets the protein in the mitochondria of tumor cells. TRAP-1 is a member of the heat shock protein 90 (HSP90) family, which are “chaperone” proteins that guide the physical formation of other proteins and serve a regulatory function within mitochondria. Tumors use HSP90 proteins, like TRAP-1, to help survive therapeutic attack. 

“In tumors, the loss of TRAP-1 is devastating, triggering a host of catastrophic defects, including metabolic problems that ultimately result in the death of the tumor cells,” Altieri said.  “Mice that lack TRAP-1 from the start, however, have three weeks in the womb to compensate for the loss of the protein.”


The researchers found that in their knockout mice, the loss of TRAP-1 causes mitochondrial proteins to misfold, which then triggers a compensatory response that causes cells to consume more oxygen and metabolize more sugar. This causes mitochondria in knockout mice to produce deregulated levels of ATP, the chemical used as an energy source to power all the everyday molecular reactions that allow a cell to function.

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Dinosaurs shrank to evolve into birds over a 50 million years time span

Dinosaurs shrank to evolve into birds over a 50 million years time span | Amazing Science | Scoop.it

Huge meat-eating dinosaurs (Theropods) underwent 12 stages of miniaturization and shrank steadily over 50 million years to evolve into small, flying birds, researchers say. The branch of theropod dinosaurs which gave rise to modern birds decreased inexorably in size from 163kg beasts that roamed the land, to birds weighing less than 1kg over the period.


The radical transformation began around 200 million years ago and was likely driven by a move to the trees where creatures with smaller, lighter bodies and other features, such as large eyes for 3D vision, fared better than others.


Scientists pieced together the dinosaurs' sustained shrinkage after analysing more than 1,500 anatomical features of 120 species of theropods and early birds.


The evolutionary tree reveals that the theropod ancestors of modern birds underwent 12 substantial decreases in size that led to archaeopteryx, the earliest known bird on Earth. The rate at which they evolved distinct features, such as feathers, wings and wishbones, was four times faster than adaptations in other dinosaurs.


"Birds evolved through a unique phase of sustained miniaturisation in dinosaurs," said Michael Lee at the University of Adelaide. "Being smaller and lighter in the land of giants, with rapidly evolving anatomical adaptations, provided these bird ancestors with new ecological opportunities, such as the ability to climb trees, glide and fly. Ultimately, this evolutionary flexibility helped birds survive the deadly meteorite impact which killed off all their dinosaurian cousins," he added. The study is published in the journal, Science.


The steady reduction in size saw the two-legged land-based theropods evolve new bird-like features, including shorter snouts, smaller teeth and insulating feathers.


Gareth Dyke, a vertebrate palaeontologist and co-author of the study at Southampton University said: "The dinosaurs most closely related to birds are all small, and many of them, such as the aptly named Microraptor, had some ability to climb and glide."


In an accompanying article, Michael Benton at Bristol University, said that the long-term trend that led to modern birds was probably shaped by the animals taking up in new habitats. "The crucial driver may have been a move to the trees, perhaps to escape from predation or to exploit new food resources," he writes.

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Diet Affects Men’s and Women’s Intestinal Microbes Differently

Diet Affects Men’s and Women’s Intestinal Microbes Differently | Amazing Science | Scoop.it

 The microbes living in the guts of males and females react differently to diet, even when the diets are identical, according to a study by scientists from The University of Texas at Austin and six other institutions published this week in the journal Nature CommunicationsThese results suggest that therapies designed to improve human health and treat diseases through nutrition might need to be tailored for each sex.


The researchers studied the gut microbes in two species of fish and in mice, and also conducted an in-depth analysis of data that other researchers collected on humans. They found that in fish and humans diet affected the microbiota of males and females differently. In some cases, different species of microbes would dominate, while in others, the diversity of bacteria would be higher in one sex than the other.

These results suggest that any therapies designed to improve human health through diet should take into account whether the patient is male or female.


Only in recent years has science begun to completely appreciate the importance of the human microbiome, which consists of all the bacteria that live in and on people’s bodies. There are hundreds or even thousands of species of microbes in the human digestive system alone, each varying in abundance.


Genetics and diet can affect the variety and number of these microbes in the human gut, which can in turn have a profound influence on human health. Obesity, diabetes, and inflammatory bowel disease have all been linked to low diversity of bacteria in the human gut.


One concept for treating such diseases is to manipulate the microbes within a person’s gut through diet. The idea is gaining in popularity because dietary changes would make for a relatively cheap and simple treatment.


Much has to be learned about which species, or combination of microbial species, is best for human health. In order to accomplish this, research has to illuminate how these microbes react to various combinations of diet, genetics and environment. Unfortunately, to date most such studies only examine one factor at a time and do not take into account how these variables interact.


“Our study asks not just how diet influences the microbiome, but it splits the hosts into males and females and asks, do males show the same diet effects as females?” said Daniel Bolnick, professor in The University of Texas at Austin's College of Natural Sciences and lead author of the study.

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Eric Chan Wei Chiang's curator insight, August 2, 2014 11:36 PM

Previously, it was assumed that men and women have mostly similar biological functions. This is an interesting paradigm shift indeed. 

 

This has future implication with our diet and how we treat diseases.

http://www.scoop.it/t/food-health-and-nutrition/?tag=Diet

http://www.scoop.it/t/biotech-and-beyond/?tag=Novel+Therapies

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Learning the smell of fear: Mothers teach babies their own fears via odor, animal study shows

Learning the smell of fear: Mothers teach babies their own fears via odor, animal study shows | Amazing Science | Scoop.it

Babies can learn what to fear in the first days of life just by smelling the odor of their distressed mothers, new research suggests. And not just "natural" fears: If a mother experienced something before pregnancy that made her fear something specific, her baby will quickly learn to fear it too -- through the odor she gives off when she feels fear.


In the first direct observation of this kind of fear transmission, a team of University of Michigan Medical School and New York University studied mother rats who had learned to fear the smell of peppermint -- and showed how they "taught" this fear to their babies in their first days of life through their alarm odor released during distress.


In a new paper in the Proceedings of the National Academy of Sciences, the team reports how they pinpointed the specific area of the brain where this fear transmission takes root in the earliest days of life.


Their findings in animals may help explain a phenomenon that has puzzled mental health experts for generations: how a mother's traumatic experience can affect her children in profound ways, even when it happened long before they were born.


The researchers also hope their work will lead to better understanding of why not all children of traumatized mothers, or of mothers with major phobias, other anxiety disorders or major depression, experience the same effects.


"During the early days of an infant rat's life, they are immune to learning information about environmental dangers. But if their mother is the source of threat information, we have shown they can learn from her and produce lasting memories," says Jacek Debiec, M.D., Ph.D., the U-M psychiatrist and neuroscientist who led the research.


"Our research demonstrates that infants can learn from maternal expression of fear, very early in life," he adds. "Before they can even make their own experiences, they basically acquire their mothers' experiences. Most importantly, these maternally-transmitted memories are long-lived, whereas other types of infant learning, if not repeated, rapidly perish."

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Extremely precise localization of sound origin

Extremely precise localization of sound origin | Amazing Science | Scoop.it

The parasitoid fly Ormia ochracea has the remarkable ability to locate crickets using audible sound. This ability is, in fact, remarkable as the fly's hearing mechanism spans only 1.5 mm which is 50× smaller than the wavelength of sound emitted by the cricket.


The hearing mechanism is, for all practical purposes, a point in space with no significant interaural time or level differences to draw from.


It has been discovered that evolution has empowered the fly with a hearing mechanism that utilizes multiple vibration modes to amplify interaural time and level differences. A team of scientist engineers now presents a fully integrated, man-made mimic of the Ormia's hearing mechanism capable of replicating the remarkable sound localization ability of the special fly.


A silicon-micromachined prototype is presented which uses multiple piezoelectric sensing ports to simultaneously transduce two orthogonal vibration modes of the sensing structure, thereby enabling simultaneous measurement of sound pressure and pressure gradient.

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Smarter than a first-grader? Caledonian crows can perform as well as 7- to 10-year-olds on cause-and-effect water displacement tasks

Smarter than a first-grader? Caledonian crows can perform as well as 7- to 10-year-olds on cause-and-effect water displacement tasks | Amazing Science | Scoop.it
In Aesop's fable about the crow and the pitcher, a thirsty bird happens upon a vessel of water, but when he tries to drink from it, he finds the water level out of his reach. Not strong enough to knock over the pitcher, the bird drops pebbles into it -- one at a time -- until the water level rises enough for him to drink his fill. New research demonstrates the birds' intellectual prowess may be more fact than fiction.


Highlighting the value of ingenuity, the fable demonstrates that cognitive ability can often be more effective than brute force. It also characterizes crows as pretty resourceful problem solvers. New research conducted by UC Santa Barbara's Corina Logan, with her collaborators at the University of Auckland in New Zealand, demonstrates the birds' intellectual prowess may be more fact than fiction. Her findings appear today in the scientific journal PLOS ONE.


Logan is lead author of the paper, which examines causal cognition using a water displacement paradigm. "We showed that crows can discriminate between different volumes of water and that they can pass a modified test that so far only 7- to 10-year-old children have been able to complete successfully. We provide the strongest evidence so far that the birds attend to cause-and-effect relationships by choosing options that displace more water."


Logan, a junior research fellow at UCSB's SAGE Center for the Study of the Mind, worked with New Caledonian crows in a set of small aviaries in New Caledonia run by the University of Auckland. "We caught the crows in the wild and brought them into the aviaries, where they habituated in about five days," she said. Keeping families together, they housed the birds in separate areas of the aviaries for three to five months before releasing them back to the wild.


The testing room contained an apparatus consisting of two beakers of water, the same height, but one wide and the other narrow. The diameters of the lids were adjusted to be the same on each beaker. "The question is, can they distinguish between water volumes?" Logan said. "Do they understand that dropping a stone into a narrow tube will raise the water level more?" In a previous experiment by Sarah Jelbert and colleagues at the University of Auckland, the birds had not preferred the narrow tube. However, in that study, the crows were given 12 stones to drop in one or the other of the beakers, giving them enough to be successful with either one.


"When we gave them only four objects, they could succeed only in one tube -- the narrower one, because the water level would never get high enough in the wider tube; they were dropping all or most of the objects into the functional tube and getting the food reward," Logan explained. "It wasn't just that they preferred this tube, they appeared to know it was more functional." However, she noted, we still don't know exactly how the crows think when solving this task. They may be imagining the effect of each stone drop before they do it, or they may be using some other cognitive mechanism. "More work is needed," Logan said.


Logan also examined how the crows react to the U-tube task. Here, the crows had to choose between two sets of tubes. With one set, when subjects dropped a stone into a wide tube, the water level raised in an adjacent narrow tube that contained food. This was due to a hidden connection between the two tubes that allowed water to flow. The other set of tubes had no connection, so dropping a stone in the wide tube did not cause the water level to rise in its adjacent narrow tube.


Each set of tubes was marked with a distinct color cue, and test subjects had to notice that dropping a stone into a tube marked with one color resulted in the rise of the floating food in its adjacent small tube. "They have to put the stones into the blue tube or the red one, so all you have to do is learn a really simple rule that red equals food, even if that doesn't make sense because the causal mechanism is hidden," said Logan.


As it turns out, this is a very challenging task for both corvids (a family of birds that includes crows, ravens, jays and rooks) and children. Children ages 7 to 10 were able to learn the rules, as Lucy Cheke and colleagues at the University of Cambridge discovered in 2012. It may have taken a couple of tries to figure out how it worked, Logan noted, but the children consistently put the stones into the correct tube and got the reward (in this case, a token they exchanged for stickers). Children ages 4 to 6, however, were unable to work out the process. "They put the stones randomly into either tube and weren't getting the token consistently," she said.


Recently, Jelbert and colleagues from the University of Auckland put the New Caledonian crows to the test using the same apparatus the children did. The crows failed. So Logan and her team modified the apparatus, expanding the distance between the beakers. And Kitty, a six-month-old juvenile, figured it out. "We don't know how she passed it or what she understands about the task," Logan said, "so we don't know if the same cognitive processes or decisions are happening as with the children, but we now have evidence that they can. It's possible for the birds to pass it.

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Bats use polarized light to calibrate their internal magnetic compass

Bats use polarized light to calibrate their internal magnetic compass | Amazing Science | Scoop.it

Scientists have discovered that greater mouse-eared bats use polarization patterns in the sky to navigate -- the first mammal that's known to do this.


The bats use the way the Sun's light is scattered in the atmosphere at sunset to calibrate their internal magnetic compass, which helps them to fly in the right direction, a study published in Nature Communications has shown.


Despite this breakthrough, researchers have no idea how they manage to detect polarized light. 'We know that other animals use polarization patterns in the sky, and we have at least some idea how they do it: bees have specially-adapted photoreceptors in their eyes, and birds, fish, amphibians and reptiles all have cone cell structures in their eyes which may help them to detect polarization,' says Dr Richard Holland of Queen's University Belfast, co-author of the study.


'But we don't know which structure these bats might be using.' Polarization patterns depend on where the sun is in the sky. They're clearest in a strip across the sky 90° from the position of the sun at sunset or sunrise. But animals can still see the patterns long after sunset. This means they can orient themselves even when they can't see the sun, including when it's cloudy. Scientists have even shown that dung beetles use the polarization pattern of moonlight for orientation.


A hugely diverse range of creatures – including bees, anchovies, birds, reptiles and amphibians – use the patterns as a compass to work out which way is north, south, east and west.

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Elephants possess a sense of smell that is likely the strongest ever identified in a single species

Elephants possess a sense of smell that is likely the strongest ever identified in a single species | Amazing Science | Scoop.it

The African elephant's genome contains the largest number of smell receptor genes - nearly 2,000 - say the researchers in the journal Genome Research.


Olfactory receptors detect odors in the environment. That means elephants' sniffers are five times more powerful than people's noses, twice that of dogs, and even stronger than the previous known record-holder in the animal kingdom: rats.


"Apparently, an elephant's nose is not only long but also superior," says lead study author Dr Yoshihito Niimura of the University of Tokyo.


Just how these genes work is not well understood, but they likely helped elephants survive and navigate their environment over the ages.


The ability to smell allows creatures to find mates and food - and avoid predators.


The study compared elephant olfactory receptor genes to those of 13 other animals, including horses, rabbits, guinea pigs, cows, rodents and chimpanzees.


Primates and people actually had very low numbers of olfactory receptor genes compared to other species, the study found.

This could be "a result of our diminished reliance on smell as our visual acuity improved," sats Niimura.

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Fecal Transplants of Bacteria Let Packrats Eat Poisonous Creosote Diet

Fecal Transplants of Bacteria Let Packrats Eat Poisonous Creosote Diet | Amazing Science | Scoop.it

Woodrats lost their ability to eat toxic creosote bushes after antibiotics killed their gut microbes. Woodrats that never ate the plants were able to do so after receiving fecal transplants with microbes from creosote-eaters, University of Utah biologists found.


The new study confirms what biologists long have suspected: bacteria in the gut – and not just liver enzymes – are “crucial in allowing herbivores to feed on toxic plants,” says biologist Kevin Kohl, a postdoctoral researcher and first author of the paper published online today in the journal Ecology Letters.


Many plants produce toxic chemicals, which they use as a defense against herbivores, or plant-eating animals. A toxic resin coats the leaves of the creosote bush; juniper toxins are found inside juniper needles.

Most mammals are herbivores. Some face serious challenges: their bodies must handle up to hundreds of toxic chemicals from the plants they consume each day. “Plant toxins determine which plants a herbivore can eat,” says Kohl.


Liver enzymes help animals detoxify such poisons. Researchers previously isolated toxin-degrading microbes from herbivores, but Kohl and Dearing say that, until now, scientists have lacked strong evidence for what has been conventional wisdom: Gut microbes also help some herbivores eat toxic plants.


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