#This is absolutely terrifying: There are really only two big patches of intact forest left On earth#A new study uncovers the ruinous consequences, to plant and animal species,
of our increasingly fragmented forests Can a forest that exists only in the spaces between roads
and patches cleared for human settlement and agricultural development truly be called a forest? Not so much, say researchers studying the growing, global problem of forest fragmentation.
And the ersistent, deleterious and often unpredictedconsequences of human activity, finds a new study conducted by a team off 24 international scientists,
and funded by the National Science Foundation, may be ruinous for plant and animal life. here are really only two big patches of intact forest left On earth the Amazon
and the Congo and they shine out like eyes from the center of the map, lead author Nick Haddad,
a professor at North carolina State university, told the New yorker. early 20 percent of the world remaining forests are the distance of a football field or about 100 meters away from forest edges,
he elaborated in a statement. eventy percent of forest lands are within a half-mile of forest edges.
That means almost no forests can really be considered wilderness. And the consequences of that forest loss, the researchers discovered, may be more profound than wee previously realized.
To figure that out, they looked at the results of seven experiments, which took place on five different continents,
that aimed to simulate the impacts of human activity on forests. Several of the studies have been going on for decades,
and the results, in aggregate, were striking: fragmented habitats, they found, can reduce plant and animal diversity by anywhere from 13 to 75 percent.
In general, the studies showed that when patches of forest become smaller and more isolated, the abundance of birds, mammal,
insects and plants decreases in kind those pressures, the authors write, reduced the speciesability to persist.
Areas surrounded by a higher proportion of edges, they also found, were a boon to predators that target birds,
which is arguably good, in the short-term, for the predators, although not so much for the birds.
Fragmented forests experienced a decline in their core ecosystem functions as well: they were less able to sequester carbon dioxide,
an important element of mitigating climate change, and displayed reduced productivity and pollination. o matter the place,
a program director in NSF Division of Environmental Biology, said, abitat fragmentation has large effects,
the harmful impacts of fragmentation on forest ecosystems only become apparent after many years. On average, they found,
fragmented forests lose more than half of their species within just 20 years; in the one experiment that still ongoing after more than two decades, the losses are continuing to compound.
and dicing of the forests has wrought. Appreciating the full extent of the damage, the authors argue,
William Laurance, a professor at Australia James Cook University and another of the study co-authors
while introducing poachers, miners, loggers and other destructive human forces. he trouble is that, for humans, if not for plants and animals,
more than fifteen million new miles worldwide, according to the International Energy Agency. That the kind of thing, according to Laurence, that care s the hell out of ecologists. g
#This special chair is saving the lives of hundreds of dogs This might be the most regal solution for a medical problem wee ever seen:
and anyone can donate money to send the specially designed chairs to shelter dogs in need.
which provide the playgrounds in which to search for new macroscopic physical properties, said Dr David Hsieh of California Institute of technology in Pasadena, California.
Dr Hsieh and his colleagues from Tel aviv University California Institute of technology, Iowa State university, and the University of Kentucky, made the discovery
while testing a laser-based measurement technique that they recently developed to look for what is called multipolar order. o understand multipolar order,
first consider a crystal with electrons moving around throughout its interior. Under certain conditions, it can be energetically favorable for these electrical charges to pile up in a regular,
repeating fashion inside the crystal, forming what is called a charge-ordered phase, the scientists said. he building block of this type of order,
namely charge, is simply a scalar quantity that is, it can be described by just a numerical value, or magnitude.
if the building block of the ordered phase was a pair of oppositely pointing spins described by what is known as a magnetic quadrupole.
When you shine a red laser pointer at a wall, for example, your eye detects red light.?However, for all materials, there is a tiny amount of light bouncing off at integer multiples of the incoming frequency.
So with the red laser pointer, there will also be some blue light bouncing off of the wall.
These multiples are called optical harmonics. he physicists exploited the fact that changes in the symmetry of a crystal will affect the strength of each harmonic differently.
Since the emergence of multipolar ordering changes the symmetry of the crystal in a very specific way
their idea was that the optical harmonic response of a crystal could serve as a fingerprint of multipolar order. e found that light reflected at the second harmonic frequency revealed a set of symmetries completely different from those of the known crystal structure,
A high enough level of doping will transform cuprates into high-temperature superconductors, and as cuprates evolve from being insulators to superconductors, they first transition through a mysterious phase known as the pseudogap,
where an additional amount of energy is required to strip electrons out of the material. For years, physicists have debated the origin of the pseudogap
and its relationship to superconductivity whether it is a necessary precursor to superconductivity or a competing phase with a distinct set of symmetry properties.
If that relationship were understood better it might be possible to develop materials that superconduct at temperatures approaching room temperature.
and temperature window where the pseudogap is present. iven the highly similar phenomenology of the iridates and cuprates,
perhaps iridates will help us resolve some of the longstanding debates about the relationship between the pseudogap and high-temperature superconductivity,
#European Researchers Create Acoustic Tractor Beam t was an incredible experience the first time we saw the object held in place by the tractor beam.
All my hard work has paid off, it brilliant, said Asier Marzo of the University of Bristol and the Public University of Navarre, a team member and the first author of a paper in the journal Nature Communications.
The tractor beam crated by Marzo and his colleagues uses high-amplitude sound waves to generate an acoustic hologram
which can pick up and move small objects. e all know that sound waves can have a physical effect,
Bruce Drinkwater of the University of Bristol. ut here we have managed to control the sound to a degree never previously achieved. n our device we manipulate objects in mid-air
added co-author Prof Sriram Subramanian of the University of Sussex and Ultrahaptics Ltd. The team used an array of 64 miniature loudspeakers (driven at 40khz with 15vpp;
whole system consumes 9 Watts of power) to create high-pitched and high-intensity sound waves to levitate a spherical bead (of up to four mm in diameter) made of expanded polystyrene.
The tractor beam works by surrounding the object with high-intensity sound and this creates a force field that keeps the objects in place.
The researchers have shown that three different shapes of acoustic force fields work as tractor beams. The first is an acoustic force field that resembles a pair of fingers or tweezers.
and then trapped at the core and the third is described best as a high-intensity cage that surrounds the objects
#Non-Genetic Cancer Mechanism Found Cancer can be caused solely by protein imbalances within cells, a study of ovarian cancer has found.
The discovery is a major breakthrough because genetic aberrations have been seen as the main cause of almost all cancer.
The research in Oncogene demonstrates that protein imbalance is a powerful prognostic tool, indicating whether or not patients are likely to respond to chemotherapy
and whether a tumor is likely to spread to other sites. The findings also open the possibility of new therapies aimed at measuring
and preventing dangerous imbalances in cells. The research led by scientists at the University of Leeds and The University of Texas MD Anderson Cancer Center, focused on the"Akt pathway,"a signaling pathway within cells that drives cancer formation and the spread of cancers
through the body. Under normal conditions, the cell receives external signals through a cell wall-bound receptor (FGFR2 in this study.
This results in the recruitment of signalling proteins and the initiation of the Akt pathway,
A conventional approach to diagnosing this cancer would be to look for genetic modification of the receptor
and found that the"Akt pathway"could be activated without genetic modifications. Two proteins; Plc? 1 (pronounced"plc-gamma-1")and Grb2 (pronounced"grab-2),
1 prevails, it triggers the Akt pathway. In this way, an imbalance in the amount of the two proteins can lead to cell proliferation and cancer formation.
Lead author Professor John Ladbury, Dean of the University of Leeds'Faculty of Biological sciences and Professor of Mechanistic Biology, said,
"There has been huge investment in sequencing the human genome with the idea that if we get all the relevant genetic information we can predict
whether you have a predisposition to cancer and, ultimately, use a precision medicine-based approach to develop a therapeutic approach.
Our study demonstrates that genetic screening alone is not enough.""Dr Zahra Timsah, University Academic Fellow at the University of Leeds'School of Molecular and Cellular biology, who was the lead researcher on the study,
said,"This competition for binding to the receptor represents an unexpected way in which cancer can occur.
We found that in cells where Grb2 is depleted, FGFR2 was vulnerable to Plc? 1 binding and that this triggered uncontrolled proliferation.
Increasing the amount of Grb2 rescued this effect to maintain normal FGFR2 activity. What we think is happening is that under normal conditions the two proteins compete fairly evenly and that the Plc?
1 binding events allow useful cell housekeeping. When the proteins get imbalanced, Plc? 1 can get out of control."
"The researchers also looked at the process in a mouse model and found that Grb2 depletion results in the development of multiple tumors in the vicinity of a primary tumour,
indicating that protein imbalance can have a role in metastasis, the spread of a cancer through the body.
This makes sense because Plc? 1 can play a role in increasing cell movement. Finally, the researchers looked at whether imbalance between Grb2 and Plc?
1 was predictive of the progress of ovarian cancers in patients. Measuring the levels of the proteins in patient tissues followed by database analysis of clinical information from The Cancer Genome Atlas
and other sources revealed that a high level of Grb2 relative to Plc? 1 and FGFR2 was associated with a significantly more favorable prognosis than patients with elevated levels of Plc?
1. Statistical data reveal that just under 40%of patients with a favorable balance were still alive seven years after samples were taken.
1 and FGFR2 binding sites survived the same length of time. The research was funded by the G. Harold and Leila Y. Mathers Charitable Foundation, the National institute of health (NIH), the RGK Foundation and the Gilder Foundation.
It involved researchers from the University of Leeds, The University of Texas MD Anderson Cancer Center and the UT Health Science Center at Houston t
#Normalization Of Testosterone Level After Testosterone Replacement Therapy Patients with low testosterone levels who have gone then on to have testosterone replacement therapy (TRT) could be at lower risk of cardiovascular events such as heart attack or stroke,
In the study, researchers from Kansas city VA Medical centre in Kansas city, USA, examined the effect of TRT on cardiovascular outcomes by comparing incidences of heart attack, stroke,
Data from 83 010 male veterans, all without history of myocardial infarction (MI) or stroke, who were treated between December 1999
Dr Rajat S. Barua, the corresponding author of the paper and a cardiologist, said:""With such widespread and ever increasing use of TRT,
#Researchers Discover Key Mechanism To Emergence Of Deadly Strep Bacteria The incidence of serious strep infections has risen dramatically in the last three decades,
Researchers at the University of California, San diego (UCSD) School of medicine and the University of Wollongong in Australia have discovered that, 30 years ago,
a virus infected the strep bacteria creating a deadly strain of lesh-eatingbacteria that has evolved to produce serious human infections worldwide. ust like a computer virus might come in
and reprogram your hard drive, this virus reprogrammed the genetic machinery of the M1t1 strep into a more virulent form,
. UCSD Professor of Pediatrics and Pharmacy. he consequences of this event on human health are still being felt three decades later.
The research focuses on the major human pathogen group A Streptococcus (trep) Among the most important of all human infectious disease agents,
strep is responsible for a wide range of diseases, ranging from simple throat and skin infections to life-threatening invasive conditions such as necrotizing fasciitis (lesh-eating disease and toxic shock syndrome.
Strep is estimated to cause over 700 million infections each year; over 650,000 of these are dangerous invasive forms.
The UCSD-Australian research team sought to identify what special characteristics make the invasive M1t1 strep clone so virulent for humans.
They observed that during the early stages of a simple skin infection, a small subpopulation of the strep bacteria hijack a protein called plasminogen from the human bloodstream.
the human immune system normally would clear a localized infection. But in the case of the M1t1 strep clone, natural selection instead favors the emergence of the invasive mutants.
The researchers found that a specific genetic mutation in the M1t1 strep clone controls the shift to this invasive form a property
can generate hypervirulent bacterial variants with an increased risk of producing invasive infections, said lead author Mark Walker, Ph d. a Professor of Biological sciences at the University of Wollongong. n the case of the invasive strep clone,
a bacteriophage provided the bacterium a genetic advantage that turned a relatively benign pathogen into a potential deadly disease agent.
A gene present on the bacteriophage acquired by the M1t1 strep encodes an enzyme that allows the bacteria to escape being trapped
The same genetic mutation that allows the strep bacteria to acquire plasminogen and activate it throughout the body also increases production of the bacteriophage-encoded enzyme that blocks neutrophil killing.
When neutrophils of the immune system are summoned to clear a simple strep infection, they apply a natural selective pressure favoring the genetic mutation. he mutation allows the bacteria
not only to survive neutrophil killing, but to spread and destroy tissues, as is seen in necrotizing fasciitis
and other severe forms of strep infection, said Walker. The research team used genetically engineered mice expressing human plasminogen
then spread throughout the body to produce a fatal infection. When the researchers eliminated the single bacteriophage gene encoding the neutrophil resistance factor
the M1t1 strep strain lost its ability to undergo the dangerous mutation and could no longer spread to produce severe infection.
Ancestral strains of the M1t1 strep, isolated before the acquisition of the bacteriophage, also failed to undergo the mutation to produce serious disease.
The collaborative study was initiated during Prof. Walker Australian-American Fulbright Commission Senior Scholar Award sabbatical in Dr. Nizet laboratory,
and financed by grants from the National institutes of health, the National Health and Medical Research Council of Australia,
and the Department of Employment Science and Technology (Australia) International Science Linkages Program. Co-authors contributing to the study were Andrew Hollands
and Jason Mcarthur of the University of Wollongong; Katrin Dinkla and Gurshan Chhatwal of the Helmholtz Centre for Infection Research in Braunschweig, Germany;
Rita Kansal and Malak Kotb of the University of Tennessee-Memphis; Ramy Aziz of the University of Cairo, Egypt;
Amy Simpson, UCSD Medical student, and John Buchanan, UCSD Assistant Research Scientist in Pediatrics
#Spontaneous Rare Mutations Cause Half Of Autism Researchers are saying a new analysis of data on the genetics of autism spectrum disorder disputes a commonly held belief that autism results from the chance combinations
of commonly occurring gene mutations, which are otherwise harmless. They find, instead, further evidence to suggest that devastating"ultra-rare"mutations of genes that they classify as"vulnerable"play a causal role in roughly half of all autism spectrum disorder cases.
The vulnerable genes to which they refer harbor what they call an LGD, or likely gene-disruption.
These LGD mutations can occur"spontaneously"between generations and when that happens they are found in the affected child
but not found in either parent. Although LGDS can impair the function of key genes,
and in this way have a deleterious impact on health, this is not always the case. The study,
whose first author is the quantitative biologist Ivan Iossifov, a Cold Spring Harbotr Laboratory assistant professor and on faculty at the New york Genome Center, finds that"autism genes"-i e.,
, those that, when mutated, may contribute to an ASD diagnosis-tend to have fewer mutations than most genes in the human gene pool.
This seems paradoxical but only on the surface. Iossifov explains that genes with devastating de novo LGD mutations,
when they occur in a child and give rise to autism, usually don't remain in the gene pool for more than one generation before they are,
in evolutionary terms, purged. This is because those born with severe autism rarely reproduce. The team's data helps the research community prioritize which genes with LGDS are most likely to play a causal role in ASD.
The team pares down a list of about 500 likely causal genes to slightly more than 200 best"candidate"autism genes.
The current study also sheds new light on the transmission to children of LGDS that are carried by parents who harbor them but
whose health is nevertheless not severely affected. Such transmission events were observed and documented in the families used in the study,
comprising the Simons Simplex Collection (SSC). When parents carry potentially devastating LGD mutations, these are more frequently found in the ASD-affected children than in their unaffected children,
and most often come from the mother. This result supports a theory first published in 2007 by senior author Michael Wigler, a CSHL professor,
and Dr. Kenny Ye, a statistician at Albert Einstein College of Medicine. They predicted that unaffected mothers are"carriers"of devastating mutations that are transmitted preferentially to children affected with severe ASD.
Females have unexplained an as yet factor that protects them from mutations which, when they occur in males,
will be significantly more likely to cause ASD. It is well known that at least four times as many males as females have ASD.
Published in PNAS
#Drug Disarms Deadly C. Difficile Bacteria Without Destroying Healthy Gut Flora Scientists successfully defeated a dangerous intestinal pathogen, Clostridium difficile,
with a drug targeting its toxins rather than its life. C. difficile is responsible for more than 250,000 hospitalizations
and 15,000 deaths per year in the United states, costing the country more than $4 billion in health-care expenses,
said the study's senior author, Matthew Bogyo, Phd, professor of pathology and of microbiology and immunology at Stanford university School of medicine.
Lead authorship of the study is shared by Kristina Bender, Phd, a former postdoctoral scholar in Bogyo's lab
and Megan Garland, a student in the Medical scientist Training program. By not aiming to kill the pathogen with antibiotics,
scientists were able to avoid wiping out sizeable numbers of beneficial gut microbes. And while their study was performed in mice,
the drug used has already been tested in clinical trials to treat other, unrelated conditions. So the researchers believe it could be moved rapidly into human trials for the treatment of C. difficile, as well.
The findings constitute the first-ever demonstration of a small molecule's ability to disarm C. difficile without incurring the collateral damage caused by antibiotics."
"Unlike antibiotics--which are both the front-line treatment for C. difficile infection and, paradoxically, possibly its chief cause--the drug didn't kill the bacteria,
Infection often recurs About one in 20 people, and possibly many more, harbor C. difficile in their gut, said study co-author Justin Sonnenburg, Phd, professor of microbiology and immunology,
who has conducted pioneering research on the trillions of microbes constituting our intestinal ecosystems. Usually, the pathogen causes no harm,
he said. But in those with immune systems weakened by age, chemotherapy or antibiotics that wipe out their"lawn"of beneficial intestinal microbes,
Plus, the pathogen can dehydrate and condense into shrunken, long-lived spores, making it difficult to get rid of.
Most C. difficile infections originate in settings such as hospitals, clinics and assisted living facilities. Making matters worse,
the infection recurs despite antibiotic treatment. When it does succeed, antibiotics in eliminating it only 25 percent of the time.
About 7 percent of infected people die within 30 days of diagnosis. Treatments for C. difficile infection include fecal transplants,
as well as in neurological changes. Bogyo's group has extensive expertise in studying the activity of proteases, proteins capable of slicing up other proteins.
a postdoctoral scholar in Bogyo's lab who is now an assistant professor at the University of Vermont,
which thrives in the new environment it has created. But it's another story for myriad other bacterial species residing in the intestine--and disastrous for the infected individual's health,
with symptoms ranging from severe diarrhea to intestinal lesions to death. Bogyo's team has developed ways of conducting high-throughput screens of small molecules to speedily test their ability to inhibit
or enhance the activity of proteases. They put this technique to work in search of small molecules that specifically blocked the C. difficile toxins'protease activity.
Helping the good guys"We figured that a molecule that interfered with the pathogen's virulence could prevent inflammation
and the disruption of colon tissue without making the intestinal environment inhospitable to normal, beneficial bacteria the way antibiotics do said
Bogyo. That would lay the groundwork for the"good guys"to make a comeback. In the first of a series of experiments, the investigators separately incubated each of 120,000 different small molecules with the protease-containing piece of C. difficile's primary toxin, Toxin B. Then,
including a number of compounds with known biological activity. Bogyo and his associates focused on a compound called ebselen because,
ebselen also has been tested in clinical trials for chemotherapy-related hearing loss and for stroke. Preclinical testing provided evidence that ebselen is safe and tolerable,
and it has shown no significant adverse effects in ensuing clinical trials. Bogyo's team conducted another test to see how ebselen affected human cells.
whose lab is adept at using mouse models of C. difficile infection. The researchers incubated Toxin B in a solution either containing
Bogyo and colleagues tested ebselen in a mouse model that more accurately mimics a clinical scenario in
The upshot of this and other experiments conducted by Bogyo's team is that using ebselen to disable a toxin in C. difficile was enough to significantly reduce the clinical symptoms of the infection and block the persistent gut damage in mice e
Professor of Complex Materials at ETH Zurich has developed a new procedure that mimics the natural model almost perfectly.
and combines it with modern material research, says Studart doctoral student Tobias Niebel, co-author of a study just published in the specialist journal Nature Materials.
Revival of a 100-year-old techniquecross-section of the artificial tooth under an electron microscope (false colour:
Ceramic platelets in the enamel are orientated vertically. In the dentin, they are aligned horizontally. Photo: Hortense Le Ferrand/ETH Zürichthis is how MASC works:
the researchers first create a plaster cast to serve as a mould. Into this mould, they pour a suspension containing magnetised ceramic platelets, such as aluminium oxide platelets.
The pores of the plaster mould slowly absorb the liquid from the suspension, which causes the material to solidify
and to harden from the outside in. The scientists create an ordered layer-like structure by applying a magnetic field during the casting process,
changing its orientation at regular intervals. As long as the material remains liquid, the ceramic platelets align to the magnetic field.
In the solidified material the platelets retain their orientation. Through the composition of the suspension and the direction of the platelets, a continuous process can be used to produce multiple layers with differing material properties in a single object.
This creates complex materials that are almost perfect imitations of their natural models, such as nacre or tooth enamel. ur technique is similar to 3d printing,
but 10 times faster and much more cost-effective, says Florian Bouville, a post-doc with Studart and co-lead author of the study.
The co-lead author of the study, doctoral student Hortense Le Ferrand, and her colleagues began by creating a plaster cast of a human wisdom tooth.
They then filled this mould with a suspension containing aluminium oxide platelets and glass nanoparticles as mortar.
the scientists poured a second suspension into the same mould. This suspension, however, did not contain glass particles.
The aluminium oxide platelets in the second layer were aligned horizontally to the surface of the tooth using the magnet.
Finally, the researchers filled the pores that remained after the sintering with a synthetic monomer used in dentistry,
the artificial tooth clearly shows that a degree of control over the microstructure of a composite material can be achieved,
However, the new production process for such complex biomimetic materials also has other potential applications.
which would allow the use of such materials in electronics. he base substances and the orientation of the platelets can be combined as required,
Overtext Web Module V3.0 Alpha
Copyright Semantic-Knowledge, 1994-2011