#Unstoppable magnetoresistance Mazhar Ali a fifth-year graduate student in the laboratory of Bob Cava the Russell Wellman Moore Professor of Chemistry at Princeton university has spent his academic career discovering new superconductors materials
coveted for their ability to let electrons flow without resistance. While testing his latest candidate the semimetal tungsten ditelluride (WTE2) he noticed a peculiar result.
Ali applied a magnetic field to a sample of WTE2 one way to kill superconductivity if present and saw that its resistance doubled.
Intrigued Ali worked with Jun Xiong a student in the laboratory of Nai Phuan Ong the Eugene Higgins Professor of Physics at Princeton to re-measure the material's magnetoresistance
which is the change in resistance as a material is exposed to stronger magnetic fields. He noticed the magnetoresistance kept going up
and up and up--that never happens. said Cava. The researchers then exposed WTE2 to a 60-tesla magnetic field close to the strongest magnetic field humans can create
and observed a magnetoresistance of 13 million percent. The material's magnetoresistance displayed unlimited growth making it the only known material without a saturation point.
The results were published on September 14 in the journal Nature. Electronic information storage is dependent on the use of magnetic fields to switch between distinct resistivity values that correlate to either a one or a zero.
The larger the magnetoresistance the smaller the magnetic field needed to change from one state to another Ali said.
Today's devices use layered materials with so-called giant magnetoresistance with changes in resistance of 20000 to 30000 percent when a magnetic field is applied.
Colossal magnetoresistance is close to 100000 percent so for a magnetoresistance percentage in the millions the researchers hoped to coin a new term.
To look at the structure with an electron microscope the research team turned to Jing Tao a researcher at Brookhaven National Laboratory.
when the magnetic field is applied in a certain direction This could be very useful in scanners where multiple WTE2 devices could be used to detect the position of magnetic fields Ali said.
#Computer science: Data smashing could unshackle automated discovery A little known secret in data mining is that simply feeding raw data into a data analysis algorithm is unlikely to produce meaningful results,
say the authors of a new Cornell University study. From recognizing speech to identifying unusual stars,
new discoveries often begin with comparison of data streams to find connections and spot outliers. But most data comparison algorithms today have one major weakness--somewhere,
they rely on a human expert to specify what aspects of the data are relevant for comparison,
and what aspects aren't . But experts aren't keeping pace with the growing amounts and complexities of big data.
Cornell computing researchers have come up with a new principle they call"data smashing"for estimating the similarities between streams of arbitrary data without human intervention,
and without access to the data sources. Hod Lipson, associate professor of mechanical engineering and computing and information science,
and Ishanu Chattopadhyay, a former postdoctoral associate with Lipson and now at the University of Chicago, have described their method in Royal Society Interface, Oct 1.
Data smashing is based on a new way to compare data streams. The process involves two steps. First, the data streams are smashed algorithmically"to"annihilate"the information in each other.
Then, the process measures what information remained after the collision. The more information remained the less likely the streams originated in the same source.
Data smashing principles may open the door to understanding increasingly complex observations, especially when experts do not know what to look for, according to the researchers.
The authors demonstrated the application of their principle to data from real-world problems, including the disambiguation of electroencephalograph patterns from epileptic seizure patients;
detection of anomalous cardiac activity from heart recordings; and classification of astronomical objects from raw photometry.
In all cases and without access to original domain knowledge, the researchers demonstrated performance on par with the accuracy of specialized algorithms and heuristics devised by experts s
#Giant leap for diabetes: From human embryonic stem cells to billions of human insulin producing cells Harvard stem cell researchers announced that they have made a giant leap forward in the quest to find a truly effective treatment for type 1 diabetes,
a condition that affects an estimated three million Americans at a cost of about $15 billion annually:
With human embryonic stem cells as a starting point, the scientists are for the first time able to produce,
in the kind of massive quantities needed for cell transplantation and pharmaceutical purposes, human insulin-producing beta cells equivalent in most every way to normally functioning beta cells.
Doug Melton, who led the work and who twenty-three years ago, when his then infant son Sam was diagnosed with type 1 diabetes,
dedicated his career to finding a cure for the disease, said he hopes to have human transplantation trials using the cells to be underway within a few years."
"We are now just one preclinical step away from the finish line, "said Melton, whose daughter Emma also has type 1 diabetes.
A report on the new work has been published by the journal Cell. Felicia W. Pagliuca, Jeff Millman,
and Mads Gurtler of Melton's lab are co-first authors on the Cell paper.
The research group and paper authors include a Harvard undergraduate.""You never know for sure that something like this is going to work until you've tested it numerous ways,
"said Melton, Harvard's Xander University Professor and a Howard hughes medical institute Investigator.""We've given these cells three separate challenges with glucose in mice
and they've responded appropriately; that was really exciting.""It was gratifying to know that we could do something that we always thought was continued possible,
"he, "but many people felt it wouldn't work. If we had shown this was not possible, then
I would have had to give up on this whole approach. Now I'm really energized.""The stem cell-derived beta cells are presently undergoing trials in animal models,
including nonhuman primates, Melton said. Elaine Fuchs, the Rebecca C. Lancefield Professor at Rockefeller University,
and a Howard hughes medical institute Investigator who is involved not in the work, hailed it as"one of the most important advances to date in the stem cell field,
and I join the many people throughout the world in applauding my colleague for this remarkable achievement."
"For decades, researchers have tried to generate human pancreatic beta cells that could be cultured and passaged long term under conditions where they produce insulin.
and opened the door for drug discovery and transplantation therapy in diabetes, "Fuchs said. And Jose Oberholtzer, M d.,Associate professor of Surgery, Endocrinology and Diabetes,
and Bioengineering at the University of Illinois at Chicago, and its Director of the Islet and Pancreas Transplant Program and the Chief of the Division of Transplantation, said work described in today's Cell"will leave a dent in the history of diabetes.
Doug Melton has put in a life-time of hard work in finding a way of generating human islet cells in vitro He made it.
This is a phenomenal accomplishment.""Melton, co-scientific director of the Harvard Stem Cell Institute, and the University's Department of Stem Cell and Regenerative Biology--both of which were created more than a decade after he began his quest--said that
when he told his son and daughter they were surprisingly calm.""I think like all kids,
they always assumed that if I said I'd do this, I'd do it, "he said with a self-deprecating grin.
Type 1 diabetes is an autoimmune metabolic condition in which the body kills off all the pancreatic beta cells that produce the insulin needed for glucose regulation in the body.
Thus the final preclinical step in the development of a treatment involves protecting from immune system attack the approximately 150 million cells that would have to be transplanted into each patient being treated.
the Samuel A. Goldblith Professor of Applied Biology, Associate professor in the Department of Chemical engineering, the Institute of Medical Engineering and Science,
Cell transplantation as a treatment for diabetes is still essentially experimental, uses cells from cadavers, requires the use of powerful immunosuppressive drugs,
MIT's Anderson said the new work by Melton's lab is"an incredibly important advance for diabetes.
human beta cells through controlled differentiation of stem cells will accelerate the development of new therapeutics.
In particular, this advance opens to doors to an essentially limitless supply of tissue for diabetic patients awaiting cell therapy."
"Richard A. Insel, M d.,chief scientific officer of the Juvenile diabetes Research Foundation, a funder of Melton's work, said the"JDRF is thrilled with this advancement toward large scale production of mature, functional human beta
This significant accomplishment has the potential to serve as a cell source for islet replacement in people with type 1 diabetes
and may provide a resource for discovery of beta cell therapies that promote survival or regeneration of beta cells and development of screening biomarkers to monitor beta cell health and survival to guide therapeutic
strategies for all stages of the disease.""Melton expressed gratitude to both the Juvenile diabetes Research Foundation and the Helmsley Trust, saying"their support has been,
"While diabetics can keep their glucose metabolism under general control by injecting insulin multiple times a day,
and that lack of control leads to devastating complications from blindness to loss of limbs.
About 10 percent of the more than 26 million Americans living with type 2 diabetes are also dependent upon insulin injections,
and would presumably be candidates for beta cell transplants, Melton said.""There have been previous reports of other labs deriving beta cell types from stem cells,
#Multiple neurodevelopmental disorders have a common molecular cause Neurodevelopmental disorders such as Down syndrome and autism-spectrum disorder can have profound lifelong effects on learning
and memory but relatively little is known about the molecular pathways affected by these diseases. A study published by Cell Press October 9th in the American Journal of Human genetics shows that neurodevelopmental disorders caused by distinct genetic mutations produce similar molecular effects in cells suggesting that a one-size-fits-all therapeutic approach could be effective
for conditions ranging from seizures to attention-deficit hyperactivity disorder. Neurodevelopmental disorders are rare meaning trying to treat them is not efficient says senior study author Carl Ernst of Mcgill University.
Once we fully define the major common pathways involved targeting these pathways for treatment becomes a viable option that can affect the largest number of people.
A large fraction of neurodevelopmental disorders are associated with variation in specific genes but the genetic factors responsible for these diseases are very complex.
For example whereas common variants in the same gene have been associated with two or more different disorders mutations in many different genes can lead to similar diseases.
As a result it has not been clear whether genetic mutations that cause neurodevelopmental disorders affect distinct molecular pathways or converge on similar cellular functions.
To address this question Ernst and his team used human fetal brain cells to study the molecular effects of reducing the activity of genes that are mutated in two distinct autism-spectrum disorders.
Changes in transcription factor 4 (TCF4) cause 18q21 deletion syndrome which is characterized by intellectual disability and psychiatric problems and mutations in euchromatic histone methyltransferase 1 (EHMT1) cause similar symptoms in a disease known as 9q34 deletion syndrome.
Interfering with the activity of TCF4 or EHMT1 produced similar molecular effects in the cells.
Strikingly both of these genetic modifications resulted in molecular patterns that resemble those of cells that are differentiating
or converting from immature cells to more specialized cells. Our study suggests that one fundamental cause of disease is that neural stem cells choose to become full brain cells too early Ernst says.
This could affect how they incorporate into cellular networks for example leading to the clinical symptoms that we see in kids with these diseases s
#Gene that drives aggressive brain cancer found by new computational approach Using an innovative algorithm that analyzes gene regulatory and signaling networks,
Columbia University Medical center (CUMC) researchers have found that loss of a gene called KLHL9 is the driving force behind the most aggressive form of glioblastoma, the most common form of brain cancer.
The CUMC team demonstrated in mice transplants that these tumors can be suppressed by reintroducing KLHL9 protein,
offering a possible strategy for treating this lethal disease. The study was published today in the online issue of Cell.
The team used the same approach to identify mutations and heritable variants that have been linked to breast cancer and Alzheimer's disease,
suggesting that the algorithm, combined with the researchers'sophisticated computer models of cellular regulation, is a powerful method for identifying genetic drivers of a wide range of diseases."
"This algorithm adds a new dimension to our ability to identify the genetic causes of complex disease.
When combined with other tools that our lab has developed, it will help identify many more genes that hold potential as genetic biomarkers of disease progression
and targets for treatment,"said study leader Andrea Califano, Phd, the Clyde and Helen Wu Professor of Chemical Biology (in Biomedical Informatics and the Institute for Cancer Genetics), chair of the Department of Systems Biology,
and director of the JP Sulzberger Columbia Genome Center, at Columbia's College of Physicians and Surgeons.
In previous studies Dr. Califano and his colleagues used high-power computer models to demonstrate that certain types of cancer have conserved highly"master regulators"--genes
whose individual or synergistic activity is necessary for disease to develop and persist. However, these models provided no information on the key genetic mutations that presumably drive the abnormal activity of these master regulators.
In the current study, the team combined its existing computational tools with a new algorithm called DIGGIT (for Driver-Gene Inference by Genetical-Genomic Information theory),
which"walks"backward from the master regulators to find the genetic events that drive cancer."
"Conventional techniques, like genome-wide association studies, must test all possible genetic mutations and variants in a disease cell, compared with a normal cell,
"said lead author James C. Chen, Phd, a postdoctoral research scientist in Dr. Califano's laboratory, who developed DIGGIT."
"These can number in the tens to hundreds of thousands. As a result, based on the number of patients we have profiled,
we have sufficient statistical power to identify only the most striking mutations. The DIGGIT algorithm, combined with
what we know about regulatory events in the cell, can help us sort through this mass of data
and identify critical hidden mutations that otherwise would have gone undetected.""The new approach was tested on mesenchymal glioblastoma, the most aggressive subtype of the disease,
by jointly analyzing the gene expression and mutational profile data of more than 250 patients collected by the Cancer Genome Atlas consortium.
The CUMC team found two genes--C/EBPD and KLHL9--that appear to activate glioblastoma's master regulators.
C/EBPD, had already been identified by the labs of Dr. Califano and of Antonio Iavarone, MD, professor of neurology and of pathology & cell biology (in the Institute for Cancer Genetics),
as a master regulator of the disease, so the researchers focused on KLHL9, which had never been tied to this or any other form of cancer.
In subsequent laboratory studies, the researchers reactivated the defective KLHL9 gene in aggressive glioblastoma cells,
which was sufficient to lose the mesenchymal phenotype. When KLHL9 protein was reintroduced into mice receiving direct transplants from patients with mesenchymal glioblastoma,
their tumors regressed, providing further evidence that KLHL9 mutations (which were found in 50 percent of the mesenchymal glioblastoma patients),
are directly responsible for driving this cancer subtype. DIGGIT may be applicable to other complex diseases. In further studies by the Califano team, the algorithm identified 35 genes as drivers of breast cancer.
Of the 25 genes previously identified in the literature 19 (76 percent) were identified by DIGGIT,
confirming that the algorithm is capable of capturing driver mutations in other types of cancer.
The analysis also revealed several novel genes that may warrant further investigation. In a study of Alzheimer's disease, DIGGIT found 14 genetic variants that appear to drive the condition,
including the APOE locus, a well-known variant associated with Alzheimer's, and TYROBP, a gene also validated as an Alzheimer's risk variant.
DIGGIT also identified novel variants, including those in four genes in the integrin pathway, that had not been connected previously with the disease
and that are currently being investigated.""It's important to stress that this constitutes an important improvement over traditional gene-association studies.
The latter can identify statistical associations between mutations and disease, but cannot explain how the mutation drives that effect,
"said Dr. Califano.""Because DIGGIT identifies disease-causing genes by tracing their aberrant activity through the regulatory network of the cell,
it provides direct information on the specific molecular interactions through which a genetic mutation causes disease--the'mechanism.'
'In traditional research, this process can take years, if not decades.""""Even in our studies of breast cancer and Alzheimer's disease, where the goal was simply to show that DIGGIT could identify mutations
and variants missed by conventional statistical methods, the algorithm identified the key molecular regulators and pathways through
which these mutations likely work to drive disease, adding significant new knowledge that can be tested rapidly in the lab"Dr. Chen said a
#Special chromosomal structures control key genes Within almost every human cell is a nucleus six microns in diameterbout one 300th of a human hair widthhat is filled with roughly three meters of DNA.
As the instructions for all cell processes the DNA must be accessible to the cell transcription machinery yet be compressed tightly enough to fit inside the nucleus. Scientists have theorized long that the way DNA is packaged affects gene expression.
Whitehead Institute researchers present the first evidence that DNA scaffolding is responsible for enhancing and repressing gene expression. or the first time we see that the structure of the chromosomes contributes to gene controlsays Whitehead Member Richard Young who is also a professor of biology at MIT. n the past there have been all kinds of ideas around how the structure might affect gene control
but now one has been tested experimentally and shown to be true. NA scaffolding has a hierarchy that ranges from beads-on-a-string where a strand of DNA is wrapped around histone proteins to form a nucleosome to topological associating domains akin to DNA balls containing multiple DNA loops interacting with various regulatory
elements to highly condensed chromosomes. Working in mouse embryonic stem cells (ESCS) the Young lab examined the scaffolding landscape found within topologically associated domains.
The researchers knew that proteins called Cohesin and CTCF are bound to the DNA around important ESC genes
but they did not know how these proteins affect the DNA three-dimensional organization. Using a technique known as Chia-PET the researchers focused on how these proteins interact. y knowing which of the Cohesin/CTCF bound sites are coming together in physical proximity we started to go from a linear view of the genome to sets of looping interactions
which led us to these domains these super enhancer domains where gene expression enhancement is contained within the loopsays Jill Dowen a postdoctoral researcher in Young lab. Dowen
and coauthors Zi Peng Fan Denes Hnisz and Gang Ren describe the structure of these loops in the latest online edition of the journal Cell.
Hnisz also a postdoctoral researcher in Young lab likens the loops to oody bagswith Cohesin
and CTCF acting as the purse strings to create a DNA loop that cradles proteins enhancing or repressing gene expression.
The enhancement or repression effects are confined to the genes within the goody bag. In the ESCS they studied the scientists identified 197 Cohesin/CTCF-flanked loops that contain active genes
but they were in similar locations as in the ESC genome. Of course the repression or enhancement role of the loops differed between ESCS and the more differentiated cells.
although they may switch their contents and therefore their effect on gene expression. The researchers plan to study the loop structure
and its effects. think wee filled in a major gap in the understanding of how gene expression is linked to the local organization of chromosomessays Hnisz. t will be exciting to explore
whether defects in these mechanisms might even contribute to human disease. tory Source: The above story is provided based on materials by Whitehead Institute for Biomedical Research.
The original article was written by Nicole Giese Rura. Note: Materials may be edited for content and length.
Led by scientists from the University of Warwick the discovery of the new particle will help provide greater understanding of the strong interaction the fundamental force of nature found within the protons of an atom's nucleus. Named Ds3*(2860) the particle
a new type of meson 1 was discovered by analysing data collected with the LHCB detector at CERN's Large hadron collider (LHC) 2. The new particle is bound together in a similar way to protons.
Lead scientist Professor Tim Gershon from The University of Warwick's Department of physics explains: Gravity describes the universe on a large scale from galaxies to Newton's falling apple
It is so strong that the binding energy of the proton gives a much larger contribution to the mass through Einstein's equation E=mc2 than the quarks themselves. 3 Due in part to the forces'relative simplicity scientists have previously been able to solve the equations behind gravity
and electromagnetic interactions but the strength of the strong interaction makes it impossible to solve the equations in the same way Calculations of strong interactions are done with a computationally intensive technique called Lattice QCD says Professor Gershon.
what the particle is adds Professor Gershon. Therefore it provides a benchmark for future theoretical calculations.
Warwick Ph d. student Daniel Craik who worked on the study adds Perhaps the most exciting part of this new result is that it could be the first of many similar discoveries with LHC data.
The above story is provided based on materials by University of Warwick. Note: Materials may be edited for content and length.
what type of chemotherapy you attack a tumor with, many cancer cells resort to the same survival tactic:
Scientists at Brigham Young University discovered the two proteins that pair up and switch on this process--known as autophagy."
"This gives us a therapeutic avenue to target autophagy in tumors, "said Josh Andersen, a BYU chemistry professor."
"The idea would be to make tumors more chemo-sensitive. You could target these proteins and the mechanism of this switch to block autophagy,
which would allow for lower doses of chemotherapy while hopefully improving patient outcomes.""Lower doses would mean milder side effects.
The prospect spurred an international hunt for this switch. For good reason, several other labs started with a protein called ATG9 as their prime suspect
and then looked for its accomplice among thousands of other proteins. But the BYU team, comprised mainly of undergraduate students,
stumbled into the race unexpectedly, coming at it from a different direction. They wanted to know why cancer cells made a surplus of protein called 14-3-3 zeta.
they forced tumor cells to undergo autophagy by depriving them of oxygen and glucose. A comparison with a control group let them see that the two proteins hook up only when under attack.
That's because stress makes Atg9 undergo a modification that enables 14-3-3 zeta to bind with it
"The study results appear in the journal Molecular and Cellular biology. Andersen notes that several medicines already exist that could block autophagy
and make chemotherapy more effective. One of them is called chloroquine, an antimalarial drug invented in 1934.
#More efficient transformer materials Almost every electronic device contains a transformer. An important material used in their construction is electrical steel.
Researchers have found a way to improve the performance of electrical steel and manufacture it more efficiently using an optimized laser process.
Transformers convert the standard voltage from the wall outlet into the lower voltages required by electronic devices.
Similar but more powerful transformers are used in electricity substations to convert the high voltages of the transmission grid into the standard AC power supply delivered to households.
All transformers have the same basic structure: a pair of iron cores around which wires of different lengths are wrapped.
These are the transformer coils one of which generates an oscillating magnetic field while the other converts this magnetic field into a voltage.
To minimize the energy loss associated with this process special types of iron-silicon alloy known as electrical steel are used to make the core.
In their native state these alloys have a grainoriented structure which determines their magnetic properties.
Grain-oriented means that the material has a crystalline structure in which each crystal or grain is arranged in a regular periodic order.
By heating selected areas of the material it is possible to reduce the size of the domains with the same magnetic orientation
which in turn alters the magnetic structure of the steel. This results in a lower heat development and thus reduces the material's hysteresis loss says Dr. Andreas Wetzig who heads the laser ablation
and cutting department at the Fraunhofer Institute for Material and Beam Technology IWS in Dresden describing the complex changes that take place inside the material.
Laser processing has long become established as the preferred method for this type of heat treatment.
While the steel sheet measuring around one meter in width moves forward at a rate of more than 100 meters per minute a focused laser beam travels at very high speed (approximately 200 meters per second) from side to side
across the surface of the material along paths spaced a few millimeters apart. The Dresden-based research team has optimized this process:
The main aim of this research is to facilitate the integration of laser processing in existing production environments in order to save time and costs.
In a further effort to reduce hysteresis loss in electrical steel the researchers have started recently working with a new type of solid-state laser:
It cuts hysteresis loss by up to 15 percent compared with the 10 percent normally achieved until now.
The IWS experts are currently working on the next important stage: that of expanding the applications of their technology to electrical steel for engine components.
However unlike transformer steel these materials do not have oriented a grain structure and therefore possess different magnetic properties.
This means that we cannot transfer our process one-to-one without modification explains Wetzig.
The benefits of laser processing in the case of non-grain-oriented electrical steel vary according to the working point of the specific engine or motor.
In high-performance machines such as vehicle engines which are designed to run at high rotational speeds energy loss can be reduced by a few percentage points In high-torque electric motors such as those used to operate pumps the reduction in energy loss can be as high as twentyfive
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