#Could flu someday be prevented without a vaccine? Researchers have discovered a way to trigger a preventive response to a flu infection without any help from the usual players the virus itself or interferon, a powerful infection fighter.
The finding, in both mouse and human cells, suggests that manipulating a natural process could someday be an alternative way to not just reduce the severity of the flu,
but prevent infection altogether. he flu vaccine needs to change every year because the virus is constantly mutating.
What wee doing is targeting a more fundamental process that is not specific to any particular strain of the virus
said Jacob Yount, assistant professor of microbial infection and immunity at The Ohio State university and senior author of the study.
After showing in cells that altering the role of one protein can stop the virus in its tracks,
Yount lab has begun using experimental drugs to test this flu prevention strategy in mice. Any possibility for human use is still many years away,
but the scientistslong-term goal is to develop a vaccine-independent method to prevent flu infections. f we were to have an outbreak of some pandemic influenza virus similar to
what we experienced in 2009, I could envision using this technique to help people who are particularly vulnerable to infection,
he said. t would work best if used before an infection, because the strategy prevents cells from becoming infected in the first place.
The research is published in the journal PLOS Pathogens. The method involves raising the level of a protein that is known to be effective against all strains of influenza ever tested.
The trick for infection prevention, however, is boosting that protein level in cells before the virus shows up.
Doing that, the scientists discovered in this study, involves suppressing the function of another protein. The protein effective against influenza is called IFITM3 (
pronounced I-fit-M-3, for interferon-induced transmembrane protein 3). Under natural conditions, IFITM3 is produced in large quantities only after the flu virus is present,
so it can reduce the severity of infection. But the way it targets the virus by trapping it
and disabling its ability to make copies of itself means that increasing the protein level before the flu ever arrives would prevent infection from occurring.
Enough IFITM3 is produced in all cells to maintain a small but steady presence, but it has a short lifespan.
If a cell doesn see a need for its virus-fighting function the protein is degraded.
and fend off an influenza attack. This enzyme, also a protein, proved to be the silver bullet in Yount work on flu prevention.
The enzyme is called NEDD4 (pronounced Ned-4), and it degrades IFITM3 by attaching a small chain of molecules to it a common process of protein clearing called ubiquitination.
In a series of experiments in mouse and human lung cells, Yount and colleagues showed that inhibiting NEDD4 from doing this job led to an accumulation of IFITM3 in the cells
and greater resistance to infection by flu viruses. IFITM3 is known to be important to humans
because previous research has shown that it is identified the only protein containing a frequent genetic mutation linked to severe flu infections.
because mice lacking the same IFITM3 protein are highly susceptible to flu infections. Being able to stimulate this response is important for many reasons, not the least
Interferon infection-fighting power is accompanied by severe side effects most commonly associated with its former use as a treatment for Hepatitis C that include, not surprisingly,
Yount said. hat was a huge finding that you don need an infection or interferon to increase the level of IFITM3.
But later in life, lacking NEDD4 might not pose any health problems which is why Yount is currently testing the effects of suppressing NEDD4 on adult mice
#Engineering a permanent solution to genetic diseases In his mind, Basil Hubbard can already picture a new world of therapeutic treatments for millions of patients just over the horizon.
It a future in which diseases like muscular dystrophy, cystic fibrosis and many others are treated permanently through the science of genome engineering.
Thanks to his latest work, Hubbard is bringing that future closer to reality. Hubbard research, published in the journal Nature Methods, demonstrates a new technology advancing the field of genome engineering.
The method significantly improves the ability of scientists to target specific faulty genes and then ditthem
replacing the damaged genetic code with healthy DNA. here is a trend in the scientific community to develop therapeutics in a more rational fashion,
rather than just relying on traditional chemical screens, says Hubbard, an assistant professor of pharmacology in the University of Alberta Faculty of medicine & Dentistry. ee moving towards a very logical type of treatment for genetic diseases,
where we can actually say, our disease is caused by a mutation in gene X, and wee going to correct this mutation to treat it.?
In theory, genome engineering will eventually allow us to permanently cure genetic diseases by editing the specific faulty genes. evolutionizing health caregenome engineering involves the targeted, specific modification of an organism genetic information.
Much like how a computer programmer edits computer code, scientists could one day replace a person broken
or unhealthy genes with healthy ones through the use of sequence-specific DNA BINDING PROTEINS attached to DNA-editing tools.
The field has made large strides over the last two decades and may one day revolutionize medical care.
One of the obstacles still to be addressed in the field before it can see widespread use in humans is how to ensure the proteins only affect the specific target genes in need of repair.
but more improvements are needed to ensure off-target genes aren modified result that could potentially cause serious health problems itself.
we can produce gene editing tools that are 100 times more specific for their target sequence. uture applicationsmuch of the current research in genome engineering is focused on treating monogenic diseasesiseases that involve a single geneecause theye much easier for researchers
Examples include diseases such as hemophilia sickle-cell anemia, muscular dystrophy and cystic fibrosis. Though the field is still in its relative infancy,
Hubbard says human clinical trials involving sequence-specific DNA-editing agents are already underway. If successful, he expects the first clinical applications could be seen in the next decade.
He hopes his current work will play a role in helping genome engineering reach its full potential
gene editing could possibly provide a permanent cure for a lot of different diseases, says Hubbard. e still have to overcome many hurdles,
but I think this technology definitely has the potential to be transformative in medicine. h
which can accurately detect malignant melanoma without a biopsy. The report, published online in Nature Scientific Reports yesterday (August 11),
During the study, led by Lancaster University and Pisa University in Italy, 55 patients with atypical moles agreed to have monitored their skin by researchers at Pisa University Hospital using a laser Doppler system.
The laser Doppler was used to record the complex interactions taking place in the minute blood vessels beneath their suspicious mole for around 30 minutes.
The fluctuations in recorded signals were analysed then using methods developed by physicists at Lancaster University.
Professor Aneta Stefanovska of Lancaster University said: e used our knowledge of blood flow dynamics to pick up on markers
and those beneath normal skin. ombining the new dynamical biomarkers we created a test which,
which means that melanoma is identified in all cases where it is ruled present, and out in 90.9%of cases where it is not. rofessor Marco Rossi of Pisa University said:
kin malignant melanoma is a particularly aggressive cancer associated with quick blood vessel growth which means early diagnosis is vital for a good prognosis.
The current diagnostic tools of examination by doctors followed by biopsy inevitably leads to many unnecessary invasive excisions. his simple, accurate,
in vivo distinction between malignant melanoma and atypical moles may lead to a substantial reduction in the number of biopsies currently undertaken. ource:
Lancaster Universit L
#Nicotine-eating bacteria could one day help smokers kick the habit Most people who smoke cigarettes know it bad for their health,
but quitting is notoriously difficult. To make it easier, scientists are taking a brand-new approach. They are turning to bacteria that thrive on nicotine, the addictive component in tobacco.
Tobacco use remains the leading cause of preventable disease, disability and death in the U s. Smokers who want to quit can turn to various pharmacological aids.
These include patches gum and other nicotine-releasing products designed to replace cigarettes, as well as drugs that sequester nicotine in the body to prevent it from reaching the brain,
#U s. Distributed Solar Prices Fell 10 to 20 Percent in 2014, with Trends Continuing into 2015 The installed price of distributed solar photovoltaic (PV) power systems in the United states continues to fall precipitously.
This is according to the latest edition of Tracking the Sun, an annual PV cost tracking report produced by the Department of energy Lawrence Berkeley National Laboratory (Berkeley Lab). Installed prices for residential and small nonresidential systems completed in 2014 were $0. 40-per-watt (W) lower,
and prices for large nonresidential systems were $0. 70/W lower, than in the prior year. his marked the fifth consecutive year of significant price reductions for distributed PV systems in the U s.,
notes Galen Barbose of Berkeley Lab Electricity Markets and Policy Group, the report lead author.
Within the first six months of 2015, installed prices within a number of large state markets fell by an additional $0. 20 to $0. 50/W,
or 6 to 13 percent, maintaining the steady pace of solar price declines in recent years.
The continued decline in PV system pricing is given especially noteworthy the relatively stable price of PV modules since 2012.
The report attributes recent system price declines, instead, to reductions in solar oftcosts. These include such things as marketing and customer acquisition
system design, installation labor, and permitting and inspections. Attention in the industry has homed-in on soft costs,
and the report suggests that these efforts are partly responsible for recent price declines. The report also highlights the tremendous variability in PV system pricing.
Among residential systems installed in 2014, for example, 20 percent sold for less than $3. 50/W,
the report finds substantial heterogeneity in pricing, and suggests that ow-price leadersin these states can serve as a benchmark for installed price reductions that could be achieved more broadly.
In Arizona, for example, 20 percent of residential installers had median prices at or below $3. 00/W in 2014, compared to the median price of $4. 30/W across all U s. residential systems in 2014.
The report examines various other drivers for PV system prices such as system size, the state in which the system is installed,
whether it is owned by the site host or a third party, whether it is installed in new construction or on existing buildings,
whether the site host is a for-profit commercial or tax-exempt entity, the module efficiency level,
whether the system uses a microinverter or a standard string inverter, and whether the system is installed on a rooftop
or is mounted ground, either with or without tracking. To varying degrees, these many factors are all found to impact PV system prices.
As Barbose stresses he fact that such variability exists underscores the need for caution and specificity when referring to the installed price of PV,
as clearly there is no single ricethat uniformly and without qualification characterizes the U s. market, or even particular market segments, as a whole. he report, Tracking the Sun VIII:
The Installed Price of Residential and Nonresidential Photovoltaic systems in the United states, is the eighth edition in Berkeley Lab Tracking the Sun report series.
It is collected based on data from more than 400,000 residential and nonresidential PV systems installed between 1998 and 2014 across 42 states,
representing more than 80 percent of all distributed PV capacity installed in the United states. The report is produced in conjunction with a number of other related and ongoing research activities at Berkeley Lab
and at the National Renewable energy Laboratory that collectively analyze trends in PV system pricing. The latest edition of Tracking the Sun
along with a summary slide deck and data file, may be downloaded at trackingthesun. lbl. gov. Source: LB g
#Researchers genetically engineer yeast to produce opioids After a decade work a team led by Stanford bioengineer Christina Smolke succeeded in finding more than 20 genes from five different organisms and engineering them into the genome of baker yeast.
In so doing they created two different microbial assembly lines, each of which took less than five days to convert sugar into one of two medicinal compounds:
either thebaine, which can be refined into painkillers, or hydrocodone which is a prescription painkiller. The circles on the left represent organisms that contributed genes to the bioengineered yeast.
From the top: California poppy, rat, goldthread, bacteria, and opium poppy. A process that had taken a year from farm to pharmaceutical factory now occurs in three to five days in yeast genetically engineered to biosynthesize the active ingredients for opioid painkillers;
this could broaden access to many plant-based medicines. For thousands of years, people have used yeast to ferment wine,
brew beer and leaven bread. Now researchers at Stanford have engineered genetically yeast to make painkilling medicines,
a breakthrough that heralds a faster and potentially less expensive way to produce many different types of plant-based medicines.
Writing today in Science, the Stanford engineers describe how they reprogrammed the genetic machinery of baker yeast
It can take more than a year to produce a batch of medicine, starting from the farms in Australia,
processed and shipped to pharmaceutical factories in the United states, where the active drug molecules are extracted
and refined into medicines. hen we started work a decade ago, many experts thought it would be impossible to engineer yeast to replace the entire farm-to-factory process,
said senior author Christina Smolke, an associate professor of bioengineering at Stanford. Now, though the output is small it would take 4,
400 gallons of bioengineered yeast to produce a single dose of pain relief the experiment proves that bioengineered yeast can make complex plant-based medicines. his is only the beginning,
Smolke said. he techniques we developed and demonstrate for opioid pain relievers can be adapted to produce many plant-derived compounds to fight cancers,
infectious diseases and chronic conditions such as high blood pressure and arthritis. rom plant to test tubesmany medicines are derived from plants,
which our ancestors chewed or brewed into teas, or later refined into pills using chemical processes to extract
to reprogram the cells into custom chemical assembly lines to produce medicinal compounds. An important predecessor to the Stanford work has been the use of genetically engineered yeast to produce the antimalarial drug artemisinin.
about one third of the world supply has shifted to bioreactors. The artemisinin experiments proved that yeast biosynthesis was involved possible,
but adding only six genes. The Stanford team had to engineer 23 genes into yeast to create their cellular assembly line for hydrocodone. his is complicated the most chemical synthesis ever engineered in yeast,
a Phd student in chemistry and a member of Smolke team. heye the action heroes of biology. o get the yeast assembly line going,
the Stanford team had to fill in a missing link in the basic science of plant-based medicines.
Many plants, including opium poppies, produce (S)- reticuline, a molecule that is a precursor to active ingredients with medicinal properties.
but even after the Stanford bioengineers added this enzyme into their microbial factory, the yeast didn create enough of the opioid compound.
Smolke said. e need options to help ensure that the bio-based production of medicinal compounds is developed in the most responsible way. molke said that in the United states,
where opioid medicines are already widely available, the focus is on potential misuse. But the World health organization estimates that 5. 5 billion people have little
with proper controls against abuse, allow bioreactors to be located where they are needed, she said. In addition to bioengineering yeast to convert sugar into hydrocodone,
Bio-produced thebaine would still need to be refined through sophisticated processes in pharmaceutical factories, but it would eliminate the time delay of growing poppies. he molecules we produced
and the techniques we developed show that it is possible to make important medicines from scratch using only yeast,
and fairly provide medicines to all who need
#Scientists pioneer method to track water flowing through glaciers Researchers for the first time have used seismic sensors to track meltwater flowing through glaciers and into the ocean,
an essential step to understanding the future of the world largest glaciers as climate changes. The brown water that can be seen at the top of the picture is the subglacial discharge,
or meltwater, that has flowed through Alaska Yahtse Glacier and into the ocean. Scientists at The University of Texas at Austin have pioneered a method to track meltwater flowing through glaciers that end in the ocean.
The University of Texas Institute for Geophysics (UTIG) helped pioneer this new method on glaciers in Greenland and Alaska.
The study will be published Aug 10 in the journal Geophysical Research Letters. Meltwater moving through a glacier into the ocean is critically important
The team also includes researchers from the University of Alaska Southeast, the U s. Geological Survey and the University of Alaska Fairbanks. Bartholomaus did his fieldwork while studying for his doctorate at the University of Alaska Fairbanks,
but he analyzed the data and wrote the study while at UTIG. UTIG is a research unit of The University of Texas at Austin Jackson School of Geosciences.
The team discovered the new method while trying to study earthquakes caused by iceberg calving
when large chunks of ice break off glaciers. Bartholomaus said the ability to identify these earthquakes, known as icequakes, varied over the season,
and that they were much more difficult to detect during summer because seismic background noise was obscuring the icequake signals.
The team set about trying to determine what was causing the background noise investigating potential causes such as rainfall, iceberg calving and the movement of the glacier over the ground.
NSF, University of Texas at Austi U
#Study shifts understanding of how bone fractures heal It time to rewrite the textbook description of bone fracture healing.
A team of Vanderbilt investigators has discovered that fibrin, a protein that was thought to play a key role in fracture healing,
is required not. Instead, the breakdown of fibrin is essential for fracture repair. The findings, reported in the August issue of the Journal of Clinical Investigation,
shift understanding of how fractures heal and have implications for efforts to promote fracture repair. any of the current pharmaceutical protocols are based on using fibrin to promote fracture healing,
said Jonathan Schoenecker, M d.,Ph d, . assistant professor of Orthopaedic Surgery and Rehabilitation. n certain instances it may help,
but wee shown for sure that you don need it. Bone biology does not require fibrin to heal a fracture.
Fibrin is involved in blood clotting; it forms a meshlike net that traps platelets to form a clot.
When bones break, so do blood vessels, and clots form to stop the bleeding. ost people don realize that bone is the most vascular organ in our bodies,
Schoenecker said. hen you have a fracture, you have a huge disruption of that vascularity.
Since fibrin is the main protein at the site of a fracture, it was thought to promote repair by providing a scaffold for the initial phase of new bone formation.
however, that fracture repair was normal in mice missing the fibrin precursor fibrinogen. The investigators had reported previously the importance of vascular re-connection for bone fracture healing.
Using imaging techniques they developed to simultaneously study angiogenesis (new blood vessel growth) and bone formation after fracture,
they found that blood vessels grow first at the ends of the fracture, extend and reconnect. Then new bone forms. herefore, any condition associated with vascular disease
and thrombosis will impair fracture healing, Schoenecker said. It follows that if fibrin is removed not efficiently,
it gets in the way, he said. In the new studies, the team demonstrated that mice missing the factor that clears fibrin had impaired vascularization and bone union.
Genetic manipulations to deplete fibrinogen in these mice restored normal fracture repair. ibrin puts a cog in the machine
and you don get the anastomosis (vessel reconnection), Schoenecker said. The findings may explain why obesity, diabetes,
smoking and advanced age impair fracture repair. They are associated all with impaired fibrin clearance, he explained.
and orthopaedic surgery. t was unexpected totally that fibrin clearance is essential to prevent heterotopic ossification,
and plates used in orthopaedic surgeries, so that those devices don disrupt the ability of blood vessels to grow
as such big injuries of an incredibly vascular structure inevitably require a clot in order not to bleed to death,
He points out that some of the medications developed for cardiovascular medicine to prevent clotting may find new purposes in enhancing tissue repair and regeneration i
#Newly discovered cells regenerate liver tissue without forming tumors Hybrid hepatocytes proliferate and replenish liver mass after chronic liver injuries in micehybrid hepatocytes proliferate
and replenish liver mass after chronic liver injuries in micethe mechanisms that allow the liver to repair
and regenerate itself have long been a matter of debate. Now researchers at University of California, San diego School of medicine have discovered a population of liver cells that are better at regenerating liver tissue than ordinary liver cells, or hepatocytes.
The study, published August 13 in Cell, is the first to identify these so-called ybrid hepatocytes
and show that they are able to regenerate liver tissue without giving rise to cancer.
While most of the work described in the study was done in mouse models, the researchers also found similar cells in human livers.
Of all major organs, the liver has the highest capacity to regenerate that why many liver diseases,
including cirrhosis and hepatitis, can often be cured by transplanting a piece of liver from a healthy donor.
In this latest study, led by Michael Karin, Phd, Distinguished Professor of Pharmacology and Pathology, researchers traced the cells responsible for replenishing hepatocytes following chronic liver injury induced by exposure to carbon tetrachloride, a common environmental toxin.
That when they found a unique population of hepatocytes located in one specific area of the liver,
and replenish liver mass after chronic liver injuries. Since the cells are similar to normal hepatocytes
While ipscs hold a lot of promise for regenerative medicine, it can be difficult to ensure that they stop proliferating
when their therapeutic job is done. As a result ipscs carry a high risk of giving rise to tumors.
To test the safety of hybrid hepatocytes, Karin team examined three different mouse models of liver cancer.
They found no signs of hybrid hepatocytes in any of the tumors, leading the researchers to conclude that these cells don contribute to liver cancer caused by obesity-induced hepatitis
or chemical carcinogens. ybrid hepatocytes represent not only the most effective way to repair a diseased liver,
but also the safest way to prevent fatal liver failure by cell transplantation, Karin said p
Two recent studies pointed to possible flaws in the methods used to identify irisin, with commercially available antibodies.
In Cell Metabolism on August 13, the Harvard scientists who discovered irisin address this contentious issue by showing that human irisin circulates in the blood at nanogram levels
Senior study author Bruce Spiegelman of Dana-Farber Cancer Institute and Harvard Medical school says that the confusion over irisin comes down to disagreement over how irisin protein is made in skeletal muscle cells and the detection limits
The authors show that human irisin is similar to the mouse hormone and that it circulates in the range previously reported.
Although irisin circulates at low levels (nanograms this range is observed comparable to that for other important biological hormones such as insulin.
Furthermore, the investigators developed a protocol, that does not rely on antibodies, to precisely measure how much irisin increases in people after exercise. he data are compelling
and clearly demonstrate the existence of irisin in circulation, says endocrinologist Francesco Celi of the Virginia Commonwealth University Medical center,
who was not involved with the study. mportantly, the authors provide a precise and reproducible protocol to measure irisin.
He adds that further studies are necessary to fully understand how the hormone works in humans
specifically how it relates to brown and beige fat tissue and energy use. Irisin discovery in 2012 was exciting
because scientists had potentially found one reason why exercise keeps us healthy. When irisin levels were increased in mice, their blood and metabolism improved.
but data suggest that high-intensity training protocols are particularly effective. The protocol described in the Cell Metabolism paper is likely to help such studies,
However, future refinement of this work should lead to more scalable protocols. piegelman and colleagues have shown unequivocally that the ythicalirisin peptide is produced
also not affiliated with the work. his data should settle the controversy surrounding the existence of irisin and its increase in blood as a function of exercise
#Telltale biomarker detects early breast cancer in NIH-funded study Researchers have shown that magnetic resonance imaging (MRI) can detect the earliest signs of breast cancer recurrence and fast-growing tumors.
breakaway tumor cells with the potential to develop into dangerous secondary breast cancer tumors elsewhere in the body.
The work was completed at Case Western Reserve University (CWRU), Cleveland and was funded by the National Institute of Biomedical Imaging and Bioengineering (NIBIB),
part of the National institutes of health. RI has a wide array of diagnostic applications and shows promise in breast cancer detection
. CWRU M. Frank Rudy and Margaret Domiter Rudy Professor of biomedical engineering and an expert in molecular imaging for cancer and other diseases. e showed with this technique that we can detect very tiny tumors of just
revealing smaller cancers than can be detected with current clinical imaging modalities. ur imaging technology has the potential to differentiate aggressive tumors from low-risk tumors.
These are two things that potentially can make a big impact on clinical practice and also management of cancer.
Since small, early-stage cancers are the most responsive to drug treatments, screening is an important aspect of follow-up care for breast cancer patients,
and early detection is critical in tailoring appropriate and effective therapeutic interventions. While multiple imaging techniques, including MRI,
they are neither able to detect specific cancer types or early cancer growth. The earliest signs of cancer spread are called micrometastases.
As the name implies, they are often too small to be detected with standard screening. Dr. Lu team used a biochemical approach combined with MRI to detect molecular changes that signal micrometastases.
To detect micrometastases Lu and his team used MRI imaging which uses a magnetic field and radio waves to produce images
and combined it with a special chemical contrast solution. The contrast solution that the team developed contains a short piece of protein,
More importantly, the fibronectin part of the complex is expressed during a cell transition to cancer and plays a role in cell growth
The researchers collected images depicting metastases where breast cancer had spread beyond the original tumors. Metal molecules within the contrast solution are magnetized during the MRI process
and enhance the image wherever the molecules of solution bind with the targeted protein. he primary tumor sends signals to distant tissue
the biomarker is enhanced, generating enough signal for MRI detection of small, high-risk cancer and micrometastases.
The researchers tested the approach in mice into which they had introduced breast cancer cells. After a two-week waiting period
and tumors compared with normal tissue. Using a microscopic imaging approach, called cryo-imaging, and MRI, the researchers verified that the MRI technique could detect micrometastases,
and the consequence of metastatic cancer make these efforts urgent and important, said Lu, adding that his research team also hopes to advance the approach for prostate cancer detection. e think this targeted approach holds great promise for earlier imaging of high-risk cancers in the clinic.
It could also become useful as a noninvasive way to assess breast cancer treatment progress.
The team plans to complete safety testing of the imaging agent during the next three years.
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