Scientists at the National institutes of health (NIH) report that newly formed brain cells in the mouse olfactory system--the area that processes smells--play a critical role in maintaining proper connections.
and receives information directly from the nose about odors in the environment. Neurons in the olfactory bulb sort that information
Olfactory loss is often an early symptom in a variety of neurological disorders including Alzheimer's and Parkinson's diseases.
In the first set of mouse experiments Dr. Belluscio's team first disrupted the organization of olfactory bulb circuits by temporarily plugging a nostril in the animals to block olfactory sensory information from entering the brain.
and amount of circuitry disruption indicating that a greater loss of stem cells led to a larger degree of disorganization in the olfactory bulb.
which could help animals adapt to a constantly varying environment. It's very exciting to find that new neurons affect the precise connections between neurons in the olfactory bulb.
but may come from a better understanding of how the sense of smell works. This is an exciting area of science said Dr. Belluscio I believe the olfactory system is very sensitive to changes in neural activity
and given its connection to other brain regions it could lend insight into the relationship between olfactory loss and many brain disorders.
#Timing is key for traumatic brain injury treatment Researchers at the University of Adelaide have discovered two potential treatments for traumatic brain injury that are most effective
when given at different stages after the injury has occurred. Laboratory studies conducted in the University's School of Medical sciences have confirmed that changes in brain water channels over time play a critical role in traumatic brain injury.
For his Phd at the University researcher Dr Joshua Burton tested two compounds that alter the natural flow of water activity in and out of the brain.
He found that recovery from brain injury can be assisted greatly when these compounds are given at the right times.
Dr Burton's work could point to the potential development of new drugs as well as new approaches to preventing brain damage and death.
The research also has implications for treatment of brain swelling after stroke. One of the serious consequences of traumatic brain injury is an increase in brain moisture content and associated brain swelling which significantly impacts patients'neurological outcomes.
This swelling can occur for days after the initial injury and is frequently life-threatening Dr Burton says.
The water channels normally function to protect the brain but in the case of traumatic injury or stroke they become a pathway of vulnerability that allows swelling.
Unfortunately the swelling creates pressure within the skull--there's nowhere for the brain to expand to--decreasing oxygen levels and blood to the brain.
Dr Burton has found that applying a drug that closes the water channels can inhibit initial water entry helping to close the window of vulnerability.
A second drug used later in the progression of the injury acts to enhance the water channel activity letting superfluous moisture out when needed.
By using both of these compounds--a blocker at the early stage of injury and an activator at the later stage--we're able to complement the brain's natural healing processes
This work builds on more than a decade of research conducted by the University of Adelaide's Professor Andrea Yool on the water channel proteins known as aquaporins.
Dr Burton's work is groundbreaking because it clarifies the roles of aquaporins in the brain during the short and long-term responses to traumatic head injury.
This work also demonstrates for the first time that recently discovered drug-like compounds can be used in series to initially reduce water entry
and then enhance water exit over time Professor Yool says. Most current therapeutic approaches are limited in their ability to reduce injury-induced brain swelling
and no treatments are available to resolve excess fluid at a later stage. While much more research is needed there is exciting potential here for new interventions in clinical situations.
New approaches that can improve the outlook for patients especially in the later stages of injury development would be of great benefit she says.
Story Source: The above story is provided based on materials by University of Adelaide. Note: Materials may be edited for content and length h
#Protein found in insect blood helps power pests immune responses Pest insects may be sickened to learn to that researchers at Kansas State university have discovered a genetic mechanism that helps compromise their immune system.
Michael Kanost university distinguished professor of biochemistry and molecular biophysics led a study by Kansas State university researchers that looked at how protein molecules in the blood of insects function in insects'immune system.
Insects use proteins that bind to the surface of pathogens to detect infections in their body.
For example when a mosquito transmits a pathogen like malaria the parasite that causes the disease spends part of its life in the mosquito's blood Kanost said.
It is recognized often by a genetic mechanism in the mosquito's immune system which kills the parasite.
This process is important in fully understanding how insects transmit diseases and how their immune system interacts with the pathogens they are transmitting
so that we can disrupt it. Researchers studied a protein called beta-13-glucan recognition protein or GRP from the blood of a caterpillar.
They found that the GRP protein binds to a carbohydrate present in the cell wall of fungi known as beta-13-glucan.
This protein complex on the surface of the pathogen may form a platform for attracting
and activating other proteins from the blood triggering immune responses that help kill pathogens in an insect's blood The findings may lead to new ways to control disease transmission from insects to humans and animals as well as new methods for biocontrol
It also sheds new light on how immune systems in organisms have evolved. The study Self-association of an Insect Beta-13-Glucan Recognition Protein Upon Binding Laminarin Stimulates Prophenoloxidase Activation as an Innate Immune response was published recently in the Journal of Biological Chemistry.
The research team included Daisuke Takahashi research associate who conducted a majority of the experiments in Kanost's lab;
Ramaswamy Krishnamoorthi associate professor of biochemistry and bimolecular physics; Huaien Dai a doctoral graduate; and former faculty member Yasuaki Hiromasa.
The team's study revolved around the tobacco hornworm. The insect's immune system has been studied by Kanost and others for more than 30 years.
Building on the decades of research on the tobacco hornworm's immune system researchers concentrated on particular molecules in the blood that form pathways in
which one molecule activates another molecule leading to production of chemicals that kill pathogens. Researchers used a variety of biochemical and biophysical experiments to understand how the protein molecules assemble on the surface of the pathogen.
They found that clusters of five GRP protein molecules bind to a polysaccharide a type of carbohydrate--beta-13-glucan in this case--along a larger carbohydrate molecule that makes a cell wall.
Their work identified the spatial orientation of the GRP proteins in the cluster and showed that the protein-carbohydrate complexes stimulate an immune response in the caterpillar.
Understanding how the biochemical mechanism activates the immune system may enable scientists to disrupt the process Kanost said.
This could reduce insects'ability to transmit diseases to humans and animals. It may also lead to new biocontrol of pest insects as exploiting the mechanism could weaken
There are fungal pathogens that are used to kill insect pests but that are harmless to humans Kanost said.
If we understand how insect immune response fights off fungal infections that might lead to better ways to use microbial control on the insects.
just as effective as invasive neck surgery for long-term prevention of fatal and disabling strokes reports an international trial led by UCL (University college London) funded by the Medical Research Council and Stroke Association.
The research paper published today in the Lancet was authored by researchers from UCL Basel University Switzerland the London School of Hygiene & Tropical Medicine the University Medical center Utrecht Netherlands Sheffield Teaching Hospitals
NHS Foundation Trust and Newcastle University. The brain's blood supply comes from the carotid arteries two large blood vessels that run through the neck.
Carotid artery disease occurs when cholesterol and fatty deposits build up in these arteries restricting blood flow
In the UK carotid artery disease is treated most commonly by an invasive surgical procedure called endarterectomy. Patients are put under general
or local anaesthetic and surgeons cut open the affected artery to remove the build up and then sew the wound up.
The operation leaves a scar on the neck and can lead to heart attack short-term facial paralysis from nerve damage and bleeding
The procedure is less invasive causing only minor bruising in the groin no risk of nerve damage and a lower heart attack risk than endarterectomy.
The study followed 1713 patients with carotid artery disease of whom 855 were assigned to stenting and 858 to endarterectomy for up to 10 years.
At the moment stenting is used not widely in the UK due to historical uncertainty over its long-term effectiveness says study leader Professor Martin Brown from the UCL Institute of Neurology.
Now that we know stenting is effective in the long term more staff should be trained to carry out the procedure and gain experience.
and staff cannot learn or observe the procedure. In other countries stenting is more widespread
A transient ischaemic attack also known as a mini-stroke can be a warning sign that someone has carotid artery stenosis
Preventative procedures to treat such carotid artery stenosis are therefore crucial. Carotid endarterectomy is a common yet invasive surgery used to treat carotid artery stenosis
and is used widely throughout the UK. Previously far less was known about the long-term effectiveness of stenting as an alternative procedure.
and accompanying death in infants with a birth weight below 750 grams or 1. 65 pounds.
NEC is a devastating neonatal illness especially in extremely low birth weight premature infants with a mean incidence of seven to nine percent and a fatality rate of 15 to 30 percent.
In addition to short-term complications such as feeding intolerance intestinal obstruction and short-bowel syndrome surviving infants have poorer neurodevelopmental outcomes
and represent a huge financial burden to the health care system. While NEC continues to be a significant cause of mortality
and morbidity in extreme preterm infants the increased use of human breast milk and implementation of standardized feeding protocols have helped to reduce its incidence.
#Sustainability in numbers: New method for estimating nutrient stocks, flows in agriculture A quantitative model for measuring sustainability in the Finnish agricultural sector has been developed in a new thesis. The new model challenges the OECD method which is used currently
when evaluating areas of potential pollution from nutrients. Research scientist Natalia Kuosmanen at MTT Agrifood Research Finland says defining sustainability quantitatively is challenging due to variety of meanings attached to this commonly used concept.
What gets measured gets done as the saying goes. The same truth applies to sustainability.
Can we define sustainability and assess it if we do not have the exact means to measure it?
Kuosmanen asks. New frontiers in ecological economyin her thesis Kuosmanen used established methods of frontier estimation to evaluate sustainability performance of Finnish dairy farms.
The methods are applied commonly for productivity and efficiency analysis in banking and industry. Moreover her thesis include a new dynamic approach to model nutrient stocks and flows.
The new model was developed in the Finnish agricultural sector where the stocks and flows of nitrogen and phosphorus were estimated from a 48-year period.
It was applied furthermore in the data of 14 EU countries in the period between 1961 and 2009.
Improvements for OECD nutrient balance modelcurrently the static nutrient balance approach of OECD is used to assess nutrient emissions from agriculture.
The new dynamic nutrient balance model has compared several advantages with the conventional static approaches. The static approach ignores the accumulation of nutrients in the environment
and overlooks the dynamic nature of the nutrient cycles Kuosmanen says. Kuosmanen's dynamic model enables the analysis of the development of nutrient stock over time and the distribution of the nutrient flows into water air and soil.
The stocks and outflows from the stock calculated using the dynamic model could be utilized in sustainability assessment as indicators of environmental pressure from agriculture.
When applied to farm and country level data the results reveal that the nutrient outflows are much more stable over time compared with the net inflows.
Unfortunately this indicator is sensitive to random fluctuations due to weather measurement errors and other noise in data
and the EU-level agri-environmental policies Kuosmanen argues. From theory to practicekuosmanen began her academic career in Kiev Polytechnic University Ukraine
and graduated in environmental sciences in Wageningen University The netherlands. She is ready to take her results from theory to practice.
Our dynamic approach would provide better estimations of the nutrient leaching from agriculture to environment than the conventional method of OECD. Story Source:
The above story is provided based on materials by MTT Agrifood Research Finland. Note: Materials may be edited for content and length h
#Personalized treatment for stress-related diabetes Researchers at Lund University in Sweden are testing a treatment for type 2 diabetes
which targets the disease mechanism itself--and not just the symptoms. For the first time knowledge about the individual patient's genetic risk profile is being used.
The treatment completely restores the capacity to secrete insulin which is impaired by the risk gene.
Our results show that it is possible to block the effects of a common risk gene for type 2 diabetes says Anders Rosengren the diabetes researcher at Lund University in charge of the project.
At the time several research teams from Lund University were able to report that a common gene variant in the population makes insulin-producing cells sensitive to stress hormones.
Continued work showed that Yohimbin a drug that had been deregistered for several years effectively blocked the gene variant's damaging effects both in animal experiments
and it is even more frequent among patients with type 2 diabetes--out of 400 000 people in Sweden who have type 2 diabetes 40 per cent of patients are carriers.
With a known disease mechanism and a method to neutralise it the obvious next step was to test it on patients. 50 patients with type 2 diabetes were recruited. 21 of them did not have the risk variant
Yohimbin must be modified to minimise side-effects in this case raised blood pressure and we need the help of a cooperation partner to achieve this.
The substance must also be tested on more patients before it can become a clinical drug says Anders Rosengren adding purely theoretically the drug should be effective for the 40 per cent of type 2 diabetes sufferers who are carriers of the genetic risk variant.
The above story is provided based on materials by Lund University t
#Big foray in the DNA pool: Retrieving small genomes from a mix of organisms Scientists from the IZW led by Alex Greenwood publish in PLOS ONE a simple way to retrieve small genomes from a mix of various organisms.
Which viruses infect the elephant? Which type of bacteria causes severe lung disease in European brown hare?
Molecular biological analyses of tissue samples always confront scientists with the same problem: how to retrieve the genome of a specific pathogen from a mixture of DNAS in a patient and its microbial cohabitants?
Very easily says Alex Greenwood from the German Leibniz Institute for Zoo and Wildlife Research.
A short single-stranded base sequence is offered to the prepared DNA soup as a bait.
What is required is to pay attention during the subsequent data analysis. Greenwood's doctoral student Kyriakos Tsangaras discovered the additional value of hybridisation capture by chance.
This technology is based on tiny magnetic beads with short baitsequences of a few base pairs (oligonucleotides
Analysis of the sequences and comparison with reference data demonstrated that the complete mitochondrial genome of the rodents had been retrieved from the DNA pool.
The authors call this bycatch process in which a single DNA fragment catches overlapping flanking sequences Capflank.
It is therefore possible to yield plenty of genetic information with just a tiny fragment. In fact entire mitochondrial genomes and almost the entire genome sequence of a bacterium were obtained
when specifically tested for the efficiency of the bycatch principle. Capflank opens doors to completely new possibilities e g. in the genetic analysis of pathogens.
We can use short preserved gene sequences to yield the genome (or at least large sections of it) from pathogenic variants of influenza viruses for example or from completely new pathogens explains Greenwood.
As their next task his team wants to retrieve simple and well characterised DNA VIRUSES such as the elephant herpes virus.
The Capflank-method is suited even for heavily fragmented ancient DNA extracted from animal bones from museum collections.
These bones are contaminated often strongly with microbial or human DNA. Greenwood's colleagues successfully applied Capflank to samples from koalas kept in museums.
From the intestinal bacterium Escherichia coli contained in a human urine sample the scientists retrieved 90 per cent of the genome in one go.
According to the research study published in Nature Communications today the Sun affects middle atmosphere ozone with potential implications on smaller scale to regional but not global climate.
Humankind is responsible for the global warming of our climate by increasing the amount of greenhouse gases in the atmosphere.
This climate variability is not a trend like climate change but rather year-to-year fluctuations following solar activity.
Auroras and ozone lossaccording to the research study conducted by the Finnish Meteorological Institute University of Otago
Earth's radiation belts are regions in near-Earth space that contain vast quantities of solar energetic electrons trapped there by Earth's magnetic field.
In their latest study Christian Seiser and his team at the Max F. Perutz Laboratories (MFPL) of the University of Vienna and the Medical University of Vienna addressed this question.
and described the molecular mechanism through which it starts the transcription of stress-activated genes.
Their results could help to develop therapeutics to treat stress-related disease and have been published in the journal Genome Research.
When people talk about stress they generally refer to feeling the strains of too high burdens at work or in their private life.
In biology the term stress has a broader meaning: discovered and first described in 1936 by Viennese physician and biochemist Hans Selye stress is a psychological and physical reaction to external stimuli
which the body initially reacts to by mobilizing its defense mechanisms. Triggers for stress so called stress factors include not only emotional strain but also physical factors such as heat cold too much sun infections injuries and toxic substances--for example in cigarette smoke.
Stressed genes share a hallmark on histone H3we all know some of the body's reactions to stress from first hand experience:
the heart is pounding we feel hot or sweaty. But what happens in our cells the building blocks of the body?
Anna Sawicka addressed this question as a Phd student in the lab of Christian Seiser at the Max F. Perutz Laboratories (MFPL) of the Medical University of Vienna.
If cells are stressed for example with certain chemicals they immediately activate a specific transcription program. That means that certain genes are activated in a tightly regulated mode that defines which gene is activated for how long explains Anna Sawicka.
It came as a big surprise that we found the same mark at fifty percent of the stress-activated genes.
The former Phd student of the FWF-funded doctoral program Molecular Mechanisms of Cell Signaling found that the hallmark is mainly present at paused gene.
Figuratively speaking these are genes that are like motor racing cars with a running engine waiting at the start of a race.
The stress signal causes the addition of a phosphate mark to the H3 proteins at the promoter the regulatory region of a gene.
which blocked transcription up to this point and stress-regulated genes are activated explains Anna Sawicka the findings.
The study has identified not only histone phosphorylation as a hallmark of stress-activated genes but also the mechanism by
Stress can make you sick. A detailed understanding of the stress reaction on a molecular level could help to develop therapeutics to treat stress-related disease.
While Anna Sawicka now works as a Postdoc at the Max Planck Institute in Goettingen Christian Seiser and his team work to understand the function of the histone mark for long term activation of genes during the stress response.
Their first cues hint to a function of the phosphate mark in combination with another histone mark as part of the so-called histone code.
Story Source The above story is provided based on materials by Medical University of Vienna. Note: Materials may be edited for content and length.
#Key step in allergic reactions revealed By studying the mode of action of the interleukin-33 protein an alarmin for white blood cells a team at the Institut de Pharmacologie et de Biologie Structurale (IPBS--CNRS
/Université Toulouse III--Paul Sabatier) has been able to evidence truncated forms of the protein that act as potent activators of the cells responsible for triggering allergic reactions.
This breakthrough in the understanding of the mechanisms underlying allergy could have important applications in the treatment of asthma and other allergic diseases such as eczema and allergic rhinitis.
and INSERM senior researcher Jean-Philippe Girard this work is published in PNAS on 13 october 2014.
It acts as an alarmin that warns the body of trauma or infection by stimulating numerous cells in the immune system.
and is truncated then by enzymes secreted by mastocytes white blood cells that are key factors in allergy.
By triggering the chain reactions responsible for the allergic symptoms of asthma eczema or allergic rhinitis these cells have an essential role in allergy.
For the research team preventing production of the truncated forms of interleukin-33 in order to reduce the allergic reactions triggered by ILC2 represents a promising strategy for the treatment of asthma and other allergic diseases.
Story Source: The above story is provided based on materials by CNRS (Délégation Paris Michel-Ange. Note:
#Unique catalysts for hydrogen fuel cells synthesized in ordinary kitchen microwave oven Swedish and Chinese researchers show how a unique nano-alloy composed of palladium nano-islands embedded in tungsten nanoparticles creates a new type of catalysts for highly efficient oxygen reduction the most important reaction in hydrogen fuel cells.
Their results are published in the scientific journal Nature Communications. The world's rapidly growing demand for energy and the requirement of sustainable energy production calls for an urgent change in today's fossil fuel based energy system.
Research groups worldwide work intensively to develop novel advanced energy conversion and storage systems with high efficiency low cost and environmental compatibility.
Fuel cell systems represent a promising alternative for low carbon emission energy production. Traditional fuel cells are limited however by the need of efficient catalysts to drive the chemical reactions involved in the fuel cell.
Historically platinum and its alloys have frequently been used as anodic and cathodic catalysts in fuel cells
but the high cost of platinum due to its low abundance motivates researchers to find efficient catalysts based on earth-abundant elements.
In our study we report a unique novel alloy with a palladium (Pd) and tungsten (W) ratio of only one to eight
which still has similar efficiency as a pure platinum catalyst. Considering the cost it would be 40 times lower says Thomas Wågberg Senior lecturer at Department of physics Umeå University.
The explanation for the very high efficiency is the unique morphology of the alloy It is neither a homogeneous alloy nor a fully segregated two-phase system but rather something in between.
By advanced experimental and theoretical investigations the researchers show that the alloy is composed of metallic Pd-islands embedded in the Pd-W alloy.
The size of the islands are about one nanometer in diameter and are composed of 10-20 atoms that are segregated to the surface.
The unique environment around the Pd-islands give rise to special effects that all together turn the islands into highly efficient catalytic hot-spots for oxygen reduction.
To stabilize the nanoparticles in practical applications they are anchored on ordered mesoporous carbon. The anchoring keep the nanoparticles stable over long time by hindering them from fusing together in the fuel cell tests.
The unique formation of the material is based on a synthesis method which can be performed in an ordinary kitchen microwave oven purchased at the local supermarket.
If we were not using argon as protective inert gas it would be fully possible to synthesize this advanced catalyst in my own kitchen!
says Thomas Wågberg. Wågberg and his fellow researchers have received recently funding from the Kempe Foundation to buy a more advanced microwave oven
and therefore they will be able to run more advanced experiments to fine tune some of the catalyst properties.
Story Source: The above story is provided based on materials by Umea University. Note: Materials may be edited for content and length.
Journal Reference r
#Evolution of extreme parasites explained by scientists Extreme adaptations of species often cause such significant changes that their evolutionary history is difficult to reconstruct.
Zoologists at the University of Basel in Switzerland have discovered now a new parasite species that represents the missing link between fungi and an extreme group of parasites.
Researches are now able to understand for the first time the evolution of these parasites causing disease in humans and animals.
Dieter Ebert from the Department of Environmental science at the University of Basel has discovered now the missing link that explains how this large group of extreme parasites the microsporidia has evolved.
and the U s. Microsporidia are a large group of extreme parasites that invade humans and animals and cost great damage for health care systems and in agriculture;
They are only able to reproduce inside the host's cells they have known the smallest genome of all organisms with a cell nucleus (eukaryotes) and they posses no mitochondria of their own (the cell's power plant.
In addition they developed a specialized infection apparatus the polar tube which they use to insert themselves into the cells of their host.
Due to their phenomenal high molecular evolution rate genome analysis has so far been rather unsuccessful:
because it possessed the unique harpoon-like infection apparatus (the polar-tube) one of the hallmarks of microsporidia.
The analysis of the entire genome had several surprises in store for them: The genome resembles more that of a fungi than a microsporidium
and in addition also has a mitochondrial genome. The new species now named Mitosporidium daphniae thus represents the missing link between fungi and microsporidia.
With the help of scientists in Sweden and the U s. the Basel researchers rewrote the evolutionary history of microsporidia.
but that its genome is rather atypical for a microsporidium. It resembles much more the genome of their fungal ancestors.
Genome modificationsthe scientists thus conclude that the microsporidia adopted intracellular parasitism first and only later changed their genome significantly.
These genetic adaptations include the loss of mitochondria as well as extreme metabolic and genomic simplification. Our results are not only a milestone for the research on microsporidia
Overtext Web Module V3.0 Alpha
Copyright Semantic-Knowledge, 1994-2011