#Researchers look to exploit females natural resistance to infection Researchers have linked increased resistance to bacterial pneumonia in female mice to an enzyme activated by the female sex hormone estrogen.
Females are naturally more resistant to respiratory infections than males. Now an international team of scientists has shown that increased resistance to bacterial pneumonia in female mice is linked to the enzyme nitric oxide synthase 3 (NOS3.
They also show that this enzyme is activated ultimately by the release of the female sex hormone estrogen.
The team lead by Professor Lester Kobzik at the Harvard university School of Public health introduced Streptococcus pneumoniae into the lungs of mice to mimic the inhalation of bacteria that occurs naturally as we breathe.
They found that deleting this gene meant that the female mice were no longer more resistant to infection.
The team hope that in the future this knowledge could be used to enhance resistance to common and serious lung infections.
Ultimately this work could be especially useful in reducing risk of secondary bacterial pneumonias during seasonal
or pandemic influenza said Professor Lester Kobzik the senior author. We were pleased quite that the work led us to NOS3-targeting drugs that are already available
and that can indeed improve resistance to pneumonia in our mouse model l
#Researchers turn to 3-D technology to examine the formation of cliffband landscapes A blend of photos
Mapping that dense molecular machinery is one of the most promising and challenging frontiers in medicine and biology.
Errors in copying DNA are found in certain cancers and this work could one day help develop new treatment methods that stall
The structural knowledge may help others engineer small molecules that inhibit DNA replication at specific moments leading to new disease prevention
#Tool enhances social inclusion for people with autism The University of Alicante has developed together with centres in the UK Spain
and Bulgaria a tool designed to assist people with autism spectrum disorders by adapting written documents into a format that is easier for them to read
and social inclusion of the users as they gain better access to education employment health care and social activities she adds.
Although in principle the tool has been designed for people with autism spectrum disorders who generally have difficulties in areas such as communication social interaction
#Prostate cancers penchant for copper may be a fatal flaw Like discriminating thieves prostate cancer tumors scavenge
Researchers at Duke Medicine have found a way to kill prostate cancer cells by delivering a trove of copper
The combination approach which uses two drugs already commercially available for other uses could soon be tested in clinical trials among patients with late-stage disease.
This proclivity for copper uptake is something we have known could be an Achilles'heel in prostate cancer tumors as well as other cancers said Donald Mcdonnell Ph d. chairman of the Duke Department of Pharmacology and Cancer Biology and senior author
of a study published Oct 15 2014 in Cancer Research a journal of the American Association of Cancer Research.
Our first efforts were to starve the tumors of copper but that was unsuccessful. We couldn't deplete copper enough to be said effective Mcdonnell.
and then use a drug that requires copper to be effective to attack the tumors.
Mcdonnell and colleagues searched libraries of thousands of approved therapies to identify those that rely on copper to achieve their results.
Disulfiram had at one time been a candidate for treating prostate cancer--it homes in on the additional copper in prostate cancer tumors
--but it showed disappointing results in clinical trials among patients with advanced disease. The Duke team found that the amount of copper cancer cells naturally hoard is not enough to make the cells sensitive to the drug.
along with the disulfiram the combination resulted in dramatic reductions in prostate tumor growth among animal models with advanced disease.
Androgens the male hormones that fuel prostate cancer increase the copper accumulation in the cancer cells.
or similar compounds and copper especially beneficial for men who have been on hormone therapies that have failed to slow tumor growth.
Unfortunately hormone therapies do not cure prostate cancer and most patients experience relapse of their disease to a hormone-refractory
or castration-resistant state Mcdonnell said. Although tremendous progress has been made in treating prostate cancer there is clearly a need for different approaches
and our findings provide an exciting new avenue to explore. Mcdonnell said clinical trials of the combination therapy are planned in upcoming months.
Andrew Armstrong M d. associate professor of medicine was involved with a recent study at Duke testing disulfiram in men with advanced prostate cancer.
While we did not observe significant clinical activity with disulfiram in men with recurrent prostate cancer in our recent clinical trial this new data suggests a potential way forward
and a reason why this trial did not have more positive results Armstrong said. Further clinical studies are warranted now to understand the optimal setting for combining copper with disulfiram
or similar compounds in men with progressive prostate cancer particularly in settings where the androgen receptor is active.
The above story is provided based on materials by Duke Medicine e
#Earths magnetic field could flip within a human lifetime Imagine the world waking up one morning to discover that all compasses pointed south instead of north.
Flip could affect electrical grid cancer ratesthe discovery comes as new evidence indicates that the intensity of Earth's magnetic field is decreasing 10 times faster than normal leading some geophysicists to predict a reversal within a few
or temporary loss of the field before a permanent reversal could increase cancer rates. The danger to life would be even greater
#Immune cells in liver drive fatty liver disease, liver cancer Fatty liver disease--alongside fatty liver due to massive alcohol consumption--is caused mainly by excessive consumption of fat
This is referred to as nonalcoholic fatty liver disease (NAFLD. If NAFLD becomes chronic--e g. through the constant uptake of high lipids
This can lead to nonalcoholic steatohepatitis (NASH)--a liver disease with clear detectable pathologic alteratons of the tissue.
These liver diseases (NAFLD and NASH) along with chronic viral infections are the most common causes of liver cancer or hepatocellular carcinoma (HCC.
In the United states HCC is the fastest-growing form of cancer at the moment. No efficient causal therapy exists for HCC patients of which approximately 800000 die every year.
T cells involved in the development of fatty liver disease NASH and HCC The mechanisms that cause diseases such as fatty liver disease steatohepatitis and HCC are still not widely understood.
However immune cells particularly CD8+T cells and NK T cells seem to play an important role.
This finding was made by a team of scientists led by Prof. Mathias Heikenwälder Prof. Matthias Tschöp Dr. Kerstin Stemmer Dr. Kristian Unger Prof.
Achim Weber from Zurich University Hospital and Dr. Monika Wolf Institute of Surgical Pathology University Hospital Zurich.
The animal model which was used to examine the long-term effects of metabolic syndrome*enabled the scientists to elucidate new mechanisms that cause fatty liver disease
and also show how it can develop into liver cancer. Inflammatory events offer starting point for prevention
The inflammation which is triggered by specific immune cells encourages the progression of fatty liver pathology
Our results provide completely new insights into the development of these serious liver diseases. Building on this knowledge we now want to develop new preventive
and therapeutic strategies to combat these diseases. The initial studies are already under way in the preclinical model.*
*Metabolic syndrome: a combination of obesity/abdominal adiposity insulin resistance raise levels of lipids in the blood and raised blood pressure.
Story Source: The above story is provided based on materials by Helmholtz Zentrum München-German Research center for Environmental Health.
At least if they live in central neighbourhoods with good access to medical services and public transit infrastructure they will not suffer so much from the loss of automobility.
#Defective gene renders diarrhea vaccine ineffective Acute diarrheal illnesses cause nearly one-fifth of all child deaths in developing countries.
Improved sanitation and hygiene have had limited a effect on the spread of the illness. Today vaccination is considered the most important method for reducing mortality.
Unfortunately several studies have shown that the two available living vaccines Rotarix and Rotateq which are recommended by bodies including the World health organization are not sufficiently effective in developing countries.
In many African countries protection has been as low as 20-50%.%The current study to be published in the Journal of Clinical Infectious diseases by Johan Nordgren from Professor Lennart Svensson's research group shows that up to four of ten children in Burkina faso are genetically resistant to the virus strains found in the vaccines.
The researchers found that children who can not express a particular sugar molecule in the small intestine called the Lewis molecule do not become infected by the rotavirus types found in existing vaccines.
This Lewis molecule is needed probably as a receptor for the rotavirus to be able to enter
This means that these children do not get the desired immunological protection from the vaccine.
and can greatly impact the evaluation of the rotavirus vaccines now being introduced in several developing countries.
The results could lead to a review of the vaccine composition and the development of vaccines better suited to the populations most affected by rotavirus.
Story Source: The above story is provided based on materials by Linköping University. Note: Materials may be edited for content and length.
#Discovery of cellular snooze button advances cancer, biofuel research The discovery of a cellular snooze button has allowed a team of Michigan State university scientists to potentially improve biofuel production and offer insight on the early stages
of cancer. The discovery that the protein CHT7 is a likely repressor of cellular quiescence
and oil production also wields control of cellular growth--and tumor growth--in humans. Christoph Benning MSU professor of biochemistry and molecular biology and his colleagues unearthed the protein's potential
Its application in cancer research however was a surprise finding that is leading Benning's lab in a new direction.
and study algae which have the genomic repertoire that make them relevant in their capacity to drive advances in human medicine.
when it's under stress said Chia-Hong Tsai doctoral candidate with MSU's Department of energy Plant Research Laboratory
In terms of human medicine this discovery gives scientists a promising new model to study tumor suppression and growth.
For cancer research it's a new paradigm Benning said. The switch that tells an organism to grow
That is the first step of tumor growth. Story Source The above story is provided based on materials by Michigan State university.
and health services. In addition the market is strong for nearly all types of new degree-holders.
Biomedical applications include microfluidic devices that can handle and process very small volumes of liquid such as samples of saliva or blood for diagnostics.
#Research leads to brain cancer clinical trial Researchers at the University of Calgary's Hotchkiss Brain Institute (HBI)
and Southern Alberta Cancer Research Institute (SACRI) have made a discovery that could prolong the life of people living with glioblastoma--the most aggressive type of brain cancer.
Samuel Weiss Phd Professor and Director of the HBI and Research Assistant professor Artee Luchman Phd and colleagues published their work today in Clinical Cancer Research
Researchers used tumour cells derived from 100 different glioblastoma patients to test drugs that could target the disease.
Researchers used the new therapy to inhibit a pathway in the cancer cells known as mtor signaling--putting the brakes on this pathway combined with the current standard therapy caused more of the cancer cells to die.
and therapies that can be tested in the clinic provides the greatest hope for brain cancer patients
and their families says Weiss leader of the university's Brain and Mental health strategic research priority.
Glioblastoma is the most common and deadly form of brain cancer among adults. The progression and complexity of the tumours are often difficult to treat.
and Dr. Greg Cairncross--director of SACRI and leader of the Terry Fox Research Institute (TFRI'Therapeutic Targeting of Glioblastoma research program at the university--are now working with cancer researchers Dr. Warren Mason (Princess
Margaret Cancer Centre in Toronto) and Dr. Lesley Seymour (Director of the NCIC Clinical Trials Group's Investigational New Drug Program) and drug manufacturer Astrazeneca to plan a clinical trial testing a similar but newer drug
This is an important initiative--to test new drugs being developed for other types of cancers in the laboratory to identify which are most promising for testing in patients with glioblastoma.
which will be funded by a grant from the TFRI as well as grants from Canadian Cancer Society Research Institute to NCIC CTG says Seymour r
Fast accurate and affordable DNA sequencing is the first step toward personalized medicine. Threading a DNA molecule through a tiny hole called a nanopore in a sheet of graphene allows researchers to read the DNA sequence;
Olfactory loss is often an early symptom in a variety of neurological disorders including Alzheimer's and Parkinson's diseases.
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.
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.
but in the case of traumatic injury or stroke they become a pathway of vulnerability that allows swelling.
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
because it clarifies the roles of aquaporins in the brain during the short and long-term responses to traumatic head injury.
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.
New approaches that can improve the outlook for patients especially in the later stages of injury development would be of great benefit she says.
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.
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.
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
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.
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
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.
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.
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
#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.
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.
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
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.
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?
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.
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.
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:
It came as a big surprise that we found the same mark at fifty percent of the stress-activated genes.
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.
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:
Researches are now able to understand for the first time the evolution of these parasites causing disease in humans and animals.
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;
In addition they developed a specialized infection apparatus the polar tube which they use to insert themselves into the cells of their host.
because it possessed the unique harpoon-like infection apparatus (the polar-tube) one of the hallmarks of microsporidia.
These mutations cause more than 200 diseases and contribute to others such as diabetes cancer Parkinson's disease and Alzheimer's disease.
Many mitochondrial diseases affect more than one system in the human body said Kateryna Makova professor of biology and one of the study's primary investigators.
They are devastating diseases and there is no cure so our findings about their transmission are very important.
The multidisciplinary research team set out to learn whether maternal age is important in the accumulation of MITOCHONDRIAL DNA (mtdna) mutations both in the mother and in the child as a result of transmission.
Collaborating with Ian Paul a pediatrician at the Penn State Milton S. Hershey Medical center they took samples of blood and of cells inside the cheek from 39 healthy mother-child pairs.
Studying healthy individuals gave the researchers a baseline for future studies of disease-causing mutations.
This finding is especially important for mothers who have a mitochondrial disease. For many mitochondrial diseases 70 to 80 percent of molecules need to have the disease-causing variant for the disease to manifest itself.
But for others only 10 percent of the mtdna molecules with the variant are needed to cause disease.
If the bottleneck is very small as we've found in our study these percentages can change dramatically Makova said.
Knowing the size of the bottleneck allows us to predict within a range the percentage of disease-carrying molecules that will be passed on to the child.
and can assist genetic counselors in advising couples about the chances of mitochondrial diseases being passed to the next generation Makova said.
Everyone is concerned about Down syndrome because that is a common genetic problem. We have added now another set of genetic disorders that also might be affected by the age of the mother.
It is good for couples to have this knowledge as they make family-planning decisions. Story Source:
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