the work showcases the new technology and its practical importance in clinical science by showing how it has given new insights into Alzheimer's disease plaques."
and collected data that may resolve several current issues regarding the pathology of Alzheimer's disease. While Superman's x-ray vision is only the stuff of comics, our method,
model of Alzheimer's disease developed at the RIKEN BSI by Takaomi Saido team. After showing how Scales treatment can preserve tissue
the researchers put the technique to practical use by visualizing in 3d the mysterious"diffuse"plaques seen in the postmortem brains of Alzheimer's disease patients that are typically undetectable using 2d imaging.
but not in later stages of the disease after the plaques have accumulated.""Clearing tissue with Scales followed by 3d microscopy has clear advantages over 2d stereology or immunohistochemistry,"states Miyawaki."
not only for visualizing plaques in Alzheimer's disease, but also for examining normal neural circuits and pinpointing structural changes that characterize other brain diseases
#Biodiesel made easier, cleaner with waste-recycling catalyst Researchers at Cardiff University have devised a way of increasing the yield of biodiesel by using the waste left over from its production process.
#New leukemia gene stops blood cells'growing up'Scientists have identified a gene--FOXC1--that, if switched on, causes more aggressive cancer in a fifth of acute myeloid leukemia (AML) patients,
according to a Cancer Research UK study published in the journal Cancer cell, today. The FOXC1 gene is switched normally on during embryonic development
and is needed to turn cells into specialised tissues, like the eyes, kidney, brain and bone.
But this new research found that in certain patients with AML--a type of blood cancer that affects white blood cells
This triggers the cancer to be more aggressive, as young cells are able to replicate more than mature cells--causing cancer cells to grow faster
Of these, around 20 per cent would have had the FOXC1 gene wrongly switched on in their cancer.
Dr Tim Somervaille, lead author from the Cancer Research UK Manchester Institute at The University of Manchester,
which makes the cancer grow more rapidly.""There are certain situations where this gene is necessary,
it causes more aggressive forms of leukemia.""Nell Barrie, senior science communication manager at Cancer Research UK, said:"
"It's essential that we continue to research basic biology to further understand how cells become cancerous.
The better we understand the nuts and bolts of each cancer, the sooner we can find new ways to stop it
#Microbiologists describe new insights into human neurodegenerative disease Microbiology researchers at the University of Georgia studying a soil bacterium have identified a potential mechanism for neurodegenerative diseases.
A role for the protein HSD10 had been suspected in patients with Alzheimer's disease and Parkinson's disease, but no direct connection had previously been established.
This new breakthrough suggests that HSD10 reduces oxidative stress, promotes cell repair and prevents cellular death.
and protects the energy-making machinery from oxidative stress. HSD10 is a versatile protein with many known functions
but its role in oxidative stress has remained a mystery. The authors showed that HSD10 preferentially degrades highly toxic cardiolipin peroxides
free radical produced during oxidative stress that would normally initiate apoptosis, or cell death. HSD10 activity is inhibited strongly
when bound to the amyloid beta peptide so prevalent in Alzheimer's disease.""Normally, apoptosis is beneficial for regulating multicellular systems,
"But with rampant oxidative stress leading to uncontrolled cellular death, you end up with diseases such as Alzheimer's and Parkinson's.
HSD10 potentially prevents this by removing these damaged lipids before they have a chance to act."
"When cardiolipin becomes damaged by oxidative stress, the newly formed cardiolipin peroxides induce apoptosis instead of energy production.
"This research suggests that HSD10 prevents neurodegeneration by destroying cardiolipin peroxides and provides a fresh perspective on the etiology of Alzheimer's disease that could inform novel drug strategies,
"Shimkets said d
#Filling a void in stem cell therapy Stem cell therapies are limited often by low survival of transplanted stem cells
and the lack of precise control over their differentiation into the terminal cell types needed to repair
and Wyss Institute Founding Director Donald Ingber, M d.,Ph d.,who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical school and Boston Children's Hospital and Professor of Bioengineering
Stem cell therapies bear tremendous hopes for the repair of many tissues and bone or even the replacement of entire organs.
and function correctly at the site of injury to be useful for clinical regenerative therapies.
To improve the therapeutic ability of transplanted stem cells, Mooney's team has drawn inspiration from naturally occurring stem cell"niches."
#Loss of cellular energy leads to neuronal dysfunction in neurodegenerative disease model A new study from the Gladstone Institutes shows for the first time that impairments in mitochondria--the brain's cellular power plants--can deplete cellular energy levels
and cause neuronal dysfunction in a model of neurodegenerative disease. A link between mitochondria, energy failure,
and neurodegeneration has long been hypothesized. However, no previous studies were able to comprehensively investigate the connection because sufficiently sensitive tests,
Using a model of Leigh's disease, a genetically inherited neurodegenerative disorder that affects mitochondria,
the researchers tested energy levels in neurons using the new assays. They found that the genetic mutation associated with Leigh's disease compromised ATP levels,
and this reduction of ATP was enough to cause significant cellular dysfunction.""It was assumed always that defects in mitochondria would result in a depletion of energy levels,
if this connection holds true in conditions like Parkinson's disease and Alzheimer's disease.""Applying their new assay in healthy neurons,
in the model of Leigh's disease, the cells did not have enough ATP to complete this step.
if boutons lacking mitochondria will still be able to function properly in diseases that disrupt the distribution of mitochondria.
in order to comprehend changes in disease, "he explains.""It's worth taking the time to study these underlying biological processes
so that we can identify the best therapeutic targets for neurodegenerative disorders
#Whole genome-sequencing uncovers new genetic cause for osteoporosis Using extensive genetic data compiled by the UK10K project,
an international team of researchers led by Dr. Brent Richards of the Lady Davis Institute at the Jewish General Hospital has identified a genetic variant near the gene EN1 as having the strongest effect on bone mineral density (BMD)
and fracture identified to date. The findings are published in the forthcoming issue of the journal Nature."
"EN1 has never before been linked to osteoporosis in humans, so this opens up a brand new pathway to pursue in developing drugs to block the disease,"Dr. Richards,
an Associate professor of Medicine at Mcgill University, says by way of explaining the importance of the discovery."
"The effect of this uncommon genetic variant that we identified in this gene is twice as large as any previously identified genetic variants for BMD
and fracture,"adds Vince Forgetta, first author on this collaborative project from the Genetic Factors for Osteoporosis Consortium,
and a Research Associate at the Lady Davis Institute. Osteoporosis is a common disease that will lead to fractures in between one-third and one-half of all women over the course of their lives.
Because osteoporosis becomes more severe with age, it is becoming more prevalent with the overall aging of the population.
There are currently few safe and effective treatments for osteoporosis and no curative therapies available. The UK10K project has measured genetic variations in 10,000 individuals in great detail,
allowing researchers to correlate rare genetic changes with human disease by comparing the DNA of healthy individuals with those who have health problems.
The use of such an extensive sample size allows for the observation of genetic variants that are not discernable among smaller groups.
This particular study also stands as proof of principle that uncommon genetic variants can have a significant impact on common diseases."
"The hypothesis is that the genetic sequencing being done by UK10K will expose previously unknown genetic factors underlying disease,
"said Dr. Celia Greenwood, a biostatistician who is Senior Investigator at the Lady Davis Institute and Associate professor at Mcgill University,
and cochaired the statistics group for a companion Nature article on the methodology behind UK10K."
and are more frequent among those with common diseases. This is precisely what has been revealed in the case of EN1
and osteoporosis."This study represents an initial realization of the hope that accompanied the development of genetic sequencing technology:
that sophisticated analysis of the genome would reveal those genes associated with disease. The promise for the contribution genetics can make to human health lies in the discovery of novel compounds that can counter the effect of deleterious genetic variants influencing these genes s
#Research breakthrough in fight against muscle wasting diseases It is estimated that half of all cancer patients suffer from a muscle wasting syndrome called cachexia.
Cancer cachexia impairs quality of life and response to therapy, which increases morbidity and mortality of cancer patients.
Currently, there is no approved treatment for muscle wasting but a new study from the Research Institute of the Mcgill University Health Centre (RI-MUHC) and University of Alberta could be a game changer for patients, improving both quality of life and longevity.
as muscle wasting is associated also with other serious illnesses such as HIV/AIDS, heart failure, rheumatoid arthritis and chronic obstructive pulmonary disease and is also a prominent feature of aging."
''says lead author Dr. Simon Wing, MUHC endocrinologist and professor of Medicine at Mcgill University."
Recent studies show that muscle wasting is much more common in cancer than we think."
They observed whether such mice were resistant to muscle wasting induced by a high level of cortisol--a stress hormone released in your body any time you have a stressful situation such as an illness or a surgery.
because muscle atrophy can occur following a stroke when people are weak and bedbound. In addition, they looked at USP19 levels in human muscle samples from the most common cancers that cause muscle wasting:
lung and gastrointestinal (pancreas, stomach, and colon.""We found that USP19 KO mice were wasting muscle mass more slowly;
''explains Dr. Wing who is also the director of the Experimental Therapeutics and Metabolism Program at the RI-MUHC."
ranging from 5 to 15 per cent in chronic heart failure and COPD, and from 60 to 80 per cent in advanced cancer.
In all of these chronic conditions, muscle wasting predicts earlier death.""Cancer patients often present with muscle wasting even prior to their initial cancer diagnosis,
''says Dr. Antonio Vigano, director of the cancer rehabilitation program and cachexia clinic at the MUHC."
"In cancer, cachexia also increases your risk of developing toxicity from chemotherapy and other oncological treatments, such as surgery and radiotherapy.
At the Mcgill Nutrition and Performance Laboratory we specialize in cachexia and sarcopenia. By treating these two pathologic conditions through inhibiting the USP19 gene, at an early,
rather than late, stage of the cancer trajectory, not only can we potentially improve the quality of life of patients,
but also allow them to better tolerate their oncological treatments, to stay at home for a longer period of time,
and to prolong their lives
#A quantum lab for everyone Topical research experiments are often too expensive or too complex to be rebuilt
The tiny particles can be bound to compounds ranging from calcium tooth building materials to antimicrobials that prevent infection.
while protecting it against further infection that could penetrate the pulp and cause irreversible damage."
and reduce contamination and risk of infection. Starstream, invented and patented by the University of Southampton and in commercial production by Ultrawave Ltd.
including brain tissue from surgical steel. Cleaning instruments between patients is critical to avoid transmission of agents leading to conditions such as Creutzfeldt-jakob disease.
It was also able to remove bacterial biofilms that typically cause dental disease and was effective at removing soft tissue from bones,
which is required prior to transplants to prevent rejection of the transplanted material by the recipient's immune system.
"In the absence of sufficient cleaning of medical instruments, contamination and infection can result in serious consequences for the health sector and remains a significant challenge.
The team that conducted the study now forms the basis of the University's Network for Antimicrobial Resistance and Infection Prevention (NAMRIP) Strategic Research Group,
a leading journal in the field of developmental biology, open up new avenues for design of drugs for ataxia, a motor coordination disorder.
called BNIP-H, was linked first to Cayman ataxia, a rare genetic disorder affecting a region of the brain involved in motor control and
which leads to difficulty in coordinating complex movements, by Professor Margit Burmeister of U-M. The research team looked at the biological roles of BNIP
The study also provides the first experimental data solidifying the link between dysfunctional cholinergic (acetylcholine) secretion and Cayman ataxia.
The researchers showed that a BNIP-H mutant associated with Cayman ataxia caused defects in the transport of the ACL enzyme.
Furthermore, they could also reproduce motor dysfunctions of Cayman ataxia in zebrafish by knocking down BNIP-H, ACL or Chat enzymes.
suggesting that the loss of acetylcholine secretion resulting from BNIP-H mutation could explain some of the symptoms of Cayman ataxia.
"We established the first ACL-based ataxia model in the zebrafish that recapitulates the ataxic phenotype seen in human patients.
cellular and organism levels on how defects in ACL trafficking impairs cholinergic signalling that leads to the development of ataxia."
Their work also serves as a foundation for further studies into acetylcholine-related diseases, and may lead to new treatments that involve BNIP-H."Our findings could provide new direction to better understand causes of cholinergic-related diseases, such as Alzheimer's disease, Down's syndrome, ataxia and schizophrenia.
Changing the activity of BNIP-H or/and its downstream effectors might be used to treat those diseases caused by dysregulation of cholinergic neurotransmission,
"said Assoc Prof Low w
#Novel role of mitochondria identified in immune function Scientists at The Scripps Research Institute (TSRI) have discovered a new role for an enzyme involved in cell death.
The new study shows that this crosstalk is important not only for launching immune responses against tumors,
but also for regulating the inflammatory responses that may result in autoimmune diseases.""This finding could be helpful for developing strategies to target cancer
and inflammatory diseases,"said TSRI Assistant professor of Immunology Young Jun Kang, who collaborated on the study with the lab of TSRI Institute Professor Richard A. Lerner,
who is also Lita Annenberg Hazen Professor of Immunochemistry. The study was published September 18, 2015 in the journal Nature Communications.
which protects the body from harmful mutations and infections. However, scientists had understood not fully RIPK3's role in the immune system.
Their research suggests that RIPK3 regulates the activation of natural killer T cells (NKTS), the immune cells that play dual roles in the development of autoimmune diseases and the destruction of cancers.
scientists may be able to develop ways to better control NKTS to attack tumors. The new study also suggests there may be a way to intervene in the pathway to block inflammation.
implying a role for RIPK3 in autoimmune diseases. Kang said future studies will focus on understanding the details of this new signaling pathway,
possibly paving the way for new therapies that can either hone the pathway's cancer-killing role or reduce its role in inflammation.
In addition to Kang and Lerner, authors of the study,"Regulation of NKT cell-mediated immune responses to tumours and liver inflammation by mitochondrial PGAM5-Drp1 signaling,"were Bo-Ram Bang, Kyung Ho Han
It's really another step in the direction of personalized medicine, since individuals carrying mutations of one of a variety of genes account for the largest group of infertile couples."
#3-D printed guide helps regrow complex nerves after injury A national team of researchers has developed a first-of-its-kind,
3d printed guide that helps regrow both the sensory and motor functions of complex nerves after injury.
The groundbreaking research has the potential to help more than 200,000 people annually who experience nerve injuries or disease.
Because of this complexity, regrowth of nerves after injury or disease is very rare according to the Mayo Clinic.
Nerve damage is often permanent. Advanced 3d printing methods may now be the solution. In a new study, published today in the journal Advanced Functional Materials,
"This represents an important proof of concept of the 3d printing of custom nerve guides for the regeneration of complex nerve injuries,
and printer right at the hospital to create custom nerve guides right on site to restore nerve function."
or cadavers that hospitals could use to create closely matched 3d printed guides for patients. In addition to Mcalpine, major contributors to the research team include Blake N. Johnson, Virginia Tech;
a journal in the field of developmental biology, open up new avenues for design of drugs for ataxia, a motor coordination disorder.
called BNIP-H, was linked first to Cayman ataxia, a rare genetic disorder affecting a region of the brain involved in motor control and
which leads to difficulty in coordinating complex movements, by Professor Margit Burmeister of U-M. The research team looked at the biological roles of BNIP
The study also provides the first experimental data solidifying the link between dysfunctional cholinergic (acetylcholine) secretion and Cayman ataxia.
The researchers showed that a BNIP-H mutant associated with Cayman ataxia caused defects in the transport of the ACL enzyme.
Furthermore, they could also reproduce motor dysfunctions of Cayman ataxia in zebrafish by knocking down BNIP-H, ACL or Chat enzymes.
suggesting that the loss of acetylcholine secretion resulting from BNIP-H mutation could explain some of the symptoms of Cayman ataxia.
"We established the first ACL-based ataxia model in the zebrafish that recapitulates the ataxic phenotype seen in human patients.
cellular and organism levels on how defects in ACL trafficking impairs cholinergic signalling that leads to the development of ataxia."
Their work also serves as a foundation for further studies into acetylcholine-related diseases, and may lead to new treatments that involve BNIP-H."Our findings could provide new direction to better understand causes of cholinergic-related diseases, such as Alzheimer's disease, Down's syndrome, ataxia and schizophrenia.
Changing the activity of BNIP-H or/and its downstream effectors might be used to treat those diseases caused by dysregulation of cholinergic neurotransmission,
"said Assoc Prof Low w
#'Safepay':'First anti-fraud system to use existing credit card readers From large-scale data breaches such as the 2013 Target case to local schemes that use skimming devices to steal data at the gas pump,
and virus biology that could translate into valuable therapeutic and diagnostic applications Dr Jonathan Loh,
With the new insights, we can better identify the good stem cells and use them more efficiently and safely in clinical therapies.
in order to bring advancement in therapeutics and improve lives. With the growing importance of stem cell therapy, this study is a fitting example of how upstream research can potentially benefit
and shape its applications
#Targeting DNA: Protein-based sensor could detect viral infection or kill cancer cells MIT biological engineers have developed a modular system of proteins that can detect a particular DNA sequence in a cell
and then trigger a specific response, such as cell death. This system can be customized to detect any DNA sequence in a mammalian cell
"says James Collins, the Termeer Professor of Medical Engineering and Science in MIT's Department of Biological engineering and Institute of Medical Engineering and Science (IMES)."
To achieve this, the researchers could program the system to produce proteins that alert immune cells to fight the infection, instead of GFP."
While treating diseases using this system is likely many years away, it could be used much sooner as a research tool,
Vaginal rings with multiple reservoirs present a promising way for preventing sexually transmitted infections (STIS) and notably HIV infection in young women with high risk of exposure.
which corresponds to doses capable of preventing viral sexual-transmitted infections such as HIV-1 infection, Hepatitis b and genital herpes.
STIS of viral origin constitute a major public health concern, notably in women from low-income countries who were shown to be infected with HIV-1 early in their sexual live,
or tissue which are telltale signs of DNA mutation or the presence of cellular malfunctions such as cancer.
The absence of light sources that cover enough of the infrared spectrum with sufficient brilliance to detect minute concentrations originating from onco-metaboloids has been the main challenge in cancer detection.
Jens Biegert and his colleagues at ICFO are currently investigating molecular sensitivity for the identification of cancer biomarkers on the single cell level using all optical techniques in the mid-wave infrared wavelength range g
This is a crucial step in creating a new generation of foldable electronics--think a flat-screen television that can be rolled up for easy portability--and implantable medical devices.
indicating it is a good material for implantable medical devices. Fatigue is a common problem for researchers trying to develop a flexible, transparent conductor,
That means the materials aren't durable enough for consumer electronics or biomedical devices.""Metallic materials often exhibit high cycle fatigue,
and fatigue has been a deadly disease for metals, "the researchers wrote.""We weaken the constraint of the substrate by making the interface between the Au (gold) nanomesh and PDMS slippery,
#Virus re-engineered to deliver therapies to cells Stanford researchers have ripped the guts out of a virus
and totally redesigned its core to repurpose its infectious capabilities into a safe vehicle for delivering vaccines
and therapies directly where they are needed. The study reported today in the Proceedings of the National Academy of Sciences breathes new life into the field of targeted delivery,
"We make it smart by adding molecular tags that act like addresses to send the therapeutic payload where we want it to go."
"Using the smart particle for immunotherapy would involve tagging its outer surface with molecules designed to teach the body's disease-fighting cells to recognize
and destroy cancers, Swartz said. For Swartz and his principal collaborator, Yuan Lu, now a pharmacology researcher at the University of Tokyo, the result is a vindication.
It will require much more effort to accomplish the second goal--packing tiny quantities of medicines into the smart particles,
"But I believe we can use this smart particle to deliver cancer-fighting immunotherapies that will have minimal side effects."
"Targeted drug delivery is one of the ultimate goals of medicine because it seeks to focus remedies on diseased cells,
while treating cancer. Looking for a model in nature, many researchers focused on viruses, which target specific cells,
to carry a significant medical payload. But in practice this had proven so difficult that when Swartz floated the idea to funding agencies they said no.
they would hang vaccine tags on the spikes. If on the other hand, they wanted the capsid to deliver medicines to a sick cell,
they would hang address tags on the spikes. Finally, the researchers had to make all these modifications without destroying the miraculous capability of the capsid's DNA code to direct 240 copies of one protein to self-assemble into a hollow sphere with a spiky surface.
Swartz said the next step is to attach cancer tags to the outside of this smart particle,
to use it to train the immune system to recognize certain cancers. Those experiments would likely occur in mice.
After that he will add the next function--further engineering the DNA code to make sure that the protein can self-assemble around a small medicinal payload."
#Identifying the'dimmer switch'of diabetes Patrick Macdonald has dedicated much of his life to diabetes research.
Macdonald, a Canada Research Chair in Islet Biology, associate professor in the University of Alberta's Faculty of medicine & Dentistry and member of the Alberta Diabetes Institute, is the senior author of a landmark study in the Journal of Clinical Investigation.
According to Macdonald, the dimmer appears to be lost in Type 2 diabetes but can be restored and'turned back on'--reviving proper control of insulin secretion from islet cells of people with Type 2 diabetes.
The discovery is a potential game-changer in Type 2 diabetes research, leading to a new way of thinking about the disease and its future treatment."
"Understanding the islet cells in the pancreas that make insulin, how they work --and how they can fail--could lead to new ways to treat the disease,
delaying or even preventing diabetes, "says Macdonald. Ten million Canadians are living with diabetes or prediabetes.
The Canadian Diabetes Association reports that more than 20 Canadians are diagnosed newly with the disease every hour of every day.
It is also the seventh leading cause of death in Canada, with associated health-care costs estimated at nearly $9 billion a year.
Type 2 diabetes accounts for 90 per cent of all cases increasing the risk of blindness, nerve damage, stroke, heart disease and several other serious health conditions.
Macdonald believes the key to his latest research has been access to the Alberta Diabetes Institute's Isletcore.
The biobank, established with funding from the Alberta Diabetes Foundation and the U of A, collects pancreatic islets from organ donors--with and without diabetes--for diabetes research in Edmonton and across North america."
"Without access to this critical tissue through the Alberta Diabetes Institute Isletcore and the generosity of organ donors and their families, we would not have been able to carry out this study,
"says Macdonald.""If we want to learn about diabetes, and how to treat and prevent it,
studying the insulin-producing cells from donors with diabetes is a powerful way to do it."
"Though important new strides in the fight against Type 2 diabetes have been taken, Macdonald stresses that much more needs to be done.
The ability to restore and fix the dimmer switch in islet cells may have been proven on a molecular level,
but finding a way to translate those findings into clinical use could yet take decades.
Despite this, Macdonald believes the findings show an important new way forward.""We don't know enough to stop Type 2 diabetes yet,
but this is a large step towards understanding what's going wrong in the first place
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