#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
As for the calcium clearance pump, the sperm needs to use it to reduce toxic calcium levels quickly.
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."
since she published her first scientific article--"Cannabis and Chromosomes,"examining the impact of marijuana on embryonic cells--in The Lancet in 1969,
#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
#Building a biofuel-boosting Swiss Army knife Researchers at Michigan State university have built a molecular Swiss Army knife that streamlines the molecular machinery of cyanobacteria,
biotechnology and medical treatments.""The very simple design rules that we have discovered provide a powerful engineering tool for many biomedical
and biotechnology applications,"said Ashutosh Chilkoti, chair of the Department of Biomedical engineering at Duke.""We can now,
however, drugs could be encapsulated in protein cages that accumulate inside of a tumor and dissolve once heated.
they could break down into additional therapeutic agents. We can now design two things into one."
a two-drug combination discovered by UF Health researchers that inhibits tumors and kills cancer cells in mouse models.
For the first time, researchers have shown that a certain protein becomes overabundant in pancreatic neuroendocrine tumors, allowing them to thrive.
The findings were published recently in the Journal of the National Cancer Institute by a group that includes Rony A. François, an M d./Ph d. student working with Maria Zajac-Kaye, Ph d.
an associate professor in the UF College of Medicine's department of anatomy and cell biology. Finding new treatments is critical
because less than 5 percent of patients with pancreatic neuroendocrine tumors respond to everolimus, the most commonly used pharmaceutical,
Neuroendocrine tumors, which form in the hormone-making islet cells, account for 3 percent to 5 percent of pancreatic malignancies
and have a five-year survival rate of about 42 percent, according to the National Cancer Institute.
Pancreatic neuroendocrine tumors are increasingly common, which medical experts and researches have attributed to better diagnostic imaging,
an aging population and heightened awareness of the disease stemming from the 2011 death of Apple Inc. cofounder Steve jobs. Zajac-Kaye's group discovered that a single protein is behind the process that allows pancreatic neuroendocrine tumors to thrive.
The protein, known as focal adhesion kinase, or FAK, activates an enzyme called AKT, which helps islet cells in the pancreas to survive.
But when islet cells begin turning into tumors, the FAK protein gets overproduced, researchers found.
This overabundance of the protein allows tumors to resist chemotherapy and evade efforts to kill them off.
After identifying FAK's role in tumor development François started looking for ways to get it in check.
One idea was finding something to make the antitumor drug everolimus more effective.""Once we figured out that FAK was started important,
Daily doses of the compound reduced tumor volume by about 50 percent after 25 days, they found.
While everolimus can extend some patients'lives by holding tumors in check, it does little to make them regress
The findings also have potential uses for most other types of solid tumors, including those affecting the lungs and ovaries,
this novel device is very suitable for applications such as soft robotics, wearable consumer electronics, smart medical prosthetic devices,
which are utilised already increasingly for monitoring critical parameters in biomedical applications, especially for those that may come in contact with human skin
With the rapid advancement of healthcare and biomedical technologies as well as consumer electronics, we are optimistic about new possibilities to commercialise our invention,
#Antimicrobial film for future implants The implantation of medical devices is not without risks. Bacterial or fungal infections can occur
and the body's strong immune response may lead to the rejection of the implant. Researchers at Unit 1121"Biomaterials and Bioengineering"(Inserm/Strasbourg university) have succeeded in creating a biofilm with antimicrobial, antifungal and anti-inflammatory properties.
It may be used to cover titanium implants (orthopaedic prostheses, pacemakers...prevent or control postoperative infections. Other frequently used medical devices that cause numerous infectious problems, such as catheters, may also benefit.
These results are published in the journal Advanced Healthcare Materials. Implantable medical devices (prosthesis/pacemakers) are an ideal interface for microorganisms,
which can easily colonize their surface. As such, bacterial infection may occur and lead to an inflammatory reaction.
This may cause the implant to be rejected. These infections are caused mainly by bacteria such as Staphylococcus aureus,
originating in the body, and Pseudomonas aeruginosa. These infections may also be caused fungal or by yeasts.
The challenge presented by implanting medical devices in the body is preventing the occurrence of these infections
which lead to an immune response that compromises the success of the implant. Antibiotics are used currently during surgery
or to coat certain implants. However, the emergence of multi-resistant bacteria now restricts their effectiveness.
A biofilm invisible to the naked eye It is within this context that researchers at the"Bioengineering
and Biomaterials"Unit 1121 (Inserm/Strasbourg University) with four laboratories1 have developed a biofilm with antimicrobial and anti-inflammatory properties.
Researchers have used a combination of two substances: polyarginine (PAR) and hyaluronic acid (HA), to develop and create a film invisible to the naked eye (between 400 and 600 nm thick) that is made of several layers.
As arginine is metabolised by immune cells to fight pathogens, it has been used to communicate with the immune system to obtain the desired anti-inflammatory effect.
Hyaluronic acid, a natural component of the body, was chosen also for its biocompatibility and inhibiting effect on bacterial growth.
Embedded antimicrobial peptides on a thin silver coating The film is also unique due to the fact that it embeds natural antimicrobial peptides
in particular catestatin, to prevent possible infection around the implant. This is an alternative to the antibiotics that are used currently.
these peptides are not toxic to the body that they are secreted into. They are capable of killing bacteria by creating holes in their cellular wall
preventing and controlling infection The results from numerous tests performed on this new film shows that it reduces inflammation
and prevents the most common bacterial and fungal infections. On the one hand, researchers demonstrate, through contact with human blood,
that the presence of the film on the implant suppresses the activation of inflammatory markers normally produced by immune cells in response to the implant.
yeast strains (Candida albicans) or fungi (Aspegillus fumigatus) that frequently cause implant-related infection"emphasises Philippe Lavalle.
Researchers conclude that this film may be used in vivo on implants or medical devices within a few years to control the complex microenvironment surrounding implants
and to protect the body from infection n
#Physiologists uncover a new code at the heart of biology UT Southwestern physiologists trying to understand the genetic code have found a previously unknown code that helps explain which protein should be created to form a particular type of cell.
The human body is made up of tens of trillions of cells. Each cell contains thousands of proteins,
"said Dr. Liu, the Louise W. Kahn Scholar in Biomedical Research.""By influencing the speed with
This can have important implications for identifying human disease-causing mutations because this study indicates that a mutation does not have to change amino acid identity to cause a disease.
In fact, most mutations in human DNA do not result in amino acid change.""Therefore, our study indicates that the new"code"--the speed limit of assembly--within the genetic code can dictate the ultimate function of a given protein,
one cancerous cell breaks off from a tumor, slips into the bloodstream and quickly lodges elsewhere in the body.
These colonizers may bloom into deadly metastatic cancer right away or lie dormant for years, only to trigger a recurrence decades after the primary tumor is removed.
Metastases cause the vast majority of cancer deaths, but their tiny seeds are so difficult to track that few researchers have managed to study them.
Now, scientists from UC San francisco describe capturing and studying individual metastatic cells from human breast cancer tumors implanted into mice as the cells escaped into the blood stream
and began to form tumors elsewhere in the body. The researchers discovered that genetic programs expressed in these cells were quite distinct from the primary tumors in
which they originated and included genes typically expressed in mammary stem cells. The findings, published online Sept. 23,2015 in Nature, could change the way researchers think about how cancer spreads
and suggest new drugs to track down and disable its deadly seeds. For the most part, modern cancer drugs ignore differences between primary
and metastatic tumors, said Zena Werb, Phd, professor and vice-chair of anatomy at UCSF, and a senior author on the new study."
"We test drugs for their ability to make primary tumors shrink, but most just don't work on metastases,
"Patients have their original tumor treated or removed, but then the cancer comes back 20,30, 40 years later because there were just a few metastatic cells sitting around."
"Catching metastatic cancer cells in the act No one really knows how dormant metastatic cells can survive incognito for decades,
"It's a big black box in the cancer field--mostly because it's very difficult to study,
only about 7 percent of all breast cancer funding goes to studying metastatic cancer, despite the fact that it causes virtually all breast cancer deaths.
Previous work by Werb's group had found a subset of cells at the edges of breast cancer tumors that seemed primed to metastasize.
and with proteins in the surrounding tumor microenvironment seemed to turn on genetic programs akin to those of mammary stem cells--the cells that allow breasts to form during puberty
These genes for self-replication could make these cells particularly apt to generate new tumors elsewhere in the body.
which involves transplanting human tumor cells into mice. Against the backdrop of healthy mouse tissue, rogue metastatic cells from the human tumor stick out like flares.
The researchers developed a new method using flow cytometry that let them capture individual human metastatic cancer cells traveling through the mouse's blood
the cancer cells'gene activity looked much like that of the primary tumor that had been transplanted into the mice,
In contrast, early-stage metastases and cancer cells traveling through the blood expressed genes typically active in mammary stem cells and quite distinct from primary tumor cells.
Remarkably, the same signature pattern of gene activity was found in metastatic cells in mice whose tumors came from genetically and clinically diverse human patients.
In other words, the genetic program that makes a cell metastatic did not depend on the genetics of its tumor of origin--suggesting that new techniques might allow researchers to find
Insights could lead to targeted therapies The research team performed a proof of principle experiment to demonstrate how valuable information about metastatic gene expression could be for drug development.
Since metastatic cells that were beginning to differentiate into secondary tumors showed high expression of genes cmyc and CDK2, the researchers treated 24 PDX mice with dinaciclib,
Whereas 44 percent of control mice (11 of 25) developed secondary tumors within four weeks, researchers could only find metastatic cells in one drug-treated mouse (4 percent.
was that the drug managed to nearly eliminate metastases without shrinking the primary tumor.""If this drug had only been tested on primary tumors,
we would have said it doesn't work, "she said.""This tells us you actually have to look at metastases
"Preventing metastatic cells from invading other parts of the body has been a priority for cancer researchers for many years,
and of medicine at UCSF and a co-corresponding author on the new study.""But practically speaking,
by the time you've detected the tumor, that horse is either already out of the barn
--which a consortium of researchers at UCSF are applying to diverse biological and clinical questions--could have a major impact on the emerging field of precision medicine."
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