#Engineering a permanent solution to genetic diseases In his mind, Basil Hubbard can already picture a new world of therapeutic treatments for millions of patients just over the horizon.
It a future in which diseases like muscular dystrophy, cystic fibrosis and many others are treated permanently through the science of genome engineering.
replacing the damaged genetic code with healthy DNA. here is a trend in the scientific community to develop therapeutics in a more rational fashion,
says Hubbard, an assistant professor of pharmacology in the University of Alberta Faculty of medicine & Dentistry. ee moving towards a very logical type of treatment for genetic diseases,
our disease is caused by a mutation in gene X, and wee going to correct this mutation to treat it.?
In theory, genome engineering will eventually allow us to permanently cure genetic diseases by editing the specific faulty genes. evolutionizing health caregenome engineering involves the targeted, specific modification of an organism genetic information.
and may one day revolutionize medical care. One of the obstacles still to be addressed in the field before it can see widespread use in humans is how to ensure the proteins only affect the specific target genes in need of repair.
but more improvements are needed to ensure off-target genes aren modified result that could potentially cause serious health problems itself.
Examples include diseases such as hemophilia sickle-cell anemia, muscular dystrophy and cystic fibrosis. Though the field is still in its relative infancy,
Hubbard says human clinical trials involving sequence-specific DNA-editing agents are already underway. If successful, he expects the first clinical applications could be seen in the next decade.
gene editing could possibly provide a permanent cure for a lot of different diseases, says Hubbard. e still have to overcome many hurdles,
but I think this technology definitely has the potential to be transformative in medicine. h
which can accurately detect malignant melanoma without a biopsy. The report, published online in Nature Scientific Reports yesterday (August 11),
55 patients with atypical moles agreed to have monitored their skin by researchers at Pisa University Hospital using a laser Doppler system.
which means that melanoma is identified in all cases where it is ruled present, and out in 90.9%of cases where it is not. rofessor Marco Rossi of Pisa University said:
kin malignant melanoma is a particularly aggressive cancer associated with quick blood vessel growth which means early diagnosis is vital for a good prognosis.
The current diagnostic tools of examination by doctors followed by biopsy inevitably leads to many unnecessary invasive excisions. his simple, accurate,
in vivo distinction between malignant melanoma and atypical moles may lead to a substantial reduction in the number of biopsies currently undertaken. ource:
Lancaster Universit L
#Nicotine-eating bacteria could one day help smokers kick the habit Most people who smoke cigarettes know it bad for their health,
Tobacco use remains the leading cause of preventable disease, disability and death in the U s. Smokers who want to quit can turn to various pharmacological aids.
These include patches gum and other nicotine-releasing products designed to replace cigarettes, as well as drugs that sequester nicotine in the body to prevent it from reaching the brain,
of which took less than five days to convert sugar into one of two medicinal compounds: either thebaine,
this could broaden access to many plant-based medicines. For thousands of years, people have used yeast to ferment wine,
Now researchers at Stanford have engineered genetically yeast to make painkilling medicines, a breakthrough that heralds a faster and potentially less expensive way to produce many different types of plant-based medicines.
Writing today in Science, the Stanford engineers describe how they reprogrammed the genetic machinery of baker yeast
It can take more than a year to produce a batch of medicine, starting from the farms in Australia,
and refined into medicines. hen we started work a decade ago, many experts thought it would be impossible to engineer yeast to replace the entire farm-to-factory process,
400 gallons of bioengineered yeast to produce a single dose of pain relief the experiment proves that bioengineered yeast can make complex plant-based medicines. his is only the beginning,
and demonstrate for opioid pain relievers can be adapted to produce many plant-derived compounds to fight cancers,
infectious diseases and chronic conditions such as high blood pressure and arthritis. rom plant to test tubesmany medicines are derived from plants,
to reprogram the cells into custom chemical assembly lines to produce medicinal compounds. An important predecessor to the Stanford work has been the use of genetically engineered yeast to produce the antimalarial drug artemisinin.
the Stanford team had to fill in a missing link in the basic science of plant-based medicines.
Many plants, including opium poppies, produce (S)- reticuline, a molecule that is a precursor to active ingredients with medicinal properties.
Smolke said. e need options to help ensure that the bio-based production of medicinal compounds is developed in the most responsible way. molke said that in the United states,
where opioid medicines are already widely available, the focus is on potential misuse. But the World health organization estimates that 5. 5 billion people have little
and the techniques we developed show that it is possible to make important medicines from scratch using only yeast,
and fairly provide medicines to all who need
#Scientists pioneer method to track water flowing through glaciers Researchers for the first time have used seismic sensors to track meltwater flowing through glaciers and into the ocean,
#Study shifts understanding of how bone fractures heal It time to rewrite the textbook description of bone fracture healing.
a protein that was thought to play a key role in fracture healing, is required not. Instead, the breakdown of fibrin is essential for fracture repair.
The findings, reported in the August issue of the Journal of Clinical Investigation, shift understanding of how fractures heal
and have implications for efforts to promote fracture repair. any of the current pharmaceutical protocols are based on using fibrin to promote fracture healing,
said Jonathan Schoenecker, M d.,Ph d, . assistant professor of Orthopaedic Surgery and Rehabilitation. n certain instances it may help,
but wee shown for sure that you don need it. Bone biology does not require fibrin to heal a fracture.
Fibrin is involved in blood clotting; it forms a meshlike net that traps platelets to form a clot.
Schoenecker said. hen you have a fracture, you have a huge disruption of that vascularity.
Since fibrin is the main protein at the site of a fracture, it was thought to promote repair by providing a scaffold for the initial phase of new bone formation.
however, that fracture repair was normal in mice missing the fibrin precursor fibrinogen. The investigators had reported previously the importance of vascular re-connection for bone fracture healing.
Using imaging techniques they developed to simultaneously study angiogenesis (new blood vessel growth) and bone formation after fracture,
they found that blood vessels grow first at the ends of the fracture, extend and reconnect. Then new bone forms. herefore, any condition associated with vascular disease
and thrombosis will impair fracture healing, Schoenecker said. It follows that if fibrin is removed not efficiently,
it gets in the way, he said. In the new studies, the team demonstrated that mice missing the factor that clears fibrin had impaired vascularization and bone union.
Genetic manipulations to deplete fibrinogen in these mice restored normal fracture repair. ibrin puts a cog in the machine
and you don get the anastomosis (vessel reconnection), Schoenecker said. The findings may explain why obesity, diabetes,
smoking and advanced age impair fracture repair. They are associated all with impaired fibrin clearance, he explained.
and orthopaedic surgery. t was unexpected totally that fibrin clearance is essential to prevent heterotopic ossification,
and plates used in orthopaedic surgeries, so that those devices don disrupt the ability of blood vessels to grow
as such big injuries of an incredibly vascular structure inevitably require a clot in order not to bleed to death,
He points out that some of the medications developed for cardiovascular medicine to prevent clotting may find new purposes in enhancing tissue repair and regeneration i
#Newly discovered cells regenerate liver tissue without forming tumors Hybrid hepatocytes proliferate and replenish liver mass after chronic liver injuries in micehybrid hepatocytes proliferate
and replenish liver mass after chronic liver injuries in micethe mechanisms that allow the liver to repair
and regenerate itself have long been a matter of debate. Now researchers at University of California, San diego School of medicine have discovered a population of liver cells that are better at regenerating liver tissue than ordinary liver cells, or hepatocytes.
and show that they are able to regenerate liver tissue without giving rise to cancer.
Of all major organs, the liver has the highest capacity to regenerate that why many liver diseases,
including cirrhosis and hepatitis, can often be cured by transplanting a piece of liver from a healthy donor.
In this latest study, led by Michael Karin, Phd, Distinguished Professor of Pharmacology and Pathology, researchers traced the cells responsible for replenishing hepatocytes following chronic liver injury induced by exposure to carbon tetrachloride, a common environmental toxin.
That when they found a unique population of hepatocytes located in one specific area of the liver,
and replenish liver mass after chronic liver injuries. Since the cells are similar to normal hepatocytes
when their therapeutic job is done. As a result ipscs carry a high risk of giving rise to tumors.
To test the safety of hybrid hepatocytes, Karin team examined three different mouse models of liver cancer.
They found no signs of hybrid hepatocytes in any of the tumors, leading the researchers to conclude that these cells don contribute to liver cancer caused by obesity-induced hepatitis
or chemical carcinogens. ybrid hepatocytes represent not only the most effective way to repair a diseased liver,
but also the safest way to prevent fatal liver failure by cell transplantation, Karin said p
Two recent studies pointed to possible flaws in the methods used to identify irisin, with commercially available antibodies.
Senior study author Bruce Spiegelman of Dana-Farber Cancer Institute and Harvard Medical school says that the confusion over irisin comes down to disagreement over how irisin protein is made in skeletal muscle cells and the detection limits
that does not rely on antibodies, to precisely measure how much irisin increases in people after exercise. he data are compelling
says endocrinologist Francesco Celi of the Virginia Commonwealth University Medical center, who was not involved with the study. mportantly,
#Telltale biomarker detects early breast cancer in NIH-funded study Researchers have shown that magnetic resonance imaging (MRI) can detect the earliest signs of breast cancer recurrence and fast-growing tumors.
breakaway tumor cells with the potential to develop into dangerous secondary breast cancer tumors elsewhere in the body.
Cleveland and was funded by the National Institute of Biomedical Imaging and Bioengineering (NIBIB), part of the National institutes of health.
CWRU M. Frank Rudy and Margaret Domiter Rudy Professor of biomedical engineering and an expert in molecular imaging for cancer and other diseases. e showed with this technique that we can detect very tiny tumors of just
revealing smaller cancers than can be detected with current clinical imaging modalities. ur imaging technology has the potential to differentiate aggressive tumors from low-risk tumors.
These are two things that potentially can make a big impact on clinical practice and also management of cancer.
Since small, early-stage cancers are the most responsive to drug treatments, screening is an important aspect of follow-up care for breast cancer patients,
and early detection is critical in tailoring appropriate and effective therapeutic interventions. While multiple imaging techniques, including MRI,
they are neither able to detect specific cancer types or early cancer growth. The earliest signs of cancer spread are called micrometastases.
As the name implies, they are often too small to be detected with standard screening. Dr. Lu team used a biochemical approach combined with MRI to detect molecular changes that signal micrometastases.
More importantly, the fibronectin part of the complex is expressed during a cell transition to cancer and plays a role in cell growth
The researchers collected images depicting metastases where breast cancer had spread beyond the original tumors. Metal molecules within the contrast solution are magnetized during the MRI process
and enhance the image wherever the molecules of solution bind with the targeted protein. he primary tumor sends signals to distant tissue
generating enough signal for MRI detection of small, high-risk cancer and micrometastases. The researchers tested the approach in mice into
and tumors compared with normal tissue. Using a microscopic imaging approach, called cryo-imaging, and MRI, the researchers verified that the MRI technique could detect micrometastases,
and the consequence of metastatic cancer make these efforts urgent and important, said Lu, adding that his research team also hopes to advance the approach for prostate cancer detection. e think this targeted approach holds great promise for earlier imaging of high-risk cancers in the clinic.
It could also become useful as a noninvasive way to assess breast cancer treatment progress.
The team plans to complete safety testing of the imaging agent during the next three years.
Andreas Velten, a Morgridge medical engineering affiliate and scientist with the University of Wisconsin-Madison Laboratory for Optical and Computational Instrumentation (LOCI
Cerebrovascular disease often entails complex tangles of vessels in sensitive brain areas. hese children had unique anatomy with deep vessels that were very tricky to operate on,
Harvard Medical school associate professor of neurosurgery at Boston Children Hospital and senior author of the paper. he 3-D printed models allowed us to rehearse the cases beforehand
who co-directs the Cerebrovascular Surgery and Interventions Center at Boston Children. ou can physically hold the 3-D models,
and get tactile feedback. s described in the Journal of Neurosurgery: Pediatrics, the models were based on the children actual brain scans.
Data from the scans were used to program a 3-D printer that laid down synthetic resins layer by layer.
I practiced those steps ahead of time. he surgery went off without complications, and last month Adam had a clean one-year follow-up angiogram.
Darren Orbach, HMS associate professor of radiology and co-director of the Cerebrovascular Surgery and Interventions Center at Boston Children, treated a 2-month-old infant who had a rare vein of Galen malformation in
Orbach used an interventional radiology technique called embolization to seal off the malformed blood vessels from the inside. ven for a radiologist who is comfortable working with
, were created in collaboration with the Boston Children Hospital Simulator Program (SIMPEDS), directed by HMS associate professor of anesthesia Peter Weinstock, the paper first author.
Measurements of the models showed 98 percent agreement with the children actual anatomy. All four children malformations were removed successfully
surgeon and operating roomhose with 3-D models had their surgical time reduced by 30 minutes,
but even a 30-minute reduction is significant for children who are especially sensitive to anesthesia.
The SIMPEDS program is tracking use of 3-D printed models across Boston Children Hospital,
but hopefully it will lead to medical applications. This gives us new opportunities to look at cell structures
and whether there any degradation of those structures in diseases. Many diseases are caused either by an invading pathogen or degradation of a cell internal structure.
Alzheimer, for example, may be related to degradation of the cytoskeleton inside neurons. he cytoskeleton system is comprised of a host of interacting subcellular structures and proteins,
#Scientists visualize critical part of basal ganglia pathways Breakthrough could help see pathways that degenerate with Parkinson and Huntingdon disease Certain diseases,
like Parkinson and Huntingdon disease, are associated with damage to the pathways between the brain basal ganglia regions.
which could potentially lead to technologies to help track disease progression for Parkinson and Huntington disease and other neurological disorders. linically,
and completed cutting-edge work in understanding the genetics of autism. Building on its strengths in biology
so that the diagnosis of heart conditions such as coronary heart disease or arrhythmia can be improved greatly. In the future, a special shield room for detecting the bio-magnetic field would be unnecessary
The device is expected to make a difference in medical treatments, preventive health care and sports p
#New synthetic tumor environments make cancer research more realistic Tumors are notoriously difficult to study in their natural habitat body tissues
but a new synthetic tissue environment may give cancer researchers the next-best look at tumor growth and behavior.
and grow into a tumor. They were able to observe how differently cells act in the three-dimensional
and expensive mouse avatars that are created by injecting human tumor cells into mice. his is really the first time that it been demonstrated that you can use a rapid methodology like this to spatially define cancer cells and macrophages,
Can therapeutics be used to disrupt that communication? What sets the team model apart from mouse avatars
and finds out theye been diagnosed with some sort of solid tumor, Kilian said. ou take a biopsy of those cells,
you put it into this device, grow them and see how they respond to different treatments. h
the optoclamp could facilitate research into new therapies for epilepsy, Parkinson disease, chronic pain and even depression. ur work establishes a versatile test bed for creating the responsive neurotherapeutic tools of the future,
said Steve Potter, an associate professor in the Wallace H. Coulter Department of Biomedical engineering at Georgia Tech and Emory University. eural modulation therapies of the future,
said Newman. his is potentially a very big deal in terms of developing therapies for aberrant forms of synaptic plasticity.
Potential applications include chronic pain, epilepsy, tinnitus, phantom limb syndrome and other nervous systems disorders where the brain has overreacted to the loss of normal inputs.
That work, recently published in the journal Nature Communications, was a collaboration with Emory University Professor Pete Wenner and former graduate student Ming-fai Fong,
#Scientists discover the mechanism behind the innate immunological memory There can be no argument it is extremely important to understand how immunity works.
Better knowledge about immunity would help scientists to come up with new, more effective ways to prevent outbreaks of diseases.
However, at this moment science is needed lacking knowledge about human immunity. For example, for a long time it was believed that acquired immunity type of immunity mediated by T-and B-cellsad memory,
whereas innate immunityhich is mediated by macrophages and other types of cells that react to certain molecules typically associated with pathogensid not.
But now scientists know things are not so simple. This was not hard to figure out
as plants and insects have innate immunity only, but seem to have immunological memory. Furthermore, scientists observed that herpes virus infection increases the resistance against bacteria in vertebrates,
which suggests that innate immunity also has memory, even though researchers have struggled to understand the mechanism behind it.
However, now scientists from the RIKEN Molecular genetics Laboratory have revealed the mechanism underlying the memory of innate immunity.
It turns out there are epigenomic changes induced by pathogen infections mediated by a transcription factor called ATF7.
Although it seems to be complicated extremely phenomenon, in the future this discovery may help everyone, including those, who struggle to understand the mechanisms behind the memory of innate immunity.
At first, research team discovered that in ATF7 knockout mice, macrophages appear similar to wild-type macrophages that have been activated by exposure to molecules that occur commonly in infections.
Even before that scientists knew heat shock or psychological stress induced epigenomic changes were mediated by ATF7-related transcription factors.
After exposure to that stress, changes remained for a long duration of time. This made researchers think that pathogen infections could induce epigenomic changes in macrophages via ATF7.
Scientists found that ATF7 transcription factor simply binds itself to a group of innate immune genes and silences their expression
which makes cells less responsive to infections. Scientists managed to make ATF7 inactive, by using a molecule found in the outer membrane of Gram-negative bacteria,
called a lipopolysaccharidel. It made ATF7 phosphorylated and immune-related genes in mice models were silenced no longer.
First of all, it may increase our understanding of the ygiene hypothesis It is the concept saying that pathogen infection
and unhygienic environment during infancy reduces the risk of allergy later in life. ygiene hypothesisis used to explain why in more developed countries with better hygiene habits the incidence of allergies
and asthma is increasing. Now scientists say that since they can explain that the pathogen-induced epigenomic changes mediated by ATF7 maintain for a long period of time,
they have a better explanation about how the changes are induced. Secondly, these new findings may be very helpful developing vaccines with more effective adjuvants.
Adjuvants are used compounds in vaccines that activate innate immunity they are necessary ingredient of efficient vaccines.
For a long time scientists thought that the effect of adjuvant can be maintained a several days only. But this new research shows that it is not necessarily true.
which would make for much more effective vaccines. As much as human immune system still remains not completely clear for science
this new research provides better understanding about how our immune system remembers appropriate reactions to stress.
Knowing how to form these memories may hide the key to creating better, more effective and long-lasting vaccines a
even though there will always be a hole in your visual field. he neuroscientists at UQ School of Psychology may have opened the way to new treatments for the developed world leading cause of blindness,
but this has proved sufficient to bring about a 10 per cent reduction in functional blindness,
suggesting that the improvement wasn simply a matter of practising the task. e did not confidently expect to see much reduction in functional blindness,
it might prove similarly effective in other cases of blindness or be used to assist developing technologies,
such as the bionic eye or retinal stem cell therapy. c
#DNA-Guided 3-D Printing of Human Tissue Is unveiled A UCSF-led team has developed a technique to build tiny models of human tissues, called organoids,
or go awry in cancer. They could be used for therapeutic drug screening and to help teach researchers how to grow whole human organs.
The new technique called DNA Programmed Assembly of Cells (DPAC) and reported in the journal Nature Methods on Aug 31 allows researchers to create arrays of thousands of custom-designed organoids,
we could be taking samples of different components of a cancer patient mammary gland and building a model of their tissue to use as a personalized drug screening platform.
But in diseases such as breast cancer, the breakdown of this order has been associated with the rapid growth and spread of tumors. ells aren lonely little automatons,
Gartner said. hey communicate through networks to make group decisions. As in any complex organization, you really need to get the group structure right to be failed successful,
it sets the stage for cancer. ut studying how the cells of complex tissues like the mammary gland self-organize,
and break down in disease has been a challenge to researchers. The living organism is often too complex to identify the specific causes of a particular cellular behavior.
but also to experiment with specifically adding in a single cell with a known cancer mutation to different parts of the organoid to observe its effects.
or more cells expressing low levels of the cancer gene Rasg12v affected the cells around them.
or structural changes in mammary glands can lead to the breakdown of tissue architecture associated with tumors that metastasize,
or stress levels in soldiers and pilots. In this study, engineers focused on uric acid, which is a marker related to diabetes and to gout.
Currently the only way to monitor the levels of uric acid in a patient is to draw blood.
and non-invasively saliva biomarkers holds considerable promise for many biomedical and fitness applications, said Wang.
Next, they collected saliva from a patient who suffers from hyperuricemia, a condition characterized by an excess of uric acid in the blood.
#Team develops quick way to determine bacteria antibiotic resistance Bacteria ability to become resistant to antibiotics is a growing issue in health care:
Staphylococcus epidermis is increasingly emerging as a cause of multi-resistant hospital-acquired infections. The ability to quickly judge whether a bacteria is resistant to antibiotics could make a major difference in a patient's treatment.
Shannon Hilton and Paul Jones Staphylococcus epidermis is increasingly emerging as a cause of multi-resistant hospital-acquired infections.
Mark Hayes National summary data from the Centers for Disease Control and Prevention indicate that each year in the United states,
at least 2 million people acquire serious infections with antibiotic-resistant strains of bacteria. At least 23,000 people die as a direct result of these infections,
and many more die from related complications. It is not just humans that are threatened by this growing adaptation.
however, Staphylococcus epidermidis has emerged increasingly as a cause of multi-resistant hospital-acquired infections. Immunocompromised patients
indwelling medical devices, and surgically implanted prostheses provide suitable environments for Staphylococcus epidermidis to propagate and form biofilms.
as a collaboration with orthopedic surgeon Dr. Alex Mclaren and his team member and bioengineer Dr. Ryan Mclemore of Banner Good samaritan Medical center, Phoenix,
along with Dr. Mark Spangehl of the Mayo Clinic College of Medicine, Arizona. By most metrics the antibiotic-resistant and susceptible strains of Staphylococcus epidermidis are phenotypically identical,
and the doctor is getting the right answer right away. By advancing a fundamental area of science,
This separation has significant potential implications for health care, as rapid and early detection will significantly improve therapeutic outcomes.
The current results establish a foundation for biophysical separations as a direct diagnostic tool, potentially improving nearly every figure of merit for diagnostics and antibiotic stewardship o
Overtext Web Module V3.0 Alpha
Copyright Semantic-Knowledge, 1994-2011