and quantify infection by parasitic worms in a drop of blood. This next generation of UC Berkeley Cellscope technology could help revive efforts to eradicate debilitating filarial diseases in Africa by providing critical information to health providers in the field. e previously showed that mobile phones can be used for microscopy,
but this is the first device that combines the imaging technology with hardware and software automation to create a complete diagnostic solution,
The UC Berkeley engineers teamed up with Dr. Thomas Nutman from the National Institute of Allergy and Infectious diseases (NIAID),
where health officials have been battling the parasitic worm diseases onchocerciasis (river blindness) and lymphatic filariasis. The video Cellscope,
May 6) in the journal Science Translational Medicine. his research is addressing neglected tropical diseases, said Fletcher. t demonstrates
but treatable, diseases. Battling parasitic worms River blindness is transmitted through the bite of blackflies and is the second-leading cause of infectious blindness worldwide.
Lymphatic filariasis, spread by mosquitoes, leads to elephantiasis, a condition marked by painful, disfiguring swelling.
It is the second-leading cause of disability worldwide and like river blindness, is highly endemic in certain regions in Africa.
The antiparasitic drug ivermectin, or IVM, can be used to treat these diseases, but mass public health campaigns to administer the medication have been stalled because of potentially fatal side effects for patients co-infected with Loa loa,
which causes loiasis, or African eye worm. When there are high circulating levels of microscopic Loa loaworms in a patient,
representing a major setback in the efforts to eradicate river blindness and elephantiasis. Next generation Cellscope uses video, automation For this latest generation of the mobile phone microscope, named Cellscope Loa, the researchers paired a smartphone with a 3d printed plastic base where the sample of blood
whether it is safe to administer IVM. he availability of a point-of-care test prior to drug treatment is a major advance in the control of these debilitating diseases,
such as premature ovarian failure and polycystic ovarian syndrome, conditions that both result in hormone imbalances and infertility in women.
developed by the Public health Agency of Canada and manufactured by the American pharmaceutical company Merck Sharp & Dome, was shown just to confer 100%protection against the disease,
said Michael Osterholm, Director of the Center for Infectious disease Research and Policy in Twin cities, Minnesota,
while current statistics on the epidemic are the most promising in well over a year last week only four new cases were observed in Guinea
#Artificial blood vessels become resistant to thrombosis Scientists from ITMO University developed artificial blood vessels that are not susceptible to blood clot formation.
Surgery, associated with cardiovascular diseases, such as ischemia, often require the implantation of vascular grafts artificial blood vessels,
#Molecular spies to fight cancer Tracking the tumor: PNA-antibodies detect initially the diseased cells (red)
and accumulate at the tumor site. Afterwards the radioactively labeled probes (blue) selectively bind to them by specific base pairing.
thus to visualize the tumor. Scientists at the Helmholtz-Zentrum Dresden-Rossendorf (HZDR), in cooperation with colleagues at the University of Zurich and the Ruhr-Universität Bochum, have tested for the first time successfully a new tumor diagnosis method under near-real conditions.
The new method first sends out an antibody as a pyto detect the diseased cells and then binds to them.
The scientists could then clearly visualize the tumor by utilizing a tomographic method. This procedure could improve cancer treatment in the future by using internal radiation.
The human immune system forms antibodies that protect the body from pathogens. Antibodies can also, however, be produced in a laboratory to precisely bind to tumor cells.
They are used in cancer research to detect and fight malignant tumors. For example, antibodies can serve as transport vehicles for radionuclides, with
which the affected regions can be visualized or can even be damaged. Until recently, a stumbling block has been their large molecular mass. his causes them to circulate in the body for too long before they reach the diseased cells
explains Dr Holger Stephan from the Institute of Radiopharmaceutical Cancer Research at HZDR. his is a disadvantage
because organs that are affected not by the disease are exposed to radiation. It also makes the exact localization of the tumor in the body more difficult
because the resulting images are less sharp. ogether with colleagues at the University of Zurich and the Ruhr-Universität Bochum,
the researchers from Dresden therefore chose an alternative strategy. y using what is known as re-targeting the antibodiestask is divided into two steps, Dr Kristof Zarschler, a member of Stephan team,
explains. n a figurative sense, we first send spies out in advance, over a longer period of time,
to scout out the enemy the tumor cells. The piesthen share their position with their troops,
In various types of tumors, there is an increase in this molecule formation or it might be found in a mutated form,
the scientists first injected the PNA-EGFR antibody into tumor-bearing mice and gave this pytime to accumulate at the tumor site.
They then administered the PNA counterpart, labeled with the radioactive substance technetium-99m. mages we took using single photon emission computed tomography show that both the antibody
The tumor could thus be visualized clearly within a short period of time. urthermore, the radioactively labeled probes had disappeared already from the bloodstream after sixty minutes,
and their matching PNA counterparts can be used in diagnosing tumors in humans. ur results however show that the PNAS we tested are suitable candidates for further preclinical studies, Stephan sums up.
it could also be used to transport therapeutically effective radioactive substances to the tumor in order to irradiate it from within
, cancer or infections), or to silence it when it mistakenly attacks the body itself (e g.,
, autoimmune disorders or allergies. Now, scientists at the Salk Institute have discovered that T cell triggering relies on a dynamic protein network at the cell surface,
in order to recognize and eliminate diseases. Lillemeier team is working to identify new principles that determine
#Nanoparticles used to breach mucus barrier in lungs Proof-of-concept study conducted in mice a key step toward better treatments for lung diseases Nanotechnology could one day provide an inhaled vehicle to deliver targeted therapeutic genes
that therapeutic genes may one day be delivered directly to the lungs to the levels sufficient to treat cystic fibrosis (CF), chronic obstructive pulmonary disease,
asthma and other life-threatening lung diseases. o our knowledge, this is the first biodegradable gene delivery system that efficiently penetrates the human airway mucus barrier of lung tissue,
Suk says their work with nanoparticles grew out of failed efforts to deliver treatments to people with lung diseases.
In patients with CF, for instance, they experience a buildup of excess mucus caused by impaired ciliary beating, resulting in an ideal breeding ground for chronic bacterial infection and inflammation.
Most of the existing drugs for CF help clear infections but do not solve the disease underlying problems.
and are capable of rapidly penetrating human airway mucus freshly collected from patients visiting the Johns Hopkins Adult Cystic fibrosis Program directed by Michael Boyle,
put stress on power generators and lead to instabilities in the power system. Grid coordinators have the daily challenge of forecasting the need for
creating an asymmetrical stress that makes the membranes fold. Zhang Jiang and Jin Wang, X-ray staff at the APS,
#Real-time data for cancer therapy In the battle against cancer, which kills nearly 8 million people worldwide each year,
Magnetic resonance imaging and other scanning technologies can indicate the size of a tumor, while the most detailed information about how well a treatment is working comes from pathologistsexaminations of tissue taken in biopsies.
Yet these methods offer only snapshots of tumor response and the invasive nature of biopsies makes them a risky procedure that clinicians try to minimize.
Now, researchers at MIT Koch Institute for Integrative Cancer Research are closing that information gap by developing a tiny biochemical sensor that can be implanted in cancerous tissue during the initial biopsy.
Making cancer treatments more targeted and precise would boost their efficacy while reducing patientsexposure to serious side effects. e wanted to make a device that would give us a chemical signal about what happening in the tumor,
says Michael Cima, the David H. Koch (1962) Professor in Engineering in the Department of Materials science and engineering and a Koch Institute investigator who oversaw the sensor development. ather than waiting months to see
if the tumor is shrinking, you could get an early read to see if youe moving in the right direction.
on-demand data concerning two biomarkers linked to a tumor response to treatment: ph and dissolved oxygen.
you can see the response chemically before you see a tumor actually shrink, Cima says.
and the inflammation will make the tumor appear to be growing, even while the therapy is effective.
since tumors thrive in low-oxygen (hypoxic) conditions. t turns out that the more hypoxic the tumor is,
could let you see how hypoxia was changing in the tumor, so you could adjust the radiation accordingly.
so we can use them to monitor tumor response, Cima says. e did a little bit of that in these experiments,
While the primary application of these sensors would be cancer care, Cima is also eager to collaborate with researchers in other fields, such as environmental science. or example,
#Researchers discover cancer markers may be visible early during human development Researchers at the Virginia Bioinformatics Institute have uncovered a link between the genomes of cells originating in the neural crest
and development of tumors a discovery that could lead to new ways to diagnose and treat cancer.
The new finding, recently published in Oncotarget, resolves why some cancer types share genomic and clinical features.
The discovery may also lead to new ways to diagnose and treat brain cancer, such as gliomas, medulloblastomas, and neuroblastomas;
and skin cancer, known as melanoma. More than 22,000 new cases of brain cancer and more than 73,000 new cases of skin cancer and were expected to arise in Americans in 2015, according to the National Cancer Institute.
To reveal when cancer-causing genomic changes occur, a research group led by Harold kipgarner, a professor in the departments of biological science, computer science,
and basic science at Virginia Tech Carilion Medical school, analyzed an often ignored part of the human genome repetitive DNA sequences referred to as microsatellites.
More than 1 million microsatellites exist in the human genome including in neural crest tissues, a thin layer of cells within an embryo that contains genetic instructions to build hundreds of cell types, from neurons to adrenal cells.
Neurological tumors, for example, may arise from glial cells that develop from the crest. Researchers with the institute Medical Informatics Systems division say cancer types can be found
or predicted from specific markers within these repetitive sequences, known as cancer-associated microsatellite loci, or CAML.
Long considered unk DNAOR ark matterwithin the genome because their function was unclear microsatellites are known for their role in certain diseases such as Fragile X and Huntington disease.
Garner group has shown that these regions can be informative about diseases ranging from cancer to autism spectrum disorder.
With more study, researchers believe interrelated hereditary and genetic traits of certain cancers can be traced to their common origin at the neural crest,
leading to potentially better therapies and easier tumor identification. The findings have been licensed to Genomeon, a company co-founded by Garner to develop new ways to assess cancer risk,
create diagnostics, and explore potential drug targets to help cancer patients p
#How chronic inflammation can lead to cancer Chronic inflammation caused by disease or exposure to dangerous chemicals has long been linked to cancer,
but exactly how this process takes place has remained unclear. Now, a precise mechanism by which chronic inflammation can lead to cancer has been uncovered by researchers at MIT a development that could lead to improved targets for preventing future tumors.
In a paper published in the Proceedings of the National Academy of Sciences, the researchers unveil how one of a battery of chemical warfare agents used by the immune system to fight off infection can itself create DNA mutations that lead to cancer.
As many as one in five cancers are believed to be caused or promoted by inflammation. These include mesothelioma,
a type of lung cancer caused by inflammation following chronic exposure to asbestos, and colon cancer in people with a history of inflammatory bowel disease, says Bogdan Fedeles,
a research associate in the Department of Biological engineering at MIT, and the paper lead author.
Innate immune response Inflammation is part of the body innate response to invading pathogens or potentially harmful irritants.
The immune system attacks the invader with a number of reactive molecules designed to neutralize it,
including hydrogen peroxide, nitric oxide and hypochlorous acid. However, these molecules can also cause collateral damage to healthy tissue around the infection site:
he presence of a foreign pathogen activates the immune response, which tries to fight off the bacteria,
but in this process it also damages some of the normal cells, Fedeles explains. Previous work by Peter Dedon, Steven Tannenbaum, Gerald Wogan,
and James Fox all professors of biological engineering at MIT had identified the presence of a lesion,
or site of damage in the structure of DNA, called 5-chlorocytosine (5clc) in the inflamed tissues of mice infected with the pathogen Helicobacter hepaticus.
This lesion, a damaged form of the normal DNA base cytosine, is caused by the reactive molecule hypochlorous acid the main ingredient in household bleach
which is generated by the immune system. The lesion 5clc, was present in remarkably high levels within the tissue,
says John Essigmann, the William R. 1956) and Betsy P. Leitch Professor in Residence Professor of Chemistry, Toxicology and Biological engineering at MIT,
who led the current research. hey found the lesions were very persistent in DNA, meaning we don have a repair system to take them out,
Essigmann says. n our field lesions that are persistent, if they are also mutagenic, are the kind of lesions that would initiate cancer,
he adds. DNA sequencing of a developing gastrointestinal tumor revealed two types of mutation: cytosine (C) bases changing to thymine (T) bases,
and adenine (A) bases changing to guanine (G) bases. Since 5clc had not yet been studied as a potentially carcinogenic mutagen,
the researchers decided to investigate the lesion further, in a bid to uncover if it is indeed mutagenic.
Using a technique previously developed in Essigmann laboratory, the researchers first placed the 5clc lesion at a specific site within the genome of a bacterial virus. They then replicated the virus within the cell.
The researchers found that, rather than always pairing with a guanine base as a cytosine would,
when triggered by infection, fires hypochlorous acid at the site, damaging cytosines in the DNA of the surrounding healthy tissue.
he explains. his scenario would best explain the work of James Fox and his MIT colleagues on gastrointestinal cancer.
the researchers replicated the genome containing the lesion with a variety of different types of polymerase,
or patterns of DNA mutations, associated with cancerous tumors. e believe that in the context of inflammation-induced damage of DNA,
says the paper provides a novel mechanistic link between chronic inflammation and cancer development. ith a combination of biochemical,
a type of mutation that is frequently observed in human cancers, Wang says. Studies of tissue samples of patients suffering from inflammatory bowel disease have found significant levels of 5clc,
Fedeles adds. By comparing these levels with his team findings on how mutagenic 5clc is,
the researchers predict that accumulation of the lesions would increase the mutation rate of a cell up to 30-fold,
who was honored with the prestigious Benjamin F. Trump award at the 2015 Aspen Cancer Conference for the research r
and hence is a promising step forward for the repair of peripheral nerve injuries. This research has just been published in the scientific journal Development at http://dev. biologists. org/Currently,
showing that they could interact with nerves in vitro. he next step is to determine, for example in animal models of peripheral nerve injury,
This study identifies a biologically relevant and accessible source of cells that could be used for generating sufficient quantities of Schwann cells and thus offers great potential in the repair of peripheral nerve injuries r
#Important regulation of cell invaginations discovered Lack of microinvaginations in the cell membrane, caveolae, can cause serious diseases such as lipodystrophy and muscular dystrophy.
resulting in diseases. Having too few invaginations is associated with atrial fibrillation. A total absence of invaginations causes lipodystrophy and muscular dystrophy combined with fatal cardiac arrhythmia. he latter is an unpleasant disease
CGL4, which usually leads to death in the patient teenage years. Many children presumably also die from this disease during their first week of life,
without any diagnosis other than udden infant death syndrome'says Karl Swärd and Catarina Rippe, researchers at Lund University.
About ten different genes contribute to the formation of caveolae. Until recently it was known not how these genes are coordinated.
and provides insight into how to combat diseases caused by a lack of caveolae. Moreover, the discovery paves the way for further studies on the significance of caveolae for cancer
and renal diseases. hese transcription factors regulate the cellsability to move and therefore play an important role in metastasis,
for example says Karl Swärd who, together with colleagues at Lund University, is also investigating whether the regulatory mechanism is activated in the case of kidney disease h
Researchers have discovered a way to trigger a preventive response to a flu infection without any help from the usual players the virus itself or interferon, a powerful infection fighter.
but prevent infection altogether. he flu vaccine needs to change every year because the virus is constantly mutating.
said Jacob Yount, assistant professor of microbial infection and immunity at The Ohio State university and senior author of the study.
but the scientistslong-term goal is to develop a vaccine-independent method to prevent flu infections. f we were to have an outbreak of some pandemic influenza virus similar to
I could envision using this technique to help people who are particularly vulnerable to infection,
he said. t would work best if used before an infection, because the strategy prevents cells from becoming infected in the first place.
The research is published in the journal PLOS Pathogens. The method involves raising the level of a protein that is known to be effective against all strains of influenza ever tested.
The trick for infection prevention, however, is boosting that protein level in cells before the virus shows up.
Doing that, the scientists discovered in this study, involves suppressing the function of another protein. The protein effective against influenza is called IFITM3 (
pronounced I-fit-M-3, for interferon-induced transmembrane protein 3). Under natural conditions, IFITM3 is produced in large quantities only after the flu virus is present,
so it can reduce the severity of infection. But the way it targets the virus by trapping it
and disabling its ability to make copies of itself means that increasing the protein level before the flu ever arrives would prevent infection from occurring.
and fend off an influenza attack. This enzyme, also a protein, proved to be the silver bullet in Yount work on flu prevention.
and greater resistance to infection by flu viruses. IFITM3 is known to be important to humans
because previous research has shown that it is identified the only protein containing a frequent genetic mutation linked to severe flu infections.
because mice lacking the same IFITM3 protein are highly susceptible to flu infections. Being able to stimulate this response is important for many reasons, not the least
Interferon infection-fighting power is accompanied by severe side effects most commonly associated with its former use as a treatment for Hepatitis C that include, not surprisingly,
Yount said. hat was a huge finding that you don need an infection or interferon to increase the level of IFITM3.
But later in life, lacking NEDD4 might not pose any health problems which is why Yount is currently testing the effects of suppressing NEDD4 on adult mice
#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.
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.
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,
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.
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,
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,
#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,
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.
as such big injuries of an incredibly vascular structure inevitably require a clot in order not to bleed to death,
#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
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,
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