Scientists discover role of skin in spreading leishmaniasis

Image result for Scientists discover role of skin in spreading leishmaniasisScientists at the University of York have discovered that parasites responsible for leishmaniasis – a globally occurring neglected tropical disease spread by sand flies – are mainly acquired from the skin rather than a person’s blood.

Visceral leishmaniasis is a parasitic infection that kills 20-40 thousand people each year across 56 countries, mainly in the developing world. There is no vaccine and drugs are prohibitively expensive or toxic.

Previously it was assumed that sand flies acquired the disease parasite directly from a host’s blood, through biting an infected person before spreading the disease to uninfected people in subsequent bites.

However, the number of parasites found in blood has often been puzzlingly low, leading some to question whether there is another source of parasites for transmission.

Now, mathematicians, experimental biologists, and immunologists have revealed a ‘patchy landscape of parasites’ found on carriers’ skin that determines how many parasites are picked up by sand flies.

Using mathematical modeling, they showed that some areas of skin can contain particularly high numbers of the parasite, while other areas may not.

This means that whether a sand fly becomes infected or not depends on where they bite a person.

This breakthrough is significant as it suggests current methods of treating leishmaniasis are too simple, as disease detection and treatment often focuses on levels of the parasite in blood samples.

The research also stresses that more attention should be focused on developing treatments that affect parasites in the skin, if the cycle of transmission is to be interrupted.

Johannes Doehl, Post-Doctoral Research Associate in York’s Centre for Immunology and Infection and lead author of the study, said: “Currently, to assess treatment success in visceral leishmaniasis, clinicians focus on monitoring parasite levels in a host’s blood.

“However, we now have conclusive proof that measuring parasites in the skin, not just the blood, is critical when assessing possible treatments. Clinical studies and elimination campaigns need to take this into account, and in particular measure how treatments affect the patchy landscape of parasites in the skin.”

Dr. Jon Pitchford, Reader in York’s Departments of Biology and Mathematics, said: “To effectively control leishmaniasis, we don’t just need to cure the disease in patients, we must also understand and try and break the transmission cycle. This research is the first step towards improving the treatment process and demonstrates how the application of mathematics can help solve important problems in medicine.”


AIDS virus almost half a billion years old: Scientists

<p>AIDS virus almost half a billion years old: Scientists<br></p>AIDS virus almost half a billion years old: Scientists

Retroviruses, the family of viruses that includes HIV, are almost half a billion years old – several hundred million years older than previously thought, claim scientists from Oxford University.

New research suggests that retroviruses have ancient marine origins, having been with their animal hosts through the evolutionary transition from sea to land.

Until now, it was thought that retroviruses were relative newcomers – possibly as recent as 100 million years in age.

“Our research shows that retroviruses are at least 450 million years old, if not older, and that they must have originated together with, if not before, their vertebrate hosts in the early Paleozoic era,” explained Dr Aris Katzourakis from Oxford University’s department of zoology.

Furthermore, they would have been present in our vertebrate ancestors prior to the colonisation of land and have accompanied their hosts throughout this transition from sea to land, all the way up until the present day.

Retroviruses are a family of viruses that includes the HIV virus responsible for the AIDS pandemic.

They can also cause cancers and immuno deficiencies in a range of animals.

The ‘retro’ part of their name comes from the fact they are made of RNA, which they can convert into DNA and insert into their host genome.

In this study, the researchers unearthed genomic fossils for foamy-like retroviruses in highly diverse hosts, including ray-finned fish and amphibians in which they had not previously been found.

“We need to consider the adaptations that vertebrates have developed to combat viruses, and the corresponding viral countermeasures, as the product of a continuous arms race that stretches back hundreds of millions of years,” Katzourakis noted in the journal Nature Communications.

Top Comment

We, humans will have final laugh on this virus”s battle to destroy human race. Not by beating the virus, but by destroying ourselves first due to religion without giving virus a chance to destroy us.Parivrajaka S

The findings will help researchers understand more about the continuing ‘arms race’ between viruses and their hosts


Scientists identify potent antibody that neutralizes HIV strains

ANI | Nov 16, 2016, 05.00 PM IST

Scientists identify potent antibody that neutralizes HIV strainsScientists identify potent antibody that neutralizes HIV strains
An antibody from an HIV-infected person can potently neutralized 98 percent of HIV isolates nearly all HIV strains, discovered scientists from the National Institutes of Health.

The remarkable breadth and potency of this antibody, named N6, make it an attractive candidate for further development to potentially treat or prevent HIV infection, say the researchers.

The scientists, led by Mark Connors, M.D., of NIH’s National Institute of Allergy and Infectious Diseases (NIAID), also tracked the evolution of N6 over time to understand how it developed the ability to potently neutralize nearly all HIV strains. This information will help inform the design of vaccines to elicit such broadly neutralizing antibodies.

Identifying broadly neutralizing antibodies against HIV has been difficult because the virus rapidly changes its surface proteins to evade recognition by the immune system. In 2010, scientists at NIAID’s Vaccine Research Center (VRC) discovered an antibody called VRC01 that can stop up to 90 percent of HIV strains from infecting human cells. Like VRC01, N6 blocks infection by binding to a part of the HIV envelope called the CD4 binding site, preventing the virus from attaching itself to immune cells.

Findings from the current study showed that N6 evolved a unique mode of binding that depends less on a variable area of the HIV envelope known as the V5 region and focuses more on conserved regions, which change relatively little among HIV strains. This allows N6 to tolerate changes in the HIV envelope, including the attachment of sugars in the V5 region, a major mechanism by which HIV develops resistance to other VRC01-class antibodies.

The new findings suggest that N6 could pose advantages over VRC01, which currently is being assessed as intravenous infusions in clinical trials to see if it can safely prevent HIV infection in humans. Due to its potency, N6 may offer stronger and more durable prevention and treatment benefits, and researchers may be able to administer it subcutaneously (into the fat under the skin) rather than intravenously. In addition, its ability to neutralize nearly all HIV strains would be advantageous for both prevention and treatment strategies.


Scientists discover way to turn carbon dioxide into useful fuel

<p>Scientists discover way to turn carbon dioxide into use<br></p>Scientists discover way to turn carbon dioxide into use

In a new twist to waste-to-fuel technology, scientists at the US Department of Energys Oak Ridge National Laboratory have accidentally discovered a process to turn carbon dioxide (CO2), a greenhouse gas, into ethanol, a renewable fuel.

The researchers used tiny spikes of carbon and copper to turn CO2 into ethanol.

“We discovered somewhat by accident that this material worked,” said lead author of the study Adam Rondinone.

“We were trying to study the first step of a proposed reaction when we realised that the catalyst was doing the entire reaction on its own,” Rondinone noted.

The team used a catalyst made of carbon, copper and nitrogen and applied voltage to trigger a complicated chemical reaction that essentially reverses the combustion process.

With the help of the nanotechnology-based catalyst which contains multiple reaction sites, the solution of carbon dioxide dissolved in water turned into ethanol with a yield of 63 per cent, showed the study published in the journal ChemistrySelect.

Typically, this type of electrochemical reaction results in a mix of several different products in small amounts.

“We’re taking carbon dioxide, a waste product of combustion, and we’re pushing that combustion reaction backwards with very high selectivity to a useful fuel,” Rondinone said.

“Ethanol was a surprise — it’s extremely difficult to go straight from carbon dioxide to ethanol with a single catalyst,” Rondinone noted.

The catalyst’s novelty lies in its nanoscale structure, consisting of copper nanoparticles embedded in carbon spikes. This nano-texturing approach avoids the use of expensive or rare metals such as platinum that limit the economic viability of many catalysts.

Given the technique’s reliance on low-cost materials and an ability to operate at room temperature in water, the researchers believe the approach could be scaled up for industrially relevant applications.

“A process like this would allow you to consume extra electricity when it’s available to make and store as ethanol,” Rondinone said.

“This could help to balance a grid supplied by intermittent renewable sources,” Rondinone pointed out.


Scientists challenge recommendation that men with more muscle need more protein

Sports nutrition recommendations may undergo a significant shift after research from the University of Stirling has found individuals with more muscle mass do not need more protein after resistance exercise.

Health and exercise scientists from Scotland’s University for Sporting Excellence found no difference in the muscle growth response to protein after a full body workout between larger and smaller participants.

Kevin Tipton, Professor of Sport, Health and Exercise Science in the Faculty of Health Sciences and Sport, said: “There is a widely-held assumption that larger athletes need more protein, with nutrition recommendations often given in direct relation to body mass.

“In our study, participants completed a bout of whole-body resistance exercise, where earlier studies — on which protein recommendations are based — examined the response to leg-only exercise. This difference suggests the amount of muscle worked in a single session has a bigger impact on the amount of protein needed afterwards, than the amount of muscle in the body.”

Experts also found participants’ muscles were able to grow and recover from exercise better after a higher dose of protein.

Consuming 40 grams of protein after exercise was more effective at stimulating muscle growth than 20 grams. This increase occurred irrespective of the size of the participants.

Professor Tipton continued: “Until now the consensus among leading sports nutritionists, including the American College of Sports Medicine and the British Nutrition Foundation, is that weightlifters do not need more than around 25 grams of protein after exercise to maximally stimulate the muscle’s ability to grow.

“In order for nutritionists to recommend the correct amount of protein we first need to consider specific demands of the workout, regardless of athletes’ size. This throws commonly held recommendations into question and suggests the amount of protein our muscles need after exercise may be dependent on the type of workout performed. These results are limited to younger, trained men so we may see different results with other groups, such as older individuals or females digesting different amounts of protein.”

Young, resistance-trained males were recruited for the study and divided into two groups, one with lower lean body mass of less than 65 kilograms and one with higher lean body mass of more than 70 kilograms.

Each volunteer participated in two trials where they consumed protein after resistance exercise. In one trial participants consumed 20 grams of whey protein and in the second, they consumed 40 grams of whey protein after exercise. Scientists measured the muscle’s ability to grow at an increased rate with metabolic tracers and muscle biopsies


Scientists sequence genome of worm that can regrow body parts, seeking stem cell insights

Adult flatworm M. lignano and diagrammatic key are shown. The tiny worm intrigues scientists because it can regenerate almost its whole body following an injury. Hence, their effort to sequence its genome.
Credit: Cold Spring Harbor Laboratory

Tourists spending a recuperative holiday on the Italian coast may be envious of the regenerative abilities of locally found flatworm Macrostomum lignano. Named for its discovery near the Italian beach town of Lignano Sabbiadoro, this tiny worm can regenerate almost its whole body following an injury, and researchers have long been trying to understand how it’s able to pull off this trick.

In work published in PNAS, a team of researchers has for the first time characterized the flatworm’s genome, paving the way for a host of new studies of the worm and its regenerative capabilities. The team was led by Cold Spring Harbor Laboratory (CSHL) Professor and HHMI Investigator Gregory Hannon, also a Professor and Senior Group Leader at the CRUK Cambridge Institute at the University of Cambridge, and CSHL Associate Professor Michael Schatz.

“This flatworm can regenerate every part of its body except the brain,” says Hannon. He was studying an important pathway in mammalian reproductive tissues when he became interested in Macrostomum. “This and other regenerating flatworms have the same kind of pathway operating in stem cells that is responsible for their remarkable regenerative capabilities. As we started to try to understand the biology of these stem cells, it very quickly became clear that we needed information about the genetic content of these organisms.”

M. lignano turned out to have an unusually complex genome filled with repetitive elements that made it challenging to assemble and analyze, says Schatz. “At the genomic level it has almost no relationship to anything else that’s ever been sequenced. It’s very strange and unique in that sense.” To overcome the extreme genomic complexity, the team used new long-read sequencing technology that boosted the quality of the genome sequence obtained by more than one hundred fold over standard short-read approaches.

The researchers used the worm’s genomic information to study how gene expression changed during regeneration. “It’s a very powerful tool to be able to see the genes that get activated that are responsible for regeneration of the animal,” Schatz explains. “We think this is going to be a very important species for stem cell research.”

The flatworm is ideal for studying stem cells, says lead author Kaja Wasik, who conducted the work as a PhD student in Hannon’s lab along with co-lead author James Gurtowski from Schatz’s lab. “The worms are just like floating sacks full of stem cells, so they’re very easily accessible,” says Wasik. “From what we looked at, it looks like many of the developmental pathways that are present in humans are also present in the worms, and we can now study whether they potentially could be involved in regeneration.”

According to co-author Peter Ladurner, an assistant professor at the University of Innsbruck, the worm has many properties that make it a good model system: “M. lignano is small, has simple tissues and organs, is transparent, and has sexual reproduction.” Well before its genome was available, M. lignano was already being studied for its insights into stem cells and tissue differentiation. The availability of the genome now enables researchers to do a lot of things they couldn’t previously, such as search within the genome, have a list of genes in hand, and gain insights into the worm’s genome organization.

Hannon says detailed analyses will be needed to figure out how the flatworm’s stem cells are able to develop into a variety of different cell types. He is also planning to examine how the pathways he has studied in other organisms operate in the worms. “The goal of this project was to enable ourselves and others to do new biology. The hope is that as these tools become more available, the community will grow.”

About 15 international research groups on three continents are actively working on Macrostomum flatworms, says co-author Lukas Schärer from the University of Basel. Schärer says he and Ladurner played a major role in helping to develop a broader Macrostomum research community. “The worm was initially used as a model to study embryology and neurobiology, and starting in the late 1990s research expanded into stem cell biology, tissue homeostasis, and regeneration, topics that are still very actively studied today,” he says. “We fully expect that the publication of the genome will lead to a surge in interest in this versatile model organism.”

Scientists grow mini human brains

Scientists in Singapore have made a big leap on research on the ‘mini-brain’. These advanced mini versions of the human midbrain will help researchers develop treatments and conduct other studies into Parkinson’s Disease (PD) and aging-related brain diseases.

These mini midbrain versions are three-dimensional miniature tissues that are grown in the laboratory and they have certain properties of specific parts of the human brains. This is the first time that the black pigment neuromelanin has been detected in an organoid model. The study also revealed functionally active dopaminergic neurons.

The human midbrain, which is the information superhighway, controls auditory, eye movements, vision and body movements. It contains special dopaminergic neurons that produce dopamine — which carries out significant roles in executive functions, motor control, motivation, reinforcement, and reward. High levels of dopamine elevate motor activity and impulsive behaviour, whereas low levels of dopamine lead to slowed reactions and disorders like PD, which is characterised by stiffness and difficulties in initiating movements.

Also causing PD is the dramatic reduction in neuromelanin production, leading to the degenerative condition of patients, which includes tremors and impaired motor skills. This creation is a key breakthrough for studies in PD, which affects an estimated seven to 10 million people worldwide. Furthermore, there are people who are affected by other causes of parkinsonism. Researchers now have access to the material that is affected in the disease itself, and different types of studies can be conducted in the laboratory instead of through simulations or on animals. Using stem cells, scientists have grown pieces of tissue, known as brain organoids, measuring about 2 to 3 mm long. These organoids contain the necessary hallmarks of the human midbrain, which are dopaminergic neurons and neuromelanin.

Jointly led by Prof Ng Huck Hui from A*STAR’s Genome Institute of Singapore (GIS) and Assistant Prof Shawn Je from Duke-NUS Medical School, this collaborative research between GIS, Duke-NUS, and the National Neuroscience Institute (NNI) is funded by the National Medical Research Council’s Translational Clinical Research (TCR) Programme In Parkinson’s disease (PD) and A*STAR. Other collaborators are from the Lieber Institute for Brain Development, the Johns Hopkins University School of Medicine, and the Nanyang Technological University.

Assistant Prof Shawn Je from Duke-NUS Medical School’s Neuroscience & Behavioural Disorders Programme said, “It is remarkable that our midbrain organoids mimic human midbrain development. The cells divide, cluster together in layers, and become electrically and chemically active in three-dimensional environment like our brain. Now we can really test how these mini brains react to existing or newly developed drugs before treating patients, which will be a game changer for drug development.”

Prof Tan Eng King, Research Director and Senior Consultant, Department of Neurology at NNI and Lead PI of the TCR Programme in PD, remarked, “The human brain is arguably the most complex organ and chronic brain diseases pose considerable challenges to doctors and patients. This achievement by our Singapore team represents an initial but momentous scientific landmark as we continue to strive for better therapies for our patients.”

GIS Executive Director Prof Ng Huck Hui said, “Considering one of the biggest challenges we face in PD research is the lack of accessibility to the human brains, we have achieved a significant step forward. The midbrain organoids display great potential in replacing animals’ brains which are currently used in research; we can now use these midbrains in culture instead to advance our understanding and future studies for the disease, and perhaps even other related diseases.”

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Scientists unpack how Toxoplasma infection is linked to neurodegenerative disease

Toxoplasma gondii, a protozoan parasite about 5 microns lengthy, infects a third of the world‘s population. Ingested via undercooked meat or unwashed veggies, the parasite infects 15-30 percent of the united states population. In France and Brazil, up to 80 percentage of the populace has the contamination.

particularly dangerous throughout being pregnantinfection in pregnant ladies can reason criticalcongenital defects or even demise of the fetus — this persistent infection has two components: the unicellular parasite, and inflammation of tissues it reasons.

working on mice (like all mammals, a herbal host for this parasite), a college of California, Riverside groupof biomedical scientists reports inside the magazine PLOS Pathogens that Toxoplasma infection ends in a disruption of neurotransmitters inside the mind and postulates that it triggers neurological disorder in the ones already predisposed to this kind of disorder.

They notice that Toxoplasma infection results in a extensive increase in glutamate — the number one andmaximum critical neurotransmitter within the mind, which transmits excitatory indicators among neurons. This glutamate boom is “extracellular,” that means out of doors the cell, and is precisely managed by using specialized cells inside the primary apprehensive system (mind and spinal cord), known asastrocytes. Glutamate buildup is visible in disturbing mind damage in addition to especially pathological and neurodegenerating diseases inclusive of epilepsy, multiple sclerosis and amyotrophic lateral sclerosis (ALS).

One position astrocytes play is to cast off extracellular glutamate, lest it growth to pathological ranges that would harm neurons. that is commonly done using a glutamate transporter, called GLT-1, tasked with regulating extracellular glutamate. GLT-1 soaks up glutamate released by means of neurons and converts itreturned into the more secure substance glutamine, which could then be utilized by cells for strength.

whilst a neuron fires it releases glutamate into the gap among itself and a close-by neuron,” defined lead researcher Emma H. Wilson, an partner professor within the department of Biomedical Sciences in thefaculty of medicine, who has worked on toxoplasmosis for greater than 15 years. “The nearby neuron detects this glutamate which triggers a firing of the neuron. If the glutamate is not cleared by way of GLT-1 then the neurons can not fireplace well the following time and they start to die.”

Wilson and her crew discovered that in toxoplasma infection, astrocytes swell and are not capable ofmodify extracellular glutamate concentrations. similarly, GLT-1 isn’t always expressed nicely. This ends ina buildup of the glutamate launched from neurons and the neurons misfire.

those effects recommend that during assessment to assuming chronic Toxoplasma infection as quiescent and benign, we need to be aware of the ability threat to regular neurological pathways andchanges in mind chemistry,” Wilson said.

when the researchers treated the infected mice with ceftriaxone, an antibiotic regarded to supplybeneficial consequences in mouse models of ALS as well as neuroprotection in an expansion of primaryanxious device accidents, they found that GLT-1 turned into upregulated. This recovery of GLT-1 expression appreciably decreased extracellular glutamate from pathological to ordinary concentrations, returning neuronal feature to a normal country.

we have shown for the primary time the direct disruption of a prime neurotransmitter in the brain as a consequence of this contamination,” Wilson stated. “more direct and mechanistic research needs to becompleted to apprehend the realities of this very commonplace pathogen.”

subsequent, Wilson and her colleagues will research what initiates the downregulation of GLT-1 at some stage in persistent Toxoplasma infection.

in spite of the significance of this transporter to retaining glutamate homeostasis, there may be littleinformation of the mechanism that governs its expression,” Wilson stated. “we’d want to understand how cells, which include peripheral immune cells, control the parasite in the brain. Toxoplasma contaminationconsequences in the lifelong presence of parasitic cysts inside the neurons inside the mind. we mightlike to similarly develop a challenge targeted on killing the cysts, that’s where the parasite hides from the immune response for the rest of the inflamed person‘s life. putting off the cyst gets rid of the threat of reactivation of the parasite and the danger of encephalitis even as additionally allowing us to limitchronic inflammation within the brain.”

Mysteriously, the parasite that causes toxoplasmosis can sexually reproduce simplest in cats. Asexually, it could reflect and stay in any mammalian cellular that has a nucleus. indeed, the parasite has beendetermined in each mammal ever examined.

put upcontamination, a equipped immune machine is needed to save you parasite reactivation and encephalitis. inflamed people with compromised immune systems need to be on prophylactic pills forlifestyles. otherwise they’re susceptible to cyst reactivation and death. The parasite lives in areas of thebrain which have the capacity to disrupt positive behaviors including dangerin search of (infected mice will run closer to cat urine instead of far from it).

The parasite isn’t always as latent or dormant as researchers once concept. cases of congenital infectionand retinal toxoplasmosis are on the upward push (the brain and retina are closely connected). peoplewho’ve schizophrenia are much more likely to be inflamed with Toxoplasma. infection shows a fewcorrelation with Alzheimer’s disorder, Parkinson’s disease and epilepsy.

although, Wilson notes that infection is no reason for principal fear.

“We have been living with this parasite for a long term,” she stated. “It does no longer want to kill its host and lose its home. The nice manner to save you infection is to cook your meat and wash your palms andveggies. And in case you are pregnant, do not trade the cat muddle.”




Scientists have discovered new genetic areas linked to an increased risk of glaucoma – the leading cause of irreversible blindness worldwide.

The investigation studied the genetic make up of about 40,000 people and identified five previously unknown genetic areas linked to an increased risk of primary angle closure glaucoma (PACG).

Co-author of the study Professor Jamie Craig from Flinders University in South Australia said PACG symptoms occurred quickly and required immediate medical attention.

“This new discovery provides a handle, to gain an understanding of the mechanisms of the disease. This will help to work out who is at risk of developing angle closure glaucoma so they can have preventative laser treatment before an emergency situation develops,” Prof Craig said.

“We also expect in time, that the improved understanding of the pathways of this disease to lead to new ways to more effectively prevent and treat this serious condition, so that permanent loss of vision does not occur.”

The genetic analysis is by far the largest genome wide association study to date on this condition. It used a combined total of 10,404 cases of angle closure glaucoma and 29,343 normal controls to identify five novel glaucoma markers.

Researchers at Flinders University, using the Australian and New Zealand Registry of Advanced Glaucoma (ANZRAG), led by Prof Craig guided international research across 23 countries in Asia, Australia, Europe and the Americas to make the discovery.

Up to 80 per cent of the estimated 15 million people afflicted with PACG live in Asia, where the disease is responsible for a high proportion of blindness.

Glaucoma generally develops later in life, initially causes loss of peripheral vision and can lead to complete blindness if untreated.

Angle closure glaucoma is a less common form of the disease than open angle glaucoma. It is caused by blocked drainage canals in the eye and is characterised by a narrow angle between the iris and cornea.

“With (PACG) it comes on quite rapidly, so they are aware something is happening. But if something is not done quickly, they can lose their vision,” Prof Craig said.

“All types of glaucoma have a strong hereditary or family influence and if there are any cases of glaucoma in the family, then people should be checked every two years from the age of 40.”

The study on angle closure glaucoma is published in Nature Genetics and was completed in association with the University of Melbourne, the University of Sydney and the Genome Institute of Singapore.


Scientists identify proteins crucial to loss of hearing

Proteins play key role in genes that help auditory hair cells grow

October 15, 2015
University of Maryland School of Medicine
Right now, there is no way to reverse hearing loss, largely because auditory hair cells, which sense sound and relay that information to the brain, do not regenerate. A new study, however, has found a key clue to how these hair cells develop. The study identified a new role for a particular group of proteins in the development and survival of the hair cells.

Almost 40 million Americans suffer from hearing loss. Right now, there is no way to reverse this condition, largely because auditory hair cells, which sense sound and relay that information to the brain, do not regenerate.

A new study led by scientists at the University of Maryland School of Medicine (UM SOM) has found a key clue to how these hair cells develop. The current study identified a new role for a particular group of proteins, known as RFX transcription factors, in the development and survival of the hair cells.

“This discovery opens up new avenues, not only for understanding the genetics of hearing, but also, eventually for treating deafness,” said the principal investigator, Ronna P. Hertzano, MD, PhD, Assistant Professor of Otorhinolaryngology-Head & Neck Surgery at the UM SOM.

The study appeared in the latest issue of the journal Nature Communications. The work was done in collaboration with scientists at several institutions, among them Ran Elkon, PhD, an Assistant Professor and computational biologist at the Sackler School of Medicine at Tel Aviv University in Israel.

Hertzano and her colleagues used mice whose auditory hair cells glow with a green fluorescent protein, allowing the cells to be identified from other kinds of cells. They then used next generation sequencing — a state-of-the-art method to rapidly measure gene expression — to sequence and quantify the thousands of genes that are expressed in hair cells, in comparison with other cells in the ear. As they generated this catalogue of genes, they were searching for key regulators of genes for hair cells. Such regulators could help researchers eventually develop techniques to regenerate hair cells. The key regulator they identified were the RFX transcription factors.

The scientists then moved on to study mice which had been genetically altered so that their hair cells lacked two of the RFX transcription factors. In these mice, hair cells initially developed normally, but then died quickly, leading to rapid hearing loss. By three months of age, the mice were profoundly deaf.

Although the experiments were done in mice, Hertzano says that it is likely that these genes work similarly in humans. Eventually, she says, it might be possible to use our increased understanding of RFX transcription factor to treat hearing loss, by either protecting hair cells from death or fostering their growth. In addition, she and her colleagues think that they will be able to identify other genes that have an important role in hair cell function.

Hertzano first got interested in the genetics of hearing as an MD-PhD student at Tel Aviv University, and then pursued residency training at the UM SOM Department of Otorhinolaryngology, where she now works as a scientist and a surgeon whose practice is focused on diseases of the ear and hearing restoration.

The current paper appeared in conjunction with another paper published inNature Communications, by Matthew W. Kelley, PhD, a neuroscientist at the National Institute on Deafness and Other Communication Disorders. Kelley and his team also used mice with fluorescent markers in different cells of the ear followed by next generation sequencing. Rather than analyzing groups of cells, they performed a comprehensive analysis of the genes that are expressed in the different cells at a single cell resolution. Their study is the first of its kind in the ear field and helps resolved the molecular aspects of the cellular complexity of the inner ear.

Story Source:

The above post is reprinted from materials provided by University of Maryland School of Medicine. Note: Materials may be edited for content and length.

Journal Reference:

  1. Ran Elkon, Beatrice Milon, Laura Morrison, Manan Shah, Sarath Vijayakumar, Manoj Racherla, Carmen C. Leitch, Lorna Silipino, Shadan Hadi, Michèle Weiss-Gayet, Emmanuèle Barras, Christoph D. Schmid, Aouatef Ait-Lounis, Ashley Barnes, Yang Song, David J. Eisenman, Efrat Eliyahu, Gregory I. Frolenkov, Scott E. Strome, Bénédicte Durand, Norann A. Zaghloul, Sherri M. Jones, Walter Reith, Ronna Hertzano. RFX transcription factors are essential for hearing in mice. Nature Communications, 2015; 6: 8549 DOI: 10.1038/ncomms9549

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