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Newly published research details how a team of scientists from the University Miguel Hernández (Spain), the Netherlands Institute of Neuroscience (Netherlands) and the John A. Moran Eye Center at the University of Utah (USA) successfully created a form of artificial vision for a blind woman using a brain implant.
In the article, “Visual percepts evoked with an Intracortical 96-channel Microelectrode Array inserted in human occipital cortex,” published in The Journal of Clinical Investigation, Eduardo Fernández, MD, PhD, from the University Miguel Hernández details how an array of penetrating electrodes produced a simple form of vision for a 58-year-old blind volunteer. The team conducted a series of experiments with the blind volunteer in their laboratory in Elche, Spain. The results represent a leap forward for scientists hoping to create a visual brain prosthesis to increase independence of the blind.
Phosphenes
A neurosurgeon implanted a microelectrode array composed of 100 microneedles into the visual cortex of the blind woman to both record from and stimulate neurons located close to the electrodes. She wore eyeglasses equipped with a miniature video camera; specialized software encoded the visual data collected by the camera and sent it to electrodes located in the brain. The array then stimulated the surrounding neurons to produce white points of light known as ‘phosphenes’ to create an image.
The blind woman was a former science teacher and had been completely blind for 16 years at the time of the study. She had no complications from the surgery, and researchers determined that the implant did not impair or negatively affect brain function. With the help of the implant, she was able to identify lines, shapes and simple letters evoked by different patterns of stimulation. To assist her in practicing with the prosthesis, researchers created a video game with a character from the popular television show The Simpsons. Due to her extensive involvement and insight, she is also co-author on the article.
“These results are very exciting because they demonstrate both safety and efficacy and could help to achieve a long-held dream of many scientists, which is the transfer information from the outside world directly to the visual cortex of blind individuals, thereby restoring a rudimentary form of sight,” said Prof. Eduardo Fernández. He also added that “although these preliminary results are very encouraging, we should be aware that there are still a number of important unanswered questions and that many problems have to be solved before a cortical visual prosthesis can be considered a viable clinical therapy.”
“This new study provides proof-of-principle and demonstrate that our previous findings in monkey experiments can be translated to humans,” said Prof. P. Roelfsema, a co-author on the study. “This work is likely to become a milestone for the development of new technologies that could transform the treatment of blindness.”
“One goal of this research is to give a blind person more mobility,” said Prof. R. A. Normann, also a co-author on the study. “It could allow them to identify a person, doorways, or cars. It could increase independence and safety. That’s what we’re working toward.”
The research team hopes that the next set of experiments will use a more sophisticated image encoder system, capable of stimulating more electrodes simultaneously and to elicit more complex visual images.
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Materials provided by Netherlands Institute for Neuroscience – KNAW. Original written by Esmeralda Schemmekes. Note: Content may be edited for style and length.

Following surgery within the abdominal or pelvic cavities, scar tissue often forms on the inner linings of these cavities and may adhere to the organs which are found within them. This adhesion occurs in 93% of these patients and can affect the intestines, liver, urinary bladder, gall bladder and female reproductive organs. In up to 20% of adhesion cases, serious complications can arise, including chronic abdominal or pelvic pain, fertility problems or intestinal obstruction. This not only results in increased patient suffering and mortality but adds over $1 billion in additional hospital costs in the United States alone.
A commonly used method of combating this problem is to use commercially available synthetic films as adhesion barriers. However, there are sometimes difficulties in applying these films with a sufficient degree of conformity to irregular surfaces and they can also be fragile and difficult to handle. Additionally, it is not possible to use the films for small-portal procedures such as catheterization and laparoscopies, and their overall efficacy is estimated at 25%.
Through a multi-institute collaborative effort, which included scientists from Harvard University and the Terasaki Institute for Biomedical Innovation (TIBI), a method was developed to overcome these challenges and to produce a more effective anti-adhesion barrier with some added advantages.
The researchers first chose a polymer called a hydrogel which was made with silicate nanoplatelets (SNPs). This hydrogel was chosen due to its shear-thinning capabilities — the ability to deform under stress and then quickly self-recover and mold itself to fit the desired space. This made it ideal for injecting or for spraying onto a surface with complete and uniform coverage. The researchers were also able to formulate this shear-thinning hydrogel barrier (STHB) to solidify without the additional polymerization or crosslinking steps that other hydrogels require. To prevent the infiltration, adherence and growth of scar tissue producing cells, a polymer called polyethylene oxide (PEO), was included in the hydrogel mixture.
Extensive testing was performed on various formulations of the hydrogel to optimize its shear-thinning ability, injectability, spray characteristics and structural stability. Microscopic observation tests were also conducted to determine the effectiveness of PEO in preventing adherence of scar-producing cells. The results showed that the optimum formulations of the STHB demonstrated superior mechanical properties and more effective prevention of cell adherence than control hydrogels prepared without either SNPs or PEO.
Animal model and staining tests confirmed these initial results. Experiments were conducted on surgically injured rats using either an STHB or a commercial film barrier implanted onto their abdominal linings. After the standard postoperative time of two weeks, the resultant adhesions were visually inspected and graded. The optimum STHB formulation exhibited the highest effectiveness in preventing cellular adhesion over the film barrier or negative control (no barrier) treatments.
The staining experiments took a closer look at scar tissue formation from the animal model adhesion tests. Microscopic examinations revealed that the rats with no barriers implanted showed high-grade bands of scar tissue formation, while the film barrier subjects exhibited low-grade scar tissue bands and the optimum STHB formulation showed no scar tissue band formation at all.
Subsequent experiments tested the STHB’s long-term biocompatibility; this is essential in obtaining normal post-surgical healing. The results showed that the STHBs produced no signs of immunological reactions against them after implantation and their degradation and resorption into the body was complete after a two-week period.
“By combining the best features of an optimized hydrogel barrier, we have created an effective way to prevent post-surgical adhesions,” said Ali Khademhosseini, Ph.D., TIBI’s Director and CEO. “This is sure to have a great impact on surgical patients and the healthcare industry.”
Authors are: Guillermo U. Ruiz-Esparza1, Xichi Wang, Xingcai Zhang, Sofia Jimenez-Vazquez1, Liliana Diaz-Gomez, Anne-Marie Lavoie, Samson Afewerki, Andres A. Fuentes-Baldemar, Roberto Parra-Saldivar, Nan Jiang, Nasim Annabi, Bahram Saleh, Ali K. Yetisen, Amir Sheikhi, Thomas H. Jozefiak, Su Ryon Shin, Nianguo Dong, Ali Khademhosseini.
This work was supported by the National Institutes of Health (1R01EB023052, 14 1R01HL140618, 1R01HL137193, 1R01GM126831).

Researchers at the University of Virginia School of Medicine have uncovered how problems in cortical microcircuits in the brain can trigger epileptic seizures. The researchers say that targeting the problem could lead to new treatments for a devastating form of the disease.
UVA epilepsy researchers Eric R. Wengert, PhD, and Manoj K. Patel, PhD, and their team determined that a particular type of brain cell called somatostatin interneurons can cause seizures when they go haywire. These interneurons are typically thought to function as a built-in brake system to safeguard against excessive activity in the brain and prevent seizures, but Wengert and colleagues found that, when dysfunctional, somatostatin interneurons actually drive excessive brain activity and seizures.
These malfunctions are triggered by mutations in a particular gene known to cause a rare epilepsy syndrome in human patients. These mutations are not inherited from the child’s parents but instead occur shortly after conception.
“Identifying the particular nerve cells that contribute to seizures is important because it helps direct the ways researchers go about developing novel therapies,” said Patel, of UVA’s Department of Anesthesiology. “Based on this research, we now have a new cellular target to try to restore balance to the brain and prevent seizures.”
Understanding the Cause of Epileptic Seizures
The researchers examined the role of somatostatin interneurons as part of their investigation of a rare neurological condition called SCN8A epilepticencephalopathy. SCN8A refers to a mutation in the SCN8A gene that causes the condition. Children with SCN8A epilepsy often suffer from recurrent seizures that do not respond to medication as well as severe developmental delays and movement disorders. They are also at significant risk of Sudden Unexpected Death in Epilepsy, the No. 1 cause of epilepsy-related death.
To better understand what occurs in SCN8A epilepticencephalopathy, the researchers developed mouse models of twoSCN8A mutations discovered in patients. These models allowed them to determine which neurons are responsible for driving the neurological dysfunction. The researchers found that both SCN8A mutations caused harmful changes to sodium channels in a way that made somatostatin interneurons fizzle out and stop functioning when they normally would be highly active.
“It’s similar to a speeding car with a broken brake system that cannot slow it down,” Wengert said. “A brain without properly functioning somatostatin interneurons to dampen brain activity ends up with runaway excitation which can result in a seizure.”
Based on their findings, the scientists believe that it may be possible to treat SCN8A epilepticencephalopathy by developing ways to fix the agitated interneurons. The results, they say, also help us better understand epilepsy more broadly.
“Although this work focused on SCN8A epilepsy, our results identify somatostatin interneurons as a general contributor to epileptic seizures” Wengert said. “If we can identify ways to restore proper functioning in these cells, these approaches may be useful in providing better anti-seizure treatments to patients with various types of epilepsy.”
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A new study from the University of Southampton has demonstrated a new method to safely clean and reuse facemask respirators with advanced low-temperature plasma technology. The discovery could help future pandemic responses by providing contingency options should a shortage of personal protective equipment (PPE) for frontline healthcare staff occur again.
The study, published in the journal AIP Advances showed that the technology can remove 99.99% of coronavirus from contaminated facemasks while maintaining their ability to filter out harmful airborne droplets.
The results also showed that this technique could reduce approximately 70% of plastic waste caused by facemasks and reduce economic burdens on low-income countries by reusing facemasks.
Dr Min Kwan Kim, Lecturer in Astronautics at the University of Southampton who led the research said, “The COVID-19 pandemic caused high demand for facemasks which led to global challenges in sustaining the supply chain. Because they are essential personal protective equipment to protect frontline healthcare against COVID-19, the chronic, global shortage of N95 and N99 facemasks is one of the most urgent threats to our collective ability to save lives from the coronavirus.
“Although most of the masks are considered one-time use, the reuse of masks may need to be considered as a crisis capacity strategy to ensure continued availability for COVID-19 and future pandemics,” he continued.
Whilst other techniques to decontaminate PPE have been trialled, including hydrogen peroxide, ultraviolet irradiation, and moist heat, these can negatively affect the masks performance in future use, either by damaging the filters or leaving residues that are harmful to skin.
In this latest study, the research team applied microdroplets containing SARS-CoV-2, the virus that causes COVID-19, to sample FFP2 and FFP3 facemasks, the most common masks used by frontline healthcare staff. A prototype decontamination system was then used to apply cold plasma to the samples for two, five and ten minutes. They then tested the samples for the presence of residual SARS-CoV-2 and transmitted aerosols of sodium chloride through the samples to monitor filter performance.
The results showed that the samples that were treated for ten minutes had been successfully decontaminated and the researchers found no significant impact on the filters for both the FFP2 and FFP3 masks.
In addition to offering a contingency strategy for health systems in the event of future rises in hospital admissions, there could also be significant benefits to the environment.
Dr Kim continued, “environmentalists warn single-use masks are adding to the glut of plastic pollution threatening the health of oceans and marine life. It has been estimated 129 billion single-use face masks are used monthly around the world, with 55 million a day in the UK. As the most of used face masks are incinerated or sent to landfills, their continued use on this scale can affect the UK’s ambitions to achieve net zero and reduce plastic waste.”
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Two new studies indicate that immunotherapy may benefit people with leptomeningeal carcinomatosis (LMD), a rare but serious complication of cancer that has spread to the brain and/or spinal cord. The research, which was led by investigators at Massachusetts General Hospital (MGH), Dana-Farber Cancer Institute and the Broad Institute, is published in Nature Communications.
Although advances in cancer treatment have extended patient survival, some cancers come back, often in a different location in the body. This may in part help explain recent increases in the incidence of LMD — when tumor cells infiltrate the leptomeninges (layers of tissue that cover the brain and spinal cord) and cerebrospinal fluid. Approximately 5-8% of all patients with cancer develop LMD after first being diagnosed with breast cancer, lung cancer, melanoma or other malignancies. Current treatment options rarely benefit patients with LMD, and there is an urgent need for new therapies.
Immune checkpoint inhibitors are important medications that boost the immune system’s response against various cancers, but their effects against LMD are unclear. To investigate, researchers conducted two phase II clinical trials. When they collected and analyzed immune cells and cancer cells from the cerebrospinal fluid of patients in the trials both before and after treatment with immune checkpoint inhibitors, the scientists found signs that the therapy was having an effect. For example, the number of certain cancer-killing immune cells and the expression of particular genes within cells were higher following treatment.
The second article in Nature Communications presents the results of one of the phase II studies, which included 18 patients with LMD who received combined ipilimumab and nivolumab (two types of immune checkpoint inhibitors) until the cancer progressed or the patient experienced unacceptable toxicity. The primary endpoint was overall survival at 3 months, and 8 of the 18 patients were alive at that time. (Historically, patients survive for a median of 3-7 weeks after being diagnosed with LMD.) One-third of patients experienced one or more serious adverse events. Two patients discontinued treatment due to unacceptable toxicity. The most frequent adverse events include fatigue, nausea, fever, anorexia and rash.
The authors noted that larger, multicenter clinical trials are needed to validate their results.
“In these two published studies, we demonstrated — in patients through a clinical trial and microscopically in the laboratory — that immune checkpoint blockade has promising activity for patients with LMD. More data is needed, but this is an exciting first step towards showing that immune checkpoint blockade may have a role in treating this devastating disease,” says co-author Priscilla K. Brastianos, MD, who is the director of the Central Nervous System Metastasis Center at MGH and an associate professor of medicine at Harvard Medical School.
Funding for the trial was provided by Bristol Myers Squibb and MGH.
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The ability to edit the genome by altering the DNA sequence inside a living cell is powerful for research and holds enormous promise for the treatment of diseases. However, existing genome editing technologies frequently result in unwanted mutations or can fail to introduce any changes at all. These problems have kept the field from reaching its full potential.
Now, new research from the laboratory of Princeton University researcher Britt Adamson, conducted with collaborators in the lab of Jonathan Weissman, a member of Whitehead Institute and a professor of biology at the Massachussetts Insittute of Technology and an investigator with the Howard Hughes Medical Institute, and Cecilia Cotta-Ramusino, formerly at Editas Medicine, details a novel method called Repair-seq that reveals in exquisite detail how genome editing tools work.
“We’ve known for a long time that the mechanisms involved in fixing broken DNA are essential for genome editing because to change the sequence of DNA you first have to break it,” said Britt Adamson, senior author on the study and assistant professor in the Princeton Department of Molecular Biology and the Lewis-Sigler Institute of Integrative Genomics. “But those processes are incredibly complex and thus often difficult to untangle.”
To repair DNA, cells use many different mechanisms, each involving sets of genes working together in distinct pathways. Repair-seq allows researchers to probe the contribution of these pathways to repair of specific DNA lesions by simultaneously profiling how hundreds of individual genes affect mutations produced at damaged sites. The researchers can then generate mechanistic models of DNA repair and learn how those mechanisms impact genome editing. Adamson and colleagues applied their method to one of the most commonly used genome editing approaches, CRISPR-Cas9, which employs the bacterial Cas9 nuclease to cut across both strands of the double-stranded DNA molecule, creating lesions called double-strand breaks.
“Editing with double-strand breaks has been the bread and butter of genome editing for a long time, but making intended changes without unwanted mutations has been an enormous challenge,” said the study’s first author Jeffrey Hussmann, who conducted the work while a postdoctoral researcher in the laboratory of Jonathan Weissman. “We set out to understand the mechanisms behind as many of the induced mutations as possible, reasoning that this could help us optimize the system.”
Repair-seq experiments generate an enormous amount of data. Analysis of that data, led by Hussmann, produced a map of how different DNA repair pathways are linked to particular types of Cas9-induced mutations. Building on a rich history of research in the field, Hussmann’s analysis illuminated pathways that were already known, and identified new ones, which together highlight the enormous complexity and myriad of systems involved in double-strand break repair. The deep set of data unearthed in this work is now posted on an online portal that others can use to interrogate DNA repair genes and pathways.

Like so many other good things in life, sleep is best in moderation. A multiyear study of older adults found that both short and long sleepers experienced greater cognitive decline than people who slept a moderate amount, even when the effects of early Alzheimer’s disease were taken into account. The study was led by researchers at Washington University School of Medicine in St. Louis.
Poor sleep and Alzheimer’s disease are both associated with cognitive decline, and separating out the effects of each has proven challenging. By tracking cognitive function in a large group of older adults over several years and analyzing it against levels of Alzheimer’s-related proteins and measures of brain activity during sleep, the researchers generated crucial data that help untangle the complicated relationship among sleep, Alzheimer’s and cognitive function. The findings could aid efforts to help keep people’s minds sharp as they age.
The findings are published Oct. 20 in the journal Brain.
“It’s been challenging to determine how sleep and different stages of Alzheimer’s disease are related, but that’s what you need to know to start designing interventions,” said first author Brendan Lucey, MD, an associate professor of neurology and director of the Washington University Sleep Medicine Center. “Our study suggests that there is a middle range, or ‘sweet spot,’ for total sleep time where cognitive performance was stable over time. Short and long sleep times were associated with worse cognitive performance, perhaps due to insufficient sleep or poor sleep quality. An unanswered question is if we can intervene to improve sleep, such as increasing sleep time for short sleepers by an hour or so, would that have a positive effect on their cognitive performance so they no longer decline? We need more longitudinal data to answer this question.”
Alzheimer’s is the main cause of cognitive decline in older adults, contributing to about 70% of dementia cases. Poor sleep is a common symptom of the disease and a driving force that can accelerate the disease’s progression. Studies have shown that self-reported short and long sleepers are both more likely to perform poorly on cognitive tests, but such sleep studies typically do not include assessments of Alzheimer’s disease.
To tease apart the separate effects of sleep and Alzheimer’s disease on cognition, Lucey and colleagues turned to volunteers who participate in Alzheimer’s studies through the university’s Charles F. and Joanne Knight Alzheimer Disease Research Center. Such volunteers undergo annual clinical and cognitive assessments, and provide a blood sample to be tested for the high-risk Alzheimer’s genetic variant APOE4. For this study, the participants also provided samples of cerebrospinal fluid to measure levels of Alzheimer’s proteins, and each slept with a tiny electroencephalogram (EEG) monitor strapped to their foreheads for four to six nights to measure brain activity during sleep.
In total, the researchers obtained sleep and Alzheimer’s data on 100 participants whose cognitive function had been monitored for an average of 4 1/2 years. Most (88) had no cognitive impairments, 11 were very mildly impaired, and one had mild cognitive impairment. The average age was 75 at the time of the sleep study.
The researchers found a U-shaped relationship between sleep and cognitive decline. Overall, cognitive scores declined for the groups that slept less than 4.5 or more than 6.5 hours per night — as measured by EEG — while scores stayed stable for those in the middle of the range. EEG tends to yield estimates of sleep time that are about an hour shorter than self-reported sleep time, so the findings correspond to 5.5 to 7.5 hours of self-reported sleep, Lucey said.
The U-shaped relationship held true for measures of specific sleep phases, including rapid-eye movement (REM), or dreaming, sleep; and non-REM sleep. Moreover, the relationship held even after adjusting for factors that can affect both sleep and cognition, such as age, sex, levels of Alzheimer’s proteins, and the presence of APOE4.
“It was particularly interesting to see that not only those with short amounts of sleep but also those with long amounts of sleep had more cognitive decline,” said co-senior author David Holtzman, MD, a professor of neurology. “It suggests that sleep quality may be key, as opposed to simply total sleep.”
Each person’s sleep needs are unique, and people who wake up feeling rested on short or long sleep schedules should not feel compelled to change their habits, Lucey said. But those who are not sleeping well should be aware that sleep problems often can be treated.
“I ask many of my patients, ‘How’s your sleep?'” said co-senior author Beau M. Ances, MD, PhD, the Daniel J. Brennan, MD, Professor of Neurology. Ances treats patients with dementia and other neurodegenerative conditions at Barnes-Jewish Hospital. “Often patients report that they’re not sleeping well. Often once their sleep issues are treated, they may have improvements in cognition. Physicians who are seeing patients with cognitive complaints should ask them about their quality of sleep. This is potentially a modifiable factor.”

In recent years, there has been some evidence that dietary interventions can help to slow the growth of tumors. A new study from MIT, which analyzed two different diets in mice, reveals how those diets affect cancer cells, and offers an explanation for why restricting calories may slow tumor growth.
The study examined the effects of a calorically restricted diet and a ketogenic diet in mice with pancreatic tumors. While both of these diets reduce the amount of sugar available to tumors, the researchers found that only the calorically restricted diet reduced the availability of fatty acids, and this was linked to a slowdown in tumor growth.
The findings do not suggest that cancer patients should try to follow either of these diets, the researchers say. Instead, they believe the findings warrant further study to determine how dietary interventions might be combined with existing or emerging drugs to help patients with cancer.
“There’s a lot of evidence that diet can affect how fast your cancer progresses, but this is not a cure,” says Matthew Vander Heiden, director of MIT’s Koch Institute for Integrative Cancer Research and the senior author of the study. “While the findings are provocative, further study is needed, and individual patients should talk to their doctor about the right dietary interventions for their cancer.”
MIT postdoc Evan Lien is the lead author of the paper, which appears today in Nature.
Metabolic mechanism
Vander Heiden, who is also a medical oncologist at Dana-Farber Cancer Institute, says his patients often ask him about the potential benefits of various diets, but there is not enough scientific evidence available to offer any definitive advice. Many of the dietary questions that patients have focus on either a calorie-restricted diet, which reduces calorie consumption by 25 to 50 percent, or a ketogenic diet, which is low in carbohydrates and high in fat and protein.

Researchers at the Francis Crick Institute have uncovered a fundamental role of glial cells in the nervous system of the gut in maintaining a healthy intestine. These cells have been found to coordinate the immune responses of the gut following pathogen invasion and could be key targets when exploring new treatments for inflammatory bowel conditions.
Maintaining a healthy intestine and repairing tissue after infection or other types of injury is a complex process, and if this goes wrong, it can lead to inflammatory bowel diseases, such as Crohn’s disease and colitis. While much previous research in this area has focused on the activity of different immune cells, a lot of mysteries about the mechanisms behind these diseases still remain unanswered, which suggests that other cells may play a critical role.
In their study, published in Nature today (20 October), researchers studied the role of enteric glial cells in response to tissue damage. These cells lie within the gut wall and form part of the enteric nervous system which governs the contractions of intestinal muscles and other aspects of digestive function.
They infected mice with a common roundworm parasite, Heligmosomoides polygyrus, and found that when the parasite invades the gut wall, a protein, called interferon gamma, is quickly released by immune cells. Although this protein so far was thought to target cells of the immune system, this new study found that one of its first targets are the nearby glial cells. The protein activates these cells which then release signals that attract other immune cells to the site of damage to fight the infection.
To identify if similar mechanisms occur in humans, the researchers analysed data previously collected by others of colon samples from people with ulcerative colitis, a long-term condition where the colon and rectum become inflamed, and which causes severe diarrhea and stomach cramps. Similar to the mouse cells, genes associated with interferon gamma were also activated in the human glial cells. This suggests that glial cells in the human gut are also implicated in inflammatory conditions of this organ.
Fränze Progatzky, author and postdoctoral scientist in the Crick’s Development and Homeostasis of the Nervous System Lab, says: “Sadly, currently treatments for inflammatory bowel disease are often limited to alleviating the symptoms, rather than tackling the cause. Our insights into the importance of enteric glial cells in maintaining a healthy intestine open the door to further studies into how these cells work and interact with the immune system and in the future could help us develop potential new treatments for these conditions.”
The team also studied the role of glial cells in maintaining healthy intestinal gut tissues, in the absence of infection. To do this, they blocked the ability of enteric glial cells to be activated by interferon gamma and found that this led to tissue inflammation even in normal mice. This shows the cells are also important outside of disease or injury, in maintaining healthy intestinal tissue.
Vassilis Pachnis, author and group leader of the Development and Homeostasis of the Nervous System Lab at the Crick, says: “Glial cells are present in many organs, and so it’s possible they also play similar roles in maintaining healthy tissue and mounting appropriate responses to pathogens or toxins in other parts of the body. It will be exciting to explore this possibility further.”
This research was carried out in collaboration with the AhRimmunity Laboratory at the Crick, led by Gitta Stockinger, and is part of an ongoing collaboration between the labs to study the processes which influence health and disease in the gut.
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Rutgers researchers have discovered that people with asthma and chronic obstructive pulmonary disease have a protein in their lungs that leaks a small molecule into their bloodstream that restricts their breathing instead of relaxing their airways.
The findings, published in the American Journal of Respiratory Cell and Molecular Biology, will help clinicians diagnose and determine the severity of chronic lung diseases and make bronchodilators more effective. In the United States, 25 million people suffer with asthma and another 14 million with COPD.
“This protein has been recognized as important in some diseases, but it has never been defined before in airway diseases, such as asthma and COPD, until now,” said co-author Reynold Panettieri, vice chancellor of translational medicine at Rutgers. “In addition to identifying this protein, we demonstrated that if you decrease the leakage, the smooth muscles in the airways relax, which could be potentially very important in improving asthma and COPD management. In addition, the presence of too much cAMP in a patient’s blood is a new biomarker that can help characterize specific types of asthma and COPD.”
The study discovered that a protein in the cell membranes of smooth muscles in the lungs of patients with chronic airway disease can leak cyclic adenosine monophosphate (cAMP), which transmits biological information to help relax muscles in the lungs and widen the airways. The leakage causes the airways to become constricted and cAMP can be found in the bloodstream, which can improve diagnosis of chronic airway diseases.
Rutgers and Yale School of Medicine researchers collaborated to discover the leak of cAMP from human airway smooth muscle cells from patients with and without asthma. These cells control constriction of the airways in asthma and by losing cAMP the cells are more apt to constrict and worsen asthma. They next defined cAMP in the bloodstream as a biomarker by analyzing blood samples from a well-defined cohort of asthma patients.
“We determined that cAMP blood levels are higher in asthma patients,” Panettieri said. “This knowledge allows for better diagnostics of the illness and forms the basis for new therapeutics that will plug the leak of cAMP in the protein.”
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Materials provided by Rutgers University. Original written by Patti Verbanas. Note: Content may be edited for style and length.