Culture

Dublin, Ireland: Treatment with capivasertib, a drug designed to work against a particular gene mutation found in some tumours, shows signs of being effective in a trial of 35 patients presented today (Tuesday) at the 30th EORTC-NCI-AACR [1] Symposium on Molecular Targets and Cancer Therapeutics in Dublin, Ireland.

The phase 2 trial (EAY131-Y) is part of a larger USA study, called NCI-MATCH (EAY131) [2], that aims to determine whether cancer patients can be treated successfully by selecting therapies that target gene abnormalities found in their tumours, rather than by cancer type.

Researchers say their results provide further evidence that the approach of tailoring treatment according to tumour genes could offer more effective treatments for individual patients in the future. The more traditional approach is to treat patients based on what has worked in the past for other patients with the same type of cancer.

The research was presented by Dr Kevin Kalinsky, Assistant Professor of Medicine, New York Presbyterian-Columbia University Irving Medical Centre, USA. He explained: "Capivasertib can be taken by mouth and it's a type of drug called an AKT inhibitor. This means it binds to a molecule called AKT that has mutated a change that plays a role in helping cancer cells grow. In a prior phase 2 study, capivasertib has shown potential in treating an aggressive form of breast cancer.

"In this trial, we wanted to see if capivasertib could be used in patients with any type of cancer whose tumours have the mutation that leads the AKT molecule to become over-active and make the cancer grow."

Patients were selected by having the cells from their tumours tested. Each of the 35 patients in the trial was carrying the AKT mutation in the cells of their tumour. Although this mutation occurs in several different types of cancer, overall it is rare. Researchers found the mutation in 1.3% of patients (70 of 5548) tested centrally in the NCI-MATCH trial.

In all patients on the EAY131-Y study, the cancer had spread to other parts of the body, and most had already received three or more previous treatments. The patients were treated with capivasertib, taken by mouth twice a day, in weekly cycles of four days with treatment and three days without treatment.

Patients' tumours were measured by imaging, such as CT scans, before and after treatment. In the best confirmed responses, the tumour reduced in size in eight patients (23%), and in 16 patients (46%) the tumour did not grow but did not shrink either. In three patients (9%), the tumour grew.

Researchers observed the following side effects from the drug, saying that physicians should carefully manage these in patients being treated with capivasertib: high blood sugar, fatigue, diarrhoea, nausea, vomiting, and skin rash.

Dr Kalinsky said: "Overall, 23% of the patients in our trial experienced a positive response, which was defined as tumour shrinkage from before they started capivasertib. We determined in advance that if 16% of patients experienced this response from the treatment, it would be a signal to move the drug on to a larger trial. This is a positive finding in a trial with patients whose cancers continued to grow despite previous treatments."

Researchers estimate that, six months after the treatment, the percentage of patients alive and without their tumours growing was 52%.

"This study is a limited but important piece of evidence. More trials are needed to learn the benefit in each tumour type and to understand why some patients did not have a response while others had a prolonged time without tumour growth," Dr Kalinsky added.

Professor Charles Swanton of the Francis Crick Institute, London, UK, is scientific co-chair of the EORTC-NCI-AACR Symposium and was not involved in the research. He said: "Although we understand more than ever about the role of genes in different cancers, there is still a lack of evidence on using this knowledge to guide treatments and improve patient survival. Outside of a trial setting, this approach is not widely available.

"This study is a small but important piece of evidence and it's part of a larger study that will help us move towards more personalised cancer treatments.

"This trial approach is particularly important for those with rarer cancers where we know less about which treatments are most effective and conducting patient trials is difficult."

Researchers at University of California San Diego School of Medicine, Scripps Institution of Oceanography, and international collaborators have evidence that Kawasaki Disease (KD) does not have a single cause. By studying weather patterns and geographical distributions of patients in San Diego, the research team determined that this inflammatory disease likely has multiple environmental triggers influenced by a combination of temperature, precipitation and wind patterns. Results will be published in the November 12 online edition of Scientific Reports.

"We are seeing firsthand evidence of these weather patterns in San Diego, where eight children have recently been diagnosed with Kawasaki Disease. Recent low pressure systems in San Diego have been associated with two distinct clusters of the disease," said Jane C. Burns, MD, pediatrician at Rady Children's Hospital-San Diego and director of the Kawasaki Disease Research Center at UC San Diego School of Medicine. "Our research is pointing towards an association between the large-scale environment, what's going on with our climate on a large scale, and the occurrence of these clusters."

Kawasaki disease is the most common acquired heart disease in children. Untreated, roughly one-quarter of children with KD develop coronary artery aneurysms -- balloon-like bulges of heart vessels -- that may ultimately result in heart attacks, congestive heart failure or sudden death.

Burns and her team examined 1,164 cases of KD treated at Rady Children's Hospital over 15 years. Noticeable clusters of KD cases were often associated with distinct atmospheric patterns that are suspected to transport or concentrate agents that result in KD. Days preceding and during the KD clusters exhibited higher than average atmospheric pressure and warmer conditions in Southern California, along with a high pressure feature south of the Aleutian Islands.

"For the first time, we have evidence that there is more than one trigger for Kawasaki Disease. Up until now, scientists have been looking for one 'thing' that triggers KD," said Burns. "Now we see that there are distinct clusters of the disease with different patterns suggesting varying causes."

Gene expression analysis further revealed distinct groups of KD patients based on their gene expression pattern, and that the different groups were associated with certain clinical characteristics.

"Our data suggest that one or more environmental triggers exist, and that episodic exposures are influenced at least in part by regional weather conditions. We propose that characterization of the environmental factors that trigger KD in genetically susceptible children should focus on aerosols inhaled by patients who share common disease characteristics," said Burns who has studied KD for more than 35 years.

Although KD is estimated to affect fewer than 6,000 children in the U.S. each year, the incidence is rising in San Diego County. While the average incidence per 100,000 children less than 5 years of age residing in San Diego County was approximately 10 for the decade of the 1990s, the estimate from 2006 to 2015 was 25.5. This increase may be attributed to the efforts of the KD team at Rady Children's Hospital to teach local physicians how to diagnose KD. Or it may be due to increasing exposure to the environmental triggers of the disease.

Prevalence rates of KD are increasing among children in Asia. Japan has the highest incidence rate, with more than 16,000 new cases per year. One in every 60 boys and one in every 75 girls in Japan will develop KD during childhood.

Incidence rates in the U.S. are approximately 19 to 25 cases per 100,000 children under age 5 -- but are higher in children of Asian descent. Predictive models estimate that by 2030, 1 in every 1,600 American adults will have been affected by the disease.

Boston, Mass. -- Bacteria are present in just about every breath of air we take in. How the airway protects itself from infection from these bacteria has largely remained a mystery -- until now. When bacteria are inhaled, exosomes, or tiny fluid-filled sacs, are immediately secreted from cells which directly attack the bacteria and also shuttle protective antimicrobial proteins from the front of the nose to the back along the airway, protecting other cells against the bacteria before it gets too far into the body.

A research team from Massachusetts Eye and Ear describes this newly discovered mechanism in a report published online today in the Journal of Allergy and Clinical Immunology (JACI). The findings shed new light on our immune systems -- and also pave the way for drug delivery techniques to be developed that harness this natural transportation process from one group of cells to another.

"Similar to kicking a hornets nest, the nose releases billions of exosomes into the mucus at the first sign bacteria, killing the bacteria and arming cells throughout the airway with a natural, potent defense" said senior author Benjamin Bleier, MD, a sinus surgeon at Massachusetts Eye and Ear and associate professor of otolaryngology at Harvard Medical School. "It's almost like this swarm of exosomes vaccinates cells further down the airway against a microbe before they even have a chance to see it."

The JACI study was motivated by a perplexing previous finding from Dr. Bleier's lab a few years ago. In studies of sinus inflammation, researchers found that proteins in the cells of the nasal cavity were also present in patients' nasal mucus. The team wanted to know why and how these proteins were moving from the cells into the nasal mucus, hypothesizing that exosomes had something to do with that process.

The new findings described in the JACI study shed light on this process. When cells at the front of the nose detect a bacterial molecule, they trigger a receptor called TLR4, which stimulates exosome release. When that happens, an innate immune response occurs within 5 minutes. First, it doubles the number of exosomes that are released into the nose. Second, within those exosomes, a protective enzyme, nitric oxide synthase, also doubles in amount. As a well-known antimicrobial molecule, nitric oxide potently arms each exosome to defend against bacteria.

The exosome "swarm" process gets an assist from another natural mechanism of the nose -- mucocilliary clearance. Mucocilliary clearance sweeps the activated exosomes over to the back of the nose, along with information from cells that have already been alerted to the presence of bacteria. This process prepares the cells in the back of the nose to immediately fight off the bacteria, arming them with defensive molecules and proteins.

In their experiments described in the JACI report, Dr. Bleier's team sampled patients' mucus and grew up their own cells in culture. They then simulated an exposure to bacteria and measured both the number and composition of the released exosomes. They found a doubling of both the number of exosomes and of antibacterial molecules after stimulation. The team then confirmed this finding in live patients and further showed that these stimulated exosomes were as effective as antibiotics at killing the bacteria. Finally, the team showed that the exosomes were rapidly taken up by other epithelial cells, where they were able to "donate" their antimicrobial molecules.

Along with this new understanding of the innate immune system, the authors on the JACI paper suggest that their findings may have implications for new methods of delivering drugs through the airway to be developed. More specifically, as natural transporters, exosomes could be used to transfer inhaled packets of therapeutics to cells along the upper airway -- and possibly even into the lower airways and lungs.

"The nose provides a unique opportunity to directly study the immune system of the entire human airway -- including the lungs," said Dr. Bleier.

Urban planning decisions from decades past are likely a contributing factor to the rise of right-wing populism, a study from the University of Waterloo has found.

The study looked at urban planning and voting data from post-World War Two to 2010 outside Toronto, Canada. It found that development patterns that led to the reliance on the automobiles may also be fueling political attitudes that favour comfort and convenience and resist sustainable development.

"As planners kept building suburbs they created scores of new electoral ridings and suburban voters who predictably voted for politicians and policies catering to their lifestyles," said Pierre Filion. "This translated into increasing automobile dependence, less land devoted to public space, and the continued cycle of building more suburbs.

"A careful look at the results of the recent mid-term elections in the United States shows the clear ideological division between urban and suburban areas."

In reviewing the data, the researchers found that the increasing use of the automobile heavily influenced land-use decisions and life-style choices. The combination of automobile dependency and continued urban sprawl normalized economic and cultural norms associated with unsustainable suburban living.

It has also led to many suburbanites resisting calls for change that would impact them personally.

"It's understandable that people whose recreation and livelihood depends on cars, would be less willing to accept transformative changes that could disproportionately impact their comfort and convenience," says Filion. "This contributes to a sense of having their values attacked, and could explain some of the waves of right-wing populism in North America.

"It's something we saw in 2016 as well as the most recent election in Ontario, Canada."

Can your smart phone determine if you're having the most serious - and deadly - form of heart attack? A new research study says it can - and may be a valuable tool to save lives.

The international study, led by researchers from the Intermountain Medical Center Heart Institute in Salt Lake City, found that a smartphone app to monitor heart activity and determine if someone is having an ST-Elevation Myocardial Infarction (STEMI), a heart attack in which the artery is completely blocked, has nearly the same accuracy as a standard 12-lead electrocardiogram (ECG), which is used to diagnose heart attacks.

Researchers say the findings are significant because the speed of treatment after a STEMI heart attack helps save lives.

"The sooner you can get the artery open, the better the patient is going to do. We found this app may dramatically speed things up and save your life," said J. Brent Muhlestein, MD, lead investigator of the study and cardiovascular researcher at the Intermountain Medical Center Heart Institute.

In the study, 204 patients with chest pain received both a standard 12-lead ECG and an ECG through the AliveCor app, which is administered through a smartphone with a two-wire attachment. Researchers found the app with the wire set-up effective in distinguishing STEMI from not-STEMI ECGs accurately and with high sensitivity compared to a traditional 12-lead ECG.

"We found the app helped us diagnose heart attacks very effectively -- and it didn't indicate the presence of a heart attack when one wasn't occurring," Dr. Muhlestein said.

A STEMI is a very serious type of heart attack during which one of the heart's major arteries -- which supplies oxygen and nutrient-rich blood to the heart muscle -- is blocked. ST-segment elevation is an abnormality that's detectable on the 12-lead ECG.

Researchers presented results from the study at the American Heart Association's 2018 Scientific Session in Chicago.

Researchers conducted the study, called the ST LEUIS International Multicenter Study, at five international sites that are all associated with the Duke University Cooperative Cardiovascular Society (DUCCS), with Intermountain Medical Center Heart Institute serving as the coordinating institution where they collected and collated data.

Other participating research centers include: Duke University, Integris Heart Hospital (Oklahoma City), Catholic University (Argentina), Mayo Clinic, Stanford University, Erlanger Institute for Clinical Research (Tennessee), University of Utah Health, AliveCor Corporation, and the Rocky Mountain University of Health Professions.

The idea for this kind of ECG set-up perhaps came from the use of treadmills for personal fitness development, said Dr. Muhlestein. Many people using treadmills wear a simple device that can detect their heart rate, through a single ECG lead, more accurate than just checking the pulse. "It's a simple jump from there to putting it on a smartphone, and then recording the same ECG lead from several body positions." he said.

The new Apple 4 smartwatch also comes with a single-lead ECG. A typical ECG has 12 leads, which improves the accuracy of a diagnosis because heart attacks happen in different parts of the heart, and each lead looks at a different part. With the AliveCor app, the two wire leads are moved around the body in order to record all 12 parts.

The findings of the study are important for two reasons, said Dr. Muhlestein.

The first is it could speed up the urgent treatment a patient needs after suffering a STEMI. American College of Cardiology/American Heart Association guidelines recommend that the "door-to-balloon time" - or the time from when a patient enters the hospital to when a catheter with a balloon on the tip is inserted into the patient's blocked artery, then inflated to flatten plaque against the wall of the artery - be less than 90 minutes.

"If somebody gets chest pain and they haven't ever had chest pain before, they might think it's just a bug or it's gas and they won't go to the emergency room," Dr. Muhlestein said. "That's dangerous, because the faster we open the blocked artery, the better the patient's outcome will be."

The app can take the electrocardiogram on the spot, send the results into the cloud where a cardiologist reviews it immediately and, if a STEMI is found, tell the person so they can be rushed to the hospital.

Secondly, the price of the app with the two-wire extension is low, which could put the power of an ECG into the hands of anyone with a smartphone or smartwatch, and make ECGs accessible in places like third world countries where people have smartphones but where expensive ECG machines are hard to find, if they're available at all.

New Haven, Conn. -- A drug therapy used for patients with chronic heart failure also improves markers of poor prognosis in individuals who are hospitalized with acute heart failure, new Yale-led research shows. The findings suggest that the drug can improve outcomes for acutely ill heart patients and potentially become the new standard of care for treating this serious condition, the researchers said.

The study was published in the New England Journal of Medicine, and presented at the American Heart Association Scientific Sessions in Chicago on Nov. 11, 2018.

Acute heart failure, a condition in which the heart fails to pump blood efficiently, is the leading cause of hospitalizations for older adults. Affected individuals experience high rates of re-hospitalization and death. The standard of care, which consists of diuretics and medications that enhance blood flow, has remained largely unchanged for decades.

To test whether the FDA-approved drug sacubitril-valsartan could improve outcomes for individuals with acute heart failure, the research team conducted a randomized, double-blind clinical trial called PIONEER-HF. More than 800 patients hospitalized with heart failure at 129 U.S. sites were treated with either sacubitril-valsartan or the standard therapy, enalapril, an ACE inhibitor. Over the trial period of eight weeks, the researchers monitored participants' blood pressure and other safety parameters, such as kidney function, and analyzed blood and urine samples.

The research team found that in patients taking sacubitril-valsartan, levels of a key measure of heart failure severity -- NT-proBNP -- reduced more quickly than with the standard therapy. Evidence of improvement was observed as early as one week into the trial, they said.

"It worked to reduce NT-proBNP rapidly and to a greater extent than enalapril," said corresponding author Eric Velazquez, M.D., the Berliner Professor of Cardiology at Yale School of Medicine and PIONEER-HF principal study investigator. "There were multiple markers including troponin T, a marker of heart cell injury, that suggested substantial improvement."

Velazquez and his co-authors also reported no significant differences between the two therapies in terms of safety, including impact on renal function, blood pressure, and other indicators. "The results of this landmark study should help inform our basic approach to treating hospitalized patients with acute heart failure," said Velazquez. "Once acute heart failure is diagnosed, patients are stabilized, and a low ejection fraction is confirmed, sacubitril/valsartan should be started promptly to reduce NT-proBNP and reduce the risk of post-discharge heart failure hospitalization."

Combined with results of a previous trial, PARADIGM-HF, which showed the drug's effectiveness for patients with chronic heart failure, these findings could make sacubitril-valsartan the go-to standard of care for acute and chronic heart failure, said the researchers.

"There are consistent results from both trials," Velazquez said. "It is safe and there's a rapid outcome. If it becomes the standard, we are likely to reduce the risk of hospitalization for heart failure, and that will have a positive clinical impact and societal impact."

For patients who take medication to treat hypothyroidism, being treated with too much medication can lead to an increased risk of atrial fibrillation, a common heart rhythm disorder associated with stroke, a new study of more than 174,000 patients has found.

The findings were presented by researchers from the Intermountain Medical Center Heart Institute in Salt Lake City at the American Heart Association Scientific Session conference in Chicago.

"We know patients with hypothyroidism have a higher risk of atrial fibrillation, but we didn't consider increased risk within what's considered the normal range of thyroid hormones," said lead researcher Jeffrey L. Anderson, MD, Distinguished Clinical and Research Physician at the Intermountain Medical Center Heart Institute, which is part of the Intermountain Healthcare system. "These findings show we might want to re-consider what we call normal."

In the new study, researchers surveyed the electronic medical records of 174,914 patients treated at Intermountain Healthcare facilities whose free thyroxine (fT4) levels were recorded and who were not on thyroid replacement medication. Researchers then took what's considered a normal range of fT4 levels, divided it into four quartiles, then looked at those patients' records for a current or future diagnosis of atrial fibrillation.

They found a 40 percent increase in existing atrial fibrillation for patients in the highest quartile of fT4 levels compared to patients in the lowest, and a 16 percent increase in newly developing atrial fibrillation during 3-years of follow up.

These findings, said Dr. Anderson, suggest that the optimal healthy range of fT4 should be reconsidered and redefined.

"Thyroid hormones are associated with losing weight and having more energy, which may lead to people being treated at the high end of the normal range," said Dr. Anderson. "Are we harming people by putting them at a higher risk of atrial fibrillation, and therefore stroke?"

The study also showed that fT4 should be measured, along with thyroid-stimulating hormone (TSH), which is more commonly tested for in patients with irregular thyroid hormone levels but was not helpful within the normal range in refining risk.

The link between fT4 and atrial fibrillation was recently recognized in the Rotterdam Study, a population-based cohort study first started in 1990. However, with any new and unexpected report requires replication and independent confirmation. The new study by Intermountain Medical Center Heart Institute researchers establishes the link between fT4 level and atrial fibrillation in patients treated in the United States.

"The next step for researchers is to conduct a randomized trial to see if targeting a lower versus a higher upper range of fT4 in patients receiving thyroid hormone replacement therapy leads to a lower risk of atrial fibrillation and stroke along with other possible heart-related issues, like atherosclerosis," Dr. Anderson said.

SYRACUSE, NY (November 9, 2018) -- Newly published research shows that a saliva-based biomarker panel and associated algorithm could improve the ability to accurately identify children with autism spectrum disorder (ASD) in its earliest stages, announced Quadrant Biosciences Inc. In a study of more than 450 children ages 18 months to 6 years, researchers demonstrated that a panel of 32 small RNAs could differentiate children with autism from children exhibiting typical development or non-ASD developmental delay with 85% accuracy. This test accuracy was achieved both during the model development and during validation of the test in a separate set of children.

The publication, entitled "Validation of a salivary RNA test for childhood autism spectrum disorder," was published online in Frontiers in Genetics by researchers Steven Hicks, M.D., Ph.D., of the Pennsylvania State College of Medicine and Frank Middleton, Ph.D., of SUNY Upstate Medical University in collaboration with scientists from Quadrant Biosciences.

Following a pilot study demonstrating that many of these RNA elements could be detected in the saliva of children with ASD, the researchers determined that saliva-based testing could provide the means to broadly interrogate genomic, physiologic, microbiome, and environmental factors implicated in ASD in a single, non-invasive, high-throughput analysis.

"Growing evidence suggests that autism arises from interactions between a child's genes and the environment. This study measured factors that may control interactions between genes and the environment, especially the microbiome," said Dr. Hicks. "Though children with autism have diverse genetic backgrounds, we found that a set of 32 RNA factors in their saliva could accurately distinguish them from peers without autism. Given this array of ASD risk factors, we believe a 'poly-omics' RNA-based approach that integrates genetic, epigenetic, and metagenomics methods would be well suited to the development of an objective biomarker-based test."

The Study

The multi-center study included 456 children recruited during the past three years. The authors compared saliva samples from 238 children with ASD to 218 children without ASD (including 84 children with developmental delay and 134 with typical development). Levels of human and bacterial RNAs were measured in the saliva samples using comprehensive next-generation sequencing. The top RNAs were identified using robust machine-learning algorithms from the first 372 children and then validated in the remaining 84 samples that were not used in the machine learning. Notably, this validation set also included samples collected from children at the University of California, Irvine, to verify that the RNA algorithm performed accurately in samples from different geographic regions.

Need for Earlier Autism Diagnosis

Screening for autism typically relies on a parent-based questionnaire called the Modified Checklist for Autism in Toddlers Revised (MCHAT-R). Children with a positive MCHAT-R score are generally referred for diagnostic evaluation. However, due to the high number of false-positive results on the MCHAT-R, wait times for autism evaluation often exceed one year. While diagnosis is possible in children as young as 24 months, the average age of ASD diagnosis in the United States today is greater than 4 years. Early diagnosis is important because intensive behavioral therapy has been shown to improve the symptoms of autism, and children benefit more from such intervention the earlier it is started.

Daniel Coury, M.D., Professor of Clinical Pediatrics and Psychiatry at The Ohio State University College of Medicine and a member of the Section of Developmental & Behavioral Pediatrics at Nationwide Children's Hospital, sees the benefit of this RNA biomarker-based test in a clinical setting. "Often autism-specific interventions are delayed while awaiting a diagnosis. It frequently takes months to obtain an autism evaluation due to the large number of referrals, many of whom will not receive a diagnosis of autism," he explained. "A test which can separate children who have screened M-CHAT-positive into high likelihood of autism or low likelihood of autism could help streamline waitlists and permit earlier diagnosis and enrollment in autism treatment."

Dr. Middleton from SUNY Upstate Medical University agreed. "The ability to accurately discriminate between children with autism and their peers with non-ASD developmental delay is of paramount importance in the field. While the algorithm is not designed as a screening tool, it can provide valuable information in children with a positive MCHAT-R screen, over 80% of whom will not have ASD. In this way, it can be used to prioritize specialist referral or to provide an objective aid to an autism diagnosis."

WEST LAFAYETTE, Ind - Purdue University researchers have developed a new flexible and translucent base for silicon nanoneedle patches to deliver exact doses of biomolecules directly into cells and expand observational opportunities.

"This means that eight or nine silicon nanoneedles can be injected into a single cell without significantly damaging a cell. So we can use these nanoneedles to deliver biomolecules into cells or even tissues with minimal invasiveness," said Chi Hwan Lee, an assistant professor in Purdue University's Weldon School of Biomedical Engineering and School of Mechanical Engineering.

A surgeon performs surgery on the back of a hand of a patient who has melanoma. Purdue researchers are developing a new flexible and translucent base for silicon patches to deliver exact doses of biomolecules directly into cells and expand observational opportunities. The researchers say skin cancer could be one of the applications for the patches.

Silicon nanoneedles patches are currently placed between skin, muscles or tissues where they deliver exact doses of biomolecules. Commercially available silicon nanoneedles patches are usually constructed on a rigid and opaque silicon wafer. The rigidity can cause discomfort and cannot be left in the body very long.

"These qualities are exactly opposite to the flexible, curved and soft surfaces of biological cells or tissues," Lee said.

Lee said the researchers have resolved that problem.

"To tackle this problem, we developed a method that enables physical transfer of vertically ordered silicon nanoneedles from their original silicon wafer to a bio-patch," Lee said. "This nanoneedle patch is not only flexible but also transparent, and therefore can also allow simultaneous real-time observation of the interaction between cells and nanoneedles."
A study on the new procedure was published today (Nov. 9) in Science Advances. The collaborators from South Korea's Hanyang University and Purdue's Weldon School of Biomedical Engineering and School of Mechanical Engineering received joint support from the United States Air Force Office of Scientific Research and the Korean Ministry of Science and ICT to complete this study.
The nanoneedles are partly embedded in a thin flexible and transparent bio-patch that can be worn on the skin and can deliver controlled doses of biomolecules.

Lee said the researchers hope to develop the patch's functionality to act as an external skin patch, lowering the pain, invasiveness and toxicity associated with long-term drug delivery.

In this technology's next iterations, Lee said the researchers plan to test operational validity of the patch's capabilities monitoring cellular electrical activity or treating cancerous tissue.

This technology aligns with Purdue's "Giant Leaps" celebrating the university's global advancements made in health, space, artificial intelligence and sustainability highlights as part of Purdue's 150th anniversary. Those are the four themes of the yearlong celebration's Ideas Festival, designed to showcase Purdue as an intellectual center solving real-world issues.

Genetics may predispose some people to both Alzheimer's disease and high levels of blood lipids such as cholesterol, a common feature of cardiovascular disease, according to a new study by an international team of researchers led by scientists at UC San Francisco and Washington University School of Medicine in St. Louis.

The research analyzed genome-wide data from over 1.5 million individuals, making it one of the largest-ever studies of Alzheimer's genetics. The authors hope the findings will lead to improved early diagnosis and potentially new preventative strategies for Alzheimer's disease, which currently affects 5.7 million people in the U.S. and has no cure.

Mounting clinical and epidemiological evidence has pointed to a link between heart disease and Alzheimer's disease, but a biological relationship between the two conditions has remained controversial. Many patients diagnosed with Alzheimer's disease also show signs of cardiovascular disease, and postmortem studies reveal that the brains of many Alzheimer's patients show signs of vascular disease, which some scientists speculate could drive the onset of dementia. These observations led to hopes of preventing Alzheimer's by treating cardiovascular symptoms, but initial genetic studies and failed clinical trials of cardiovascular drugs called statins in Alzheimer's disease have cast doubt on this possibility.

The new study, published November 9, 2018 in Acta Neuropathologica, shows that Alzheimer's and cardiovascular disease do share common genetics in some individuals, raising new questions about whether this shared biology could be targeted to slow down or prevent both diseases.

"These results imply that irrespective of what causes what, cardiovascular and Alzheimer's pathology co-occur because they are linked genetically. That is, if you carry this handful of gene variants you may be at risk for not only heart disease but also Alzheimer's," said UCSF neurodegeneration researcher Rahul Desikan, MD, PhD, a clinician-scientist whose lab is known for developing a so-called polygenic hazard score for Alzheimer's that predicts the age at which an individual is likely to begin experiencing symptoms of dementia based on their genetic background.

To identify genetic variants that confer risk of both cardiovascular disease and Alzheimer's disease, the researchers used statistical techniques pioneered by Desikan's lab in collaboration with Ole Andreassen, MD, PhD, at the University of Oslo, and Anders Dale, PhD, at UC San Diego, that allowed them to combine multiple large-scale genome-wide association studies (GWAS) -- a type of genetic study that makes statistical links between various disease states and widely shared variations in the genetic code.

Ultimately Desikan's team was able to analyze the combined impact of such genetic markers on both cardiovascular disease risk -- based on five GWAS studies of more than one million individuals -- and on Alzheimer's risk -- based on three GWAS studies of nearly 30,000 Alzheimer's patients and more than 50,000 age-matched controls.

"Our approach works by combining and leveraging these massive GWAS studies to make discoveries that would otherwise be invisible," Desikan said. "We are essentially borrowing statistical power."

This analysis enabled the researchers to identify 90 spots in the genome where specific DNA variants increased patients' combined chance of developing both Alzheimer's disease and heightened blood levels of lipid molecules, including HDL and LDL cholesterol and triglycerides, which are common risk factors for cardiovascular disease.

The researchers confirmed that six of these 90 regions had very strong "genome-wide significant" effects on Alzheimer's and heightened blood lipid levels, including several within genes that had never before been linked to dementia risk. These included several sites within the CELF1/MTCH2/SPI1 region on chromosome 11, which had previously been linked to immune system biology.

In contrast, though patients diagnosed with Alzheimer's also often exhibit other cardiovascular risk factors, such as unhealthy levels of belly fat, type 2 diabetes, and chest pain or other symptoms of coronary artery disease, the authors could find no clear overlapping genetics between Alzheimer's disease and these risk factors.

"These results suggest that Alzheimer's and cardiovascular disease could both be influenced by genetic defects that impair the body's ability to processes lipids properly," said study first author Iris Broce-Diaz, PhD, a postdoctoral researcher in Desikan's lab. "But they also suggest that the link between Alzheimer's and other cardiovascular risk factors are not likely due to common genetics, though they could be linked by diet or other lifestyle factors."

"This is exciting because we know that levels of cholesterol and other lipids in the blood are highly modifiable through changes in diet or with drugs," Broce added. "This raises the possibility that we might be able to help delay or even prevent the onset of Alzheimer's in these patients, though we'll need more data before we can say that for sure."

Desikan's team then examined whether currently healthy individuals with a family history of Alzheimer's disease were more likely to carry these newfound genetic variants, a relatively new method for studying early Alzheimer's risk factors called "Alzheimer's-by-proxy." Taking advantage of a large British research cohort called UK Biobank, the researchers found these variants were much more likely to be present in the genomes of 50,000 individuals who had one or more parents diagnosed with Alzheimer's disease than in nearly 330,000 individuals without a family history of the disease.

"It's remarkable that among these healthy adults with a family history of Alzheimer's, a subset of cardiovascular risk genes themselves appear to strongly influence risk of eventually developing Alzheimer's," Desikan said. "This is exactly the population we should study to see if reducing cardiovascular disease risk through lifestyle or medication can delay or prevent the onset of dementia later in life."

The researchers further confirmed their findings in a collaboration with Celeste M. Karch, PhD, an Alzheimer's expert at Washington University School of Medicine in St. Louis and co-corresponding author on the new study. Karch's team showed that the novel genes most closely tied to Alzheimer's/cardiovascular risk in the new study were differently expressed in the brains of Alzheimer's patients compared to control brains.

"This study emphasizes that we should be thinking about Alzheimer's disease holistically," Karch said. "There's a lot to learn about how the genes that are driving Alzheimer's disease risk also are driving changes throughout the body."

"This is also an exciting opportunity because we already know a great deal about these cardiovascular traits and how to target them," she added.

Desikan and Broce-Diaz are now integrating these findings into the lab's previously developed polygenic risk score, which will allow clinicians to calculate, based on a patient's genome, their combined risk for cardiovascular disease and Alzheimer's. The researchers hope that their work will help launch a precision medicine approach to testing whether controlling blood lipid levels in individuals with the newly discovered risk factors, either through diet or using established drugs such as statins, might delay or prevent the onset of Alzheimer's disease.

"That's really the goal," said Broce-Diaz. "If we can identify the subset of individuals whose cardiovascular and brain health is linked genetically, we think there's a possibility that reducing their blood lipid levels could help reduce their risk of developing dementia later in life. Such treatments haven't worked in clinical trials before, but this could be because we haven't had a good way of selecting who is most likely to benefit based on their genetics."

Nov. 9, 2018--Babies with cystic fibrosis may breathe better by inhaling hypertonic saline, according to a randomized controlled trial conducted in Germany and published in the American Thoracic Society's American Journal of Respiratory and Critical Care Medicine.

In "Preventive Inhalation of Hypertonic Saline in Infants with Cystic Fibrosis (PRESIS): A Randomized, Double-blind, Controlled Study," Mirjam Stahl, MD, and co-authors describe a study of 40 young infants (average age three months at enrollment) with CF. The babies were randomly assigned to receive either hypertonic saline (saline with a 6 percent salt concentration) or isotonic (.9 percent) saline. They were followed for 12 months.

Previous studies in mice found that the salt content of hypertonic saline decreased mucous plugging that can lead to airway obstruction and repeated infections. Other studies found hypertonic saline benefited older infants and children with CF.

"Several studies from teams worldwide investigating infants and preschool children with CF identified by newborn screening revealed that CF lung disease starts in the first months of life, leaving only a narrow window of opportunity for preventive therapeutic interventions," said Dr. Stahl, the lead study author and a pediatric pulmonologist at the Cystic Fibrosis Centre and the Translational Lung Research Center at the University of Heidelberg. "Because lung disease is the most important factor for morbidity and mortality in patients with CF, prevention, or at least delay, of the onset and progression of CF lung disease may be a promising therapeutic strategy."

The researchers also tested whether lung clearance index and chest magnetic resonance imaging (MRI) could be safely performed on the infants and serve as quantitative outcome measures.

Lung clearance index measures how well air is flowing through the lungs. Mucous obstruction of the smallest airways is one of the earliest features of CF lung disease, and lung clearance index can detect these changes in breathing. MRI can detect early abnormalities in lung structure.

The authors report that both procedures could be safely performed in the infants and were well tolerated, though lung clearance index in this particular study provided a better yardstick to measure the benefits of this treatment.

After one year, the infants who received the hypertonic saline had a better lung clearance index. Furthermore, they gained significantly more weight (500 grams or 1.1 pounds higher mean weight after one year of treatment) and height (1.5 centimeters or just under an inch higher mean height after one year of treatment). The weight gain confirmed previous studies of hypertonic saline in a mouse model for CF lung disease. Pulmonary exacerbation rates and adverse events between the treatment groups were similar.

Study limitations include the fact that isotonic saline (sodium chloride concentration: .9 percent) is not a true placebo because it may, itself, have therapeutic benefits. The authors added that the infants were followed for only one year, so whether hypertonic saline therapy is beneficial over the long term is unknown.

The study is believed to be the first randomized controlled trial in infants with CF.

"We demonstrated that early studies are feasible in this challenging age group using innovative, sensitive outcome parameters such as lung clearance index," Dr. Stahl said. "Treatment with hypertonic saline in infants with CF is safe from diagnosis onwards, and our results suggest this preventive therapy benefits lung function and improves thriving."

Brazil's Ministry of Health received reports of 11,524 outbreaks of foodborne diseases between 2000 and 2015, with 219,909 individuals falling sick and 167 dying from the diseases in question. Bacteria caused most outbreaks of such illnesses, including diarrhea and gastroenteritis. The most frequent were Salmonella spp., with 31,700 cases diagnosed in the period (14.4% of the total), Staphylococcus aureus (7.4%), and Escherichia coli (6.1%).

According to a survey by the Ministry of Social Development, bacteria of the genus Salmonella were the etiological agents in 42.5% of the laboratory-confirmed foodborne disease outbreaks reported in Brazil between 1999 and 2009.

Whole-genome sequencing of the main bacteria that cause acute diarrhea is the research focus for a group at the University of São Paulo led by Juliana Pfrimer Falcão, a professor at the university's Ribeirão Preto School of Pharmaceutical Sciences (FCFRP-USP).

In an article published in PLOS ONE, biomedical scientists Amanda Aparecida Seribelli and Fernanda Almeida, who belong to Falcão's lab, describe how they sequenced and investigated the genomes of 90 strains of a specific serovar of Salmonella enterica known as S. Typhimurium (an abbreviation of Salmonella enterica subspecies serovar Typhimurium).

The 90 strains were isolated between 1983 and 2013 at Adolfo Lutz Institute in Ribeirão Preto (São Paulo State, Brazil) and Oswaldo Cruz Foundation (Fiocruz) in Rio de Janeiro. They provide a portrait of the epidemiology of salmonellosis in Brazil in the last 30 years, coming from all regions of the country and having been collected from patients with foodborne infections or from contaminated food such as poultry, pork, or lettuce and other vegetables.

"From humans, we received samples of blood, brain abscesses, and diarrheic feces," Seribelli told.

When the action of antibiotics in each of the 90 strains was tested, it was discovered that the vast majority were resistant to different classes of antibiotics that are part of the arsenal of medicine. The study also identified 39 genes responsible for resistance to antibiotics.

Researchers affiliated with Fiocruz, São Paulo State University's School of Agrarian and Veterinary Sciences (FCAV-UNESP) and Adolfo Lutz Institute participated in the study. The 90 strains of S. Typhimurium were sequenced at the United States Food and Drug Administration (FDA) during Almeida's doctoral stay.

The comparative analysis of the genomes, transcriptomes, and phenotypes of S. Typhimurium strains isolated from humans and food in Brazil was supported by São Paulo Research Foundation - FAPESP, the FDA, and the Ministry of Education's Office for Faculty Development (CAPES).

Salmonellosis

Salmonella comprises two species, S. bongori and S. enterica. The latter is the type species, with a large number of subspecies and serovars that cause more foodborne infections than any other species in Brazil and worldwide. The human and animal intestinal tract is the main natural reservoir for this pathogen, with poultry, pork and related food products serving as major transmission vectors.

The six subspecies of S. enterica are subdivided into 2,600 serovars. A serovar (short for serological variant) is a distinct variation within a species of bacteria or virus characterized by having the same number of specific surface antigens.

The most important subspecies of S. enterica from the epidemiological standpoint is S. enterica subspecies enterica, which causes the foodborne infection known as salmonellosis. The symptoms are diarrhea, fever, stomach cramps, and vomiting.

S. enterica subsp. enterica was the main cause of the 31,700 cases of salmonellosis reported in Brazil between 2000 and 2015. The most frequently isolated serovars of this subspecies are S. Typhimurium and S. Enteritidis.

S. Enteritidis is one of the leading salmonellosis-causing serovars. It first spread in a pandemic that started in Europe in the 1990s. S. Typhimurium was the most prevalent serovar before the pandemic and has continued to cause infections.

According to Almeida, all 90 strains analyzed in the study belonged to S. Typhimurium. Another researcher at FCFRP-USP (also working at the university's Clinical, Toxicological and Bromatological Analysis Laboratory) is currently sequencing and analyzing samples containing the serovar S. Enteritidis.

Almeida took the 90 strains of S. Typhimurium to the US in 2015. "Their genomes were sequenced at the FDA's Center for Food Safety and Applied Nutrition in Maryland under the supervision of researcher Marc W. Allard," he said.

S. Typhimurium's genome contains 4.7 million base pairs. Brief reflection tells us that the study generated a mountain of data, more specifically 423 million bases corresponding to the sum of 90 genomes.

After his return to Ribeirão Preto, Almeida worked with Seribelli on a comparative analysis of the various strains' genomes to understand their diversity and the evolutionary relationships between them.

According to Almeida, the technique used was high-throughput genotyping with SNPs (pronounced "snips" and short for single-nucleotide polymorphisms), which enabled them to identify the genetic composition (genotype) of each strain by means of DNA sequencing. SNPs are the most common markers of genetic variation. The phylogenetic results separated the 90 strains of S. Typhimurium into two groups, A and B.

"The group of samples collected from food differed from the group collected from humans," Seribelli explained. "Food isolates were distributed between groups A and B in relatively similar numbers, suggesting that more than one subtype is circulating in foods in Brazil. Human isolates were more prevalent in group B, suggesting that a specific subtype has probably adapted to humans."

In another important part of their research funded by FAPESP, the scientists measured antibiotic resistance in each of the 90 strains. According to the study, 65 (72.2%) of the strains proved resistant to sulfonamides, 44 (48.9%) to streptomycin, 27 (30%) to tetracycline, 21 (23.3%) to gentamicin and seven (7.8%) to ceftriaxone, a cephalosporin antibiotic.

Origin of resistance

The analysis of SNPs identified 39 genes for resistance to different classes of antimicrobial or antibiotic, such as aminoglycoside, tetracycline, sulfonamide, trimethoprim, beta-lactam, fluoroquinolone, phenicol and macrolide. Point mutations were also found in some of the genes, such as gyrA, gyrB, parC and parE.

"It's striking that S. Typhimurium is resistant to antibiotics that can be used to treat the disease," Seribelli said. "These drugs are available to physicians for use in combating infections that display resistance. They're a second line of defense when microorganisms aren't killed by the patient's immune system since salmonellosis is normally self-limiting and doesn't require the use of antibiotics. The main problem is when this fails and the bacteria become invasive."

Another point that drew the scientists' attention was the difference between the strains' resistance over the 30-year sample collection period. "The samples of S. Typhimurium collected in the mid-1990s showed more resistance to antibiotics than samples from later years. This could be explained by the emergence in the early 1990s of the serovar S. Enteritidis, which has since become one of the main causes of salmonella infection," Seribelli said.

S. Enteritidis has been known since the 1950s, but for a time, it caused fewer cases of the disease. This was radically changed by the S. Enteritidis pandemic, which began in the late 1980s and early 1990s in Europe and then spread around the world.

"Since then, S. Enteritidis has been one of the most prevalent serovars in Brazil and worldwide. As a result, it's a serovar that can also be combated with antibiotics if necessary," Seribelli said.

According to Almeida, S. Typhimurium remains one of the main serovars isolated from humans, animals and food in Brazil and worldwide.

As of the S. Enteritidis pandemic in the mid-1990s, the number of resistant strains apparently decreased compared with the number prevalent before the 1990s, but whether the virulence of these strains increased to allow them to adapt to this new niche is unknown.

"The key finding of this research is the discovery of a large number of resistance genes in the samples, considering that they were isolated from humans and food. This points to the very significant risk of contamination in Brazil today from food containing strains of Salmonella that are resistant to antimicrobials," Almeida said.

MINNEAPOLIS - Researchers have been searching for possible treatments for the polio-like illness causing paralysis in children, called acute flaccid myelitis. But a new study shows no signal of efficacy for one potential treatment, the antidepressant fluoxetine. The study is published in the November 9, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Research suggests that the virus called enterovirus D68, or EV-D68, is one possible cause of acute flaccid myelitis. Lab tests showed that fluoxetine had antiviral effects against EV-D68, so the antidepressant was suggested by various experts as a possible treatment for acute flaccid myelitis, which can cause sudden muscle weakness in the arms, legs or neck, drooping eyelids and difficulty swallowing, speaking and breathing.

"The lack of an efficacy signal for the treatments for acute flaccid myelitis evaluated in this study emphasizes the need for development and prospective evaluation of more effective treatment and prevention strategies for this potentially devastating condition," said study author Kevin Messacar, MD, of Children's Hospital Colorado in Aurora.

For the retrospective study, researchers looked at the cases of 56 children with acute flaccid myelitis in 2015-2016 from 12 medical centers across the country. The children ranged in age from 2-1/2 to 9 years old.

The 28 children who received more than one dose of fluoxetine were compared to the 26 children who did not receive the drug and two who had only one dose and were considered part of the untreated group. The children's muscle strength in their arms and legs was recorded to determine whether the drug was effective.

At their first exams, there was no difference between the two groups in muscle strength. But by the end of the study an average of seven months later, the children who had taken the drug had lower strength scores than the children who did not receive treatment. After adjusting for factors that could affect the results, such as age, sex, other treatments the children received and their strength level at the first exam, the researchers found that on a scale of 0 to 20 that grades muscle strength throughout all four limbs, the strength scores of children who received the drug worsened by 0.2, while the scores of those who did not receive the drug improved by 2.5.

The researchers also looked at the strength score of the weakest limb in each child and found the difference in this score from initial examination to latest follow-up was worse for children who received the drug than those who did not.

The drug was well-tolerated by the children, with the number of side effects similar between those receiving the drug and those who did not.

A total of 91 percent of the children were sick before developing acute flaccid myelitis, with 71 percent having fever and 73 percent having respiratory symptoms. Weakness started an average of 8.5 days after the start of the illness.

More than 40 percent of the children had an enterovirus in their system, with 36 percent having EV-D68. A total of 57 percent of those who received the drug had EV-D68, compared to 14 percent of those who did not receive the drug.

Messacar noted that the study has several inherent limitations in that it was looking back in time, patients were not chosen at random to receive the treatment or not and doctors and patients and their families were aware that they were receiving the drug. In addition, the small number of patients may make it difficult to draw definite conclusions.

UNIVERSITY PARK, Pa. -- Helping residents become more physically fit may not just be a walk in a park, it could also be a walk to a park, according to a team of Penn State researchers.

In a study, the researchers found that small improvements to a city's ParkScore - an evaluation of a city's park system -- could lead to more physical exercise for its residents. The Trust for Public Land created the ParkScore as an index to rank the park systems of the nation's largest 100 cities, they added.

"What we found was that the higher the ParkScore -- which is a way of saying the better the park system -- the larger the proportion of the population that was engaged in physical activity and just a small positive change in that score can mean quite a bit as far as helping residents taking part in physical activity," said Lauren Mullenbach, a doctoral candidate in recreation, park and tourism management.

For example, the researchers said that a 10 point increase in improvement to the ParkScore of Atlanta, a city with 420,003 residents in 2014, would mean an additional 2,688 people would engage in leisure-related physical activity.

Cities with parks that are more accessible, spacious and adequately funded rank higher on the list, according to Mullenbach. The top five cities on the list include Minneapolis and St. Paul, Minnesota; Washington, D.C.; Arlington, Virginia, and San Francisco. Pennsylvania cities are in the top third of the list. Pittsburgh is ranked at 23 and Philadelphia is placed at 30 on the list.

According to the researchers, who present their findings in the current issue of Preventing Chronic Disease, city planners do not need to undertake dramatic programs to improve their parks to increase their resident's physical activity.

"Cities could do any number of things to increase their score, and some of the improvements are relatively straightforward," said Mullenbach. "They could spend more money on parks or park programming, expand their park acreage, or they could increase walking access by putting in sidewalks to the parks, or adding a few more entrances."

The researchers combined three nationwide public data sets to study possible relationships between parks, health and physical activity levels in 59 American cities. They used data from the Center for Disease Control and Prevention's 500 Cities Project, the Trust for Public Land's City Park Facts Report and the U.S. Census Bureau.

"We've known for years that there are aspects of city park systems that link to health outcomes, but we really never had the data -- the evidence -- to put this all together well," said Andrew Mowen, professor of recreation, park and tourism management, who worked with Mullenbach. "Lauren was able to tie this all together with those data sets."

Part of the problem with trying to research the health effects of city parks prior to the availability of these data sets was that earlier data might include data from suburban and county parks, according to the researchers.

"Normally, there's an effort from the Center for Disease Control to collect health information about people on a yearly basis from different municipalities -- a mix of both metro counties and non-metro counties -- across the country and they aggregate that health data to the metropolitan statistical area, so that could include the city and surrounding suburbs," said Mullenbach. "But, for this particular project, the CDC received funding to aggregate data just to the city boundary level, which has never been done before."

While the researchers found that a good park system was positively related to the residents' physical health, the effect was not statistically significant when accounting for demographics and other lifestyle factors.

"This could be because so many other factors -- smoking, access to health care, are some examples -- are crucial to health, too, that parks, or access to parks, really can't affect," said Mowen.

In the future, the researchers would like to examine how investments in park from public and private sources may affect physical fitness and health. They may also examine each contribution -- access, funding and investment - separately to determine how they individually affect park quality and physical fitness and health.

"Another big message in this is that this is a collective effect," said Mowen. "It's not just the spending that planners have to work on, it's the collective of those three factors that have that impact."

Birgitta L. Baker, associate professor of professor of recreation, park and tourism management, also worked on the study.

Drawing from almost 200 scientific studies on workplace meetings, a team of psychological scientists provides recommendations for making the most out of meetings before they start, as they're happening, and after they've concluded. Their report is published in Current Directions in Psychological Science, a journal of the Association for Psychological Science.

Meetings are a near-ubiquitous aspect of today's professional workplace and there is abundant trade wisdom and written guidance about how meetings should be run. But, as researchers Joseph Mroz and Joseph Allen (University of Nebraska Omaha) and Dana Verhoeven and Marissa Shuffler (Clemson University) point out, very little of this guidance is informed by the available science.

"Meetings are generally bad, but meeting science shows us there are concrete ways we can improve them," says Allen. "Leaders can be more organized, start on time, and encourage a safe sharing environment. Attendees can come prepared, be on time, and participate."

Science shows that, under the right circumstances, meetings can provide a place for creative thinking, problem solving, discussion, and idea generation. And yet, a large body of employee research suggests that most meetings are inefficient despite the organizational resources devoted to them, including time, wages, mental resources, and technology.

Improving meetings isn't a trivial matter. According to the researchers' findings, employees average 6 hours per week in meetings, and managers spend an average of 23 hours in them. Studies suggest that employees' attitudes toward meetings can influence their overall attitudes toward work and their well-being.

In their report, Mroz, Allen, Verhoeven, and Shuffler highlight the ingredients of good meetings, including how people can prepare for meeting success, how certain aspects of meetings can make or break them, and how what happens after a meeting can improve team outcomes.

Before the Meeting

Assess current needs: Meetings should involve problem solving, decision making, or substantive discussion. They should not be held to share routine or non-urgent information.

Circulate an agenda: Having an agenda makes the meeting priorities clear to all stakeholders and allows attendees to prepare beforehand.

Invite the right people: Leaders should ask what the goal of the meeting is and whose expertise can help the team get there.

During the Meeting

Encourage contribution: Findings suggest that high-level performers use meetings to set goals, facilitate group understanding of work problems, and seek feedback.

Make space for humor: Humor and laughter can stimulate positive meeting behaviors, encouraging participation and creative problem solving, research shows. These positive meeting behaviors predict team performance concurrently and two years later.

Redirect complaining: Attendees should be aware that complaining can quickly lead to feelings of futility and hopelessness, and leaders should quell complaining as quickly as they can.

Keep discussions focused: Leaders also make sure the purpose of the meeting and the agenda are followed. Leaders should be ready to identify dysfunctional behaviors and intervene to refocus the meeting.

After the Meeting

Share minutes: Sending meeting minutes serves as a record of the decisions that were made, a plan of action for next steps, and an outline of designated roles and responsibilities. This step also loops in people who weren't able to attend the meeting but need the information.

Seek feedback: Feedback can inform the structure and content of future meetings. In particular, leaders can identify meeting problems to increase attendee satisfaction.

Look ahead: To build on progress made during the meeting, stakeholders should think about future actions, follow-through, and immediate and long-term outcomes of the meeting.

Mroz, Allen, Verhoeven, and Shuffler note that video, audio, and motion-tracking technology is allowing for better video and audio analysis of meetings. These improvements could help researchers analyze behaviors rather than attitudes and self-reports after the fact. They point out that "tele-meetings" and video conferences need more study, as they may present their own dynamics, advantages, or challenges.