Healthy Living Linked To Higher Brain Function, Delay Of Dementia

Newswise, November 7, 2016- It's tempting to dip into the leftover Halloween treats, but new research out of York University has found eating plenty of fruits and vegetables, combined with regular exercise, leads to better cognitive functioning for younger and older adults, and may delay the onset of dementia.

York U post-doctoral fellow Alina Cohen and her team, including Professors Chris I. Ardern and Joseph Baker, looked at cross-sectional data of 45,522 participants, age 30 to 80+, from the 2012 annual component of the Canadian Community Health Survey.

What they found was that for those who are normal weight or overweight, but not obese, eating more than 10 servings of fruit and vegetable daily was linked to better cognitive functioning. When moderate exercise was added, those eating less than five servings, reported better cognitive functioning.

Higher levels of physical activity were linked to the relationship between higher daily fruit and vegetable consumption and better cognitive performance. Those with higher body mass indexes, low activity levels and fruit and vegetable consumption were associated with poorer cognitive functioning.

"Factors such as adhering to a healthy lifestyle including a diet that is rich in essential nutrients, regular exercise engagement, and having an adequate cardiovascular profile all seem to be effective ways by which to preserve cognitive function and delay cognitive decline," said Cohen.

With rising rates of inactivity and obesity, the researchers wanted to know if there was a relationship between clusters of risk factors for cognitive decline, and how lifestyle factors might help prevent or delay it.

 Few studies have looked at the relationship between physical activity and eating fruit and vegetables and the effect it has on the brain for both younger and older adults.

"It is pertinent that we develop a better understanding of the lifelong behaviours that may contribute to cognitive decline in late life by implementing a life-span approach whereby younger, middle-aged, and older adults are collectively studied, and where lifestyle risk factors are evaluated prior to a diagnosis of dementia," said Cohen.

The paper, "Physical Activity Mediates the Relationship between Fruit and Vegetable Consumption and Cognitive Functioning: A Cross-Sectional Analysis," was published today in the Journal of Public Health, Oxford University Press.

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York University is known for championing new ways of thinking that drive teaching and research excellence. Our students receive the education they need to create big ideas that make an impact on the world. Meaningful and sometimes unexpected careers result from cross-discipline programming, innovative course design and diverse experiential learning opportunities. York students and graduates push limits, achieve goals and find solutions to the world's most pressing social challenges, empowered by a strong community that opens minds. York U is an internationally recognized research university - our 11 faculties and 26 research centres have partnerships with 200+ leading universities worldwide. Located in Toronto, York is the third largest university in Canada, with a strong community of 53,000 students, 7,000 faculty and administrative staff, and more than 295,000 alumni. York U's fully bilingual Glendon campus is home to Southern Ontario's Centre of Excellence for French Language and Bilingual Postsecondary Education.

Words Matter When Talking About Alzheimer’s

Newswise, November 7, 2016 — Using war metaphors in reference to Alzheimer’s disease should be replaced with messages of resilience against a complex, age-associated condition that may not be fully defeatable, according to a team of researchers.

Framing a health issue through comparisons to warfare is common in popular media and medical and research communities.

While it can motivate efforts to deal with the issue, this type of language and messaging can also create fear and stigma, turn patients into victims and divert resources from critically important prevention and care, said Daniel R. George, assistant professor of medical humanities, Penn State College of Medicine.

Despite decades of failures in Alzheimer’s drug development, scientific attention continues to focus on drugs that “attack” a molecular compound called beta amyloid, with the goal of curing the disease.

Amyloid is a key component of the plaques in the brain that are a hallmark of Alzheimer’s disease.

Research, however, shows that the appearance of amyloid does not correlate with clinical symptoms and beta amyloid has repeatedly been found in the brains of one-third of “normal” elderly people.

This suggests that amyloid may be a symptom rather than a cause of damage. A growing number of researchers believe that declaring “war” on Alzheimer’s by “attacking” amyloid may ultimately be an exercise in self-harm, particularly if amyloid is representative of the brain’s repair response, and may be channeling resources away from other drug-based approaches that do not assume amyloid toxicity.

Scholars have argued that metaphors and narratives that treat disease as something to be attacked can be socially damaging to those affected.

The value of such metaphors may be clearer for infectious diseases caused by single pathogens.

It becomes more problematic when discussing diverse, age-associated syndromes like Alzheimer’s that may not be fully curable. In this way, war metaphors in medicine can invite ways of thinking that may not be scientifically or socially productive.

“If applied in a careless manner, war metaphors can delude our sense of what’s possible therapeutically, and give false hope to people and caregivers who are suffering,” George said.

George and his co-authors propose moving toward different types of metaphors – those that encourage use of words like “slow” or “postpone” rather than “prevent” or “cure,” and emphasize building “resilience” to aging processes in the brain rather than aiming at “absolute victory” over a disease.

While “fighting” and “defeating” Alzheimer’s through drug development is important, the authors argue it may be wiser to acknowledge that Alzheimer’s is not a disease disconnected from the aging process like polio or malaria.

The authors note that Alzheimer’s has been classified as a disease for the past 40 years.

They suggest it may be more beneficial to take a lifespan-oriented approach that includes education about known biological, psychosocial and environmental risk factors, investment in societal programs and infrastructure that support brain health, and ensuring proper care for those affected and their caregivers.

“While not as profitable as drug development, public health initiatives that reduce vascular risk factors, modulate oxidative stress and inflammation, guard against traumatic brain injuries, promote social engagement and lifelong learning, and reduce exposure to neurotoxins, and other commonsense actions should be an explicit component of our societal response (to Alzheimer’s)," the researchers wrote in the American Journal of Bioethics.

George drew particular attention to the residents of Flint, Michigan being exposed to lead, a neurotoxin, through the water supply.

“It is inexcusable that we could let our public infrastructure fail to the point where it becomes a contributor to Alzheimer’s disease risk for socio-economically disadvantaged citizens,” George said.

“If we’re really serious about addressing the problem of Alzheimer’s, we must start by not poisoning our citizens.”

Moving beyond the notion of being at war against Alzheimer’s could also serve to humanize cognitive aging.

“There’s a widely-accepted myth that people who have Alzheimer’s are sort of non-people, akin to zombies,” George said.

“There are ways to construct meaning around memory loss that show greater compassion and solidarity toward people with cognitive frailty rather than seeing them as passive victims in our biological war against the disease.

“We believe in a more humane message – that even if you have a diagnosis of ‘probable Alzheimer’s’ you can still have a life with deep purpose, social contribution and meaningful relationships.”

Other researchers on this paper were Erin R. Whitehouse, Johns Hopkins University School of Nursing; and Peter J. Whitehouse, Case Western Reserve University.

About Penn State College of Medicine
Located on the campus of Penn State Health Milton S. Hershey Medical Center in Hershey, Pa., Penn State College of Medicine boasts a portfolio of nearly $82 million in funded research. Projects range from the development of artificial organs and advanced diagnostics to groundbreaking cancer treatments and understanding the fundamental causes of disease. Enrolling its first students in 1967, the College of Medicine has more than 1,600 students and trainees in medicine, nursing, the health professions and biomedical research on its campus.

Electronic Records Help Link Genes To Age-Related Hearing Loss

 UCSF-Kaiser collaboration studied more than 6,000 cases of hearing impairment

Newswise, October 26, 2016 — A study of patient electronic medical records and genome sequences from adults with age-related hearing impairment by researchers at UC San Francisco and Kaiser Permanente Northern California, identified two genetic variations linked to the hearing disorder.

The research—led by Thomas Hoffmann, PhD, a professor of epidemiology and biostatistics and member of the Institute for Human Genetics at UCSF—was published October 20, 2016 in PLOS Genetics.

“This is one of the first studies that has found and replicated genes linked with age-related hearing impairment,” Hoffmann says.

“And it provides some of the best evidence to date that age-related hearing loss may share a common biological basis with other forms of hearing impairment.”

Age-related hearing impairment (ARHI) is a common condition, affecting one quarter of individuals aged 65, and half of individuals aged 80 and older.

While hearing aids and other technologies offer treatments, scientists hope that a better understanding of the underlying genetics of the disorder may one day yield a cure.

To find genetic variations linked to ARHI, the scientists conducted a genome-wide association study using 6,527 age-related hearing impairment cases and 45,882 controls among white participants in the Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort, a collaboration between UCSF and the Kaiser Permanente Research Program on Genes, Environment, and Health (RPGEH).

“Our collaboration with Kaiser is incredibly powerful,” Hoffmann said. “They have a very long history of electronic health records on all of their patients in the system, so as a researcher you have this rich set of information that you can look at to understand the factors that drive health and disease.”

The researchers discovered two genome variants that contribute to the disorder: a novel variation near the ISG20 gene, and a second variant within TRIOBP, a gene previously associated with another type of hearing loss.

To verify their findings, the scientists replicated the experiment in Latino, East Asian, and African American cohorts within GERA and in an independent cohort of individuals from the UK Biobank.

They also looked at genes known to play a role in hearing loss and identified two additional genetic variations linked to ARHI.

This study provides novel insights into the genetic factors involved in ARHI. In particular, the discovery of the two additional variations in known hearing loss genes suggests that these may be regions of the genome to focus on in future studies of ARHI.

The findings also highlight the utility of large cohorts with matched genomic data and electronic health records for revealing the underlying genetic basis of ARHI and other disorders.

“This has been a long process,” Hoffmann says of the project to collect genomic data and link it with GERA health records.

“It’s really nice to see at the end that all the collaborative work that we’ve done is producing interesting results that help advance the field.”

Additional authors on the paper include Bronya J. Keats, PhD, of Louisiana State University Health Sciences Center; Noriko Yoshikawa, MD, of Kaiser Permanente Medical Center, Oakland; Catherine Schaefer, PhD, of Kaiser Permanente Northern California Division of Research, Oakland; Neil Risch, PhD, who is Lamond Family Foundation Distinguished Professor in Human Genetics, professor of epidemiology and biostatistics, and director of the Institute for Human Genetics at UCSF and an adjunct investigator at the Kaiser Permanente Northern California Division of Research; and Lawrence R. Lustig, MD, of Columbia University Medical Center.

Funders of the research include the National Institute of Deafness and Other Communication Disorders (grant K01 DC013300), the National Institute on Aging, National Institute of Mental Health, the National Institutes of Health Common Fund (RC2 AG036607), the Robert Wood Johnson Foundation, the Wayne and Gladys Valley Foundation, the Ellison Medical Foundation, and Kaiser Permanente National and Regional Community Benefit Programs. The authors have declared no competing financial interests.

About UCSF: UC San Francisco (UCSF) is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy; a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences; and a preeminent biomedical research enterprise. It also includes UCSF Health, which comprises top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospitals in San Francisco and Oakland – and other partner and affiliated hospitals and healthcare providers throughout the Bay Area. Please visit www.ucsf.edu/news and follow @ucsf.

About the Kaiser Permanente Division of Research: The Kaiser Permanente Division of Research conducts, publishes and disseminates epidemiologic and health services research to improve the health and medical care of Kaiser Permanente members and society at large. It seeks to understand the determinants of illness and well-being, and to improve the quality and cost-effectiveness of health care. Currently, DOR’s 550-plus staff is working on more than 350 epidemiological and health services research projects. For more information, visit http://www.dor.kaiser.org or follow us @KPDOR. 

Exercise May Help Ward Off Memory Decline

Newswise, October 24, 2016– Exercise may be associated with a small benefit for elderly people who already have memory and thinking problems, according to new research published in the October 19, 2016, online issue of Neurology®, a medical journal of the American Academy of Neurology.

The research involved people with vascular cognitive impairment, which is the second most common cause of dementia after Alzheimer’s disease. In vascular cognitive impairment, problems with memory and thinking skills result from damage to large and small blood vessels in the brain.

“Studies have shown that exercise can help reduce the risk of developing memory problems, but few studies have looked at whether it can help people who already have these problems get better or keep from getting worse,” said study author Teresa Liu-Ambrose, PT, PhD, of the University of British Columbia in Vancouver, Canada.

The study involved 70 people with an average age of about 74 who had mild vascular cognitive impairment.

Half of the participants took part in one-hour exercise classes three times a week for six months. The other half received information each month about vascular cognitive impairment and a healthy diet, but no information on physical activity.

All of the participants were tested before the study started, at the end of the study and again six months later on their overall thinking skills, executive function skills such as planning and organizing and how well they could complete their daily activities.

Those who exercised had a small improvement on the test of overall thinking skills compared to those who did not exercise. The scores of those who exercised improved by 1.7 points compared to those who did not exercise.

“This result, while modest, was similar to that seen in previous studies testing the use of drugs for people with vascular cognitive impairment,” Liu-Ambrose said.

 “However, the difference was less than what is considered to be a the minimal clinically important difference of three points.”

Six months after the participants stopped the exercise program, their scores were no different than those who did not exercise. Also, there was no difference between the two groups at any point on the tests of executive function skills or daily activities.

Those who exercised also improved compared to the other group in their blood pressure and on a test of how far they could walk in six minutes, which measured overall cardiovascular capacity.

These findings are also important to note given that high blood pressure is a risk factor for developing vascular cognitive impairment.

Liu-Ambrose said more studies are needed to determine whether exercise can improve thinking abilities in people with mild vascular cognitive impairment.

Because the study sample size was based on detecting a difference on the overall thinking skills test, large samples might be needed to detect differences in specific thinking abilities, such as planning, and everyday skills, such as managing one’s finances.

The study was supported by the Canadian Stroke Network and the Heart and Stroke Foundation of Canada.

To learn more about brain health, visit www.aan.com/patients.

The American Academy of Neurology is the world’s largest association of neurologists and neuroscience professionals, with 30,000 members. The AAN is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, concussion, Parkinson’s disease and epilepsy.

For more information about the American Academy of Neurology, visit http://www.aan.com or find us on Facebook, Twitter, LinkedIn and YouTube.

Alzheimer's Disease Could Be Treated With Gene Therapy, Suggests Animal Study

Researchers have prevented the development of Alzheimer's disease in mice by using a virus to deliver a specific gene into the brain

Newswise, October 17, 2016— Researchers have prevented the development of Alzheimer's disease in mice by using a virus to deliver a specific gene into the brain.

The early-stage findings, by scientists from Imperial College London, open avenues for potential new treatments for the disease.

In the study, published in the journal Proceedings of the National Academy of Sciences, the team used a type of modified virus to deliver a gene to brain cells.

The research was funded by Alzheimer's Research UK and the European Research Council.

Previous studies by the same team suggest this gene, called PGC1 - alpha, may prevent the formation of a protein called amyloid-beta peptide in cells in the lab.

Amyloid-beta peptide is the main component of amyloid plaques, the sticky clumps of protein found in the brains of people with Alzheimer's disease. These plaques are thought to trigger the death of brain cells.

Alzheimer's disease affects around 520,000 people in the UK. Symptoms include memory loss, confusion, and change in mood or personality. Worldwide 47.5 million people are affected by dementia - of which Alzheimer's is the most common form.

There is no cure, although current drugs can help treat the symptoms of the disease.

Dr Magdalena Sastre, senior author of the research from the Department of Medicine at Imperial, hopes the new findings may one day provide a method of preventing the disease, or halting it in the early stages.

She explained: "Although these findings are very early they suggest this gene therapy may have potential therapeutic use for patients. There are many hurdles to overcome, and at the moment the only way to deliver the gene is via an injection directly into the brain. However this proof of concept study shows this approach warrants further investigation."

The modified virus used in the experiments was called a lentivirus vector, and is commonly used in gene therapy explained Professor Nicholas Mazarakis, co-author of the study from the Department of Medicine: "Scientists harness the way lentivirus infects cells to produce a modified version of the virus, that delivers genes into specific cells. It is being used in experiments to treat a range of conditions from arthritis to cancer. We have previously successfully used the lentivirus vector in clinical trials to deliver genes into the brains of Parkinson's disease patients."

In the new study, the team injected the virus, containing the gene PGC-1 - alpha, into two areas of the brain in mice susceptible to Alzheimer's disease.

The areas targeted were the hippocampus and the cortex, as these are the first regions to develop amyloid plaques in Alzheimer's disease.

Damage to the hippocampus affects short-term memory, and leads to a person forgetting recent events, such as a conversation or what they ate for breakfast. The hippocampus is also responsible for orientation, and damage results in a person becoming lost on familiar journeys, such as driving home from the shops.

The cortex, meanwhile, is responsible for long-term memory, reasoning, thinking and mood. Damage can trigger symptoms such as depression, struggling to work out how much money to give at a checkout, how to get dressed or how to cook a familiar recipe.

The animals were treated at the early stages of Alzheimer's disease, when they still had not developed amyloid plaques. After four months, the team found that mice who received the gene had very few amyloid plaques, compared with the untreated mice, who had multiple plaques in their brain.

Furthermore, the treated mice performed as well in memory tasks as healthy mice. The tasks included challenges such as replacing a familiar object in the mouse's cage with a new one. If the mice had a healthy memory, they would explore the new object for longer.

The team also discovered there was no loss of brain cells in the hippocampus of the mice who received the gene treatment. In addition to this, the treated mice had a reduction in the number of glial cells, which in Alzheimer's disease can release toxic inflammatory substances that cause further cell damage.

The protein PGC-1 - alpha, which is coded by the gene, is involved in metabolic processes in the body, including regulation of sugar and fat metabolism.

Dr Sastre added that other studies from different institutions suggest physical exercise and the compound resveratrol, found in red wine, may increase levels of PGC-1 - alpha protein. However, resveratrol has only been found to have benefits as a pill, rather than in wine, as the alcohol counteracts any benefit.

The team suggest injections of the gene would be most beneficial in the early stages of the disease, when the first symptoms appear.

They now hope to explore translating their findings into human treatments, said Dr Sastre.

"We are still years from using this in the clinic. However, in a disease that urgently needs new options for patients, this work provides hope for future therapies."

Dr David Reynolds, Chief Scientific Officer at Alzheimer's Research UK, said: "There are currently no treatments able to halt the progression of damage in Alzheimer's, so studies like this are important for highlighting new and innovative approaches to take us towards that goal.

“This research sets a foundation for exploring gene therapy as a treatment strategy for Alzheimer's disease, but further studies are needed to establish whether gene therapy would be safe, effective and practical to use in people with the disease.

“The findings support PGC-1-alpha as a potential target for the development of new medicines, which is a promising step on the road towards developing treatments for this devastating condition."

Secrets of Age-Related Diseases May Lie in Cellular Targets Identified

Newswise, August 3, 2016— New insights on age-related diseases may hold the key to both delaying aging and, in the process, reducing the occurrence of diseases including cancer.

These findings have been reported by a team from Roswell Park Cancer Institute and Everon Biosciences in the journal Aging.

“The majority of aging theories agree that chronic inflammation associated with secretions by senescent, or aging, cells are the underlying cause of frailty and of multiple age-related diseases, including cancer,” says senior author Andrei Gudkov, PhD, DSci, Senior Vice President for Basic Science at Roswell Park.

“Our study has redefined a subset of these cells as belonging to the category of macrophages. This finding requires a re-interpretation of the mechanisms underlying these cellular targets and a reconsideration of their potential for anti-aging treatments.”

Scientists have named the subtype “senescence-associated macrophages,” or SAMS.

“Our research allowed us to redefine the nature of cells that are sources of poisonous inflammation associated with aging. These cells appear to be not senescent cells, but are actually part of our natural immune system. This finding allows us to identify targets as well as agents that can eradicate senescence-associated macrophages, with the ultimate goal of finding new ways to treat cancer and other age-related diseases,” adds Dr. Gudkov.

How the Brain Improves Motor Control

Error signals in motor cortices drive adaptation in reaching

Newswise, July 29, 2016--Adaptation in reaching -- gradual improvement of motor control in response to a perturbation -- is a central issue in motor neuroscience.However, even the cortical origin of errors that drive adaptation has remained elusive. In a new paper published in Neuron, Inoue, Uchimura and Kitazawa have shown that error signals encoded by motor cortical neurons drive adaptation in reaching.

• The premotor and primary motor cortices encoded visual error in reaching.
• Stimulation to the motor cortices induced trial-by-trial increases in reach errors.
• The error increased opposite to the preferred direction of errors at each location.
• The after-effect of stimulation subsided gradually as in ordinary adaptation.

The neural mechanisms of motor learning and adaptation constitute a central issue in both basic and clinical neuroscience.

However, it is surprising that very little is known about the neural mechanisms underlying the motor learning and adaptation of voluntary arm movements. For example, the origin of cortical error signals that drive adaptation in reaching remains an unanswered question.

A major theory in motor learning (feedback error learning) proposed by Kawato and Gomi (1992) hypothesized that error signals are provided by premotor circuits, including the motor cortical circuits.

However, neuroimaging studies to date have not indicated whether motor cortices encode error signals. Preceding human imaging studies unanimously implicated parietal regions, such as areas 2, 5 and 7, in representing reaching errors.

In the current study, Inoue and colleagues were successful for the first time in inducing trial-by-trial "adaptation" in voluntary arm movements by artificial electrical stimulation of the premotor cortex (PM) or the primary motor cortex (M1).

When the stimulation was terminated, the error (after-effect) did not decrease at once but recovered with practice, as observed after typical adaptation.

The direction of the increase in the error was opposite to the "preferred" error direction of the neuron recorded in the stimulation site. The results clearly show that the motor cortices submit error signals that drive adaptation in voluntary arm movements, as predicted by the feedback error learning scheme.

The novel technique to artificially "improve" a motor skill by a small amount of stimulation would be applicable to performance enhancement in athletes as well as for restoring motor control in neurological patients.

Radar, Bed Sensors Help Health Providers Detect Problems Early

By Molly Peterson

Newswise, June 17, 2016 — Developing and evaluating motion-capture technology to help older adults “age in place” has been the focus of researchers at the University of Missouri for more than a decade.

Previous research has utilized video game technology and various web-cameras to detect health changes in Tiger Place residents. Now, two new studies demonstrate how monitoring walking speed using radar and heart health by utilizing bed sensors help maintain older adults’ health and warn of impeding issues.

“In-home sensors have the ability to capture early signs of health changes before older adults recognize problems themselves,” said Marjorie Skubic, professor of electrical and computer engineering in the MU College of Engineering and director of MU’s Center for Eldercare and Rehabilitation Technology.

“The radar enhances our ability to monitor walking speed and determine if a senior has a fall risk; the bed sensors provide data on heart rate, respiration rate, and overall cardiac activity when a senior is sleeping. Both sensors are non-invasive and don’t require seniors to wear monitoring devices.”

The radar sensors were used to monitor the walking speed of residents in 10 Tiger Place apartments for two years. The radar devices were concealed in a wooden box and placed in the living room of each senior resident. Residents also were provided monthly assessments by professionals to establish whether they were at risk for potential falls. The data collected were then compared to the data captured by the radar.

“Before using radar, we were able to estimate an individual’s walking speed and have an idea of their health status,” said Dominic Ho, co-author and professor of electrical and computer engineering in the MU College of Engineering. “Now, we have data that definitely shows how declines in walking speed can determine the risk for falls.”

Skubic and her team also developed a bed sensor with the ability to continuously monitor heart rate, respiration rate and overall cardiac activity. The bed sensors are made using a hydraulic transducer, which is a flexible tube of water.

The transducer measures the ballistocardiogram, which is the mechanical effect of the blood flowing through the body as a result of the heart beating. In the study, four hydraulic transducers were placed under a mattress to capture cardiac data of the participants.

“Heart disease is a major cause of death for both men and women,” Skubic said.

“Having a sensor continuously monitoring heart rate provides a significant benefit for older adults. The bed sensors also allow us to collect data on sleeping patterns– when people are in bed, how often they are in bed, and how long they are in bed. Similar to walking speed, sleep patterns can detect early signs of illness.”

The radar study and the bed sensor study provide non-invasive monitoring systems that help detect early signs of illness. Skubic and her team are working to investigate other sensors that can further improve very early detection of health changes so that health problems can be addressed while they are still small and manageable.

The study “Estimation of Human Walking Speed by Doppler Radar for Elderly Care” recently was accepted by the Journal of Ambient Intelligence and Smart Environments. Funding for the study was provided by the Agency for Healthcare Research and Quality.

The study “Heart Rate Monitoring Using Hydraulic Bed Sensors Ballistocardiogram” recently was accepted by the Journal of Ambient Intelligence and Smart Environments. Marilyn Rantz, Curators’ Professor Emerita of Nursing in the Sinclair School of Nursing also contributed to the study. Funding for this work was provided by the National Science Foundation. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funding agency.