Wearable Sensors Styled into T-shirts and Face Masks

Caroline Brogan wrote . . . . . . . . .

Imperial researchers have embedded new low-cost sensors that monitor breathing, heart rate, and ammonia into t-shirts and face masks.

Potential applications range from monitoring exercise, sleep, and stress to diagnosing and monitoring disease through breath and vital signs.

Spun from a new Imperial-developed cotton-based conductive thread called PECOTEX, the sensors cost little to manufacture. Just $0.15 produces a metre of thread to seamlessly integrate more than ten sensors into clothing, and PECOTEX is compatible with industry-standard computerised embroidery machines.

First author of the research Fahad Alshabouna, PhD candidate at Imperial’s Department of Bioengineering, said: “The flexible medium of clothing means our sensors have a wide range of applications. They’re also relatively easy to produce which means we could scale up manufacturing and usher in a new generation of wearables in clothing.”

The researchers embroidered the sensors into a face mask to monitor breathing, a t-shirt to monitor heart activity, and textiles to monitor gases like ammonia, a component of the breath that can be used to detect liver and kidney function. The ammonia sensors were developed to test whether gas sensors could also be manufactured using embroidery.

Fahad added: “We demonstrated applications in monitoring cardiac activity and breathing, and sensing gases. Future potential applications include diagnosing and monitoring disease and treatment, monitoring the body during exercise, sleep, and stress, and use in batteries, heaters, and anti-static clothing.”

The research is published in Materials Today.

Seamless sensors

Wearable sensors, like those on smartwatches, let us continuously monitor our health and wellbeing non-invasively. Until now, however, there has been a lack of suitable conductive threads, which explains why wearable sensors seamlessly integrated into clothing aren’t yet widely available.

Enter PECOTEX. Developed and spun into sensors by Imperial researchers, the material is machine washable, and is less breakable and more electrically conductive than commercially available silver-based conductive threads, meaning more layers can be added to create complex types of sensor.

The researchers tested the sensors against commercially available silver-based conductive threads during and after they were embroidered into clothing.

During embroidery, PECOTEX was more reliable and less likely to break, allowing for more layers to be embroidered on top of each other.

After embroidery, PECOTEX demonstrated lower electrical resistance than the silver-based threads, meaning they performed better at conducting electricity.

Lead author Dr Firat Güder, also of the Department of Bioengineering, said: “PECOTEX is high-performing, strong, and adaptable to different needs. It’s readily scalable, meaning we can produce large volumes inexpensively using both domestic and industrial computerised embroidery machines.

“Our research opens up exciting possibilities for wearable sensors in everyday clothing. By monitoring breathing, heart rate, and gases, they can already be seamlessly integrated, and might even be able to help diagnose and monitor treatments of disease in the future.”

The embroidered sensors retained the intrinsic properties of the fabric such as wearability, breathability and feel-on-the-skin. They are also machine washable at up to 30°C.

Next, the researchers will explore new application areas like energy storage, energy harvesting and biochemical sensing for personalised medicine, as well as finding partners for commercialisation.

Source: Imperial College

 

 

 

 

Researchers Discover How Prostate Cancer May Begin

A new study published today reveals that the prostate as a whole, including cells that appear normal, is different in men with prostate cancer.

It suggests that tissue cells throughout the whole prostate are primed and ready to develop prostate cancer.

This means that it may be better to treat the whole prostate rather than only the areas in the prostate that have cancer.

The team hope their work could help scientists better understand the causes of prostate cancer, and even prevent it altogether.

Lead researcher Prof Daniel Brewer, from UEA’s Norwich Medical School, said: “Prostate cancer is the most common cancer in men and kills one man every 45 minutes in the UK.

“Often, when men are diagnosed with prostate cancer, groups of cancer cells can be found in more than one location within the prostate.

“We wanted to know if this is because of changes in ‘normal’ prostate cells throughout the prostate.”

Cancer is driven by changes in DNA, the genetic code of life, that appear in every cell. The team studied the DNA code in 121 tissue samples from 37 men with and without prostate cancer.

Prof Brewer said: “The samples we studied included tissue that comes from the cancer and tissue from elsewhere in the prostate, which looks normal down the microscope.

“This produces a massive amount of data and by applying a large amount of computer power we can determine the differences that have occurred in the DNA, giving us insight into how the cancer grows.

“We found that ‘normal’ prostate cells in men who had prostate cancer had more mutations (changes in the DNA) than ‘normal’ prostate cells from men without prostate cancer.

“Based on the genetics of the samples analysed, we created maps to understand where the different mutations occurred. And we showed that in most men, the mutations in normal cells are different to mutations in cancer cells.

“The ‘normal’ prostate cells in men who have prostate cancer appear to provide a beneficial environment for prostate cancer cells to develop and grow.

“In other words, the whole prostate is primed and ready to develop prostate cancer driven by an, as yet unknown, biological process.

“This work has improved our knowledge of how prostate cancer first starts to develop and might one day give us clues as to how to prevent or treat it.

“And it shows that it may be better to treat the whole prostate rather than only the areas in the prostate that have cancer,” he added.

Dr Hayley Luxton, Senior Research Impact Manager at Prostate Cancer UK, said: “This exciting new research shows for the first time how normal cells in the prostate can facilitate the growth and spread of prostate cancer.

“The researchers found that normal prostate cells in men with prostate cancer have specific genetic changes that make them act like a rich compost, providing the perfect environment for prostate cancer cells to grow and develop. These findings give us important new insights into the early development of prostate cancer, which might one day give us clues as to how to prevent it.”

The study is published in the journal Molecular Oncology.

Source: University of East Anglia

 

 

 

 

How Does What We Eat Affect Our Healthspan and Longevity? It’s a Complex Dynamic System

The answer to a relatively concise question – how does what we eat affect how we age — is unavoidably complex, according to a new study at the Butler Columbia Aging Center at Columbia University Mailman School of Public Health. While most analyses had been concerned with the effects of a single nutrient on a single outcome, a conventional, unidimensional approach to understanding the effects of diet on health and aging no longer provides us with the full picture: healthy diet needs to be considered based on the balance of ensembles of nutrients, rather than by optimizing a series of nutrients one at a time. Until now little was known about how normal variation in dietary patterns in humans affects the aging process. The findings are published online in the journal BMC Biology.

“Our ability to understand the problem has been complicated by the fact that both nutrition and the physiology of aging are highly complex and multidimensional, involving a high number of functional interactions,” said Alan Cohen, PhD, associate professor of environmental health sciences at Columbia Mailman School. “This study therefore provides further support to the importance of looking beyond ‘a single nutrient at a time’ as the one size fits all response to the age-old question of how to live a long and healthy life.” Cohen also points that the results are also concordant with numerous studies highlighting the need for increased protein intake in older people, in particular, to offset sarcopenia and decreased physical performance associated with aging.

Using multidimensional modelling techniques to test the effects of nutrient intake on physiological dysregulation in older adults, the researchers identified key patterns of specific nutrients associated with minimal biological aging. “Our approach presents a roadmap for future studies to explore the full complexity of the nutrition-aging landscape,” observed Cohen, who is also affiliated with the Butler Columbia Aging Center.

The researchers analyzed data from 1560 older men and women, aged 67-84 years selected randomly between November 2003 and June 2005 from the Montreal, Laval, or Sherbrooke areas in Quebec, Canada, who were re-examined annually for 3 years and followed over four years to assess on a large-scale how nutrient intake associates with the aging process.

Aging and age-related loss of homeostasis (physiological dysregulation) were quantified via the integration of blood biomarkers. The effects of diet used the geometric framework for nutrition, applied to macronutrients and 19 micronutrients/nutrient subclasses. Researchers fitted a series of eight models exploring different nutritional predictors and adjusted for income, education level, age, physical activity, number of comorbidities, sex, and current smoking status.

Four broad patterns were observed:

  • The optimal level of nutrient intake was dependent on the aging metric used. Elevated
    protein intake improved/depressed some ageing parameters, whereas elevated carbohydrate levels improved/depressed others;

  • There were cases where intermediate levels of nutrients performed well for many outcomes (i.e. arguing against a simple more/less is better perspective);
  • There is broad tolerance for nutrient intake patterns that don’t deviate too much from norms
    (‘homeostatic plateaus’).

  • Optimal levels of one nutrient often depend on levels of another (e.g. vitamin E and vitamin C). Simpler analytical approaches are insufficient to capture such associations.

The research team also developed an interactive tool to allow users to explore how different combinations of micronutrients affect different aspects of aging.

The results of this study are consistent with earlier experimental work in mice showing that high-protein diets may accelerate aging earlier in life, but are beneficial at older ages.

“These results are not experimental and will need to be validated in other contexts. Specific findings, such as the salience of the combination of vitamin E and vitamin C, may well not replicate in other studies. But the qualitative finding that there are no simple answers to optimal nutrition is likely to hold up: it was evident in nearly all our analyses, from a wide variety of approaches, and is consistent with evolutionary principles and much previous work,” said Cohen.

Source: Columbia University

 

 

 

 

Not Just Obesity: Everyone May Have a ‘Fat Threshold’ for Type 2 Diabetes

Denise Mann wrote . . . . . . . . .

If you are one of the millions of people with type 2 diabetes, losing weight can help reverse the blood sugar disease even if you aren’t overweight or obese, new research reveals.

Here’s the proof: 70% of people with type 2 diabetes who were a normal weight during the study went into remission after they lost roughly 10% of their body weight.

Type 2 diabetes is the form of the disease most closely tied to obesity, yet around 15% of patients aren’t overweight or obese. They may, however, be pushing their personal “fat threshold.”

“Everyone has a level at which they can no longer store fat safely inside the body — that is determined by genes,” said study author Dr. Roy Taylor, a professor of medicine and metabolism at Newcastle University in the United Kingdom.

“If you can’t store more fat under your skin, the fat spills over and starts building up inside the liver,” he explained. When this happens, too much fat goes to the rest of the body, including the pancreas. Insulin-producing cells in the pancreas then stop working correctly, triggering diabetes.

“Type 2 diabetes happens to those who are susceptible, but only when they have become too heavy for their own body,” Taylor noted.

No test can say “you have exceeded your personal fat threshold” yet, but some blood markers of stress in fat may one day prove to be a reliable way to measure that threshold, he added.

For the study, 20 people with diabetes who weren’t overweight or obese ate 800 calories a day (from low-calorie soups and shakes and non-starchy vegetables) for two to four weeks. They did these three times, with each cycle followed by four to six weeks of weight maintenance.

They lost about 10.7% of their weight overall, and kept it off for six months to a year.

Fourteen people achieved diabetes remission, based on their HbA1c levels. This provides a snapshot of average blood glucose levels over several weeks. Folks in remission no longer needed to take diabetes medication.

This mirrors what is seen among people with type 2 diabetes who are overweight or obese and lose weight, Taylor said.

MRI scans showed declines of fat inside the liver and pancreas that were in line with what is seen in people without diabetes. Specifically, fat in the pancreas fell from an average of 5.8% to 4.3% among people with diabetes, and the activity of the insulin-producing cells returned to normal.

It doesn’t take much extra fat to thwart the activity of insulin-producing cells in the pancreas. “You only need an extra half gram of fat in the pancreas to prevent normal insulin production,” Taylor said.

“Regardless of body mass index [BMI], people diagnosed with type 2 diabetes have more fat inside the body than they can cope with,” he said. “There is a good chance of remission if they can lose around 10% of their starting weight.”

The study was presented this week at the European Association for the Study of Diabetes meeting in Stockholm. Findings presented at medical meetings should be considered preliminary until published in a peer-reviewed journal.

The relationship between obesity and diabetes is consistent and strong, said Dr. Scott Kahan, director of the National Center for Weight and Wellness, in Washington, D.C.

“Even exceedingly small amounts of weight gain or excess weight can increase the risk for type 2 diabetes significantly — even in people who are relatively thin,” Kahan noted.

The good news is that small weight losses, often on the order of just a few pounds, can improve blood sugar control and diabetes risk.

“This study further supports the importance of weight management for the prevention and treatment of type 2 diabetes, and strongly suggests that weight management guidance, support and intervention will likely be valuable even in persons with only small amounts of excess weight,” Kahan said.

Source: HealthDay

 

 

 

 

COVID-19 Infections Increase Risk of Long-term Brain Problems


Enlarge image . . . . .

Kristina Sauerwein wrote . . . . . . . . .

A comprehensive analysis of federal data by researchers at Washington University School of Medicine in St. Louis shows people who have had COVID-19 are at an elevated risk of developing neurological conditions within the first year after infection. Movement disorders, memory problems, strokes and seizures are among the complications.

If you’ve had COVID-19, it may still be messing with your brain. Those who have been infected with the virus are at increased risk of developing a range of neurological conditions in the first year after the infection, new research shows. Such complications include strokes, cognitive and memory problems, depression, anxiety and migraine headaches, according to a comprehensive analysis of federal health data by researchers at Washington University School of Medicine in St. Louis and the Veterans Affairs St. Louis Health Care system.

Additionally, the post-COVID brain is associated with movement disorders, from tremors and involuntary muscle contractions to epileptic seizures, hearing and vision abnormalities, and balance and coordination difficulties as well as other symptoms similar to what is experienced with Parkinson’s disease.

The findings are published in Nature Medicine.

“Our study provides a comprehensive assessment of the long-term neurologic consequences of COVID-19,” said senior author Ziyad Al-Aly, MD, a clinical epidemiologist at Washington University. “Past studies have examined a narrower set of neurological outcomes, mostly in hospitalized patients. We evaluated 44 brain and other neurologic disorders among both nonhospitalized and hospitalized patients, including those admitted to the intensive care unit. The results show the devastating long-term effects of COVID-19. These are part and parcel of long COVID. The virus is not always as benign as some people think it is.”

Overall, COVID-19 has contributed to more than 40 million new cases of neurological disorders worldwide, Al-Aly said.

Other than having a COVID infection, specific risk factors for long-term neurological problems are scarce. “We’re seeing brain problems in previously healthy individuals and those who have had mild infections,” Al-Aly said. “It doesn’t matter if you are young or old, female or male, or what your race is. It doesn’t matter if you smoked or not, or if you had other unhealthy habits or conditions.”

Few people in the study were vaccinated for COVID-19 because the vaccines were not yet widely available during the time span of the study, from March 2020 through early January 2021. The data also predates delta, omicron and other COVID variants.

A previous study in Nature Medicine led by Al-Aly found that vaccines slightly reduce — by about 20% — the risk of long-term brain problems. “It is definitely important to get vaccinated but also important to understand that they do not offer complete protection against these long-term neurologic disorders,” Al-Aly said.

The researchers analyzed about 14 million de-identified medical records in a database maintained by the U.S. Department of Veterans Affairs, the nation’s largest integrated health-care system. Patients included all ages, races and sexes.

They created a controlled data set of 154,000 people who had tested positive for COVID-19 sometime from March 1, 2020, through Jan. 15, 2021, and who had survived the first 30 days after infection. Statistical modeling was used to compare neurological outcomes in the COVID-19 data set with two other groups of people not infected with the virus: a control group of more than 5.6 million patients who did not have COVID-19 during the same time frame; and a control group of more than 5.8 million people from March 2018 to December 31, 2019, long before the virus infected and killed millions across the globe.

The researchers examined brain health over a year-long period. Neurological conditions occurred in 7% more people with COVID-19 compared with those who had not been infected with the virus. Extrapolating this percentage based on the number of COVID-19 cases in the U.S., that translates to roughly 6.6 million people who have suffered brain impairments associated with the virus.

Memory problems — colloquially called brain fog — are one of the most common brain-related, long-COVID symptoms. Compared with those in the control groups, people who contracted the virus were at a 77% increased risk of developing memory problems. “These problems resolve in some people but persist in many others,” Al-Aly said. “At this point, the proportion of people who get better versus those with long-lasting problems is unknown.”

Interestingly, the researchers noted an increased risk of Alzheimer’s disease among those infected with the virus. There were two more cases of Alzheimer’s per 1,000 people with COVID-19 compared with the control groups. “It’s unlikely that someone who has had COVID-19 will just get Alzheimer’s out of the blue,” Al-Aly said. “Alzheimer’s takes years to manifest. But what we suspect is happening is that people who have a predisposition to Alzheimer’s may be pushed over the edge by COVID, meaning they’re on a faster track to develop the disease. It’s rare but concerning.”

Also compared to the control groups, people who had the virus were 50% more likely to suffer from an ischemic stroke, which strikes when a blood clot or other obstruction blocks an artery’s ability to supply blood and oxygen to the brain. Ischemic strokes account for the majority of all strokes, and can lead to difficulty speaking, cognitive confusion, vision problems, the loss of feeling on one side of the body, permanent brain damage, paralysis and death.

“There have been several studies by other researchers that have shown, in mice and humans, that SARS-CoV-2 can attack the lining of the blood vessels and then then trigger a stroke or seizure,” Al-Aly said. “It helps explain how someone with no risk factors could suddenly have a stroke.”

Overall, compared to the uninfected, people who had COVID-19 were 80% more likely to suffer from epilepsy or seizures, 43% more likely to develop mental health disorders such as anxiety or depression, 35% more likely to experience mild to severe headaches, and 42% more likely to encounter movement disorders. The latter includes involuntary muscle contractions, tremors and other Parkinson’s-like symptoms.

COVID-19 sufferers were also 30% more likely to have eye problems such as blurred vision, dryness and retinal inflammation; and they were 22% more likely to develop hearing abnormalities such as tinnitus, or ringing in the ears.

“Our study adds to this growing body of evidence by providing a comprehensive account of the neurologic consequences of COVID-19 one year after infection,” Al-Aly said.

Long COVID’s effects on the brain and other systems emphasize the need for governments and health systems to develop policy, and public health and prevention strategies to manage the ongoing pandemic and devise plans for a post-COVID world, Al-Aly said. “Given the colossal scale of the pandemic, meeting these challenges requires urgent and coordinated — but, so far, absent — global, national and regional response strategies,” he said.

Source: Washington University School of Medicine