Rising health care prices in the U.S. are leading employers outside the health care sector to reduce their payroll and decrease their number of employees, according to a new study co-authored by Yale economist Zack Cooper.
The study, published June 24 as a working paper by the National Bureau of Economic Research (NBER), found that when health care prices increased, non-health care employers responded by reducing their payroll and cutting the jobs of middle-class workers. For the average county, a 1% increase in health care prices would reduce aggregate income in the area by approximately $8 million annually.
The study was conducted by a team of leading economists from Yale, the University of Chicago, the University of Wisconsin-Madison, Harvard University, the U.S. Internal Revenue Service (IRS), and the U.S. Department of the Treasury.
“When health care prices go up, jobs outside the health care sector go down,” said Cooper, an associate professor of health policy at the Yale School of Public Health and of economics in the Faculty of Arts and Sciences. “It’s broadly understood that employer-sponsored health insurance creates a link between health care markets and labor markets. Our research shows that middle- and lower-income workers are shouldering rising health care prices, and in many cases, it’s costing them their jobs. Bottom line: Rising health care costs are increasing economic inequality.”
To better understand how rising health care prices affect labor market outcomes, the researchers brought together insurance claims data on approximately a third of adults with employer-sponsored insurance, health insurance premium data from the U.S. Department of Labor, and IRS data from every income tax return filed in the United States between 2008 and 2017. They then used these data to trace out how an increase in health care prices — such as a $2,000 increase on a $20,000 hospital bill — flows through to health spending, insurance premiums, employer payrolls, income and unemployment in counties, and the tax revenue collected by the federal government.
“Many think that it’s insurers or employers who bear the burden of rising health care prices. We show that it’s really the workers themselves who are impacted,” said Zarek Brot-Goldberg, an assistant professor at the Harris School of Public Policy at the University of Chicago. “It’s vital to understand that rising health care prices aren’t just impacting patients. Rising prices are hurting the employment outcomes for workers who never went to the hospital.”
For the new study, the authors used hospital mergers as a vehicle to assess the effect of price increases. From 2000 to 2020, there were over 1,000 hospital mergers among the approximately 5,000 U.S. hospitals. In past work, the authors found that approximately 20% of hospital mergers should have been expected to raise prices by lessening competition, according to merger guidelines from the Department of Justice and the Federal Trade Commission. These mergers, on average, raised prices by 5%.

“We can use our analysis to estimate the effect of hospital mergers,” said Stuart Craig, an assistant professor at the University of Wisconsin-Madison Business School. “Our results show that a hospital merger that raised prices by 5% would result in $32 million in lost wages, 203 lost jobs, a $6.8 million reduction in federal tax revenue, and a death from suicide or overdose of a worker outside the health sector.”
The study also showed that because rising health care prices leads firms to let go of workers, a knock-on effect of hospital mergers is that they lead to increases in government spending on unemployment insurance and reductions in the tax revenue collected by the federal government.
“It’s vital to point out that hospital mergers raise spending by the federal government and lower tax revenue at the same time,” said Cooper. “When prices in the U.S health sector rise, it’s actually a net negative for the economy. It’s leading to fewer jobs and precipitating all the consequences we associate with workers becoming unemployed.”
Other authors of the study were Lev Klarnet from Harvard University, Ithai Lurie from U.S. Department of Treasury, and Corbin Miller from the U.S. Internal Revenue Service.

In a new article, researchers at the University of Illinois Chicago debunk four common myths about the safety of intermittent fasting.
Intermittent fasting has become an increasingly popular way to lose weight without counting calories. And a large body of research has shown it’s safe. Still, several myths about fasting have gained traction among clinicians, journalists and the general public: that fasting can lead to a poor diet or loss of lean muscle mass, cause eating disorders, or decrease sex hormones.
In a new commentary in Nature Reviews Endocrinology, UIC researchers debunk each of these. They base their conclusions on clinical studies, some of which they conducted and some done by others.
“I’ve been studying intermittent fasting for 20 years, and I’m constantly asked if the diets are safe,” said lead author Krista Varady, professor of kinesiology and nutrition at UIC. “There is a lot of misinformation out there. However, those ideas are not based on science; they’re just based on personal opinion.”
There are two main types of intermittent fasting. With alternate-day eating, people alternate between days of eating a very small number of calories and days of eating what they want. With time-restricted eating, people eat what they want during a four- to 10-hour window each day, then don’t eat during the rest of the day. The researchers conclude both types are safe despite the popular myths.
Here’s a look at their conclusions:
Intermittent fasting does not lead to a poor diet: The researchers point to studies showing the intake of sugar, saturated fat, cholesterol, fiber, sodium and caffeine do not change during fasting compared with before a fast. And the percentage of energy consumed in carbohydrates, protein and fat doesn’t change, either.

Intermittent fasting does not cause eating disorders: None of the studies show that fasting caused participants to develop an eating disorder. However, all the studies screened out participants who had a history of eating disorders, and the researchers say that those with a history of eating disorders should not try intermittent fasting. They also urge pediatricians to be cautious when monitoring obese adolescents if they start fasting, because this group has a high risk of developing eating disorders.
Intermittent fasting does not cause excessive loss of lean muscle mass: The studies show that people lose the same amount of lean muscle mass whether they’re losing weight by fasting or with a different diet. In both cases, resistance training and increased protein intake can counteract the loss of lean muscle.
Intermittent fasting does not affect sex hormones: Despite concerns about fertility and libido, neither estrogen, testosterone nor other related hormones are affected by fasting, the researchers said.
The other authors of the article are Vanessa Oddo and Sofia Cienfuegos at UIC and Shuhao Lin, formerly at UIC and now at the Mayo Clinic.

Researchers at the University of Toronto have harnessed a bacterial immune defense system, known as CRISPR, to efficiently and precisely control the process of RNA splicing.
The technology opens the door to new applications, including systematically interrogating the functions of parts of genes and correcting splicing deficiencies that underlie numerous diseases and disorders.
“Almost all human genes produce RNA transcripts that undergo the process of splicing, whereby coding segments, called exons, are joined together and non-coding segments, called introns, are removed and typically degraded,” said Jack Daiyang Li, first author on the study and PhD student of molecular genetics, working in the labs of Benjamin Blencowe and Mikko Taipale at U of T’s Donnelly Centre for Cellular and Biomolecular Research.
Exons can be alternatively spliced, such that the regulation and function of the approximately 20,000 human genes that encode proteins are greatly diversified, allowing the development and functional specialization of different types of cells.
However, it is unclear what most exons or introns do, and the mis-regulation of normal alternative splicing patterns is a frequent cause or contributing factor to various diseases, such as cancers and brain disorders. However, existing methods that allow for the precise and efficient manipulation of splicing have been lacking.
In the new research study, a catalytically-deactivated version of an RNA targeting CRISPR protein, referred to as dCasRx, was joined to more than 300 splicing factors to discover a fusion protein, dCasRx-RBM25. This protein is capable of activating or repressing alternative exons in an efficient and targeted manner.
“Our new effector protein activated alternative splicing of around 90 percent of tested target exons,” said Li. “Importantly, it is capable of simultaneously activating and repressing different exons to examine their combined functions.”
This multi-level manipulation will facilitate the experimental testing of functional interactions between alternatively spliced variants from genes to determine their combined roles in critical developmental and disease processes.

“Our new tool makes possible a broad range of applications, from studying gene function and regulation, to potentially correcting splicing defects in human disorders and diseases,” said Blencowe, principal investigator on the study, Canada Research Chair in RNA Biology and Genomics, Banbury Chair in Medical Research and professor of molecular genetics at the Donnelly Centre and the Temerty Faculty of Medicine.
“We have developed a versatile engineered splicing factor that outperforms other available tools in the targeted control of alternative exons,” said Taipale, also principal investigator on the study, Canada Research Chair in Functional Proteomics and Proteostasis, Anne and Max Tanenbaum Chair in Molecular Medicine and associate professor of molecular genetics at the Donnelly Centre and Temerty Medicine. “It is also important to note that target exons are perturbed with remarkably high specificity by this splicing factor, which alleviates concerns about possible off-target effects.”
The researchers now have a tool in hand to systematically screen alternative exons to determine their roles in cell survival, cell type specification and gene expression.
When it comes to the clinic, the splicing tool has potential to be used to treat numerous human disorders and diseases, such as autism and cancers, in which splicing is often disrupted.
This research was supported by the Canadian Institutes of Health Research and the Simons Foundation.

Magnetic stimulation therapy may assist patients for whom antidepressants are ineffective. Researchers from the University of Helsinki and Stanford University have developed more precise methods that could, in the future, help to develop individually tailored magnetic stimulation therapies for depression.
Not all patients with depression respond to medication. Two recently published studies provide additional information on how an alternative treatment, transcranial magnetic stimulation (TMS), could be further enhanced. TMS differs from electroconvulsive therapy (ECT), which is also used to treat depression.
Researchers from the University of Helsinki and Stanford University investigated which factors in targeting TMS influence the brain’s electrical responses. They examined the behavior of a specific electrophysiological marker. This marker could potentially be used as a biomarker in the future to measure the efficacy of TMS treatment and thus help target and tailor the therapy.
“Magnetic stimulation is an effective treatment for patients whose depression is not alleviated by medication. However, currently, about half of these patients do not receive significant help from TMS. The biomarker we studied may help predict who will benefit from the therapy. In the future, it may also be possible to tailor the treatment individually,” says postdoctoral researcher Juha Gogulski from Stanford, University of Helsinki and Aalto University.
Individual optimization is worthwhile
The first study addressed an electrophysiological marker that describes cortical excitability and the sources of error affecting its measurement. Researchers studied healthy subjects to determine how magnetic stimulation targeted to the prefrontal cortex and the angle of the stimulation coil affected cortical excitability, that is, the responses measured on an electroencephalogram (EEG) immediately after the stimulation pulse.
“The results showed that targeting of the stimulation coil in different parts of the prefrontal cortex significantly affected the quality of electrical responses. Additionally, we found indications that individual optimization of the stimulation site and coil angle may further improve the quality of this metric,” says Gogulski.

The second study dealt with the reliability of the same electrophysiological marker in the prefrontal cortex. The study revealed that the most significant factor affecting reliability was the stimulation site.
“Before we can develop personalized TMS therapy, we must ensure that the excitability of the prefrontal cortex can be measured as accurately as possible in individual patients to be able to monitor how TMS treatment changes brain excitability. Determining reliability is also essential before this type of biomarker can be applied clinically,” says Gogulski.
Potential benefits are significant, more research needed
Magnetic stimulation already helps some people with depression, but according to Gogulski, the effectiveness of TMS therapy varies between individuals. More precisely tailored treatment might improve outcomes.
“There are many possible factors in TMS therapy that could be used for individual tailoring, such as the stimulation site, the number and frequency of pulses, the intensity of the stimulation, and the number of treatment sessions. The side effects of TMS therapy are minimal, with the most common being a temporary, mild headache.”
According to Gogulski, what makes the new studies significant is that this detailed systematic mapping of the electrical responses of the prefrontal cortex and their reliability has not been done before. The researchers hope that in the future, the effectiveness of TMS therapy can be monitored by measuring the brain’s electrical responses during treatment. Based on these measurements, it might be possible to fine-tune the stimulation if necessary, even during the treatment.
“The results of both studies will be utilized in the future when designing individual brain stimulation therapies based on electrical biomarkers. However, more research is needed before new treatment methods can be implemented,” says Gogulski.

A study of 17 commonly used synthetic ‘forever chemicals’ has shown that these toxic substances can readily be absorbed through human skin.
New research, published today in Environment International proves for the first time that a wide range of PFAS (perfluoroalkyl substances) — chemicals which do not break down in nature — can permeate the skin barrier and reach the body’s bloodstream.
PFAS are used widely in industries and consumer products from school uniforms to personal care products because of their water and stain repellent properties. While some substances have been banned by government regulation, others are still widely used and their toxic effects have not yet been fully investigated.
PFAS are already known to enter the body through other routes, for example being breathed in or ingested via food or drinking water, and they are known to cause adverse health effects such as a lowered immune response to vaccination, impaired liver function and decreased birth weight.
It has commonly been thought that PFAS are unable to breach the skin barrier, although recent studies have shown links between the use of personal care products and PFAS concentrations in human blood and breast milk. The new study is the most comprehensive assessment yet undertaken of the absorption of PFAS into human skin and confirms that most of them can enter the body via this route.
Lead author of the study, Dr Oddný Ragnarsdóttir carried out the research while studying for her PhD at the University of Birmingham. She explained: “The ability of these chemicals to be absorbed through skin has previously been dismissed because the molecules are ionised. The electrical charge that gives them the ability to repel water and stains was thought to also make them incapable of crossing the skin membrane.
“Our research shows that this theory does not always hold true and that, in fact, uptake through the skin could be a significant source of exposure to these harmful chemicals.”
The researchers investigated 17 different PFAS. The compounds selected were among those most widely used, and most widely studied for their toxic effects and other ways through which humans might be exposed to them. Most significantly, they correspond to chemicals regulated by the EU’s Drinking Water Directive.

In their experiments the team used 3D human skin equivalent models — multilayered laboratory grown tissues that mimic the properties of normal human skin, meaning the study could be carried out without using any animals. They applied samples of each chemical to measure what proportions were absorbed, unabsorbed, or retained within the models.
Of the 17 PFAS tested, the team found 15 substances showed substantial dermal absorption — at least 5% of the exposure dose. At the exposure doses examined, absorption into the bloodstream of the most regulated PFAS (perfluoro octanoic acid (PFOA)) was 13.5% with a further 38% of the applied dose retained within the skin for potential longer-term uptake into the circulation.
The amount absorbed seemed to correlate with the length of the carbon chain within the molecule. Substances with longer carbon chains showed lower levels of absorption, while compounds with shorter chains that were introduced to replace longer carbon chain PFAS like PFOA, were more easily absorbed. Absorption of perfluoro pentanoic acid for example was four times that of PFOA at 59%.
Study co-author, Dr Mohamed Abdallah, said “our study provides first insight into significance of the dermal route as pathway of exposure to a wide range of forever chemicals. Given the large number of existing PFAS, it is important that future studies aim to assess the risk of broad ranges of these toxic chemicals, rather than focusing on one chemical at a time.”
Study co-author, Professor Stuart Harrad, of the University of Birmingham’s School of Geography, Earth and Environmental Sciences, added: “This study helps us to understand how important exposure to these chemicals via the skin might be and also which chemical structures might be most easily absorbed. This is important because we see a shift in industry towards chemicals with shorter chain lengths because these are believed to be less toxic — however the trade-off might be that we absorb more of them, so we need to know more about the risks involved.”

A recent study led by researchers at Tampere University investigated whether a transglutaminase 2 inhibitor has potential as a drug to treat celiac disease. Previous tissue studies have shown that the ZED1227 transglutaminase 2 inhibitor prevents gluten-induced intestinal damage. The results of the new study, based on an analysis of the molecular activity of more than 10,000 genes, provide very strong evidence that the first successful drug to treat celiac disease may be at hand.
Consuming gluten-containing cereals, i.e. wheat, barley, and rye, leads to an abnormal immune response in the small intestine and the development of celiac disease in up to 2% of the population. Currently, no drug therapy exists, and a life-long strict gluten-free diet is the only available treatment. However, symptoms and intestinal damage caused by hidden gluten can occur even in patients who are following a strict diet.
“Blood antibody tests and traditional tissue tests do not necessarily tell the whole truth about the condition of the intestinal mucosa. Our previous studies have shown that even though the intestinal tissue may look healthy, it can still have a molecular ‘scar’ and, for example, the expression of genes promoting the absorption of vitamins and trace elements may be deficient. This probably explains the often-observed deficiencies of trace elements in celiac patients despite a gluten-free diet,” says Keijo Viiri, Adjunct Professor of Cellular and Molecular Biology.
In a previous tissue study coordinated by Professor Emeritus Markku Mäki from Tampere University, the ZED1227 transglutaminase 2 inhibitor was shown to prevent gluten-induced intestinal damage in patients with celiac disease. However, its mechanisms of action are not fully understood yet. A new international study led by Tampere University analysed molecular mechanisms to investigate whether ZED1227 is a potential drug candidate for treating celiac disease.
The study evaluated the efficacy and molecular mechanisms of ZED1227 by analysing intestinal biopsies collected from celiac patients. The biopsies were taken after a long-term gluten-free diet and again after six weeks of gluten exposure, during which the patients were given 3 grams of gluten per day. At the same time, some patients were given a daily dose of 100 milligrams of ZED1227 and others a placebo.
“By measuring gene activity, we found that orally ingested ZED1227 effectively prevented gluten-induced intestinal mucosal damage and inflammation. In the drug group, the activity of the genes responsible for the absorption of nutrients and trace elements also returned to the pre-gluten exposure level,” Viiri says.
In the intestines of celiac patients, inflammation and mucosal damage occur through several cellular and molecular events when gluten binds to human leukocyte antigen (HLA) molecules. However, gluten can only bind to HLA when the small intestine’s transglutaminase 2 enzyme first chemically modifies, i.e. deamidates, the structure of gluten. The effectiveness of ZED1227 is based on its ability to prevent deamidation.
“It is still premature to say that ZED1227 will be the celiac medicine of the future eliminating the need for a gluten-free diet. However, it is a strong drug candidate that could potentially be used in conjunction with a gluten-free diet. If or when the ZED1227 medicine becomes available, it would also be useful to apply personalised medicine especially to celiac patients with the high-risk HLA genotype,” Viiri points out.

Whether it’s physical phenomena, share prices or climate models — many dynamic processes in our world can be described mathematically with the aid of partial differential equations. Thanks to stochastics — an area of mathematics which deals with probabilities — this is even possible when randomness plays a role in these processes. Something researchers have been working on for some decades now are so-called stochastic partial differential equations. Working together with other researchers, Dr. Markus Tempelmayr at the Cluster of Excellence Mathematics Münster at the University of Münster has found a method which helps to solve a certain class of such equations. The results have been published in the journal Inventiones Mathematicae.
The basis for their work is a theory by Prof. Martin Hairer, recipient of the Fields Medal, developed in 2014 with international colleagues. It is seen as a great breakthrough in the research field of singular stochastic partial differential equations. “Up to then,” Markus Tempelmayr explains, “it was something of a mystery how to solve these equations. The new theory has provided a complete ‘toolbox’, so to speak, on how such equations can be tackled.”
The problem, Tempelmayr continues, is that the theory is relatively complex, with the result that applying the ‘toolbox’ and adapting it to other situations is sometimes difficult. “So, in our work, we looked at aspects of the ‘toolbox’ from a different perspective and found and proved a method which can be used more easily and flexibly.” The study, in which Markus Tempelmayr was involved as a doctoral student under Prof. Felix Otto at the Max Planck Institute for Mathematics in the Sciences, published in 2021 as a pre-print. Since then, several research groups have successfully applied this alternative approach in their research work.
Stochastic partial differential equations can be used to model a wide range of dynamic processes, for example the surface growth of bacteria, the evolution of thin liquid films, or interacting particle models in magnetism. However, these concrete areas of application play no role in basic research in mathematics as, irrespective of them, it is always the same class of equations which is involved. The mathematicians are concentrating on solving the equations in spite of the stochastic terms and the resulting challenges such as overlapping frequencies which lead to resonances.
Various techniques are used for this purpose. In Hairer’s theory, methods are used which result in illustrative tree diagrams. “Here, tools are applied from the fields of stochastic analysis, algebra and combinatorics,” explains Markus Tempelmayr. He and his colleagues selected, rather, an analytical approach. What interests them in particular is the question of how the solution of the equation changes if the underlying stochastic process is changed slightly.
The approach they took was not to tackle the solution of complicated stochastic partial differential equations directly, but, instead, to solve many different simpler equations and prove certain statements about them. “The solutions of the simple equations can then be combined — simply added up, so to speak — to arrive at a solution for the complicated equation which we’re actually interested in.” This knowledge is something which is used by other research groups who themselves work with other methods.

West Virginia University research illustrates that American Heart Association and American Stroke Association guidelines are effective at speeding up hospitals’ response times for stroke treatment and can be mastered even by members of “ad hoc” medical teams that assemble rapidly on the fly.
Swift stroke treatment is critical, so when a stroke patient arrives at an emergency room, specialists from across hospital departments — EMS, neurologists, pharmacists, physicians, nurses, radiologists and technicians — rush to coordinate a team response. AHA and ASA guidelines, or “best practices,” put specific limits on how much time can optimally elapse between the onset of ischemic stroke, in which blood flow to the brain is blocked, and subsequent events like arrival at the hospital and delivery of an infusion.
However, experts have questioned whether the communication of those best practices helps medical teams that assemble temporarily and whose members don’t typically collaborate. A Journal of Operations Management paper by WVU John Chambers College of Business and Economics associate professor Bernardo Quiroga and coauthors answers that question using data about more than 8,000 patients who received stroke care at a large hospital (not WVU Hospitals) between 2009 and 2017.
“‘Time is brain’ for stroke victims,” Quiroga explained. “Blocked blood flow to the brain kills almost two million neurons a minute, so your life or ability to walk or talk hinges on how quickly multiple professionals coordinate to restore blood flow. If you’re lucky, you’re treated within the first hour of symptom onset. Better yet, you receive a shot of Tissue Plasminogen Activator, which dissolves clots. TPA works better the earlier it’s given and usually isn’t effective after 4.5 hours.”
In 2010, the AHA and ASA launched Target: Stroke, a program that identifies stroke care best practices and standardizes each step in the process. Participating hospitals reduced median treatment times from 79 minutes in 2009 to 51 minutes in 2017, but it wasn’t clear if that improvement was driven by adherence to best practices or by clinicians learning through repetition as they handled more stroke cases.
To figure that out, the researchers investigated whether repeated “learning by doing” decreased the hospital’s stroke care time. Then, they evaluated whether deliberate, “induced” learning and implementation of AHA/ASA best practices decreased the time further.
Learning through repetition worked. The more strokes the hospital treated, the faster it responded. For each doubling of cumulative stroke alerts, “door-to-needle time” — the time to get patients from the hospital door to a TPA infusion — decreased by 10.2%.

Best practices also worked. Specifically, the researchers examined two best practices: the Helsinki Model protocol, which directs that EMS staff keep stroke patients on the stretcher for transport to the CT room rather than transferring them to ER beds; and the Rapid Administration of TPA protocol, which requires the pharmacist to be in the CT room with TPA before completion of the CT scan. Those protocols significantly reduced the hospital’s door-to-needle time beyond improvements from repetition-based learning.
According to Quiroga’s coauthor and former PhD student Brandon Lee, that matters because it demonstrates the efficacy of best practices and shows ad hoc teams learning guidelines and implementing them long-term.
However, Lee emphasized the importance of the presence of the hospital’s stroke advisory committee, which set targets, evaluated stroke teams’ performances and gave feedback.
Without similar “countermeasures to organizational forgetting,” Quiroga acknowledged that best practices aren’t always sustainable, especially on ad hoc teams.
“In the case of the best practice indicated by the Helsinki Model, compliance is difficult because the hospital needs to coordinate with multiple independent EMS systems. Some EMS providers may be reluctant to commit resources to extended time in the CT room, and EMS staff turnover may lead to forgetting,” Quiroga said.
Lee added, “Overall, because ad hoc teams are fluid, information sharing is harder. And when a group of people don’t know each other well, group learning slows. But although ad hoc teams learn more slowly, we determined they still learn.”
The research also assessed whether neurologists’ abilities to meet time goals were affected by their recent experiences treating prior stroke patients.

“As team leaders, neurologists can have an outsized influence on performance,” Quiroga said. “Because other members of the ad hoc team aren’t familiar with each other, they lean on their leader.”
But data showed stroke teams improving response times regardless of how many stroke cases the neurologist had treated individually or what the neurologist’s recent success rate was. Quiroga said that’s good news.
“The implication is that learning and sustaining best practices ensures an even quality of care for patients, regardless of individual neurologists’ experience levels.”

One of the first studies to examine patient acceptability of teleneurology and determine factors influencing acceptability across neurological conditions, has found teleneurology was highly acceptable across the full range of patients with different neurological diagnoses, including headache, movement disorders and other neurological symptoms and diagnoses. The study also determined that the more medical complexity — having additional diseases — was associated with increased patient satisfaction with teleneurology.
Older patients were as accepting of teleneurology as younger patients, individuals often viewed as more comfortable with technology. Living in a rural area, typically with inconvenient access to in-person appointments, was also not associated with acceptability of teleneurology.
“There are always going to be certain clinical conditions or patient preferences where in- person visits are essential. But for most patients a large portion of what we’re trying to do — understanding the patients’ symptoms, when they started, what helps them and what makes their symptoms worse — all those basics that we learn in medical school that we know are at least 75 percent of getting the right diagnosis can be done via video; we can then adapt most parts of our physical exam to be done via video too,” said study senior author Linda S. Williams, M.D., a U.S. Department of Veterans Affairs and Regenstrief Institute research scientist, whose clinical neurology practice focuses on stroke patients. “This is true, no matter the healthcare system.
“Telehealth is more efficient. It may help us make better use of scarce resources when we have physician shortages and, most importantly, it may help us meet patients where they are at home, when they’re having trouble or can’t drive from perhaps conditions like epilepsy, which are very important in neurology.”
Patients in the study were surveyed two weeks after accessing clinicians via teleneurology. Visits were conducted via video to home or an outpatient primary care clinic with telehealth capabilities.
“Older patients and those with more medical complexity often make up a large portion of the patients requiring care by a neurologist. These findings will help healthcare providers realize they should not exclude consideration of teleneurology for patients that fall into these groups,” said first author Courtney R. Seigel, an Indiana University School of Medicine student.
“There is a tremendous shortage of neurologists in the United States and neurologists, like many specialists, tend to be at a higher density in urban areas and lower density in rural areas,” said Dr. Williams. “Teleneurology is one way that care can be more efficient. We can see many more patients in a given day via telehealth compared to driving to a single remote clinic and so can spread a scarce resource.”

Metabolic disorders, like diabetes and osteoporosis, are burgeoning throughout the world, especially in developing countries.
The diagnosis for these disorders is typically a blood test, but because the existing healthcare infrastructure in remote areas is unable to support these tests, most individuals go undiagnosed and without treatment. Conventional methods also involve labor-intensive and invasive processes which tend to be time-consuming and make real-time monitoring unfeasible, particularly in real life settings and in country-side populations.
Researchers at the University of Pittsburgh and University of Pittsburgh Medical Center are proposing a new device that uses blood to generate electricity and measure its conductivity, opening doors to medical care in any location.
“As the fields of nanotechnology and microfluidics continue to advance, there is a growing opportunity to develop lab-on-a-chip devices capable of surrounding the constraints of modern medical care,” said Amir Alavi, assistant professor of civil and environmental engineering at Pitt’s Swanson School of Engineering. “These technologies could potentially transform healthcare by offering quick and convenient diagnostics, ultimately improving patient outcomes and the effectiveness of medical services.”
Now, We Got Good Blood
Blood electrical conductivity is a valuable metric for assessing various health parameters and detecting medical conditions.
This conductivity is predominantly governed by the concentration of essential electrolytes, notably sodium and chloride ions. These electrolytes are integral to a multitude of physiological processes, helping physicians pinpoint a diagnosis.

“Blood is basically a water-based environment that has various molecules that conduct or impede electric currents,” explained Dr. Alan Wells, the medical director of UPMC Clinical Laboratories, Executive Vice Chairman, Section of Laboratory Medicine at University of Pittsburgh and UPMC, and Thomas Gill III Professor of Pathology, Pitt School of Medicine, Department of Pathology. “Glucose, for example, is an electrical conductor. We are able to see how it affects conductivity through these measurements. Thus, allowing us to make a diagnosis on the spot.”
Despite its vitality, the knowledge of human blood conductivity is limited because of its measurement challenges like electrode polarization, limited access to human blood samples, and the complexities associated with blood temperature maintenance. Measuring conductivity at frequencies below 100 Hz is particularly important for gaining a deeper understanding of the blood electrical properties and fundamental biological processes, but is even more difficult.
A Pocket-Sized Lab
The research team is proposing an innovative, portable millifluidic nanogenerator lab-on-a-chip device capable of measuring blood at low frequencies. The device utilizes blood as a conductive substance within its integrated triboelectric nanogenerator, or TENG. The proposed blood-based TENG system can convert mechanical energy into electricity via triboelectrification.
This process involves the exchange of electrons between contacting materials, resulting in a charge transfer. In a TENG system, the electron transfer and charge separation generate a voltage difference that drives electric current when the materials experience relative motion like compression or sliding. The team analyzes the voltage generated by the device under predefined loading conditions to determine the electrical conductivity of the blood. The self-powering mechanism enables miniaturization of the proposed blood-based nanogenerator. The team also used AI models to directly estimate blood electrical conductivity using the voltage patterns generated by the device.
To test its accuracy, the team compared its results with a traditional test which proved successful. This opens the door to taking the testing to where people live. In addition, blood-powered nanogenerators are capable of functioning in the body wherever blood is present, enabling self-powered diagnostics using the local blood chemistry.