Publisher Health

For years, automotive companies have developed intelligent sensors to provide real-time monitoring of a vehicle’s health, including engine oil pressure, tire pressure and air-fuel mixture. Together, these sensors can provide an early warning system for a driver to identify a potential problem before it may need to be repaired.
Now, in a similar vein biologically, Zheng Yan, an assistant professor in the MU College of Engineering at the University of Missouri, has recently published two studies demonstrating different ways to improve wearable bioelectronic devices and materials to provide better real-time monitoring of a person’s health, including vital signs.
Developing a ‘smart’ face mask
The onset of the COVID-19 pandemic has brought the idea of mask-wearing to the forefront of many people’s minds. In response, one focus of Yan’s lab has been to develop breathable soft bioelectronics. He said it was natural for him and his team to come up with the idea for integrating bioelectronics in a breathable face mask, which can monitor someone’s physiological status based on the nature of the person’s cough. Their findings were recently published in ACS Nano, a journal of the American Chemical Society.
“Different respiratory problems lead to different cough frequencies and degrees,” Yan said. “Taking chronic obstructive pulmonary disease (COPD) as an example, the frequency of cough in the early morning is higher than that in the daytime and night. Our smart face mask can effectively monitor cough frequencies, which may assist physicians with knowing disease development and providing timely, customized interventions.”
In addition to monitoring someone’s physiological status, the mask can also help identify proper mask wearing in public places using a bioelectronic sensor, Yan said. At this time, the mask does not have the capability to provide automatic reminders, but they would like to develop that function in the future.

As they grow, solid tumors surround themselves with a thick, hard-to-penetrate wall of molecular defenses. Getting drugs past that barricade is notoriously difficult. Now, scientists at UT Southwestern have developed nanoparticles that can break down the physical barriers around tumors to reach cancer cells. Once inside, the nanoparticles release their payload: a gene editing system that alters DNA inside the tumor, blocking its growth and activating the immune system.
The new nanoparticles, described in Nature Nanotechnology, effectively stopped the growth and spread of ovarian and liver tumors in mice. The system offers a new path forward for the use of the gene editing tool known as CRISPR-Cas9 in cancer treatment, said study leader Daniel Siegwart, Ph.D., Associate Professor of Biochemistry at UT Southwestern.
“Although CRISPR offers a new approach for treating cancer, the technology has been severely hindered by the low efficiency of delivering payloads into tumors,” said Dr. Siegwart, a member of the Harold C. Simmons Comprehensive Cancer Center.
In recent years, CRISPR-Cas9 technology has given researchers a way to selectively edit the DNA inside living cells. While the gene editing system offers the potential to alter genes that are driving cancer growth, delivering CRISPR-Cas9 to solid tumors has been challenging.
For more than a decade, Dr. Siegwart and his colleagues have been studying and designing lipid nanoparticles (LNPs), small spheres of fatty molecules which can carry molecular cargo (including recent mRNA COVID-19 vaccines) into the human body. In 2020, Dr. Siegwart’s group showed how to direct nanoparticles to specific tissues, which had been a challenge limiting the field.
In the new work, to target cancer, the researchers began with the nanoparticles that they had already optimized to travel to the liver. They added a small piece of RNA (called short interfering RNA or siRNA) that could shut off focal adhesion kinase (FAK), a gene that plays a central role in holding together the physical defenses of a number of tumors.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia, affecting more than 5.8 million individuals in the U.S. Scientists have discovered some genetic variants that increase the risk for developing Alzheimer’s; the most well-known of these for people over the age of 65 is the APOE ε4 allele. Although the association between APOE4 and increased AD risk is well-established, the mechanisms responsible for the underlying risk in human brain cell types has been unclear until now.
Researchers from Boston University School of Medicine (BUSM) have discovered two important novel aspects of the gene:
1) human genetic background inherited with APOE4 is unique to APOE4 patients and
2) the mechanistic defects due to APOE4 are unique to human cells.
“Our study demonstrated what the APOE4 gene does and which brain cells get affected the most in humans by comparing human and mouse models. These are important findings as we can find therapeutics if we understand how and where this risk gene is destroying our brain,” says corresponding author Julia TCW, PhD, assistant professor of pharmacology & experimental therapeutics at BUSM.
To investigate the effects of APOE4 on brain cell types, the researchers used three models, human induced pluripotent stem cells (hiPSCs), post-mortem human brains and experimental models. They used a population hiPSC model, comparing APOE4 (mutation) vs. APOE3 (mutation-free) of AD patients and normal people. For the second model, they compared AD brains against a control brain with different APOE genotypes. For the third model, they used an experimental model carrying human APOE genes. With all, they used genetic screening and RNA sequencing to identify human cell-type specific defects due to APOE4.
“Our study supports that the genetic background around APOE region can modify the APOE4 risk effects. Therefore, apart from finding drugs to reduce the APOE4 risk, modulating targets to mimic brains carrying protective genes or genetic backgrounds can be another strategy to reduce the risk of developing AD,” adds TCW.
While this study is about APOE4 gene using Alzheimer’s patient samples, it is also known that APOE4 is risk for Parkinson’s disease (PD). According to TCW, this study has implications for any disease associated with APOE as risk such as AD and PD, or for any disease phenotype found similar to the one caused by APOE4, such as rare genetic diseases.
These findings appear online in the journal Cell.
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Participation in cardiac rehabilitation is low among Asian, Black and Hispanic adults compared to white adults, with significant disparities by race/ethnicity regardless of income, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
Cardiac rehabilitation programs combine physical activity with counseling about healthy living and stress reduction to help improve recovery after a major cardiovascular event, such as a heart attack, heart failure, heart surgery or angioplasty. Cardiac rehabilitation is proven to be an effective method to for reducing recurrent cardiac events among people who have had a heart attack, heart failure, heart surgery or coronary intervention including angioplasty. A previous meta-analysis found that cardiac rehabilitation decreases the chances of death following a heart attack, or bypass surgery by about 25% and hospital re-admissions by 18%.
In this study, researchers reviewed health insurance claims data for more than 107,000 people across the U.S. who had diagnoses and/or procedures designated for cardiac rehabilitation. The data came from Optum Clinformatics Data Mart, an administrative database including inpatient, outpatient, emergency department, pharmacy and lab health claims for people with commercial health insurance and Medicare Advantage (C and D). The average age of the people who met the criteria was 70 years; 37% were women; and 76% were white adults, while 2.5% were Asian race, 9.8% were Hispanic ethnicity, and 11.8% were Black race. Each person had experienced one or more of the following cardiovascular events between 2016 and 2018: a heart attack, bypass surgery, heart valve repair or replacement surgery, or angioplasty. Annual household income was estimated and validated from surveys of U.S. households using a comprehensive set of variables that encompass ZIP code data, Internal Revenue Service data, address-level home value, accumulated credit and short-term loans. Among all participants, 34.2% had a high school diploma or lower education level, and 31.5% had an annual household income of less than $40,000. Black individuals were most likely to have a history of high blood pressure, ischemic stroke or other chronic health conditions.
The study evaluated racial and ethnic differences in cardiac rehabilitation participation to determine if household income may affect attendance in cardiac rehabilitation programs.
Researchers found: Overall, only about 26% of all study participants attended one or more cardiac rehabilitation sessions, which included 29.6% of the white individuals, 22.5% of the Asian individuals, 17.6% of the Black individuals and 14.4% of the Hispanic individuals. After adjusting for age, sex, hypertension, diabetes, depression, ischemic stroke, income and education, the probability of attending cardiac rehabilitation was 31% lower among Asian individuals, 19% lower for Black individuals and 43% lower for Hispanic individuals compared to White individuals. Compared to white individuals, the time to attendance in the first cardiac rehabilitation session averaged 9 days longer for Asian and Black people and 10 days longer for Hispanic people. Asian, Black and Hispanic individuals were overall less likely to attend cardiac rehabilitation at all income levels compared to white adults: ranging from 53% less likely among Hispanic people with an annual household income of $60K — $75K; to 13% less likely among Black people earning more than $100K annually.”Disparities in cardiac rehabilitation participation have been well-documented; however, it is alarming to see the magnitude of the disparities that persist,” said Joshua H. Garfein, M.P.H., co-lead study author and a medical student at the University of Pittsburgh. “We were surprised to find that the racial or ethnic disparities did not decrease at higher income levels, which means we need to do more research to identify the barriers.”
New initiatives are urgently needed to optimize the secondary prevention benefits of cardiac rehabilitation and promote equitable cardiovascular outcomes, researchers said.

Black and Asian women are more likely than white women to experience significant delays in getting breast biopsies after a mammogram identifies an abnormality. Moreover, those delays appear to be influenced by screening site-specific factors that may stem from structural racism, according to research published today in JAMA Oncology.
“Even after adjusting for multiple factors thought to contribute to delayed diagnosis, we still see persistent disparities among minority women, particularly Black women. To me, this suggests that other underlying factors are contributing to these differences in time to biopsy,” said Dr. Marissa Lawson, the study’s lead author. She is an acting instructor of radiology at the University of Washington School of Medicine.
The study reviewed the cases of 45,186 women whose screening mammograms had shown a tissue abnormality that called for a biopsy to ascertain whether it was cancerous. Across the study population, 34.6% of women were not biopsied within 30 days, 16% were not biopsied at 60 days, and 12% were not biopsied within 90 days.
The delays are concerning because previous studies have indicated that the benefit of screening diminishes with time, and these lags are associated with later-stage disease at time of diagnosis.
Using the time-to-biopsy of white patients as the benchmark, the researchers found that: At 30 days out, Asian women had a 66% higher risk of not undergoing a biopsy, Black women, 52% higher, and Hispanic women, 50% higher. At 90 days out, Black women had a 28% higher risk of not undergoing a biopsy. Among Asian women and Hispanic women, the risk was 21% higher and 12 % higher, respectively.With that unadjusted model, the researchers then examined whether specific factors of individual patients, their neighborhoods and their screening facilities influenced the time to biopsy among women of different races and ethnicities.

Salk scientists have uncovered an unexpected molecular target of a common treatment for alopecia, a condition in which a person’s immune system attacks their own hair follicles, causing hair loss. The findings, published in Nature Immunology on June 23, 2022, describe how immune cells called regulatory T cells interact with skin cells using a hormone as a messenger to generate new hair follicles and hair growth.
“For the longest time, regulatory T cells have been studied for how they decrease excessive immune reactions in autoimmune diseases,” says corresponding author Ye Zheng, associate professor in Salk’s NOMIS Center for Immunobiology and Microbial Pathogenesis. “Now we’ve identified the upstream hormonal signal and downstream growth factor that actually promote hair growth and regeneration completely separate from suppressing immune response.”
The scientists didn’t begin by studying hair loss. They were interested in researching the roles of regulatory T cells and glucocorticoid hormones in autoimmune diseases. (Glucocorticoid hormones are cholesterol-derived steroid hormones produced by the adrenal gland and other tissues.) They first investigated how these immune components functioned in multiple sclerosis, Crohn’s disease and asthma.
They found that glucocorticoids and regulatory T cells did not function together to play a significant role in any of these conditions. So, they thought they’d have more luck looking at environments where regulatory T cells expressed particularly high levels of glucocorticoid receptors (which respond to glucocorticoid hormones), such as in skin tissue. The scientists induced hair loss in normal mice and mice lacking glucocorticoid receptors in their regulatory T cells.
“After two weeks, we saw a noticeable difference between the mice — the normal mice grew back their hair, but the mice without glucocorticoid receptors barely could,” says first author Zhi Liu, a postdoctoral fellow in the Zheng lab. “It was very striking, and it showed us the right direction for moving forward.”
The findings suggested that some sort of communication must be occurring between regulatory T cells and hair follicle stem cells to allow for hair regeneration.
Using a variety of techniques for monitoring multicellular communication, the scientists then investigated how the regulatory T cells and glucocorticoid receptors behaved in skin tissue samples. They found that glucocorticoids instruct the regulatory T cells to activate hair follicle stem cells, which leads to hair growth. This crosstalk between the T cells and the stem cells depends on a mechanism whereby glucocorticoid receptors induce production of the protein TGF-beta3, all within the regulatory T cells. TGF-beta3 then activates the hair follicle stem cells to differentiate into new hair follicles, promoting hair growth. Additional analysis confirmed that this pathway was completely independent of regulatory T cells’ ability to maintain immune balance.
However, regulatory T cells don’t normally produce TGF-beta3, as they did here. When the scientists scanned databases, they found that this phenomenon occurs in injured muscle and heart tissue, similar to how hair removal simulated a skin tissue injury in this study.
“In acute cases of alopecia, immune cells attack the skin tissue, causing hair loss. The usual remedy is to use glucocorticoids to inhibit the immune reaction in the skin, so they don’t keep attacking the hair follicles,” says Zheng. “Applying glucocorticoids has the double benefit of triggering the regulatory T cells in the skin to produce TGF-beta3, stimulating the activation of the hair follicle stem cells.”
This study revealed that regulatory T cells and glucocorticoid hormones are not just immunosuppressants but also have a regenerative function. Next, the scientists will look at other injury models and isolate regulatory T cells from injured tissues to monitor increased levels of TGF-beta3 and other growth factors.
This work was supported by a NOMIS fellowship and the NOMIS Foundation, the National Institute of Health (NCI CCSG P30-014195, NIA P01- 454 AG073084, NIA-NMG RF1-AG064049, NIA P30-AG068635, R01-AI107027, R01-AI1511123, R21-AI154919, and S10-OD023689), the Leona M. and Harry B. Helmsley Charitable Trust, the Crohn’s and Colitis Foundation, the National Cancer Institute, and Salk’s Cancer Center Core Facilities (P30-CA014195).
Other authors included Xianting Hu, Yuqiong Liang, Jingting Yu, and Maxim N. Shokhirev of Salk; and Huabin Li of Fudan University in Shanghai.
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Materials provided by Salk Institute. Note: Content may be edited for style and length.

Millions of children in low- and middle-income nations suffer from environmental enteric dysfunction (EED), a chronic inflammatory disease of the intestine that is the second leading cause of death in children under five years old. EED is a devastating condition that is associated with malnutrition, stunted growth, and poor cognitive development, permanently impacting patients’ quality of life. In addition, oral vaccines are less effective in children with EED, leaving them vulnerable to otherwise preventable diseases. While some cases of EED are treatable by simply improving a patient’s diet, better nutrition doesn’t help all children. A lack of adequate nutrients and exposure to contaminated water and food contribute to EED, but the underlying mechanism of the disease remains unknown.
Now, a team of researchers at the Wyss Institute at Harvard University has created an in vitro human model of EED in a microengineered Intestine Chip device, providing a window into the complex interplay between malnutrition and genetic factors driving the disease. Their EED Chips recapitulate several features of EED found in biopsies from human patients, including inflammation, intestinal barrier dysfunction, reduced nutrient absorption, and atrophy of the villi (tiny hair-like projections) on intestinal cells.
They also found that depriving healthy Intestine Chips of two crucial nutrients — niacinamide (a vitamin) and tryptophan (an essential amino acid) — caused morphological, functional, and genetic changes similar to those found in EED patients, suggesting that their model could be used to identify and test the effects of potential treatments.
“Functionally, there is something very wrong with these kids’ digestive system and its ability to absorb nutrients and fight infections, which you can’t cure simply by giving them the nutrients that are missing from their diet. Our EED model allowed us to decipher what has happened to the intestine, both physically and genetically, that so dramatically affects its normal function in patients with EED,” said co-first author Amir Bein, R.D., Ph.D., a former Senior Postdoctoral Research Fellow at the Wyss Institute who is now the VP of Biology at Quris Technologies.
The research is published today in Nature Biomedical Engineering.
Modeling a complex disease on-a-chip
The EED Chip project grew out of conversations between the Wyss Institute’s Founding Director Donald Ingber, M.D., Ph.D. and the Bill and Melinda Gates Foundation, which has an established interest in supporting research to understand and treat enteric diseases. Recognizing that there had been no in vitro studies of EED to study its molecular mechanisms, a Wyss team of more than 20 people set about creating a model of EED using its Human Organ Chip technology developed in Ingber’s lab.

A new report led by researchers at the American Cancer Society (ACS) in collaboration with the National Cancer Institute (NCI) shows more than 18 million Americans (8.3 million males and 9.7 million females) with a history of cancer were living in the United States as of January 1, 2022, with a little over 12 million (67%) aged 65 years or older. The study also found substantial racial disparities in treatment and survival for common cancers. The findings were published today as an article in CA: A Cancer Journal for Clinicians and a companion consumer version, Cancer Treatment & Survivorship Facts & Figures 2022-2024.
To assist the public health community in better serving cancer survivors, the ACS and the NCI collaborate every three years to estimate cancer prevalence in the U.S. The most prevalent cancers are prostate (3,523,230), melanoma of the skin (760,640), and colorectal (726,450) among men and breast (4,055,770), uterine corpus (891,560), and thyroid (823,800) among women. More than one-half (53%) of survivors were diagnosed within the past 10 years.
As the population of cancer survivors continues to grow and age, there is an increased need for guidance for health professionals, caregivers, and patients on how to manage late and long-term effects of cancer and its treatment, maintain healthy behaviors and limit financial toxicity,” said Kimberly Miller, scientist, surveillance and health equity science at the ACS and lead author of the study. “In addition, the survivor population is increasingly diverse, and further resources are needed to ensure equitable access to survivorship care.”
According to the report, contemporary treatment patterns based on information from the National Cancer Database show evidence of increased uptake of recent treatment advances. For example, receipt of immunotherapy for stage IV non-small cell lung cancer increased from 12% in 2016 to 33% in 2018.
However, there are substantial racial disparities in treatment. For example, receipt of surgery is substantially lower among Black patients than White patients with non-small cell lung cancer, 49% versus 55% for stages I-II and 16% versus 22% for stage III. One of the largest racial disparities occurs in the treatment of rectal cancer, for which only 41% of Black patients with stage I disease receive proctectomy or proctocolectomy compared to 66% of White patients. Treatment disparities are exacerbated by later stage diagnosis in Black people than in White people for most cancers, with one of the largest disparities for uterine corpus cancer (59% vs 73% diagnosed with stage I disease, respectively).
“We are encouraged by a growing number of tools to assist patients, caregivers, and clinicians in navigating the various phases of cancer survivorship,” said Miller. For example, the ACS has developed guidelines for posttreatment care and nutrition and physical activity among survivors. “However, more evidence-based strategies and equitable access to available resources are needed to mitigate disparities for communities of color.”
The study authors add that the increasing number of cancer survivors cannot be used as a measure of progress by itself against cancer because the increase in part reflects population growth. In addition, these estimates do not reflect the impact of the COVID-19 pandemic, as they are based on observed population-based data through 2018.
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Materials provided by American Cancer Society. Note: Content may be edited for style and length.

Many of us will have likely heard of music therapy and art therapy — but what about ‘travel therapy’?
A new cross-disciplinary paper from Edith Cowan University (ECU) proposes we change the way we view tourism, seeing it not just as a recreational experience but as an industry that can provide real health benefits.
The collaboration between ECU’s Centre for Precision Health and School of Business and Law found many aspects of going on holiday could have a positive impact on those with mental health issues or conditions.
Lead researcher Dr Jun Wen said the diverse team of tourism, public health and marketing experts investigated how tourism could benefit those living with dementia.
“Medical experts can recommend dementia treatments such as music therapy, exercise, cognitive stimulation, reminiscence therapy, sensory stimulation and adaptations to a patient’s mealtimes and environment,” Dr Wen said.
“These are all also often found when on holidays.

COVID-19 vaccination is not associated with an increased risk of heart attack or stroke in patients with established cardiovascular disease, according to a large study published today in Cardiovascular Research, a journal of the European Society of Cardiology (ESC).
“Our study showed that pre-existing cardiovascular disease should not prevent people from getting vaccinated against COVID-19,” said study author Dr. Esther W. Chan of the Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China. “Vaccination is particularly important for this group since cardiovascular disease is associated with worse outcomes and a higher risk of death after COVID-19 infection.”
This was the first study to examine the association between COVID-19 vaccines and the risk of major adverse cardiovascular events (MACE) in patients with cardiovascular disease. The study focused on BNT162b2 and CoronaVac, the only COVID-19 vaccines authorised for emergency use in Hong Kong.2
The researchers linked data from electronic health records managed by the Hong Kong Hospital Authority, which covers around 80% of hospital admissions, and vaccination records provided by the Hong Kong Department of Health. The first two doses of vaccine were included in the analyses. Individuals were not permitted to switch between vaccine types for the first two doses.
The investigators identified patients with existing cardiovascular disease and a new MACE diagnosis between 23 February 2021, when the mass COVID-19 vaccination programme started in Hong Kong, and 31 January 2022. Established cardiovascular disease included coronary heart disease, cerebrovascular disease, peripheral vascular disease, and prior interventions such as stenting. MACE included myocardial infarction, stroke, revascularisation or cardiovascular death.
The researchers used the self-controlled case series study design, which was developed to assess the risk of adverse events after vaccination. Each patient was compared with himself/herself for the risk of MACE up to 27 days after each vaccine dose (exposure period) versus the non-exposure baseline period. Dr. Chan explained: “A traditional cohort study would compare the vaccinated group with the unvaccinated group but the two groups could have different baseline characteristics. A self-controlled case series avoids the issue of differences between groups since each individual acts as his/her own control.”
A total of 229,235 patients with cardiovascular disease were identified, of which 1,764 were vaccinated and experienced MACE during the study period (662 received BNT162b2 and 1,102 received CoronaVac). For BNT162b2 and CoronaVac, the researchers estimated incidence rate ratios (IRRs) to compare the risk of MACE during the 13 days after vaccination compared to the baseline period. IRRs were also calculated for the risk of MACE during days 14 to 27 post-vaccination versus the baseline period. The analyses were conducted for the first and second doses.
There was no evidence of an elevated risk of MACE after the first or second dose of BNT162b2 or CoronaVac. For the first dose of BNT162b2, the IRRs were 0.48 (95% confidence interval [CI] 0.23-1.02) during the first 13 days post-vaccination and 0.40 (95% CI 0.18-0.93) during days 14 to 27 days after vaccination. For the second dose, the IRRs were 0.87 (95% CI 0.50-1.52) during the first 13 days and 1.13 (95% CI 0.70-1.84) during days 14 to 27 after vaccination.
For the first CoronaVac dose, the IRRs were 0.43 (95% CI 0.24-0.75) during the first 13 days and 0.54 (95% CI 0.33-0.90) during days 14 to 27 post-vaccination. For the second dose, the IRRs were 0.73 (95% CI 0.46-1.16) for the first 13 days and 0.83 (95% CI 0.54-1.29) during days 14 to 27 days after vaccination.
Dr. Chan said: “The findings were consistent for women and men, individuals aged under and above 65 years old, and patients with different underlying cardiovascular conditions. The results should provide reassurance about the cardiovascular safety of these two vaccines.”
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Materials provided by European Society of Cardiology. Note: Content may be edited for style and length.