Publisher Health

A new study suggests structural racism measured by the racial economic mobility gap between Black and White persons with a similar parental income (as an indicator of similar childhood socioeconomic status) is strongly associated with Black-White disparities in mortality in the United States, both in a recent birth cohort and in all ages combined. These findings, appearing in Cancer Epidemiology, suggest that the effects of structural racism on mortality have persisted with a similar magnitude across generations in the past century.
Social inequalities and discriminatory policies by race/ethnicity, also collectively known as structural racism, is a major factor contributing to health disparities. Structural racism can adversely affect economic, social, service, and physical living environments leading to limited educational and job opportunities; lower income; poorer housing, transportation, and public safety; food insecurity; and limited health care.
This is one of the few studies to examine the association of structural racism to death from multiple specific causes. Investigators led by Farhad Islami, MD, PhD of the American Cancer Society, examined county-level data on economic mobility and death from all causes, heart diseases, cerebrovascular diseases, chronic obstructive pulmonary disease (COPD), injury/violence, all malignant cancers, and 14 cancer types in all ages combined and on all-cause mortality in ages 30-39 years. Data for ages 30-39 years covered 69% of individuals in that age group nationally and for all ages combined covered 82% to 90% of the U.S. population.
“Although more research is needed to identify factors mediating these associations and appropriate interventions to mitigate them, equitable and broad implementation of proven interventions to increase health equity, such as equitable access to care and preventive measures can help reduce health disparities,” said Dr. Islami.
Findings show that in the U.S., death rates are higher among non-Hispanic Black (Black) persons than among non-Hispanic White (White) persons. In ages 30-39 years, a one percentile increase in the economic mobility gap was associated with a 6.8% increase in the Black-White mortality gap among males and a 10.7% increase among females, based on data from 471 counties.
In all ages combined, the corresponding percentages based on data from 1,572 counties were 10.2% among males and 14.8% among females, equivalent to an increase of 18.4 and 14.0 deaths per 100,000 in the mortality gap, respectively. Similarly, strong associations between economic mobility gap and mortality gap in all ages were found for major causes of death, notably for potentially preventable conditions, including COPD, injury/violence, and cancers of the lung, liver, and cervix.
“Dismantling structural racism will require greater efforts to implement meaningful institutional changes, with broad societal engagement to create equitable local, state, and federal policies,” write the authors. “Results of this study could help advocate for and inform public policies to improve equity and establish a benchmark by which to evaluate progress in reducing structural racism and its adverse health effects.”
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Materials provided by American Cancer Society. Note: Content may be edited for style and length.

A study by University of Liverpool researchers has identified new factors accompanying previous findings that frequent consumption of peanuts by cancer patients could increase risk of cancer spread.
The study, published in Carcinogenesis, shows that Peanut agglutinin (PNA) — a carbohydrate-binding protein that rapidly enters into the blood circulation after peanuts are eaten — interacts with blood vascular wall (endothelial) cells to produce molecules called cytokines.
The cytokines in question, IL-6 and MCP-1 are well-known promoters of cancer metastasis. The increased cytokine production causes other endothelial cells to express more cell surface adhesion molecules, making them more attractive to the circulating tumour cells and thus potentially promoting metastasis.
In an earlier study, Corresponding Author Professor Lu-Gang Yu and colleagues reported that circulating PNA binds to a special sugar chain, which occurs mainly on pre-cancerous and cancer cells, and interacts with a larger protein expressed on the surface of tumour cells in the bloodstream.
This interaction triggers changes in the larger protein, resulting in underlying adhesion molecules on the surface of the cancer cell to become exposed, making the cancer cells stickier and easier to attach themselves to the blood vessels. It also allows the cancer cells to form small clumps that prolong the survival of cancer cells in the body’s circulation. Many epithelial cancers spread to the other organs through traveling through the bloodstream.
Professor Lugang Yu said: “Although further research and investigation are still needed, these studies suggest that very frequent consumption of peanuts by cancer patients might increase the risk of metastatic spread.
“Reassuringly though, a large US study reported no significant impact of peanut consumption on cancer mortality. In another study, peanut consumption was reported to have no significant effect on prognosis in men with established prostate cancer. In our previous healthy volunteer study, substantial blood concentrations of PNA were only seen transiently one hour or so after consumption of a large dose (250g) of peanuts, so it may be that ‘normal’ peanut consumption yielding lower PNA concentrations is harmless.
“Nevertheless, the possibility remains that circulating PNA, at least at the relatively high levels found shortly after a large “dose” of peanuts, could have a significant biological effect on tumour cells circulating at that time, with a potential for increased risk of metastasis. Heavy or very frequent peanut consumption therefore might be better avoided by cancer patients.”
The possible impact of heavy peanut consumption by cancer patients on survival will need to be investigated in further population-based epidemiological studies.
This study was supported by the American Institute for Cancer Research.
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Materials provided by University of Liverpool. Note: Content may be edited for style and length.

X-ray imaging is a fast and painless way for doctors to see inside a person. But radiation detectors, which go under the body part being imaged, are rigid panels that contain harmful heavy metals, such as lead and cadmium. Now, researchers in ACS’ Nano Letters report a proof-of-concept wearable X-ray detector prepared from nontoxic metal-organic frameworks (MOFs) layered between flexible plastic and gold electrodes for high-sensitivity sensing and imaging.
Most X-ray detectors are integrated into big, immobile instruments, such as computerized tomography (known as CT) and mammography equipment, or are stiff, like the sharp-edged bitewing detectors used in dental offices. Detectors that could conform to rounded body parts or mold to the inside of confined spaces could be beneficial in some radiation monitoring and medical imaging applications. Previous researchers have used MOFs for flexible radiation detectors because they are semiconducting materials that respond to electromagnetic radiation by creating an electrical current. However, some of these MOFs still include lead, just like the X-ray detectors that are currently in use. So, Shuquan Chang, Shenqiang Ren and colleagues wanted to create a heavy-metal-free MOF for a flexible X-ray detector and imager.
The researchers mixed a solution of nickel chloride salt and 2,5-diaminobenzene-1,4-dithiol (DABDT) for several hours, creating a MOF in which nickel linked the DABDT molecules. In initial tests, the nickel-containing MOF was more sensitive than recently reported detectors when irradiated with 20 keV X-rays, equivalent to the energy released during medical diagnostic imaging. Then, to make a flexible X-ray radiation detector, the team sandwiched the nickel-containing MOF between gold film electrodes, one of which was on a flexible plastic surface. They used copper wires to transmit current from each pixel of a 12×12 array and covered the whole device with a silicone-based flexible polymer. Finally, they placed an aluminum letter “H” on the detector and irradiated it with X-rays, measuring a much lower current output underneath the H than under the unimpeded material. The researchers say that their proof-of-concept device is promising for the next generation of radiology imaging equipment and radiation detection when wearable or flexible devices are needed.
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Materials provided by American Chemical Society. Note: Content may be edited for style and length.

Last month, New York City and other cities along the east coast experienced some of the worst air pollution in the world. The cause? Wildfires in Canada, California, and Oregon so large they produced smoke that drifted thousands of miles. If smoke that dense can travel from one end of the U.S. to the other, imagine what it could do to your lungs.
Using satellites scientists can accurately see how far and wide wildfire smoke spreads across an area, but they have a more difficult time predicting whether the plumes are high in altitude or lower to the ground where it can gravely affect people’s health.
But a team of researchers led by University of Utah chemical engineering associate professor Heather A. Holmes has developed a method of combining a meteorological model with NASA satellite data to determine whether the wildfire smoke will stay high up or come down to the ground. That will lead to more accurate predictions of whether and when smoke from a nearby wildfire could reach people on the ground.
“Our hope is this technique gets incorporated into smoke forecasting as a way to improve warning systems related to smoke exposure,” says Holmes, whose research is focused on the physics and chemistry of air pollution.
Holmes’ research was published in the most recent issue of the Journal of Geophysical Research: Atmospheres. The first author was one of Holmes’s former graduate students, S. Marcela Loría-Salazar, who is now an assistant professor at the University of Oklahoma’s School of Meteorology.
Before, scientists could not accurately predict whether wildfire smoke would actually reach the lower altitudes of an area where it can affect residents, even by examining satellite data of the smoke’s spread. For example, during the 2013 Yosemite Rim Fire in 2013, one of California’s largest wildfires that scorched more than 257,000 acres, they initially couldn’t explain why Fresno, Calif., had low levels of pollution even though satellite images from the fire showed smoke covering the city. It turns out the mountains created complex winds, and the smoke was actually in the upper level of the troposphere (the lowest region of the atmosphere) where it was separated from the Earth’s surface.
So Holmes and Loria-Salazar collaborated with NASA scientists and analyzed satellite data from the Yosemite Rim Fire along with ground observation data and developed a method to better understand the vertical smoke patterns. They examined what is called the “plume injection height” data from the satellite, an estimate of the top layer of the pollution, and the vertical meteorology at the time of the fire. With that, they developed a “smoke height/boundary ratio,” an estimate of how much of the smoke is going down to the surface of the Earth. Better understanding where the smoke is in the atmosphere vertically can help scientists also understand where the smoke will be downwind, says Holmes.
“There’s a lot of uncertainties in understanding the vertical mixing in the atmosphere, and that really drives where the smoke will end up,” she says.
With this new information, Holmes believes meteorologists, climatologists or air quality experts could possibly predict up to two or three days whether smoke from a wildfire could affect the health of residents in a nearby city.
“If you can forecast this, you can make more informed decisions on whether to have school closures, or you can give alerts on when to not go outside to exercise,” she says. “You can give people information to protect themselves better.”
Wood smoke produces microscopic particulate matter that can penetrate the lungs and adversely affect a person’s health, particularly those with lung and heart conditions, diabetes, older adults, younger children and pregnant women, according to the U.S. Environmental Protection Agency. And studies show that wildfire smoke not only affects people while they are outside, but it also seeps into homes and affects indoor air quality.
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Materials provided by University of Utah. Original written by Vince Horiuchi. Note: Content may be edited for style and length.

In a newly published study, physician-scientists at the University of Miami Miller School of Medicine have shown that the flu vaccine may provide vital protection against COVID-19.
The study, titled “Examining the potential benefits of the influenza vaccine against SARS-CoV-2: A retrospective cohort analysis of 74,754 patients,” was published in the peer-reviewed scientific journal PLoS One on August 3. This was the largest study of its kind and analyzed deidentified patient records from around the world, which strongly suggested that the annual flu shot reduces the risks of stroke, sepsis, and DVT in patients with COVID-19. Patients with COVID-19 who had been vaccinated against the flu were also significantly less likely to visit the emergency department and be admitted to the intensive care unit.
“Only a small fraction of the world has been fully vaccinated against COVID-19 to date, and with all the devastation that has occurred due to the pandemic, the global community still needs to find solutions to reduce morbidity and mortality,” said senior study author Devinder Singh, M.D., chief of plastic surgery, and professor of clinical surgery at the Miller School.
“Having access to the real-time data of millions of patients is an incredibly powerful research tool,” added Dr. Singh, who conducted the study with medical student Susan Taghioff and plastic surgery resident Benjamin Slavin, M.D., both of whom were lead authors. “Together with asking important questions, my team has been able to observe an association between the flu vaccine and reduced morbidity in COVID-19 patients.”
Sharing Findings with Scientists and General Public
The researchers previously presented their preliminary data findings at the European Congress of Clinical Microbiology & Infectious Diseases (ECCMID), receiving international attention. Now that the full study has been published, the authors are extremely excited to share their detailed findings for the first time with both the general public and scientific community.

A protein that causes a cell’s skeleton to bend, allowing it to twist the cell into different shapes, could be key to how cells divide according to University of Warwick scientists.
By making the cytoskeleton bend inwards to a tight point at its centre, one cell divides into two — much like how you would make a balloon animal by twisting. The protein, named ‘curly’, has been observed bending the material that makes up the cytoskeleton for the first time.
Their results, from research supported by the European Research Council and Wellcome Trust, are published in the journal eLife and point to new ways to modify and engineer cells, as well as a better understanding of how they replicate — a process essential to all living organisms.
All living matter is made up of cells, which are surrounded by a fragile and flexible membrane much like a balloon. This is supported by a cytoskeleton composed of a material called actin that give structure and stability to cells. Filaments of actin are semi-flexible and normally straight and it has long been thought that they form structures by stacking together like matchsticks.
During cell division a cell will create a cytokinetic ring, a type of machinery comprised of actin and motor proteins called myosin, along the centre of the surrounding membrane. The myosins then constrict the actin filaments together and squeeze the cell down its middle until it divides — as if making the parts of a balloon animal, except from the inside.
Until now, it was thought that the actin filaments that comprise the cytokinetic ring break up as the cell is squeezed tighter. An interdisciplinary collaboration between Professor Mohan Balasubramanian, Dr Saravanan Palani (now at the Indian Institute of Science) and Dr Darius Köster at the University of Warwick was astonished to find that a segment of the protein Rng2, nicknamed ‘curly’, can naturally curve actin, with 10 micrometres of actin forming a ring less than a micrometre in diameter.

A new study from Tel Aviv University discovered changes in healthy lung tissue which indicate preparation to receive metastases. The changes were identified in the area known as “the micro-environment” of the tumor, and specifically in connective tissue known as fibroblasts. Researchers claim that these changes in the tissues are an early sign for the possible development of disseminated cancerous cells — metastases. According to them, understanding the metastatic process and its diagnosis at such an early stage may lead to life-saving prophylactic treatment.
The study conducted was led by Prof. Neta Erez, Chair of the Dept. of Pathology at the Sackler Faculty of Medicine, along with the research team of her laboratory, Dr. Ophir Shani and Dr. Yael Raz, as well as additional researchers from Tel Aviv University, Tel Aviv Medical Center (Ichilov), Sheba Medical Center and the Weizmann Institute. The paper was published in the journal eLife.
Researchers explain that in many types of cancers, among them breast cancer, patients do not necessary die from the primary tumor. In the end, the main cause of mortality are metastases, which arrive at the essential organs and proliferate there. Metastases may appear after several years even in patients who have undergone all the treatments offered, including surgical removal of the primary tumor, subsequent chemotherapy and radiation intended to destroy any residual tumor. Methods used for follow-up today locate metastases only when they are quite large — when the disease is at an advanced stage, and medicine does not have curative solutions.
For this reason, Prof. Erez’s research group is investigating the ‘black box’ — the time period between apparent recovery and the appearance of metastases, for the purpose of understanding the metastatic process and to identify it in early stages. Their research in the last years has revealed that designated tissues, in organs where the metastases are set to arrive, ‘prepare the area’ for reception and produce a hospitable environment for them, a long time before the appearance of the metastases themselves.
In the present study, the research team led by Prof. Erez searched for signs of these changes, which may be used in the future to identify the start of the process. The researchers focused on connective tissue cells known as fibroblasts which are found in the lungs among other places.
Prof. Erez: “In a normal situation, fibroblasts play a central role in healing wounds and injury to the lungs, but recent studies revealed that cancer is successful in recruiting them and causing them to produce a supportive environment for it. Within the framework of the present study, we performed sequencing of all the genes which are expressed (transcriptome sequencing) in fibroblasts taken from the lungs of mice in a model of breast cancer metastasis.”
The researchers compared the sequencing results sampled from healthy lungs, from lungs with micro-metastases (very small metastases which cannot be identified using existing clinical tools), and from lungs with large metastases, in a state of advanced disease. According to the changes identified from stage to stage, researchers have succeeded, for the first time, in characterizing the process occurring in the micro-environment of the metastases, already in the early stages of preparation of the area for its reception.
In addition, they specifically identified the proteins that initiate the ‘rewiring’ processes in fibroblasts, and discovered that one of the central proteins in the process is MYC — known as a central driver in accelerating the division of cancerous cells. This study revealed that MYC also plays an important role in the changes occurring in fibroblasts towards reception of the metastases.
Prof. Erez summarizes: “in our study, we have succeeded in characterizing processes which occur in lung tissue in preparation for the reception of breast cancer metastases. We believe that in the future, our findings can aid in the identification of the metastatic process even before the disseminated cancer cells thrive and colonize the metastatic organ, with the purpose of providing prophylactic treatment. Such treatment, that will prevent the development of metastases, may save the lives of millions of people, worldwide.”
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Materials provided by Tel-Aviv University. Note: Content may be edited for style and length.

An artificial pancreas could soon help people living with type 2 diabetes and who also require kidney dialysis. Tests led by the University of Cambridge and Inselspital, University Hospital of Bern, Switzerland, show that the device can help patients safely and effectively manage their blood sugar levels and reduce the risk of low blood sugar levels.
Diabetes is the most common cause of kidney failure, accounting for just under a third (30%) of cases. As the number of people living with type 2 diabetes increases, so too does the number of people requiring dialysis or a kidney transplant. Kidney failure increases the risk of hypoglycaemia and hyperglycaemia — abnormally low or high levels of blood sugar respectively — which in turn can cause complications from dizziness to falls and even to coma.
Managing diabetes in patients with kidney failure is challenging for both patients and healthcare professionals. Many aspects of their care are poorly understood, including targets for blood sugar levels and treatments. Most oral diabetes medications are not recommended for these patients, so insulin injections are the most commonly used diabetes therapy — though optimal insulin dosing regimens are difficult to establish.
A team at the University of Cambridge and Cambridge University Hospitals NHS Foundation Trust has previously developed an artificial pancreas with the aim of replacing insulin injections for patients living with type 1 diabetes. In research published today in Nature Medicine, the team — working with researchers at Bern University Hospital and University of Bern, Switzerland — has shown that the device can be used to support patients living with both type 2 diabetes and kidney failure.
The artificial pancreas is powered by software in the user’s smartphone that sends a signal to an insulin pump to adjust the level of insulin the patient receives. A glucose monitor measures the patient’s blood sugar levels and sends these back to the smartphone to enable it to make further adjustments.
Unlike the artificial pancreas being used for type 1 diabetes, this version is a fully closed loop system — whereas patients with type 1 diabetes need to tell their artificial pancreas that they are about to eat to allow adjustment of insulin, for example, with this new version they can leave the device to function entirely automatically.

Collagen is the most abundant protein in the human body. It makes up a third of protein content and single strands assemble to form stable fibres that give structure to connective tissue such as skin, tendons, cartilage and bones. Researchers at ETH Zurich have now developed a multi-component molecule that interacts with collagen and can be used to illuminate new tissue growth in the body.
Our bodies start producing more collagen as wounds heal — or as tumours grow. During this process, the fibrous collagen molecules cross-link to create stable fibres. This requires LOX enzymes, which oxidise certain sites in the collagen molecules. Subsequently, the chemically altered sites on different collagen strands react with each other, causing the strands to fuse together.
Sensor combined with functional peptide
Led by Professor Helma Wennemers, a professor at the Laboratory of Organic Chemistry at ETH Zurich, the team of researchers developed a sensor molecule with inducible fluorescence. The molecule itself isn’t fluorescent, but after reacting with the LOX enzyme, it begins to light up. In this way, the sensor molecule acts as a marker for LOX activity. Next, the scientists combined this molecule with a short fibrous peptide similar to collagen. They conjugated this peptide with a what is known as a reactive group that reacts with collagen only if the latter has been oxidised.
In collaboration with researchers from the group led by Sabine Werner, Professor of Cell Biology, the scientists conducted experiments with mice whose skin had been injected with the multi-component molecule. They also performed in vitro experiments with tissue sections. Their investigations revealed that the molecule anchors itself to collagen fibres where new tissue is being formed. And it lights up when new tissue starts growing and the LOX enzyme is being formed. “Thanks to its modular design with three components — the sensor, the peptide and the reactive group — our system is exceptionally specific and precise,” says Matthew Aronoff, senior scientist in Wennemers’ group and lead author of the study.
Applications in oncology and wound healing
Because new tissue forms primarily at the edges of tumours as they grow, one application for the new molecule is in biopsy examinations to show the boundaries of a tumour. “One of our visions is that surgeons will one day use this molecule in an operating theatre when removing a tumour,” Wennemers says. The molecule would show surgeons the boundary of the tumour and help them to remove it entirely.
Other potential applications for the new marker molecule are in the field of wound healing, for example to investigate tissue formation in general or healing disorders in patients suffering from diabetes or other diseases. Such questions are also addressed within the framework of the interdisciplinary skin research project Skintegrity, in which ETH Zurich is involved.
Having applied for a patent for their system, the scientists are currently exploring various options for bringing it to market and developing it for a wider range of applications.
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Materials provided by ETH Zurich. Original written by Fabio Bergamin. Note: Content may be edited for style and length.

In a proof-of-concept study, researchers at Children’s Hospital of Philadelphia (CHOP) have created a coating that can be applied to endotracheal tubes and release antimicrobial peptides that target infectious bacteria with specificity. The innovation could reduce upper-airway bacterial inflammation during intubation, a situation that can lead to chronic inflammation and a condition called subglottic stenosis, the narrowing of the airway by an accumulation of scar tissue. The findings were published recently in the journal The Laryngoscope.
“We have created a novel device to modulate the upper-airway microbiome, which could be used to prevent bacterial infections during intubation and help prevent subglottic stenosis and other airway diseases,” said senior study author Riccardo Gottardi, PhD, Assistant Professor of Pediatrics and head of the Bioengineering and Biomaterials Laboratory at CHOP. “Not only does this technology work predictably and continuously over the normal duration of chronically intubated patients, but it is also fast and easy to produce and could easily be modulated to target any bacteria of interest.”
Recent studies have shown that the endotracheal microbiome of intubated patients with subglottic stenosis is unbalanced. However, addressing the overgrowth of certain bacteria with conventional antibiotics is not ideal, as their use can disrupt the balance of both “good” and “bad” bacteria, while also causing antimicrobial resistance.
Instead, the investigators explored the use of antimicrobial peptides (AMPs), which are small proteins that destabilize bacterial membranes, causing bacterial cells to fall apart and die. This mechanism of action allows them to target specific bacteria and makes them unlikely to promote antimicrobial resistance. Prior studies have shown that it is possible to coat endotracheal tubes with conventional antibiotics, so the research team investigated the possibility of incorporating AMPs into polymer-coated tubes to inhibit bacterial growth and modulate the upper-airway microbiome.
The researchers, led by Matthew Aronson, a graduate student in Penn Engineering’s Department of Bioengineering, tested their theory by creating a polymer coating that would release Lasioglossin-III, an AMP with broad-spectrum antibacterial activity. They found that Lasio released from coated endotracheal tubes, reached the expected effective concentration rapidly and continued to release at the same concentration for a week, which is the typical timeframe that an endotracheal is used before being changed. The investigators also tested their drug-eluting tube against airway microbes, including S. epidermidis, S. pneumoniae, and human microbiome samples and observed significant antibacterial activity, as well as prevention of bacterial adherence to the tube.
“This study shows that it is possible to create a drug-eluting endotracheal tube to prevent airway complications, which opens the door to future research on targeting specific pathogens that are responsible for laryngotracheal stenosis,” said study co-author Ian N. Jacobs, MD, Medical Director of the Center for Pediatric Airway Disorders in the Division of Otolaryngology and Endowed Chair in Pediatric Otolaryngology and Pediatric Airway Disorders at Children’s Hospital of Philadelphia. “Moreover, the ability to purposefully select AMPs against certain microbes in the trachea and other organs could have significant implications in the prevention of specific diseases, even beyond airway disorders.”
The study was supported in part by the Ri.MED Foundation, the Children’s Hospital of Philadelphia Research Institute, the Frontier Program in Airway Disorders of the Children’s Hospital of Philadelphia, and the National Science Foundation Graduate Research Fellowship No. DGE 1845298.
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Materials provided by Children’s Hospital of Philadelphia. Note: Content may be edited for style and length.