Publisher Health

People with lower incomes are exposed to heat waves for longer periods of time compared to their higher income counterparts due to a combination of location and access to heat adaptations like air conditioning. This inequality is expected to rise as temperatures increase, according to new research.
Lower income populations currently face a 40% higher exposure to heat waves than people with higher incomes, according to a new study. By the end of the century, the poorest 25% of the world’s population will be exposed to heat waves at a rate equivalent to the rest of the population combined.
Poorer populations may be hit with a one-two punch of more heat waves from climate change due to their location and an inability to keep up with it as a result of lack of heat adaptations like air conditioning.
The study analyzed historical income data, climate records and heat adaptations to quantify the level of heat wave exposure that people in different income levels face around the world. Exposure to heat waves was measured by the number of people exposed to heat waves times the number of heat wave days. Researchers paired those observations with climate models to predict how exposure will change over the next eight decades.
The study was published in the AGU journal Earth’s Future, which publishes interdisciplinary research on the past, present and future of our planet and its inhabitants.
The study found the lowest-income quarter of the world’s population will face a pronounced increase in exposure to heat waves by 2100, even taking into account access to air conditioning, cool air shelters, safety regulations for outdoor workers and heat safety awareness campaigns. The highest-income quarter, comparatively, will experience little change in exposure as their ability to keep up with climate change is generally greater.
People in the lowest-income population quarter will face 23 more days of heat waves per year than those in the highest income quarters by 2100. Many populous, low-income regions are in the already-warm tropics, and their populations are expected to grow, contributing to the discrepancies in heat wave exposure.
The study adds to a growing body of evidence that populations who have contributed the least to anthropogenic climate change often bear the brunt of climate change impacts, said lead study author Mojtaba Sadegh, a climatologist at Boise State University. Historically, higher-income countries contribute a majority of greenhouse gases.
“We expected to see a discrepancy, but seeing one quarter of the world facing as much exposure as the other three quarters combined… that was surprising,” Sadegh said.
While higher-income regions often have greater access to adaptations, they will likely face rolling blackouts or brownouts as electricity demand swamps the grid. An increase in geographic area affected by heat waves, which the study found has already increased by 2.5 times since the 1980s, will limit our ability to “borrow” electricity from unaffected neighboring regions, like California importing electricity from the Pacific Northwest, Sadegh said.
“We know from far too much experience that issuing a heat wave forecast is insufficient to ensure that people know what appropriate actions they need to take during a heatwave and to do so,” said Kristie Ebi, a professor in the Center for Health and the Global Environment at the University of Washington who was not involved in the study. Collecting more data on heat wave frequency and responses in low-income countries, she said, is critical.
Sadegh hopes the study will prompt innovations into affordable, energy-efficient cooling solutions as well as highlight the need for short-term solutions. “We need to raise awareness of dangers and heat safety, and to improve early warning systems — and access to those early warning systems,” he said.
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Materials provided by American Geophysical Union. Note: Content may be edited for style and length.

Ulcerative colitis is an inflammatory bowel disease (IBD) that causes inflammation and ulcers (sores) in the digestive tract. Ulcerative colitis affects the innermost lining of the colon and rectum. It can be a debilitating condition and can sometimes lead to life-threatening complications. Most importantly, it does not have a cure at the moment.
In a recently published article, researchers from Tokyo Medical and Dental University (TMDU) have presented a detailed protocol for transplanting 3D cellular structures that can regenerate the intestinal tissue that gets damaged in colitis. To develop this approach, they used a mouse model of colitis, obtained by the administration of dextran sulfate sodium, which destroys the intestinal epithelium in a way similar to colitis.
The 3D cellular structures that the team transplanted are called organoids and represent one of the biggest revolutions in the field of biomedicine in the last decade. Organoids are a miniaturized and simplified version of an organ produced in the laboratory, made of agglomerates of cells; they are three-dimensional and show realistic micro-anatomy. Organoids are used for several applications, including as an in vitro tool to study diseases, for regenerative medicine, and to develop precision medicine approaches.
In the present study, the investigators used intestinal organoids to replace damaged intestinal tissue, a regenerative medicine application. “We infused around 1000 organoids via a flexible catheter into the colon where most epithelial damage occurred. The cultured epithelial cells of the organoids attached to the injured surfaces and integrated into the host epithelium, the cell layer lining the inside of the colon,” explains Satoshi Watanabe, lead author of the paper. “This resulted in an intact epithelium where part of the recipients’ epithelial lining has been replaced by donor cells.”
The total time taken for the rectal infusion of the organoids was 10 minutes, and, importantly, the researchers found that the method was reproducible across different culture conditions of the organoids. These features make it very attractive for a clinical application as it is a quick, reproducible, and minimally invasive method. Moreover, organoids can potentially be derived from the cells of the recipient patient, minimizing the risk of rejection after transplantation.
“This is a versatile protocol, which has been previously used to investigate cellular function, and formed the basis for the first-in-human clinical trial using colonic organoid transplantation therapy for hard-to-treat cases of ulcerative colitis,” explains Shiro Yui, senior author on the study. Thus, the protocol developed in this study has already been translated into clinical practice, and both the scientific and clinical communities are excited about the future clinical applications.
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Materials provided by Tokyo Medical and Dental University. Note: Content may be edited for style and length.

Human primordial germ cells (PGCs) are the early precursors of the eggs (oocytes) and sperm that are necessary to keep humankind alive and reproducing. Medical researchers attempt to study their function and development using models of these cells called human primordial germ-cell-like cells (PGCLCs).
Human PGCLCs have been developed in several research centers, including the laboratory headed by Toshi Shioda, MD, PhD, in the Center for Cancer Research at Massachusetts General Hospital (MGH) and Harvard Medical School.
Natural PGCs exist only in embryos. The models were created to overcome the ethical and technical barriers surrounding the use of human embryonic tissues in experiments.
“My primary interest is the use of PGCLCs for toxicological research to understand how exposure to chemicals or prescription drugs might affect human reproduction,” Shioda says.
He and his colleagues are using the cells to study in the lab how exposure of women to chemicals such as general anesthetic could introduce heritable changes that can then be passed on to future generations without creating DNA mutations. This process is known as epigenetic inheritance.
They are also using this model to investigate how PGCs become testicular cancer, the most common malignancy in boys and young men.
The catch is that hPGCLCs don’t survive long in the laboratory and quickly lose their germ-cell-like features unless they are carefully and painstakingly nursed along with the use of blood serum or added chemicals. And even when these special cells survive and grow in laboratory dishes, they tend to drift away from their germ-cell-like identity and become other types of cells.
But as Shioda and colleagues explain in the journal Stem Cell Reports, they have developed a method for maintaining hPGCLCs and their germ-cell-like functions in cell culture without the need for special handling, with the cells surviving and continuing to replicate for at least five months without losing their primordial germ-cell-like features.
Using these cells, they have successfully generated hPGCLCs that carry various genetic mutations linked to testicular cancer, and are working to create the first synthetic tumor model of human testicular cancer with defined genetic mutations to aid in research into cancer prevention and treatment.
The work was supported by gifts from the RICBAC Foundation and the Escher Fund for Autism as well as grants from the National Institutes of Health.
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Materials provided by Massachusetts General Hospital. Note: Content may be edited for style and length.

Uppsala researchers have succeeded in designing a molecule that inhibits the replication of coronaviruses and that has great potential for development into a drug suitable for treating COVID-19. The molecule is effective against both the new variant and previously identified coronaviruses. The article has been published in the Journal of the American Chemical Society.
The new coronavirus has caused more than five million deaths. Many lives could have been saved with antiviral drugs, but no treatment of this type has been available to the healthcare system. During the pandemic, researchers around the world have tried to find a pharmaceutical, but the development of new medications often takes a long time.
During the first months of the pandemic, researchers were able to determine the structure of the coronavirus and how it functions at the molecular level. One of the viral enzymes was identified as a promising target for a drug, which is a strategy that has been successful for other viral diseases, such as AIDS. The idea is to design a molecule with the ability to recognise and bind to the enzyme. This would block its activity and thereby prevent the virus from producing new virus particles, stopping the spread of the virus.
In 2020, researchers at Uppsala University, in collaboration with the Drug discovery and Development platform at Scilifelab, began to screen for inhibitors of the enzyme. They used computer models to identify molecules that can inhibit the enzyme’s activity. This proved to be a fast way to discover starting points for the design of pharmaceuticals. Access to Swedish supercomputers has made it possible to evaluate several hundred million different molecules to find those that can bind to the enzyme. The molecules predicted by the models were then synthesised and tested in experiments.
“The most promising molecule shows the same ability to inhibit the replication of the new coronavirus as the active substance in Paxlovid, a combination drug recently approved for treating COVID-19. Our molecule works well on its own, and we have shown that the molecule is also effective against previously identified variants of the coronavirus,” says Jens Carlsson, associate professor and the article’s lead author.
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Materials provided by Uppsala University. Note: Content may be edited for style and length.

Oregon State University scientists have discovered a new class of potential drug targets for people suffering from neurodegenerative conditions such as Alzheimer’s, Parkinson’s and Lou Gehrig’s disease.
The possible targets are oxidized proteins, and researchers in the OSU College of Science are now in pursuit of the best way to attack them. A drug target is any molecule critical to the process a disease follows, meaning its disruption can prevent or slow illness progression.
Findings were published in Redox Biology.
Neurodegenerative diseases happen because nerve cells lose function over time and ultimately perish. The diseases affect millions of people worldwide, and Alzheimer’s and Parkinson’s are the most common ones, according to the National Institutes of Health.
The Alzheimer’s Disease Association estimates more than 6 million Americans suffer from that condition, and another 1 million have Parkinson’s, according to the Parkinson’s Foundation.
Any individual’s risk of developing a neurological disease increases with age, which means that with people living longer, a growing number of cases is likely coming over the next few decades, the NIH says.

A BBC News investigation revealed last year there were 100 people with learning disabilities and autism who have been detained in specialist hospitals for more than 20 years. Since then, families across the UK have contacted the BBC to tell their own stories. One of those is a woman from Northern Ireland whose brother was hospitalised 34 years ago, but has been fit for discharge for 25 years. He is in Muckamore Abbey Hospital, which is at the heart of the biggest abuse investigation in NHS history.Watch as Brigene tells the BBC’s Jayne McCubbin about her fight to bring her brother home.

Three members of a family of proteins have been identified that are important to helping us fine tune the activity of brain chemicals which enable us to walk or stand at will, scientists report.
The findings point toward the proteins KCTD5, KCTD17 and KCTD2 as potential new therapeutic targets in conditions like Parkinson’s and dystonia where control of movement is lost, says Dr. Brian Muntean, pharmacologist and toxicologist at the Medical College of Georgia at Augusta University and co-corresponding author of the study published in the journal PNAS.
Dr. Kirill A. Martemyanov, chair of the Department of Neuroscience at the Florida Campus of the Scripps Research Institute in Jupiter, Florida, also is a corresponding author.
The fine tuning these KCTD family members appear to enable is called neuromodulation, which involves hundreds if not thousands of proteins inside neurons that are part of the complex pathway that precisely fine tunes the fast-moving sharing of neurotransmitters, or chemical messengers, between these brain cells so we can accomplish a desired function of our brain and body like walking across the room.
It’s the first discovery about the role these KCTD proteins play in neurons called striatal neurons, which are essential to movement and a variety of other fundamental functions.
One of the key pathways neuromodulators use is cyclic AMP, or cAMP, which is called a “second messenger” because it’s a response inside a cell that occurs in response to something that happens outside a cell.

UBC researchers have developed an inexpensive, non-toxic coating for almost any fabric that decreases the infectivity of the virus that causes COVID-19 by up to 90 per cent.
And in the future, you might be able to spray it on fabric yourself.
“When you’re walking into a hospital, you want to know that pillow you’re putting your head onto is clean,” says lead author Taylor Wright, a doctoral student in the department of chemistry. “This coating could take a little bit of the worry off frontline workers to have Personal Protection Equipment with antimicrobial properties.”
Researchers soaked fabric in a solution of a bacteria-killing polymer which contains a molecule that releases sterilizing forms of oxygen when light shines on it. They then used an ultraviolet (UV) light to turn this solution to a solid, fixing the coating to the fabric. “This coating has both passive and active antimicrobial properties, killing microbes immediately upon contact, which is then amped up when sunlight hits the cloth,” says senior author Dr. Michael Wolf (he/him), a professor of chemistry.
Both components are safe for human use, and the entire process takes about one hour at room temperature, says Wright. It also makes the fabric hydrophobic, meaning microbes are less likely to stick to the cloth, and doesn’t seem to affect the strength of the fabric.
In addition, the coating can be used on almost any fabric, including cotton, polyester, denim, and silk, with applications in hospital fabrics, masks, and activewear. Whereas other such technologies can involve chemical waste, high energy use, or expensive equipment, the UBC method is relatively easy and affordable, says Wright. “All we need is a beaker and a light bulb. I’m fairly certain I could do the whole process on a stove.”
To test the coating’s bug-killing properties, the researchers bathed treated fabric in bacterial soups of Escherichia coli (E. coli) andMethicillin-resistant Staphylococcus aureus (MRSA), both major sources of hospital-acquired infections. They found there were 85 per cent of viable E. coli bacteria remaining after 30 minutes, which fell to three per cent when the treated cloth was exposed to green light for the same amount of time. Similarly, 95 per cent of viable MRSA bacteria remained, dropping to 35 per cent under green light. No bacteria remained after four hours.

Drugs to increase insulin signaling may be effective for treating autism say Lancaster University researchers, who have discovered how a genetic change impacts on insulin signaling and glucose metabolism in the brain.
In the human genome small sections of DNA have been found to be duplicated or deleted in some people, a phenomenon known as Copy Number Variation.
Some of these genetic changes cause neurodevelopmental problems and dramatically increase someone’s risk of developing disorders such as autism, schizophrenia and Tourette’s syndrome.
For example, people with a DNA deletion at chromosome 2p16.3, which results in deletion of the Neurexin1 gene, commonly experience neurodevelopmental delay and cognitive problems.
People with the 2p16.3 deletion are also around 14 to 20 times more likely to develop neurodevelopmental disorders including autism, schizophrenia and Tourette’s syndrome than people without the deletion.
There are an estimated two to three million people worldwide who have this type of DNA deletion but there are currently no effective drug treatments for their resulting cognitive problems.

Infants and children with poor nutrition and growth are more likely to suffer from a serious respiratory condition that has been linked to comorbidities and early mortality as adults, according to an international investigation led by researchers at the University of Arizona Health Sciences.
The study, published in The Lancet Respiratory Medicine, is the first to identify early-life risk factors for spirometric restriction in adult life. A team led by Stefano Guerra, MD, PhD, MPH, director of population sciences at the UArizona Health Sciences Asthma and Airway Disease Research Center, found three risk factors that were significantly linked to adult spirometric restriction: maternal nutritional problems during pregnancy, low birth weight for gestational age, and below normal weight in childhood.
Spirometric restriction, a restrictive lung disease that decreases total lung capacity, is an important marker of poor general health and has been linked to an increase in cardiovascular disease, diabetes and metabolic syndrome, as well as a higher risk of dying of any cause.
“Participants who were underweight in childhood had a risk of developing lung restriction that was three times higher than children with normal weight,” said Dr. Guerra, a professor of medicine and the Henry E. Dahlberg Chair in Asthma Research at the UArizona College of Medicine — Tucson.
“Similar increased risks for spirometric restriction were found for infants who were born small for gestational age. This may be an indicator that during early development, perhaps even in utero, something went wrong, and that’s affecting your lungs as well as your cardiovascular system and other organs. That might explain the comorbidity and increased mortality risk that we see with this restrictive pattern.”
Researchers examined data from participants who were tracked over two to four decades, from infancy to adulthood, in long-term respiratory studies including the Tucson Children’s Respiratory Study at the Asthma and Airway Disease Research Center and two similar studies in Great Britain and Sweden.
Study participants whose mothers had nutritional problems such as anemia and excessive vomiting during pregnancy were twice as likely to have spirometric restriction at ages 22-36. Infants who were born small for their gestational age were nearly three times more likely to develop spirometric restriction as adults. And when childhood nutritional status was evaluated from ages 6 to 16, participants who were underweight — particularly those with deficits in lean body mass — were three times more likely than those with a normal weight to develop spirometric restriction as adults.
“What was striking is how consistent the findings were. This association was pretty much identical in each of the three cohorts,” said Dr. Guerra, who is a member of the BIO5 Institute.
“Our findings really highlight that growth and nutrition problems very early in life have a long-term effect or consequence on adult lung health,” added co-author Nipasiri Trudeau, née Voraphani, a statistician in the Asthma and Airway Disease Research Center who earned a doctorate in medicine in Thailand before emigrating to the U.S.
Dr. Guerra and other UArizona Health Sciences investigators are now studying whether children can “catch up” and improve their long-term health through better nutrition or other interventions.
This study was supported in part by the National Institute of Allergy and Infectious Diseases (AI135108) and the National Heart, Lung, and Blood Institute (HL132523), both divisions of the National Institutes of Health.