Methane is particularly targeted for curbing greenhouse gas emissions because its significant global-warming potential in the short term exceeds carbon dioxide by over 80-fold. However, monitoring methane emissions and compiling their quantities have been challenging due to limiting trade-offs with existing detection methods. Researchers developed a method to automatically detect methane emissions at a global scale, potentially providing methane detection at high frequency and high resolution from point sources.
As global temperatures rise to record highs, the pressure to curb greenhouse gas emissions has intensified. Methane is particularly targeted because its significant global-warming potential in the short term exceeds carbon dioxide by over 80-fold.
However, monitoring methane emissions and compiling their quantities have been challenging due to limiting trade-offs with existing detection methods.
Now, a research team including Kyoto University and Geolabe, USA has developed a method to automatically detect methane emissions at a global scale.
“Our approach can potentially provide methane detection at high frequency and high resolution from point sources, paving the way for a systematic quantification method,” says lead author Bertrand Rouet-Leduc of KyotoU’s Disaster Prevention Research Institute and Geolabe.
Rouet-Leduc further suggests that their method may help prioritize and automatically validate atmospheric mitigation of methane, which currently accounts for approximately one third of global warming.
Multispectral satellite data has emerged as a viable methane detection tool in recent years, enabling routine measurements of methane plumes at a global scale every few days. However, significant noise plagues these methane data, and until now, detections have been limited to very large emissions and have required human verification.

In contrast, the team has trained an AI to automatically detect methane leaks over 200kg/h, accounting for over 85% of the methane emissions in well-studied, large oil and gas basins.
“With satellite measurements, trade-offs must be made between spatial coverage, spatial and temporal resolution, and spectral resolution and associated detection accuracy. AI partially offsets these trade-offs,” explains co-author Claudia Hulbert, also of Geolabe.
Methane plumes are invisible and odorless, so they are typically detected with specialized equipment such as infrared cameras. The difficulty in finding these leaks from space goes without saying, akin to finding a needle in a haystack. Leaks are distributed around the globe, and most of the methane plumes are relatively small, making them easy to miss in satellite data.
The group’s collaborative work represents a key step towards the precise, systematic monitoring of methane emissions, anywhere on Earth, every few days.
“Automation is paramount when analyzing large areas. We were surprised that AI can automate the process and dramatically outperform the human eye in detecting small methane plumes, ” reflects Rouet-Leduc.
“In our next phase, we plan to integrate additional satellites in a global study of methane emissions.”

Same-sex couples with non-transmissible HIV will now be able to donate eggs or sperm and become parents.

Published26 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Jamie Niblock/BBCBy Nikki Fox & Matt PreceyBBC NewsnightMore and more UK hospitals are leaving patients in corridors due to a lack of bed space. NHS bosses say so-called corridor care is freeing up ambulances and saving lives, but BBC Newsnight has spoken to patients who say the growing practice is humiliating and degrading.Gregory Knowles counted 13 other patients alongside him on a corridor at the Norfolk and Norwich University Hospital (NNUH) in March. Complications after an operation put him back in hospital and on to a ward but at 04:00 one morning he was moved.The 68-year-old was wheeled in his bed to reception. “I was waking up with people around me. It was horrendous,” he told the BBC. “I had no screens and no facilities for water or for really getting changed. My possessions were on the bottom of the bed. My daughter and partner were as horrified as I was,” he said.His partner Alicia Goulty described how staff had been too rushed to attend to him.”One day when we got there his catheter had leaked in the bed when he was on the corridor. He was wet with no covers or any screens and I had to take him to the bathroom to get him cleaned”. Ms Goulty said her partner’s medication had been missed.”We had to ask for water for him. We had to ask sometimes for his meals because he got forgotten.” It would be three days until there was room to move Mr Knowles from the corridor and back to a ward.Another patient admitted to NNUH in March described being “distraught” when she was put in a corridor opposite a nursing station alongside three others. A nurse at the hospital, who asked to remain anonymous, said: “It’s horrible for your patient to say to them, ‘This is where I’m going to leave you’. You come into work to be a carer. You want to do it in the best way possible and sometimes you’re coming into a situation where you can’t do that.”‘Drip-feeding patients’Since 2022, hospitals like NNUH have increasingly adopted a new way of working called the Continuous Flow Model, in which patients are sent from A&E to wards and other areas even if they are full.They have done this to address soaring ambulance waits outside A&E as paramedics try to offload patients.In the UK, the model started at the North Bristol NHS Trust and was then implemented at the 10 hospitals with the most delays, according to NHS board papers.These documents indicate at least 36 hospitals have now adopted the system or a version of it. Some implementations involve “drip-feeding” patients from A&E. But it often means hospitals will have to put patients on beds in corridors, albeit in a planned and risk-assessed manner. Trusts have adopted it reluctantly, they say, but it now allows ambulances to get to the sickest patients quicker.Lesley Dwyer, NNUH chief executive, said demand for beds was forcing tough choices. “We are committed to reducing ambulance delays outside our hospital, which we know is saving lives by improving 999 response times by freeing up ambulances quicker to get to patients in our community.”Back in February, the interim chief executive of NNUH, Nick Hulme, said they had cut ambulance handover delays – but that it had come at a cost. He said the risk had been moved from outside hospital into corridors but that it was “better for the community”.’It is the right thing for us to have done’Image source, Matt Precey/BBCProf Steve Hams says the Continuous Flow Model has “without question” saved lives. The chief nursing officer at North Bristol NHS Trust points to a dramatic improvement in ambulance performance. The trust pioneered the model during the summer 2022 heatwave amid a spike in admissions. It still struggles to discharge mostly elderly patients deemed fit to leave. Prof Hams described how ambulance response times to heart attack and stroke patients had more than halved. Average hours lost to ambulance waits outside of A&E had plummeted from 139 hours a day to just six, he said. Image source, Jamie Niblock/BBCNewsnight was taken to a complex care ward at Bristol’s Southmead Hospital. In the corridor was a bed on stand-by but the trust ensures nobody spends the night there with just one such patient per ward. Screens are available to protect patient privacy. Prof Hams adds what while the model works at his trust, it may not be right for others.”Caring for people at the end of a corridor is something none of us aspire to do and it is certainly something we would not wish to do here. But on the balance of risk, the safety risk of both our patients and citizens in the community, it’s the right thing for us to have done,” he said.However, the Royal College of Nursing has criticised the model for just moving risk, rather than solving it. And the Royal College of Emergency Medicine warned the model was not a “silver bullet”.Dr Louella Vaughan, a medical researcher, said she had concerns about safety.”If you look at the literature there is absolutely evidence that overcrowding on a ward increases mortality,” she said, adding trusts were “rushing” to implement the model because it appeared to work.Image source, Jamie Niblock/BBC”I know of places where an email was sent on a Thursday to say it was being put in on a Monday.”One of the major impediments to freeing hospital bed capacity appears to be worsening. Across England, patients fit for discharge but unable to leave was on average 59% higher in April than three years ago, according to NHS data.,

Published26 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Philippa RoxbyHealth reporterMillions of middle-aged people have been mistakenly led to believe they are not obese, according to an Italian study that looked at body-fat percentage instead of body-mass index.Using a new, lower BMI cut-off for obesity would give a truer picture of who is affected, the researchers say.With age, muscle declines and fat builds up around organs in the waist region, often with no change in weight.The challenge is to find a tool that easily screens for obesity.BMI is calculated by dividing an adult’s weight in kilograms by the square of their height in metres.18.5-25 is said to suggest a healthy weight25-29 that they are overweight30 or above that they are obeseIt is a quick and easy method, supported by the World Health Organization,

As a student competing in track and field at his Parlier high school, Robert Leija was obsessed with how to improve his performance and, in particular, prevent the buildup of lactic acid in his muscles during training. Like many athletes, he blamed it for the performance fatigue and muscle soreness he experienced after intense workouts.
But as a kinesiology student at Fresno State, he was handed an out-of-print textbook that told him he had it all wrong. Lactate wasn’t a danger sign that athletes had depleted their body’s supply of oxygen, but likely a normal product of the metabolic activity required to fuel the muscles during sustained exercise.
Now, as a graduate student in the University of California, Berkeley, laboratory of the scientist who wrote that textbook, George Brooks, his research is providing a much clearer picture of lactate’s role in the body, further refuting the notion that lactate is a sign of oxygen deprivation in the muscles.
In a paper published in February in the journal Nature Metabolism, Leija, Brooks and their colleagues showed conclusively that lactate is produced normally in humans after ingestion of carbohydrates. Lactate rapidly enters the bloodstream, even before glucose shows up. Far from being a toxic byproduct to be eliminated during hard exercise, dietary glucose is converted so rapidly to lactate that it preempts or shares top billing with glucose as the two main carbon-energy carriers in the body.
The results show that the rapid conversion of glucose to lactate, starting initially in the intestines, is a way for the body to deal with a sudden dose of carbohydrates. Lactate, working with insulin, buffers the appearance of dietary glucose in the blood.
“Instead of a big glucose surge, we have a lactate and glucose surge after eating,” said Brooks, a UC Berkeley professor of integrative biology. “And the more of it that is converted into lactate from glucose, the better it is to manage glucose. Lactate is a carbohydrate buffer.”
Brooks and his colleagues had earlier shown this to be true during intense exercise. The new study confirms that lactate plays the same role during normal non-exercise activity and resting.

“It’s evidence to show that lactate shouldn’t be associated with anaerobic metabolism — that is oxygen-limited metabolism. It’s just a normal response to consuming carbohydrates or to exercise,” Leija said. “In exercise, lactate is utilized as the dominant fuel source. That’s why your blood lactate increases as you exercise a little harder. It’s not that you’re making it as a waste product. It’s getting into the blood because it needs to go to tissues that need it to continue their physiological performance.”
Glucose tolerance
The study was conducted on 15 healthy, physically active young adults — eight women and seven men — as part of a larger NIH-funded study to determine how well people switch from fat to carbohydrate metabolism as they age. The volunteers were asked to fast overnight (12 hours) to deplete their carbohydrate and glycogen stores so that they were getting energy primarily by breaking down fats into fatty acids and using them to power basic bodily functions.
They then drank 75 grams of glucose, a rapidly absorbed sugar, to stimulate a switchover from fatty acid to carbohydrate metabolism. This is similar to the glucose tolerance test used to diagnose diabetes and is commonly given to pregnant women to screen for gestational diabetes.
Brooks’ study differed from previous similar studies in that he and his colleagues, including Leija, closely monitored the volunteers’ blood lactate levels over a two-hour period following ingestion of the glucose, and periodically measured the ratio of oxygen and carbon dioxide in their breath, which indicates the proportion of fatty acids versus carbohydrates being burned.
In order to calculate the amount of lactate that entered the blood compared to glucose, they infused lactate and glucose tracers — lactate labeled with a stable, non-radioactive isotope, carbon-13, and glucose labeled with deuterium — for 90 minutes beforehand to bring the levels of labeled lactate and glucose in the blood to between 1% and 2%. The dilution of the labeled lactate and glucose by incoming, unlabeled dietary glucose allowed them to establish the kinetics, that is, the appearance, disappearance and clearance of blood lactate and glucose. Most such experiments measure static venous blood concentration, which provides little information about glucose and lactate kinetics.

Sampling of arterialized blood was also key to success of the study, Leija said. That allowed the researchers to see what happened in the gut. Typically, a forearm vein is used to sample blood 30 minutes after a glucose challenge, but that sampling yields muddled results.
The researchers found that the volunteers began converting the dietary glucose into lactate before it even left the intestines. Levels of lactate began rising in arterial blood a mere five minutes after the meal, while glucose, often touted as the energy currency of the body, only showed up in the bloodstream 15 to 30 minutes after glucose ingestion.
“The first carbohydrate after a glucose meal gets into the blood as lactate because that’s what intestinal cells do and because most of the glucose is captured by the liver before it is released into the blood for the muscles, where glucose is going to be converted to lactate,” Brooks said. “We could see that because of lactate clearance and oxidation and because carbon-13 from the lactate tracer appeared in blood glucose. This shows that lactate is just a major energy highway for distributing carbohydrate — carbon energy flux.”
The lactate shuttle
Brooks has conducted human and animal studies for more than 50 years to investigate the role of lactate in the body, each study providing more evidence that it’s not a toxic byproduct of oxygen-limited, anaerobic metabolism, which does not happen in the human body, he said. That assumption, however, has colored the way athletes as well as physicians have looked at lactate. Many physicians still perceive high levels of lactate — often incorrectly called lactic acid — in the blood as a symptom of illness that needs to be fixed with supplemental oxygenor drugs.
“Measuring lactate is one of the major things that sports medicine practitioners do. And now we understand what’s happening,” Brooks said. “Athletes are producing lactate all the time and clearing it all the time. And when they get to the point where they can’t clear it, mostly by oxidation and making it into glucose, we know the person can’t persist very long.
“I think this is so revolutionary. But it’s really confusing to people. What was bad now is good. All the books are wrong.”
Except for Brooks’ textbook, “Exercise Physiology: Human Bioenergetics and Its Applications.” Originally written in 1984 with Thomas Fahey, it’s now in its 5th edition. Text for the 6th edition is already being uploaded to the publisher.
“When I read through Dr. Brooks’ 1984 book it was a complete mind blow to me, to be honest,” Leija said. “I had always associated lactic acid with exercising so hard that I was running out of oxygen and I wasn’t putting anything together in terms of physiology. Then it started to make a lot more sense.”
In his book, Brooks coined the term “lactate shuttle” to describe the body’s metabolic feedback loop in which lactate is the intermediary sustaining most if not all tissues and organs.
He has showed, for example, that in many tissues, lactate is preferred as a fuel over glucose. During intense activity, the muscle mitochondria burn it preferentially and even shut off glucose and fatty acid fuel use. Brooks used tracers to show that human skeletal muscle, heart muscle and the brain prefer lactate to glucose as fuel and run more strongly on lactate. Lactate also signals fat tissue to stop breaking down fat for fuel.
One gap in these studies was what happens during normal non-exercise activity and resting. The current study fills that gap and supports the idea that when lactate levels in the blood remain high, it is a signal that something is disrupting the lactate shuttle cycle, not that lactate itself is harming the body.
“It’s really informative about various medical conditions,” Brooks said. “I think what’s significant about the current result is that it’s just not a muscle thing. It starts with dietary carbohydrate. This was a missing piece in the puzzle.”
The recent study is part of Leija’s Ph.D. thesis, after which he hopes to conduct further research on the metabolic role of lactate.
“Since before college I would read physiology books trying to improve my training and I would see all these science terms that I kind of ignored back then because I was just looking for, How can I get faster? How can I run longer?” Leija said. “But now, wow, it ended up helping me out indirectly. Still to this day, there’s so much I think that’s left to be uncovered about it.”
Other coauthors of the study are graduate students Casey Curl, Jose Arevalo, Adam Osmond and Justin Duong, Melvin Huie, MD, a UC Berkeley graduate affiliated with Brooks’ Exercise Physiology Laboratory, and Umesh Masharani, MD, an endocrinologist with UC San Francisco’s Diabetes Center.

A research team led by the University of California, Irvine has revealed the link between the frequency of sleep apnea events during the rapid-eye-movement stage and the severity of verbal memory impairment in older adults at risk for Alzheimer’s disease. Verbal memory refers to the cognitive ability to retain and recall information presented through spoken words or written text and is particularly vulnerable to Alzheimer’s.
The study, recently published online in the journal Alzheimer’s Research & Therapy, discovered a specific correlation between the severity of sleep apnea — when breathing pauses while an individual is sleeping — and diminished cognition. Higher ratios during REM compared to non-REM stages were associated with worse memory performance.
“Our findings identified the specific features of sleep apnea that are associated with memory, which is important because clinically, events occurring during REM sleep are often overlooked or minimized,” said co-corresponding author Bryce Mander, UC Irvine associate professor of psychiatry & human behavior. “Most hours of sleep are non-REM, so the overall averages of apnea severity can look much lower than what is typically observed during REM sleep. This means that someone at risk can be misdiagnosed and undertreated because current evaluation standards are not focused on sleep-stage-specific apnea severity.”
“Furthermore,” said co-corresponding author Ruth Benca, professor and chair of psychiatry and behavioral medicine at Wake Forest University School of Medicine, “we found that women are more likely to have a greater proportion of their apneic events in REM sleep in comparison to men, which could potentially be contributing to their greater risk for Alzheimer’s disease.”
The study involved 81 middle-aged and older adults from the Wisconsin Alzheimer’s Disease Research Center with heightened risk factors, of whom 62 percent were female. Participants underwent polysomnography — a comprehensive test that records brain waves, eye movements, muscle activity, blood oxygen levels, heart rate and breathing during sleep — and verbal memory assessments. Results showed apnea events during REM to be a critical factor contributing to verbal memory decline, especially among individuals with a genetic predisposition to Alzheimer’s and those with a parental history of the disease.
“Our findings highlight the intricate relationship among sleep apnea, memory function and Alzheimer’s risk,” Mander said. “Identifying and addressing REM-specific events are crucial for developing proactive, personalized approaches to assessment and treatment that are tailored to individual sleep patterns.”
The team also included lead author Kitty K. Lui, a graduate student in the San Diego State University/University of California, San Diego joint doctoral program in clinical psychology, and faculty and graduate students from UC Irvine, UC San Diego, the Wisconsin Alzheimer’s Disease Research Center and the University of Kentucky.
This work was supported by the National Institute on Aging under grants R56 AG052698, R01 AG027161, R01 AG021155, ADRC P50 AG033514, R01 AG037639 and K01 AG068353; by the National Institutes of Health’s Ruth L. Kirschstein National Research Service Award F31 AG048732; and by the National Center for Advancing Translational Sciences’ Clinical and Translational Science Awards Program under grant UL1TR000427.

A new study from the University of Hawai’i at Manoa shows that chlorine mixed with petroleum in water can potentially produce inadvertent byproducts harmful to human health.
Small amounts of chlorine, within safe industry standards, are added to disinfect Oʻahu’s drinking water by the Honolulu Board of Water Supply (BWS) and military installations, according to BWS. In late November 2021, a petroleum release from the Red Hill Bulk Fuel Storage Facility contaminated the Red Hill drinking water well. Hundreds of families, living on Joint Base Pearl Harbor-Hickam and the Army’s Aliamanu Military Reservation and Red Hill Housing, reported petroleum odors coming from tap water supplied by the U.S. Navy water system.
Lab experiments conducted by researchers in UH Manoa’s College of Engineering and Water Resources Research Center (WRRC), showed elevated levels of THM4 (Total Trihalomethanes) and HAA5 (Haloacetic Acids), which are both classified as disinfection byproducts, can form during chlorination of petroleum contaminated water. THM4 was the most abundant, and additionally, various unregulated disinfection byproducts were produced. The researchers stress that their findings are from controlled lab conditions, and further research is needed to understand real-world implications.
According to the Centers for Disease Control and Prevention, “Chronic exposure to disinfection byproducts may increase risk of cancer. Humans exposed to unusually large amounts of some disinfection byproducts could experience liver damage and decreased nervous system activity.”
“These findings highlight the potential health risks associated with chlorinating petroleum-contaminated water, and further research is needed to fully understand these risks in real-world conditions,” said study co-author and Professor Tao Yan from the UH Manoa Department of Civil, Environmental and Construction Engineering and WRRC.
During the lab process, control reactors containing either only free chlorine or only petroleum hydrocarbons produced significantly lower or no detectable levels of disinfection byproducts, which indicated that the presence of petroleum hydrocarbons and free chlorine together was responsible for the elevated disinfection byproduct concentrations.
“Recent contamination events in the Pearl Harbor aquifer show that petroleum hydrocarbons can directly enter groundwater wells without undergoing natural breakdown processes,” Yan said. “This study reveals that when unaltered petroleum hydrocarbons come into contact with free chlorine, commonly used in water treatment, they can produce higher levels of regulated disinfection byproducts. Understanding the potential risks during both water treatment and distribution is important for safeguarding water quality and protecting human health.”

A study from North Carolina State University has found that environmentally caused alterations to specific areas of the genome — known as imprint control regions — during early development may contribute to the risk of developing Alzheimer’s disease, and that Black people may be more affected than white people. The work adds to our understanding of the ways in which environmental factors can contribute to genetic alterations and disease susceptibility.
“In terms of genetics and disease, I always think of Dr. Kenneth Olden’s analogy: genetics loads the gun and the environment pulls the trigger,” says Cathrine Hoyo, professor of biological sciences at NC State and co-corresponding author of the research.
“In fact, the Institute of Medicine has estimated that epigenetic response to the environment -how our genes respond to the environment — contributes between 70% to 90% of chronic disease risk. And we know that in the case of Alzheimer’s disease, only about 5% of cases are familial, or inherited.
“We also know that the risk of developing non-familial, or sporadic, Alzheimer’s differs according to race — Black people have twice the incidence of white people,” Hoyo continues. “So we wanted to see if we could identify stable epigenetic features — parts of the epigenome that are unlikely to change once established — that distinguished Alzheimer’s brains from those without the disease.”
Specifically, the research team used the imprintome — the imprint control regions (ICRs) in the human genome that regulate the expression of imprinted genes — to identify stable epigenetic features that distinguished people with Alzheimer’s disease from those without.
Imprinted genes differ from other genes because only one parental copy of an imprinted gene is active. The other copy is methylated, or silenced, early in development. Additionally with these genes, the methylation marks that control their expression are susceptible to environmental influences.
“With imprinted genes, there isn’t a backup copy in the event of mutation,” says Randy Jirtle, professor of epigenetics at NC State and co-corresponding author of the research. “ICRs control the expression of these genes — in other words, they tell imprinted genes where, when and how to work through DNA methylation. And these methylation marks in ICRs don’t normally change unless altered early in development, either at conception or shortly thereafter.”
For the study, the team had brain tissue samples from 17 donors — eight normal brains and nine with Alzheimer’s. Each group was divided between non-Hispanic white and non-Hispanic Black donors (the Alzheimer’s group had five samples from Black donors and four from white donors).

The team sequenced the entire genome for each sample, then looked for ICRs in the Alzheimer’s brains that were either over- or under-methylated compared to the healthy brains.
They found 120 differently methylated ICRs in the Alzheimer’s brains. Forty were found in the combined Black and white populations; however, 81 ICRs were found only in the Black population, and 27 were found only in the white population.
The differently methylated ICRs common to both populations are associated with (MEST/MESTIT1), a paternally expressed imprinted gene, and NLRP1, a predicted imprinted gene involved in brain inflammation.
“The importance of finding the common ICRs is that it could help us develop universal tests for potential disease markers,” says Hoyo. “But it was very puzzling to discover that the Black population had almost three times as many affected ICRs as the white population.
“When you see that level of difference, and you know that the changes you’re finding are likely caused early by environmental interactions, one possible explanation is that there are unique or different stressors in that population, and those epigenetic effects are being passed along.”
The researchers hope the work could lead to testing and targeted early interventions to prevent Alzheimer’s disease.

“We know that targeted prevention over long periods can alter risk,” Hoyo says. “So if you can alert people early on about their risk and apply targeted interventions, you could prevent disease onset.”
“Epigenetics is the science of hope,” Jirtle says. “You can’t necessarily reverse genetic mutations, but when you know disease risks result from changes in the epigenome you can potentially negate them.”
The work appears in Clinical Epigenetics and was supported by the National Institutes of Health under grants R01HD098857, R01MD017696, R01MD011746, P30ES025128, and R01ES032462. Brain tissue samples were provided by Duke University School of Medicine. Former NC State Ph.D. student Sebnam Cevik is first author. Other NC State contributors were David Skaar, associate research professor of biology; Antonio Planchart, associate professor of biology; and Ph.D. student Dereje Jima. Dr. Andy Liu, Dr. Truls Østbye and Dr. Heather E. Whitson of Duke University School of Medicine also contributed to the work.

The declining population in Osaka is related to an aging society that is driving up health expenditures. Dr. Haruka Kato, a junior associate professor at Osaka Metropolitan University, teamed up with the Future Co-creation Laboratory at Japan System Techniques Co., Ltd. to conduct natural experiments on how a new train station might impact healthcare expenditures.
JR-Sojiji Station opened in March 2018 in a suburban city on the West Japan Railway line connecting Osaka and Kyoto. The researchers used a causal impact algorithm to analyze the medical expenditure data gathered from the time series medical dataset REZULT provided by Japan System Techniques.
Their results indicate that opening this mass transit station was significantly associated with a decrease in average healthcare expenditures per capita by approximately 99,257.31 Japanese yen (USD 929.99) over four years, with US dollar figures based on March 2018 exchange rates. In addition, the 95% confidence interval indicated the four-year decreasing expenditure of JPY 136,194.37 ($1276.06) to JPY 62,119.02 ($582.02). This study’s findings are consistent with previous studies suggesting that increased access to transit might increase physical activity among transit users. The results provided evidence for the effectiveness of opening a mass transit station from the viewpoint of health expenditures.
“From the perspective of evidence-based policymaking, there is a need to assess the social impact of urban designs,” said Dr. Kato. “Our findings are an important achievement because they enable us to assess this impact from the perspective of health care expenditures, as in the case of JR-Sojiji Station.”

In the stomach, so-called parietal cells are responsible for acid production. They react not only to the body’s own messenger molecules, but also to bitter-tasting food constituents such as caffeine. A research team from the Leibniz Institute for Food Systems Biology at the Technical University of Munich has now carried out a study on a human gastric cell line. Their results help to clarify the molecular regulatory mechanisms by which bitter substances influence gastric acid production.
It is known that taste receptors for bitter substances are not only found on the tongue, but also on the surface of other tissues and cells. These include the parietal cells of the stomach, which secrete protons into the stomach — i.e. produce gastric acid. Recent studies have already shown that the bitter taste receptors found in parietal cells are involved in the regulation of gastric acid release. However, the underlying molecular signaling pathways are not yet fully understood.
Gastric cells as a test system
To further clarify the molecular interaction between bitter substances, bitter taste receptors, and gastric acid production, a research team led by Veronika Somoza, Director of the Leibniz Institute in Freising, has carried out a study on a cellular test system. This involves human parietal HGT-1 cells, which are able to secrete protons and, like taste cells, have bitter taste receptors.
Veronika Somoza’s team initially developed a working hypothesis based on the results of previous studies and the findings on signal transduction pathways in taste cells. According to this hypothesis, bitter tasting food constituents stimulate bitter taste receptors that are embedded in the cell membrane. This releases calcium ions inside the cells, leading to ion channel opening. This, in turn, allows sodium ions to flow into the gastric cells from the outside, ultimately contributing to the release of protons.
Hypothesis confirmed
First author Phil Richter explains: “We have successfully tested this mechanism with the two bitter substances caffeine and l-arginine. As expected from previous results, both food constituents were shown to stimulate gastric cell proton secretion in our test system.” The PhD student adds: “For the first time, we were able to demonstrate that the transient receptor potential channelsM4 and M5 are involved in the signaling cascade not only in taste cells but also in gastric cells and ensure an influx of sodium ions into the cells.”
Senior Scientist Gaby Andersen says: “By using knock-out experiments, in which we specifically switched off one type of bitter taste receptor in the cells, we were also able to show for the first time that there is a link between bitter taste receptors and the activation of the ion channels.” The scientist emphasizes that the results not only contribute to a better understanding of the role of taste receptors in the stomach but would also show that HGT-1 cells could be suitable as a replacement model for taste cells.
The research team agrees that the results will provide new insights into the regulation of gastric acid production and thus lead to innovative approaches in treating gastric diseases in the long term. However, further studies are needed to deepen knowledge of the molecular regulatory mechanisms and intracellular signaling pathways.