Friday, June 09, 2023

 

Colorful foods improve athletes’ vision

Visual range is a critical asset for top athletes in almost any sport

Peer-Reviewed Publication

UNIVERSITY OF GEORGIA

Nutrition is an important part of any top athlete’s training program. And now, a new study by researchers from the University of Georgia proposes that supplementing the diet of athletes with colorful fruits and vegetables could improve their visual range.

The paper, which was published in Exercise and Sport Sciences Reviews, examines how a group of plant compounds that build up in the retina, known as macular pigments, work to improve eye health and functional vision.

Previous studies done by UGA researchers Billy R. Hammond and Lisa Renzi-Hammond have shown that eating foods like dark leafy greens or yellow and orange vegetables, which contain high levels of the plant compounds lutein and zeaxanthin, improves eye and brain health.

“A lot of the research into macular lutein and zeaxanthin has focused on health benefits, but from a functional perspective, higher concentrations of these plant pigments improve many aspects of visual and cognitive ability. In this paper, we discuss their ability to improve vision in the far distance or visual range,” said lead author Jack Harth, a doctoral candidate in UGA’s College of Public Health.

Visual range, or how well a person can see a target clearly over distance, is a critical asset for top athletes in almost any sport.

The reason why objects get harder to see and appear fuzzier the farther they are from our eyes is thanks in part to the effects of blue light.

“From a center fielder's perspective, if that ball's coming up in the air, it will be seen against a background of bright blue sky, or against a gray background if it's a cloudy day. Either way, the target is obscured by atmospheric interference coming into that path of the light,” said Harth.

Many athletes already take measures to reduce the impact of blue light through eye black or blue blocker sunglasses, but eating more foods rich in lutein and zeaxanthin can improve the eye’s natural ability to handle blue light exposure, said Harth.

When a person absorbs lutein and zeaxanthin, the compounds collect as yellow pigments in the retina and act as a filter to prevent blue light from entering the eye.

Previous work had been done testing the visual range ability of pilots in the 1980s, and Hammond and Renzi-Hammond have done more recent studies on how macular pigment density, or how much yellow pigment is built up in the retina, is linked to a number of measures of eye health and functional vision tests.

“In a long series of studies, we have shown that increasing amounts of lutein and zeaxanthin in the retina and brain decrease glare disability and discomfort and improve chromatic contrast and visual-motor reaction time, and supplementing these compounds facilitates executive functions like problem-solving and memory. All of these tasks are particularly important for athletes,” said corresponding author Billy R. Hammond, a professor of psychology in the Behavior and Brain Sciences Program at UGA’s Franklin College of Arts and Sciences.

This paper, Harth said, brings the research on these links between macular pigment and functional vision up to date and asks what the evidence suggests about optimizing athletic performance.

“We're at a point where we can say we've seen visual range differences in pilots that match the differences found in modeling, and now, we've also seen it in laboratory tests, and a future goal would be to actually bring people outside and to measure their ability to see contrast over distance through real blue haze and in outdoor environments,” said Harth.

But before you start chowing down on kale in the hopes of improving your game, he cautions that everybody is different. That could mean the way our bodies absorb and use lutein and zeaxanthin varies, and it could take a while before you notice any improvements, if at all.

Still, the evidence of the overall health benefits of consuming more lutein and zeaxanthin are reason enough to add more color to your diet, say the authors.

“We have data from modeling and empirical studies showing that higher macular pigment in your retina will improve your ability to see over distance. The application for athletes is clear,” said Harth.

 

Single-cell atlas of the whole human lung


First integrated Human Lung Cell Atlas provides insights into lung diseases

Peer-Reviewed Publication

WELLCOME TRUST SANGER INSTITUTE

The largest and most comprehensive cell map of the human lung is announced in Nature Medicine today (8 June).  Revealing the great diversity of cell types in the lung and key differences between health and disease, the Human Lung Cell Atlas will be a valuable resource for lung researchers.


By combining data from nearly 40 studies, researchers created the first integrated single-cell atlas of the lung, revealing rare cell types and highlighting cellular differences between healthy people. In addition, the study found common cell states between lung fibrosis, cancer and COVID-19, offering new ways of understanding lung disease, which could help identify new therapeutic targets.

The study is part of the global Human Cell Atlas* (HCA) initiative to map every cell type in the human body, to transform our understanding of health, infection and disease.

Lung research has benefited greatly from recent single-cell studies that show which genes are active in each cell. Despite this, the research has been limited so far by the number of samples and individuals included per study. To better understand healthy lungs and determine what goes wrong in disease, a comprehensive atlas has been needed, however this has been difficult to achieve.

Now, a large team of researchers has successfully combined 49 lung datasets, from nearly 40 separate studies, into a single integrated Atlas, using advanced machine learning.  By pooling and integrating datasets from every major single-cell RNA-sequencing lung study published to date, the team created the first integrated Human Lung Cell Atlas. This Atlas spans over 2.4 million cells from 486 individuals and gives new insights into lung biology that were not possible before.

Dr Malte Luecken, a senior author on the paper and Group leader at the Institute of Computational Biology and the Institute of Lung Health and Immunity at Helmholtz Munich, Germany, said: “A comprehensive organ atlas requires many datasets to capture the diversity between both cells and individuals, but combining different datasets is a huge challenge. We developed a benchmarking pipeline to find the optimal method to integrate all datasets into the Atlas, using artificial intelligence, and successfully combined knowledge and data from almost 40 previous lung studies.”

Professor Fabian Theis, a senior author on the paper and Director of the Institute of Computational Biology at Helmholtz Munich, said: “We have created a first reference atlas of the human lung, which includes data from more than a hundred healthy people and reveals how the cells from individuals vary with age, sex, and smoking history. The sheer numbers of cells and individuals involved now gives the power to see rare cell types and identify new cell states that have not previously been described.”

While the core of the Human Lung Cell Atlas is data from healthy lungs, the team also took datasets from more than 10 different lung diseases and projected these onto the healthy data, to understand disease states.

The team discovered that different lung diseases shared common immune cell states, including the finding that a subset of macrophages (a type of immune cell) shared similar gene activity in lung fibrosis, cancer and COVID-19. The shared states indicate that these cells could play a similar role in scar formation in the lung in all three diseases, and provide pointers for potential therapeutic targets. 

Professor Martijn Nawijn, a senior author on the paper and Professor at the University Medical Center Groningen, the Netherlands, said: “This is the first effort to compare healthy and diseased lungs in one study in an integrated way.  Our study not only supports the presence of lung fibrosis in COVID-19, it allows us to identify and define a shared cell state between lung fibrosis, COVID-19 and lung cancer patients.  Finding these shared disease-associated cells is really exciting, and reveals a totally different way of looking at lung diseases, opening possibilities for novel treatment targets and developing treatment response biomarkers. Our findings also suggest that therapies working for one disease may help alleviate others.”

The Lung Atlas Integration project was an international collaborative effort with nearly 100 partners from more than 60 departments, including key researchers from Helmholtz Munich, University Medical Center Groningen and Northwestern University. The team are part of the Human Cell Atlas Lung Biological Network**, which has its roots in the Chan Zuckerberg Initiative Seed Networks for the Human Cell Atlas, and the European Union funded lung network DiscovAIR. At the start of the COVID-19 pandemic in 2020, the single-cell lung communities came together rapidly, forming the HCA Lung Biological Network to help understand COVID-19, which then led to the global effort to integrate all the data.

Lisa Sikkema, the first author on the paper and PhD student at the Institute of Computational Biology at Helmholtz Munich, said: “One of the big problems in creating the integrated lung cell atlas was with cell type annotation. Different research groups used different names for the same cell type, or the same name for different cells, so as a team we worked to standardise them using the data in the atlas. The atlas is a first step towards a consensus annotation of the human lung, which will help bring together the field of lung research.”

The first integrated major organ within the Human Cell Atlas initiative, the Human Lung Cell Atlas is publically available for researchers globally, as a central resource to study the lung in health and disease.

Dr Alexander Misharin, a senior author on the paper and Associate Professor at Northwestern University Feinberg School of Medicine, USA, said: “The Human Lung Cell Atlas is a huge resource for the scientific and medical community. Openly available to researchers, new disease data can be mapped onto the HLCA, transforming research into lung biology and disease. As the first whole reference atlas of a major organ, the HLCA also represents a milestone towards achieving a full Human Cell Atlas which will transform our understanding of biology and disease and lay the foundation for a new era of healthcare”.

ENDS

Contact Details:
Dr Samantha Wynne,
Human Cell Atlas Scientific Communications Manager,
HCA UK Office, Wellcome Sanger Institute,
Cambridge, CB10 1SA, UK
Email: press@humancellatlas.org
 

Notes to Editors:

*The Human Cell Atlas (HCA)
The Human Cell Atlas (HCA) is an international collaborative consortium which is creating comprehensive reference maps of all human cells—the fundamental units of life—as a basis for understanding human health and for diagnosing, monitoring, and treating disease. The HCA is likely to impact every aspect of biology and medicine, propelling translational discoveries and applications and ultimately leading to a new era of precision medicine.

The HCA was co-founded in 2016 by Dr Sarah Teichmann at the Wellcome Sanger Institute (UK) and Dr Aviv Regev, then at the Broad Institute of MIT and Harvard (USA). A truly global initiative, there are now more than 2,900 HCA members, from 94 countries around the world. https://www.humancellatlas.org

**The Human Cell Atlas Lung Biological Network is a group of scientists who collaborate to map the cell types and states present in human airways. This group is coordinated by Pascal Barbry, Alexander Misharin, Martijn Nawijn and Jay Rajagopal.

Publication:
An integrated cell atlas of the lung in health and disease. Lisa Sikkema et al. (2023). Nature MedicineDOI :10.1038/s41591-023-02327-2

Funding:
This work was supported by many funders including: The Chan Zuckerberg Initiative, European Union H2020 (Discovair), Fondation pour la Recherche Médicale, National Infrastructure France Génomique, Wellcome, The Netherlands Lung Foundation, The German Center for Lung Research, the Helmholtz Association and the European Respiratory Society. Please see the paper for full list of funders.


Selected Websites:

Helmholtz Munich
Helmholtz Munich is a leading biomedical research center. Its mission is to develop breakthrough solutions for better health in a rapidly changing world. Interdisciplinary research teams focus on environmentally triggered diseases, especially the therapy and prevention of diabetes, obesity, allergies, and chronic lung diseases. With the power of artificial intelligence and bioengineering, researchers accelerate the translation to patients. Helmholtz Munich has more than 2,500 employees and is headquartered in Munich/Neuherberg. It is a member of the Helmholtz Association, with more than 43,000 employees and 18 research centers the largest scientific organization in Germany. More about Helmholtz Munich (Helmholtz Zentrum München Deutsches Forschungszentrum für Gesundheit und Umwelt GmbH): www.helmholtz-munich.de/en [helmholtz-munich.de] 

University Medical Center Groningen
The University Medical Center Groningen (UMCG) is one of the largest hospitals in the Netherlands and is the largest employer in the Northern Netherlands. More
characterized by a combination of fundamental and patient oriented clinical research. The interaction between these two stimulates the development of new clinical and research opportunities. Problems that occur in the clinical practice act as a catalyst which sets new fundamental research in motion, whereas fundamental research can come up with new clinical possibilities. The UMCG focuses on healthy ageing in all priority areas: research, clinical care and education. Together we push boundaries for a sustainable future of health. https://umcgresearch.org/

Mouse models of adolescent binge drinking reveal key long-lasting brain changes

Peer-Reviewed Publication

PENN STATE

Avery Sicher 

IMAGE: PENN STATE NEUROSCIENCE DOCTORAL STUDENT AVERY SICHER WORKS IN THE LAB, DOING PATCH-CLAMP ELECTROPHYSIOLOGY. view more 

CREDIT: DAN LESHER / PENN STATE




UNIVERSITY PARK, Pa — Heavy alcohol consumption may cause permanent dysregulation of neurons, or brain cells, in adolescents, according to a new study in mice. The findings suggest that exposure to binge-levels of alcohol during adolescence, when the brain is still developing, lead to long-lasting changes in the brain’s ability to signal and communicate — potentially setting the stage for long-term behavioral changes and hinting towards the mechanisms of alcohol-induced cognitive changes in humans.

“What we’re seeing here,” said Nikki Crowley, assistant professor in biology and biomedical engineering and Huck Early Chair in Neurobiology and Neural Engineering, “is that if adolescent binge drinking knocks neurons off this trajectory, they might not be able to get back, even if the alcohol consumption stops.”

The prefrontal cortex is a key brain region for executive functioning, risk assessment and decision-making. According to Crowley, it’s not fully formed in adolescents and is still maturing in humans until around age 25. Disruptions to its development in young people may have serious and long-lasting consequences, added Crowley.

“Heavy binge drinking is problematic for everyone, and should be avoided, but adolescent brains appear to be particularly vulnerable to the consequences, which in humans, will follow them for decades,” Crowley said.

The team, led by Avery Sicher, a doctoral student in Penn State’s neuroscience program, used a model of adolescent ethanol exposure in mice to understand how different populations of neurons in the cortex, the outermost layer of the brain, are changed by voluntary binge alcohol consumption. In this model, mice are known to consume alcohol in patterns that approximate human binge drinking — defined by the National Institute on Alcohol Abuse and Alcoholism as a pattern of alcohol consumption that leads to a blood alcohol concentration of 0.08% or higher, usually in about two hours. Binge drinking is considered to be one of the most dangerous patterns of alcohol misuse, and understanding its impact on the developing brain can help inform treatment.

Sicher and her colleagues gave mice access to alcohol during a 30-day period. Due to their faster development and shorter lifespan, this corresponded to roughly ages 11-18 in human years. They then looked at the electrophysiological properties of different neurons throughout the prefrontal cortex to understand how adolescent binge drinking influenced the wiring and firing of these circuits. Sicher et al. used whole-cell patch clamp electrophysiology, combined with techniques such as optogenetics, which allowed the team to isolate individual neurons and record measurements related to intrinsic excitability, such as the resting membrane potential and the ability for each neuron to fire action potentials. This allowed them to understand how these neurons had changed their ability to signal with other neurons.

They found that somatostatin neurons, a key population of cells that provides inhibition of neurotransmitter release from other cell types throughout the brain and helps to “dampen the noise,” appeared to be permanently dysregulated in the mice that binge drank as compared to mice that were only provided water throughout development. Somatostatin neurons release both inhibitory neurotransmitters, like GABA, as well as inhibitory peptides like somatostatin, and proper functioning of these neurons is necessary for a healthy brain. The neurons were more excitable — meaning they were signaling too much and dampening the activity of other key neurons — as far out as 30 days after the mice stopped drinking alcohol, when the mice have transitioned into adulthood.

“Neurons have a relatively fixed developmental trajectory — they need to get where they are going and sync up with the right partners during specific periods of development in order to function properly,” explained Crowley.

David Starnes, an undergraduate biology student in Schreyer’s Honor College, performed somatostatin cell counts to quantify cell density before and after ethanol consumption. He found that while the electrophysiology data suggested these neurons wire differently, the number of SST neurons does not appear to change as a result of binge drinking.

Other authors on the paper include Keith Griffith, a research technician in the lab and former undergraduate in Engineering Science and Mechanics, Grace Smith, a graduate student in Biomedical Engineering, Dakota Brockway, a graduate student in neuroscience, and Nigel Dao, a former research technician in the lab and current doctoral student at New York University. This research was supported by the National Institutes of Health and the Huck Institutes of the Life Sciences at Penn State.

To learn more about Sicher’s neuroscience research, watch this short video from the Huck Institutes’ Student Spotlight series. The paper is currently available in the online version of the journal Neuropharmacology and will be published in the Aug. 15 issue.

Black, Hispanic survivors of breast cancer have higher death rates from second cancers

Peer-Reviewed Publication

JOHNS HOPKINS MEDICINE

Cancer mortality 

IMAGE: THIS GRAPHIC SHOWS THE PERCENT OF CANCER DEATHS FROM A SECOND CANCER AMONG BREAST CANCER SURVIVORS OVER TIME. EACH COLOR LINE REPRESENTS A DIFFERENT RACE/ETHNICITY, WITH PURPLE REPRESENTING ASIANS, BLACK REPRESENTING HISPANICS, RED REPRESENTING NON-HISPANIC BLACKS AND BLUE REPRESENTING NON-HISPANIC WHITES. view more 

CREDIT: IMAGE COURTESY OF KALA VISVANATHAN



Hispanic and non-Hispanic Black female survivors of breast cancer experience higher death rates after being diagnosed with a second primary cancer than members of other ethnic and racial groups, according to recent research from investigators at the Johns Hopkins Kimmel Cancer Center.

In a study of nearly 40,000 adult survivors of breast cancer, the risk of death from a second cancer was 12% higher among non-Hispanic Black survivors and 8% higher among Hispanic survivors compared with non-Hispanic white survivors. Survivors in racial and ethnic minorities were diagnosed with second cancers up to six years younger than non-Hispanic white survivors, and within a shorter time from their first cancer.

Additionally, non-Hispanic Black survivors had a 44% higher risk of cardiovascular disease-related death after a second cancer diagnosis than non-Hispanic white survivors. These results were published March 9 in the Journal of the National Cancer Institute.

Nearly half of cancer survivors live for more than 10 years, and approximately one in five people diagnosed with cancer has a prior cancer history, according to the National Cancer Institute. Therefore, says senior study author Kala Visvanathan, M.D., M.H.S., director of the Cancer Genetics and Prevention Service at the Kimmel Cancer Center and a member of the Women’s Malignancy Program at Johns Hopkins, it’s important to determine risk factors associated with second cancers so they can best be prevented, or diagnosed and managed as early as possible.

There could be many contributing factors to the poor survival observed after a second cancer, including diagnosis of aggressive tumors, cumulative treatment and type of treatment received, lifestyle factors and social determinants of health, says Visvanathan, who is also director of the cancer epidemiology track at the Johns Hopkins Bloomberg School of Public Health.

“We believe this to be one of the first studies to comprehensively examine the racial and ethnic disparities in survival outcomes after a second cancer,” Visvanathan says. “The findings are extremely concerning given the increasing prevalence of second cancer at a young age among women diagnosed with breast cancers. A multipronged approach is needed to identify biological factors, and patient-, provider- and systems-level contributors to survival outcomes among breast cancer survivors.”

Zhengyi Deng, Ph.D., a former doctoral student at the Bloomberg School of Public Health, was the study’s lead author. The research team evaluated information from 39,029 adult female survivors of breast cancer who developed a second primary cancer in 2000–2014, as recorded in the national Surveillance, Epidemiology and End Results (SEER) 18 Program database. The database, maintained by the National Cancer Institute, covers 18 U.S. cancer registries and represents nearly 28% of the population. Participants were followed until Dec. 31, 2016, or at least two years after the second cancer diagnosis.

Participants’ ethnicity was categorized as Hispanic, non-Hispanic Asian, non-Hispanic Black and non-Hispanic white. Non-Hispanic American Indian or Alaska Native, and Pacific Islander, were excluded from study due to a small number of records. Investigators looked at several variables, including five-year survival rate; demographics including age and year of diagnosis, marital and insurance status, and initial treatments; median household income and education level; and cause of death.

Overall, there were 39,029 second cancers and 15,117 deaths after second cancers. The strongest associations with cancer deaths were among non-Hispanic Black survivors with a second breast or uterine cancer and among Hispanic survivors with a second breast cancer. Secondary cancers occurred at an earlier age in Hispanic (mean age: 62.2), non-Hispanic Asian (mean age: 63.4) and non-Hispanic Black (mean age: 63.5) survivors compared with non-Hispanic white survivors (mean age: 68.8).

Breast cancer was the most common second cancer across all racial and ethnic groups, followed by lung, colorectal and uterine cancer. Second cancers in non-Hispanic Black women were less likely to be diagnosed at a local stage compared with other groups. And, Hispanic and non-Hispanic Black survivors were more likely than members of other groups to need chemotherapy for their first and second cancer.

Looking at cancer mortality, non-Hispanic Black survivors had the highest cumulative mortality during the entire follow-up, followed by Hispanic, non-Hispanic white and non-Hispanic Asian survivors. Later stage at presentation and more aggressive tumor characteristics contributed to increased cancer mortality among Hispanic and non-Hispanic Black survivors after second cancers.

A prior study from the team, the results of which were published last summer in NPJ Breast Cancer, found that cancer survivors with a second cancer had a 27% increased risk of cancer death and 18% increased risk of death from any cause compared to survivors with primary cancers. The research team is continuing studies of patients with second cancers.

Study co-authors were Miranda Jones, Mei-Cheng Wang and Antonio Wolff of Johns Hopkins. The work was supported by the Breast Cancer Research Foundation. Visvanathan received research funding from Cepheid and holds a patent. Wolff also holds a patent. The Johns Hopkins University is managing these relationships in accordance with its conflict-of-interest policies.

Study shows metformin lowers the risk of getting long COVID


Peer-Reviewed Publication

UNIVERSITY OF MINNESOTA MEDICAL SCHOOL




MINNEAPOLIS/ST. PAUL (06/09/2023) — In a new study published in The Lancet Infectious Diseases, University of Minnesota researchers found that metformin, a drug commonly used to treat diabetes, prevents the development of long COVID. 

The study, called COVID-OUT, investigated if early outpatient COVID-19 treatment with metformin, ivermectin or fluvoxamine could prevent long COVID. Long COVID is a chronic illness that can affect up to 10% of people who have had COVID-19. 

“The results of this study are important because long COVID can have a significant impact on people's lives,” said Carolyn Bramante, MD, principal investigator and an assistant professor at the U of M Medical School. “Metformin is an inexpensive, safe and widely available drug, and its use as a preventive measure could have significant public health implications.”

This was a large, placebo-controlled randomized clinical trial which enrolled volunteers across the United States. The study found: 

  • Those who received metformin were more than 40% less likely to develop long COVID than those who received an identical looking placebo. 
  • For participants who started metformin less than four days after their COVID symptoms started, metformin decreased the risk of long COVID by 63%. 
  • The effect was consistent across different demographic populations of volunteers who participated and across multiple viral variants, including the Omicron variant. 
  • Ivermectin and fluvoxamine did not prevent long COVID.

The study included more than 1,200 participants who were randomly chosen to receive either metformin or placebo, and an additional subset received ivermectin, fluvoxamine or their placebos. Participants were between 30 and 85 years old who qualified as overweight or obese. Over 1,100 of the participants reported on their symptoms for up to 10 months after their initial COVID-19 diagnosis. 

“This long-term outcome from a randomized trial is high-quality evidence that metformin prevents harm from the SARS-CoV-2 virus,” said Dr. Bramante, who is also an internist and pediatrician with M Health Fairview. “While half of our trial had been vaccinated, none had been previously infected with the COVID-19 virus. Further research could show whether it is also effective in those with previous infection or in adults with lower body mass index.” 

Metformin’s ability to stop the virus was predicted by a simulator developed by U of M Medical School and College of Science and Engineering Biomedical Engineering faculty. The model has been highly accurate to date, successfully predicting, among others, the failure of hydroxychloroquine and the success of remdesivir before the results of clinical trials testing these therapies were announced.

Funding was provided by the Parsemus Foundation, Rainwater Charitable Foundation, Fast Grants and the United Health Foundation.This research was also supported by the National Institutes of Health’s National Center for Advancing Translational Sciences under award number [UL1TR002494, KL2TR002492, and UM1TR004406]. 

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The University of Minnesota Medical School, School of Public Health, College of Science and Engineering and M Health Fairview served as the lead site. The trial was also conducted at Northwestern University; University of Colorado, Denver; Olive View – UCLA Education & Research Institute in Los Angeles; Optum Health, and with scientific collaboration from partners at the University of North Carolina at Chapel Hill, Vanderbilt University, and Emory University School of Medicine. 

The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health’s National Center for Advancing Translational Sciences.

About the University of Minnesota Medical School
The University of Minnesota Medical School is at the forefront of learning and discovery, transforming medical care and educating the next generation of physicians. Our graduates and faculty produce high-impact biomedical research and advance the practice of medicine. We acknowledge that the U of M Medical School, both the Twin Cities campus and Duluth campus, is located on traditional, ancestral and contemporary lands of the Dakota and the Ojibwe, and scores of other Indigenous people, and we affirm our commitment to tribal communities and their sovereignty as we seek to improve and strengthen our relations with tribal nations. For more information about the U of M Medical School, please visit med.umn.edu.

Worker dies at Fort McMurray ammonium sulphate production plant

Story by Emily Mertz 

Suncor's base plant with upgraders in the oilsands in Fort McMurray Alta, on Monday June 13, 2017. New federal research suggests greenhouse gas emissions from the oilsands may be significantly underestimated, adding to a growing pile of studies that say our understanding of what is going into the atmosphere is incomplete.© Jason Franson, The Canadian Press

A contractor working on the roof of the Chemtrade site in Fort McMurray, Alta., died Thursday.

The company's website says the northern Alberta location is an ammonium sulphate production plant.

The vice-president of the water chemical production company said it was an isolated incident and there was no public danger.

Tim Montgomery said a roofing contractor was doing work on a maintenance building for Chemtrade, which has an operation within the Suncor/Syncrude site. The contractor had done contract work for Chemtrade in the past. Montgomery estimates the man fell more than 25 feet.

"Our deepest sympathy is extended to the family, friends, and colleagues of the individual who sustained fatal injuries while performing services on the roof of our site," Montgomery said in a statement.

"We are working closely with the authorities to support all investigations into this incident.

"Our plant has been safely shut down and our immediate focus is supporting our on-site personnel and all those affected by this tragedy."

The name or age of the worker has not been released.

Counselling services are being provided to staff, Montgomery said.

Occupational Health and Safety is investigating and Chemtrade is fully complying.

Unlocking early Earth chemistry: Salt-induced changes in polyester microdroplet structure


Peer-Reviewed Publication

TOKYO INSTITUTE OF TECHNOLOGY

Differential Salt Uptake in Polyester Microdroplets 

IMAGE: - view more 

CREDIT: TOKYO TECH




Billions of years ago, Earth was an extremely hostile planet with active volcanoes, a harsh atmosphere, and certainly no life! This prebiotic Earth, however, was filled with a wide array of abiotic organic molecules derived from its early environment, which underwent chemical reactions that eventually led to the origin of life. A class of such abiotic molecules abundant during the prebiotic era was the 𝛼-hydroxy acid (𝛼HA)–monomers with structures somewhat similar to those of the 𝛼-amino acids essential to modern life. However, their present abundance in biology is low.

Polyester microdroplets generated from dehydration and rehydration of 𝛼HA monomers were proposed as protocell models and could have been a type of primitive compartment that interacted with and took up various primitive analytes, such as salts within primitive aqueous environments. However, salt–polyester interactions and salt-uptake within polyester microdroplets remains poorly studied due to a lack of appropriate analytical techniques.

To bridge this gap in understanding, a team of researchers led by Special Postdoctoral Researcher Chen Chen from RIKEN (formerly of Tokyo Institute of Technology) and Specially Appointed Associate Professor Tony Z. Jia from the Earth-Life Science Institute at Tokyo Institute of Technology have recently come up with a new strategy for investigating the effect of salt uptake on polyester microdroplets. Their breakthrough, published in Small Methods on May 18, 2023, proposed a novel way of using existing spectroscopic and biophysical methods to characterize salt uptake by polyester microdroplets and understand their salt-mediated behavior.

“Primitive molecules such as 𝛼HAs and polyesters, though not as commonly used by current living systems as amino acids, may have laid the ground for the evolution of primitive chemical systems that led to the origin of life on Earth. Examining the interaction of polyesters with different prebiotic analytes such as salts and determining whether polyester droplets can uptake salts can provide insights into the relevant functions exhibited by primitive compartments,” explains Prof. Jia.

𝛼HAs such as ᴅʟ-3-phenyllactic acid (PA) can undergo dehydration under early Earth mimicking conditions to form gel-like polyesters; further rehydration results in assembly of membraneless microdroplets. These membraneless droplets have previously been found to segregate primitive analytes such as nucleic acids, small organic molecules, and proteins.

Studies have hypothesized that life originated and evolved in ancient aqueous environments. If polyester microdroplets existed in primitive aqueous environments, then they might have also uptaken salts, a major analyte found in primitive aqueous environments, which could have subsequently changed the microdroplets’ structure as well. Thus, the team subjected various 𝛼HAs, such as PA (a neutral monomer), malic acid (a monomer with an acidic side chain), and 4-amino-2-hydroxybutyric acid (a monomer with a basic side chain) to dehydration synthesis, followed by rehydration in aqueous medium to generate neutral, acidic residue-containing, and basic residue-containing polyester microdroplets. In fact, this study was the first to show the plausibility of acidic residue-containing polyester microdroplets! They then incubated the polyester microdroplets in aqueous solutions consisting of different concentrations of different chloride salts (NaCl, KCl, MgCl2, and CaCl2) that may have been abundant in early oceans.

Post salt uptake, the polyester microdroplets were subjected to a novel analytical technique utilizing inductively coupled plasma mass spectrometry (ICP–MS) to analyze the salt cation concentration within the microdroplets. The analyses were performed in collaboration with researchers from the Pheasant Memorial Lab at the Institute of Planetary Materials at Okayama University, where the ICP–MS was located, as part of a joint use collaborative grant. Furthermore, in collaboration with other members, each with unique specialties, the team then coupled ICP–MS with other spectroscopic and biophysical analytical methods, such as zeta potential analysis, optical density, dynamic light scattering, and micro-Raman imaging to study in detail how salt uptake affects the surface potential, droplet turbidity, size, and internal water distribution, respectively, of the microdroplets.

The results indicated that microdroplets possessed the ability to selectively partition salt cations, leading to differential coalescence of microdroplets, likely due to reduced electrostatic repulsions between the microdroplets as a result of surface charge neutralization by the uptaken salts, which preferentially localized to the droplet surface. The present study highlights that even slight changes in salt-uptake could significantly affect protocell structure, which could potentially account for diversity in chemistries of primitive systems that emerged in different aqueous systems—ranging from freshwater to oceanic to hypersaline under-ocean brines. “The adoption of a novel and highly sensitive strategy for analyzing salt uptake by polyester microdroplets widened the range of known primitive chemicals that could have had an effect on primitive protocell structure and function. This opens new avenues for future investigations regarding the relevance of polyester microdroplets during the origins of life both on and off Earth,” concludes Dr. Chen.