. Scientific Frontline

Friday, June 17, 2022

Chemical pollution threatens biodiversity

Chemicals threaten biodiversity - not only because they can directly poison animals and plants, but because they affect the living conditions and functions of living things.
Credit: Gabriel Sigmund & Aaron Kintz

Pollution of the environment with chemicals threatens biodiversity. The complexity of this pollution has so far been insufficiently recorded by decision-makers - this is what international researchers around Gabriel Sigmund from the University of Vienna and Ksenia Groh from the Eawag water research institute (Dübendorf, Switzerland) are writing in the current issue of the journal Science. They appeal to decision-makers and researchers to consider more chemicals than previously planned. Your contribution will appear shortly before the international negotiations on a new biodiversity agreement, the "post-2020 Global Biodiversity Framework". These take place from the 21st. June in Nairobi (Kenya).

"Design to the agreement mentions chemical pollution, but it only takes nutrients, pesticides and plastic waste into account and falls short of it," explains environmental scientist Gabriel Sigmund. "Many highly problematic chemicals that pollute the environment and thus threaten the diversity of animal and plant species are simply overlooked," added ecotoxicologist Ksenia Groh. This does not do justice to the immense variety of man-made chemicals. So far not considered in the draft agreement, but from the perspective of the researchers toxic metals, industrial chemicals, chemicals from consumer goods, pharmaceuticals and the often-unknown conversion products of these chemicals are problematic.

Research reveals the northernmost glaciers on the globe are melting at record speed

Coastal glaciers in northern Greenland
image resized using AI by SFLORG
Credit: William Colgan

Greenland's many small glaciers are melting at great speed, and the melting is increasing, especially in the Arctic regions, where the temperature rise is worst.

Now, researchers have studied precisely how much mass these glaciers – not connected to the ice sheet – have lost in recent decades.

In the Arctic, temperatures are rising more than in the rest of the world, and this is causing the northernmost glaciers in Greenland to melt at record speed. This is shown in a new study by researchers led by DTU Space in collaboration with Geological Survey of Denmark and Greenland (GEUS), NASA Goddard Space Flight Center, Utrecht University, University of Bristol, Technical University Munich, and the University of Copenhagen.

The study focuses on smaller glaciers with no connection to the Greenland Ice Sheet. These peripheral glaciers make up only about four percent of Greenland's ice-covered areas, corresponding to approximately the same area as Ireland (72,000 km2), but they contribute as much as 11 percent of the total loss of ice from Greenland's ice-covered areas. Thus, they are a major contributor to global sea level rise.

"The loss of ice from these small glaciers occurs because they are more sensitive to ongoing temperature changes and therefore melt faster than we see in many other places in the Arctic," said Professor Shfaqat Abbas Khan from DTU Space, lead author of the paper published in Geophysical Research Letters.

Heart surgery delays will cost lives


Urgent action is needed to clear the backlog of people with a common heart condition who are waiting for lifesaving treatment, according to research published in the journal BMJ Open. Researchers have warned that a lack of action could result in thousands of people dying while waiting for treatment.

The COVID-19 pandemic has led to thousands of heart procedures being postponed and record waiting lists. Previous work has estimated that 4,989 people in England with severe aortic stenosis missed out on life-saving treatment between March and November 2020.

Aortic stenosis develops when the heart’s aortic valve becomes narrowed, restricting blood flow out of the heart. Prompt treatment is vital for people diagnosed with severe aortic stenosis, as around 50 percent will die within two years of symptoms beginning.

Now, an international team of researchers, including those from the University of Cambridge, has modelled the impact that increasing treatment capacity and using a quicker, less invasive treatment option would have on waiting lists. Even in the best-case scenario, they found that the waiting list would take nearly a year to clear and over 700 people would die while waiting for treatment. The research was funded by the British Heart Foundation and the EPSRC Cambridge Centre for Mathematics of Information in Healthcare.

An Experimental Treatment Failed in Mice, and Researchers Did the Right Thing: They Published About It

Treatment of FOP mice with an antibody to ACVR1 greatly exacerbates abnormal bone formation (heterotopic ossification) following muscle injury. This is a 3D-rendered microCT image in which the heterotopic bone has been colorized green.
Source: University of Connecticut

Blocking the mutant protein with an antibody didn’t stop the strange, abnormal bone growths in mice. But the knowledge gained could steer scientists toward more promising approaches, report researchers from UConn and Alexion Pharmaceuticals in the The Journal of Clinical Investigation.

Fewer than 4,000 people worldwide are afflicted with fibrodysplasia ossificans progressiva (FOP), an inherited disease in which small injuries or bruises to skeletal muscle provoke the growth of massive, abnormal bone and cartilage. Gradually much of the body’s soft tissue turns to bone. Now, researchers at UConn and Alexion Pharmaceuticals who were investigating a potential cure instead found a concerning surprise–blocking the protein responsible for the disease with a monoclonal antibody made the abnormal bone growth worse in mice.

Normally, stem cells help repair muscle damaged by injury or disease. But in people with FOP, certain stem cells get the wrong message from a mutant receptor on their surface. Instead of promoting muscle regeneration, the stem cells develop into bone.

UConn Professor of Molecular and Cell Biology David Goldhamer, Alexion Pharmaceuticals researcher Jeffrey Hunter, and colleagues worked for years to discover a potential antibody therapy for FOP using accurate genetic mouse models of the disease developed by the two groups. The idea was that the antibody would block the mutant receptor and prevent the responsible stem cells from making new bone. But the results were exactly the opposite.

A new hope for a therapy against retinitis pigmentosa

Retinitis pigmentosa is the most common hereditary retinal disease in humans, with a prevalence of one in every 4,000 people worldwide.
Photo by Danish Ahmad

Retinitis pigmentosa, a degenerative genetic disease of the eye, is characterized by progressive vision loss, usually leading to blindness. In some patients, structural defects in the photoreceptor cells have been observed, but the molecular mechanisms involved are not understood. A team from the University of Geneva (UNIGE), in collaboration with the University of Lausanne (UNIL), has identified the essential role played by a molecular zipper formed by four proteins. The absence of this zipper leads to cell death in retinal cells. This discovery could lead to the development of therapeutic approaches for retinitis pigmentosa. This work can be read in the journal PLOS Biology.

Retinitis pigmentosa is the most common hereditary retinal disease in humans, with a prevalence of one in every 4,000 people worldwide. The first symptoms usually appear between the ages of 10 and 20 with a loss of night vision. Thereafter, the visual field narrows into a “tunnel vision” to finally lead to blindness around the age of 40. This disease is characterized by a degeneration of the light sensitive cells, the photoreceptors.

These specialized neuronal cells of the retina are responsible for the conversion of light into a nerve signal. The outer segment of the cell is made up of stacks of discs on which the light-sensitive pigments are located. The inner segment contains all the metabolic machinery essential to the functioning of the cell and is linked to the outer segment by the connecting cilium.

Flawed research not retracted fast enough to prevent spread of misinformation

People who engage with research critically on Twitter may contribute to valuable conservations about science, new research suggests.
Illustration by ijmaki via Pixabay

A new analysis by Northwestern University and University of Michigan researchers suggests retracting academic papers does not dampen the reach of problematic research as intended. Instead, papers that are later retracted are often widely circulated online, both by news outlets and social media, and the cycle of attention that they receive typically dies away before the retraction even happens.

The finding has concerning implications for the spread of misinformation and public trust in science. However, retracted papers included in the analysis were often the subject of more critical discourse on Twitter before their retraction, suggesting that while Twitter should not be an official judge of science, it’s possible that in some communities, it could provide early signals of dubious research.

When a paper is retracted, the goal is to officially discredit it and acknowledge the research as flawed, thereby maintaining the overall integrity of the research enterprise. However, many people who hear about the initial finding may never learn of the retraction.

“Social media and even top news outlets — the most prestigious venues that cover science — are more prone to talk about papers that end up being retracted,” said Ágnes Horvát, an assistant professor of communication and computer science at Northwestern who was an author on the paper, published in the Proceedings of the National Academy of Sciences.

Going Platinum: A Non-Toxic Catalyst for Clean, Re-Usable Water

Harmful aldehydes (found in treated wastewater can be transformed to carboxylic acids by using the existing oxygen found in water and platinum as a catalyst to speed up the reaction. note: The reaction scheme shown appears not to be balanced. The illustration is used to simplify the presentation of the multiple reactions occurring and which are balanced. details are available in the material cited.
Image Credit: Daniel McCurry.

Platinum has set a new “gold standard” in jewelry, and now it’s about to upscale the quality of your water.

As wastewater treatment for potable – drinkable – reuse becomes a more viable and popular option to address water shortages, the question of what harmful byproducts might form in treatment and how to address them looms large. One group of these chemicals, aldehydes, are known to stubbornly persist through treatment. Toxic to humans, aldehydes will be at the top of the list of regulated byproducts in forthcoming reuse regulations, USC researchers believe, and require sustainable methodology to be removed from our drinking water.

In research published in Environmental Science & Technology, USC Viterbi School of Engineering researchers introduced platinum to help clean even the most stubborn toxins from wastewater. Platinum, the same metal used in catalytic converters to clean up air pollutants in car exhaust, can serve as a catalyst, said Dan McCurry, assistant professor in civil and environmental engineering, speeding up oxidation to transform once-toxic aldehydes into harmless carboxylic acids.

New research on dust mites and respiratory infections

Lena Uller
Credit: Agata Garpenlind
When asthmatics’ respiratory tracts are exposed to dust mites, their immune response becomes less effective, which can lead to a weaker immune system. People who suffer from asthma associated with infection may therefore be more susceptible to secondary viral or bacterial infections. According to the researchers, the results suggest that asthmatics should avoid house dust mites and that patients who are also allergic to the mites should consider undergoing so-called hyposensitization. The study was recently published in Allergy.

In an earlier study, Professor Lena Uller and her research team have shown that house dust mites, when compared to other common allergens, give rise to a more powerful inflammatory response in the epithelium cells in the lungs of asthmatics. These epithelium cells are a barrier intended to protect the lungs from harmful microbes and particles that we breathe in.

Clinical data has shown that asthma patients with allergies are more frequently prescribed antibiotics, compared to non-allergic asthmatics, according to Samuel Cerps, first author of the study, which was part of the doctoral thesis he submitted in late May.

“This suggests that allergy is a risk factor in bacterial infections and that got us interested in studying how exposure to house dust mites affects the immune system of asthmatics,” says Cerps.

Using bronchial brushing, the researchers collected and cultivated epithelial cells from asthmatics including those with and without a dust mite allergy. The cells were then exposed to dust mites for 24 hours before being exposed to a virus. Through this method, the researchers were able to investigate how a viral infection affects the immune system in terms of both viral and bacterial infections.

Tenascin proteins inhibit cell sheath regeneration

Juliane Bauch (left) and Andreas Faissner from the Chair of Cell Morphology and Molecular Neurobiology
Credit: RUB, Kramer

In multiple sclerosis, nerve cells lose their insulating layer. Researchers from Bochum are looking for starting points to promote regeneration processes. They have identified two relevant proteins.

Researchers at the Ruhr University Bochum have investigated the role that the two proteins tenascin C and tenascin R play in multiple sclerosis. In the disease, cells of the immune system destroy the myelin sheaths, i.e. the sheathing of the nerve cells. As the Bochum team showed in experiments with mice, the presence of the two Tenascins inhibits the regeneration of the myelin sheaths. Dr. Juliane Bauch and Prof. Dr. Andreas Faissner from the Bochum Chair for Cell Morphology and Molecular Neurobiology describes the results in the journal Cells.

The cause of the destruction of myelin sheaths in multiple sclerosis has not yet been clarified. "But the organism has various mechanisms to partially compensate for the lesions," says Juliane Bauch, who dealt intensively with the topic in her doctorate. The aim of the work is to identify starting points with which the regeneration of myelin sheaths could be improved.

Thursday, June 16, 2022

Experiment results confirm anomaly suggesting new physics possibility

Located deep underground at the Baksan Neutrino Observatory in the Caucasus mountains in Russia, the completed two-zone gallium target, at left, contains an inner and outer tank of gallium, which is irradiated by an electron neutrino source.
image resized using AI by SFLORG
Credit: A.A. Shikhin

New scientific results confirm an anomaly seen in previous experiments, which may point to an as-yet-unconfirmed new elementary particle, the sterile neutrino, or indicate the need for a new interpretation of an aspect of standard model physics, such as the neutrino cross section, first measured 60 years ago. Los Alamos National Laboratory is the lead American institution collaborating on the Baksan Experiment on Sterile Transitions (BEST) experiment, results of which were recently published in the journals Physical Review Letters and Physical Review C.

“The results are very exciting,” said Steve Elliott, lead analyst of one of the teams evaluating the data and a member of Los Alamos’ Physics division. “This definitely reaffirms the anomaly we’ve seen in previous experiments. But what this means is not obvious. There are now conflicting results about sterile neutrinos. If the results indicate fundamental nuclear or atomic physics are misunderstood, that would be very interesting, too.” Other members of the Los Alamos team include Ralph Massarczyk and Inwook Kim.

More than a mile underground in the Baksan Neutrino Observatory in Russia’s Caucasus Mountains, BEST used 26 irradiated disks of chromium 51, a synthetic radioisotope of chromium and the 3.4 megacurie source of electron neutrinos, to irradiate an inner and outer tank of gallium, a soft, silvery metal also used in previous experiments, though previously in a one-tank set-up. The reaction between the electron neutrinos from the chromium 51 and the gallium produces the isotope germanium 71.

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