SwRI Models Point to a Potentially Diverse Metabolic Menu at Enceladus (Planetary Science)

Discovery provides more evidence that the Saturn moon could support life in its subsurface ocean.

Using data from NASA’s Cassini spacecraft, scientists at Southwest Research Institute (SwRI) modeled chemical processes in the subsurface ocean of Saturn’s moon Enceladus. The studies indicate the possibility that a varied metabolic menu could support a potentially diverse microbial community in the liquid water ocean beneath the moon’s icy facade.

This figure illustrates a cross-section of Enceladus, showing a summary of the processes SwRI scientists modeled in the Saturn moon. Oxidants produced in the surface ice when water molecules are broken apart by radiation can combine with reductants produced by hydrothermal activity and other water-rock reactions, creating an energy source for potential life in the ocean. © SwRI

Prior to its deorbit in September of 2017, Cassini sampled the plume of ice grains and water vapor erupting from cracks on the icy surface of Enceladus, discovering molecular hydrogen, a potential food source for microbes. A new paper published in the planetary science journal Icarus explores other potential energy sources.

“The detection of molecular hydrogen (H2) in the plume indicated that there is free energy available in the ocean of Enceladus,” said lead author Christine Ray, who works part time at SwRI as she pursues a Ph.D. in physics from The University of Texas at San Antonio. “On Earth, aerobic, or oxygen-breathing, creatures consume energy in organic matter such as glucose and oxygen to create carbon dioxide and water. Anaerobic microbes can metabolize hydrogen to create methane. All life can be distilled to similar chemical reactions associated with a disequilibrium between oxidant and reductant compounds.”

This disequilibrium creates a potential energy gradient, where redox chemistry transfers electrons between chemical species, most often with one species undergoing oxidation while another species undergoes reduction. These processes are vital to many basic functions of life, including photosynthesis and respiration. For example, hydrogen is a source of chemical energy supporting anaerobic microbes that live in the Earth’s oceans near hydrothermal vents. At Earth’s ocean floor, hydrothermal vents emit hot, energy-rich, mineral-laden fluids that allow unique ecosystems teeming with unusual creatures to thrive. Previous research found growing evidence of hydrothermal vents and chemical disequilibrium on Enceladus, which hints at habitable conditions in its subsurface ocean.

“We wondered if other types of metabolic pathways could also provide sources of energy in Enceladus’ ocean,” Ray said. “Because that would require a different set of oxidants that we have not yet detected in the plume of Enceladus, we performed chemical modeling to determine if the conditions in the ocean and the rocky core could support these chemical processes.”

For example, the authors looked at how ionizing radiation from space could create the oxidants O2 and H2O2, and how abiotic geochemistry in the ocean and rocky core could contribute to chemical disequilibria that might support metabolic processes. The team considered whether these oxidants could accumulate over time if reductants are not present in appreciable amounts. They also considered how aqueous reductants or seafloor minerals could convert these oxidants into sulfates and iron oxides.

“We compared our free energy estimates to ecosystems on Earth and determined that, overall, our values for both aerobic and anaerobic metabolisms meet or exceed minimum requirements,” Ray said. “These results indicate that oxidant production and oxidation chemistry could contribute to supporting possible life and a metabolically diverse microbial community on Enceladus.”

“Now that we’ve identified potential food sources for microbes, the next question to ask is ‘what is the nature of the complex organics that are coming out of the ocean?'” said SwRI Program Director Dr. Hunter Waite, a coauthor of the new paper, referencing an online Nature paper authored by Postberg et al. in 2018. “This new paper is another step in understanding how a small moon can sustain life in ways that completely exceed our expectations!”

The paper’s findings also have great significance for the next generation of exploration.

“A future spacecraft could fly through the plume of Enceladus to test this paper’s predictions on the abundances of oxidized compounds in the ocean,” said SwRI Senior Research Scientist Dr. Christopher Glein, another coauthor. “We must be cautious, but I find it exhilarating to ponder whether there might be strange forms of life that take advantage of these sources of energy that appear to be fundamental to the workings of Enceladus.”

References: Christine Ray, Christopher R. Glein, J. Hunter Waite, Ben Teolis, Tori Hoehler, Julie Huber, Jonathan Lunine, Frank Postberg, “Oxidation processes diversify the metabolic menu on Enceladus”, Icarus, 2020, 114248, ISSN 0019-1035,
https://doi.org/10.1016/j.icarus.2020.114248.
(http://www.sciencedirect.com/science/article/pii/S001910352030573X)

Provided by Southwest Research Institute

Information Transport in Antiferromagnets via Pseudospin-magnons (Physics)

A team of researchers from the Technical University of Munich, the Walther-Meissner-Institute of the Bavarian Academy of Sciences and Humanities, and the Norwegian University of Science and Technology in Trondheim has discovered an exciting method for controlling spin carried by quantized spin wave excitations in antiferromagnetic insulators.

A research team from the Technical University of Munich (TUM), the Bavarian Academy of Sciences and Humanities, and the Norwegian University of Science and Technology (NTNU) in Trondheim has succeeded in creating excitations in the magnetic order in a thin layer of hematite that can be moved through the layer in order to transmit information. © Christoph Hohmann / MCQST

Elementary particles carry an intrinsic angular momentum known as their spin. For an electron, the spin can take only two particular values relative to a quantization axis, letting us denote them as spin-up and spin-down electrons. This intrinsic two-valuedness of the electron spin is at the core of many fascinating effects in physics.

In today’s information technology, the spin of an electron and the associated magnetic momentum are exploited in applications of information storage and readout of magnetic media, like hard disks and magnetic tapes.

Antiferromagnets: future stars in magnetic data storage?

Both, the storage media and the readout sensors utilize ferromagnetically ordered materials, where all magnetic moments align parallel. However, the moments may orient in a more complex way. In antiferromagnets, the “antagonist to a ferromagnet”, neighboring moments align in an anti-parallel fashion. While these systems look “non-magnetic” from outside, they have attracted broad attention as they promise robustness against external magnetic fields and faster control. Thus, they are considered as the new kids on the block for applications in magnetic storage and unconventional computing.

One important question in this context is, whether and how information can be transported and detected in antiferromagnets. Researchers at the Technical University of Munich, the Walther-Meissner-Institute and the Norwegian University of Science and Technology in Trondheim studied the antiferromagnetic insulator hematite in this respect.

In this system, charge carriers are absent and therefore it is a particularly interesting testbed for the investigation of novel applications, where one aims at avoiding dissipation by a finite electrical resistance. The scientists discovered a new effect unique to the transport of antiferromagnetic excitations, which opens up new possibilities for information processing with antiferromagnets.

Unleashing the pseudospin in antiferromagnets

Dr Matthias Althammer, the lead researcher on the project describes the effect as follows: “In the antiferromagnetic phase, neighboring spins are aligned in an anti-parallel fashion. However, there are quantized excitations called magnons. Those carry information encoded in their spin and can propagate in the system. Due to the two antiparallel-coupled spin species in the antiferromagnet the excitation is of a complex nature, however, its properties can be cast in an effective spin, a pseudospin. We could experimentally demonstrate that we can manipulate this pseudospin, and its propagation with a magnetic field.”

Dr Akashdeep Kamra, the lead theoretician from NTNU in Trondheim adds that “this mapping of the excitations of an antiferromagnet onto a pseudospin enables an understanding and a powerful approach which has been the crucial foundation for treating transport phenomena in electronic systems. In our case, this enables us to describe the dynamics of the system in a much easier manner, but still maintain a full quantitative description of the system. Most importantly, the experiments provide a proof-of-concept for the pseudospin, a concept which is closely related to fundamental quantum mechanics.”

Unlocking the full potential of antiferromagnetic magnons

This first experimental demonstration of magnon pseudospin dynamics in an antiferromagnetic insulator not only confirms the theoretical conjectures on magnon transport in antiferromagnets, but also provides an experimental platform for expanding towards rich electronics inspired phenomena.

“We may be able to realize fascinating new stuff such as the magnon analogue of a topological insulator in antiferromagnetic materials” points out Rudolf Gross, director of the Walther-Meissner-Institute, Professor for Technical Physics (E23) at the Technical University of Munich and co-speaker for the cluster of excellence Munich Center for Quantum Science and Technology (MCQST). “Our work provides an exciting perspective for quantum applications based on magnons in antiferromagnets”

The research was funded by the Deutsche Forschungsgemeinschaft (DFG) via the cluster of excellence Munich Center for Quantum Science and Technology (MCQST) and by the Research Council of Norway.

References: (1) A. Kamra, T. Wimmer, H. Huebl, M. Althammer, “Antiferromagnetic magnon pseudospin: Dynamics and diffusive transport”, Physical Review B 102, 174445 (2020) – DOI: 10.1103/PhysRevB.102.174445 https://journals.aps.org/prb/abstract/10.1103/PhysRevB.102.174445 (2) T. Wimmer, A. Kamra, J. Gückelhorn, M. Opel, S. Geprägs, R. Gross, H. Huebl, M. Althammer, “Observation of Antiferromagnetic Magnon Pseudospin Dynamics and the Hanle Effect”, Physical Review Letters 125, 247204 (2020) – DOI: 10.1103/PhysRevLett.125.247204 https://journals.aps.org/prl/abstract/10.1103/PhysRevLett.125.247204

Provided by Technical University of Munich

Cancer: Tumor Driver Promoting EMT, Metastasis And Resistance to Therapy (Medicine / Oncology)

Cancer metastasis, which is the dissemination of tumor cells into distant organs, is the leading cause of mortality in cancer patients. To undergo metastasis, cells must leave the primary tumor, circulate into the blood, colonize distant organs, and form distant metastasis. It has been proposed that epithelial to mesenchymal transition (EMT), a process in which epithelial cells detach from their neighboring cells, and acquire mesenchymal migrating properties, is important to initiate the metastatic cascade allowing the cancer cells to leave the primary tumor. However, the role of genetic mutations in promoting EMT is unknown.

FAT1 is among the most frequently mutated driver genes in a broad range of human cancers. The loss of function mutations in this gene suggest that FAT1 acts as tumour suppressor, preventing cancer development. However, and despite the high frequency of FAT1 mutations, its role in cancer is poorly understood.

In a study published in Nature, researchers led by Prof. Cedric Blanpain, MD/PhD, WELBIO investigator, Director of the Laboratory of Stem Cells and Cancer and Professor at the Université libre de Bruxelles, Belgium, demonstrated, for the first time, that loss of FAT1, promote EMT, invasive features and metastasis in skin squamous cell carcinoma -the second most frequent cancer in humans-, lung cancer -the deadliest cancer – and head and neck tumors.

Ievgenia Pastushenko and colleagues used state of the art genetic models of skin and lung cancers, as well as human skin, lung and head and neck tumors to assess the role of FAT1 in cancer.

The authors discovered that loss of function of FAT1, promotes hybrid EMT phenotype, characterized by the co-expression of epithelial and mesenchymal genes in tumor cells. The authors demonstrated that this hybrid EMT state occurring following FAT1 loss of function, promotes metastasis and was associated with poor clinical outcome in patients with lung cancers. “It was particularly exciting to identify that mutations in a single gene, FAT1, promote hybrid EMT state, leading to metastasis and associated with poor prognosis in cancer patients” comments Ievgenia Pastushenko, the first author of this study.

Using different molecular approaches, the authors decipher the mechanisms by which FAT1 mutations promote hybrid EMT state. “The identification of the mechanisms that promote this highly metastatic tumor state, allowed us to identify drug resistance and vulnerabilities in FAT1 mutated cancers. We found that Fat1 mutated cancers are highly resistant to several drugs including EGFR inhibitor that are frequently used to treat patients with lung cancers. Most interestingly, we identify that FAT1 mutated cancers are particularly sensitive to other drugs including Src inhibitor that are currently used to treat patients with blood cancer. These findings will have very important and immediate implications for personalized therapy in patients FAT1 mutated cancers”, comments Pr Cedric Blanpain, the senior author of this study.

This study is a result of a fruitful collaboration between different research groups and clinical departments in Belgium, France and Spain. In Belgium, the teams of Pr Isabelle Salmon and other departments from the Hospital Erasme, Brugman Hospital, as well as Institute Bordet, Cliniques d’Europe, KU Leuven and VIB participated in the study. In France, Francoise Helmbacher from Universités de Marseille et Manuel Thery from Université de Paris participated in this study. In Spain, Spanish Academy of Dermatology and the Hospitals Ramon y Cajal (Madrid), Hospital Clinic (Barcelona), Hospital Clinico Lozano Blesa (Zaragoza), Complejo Asistencial de Leon (Leon), Clinica Universitaria de Navarra (Pamplona), Hospital Costa del Sol (Marbella) and Instituto Valenciano de Oncologia (Valencia) participated in the study.

This work was supported by the FNRS, TELEVIE, WELBIO, the Fondation Contre le Cancer, the ULB fondation, Fonds Erasme, the European Research Council (ERC), and the foundation Baillet Latour.

References: Pastushenko, I., Mauri, F., Song, Y. et al. Fat1 deletion promotes hybrid EMT state, tumour stemness and metastasis. Nature (2020). https://www.nature.com/articles/s41586-020-03046-1 https://doi.org/10.1038/s41586-020-03046-1

Provided by Université libre de Bruxelles

Some Neurons Target Tiny Cerebral Blood Vessel Dilation (Neuroscience)

Neurons control blood flow in tiny vessels in the brain, but researchers know little about this relationship. Now a team of Penn State engineers has found a connection between nitric oxide expressing neurons and changes in arterial diameters in mice, which may shed light on brain function and aging.

Section of a brain showing neurons that have nNOS-expressing neurons labeled in green, DREADD-expressing neurons in magenta. Neurons that express both show up as white. © Jordan Norwood, Penn State

“The brain has many types of neurons,” said Patrick J. Drew, Huck Distinguished Associate Professor of Engineering Science and Mechanics, Neurosurgery and Biomedical Engineering. “People have observed that blood flow and neural activity go together, and we wanted to measure the blood flow and activity in specific subtypes of neurons.”

The researchers looked for a way to turn neurons off and on so that they could determine which neurons dilated the blood vessels.

“We knew that when animals run, all the neurons become more active and this causes the blood vessels to react,” said Drew. “There are excitatory and inhibitory neurons and there is some evidence that if you stimulate inhibitory neurons you get vasodilation, but there are lots of inhibitory neuron types. We wanted to find out which ones were responsible.”

The researchers used two-photon microscopy to look at the surface and deep arteries in the somatosensory cortex of mice while the mice were awake. They were able to make multiple observations of the same arteries in the same animals over a series of different neural perturbations, so they could compare results in individuals rather than across individuals. They reported their results in eLife.

Lower magnification section of a brain showing neurons that have nNOS-expressing neurons labeled in green, DREADD-expressing neurons in magenta. Neurons that express both show up as white. © Jordan Norwood, Penn State

“Thirty years ago people realized that nitric oxide is a vasodilator,” said Drew. “Other researchers have seen an enzyme of nitric oxide stimulate a subset of neurons giving us a hint that this could help locate the responsible neurons.”

Drew and his team showed that with an increase or decrease of the nitric oxide enzyme there was a change in dilation without there being a change in electrical activity. According to Drew, the brain is oversupplied with oxygen, so an increase in dilation when running or for other reasons is not necessarily to increase oxygen supply.

“The changes do not seem to be linked with need,” said Drew. “It is a mystery why it happens.”

Because the researchers could track changes in the same blood vessel over time and with different stimuli, they could compare these changes to the baseline in the individual animals. They could also inhibit certain groups of neurons for various lengths of time.

“Our results suggest a model where approximately half of the dynamic range in the basal and evoked blood arterial diameter is controlled by a small group of neurons and the rest is controlled by other neurons and astrocytes,” the researchers report. “Any damage to or dysfunction of nNOS neurons (producing nitric oxide enzymes) could result in decreased basal blood flow, regardless of the metabolic need.”

The researchers also noted that changes in the diameter of blood vessels affects the amplitude of fmri signals. Because fmri is used to image blood vessels in animals and humans, this can produce signals not related to neural activity.

“This tells us that fmri signals may not represent overall activity,” said Drew. “It suggests that if these neurons die, it might cause the development of dementia.”

The researchers would like to know what happens if these neurons are shut down for a long time. They would also like to know what happens if these same neurons are stimulated for a long time. Another goal is to understand what drives these neurons, what modulatory input do they receive and in what other parts of the brain do they function?

Reference: http://dx.doi.org/10.7554/eLife.60533

Provided by Penn State

Blocking DNA Repair Enzyme Could Help Treat Certain Cancers (Medicine)

Researchers at the Francis Crick Institute have found a new way to prevent some tumours from repairing their own DNA, a function that is essential for cancer cell survival. This discovery could lead to much needed new treatments for certain types of the disease.

Images showing tumours developing in the stomach and spleen of mice in the presence of ALC1 but not in the mice without ALC1. ©Francis Crick Institute

In their study, published in Molecular Cell today [16th December], the researchers showed that blocking an enzyme called ALC1 in certain human cancer cells in the lab caused the cells to die.

It has emerged that many cancers lose specific DNA repair processes. As a consequence, these cancers become critically dependent on backup DNA repair pathways, which present an ‘Achilles heel’ that can be targeted to kill cancer cells.

“This work provides strong evidence for developing new drugs that block the ALC1 enzyme.”, said Simon Boulton.

Cancers that lack homologous recombination (HR), a key pathway involved in DNA repair, including some breast and ovarian cancers, can be selectively killed by PARP inhibitors. However, in about half of cases, people do not respond to these drugs and of those who do, many will eventually develop resistance.

In the search for urgently needed new drug targets to exploit DNA repair deficiencies, the team studied the effect of removing ALC1, an enzyme which plays an important role in repair of damaged DNA bases. Unexpectedly, cells lacking ALC1 were found to be exquisitely sensitive to PARP inhibitor treatment. Removing ALC1 also conferred synthetic lethality in HR deficient cancers.* The researchers also found that HRD cancer patients with higher levels of ALC1 in their tumours were predicted to be less likely to survive.

Simon Boulton, senior author and group leader of the DSB Repair Metabolism Laboratory at the Crick says, “This work provides strong evidence for developing new drugs that block the ALC1 enzyme. If shown to be effective in further studies, these drugs could be used alone or in combination with existing PARP inhibitors to target HRD cancers.”

To understand why this enzyme has this particular effect, the team also analysed the genomes of human cancer cells where ALC1 had been removed. They observed that without this enzyme, DNA gaps accumulated in the cancer cells, which are normally repaired by HR.

Graeme Hewitt, author and postdoc in the DSB Repair Metabolism Laboratory at the Crick says, “Many different types of cancer have weaknesses in their ability to repair DNA that could be targeted with new treatments.”

“Not only have we shown that inhibiting ALC1 effectively leads to cancer cell death, we have also found out the detailed mechanism behind this. Our increased understanding of this enzyme could help in the development of drugs which stop it working.”

*Synthetic lethality is when a combination of deficiencies in the expression of two or more genes leads to cell death. In this case it refers to the homologous recombination deficiency and the ALC1 deficiency.

References: Graeme Hewitt, Valerie Borel, Sandra Segura-Bayona, J. Ross Chapman, Sebastian Deindl, Simon J. Boulton, “Defective ALC1 nucleosome remodeling confers PARPi sensitization and synthetic lethality with HRD”, Molecular Cell, 2020. DOI: https://doi.org/10.1016/j.molcel.2020.12.006

Provided by Francis Crick Institute

New Theranostic Approach Reduces Tumor Volume and Increases Survival in NET Study (Medicine)

A pair of copper radionuclides that target the somatostatin receptor overexpressed in neuroendocrine tumors has proven successful in identifying tumors and improving survival. According to new research published in the December issue of The Journal of Nuclear Medicine, the imaging agent 64Cu-CuSarTate produced high-quality positron emission tomography (PET) images in a mouse model of neuroendocrine tumors, while its therapeutic counterpart, 67Cu-CuSarTate, was highly effective in reducing tumor volume and extending lifespan. The research also demonstrated the advantages of delivering the radionuclide therapy as two fractionated doses, as opposed to one.

Representative maximum intensity projection PET/CT images of AR42J tumor-bearing female Balb/c nude mice following injection of 64Cu-CuSarTATE (3 MBq, 0.24 nmol of peptide) at 1 and 4 hours post injection. Images created by associate professor Carleen Cullinane (Peter MaCallum Cancer Centre).

Neuroendocrine tumors typically are diagnosed with 68Ga-DOTA-octreotate and treated with 177Lu-LuTATE peptide receptor radionuclide therapy. However, using two different chemical elements (Ga and Lu) can lead to inconsistent tissue biodistribution, as they do not have the same binding and internalizations interactions. “Ideally, a chemically identical ‘imaging-therapeutic’ pair of radionuclides bound to the same targeting agent should be used for diagnosis and treatment,” said Paul S. Donnelly, BSc(Hons), PhD, professor in the School of Chemistry at the University of Melbourne in Melbourne, Victoria, Australia.

In the study, researchers utilized a preclinical mouse model to explore the chemically identical radionuclide pair 64Cu-CuSarTate and 67Cu-CuSarTate. To assess the ability of 64Cu-CuSarTate to positively identify tumors, PET imaging occurred at one hour and four hours after injection of the radiotracer. On completion of the four-hour imaging, mice were euthanized and biodistribution studies were performed.

Multiple therapy experiments were also performed to evaluate the efficacy of 67Cu-CuSarTate. In the first, mice were injected with five MBq of 177Lu-LuTATE, five MBq of 67Cu-CuSarTate or saline and monitored for tumor growth. In the second experiment, mice were injected with a total of 30 MBq of 177Lu-LuTATE, 67Cu-CuSarTate or saline either as a single intravenous injection or as two 15 MBq fractions, two weeks apart; tumor growth was then monitored.

64Cu-CuSarTate PET images acquired at both one hour and four hours post-injection revealed very high tumor uptake and excellent tumor-to-background ratios. The high tumor uptake was confirmed with the ex vivo biodistribution analysis. Tumor growth was inhibited by 75 percent with 67Cu-CuSarTate treatment and by 89 percent with 177Lu-LuTATE, and survival was extended from 12 days in the control group to 21 days following treatment with both therapies. Treatment of tumors with two fractions of either 177Lu-LuTATE or 67Cu-CuSarTate significantly improved survival when compared to delivery as a single fraction. Equivalent efficacy was observed between the two therapies following treatment on both the single and fractionated schedules.

“Copper radionuclides are beneficial for several reasons,” said Rodney J. Hicks, MBBS, MD, FRACP, FAHMS, professor in the Sir Peter MacCallum department of oncology at the University of Melbourne, in Melbourne, Victoria, Australia. “The strong binding of copper within the tumor allows for increased detection of disease, which can serve to limit radiation exposure to normal tissues during therapy. The ability to image at multiple time points with 64Cu-CuSarTate supports prospective dosimetry for therapeutic treatment planning with 67Cu-CuSarTATE, which could potentially offer shorter cycling of treatment, particularly for more aggressively growing tumors.”

In terms of potential translation of the copper-64/67 theranostic pair to clinical studies, it is pertinent that copper-64 is produced in a cyclotron. The longer half-life of 64Cu-CuSarTATE as compared to 68Ga-DOTA-octreotate means that the tracer can be easily produced under good manufacturing practice conditions and transported regionally. 67Cu-CuSarTATE can be produced with linear-accelerators in high specific activity and radionuclide purity, so it is not reliant on nuclear reactors.

“Looking to the future of molecular imaging and nuclear medicine, the chemistry and general concepts presented in this study could be expanded to other peptides that target different receptors, as well as antibodies and engineered antibody fragments. This offers the potential to provide diagnostic imaging using copper-64 to plan individualized treatments with copper-67 agents for a wide range of cancer patients,” noted Donnelly.

References: Carleen Cullinane, Charmaine M. Jeffery, Peter D. Roselt, Ellen M. van Dam, Susan Jackson, Kevin Kuan, Price Jackson, David Binns, Jessica van Zuylekom, Matthew J. Harris, Rodney J. Hicks and Paul S. Donnelly, “Peptide Receptor Radionuclide Therapy with 67Cu-CuSarTATE Is Highly Efficacious Against a Somatostatin-Positive Neuroendocrine Tumor Model”, Journal of Nuclear Medicine December 2020, 61 (12) 1800-1805; https://jnm.snmjournals.org/content/61/12/1800 DOI: https://doi.org/10.2967/jnumed.120.243543

Provided by Society of Nuclear Medicine and Molecular Imaging

About the Society of Nuclear Medicine and Molecular Imaging

The Journal of Nuclear Medicine (JNM) is the world’s leading nuclear medicine, molecular imaging and theranostics journal, accessed close to 10 million times each year by practitioners around the globe, providing them with the information they need to advance this rapidly expanding field. Current and past issues of The Journal of Nuclear Medicine can be found online at http://jnm.snmjournals.org.

JNM is published by the Society of Nuclear Medicine and Molecular Imaging (SNMMI), an international scientific and medical organization dedicated to advancing nuclear medicine and molecular imaging–precision medicine that allows diagnosis and treatment to be tailored to individual patients in order to achieve the best possible outcomes. For more information, visit http://www.snmmi.org.

Cornell Postdoc Detects Possible Exoplanet Radio Emission (Planetary Science)

By monitoring the cosmos with a radio telescope array, an international team of scientists has detected radio bursts emanating from the constellation Boötes – that could be the first radio emission collected from a planet beyond our solar system.

In this artistic rendering of the Tau Boötes b system, the lines representing the invisible magnetic field are shown protecting the hot Jupiter planet from solar wind. © Jack Madden/Cornell University

The team, led by Cornell postdoctoral researcher Jake D. Turner, Philippe Zarka of the Observatoire de Paris – Paris Sciences et Lettres University and Jean-Mathias Griessmeier of the Université d’Orléans will publish their findings in the forthcoming research section of Astronomy & Astrophysics, on Dec. 16.

“We present one of the first hints of detecting an exoplanet in the radio realm,” Turner said. “The signal is from the Tau Boötes system, which contains a binary star and an exoplanet. We make the case for an emission by the planet itself. From the strength and polarization of the radio signal and the planet’s magnetic field, it is compatible with theoretical predictions.”

Among the co-authors is Turner’s postdoctoral advisor Ray Jayawardhana, the Harold Tanner Dean of the College of Arts and Sciences, and a professor of astronomy.

“If confirmed through follow-up observations,” Jayawardhana said, “this radio detection opens up a new window on exoplanets, giving us a novel way to examine alien worlds that are tens of light-years away.”

Using the Low Frequency Array (LOFAR), a radio telescope in the Netherlands, Turner and his colleagues uncovered emission bursts from a star-system hosting a so-called hot Jupiter, a gaseous giant planet that is very close to its own sun. The group also observed other potential exoplanetary radio-emission candidates in the 55 Cancri (in the constellation Cancer) and Upsilon Andromedae systems. Only the Tau Boötes exoplanet system – about 51 light-years away – exhibited a significant radio signature, a unique potential window on the planet’s magnetic field.

Observing an exoplanet’s magnetic field helps astronomers decipher a planet’s interior and atmospheric properties, as well as the physics of star-planet interactions, said Turner, a member of Cornell’s Carl Sagan Institute.

Earth’s magnetic field protects it from solar wind dangers, keeping the planet habitable. “The magnetic field of Earth-like exoplanets may contribute to their possible habitability,” Turner said, “by shielding their own atmospheres from solar wind and cosmic rays, and protecting the planet from atmospheric loss.”

Two years ago, Turner and his colleagues examined the radio emission signature of Jupiter and scaled those emissions to mimic the possible signatures from a distant Jupiter-like exoplanet. Those results became the template for searching radio emission from exoplanets 40 to 100 light-years away.

After poring over nearly 100-hours of radio observations, the researchers were able to find the expected hot Jupiter signature in Tau Boötes. “We learned from our own Jupiter what this kind of detection looks like. We went searching for it and we found it,” Turner said.

The signature, though, is weak. “There remains some uncertainty that the detected radio signal is from the planet. The need for follow-up observations is critical,” he said.

Turner and his team have already begun a campaign using multiple radio telescopes to follow up on the signal from Tau Boötes.

In addition to Turner, Jayawardhana, Griessmeier and Zarka, the co-authors are Laurent Lamy and Baptiste Cecconi of the Observatoire de Paris, France; Joseph Lazio from NASA’s Jet Propulsion Laboratory; J. Emilio Enriquez and Imke de Pater from the University of California, Berkeley; Julien N. Girard from Rhodes University, Grahamstown, South Africa; and Jonathan D. Nichols from the University of Leicester, United Kingdom.

Turner, who laid the groundwork for this research while earning his doctorate at the University of Virginia, received funding from the National Science Foundation.

References: J.D. Turner, P. Zarka, J.-M. Griessmeier, J. Lazio, B. Cecconi, J.-E. Enriquez, J.N. Girard, R. Jayawardhana, L. Lamy, J.D. Nichols, and I. Pater, “The search for radio emission from the exoplanetary systems 55 Cancri, upsilon Andromedae, and tau Boötis using LOFAR beam-formed observations”, A&A, 2020. https://www.aanda.org/component/article?access=doi&doi=10.1051/0004-6361/201937201

Provided by Cornell University

When Dinosaurs Disappeared, Forests Thrived (Paleontology)

Rainfall patterns remained largely unaffected despite dramatic climate changes.

It’s known that the primary cause of the mass extinction of dinosaurs, about 66 million years ago, was a meteorite impact. But the exact mechanisms that linked the meteorite impact to mass extinction remain unclear, though climactic changes are thought to have played a part.

Researcher overlooking one of the two field sites for the study, the Frenchman Valley in Chambery Coulee Saskatchewan in July 2017. © McGill University

To understand how the mass extinction and associated climate changes affected specific ecosystems, a team of McGill scientists has analyzed the microscopic remains of plants from this period, found in the sediment of rivers in southern Saskatchewan. In a recent article in Palaeogeography, Palaeoclimatology, Palaeoecology they show that in this area, local plant communities and ecosystems experienced a long-term shift towards fewer aquatic plants and an increase in terrestrial plants, including trees such as birches and elms. The researchers speculate that this increase was due to the extinction of large plant-eating dinosaurs. They also found, unexpectedly, that changes in rainfall patterns during the extinction event were relatively minor and short-lived.

“This could be important as we look to the future of global warming, where many scientists have predicted that changes in precipitation could have big impacts on humans and ecosystems,” says Peter Douglas from McGill’s Department of Earth and Planetary Scientists and senior author on the paper. “At other times of major climate change in Earth’s history we typically do see evidence for such changes. The absence of such a signal during the most recent mass extinction event is intriguing.”

Douglas adds, “Surprisingly, scientists know more about what happened in the oceans at the end-Cretaceous extinction than on land. By clarifying the environmental changes occurring during this period, we narrowed down the factors that are likely to have caused the disappearance of dinosaurs. The research also provides an important analogue for environmental changes humans are causing to the planet, and the potential for future mass extinction.”

References: Robert D. Bourque, Peter M.J. Douglas, Hans C.E. Larsson, “Changes in terrestrial ecosystems across the Cretaceous-Paleogene boundary in western Canada inferred from plant wax lipid distributions and isotopic measurements”, Palaeogeography, Palaeoclimatology, Palaeoecology, 2020,
110081, ISSN 0031-0182,
https://doi.org/10.1016/j.palaeo.2020.110081.
(http://www.sciencedirect.com/science/article/pii/S0031018220305290)

Provided by McGill University

About McGill University

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Novel Principle For Cancer Treatment Shows Promising Effect (Medicine)

Researchers at Karolinska Institutet in Sweden report in the journal Nature that they have developed novel first-in-class inhibitors that compromise mitochondrial function in cancer cells. Treatment with the inhibitors stopped cancer cells from proliferating and reduced tumor growth in mice without significantly affecting healthy cells.

The small-molecule inhibitors (green) target the expression of mitochondrial DNA and cause a cellular energy crisis in cancer cells to stop their growth. Illustration: Mattias Karlén. Credit: Mattias Karlén

“We are excited to have shown that this novel principle for cancer treatment works in animal models and hopefully the inhibitors can now be developed further for anti-cancer treatment in humans,” says Nils-Göran Larsson, professor at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet, who led the study.

Mitochondria are the power plants of our cells. They are essential for converting the energy in the food we eat into the common energy currency that is required for a variety of cellular functions. Cancer cells are critically dependent on mitochondria, not only for providing energy but also for producing a variety of building blocks needed to make more cells as the cancer cells divide. The continuous cell division means that a cancer cell must constantly make new mitochondria in order to grow.

Previous attempts to target mitochondria for cancer treatment have focused on acutely inhibiting mitochondrial function. However, this strategy has often resulted in severe side effects due to the crucial role of mitochondria for normal tissue function. As an alternative, researchers from Karolinska Institutet and the University of Gothenburg in Sweden, in collaboration with the Max Planck Society and the Lead Discovery Center GmbH in Germany, developed a novel strategy that does not directly interfere with the function of existing mitochondria. Instead, they designed highly selective inhibitors that target the mitochondria’s own genetic material, mtDNA, which has a critical role in the formation of new mitochondria.

“Previous findings from our research group have shown that rapidly dividing cells, such as cancer cells, are crucially dependent on mtDNA to form new functional mitochondria,” says Nils-Göran Larsson. “Consequently, treatment with our inhibitors specifically affects proliferation of tumor cells, whereas healthy cells in tissues such as skeletal muscle, liver or heart remain unaffected for a surprisingly long time.”

When investigating the mechanism of action of these novel inhibitors, the researchers observed that the inhibitors put cancer cells into a state of severe energy and nutrient depletion. This leads to loss of necessary cellular building blocks, reduced tumor cell growth and ultimately cell death.

“The findings are very promising, but many years of further development will be required before human use can be considered,” concludes Nils-Göran Larsson.

References: Bonekamp, N.A., Peter, B., Hillen, H.S. et al. Small-molecule inhibitors of human mitochondrial DNA transcription. Nature (2020). https://www.nature.com/articles/s41586-020-03048-z https://doi.org/10.1038/s41586-020-03048-z

Provided by Karolinska Institutet