Culture

New research from Cass Business School has found that global liquidity shocks do impact house prices in both emerging and advanced economies but this can be mitigated by government policy.

In Global liquidity, house prices and policy responses, which is published in the Journal of Financial Stability, researchers investigated the impact of global liquidity on house prices around the world. They used a new measure of liquidity, which focused on the private component of liquidity of the major wholesale funding markets for financial intermediaries - the repurchase agreement (repo) market not only in the US, but also in the UK and Europe from 2000-2014.

The study is the first to investigate the effect of macroprudential policy on house prices and credit growth and examines its ability to shield countries from global shocks, as opposed to domestic credit conditions. Macroprudential policy is the approach to financial regulation that aims to mitigate risk to the financial system as a whole.

"Although it is understood that global liquidity triggers global house price movements, we discovered that this effect does not only originate from the US but from other important financial systems including the UK," explained co-author, Professor Kate Phylaktis of Cass Business School.

"We can now confirm that while house prices in advanced countries such as Switzerland, Canada and Australia react to liquidity shocks regardless of their origin, the effect is short-lived and turns insignificant within one year. In emerging markets, the response is greater and more persistent.

"This impact is channelled through increases in cross border bank flows, which feed into the local banking system triggering long lasting effects in the domestic housing markets. This signals the important role that banks play in the transmission of global shocks to the real economy."

Professor Phylaktis said an example of a global liquidity shock is the increase in liquidity by the Federal Reserve Board, the Bank of England and the European Central Bank in the aftermath of the Global Financial Crisis, which spurred the resumption of the upward trend in bank flows and house prices, following the liquidity dry-ups and the worsening of credit conditions around the world during the crisis. In response to potential vulnerabilities to financial stability and economic growth, arising from credit cycles, countries have developed policy frameworks, such as a variety of macroprudential policies.

The researchers found that countries' exposure to shocks can be mitigated by housing-related macroprudential and monetary policies but there are striking differences in effectiveness of these policies in advanced and emerging markets.

Professor Phylaktis said advanced economies can rely on monetary policy and macroprudential instruments, especially housing-related measures such as caps on loan to value (LTV), housing capital buffers, and housing loan loss provision, to shield their housing markets from global shocks.

"However, we found that the majority of the instruments in emerging markets are only marginally effective, and monetary policy only mitigates the impact of global shocks to emerging economies. We suggest that emerging markets adopt focused restrictions to non-resident investments in the local real estate sector, as these have been found to be effective in limiting the liquidity impact on house prices."

Researchers have outlined how fishing and farming policies could be created to protect employment opportunities and the environment after Brexit.

The team of researchers, led by scientists at the University of York, consulted with key figures from the agriculture and fishing industries nationwide to produce a framework for managing land and seas after the UK has left the EU.

The results highlight how leaving both the EU's Common Agricultural Policy and the Common Fisheries Policy is an opportunity for the UK to shift its focus to protecting the environment and livelihoods, rather than maximising production.

However, the ability to deliver on this vision will be severely compromised by a no-deal Brexit, the researchers warn.

Lead author of the study, Dr Bryce Stewart, from the Department of Environment and Geography at the University of York, said: "The UK has a rare opportunity to rewrite the rulebook to focus on effective agricultural, environmental and fisheries management and become a world-leader in these spheres.

"However, we have grave concerns about a no-deal Brexit across the board. For example, in the fishing industry the imposition of WTO rules could lead to tariffs of 7.5% to 24% on seafood exported to the EU.

"The UK would find itself under pressure to lower environmental protections and welfare standards across the farming and fishing industries to be competitive in markets outside of the EU.

"With widespread agreement that a no-deal Brexit will lead to a decline in economic growth, the resources and political will to deliver on sustainable practices may also be in short supply."

The report highlights the need for UK policy makers to adopt an "ecosystem based" approach, which prioritises the protection of natural assets and provides enough resources to fund and reward sustainable farming and fishing practices so that products can remain competitively priced, while protecting principles of environmental justice; sustainable environmental management and community livelihoods.

High levels of cooperation with other European nations would also continue to be required after Brexit to ensure consistency, collaboration and the efficient movement of goods and labour, the researchers say.

The recommendations of the report include:

Give greater voice to local and regional stakeholders (such as inshore fishing communities, which make up over 75% of the UK fleet) to ensure more locally appropriate and informed management decisions.

Sustainable management and redesign of agricultural practices in the environment based on developing and implementing joint land use, food and rural policy strategies.

Reforming farming subsidies so that farmers are paid for producing public goods that benefit nature and society.

Further develop partnerships between the fishing industry and scientists to improve knowledge of stocks and marine ecosystems.

Conserve Marine Protected Areas.

Co-author, Professor Sue Hartley, Director of the York Environmental Sustainability Institute, said: "Our research highlights that policy makers should recognise that healthy environments deliver 'public goods' such as clean air and water, food provision and places for leisure, that belong to all of us, and that the continued provision of these goods means providing sufficient resource to publicly reward sustainable farming and fishing practices."

Professor Charlotte Burns, joint lead author of the study, from the University of Sheffield, added: "Significant challenges lie ahead. In the face of continued uncertainty over Brexit, much of the UK's new policy on the environment, agriculture and fisheries is currently ambitious in vision but light on detail. There is also a risk that leaving the EU will weaken existing environmental protection."

"The development of innovative policies, with significant input from the major players in the industries across UK countries, will therefore be essential for ensuring environmental sustainability and prosperity after Brexit."

The impostor syndrome, a phenomenon that manifests when people feel like frauds even if they are actually capable and well-qualified, affects people both in the workplace and in the classroom. A new study reveals that perceptions of impostorism are quite common and uncovers one of the best -- and worst -- ways to cope with such feelings.

Findings of the study, co-authored by Brigham Young University professors Jeff Bednar, Bryan Stewart, and James Oldroyd, revealed that 20 percent of the college students in their sample suffered from very strong feelings of impostorism. The researchers conducted interviews with students in an elite academic program to understand the various coping mechanisms students used to escape these feelings, but one particular method stood out above the rest: seeking social support from those outside their academic program.

The findings of their interview study suggest that if students "reached in" to other students within their major, they felt worse more often than they felt better. However, if the student "reached out" to family, friends outside their major, or even professors, perceptions of impostorism were reduced.

"Those outside the social group seem to be able to help students see the big picture and recalibrate their reference groups," said Bednar, a BYU management professor and co-author on the study. "After reaching outside their social group for support, students are able to understand themselves more holistically rather than being so focused on what they felt they lacked in just one area."

Along with seeking social support, the study also uncovered negative ways students coped with impostorism. Some students tried to get their mind off schoolwork through escapes such as video games but ended up spending more time gaming than studying. Other students tried to hide how they really felt around their classmates, pretending they were confident and excited about their performance when deep down they questioned if they actually belonged.

In a second study, the researchers surveyed 213 students to confirm what was revealed in their interview study about seeking social support: reaching out to individuals outside the major proved to be more effective than reaching in to individuals within the major.

Surprisingly, the study also reveals that perceptions of impostorism lack a significant relationship with performance. This means that individuals who suffer with the impostor syndrome are still capable of doing their jobs well, they just don't believe in themselves. Researchers also explain that social-related factors impact impostorism more than an individual's actual ability or competence.

"The root of impostorism is thinking that people don't see you as you really are," said Stewart, an accounting professor at BYU and co-author on the study. "We think people like us for something that isn't real and that they won't like us if they find out who we really are."

Outside the classroom, researchers believe that implications from this study can and should be applied in the workplace as well. "It's important to create cultures where people talk about failure and mistakes," Bednar said. "When we create those cultures, someone who is feeling strong feelings of impostorism will be more likely to get the help they need within the organization."

One fundamental problem of quantum electrodynamics is the fate of the superheavy atomic nucleus, which is proposed to collapse when the atomic number exceeds certain value. However, this intriguing supercritical collapse phenomenon remains elusive in experiments. Discrete scale invariance (DSI) is a scale anomaly with the violation of the continuous scale symmetry. The intriguing log-periodicity is the characteristic signature of DSI, which exists in rupture, growth processes, turbulence, finance, and so on. The DSI feature is of high interest in quantum physics, while it can be rarely realized in quantum systems experimentally. The previously known example with DSI in quantum physics only focuses on the Efimov trimer state.

A novel type of quantum magneto-resistance oscillations has been observed in topological material ZrTe5 (Science Advances 4, eaau5096 (2018)), constituting the third known distinctive type of periodicity in the nearly 90 years searching for quantum oscillations in solids. Moreover, the discovery of the exotic logB periodic oscillations can virtually represent the discrete scale invariance associated with the quasi-bound states formed through supercritical atomic collapse in Dirac materials. Such peculiar feature is supposed to be universal in Dirac materials with Coulomb attraction. Thus, it is desirable to extend the investigations to other topological systems, and more importantly to other physical observables. In a new work published in the National Science Review, Beijing-based research collaboration led by Prof. Jian Wang, Prof. Haiwen Liu and Prof. Jiyan Dai has revealed the universality of the log-periodic quantum magneto-oscillations and DSI phenomenon in Dirac materials by magneto-transport results of HfTe5 crystals.

Scientists measured the magneto- and Hall resistance of the HfTe5 crystals at pulsed magnetic fields up to 58 T and static magnetic fields up to 25 T. Clear logB-periodic quantum oscillations signaling of DSI are observed in the longitudinal magneto-resistance (MR) (subfigure (a)), independent on the minor differences of the sample quality. The temperature dependence of the logB-periodic oscillations in HfTe5 is shown in subfigure (b). One can see that the log-periodic features become invisible when the temperature is increased to be above 80 K. Furthermore, for the first time, the DSI signal with remarkable logB-periodicity is discovered in the Hall traces of the HfTe5 crystals. The finding indicates an overall effect of the DSI feature on the transport properties of the system. The second derivate results of the Hall data are shown in the subfigure (c). In addition, the MR and Hall results on the same sample are shown in subfigure (d). It is found that in the oscillations the phase of Hall data is slightly ahead of MR, reminiscent of that in the two-dimensional quantum Hall effect.

The log-periodic oscillations in Dirac materials were attributed to the supercritical atomic collapse phenomenon and the concomitant quasi-bound states featuring discrete scale invariance in Dirac materials. The quasi-particle in Dirac materials obeys the relativistic equation, and the Fermi velocity is much smaller than the speed of light in vacuum. Thus, the value of the fine-structure constant in Dirac materials is much larger than that in vacuum, which provides a promising platform to investigate the supercritical atomic collapse phenomenon. Owing to the large value of the fine-structure constant in these solid state systems, the Coulomb attraction gives rise to the supercritical atomic collapse in analogy to the phenomenon proposed to exist in superheavy atoms. Moreover, the massless Dirac equation with Coulomb attraction preserves the discrete scale invariance, in contrast to the discrete scale symmetry breaking in massive Dirac equation of superheavy atoms.

In topological material HfTe5, the log-periodic quantum oscillations in both the longitudinal MR and the Hall resistance are closely related to the quasi-bound states of Weyl particles from the hole band with long-range Coulomb attraction when the carrier density is so dilute, and the long-range Coulomb attraction is generated by the charge impurity or the opposite type of carriers. Aside from the quasi-bound states near the Coulomb center, large number of mobile carriers also exist in the Fermi surface. Thus, the resonant scattering between the mobile carriers and the quasi-bound states around the Fermi level determine the transport properties of the material, e.g. the longitudinal MR and the Hall traces. Further theoretical analysis signify that the π/2 phase shift originates from the resonant scattering between the mobile carriers and the quasi-bound states, sharing the same origin of the log-periodic oscillations. Moreover, scientists have analyzed the influence of a small band gap on the DSI feature and clarified its relevance to various topological materials.

Dirac materials showing log-periodicity provide promising platforms to investigate the rarely observed supercritical atomic collapse phenomenon and the discrete scale invariance feature. This work provides new insights towards further understanding of the universality and the physical nature of the log-periodic quantum oscillations in Dirac materials.

A research team led by Dr Xiang David Li, Associate Professor from the Department of Chemistry, in collaboration with Dr Karen Wing Yee Yuen from the School of Biological Sciences and Dr Jason Wing Hon Wong from the School of Biomedical Sciences at The University of Hong Kong (HKU), revealed a new fundamental mechanism by which a cell can make necessary changes in its chromatin structure in response to different DNA-associated processes such as gene expression and DNA damage repair. The findings were recently published in the prestigious scientific journal Molecular Cell.

Imagine, for a moment, that you are now living in the centre of an ever-shifting maze: paths moving about and breaking apart, wide, straight roads curling up and shrinking into tight, winding tracks, new roads appearing from what used to be dead-ends. Travelling through this labyrinth, the only thing guiding you on the way is various road signs (e.g., "STOP", "SLOW", "ONE WAY" and "DO NOT ENTER") that indicate whether and how you may traverse different paths.

One such maze lies within our every cell: the chromatin, in which DNA is packaged with proteins called histones. Packaging of DNA can be tighter or looser in different regions of chromatin. While a loose packaging indicates an "active" or a gene "ON" region, a tight compaction means a "silent" or a gene "OFF" region. Interestingly, the chromatin also contains various "road signs" in the form of chemical modifications to histones (or histone marks) that indicate the active, inactive or damaged regions of the chromatin and give order to various chromatin-associated machineries in the regulation of gene expression, DNA replication and damage repair. While some well-known chromatin "road signs" such as lysine acetylation (Kac) and methylation (Kme) have been well characterised, the biological meanings of many other "signs", particularly those newly identified histone marks, remain mysterious.

In a search for new chromatin "road sign", Dr Li's team discovered a novel histone mark, lysine glutarylation (Kglu) at histone H4, Lysine-91 (H4K91glu) from human cells. "I was so excited to find this new histone mark. Now imagine that in the maze you come across a new sign that you've not seen before. Who puts it there? What does it mean?" said Dr Xiucong Bao, a postdoctoral fellow in Dr Li's lab and the first author of the study, but she also notes the great challenge to uncover these mysteries, for which she has spent more than five years on the project. The researchers finally found that this mark is especially abundant in promoter regions of active, "open" chromatin where genes are highly expressed - equivalent to a road sign in the maze showing "expressway". "We believe that H4K91glu is a "sign" for activation of gene expression," said Dr Li. "And this 'sign' seems to be conserved in evolution, as we found it in not only human but also mouse, fly, worm and even baker's yeast cells."

Besides marking the active genomic region, H4K91glu in fact directly contributes to the formation of the more open accessible chromatin structure facilitating gene expression. Dr Li's team found in this study that H4K91glu destabilizes nucleosome, the basic repeating unit of chromatin, and leads to activation or "opening" of chromatin. "It makes perfect sense if you know chemistry, as the mark puts a negative charge on an originally positively charged lysine residue. It therefore causes a charge-charge repulsion within the nucleosome and makes it more prone to falling apart," says Dr Li.

Much like the ever-shifting maze, chromatin packaging is highly dynamic. A compacted region of chromatin at this moment can quickly change to a relaxed one at the next moment, which allows fast switching between gene ON and OFF states. Meanwhile, when chromatin structure is changed at a specific region, the old "road signs" (i.e., histone marks) are taken off and the new ones are installed by enzymes called histone mark "erasers" and "writers", respectively. "To understand a histone mark, it is key to find its "writer" and "eraser", says Li, whose team further identified the enzymes that "write" and "erase'"= the H4K91glu mark: KAT2A, working together with the α-ketoadipate dehydrogenase (α-KADH) complex, adds the H4K91glu mark, while SIRT7 works to remove it. The researchers went on to demonstrate that H4K91glu must be removed by SIRT7 such that the open chromatin region could be inactivated and condensed during cell division or at local DNA damage site.

In summary, Dr Li's study identified H4K91glu as a novel histone mark and unraveled its regulation and function in chromatin structure and dynamics, putting us one step closer towards deciphering the yet mysterious chromatin maze. The findings from this study also laid the foundation for elucidating how this novel histone mark contributes to human health and disease and will open opportunities for development of therapeutic agents for the treatment of human diseases associated with mis-regulation of histone H4K91glu and chromatin structure.

Artificial intelligence (AI) appears to detect diseases from medical imaging with similar levels of accuracy as health-care professionals, according to the first systematic review and meta-analysis, synthesising all the available evidence from the scientific literature published in The Lancet Digital Health journal.

Nevertheless, only a few studies were of sufficient quality to be included in the analysis, and the authors caution that the true diagnostic power of the AI technique known as deep learning--the use of algorithms, big data, and computing power to emulate human learning and intelligence--remains uncertain because of the lack of studies that directly compare the performance of humans and machines, or that validate AI's performance in real clinical environments.

"We reviewed over 20,500 articles, but less than 1% of these were sufficiently robust in their design and reporting that independent reviewers had high confidence in their claims. What's more, only 25 studies validated the AI models externally (using medical images from a different population), and just 14 studies actually compared the performance of AI and health professionals using the same test sample," explains Professor Alastair Denniston from University Hospitals Birmingham NHS Foundation Trust, UK, who led the research. [1]

"Within those handful of high-quality studies, we found that deep learning could indeed detect diseases ranging from cancers to eye diseases as accurately as health professionals. But it's important to note that AI did not substantially out-perform human diagnosis." [1]

With deep learning, computers can examine thousands of medical images to identify patterns of disease. This offers enormous potential for improving the accuracy and speed of diagnosis. Reports of deep learning models outperforming humans in diagnostic testing has generated much excitement and debate, and more than 30 AI algorithms for healthcare have already been approved by the US Food and Drug Administration.

Despite strong public interest and market forces driving the rapid development of these technologies, concerns have been raised about whether study designs are biased in favour of machine learning, and the degree to which the findings are applicable to real-world clinical practice.

To provide more evidence, researchers conducted a systematic review and meta-analysis of all studies comparing the performance of deep learning models and health professionals in detecting diseases from medical imaging published between January 2012 and June 2019. They also evaluated study design, reporting, and clinical value.

In total, 82 articles were included in the systematic review. Data were analysed for 69 articles which contained enough data to calculate test performance accurately. Pooled estimates from 25 articles that validated the results in an independent subset of images were included in the meta-analysis.

Analysis of data from 14 studies comparing the performance of deep learning with humans in the same sample found that at best, deep learning algorithms can correctly detect disease in 87% of cases, compared to 86% achieved by health-care professionals.

The ability to accurately exclude patients who don't have disease was also similar for deep learning algorithms (93% specificity) compared to health-care professionals (91%).

Importantly, the authors note several limitations in the methodology and reporting of AI-diagnostic studies included in the analysis. Deep learning was frequently assessed in isolation in a way that does not reflect clinical practice. For example, only four studies provided health professionals with additional clinical information that they would normally use to make a diagnosis in clinical practice. Additionally, few prospective studies were done in real clinical environments, and the authors say that to determine diagnostic accuracy requires high-quality comparisons in patients, not just datasets. Poor reporting was also common, with most studies not reporting missing data, which limits the conclusions that can be drawn.

"There is an inherent tension between the desire to use new, potentially life-saving diagnostics and
the imperative to develop high-quality evidence in a way that can benefit patients and health systems in clinical practice," says Dr Xiaoxuan Liu from the University of Birmingham, UK. "A key lesson from our work is that in AI--as with any other part of healthcare--good study design matters. Without it, you can easily introduce bias which skews your results. These biases can lead to exaggerated claims of good performance for AI tools which do not translate into the real world. Good design and reporting of these studies is a key part of ensuring that the AI interventions that come through to patients are safe and effective." [1]

"Evidence on how AI algorithms will change patient outcomes needs to come from comparisons with alternative diagnostic tests in randomised controlled trials," adds Dr Livia Faes from Moorfields Eye Hospital, London. "So far, there are hardly any such trials where diagnostic decisions made by an AI algorithm are acted upon to see what then happens to outcomes which really matter to patients, like timely treatment, time to discharge from hospital, or even survival rates." [1]

Writing in a linked Comment, Dr Tessa Cook from the University of Pennsylvania, USA, discusses whether AI can be effectively compared to the human physician working in the real world, where data are "messy, elusive, and imperfect". She writes: "Perhaps the better conclusion is that, the narrow public body of work comparing AI to human physicians, AI is no worse than humans, but the data are sparse and it may be too soon to tell."

In adults that are born blind, the "visual" cortex is activated in a similar way during a listening task, according to new research in JNeurosci. The results answer questions about how development can override anatomy to influence brain function.

Previous research observed that the "visual" cortex in blind people is recruited for other functions, but it was not known if the new purpose was consistent or varied from person to person.

Loiotile et al. used functional magnetic resonance imaging to compare how the auditory and visual cortices of the brain were activated in blind and blindfolded, sighted participants while listening to audio clips from movies. Sixty-five percent of the regions in the visual cortex had similar activation among the blind participants when they listened to the movie clips. The similarity diminished when the sentences were played in a random order or the track was played backwards, indicating that the region is used for higher-order processing. These results suggest that there is an underlying organization that dictates how the visual cortex is repurposed in blind people, and that it is not random.

ANN ARBOR--Research led by the University of Michigan Life Sciences Institute has solved a nearly 50-year-old mystery of how nature produces a large class of bioactive chemical compounds.

The findings are scheduled for publication on Sept. 23 in the journal Nature Chemistry.

The compounds, called prenylated indole alkaloids, were first discovered in fungi in the 1970s. Since then, they have attracted considerable interest for their wide range of potential applications as useful drugs. One compound is already used worldwide as an antiparasitic for livestock.

Understanding how the fungi build these chemicals is essential to reproducing them and creating variants in the lab for new applications. The fungi's genes encode enzymes, and these enzymes use very simple building blocks to perform each step to build the complex molecule.

But despite the longstanding knowledge about these compounds, researchers have not been able to tease apart the precise enzymes and reactions that the fungi use to produce them.

"But if we can actually isolate the genes involved and make these enzymes, we should be able to recreate the entire bio-assembly line in a test tube," said Qingyun Dan, a researcher in the lab of Janet Smith at the Life Sciences Institute and a lead author on the study. "But, until now, no lab has been able to do so."

Using a collaborative approach that combined synthetic chemistry, genetics, enzymology, computational chemistry and structural biology over the course of a decade, the researchers have revealed the process--and uncovered a surprising chemical twist. The final step in the assembly process is a reaction that is nearly unprecedented in nature: the Diels-Alder reaction.

"This reaction is one of the fundamentals of synthetic organic chemistry, going back to the 1920s when it was first discovered," said LSI faculty member David Sherman, one of the senior authors of the study.

"But even within the last few years, there has been major debate in the field about whether this reaction actually exists in nature. It's just the most phenomenal, unexpected path to this fascinating class of indole alkaloids."

The researchers believe that discovering the enzyme that enables the Diels-Alder reaction--and resolving how these compounds are made in nature--now opens two exciting paths forward.

First, the particular enzyme that catalyzes this Diels-Alder reaction could help improve one of the most commonly used chemical reactions. This enzyme performs the reaction with specificity that far outperforms what can commonly be achieved in the lab, meaning it creates only the one desired compound and no unintended byproducts.

Second, because the researchers were able to obtain a crystal structure of the enzyme performing the Diels-Alder reaction, they now have a clear picture of how the enzyme directs the reaction in nature--and how it might be harnessed to create new compounds in the future.

"This is a very good example of the explanatory power of crystal structures," said Sean Newmister, a researcher in Sherman's lab and a lead author on the study. "We gain mechanistic insight into the activity of the enzyme we're studying, but also insight into how to use this as a tool to synthesize new chemical compounds with biological activities. And that's really exciting."

A University of Calgary-led international study is highlighting the importance of magnetic resonance imaging (MRI) in helping to diagnose minor stroke and transient ischemic attacks (TIAs).

The six-year study, which included researchers from hospitals in Canada, Australia and the Czech Republic, involved 1028 patients who experienced a number of symptoms that aren't always associated with stroke--such as numbness, dizziness, or very short episodes of weakness or difficulty with speech.

Principal investigator Dr. Shelagh Coutts, MD, a member of the Cumming School of Medicine's (CSM), Hotchkiss Brain Institute, and a neurologist at Alberta Health Services' Foothills Medical Centre, says that, because the risk of stroke increases after a first TIA, it is important that physicians are certain of the diagnosis in low-risk cases with non-traditional symptoms.

Patients with motor or speech symptoms lasting more than five minutes are at high risk of having a stroke and must been seen urgently. The problem is that over 50 per cent of patients with possible symptoms of a TIA do not have these symptoms.

"If you don't have motor and speech symptoms, the diagnosis is a lot less clear--so patients with numbness, dizziness or with difficulty walking may not be diagnosed with a stroke syndrome. These patients are, overall, felt to be at low-risk of having stroke," says Coutts, a professor in the departments of Clinical Neurosciences, Radiology, and Community Health Sciences at the CSM.

Physicians involved in the study group--Diagnosis of Uncertain-Origin Benign Transient Neurological Symptoms (DOUBT)--examined patients within eight days of the start of their symptoms. They performed a detailed neurological assessment, took a patient history, made a diagnosis, and then did an MRI scan within the first week--followed by a second diagnosis.

"We found in this study that there was a 13 per cent risk of having had a stroke," adds Coutts. "This was far higher than we expected in this low risk population."

Further, in 30 per cent of patients in the study, the physicians changed their diagnosis based on the MRI scan.

"That's not just to change patients to having a stroke," notes Coutts. "There's also the reverse where we thought they might have had a stroke or TIA but based on a negative MRI scan (and other clinical symptoms) we decided it wasn't."

In many patients with minor stroke or TIA, Coutts says that symptoms are straightforward and a stroke can be diagnosed--or ruled out--without the need for MRI scans.

"In a patient in whom it is quite clear to the physician treating them that they have had a transient ischemic attack, then usually an MRI scan isn't actually that helpful. The MRI is really useful in patients in whom we are unclear what the diagnosis is."

And from a patient perspective (if the MRI is negative), knowing they haven't had a TIA is very important, she says, as it reduces the use of unnecessary medication.

"The MRI can be done in the first week as an outpatient," notes Dr. Michael Hill, MD, a co-author of the paper, and neurologist at Alberta Health Services' Foothills Medical Centre and member of the CSM's Hotchkiss Brain Institute and the O'Brien Institute for Public Health.

"It is not an emergency, same-day test. The MRI has an important predictive value. A normal test means that the patient most likely has not suffered a stroke syndrome and the risk of future stroke is very, very low," adds Hill, a professor in the departments of Clinical Neurosciences, Community Health Sciences, Medicine, and Radiology, at the CSM.

A key theory that attributes the climate evolution of the Earth to the breakdown of Himalayan rocks may not explain the cooling over the past 15 million years, according to a Rutgers-led study.

The study in the journal Nature Geoscience could shed more light on the causes of long-term climate change. It centers on the long-term cooling that occurred before the recent global warming tied to greenhouse gas emissions from humanity.

"The findings of our study, if substantiated, raise more questions than they answered," said senior author Yair Rosenthal, a distinguished professor in the Department of Marine and Coastal Sciences in the School of Environmental and Biological Sciences at Rutgers University-New Brunswick. "If the cooling is not due to enhanced Himalayan rock weathering, then what processes have been overlooked?"

For decades, the leading hypothesis has been that the collision of the Indian and Asian continents and uplifting of the Himalayas brought fresh rocks to the Earth's surface, making them more vulnerable to weathering that captured and stored carbon dioxide - a key greenhouse gas. But that hypothesis remains unconfirmed.

Lead author Weimin Si, a former Rutgers doctoral student now at Brown University, and Rosenthal challenge the hypothesis and examined deep-sea sediments rich with calcium carbonate.

Over millions of years, the weathering of rocks captured carbon dioxide and rivers carried it to the ocean as dissolved inorganic carbon, which is used by algae to build their calcium carbonate shells. When algae die, their skeletons fall on the seafloor and get buried, locking carbon from the atmosphere in deep-sea sediments.

If weathering increases, the accumulation of calcium carbonate in the deep sea should increase. But after studying dozens of deep-sea sediment cores through an international ocean drilling program, Si found that calcium carbonate in shells decreased significantly over 15 million years, which suggests that rock weathering may not be responsible for the long-term cooling.

Meanwhile, the scientists - surprisingly - also found that algae called coccolithophores adapted to the carbon dioxide decline over 15 million years by reducing their production of calcium carbonate. This reduction apparently was not taken into account in previous studies.

Many scientists believe that ocean acidification from high carbon dioxide levels will reduce the calcium carbonate in algae, especially in the near future. The data, however, suggest the opposite occurred over the 15 million years before the current global warming spell.

Rosenthal's lab is now trying to answer these questions by studying the evolution of calcium and other elements in the ocean.

"These ancient fossils provide us with evidence of how at least two predator species hunted these vegetarian dinosaurs 210 million-years-ago. It is amazing to follow the clues left behind in fossilised teeth, jaws, limbs and other fossils to help us tell the ancient story of life in southern Africa," says Tolchard.

The fossils studied by Tolchard include teeth, pieces of jaws, hind limbs and body armour, all of which are can be described as parts of rauisuchians.

Rauisuchians are closely related to crocodiles as we know them today. They had a diversity of body shapes and sizes during the Triassic period. The specimens described in this research include some of the largest carnivorous members of this group, that were possibly up to 10 metres long, with huge skulls full of serrated, curved teeth.

The study, published online in the Journal of African Earth Sciences last week, shows that the rauisuchians were some of the latest-surviving members of their group, and that when they were alive, they were thriving close to the Antarctic Circle - the theoretical limit for their physiology.

"In the Triassic period, rauisuchians were widespread and their fossils are known from all continents except Antarctica," adds Tolchard. "They went extinct about 200 million years ago, paving the way for dinosaurs to become the dominant large land animals."

"Rick's study demonstrates the value of re-examining old specimens, and now we finally know what was preying on all those herbivorous dinosaurs!" says Professor Jonah Choiniere, Rick's advisor and Professor of Comparative Palaeobiology at the Wits Evolutionary Studies Institute.

Tolchard studied fossils from collections based at the the University of the Witwatersrand, the Iziko South African Museum and the National Museum in Bloemfontein. He was joined in the research by an international team, including researchers from the USA, Argentina and the UK.

DEVELOPED by an influential U.S. psychologist, the Micro-Expressions Training Tool, or METT, inspired the hit TV show Lie to Me, which revolved around the uncanny ability of its lead character to tell truth from falsehood by analysing minute facial tics. And in the real world, METT is being used to train airport personnel to spot people who pose potential security risks.

But a research project involving a University of Huddersfield lecturer has concluded that METT training fails to improve lie detection rates beyond levels that can be achieved by guesswork.

The verdict is reported in a new article which concludes that the failure of METT is highly problematic "given that training in the recognition of micro-expressions composes a large part of a screening system that has become ever more pervasive in our aviation security".

METT is now an element of the Screening Passengers by Observation Technique (SPOT) used in airport security in the USA. This meant that research into its effectiveness was critical, state the article's authors.

One of them is the University of Huddersfield's Reader in Cognitive Psychology Dr Chris Street, who has made a speciality out of lie detection. He formed a collaboration with colleagues at two universities in the USA who had decided to carry out the first known full test of METT as a lie detection tool.

The findings are revealed in an article that appears in the Journal of Investigative Psychology and Offender Profiling.

METT-trained individuals performed no better

METT was developed by the psychologist Dr Paul Ekman, whose research group was the inspiration for TV series Lie to Me, starring Tim Roth. It is a form of training that aims to improve the detection of the micro-expressions sadness, anger, fear, disgust, contempt and happiness - fleeting expressions can last for as little as half a second.

"Recognising micro-expressions may have some utility as an aid for better recognising facial expressions, but it is more prominently promoted as a potential to aid in detecting deception," according to the new article, which then goes on to state that its research "does not paint an optimistic picture for the utility of METT".

The article describes the research process, which involved 90 students at a U.S. university. Some were randomly selected to receive METT training and some received bogus "placebo" training or none at all. They were shown stimulus videos containing truths and lies, taken from five different deception detection studies. One them was developed by Dr Street and colleagues.

The success rate of participants in telling truth from lies was then compiled. One of the findings was that METT-trained individuals performed no better than those who received bogus or no training and indeed performed worse than chance - "guessing would have produced marginally better results".

Commenting on the research project, Dr Street said: "METT is something that most people in the field felt didn't really hold up. The Ekman group argue that these micro-expressions help you to detect lies. But there really hasn't been any evidence to that effect. The problem now is that it has been brought into government usage in the U.S."

Scientists are one step closer to discovering the causes of immune diseases such as asthma, multiple sclerosis and arthritis. Research from the Wellcome Sanger Institute, GSK and Biogen, under the Open Targets initiative, has shown that thousands of differences in DNA between individuals, associated with immune diseases, are linked with the switching-on of a specific subtype of immune cells.

Published today (23rd September) in Nature Genetics, this study will help narrow down the search for the molecular pathways involved in immune diseases and could lead to finding drug targets for developing new treatments.

The immune system keeps us healthy by fighting infections. However, if something goes wrong, the cells in our immune system can mistakenly cause inflammation, leading to immune diseases like asthma, multiple sclerosis and inflammatory bowel disease (IBD). These diseases affect millions of people worldwide, with more than 5 million asthma patients in the UK alone*, yet it is not known what triggers the immune system to respond in this way, or even the exact cell types involved.

Previous research found that there are thousands of genetic changes - known as genetic variants - that are more common in patients with immune diseases than in healthy people. Understanding these genetic changes could provide clues to the causes and biological pathways involved in immune disease, and in time, lead to identifying new drug targets.

Many of these genetic variants are in poorly understood areas of the genome and are thought to be involved in regulating functions of immune cells. Add to this, cytokines - the signalling proteins released to allow communication between the immune cells during inflammation - and the picture becomes even more complex, making it extremely difficult to pinpoint what is causing the disease.

Researchers at the Sanger Institute and their collaborators aim to understand which immune cell states are most important for immune diseases, in an effort to hone in on potential new drug targets for diseases like asthma and IBD.

In this new study, the team looked at which parts of the genome were active in three types of immune cells from healthy volunteers, and cross-checked these positions against all the genetic variants implicated in different immune diseases. They also added different cytokines, creating a total of 55 different cell states, to mimic immune disease inflammation and understand the effects of the signalling chemicals in these cells.

The study revealed that one particular cell type and cell state - early activation of memory T cells - had the most active DNA across the same regions as the genetic variants implicated in immune diseases. This pointed towards the initial activation of these T cells being important in disease development. Surprisingly, the research showed that the cytokines generally only had subtle effects on the DNA activity, and played a lesser role in most of the diseases studied.

Dr Blagoje Soskic, a lead author on the paper from the Wellcome Sanger Institute and Open Targets, said: "Our study is the first in depth analysis of immune cells and cytokine signals in the context of genetic differences linked to immune diseases. We found links between the disease variants and early activation of memory T cells, suggesting that problems with regulating this early T cell activation could lead to immune diseases."

Dr Rab Prinjha, Chair of the Open Targets Governance Board and Head of Adaptive Immunity and Immuno-Epigenetics Research Unit, GSK said: "At GSK, we deploy both genetics and genomics to identify which parts of the immune system are central to a range of human diseases and to yield better validated targets that could become transformational medicines. To investigate the science of the immune system, functional genomics helps us better understand the role that individual genes may or may not play in triggering pathogenic immune mechanisms. This paper is yet another result from our 5-year collaboration with Open Targets to advance the field and shows our focus on advanced technologies to drive our science."

To enable this complex analysis, the researchers developed a new computational method, called CHEERS, which enabled them to identify cell states relevant for immune diseases. Openly available**, this resource could also be used to find links between genetic variation and mechanisms for other complex diseases.

Dr Gosia Trynka, the senior author from the Wellcome Sanger Institute and Open Targets, said: "There are thousands of different cell types and states in the body, and finding the cause of autoimmune diseases is like finding a needle in a haystack. We have identified early activation of memory T cells as being particularly relevant to immune diseases, and will now be able to dive deeper into studying how this is regulated, to discover genes and pathways that could be used as drug targets."

New Iridium compounds effective towards killing cancer cells even without the presence of oxygen - expanding the range of tumours that can be targeted

When activated by light, compound cuts off the cancer cell's 'power source'

Technique could reduce side effects of cancer treatment and potentially immunise against future cancer

Most Iridium is believed to have come from the meteorite that wiped out dinosaurs, and uses include in spacecraft and satellites

A space-age metal that formed part of the asteroid that destroyed the dinosaurs could provide a new method of treating cancer tumours selectively using light.

Scientists at the University of Warwick in collaboration with colleagues in China, France, Switzerland and Heriot-Watt University have developed a technique that uses light to activate a cancer-killing compound of Iridium that attacks, for the first time, a vital energy source in cancer cells even under hypoxia, significantly opening up the range of cancers that can be treated using the technique.

The technique is detailed in a paper published today (23 September 2019) in Nature Chemistry and could lead to another tool for clinicians to use in the fight against cancer, and potentially even vaccinate patients against future cancers.

Photodynamic therapy (PDT) uses light to kill cancer tumours in the body by activating a chemical compound called a photosensitiser, which creates species that can attack cancer cells in the presence of light. Using this method, clinicians can direct the light to specific regions of the cancer tumour and spare normal tissue from damage.

Current methods mainly rely on the presence of oxygen and many tumours are 'hypoxic', which means that they are deficient in normal oxygen often due to poor blood supplies. The international team of scientists have now developed a compound of the metal Iridium that will kill cancer cells in culture even when oxygen concentration is low.

The technique can treat any tumours where light can be administered, and would be particularly suited to treat bladder, lung, oesophageal, brain and skin cancers. There are around 10,000 bladder cancer cases in the UK per year, of which about 5,000 might potentially benefit from this kind of treatment.

Professor Peter Sadler from the University of Warwick's Department of Chemistry said: "All the time in cancer treatment, clinicians are trying to fight resistance. Drugs can kill the cancer cells initially, but with repeated treatment the cells become resistant, they learn how to chemically modify the drug or counteract its mechanism of action. Researchers are looking for novel ways in which the cancer cell will die. If they have become resistant to other cancer drugs, they may not be resistant to this treatment because the way it kills the cancer cells is different.

"There is an increasing interest in reducing the side effects of cancer treatment as much as possible and anything that can be selective in what it targets will help with that. The compound that we have developed would not be very toxic at all, we would give it to the cancer cells, allow a little time for it to be taken up, then we would irradiate it with light and activate it in those cells. We would expect killing of those cancer cells to occur very quickly compared with current methods."

Once light-activated, the Iridium compound attacks the energy producing machinery in the cancer cells - a vital co-enzyme called nicotinamide adenine dinucleotide (NADH) - and catalytically destroys that co-enzyme or changes it into its oxidised form. This upsets the energy-producing machinery in a cancer cell and effectively cuts off the tumour's power source.

Our bodies need coenzyme nicotinamide adenine dinucleotide (NADH) to generate energy. Cancer cells have a very high requirement for NADH, because they need a lot of energy to divide and multiple rapidly.

The researchers even found that the compound still works in the presence of oxygen, by converting it into a 'toxic' type of oxygen that will kill the cancer cells.

The team of scientists also noted that as the cancer cells die, they change their chemistry in such a way that they will generate an immune reaction in the body, what is known as an immunotherapeutic response. This suggests that those treated by this technique might be immunised against attack by that cancer, and will be investigated further in future research.

Professor Vas Stavros (University of Warwick) commented: "The power of light to change the reactivity of chemical molecules dramatically within a thousandth of a millionth of a second can now be harnessed to treat resistant cancers."

Professor Martin Paterson (Heriot-Watt University) commented: "This breakthrough illustrates the power of modern computation to understand the effects of light on chemical molecules to provide drugs of the future with truly unique mechanisms of action."

Professor Hui Chao (Sun Yat-Sen University) commented: "Now we have a potential new drug which can not only selectively kill cancer cells with normal oxygen supplies, but also hypoxic cancer cells which often resist treatment by photodynamic therapy."

Professor Peter Sadler added: "The ability of metal compounds to induce an immunogenic response in the body that may effectively vaccinate a person against future attack by cancer is an exciting development. It is very speculative, but we are looking further into the hallmarks of that.

"Importantly we were fortunate to have had 3 highly talented young Royal Society Newton International Fellows in our team working on this challenging interdisciplinary project, who will undeniably contribute towards the future of this crucially important research."

Iridium was first discovered in 1803, and its name comes from the Latin for 'rainbow'. From the same family as platinum, it is hard, brittle, and is the world's most corrosion-resistant metal. Yellow in colour, its melting point is more than 2400° Celsius. It is used in satellites and spacecraft due to its resistance to extreme environments, and is commonly believed to have been enriched in the earth's crust by a meteorite that wiped out the dinosaurs 66 million years ago.

HOUSTON - (Sept. 23, 2019) - Rice University researchers have found a way to track the formation of soluble amyloid beta peptide aggregates implicated in the onset of Alzheimer's disease.

The Rice lab of Angel Martí reported its development of a ruthenium-based fluorescent complex that binds to soluble, oligomeric amyloid beta peptides. As the peptides come together to form the large biomolecules called oligomers, the fluorescent additive binds and labels them.

That will allow researchers to easily track the progress and movements of aggregates as they grow over time. Details of the work appear in the Journal of the American Chemical Society.

Amyloid plaques have long been suspected as the root cause of Alzheimer's, but recent studies suggest that oligomers -- floating molecules with repeating peptide units -- do far more damage.

"There's a view in the field that soluble oligomers are the main cause of neuronal degeneration, because these oligomers are toxic to neurons," said Martí, an associate professor of chemistry, of bioengineering and of materials science and nanoengineering.

"These oligomers are definitely associated with Alzheimer's pathology, so there's been a need for tools to help us study them."

He said oligomers are "virtually invisible" to Thioflavin T dyes commonly used to tag amyloid fibrils in lab studies. The ruthenium complexes solve that problem.

The complexes take advantage of fluorescence anisotropy, in which the fluorescent response is polarized, glowing brighter in some directions than others. "It's a very old technique related to the rotation of molecules," Martí said. "When the molecule is in solution, it moves and is constantly rotating. When it's very small, it rotates very fast and the anisotropy is nearly zero.

"But when the same probe binds to a big macromolecule, it rotates more slowly," he said. "That's how we know we have oligomers, and then we can track their growth and propagation."

Lab tests showed oligomers forming in solution at different temperatures over hours. Martí noted cold solutions slow the process, but at body temperatures, oligomers form "very fast and in large amounts. The speed at which they form at physiological temperatures is remarkable."

The Rice lab also used its probes to see how neuroblastoma cells were affected in real time when injected with amyloid beta peptides. They revealed only 60% of cells injected with oligomers remained viable, while those treated with amyloid fibrils and monomers had higher viability, about 80%, suggesting the oligomers are indeed toxic, Martí said.

For now, he said, the ruthenium probes are meant for use only in the laboratory. "It will be difficult to use these in the brain because there's too much scattering of light," Martí said. "They are made to take advantage of polarized light, and scattering would dampen that."

"But as a lab tool, they will allow researchers around the world to test the effects of other molecules on the rate of oligomer formation, and that's a big deal," he said. "They can quickly see if a drug delays or halts the formation of oligomers."