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  • Looking at the rare earth elements | Scientia News

    The advent of recent technology has driven a surge in the use of the REEs Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Looking at the rare earth elements Last updated: 23/02/26, 21:36 Published: 26/02/26, 08:00 The advent of recent technology has driven a surge in the use of the REEs Introduction President Trump said in reference to a proposed minerals deal with Ukraine: We're telling Ukraine they have very valuable rare earths. Over the past few decades, the technological revolution has expanded the applications of the rare earth elements (REEs) from modern electronics to renewable energy sources. Despite the name, the REEs are relatively abundant in the Earth's crust, but their perceived scarcity is centred around difficulties in extracting and processing. As REE refining is currently monopolised by China, access to these materials is a constant source of geopolitical tension. The REEs comprise the lanthanide series as well as scandium (Sc) and yttrium (Y), and are characterised by the similarity of their chemical properties. Therefore, this article aims to introduce some of the fundamental chemistry of the rare earth elements to contextualise their role in modern technologies. Chemical properties of the REEs Scandium and yttrium are considered “honorary lanthanides,” as they form highly ionic, charge‑dense +3 cations when ionised. However, as they are transition metals, their properties cannot be explained by considering the f‑orbitals. The f‑orbitals are a set of seven orbitals which can hold a maximum of 14 electrons. For the lanthanides, each element has a set of 4f and 6s valence orbitals, with cerium (Ce),lanthanum (La), gadolinium (Gd), and lutetium (Lu) also having an occupied 5d¹ orbital. The 4f orbitals are generally contracted because of the nuclear charge felt by the electrons in these orbitals. As the atomic radius across the period decreases, this contraction is felt more strongly, meaning the resulting ions become more charge‑dense. This phenomenon is known as the lanthanide contraction. The contracted nature of the 4f orbitals explains why the lanthanides preferentially adopt a +3 oxidation state (O.S). The 4f electrons are strongly attracted to the nucleus, making them energetically unfavourable to remove. Therefore, once the two 6s electrons and one 4f (or sometimes 5d) electron are removed, further ionisation becomes much more difficult. This is reflected by the ionisation potentials of the lanthanides ( Figure 1 ). However, some lanthanides can form stable +2 O.S (samarium (Sm), europium (Eu), and ytterbium (Yb)), while Ce can form a +4 O.S ( Figure 2 ). This is because of the electronic configurations of these elements. For example, Eu has an electronic configuration of [Xe] 4f⁷ 6s²; therefore, by removing two electrons, the ion becomes exchange‑energy stabilised (Eu²⁺ [Xe] 4f⁷). Another notable property of the lanthanides is their large magnetic moments. This again is a consequence of the 4f orbitals. Magnetism is determined by the number of unpaired electrons an element has and its orbital angular momentum. Orbital angular momentum is an intrinsic property and becomes more prevalent with larger elements. Therefore, as the 4f orbitals can hold up to seven unpaired electrons, coupled with the intrinsic heaviness of the lanthanides, they often exhibit strong magnetic behaviour. Applications Catalytic Converters As previously mentioned, most lanthanides preferentially adopt a +3 O.S, Ce being a key exception due to its ability to cycle between +3 and +4. This property makes Ce particularly valuable in catalytic converters — vehicle exhaust devices which help reduce emissions of toxic pollutants such as carbon monoxide (CO) and nitric oxide (NO). Using CeO₂ as a catalyst, CO₂ and N₂ are generated as less harmful by‑products ( Figure 2 ). Chemical Reagents The redox flexibility of certain lanthanides is also exploited in organic chemistry. Ce(IV) and Sm(II) compounds serve as effective oxidising and reducing agents respectively. Reagents such as ceric ammonium nitrate (CAN) and cerium ammonium sulphate (CAS) are frequently used as selective oxidants, while samarium bromide (SmBr₂) is an effective reductant. MRI & Chiral Shift Reagents The magnetic properties of the lanthanides can be exploited in medical imaging, particularly in magnetic resonance imaging (MRI). Prior to an MRI scan, patients may be injected with a gadolinium (Gd³⁺) complex, such as [Gd(DTPA)]²⁻ ( Figure 4 ), to enhance image contrast. By coordinating water molecules and increasing the proton relaxation rate, these complexes cause certain regions of tissue to appear brighter and more easily distinguishable. Chemically, this principle is utilised when NMR spectroscopy is conducted in the laboratory. Fundamentally, MRI and NMR machines work in the same way, so by adding small quantities of paramagnetic lanthanide reagents to a proton NMR sample, changes in the chemical shift can be induced. These “lanthanide shift reagents” increase the proton relaxation rate, which reduces signal overlap and allows specific proton environments to be more easily identified. Commonly used lanthanide reagents include Eu³⁺ and Pr³⁺ complexes. Conclusion In conclusion, the advent of recent technology has driven a surge in the use of the REEs. While chemically similar, each element has a broad range of diverse applications, whether as magnets, reagents, or even phosphors in TV sets. Certain to dominate geopolitics for the foreseeable future, understanding the chemistry and applications of the REEs has never been more important. Written by Antony Lee Project Gallery

  • A comprehensive guide to the Relative Strength Index (RSI) | Scientia News

    The maths behind trading Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A comprehensive guide to the Relative Strength Index (RSI) 08/07/25, 14:37 Last updated: Published: 27/12/23, 11:02 The maths behind trading In this piece, we will delve into the essential concepts surrounding the Relative Strength Index (RSI). The RSI serves as a gauge for assessing the strength of price momentum and offers insights into whether a particular stock is in an overbought or oversold condition. Throughout this exploration, we will demystify the underlying calculations of RSI, explore its significance in evaluating market momentum, and unveil its practical applications for traders. From discerning opportune moments to buy or sell based on RSI values to identifying potential shifts in market trends, we will unravel the mathematical intricacies that underpin this critical trading indicator. Please note that none of the below content should be used as financial advice, but for educational purposes only. This article does not recommend that investors base their decisions on technical analysis alone. As indicated in the name, RSI measures the strength of a stock's momentum and can be used to show when a stock can be considered over- or under-bought, allowing us to make a more informed decision as to whether we should enter a position or hold off until a bit longer. It’s all very well and good to know that ‘you should buy when RSI is under 30 and sell when RSI is over 70' , but in this article, I will attempt to explain why this is the case and what RSI is really measuring. The calculations The relative strength index is an index of the relative strength of momentum in a market. This means that its values range from 0 to 100 and are simply a normalised relative strength. But what is the relative strength of momentum? Initial Average Gain = Sum of gains over the past 14 days / 14 Initial Average Loss = Sum of losses over the past 14 days / 14 Relative strength is the ratio of higher closes to lower closes. Over a fixed period of usually 14 days (but sometimes 21), we measure how much the price of the stock has increased in each trading day and find the mean average between them. We then repeat and do the same to find the average loss. The subsequent average gains and losses can then be calculated: Average Gain = [(Previous Avg. Gain * 13) + Current Day's Gain] / 14 Average Loss = [(Previous Avg. Loss * 13) + Current Day's Loss] / 14 With this, we can now calculate relative strength! Therefore, if our stock gained more than it lost in the past 14 days, then our RS value would be >1. On the other hand, if we lost more than we gained, then our RS value would be <1. Relative strength tells us whether buyers or sellers are in control of the price. If buyers were in control, then the average gain would be greater than the average loss, so the relative strength would be greater than 1. In a bearish market, if this begins to happen, we can say that there is an increase in buyers’ momentum; the momentum is strengthening. We can normalise relative strength into an index using the following equation: Relative Strength= Average Gain / Average Loss Traders then use the RSI in combination with other techniques to assess whether to buy or sell. When a market is ranging, which means that price is bouncing between support and resistance (has the same highs and lows for a period), we can use the RSI to see when we may be entering a trend. When the RSI is reaching 70, it is an indication that the price is being overbought, and in a ranging market, there is likely to be a correction and the price will fall so that the RSI stays at around 50. The opposite is likely to happen when the RSI dips to 30. Price action is deemed to be extreme, and a correction is likely. It should, however, be noted that this type of behaviour is only likely in assets presenting mean-reversion characteristics. In a trending market, RSI can be used to indicate a possible change in momentum. If prices are falling and the RSI reaches a low and then, a few days later, it reaches a higher low (therefore, the low is not as low as the first), it indicates a possible change in momentum; we say there is a bullish divergence. Divergences are rare when a stock is in a long-term trend but is nonetheless a powerful indicator. In conclusion, the relative strength index aims to describe changes in momentum in price action through analysing and comparing previous day's highs and lows. From this, a value is generated, and at the extremes, a change in momentum may take place. RSI is not supposed to be predictive but is very helpful in confirming trends indicated by other techniques. Written by George Chant Project Gallery

  • Why representation in STEM matters | Scientia News

    Tackling stereotypes and equal access Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why representation in STEM matters Last updated: 03/04/25, 10:38 Published: 13/03/25, 08:00 Tackling stereotypes and equal access In collaboration with Stemmettes for International Women's Month Representation in Science, Technology, Engineering, and Mathematics (STEM) and Science, Technology, Engineering, Art and Mathematics (STEAM), is crucial for everyone. Historically, STEM fields have been dominated by certain demographics that don’t show the true picture of our world. Maybe you grew up seeing no (or very few) women, people of colour, or other marginalised groups mentioned in your science curriculum. This needs to change because your voice, experiences and talents should be celebrated in any career you choose. Below, we’ll list some of the top reasons why representation is so important. Equal access Why does representation matter? Because it promotes equal access! Whether in an educational or career setting, seeing someone who looks like you do something you never thought possible can be life-changing. After all, you can’t be what you can’t see . Showing up in your role and sharing what you do or your STEM/STEAM interests show other people that these fields are accessible to everyone. Also, finding someone in a field you are (or would like to) get into is a great way to find a mentor, build a network, and boost your knowledge. Feeling excluded or discouraged is bound to happen at some point in your career, but anyone can succeed, no matter their background. Innovation When STEM fields are equally represented, better (and more innovative) ideas come to the table. Everything you’ve experienced can be useful in developing solutions to STEM and STEAM problems, no matter your level of education or upbringing. A lot of STEM doesn’t rely so much on your qualifications, but instead on your problem-solving, creativity, and innovation skills. For example, if you’re part of a culture that nobody else in your team has experienced, or you’ve experienced a disability and made adaptations for yourself, you bring a unique set of ideas to the table that can help solve many different problems. Inclusion There are many examples of when certain demographics haven’t been included in STEM decision-making processes. For example, many face recognition apps have failed to recognise the faces of people of colour, and period trackers have been made with misinformation about cycle lengths. If more diversity were seen throughout the process of creating a STEM product or service, we would see a lot fewer issues and a lot better products! Now, more than ever, your voice is important in STEM because science and technology are shaping the future at a fast rate. With the boom in artificial intelligence (AI) technology and its impact on almost every industry, we can’t afford to have models being trained from an unrepresentative data set. Look at people like Katherine Johnson, who despite facing setbacks as an African American at the time, was a pivotal part of sending astronauts aboard Apollo 11 into space. Or, more recently, Dr Ronx, who is paving the way as a trans-non-binary emergency medicine doctor. Tackling stereotypes Showing up in STEM & STEAM fields is a great way to tackle stereotypes. So many underrepresented groups are usually stereotyped into different career paths that are based on old, outdated notions about what certain people should do. By showing up and talking about what you love, you show that you’re not less capable than anyone else. Shout about your achievements, no matter how big or small, no matter where you are on your career journey so that we can encourage a new idea of what STEM looks like. Conclusion If this article hasn’t already given you the confidence to explore STEM and STEAM fields and all they have to offer, there are so many other reasons why you’re important to these fields and capable of achieving your dreams. Representation from you and others helps us create a more equitable, innovative, and inclusive future. It matters because the progress of science and society depends on the contributions of all, not a select few. Written by Angel Pooler -- Scientia News wholeheartedly thanks Stemmettes for this pertinent piece on the importance of representation in STEM. We hope you enjoyed reading this International Women's Month Special piece! Check out their website , and Zine / Futures youth board (The Stemette Futures Youth Board is made up of volunteers aged 15-25 from the UK and Ireland who will ensure the voices of girls, young women and non-binary young people are heard. They will work alongside the Stemette Futures charity board to guide and lead the mission to inspire more girls, young women and non-binary young people in to STEAM). -- Related articles: Sisterhood in STEM / Women leading in biomedical engineering / African-American women in cancer research Project Gallery

  • Proving causation: causality vs correlation | Scientia News

    Establishing causation through Randomised Controlled Trials and Instrumental Variables Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Proving causation: causality vs correlation Last updated: 03/06/25, 13:43 Published: 12/06/25, 07:00 Establishing causation through Randomised Controlled Trials and Instrumental Variables Does going to the hospital lead to an improvement in health? At first glance, one might assume that visiting a hospital should improve health outcomes. However, if we compare the average health status of those who go to the hospital with those who do not, we might find that hospital visitors tend to have worse health overall. This apparent contradiction arises due to confounding – people typically visit hospitals due to existing health issues. Simply comparing these two groups does not tell us whether hospitals improve health or if the underlying health conditions of patients drive the observed differences. A similar challenge arises when examining the relationship between police presence and crime rates. Suppose we compare two cities—one with a large police force and another with a smaller police force. If the city with more police also has higher crime rates, does this mean that police cause crime? Clearly not. Instead, it is more likely that higher crime rates lead to an increased police presence. This example illustrates why distinguishing causation from correlation is crucial in data analysis, and that stating that two variables are correlated does not imply causation. First, let’s clarify the distinction between causation and correlation. Correlation refers to a relationship between two variables, but it does not imply that one causes the other. Just because two events occur together does not mean that one directly influences the other. To establish causation, we need methods that separate the true effect of an intervention from other influencing factors. Statisticians, medical researchers and economists have ingeniously come up with several techniques that allow us to separate correlation and causation. In medicine, the gold standard for researchers is the use of Randomised Controlled Trials (RCTs). Imagine a group of 100 people, each with a set of characteristics, such as gender, age, political views, health status, university degree, etc. RCTs randomly assign each individual to one of two groups. Consequently, each group of 50 individuals should, on average, have similar ages, gender distribution, and baseline health. Researchers then examine both groups simultaneously while changing only one factor. This could involve instructing one group to take a specific medicine or asking individuals to drink an additional cup of coffee each morning. This results in two statistically similar groups differing in only one key aspect. Therefore, if the characteristics of one group change while those of the other do not, we can reasonably conclude that the change caused the difference between the groups. This is great for examining the effectiveness of medicine, especially when you give one group a placebo, but how would we research the causation behind the police rate and crime example? Surely it would be unwise and perhaps unethical to randomise how many police officers are present in each city? And because not all cities are the same, the conditions for RCTs would not hold. Instead, we use more complex techniques like Instrumental Variables (IV) to overcome those limitations. A famous experiment using IV to explain police levels and crime was published by Steven Levitt (1997). Levitt used the timings of mayoral and gubernatorial elections (the election of a governor) as an instrument for changes in police hiring. Around election time, mayors and governors have incentives to look “tough on crime.” This can lead to politically motivated increases in police hiring before an election. Crucially, hiring is not caused by current crime rates but by the electoral calendar. So, by using the timing of elections to predict an increase in police, we can use those values to estimate the effect on crime. What he found was that more police officers reduce violent and property crime, with a 10% increase in police officers reducing violent crime by roughly 5%. Levitt’s paper is a clever application of IV to get around the endogeneity problem and takes correlation one step further into causation, through the use of exogenous election timing. However, these methods are not without limitations. IV analysis, for instance, hinges on finding a valid instrument—something that affects the independent variable (e.g., police numbers) but has no direct effect on the outcome (e.g., crime) other than through that variable. Finding such instruments can be extremely challenging, and weak or invalid instruments can lead to biased or misleading results. Despite these challenges, careful causal inference allows researchers to better understand the true drivers behind complicated relationships. In a world where influencers, media outlets, and even professionals often mistake correlation for causation, developing a critical understanding of these concepts is an essential skill required to navigate through the data, as well as help drive impactful change in society through exploring the true relationships behind different phenomena. Written by George Chant Related article: Correlation between HDI and mortality rate REFERENCE Steven D. Levitt (1997). “Using Electoral Cycles in Police Hiring to Estimate the Effect of Police on Crime”. American Economic Review 87.3, pp. 270–290 Project Gallery

  • Why South Asian genes remember famine | Scientia News

    Famine-induced epigenetic changes and public health strategies in affected populations Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why South Asian genes remember famine Last updated: 18/09/25, 08:44 Published: 23/01/25, 08:00 Famine-induced epigenetic changes and public health strategies in affected populations Our genes are often thought of as a fixed blueprint, but what if our environment could change how they work? This is the intriguing idea behind epigenetics—a field that shows how our environment, combined with the body’s adaptive responses for survival, can influence gene expression without altering our DNA. In South Asia, famines such as the infamous Bengal Famine of 1943 caused immense suffering, and these hardships may have triggered genetic changes that continue to affect generations. Today, South Asians face an increased risk of developing Type 2 diabetes by age 25, whereas White Europeans generally encounter this risk around age 40. What is driving this difference in risk? This article will explore the science behind these epigenetic changes, their impact on the descendants of famine survivors and how these insights can shape public health, policy, and research. The legacy of historical famines In 1943, the Bengal Famine claimed around three million lives. Nobel laureate Amartya Sen argues that the severity of the famine was not merely a result of prior natural disasters and disease outbreaks in crops. Instead, it was primarily driven by wartime inflation, speculative buying, and panic hoarding, which disrupted food distribution across the Bengal region. Consequently, for the average Bengali citizen, death from starvation, disease, and malnutrition became widespread and inevitable. The impact of the famine extended well beyond the immediate loss of life. Dr Mubin Syed, a radiologist specialising in vascular and obesity medicine, emphasises that these famines have left a lasting mark on the health of future generations. Dr Syed explains that South Asians, having endured numerous famines, have inherited "starvation-adapted" traits. These traits are characterised by increased fat storage. As a result, the risk of cardiovascular diseases, diabetes, and obesity is heightened in their descendants. This tendency towards fat storage is believed to be closely tied to epigenetic factors, which play a crucial role in how these traits are passed down through generations. Epigenetic mechanisms and their impact These inherited traits are shaped by complex epigenetic mechanisms, which regulate gene expression in response to environmental stressors like famines without altering the underlying DNA sequence. DNA methylation, a process involving the addition of small chemical groups to DNA, plays a crucial role in regulating gene expression. When a gene is 'on,' it is actively transcribed into messenger RNA (mRNA), resulting in the synthesis of proteins such as enzymes that regulate energy metabolism or hormones like insulin that manage blood sugar levels. Conversely, when a gene is 'off,' it is not transcribed, leading to a deficiency of these essential proteins. During periods of famine, increased DNA methylation can enhance the body's ability to conserve and store energy by altering the activity of metabolism-related genes. Epigenetic inheritance, a phenomenon where some epigenetic tags escape the usual reprogramming process and persist across generations, plays a crucial role in how famine-induced traits are passed down. Typically, reproductive cells undergo a reprogramming phase where most epigenetic tags are erased to reset the genetic blueprint. However, certain DNA methylation patterns can evade this erasure and remain attached to specific genes in the germ cells, the cells that develop into sperm and egg cells. These persistent modifications can influence gene expression in the next generation, affecting metabolic traits and responses to environmental stressors. This means the metabolic adaptations seen in famine survivors, such as increased fat storage and altered hormone levels, can be transmitted to their descendants, predisposing them to similar health risks. Research has highlighted how these inherited traits manifest in distinct hormone profiles across different ethnic groups. A study published in Diabetes Care found that South Asians had higher leptin levels (11.82 ng/mL) and lower adiponectin levels (9.35 µg/mL) compared to Europeans, whose leptin levels were 9.21 ng/mL and adiponectin levels were 12.96 µg/mL. Leptin, encoded by the LEP gene, is a hormone that reduces appetite and encourages fat storage. Adiponectin, encoded by the ADIPOQ gene, improves insulin sensitivity and supports fat metabolism. Epigenetic changes, such as DNA methylation in the LEP and ADIPOQ genes, have led to these imbalances which were advantageous for South Asian populations during times of famine. Elevated leptin levels helped ensure the body could maintain energy reserves for survival, while lower adiponectin levels slowed fat breakdown, preserving stored fat for future use. This energy-conservation mechanism allowed individuals to endure long periods of food scarcity. Remarkably, these epigenetic changes can be passed down to subsequent generations. As a result, descendants continue to exhibit these metabolic traits, even in the absence of famine conditions. This inherited imbalance—higher leptin levels and lower adiponectin—leads to a higher predisposition to metabolic disorders. Increased leptin levels can cause leptin resistance, where the body no longer responds properly to leptin’s signals, driving overeating and fat accumulation. Simultaneously, reduced adiponectin weakens the body’s ability to regulate insulin and break down fats efficiently, resulting in higher blood sugar levels and greater fat storage. These combined effects heighten the risk of obesity and Type 2 diabetes in South Asian populations today. Integrating cultural awareness in health strategies Understanding famine-induced epigenetic changes provides a compelling case for rethinking public health strategies in affected populations. While current medicine cannot reverse famine-induced epigenetic changes in South Asians, culturally tailored interventions and preventive measures are crucial to reducing metabolic risks. These should include personalised dietary plans, preventive screenings, and targeted healthcare programmes. For example, the Indian Diabetes Prevention Programme showed that lifestyle changes reduced diabetes risk by 28.5% among high-risk individuals. Equally, policymakers must consider the broader societal factors that contribute to these health risks, and qualitative studies highlight challenges in shifting cultural attitudes. Expectations that women prepare meals in line with traditional norms often limit healthier dietary options.Differing perceptions of physical activity can complicate efforts to promote healthier lifestyles. For example, a study in East London found that some communities consider prayer sufficient exercise, which adds complexity to changing attitudes. Facing our past to secure a healthier future As we uncover the long-term effects of environmental stressors like historical famines, it becomes clear that our past is not just a distant memory but an active force shaping our present and future health. Epigenetic changes inherited from South Asian ancestors who endured famine have heightened the risk of metabolic disorders in their descendants. For instance, UK South Asian men have been found to have nearly double the risk of coronary heart disease (CHD) compared to White Europeans. Consultant cardiologist Dr Sonya Babu-Narayan has stated, “Coronary heart disease is the world’s biggest killer and the most common cause of premature death in the UK.” With over 5 million South Asians in the UK alone, this stark reality requires immediate action. We must not only address the glaring gaps in scientific research but also develop targeted public health policies to tackle these inherited health risks. These traits are not relics of the past; they are living legacies that, without swift intervention, will continue to affect generations to come. To truly address the inherited health risks South Asians face, we must go beyond surface-level awareness and commit to long-term, systemic change. Increasing funding for research that directly focuses on the unique health challenges within this population is non-negotiable. Equally crucial are culturally tailored public health initiatives that resonate with the affected communities, alongside comprehensive education programmes that empower individuals to take control of their health. These steps are not just about improving outcomes—they’re about breaking a cycle. The question, therefore, is not simply whether we understand these epigenetic changes, but whether we have the resolve to confront their full implications. Can we muster the political will needed to confront these inherited risks? Can we unite our efforts to stop these risks from affecting the health of entire communities? The cost of inaction is not just measured in statistics—it will be felt in the lives lost and the potential unrealised. The time to act is now. Written by Naziba Sheikh Related articles: Epigenetics / Food deserts and malnutrition / Mental health in South Asian communities / Global health injustices- Kashmir , Bangladesh REFERENCES Safi, M. (2019). Churchill’s policies contributed to 1943 Bengal famine – study. [online] the Guardian. Available at: https://www.theguardian.com/world/2019/mar/29/winston-churchill-policies-contributed-to-1943-bengal-famine-study . Bakar, F. (2022). How History Still Weighs Heavy on South Asian Bodies Today. [online] HuffPost UK. Available at: https://www.huffingtonpost.co.uk/entry/south-asian-health-colonial-history_uk_620e74fee4b055057aac0e9f . Sayed, M., Deek, F. and Shaikh, A. (2022). The Susceptibility of South Asians to Cardiometabolic Disease as a Result of Starvation Adaptation Exacerbated During the Colonial Famines. [online] Research Gate. Available at: https://www.researchgate.net/publication/366596806_The_Susceptibility_of_South_Asians_to_Cardiometabolic_Disease_as_a_Result_of_Starvation_Adaptation_Exacerbated_During_the_Colonial_Famines#:~:text=This%20crisis%20could%20be%20the,adapted%20physiology%20can%20become%20harmful . Utah.edu . (2009). Epigenetics & Inheritance. [online] Available at: https://learn.genetics.utah.edu/content/epigenetics/inheritance/ . Palaniappan, L., Garg, A., Enas, E., Lewis, H., Bari, S., Gulati, M., Flores, C., Mathur, A., Molina, C., Narula, J., Rahman, S., Leng, J. and Gany, F. (2018). South Asian Cardiovascular Disease & Cancer Risk: Genetics & Pathophysiology. Journal of Community Health, 43(6), pp.1100–1114. doi: https://doi.org/10.1007/s10900-018-0527-8 . Diabetes UK (2022). Risk of Type 2 Diabetes in the South Asian Community. [online] Diabetes UK. Available at: https://www.diabetes.org.uk/node/12895 . King, M. (2024). South Asian Heritage Month: A Journey Through History and Culture . [online] Wearehomesforstudents.com . Available at: https://wearehomesforstudents.com/blog/south-asian-heritage-month-a-journey-through-history-and-culture . Project Gallery

  • Genetically-engineered bacteria break down plastic in saltwater | Scientia News

    Unlocking the potential to tackle plastic pollution in oceans Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Genetically-engineered bacteria break down plastic in saltwater 09/07/25, 14:14 Last updated: Published: 29/09/23, 20:19 Unlocking the potential to tackle plastic pollution in oceans Groundbreaking discovery in the fight against plastic pollution North Carolina State University researchers have made a groundbreaking discovery in the fight against plastic pollution in marine environments. They have successfully genetically engineered a marine microorganism capable of breaking down polyethylene terephthalate (PET), a commonly used plastic found in water bottles and clothing, contributing to the growing problem of ocean microplastic pollution. Introducing foreign enzymes to V. natriegens The modified organism, created by incorporating genes from the bacterium Ideonella sakaiensis into the genome of Vibrio natriegens , can effectively degrade PET in saltwater conditions. This achievement marks the first time foreign enzymes have been successfully expressed on the surface of V. natriegens cells, making it a significant scientific breakthrough. PET microplastics pose a significant challenge in marine ecosystems, and current methods of removing them, such as extracting and disposing of them in landfills, are not sustainable. The researchers behind this study aim to find a more environmentally friendly solution by breaking down PET into reusable products, like thermoformed packaging (takeaway cartons) or textiles (clothing, duvets, pillows, carpeting). The team worked with two bacteria species, V. natriegens and I. sakaiensis . V. natriegens , known for its rapid reproduction in saltwater, served as the host organism, while I. sakaiensis provided the enzymes necessary for PET degradation. The researchers first rinsed the plastics collected from the ocean to remove high-concentration salts before initiating the plastic degradation process. Challenges ahead While this breakthrough is a significant step forward, three key challenges are still ahead. The researchers aim to incorporate the DNA responsible for enzyme production directly into the genome of V. natriegens to enhance stability. Because DNA is the genetic material responsible for the production of enzymes, and enzymes are proteins that are responsible for carrying out various chemical reactions in the body, by incorporating the DNA responsible for enzyme production into the genome of V. natriegens , the researchers can enhance the stability of the enzyme production. Thus, this DNA is essential for producing the enzymes necessary for PET degradation, as it contains the genetic information vital for encoding the proteins needed for PET breakdown. Additionally, the research team plans to modify V. natriegens further to feed on the byproducts generated during PET degradation. Lastly, they seek to engineer V. natriegens to produce a desirable end product from PET, such as a molecule that can be utilised in the chemical industry. Collaboration with industry groups Collaboration with industry groups is also crucial in determining the market demand for the molecules that V. natriegens can produce. The researchers are open to working with industry partners to explore the vast production scale and identify the most desirable molecules for commercial use. By introducing the genes responsible for PET degradation into V. natriegens using a plasmid, the researchers successfully induced the production of enzymes on the surface of the bacterial cells. The modified V. natriegens demonstrated its ability to break down PET microplastics in saltwater, providing a practical and economically feasible solution for addressing plastic pollution in marine environments. This research represents a significant advancement in the field, as it is the first time that V. natriegens has been genetically engineered to express foreign enzymes on its cell surface. This breakthrough opens up possibilities for further modifications, such as incorporating the DNA from I. sakaiensis directly into the genome of V. natriegens to make the production of plastic-degrading enzymes a more stable feature of the organism. The researchers aim to modify V. natriegens to feed on the byproducts produced during the breakdown of PET and create a desirable end product for the chemical industry. The researchers are open to collaborating with industry groups to identify the most desirable molecules to be engineered into V. natriegens for production. This groundbreaking research, published in the AIChE Journal with the support of the National Science Foundation under grant 2029327, paves the way for developing more efficient and sustainable methods for addressing plastic pollution in saltwater environments. Conclusion The research has made a breakthrough in the fight against plastic pollution in marine environments. By incorporating genes from the bacterium I. sakaiensis into the genome of V. natriegens , they created a genetically modified marine microorganism capable of breaking down PET. This achievement provides a practical and economically feasible solution to address plastic pollution in aquatic ecosystems. The researchers are now looking into further modifications to the organism to enable it to feed on byproducts and to produce a desirable end product that can be used in the chemical industry. This research highlights the potential of genetic engineering to create sustainable solutions to the growing problem of plastic pollution. Written by Sara Maria Majernikova Related article: Plastics and their environmental impact Project Gallery

  • The Survival Secrets of the Arctic Springtail | Scientia News

    Antifreeze proteins and frozen foods Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Survival Secrets of the Arctic Springtail 04/07/25, 12:59 Last updated: Published: 21/09/24, 16:09 Antifreeze proteins and frozen foods Introduction Approximately 450 million years ago, during the Ordovician period, the Earth was characterised by a hot and humid globe. The sea was teeming with life, with early squids, eel-like fish, and sea worms hunting smaller animals. However, there was no sign of movement above ground as the animals had not yet crawled ashore. This period of warmth created ideal living conditions for wildlife, but it was about to change dramatically. Shortly after, the land masses began to freeze, and an ice cap started to spread. The once warm and accommodating waters turned cold and inhospitable, leading to the second-worst mass extinction in the history of the planet. Many species succumbed to the harsh conditions, but one animal survived - the springtail. The springtail, a small insect-like animal, had developed a special strategy to combat the cold. Its cells started producing proteins that could protect them from freezing. This discovery challenges the previous belief that animals did not develop antifreeze proteins until much later. Research from Aarhus University has shown that the springtail might have been the first animal to develop such proteins. Applications in the Food Industry Since then, scientists have found antifreeze proteins in various animals, plants, and microorganisms. These proteins have also found applications in different industries. One of the industries utilising antifreeze proteins is the food industry, especially in producing frozen foods. Frozen foods often suffer from changes in taste and texture due to the formation of ice crystals. However, by incorporating antifreeze proteins, these undesirable effects can be prevented. Industrial yeast cell cultures have been engineered to produce antifreeze proteins derived from fish genes. These proteins can then be added to different foods, including ice cream, to improve texture and prevent the formation of ice crystals. Exploring Arctic Fish Aside from their contribution to the food industry, springtails have also fascinated scientists due to their ability to survive in extremely cold regions. The discovery of antifreeze proteins explained how arctic fish could swim in icy seawater. The proteins prevent ice from forming in the cells and blood of the fish, allowing them to survive in freezing conditions. Martin Holmstrup, a researcher at Aarhus University, oversees colonies of springtails in his laboratory. These small animals require minimal space and can be easily maintained in Petri dishes with a base of moist plaster and a feed of dry yeast. Researchers have determined that springtails developed these proteins long before other animals by studying the DNA sequences responsible for building antifreeze proteins. The discovery of antifreeze proteins in springtails opens up possibilities for various applications, including in the food industry. These proteins have been found to prevent ice crystal formation, which can affect the taste and texture of frozen foods. The genes responsible for their production have been copied into industrial yeast cell cultures to utilise these proteins. This allows the yeast to produce the antifreeze proteins, which can then be added to different foods. One example is the use of these proteins in ice cream, where they help create a delightful texture and allow the ice cream to be thawed and refrozen without compromising its quality. Conclusion The discovery of antifreeze proteins in springtails has revolutionised various industries, particularly the food industry. These proteins have been found to prevent ice crystal formation, improving the taste and texture of frozen foods. Incorporating antifreeze proteins derived from fish genes into yeast cell cultures can produce and add these proteins to different foods, such as ice cream, ensuring a delightful texture and the ability to thaw and refreeze without compromising quality. This remarkable adaptation of springtails has provided insight into their survival in extremely cold regions and opened up possibilities for further applications of antifreeze proteins in various fields. Written by Sara Maria Majernikova Related articles: p53 protein / Zinc finger proteins / Emperor penguins, kings of ice Project Gallery

  • Breaking down Tay-Sachs | Scientia News

    Exploring the genetic roots of a neurological tragedy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Breaking down Tay-Sachs 15/05/25, 10:43 Last updated: Published: 20/04/24, 11:29 Exploring the genetic roots of a neurological tragedy This is article no. 9 in a series on rare diseases. Next article: Ehlers-Danlos Syndrome . Previous article: Pseudo-Angelman Syndrome . Tay-Sachs disease is a heritable metabolic condition that affects the neurons in the brain. The disease is more common in infants and young children as well as people of Ashkenazi Jewish descent, although it can occur in any ethnicity. Symptoms of the disease most commonly manifest themselves in children around six months of age. However, it is possible to develop symptoms from five years old to the teenage years. There are three different forms of the disease, each appearing at different stages of life: infantile, juvenile, and adult. The adult form is much rarer and non-fatal but can still cause neuron dysfunction and psychosis. Early symptoms of the disease include mobility issues such as difficulty crawling, and as the disease progresses, the child may suffer from seizures, vision, and hearing loss. In the classic infantile form, the disease is fatal within the first few years of life or by three to five years old. In infants, infection and respiratory complications, such as pneumonia, are the most common cause of death. Being categorised as an autosomal recessive disease means that in order to display the phenotype, two copies of the mutated HEXA gene must be present in an individual. This HEXA gene is located on chromosome 15 and is responsible for producing enzymes that affect the nerve cells. The carrier frequency of Tay-Sachs is highly dependent on ethnic backgrounds, with carrier frequency being 1 in 30 for those of Ashkenazi Jewish descent and 1 in 300 for others. The chance of developing the disease early or late is predicated on the specific type of HEXA mutation that is inherited within the family. Meaning, if one child in a family possesses the infantile form, all other members of the family will also possess the infantile form (if they express the phenotype). When both parents are carriers of the Tay-Sachs gene mutation, there is a 25% chance with each pregnancy that the child will inherit two mutated copies of the HEXA gene and thus be affected by the disease. Also, there is a 50% chance the child will be a carrier like the parents and a 25% chance the child will inherit two normal copies of the gene and be unaffected. Furthermore, this particular type of gene mutation results in the disease being commonly labelled as a hexosaminidase A deficiency. The HEXA gene’s significance in the disease is further highlighted due to its ability to code for specific alpha subunits in the enzyme β-hexosaminidase A. This enzyme is involved in breaking down molecules that can be recycled in a cell through the use of lysosomes. This key cellular function helps a cell undergo apoptosis (programmed cell death) or help evade bacteria that can damage a cell. However, in individuals with this HEXA gene mutation, less of the enzyme β-hexosaminidase A is produced, which results in less degradation of GM2 ganglioside. GM2 ganglioside is a lipid involved in a host of processes such as membrane organisation, neuronal differentiation, and signal transduction. In addition, due to its lack of degradation, it accumulates inside the body. The rate at which the lipid accumulates inside the cell ultimately determines the form of Tay-Sachs an individual will possess. It is worth noting that this GM2 ganglioside pathology also includes other diseases, such as Sandhoff disease and the AB variant, which have similar disease prognoses. Furthermore, the disease specifically targets the brain as gangliosides are the main lipids that compose neuronal plasma membranes. Their expression is specific to brain regions, impacting key neurodevelopmental processes like neural tube formation and synaptogenesis. Furthermore, ganglioside synthesis is a highly regulated process facilitated by glycosyltransferases during transcription and post-transcription. They also modulate ion channels and receptor signalling, which are crucial for neurotransmission, memory, and learning. The exact mechanism of how this ganglioside accumulation due to HEXA malfunction leads to neuronal death remains unclear. Figure 1 illustrates the dysfunction of the alpha subunit in HEXA as it cannot break down GM2 gangliosides. This results in an accumulation of GM2 within the liposome, contrasting with its concentration in the external environment. This accumulation of GM2 causes lysosomal dysfunction and eventually cell damage, which leads to the symptoms commonly associated with Tay-Sachs. Mouse models have been created to understand this GM2 pathway in greater detail to develop treatments. However, this is quite limited as mice do not have the same pathway of breaking down GM2 as humans. Also, since the disease may be prevalent before birth, it is hard to establish the damage done to a baby inside the womb, making reversing this disease in infants very challenging. However, the later onset types of Tay-Sachs disease might respond to treatment. Implementing ganglioside synthesis inhibitors in combination with existing DNA and enzymatic screening programs holds promise for eventually managing and controlling this condition. Parents can undergo genetic screening to assess their risk of carrying the Tay-Sachs gene, which is done by doing a simple blood test that examines the DNA for mutations in the HEXA gene. Genetic screening is particularly important for couples who have a family history of Tay-Sachs disease or who belong to ethnic groups with a higher prevalence of the condition. Early detection through genetic screening allows couples to make informed reproductive decisions, such as pursuing in vitro fertilisation with preimplantation genetic testing or opting for prenatal testing during pregnancy to determine if the foetus has inherited the mutated gene. Utilising the acronym SHADES as a mnemonic to recognise potential signs of Tay-Sachs disease in their child can help parents get a prompt medical evaluation if any symptoms arise. SHADES: S tartle response H earing loss A ffecting vision D evelopmental delay E pileptic seizures S wallowing difficulties Written by Imron Shah REFERENCES Center, N. (2015). Tay-Sachs disease. Nih.gov . Available at: https://www.ncbi.nlm.nih.gov/books/NBK22250/ . Leal, A.F., Benincore-Flórez, E., Solano-Galarza, D., Garzón Jaramillo, R.G., Echeverri-Peña, O.Y., Suarez, D.A., Alméciga-Díaz, C.J. and Espejo-Mojica, A.J. (2020). GM2 Gangliosidoses: Clinical Features, Pathophysiological Aspects, and Current Therapies. International Journal of Molecular Sciences, 21(17), p.6213. doi: https://doi.org/10.3390/ijms21176213 . Ramani, P.K. and Parayil Sankaran, B. (2022). Tay-Sachs Disease. PubMed. Available at: https://www.ncbi.nlm.nih.gov/books/NBK564432/ . Project Gallery

  • Electricity in the body | Scientia News

    Luigi Galvani was an Italian physician and biologist, and is known for his work on bioelectricity, and for laying the foundations of electrophysiology- the branch of science focusing on electricity in the body. He was born in 1737 in Bologna, Italy, and died in 1798 when the age of electricity was approaching. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Electricity in the body: Luigi Galvani Last updated: 07/11/24 Published: 05/12/23 Luigi Galvani (1737- 1798) Luigi Galvani was an Italian physician and biologist, and is known for his work on bioelectricity, and for laying the foundations of electrophysiology- the branch of science focusing on electricity in the body. He was born in 1737 in Bologna, Italy, and died in 1798 when the age of electricity was approaching. Galvani began his career as a doctor after he graduated with a thesis in 1762, at the University of Bologna. The same year, he became a Reader in Anatomy at the university. He was then given the Chair of Obstetrics at the Institute of Sciences, owing to his surgical skills, and became its president in 1772. He held his chair for 33 years but was dismissed in 1797 when Napoleon’s army invaded but was reinstated sometime later. Galvani's discovery Galvani was performing experiments on frog legs at the University of Bologna, when his assistant touched his scalpel to the crural nerves of the frog, when he was drawing spark from the brass conductor of the electrostatic machine, and the frog leg twitched. Due to the current, muscular spasms were generated throughout the body. Galvani was intrigued and performed more experiments to see if he would get the same result. He did- the experiment was reproducible. Galvani used a Leyden jar (a device which stores static electricity, an early form of capacitor), and an electrostatic machine to produce this electricity. He knew that metals transmitted something called electricity, and a form of this electricity was presumably generated in the frog tissue to allow muscular contraction- he named this ‘animal electricity’. He believed this ‘animal electricity’ was different from static, and natural electricity e.g. lightning. Indeed, in 1786, during a lightning storm, he touched some frog nerves with a pair of scissors and the muscle contracted. Galvani thought ‘animal electricity’ as a fluid secreted by the brain, which flows though nerves and activates the muscles. This is how his experiments helped pave the way for electrophysiology in neuroscience. In 1786, during a lightning storm, Galvani touched some frog nerves with a pair of scissors and the muscle contracted. Galvani's experimental setup consisted of frog legs, a Leyden jar, and an electrostatic machine. He knew that metals transmitted something called electricity, and a form of this electricity was presumably generated in the frog tissue to allow muscular contraction- he named this ‘animal electricity’. A first step in the branch of electrophysiology. Galvani's progress in the field Galvani’s work was accepted by all his colleagues except for Volta, the professor of physics at the University of Pavia. Though Volta could reproduce Galvani’s experiments, he did not like Galvani’s explanation of ‘animal electricity’. Volta believed it was the two dissimilar metals producing the electricity, he named it ‘metallic electricity’, and there was no current running inside the frogs- there was no ‘animal electricity’. Galvani argued that there were electric forces inside organisms, and in 1794 he published an anonymous book Dell’uso e dell’attivita dell’arco conduttore nella contrazione dei muscoli (“On the Use and Activity of the Conductive Arch in the Contraction of Muscles”), where Galvani described his work on how he obtained electricity inside the frog, without the use of any metal. It was reported that he did this by touching the exposed muscle of one frog with a nerve of another, and the muscle contracted (Dibner 2020). This seems doubtful as Galvani’s forceps must have been in contact with spark for there to be movement. Still, it was the first attempt to demonstrate the existence of bioelectric forces. Outside of neuroscience The term ‘animal fluid’ Galvani used, is reminiscent of ‘animal spirits’, which was used by Rene Descartes, French philosopher, in the 1600s. Descartes described ‘animal spirits’ as a fluid flowing through the brain and the body, and Galvani unwittingly built on this belief with his findings on bioelectricity; the spirits ‘became’ “electricity”. There was a paradigm shift as Descartes thought that nerves were water pipes, but they were electrical conductors. This illustrates how Galvani was able to build on existing ideas in science. Limitations Even with the vigorous experiments and support, there was one limitation. For a direct correlation between frog muscle contraction and electricity generation, Galvani needed to be able to quantitatively measure the electrical currents generated in the muscle. This was difficult to do at the time since there was not enough technology to measure the currents- the currents were too small. Eventually, in the early 1900s when there were major advances in technology, Muller, Bois-Reymond, and Helmholtz, three German physiologists, managed to successfully measure the conduction of electrical activity along the nerve axon. This breakthrough furthered the branch of electrophysiology which Galvani had started. Summary In conclusion, Luigi Galvani was an influential physician and biologist, who founded the branch of electrophysiology with his experiments on frogs and metals. His results were crucial to the development of neuroscience, particularly the beginning of understanding electrical activity along the axon. Written by Manisha Halkhoree Related article: Nikola Tesla and wireless electricity

  • Protecting rock-wallabies in Australia | Scientia News

    Rock-wallabies are adapted to occupy specific rocky habitats, like outcrops, cliffs and caves Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Protecting rock-wallabies in Australia Last updated: 06/11/25, 11:54 Published: 29/05/25, 07:00 Rock-wallabies are adapted to occupy specific rocky habitats, like outcrops, cliffs and caves This is the final article (article no. 7) in a series on animal conservation. Previous article: Emperor penguins, kings of ice . First article: 55 years of vicuna conservation . Australia is home to many unique mammals because they have evolved in geographic isolation for millennia. Over 200 years ago, European colonists brought their own mammals to Australia, devastating this unique wildlife in ways that can still be seen today. One example is the rock-wallabies ( Petrogale spp. ), a group of 25 animal species and subspecies related to kangaroos. Australian scientists are monitoring rock-wallaby populations to ensure they remain safe from natural and human-caused threats. This article will describe those threats and how rock wallabies are being conserved. Rock-wallaby habitat As their name suggests, rock-wallabies are adapted to occupy specific rocky habitats, including outcrops, cliffs and caves. Since they are primarily nocturnal, these habitats provide shelter in the daytime. Rock-wallabies have modified foot pads to grip tricky surfaces and access places their predators cannot. Recent research found that for two rock-wallaby species, their abundance is associated with more complex and rocky habitats. Because their habitat type is so niche and they rarely migrate, one small disturbance could wipe out an entire rock-wallaby population. This is reflected by their protections under Australian law: five types of rock-wallaby are classified as ‘vulnerable’, six as ‘endangered’, and one as ‘critically endangered’. Thus, the complex habitat of rock-wallabies is both a blessing and a curse. Threats to rock-wallabies Rock-wallabies are vulnerable or endangered mainly because of invasive predators such as foxes, cats, and goats. After being introduced from Europe during colonisation, these predators have eaten many wallabies and scared the rest into foraging elsewhere. If predators live between two rock-wallaby populations, there will be less migration and interbreeding, reducing overall genetic health ( Figure 1 ). In addition, rock-wallabies will not forage if predators are in an area, so they have limited food sources under high pressure ( Figure 1 ). Combined with these indirect reasons, direct predation by invasive mammals is the biggest threat to rock-wallaby survival. Invasive predators are not the only threats to rock-wallaby populations. Wildfires kill the plants that wallabies rely on for food and shelter, such as rock figs. For example, one wildfire in the 2019/2020 season destroyed about 38% of brush-tailed rock-wallaby habitat. The already dwindling rock-wallaby populations may disappear if the climate crisis makes wildfires less predictable and more severe. Native herbivores like the euro and invasive herbivores like goats may also compete with rock-wallabies for food. There is evidence that euros out-compete rock-wallabies when food supplies are limited, but no evidence for goats yet. Thus, fires and competition combine with invasive predators to endanger rock-wallabies. Translocation and monitoring Monitoring existing rock-wallaby populations and creating new ones by translocation are reducing the threats of predation, fire, and competition. Brush-tailed rock-wallabies were translocated to Grampians National Park in 2008, but most animals died by 2013. Scientists thought manually handling wallabies might make them stressed and more vulnerable to predators. From 2014 onwards, non-invasive monitoring procedures like cameras and faecal DNA monitoring reduced predation and increased the survival rate of young rock-wallabies. Meanwhile, black-flanked rock-wallabies were being translocated from four different source populations to Kalbarri National Park, hoping they would interbreed and create a new genetically diverse population. The project was successful, as microsatellite genotyping found that the translocated population had more heterozygotes and more alleles per locus than the source populations ( Figure 2 ). This population is predicted to grow until at least 2028 because it is diverse enough to avoid the inbreeding mentioned earlier. The Grampians and Kalbarri translocations show the importance of careful monitoring and genetic considerations for conserving rock-wallabies. Conclusion After invasive mammalian predators have decimated rock-wallaby populations throughout Australia for over 200 years, wildfires and herbivore competition make survival even more difficult. Conservation efforts are made harder by the specific and limited habitats that rock-wallabies need. However, translocation efforts which consider genetic diversity and the stress of manual handling keep rock-wallaby populations afloat. Written by Simran Patel Related article: Wildlife corridors REFERENCES Campbell, I. & Woods, S. (2013) Wildlife of Australia . Princeton, UNITED STATES: Princeton University Press. Kleemann, S., Sandow, D., Stevens, M., Schultz, D.J., Taggart, D.A. & Croxford, A. (2022) Non-invasive monitoring and reintroduction biology of the brush-tailed rock-wallaby (Petrogale penicillata) in the Grampians National Park, Australia. Australian Journal of Zoology . 69 (2): 41–54. Available from: https://www.publish.csiro.au/zo/ZO21009 (Accessed 10th December 2024). Lavery, T.H., Eldridge, M., Legge, S., Pearson, D., Southwell, D., Woinarski, J.C.Z., Woolley, L.-A. & Lindenmayer, D. (2021) Threats to Australia’s rock-wallabies (Petrogale spp.) with key directions for effective monitoring. Biodiversity and Conservation . 30 (14): 4137–4161. Available from: https://doi.org/10.1007/s10531-021-02315-3 (Accessed 9th December 2024). Morris, S.D., Johnson, C.N. & Brook, B.W. (2020) Roughing it: terrain is crucial in identifying novel translocation sites for the vulnerable brush-tailed rock-wallaby (Petrogale pencillata). Royal Society Open Science . 7 (12): 201603. Available from: https://royalsocietypublishing.org/doi/full/10.1098/rsos.201603 (Accessed 10th December 2024). Nilsson, K., Pearson, D., Paxman, M., Desmond, A., Kennington, J., Byrne, M. & Ottewell, K. (2023) Translocations restore a population of a threatened rock-wallaby and bolster its genetic diversity. Conservation Genetics . 24 (5): 547–561. Available from: https://doi.org/10.1007/s10592-023-01520-7 (Accessed 9th December 2024). Silcock, J.L., Gynther, I.C., Horsup, A., Molyneux, J., Wattz, T.L., Fairfax, R.J., Healy, A.J., Murphy, D. & McRae, P.D. (2024) Half a century of survey data reveal population recovery but persistent threats for the Vulnerable yellow-footed rock-wallaby in Queensland, Australia. Oryx . 1–13. Available from: https://www.cambridge.org/core/journals/oryx/article/half-a-century-of-survey-data-reveal-population-recovery-but-persistent-threats-for-the-vulnerable-yellowfooted-rockwallaby-in-queensland-australia/D976E61ABE458B9FADA059372117382E (Accessed 10th December 2024). Project Gallery

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