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Our planet's ecosystems are teeming with life! Navigate the intricate web of interactions in these intriguing articles. How do organisms relate to one another and their surroundings? Ecology Articles Our planet's ecosystems are teeming with life! Navigate the intricate web of interactions in these intriguing articles. How do organisms relate to one another and their surroundings? You may also like: Biology, Zoology Galápagos Tortoises An end at the beginning: their conservation Beavers are back in Britain The role of beavers in the ecosystem and their reintroduction in the UK. Article #3 in a series on animal conservation around the world. Pangolins in China From poached to protected. Article #4 in a series on animal conservation around the world. Gorongosa National Park, Mozambique From conflict to community. Article #5 in a series on animal conservation around the world. Wildlife corridors Why did the sloth cross the road? Meet the microbes that feed phosphorus to plants Plants need phosphorus to make biological molecules like DNA, ATP, and the phospholipid bilayers that form cell membranes How human activity impacts the phosphorus cycle Discussing eutrophication and industrial activities

In today's fast-paced and often overwhelming world, taking care of our mental well-being is more crucial than ever. In this article, we will explore practical strategies that can easily be incorporated into our day-to-day lives, allowing us to establish a solid foundation for our mental well-being and sustain it in the long run. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Empowering your mental health journey with practical strategies Last updated: 22/05/25 Published: 18/05/23 In today's fast-paced and often overwhelming world, taking care of our mental well-being is more crucial than ever. In this article, we will explore practical strategies that can easily be incorporated into our day-to-day lives, allowing us to establish a solid foundation for our mental well-being and sustain it in the long run. 1. Embracing mindfulness Mindfulness is a powerful practice that helps us stay present, cultivate awareness, and manage stress. Imagine starting your day by dedicating a few minutes to mindful breathing or meditation, allowing yourself to set a calm and focused tone for the day. Engage in activities with a mindful mindset, whether it's taking a peaceful walk in nature, relishing a cup of tea, or fully immersing yourself in the present moment. 2. Exercise Physical activity is another essential self-care strategy that not only benefits our physical health but also plays a profound role in nurturing our mental well-being. Find an exercise routine that that brings you joy and that easily fits into your life. Whether it's walking, jogging, yoga, or any other form of movement that resonates with you, the key is to find something you enjoy and can stick to. Even small bursts of exercise throughout the day, like a short walk during your lunch break or opting for the stairs instead of the elevator, can make a significant difference in your overall well-being. 3. Sleep Hygiene Adequate sleep is vital for mental and emotional wellbeing. Establishing good sleep hygiene is crucial. Maintain a consistent sleep schedule by going to bed and waking up at the same time each day. Create a relaxing bedtime routine that signals to your body that it's time to unwind. Consider reading a book, taking a warm bath, or practicing gentle stretches to prepare your mind and body for restful sleep. Ensure your bedroom provides an optimal sleep environment by keeping it dark, quiet, and cool, and minimize exposure to screens before bed. 4. Online mental health platforms In our digital age, online mental health platforms have become invaluable resources for supporting our mental well-being. Platforms like Headspace , Better Help , and Calm offer a range of services, including meditation exercises, therapy sessions with licensed professionals, and stress reduction tools. Exploring these platforms can provide the support and guidance needed on your mental health journey. Self-care apps that can be installed on phones Prioritising self-care is essential for maintaining good mental health. By incorporating these practices into your daily routine, you can nurture your mind, body, and soul. By investing time and energy into yourself, you are fostering a stronger foundation for a happier and healthier life. Written by Viviana Greco Related articles: Physical and mental health / Imposter syndrome in STEM / Mental health in the South Asian community

Lyra is a prominent constellation, largely due to Vega which forms one of its corners, and is one of the brightest stars in the sky. Interestingly, Vega is defined as the zero point of the magnitude scale - a logarithmic system used to measure the brightness of celestial objects. Technically, the brightness of all stars and galaxies are measured relative to Vega! Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Lyrids meteor shower Last updated: 14/11/24 Published: 10/06/23 The Lyrids bring an end to the meteor shower drought that exists during the first few months of the year. On April 22nd, the shower is predicted to reach its peak, offering skygazers an opportunity to witness up to 20 bright, fast-moving meteors per hour which leave long, fiery trails across the sky, without any specialist equipment. The name Lyrids comes from the constellation Lyra - the lyre, or harp - which is the radiant point of this shower, i.e. the position on the sky from which the paths of the meteors appear to originate. In the Northern Hemisphere Lyra rises above the horizon in the northeast and reaches the zenith (directly overhead) shortly before dawn, making this the optimal time to observe the shower. Lyra is a prominent constellation, largely due to Vega which forms one of its corners, and is one of the brightest stars in the sky. Interestingly, Vega is defined as the zero point of the magnitude scale - a logarithmic system used to measure the brightness of celestial objects. Technically, the brightness of all stars and galaxies are measured relative to Vega! Have you ever wondered why meteor showers occur exactly one year apart and why they always radiate from the same defined point in the sky? The answer lies in the Earth's orbit around the Sun, which takes 365 days. During this time, Earth may encounter streams of debris left by a comet, composed of gas and dust particles that are released when an icy comet approaches the Sun and vaporizes. As the debris particles enter Earth’s atmosphere, they burn up due to friction, creating a streak of light known as a meteor. Meteorites are fragments that make it through the atmosphere to the ground. The reason that the Lyrids meteor shower peaks in mid-late April each year is that the Earth encounters the same debris stream at the point on its orbit corresponding to mid-late April. Comets and their debris trails have very eccentric, but predictable orbits, and the Earth passes through the trail of Comet Thatcher in mid-late April every year. Additionally, Earth’s orbit intersects the trail at approximately the same angle every year, and from the perspective of an observer on Earth, the constellation Lyra most accurately matches up with the radiant point of the meteors when they are mapped onto the canvas of background stars in the night sky. The Lyrids meteor shower peaks in mid-late April each year. Image/ EarthSky.org This year, there is a fortunate alignment of celestial events. New Moon occurs on April 20th, meaning that by the time the Lyrids reach their maximum intensity, the Moon is only 6% illuminated, resulting in darker skies and an increased chance to see this dazzling display. Written by Joseph Brennan Related article: L onar Lake

An introductory and comprehensive review of complex diseases and their environmental influences. Using schizophrenia as an example, we are interested in exploring one of the biggest questions that underlie complex diseases. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The environment on complex diseases: schizophrenia Last updated: 18/11/24 Published: 08/05/23 An introductory and comprehensive review of complex diseases and their environmental influences. Using schizophrenia as an example, we are interested in exploring one of the biggest questions that underlie complex diseases. Introduction: Not Exactly a Yes or No Question Many things in science revolve around questions. It is remarkable to find the number of questions left for scientists to answer or those that will remain unanswered. Indeed, one of the most daunting tasks for any scientist would be to see through every detail of a piece of information, even if everyone has seen it, but with different sets of lenses and asking different sets of questions. After all, “why did the apple fall from its tree?”. However, asking questions is one thing. Finding answers and, more importantly, the evidence or proof that supports them does not always yield conclusive results. Nevertheless, perhaps some findings may shine a new light on a previously unanswered question. We can categorise the study of genetics into two questions: “What happens if everything goes well?” and “What happens if it goes wrong?”. Whilst there are virtually limitless potential causes of any genetic disease, most genetic diseases are known to be heritable. A mutation in one gene that causes a disease can be inherited from the parents to their offspring. Often, genetic diseases are associated with a fault in one gene, known as a single-gene disorder, with notorious names including Huntington’s disease, cystic fibrosis, sickle cell anaemia, and familial hypercholesterolaemia. These diseases have different mechanisms, and the causes are also diverse. But all these diseases have one thing in common: they are all caused by a mutation or fault in one gene, and inheriting any specific genes may lead to disease development. In other words, “either you have it, or you do not”. The role of DNA and mutations in complex diseases. Image/ craiyon.com Multifactorial or complex diseases are a classification geneticists give to diseases caused by factors, faults or mutations in more than one gene. In other words, a polygenic disease. As a result, the research, diagnosis, and identification of complex diseases may not always produce a clear “black-and-white” conclusion. Furthermore, complex diseases make up most non-infectious diseases known. The diseases associated with leading causes of mortality are, in their respective ways, complex. Household names include heart diseases, Alzheimer’s and dementia, cancer, diabetes, and stroke. All of these diseases may employ many mechanisms of action, involving multiple risk factors instead of direct cause and effect, using environmental and genetic interactions or factors to their advantage, and in contrast to single-gene disorders, do not always follow clear or specific patterns of inheritance and always involve more than one problematic genes before the complete symptoms manifest. For these reasons, complex diseases are infamously more common and even more challenging to study and treat than many other non-infectious diseases. No longer the easy “yes or no” question. The Complex Disease Conundrum: Schizophrenia Here we look at the case of a particularly infamous and, arguably, notorious complex disease, schizophrenia (SCZ). SCZ is a severely debilitating and chronic neurodevelopmental disorder that affects around 1% of the world’s population. Like many other complex diseases, SCZ is highly polygenic. The NHS characterise SCZ as a “disease that tends to run in families, but no single gene is known to be directly responsible…having these genes does not necessarily mean one will develop SCZ”. As previously mentioned, many intricate factors are at play behind complex diseases. In contrast, there is neither a single known cause for SCZ nor a cure. Additionally, despite its discovery a century ago, SCZ is arguably not well understood, giving a clue to the sophisticated mechanisms that underlie SCZ. To further illustrate how such complexities may pose a challenge to future medical treatments, we shall consider a conundrum that diseases like SCZ may impose. The highly elaborate nature of complex diseases means that it is impossible to predict disease outcomes or inheritance with absolute certainty nor rule out potential specific causes of diseases. One of the most crucial aspects of research on complex diseases is their genetic architecture, just as a house is arguably only as good as its blueprint. Therefore, a fundamental understanding of the genes behind diseases can lead to a better knowledge of diseases’ pathogenesis, epidemiology, and potential drug target, and hopefully, one day bridge our current healthcare with predictive and personalised medicine. However, as mentioned by the NHS, one of the intricacies behind SCZ is that possessing variants of diseased genes does not translate to certainty in disease development or symptom manifestation. Our conundrum, and perhaps the biggest question on complex diseases like SCZ is: “Why, even when an individual possesses characteristic genes of a complex disease, they may not necessarily exhibit symptoms or have the disease?”. The enigma surrounding complex diseases lies in the elegant interactions between our genes, the blueprint of life, and “everything else”. Understanding the interplay of factors behind complex diseases may finally explain many of the intricacies behind diseases like SCZ. Genes and Environment: an Obvious Interaction? The gene-environment important implications on complex disease development were demonstrated using twin studies. A twin study, as its name suggests, is the study of twins by their similarities, differences, and many other traits that twins may exhibit to provide clues to the influences of genetic and external factors. Monozygotic (MZ) twins each share the same genome and, therefore, are genetically identical. Therefore, if one twin shows a phenotype, the other twin would theoretically also have said genes and should exhibit the corresponding trait. Experimentally, we calculate the concordance rate, which means the probability of both twins expressing a phenotype or characteristic, given that one twin has said characteristic. Furthermore, the heritability score may be mathematically approximated using MZ concordance and the concordance between dizygotic twins (twins that share around half a genome). These studies are and have been particularly useful in demonstrating the exact implications genetic factors have on phenotypes and how the expression of traits may have been influenced by confounding factors. In the case of SCZ, scientists have seen, over decades, a relatively low concordance rate but high heritability score. A recent study (published in 2018) through the Danish SCZ research cohort involved the analysis of around 31,500 twins born between the years 1951 and 2000, where researchers reported a concordance rate of 33% and estimated heritability score of 79%, with other older studies reporting a concordance rate up to and around 50%. The percentages suggest that SCZ is likely to be passed down. In other words, a genetically identical twin only has approximately 1 in 2 risks of also developing symptoms of SCZ if its opposite twin also displays SCZ. The scientists concluded that although genetic predisposition significantly affects one’s susceptibility or vulnerability against SCZ, it is not the single cause of SCZ. Demographically, there have been studies that directly link environmental risks to SCZ. Some risk factors, such as famines and malnutrition, are more evident than others. However, some studies also associate higher SCZ risk among highly industrialised countries and first or second-generation migrants. For instance, few studies point out an increased risk of SCZ within ethnic minorities and Afro-Caribbean immigrants in the United Kingdom. Hypotheses that may explain such data include stress during migration, potential maternal malnutrition, and even exposure to diseases. With this example, hopefully, we all may appreciate how the aetiology of SCZ and other complex diseases are confounded by environmental factors. In addition, how such factors may profoundly influence an individual’s genome. SCZ is a clear example of how genetic predisposition, the presence of essential gene variants characteristic of a disease, may act as a blueprint to a terrible disease waiting to be “built” by certain factors as if they promote such development. It is remarkable how genetic elements and their interactions with many other factors may contribute almost collectively to disease pathogenesis. We can reflect this to a famous quote amongst clinical geneticists: “genetics loads the gun, and environment pulls the trigger.” Carrying high-risk genes may increase the susceptibility to a complex disease, and an environment that promotes such disease may tip the balance in favour of the disease. However, finding and understanding the “blueprints” of SCZ, what executes this “blueprint”, and how it works is still an area of ongoing research. Furthermore, how the interplay between genetics and external factors can lead to profound effects like disease outcomes is still a relatively new subject. The Epigenome: the Environment’s Playground To review, it is clear that genes are crucial in complex disease aetiology. In the case of SCZ, high-risk genes and variances are highly attributed to disease onset and pathogenesis. However, we also see with twin studies that genetics alone cannot explain the high degree of differences between twins, particularly when referring to SCZ concordance between identical twins. In other words, external factors are at play, influencing one’s susceptibility and predisposition to SCZ. These differences can be explained by the effects epigenetics have on our genome. Epigenetic mechanisms regulate gene expression by modifying the genome. In short, on top of the DNA double strands, the genome consists of additional proteins, factors, and even chemical compounds that all aid the genetic functions our body heavily relies on. The key to epigenetics lies in these external factors’ ability to regulate gene expression, where some factors may promote gene expression whilst others may prevent it. Epigenetic changes alter gene functions as they can turn gene expression “on” and “off”. Furthermore, many researchers have also shown how epigenetic changes may accumulate and be inherited somatically with cell division and even passed down through generations. Therefore, epigenetic changes may occur without the need to change any of the DNA codes, yet, they may cause a profound effect by controlling gene expression throughout many levels of the living system. These underlying mechanisms are crucial for the environment’s effect on complex diseases. Some external factors may directly cause variances or even damage to the genome (e.g. UV, ionising radiation), and other sources may indirectly change gene expression by manipulating epigenetic changes. The exact molecular genetics behind epigenetic mechanisms are elaborate. However, we can generally find three common epigenetic mechanisms: DNA Methylation, Histone Modification, and Non-coding RNA. Although each method works differently, they achieve a common goal of promoting or silencing gene expression. All of these are done by the many molecular components of epigenetics, altering the genome without editing the gene sequence. We refer to the epigenome, which translates to “above the genome”, the genome itself and all the epigenetic modifiers that regulates gene expression on many levels. Environmental factors and exposure may influence epigenetic mechanisms, affecting gene expression in the cell or throughout the body, sometimes permanently. Therefore, it is clear how the epigenome may change throughout life as different individuals are exposed to numerous environmental factors. Furthermore, each individual may also have a unique epigenome. Depending on which tissues or cells are affected by these mechanisms, tissues or cells may even have a distinct epigenome, unlike the genome, which is theoretically identical in all cells. One example of this is the potential effects of DNA methylation on schizophrenia epidemiology. DNA methylation can silence genes via the enzymes DNA methyltransferases (DNMT), a family of enzymes capable of catalysing the addition of methyl groups directly into the DNA. The DNMT enzymes may methylate specific nucleotides on the gene, which usually would silence said gene. Many researchers have found that the dysregulation of DNA methylation may increase the risk towards the aetiology of numerous early onset neuro-developmental disorders. However, SCZ later-onset development also points towards the influence of environmental risk factors that target DNA methylation mechanisms. Studies show links between famines and SCZ increased prevalence, as the DNMT enzymes heavily rely on nutrients to supply essential amino acids. Malnutrition is thought to play a considerable role in DNA methylation changes and, therefore, the risk of SCZ. Small Piece of a Changing Puzzle Hopefully, we can see a bigger picture of the highly intricate foundation beneath complex diseases. Bear in mind that SCZ is only one of many complex diseases known. SCZ is ultimately not a pristine and impartial model to study complex disorders. For instance, concordance rates of complex diseases change depending on their genetic background. In addition, they may involve different mutations, variance, or dysregulation of differing pathways and epigenetic mechanisms. After all, complex diseases are complex. Finally, this article aimed to give a rundown of the epigenetics behind complex diseases like SCZ. However, it is only a snapshot compared to the larger world of the epigenome. Furthermore, some questions remain unanswered: the genetic background and architecture of complex diseases, and ways to study, diagnose, and treat complex diseases. This Scientia article is one of the articles in Scientia on the theme of complex disease science and genetics. Hopefully, this introductory article is an insight and can be used to reflect upon, especially when tackling more complicated subjects of complex diseases and precision medicine. Written by Stephanus Steven Related articles: Schizophrenia, Inflammation, and Accelerated Ageing / An Introduction to Epigenetics

It's extremely pronounced in a technical environment Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link You're not a fraud: battling imposter syndrome in STEM Last updated: 22/05/25, 10:01 Published: 17/04/25, 07:00 It's extremely pronounced in a technical environment Background If you work in STEM or take even a keen interest in the field, it’s highly likely you’d have heard of and possibly experienced the term 'imposter syndrome'. Despite the glamorised success stories and carefully curated achievements we see in professional circles and on social media, let’s take a realistic step back - people struggle no matter how qualified they are. It’s okay to admit that, and it’s time we remove the stigma of this common experience. Coming into the Scientist Training Programme, I felt a sense of excitement and pride in my achievement of having even managed to get a place on the programme. As I settled in, this quickly turned into something else – fear, anxiety, worry. Feelings that I may not be good enough or I’m not where I belong. I seemed like the only one in my department without a postgraduate qualification. I began feeling out of place. It was only until I was able to put a label on this feeling – imposter syndrome, that I could take active steps to fix it. So, what is imposter syndrome? Put simply, it's the persistent feeling of self-doubt and inadequacy despite evident success. It makes you question whether you truly deserve your accomplishments, fearing that at any moment, someone will expose you as a fraud. This is extremely pronounced in a technical environment where your success is largely measured by your ability to tackle complex problems. Understanding its purpose While frustrating, imposter syndrome stems from a mechanism designed to keep us grounded and striving for growth. As social beings, we evolved to be highly attuned to hierarchies and belonging, and self-doubt may have once served as a protective mechanism, preventing reckless decisions. However, in today’s world, particularly in STEM fields, this innate caution can turn into chronic self-evaluation. The role of social media Imposter syndrome can be exacerbated through the often-unrealistic lens of social media. As I scroll through various social media platforms, I encounter countless posts showcasing often unrealistically flawless careers. Despite what you see in those 'day in the life' posts, not every STEM professional wakes up at 4am and has a cold shower. Rarely do we see the setbacks, rejections, or moments of self-doubt behind those polished posts, yet they exist for everyone. The distortion of what we see online is undoubtably a catalyst for imposter syndrome, but we can take a sensible step back and look at things through a realistic lens. Comparison truly can be the thief of joy if you let it. Coping strategies The good news is, it’s not all doom and gloom and there are strategies we can employ to handle our mischievous minds. As STEM professionals, sometimes we become isolated in our work, deeply ingrained in fixing a problem and not realising there are countless others to share your thoughts and feelings with. This is something I pushed myself to do and as I reached out to the wider community of trainee scientists, I quickly realised that I wasn’t alone. Almost everyone I had spoken to had shared a similar sentiment of having experienced imposter syndrome to some extent. It is important to remember that imposter syndrome is something that has been a universal experience for a very long time. It is certainly not a feeling that is exclusive to those in the early stages of their career as I surprisingly found out having networked with senior figures in the STEM community. My supervisor – a consultant clinical scientist with over 40 years of experience still experiences imposter syndrome as he tackles new challenges in the ever-evolving world of science. I have found that keeping a journal has been incredibly beneficial in logging my achievements -whether personal or career-related. Having a record of successes, no matter how small, serves as a tangible reminder that progress is being made, even when self-doubt tries to convince me otherwise. But the most effective tool I’ve discovered is something I’m still learning myself - self-compassion instead of self-criticism. It’s easy to be too hard on yourself, especially in STEM, where learning new things daily is the norm. The pressure to always have the right answers can make mistakes feel like failures rather than part of the learning process. But the reality is that growth comes from pushing through discomfort, not from perfection. Learning to extend yourself the same kindness you would offer a friend can make a world of difference in battling imposter syndrome. Reframing its meaning If you have experienced imposter syndrome I do have some good news for you – you’re pushing yourself out of your comfort zone in some way and challenging yourself. That is something to be proud of and its important to realise that experiencing imposter syndrome can sometimes simply be a mandatory byproduct of self-growth. You are exactly where you need to be. Even the greatest of minds can experience imposter syndrome. Albert Einstein himself once remarked: The exaggerated esteem in which my lifework is held makes me very ill at ease. I feel compelled to think of myself as an involuntary swindler. So, remember, you’re not alone in this struggle. When to seek help While imposter syndrome is something that a large majority of people experience, you should know when to seek help. If it manifests into something much more than occasional self-doubt, there is no shame in reaching out for help. Speaking to trusted friends or family about how you’re feeling is crucial to keep your mind in the right place. A qualified therapist will be well equipped to help you deal with imposter syndrome and keep you grounded. There are a wealth of online resources that can be used to help you; such as articles, self-help guides, and professional development communities – including the team here at Scientia News who offer strategies to build confidence and reframe negative thinking. Acknowledging imposter syndrome is the first step, but learning to challenge it is what truly allows you to move forward. And the next time you begin to doubt yourself, take a step back and think about your achievements and how they themselves were born from the ashes of self-doubt. Written by Jaspreet Mann Related articles: My role as a clinical computer scientist / Mental health strategies / Mental health in South Asian communities REFERENCES “Imposter Syndrome: A Curse You Share with EinsteinThesislink « Thesislink.” Thesislink, 10 July 2018, https://thesislink.aut.ac.nz/?p=6630 . NHS Inform (2023) ‘Imposter syndrome’, NHS Inform. Available at: https://www.nhsinform.scot/healthy-living/mental-wellbeing/stress/imposter-syndrome . Mind (2022) ‘Understanding imposter syndrome’, Mind. Available at: https://www.mind.org.uk/information-support/types-of-mental-health-problems/imposter-syndrome/ . Healthline (2021) ‘What is imposter syndrome and how can you combat it?’, Healthline. Available at: https://www.healthline.com/health/mental-health/imposter-syndrome . Psychology Today (2020) ‘Overcoming imposter syndrome’, Psychology Today. Available at: https://www.psychologytoday.com/gb/blog/think-well/202002/overcoming-imposter-syndrome . beanstalk. Feel Like a Fraud? How to Overcome Imposter Syndrome - Employee and Family Resources . 1 Jan. 2023, https://efr.org/blog/feel-like-a-fraud . Ling, Ashley. “3 Ways to Get Past Imposter Syndrome.” Thir.St , 13 Aug. 2024, https://thirst.sg/3-ways-to-get-past-imposter-syndrome/ . Project Gallery

Malaria is a vicious parasitic disease spread through the bite of the female Anopheles mosquito, with young children being its most prevalent victim. In 2021, there were over 600,000 reported deaths, giving us an insight into its Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Could this new vaccine spell the end of malaria? Last updated: 20/01/25 Published: 01/02/23 Malaria is a vicious parasitic disease spread through the bite of the female Anopheles mosquito, with young children being its most prevalent victim. In 2021, there were over 600,000 reported deaths, giving us an insight into its alarming virulence. The obstacle in lessening malaria's disease burden is the challenge of creating a potent vaccine. The parasite utilises a tactic known as antigenic variation, where its extensive genetic diversity of antigens allows it to modulate its surface coat, allowing it to effectively evade the host immune system. However, unlike other variable malaria surface proteins, RH5, the protein required to invade red blood cells (RBC), does not vary and is therefore a promising target. Researchers at the University of Oxford have demonstrated various human antibodies that block the interaction between the RH5 malaria protein to host RBCs, providing hope for a new way to combat this deadly disease. The researchers have reported up to an 80% vaccine efficacy, surpassing the WHO's goal of developing a malaria vaccine with 75% efficacy. Therefore, this vaccine has the potential to be the world’s first highly effective malaria vaccine, and with adequate support in releasing this vaccine, we could be well on our way to seeing a world without child deaths from malaria. Written by Bisma Butt Related articles: Rare zoonotic diseases / mRNA vaccines

In bones, neural communications, fertilisation and more Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The importance of calcium in life Last updated: 12/03/25, 16:45 Published: 10/04/25, 07:00 In bones, neural communications, fertilisation and more Did you know that the same mineral that gives your bones strength also helps to maintain your heartbeat and even plays a role in the very start of life? Calcium, the most abundant mineral in the human body, is primarily found in bones and teeth as calcium phosphate (Ca₃(PO₄)₂). But beyond its structural role, calcium ions are essential for nearly every biological function, from muscle contractions to nerve signalling. What makes calcium so versatile, while other minerals like iron, have far more limited roles? To truly understand its significance, we must explore its underlying chemical properties. Calcium and bones The calcium ion carries a 2+ charge allowing it to form stronger ionic bonds and interact strongly with negatively charged molecules like nucleotides and ATP. This makes it essential for energy transfer in cells. In comparison to monovalent ions like Na+ and K+, calcium, therefore, has a more significant charge density, increasing affinity for anions. However, the ion also has more shells than beryllium and magnesium in the same group (Group 2), contributing to reduced charge density. These properties are very crucial in determining the strength of Calcium compounds, as a high charge density may result in problems with toxicity and difficulty in the breakdown of the product. Calcium phosphate exists as hydroxyapatite in bones and teeth, giving them hardness and rigidity. Hydroxyapatite forms hexagonal crystals that are tightly packed, contributing to the dense, durable structure of bones. These crystals are organised into a matrix along collagen fibres, creating a composite material that combines rigidity (from hydroxyapatite) and flexibility (from collagen). The properties of hydroxyapatite make it uniquely suited for its roles in the body. Its hardness provides bones with the ability to resist deformation and compression, while its porous structure allows space for blood vessels, bone marrow, and the exchange of nutrients and waste. Osteoclasts break down the bone releasing calcium and phosphate ions while osteoblasts can reabsorb this calcium to reform bones in another area of the body, maintaining skeletal health and strength. Neural communication Imagine a relay race where one runner must pass the baton to the next for the race to continue. In a similar way, calcium ions act as messengers in the nervous system, triggering the release of neurotransmitters which allow nerve cells to communicate with each other. Upon experiencing a stimulus, sodium ions begin to enter neurones through voltage-gated sodium channels, causing depolarisation, which sends an electrical signal throughout the neurone that results in the opening of other sodium channels, carrying the electrical signal throughout the neurone until the signal reaches the axon terminal. When the action potential reaches the axon terminal, it triggers the opening of voltage-gated calcium channels in the membrane of the presynaptic neurone. Calcium ions from the extracellular fluid flow into the neurone due to the concentration gradient. This influx of calcium ions is a critical step in neural communication, as it directly facilitates the release of neurotransmitters stored in synaptic vesicles. This action helps to coordinate the strength and the timing of each heartbeat. Calcium ions bind to proteins on the surface of these vesicles, which enables the vesicles to fuse with the presynaptic membrane. This fusion releases neurotransmitters, such as acetylcholine, into the synaptic cleft—a tiny gap between the presynaptic and postsynaptic neurones. These neurotransmitters then bind to specific receptors on the postsynaptic neurone, leading to either an excitatory or inhibitory response. For example, acetylcholine often causes an excitatory response, such as muscle contraction or memory formation. Fertilisation Calcium ions are crucial for fertilisation, facilitating key events from sperm-egg interaction to the activation of embryonic development. When a sperm binds to the egg’s outer layer, calcium ions trigger the release of enzymes from the sperm, enabling it to penetrate the egg. Following the sperm-egg fusion, calcium ions are released within the egg, creating a wave-like signal. The rise in intracellular calcium levels in the egg has several critical effects triggers the cortical reaction, in which cortical granules – small vesicles located beneath the egg’s plasma membrane- release their contents into the space between the plasma membrane and the zona pellucida. The enzymes released during this reaction modify the zona pellucida, making it impermeable to other sperm. This process prevents polyspermy, ensuring that only one sperm fertilises the egg. This precise calcium signalling achieves successful fertilisation and the initiation of new life. Role of calcium in other organisms Calcium is a vital element essential for initiating and sustaining human life, but its importance extends far beyond the human body. Its role is not confined to animals as calcium is equally critical in the physiology of plants and fungi, where it contributes to a wide range of biological processes. In plants, calcium ions are used to form calcium pectate, a chemical used to strengthen the cell walls of the cell and make plant cells stick together. Additionally, calcium is vital for root development and nutrient uptake. It helps in the formation of root nodules in legumes, where nitrogen-fixing bacteria establish symbiotic relationships, and it influences the movement of ions across cell membranes to regulate nutrient transport. Furthermore, calcium oscillations play a crucial role in regulating the polarised growth of fungal hyphae, which are essential for environmental exploration and host infection. Hyphal growth is characterised by a highly localised expansion at the tip, requiring cytoplasmic movement and continuous synthesis of the cell wall. Calcium ions are central to these processes, functioning as dynamic signalling molecules. Calcium concentration is highest at the growing hyphal tip, forming a steep gradient essential for maintaining growth direction. This gradient is not static but oscillatory, with periodic fluctuations in cytosolic calcium levels. These oscillations arise from the interplay of calcium influx through plasma membrane channels like voltage-gated channels. These are critical for coordinating key processes at the hyphal tip. Calcium regulates vesicle trafficking by triggering the fusion of vesicles carrying enzymes with the plasma membrane. Additionally, calcium modulates the actin cytoskeleton, which provides tracks for vesicle transport and maintains the structural polarity of the hypha. Periodic calcium signals promote the dynamic assembly and disassembly of actin filaments, ensuring flexibility and responsiveness to physical barriers to mobility during growth. Through its oscillatory signalling, calcium enables the precise regulation required for hyphal growth and network formation. Conclusion In conclusion, calcium is a remarkably versatile element, playing vital roles across a diverse range of organisms. In humans and animals, it not only provides structural integrity through bones and teeth but also regulates critical physiological processes such as nerve signalling. Beyond animal systems, calcium is also essential in plants, where it strengthens cell walls and improves structure. In fungi, calcium oscillations are fundamental to hyphal growth, coordinating vesicle trafficking. From building bones to driving vital biological processes, calcium is a silent powerhouse in life. Its influence stretches across humans, plants, and even fungi. Its role is truly indispensable. Written by Barayturk Aydin Related articles: Bone cancer / Tooth decay REFERENCES Haider, A. et al. (2017) Recent advances in the synthesis, functionalization and biomedical applications of Hydroxyapatite: A Review, RSC Advances. Available at: https://pubs.rsc.org/en/content/articlehtml/2017/ra/c6ra26124h (Accessed: 24 November 2024). Splettstoesser, T. (2024) Action potentials and synapses, Queensland Brain Institute - University of Queensland. Available at: https://qbi.uq.edu.au/brain-basics/brain/brain-physiology/action-potentials-and-synapses (Accessed: 01 December 2024). Abbott, A., L. (2001) ‘Calcium and the control of mammalian cortical granule exocytosis’, Frontiers in Bioscience, 6(1), p. d792. doi:10.2741/abbott. Vaz Martins, T. and Livina, V.N. (2019) What drives symbiotic calcium signalling in legumes? insights and challenges of imaging, International journal of molecular sciences. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC6539980/#:~:text=Currently%2C%20two%20different%20calcium%20signals,formation%20of%20the%20root%20nodule%2C (Accessed: 01 December 2024). Lew, R.R. (2011) ‘How does a hypha grow? the biophysics of pressurized growth in fungi’, Nature Reviews Microbiology, 9(7), pp. 509–518. doi:10.1038/nrmicro2591. Project Gallery

Since 2006 when the link between amyotrophic lateral sclerosis (ALS), frontotemporal degeneration and TDP-43 mutations was demonstrated by Arai et al., it has remained a focus in neurological academia. This is for good reason; the research boom around the role of TDP-43 in neurodegeneration has elucidated links between TDP-43, parkinsonism and frontotemporal dementia (FTD). Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link TDP-43 and Me: the Neurodegenerative Impact of Gene Misplacement in Parkinsonism Last updated: 18/11/24 Published: 06/04/23 Practice and Progress in Neurology Since 2006 when the link between amyotrophic lateral sclerosis (ALS), frontotemporal degeneration and TDP-43 mutations was demonstrated by Arai et al., it has remained a focus in neurological academia. This is for good reason; the research boo m around the role of TDP-43 in neurodegeneration has elucidated link s between TDP-43, parkinsonism and frontotemporal dementia (FTD). The link between point mutations, deletions and loss of gene function in PRKN has long been established, but has yet to lead to the development of a targeted therapeutic treatment. PRKN is involved in the tagging of excess or faulty proteins with ubiquitin, which leads to degradation of the proteins in the ubiquitin/proteasome system (UPS)- a system characterised in medical neurology by its potential to cause serious neurological disorders. This places parkinsonism in a domain of neurodegenerative disorders sharing a common root in UPS dysfunction, including Alzheimer’s Disease, multiple sclerosis and Huntington’s Disease. Panda et al. (2022) demonstrated how the dysfunction of the UPS due to PRKN aberration inhibits the breakdown of the damaging TDP-43 aggregates which develop in human brains in response to mutation or stress. In healthy people, autophagic granules would attack and kill off these TDP-43 aggregates as an end result of the UPS , but due to aberrations in PRKN the UPS is inhibited in those afflicted with parkinsonism, causing neurodegeneration. The discovery of how TDP-43 and parkinsonism are linked could lead to the development of a treatment mimicking the organic catalyst of the TDP-43 aggregate breakdown to replicate UPS, reducing TDP-43 aggregate volume and by proxy, inhibiting neurodegeneration. In 2007, research by Esper et al. catalysed recognition of drug-induced Parkinsonism as severely underdiagnosed, with evidence proving even neurologists fail to effectively remember which medications cause parkinsonism. Fast halting of the inciting agent is necessary for the reversal of all parkinsonism symptoms, but in some patients, cognitive symptoms may persist for a time after the medication is stopped. In response to the novel discoveries of Panda et al. (2022), it is likely due to the aggregation of TDP-43. Another possibility is that permanent cognitive symptoms after inciting agent cessation in DIP may be due to large TDP-43 aggregates unable to be destroyed by the UPS. Further research will demonstrate whether TDP-43 aggregates become more resistant to UPS or autophagy through the progression of DIP, whether due to size or other extraneous factors. The implications of such a promising lead in neurotherapeutics for refractory parkinsonism cannot be understated. Surgical therapies have long since remained the industry standard in treating refractory parkinsonism, though this option remains prone to risk since many of those afflicted with parkinsonism are elderly, with drug-induced parkinsonism from treatment with antipsychotics, calcium channel blockers or other medications always heightening the number of the geriatric population requiring care for parkinsonism . Furthermore, the adequate treatment of those with parkinsonism in their youth could inhibit their progression to a refractory disease state in old age. Overall, the future looks very promising for those around the world suffering from all different forms of parkinsonism. Written by Aimee Wilson Related articles: A common diabetes drug treating Parkinson's disease / Lifestyle and PD risk

- And face masks! No need to say they don’t work either. No matter the number of layers in the mask. Nothing is ever 100% efficient, and face masks are not exempt from this. Face masks help a lot by stopping you from inhaling COVID-19 particles in the air, indeed spread by people not wearing, or cannot wear, masks. Not just COVID-19 particles, Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Misconceptions about COVID-19 and its vaccine Last updated: 07/11/24 Published: 28/12/22 Three years into the pandemic, after huge losses in lives, livelihoods, and freedoms, misinformation about the coronavirus and now its vaccines, are still in circulation on the internet. It will take time to completely eradicate these misconstructions, but it is not impossible. I will begin discussing some myths and theories about the coronavirus itself, and then continue on to the vaccines science has developed to battle the virus. The misunderstandings are not listed in any order. Coronavirus The virus is called many different names: coronavirus, SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). The disease it causes is called COVID-19, or simply COVID. – Getting COVID is no big deal. It is just another flu. It is true yes that COVID-19 is only a mild condition for most people, however for those who are elderly and/ or clinically vulnerable it is anything but mild. Getting COVID-19 depends on the immune system, and if the immune system is already weakened, it is a big deal. As for the flu, it has been around for years mutating each time, but it is never less of a threat. – Only the elderly contract it. In most cases, it is the elderly who fall victim to the disease. But there are many factors at play; age is only one of them. Pre-existing health conditions regardless of age (for those clinically vulnerable), ethnicity, wealth, gender (does not factor that much), all determine who contracts it and how long it will take for someone to recover from the disease. – Children and teenagers are immune to it. Not necessarily true. For the better part of a year, children and younger adults seemed to evade COVID-19 but now more and more are falling ill to it. It is probably due to the emerging variants and how vulnerable children are. – Herd immunity is the way out. We do this by sacrificing said elderly to save the economy. It would have been the ideal solution to continue working and travelling while the virus ravages entire nations to protect the economy, but it would also have meant exposing society’s most vulnerable, namely the elderly, to the virus. Not a good solution to only protect one generation of society and not another. – Yes, because lockdowns don’t work. Lockdowns tend to have a rapid effect; they act to break the circuit of virus transmission up and down the country. They work. This is the reason why they last no more than one month or so when put in place. However, lockdown costs people’s freedoms and mental health so it should only be imposed when crucial. – But we need to work! How will we support ourselves? Very understandable. But if you suddenly contract COVID, you will not be able to work anyway. Many government initiatives have been started to support workers in the past year or so. - What is this 2m/ 6ft rule? No social contact whatsoever? The particles don’t even travel that far. The major way coronavirus travels is by droplets in the air between human contact. Not through surfaces (very little evidence supporting this), not by sharing needles, not by parasites and animals (vectors that bring the virus to humans). - And face masks! No need to say they don’t work either. No matter the number of layers in the mask. Nothing is ever 100% efficient, and face masks are not exempt from this. Face masks help a lot by stopping you from inhaling COVID-19 particles in the air, indeed spread by people not wearing, or cannot wear, masks. Not just COVID-19 particles, but any other harmful particles. You’re still able to take oxygen in and carbon dioxide out- these molecules are much smaller, 1-3 atoms big, so they can pass through the mask. Multiple layers of the mask offer more protection, however one is enough. - Antibiotics can be used to treat COVID-19. Antibiotics are anti-bacteria. Coronavirus is a virus- only antivirals will help. - Surely if bleach cleans and wipes out pathogens on surfaces and on just about anything else, it can do the same inside our bodies. Bleach is for surfaces only; they are not for consumption or administration as medicine. They will cause untold amount of damage inside the body. Bleach also turns things white. Whatever cleaning and wiping of pathogen need to be done, your immune system will do it. No need for bleach. - How does opening windows help prevent the spread of COVID-19? As mentioned before, COVID-19 respiratory particles travel by air. So opening windows and increasing the circulation of air, helps the particles to be blown away from you and the people with you and reduces the chance of becoming infected with the virus. Going outside for this reason helps (if not under lockdown or other restrictions). - How does fresh air help? As above. Vaccine – I think they will inject a microchip under the pretence of a vaccine and will track my every movement. There is no microchip. All the ingredients and chemicals used to produce the vaccines are available to view on the respective pharmaceutical website. None of the ingredients have any tracking potential. – Or they are just making money. Usually the government or state orders and buys the vaccines from the different companies. The expenses are on them. The rest of the population get the vaccine for free. - Vaccines hurt. Only a pinprick when the vaccine is being administered. After that only mild side effects and taking paracetamol or other painkillers will help. - And we are part of a big experiment. All the testing and experimenting was done during the three phases of clinical trials. The vaccines have been approved for (temporary) nationwide use. - Vaccines don’t work anyway. There is always a story in the news detailing the efficacies of the vaccines. They have an efficiency of 70-96% depending on the vaccine, and vaccine dose. Generally, the benefits of the vaccine far outweigh the risks that come from it. - Yes, because they cause shedding. Check the context and definition of this word. ‘Shedding’ here refers to the vaccine releasing or discharging its viral components onto others and infecting them. Once inside the body, the vaccine has no way to expel the viral contents.The only way the virus will shed its components is when the person is infected and sneezes, coughs, or causes the particles to travel in the air (i.e. when NOT vaccinated). - And, fertility issues. No biological mechanism or pathway has been discovered over the centuries that shows vaccines cause fertility issues. In fact, the reproductive system itself suppresses the immune system (not the other way round). - They will definitely cause issues if given to children. Vaccines were originally produced to provide protection to adults 18 years and older. Though there are vaccines that only children take as routine e.g. MMR (measles, mumps, rubella) and children don’t typically have any problems with them, COVID-19 vaccines aren’t among them. - Vaccines contain meat, and/ or made from animal products (and I am against this). As mentioned already, all the ingredients of the different vaccines can be found on the individual drug company websites. None of the vaccines contain meat, and if religion-conscious, scriptures advise the use of health agents even if they contain meat, to better your well-being. Anyway, the vaccine is used as medicine and not as an item for consumption. – You can pay to get a vaccine made from glucose sugar and water, and I believe it does the same thing as the official vaccine. Sugar solution is not a vaccine. It does not prevent against COVID-19. No trials have been conducted in favour of this. For a vaccine to be a vaccine, it is essential to have the actual weakened version or mRNA form of the virus. - Please take the time to read, watch, or listen to official government or health system information on coronavirus and vaccines. Millions if not billions have listened so far, be a part of this number. As with any public health guidance, education and spreading awareness are always key. Written by Manisha Halkhoree Related articles: COVID-19 glossary / Origins of COVID-19 / Digital disinformation / Fake science websites

At Scientia News, we provide free help with personal statements for students applying to UK universities. From proofreading and checking to detailed feedback reports, there is a lot of support. We check UCAS personal statements for free! What are UCAS personal statements? For UK-based universities UCAS personal statements are a chance for students to show a UK university why they should be offered a place to study a particular subject there. Academics or more? Whilst academics are important to talk about, it is just as necessary to talk about who you are beyond your grades, too. This is the third mandatory question of the statement. Page and character limited It is critical to note that the statements must not be longer than 1 page: anything beyond this will not be read. The character limit is 4000, with a minimum of 350 characters per question. You can v isit UCAS for more information... Deadline! All statements must be submitted through UCAS by 14th January 2026 at 18:00 (UK time). However, the earlier the better as universities accept students on a rolling deadline. The process of submitting a personal statement: 1. Research university courses interested in 2. Pick a course & answer the 3 statement questions 3. Check and edit statement for approval 4. Submit to your top 5 university choices Note for those that are considering medicine or dentistry: You (normally) will have to choose 1 university out of the 5 where you will do a back up course i.e. something that is not medicine or dentistry. What we offer to you: Proofreading To catch any remaining errors or inconsistencies in draft statements Expert advisors Graduates or current university students will provide personalised advice to highlight your unique qualities, and align your statement with your chosen field of study Goals We'll assist in articulating your passion and long-term goals effectively Feedback Get detailed feedback reports with specific improvement suggestions Guidance Giving example guideline questions for you to answer and include in your statement. This will help to create flow and making adjustments easier. Structure Advice on approaching your introduction, main body paragraphs and ending Examples of universities where some of our volunteers currently attend, or have graduated from: Queen Mary University of London, Imperial College London, Kings College London, University of Liverpool and so on. Fill the form out below and we will contact you* * Alternatively, you can email us at scientianewsorg@gmail.com . Please keep the subject as 'Personal Statement'. * Disclaimer: there must be no plagiarism or use of AI in all statements submitted - we will assume there has been no copying. Scientia News will not be responsible for any plagiarism or AI detection by UCAS, as we only give advice. Email Subject Your message Send Thanks for submitting!