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Understanding the cause of bullying can provide effective prevention and intervention Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The brain of a bully Last updated: 13/05/25, 14:22 Published: 29/05/25, 07:00 Understanding the cause of bullying can provide effective prevention and intervention Introduction Bullying is a global social issue affecting any individual regardless of sex, age, or gender, particularly in childhood and adolescence. Approximately one-third of the youth is bullied worldwide; the range could be as low as 7% in Tajikistan to 74% in Samoa. While much neuroscientific research focuses on bullying victimisation and social exclusion, there is a growing field to understand the brain mechanisms behind bullying behaviour. Why does bullying occur? Is there a neurological basis for such behaviour? This article will answer these questions with insights into prevention and intervention strategies. The neural basis of bullying As per Johnna R. Swartz, an assistant professor at the University of California, Davis : Bullying is fairly common during adolescence, with about 25-50% of teenagers in the U.S. reporting that they have bullied or been a victim of bullying. The Swartz team focused on the amygdala, a small almond-shaped structure deep within the brain. The amygdala is critical for processing emotions, particularly fear and aggression. Swartz and her colleagues conducted a functional resonance imaging (fMRI) study on 49 adolescents, examining how their amygdala responded to different emotional expressions during a face-matching task. The findings indicated that the adolescents who engaged in bullying behaviour exhibited a heightened amygdala response to angry faces and a diminished amygdala response to fearful faces. This pattern suggests that bullies may struggle to recognise fear in others, potentially making them less likely to empathise with their victims. Moreover, a study revealed that adolescents who reported higher rates of bullying showed increased activation of the ventral striatum (the area that responds to rewarded feelings), amygdala (emotion processing), medial prefrontal cortex (involved with social cognition, decision-making), and insula (salience detection) while observing social exclusion scenarios. The findings suggest that bullying is not just about aggression but also about maintaining social dominance and hierarchy. Another study by the University of Chicago conceded that bullies might enjoy others in pain by observing a robust activation of the amygdala and ventral striatum when watching pain inflicted on others. Why is knowing the neural basis of bullying useful? Understanding the root cause of bullying can provide effective prevention and intervention strategies: Social-emotional training (SET) to improve emotional regulation and empathy, which can help reshape neural pathways. For example, programmes like the ‘Roots of Empathy’ initiative have shown that training children to recognise emotions can reduce bullying behaviours in schools. Cognitive-behavioural therapy (CBT) allows bullies to reframe negative thoughts and develop a healthier response to social interactions. For instance, the CBT techniques, like role-playing social situations, have been successfully used in school-based interventions. Mindfulness and cognitive training strengthen the prefrontal cortex by meditation and improve decision-making skills and impulse control. School-based interventions (like anti-bullying programs) create supportive environments that reward prosocial behaviour rather than only punishing aggressive behaviour. Conclusion The neuroscience of bullying helps us understand the root cause of bullying scientifically. Bullying is not simply a matter of choice; there is a deeper scientific basis to consider. This knowledge can help to develop comprehensive solutions to prevent bullying and create a healthier social environment. Future studies should focus on longitudinal studies that track brain development in children and adolescents involved in bullying, thereby informing how early interventions can reshape them for positive change. Written by Prabha Rana Related articles: Aggression / Depression in childhood / Forensic neurology REFERENCES Assistant Secretary for Public Affairs (ASPA). “Facts about Bullying.” StopBullying.Gov , 9 Oct. 2024, www.stopbullying.gov/resources/facts . “Bullies May Enjoy Seeing Others in Pain: Brain Scans Show Disruption in Natural Empathetic Response.” University of Chicago News , news.uchicago.edu/story/bullies-may-enjoy-seeing-others-pain-brain-scans-show-disruption-natural-empathetic-response . Accessed 15 Feb. 2025. Dolan, Eric W. “Neuroscience Study Finds Amygdala Activity Is Related to Bullying Behaviors in Adolescents.” PsyPost , 7 Dec. 2019, www.psypost.org/neuroscience-study-finds-amygdala-activity-is-related-to-bullying-behaviors-in-adolescents/ . Perino, Michael T., et al. “Links between adolescent bullying and neural activation to viewing social exclusion.” Cognitive, Affective, & Behavioral Neuroscience , vol. 19, no. 6, 10 July 2019, pp. 1467–1478, https://doi.org/10.3758/s13415-019-00739-7 . Project Gallery ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us.

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

Chemistry is such a diverse science branching into many industries and its understanding is fundamental in unlocking solutions to overcome diseases, viruses and infections. The science has a central application in the pharmaceutical drug manufacturing process. In medicine, Chemistry helps understand diseases and medical samples through the various analytical and instrumental methods – which in turn aids medical research and the development and discovery of drugs. Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The role of chemistry in medicine Last updated: 17/11/24 Published: 13/04/23 Chemistry is such a diverse science branching into many industries and its understanding is fundamental in unlocking solutions to overcome diseases, viruses and infections. The science has a central application in the pharmaceutical drug manufacturing process. In medicine, chemistry helps understand diseases and medical samples through the various analytical and instrumental methods – which in turn aids medical research and the development and discovery of drugs. Chemical synthesis has allowed scientists to synthesise new compounds which can be used to treat a range of diseases and medical conditions. The study and knowledge of chemistry is very essential for professionals involved in the healthcare sector including doctors and nurses. The fact is that it cannot be denied that chemistry plays a dominant role in the day-to-day life of a healthcare professional. With the help of chemistry alongside biochemistry and biology, diseases and disorders can be easily diagnosed. The knowledge of chemistry has allowed for the understanding of the science behind pregnancy tests and COVID-19 PCR tests using UV-VIS Spectroscopy. Chemistry also plays a key role in the development of new medical technologies, such as diagnostic tools and imaging equipment. Magnetic resonance imaging (MRI) relies on principles of chemistry and is an application of nuclear magnetic resonance (NMR), an analytical tool for chemists found in laboratories. The technique uses strong magnetic fields and radio waves to produce detailed images of organs and body tissues. The scan uses contrast agents using elements iron and gadolinium to enhance the clarity of images. Overall, chemistry is an essential discipline for advancing our understanding of health and disease, and for developing new treatments and technologies to improve human health. Interesting fact: vaccines for rabies and anthrax were discovered by Louis Pasteur – a famous chemist. Written by Khushleen Kaur Related articles: AI in medicinal chemistry / The role of chemistry in space

Uncovering the role of IGF2BP1 in neuroblastoma and its potential as a therapeutic target Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Novel neuroblastoma driver: a potential target for therapeutics Last updated: 24/06/25, 14:16 Published: 03/07/25, 07:00 Uncovering the role of IGF2BP1 in neuroblastoma and its potential as a therapeutic target Introduction Neuroblastoma is a complicated cancer of the nervous system that primarily affects children, particularly those under the age of five. It is characterised by the development of tumours originating from neural crest cells involved in the formation of the adrenal glands and sympathetic nervous system. As the most common extracranial solid tumour in infancy and childhood, neuroblastoma represents a significant challenge in paediatric oncology due to its complex biology and variable prognosis. Recent advancements have brought hope by identifying a novel genetic driver, IGF2BP1 , implicated in the aggressive progression of the disease. The University Medicine Halle team's breakthrough in pinpointing IGF2BP1 's role is significant. It paves the way for understanding the molecular underpinnings of neuroblastoma. Additionally, it opens the door to potentially transformative targeted therapies. By elucidating the mechanisms through which IGF2BP1 drives tumour growth—specifically through its interaction with oncogenes such as MYCN —researchers are making significant progress. They are closer than ever to devising strategies that could arrest the disease's development. This progress could significantly improve patient outcomes. The importance of this discovery cannot be overblown, as it provides a crucial target for therapeutic intervention, potentially leading to the development of more effective, less toxic treatments. This is a significant step towards not only enhancing survival rates but also the quality of life for affected children worldwide. IGF2BP1: a key player in neuroblastoma and potentially other tumours The IGF2BP1 gene has emerged as a crucial element in neuroblastoma pathogenesis. It functions as an RNA-binding protein that enhances the stability and translation of mRNA transcripts. These transcripts encode oncogenic proteins, significantly impacting tumour behaviour. Oncogenes are genes that have the potential to cause cancer by promoting uncontrolled cell division and tumour growth. The activation of IGF2BP1 leads to the increased expression of several key oncogenes, including BIRC5 and MYCN. These are known to drive the growth and malignancy of neuroblastoma cells. This discovery marks a substantial leap in understanding the molecular dynamics at play within neuroblastoma cells, offering a novel avenue for targeted intervention. By stabilising and enhancing the translation of mRNA transcripts encoding these oncogenic proteins, IGF2BP1 plays a crucial role in promoting tumour growth and malignancy. Understanding this interaction provides a strategic point of intervention, potentially leading to targeted therapies that could inhibit the harmful effects of IGF2BP1 and significantly improve patient outcomes. Moreover, the IGF2BP1 role extends beyond neuroblastoma. Its expression has been detected in various other cancers, where it similarly promotes tumour growth and survival. For example, IGF2BP1 has been implicated in the progression of colorectal, breast, and lung cancers, suggesting a broader oncogenic role. This consistent pattern across different cancers underscores its potential as a universal therapeutic target. The broad impact of IGF2BP1 on multiple tumour types also highlights the potential for developing cross-cancer therapeutic strategies. By targeting IGF2BP1 , it may be possible to design treatments that are effective against multiple forms of cancer, thus maximising the impact of research and development efforts in oncology. This could lead to the creation of a new class of anticancer drugs that inhibit IGF2BP1 , offering hope to patients with various malignancies. However, targeting this gene presents challenges. IGF2BP1 is involved in beneficial processes such as normal cell growth and repair. For instance, it plays a role in stabilising mRNA during cell division, which is crucial for tissue regeneration. Inhibiting IGF2BP1 might impair these processes, leading to issues such as poor wound healing or reduced immune function. Additionally, its inhibition could potentially affect other normal cellular functions, posing a risk of unintended side effects. Thus, while targeting IGF2BP1 holds promise, understanding its role in healthy cells is essential to developing therapies that are both effective and safe. Research into IGF2BP1’s mechanisms has also revealed that it might be instrumental in initiating an “oncogene storm”. This is a rapid and intense expression of oncogenes that drives aggressive tumour growth. It also leads to resistance to conventional therapies. Conventional therapies typically refer to standard cancer treatments such as chemotherapy, radiation therapy, and surgery. For example, chemotherapy drugs like doxorubicin and cisplatin are designed to kill rapidly dividing cells, but the oncogene storm can enable tumour cells to become resistant to these drugs by enhancing their survival mechanisms. Similarly, radiation therapy aims to damage the DNA of cancer cells, but the increased expression of oncogenes can repair this damage more effectively, allowing the tumour to persist. This understanding provides a crucial insight into how cancer cells exploit molecular mechanisms to thrive and evade treatment, thereby pointing to strategic points of intervention. Current research is exploring how targeted therapies can be developed to specifically inhibit the effects of the oncogene storm, potentially overcoming resistance to these conventional treatments. This understanding provides a crucial insight into how cancer cells exploit molecular mechanisms to thrive and evade treatment, thereby pointing to strategic points of intervention. MYCN’s role in neuroblastoma: a pivotal transcriptional driver MYCN is a member of the MYC family of transcription factors, which play critical roles in cell cycle progression, apoptosis, and cellular transformation. In neuroblastoma, MYCN is particularly notorious for its strong association with high-risk disease and poor clinical outcomes, making it a main point of cancer research. High-risk disease in neuroblastoma is characterised by factors such as advanced stage at diagnosis, unfavourable histology, and the presence of MYCN amplification. For example, Stage 4 neuroblastoma, where the cancer has spread to distant lymph nodes, bone, bone marrow, liver, skin, or other organs, is considered high-risk. Poor clinical outcomes in these cases often include a lower survival rate and a higher likelihood of relapse after treatment. Studies have shown that children with MYCN -amplified neuroblastoma have a significantly lower 5-year survival rate compared to those without MYCN amplification. This is because MYCN amplification drives rapid tumour growth and metastasis, making the cancer more aggressive and difficult to treat. Additionally, these patients often exhibit resistance to conventional therapies such as chemotherapy and radiation, which further complicates treatment and negatively impacts prognosis. Specific examples of poor clinical outcomes include frequent relapses and the development of resistance to multiple lines of therapy. Despite intensive treatment regimens, including high-dose chemotherapy followed by stem cell transplant and radiation therapy, the overall survival rate for high-risk neuroblastoma remains below 50%. This bare reality underscores the critical need for novel therapeutic strategies that can effectively target MYCN and improve outcomes for patients with high-risk neuroblastoma. In general, MYCN amplifies in approximately 20% to 25% of neuroblastoma cases, leading to a dramatic increase in its protein expression. This overexpression is a known marker for aggressive disease and has been linked to rapid tumour progression and resistance to standard therapies. Standard therapies for neuroblastoma typically include a combination of surgery, chemotherapy, and radiation therapy. For instance, chemotherapy drugs such as cyclophosphamide and vincristine are commonly used to shrink tumours before surgical removal. However, the overexpression of MYCN can enhance the tumour’s ability to repair DNA damage caused by these treatments, making them less effective. Radiation therapy, which uses high-energy particles to destroy cancer cells, also becomes less effective as MYCN overexpression promotes survival pathways within the cells. The interaction between MYCN and IGF2BP1 creates a formidable axis that drives the malignant characteristics of neuroblastoma cells. Functionally, MYCN amplifies the effects of IGF2BP1 by synergising its activity. This synergy is evident in their mutual enhancement of oncogenic signalling pathways. MYCN enhances the transcription of numerous genes involved in cellular proliferation and survival. While IGF2BP1 stabilises the mRNAs of these genes, ensuring their sustained expression and activity within the cell. This interaction not only accelerates tumour growth but also contributes to the genomic instability that is characteristic of high-risk neuroblastoma. Besides, the role of MYCN extends beyond merely amplifying gene expression. It fundamentally alters the cellular landscape by modulating the expression of genes involved in metabolism, differentiation, and angiogenesis, thus shaping the tumour microenvironment to favour cancer growth and metastasis. Recent studies have also uncovered MYCN ’s role in repressing the transcription of genes involved in cellular differentiation, thereby maintaining the cells in a more primitive, stem-like state that is conducive to cancer progression. The discovery of the “oncogene storm”, a phenomenon triggered by the cooperative action of MYCN and IGF2BP1 , highlights the critical need for targeted therapeutic strategies that can disrupt this deleterious synergy. By focusing on this interaction, researchers aim to develop novel treatments that can more effectively curb the aggressive nature of MYCN -amplified neuroblastoma. The potential for therapeutic intervention The discovery of the IGF2BP1 and MYCN interaction not only deepens our understanding of neuroblastoma pathogenesis but also marks a significant step towards developing targeted therapeutic interventions. The small molecule BTYNB , which disrupts this interaction, has shown promising results in preclinical studies. By inhibiting the oncogene-enhancing effect of IGF2BP1 on MYCN , BTYNB effectively reduces tumour growth and could potentially improve the efficacy of existing treatment protocols. Current research is exploring the application of BTYNB in combination with other therapeutic agents. Combining BTYNB with existing chemotherapy drugs or novel targeted therapies may enhance treatment efficacy and prevent the onset of resistance. This combinatorial approach could be particularly effective in high-risk neuroblastoma cases, where conventional treatments often fall short. Additionally, understanding the pharmacodynamics and optimising the dosing schedule of BTYNB are critical areas of ongoing research to maximise its therapeutic potential and minimise side effects. This includes studying how the drug is absorbed, distributed, metabolised, and excreted in the body to ensure optimal efficacy. For instance, researchers are investigating the timing and dosage that maximise tumour reduction while minimising toxicity. Examples include adjusting the frequency of administration to maintain therapeutic levels and combining BTYNB with other agents to enhance its effects. These efforts aim to maximise its therapeutic potential and minimise side effects. Furthermore, the ability of BTYNB to impair tumour growth without the severe side effects associated with conventional chemotherapy presents an opportunity to reduce the treatment burden on patients. This aspect is crucial, especially in paediatric oncology, where the long-term health of young patients is a significant concern. Future therapeutic strategies could see BTYNB becoming part of a first-line treatment for neuroblastoma, either as a standalone therapy or in combination with other treatments. Future directions The ground-breaking discovery of the IGF2BP1 - MYCN interaction in neuroblastoma provides solid initial results with BTYNB , and the identification of IGF2BP1 as a key driver in neuroblastoma opens several avenues for future research. One critical area involves further elucidation of the molecular mechanisms underlying IGF2BP1 ’s influence on neuroblastoma progression. Continued research is necessary to dissect the finer details of the molecular pathways modulated by IGF2BP1 and MYCN . This includes understanding the downstream effects of their interaction and identifying other molecular players involved in the signalling cascade. Insights from such studies could reveal novel personalised therapeutic targets and help in designing drugs that can more precisely disrupt these pathways. Additionally, given the role of IGF2BP1 in various cancers, research should also explore its potential as a universal cancer target. Comparative studies across different cancer types could identify shared patterns of IGF2BP1 activity, offering opportunities to develop broad-spectrum anticancer strategies. Developing targeted delivery mechanisms that can direct BTYNB or other similar drugs specifically to neuroblastoma cells could significantly enhance therapeutic outcomes and reduce side effects. Research into nanoparticle-based delivery systems or conjugated molecules that seek out cancer-specific markers could be particularly fruitful. Additionally, investigating other compounds that can target IGF2BP1 or MYCN could provide alternative therapeutic options or complementary strategies to overcome resistance. Strategic integration of new therapies into existing treatment protocols needs careful planning. This includes determining the optimal sequencing of therapies and identifying which combinations are most effective for various subtypes of neuroblastoma based on genetic characteristics. Clinical trials are essential to transitioning laboratory findings to clinical applications. Designing and implementing rigorous clinical trials to test the efficacy and safety of BTYNB , both as a monotherapy and in combination with other therapies, is crucial. These trials should incorporate robust biomarker studies to tailor therapies based on genetic profiles and monitor patient responses more effectively. Lastly, addressing the challenge of drug delivery remains paramount. Developing drug delivery systems that can effectively target tumour sites with minimal off-target effects could improve the therapeutic index of treatments like BTYNB . Research in this area will not only benefit neuroblastoma patients but also advance the field of targeted cancer therapy in general. Importantly, given the young age of neuroblastoma patients, it is imperative to consider long-term outcomes and quality of life in therapeutic development. Efforts must be made to ensure that new treatments are not only effective but also minimise the long-term health impacts often associated with aggressive cancer therapies. Conclusion The identification of IGF2BP1 as a pivotal driver in the pathogenesis of neuroblastoma, particularly in concert with MYCN , marks a significant milestone in paediatric oncology. This discovery not only enhances our molecular understanding of one of the most challenging childhood cancers but also sets the stage for the development of targeted therapeutic strategies that could revolutionise treatment paradigms. The potential of BTYNB , a small molecule inhibitor that disrupts the IGF2BP1 - MYCN interaction, underscores the power of targeted therapy. In preclinical models, BTYNB has demonstrated a promising ability to inhibit tumour growth effectively and with fewer side effects compared to traditional chemotherapy. Such advancements herald a new era in treatment where therapy is not only about fighting the disease but also preserving the quality of life for the youngest patients. However, the journey from laboratory to clinic is filled with challenges that require innovative solutions and collaborative efforts. These challenges include ensuring the safety and efficacy of new treatments, overcoming drug resistance, and achieving precise delivery to tumour sites. The future of neuroblastoma treatment lies in the ability to refine these emerging therapies through rigorous research, optimise their delivery, and integrate them seamlessly into existing treatment protocols. Additionally, the exploration of IGF2BP1 's role across various cancer types may provide insights that transcend paediatric oncology, offering new hope for comprehensive cancer treatment strategies. As the research advances, it will be crucial to maintain a multidisciplinary approach, combining the expertise of molecular biologists, clinical researchers, and pharmacologists to ensure that these new discoveries translate into safe and effective treatments. The engagement of global health communities in these efforts will be essential to address the diverse and complex nature of cancer treatment across different populations. All in all, the path forward is marked by significant potential and profound responsibility—to continue the search for knowledge and to translate that knowledge into therapies that not only extend life but also enhance the lived experiences of patients during and after treatment. With continued dedication and innovation, the future for children battling neuroblastoma looks increasingly hopeful. Written by Sara Maria Majernikova Related articles: Cancer on the move (metastasis) REFERENCES Hagemann, S., Misiak, D., Bell, J. L., Fuchs, T., Lederer, M. I., Bley, N., Hämmerle, M., Ghazy, E., Sippl, W., Schulte, J. H., & Hüttelmaier, S. (2023). IGF2BP1 induces neuroblastoma via a druggable feedforward loop with MYCN promoting 17q oncogene expression. Molecular cancer , 22 (1), 88. https://doi.org/10.1186/s12943-023-01792-0 Liu, Y., Guo, Q., Yang, H., Zhang, X. W., Feng, N., Wang, J. K., Liu, T. T., Zeng, K. W., & Tu, P. F. (2022). Allosteric Regulation of IGF2BP1 as a Novel Strategy for the Activation of Tumor Immune Microenvironment. ACS central science , 8 (8), 1102–1115. https://doi.org/10.1021/acscentsci.2c00107 Project Gallery

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