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The main difference between children and adults lies in what needs to be rebuilt Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why brain injuries affect children and adults differently Last updated: 12/11/25, 12:09 Published: 13/11/25, 08:00 The main difference between children and adults lies in what needs to be rebuilt When we think about a brain injury, it is easy to assume that the same thing happens in everyone; a bump to the head, swelling, and hopefully a recovery. In reality, things aren’t quite that simple. A child’s brain is not a smaller version of an adult’s, it is still developing, which makes it both incredibly adaptable and, at the same time, especially vulnerable. Smaller bodies, bigger risks Although the brain’s basic reaction to injury is similar in children and adults, injuries in younger people tend to cause more widespread and severe damage. This is due to the differences in anatomical development. Children’s heads are proportionally larger compared to the rest of their bodies, and their neck muscles are much weaker than those of adults. This means that when a child falls or is knocked, their head can move suddenly and forcefully, placing extra strain on the brain. On top of that, children’s brains have a higher water content and are softer in texture, which makes them more vulnerable to rotational forces and acceleration-deceleration injuries. These types of movements can lead to diffuse axonal injury, where nerve fibres are torn across large areas, and cerebral swelling, both of which are less common in adults experiencing similar trauma. A clear example of this vulnerability is seen in abusive head trauma. When an infant is shaken, their softer skull and brain structure can lead to a combination of skull fractures, internal bleeding, and swelling. Sadly, these injuries are often linked to very poor outcomes. The double-edged sword of brain plasticity One of the most remarkable things about the young brain is its plasticity, which is its ability to reorganise itself and form new connections after injury. This flexibility often means that children recover some functions, such as movement or daily activities, more quickly than adults do in the early months after a brain injury. However, this adaptability has limits. During childhood, the brain is constantly developing new skills and abilities. If an injury occurs during one of these critical periods, it can interrupt processes essential for normal development. This means that difficulties might not appear straight away. A child could seem to recover well at first but then struggle later when their brain is expected to handle more complex tasks, such as problem-solving or emotional regulation. Over time, recovery often plateaus, and children may continue to face long-term challenges with learning, behaviour, and social interaction. Research also shows that injury severity is a major factor in long-term outcomes. Children who suffer severe traumatic brain injuries are more likely to experience lower academic performance and, later in life, face higher rates of unemployment or lower paid work compared with their peers. Behaviour, learning and life after injury Brain injuries in childhood can also affect behaviour and mental health. Conditions such as ADHD are especially common following injury, affecting between 20-50% of children. These difficulties can make returning to school and social life far more challenging. Children from lower socioeconomic backgrounds often experience extra barriers, including limited access to rehabilitation and educational support. This can increase the risk of social isolation and mental health difficulties. Children are also more likely than adults to develop secondary brain conditions, such as epilepsy, after an injury which adds further complexity to their recovery. Why recovery is not the same The main difference between children and adults lies in what needs to be rebuilt. Adults are generally trying to re-learn skills they already had, while children are still learning those skills for the first time. That makes recovery a much more delicate and unpredictable process. Moreover, most rehabilitation is concentrated in the first few months after the injury, but children’s challenges often become clearer years later, when their brains, and the demands placed on them, have developed further. In summary The developing brain is both fragile and flexible . While its biological features make it more prone to injury, its capacity for plasticity allows for impressive short-term recovery. Yet the same developmental processes that support growth also make it more vulnerable to long-term disruption. Injuries sustained during childhood can alter the course of brain development, leading to lasting effects on thinking, learning, and behaviour. These consequences can shape a person’s future long after the initial recovery period has ended. Understanding these differences is crucial, not just for doctors, but also for teachers, parents, and anyone supporting a young person recovering from a brain injury. Written by Alice Greenan Related articles: Synaptic plasticity / Traumatic Brain Injury (TBI) / Childhood intelligence REFERENCES Anderson, V. (2005). Functional Plasticity or Vulnerability After Early Brain Injury? PEDIATRICS , 116 (6), 1374–1382. https://doi.org/10.1542/peds.2004-1728 Anderson, V., Brown, S., Newitt, H., & Hoile, H. (2011). Long-term outcome from childhood traumatic brain injury: Intellectual ability, personality, and quality of life. Neuropsychology , 25 (2), 176–184. https://doi.org/10.1037/a0021217 Anderson, V., & Yeates, K. O. (2010). Pediatric Traumatic Brain Injury. In Cambridge University Press eBooks . Cambridge University Press. https://doi.org/10.1017/cbo9780511676383 ARAKI, T., YOKOTA, H., & MORITA, A. (2017). Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurologia Medico-Chirurgica , 57 (2), 82–93. https://doi.org/10.2176/nmc.ra.2016-0191 Blackwell, L. S., & Grell, R. M. (2023). Pediatric Traumatic Brain Injury: Impact on the Developing Brain. Pediatric Neurology . https://doi.org/10.1016/j.pediatrneurol.2023.06.019 Figaji, A. A. (2017). Anatomical and Physiological Differences between Children and Adults Relevant to Traumatic Brain Injury and the Implications for Clinical Assessment and Care. Frontiers in Neurology , 8 (685). https://doi.org/10.3389/fneur.2017.00685 Manfield, J., Oakley, K., Macey, J.-A., & Waugh, M.-C. (2021). Understanding the Five-Year Outcomes of Abusive Head Trauma in Children: A Retrospective Cohort Study. Developmental Neurorehabilitation , 24 (6), 1–7. https://doi.org/10.1080/17518423.2020.1869340 Narad, M. E., Kaizar, E. E., Zhang, N., Taylor, H. G., Yeates, K. O., Kurowski, B. G., & Wade, S. L. (2022). The Impact of Preinjury and Secondary Attention-Deficit/Hyperactivity Disorder on Outcomes After Pediatric Traumatic Brain Injury. Journal of Developmental & Behavioral Pediatrics , 43 (6), e361–e369. https://doi.org/10.1097/dbp.0000000000001067 Neumane, S., Câmara-Costa, H., Francillette, L., Araujo, M., Toure, H., Brugel, D., Laurent-Vannier, A., Ewing-Cobbs, L., Meyer, P., Dellatolas, G., Watier, L., & Chevignard, M. (2021). Functional outcome after severe childhood traumatic brain injury: Results of the TGE prospective longitudinal study. Annals of Physical and Rehabilitation Medicine , 64 (1), 101375. https://doi.org/10.1016/j.rehab.2020.01.008 Parker, K. N., Donovan, M. H., Smith, K., & Noble-Haeusslein, L. J. (2021). Traumatic Injury to the Developing Brain: Emerging Relationship to Early Life Stress. Frontiers in Neurology , 12 . https://doi.org/10.3389/fneur.2021.708800 Project Gallery

An overview Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Crab Nebula 14/02/25, 13:44 Last updated: Published: 23/03/24, 17:45 An overview Of the 270 known supernova remnants, the Crab Nebula is one of the more well known in popular science, originating from a violent supernova explosion first discovered by Chinese astronomer Wang Yei-te in July of 1054 AD. Yei-te reported the appearance of a “guest star” so bright that it was visible during the day for three weeks, and at night for 22 months. In 1731, English astronomer John Bevis rediscovered the object, which was then observed by Charles Messier in 1758 prompting the nebula’s lesser-known name, Messier 1. Located approximately 6,500 light years from Earth, the nebula cannot be seen with the naked eye but observations in different wavelengths gives rise to the beautiful colored images often published. The Crab Nebula is the result of a violent explosion process that signals what astronomers call “star death.” This occurs when the star runs out of fuel for the fusion process in its core that produces an outward pressure counteracting the constant inward pressure of the star’s outer shells. With the loss of outward pressure, these layers suddenly collapse inwards and produce an explosion astrophysicists call a supernova. Following the explosion, the original star, named SN1054 in this case, collapsed into a rapidly spinning neutron star, also known as a pulsar, which is generally roughly the size of Manhattan, New York. The pulsar is situated at the center of the nebula and ejects two beams of radiation that, while the pulsar rotates, makes it appear as if the object is pulsing 30 times per second. Studies of the Crab Nebula were primarily conducted by the Hubble Space Telescope. Hubble spent three months capturing 24 images that were assembled into a colorful mosaic resembling not what is visible with human eyes, but rather a kind of paint-by-number image where each color mapped to a particular element. Traces of hydrogen, neutral oxygen, doubly ionized oxygen, and sulfur have been detected across multiple wavelengths as the remains span an expanding six to eleven light-year-wide remnant of the supernova event. It was not until 1942 that the Crab Nebula was officially found to be related to the recorded supernova explosion of 1054. This establishment was jointly provided by Professor J. J. L. Duyvendak of Leiden University as well as astronomers N. U. Mayall and J. Oort. Due to its long history of rediscovery and inherent beauty, the Crab Nebula remains as one of the most studied celestial objects today and continues to provide valuable insight into astrophysical processes. Written by Amber Elinsky REFERENCES Hester, J. Jeff. “The Crab Nebula: An Astrophysical Chimera,” Annual Review of Astronomy and Astrophysics 46 (2008): 127-155. https://doi.org/10.1146/annurev.astro.45.051806.110608 . Hester, J. and A. Loll. “Messier 1 (The Crab Nebula),” NASA. https://science.nasa.gov/mission/hubble/science/explore-the-night-sky/hubble-messier-catalog/messier-1/ . Image ref.: European Space Agency; Space Australia; dreamstime. Mayall, N. U., and J. H. Oort. “FURTHER DATA BEARING ON THE IDENTIFICATION OF THE CRAB NEBULA WITH THE SUPERNOVA OF 1054 A. D. PART II. THE ASTRONOMICAL ASPECTS.” Publications of the Astronomical Society of the Pacific 54, no. 318 (1942): 95–104. http://www.jstor.org/stable/40670293 Project Gallery

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

Linking a country's HDI with its COVID-19 mortality rate Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Correlation between wealthy countries and COVID-19 mortality rate 09/07/25, 13:35 Last updated: Published: 24/08/23, 16:20 Linking a country's HDI with its COVID-19 mortality rate Investigation title: Could there have been a correlation between very rich countries and COVID-19 mortality rate? Investigation period: December 2019- November 2020 (Approx. 1 year) Background The World Health Organisation (WHO) were first alerted about coronavirus on the 31st December 2019, by a lot of pneumonia cases in Wuhan, China that has a population of 11 million. Furthermore, by 15th January 2020 there were precisely 289 cases recorded in countries such as: Thailand, Japan, S.Korea, and other places in China. And of the original cases there were 6 deaths, 51 severe cases - 12 of which were in critical condition. Meanwhile, the virus responsible for the cases was isolated and had its genome mapped, and was shared on 12th January. HDI represents the measurement of development. This is a composite of Gross National Income (GNI) per capita, mean years of education and life expectancy at birth, to measure the development of a country. It is calculated between a scale of 0 (least developed) to 1 (most developed) and all its values are to 3 significant figures. HDI values of 2019 and countries of HDI greater than 0.800 were used, as these are all regarded as very high HDI-countries so were in the scope of this investigation. Therefore, this research aimed to determine the impact of human development on the number of mortalities caused by SARS-CoV-2; where human development is measured by HDI, and the number of mortalities per hundred thousand from December 2019 to November 2020. Method Stratified sampling produced 12 countries, in descending order of HDI value: - Australia, Netherlands, UK, Austria, Spain, Estonia, UAE, Portugal, Bahrain, Kazakhstan, Romania, Malaysia See Table 4 . Results See Chart 2 . r= 0.321 (3 s.f.) – Pearson’s test ∴ There is a moderate positive linear correlation between HDI and mortality rate due to SARS-CoV-2 per 100,000. Further stats testing- Spearman’s Rank ∑D^2 = 216 n = 12 Rs = 1 - (6 ∑D^2 )/ n(n^2 – n) = 1 - (6 x 216) 1584 = 0.182 (3 d.p.) Rs = 0.245 ＜ Critical Value (0.0.587591) ∴ There is no correlation between HDI and mortality rate due to coronavirus per 100,000. Conclusion The null hypothesis was accepted: there is no correlation between a country’s HDI and its mortality rate due to SARS-CoV-2. A biogeographical reason for this is that the more developed countries (such as those in my investigation- for example, the UK) have a higher level of immigration from latitudes closer to the equator, therefore there is a section of their society with increased susceptibility to SARS-CoV-2 due to vitamin D deficiency. It is known that low vitamin D levels have a negative impact on immune function and that low vitamin D levels are common in the immigrant population. Therefore, it is likely that there is a link between vitamin D deficiency and mortality rate per 100,000, however this could be overstated due to confounding factors such as socioeconomic status, residence and employment. This would explain why countries at higher latitudes like the Netherlands have higher mortality rates per 100,000 (41.80) which is the third highest HDI-country in this investigation. Another explanation for this non-correlation could be that the less developed countries could be more used to dealing with a pandemic, or stress on a healthcare system, due to previous experience. For example, after the SARS outbreak, many countries decided to prepare in case of a pandemic, however some large HDI-countries such as the UK chose not to and even ignored other warnings on the effects of a pandemic (like the exercise signs simulation). Moreover, studies have shown that as a very high HDI-country becomes more developed, its healthcare system continues to develop until it reaches a peak where its effectiveness is undermined by economic benefit or interest. This would explain why the UK had a death rate of 68.00 per 100,000 and a total death count of over 45,000 (as of December 2020). Implications Since there is no correlation between a country’s HDI index and its mortality rate of COVID-19, this may apply to other diseases that became pandemics such as 1918’s Spanish Flu, or more recent ones like the SARS outbreak in the early 21st century. As for tropical diseases (malaria, dengue, chikungunya and others) and other illnesses such as the common cold and the flu, these diseases present in only certain geographies. This means that the countries with these ailments will be of a similar HDI and economical status; therefore there would be a correlation between a country’s HDI index and its mortality rate of these diseases, to a certain extent. Investigation conducted and written by Roshan Gill Tables, charts, stats and calculations by Roshan Gill This summary by Manisha Halkhoree ‘Implications’ section by Manisha Halkhoree Related articles: Causality vs correlation / Impacts of global warming on dengue fever / Global Health Injustices (series) Project Gallery

Research confirms anxiety disorders do have a genetic side Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Does anxiety run in families? Here's what genetics tells us Last updated: 10/07/25, 18:26 Published: 19/06/25, 07:00 Research confirms anxiety disorders do have a genetic side Have you ever noticed anxiety can pop up in several members of the same family? Maybe your sister worries constantly, or your brother gets nervous around people. It might feel like anxiety is passed down through generations. But is that really how it works, or is it just a coincidence? Here's what science has to say. Your DNA can affect anxiety Research confirms anxiety disorders do have a genetic side. That means you're more likely to have anxiety if someone in your family, like your mum, dad, sibling, or even a grandparent, has it too. But this doesn't mean anxiety is certain. Instead, genes increase your chances, accounting for about 30% to 40% of your risk. Scientists work this out by comparing identical and fraternal twins and by following anxiety diagnoses across generations; those studies repeatedly find that roughly one-third to two-fifths of a person’s risk is genetic. So, if genetics only make up part of the picture, what's the rest? That's where your environment steps in. Your life experiences matter a lot. Things like your relationships, stressful situations, and even your physical health can tip the scales one way or another. Genes set the stage, but they don't control the outcome. Think of your genes as nudging you towards anxiety rather than pushing you into it completely. The rest depends on what happens to you. How genes shape your brain Scientists have pinpointed several genes linked to anxiety. One of these genes affects serotonin, a brain chemical that helps regulate your mood and manage stress. When serotonin works well, you feel calm and can handle stressful events better. But if your genes make serotonin less effective, stress hits you harder. This can make anxiety more likely during tough times, even when others around you seem okay. There's another important point: your brain structure. Genes influence parts of your brain, especially the amygdala. Think of the amygdala as your internal alarm system. It warns you when something feels dangerous. In people with certain genes, the amygdala is extra sensitive. That means their "alarm" goes off more easily, causing anxiety even when there's no real danger present. However, not everyone with these genetic variations experiences anxiety. Your brain adapts throughout life, changing how genes affect you. This ongoing flexibility is called neuroplasticity: experience can strengthen or weaken neural circuits and can even add or remove chemical tags, such as DNA methylation, that switch genes on or off, reshaping how your stress system responds. Anxiety isn't just genetic; here's why It's tempting to blame your genes entirely if anxiety runs in your family. But life is more complicated. Even if you inherit genes that make anxiety more likely, the disorder usually develops when certain environmental conditions come into play. Stressful life events like losing a loved one, ongoing conflict at home, bullying, or trauma can trigger anxiety symptoms. Someone might have anxiety-related genes but never experience anxiety if their life stays relatively stress-free. On the other hand, someone without these genes can still develop anxiety if they experience severe stress or trauma. Lifestyle choices also make a big difference. Regular exercise, healthy eating, good sleep, and support from friends and family can protect against anxiety. Studies show these lifestyle habits are powerful, even if your genes are pushing in the opposite direction. Can you change your genetic destiny? Understanding that anxiety has a genetic basis can help. It means anxiety isn't just a character flaw or personal weakness. It's something partly built into your biology, something real and valid. Realising this can reduce shame and make people more willing to seek help. And here's another benefit: knowing your family history allows you to spot anxiety sooner. If you understand that anxiety might run in your family, you can pay attention to early signs, like trouble sleeping, excessive worry, or panic in social settings. Catching anxiety early means getting support earlier, making treatments like therapy or lifestyle changes more effective. Anxiety might run in your family, but you get to decide how far it goes. Written by Rand Alanazi Related articles: Depression / South Asian mental health / Physical and mental health / Does insomnia run in families? REFERENCES National Institute of Mental Health. Anxiety disorders [Internet]. Bethesda (MD): National Institute of Mental Health; 2024 [cited 2025 May 29]. Available from: https://www.nimh.nih.gov/health/topics/anxiety-disorders Mayo Clinic. Anxiety disorders [Internet]. Rochester (MN): Mayo Foundation for Medical Education and Research; 2018 [cited 2025 May 29]. Available from: https://www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-20350961 Leyfer O, Woodruff-Borden J, Mervis CB. Anxiety disorders in children with Williams syndrome, their mothers, and their siblings: implications for the aetiology of anxiety disorders. J Neurodev Disord . 2009 Feb 13;1(1):4-14. Martin EI, Ressler KJ, Binder EB, Nemeroff CB. The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. Psychiatr Clin North Am [Internet]. 2009 Sep;32(3):549-75. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684250/ McEwen BS, Eiland L, Hunter RG, Miller MM. Stress and anxiety: structural plasticity and epigenetic regulation as a consequence of stress. Neuropharmacology . 2012 Jan;62(1):3-12. Xie S, Zhang X, Cheng W, Yang Z. Adolescent anxiety disorders and the developing brain: comparing neuroimaging findings in adolescents and adults. Gen Psychiatry [Internet]. 2021 Aug 4;34(4):e100542. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8340272/ Zhang K, Ibrahim GM, Venetucci Gouveia F. Molecular pathways, neural circuits and emerging therapies for self-injurious behaviour. Int J Mol Sci [Internet]. 2025 Feb 24;26(5):1938. Available from: https://www.mdpi.com/1422-0067/26/5/1938 Chaves T, Fazekas CL, Horváth K, Correia P, Szabó A, Török B, et al. Stress adaptation and the brainstem with focus on corticotropin-releasing hormone. Int J Mol Sci [Internet]. 2021 Jan 1;22(16):9090. Available from: https://www.mdpi.com/1422-0067/22/16/9090 Project Gallery

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

The slippery property of a superfluid is caused by its ability to flow very easily Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The incredibly slippery nature of superfluids 03/04/25, 10:33 Last updated: Published: 24/05/23, 08:53 The slippery property of a superfluid is caused by its ability to flow very easily Slipperiness is a property that we often associate with everyday objects like ice, soap, and banana peels. However, there is a substance that is even more slippery than these: superfluids. A normal liquid becomes a superfluid when it is cooled down below a certain temperature. This temperature is unique to all fluids, for example for helium it is 2.17 K. Below this temperature, the superfluid will behave in completely unique ways. For example, if a container of water at room temperature was spun, you’d expect the water to also spin around, creating a whirlpool. Whereas a superfluid in a spinning container doesn’t spin at all, until it reaches a certain speed! The slippery property of a superfluid is caused by its ability to flow very easily. Usually it’s safe to leave a glass of water on a countertop (unless of course you’ve got a particularly excitable dog), but if you were to leave a glass of superfluid on a table, the liquid would creep out and escape. The tiny changes in temperature or pressure in the container cause it to flow, seemingly defying gravity. Unfortunately, superfluids cannot just be bought in the local supermarket! To produce a superfluid, devices known as cryostats can be used to cool a substance down to low temperatures. Using the ideal gas model, pressure, and volume can be related, so by reducing the pressure, the temperature of the device can also be decreased. The pressure is reduced using a vacuum pump, which works by removing particles from the cryostat. The applications of superfluids are limited as, due to the typically very low temperatures needed for a normal fluid to transition to a superfluid, there is difficulty in producing superfluids. Currently, scientists are working on finding fluids that enter a stable superfluid state at room temperatures. However, superfluids are used within many fields of physics to explain certain phenomena. One theory is that the core of collapsed large stars (neutron stars) is a superfluid, despite the very hot temperatures. The idea is that below a certain temperature, it uses less energy for the core to behave like a superfluid which cools the star down at an increased rate. The superfluid theory of neutron stars is just a hypothesis, however hints at the role superfluids play in all areas of physics. Written by Madeleine Hales REFERENCES/ FURTHER READING: https://www.aps.org/publications/apsnews/200601/history.cfm#:~:text=In%201927%20Willem%20Keesom%20and,helium%20I%20and%20helium%20II . https://physicsworld.com/a/neutron-star-has-superfluid-core/ Project Gallery

Looking at silicon dioxide Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The effects of nanoparticles on health Last updated: 17/07/25, 10:50 Published: 01/05/25, 07:00 Looking at silicon dioxide There are around 100 trillion harmless and beneficial microbes in the gut, representing as many as 5,000 different species! They are called the gut microbiota and are essential for regulating brain function through the microbiota-gut-brain axis, controlling intestinal inflammation and more. Nanoparticles may alter the gut microbiota, posing a risk to health and well-being. Read on to find out more about how. What are nanoparticles? Nanoparticles are small particles that are usually less than 100 nm in diameter. One example of a common nanoparticle is silicon dioxide, which can be found as the food additive E551. Silicon dioxide nanoparticles (SiO2NPs) are commonly used as anti-caking agents in free-flowing powdery food products, such as spices and coffee. These nanoparticles can be toxic, damaging cells, tissues, and organs including the liver, kidneys, and lungs. The damage is primarily due to the way SiO2NPs react in the body as a result of their size: even though SiO2NPs are bigger than 100 nm in the form of E551, when the SiO2NPs are in the gastrointestinal tract, they can clump together and degrade into a smaller size of 10-50 nm. The experiment Researchers completed several experiments to examine the effects of exposure to SiO2NPs on health. This article will specifically talk about one experiment where they looked at the impacts of SiO2NPs on the gut microbiota. For this experiment, the researchers hypothesised that oral exposure to SiO2NPs will cause changes in the gut microbiota, affecting diversity and function in mice. 20 healthy male 4-week-old mice were used, weighing 8 to 12 grams. Researchers administered either SiO2NPs solution or vehicle solution for 28 days. The vehicle solution can be considered the control and was created out of a sterile saline solution. All bacteria contain the 16S rRNA gene which is highly conserved, meaning that the sequence remains mostly unchanged across different species. After 28 days, the researchers took faecal samples from the mice and conducted 16S rRNA gene sequencing of the bacterial DNA in the faeces to analyse the gut microbiota. Figure 1 shows the process of 16S rRNA gene sequencing, a method used to identify and compare bacterial diversity without needing to grow bacterial cultures. Because it is culture-free, 16S sequencing can survey complex microbiomes or difficult environments to study. This technique is commonly used to identify bacteria down to the genus or species level, depending on the needs of the experiments. Researchers looked at the alpha diversity of the gut microbiota, with Sob, Ace, Chao, Simpson, and Shannon indices being used. Sob, Ace and Chao give information about the number of species, while Simpson and Shannon give information about the community diversity, including the species evenness. The results The results of this experiment, as seen in Figure 2 , show that there was a significant increase in Sob, Ace, and Chao indices, but there was no substantial change in Simpson or Shannon indices. This suggests that SiO2NPs can change the diversity of gut microbiota, which could impact their biological functions. For example, if there are changes to the gut microbiota, it could result in increased inflammation in the intestine. This could potentially lead to the immune system’s defences in the gut being weaker, allowing harmful pathogens to pass through the epithelial barrier more easily. Conclusion One of the main weaknesses of this experiment is that it was conducted on mice. Because of this, the study's findings cannot be directly translated to humans. In addition, the study was conducted over only 28 days, meaning we don’t know the long-term effects and consequences of the impacts of SiO2NPs on the gut microbiota. Nevertheless, this is still a critical study as it shows that SiO2NPs do impact the gut microbiota. It also shows that maintaining healthy gut microbiota is important. This can be done by being mindful of what we eat. So next time, instead of having instant noodles full of additives, think about making a home-made soup with your favourite vegetables! Eating unprocessed whole foods is not just good for us, but also for our gut microbiota! Written by Naoshin Haque Related articles: Nanomedicine / Nanoparticles as diabetes treatment / Nanogels / Nanocarriers / Silicon hydrogel lenses / Microbiota Project Gallery

How kidney damage can be detected Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link NGAL: A Valuable Biomarker for Early Detection of Renal Damage 10/07/25, 10:22 Last updated: Published: 04/04/24, 16:20 How kidney damage can be detected Nestled under the ribcage, the kidneys are primarily responsible for the filtration of toxins from the bloodstream and their elimination in urine. In instances of Acute Kidney Injury (AKI), however, this vital function is compromised. AKI is the sudden loss of kidney function, which is commonly seen in hospitalised patients. Because patients don’t usually experience pain or distinct symptoms, AKI is difficult to identify. Early detection of AKI is paramount to prevent kidney damage from progressing into more enduring conditions such as Chronic Kidney Disease (CKD). So, how can we detect AKI promptly? This is where Neutrophil Gelatinase-Associated Lipocalin (NAGL), a promising biomarker for the early detection of renal injury, comes into focus. Until recently, assessing the risk of AKI has relied on measuring changes in serum creatinine (sCr) and urine output. Creatinine is a waste product formed by the muscles. Normally, the kidney filters creatinine and other waste products out of the blood into the urine. Therefore, high serum creatinine levels indicate disruption to kidney function, suggesting AKI. However, a limitation of the sCr test is that it is affected by extrarenal factors such as muscle mass; people with higher muscle mass have higher serum creatinine. Additionally, an increase in this biomarker becomes evident once the renal function is irreversibly damaged. NGAL’s ability to rapidly detect kidney damage hours to days before sCr, renders it a more fitting biomarker to prevent total kidney dysfunction. Among currently proposed biomarkers for AKI, the most notable is NGAL. NGAL is a small protein rapidly induced from the kidney tubule upon insult. It is detected in the bloodstream within hours of renal damage. NGAL levels swiftly rise much before the appearance of other renal markers. Such characteristics render NGAL a promising biomarker in quickly pinpointing kidney damage. The concentration of NGAL present in a patient's urine is determined using a particle-enhanced laboratory technique. This involves quantifying the particles in the solution by measuring the reduced transmitted light intensity through the urine sample. In conclusion, the early detection of AKI remains a critical challenge, but NGAL emerges as a promising biomarker for promptly detecting renal injury before total loss of kidney function unfolds. NGAL offers a significant advantage over traditional biomarkers like serum creatinine- its swift induction upon kidney injury allows clinicians and healthcare providers to intervene before renal dysfunction manifests. Written by Fozia Hassan Related article: Cancer biomarkers and evolution REFERENCES Bioporto. (n.d.). NGAL . [online] Available at: https://bioporto.us/ngal/ [Accessed 5 Feb. 2024]. Branislava Medić, Branislav Rovčanin, Katarina Savić Vujović, Obradović, D., Duric, D. and Milica Prostran (2016). Evaluation of Novel Biomarkers of Acute Kidney Injury: The Possibilities and Limitations. Current Medicinal Chemistry , [online] 23(19). doi: https://doi.org/10.2174/0929867323666160210130256 . Buonafine, M., Martinez-Martinez, E. and Jaisser, F. (2018). More than a simple biomarker: the role of NGAL in cardiovascular and renal diseases. Clinical Science , [online] 132(9), pp.909–923. doi: https://doi.org/10.1042/cs20171592 . Giasson, J., Hua Li, G. and Chen, Y. (2011). Neutrophil Gelatinase-Associated Lipocalin (NGAL) as a New Biomarker for Non – Acute Kidney Injury (AKI) Diseases. Inflammation & Allergy - Drug Targets , [online] 10(4), pp.272–282. doi: https://doi.org/10.2174/187152811796117753 . Haase, M., Devarajan, P., Haase-Fielitz, A., Bellomo, R., Cruz, D.N., Wagener, G., Krawczeski, C.D., Koyner, J.L., Murray, P., Zappitelli, M., Goldstein, S.L., Makris, K., Ronco, C., Martensson, J., Martling, C.-R., Venge, P., Siew, E., Ware, L.B., Ikizler, T.A. and Mertens, P.R. (2011). The Outcome of Neutrophil Gelatinase-Associated Lipocalin-Positive Subclinical Acute Kidney Injury. Journal of the American College of Cardiology , [online] 57(17), pp.1752–1761. doi: https://doi.org/10.1016/j.jacc.2010.11.051 . Moon, J.H., Yoo, K.H. and Yim, H.E. (2020). Urinary Neutrophil Gelatinase – Associated Lipocalin: A Marker of Urinary Tract Infection Among Febrile Children. Clinical and Experimental Pediatrics . doi: https://doi.org/10.3345/cep.2020.01130 . Vijaya Marakala (2022). Neutrophil gelatinase-associated lipocalin (NGAL) in kidney injury – A systematic review. International Journal of Clinical Chemistry and Diagnostic Laboratory Medicine , [online] 536, pp.135–141. doi: https://doi.org/10.1016/j.cca.2022.08.029 . www.nice.org.uk . (2014). Overview | The NGAL Test for early diagnosis of acute kidney injury | Advice | NICE . [online] Available at: https://www.nice.org.uk/advice/mib3 [Accessed 6 Feb. 2024]. Project Gallery

Using toxins for pain management Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Anthrax Toxin Last updated: 18/09/25, 08:45 Published: 03/04/25, 07:00 Using toxins for pain management Introduction Pain is a response and signal to organisms that there is damage to the body. This could be due to an infection, tissue damage or organ damage. Different types of pain medication have been manufactured in the last decade. This includes the artificial manufacture of opioids, non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, using pathogens like bacteria and other substances. Bacteria have been investigated for managing and treating pain, with varying levels of effectiveness. Research by Yang et al. (2021) has shown that bacteria can interact with organisms and communicate with the nervous system, leading to analgesia (pain relief). Bacteria can also activate nociceptors, receptors that respond to pain, to alert the organism of damage. These nociceptors can also detect bacterial processes that release pain-producing toxins. Yang et al.’s research specifically looked at the bacterial toxin Bacillus anthracis ( Figure 1 ). It is a significant factor in the spread of anthrax, an infectious disease, and their experiments showed that it can lead to analgesia, as Bacillus anthracis and nociceptors can work together to suppress pain. The experiment The experiment by Yang et al. looked at different methods to target and suppress specific nociceptive neurons to decrease pain in mammals using bacteria. The study focused on the interactions between nociceptors and Bacillus anthracis . The researchers found that Bacillus anthracis toxin was made up of three substances: protective antigen (PA), lethal factor (LF), and edema factor (EF), as shown in Figure 2 . They created edema toxin (ET) using PA and EF, and administered the ET to mice via the intrathecal route (through the spinal canal, also shown in Figure 2 ). The scientists used different doses of PA, LF and EF. The intrathecal route was used to limit the diffusion of ET to the spinal cord and sensory neurons, preventing ET from moving into other organs. The researchers then analysed the mouse neurons to compare the sequences before and after the experiments and determine the effectiveness of the treatments. The results indicated high levels of ANTXR2 receptors (high-affinity receptors for anthrax toxins), meaning the response to pain was faster. The results The researchers examined the mechanical sensitivity and thermal latency. Mechanical sensitivity is the ability to differentiate between and respond to mechanical stimuli, and thermal latency is the ability to differentiate between and respond to heat stimuli. In mammals, signs of pain can be quantified using these indicators. The higher the threshold, the lower the pain. The threshold levels of these factors were compared up to 24 hours after the injections of the PA, PA + LF and PA + EF, as shown in Figure 3. Figure 3 : Line graphs showing the results of the intrathecal injections. (A) Line graph of mechanical sensitivity thresholds after intrathecal administration. (B) Line graph of thermal sensitivity thresholds after intrathecal administration. (C) Line graph of mechanical sensitivity thresholds on the day and 24 hours after the second injection. After administration of the injections via the intrathecal route, thresholds of mechanical sensitivity, Figure 3A , were increased significantly for several hours. The injection of PA + EF resulted in the highest threshold, remaining at 1.0 g 6 hours post-injection, compared to the injections of PA and PA + LF, which both had a threshold of below 0.5 g 6 hours post-injection. The thresholds of thermal latency, shown in Figure 3B , also increased significantly for several hours. Again, the injection of PA + EF resulted in the highest latency, remaining for more than 20 seconds 6 hours post-injection, compared to the injections of PA and PA + LF, which both had a latency of below 20 seconds 6 hours post-injection. The results from Figures 3A and 3B suggest that the injections of PA + EF were the most effective in increasing the thresholds of both mechanical sensitivity and thermal latency. A second injection of ET was administered, and thresholds of mechanical sensitivity were again elevated, as shown in Figure 3C . After the second injection, the effects of pain relief were more potent. In the graph, at D2, the threshold of mechanical sensitivity 6 hours after the second injection was above 1.5 g for mice given ET, compared to below 1.0 g 6 hours after the first injection for mice given ET. This could be due to the upregulation of the ANTXR2 receptors induced by ET. Upregulation is when hormone secretion is suppressed, and the number of receptors (in this case, ANTXR2) increases, causing a faster response to the stimulus (in this case, pain). This suggests that ET can result in pain receptors being affected, leading to a faster analgesic response. The researchers concluded that this experiment did result in analgesia in mice as ET targeted specific nociceptors. The results from this experiment are significant because they indicate that pain behaviour can be blocked by intrathecal administration of a harmful bacterial toxin such as Bacillus anthracis . Conclusion Yang et al. (2021) found that the injection of the ET via the intrathecal route results in blocked pain behaviour in mice. The experiment is significant as it has shown that a harmful toxin can have positive effects. However, it is difficult to know if the effects will be replicated in humans as human trials have not yet been carried out. In addition, the sample size was very small, with a maximum of eight mice observed after each injection. This could result in high variability (the data points would be more spread out from the mean and, therefore, less consistent) and inconclusive results. Nevertheless, with further study, experimentation, and refinement of the ET via the intrathecal method, new therapies for people with pain, especially chronic pain, could be created in the future. Different dosages of the ET could be experimented upon to see whether a higher dosage has better results, with a bigger sample size, and human trials. The results from Yang et al. (2021) showed that intrathecal ET injections are promising, and if successful in humans, this method would ease the burden on healthcare systems worldwide. Written by Naoshin Haque Related articles: Ibuprofen / The Pain Gate Theory Project Gallery