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Exploring the microscopic world of molecules Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Quantum Chemistry Last updated: 24/02/25, 11:29 Published: 06/02/25, 08:00 Exploring the microscopic world of molecules Quantum chemistry provides a glimpse into the strange and fascinating world of molecules and atoms, where the principles of traditional chemistry and physics no longer apply. While classical chemistry can explain molecular interactions and bonding, it cannot fully account for particles' unusual, frequently contradictory behaviour at the atomic and subatomic levels. Quantum mechanics provides scientists with a powerful framework for understanding the complicated behaviour of electrons and nuclei in molecules. The basics of quantum chemistry The notion of wave-particle duality, which states that particles, such as electrons, act not just like objects with mass but also like waves, is central to quantum chemistry. Because the exact position and momentum of an electron cannot be known at the same time (according to the Heisenberg Uncertainty Principle), probability distributions are used to describe electrons rather than accurate orbits. These distributions are represented by mathematical functions known as wave functions, which describe the probability of finding an electron in a specific location surrounding the nucleus. This fundamentally affects our understanding of chemical bonding. Instead of conceiving a bond as a solid connection between two atoms, quantum chemistry defines it as the overlap of electron wave functions, which can result in a variety of molecular topologies depending on their energy levels. Quantum mechanics and bonding theories Quantum mechanics has fundamentally altered our knowledge of chemical bonding. The classic Lewis structure model, which explains bonding as the sharing or transfer of electrons, is effective for simple molecules but fails to convey the complexities of real-world interactions. In contrast, quantum chemistry introduces the concept of molecular orbitals. In molecular orbital theory, electrons are not limited to individual atoms but can spread across a molecule in molecular orbitals, which are combinations of atomic orbitals from the participating atoms. These molecular orbitals provide a more detailed explanation for bonding, especially in compounds that do not match simple bonding models, such as delocalised systems like benzene or metals. For example, quantum chemistry explains why oxygen is paramagnetic (it possesses unpaired electrons), a characteristic that classical bonding theories cannot explain. Quantum chemistry and quantum computing One of the most interesting frontiers in quantum chemistry is its application to the development of quantum computers. Traditional computers, despite their enormous processing power, struggle to model the complicated behaviour of molecules, particularly large ones. This is because simulating molecules at the quantum level necessitates tracking all conceivable interactions between electrons and nuclei, which can quickly become computationally challenging. Quantum computers use fundamentally different ideas. They employ qubits, which, unlike classical bits, can exist in a state of both 0 and 1. This enables quantum computers to execute several calculations concurrently and manage the complexity of molecular systems considerably more effectively. This could lead to advancements in quantum chemistry, such as drug discovery, where precisely modelling molecular interactions is critical. Instead of depending on trial and error, scientists may utilise quantum computers to model how possible pharmaceuticals interact with biological molecules at the atomic level, thereby speeding up the creation of novel therapies. Similarly, quantum chemistry could help in the development of novel materials with desirable qualities, such as stronger alloys and more efficient energy storage devices. Why quantum chemistry matters The consequences of quantum chemistry go well beyond the lab. Understanding molecular behaviour at its most fundamental level allows us to create new technologies and materials that have an impact on everyday life. Nanotechnology, for example, relies largely on quantum principles to generate innovative materials with applications in medicine, electronics, and clean energy. Catalysis, the technique of speeding up reactions, also benefits from quantum chemistry insights, making industrial operations more efficient, such as cleaner fuel generation and more effective environmental remediation. Furthermore, quantum chemistry provides insights into biological processes. Enzymes, the proteins that catalyse processes in living organisms, work with a precision that frequently defies standard chemistry. Tunnelling, quantum phenomena in which particles slip past energy barriers, helps to explain these extraordinarily efficient biological processes. In brief, quantum chemistry provides the fundamental understanding required to push the limits of chemistry and physics by exposing how molecules interact and react in ways that traditional theories cannot fully explain. Quantum chemistry has the potential to radically alter our understanding of the microscopic world, whether through theoretical models, practical applications, or future technology advancements. Written by Laura K Related articles: Quantum computing / Topology Project Gallery

Knowing which species menstruate lets us pick suitable animal models Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Do other animals get periods? Last updated: 16/06/25, 16:25 Published: 26/06/25, 07:00 Knowing which species menstruate lets us pick suitable animal models Periods, formally called menstruation, happen to female mammals every menstrual cycle when an egg cell is not fertilised. Levels of the progesterone hormone decrease, causing the lining of the uterus to self-destruct and shed. This lining is called the endometrium and is flushed out of the body with blood during menstruation. Some primates, bats, the spiny mouse, and elephant shrews get periods ( Figure 1 ). Since these groups are distantly related, menstruation likely evolved multiple times independently. Knowing which species menstruate lets us pick animal models which best reflect the human female reproductive system. Why do we get periods? Despite being painful and inconvenient, menstruation must have some benefit; otherwise, natural selection would not favour it on multiple separate occasions. Hypotheses put forward to explain menstruation include clearing the uterus of pathogens and saving energy compared to maintaining an endometrium all the time. A 2012 paper argues that neither of these hypotheses are true and that menstruation is an unfortunate byproduct of the way pregnancy occurs in certain animals. In non-menstruating animals, an embryo induces morphological and biological changes in the uterus, so those changes do not happen if they are not pregnant. The uterus of a menstruating animal undergoes regular changes even without an embryo, and one of those changes is shedding the endometrium. However, there is no consensus on the benefits of menstruation. Non-human primates Old World monkeys, apes, and humans menstruate conspicuously. This could be because their endometria have spiral arteries, which dilate and weaken in response to hormones. Eventually, the weakened arteries break and release blood, which carries dead and detached endometrial tissue out of the body. While chimpanzee menstruation is visible to the naked eye, menstrual blood in orangutans and gorillas is detected with a chemical urine strip. Gorillas bleed for 3 days, while orangutans bleed for 1-4 days. Humans have the most obvious, and possibly the most prolonged, menstruation out of the Old World primates. (Aren’t we unlucky?). On the other hand, the very few New World monkey species which menstruate need a microscope to detect it. Pedro Mayor and colleagues sampled the endometria of various New World monkeys and viewed those samples under a microscope. They found that monkeys from the Aotus nancymaae and Sapajus macrocephalus species had weakened endometria with dilated blood vessels and blood clots ( Figure 2 ). Combined with other context clues from those endometrium samples, they concluded that those monkeys must be menstruating. Bats Microscopy also identified menstruation in some bat species. In a 2011 study, uterus sections from Carollia perspicillata bats showed the endometrium getting thinner over a few days with associated bleeding. Some sections had endometrial debris in the lumen of the uterus – but unlike in Old World primates and humans, this debris was reabsorbed by the body rather than released. Menstruating Molossus ater bats had blood and endometrial cells in their cervix under a microscope, while one individual was visibly bleeding in its vagina. In contrast, a colony of female Rousettus leschenaulti bats all had visible vaginal bleeding on the same day. On that day, two-thirds of their endometria were shed, and they had low progesterone levels – meaning those bats were menstruating. Bat menstruation differs from primates in at least two ways. Firstly, menstruation happens simultaneously with ovary development in Carollia perspicillata and before ovary development in primates. Secondly, some bat species only menstruate after an interrupted mating attempt – which scientists call coitus , and the public would call “pulling out”. Perhaps menstruation gives these bats a second chance at successful mating in that breeding season. Conclusion We rarely see other animals on their period because if the species does menstruate, they do not bleed as much as humans do. Evidence of menstruation in New World monkeys and bats usually came from microscopy, where the endometrium was seen to detach, and blood was seen in the uterine lumen. These monkeys and bats could be used as rudimentary animal models to study what happens in humans during a period. Written by Simran Patel Related article: Monkey see, monkey clone REFERENCES Catalini L, Fedder J. Characteristics of the endometrium in menstruating species: lessons learned from the animal kingdom. Biology of Reproduction [Internet]. 2020 May 26 [cited 2025 Jan 8];102(6):1160–9. Available from: https://doi.org/10.1093/biolre/ioaa029 Mayor P, Pereira W, Nacher V, Navarro M, Monteiro FOB, El Bizri HR, et al. Menstrual cycle in four New World primates: Poeppig’s woolly monkey (Lagothrix poeppigii), red uakari (Cacajao calvus), large-headed capuchin (Sapajus macrocephalus) and nocturnal monkey (Aotus nancymaae). Theriogenology [Internet]. 2019 Jan 1 [cited 2025 Jan 7];123:11–21. Available from: https://www.sciencedirect.com/science/article/pii/S0093691X18302796 Rasweiler IV JJ, Badwaik NK, Mechineni KV. Ovulation, Fertilization, and Early Embryonic Development in the Menstruating Fruit Bat, Carollia perspicillata. The Anatomical Record [Internet]. 2011 [cited 2025 Jan 8];294(3):506–19. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/ar.21304 Graham C. Reproductive Biology of the Great Apes: Comparative and Biomedical Perspectives. Elsevier; 2012. 456 p. Rasweiler IV JJ. Spontaneous decidual reactions and menstruation in the black mastiff bat, Molossus ater. American Journal of Anatomy [Internet]. 1991 [cited 2025 Jan 8];191(1):1–22. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/aja.1001910102 Martin RD. The evolution of human reproduction: A primatological perspective. American Journal of Physical Anthropology [Internet]. 2007 [cited 2025 Jan 8];134(S45):59–84. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.20734 Emera D, Romero R, Wagner G. The evolution of menstruation: A new model for genetic assimilation. BioEssays [Internet]. 2012 [cited 2025 Jan 8];34(1):26–35. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/bies.201100099 Zhang X, Zhu C, Lin H, Yang Q, Ou Q, Li Y, et al. Wild Fulvous Fruit Bats (Rousettus leschenaulti) Exhibit Human-Like Menstrual Cycle1. Biology of Reproduction [Internet]. 2007 Aug 1 [cited 2025 Jan 8];77(2):358–64. Available from: https://doi.org/10.1095/biolreprod.106.058958 Project Gallery

Civil wars and arms trade Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Yemen- a neglected humanitarian crisis Last updated: 19/06/25, 10:06 Published: 15/05/25, 07:00 Civil wars and arms trade This is article no. 3 in a series about global health injustices. Previous article: Civil war in Sudan . Next article: Injustices in Lebanon and Syria . Introduction Welcome to the third article of the Global Health Injustices Series. Building on the last article on Sudan , the focus is now on Yemen, by analysing the health inequalities and inequities the broader Yemeni population encounters. Similar to Sudan, there is a civil war between the government and the Houthis, among other political factions in Yemen, producing detrimental population health outcomes that will be delved into after an overview of Yemen's history and current state. Yemen: a distinct past and its current challenges Yemen is a country in the Middle East bordered by Saudi Arabia and Oman. Like Palestine and Sudan, Yemen is noteworthy for its distinct culture, languages and traditions. Moreover, Yemen has been part of trade routes with other surrounding countries for centuries and even now, as it is adjacent to the Red and Arabian Seas. However, as far back as the 1990s, when Yemen gained independence after varying degrees of resisting colonialism, internal friction within the government has led to civil wars even before this current one. At the moment, Yemen has one of the highest rates of mal- and undernutrition in the Middle East due to approximately half of the Yemeni people living in poverty and lacking access to clean water. Additionally, around 4.5 billion people are displaced in Yemen, and have been displaced in many instances since 2015. Furthermore, in spite of the ongoing civil war, Yemen has at least 97,000 asylum seekers and refugees from countries like Somalia and Ethiopia. Taking into account this important context, it is vital to support the Yemeni population as well as the refugees and asylum seekers. This is because they are facing injustices, which then lead to worsening outcomes for numerous people in Yemen. Although this crisis is ongoing, the Yemeni people, the refugees and asylum seekers stay resilient within their communities. Civil war and the consequences of the arms trade Unfortunately, Yemen has been noted by the WHO as an ignored humanitarian crisis, where approximately 20 million people need emergency healthcare. Specifically, 17.3 million people are driven to starvation, including 1.15 million children under 5 years old being acutely malnourished, having a 30-50% mortality risk. Although these statistics are driven by the ongoing civil war fueled by the arms trade between the Yemeni government, others in the Middle East and notably the United States, it is essential to highlight the other factors in Yemen driving childhood malnutrition. One study found that as maternal education, social and economic status increase, the likelihood of malnutrition in children decreases. Moreover, cigarette smoking during pregnancy increased the number of children with malnutrition. It could be inferred that there was a lot of internal instability within Yemen when this study occurred, leading to these health outcomes for the children, which have been currently worsened by the ongoing civil war, with further fuel from the arms trade. Regarding mental health in Yemen, one article noted how the COVID-19 pandemic, on top of the civil war, has impacted access to mental health care. Approximately 20% of Yemenis suffer from at least one mental health disorder, which includes anxiety, depression and schizophrenia. However, seeking help for mental health has been hindered by stigma and superstition, notably how people with these concerns may be described as dangerous. These gaps underline a lack of resources and facilities in Yemen attributed to damage from the ongoing civil war. Shifting to infectious diseases, the civil war in Yemen has contributed to a high burden of neglected tropical diseases (NTDs), which are diseases affecting low-income countries that lack healthcare resources, infrastructure and sanitation and hygiene facilities. The most notable include dengue fever, salmonella, and schistosomiasis ( Figure 1 ). The exact epidemiological data of NTDs in Yemen is difficult to find because there is a lack of infectious disease surveillance, and the healthcare system is fractured. Focusing on Yemen’s healthcare system, one review noted six key areas from the World Health Organisation that are involved in a strong healthcare system: health information systems, health workforce, governance, service delivery, access to essential medicines, and financing. Each area is weakened by the civil war, but here is a glimpse of each area, with some of the steps forward. Firstly, the review suggested that health information systems are deficient, so the authors urged the creation of a health survey system for Yemen. Since 2015, the health workforce has decreased by 50%, where more than half of workers left their jobs as they were not getting paid; retaining them could be through voucher programs and payment contracts. Also, access to essential medicines, particularly for chronic diseases, is scarce due to lack of funding, limited imports and damage to infrastructure. As for service delivery, at least 50% of healthcare buildings are operating, with airstrikes destroying more than 500 buildings, leaving vital services like emergency obstetric care very restricted. Although financing on healthcare has increased from 0.8% in 2004 to approximately 2.9-4.1%, with further investment to up to 12%, the population still has to pay out-of-pocket for healthcare. To move forward, the author noted how crucial it is to increase government spending on health. However, enhancing these areas must begin with improving governance, or the key leaders in Yemen congregating to make decisions that lead to a more robust healthcare system. Currently, there are issues due to bureaucracy, top-down management and friction between the Yemeni government, the Houthis and the other political factions. As mentioned above, one area of service delivery severely impacted by the ongoing war is obstetric care, along with newborn and child health. One case study noted that although these areas are a priority, there were instances, like tackling cholera outbreaks ( Figure 2 ) and treating malnutrition, which were offered priority over other forms of care. This imbalance reflects that more funding is required for all of the healthcare service areas to run optimally. One way forward is to include not only the leaders in Yemen, but also international NGOs to bring in their expertise to support the re-development of the healthcare system. The role of NGOs in supporting the Yemeni population At this present moment, NGOs have a vital role in supporting vulnerable populations, especially in Yemen. In a 2023 report from Amnesty International, they noted several breaches of international law and human rights: Parties to the conflict continued to harass, threaten, arbitrarily detain, forcibly disappear and prosecute individuals for peacefully exercising their right to freedom of expression, religion and belief. Parties to the conflict continued to restrict movement and the delivery of aid, including by imposing bureaucratic constraints such as delayed approvals, travel permit denials or delays, cancellation of humanitarian initiatives, and interference in the project design, implementation and assessment of humanitarian activities. Other NGOs, such as the United Nations High Commissioner for Refugees (UNHCR), stated their provision of lifesaving aid to refugees, asylum seekers and displaced Yemenis, along with other forms of support through cash and essential supplies. The first way forward towards upholding the health and wellbeing of the broader population is to establish clearer governance among the leaders in Yemen. This could be facilitated by NGOs and other stakeholders, perhaps the other governments too, by stopping arms trade and increasing humanitarian aid. Conclusion: looking ahead at clearer governance Throughout this article, evidence indicates that the civil war in Yemen has devastating impacts on the health and wellbeing of the population. From individuals unable to seek appropriate mental health support, to a divided healthcare system with limited funding and other deficits. Consequently, the leaders in Yemen must come together to uphold international law and human rights, while NGOs are vital in facilitating this dynamic. My previous words on holding people in power worldwide accountable to human rights and international law are very relevant for Yemen. This is because they are responsible for enabling the ongoing civil war through the arms trade, so urging these people in power, particularly in Western countries, to stop would be a major step forward in de-escalating the humanitarian crisis. For the next article in the Global Health Injustices Series, it will be a collaborative endeavour that focuses on both Syria and Lebanon, two bordering countries that have diverging yet connected struggles; by understanding them, we can ensure that the populations in both countries obtain as much support as possible to improve their health outcomes. Written by Sam Jarada Related article: Understanding health through different stances REFERENCES UNHCR. Yemen Crisis Explained. 2024. Available from: https://www.unrefugees.org/news/yemen-crisis-explained/ WHO. Achieving health for all in Yemen. 2023. Available from: https://www.emro.who.int/images/stories/yemen/achieving-health-for-all-in-yemen.pdf Capitalizing on Conflict: How U.S. arm sales fuel the humanitarian crisis in Yemen. OpenSecrets. 2024. Available from: https://www.opensecrets.org/news/reports/capitalizing-on-conflict/yemen-case-study Sunil TS. Effects of socio‐economic and behavioural factors on childhood malnutrition in Yemen. Maternal and Child Nutrition. 2009 Feb 3;5(3):251–9. Available from: https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1740-8709.2008.00174.xm Waleed Alhariri, Mcnally A, Knuckey S. The Right to Mental Health in Yemen: A Distressed and Ignored Foundation for Peace. Health and Human Rights. 2021 Jun;23(1):43. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC8233030/ Ahmed A, Rahmat Dapari, Dom NC. Neglected tropical diseases in Yemen: a systematic review of epidemiology and public health challenges. BMC Public Health. 2025 Feb 7;25(1). Available from: https://bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-025-21700-z#Fig3 Ali Alraimi A, Shelke A. Strengthening Health Systems in Conflict: Evidence-Based Policies for Quality Care in Yemen. Journal of Cardiovascular and Cardiology. 2024 Mar 31;1–4. Available from: https://oaskpublishers.com/assets/article-pdf/strengthening-health-systems-in-conflict-evidence-based-policies-for-quality-care-in-yemen.pdf Tappis H, Elaraby S, Shatha Elnakib, Abdulghani A, Huda BaSaleem, Saleh A, et al. Reproductive, maternal, newborn and child health service delivery during conflict in Yemen: a case study. Conflict and Health. 2020 May 27;14(1). Available from: https://conflictandhealth.biomedcentral.com/articles/10.1186/s13031-020-00269-x Human rights in Yemen. Amnesty International. 2023. Available from: https://www.amnesty.org/en/location/middle-east-and-north-africa/middle-east/yemen/report-yemen/ Project Gallery

The neural pathways behind movement Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Mastering motion- reflex, rhythmic and complex movements Last updated: 12/03/25, 11:49 Published: 03/04/25, 07:00 The neural pathways behind movement Introduction Movement is arguably the most fundamental aspect of human behaviour and is one of the most obvious features distinguishing plants and animals. The ability to physically respond to stimuli has enhanced our chances of survival an immeasurable amount. As such, our body’s ability to move has evolved and refined itself over many millennia, even developing new ways to move that protect us in many ways. For example, involuntary reflexes have reduced the computational demand on our brain to move parts of our body away from hot or painful objects, making the process almost instantaneous. Meanwhile, central pattern generators (CPGs) in our spinal cord have also reduced cognitive load by carrying out subconscious movement. This has allowed the motor cortex and cerebellum to focus on planning, coordinating, and refining purposeful movements in response to sensory feedback. While movement can be separated into even more categories, understanding the neural pathways of these three types can be beneficial to uncover core concepts of human neurophysiology, and even pave the way for treating movement disabilities. With that said, let’s take a deep dive into the circuitry and principles of reflex, rhythmic, and voluntary movement. Reflex movements Reflex movements are rapid, involuntary responses to stimuli that are commonly used to help us avoid danger or harm. An example includes touching a hot object and immediately jerking our hand away from it. The goal of this form of movement is to be as quick as possible in order to avoid injury. As such the neural pathway, known as a reflex arc, is simple and can take as few as three neurons. Firstly, sensory receptors detect a stimulus, such as heat, and send a signal up towards the central nervous system (CNS) through sensory neurons. Instead of going up to the brain for processing and movement planning, the sensory neuron connects with a relay neuron in the spinal cord, and then to motor neurons. This reduces the time taken to respond as it bypasses the brain’s processing circuitry. Motor neurons then carry a signal to relevant muscles to contract and move the body away from danger. Because the signal from the sensory receptors bypasses the brain, this movement is subconscious, meaning it happens without consciously deciding to move. This makes the movement rapid and stereotyped – the motion is predictable as there is minimal planning; just a need to move anywhere away from the stimulus. Central Pattern Generators (CPGs) CPGs are networks of neurons in the spinal cord that, when activated, produce rhythmic pattern-like movement such as walking or running. This type of movement is also subconscious as it does not require active focus to perform. However, unlike reflex movements, CPG output does not require sensory activation or feedback. Instead CPGs are activated by descending pathways from the medulla – a region of the brainstem that is responsible for performing involuntary movement. CPGs typically control movements that are necessary for survival such as breathing and heartbeats. The lack of need to consciously focus on these movements allows us to instead direct our attention to more complex situations, such as responding to stimuli or achieving a specific goal. This is where voluntary movements are required. Voluntary movements Any movement performed via conscious decision-making requires activity from a range of areas in the brain. To respond to our environment, we firstly need information on what is around us. This is largely handled by the frontal lobe which perceives our external environment through sensory input and attention. Human fMRI studies have highlighted increased activity in the frontal lobe as we switch our attention, thus perceiving different parts of our external environment. This information of our environment is sent to the motor cortex which plans our next movement. Complex multi-limb movements may require additional processing from premotor and association areas. Once the movement has been planned, it then has to pass through the cerebellum, which refines specific parts of the movement, such as precise finger motion. After refinement, the movement signal is then sent to relevant muscles via motor neurons to carry out the intended movement. An example of a complex movement is reaching out and grabbing an object. This seemingly simple task requires coordinated movement of the hand, arm, shoulder, and torso to ensure we move our arm the right amount – not too far so that we go past the object, and not too near so that we do not reach it. This also requires great precision to grab the object with appropriate force, to gain a firm grip while ensuring we do not break the object. A lot of planning goes into rudimentary movements, and yet sometimes we can still get things wrong. For instance, suppose we couldn’t see the object too well so we end up going too far and missing it. This will be picked up by our sensory organs, giving our brain feedback on what we ended up doing. By comparing the actual movement with our intended movement, we can create an error signal of how far we missed and in what direction. This drives learning – by using our previous errors, we can refine our future movements to eventually achieve our intended goal. In this example, we may learn that we keep extending our arm too far, and so with repetitive trials we eventually move the right amount in order to grab the object, as we intended. The cerebellum is largely seen as responsible for motor learning, however the deep underlying mechanism is still being researched. When the same complex movement is performed again and again, it can be trained to become subconscious movements activated by spinal CPGs, gradually requiring less coordination from the motor cortex to perform. This is how common movements such as walking, go from being a strenuous task as a toddler to a simple ability requiring minimal focus as an adult. Conclusion Overall, we can see a general trend of movements requiring more parts of the CNS as they become more complex. Precise, unfamiliar movements requiring multiple limbs are the most complex, thus recruiting decision-making and motor coordination areas in order to perform. By repeating an action again and again, we can train ourselves to perform it with less and less input from higher brain regions, until it eventually becomes a subconscious coordinated act that can be performed on demand. Written by Ramim Rahman Related articles: Dopamine in the movement pathway / Mobility disorders REFERENCES Dickinson, P.S. (2006) ‘Neuromodulation of central pattern generators in invertebrates and vertebrates’, Current Opinion in Neurobiology , 16(6), pp. 604–614. doi:10.1016/j.conb.2006.10.007. Latash, M.L. (2020) Physics of biological action and perception . London, United Kingdom: Academic Press. Brent Cornell (no date) BioNinja . Available at: https://old ib.bioninja.com.au/options/option-a-neurobiology-and/a4-innate-and-learned-behav/reflex-arcs.html (Accessed: 11 February 2025). Berni, D.J. (2023) The motor system , Introduction to Biological Psychology . Available at: https://openpress.sussex.ac.uk/introductiontobiologicalpsychology/chapter/the-motor-system/ (Accessed: 11 February 2025). Rossi, A.F. et al. (2008) ‘The prefrontal cortex and the executive control of attention’, Experimental Brain Research , 192(3), pp. 489–497. doi:10.1007/s00221-008-1642 z. Project Gallery

Looking at caspase-8’s inability to trigger cell death Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link CEDS: a break in cell death Last updated: 12/09/25, 11:08 Published: 11/09/25, 07:00 Looking at caspase-8’s inability to trigger cell death This is article no. 11 in a series on rare diseases. Next article coming soon. Previous article: Ehlers-Danlos syndrome . Cell death, as we know it, is a crucial phenomenon by which our bodies remove unnecessary or damaged cells to maintain internal stability, a process known as homeostasis. Cell death can occur in many ways, but the mechanisms by which cells die follow two main paths. It may occur as naturally programmed, as in apoptosis, or as a result of toxic trauma or physical damage, like necrosis. While cell death due to trauma can often be more noticeable and dramatic, programmed cell death happens continually, not only because of cell damage but also because it is a normal part of development, and inducing it is a core function of immune system cells. In essence, cell death comes naturally, removing cells that are possibly damaged or infected to maintain the body as a whole. But what if cell death stops? As many fiction stories will tell you, immortality is never a good thing, and this is accurate for our cells, too. Although excessive cell death is also destructive, cell death in its natural controlled manner not only stops the spread of infection but also prevents the survival of cancer cells and auto-reactive immune cells, which can damage the body by forming cancerous tumours and triggering autoimmune diseases, respectively. This demonstrates that a careful balance of life and death must always be in place to maintain homeostatic conditions and allow our unimpeded survival. However, as cell death is a multi-step mechanism, it can go wrong in several ways. Furthermore, diseases causing faults in the cell death process can be challenging to diagnose. Not only can there be numerous reasons for patients to exhibit symptoms associated with the loss of cell death, but some of these reasons may also be rare disorders and, therefore, difficult for healthcare professionals to identify. One rare disease that researchers recently recognised is Caspase-8 Deficiency Syndrome (CEDS). This disease, stemming from a genetic mutation in the gene coding for caspase-8, results in extensive issues related to immunodeficiency, and they are all caused by caspase-8’s inability to trigger cell death. So what is Caspase-8? Caspase-8 is a pivotal regulator of the apoptotic pathway. Essentially, apoptosis can happen through two key pathways: the extrinsic pathway, when triggers originate outside the cell; and the intrinsic pathway, when the cell itself activates the cell death pathway. Whilst there are several key players in apoptosis, caspase-8 is a central mediator of the extrinsic apoptotic pathway. Caspase-8 can be activated through numerous ways, but it is often through so-called death receptors, which are typically members of the Tumour Necrosis Factor Receptor (TNFR) family of transmembrane proteins. Upon their activation, a chain reaction occurs, involving the recruitment of caspase-8 into a complex, known as the death-inducing signalling complex (DISC). This complex then cleaves further downstream caspases or the BH3 Bcl2-interacting protein. This cascade leads to DNA fragmentation, degradation of the cytoskeleton, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors, and finally, uptake by phagocytes, thus completing the death of the cell and its cleanup ( Figure 2. ). Caspase-8 therefore plays a crucial role in completing the death inducing pathway. While there are other methods of cell death, the loss of Caspase-8 undoubtedly leads to significant consequences. Caspase-8 deficiency syndrome (CEDS) Scientists first discovered CEDs in the early 2000s. By this time, there had already been extensive research into a similar disease known as Autoimmune Lymphoproliferative Syndrome (ALPS), which results from defective apoptosis leading to abnormal immune cell survival. However, at the time of ALPS discovery, there was no identified link to a loss of Caspase-8. Furthermore, there was a lack of available mouse models to study, as inducing homozygous caspase-8 deficiency caused embryonic lethality in mice, significantly limiting research. Therefore, a loss of caspase-8 was also considered to have the same effect in humans. This train of thought continued until 2002, when Chun et al. conducted major studies into apoptosis-related diseases. During one of their many trials, two siblings—a 12-year-old girl and an 11-year-old boy—were found to exhibit symptoms similar to those of ALPS (lymphadenopathy, splenomegaly, and defective CD95-induced apoptosis of peripheral blood lymphocytes). However, unlike ALPS, the siblings were also immunodeficient and suffered from recurrent sinopulmonary and herpes simplex virus (HSV) infections, as well as a poor response to immunisation. Following the discovery of these additional symptoms in the siblings, researchers examined their other family members but were surprised to find that neither the parents nor another sibling suffered in a similar fashion. The only symptom they had was a partial defect in apoptosis mediated by CD95. It was determined that the mother, father, sibling, and several other extended family members were potentially heterozygous carriers of the mutation found in the affected siblings. Subsequently, a DNA analysis was conducted, and a mutation was found in the CASP8 gene. This mutation was a homozygous deletion, which ultimately led to a loss of function of the caspase-8 protein. This loss of function in caspase-8 resulted in defective interleukin 2 production and diminished T-cell proliferation, explaining the immunodeficiency associated with CEDS and highlighting the important role caspase-8 plays in regulating cell death and immune responses. Since CEDS was first identified in the 2002 study, very few cases have been reported in medical literature. However, despite this, research continues, and it has allowed further insights into caspase-8’s pathophysiology and, in many studies, new genetic variants have been identified. One such variant is a homozygous missense mutation resulting in significant immune dysregulation in an affected individual, which results in immune responses and inflammatory conditions associated with the disease. Alongside research into the causes of this disease, focus has also shifted to how we might best diagnose and treat the disease and provide patients with the good quality of life they deserve. Diagnosis As with all rare diseases, one of the main issues stopping correct diagnosis of CEDS and delaying treatment is the fact healthcare providers are not familiar with disease symptoms, let alone the genetic basis of the disease. To make matters worse, the presentation of disease varies depending on the age of onset, which makes it even more difficult to recognise CEDS as the common underlying cause. For instance, early-onset often results in symptoms, such as severe infections and organomegaly, while adult-onset patients may present with neurological issues, multi-organ failure and chronic inflammatory conditions. Further adding to these diagnostic difficulties is the fact CEDS overlaps with other conditions, such as the previously mentioned ALPs. As a result, a patient could receive multiple different diagnoses before CEDS is identified as the cause of their suffering. For effective CEDS diagnosis, expertise in immunology, genetics and infectious diseases is required. However, this specialised knowledge is hard to come by, and as with all diseases, the familiarity the healthcare provider has with it contributes greatly to whether you will get diagnoses, and this familiarity does not exist for rare diseases. Furthermore, diagnostic methods in general are tricky for this disease, with multiple tests often being required including an analysis of patient history alongside genetic testing through methods like whole exome sequencing and immunological tests analysing the types and states of immune cells and abnormal levels of immunoglobulins. Each of these diagnostic methods takes time, in an often-strained healthcare system, which can lead to a sense of helplessness in disease sufferers who only suffer more the longer they do not know what is wrong. Treatments Unfortunately for patients, a difficult diagnosis is not the only challenge they face, as there is currently no cure for CEDS, and no specific treatments. However, there are more general treatments available that could potentially alleviate symptoms and help individuals achieve some level of normality in their lives. The best possible way to approach treatment of CEDS, as with most immunodeficiency related diseases, would be to treat both the immune dysfunction and prevent recurrent infections. This could involve a multifaceted treatment plan tailored to the individual, aiming to avoid complications from immune dysfunction and improve quality of life. Potential treatment plans could include the use of antibiotic and antiviral medications for recurrent infections, and also more complex treatments such as Immunoglobulin replacement therapy (IVIG). IVIG provides necessary antibodies to bolster patients’ immune system, when they are not able to themselves, which both helps avoid overuse of antibiotic and antiviral treatments and prevents infections in the first place before treatment is required. Alongside these treatment methods, due to it being a relatively unknown disease, CEDS patients will also require a great deal of supportive and hands on care. As part of this care patients could potentially be provided with a specialised diet plan with all the correct nutrition to help them combat any gastrointestinal issues (GI’s) associated with CEDS, as primary immunodeficiency patients have found this method to help with control of GIs. In addition to current therapies several innovative approaches to treatment of genetic diseases are in development which could be used in CEDS treatment. Recent advances in gene therapy research offer new hope for treating immune deficiencies resulting from genetic defects, which means these therapies could potentially benefit CEDS patients. One promising method for gene therapy utilises CRISPR-Cas9 to correct the genetic mutations, such as those in CASP8 leading to CEDS. Another approach uses viral vectors to deliver functional genes into patients’ cells, and this could potentially deliver a functional CASP8 gene. Additionally, another very promising therapy, previously used for ALPS patients, involves genetically modifying stem cells to correct a faulty gene (such as the faulty CASP8 gene) before re-infusing them into the patient to produce healthy immune cells. These treatments could revolutionise the management of rare genetic diseases like CEDS. The future for CEDS as a rare disease Rare diseases like CEDS are often chronic and, in many cases, life threatening. Due to the scarcity of information on these conditions, few if any treatments exist. Furthermore, due to their rarity, patients of rare diseases are not only small in number but also dispersed worldwide, leading to a feeling of isolation as they rarely meet someone who shares in their experiences. However, as scientific research progresses, treatments and therapies become more effective and accessible, and with 72% of rare diseases, including CEDS, having a genetic basis, gene therapies appear incredibly promising. Yet, there is still a long way to go to fully realize their potential, and even more that can be done to help and support those who continue to suffer alone with rare diseases. Written by Faye Boswell REFERENCES Telford WG. Multiparametric analysis of apoptosis by flow cytometry. Methods Mol Biol. 2018;1678:167–202. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC8063493/ Smith C. Monitoring apoptosis by flow cytometry. Biocompare. 2017 Jan 17. Available from: https://www.biocompare.com/Editorial-Articles/332620-Monitoring-Apoptosiby-Flow-Cytometry/ Tummers B, Green DR. Caspase-8; regulating life and death. Immunol Rev. 2017 May;277(1):76–89. doi: 10.1111/imr.12541. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC5417704/ Leeies M, Flynn E, Turgeon AF, Paunovic B, Loewen H, Rabbani R, Abou-Setta AM, Ferguson ND, Zarychanski R. High-flow oxygen via nasal cannulae in patients with acute hypoxemic respiratory failure: a systematic review and meta-analysis. Syst Rev. 2017 Oct 18;6(1):202. doi: 10.1186/s13643-017-0607-1. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439260/ Goyal A, Moitra D, Goldstein DB, Savage H, Lisco A, Rosenzweig SD, et al. Caspase-8 deficiency presenting as a novel immune dysregulation syndrome: case report and literature review. Allergy Asthma Clin Immunol. 2023;19(1):57. doi:10.1186/s13223-023-00778-3. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10084589/ Chun HJ, Zheng L, Ahmad M, Wang J, Speirs CK, Siegel RM, et al. Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency. Nature. 2002 Sep 26;419(6905):395–9. doi:10.1038/nature01063. Available from: https://pubmed.ncbi.nlm.nih.gov/12353035/ Khan S, Saha S, Saha S, et al. Early and frequent exposure to antibiotics in early childhood and risk of overweight: a systematic review and dose-response meta-analysis. Obes Rev. 2021;22(3):e13113. doi:10.1111/obr.13113. Available from: https://www.gastrojournal.org/article/S0016-5085(18)35036-4/fulltext Casanova JL, Abel L. Caspase-8 deficiency syndrome. Front Immunol. 2019;10:104. doi:10.3389/fimmu.2019.00104. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7750663/ Castiello MC, Villa A. Stem cell editing repairs severe immunodeficiency. The Scientist. 2024 Mar 6. Available from: https://www.the-scientist.com/stem-cell-editing-repairs-severe-immunodeficiency-71733 Ha TC, Morgan M, Schambach A. Base editing: a novel cure for severe combined immunodeficiency. Signal Transduct Target Ther. 2023;8(1):354. doi:10.1038/s41392-023-01586-2. Available from: https://www.nature.com/articles/s41392-023-01586-2https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7750663/ Project Gallery

Dysregulation of this pathway occurs in many different types of cancers Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The MAPK/ERK signalling pathway in cancer Last updated: 24/02/25, 11:29 Published: 20/02/25, 08:00 Dysregulation of this pathway occurs in many different types of cancers Introduction The mitogen-activated protein kinase (MAPK) signalling pathway is an important pathway in apoptosis, proliferation, differentiation, angiogenesis and metastasis. It is a protein kinase pathway (causes phosphorylation) with between 3-5 sets of kinases and is known to be activated via Ras, KC-mediated (Kupffer cells/liver macrophages), Ca2+, or G protein-coupled receptors. The MAPK/ERK pathway, also known as the Ras-Raf-MEK-ERK pathway, is conserved in mammals, and dysregulation of this pathway occurs in many different types of cancers. MAPK/ERK function Ras (GTPase) activates Raf (serine/threonine kinase), which activates MEK1/2 (tyrosine & serine/threonine kinases) and ERK1/2 (serine/threonine kinases), which controls certain transcription factors. ERK1/2 also phosphorylates various substrates in the cytoplasm (not shown). This results in gene expression, which can cause apoptosis, cell cycle regulation, differentiation, proliferation, etc. (Fig. 1). It is estimated that there are more than 150 target substrates of ERK1/2, either directly or indirectly. Furthermore, Ras and RAF have several different subtypes which have different functions. Ras has four different subtypes, which are the GTPases: HRAS, KRAS4A/4B, and NRAS, with KRAS being the common form found in human cancers. RAF has subtypes, which are the kinases: ARAF, BRAF, and CRAF (in humans). Ras is activated when GRB2 (growth-factor-receptor bound protein 2) binds to SOS (son of sevenless). This occurs via the complex moving to the cell membrane upon activation of a transmembrane receptor, such as EGFR (epidermal growth factor receptor). SOS transports the signal from the receptor to RAS and aids in the conversion of RAS-GDP to RAS-GTP. This switches ‘on’ RAF, which leads to the phosphorylation of MEK and ERK (Fig. 1). ERK is then able to move into the nucleus and alter gene expression, of genes such as CREB, MYC, FOS, MSK, ELK, JUN, etc., which are involved in processes such as metabolism, proliferation, angiogenesis (formation of blood vessels), haematopoiesis (formation of blood cells), wound healing, differentiation, inflammation, and cancer. However, ERK is also able to activate other substrates in the cytoplasm, such as BIM, RSK, MNK, and MCL, which are involved in processes such as apoptosis and blood pressure regulation. A regular level of ERK expression is needed for activation of genes involved in the cell cycle and to inhibit negative cell cycle control. ERK phosphorylates Cyclin D and Cdk4/6, which are bound together and aid the cell in the movement from G1 (gap) to the S phase (DNA synthesis/repair) of the cell cycle. MAPK/ERK pathway in cancer The MAPK/ERK pathway has been linked with many cancers, such as colon, thyroid, melanoma, pancreatic, lung, and glioblastoma. Mutations in epidermal growth factor receptor (EGFR), Ras, and Raf are well-known to cause cancer, with an estimated 33% of cancers containing Ras mutations, and an estimated 8% being caused by Raf mutations. It is also estimated that 85% of cancers have elevated activity of MEK. The MAPK/ERK pathway has also been shown to interact with the PI3K/Akt pathway, which controls the cell cycle and causes increased cell proliferation, which is obviously an important factor in tumourigenesis (tumour initiation). Regulation of the MAPK/ERK pathway There is a negative feedback mechanism of ERK1/2 on RAS/RAF/MEK, by ERK1/2 phosphorylating SOS, which causes the RAF-RAS link to be disrupted. ERK also inhibits MEK via the phosphorylation of BRAF and CRAF. There are inhibitors for Ras/Raf/MEK/ERK, but not all of these inhibitors work well/are without issues. ERK is problematic, in that their ATP-binding sites are very like cell cycle proteins, so are more difficult to inhibit. Also, it is difficult to target Ras due to its high GTP binding affinity, profuse cellular GTP, and lack of appropriate binding pockets. Therefore, the main focus currently appears to be on Raf/MEK inhibition. Raf inhibitors include drugs such as sorafenib, vemurafenib, encorafenib, and dabrafenib (these drugs are used on specific BRAF mutations). On the other hand, MEK inhibitors include drugs such as trametinib, cobimetinib, binimetinib, and selumetinib (these drugs can be used on specific mutations in Ras and Ras/Raf). Negative feedback mechanisms tightly control the MEK/ERK pathway and therefore great care is taken with inhibitor drug doses. To illustrate, if the doses are too low, the negative feedback loops are activated, which can lead to drug resistance/ poor therapeutic outcome. Conclusion The MAPK/ERK pathway is essential for several cellular processes, such as apoptosis, cell cycle regulation, differentiation, and proliferation. Therefore, it has a critical role in tumourigenesis. Raf and MEK in particular are susceptible to inhibition, which has led to the production of several different drugs for use in various types of cancer. There are currently other clinical trials in progress, and these will hopefully lead to further therapies for other cancers involved in this pathway. Written by Eleanor R Markham Related articles: HIPPO signalling pathway / Thyroid cancer REFERENCES Lake, D., Corrêa, S.A.L. & Müller, J. Negative feedback regulation of the ERK1/2 MAPK pathway. Cell. Mol. Life Sci. 73 , 4397–4413 (2016). https://doi.org/10.1007/s00018-016-2297-8 Song Y, Bi Z, Liu Y, Qin F, Wei Y, Wei X. Targeting RAS-RAF-MEK-ERK signaling pathway in human cancer: Current status in clinical trials. Genes Dis. 2022 May 20;10(1):76-88. doi: 10.1016/j.gendis.2022.05.006. PMID: 37013062; PMCID: PMC10066287 Ullah R, Yin Q, Snell AH, Wan L. RAF-MEK-ERK pathway in cancer evolution and treatment. Semin Cancer Biol. 2022 Oct;85:123-154. doi: 10.1016/j.semcancer.2021.05.010. Epub 2021 May 13. PMID: 33992782. Project Gallery

The future of precision healthcare: nanocarriers Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nanomedicine and targeted drug delivery Last updated: 17/07/25, 10:53 Published: 17/07/25, 07:00 The future of precision healthcare: nanocarriers In recent years, nanomedicine - the application of nanotechnology in healthcare - has emerged as a powerful and versatile area of research and is rapidly developing with many promising opportunities in the medical sciences. Nanocarriers are being developed for pharmaceuticals for example, with uses in cancer treatment and in particular targeted drug delivery. In nanomedicine, the materials are engineered at the nanoscale, with sizes ranging from 100 to 1000 nm, and can be used to perform specific biomedical tasks. These nanomaterials, such as nanoparticles, are often made from crosslinked polymer chains and can encapsulate therapeutic molecules for delivery within the body. Their small sizes give them unique properties, as they can interact with cells at a molecular level, and be designed to respond at specific times and locations, which can be directed to specific tissues or environments. Since the coronavirus disease (COVID-19) pandemic, nanoparticle-based drug delivery platforms have been widely studied - lipid nanoparticles were used in the vaccine to combat the virus. Being highly successful, and looking ahead, research and development in nanomedicine-based drug delivery is expected to keep growing, as the interest in more precise and effective treatments continues to rise. How can nanoparticles be used for drug delivery? A significant challenge in conventional drug therapies lies in their limited solubility, which can reduce the effectiveness of a drug and cause harmful side effects. Nanoparticles offer a solution to this: they can encapsulate poorly soluble drugs, protecting them from degradation in the body, and this allows them to be carried safely to the targeted tissues. This localised delivery improves the drugs’ biodistribution, and reduces systemic toxicity, which is a common concern in treatments such as chemotherapy, where healthy tissues in the body are damaged. Nanoparticles in particular are exciting as they have tuneable surface properties and a high surface to area volume ratio. This means their physical and chemical behaviours can be adjusted - for example through changing their sizes, shapes, or surface chemistries - to match a specific medical application or target. In addition to this, nanoparticles undergo the enhanced permeability and retention (EPR) effect; a phenomenon where they naturally accumulate in tumour tissues due to the leaky nature of tumour blood vessels. This effect improves the targeting precision, and drugs can be delivered more efficiently to cancer cells, while sparing healthy ones one, avoiding unnecessary damage and side effects to the patient. While drug delivery is a major focus, nanomedicine research also plays a role in diagnostics. Nanoparticles can be engineered to function as contrast agents in medical imaging, helping doctors detect diseases earlier and monitor treatments more accurately. There is also a growing interest in using nanomaterials for tissue regeneration, by creating scaffolds that support the repair and regrowth of damaged tissues. As research continues, nanomedicine holds promise for tacking some of the most pressing challenges in modern healthcare - from treating cancer more safely to developing new vaccines and personalised therapies. Though there are some hurdles, particularly around large-scale manufacturing and regularly approval, the path ahead for nanomedicine has huge potential. As the field of nanomedicine continues to grow, it shows great promise in reshaping healthcare with treatments that are smarter, safer, and more effective - ultimately improving patient outcomes and transforming the way we fight disease. Written by Saanchi Agarwal Related articles: Nanomedicine / Nanoparticles and diabetes treatment / Nanoparticles and health / Nanogels Project Gallery

Global warming can lead to higher transmission rates of dengue fever Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The impacts of global warming on dengue fever Last updated: 08/10/25, 16:42 Published: 19/06/25, 07:00 Global warming can lead to higher transmission rates of dengue fever Introduction Dengue fever is a viral disease transmitted by two mosquitoes: Aedes aegypti and Aedes albopictus . These mosquitoes are called ‘vectors’. Symptoms of dengue fever include a sudden high fever and severe headaches, making it hard to diagnose. Transmission suitability is endemic, meaning the virus spreads where the conditions are suitable for the vectors to survive and reproduce for 10-12 months. This disease is endemic in the tropics, including much of Sub-Saharan Africa and Central Africa, Northern South America, Brazil, South and Southeast Asia, and parts of Northern Australia. The World Health Organisation (WHO) has stated that it is “the most important mosquito-borne viral disease in the world”. Dengue fever does not currently have a vaccine. There are many areas of transmission, and dengue fever impacts communities worse if they have weaker health systems. Severe dengue can be fatal, especially in children, who have a weaker immune system. Due to climate change and increasing temperatures, more areas will be habitable for the vectors in the future. This could lead to higher transmission rates of dengue fever. Researchers used a modelling approach using different datasets to make projections of the impact of changing temperatures and predict the future spread of dengue fever. They specifically looked at locations and months suitable for dengue transmission if conditions were suitable for both vectors. Method The researchers used temperature data from the Berkeley Earth Surface Temperatures dataset for the present day (2001-2020). They also used projected temperature data for 2050 based on the Coupled Model Intercomparison Project Phase 6 (CMIP6) projections for the socio-economic pathway (SSP) 1-2.6 scenario and SSP5-8.5 scenario, as used in the Intergovernmental Panel on Climate Change Sixth Assessment Report. The SSP1-2.6 scenario is the best-case scenario and assumes international policy agreements and emissions reductions will be followed, limiting the average global temperature to 1.5 °C above pre-industrial levels. The SSP5-8.5 scenario is the “business as usual” scenario and assumes that continued fossil fuel use and development will occur. Researchers used the most recent climate projections from the CMIP6, which gave an up-to-date, holistic view of the impact of potential differences between climate change trajectories on vulnerable populations. This information can be used to support climate change mitigation strategies and disease prevention and control. Thermal limits for the mosquito vectors used in this study were 19.9 - 29.4 °C for Aedes aegypti and 21.3 - 34 °C for Aedes albopictus , since the vectors can only survive and reproduce within these temperatures. Modelling the thermal limits of both vectors, instead of just one, made the analysis more comprehensive. The researchers also applied an aridity mask using the Normalised Difference Vegetation Index (NDVI), which excluded areas too dry for mosquito survival and reproduction. They then applied the thermal limits and aridity mask to the climate data to predict areas with suitable conditions for the vectors and estimate the number of months suitable for transmission. Using aridity masks (previously only done with malaria) enhanced the model's accuracy because moisture is an important factor for mosquito breeding. Results Figure 1 shows that under the SSP1-2.6 (best-case) scenario, there will be new suitability for dengue transmission in temperate regions by 2050, lasting about 1 to 2 months. In addition, northwestern South America could see increases of up to 5 months of new suitability, and Eastern Africa up to 6 months of new suitability. In addition, eastern and southern Central America, central and northwestern South America, northern Australia, and parts of Southeast Asia are also becoming suitable for year-round transmission. Figure 2 shows that under the SSP5-8.5 (“business as usual”) scenario, areas will become suitable for year-round transmission in similar locations as under the SSP1-2.6 scenario by 2050. Dengue transmission suitability could increase by up to 6 months in Eastern Africa, and up to 10 months in parts of northwestern South America. Areas as far north as the Arctic Circle also have new suitability under this scenario. This demonstrates that climate change could result in the expansion of areas and the length of time during which dengue fever transmission is possible. Evaluation It’s essential to also acknowledge the study's limitations. For example, the model did not account for other variables impacting disease transmission, such as mosquito adaptation and extreme weather. The potential adaptation of mosquitoes and parasites to changing environmental conditions could alter transmission dynamics. In addition, extreme weather events, such as heavy rain, could eliminate breeding sites. Furthermore, the method of using modelling and projections is unreliable, because many things could change between now and 2050. For example, there could be temperature fluctuations, or temperatures could fall between SSP1-2.6 and SSP5-8.5, rather than being fixed in either scenario. This could affect the reliability of predicting future dengue fever transmission suitability. The study also did not include aridity projections under climate change scenarios. As future projections of NDVI are not currently available, NDVI values for 2020 were held constant for the 2050 projections. There will likely be changes in aridity by 2050, which will affect mosquito reproduction and dengue transmission. Nevertheless, this study's results are still important because they suggest that with increasing climate change, dengue fever transmission could increase, which would be a public health issue. Further listening and reading If you would like to know more about dengue fever, consider listening to this short 5-minute podcast from the World Health Organisation. If you would like to know more about the impacts of climate change on health, consider listening to this podcast , also from the World Health Organisation. If you would like to know more about the impacts of climate change on neglected tropical diseases (NTDs), consider reading the full open-access paper mentioned in this article . Written by Naoshin Haque Related articles: Potential vaccine for malaria / Correlation between HDI and mortality rate / Healthcare challenges during civil war in Sudan / Rising temperatures impacts 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

Richard Dawkins's work and the Modern Evolutionary Synthesis Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Is the immune system ‘selfish’? – a Dawkins perspective Last updated: 22/09/25, 10:59 Published: 25/09/25, 07:00 Richard Dawkins's work and the Modern Evolutionary Synthesis Evolution and Dawkins’ perspective Charles Darwin introduced the unprecedented theory of evolution by natural selection in his famous work ‘On the Origin of Species’, published in 1859. Gregor Mendel, who explained the concept of Mendelian genetics (the inheritance of genes), was a contemporary of Darwin, but his research was recognised much later on, beyond his time. In the 20 th century, the Modern Evolutionary Synthesis was formed and gave a foundation for how biological life has formed as we see it today. The Modern Evolutionary Synthesis is widely accepted and strongly supported by experimental and observational evidence across an array of life. Human beings have even leveraged these concepts for hundreds of years through artificial selection, imposing our own sometimes superficial selective pressures on organisms to express characteristics that we desire (such as the case of the Belgian Blue cattle, with a mutation in the myostatin gene making it a muscular, lean beef, or perhaps artificial selection in dog breeding). Richard Dawkins’ breakout book, ‘The Selfish Gene’, published in 1976, took him from an unknown voice at the University of Oxford passionate about the works of evolution across all animals, to a lauded voice in the scientific community. His concept of genes being selfish is the idea that natural selection works at the gene level, whereby genes over time become better at replication, with the organism acting as a ‘survival machine’ built to help genes propagate. It is important to note that the term ‘selfish’ is not meant metaphysically or philosophically. Figure 1 explains what ‘selfish’ means. Taking this further, it can be argued that genes helping organisms resist pathogenic attack are more likely to survive and propagate. This means the immune system does not exist to protect the body holistically but rather to protect its genes individually. The immune system evolved through the gene-centric lens As previously mentioned, the immune system has become integral to all complex organisms responding to pathogens as a selective pressure. Those genes that have conferred a greater ability to combat or resist a particular pathogen allow the organism an improved survival chance until reproductive age has been achieved. The window whereby the organism has reached reproductive maturity and is reproducing is what the genes have been selected to get, which is why many genetic pathways end up becoming detrimental to an organism in old age (explained by the antagonistic pleiotropy hypothesis- APT- and the disposable soma theory). This remains especially true for the immune system. One must also understand that only vertebrates are biologically equipped with an adaptive immune system (allowing for memory and effective response to previous pathogens), with Figure 2 explaining this difference. This supports that the immune system is a ‘selfish system’, as while many organisms survive without adaptive immunity, more complex organisms have evolved to include it because of our prolonged individual survival and delay in reproductive maturity (indicating that survivability until our reproductive window is an intense selective pressure). Immune imperfection through the ‘Selfish System’ lens We now understand there is a compelling point to be made that the immune system has evolved with the reproductive window in mind and to allow as much gene propagation in a population as possible. If we accept this point of view, it explains many of the trade-offs and imperfections of the immune system when we look at the potential harm caused by immunity. Allergies are one such example, whereby hypersensitivity causes an immune response to harmless substances, which, through the gene-centric lens, may have evolved to detect pathogens such as parasites. This further supports the ‘selfish system’ idea as reproductive success on a population scale is not impaired by a significant amount by allergies. One such study showed that women with allergies and asthma, despite having systemic inflammation, did not have a reduced fertility rate when analysing the relationship between an increase in allergic diseases in the 20 th century and a decrease in fertility globally. Chronic inflammation through persistent immune activation in old age (a concept termed inflammaging) is another such example. We previously mentioned that past reproductive age natural selection weakens, meaning that our genes are selected for early life immune optimisation, even if that means they cause problems later in old age. Processes such as cellular senescence, inflammasome activation, oxidative stress, immune cell dysregulation and so on begin to occur, leading to an increased risk of age-related diseases such as cardiovascular disease, cancer, dementia, sarcopenia and so on. Immune evolution is therefore a ‘selfish system’ because it seems to care more about gene propagation in the young to middle-aged years in comparison to long-term organism health, as many immune systems rapidly decline and become detrimental. Conclusion This perspective of the immune system as a ‘selfish system’ allows us to understand that it is not a protector of the organism throughout its life span, as we may perceive it to be, but rather that it is a mechanism evolved and optimised to propagate genetic material during the organism’s reproductive window (expanding beyond humans). This analysis of the immune system through Richard Dawkins' lens of the “selfish gene” helps us to understand many of the limitations of the immune system. Working on treatments to preserve and maintain the immune system’s healthy state, which reflects young adult life, appears to be a promising approach for future clinical prevention plans for old age diseases. There are many currently being researched and emerging treatments with this principle in mind, such as senotherapeutics and mTOR inhibitors (such as rapamycin and other rapalogs), making this an interesting field to keep up to date with. Written by Yaseen Ahmad Related article: Darwin and Galápagos Tortoises Project Gallery