Peering into the mind Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Neuroimaging and spatial resolution 10/07/25, 11:24 Last updated: Published: 04/11/24, 14:35 Peering into the mind Introduction Neuroimaging has been at the forefront of brain discovery ever since the first ever images of the brain were recorded in 1919 by Walter Dandy, using a technique called pneumoencephalography (PET). Fast-forward over a decade and neuroimaging is more than just blurry singular images. Modern techniques allow us to observe real time changes in brain activity with millisecond resolution, leading to breakthroughs in scientific discovery that would not be possible without it. Memory is a great example - with functional magnetic resonance imaging (fMRI) techniques we have been able to demonstrate that more recent long-term memories are stored and retrieved with brain activity in the hippocampus, but as memories become more in the distant past, they are transferred to the medial temporal lobe. While neuroimaging techniques keep the doors open for new and exciting discoveries, spatial limitations leave many questions unanswered, especially at a cellular and circuit level. For example - within the hippocampus, is each memory encoded via complete distinct neural circuits? Or do similar memories share similar neural pathways? Within just a millimetre cubed of brain tissue we could have up to 57,000 cells (most of them neurons), all of which may have different properties, be part of different circuits, and produce different outcomes. This almost makes revolutionary techniques such as fMRI, with almost unparalleled image quality, seem pointless. To truly understand how neural circuits work, we have to dig as deep as possible to record the smallest regions possible. So that begs the question, how small can we actually record in the human brain? EEG 2024 marks a decade since the first recorded electroencephalography (also known as EEG) scan by Hans Berger in Germany. This technique involves placing electrodes all around the scalp to record activity throughout the whole outer surface of the brain ( Figure 1 ). Unlike the methods we see later on, EEG scans provide a direct measure of activity in the brain, by measuring electrical activity when the brain is active. However, because electrodes are only placed across the scalp, EEG scans are only able to pick up activity from the outer cortex, missing important activity in deeper parts of the brain. In our memory example, this means it would completely miss any activity in the hippocampus. EEG resolution is also quite underwhelming, typically being able to resolve activity with a few centimetres’ resolution - not great for mapping behaviours to specific structures in the brain. EEG scans are used in a medical environment to measure overall activity levels, assisting with epilepsy diagnosis. Let's look at what we can use to dig deeper into the brain and locate signals of activity… PET Position emission tomography (PET) scans offer a chance to record activity throughout the whole brain by ingesting a radioactive tracer, typically glucose labelled with a mildly radioactive substance. This tracer is tracked and uptake in specific parts of the brain is a sign for greater metabolic activity, indicating a higher signalling rate. PET scans already offer a resolution far beyond the capacities of EEG scans, distinguishing activity between areas with a resolution of up to 4mm. With the use of different radioactive labels, we can also detect activity of specific populations of neurons such as dopamine neurons to diagnose Parkinson's disease. In fact, many studies have reliably demonstrated the ability of PET scans to detect the root cause of Parkinson's disease, which is a reduced number of dopamine neurons in the basal ganglia, before symptoms become too extreme. As impressive as it sounds, a 4mm resolution can locate activity in large areas of the cortex, but is limited in its resolving power for discrete cortical layers. Take the human motor cortex for example - all 6 layers have an average width of only 2.79mm. A PET scan would not be powerful enough to determine which layer is most active, so we need to dig a little deeper… fMRI Since its inception in the early 90's, fMRI has gained the reputation of becoming the gold standard for human neuroimaging, thanks to its non-invasiveness, lack of artefacts, and reliable signalling. fMRI uses Nuclear Magnetic Resonance to measure changes in oxygenated blood flow, which is correlative of neural activity, known as BOLD signals. In comparison to EEG, measuring blood oxygen levels cannot reach a highly impressive temporal resolution, and is also not a direct measure of neural activity. fMRI makes up for this with its superior spatial resolution, resolving spaces as small as 1mm apart. Using our human motor cortex example, this would allow us to resolve activity between every 2-3 layers - not a bad return considering it doesn’t even leave a scar. PET, and especially EEG, pales in comparison to the capabilities of fMRI that has since been used for a wide range of neuroimaging research. Most notably, structural MRI has been used to support the idea of hippocampal involvement during spatial navigation from memory tasks ( Figure 2 ). Its resolving power and highly precise images also make it suitable to be used for mapping surgical procedures. Conclusion With a resolution of up to 1mm, fMRI takes the crown as the human neuroimaging technique with the best spatial resolution! Table 1 shows a brief summary of each neuroimaging method. Unfortunately though, there is still so much more we need to do to look at individual circuits and connections. As mentioned before, even within a millimetre cubed of brain, we have 5 figures worth of cells, making the number of neurons that make up the whole brain impossible to comprehend. To observe the activity of a single neuron, we would need an imaging technique with the power of viewing cells in the 10’s of micrometre range. So what can we do to get to the resolution we desire while still being suitable for humans? Maybe there isn't a solution. Instead, maybe if we want to record singular neuron activity, we have to take inspiration from invasive animal techniques such as microelectrode recordings. Typically used in rats and mice, these can achieve single-cell resolution to look at neuroscience from the smallest of components. It would be unethical to stick an electrode into a healthy human's brain and record activity, but perhaps in the future a non-invasive form of electrode recording could be developed? The current neuroscience field is foggy and shrouded in mystery. Most of these mysteries simply cannot be solved with the current research techniques we have at our disposal. But this is what makes neuroscience exciting - there is still so much to explore! Who knows when we will be able to map behaviours to neural circuits with single-cell precision, but with how quickly imaging techniques are being enhanced and fine-tuned, I wouldn't be surprised if it's sooner than we think. Written by Ramim Rahman Related articles: Neuromyelitis optica / Traumatic brain injuries REFERENCES Hoeffner, E.G. et al. (2011) ‘Neuroradiology back to the future: Brain Imaging’, American Journal of Neuroradiology, 33(1), pp. 5–11. doi:10.3174/ajnr.a2936. Maguire, E.A. and Frith, C.D. (2003) ‘Lateral asymmetry in the hippocampal response to the remoteness of autobiographical memories’, The Journal of Neuroscience, 23(12), pp. 5302–5307. doi:10.1523/jneurosci.23-12-05302.2003. Wong, C. (2024) ‘Cubic millimetre of brain mapped in spectacular detail’, Nature, 629(8013), pp. 739–740. doi:10.1038/d41586-024-01387-9. Butman, J. A., & Floeter, M. K. (2007). Decreased thickness of primary motor cortex in primary lateral sclerosis. AJNR. American journal of neuroradiology, 28(1), 87–91. Loane, C., & Politis, M. (2011). Positron emission tomography neuroimaging in Parkinson's disease. American journal of translational research, 3(4), 323–341. Maguire, E.A. et al. (2000) ‘Navigation-related structural change in the hippocampi of taxi drivers’, Proceedings of the National Academy of Sciences, 97(8), pp. 4398–4403. doi:10.1073/pnas.070039597. [Figure 1] EEG (electroencephalogram) (2024) Mayo Clinic . Available at: https://www.mayoclinic.org/tests-procedures/eeg/about/pac-20393875 (Accessed: 18 October 2024). [Figure 2] Boccia, M. et al. (2016) ‘Direct and indirect parieto-medial temporal pathways for spatial navigation in humans: Evidence from resting-state functional connectivity’, Brain Structure and Function, 222(4), pp. 1945–1957. doi:10.1007/s00429-016-1318-6. Project Gallery

New research suggests that the cause extends far beyond the nervous system Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can what we eat, breathe, and do for a living affect our Parkinson’s risk? Last updated: 21/03/25, 11:59 Published: 10/04/25, 08:00 New research suggests that the cause extends far beyond the nervous system Introduction Parkinson’s disease (PD) is the most prevalent movement disorder and the second most common neurodegenerative disorder worldwide. PD is best known for causing tremors and stiffness, but it’s much more than a movement disorder. It also affects mood and speech. While PD is caused by the loss of dopamine-producing neurons in the brain’s substantia nigra, new research suggests that its roots may extend far beyond the nervous system. Surprisingly, the gut microbiome – trillions of bacteria living in our digestive tract – may play a key role in both the development and prevention of PD. These microbes help regulate inflammation and support brain health by influencing microglia, the brain’s immune cells. Diet also seems to matter: a Mediterranean-style diet rich in fruits, vegetables, and healthy fats appears to lower PD risk, while smoking – despite its well-known dangers – has been linked to a puzzling protective effect, possibly due to nicotine’s impact on the brain. Meanwhile, specific jobs, like farming, may increase PD risk due to pesticide exposure, which has been associated with neurodegeneration. The idea that what we eat, breathe, and do for a living could shape our brain health is intriguing. As research continues to uncover these surprising links, it raises an important question: could simple lifestyle changes help protect against neurodegenerative diseases? Gut-Brain Axis The gut-brain axis (GBA) is a two-way communication network between the enteric nervous system of the gastrointestinal (GI) tract and the central nervous system, connecting emotions and cognition with the intestines’ functions. This involves the brain sending signals to the gut and vice versa, which happens through the vagus nerve, gut hormones and the gut microbiome, which can produce chemicals to impact brain activity. This usually explains why stress signals from the brain can influence the digestion of food, causing symptoms such as stomach pain, bloating or changes in bowel movements. Alternatively, signals travelling from the gut to the brain can be seen when we eat something that makes us feel sick – we naturally avoid that food and the place where we ate it. Gut dysbiosis can be triggered by multiple factors, including diet, antibiotic use, infection, inflammation, and chronic stress. Dysbiosis is the imbalance in the composition and activity of the microbiota (microorganisms present in the gut). It is considered a risk factor for PD, but is not a direct cause of it. Changes in the microbiota can induce metabolic changes, which can result in increased local and systemic inflammation in addition to increased permeability of the intestines, making the gut ‘leaky’. Additionally, this can cause increased harmful gut bacteria (such as E. coli or Salmonella ) as they leak through the intestinal lining, producing amyloid proteins which can travel to the brain and cause the accumulation of α-synuclein – a protein linked to neurodegenerative diseases such as PD. There is also a reduction in healthy gut bacteria – which usually produce short-chain fatty acids (SCFAs) such as butyrate – which reduce inflammation and protect the brain cells. Less SCFAs cause an increase in inflammation and loss of the neuroprotective effects of SCFAs. Increased inflammation can eventually cause the weakening of the gut lining and a cycle of worsening dysbiosis, increased inflammation and increased α-synuclein accumulation, which spreads to the brain. Furthermore, gut dysbiosis can decrease the efficacy of dopaminergic treatments, which may be used to treat PD. In gut dysbiosis, harmful bacteria can produce an enzyme called dopa-decarboxylase – which converts Levodopa (a drug used to treat PD) into dopamine within the intestines. Hence, less Levodopa reaches the bloodstream and the brain, where it primarily acts and is converted to dopamine. This results in less Levodopa being converted to dopamine within the brain, reducing the effectiveness of the treatment. Consequently, this leads to motor symptoms and impairments such as tremors, which is a characteristic symptom of PD. Can food protect the brain? Could your diet be influencing your brain health in ways you never imagined? Research suggests that what you eat might play a critical role in either protecting your brain from PD or increasing your risk. People who follow a Mediterranean diet (MD) – rich in olive oil, fish, fruits, vegetables, whole grains, and nuts – may have up to a 25% lower risk of developing PD. Interestingly, this protective effect appears stronger in younger individuals and those in the early stages of PD. So.. what makes the MD so powerful? Gut microbiome boost: the MD promotes beneficial gut bacteria while reducing harmful microbes, supporting overall brain health. Anti-inflammatory effects: fibre from plant-based foods fuels the gut microbiome, leading to the production of SCFAs, which reduce inflammation and may slow PD progression. Mitochondrial protection: compounds in the MD, such as polyphenols in olive oil and omega-3 fatty acids in fish, help repair and protect mitochondria – the powerhouses of our cells. This helps prevent brain cell damage and maintain dopamine function. Neural growth & repair: walnuts and omega-3s may support neuronal growth and reduce protein clumping, a hallmark of PD. On the other hand, a Western diet – high in processed foods, saturated fats, refined sugars, and excess salt – may increase the risk of developing and worsening PD symptoms. Foods commonly associated with faster PD progression include canned fruits and vegetables, soda, fried foods, beef, ice cream, and cheese. Why does this happen? Microbiome disruption: the Western diet fosters an imbalance in gut bacteria, leading to inflammation and potential brain damage. Gut leakiness and neuroinflammation: a diet high in unhealthy fats and low in fibre can damage the gut lining, allowing harmful substances to enter the bloodstream and trigger brain inflammation. Hormonal imbalance: key gut-derived hormones (GLP-1, GIP, and IGN) that help protect neurons are disrupted by poor diet but can be restored through healthier food choices. While diet alone cannot cure PD, growing evidence suggests it can modify the disease course. A diet rich in fibre, healthy fats, and plant-based foods supports gut health, reduces inflammation, and may protect neurons from degeneration. Understanding these diet-microbiome-brain interactions could open new doors to PD prevention and treatment – proving once again that food truly is medicine. The smoking paradox One of the most intriguing findings in PD research is that smokers appear to have a lower risk of developing the disease. Epidemiological studies consistently show that people who smoke are less likely to be diagnosed with PD compared to non-smokers. But why? Scientists believe that nicotine, a key compound in tobacco, may play a neuroprotective role by affecting dopamine-producing neurons – the same cells that are progressively lost in PD disease. Nicotine interacts with receptors in the brain that influence dopamine release, which could help protect these neurons from degeneration. However, clinical trials testing nicotine as a treatment for PD have not shown significant benefits, suggesting that other compounds in tobacco or alternative mechanisms might be involved. Some researchers propose that additional chemicals in cigarette smoke, such as monoamine oxidase inhibitors, antioxidants, or even carbon monoxide at low levels, might contribute to this protective effect. Others suggest that genetic factors or lifestyle differences between smokers and non-smokers could also explain the association. Despite this fascinating link, smoking is not a recommended strategy for preventing PD. The well-documented risks – including cancer, cardiovascular disease, and lung damage – far outweigh any potential benefit. Instead, scientists are investigating whether specific compounds found in tobacco could be harnessed for new treatments without the harmful effects of smoking itself. What about my job? Can your job affect your risk of developing PD? Some studies suggest that certain occupations – like farming – might increase the risk, while others find no clear connection. So, what’s the truth? Let’s break it down. Some research suggests that farmers are more likely to develop PD, possibly due to exposure to pesticides like paraquat and rotenone, which have been linked to brain cell damage. Additionally, heavy metals found in agricultural environments – such as lead and manganese – may contribute to brain inflammation and oxidative stress, both of which play a role in PD. Furthermore, certain metals, including iron, mercury, copper, and manganese, can build up in the brain over time. Scientists believe that long-term exposure could damage the neurons that produce dopamine. However, the exact link isn’t fully understood, and not everyone exposed to these metals develops PD. That said, not all studies agree. Some large-scale research has found no significant link between farming, pesticide exposure, heavy metals and PD risk. This means that while environmental factors might play a role, other things – like genetics, lifestyle, or how long and intensely someone is exposed – could be just as important. So.. should you worry? If you work in farming or are regularly exposed to pesticides and heavy metals, it might be a good idea to take precautions, like using protective equipment and following safety guidelines. However, more research is needed to fully understand how these exposures contribute to PD. For now, staying informed and taking steps to reduce unnecessary exposure to harmful chemicals is a smart approach. What can you do? While there’s no guaranteed way to prevent PD, research suggests that certain lifestyle choices may help reduce the risk. Here are some science-backed steps you can take: 1. Adopt a Mediterranean-style diet: eating a diet rich in whole, plant-based foods, healthy fats (like olive oil and nuts), and lean proteins has been linked to a lower risk of PD. The Mediterranean diet is packed with antioxidants and anti-inflammatory compounds that may help protect brain cells. 2. Stay active: regular exercise isn’t just good for your muscles and heart – it may also help maintain gut health and protect neurons. Activities like walking, swimming, or strength training have been associated with a reduced risk of PD and other neurodegenerative diseases. 3. Limit pesticide exposure: for those in agricultural or industrial settings, protective measures, such as wearing gloves and masks and following safety guidelines, can help reduce exposure to potentially harmful chemicals linked to PD. 4. Monitor gut health: emerging research suggests that the gut microbiome may play a key role in PD. While scientists are still exploring microbiome-targeted therapies, maintaining good gut health by eating fibre-rich foods, fermented foods (like yogurt and kimchi), and staying hydrated may support overall well-being. Conclusion The connection between diet, gut health, lifestyle, and PD is an exciting area of research. While we don’t yet have all the answers, it’s clear that healthy habits – such as eating well, staying active, and minimising harmful exposures – can support both brain and overall health. As science continues to uncover new insights, making informed choices today can help protect your well-being in the long run! Written by Joecelyn Kirani Tan, Hanin Salem, Devikka Sivashanmuganathan & Barayturk Aydin Related articles: TDP43 and Parkinsonism / Diabetes drug to treat Parkinson's REFERENCES Berthouzoz E, Lazarevic V, Zekeridou A, Castro M, Debove I, Aybek S, Schrenzel J, Burkhard PR, Fleury V. Oral and intestinal dysbiosis in Parkinson's disease. Rev Neurol (Paris). 2023 Nov;179(9):937-946. doi: 10.1016/j.neurol.2022.12.010. Epub 2023 Mar 16. PMID: 36934020. Bisaglia M. Mediterranean Diet and Parkinson's Disease. Int J Mol Sci. 2022 Dec 20;24(1):42. doi: 10.3390/ijms24010042. PMID: 36613486; PMCID: PMC9820428. Firestone JA, Lundin JI, Powers KM, Smith-Weller T, Franklin GM, Swanson PD, Longstreth WT Jr, Checkoway H. Occupational factors and risk of Parkinson's disease: A population-based case-control study. Am J Ind Med. 2010 Mar;53(3):217-23. doi: 10.1002/ajim.20788. PMID: 20025075; PMCID: PMC3299410. Gorell JM, Johnson CC, Rybicki BA, Peterson EL, Richardson RJ. The risk of Parkinson's disease with exposure to pesticides, farming, well water, and rural living. Neurology. 1998 May;50(5):1346-50. doi: 10.1212/wnl.50.5.1346. PMID: 9595985. hms.harvard.edu . (2017). The Gut and the Brain. [online] Available at: https://hms.harvard.edu/news-events/publications-archive/brain/gut-brain . Hrncir, T. (2022). Gut Microbiota Dysbiosis: Triggers, Consequences, Diagnostic and Therapeutic Options. Microorganisms, [online] 10(3), p.578. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC8954387/#:~:text=Dysbiosis%20can%20be%20caused%20by,food%20additives)%2C%20and%20hygiene .. Jackson A, Forsyth CB, Shaikh M, Voigt RM, Engen PA, Ramirez V, Keshavarzian A. Diet in Parkinson's Disease: Critical Role for the Microbiome. Front Neurol. 2019 Dec 10;10:1245. doi: 10.3389/fneur.2019.01245. PMID: 31920905; PMCID: PMC6915094. Johns Hopkins Medicine (2025). Can Environmental Toxins Cause Parkinson’s Disease? https://www.hopkinsmedicine.org/health/conditions-and-diseases/parkinsons-disease/can-environmental-toxins-cause-parkinson-disease Kwon, D. et al. (2024) ‘Diet and the gut microbiome in patients with parkinson’s disease’, npj Parkinson’s Disease , 10(1). doi:10.1038/s41531-024-00681-7. Physiopedia. (n.d.). Gut Brain Axis (GBA). [online] Available at: https://www.physio-pedia.com/Gut_Brain_Axis_(GBA) . Project Gallery

A (possibly) new class of semiconductors Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The search for a room-temperature superconductor 14/07/25, 16:02 Last updated: Published: 13/01/24, 15:19 A (possibly) new class of semiconductors In early August, the scientific community was buzzing with excitement over the groundbreaking discovery of the first room-temperature superconductor. As some rushed to prove the existence of superconductivity in the material known as LK-99, others were sceptical of the validity of the claims. After weeks of investigation, experts have concluded that LK-99 was likely not the elusive room-temperature superconductor but rather a different type of magnetic material with interesting properties. But what if we did stumble upon a room-temperature superconductor? What could this mean for the future of technology? Superconductivity is a property of some materials at extremely low temperatures that allows the material to conduct electricity with no resistance. Classical physics cannot explain this phenomenon, and instead, we have to turn to quantum mechanics to provide a description of superconductors. Inside superconductors, electrons are paired up and can move through the structure of the material without experiencing any friction. The pairs of electrons are broken up by the thermal energy from temperature, so they will only exist for low temperatures. Therefore, this theory, known as BCS theory after the physicists who formulated it, does not explain the existence of a high-temperature superconductor. To describe high-temperature superconductors, such as those occurring at room temperature, more complicated theories are needed. The magic of superconductors lies in their property of zero resistance. Resistance is a cause of energy waste in circuits due to heating, which leads to the unwanted loss of power, making for inefficient operation. Physically, resistance is caused by electrons colliding with atoms in the structure of a material, causing energy to be lost in the process. The ability for electrons to move through superconductors without experiencing any collisions results in no resistance. Superconductors are useful as components in circuits as they cause no wasted power due to heating effects and are completely energy-efficient in this aspect. Normally, using superconductors requires complex methods of cooling them down to typical superconducting temperatures. For example, the temperature at which copper becomes superconducting is 35 K, or in other words, around 130 °C colder than the temperature at which water freezes. These methods are expensive to implement, which prevents them from being implemented on a wide scale. However, having a room-temperature superconductor would allow access to the beneficial properties of the material, such as its resistance, without the need for extreme cooling. The current record holders for highest-temperature superconductors are the cuprate superconductors at around −135 °C. These are a family of materials made up of layers of copper oxides alternating with layers of other metal oxides. As the mechanism for superconductivity is yet to be revealed, scientists are still scratching their heads over how this material can exhibit superconducting properties. Once this mechanism is discovered, it may be easier to predict and find high-temperature superconducting materials and may lead to the first room-temperature superconductor. Until then, the search continues to unlock the next frontier in low-temperature physics… For more information on superconductors: [1] Theory behind superconductivity [2] Video demonstration Written by Madeleine Hales Related articles: Semiconductor manufacturing / Semiconductor laser technology / Silicon hydrogel lenses / Titan Submersible Project Gallery

Unveiling the dance between genes and the environment Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link An introduction to epigenetics 09/07/25, 11:47 Last updated: Published: 04/10/23, 18:01 Unveiling the dance between genes and the environment In recent times, a new area of genetics termed epigenetics has emerged. It seeks to uncover the relationship between our genes and environment. At the core of this novel field is the principle that gene expression can be altered without modifications to the DNA sequence itself. Epigenetic changes to DNA involve the addition of methyl or acetyl groups. Methyl groups decrease gene expression by making DNA more tightly bound around histones, forming heterochromatin, whereas acetyl groups do the opposite; they increase gene expression by loosening histone-bound DNA, forming euchromatin. The addition of these chemical groups to DNA is mediated by enzymes that act on signals our bodies receive from our environment such as diet, stressors, and exercise. Epigenetic mechanisms of gene regulation have gained notoriety in the scientific community as it is suggested that these changes can be passed down to future generations through germline cells. This means that our grandparents’ diets can influence whether we develop diabetes or not. This neo-Lamarckian concept of evolution challenges the current Darwinian understanding of evolutionary genetics where phenotypic traits are believed to emerge due to genetic mutations and natural selection. Understanding epigenetic modifications opens new doors for potential clinical therapies as by modifying harmful epigenetic changes, we may be able to treat various diseases. This field also highlights the importance of a healthy lifestyle, proper nutrition, and avoiding stressors like smoking and radiation, not only for us but for future generations as well. A noteworthy study on exercise A study conducted by Sailani et. al delves into the effects of lifelong exercise on DNA methylation patterns in genes related to metabolism, skeletal muscle properties, and myogenesis. They used two groups with different levels of physical activity. Individuals from one group reported being physically active by playing various sports and engaging in other forms of activity such as cycling, hiking, running, and swimming; the other group were reported to be physically inactive but healthy. The active group exhibited promoter hypomethylation in genes related to insulin sensitivity, muscle repair and development, and mitochondrial respiratory complexes. Compared to the inactive individuals, a significant increase in hypomethylation was seen in 714 promoters in the active group. Bearing in mind that the inactive group were healthy despite being inactive, this significant difference in methylation pattern is remarkable to see and hits home the gravity of epigenetic influence in our lives. As a result of hypomethylation, these genes would have a higher rate of expression in the active individuals. An example of one such gene is GYG2 which codes for the glycogenin 2 enzyme involved in glycogen synthesis. With enhanced glycogen synthesis we can expect to see improved physical performance and recovery in the active individuals. Along with improved skeletal muscle properties and metabolic profiles, we can assume that the active group will have a higher life expectancy and quality of life than the inactive group. As we can see, epigenetics holds a lot of promise for the future of genetic research. By understanding the extent to which epigenetic modifications affect our lives, we can take measures to encourage positive changes to our genomes for greater health, happiness, and vitality. Written by Malintha Hewa Batage Related articles: How epigenetic modifications give the queen bee her crown / Complex disease I- schizophrenia / Famine-induced epigenetic changes Project Gallery

The importance of implementing Maths into our lives Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Teaching maths like it matters 11/07/25, 10:54 Last updated: Published: 03/10/23, 14:43 The importance of implementing Maths into our lives …But I’m never going to use Algebra in my life! The above is a typical response from students across the country when walking into a Maths class. I did not understand others’ disdain, because I love Maths. I got satisfaction from solving numerical problems, stimulation from equations, and excitement from learning new variables like alpha, or constants like Pi. The abstract nature of Maths was like art to me. Later, I realised that not all my peers felt the same way, that somehow, I was the anomaly and that they were the norm. Many maths teachers feel the same way. They get lost in the subject that they love and try to teach it in the way that makes sense to them, without thinking on how the lack of context in equations and processes means nothing to disengaged students. As teachers, our job is to show how applicable Maths can be to our students on an individual basis. Rather than using real-life questions as extensions after the core activity, we must utilise them from the beginning when introducing topics, showing student’s how the methods that they learn can be applied to have some use beyond a pass mark in their exams. I am not talking about examples of ladders leaning against walls when teaching Pythagoras’ theorem and SOHCAHTOA, or, taking counters from a bag, to explain Probability. The examples here are forced, no student will connect with them because they are not lived examples or likely scenarios in most of their lives. We need to build strong relationships with our students, understand their demographic and interests, then introduce topics based on this. For example: If I know that my class enjoys football, I will begin with a video of Messi playing the game, pausing the video, and splitting the pitch up into segments, which can lead a conversation into areas of segments and circles, or, I can discuss the trajectory of the ball after a kick, to talk about quadratic equations. In another class, we can ask what students are budgeting for, perhaps concert tickets or new clothes, and use that to open a discussion into arithmetic series. Another great example is asking students to find an event happening somewhere in the country that they would like to go to, and as a class, plan for this. We would use research skills, calculate speed, distance and time if going by car, or pull up a train timetable where we can teach two-way tables and time conversions. To create meaningful connections to Math topics will take time, effort, and research, and the difficulty will be that not every application will be relatable to every cohort. We will need to build a portfolio of contextual examples related to each topic, however, if there is buy-in from others in our departments, it is an achievable target. In conclusion, we must teach Maths to students in meaningful ways that applies to their life, to keep up engagement and motivation as well as providing opportunities to deepen understanding. Maths should be based around conversation and interests, rather than an exercise of memorising and processes. It should make sense to students, it should matter. Written by Sara Altaf Related article: The game of life Project Gallery

iPSCs are one of the most powerful tools of biosciences Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The endless possibilities of iPSCs and organoids 11/07/25, 11:02 Last updated: Published: 20/01/24, 11:50 iPSCs are one of the most powerful tools of biosciences On the 8th of October 2012, the Nobel Prize in Physiology was given to Shinya Yamanaka and John B. Gurdon for a groundbreaking discovery; induced Pluripotent Stem Cells (iPSCs). The two scientists discovered that mature, specialised cells can be reprogrammed to their initial state and consequently transformed into any cell type. These cells can be used to study disease, examine genetic variations and test new treatments. The science behind iPSCs The creation of iPSCs is based on the procedure of cell potency during mammalian development. While the organism is still in the embryonic stage, the first cell developed is a totipotent stem cell, which has the unique ability to differentiate into any cell type in the human body. “Totipotent” refers to the cell’s potential to give rise to all cell types and tissues needed to develop an entire organism. As the totipotent cell grows, it develops into the pluripotent cell, which can differentiate into the three types of germ layers; the endoderm line, the mesoderm line and the ectoderm line. The cells of each line then develop into multipotent cells, which are derived into all types of human somatic cells, such as neuronal cells, blood cells, muscle cells, skin cells, etc. Creation of iPSCs and organoids iPSCs are produced through a process called cellular reprogramming, which involves the reprogramming of differentiated cells to revert to a pluripotent state, similar to that of embryonic stem cells. The process begins with selecting any type of somatic cell from the individual (in most cases, the individual is a patient). Four transcription factors, Oct4, Sox2, Klf4 and c-Myc, are introduced into the selected cells. These transcription factors are important for the maintenance of pluripotency. They are able to activate the silenced pluripotency genes of the adult somatic cells and turn off the genes associated with differentiation. The somatic cells are now transformed into iPSCs, which can differentiate into any somatic cell type if provided with the right transcription factor. Although iPSCs themselves have endless applications in biosciences, they can also be transformed into organoids, miniature three-dimensional organ models. To create organoids, iPSCs are exposed to a specific combination of signalling molecules and growth factors that mimic the development of the desired organ. Current applications of iPSCs As mentioned earlier, iPSCs can be used to study disease mechanisms, develop personalised therapies and test the action of drugs in human-derived tissues. iPSCs have already been used to model cardiomyocytes, neuronal cells, keratinocytes, melanocytes and many other types of cells. Moreover, kidney, liver, lung, stomach, intestine, and brain organoids have already been produced. In the meantime, diseases such as cardiomyopathy, Alzheimer’s disease, cystic fibrosis and blood disorders have been successfully modelled and studied with the use of iPSCs. Most importantly, the use of iPSCs in all parts of scientific research reduces or replaces the use of animal models, promising a more ethical future in biosciences. Conclusion iPSCs are one of the most powerful tools of biosciences at the moment. In combination with gene editing techniques, iPSCs give accessibility to a wide range of tissues and human disorders and open the doors for precise, personalised and innovative therapies. iPSCs not only promise accurate scientific research but also ethical studies that minimise the use of animal models and embryonic cells. Written by Matina Laskou Related articles: Organoids in drug discovery / Introduction to stem cells Project Gallery

Protective bodies regulate animal use in research worldwide Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Animal ethics: the good, the bad, and the ugly? 03/04/26, 17:04 Last updated: Published: 09/06/24, 12:07 Protective bodies regulate animal use in research worldwide Many research trials involve using animals, specifically those labelled as ‘model organisms’. This refers to species of animals that are desirable for scientific research as they are usually cost-effective, easily manipulated, and well understood in terms of their genetic background. Good knowledge of their genetic background allows for these experiments to be applied with the intention of human benefit. Protective bodies regulate animal use in research worldwide, albeit with various degrees of severity. One of the strictest regions when it comes to animal legislation is the United Kingdom. The Animal Scientific Procedures Act 1986 protects the use of animals in the UK; they, do this by only licensing trusted individuals and experiments that follow the principle of the ‘3Rs’. This principle aims to; r educe the number of animals used r efine procedures to reduce pain r eplace experiments on animals with artificial systems such as cell cultures. In November 2025, the UK government published its official roadmap to accelerate the transition away from animal use in science; "This includes an end to regulatory testing on animals to assess the potential for new treatments to cause skin and eye irritation and skin sensitisation by the end of 2026." Research by Byron Blagburn and coworkers had some controversy as they tested four commercially available heartworm preventatives in dogs, as they first had to infect them. This parasitic worm that was infected in the dogs is extremely severe and life-threatening. The point of the experiment was to see which was the most effective treatment, and they did find that the combination of imidacloprid and moxidectin was 100% effective at eradicating the infection. Despite this research being approved by the Auburn University, Alabama USA Institutional Animal Care and Use Committee, many ethical principles were breached. As the dogs had no choice but to participate in the experiment which completely disregards the autonomy of the dogs. However, Byron and his colleagues would counteract that argument by saying they acted with beneficence as the study’s intention was to find out what was the best treatment for the dogs to improve their health. But for this beneficence to be achieved, non-maleficence was broken as the dogs were given parasitic infections that inflicted pain. Unfortunately, according to the DxE investigators (Direct Action Everywhere), after 5 months the dogs were euthanised. Although the researchers defended the morality of their study by pointing out that all treatments were already in commerce, some have argued that the infection of a previously healthy dog with a parasite is morally wrong. Many religions and groups oppose the use of animals in research as they value animal life as much as human life. Buddhists, for example, believe that animals have moral significance, as the Buddha condemns occupations that involve harming animals and encourages his followers to help animals where they can. While many groups stand against this research, most of our findings and medicine today would not be available without the contribution of animals. According to the American Medical Association: Virtually every advance in medical science in the 20th century, from antibiotics and vaccines to antidepressant drugs and organ transplants, has been achieved either directly or indirectly through the use of animals in laboratory experiments. Thus, showing how important the use of animals is in terms of medical advancements and improvement of human life. One of the most vocal groups is People for the Ethical Treatment of Animals ( PETA): PETA is an organisation advocating for animal rights and strongly opposing many of the current research studies. For example, the research of sepsis is undertaken at many universities like Pittsburgh and California involves puncturing of mice intestines while awake and then stitching multiple of these punctured mice together. This then leads to the excruciating death of these animals. Now, this has aided in the knowledge of sepsis and potential treatment. However, the autonomy of the animals is disregarded whilst the researchers act with maleficence. Therefore, we are at a vital stage with animal experimentation as the intention is for improving health and can be argued to be necessary for the advancing medicine for humans and animals. Nevertheless, religious groups and animal rights groups believe that justice is not being served as the animals are subject to harm without a choice. Despite the advancements of artificial systems such as organ-on-a-chip (OOC) - multi-channel 3-D microfluidic cell culture that simulates the activities, mechanics and physiological response of an entire organ or an organ system, the findings of animal studies are required before trialling within humans. When artificial systems improve and become more available there could be a world where animal studies are limited or non-existent to please animal rights activists and still aid the enhancements of modern-day medicine. Written by Harvey Wilkes Related articles: Regulation and policy of stem cell research / Miniature organs in biomedicine REFERENCES Blagburn, B.L., Arther, R.G., Dillon, A.R., Butler, J.M., Bowles, J.V., von Simson, C. and Zolynas, R., 2016. Efficacy of four commercially available heartworm preventive products against the JYD-34 laboratory strain of Dirofilaria immitis. Parasites & vectors, 9, pp.1-10. Mice stitched together, injected with bacteria-take action! (no date) PETA. Available at: https://support.peta.org/page/6980/action/1?locale=en-US (Accessed: 29 May 2024). 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

How colonialism, interventionism and health are interwoven Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How colonialism and geopolitics shape health injustices: a deep, critical reflection Last updated: 02/04/26, 18:29 Published: 16/10/25, 08:00 How colonialism, interventionism and health are interwoven This is the final article (article no. 7) in a series about global health injustices. Previous article: Addressing the health landscape in Bangladesh's Rohingya community Introduction Welcome to the reflective article of the Global Health Injustices Series. Before I begin, I want to thank Jana Antar again for her contributions to the Lebanon and Syria article, and Dr Nasif Mahmood for his contributions to the Rohingya people in Bangladesh article. Writing and researching about these different countries was an incredible experience. Although I initially planned for this series to go beyond ten articles, focusing on the most enduring and neglected injustices was vital, particularly as the world is becoming more dynamic with geopolitical power shifts. With this in mind, I want to emphasise that each vulnerable population faces unique challenges, but they have challenges shared with others that are not mentioned in this series. I wanted to address these injustices because they are urgent and demonstrate how interconnected global struggles truly are. Through writing this last article, I deepened my understanding of how colonialism, interventionism, and health are interwoven. How the past impacts present reality (colonialism) The injustices we see in news headlines, social media, or the ones we directly experience should not be understood as isolated examples ( Table 1 ). Instead, they stem from European colonialism and later foreign interventionism, shaping how regional governments were created. The ongoing Gaza genocide and expanding illegal settlements pushing out Palestinians in the West Bank are due to Israel’s brutal military occupation and apartheid for 70+ years, and its acts, including the Nakba. Sudan had external rulers (notably Egypt and the British Empire) contributing to its civil wars through political destabilisation, among other factors. This similarly happened in Yemen, though it is also important to note that foreign intervention from the United States (US) and Saudi Arabian governments contributed to the country's existing crises. Lebanon and Syria were divided up and governed by Britain and France after the Ottoman Empire collapsed shortly after World War 1, a significant event leading to political destabilisation and ongoing catastrophes, which also happened to Palestine. In Kashmir, the people’s plight erupted through the British Empire partitioning the Indian subcontinent into multiple nations in 1947 (India, West Pakistan becoming Pakistan and East Pakistan becoming Bangladesh), with Kashmir being a disputed territory between Pakistan and India. As for the Rohingya population and Bangladesh, civil wars during the 20th century and ensuing persecution by the government of Myanmar have contributed to their crises. Therefore, it is clear that all of these events I summarised showcase how their root causes lead to the substantial effects of the current daily injustices. Moreover, what connects these substantial injustices and many others worldwide traces back to the consequences of European colonialism; these powers dispossessed indigenous peoples of their lands and resources through violence, subsequently broken treaties, or legal frameworks that did not identify Indigenous land tenure systems. While they did disrupt indigenous governments, some recent injustices prevail because post-colonial elites embraced or exacerbated these exploitative systems. This severed deep cultural, spiritual, and economic ties that indigenous communities had with their land. For example, Canada’s colonial legacy, notably its Indian Residential Schools, involved forcibly removing children from their families, leading to negative outcomes for the Indigenous communities. Moreover, it is vital to acknowledge the impact of settler colonialism on Indigenous communities globally across South America, Africa, Asia and the Aboriginal people of Australia and New Zealand. If we do not critically think and learn about these past events, how will we improve our present reality and build a future for everyone? Table 1: Summary of the historical and modern perpetrators of injustices affecting the countries/communities explored in the Global Health Injustices Series Country/ community explored in the Global Health Injustices Series Main perpetrator(s) of their injustices Palestine Israel + foreign military aid from the US, UK + other countries Sudan RSF + other local political factions with foreign military aid from the UAE + other countries Yemen Houthis + other local political factions + foreign Interventionism from Saudi Arabia + US + foreign military aid Lebanon Local political factions + US, UK + other countries Syria Local political factions + US, UK + other countries Kashmir Indian + Pakistani militaries + foreign military aid Rohinyga Government of Myanmar + foreign military aid Bangladesh UK via the partition of Subcontinental India (1947), contributing to later injustices Current major health problems Health is essential in global injustices because it is a mirror and a driver of the disparities among various populations. Accessing quality healthcare is usually affected by factors, such as race and ethnicity, which accentuate deep-rooted inequalities. For example, communities with lower incomes encounter challenges, ranging from a lack of healthcare infrastructure to environmental hazards, leading to worse health outcomes. Therefore, tackling them is essential for achieving justice, as improved health outcomes can empower marginalised groups. Aside from warfare being a major determinant of health and injustice, I want to highlight migration as a significant co-occurring determinant. Although research is expanding, the bidirectional relationship between migration and health remains inadequately incorporated into practice and laws. Migration is a complicated and heterogeneous multiphase process ( Figure 1 ). Meanwhile, collecting migration data remains difficult due to polarised political views, unwillingness to finance research on discriminatory laws, varying migration definitions, and limited comparable global data. Unfortunately, political rhetoric and media depictions form incorrect assumptions, stereotypes, and negative views of migrants and refugees, leading to a weakened understanding of the severity and positive aspects of migration. Also, this manifests into hatred and scapegoating of migrants and refugees through their “perceived” impact on countries like employment and healthcare. In reality, accessing employment and healthcare is very difficult for them, leading to negative health outcomes. Thinking more broadly, health behaviours are not solely individual choices, but are deeply rooted in and affected by social, cultural, and political environments. For example, when looking at politics and health through a framework ( Figure 2 ), it is clear how politics is influential through labour markets and welfare states, leading to socioeconomic, income and wealth inequalities and poor health. One systematic review found that a generous welfare state is typically associated with positive population health outcomes, with the Nordic model as an example. This suggests that political leaders are vital in affecting agendas, encouraging intersectoral partnerships, and showing political will to promote health equity. Another review supported the benefits of a generous welfare state through maternal and child health outcomes. Therefore, health and politics are intertwined, as addressed in previous articles through specific contexts. Now I will discuss it more broadly. Current major geopolitical problems Geopolitical dynamics are crucial to shaping the lives of vulnerable populations by influencing their access to security, resources, and fundamental human rights; this is impacted by governments, policies, geographies, and the relationships and interests between countries. In countries or regions plagued by continuous conflict or authoritarian governments, these communities often find themselves at greater risk of challenges like displacement, violence, and systemic discrimination. Moreover, the complicated relationship between global and local power systems results in specific communities being neglected, as more powerful geopolitical interests repeatedly overshadow their needs. To truly support these communities, it is vital to consider how foreign interventionism from countries like the US and the UK impacts the Palestinians, Sudanese, Lebanese, Syrian, Yemeni, Kashmiri, and the Rohingya populations. Foreign interventionism, which typically occurs through militarism, is characterised as the international and social relations of training for and executing organised political violence; this is a pervasive feature of geopolitics, rising into civilian domains by shaping countries and regions. Then, humanitarianism is typically seen as an unbiased moral discourse centred on universal humanity and aid. Yet, it is historically linked to militarism, particularly in Western countries and has deepened in recent decades. Humanitarian standards, like International Humanitarian Law (IHL), are supposed to limit wars’ consequences, but IHL may implicitly tolerate particular levels of ‘collateral damage’ as allowable. IHL is embedded in a hierarchy that determines who can be saved and who cannot, possibly causing inequalities and unstable power relations tied to imperial dynamics. Hence, I see Western humanitarianism as deeply entangled with militarism because of how it can serve to justify and expand political violence across diverse countries and regions, as seen in modern news headlines. More importantly, this dynamic drives a vicious cycle of violence, where armed conflicts cause vulnerability by destroying infrastructure, destabilising nations and other negative consequences, like climate change and rising extremism, leading to civil wars and genocide. Moving forward To truly move forward, adopting a multifaceted approach (e.g. decolonising global health) to addressing all the injustices and health disparities is vital; this can work, but I think that should involve giving all the most vulnerable communities their autonomy, liberation and fundamental human rights. There is the notion of peace plans coming from Western governments like the US, yet that cannot start without putting those directly experiencing war, genocide, displacement, ethnic cleansing and other atrocities as the central voice in those conversations. Moreover, we should highlight those most accountable for making amends. For example, they should allow a right to return and a payment of extensive reparations to the displaced Palestinians, Sudanese, Lebanese, Syrian, Yemeni, Kashmiri, and the Rohingya populations to their homelands, among numerous others. The big question is whether these suggestions will become tangible realities. Although reparations and the right to return may seem distant from contemporary political realities, they are moral imperatives for real justice to occur. Continuously raising awareness and rallying support for affected communities so they can tackle their needs and challenges is important. There is also advocacy, which is vital in showcasing the issues they encounter, which can pave the way for significant policy changes. Moreover, the participation of local and international non-governmental organisations (NGOs), like Amnesty International, is crucial for enforcing ongoing solutions, as they better grasp the vulnerable communities’ needs. When these efforts are done collaboratively, fostering a more supportive environment for those needing it most is vital. Unfortunately, NGOs cannot replace genuine international political will because their impact will always be limited without structural change. Importantly, recognising how interconnected everyone is as a global community is crucial. Engaging in different cultures and experiences should foster empathy and build a collective strength to face challenges, notably climate change and warfare driven by the weapons industry. Uniting and sharing knowledge can encourage real change and all countries actually following international law, which requires powerful countries to be held responsible in ways that have been avoided so far; this should involve acknowledging that the vulnerable communities have a right to resist and defend themselves against their oppressors. Conclusion The global health injustices seen today have historical roots in European colonialism, which has stripped indigenous global communities of their homelands and disrupted their cultural connections. Furthermore, they are influenced by many factors. Moreover, health behaviours are influenced by the broader social, cultural, and political landscapes. Geopolitical dynamics impact vulnerable populations by undermining their security, access to resources, and fundamental human rights; foreign interventionism via militarism makes them worse. Humanitarianism with militarism can reinforce cycles of violence by legitimising unequal power dynamics despite its good intentions. To effectively tackle the global health injustices, uplifting vulnerable communities by prioritising their human rights is vital. The perpetrators should pay reparations and grant the right of return to the most impacted. As individuals, we must raise awareness and push for policy changes. Local and international organisations are pivotal in understanding and addressing community needs. With everything said, I enjoyed writing this series because it showed me how connected all these injustices are and how we can act, listen and reflect together. Ultimately, we must focus on all the countries and communities highlighted in this series, as well as others currently facing injustices like the Uyghurs in China and Afghanistan. We must open our eyes, hearts, souls, and minds to nurture global connections and share knowledge for impactful change. Written by Sam Jarada Related articles: How does physical health affect mental health? / Beyond medicine: health through different stances / Addressing Health Inequalities REFERENCES Banat BYI, Entrena-Durán F, Dayyeh J. Palestinian Refugee Youth: Reproduction of Collective Memory of the Nakba. Asian Social Science. 2018 Nov 29;14(12):147.2. Amiad Haran Diman, Miodownik D. Bloody Pasts and Current Politics: The Political Legacies of Violent Resettlement. Comparative Political Studies. 2023 Aug 13;57(9). Abubakar M, Yahaya TB. Secession and border disputes in Africa: The case of Sudan and South Sudan border. African Journal of Political Science and International Relations. 2021 Oct 31;15(4):131–8. Tamer Abd Elkreem, Jaspars S. Sudan’s catastrophe: the role of changing dynamics of food and power in the Gezira agricultural scheme. Disasters [Internet]. 2024 Oct 30 [cited 2025 Sep 18];49(1). Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC11603519/ eClinicalMedicine. Under the shade of world events: a never-ending crisis in Yemen. EClinicalMedicine [Internet]. 2023 Oct 1 [cited 2025 Sep 18];64:102302–2. Available from: https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(23)00479-0/fulltext Bordón J, Eyad Alrefai. Saudi Arabia’s Foreign aid: the Singularity of Yemen as a Case Study. Third World Quarterly. 2023 Jul 14;45:1–18. Osman O. Western Domination, Destructive Governance, and the Perpetual Development Crisis in the Arab Region. World review of political economy. 2024 Apr 15;15(1). Huber D, Woertz E. Resilience, conflict and areas of limited statehood in Iraq, Lebanon and Syria. Democratization. 2021 Jun 25;28(7):1–19. Gupta H. 1947 Partition of India and its lessons. Journal of Family Medicine and Primary Care [Internet]. 2024 Jul 26 [cited 2025 Sep 18];13(8):3471–2. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC11368293/ Jong K de, van, Ford N, Kamalini Lokuge, Fromm S, Galen R van, et al. Conflict in the Indian Kashmir Valley II: psychosocial impact. Conflict and Health [Internet]. 2008 Oct 14 [cited 2025 Sep 18];2(1). Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC257762/ Project Gallery

Pathology and promising therapeutics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Secondary bone cancer 11/07/25, 10:52 Last updated: Published: 13/12/23, 17:27 Pathology and promising therapeutics Introduction: what is secondary bone cancer? Secondary bone cancer occurs when cancer cells spread to the bones from a tumour that started somewhere else in the body. The site where the tumour first develops is called primary cancer. Cancer cells can break away from the primary cancer, travel through the bloodstream or lymphatic system, and establish secondary cancers, known as metastasis. Bones are among the most common sites to which cancer can spread. Most type of cancer has the potential to metastasise to the bones, with the most frequent occurrences seen in prostate, breast, lung, thyroid, kidney, and myeloma cancers. Throughout the literature, secondary cancer in the bones is referred to as bone secondaries or bone metastases. The most common areas of secondary bone cancer are the spine, ribs, pelvis, humerus (upper bone of the arm), femur (upper bone of the leg) and skull. There are two main types of bone cancer referred to as osteolytic and osteoblastic metastases. In osteolytic metastases, cancer cells break down the bone, leading to significant weakening. This type of metastasis is more common than osteoblastic metastases and often occurs when breast cancer spreads to the bone. In osteoblastic metastases, cancer cells invade the bone and stimulate excessive bone cell formation. This process results in the bone becoming very dense (sclerotic). Osteoblastic metastases frequently occur when prostate cancer spreads to the bone. Although new bone forms, it grows abnormally, which weakens the overall bone structure. Hormone therapy Like primary bone cancer, treatment for secondary bone cancer includes surgical excision, chemotherapy, and radiation therapy. Treatment for secondary bone cancer aims to control the cancer growth and symptoms. Treatment depends on several factors, including the type of primary cancer, previous treatment, the number of bones affected by cancer, whether cancer has spread to other body parts, overall health, and symptoms. Breast and prostate cancers rely on hormones for their growth. Reducing hormone levels in the body can be effective in managing the proliferation of secondary cancer. Hormone therapy, also known as endocrine therapy, uses synthetic hormones to inhibit the impact of the body’s innate hormones. Typical side effects include hot flashes, mood fluctuations, changes in weight, and sweating. Bisphosphonates Bone is a dynamic tissue with a continuous process of bone formation and resorption. Osteoclasts are cells responsible for breaking down bone tissue. In secondary bone cancer, cancer cells often produce substances that stimulate the activity of osteoclasts. This leads to elevated levels of calcium in the blood (hypercalcemia), resulting in feelings of nausea and excessive thirst. Treating secondary bone cancer involves strengthening bones, alleviating bone pain and managing hypercalcaemia). One option for bone-strengthening is bisphosphonates. Bisphosphonates can be administered orally or intravenously. They have been in clinical practice for over 50 years and are used to treat metabolic bone diseases, osteoporosis, osteolytic metastases, and hypercalcaemia. These compounds selectively target osteoclasts to inhibit their function. Bisphosphonates can be classified into two pharmacologic categories based on their mechanism of action. Nitrogen-containing bisphosphonates, the most potent class, function by suppressing the activity of farnesyl pyrophosphate synthase, a key factor in facilitating the binding of osteoclasts to bone. Consequently, this interference causes the detachment of osteoclasts from the bone surface, effectively impeding the process of bone resorption. Examples of these bisphosphonates include alendronate and zoledronate. Bisphosphonates without nitrogen in their chemical structure are metabolised intracellularly to form an analogue of adenosine triphosphate (ATP), known as 5'-triphosphate pyrophosphate (ApppI). ApppI is a non-functional molecule that disrupts cellular energy metabolism, leading to osteoclast cell death (apoptosis) and, consequently, reduced bone resorption. Examples of these bisphosphonates include etidronate and clodronate. Non-nitrogen-containing bisphosphonates can inhibit bone mineralisation and cause osteomalacia, a condition characterised by bones becoming soft and weak. Due to these considerations, they are not widely utilised. Denosumab Denosumab is another option for bone strengthening. It is administered as an injection under the skin (subcutaneously). Denosumab is a human monoclonal antibody that inhibits RANKL to prevent osteoclast-mediated bone resorption. Denosumab-mediated RANKL inhibition hinders osteoclast maturation, function, and survival in contrast to bisphosphonates, which bind to bone minerals and are absorbed by mature osteoclasts. In some studies, Denosumab demonstrated equal or superior efficacy compared to bisphosphonates in preventing skeletal-related events (SREs) associated with bone metastasis. Denosumab’s mechanism of action provides a targeted approach that may offer benefits for specific populations, such as patients with renal impairment. Bisphosphonates are excreted from the human body by the kidneys. A study by Robinson and colleagues demonstrated that bisphosphonate users had a 14% higher risk of chronic kidney disease (CKD) stage progression (including dialysis and transplant) than non-users. On the other hand, denosumab is independent of renal function and less likely to promote deteriorations in kidney function. Take-home message Secondary bone cancer, resulting from the spread of cancer cells to the bones, poses challenges across various cancers. Two main types, osteolytic and osteoblastic metastases, impact bone structure differently. Hormone therapy, bisphosphonates, and Denosumab have shown promising results and offer effective management of secondary bone cancers. Ultimately, the decision between treatments should be made in consultation with a healthcare professional who can evaluate the specific clinical situation and individual patient factors. The choice should be tailored to meet the patient’s needs and treatment goals. Written by Favour Felix-Ilemhenbhio Related article: Bone cancer Project Gallery