How botox works in the cosmetic industry Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link From botulism to beauty: the evolution of botulinum toxins and botox 09/07/25, 15:10 Last updated: Published: 03/10/23, 15:07 How botox works in the cosmetic industry Botulinum neurotoxins (BoNTs) rank amongst the most potent and lethal neurotoxins known to science. Yet, it's a fascinating journey to discover how these deadly substances have found their way into one of the most renowned cosmetic procedures in the world: Botox. BoNTs originate from the bacterium Clostridium botulinum , which produces some of the most potent neurotoxins in existence. They are central to the development of botulism, a condition that relentlessly targets the body's nervous system, resulting in challenges in breathing and muscle paralysis. Despite their perilous origins, these toxins have undergone a fascinating metamorphosis into a popular cosmetic procedure. They have been studied substantially due to their ability to block nerve functions leading to muscle paralysis and their unique pharmacological properties in therapeutic and cosmetic uses. They affect the neurotransmission process by blocking the release of acetylcholine that allows muscle contraction in the body. The toxins bind pre-synaptically to recognition sites on cholinergic nerve terminals resulting in the inhibition of neurotransmitter release. The toxin consists of a heavy chain and a light chain connected by a disulphide bond. This disulphide bond is vital in the entry of the metalloprotease chain in the cytosol. BoNTs have a unique binding characteristic as a dual receptor binder, which allows them to achieve a high affinity for neurons. These proteins possess the remarkable ability to specifically target and interfere with the neurotransmission process. At their core, BoNTs are proteases, enzymes specialised in cleaving specific proteins involved in nerve signal transmission. When administered as Botox, BoNTs are skillfully harnessed to their advantage due to these properties. By injecting small, controlled amounts into specific facial muscles, they temporarily disrupt the nerve signals that stimulate muscle contraction. This action leads to muscle relaxation, smoothing out wrinkles and lines on the skin's surface. Importantly, the effects are localised, preserving the natural expressiveness of the face. In 1989, BoNTs made their debut in the medical community by being recognised as a safe and effective treatment by the FDA for blepharospasm, which affects eye muscle control. However, in 2002 the FDA extended its endorsement, propelling Botox into the realm of beauty. This pivotal decision forever reshaped the landscape of cosmetic procedures, solidifying Botox's status as an iconic treatment for rejuvenation and enhancement. In conclusion, the evolution of botulinum toxins and the rise of Botox is a captivating journey that traverses the realms of science, medicine, and evolving beauty ideals. Written by Anam Ahmed Project Gallery

Discussing Peto's Paradox in cancer Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why blue whales don't get cancer 09/05/26, 14:57 Last updated: Published: 16/10/23, 22:22 Discussing Peto's Paradox in cancer Introduction: What is Peto’s Paradox? Cancer is a disease that occurs when cells divide uncontrollably, owing to genetic and epigenetic factors . Theoretically, the more cells an organism possesses, the higher the probability should be for it to develop cancer. Imagine that you have one tiny organism – a mouse, and a huge organism – an elephant. Since an elephant has more cells than a mouse, it should have a higher chance of developing cancer, right? This is where things get mysterious. In reality, animals with 1,000 times more cells than humans are not more likely to develop cancer. Notably, blue whales, the largest mammals, hardly develop cancer. Why? In order to understand this phenomenon, we must dive deep into Peto’s Paradox. Peto’s paradox is the lack of correlation between body size and cancer risk. In other words, the number of cells you possess does not dictate how likely you are to develop cancer. Furthermore, research has shown body mass and life expectancy are unlikely to impact the risk of death from cancer . (see figure 1) Peto’s Paradox: Protective Mechanisms Mutations, otherwise known as changes or alterations in the deoxyribonucleic acid (DNA) sequence, play a role in cancer and ageing. Research scientists have analysed mutations in the intestines of several mammalian species , ranging from mice, monkeys, cats, dogs, humans, and giraffes, to tigers and lions. Their results reveal that these mutations mostly come from processes that occur inside the body, such as chemicals causing changes in DNA. These processes were similar in all the animals they studied, with slight differences. Interestingly, annually, animals with longer lifespans were found to have fewer mutations in their cells ( figure 2 ). These findings suggest that the rate of mutations is associated with how long an animal lives and might have something to do with why animals age. Furthermore, even though these animals have very different lifespans and sizes, the amount of mutations in their cells at the end of their lives was not significantly different – this is known as cancer burden. Since animals with a larger size or longer lifespan have a larger number of cells (and hence DNA) that could undergo mutation, and a longer time of exposure to mutations, how is it possible that they do not have a higher cancer burden? Evolution has led to the formation of mechanisms in organisms that suppress the development of cancerous cells . Animals possessing 1,000 times as many cells as humans do not display a higher susceptibility to cancer, indicating that natural mechanisms can suppress cancer roughly 1,000 times more efficiently than they operate in human cells . Does this mean larger animals have a more efficient protective mechanism against cancer? A tumour is an abnormal lump formed by cells that grow and multiply uncontrollably. A tumour suppressor gene acts like a bodyguard in your cells. They help prevent the uncontrollable division of cells that could form tumours. Previous analyses have shown that the addition of one or two tumour suppressor gene mutations would be sufficient to reduce the cancer risk of a whale to that of a human. However, evidence does not suggest that an increased number of tumour suppressor genes correlated with increasing body mass and longevity. Although a study by Caulin et al . identified biomarkers in large animals that may explain Peto’s paradox, more experiments need to be conducted to confirm the biological mechanisms involved. Perillo et. al (2023) was an investigation of existing evidence on such mechanisms, and revealed a list of factors that may contribute to Peto’s paradox. This includes replicative immortality, cell senescence, genome instability and mutations, proliferative signalling, growth suppression evasion and cell resistance to death. As far as we know, different strategies have been followed to prevent cancer in species with larger sizes or longer lifespans . However, more studies must be conducted in the future in order to truly explain Peto’s paradox. Peto’s Paradox: Other Theories There are several theories that attempt to explain Peto’s paradox. One of which explains that large organisms have a lower basal metabolic rate, leading to less reactive oxygen species. This means that cells in larger organisms incur less oxidative damage, causing a lower mutation rate and lower risk of developing cancer. Another popular theory is the formation of hypertumours . As cells divide uncontrollably in a tumour, “cheaters” could emerge. These “cheaters”, known as hypertumours, are cells which grow and feed on their original tumour, ultimately damaging or destroying the original tumour. In large organisms, tumours have more time to reach lethal size. Therefore, hypertumours have more time to evolve, thereby destroying the original tumours. Hence, in large organisms, cancer may be more common but is less lethal. Clinical Implications Curing cancer has posed significant challenges. Consequently, the focus on cancer treatment has shifted towards cancer prevention . Extensive research is currently underway to investigate the behaviour and response of cancer cells to the treatment process. This is done through a multifaceted approach; investigating the tumour microenvironment and diagnostic or prognostic biomarkers. Going forward, a deeper understanding of these fields enables the development of prognostic models as well as targeted treatment methods. One example of an exciting discovery is the revelation of TP53 . The discovery of this tumour suppressor gene indicates that it plays a role in making elephant cells more responsive to DNA damage and in triggering apoptosis by regulating the TP53 signaling pathway. These findings imply that having more copies of TP53 may have directly contributed to the evolution of extremely large body sizes in elephants, helping resolve Peto’s paradox . Particularly, there are 20 copies of the TP53 gene in elephants, but only one copy of the TP53 gene in humans (see figure 3 ). Through more robust studies and translational medicine, it would be fascinating to see how such discoveries could be applied into human medicine ( figure 4 ). Conclusion The complete mechanism of how evolution has enabled organisms that are larger in size and have longer lifespans than humans is still a mystery. There is a multitude of hypotheses that need to be extensively investigated with large-scale experiments. By unravelling the mysteries of Peto’s paradox, these studies could provide invaluable insights into cancer resistance and potentially transform cancer prevention strategies for humans. Written by Joecelyn Kirani Tan Related articles: Biochemistry of cancer / Orcinus orca (killer whale) / Canine friends and cancer Project Gallery

Differences in brain structure Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Brief neuroanatomy of autism 26/04/26, 15:18 Last updated: Published: 26/12/23, 20:38 Differences in brain structure Autism is a neurodevelopmental condition present in both children and adults worldwide. The core symptoms include difficulties understanding social interaction and communication, and restrictive or repetitive behaviours such as strict routines and stimming. When the term autism was first coined in the 20th century, it was thought of as a disease. However, it is now described as a cognitive difference rather than a disease; that is, the brains of autistic individuals – along with people diagnosed with dyslexia, dyspraxia, or attention deficit hyperactive disorder – are not defective, but simply wired differently. The exact cause or mechanism for autism has not been determined; the symptoms are thought to be brought about by a combination of genetic and environmental factors. Currently, autism disorders are diagnosed solely by observing behaviours, without measuring the brain directly. However, behaviours may be seen as the observable consequence of brain activity. So, what is it about their brains that might make autistic individuals behave differently to neurotypicals? Total brain volume Back before sophisticated imaging techniques were in use, psychiatrics had already observed the head size of autistic infants was often larger than that of other children. Later studies provided more evidence that most children who would go on to be diagnosed had a normal-sized head at birth, but an abnormally large circumference by the time they had turned 2 to 4 years old. Interestingly, increase in head size has been found to be correlated with the onset of main symptoms of autism. However, after childhood, growth appears to slow down, and autistic teenagers and adults present brain sizes comparable to those of neurotypicals. The cortex Research from the UC Davis MIND Institute (May 2024) found that at the age of 3, autistic girls have a thicker cortex than non-autistic girls, with these differences becoming less pronounced by age 12- due to faster cortical thinning in autistic girls. A major study published in Molecular Psychiatry (Oct 2024) found that, for the first time in living adults, autistic brains have approximately 17% lower synaptic density compared to neurotypical individuals. A lower density of these nerve cell connections was directly correlated with more pronounced differences in communication. The amygdala As well transient increase of total brain volume and differences in the cortex, the size and volume of several brain structures in particular seems to differ between individuals with and without autism. Most studies have found that the amygdala, a small area in the centre of the brain that mediates emotions such as fear, appears enlarged in autistic children. The amygdala is a particularly interesting structure to study in autism, as individuals often have difficulty interpreting and regulating emotions and social interactions. Its increased size seems to persist at least until early adolescence. However, studies in adolescents and adults tend to show that the enlargement slows down, and in some cases is even reversed so that the number of amygdala neurons may be lower than normal in autistic adults. Moreover, higher neuron density was found in the amygdala in children, with lower neuron density in other brain areas- as described by a study in Autism Research (Oct 2024). The cerebellum Another brain structure that tends to present abnormalities in autism is the cerebellum. Sitting at the back of the head near the spinal cord, it is known to mediate fine motor control and proprioception. Yet, recent literature suggests it may also play an important role in some higher other cognitive functions, including language and social cognition. Specifically, it may be involved in our ability to imagine hypothetical scenarios and to abstract information from social interactions. In other words, it may help us recognise similarities and patterns in past social interactions that we can apply to understand a current situation. This ability is poor in autism; indeed, some investigations have found the volume of the cerebellum may be smaller in autistic individuals, although research is not conclusive. Nevertheless, most research agrees that the number of Purkinje cells is markedly lower in people with autism. Purkinje cells are a type of neuron found exclusively in the cerebellum, able to integrate large amounts of input information into a coherent signal. They are also the only source of output for the cerebellum; they are responsible for connecting the structure with other parts of the brain such as the cortex and subcortical structures. These connections eventually bring about a specific function, including motor control and cognition. Therefore, a low number of Purkinje cells may cause underconnectivity between the cerebellum and other areas, which might be the reason for functions such as social cognition being impaired in autism. Written by Julia Ruiz Rua Related article: Epilepsy Project Gallery

Observations suggest that aspects of their design were purposeful for other reasons Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The astronomical symbolism of the Giza Pyramids Last updated: 09/10/25, 11:03 Published: 06/03/25, 08:00 Observations suggest that aspects of their design were purposeful for other reasons This is Article 2 in a series about astro-archaeology. Next article: The celestial blueprint of time: Stonehenge, UK . Previous article: Cities designed to track the heavens: Chaco Canyon, New Mexico The Giza Pyramids of the ancient Egyptian civilisation may be most well known as one of the Seven Wonders of the Ancient World, but they also harbour astronomical secrets. The three Great Pyramids (Khafre, Khufu, and Menkaure) are incredible feats of engineering, with heights measuring 146.6 meters, 143.5 meters, and 64.5 meters, respectively. No documentation has been found explaining the planning or construction processes behind the creation of these magnificent structures, yet observations suggest that aspects of their design were purposeful for reasons other than simply erecting the pyramid. Example 1: The square bases of the pyramids are very carefully oriented to the cardinal points with the Khufu Pyramid aligning within 4 arc minutes of the north-south line. For context, if you were to hold your index finger up, it would cover a portion of the sky that measures about 10 degrees across. 1 arc minute is a unit of measurement equal to 1/60 of 1 degree, which means that the orientation of the Khufu Pyramid only deviates from the north-south line by less than 4/60-degree error. Today, we would calculate this using a GPS or other technical equipment, but what did the ancient Egyptians use? Well, astronomy! While the exact method of calculation is not known, researchers believe that the ancient engineers aligned the pyramids to the constellation Orion and the star Sirius as they are circumpolar stars, never rising nor setting, and are therefore visible every night as a useful guide. This may also have religious implications relating to immortality, perhaps adding to the desire to align the Pharoah’s tombs with such a symbolic constellation. Example 2: The south-eastern corners of the three Giza Pyramids all point toward the nearby great solar temple of Heliopolis, which was a major religious centre of the sun god Atum-Ra. According to the Pyramid Texts, Heliopolis was the location that the god-creator Atum emerged from chaos and begun creation. These texts suggest that the ancient Egyptians believed that the Pharaohs join Atum-Ra in the afterlife, and they together cross the sky in Atum-Ra’s sun boat as part of the rebirth process. Upon investigation, the three pyramids seem to be aligned with various solar events as well as the city of the sun god: the setting sun is aligned with the northern side of the Khafre pyramid and the southern side of the Khufu pyramid during the equinoxes the causeways point to the setting sun behind the pyramid twice per year, which are distanced the same number of days from the winter/summer solstices each of the two causeways point towards sunset in two separate locations that are halfway between the equinoxes and solstices, respectively (not according to the calendar year, but according to the astronomical year) on the summer solstice, the sun sets directly between the two great pyramids when viewing from the Sphinx area of the pyramidal complex Example 3: the position of three Great Pyramids with respect to each other mimics the position of the stars in the constellation Orion’s belt with respect to each other. Astronomical calculations show that the orientation and position of the Khufu, Khafre, and Menkaure pyramids align together in exactly the same way that the Alnitak, Alnilam, and Mintaka stars align in Orion’s belt. Of course, there is a small percentage of error, but it is because of naked eye observations instead of mathematical miscalculations. While there are still many secrets hidden in and around the Great Pyramids of ancient Egypt, they can continue to provide insight into how ancient peoples interconnected architecture, astronomy/mathematics, and religious beliefs within their societies. Written by Amber Elinsky REFERENCES Magli, G. (2009). Archaeoastronomy at Giza: the ancient Egyptians’ mathematical astronomy in action. In: Emmer, M., Quarteroni, A. (eds) Mathknow. MS&A, vol 3. Springer, Milano. https://doi.org/10.1007/978-88-470-1122-9_10 . Orofino, V. and P. Bernardini. Archaeoastronomical Study of the Main Pyramids of Giza, Egypt: Possible Correlations with the Stars?. Archaeological Discovery: 1 (2016), vol 3. https://www.scirp.org/journal/paperinformation?paperid=61389 . Verner, Miroslav, 'Heliopolis: The City of the Sun', in Anna Bryson-Gustová (ed.), Temple of the World: Sanctuaries, Cults, and Mysteries of Ancient Egypt (Cairo, 2013; online edn, Cairo Scholarship Online, 18 Sept. 2014), https://doi.org/10.5743/cairo/9789774165634.003.0002 . https://pyramidtextsonline.com/translation.html Project Gallery

Research confirms anxiety disorders do have a genetic side Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Does anxiety run in families? Here's what genetics tells us Last updated: 10/07/25, 19:26 Published: 19/06/25, 08:00 Research confirms anxiety disorders do have a genetic side Have you ever noticed anxiety can pop up in several members of the same family? Maybe your sister worries constantly, or your brother gets nervous around people. It might feel like anxiety is passed down through generations. But is that really how it works, or is it just a coincidence? Here's what science has to say. Your DNA can affect anxiety Research confirms anxiety disorders do have a genetic side. That means you're more likely to have anxiety if someone in your family, like your mum, dad, sibling, or even a grandparent, has it too. But this doesn't mean anxiety is certain. Instead, genes increase your chances, accounting for about 30% to 40% of your risk. Scientists work this out by comparing identical and fraternal twins and by following anxiety diagnoses across generations; those studies repeatedly find that roughly one-third to two-fifths of a person’s risk is genetic. So, if genetics only make up part of the picture, what's the rest? That's where your environment steps in. Your life experiences matter a lot. Things like your relationships, stressful situations, and even your physical health can tip the scales one way or another. Genes set the stage, but they don't control the outcome. Think of your genes as nudging you towards anxiety rather than pushing you into it completely. The rest depends on what happens to you. How genes shape your brain Scientists have pinpointed several genes linked to anxiety. One of these genes affects serotonin, a brain chemical that helps regulate your mood and manage stress. When serotonin works well, you feel calm and can handle stressful events better. But if your genes make serotonin less effective, stress hits you harder. This can make anxiety more likely during tough times, even when others around you seem okay. There's another important point: your brain structure. Genes influence parts of your brain, especially the amygdala. Think of the amygdala as your internal alarm system. It warns you when something feels dangerous. In people with certain genes, the amygdala is extra sensitive. That means their "alarm" goes off more easily, causing anxiety even when there's no real danger present. However, not everyone with these genetic variations experiences anxiety. Your brain adapts throughout life, changing how genes affect you. This ongoing flexibility is called neuroplasticity: experience can strengthen or weaken neural circuits and can even add or remove chemical tags, such as DNA methylation, that switch genes on or off, reshaping how your stress system responds. Anxiety isn't just genetic; here's why It's tempting to blame your genes entirely if anxiety runs in your family. But life is more complicated. Even if you inherit genes that make anxiety more likely, the disorder usually develops when certain environmental conditions come into play. Stressful life events like losing a loved one, ongoing conflict at home, bullying, or trauma can trigger anxiety symptoms. Someone might have anxiety-related genes but never experience anxiety if their life stays relatively stress-free. On the other hand, someone without these genes can still develop anxiety if they experience severe stress or trauma. Lifestyle choices also make a big difference. Regular exercise, healthy eating, good sleep, and support from friends and family can protect against anxiety. Studies show these lifestyle habits are powerful, even if your genes are pushing in the opposite direction. Can you change your genetic destiny? Understanding that anxiety has a genetic basis can help. It means anxiety isn't just a character flaw or personal weakness. It's something partly built into your biology, something real and valid. Realising this can reduce shame and make people more willing to seek help. And here's another benefit: knowing your family history allows you to spot anxiety sooner. If you understand that anxiety might run in your family, you can pay attention to early signs, like trouble sleeping, excessive worry, or panic in social settings. Catching anxiety early means getting support earlier, making treatments like therapy or lifestyle changes more effective. Anxiety might run in your family, but you get to decide how far it goes. Written by Rand Alanazi Related articles: Depression / South Asian mental health / Physical and mental health / Does insomnia run in families? REFERENCES National Institute of Mental Health. Anxiety disorders [Internet]. Bethesda (MD): National Institute of Mental Health; 2024 [cited 2025 May 29]. Available from: https://www.nimh.nih.gov/health/topics/anxiety-disorders Mayo Clinic. Anxiety disorders [Internet]. Rochester (MN): Mayo Foundation for Medical Education and Research; 2018 [cited 2025 May 29]. Available from: https://www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-20350961 Leyfer O, Woodruff-Borden J, Mervis CB. Anxiety disorders in children with Williams syndrome, their mothers, and their siblings: implications for the aetiology of anxiety disorders. J Neurodev Disord . 2009 Feb 13;1(1):4-14. Martin EI, Ressler KJ, Binder EB, Nemeroff CB. The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. Psychiatr Clin North Am [Internet]. 2009 Sep;32(3):549-75. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684250/ McEwen BS, Eiland L, Hunter RG, Miller MM. Stress and anxiety: structural plasticity and epigenetic regulation as a consequence of stress. Neuropharmacology . 2012 Jan;62(1):3-12. Xie S, Zhang X, Cheng W, Yang Z. Adolescent anxiety disorders and the developing brain: comparing neuroimaging findings in adolescents and adults. Gen Psychiatry [Internet]. 2021 Aug 4;34(4):e100542. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8340272/ Zhang K, Ibrahim GM, Venetucci Gouveia F. Molecular pathways, neural circuits and emerging therapies for self-injurious behaviour. Int J Mol Sci [Internet]. 2025 Feb 24;26(5):1938. Available from: https://www.mdpi.com/1422-0067/26/5/1938 Chaves T, Fazekas CL, Horváth K, Correia P, Szabó A, Török B, et al. Stress adaptation and the brainstem with focus on corticotropin-releasing hormone. Int J Mol Sci [Internet]. 2021 Jan 1;22(16):9090. Available from: https://www.mdpi.com/1422-0067/22/16/9090 Project Gallery

Understanding the cause of bullying can provide effective prevention and intervention Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The brain of a bully Last updated: 26/04/26, 15:22 Published: 29/05/25, 08:00 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. The immediate brain 'alarm' system: research published in Journal of Neuroscience found that witnessing or experiencing bullying activates social and emotional brain networks and autonomic threat systems, in both children (11–14 years old) and adults. This response is similar to how the brain reacts to physical threats. Another finding is that adolescents show stronger, more profound brain activity in regions processing bodily sensations during bullying compared to adults, suggesting it acts as a severe, acute, and physical threat during this developmental stage. Lastly, a January 2026 study in European Child & Adolescent Psychiatry found that while some victims show high stress responses, those frequently exposed to bullying (more than twice a month) exhibit lower amygdala activation, in response to further social exclusion. This suggests a neural adaptation to chronic trauma, known as 'emotional numbing'. 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

A disease of the blood Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Anaemia 09/05/26, 14:44 Last updated: Published: 17/06/23, 13:40 A disease of the blood This is article no. 1 in a series about anaemia. Next article: iron-deficiency anaemia Introduction Erythrocytes in their typical state are a biconcave and nucleus free cell, responsible for carrying oxygen and carbon dioxide. The production is controlled by erythropoietin and as they mature in the bone marrow, they lose their nuclei. These red blood cells (RBC) contain haemoglobin, which aids in the transport of oxygen and iron. Iron is a key component of haem; insufficient levels of iron leads to anaemic disorders. Low oxygen-carrying capacity may be defined by too few RBC in circulation, or RBC dysfunction. Haem iron is acquired through the digestion of meat, and transported through enterocytes of the duodenum, in its soluble form. Erythrocytic iron accounts for approximately 50% of the iron in blood. Metals cannot move freely throughout the body so they must be transported; the molecule involved in transporting iron is known as transferrin. Plasma transferrin saturation refers to the iron that is attached to transferrin. In iron deficient anaemia (IDA), this will always be low. Anaemia is physiological or pathological. These changes can be due to a plethora of causes; malabsorption due to diet or gastrointestinal (GI) conditions, genetic dispositions such as sideroblastic anaemias (SA), thalassaemia, or deficiency in erythropoietin due to comorbidities and chronic disease; where haemolysis is caused by autoimmune disorders, infections and drugs, or blood loss. Haem The iron is in a protoporphyrin ring at the centre of a haem molecule. The structure of haem consists of two alpha and two beta polypeptide chains, to form a single haemoglobin macromolecule. Microcytic anaemias arise from problems in the creation of haemoglobin; sourcing through diet (IDA), synthesising protoporphyrin (SA) or from globin chain defects caused by thalassaemia. Summary Anaemia is a multifactorial condition with many different mechanisms involved. Microcytic anaemias have an issue at the haemoglobin level. these can be acquired or inherited. A microcytic anaemia is caused by a failure to efficiently synthesise haemoglobin, whether from iron, protoporphyrin rings or globin chains. The diagnosis of anaemias is reliant on a patient’s background and medical history, as there are many factors involved in an anaemic disorder. A diagnosis should be patient led, as the age and sex of the patient can significantly highlight the origin and pathogenesis, as well as the prognosis and follow up care. Written by Lauren Kelly Related article: Blood Project Gallery

Civil wars and arms trade Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Yemen- a neglected humanitarian crisis Last updated: 03/05/26, 18:20 Published: 15/05/25, 08:00 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 NGOs have a vital role in supporting vulnerable populations, especially in Yemen. In a 2025 report from Amnesty International, they noted several breaches of international law and human rights: Parties to the conflict in Yemen continued to arbitrarily detain, forcibly disappear and unjustly prosecute people who criticized their human rights records and policies, including human rights defenders, journalists and humanitarian workers. All parties to the conflict failed to protect economic and social rights amid international funding cuts that further worsened the humanitarian crisis. Parties to the conflict contributed to environmental degradation. 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

Is bacteria the key to unlocking this treatment? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A breakthrough in endometriosis treatment 27/03/25, 12:05 Last updated: Published: 29/06/23, 10:16 Is bacteria the key to unlocking this treatment? In a giant leap forward, scientists have linked a specific bacterial infection to endometriosis for the very first time. Endometriosis is a condition in which the endometrium (lining of the uterus wall) grows outside of the uterus. For many women, the condition is characterised by debilitating pain, fatigue and infertility. The average time span for an accurate diagnosis is 7.5 years, with some women opting for a complete hysterectomy (removal of the uterus) to curb the pain. Unfortunately, the pathogenesis (the process by which a disease develops) of endometriosis is still relatively unknown. With previous scientific theories including retrograde menstruation, immune dysregulation, hormonal imbalance, stem cells and benign metastasis- this is the first time a bacterial theory has been forwarded. Dr Muraoka and his team theorised a link between bacterial localisation within the female reproductive tract and endometriosis- following promising research carried out on mice models. The Japanese study discovered a bacterium known as Fusobacterium to be present in the uteruses of 65% of women suffering from endometriosis, compared to less than 7% of women without the disease. Fusobacterium is a bacterium which is mostly found within the microbe of the mouth, gut and vagina. This bacterium has been linked to other inflammatory diseases such as gum disease. Follow-up studies- undertaken on mice- discovered that those treated with antibiotics saw a significant reduction in both size and frequency of lesions associated with the disease. Clinical trials are now forging ahead to investigate the effects of antimicrobials as a viable treatment option for endometriosis patients. This revolutionary study is the first of its kind and could see patient disease management progress away from medieval invasive procedures and decades of pain. For more information on Dr Muraoka and his team's work check out his study . Written by Kellie Leonard Related articles: Underreporting of endometriosis / Are PCOS and endometriosis sisters? / Gynaecology Project Gallery

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