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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

Discussing Peto's Paradox Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why blue whales don't get cancer 14/07/25, 15:16 Last updated: Published: 16/10/23, 21:22 Discussing Peto's Paradox 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. Just over a month ago, an investigation of existing evidence on such mechanisms 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

An exploration of this genetic concept Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Delving into the world of chimeras 09/07/25, 14:03 Last updated: Published: 03/02/24, 11:13 An exploration of this genetic concept The term chimera has been borrowed from Greek mythology, transcending ancient tales to become a captivating concept within the fields of biology and genetics. In mythology, the chimera was a monstrous hybrid creature. However, in the biological context, a chimera refers to an organism with cells derived from two or more zygotes. While instances of natural chimerism exist within humans, researchers are pushing the boundaries of genetics via the intentional creation of chimeras, consequentially sparking debates and breakthroughs in various fields, spanning from medicine to agriculture. Despite the theory that every cell in the body should share identical genomes, chimeras challenge this notion. For example, the fusion of non-identical twin embryos in the womb is a way chimeras can emerge. While visible cues, such as heterochromia or varied skin tone patches, may provide subtle hints of its existence, often individuals with chimerism show no overt signs, making its prevalence uncertain. In cases where male and female cells coexist, abnormalities in reproductive organs may exist. Furthermore, advancements in genetic engineering and CRISPR genome editing have also allowed the artificial creation of chimeras, which may aid medical research and treatments. In 2021, the first human-monkey chimera embryo was created in China to investigate ways of using animals to grow human organs for transplants. The organs could be genetically matched by taking the recipient’s cells and reprogramming them into stem cells. However, the process of creating a chimera can be challenging and inefficient. This was shown when researchers from the Salk Institute in California tried to grow the first embryos containing cells from humans and pigs. From 2,075 implanted embryos, only 186 developed up to the 28-day time limit for the project. Chimeras are not exclusive to the animal kingdom; plants exhibit this genetic complexity as well. The first non-fictional chimera, the “Bizzaria” discovered by a Florentine gardener in the seventeenth century, arose from the graft junction between sour orange and citron. Initially thought to be an asexual hybrid formed from cellular fusion, later analyses revealed it to be a chimera, a mix of cells from both donors. This pivotal discovery in the early twentieth century marked a turning point, shaping our understanding of chimeras as unique biological phenomena. Chimera is a common form of variegation, with parts of the leaf appearing to be green and other parts white. This is because the white or yellow portions of the leaf lack the green pigment chlorophyll, which can be traced to layers in the meristem (areas found at the root and shoot tip that have active cell division) that are either genetically capable or incapable of making chlorophyll. As we conclude this exploration into the world of chimeras, from the mythological realm to the scientific frontier, it’s evident that these entities continue to mystify and inspire, broadening our understanding of genetics, development, and the interconnectedness of organisms. Whether natural wonders or products of intentional creation, chimeras beckon further exploration, promising a deeper comprehension of the fundamental principles that govern the tapestry of life. Written by Maya El Toukhy Related article: Micro-chimerism and George Floyd's death Project Gallery

Its significant role in immunity Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The mast cell 14/07/25, 14:57 Last updated: Published: 05/08/23, 09:55 Its significant role in immunity The mast cell The mast cell is the first white blood cell to respond to infection or injury; they are located in many connective tissues throughout the body, especially in areas that introduce foreign bodies such as the gastrointestinal tract, respiratory epithelium and the skin. Mast cells are a crucial part in adaptive and innate immunity- in response to pathogens, allergens and toxin exposure they release chemicals and recruit other immune cells. They are created from pluripotent progenitor cells of myeloid lineages; these cells differentiate due to exposure and influence of stem cell factors. There are two types of mast cells in the human body, the first is called TC mast cells and contains tryptase, proteases and chymotryptic proteinase, the second is know as a T mast cell which contains only tryptase. The two types of mast cells are mucosal and connective tissue mast cells: mucosal mast cell are found mostly in the respiratory tract and the gut. Mast cells are found in three forms, granulated, spreading and intact. Intact mast cells lay in the epithelial tissue, the less common spreading mast cells are found in the connective tissues, and granulated mast cells are those which have released their mediators. These mediators reside in the cytoplasm of the mast cell- these include tryptases, heparin, histamine, cytokines, chymase, leukotrienes, TNF- alpha and many more. Mast cells are coated in IgE antibodies that crosslink (bind) to allergen proteins, which ultimately triggers degranulation. Mast cell disorders Abnormal growth of mast cells leads to a variety of issues. Mast cell activation syndrome in its primary state is caused by mast cell clone overproduction resulting in mastocytosis. This can lead to hives, gastric symptoms, and anaphylaxis. In some cases aggressive mastocytosis can lead to death. Cutaneous mastocytosis causes redden lesions of the skin and is most common in infants; systemic mastocytosis is most common in adults, led by the accumulation of mast cells in the intestines, organs, and bone marrow. Systemic mastocytosis includes the rare leukaemia and sarcoma forms. Mast cell activation syndrome in its secondary state is in an IgE -mediated hypersensitive response to external factors, that contributes to the release of pro-inflammatory cytokines and increases blood flow. However, it is too abundant, as the mast cells trigger far more granulation than that which is required. Idopathic mast cell activation is severe responses to the exposure of pathogens, toxins and other triggers. In idiopathic mast cell activation many patients can develop anaphylactic allergic reactions, which can present as difficulty breathing, swelling and hives. Conclusion Mast cells play a crucial role in biological defence and are derived from stem cells in the bone marrow. They come in different forms and locations, delivering an efficient response to injury and infection. When unregulated, they can lead to the development of disorders- ranging from mild rashes to severe anaphylaxis. Written by Lauren Kelly Project Gallery

Unlocking the secrets to gut health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The power of probiotics 14/07/25, 14:59 Last updated: Published: 18/08/23, 19:58 Unlocking the secrets to gut health What are probiotics? Probiotics are dietary supplements that consist of live cultures of bacteria or yeast. In the human body, more precisely in the microbiome, there are about 4 trillion bacteria, which include almost 450 species. These bacteria are necessary for the proper functioning of the entire body, especially the intestines and digestive system. In probiotics, bacteria from the Lactobacillus and Bifidobacterium families are most often used, as well as yeasts such as Saccharomyces cerevisiae. How probiotics work? Probiotics have a wide range of effects on our body. Their main task is to strengthen immunity and improve the condition of the digestive tract. This is because microorganisms produce natural antibodies, and also constitute a kind of protective barrier that does not allow factors conducive to infection to our intestine. Types of probiotics Most often, lactic acid bacteria of the genera Lactobacillus and Bifidobacterium are used as probiotics, but some species of Escherichia and Bacillus bacteria and the yeast Saccharomyces cerevisiae boulardi also have pro-health properties. Probiotics for your gut health The composition of our bacterial flora in the intestines determines the proper functioning of the digestive and immune systems. Probiotics have a positive effect primarily on the intestinal flora. They speed up metabolism and lower bad cholesterol (LDL). Live cultures of bacteria protect our digestive system. They improve digestion, regulate intestinal peristalsis, and prevent diarrhoea. They also increase the nutritional value of products - they facilitate the absorption of minerals such as magnesium and iron as well as vitamins from group B and K. In addition, probiotics strengthen immunity and protect us from infections caused by pathogenic bacteria. Therefore, it is very important to take as many probiotics as possible during and after antibiotic treatment. They will then regenerate the intestinal flora damaged by antibiotic therapy and reduce inflammation. Main benefits · facilitate the digestive process · increase the absorption of vitamins and minerals · during antibiotic treatments, they protect our intestinal microflora · affect the immune system by increasing resistance to infections · some strains have anti-allergic and anti-cancer properties · lower cholesterol · relieve the symptoms of lactose intolerance · ability to synthesize some B vitamins, vitamin K, folic acid Written by Aleksandra Zurowska Related articles: The gut microbiome / Vitamins / Interplay of hormones and microbiome Project Gallery

Understanding what goes wrong in the brain Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Epilepsy 101 29/04/25, 16:10 Last updated: Published: 09/10/24, 11:32 Understanding what goes wrong in the brain Epilepsy is a condition that affects millions of people worldwide, often causing unprovoked seizures due to irregular brain activity. But what exactly happens in the brain when someone has epilepsy? It is important to establish that not everyone with seizures has epilepsy. While epilepsy can start at any age, it often begins in childhood, or in people over the age of 60. Epilepsy can be due to genetic factors - 1 in 3 people with epilepsy have family history- or brain damage from causes like stroke, infection, severe head injury or a brain tumour. However, around half of epilepsy cases have an unknown cause. Now, imagine your brain as a big city with lots of lights. Each light represents a part of your brain that controls things like movement, feelings, and thoughts. Epilepsy is like when the lights in the city start flickering or shut completely. There are three main types of epilepsy, and each affects the lights in different ways: 1) Generalized epilepsy: when all the lights in the city flicker or go out at once, affecting the whole brain. There are two main kinds: Generalized Motor (Grand Mal) Seizures: Imagine the lights in the city going wild, making everything shake. This is like the shaking or jerking movements during myoclonic or tonic-clonic seizures. Generalized Non-Motor (Absence) Seizures: Picture the lights suddenly pausing, making everything freeze. During these seizures, a person might stare into space or make small, repeated movements, like lip-smacking. 2) Focal epilepsy: when only the lights in one part of the city flicker or go out. This means only one part of the brain is affected: Focal Aware Seizures: The lights flicker, but people in that part of the city know what’s happening. The person stays aware during the seizure. Focal Impaired Awareness Seizures: The lights flicker, and people lose track of what’s going on. The person might not remember the seizure. Focal Motor Seizures: Some lights flicker, causing strange movements, like twitching, rubbing hands, or walking around. Focal Non-Motor Seizures: The lights stay on, but everything feels strange, like sudden change in mood or temperature. The person might feel odd sensations without moving in unusual ways. 3) ‘Unknown’ epilepsy: ‘Unknown’ epilepsy is like a power outage where no one knows where it happened because the person was alone or asleep during the seizure. Doctors might later figure out if it's more like generalized or focal epilepsy. Some people can even have both types. But how do doctors find out if someone has epilepsy? A range of tests could be used to look at the brain’s activity and structure, including: Electroencephalogram (EEG): detects abnormal electrical activities in the brain using electrodes. This procedure can be utilised in Stereoelectroencephalography (SEEG), a more invasive method where the electrodes are placed directly on or within the brain to locate the abnormal electrical activities more precisely. Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI): form images of the brain to detect abnormal brain structures such as brain scarring, tumours or damage that may cause seizures. Blood tests: test for genetic or metabolic disorders, or health conditions such as anaemia, infections or diabetes that can trigger seizures. Magnetoencephalogram (MEG): measures magnetic signals generated by nerve cells to identify the specific area where seizures are starting, to diagnose focal epilepsy. Positron emission tomography (PET): detects biochemical changes in the brain, detecting regions of the brain with lower-than-normal metabolism linked to seizures. Single-photon emission computed tomography (SPECT): identifies seizure focus by measuring changes in blood flow in the brain during or between seizures, using a tracer injected into the patient. The seizure focus in this scan is seen by an increase in blood flow to that region. So, how does epilepsy affect the brain? For most people, especially those with infrequent or primarily generalised seizures, cognitive issues are less likely compared to those with focal seizures, particularly in the temporal lobe. The following cognitive functions can be affected: Memory : seizures can disrupt the hippocampus in the temporal lobe, responsible for storing and receiving new information. This can lead to difficulties in remembering words, concepts, names and other information. Language : seizures can affect areas of the brain responsible for speaking, understanding and storing words, which can lead to difficulties in finding familiar words. Executive function: seizures can impact the frontal lobe of the brain which is responsible for planning, decision making and social behaviour, leading to challenges in interacting, organising thoughts and controlling unwanted behaviour. While epilepsy itself cannot be cured, treatments exist to control seizures including: Anti-Epileptic Drugs (AEDs): suppress the brain’s ability of sending abnormal electrical signals - effective in 70% of patients. Diet: ketogenic diets can reduce seizures in some medication- resistant epilepsies and in children as they alter the chemical activity in the brain. Surgery: 1) Resective Surgery: removal of the part of the brain causing the seizures, such as temporal lobe resection, mainly for focal epilepsy. 2) Disconnective Surgery: cutting the connections between the nerves through which the seizure signals travel in the brain, such as in corpus callosotomy, mainly for generalised epilepsy. 3) Neurostimulation device implantation (NDI): insertion of devices in the body to control seizures by stimulating brain regions to control the electrical impulses causing the seizures. This includes vagus nerve stimulation and Deep Brain Stimulation (DBS). Even though epilepsy can be challenging, many people manage it successfully with the right treatment. Continued research offers hope for even better, long lasting treatments in the future. Written by Hanin Salem Related articles: Different types of epilepsy seizures / Alzheimer's disease / Parkinson's disease / Autism REFERENCES D’Arrigo, T. (n.d.). What Are the Types of Epilepsy? [online] WebMD. Available at: https://www.webmd.com/epilepsy/types-epilepsy [Accessed 5 Aug. 2024]. Epilepsy Foundation. (n.d.). Thinking and Memory. [online] Available at: https://www.epilepsy.com/complications-risks/thinking-and-memory [Accessed 10 Aug. 2024]. GOSH Hospital site. (n.d.). Invasive EEG monitoring. [online] Available at: https://www.gosh.nhs.uk/conditions-and-treatments/procedures-and- treatments/invasive-monitoring/ [Accessed 9 Aug. 2024]. My Epilepsy Team.com. (2016). Epilepsy: What People Don’t See (Infographic) | MyEpilepsyTeam. [online] Available at: https://www.myepilepsyteam.com/resources/epilepsy-what-people-dont-see- infographic [Accessed 29 Aug. 2024]. National institute of Neurological Disorders and stroke (2023). Epilepsy and Seizures | National Institute of Neurological Disorders and Stroke. [online] www.ninds.nih.gov . Available at: https://www.ninds.nih.gov/health- information/disorders/epilepsy-and-seizures [Accessed 10 Aug. 2024]. NHS (2020). Epilepsy. [online] NHS. Available at: https://www.nhs.uk/conditions/epilepsy/ [Accessed 10 Aug. 2024]. Project Gallery

A life of neurology and literature Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Oliver Sacks 10/07/25, 10:26 Last updated: Published: 21/01/24, 11:54 A life of neurology and literature If I had to credit one person for introducing me to the subject that would become my career choice, it would be Oliver Sacks. Trying to develop my interests and finding myself in a world of science textbooks that sounded too complicated – and often simply pedantic – made me desperate to find something that could somehow combine my love for science and my fondness for literature. Luckily, I managed to stumble upon “the poet laureate of literature”, a physician who presented real characters with true medical cases without putting a teenage girl to sleep. Oliver Wolf Sacks was born in London in 1933. He grew up in a family of doctors; his mother was one of the first female surgeons in England and his father, a general practitioner. His interest in science started at a young age, experimenting with his home chemistry set. Following in his parents’ footsteps, he went on to study medicine at The University of Oxford before moving to the US for residency opportunities in San Francisco and Los Angeles. Although he enjoyed the sweeter life on the West Coast, by 1965 he decided to take a more permanent residence in New York, where he continued to work as a neurologist as well as eventually teaching at Columbia and NYU. It was in the city of dreams where he started his literary journey. One of his main creative inspirations was born from his time as a consultant neurologist at Beth Abraham Hospital in the Bronx. There, he found a group of patients who had been in a catatonic state due to encephalitis lethargica. They appeared frozen, trapped in their own bodies, unable to come out. Sacks decided to start a series of trials with L-Dopa, a dopamine precursor drug which was then still in the experimental stage as a treatment for Parkinson’s. Almost miraculously, some of the patients started “waking up” and regaining some movement ability. Although the treatment was not without flaws, the satisfaction of helping his patients and the close relationships he came to develop with them after caring for them for months really touched Sacks. In 1973, he published his narration of the events in Awakenings , a bestseller that was later adapted into a film of the same name starring Robin Williams and Robert de Niro. Oliver Sacks went on to write about music therapy, a rare community of colourblind individuals and his own experience both as a doctor and as a patient, among others. His most notable works are probably “The Man Who Mistook His Wife for a Hat” and “An Anthropologist on Mars”. Both describe in detail fascinating case studies, ranging from more known conditions such as Parkinson’s, epilepsy and schizophrenia, to other relatively more obscure diagnoses at the time including Tourette’s, musical hallucinations and autism. The condition that took my attention the most when reading “The Man Who Mistook His Wife for a Hat” was that which gives the book its title. The man who could not tell apart his hat from his spouse was diagnosed with agnosia: the inability to recognise objects, people or animals as a result of neurological damage along pathways connecting primary sensory areas. Agnosia can affect visual, auditory, tactile or facial recognition (prosopagnosia), or a combination of these. Crucially, Sacks’s works showcase not only a recount of symptoms and abnormalities, but a tale of people who retained their humanity and individuality beyond their medical diagnoses. As he told People magazine in 1986, he loved to discover potential in people who weren’t thought to have any. Instead of merely fitting patients into disease, he liked. To observe how they experienced the world in their unique ways, recognising difference as a path to resilience rather than just a handicap. Written by Julia Ruiz Rua Project Gallery

The mechanisms of the disease Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Alzheimer's disease 09/07/25, 10:46 Last updated: Published: 21/07/23, 09:36 The mechanisms of the disease Introduction to Alzheimer’s disease Alzheimer’s disease is a neurodegenerative disease that results in cognitive decline and dementia with increasing age, environmental and genetic factors contributing to its onset. Scientists believe this is the result of protein biomarkers that build-up in the brain and accumulate within neurones. As of 2020, 55 million people suffer with dementia, with Alzheimer’s being a leading cause. Thus, it is crucial we develop efficacious treatments, with final adverse effects. A new drug called Iecanemab, may be the key to a new era of Alzheimer’s treatment… The disease is most common in people over 65, with 1/14 affected in the UK, thus, there is a huge emphasis on defining the disorder and developing drug treatments. The condition results in difficulty with memory, planning, decision making and can result in co-morbidities such as depression or personality change. This short article will explain the pathology of the disorder and the genetic predispositions for its onset. It will also explore future avenues for treatment, such as the drug I ecanemab that may provide, “a new era for Alzheimer’s disease”. Pathology and molecular aspects The neurodegeneration seen in Alzheimer’s has, as far, been associated protein dispositions in the brain, such as the amyloid precursor protein (APP) and Tau tangles. This has been deduced by PET scans and post-mortem study. APP, located on chromosome 21, is responsible for synapse formation and signalling. It is cleaved to b-amyloid peptides by enzymes called secretases, but overexpression of both these factors can be neurotoxic (figure 1). The result is accumulation of protein aggregates called beta-amyloid plaques in neurons, impairing their survival. This deposition starts in the temporo-basal and front-medial areas of the brain and spreads to the neocortex and sensory-motor cortex. Thus, many pathways are affected, resulting in the characteristic cognitive decline. Tau proteins support nerve cells structurally and can be phosphorylated at various regions, changing the interactions they have with surrounding cellular components. Hyperphosphorylation of these proteins result in the Tau pathology in the form of tau oligomer (short peptides) that is toxic to neurons. These enter the limbic regions and neocortex. It is not clearly defined which protein aggregate proceeds the other, however, the amyloid cascade hypothesis suggests that b-amyloid plaque pathology comes first. It is speculated that b-amyloid accumulation leads to activation of the brain’s immune response, the microglial cells, which then promotes the hyperphosphorylation of Tau. Sometimes, there is a large release of pro-inflammatory cytokines, known as a cytokine storm, that promotes neuroinflammation. This is common amongst older individuals, due to a “worn-out” immune system, which may in part explain Alzheimer’s disease. Genetic component to Alzheimer’s disease There is strong evidence obtained through whole genome-sequencing studies (WGS), that suggests there is a genetic element to the disease. One gene is the Apoliprotein E (APOE) gene, responsible for b-amyloid clearance/metabolism. Some alleles of this gene show association with faulty clearance, leading to the characteristic b-amyloid build-up. In the body, proteins are made consistently depending on need, a dysregulation of the recycling process can be catastrophic for the cells involved. PSEN1 gene that codes for the presenilin 1 protein, part of a secretase enzyme complex. As mentioned, the secretase enzyme is responsible for the cleavage of APP, the precursor for b-amyloid. Variants of this gene have been associated with early onset Alzheimer’s disease, due to APP processing being altered to produce a longer form of the b-amyloid plaque. The genetic aspects to Alzheimer’s disease are not limited to these genes, and in actuality, one gene can have an assortment of mutation that results in a faulty protein. Understanding the genetic aspects, may provide avenue for gene therapy in the future. Treatment Understanding the point in which the “system goes wrong” is crucial for directing treatment. For example, we may use secretase inhibitors to reduce the rate of plaque formation. An example of this is the g- secretase BACE1 inhibitor. There is a need for this drug-type to be more selective to its target, as has been found to produce unwanted adverse effects. A more selective approach may be to target the patient’s immune system with the use of monoclonal antibodies (mAb). This means designing an antibody that recognises a specific component, such as the b-amyloid plaque, so it may bind and then encourage immune cells to target the plaque (figure 3). An example is Aducanumab mAb, which targets b-amyloid as fibrils and oligomers. The Emerge study demonstrated a decrease in amyloid by the end of the 78-week study. As of June 2021, Aducanumab received approval from the FDA for prescription of this drug, but this is controversial as there are claims it brings no clinical benefit to the patient. The future of Alzheimer’s disease Of note, drug development and approval is a slow process, and there must be a funding source in order to carry out plans. Thus, particularly in Alzheimer’s, it is relevant to educate the public and funding bodies to supply the financial support to the process. However, with many hits (potential drug candidates), these often fail at phase III clinical trials. Despite this, another mAb, lecanemab, has recently been approved by the FDA (2023), due to its ability to slow cognitive decline by 27% in early Alzheimer’s disease. The Clarity AD study on Iecanemab, found the drug benefited memory and thinking, but also allowed for better performance of daily tasks. This drug is currently being prescribed on a double-blind basis, meaning a patient may either receive the drug or the placebo. This study shows a hope for those suffering from the disease. Drugs that have targeted the Tau tangles, have as far, not been successful in clinical trials. However, the future of Alzheimer’s treatment may be in the combination therapy directed to both Tau protein and b-amyloid. Washington universities neurology department have launched a trial known as Tau NextGen, in which participants will receive both Iecanemab and tau-reducing antibody. Conclusion This article provides a summary to what we know about Alzheimer’s disease and the potential treatments of the future. Overall, the future of Alzheimer’s treatment lies in the combination therapy to target known biomarkers of the disease. Written by Holly Kitley Related articles: CRISPR-Cas9 as Alzheimer's treatment / Hallmarks of Alzheimer's / Sleep and memory loss Project Gallery

The closest planet to the Sun Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Exploring the solar system: Mercury 09/07/25, 14:08 Last updated: Published: 27/06/23, 15:46 The closest planet to the Sun Mercury, the closest planet to the Sun, holds a significant place in our understanding of the solar system and serves as our first stepping stone in the exploration of the cosmos. Its intriguing history dates back to ancient times when it was studied and recorded by the Babylonians in their celestial charts. Around 350 BC the ancient Greeks, recognized that the celestial body known as the evening and morning star was, in fact, a single entity. Impressed by its swift movement, they named it Hermes, after the swift messenger of their mythology. As time passed, the Roman Empire adopted the Greek discovery and bestowed upon it the name of their equivalent messenger god, Mercury, a name by which the planet is known today. This ancient recognition of Mercury's uniqueness paved the way for our continued exploration and study of this fascinating planet. Mercury's evolution As Mercury formed from the primordial cloud of gas and dust known as the solar nebula, it went through a process called accretion. Small particles collided and gradually merged together, forming larger bodies called planetesimals. Over time, these planetesimals grew in size through further collisions and gravitational attraction, eventually forming the protoplanet that would become Mercury. However, the proximity to the Sun presented unique challenges for Mercury's formation. The Sun emitted intense heat and powerful solar winds that swept away much of the planet's initial atmosphere and surface materials. This process, known as solar stripping or solar ablation, left behind a relatively thin and tenuous atmosphere compared to other planets in the solar system. The intense heat also played a crucial role in shaping Mercury's surface. The planet's surface rocks melted and differentiated, with denser materials sinking towards the core while lighter materials rose to the surface. This process created a large iron-rich core, accounting for about 70% of the planet's radius. Mercury's lack of significant geological activity, such as plate tectonics, has allowed its surface to retain ancient features and provide insights into the early history of our solar system. The planet's surface is dominated by impact craters, much like the Moon. These craters are the result of countless collisions with asteroids and comets over billions of years. The largest and most prominent impact feature on Mercury is the Caloris Basin, a vast impact crater approximately 1,525 kilometres in diameter. The impact of such large celestial bodies created shockwaves and volcanic activity, leaving behind a scarred and rugged terrain. Scientists estimate that the period known as the Late Heavy Bombardment, which occurred around 3.8 to 4.1 billion years ago, was particularly tumultuous for Mercury. During this time, the inner planets of our solar system experienced a high frequency of cosmic collisions. These impacts not only shaped Mercury's surface but also influenced the evolution of other rocky planets like Earth and Mars. Studying Mercury's geology and surface features provides valuable insights into the early stages of planetary formation and the impact history of our solar system. Exploration history Our understanding of Mercury has greatly benefited from a series of pioneering missions that ventured close to the planet and provided valuable insights into its characteristics. Let's delve into the details of these key exploratory endeavours: Mariner 10 (1974-1975): Launched by NASA, Mariner 10 was the first spacecraft to conduct a close-up exploration of Mercury. It embarked on a series of three flybys, passing by the planet in 1974 and 1975. Mariner 10 captured images of approximately 45% of Mercury's surface, revealing its heavily cratered terrain. The spacecraft's observations provided crucial information about the planet's rotation period, which was found to be approximately 59 Earth days. Mariner 10 also discovered that Mercury possessed a magnetic field, albeit weaker than Earth's. MESSENGER (2004-2015): The MESSENGER mission, short for Mercury Surface, Space Environment, Geochemistry, and Ranging, was launched by NASA in 2004. It became the first spacecraft to enter into orbit around Mercury in 2011, marking a significant milestone in the exploration of the planet. Over the course of more than four years, MESSENGER conducted an extensive study of Mercury's surface and environment. It captured detailed images of previously unseen regions, revealing the planet's diverse geological features, including vast volcanic plains and cliffs. MESSENGER's data also indicated the presence of water ice in permanently shadowed craters near Mercury's poles, surprising scientists. Furthermore, the mission discovered that Mercury possessed a global magnetic field, challenging previous assumptions about the planet's magnetism. MESSENGER's observations greatly expanded our knowledge of Mercury's geology, composition, and magnetic properties. BepiColombo (2018-Present): The BepiColombo mission, a joint endeavour between the European Space Agency (ESA) and the Japan Aerospace Exploration Agency (JAXA), aims to further enhance our understanding of Mercury. The mission consists of two separate orbiters: the Mercury Planetary Orbiter (MPO) developed by ESA and the Mercury Magnetospheric Orbiter (MMO) developed by JAXA. Launched in 2018, BepiColombo is currently on its journey to Mercury, with an expected arrival in 2025. Once there, the mission will study various aspects of the planet, including its magnetic field, interior structure, and surface composition. The comprehensive data collected by BepiColombo's orbiters will contribute significantly to our knowledge of Mercury and help answer remaining questions about its formation and evolution. These missions have played pivotal roles in advancing our understanding of Mercury. They have provided unprecedented insights into the planet's surface features, composition, magnetic field, and geological history. As exploration efforts continue, we can anticipate further revelations and a deeper understanding of this intriguing world. Future exploration While significant advancements have been made in understanding Mercury, there is still much more to learn. Scientists hope to explore areas of the planet that have not yet been observed up close, such as the north pole and regions where water ice may be present. They also aim to study Mercury's thin atmosphere, which consists of atoms blasted off the surface by the solar wind. Moreover, the advancement of technology may lead to the development of innovative missions to Mercury. Concepts such as landing missions and even manned exploration have been proposed, although the challenges associated with the planet's extreme environment and proximity to the Sun make such endeavours highly demanding. Nevertheless, the quest to unravel Mercury's mysteries continues, driven by the desire to deepen our knowledge of planetary formation, evolution, and the unique conditions that shaped this enigmatic world. Exploring the uncharted areas of Mercury, particularly the north pole, holds great scientific potential. The presence of water ice in permanently shadowed regions has been suggested by previous observations, and investigating these areas up close could provide valuable insights into the planet's volatile history and the potential for water resources. Additionally, studying Mercury's thin atmosphere is of significant interest. Comprised mostly of atoms blasted off the surface by the intense solar wind, understanding the composition and dynamics of this atmosphere could shed light on the processes that shape Mercury's exosphere. In conclusion, while significant progress has been made in unravelling the mysteries of Mercury, there is still much to explore and discover. Scientists aspire to investigate untouched regions, study the planet's thin atmosphere, and employ innovative mission concepts. The future may hold ambitious missions, including landing missions and potentially even manned exploration. As our knowledge and capabilities expand, Mercury continues to beckon us with its fascinating secrets, urging us to push the boundaries of exploration and expand our understanding of the wonders of the solar system. And with that we finish our journey into the history and exploration of Mercury and will move to Venus in the next article. Written by Zari Syed Related articles: Fuel for the colonisation of Mars / Nuclear fusion Project Gallery

The different models of health and disease Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Beyond medicine: understanding health through various stances 16/10/25, 10:21 Last updated: Published: 22/04/24, 10:24 The different models of health and disease Introduction Various models can show what factors produce health outcomes between individuals and populations. This article looks at the biomedical, social, humanistic and biopsychosocial models, reviewing each through examples and its applications to the real world. With this said, every model has advantages and disadvantages because they are imperfect. Each one is essential as it provides a way to treat patients, so they need to be used alongside one another to address the different aspects involved in a person’s health. Biomedical model- figure 1 To start with the most familiar, the biomedical model looks at finding the cause of illness through a physiological perspective, i.e. finding malfunctions in organs and cells. For example, infections are caused by microorganisms, or metabolic disorders usually occur due to at least one critical genetic mutation. This model has some advantages, such as using evidence-based strategies to treat patients, and it has contributed to medical breakthroughs that have improved overall health. Also, it can lead to effective treatment plans through medical interventions to handle specific diseases. However, the biomedical model does not consider external factors involved in illness. Moreover, it focuses on curing diseases instead of preventative plans that may be more successful, and its recommendation of pharmaceutical drugs for certain conditions may cause addiction, which is another health problem. Social-ecological model- figure 2 Now, the social-ecological model considers societal factors, ranging from economic to political, that are influential in population health. It helps investigate non-communicable and infectious diseases. An advantage of this model is it emphasises preventative strategies, which can lead to long-term advancements in health. Moreover, it encourages cooperation within communities in shaping initiatives that benefit everyone and regards collaboration between multiple work sectors like education and law enforcement as vital to progressing society. A significant downside of the social model is that it is complicated, suggesting it is difficult to tackle all of these determinants of health effectively. In turn, allocating resources to resolve specific issues would take much work. Lastly, some detractors of this model believe it absolves people’s responsibility for their health. Humanistic model- figure 3 Subsequently, the humanistic model is about an individual’s wellbeing, experiences, and self-exploration. Its applications are mainly in psychology, though it can manifest in other areas of life through a person making decisions they are satisfied with. A few advantages of this model include prioritising a person’s autonomy, encouraging their psychological well-being, and facilitating collaboration between clinicians and patients in treatment. On the other hand, only some can think for themselves or their experiences; the model relies on subjectivity, so it can be challenging to measure parts of well-being, and it is more beneficial for chronic conditions than acute ailments. Biopyschosocial model- figure 4 The biopsychosocial (BPS) model includes biological, psychological and social factors related to a patient’s health. Therefore, it can be used for any individual with chronic or acute disease(s) and is used broadly in psychology between the psychiatrist/ counsellor and the patient. One advantage is that it aids primary care doctors in comprehending the interrelations between an illness's biological and psychosocial parts. In turn, this strengthens the patient-clinician relationship. Similar to the social model, this can promote preventative measures against diseases. However, the addition of biological and psychosocial factors makes the model complicated to implement in clinical contexts. Moreover, there needs to be more distinct guidelines for its use in treating patients compared to the biomedical model. Lastly, applying the biopsychosocial can change between healthcare practices, possibly leading to different standards of care. Conclusion Reflecting on the models outlined, the biopsychosocial model seems to be the perfect one compared to the others because it includes all of the models above or others not mentioned in this article. In turn, it succeeds in providing a balanced view of health. On the other hand, as iterated before, the BPS model has its disadvantages. Thus, it may require more refinements to be widely implemented across healthcare settings. Written by Sam Jarada Related articles: Key discoveries in public health / Healthcare challenges in Sudan / Conflicted Kashmir / Colonialism, geopolitics and health REFERENCES Leeper HE. Survivorship and Caregiver Issues in Neuro-oncology. Current Treatment Options in Oncology. 2019 Nov;20(11). Rocca E, Anjum RL. Complexity, Reductionism and the Biomedical Model. Rethinking Causality, Complexity and Evidence for the Unique Patient. 2020 Jun 3;1(1):75–94. Williams H. What Is the Biomedical Model? The Health Board. 2011. Golden TL, Wendel ML. Public Health’s Next Step in Advancing Equity: Re-evaluating Epistemological Assumptions to Move Social Determinants From Theory to Practice. Frontiers in Public Health. 2020 May 7;8. Isaacs P. A Humanistic Psychological Approach To Autism. Paul Isaacs’ Blog. 2017. Flow Psychology. 10 Humanistic Approach Strengths and Weaknesses | Flow Psychology. Flowpsychology.com . 2016. Hardie M. Three Aspects of Health and Healing: The Biopsychosocial Model in Medicine. Department of Surgery. 2021. Kusnanto H, Agustian D, Hilmanto D. Biopsychosocial model of illnesses in primary care: A hermeneutic literature review. Journal of Family Medicine and Primary Care. 2018 May;7(3):497–500. Project Gallery