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Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and the other sciences. Log In Welcome to Scientia News DELIVERING INFORMATIVE CONTENT Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and other sciences. We hope this platform helps you discover something that inspires your curiosity, and encourages you to learn more about important topics in STEM. Meet the Official Team NAVIGATE AND CLICK THE PHOTOS BELOW TO LEARN MORE ABOUT US! To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. Latest Articles biology Socioeconomic Health Inequalities View More ecology How human activity impacts the phosphorus cycle View More chemistry Not all chemists wear white coats: computational organic chemistry View More chemistry The importance of symmetry in chemistry View More CONTACT CONTACT US Scientia News welcomes anyone who wants to share their ideas and write for our platform. If you are interested in realising your writing potential with us AND live in the UK; and/ or would like to give feedback: Email us at scientianewsorg@gmail.com or fill in our GET IN TOUCH form below and we'll be in contact... Follow us on our socials for the latest updates. Comment, like and share! Join our mailing list below for latest site content. You can also sign up to become a site member . SUBSCRIPTION Join our mailing list to receive alerts for new articles and other site content. Be sure to check your spam/ junk folders in case emails are sent there. Email Subscribe GET IN TOUCH First Name Last Name Email Message Send Thanks for submitting!

Tesla’s vision was to develop wireless power across the globe Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nikola Tesla, wireless electricity, and the failure of Wardenclyffe Tower 10/07/25, 10:25 Last updated: Published: 04/09/24, 10:37 Tesla’s vision was to develop wireless power across the globe Nikola Tesla Nikola Tesla (1856-1943) was a Serbian-American engineer and one of the most brilliant inventors of his time. His discoveries on how to utilise alternating current laid the foundation for the industrial revolution and today makes up the majority of power distribution systems globally. Finding inspiration from his mother Duka Mandic, whom he called a first-class inventor and credited for passing on her gift of discovery*, he went on to make significant contributions to the development of X-ray technology, radio, and robotics, as well as inventing the brushless AC motor, the rotating magnetic field, neon lights, and remote control. However, despite his many revolutionary inventions and around 300 patents to his name, Tesla died poor and ultimately failed in his greatest pursuit: to develop a free system of clean, wireless, electric power. Wardenclyffe Tower, also known as the Tesla Tower, was the first step in Tesla’s ‘World Wireless System’, a system designed to wirelessly broadcast electrical power across the globe, based on 20th century knowledge of resonance, the earth’s conductivity, and the Tesla coil. The Tesla coil: working principle The Tesla coil, invented by Nikola Tesla in 1894, is an alternating current resonant transformer that produces a high voltage from a low current. The high voltage produces sparks of ‘lightning’ or electrical discharge which can power lightbulbs. This experiment was a key motivator for Tesla’s later works with Wardenclyffe, although today the main use of the Tesla coil is for filming, entertainment, and educational displays. In a typical transformer, the ratio of turns determines the output voltage. The resonant properties of the secondary coil in a Tesla coil allows the transformer to achieve much higher voltages. A high voltage power supply from the first transformer is applied to a small primary coil, creating a large magnetic field. Current flow through the primary coil charges up a capacitor until the voltage across it exceeds the breakdown voltage of the spark gap (air). The capacitor discharges through the secondary coil in the opposite direction. This reverse current flow induces a magnetic field around the primary coil in the opposite direction. The constant changing of field direction induces a current in the secondary coil and produces a voltage proportional to the winding ratio of the coils. The resulting high voltage produces arcs of electricity similar to lightning from the terminal (typically torus shaped to direct sparks outward and prevent interference). Despite the high voltage, these electric discharges only produce a very small current in people who interact with it because of the high impedance of the coil and are not dangerous unless a person has a pacemaker or other medical device that could be affected by the high voltages. The frequency of the current has little interaction with nerve cells. Wardenclyffe Tower Following the same principles as the small-scale Tesla coil, Tesla’s vision was to replicate this on a large scale to develop wireless power across the globe, so that information could be transmitted from one tower to another by resonance. His early design featured two towers placed next to each other, so that the gap between the two domes could act as a spark gap. After cost revisions, the tower was redesigned to feature the entire transmitter circuit in one tower (see Figure 2 ). Figure 3 shows Tesla’s plan for the World Wireless System. An oscillator tower stands at 187 feet with a large dome of conductive metals on top, and an iron root system 300 feet into the earth. When the tower and Tesla receivers are tuned to the same resonant frequency, Tesla theorised that energy could be efficiently transferred between them. After obtaining funding from financier J.P. Morgan, Wardenclyffe tower began construction in 1901 in Shoreham, New York. The 187-foot tower featured a large spherical terminal, which was intended to ionize the atmosphere and create a conductive path for the energy. Below ground, a network of metal rods and plates would transmit energy into the Earth, relying on the Earth’s conductivity to complete the circuit. The working of the tower fundamentally relied on two highly under-researched principles, which were: 1. Earth as a conductor : In 1899 before Tesla began work on Wardenclyffe, he studied the periodicity of lightning in Colorado Springs, USA, and discovered what he called earth resonance. He found that large electrical impulses travel longitudinally through the earth to the antipode and are reflected (i.e., ‘resonate’) creating terrestrial stationary waves. He planned to use the tower to send electrical energy through the ground, which would then be picked up by receivers located anywhere on the planet. 2. Air as a conductor: Although air is normally a good insulator, at high altitudes (the earth’s ionosphere) it becomes an excellent conductor of high frequencies and voltages. The tower was designed to generate extremely high-frequency alternating currents, however reaching the earth’s ionosphere would require an antenna of at least 15 miles tall. Tesla apparently discovered a way to bypass this but did not make his methods public. There was very little knowledge about these phenomena at the time and even today are still not fully validated. Why Wardenclyffe failed Tesla initially pitched the project to J.P. Morgan as a world system of wireless communication to send messages, reports, and secure military messages, and to broadcast news and music. Morgan invested around $150,000 which Tesla accepted and instead began working on wireless electricity transmission, despite the investment being far below a realistic sum for the cost of the project. As Wardenclyffe tower required frequent modifications to the tower’s design during construction as well as expensive materials, the project was very costly. At the same time, Guglielmo Marconi achieved his less ambitious and inexpensive aim of wirelessly communicating the letter ‘s’ in Morse code (using some of Tesla’s patents). Combined with the Panic of 1907 and realising Tesla’s primary aim was for electricity to be free worldwide, which would be difficult to monetise, J.P. Morgan withdrew financial support and Tesla was forced to abandon the project. The scientific community and further potential investors were also sceptical about the feasibility of wireless energy transmission particularly considering energy losses over long distances, which made it difficult to obtain further funding. At the same time as Wardenclyffe Tower was being developed, Tesla’s AC power distribution system was being implemented rapidly. The established infrastructure of wired electricity transmission made it even more difficult for Tesla's wireless system to gain traction and funding, and the tower was demolished in 1917 to satisfy Tesla’s debts. Conclusion Wardenclyffe tower was an ambitious and audacious project which ultimately was not financially feasible. Even with modern day technology, efficiency, safety, and economic considerations prevent the system being a practical reality. Nevertheless, Tesla was undeniably an ingenious inventor, and his futuristic and daring approach to engineering continues to inspire innovations as well as debate. Today the site of Wardenclyffe tower is home to the Tesla Science Centre, a memorial to Tesla’s life and work. Footnotes * A highly skilled and intelligent woman despite no formal education, she invented various household tools and devices like the loom and egg whisk. Written by Varuna Ganeshamoorthy Related articles: Transformers / Mobile networks / Electricity in the body REFERENCE Tesla, N., & Johnston, B. (1982). My inventions: the autobiography of Nikola Tesla. 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

Total solar eclipses Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Totality- Our Perfect Eclipse 14/07/25, 15:05 Last updated: Published: 24/05/23, 10:05 Total solar eclipses We are all familiar with the characteristic depiction of a solar eclipse, when the Moon passes directly between the Sun and the Earth. However, the significance of solar eclipses extends far beyond their aesthetic appeal. Major scientific discoveries, cultural practices, and even the behaviour of wild animals are derived from total solar eclipses that we have the privilege of experiencing (See image 1). A solar eclipse occurs when the Earth, Moon, and Sun all appear to lie on a straight line. They are collinear. Total solar eclipses occur when the Moon completely obscures the Sun's photosphere, enabling prominences and coronal filaments to be seen along the limb. This phenomenon is unique to the Earth, Sun, and Moon system and to understand why we must explore the mathematics underlying these ‘orbital gymnastics’. We wish to compare the ‘apparent’ size of the Sun and Moon, a quantity proportional to the ratio of their size and distance from Earth. The Moon has a radius of around 3,400 km, and is approximately 384,000 km from Earth. The Sun has a much larger radius of 1.4 million km, and is located at a distance of 150 million km. By dividing the Sun's radius by the Moon's radius and dividing the Earth-Sun distance by the Earth-Moon distance, we can determine that the Sun is 400 times larger than the Moon and 400 times further away. This unique relationship allows for total solar eclipses, where totality indicates **the complete blocking of sunlight from the Sun’s disk by the Moon. In partial eclipses, only part of the Sun is obscured. One might wonder why we don’t have total solar eclipses every month, and the reason is that the plane of the Moon’s orbit around Earth is tilted at 5 degrees relative to Earth’s orbital plane. This hugely decreases the likelihood of such perfect alignment. Of the hundreds of moons orbiting planets in our Solar System, only our Moon totally eclipses the Sun. For example, none of Jupiter’s 95 moons have the correct size and orbital separation that completely block out the Sun from any point on Jupiter’s surface! Surely this serendipitous interplay of Earth, Sun, and Moon cannot be a coincidence? (See image 2) It is at this point where divine intervention is typically invoked. There are a few problems with doing this. The Moon's eccentric orbit around Earth means that it will be closer during some total solar eclipses than others, resulting in annular eclipses when the Moon is furthest from Earth. Additionally, the Moon is receding from the Earth at a rate of 4 cm/year, which means that total solar eclipses will only be observable for another 250 million years. (See image 3) For those of you who wish to make the most of this brief window of opportunity, this website shows the dates and locations of upcoming total solar eclipses. Written by Joseph Brennan REFERENCE Guillermo Gonzalez, Wonderful eclipses, Astronomy & Geophysics , Volume 40, Issue 3, June 1999, Pages 3.18–3.20, https://doi.org/10.1093/astrog/40.3.3.18 Project Gallery

Properties of space Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Topology in action 17/02/25, 14:51 Last updated: Published: 29/09/23, 20:09 Properties of space Let’s say I put a sphere in front of you. I’m sure you could go through and tell me the basic facts and formulas surrounding it, many if which containing Pi. And even better, if you were a bit more fluent in maths, you could go further and start telling me about the geometry of the shape, say how the gradient had to disappear at a certain point or an assortment of many other things. But if we dive a little deeper into pure maths, it starts getting a little more complicated. When labels like Hausdorff get casually thrown about (meaning you can always separate two distinct points with an open boundary, which you certainly can do on a sphere!) it can really build up and become quite hard, especially if someone then puts in front of you two spheres stuck together. This is where the study of topology comes in and starts helping out, allowing us to start to categorise certain spaces without having to worry about all the small details that could catch you out. Topology is certainly found in the purer side of maths, generally seen as one of the more abstract modules to be taking at undergraduate level (as seen by the exam scores). But thinking of it just as some far away concept disconnected with the rest of the world would be foolish. Thinking back to what I said before about gradient fields on a sphere, this is more commonly known in maths as the “Hairy Ball Theorem” named as such as if you had a ball of hair, you wouldn’t be able to smooth it all out without a cow’s lick. And in mathematical terms it means that a continuous vector field has to disappear at a certain point. And maybe not readily apparent but this comes up in loads of places, the most obvious of which is that two points on the Earth will always have the exact temperature! But moving to Biology we see a lot more applications, even as early as in A-level study. Just thinking about how a protein will fold is all to do with the topological properties of them. DNA is a bit more complex understandably, with more base pairs it becomes incredibly flexible, able to bend into many shapes, but like topological spaces this flexible has limits. It doesn’t pass through itself nor tear, so it allows us to start applying our theorems to it. A key one of these is Knot theory, which of course is the study of knots. Knots in maths are defined as having no open ends and being complex, which helpfully is exactly like DNA! As you hopefully know, its coiled form has no open ends, and in order to untangle it we have to go through the process of cutting at double points. The amount of times this is needed to untangle is called the 'unknotting number' in topology and this mathematical modelling of the process allows biologists to move away from the microscope and still get a more accurate look on what’s happening. Written by Tom Murphy Related article: Quantum chemistry Project Gallery

Molecular gastronomy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Exploring food at a molecular level 09/07/25, 14:07 Last updated: Published: 13/05/24, 14:46 Molecular gastronomy Imagine taking a bite of your favourite dish, not just savouring the flavours, but peering into the very essence of its existence. That's the realm of molecular gastronomy, a fascinating exploration of food through the lens of science. This article takes you on a journey at the microscopic level of what fuels the human body. The foundation of all food lies in macromolecules, large molecules formed from the intricate assembly of smaller ones. Carbohydrates, proteins, and lipids are the main players, each with unique structures and roles. Carbohydrates: These sugary giants, like starches and sugars, provide our bodies with energy. Imagine them as long chains of sugar molecules linked together, like beads on a necklace. Proteins: The workhorses of the cellular world, proteins are responsible for countless functions. They're built from amino acids, each with a distinct side chain, creating a diverse and essential cast of characters. Lipids: Fats and oils, these slippery molecules store energy and form cell membranes. Think of them as greasy chains with attached rings, like chubby tadpoles swimming in oil. The symphony of cooking and the final dance Applying heat, pressure, and chemical reactions, chefs become culinary alchemists at the molecular level. Water, the universal solvent, facilitates the movement and interaction of these molecules. As we cook, proteins unfold and rearrange, starches break into sugars, and fats melt and release flavours. Maillard Reaction: This browning phenomenon, responsible for the delicious crust and crunch on your food, arises from the dance between sugars and amino acids. Imagine them waltzing and exchanging partners, creating new flavorful molecules that paint your food with golden hues. Emulsification: Oil and water don't mix, but lecithin, a molecule found in egg yolks, acts as a matchmaker. It bridges the gap between these unlikely partners, allowing for the creation of creamy sauces and fluffy cakes. Think of lecithin as a tiny cupid, shooting arrows of attraction between oil and water droplets. Saponification: Techniques like spherification use alginate and calcium to create edible spheres filled with liquid, transforming into playful pearls that burst with flavor in your mouth. A world of potential Understanding food at the molecular level unlocks a treasure trove of possibilities. It can help us create healthier, more sustainable food choices, develop personalized nutrition plans, and even combat food-borne illnesses. By peering into the microscopic world of our meals, we gain a deeper appreciation for the magic that happens on our plates, bite after delicious bite. So next time you savor a meal, remember the intricate dance of molecules that brought it to life. From the building blocks of carbohydrates to the symphony of cooking, food is a story written in the language of chemistry, waiting to be deciphered and enjoyed. Written by Navnidhi Sharma Related articles: Emotional chemistry on a molecular level / Food prices and malnutrition / Vitamins References and further readings: Chapter 2: Protein structure . (2019, July 10). Chemistry. https://wou.edu/chemistry/courses/online-chemistry-textbooks/ch450-and-ch451-biochemistry-d efining-life-at-the-molecular-level/chapter-2-protein-structure/ Gan, J., Siegel, J. B., & German, J. B. (2019). Molecular annotation of food - Towards personalized diet and precision health. Trends in Food Science & Technology , 91 , 675–680. https://doi.org/10.1016/j.tifs.2019.07.016 Grant, P. (2020, August 4). Sugar, fiber, starch: What’s A carbohydrate? — Pamela Grant, L.Ac , NTP. Pamela Grant, L.Ac , NTP . https://pamela-grant.com/blog-ss/sugar-fiber-starch Helmenstine, A. (2022, October 25). Examples of carbohydrates . Science Notes and Projects. https://sciencenotes.org/examples-of-carbohydrates/ Project Gallery

A potential gene therapy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Antisense oligonucleotide gene therapy for treating Huntington's disease 27/09/25, 11:03 Last updated: Published: 25/02/24, 14:38 A potential gene therapy Huntington’s disease (HD) is an inherited neurodegenerative disease caused by a CAG extension in exon 1 of the huntingtin gene. An extended polyglutamine tract in the huntingtin protein is developed due to the expanded alleles, resulting in intracellular signalling defects. Antisense Oligonucleotide (ASO) gene therapy is currently being pioneered to treat HD. In this therapy, oligonucleotides are inserted into cells and bind to the target huntingtin mRNA. Thus, inhibiting the formation of the huntingtin protein by either physically blocking the translation of mRNA (figure 1) or by utilising RNase H to degrade the mRNA. Previous ASO gene therapy experiments conducted on R6/2 mice that express the human huntingtin gene have been successful. In HD research, the R6/2 mouse model is commonly used to replicate HD symptoms and is therefore useful for testing potential treatments. The transgenic R6/2 mouse has an N-terminally mutant Huntingtin gene with a CAG repeat expansion within exon 1. In this successful experiment, scientists treated one group of R6/2 mice with the ASO treatment that suppresses the production of human huntingtin mRNA, and saline solution was administered to the control group of mice. This experiment aimed to confirm if ASO therapy improves the survival rate in the R6/2 mice. The results showed that human huntingtin mRNA levels of the mice treated with ASO therapy were lower than the control group. Furthermore, the mice treated with ASO therapy had a higher percentage of survival and lived longer (21 weeks), in comparison to the control group mice that survived until 19 weeks. Thus, it could be concluded that if less human huntingtin mRNA was present in the ASO group, then less human huntingtin mRNA would be translated, and so there would be less synthesis of the huntingtin protein, in contrast to the control group. The results of this study are enormously informative in understanding how gene therapy can be used in the future to treat other neurological diseases. However, before ASO therapy is approved for clinical use, further trials will need to be conducted in humans to verify the same successful outcomes as the R6/2 mice. If approved, then the symptoms of HD, including dystonia could be safely controlled with ASO therapy. Furthermore, scientists need to consider that an increased survival rate of only an additional two weeks, as shown in the experiment does not always correlate to an increased quality of life for the patient. Therefore, it needs to be established if the benefits of ASO gene therapy will outweigh the risks associated with it. Furthermore, the drug PBT2, which influences copper interactions between abnormal proteins, is currently being studied as a potential treatment option for HD. Some studies have inferred that the aggregation of mutant huntingtin proteins could be due to interactions with metals, including copper. Therefore, this drug is designed to chelate metals and consequently, decrease abnormal protein aggregations in the body. This treatment has been shown to improve motor tasks and increase the lifespan in R6/2 mice. However, as this treatment has a lot of shortcomings, further studies need to be conducted over a large period of time to confirm a successful outcome of this drug on HD patients. Written by Maria Z Kahloon Related article: Overview of Huntington's disease REFERENCES Kordasiewicz HB, Stanek LM, Wancewicz EV, Mazur C, McAlonis MM, Pytel KA, et al. Sustained therapeutic reversal of Huntington’s disease by transient repression of huntingtin synthesis. Neuron. 2012;74(6):1031–44. Valcárcel-Ocete L, Alkorta-Aranburu G, Iriondo M, Fullaondo A, García-Barcina M, Fernández-García JM, et al. Exploring genetic factors involved in Huntington disease age of onset: E2F2 as a new potential modifier gene. PLoS One. 2015;10(7):e0131573. Liou S. Antisense gene therapy [Internet]. Stanford.edu . 2010 [cited 2021 Aug 6]. Available from: https://hopes.stanford.edu/antisense-gene-therapy/ Huntington's disease research study in R6/2 MOUSE model: Charles River [Internet]. Charles River Labs. [cited 2021 Aug 26]. Available from: https://www.criver.com/products-services/discovery-services/pharmacology-studies/neuroscience-models-assays/huntingtons-disease-studies/r62-mouse?region=3696 Frank S. Treatment of Huntington's disease. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. Springer US; 2014;11(1):153-160. Potkin KT, Potkin SG. New directions in therapeutics for HUNTINGTON DISEASE. Future neurology. 2018;13(2):101-121. Project Gallery