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Physics Articles These articles range from astrophysics and space science to nuclear physics, harmonic motion, and thermodynamics. You may also like: Maths, Technology , Engineering The liquid viscosity of castor oil An experiment determining the liquid viscosity of castor oil using spheres Summary of a pendulum experiment An experiment on the pendulum and its relation to gravity Female Nobel Prize winners in physics Who were they and what did they achieve? The Northern Lights in the UK What determines the Northern Lights to be seen in your country? The James Webb Space Telescope And its significance in space exploration Geoengineering Will it work to save the environmental crisis? The Lyrids meteor shower What is it and when does it happen? Nuclear fusion Unleashing the power of the stars Colonising Planet Mars Which fuel would be used to colonise Mars? Superfluids And their incredibly slippery nature Total solar eclipses A description of them Mercury The closest planet to the Sun The DESI instrument DESI stands for the Dark Energy Spectroscopic Instrument Cumulus clouds How they form and their link to the weather Hubble Tension The cause of the Hubble Tension discrepancy is unknown Artemis The lunar south pole base A room-temperature superconductor? The search for one Physics in healthcare Incorporating nuclear medicine The Crab nebula In the constellation of Taurus The physics of LIGO LIGO stands for Laser Interferometer Gravitational-Wave Observatory Next

We check UCAS personal statements for free! What are UCAS personal statements? For UK-based universities UCAS personal statements are a chance for students to show a UK university why they should be offered a place to study a particular subject there. Academics or more? Whilst academics are important to talk about, it is just as necessary to talk about who you are beyond your grades, too. We can inform you on what this may look like. Page limited It is critical to note that the statements must not be longer than 1 page: anything beyond this will not be read. You can v isit UCAS for more information... Deadline! All statements must be submitted through UCAS by 31st January 2024 at 18:00 (UK time). However, the earlier the better as universities accept students on a rolling deadline. The process of submitting a personal statement: 1. Research university courses interested in 2. Pick a course & write statement on why this subject 3. Check and edit statement for approval 4. Submit to your top 5 university choices Note for those that are considering medicine or dentistry: You (normally) will have to choose 1 university out of the 5 where you will do a back up course i.e. something that is not medicine or dentistry. What we offer to you: Proofreading To catch any remaining errors or inconsistencies in draft statements Expert advisors Graduates or current university students will provide personalised advice to highlight your unique qualities, and align your statement with your chosen field of study Goals We'll assist in articulating your passion and long-term goals effectively Feedback Get detailed feedback reports with specific improvement suggestions Guidance Giving example guideline questions for you to answer and include in your statement. This will help to create flow and making adjustments easier. Structure Advice on approaching your introduction, main body paragraphs and ending Example universities where some of our volunteers currently attend, or have graduated from: Queen Mary University of London, Imperial College London, Kings College London, University of Liverpool and so on. Fill the form out below and we will contact you* * Alternatively, you can email us at scientianewsorg@gmail.com . Please keep the subject as 'Personal Statement'. * Disclaimer: there must be no plagiarism in all statements submitted - we will assume there has been no copying. Scientia News will not be responsible for any plagiarism detection by UCAS, as we only give advice. Email Subject Your message Send Thanks for submitting!

Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Stress and neurodegeneration Last updated: 07/01/25 Cortisol is a glucocorticoid steroid hormone produced by the zona fasciculata segment of the adrenal gland, following stimulation by the release of adrenocorticotropic hormones from the pituitary gland. Chronic stress is associated with excessive cortisol production and the development of neurodegenerative diseases. Once cortisol is produced and released into circulation, it crosses the blood-brain barrier to bind to and activate nuclear glucocorticoid receptors (GR) in the hippocampus. Upon cortisol binding, the GR undergoes conformational changes, causing it to dissociate from its chaperone complex and consequently allowing for the transcription of target genes. One such pathway that is activated as a result of GR binding is the brain-derived neurotrophic factor (BDNF) and the cAMP response element-binding protein (CREB) pathway, which is important for long-term memory formation and consolidation. However, memory formation can be impaired following abnormal BDNF/ CREB pathway activation due to elevated cortisol levels. Moreover, high cortisol levels have been found to cause increased amyloid-beta (AB) deposition, which is evident in Alzheimer's disease patients. Therefore, increased blood cortisol levels result in increased activation of GR, causing impaired gene expression and affecting cellular functions. When GR are exposed to cortisol over a long period of time, such pathways become further impaired, resulting in the characteristic neurodegenerative disease pathology in affected individuals. A study conducted by Kline et. al assessed the relationship between high cortisol levels and neurodegenerative disease pathology in mice. In this study, it was noted that chronic stress reduced the diversity of the gut microbiome in mice, and such alterations resulted in increased gut permeability, promoting the movement of pathogens across the epithelial lining, and increasing AB deposition in affected mice. However, AB deposition can be reduced if cortisol levels are controlled. For example, xanamem, a drug currently in clinical trials, reduces cortisol levels by inhibiting the 11B-hydroxysteroid-1 ezyme, known to play a role in the activation of cortisol via the hypothalamus-pituitary-adrenal axis. Therefore, xanamem or similar compounds, if suitable following clinical testing, could be a means of decreasing AB deposition, thereby targeting one component of neurodegnerative disease pathology. If the putative hypotheses of Alzheimer's disease aetiology are correct, this would potentially ameliorate patient symptoms and offer a degree of improved quality of life for affected individuals. Written by Maria Zareef Kahloon Related articles: Tetris and PTSD / Mental health awareness

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Behavioural Economics II 06/01/25, 14:01 Last updated: The endowment effect This article is part 2 in a four-part series on behavioural economics. Next article: Loss aversion . Previous article- The role of honesty . In microeconomics, we say preferences are reversible. If you would pay £2 for a bar of chocolate, then you would be happy to sell a bar of chocolate for £2, especially if I gave it to you for free. Sounds reasonable? Well, in fact, this is not the case. Once again, consumers, just like you and me, are irrational, and thanks to what’s known as the endowment effect, classical economics falls flat once again. The endowment effect In an experiment conducted by Knetsch, participants were randomly allocated into three different categories. The first were given a coffee mug, the second were given some candy, and the third were given nothing. We say that the first two groups were endowed; they were given an item for free at no cost to them. Then the participants in the first two groups were given the option to either swap their item for either the mug or the candy or keep the item they were endowed with. The third group, treated as a control, was given the option to choose between the two and keep which they preferred the most. In the control group, we saw that about half of the participants chose the mug and half chose the candy. But in the endowed groups, an overwhelming majority decided to keep the item they were given rather than swapping! Therefore, as we can clearly see, when someone is endowed with an item, their perception of its utility (or benefit) seems to increase, so when given the opportunity to switch items, they often decline. Clearly, from an economic perspective, when endowed with an item, your utility curve for that item differs from when given the opportunity to choose. But why might that be the case? When you are endowed with an item, you own that item and, in a sense, hold responsibility over it. You become possessive, and this sense of ownership seems to have its own psychological value; therefore, the act of giving it up for something of equal worth is no longer treated as a fair trade-off. Whereas when not endowed, you have no sentiment value attached to the items, and for the most part, people are indifferent between them! A good example of this could be an old, run-down car. Buyers of this car see it for what it is—something that is barely functional. But owners of the car who have driven it for 20 years see it as more than that. There is an emotional attachment to the car that makes it more valuable in their eyes. Is the endowment effect always true? List conducted a similar experiment. A survey was undertaken by both unexperienced and experienced 'traders', and then after the survey, they were given trading cards as a reward. They were then given the opportunity to trade their cards if they wanted to. Non-experienced traders were subject to the endowment effect, so they kept the cards they worked hard for, but experienced traders knew that some cards may be more valuable, even if only slightly, which meant that they were able to overcome this effect. Additionally, what was found was that when participants were aware and went into the experiment knowing that there would be a trade, they had the intention to trade, which also managed to remove the endowment effect. In essence, the endowment effect serves as a reminder of the complexities inherent in human psychology and decision-making. There are many limitations in traditional economic models, which emphasises the need for behavioural economics and the inclusion of multidisciplinary thinking. To discover more about behavioural economics and in particular how honesty plays a big role in restructuring economic thinking, click here to read my prior article, and be sure to look out for more articles to come in the future! Written by George Chant Related articles: Explaining altruism / Mathematical models in cognitive decision-making References: Knetsch, Jack L. “The Endowment Effect and Evidence of Nonreversible Indifference Curves.” The American Economic Review 79, no. 5 (1989): 1277–84. John A. List, Does Market Experience Eliminate Market Anomalies?, The Quarterly Journal of Economics , Volume 118, Issue 1, February 2003, Pages 41–71,33 Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Artificial Intelligence in Drug Research and Discovery 13/12/24, 11:30 Last updated: Using the new technology AI to develop drugs Drug research has been transformed by artificial intelligence (AI), which has become a game-changing technology in several industries. Only a small portion of potential drugs make it to the market after the lengthy and expensive traditional drug discovery process. A drug's discovery and development can take over ten years and cost an average of US$2.8 billion. Even then, nine out of 10 medicinal compounds fall short of passing regulatory approval and Phase II clinical trials. The use of AI in this process, however, has the potential to greatly improve effectiveness, accuracy, and success rates. Given that AI can help with rational drug design, support decision-making, identify the best course of treatment for a patient, including personalised medicines, manage the clinical data generated, and use it for future drug development, it is reasonable to assume that it will play a role in the development of pharmaceutical products from the laboratory bench to bedside table. There are several ways in which AI is currently being used to enhance the drug discovery process. One of the primary applications is virtual screening ( Figure 2 ), which involves using machine learning algorithms to analyse large libraries of chemical compounds and predict which ones are likely to be effective against a specific disease target. This can significantly reduce the time and cost required for drug discovery by narrowing down the number of compounds that need to be tested in the lab. Another way AI is being used in drug discovery is through generative models, which use deep learning algorithms to design molecules that are optimised for specific therapeutic targets. This approach can be used to design molecules that are effective against a specific target while also minimising toxicity or other undesirable properties. Data analysis is another area where AI can be applied in drug discovery. By analysing large datasets of biological and chemical information, AI can help researchers identify patterns and relationships that may be relevant to drug discovery. For example, AI can be used to analyse genomic data to identify potential drug targets or to analyse drug-drug interactions to identify potential safety issues. However, one of the main challenges is the need for high-quality data, as AI models rely on large amounts of data to make accurate predictions. Additionally, there is a risk that AI models may miss important insights or make incorrect predictions if the data used to train them is biased or incomplete. Nevertheless, the continued development of AI and its amazing tools seeks to lessen the difficulties experienced by pharmaceutical firms, impacting both the medication development process and the full lifecycle of the product, which may account for the rise in the number of start-ups in this industry. The importance of automation will increase as a result of using the most up-to-date AI-based technologies, which will not only shorten the time needed for products to reach the market but also enhance product quality, increase overall production process safety, and make better use of available resources while also being cost-effective. In conclusion, the use of AI in drug discovery has the potential to revolutionize the field and significantly improve the success rate of potential drug candidates. Despite the challenges and limitations, the continued research and development of AI in drug discovery will undoubtedly lead to faster, cheaper, and more accurate drug development. Written by Navnidhi Sharma Related articles: A breakthrough procedure in efficient drug discovery / AI in medicinal chemistry / AI advancing genetic disease diagnosis Project Gallery

Engineering Articles Recognising the remarkable contributions in the vast field of engineering, including silicon hydrogel contact lenses, wireless electricity, hydrogen cars and many other innovations. You may also like: Maths , Physics , Technology Pioneers in biomedical engineering An International Women's Month collab with Kameron's Lab Silicon hydrogel contact lenses A case study on this latest innovation in eye vision correction Nikola Tesla and wireless electricity Tesla's dream of Wardenclyffe Tower: why did it not become a reality? Hydrogen cars Are they the future model of cars in the UK?

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Epilepsy 101 10/10/24, 10:40 Last updated: 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: 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

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Secondary bone cancer 24/09/24, 13:05 Last updated: Pathology and promising therapeutics Introduction: what is secondary bone cancer? Secondary bone cancer occurs when cancer cells spread to the bones from a tumour that started somewhere else in the body. The site where the tumour first develops is called primary cancer. Cancer cells can break away from the primary cancer, travel through the bloodstream or lymphatic system, and establish secondary cancers, known as metastasis. Bones are among the most common sites to which cancer can spread. Most type of cancer has the potential to metastasise to the bones, with the most frequent occurrences seen in prostate, breast, lung, thyroid, kidney, and myeloma cancers. Throughout the literature, secondary cancer in the bones is referred to as bone secondaries or bone metastases. The most common areas of secondary bone cancer are the spine, ribs, pelvis, humerus (upper bone of the arm), femur (upper bone of the leg) and skull. There are two main types of bone cancer referred to as osteolytic and osteoblastic metastases. In osteolytic metastases, cancer cells break down the bone, leading to significant weakening. This type of metastasis is more common than osteoblastic metastases and often occurs when breast cancer spreads to the bone. In osteoblastic metastases, cancer cells invade the bone and stimulate excessive bone cell formation. This process results in the bone becoming very dense (sclerotic). Osteoblastic metastases frequently occur when prostate cancer spreads to the bone. Although new bone forms, it grows abnormally, which weakens the overall bone structure. Hormone therapy Like primary bone cancer, treatment for secondary bone cancer includes surgical excision, chemotherapy, and radiation therapy. Treatment for secondary bone cancer aims to control the cancer growth and symptoms. Treatment depends on several factors, including the type of primary cancer, previous treatment, the number of bones affected by cancer, whether cancer has spread to other body parts, overall health, and symptoms. Breast and prostate cancers rely on hormones for their growth. Reducing hormone levels in the body can be effective in managing the proliferation of secondary cancer. Hormone therapy, also known as endocrine therapy, uses synthetic hormones to inhibit the impact of the body’s innate hormones. Typical side effects include hot flashes, mood fluctuations, changes in weight, and sweating. Bisphosphonates Bone is a dynamic tissue with a continuous process of bone formation and resorption. Osteoclasts are cells responsible for breaking down bone tissue. In secondary bone cancer, cancer cells often produce substances that stimulate the activity of osteoclasts. This leads to elevated levels of calcium in the blood (hypercalcemia), resulting in feelings of nausea and excessive thirst. Treating secondary bone cancer involves strengthening bones, alleviating bone pain and managing hypercalcaemia). One option for bone-strengthening is bisphosphonates. Bisphosphonates can be administered orally or intravenously. They have been in clinical practice for over 50 years and are used to treat metabolic bone diseases, osteoporosis, osteolytic metastases, and hypercalcaemia. These compounds selectively target osteoclasts to inhibit their function. Bisphosphonates can be classified into two pharmacologic categories based on their mechanism of action. Nitrogen-containing bisphosphonates, the most potent class, function by suppressing the activity of farnesyl pyrophosphate synthase, a key factor in facilitating the binding of osteoclasts to bone. Consequently, this interference causes the detachment of osteoclasts from the bone surface, effectively impeding the process of bone resorption. Examples of these bisphosphonates include alendronate and zoledronate. Bisphosphonates without nitrogen in their chemical structure are metabolised intracellularly to form an analogue of adenosine triphosphate (ATP), known as 5'-triphosphate pyrophosphate (ApppI). ApppI is a non-functional molecule that disrupts cellular energy metabolism, leading to osteoclast cell death (apoptosis) and, consequently, reduced bone resorption. Examples of these bisphosphonates include etidronate and clodronate. Non-nitrogen-containing bisphosphonates can inhibit bone mineralisation and cause osteomalacia, a condition characterised by bones becoming soft and weak. Due to these considerations, they are not widely utilised. Denosumab Denosumab is another option for bone strengthening. It is administered as an injection under the skin (subcutaneously). Denosumab is a human monoclonal antibody that inhibits RANKL to prevent osteoclast-mediated bone resorption. Denosumab-mediated RANKL inhibition hinders osteoclast maturation, function, and survival in contrast to bisphosphonates, which bind to bone minerals and are absorbed by mature osteoclasts. In some studies, Denosumab demonstrated equal or superior efficacy compared to bisphosphonates in preventing skeletal-related events (SREs) associated with bone metastasis. Denosumab’s mechanism of action provides a targeted approach that may offer benefits for specific populations, such as patients with renal impairment. Bisphosphonates are excreted from the human body by the kidneys. A study by Robinson and colleagues demonstrated that bisphosphonate users had a 14% higher risk of chronic kidney disease (CKD) stage progression (including dialysis and transplant) than non-users. On the other hand, denosumab is independent of renal function and less likely to promote deteriorations in kidney function. Take-home message Secondary bone cancer, resulting from the spread of cancer cells to the bones, poses challenges across various cancers. Two main types, osteolytic and osteoblastic metastases, impact bone structure differently. Hormone therapy, bisphosphonates, and Denosumab have shown promising results and offer effective management of secondary bone cancers. Ultimately, the decision between treatments should be made in consultation with a healthcare professional who can evaluate the specific clinical situation and individual patient factors. The choice should be tailored to meet the patient’s needs and treatment goals. Written by Favour Felix-Ilemhenbhio Related article: Bone cancer Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link 'The Emperor of All Maladies' by Siddhartha Mukherjee 28/11/24, 15:25 Last updated: Book review Stretching nearly 4,000 years of history, Pulitzer Prize winner, Siddhartha Mukherjee sets on a journey to document the biography of cancer in ‘The Emperor of All Maladies’. Drawing from a vast array of books, studies, interviews, and case studies, Mukherjee crafts a narrative that is as comprehensive as it is compelling. Driven by curiosity and a desire to understand the origins of cancer, Mukherjee sets the tone by reflecting on his experiences as an oncology trainee, drawing insightful parallels to contemporary perspectives on the fight against this relentless disease. Mukherjee also pays homage to Ancient Egyptian and Greek physicians for their early observations on cancer, from the work on Imhotep to Claudius Galen. He then introduces Sidney Farber, whose monumental contributions to modern chemotherapy are brought to life through Mukherjee's exceptional storytelling—tracing Farber's journey from his initial observations to his unprecedented success in treating children with leukaemia. As you progress through each chapter of this six-part book, your appreciation deepens for how far cancer treatments have advanced - and how much further they can go. Mukherjee’s unparalleled skill as a science communicator shines through, seamlessly weaving together groundbreaking scientific discoveries with the historical contexts in which they emerged contributing to an immersive reading experience. Siddhartha Mukherjee, The Emperor of All Maladies : In 2005, a man diagnosed with multiple myeloma asked me if he would be alive to watch his daughter graduate from high school in a few months. In 2009, bound to a wheelchair, he watched his daughter graduate from college. The wheelchair had nothing to do with his cancer. The man had fallen down while coaching his youngest son's baseball team. Mukherjee also makes an effort to highlight the critical role of raising awareness in shaping public health outcomes. ‘Jimmy’ was a cancer patient that represented children with cancer, his real name was Einar Gustafson, but his individual story was able to galvanise large-scale support. As the face of the ‘Jimmy Fund’, he was able to assist in raising $231,485.51 for the Dana-Farber Institute subsequently becoming the official charity for the Boston Red Sox. Mukherjee underscores how storytelling can serve as a catalyst for change, not just in raising money, but also in enacting larger societal and governmental shifts. In 1971, President Richard Nixon signed the ‘National Cancer Act’, the first of its kind where federal funding went directly into advancing cancer research. What struck me most was how Mukherjee connects this historical event to the broader need for advocacy, as science doesn’t just happen in the lab. It is a collective effort, driven by awareness, to push funding and influence policy. The ability to link individual stories to broader missions, as Mukherjee illustrates, continues to be one of the most effective strategies in keeping cancer research in the public eye. Mukherjee delves into the pivotal role of genetics in cancer research, tracing its evolution from the discovery of DNA's structure by Francis Crick, James Watson, and Rosalind Franklin to Robert Weinberg's ground-breaking work on how proto-oncogenes and tumour suppressors drive cancer progression. These discoveries ushered in a new era in cancer drug development. Mukherjee also emphasises the importance of collaboration and the rise of the internet, which gave birth to The Cancer Genome Atlas, a landmark program, that unites various research disciplines to diagnose, treat, and prevent cancer. In concluding the book, Mukherjee looks ahead to the future of cancer treatment, seamlessly connecting this discussion to his second book, ‘ The Gene’ . This book takes readers on a remarkable journey through the history of cancer, from the earliest recorded cases to groundbreaking discoveries in genetics. It weaves together compelling personal stories as well as pivotal moments in governmental policy. The storytelling is rich and immersive, drawing you in with its detail and depth. By the time you finish, you'll find yourself returning to its pages, eager to revisit the knowledge and insights it offers. Written by Saharla Wasarme Related book review: Intern Blues Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Emotional chemistry on a molecular level 16/01/25, 11:19 Last updated: From bonds to emotions Emotions have a crucial role in how we perceive the world, behave, and interact with others. Our emotional states significantly influence how our lives are shaped, from the happiness of a long-awaited reunion to the grief of a heartbreaking farewell. But have you ever wondered what happens on a molecular level when we experience emotions? In this article, we will delve into the fascinating world of the chemistry behind emotions and explore how neurotransmitters, hormones, and brain regions collaborate to orchestrate the symphony of our feelings. Neurotransmitters , the chemical messengers in charge of transferring impulses between brain neurons, lie at the core of the chemistry of emotions. The "happiness hormone," Serotonin , is known for its critical function in controlling mood, appetite, and sleep. Anxiety and sadness have been associated with low serotonin levels. Dopamine : This "reward neurotransmitter" is linked to reinforcement and pleasure. Dopamine is released when we like or receive a reward, which reinforces the behaviour and motivates us to seek out more of those kinds of experiences. Norepinephrine is a component of the body's fight-or-flight response that causes increased attention and arousal in reaction to stress or danger. Lastly, Gamma-Aminobutyric Acid (GABA) , an inhibitory neurotransmitter, counteracts the effects of excitatory neurotransmitters to maintain emotional stability by calming and soothing the brain. Our emotional experiences are significantly shaped by hormones as well. These chemical messengers affect the brain and other organs by entering the circulation after being released by numerous glands throughout the body. Cortisol , also referred to as the "stress hormone," is a key component of the body's fight-or-flight response and is released while under stress. Anxiety and a sense of being overpowered might result from elevated cortisol levels. The "love hormone" or "bonding hormone," Oxytocin , is a chemical that is released during social interactions, particularly during times of closeness, trust, and bonding. The body's own natural mood lifters and painkillers are called Endorphins . Exercise, laughing, and other enjoyable activities all produce endorphins, which contribute to a feeling of pleasure. Emotions are orchestrated within various brain regions , each with its own role in processing and interpreting emotional stimuli. Some key brain regions associated with emotions are: Amygdala : The "emotional hub" of the brain is commonly referred to as the amygdala. It analyses emotional inputs, particularly those connected to aggressiveness and fear, and participates in the development of emotional memories. Prefrontal Cortex : This part of the brain controls rational higher-order thought, judgement, and emotional regulation. Even in highly emotional situations, it supports our ability to control our emotions and make logical decisions. Hippocampus : The hippocampus helps people remember emotional memories in particular. It is essential for remembering previous emotional experiences and creating emotional bonds. In conclusion, the chemistry of emotion is a gorgeously sophisticated dance of neurotransmitters, hormones, and different parts of the brain. It highlights the delicate balance that shapes our emotional experiences and influences our behaviour and well-being. Understanding this molecular magic can provide insight into our emotional reactions and open the door to novel treatment strategies for treating emotional disorders and mental health issues. Next time you feel overwhelmed with joy, anger, or any emotion in between, remember that there's a symphony of chemicals and brain activity behind the scenes, composing the unique melody of your emotional journey. Embrace your emotions, for they are an essential part of what makes us human. Written by Navnidhi Sharma Related articles: Exploring food at the molecular level / Psychology of embarrassment / Unmasking aggression Project Gallery