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Lesser-known illnesses Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Rare zoonotic diseases 10/07/25, 10:33 Last updated: Published: 08/07/23, 13:34 Lesser-known illnesses This is article no. 1 in a series on rare diseases. Next article: Breast cancer in males . Introduction From COVID-19 possibly coming from livestock in Wuhan market to HIV resulting from numerous transmissions between African primates, it seems that zoonotic diseases are difficult to control. They occur when pathogenic microorganisms are spread from animals to humans or vice-versa. Their impact on human civilization is alarming because they are responsible for 2.5 billion cases of illness and 2.7 million deaths in humans annually around the world. Although there is a lot of information regarding more familiar zoonotic diseases such as rabies and malaria, this article focuses on those that may be less discussed as they could become more problematic in the future. Crimean-Congo haemorrhagic fever (virus) To begin, Crimean-Congo haemorrhagic fever (CCHF) is a viral disease, which spreads when humans are bitten by ticks carrying the virus along with farmers killing infected livestock. It is endemic in more than 30 European, African and Asian countries with the exact factors contributing to the increased cases of CCHF being a mystery. Diagnosing the disease involves detecting the virus through Enzyme-linked immunosorbent assay (ELISA), real time polymerase chain reaction (RT-PCR) along with detecting IgM and IgG antibodies using ELISA. As for the treatment options for CCHF, they are finite as there are no available vaccines and the only antiviral drug used against the virus is ribavirin, which prevents replication of various DNA and RNA viruses in-vitro. Given all this information, it is evident that extensive research is necessary to better understand the disease holistically and design drugs that can stop more fatalities associated with CCHF. Trichinellosis (parasite) The next zoonotic disease to address is trichinellosis or trichinosis , which is caused by Trichinella spiralis and so it is a parasitic infection. It can spread by eating poorly prepared meat such as pork and mammals like horses and wild carnivores are typically the reservoirs of infection. Its epidemiology in humans seems to be limited because it has 10,000 cases and 0.2% death rate annually. Moreover, an important factor that can contribute to the spread of trichinellosis is culture because certain communities have dishes containing raw meat. For example, a review referenced more than 600 outbreaks, 38,797 infections and 336 deaths in humans between 1964 and 2011 in China. As for diagnosing trichinellosis, it is challenging because it has general signs. With this in mind, the common method to spot the disease is detecting IgG antigens that work against Trichinella spiralis . On the other hand, its major drawback is getting a false negative in early trichinellosis infection. Like CCHF, trichinellosis is not as prevalent compared to other zoonotic diseases but it can have devastating impacts on specific countries, so increasing the supply of antiparasitic drugs like albendazole and/or mebendazole would be beneficial to stop the spread of Trichinella spiralis. Brucellosis (bacteria) The next zoonotic disease which is caused by a bacterial pathogen is brucellosis and is common worldwide, though certain places have higher prevalence of the disease compared to others. The pathogen can be transmitted through various ways such as direct contact with infected animal tissue on broken skin and consuming contaminated meat or dairy. Interestingly, it has been linked to childhood pulmonary infections as 18 out of 98 brucellosis patients have experienced such symptoms, but this is rare. The graph above indicates that when brucellosis occurs in animals, it has a high likelihood of being passed onto humans. For example, the years 2004-2007 could be when brucellosis cases were most frequent. This could have been alleviated through specific antibiotics used to treat brucellosis that include rifampin, doxycycline and streptomycin. Similar to trichinellosis, brucellosis diagnosis can be difficult because the symptoms can vary and are not exclusive to one disease, suggesting that different laboratory techniques are needed to find brucellosis in patients. Conclusion It looks like there is a recurring pattern of the zoonotic diseases outlined in this article occurring in developing countries as opposed to developed countries. As such, there have to be more effective interventions to prevent their ramifications on populations living in these countries. For this to occur, there has to be sufficient information, awareness, and education of these rarer zoonotic diseases to begin with. Furthermore, the current treatments for CCHF, trichinellosis and brucellosis may be unsuccessful due to the threat of antimicrobial resistance, hence finding alternative treatments for the aforementioned zoonotic diseases is vital in the future. Written by Sam Jarada Related articles: Rabies / Canines and cancer / Vaccine for malaria Project Gallery

They are on the IUCN red list as 'vulnerable' Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Conservation of marine iguanas 09/07/25, 13:34 Last updated: Published: 06/01/24, 10:40 They are on the IUCN red list as 'vulnerable' The marine iguana ( Amblyrhynchus cristatus ), also known as the sea iguana, is a unique species. It is the world’s only ocean- going lizard. Their main food source is algae; large males can dive to forage for this source, while females feed during low tide. They can be found on rocky shorelines, but also on marshes, mangrove swamps and beaches of the Galapagos. Their range is limited to the Galapagos islands, so they are an isolated species. Currently, they are on the IUCN red list as ‘vulnerable’ with a current population estimated at 200,000, and conservation efforts are needed to stabilise populations. Key threats There are three key threats to iguana populations. The first is invasive species; animals such as pigs, dogs and cats feed on young hatchlings and iguana eggs, which reduces the long-term survival rate of the species. Marine iguanas have not yet developed defence strategies against these predators. Even humans introduce pathogens to the islands that pose a threat to the species, because of their isolated habitat, the marine iguana lacks immunity to many pathogens and so has a higher risk of contracting diseases. Climate change is another key threat. El Niño is a weather event that prevents cold, nutrient-rich waters, that the marine wildlife depends on, from reaching the Eastern Tropical Pacific. This depletes algae populations, and this food drop drastically reduces iguana populations ( Figure 1 ). With global warming, El Niño events are expected to be more prominent and more frequent. In addition, pollution from humans like oil spills and microplastics are damaging their habitat. Current and future conservation methods Under the laws of Ecuador, marine iguanas are completely protected. Their land range is in the Galapagos National Park, and their sea range is within the Galapagos Marine Reserve. They are also listed on the CITES, which ensures monitoring the trade of endangered animals to inhibit damage to their numbers. Sanctuaries are also in place to mitigate against extinction, but their specialised diet is challenging. So, what does the future hold for marine iguanas? The biggest challenge is the distribution of the species. The population is scattered across the different islands of the Galapagos as such, there are at least 11 subspecies. This brings more complications to marine iguana conservation. As these subspecies specialise, it becomes less likely they will breed, thus more difficult to maintain the species population. Introducing education and awareness programmes will better equip us to the dangers faced by marine iguanas and could be a tourism idea for the Galapagos. This species is one of a kind, which is why it is so important for them to be protected.There should be a monitoring scheme, as suggested by MacLeod and Steinfartz, 2016 ( Figure 2 ), but the location of these subspecies makes it difficult to monitor them. However, there was a recent study using drone-based methods which showed promising results ( Figure 3 ). The overarching question remains: do we continue to conserve the current population in the Galapagos, or should we relocate the species to a less endangered habitat. Written by Antonio Rodrigues Related articles: Conservation of Galapagos Tortoises / 55 years of vicuna conservation Project Gallery

Also known as Major Depressive Disorder (MDD) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What does depression do to your brain? 14/07/25, 15:12 Last updated: Published: 10/10/24, 11:19 Also known as Major Depressive Disorder (MDD) This is Article 1 in a series on psychiatric disorders and the brain. Next article: Inside out: the chemistry of depression. -- I affect 3.8% of the population wide, With 280 million voices struggling inside. In women, my reach is 6%, And 5.7% of those over 60 feel me. Among new mothers, I reach 10%, With over 700,000 lost to my torment each year. What am I? Depression. The most prevalent psychiatric disorder that costs both money and lives. -- Also known as Major Depressive Disorder (MDD), depression is a heterogenous disease, which means the manifestation of the disorder is influenced by multiple genes. It is commonly known that consistent low mood, loss of interest in hobbies you used to enjoy, lethargy, feeling of hopelessness etc. are physical symptoms of depression. However, have you ever wondered what happens in the brain in a depression sufferer, from the neuroscience aspect? Structurally, research into the neuroscience of depression reveals significant structural abnormalities in the brains of affected individuals. Studies using structural magnetic resonance imaging (MRI) have shown that those with MDD show reductions in gray matter volume in regions responsible for emotion regulation. The limbic system of the brain is responsible for producing and regulating emotions. In depressed individuals, the hippocampus—a key component of the limbic system—shows reduced gray matter volume, which is linked to abnormalities in the associated white matter tracts. White matter consists of myelinated axons that facilitate communication between different brain regions, while grey matter contains the neuronal cell bodies responsible for processing information. The presence of abnormalities in white matter suggests a disconnection between regions within the limbic system, potentially impairing their ability to communicate effectively. This disconnection may contribute to the emotional dysregulation observed in depression, highlighting the intricate relationship between grey and white matter in the pathology of this disorder. Depression is a complex disorder that not only affects mood but changes the structure and function of the brain. By understanding the neurobiological changes—including reductions in grey matter and white matter disconnections—we can better grasp the pathogenesis of this condition. Continued research in the neuroscience behind depression is essential for developing more effective treatments. There is still much more to explore and understand in depression research; with each new discovery, we realise how much more there is to learn. Written by Chloe Kam Related article: Depression in children Project Gallery

Delving into the impacts of gut bacteria on health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Gut Microbiome 11/07/25, 09:58 Last updated: Published: 04/04/24, 16:41 Delving into the impacts of gut bacteria on health Inflammatory Bowel Disease The microbiome is hugely important to human health, and has been shown to beneficial to digestion, the immune system and even our mental health when in good working condition. However, disruption to the balance of the microbial flora has likewise been associated with multiple diseases and poor general health. Dysbiosis, or a poor balance, of human microbiome communities has been implicated in a wide range of disease, such as cardiovascular disease, chronic inflammation, obesity and even mental health issues. A diverse and well-balanced microbial community is important for disease prevention, however modern over usage of antibiotics as well as poor diets low in dietary fibre and high in artificial additives can lead to compromised communities dominated by single pathogenic strains of bacteria. The human microbiome plays a critical role in overall health, from providing valuable metabolites to aiding the immune system. Friendly commensal bacteria colonise major regions in our gut, with characteristic diverse communities of microbes inhabiting them. These microbes occupy these niches and outcompete pathogenic organisms, actively preventing infection and disease. In this article we will be specifically looking into the link between the gut microbiome and Inflammatory Bowel disease (IBD), as this is currently one of the most well researched cases of a causal relationship between the microbiome and disease state. Dysbiosis and Disease state Disruption of the gut flora is associated with painful inflammation of the gastrointestinal tract, diagnosed as IBD. Crohn’s disease and Ulcerative Colitis are conditions under the umbrella term of IBD and cause painful swelling and eventually ulcers in the gastrointestinal tract. The exact cause of IBD remains unclear, with the true cause likely a combination of genetics, environmental factors and the gut microbiome. Evidence has come to light that shows a link between disease state and the gut dysbiosis, where they influence each other and are potentially both each other’s cause and effect. Successfully treating IBD has proved difficult; medications focus on alleviating inflammation or other symptoms as antibiotics have shown limited effectiveness in curing the disease. Antibiotics have even been suggested to weaken the immune system long-term, as evidence suggests that antibiotic clearance of commensal bacteria can provide opportunity for pathogenic strains to establish themselves. Medical treatments destabilizing the microbiome can lead to a change in overall metabolism and chronic Clostridium difficile infection. When colonization resistance is compromised there is more opportunity for single bacteria to dominate the community, with antibiotic-associated diarrhoea a common side effect associated with antibiotic induced dysbiosis. Microbial-based therapies Recently potential therapies pivoted to target the microbiota, as reinstating a healthy colony of gut microbials should alleviate the cause of IBD. Previous treatments relied on antibiotics followed by a course of probiotics; however, this has had variable levels of success as the antibiotic treatment can further reduce bacterial diversity in the gut. Probiotics have limited effectiveness in alleviating symptoms; any effect is transient as no probiotic microbial strains are detectable after 2 weeks of stopping intake. In modern clinical trials we have already seen positive results from microbiome treatments in clearing C. difficile infection, such as faecal microbiota transplantation (FMT) therapy. FMT uses faeces from a healthy donor, which are processed and delivered to the gastrointestinal tract of patients. Faeces contain a high microbial load, with up to 1011 bacterium per gram and multiple archaea, fungi and viruses that could not be delivered orally in a probiotic form. Success in resolving dysbiosis through FMT is variable but shows more promise than other therapies. Future Potential Specific forms of IBD such as ulcerative colitis (UC) was first treated with FMT in 1989, with patients reducing medications within a week of enema treatments and remaining clinically disease free for multiple years after treatment. More recent trials have had more variable levels of remission, suggesting donor compatibility, disease prevalence and engraftment of the microbiota all factor into the success of FMT. There is potential in this therapy, as FMT has proved more robust than previous treatments for IBD. Modern research into the relationship between disease and gut flora has come a long way in a relatively short time and shows there is much potential for future research in this area. Written by Charlotte Jones Related articles: the power of probiotics / Crohn's disease / the dopamine connection / Diverticular disease / Nanoparticles on gut health / Microbes in charge Project Gallery

The rabies virus infects neurons Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Rabies- the scariest disease ever? 10/07/25, 10:31 Last updated: Published: 10/10/24, 11:05 The rabies virus infects neurons Rabies is a viral disease that primarily affects the central nervous system (CNS), usually in mammals. Wild animals such as foxes, dogs, and raccoons are frequent carriers of the virus. Transmission occurs through the saliva of an infected animal through a bite or a scratch, allowing the virus to enter the body and travel through the nervous system toward the brain. While rabies can be prevented with a vaccine, once symptoms begin to show, the disease is nearly always fatal once symptoms begin to show. What makes this virus so deadly, and how can it take control of the human body with just five genes in its genome? Why is the virus so hard to kill? To arrive at a sensible answer, we must first understand the ‘tropism’ of the virus – the cell type it likes to infect. Rabies virus infects the neurones (neurotropic), which creates a massive problem for the immune system. Macrophages and neutrophils, which are the prominent cells in killing foreign pathogens that kill foreign pathogens, usually deal collateral damage to the body’s own cells to some extent. This must be avoided with neurones, as neurones cannot replenish themselves after cell death. An inflammation of the nerve cells could lead to paralysis and seizures, compromising the CNS. As a result, the immune system response is significantly lowered around nerve cells to prevent accidental damage, which allows the virus to infect the neural pathway easily. Transmission of the virus See Figure 1 The strategy of the immune system is that the neurones can be protected if the pathogens are intercepted before they travel to their destination. However, this strategy ultimately fails when it comes to rabies, because the transmission is through a bite, which can penetrate and cut through many layers of tissue, providing a direct access to nerve cells. If you were bitten on the leg, then the time it takes for the rabies virus to travel to your brain would be the time it takes for you to travel from Florida, USA to Sweden. This may seem like a long time, but the rabies virus has evolved a technique that is able to hijack the cellular transport system can trick your cells’ transport system to travel quickly through the nerves by binding to a protein called dynein . Dynein is a motor protein that move along the microtubules in cells, converting the chemical energy of ATP into mechanical work. Microtubules are polarized structures, with a plus end (typically towards the axon terminal in neurones) and a minus end (towards the cell body). Dynein moves toward the minus end, facilitating retrograde transport, meaning it moves materials from the periphery of the cell, such as the axon terminals, back toward the cell body. Dynein is transports chemicals inside cells via endocytosis and plays a vital role in the movement of eukaryotic flagella. Rabies has evolved to stick to dynein via the Glycoprotein (G) present on its viral envelope, which allows rabies to travel to the brain much quicker. Dynein may be small, weighing around two megadaltons (3 x 10-18 grams), but it can move at a speed of 800 nanometres per second. At this speed, it takes rabies around 14 days to move up a metre- long neuron. This implies that the closer the animal bites you to the brain, the less time it takes for the symptoms to appear. If you’re bitten on the foot, it could take months for the virus to reach your brain. But if you’re bitten on the neck or face, the virus can get to your brain in just a few days, making it much more dangerous. This explains the broad range in the incubation time which is between 20 to 90 days. Infection and replication- see Figure 2 As the rabies travels through neuronal tracks, it sets up points of concentrated viral production centres called Negri bodies. These replicate the rabies virus within the neurones and inhibit interferon action, which are chemicals that alert white blood cells to the area of infection. Interferon inhibition along with lowered immune response to neurones make rabies extremely effective. However, neurones can undergo apoptosis—controlled cell death—to limit the spread of the virus and allow macrophages to clear the debris. Research in mice suggests that some strains of rabies may prevent this apoptotic response in cells. Additionally, studies indicate that rabies promotes apoptosis in killer T cells, which are responsible for inducing apoptosis in other cells. This mechanism helps to shield nerve cells from immune system attacks. Symptoms Patients with rabies initially experience flu-like symptoms and muscle pain. Once these early symptoms appear, treatment is virtually impossible. As the disease progresses, neurological symptoms develop including hydrophobia due to painful throat spasms when swallowing liquids. About 10 days after these neurological symptoms start, patients enter a coma, often accompanied by prolonged sleep apnoea. As virus attacks the brain throughout this stage, patients develop the urge to bite other organisms to transmit the virus. The virus can reach the salivary glands, allowing for transmission through a bite to occur again. Most patients typically die within three days of reaching this coma stage. Legends Rabies may have influenced the development of vampire and zombie myths due to its distinct symptoms. The disease causes aggression and sensitivity to light, which could have inspired some characteristics of vampires, such as their aversion to light and erratic movements. Additionally, rabies leads to excessive salivation and a tendency to bite, traits that align with vampire lore. Similarly, the delirium and motor dysfunction seen in rabies may have contributed to the depiction of zombies as shuffling, incoherent beings. Conclusion Rabies is a uniquely deadly virus due to its mechanism of hijacking the nervous system. After entering the body, the virus binds to dynein, using it to travel along neuronal pathways toward the brain. It replicates rapidly, forming Negri bodies disrupting neurone function. The virus effectively suppresses immune responses, making it nearly impossible to treat once symptoms appear, leading to almost 100% fatality. Beyond its biological impact, rabies has influenced cultural stories like those of vampires and zombies, with its symptoms—such as aggression, fear of water, and neurological decay—providing eerie parallels to these myths. Despite modern medical advances, rabies remains one of the most feared infectious diseases due to its fatal nature. Written by Baraytuk Aydin Related articles: Rare zoonotic diseases / rAAV gene therapy REFERENCES CUSABIO (2020) Rabies virus overview: Structure, transmission, pathogenesis, symptoms, etc, CUSABIO. Available at: https://www.cusabio.com/infectious-diseases/rabies-virus.html (Accessed: 12 September 2024). Hendricks, A.G. et al. (2012) Dynein tethers and stabilizes dynamic microtubule plus ends, Current biology : CB. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3347920/ (Accessed: 13 September 2024). Lahaye, X. et al. (2009) Functional Characterization of Negri Bodies (NBS) in rabies virus-infected cells: Evidence that NBS are sites of viral transcription and replication, Journal of virology. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715764/ (Accessed: 13 September 2024). Tarantola, A. (2017) Four thousand years of concepts relating to rabies in animals and humans, its prevention and its cure , MDPI . Available at: https://www.mdpi.com/2414-6366/2/2/5 (Accessed: 15 September 2024). Project Gallery

Strategies for success and mathematical mastery Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How to excel in maths 09/07/25, 14:19 Last updated: Published: 01/10/23, 20:00 Strategies for success and mathematical mastery Mathematics is a subject that can be both daunting and rewarding. While some individuals seem to effortlessly grasp mathematical concepts, most of us need to put in extra effort to excel. This article is dedicated to the majority—the ones willing to work hard to achieve success in their A-level maths exams and beyond. By following a structured approach and embracing a growth mindset, you can unlock your mathematical potential and reach heights you may have never thought possible. Understanding the concepts Fundamentally, to be able to get anywhere in mathematics, you need to understand what you are doing with numbers and why. There is no point in knowing how to differentiate if you don’t know why you want to differentiate and why it works. Now, I am a strong believer that anyone can learn anything if they approach it with an open mind and determination to succeed. This is called having a growth mindset. However, there is a caveat with how maths is taught at school. When maths is taught, it is taught by someone who understands a concept in a particular way. We are all inherently different, and similarly, our minds all work slightly differently. So when your teacher explains how they understand something, it does not mean that you should also understand it as you both think differently. Now for some, they manage to grasp what their teacher is saying easily as they think similarly, but for others this may need an alternative approach. Some examples could be supplementary lessons with a tutor, buying a subscription to online lessons or asking for some 1-on-1 time with your teacher. But sometimes this may still not even work. If my teacher can’t help me, how can I learn? Well, for A-Levels and GCSEs, we are extremely blessed that there is a plethora of different resources that we can use, both written and in video format! Some of my favourites include, but are not limited to, TLMaths (Youtube), BBC Bitesize (GCSE only), and Khan Academy. (Also see: Extra Resources for more maths resources). YouTube really can be your best friend. There are thousands of videos explaining mathematical concepts, and they are not all as trivial as those shared by Numberphile. By simply searching for a topic that you are stuck on, you can get many different professionals to explain the same problem; with enough grit and determination, you’ll be able to find a video that you can easily understand! If, however, that does not seem to work, it may be an indicator that you need to step back and learn the fundamentals a bit better. There is little point in using the integral to calculate the area under a line graph if you don’t know what a line graph actually shows. Practice the concepts Once you’ve got the concepts down to the tee, there is only one option to go with. Practice. Practice. Practice. I foolishly made the mistake during my year 10 final exams, where instead of doing practice questions, I made notes from watching videos and thought that was enough. Not only is this not engaging, but when it comes to maths, practice is the only way to revise. Truthfully, I would never recommend taking notes in maths as it is not only quicker to look something up, but I believe the time spent making notes could be spent better elsewhere. The best way to practice for an exam is through practice papers. You may now be dashing off to find practice papers for your exam board; however, I would recommend not touching these until you are around 1 month away from your exam. If you are as crazy as I am, you could even leave it until the last week and complete 2 or 3 per day, but maybe for your sanity, I’d advise against this. Instead, use all of the resources that you are fortunate enough to have available to you thanks to the internet. Complete every question in your textbook and revision guide; complete predicted papers; do it all! This is the surefire way to get top marks and become a competent mathematician. But maybe you’re not studying for a big A-level exam just yet. By completing the questions that you may not have done in class and researching topic-specific questions (Math’s Genie and Physics and Maths Tutor are both excellent resources for this), you will, with time, start to develop your skills and put the theory into practice. By better applying these concepts, you begin to understand them and maybe even start to enjoy them. (Bonus tip: do your homework. It’s given out for a reason.) Apply the concepts to unfamiliar situations Now that you have mastered the concepts and put them to the test by answering every question you can get your hands on, comes the trickiest part of mathematical mastery: These are the questions that separate the A’s and the A*’s. The geniuses and the sedulous, but more importantly, those who can do maths, and those who understand maths. By applying the mathematical concepts that you’ve learned to unfamiliar situations, you start to develop an extremely sought-after skill. Problem solving. By using maths in an unfamiliar context, most students are hasty to give up, and this is why the last question on the test is so ‘difficult’, but in fact it's the same as the prior questions but in disguise. To conquer these questions, you have to be able to decipher what the question is asking and then apply the appropriate techniques to solve it. The only way that you will know which techniques to use is by attempting similar questions that push you, and in time, your brain's pattern recognition will kick in and you’ll start to find that you just know what to do. You can't explain it; you just want to differentiate here, factor out here, and expand these brackets here, and bam! You’ve got the answer. But the only way you can get there is by putting in the hours and attempting questions that are outside your comfort zone. At the beginning of the article, I said it would be tough, but maths does not require you to spend 4 hours every night (until you are smack in the middle of your A-level exams), but instead a mere 20 minutes, maybe only 5 days a week, but I promise you that this small amount of time after school, before bed, or during break, if uninterrupted and follows the rules that I have just suggested, will work absolute wonders on your mathematical ability. Imagine the impact of dedicating just 20 minutes a day to math starting right now. If you're in year 13, with your first math paper 38 weeks away on June 4th, time will fly. By committing to 20 minutes daily, five days a week, you'll accumulate over 63 hours of revision. Bump it up to half an hour, and you'll hit almost 100 hours. This early start saves you precious time closer to exams, allowing you to focus on other subjects. Unlike some subjects, math doesn't require rote memorisation. Building these skills gradually pays off. Yes, 20 minutes daily may seem modest, but consistency can be challenging. Skipping just one day can turn into a week, then a month. Dedication, determination, and discipline are essential for success. If you maintain this routine, you can achieve remarkable results, even surpassing natural mathematical geniuses. Now with the three steps to mathematical freedom: Understand the concepts. Practice the concepts. Apply the concepts to unfamiliar situations. Go out there and give it your best shot! I wish you all the best of luck in your journey to mathematical mastery! Written by George Chant Related articles: The game of life / Teaching maths / Topology Project Gallery

From bonds to emotions Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Emotional chemistry on a molecular level 26/06/25, 10:12 Last updated: Published: 16/01/24, 00:03 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 / Chemistry of depression / Music and emotions Project Gallery

What matters most for the development of intelligence in childhood? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nature vs nurture in childhood intelligence 11/12/25, 14:14 Last updated: Published: 21/09/24, 15:38 What matters most for the development of intelligence in childhood? Introduction Intelligence is reasoning, planning, solving problems, thinking abstractly, comprehending complex ideas, and learning from experience. This broad and deep capacity for understanding our surroundings can be measured using standardised tests, such as Intelligence Quotient (IQ) tests, picture vocabulary tests for verbal ability and matrix reason tasks for non-verbal ability. This article explores how nature facilitates the development of intelligence in childhood through twin studies, which highlight genome-wide association studies. On the other hand, how nurture can further aid in developing intelligence in childhood through social environmental influences and investigate the association between parent socio-economic status (SES) and intelligence. However, there is no definite answer to whether only nature or nurture leads to the development of intelligence in childhood. Therefore, genotype-environment correlations are also explored. Nature Argument Nativists such as Jensen (1969) believe that intelligence is determined by nature-genetic makeup and estimate that 80% of the heritability in IQ is accounted for by genes. One way to determine the heritability of intelligence is by using twin studies. McGue and Bouchard (1998) reviewed five studies of monozygotic (MZ) twins who were reared apart and found that when accounting for heritability of intelligence, there was a correlation of 0.86 in MZ twins compared to the 0.60 correlation in dizygotic (DZ) twins. Hence, nature does play a role in the development of intelligence in childhood, because the monozygotic/MZ twins didn’t share the same environment but did share the same genes and had a higher correlation than dizygotic/DZ twins, suggesting that intelligence is heritable. Genome-wide association studies (GWAS) further investigate the relationship between genetic sequences and intelligence by examining individual chromosomal markers, such as single nucleotide polymorphisms (SNPs). Butcher et al (2008) conducted a genome scan using 7000 subjects and found six SNPs associated with intelligence, indicating that it is polygenic. The correlation between SNP-set scores and g scores is 0.105. Squaring this correlation indicates an effect size of 1.1% comparable to the sum of the effect sizes of the six SNPs. Figure 2 depicts a genotype-by-phenotype plot illustrating the relationship between SNP-set scores and standardised g . Identifying target alleles and SNP associations in genome polygenic scores has helped account for the heritability of intelligence in childhood. However, due to intelligence being polygenic, the contribution of any individual locus is small. Therefore, genomic variance only explains 10%, which makes it very difficult to detect relevant SNPS without huge samples. Foreseeable advances in genetic technology can mitigate this problem. Nurture Argument Alternatively, empiricists emphasise the family environment, socioeconomic status, and schooling, where schooling is a social influence. Sternberg et al., 2001 claim that pursuing higher education and schooling is associated with higher IQs. Dearey et al (2007), in their 5-year longitudinal study, recruited approximately 70,000 children and found a large overall contribution of intelligence to educational attainment, with an average chance of 58% of attaining grades between A and C. Therefore, their study establishes educational attainment for intelligence as an environmental outcome. However, the decision to pursue education may not be motivated by intelligence but may result from social causation, suggesting that social-economic conditions influence intelligence. The relationship between a parent's SES and a child's intelligence also exemplifies the role of nurture in the development of intelligence. This is further supported by Turkheimer et al (2003), where the authors concluded that in families with low levels of SES, 60% of the variance in IQ is explained by the shared environment, while in affluent families, all variation was accounted for by genes. However, parents with higher levels of intelligence may qualify for better-paying jobs. Hence, they have higher levels of SES, referring to social selection — when individuals influence the quality of their socio-economic environment — and genetics. Meanwhile, impoverished families do not get to develop their full genetic potential, and thus, the heritability of IQ is very low. Conversely, adoption can be seen as a social intervention that moves children from lower to higher SES homes and explores the gene-environment interplay in the development of intelligence. Kendler et al. (2015) studied 436 full male siblings, separated at birth, and tested at 18–20 years. A comparison was made between pairs of separated siblings (one raised in their biological family, the other in an adoptive family). Adopted-away siblings tested 7.6 points higher than their biological siblings when their adoptive parents had higher education levels than their biological parents (such as high school versus some postsecondary education). Gene-environment interplay According to Lerner et al. (2015), nature and nurture are inextricably linked and never exist independently of each other. In this way, the nature-nurture dichotomy presented in the title may be false. Gene-environment (GE) interplay offers two concepts: GE interaction and GE correlation. GE interaction is where the effects of genes on intelligence depend on the environment. GE correlation can be explained through adoption studies that compare genetically unrelated and related individuals. Supporting evidence from Van Ijzendoorn et al (2005) indicates that children who were adopted away from institutions had a better IQ than those children who remained in institutional care. Using 75 studies involving 3,800 children from 19 countries, a meta-analysis compared the intellectual development of children living in orphanages to those living with their adoptive families. On average, children growing up in orphanages had an IQ of 16.5 points lower than their adopted peers. This illustrates how adoptive families who typically have higher SES levels can assist children in achieving higher levels of IQ. However, the generalisability of Ijzendoorn's findings can be questioned as they used participants who were highly deprived in institutional settings, suggesting that their cognitive development is at risk. Furthermore, Neiss and Rowe (2000) contradicted Ijzendoorn’s findings by comparing adopted children to birth children to estimate the genetic-environmental effect of the mother's and father's years of education on the child's verbal intelligence. In biological families, mother-child (0.41) and father-child (0.36) correlations were significantly higher than in adoptive families (0.16). This implies that the adoptive parent's home environment has modest effects on the children's cognitive abilities, whereas the heredity and environment of the birth parents exert a profound influence. Conclusion In conclusion, both nature and nurture represent their significant role in childhood intelligence development, as they both offer testable evidence through twin studies and socio-economic correlations. Nevertheless, scientists have claimed that both genetics and environmental factors will predominantly influence the development of intelligence in childhood. This essay and future research in this field demonstrate that intelligence can be malleable, especially in children, through major social interventions and that the environment will continuously affect gene action. Written by Pranavi Rastogi Related articles: Mutualism theory of intelligence / Depression in children / Childhood stunting / Intellectual deficits / Does being bilingual make you smarter? Project Gallery

Exploring the distinctive features that define and disrupt the brain Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A deep dive into the hallmarks defining Alzheimer’s disease 08/07/25, 14:39 Last updated: Published: 06/11/24, 12:02 Exploring the distinctive features that define and disrupt the brain The progressive decline in neurocognition, resulting in a detrimental effect on one’s activities of daily living, is referred to as dementia. It typically affects people over the age of 65. Multiple theories have been proposed to explain the pathogenesis of Alzheimer’s disease (AD), including the buildup of amyloid plaques in the brain and the formation of neurofibrillary tangles (NFT) in cells. Understanding the pathophysiology of AD is imperative to the development of therapeutic strategies. Therefore, this article will outline the major hallmarks and mechanisms of AD. Hallmark 1: amyloid plaques One of the most widely accepted hypotheses for AD is the accumulation of amyloid beta protein (Aβ) in the brain. Aβ is a 4.2 kDa peptide consisting of approximately 40–42 amino acids, originating from a precursor molecule called amyloid precursor protein. This process, defined as amyloidosis, is strongly linked to brain aging and neurocognitive decline. How do the amyloid plaques form? See Figure 1 . Reasons for the accumulation of amyloid plaques: Decreased autophagy: Amyloid proteins are abnormally folded proteins. Autophagy in the brain is primarily carried out by neuronal and glial cells, involving key structures known as autophagosomes and lysosomes. When autophagy becomes downregulated, the metabolism of Aβ is impaired, eventually resulting in plaque buildup. Overproduction of acetylcholinesterase (AChE): Acetylcholine (Ach) is the primary neurotransmitter involved in memory, awareness, and learning. Overproduction of ACHE by astrocytes into the synaptic cleft can lead to excessive breakdown of Ach, with detrimental effects on cognition. Reduced brain perfusion: Blood flow delivers necessary nutrients and oxygen for cellular function. Reduced perfusion can lead to “intracerebral starvation”, depriving cells of the energy needed to clear Aβ. Reduced expression of low-density lipoprotein receptor-related protein 1: Low-density lipoprotein receptor-related protein 1 (LRP1) receptors are abundant in the central nervous system under normal conditions. They are involved in speeding up the metabolic pathway of Aβ by binding to its precursor and transporting them from the central nervous system into the blood, thereby reducing buildup. Reduced LRP1 expression can hinder this process, leading to amyloid buildup. Increased expression of the receptor for advanced glycation end products (RAGE): RAGE is expressed on the endothelial cells of the BBB, and its interaction with Aβ facilitates the entry of Aβ into the brain. Hallmark 2: neurofibrillary tangles See Figure 2 Neurofibrillary tangles are excessive accumulations of tau protein. Microtubules typically support neurons by guiding nutrients from the soma (cell body) to the axons. Furthermore, tau proteins stabilise these microtubules. In AD, signalling pathways involving phosphorylation and dephosphorylation cause tau proteins to detach from microtubules and stick to each other, eventually forming tangles. This results in a disruption in synaptic communication of action potentials. However, the exact mechanism remains unclear. Recent studies suggest an interaction between Aβ and tau, where Aβ can cause tau to misfold and aggregate, forming neurofibrillary tangles inside brain cells. Both Aβ and tau can self-propagate, spreading their toxic effects throughout the brain. This creates a vicious cycle, where Aβ promotes tau toxicity, and toxic tau can further exacerbate the harmful effects of Aβ, ultimately causing significant damage to synapses and neurons in AD. Hallmark 3: neuroinflammation Microglia are the primary phagocytes in the central nervous system. They can be activated by dead cells and protein plaques, where they initiate the innate immune response. This involves the release of chemokines to attract other white blood cells and the activation of the complement system which is a group of proteins involved in initiating inflammatory pathways to fight pathogens. In AD, microglia bind to Aβ via various receptors. Due to the substantial accumulation of Aβ, microglia are chronically activated, leading to sustained immune responses and neuroinflammation. Conclusion The contributions of amyloid beta plaques, neurofibrillary tangles and chronic neuroinflammation provide a framework for understanding the pathophysiology of AD. AD is a highly complex condition with unclear mechanisms. This calls for the need of continued research in the area as it is crucial for the development of effective treatments. Written by Blessing Amo-Konadu Related articles: Alzheimer's disease (an overview) / CRISPR-Cas9 to potentially treat AD / Sleep and memory loss REFERENCES 2024 Alzheimer’s Disease Facts and Figures. (2024). Alzheimer’s & dementia, 20(5). doi:https://doi.org/10.1002/alz.13809. A, C., Travers, P., Walport, M. and Shlomchik, M.J. (2001). The complement system and innate immunity. [online] Nih.gov. Available at: https://www.ncbi.nlm.nih.gov/books/NBK27100/ . Bloom, G.S. (2014). Amyloid-β and tau: the Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA neurology, [online] 71(4), pp.505–8. doi:https://doi.org/10.1001/jamaneurol.2013.5847. Braithwaite, S.P., Stock, J.B., Lombroso, P.J. and Nairn, A.C. (2012). Protein Phosphatases and Alzheimer’s Disease. Progress in molecular biology and translational science, [online] 106, pp.343–379. doi:https://doi.org/10.1016/B978-0-12-396456-4.00012-2. Heneka, M.T., Carson, M.J., El Khoury, J., Landreth, G.E., Brosseron, F., Feinstein, D.L., Jacobs, A.H., Wyss-Coray, T., Vitorica, J., Ransohoff, R.M., Herrup, K., Frautschy, S.A., Finsen, B., Brown, G.C., Verkhratsky, A., Yamanaka, K., Koistinaho, J., Latz, E., Halle, A. and Petzold, G.C. (2015). Neuroinflammation in Alzheimer’s disease. The Lancet. Neurology, 14(4), pp.388–405. doi:https://doi.org/10.1016/S1474-4422(15)70016-5. Kempf, S. and Metaxas, A. (2016). Neurofibrillary Tangles in Alzheimer′s disease: Elucidation of the Molecular Mechanism by Immunohistochemistry and Tau Protein phospho- proteomics. Neural Regeneration Research, 11(10), p.1579. doi:https://doi.org/10.4103/1673-5374.193234. Kumar, A., Tsao, J.W., Sidhu, J. and Goyal, A. (2022). Alzheimer disease. [online] National Library of Medicine. Available at: https://www.ncbi.nlm.nih.gov/books/NBK499922/. Ma, C., Hong, F. and Yang, S. (2022). Amyloidosis in Alzheimer’s Disease: Pathogeny, Etiology, and Related Therapeutic Directions. Molecules, 27(4), p.1210. doi:https://doi.org/10.3390/molecules27041210. National Institute on Aging (2024). What Happens to the Brain in Alzheimer’s Disease? [online] National Institute on Aging. Available at: https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/what-happens-brain- alzheimers-disease. Stavoe, A.K.H. and Holzbaur, E.L.F. (2019). Autophagy in Neurons. Annual Review of Cell and Developmental Biology, 35(1), pp.477–500. doi: https://doi.org/10.1146/annurev-cellbio-100818-125242 . Project Gallery

Natural substances and their treatment potential Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Using Natural Substances to Tackle Infectious Diseases 14/07/25, 15:11 Last updated: Published: 06/06/23, 17:06 Natural substances and their treatment potential Introduction There is increased concern of antimicrobial resistance, especially when referring to bacteria with superbugs such as Methicillin-resistant Staphylococcus aureus (MRSA) and Carbapenem-resistant Enterobacteriaceae (CRE) as they impact lives globally, mainly through fatalities. Given this predicament, It seems that humanity is losing as a result of this pressing issue. However, it is possible for healthcare professionals to utilise more natural products, which are chemicals made by plants, animals and even microorganisms. This includes resources such as wood and cotton aside from food like milk and cacao. In the context of medicinal treatments, an important justification for using more natural products is because although synthetic or partially synthetic drugs are effective for treating countless diseases, an article found that 8% of hospital admissions in the United States and approximately 100,000 fatalities per year were due to people experiencing unfortunate side effects from these drugs. This article explores three specific natural products, where each have similar and unique health properties that can be harnessed to tackle infectious diseases and its subsequent consequences when left sufficiently unaddressed (i.e. antimicrobial resistance). Honey One of the most famous natural products that has been referenced in various areas of research and has been a food and remedial source for thousands of years is honey. It has properties ranging from antibacterial to antioxidant, suggesting that when honey is applied clinically, they have the potential to stop pathogenic bacteria. For example, honey can protect the gastrointestinal system against Helicobacter pylori , which causes stomach ulcers. In disc diffusion assays, the inhibitive properties of honey were shown when honey samples were evaluated holistically as opposed to its individual ingredients. This implies that the macromolecules in honey (carbohydrates, proteins and lipids) work in unison with other biomolecules, illustrating that honey is a distinctive remedy for preventing bacterial growth. For tackling infectious diseases, particularly against wound infections among others, honey’s medicinal properties provide a lot of applications and because it is a natural product, honey would not present any drastic side effects to a patient upon its administration. Garlic Another natural product that can be effective against microorganisms is garlic because similar to honey, it has antimicrobial and antioxidative compounds. A study judged different garlic phenotypes originating from Greece and discovered that they were beneficial against Proteus mirabilis and Escherichia coli aside from inhibiting Candida albicans and C. kruzei . As for fresh garlic juice (FGJ), it increases the zone of inhibition in various pathogens at 10% and more along with it displaying minimum inhibitory concentrations (MICs) in the 4-16% range. Therefore, garlic in solid or liquid form does show potential as a natural antimicrobial agent, especially against pathogenic bacteria and fungi. With this in mind, it too has multiple applications like honey and should be further studied to best isolate the chemical compounds that could be involved in fighting infectious diseases. Turmeric Curcuma longa (also known as turmeric) is one other natural product with unique properties like garlic and honey, making it a suitable candidate against various microbes. One specific pigment that is part of the ginger family and found in turmeric is curcumin, which can tackle diverse microbes through numerous mechanisms illustrated below in Figure 2 . With this said, curcumin has drawbacks: it is highly hydrophobic, has low bioavailability and quickly breaks down. Although when paired with nanotechnology for delivery into the human body, its clinical applications can be advantageous and an additional observation about curcumin is that it can work collaboratively with other plant derived chemicals to stop antibiotic resistant bacteria. One specific bacterial strain that turmeric can attack is Clostridium difficile, a superbug that causes diarrhoea. A study had 27 strains to measure the MICs of turmeric constituents, particularly curcuminoids and curcumin. The results showed reduced C. difficile growth in the concentration range 4-32 μg/mL. Moreover, they had no negative impacts on the gut microbiome and curcumin had more efficacy in stopping C. difficile toxin production compared to fidaxomicin. Thus, turmeric is efficacious as a natural antimicrobial chemical and with further experimentation (same as honey and garlic), it can be harnessed to prevent infectious diseases besides their impact on human lives. Conclusion Considering the above examples of natural products in this article and others not mentioned, it is clear that they can be powerful in the battle against infectious diseases and the problems associated with them, mainly antimicrobial resistance. They are readily available to purchase in markets and shops at low cost, making them convenient. Moreover, populations in Eastern countries like China and India traditionally have used, and are still using these materials for curing pain and illness. In turn, manufacturing medicines from natural products on a larger scale has the prospect of preventing infectious diseases and even alleviating those that patients currently have. Written by Sam Jarada Related article: Mechanisms of pathogen evasion Project Gallery