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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

The same condition after all? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorder 09/07/25, 14:21 Last updated: Published: 20/01/24, 11:38 The same condition after all? Practice and progress in rheumatology The relationship between hypermobile Ehlers-Danlos Syndrome (hEDS) and Hypermobility Spectrum Disorder (HSD) has been hotly debated in recent years, with research being published on a near-constant basis attempting to establish a valid symptomatological or causalogical difference between the two disorders. Now, a paper by Ritelli et al. (2022) threatens to end the savage cycle for all. Using RNA sequencing techniques and immunofluorescence, Ritelli et al. found identical gene expression and cellular characteristics in dermal biopsies from those with both conditions. Through immunofluorescence of biopsies from 20 women with hEDS, 16 women and 4 men with HSD and 40 controls, it was found that the shape and components of the extracellular matrix were greatly different in those with HSD/hEDS in comparison to those in the healthy control group. Abnormalities were discovered in the expression of cadherin-11, snail1, and αvβ3, α5β1 and α2β1 integrins. Integrins mediate the connections between the cell cytoskeleton and extracellular matrix to ensure they stay together, cell-to-cell adhesion is initiated by cadherin-11, and snail1 is localised close to the cyclin-dependent kinase inhibitor 2B (CDKN2B) gene. Snail1 can activate CDKN2B gene products when Snail1 is overexpressed to the point of reaching the general localisation of the CDKN2B domain. This demonstrates that there may be a similar causative link between the widespread inflammation and chronic pain in HSD/hEDS and rheumatoid arthritis. Li et al. (2021) proved that the polarisation of macrophages (white blood cells which destroy foreign products) was carefully controlled by the CDKN2B-AS1/ MIR497/TXNIP axis- the increased activation of which in rheumatoid arthritis catalyses the excessive polarisation of macrophages, which causes the macrophages to attack healthy cells. In rat studies published by Tan et al. (2022), it was found that rats with diabetes and induced sepsis experienced greater intestinal injury that control rats without any medical pathology who experienced induced sepsis. This was demonstrated to be due to interruptions in the miR-3061/Snail1 communication pathway. Research on this phenomenon in humans may elucidate the relevance of snail1 overproduction in hEDS/HSD sufferers to their complex gastrointestinal symptoms. If this pathway works similarly in human models of sepsis or localised GI infection, it may intimate that snail1 overproduction is responsible for the hyperpolarisation of macrophages in response to foreign product detection, which may cause immunological damage in the intestines. However, the relevance of this study to hEDS/HSD should be considered questionable until further human research into this avenue has been completed. The result of this research is that academia can potentially derive a genetic cause of the complex phenotypes demonstrated by sufferers of hEDS/HSD. This can be achieved by visualising the human genome, and testing genes like those above, or those implicated in modulating the activity of the genes above. Once garnered, this genetic evidence will elucidate whether or not hEDS and HSD are one disorder, or both variants of the same disorder with differing genetic causes. This, in turn, could lead to the development of medications or treatments based on genetic phenotype. Written by Aimee Wilson Related articles: Ehlers-Danlos syndrome / Types of movement Project Gallery

Comparative oncology Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What can our canine friends tell us about cancer? 14/07/25, 15:12 Last updated: Published: 02/07/24, 10:04 Comparative oncology Comparative oncology is a field of study within cancer that has been adopted to study cancer and develop new therapies. It involves studying cancer in animals to uncover similarities between human and animal cancers. By combining scientific findings across a range of species, including companion animals such as dogs and horses or non-human primates such as monkeys, comparative oncology will advance cancer research and help develop effective novel therapies. This approach not only explores cancers in both animals and humans but also aims to bridge the gap between human and veterinary medicine. By examining similarities and differences in cancer biology, progression and treatment responses across species, comparative oncology provides valuable insights that can benefit both fields. Understanding how cancer behaves in animals can offer new perspectives and potential therapies for human patients. Conversely, while findings in human oncology can inform veterinary medicine, leading to improved diagnostics and treatments for animals. ( Figure 1 summarises the aims of comparative oncology). This article aims to explore this field of oncology further by discussing what it entails, the methodologies utilised, some recent advancements, and finally, things to look out for in the future. Comparative oncology has been developed and expanded into two areas of study. This includes spontaneous oncology and experimental oncology. Spontaneous oncology focuses on naturally occurring tumours in animals by investigating aspects of carcinogenesis, epidemiology, diagnosis, and treatment. It provides unique insights by drawing comparisons with human oncology research. These results can then be extrapolated to human oncology to gain a better understanding of cancer. This is because the similarities and differences observed in naturally occurring tumours across species provide valuable insights into underlying mechanisms within tumours and treatment responses. Experimental oncology serves as a distinct discipline where there are specialisations such as studying viral, chemical, and radiation oncogenesis alongside studying environmental factors such as pollution residues and food additives. This area involves studying both spontaneous tumours in animals and lab settings, where controlled conditions are used to explore different parts of cancer biology and treatment strategies. Additionally, the primary methodology utilised in comparative oncology involves studying spontaneous tumours in animals. Unlike artificially induced tumours in lab animals, these spontaneous tumours in pets closely mimic the complexity and heterogeneity of human cancers. For example, canines will live in similar living environments and experience similar external stimuli to their owner, such as pollution. The nature of these external stimuli means that they develop cancer in similar ways caused by epigenetic alterations, metabolic, and immune changes. (Figure 2 illustrates this process). Furthermore, comparative oncology uses advanced imaging techniques, genetic analysis, and immunological studies to predict pathways that may be shared among animals and humans which, could drive cancer development. Overall, these methods will allow the identification of promising therapies which directly target cancer and expand on current treatment choices such as chemotherapy and immunotherapy. One of the recent advancements in comparative oncology relates to osteosarcomas. This refers to cancer cells which begin to grow in the bones. For this specific form of cancer, molecular signatures were identified to predict clinical outcomes for both humans and canines, which can help improve treatment outcomes. Led by Amy K. LeBlanc, scientists have identified gene activity patterns in osteosarcoma tumours in nearly 200 dogs, revealing distinct groups with varying prognoses. These findings help us understand the biology behind osteosarcomas further and can potentially help us develop targeted therapies that take advantage of the immune system to treat the disease in both species. This potentially includes a range of therapies including PD-L1 inhibitors and cancer vaccines targeting the immune system. Moreover, breakthroughs in immunotherapies such as checkpoint inhibitors and CAR-T cell therapy are effective in treating haematological malignancies in both humans and canines. Furthermore, studies in canine melanoma reveal similar gene expression changes to human melanoma, such as in the PI3K/AKT/mTOR and MAPK pathways, even when the driver mutations are different. (Figure 3 shows how the pathway contributes to cancer). Useful data was provided in trials using companion animals with spontaneous tumours, providing an insight into safety, dosage, and efficacy, which have paved the way to develop treatments for both species. To conclude, it is clear with comparative oncology, researchers will be able to identify new molecular targets, assess novel drugs, and identify patient populations which will benefit the most from these therapies. It holds great promise in helping streamline cancer diagnosis further and even plays a role in preventing cancer. While the field shows great potential, more studies still need to be conducted to understand the similarities and differences in cancers between animals and humans. Additionally, more collaboration is needed amongst oncologists, veterinarians, and researchers across these disciplines to harness collective expertise to address questions relating to cancer diagnosis, treatment, and prevention. Ultimately, this field will help us identify new avenues of treating and diagnosing cancer whilst improving healthcare outcomes for humans and animals alike. Written by Harene Elayathamby Related articles: Why blue whales don't get cancer / Rare zoonotic diseases REFERENCES Schiffman, J.D. and Breen, M. (2015) ‘Comparative oncology: What dogs and other species can teach us about humans with cancer’, Philosophical Transactions of the Royal Society B: Biological Sciences , 370(1673), p. 20140231. doi:10.1098/rstb.2014.0231. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Al, B. and C., C. (2007) ‘Chapter 1 COMPARATIVE ONCOLOGY ’, in Comparative oncology . Bucharest (RO): The Publishing House of the Romanian Academy, p. 1. Vail, D.M., LeBlanc, A.K. and Jeraj, R. (2020) ‘Advanced cancer imaging applied in the comparative setting’, Frontiers in Oncology , 10. doi:10.3389/fonc.2020.00084. New findings highlight shared features of human and canine osteosarcoma (2023) Center for Cancer Research . Available at: https://ccr.cancer.gov/news/article/new-findings-highlight-shared-features-of-human-and-canine-osteosarcoma (Accessed: 02 March 2024). Mochel, J.P. et al. (2018) Car T-cell immunotherapy in human and veterinary oncology: Changing the odds against hematological malignancies [Preprint]. doi:10.20944/preprints201811.0525.v1. LeBlanc AK, Mazcko CN, Khanna C. (2016) ‘Defining the Value of a Comparative Approach to Cancer Drug Development’, Clinical cancer research : an official journal of the American Association for Cancer Research , 22(9). p. 2133-2138. doi: 10.1158/1078-0432.CCR-15-2347 FIGURE REFERENCES Boddy, A.M., Harrison, T.M. and Abegglen, L.M. (2020) ‘Comparative oncology: New insights into an ancient disease’, iScience , 23(8), p. 101373. doi:10.1016/j.isci.2020.101373. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Rascio, F. et al. (2021) ‘The pathogenic role of PI3K/Akt pathway in cancer onset and drug resistance: An updated review’, Cancers , 13(16), p. 3949. doi:10.3390/cancers13163949. Project Gallery

Aggression has the confluence of individual predisposition and maintenance via social context Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unmasking aggression: a result of personal or social triggers? 14/07/25, 15:10 Last updated: Published: 01/01/25, 14:02 Aggression has the confluence of individual predisposition and maintenance via social context Introduction Anderson & Bushman (2002) define aggression as behaviour aimed at causing harm to another individual. Aggression can be measured by observing a signal of intention or aggression rating by self or others. The social theories of aggression include Dollard's frustration-aggression theory and Bandura's Social Learning Theory, while the individual factors theories account for personality traits and the influence of alcohol. However, there is no definite answer to whether social or individual factors are most important in explaining human behaviour. The interaction between social and individual factors will be explored to gain a deeper understanding of aggression. Social theories The frustration-aggression hypothesis proposed by Dollard et al. (1939) defines frustration as the emotion that follows when the occurrence of an instigated goal-response is interfered with, in turn leading to anger and aggression. According to this hypothesis, a person’s aggressive tendencies will be more intense the closer the individual is to achieving a goal before an obstacle appears. Many support this hypothesis, including Dill and Anderson (1995), who found that levels of aggression resulting from unjustified frustration were higher than justified frustration because they were caused by situational constraints rather than dispositional qualities. However, Berkowitz (1989) criticises Dollard et al.'s hypothesis, saying that frustration can only produce aggressive behaviour if it causes adverse effects. Due to the wide variety of negative and positive effects of frustration, it is important to revisit and clarify the frustration-aggression hypothesis. Additionally, aggression is often explained by the Social Learning Theory (SLT), proposed by Bandura et al. (1963), which states that aggressive behaviour is a learned behaviour reinforced by imitation and rewards or punishment. Bandura conducted the renowned Bobo Doll Study in 1961, in which children mimicked adult behaviour and attacked the doll after watching the researchers physically and verbally abuse a clown-faced inflatable toy in front of them, making this study extremely influential in understanding the role that families and household dynamics play in human behaviour. Based on this theory, exposure to TV violence can teach aggressive conduct and provide a model of behaviour to base actions upon. In SLT, rather than frustration generating an aggressive drive that can only be reduced by injurious behaviour, aversive stimulation creates general emotional arousal that can result in aggressive behaviour. Therefore, social theories encompass a broad range of disinhibitory factors and provide a broad theory explaining both impulsive and principled aggressive conduct. Individual factors theories Individual differences and variables, like personality traits, have also contributed to the study of aggressive behaviour. Hyatt et al. (2019) stated that certain personality traits such as narcissism and sadism have been meta-analytically linked to aggression shown in a lab setting. The lab paradigm captures aggression as it manifests whilst controlling for confounding variables, such as different types of aggression. However, the lab paradigm lacks construct validity because researchers don’t interpret the subjects’ intentions and motives when operationalising aggression. Further evaluation comes from Bettencourt et al. (2006), who meta-analysed personality dimensions and stated that provocation can cause aggression. They note that individuals with Type A personalities often exhibit impulsivity and emotional reactivity, which are positively associated with aggression. Thus, situational circumstances such as provocation and aggressive cues interact with these personality factors, together shaping the likelihood and intensity of aggressive behaviour. Additionally, the interplay between personality and alcohol can explain aggression. Alcohol reduces inhibitions that regulate 'normal' behaviour and increases aggression. Miller et al. (2009) concluded that alcohol may facilitate aggression in high-trait individuals specifically, those who score high on traits associated with aggression, such as impulsivity, hostility, or a predisposition toward anger—by impairing the drinker’s inhibition. Moreover, further research indicates a strong relationship between alcohol consumption and antisocial personality. Therefore, any discussion of personal factors and personality in aggression would be incomplete without considering the influence of alcohol. The interplay between social and individual trait theories Allen et al. (2018) created a model that encompasses both the social and the individual trait theories. The General Aggression Model (GAM) considers social, biological, and individual factors in aggression. This model consists of three stages: input, appraisal, and action. The input stage determines the likelihood of personal and situational factors causing aggression. For instance, individual differences, such as personality, social rejection, and provocation, are identified as risk factors for aggression. During the appraisal stage, the individual decides how to respond. Their response can be aggressive or non-aggressive, depending on the resources, time, and event. The action then influences the social encounter, which can alter personal and situational factors, leading to those factors restarting the cycle. Hence, this model proposes that individuals learn situations that lead to aggressive outcomes. To reduce aggression and offer treatment, the GAM has been applied to intergroup violence and therefore can be applied to a wide range of situations in real life. Conclusion In conclusion, aggression has the confluence of individual predisposition and maintenance via social context. For instance, as discussed previously, socialisation experiences may contribute to aggressive behaviour in individuals with certain personality traits. Thus, it is difficult to distinguish social and individual factors when explaining aggression, as most human behaviour is a multifaceted phenomenon with multiple determinants. Therefore, future research should be more holistic in the explanations of aggression, encompassing both social and individual factors. Written by Pranavi Rastogi Related articles: Emotional chemistry / Psychology of embarrassment / Brain of a bully REFERENCES Allen, J. J., Anderson, C. A., & Bushman, B. J. (2018). The general aggression model. Current Opinion in Psychology,19 , 75-80. doi:10.1016/j.copsyc.2017.03.034 Anderson, C. A., & Bushman, B. J. (2002). Human aggression. Annual Review of Psychology, 53 (1), 27-51. doi:10.1146/annurev.psych.53.100901.135231 Bandura, A., Ross, D., & Ross, S. A. (1963). Imitation of film-mediated aggressive models. Journal of Abnormal and Social Psychology, 66, 3-11 Berkowitz, L. (1989). Frustration-aggression hypothesis: Examination and reformulation. Psychological Bulletin, 106 (1), 59-73. doi:10.1037/0033-2909.106.1.59 Bettencourt, B.A. et al. (2006) ‘Personality and aggressive behavior under provoking and neutral conditions: A meta-analytic review.’, Psychological Bulletin , 132(5), pp. 751–777. doi:10.1037/0033-2909.132.5.751. Dill, J. C., & Anderson, C. A. (1995). Effects of frustration justification on hostile aggression. Aggressive Behavior, 21 (5), 359-369. doi:10.1002/1098-2337(1995)21:5<359::aid-ab2480210505> 3.0.co ;2-6 Dollard, J., Miller, N. E., Doob, L. W., Mowrer, O. H., & Sears, R. R. (1939). Frustration and aggression. doi:10.1037/10022-000 Hyatt, C. S., Chester, D. S., Zeichner, A., & Miller, J. D. (2019). Analytic flexibility in laboratory aggression paradigms: Relations with personality traits vary (slightly) by operationalization of Aggression. Aggressive Behavior, 45 (4), 377-388. doi:10.1002/ab.21830 Miller, C.A., Parrott, D.J. and Giancola, P.R. (2009) ‘Agreeableness and -related aggression: The mediating effect of trait aggressivity.’, Experimental and Clinical Psychopharmacology , 17(6), pp. 445–455. doi:10.1037/a0017727. Project Gallery

A short exploration of the genetic predisposition behind human behaviours Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can we blame our genes for excessive smoking and drinking? 09/07/25, 13:31 Last updated: Published: 13/01/24, 15:33 A short exploration of the genetic predisposition behind human behaviours The advancing research on how tobacco, alcohol addictions, and other detrimental behaviors are consequences of complex interplays between genetic and environmental factors has gradually developed and gained credibility. A collaborative effort involving over 100 international scientists, including researchers from the National Institutes of Health (NIH) and the National Institute on Drug Abuse (NIDA), embarked on a genome-wide association study (GWAS) to explore the heritable traits associated with tobacco and alcohol addiction. The study analyzed data from a sample size of 1.2 million biobanks, epidemiological research, and genetic testing companies, shedding light on the relationship between genetics and addiction behaviors. Researchers discovered that phenotypes related to smoking, such as when individuals began smoking habits, are genetically correlated with various diseases. In contrast, increased genetic risk for alcohol consumption is linked to reduced risk of many diseases. Previous studies pinpointed 10 genes involved in the risk of tobacco and alcohol addiction. In addition, this study further contributed to genetic links by identifying more than 400 locations in the genomes with over 500 variants associated with critical functions involving dopamine regulation, glutamate transmission and acetylcholine activation in the brain. Another study involving 3.4 million people with diverse ancestries suggested that approximately 3,823 genetic variants may impact addiction behaviors, with specific variants associated with the age at which individuals start smoking and the number of cigarettes or alcoholic drinks consumed. These studies could indicate a future where genetic screening for genes relevant to addiction behaviors is available, and this could be especially useful for those with relatives involved in certain addictions. Furthermore, it also provides perspective on whether certain genes can increase the likelihood of addiction to illegal drugs like cocaine, heroin or MDMA. However, increasing people’s awareness of whether they are at risk of developing addictions may be insufficient in deterring them from pursuing risky behaviors, which suggests that genetic screening for these genes would be beneficial as an optional screening assessment for individuals. While the influence of environmental and social factors on tobacco and alcohol addictions has long been acknowledged and explored, these studies underscore the significant role genetics plays in determining an individual’s susceptibility to nicotine and alcohol dependence. The prospect of predicting a person’s risk of addiction can lead to early interventions. Furthermore, it prevents countless health-related fatalities associated with smoking and alcoholic beverages. This primary prevention provides a different aspect to risk factors for smoking and alcohol addiction while also reducing the burden of these highly prevalent public health concerns. Written by Maya El Toukhy Related article: Smoking cessation References: New Scientist (n.d.). Thousands of genetic variants may influence smoking and alcohol use. [online] New Scientist. Available at: https://www.newscientist.com/article/2350516thousandsofgenetic-variants-may-influence-smoking-and-alcohol-use/ [Accessed 23 Oct. 2023]. Today’s Clinical Lab. (n.d.). Do Your Genes Predispose You to Smoking and Drinking? [online] Available at: https://www.clinicallab.com/do-your-genes-predispose-you-tosmokinganddrinking-26963 [Accessed 23 Oct. 2023]. University of Minnesota. (2019). Hundreds of genes affecting tobacco and alcohol use discovered. [online] Available at: https://twin-cities.umn.edu/newsevents/hundredsgenesaffecting-tobacco-and-alcohol-use-discovered [Accessed 23 Oct. 2023]. Schlaepfer, I., Hoft, N. and Ehringer, M. (2008). The Genetic Components of Alcohol and Nicotine Co-Addiction: From Genes to Behavior. Current Drug Abuse Reviewse, 1(2), pp.124– 134. doi: https://doi.org/10.2174/1874473710801020124 . Project Gallery

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

Chemistry is such a diverse science branching into many industries and its understanding is fundamental in unlocking solutions to overcome diseases, viruses and infections. The science has a central application in the pharmaceutical drug manufacturing process. In medicine, Chemistry helps understand diseases and medical samples through the various analytical and instrumental methods – which in turn aids medical research and the development and discovery of drugs. Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The role of chemistry in medicine Last updated: 17/11/24 Published: 13/04/23 Chemistry is such a diverse science branching into many industries and its understanding is fundamental in unlocking solutions to overcome diseases, viruses and infections. The science has a central application in the pharmaceutical drug manufacturing process. In medicine, chemistry helps understand diseases and medical samples through the various analytical and instrumental methods – which in turn aids medical research and the development and discovery of drugs. Chemical synthesis has allowed scientists to synthesise new compounds which can be used to treat a range of diseases and medical conditions. The study and knowledge of chemistry is very essential for professionals involved in the healthcare sector including doctors and nurses. The fact is that it cannot be denied that chemistry plays a dominant role in the day-to-day life of a healthcare professional. With the help of chemistry alongside biochemistry and biology, diseases and disorders can be easily diagnosed. The knowledge of chemistry has allowed for the understanding of the science behind pregnancy tests and COVID-19 PCR tests using UV-VIS Spectroscopy. Chemistry also plays a key role in the development of new medical technologies, such as diagnostic tools and imaging equipment. Magnetic resonance imaging (MRI) relies on principles of chemistry and is an application of nuclear magnetic resonance (NMR), an analytical tool for chemists found in laboratories. The technique uses strong magnetic fields and radio waves to produce detailed images of organs and body tissues. The scan uses contrast agents using elements iron and gadolinium to enhance the clarity of images. Overall, chemistry is an essential discipline for advancing our understanding of health and disease, and for developing new treatments and technologies to improve human health. Interesting fact: vaccines for rabies and anthrax were discovered by Louis Pasteur – a famous chemist. Written by Khushleen Kaur Related articles: AI in medicinal chemistry / The role of chemistry in space

Peruse through the current treatment discoveries for one of the deadliest diseases in the world. With key breakthroughs in research, take a deep dive into specific cancers like bone, breast, and ovarian cancer. Learn about cancer biomarker evolution. Cancer Articles Peruse through the current treatment discoveries for one of the deadliest diseases in the world. With key breakthroughs in research, take a deep dive into specific cancers like bone, breast, and ovarian. Learn about cancer biomarker evolution. You may also like: Biology, Medicine Cancer biomarkers What does cancer evolution mean to cancer diagnosis and prognosis? Breast cancer and asbestos A collaboration with the Mesothelioma Centre (Asbestos), US Bone cancer How bone cancer forms Breast cancer in men How this killer disease affects the male population. Article #2 in a series on Rare diseases. Secondary bone cancer What is secondary bone cancer? Cancer treatment A breakthrough drug discovery process Liquid biopsies A novel diagnostic tool Cancer on the move Metastasis Epithelioid hemangioendothelioma A rare type of cancer. Article #4 in a series on Rare diseases. Ovarian cancer A deep dive Prostate cancer A breakthrough in treatment for this disease African-American women in cancer research Celebrating trailblazers in skin cancer, chemotherapy and cervical cancer cells Polly Matzinger A summary of the influential cancer immunologist's works The Hippo signalling pathway Also known as the Salvador-Warts-Hippo (SWH) pathway Illuminating thyroid cancer Shedding light on this disease Canines and cancer What can our canine friends tell us about cancer? Apocrine carcinoma A rare form of breast cancer. Article #9 in a series on Rare diseases. Metastasis caused by immue signals Chromosomal instability initiates immune signals, which lead to metastasis The Emperor of All Maladies by Siddhartha Mukherjee Book review The MAPK/ ERK pathway The mitogen-activated protein kinase/extracellular signal regulated kinase pathway Next

Recognising the remarkable contributions in the vast field of engineering, including silicon hydrogel contact lenses, wireless electricity, hydrogen cars and many other innovations. 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; looking at hydroxyapatite polyethylene, imaging and therapeutic tools for cancer and cancer-cell surfaces 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? The Titan Submersible Investigating its failure due to its design and engineering

Uncovering the truth behind the origins of the virus Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Origins of COVID-19 10/07/25, 10:27 Last updated: Published: 08/10/23, 16:07 Uncovering the truth behind the origins of the virus The quest for the crime of the century begins now! Suspicion of the Wuhan Institute of Virology Since the early epidemic reports in Wuhan, the origin of COVID-19 has been a matter of contention. Was SARS-CoV-2 the outcome of spontaneous transmission from animals to humans or scientific experimentation? Although most of the recorded initial cases occurred near a seafood market, Western Intelligence Agencies knew that the Wuhan Institute of Virology (WIV) was situated nine miles to the south. Researchers at the biosafety centre combed Yunnan caves for bats harbouring SARS-like viruses. They have been extracting genetic material from their saliva, urine, and faeces. Additionally, bat coronavirus RaTG13 (BatCoV RaTG13) shared 96% of its genome with SARS-CoV-2. Suspicion increased when it was discovered that WIV researchers dealt with chimeric versions of SARS-like viruses capable of infecting human cells. However, similar "gain-of-function" studies in Western biosecurity institutions have shown that such slow virulence increases may occur naturally. The coincidence that the pandemic began in the same city as the WIV outbreak was too obvious to ignore. According to two Chinese specialists , "the likelihood of bats flying to the market was quite remote". Chan and Ridley's "Quest for the Origin of COVID-19" Chan and Ridley have created a viral whodunit titled "Quest for the origin of COVID-19" to excite the curiosity of armchair detectives and scientific sceptics. Both need clarification as to why a virus of unknown origin was detected in Wuhan and not in Yunnan, 900 kilometres to the south. The stakes could not be more significant; if the virus were deliberately developed and spread by a Chinese laboratory, it would be the crime of the century. They are prudent in not going that far. They are, however, within their rights to cast doubt on the findings since their concerns were shared by numerous coronavirus experts who openly discounted the possibility of a non-natural origin and declared that the virus displayed no evidence of design at the time. Is this the impartial and fair probe the world has been waiting for? They present no evidence for the development of SARS-CoV-2. For example, Chan asserts that it seemed pre-adapted to human transmission " to an extent comparable to the late SARS-CoV-2 outbreak ". This statement is based on a single spike protein mutation that appears to "substantially enhance" its potential to connect to human receptor cells, meaning it had "apparently stabilised genetically" when identified in Wuhan. Nonetheless, this is a staggeringly misleading statement. As seen by the alphabet soup of mutations, the coronavirus has undergone multiple alterations that have consistently increased its suitability. Additionally, viruses isolated from pangolins attach to human receptor cells more efficiently than SARS-CoV-2, indicating the possibility of additional adaptation. According to two virologists, although the SARS-CoV-2 virus was not wholly adapted to humans, it was "merely enough". Evidence for design of SARS-CoV-2 and possible natural origins of the virus Another concerning feature of SARS-CoV-2 is a furin cleavage site, which enables it to infect human cells by interfering with the receptor protein. The identical sequence is present in highly pathogenic influenza viruses and was previously utilised to modify the spike protein of COVID-19. Chan and Ridley explain that this is the kind of insertion that would occur in a laboratory-modified bat virus. As a result, 21 leading experts have concluded that the furin sequence is insufficient. Coronaviruses have been shown to possess " near identical " genomes that often can infect humans and animals. Because the furin cleavage site characteristic is not seen in known bat coronaviruses, it is possible that it evolved naturally. Surprisingly, Chan and Ridley do not suggest that the SARS virus's high human infectivity feature was inserted on purpose since "there is no way to determine". There is also no way to determine if a RaTG13 is the pandemic virus's progenitor since history is replete with pandemics that began with zoonotic jumps. This argument is based on the strange fact that WIV researchers retrieved the bat isolate in 2013 from a decommissioned mine shaft in Yunnan. Six people were removing bat guano from the cave that year when they suffered an unexplained respiratory ailment. As a consequence, half of them perished. The 4% genetic diversity between RaTG13 and SARS-CoV-2, on the other hand, is similar to 40 years of evolutionary change. While exploring caves in northern Laos, researchers discovered three more closely related bat coronaviruses, which have a higher affinity to attach to human cells than the early SARS-CoV-2 strains. This indicates an organic origin, either through another animal host or directly from a bat, maybe when a farmer went into a cave. This is arguably the most reasonable explanation since it is consistent with forensic and epidemiological data. The food sample isolates collected from the Wuhan seafood market are similar to human isolates, and the majority of original human cases had a history of market exposure, in contrast to the absence of an epidemiological connection to the WIV or any other Wuhan research institution. Lack of evidence for a laboratory origin If scientists could demonstrate prior infection at the Wuhan market or other Chinese wildlife markets that sell the most likely intermediary species, including pangolins, civet cats, and raccoon dogs, the case for a natural origin would be strengthened. Although multiple animals tested positive for sister human viruses during the SARS epidemic, scientists have yet to find evidence of earlier infections in animals in the instance of Sars-CoV-2. Nonetheless, the absence of evidence does not confirm the absence and may indicate that samples were not taken from the appropriate animal. The same may be said of the lab leak argument's lack of evidence. However, even though history is littered with pandemics, no significant pandemic has ever been traced back to a laboratory. In other words, the null hypothesis is a zoonotic occurrence; Chan and Ridley must demonstrate otherwise. The irony is their drive to construct a compelling case for a laboratory accident. They are oblivious to the much more pressing story of how the commerce in wild animals, global warming, and habitat degradation increase the likelihood of pandemic viral development. This is the most plausible origin story that should concern us. Summary Although Chan and Ridley's "Quest for the Origin of COVID-19" has cast suspicion on the Wuhan Institute of Virology, there is still insufficient evidence to support the lab leak theory. There is, however, growing evidence for a natural origin of SARS-CoV-2, with multiple animals testing positive for sister human viruses during the SARS epidemic and the discovery of more closely related bat coronaviruses in northern Laos. As such, we should be more concerned with the increasing likelihood of pandemic viral development due to the commerce in wild animals, global warming, and habitat degradation. Written by Sara Maria Majernikova Project Gallery