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This page features articles which tackle imminent health problems such as smoking, childhood obesity and depression, and pre-diabetes. Skin disease, Crohn's disease, anaemias, and endometriosis are also explored.  Medicine Articles This page features articles which tackle imminent health problems such as smoking, childhood obesity and depression, and pre-diabetes. Skin disease, Crohn's disease, anaemias, and endometriosis are also explored. You may also like: Dentistry , Biology Interventions for smoking cessation Public smoking health interventions The problem with childhood obesity What is childhood obesity? How many does it affect, and what can we do to tackle this? Pre-diabetes Pre-diabetes is the period before the onset of diabetes Anaemias Anaemia is a blood disease. Article #1 in a series about anaemia. Endometriosis breakthrough The latest breakthrough in endometriosis: the bacterium theory AI in medicinal chemistry How can it help the field? Depression in children And how we can help them Iron-deficiency anaemia Anaemia is a blood disease. Article #2 in a series about anaemia. The power of probiotics And how they are effective Blood: a vital fluid The role and importance of blood Smart bandages What are they and how can they be better than traditional bandages? Why whales don't get cancer Discussing from Peter's Paradox perspective Anaemia of chronic disease The second most-common anaemia. Article #3 in a series about anaemia. Erasing memory Is it possible to wipe your memories clean? Herpes vs. skin disease From foe to ally: a Herpes-based gene therapy treats dystrophic epidermolysis bullosa. Article #3 in a series on Rare diseases. The foremothers of gynaecology An International Women's Month collab with Publett Healthcare serial killers A disturbing reality The gut microbiome Also known as: the microbiota, gut microflora Crohn's disease A summary of the condition Sideroblastic anaemia A problem synthesising haem. Article #4 in a series about anaemia. Next

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

Step into the intricate field of dentistry and learn about dental tourism, tooth decay, water fluoridation- and more. Dentistry Articles Step into the intricate field of dentistry and learn about dental tourism, tooth decay, water fluoridation- and more. You may also like: Medicine Water fluoridation Diving deep Dental tourism What is 'Turkey teeth'? Tooth decay And how to prevent it COMING SOON

Setting Neuropsychiatry In a Wider Medical Context Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Schizophrenia, Inflammation and Accelerated Aging: a Complex Medical Phenotype 20/02/25, 11:54 Last updated: Published: 24/05/23, 09:45 Setting Neuropsychiatry In a Wider Medical Context In novel research by Campeau et al. (2022), the proteomic analysis of 742 proteins from the blood plasma of 54 schizophrenic participants and 51 age-matched healthy volunteers. This investigation resulted in the validation of the previously-contentious link between premature aging and schizophrenia by testing for a wide variation of proteins involved in cognitive decline, aging-related comorbidities, and biomarkers of earlier-than-average mortality. The results from this research demonstrated that age-linked changes in protein abundance occur earlier on in life in people with schizophrenia. This data also helps to explain the heightened incidence rate of age-related disorders and early all-cause death in schizophrenic people too, with protein imbalances associated with both phenomena being present in all schizophrenic age strata over age 20. This research is the result of years of medical intrigue regarding the biomedical underpinnings of schizophrenia. The comorbidities and earlier death associated with schizophrenia were focal points of research for many years, but only now have valid explanations been posed to answer the question of the presence of such phenomena. The explanation for the greater incidence rate of early death in schizophrenia was described in this study as the increased volume of certain proteins. Specifically, these included biomarkers of heart disease (Cystatin-3, Vitronectin), blood clotting abnormalities (Fibrinogen-B) and an inflammatory marker (L-Plastin). These proteins were tested for due to their inclusion in a dataset of protein biomarkers of early all-cause mortality in healthy and mentally-ill people published by Ho et al. (2018) for the Journal of the American Heart Association. Furthermore, a protein linked to degenerative cognitive deficit with age, Cystatin C, was present in increased volume in schizophrenic participants both under and over the age of 40. This explains why antipsychotics have limited effectiveness in reducing the cognitive effects of schizophrenia. In this study, schizophrenics under 40 had similar plasma protein content as the healthy over-60 strata set, including both biomarkers of cognitive decline, age-related diseases and death. Schizophrenics under-40 showed the same likelihood for incidence of the latter phenomena compared to the healthy over-60 set. These results could demonstrate the necessity for use of medications often used to treat age-related cognitive decline and mortality-linked protein abundances to treat schizophrenia. One of these options include polyethylene glycol-Cp40, a C3 inhibitor used to treat nocturnal haemoglobinuria, which could be used to ameliorate the risk of developing age-related comorbidities in schizophrenic patients. This treatment may be effective in the reduction of C3 activation, which would reduce the opsonisation (tagging of detected foreign products in blood). When overexpressed, C3 can cause the opsonisation of healthy blood cells in a process called haemolysis, which can catalyse the reduction of blood volume implicated in cardiac events and other comorbidities. However, whether or not this treatment would benefit those with schizophrenia is yet to be proven. The potential of this research to catalyse new treatment options for schizophrenia cannot be understated. Since the publication of Kilbourne et al. in 2009, the impact of cardiac comorbidities in catalysing early death in schizophrenic patients has been accepted medical dogma. The discovery of exact protein targets to reduce the incidence rate of age-linked conditions and early death in schizophrenia will allow the condition to be treated more holistically, with greater observance to the fact that schizophrenia is not only a psychiatric illness, but also a neurocognitive disorder with affiliated comorbidities that have to be prevented adequately. Written by Aimee Wilson Related articles: Genetics of ageing and longevity / Ageing and immunity / Inflammation therapy Project Gallery

Resources to help you prepare for university admission. Entrance Exam Preparation Resources to help you with university admission for: medicine , dentistry, natural sciences , physics , maths , engineering . Do note these entrance exams are mainly for UK universities, but can be used for international unis too. It is advised to check with the university when applying. You may also like: Personal statements , A-level resources, IB resources and Extra resources MEDICINE: University Clinical Aptitude Test (UCAT) UCAT resources: UCAT website / The Medic Portal / 6med UCAT Books: 1300 UCAT Practice Questions / 1250 UKCAT Practice Questions / UCAT 700+ UCAT online course: Medify Help with medical exams DENTISTRY: UCAT and BioMedical Admissions Test (BMAT; for University of Leeds only) Dentistry application preparation BMAT: online mastery course / Medify guide / Past papers / 700 BMAT Practice Questions / BMAT ebook For UCAT resources, see above OTHER ADMISSION TESTS Engineering: STEP / PAT University of Cambridge: natural sciences (NSAA) / engineering (ENGAA) / maths (STEP) / physics (PAT)

- And face masks! No need to say they don’t work either. No matter the number of layers in the mask. Nothing is ever 100% efficient, and face masks are not exempt from this. Face masks help a lot by stopping you from inhaling COVID-19 particles in the air, indeed spread by people not wearing, or cannot wear, masks. Not just COVID-19 particles, Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Misconceptions about COVID-19 and its vaccine Last updated: 07/11/24 Published: 28/12/22 Three years into the pandemic, after huge losses in lives, livelihoods, and freedoms, misinformation about the coronavirus and now its vaccines, are still in circulation on the internet. It will take time to completely eradicate these misconstructions, but it is not impossible. I will begin discussing some myths and theories about the coronavirus itself, and then continue on to the vaccines science has developed to battle the virus. The misunderstandings are not listed in any order. Coronavirus The virus is called many different names: coronavirus, SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). The disease it causes is called COVID-19, or simply COVID. – Getting COVID is no big deal. It is just another flu. It is true yes that COVID-19 is only a mild condition for most people, however for those who are elderly and/ or clinically vulnerable it is anything but mild. Getting COVID-19 depends on the immune system, and if the immune system is already weakened, it is a big deal. As for the flu, it has been around for years mutating each time, but it is never less of a threat. – Only the elderly contract it. In most cases, it is the elderly who fall victim to the disease. But there are many factors at play; age is only one of them. Pre-existing health conditions regardless of age (for those clinically vulnerable), ethnicity, wealth, gender (does not factor that much), all determine who contracts it and how long it will take for someone to recover from the disease. – Children and teenagers are immune to it. Not necessarily true. For the better part of a year, children and younger adults seemed to evade COVID-19 but now more and more are falling ill to it. It is probably due to the emerging variants and how vulnerable children are. – Herd immunity is the way out. We do this by sacrificing said elderly to save the economy. It would have been the ideal solution to continue working and travelling while the virus ravages entire nations to protect the economy, but it would also have meant exposing society’s most vulnerable, namely the elderly, to the virus. Not a good solution to only protect one generation of society and not another. – Yes, because lockdowns don’t work. Lockdowns tend to have a rapid effect; they act to break the circuit of virus transmission up and down the country. They work. This is the reason why they last no more than one month or so when put in place. However, lockdown costs people’s freedoms and mental health so it should only be imposed when crucial. – But we need to work! How will we support ourselves? Very understandable. But if you suddenly contract COVID, you will not be able to work anyway. Many government initiatives have been started to support workers in the past year or so. - What is this 2m/ 6ft rule? No social contact whatsoever? The particles don’t even travel that far. The major way coronavirus travels is by droplets in the air between human contact. Not through surfaces (very little evidence supporting this), not by sharing needles, not by parasites and animals (vectors that bring the virus to humans). - And face masks! No need to say they don’t work either. No matter the number of layers in the mask. Nothing is ever 100% efficient, and face masks are not exempt from this. Face masks help a lot by stopping you from inhaling COVID-19 particles in the air, indeed spread by people not wearing, or cannot wear, masks. Not just COVID-19 particles, but any other harmful particles. You’re still able to take oxygen in and carbon dioxide out- these molecules are much smaller, 1-3 atoms big, so they can pass through the mask. Multiple layers of the mask offer more protection, however one is enough. - Antibiotics can be used to treat COVID-19. Antibiotics are anti-bacteria. Coronavirus is a virus- only antivirals will help. - Surely if bleach cleans and wipes out pathogens on surfaces and on just about anything else, it can do the same inside our bodies. Bleach is for surfaces only; they are not for consumption or administration as medicine. They will cause untold amount of damage inside the body. Bleach also turns things white. Whatever cleaning and wiping of pathogen need to be done, your immune system will do it. No need for bleach. - How does opening windows help prevent the spread of COVID-19? As mentioned before, COVID-19 respiratory particles travel by air. So opening windows and increasing the circulation of air, helps the particles to be blown away from you and the people with you and reduces the chance of becoming infected with the virus. Going outside for this reason helps (if not under lockdown or other restrictions). - How does fresh air help? As above. Vaccine – I think they will inject a microchip under the pretence of a vaccine and will track my every movement. There is no microchip. All the ingredients and chemicals used to produce the vaccines are available to view on the respective pharmaceutical website. None of the ingredients have any tracking potential. – Or they are just making money. Usually the government or state orders and buys the vaccines from the different companies. The expenses are on them. The rest of the population get the vaccine for free. - Vaccines hurt. Only a pinprick when the vaccine is being administered. After that only mild side effects and taking paracetamol or other painkillers will help. - And we are part of a big experiment. All the testing and experimenting was done during the three phases of clinical trials. The vaccines have been approved for (temporary) nationwide use. - Vaccines don’t work anyway. There is always a story in the news detailing the efficacies of the vaccines. They have an efficiency of 70-96% depending on the vaccine, and vaccine dose. Generally, the benefits of the vaccine far outweigh the risks that come from it. - Yes, because they cause shedding. Check the context and definition of this word. ‘Shedding’ here refers to the vaccine releasing or discharging its viral components onto others and infecting them. Once inside the body, the vaccine has no way to expel the viral contents.The only way the virus will shed its components is when the person is infected and sneezes, coughs, or causes the particles to travel in the air (i.e. when NOT vaccinated). - And, fertility issues. No biological mechanism or pathway has been discovered over the centuries that shows vaccines cause fertility issues. In fact, the reproductive system itself suppresses the immune system (not the other way round). - They will definitely cause issues if given to children. Vaccines were originally produced to provide protection to adults 18 years and older. Though there are vaccines that only children take as routine e.g. MMR (measles, mumps, rubella) and children don’t typically have any problems with them, COVID-19 vaccines aren’t among them. - Vaccines contain meat, and/ or made from animal products (and I am against this). As mentioned already, all the ingredients of the different vaccines can be found on the individual drug company websites. None of the vaccines contain meat, and if religion-conscious, scriptures advise the use of health agents even if they contain meat, to better your well-being. Anyway, the vaccine is used as medicine and not as an item for consumption. – You can pay to get a vaccine made from glucose sugar and water, and I believe it does the same thing as the official vaccine. Sugar solution is not a vaccine. It does not prevent against COVID-19. No trials have been conducted in favour of this. For a vaccine to be a vaccine, it is essential to have the actual weakened version or mRNA form of the virus. - Please take the time to read, watch, or listen to official government or health system information on coronavirus and vaccines. Millions if not billions have listened so far, be a part of this number. As with any public health guidance, education and spreading awareness are always key. Written by Manisha Halkhoree Related articles: COVID-19 glossary / Origins of COVID-19 / Digital disinformation / Fake science websites

Beavers alter their landscape through dams, canals, and felling trees Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Beavers are back in Britain, ‘wood’ you like to know why? 08/03/26, 18:09 Last updated: Published: 03/12/24, 12:05 Beavers alter their landscape through dams, canals, and felling trees This is article no. 3 in a series on animal conservation. Next article: Pangolins: from poached to protected . Previous article: Conserving the California condor Eurasian beavers ( Castor fiber ) transform freshwater habitats so dramatically that they are nicknamed ‘ecosystem engineers’. Their dam-building and tree-felling activities could reduce flood risk and increase biodiversity. After being hunted to extinction centuries ago, beavers have been reintroduced to Britain in both organised and illicit ways. This article will describe where they have been reintroduced in Britain, and the impact they could have. Ecological importance of beavers By building dams, Eurasian beavers alter their habitat - often for the better. Beaver dams are made from wood, stones, and mud. They control the flow of river water, reducing the risk of floods and droughts. The resulting slower water is a good place for amphibians to lay eggs and undergo the aquatic part of their life cycle. As water builds up behind the dam, it converts the area into a wetland - a source of drinking water for animals like bats and an excellent carbon sink. Meanwhile, invertebrates can lay eggs or hide from predators in the spaces within beaver dams ( Figure 1 ). Further up the food chain, beaver dams have complex effects on fish. Although the still water provides habitat for overwintering and rearing young, dams restrict the movement of fish species like salmon. However, most studies have concluded that beaver dams benefit freshwater biodiversity. Dams are not the only way Eurasian beavers improve their landscape. To access food and construction materials easily, beavers dig canals – which make the habitat better drained and more complex. Moreover, beavers gnaw at tree trunks and branches, sometimes knocking over entire trees. This creates deadwood where terrestrial invertebrates can live. Felling trees also allow sunlight to reach the river surface, promoting aquatic plant growth. When beavers gnaw at willow trees, they create propagules, which disperse along the beaver-made canal network and grow downstream. These new willow trees stabilise the river bank and further reduce the flood risk. Humans often trim back trees to stimulate their growth – called coppicing – but beavers do this free of charge. Coppicing, dam building, and canal digging are just a few ways beavers save the human costs of restoring and protecting natural habitats. Extinction and reintroduction However, Eurasian beavers used to be more exploited than appreciated. They were hunted for their fur, meat, and a secretion called castoreum, which is used in perfume and pharmaceuticals. Exactly when and how the beaver population went extinct from Britain is unclear, but the last written record of a beaver is from 1526 in Scotland and 1780 in England. Since then, the British turned wetlands into farmland and forgot about beavers … until recently. After centuries, beavers returned to Scotland in the late 2000s. A handful of beavers were spotted in River Tay about 15 years ago, after either an enclosure escape or an illegal release. There are 114 families in this illegal population, which has genetic origins in Germany. The first official beaver reintroduction occurred in Knapdale Forest, Scotland, in 2009 – but this population did not grow as quickly as the River Tay one. With scepticism, the reintroduction of Eurasian beavers to Scotland was deemed a success, and they became a ‘European Protected Species’ in Scotland in 2019. Seeing Eurasian beavers thriving in Scotland encouraged reintroduction plans in England. In the English county of Devon, River Otter showed signs of beaver presence since 2008 and breeding since 2013. Authorities were worried these illegally released beavers would spread foreign diseases to local wildlife, but the public campaigned to let the beavers be. Public affection for beavers led to the River Otter Beaver Trial in 2015, where two breeding pairs were released into the river after thorough health checks. By 2019, the number of breeding pairs grew to seven ( Figure 2 ). Therefore, beavers have successfully returned to England. Encouraged by the unofficial projects, in February 2025 the UK government announced a new programme to officially re-introduce beavers to England. This programme ensures existing beaver populations are carefully managed and new reintroductions are licensed. Since then, beavers have been legally released in Dorset (March 2025) and Cornwall (February 2026). Thus, the UK government has joined the British public in returning Eurasian beavers to their ancestral home. Conclusion Beavers alter their landscape through dams, canals, and felling trees. However, in Britain, they were hunted to extinction a long time ago. Although beavers first returned to England and Scotland illegally, they now live in healthy, growing populations supported by the government . Hopefully they will remain protected and loved by the public, helping us to restore wetlands and improve British freshwater biodiversity. Written by Simran Patel Related article: Vicuna conservation REFERENCES Andersen, L.H. et al. (2023) ‘Can reintroduction of beavers improve insect biodiversity?’, Journal of Environmental Management , 337, p. 117719. Available at: https://doi.org/10.1016/j.jenvman.2023.117719 . Brazier, R.E., Elliott, M., Andison, E., Auster, R.E., Bridgewater, S., Burgess, P., Chant, J., Graham, H., Knott, E., Puttock, A.K., Sansum, P., Vowles, A., (2020) ‘River Otter Beaver Trial: Science and Evidence Report’. Brazier, R.E. et al. (2021) ‘Beaver: Nature’s ecosystem engineers’, WIREs Water , 8(1), p. e1494. Available at: https://doi.org/10.1002/wat2.1494 . Campbell-Palmer, R. et al. (2020) ‘Beaver genetic surveillance in Britain’, Global Ecology and Conservation , 24, p. e01275. Available at: https://doi.org/10.1016/j.gecco.2020.e01275 . Department for Environment, Food & Rural Affairs and Natural England (2025) Wild beavers: Nature’s engineers to return to English waterways , GOV.UK . Available at: https://www.gov.uk/government/news/wild-beavers-natures-engineers-to-return-to-english-waterways (Accessed: 7 March 2026). Gaywood, M., Batty, D. and Galbraith, C. (2008) ‘Reintroducing the European Beaver in Britain’, British Wildlife , 19, pp. 381–391. Halley, D.J., Saveljev, A.P. and Rosell, F. (2021) ‘Population and distribution of beavers Castor fiber and Castor canadensis in Eurasia’, Mammal Review , 51(1), pp. 1–24. Available at: https://doi.org/10.1111/mam.12216 . Harris, S. (2025) ‘Wild beavers make historic return to England at Dorset nature reserve’, BBC News , 5 March. Available at: https://www.bbc.co.uk/news/articles/cwygxvzpkevo (Accessed: 7 March 2026). Hooker, J. et al. (2024) ‘Re-establishing historic ecosystem links through targeted species reintroduction: Beaver-mediated wetlands support increased bat activity’, Science of The Total Environment , 951, p. 175661. Available at: https://doi.org/10.1016/j.scitotenv.2024.175661 . Robinson, C. (2026) Two pairs of beavers released in Cornwall by wildlife trust , BBC News . Available at: https://www.bbc.co.uk/news/articles/cm2x9ndl4l9o (Accessed: 7 March 2026). Wilson, J.B., Bradley, J. and Bremner-Harrison, S. (2024) ‘The short-term impact of Eurasian beavers ( Castor fiber ) post-reintroduction on amphibian abundance and diversity in a lentic environment’, The Glasgow Naturalist , 28(2). Available at: https://doi.org/10.37208/tgn28224 . Project Gallery

Ways in which pathogens avoid being detected by the immune system Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Mechanisms of pathogen evasion 27/03/25, 11:23 Last updated: Published: 05/09/24, 10:54 Ways in which pathogens avoid being detected by the immune system Introduction Pathogens such as bacteria and viruses have evolved strategies to deceive and outsmart the immune system's defences. From hiding within cells to avoiding immune detection to blocking signals crucial for immune function, pathogens have developed an array of tactics to stay one step ahead of the immune system. This article introduces some key strategies pathogens employ to evade the immune system. Antigenic variation The influenza virus is a persistent and challenging pathogen to treat because it employs a clever strategy known as antigenic variation to evade the immune system. Antigenic variation is the pathogen’s ability to alter the proteins on its surface (antigens), particularly hemagglutinin (HA) and neuraminidase (NA), which are the primary targets of the immune system. As the virus conceals itself, it is no longer recognised and attacked by the host's defences. But how do the surface antigens change? This occurs through two primary mechanisms: antigenic drift and antigenic shift. The former process involves gradual changes in the virus's surface proteins by progressive accumulation of genetic mutations. Meanwhile, the latter requires a slightly different explanation. Antigenic shift is an abrupt process. It occurs when two influenza virus strains infect the same host cell and exchange genetic material. The exchange can lead to a new hybrid strain. This hybrid strain usually presents a new combination of surface proteins. It is a more abrupt process, and because the immune system lacks prior exposure to these new proteins, it fails to clear the viral pathogen. Antigenic shifts can lead to the emergence of strains to which the population has little to no pre-existing immunity. Some examples are the 1968 Hong Kong flu and the 2009 swine flu pandemic. Variable serotypes- Streptococcus pneumoniae When the host encounters a pathogen, the body creates antibodies against specific proteins on the pathogen's surface, ensuring long-term immunity. However, some species of pathogens evade this protection by evolving different strains. These strains involve multiple serotypes, each defined by distinct variations in the structure of their capsular polysaccharides. This variability allows them to infect the same host repeatedly, as immunity to one serotype does not confer protection against other serotypes. A perfect example of such a pathogen is the pneumonia-causing bacterium, Streptococcus pneumoniae , which has more than 90 strains. After successful infection with a particular S. pneumoniae serotype, a person will have devised antibodies that prevent reinfection with that specific serotype. However, these antibodies do not prevent an initial infection with another serotype, as illustrated in Figure 1 . Therefore, by evading the immune response, a new primary immune response is required to clear the infection. Latency- chicken pox & Human Immunodeficiency Virus (HIV) Pathogens can cleverly persist in the host by entering a dormant state where they are metabolically inactive. In this state, they are invisible to the immune system. Human Immunodeficiency Virus is well known for its use of HIV latent reservoirs. These reservoirs, consisting of metabolically inactive T-cells infected with HIV, can exist for years on end. When the host becomes immunocompromised at any stage in life, the T-cells in these reservoirs are suddenly activated to renew HIV production. The Varicella-Zoster Virus (VZV) is responsible for causing varicella (chickenpox) and zoster (shingles). Similarly, this virus can remain latent in the host to evade immune detection. VZV establishes latency in sensory ganglia, particularly in neurons. Since neurons are relatively immune-privileged sites, they are less accessible to immune surveillance mechanisms. This provides a safe haven from immune detection. When the host is immunocompromised, the virus reactivates. This renewed viral activity results in the production of viral particles which travel along the sensory nerve fibres towards mucous membranes. When the virus reaches the skin, it causes an inflammatory response. This results in painful vesicular skin lesions, commonly known as shingles (herpes zoster). Conclusion Pathogens employ diverse mechanisms to evade the host immune system, ensuring their survival and propagation through host cells. These evasion mechanisms can hinder the development of treatments for certain infectious diseases. For instance, the diversity in Strep A serotypes challenges vaccine development because immunity to one serotype may not confer protection against another. Additionally, the influenza virus constantly evolves via antigenic variation, always one step ahead of the immune system. The strategies employed by pathogens to evade the immune system are as diverse as they are sophisticated. Scientists continue to study these mechanisms, paving the way for developing more effective vaccines, treatments, and public health strategies to out-manoeuvre these organisms. We can better protect human health by staying one step ahead of pathogen evolution. Written by Fozia Hassan Related articles: Allergies / Plant diseases REFERENCES Abendroth, Allison, et al. “Varicella Zoster Virus Immune Evasion Strategies.” Current Topics in Microbiology and Immunology , 2010, pp. 155–171, www.ncbi.nlm.nih.gov/pmc/articles/PMC3936337/ , https://doi.org/10.1007/82_2010_41 . Accessed 24 July 2024. Gougeon, M-L. “To Kill or Be Killed: How HIV Exhausts the Immune System.” Cell Death & Differentiation , vol. 12, no. S1, 15 Apr. 2005, pp. 845–854, www.nature.com/articles/4401616 , https://doi.org/10.1038/sj.cdd.4401616 . Accessed 24 July 2024. Parham, Peter. The Immune System . 5th ed., New York, Garland Science, 2015, read.kortext.com/reader/epub/1743564 . Accessed 24 July 2024. Shaffer, Catherine. “How HIV Evades the Immune System.” News-Medical.net , 21 Feb. 2018, www.news-medical.net/life-sciences/How-HIV-Evades-the-Immune-System.aspx . Accessed 24 July 2024. Project Gallery

The endowment effect Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Behavioural Economics II 31/10/25, 12:46 Last updated: Published: 22/03/24, 19:51 The endowment effect This is article no. 2 in a series on behavioural economics. Next article: Loss aversion . Previous article: The role of honesty . In microeconomics, we say preferences are reversible. If you would pay £2 for a bar of chocolate, then you would be happy to sell a bar of chocolate for £2, especially if I gave it to you for free. Sounds reasonable? Well, in fact, this is not the case. Once again, consumers, just like you and me, are irrational, and thanks to what’s known as the endowment effect, classical economics falls flat once again. The endowment effect In an experiment conducted by Knetsch, participants were randomly allocated into three different categories. The first were given a coffee mug, the second were given some candy, and the third were given nothing. We say that the first two groups were endowed; they were given an item for free at no cost to them. Then the participants in the first two groups were given the option to either swap their item for either the mug or the candy or keep the item they were endowed with. The third group, treated as a control, was given the option to choose between the two and keep which they preferred the most. In the control group, we saw that about half of the participants chose the mug and half chose the candy. But in the endowed groups, an overwhelming majority decided to keep the item they were given rather than swapping! Therefore, as we can clearly see, when someone is endowed with an item, their perception of its utility (or benefit) seems to increase, so when given the opportunity to switch items, they often decline. Clearly, from an economic perspective, when endowed with an item, your utility curve for that item differs from when given the opportunity to choose. But why might that be the case? When you are endowed with an item, you own that item and, in a sense, hold responsibility over it. You become possessive, and this sense of ownership seems to have its own psychological value; therefore, the act of giving it up for something of equal worth is no longer treated as a fair trade-off. Whereas when not endowed, you have no sentiment value attached to the items, and for the most part, people are indifferent between them! A good example of this could be an old, run-down car. Buyers of this car see it for what it is—something that is barely functional. But owners of the car who have driven it for 20 years see it as more than that. There is an emotional attachment to the car that makes it more valuable in their eyes. Is the endowment effect always true? List conducted a similar experiment. A survey was undertaken by both unexperienced and experienced 'traders', and then after the survey, they were given trading cards as a reward. They were then given the opportunity to trade their cards if they wanted to. Non-experienced traders were subject to the endowment effect, so they kept the cards they worked hard for, but experienced traders knew that some cards may be more valuable, even if only slightly, which meant that they were able to overcome this effect. Additionally, what was found was that when participants were aware and went into the experiment knowing that there would be a trade, they had the intention to trade, which also managed to remove the endowment effect. In essence, the endowment effect serves as a reminder of the complexities inherent in human psychology and decision-making. There are many limitations in traditional economic models, which emphasises the need for behavioural economics and the inclusion of multidisciplinary thinking. To discover more about behavioural economics and in particular how honesty plays a big role in restructuring economic thinking, click here to read my prior article, and be sure to look out for more articles to come in the future! Written by George Chant Related articles: Explaining altruism / Mathematical models in cognitive decision-making References: Knetsch, Jack L. “The Endowment Effect and Evidence of Nonreversible Indifference Curves.” The American Economic Review 79, no. 5 (1989): 1277–84. John A. List, Does Market Experience Eliminate Market Anomalies?, The Quarterly Journal of Economics , Volume 118, Issue 1, February 2003, Pages 41–71,33 Project Gallery

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