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Looking at p53 mutations and cancer predisposition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Decoding p53: the guardian against cancer 05/02/25, 16:21 Last updated: Published: 23/11/23, 11:38 Looking at p53 mutations and cancer predisposition Being a tumour suppressor protein, p53 encoded by the TP53 gene plays a critical role in regulating cell division and preventing the formation of tumours. Its function in maintaining genome stability is vital in inhibiting cancer development. Understanding p53 Located on chromosome locus 17p13.1, TP53 encodes the p53 transcription factor 1. Consisting of three domains, p53 can directly initiate or suppress the expression of 3661 different genes involved in cell cycle control and DNA repair 2. With this control, p53 can influence cell division on a massive scale. Cancer is characterised by uncontrolled cell division, which can occur due to accumulated mutations in either proto-oncogenes or tumour suppressor genes. Wild-type p53 can repair mutations in oncogenes such that they will not affect cell division. However, if p53 itself is mutated, then its ability to repair DNA and control the cell cycle is inhibited, leading to the emergence of cancer. Mutations in TP53 are actually the most prevalent genetic alterations found in patients with cancer. The mechanisms by which mutated p53 leads to cancer are manifold. One such mechanism is p53’s interaction with p21. Encoded by CDKN1A , p21 is activated by p53 and prevents cell cycle progression by inhibiting the activity of cyclin-dependent kinases (CDKs). Therefore, we can see that a non-functional p53 would lead directly to uncontrolled cell division and cancer. Clinical significance The importance of p53 in preventing cancer is highlighted by the fact that individuals with inherited TP53 mutations (a condition known as Li-Fraumeni syndrome or LFS) have a significantly greater risk of developing any cancer. These individuals inherit one defective TP53 allele from one parent, making them highly susceptible to losing the remaining functional TP53 allele, ultimately leading to cancer. Loss of p53 also endows cells with the ability to ignore pro-apoptotic signals such that if a cell becomes cancerous, it is far less likely to undergo programmed cell death 3. Its interactions with the apoptosis-inducing proteins Bax and Bak, are lost when mutated, thus leading to cellular apoptosis resistance. The R337H mutation in TP53 is an example of the founder effect at work. The founder effect refers to the loss of genetic variation when a large population descends from a smaller population of fewer individuals. The descendants of the initial population are much more likely to harbour genetic variations that are less common in the species as a whole. In southern Brazil, the R337H mutation in p53 is present at an unusually high frequency 4 and is thought to have been introduced by European settlers several hundred years ago. It is responsible for a widespread incidence of early-onset breast cancers, LFS, and paediatric adrenocortical tumours. Interestingly, individuals with this mutation can trace their lineage back to the group of European settlers that set foot in Brazil hundreds of years ago. Studying p53 has enabled us to unveil its intricate web of interactions with other proteins and molecules within the cell and unlock the secrets of cancer development and potential therapeutic strategies. By restoring or mimicking the functions of p53, we may be able to provide cancer patients with some relief from this life-changing condition. Written by Malintha Hewa Batage Related articles: Zinc finger proteins / Anti-freeze proteins Project Gallery

A hereditary neurodegenerative disorder Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Huntington's disease 07/02/25, 16:19 Last updated: Published: 18/10/23, 16:12 A hereditary neurodegenerative disorder Huntington’s disease (HD) is a neurodegenerative disorder causing cognitive decline, behavioural difficulties, and uncontrollable movements. It is a hereditary disease that has a devastating effect on the individual’s life and unfortunately is incurable. Genetic component What may come as a surprise, is that in everyone’s genetics there are two copies (one from each parent) of the Huntingtin’s gene coding for the Huntingtin protein. This gene is coded by CAG repeats. In healthy genes, the CAG sequence is repeated between 10 and 26 times. However, if the gene is faulty, CAG repeats over 40 times resulting in a dysfunctional Huntingtin protein. The disease is autosomal dominant meaning regardless of gender, if either parent is a carrier, their child has a 50% chance of inheriting the faulty gene. REMINDER: because the gene is dominant, it means those who inherit even one copy will develop the disease Effect on the brain The faulty Huntingtin protein accumulates in cells, leading to cell death and damage to the brain. If you were to look at the brains of individuals with Huntington’s Disease, you would see a reduction in volume of the caudate and putamen. These areas are part of the striatum, which is a subdivision of the basal ganglia, involved in fine tuning our voluntary movements, i.e., reaching out to grab a cup. As the disease progresses, this atrophy can extend to other areas of the brain including the thalamus, frontal lobe, and cerebellum. Symptoms The symptoms normally manifest in three categories: motor, cognitive and psychiatric. We know that the basal ganglia is involved in our voluntary movement, so the damage causes one of the most visible symptoms in HD- uncontrollable and jerky movements. Cognitive symptoms include personality changes, difficulties with planning and attention. There can also be impairments to how those with HD recognise emotions- all these symptoms can interact to make social interaction more difficult. Finally, the psychiatric symptoms often seen include irritability and aggression, depression, anxiety, and apathy. Impact on life and family At the age when diagnosis usually occurs (around 30 years old), patients are often buying houses, getting married and either having children or deciding to start a family. The diagnosis may change peoples outlook on having children and can put a great psychological burden on them if they have unknowingly passed it along to those already born. Diagnosis also brings consequences to seemingly mundane, but incredibly important issues such as gaining life insurance, with some companies not covering individuals with an official diagnosis. Subsequently this makes life harder for their families, as the patient will eventually be unable to work and there could be associated costs with the need for care facilities as the disease progresses. Unfortunately, this is a progressive neurodegenerative condition with no cure. The only treatment options available at present, are interventions which aim to alleviate the patients’ symptoms. Whilst these treatments will reduce the motor and psychiatric symptoms, they cannot stop the progression of Huntington’s disease. We have only scratched the surface on the impact Huntington’s disease has on a patient and their families. It is so important to understand ways in which everyone that is affected can be best supported during the disease progression, to give all those involved a better quality of life. Written by Alice Jayne Greenan Related article: Epilepsy Project Gallery

When misfolded proteins lead to disease Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unfolding prion diseases and their inheritance 22/04/25, 14:11 Last updated: Published: 06/03/24, 11:32 When misfolded proteins lead to disease This is article no. 5 in a series on rare diseases. Next article: Neuromyelitis optica . Previous article: Epitheliod hemangioendothelioma . Prion proteins are found abundantly in the brain; their function is unclear, but they are involved in a multitude of physiological mechanisms, including myelin homeostasis and the circadian rhythm. Correctly folded prion proteins in the cellular form are termed PrP C , while their infectious isoform is called PrP Sc . As shown in Figure 1, the misfolded PrP Sc is largely made up of β-pleated sheets instead of α-helices; PrP Sc is prone to forming aggregates that cause transmissible spongiform encephalopathies (TSEs). Prion diseases can be categorised by their aetiology: acquired, sporadic, and hereditary. Acquired prion diseases are caused by the inadvertent introduction of PrP Sc prions into an individual. Sporadic prion diseases are the most common type, where PrP C misfolds into PrP Sc for an unknown reason and propagates this misfolding within other prion proteins. Hereditary prion diseases are caused by genetic mutation of the human prion protein gene (PRNP), which causes misfolding into the infectious isoform. Consequently, these mutations can be passed to offspring, resulting in the same misfolding and disease. Interestingly, different types of PRNP mutations cause different types of prion diseases. Creutzfeldt-Jakob disease (CJD) is a type of TSE found in humans which causes mental deterioration and involuntary muscle movement; symptoms tend to worsen as the disease progresses, making it a degenerative disorder. Familial CJD (fCJD) is a rare type of hereditary prion disease and can sometimes result in a faster rate of disease progression compared to sporadic cases. Due to a dominant inheritance pattern, relatives of fCJD patients are often also affected by the disease. The most common mutation observed in familial CJD is an E200K mutation denoting the substitution of glutamic acid with lysine in the prion protein. Other common mutations resulting in fCJD include mutations at positions 178 and 210 on the prion protein. However, there are, less frequently, a multitude of other mutations correlated with familial CJD development. Familial CJD can be caused by STOP codon mutations, which result in a truncated protein, some of which show similar pathology to Alzheimer’s disease, such as Q16OX and Q227X. fCJD can also be caused by insertional mutations, possibly caused by unbalanced crossover and recombination. The prion protein consists of a nona-peptide (made up of nine amino acids) followed by four repeats of an octa-peptide (made up of eight amino acids). During insertion mutations, additional repeats of the octa-peptide are present in the prion protein. Interestingly, different numbers of inserts result in different pathological characteristics; patients with 1, 2 or 4 extra repeats show similarity to sporadic CJD, while those with 5-9 extra repeats show similarity to Gerstmann-Sträussler-Scheinker syndrome. Hereditary prion diseases are important to study in order to develop an understanding of not only prion misfolding diseases but also diseases associated with misfolding of other proteins, such as Alzheimer’s and Parkinson’s. Understanding the mechanisms of hereditary prion diseases will aid the development of treatments for such conditions. In particular, observing and investigating particular genetic mutations observed to play a part in prion misfolding is crucial alongside using genetic information to infer the risk of disease an individual may have. Written by Isobel Cunningham Project Gallery

Unmasking the complexities of the condition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Crohn's disease 06/02/25, 11:54 Last updated: Published: 22/03/24, 20:16 Unmasking the complexities of the condition Introduction Crohn's disease is a chronic inflammatory condition that primarily targets the gastrointestinal tract. While it commonly afflicts individuals aged 20 to 50, it can also manifest in children and older adults, albeit less frequently. Symptoms of Crohn's disease vary widely and may include skin lesions spanning from the mouth to the anus, along with prevalent issues such as diarrhoea, abdominal pain, weight loss, rectal bleeding, fatigue, and fever. Diagnosis Diagnosing Crohn's disease can be challenging due to its similarity to other conditions. However, specific symptoms like bloody diarrhoea, iron deficiency, and unexplained weight loss are significant indicators that warrant further investigation by a gastroenterologist. Many tests that can confirm Crohn’s disease: Endoscopy: endoscopy, including procedures like colonoscopy and upper endoscopy, is a dependable method for diagnosing Crohn's disease and distinguishing it from other conditions with similar symptoms. During an endoscopy, a thin tube called an endoscope is inserted into the rectum to visually inspect the entire gastrointestinal tract and collect small tissue samples for further analysis. Imaging: Computed tomography (CT), magnetic resonance imaging (MRI), and ultrasonography are valuable tools for assessing disease activity and detecting complications associated with Crohn's disease. These imaging techniques can examine areas of the gastrointestinal tract that may not be accessible via endoscopy, providing comprehensive insights into the condition's progression and associated issues. Laboratory testing: various laboratory tests, including complete blood count, C-reactive protein levels, pregnancy tests, and stool samples, are conducted to screen for Crohn's disease. These tests are typically the initial step in diagnosis, helping to avoid the necessity for more invasive procedures like endoscopies and imaging. Additionally, laboratory testing may involve assessing inflammatory markers such as erythrocyte sedimentation rate (ESR) and faecal calprotectin to further aid in diagnosis and monitoring of the condition. Treatment and prevention While there is currently no cure for Crohn’s disease, numerous treatments have been developed over time to effectively manage symptoms and sometimes even induce remission. When determining a treatment plan for patients, factors such as age, specific symptoms, and the severity of inflammation are taken into careful consideration. Corticosteroids and immunomodulators are medications commonly used to manage Crohn’s disease. Corticosteroids work by reducing inflammation and suppressing the immune system, typically employed to address flare-ups due to their rapid action. However, they are not suitable for long-term use as they may lead to significant side effects. In contrast, maintenance therapy often involves immunomodulators such as azathioprine, methotrexate, or biologic agents like anti-TNF drugs (such as infliximab or adalimumab). These medications target specific immune pathways to enhance the effectiveness of the immune system. Research indicates that immunomodulators are associated with fewer adverse effects compared to corticosteroids and are effective in maintaining remission. Monoclonal antibody treatment is another approach used to manage symptoms and sustain remission in Crohn's disease. These therapies are categorised as biologic treatments, targeting precise molecules involved in inflammation and the immune response. Despite carrying certain risks, such as infections, the likelihood of developing cancer with these treatments is typically deemed low. Crohn’s disease frequently leads to complications that may necessitate surgical intervention. Gastrointestinal surgeries can greatly alleviate symptoms and enhance the quality of life for patients. However, surgery is usually considered only when medical therapy proves insufficient in controlling the disease or when complications arise. Although the exact cause of Crohn’s disease remains uncertain, factors such as genetics, immune system dysfunction, and environmental influences are believed to contribute to its development. While there is no definitive evidence pinpointing specific causative factors, numerous studies suggest potential links to an unhealthy diet and lifestyle, dysbiosis (imbalance of healthy and unhealthy gut bacteria), smoking, and a family history of the disease. Therefore, it is crucial to minimise exposure to these risk factors in order to decrease the likelihood of developing Crohn’s disease. Written by Sherine Abdul Latheef Related articles: the gut microbiome / the dopamine connection / Diverticular disease / Mesenchymal stem cells REFERENCES Veauthier B, Hornecker JR. Crohn's Disease: Diagnosis and Management. Am Fam Physician. 2018;98(11):661-669. Torres J, Mehandru S, Colombel JF, Peyrin-Biroulet L. Crohn's disease. Lancet. 2017;389(10080):1741-1755. doi:10.1016/S0140-6736(16)31711-1 Mills SC, von Roon AC, Tekkis PP, Orchard TR. Crohn's disease. BMJ Clin Evid. 2011;2011:0416. Published 2011 Apr 27. Sealife, A. (2024) Crohn’s disease, Parkland Natural Health. Available at: https://wellness-studio.co.uk/crohns-disease/ (Accessed: 09 March 2024). How to stop anxiety stomach pain & cramps (2022) Calm Clinic - Information about Anxiety, Stress and Panic. Available at: https://www.calmclinic.com/anxiety/symptoms/stomach-pain (Accessed: 09 March 2024). Project Gallery

From confusion to career opportunities Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unlocking the power of statistics 21/02/25, 12:19 Last updated: Published: 19/09/23, 16:23 From confusion to career opportunities During my time studying maths there was always one topic that would trip me up: statistics. Being an A-level physics student, I could understand why calculus is useful in real life, using differentiation to calculate the velocities of projectiles. And I could look and see how geometry is used in buildings and structures. However, statistics often made me feel unrelatable and lost, as I was unable to see real-world applications. But today, I wish to alter my old perspective. First and foremost, you might be pleasantly surprised to learn that statistics opens doors to some of the most lucrative careers available today. We'll delve into roles such as quantitative analysts, who boast a national average salary of £99,000 per year. But if finance is not your cup of tea, there are many other rewarding career paths to explore, from becoming a data scientist to forecasting the weather as a meteorologist. In this article, I wish to unveil the world of statistics, revealing its importance and shedding light on its real-life applications. My hope is to not only inspire those who are already passionate about statistics but also to ignite motivation in individuals who, like me, found themselves in a similar predicament a few years ago. The Actuary Less well known when compared to a banker or engineer, an actuary’s sole purpose is to analyse risk for multiple different scenarios. It may sound simple on first inspection, but being an actuary is a very well-established career requiring many years of learning followed by some of the most challenging exams in the job market. An actuary attempts to quantify the risk of an event happening so that financial decisions can be made with an objective view. A good and close-to-home example of this is being either accepted or rejected from a credit card. As a younger person below the age of 21, the chances of you getting accepted for a credit card are extremely and quite painfully low. This is because banks, and more specifically, credit score providers, deem you to be a high-risk person to lend to. They think this because you have a very short credit history, are unaware of how responsible you are with money, and are more afraid to lend you their cash. In other words, they don’t want you to spend their money on going out and drinking booze. The insurance industry is, however, the biggest industry when it comes to actuaries. Both life and non-life actuaries work in teams with insurance providers to establish whether a client, company, or investment is worthwhile. Actuaries apply both statistics and actuarial science (similar to applied statistics) to real-life situations, evaluate whether to offer a premium to a customer, and then establish what that premium is. You may see in advertisements that life insurance costs as little as £10 a month for a 20-year-old compared to someone who is 65. This is because the younger you are, the less likely you are to claim against your policy. Actuaries put together vast amounts of information about people, lifestyle choices, and other factors to help determine the probability that someone may claim, suggesting a ‘fair’ premium that an insurance company may offer. Without the help of an actuary, insurance companies would either charge too much, making people disadvantaged, or charge too little, in which case they would have to default on their policy and be unable to pay out any claims. Although this seems very specific, the role of an actuary is becoming increasingly important as people live longer lives and insurance companies become more fearful of defaulting.To put it into perspective, actuaries on average earn £80,000 working in London, putting you well in the top 10% of earners in the UK. The Quantitative Analyst Similar to an actuary, quantitative analysts do exactly what is said on the tin. They use quantitative methods to analyse data. Often, companies like investment banks, hedge funds, and pension funds will hire front-office ‘quants’. The aim of the game is to send out trades as quickly as possible before all the other trading offices do. These big companies have links directly to the trading floor, so every millisecond counts, and it’s a quant's job to devise a trading strategy that beats the rest and operates in the least amount of time. Quants are masters of statistics and mathematics, and for this reason, high-frequency trading firms like Hudson River Trading offer salaries to top mathematical minds in excess of $500,000. The role of quantitative researchers is to explore the latest statistical articles being published by top universities and generate strategies that can be implemented in the stock market. This job is not one to be taken lightly, as salary is often based on performance, but someone who is motivated to explore the ins and outs of statistics may find themselves loving the life of a quant. The Meteorologist Meteorologists are the people that we incorrectly blame for the bad weather that we have. And they are also the people we blame when we forget to take a coat and get soaked on the long walk back home. But what do meteorologists actually do? And is it any more than just an educated guess? Meteorologists, along with climatologists, collect millions of pieces of information every hour of every day across their 195,000 weather stations spread all around the globe. These stations collect key pieces of information, including atmospheric pressure, temperature, speed, rain, humidity, and many other components of current weather conditions. With this information, meteorologists begin to paint a picture of what the current weather climate is like and then use forecasting methods and statistical models to estimate how the weather is going to change. The probability that it might rain is much more than an educated guess; it is the probability that if this situation happened 100 times, it would rain the estimated number of times (i.e., if there was an 80% chance of rain, it would rain 80 times out of the hundred over a large enough sample). As a forecaster, you will collect this information and input it into very advanced systems to analyse and give an outcome, but as a researcher, you will help derive these statistical forecasting models and improve them so that our apps and news channels are even more precise. Not only that, but you may also find yourself researching the effects of climate change from the data that you analyse, and maybe even how the weather affects the spread of pollution and disease. Meteorologists get paid a modest salary of around £32,000 per year, which may seem small when compared to that of a quant, but the quality of life is far more generous than some careers in finance. To conclude In conclusion, statistics, once a perplexing subject for many, can offer an exciting and rewarding career. From the meticulous work of actuaries, assessing risks and financial decisions, to the world of quantitative analysts, where every millisecond counts, and even to the indispensable role of meteorologists, who help us navigate the weather and climate change, statistics holds the power to transform lives and industries. As we've explored, statistics is not just about numbers and formulas; it's about making sense of the world, predicting outcomes, and creating informed decisions. So, whether you're a seasoned statistician or someone who, like me, once felt lost in its complexities, remember that statistics isn't merely a subject to conquer—it's a key that unlocks doors to some of the most intriguing and well-compensated careers out there. Written by George Chant Project Gallery

Navigating the silence Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unveiling the underreported challenges of endometriosis 16/03/25, 14:13 Last updated: Published: 25/11/23, 11:22 Navigating the silence What is endometriosis? Endometriosis is a chronic, neuro-inflammatory disease that affects 1 in 10 women in the UK. It is associated with debilitating chronic pelvic pain caused by tissue alike the lining of the womb (uterus) grows outside the uterus in other places like the ovaries and fallopian tubes. Endometriosis can affect any woman of reproductive age with a lifelong impact and can even lead to infertility. During a normal menstrual cycle, the body undergoes monthly hormonal changes. Natural hormonal release causes the uterus lining to thicken in preparation of a fertilised egg. If there is no pregnancy, the uterus lining will break down and bleed and is then released from the body in the form of a period. In endometriosis, tissue alike to the uterus lining tissue behaves in the same way the uterus tissue behaves every month during the menstrual period: building up, breaking down then bleeding. Unlike the womb tissue broken down blood, this blood has no way to leave. The internal bleeding causes inflammation, debilitating pain, and scar tissue formation. The symptoms are: · Painful, heavy, long periods · Infertility · Pain during or after sex · Painful bowel movements · Mood disorders like anxiety or depression · Chronic fatigue · Chronic pelvic pain The challenges of endometriosis Contrary to popular belief, period pain is not normal and can be experienced by those without endometriosis. The main point is if your period pain is interfering with your daily life, please consult your doctor. There are many challenges behind endometriosis from the hard time a patient has to get a diagnosis, to the severely under-research of the condition. Unfortunately, since endometriosis shares symptoms with many other conditions, diagnosis can be delayed and strenuous with recent research showing the average time to get a firm diagnosis being 7.5 years. A 2021 focus group in the Netherlands also shows the many issues with diagnosing endometriosis. Many of the focus group reported having a hard time finding a doctor who does not dismiss their concerns, undermine their pain, or dismiss them with paracetamol or ibuprofen which patients have reported as not strong for the pain endometriosis causes. Little research has been done on how effective paracetamol or ibuprofen is with endometriosis pain, but anecdotal evidence suggests it is not effective. Many of them reported their concerns being unheard, told to come back when they want to have a child and that their pain is normal, so they don’t need to see a doctor. Research for endometriosis is heavily underfunded, women reproductive health disorders are generally underfunded. There is a huge gender disparity with disorders that mostly affect men being over-funded while disorders affecting mostly women being underfunded. A 2018 analysis by the UK Clinical Research Collaboration reported findings of only 2.1% of public funded medical research going towards childbirth and reproductive health which is down from 2.5% in 2014. A 16% funding decrease over a 4-year period. The UK Research and Innovation (UKRI) has funded just over 40 endometriosis-related projects since 2003. However, diabetes which has the same incident rate but affecting both sexes instead of one like endometriosis has been funded 1891 projects in the same time. Just over 1m was funded to 6 of the endometriosis projects compared almost 250 diabetes projected with more than 10 receiving funding greater than £10 million. In 2020 the UK’s All-Part Parliament Group (APPG) report on Endometriosis calls the attention of the cause of the disorder being unclear: Historically, with limited investment in research into women’s health in general, there’s been so little investment in research into endometriosis that we don’t even know what causes it, and without knowing the cause, a cure cannot be found. - APPG The APPG called for more investment into the cause, diagnosis, treatment, and management options of endometriosis. Without investment in research, this condition will rob the next generation of women [of] the education, care, and support they deserve. – APPG With more awareness being brought up by endometriosis charities, researchers and the affected group, the hard work and motivation may pay off soon. Written by Blessing O. Related articles: Breakthrough in endometriosis treatment / Gynaecology Project Gallery

A vital fluid Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Blood 20/03/25, 12:02 Last updated: Published: 07/09/23, 10:16 A vital fluid A comprehensive guide to the human blood system and alternatives Human blood Blood is a vital fluid for humans and vertebrates. It transports nutrients, including oxygen, to cells and tissues. Blood is made of different components: red blood cells, white blood cells, platelets and plasma. Red blood cells (also called erythrocytes) contain haemoglobin, which gives blood its red colour. Haemoglobin helps to carry oxygen to the body from the lungs. White blood cells (also called leukocytes) defend the body against infections. Lymphocytes are a type of white blood cell, and the two types are T lymphocytes and B lymphocytes. T lymphocytes target infected cells and regulate the function of other immune cells. B lymphocytes create antibodies, which are proteins that can destroy foreign substances like bacteria and viruses. Platelets (also called thrombocytes) are small cell fragments. They are essential in blood clotting, a process known as coagulation. They also help wounds heal and contribute to the immune response. Plasma is the liquid component in blood, made of water, ions, proteins, nutrients, wastes and gases. Its main role is transporting substances such as blood cells and other nutrients throughout the body. Artificial blood There are two main types of artificial blood: haemoglobin-based oxygen carriers (HBOCs) and perfluorocarbons (PFCs). HBOCs are synthetic solutions designed to carry oxygen. They are usually a smaller size than RBCs. The haemoglobin is modified and covered with carriers to ensure the HBOCs do not break down inside the body. They can be used for blood transfusions that need to be done immediately or when there is too much blood loss. PFCs are derived from fluorine-containing and carbon-containing chemicals. They have a high capacity for carrying and delivering oxygen. Advantages and disadvantages of artificial blood Artificial blood can be beneficial because it can be used for any patient who needs a blood transfusion, regardless of their blood type, if the substitute has the universal O blood group. There is also less chance of diseases being passed to patients using artificial blood. However, artificial blood has been shown to have adverse side effects, including high blood pressure and a higher chance of heart attacks. The future of artificial blood As of 2022, there have been experiments in the NHS with laboratory-grown RBCs in the RESTORE randomised controlled clinical trial. With further research, artificial blood can be refined and used more, especially when there is low blood availability for transfusions or for people with blood-related diseases. Written by Naoshin Haque Related articles: Sideroblastic anaemia / Kawasaki disease Project Gallery

Characteristics, triggers and theoretical models of embarrassment Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Psychology of embarrassment: why do we get embarrassed? 28/03/25, 11:39 Last updated: Published: 06/09/24, 11:07 Characteristics, triggers and theoretical models of embarrassment The six basic emotions proposed by Ekman and recognised worldwide are sadness, happiness, fear, anger, surprise and disgust- Ekman (1999). Recently, the list of basic emotions has expanded to include self-conscious emotions, such as embarrassment, pride and shame, as all of those emotions show evidence for cross-cultural and cross-species production and perception. According to Miller (1995), embarrassment is the self-conscious feeling individuals get after realising they have done something stupid, silly or dishonourable. Embarrassment is a social emotion that emerges at around 18 months of age and the development of which is related to self-recognition. Characteristics of embarrassment in humans are gaze aversion, downward head movements, controlled smile and face touching. Embarrassment has been linked to the two main personality dimensions proposed by Eysenck (1983): extraversion/introversion and neuroticism/emotional stability. Kelly & Jones (1997) found that neuroticism is positively associated with embarrassment, suggesting that the individuals who score highly in neuroticism are more prone to experiencing embarrassment. The same researchers also concluded that embarrassment is negatively related to extraversion, implying that introverted individuals are more likely to feel embarrassed than extroverted individuals. The three triggers of embarrassment, according to Sabini, Siepmann & Meyerowitz (2000), are faux pas, sticky situations and centre of attention. Faux pas causes embarrassment when an individual creates a social mistake that forces them to think of others’ evaluation, like misspelling a word in a presentation and only realising when presenting it to a supervisor. Sticky situations lead to embarrassment when they threaten an individual's role, not their self-esteem, such as a leader being challenged publicly by their second in command. Centre of attention describes an anomaly when embarrassment is not a result of failure but of increased attention, for example being at your own birthday party. The faux pas trigger aligns with the social evaluation model of embarrassment, whilst sticky situations are in line with the dramaturgic model of embarrassment. There are four prominent theories of embarrassment: the dramaturgic model, the social evaluation model, the situational self-esteem model and the personal standards model. The dramaturgic model proposed by Silver, Sabini and Parrott (1987) says that embarrassment is the flustered uncertainty that follows a poor public performance and leaves the individual at a loss of what to do. This model suggests that anxiety and aversive arousal trigger embarrassment after realising a performance has gone wrong (see Figure 4 ). In this model, concern about what others think accompanies embarrassment but does not cause it. Miller (1996) suggests that whilst the dramaturgic model has substantial support, it is difficult for a dramaturgic dilemma to cause embarrassment without simultaneously creating unwanted social evaluations, highlighting a limitation of this model. The social evaluation model of embarrassment put forward by Edelmann (1987) suggests that embarrassed individuals fear failure to impress others and feeling at a loss of what to do is a result of embarrassment, not the cause (see Figure 5 ). This model assumes that individuals are concerned about others’ opinions. Miller (1996) supports this theory, saying that negative evaluation from others is crucial to embarrassment. The situational self-esteem model by Modigliani (1971) proposes that the root cause of embarrassment is the temporary loss of self-esteem that results from public failures based on one’s own opinions of self and performance in faulty situations (see Figure 6). Miller (1995) does not support this theory, arguing that self-esteem plays a secondary role in embarrassment and states that susceptibility to embarrassment depends more on the persistent concern about others’ evaluations of us. The personal standards model of embarrassment introduced by Babcock (1988) presents the view that embarrassment is caused by the individual realising they have failed the standards of behaviour that they have set for themselves, implying that the situation does not matter and that individuals can feel embarrassment when they are alone (see Figure 7 ). Miller (1992) disagrees with this theory, saying that guidelines for self are linked to impressions made on other people and that embarrassment can happen due to poor audience reaction, not letting yourself down. Therefore, there are many plausible theories behind embarrassment that have been linked to various causes like dispositional, situational and personality factors. Whilst it is unlikely that one theory can perfectly explain such a complex social emotion like embarrassment, the consensus among psychologists in the recent years has created the most support for a combination of the dramaturgic and the social evaluation models. I agree with the consensus and think that the different theories behind embarrassment may all apply to a given situation. For instance, forgetting someone’s name may lead to embarrassment due to being at a loss of what to say (the dramaturgic model), unwanted social judgements (the social evaluation model), the negative effects of this situation on the self-esteem (the situational self-esteem model) and the painful realisation of letting yourself down (the personal standards model). Thus, like many subjects in psychology, embarrassment is a multidimensional concept that can be looked at from many different angles. Written by Aleksandra Lib Related articles: Chemistry of emotions / Unmasking aggression REFERENCES Babcock, M. K. (1988). Embarrassment: A window on the self. Journal for the Theory of Social Behaviour . Edelmann, R. J. (1987). The psychology of embarrassment . John Wiley & Sons. Ekman, P. (1999). Basic emotions. Handbook of cognition and emotion , 98 (45-60), 16. Eysenck, H. J. (1983). Psychophysiology and personality: Extraversion, neuroticism and psychoticism. In Individual differences and psychopathology (pp. 13-30). Academic Press. Kelly, K. M., & Jones, W. H. (1997). Assessment of dispositional embarrassability. Anxiety, Stress, and Coping, 10 (4), 307-333. Lewis, M., Sullivan, M. W., Stanger, C., & Weiss, M. (1989). Self development and self-conscious emotions. Child development , 146-156. Miller, R. S. (1992). The nature and severity of self-reported embarrassing circumstances. Personality and Social Psychology Bulletin , 18 (2), 190-198. Miller, R. S. (1995). On the nature of embarrassabllity: Shyness, social evaluation, and social skill. Journal of personality , 63 (2), 315-339. Miller, R. S. (1996). Embarrassment: Poise and peril in everyday life. Guilford Press. Modigliani, A. (1971). Embarrassment, facework, and eye contact: Testing a theory of embarrassment. Journal of Personality and social Psychology , 17 (1), 15. Sabini, J., Siepmann, M., Stein, J., & Meyerowitz, M. (2000). Who is embarrassed by what?. Cognition & Emotion , 14 (2), 213-240. Silver, M., Sabini, J., Parrott, W. G., & Silver, M. (1987). Embarrassment: A dramaturgic account. Journal for the Theory of Social Behaviour , 17 (1), 47-61. Tracy, J. L., Robins, R. W., & Tangney, J. P. (2007). The self-conscious emotions. New York: Guilford . Project Gallery

Psychology delves into the human mind and behaviour. Read on for compelling articles ranging from reward sensitivity to evolutionary, and empathy-altruism theories. Discover the psychology of emotions: embarrassment, and aggression. Psychology Articles Psychology delves into the human mind and behaviour. Read on for compelling articles ranging from reward sensitivity to evolutionary, and empathy-altruism theories. Discover the psychology of emotions: embarrassment, and aggression. You may also like: Biology, Medicine Motivating the mind Effect of socioeconomic status on reward sensitivity The evolutionary theory by Darwin vs empathy-altruism Explaining altruism through different theories A perspective on well-being Hedonic vs eudaimonic: based on the principles of Aristotle and Aristippus Nature vs. nurture in childhood intelligence What matters most? The psychology of embarrassment Why do we feel this emotion? Models and theories A primer on the Mutualism theory of intelligence A detailed review on different studies Unmasking aggression Is this fierce emotion the result of personal, or social triggers? Mental health strategies Raising awareness to look after mental health Imposter syndrome in STEM Have you ever had this feeling in your STEM education or job? Mental health in the South Asian community Why is it not yet such an open discussion?

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