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The specific research that was recognised for a Nobel Prize in Physics was the discovery of radioactivity. Radioactivity is the spontaneous emission of energy, in the form of radiation, a term that Curie herself coined. Marie Curie researched whether uranium, a weakly radioactive element, was found in other materials. She then analysed pitchblende, Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Women who have won the Nobel Prize in Physics Last updated: 13/11/24 Published: 01/03/23 March is International Women’s month, so it seems like the perfect time to celebrate the women who have been awarded Nobel Prizes in Physics. There have only been a total of four women to receive this prestigious award, namely Marie Curie, Maria Goeppert Mayer, Donna Strickland, and Andrea Ghez. This article will detail the research each woman did to achieve the Nobel Prize, as well as the context of their discoveries. Marie Curie (1903) Arguably the most famous of these Nobel Prize winners, Marie Curie won her award for research on radioactive phenomena. Curie received half the Nobel Prize for Physics, shared with her husband, but at first, the committee had only intended to award it to him. This was the first Nobel Prize for Physics ever awarded to a woman. The specific research that was recognised for a Nobel Prize in Physics was the discovery of radioactivity. Radioactivity is the spontaneous emission of energy, in the form of radiation, a term that Curie herself coined. Marie Curie researched whether uranium, a weakly radioactive element, was found in other materials. She then analysed pitchblende, a mineral made partially of uranium but had a higher amount of radiation. Curie investigated other elements that pitchblende could be made up of and, as a result of this, discovered new elements: polonium and radium. Following this, she had ambitions of obtaining pure radium, and following this achievement, she was awarded the Nobel Prize in Physics in 1903. Maria Goeppert Mayer (1963) 60 years after Marie Curie was awarded her Nobel Prize for Physics, Maria Goeppert Mayer became the second female recipient. She received the Prize for her work in 1963 on the nuclear shell model of the atomic nucleus. Goeppert Mayer shared her award with two other physicists who came to the same conclusion as her. The nuclear shell model describes the exact makeup of the atomic nucleus, through the exact numbers of protons and neutrons. Maria Goeppert Mayer’s mathematical work on this model described why there are certain amounts of neutrons and protons in stable atoms. She beautifully described the model in terms of waltzers dancing and spinning in circles. Donna Strickland (2018) The next female Nobel Prize in Physics award winner wouldn’t be until another half-century later, with Donna Strickland. Strickland was awarded the Prize for her work on chirped pulse amplification and its applications. Although the research itself was published in 1985, she didn’t receive the award until 2018. Chirped pulse amplification (CPA) is a technique that takes a very short laser pulse (a light flash) and makes it brighter. The technique is useful for making extremely precise cuts, so is used for many laser-related applications, such as laser eye surgery. The wide range of uses CPA has in medicine makes this an important discovery for physics which led to Strickland being awarded the Nobel Prize award. Andrea Ghez (2020) The result of the work of Andrea Ghez, the fourth female Nobel Prize in Physics recipient, may be the most exciting conclusion of the research described in this article. Ghez won the award for her role in discovering a black hole in the centre of our galaxy. A black hole is a very dense, compact object with gravity so strong that not even light can escape it. Until recently, physicists have not been able to visually observe black holes but instead can detect them by looking at how other objects, such as stars, behave around one. Andrea Ghez and her team used the movement of Sagittarius A* to prove that there was a black hole in the centre of the Milky Way. Written by Madeleine Hales Related articles: Female Nobel prize winners in chemistry / African-American women in cancer research

Read articles delving into the universal genetic code: from specific examples of epigenetic modifications, to rare genetic diseases. Genetics Articles Read articles delving into the universal genetic code: from specific examples of epigenetic modifications, to rare genetic diseases. You may also like: Biology Why South Asian genes remember famine An example of epigenetic modification CEDS- a break in cell death Looking at caspase-8’s inability to trigger cell death. Article #11 in a series on Rare diseases. COMING SOON COMING SOON Previous

Study the plethora of interactions between drug and target with these articles focusing on antibiotic resistance, analgesics, and drug treatments for diseases with presently no cure. Pharmacology Articles Study the plethora of interactions between drug and target with these articles focusing on antibiotic resistance, analgesics, and drug treatments for diseases with presently no cure. You may also like: Chemistry , Medicine Effect of heat on medicine When medication is exposed to extreme heat, what happens? Antibiotic resistance Its rising threat Exploring ibuprofen Ibuprofen is a painkiller A treatment for Parkinson's disease By using a common diabetes drug mRNA vaccines What they are, and how they are different to traditional (live, attenuated, or viral-vectored) vaccines Anthrax toxin Using bacterial toxins to treat pain

Cortisol is a glucocorticoid steroid hormone produced by the zona fasciculata segment of the adrenal gland, following stimulation by the release of adrenocorticotropic hormones from the pituitary gland. Chronic stress is associated with excessive cortisol production and the development of neurodegenerative diseases.  Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Stress and neurodegeneration Last updated: 30/01/25 Published: 10/03/23 Cortisol is a glucocorticoid steroid hormone produced by the zona fasciculata segment of the adrenal gland, following stimulation by the release of adrenocorticotropic hormones from the pituitary gland. Chronic stress is associated with excessive cortisol production and the development of neurodegenerative diseases. Once cortisol is produced and released into circulation, it crosses the blood-brain barrier to bind to and activate nuclear glucocorticoid receptors (GR) in the hippocampus. Upon cortisol binding, the GR undergoes conformational changes, causing it to dissociate from its chaperone complex and consequently allowing for the transcription of target genes. One such pathway that is activated as a result of GR binding is the brain-derived neurotrophic factor (BDNF) and the cAMP response element-binding protein (CREB) pathway, which is important for long-term memory formation and consolidation. However, memory formation can be impaired following abnormal BDNF/ CREB pathway activation due to elevated cortisol levels. Moreover, high cortisol levels have been found to cause increased amyloid-beta (AB) deposition, which is evident in Alzheimer's disease patients. Therefore, increased blood cortisol levels result in increased activation of GR, causing impaired gene expression and affecting cellular functions. When GR are exposed to cortisol over a long period of time, such pathways become further impaired, resulting in the characteristic neurodegenerative disease pathology in affected individuals. A study conducted by Kline et. al assessed the relationship between high cortisol levels and neurodegenerative disease pathology in mice. In this study, it was noted that chronic stress reduced the diversity of the gut microbiome in mice, and such alterations resulted in increased gut permeability, promoting the movement of pathogens across the epithelial lining, and increasing AB deposition in affected mice. However, AB deposition can be reduced if cortisol levels are controlled. For example, xanamem, a drug currently in clinical trials, reduces cortisol levels by inhibiting the 11B-hydroxysteroid-1 ezyme, known to play a role in the activation of cortisol via the hypothalamus-pituitary-adrenal axis. Therefore, xanamem or similar compounds, if suitable following clinical testing, could be a means of decreasing AB deposition, thereby targeting one component of neurodegnerative disease pathology. If the putative hypotheses of Alzheimer's disease aetiology are correct, this would potentially ameliorate patient symptoms and offer a degree of improved quality of life for affected individuals. Written by Maria Zareef Kahloon Related articles: Tetris and PTSD / Mental health awareness / Physical and mental health

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

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? The cognitive orchestra How music can manipulate emotional processes The attentional blink An exploration of this concept in rapid serial visual presentation studies Postpartum depression in adolescent mothers An analysis of risk and protective factors

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

An introductory and comprehensive review of complex diseases and their environmental influences. Using schizophrenia as an example, we are interested in exploring one of the biggest questions that underlie complex diseases. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The environment on complex diseases: schizophrenia Last updated: 18/11/24 Published: 08/05/23 An introductory and comprehensive review of complex diseases and their environmental influences. Using schizophrenia as an example, we are interested in exploring one of the biggest questions that underlie complex diseases. Introduction: Not Exactly a Yes or No Question Many things in science revolve around questions. It is remarkable to find the number of questions left for scientists to answer or those that will remain unanswered. Indeed, one of the most daunting tasks for any scientist would be to see through every detail of a piece of information, even if everyone has seen it, but with different sets of lenses and asking different sets of questions. After all, “why did the apple fall from its tree?”. However, asking questions is one thing. Finding answers and, more importantly, the evidence or proof that supports them does not always yield conclusive results. Nevertheless, perhaps some findings may shine a new light on a previously unanswered question. We can categorise the study of genetics into two questions: “What happens if everything goes well?” and “What happens if it goes wrong?”. Whilst there are virtually limitless potential causes of any genetic disease, most genetic diseases are known to be heritable. A mutation in one gene that causes a disease can be inherited from the parents to their offspring. Often, genetic diseases are associated with a fault in one gene, known as a single-gene disorder, with notorious names including Huntington’s disease, cystic fibrosis, sickle cell anaemia, and familial hypercholesterolaemia. These diseases have different mechanisms, and the causes are also diverse. But all these diseases have one thing in common: they are all caused by a mutation or fault in one gene, and inheriting any specific genes may lead to disease development. In other words, “either you have it, or you do not”. The role of DNA and mutations in complex diseases. Image/ craiyon.com Multifactorial or complex diseases are a classification geneticists give to diseases caused by factors, faults or mutations in more than one gene. In other words, a polygenic disease. As a result, the research, diagnosis, and identification of complex diseases may not always produce a clear “black-and-white” conclusion. Furthermore, complex diseases make up most non-infectious diseases known. The diseases associated with leading causes of mortality are, in their respective ways, complex. Household names include heart diseases, Alzheimer’s and dementia, cancer, diabetes, and stroke. All of these diseases may employ many mechanisms of action, involving multiple risk factors instead of direct cause and effect, using environmental and genetic interactions or factors to their advantage, and in contrast to single-gene disorders, do not always follow clear or specific patterns of inheritance and always involve more than one problematic genes before the complete symptoms manifest. For these reasons, complex diseases are infamously more common and even more challenging to study and treat than many other non-infectious diseases. No longer the easy “yes or no” question. The Complex Disease Conundrum: Schizophrenia Here we look at the case of a particularly infamous and, arguably, notorious complex disease, schizophrenia (SCZ). SCZ is a severely debilitating and chronic neurodevelopmental disorder that affects around 1% of the world’s population. Like many other complex diseases, SCZ is highly polygenic. The NHS characterise SCZ as a “disease that tends to run in families, but no single gene is known to be directly responsible…having these genes does not necessarily mean one will develop SCZ”. As previously mentioned, many intricate factors are at play behind complex diseases. In contrast, there is neither a single known cause for SCZ nor a cure. Additionally, despite its discovery a century ago, SCZ is arguably not well understood, giving a clue to the sophisticated mechanisms that underlie SCZ. To further illustrate how such complexities may pose a challenge to future medical treatments, we shall consider a conundrum that diseases like SCZ may impose. The highly elaborate nature of complex diseases means that it is impossible to predict disease outcomes or inheritance with absolute certainty nor rule out potential specific causes of diseases. One of the most crucial aspects of research on complex diseases is their genetic architecture, just as a house is arguably only as good as its blueprint. Therefore, a fundamental understanding of the genes behind diseases can lead to a better knowledge of diseases’ pathogenesis, epidemiology, and potential drug target, and hopefully, one day bridge our current healthcare with predictive and personalised medicine. However, as mentioned by the NHS, one of the intricacies behind SCZ is that possessing variants of diseased genes does not translate to certainty in disease development or symptom manifestation. Our conundrum, and perhaps the biggest question on complex diseases like SCZ is: “Why, even when an individual possesses characteristic genes of a complex disease, they may not necessarily exhibit symptoms or have the disease?”. The enigma surrounding complex diseases lies in the elegant interactions between our genes, the blueprint of life, and “everything else”. Understanding the interplay of factors behind complex diseases may finally explain many of the intricacies behind diseases like SCZ. Genes and Environment: an Obvious Interaction? The gene-environment important implications on complex disease development were demonstrated using twin studies. A twin study, as its name suggests, is the study of twins by their similarities, differences, and many other traits that twins may exhibit to provide clues to the influences of genetic and external factors. Monozygotic (MZ) twins each share the same genome and, therefore, are genetically identical. Therefore, if one twin shows a phenotype, the other twin would theoretically also have said genes and should exhibit the corresponding trait. Experimentally, we calculate the concordance rate, which means the probability of both twins expressing a phenotype or characteristic, given that one twin has said characteristic. Furthermore, the heritability score may be mathematically approximated using MZ concordance and the concordance between dizygotic twins (twins that share around half a genome). These studies are and have been particularly useful in demonstrating the exact implications genetic factors have on phenotypes and how the expression of traits may have been influenced by confounding factors. In the case of SCZ, scientists have seen, over decades, a relatively low concordance rate but high heritability score. A recent study (published in 2018) through the Danish SCZ research cohort involved the analysis of around 31,500 twins born between the years 1951 and 2000, where researchers reported a concordance rate of 33% and estimated heritability score of 79%, with other older studies reporting a concordance rate up to and around 50%. The percentages suggest that SCZ is likely to be passed down. In other words, a genetically identical twin only has approximately 1 in 2 risks of also developing symptoms of SCZ if its opposite twin also displays SCZ. The scientists concluded that although genetic predisposition significantly affects one’s susceptibility or vulnerability against SCZ, it is not the single cause of SCZ. Demographically, there have been studies that directly link environmental risks to SCZ. Some risk factors, such as famines and malnutrition, are more evident than others. However, some studies also associate higher SCZ risk among highly industrialised countries and first or second-generation migrants. For instance, few studies point out an increased risk of SCZ within ethnic minorities and Afro-Caribbean immigrants in the United Kingdom. Hypotheses that may explain such data include stress during migration, potential maternal malnutrition, and even exposure to diseases. With this example, hopefully, we all may appreciate how the aetiology of SCZ and other complex diseases are confounded by environmental factors. In addition, how such factors may profoundly influence an individual’s genome. SCZ is a clear example of how genetic predisposition, the presence of essential gene variants characteristic of a disease, may act as a blueprint to a terrible disease waiting to be “built” by certain factors as if they promote such development. It is remarkable how genetic elements and their interactions with many other factors may contribute almost collectively to disease pathogenesis. We can reflect this to a famous quote amongst clinical geneticists: “genetics loads the gun, and environment pulls the trigger.” Carrying high-risk genes may increase the susceptibility to a complex disease, and an environment that promotes such disease may tip the balance in favour of the disease. However, finding and understanding the “blueprints” of SCZ, what executes this “blueprint”, and how it works is still an area of ongoing research. Furthermore, how the interplay between genetics and external factors can lead to profound effects like disease outcomes is still a relatively new subject. The Epigenome: the Environment’s Playground To review, it is clear that genes are crucial in complex disease aetiology. In the case of SCZ, high-risk genes and variances are highly attributed to disease onset and pathogenesis. However, we also see with twin studies that genetics alone cannot explain the high degree of differences between twins, particularly when referring to SCZ concordance between identical twins. In other words, external factors are at play, influencing one’s susceptibility and predisposition to SCZ. These differences can be explained by the effects epigenetics have on our genome. Epigenetic mechanisms regulate gene expression by modifying the genome. In short, on top of the DNA double strands, the genome consists of additional proteins, factors, and even chemical compounds that all aid the genetic functions our body heavily relies on. The key to epigenetics lies in these external factors’ ability to regulate gene expression, where some factors may promote gene expression whilst others may prevent it. Epigenetic changes alter gene functions as they can turn gene expression “on” and “off”. Furthermore, many researchers have also shown how epigenetic changes may accumulate and be inherited somatically with cell division and even passed down through generations. Therefore, epigenetic changes may occur without the need to change any of the DNA codes, yet, they may cause a profound effect by controlling gene expression throughout many levels of the living system. These underlying mechanisms are crucial for the environment’s effect on complex diseases. Some external factors may directly cause variances or even damage to the genome (e.g. UV, ionising radiation), and other sources may indirectly change gene expression by manipulating epigenetic changes. The exact molecular genetics behind epigenetic mechanisms are elaborate. However, we can generally find three common epigenetic mechanisms: DNA Methylation, Histone Modification, and Non-coding RNA. Although each method works differently, they achieve a common goal of promoting or silencing gene expression. All of these are done by the many molecular components of epigenetics, altering the genome without editing the gene sequence. We refer to the epigenome, which translates to “above the genome”, the genome itself and all the epigenetic modifiers that regulates gene expression on many levels. Environmental factors and exposure may influence epigenetic mechanisms, affecting gene expression in the cell or throughout the body, sometimes permanently. Therefore, it is clear how the epigenome may change throughout life as different individuals are exposed to numerous environmental factors. Furthermore, each individual may also have a unique epigenome. Depending on which tissues or cells are affected by these mechanisms, tissues or cells may even have a distinct epigenome, unlike the genome, which is theoretically identical in all cells. One example of this is the potential effects of DNA methylation on schizophrenia epidemiology. DNA methylation can silence genes via the enzymes DNA methyltransferases (DNMT), a family of enzymes capable of catalysing the addition of methyl groups directly into the DNA. The DNMT enzymes may methylate specific nucleotides on the gene, which usually would silence said gene. Many researchers have found that the dysregulation of DNA methylation may increase the risk towards the aetiology of numerous early onset neuro-developmental disorders. However, SCZ later-onset development also points towards the influence of environmental risk factors that target DNA methylation mechanisms. Studies show links between famines and SCZ increased prevalence, as the DNMT enzymes heavily rely on nutrients to supply essential amino acids. Malnutrition is thought to play a considerable role in DNA methylation changes and, therefore, the risk of SCZ. Small Piece of a Changing Puzzle Hopefully, we can see a bigger picture of the highly intricate foundation beneath complex diseases. Bear in mind that SCZ is only one of many complex diseases known. SCZ is ultimately not a pristine and impartial model to study complex disorders. For instance, concordance rates of complex diseases change depending on their genetic background. In addition, they may involve different mutations, variance, or dysregulation of differing pathways and epigenetic mechanisms. After all, complex diseases are complex. Finally, this article aimed to give a rundown of the epigenetics behind complex diseases like SCZ. However, it is only a snapshot compared to the larger world of the epigenome. Furthermore, some questions remain unanswered: the genetic background and architecture of complex diseases, and ways to study, diagnose, and treat complex diseases. This Scientia article is one of the articles in Scientia on the theme of complex disease science and genetics. Hopefully, this introductory article is an insight and can be used to reflect upon, especially when tackling more complicated subjects of complex diseases and precision medicine. Written by Stephanus Steven Related articles: Schizophrenia, Inflammation, and Accelerated Ageing / An Introduction to Epigenetics

Elements, compounds, and mixtures make up the building blocks of materials that shape our world. Read on to uncover the latest contributions in chemistry, such as advances in mass spectrometry and quantum chemistry. Chemistry Articles Elements, compounds, and mixtures make up the building blocks of materials that shape our world. Read on to uncover the latest contributions in chemistry, such as advances in mass spectrometry and quantum chemistry. You may also like: Medicine , Pharmacology Advances in mass spectrometry Analytical chemistry Bioorthogonal chemistry Chemical reactions with high yields Polypharmacy Multiple medications Plastics and their environmental impact The same property that makes plastics so strong endangers the environment Quantum chemistry A relatively new field of chemistry Nanomedicine and targeted drug delivery An overview as to why nanoparticles are suitable for drug delivery Nanogels Smarter drug delivery Previous

Pre-diabetes is a period before the diagnosis of diabetes mellitus. When level of blood sugar rise above the normal level but it is not high enough to considered as a diabetes. The blood sugar level range between 100-125mg/dl is considered as a pre-diabetes. Causes of pre-diabetes: Obesity Family Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Pre-diabetes Last updated: 14/11/24 Published: 14/06/23 Pre-diabetes is the period before the diagnosis of diabetes mellitus; when the level of blood sugar rises above the normal level but it is not high enough to considered as diabetes. The blood sugar level ranges between 100 and 125mg/dl in pre-diabetes. Causes of pre-diabetes: Obesity Family history Genetic history Lack of physical activity High calories diet Sign and symptoms: Pre-diabetes does not have any sign and symptoms. Though some of these symptoms may appear: Increase thirst Frequent urination Increased appetite Fatigue Frequent infections Prevention: In medical science, ‘prevention is better than cure’. So, pre-diabetes is one of the most preventable diseases. There are several ways to prevent diabetes such as dietary intervention, physical activities and lifestyle modifications. A low carbohydrate diet focuses on protein and non-starchy food. Low carbohydrate diets help in reducing weight; if patients have diabetes already, then it will help to lower medication dose and reducing morbidity overall. APPLICATION OF LOW CARBOHYDRATE DIET FOR PRE-DIABETES: Low carbohydrate diets are sometimes recommended to individuals who are being treated for diabetes. These diets can be safe and effective in helping people with type 2 diabetes to manage their weight, blood glucose level, and risk of heart disease in the short term . A healthy, balanced meal. Overall, medium-low carbohydrate diets (30%) are effective and sustainable in the long term for most people. As well as reducing your overall carbohydrate intake, replace refined carbohydrate (e.g. white bread and white rice) with high fibre, and complex carbohydrates (e.g. oats and sweet potato) where possible. Reducing your intake of ultra-processed foods (e.g. biscuits and cakes) will also help you avoid refined carbohydrates and reduce sweet cravings. When adapting to a new way of eating, it can be tricky to know how your plate should look. Above is a plate which is an example of how your plate might look, depending on whether you are including complex carbohydrates. Altogether, low carbohydrate diets are helpful for prediabetic or diabetic individuals to maintain their sugar level and ultimately reduce the incidence rate of diabetes globally. Written by Chhaya Dhedi Related articles: Diabetes to become an epidemic? / Diabetes drug to treat Parkinson's