How botox works in the cosmetic industry Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link From botulism to beauty: the evolution of botulinum toxins and botox 09/07/25, 15:10 Last updated: Published: 03/10/23, 15:07 How botox works in the cosmetic industry Botulinum neurotoxins (BoNTs) rank amongst the most potent and lethal neurotoxins known to science. Yet, it's a fascinating journey to discover how these deadly substances have found their way into one of the most renowned cosmetic procedures in the world: Botox. BoNTs originate from the bacterium Clostridium botulinum , which produces some of the most potent neurotoxins in existence. They are central to the development of botulism, a condition that relentlessly targets the body's nervous system, resulting in challenges in breathing and muscle paralysis. Despite their perilous origins, these toxins have undergone a fascinating metamorphosis into a popular cosmetic procedure. They have been studied substantially due to their ability to block nerve functions leading to muscle paralysis and their unique pharmacological properties in therapeutic and cosmetic uses. They affect the neurotransmission process by blocking the release of acetylcholine that allows muscle contraction in the body. The toxins bind pre-synaptically to recognition sites on cholinergic nerve terminals resulting in the inhibition of neurotransmitter release. The toxin consists of a heavy chain and a light chain connected by a disulphide bond. This disulphide bond is vital in the entry of the metalloprotease chain in the cytosol. BoNTs have a unique binding characteristic as a dual receptor binder, which allows them to achieve a high affinity for neurons. These proteins possess the remarkable ability to specifically target and interfere with the neurotransmission process. At their core, BoNTs are proteases, enzymes specialised in cleaving specific proteins involved in nerve signal transmission. When administered as Botox, BoNTs are skillfully harnessed to their advantage due to these properties. By injecting small, controlled amounts into specific facial muscles, they temporarily disrupt the nerve signals that stimulate muscle contraction. This action leads to muscle relaxation, smoothing out wrinkles and lines on the skin's surface. Importantly, the effects are localised, preserving the natural expressiveness of the face. In 1989, BoNTs made their debut in the medical community by being recognised as a safe and effective treatment by the FDA for blepharospasm, which affects eye muscle control. However, in 2002 the FDA extended its endorsement, propelling Botox into the realm of beauty. This pivotal decision forever reshaped the landscape of cosmetic procedures, solidifying Botox's status as an iconic treatment for rejuvenation and enhancement. In conclusion, the evolution of botulinum toxins and the rise of Botox is a captivating journey that traverses the realms of science, medicine, and evolving beauty ideals. Written by Anam Ahmed Project Gallery

CRISPR-Cas9, CAR T-cells, incretins, and iPSCs Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Biggest Innovations in Biosciences 09/03/26, 15:00 Last updated: Published: 25/03/24, 11:43 CRISPR-Cas9, CAR T-cells, incretins, and iPSCs We are in the era of innovation and cutting-edge technology in biosciences and health. This article goes through some of the most remarkable technologies slowly conquering the world of biosciences. Gene editing and CRISPR-Cas9 Gene editing is based on the idea that correcting the genetic mistake that causes a disease offers a permanent result than curing the symptoms. This technique allows scientists to alter the DNA of cells by deleting, adding or modifying genes. There are numerous ways to edit a gene. The most widely used and revolutionary method for gene editing is CRISPR-Cas9, which stands for Clustered Regularly Interspaced Short Palindromic Repeats and CRISPR- associated protein 9. The process begins with the design of a synthetic RNA molecule, known as guide RNA (gRNA) that matches the target gene sequence. The gRNA, combined with the Cas9 protein, forms a complex that is then introduced into the target cells. Cas9 acts like scissors, guided by the gRNA, to locate the precise location on the DNA where the genetic modification is intended. Once the target site is identified, Cas9 induces a break in the DNA strand. The cell's natural DNA repair mechanisms then come into play. The non- homologous end joining pathway introduces insertions and deletions at the site, resulting in gene knockout or inactivation. On the other hand, once a DNA template with homology to the sequences is present, the homology-directed repair pathway allows the incorporation of a desired genetic sequence, facilitating gene insertion or replacement. Several other gene-editing techniques have been developed, each with unique approaches. Zinc Finger Nucleases (ZFNs) and Transcription Activator-Like Effector Nucleases (TALENs) are two examples. These methods also use proteins that act as molecular scissors to cut the DNA at specific locations. ZFNs use zinc finger proteins to bind to target DNA sequences, while TALENs use transcription activator-like effector proteins. As the field of gene editing rapidly advances, these diverse methods contribute to the expanding toolkit available for researchers and hold promise for addressing a wide array of applications, from medical treatments to agricultural improvements. CAR T-cells Chimeric antigen receptor T-cells (CAR T-cells) are a new type of immunotherapy, considered to be the new fighters in the war on cancer. In general, immunotherapies use the patient’s immune system to fight the cancer. This therapy promises more specificity than traditional therapies and more permanent results. T-cells naturally exist in the human organism, supporting the adaptive immune system. They are a group of lymphocytes in the blood or lymph tissue that target or kill specific pathogens. Each type of T-cell recognises specific pathogens. T-cells have proteins on their outer surface, called receptors and these receptors recognize specific proteins on the outer surface of the pathogen. Depending on the type of T-cell, after recognizing the specific pathogen, they are either killing the pathogen (killer T-cells) or signaling to other elements of immune system to attack the pathogen (helper T-cells). CAR T-cell therapy involves modifying a patient’s own T-cells to express a specific CAR on their surface. The receptor is designed to recognise antigens commonly found on the surface of cancer cells. To introduce CARs on the outer surface of T-cells, the patient’s T-cells are genetically modified in the lab. A viral vector is often used to knock out the original T-cell receptors and express the CAR construct. The newly created CAR-T-cells are introduced into the patients, where they target and destroy cancer cells expressing the specific antigen for which the CAR is designed. Incretins The scientific journal “Science” proclaimed glucagon-like peptide-1 (GLP-1) receptor agonists The Breakthrough of 2023. These medications, originally approved for type 2 diabetes, demonstrated remarkable weight-loss benefits. GLP-1 is a natural hormone produced in the intestines that plays a role in regulating blood sugar levels. When we eat a meal, incretins, GLP-1 and Glucose-dependent insulinotropic polypeptide (GIP), are released into the bloodstream. They bind to specific receptors on the beta cells of the pancreas, triggering insulin release. Incretins also suppress the release of glucagon, a hormone that increases blood sugar levels by promoting the breakdown of stored glucose. GLP-1 receptor agonists are medications that mimic the effects of GLP-1. They bind to the GLP-1 receptors on pancreatic beta cells, promoting insulin secretion and suppressing glucagon release. By mimicking the actions of GLP-1, these medications help to lower sugar levels, improve glucose control, and reduce the risk of hypoglycemia. At the same time, they seem to regulate the appetite and delay gastric emptying. New GLP-1 medicines have been produced to combat weight loss with high efficacies; some are available on the NHS while others can be purchased privately. iPSCs Induced pluripotent stem cells (iPSCs) are becoming a new powerful weapon in lab research. They are a type of stem cell that can be generated from adult cells, such as skin or blood cells, through reprogramming. The process of creating iPSCs involves introducing a set of specific genes into the adult cells. These reprogramming factors reset the adult cells' developmental clock, turning them back into a pluripotent state, similar to embryonic stem cells. Once iPSCs are generated, they can be expanded indefinitely in the laboratory and induced to differentiate into various cell types. iPSCs are a valuable tool for studying human development and disease, as well as for drug discovery and regenerative medicine. iPSCs can be derived from patients with genetic diseases or other conditions, allowing researchers to study disease mechanisms in a dish. By differentiating iPSCs into the relevant cell types affected by the disease, researchers can observe how the disease develops and test potential treatments. Moreover, iPSC-derived cells can screen potential drugs for safety and efficacy. Because iPSCs can differentiate into many different cell types, they provide a more accurate model of human biology than traditional cell culture methods. Finally, because iPSCs can be derived from individual patients, they offer the potential for personalised therapies. iPSCs could be used to generate patient-specific cells for transplantation or to test drugs for individual patients. Conclusion These cutting-edge technologies offer unprecedented opportunities for targeted interventions in the treatment of genetic disorders, cancer, diabetes, and a myriad of other diseases. However alongside their immense promise, these biotechnological techniques and therapies also raise important ethical, social and regulatory considerations. The implications of gene editing on human germline cells, the accessibility of advanced therapies, and the long-term safety of these interventions are critical areas that warrant careful attention and thoughtful deliberation. Embracing these innovative techniques with diligence holds the key to unlocking a future where previously incurable conditions become manageable, and where the boundaries of medical possibility are continually expanded. Written by Matina Laskou Related articles: Medical biotechnology / Mesenchymal stem cells Project Gallery

Unveiling the dance between genes and the environment Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link An introduction to epigenetics 09/07/25, 11:47 Last updated: Published: 04/10/23, 18:01 Unveiling the dance between genes and the environment In recent times, a new area of genetics termed epigenetics has emerged. It seeks to uncover the relationship between our genes and environment. At the core of this novel field is the principle that gene expression can be altered without modifications to the DNA sequence itself. Epigenetic changes to DNA involve the addition of methyl or acetyl groups. Methyl groups decrease gene expression by making DNA more tightly bound around histones, forming heterochromatin, whereas acetyl groups do the opposite; they increase gene expression by loosening histone-bound DNA, forming euchromatin. The addition of these chemical groups to DNA is mediated by enzymes that act on signals our bodies receive from our environment such as diet, stressors, and exercise. Epigenetic mechanisms of gene regulation have gained notoriety in the scientific community as it is suggested that these changes can be passed down to future generations through germline cells. This means that our grandparents’ diets can influence whether we develop diabetes or not. This neo-Lamarckian concept of evolution challenges the current Darwinian understanding of evolutionary genetics where phenotypic traits are believed to emerge due to genetic mutations and natural selection. Understanding epigenetic modifications opens new doors for potential clinical therapies as by modifying harmful epigenetic changes, we may be able to treat various diseases. This field also highlights the importance of a healthy lifestyle, proper nutrition, and avoiding stressors like smoking and radiation, not only for us but for future generations as well. A noteworthy study on exercise A study conducted by Sailani et. al delves into the effects of lifelong exercise on DNA methylation patterns in genes related to metabolism, skeletal muscle properties, and myogenesis. They used two groups with different levels of physical activity. Individuals from one group reported being physically active by playing various sports and engaging in other forms of activity such as cycling, hiking, running, and swimming; the other group were reported to be physically inactive but healthy. The active group exhibited promoter hypomethylation in genes related to insulin sensitivity, muscle repair and development, and mitochondrial respiratory complexes. Compared to the inactive individuals, a significant increase in hypomethylation was seen in 714 promoters in the active group. Bearing in mind that the inactive group were healthy despite being inactive, this significant difference in methylation pattern is remarkable to see and hits home the gravity of epigenetic influence in our lives. As a result of hypomethylation, these genes would have a higher rate of expression in the active individuals. An example of one such gene is GYG2 which codes for the glycogenin 2 enzyme involved in glycogen synthesis. With enhanced glycogen synthesis we can expect to see improved physical performance and recovery in the active individuals. Along with improved skeletal muscle properties and metabolic profiles, we can assume that the active group will have a higher life expectancy and quality of life than the inactive group. As we can see, epigenetics holds a lot of promise for the future of genetic research. By understanding the extent to which epigenetic modifications affect our lives, we can take measures to encourage positive changes to our genomes for greater health, happiness, and vitality. Written by Malintha Hewa Batage Related articles: How epigenetic modifications give the queen bee her crown / Complex disease I- schizophrenia / Famine-induced epigenetic changes Project Gallery

Resources such as: other websites, textbooks, YouTube videos, and books to help! Aiding university students studying STEM subjects. Extra Resources A masterlist of other websites, textbooks, YouTube videos, and books to help with your studies, research and revision. You may also like: A-level resources, IB resources, Entrance exam preparation, FREE CV and PS checks!, STEM book reviews Representation in STEM Sisterhood in STEM GENERAL INFORMATION Referencing guide: Cite Them Right Cite this for me ZoteroBib (fast, free reference generator) Phrasebank to help with essays Free notes and textbooks: Studocu Grammar checker: Grammarly (available as a browser extension) Money financing for students: Save the Student Others: New Scientist (print and online magazine) BBC iPlayer science and nature documentaries WEBSITES TO AID STUDIES Science and maths: MME Revise Cognito Resources Access Tuition Maths Genie LibreTexts: biology , chemistry , physics , maths , engineering , and medicine HELP WITH RESEARCH Databases: - PubMed - MEDLINE (by National Library of Medicine) - ScienceDirect - Web of Science - Literature search: Google Scholar - Participate in actual research: Zooniverse - citizen science - Top multi-disciplinary journal in the field: Nature PHARMACOLOGY AND RELATED Reference sites: - Pharmgkb - Drug Bank - Check which drugs are in trial Textbooks: - Katzung's Basic & Clinical Pharmacology, 16th edition by Todd Vanderah, PhD - The Top 100 Drugs: Clinical Pharmacology and Practical Prescribing by Andrew Hitchings, Daniel Burrage, Dagan Lonsdale and Emma Baker BIOLOGICAL SCIENCES TEXTBOOKS Biology: - Campbell & Reece - Molecular biology and genetics: Molecular Biology of the Cell. 4th edition - Molecular Cell Biology by Lodish et al - Anatomy and physiology: Marieb - Principles of Animal Physiology by Moyes and Schulte - Animal Physiology by Hill, Wyse, and Anderson - Developmental Biology by Barresi and Gilbert - Cancer: The Biology of Cancer by Robert A. Weinberg Biochemistry: - Medical Biochemistry b y N. Mallikarjuna Rao Neuroscience: - Purves et. al - Kandel Immunology: - Immunobiology, 5th edition The Immune System in Health and Disease Genetics: - Emery's Elements of Medical Genetics and Genomics by Turnpenny & Ellard - Lewin’s Genes by Krebs, Goldstein, and Kilpatrick - Human Molecular Genetics by Strachan and Read CHEMISTRY TEXTBOOKS Physical chemistry: - Atkins Physical Chemistry (latest edition) - Solid State Chemistry (Fourth Edition) by Lesley Smart and Elaine Moore Organic chemistry: - Jonathan Clayden Organic Chemistry (latest edition) Inorganic chemistry: - Atkins Physical Chemistry (latest edition) - Housecroft Inorganic Chemistry (latest edition) - Electronic Structure (Basic Theory and Practical Methods) by Richard M. Martin PSYCHOLOGY Resources: - QMUL resource guides - Psychology Today - Royal Holloway activities and research - Verywell Mind - Two-minute Neuroscience - Amoeba Sisters (biology related) - Khan Academy (all STEM based) - TEDx Talk - Royal Society (range of science videos) - NumberPhile - patrickJMT (maths) - Tyler DeWitt (general chemistry) - Crash Course - Stanford Medicine (wellness) PHYSICS Resources: - Astronomy Picture of the Day - NASA STEM activities Textbooks- Foundational: - University Physics by Young and Freedman - Space, Time, and Geometry by Sean M. Classical electromagnetism: - Introduction to Electrodynamics by Griffiths - Electricity and Magnetism by Morin and Purcell - ' SQUIDs, the Josephson Effects and Superconducting Electronics' by J.C Gallop Thermal physics & classical mechanics: - Introductory Statistical Mechanics by Bowley & Sanchez - Statistical Mechanics: A Survival Guide by Glazer & Wark - Concepts in Thermal Physics by Blundell and Blundell Quantum mechanics: - Introduction to Quantum Mechanics by Griffiths - Modern Quantum Mechanics (Third Edition) by J. J. Sakurai and Jim Napolitano Quantum field theory: - Quantam Field Theory for the Gifted Amateur by Tom Lancaster & Stephen J. Blundell - Condensed Matter Field Theory (Second Edition) by Alexander Altland and Ben Simons Particle physics: - Introduction to Elementary Particles by Griffiths Condensed matter physics: - Introduction to Solid State Physics by Mittel & McEuen - Solid State Physics by Ashcroft and Mermin - Condensed Matter Physics by Michael P. Marder - The Physics of Semiconductors: An Introduction Including Nanophysics and Applications by Marius Grundmann - Density Functional Theory by David S. Sholl and Janice A. Steckel MATHS Textbooks: - Mathematical Methods for Physicists and Engineers by Riley Benson and Hobson - Mathematics for Natural Scientists 1 and 2 by Lev Kantorovich - Advanced Engineering Mathematics by Kreyszig - Thomas's Calculus by George B. Thomas - Mathematical Methods for Science students by G Stephenson - Contemporary Abstract Algebra by Joseph A. Gallian Read this article on how to excel in maths COMPUTER SCIENCE AND RELATED Resources: - Codeacademy - W3Schools ( has tutorials for HTML/ CSS/ Javascript, Python, Java, and many other languages) - Adacomputerscience - TeachComputing - Codewars (practise coding with your friends) - freeCodeCamp ENGINEERING Resources: - eFunda- formulae - Engineering statistics handbook - The Engineering Toolbox - free tools, calculators, and more - Engineers Edge - Online Ethics - ethics in engineering and science INFORMATIVE YOUTUBE CHANNELS

When deciding on the treatment of diseases, experts must gain as much relevant information as they can about that disease, before acting on an informed decision. When cancer is suspected, it might be that the decision for future treatment and prognosis be heavily weighted on the results of biopsies Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Cancer biomarker and evolution Last updated: 27/02/25 Published: 30/01/23 Development of Novel Biomarkers by Studying Cancer Evolution What does cancer evolution mean to cancer diagnosis and prognosis? How does studying it provide a better outlook on cancer precision medicine? =================== When deciding on the treatment of diseases, experts must gain as much relevant information as they can about that disease, before acting on an informed decision. When cancer is suspected, it might be that the decision for future treatment and prognosis be heavily weighted on the results of biopsies. After all, this is the standard for diagnosing many cancers. It takes one needle to take “information” that is used to predict patients’ outcomes and their respective treatment options, in other words, a test that might just predict their future. Cancer is an evolving disease. There have been many studies over the decades that demonstrate solid cancers’ singular-cell origins. Other studies show how cancer may evolve from a single cell to a mass of cells through Darwinian or branched evolution. This also implies that many things that apply to other evolutionary phenomena also apply to evolving cancer lines: mutation, genetic drift, selection and their selection pressures. In the end, what originated from one cell turns out to be a tumour with a unique genetic landscape, made up of numerous cancer subpopulations, each with its own unique genotypic and phenotypic profile and each of these subpopulations of cancerous cells evolving on its own. This phenomenon is more commonly referred to as intratumor heterogeneity (ITH). What all of this means to biopsies, is that when a single-site needle biopsy is done, it might not give an accurate representation of the whole tumour. The tumour itself, depending on its stage of development may be quite uniform with minimal ITH, however, it may also, in the eyes of a geneticist, look like a mosaic with multiple different “populations” of cancerous cells. Say, for example, the biopsy is aimed to target certain biomarkers (e.g. single nucleotide polymorphisms (SNPs)) or other “landmarks” such as satellites, the biopsy will only view whatever the needle so happened to have sampled. In other words, sampling could have made it look like a mosaic is red, even though the majority of the mosaic at the time is blue, but it seemed red for we only found red during the biopsy. Additionally, this mosaic is changing, new colours may emerge just like new lines arise within the same tumour. ITH introduces what is known as sampling bias, where samples taken from biopsies only provide an overview or snapshot of the tumour at its state and only pick up on one piece of the actively evolving puzzle, potentially missing many details, in this case, biomarkers from other tumour subpopulations. To solve the issues of ITH, scientists participating in the TRACERx research consortium are employing unique methods to sample tumours in an approach to cancer evolution. The research involved using multiregional sampling and RNA sequencing to sample tumours from patients with non-small cell lung cancers (NSCLC) at different timestamps, i.e. during the various stages of cancer development, metastasis and relapse. By using this approach, the team managed to document better how cancer evolves and how the genomic landscape and tumour architecture changes over time. Furthermore, they succeeded in honing genes that are uniformly conserved and expressed throughout the tumour, even after the effects of ITH. The research looked over 20,000 expressed genes and found 1,080 genes that despite cancer evolution and ITH, are relatively conserved and clonally expressed, relatively unaffected by sampling bias. Furthermore, using machine learning, 23 genes (from the 1,080) were found to be predictive of patient outcomes. Meaning, this novel set of genes or “biomarkers” may be used as a basis for prognosis and to predict mortality in NSCLC. This novel biomarker is named ORACLE or Outcome Risk Associated Clonal Lung Expression signature and scientists are hopeful that it may be used to determine the relative aggressiveness of lung cancers, whilst maintaining a robust function unaffected by ITH. By targeting ORACLE, it mattered less where the biopsy needle is placed on the tumour, as these genes are found clonally. In terms of its effectiveness, a trial shows that having high scores of ORACLE signatures is associated with an increased risk of death within five years of diagnosis. In addition, other trials show that by targeting ORACLE, scientists were able to identify patients with a substantial risk of poor clinical outcomes. Overall, research on the application of ORACLE has shown satisfactory results in predicting patient outcomes and is found to be relatively resistant to the confounding effects of ITH. In summary, we have seen what cancer evolution may cause, and how it shadows the effectiveness of conventional biopsies and biomarkers due to sampling bias in ITH. We also find the research by the TRACERx Consortium and how they aim to study the effects of cancer evolution and ITH, finding a set of genes that are found and expressed throughout the tumour, yet still provide a favourable measure to patient outcomes. Whilst these topics are still under active research, it is clear, how studying cancer evolution and changing the approach to biopsies and biomarker designs can improve the overall quality of diagnosis and cancer prognosis. After all, finding what is wrong is as important as fixing the problem. We hope that similar biomarkers may be developed in the future, applicable to many other types of cancers. Written by Stephanus Steven Related articles: Thyroid cancer / Arginine and tumour growth / NGAL- a marker for kidney damage REFERENCES Biswas, D. et al. (2019) “A clonal expression biomarker associates with lung cancer mortality,” Nature Medicine, 25(10), pp. 1540–1548. Available at: https://doi.org/10.1038/s41591-019-0595-z. Header image: Lung cancer cells. Anne Weston, Francis Crick Institute. Attribution-Non-Commercial 4.0 International (CC BY-NC 4.0)

Evaluating the advantages and disadvantages of gentrification in the context of health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How does moving houses impact your health and well-being? 01/10/26, 17:11 Last updated: Published: 13/07/24, 12:02 Evaluating the advantages and disadvantages of gentrification in the context of health Introduction According to the World Health Organization (WHO), health is “a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity". Another way to define health is an individual being in a condition of equilibrium within themselves and the surrounding environment, which includes their social interactions and other factors. Reflecting on historical views of health, ancient Indian and Chinese medicine and society in Ancient Greece thought of health as harmony between a person and their environment, which underlines the cohesion between the soul and body; this is similar to the WHO’s definition of health. Considering these ideas, one key determinant of health is gentrification (see Figure 1 ). It was first defined in 1964 by British sociologist Ruth Glass, who witnessed the dilapidated houses in the London Borough of Islington being taken over and renovated by middle-class proprietors. The broader consequences of gentrification include enhanced living conditions for the residents, differences in ownership prerequisites, increased prices of land and houses, and transformations in the social class structure. Also, these changes cause lower-income inhabitants to be pushed out or go to poorer neighbourhoods, and the conditions in these neighbourhoods, which can include racial separation, lead to inequities and discrepancies in health. For example, a systematic review discovered that elderly and Black residents were affected more by gentrification compared to younger and White citizens; this highlights the importance of support and interventions for specific populations during urban renewal. Given the knowledge provided above, this article will delve further into the advantages and disadvantages of gentrification in the context of health outcomes. Advantages of gentrification Gentrification does have its benefits. Firstly, it is positively linked with collective efficacy, which is about enhancing social cohesion within neighbourhoods and maintaining etiquette; this has health benefits for residents, like decreased rates of obesity, sexually transmitted diseases, and all-cause mortality. Another advantage of gentrification is the possibility of economic growth because as more affluent tenants move into specific neighbourhoods, they can bring companies, assets, and an increased demand for local goods and services, creating more jobs in the area for residents. Additionally, gentrification can be attributed to decreased crime rates in newly developed areas because the inflow of wealthier citizens often conveys a more substantial sense of community and investment in regional security standards. Therefore, this revitalised feeling of safety can make these neighbourhoods more appealing to existing and new inhabitants, which leads to further economic development. Moreover, reducing crime can improve health outcomes by reducing stress and anxiety levels among residents, for example. As a result, the community's general well-being can develop, leading to healthier lifestyle choices and more lively neighbourhoods. Furthermore, the longer a person lives in a gentrifying neighbourhood, the better their self-reported health, which does not differ by race or ethnicity, as observed in Los Angeles. Disadvantages of gentrification However, it is also essential to mention the drawbacks of gentrification, which are more numerous. In a qualitative study involving elderly participants, for example, one of them stated that, “The cost of living increases, but the money that people get by the end of the month is the same, this concerning those … even retired people, and people receiving the minimum wage, the minimum wage increases x every year, isn’t it? But it is not enough”. Elderly residents in Barcelona faced comparable challenges of residential displacement between 2011 and 2017 due to younger adults with higher incomes and those pursuing university education moving into the city. These cases spotlight how gentrification can raise the cost of living without an associated boost in earnings, making it problematic for people with lower incomes or vulnerable individuals to live in these areas. Likewise, a census from gentrified neighbourhoods in Pittsburgh showed that participants more typically conveyed negative health changes and reduced resources. Additionally, one study examined qualitative data from 14 cities in Europe and North America and commonly noticed that gentrification negatively affects the health of historically marginalised communities. These include threats to housing and monetary protection, socio-cultural expulsion, loss of services and conveniences, and raised chances of criminal behaviour and compromised public security. This can be equally observed during green gentrification, where longtime historically marginalised inhabitants feel excluded from green or natural spaces, and are less likely to use them compared to newer residents. To mitigate these negative impacts of gentrification, inclusive urban renewal guidelines should be drafted that consider vulnerable populations to boost health benefits through physical and social improvements. The first step would be to provide residents with enough information and establish trust between them and the local authorities because any inequality in providing social options dramatically affects people’s health-related behaviours. Intriguingly, gentrification has been shown to increase the opportunity for exposure to tick-borne pathogens by populations staying in place, displacement within urban areas, and suburban removal. This increases tick-borne disease risk, which poses a health hazard to impacted residents ( Figure 2 ). As for mental health, research has indicated that residing in gentrified areas is linked to greater levels of anxiety and depression in older adults and children. Additionally, one study found young people encountered spatial disconnection and affective exclusion due to gentrification and felt disoriented by the quickness of transition. Lastly, there is something called Relocation Stress Syndrome (RSS), which occurs when a person, especially an older adult, moves to a new environment. This syndrome is also called transfer trauma. Therefore, all of these problems associated with gentrification reveal that it can harm public health and well-being, aggravating disparities and creating feelings of isolation and aloneness in impacted communities. Conclusion Gentrification is a complicated and controversial approach that has noteworthy consequences for the health of neighbourhoods. Its advantages include enhanced infrastructure and boosted economic prospects, potentially leading to fairer access to healthcare services and improved health outcomes for residents. However, gentrification often leads to removal and the loss of affordable housing, which can harm the health of vulnerable populations. Therefore, it is vital for policymakers and stakeholders to carefully evaluate the likely health effects of gentrification and enforce alleviation strategies to safeguard the well-being of all citizens (see Table 1 ). Written by Sam Jarada Related articles: A perspective on well-being / Socioeconomics health inequalities / Life under occupation / The 'New' scheme for first-time home buyers REFERENCES WHO. Health and Well-Being. Who.int . 2015. Available from: https://www.who.int/data/gho/data/major-themes/health-and-well-being Sartorius N. The meanings of health and its promotion. Croatian Medical Journal. 2006;47(4):662–4. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080455/ Krahn GL, Robinson A, Murray AJ, Havercamp SM, Havercamp S, Andridge R, et al. It’s time to Reconsider How We Define Health: Perspective from disability and chronic condition. Disability and Health Journal. 2021 Jun;14(4):101129. Available from: https://www.sciencedirect.com/science/article/pii/S1936657421000753 Svalastog AL, Donev D, Jahren Kristoffersen N, Gajović S. Concepts and Definitions of Health and health-related Values in the Knowledge Landscapes of the Digital Society. Croatian Medical Journal. 2017 Dec;58(6):431–5. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5778676/ Foryś I. Gentrification on the Example of Suburban Parts of the Szczecin Urban Agglomeration. remav. 2013 Sep 1;21(3):5–14. Uribe-Toril J, Ruiz-Real J, de Pablo Valenciano J. Gentrification as an Emerging Source of Environmental Research. Sustainability. 2018 Dec 19;10(12):4847. Schnake-Mahl AS, Jahn JL, Subramanian SV, Waters MC, Arcaya M. Gentrification, Neighborhood Change, and Population Health: a Systematic Review. Journal of Urban Health. 2020 Jan 14;97(1):1–25. Project Gallery

Role of neurotransmitters in depression Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Inside out: the chemistry of depression Last updated: 19/02/26, 19:35 Published: 05/06/25, 08:00 Role of neurotransmitters in depression This is Article 2 in a series on psychiatric disorders and the brain. Next article: The promising effects of magic mushrooms for depression . Previous article: What does depression do to your brain? Ever wondered what’s going on inside your brain when you’re feeling down? Imagine the scene from Inside Out , where Sadness takes over the control room, overshadowing the other emotions. That’s actually not too far from what happens during depression, but the changes in your brain are much more than just a battle of emotions. Depression is the most common mental illness globally. It is typically marked by a persistently low mood and energy, and a loss of interest or pleasure in everyday activities. Risk factors include chronic stress, traumatic life events, genetic vulnerability, ageing, and female sex. While these influences are widely recognised, have you ever thought about what is actually happening inside your brain when you're depressed? You've probably heard phrases like “I need a serotonin boost,” but what does that really mean? What is serotonin, and how does it influence our emotions and mental health? What are neurotransmitters? Think of neurotransmitters as messenger pigeons between neurons. They are involved in communication between different neurons. Communication between neurons is called synaptic transmission. In synaptic transmission, neurotransmitters are released from vesicles in one neuron into the synaptic cleft (the gap between two neurons) and then bind to receptors on the receiving neuron. This is how information travels through the brain, allowing us to think, feel, and act. Serotonin is an example of a neurotransmitter. Others include dopamine, noradrenaline, acetylcholine. The monoamine theory of depression One of the most widely supported explanations for the neurobiology of depression is the monoamine theory. This theory suggests that depression results from an imbalance or deficiency of monoamines in the brain. Monoamines are a group of neurotransmitters, including serotonin, dopamine, and noradrenaline, that are synthesised from the amino acids L-tryptophan and L-tyrosine. Fun fact: Did you know around 95% of the body's serotonin is produced in the gut? This is why there is growing interest in the gut-brain axis in mental health! Different neurotransmitter systems are involved in depression and even everyday emotion processing and regulation. The dopamine (DA) system plays a key role in experiencing reward and pleasure, often linked to feelings of joy. In contrast, the serotonin (5-HT) system is more associated with responses to punishment and aversive experiences, such as sadness or disgust. Noradrenaline (NE), on the other hand, is closely tied to fear, anger, and the activation of the "fight or flight" response during stressful situations. These neurotransmitters are thought to underlie three fundamental emotional states, which can combine in different ways to form a wide range of complex emotions. In the brain, these monoamines regulate mood, motivation, pleasure, and emotional stability. When levels are low, people may experience sadness, fatigue, apathy, and changes in appetite or sleep. This is why many antidepressant medications, such as selective serotonin reuptake inhibitors (SSRIs), aim to increase the availability of these monoamines in the synapse, improving communication between neurons and, over time, alleviating symptoms. SSRI treatment, in particular, is based on the serotonin hypothesis, a subset of the broader monoamine theory of depression, which suggests that reduced serotonin levels contribute to depressive symptoms. Conclusion: why depression is more than a mood Depression isn’t just “feeling sad”; it is a real condition that involves real chemical changes in the brain. The monoamine theory helps explain this by focusing on key neurotransmitters like serotonin, dopamine, and noradrenaline, which help control mood, motivation, and emotional balance. When these chemicals are out of sync, too low or not working properly, it can lead to the emotional numbness, low energy, and hopelessness that many people with depression experience. These neurotransmitters do not work in isolation; they influence how we respond to rewards, stress, and even daily activities. By understanding the biological changes behind depression, we take an important step toward not only understanding the condition but also reducing the stigma around it. Written by Chloe Kam Related articles: Emotional chemistry / Embarrassment / Postpartum depression in adolescent mothers REFERENCES Barchas, J.D. and Altemus, M. (1999) ‘Monoamine Hypotheses of Mood Disorders’, in Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition . Lippincott-Raven. Available at: https://www.ncbi.nlm.nih.gov/books/NBK28257/ (Accessed: 3 May 2025). Jiang, Y. et al. (2022) ‘Monoamine Neurotransmitters Control Basic Emotions and Affect Major Depressive Disorders’, Pharmaceuticals , 15(10), p. 1203. Available at: https://doi.org/10.3390/ph15101203 . Project Gallery

Dive into the latest biological research! Explore the profound impact of negligent exercise on well-being, discover breakthroughs in organoid and iPSC research, and gain insights into how biomarkers are enabling disease diagnosis and prevention- along with public health news. Biology Articles Dive into the latest biological research! Explore the profound impact of negligent exercise on well-being, discover breakthroughs in organoid and iPSC research, and gain insights into how biomarkers are enabling disease diagnosis and prevention- along with public health news. You may also like: Cancer , Ecology , Genetics , Immunology , Neuroscience , Zoology , and Medicine Can a human brain be uploaded to a computer? Uncovering the possibilities of transferring information from your brain to a computer Impacts of negligent exercise on physiology How to avoid negligent personal training as it can harm the individual Key historical events in public health A timeline of discoveries in the history of public health Influence of different environmental factors on exercise How different environmental factors can affect exercise Why bacteria are essential to human survival The benefits of bacteria Will diabetes mellitus become an epidemic? Diabetes mellitus is when the body is unable to produce enough insulin or becomes resistant to it Correlation between a country's HDI and COVID-19 mortality rate HDI stands for Human Development Index, i.e. how much a country is developed considering various factors such as wealth Rising food prices Food deserts and malnutrition Organoids in drug discovery What organoids are, their applications in drug discovery and more The genesis of life What came first: the chicken or the egg? Challenges in endometriosis From underreporting to under-research iPSCs and organoids iPSC stands for induced pluripotent stem cells PMOS and endometriosis These two diseases are very similar, but how are they different? Neutrophil gelatinase-associated lipocalin (NGAL) A biomarker for renal damage Childhood stunting Its issue in developing countries Innovations in the biosciences The biggest ones currently Various health models Understanding health through different stances Medicinal Manuka The benefits of using Manuka honey as medicine The dual role of mitochondria A mechanism for survival, or death? Next

The rabies virus infects neurons Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Rabies- the scariest disease ever? 13/06/26, 16:29 Last updated: Published: 10/10/24, 12:05 The rabies virus infects neurons Rabies is a viral disease that primarily affects the central nervous system (CNS), usually in mammals. Wild animals such as foxes, dogs, and raccoons are frequent carriers of the virus. Transmission occurs through the saliva of an infected animal through a bite or a scratch, allowing the virus to enter the body and travel through the nervous system toward the brain. While rabies can be prevented with a vaccine (the latest one, ChAdOx2 RabG, is single-shot), once symptoms begin to show, the disease is nearly always fatal once symptoms begin to show. What makes this virus so deadly, and how can it take control of the human body with just five genes in its genome? Why is the virus so hard to kill? To arrive at a sensible answer, we must first understand the ‘tropism’ of the virus – the cell type it likes to infect. Rabies virus infects the neurones (neurotropic), which creates a massive problem for the immune system. Macrophages and neutrophils, which are the prominent cells in killing foreign pathogens that kill foreign pathogens, usually deal collateral damage to the body’s own cells to some extent. This must be avoided with neurones, as neurones cannot replenish themselves after cell death. An inflammation of the nerve cells could lead to paralysis and seizures, compromising the CNS. As a result, the immune system response is significantly lowered around nerve cells to prevent accidental damage, which allows the virus to infect the neural pathway easily. Transmission of the virus See Figure 1 The strategy of the immune system is that the neurones can be protected if the pathogens are intercepted before they travel to their destination. However, this strategy ultimately fails when it comes to rabies, because the transmission is through a bite, which can penetrate and cut through many layers of tissue, providing a direct access to nerve cells. If you were bitten on the leg, then the time it takes for the rabies virus to travel to your brain would be the time it takes for you to travel from Florida, USA to Sweden. This may seem like a long time, but the rabies virus has evolved a technique that is able to hijack the cellular transport system can trick your cells’ transport system to travel quickly through the nerves by binding to a protein called dynein . Dynein is a motor protein that move along the microtubules in cells, converting the chemical energy of ATP into mechanical work. Microtubules are polarized structures, with a plus end (typically towards the axon terminal in neurones) and a minus end (towards the cell body). Dynein moves toward the minus end, facilitating retrograde transport, meaning it moves materials from the periphery of the cell, such as the axon terminals, back toward the cell body. Dynein is transports chemicals inside cells via endocytosis and plays a vital role in the movement of eukaryotic flagella. Rabies has evolved to stick to dynein via the Glycoprotein (G) present on its viral envelope, which allows rabies to travel to the brain much quicker. Dynein may be small, weighing around two megadaltons (3 x 10-18 grams), but it can move at a speed of 800 nanometres per second. At this speed, it takes rabies around 14 days to move up a metre- long neuron. This implies that the closer the animal bites you to the brain, the less time it takes for the symptoms to appear. If you’re bitten on the foot, it could take months for the virus to reach your brain. But if you’re bitten on the neck or face, the virus can get to your brain in just a few days, making it much more dangerous. This explains the broad range in the incubation time which is between 20 to 90 days. Infection and replication- see Figure 2 As the rabies travels through neuronal tracks, it sets up points of concentrated viral production centres called Negri bodies. These replicate the rabies virus within the neurones and inhibit interferon action, which are chemicals that alert white blood cells to the area of infection. Interferon inhibition along with lowered immune response to neurones make rabies extremely effective. However, neurones can undergo apoptosis—controlled cell death—to limit the spread of the virus and allow macrophages to clear the debris. Research in mice suggests that some strains of rabies may prevent this apoptotic response in cells. Additionally, studies indicate that rabies promotes apoptosis in killer T cells, which are responsible for inducing apoptosis in other cells. This mechanism helps to shield nerve cells from immune system attacks. Symptoms Patients with rabies initially experience flu-like symptoms and muscle pain. Once these early symptoms appear, treatment is virtually impossible. As the disease progresses, neurological symptoms develop including hydrophobia due to painful throat spasms when swallowing liquids. About 10 days after these neurological symptoms start, patients enter a coma, often accompanied by prolonged sleep apnoea. As virus attacks the brain throughout this stage, patients develop the urge to bite other organisms to transmit the virus. The virus can reach the salivary glands, allowing for transmission through a bite to occur again. Most patients typically die within three days of reaching this coma stage. Legends Rabies may have influenced the development of vampire and zombie myths due to its distinct symptoms. The disease causes aggression and sensitivity to light, which could have inspired some characteristics of vampires, such as their aversion to light and erratic movements. Additionally, rabies leads to excessive salivation and a tendency to bite, traits that align with vampire lore. Similarly, the delirium and motor dysfunction seen in rabies may have contributed to the depiction of zombies as shuffling, incoherent beings. Conclusion Rabies is a uniquely deadly virus due to its mechanism of hijacking the nervous system. After entering the body, the virus binds to dynein, using it to travel along neuronal pathways toward the brain. It replicates rapidly, forming Negri bodies disrupting neurone function. The virus effectively suppresses immune responses, making it nearly impossible to treat once symptoms appear, leading to almost 100% fatality. Beyond its biological impact, rabies has influenced cultural stories like those of vampires and zombies, with its symptoms—such as aggression, fear of water, and neurological decay—providing eerie parallels to these myths. Despite modern medical advances, rabies remains one of the most feared infectious diseases due to its fatal nature. Written by Baraytuk Aydin Related articles: Rare zoonotic diseases / rAAV gene therapy REFERENCES CUSABIO (2020) Rabies virus overview: Structure, transmission, pathogenesis, symptoms, etc, CUSABIO. Available at: https://www.cusabio.com/infectious-diseases/rabies-virus.html (Accessed: 12 September 2024). Hendricks, A.G. et al. (2012) Dynein tethers and stabilizes dynamic microtubule plus ends, Current biology : CB. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3347920/ (Accessed: 13 September 2024). Lahaye, X. et al. (2009) Functional Characterization of Negri Bodies (NBS) in rabies virus-infected cells: Evidence that NBS are sites of viral transcription and replication, Journal of virology. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715764/ (Accessed: 13 September 2024). Tarantola, A. (2017) Four thousand years of concepts relating to rabies in animals and humans, its prevention and its cure , MDPI . Available at: https://www.mdpi.com/2414-6366/2/2/5 (Accessed: 15 September 2024). Project Gallery

Examining disconnection strategies and Functional Group Interconversion (FGI) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Molecular blueprints: the art of synthetic planning Last updated: 05/03/26, 14:47 Published: 19/02/26, 08:00 Examining disconnection strategies and Functional Group Interconversion (FGI) This is article no. 1 in a two-part series on retrosynthesis. Next article: Synthesis of ibuprofen . Introduction Science is often seen as rigid, driven solely by facts and logic. Yet, in the world of chemical synthesis, molecular design and retrosynthetic analysis can be considered an art form. Synthetic creativity can be measured by the number of steps, environmental considerations, or the clever assembly of chemical building blocks. Widely used in the pharmaceutical industry and responsible for many Nobel Prize‑winning discoveries, retrosynthetic planning is central to modern synthetic chemistry. 1. Disconnection Strategy Retrosynthesis begins with deconstructing a target molecule into simpler starting materials known as synthons. A synthon is hypothetical but represents a fragment that could react to form a target molecule. Chemists then match synthons to real‑life equivalents (R.L.E.) which can be used in the lab. For example, if a target molecule contains an ester group, cleaving the oxygen–carbonyl bond produces four possible synthons ( Figure 1 ). Of these synthons, the positively charged oxygen has no R.L.E., so pairing the negatively charged oxygen with a carbonyl‑containing R.L.E., such as a carboxylic acid or acid chloride, and an alcohol will effectively synthesise the desired ester. 2. Functional Group Interconversion (FGI) FGIs are exploited by chemists when a functional group is difficult to manipulate directly. In these cases, the target functional group is converted to another functional group which is easier to work with. For instance, this strategy is commonly used to synthesise alkene and carboxylic acid fragments. As alkenes mainly participate in addition reactions, forming C–C bonds can prove difficult; therefore, converting the alkene to an alkyne can make this simpler. As an alkyne‑to‑alkene transformation is relatively simple, using either Lindlar’s catalyst (Z‑alkene) or Na/NH₃ (E‑alkene), alkynes can be used to build up the carbon chain before a final reduction. This is done by simple nucleophilic substitutions promoted by base deprotonation (NaNH₂) of the alkyne. The same idea is used for installing carboxylic acids, as a common FGI is to use a nitrile group (CN). These can be easily transformed back to the target carboxylic acid using acid in aqueous conditions. 3. Synthesis of Aspirin Retrosynthetic analysis can be used to design synthetic routes to common pharmaceuticals. For aspirin, a good disconnection strategy would be to break the ester bond and derive R.L.E. as shown above. To install the carboxylic acid, an FGI can be used. In Figure 3, two possible syntheses are highlighted utilising these strategies. While the synthetic methods presented previously will produce aspirin in high yields, they often create large amounts of waste and use harsh acidic conditions. Bhuyan et al. have proposed a more sustainable synthesis using blue LED light to catalyse the reaction under an O₂ atmosphere ( Figure 4) . Conclusion In conclusion, retrosynthesis and synthetic planning are essential tools for designing complex molecules. While the disconnection strategy and FGIs are relatively simple concepts, their application is used routinely in both industry and academia, regardless of the complexity of the target molecule. While one strategy may be used routinely, there are often many more ways to synthesise a particular compound more efficiently or with more flair. Stay tuned for Part 2, where the techniques discussed here are applied to the synthesis of ibuprofen. Written by Antony Lee Project Gallery