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Molecular gastronomy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Exploring food at a molecular level 09/07/25, 14:07 Last updated: Published: 13/05/24, 14:46 Molecular gastronomy Imagine taking a bite of your favourite dish, not just savouring the flavours, but peering into the very essence of its existence. That's the realm of molecular gastronomy, a fascinating exploration of food through the lens of science. This article takes you on a journey at the microscopic level of what fuels the human body. The foundation of all food lies in macromolecules, large molecules formed from the intricate assembly of smaller ones. Carbohydrates, proteins, and lipids are the main players, each with unique structures and roles. Carbohydrates: These sugary giants, like starches and sugars, provide our bodies with energy. Imagine them as long chains of sugar molecules linked together, like beads on a necklace. Proteins: The workhorses of the cellular world, proteins are responsible for countless functions. They're built from amino acids, each with a distinct side chain, creating a diverse and essential cast of characters. Lipids: Fats and oils, these slippery molecules store energy and form cell membranes. Think of them as greasy chains with attached rings, like chubby tadpoles swimming in oil. The symphony of cooking and the final dance Applying heat, pressure, and chemical reactions, chefs become culinary alchemists at the molecular level. Water, the universal solvent, facilitates the movement and interaction of these molecules. As we cook, proteins unfold and rearrange, starches break into sugars, and fats melt and release flavours. Maillard Reaction: This browning phenomenon, responsible for the delicious crust and crunch on your food, arises from the dance between sugars and amino acids. Imagine them waltzing and exchanging partners, creating new flavorful molecules that paint your food with golden hues. Emulsification: Oil and water don't mix, but lecithin, a molecule found in egg yolks, acts as a matchmaker. It bridges the gap between these unlikely partners, allowing for the creation of creamy sauces and fluffy cakes. Think of lecithin as a tiny cupid, shooting arrows of attraction between oil and water droplets. Saponification: Techniques like spherification use alginate and calcium to create edible spheres filled with liquid, transforming into playful pearls that burst with flavor in your mouth. A world of potential Understanding food at the molecular level unlocks a treasure trove of possibilities. It can help us create healthier, more sustainable food choices, develop personalized nutrition plans, and even combat food-borne illnesses. By peering into the microscopic world of our meals, we gain a deeper appreciation for the magic that happens on our plates, bite after delicious bite. So next time you savor a meal, remember the intricate dance of molecules that brought it to life. From the building blocks of carbohydrates to the symphony of cooking, food is a story written in the language of chemistry, waiting to be deciphered and enjoyed. Written by Navnidhi Sharma Related articles: Emotional chemistry on a molecular level / Food prices and malnutrition / Vitamins References and further readings: Chapter 2: Protein structure . (2019, July 10). Chemistry. https://wou.edu/chemistry/courses/online-chemistry-textbooks/ch450-and-ch451-biochemistry-d efining-life-at-the-molecular-level/chapter-2-protein-structure/ Gan, J., Siegel, J. B., & German, J. B. (2019). Molecular annotation of food - Towards personalized diet and precision health. Trends in Food Science & Technology , 91 , 675–680. https://doi.org/10.1016/j.tifs.2019.07.016 Grant, P. (2020, August 4). Sugar, fiber, starch: What’s A carbohydrate? — Pamela Grant, L.Ac , NTP. Pamela Grant, L.Ac , NTP . https://pamela-grant.com/blog-ss/sugar-fiber-starch Helmenstine, A. (2022, October 25). Examples of carbohydrates . Science Notes and Projects. https://sciencenotes.org/examples-of-carbohydrates/ Project Gallery

What they are, uses, and future outlook Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Advancements in Semiconductor Laser Technology 08/07/25, 16:19 Last updated: Published: 23/06/24, 09:39 What they are, uses, and future outlook Lasers have revolutionised many fields starting from the telecommunications, data storage to medical diagnostics and consumer electronics. And among the semiconductor laser technologies, Edge Emitting Lasers (EEL) and Vertical Cavity Surface Emitting Lasers (VCSEL) emerged as critical components due to their unique properties and performance. These lasers generate light through the recombination of electrons and holes in a semiconductor material. EELs are known for their high power and efficiency and they are extensively used in fiber optic communications and laser printing. VCSELs on the other hand are compact and are used for applications like 3D sensing. Traditionally VCSELs have struggled to match the efficiency levels of EELs however a recent breakthrough particularly in multi junction VCSEL, has demonstrated remarkable efficiency improvements which place the VCSELs to surpass EELs in various applications. This article focuses on the basics of these laser technologies and their recent advancements. EELs are a type of laser where light is emitted from the edge of the semiconductor wafer. This design contrasts with the VCSELs which emit light perpendicular to the wafer surface. EELs are known for their high power output and efficiency which makes them particularly suitable for applications that require long-distance light transmission such as fiber optic communications, laser printing and industrial machining. EELs consist of an active region where electron hole recombination occurs to produce light. This region is sandwiched between two mirrors forming a resonant optical cavity. The emitted light travels parallel to the plane of the semiconductor layers and exits from the edge of the device. This design allows EELs to achieve high gain and power output which makes them effective for transmitting light over long distances with minimal loss. VCSELs are a type of semiconductor laser that emits light perpendicular to the surface of the semiconductor wafer unlike the EELs which emit light from the edge. VCSELs have gained popularity due to their lower threshold currents and ability to form high density arrays. VCSELs consist of an active region where electron-hole recombination occurs to produce light. This region is situated between two highly reflective mirrors which forms a vertical resonant optical cavity. The light is emitted perpendicular to the wafer surface which allows for efficient vertical emission and easy integration into arrays. Recent advancements in VCSEL technology marked a significant milestone in the field of semiconductor lasers. And in particular the development of multi junction VCSEL which led to the improvements in power conversion efficiency (PCE) of the laser. Research conducted by Yao Xiao et al. and team has demonstrated the potential of a multi junction VCSELs to achieve efficiency levels which were previously thought unattainable. This research focuses on cascading multiple active regions within a single VCSEL to enhance gain and reduce threshold current which leads to higher overall efficiency. The study employed a multi-junction design where several active regions are stacked vertically within the VCSEL. This design increases the volume of the gain region and lowers the threshold current density resulting in higher efficiency. Experimental results from the study revealed that a 15-junction VCSEL achieved a PCE of 74% at room temperature when driven by nanosecond pulses. This efficiency is the highest ever reported for VCSELs and represents a significant leap forward from previous records. Simulations conducted as part of the study indicated that a 20-junction VCSEL could potentially reach a PCE exceeding 88% at room temperature. This suggests that further optimization and refinement of the multi-junction approach could yield even greater efficiencies. The implications of this research are profound for the future of VCSEL technology. Achieving such high efficiencies places VCSELs as strong competitors to EELs particularly in applications where energy efficiency and power density are critical. The multi junction VCSELs demonstrated in the study shows promise for a wide range of applications and future works may focus on optimizing the fabrication process, reducing thermal management issues and exploring new materials to further enhance performance. Integrating these high-efficiency VCSELs into commercial products could revolutionize industries reliant on laser technology. Written by Arun Sreeraj Related articles: The future of semi-conductor manufacturing / The search for a room-temperature superconductor / Advances in mass spectrometry Project Gallery

An overview Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Epithelioid hemangioendothelioma (EHE) 09/07/25, 14:05 Last updated: Published: 25/02/24, 14:52 An overview This is article no. 4 in a series on rare diseases. Next article: Unfolding prion disease . Previous article: Herpes vs devastating skin disease . Gene fusion and EHE Epithelioid hemangioendothelioma (EHE) is a rare cancer which arises from the cells lining the blood vessels (endothelial cells). This occurs when two genes fuse together. Generally, there are several different gene fusions which lead to cancer, predominantly in prostate, ovarian, blood, and sarcomas (soft tissue cancer). These arise from two genes which bind together to create a fusion oncogene, such as the classical example of the BCR-ABL1 fusion gene, called the “Philadelphia chromosome,” in chronic myeloid leukaemia . EHE is a rare vascular sarcoma caused by a fusion between two genes, primarily TAZ and CAMTA1. TAZ is part of the Hippo signalling pathway (see below) and is a transcriptional co-activator (it binds to a transcription factor to activate the first step in gene expression, which is the conversion of DNA to RNA). Less is known about CAMTA1, although it is a transcription activator found primarily in the brain. However, there are also a small number of cases (10%) caused by a YAP1-TFE3 fusion. YAP1 is also part of the Hippo pathway, whilst TFE3 is a transcription factor. EHE is a prime example of the importance of gene fusions (and other chromosomal rearrangements) in the genetic origin of many cancers. Therefore, further understanding of this disease may provide clues into the tumourigenesis of other different cancers. EHE is extremely rare at a prevalence of 1 in 1 million and presents more often in females, but it can occur in either sex at any age. It is most common in the liver and lung and has an unusual pathology, as it can present as an aggressive or indolent (slow-growing) cancer. Similarly to many cancers, symptoms can present as any or all the following: a mass, fever, fatigue, pain, and weight loss. It may also have no symptoms and be highlighted by chance whilst undergoing other investigations. Cellular signalling behind EHE: the Hippo pathway The Hippo pathway controls tissue growth and is the signalling mechanism behind EHE. YAP/TAZ are vital members of this pathway and are oncogenic transcription (co-) factors in many solid tumours. They have also been shown to be crucial for cancer initiation, progression, and metastasis. However, surprisingly, certain blood cancers, such as leukaemia, myeloma, and lymphoma, show reduced levels of YAP/TAZ. Therefore, it seems YAP/TAZ behave differently depending on cell type. High expression of YAP/TAZ (or nuclear localization) is related to poor prognosis in breast, colorectal, liver, lung, gastric, pancreatic, ovarian, endometrial, oesophageal, and bladder cancers. YAP/TAZ are phosphorylated and degraded in the cytoplasm when the Hippo pathway is ‘on.’ However, when the Hippo pathway is ‘off,’ YAP/TAZ move to the nucleus, where they are involved in transcription (see the signalling pathway diagram). However, in EHE disease, even when Hippo is ‘on,’ TAZ-CAMTA1/YAP1-TFE3 override this and move to the nucleus to be involved in aberrant (atypical) transcription. YAP/TAZ bind to TEAD ( DNA-binding domain ) in the nucleus, whilst CAMTA1 and TFE3 are thought to be involved in chromatin remodelling. Chromatin consists of tightly packed DNA and histones (proteins). Chromatin remodelling results in the chromatin unwinding and the DNA becoming more accessible for transcription (i.e. ‘switching on’ certain genes). Therefore, this may lead to overexpression and subsequently, cancer. EHE treatment There are no standard treatments for EHE, but indolent cancers are often treated by monitoring, a ‘watch-and-wait’ strategy. Surgery is a common form of treatment for single tumours. Ablation (burning/freezing), isolated limb perfusion (drug treatment to one limb), vascular embolization (blocking tumour blood supply), and radiation therapy are also other forms of possible treatment, along with the mammalian target of rapamycin (mTOR) inhibitors (the mTOR pathway controls cell proliferation/metabolism). Tyrosine kinase inhibitors (tyrosine kinases activate proteins in related pathways) and interferon (immune system modulators) are two other possible treatments. A transplant could also be an option if there is an organ with multiple tumours (most often the liver). However, more effective treatments are needed and research into this disease is currently underway. Summary EHE is a rare cancer which arises from the cells lining the blood vessels. It occurs from gene fusions, primarily TAZ-CAMTA1. TAZ is part of the Hippo signalling pathway, which controls tissue growth. Therefore, Hippo is a vital pathway involved in many cancers, and understanding this pathway in EHE disease may provide clues as to the tumourigenesis of other cancers. Written by Eleanor R. Markham Related articles: The Hippo signalling pathway / Apocrine carcinoma (a rare form of breast cancer) Project Gallery

Landing on the moon (again!) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Artemis: the Lunar South Pole Base 09/07/25, 10:55 Last updated: Published: 13/01/24, 15:44 Landing on the moon (again!) Humans have not visited the moon since 1972, but that’s about to change. Thanks to NASA’s Artemis missions, we have already taken the first small step towards our own lunar home for astronauts. NASA has established the second generation of its lunar missions- “Artemis”, fittingly named after the ancient Greek Goddess of the Moon, and Apollo’s twin. The ultimate aim of the Artemis missions is to solidify a stepping stone to Mars. Technologies will be developed, tested, and perfected, before confidence is built to travel on to Mars. NASA has to consider the natural conditions of the Moon, since doing so will allow astronauts to limit their reliance on resources from Earth, and increase their length of stay and therefore potential for research. The amount achieved would be extremely limited if a lunar mission relied solely on resources from Earth, due to the limitation of rocket payloads. This is known as In-Situ Resource Utilisation, and in addition to extended lunar stays, its success on the Moon is essential if we hope to one day establish a base on Mars. As a priority, astronauts need to have access to energy and water. Luckily, the conditions at the lunar south pole may be ideal for this. Unlike Earth, where we experience seasons due to its 23.5° tilt, the Moon’s tilt is tiny, at only 1.5°. This means some areas at the lunar poles are almost always exposed to sunlight, providing a reliable source of solar energy generation for a potential Artemis Base Camp. And since the Sun is always near the horizon at the poles, there are even areas in deep craters that never see the light. These areas of “eternal darkness” can reach temperatures of -235°, possibly allowing astronauts access to water ice. Aside from access to resources, Artemis has to consider the dangers that come from living in space. Away from the safety of Earth’s protective atmosphere and magnetosphere, astronauts would be exposed to harsh solar winds and cosmic rays. To combat this, NASA hopes to make use of the terrain surrounding the base, highlighting another advantage of the hilly south pole [3]. The exact location for the Artemis Base is currently undecided. We just know it will most likely be near a crater rim by the south pole, and on the Earth-facing side to allow for communication to and from Earth. Not only is the south pole ideal from a practical standpoint, it is also an area of exciting scientific interest. Scientists will have access to the South Pole–Aitken basin, not only the oldest and largest confirmed impact crater on the Moon, but the second largest confirmed impact crater in the entire Solar System. With a depth of up to 8.2 km, and diameter of 2500 km, it is thought this huge crater will contain exposed areas of lower crust and mantle, providing an insight into the Moon’s history and formation. Additionally, thanks to areas of “eternal darkness” the ice water found deep within craters at the south pole may hold trapped volatiles up to 3.94 billion years old, which, although not as ancient as previously expected, can still provide an insight into the evolution of the Moon. The scientific potential of the Artemis Base Camp extends far beyond location specific investigations to our most fundamental understanding of physics, from Quantum Physics to General Relativity. Not to mention the astronauts themselves, as well as “model organisms” which will be the focus of physiological studies into the effects of extreme space environments. Artemis Timeline Overview Artemis 1 launched on 16th November 2022. It successfully tested the use of two key elements of the Artemis mission- Orion and the Space Launch System (SLS)- with an orbit around the moon. Orion, named after the Goddess Artemis' hunting partner, is the spacecraft that will carry the Artemis crew into lunar orbit. It is carried by the SLS, NASA’s super heavy-lift rocket, one of the most powerful rockets in the world. Artemis 2 plans to launch late 2024 and will be the first crewed Artemis mission, with a lunar flyby bringing four astronauts further than humans have ever travelled beyond Earth. Artemis 3 plans to launch the following year. It will be the historic moment that will see humans step foot on the surface of the moon for the first time since we left in 1972. The mission will be the first use of another key element of the Artemis missions- the Human Landing System (HLS). Astronauts will use a lunar version of SpaceX’s Starship rocket as the HLS for Artemis 3 and 4. (Starship is currently in its test stage, with its second test launch carried out very recently on the 18th November 2023.) Two astronauts will stay on the lunar surface for about a week, beating the current record of 75 hours on the Moon by Apollo 17. Artemis 4 plans to launch in 2028. The mission will include the first use of Gateway, another key element to the Artemis missions. Gateway will be a multifunctional lunar space station, designed to transfer astronauts between Orion and HLS, as well as hosting astronauts to live and research in lunar orbit. Gateway will be constructed over Artemis 4-6 , with each mission completing an additional module. NASA plans to have Artemis missions extending for years beyond this, with over 10 proposed and more expected. Eventually we will have a working base on the Moon with astronauts able to stay for months at a time. Having already started a year ago, Artemis will continue to expand our horizons. We can look forward to uncovering long held secrets of the Moon, and soon, setting our sights confidently on Mars. Written by Imo Bell Related articles: Exploring Mercury / Fuel for the colonisation of Mars / Nuclear fusion REFERENCES How could we live on the Moon? - Institute of Physics. Available at: https://www.iop.org/explore-physics/moon/how-could-we-live-on-the-moon Understanding Physical Sciences on the Moon - NASA. Available at: https://science.nasa.gov/lunar-science/focus-areas/understanding-physical-sciences-on-themoon NASA’s Artemis Base Camp on the moon will need light, water, elevation - NASA. Available at: https://www.nasa.gov/humans-in-space/nasas-artemis-base-camp-on-the-moon-will-need-ligh t-water-elevation Zuber, M.T. et al. (1994) ‘The shape and internal structure of the Moon from the Clementine Mission’, Science, 266(5192), pp. 1839–1843. doi:10.1126/science.266.5192.1839. Flahaut, J. et al. (2020) ‘Regions of interest (ROI) for future exploration missions to the Lunar South Pole’, Planetary and Space Science, 180, p. 104750. doi:10.1016/j.pss.2019.104750. Moriarty, D.P. et al. (2021) ‘The search for lunar mantle rocks exposed on the surface of the Moon’, Nature Communications, 12(1). doi:10.1038/s41467-021-24626-3. Estimates of water ice on the Moon get a ‘dramatic’ downgrade - Physics World. Available at: https://physicsworld.com/a/estimates-of-water-ice-on-the-moon-get-a-dramatic-downgrade Biological Systems in the lunar environment - NASA. Available at: https://science.nasa.gov/lunar-science/focus-areas/biological-systems-in-the-lunar-environme Https://www.nasa.gov/wp-content/uploads/static/artemis/NASA : Artemis - NASA. Available at: https://www.nasa.gov/specials/artemis Project Gallery

iPSCs are one of the most powerful tools of biosciences Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The endless possibilities of iPSCs and organoids 11/07/25, 10:02 Last updated: Published: 20/01/24, 11:50 iPSCs are one of the most powerful tools of biosciences On the 8th of October 2012, the Nobel Prize in Physiology was given to Shinya Yamanaka and John B. Gurdon for a groundbreaking discovery; induced Pluripotent Stem Cells (iPSCs). The two scientists discovered that mature, specialised cells can be reprogrammed to their initial state and consequently transformed into any cell type. These cells can be used to study disease, examine genetic variations and test new treatments. The science behind iPSCs The creation of iPSCs is based on the procedure of cell potency during mammalian development. While the organism is still in the embryonic stage, the first cell developed is a totipotent stem cell, which has the unique ability to differentiate into any cell type in the human body. “Totipotent” refers to the cell’s potential to give rise to all cell types and tissues needed to develop an entire organism. As the totipotent cell grows, it develops into the pluripotent cell, which can differentiate into the three types of germ layers; the endoderm line, the mesoderm line and the ectoderm line. The cells of each line then develop into multipotent cells, which are derived into all types of human somatic cells, such as neuronal cells, blood cells, muscle cells, skin cells, etc. Creation of iPSCs and organoids iPSCs are produced through a process called cellular reprogramming, which involves the reprogramming of differentiated cells to revert to a pluripotent state, similar to that of embryonic stem cells. The process begins with selecting any type of somatic cell from the individual (in most cases, the individual is a patient). Four transcription factors, Oct4, Sox2, Klf4 and c-Myc, are introduced into the selected cells. These transcription factors are important for the maintenance of pluripotency. They are able to activate the silenced pluripotency genes of the adult somatic cells and turn off the genes associated with differentiation. The somatic cells are now transformed into iPSCs, which can differentiate into any somatic cell type if provided with the right transcription factor. Although iPSCs themselves have endless applications in biosciences, they can also be transformed into organoids, miniature three-dimensional organ models. To create organoids, iPSCs are exposed to a specific combination of signalling molecules and growth factors that mimic the development of the desired organ. Current applications of iPSCs As mentioned earlier, iPSCs can be used to study disease mechanisms, develop personalised therapies and test the action of drugs in human-derived tissues. iPSCs have already been used to model cardiomyocytes, neuronal cells, keratinocytes, melanocytes and many other types of cells. Moreover, kidney, liver, lung, stomach, intestine, and brain organoids have already been produced. In the meantime, diseases such as cardiomyopathy, Alzheimer’s disease, cystic fibrosis and blood disorders have been successfully modelled and studied with the use of iPSCs. Most importantly, the use of iPSCs in all parts of scientific research reduces or replaces the use of animal models, promising a more ethical future in biosciences. Conclusion iPSCs are one of the most powerful tools of biosciences at the moment. In combination with gene editing techniques, iPSCs give accessibility to a wide range of tissues and human disorders and open the doors for precise, personalised and innovative therapies. iPSCs not only promise accurate scientific research but also ethical studies that minimise the use of animal models and embryonic cells. Written by Matina Laskou Related articles: Organoids in drug discovery / Introduction to stem cells Project Gallery

The importance of implementing Maths into our lives Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Teaching maths like it matters 11/07/25, 09:54 Last updated: Published: 03/10/23, 13:43 The importance of implementing Maths into our lives …But I’m never going to use Algebra in my life! The above is a typical response from students across the country when walking into a Maths class. I did not understand others’ disdain, because I love Maths. I got satisfaction from solving numerical problems, stimulation from equations, and excitement from learning new variables like alpha, or constants like Pi. The abstract nature of Maths was like art to me. Later, I realised that not all my peers felt the same way, that somehow, I was the anomaly and that they were the norm. Many maths teachers feel the same way. They get lost in the subject that they love and try to teach it in the way that makes sense to them, without thinking on how the lack of context in equations and processes means nothing to disengaged students. As teachers, our job is to show how applicable Maths can be to our students on an individual basis. Rather than using real-life questions as extensions after the core activity, we must utilise them from the beginning when introducing topics, showing student’s how the methods that they learn can be applied to have some use beyond a pass mark in their exams. I am not talking about examples of ladders leaning against walls when teaching Pythagoras’ theorem and SOHCAHTOA, or, taking counters from a bag, to explain Probability. The examples here are forced, no student will connect with them because they are not lived examples or likely scenarios in most of their lives. We need to build strong relationships with our students, understand their demographic and interests, then introduce topics based on this. For example: If I know that my class enjoys football, I will begin with a video of Messi playing the game, pausing the video, and splitting the pitch up into segments, which can lead a conversation into areas of segments and circles, or, I can discuss the trajectory of the ball after a kick, to talk about quadratic equations. In another class, we can ask what students are budgeting for, perhaps concert tickets or new clothes, and use that to open a discussion into arithmetic series. Another great example is asking students to find an event happening somewhere in the country that they would like to go to, and as a class, plan for this. We would use research skills, calculate speed, distance and time if going by car, or pull up a train timetable where we can teach two-way tables and time conversions. To create meaningful connections to Math topics will take time, effort, and research, and the difficulty will be that not every application will be relatable to every cohort. We will need to build a portfolio of contextual examples related to each topic, however, if there is buy-in from others in our departments, it is an achievable target. In conclusion, we must teach Maths to students in meaningful ways that applies to their life, to keep up engagement and motivation as well as providing opportunities to deepen understanding. Maths should be based around conversation and interests, rather than an exercise of memorising and processes. It should make sense to students, it should matter. Written by Sara Altaf Related article: The game of life Project Gallery

Navigating the silence Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unveiling the underreported challenges of endometriosis 14/07/25, 15:10 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

Mutations in collagen and related proteins are the primary cause of EDS Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link From genes to joints: how Ehlers-Danlos Syndrome is shaped by genetics 12/09/25, 11:12 Last updated: Published: 08/11/24, 11:40 Mutations in collagen and related proteins are the primary cause of EDS This is article no. 10 in a series on rare diseases. Next article: CEDS- a break in cell death . Previous article: Breaking down Tay-Sachs . Ehlers-Danlos Syndrome (EDS) is a group of 13 inherited disorders that affect connective tissues, particularly collagen. Collagen is a crucial protein in the body that provides structure and strength to skin, joints, and blood vessels. Mutations in collagen or collagen-modifying proteins are the primary cause of the types of EDS. EDS manifests through a range of symptoms that vary significantly depending on the specific type of EDS. However, there are common symptoms that many individuals with EDS experience, particularly related to joint and skin issues. For instance, joints can move beyond the normal range, leading to frequent dislocations and subluxations, also called joint hypermobility. Additionally, the skin can be stretched more than usual, which creates a soft and velvety appearance known as skin hyperextensibility. As mentioned in Figure 1 , skin bruising, scarring and tearing are common symptoms, leading to individuals often experiencing chronic pain. Life expectancy for individuals with EDS varies depending on the type of disorder an individual has. This is due to how specific forms can have structural changes in organs and tissues, which can lead to serious life-threatening complications. For example, vascular EDS (vEDS) is associated with a significantly reduced life expectancy due to the risk of spontaneous rupture of major blood vessels, intestines, and other hollow organs. Most other forms of EDS, such as classical EDS (cEDS), hypermobile EDS (hEDS), and kyphoscoliotic EDS (kEDS), generally do not significantly affect life expectancy. However, the health complications that patients have can substantially impact their quality of life. Genetic basis As stated, the various types of EDS encompass many genetic defects, for example, cEDS is linked to mutations in the COL5A1 or COL5A2 genes, which encode the α1 and α2 chains of type V collagen. Following an autosomal dominant inheritance pattern, 50% of cEDS diagnoses inherit the condition from an affected parent, while the other half from a new (de novo) pathogenic variant. Diagnosing EDS encompasses a variety of methods. Firstly, differential diagnosis may be used to distinguish between subtypes like cEDS and hEDS by evaluating clinical features such as the presence of joint hypermobility, skin characteristics, and scarring patterns. Clinicians use these specific symptoms along with family history to differentiate between the subtypes since some, like hEDS, lack identified genetic markers, making this clinical assessment essential for accurate diagnosis and management. This process helps exclude other conditions and accurately identify the EDS subtype. Also, suggestive clinical features identifying pathogenic or likely pathogenic variants in the COL5A1 or COL5A2 genes can be done through molecular genetic testing. This testing can be approached in two ways: targeted multigene panels, which focus on specific genes like COL5A1 and COL5A2 . Alternatively, comprehensive genomic testing, such as exome or genome sequencing, does not require preselecting specific genes and is useful when the clinical presentation overlaps with other inherited disorders. Mutations in COL5A1 and COL5A2 can include missense, nonsense, splice site variants, or small insertions and deletions, all of which impair the function of type V collagen. Missense mutations result in the substitution of one amino acid for another, disrupting the collagen triple helix structure and affecting its stability and function. On the other hand, nonsense mutations lead to a premature stop codon, producing a truncated and usually non-functional protein. Splice site mutations interfere with the normal splicing of pre-mRNA, resulting in aberrant proteins. These mutations in COL5A1 and COL5A2 lead to the characteristic features of cEDS, such as highly elastic skin and joint hypermobility. Furthermore, different types of EDS are caused by specific genetic mutations, each affecting collagen in distinct ways and necessitating varied treatment approaches. VEDS is caused by mutations in the COL3A1 gene, which affects type III collagen and leads to fragile blood vessels and a higher risk of organ rupture. kEDS results from mutations in the PLOD1 or FKBP14 genes, impacting collagen cross-linking, and presents with severe scoliosis and muscle hypotonia. Arthrochalasia EDS (aEDS), due to mutations in the COL1A1 or COL1A2 genes that affect type I collagen, features severe joint hypermobility and congenital hip dislocation. Dermatosparaxis EDS (dEDS) is caused by mutations in the ADAMTS2 gene, which is crucial for processing type I collagen, leading to extremely fragile skin and severe bruising. Each type of EDS highlights the critical role of specific genetic mutations in the structural integrity and function of collagen, which consequently influences treatment approaches. Treatment Treatments for EDS primarily focus on managing symptoms and preventing complications due to the underlying genetic defects affecting collagen. Pain relief through nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and sometimes opioids is common, addressing chronic pain related to joint and muscle issues. Moreover, physical therapy may help strengthen muscles around hypermobile joints, reducing the risk of dislocations and improving stability. Orthopaedic interventions, such as braces and orthotics, are also used to support joint function, and surgery may be considered in severe cases. Cardiovascular care is crucial, especially for vEDS, involving regular monitoring with imaging techniques to detect arterial problems early. Preventive vascular surgery might be necessary to repair aneurysms or other vascular defects. Wound care includes using specialised dressings to handle fragile skin and prevent extensive scarring, relevant to mutations in genes like COL5A1 and COL5A2 in classical EDS. Understanding the specific genetic mutations helps tailor these treatments to address the particular collagen-related defects and associated complications in different EDS types. Moreover, clinical trials for treating EDS have shown both positive and negative results. For example, trials investigating the efficacy of physical therapy in strengthening muscles around hypermobile joints have shown positive outcomes in reducing joint instability and improving function. On the other hand, trials aiming to directly modify the underlying genetic defects in collagen production have faced significant challenges. Gene therapy approaches and other experimental treatments targeting specific mutations, such as those in COL5A1 or COL3A1 genes, have shown limited success and faced hurdles in achieving sufficient therapeutic benefit without adverse effects. This is evident as in mouse models the deletion of COL3A1 resulted in aortic and gastrointestinal rupture meaning that simply restoring one functional copy may not be sufficient to prevent the disease. Moreover, the unknown and partial success in identifying mutations responsible for all EDS cases has further bolstered the struggle for researchers to establish comprehensive treatment strategies. In vEDS, as it is a dominantly inherited disorder, adding a healthy copy of the gene (a common strategy in gene therapy) is ineffective because the defective gene still produces harmful proteins. Research has highlighted, however, that the combination of RNAi-mediated mutant allele-specific gene silencing and transcriptional activation of a normal allele could help as a promising strategy for vascular Ehlers-Danlos Syndrome. In the experiment, researchers used small interfering RNA (siRNA) to selectively reduce the mutant COL3A1 mRNA levels by up to 80%, while simultaneously using lysyl oxidase (LOX) to boost the expression of the normal COL3A1 gene. This dual approach successfully increased the levels of functional COL3A1 mRNA in patient cells, suggesting a potential therapeutic strategy for this condition. Conclusion In conclusion, EDS represents a diverse group of inherited connective tissue disorders, primarily caused by mutations in collagen or collagen-modifying proteins. These genetic defects result in a wide range of symptoms, including joint hypermobility, skin hyperextensibility, and vascular complications, which vary significantly across the 13 different types of EDS. Diagnosing and treating EDS is complex and largely dependent on the specific genetic mutations involved. While current treatments mainly focus on managing symptoms and preventing complications, advances in genetic research, such as RNAi-mediated gene silencing and transcriptional activation, show promise for more targeted therapies, especially for severe forms like vascular EDS. However, challenges remain in developing comprehensive and effective treatments, underscoring the need for ongoing research and personalised medical approaches to improve the quality of life for individuals with EDS. Written by Imron Shah Related articles: Hypermobility spectrum disorders / Therapy for skin disease REFERENCES Malfait, F., Wenstrup, R.J. and De Paepe, A. (2010). Clinical and genetic aspects of Ehlers-Danlos syndrome, classic type. Genetics in Medicine, 12(10), pp.597–605. doi: https://doi.org/10.1097/gim.0b013e3181eed412 . Miklovic, T. and Sieg, V.C. (2023). Ehlers Danlos Syndrome. [online] PubMed. Available at: https://www.ncbi.nlm.nih.gov/books/NBK549814/ . Sobey, G. (2014). Ehlers–Danlos syndrome – a commonly misunderstood group of conditions. Clinical Medicine, [online] 14(4), pp.432–436. doi: https://doi.org/10.7861/clinmedicine.14-4-432 . Watanabe, A., Wada, T., Tei, K., Hata, R., Fukushima, Y. and Shimada, T. (2005). 618. A Novel Gene Therapy Strategy for Vascular Ehlers-Danlos Syndrome by the Combination with RNAi Mediated Inhibition of a Mutant Allele and Transcriptional Activation of a Normal Allele. Molecular Therapy, [online] 11, p.S240. doi: https://doi.org/10.1016/j.ymthe.2005.07.158 . FURTHER READING The Ehlers-Danlos Society - A global organisation dedicated to supporting individuals with EDS and raising awareness about the condition by providing extensive information on the different types of EDS, updates on research, and resources for patients https://www.ehlers-danlos.com/ PubMed - For those interested in academic research, articles and studies on EDS. https://www.ncbi.nlm.nih.gov/pmc/?term=ehlers-danlos+syndrome Cleveland Clinic – A clinic with an extensive health library providing easy to understand and informative information about the syndrome. https://my.clevelandclinic.org/health/diseases/17813-ehlers-danlos-syndrome Project Gallery

Total solar eclipses Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Totality- Our Perfect Eclipse 14/07/25, 15:05 Last updated: Published: 24/05/23, 10:05 Total solar eclipses We are all familiar with the characteristic depiction of a solar eclipse, when the Moon passes directly between the Sun and the Earth. However, the significance of solar eclipses extends far beyond their aesthetic appeal. Major scientific discoveries, cultural practices, and even the behaviour of wild animals are derived from total solar eclipses that we have the privilege of experiencing (See image 1). A solar eclipse occurs when the Earth, Moon, and Sun all appear to lie on a straight line. They are collinear. Total solar eclipses occur when the Moon completely obscures the Sun's photosphere, enabling prominences and coronal filaments to be seen along the limb. This phenomenon is unique to the Earth, Sun, and Moon system and to understand why we must explore the mathematics underlying these ‘orbital gymnastics’. We wish to compare the ‘apparent’ size of the Sun and Moon, a quantity proportional to the ratio of their size and distance from Earth. The Moon has a radius of around 3,400 km, and is approximately 384,000 km from Earth. The Sun has a much larger radius of 1.4 million km, and is located at a distance of 150 million km. By dividing the Sun's radius by the Moon's radius and dividing the Earth-Sun distance by the Earth-Moon distance, we can determine that the Sun is 400 times larger than the Moon and 400 times further away. This unique relationship allows for total solar eclipses, where totality indicates **the complete blocking of sunlight from the Sun’s disk by the Moon. In partial eclipses, only part of the Sun is obscured. One might wonder why we don’t have total solar eclipses every month, and the reason is that the plane of the Moon’s orbit around Earth is tilted at 5 degrees relative to Earth’s orbital plane. This hugely decreases the likelihood of such perfect alignment. Of the hundreds of moons orbiting planets in our Solar System, only our Moon totally eclipses the Sun. For example, none of Jupiter’s 95 moons have the correct size and orbital separation that completely block out the Sun from any point on Jupiter’s surface! Surely this serendipitous interplay of Earth, Sun, and Moon cannot be a coincidence? (See image 2) It is at this point where divine intervention is typically invoked. There are a few problems with doing this. The Moon's eccentric orbit around Earth means that it will be closer during some total solar eclipses than others, resulting in annular eclipses when the Moon is furthest from Earth. Additionally, the Moon is receding from the Earth at a rate of 4 cm/year, which means that total solar eclipses will only be observable for another 250 million years. (See image 3) For those of you who wish to make the most of this brief window of opportunity, this website shows the dates and locations of upcoming total solar eclipses. Written by Joseph Brennan REFERENCE Guillermo Gonzalez, Wonderful eclipses, Astronomy & Geophysics , Volume 40, Issue 3, June 1999, Pages 3.18–3.20, https://doi.org/10.1093/astrog/40.3.3.18 Project Gallery

And its chemical effects Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Exposing medication to extreme heat 09/07/25, 14:09 Last updated: Published: 08/10/23, 16:18 And its chemical effects Introduction The majority of us look forward to when summer is just around the corner. It is a time for parents to start planning days off to be able to go on holiday with their kids to relax from their studies and enjoy sunsets at the beach. But for people who take medication, whether this just be a week-long course of antibiotics or for long-term conditions, summer may also be a chance for some negligence to occur. Specifically, alongside making sure you have applied SPF to protect your skin from the sun’s rays, you should also protect your medicine as well. This applies to both oral and non-oral drugs. Experts at The Montreal Children’s Hospital say that “many prescription drugs are very sensitive to changes in temperature and humidity”; in this article, we will therefore discuss the effect of extreme heat on drugs from a medicinal chemistry perspective. Factors affecting drug activity due to heat Certain drugs may begin to degrade before their expiry date if not stored appropriately. This affects the efficacy, which is the maximum biological response that is achievable with a certain drug. A dose-response curve can be plotted (see Figure 1 ) to show the relationship between the two variables; the label Emax refers to the efficacy. During hot weather, the structure of the drug can change and therefore unable to bind to its target, causing a lowered and shifted Emax to be seen. Simply put, the medication will not relieve your symptoms as effectively. Another physiochemical property of a drug that can be altered in the heat is the potency. Many people confuse this term with efficacy, but potency refers to the concentration of a drug required to achieve 50% of its maximum therapeutic effect i.e., half the Emax. Potency is therefore also known as EC50, which abbreviates for ‘half maximal effective concentration’. The lower the concentration needed, the more potent your drug is. Like reduced efficacy, the drug’s potency will also decrease in the heat due to altered chemical structure. For drugs like antibiotics, it is crucial to note that if potency is reduced significantly, it could risk infection spreading to other parts of the body as the medication will not fight off bacteria as well as it should. Potentially dangerous! Finally, drug absorption is when a drug moves into the bloodstream after being administered. The chemical structure of the drug and the environment in which it is present hugely affects this; for example, if a lipophilic (‘fat loving’) drug is also present in a lipophilic surrounding, fast absorption is seen as they work well with each other. As you have probably guessed, high temperatures outside of the body can reduce drug absorption due to the above factors mentioned, as the drug is not in its optimal structure to be absorbed effectively. Examples of medicine that are heat sensitive Here is a list of some medicines that require extra care to prevent the above: 1) Nitroglycerin – used to treat chest pains for those with cardiovascular disease. It is especially sensitive to heat or light as it degrades very fast. Dr. Sarah Westberg, a professor at The University of Minnesota College of Pharmacy, says you should follow the storage instructions and replace them regularly. 2) Some antibiotics – research has shown that ampicillin, erythromycin, and furosemide show a reduction in activity in the heat, although this was found after storing them for a year in a car with a temperature exceeding 25 degrees Celsius. Other antibiotics such as cefoxitin are shown to have some “stability in warmer climates”. 3) Levothyroxine – used to treat an underactive thyroid, also known as hypothyroidism. This drug should be stored between 15 to 30 degrees Celsius, although even 30 is quite high so the lower the temperature the better. Interestingly, levothyroxine isn’t heat sensitive itself, it is the fact that the body becomes sensitive to the drug and may make a person feel strange in the heat. 4) Metoprolol succinate – used to treat high blood pressure, also known as hypertension, and heart failure in emergencies . The ideal storage conditions for this drug are 15 to 30 degrees Celsius, like Levothyroxine. Key things to look out for with your medicine in the heat Below are the 2 main things you should be checking for before taking your medicine in the summer: 1) Change in colour – Light can initiate all sorts of reactions, such as oxidation. If, for example, your medicine that is normally white has now changed into a different colour, this suggests that a reaction has taken place within your drug and will not be effective when administered. 2) Change in texture – Similar to change in colour, if a normally solid, oral tablet has become soft then this also suggests that the medication will not be as effective when consumed. How you can prevent your medicine from degrading To make sure you do not contribute to wasting medicine, you should do the following: 1) Check storage information – for any medication that you take, this will let you know how to store them correctly. 2) Travel with care – do not pack prescription drugs into your luggage, as it will almost always become very warm due to the surrounding environment. Instead, carry your medicine with you with the labels still on. 3) Do not leave medicine in any vehicle – everyday vehicles such as cars tend to get warm after a period , which can affect the colour and texture of your medicine. 4) Careful deliveries – for those who have their medicine delivered to them, you can request for your local pharmacy to deliver your medicine in temperature-controlled packages. Summary As discussed, chemicals in the majority of over-the-counter prescription drugs are heat sensitive and should therefore be handled with care, to prevent degradation of the drug. Changes in colour and texture are signs of degradation, which result in loss of efficacy, absorption, and potency. However, many other pharmacological factors interfere, so scientists especially involved in drug synthesis should (or continue to) take great precautions with the manufacturing process. Drugs are costly to make and require a lot of time, so the takeaway is to store them correctly! You should contact your pharmacist if you are still unsure about your prescription(s). Written by Harsimran Kaur Sarai Project Gallery