Rising temperatures can affect brain health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Brain-Climate Connection: The Hidden Impact of Rising Temperatures 08/03/26, 20:01 Last updated: Published: 24/05/23, 10:55 Rising temperatures can affect brain health Global warming is not only disrupting ecosystems, affecting the food we eat and the air we breathe, but it’s also impacting our neurological health. According to the Met Office and ECMWF, 2025 was confirmed as one of the top three warmest years on record globally - following 2024 and 2023- with temperatures ~1.41°C to 1.44°C above the 1850-1900 average. To understand this better, let’s start with the basics. The brain is made up of billions of tiny cells called neurons that communicate with each other by generating electrochemical signals. Think of neurons as small batteries capable of producing electricity when triggered by electrically charged chemicals, called ions. When a neuron is at rest, so when it’s not transmitting an electrical signal, it maintains a negative charge inside compared to the outside. This difference in charge is created by the selective movement of ions across the neuron’s membrane through ion channels and pumps. The resting membrane potential of a neuron is typically around -70 millivolts (mV). When a neuron needs to send information, it generates electrical activity called action potential , which causes the electrical charge to become less negative and closer to zero. To trigger a full-sized action potential, the electrical charge needs to reach a threshold of approximately -55 mV. If the charge reaches this threshold, a full-sized action potential is triggered and the neuron will send a signal down to other neurons. However, if the electrical charge does not reach this threshold, the neuron will not send a signal at all. This is known as the “ALL OR NONE” principle. The action potential is a crucial part of the neuron’s communication process, as it allows the neuron to send signals quickly and efficiently to other neurons. But here’s the catch: temperature fluctuations can affect the ion channels that generate and propagate action potentials, which are critical for the neuron’s communication process. It turns out that an increase in temperature can influence the generation , speed , and duration of action potentials. But that’s not all! Hotter temperatures can trigger seizures in individuals with epilepsy or a history of seizures. One of the most concerning findings from scientific research is that climate change, among other factors, may contribute to an increase in seizure severity and frequency, as well as the development of cerebrovascular and neurodegenerative diseases, such as strokes or dementia . Triggering stress and sleep deprivation, heat waves can also exacerbate the symptoms of such pre-existing disorders. The good news is that we can take action to address the direct impact of climate change on our planet and health. Joining initiatives like Climatematch Academy (CMA) , a 2-week interactive online summer school, can help you learn more about climate science and become part of a global community that is working towards a more sustainable future. CMA is an all-volunteer organization run by dozens of science enthusiasts. It aims at introducing computational methods for climate science taking advantage of available open-source tools and datasets to make science accessible to students worldwide. This is your chance to learn cutting-edge techniques from climate science experts and make a difference in the world, ensuring a brighter future for ourselves and future generations. Written by Viviana Greco Related articles: The environmental impact of EVs / Emperor penguins / Impacts of global warming on NTDs Project Gallery

From the Big Bang to the current model Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Story of the atom 11/02/25, 12:23 Last updated: Published: 20/04/24, 12:16 From the Big Bang to the current model The Greek philosopher and physicist Democritus proposed the idea of an atom at around 440 B.C. The atom is first explained by him using a stone. When a stone is split in half, it becomes two separate stones. There would eventually come to be a portion of the stone that would be too small to be cut if it were to be cut continuously i.e., indivisible. Since then, many scientists have adopted, discarded, or published their own theories about the nature, structure, and size of atoms. However, the most widely accepted, and still the basic model used to study atoms is Rutherford’s model. Rutherford published his theory of the atom suggesting that it had an electron orbiting a positively charged nucleus. This model was created after a series of experiments which included shooting alpha particles at thin gold sheets. Most of the alpha particles flowed through with little disturbance, but a tiny fraction was scattered at extreme angles to their initial direction of motion. Rutherford calculated the estimated size of the gold atom's nucleus and discovered that it was at least 10,000 times smaller than the atom's total size, with a large portion of the atom made up of empty space. This theory paved the way to further the atomic models by various other scientists. (Figure 1) Researchers have discovered unidentified molecules in space which are believed to be the precursor of all chemistry in the universe. The earliest "atoms" in the cosmos were actually nuclei without any electrons. The universe was incredibly hot and dense in the earliest seconds following the Big Bang. The quarks and electrons that make up matter first appeared when the cosmos cooled, and the ideal conditions were met for them to do so. Protons and neutrons were created by quarks aggregating a few millionths of a second later. These protons and neutrons joined to form nuclei in a matter of minutes. (Figure 2) Things started to happen more slowly as the cosmos cooled and expanded. The first atoms were formed 380,000 years ago when electrons were locked into orbits around nuclei. These were mostly hydrogen and helium, which are still the elements that are found in the universe in the greatest quantities. Even now, the most basic nucleus, found in ordinary hydrogen, is only a single, unadorned proton. There were other configurations of protons and neutrons that also developed, but since the number of protons in an atom determines its identity, all these other conglomerations were essentially just variations of hydrogen, helium, and lithium traces. To say that this is an exciting time for astrochemistry is an understatement. Furthermore, the formation mechanism of amino acids and nucleobases is being demonstrated by laboratory simulations of interstellar environments. Now that we are finding answers to these known problems, even more are arising. Hopefully, a more thorough understanding of these chemical processes will enable us to make more precise deductions about the general history of the universe and astrophysics. Written by Navnidhi Sharma REFERENCES CERN (n.d.). The early universe. [online] CERN. Available at: https://home.cern/science/physics/earlyuniverse#:~:text=As%20the%20universe%20continued%20to . Compound Interest (2016). The History of the Atom – Theories and Models | Compound Interest. [online] Compound Interest. Available at: https://www.compoundchem.com/2016/10/13/atomicmodels/ . Fortenberry, R.C. (2020). The First Molecule in the Universe. Scientific American. [online] doi: https://doi.org/10.1038/scientificamerican0220-58 . Sharp, T. (2017). What is an Atom? [online] Live Science. Available at: https://www.livescience.com/37206-atom-definition.html . Project Gallery

Comparative oncology Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What can our canine friends tell us about cancer? 14/07/25, 16:12 Last updated: Published: 02/07/24, 11:04 Comparative oncology Comparative oncology is a field of study within cancer that has been adopted to study cancer and develop new therapies. It involves studying cancer in animals to uncover similarities between human and animal cancers. By combining scientific findings across a range of species, including companion animals such as dogs and horses or non-human primates such as monkeys, comparative oncology will advance cancer research and help develop effective novel therapies. This approach not only explores cancers in both animals and humans but also aims to bridge the gap between human and veterinary medicine. By examining similarities and differences in cancer biology, progression and treatment responses across species, comparative oncology provides valuable insights that can benefit both fields. Understanding how cancer behaves in animals can offer new perspectives and potential therapies for human patients. Conversely, while findings in human oncology can inform veterinary medicine, leading to improved diagnostics and treatments for animals. ( Figure 1 summarises the aims of comparative oncology). This article aims to explore this field of oncology further by discussing what it entails, the methodologies utilised, some recent advancements, and finally, things to look out for in the future. Comparative oncology has been developed and expanded into two areas of study. This includes spontaneous oncology and experimental oncology. Spontaneous oncology focuses on naturally occurring tumours in animals by investigating aspects of carcinogenesis, epidemiology, diagnosis, and treatment. It provides unique insights by drawing comparisons with human oncology research. These results can then be extrapolated to human oncology to gain a better understanding of cancer. This is because the similarities and differences observed in naturally occurring tumours across species provide valuable insights into underlying mechanisms within tumours and treatment responses. Experimental oncology serves as a distinct discipline where there are specialisations such as studying viral, chemical, and radiation oncogenesis alongside studying environmental factors such as pollution residues and food additives. This area involves studying both spontaneous tumours in animals and lab settings, where controlled conditions are used to explore different parts of cancer biology and treatment strategies. Additionally, the primary methodology utilised in comparative oncology involves studying spontaneous tumours in animals. Unlike artificially induced tumours in lab animals, these spontaneous tumours in pets closely mimic the complexity and heterogeneity of human cancers. For example, canines will live in similar living environments and experience similar external stimuli to their owner, such as pollution. The nature of these external stimuli means that they develop cancer in similar ways caused by epigenetic alterations, metabolic, and immune changes. (Figure 2 illustrates this process). Furthermore, comparative oncology uses advanced imaging techniques, genetic analysis, and immunological studies to predict pathways that may be shared among animals and humans which, could drive cancer development. Overall, these methods will allow the identification of promising therapies which directly target cancer and expand on current treatment choices such as chemotherapy and immunotherapy. One of the recent advancements in comparative oncology relates to osteosarcomas. This refers to cancer cells which begin to grow in the bones. For this specific form of cancer, molecular signatures were identified to predict clinical outcomes for both humans and canines, which can help improve treatment outcomes. Led by Amy K. LeBlanc, scientists have identified gene activity patterns in osteosarcoma tumours in nearly 200 dogs, revealing distinct groups with varying prognoses. These findings help us understand the biology behind osteosarcomas further and can potentially help us develop targeted therapies that take advantage of the immune system to treat the disease in both species. This potentially includes a range of therapies including PD-L1 inhibitors and cancer vaccines targeting the immune system. Moreover, breakthroughs in immunotherapies such as checkpoint inhibitors and CAR-T cell therapy are effective in treating haematological malignancies in both humans and canines. Furthermore, studies in canine melanoma reveal similar gene expression changes to human melanoma, such as in the PI3K/AKT/mTOR and MAPK pathways, even when the driver mutations are different. (Figure 3 shows how the pathway contributes to cancer). Useful data was provided in trials using companion animals with spontaneous tumours, providing an insight into safety, dosage, and efficacy, which have paved the way to develop treatments for both species. To conclude, it is clear with comparative oncology, researchers will be able to identify new molecular targets, assess novel drugs, and identify patient populations which will benefit the most from these therapies. It holds great promise in helping streamline cancer diagnosis further and even plays a role in preventing cancer. While the field shows great potential, more studies still need to be conducted to understand the similarities and differences in cancers between animals and humans. Additionally, more collaboration is needed amongst oncologists, veterinarians, and researchers across these disciplines to harness collective expertise to address questions relating to cancer diagnosis, treatment, and prevention. Ultimately, this field will help us identify new avenues of treating and diagnosing cancer whilst improving healthcare outcomes for humans and animals alike. Written by Harene Elayathamby Related articles: Why blue whales don't get cancer / Rare zoonotic diseases REFERENCES Schiffman, J.D. and Breen, M. (2015) ‘Comparative oncology: What dogs and other species can teach us about humans with cancer’, Philosophical Transactions of the Royal Society B: Biological Sciences , 370(1673), p. 20140231. doi:10.1098/rstb.2014.0231. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Al, B. and C., C. (2007) ‘Chapter 1 COMPARATIVE ONCOLOGY ’, in Comparative oncology . Bucharest (RO): The Publishing House of the Romanian Academy, p. 1. Vail, D.M., LeBlanc, A.K. and Jeraj, R. (2020) ‘Advanced cancer imaging applied in the comparative setting’, Frontiers in Oncology , 10. doi:10.3389/fonc.2020.00084. New findings highlight shared features of human and canine osteosarcoma (2023) Center for Cancer Research . Available at: https://ccr.cancer.gov/news/article/new-findings-highlight-shared-features-of-human-and-canine-osteosarcoma (Accessed: 02 March 2024). Mochel, J.P. et al. (2018) Car T-cell immunotherapy in human and veterinary oncology: Changing the odds against hematological malignancies [Preprint]. doi:10.20944/preprints201811.0525.v1. LeBlanc AK, Mazcko CN, Khanna C. (2016) ‘Defining the Value of a Comparative Approach to Cancer Drug Development’, Clinical cancer research : an official journal of the American Association for Cancer Research , 22(9). p. 2133-2138. doi: 10.1158/1078-0432.CCR-15-2347 FIGURE REFERENCES Boddy, A.M., Harrison, T.M. and Abegglen, L.M. (2020) ‘Comparative oncology: New insights into an ancient disease’, iScience , 23(8), p. 101373. doi:10.1016/j.isci.2020.101373. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Rascio, F. et al. (2021) ‘The pathogenic role of PI3K/Akt pathway in cancer onset and drug resistance: An updated review’, Cancers , 13(16), p. 3949. doi:10.3390/cancers13163949. Project Gallery

Arginine, the key to metabolic reprogramming in liver cancer Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Linking arginine and tumour growth: a breakthrough in cancer research Last updated: 20/02/25, 15:29 Published: 27/02/25, 08:00 Arginine, the key to metabolic reprogramming in liver cancer Unpicking the secrets of tumour growth: arginine, the key to metabolic reprogramming in liver cancer. We will look at how unleashing the power of arginine and elevating levels of this amino acid drive metabolic reprogramming and fuel tumour growth. Introduction In recent years, the field of cancer research has made significant progress in unravelling the complexities of this devastating disease. Scientists at the University of Basel have made a groundbreaking discovery regarding the role of the amino acid arginine in promoting tumour growth. Their findings shed light on the mechanisms underlying metabolic reprogramming in cancer cells and present new avenues for improving liver cancer treatment. Elevated levels of arginine: a surprising revelation An intriguing aspect of the study conducted by the researchers is the observation that tumour cells accumulate high levels of arginine despite producing less or none of this amino acid. Through careful analysis of liver tumour samples from both mice and patients, the team discovered that the tumour cells achieve this accumulation by increasing the uptake of arginine and suppressing its consumption. The role of arginine in tumorigenicity Upon further investigation, the scientists at the University of Basel found that high concentrations of arginine bind to a specific factor, triggering metabolic reprogramming in the tumour cells. This reprogramming, in turn, promotes tumour growth by regulating the expression of metabolic genes. The tumour cells revert to an undifferentiated embryonic cell state, enabling them to divide indefinitely. Immune system escape: a beneficial effect for tumour cells Another fascinating discovery made by the researchers is the role of arginine in aiding tumour cells in evading the immune system. Immune cells rely on arginine to function properly. By depleting arginine in the tumour environment, the tumour cells can escape immune surveillance. This finding opens up new possibilities for targeted therapies. Targeting the arginine-binding factor: a novel approach Instead of depleting arginine levels overall, which can have unwanted side effects, the scientists propose targeting the specific arginine-binding factor responsible for promoting metabolic reprogramming. By inducing the degradation of this factor, the researchers were able to prevent metabolic reprogramming in liver tumours. This approach offers a promising alternative to liver cancer treatment. Metabolic changes as biomarkers for early cancer detection Furthermore, the study suggests that metabolic changes, such as increased arginine levels, may serve as biomarkers for the early detection of cancer. Early detection is crucial for successful cancer treatment and patient survival. This finding provides hope for the development of non-invasive diagnostic methods that can detect elevated arginine levels. By measuring arginine levels in patients, these diagnostic methods can potentially identify liver cancer at an early stage. By identifying the elevated levels of arginine in liver tumour cells, these diagnostic methods could potentially use metabolic changes, such as increased arginine levels, as biomarkers for detecting cancer. Therefore, this would be crucial for successful cancer treatment and patient survival, as early detection allows for prompt intervention and improved outcomes. Conclusion The discovery of the role of arginine in driving metabolic reprogramming and promoting tumour growth opens up new avenues for liver cancer treatment. Additionally, the elevated levels of arginine observed in liver cancer patients suggest the potential for using arginine as a biomarker for non-invasive cancer detection. Further research is needed to explore the full potential of arginine as a diagnostic marker and to develop targeted therapies that exploit the metabolic vulnerabilities of cancer cells. With continued advancements in our understanding of cancer metabolism and the role of arginine in tumour growth, further research is needed to explore the full potential of arginine as a diagnostic marker and to develop targeted therapies that exploit the metabolic vulnerabilities of cancer cells. By studying the specific arginine-binding factor and its role in promoting metabolic reprogramming, scientists may be able to develop new treatments that selectively target tumour cells while minimising harm to immune cells that rely on arginine. Additionally, investigating the metabolic changes associated with increased arginine levels may lead to new biomarker designs for early cancer detection, which is crucial for successful treatment and patient survival. Written by Sara Maria Majernikova Related articles: Immune signals and metastasis / Cancer research treatment / Prostatate cancer treatment REFERENCE MOSSMANN, D., MÜLLER, C., PARK, S., RYBACK, B., COLOMBI, M., RITTER, N., WEISSENBERGE, D., DAZERT, E., COTO-LLERENA, M., NUCIFORO, S., BLUKACZ, L., ERCAN, C., JIMENEZ, V., PISCUOGLIO, S., BOSCH, F., TERRACCIANO, L. M., SAUER, U., HEIM, M. H. & HALL, M. N. Arginine reprograms metabolism in liver cancer via RBM39. Cell . DOI: https://doi.org/10.1016/j.cell.2023.09.011 Project Gallery

Code to cure Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How did bioinformatics allow for swift development of the SARS-CoV-2 vaccine? 30/01/25, 12:36 Last updated: Published: 03/09/24, 14:05 Code to cure Traditionally, vaccine development takes years. However, the urgent need for a vaccine to mitigate the effects of this pandemic sped up the process. Bioinformaticians played a crucial role in enabling the swift development of effective SARS-CoV-2 vaccines in many ways. Bioinformatics is the science of performing computational analysis and applying computational tools to capture and interpret biological data. The SARS-CoV-2 virus, with its rapid transmission and mutation rates, quickly became one of the most widespread and economically disruptive pandemics in history. According to Naseer et al. (2022), the global economy has been estimated to lose nearly 9 trillion due to the pandemic by the chief of the International Monetary Fund (IMF). Scientists sequenced the SARS-CoV-2 virus within the first few months of the viral outbreak, and the first SARS-CoV-2 genome sequence was published on GenBank on 10 January 2020. However, a sequence on its own means little, that is until the genes and regulatory elements present in the genome are determined. This was made possible by many bioinformatic tools and pipelines such as: - BLAST (Basic Local Alignment Search Tool): A sequence alignment tool used to find on regions of similarity and infer function and evolutionary relationships. - VADR (Viral Annotation DefineR): An automated annotation tool specifically for viral genomes - Velvet: A de novo sequence assembler i.e. it constructs a longer, full sequence from short read data obtained from next-generation sequencing. The information collected by different labs was shared worldwide, which allowed for a global collaborative effort towards developing a SARS-CoV-2 vaccine. Bioinformaticians also played a role in predicting the 3D structures of the proteins on the surface of the SARS-CoV-2 virus including the spike protein, which is protein against which vaccines build immunity. By using computational tools such as AlphaFold, they could model the structure of the spike protein and identify key sites to target in immunisation strategies. Another method used to identify key sites to target is Epitope Mapping, which is the identification of specific regions on an antigen that are recognised by parts of the immune system such as T Cell Receptors and antibodies. Tools such as IEDB Analysis Resource and BepiPred allow for the identification of epitopes on the SARS-CoV-2 spike that are highly immunogenic, meaning they are able to stimulate a strong immune response, and are therefore ideal targets for vaccines. SARS-CoV-2 is a highly mutagenic virus and one incredibly important bioinformatic platform known as GISAID which has enabled the real-time monitoring of these mutations. This comprehensive and open-access database was key to updating vaccine formulations and maintaining efficacy against emerging variants. In conclusion, although sometimes overlooked, bioinformatics played a crucial factor in fighting SARS-CoV-2 as efficiently and quickly as we did. From genome sequencing to mutation mapping, bioinformaticians have taken arms at every stage of battling the SARS-CoV-2 pandemic. Written by Devanshi Shah Related articles: Origins of COVID / COVID-19 glossary / Correlation between HDI and mortality rate during the pandemic / mRNA vaccines REFERENCES Chatterjee, R., Ghosh, M., Sahoo, S., Padhi, S., Misra, N., Raina, V., Suar, M. & Son, Y.-O. (2021) Next-Generation Bioinformatics Approaches and Resources for Coronavirus Vaccine Discovery and Development—A Perspective Review. Vaccines . 9 (8), 812. doi: 10.3390/vaccines9080812 . Hufsky, F., Lamkiewicz, K., Almeida, A., Aouacheria, A., Arighi, C., et al. (2020) Computational strategies to combat COVID-19: useful tools to accelerate SARS-CoV-2 and coronavirus research. Briefings in Bioinformatics . 22 (2), 642–663. doi: 10.1093/bib/bbaa232 . Ma, L., Li, H., Lan, J., Hao, X., Liu, H., Wang, X. & Huang, Y. (2021) Comprehensive analyses of bioinformatics applications in the fight against COVID-19 pandemic. Computational Biology and Chemistry . 95, 107599. doi: 10.1016/j.compbiolchem.2021.107599 . Torrington, E. (2022) Bioinformaticians: the Hidden Heroes of the COVID-19 Pandemic. BioTechniques . 72 (5), 171–174. doi: 10.2144/btn-2022-0039 . PYMOL: Schrödinger, LLC. (2024). PyMOL Molecular Graphics System (Version 2.5.4) [Software]. Available at: https://pymol.org/2/ [Accessed 3 Jul. 2024]. RCSB PDB 7T3M: Protein Data Bank. (2024). PDB ID: 7T3M, [online] Available at: https://www.rcsb.org/structure/7T3M [Accessed 3 Jul. 2024]. Project Gallery

The slippery property of a superfluid is caused by its ability to flow very easily Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The incredibly slippery nature of superfluids 03/04/25, 11:33 Last updated: Published: 24/05/23, 09:53 The slippery property of a superfluid is caused by its ability to flow very easily Slipperiness is a property that we often associate with everyday objects like ice, soap, and banana peels. However, there is a substance that is even more slippery than these: superfluids. A normal liquid becomes a superfluid when it is cooled down below a certain temperature. This temperature is unique to all fluids, for example for helium it is 2.17 K. Below this temperature, the superfluid will behave in completely unique ways. For example, if a container of water at room temperature was spun, you’d expect the water to also spin around, creating a whirlpool. Whereas a superfluid in a spinning container doesn’t spin at all, until it reaches a certain speed! The slippery property of a superfluid is caused by its ability to flow very easily. Usually it’s safe to leave a glass of water on a countertop (unless of course you’ve got a particularly excitable dog), but if you were to leave a glass of superfluid on a table, the liquid would creep out and escape. The tiny changes in temperature or pressure in the container cause it to flow, seemingly defying gravity. Unfortunately, superfluids cannot just be bought in the local supermarket! To produce a superfluid, devices known as cryostats can be used to cool a substance down to low temperatures. Using the ideal gas model, pressure, and volume can be related, so by reducing the pressure, the temperature of the device can also be decreased. The pressure is reduced using a vacuum pump, which works by removing particles from the cryostat. The applications of superfluids are limited as, due to the typically very low temperatures needed for a normal fluid to transition to a superfluid, there is difficulty in producing superfluids. Currently, scientists are working on finding fluids that enter a stable superfluid state at room temperatures. However, superfluids are used within many fields of physics to explain certain phenomena. One theory is that the core of collapsed large stars (neutron stars) is a superfluid, despite the very hot temperatures. The idea is that below a certain temperature, it uses less energy for the core to behave like a superfluid which cools the star down at an increased rate. The superfluid theory of neutron stars is just a hypothesis, however hints at the role superfluids play in all areas of physics. Written by Madeleine Hales REFERENCES/ FURTHER READING: https://www.aps.org/publications/apsnews/200601/history.cfm#:~:text=In%201927%20Willem%20Keesom%20and,helium%20I%20and%20helium%20II . https://physicsworld.com/a/neutron-star-has-superfluid-core/ Project Gallery

The same condition after all? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorder 26/04/26, 15:06 Last updated: Published: 20/01/24, 11:38 The same condition after all? Practice and progress in rheumatology The relationship between hypermobile Ehlers-Danlos Syndrome (hEDS) and Hypermobility Spectrum Disorder (HSD) has been hotly debated in recent years, with research being published on a near-constant basis attempting to establish a valid symptomatological or causalogical difference between the two disorders. Now, a paper by Ritelli et al. (2022) threatens to end the savage cycle for all. Using RNA sequencing techniques and immunofluorescence, Ritelli et al. found identical gene expression and cellular characteristics in dermal biopsies from those with both conditions. Through immunofluorescence of biopsies from 20 women with hEDS, 16 women and 4 men with HSD and 40 controls, it was found that the shape and components of the extracellular matrix were greatly different in those with HSD/hEDS in comparison to those in the healthy control group. Abnormalities were discovered in the expression of cadherin-11, snail1, and αvβ3, α5β1 and α2β1 integrins. Integrins mediate the connections between the cell cytoskeleton and extracellular matrix to ensure they stay together, cell-to-cell adhesion is initiated by cadherin-11, and snail1 is localised close to the cyclin-dependent kinase inhibitor 2B (CDKN2B) gene. Snail1 can activate CDKN2B gene products when Snail1 is overexpressed to the point of reaching the general localisation of the CDKN2B domain. This demonstrates that there may be a similar causative link between the widespread inflammation and chronic pain in HSD/hEDS and rheumatoid arthritis. Li et al. (2021) proved that the polarisation of macrophages (white blood cells which destroy foreign products) was carefully controlled by the CDKN2B-AS1/ MIR497/TXNIP axis- the increased activation of which in rheumatoid arthritis catalyses the excessive polarisation of macrophages, which causes the macrophages to attack healthy cells. In rat studies published by Tan et al. (2022), it was found that rats with diabetes and induced sepsis experienced greater intestinal injury that control rats without any medical pathology who experienced induced sepsis. This was demonstrated to be due to interruptions in the miR-3061/Snail1 communication pathway. Research on this phenomenon in humans may elucidate the relevance of snail1 overproduction in hEDS/HSD sufferers to their complex gastrointestinal symptoms. If this pathway works similarly in human models of sepsis or localised GI infection, it may intimate that snail1 overproduction is responsible for the hyperpolarisation of macrophages in response to foreign product detection, which may cause immunological damage in the intestines. However, the relevance of this study to hEDS/HSD should be considered questionable until further human research into this avenue has been completed. The result of this research is that academia can potentially derive a genetic cause of the complex phenotypes demonstrated by sufferers of hEDS/HSD. This can be achieved by visualising the human genome, and testing genes like those above, or those implicated in modulating the activity of the genes above. Given this, the 2025 symposium discussed whether HSD and hEDS should be considered separate at all, with discussions around potentially reclassifying or merging them in the future, to improve access to care to patients. Written by Aimee Wilson Related articles: Ehlers-Danlos syndrome / Types of movement Project Gallery

Uncovering the truth behind the origins of the virus Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Origins of COVID-19 03/05/26, 18:31 Last updated: Published: 08/10/23, 17:07 Uncovering the truth behind the origins of the virus The quest for the crime of the century begins now! Suspicion of the Wuhan Institute of Virology Since the early epidemic reports in Wuhan, the origin of COVID-19 has been a matter of contention. Was SARS-CoV-2 the outcome of spontaneous transmission from animals to humans, or scientific experimentation? Although most of the recorded initial cases occurred near a seafood market, Western Intelligence Agencies knew that the Wuhan Institute of Virology (WIV) was situated nine miles to the south. Researchers at the biosafety centre combed Yunnan caves for bats harbouring SARS-like viruses. They have been extracting genetic material from their saliva, urine, and faeces. Additionally, bat coronavirus RaTG13 (BatCoV RaTG13) shared 96% of its genome with SARS-CoV-2. Suspicion increased when it was discovered that WIV researchers dealt with chimeric versions of SARS-like viruses capable of infecting human cells. However, similar "gain-of-function" studies in Western biosecurity institutions have shown that such slow virulence increases may occur naturally. The coincidence that the pandemic began in the same city as the WIV outbreak was too obvious to ignore. According to two Chinese specialists , "the likelihood of bats flying to the market was quite remote". Chan and Ridley's "Quest for the Origin of COVID-19" Chan and Ridley have created a viral whodunit titled "Quest for the origin of COVID-19" to excite the curiosity of armchair detectives and scientific sceptics. Both need clarification as to why a virus of unknown origin was detected in Wuhan and not in Yunnan, 900 kilometres to the south. The stakes could not be more significant; if the virus were deliberately developed and spread by a Chinese laboratory, it would be the crime of the century. They are prudent in not going that far. They are, however, within their rights to cast doubt on the findings since their concerns were shared by numerous coronavirus experts who openly discounted the possibility of a non-natural origin and declared that the virus displayed no evidence of design at the time. Is this the impartial and fair probe the world has been waiting for? They present no evidence for the development of SARS-CoV-2. For example, Chan asserts that it seemed pre-adapted to human transmission " to an extent comparable to the late SARS-CoV-2 outbreak ". This statement is based on a single spike protein mutation that appears to "substantially enhance" its potential to connect to human receptor cells, meaning it had "apparently stabilised genetically" when identified in Wuhan. Nonetheless, this is a staggeringly misleading statement. As seen by the alphabet soup of mutations, the coronavirus has undergone multiple alterations that have consistently increased its suitability. Additionally, viruses isolated from pangolins attach to human receptor cells more efficiently than SARS-CoV-2, indicating the possibility of additional adaptation. According to two virologists, although the SARS-CoV-2 virus was not wholly adapted to humans, it was "merely enough". Evidence for design of SARS-CoV-2 and possible natural origins of the virus Another concerning feature of SARS-CoV-2 is a furin cleavage site, which enables it to infect human cells by interfering with the receptor protein. The identical sequence is present in highly pathogenic influenza viruses and was previously utilised to modify the spike protein of COVID-19. Chan and Ridley explain that this is the kind of insertion that would occur in a laboratory-modified bat virus. As a result, 21 leading experts have concluded that the furin sequence is insufficient. Coronaviruses have been shown to possess " near identical " genomes that often can infect humans and animals. Because the furin cleavage site characteristic is not seen in known bat coronaviruses, it is possible that it evolved naturally. Surprisingly, Chan and Ridley do not suggest that the SARS virus's high human infectivity feature was inserted on purpose since "there is no way to determine". There is also no way to determine if a RaTG13 is the pandemic virus's progenitor since history is replete with pandemics that began with zoonotic jumps. This argument is based on the strange fact that WIV researchers retrieved the bat isolate in 2013 from a decommissioned mine shaft in Yunnan. Six people were removing bat guano from the cave that year when they suffered an unexplained respiratory ailment. As a consequence, half of them perished. The 4% genetic diversity between RaTG13 and SARS-CoV-2, on the other hand, is similar to 40 years of evolutionary change. While exploring caves in northern Laos, researchers discovered three more closely related bat coronaviruses, which have a higher affinity to attach to human cells than the early SARS-CoV-2 strains. This indicates an organic origin, either through another animal host or directly from a bat, maybe when a farmer went into a cave. This is arguably the most reasonable explanation since it is consistent with forensic and epidemiological data. The food sample isolates collected from the Wuhan seafood market are similar to human isolates, and the majority of original human cases had a history of market exposure, in contrast to the absence of an epidemiological connection to the WIV or any other Wuhan research institution. Lack of evidence for a laboratory origin If scientists could demonstrate prior infection at the Wuhan market or other Chinese wildlife markets that sell the most likely intermediary species, including pangolins, civet cats, and raccoon dogs, the case for a natural origin would be strengthened. Although multiple animals tested positive for sister human viruses during the SARS epidemic, scientists have yet to find evidence of earlier infections in animals in the instance of Sars-CoV-2. Nonetheless, the absence of evidence does not confirm the absence and may indicate that samples were not taken from the appropriate animal. The same may be said of the lab leak argument's lack of evidence. However, even though history is littered with pandemics, no significant pandemic has ever been traced back to a laboratory. In other words, the null hypothesis is a zoonotic occurrence; Chan and Ridley must demonstrate otherwise. The irony is their drive to construct a compelling case for a laboratory accident. They are oblivious to the much more pressing story of how the commerce in wild animals, global warming, and habitat degradation increase the likelihood of pandemic viral development. This is the most plausible origin story that should concern us. Summary and future direction Although Chan and Ridley's "Quest for the Origin of COVID-19" has cast suspicion on the Wuhan Institute of Virology, there is still insufficient evidence to support the lab leak theory. There is, however, growing evidence for a natural origin of SARS-CoV-2, with multiple animals testing positive for sister human viruses during the SARS epidemic and the discovery of more closely related bat coronaviruses in northern Laos. A World Health Organization advisory group in 2025 has concluded its independent assessment of how the COVID pandemic started . As mentioned, most of the peer-reviewed scientific evidence supports the hypothesis that SARS-CoV-2 has a zoonotic origin. "But," the group say, "until requests for additional information are met or more data become available, there can be no certainty about when, where and how SARS-CoV-2 entered the human population. There is a continued need for a thorough, unbiased investigation". As such, we should be more concerned with the increasing likelihood of pandemic viral development due to the commerce in wild animals, global warming, and habitat degradation. Written by Sara Maria Majernikova Project Gallery

Looking at p53 mutations and cancer predisposition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Decoding p53: the guardian against cancer 09/07/25, 15:03 Last updated: Published: 23/11/23, 11:38 Looking at p53 mutations and cancer predisposition Being a tumour suppressor protein, p53 encoded by the TP53 gene plays a critical role in regulating cell division and preventing the formation of tumours. Its function in maintaining genome stability is vital in inhibiting cancer development. Understanding p53 Located on chromosome locus 17p13.1, TP53 encodes the p53 transcription factor 1. Consisting of three domains, p53 can directly initiate or suppress the expression of 3661 different genes involved in cell cycle control and DNA repair 2. With this control, p53 can influence cell division on a massive scale. Cancer is characterised by uncontrolled cell division, which can occur due to accumulated mutations in either proto-oncogenes or tumour suppressor genes. Wild-type p53 can repair mutations in oncogenes such that they will not affect cell division. However, if p53 itself is mutated, then its ability to repair DNA and control the cell cycle is inhibited, leading to the emergence of cancer. Mutations in TP53 are actually the most prevalent genetic alterations found in patients with cancer. The mechanisms by which mutated p53 leads to cancer are manifold. One such mechanism is p53’s interaction with p21. Encoded by CDKN1A , p21 is activated by p53 and prevents cell cycle progression by inhibiting the activity of cyclin-dependent kinases (CDKs). Therefore, we can see that a non-functional p53 would lead directly to uncontrolled cell division and cancer. Clinical significance The importance of p53 in preventing cancer is highlighted by the fact that individuals with inherited TP53 mutations (a condition known as Li-Fraumeni syndrome or LFS) have a significantly greater risk of developing any cancer. These individuals inherit one defective TP53 allele from one parent, making them highly susceptible to losing the remaining functional TP53 allele, ultimately leading to cancer. Loss of p53 also endows cells with the ability to ignore pro-apoptotic signals such that if a cell becomes cancerous, it is far less likely to undergo programmed cell death 3. Its interactions with the apoptosis-inducing proteins Bax and Bak, are lost when mutated, thus leading to cellular apoptosis resistance. The R337H mutation in TP53 is an example of the founder effect at work. The founder effect refers to the loss of genetic variation when a large population descends from a smaller population of fewer individuals. The descendants of the initial population are much more likely to harbour genetic variations that are less common in the species as a whole. In southern Brazil, the R337H mutation in p53 is present at an unusually high frequency 4 and is thought to have been introduced by European settlers several hundred years ago. It is responsible for a widespread incidence of early-onset breast cancers, LFS, and paediatric adrenocortical tumours. Interestingly, individuals with this mutation can trace their lineage back to the group of European settlers that set foot in Brazil hundreds of years ago. Studying p53 has enabled us to unveil its intricate web of interactions with other proteins and molecules within the cell and unlock the secrets of cancer development and potential therapeutic strategies. By restoring or mimicking the functions of p53, we may be able to provide cancer patients with some relief from this life-changing condition. Written by Malintha Hewa Batage Related articles: Zinc finger proteins / Anti-freeze proteins Project Gallery

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