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Through AI Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Revolutionising sustainable agriculture 11/07/25, 09:51 Last updated: Published: 27/06/23, 15:34 Through AI Artificial Intelligence (AI) is taking the world by storm. Recent developments now allow scientists to integrate AI into sustainable farming. Through transforming the way we grow crops, manage resources and pests, and most importantly- protect the environment. There are many applications for AI in agriculture. Outlined below are some of the areas in which the incorporation of AI systems improves sustainability: Precision farming Artificial intelligence systems help improve the overall quality and accuracy of harvesting – known as precision farming. Artificial intelligence technology helps detect plant diseases, pests, and malnutrition on farms. AI sensors can detect and target weeds, then decide what herbicide to use in an area. This helps reduce the use of herbicides and lower costs. Many tech companies have developed robots that use computer vision and AI to monitor and precisely spray weeds. These robots can eliminate 80% of the chemicals normally sprayed on crops and reduce herbicide costs by 90%. These intelligent AI sprayers can drastically reduce the amount of chemicals used in the field, improving product quality, and lowering costs. Vertical farming Vertical farming is a technique in which plants are grown vertically by being stacked on top of each other (usually indoors) as opposed to the ‘traditional way’ of growing plants and crops on big strips of land. This approach offers several benefits for sustainable agriculture and waste reduction. The use of AI brings even more significant advancements making vertical farming more sustainable and efficient- Intelligent Climate Control: AI can use algorithms to measure and monitor temperature, humidity, and lighting conditions to optimise climate control in vertical farms. Thus, reducing energy consumption and improving resource efficiency. Creating an enhanced climate-controlled environment also allows for repeatable and programmable crop production. Predictive Plant Modelling: the difference between a profitable year and a failed harvest can just be the specific time the seeds were sowed. By using AI, farmers can use predictive analysis tools to determine the exact date suitable for sowing seeds for maximum yield and reduce waste from overproduction. Automated Nutrient Monitoring: to optimise plant nutrition, AI systems monitor and adjust nutrient levels in hydroponic (plants immersed in nutrient containing water) and aeroponic setups (plants growing outside the soil, with nutrients being provided by spraying the roots). Genetic engineering AI plays a pivotal role in genetic engineering, enhancing the sustainability and precision of crop modification through- Targeted Gene Editing: AI algorithms help in gene editing to produce desirable traits in crops, such as resistance to disease or improved nutritional content. This allows genetic modification without the need to conduct extensive field trials. Thus, saving time and resources. Computational Modelling: by combining AI modelling with gene prediction, farmers will be able to predict which combinations of genes have the potential to increase crop yield. Pest management and disease detection Artificial intelligence solutions such as smart pest detection systems are being used to monitor crops for signs of pests and diseases. These systems detect changes in the environment such as temperature, humidity, and soil nutrients, then alert farmers when something is wrong. This allows farmers to act quickly and effectively, taking preventive measures before pests cause significant damage. Another way to achieve this is by using computer vision and image processing techniques. AI can detect signs of pest infestation, nutrient deficiencies and other issues that can affect yields. This data can help farmers make informed decisions about how to protect their crops. By incorporating AI into these aspects of sustainable agriculture, farmers can achieve high yields, reduce waste and enable more sustainable farming practices, reducing environmental impacts while ensuring efficient food production. Written by Aleksandra Zurowska Related articles: Digital innovation in rural farming / Plant diseases and nanoparticles 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

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

Book review Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link 'The Emperor of All Maladies' by Siddhartha Mukherjee 08/01/26, 18:58 Last updated: Published: 28/11/24, 14:55 Book review Stretching nearly 4,000 years of history, Pulitzer Prize winner Siddhartha Mukherjee sets on a journey to document the biography of cancer in The Emperor of All Maladies. Drawing from a vast array of books, studies, interviews, and case studies, Mukherjee crafts a narrative that is as comprehensive as it is compelling. Driven by curiosity and a desire to understand the origins of cancer, Mukherjee sets the tone by reflecting on his experiences as an oncology trainee, drawing insightful parallels to contemporary perspectives on the fight against this relentless disease. Mukherjee also pays homage to Ancient Egyptian and Greek physicians for their early observations on cancer, from the work on Imhotep to Claudius Galen. He then introduces Sidney Farber, whose monumental contributions to modern chemotherapy are brought to life through Mukherjee's exceptional storytelling—tracing Farber's journey from his initial observations to his unprecedented success in treating children with leukaemia. As you progress through each chapter of this six-part book, your appreciation deepens for how far cancer treatments have advanced - and how much further they can go. Mukherjee’s unparalleled skill as a science communicator shines through, seamlessly weaving together groundbreaking scientific discoveries with the historical contexts in which they emerged contributing to an immersive reading experience. Siddhartha Mukherjee, The Emperor of All Maladies : In 2005, a man diagnosed with multiple myeloma asked me if he would be alive to watch his daughter graduate from high school in a few months. In 2009, bound to a wheelchair, he watched his daughter graduate from college. The wheelchair had nothing to do with his cancer. The man had fallen down while coaching his youngest son's baseball team. Mukherjee also makes an effort to highlight the critical role of raising awareness in shaping public health outcomes. ‘Jimmy’ was a cancer patient that represented children with cancer, his real name was Einar Gustafson, but his individual story was able to galvanise large-scale support. As the face of the ‘Jimmy Fund’, he was able to assist in raising $231,485.51 for the Dana-Farber Institute subsequently becoming the official charity for the Boston Red Sox. Mukherjee underscores how storytelling can serve as a catalyst for change, not just in raising money, but also in enacting larger societal and governmental shifts. In 1971, President Richard Nixon signed the National Cancer Act, the first of its kind where federal funding went directly into advancing cancer research. What struck me most was how Mukherjee connects this historical event to the broader need for advocacy, as science doesn’t just happen in the lab. It is a collective effort, driven by awareness, to push funding and influence policy. The ability to link individual stories to broader missions, as Mukherjee illustrates, continues to be one of the most effective strategies in keeping cancer research in the public eye. Mukherjee delves into the pivotal role of genetics in cancer research, tracing its evolution from the discovery of DNA's structure by Francis Crick, James Watson, and Rosalind Franklin to Robert Weinberg's ground-breaking work on how proto-oncogenes and tumour suppressors drive cancer progression. These discoveries ushered in a new era in cancer drug development. Mukherjee also emphasises the importance of collaboration and the rise of the internet, which gave birth to The Cancer Genome Atlas, a landmark program, that unites various research disciplines to diagnose, treat, and prevent cancer. In concluding the book, Mukherjee looks ahead to the future of cancer treatment, seamlessly connecting this discussion to his second book, The Gene . This book takes readers on a remarkable journey through the history of cancer, from the earliest recorded cases to groundbreaking discoveries in genetics. It weaves together compelling personal stories as well as pivotal moments in governmental policy. The storytelling is rich and immersive, drawing you in with its detail and depth. By the time you finish, you'll find yourself returning to its pages, eager to revisit the knowledge and insights it offers. Written by Saharla Wasarme Related book reviews: Intern Blues / The Molecule Project Gallery

The rabies virus infects neurons Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Rabies- the scariest disease ever? 10/07/25, 10:31 Last updated: Published: 10/10/24, 11:05 The rabies virus infects neurons Rabies is a viral disease that primarily affects the central nervous system (CNS), usually in mammals. Wild animals such as foxes, dogs, and raccoons are frequent carriers of the virus. Transmission occurs through the saliva of an infected animal through a bite or a scratch, allowing the virus to enter the body and travel through the nervous system toward the brain. While rabies can be prevented with a vaccine, once symptoms begin to show, the disease is nearly always fatal once symptoms begin to show. What makes this virus so deadly, and how can it take control of the human body with just five genes in its genome? Why is the virus so hard to kill? To arrive at a sensible answer, we must first understand the ‘tropism’ of the virus – the cell type it likes to infect. Rabies virus infects the neurones (neurotropic), which creates a massive problem for the immune system. Macrophages and neutrophils, which are the prominent cells in killing foreign pathogens that kill foreign pathogens, usually deal collateral damage to the body’s own cells to some extent. This must be avoided with neurones, as neurones cannot replenish themselves after cell death. An inflammation of the nerve cells could lead to paralysis and seizures, compromising the CNS. As a result, the immune system response is significantly lowered around nerve cells to prevent accidental damage, which allows the virus to infect the neural pathway easily. Transmission of the virus See Figure 1 The strategy of the immune system is that the neurones can be protected if the pathogens are intercepted before they travel to their destination. However, this strategy ultimately fails when it comes to rabies, because the transmission is through a bite, which can penetrate and cut through many layers of tissue, providing a direct access to nerve cells. If you were bitten on the leg, then the time it takes for the rabies virus to travel to your brain would be the time it takes for you to travel from Florida, USA to Sweden. This may seem like a long time, but the rabies virus has evolved a technique that is able to hijack the cellular transport system can trick your cells’ transport system to travel quickly through the nerves by binding to a protein called dynein . Dynein is a motor protein that move along the microtubules in cells, converting the chemical energy of ATP into mechanical work. Microtubules are polarized structures, with a plus end (typically towards the axon terminal in neurones) and a minus end (towards the cell body). Dynein moves toward the minus end, facilitating retrograde transport, meaning it moves materials from the periphery of the cell, such as the axon terminals, back toward the cell body. Dynein is transports chemicals inside cells via endocytosis and plays a vital role in the movement of eukaryotic flagella. Rabies has evolved to stick to dynein via the Glycoprotein (G) present on its viral envelope, which allows rabies to travel to the brain much quicker. Dynein may be small, weighing around two megadaltons (3 x 10-18 grams), but it can move at a speed of 800 nanometres per second. At this speed, it takes rabies around 14 days to move up a metre- long neuron. This implies that the closer the animal bites you to the brain, the less time it takes for the symptoms to appear. If you’re bitten on the foot, it could take months for the virus to reach your brain. But if you’re bitten on the neck or face, the virus can get to your brain in just a few days, making it much more dangerous. This explains the broad range in the incubation time which is between 20 to 90 days. Infection and replication- see Figure 2 As the rabies travels through neuronal tracks, it sets up points of concentrated viral production centres called Negri bodies. These replicate the rabies virus within the neurones and inhibit interferon action, which are chemicals that alert white blood cells to the area of infection. Interferon inhibition along with lowered immune response to neurones make rabies extremely effective. However, neurones can undergo apoptosis—controlled cell death—to limit the spread of the virus and allow macrophages to clear the debris. Research in mice suggests that some strains of rabies may prevent this apoptotic response in cells. Additionally, studies indicate that rabies promotes apoptosis in killer T cells, which are responsible for inducing apoptosis in other cells. This mechanism helps to shield nerve cells from immune system attacks. Symptoms Patients with rabies initially experience flu-like symptoms and muscle pain. Once these early symptoms appear, treatment is virtually impossible. As the disease progresses, neurological symptoms develop including hydrophobia due to painful throat spasms when swallowing liquids. About 10 days after these neurological symptoms start, patients enter a coma, often accompanied by prolonged sleep apnoea. As virus attacks the brain throughout this stage, patients develop the urge to bite other organisms to transmit the virus. The virus can reach the salivary glands, allowing for transmission through a bite to occur again. Most patients typically die within three days of reaching this coma stage. Legends Rabies may have influenced the development of vampire and zombie myths due to its distinct symptoms. The disease causes aggression and sensitivity to light, which could have inspired some characteristics of vampires, such as their aversion to light and erratic movements. Additionally, rabies leads to excessive salivation and a tendency to bite, traits that align with vampire lore. Similarly, the delirium and motor dysfunction seen in rabies may have contributed to the depiction of zombies as shuffling, incoherent beings. Conclusion Rabies is a uniquely deadly virus due to its mechanism of hijacking the nervous system. After entering the body, the virus binds to dynein, using it to travel along neuronal pathways toward the brain. It replicates rapidly, forming Negri bodies disrupting neurone function. The virus effectively suppresses immune responses, making it nearly impossible to treat once symptoms appear, leading to almost 100% fatality. Beyond its biological impact, rabies has influenced cultural stories like those of vampires and zombies, with its symptoms—such as aggression, fear of water, and neurological decay—providing eerie parallels to these myths. Despite modern medical advances, rabies remains one of the most feared infectious diseases due to its fatal nature. Written by Baraytuk Aydin Related articles: Rare zoonotic diseases / rAAV gene therapy REFERENCES CUSABIO (2020) Rabies virus overview: Structure, transmission, pathogenesis, symptoms, etc, CUSABIO. Available at: https://www.cusabio.com/infectious-diseases/rabies-virus.html (Accessed: 12 September 2024). Hendricks, A.G. et al. (2012) Dynein tethers and stabilizes dynamic microtubule plus ends, Current biology : CB. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3347920/ (Accessed: 13 September 2024). Lahaye, X. et al. (2009) Functional Characterization of Negri Bodies (NBS) in rabies virus-infected cells: Evidence that NBS are sites of viral transcription and replication, Journal of virology. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715764/ (Accessed: 13 September 2024). Tarantola, A. (2017) Four thousand years of concepts relating to rabies in animals and humans, its prevention and its cure , MDPI . Available at: https://www.mdpi.com/2414-6366/2/2/5 (Accessed: 15 September 2024). Project Gallery

Can CRISPR/Cas9 overcome the challenges posed by current HIV treatments? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A potential treatment for HIV 08/07/25, 16:16 Last updated: Published: 21/07/23, 09:50 Can CRISPR/Cas9 overcome the challenges posed by current HIV treatments? The human immunodeficiency virus (HIV) was recorded to affect 38.4 million people globally at the end of 2021. This virus attacks the immune system, incapacitating CD4 cells: white blood cells (WBCs) which play a vital role in activating the innate immune system and fighting infection. The normal range of CD4 cells in our body is from 500 to 1500 cells/mm3 of blood; HIV can rapidly deplete the CD4 count to dangerous levels, damaging the immune system and leaving the body highly susceptible to infections. Whilst antiretroviral therapy (ART) can help manage the virus by interfering with viral replication and helping the body manage the viral load, it fails to eliminate the virus altogether. The reason for this is due to the presence of latent viral reservoirs where HIV can lay dormant and reignite infection if ART is stopped. Whilst a cure has not yet been discovered, a promising avenue being explored in the hopes of eradicating HIV has been CRISPR/Cas9 technology. This highly precise gene-editing tool has been shown to have the ability to induce mutations at specific points in the HIV proviral DNA. Guide RNAs pinpoint the desired genome location and Cas9 nuclease enzymes act as molecular scissors that remove selected segments of DNA.  Therefore, CRISPR/Cas9 technology provides access to the viral genetic material integrated into the genome of infected cells, allowing researchers to cleave HIV genes from infected cells, clearing latent viral reservoirs. Furthermore, the CRISPR/Cas9 gene-editing tool can also prevent HIV from attacking the CD4 cells in the first place. HIV binds to the chemokine receptor, CCR5, expressed on CD4 cells, in order to enter the WBC. CRISPR/Cas9 can cleave the genes for the CCR5 receptor and therefore preventing the virus from entering and replicating inside CD4 cells. CRISPR/Cas9 technology provides a solution that current antiretroviral therapies cannot solve. Through gene-editing, researchers can dispel the lasting reservoirs unreachable by ART that HIV is able to establish in our bodies. However, further research and clinical trials are still required to fully understand the safety and efficacy of this approach to treating HIV before it can be implemented as a standard treatment. Written by Bisma Butt Related articles: Antiretroviral therapy / mRNA vaccines Project Gallery

Investigating the outbreak in Devon, UK in May 2024 Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Cryptosporidium: bridging local outbreaks to global health disparities 20/03/25, 12:06 Last updated: Published: 01/09/24, 12:50 Investigating the outbreak in Devon, UK in May 2024 In early May, news emerged of numerous Devon (UK) residents experiencing vomiting and diarrhoea. Majorly affecting the Brixham region, over 40 people were diagnosed with cryptosporidiosis, and over 16,000 homes were advised to boil water before consuming it to kill potential pathogens ( Figure 1 ). Despite a controversial handling of the situation from South West Water (SWW) (from initial denial of the ‘crisis’, to major profit increases for the company), the outbreak was eventually linked to a broken pipe from where animal faeces could have entered, contaminating the water supply, a SWW representative suggested. In this article, we will investigate the disease and its relevance worldwide. So, what is Cryptosporidiosis? Cryptosporidiosis is commonly associated with gastrointestinal symptoms, such as vomiting, diarrhoea and severe abdominal cramps. It is caused by cryptosporidium, from the Apicocomplexa family. This microorganism is an intra-cellular gut parasite which invades the microvilli in the gut and depletes host nutrients. The parasite is spread via faecal-oral transmission, and it is commonly found in contaminated water, food and animals. Its life cycle starts with oocyst (egg) ingestion, leading to attachment to host gut epithelia, and asexual reproduction. This allows sexual reproduction to ensue, and oocyst formation. Eventually, the oocysts are released via faeces, for the cycle of infection to continue. Cryptosporidium species are often identified by the immune system via Toll-Like Receptors, specifically TLR-4, in the gut epithelia; Cryptosporidium-derived molecules are treated as TLR-4 ligands, since the microbe does not produce LPS molecules. Adaptive immune signalling pathways, such as NF-kB, are triggered, encouraging IL-8, CXCL1 and other chemokine secretion from the gut ( Figure 2 ). Consequently, gut inflammation is increased, as well as levels of Intracellular Adhesion Molecule-1 (ICAM-1), to aid immunocyte recruitment and improve pathogenic clearance. Other mechanisms the epithelial barrier uses to eliminate cryptosporidium infection include NO secretion and mucin production, to kill the pathogen, and prevent further infection by blocking extracellular oocyst binding, respectively. In some individuals, cryptosporidium can evade immune response due to its intracellular nature. Most immunocompetent patients suffer mild symptoms and so are offered symptomatic treatment, but some immunocompromised patients (those with HIV, for example) can develop chronic diarrhoea as a result of cryptosporidium infection. In this instance, managing fluid loss and rest is often insufficient; these patients are prescribed nitazoxanide, a broad-spectrum antiparasitic, to manage their diarrhoea. Cryptosporidiosis on a global scale Although controversial, the management of the cryptosporidium ‘crisis’ in Devon was resolved relatively quickly compared to outbreaks in other countries ( Figure 3 ). There are clear links between socio-economic dynamics and water-borne illness prevalence. In some developing regions, such as areas in the Middle East and North Africa (MENA), cryptosporidiosis is considered endemic, due to poor quality water-sanitation centres, rapid population growth and inadequate potable water supply. Globally, 3.4 million people die each year from water-borne illnesses - and poor sanitation ranks higher in causes of human morbidity than war and terrorism. Additionally, in 2015, cryptosporidium was the fourth leading cause of death amongst children under 5, clearly highlighting the danger this parasite can cause. For children in developing countries, who are already predisposed to starvation, cryptosporidiosis can kick-start a malnutrition cycle. Here, cryptosporidium exacerbates host malnutrition due to its parasitic nature, potentially causing cognitive impairment and growth stunting. Cryptosporidiosis, although typically mild, can be devastating for some people (the immunocompromised and young children). Particularly, those who are malnourished can suffer severe effects. The water contamination in Devon (UK), handled by SWW, was unfortunate and many in the region experienced severe illness. Globally, cryptosporidiosis is a major problem and in some regions, it is considered endemic. Thus, it is important we spread awareness of the devastating effects of this disease, continue efforts to prevent transmission and strive for eradication. Written by Eloise Nelson REFERENCES Abuseir, S. (2023) ‘A systematic review of frequency and geographic distribution of water-borne parasites in the Middle East and North Africa’, Eastern Mediterranean Health Journal , 29(2), pp. 151–161. doi:10.26719/emhj.23.016. Chalmers, R.M., Davies, A.P. and Tyler, K. (2019) ‘Cryptosporidium’, Microbiology , 165(5), pp. 500–502. doi:10.1099/mic.0.000764. Hassan, E.M. et al. (2020) ‘A review of cryptosporidium spp. and their detection in water’, Water Science and Technology , 83(1), pp. 1–25. doi:10.2166/wst.2020.515. News, S. (2024) ‘Brixham: More than 50 people in Devon ill from contaminated water - as South West Water’s owner posts £166m profit’, Sky News , 21 May. Available at: https://news.sky.com/story/brixham-more-than-50-people-in-devon-ill-from-contaminated-water-as-south-west-waters-owner-posts-166m-profit-13140820#:~:text=More%20than%2050%20cases%20of,water%2C%20health%20bosses%20have%20said . Sparks, H. et al. (2015) ‘Treatment of cryptosporidium: What we know, gaps, and the way forward’, Current Tropical Medicine Reports , 2(3), pp. 181–187. doi:10.1007/s40475-015-0056-9. Caccio SM. Cryptosporidium : parasite and disease, Immunology of Cryptosporidiosis. Springer Verlag Gmbh; 2016. Project Gallery

Observations suggest that aspects of their design were purposeful for other reasons Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The astronomical symbolism of the Giza Pyramids Last updated: 09/10/25, 10:03 Published: 06/03/25, 08:00 Observations suggest that aspects of their design were purposeful for other reasons This is Article 2 in a series about astro-archaeology. Next article: The celestial blueprint of time: Stonehenge, UK . Previous article: Cities designed to track the heavens: Chaco Canyon, New Mexico The Giza Pyramids of the ancient Egyptian civilisation may be most well known as one of the Seven Wonders of the Ancient World, but they also harbour astronomical secrets. The three Great Pyramids (Khafre, Khufu, and Menkaure) are incredible feats of engineering, with heights measuring 146.6 meters, 143.5 meters, and 64.5 meters, respectively. No documentation has been found explaining the planning or construction processes behind the creation of these magnificent structures, yet observations suggest that aspects of their design were purposeful for reasons other than simply erecting the pyramid. Example 1: The square bases of the pyramids are very carefully oriented to the cardinal points with the Khufu Pyramid aligning within 4 arc minutes of the north-south line. For context, if you were to hold your index finger up, it would cover a portion of the sky that measures about 10 degrees across. 1 arc minute is a unit of measurement equal to 1/60 of 1 degree, which means that the orientation of the Khufu Pyramid only deviates from the north-south line by less than 4/60-degree error. Today, we would calculate this using a GPS or other technical equipment, but what did the ancient Egyptians use? Well, astronomy! While the exact method of calculation is not known, researchers believe that the ancient engineers aligned the pyramids to the constellation Orion and the star Sirius as they are circumpolar stars, never rising nor setting, and are therefore visible every night as a useful guide. This may also have religious implications relating to immortality, perhaps adding to the desire to align the Pharoah’s tombs with such a symbolic constellation. Example 2: The south-eastern corners of the three Giza Pyramids all point toward the nearby great solar temple of Heliopolis, which was a major religious centre of the sun god Atum-Ra. According to the Pyramid Texts, Heliopolis was the location that the god-creator Atum emerged from chaos and begun creation. These texts suggest that the ancient Egyptians believed that the Pharaohs join Atum-Ra in the afterlife, and they together cross the sky in Atum-Ra’s sun boat as part of the rebirth process. Upon investigation, the three pyramids seem to be aligned with various solar events as well as the city of the sun god: the setting sun is aligned with the northern side of the Khafre pyramid and the southern side of the Khufu pyramid during the equinoxes the causeways point to the setting sun behind the pyramid twice per year, which are distanced the same number of days from the winter/summer solstices each of the two causeways point towards sunset in two separate locations that are halfway between the equinoxes and solstices, respectively (not according to the calendar year, but according to the astronomical year) on the summer solstice, the sun sets directly between the two great pyramids when viewing from the Sphinx area of the pyramidal complex Example 3: the position of three Great Pyramids with respect to each other mimics the position of the stars in the constellation Orion’s belt with respect to each other. Astronomical calculations show that the orientation and position of the Khufu, Khafre, and Menkaure pyramids align together in exactly the same way that the Alnitak, Alnilam, and Mintaka stars align in Orion’s belt. Of course, there is a small percentage of error, but it is because of naked eye observations instead of mathematical miscalculations. While there are still many secrets hidden in and around the Great Pyramids of ancient Egypt, they can continue to provide insight into how ancient peoples interconnected architecture, astronomy/mathematics, and religious beliefs within their societies. Written by Amber Elinsky REFERENCES Magli, G. (2009). Archaeoastronomy at Giza: the ancient Egyptians’ mathematical astronomy in action. In: Emmer, M., Quarteroni, A. (eds) Mathknow. MS&A, vol 3. Springer, Milano. https://doi.org/10.1007/978-88-470-1122-9_10 . Orofino, V. and P. Bernardini. Archaeoastronomical Study of the Main Pyramids of Giza, Egypt: Possible Correlations with the Stars?. Archaeological Discovery: 1 (2016), vol 3. https://www.scirp.org/journal/paperinformation?paperid=61389 . Verner, Miroslav, 'Heliopolis: The City of the Sun', in Anna Bryson-Gustová (ed.), Temple of the World: Sanctuaries, Cults, and Mysteries of Ancient Egypt (Cairo, 2013; online edn, Cairo Scholarship Online, 18 Sept. 2014), https://doi.org/10.5743/cairo/9789774165634.003.0002 . https://pyramidtextsonline.com/translation.html Project Gallery

The Design Argument vs science Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Anthropic Principle: Science or God? 20/11/25, 15:34 Last updated: Published: 08/11/24, 11:25 The Design Argument vs science One of the most common points of tension between science and religion is the Design Argument – an argument for the existence of an intelligent designer/creator of the universe or God. Individuals who tend to identify with one of the Abrahamic religions (Christianity, Judaism, and Islam) often also believe in a God who created the universe, although it is important to note that not every person agrees here. On the other hand, public opinion often says that scientists do not support the Design Argument because they are studying how the universe was ‘actually’ created, which leads to some tension between the two groups. However, there is some logical support for the Design Argument originating from scientific data: the Anthropic Principle, also known as the Observation-Selection Hypothesis. While there are different takes on the hypothesis, this article will briefly cover how it relates to physics and the Design Argument. In general, the Anthropic Principle states that the parameters of the universe are exactly what they are so that life (intelligent, conscious life) would ultimately be produced. The following are examples of factors that happen to be just right for life to be possible: The electromagnetic force is 39 times stronger than gravity, but if they were more evenly matched, stars would not survive long enough for life to develop on an orbiting planet. If gravity were 1 part in 1040 stronger, the universe would have utterly collapsed long ago. If the combined mass of a proton and electron were slightly more than the mass of a neutron (rather than slightly less as it currently is), then the hydrogen atom would become unstable, which would collapse stars like the Sun. If the mass of neutrinos (the most abundant particles with mass in the universe) was 5 x 10-34 kg instead of 5 x 10-35 kg, the universe would be contracting rather than expanding. There are many more examples, but isn’t it strange how absolutely exact the strengths of these kinds of fundamental forces are? This is the line of reasoning that leads to the Design Argument. How could the universe be so incredibly exact to produce life, unless it was specifically created that way? Such questions are asked by Science and Religion scholars, and while there are no answers yet, it opens the conversation up to explore what information different fields have to offer. Written by Amber Elinsky Related article: Creatio ex Nihilo REFERENCES Davis, John Jefferson. “The Design Argument, Cosmic ‘Fine Tuning,’ and the Anthropic Principle.” International Journal for Philosophy of Religion 22, no. 3 (1987): 139–50. http://www.jstor.org/stable/40018832 . Gale, George. “The Anthropic Principle.” Scientific American 245, no. 6 (1981): 154–71. http://www.jstor.org/stable/24964627 . Project Gallery

Manufacturing doubt is another strategy where facts are intentionally changed to promote an agenda. It is used in the tobacco industry and against the climate crisis. Meaning articles can maintain the façade of using scientific methods by referencing sources that are difficult to interpret whilst research supported by sound evidence is labelled and downplayed. Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How fake science websites hijack our trust in experts to misinform and confuse Last updated: 07/11/24 Published: 29/12/22 In science, all research is peer-reviewed by experts. Now, fake science websites are mimicking these disciplines. These websites capitalise on our trust in experts. In some cases, these websites are paid to publish fake science. This is becoming more common. In a recent global survey, almost 50% of respondents said they see false or misleading information online daily. By understanding the methods these sites use we can prevent their influence. Hyperlinking is a technique used to convince website users. They reassure the user that the content is credible, but most people don’t have experience in analytical techniques and so these links aren’t questioned. Repetition is used to increase the visibility of fake science content but also saturate search engines. This content can be repeated and spread across different sites. Users of “lateral reading” get multiple websites that corroborate the fake science from the initial source. Many of these sites only choose articles that agree with their perspective and depend on the audience not taking time to follow up. Manufacturing doubt is another strategy where facts are intentionally changed to promote an agenda. It is used in the tobacco industry and against the climate crisis. Meaning articles can maintain the façade of using scientific methods by referencing sources that are difficult to interpret whilst research supported by sound evidence is labelled and downplayed. On fake science websites first, check the hyperlinked articles. These websites will use sites with repeated content from disreputable sites. Next, look at the number of reposts a website has. Legitimate science posts are on credible websites. Some websites investigate websites that feature fake science. Ultimately, these websites thrive on users not having the time or skills to look deeper into the evidence, so doing so will help expose the fake websites. Written by Antonio Rodrigues Related articles: Digital disinformation / COVID-19 misconceptions