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The prevalence of diverticulosis is increasing in developed countries Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Understanding diverticular disease 14/07/25, 15:08 Last updated: Published: 27/11/24, 11:31 The prevalence of diverticulosis is increasing in developed countries Diverticulosis, diverticula, diverticulum, and diverticulitis - they may sound similar, but each term describes a specific aspect of diverticular disease. Before diving into diverticular disease, let’s clarify these key terms: Diverticulum: a small, bulging pouch that forms in a weak spot in the lining of the large intestine. Diverticula: the plural form of a diverticulum, indicating multiple bulging pouches in the large intestine's lining. Diverticulosis: a condition where multiple diverticula are present in the large intestine. Diverticulitis: this occurs when one or more diverticula become inflamed or infected. What is diverticular disease? Diverticular disease can be broadly categorised into two main conditions: diverticulosis and diverticulitis. Both involve the presence of diverticula in the colon, but the key difference lies in inflammation. In diverticulitis, the diverticula become inflamed or infected, leading to symptoms. On the other hand, diverticulosis is typically asymptomatic. However, there is a third condition, referred to as symptomatic uncomplicated diverticular disease (SUDD), where diverticula are present without inflammation, but the patient still experiences symptoms. The prevalence of diverticulosis is increasing in developed countries, largely due to the typical 'Western diet', which is high in red meat and low in fibre. Additionally, lifestyle factors such as obesity, smoking, and physical inactivity contribute to this rise. Age is also a significant factor, with 85% of diverticulosis cases occurring in individuals over the age of 50. Pathophysiology The formation of diverticula in the colon is primarily due to three factors: structural abnormalities in the colonic wall, disordered intestinal motility, and a deficiency of dietary fibre. The large intestine has two layers of muscle that work together to move its contents: an inner circular layer and an outer longitudinal layer. The outer layer consists of three bands called the taeniae coli, which run longitudinally along the colon. The gaps between these muscle bands are areas of weakness, making them vulnerable to the development of diverticula. Age-related weakening of the connective tissue further increases the risk of developing diverticula in these vulnerable areas. In some patients, abnormal gut motility can lead to areas of high pressure in the bowel, causing the mucosa to bulge outward, forming diverticula. Similarly, a lack of fibre in the diet can increase bowel pressure and lead to irregular movement, which also promotes outpouching. As we've discussed, some patients with diverticula may remain asymptomatic, while others experience varying levels of discomfort. The transition from diverticulosis to diverticulitis occurs when undigested food or a fecalith becomes trapped in these pouches, causing a blockage. This leads to bacterial growth and multiplication, resulting in infection and inflammation of the pouch. Symptoms Diverticular disease comes with a range of symptoms, some of which are quite common and could be easily mistaken for other conditions. General symptoms like nausea, vomiting, diarrhoea, and fever often overlap with other digestive problems, making diagnosis tricky. However, certain symptoms can hint more strongly at diverticular disease. For instance, experiencing pain in the lower left side of the abdomen (known as the left iliac fossa) or noticing rectal bleeding are more specific indicators that may point towards this condition. Recognising these symptoms can help in getting a more accurate diagnosis and appropriate treatment. Management Managing diverticular disease depends on the individual patient and the severity of their symptoms. For some, simple, conservative treatments are enough—this might include staying hydrated, eating a high-fibre diet, and giving the bowel a short rest by temporarily avoiding food. However, if a patient is experiencing significant pain or signs of infection, medical treatment is necessary. This may involve pain relief based on the WHO pain ladder or antibiotics to tackle the infection. In more serious cases, where other treatments haven’t worked or the patient is in a life-threatening situation, surgery might be required. A common procedure for these severe cases is the Hartmann’s procedure. This surgery removes the damaged section of the large intestine, usually due to infection or blockage. The healthy end of the intestine is brought out through an opening in the abdomen, creating a temporary colostomy that allows waste to leave the body through a bag. This setup gives the intestine time to heal, and in some cases, a follow-up surgery can reconnect it for normal function. Complications There are both short-term and long-term complications associated with diverticulitis, particularly in more severe cases that require more aggressive treatment such as surgery (see Figure 4 ). Future directions Recent changes in the management of diverticulitis have shifted how clinicians approach treatment. One significant update involves the use of antibiotics. Traditionally, diverticulitis was treated with routine antibiotic prescriptions. However, newer guidelines suggest that antibiotics may not be necessary for uncomplicated cases, helping to reduce both antibiotic resistance and the potential medication side effects for patients. Another emerging trend is treating uncomplicated diverticulitis on an outpatient basis. This allows patients to be managed at home with pain relief and dietary adjustments, which in turn frees up hospital resources for those with more severe conditions. Additionally, the management of complicated diverticulitis has evolved. For instance, abscesses may now be treated with percutaneous drainage rather than resorting to emergency surgery. Conclusion In summary, diverticular disease can vary widely in its symptoms and required treatments, ranging from dietary changes to surgical interventions for severe cases. Identifying specific signs and understanding the treatment options can empower patients and help them make informed choices. Advances in treatment approaches are also helping to improve outcomes and quality of life for those affected. Written by Abbasali Gulamhussein Related articles: Crohn's disease / The gut microbiome / Interplay of hormones and microbiome REFERENCES Cater, M. (2023). Foods for Diverticulosis and Diverticulitis . [online] www.hopkinsmedicine.org . Available at: https://www.hopkinsmedicine.org/health/wellness-and-prevention/foods-for-diverticulosis-and-diverticulitis . Matrana, M.R. and Margolin, D.A. (2009a) Epidemiology and pathophysiology of diverticular disease , Clinics in colon and rectal surgery . Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC2780269/ (Accessed: 12 October 2024). Miller, A.S. et al. (2021) The Association of Coloproctology of Great Britain and Ireland consensus guidelines in emergency colorectal surgery , Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland . Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC9291558/ (Accessed: 12 October 2024). NHS (2019). Diverticular disease and diverticulitis . [online] NHS. Available at: https://www.nhs.uk/conditions/diverticular-disease-and-diverticulitis/ . Sciencedirect.com . (2019). Hartmann Procedure - an overview | ScienceDirect Topics . [online] Available at: https://www.sciencedirect.com/topics/medicine-and-dentistry/hartmann-procedure . Singh, B., May, K., Coltart, I., Moore, N. and Cunningham, C. (2008). The Long-Term Results of Percutaneous Drainage of Diverticular Abscess. The Annals of The Royal College of Surgeons of England , [online] 90(4), pp.297–301. doi: https://doi.org/10.1308/003588408x285928 . Ubhi, L. (2023). Prescribing Analgesia and the WHO Analgesic Ladder | Geeky Medics . [online] geekymedics.com . Available at: https://geekymedics.com/prescribing-analgesia-and-the-who-analgesic-ladder/ . Project Gallery

Getting treatment can prevent things from getting worse Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Depression in Children 10/07/25, 10:17 Last updated: Published: 17/06/23, 12:46 Getting treatment can prevent things from getting worse It's normal for kids to feel sad, act grouchy, or be in a bad mood at times. But when a sad or bad mood lasts for weeks or longer, and when there are other changes in a child's behavior, it might be depression. Therapy can help children who are going through sadness or depression. And there are things parents can do, too. Getting the right care can prevent things from getting worse and help a child feel better. Symptoms of depression Sad or bad mood. A child may seem sad, lonely, unhappy, or grouchy. It can last weeks or months. A child may cry more easily. They may have more tantrums than before. Being self-critical. Kids going through depression may complain a lot. They may say self-critical things like, "I can't do anything right." "I don't have any friends." "I can't do this." "It's too hard for me." Lack of energy and effort. Depression can drain a child's energy. They might put less effort into school than before. Even doing little tasks can feel like too much effort. Kids may seem tired, give up easily, or not try. Not enjoying things. Kids don't have as much fun with friends or enjoy playing like before. They may not feel like doing things they used to enjoy. Sleep and eating changes. Kids may not sleep well or seem tired even if they get enough sleep. Some may not feel like eating. Others may overeat. Aches and pains. Some children may have stomach aches or other pains. Some miss school days because of not feeling well, even though they aren't sick. Causes of depression Some common reasons include: - life events like someone dying - moving schools or other big changes - physical health problems - experiencing physical, sexual or psychological abuse or neglect - witnessing violence or a traumatic event - if you have an unstable family environment Intervention Three of the more common methods used in depression treatment include: - cognitive behavioral therapy - interpersonal therapy - psychodynamic therapy Written by Chhaya Dhedi Related articles: Childhood stunting in developing nations / What does depression do to your brain? / Brain of a bully / Anxiety / Postpartum depression in adolescent mothers Project Gallery

Pathology and emerging therapeutics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Bone cancer 25/03/26, 16:48 Last updated: Published: 12/10/23, 10:38 Pathology and emerging therapeutics Introduction: what is bone cancer? Primary bone cancer can originate in any b one. However, most cases develop in the long bones of the legs or upper arms. Each year, more than 500 new cases are diagnosed in the United Kingdom (with a projected downward trend). Primary bone cancer is distinct from secondary bone cancer, which occurs when cancer spreads to the bones from another region of the body. The focus of this article is on primary bone cancer. There are several types of bone cancer: osteosarcoma, Ewing sarcoma, and chondrosarcoma. Osteosarcoma originates in the osteoblasts that form bone. It is most common in children and teens, with the majority of cases occurring between the ages of 10 and 30. Ewing (pronounced as YOO-ing) sarcoma develops in bones or the soft tissues around the bones. Like osteosarcoma, this cancer type is more common in children and teenagers. Chondrosarcoma occurs in the chondrocytes that form the cartilage. Chondrosarcoma is most common in adults between the ages of 30 and 70 and is rare in the under-21 age group. Causes of bone cancer include genetic factors such as inherited mutations and syndromes, and environmental factors such as previous radiation exposure. Treatment will often depend on the type of bone cancer, as the specific pathogenesis of each case is unknown. What is the standard treatment for bone cancer? Most patients are treated with a combination of surgical excision, chemotherapy, and radiation therapy. Surgical excision is employed to remove the cancerous bone. Typically, it is possible to repair or replace the bone, although amputation is sometimes required. Chemotherapy involves using powerful chemicals to kill rapidly growing cells in the body. It is widely used for osteosarcoma and Ewing sarcoma but less commonly used for chondrosarcomas. Radiation therapy (also termed radiotherapy) uses high doses of radiation to damage the DNA of cancer cells, leading to the killing of cancer cells or slowed growth. Six out of every ten individuals with bone cancer will survive for at least five years after their diagnosis, and many of these will be completely cured. However, these treatments have limitations in terms of effectiveness and side effects. The limitation of surgical excision is the inability to eradicate microscopic cancer cells around the edges of the tumour. Additionally, the patient must be able to withstand the surgery and anaesthesia. Chemotherapy can harm the bone marrow, which produces new blood cells, leading to low blood cell counts and an increased risk of infection due to a shortage of white blood cells. Moreover, radiation therapy uses high doses of radiation, resulting in the damage of nearby healthy tissues such as nerves and blood vessels. Taken together, this underscores the need for a therapeutic approach that is non-invasive, bone cancer-specific, and with limited side effects. miR-140 and tRF-GlyTCC Dr Darrell Green and colleagues investigated the role of small RNAs (sRNAs) in bone cancer and its progression. Through the analysis of patient chondrosarcoma samples, the researchers identified two sRNA candidates associated with overall patient survival: miR-140 and tRF-GlyTCC. MiR-140 was suggested to inhibit RUNX2, a gene upregulated in high-grade tumours. Simultaneously, tRF-GlyTCC was demonstrated to inhibit RUNX2 expression by displacing YBX1, a multifunctional protein with various roles in cellular processes. Interestingly, the researchers found that tRF-GlyTCC was attenuated during chondrosarcoma progression, indicating its potential involvement in disease advancement. Furthermore, since RUNX2 has been shown to drive bone cancer progression, the identified miR-140 and tRF-GlyTCC present themselves as promising therapeutic targets. CADD522 Dr Darrell Green and colleagues subsequently investigated the impact of a novel therapeutic agent, CADD522, designed to target RUNX2. In vitro experiments have revealed that CADD522 reduced proliferation in chondrosarcoma and osteosarcoma. However, a bimodal effect was observed in Ewing sarcoma, indicating that lower levels of CADD522 promoted sarcoma proliferation, whereas higher levels of the same drug suppressed proliferation. In mouse models treated with CADD522, there was a significant reduction in cancer volumes observed in both osteosarcoma and Ewing sarcoma. Take-home message The results described here contribute to understanding the molecular mechanisms involved in bone cancer. They highlight the anti-proliferative and anti-tumoral effects of CADD522 in treating osteosarcoma and Ewing sarcoma. Further research is necessary to fully elucidate the specific molecular mechanism of CADD522 in bone cancer and to identify potential side effects. Written by Favour Felix-Ilemhenbhio Related articles: Secondary bone cancer / Importance of calcium / Novel neuroblastoma driver for therapeutics Project Gallery

The future of targeted cancer therapeutics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Bioorthogonal Chemistry 04/02/25, 15:42 Last updated: Published: 01/09/24, 10:47 The future of targeted cancer therapeutics ‘Bioorthogonal chemistry’ is a term coined in 2003 by American Chemist & 2022 Nobel Prize Laureate Carolyn Bertozzi. It encompasses a set of chemical reactions which can occur within biological environments, whilst exerting minimal effect on native biomolecules or interference with native biochemical processes of the host organism - these reactions exist ‘orthogonal’ (perpendicular) to biology. Key functional groups in Bioorthogonal Chemistry include the alkynes (carbon-carbon triple bonds) and the azides (⁻N=N⁺=N⁻) . The azides are particularly bioorthogonal due to their minute size (which is favourable for cell permeability and avoiding ‘perturbations’ - the alteration of a function of a biological system), metabolic stability, and how, as they don’t naturally exist in cells, they have no competing biological side reactions. Past & present uses of bioorthogonal chemistry include: ● Vehicle airbags: Modern vehicle airbags contain sodium azide (NaN₃), a shock sensitive, explosive compound. When a vehicle’s crash sensor is triggered, an electrical charge is administered which starts the chemical reaction, inflating the air bag with harmless nitrogen gas (2NaN₃ → 2Na + 3N₂). This reaction can occur in as quickly as 0.03 seconds! ● Early HIV treatment: Azidothymidine - AZT - (Fig. 1) was the first drug used to treat HIV infection. For viruses to replicate, they use an enzyme called reverse transcriptase to convert their single-stranded RNA genome to double-stranded DNA in a process termed reverse transcription. When this antiretroviral medicine is used, instead of the virus transcribing thymidine, it instead transcribes the AZT, which contains an azide Group, thus stalling DNA synthesis of HIV and producing less viruses. Another key feature to consider when discussing uses of Bioorthogonal Chemistry are Click Reactions. Click Reactions occur exclusively between the azides (⁻N=N⁺=N⁻) and alkynes (carbon-carbon triple bond), produce no by-products and therefore have a 100% atom economy. Bioorthogonal ‘Click’ Chemistry has enabled complex chemical reactions to be carried out within living organisms: the reactions do not bring harm to, interfere with or disrupt the biological processes occurring within these systems as they cannot be recognised & used by these systems. ‘Click’ Chemistry is therefore vital in understanding how we may be able to develop Targeted Cancer Therapeutics using Bioorthogonal Chemistry. Modern day cancer treatments tend to be delivered intravenously using anthracyclines (notably doxorubicin), a class of antitumour antibiotics used for cancer chemotherapy: they stop the growth of cancerous cells by preventing their enzymatic machinery from engaging in DNA duplication & cell division, causing the cells to die. The long-standing side effect of using such effective drugs is the high likelihood of ‘off-target toxicity’, where non-cancerous cells can also be harmed by the intercalating effects of the anthracyclines. Frequent targets for this ‘off-target toxicity’ tend to be fast growing body cells, like hair & nails, hence why most cancer patients experience some form of hair loss over the course of their chemotherapy treatment. So, scientists began to consider: what if there was a way to develop targeted cancer treatments? Treatments that enabled the activation of these powerful cancer drugs - anthracyclines - at the tumour sites, mitigating the harm of ‘off-target toxicity’? This is where Bioorthogonal ‘Click’ Chemistry comes in. ‘ C lick- A ctivated P rotodrugs A gainst C ancer’ (or ‘ CAPAC ’) is a platform developed by American Biotechnology Company Shasqi. Through ‘CAPAC’, Shasqi are pioneering the use of Bioorthogonal ‘Click’ Chemistry to target cancer drugs directly to the tumour site, minimising side effects and potentially improving the therapeutic index. They’ve achieved this through exploiting one of the fastest click reactions: a Diels-Alder cycloaddition between a tetrazine (C2H2N4) and a trans-cyclooctene (TCO) - 2 bioorthogonal molecules. The treatment involves two key components: a tetrazine-modified sodium hyaluronate biopolymer & doxorubicin that is connected to a TCO (trans-cyclooctene) unit. Over the course of the treatment (Fig. 2) , the patient will undergo multiple stages: ● Local hydrogel injection: The tetrazine-modified sodium hyaluron ate biopolymer is injected into a patient’s tumour ● Protodrug dose: The patient then receives five daily infusions of doxorubicin-TCO ● Concentration: The drug circulates through the body until it meets the tetrazine-modified biopolymer at the tumour site ● Activation: At the point of meeting, the click reaction brings the tetrazine and TCO together, triggering a rearrangement that frees the doxorubicin right next to the tumour cells Compared to prior cancer treatments, this process would not only mitigate the harm of the drug’s ‘off-target toxicity’, limiting the side-effects of the chemotherapy drug, it would also increase the local concentration of doxorubicin far beyond what would normally be possible in a patient, having a greater effect in preventing the growth of cancer cells. In the treatment of this life-threatening disease, Shasqi’s research into the ‘CAPAC’ platform, though still ongoing, looks excitingly promising: as recently as March 2023, they’ve proven their platform’s efficacy in humans. During a Phase 1 dose-escalation clinical trial in adult patients with advanced solid tumours, Shasqi were able to demonstrate the activation of their tetrazine-modified sodium hyaluronate biopolymer & doxorubicin-TCO at tumour sites, evidencing it’s safety, systemic pharmacokinetics, and immunological activity. With the continuation of their innovative research, the future treatment of cancer can be significantly aided with the use of Bioorthogonal ‘Click’ Chemistry. Written by Emmanuella Fernandez REFERENCES Acs.org . (2021). Click chemistry sees first use in humans . [online] Available at: https://cen.acs.org/pharmaceuticals/Click-chemistry-sees-first-use/98/web/2020/10 . Cancer Research UK (2023). Doxorubicin (Adriamycin) | Cancer drugs | Cancer Research UK . [online] www.cancerresearchuk.org . Available at: https://www.cancerresearchuk.org/about-cancer/treatment/drugs/doxorubicin . Wang, Y., Zhang, C., Wu, H. and Feng, P. (2020). Activation and Delivery of Tetrazine-Responsive Bioorthogonal Prodrugs. Molecules , 25(23), p.5640. doi: https://doi.org/10.3390/molecules25235640 . Wikipedia Contributors (2019). Reverse transcriptase . [online] Wikipedia. Available at: https://en.wikipedia.org/wiki/Reverse_transcriptase . Wikipedia. (2020). Zidovudine . [online] Available at: https://en.wikipedia.org/wiki/Zidovudine . Wikipedia. (2022). Bioorthogonal chemistry . [online] Available at: https://en.wikipedia.org/wiki/Bioorthogonal_chemistry . Project Gallery

Contributions include artificial radioactive atoms, atomic structure, ribosome research Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Female Nobel Prize Winners in Chemistry 04/04/26, 16:02 Last updated: Published: 03/06/23, 17:37 Contributions include artificial radioactive atoms, atomic structure, ribosome research Women contributing their innovative ideas has strengthened the knowledge held in the scientific world. It is important to realise that women in STEM need to be celebrated all year round – they need to be given the recognition they deserve. A total of 60 women have been awarded the Nobel Prize between 1901 and 2022. Specifically looking at the Female Nobel Prize winners in Chemistry – all of whom have changed the way society views women but also puts a spotlight on the progress that can still be made if we have more women in the field of STEM. There have been eight women to receive this prestigious award: Carolyn R. Bertozzi, Emmanuelle Charpentier, Jennifer A. Doudna, Frances H. Arnold, Ada E., Dorothy Crowfoot Hodgkin, Yonath, Irène Joliot-Curie and Marie Curie. This article celebrates their ground-breaking discoveries and contributions to the world of science and is a way to serve as an inspiration to young girls and women in the hope to raise a generation where more women are studying STEM subjects and acquiring high-ranked roles to reduce the gender gap. Nobel Prizes won in- 2022: Carolyn R. Bertozzi was awarded for her development of biorthogonal reactions which has allowed scientists to explore and track biological processes without disrupting the chemistry of the original cells (click chemistry and biorthogonal chemistry). 2020: Emmanuelle Charpentier and Jennifer Doudna were awarded for their development of a method for high-precision genome editing: CRISPR/Cas9 genetic scissors. They used the immune system of a bacterium, which disables viruses by cutting their DNA up with a type of genetic scissors. The CRISPR/Cas9 genetic scissors has led to many exciting discoveries and new ways to fight against cancer and genetic diseases. 2018: Frances Arnold was awarded because of her work on directed evolution of enzymes. In 1993, Arnold conducted the first directed evolution of enzymes, which are proteins that catalyse chemical reactions. This has led to the manufacturing of environmentally friendly chemical substances such as pharmaceuticals, and the production of renewable fuels. 2009: Ada Yonath was awarded the Nobel Prize for her studies on the structure and functions of the ribosome. In the 1970s, Ada began a project that concluded in her successful mapping of the structure of ribosomes, which consisted of thousands of atoms, using x-ray crystallography. This has been important in the production of antibiotics. 1964: Dorothy Hodgkin was awarded the 1964 Nobel Prize in Chemistry for solving the atomic structure of molecules such as penicillin and insulin, using X-ray crystallography. 1935: Irène Joliot-Curie was awarded for her discovery that radioactive atoms could be created artificially. Written by Khushleen Kaur Related articles: Female Nobel prize winners in physics / African-American women in cancer research Project Gallery

Its toxicodynamics, and balancing benefits and risks Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Exploring Ibuprofen 05/03/26, 15:06 Last updated: Published: 17/01/24, 01:28 Its toxicodynamics, and balancing benefits and risks What is Ibuprofen? Ibuprofen is a standard over-the-counter medicine which can be bought from supermarkets and pharmacies. It is primarily used for pain relief, such as back pain, period pain, toothaches, etc. It can also be used for arthritis pain and inflammation. It is available in various forms, including tablets, capsules, gels, and sprays for the skin. The Toxicodynamics of Ibuprofen Toxicodynamics refers to the biological effects of a substance after exposure to it. Scientists look at the mechanisms by which the substance produces toxic effects and the target organs or tissues it affects. Ibuprofen works by stopping the enzymes that synthesise prostaglandins, which are a group of lipid molecules that cause inflammation, including symptoms like redness, heat, swelling and pain. Therefore, after the action of Ibuprofen, inflammatory responses and pain are reduced. Ibuprofen targets organs and tissues, including the gastrointestinal tract, the kidneys, the central nervous system, blood and more. Balancing the Benefits and Risks Ibuprofen’s method of action means it is a safe and effective pain relief medication for most people. It is also easily accessible and easy to use. However, it is able to affect the target organs and tissues negatively and, therefore, can have serious side effects, especially if taken for an extended period of time and/or in high doses. They include heartburn, abdominal pain, kidney damage (especially for people who already have kidney problems), low blood count and more. Therefore, it is important to use Ibuprofen responsibly. This can be done by understanding and being well-informed about its effects on the body, particularly its impact on organs and tissues. With caution and proper use, the side effects can be minimised. One of the easiest ways to lessen side effects is by taking the medication with food. Additionally, patients should take the lowest effective dose for the shortest possible time. If patients have a history of stomach problems, avoiding Ibuprofen and using alternatives is the best solution. Patients can also talk to their GP if they are concerned about the side effects and report any suspected side effects using the Yellow Card safety scheme on the NHS website. Written by Naoshin Haque Related articles: Synthesis of ibuprofen / Anthrax toxin / The Pain Gate Theory Project Gallery

Conservation efforts Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link An end at the beginning: the tale of the Galápagos Tortoises 25/03/26, 16:39 Last updated: Published: 06/06/24, 11:20 Conservation efforts The Galápagos Islands Most who know of the name “Darwin” will be familiar with the Galápagos. These relatively uninviting islands protrude harsh, crashing waves like spears of mountainous rock, formed through millions of years of fierce volcanic activity. Even Charles Darwin himself thought life could not be sustained in such a remote and harsh environment, writing in his 1835 Journal of Researches: A broken field of basaltic lava, thrown into the most rugged waves, and crossed by great fissures, is everywhere covered by stunted, sun-burnt brushwood, which shows little signs of life. Little did the 22-year-old university graduate know at the time, these rugged islands would spark the most pivotal and influential theory in the field of modern biology. Due to the Hawaiian archipelago’s unique volcanic origins, the cluster of islands have grown jagged and fractured, with some islands showcasing altitudes as low as a few meters above sea level to others flexing spaces over 5000 feet above sea level. These extremely diverse habitats enable the observation of vastly different sub-populations of the same (or closely related) species*, exhibiting differing adaptations to their unique environments. These morphological distinctions lead to Darwin’s infamous 1859 book ‘On the Origin of Species’, detailing his evidence for the theories of evolution. *This article may refer to the Galápagos Tortoises as different subspecies or species interchanagably, as this remains a contentious area. The giant tortoises One most apparent examples of evolution that Darwin noted were the Galapagos tortoises, Chelonoidis niger ( Chelonoidis porteri) , of which there were at least 15 subspecies. Darwin devoted almost four pages of his Journal of Researches to the Galapagos tortoise, more than he did to any other Galápagos species. These captivating reptiles can grow up to 5 feet in length and weigh over 220kg, making them the largest tortoises in the world. This miraculous species can survive over a year without food or water, able to store tremendous volumes of liquid in their bladders in periods of drought - one of the many adaptive characteristics that enable them to routinely live well over 150-years-old. Darwin notably observed the species’ two unique primary shell morphologies - saddleback and domed. Some subspecies, such as the Pinta Island Tortoise ( Chelonoidis niger abingdonii ), have saddle-shaped shells which raise at the front, making it easier for the neck to stretch upwards to feed on taller vegetation on hotter, more arid islands. Whereas the populations with the dome-shaped shells, including the Chelonoidis niger porteri , occupy islands where there’s an abundance of flora lower to the ground, making upward stretching of the neck unnecessary to feed. Features such as these are well documented in Darwin’s evidence for evolutionary adaptation throughout the islands. Torment and tragedy Only two centuries ago, the Galápagos Islands were rife with life, with an estimated 250,000 giant tortoises. Today, multiple species are extinct, with only around 10% of the individuals surviving. The dramatic decline of the Galápagos tortoises has been characterised by frequent human failure, and in some instances, human design. Between the 1790s and 1800s, whalers began operating around the Galápagos, routinely taking long voyages to explore the Pacific Ocean. With whaling voyages lasting about a year, the tortoises were selected as the primary source of fresh meat for the whalers, with each taking 200 to 300 tortoises aboard. Here, in a ship’s hold, the hundreds of tortoises would live without food or water for months, before being killed and consumed. Documentation regarding how many tortoises were taken aboard by whalers is scarce, however estimates place the number between 100,000 and 200,000 by 700 whaling ships between 1800 and 1870. This initial decimation via over-consumption was then followed by the introduction of harmful invasive species. In the years since, multiple foreign species have been introduced to the archipelago, mainly for farming, including pigs (a lot of which are feral), dogs, cats, rats, goats and donkeys. These non-native species are an enduring threat to the giant tortoise populations, preying on their eggs and hatchlings, whilst also providing fierce and unprecedented competition for food. Furthermore, increasing temperatures attributed to climate change are thought to trigger atypical migrations. These migrations have the potential to reduce tortoise nesting success, further adding to the list of threats these species have had to endure. The Pinta giant tortoise, Chelonoidis niger abingdonii , a species of the unique saddleback shell variety, was thought to be extinct since the early 20th century. But then, in 1971, József Vágvölgyi, a Hungarian scientist on Pinta island made a special discovery – Lonesome George. Seemingly a sole survivor of his kind, Lonesome George became an icon of the sparking conservation movement surrounding the Galápagos species. This lone Pinta individual could have been wandering the small island for decades in search for another member of his species - a search that would unfortunately never bear fruit. Despite selective breeding efforts, on June 24, 2012, at 8:00 A.M. local time, Lonesome George would pass away without producing any offspring, found by park ranger Fausto Llerena who had looked after him for forty years. Hope and the future Despite all the devastation the Galápagos tortoises have endured, not is all lost. Just like the story of Lonesome George, a microcosm of this larger crisis, there is a small light at the end of the tunnel. Just prior to George’s passing a remarkable discovery was made. During 2008, research conducted by the Ecology and Evolutionary Biology Department of Yale University on neighbouring Isabela Island, set out to genetically sequence the local giant tortoise population. Over 1,600 tortoises were tagged and sampled for their DNA, with analyses revealing an astonishing number of tortoises with mixed genetic ancestry. Within this sample, 17 individuals contained DNA from the Pinta tortoise species (and more contained DNA from the also extinct Floreana species). Retrospective study of old whaling logbooks seems to indicate that, in order to lighten the burden of their ships, whalers and pirates dropped large numbers of tortoises in Banks Bay, near Volcano Wolf, Isabela Island, likely accounting for these hybrids. This miracle discovery opens the door to selective breeding efforts, paving a future of reintroduction of the previously-extinct Pinta Island species. While only a fraction of their original numbers remain, the Galápagos tortoises continue to personify evolution’s stunning intricacies and persist as a bright beacon of hope for the greater world of conservation. It is vital that we do our part as human beings to correct the errors of our past and to respect and nurture these gentle giants and all that they represent in this world we call home. In line with this, recently, 158 captive-bred Galápagos tortoises have returned to the Galápagos island of Floreana for the first time in more than 180 years; this has been dubbed as a significant win by conservationists. Written by Theo Joe Andreas Emberson Related articles: Conservation of marine iguanas / 55 years of vicuna conservation / Gorongosa National Park / Modern Evolutionary Synthesis REFERENCES Sulloway FJ. Tantalizing tortoises and the Darwin-Galápagos legend. J Hist Biol. 2009;42(1):3-31. doi:10.1007/s10739-008-9173-9 Patrick J. Endres. AlaskaPhotoGraphics.com Project Gallery

Loss aversion: the power of framing in decision-making and why we are susceptible to poor decisions Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Behavioural Economics III 06/11/25, 11:56 Last updated: Published: 15/10/24, 11:18 Loss aversion: the power of framing in decision-making and why we are susceptible to poor decisions This is article no. 3 in a series on behavioural economics. Next article- Libertarian Paternalism . Previous article- The endowment effect . In the realm of decision-making, the way information is presented can dramatically influence the choices people make. This phenomenon, known as framing, plays a pivotal role in how we perceive potential outcomes, especially when it comes to risks and rewards. We shall now explore the groundbreaking work of Tversky and Kahneman, who sought to explain how different framings of identical scenarios could lead to vastly different decisions. By examining their research, we can gain insight into why we are susceptible to making poor decisions and understand the underlying psychological mechanisms that drive our preferences. The power of framing Imagine that the UK is preparing for the outbreak of an unusual disease, which is expected to kill 600 people. Two alternative programs to combat the disease have been proposed. In a paper by Tversky and Kahneman, they examined the importance of how information is conveyed in two different scenarios. In scenario 1: If program A is adopted, 200 people will be saved. If program B is adopted, there is a 1/3 probability that 600 people will be saved and a 2/3 probability that no people will be saved. In scenario 2: If program A is adopted, 400 people will die. If program B is adopted, there is a 1/3 probability that nobody will die and a 2/3 probability that 600 people will die. Notice that both scenarios display the exact same information, but the way in which the information is displayed is different. So surely there should be no difference between the two scenarios? In fact, there is a huge difference. Scenario 2 has been given a loss frame, where the loss frame emphasises the potential negative outcomes. By taking a sidestep, we can examine why this is important. Loss aversion is the phenomenon where ‘losses loom larger gains’. In other words, if we lose something, then the negative impact of this is greater than the positive impact of an equal-sized gain. Image 1 illustrates a loss aversion function. As illustrated in the image, a loss of £100 results in a much larger negative reaction than the positive reaction of a gain of £100. To put this into perspective, imagine it’s your birthday and someone gifts you some money. You would hopefully feel quite grateful and happy, but perhaps this feeling isn’t overwhelming. On the contrary, if you soon discover that you lost your wallet or purse, which contained the same amount of money, the psychological impact is often much more severe. Losses are perceived to be much more significant than gains. Going back to the example involving the two scenarios, we see that in scenario 2, program A emphasises the death of 400 people compared to scenario 2, program B, which has a chance to lose more but also a chance to save everyone. Statistically, you should be indifferent between the two, but because the guaranteed loss of 400 people is so overwhelming, people would much rather gamble and take the chance. This same reason is why gambling is so addictive. When you lose money in a gamble, you feel compelled to not accept the loss and decide to continue betting in an effort to make back what you once had. What Kahneman and Tversky found was that in scenario 1, 72% of people chose program A, and in scenario 2, 78% of people chose program B. Clearly, how we frame a policy makes a huge difference in its popularity. By framing the information by saying “200 people will be saved” rather than “400 people will die” out of the same 600 people, our own perception is considerably different. But on a deeper level, why might this be, and why is knowing this distinction important? In my previous article on the endowment effect, we saw that once you own something, you feel possessive over it, and losing something that you have had to work for, like money, makes you feel as though that hard work has gone to waste. But this explanation struggles to translate into our example of people. In researching for this article, I came across the evolutionary psychology perspective and found it to be both interesting and persuasive. From an evolutionary perspective, loss aversion can be seen as an adaptive trait. For our ancestors, losses such as losing food or shelter could have dire consequences for survival, whereas gains such as finding extra food was certainly beneficial but not as crucial for immediate survival. Therefore, we may be hardwired to avoid any losses, which has translated into modern-day loss aversion. The reason why knowing about this is important comes up in two aspects of life. The first is in healthcare. As demonstrated at the beginning of the article, people’s decisions can be impacted by the way in which healthcare professionals and the government frame policies. By understanding this, it allows you to make your own decision on the risks and determine whether you believe it is right for you. Similarly, policymakers can shape public opinion by highlighting the benefits or costs of action or inaction such that it meets their own political agenda. So recognising loss aversion allows for more informed decision-making. Additionally, when it comes to the world of investing, people tend to keep hold of an investment that is performing badly or perhaps at a loss in the hopes that it will go back up in the future. If this belief is justified through analysis or good judgement, then deciding to hold may be a good decision; however, often loss aversion creates a false sense of hope similar to the example I gave for gambling. If you are a keen investor, it’s important to be aware of your own investment psychology so that it allows you to maintain an objective view of a company throughout the time you decide to remain invested. Evidently, understanding how we think and make decisions can play an important role in improving the choices we make in our personal and professional lives. By recognising the impact of loss aversion and framing, we can become more aware of the unconscious biases that drive us to avoid losses at all costs, even when those decisions may not be in our best interest. Whether it’s in healthcare, investing, or everyday life, cultivating this awareness allows for more rational, informed choices that better align with long-term goals rather than short-term fears. In a world where information is constantly framed to sway public opinion, knowing the psychology behind our decision-making processes is a powerful tool that can help us make wiser, more deliberate decisions. Written by George Chant REFERENCES Tversky A, Kahneman D. The framing of decisions and the psychology of choice. Science. 1981 Jan 30;211(4481):453-8. doi: 10.1126/science.7455683. PMID: 7455683. Image provided by Economicshelp.org , a link to the website: https://www.economicshelp.org/blog/glossary/loss-aversion/ Project Gallery

When misfolded proteins lead to disease Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unfolding prion diseases and their inheritance 22/04/25, 14:11 Last updated: Published: 06/03/24, 11:32 When misfolded proteins lead to disease This is article no. 5 in a series on rare diseases. Next article: Neuromyelitis optica . Previous article: Epitheliod hemangioendothelioma . Prion proteins are found abundantly in the brain; their function is unclear, but they are involved in a multitude of physiological mechanisms, including myelin homeostasis and the circadian rhythm. Correctly folded prion proteins in the cellular form are termed PrP C , while their infectious isoform is called PrP Sc . As shown in Figure 1, the misfolded PrP Sc is largely made up of β-pleated sheets instead of α-helices; PrP Sc is prone to forming aggregates that cause transmissible spongiform encephalopathies (TSEs). Prion diseases can be categorised by their aetiology: acquired, sporadic, and hereditary. Acquired prion diseases are caused by the inadvertent introduction of PrP Sc prions into an individual. Sporadic prion diseases are the most common type, where PrP C misfolds into PrP Sc for an unknown reason and propagates this misfolding within other prion proteins. Hereditary prion diseases are caused by genetic mutation of the human prion protein gene (PRNP), which causes misfolding into the infectious isoform. Consequently, these mutations can be passed to offspring, resulting in the same misfolding and disease. Interestingly, different types of PRNP mutations cause different types of prion diseases. Creutzfeldt-Jakob disease (CJD) is a type of TSE found in humans which causes mental deterioration and involuntary muscle movement; symptoms tend to worsen as the disease progresses, making it a degenerative disorder. Familial CJD (fCJD) is a rare type of hereditary prion disease and can sometimes result in a faster rate of disease progression compared to sporadic cases. Due to a dominant inheritance pattern, relatives of fCJD patients are often also affected by the disease. The most common mutation observed in familial CJD is an E200K mutation denoting the substitution of glutamic acid with lysine in the prion protein. Other common mutations resulting in fCJD include mutations at positions 178 and 210 on the prion protein. However, there are, less frequently, a multitude of other mutations correlated with familial CJD development. Familial CJD can be caused by STOP codon mutations, which result in a truncated protein, some of which show similar pathology to Alzheimer’s disease, such as Q16OX and Q227X. fCJD can also be caused by insertional mutations, possibly caused by unbalanced crossover and recombination. The prion protein consists of a nona-peptide (made up of nine amino acids) followed by four repeats of an octa-peptide (made up of eight amino acids). During insertion mutations, additional repeats of the octa-peptide are present in the prion protein. Interestingly, different numbers of inserts result in different pathological characteristics; patients with 1, 2 or 4 extra repeats show similarity to sporadic CJD, while those with 5-9 extra repeats show similarity to Gerstmann-Sträussler-Scheinker syndrome. Hereditary prion diseases are important to study in order to develop an understanding of not only prion misfolding diseases but also diseases associated with misfolding of other proteins, such as Alzheimer’s and Parkinson’s. Understanding the mechanisms of hereditary prion diseases will aid the development of treatments for such conditions. In particular, observing and investigating particular genetic mutations observed to play a part in prion misfolding is crucial alongside using genetic information to infer the risk of disease an individual may have. Written by Isobel Cunningham Project Gallery

Vicuñas are members of the camelid family Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The cost of coats: celebrating 55 years of vicuña conservation 08/03/26, 18:25 Last updated: Published: 09/10/24, 14:03 Vicuñas are members of the camelid family This is article no. 1 in a series on animal conservation. Next article: Conserving the California condor . Is the softest coat in the world worth the near-extinction of a species? Just ask a vicuña, the wild cousin of llamas and alpacas. After being widely hunted in South America in the mid-20th century, the vicuña population thrives. Their recovery is considered one of the earliest successes in modern wildlife conservation, setting a precedent for sustainable development. October 2024 marked the 55th anniversary of the first international agreement to conserve these furry friends. In its honour, here is the story of vicuña conservation. What are vicuñas? Vicuñas have a unique biology. They are members of the camelid family ー which includes llamas, alpacas, and camels. Vicuñas live in high-altitude arid grasslands in South America (Figure 1). Their families consist of one alpha male, multiple females, and their offspring – while bachelor males form their own groups. Unlike other camelids, vicuña families remain together for most of the year. Vicuñas are herbivores with characteristic grazing and defecating behaviours that shape the surrounding plant community. Therefore, their ecological role cannot be underestimated. How vicuñas nearly went extinct However, vicuñas are hunted by humans because their wool is the finest and softest in the world. They are difficult to domesticate, and their habitat has no hiding spots, so they are easy poaching targets. Their intricate social structure means killing one vicuña has unforeseen impacts on the rest of the population. Consequently, expensive wool comes at the expense of a fascinating species. Demand for ultra-fine vicuña wool made hunting the animals a lucrative business in South America. Although 15th-16th century Inca rulers wore high-end clothing made from vicuña wool, it was usually harvested without killing the animals. European colonisation in the 19th-20th centuries opened vicuña wool to a wealthy international market, making poaching more popular and reckless than under Inca rule. These inconsiderate hunting practices continued after South American countries gained independence. As the luxurious wool remained in demand, the vicuña population decreased by over 99% between 1940 and 1965. Conservation policies saved the vicuñas South American national governments soon realised that indiscriminate vicuña hunting had to stop. As well as being ecologically important, vicuñas should not be allowed to go extinct because of their economic value. Peru had the largest proportion of the vicuña population, so in 1966 its government set up a nature reserve called Pampa Galeras. Creating this reserve involved negotiating with rural communities so that both people and vicuñas benefitted, for example, by employing locals at the reserve. This was one of the earliest examples of what is now known as sustainable development, which provides rural communities with a way of life that works alongside ecosystems rather than damaging them. Scientists found that vicuñas changed their social structures inside Pampa Galeras to maximise reproductive success. A 1987 study suggested that because females had more time to graze without the constant threat of predators and poachers, their reproductive success was higher. The creation of this reserve was the first of many successful steps South America took in the 1960s towards vicuña recovery. In October 1969, Argentina, Chile, Ecuador, and Bolivia joined Peru in the efforts to conserve vicuñas. Their Convention for the Conservation of the Vicuña banned international trade and massively restricted hunting. Since the convention successfully led to a rise in vicuña numbers, it was modified in 1979 so that sustainable vicuña wool could be sold. Meanwhile, conservation laws were being established in the United States and European Union, the wildlife trade regulator CITES was established, and public awareness about the biodiversity crisis was rising. This international effort saved vicuñas from extinction, and today there are 350,000 to 500,000 of them ( Figure 2 ). Although governments have played a huge role in conserving the vicuña, local communities have also contributed. People in Chile and Peru have revived the non-lethal, Inca traditional way of shearing vicuña to harvest their wool. This has many benefits: locals are de-colonising their culture and re-connecting with their heritage, the wool provides a source of income, and the vicuña population remains stable. Vicuñas were classified as ‘least concern’ for conservation by the International Union for Conservation of Nature in 2018. Climate change, mite infestations, and competition with livestock are affecting the population today – but to a much smaller extent than poaching was. Thus, vicuñas are back to freely roaming the Andes. Conclusion Conserving the vicuña relied on political willpower and community involvement. In the 55+ years since, ecologists have used this charismatic and distinctive animal to galvanise wildlife conservation worldwide. The vicuña’s story should also remind us that what we wear has financial and ecological costs. Written by Simran Patel Related articles: Conservation of marine igunanas / Gal á gapos tortoises REFERENCES Acebes, P., Wheeler, J., Baldo, J.L., Tuppia, P., Lichtenstein, G., Hoces, D. & Franklin, W.L. (2018) Vicuna: Vicugna vicugna . The IUCN Red List of Threatened Species 2018 . Available from: https://ri.conicet.gov.ar/handle/11336/178499 (Accessed 12th September 2024). Bosch, P.C. & Svendsen, G.E. (1987) Behavior of Male and Female Vicuna (Vicugna vicugna Molina 1782) as It Relates to Reproductive Effort. Journal of Mammalogy . 68 (2): 425–429. Available from: https://doi.org/10.2307/1381491 (Accessed 23rd September 2024). González, B. et al. (2019) Phylogeography and Population Genetics of Vicugna vicugna : Evolution in the Arid Andean High Plateau. Frontiers in Genetics . 10. Available from: https://doi.org/10.3389/fgene.2019.00445 (Accessed 22nd September 2024). Karandikar, H., Donadio, E., Smith, J.A., Bidder, O.R. & Middleton, A.D. (2023) Spatial ecology of the Vicuña ( Lama vicugna ) in a high Andean protected area. Journal of Mammalogy . 104 (3): 509–518. Available from: https://doi.org/10.1093/jmammal/gyad018 (Accessed 11th September 2024). Lyster, S. (1985) VICUNA. In: International Wildlife Law: An Analysis of International Treaties concerned with the Conservation of Wildlife . Cambridge: Cambridge University Press: 88–94. Nolan, D. (2025) How an Ancestral Peruvian Ceremony Is Saving the Once-Endangered Vicuña . Smithsonian Magazine . Available at: https://www.smithsonianmag.com/travel/how-an-ancestral-peruvian-ceremony-is-saving-the-once-endangered-vicuna-180986933/ (Accessed: 7 March 2026). Reider, K.E. & Schmidt, S.K. (2021) Vicuña dung gardens at the edge of the cryosphere. Ecology . 102 (2): 1–3. Available from: https://www.jstor.org/stable/26998110 (Accessed 11th September 2024). UNESCO (2024) Ancestral practice promotes vicuña conservation and sustainable . unesco.org . Available at: https://www.unesco.org/en/articles/ancestral-practice-promotes-vicuna-conservation-and-sustainable-development-chiles-lauca-biosphere (Accessed: 7 March 2026). Vilá, B. & Arzamendia, Y. (2022) Weaving a vicuña shawl. Pastoralism . 12 (1): 46. Available from: https://doi.org/10.1186/s13570-022-00260-6 (Accessed 11th September 2024). Wakild, E. (2020) Saving the Vicuña: The Political, Biophysical, and Cultural History of Wild Animal Conservation in Peru, 1964–2000. The American Historical Review . 125 (1): 54–88. Available from: https://doi.org/10.1093/ahr/rhz939 (Accessed 11th September 2024). Yacobaccio, H. (2009) The Historical Relationship Between People and the Vicuña. In: Gordon, I.J., ed. The Vicuña: The Theory and Practice of Community Based Wildlife Management . Boston, MA: Springer US: 7–20. Project Gallery