Search Index

Captive breeding has grown the California condor population over 18-fold Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Conserving the California condors 24/04/25, 11:46 Last updated: Published: 04/11/24, 14:56 Captive breeding has grown the California condor population over 18-fold This is article no. 2 in a series on animal conservation. Next article: Beavers are back in Britain . Previous article: The cost of coats: celebrating 55 years of vicuna conservation . California condors are critically endangered birds living on the west coast of North America. Their population decline was first reported in 1953, and they were nearly extinct by 1987. Since then, a captive breeding and reintroduction program has saved the species in the face of multiple human threats. This article will describe some of those threats and available measures to mitigate them. Why California condors became endangered Lead poisoning was the main cause of California condor mortality in the late 20th century. Like vultures, California condors eat dead mammals. When these mammals were shot dead with lead bullets, condors ingested fragments of the bullets, and the lead poisoned their bloodstream. Multiple condors feeding on the same carcass got poisoned, which could be why the population crashed so badly. Today, lead poisoning is the biggest, but not the only, threat to California condor survival ( Figure 1 ). The birds used to be hunted for museums and private collections in the early 20th century, but nowadays, any shootings are accidental. A bigger concern, and the second-most common human-related cause of mortality, is condors colliding with utility poles and power lines. The third-most common is fires: a 2015 study found that every recent wildfire in California has coincided with at least one condor death. Climate change will make these fires more frequent and severe. These threats mainly apply to inland California condors - halogenated organic compound (HOC) pollution is an issue for coastal birds. When coastal condors eat marine mammals contaminated with HOCs, the compounds disrupt their reproductive system and thin their eggshells. In short, humans have created a hostile environment for California condors. Successful captive breeding and population recovery Despite these threats, captive breeding has grown the California condor population over 18-fold ( Figure 2 ). In 1987, all remaining wild condors were captured and bred, with juveniles released to the wild from 1992 onwards. Reintroduced birds are monitored regularly, and poisoned birds are treated with chelation therapy - where a drug binds to lead in the bloodstream and takes it to the kidneys to be filtered out. Since 1995, power line collisions have been avoided by giving juveniles behavioural training before reintroduction. Because of these measures, the California condor mortality rate in the wild decreased from 37.2% in 1992-1994 to 5.4% in 2001-2011. Challenges of conserving California condors Although captive breeding has saved the California condor population, it has also altered behaviours. The original condors stay with one mate longer than reintroduced condors, which may form polygamous relationships. Scientists think that spending so much time with non-family members in captivity has made juveniles promiscuous when reintroduced. Captive bred condors have also gotten used to being fed by people - so they approach people more often, spend longer in areas of human activity, and forage over a smaller area than the original condors. Moreover, condors in southern California were spotted feeding their chicks human litter. These behavioural changes mean the wild California condor population is not self-sustaining. The wild population is also not self-sustaining because condors are still being poisoned ( Figure 3 ). Banning lead bullets is the most effective way to guarantee population growth, but enforcing it has been challenging. Non-toxic alternative bullets like copper cannot find popularity. For population growth, every adult California condor killed is estimated to be worth 2-3 reintroduced juveniles. This is because released juveniles are more vulnerable and take years to reach breeding age. Therefore, American conservationists must keep pressuring authorities to reduce threats to adult California condors. Conclusion Pollution, urbanisation, and climate change have made it hard for the California condor population to recover from decades of lead poisoning. Long generation times and behavioural changes mean captive breeding is the species’ only hope of survival. Perhaps humans are the ones who need to change their behaviour - not feeding California condors and switching to copper bullets would allow these majestic birds to keep roaming the skies. Written by Simran Patel Related articles: Marine iguana conservation / Deception by African birds / Emperor penguins REFERENCES Bakker, V.J. et al. (2024) Practical models to guide the transition of California condors from a conservation-reliant to a self-sustaining species. Biological Conservation . 291: 110447. Available from: https://www.sciencedirect.com/science/article/pii/S0006320724000089 (Accessed 19th September 2024). D’Elia, J., Haig, S.M., Mullins, T.D. & Miller, M.P. (2016) Ancient DNA reveals substantial genetic diversity in the California Condor (Gymnogyps californianus) prior to a population bottleneck. The Condor . 118 (4): 703–714. Available from: https://doi.org/10.1650/CONDOR-16-35.1 (Accessed 28th September 2024). Finkelstein, M.E. et al. (2023) California condor poisoned by lead, not copper, when both are ingested: A case study. Wildlife Society Bulletin . 47 (3): e1485. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/wsb.1485 (Accessed 28th September 2024). Kelly, T.R. et al. (2015) Two decades of cumulative impacts to survivorship of endangered California condors in California. Biological Conservation . 191: 391–399. Available from: https://www.sciencedirect.com/science/article/pii/S0006320715300173 (Accessed 28th September 2024). Mee, A. & Snyder, N. (2007) California Condors in the 21st Century - conservation problems and solutions. In: 243–279. Meretsky, V.J., Snyder, N.F.R., Beissinger, S.R., Clendenen, D.A. & Wiley, J.W. (2000) Demography of the California Condor: Implications for Reestablishment. Conservation Biology . 14 (4): 957–967. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1523-1739.2000.99113.x (Accessed 29th September 2024). Stack, M.E. et al. (2022) Assessing Marine Endocrine-Disrupting Chemicals in the Critically Endangered California Condor: Implications for Reintroduction to Coastal Environments. Environmental Science & Technology . 56 (12): 7800–7809. Available from: https://doi.org/10.1021/acs.est.1c07302 (Accessed 19th September 2024). U.S. Fish and Wildlife Service (2023) California Condor Population Graph, 1980-2022 | FWS.gov . 18 April 2023. Available from: https://www.fws.gov/media/california-condor-population-graph-1980-2022 (Accessed 28th September 2024). U.S. Fish and Wildlife Service (2020) California Condor Recovery Program 2020 Annual Population Status . Available from: https://www.fws.gov/sites/default/files/documents/2020-California-Condor-Population-Status.pdf (Accessed 28th September 2024). Project Gallery

Beavers alter their landscape through dams, canals, and felling trees Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Beavers are back in Britain, ‘wood’ you like to know why? 09/07/25, 10:58 Last updated: Published: 03/12/24, 12:05 Beavers alter their landscape through dams, canals, and felling trees This is article no. 3 in a series on animal conservation. Next article: Pangolins: from poached to protected . Previous article: Conserving the California condor Eurasian beavers ( Castor fiber ) transform freshwater habitats so dramatically that they are nicknamed ‘ecosystem engineers’. Their dam-building and tree-felling activities could reduce flood risk and increase biodiversity. After being hunted to extinction centuries ago, beavers have been reintroduced to Britain in both organised and illicit ways. This article will describe where they have been reintroduced in Britain, and the impact they could have. Ecological importance of beavers By building dams, Eurasian beavers alter their habitat - often for the better. Beaver dams are made from wood, stones, and mud. They control the flow of river water, reducing the risk of floods and droughts. The resulting slower water is a good place for amphibians to lay eggs and undergo the aquatic part of their life cycle. As water builds up behind the dam, it converts the area into a wetland - a source of drinking water for animals like bats and an excellent carbon sink. Meanwhile, invertebrates can lay eggs or hide from predators in the spaces within beaver dams ( Figure 1 ). Further up the food chain, beaver dams have complex effects on fish. Although the still water provides habitat for overwintering and rearing young, dams restrict the movement of fish species like salmon. However, most studies have concluded that beaver dams benefit freshwater biodiversity. Dams are not the only way Eurasian beavers improve their landscape. To access food and construction materials easily, beavers dig canals – which make the habitat better drained and more complex. Moreover, beavers gnaw at tree trunks and branches, sometimes knocking over entire trees. This creates deadwood where terrestrial invertebrates can live. Felling trees also allow sunlight to reach the river surface, promoting aquatic plant growth. When beavers gnaw at willow trees, they create propagules, which disperse along the beaver-made canal network and grow downstream. These new willow trees stabilise the river bank and further reduce the flood risk. Humans often trim back trees to stimulate their growth – called coppicing – but beavers do this free of charge. Coppicing, dam building, and canal digging are just a few ways beavers save the human costs of restoring and protecting natural habitats. Extinction and reintroduction However, Eurasian beavers used to be more exploited than appreciated. They were hunted for their fur, meat, and a secretion called castoreum, which is used in perfume and pharmaceuticals. Exactly when and how the beaver population went extinct from Britain is unclear, but the last written record of a beaver is from 1526 in Scotland and 1780 in England. Since then, the British turned wetlands into farmland and forgot about beavers … until recently. After centuries, beavers returned to Scotland in the late 2000s. A handful of beavers were spotted in River Tay about 15 years ago, after either an enclosure escape or an illegal release. There are 114 families in this illegal population, which has genetic origins in Germany. The first official beaver reintroduction occurred in Knapdale Forest, Scotland, in 2009 – but this population did not grow as quickly as the River Tay one. With scepticism, the reintroduction of Eurasian beavers to Scotland was deemed a success, and they became a ‘European Protected Species’ in Scotland in 2019. Seeing Eurasian beavers thriving in Scotland encouraged reintroduction plans in England. In the English county of Devon, River Otter showed signs of beaver presence since 2008 and breeding since 2013. Authorities were worried these illegally released beavers would spread foreign diseases to local wildlife, but the public campaigned to let the beavers be. Public affection for beavers led to the River Otter Beaver Trial in 2015, where two breeding pairs were released into the river after thorough health checks. By 2019, the number of breeding pairs grew to seven ( Figure 2 ). Therefore, beavers have successfully returned to England. Conclusion Beavers alter their landscape through dams, canals, and felling trees. However, in Britain, they were hunted to extinction a long time ago. Although beavers first returned to England and Scotland illegally, they now live in healthy, growing populations. Hopefully they will remain protected and loved by the public, helping us to restore wetlands and improve British freshwater biodiversity. Written by Simran Patel Related article: Vicuna conservation REFERENCES Andersen, L.H. et al. (2023) ‘Can reintroduction of beavers improve insect biodiversity?’, Journal of Environmental Management , 337, p. 117719. Available at: https://doi.org/10.1016/j.jenvman.2023.117719 . Brazier, R.E., Elliott, M., Andison, E., Auster, R.E., Bridgewater, S., Burgess, P., Chant, J., Graham, H., Knott, E., Puttock, A.K., Sansum, P., Vowles, A., (2020) ‘River Otter Beaver Trial: Science and Evidence Report’. Brazier, R.E. et al. (2021) ‘Beaver: Nature’s ecosystem engineers’, WIREs Water , 8(1), p. e1494. Available at: https://doi.org/10.1002/wat2.1494 . Campbell-Palmer, R. et al. (2020) ‘Beaver genetic surveillance in Britain’, Global Ecology and Conservation , 24, p. e01275. Available at: https://doi.org/10.1016/j.gecco.2020.e01275 . Gaywood, M., Batty, D. and Galbraith, C. (2008) ‘Reintroducing the European Beaver in Britain’, British Wildlife , 19, pp. 381–391. Halley, D.J., Saveljev, A.P. and Rosell, F. (2021) ‘Population and distribution of beavers Castor fiber and Castor canadensis in Eurasia’, Mammal Review , 51(1), pp. 1–24. Available at: https://doi.org/10.1111/mam.12216 . Hooker, J. et al. (2024) ‘Re-establishing historic ecosystem links through targeted species reintroduction: Beaver-mediated wetlands support increased bat activity’, Science of The Total Environment , 951, p. 175661. Available at: https://doi.org/10.1016/j.scitotenv.2024.175661 . Wilson, J.B., Bradley, J. and Bremner-Harrison, S. (2024) ‘The short-term impact of Eurasian beavers ( Castor fiber ) post-reintroduction on amphibian abundance and diversity in a lentic environment’, The Glasgow Naturalist , 28(2). Available at: https://doi.org/10.37208/tgn28224 . Project Gallery

Revolutionising drug discovery Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A breakthrough procedure for efficient and effective development 08/07/25, 14:35 Last updated: Published: 07/01/24, 14:05 Revolutionising drug discovery Discover how researchers have transformed the early stages of drug development with a ground-breaking test that identifies the most promising compounds. "Saving time and resources by focusing on the most potential compounds". Researchers at the Centre for Cancer Drug Discovery at The Institute of Cancer Research (ICR), London have made a significant breakthrough in the field of drug discovery. Their new investigative procedure promises to revolutionize the early stages of drug development by making it more efficient and effective. This ground-breaking test allows scientists to identify new biologically active compounds with the highest potential, saving valuable time and resources. Thanks to this procedure, researchers worldwide can now select only the most promising compounds to develop into effective medications. The study, funded by Cancer Research UK, has been published in the prestigious Journal of Medicinal Chemistry, highlighting its importance and impact on the field. A new approach to fragment-based drug discovery Fragment-based drug discovery has become the standard method for identifying the starting point of a drug discovery program. Scientists screen libraries of compounds, known as fragments, to determine their interaction with a potential anti-cancer target. Previously, scientists could only qualify the interactions between fragments and target proteins as a simple "yes" or "no". However, weak, or nonspecific interactions were challenging to evaluate accurately. Now, thanks to this latest research, researchers have developed a quantitative approach to measure the strength of these interactions. By ranking the fragments based on their interaction strength, research teams can confidently identify the most active compounds to move forward in the drug development process. This additional information allows scientists to refine the selected fragments by optimizing their shape, combining them with other fragments, or both. The result is a more streamlined and efficient drug discovery workflow. Realising the potential of the new procedure Dr. Maggie Liu, the first author of the study and a Senior Scientific Officer at the ICR, expressed confidence that this new procedure will become an integral part of the standard drug discovery workflow. The method is accessible to any team with the right equipment, providing a valuable tool for the wider drug discovery community. The ICR has already started follow-up work on one of the identified fragments using this new test. They plan to utilize this procedure for all future projects, recognizing its potential to accelerate the development of life-saving drugs. Compounds discovered from fragment-based drug discovery (FBDD) and their potential effects FBDD has emerged as an effective strategy in drug discovery, leading to the identification of several compounds with promising potential, including: 1. Vemurafenib: FDA approved in 2011, Vemurafenib has shown efficacy against specific targets, potentially offering treatment options for certain conditions. 2. Venetoclax: Another FBDD-derived drug, Venetoclax, received FDA approval in 2016. It has demonstrated positive outcomes in clinical trials, indicating its potential as a therapeutic agent. 3. Pexidartinib: Approved in 2019, Pexidartinib is a fragment-derived drug that has exhibited promising effects against its intended targets. 4. Erdafitinib: Similarly, Erdafitinib, developed through FBDD, obtained FDA approval in 2019. It has shown potential in clinical trials, highlighting its significance as a therapeutic option. 5. Sotorasib: This compound, approved in 2021, is another example of a fragment-derived drug with potential therapeutic benefits against specific targets. 6. Asciminib: Lastly, Asciminib, also approved in 2021, is a fragment-based drug that has demonstrated efficacy in clinical trials, showcasing its potential as a therapeutic intervention. These compounds represent a fraction of the molecules discovered through FBDD, and their effects vary depending on the specific targets they interact with. Further research and clinical trials are necessary to fully understand the therapeutic potential of these compounds and their broader impact on various diseases and conditions. Testing the R2KD tool Dr. Liu and her team successfully used the R2KD tool to identify new biologically active compounds. This tool utilizes a ligand-observed nuclear magnetic resonance (LONMR) approach, similar to an MRI scanner, to observe fragment interactions. By measuring the transverse relaxation rate (R2) of the fragments, which indicates their speed in the solution, the researchers could determine the fragments' interaction with the target protein. They then applied a new mathematical formulation to calculate a binding affinity value (Kd) for each fragment and compare their Kd values. This allowed them to identify the fragments with the strongest interactions. The researchers named their test 'R2KD'; based on these steps. By using this method, scientists can now quantitatively determine the binding affinity of fragments, which helps in selecting compounds with the most potential for further development. This new procedure makes the early stages of drug discovery more efficient, saving time and resources by focusing on the most promising compounds. Written by Sara Maria Majernikova Related articles: AI in drug discovery / AI in medicinal chemistry / A breakthrough in prostate cancer treatment / Arginine and tumour growth Project Gallery

Powering life and causing death Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Dual Role of Mitochondria 11/07/25, 09:57 Last updated: Published: 13/05/24, 13:38 Powering life and causing death Mitochondria as mechanisms of apoptosis Mitochondria are famous for being the “powerhouse of cells” and producing ATP for respiration by being the site for the Krebs cycle, the electron transport chain and the location of electron carriers. However, one thing mitochondria are not known for is mediating programmed cell death, or apoptosis. This is a tightly controlled process within a cell to prevent the growth of cancer cells. One way apoptosis occurs is through the mitochondria initiating protein activation in the cytosol (a part of the cytoplasm). Proteins such as cytochrome c activate caspases by binding to them, causing cell death. Caspases are enzymes that degrade cellular components so they can be removed by phagocytes. Mitochondrial apoptosis is also controlled by the B cell lymphoma 2 (BCL-2) family of proteins. They are split into pro-apoptotic and pro-survival proteins, so the correct balance of these two types of BCL-2 proteins is important in cellular life and death. Regulation and initiation of mitochondrial apoptosis Mitochondrial apoptosis can be regulated by the BCL-2 family of proteins. They can be activated due to things such as transcriptional upregulation or post-translational modification. Transcriptional upregulation is when the production of RNA from a gene is increased. Post-translational modification is when chemical groups (such as acetyl groups and methyl groups) are added to proteins after they have been translated from RNA. This can change the structure and interactions of proteins. After one of these processes, BAX and BAK (some examples of pro-apoptotic BCL-2 proteins) are activated. They form pores in the mitochondrial outer membrane in a process called mitochondrial outer membrane permeabilisation (MOMP). This allows pro-apoptotic proteins to be released into the cytosol, leading to apoptosis. Therapeutic uses of mitochondria Dysregulation of mitochondrial apoptosis can lead to many neurological and infectious diseases, such as neurodegenerative diseases and autoimmune disorders, as well as cancer. Therefore, mitochondria can act as important drug targets, providing therapeutic opportunities. Some peptides and proteins are known as mitochondriotoxins or mitocans, and they are able to trigger apoptosis. Their use has been investigated for cancer treatment. One example of a mitochondriotoxin is melittin, the main component in bee venom. This compound works by incorporating into plasma membranes and interfering with the organisation of the bilayer by forming pores, which stops membrane proteins from functioning. Drugs consisting of melittin have been used as treatments for conditions such as rheumatoid arthritis and multiple sclerosis. It has also been investigated as a potential treatment for cancer, and it induced apoptosis in certain types of leukaemia cells. This resulted in the downregulation of BCL-2 proteins, meaning there was decreased expression and activity.The result of the melittin-induced apoptosis is a preclinical finding, and more research is needed for clinical applications. This shows that mechanisms of mitochondrial apoptosis can be harnessed to create novel therapeutics for diseases such as cancer. It is evident that mitochondria are essential for respiration but also involved in apoptosis. Moreover, mitochondria are regulated by the activation of proteins like BCL-2, BAX and BAK. With further research, scientists can develop more targeted and effective drugs to treat various diseases associated with mitochondria. Written by Naoshin Haque Project Gallery

Second most common anaemia Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Anaemia of chronic disease 09/07/25, 10:49 Last updated: Published: 24/08/23, 16:06 Second most common anaemia This article is no. 3 of the anaemia series. Next article: sideroblastic anaemia . Previous article: Iron-deficiency anaemia. Pathogenesis The second most prevalent anaemia is anaemia of chronic disease (ACD), it is more often seen alongside chronic infections or malignancies, other causes include infections, autoimmune diseases, and transplant rejection. The pathogenesis of the condition is greatly lead by the effectiveness of the immune system, the immune response to tumour cells and pathogens is to remove and deny access to iron, which is needed to thrive. The processes are mainly thought to be mediated through cytokines such as TNF, IL-6s and IFN as well as the acute phase protein hepcidin. IL-6 is a very powerful cytokine in that it can inhibit erythropoiesis through the downregulation of gene expression; SLC4a1 reducing haemoglobin production, it increases ferratin production whilst inhibiting TNF-α, it upregulates DMT-1 which is a protein (transmembrane) involved in iron uptake in macrophages and it upregulates the production of hepcidin. Hepicidin Hepcidin is a peptide hormone, 25 amino acid chain protein, derived mainly from hepatic cells its synthesis is induced as a response to iron overload or inflammation, its presence crucial in the diagnosis of ACD. IL-6 induces hepcidin release from hepatocytes, upregulation causes the transport protein (ferroportin) degradation inhibiting iron absorption in duodenum enterocytes and macrophage recycling via upregulation of dMT-1 and mobilization of stored iron resulting in low iron plasma. Clinical presentation A patient with ACD may have low haemoglobin (Hb) and the reticulocyte index (new RBC) count may be reduced also, this is a common feature of an iron deficient anaemia. A blood film may help diagnose the underlying condition, but the red cell morphology varies greatly, less than half can be microcytic or hypochromic. Iron studies are what helps ACD stand out from the other anaemias, raised IL-6, hepcidin and ferratin are the key markers; the presence of iron results with raised ferratin and iron will be seen if a blood film is stained correctly. There may also be reduced serum iron, % saturation and TIBC. Should erythrocyte sedimentation rates be high Rouleaux’s may be seen, which are aggregations of RBC. Conclusion The most efficient way to diagnose an anaemia is through serum biomarkers in a FBC and iron studies. Hepcidin and other chemical markers play a key role in the diagnosis of ACD. Iron studies help to paint a clearer picture when diagnosing anaemias but should be supported with a medical history alongside a clinical examination, as comorbidities may influence chronic inflammatory markers. Written by Lauren Kelly Project Gallery

Its significant role in immunity Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The mast cell 14/07/25, 14:57 Last updated: Published: 05/08/23, 09:55 Its significant role in immunity The mast cell The mast cell is the first white blood cell to respond to infection or injury; they are located in many connective tissues throughout the body, especially in areas that introduce foreign bodies such as the gastrointestinal tract, respiratory epithelium and the skin. Mast cells are a crucial part in adaptive and innate immunity- in response to pathogens, allergens and toxin exposure they release chemicals and recruit other immune cells. They are created from pluripotent progenitor cells of myeloid lineages; these cells differentiate due to exposure and influence of stem cell factors. There are two types of mast cells in the human body, the first is called TC mast cells and contains tryptase, proteases and chymotryptic proteinase, the second is know as a T mast cell which contains only tryptase. The two types of mast cells are mucosal and connective tissue mast cells: mucosal mast cell are found mostly in the respiratory tract and the gut. Mast cells are found in three forms, granulated, spreading and intact. Intact mast cells lay in the epithelial tissue, the less common spreading mast cells are found in the connective tissues, and granulated mast cells are those which have released their mediators. These mediators reside in the cytoplasm of the mast cell- these include tryptases, heparin, histamine, cytokines, chymase, leukotrienes, TNF- alpha and many more. Mast cells are coated in IgE antibodies that crosslink (bind) to allergen proteins, which ultimately triggers degranulation. Mast cell disorders Abnormal growth of mast cells leads to a variety of issues. Mast cell activation syndrome in its primary state is caused by mast cell clone overproduction resulting in mastocytosis. This can lead to hives, gastric symptoms, and anaphylaxis. In some cases aggressive mastocytosis can lead to death. Cutaneous mastocytosis causes redden lesions of the skin and is most common in infants; systemic mastocytosis is most common in adults, led by the accumulation of mast cells in the intestines, organs, and bone marrow. Systemic mastocytosis includes the rare leukaemia and sarcoma forms. Mast cell activation syndrome in its secondary state is in an IgE -mediated hypersensitive response to external factors, that contributes to the release of pro-inflammatory cytokines and increases blood flow. However, it is too abundant, as the mast cells trigger far more granulation than that which is required. Idopathic mast cell activation is severe responses to the exposure of pathogens, toxins and other triggers. In idiopathic mast cell activation many patients can develop anaphylactic allergic reactions, which can present as difficulty breathing, swelling and hives. Conclusion Mast cells play a crucial role in biological defence and are derived from stem cells in the bone marrow. They come in different forms and locations, delivering an efficient response to injury and infection. When unregulated, they can lead to the development of disorders- ranging from mild rashes to severe anaphylaxis. Written by Lauren Kelly Project Gallery

CRISPR-Cas9, CAR T-cells, incretins, and iPSCs Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Biggest Innovations in Biosciences 11/07/25, 09:55 Last updated: Published: 25/03/24, 11:43 CRISPR-Cas9, CAR T-cells, incretins, and iPSCs We are in the era of innovation and cutting-edge technology in biosciences and health. This article goes through some of the most remarkable technologies slowly conquering the world of biosciences. Gene editing and CRISPR-Cas9 Gene editing is based on the idea that correcting the genetic mistake that causes a disease offers a permanent result than curing the symptoms. This technique allows scientists to alter the DNA of cells by deleting, adding or modifying genes. There are numerous ways to edit a gene. The most widely used and revolutionary method for gene editing is CRISPR-Cas9, which stands for Clustered Regularly Interspaced Short Palindromic Repeats and CRISPR- associated protein 9. The process begins with the design of a synthetic RNA molecule, known as guide RNA (gRNA) that matches the target gene sequence. The gRNA, combined with the Cas9 protein, forms a complex that is then introduced into the target cells. Cas9 acts like scissors, guided by the gRNA, to locate the precise location on the DNA where the genetic modification is intended. Once the target site is identified, Cas9 induces a break in the DNA strand. The cell's natural DNA repair mechanisms then come into play. The non- homologous end joining pathway introduces insertions and deletions at the site, resulting in gene knockout or inactivation. On the other hand, once a DNA template with homology to the sequences is present, the homology-directed repair pathway allows the incorporation of a desired genetic sequence, facilitating gene insertion or replacement. Several other gene-editing techniques have been developed, each with unique approaches. Zinc Finger Nucleases (ZFNs) and Transcription Activator-Like Effector Nucleases (TALENs) are two examples. These methods also use proteins that act as molecular scissors to cut the DNA at specific locations. ZFNs use zinc finger proteins to bind to target DNA sequences, while TALENs use transcription activator-like effector proteins. As the field of gene editing rapidly advances, these diverse methods contribute to the expanding toolkit available for researchers and hold promise for addressing a wide array of applications, from medical treatments to agricultural improvements. CAR T-cells Chimeric antigen receptor T-cells (CAR T-cells) are a new type of immunotherapy, considered to be the new fighters in the war on cancer. In general, immunotherapies use the patient’s immune system to fight the cancer. This therapy promises more specificity than traditional therapies and more permanent results. T-cells naturally exist in the human organism, supporting the adaptive immune system. They are a group of lymphocytes in the blood or lymph tissue that target or kill specific pathogens. Each type of T-cell recognises specific pathogens. T-cells have proteins on their outer surface, called receptors and these receptors recognize specific proteins on the outer surface of the pathogen. Depending on the type of T-cell, after recognizing the specific pathogen, they are either killing the pathogen (killer T-cells) or signaling to other elements of immune system to attack the pathogen (helper T-cells). CAR T-cell therapy involves modifying a patient’s own T-cells to express a specific CAR on their surface. The receptor is designed to recognise antigens commonly found on the surface of cancer cells. To introduce CARs on the outer surface of T-cells, the patient’s T-cells are genetically modified in the lab. A viral vector is often used to knock out the original T-cell receptors and express the CAR construct. The newly created CAR-T-cells are introduced into the patients, where they target and destroy cancer cells expressing the specific antigen for which the CAR is designed. Incretins The scientific journal “Science” proclaimed glucagon-like peptide-1 (GLP-1) receptor agonists The Breakthrough of 2023. These medications, originally approved for type 2 diabetes, demonstrated remarkable weight-loss benefits. GLP-1 is a natural hormone produced in the intestines that plays a role in regulating blood sugar levels. When we eat a meal, incretins, GLP-1 and Glucose-dependent insulinotropic polypeptide (GIP), are released into the bloodstream. They bind to specific receptors on the beta cells of the pancreas, triggering insulin release. Incretins also suppress the release of glucagon, a hormone that increases blood sugar levels by promoting the breakdown of stored glucose. GLP-1 receptor agonists are medications that mimic the effects of GLP-1. They bind to the GLP-1 receptors on pancreatic beta cells, promoting insulin secretion and suppressing glucagon release. By mimicking the actions of GLP-1, these medications help to lower sugar levels, improve glucose control, and reduce the risk of hypoglycemia. At the same time, they seem to regulate the appetite and delay gastric emptying. iPSCs Induced pluripotent stem cells (iPSCs) are becoming a new powerful weapon in lab research. They are a type of stem cell that can be generated from adult cells, such as skin or blood cells, through reprogramming. The process of creating iPSCs involves introducing a set of specific genes into the adult cells. These reprogramming factors reset the adult cells' developmental clock, turning them back into a pluripotent state, similar to embryonic stem cells. Once iPSCs are generated, they can be expanded indefinitely in the laboratory and induced to differentiate into various cell types. iPSCs are a valuable tool for studying human development and disease, as well as for drug discovery and regenerative medicine. iPSCs can be derived from patients with genetic diseases or other conditions, allowing researchers to study disease mechanisms in a dish. By differentiating iPSCs into the relevant cell types affected by the disease, researchers can observe how the disease develops and test potential treatments. Moreover, iPSC-derived cells can screen potential drugs for safety and efficacy. Because iPSCs can differentiate into many different cell types, they provide a more accurate model of human biology than traditional cell culture methods. Finally, because iPSCs can be derived from individual patients, they offer the potential for personalised therapies. iPSCs could be used to generate patient-specific cells for transplantation or to test drugs for individual patients. Conclusion These cutting-edge technologies offer unprecedented opportunities for targeted interventions in the treatment of genetic disorders, cancer, diabetes, and a myriad of other diseases. However alongside their immense promise, these biotechnological techniques and therapies also raise important ethical, social and regulatory considerations. The implications of gene editing on human germline cells, the accessibility of advanced therapies, and the long-term safety of these interventions are critical areas that warrant careful attention and thoughtful deliberation. Embracing these innovative techniques with diligence holds the key to unlocking a future where previously incurable conditions become manageable, and where the boundaries of medical possibility are continually expanded. Written by Matina Laskou Related articles: Medical biotechnology / Mesenchymal stem cells Project Gallery

An exposé to the undisclosed condition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Breast cancer in males 03/07/25, 10:26 Last updated: Published: 17/11/23, 16:51 An exposé to the undisclosed condition This is article no. 2 in a series on rare diseases. Next article: Herpes vs devastating skin disease . Previous article: Rare zoonotic diseases . Following the breakthroughs and increasingly successful screening programmes in most recent years, breast cancer in women has become increasingly talked about. Throughout October, social media is filled with information on breast cancer in women, what to do if diagnosed, memorable fundraising events that will generate thousands of pounds, and the heartwarming stories of survivors and patients fighting against this horrible disease. In the UK, 1 in 7 females will be diagnosed with breast cancer at some point in their lifetime. If we look at other areas in the world, this statistic shifts significantly: in the USA 1 in 8 females will develop the condition, whilst in Japan, it is 1 in 38 females. Although the percentages of breast cancer incidence differ around the globe, they all underline one common characteristic: many women and their families throughout the globe will suffer because of breast cancer ( Figure 1 ). Interestingly, though, with how prevalent breast cancer is in women, breast cancer in men is hardly ever mentioned. Whilst breast cancer is much more common in women, with around 55 thousand diagnoses every year, only 400 males a are diagnosed annually, which is equivalent to 1% of breast cancer diagnoses in the UK. However, the unlikelihood of a disease does not mean that it is any less significant. Conditions like epilepsy, strangulated inguinal hernias, alpha-1 antitrypsin, and Paget’s disease are all conditions with an incidence of around 1% or less. Nevertheless, they all may severely change the lifestyle of patients and even cause death - the fact that they have a low presence makes them no less important. This makes one wonder, what causes breast cancer in men and women to differ so extensively in numbers, and why is breast cancer in men so undisclosed? To answer this question, we must first understand what breast cancer is. Cancers are cells that grow uncontrollably, often forming tumours in the tissue or organs of the body and usually caused by a mutation or environmental factors, such as carcinogens. Cancers can be classified as benign and malignant, the difference being that benign cancers will stay in the original location, whilst malignant cancers are invasive. In other words, the tumour may spread to nearby tissues and lymph nodes or metastasise, spreading to other locations in the body. Breast cancer can be divided further into several types – this is one of the reasons finding a “cure” for breast cancer is so complicated. In men, the two most common types of breast cancer are invasive ductal carcinoma, which can spread through the ducts to the body, and ductal carcinoma in situ, which arises in the ductal lining of the breast tissue. But what causes these cancers to develop in men? There are multiple risk factors to consider when it comes to breast cancer in men, one of the most common being genetic mutations. Genetic mutations are when a copy of the DNA sequence in a gene has a change, and it can cause a different function or phenotype of the gene. In breast cancer, two critical and potentially inheritable mutations are in the genes BRCA1 and BRCA2, which increase the risk of breast cancer in both men and women. Furthermore, this is why taking the family history of breast cancer is essential: an individual with a positive family history for breast cancer may wish to take a genetic test to confirm whether they have the mutated genes. After all, genes are inherited. Hence, if one parent has the mutated gene, they could pass it on to their children. In addition, it is important to understand how breast cancer can only occur in breast tissue. Therefore, even if a male has the mutated gene, they could only have said cancer if there is breast tissue where the hormones oestrogen and progesterone can bind to and lead to mutation, causing the cancer to further multiply and spread – this is not always the case. Another genetic risk for breast cancer is a diagnosis of Klinefelter syndrome. This syndrome, which affects less than 1% of newborn males, involves having an extra X chromosome, leading to the body producing higher levels of oestrogen and lower levels of androgen. Androgens are a group of sex hormones, usually found at higher levels in men, one example being testosterone. Meanwhile, oestrogen appears to be another risk factor. This natural hormone has been shown to correlate with breast cancer. A study in the Nature Journal found that the inhibition of oestrogen has decreased the incidence of cancer in patients considered high-risk. But how are men exposed to the hormone? Aside from being diagnosed with Klinefelter syndrome, men can be exposed to hormone therapy treatments, which include drugs that could contain oestrogen. Likewise, another treatment that’s considered a risk factor is chest radiation therapy. Radiation is one of the known carcinogens of cancer, causing cells to mutate. Therefore, elevated levels of radiation could increase the risk for a patient. Other factors such as obesity, age and liver disease should also be carefully considered. As you can see, the list of risk factors for men is abundant, so why is it that breast cancer is still more present in women? And why is the general male public less aware of these risks, as they are for women? The answer to the first question is easy enough. Although the list of risk factors for breast cancer in men seems extensive, it is even longer for women. Furthermore, women are considered at higher risk as certain risk factors that both men and women share are more prevalent in women. For instance, oestrogen is produced in larger quantities by women. Additionally, a higher proportion of women are taking hormone replacement therapy drugs. Hormone replacement therapy (HRT) drugs are usually given to post-menopausal women to supplement more hormones, such as oestrogen. In the 90s alone, one study found that 22% of post-menopausal women took HRT whilst another study found that 51% of women have discussed taking the drug with their doctors. Meanwhile, the number of men taking HRT is much smaller, and usually these have a lower quantity of oestrogen, focusing more on testosterone. Although it is important to consider that within this time, incidences of individuals taking the hormones could change as the culture, awareness and research into hormone therapy changes. The second question, on the other hand, is slightly more complicated to answer. Of course, regardless of the rarity and prevalence of a condition in the population, the aim would be to treat and cure all. However, despite the significant impact and importance the NHS has on British healthcare, its limited resources meant that the most pressing and widespread issues were given priority. For instance, concentrating resources towards the C-19 virus during the last few years. Similarly, all healthcare systems globally are under constant pressure of this public health issue, managing its resources. Nevertheless, this does not mean that treating and raising awareness towards male breast cancer is less urgent and necessary. Another issue is the misinformation towards male breast cancer. In March 2023, a study in the American Journal of Men’s Health found that 61.1% of the participants (a total of 270 women and 141 men) were unaware that men could, in theory, have breast cancer. If we think about breast cancer, it is in many incorrect ways associated with femininity, perhaps from the organ it is found it arises on and to the colour (pink) used to represent breast cancer. Therefore, it all boils down to a convenient misconception, often following illogical stereotypes, that “large, strong, macho men” would never have this “women-only condition”. But how do we diagnose men with a condition they may not even know they could have? Following the process for diagnoses, specialists may recommend men with a strong family history to do regular screenings from the age of 35. Whilst screening is found to be an effective method when diagnosing women, its success in men is limited. For a majority of men, their process for diagnosis will start by noticing symptoms. Symptoms can be as obscure as a “different feel” to the breast tissue, or something more visible like a lump or hard mass. In theory, this would encourage men to approach their GPs which can then lead to the next steps of screening. However, many go seek experts late, often when seriously ill. This can both be explained culturally (such as Hispanics) and generationally, where older generations avoid medical consultations. This is very dangerous, as men often only received an official diagnosis of breast cancer six months after noticing symptoms, allowing the cancer to significantly grow within this time. On the other hand, an early diagnosis can allow for a swifter start to treatment, greater possibilities in treatment options, and could be less brutal for the patient. Hence, a better chance of treatment success and recovery. In summary, the procedures for the treatment of breast cancer in men do exist. However, for this treatment to be effective, healthcare professionals could consider increasing the awareness of the importance of regular screenings and appointments for early treatment. Overall, breast cancer in men is indeed rare. However, one must not overlook its consequences or its significance solely due to statistics. Breast cancer in men impacts many lives of both the patient and their families. Understanding the risks and the process for diagnosis could be essential in the early treatment of male patients. However, a further understanding of the astigmatisms and culture around breast cancer could be useful when educating the public on this condition. This article used “men” and “women” when describing breast cancer in patients. However, note that many individuals may not identify within these categories but could still be diagnosed and affected by breast cancer. Written by Inês Isabel Couto André ------------------ Learn more about this disease with Against Breast Cancer Take action and donate to Breast Cancer UK , and Cancer Research UK ------------------ Related articles: New radiation therapy to treat cancer / Apocrine carcinoma (a rare form of breast cancer) / Novel neuroblastoma driver for therapeutics Project Gallery

It's in the diet Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How epigenetic modification gives the queen bee her crown 23/01/25, 11:52 Last updated: Published: 26/11/23, 10:46 It's in the diet Honey bee colonies are comprised of three kinds of adult bees: workers, drones and a single queen. While all drones are male, the queen and the worker bees are female. Within the female population, only the queen bee is fertile and is thus responsible for laying eggs which are fertilised by drones. Additionally, a queen bee is larger than worker bees and produces pheromones to allow the colony to function. However, worker and queen bees are genetically identical, so how is it possible that they are so fundamentally different? ( Figure 1 ) The answer lies in epigenetic modification , defined as the alteration in gene function without a change in the DNA sequence. Types of epigenetic regulation include histone modification, DNA methylation and action of noncoding RNA. The honey bee Apis mellifera is amongst the many species that can produce different characteristics of organisms using the same genome. The mechanism by which honey bees do this derives from epigenetic modification resulting from the difference in diet during larval development. All larvae feed on royal jelly during the first three days of their development ( Figure 2 ). However, worker larvae will then feed on a diet of honey and pollen, which constitutes worker jelly. In comparison, the queen larva maintains a diet of royal jelly; this is a complex mixture produced by nurse bees and contains water, crude protein, monosaccharides, and fatty acids. Subsequently, the difference in dietary intake provides information to facilitate the correct epigenome which in turn allows correct transcription. Thus, key studies have taken place to investigate the effect of epigenetic marks on the development of bees. DNA methyltransferase DNMT3 is responsible for the methylation of DNA and is a repressive mark; a study found that the silencing of DNMT3 resulted in worker larvae developing into queens that had developed ovaries. Consequently, this shows that royal jelly gives information to larvae destined to be queens that can be interpreted to apply the correct epigenome. Additionally, certain histone deacetylase inhibitors have been observed in royal jelly including the compound 10 HDA and phenylbutyrate. Histone acetylation within regions of the genome results in chromatin opening; acetylation is associated with active regions. HDACi activity will inhibit the removal of such acetylation and maintain open regions of DNA. However, note that worker bees are not just a repressed version of queen bees, as they have overexpressed genes of their own to facilitate their specific behaviours. On examination of the methylome (see Figure 3 ), different genes were identified as being hypo- or hyper- methylated within worker vs queen bees. See the table below for a detailed analysis of worker and queen bees on days 3-5 of development. How exactly the specificity of epigenetic modifications is accomplished is not completely realised. To exemplify this, DNMTs do not have specificity, and thus, there must be an interplay between chromatin modifiers and cellular components to accomplish the correct recruitment of enzymes involved in epigenetic modification. However, it is clear that the epigenomes of workers vs queen bees are decidedly different and thus are the cause of different physiological and behavioural characteristics. Written by Isobel Cunningham Related articles: An introduction to epigenetics / Famine-induced epigenetic changes Project Gallery

From the eyes of a chemist Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Polypharmacy: the complex landscape of multiple medications 10/07/25, 10:30 Last updated: Published: 21/09/24, 15:48 From the eyes of a chemist The concurrent use of many medications by a patient, known as polypharmacy, poses a complex challenge to modern healthcare, especially for the elderly and those with chronic diseases. Polypharmacy raises the risk of adverse drug responses, drug interactions, and medication non-adherence, even though it is essential for managing complicated health concerns. To maximise patient outcomes and guarantee safe treatment regimens, it is crucial to recognise the chemical interactions and effects of different medications. The chemistry behind polypharmacy Polypharmacy stems from the intricate interactions between several chemicals in the human body. Every drug has unique chemical components intended to interact with biological targets in order to provide therapeutic benefits. Nevertheless, when several medications are taken at once, their combinations may have unexpected effects. Understanding polypharmacy requires a thorough understanding of pharmacokinetics—the way the body absorbs, distributes, metabolises, and excretes medications—and pharmacodynamics—the effects of pharmaceuticals on the body. For example, some pharmaceuticals may cause or inhibit the enzymes that metabolise other drugs, changing the levels of the drug and possibly increasing its toxicity or decreasing its effectiveness. Analytical methods in polypharmacy management Chemistry offers a number of analytical and instrumental techniques for efficient polypharmacy management. Drug levels in the blood are tracked using methods like mass spectrometry (MS) and high-performance liquid chromatography (HPLC) to make sure they stay within therapeutic ranges. These techniques support dose modifications by identifying possible medication interactions. Furthermore, it is impossible to exaggerate the importance of chemistry in the creation of drug interaction databases and predictive modelling instruments. By helping medical professionals foresee and minimise harmful medication interactions, these materials help to ensure patient safety. The role of healthcare professionals To successfully manage the complexity of polypharmacy, healthcare professionals—including physicians, chemists, and nurses—need to have a solid understanding of chemistry. Their expertise is essential for assessing each drug's requirement, taking possible interactions into account, and coming up with methods to make drug regimens easier to follow. Managing polypharmacy is especially important for chemists. They assess patients' prescriptions, look for any interactions, and suggest changes or substitutes using their knowledge of medicinal chemistry. Pharmacists who participate in collaborative care can greatly lower the hazards related to polypharmacy. Innovations in medication management Chemistry-driven advances in medical technology are improving polypharmacy management. Real-time alerts regarding potential drug interactions can be provided to prescribers through computerised physician order entry (CPOE) systems that are coupled with clinical decision support systems (CDSS). Optimising polypharmacy may also be possible with the emergence of personalised medicine, which adjusts drug regimens according to a patient's genetic profile. Conclusion Polypharmacy remains a significant challenge in healthcare, demanding a comprehensive understanding of chemistry and pharmacology to manage effectively. Healthcare practitioners can minimise the hazards associated with several medications and provide safer and enhanced patient care by utilising modern analytical methods, prediction technologies, and multidisciplinary teamwork. Written by Laura K Project Gallery