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Nanoparticles have unique properties Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nanoparticles: the future of diabetes treatment? 17/07/25, 10:52 Last updated: Published: 06/05/24, 13:20 Nanoparticles have unique properties Diabetes mellitus is a chronic metabolic disorder affecting millions worldwide. Given its myriad challenges, there is a substantial demand for innovative therapeutic strategies in its treatment. The global diabetic population is expected to increase to 439 million by 2030, which will impose a significant burden on healthcare systems. Diabetes occurs when the body cannot produce enough insulin, a hormone crucial for regulating glucose levels in the blood. This deficiency leads to increased glucose levels, causing long-term damage to organs such as the eyes, kidneys, heart, and nervous system, due to defects in insulin function and secretion. Nanoparticles have unique properties making them versatile in their applications and are promising to help revolutionise the future of the treatment of diabetes. This article will explore the potential of this emerging technology in medicine and will address the complexities and issues that arise with the management of diabetes. Nanoparticles have distinct advantages: biocompatibility, bioavailability, targeting efficiency and minimal toxicity, making them ideal for antidiabetic treatment. The drug delivery is targeted, making the delivery precise and efficient, avoiding off-target effects. Modifying nanoparticle surfaces enhances therapeutic efficacy, enabling targeted delivery to specific tissues and cells, while reducing systemic side effects. Another currently researched key benefit is real-time glucose sensing and monitoring, which addresses a critical aspect in managing diabetes, as nanoparticle-based glucose sensors can detect glucose levels with high sensitivity and selectivity. This avoids the use of invasive blood sampling and allows for continuous monitoring of glucose levels. These can be functionalised and integrated into wearable devices, or implanted sensors, making it convenient and reliable to monitor and to be able to optimum insulin therapy. Moreover, nanoparticle-based approaches show potential in tissue regeneration, aiding insulin production restoration. For example, in particular, nanomedicine is a promising tool in theranostics of chronic kidney disease (CKD), where one radioactive drug can diagnose and a second delivers the therapy. The conventional procedure to assess renal fibrosis is by taking a kidney biopsy, which is then followed by a histopathological assessment. This method is risky, invasive, and subjective, and less than 0.01 % of kidney tissue is examined which results in diagnostic errors, limiting the accuracy of the current screening method. The standard use of pharmaceuticals has been promising but can cause hypoglycaemia, diuresis, and malnutrition because of the low caloric intake. Nanoparticles offer a new approach to both diagnosis and treatment and are an attractive candidate for managing CKD as they can carry drugs and enhance image contrast, controlling the rate and location of drug release. In the treatment of this multifaceted disease, nanoparticle delivery systems seem to be a promising and innovative therapeutic strategy, with the variety in the methods of delivery. The range of solutions that are currently being developed are promising, from enhancing the drug delivery to monitoring the glucose level, to direct tissue regeneration. There is immense potential for the advancement of nanomedicines, helping improve patient outcomes, the treatment efficacy, and allowing the alleviation of the burden and side effects of the disorder. With ongoing efforts and innovation, the future treatment of diabetes can be greatly helped with the use of nanoparticles, and these advancements will improve strategies for the management and future treatment of diabetes. Written by Saanchi Agarwal Related articles: Pre-diabetes / Can diabetes mellitus become an epidemic? / Nanomedicine / Nanoparticles on gut health / Nanogels / Nanocarriers REFERENCES Lemmerman LR, Das D, Higuita-Castro N, Mirmira RG, Gallego-Perez D. Nanomedicine-Based Strategies for Diabetes: Diagnostics, Monitoring, and Treatment. Trends Endocrinol Metab. 2020 Jun;31(6):448-458. doi: 10.1016/j.tem.2020.02.001. Epub 2020 Mar 4. PMID: 32396845; PMCID: PMC7987328. Dehghani P, Rad ME, Zarepour A, Sivakumar PM, Zarrabi A. An Insight into the Polymeric Nanoparticles Applications in Diabetes Diagnosis and Treatment. Mini Rev Med Chem. 2023;23(2):192-216. doi: 10.2174/1389557521666211116123002. PMID: 34784864. Luo XM, Yan C, Feng YM. Nanomedicine for the treatment of diabetes-associated cardiovascular diseases and fibrosis. Adv Drug Deliv Rev. 2021 May;172:234-248. doi: 10.1016/j.addr.2021.01.004. Epub 2021 Jan 5. PMID: 33417981. L. Tillman, T. A. Tabish, N. Kamaly, A. El-Briri F, C. Thiemermann, Z. I. Pranjol and M. M. Yaqoob, Review Advancements in nanomedicines for the detection and treatment of diabetic kidney disease, Biomaterials and Biosystems, 2022, 6, 100047. J. I. Cutler, E. Auyeung and C. A. Mirkin, Spherical nucleic acids, J Am Chem Soc, 2012, 134, 1376–1391. Veiseh, O., Tang, B., Whitehead, K. et al. Managing diabetes with nanomedicine: challenges and opportunities. Nat Rev Drug Discov 14, 45–57 (2015). https://doi.org/10.1038/nrd4477 Project Gallery

Nanogels are tiny, water swollen polymer networks and encapsulate therapeutic agents Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nanogels: the future of smart drug delivery Last updated: 17/07/25, 10:54 Published: 17/07/25, 07:00 Nanogels are tiny, water swollen polymer networks and encapsulate therapeutic agents Nanomedicine is a rapidly advancing field, with nanogels emerging as promising innovations for drug delivery applications. Nanogels are soft nanoscale hydrogels that are transforming how we deliver drugs and treat diseases. Whilst hydrogels themselves have long been used in biomedical applications such as tissue engineering and wound healing, their relatively larger sizes (above 100 micrometres) limits their ability to interact with cells and cross biological barriers. Nanogels, however, are thousands of times smaller, and offer unique advantages as a result. What are nanogels? Nanogels are tiny, water swollen polymer networks and are made up of crosslinked polymer chains to form a 3D matrix. Nanogels can encapsulate therapeutic agents inside their porous core shell structure. This swelling allowing nanogels to carry payloads, such as drugs, proteins, nucleic acids and these cargo materials are protected from degradation in the body whilst enabling controlled and targeted delivery. Due to their small sizes, nanogels can penetrate tissues and even enter cells, which overcomes the limitations faced with hydrogels. The surface of nanogels can also be engineered for specificity, to allow for precise targeting of drugs to receptors on diseased cells or inflamed tissues. Advantages over other nanocarriers Compared to liposomes and polymeric micelles, nanogels have a larger inner surface, which means they can carry more payload. The higher loading capacity improves the therapeutic efficiency whilst reducing the risks of side effects cause by off-target drug release. Nanogels also undergo the enhanced permeability and retention (EPR) effect - a phenomenon where the nanoparticles naturally accumulate in tumour or inflamed tissues due to leaky blood vessel, and as a result this improves drug delivery to targeted disease sites. Stimuli responsive ‘smart’ nanogels A key feature of nanogels is their stimuli responsiveness, or ability to act as ‘smart’ materials. The nanogels can be designed to respond to environmental triggers such as changes in pH, temperature, light, redox conditions, pressure and more. This responsiveness enables controlled release of drugs exactly when and where they are needed12. For example, thermoresponsive nanogels can change their structure at body temperature or when exposed to localised heating, making them ideal for applications like wound healing and cancer therapy. This controlled release prevents premature drug leakage, reduces systemic toxicity and overall improves the precision of the treatment. The future of nanogels in medicine Nanogels have huge potential as customisable drug delivery systems to target specific disease systems. They are biocompatible, stable, and have high drug loading capacities and are stimuli responsive; these properties combined make them a powerful tool in applications such as targeted drug delivery and gene therapy. As nanomedicine research progresses, nanogels are set to revolutionise healthcare with smarter, safer and more targeted therapies. Written by Saanchi Agarwal Related articles: Nanomedicine / Nanoparticles and diabetes treatment / Nanoparticles and health / Nanocarriers / Silicon hydrogel REFERENCES L. Blagojevic and N. Kamaly, Nanogels: A chemically versatile drug delivery platform, Nano Today, 2025, 61, 102645. F. Carton, M. Rizzi, E. Canciani, G. Sieve, D. Di Francesco, S. Casarella, L. Di Nunno and F. Boccafoschi, Use of Hydrogels in Regenerative Medicine: Focus on Mechanical Properties, Int. J. Mol. Sci. , 2024, 25 , 11426. N. Rabiee, S. Hajebi, M. Bagherzadeh, S. Ahmadi, M. Rabiee, H. Roghani-Mamaqani, M. Tahriri, L. Tayebi and M. R. Hamblin, Stimulus-Responsive Polymeric Nanogels as Smart Drug Delivery Systems, Acta Biomater. , 2019, 92 , 1–18. N. Rabiee, S. Hajebi, M. Bagherzadeh, S. Ahmadi, M. Rabiee, H. Roghani-Mamaqani, M. Tahriri, L. Tayebi and M. R. Hamblin, Stimulus-Responsive Polymeric Nanogels as Smart Drug Delivery Systems, Acta Biomater. , 2019, 92 , 1–18. A. Vashist, G. P. Alvarez, V. A. Camargo, A. D. Raymond, A. Y. Arias, N. Kolishetti, A. Vashist, P. Manickam, S. Aggarwal and M. Nair, Recent advances in nanogels for drug delivery and biomedical applications, Biomater. Sci. , 2024, 12 , 6006–6018. K. S. Soni, S. S. Desale and T. K. Bronich, Nanogels: an overview of properties, biomedical applications and obstacles to clinical translation, J. Control. Release Off. J. Control. Release Soc. , 2016, 240 , 109–126. A. Bordat, T. Boissenot, J. Nicolas and N. Tsapis, Thermoresponsive polymer nanocarriers for biomedical applications, Adv. Drug Deliv. Rev. , 2019, 138 , 167–192. K. S. Soni, S. S. Desale and T. K. Bronich, Nanogels: an overview of properties, biomedical applications and obstacles to clinical translation, J. Control. Release Off. J. Control. Release Soc. , 2016, 240 , 109–126. T. Alejo, L. Uson, G. Landa, M. Prieto, C. Yus Argón, S. Garcia-Salinas, R. de Miguel, A. Rodríguez-Largo, S. Irusta, V. Sebastian, G. Mendoza and M. Arruebo, Nanogels with High Loading of Anesthetic Nanocrystals for Extended Duration of Sciatic Nerve Block, ACS Appl. Mater. Interfaces , 2021, 13 , 17220–17235. S. V. Vinogradov, Nanogels in The Race for Drug Delivery, Nanomed. , 2010, 5 , 165–168. Project Gallery

Global warming can lead to higher transmission rates of dengue fever Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The impacts of global warming on dengue fever Last updated: 08/10/25, 16:42 Published: 19/06/25, 07:00 Global warming can lead to higher transmission rates of dengue fever Introduction Dengue fever is a viral disease transmitted by two mosquitoes: Aedes aegypti and Aedes albopictus . These mosquitoes are called ‘vectors’. Symptoms of dengue fever include a sudden high fever and severe headaches, making it hard to diagnose. Transmission suitability is endemic, meaning the virus spreads where the conditions are suitable for the vectors to survive and reproduce for 10-12 months. This disease is endemic in the tropics, including much of Sub-Saharan Africa and Central Africa, Northern South America, Brazil, South and Southeast Asia, and parts of Northern Australia. The World Health Organisation (WHO) has stated that it is “the most important mosquito-borne viral disease in the world”. Dengue fever does not currently have a vaccine. There are many areas of transmission, and dengue fever impacts communities worse if they have weaker health systems. Severe dengue can be fatal, especially in children, who have a weaker immune system. Due to climate change and increasing temperatures, more areas will be habitable for the vectors in the future. This could lead to higher transmission rates of dengue fever. Researchers used a modelling approach using different datasets to make projections of the impact of changing temperatures and predict the future spread of dengue fever. They specifically looked at locations and months suitable for dengue transmission if conditions were suitable for both vectors. Method The researchers used temperature data from the Berkeley Earth Surface Temperatures dataset for the present day (2001-2020). They also used projected temperature data for 2050 based on the Coupled Model Intercomparison Project Phase 6 (CMIP6) projections for the socio-economic pathway (SSP) 1-2.6 scenario and SSP5-8.5 scenario, as used in the Intergovernmental Panel on Climate Change Sixth Assessment Report. The SSP1-2.6 scenario is the best-case scenario and assumes international policy agreements and emissions reductions will be followed, limiting the average global temperature to 1.5 °C above pre-industrial levels. The SSP5-8.5 scenario is the “business as usual” scenario and assumes that continued fossil fuel use and development will occur. Researchers used the most recent climate projections from the CMIP6, which gave an up-to-date, holistic view of the impact of potential differences between climate change trajectories on vulnerable populations. This information can be used to support climate change mitigation strategies and disease prevention and control. Thermal limits for the mosquito vectors used in this study were 19.9 - 29.4 °C for Aedes aegypti and 21.3 - 34 °C for Aedes albopictus , since the vectors can only survive and reproduce within these temperatures. Modelling the thermal limits of both vectors, instead of just one, made the analysis more comprehensive. The researchers also applied an aridity mask using the Normalised Difference Vegetation Index (NDVI), which excluded areas too dry for mosquito survival and reproduction. They then applied the thermal limits and aridity mask to the climate data to predict areas with suitable conditions for the vectors and estimate the number of months suitable for transmission. Using aridity masks (previously only done with malaria) enhanced the model's accuracy because moisture is an important factor for mosquito breeding. Results Figure 1 shows that under the SSP1-2.6 (best-case) scenario, there will be new suitability for dengue transmission in temperate regions by 2050, lasting about 1 to 2 months. In addition, northwestern South America could see increases of up to 5 months of new suitability, and Eastern Africa up to 6 months of new suitability. In addition, eastern and southern Central America, central and northwestern South America, northern Australia, and parts of Southeast Asia are also becoming suitable for year-round transmission. Figure 2 shows that under the SSP5-8.5 (“business as usual”) scenario, areas will become suitable for year-round transmission in similar locations as under the SSP1-2.6 scenario by 2050. Dengue transmission suitability could increase by up to 6 months in Eastern Africa, and up to 10 months in parts of northwestern South America. Areas as far north as the Arctic Circle also have new suitability under this scenario. This demonstrates that climate change could result in the expansion of areas and the length of time during which dengue fever transmission is possible. Evaluation It’s essential to also acknowledge the study's limitations. For example, the model did not account for other variables impacting disease transmission, such as mosquito adaptation and extreme weather. The potential adaptation of mosquitoes and parasites to changing environmental conditions could alter transmission dynamics. In addition, extreme weather events, such as heavy rain, could eliminate breeding sites. Furthermore, the method of using modelling and projections is unreliable, because many things could change between now and 2050. For example, there could be temperature fluctuations, or temperatures could fall between SSP1-2.6 and SSP5-8.5, rather than being fixed in either scenario. This could affect the reliability of predicting future dengue fever transmission suitability. The study also did not include aridity projections under climate change scenarios. As future projections of NDVI are not currently available, NDVI values for 2020 were held constant for the 2050 projections. There will likely be changes in aridity by 2050, which will affect mosquito reproduction and dengue transmission. Nevertheless, this study's results are still important because they suggest that with increasing climate change, dengue fever transmission could increase, which would be a public health issue. Further listening and reading If you would like to know more about dengue fever, consider listening to this short 5-minute podcast from the World Health Organisation. If you would like to know more about the impacts of climate change on health, consider listening to this podcast , also from the World Health Organisation. If you would like to know more about the impacts of climate change on neglected tropical diseases (NTDs), consider reading the full open-access paper mentioned in this article . Written by Naoshin Haque Related articles: Potential vaccine for malaria / Correlation between HDI and mortality rate / Healthcare challenges during civil war in Sudan / Rising temperatures impacts 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

Recent prospects for carbon monoxide indicate so Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can carbon monoxide unlock new pathways in inflammation therapy? 20/03/25, 12:03 Last updated: Published: 01/09/24, 10:31 Recent prospects for carbon monoxide indicate so Carbon monoxide (CO) is a colourless, odourless and tasteless gas which is a major product of the incomplete combustion of carbon-containing compounds. The toxic identity CO stems from its strong affinity for the haemoglobin in our blood which is around 300 times as strong as the affinity of oxygen. As a result, once the gas is inhaled, CO binds to the haemoglobin instead and reduces the amount of oxygen our blood can transport, which can cause hypoxia (low levels of oxygen in tissue) and dizziness, eventually leading to death. However, an intriguing fact is that CO is also endogenously produced in our body, due to the degradation of haem in the blood. Moreover, recent prospects for CO indicate that it may even be developed as an anti-inflammatory drug. How CO is produced in the body See Figure 1 Haem is a prosthetic (non-peptide) group in haemoglobin, where the oxygen binds to the iron in the molecule. When red blood cells reach the end of their lifespan of around 120 days, they are broken down in a reaction called haemolysis. This occurs in the bone marrow by macrophages that engulf the cells, which contain the necessary haem-oxygenase enzyme. Haem-oxygenase converts haem into CO, along with Fe2+ and biliverdin, the latter being converted to bilirubin for excretion. The breakdown of haem is crucial because the molecule is pro-oxidant. Therefore, free haem in the blood can lead to oxidative stress in cells, potentially resulting in cancers. Haem degradation also contributes to the recycling of iron for the synthesis of new haem molecules or proteins like myoglobin. This is crucial for maintaining iron homeostasis in the body. The flow map illustrates haemolysis and the products produced, which either protect cells from further stress or result in cell injury. CO can go on to induce anti-inflammatory effects- see Figure 2 . Protein kinases and CO Understanding protein kinases is crucial before exploring carbon monoxide (CO) reactions. Protein kinases phosphorylate (add a phosphate group to) proteins using ATP. Protein kinases are necessary to signal the release of a hormone or regulating cell growth. Each kinase has two regulatory (R) subunits and two catalytic (C) subunits. ATP as a reactant is usually sufficient for protein kinases. However, some kinases require additional mitogens – specific activating molecules like cytokines (proteins regulating immune cell growth), that are involved in regulating cell division and growth. Without the activating molecules, the R subunits bind tightly to the C subunits, preventing phosphorylation. Research on obese mice showed that CO binding to a Mitogen-Activated Protein Kinase (MAPK) called p38 inhibits inflammatory responses. This kinase pathway enhances insulin sensitivity, reducing obesity effects. The studies used gene therapy, modifying haem-oxygenase levels in mice. Mice with reduced haem-oxygenase levels had more adipocytes (fat-storing cells) and increased insulin resistance, suggesting CO treatment potential for chronic obstructive pulmonary disease (COPD), which causes persistent lung inflammation and results in 3 million deaths annually. Carbon-monoxide-releasing molecules As a result of these advancements, specific CO-releasing molecules (CORMs) have been developed to release carbon monoxide at specific doses. Researchers are particularly interested in the ability of CORMs to regulate oxidative stress and improve outcomes in conditions during organ transplantation, and cardiovascular diseases. Advances in the design of CORMs have focused on improving their stability, and targeted release to specific tissues or cellular environments. For instance, CORMs based on transition metals like ruthenium, manganese, and iron have been developed to enhance their efficacy and minimize side effects. This is achieved through carbon monoxide forming a stable ‘ligand’ structure with metals to travel in the bloodstream. Under an exposure to light or a chemical, or even by natural breakdown, these structures can slowly distribute CO molecules. Although the current research did not find any notable side effects within mouse cells, this does not reflect the mechanisms in human organ systems, therefore there is still a major risk of incompatibility due to water insolubility and toxicity issues. These problems could lead to potentially lead to disruption in the cell cycle, which may promote neurodegenerative diseases. Conclusion: the future of carbon monoxide Carbon monoxide has transitioned from being a notorious toxin to a valuable therapeutic agent. Advances in CO-releasing molecules have enabled its safe and controlled use, elevating its anti-inflammatory and protective properties to treat various inflammatory conditions effectively. This shift underpins the potential of CO to revolutionise inflammation therapy. It is important to remember that while carbon monoxide-releasing molecules (CORMs) have potential in controlled therapeutic settings, carbon monoxide gas itself remains highly toxic and should be handled with extreme caution to avoid serious health risks. Written by Baraytuk Aydin Related articles: Schizophrenia, inflammation and ageing / Kawasaki disease REFERENCES Different Faces of the Heme-Heme Oxygenase System in Inflammation - Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/The-colorimetric-actions-of-the-heme-HO-system-heme-oxygenase-mediated-heme-degradation_fig3_6531826 (accessed 11 Jul, 2024). Nath, K.A. (2006) Heme oxygenase-1: A provenance for cytoprotective pathways in the kidney and other tissues, Kidney International. Available at: https://www.sciencedirect.com/science/article/pii/S0085253815519595 (Accessed: 12 July 2024). Gáll, T. et al. (2020) ‘Therapeutic potential of carbon monoxide (CO) and hydrogen sulfide (H2S) in hemolytic and hemorrhagic vascular disorders—interaction between the heme oxygenase and H2S-producing systems’, International Journal of Molecular Sciences, 22(1), p. 47. doi:10.3390/ijms22010047. Venkat, A. (2024) Protein kinase, Wikipedia. Available at: https://en.wikipedia.org/wiki/Protein_kinase (Accessed: 12 July 2024). Goebel, U. and Wollborn, J. (2020) Carbon monoxide in intensive care medicine-time to start the therapeutic application?! - intensive care medicine experimental, SpringerOpen. Available at: https://icm-experimental.springeropen.com/articles/10.1186/s40635-020-0292-8 (Accessed: 07 July 2024). Bansal, S. et al. (2024) ‘Carbon monoxide as a potential therapeutic agent: A molecular analysis of its safety profiles’, Journal of Medicinal Chemistry, 67(12), pp. 9789–9815. doi:10.1021/acs.jmedchem.4c00823. DeSimone, C.A., Naqvi, S.L. and Tasker, S.Z. (2022) ‘Thiocormates: Tunable and cost‐effective carbon monoxide‐releasing molecules’, Chemistry – A European Journal, 28(41). doi:10.1002/chem.202201326. Project Gallery

Unmasking the complexities of the condition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Crohn's disease 09/07/25, 14:01 Last updated: Published: 22/03/24, 20:16 Unmasking the complexities of the condition Introduction Crohn's disease is a chronic inflammatory condition that primarily targets the gastrointestinal tract. While it commonly afflicts individuals aged 20 to 50, it can also manifest in children and older adults, albeit less frequently. Symptoms of Crohn's disease vary widely and may include skin lesions spanning from the mouth to the anus, along with prevalent issues such as diarrhoea, abdominal pain, weight loss, rectal bleeding, fatigue, and fever. Diagnosis Diagnosing Crohn's disease can be challenging due to its similarity to other conditions. However, specific symptoms like bloody diarrhoea, iron deficiency, and unexplained weight loss are significant indicators that warrant further investigation by a gastroenterologist. Many tests that can confirm Crohn’s disease: Endoscopy: endoscopy, including procedures like colonoscopy and upper endoscopy, is a dependable method for diagnosing Crohn's disease and distinguishing it from other conditions with similar symptoms. During an endoscopy, a thin tube called an endoscope is inserted into the rectum to visually inspect the entire gastrointestinal tract and collect small tissue samples for further analysis. Imaging: Computed tomography (CT), magnetic resonance imaging (MRI), and ultrasonography are valuable tools for assessing disease activity and detecting complications associated with Crohn's disease. These imaging techniques can examine areas of the gastrointestinal tract that may not be accessible via endoscopy, providing comprehensive insights into the condition's progression and associated issues. Laboratory testing: various laboratory tests, including complete blood count, C-reactive protein levels, pregnancy tests, and stool samples, are conducted to screen for Crohn's disease. These tests are typically the initial step in diagnosis, helping to avoid the necessity for more invasive procedures like endoscopies and imaging. Additionally, laboratory testing may involve assessing inflammatory markers such as erythrocyte sedimentation rate (ESR) and faecal calprotectin to further aid in diagnosis and monitoring of the condition. Treatment and prevention While there is currently no cure for Crohn’s disease, numerous treatments have been developed over time to effectively manage symptoms and sometimes even induce remission. When determining a treatment plan for patients, factors such as age, specific symptoms, and the severity of inflammation are taken into careful consideration. Corticosteroids and immunomodulators are medications commonly used to manage Crohn’s disease. Corticosteroids work by reducing inflammation and suppressing the immune system, typically employed to address flare-ups due to their rapid action. However, they are not suitable for long-term use as they may lead to significant side effects. In contrast, maintenance therapy often involves immunomodulators such as azathioprine, methotrexate, or biologic agents like anti-TNF drugs (such as infliximab or adalimumab). These medications target specific immune pathways to enhance the effectiveness of the immune system. Research indicates that immunomodulators are associated with fewer adverse effects compared to corticosteroids and are effective in maintaining remission. Monoclonal antibody treatment is another approach used to manage symptoms and sustain remission in Crohn's disease. These therapies are categorised as biologic treatments, targeting precise molecules involved in inflammation and the immune response. Despite carrying certain risks, such as infections, the likelihood of developing cancer with these treatments is typically deemed low. Crohn’s disease frequently leads to complications that may necessitate surgical intervention. Gastrointestinal surgeries can greatly alleviate symptoms and enhance the quality of life for patients. However, surgery is usually considered only when medical therapy proves insufficient in controlling the disease or when complications arise. Although the exact cause of Crohn’s disease remains uncertain, factors such as genetics, immune system dysfunction, and environmental influences are believed to contribute to its development. While there is no definitive evidence pinpointing specific causative factors, numerous studies suggest potential links to an unhealthy diet and lifestyle, dysbiosis (imbalance of healthy and unhealthy gut bacteria), smoking, and a family history of the disease. Therefore, it is crucial to minimise exposure to these risk factors in order to decrease the likelihood of developing Crohn’s disease. Written by Sherine Abdul Latheef Related articles: the gut microbiome / the dopamine connection / Diverticular disease / Mesenchymal stem cells REFERENCES Veauthier B, Hornecker JR. Crohn's Disease: Diagnosis and Management. Am Fam Physician. 2018;98(11):661-669. Torres J, Mehandru S, Colombel JF, Peyrin-Biroulet L. Crohn's disease. Lancet. 2017;389(10080):1741-1755. doi:10.1016/S0140-6736(16)31711-1 Mills SC, von Roon AC, Tekkis PP, Orchard TR. Crohn's disease. BMJ Clin Evid. 2011;2011:0416. Published 2011 Apr 27. Sealife, A. (2024) Crohn’s disease, Parkland Natural Health. Available at: https://wellness-studio.co.uk/crohns-disease/ (Accessed: 09 March 2024). How to stop anxiety stomach pain & cramps (2022) Calm Clinic - Information about Anxiety, Stress and Panic. Available at: https://www.calmclinic.com/anxiety/symptoms/stomach-pain (Accessed: 09 March 2024). Project Gallery

Exploring the distinctive features that define and disrupt the brain Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A deep dive into the hallmarks defining Alzheimer’s disease 08/07/25, 14:39 Last updated: Published: 06/11/24, 12:02 Exploring the distinctive features that define and disrupt the brain The progressive decline in neurocognition, resulting in a detrimental effect on one’s activities of daily living, is referred to as dementia. It typically affects people over the age of 65. Multiple theories have been proposed to explain the pathogenesis of Alzheimer’s disease (AD), including the buildup of amyloid plaques in the brain and the formation of neurofibrillary tangles (NFT) in cells. Understanding the pathophysiology of AD is imperative to the development of therapeutic strategies. Therefore, this article will outline the major hallmarks and mechanisms of AD. Hallmark 1: amyloid plaques One of the most widely accepted hypotheses for AD is the accumulation of amyloid beta protein (Aβ) in the brain. Aβ is a 4.2 kDa peptide consisting of approximately 40–42 amino acids, originating from a precursor molecule called amyloid precursor protein. This process, defined as amyloidosis, is strongly linked to brain aging and neurocognitive decline. How do the amyloid plaques form? See Figure 1 . Reasons for the accumulation of amyloid plaques: Decreased autophagy: Amyloid proteins are abnormally folded proteins. Autophagy in the brain is primarily carried out by neuronal and glial cells, involving key structures known as autophagosomes and lysosomes. When autophagy becomes downregulated, the metabolism of Aβ is impaired, eventually resulting in plaque buildup. Overproduction of acetylcholinesterase (AChE): Acetylcholine (Ach) is the primary neurotransmitter involved in memory, awareness, and learning. Overproduction of ACHE by astrocytes into the synaptic cleft can lead to excessive breakdown of Ach, with detrimental effects on cognition. Reduced brain perfusion: Blood flow delivers necessary nutrients and oxygen for cellular function. Reduced perfusion can lead to “intracerebral starvation”, depriving cells of the energy needed to clear Aβ. Reduced expression of low-density lipoprotein receptor-related protein 1: Low-density lipoprotein receptor-related protein 1 (LRP1) receptors are abundant in the central nervous system under normal conditions. They are involved in speeding up the metabolic pathway of Aβ by binding to its precursor and transporting them from the central nervous system into the blood, thereby reducing buildup. Reduced LRP1 expression can hinder this process, leading to amyloid buildup. Increased expression of the receptor for advanced glycation end products (RAGE): RAGE is expressed on the endothelial cells of the BBB, and its interaction with Aβ facilitates the entry of Aβ into the brain. Hallmark 2: neurofibrillary tangles See Figure 2 Neurofibrillary tangles are excessive accumulations of tau protein. Microtubules typically support neurons by guiding nutrients from the soma (cell body) to the axons. Furthermore, tau proteins stabilise these microtubules. In AD, signalling pathways involving phosphorylation and dephosphorylation cause tau proteins to detach from microtubules and stick to each other, eventually forming tangles. This results in a disruption in synaptic communication of action potentials. However, the exact mechanism remains unclear. Recent studies suggest an interaction between Aβ and tau, where Aβ can cause tau to misfold and aggregate, forming neurofibrillary tangles inside brain cells. Both Aβ and tau can self-propagate, spreading their toxic effects throughout the brain. This creates a vicious cycle, where Aβ promotes tau toxicity, and toxic tau can further exacerbate the harmful effects of Aβ, ultimately causing significant damage to synapses and neurons in AD. Hallmark 3: neuroinflammation Microglia are the primary phagocytes in the central nervous system. They can be activated by dead cells and protein plaques, where they initiate the innate immune response. This involves the release of chemokines to attract other white blood cells and the activation of the complement system which is a group of proteins involved in initiating inflammatory pathways to fight pathogens. In AD, microglia bind to Aβ via various receptors. Due to the substantial accumulation of Aβ, microglia are chronically activated, leading to sustained immune responses and neuroinflammation. Conclusion The contributions of amyloid beta plaques, neurofibrillary tangles and chronic neuroinflammation provide a framework for understanding the pathophysiology of AD. AD is a highly complex condition with unclear mechanisms. This calls for the need of continued research in the area as it is crucial for the development of effective treatments. Written by Blessing Amo-Konadu Related articles: Alzheimer's disease (an overview) / CRISPR-Cas9 to potentially treat AD / Sleep and memory loss REFERENCES 2024 Alzheimer’s Disease Facts and Figures. (2024). Alzheimer’s & dementia, 20(5). doi:https://doi.org/10.1002/alz.13809. A, C., Travers, P., Walport, M. and Shlomchik, M.J. (2001). The complement system and innate immunity. [online] Nih.gov. Available at: https://www.ncbi.nlm.nih.gov/books/NBK27100/ . Bloom, G.S. (2014). Amyloid-β and tau: the Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA neurology, [online] 71(4), pp.505–8. doi:https://doi.org/10.1001/jamaneurol.2013.5847. Braithwaite, S.P., Stock, J.B., Lombroso, P.J. and Nairn, A.C. (2012). Protein Phosphatases and Alzheimer’s Disease. Progress in molecular biology and translational science, [online] 106, pp.343–379. doi:https://doi.org/10.1016/B978-0-12-396456-4.00012-2. Heneka, M.T., Carson, M.J., El Khoury, J., Landreth, G.E., Brosseron, F., Feinstein, D.L., Jacobs, A.H., Wyss-Coray, T., Vitorica, J., Ransohoff, R.M., Herrup, K., Frautschy, S.A., Finsen, B., Brown, G.C., Verkhratsky, A., Yamanaka, K., Koistinaho, J., Latz, E., Halle, A. and Petzold, G.C. (2015). Neuroinflammation in Alzheimer’s disease. The Lancet. Neurology, 14(4), pp.388–405. doi:https://doi.org/10.1016/S1474-4422(15)70016-5. Kempf, S. and Metaxas, A. (2016). Neurofibrillary Tangles in Alzheimer′s disease: Elucidation of the Molecular Mechanism by Immunohistochemistry and Tau Protein phospho- proteomics. Neural Regeneration Research, 11(10), p.1579. doi:https://doi.org/10.4103/1673-5374.193234. Kumar, A., Tsao, J.W., Sidhu, J. and Goyal, A. (2022). Alzheimer disease. [online] National Library of Medicine. Available at: https://www.ncbi.nlm.nih.gov/books/NBK499922/. Ma, C., Hong, F. and Yang, S. (2022). Amyloidosis in Alzheimer’s Disease: Pathogeny, Etiology, and Related Therapeutic Directions. Molecules, 27(4), p.1210. doi:https://doi.org/10.3390/molecules27041210. National Institute on Aging (2024). What Happens to the Brain in Alzheimer’s Disease? [online] National Institute on Aging. Available at: https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/what-happens-brain- alzheimers-disease. Stavoe, A.K.H. and Holzbaur, E.L.F. (2019). Autophagy in Neurons. Annual Review of Cell and Developmental Biology, 35(1), pp.477–500. doi: https://doi.org/10.1146/annurev-cellbio-100818-125242 . Project Gallery

Looking at p53 mutations and cancer predisposition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Decoding p53: the guardian against cancer 09/07/25, 14:03 Last updated: Published: 23/11/23, 11:38 Looking at p53 mutations and cancer predisposition Being a tumour suppressor protein, p53 encoded by the TP53 gene plays a critical role in regulating cell division and preventing the formation of tumours. Its function in maintaining genome stability is vital in inhibiting cancer development. Understanding p53 Located on chromosome locus 17p13.1, TP53 encodes the p53 transcription factor 1. Consisting of three domains, p53 can directly initiate or suppress the expression of 3661 different genes involved in cell cycle control and DNA repair 2. With this control, p53 can influence cell division on a massive scale. Cancer is characterised by uncontrolled cell division, which can occur due to accumulated mutations in either proto-oncogenes or tumour suppressor genes. Wild-type p53 can repair mutations in oncogenes such that they will not affect cell division. However, if p53 itself is mutated, then its ability to repair DNA and control the cell cycle is inhibited, leading to the emergence of cancer. Mutations in TP53 are actually the most prevalent genetic alterations found in patients with cancer. The mechanisms by which mutated p53 leads to cancer are manifold. One such mechanism is p53’s interaction with p21. Encoded by CDKN1A , p21 is activated by p53 and prevents cell cycle progression by inhibiting the activity of cyclin-dependent kinases (CDKs). Therefore, we can see that a non-functional p53 would lead directly to uncontrolled cell division and cancer. Clinical significance The importance of p53 in preventing cancer is highlighted by the fact that individuals with inherited TP53 mutations (a condition known as Li-Fraumeni syndrome or LFS) have a significantly greater risk of developing any cancer. These individuals inherit one defective TP53 allele from one parent, making them highly susceptible to losing the remaining functional TP53 allele, ultimately leading to cancer. Loss of p53 also endows cells with the ability to ignore pro-apoptotic signals such that if a cell becomes cancerous, it is far less likely to undergo programmed cell death 3. Its interactions with the apoptosis-inducing proteins Bax and Bak, are lost when mutated, thus leading to cellular apoptosis resistance. The R337H mutation in TP53 is an example of the founder effect at work. The founder effect refers to the loss of genetic variation when a large population descends from a smaller population of fewer individuals. The descendants of the initial population are much more likely to harbour genetic variations that are less common in the species as a whole. In southern Brazil, the R337H mutation in p53 is present at an unusually high frequency 4 and is thought to have been introduced by European settlers several hundred years ago. It is responsible for a widespread incidence of early-onset breast cancers, LFS, and paediatric adrenocortical tumours. Interestingly, individuals with this mutation can trace their lineage back to the group of European settlers that set foot in Brazil hundreds of years ago. Studying p53 has enabled us to unveil its intricate web of interactions with other proteins and molecules within the cell and unlock the secrets of cancer development and potential therapeutic strategies. By restoring or mimicking the functions of p53, we may be able to provide cancer patients with some relief from this life-changing condition. Written by Malintha Hewa Batage Related articles: Zinc finger proteins / Anti-freeze proteins Project Gallery

A hereditary neurodegenerative disorder Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Huntington's disease 25/03/26, 16:52 Last updated: Published: 18/10/23, 16:12 A hereditary neurodegenerative disorder Huntington’s disease (HD) is a neurodegenerative disorder causing cognitive decline, behavioural difficulties, and uncontrollable movements. It is a hereditary disease that has a devastating effect on the individual’s life and unfortunately is incurable. Genetic component What may come as a surprise, is that in everyone’s genetics there are two copies (one from each parent) of the Huntingtin’s gene coding for the Huntingtin protein. This gene is coded by CAG repeats. In healthy genes, the CAG sequence is repeated between 10 and 26 times. However, if the gene is faulty, CAG repeats over 40 times resulting in a dysfunctional Huntingtin protein. The disease is autosomal dominant meaning regardless of gender, if either parent is a carrier, their child has a 50% chance of inheriting the faulty gene. REMINDER: because the gene is dominant, it means those who inherit even one copy will develop the disease Effect on the brain The faulty Huntingtin protein accumulates in cells, leading to cell death and damage to the brain. If you were to look at the brains of individuals with Huntington’s Disease, you would see a reduction in volume of the caudate and putamen. These areas are part of the striatum, which is a subdivision of the basal ganglia, involved in fine tuning our voluntary movements, i.e., reaching out to grab a cup. As the disease progresses, this atrophy can extend to other areas of the brain including the thalamus, frontal lobe, and cerebellum. Symptoms The symptoms normally manifest in three categories: motor, cognitive and psychiatric. We know that the basal ganglia is involved in our voluntary movement, so the damage causes one of the most visible symptoms in HD- uncontrollable and jerky movements. Cognitive symptoms include personality changes, difficulties with planning and attention. There can also be impairments to how those with HD recognise emotions- all these symptoms can interact to make social interaction more difficult. Finally, the psychiatric symptoms often seen include irritability and aggression, depression, anxiety, and apathy. Impact on life and family At the age when diagnosis usually occurs (around 30 years old), patients are often buying houses, getting married and either having children or deciding to start a family. The diagnosis may change people's outlook on having children and can put a great psychological burden on them if they have unknowingly passed it along to those already born. Diagnosis also brings consequences to seemingly mundane, but incredibly important, issues such as gaining life insurance, with some companies not covering individuals with an official diagnosis. Subsequently this makes life harder for their families, as the patient will eventually be unable to work and there could be associated costs with the need for care facilities as the disease progresses. Unfortunately, this is a progressive neurodegenerative condition with no cure. The only treatment options available at present, are interventions which aim to alleviate the patients’ symptoms. Whilst these treatments will reduce the motor and psychiatric symptoms, they cannot stop the progression of Huntington’s disease. We have only scratched the surface on the impact Huntington’s disease has on a patient and their families. It is so important to understand ways in which everyone that is affected can be best supported during the disease progression, to give all those involved a better quality of life. Written by Alice Jayne Greenan Related articles: A potential gene therapy for HD / Epilepsy Project Gallery

The emperor penguin's life cycle is intertwined with sea ice freezing and melting over the year Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Emperor penguins, the kings of the ice Last updated: 29/03/26, 15:57 Published: 24/04/25, 07:00 The emperor penguin's life cycle is intertwined with sea ice freezing and melting over the year This is article no. 6 in a series on animal conservation. Next article: Protecting rock-wallabies in Australia . Previous article: Gorongosa National Park . In November 2024, a malnourished emperor penguin was spotted in Australia, over 2000 miles from its home in Antarctica. It is said to be the furthest north a wild emperor has ever been seen. While scientists do not know why or how the penguin ended up there, it sparked conversations about climate change and the survival of this fascinating species. This article will describe the characteristics of the emperor penguin, and how climate change could affect it. Introduction to emperor penguins Emperor penguins ( Aptenodytes forsteri ) are the largest living penguin species, weighing 20-40 kilograms and standing about 1 metre tall. It is estimated that there are around 260,000 breeding pairs of emperor penguins across 61 colonies, which are spread out along the entire coast of Antarctica. Their diet consists of krill, fish, and squid - and they can dive over 500m deep to find food. Emperor penguins are the only warm-blooded animal to breed during the Antarctic winter, one of the world's coldest and darkest times of the year. Therefore, they are adapted to the cold days, harsh winds, and high water pressure in which they live. For example, they have over 20 kinds of feathers - some of which help with waterproofing while swimming, and others help with thermal insulation. Many penguin species huddle together as juveniles to conserve body heat, but emperors are the only species to do so as adults. Thus, emperor penguins are a unique and ecologically fascinating species. Life cycle and fast ice The emperor penguin's life cycle is intertwined with sea ice freezing and melting over the year ( Figure 1 ). For most of the year, emperors live on fast ice, which are ice sheets floating on the sea but attached to the coast. The first reason they need fast ice is moulting, when emperor penguins replace all their feathers in late summer. They moult on ice because they cannot swim until their new layer of waterproof feathers has grown. Emperor penguins return to fast ice at the onset of winter to mate, lay eggs, and raise chicks. While one parent stays on the fast ice to look after the chick, the other parent goes to sea to find food for the family. The chick grows waterproof adult feathers for fast ice to break up in summer. At this point, the penguins live at sea until moulting time. This way, emperor penguin survival is linked to fast ice availability. Threat from climate change Because emperor penguins are so heavily dependent on fast ice, scientists are concerned about the potential impacts of global warming. Rising sea surface temperatures mean fast ice may not form long enough in the year for emperor penguins to complete their life cycle. In late 2022, sea ice was dramatically reduced in the Bellingshausen Sea in Antarctica, and 4 of the 5 nearby emperor penguin colonies had a failed breeding season. These failed seasons may become more common in the future with climate change. A 2020 study predicted that in the worst case climate scenario, 80% of penguin colonies will see population declines of over 90% by 2100. If international climate targets are met, only 19% of colonies are expected to decline that badly ( Figure 2 ). Because the International Union for Conservation of Nature classified emperors as Near Threatened, they do not meet Antarctica's criteria for being a protected species. Scientists have requested this conservation status be upgraded to better reflect the inability of emperor penguins to adapt or disperse away from the effects of climate change. Emperor penguins face no threats from humans other than global warming, so reducing greenhouse gas emissions is crucial to protect them. Conclusion Emperor penguins are charismatic creatures with unique adaptations to live during the cold Antarctic winter. Their survival is strongly linked to the availability of sea ice because they moult, breed, and care for their offspring on ice sheets. Global warming is making these ice sheets disappear, so emperor penguins must be monitored and protected to ensure survival through a changing climate. Written by Simran Patel Related articles: The Arctic Springtail / California Condors / Brain-climate connection REFERENCES CBS News. (2024) Malnourished emperor penguin that swam ashore in Australia 2,000 miles from home a quandary for rescuers. CBS News . Available from: https://www.cbsnews.com/news/emperor-penguin-australia-2000-miles-from-antarctic-ice-melting-climate-change/ (Accessed 11th November 2024). Fretwell, P.T., Boutet, A. & Ratcliffe, N. (2023) Record low 2022 Antarctic sea ice led to catastrophic breeding failure of emperor penguins. Communications Earth & Environment . 4 (1): 1–6. Garnier, J., Clucas, G., Younger, J., Sen, B., Barbraud, C., Larue, M., Fraser, A.D., Labrousse, S. & Jenouvrier, S. (2023) Massive and infrequent informed emigration events in a species threatened by climate change: the emperor penguins . Available from: https://hal.science/hal-03822288 (Accessed 10th November 2024). Hooper, S. (11th November 2024) Experts baffled after penguin shows up on beach 2,200 miles away from home Metro . Available from: https://metro.co.uk/2024/11/11/experts-baffled-penguin-shows-beach-2-200-miles-away-home-21970144/ (Accessed 11th November 2024). Fretwell, P. (2024) Four unreported emperor penguin colonies discovered by satellite. Antarctic Science , 36(4), 277–279. Jenouvrier, S. et al. (2020) The Paris Agreement objectives will likely halt future declines of emperor penguins. Global Change Biology . 26 (3): 1170–1184. Labrousse, S., Nerini, D., Fraser, A.D., Salas, L., Sumner, M., Le Manach, F., Jenouvrier, S., Iles, D. & LaRue, M. (2023) Where to live? Landfast sea ice shapes emperor penguin habitat around Antarctica. Science Advances . 9 (39): eadg8340. LaRue, M. et al. (2024) Advances in remote sensing of emperor penguins: first multi-year time series documenting trends in the global population. Proceedings of the Royal Society B: Biological Sciences . 291 (2018): 20232067. Le Maho, Y. (1977) The Emperor Penguin: A Strategy to Live and Breed in the Cold: Morphology, physiology, ecology, and behavior distinguish the polar emperor penguin from other penguin species, particularly from its close relative, the king penguin. American Scientist . 65 (6): 680–693. Trathan, P.N. et al. (2020) The emperor penguin - Vulnerable to projected rates of warming and sea ice loss. Biological Conservation . 241: 108216. Williams, C.L., Hagelin, J.C. & Kooyman, G.L. (2015) Hidden keys to survival: the type, density, pattern and functional role of emperor penguin body feathers. Proceedings of the Royal Society B: Biological Sciences . 282 (1817): 20152033. Project Gallery