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Conservation, diseases, animal behaviour, adaptation and survival. Expand your knowledge on the incredible diversity of life on Earth with these articles. Zoology Articles Conservation, diseases, animal behaviour, adaptation and survival. Expand your knowledge on the incredible diversity of life on Earth with these articles. You may also like: Biology , and Ecology Deception by African birds The species Dicrurus adsimilis uses deception by flexible alarm mimicry to target and carry out food-theft attempts An experiment on ochre stars Investigating the relative fitness of the species Pisaster ocharceus Orcinus orca A species report Rare zoonotic diseases We all know about COVID-19. But what about the other zoonotic diseases? Article #1 in a series on Rare diseases. Marine iguanas Their conservation The cost of coats 55 years of vicuna conservation in South America. Article #1 in a series on animal conservation around the world. Conserving the California condor These birds live on the west coast of North America. Article #2 in a series on animal conservation around the world. Emperor penguins Kings of ice. Article #6 in a series on animal conservation around the world. Protecting rock-wallabies in Australia A group of 25 animal species, and subspecies related to kangaroos. Article #7 in a series on animal conservation around the world. Do other animals get periods? Looking at menstruation in non-human animals e.g. monkeys, bats Same-sex attraction in non-human animals SSSB in birds, mammals, and invertebrates Changing sex in fish Why some fish change sex during their lifetimes

Delving into the impacts of gut bacteria on health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Gut Microbiome 11/07/25, 09:58 Last updated: Published: 04/04/24, 16:41 Delving into the impacts of gut bacteria on health Inflammatory Bowel Disease The microbiome is hugely important to human health, and has been shown to beneficial to digestion, the immune system and even our mental health when in good working condition. However, disruption to the balance of the microbial flora has likewise been associated with multiple diseases and poor general health. Dysbiosis, or a poor balance, of human microbiome communities has been implicated in a wide range of disease, such as cardiovascular disease, chronic inflammation, obesity and even mental health issues. A diverse and well-balanced microbial community is important for disease prevention, however modern over usage of antibiotics as well as poor diets low in dietary fibre and high in artificial additives can lead to compromised communities dominated by single pathogenic strains of bacteria. The human microbiome plays a critical role in overall health, from providing valuable metabolites to aiding the immune system. Friendly commensal bacteria colonise major regions in our gut, with characteristic diverse communities of microbes inhabiting them. These microbes occupy these niches and outcompete pathogenic organisms, actively preventing infection and disease. In this article we will be specifically looking into the link between the gut microbiome and Inflammatory Bowel disease (IBD), as this is currently one of the most well researched cases of a causal relationship between the microbiome and disease state. Dysbiosis and Disease state Disruption of the gut flora is associated with painful inflammation of the gastrointestinal tract, diagnosed as IBD. Crohn’s disease and Ulcerative Colitis are conditions under the umbrella term of IBD and cause painful swelling and eventually ulcers in the gastrointestinal tract. The exact cause of IBD remains unclear, with the true cause likely a combination of genetics, environmental factors and the gut microbiome. Evidence has come to light that shows a link between disease state and the gut dysbiosis, where they influence each other and are potentially both each other’s cause and effect. Successfully treating IBD has proved difficult; medications focus on alleviating inflammation or other symptoms as antibiotics have shown limited effectiveness in curing the disease. Antibiotics have even been suggested to weaken the immune system long-term, as evidence suggests that antibiotic clearance of commensal bacteria can provide opportunity for pathogenic strains to establish themselves. Medical treatments destabilizing the microbiome can lead to a change in overall metabolism and chronic Clostridium difficile infection. When colonization resistance is compromised there is more opportunity for single bacteria to dominate the community, with antibiotic-associated diarrhoea a common side effect associated with antibiotic induced dysbiosis. Microbial-based therapies Recently potential therapies pivoted to target the microbiota, as reinstating a healthy colony of gut microbials should alleviate the cause of IBD. Previous treatments relied on antibiotics followed by a course of probiotics; however, this has had variable levels of success as the antibiotic treatment can further reduce bacterial diversity in the gut. Probiotics have limited effectiveness in alleviating symptoms; any effect is transient as no probiotic microbial strains are detectable after 2 weeks of stopping intake. In modern clinical trials we have already seen positive results from microbiome treatments in clearing C. difficile infection, such as faecal microbiota transplantation (FMT) therapy. FMT uses faeces from a healthy donor, which are processed and delivered to the gastrointestinal tract of patients. Faeces contain a high microbial load, with up to 1011 bacterium per gram and multiple archaea, fungi and viruses that could not be delivered orally in a probiotic form. Success in resolving dysbiosis through FMT is variable but shows more promise than other therapies. Future Potential Specific forms of IBD such as ulcerative colitis (UC) was first treated with FMT in 1989, with patients reducing medications within a week of enema treatments and remaining clinically disease free for multiple years after treatment. More recent trials have had more variable levels of remission, suggesting donor compatibility, disease prevalence and engraftment of the microbiota all factor into the success of FMT. There is potential in this therapy, as FMT has proved more robust than previous treatments for IBD. Modern research into the relationship between disease and gut flora has come a long way in a relatively short time and shows there is much potential for future research in this area. Written by Charlotte Jones Related articles: the power of probiotics / Crohn's disease / the dopamine connection / Diverticular disease / Nanoparticles on gut health / Microbes in charge Project Gallery

You can have endometriosis and PCOS at the same time Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Are PCOS and endometriosis sisters? 09/07/25, 10:52 Last updated: Published: 30/01/24, 21:33 You can have endometriosis and PCOS at the same time The label of PCOS or endometriosis can have physical and emotional consequences for women. It is important for both male and females to gain a better understanding of such conditions, the symptoms and the challenges they pose. Such knowledge can act as physical and emotional support in times of need. It creates a safe space where the person with PCOS is comfortable discussing their experiences, feelings and concerns knowing they are being heard and supported by the right people. With research fast developing there is a plethora of information out there, so WHAT do you believe in and WHAT do you ignore and WHOM do you believe and WHOM do you ignore? Endometriosis and polycystic ovary syndrome (PCOS) both affect females and can have similar symptoms. However, the causes and some key symptoms are different. Endometriosis is a painful disorder in which tissue that normally lines the inside of your uterus grows outside the uterus. (Read more on Endometriosis breakthrough ). PCOS is an endocrine system disorder where small fluid-filled sacs develop in the ovaries. You can have endometriosis and PCOS at the same time. A 2015 study found that women with PCOS had a higher risk for a diagnosis of endometriosis. Another 2014 study determined that there is a strong link between endometriosis and PCOS with pelvic pain and trouble getting pregnant. What is a normal menstrual cycle? Let’s polish up the basics! The brain, ovaries and uterus work together to prepare the body per month for pregnancy. Follicle-stimulating Hormone (FSH) and Luteinising Hormone (LH) are made by the pituitary gland and progesterone and oestrogen are made in the ovaries. Many females with PCOS do not ovulate regularly and it may take these females longer to become pregnant. Irregular periods results in months where ovulation does not occur. Where the ovaries do not produce progesterone the lining of the uterus becomes thicker but shedding is very irregular which can lead to heavy and prolonged bleeding. PCOS affects 1 in 10 women in the UK. Women with PCOS experience irregular menstrual cycles, acne, excess hair growth, infertility, pregnancy complications and cardiovascular disease. PCOS can be associated with weight gain and obesity in approximately one-half of females. Females with PCOS can also be at increased risk of other problems that can impact quality of life. These include depression and anxiety, sexual dysfunction and eating disorders. Although PCOS is not ‘completely’ reversible there are many ways you can minimise the symptoms. Most females can lead a normal life and are able to conceive without significant complications. A pelvic examination is requested by your GP to assess the ovaries for a diagnosis to be made. Imaging tests for examining the ovaries are pelvic and intravaginal ultrasonography, however, the latter may be extremely uncomfortable if sexually inactive. Please be aware this article acts to capture your attention, encouraging you to delve further into the subject and continue your self-education on this topic and by no means is everything about PCOS. It is essential to consult with a healthcare professional if you suspect you may have symptoms of either PCOS or endometriosis. Proper diagnosis and management can help address specific concerns and improve overall reproductive health. Written by Khushleen Kaur Related articles: Endometriosis breakthrough / Underreporting in endometriosis / Gynaecology REFERENCES R. Hart and D. A. Doherty, Fertility Specialists of Western Australia (R.H.), Bethesda Hospital, 6008. K. J. Holoch, R. F. Savaris, D. A. Forstein, P. B. Miller, H. Lee Higdon, C. E. Likes and B. A. Lessey, https://doi.org/10.5301/je.5000181 , 2014, 6, 79–83. R. J. Norman, D. Dewailly, R. S. Legro and T. E. Hickey, The Lancet, 2007, 370, 685–697. Project Gallery

A type of anaemia Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Iron deficiency anaemia 10/07/25, 10:20 Last updated: Published: 27/06/23, 17:10 A type of anaemia This article is no. 2 of the anaemia series. Next article: anaemia of chronic disease . Previous article: Anaemia . Aetiology Iron deficiency anaemia (IDA) is the most frequent in children due to rapid growth (adolescence) and poor diets (infants), and in peri and post -menopausal women due to rapid growth (pregnancy) and underlying conditions. Anaemia typically presents, in around 50% of cases as headache, lethargy and pallor depending on the severity. Less common side effects include organomegaly and Pica which occurs in patients with zinc and iron deficiency and is defined by the eating of things with little to no nutritional value. Pathophysiology Iron is primarily sourced through diet, as haem (Fe2+) and non-haem iron (Fe3+). Fe2+ is sourced through meat, fish, and other animal-based products, Fe2+ can be absorbed directly through the enterocyte via the haem carrier protein1 (HCP1). Fe3+ is less easily absorbed and is mostly found in plant-based products. Fe3+ must be reduced and transported through the duodenum by the enzyme duodenal cytochrome B (DcytB) and the divalent metal transporter 1 (DMT1), respectively. Diagnosis As with any diagnosis, the first test to run would be a full blood count and this will occur with all the anaemias. In suspected cases of anaemia, the Haemoglobin (Hb) levels would be lower than 130 in males and 120 in females. The mean cell volume (MCV) is a starting point for pinpointing the type of anaemia, for microcytic anaemias you would expect to see an MCV < 80. Iron studies are best for diagnosing anaemias, for IDA you would expect most of the results to be low. A patient with IDA has little to no available iron so the body would halt the mechanism’s for storing iron. As ferratin is directly related to storage, low ferratin can be a lone diagnostic of IDA. Total iron-binding capacity (TIBC) would be expected to be raised, as transferrin transports iron throughout the body, the higher it is the more iron it would be capable of binding to. Elliptocytes (tear drop) are elongated RBC, often described as pencil like in structure and are regularly seen in IDA and other anaemias. Typically, one would see hypochromic RBC as they contain less Hb than normal cells, the Hb is what gives red cells their pigment. It’s not uncommon to see other changes in RBC such as target cells, given their name due to the bullseye appearance. Target cells are frequently seen in cases with blood loss. Summary IDA is the most frequent anaemia affecting patients of all age ranges and usually presents with lethargy and headaches. Dietary iron from animal derivatives are the most efficient source of iron uptake. Diagnosis of IDA is through iron studies, red cell morphological investigations alongside clinical presentation, to rule out other causes. Written by Lauren Kelly Project Gallery

Ways in which pathogens avoid being detected by the immune system Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Mechanisms of pathogen evasion 27/03/25, 11:23 Last updated: Published: 05/09/24, 10:54 Ways in which pathogens avoid being detected by the immune system Introduction Pathogens such as bacteria and viruses have evolved strategies to deceive and outsmart the immune system's defences. From hiding within cells to avoiding immune detection to blocking signals crucial for immune function, pathogens have developed an array of tactics to stay one step ahead of the immune system. This article introduces some key strategies pathogens employ to evade the immune system. Antigenic variation The influenza virus is a persistent and challenging pathogen to treat because it employs a clever strategy known as antigenic variation to evade the immune system. Antigenic variation is the pathogen’s ability to alter the proteins on its surface (antigens), particularly hemagglutinin (HA) and neuraminidase (NA), which are the primary targets of the immune system. As the virus conceals itself, it is no longer recognised and attacked by the host's defences. But how do the surface antigens change? This occurs through two primary mechanisms: antigenic drift and antigenic shift. The former process involves gradual changes in the virus's surface proteins by progressive accumulation of genetic mutations. Meanwhile, the latter requires a slightly different explanation. Antigenic shift is an abrupt process. It occurs when two influenza virus strains infect the same host cell and exchange genetic material. The exchange can lead to a new hybrid strain. This hybrid strain usually presents a new combination of surface proteins. It is a more abrupt process, and because the immune system lacks prior exposure to these new proteins, it fails to clear the viral pathogen. Antigenic shifts can lead to the emergence of strains to which the population has little to no pre-existing immunity. Some examples are the 1968 Hong Kong flu and the 2009 swine flu pandemic. Variable serotypes- Streptococcus pneumoniae When the host encounters a pathogen, the body creates antibodies against specific proteins on the pathogen's surface, ensuring long-term immunity. However, some species of pathogens evade this protection by evolving different strains. These strains involve multiple serotypes, each defined by distinct variations in the structure of their capsular polysaccharides. This variability allows them to infect the same host repeatedly, as immunity to one serotype does not confer protection against other serotypes. A perfect example of such a pathogen is the pneumonia-causing bacterium, Streptococcus pneumoniae , which has more than 90 strains. After successful infection with a particular S. pneumoniae serotype, a person will have devised antibodies that prevent reinfection with that specific serotype. However, these antibodies do not prevent an initial infection with another serotype, as illustrated in Figure 1 . Therefore, by evading the immune response, a new primary immune response is required to clear the infection. Latency- chicken pox & Human Immunodeficiency Virus (HIV) Pathogens can cleverly persist in the host by entering a dormant state where they are metabolically inactive. In this state, they are invisible to the immune system. Human Immunodeficiency Virus is well known for its use of HIV latent reservoirs. These reservoirs, consisting of metabolically inactive T-cells infected with HIV, can exist for years on end. When the host becomes immunocompromised at any stage in life, the T-cells in these reservoirs are suddenly activated to renew HIV production. The Varicella-Zoster Virus (VZV) is responsible for causing varicella (chickenpox) and zoster (shingles). Similarly, this virus can remain latent in the host to evade immune detection. VZV establishes latency in sensory ganglia, particularly in neurons. Since neurons are relatively immune-privileged sites, they are less accessible to immune surveillance mechanisms. This provides a safe haven from immune detection. When the host is immunocompromised, the virus reactivates. This renewed viral activity results in the production of viral particles which travel along the sensory nerve fibres towards mucous membranes. When the virus reaches the skin, it causes an inflammatory response. This results in painful vesicular skin lesions, commonly known as shingles (herpes zoster). Conclusion Pathogens employ diverse mechanisms to evade the host immune system, ensuring their survival and propagation through host cells. These evasion mechanisms can hinder the development of treatments for certain infectious diseases. For instance, the diversity in Strep A serotypes challenges vaccine development because immunity to one serotype may not confer protection against another. Additionally, the influenza virus constantly evolves via antigenic variation, always one step ahead of the immune system. The strategies employed by pathogens to evade the immune system are as diverse as they are sophisticated. Scientists continue to study these mechanisms, paving the way for developing more effective vaccines, treatments, and public health strategies to out-manoeuvre these organisms. We can better protect human health by staying one step ahead of pathogen evolution. Written by Fozia Hassan Related articles: Allergies / Plant diseases REFERENCES Abendroth, Allison, et al. “Varicella Zoster Virus Immune Evasion Strategies.” Current Topics in Microbiology and Immunology , 2010, pp. 155–171, www.ncbi.nlm.nih.gov/pmc/articles/PMC3936337/ , https://doi.org/10.1007/82_2010_41 . Accessed 24 July 2024. Gougeon, M-L. “To Kill or Be Killed: How HIV Exhausts the Immune System.” Cell Death & Differentiation , vol. 12, no. S1, 15 Apr. 2005, pp. 845–854, www.nature.com/articles/4401616 , https://doi.org/10.1038/sj.cdd.4401616 . Accessed 24 July 2024. Parham, Peter. The Immune System . 5th ed., New York, Garland Science, 2015, read.kortext.com/reader/epub/1743564 . Accessed 24 July 2024. Shaffer, Catherine. “How HIV Evades the Immune System.” News-Medical.net , 21 Feb. 2018, www.news-medical.net/life-sciences/How-HIV-Evades-the-Immune-System.aspx . Accessed 24 July 2024. Project Gallery

Properties of space Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Topology in action 17/02/25, 14:51 Last updated: Published: 29/09/23, 20:09 Properties of space Let’s say I put a sphere in front of you. I’m sure you could go through and tell me the basic facts and formulas surrounding it, many if which containing Pi. And even better, if you were a bit more fluent in maths, you could go further and start telling me about the geometry of the shape, say how the gradient had to disappear at a certain point or an assortment of many other things. But if we dive a little deeper into pure maths, it starts getting a little more complicated. When labels like Hausdorff get casually thrown about (meaning you can always separate two distinct points with an open boundary, which you certainly can do on a sphere!) it can really build up and become quite hard, especially if someone then puts in front of you two spheres stuck together. This is where the study of topology comes in and starts helping out, allowing us to start to categorise certain spaces without having to worry about all the small details that could catch you out. Topology is certainly found in the purer side of maths, generally seen as one of the more abstract modules to be taking at undergraduate level (as seen by the exam scores). But thinking of it just as some far away concept disconnected with the rest of the world would be foolish. Thinking back to what I said before about gradient fields on a sphere, this is more commonly known in maths as the “Hairy Ball Theorem” named as such as if you had a ball of hair, you wouldn’t be able to smooth it all out without a cow’s lick. And in mathematical terms it means that a continuous vector field has to disappear at a certain point. And maybe not readily apparent but this comes up in loads of places, the most obvious of which is that two points on the Earth will always have the exact temperature! But moving to Biology we see a lot more applications, even as early as in A-level study. Just thinking about how a protein will fold is all to do with the topological properties of them. DNA is a bit more complex understandably, with more base pairs it becomes incredibly flexible, able to bend into many shapes, but like topological spaces this flexible has limits. It doesn’t pass through itself nor tear, so it allows us to start applying our theorems to it. A key one of these is Knot theory, which of course is the study of knots. Knots in maths are defined as having no open ends and being complex, which helpfully is exactly like DNA! As you hopefully know, its coiled form has no open ends, and in order to untangle it we have to go through the process of cutting at double points. The amount of times this is needed to untangle is called the 'unknotting number' in topology and this mathematical modelling of the process allows biologists to move away from the microscope and still get a more accurate look on what’s happening. Written by Tom Murphy Related article: Quantum chemistry Project Gallery

'Manis pentadactyla' is the dominant pangolin species in China Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Pangolins: from poached to protected Last updated: 27/03/25, 11:15 Published: 27/02/25, 08:00 'Manis pentadactyla' is the dominant pangolin species in China This is article no. 4 in a series on animal conservation. Next article: How Gorongosa National Park went from conflict to community . Previous article: Beavers are back in Britain Pangolins are a group of eight scaled mammal species from Asia and Africa. They are being poached mainly for their scales and meat, driving them to dangerously low numbers. Although commercial trade is banned for all species, pangolins are the most illegally trafficked animals in the world. One pangolin species has a fascinating story because of its appeal to traditional medicine and demand in a populated country. That species is the Chinese pangolin Manis pentadactyla , and this article will describe its threats and conservation efforts. About pangolins in China Manis pentadactyla is the dominant pangolin species in China, living south of the Yangtze River ( Figure 1 ). The Sunda pangolin Manis javanica has a tiny habitat in southwest China ( Figure 1 ). Pangolins prefer natural forests, with an ambient temperature of 18-27°C and plenty of termites and ants to eat. Both Chinese species were classified as critically endangered in 2014, though accurately estimating pangolins' distribution and population size is complex. This is because they are nocturnal, solitary, and live underground. Pangolins also make no obvious sounds, or leave no apparent traces, for scientists to detect their presence. Despite these challenges, Chinese scientists are learning more about pangolin habitat to improve conservation strategies. Threats facing Chinese pangolins Chinese pangolins are critically endangered for various human-caused reasons ( Figure 2 ). The biggest reason is poaching because pangolin meat is a local delicacy, and its scales, bones, and blood are used in traditional Chinese medicine. Pangolin scales have recently been removed from the official list of ingredients for Chinese medicine, but that has not stopped hospitals from selling them. In a recent study, only a third of Chinese hospitals selling roasted pangolin scales had the required permit. Permits are also needed to sell or manufacture patented medicines containing pangolin scales, considered the gold standard for treating many conditions. Because these medicines and pangolin meat are so revered, one hunted pangolin sells for up to 90,000 yuan (≈£9800). This has incentivised the hunting and illegal trafficking of non-native pangolin species into China - where they could outcompete, or spread diseases to native species. Thus, illicit trade for traditional medicine threatens Chinese pangolins. Habitat destruction has made Chinese pangolins more vulnerable to poaching. Natural forests are being destroyed to grow crops, grow economic trees like rubber, or build human infrastructure. Farms or rubber plantations have fewer ants and termites than natural forests, so pangolins cannot survive there. As a result, in some parts of China, the pangolin geographical range halved in 30 years. With acres of this unsuitable habitat separating fragments of forest, pangolins may struggle to find mates, and inbreeding could be an issue. Thus, habitat loss is contributing to the decline of the Chinese pangolin. Conservation Conservation measures were taken in the last few decades in response to the pangolin population decline. In China, hunting pangolins was first restricted in 1987, and they were given legal protection in 1989. The Chinese government tightened this protection in 2020 after suggestions that pangolins were an intermediate species for SARS-CoV-2 to transmit from bats to humans. In addition to national restrictions, international authorities restricted pangolin trade, and the Chinese government ran public awareness campaigns about their endangered status ( Figure 3 ). Pangolins also have 100,000 squared kilometres of protected habitat in China, though this is only 9% of what models predict as a suitable pangolin habitat. Habitat protection and trade restrictions are essential to protect pangolins because captive breeding has either failed or acted as a front for illegal trafficking. Although Chinese pangolin conservation has come far in the last 40 years, more can be done. Conclusion Humans have driven Chinese pangolins to near extinction, mainly by hunting for traditional medicine ingredients and destroying native habitats. Conservation efforts have primarily involved legal and habitat protection, but pangolins are challenging to monitor and impossible to breed in captivity. Hopefully, public awareness and a clampdown on illegal trafficking will help to save this unique mammal species. Written by Simran Patel Related articles: Conservation of marine iguanas / Galapagos tortoises REFERENCES Challender, D. et al. (2013) IUCN Red List of Threatened Species: Manis pentadactyla . IUCN Red List of Threatened Species . Available from: https://www.iucnredlist.org/en (Accessed 23rd October 2024). Convention On International Trade In Endangered Species Of Wild Fauna And Flora (2017) Appendices I, II and III valid from 4 October 2017 . Available from: https://cites.org/sites/default/files/eng/app/2017/E-Appendices-2017-10-04.pdf . Mammoser, G. (20th February 2017) Chinese Police Go After ‘Pangolin Princess’ Who Proudly Eats Endangered Species. VICE . Available from: https://www.vice.com/en/article/chinese-police-go-after-pangolin-princess-who-proudly-eats-endangered-species/ (Accessed 23rd October 2024). Wang, Y., Turvey, S.T. & Leader-Williams, N. (2023) The scale of the problem: understanding the demand for medicinal pangolin products in China. Nature Conservation . 52: 47–61. Available from: https://doi.org/10.3897/natureconservation.52.95916 (Accessed 23rd October 2024). Xinhua News Agency (2015) Opinions of the Central Committee of the Communist Party of China and the State Council on Accelerating the Construction of Ecological Civilization . Beijing: The Central Government of the People’s Republic of China. Available from: https://www.gov.cn/xinwen/2015-05/05/content_2857363.htm (Accessed 23rd October 2024). Zhang, F., Chen, Y., Tang, X., Xi, F., Cen, P., Pan, Z., Ye, W. & Wu, S. (2024) Predicting the distribution and characteristics of Chinese pangolin habitat in China: Implications for conservation. Global Ecology and Conservation . 51: e02907. Available from: https://www.sciencedirect.com/science/article/pii/S2351989424001112 (Accessed 23rd October 2024). Zhang, F., Wang, W., Mahmood, A., Wu, S., Li, J. & Xu, N. (2021) Observations of Chinese pangolins ( Manis pentadactyla ) in mainland China. Global Ecology and Conservation . 26: e01460. Available from: https://www.sciencedirect.com/science/article/pii/S235198942100010X (Accessed 23rd October 2024). Zhang, F., Wu, S. & Cen, P. (2022) The past, present and future of the pangolin in Mainland China. Global Ecology and Conservation . 33: e01995. Available from: https://www.sciencedirect.com/science/article/pii/S235198942100545X (Accessed 19th October 2024). Project Gallery

When we think of bacteria, we tend to focus on their pathogenicity and ability to cause diseases such as tuberculosis, which infects around one-quarter of the world’s population. However, whilst bacteria do have the potential to become parasitic, if the trillions of bacterial cells that make up the human microbiome ceased to exist, human health would experience a rapid decline. Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why bacteria are essential for human survival Last updated: 13/11/24 Published: 13/04/23 When we think of bacteria, we tend to focus on their pathogenicity and ability to cause diseases such as tuberculosis, which infects around one-quarter of the world’s population. However, whilst bacteria do have the potential to become parasitic, if the trillions of bacterial cells that make up the human microbiome ceased to exist, human health would experience a rapid decline. One reason for this is due to the critical role bacteria play in inducing the immune system against pathogenic threats. Upon viral infection, the interferon (IFN) defence system is initiated where the synthesis of antiviral cytokines is upregulated. Evidence suggests bacteria in the gut are capable of modulating the IFN system. They work by inducing macrophages and plasmacytoid dendritic cells to express type 1 IFN, which in turn primes natural killer cells and prepares cytotoxic CD8+ T cells for action. Erttmann et al (2022) demonstrate that a depletion of the gut microbiota diminishes the cell signalling pathways modulated by these commensal bacteria. This causes a reduction in type 1 IFN production, and thus an impairment in the activation of NK and CD8+ T cells. As a result, the body becomes more susceptible to attack by viral infections and less able to defend itself. This highlights just how vital the role bacteria in our microbiome play in providing us with innate immunity against viral pathogens and protecting our health. This also brings attention to our use of antibiotics, and the potential negative effects they may have on the commensal bacteria residing in our body. Erttmann et al (2022) further showed that mice treated with a variety of antibiotics exhibited a major reduction in gut microbiota diversity, thus severely comprising their ability to fight off viral infections. Research like this is important in informing doctors to be sensible in their administration of antibiotics, as well as informing patients to not self-medicate and unnecessarily ingest antibiotics. Ultimately, the commensal bacteria living in our bodies play essential roles in protecting human health, and it is, therefore, vital we take the necessary steps to also protect these remarkable microorganisms in return. Written by Bisma Butt Related article: The rising threat of antibiotic resistance REFERENCES Erttmann, S.F., Swacha, P., Aung, K.M., Brindefalk, B., Jiang, H., Härtlova, A., Uhlin, B.E., Wai, S.N. and Gekara, N.O., 2022. The gut microbiota prime systemic antiviral immunity via the cGAS-STING-IFN-I axis. Immunity, 55(5), pp.847-861. Ganal, S.C., Sanos, S.L., Kallfass, C., Oberle, K., Johner, C., Kirschning, C., Lienenklaus, S., Weiss, S., Staeheli, P., Aichele, P. and Diefenbach, A., 2012. Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota. Immunity, 37(1), pp.171-186.

Exenatide as a potential drug Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A common diabetes drug treating Parkinson’s disease 08/07/25, 14:37 Last updated: Published: 24/01/24, 21:15 Exenatide as a potential drug A new investigational drug, originally developed for type 2 diabetes, is being readied for human clinical trials in search of the world's first treatment to impede Parkinson's disease progression. Parkinson's (PD) is the second most common neurodegenerative disorder. The connection between type 2 diabetes (T2DM) and PD was discovered in 1993, when PD patients with co-existing T2DM had worse motor symptoms and response to therapy. Dopaminergic neurons promote eating behaviour in hypoglycaemic states, mediated via insulin receptors in the substantia nigra, because dopaminergic neuronal loss affects glycaemic control. Thus, T2DM patients are more likely to acquire PD than people without diabetes. Excess glucose in the brain, as found in uncontrolled T2DM, may interact randomly with surrounding proteins and interfere with their function. These interactions also result in toxic end products promoting inflammation and α-synuclein clustering, both of which are PD characteristics. Over a 12-year period, retrospective data (N=8,190,323) showed that T2DM responders had considerably greater PD rates when compared to those without diabetes. The rise was significantly more pronounced among individuals with complex T2DM and those aged 25-44. Exenatide: Overview and Mechanism of Action Exenatide is a synthetic form of exendin-4, a naturally occurring protein identified in the saliva of the Gila monster (poisonous lizard endemic to the Southwest US) by Dr. Eng in the early 1990s. In humans, the chemical is produced after a meal to increase insulin production, decreasing blood sugar. GLP-1 degrades fast in humans, and its benefits are short-lived. However, investigations have shown effects of exendin-4 continue longer in people. This finally led to FDA clearance in 2005, when the product was sold as Byetta TM . Its current indications are for the treatment of balancing glucose levels in T2DM with or without additional oral hypoglycemic medications. This glycaemic control is an analogue of human GLP-1, used in T2DM treatment, either alone or in conjunction with other antidiabetic medications. Exendin-4's neuroprotective characteristics may aid in rescuing degenerating cells and neuron protection. Because T2DM and PD are linked, researchers want to explore its effectiveness as a PD therapy. Patients treated with exenatide for one year (in addition to standard medication) experienced less deterioration in motor symptoms when tested without medication compared to the control group. Research on Exenatide as a Potential Parkinson's Disease Therapy 21 patients with intermediate PD were assessed over a 14-month period, and their progress was compared to 24 other people with Parkinson's who served as controls. Exenatide was well accepted by participants, albeit some individuals complained about weight loss. Significantly, exenatide-treated participants improved their PD movement symptoms, while the control patients continued to deteriorate. The researchers investigate exenatide, a possible PD therapy, in an upcoming clinical study, lending support to the repurposing of diabetes drugs for Parkinson's patients. This research adds to the evidence for a phase 3 clinical trial of exenatide for PD patients. Data on 100,288 T2DM revealed that people using two types of diabetic medications, GLP-1 agonists and DPP4-inhibitors, were less likely to be diagnosed with Parkinson's up to 3.3 years follow-up. Those who used GLP-1 agonists were 60% less likely to acquire PD than those who did not. The results revealed that T2DM had a higher risk of Parkinson's than those without diabetes, although routinely given medicines, GLP-1 agonists, and DPP4-inhibitors seemed to reverse the association. Furthermore, a 2-year follow-up research indicated individuals previously exposed to exenatide displayed a substantial improvement in their motor characteristics 12 months after they ceased taking the medication. However, this experiment was an open-label research so the gains may be explained by a placebo effect. The research adds to the evidence that exenatide may assist to prevent or treat PD, perhaps by altering the course of the illness rather than just lowering symptoms. Other risk factors for PD should be considered by clinicians when prescribing T2DM drugs, although further study is required to clarify clinical significance. Findings from Clinical Trials and Studies Based on these findings, the UCL team broadened their investigation and conducted a more extensive, double-blind, placebo-controlled experiment. The findings establish the groundwork for a new generation of PD medicines, but they also confirm the repurposing of a commercially existing therapy for this illness. Patients were randomly randomised (1:1) to receive exenatide 2 mg or placebo subcutaneous injections once weekly in addition to their current medication for 48 weeks, followed by a 12-week washout period. Web-based randomisation was used, with a two-stratum block design depending on illness severity. Treatment allocation was concealed from both patients and investigators. The main outcome was the adjusted difference in the motor subscale of the Movement Disorders Society Unified Parkinson's Disease Rating Scale after 60 weeks in the realistically defined off-medication condition. Six major adverse events occurred in the exenatide group and two in the placebo group, but none were deemed to be connected to the research treatments in either group. It is unclear if exenatide alters the underlying illness mechanism or causes long-term clinical consequences. Implications and Future Directions Indeed, the UCL study showed that exenatide decreases deterioration compared to a placebo. However, participants reported no change in their quality of life. The study team would broaden their study to include a broader sample of people from several locations. Because PD proceeds slowly, longer-term trials might provide a better understanding of how exenatide works in these responders. Overall, findings suggest that gathering data on this class of medications should be the topic of additional inquiry to evaluate their potential. Exenatide is also being studied to see whether it might postpone the onset of levodopa-induced problems (e.g., dyskinesias). Furthermore, if exenatide works for Parkinson's, why not for other neurodegenerative illnesses (Alzheimer's, amyotrophic lateral sclerosis, Huntington's disease, multiple sclerosis) or neurological diseases (including cerebrovascular disorders, traumatic brain injury...)? Exenatide has been FDA-approved for diabetes for many years and has a good track record, but it does have some adverse side effects in Parkinson's patients, namely gastrointestinal difficulties (nausea, constipation). Exenatide as a prospective PD therapy is an example of medication repurposing or repositioning, an essential method for bringing novel therapies to patients in a timely and cost-effectively. However, further research is required, so it will be many years before a new therapy is licenced and available. Drug repurposing, or using authorised medicines for one ailment to treat another, opens up new paths for Parkinson's therapeutic development. Conclusion Exenatide shows potential as a therapy for Parkinson's disease (PD). Studies have shown that exenatide may help improve motor symptoms and slow down the progression of PD. However, further research and clinical trials are needed to fully understand its effectiveness and long-term effects. The findings also suggest that repurposing existing medications, like exenatide, could provide new avenues for developing PD therapies. While exenatide shows promise, it will likely be many years before it is licensed and widely available as a PD treatment. PROJECT GALLERY IMAGES DESCRIPTION Figure 1- The use of GLP-1 is beyond diabetes treatment. Nineteen clinical studies found that GLP-1 agonists can improve motor scores in Parkinson's Disease, improve glucose metabolism in Alzheimer's, and improve quality of. They can also treat chemical dependency, improve lipotoxicity, and reduce insulin resistance. However, adverse effects are primarily gastrointestinal. Thus, GLP-1 analogues may be beneficial for other conditions beyond diabetes and obesity. Figure 2- Potent GLP-1 agonists suppress appetite through a variety of mechanisms, including delayed gastric emptying, increased glucose-dependent insulin secretion, decreased glucagon levels, and decreased food ingestion via central nervous system effects. Short-acting agents, including exenatide, primarily function by impeding gastric evacuation, thereby leading to a decrease in postprandial glucose levels. On the contrary, extended-release exenatide and other long-acting agonists (e.g., albiglutide, dulaglutide) exert a more pronounced impact on fasting glucose levels reduction via their mechanism of action involving the release of insulin and glucagon. The ineffectiveness of long-acting GLP-1 receptor agonists on gastric evacuation can be attributed to the development of tolerance to GLP-1 effects, which is regulated by parasympathetic tone alterations. Figure 3- Illustrated is the cross-communication with insulin receptor signalling pathways and downstream effectors . Biomarkers can be derived from the formation and origin of extracellular vesicles, which indicate the initial inward budding of the plasma membrane. An early endosome is formed when this membrane fuses; it subsequently accumulates cytoplasmic molecules. As a consequence, multivesicular bodies are generated, which subsequently fuse with the plasma membrane and discharge their constituents into the extracellular milieu. Akt denotes protein kinase B; Bcl-2 signifies extracellular signal-related kinase; Bcl-2 antagonist of death; Bcl-2 extra large; Bcl-XL signifies Bcl-2; Bim signifies Bcl-2-like protein 11; cAMP signifies cyclic adenosine monophosphate; CREB signifies cAMP response element-binding protein; Erk1/2 signifies extracellular signal-related kinase IDE, insulin-degrading enzyme; IL-1α, interleukin 1α; IRS-1, insulin receptor signalling substrate 1; MAPK, mitogen-associated protein kinase; mTOR, mechanistic target of rapamycin; mTORC1, mTOR complex 1; mTORC2, mTOR complex 2; NF-kB, nuclear factor–κB; PI3-K, phosphoinositide 3-kinase; PKA, protein kinase; FoxO1/O3, forkhead box O1/O3, forkhead box O1/O3; GRB2, growth factor receptor-bound protein 2; GSK-3β, Written by Sara Maria Majernikova Related articles: Pre-diabetes / Will diabetes mellitus become an epidemic? / Parkinson's risk / Markers for Parkinsonism Project Gallery

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