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Antimicrobial Resistance (AMR) is a growing concern for healthcare systems globally Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Are we doing enough to fight anti-fungal resistance? 26/04/26, 14:30 Last updated: Published: 04/11/24, 15:29 Antimicrobial Resistance (AMR) is a growing concern for healthcare systems globally Introduction to fungi Fungi are a fascinating yet relatively untouched area of microbiology. From growing in damp forest soil to the human body, these eukaryotes (surprisingly more closely related to animals than plants!) reproduce sexually and asexually, producing hyphae (long, branching filaments) to absorb nutrients. Even in the human body, fungal infections can range from athletes' foot to severe cases of invasive pneumonia. Despite its diverse and incredibly interesting nature, only 5% of all estimated fungal species worldwide have been discovered. There is a significant lack of knowledge regarding these amazing microorganisms. The challenge of antimicrobial resistance Antimicrobial Resistance (AMR) is a growing concern for healthcare systems globally. AMR is the process by which microbes develop decreased sensitivity to antimicrobial drugs, meaning they can evade drug and immune response, creating the potential for superbugs (i.e. Multi-Drug Resistant Staphylococcus Aureus/MRSA). An increasing number of resistant fungal species are emerging, with more than 90% of Candida Auris strains in the US now fluconazole resistant. Microorganisms can confer resistance in various ways, such as the misuse of antimicrobial drugs and pesticides in healthcare and agriculture or random genetic evolution (secondary vs primary resistance). Biofilm formation can also contribute to this, particularly for those with inserted medical devices. This can be seen in Candidiasis, for example on inserted catheters, as can be seen in Figure 2 . AMR was thought to be responsible for 1.27 million deaths globally in 2019, with an 8% increase in resistant infections in the UK from 2021-22. Global efforts regarding resistance appear to focus on antibiotic resistance, much reflective of worldwide research efforts. This leaves us wondering, are we doing enough to fight antifungal resistance? Mechanisms of fungal resistance Fungal infections, although typically mild, often present most severely in the immunocompromised, particularly those with cancer or who have had recent organ transplants. Invasive infections are cleared using five classes of antifungal drugs: azoles, polyenes, allylamines, flucytosine, and echinocandins, the two most common being azoles and echinocandins. Azoles aim to inhibit ergosterol synthesis, which is crucial for cell membrane stability, whilst echinocandins interfere with beta-1,3-D-glucan synthesis (a major component of fungal cell walls). Fungi can come in two forms: mould fungi (multicellular units containing branching hyphae), and yeast fungi (unicellular with the ability to ferment carbohydrates). In yeasts, azoles target the Erg11 protein (or Cyp51A for mould fungi), which disrupts ergosterol synthesis and causes the build up of 14a-methyl sterols. In turn, this disrupts membrane activity. Azole resistance can develop through different pathways: changes in the Erg11 amino acid structure, changes in Erg11 expression, and alterations to drug efflux pathways. For Candida species, amino acid substitutions occurring at the Erg11 enzyme binding site often lead to azole resistance, whilst in Aspergillus fumigatus, changes occur at codons 54-220 in Cyp51A. Resistant Candida albicans can also overexpress Erg11, meaning a higher drug concentration is needed to combat infection. Some fungal species, such as Candida spp. confer azole resistance by utilising drug efflux systems, particularly the ABC transporter MDR1, where a gain of function mutation can lead to multidrug resistance. Loss of heterozygosity, for example, by aneuploidy, can lead to resistance if this occurs across Erg11 or MDR1 gene loci. Inhibition of the Hsp90 pathway (a component of the cellular stress response) can alleviate both azole and echinocandin resistance and regulate biofilm resistance. Hsp90 stabilises the terminal MAPK component, increasing cell wall integrity (most antifungal drugs target the fungal cell wall). Global nature of AMR Global schemes have emerged to combat AMR, with fungal efforts appearing to lag behind its bacterial equivalent; The WHO published its first priority bacterial pathogens list in 2017, which has been effectively used by pharmaceutical companies, researchers, and local health trusts to target bacterial species, asserting themselves as an increasing risk. WHO Fungal Priority lists didn’t emerge until 2022, which was the first global effort to establish fungal species of risk. The One Health approach, another global strategy, aims to combat AMR by emphasising collaboration between multiple sectors, increasing innovation and creating clear communication. Its main aims lay in identifying knowledge gaps, involving policymakers, creating networks and sharing data. In addition to global strategies, national ones exist. The UK government made its own five year AMR-combatting plan, implementing a One Health approach; Previous plans have proven successful; antimicrobial exposure was reduced by 8%, with a further 81% reduction in antibiotic sales for food-producing mammals. It is clear AMR (particularly fungal resistance) is becoming an increasingly worrying issue. In 2019, UK deaths directly arising from drug resistant infections nearly matched those from stomach cancer, with an estimated further 35,000 deaths indirectly resulting from resistant infections. Hence, measures must be in place to contain its potential for worldwide damage. Insufficient action against AMR was predicted to have long-lasting effects like the COVID-19 pandemic every five years. Since drug-resistant fungi have the potential to cause significant burden on healthcare systems globally, what is currently being done to combat Fungal AMR? What more can we do? Fungal infections are the fifth leading cause of death worldwide, yet less than 1.5% of infectious disease funding goes towards research of fungal infections. This could be because fungal infections present mildly in most healthy people. However, we cannot ignore the fatal consequences for those with pre-existing illnesses or the devastating effects that could ensue if we do not make significant efforts to eliminate fungal resistance. In its most recent five-year plan, the UK government stated its support for initiatives to increase agrochemical stewardship, particularly focussing on fungicides. The efforts outlined include establishing a pharmaceutical monitoring programme, funding research into AMR-driving chemicals, and a pilot AMR surveillance scheme. This is significant progress, however, it focuses on environmental fungal resistance, with a tendency to ignore research efforts and failing to actively address fungi in most sections. In April 2026, £4.5 million was awarded to an international collaboration including the University of Edinburgh, to help improve understanding of fungal diseases. This is a significant contribution, and can accelerate endeavours in research. To move forward, more efforts are needed to drive antifungal research - whether in expanding the number of antifungal classes available to patients or improving existing antifungal therapies (e.g. improvements in pharmacokinetics and efficacy). This is evidenced by the sheer number of antibiotics and respective classes compared to fungal counterparts; bacterial infections can be treated with a whopping two-fold more drug classes than their fungal equivalent. Moreover, the One Health approach emphasises the importance of diagnostics and testing; whilst most modern fungal testing methods are very sensitive and specific, some tests can only report positive results very late into disease progression (read more about One Health ). Hence, fungal diagnostic and testing approaches need to be optimised. This all can be achieved by pushing more funding towards fungal research and development, encouraged with government spending, and an emphasis on collaboration between academia and industry. How can we relay the importance of stewardship in agriculture, or bring more treatments to the bedside without collaboration and education? Written by Eloise Nelson Related article: The increasing threat of anti-microbial resistance REFERENCES Gaya E., Fungarium: Welcome to the Museum, 2019. Kundu R, Srinivasan R. Cytopathology of Fungal Infections. Current Fungal Infection Reports. 2021;15(3):81-92. The Role of Plant Agricultural Practices on Development of Antimicrobial Resistant Fungi Affecting Human Health: Proceedings of a Workshop Series.: Hearing before the National academies of Sciences, Engineering and Medicine (05.04.2023, 2023). Government U. Confronting antimicrobial resistance 2024 to 2029. In: Care DoHaS, editor. 2024. Fisher CM, Alastruey-Izquierdo A, Berman J, Bicanic T, Bignell ME, Bowyer P, et al. Tackling the emerging threat of antifungal resistance to human health. Nature Reviews Microbiology. 2022;20(9):557-71. Cowen EL, Sanglard D, Howard JS, Rogers DP, Perlin SD. Mechanisms of Antifungal Drug Resistance. Cold Spring Harbor Perspectives in Medicine. 2015;5(7):a019752. Fisher CM, Alastruey-Izquierdo A, Berman J, Bicanic T, Bignell ME, Bowyer P, et al. Tackling the emerging threat of antifungal resistance to human health. Nature Reviews Microbiology. 2022;20(9):557-71. WHO fungal priority pathogens list to guide research, development and public health action. WHO; 2022. Greener M. Why have we neglected fungal infections? Prescriber. 2022;33(8-9):20-3. Baker J, Denning WD. The SSS revolution in fungal diagnostics: speed, simplicity and sensitivity. British Medical Bulletin. 2023;147(1):62-78. Project Gallery

Richard Dawkins's work and the Modern Evolutionary Synthesis Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Is the immune system ‘selfish’? – a Dawkins perspective Last updated: 26/04/26, 14:38 Published: 25/09/25, 07:00 Richard Dawkins's work and the Modern Evolutionary Synthesis Evolution and Dawkins’ perspective Charles Darwin introduced the unprecedented theory of evolution by natural selection in his famous work ‘On the Origin of Species’, published in 1859. Gregor Mendel, who explained the concept of Mendelian genetics (the inheritance of genes), was a contemporary of Darwin, but his research was recognised much later on, beyond his time. In the 20 th century, the Modern Evolutionary Synthesis was formed and gave a foundation for how biological life has formed as we see it today. The Modern Evolutionary Synthesis is widely accepted and strongly supported by experimental and observational evidence across an array of life. Human beings have even leveraged these concepts for hundreds of years through artificial selection, imposing our own sometimes superficial selective pressures on organisms to express characteristics that we desire (such as the case of the Belgian Blue cattle, with a mutation in the myostatin gene making it a muscular, lean beef, or perhaps artificial selection in dog breeding). Richard Dawkins’ breakout book, ‘The Selfish Gene’, published in 1976, took him from an unknown voice at the University of Oxford passionate about the works of evolution across all animals, to a lauded voice in the scientific community. His concept of genes being selfish is the idea that natural selection works at the gene level, whereby genes over time become better at replication, with the organism acting as a ‘survival machine’ built to help genes propagate. It is important to note that the term ‘selfish’ is not meant metaphysically or philosophically. Figure 1 explains what ‘selfish’ means. Taking this further, it can be argued that genes helping organisms resist pathogenic attack are more likely to survive and propagate. This means the immune system does not exist to protect the body holistically but rather to protect its genes individually. The immune system evolved through the gene-centric lens As previously mentioned, the immune system has become integral to all complex organisms responding to pathogens as a selective pressure. Those genes that have conferred a greater ability to combat or resist a particular pathogen allow the organism an improved survival chance until reproductive age has been achieved. The window whereby the organism has reached reproductive maturity and is reproducing is what the genes have been selected to get, which is why many genetic pathways end up becoming detrimental to an organism in old age (explained by the antagonistic pleiotropy hypothesis- APT- and the disposable soma theory). This remains especially true for the immune system. One must also understand that only vertebrates are biologically equipped with an adaptive immune system (allowing for memory and effective response to previous pathogens), with Figure 2 explaining this difference. This supports that the immune system is a ‘selfish system’, as while many organisms survive without adaptive immunity, more complex organisms have evolved to include it because of our prolonged individual survival and delay in reproductive maturity (indicating that survivability until our reproductive window is an intense selective pressure). Immune imperfection through the ‘Selfish System’ lens We now understand there is a compelling point to be made that the immune system has evolved with the reproductive window in mind and to allow as much gene propagation in a population as possible. If we accept this point of view, it explains many of the trade-offs and imperfections of the immune system when we look at the potential harm caused by immunity. Allergies are one such example, whereby hypersensitivity causes an immune response to harmless substances, which, through the gene-centric lens, may have evolved to detect pathogens such as parasites. This further supports the ‘selfish system’ idea as reproductive success on a population scale is not impaired by a significant amount by allergies. One such study showed that women with allergies and asthma, despite having systemic inflammation, did not have a reduced fertility rate when analysing the relationship between an increase in allergic diseases in the 20 th century and a decrease in fertility globally. Chronic inflammation through persistent immune activation in old age (a concept termed inflammaging) is another such example. We previously mentioned that past reproductive age natural selection weakens, meaning that our genes are selected for early life immune optimisation, even if that means they cause problems later in old age. Processes such as cellular senescence, inflammasome activation, oxidative stress, immune cell dysregulation and so on begin to occur, leading to an increased risk of age-related diseases such as cardiovascular disease, cancer, dementia, sarcopenia and so on. Immune evolution is therefore a ‘selfish system’ because it seems to care more about gene propagation in the young to middle-aged years in comparison to long-term organism health, as many immune systems rapidly decline and become detrimental. Conclusion This perspective of the immune system as a ‘selfish system’ allows us to understand that it is not a protector of the organism throughout its life span, as we may perceive it to be, but rather that it is a mechanism evolved and optimised to propagate genetic material during the organism’s reproductive window (expanding beyond humans). This analysis of the immune system through Richard Dawkins' lens of the “selfish gene” helps us to understand many of the limitations of the immune system. Working on treatments to preserve and maintain the immune system’s healthy state, which reflects young adult life, appears to be a promising approach for future clinical prevention plans for old age diseases. There are many currently being researched and emerging treatments with this principle in mind, such as senotherapeutics and mTOR inhibitors (such as rapamycin and other rapalogs), making this an interesting field to keep up to date with. Written by Yaseen Ahmad Related articles: Darwin and Galápagos Tortoises / The genetics of ageing and longevity Project Gallery

Understanding the cause of bullying can provide effective prevention and intervention Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The brain of a bully Last updated: 26/04/26, 14:22 Published: 29/05/25, 07:00 Understanding the cause of bullying can provide effective prevention and intervention Introduction Bullying is a global social issue affecting any individual regardless of sex, age, or gender, particularly in childhood and adolescence. Approximately one-third of the youth is bullied worldwide; the range could be as low as 7% in Tajikistan to 74% in Samoa. While much neuroscientific research focuses on bullying victimisation and social exclusion, there is a growing field to understand the brain mechanisms behind bullying behaviour. Why does bullying occur? Is there a neurological basis for such behaviour? This article will answer these questions with insights into prevention and intervention strategies. The neural basis of bullying As per Johnna R. Swartz, an assistant professor at the University of California, Davis : Bullying is fairly common during adolescence, with about 25-50% of teenagers in the U.S. reporting that they have bullied or been a victim of bullying. The Swartz team focused on the amygdala, a small almond-shaped structure deep within the brain. The amygdala is critical for processing emotions, particularly fear and aggression. Swartz and her colleagues conducted a functional resonance imaging (fMRI) study on 49 adolescents, examining how their amygdala responded to different emotional expressions during a face-matching task. The findings indicated that the adolescents who engaged in bullying behaviour exhibited a heightened amygdala response to angry faces and a diminished amygdala response to fearful faces. This pattern suggests that bullies may struggle to recognise fear in others, potentially making them less likely to empathise with their victims. Moreover, a study revealed that adolescents who reported higher rates of bullying showed increased activation of the ventral striatum (the area that responds to rewarded feelings), amygdala (emotion processing), medial prefrontal cortex (involved with social cognition, decision-making), and insula (salience detection) while observing social exclusion scenarios. The findings suggest that bullying is not just about aggression but also about maintaining social dominance and hierarchy. Another study by the University of Chicago conceded that bullies might enjoy others in pain by observing a robust activation of the amygdala and ventral striatum when watching pain inflicted on others. The immediate brain 'alarm' system: research published in Journal of Neuroscience found that witnessing or experiencing bullying activates social and emotional brain networks and autonomic threat systems, in both children (11–14 years old) and adults. This response is similar to how the brain reacts to physical threats. Another finding is that adolescents show stronger, more profound brain activity in regions processing bodily sensations during bullying compared to adults, suggesting it acts as a severe, acute, and physical threat during this developmental stage. Lastly, a January 2026 study in European Child & Adolescent Psychiatry found that while some victims show high stress responses, those frequently exposed to bullying (more than twice a month) exhibit lower amygdala activation, in response to further social exclusion. This suggests a neural adaptation to chronic trauma, known as 'emotional numbing'. Why is knowing the neural basis of bullying useful? Understanding the root cause of bullying can provide effective prevention and intervention strategies: Social-emotional training (SET) to improve emotional regulation and empathy, which can help reshape neural pathways. For example, programmes like the ‘Roots of Empathy’ initiative have shown that training children to recognise emotions can reduce bullying behaviours in schools. Cognitive-behavioural therapy (CBT) allows bullies to reframe negative thoughts and develop a healthier response to social interactions. For instance, the CBT techniques, like role-playing social situations, have been successfully used in school-based interventions. Mindfulness and cognitive training strengthen the prefrontal cortex by meditation and improve decision-making skills and impulse control. School-based interventions (like anti-bullying programs) create supportive environments that reward prosocial behaviour rather than only punishing aggressive behaviour. Conclusion The neuroscience of bullying helps us understand the root cause of bullying scientifically. Bullying is not simply a matter of choice; there is a deeper scientific basis to consider. This knowledge can help to develop comprehensive solutions to prevent bullying and create a healthier social environment. Future studies should focus on longitudinal studies that track brain development in children and adolescents involved in bullying, thereby informing how early interventions can reshape them for positive change. Written by Prabha Rana Related articles: Aggression / Depression in childhood / Forensic neurology REFERENCES Assistant Secretary for Public Affairs (ASPA). “Facts about Bullying.” StopBullying.Gov , 9 Oct. 2024, www.stopbullying.gov/resources/facts . “Bullies May Enjoy Seeing Others in Pain: Brain Scans Show Disruption in Natural Empathetic Response.” University of Chicago News , news.uchicago.edu/story/bullies-may-enjoy-seeing-others-pain-brain-scans-show-disruption-natural-empathetic-response . Accessed 15 Feb. 2025. Dolan, Eric W. “Neuroscience Study Finds Amygdala Activity Is Related to Bullying Behaviors in Adolescents.” PsyPost , 7 Dec. 2019, www.psypost.org/neuroscience-study-finds-amygdala-activity-is-related-to-bullying-behaviors-in-adolescents/ . Perino, Michael T., et al. “Links between adolescent bullying and neural activation to viewing social exclusion.” Cognitive, Affective, & Behavioral Neuroscience , vol. 19, no. 6, 10 July 2019, pp. 1467–1478, https://doi.org/10.3758/s13415-019-00739-7 . Project Gallery

Differences in brain structure Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Brief neuroanatomy of autism 26/04/26, 14:18 Last updated: Published: 26/12/23, 20:38 Differences in brain structure Autism is a neurodevelopmental condition present in both children and adults worldwide. The core symptoms include difficulties understanding social interaction and communication, and restrictive or repetitive behaviours such as strict routines and stimming. When the term autism was first coined in the 20th century, it was thought of as a disease. However, it is now described as a cognitive difference rather than a disease; that is, the brains of autistic individuals – along with people diagnosed with dyslexia, dyspraxia, or attention deficit hyperactive disorder – are not defective, but simply wired differently. The exact cause or mechanism for autism has not been determined; the symptoms are thought to be brought about by a combination of genetic and environmental factors. Currently, autism disorders are diagnosed solely by observing behaviours, without measuring the brain directly. However, behaviours may be seen as the observable consequence of brain activity. So, what is it about their brains that might make autistic individuals behave differently to neurotypicals? Total brain volume Back before sophisticated imaging techniques were in use, psychiatrics had already observed the head size of autistic infants was often larger than that of other children. Later studies provided more evidence that most children who would go on to be diagnosed had a normal-sized head at birth, but an abnormally large circumference by the time they had turned 2 to 4 years old. Interestingly, increase in head size has been found to be correlated with the onset of main symptoms of autism. However, after childhood, growth appears to slow down, and autistic teenagers and adults present brain sizes comparable to those of neurotypicals. The cortex Research from the UC Davis MIND Institute (May 2024) found that at the age of 3, autistic girls have a thicker cortex than non-autistic girls, with these differences becoming less pronounced by age 12- due to faster cortical thinning in autistic girls. A major study published in Molecular Psychiatry (Oct 2024) found that, for the first time in living adults, autistic brains have approximately 17% lower synaptic density compared to neurotypical individuals. A lower density of these nerve cell connections was directly correlated with more pronounced differences in communication. The amygdala As well transient increase of total brain volume and differences in the cortex, the size and volume of several brain structures in particular seems to differ between individuals with and without autism. Most studies have found that the amygdala, a small area in the centre of the brain that mediates emotions such as fear, appears enlarged in autistic children. The amygdala is a particularly interesting structure to study in autism, as individuals often have difficulty interpreting and regulating emotions and social interactions. Its increased size seems to persist at least until early adolescence. However, studies in adolescents and adults tend to show that the enlargement slows down, and in some cases is even reversed so that the number of amygdala neurons may be lower than normal in autistic adults. Moreover, higher neuron density was found in the amygdala in children, with lower neuron density in other brain areas- as described by a study in Autism Research (Oct 2024). The cerebellum Another brain structure that tends to present abnormalities in autism is the cerebellum. Sitting at the back of the head near the spinal cord, it is known to mediate fine motor control and proprioception. Yet, recent literature suggests it may also play an important role in some higher other cognitive functions, including language and social cognition. Specifically, it may be involved in our ability to imagine hypothetical scenarios and to abstract information from social interactions. In other words, it may help us recognise similarities and patterns in past social interactions that we can apply to understand a current situation. This ability is poor in autism; indeed, some investigations have found the volume of the cerebellum may be smaller in autistic individuals, although research is not conclusive. Nevertheless, most research agrees that the number of Purkinje cells is markedly lower in people with autism. Purkinje cells are a type of neuron found exclusively in the cerebellum, able to integrate large amounts of input information into a coherent signal. They are also the only source of output for the cerebellum; they are responsible for connecting the structure with other parts of the brain such as the cortex and subcortical structures. These connections eventually bring about a specific function, including motor control and cognition. Therefore, a low number of Purkinje cells may cause underconnectivity between the cerebellum and other areas, which might be the reason for functions such as social cognition being impaired in autism. Written by Julia Ruiz Rua Related article: Epilepsy Project Gallery

The same condition after all? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorder 26/04/26, 14:06 Last updated: Published: 20/01/24, 11:38 The same condition after all? Practice and progress in rheumatology The relationship between hypermobile Ehlers-Danlos Syndrome (hEDS) and Hypermobility Spectrum Disorder (HSD) has been hotly debated in recent years, with research being published on a near-constant basis attempting to establish a valid symptomatological or causalogical difference between the two disorders. Now, a paper by Ritelli et al. (2022) threatens to end the savage cycle for all. Using RNA sequencing techniques and immunofluorescence, Ritelli et al. found identical gene expression and cellular characteristics in dermal biopsies from those with both conditions. Through immunofluorescence of biopsies from 20 women with hEDS, 16 women and 4 men with HSD and 40 controls, it was found that the shape and components of the extracellular matrix were greatly different in those with HSD/hEDS in comparison to those in the healthy control group. Abnormalities were discovered in the expression of cadherin-11, snail1, and αvβ3, α5β1 and α2β1 integrins. Integrins mediate the connections between the cell cytoskeleton and extracellular matrix to ensure they stay together, cell-to-cell adhesion is initiated by cadherin-11, and snail1 is localised close to the cyclin-dependent kinase inhibitor 2B (CDKN2B) gene. Snail1 can activate CDKN2B gene products when Snail1 is overexpressed to the point of reaching the general localisation of the CDKN2B domain. This demonstrates that there may be a similar causative link between the widespread inflammation and chronic pain in HSD/hEDS and rheumatoid arthritis. Li et al. (2021) proved that the polarisation of macrophages (white blood cells which destroy foreign products) was carefully controlled by the CDKN2B-AS1/ MIR497/TXNIP axis- the increased activation of which in rheumatoid arthritis catalyses the excessive polarisation of macrophages, which causes the macrophages to attack healthy cells. In rat studies published by Tan et al. (2022), it was found that rats with diabetes and induced sepsis experienced greater intestinal injury that control rats without any medical pathology who experienced induced sepsis. This was demonstrated to be due to interruptions in the miR-3061/Snail1 communication pathway. Research on this phenomenon in humans may elucidate the relevance of snail1 overproduction in hEDS/HSD sufferers to their complex gastrointestinal symptoms. If this pathway works similarly in human models of sepsis or localised GI infection, it may intimate that snail1 overproduction is responsible for the hyperpolarisation of macrophages in response to foreign product detection, which may cause immunological damage in the intestines. However, the relevance of this study to hEDS/HSD should be considered questionable until further human research into this avenue has been completed. The result of this research is that academia can potentially derive a genetic cause of the complex phenotypes demonstrated by sufferers of hEDS/HSD. This can be achieved by visualising the human genome, and testing genes like those above, or those implicated in modulating the activity of the genes above. Given this, the 2025 symposium discussed whether HSD and hEDS should be considered separate at all, with discussions around potentially reclassifying or merging them in the future, to improve access to care to patients. Written by Aimee Wilson Related articles: Ehlers-Danlos syndrome / Types of movement Project Gallery

Testing cancerous tumours Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A new tool to diagnose: liquid biopsies 26/04/26, 13:55 Last updated: Published: 15/01/24, 23:48 Testing cancerous tumours Liquid biopsies are an example of integrating next-generation sequencing to diagnose and study tumours using only blood or other fluid samples rather than solid tissue. These biopsies are significant in modern medicine, particularly in treating cancer, as they enable the earlier detection of cancers in a less invasive manner. As of 2025-26, England's NHS is implementing liquid biopsy tests for thousands of lung and breast cancer patients, enabling faster access to targeted therapies. In this article, I aim to explore liquid biopsies, their role in disease detection and issues which arise from their usage. A liquid biopsy is a test which detects cancerous tumours from the pieces of tumour that break off and circulate in the bloodstream. A liquid biopsy involves a simple blood test and analysis in the lab with a machine that separates blood cells from the plasma, allowing a pathologist to examine the fluid and look for biomarkers. These include circulating tumour cells (CTC) or circulating tumour DNA (ctDNA). CTCs are cancer cells that disseminate from a tumour and travelling in the bloodstream, whereas ctDNA is a DNA fragment from the tumour circulating in the blood. See Figure 1 for a diagram summarising this process in more detail. Finding these biomarkers shows evidence of a malignant tumour, possibly revealing its stage of development and potential metastases. Oncologists use this information to form the basis of cancer prognosis. Furthermore, genetic data from these tests provides information on suitable and effective treatments specific to the patient. In particular, the suitability for targeted therapies, which target specific genes or proteins within the cancer. Furthermore, it can monitor how well a treatment is working by seeing if the tumour has stopped growing after treatment. Finally, it can be used to predict and help prevent recurrence of cancer or progression of cancer by detecting minimal residual disease (where a small number of cancer cells remain in the body after treatment). Liquid biopsies are perhaps better and more advantageous than normal biopsies, as the method is quicker without requiring surgical intervention. In addition, liquid biopsies provide a more comprehensive tissue profile by taking tumour heterogeneity into account. This includes revealing more information about genetic variations, monitoring clonal evolution, assessing treatment resistance, and aiding in the customisation of targeted therapies. This means a more comprehensive view is provided compared to tissue biopsies, which do not represent the entire genetic diversity of a tumour. Liquid biopsies excel in overcoming these limitations by providing a systematic and dynamic assessment of the entire tumour’s genetic diversity. Unlike tissue biopsies, which may miss subclones, liquid biopsies offer a more comprehensive understanding of the overall tumour, making them a valuable tool for precision oncology. The process is also minimally invasive and only causes minimal pain. While liquid biopsies offer a less invasive means of monitoring diseases, their sensitivity and specificity in detecting biomarkers, such as circulating tumour DNA (ctDNA) or circulating tumour cells (CTCs), might vary, leading to potential false positives or negatives. Additionally, the quantity and quality of biomarkers present in bodily fluids can fluctuate, impacting the reliability of liquid biopsy results for consistent monitoring. Furthermore, the associated cost of analysing liquid biopsy samples and the technology required for accurate detection can pose financial constraints for widespread implementation in healthcare systems. See Figure 2 which summarises the advantages and disadvantages of each method. Currently, there are a few liquid biopsy tests approved by the FDA to detect cancer within a patient. One example is the “Guardant 360 CDx”, approved for use in people with non-small cell lung cancer (NSCLC). Another example is the “Foundation One liquid CDx”, which is approved for use in people with a range of cancers such as NSCLC, prostate, ovarian and breast cancer. However, more research is needed to clinically evaluate the efficacy of liquid biopsies when compared to tissue biopsies. Nevertheless, liquid biopsies show a positive prospect for cancer diagnosis. Furthermore, liquid biopsies have also been used outside of cancer, such as in cardiovascular conditions such as myocardial infarction. In myocardial infarction, specific miRNA signatures released during myocardial necrosis provide accurate early detection of myocardial infarction. Further highlighting the multilevel potential of liquid biopsies. One of the main ethical concerns surrounding liquid biopsies involves the revealing of sensitive genetic information about a patient, encompassing medical history, and genetic identity, and potentially impacting familial relationships and legal affairs. This raises critical issues regarding privacy, consent, and the secure storage of such sensitive data. Additionally, challenges surrounding standardisation, cost-effectiveness, and the establishment of robust regulatory frameworks for the handling and storage of this genetic information further underscore the ethical complexities and necessity for stringent protocols in the implementation and management of liquid biopsy technologies. To conclude, it is clear that liquid biopsies have a lot of potential in diagnosing patients and, therefore, treating patients by aiding clinical decisions made by healthcare professionals. It has proven to be useful not just in diagnosing cancer but also in cardiovascular conditions such as myocardial infarction. The process has the potential to improve future patient outcomes. However, for this to happen, issues such as costs and ethics must be addressed so that liquid biopsies can be utilised more effectively in clinical practice. Written by Harene Elayathamby References: professional, C.C. medical Liquid biopsy: What it is & procedure details , Cleveland Clinic . Available at: https://my.clevelandclinic.org/health/diagnostics/23992-liquid-biopsy (Accessed: 19 December 2023). A tale of two biopsies: Liquid biopsy vs tissue biopsy (no date) Biochain Institute Inc. Available at: https://www.biochain.com/blog/a-tale-of-two-biopsies-liquid-biopsy-vs-tissue-biopsy/ (Accessed: 19 December 2023). Adhit, K.K. et al. (2023) ‘Liquid biopsy: An evolving paradigm for non-invasive disease diagnosis and monitoring in medicine’, Cureus [Preprint]. doi:10.7759/cureus.50176. Mannelli, C. (2019) ‘Tissue vs liquid biopsies for cancer detection: Ethical issues’, Journal of Bioethical Inquiry , 16(4), pp. 551–557. doi:10.1007/s11673-019-09944-y. Figures: Journey of a liquid biopsy (no date) Diagnostics . Available at: https://diagnostics.roche.com/global/en/article-listing/infographic-journey-of-a-liquid-biopsy.html (Accessed: 19 December 2023). A tale of two biopsies: Liquid biopsy vs tissue biopsy (no date) Biochain Institute Inc. Available at: https://www.biochain.com/blog/a-tale-of-two-biopsies-liquid-biopsy-vs-tissue-biopsy/ (Accessed: 19 December 2023) Project Gallery

An extensive collection of insightful reviews on the best STEM books available. Whether you're a student looking to deepen your knowledge or something to aid your revision and research, an educator seeking great resources for your classroom, or simply a curious mind passionate about science, technology, engineering, mathematics, medicine and more, you'll find something here to inspire and inform you.  Discover Your Next Great Read Deep Dive into STEM Books Here you can explore an extensive collection of insightful reviews on the best STEM books available. Whether you're a student looking to deepen your knowledge or something to aid or complement your revision and research, an educator seeking great resources for your classroom, or simply a curious mind passionate about science, technology, engineering, mathematics, medicine and more, you'll find something here to inspire and inform you. Our Curated Selections: Intern Blues by Robert Marion, M.D. The Emperor of All Maladies by Siddhartha Mukherjee The Molecule by Dr Rick Sax and Marta New

The unique condition of microgravity Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Astronauts in space… losing gravity, losing immunity? 26/04/26, 14:42 Last updated: Published: 08/09/24, 13:39 The unique condition of microgravity Introduction Since the first successful human launch to space on April 12th, 1961, over 600 astronauts have travelled beyond the Earth’s atmosphere. Space travel is essential in driving technological innovation and consistently increases our understanding of the cosmos. However, alongside the thrill of space exploration, astronauts face significant challenges, including profound risks to their immune systems. Astronauts in space endure a unique condition of near weightlessness known as microgravity, which often causes dysregulation of their immune systems. Effect of microgravity on T-cell immunity One of the critical studies emphasising the effects of microgravity on the immune system is a twin study conducted by NASA, where they compared various gene expression datasets between an astronaut who had been on the International Space Station (ISS) for one year and their identical twin who had not travelled to space. They discovered changes in the methylation patterns of immunologically relevant genes such as NOTCH3 and SLC1A5 , which are both crucial in T cell development. They also found microgravity caused an increase in pro-inflammatory molecules and decreased anti-inflammatory molecules, alluding to spaceflight causing an increased inflammatory state. These patterns are consistent with other experiments simulating microgravity conditions, such as prolonged bed rest models. Microgravity has also been shown to induce thymic atrophy, which is when the thymus slowly shrinks and loses its function. The thymus is a primary lymphoid organ that is crucial in T cell development. An experiment performed on the International Space Station (ISS) has shown that exposing mice to 1g gravity can alleviate microgravity-induced thymic atrophy ( Figure 1 ), suggesting that exposure to a standard gravitational field is a potential treatment. The thymic environment is altered due to microgravity. In particular, thymic epithelial cells (TECs) are misplaced and, therefore cannot perform their role in T cell maturation. Overall, there is a significant decrease in the output of T cells from the thymus, shown by a clear decrease in thymic mass and alterations in gene expression related directly to the process of T cell differentiation. Effect of microgravity on the bone marrow Furthermore, microgravity affects the bone marrow, another primary lymphoid organ. The bone marrow consists of many mesenchymal stem cells (MSCs), which differentiate hematopoietic stem cells (HSCs) into leukocytes. Microgravity inhibits osteogenesis and promotes adipogenesis, which means that bone formation is slowed down, but fat cell production is increased. This happens due to the changes to the structure inside the cell, known as actin cytoskeleton, which affects transcriptional regulators, which generally control cell differentiation. In space, there is also suppression of the cytokine CXCL2 in MSCs, which affects HSC differentiation into immune cells, indicating a link between MSC dysfunction and immunosuppression faced by astronauts. Other factors affecting the immune system Microgravity is the main factor behind immune system dysregulation in astronauts, but other factors, such as stress and exposure to cosmic radiation, also play a role. Cosmic radiation can damage DNA, leading to mutations that impair the immune system’s ability to function properly. Stress hormones are known to affect immune system function. For instance, cortisol can reduce the number of leukocytes in circulation. Conclusion Due to the compromised state of the astronauts’ immune systems, latent viruses often reactivate. Herpes viruses, such as varicella-zoster virus (chickenpox!) and Epstein-Barr virus, have been documented to be reactivated in astronauts during and after space flight. This is mainly due to the loss of T cell immunity ( Figure 2 ) and a reduction in NK cell potency and number. Microgravity affects NK cells by changing their cytoskeletal form, which they need to perform cytotoxic functions. Understanding and mitigating the risks of space travel is crucial as more prolonged and ambitious missions are planned, such as sending humans to Mars. The primary medical countermeasure for the reactivation of herpes viruses is re-vaccination. However, at this current point, only a vaccine for varicella-zoster virus is available. Future research focusing on artificial gravity and environmental changes on spacecraft and the ISS may provide a safer journey for astronauts spending extended time in space. Written by Devanshi Shah Related articles: AI in space / The role of chemistry in space / Colonisation of Mars / Artemis: the lunar south pole base REFERENCES Akiyama, T., Horie, K., Hinoi, E., Hiraiwa, M., Kato, A., Maekawa, Y., Takahashi, A. & Furukawa, S. (2020) How does spaceflight affect the acquired immune system? npj Microgravity. 6 (1), 1–7. doi:10.1038/s41526-020-0104-1. Simon N. Archer, Carla Möller-Levet, María-Ángeles Bonmatí-Carrión, Emma E. Laing, Derk-Jan Dijk. Extensive dynamic changes in the human transcriptome and its circadian organization during prolonged bed rest -ScienceDirect. https://www-sciencedirect.com.iclibezp1.cc.ic.ac.uk/science/article/pii/S2589004224005522?via%3Dihub [Accessed: 16 August 2024]. Hicks J, Olson M, Mitchell C, Juran CM, Paul AM. The Impact of Microgravity on Immunological States. Immunohorizons. 2023 Oct 1;7(10):670-682. doi: 10.4049/immunohorizons.2200063. PMID: 37855736; PMCID: PMC10615652. The NASA Twins Study: A multidimensional analysis of a year-long human spaceflight | Science. https://www.science.org/doi/10.1126/science.aau8650 [Accessed: 16 August 2024]. Hicks, J., Olson, M., Mitchell, C., Juran, C.M. & Paul, A.M. (2023) The Impact of Microgravity on Immunological States. ImmunoHorizons. 7 (10), 670–682. doi:10.4049/immunohorizons.2200063. Hobbs, Z. (2023) How many people have gone to space? | Astronomy.com. Astronomy Magazine. https://www.astronomy.com/space-exploration/how-many-people-have-gone-to-space/ . Mehta, S.K., Laudenslager, M.L., Stowe, R.P., Crucian, B.E., Feiveson, A.H., Sams, C.F. & Pierson, D.L. (2017) Latent virus reactivation in astronauts on the international space station. npj Microgravity. 3 (1), 1–8. doi:10.1038/s41526-017-0015-y. Surrey, U. Microgravity found to cause marked changes in gene expression rhythms in humans. https://phys.org/news/2024-03-microgravity-gene-rhythms-humans.html [Accessed: 16 August 2024]. Project Gallery

Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and the other sciences. Log In Welcome to Scientia News DELIVERING INFORMATIVE CONTENT Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and other sciences. We hope this platform helps you discover something that inspires your curiosity, and encourages you to learn more about important topics in STEM. Meet the Official Team NAVIGATE AND CLICK THE PHOTOS BELOW TO LEARN MORE ABOUT US! To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. Latest Articles ecology Rock, paper, survival? View More chemistry Diels–Alder Reaction View More biology Addressing Health Inequalities View More chemistry Molecular blueprints: the synthesis of ibuprofen View More CONTACT CONTACT US Scientia News welcomes anyone who wants to share their ideas and write for our platform. If you are interested in realising your writing potential with us AND live in the UK; and/ or would like to give feedback: Email us at scientianewsorg@gmail.com or fill in our GET IN TOUCH form below and we'll be in contact... Follow us on our socials for the latest updates. Comment, like and share! Join our mailing list below for latest site content. You can also sign up to become a site member . SUBSCRIPTION Join our mailing list to receive alerts for new articles and other site content. Be sure to check your spam/ junk folders in case emails are sent there. Email Subscribe GET IN TOUCH First Name Last Name Email Message Send Thanks for submitting!

Jennifer Doudna and Emmanuelle Charpentier were jointly awarded the Nobel Prize in Chemistry in the year 2020, for their major contributions in reducing the number of components in the CRISPR-Cas9 system. An outline of their discovery CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats) can be used, by removing, adding, or altering particular DNA sequences and may edit specific parts of the genome. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Who were the winners of the Nobel Prize in Chemistry in 2020? Last updated: 26/04/26 Published: 02/02/23 Jennifer Doudna and Emmanuelle Charpentier were jointly awarded the Nobel Prize in Chemistry in the year 2020, for their major contributions in assembling and demonstrating Cas9 gene editing capabilities in vitro. An outline of their discovery Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR-Cas9) can be used, by removing, adding, or altering particular DNA sequences and may edit specific parts of the genome. A four-part mechanism called the Cas9 endonuclease consists of two small molecules. Charpentier discovered the tracrRNA, which, when combined with the crRNA (discovered in 2007 by a different group), they could assemble and demonstrate Cas9 gene editing capabilities in vitro. The two types of sequences were later combined to the now well-known "single-guide RNA" (sgRNA)- done in collaboration with Doudna in 2012. By combining these two RNA molecules into a sgRNA, the Cas9 endonuclease was redesigned into a more manageable two-component system that could locate and cut the DNA target defined by the guide RNA- CRISPR/Cas9 ‘genetic scissors’. It can silence or activate genes as well as add or remove others. The Nobel Prize in Chemistry was awarded in 2020 in recognition of this contribution. Some advantages of this technology: quick easy adaptable innovative, unique Disadvantages: distribution challenges extremely conservative ethical issues some off-target effects some negative outcomes Significance of this discovery This discovery is important in preventing disease and is such a revolutionary tool. It does not just help humans but also animals, plants and even bacteria. CRISPR has already been applied to various disorders, such as cancer and infectious diseases. By making it possible to make changes to the target cells' genomes, which were previously challenging to do, the procedure offers a new perspective on biological treatment and demonstrates how important this tool is. But since this technology is still recent, scientists must develop straightforward processes and techniques to monitor and test its progress, performance, and outcomes. Jennifer Doudna Hailing from Washington DC., USA, Jennifer Doudna was born in 1964. As a professor of biochemistry, biophysics, and structural biology, Doudna’s main research focus is on RNA, and its variety of structures and functions. It was her research lab’s work that led to the discovery of CRISPR-Cas9 as an extraordinarily powerful tool to cut and edit the human genome to treat disease. This remarkable discovery was a decade ago in 2012, when Doudna and others were able to copy a bacterial system to create molecular scissors, in order to edit the genetic code. In October 2020, at the time of her being awarded the Nobel Prize in Chemistry, Doudna was affiliated to the University of Berkeley, in California. Emmanuelle Charpentier Coming from a French background, Emmanuelle Charpentier is a professor and researcher in microbiology, genetics, and biochemistry. Born in 1968, researcher Charpentier has made tremendous progress in her respective field. From being the director at the Berlin Max Planck Institute for Infection Biology in 2015, to founding her own independent research institute- the Max Planck Unit for the Science of Pathogens in the year 2018, and of course being jointly awarded the Nobel Prize in Chemistry in 2020; it is true that Charpentier has added new, valuable research in her work and has come a long way in her career. Why the CRISPR/ Cas9 system fascinates us We find CRISPR fascinating because as biological science students, we know this tool is vital for genetics and can help cure present incurable diseases such as sickle cell disease as well as cancer, showing what a revolutionary tool this is. It does not just help humans but also animals, plants and even bacteria showing how broad biology is and different fields can be linked to one another. Researchers are constantly coming up with new ways to use CRISPR-Cas9 gene editing technology to solve problems in the real world, such as epigenome editing, new cell and gene therapies, infectious disease research, and the conservation of endangered species. The advantages of this technology are that it is quick, easy and adaptable, but its disadvantages include distribution challenges, extremely conservative ethical issues, some off-target effects, and some negative outcomes. By making it possible to make changes to the target cells' genomes, which were previously challenging to do, the procedure offers a new perspective on biological treatment and demonstrates how important this tool is. Written by Jeevana Thavarajah, and Manisha Halkhoree Scientia News Founder and Managing Director Related articles: Female Nobel prize winners in Chemistry and in Physics