Search Index

The natural body clock and the involvement of genetics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The chronotypes 26/04/26, 14:33 Last updated: Published: 27/11/24, 11:47 The natural body clock and the involvement of genetics Feeling like heading to bed at 9 pm and waking up at the crack of dawn? These tendencies define your chronotype, backed up by changes within your body. A generally overlooked topic, chronotypes affect our everyday behaviour. Many people innately associate themselves with a certain chronotype, but what do we know about how these physiological differences are caused at a molecular level? The word ‘chronotype’ was first coined in the 1970s, combining the Greek words chrono (time) and type (kind or form). While the term is relatively modern, the concept emerged in the 18th century. Researchers in the 1960s and 1970s, like Jürgen Aschoff, explored how internal biological clocks influence our sleep-wake cycles, leading to the classification of people into morning or evening types based on their activity patterns. The first evidence of body clocks was found in plants rather than humans, thus leading to the invention of flower clocks, which were used to tell the time of the day. Before delving into the details, let us be introduced to the general categories of chronotypes, which describe a person’s inclination to wake up and sleep while also affecting productivity periods. We know of the following three categories: The morning type (also referred to as larks): they are inclined to wake up and go to bed early because they feel most alert and productive in the mornings. The evening type (also called the owls): they feel most alert and productive in the evenings and onwards, so they are inclined to wake up and go to bed later. The intermediate types (also referred to as the doves): they fall in the middle of this range. Let’s explore what we know about the genetics that prove that chronotypes are a natural phenomenon. Genetics of chronotypes The main determining factor in our chronotypes is the circadian period. This is the body’s 24 hour cycle of changes that manifest into feelings of productivity and energy or tiredness. The length of this is crucial in determining our chronotypes. More importantly, specific physiological changes that cause these effects are melatonin and core body temperature. One study suggested that the morning types might have circadian periods shorter than 24 hours, whereas evening chronotypes might have circadian periods longer than 24 hours. A major clock gene is PER, which includes a collection of genes known as PER1, PER2 and PER3, which are thought to regulate circadian period factors. Specifically, it has been observed that a delay in the expression of the PER1 gene in humans causes an increased circadian period. Possible causes for this delay may be rendered to a variation within the negative feedback loop that PER1 operates in, including hereditary differences, environmental causes, changes to hormonal signals and age. This process may describe the mechanism behind the evening chronotype. Molecular polymorphs in the PER3 gene are thought to cause shorter circadian rhythms and the manifestation of the morning types. Similarly, a polymorph in the PER3 gene can be caused by a plethora of causes, as described for PER1. These nuances cause differences in the periodic release and stop of hormones which control the circadian rhythm, such as melatonin and body temperature. This is important in its power to control our energy levels, windows of productivity, and sleep cycles. The consensus remains that chronotypes are attributable to genetic premeditation by 50%, however, it has also been observed that chronotypes are prone to change with advancing age. Increased age is associated with an inclination towards an earlier phase chronotype. Age-related variation has been observed to be higher in men. There also exists an association between geographical locations and phase preference; increasing latitude (travelling North or South) from the earth's equator is associated with later chronotypes. Of course, many variations and factors come into play to affect these findings, such as ethnic genetics, climate, work culture and even population density. The effect on core body temperature and melatonin Polymorphisms in the PER3 cause a much earlier peak in body temperature and melatonin in the morning than in the evening and intermediate types. These manifest as the need to sleep much earlier in the morning and a decreased feeling of productivity later in the day. In contrast, the evening types experience a later release of melatonin and a drop in core body temperature, causing a later onset of tiredness and lack of energy. It can then be inferred that the intermediate types are affected by the expression of these genes in a way that falls in the middle of this spectrum. The Morning-Eveningness Questionnaire (MEQ) The MEQ is a self-reported questionnaire you may complete to gain more insight into your chronotype category. Clinical psychologist Micheal Breus created it and uses different animals to categorise the chronotypes further. The framework suggests that the Bear represents individuals whose energy patterns are entrained to the rising and the sun's setting and are the most common types in the general population. The Lions describe the early risers, and Wolves roughly equate to the evening types. Recently, a fourth chronotype has been proposed: the Dolphin, whose responses to the questionnaire suggest that they switch between modes. Whether you're a Bear, Lion, Wolf, or Dolphin, understanding your chronotype can be a game-changer in optimising your daily routine. So, what’s your chronotype—and how can you start working with your body’s natural rhythms to unlock your full potential? A sleep study ? The MEQ ? Maybe keeping a tracker. Conclusion Understanding differences in circadian rhythms and sleep-wake preferences offers valuable insights into human behaviour and health. Chronotypes influence various aspects of daily life, including sleep patterns and quality, cognitive performance and susceptibility to specific health conditions, including sleep-wake conditions. An extreme deviation in circadian rhythms and sleep cycles may lead to such conditions as Advanced sleep-wake phase Disorder (ASPD) and Delayed sleep-wake phase Disorder (DSPD). Recognising these variations is also helpful in optimising work schedules and aligning to jet lags, improving mental and physical health by tailoring our biological rhythms to our environments. Many individuals opt to do a sleep study at an institution to gain insights into their circadian rhythms. A healthcare professional may also prescribe this if they suspect you have a circadian disturbance such as insomnia. Written by B. Esfandyare Related articles: Circadian rhythms and nutrition / Does insomnia run in families? REFERENCES Emens JS, Yuhas K, Rough J, Kochar N, Peters D, Lewy AJ. Phase Angle of Entrainment in Morning‐ and Evening‐Types under Naturalistic Conditions. Chronobiology International. 2009 Jan;26(3):474–93. Lee, J.H., Kim, I.S., Kim, S.J., Wang, W. and Duffy, J.F. (2011). Change in Individual Chronotype Over a Lifetime: A Retrospective Study. Sleep Medicine Research , 2(2), pp.48–53. doi: https://doi.org/10.17241/smr.2011.2.2.48 . Ujma, P.P. and Kirkegaard, E.O.W. (2021). The overlapping geography of cognitive ability and chronotype. PsyCh Journal , 10(5), pp.834–846. doi: https://doi.org/10.1002/pchj.477 . Shearman LP, Jin X, Lee C, Reppert SM, Weaver DR. Targeted Disruption of the mPer3 Gene: Subtle Effects on Circadian Clock Function. Molecular and Cellular Biology. 2000 Sep 1;20(17):6269–75. Viola AU, Archer SN, James Lynette M, Groeger JA, Lo JCY, Skene DJ, et al. PER3 Polymorphism Predicts Sleep Structure and Waking Performance. Current Biology. 2007 Apr;17(7):613–8. 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

A leap forward in primate research Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Monkey see, monkey clone 26/04/26, 14:26 Last updated: Published: 07/09/24, 19:20 A leap forward in primate research Chinese scientists have recently unlocked the secrets of cloning Rhesus monkeys offering new hope for medical breakthroughs. Introduction When we think of cloning, perhaps the first thing that comes to mind is Dolly the sheep, the first mammal ever cloned from an adult cell back in 1996. This groundbreaking achievement inspired a revolution leading to the successful cloning of other mammals such as cattles and pigs. However, cloning primates, especially Rhesus monkeys, has proven to be a significant challenge due to the low success rates and high embryonic losses during development. What is cloning? Cloning is the process of creating an identical genetic copy of an organism. In mammals, this is typically done through a technique called somatic cell nuclear transfer (SCNT). In SCNT, the nucleus (the compartment storing genetic material) from a cell of the animal to be cloned is transferred into an egg cell that has had its own nucleus removed. This hybrid egg cell then develops into an embryo which is implanted into a surrogate mother to grow into a new individual. Despite the success in cloning other mammals, cloning primates has proven to be a significant challenge. However, the potential benefits of cloning primates for medical research make it a worthwhile endeavour. The importance of cloning primates You might be wondering why being able to clone primates is so important. Well, primates like the Rhesus monkey are invaluable models for studying human diseases and create new therapies! The reason we can use them as disease models is because they share about 93% genetic identity and have very similar physiological characteristics with humans. For instance, Rhesus monkeys also experience a decline in their cognitive abilities as they age, and they lose important connections between brain cells in the part of the brain responsible for complex thinking, even when there's no severe brain damage. Moreover, Rhesus monkeys also develop the same kinds of brain changes that we see in people with Alzheimer's disease, such as the buildup of sticky proteins called amyloid-beta and tangled fibres of another protein called tau.These similarities make them excellent models for understanding how human diseases progress and for developing new treatments. So, by cloning these animals, researchers might be able to create monkeys with specific genetic changes that mimic human diseases even more closely. This could allow scientists to study these diseases in greater detail and develop more effective therapies. Cloning primates could give us a powerful tool to fight against some of the most challenging disorders that affect the human brain! A breakthrough in primate cloning Now, a group of scientists in China have made a breakthrough in primate cloning. They successfully cloned a Rhesus monkey using a novel technique called trophoblast replacement (TR). This innovative approach not only helps us better understand the complex process of cloning but also offers a promising way to improve the efficiency of primate cloning, bringing us one step closer to unlocking the full potential of this technology for medical research and beyond. The awry DNA methylation of cloned conkey embryos To understand why cloning monkeys is so challenging, Liao and colleagues (2024) took a closer look at the genetic material of embryos created in two different ways. They compared embryos made through a standard fertility treatment called intracytoplasmic sperm injection (ICSI) with those created via the cloning technique, SCNT. What they found was quite surprising! To make matters worse, the scientists also noticed that certain genes, known as imprinted genes, were not functioning properly in the SCNT embryos. Imprinted genes are a special group of genes that play a crucial role in embryo development. In a healthy embryo, only one copy of an imprinted gene (either from the mother or the father) is active, while the other copy is silenced. But in the cloned embryos, both copies were often incorrectly switched on or off. Here's the really concerning part: these genetic abnormalities were not just present in the early embryos but also in the placentas of the surrogate monkey mothers carrying the cloned offspring. This suggests that the issues arising from the cloning process start very early in development and continue to affect the pregnancy. Liao and colleagues suspect that the abnormal DNA methylation patterns might be responsible for the imprinted gene malfunction. It's like a game of genetic dominos – when one piece falls out of place, it can cause a whole cascade of problems down the line. Piecing together this complex genetic puzzle is crucial for understanding why primate cloning is so difficult and how we can improve its success in the future. By shedding light on the mysterious world of DNA methylation and imprinted genes, Liao and colleagues have brought us one step closer to unravelling the secrets behind monkey cloning. Digging deeper: what does the data reveal? Liao et al. (2024) discovered that nearly half of the cloned monkey foetuses died before day 60 of the gestation period, indicating developmental defects in the SCNT embryos during implantation. They also found that the DNA methylation level in SCNT blastocysts was 25% lower compared to those created through ICSI (30.0% vs. 39.6%). Furthermore, out of the 115 human imprinting genes they examined in both the embryos and placentas, four genes - THAP3, DNMT1, SIAH1, and RHOBTB3 - showed abnormal expression and loss of DNA methylation in SCNT embryos. These findings highlight the complex nature of the reprogramming process in SCNT and the importance of imprinted genes in embryonic development. By understanding these intricacies, scientists can develop targeted strategies to improve the efficiency of primate cloning. The power of trophoblast replacement To avoid the anomalies in SCNT placentas, the researchers developed a new method called TR. In this method, they transferred the inner cell mass (the part of the early embryo that develops into the baby) from an SCNT embryo into the hollow cavity of a normal embryo created through fertilisation, after removing its own inner cell mass. The idea behind this technique is to replace the abnormal placental cells in the SCNT embryo with healthy ones from the normal embryo. And it worked! Using this method, along with some additional treatments, Liao et al. (2024) successfully cloned a healthy male Rhesus monkey that has survived for over two years (FYI his name is Retro!). The ethics of cloning While the scientific advances in primate cloning are exciting, they also raise important ethical questions. Some people worry about the potential misuse of this technology, for instance to clone humans, which is widely considered unethical. Others are concerned about the well-being of cloned animals, as the cloning process can sometimes lead to health problems. As scientists continue to make progress in cloning technology, it is essential to have open discussions about the ethical implications of their work. Rules and guidelines must be put in place to ensure that this technology is developed and used responsibly, with the utmost care for animal welfare and the concerns of society. Looking to the future The successful cloning of a rhesus monkey using TR opens up new avenues for primate research. This technology can help scientists create genetically identical monkeys to study a wide range of human diseases, from neurodegenerative disorders like Alzheimer's and Parkinson's to infectious diseases like HIV and COVID-19. The trophoblast replacement technique developed by Liao et al. (2024) increases the likelihood of successful cloning by replacing the abnormal placental cells in the SCNT embryo with healthy ones from a normal embryo. However, it is important to note that this technique does not affect the genetic similarity between the clone and the original monkey, as the inner cell mass, which gives rise to the foetus, is still derived from the SCNT embryo. Moreover, this research provides valuable insights into the mechanisms of embryonic development and the role of imprinted genes in this process. By understanding these fundamental biological processes, scientists can not only improve the efficiency of cloning but also develop new strategies for regenerative medicine and tissue engineering. As we look to the future, cloning monkeys could help us make groundbreaking discoveries in medical research and develop new treatments for human diseases. However, we must also carefully consider the ethical implications of cloning primates and ensure that this powerful tool is used responsibly and for the benefit of society. Written by Irha Khalid Related articles: Do other animals get periods? / Germline gene therapy (GGT) REFERENCES Beckman, D. and Morrison, J.H. (2021). Towards developing a rhesus monkey model of early Alzheimer’s disease focusing on women’s health. American Journal of Primatology , [online] 83(11). doi: https://doi.org/10.1002/ajp.23289 . Liao, Z., Zhang, J., Sun, S., Li, Y., Xu, Y., Li, C., Cao, J., Nie, Y., Niu, Z., Liu, J., Lu, F., Liu, Z. and Sun, Q. (2024). Reprogramming mechanism dissection and trophoblast replacement application in monkey somatic cell nuclear transfer. Nature Communications , [online] 15(1), p.5. doi: https://doi.org/10.1038/s41467-023-43985-7 . Morrison, J.H. and Baxter, M.G. (2012). The ageing cortical synapse: hallmarks and implications for cognitive decline. Nature Reviews Neuroscience , [online] 13(4), pp.240–250. doi: https://doi.org/10.1038/nrn3200 . Paspalas, C.D., Carlyle, B.C., Leslie, S., Preuss, T.M., Crimins, J.L., Huttner, A.J., Dyck, C.H., Rosene, D.L., Nairn, A.C. and Arnsten, A.F.T. (2017). The aged rhesus macaque manifests Braak stage III/IV Alzheimer’s‐like pathology. Alzheimer’s & Dementia , [online] 14(5), pp.680–691. doi: https://doi.org/10.1016/j.jalz.2017.11.005 . Shi, L., Luo, X., Jiang, J., Chen, Y., Liu, C., Hu, T., Li, M., Lin, Q., Li, Y., Huang, J., Wang, H., Niu, Y., Shi, Y., Styner, M., Wang, J., Lu, Y., Sun, X., Yu, H., Ji, W. and Su, B. (2019). Transgenic rhesus monkeys carrying the human MCPH1 gene copies show human-like neoteny of brain development. National Science Review , [online] 6(3), pp.480–493. doi: https://doi.org/10.1093/nsr/nwz043 . Project Gallery

Differences in brain structure Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Brief neuroanatomy of autism 26/04/26, 14:17 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

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, 14:27 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. 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

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

When deciding on the treatment of diseases, experts must gain as much relevant information as they can about that disease, before acting on an informed decision. When cancer is suspected, it might be that the decision for future treatment and prognosis be heavily weighted on the results of biopsies Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Cancer biomarker and evolution Last updated: 27/02/25 Published: 30/01/23 Development of Novel Biomarkers by Studying Cancer Evolution What does cancer evolution mean to cancer diagnosis and prognosis? How does studying it provide a better outlook on cancer precision medicine? =================== When deciding on the treatment of diseases, experts must gain as much relevant information as they can about that disease, before acting on an informed decision. When cancer is suspected, it might be that the decision for future treatment and prognosis be heavily weighted on the results of biopsies. After all, this is the standard for diagnosing many cancers. It takes one needle to take “information” that is used to predict patients’ outcomes and their respective treatment options, in other words, a test that might just predict their future. Cancer is an evolving disease. There have been many studies over the decades that demonstrate solid cancers’ singular-cell origins. Other studies show how cancer may evolve from a single cell to a mass of cells through Darwinian or branched evolution. This also implies that many things that apply to other evolutionary phenomena also apply to evolving cancer lines: mutation, genetic drift, selection and their selection pressures. In the end, what originated from one cell turns out to be a tumour with a unique genetic landscape, made up of numerous cancer subpopulations, each with its own unique genotypic and phenotypic profile and each of these subpopulations of cancerous cells evolving on its own. This phenomenon is more commonly referred to as intratumor heterogeneity (ITH). What all of this means to biopsies, is that when a single-site needle biopsy is done, it might not give an accurate representation of the whole tumour. The tumour itself, depending on its stage of development may be quite uniform with minimal ITH, however, it may also, in the eyes of a geneticist, look like a mosaic with multiple different “populations” of cancerous cells. Say, for example, the biopsy is aimed to target certain biomarkers (e.g. single nucleotide polymorphisms (SNPs)) or other “landmarks” such as satellites, the biopsy will only view whatever the needle so happened to have sampled. In other words, sampling could have made it look like a mosaic is red, even though the majority of the mosaic at the time is blue, but it seemed red for we only found red during the biopsy. Additionally, this mosaic is changing, new colours may emerge just like new lines arise within the same tumour. ITH introduces what is known as sampling bias, where samples taken from biopsies only provide an overview or snapshot of the tumour at its state and only pick up on one piece of the actively evolving puzzle, potentially missing many details, in this case, biomarkers from other tumour subpopulations. To solve the issues of ITH, scientists participating in the TRACERx research consortium are employing unique methods to sample tumours in an approach to cancer evolution. The research involved using multiregional sampling and RNA sequencing to sample tumours from patients with non-small cell lung cancers (NSCLC) at different timestamps, i.e. during the various stages of cancer development, metastasis and relapse. By using this approach, the team managed to document better how cancer evolves and how the genomic landscape and tumour architecture changes over time. Furthermore, they succeeded in honing genes that are uniformly conserved and expressed throughout the tumour, even after the effects of ITH. The research looked over 20,000 expressed genes and found 1,080 genes that despite cancer evolution and ITH, are relatively conserved and clonally expressed, relatively unaffected by sampling bias. Furthermore, using machine learning, 23 genes (from the 1,080) were found to be predictive of patient outcomes. Meaning, this novel set of genes or “biomarkers” may be used as a basis for prognosis and to predict mortality in NSCLC. This novel biomarker is named ORACLE or Outcome Risk Associated Clonal Lung Expression signature and scientists are hopeful that it may be used to determine the relative aggressiveness of lung cancers, whilst maintaining a robust function unaffected by ITH. By targeting ORACLE, it mattered less where the biopsy needle is placed on the tumour, as these genes are found clonally. In terms of its effectiveness, a trial shows that having high scores of ORACLE signatures is associated with an increased risk of death within five years of diagnosis. In addition, other trials show that by targeting ORACLE, scientists were able to identify patients with a substantial risk of poor clinical outcomes. Overall, research on the application of ORACLE has shown satisfactory results in predicting patient outcomes and is found to be relatively resistant to the confounding effects of ITH. In summary, we have seen what cancer evolution may cause, and how it shadows the effectiveness of conventional biopsies and biomarkers due to sampling bias in ITH. We also find the research by the TRACERx Consortium and how they aim to study the effects of cancer evolution and ITH, finding a set of genes that are found and expressed throughout the tumour, yet still provide a favourable measure to patient outcomes. Whilst these topics are still under active research, it is clear, how studying cancer evolution and changing the approach to biopsies and biomarker designs can improve the overall quality of diagnosis and cancer prognosis. After all, finding what is wrong is as important as fixing the problem. We hope that similar biomarkers may be developed in the future, applicable to many other types of cancers. Written by Stephanus Steven Related articles: Thyroid cancer / Arginine and tumour growth / NGAL- a marker for kidney damage REFERENCES Biswas, D. et al. (2019) “A clonal expression biomarker associates with lung cancer mortality,” Nature Medicine, 25(10), pp. 1540–1548. Available at: https://doi.org/10.1038/s41591-019-0595-z. Header image: Lung cancer cells. Anne Weston, Francis Crick Institute. Attribution-Non-Commercial 4.0 International (CC BY-NC 4.0)

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