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Read articles delving into the universal genetic code: from CRISPR-Cas9 and epigenetics, to AI diagnosis, schizophrenia, and ancestry. Genetics Articles Read articles delving into the universal genetic code: from CRISPR-Cas9 and epigenetics, to AI diagnosis, schizophrenia, and ancestry. You may also like: Biology The CRISPR- CAS9 system Who were the Nobel Prize winners of Chemistry in 2020? What did they discover? Micro-chimerism, and George Floyd's death A Publett collaboration Schizophrenia Complex disease series: the influence of the environment on complex diseases. Article #1 Genetically-engineered bacteria decompose plastic A solution to plastic pollution Gene therapy by rAAVs rAAVs- recombinant adeno-associated viruses An introduction to epigenetics Interactions between genes and the environment Are aliens on Earth? Applications of ancient DNA analysis New horizons in Alzheimer's Reaching new potential in research The Y chromosome unveiled A remarkable discovery Decoding p53 A fundamental tumour supressor protein Epigenetics and queen bees What distinguishes queen bees from worker bees? Genetics of excessive smoking and drinking What are their contribution? SNPs and haplogroups Solving the mystery of ancestry Germline gene therapy A Scientia News Biology and Genetics collaboration Chimeras A genetic phenomenon Unfolding prion diseases What happens when proteins don't fold properly? Article #5 in a series on Rare diseases. Diagnosing genetic diseases with AI The advancements made by AI in diagnosis Breaking down Tay-Sachs A rare inherited disease caused by a missing enzyme. Article #6 in a series on Rare diseases. Genetics of ageing and longevity What genes and transcription factors are involved in these processes? Ehlers-Danlos syndrome How it's caused. Article #7 in a series on Rare diseases. Next

Mortality trends, mechanisms, and future strategies Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Illuminating Thyroid Cancer 09/07/25, 14:22 Last updated: Published: 23/06/24, 09:24 Mortality trends, mechanisms, and future strategies Introduction The thyroid gland is situated at the front of the neck, below the larynx and it is butterfly-shaped with two lobes located on either side of the trachea. The thyroid gland produces hormones such as thyroid hormone and calcitonin, which are necessary for regulating metabolism in the body. The thyroid hormone is responsible for regulating the human body's metabolic rate, growth, and development. It plays an important role in controlling heart, muscle and digestive function, brain development and bone maintenance. Calcitonin produced by the thyroid gland helps the body control calcium balance. Here in this short article, we discuss and understand the molecular mechanisms, mortality trends, and future strategies for improving diagnosis, treatment, and prevention of thyroid cancer. What is thyroid cancer? Thyroid cancer occurs due to the abnormal growth of cells in the thyroid gland. Over the past few years, the number of thyroid cancers has been continuously increasing, and it has become a topic of growing concern in both medical society and the general public. Understanding the severity of thyroid cancer is important for individuals affected by the disease, as well as for researchers, scientists, and healthcare professionals. Thyroid cancer occurs in both men and women, and it is most common in women between the ages of 30 and 60. Most cases of thyroid cancer occur without risk factors, although a few have inherited forms of thyroid cancer. After the removal of cancer or tumour cells, thyroid cancer is grouped by the appearance of the tumour cells on biopsy. The most common types of thyroid cancers are well-differentiated thyroid cancers, where the cells keep essential characteristics of normal thyroid cells when they become malicious and they can be further classified as papillary thyroid cancer, and follicular thyroid cancer. The other less common types of thyroid cancer are medullary thyroid carcinoma, poorly differentiated thyroid carcinoma, and anaplastic thyroid carcinoma, which is most difficult to treat. Understanding thyroid cancer molecular mechanisms Thyroid cancer, a complicated disease, is caused by several molecular pathways that contribute to its onset and progression. Thyroid cancer develops mostly in the thyroid gland, which regulates metabolism and growth. Several genetic abnormalities within this gland play an important role in the initiation and progression of malignant cells. The BRAF gene is important in thyroid cancer because alterations, particularly the BRAF V600E variant, are usually associated with disease development and progression, particularly in papillary thyroid carcinoma (PTC). This mutation causes the MAPK signalling pathway to be activated indefinitely, resulting in uncontrolled cell proliferation. As a result, BRAF-mutated thyroid tumours frequently exhibit aggressive behaviour and a poor prognosis, providing problems for traditional treatments. Understanding the involvement of the BRAF gene allows for the creation of targeted medicines that selectively inhibit the aberrant signalling pathways induced by BRAF mutations, presenting intriguing paths for improved treatment outcomes. Furthermore, BRAF mutations serve as important biomarkers for identifying patients who may benefit from targeted medicines, allowing personalised therapy methods customised to specific genetic profiles in thyroid cancer management. The BRAF V600E mutant, which is typically seen in papillary thyroid carcinoma (PTC), the most prevalent subtype of thyroid cancer, is one of the most extensively researched genetic variants in thyroid cancer. This mutation activates the MAPK signalling pathway, which drives excessive cell growth and proliferation. Understanding the specific genetic abnormalities found in thyroid cancer can provide vital information about the disease's underlying causes. Furthermore, mutations in the RET gene are linked to medullary thyroid carcinoma (MTC), another kind of thyroid cancer. These mutations cause the RET tyrosine kinase receptor to be constitutively activated, resulting in aberrant cell proliferation and tumour formation. By understanding the impact of genetic abnormalities in thyroid cancer, researchers can identify possible therapeutic targets and create more effective treatment techniques. Unveiling thyroid cancer mortality trends Analysing mortality rates in thyroid cancer provides valuable insights into the disease's influence on public health and healthcare systems. While average mortality rates have decreased over time, various demographic groups continue to face discrepancies in survival rates. Age, gender, and financial position are important factors in determining prognosis and access to care. For example, older persons may have worse results due to comorbidities and delays in identification and treatment. Similarly, those from poorer socioeconomic origins may experience challenges in getting healthcare services, resulting in differences in survival rates. By recognising these discrepancies and understanding the underlying causes, healthcare practitioners and governments can design focused initiatives to improve outcomes for all thyroid cancer patients. The expected increase in thyroid cancer mortality rates in the United Kingdom from around 480 deaths per year in 2023-2025 to around 640 deaths per year in 2038-2040 is a troubling trend. Mortality rates are predicted to climb by 6% overall throughout this time, reaching one death per 100,000 people per year by 2038-2040. This increase is mostly driven by a projected 10% increase in female mortality rates, with rates reaching one death per 100,000 by 2038-2040. In contrast, male mortality rates are expected to fall somewhat, by less than 1%, reaching one death per 100,000 people per year by 2038-2040. These forecasts highlight the need for ongoing research, preventive, and treatment initiatives to meet the rising burden of thyroid cancer mortality. The expected increase in thyroid cancer mortality rates in the United Kingdom from around 480 deaths per year in 2023-2025 to around 640 deaths per year in 2038-2040 is a troubling trend. Mortality rates are predicted to climb by 6% overall throughout this time, reaching one death per 100,000 people per year by 2038-2040. This increase is mostly driven by a projected 10% increase in female mortality rates, with rates reaching one death per 100,000 by 2038-2040. In contrast, male mortality rates are expected to fall somewhat, by less than 1%, reaching one death per 100,000 people per year by 2038-2040. These forecasts highlight the need for ongoing research, preventive, and treatment initiatives to meet the rising burden of thyroid cancer mortality. Intersections and insights The interaction of molecular mechanisms and mortality trends provides crucial information about thyroid cancer biology and therapeutic therapy. For example, studies on radiation-induced thyroid cancer emphasise the long-term effects of environmental exposures on disease risk. According to studies, being exposed to ionising radiation, whether from medical treatments or nuclear accidents, increases the risk of acquiring thyroid cancer later in life. Furthermore, combining genomic research findings with epidemiological data improves our understanding of illness aetiology and influences public health measures. Identifying patients at high risk of getting thyroid cancer allows healthcare providers to adopt focused screening programmes and preventive measures to discover the disease at an early stage when treatment is most successful. Strategies for the future Future thyroid cancer management strategies include precision medicine, immunotherapy, and public health initiatives. These approaches have great opportunities for improving patient outcomes and lowering the impact of thyroid cancer on individuals and healthcare systems. Precision Medicine entails adjusting treatment procedures based on individual genetic profiles, resulting in more targeted and effective medications. Understanding the exact genetic abnormalities that cause thyroid cancer in each patient allows clinicians to select treatments that are most likely to be beneficial while minimising side effects. Targeted medicines, such as tyrosine kinase inhibitors, have shown promise in treating advanced thyroid cancer with specific genetic abnormalities. Furthermore, advances in molecular diagnostics, like next-generation sequencing, allow for more extensive profiling of tumour genomes, allowing doctors to pinpoint possible therapy targets with higher precision. For example, in a groundbreaking clinical trial, researchers assessed the efficacy of vemurafenib, a BRAF inhibitor, in patients with BRAF-mutated thyroid cancer. The research included a cohort of patients with advanced thyroid cancer who carried the BRAF V600E mutation, a common genetic change associated with aggressive tumour behaviour and a worse prognosis. Treatment with vemurafenib produced outstanding results, with a considerable proportion of patients having tumour reduction and improved progression-free survival. This personalised strategy, which targets the exact genetic aberration causing the cancer, demonstrates the power of precision medicine in oncology. Furthermore, advances in next-generation sequencing technologies have aided in the detection of such genetic abnormalities in thyroid tumours, allowing oncologists to tailor treatment plans to specific patients' genetic profiles. A new era in personalised cancer care can be brought about by physicians utilising precision medicine to maximise therapeutic success while minimising side effects. Immunotherapy is a breakthrough method of cancer treatment that uses the immune system to recognise and eliminate cancer cells. Immune checkpoint inhibitors, such as pembrolizumab and nivolumab, have demonstrated extraordinary success in treating a variety of malignancies, including advanced thyroid carcinoma. These medications operate by disrupting inhibitory signals that cancer cells employ to avoid detection by the immune system, boosting the body's natural ability to fight the disease. While immunotherapy has shown promise in some individuals, more research is needed to uncover biomarkers that might predict treatment response and to develop combination medicines that improve efficacy while also overcoming resistance. Case study articles: 1) The Phase 2 KEYNOTE-158 trial examined the effectiveness and safety of pembrolizumab monotherapy in patients with advanced thyroid cancer and found positive results. Pembrolizumab indicated remarkable efficacy, particularly in patients who had received many prior treatments, with large objective response rates and long-lasting responses. Furthermore, the medication demonstrated improved progression-free survival and overall survival rates. Importantly, pembrolizumab had a manageable safety profile, with treatment-related side events often mild to moderate. These data demonstrate pembrolizumab's potential as a significant treatment choice for advanced thyroid cancer, providing hope to patients who have exhausted traditional medications. Article: Oh, Y., Algazi, A., Capdevila, J., Longo, F., Miller, W., Chun Bing, J. T., Bonilla, C. E., Chung, H. C., Guren, T. K., Lin, C., Motola-Kuba, D., Shah, M., Hadoux, J., Yao, L., Jin, F., Norwood, K., & Lebellec, L. (2023). Efficacy and safety of pembrolizumab monotherapy in patients with advanced thyroid cancer in the phase 2 KEYNOTE-158 study. Cancer , 129 (8), 1195-1204. 2) The efficacy and safety evidence for the combination of lenvatinib and pembrolizumab in anaplastic thyroid cancer is based on complementary mechanisms of action and encouraging preclinical and clinical data. Lenvatinib, a multi-kinase inhibitor, targets numerous pathways involved in tumour growth and angiogenesis, whereas pembrolizumab, an immune checkpoint inhibitor, boosts anti-tumour immunity by inhibiting the PD-1 pathway. In animal models of anaplastic thyroid carcinoma, preclinical studies have shown that combining lenvatinib and pembrolizumab has synergistic effects, resulting in increased tumour regression and prolonged survival. Clinical trials of this combination therapy have yielded promising results, with high response rates and prolonged survival found in patients with advanced anaplastic thyroid carcinoma, a disease with a traditionally dismal prognosis and few therapeutic alternatives. Article: Boudin, L., Morvan, B., Thariat, J., Métivier, D., Marcy, Y., & Delarbre, D. (2022). Rationale Efficacy and Safety Evidence of Lenvatinib and Pembrolizumab Association in Anaplastic Thyroid Carcinoma. Current Oncology , 29 (10), 7718-7731. In addition to precision medicine and immunotherapy, current research is looking into new therapeutic techniques and technologies for treating thyroid cancer. One potential area of research is the creation of tailored radiotherapies, which deliver radiation to cancer cells while sparing healthy tissue. This method reduces adverse effects while increasing the therapeutic benefit of radiation treatment. Furthermore, advances in molecular imaging techniques such as positron emission tomography (PET) and magnetic resonance imaging (MRI) improve cancer staging and monitoring accuracy, allowing for more precise treatment planning and response evaluation. To reduce the incidence and fatality rates of thyroid cancer, a multimodal approach is required that addresses both primary prevention and early detection. Public health activities targeted at reducing modifiable risk factors, such as smoking cessation programmes and attempts to decrease environmental exposure to radiation and other carcinogens, can aid in the prevention of thyroid cancer. Furthermore, raising awareness of the signs and symptoms of thyroid cancer among healthcare providers and the general public can lead to earlier detection and treatment, which improves patient outcomes. Finally, maintaining equal access to high-quality healthcare services, such as cancer screening and treatment, is critical to reducing disparities in thyroid cancer outcomes across demographic groups. Finally, future thyroid cancer management options show significant promise for improving patient outcomes and lowering the disease's burden. We can make more progress against thyroid cancer by adopting precision medicine, immunotherapy, and other novel techniques. Addressing the underlying causes of thyroid cancer, as well as providing prompt and equitable access to healthcare, are critical for long-term reductions in incidence and fatality rates. Collaboration among academics, physicians, politicians, and patient advocates will be critical to achieving these objectives and improving the lives of those impacted by thyroid cancer. Conclusion Genetic, environmental, and socioeconomic variables all contribute to the complexity of thyroid cancer. Significant progress in illness management can be made by unravelling molecular pathways, monitoring mortality trends, and implementing novel interventions. Collaboration among stakeholders, such as researchers, physicians, policymakers, and patient advocates, is essential for turning scientific discoveries into practical advances in patient treatment and outcomes. Written by Sindhu Mohan Related articles: Prostate cancer research / Apocrine carcinoma / MAPK/ ERK signalling pathway Project Gallery

Step into the intricate field of dentistry and learn about dental tourism, tooth decay, water fluoridation- and more. Dentistry Articles Step into the intricate field of dentistry and learn about dental tourism, tooth decay, water fluoridation- and more. You may also like: Medicine Water fluoridation Diving deep Dental tourism What is 'Turkey teeth'? Tooth decay And how to prevent it COMING SOON

Exploring the microscopic world of molecules Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Quantum Chemistry Last updated: 05/02/26, 10:12 Published: 06/02/25, 08:00 Exploring the microscopic world of molecules Quantum chemistry provides a glimpse into the strange and fascinating world of molecules and atoms, where the principles of traditional chemistry and physics no longer apply. While classical chemistry can explain molecular interactions and bonding, it cannot fully account for particles' unusual, frequently contradictory behaviour at the atomic and subatomic levels. Quantum mechanics provides scientists with a powerful framework for understanding the complicated behaviour of electrons and nuclei in molecules. The basics of quantum chemistry The notion of wave-particle duality, which states that particles, such as electrons, act not just like objects with mass but also like waves, is central to quantum chemistry. Because the exact position and momentum of an electron cannot be known at the same time (according to the Heisenberg Uncertainty Principle), probability distributions are used to describe electrons rather than accurate orbits. These distributions are represented by mathematical functions known as wave functions, which describe the probability of finding an electron in a specific location surrounding the nucleus. This fundamentally affects our understanding of chemical bonding. Instead of conceiving a bond as a solid connection between two atoms, quantum chemistry defines it as the overlap of electron wave functions, which can result in a variety of molecular topologies depending on their energy levels. Quantum mechanics and bonding theories Quantum mechanics has fundamentally altered our knowledge of chemical bonding. The classic Lewis structure model, which explains bonding as the sharing or transfer of electrons, is effective for simple molecules but fails to convey the complexities of real-world interactions. In contrast, quantum chemistry introduces the concept of molecular orbitals. In molecular orbital theory, electrons are not limited to individual atoms but can spread across a molecule in molecular orbitals, which are combinations of atomic orbitals from the participating atoms. These molecular orbitals provide a more detailed explanation for bonding, especially in compounds that do not match simple bonding models, such as delocalised systems like benzene or metals. For example, quantum chemistry explains why oxygen is paramagnetic (it possesses unpaired electrons), a characteristic that classical bonding theories cannot explain. Quantum chemistry and quantum computing One of the most interesting frontiers in quantum chemistry is its application to the development of quantum computers. Traditional computers, despite their enormous processing power, struggle to model the complicated behaviour of molecules, particularly large ones. This is because simulating molecules at the quantum level necessitates tracking all conceivable interactions between electrons and nuclei, which can quickly become computationally challenging. Quantum computers use fundamentally different ideas. They employ qubits, which, unlike classical bits, can exist in a state of both 0 and 1. This enables quantum computers to execute several calculations concurrently and manage the complexity of molecular systems considerably more effectively. This could lead to advancements in quantum chemistry, such as drug discovery, where precisely modelling molecular interactions is critical. Instead of depending on trial and error, scientists may utilise quantum computers to model how possible pharmaceuticals interact with biological molecules at the atomic level, thereby speeding up the creation of novel therapies. Similarly, quantum chemistry could help in the development of novel materials with desirable qualities, such as stronger alloys and more efficient energy storage devices. Why quantum chemistry matters The consequences of quantum chemistry go well beyond the lab. Understanding molecular behaviour at its most fundamental level allows us to create new technologies and materials that have an impact on everyday life. Nanotechnology, for example, relies largely on quantum principles to generate innovative materials with applications in medicine, electronics, and clean energy. Catalysis, the technique of speeding up reactions, also benefits from quantum chemistry insights, making industrial operations more efficient, such as cleaner fuel generation and more effective environmental remediation. Furthermore, quantum chemistry provides insights into biological processes. Enzymes, the proteins that catalyse processes in living organisms, work with a precision that frequently defies standard chemistry. Tunnelling, quantum phenomena in which particles slip past energy barriers, helps to explain these extraordinarily efficient biological processes. In brief, quantum chemistry provides the fundamental understanding required to push the limits of chemistry and physics by exposing how molecules interact and react in ways that traditional theories cannot fully explain. Quantum chemistry has the potential to radically alter our understanding of the microscopic world, whether through theoretical models, practical applications, or future technology advancements. Written by Laura K Related articles: Quantum computing / Topology / Computational organic chemistry Project Gallery

The endowment effect Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Behavioural Economics II 31/10/25, 12:46 Last updated: Published: 22/03/24, 19:51 The endowment effect This is article no. 2 in a series on behavioural economics. Next article: Loss aversion . Previous article: The role of honesty . In microeconomics, we say preferences are reversible. If you would pay £2 for a bar of chocolate, then you would be happy to sell a bar of chocolate for £2, especially if I gave it to you for free. Sounds reasonable? Well, in fact, this is not the case. Once again, consumers, just like you and me, are irrational, and thanks to what’s known as the endowment effect, classical economics falls flat once again. The endowment effect In an experiment conducted by Knetsch, participants were randomly allocated into three different categories. The first were given a coffee mug, the second were given some candy, and the third were given nothing. We say that the first two groups were endowed; they were given an item for free at no cost to them. Then the participants in the first two groups were given the option to either swap their item for either the mug or the candy or keep the item they were endowed with. The third group, treated as a control, was given the option to choose between the two and keep which they preferred the most. In the control group, we saw that about half of the participants chose the mug and half chose the candy. But in the endowed groups, an overwhelming majority decided to keep the item they were given rather than swapping! Therefore, as we can clearly see, when someone is endowed with an item, their perception of its utility (or benefit) seems to increase, so when given the opportunity to switch items, they often decline. Clearly, from an economic perspective, when endowed with an item, your utility curve for that item differs from when given the opportunity to choose. But why might that be the case? When you are endowed with an item, you own that item and, in a sense, hold responsibility over it. You become possessive, and this sense of ownership seems to have its own psychological value; therefore, the act of giving it up for something of equal worth is no longer treated as a fair trade-off. Whereas when not endowed, you have no sentiment value attached to the items, and for the most part, people are indifferent between them! A good example of this could be an old, run-down car. Buyers of this car see it for what it is—something that is barely functional. But owners of the car who have driven it for 20 years see it as more than that. There is an emotional attachment to the car that makes it more valuable in their eyes. Is the endowment effect always true? List conducted a similar experiment. A survey was undertaken by both unexperienced and experienced 'traders', and then after the survey, they were given trading cards as a reward. They were then given the opportunity to trade their cards if they wanted to. Non-experienced traders were subject to the endowment effect, so they kept the cards they worked hard for, but experienced traders knew that some cards may be more valuable, even if only slightly, which meant that they were able to overcome this effect. Additionally, what was found was that when participants were aware and went into the experiment knowing that there would be a trade, they had the intention to trade, which also managed to remove the endowment effect. In essence, the endowment effect serves as a reminder of the complexities inherent in human psychology and decision-making. There are many limitations in traditional economic models, which emphasises the need for behavioural economics and the inclusion of multidisciplinary thinking. To discover more about behavioural economics and in particular how honesty plays a big role in restructuring economic thinking, click here to read my prior article, and be sure to look out for more articles to come in the future! Written by George Chant Related articles: Explaining altruism / Mathematical models in cognitive decision-making References: Knetsch, Jack L. “The Endowment Effect and Evidence of Nonreversible Indifference Curves.” The American Economic Review 79, no. 5 (1989): 1277–84. John A. List, Does Market Experience Eliminate Market Anomalies?, The Quarterly Journal of Economics , Volume 118, Issue 1, February 2003, Pages 41–71,33 Project Gallery

An influential immunologist Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link From Playboy Model to Danger Model: The (brief) Story of Polly Matzinger 13/02/25, 12:47 Last updated: Published: 11/05/24, 11:06 An influential immunologist Polly Matzinger may be one of the most influential and important immunologists, even if her research is still a little controversial. She took the already known ‘Self/Non-self’ model by Frank Macfarlane Burnet and Frank Fenner from 1949 and expanded it to incorporate ‘danger signals’. However, her life prior to becoming a world-leading immunologist might be the most unexpected thing about her. Born into an artistic French-Dutch family in La Seyne she grew up playing instruments and composing music alongside her brother and sister, who would themselves go on to become a rock musician and artist, respectively. By the early 70s, she had already done stints as a dog trainer, jazz musician, and a Playboy Bunny, before settling as a cocktail waitress in California. At this point, she had been in and out of studying biology at the University of California. After eleven years, she completed her Bachelor of Science. While working at the bar, her professor, Robert Schwab brought in scientific articles for her to read after she asked him about animal mimicry. Matzinger would later credit Professor Robert Schwab for her foray into science and her life. While at graduate school, Matzinger began to question the generally accepted idea that the body rejects anything that is ‘non-self’. At first glance, the idea makes sense; the immune system should attack things it does not recognise to keep us healthy. But upon further analysis, it might seem to be counterintuitive. We do not reject food, water, or even foetuses. For example, in organ transplants, it is thought that the body needs immunosuppression so that the immune system does not reject the new organ. But why would the body have evolved for this when not until the mid-20th century, an organ had never been transplanted? Equally, why did the body sometimes attack itself in the case of autoimmune diseases? Matzinger did not pursue this line of thought until ten years later. Thus, the ‘Danger Model’ was derived. Matzinger proposed that in order for the immune response to be activated, there must first be a ‘danger signal’. This danger signal is emitted by unhealthy cells, which might be stressed or infected or have been mutated or damaged. Examples of danger signals include heat-shock proteins, extracellular matrix breakdown products, and cytokines, as well as other proteins and substances released by these stressed cells. Danger signals, or ‘alarmins’, are detected by dendritic cells, which activate T cells and start the immune response. While this model was originally met with scepticism, it has gained more and more support over the years, as the research into it expands and deepens. With the ‘Danger Model’, many routes for potential therapies have opened, including cancer vaccines. Matzinger believes that vaccinations can cure up to 80% of all cancers. If danger signals are induced within tumour cells, the tumour will be visible to the immune system. This is different to the current way that cancer vaccines target the tumour. In current therapeutic cancer vaccines (as opposed to preventative vaccines), the vaccines induce the immune system by showing them what the cancer cell ‘looks like’. It does this by introducing cancer antigens (or tumour-specific antigens, i.e. a protein that is only on the cancer and not on other healthy cells in the body) to the body and, thus, the immune system. Now that the immune cells have seen and identified the cancer antigens, they can search the body for the antigen, induce an immune response against them, and hopefully kill the cancer cells. This means that if the cancer mutates and the antigen changes, which is not unlikely, the vaccine may cease to have any effect because what the immune system is searching for no longer exists. In contrast, with this new method, the actual antigen does not matter. The vaccine works by inducing the danger signals, making the tumours visible to the immune system without the need for the tumour-specific antigen to be identified. This means that even if the cancer undergoes mutation, the vaccine will still be active and working, as its effectiveness does not depend on the cancer molecule itself. In addition to describing the ‘Danger Model’, Matzinger also made a name for herself when she cited ‘Galadriel Mirkwood’ as her co-author on a paper published in the Journal of Experimental Medicine. What is surprising about this, is that Galadriel Mirkwood is not another scientist, but her pet Afghan Hound. It is unknown why she did this, potentially to challenge the strict and rigid rules in the scientific community, to garner more interest in the paper, or just to be funny. Either way, it got her banned from publishing in the journal for more than ten years, but it certainly made her a scientist with a sense of humour and a memorable story. Written by Henrietta Owen Related article: Immune signals and metastasis Project Gallery

It’s been found that the species Dicrurus adsimilis (fork-tailed drongos) uses deception by flexible alarm mimicry to target and carry out food-theft attempts. The deceptive tactics of the fork-tailed drongo were studied which includes the use of false alarm calls and mimicked calls. Research was done on 64 wild drongos in the Kalahari Desert and it was found that the drongos spent more than a quarter of their time watching their target species which included southern pied babblers and meerkats Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Deception by flexible alarm mimicry in an African bird Last updated: 05/11/24 Published: 28/12/22 It’s been found that the species Dicrurus adsimilis (fork-tailed drongos) uses deception by flexible alarm mimicry to target and carry out food-theft attempts. The deceptive tactics of the fork-tailed drongo were studied which includes the use of false alarm calls and mimicked calls. Research was done on 64 wild drongos in the Kalahari Desert and it was found that the drongos spent more than a quarter of their time watching their target species which included southern pied babblers and meerkats. The other species’ would listen to the alarm calls made by drongos and would rush to take cover as they would if it was an alarm call from their species. These alarm calls were beneficial to them as it increased the number of returns from foraging and reduced their vigilance. However, the drongos used this to their advantage and if the target species was to find a large item of food the drongos could produce a false alarm call to make the target species run to cover out of fear which allowed the observing drongo to steal the deserted food. In 42% of cases of false alarms the drongos used a mimicked cry and in another 27% it was a mixture of mimicked and drongo-specific. This could be because target species are more likely to respond to a mimicked alarm call. In the case of babblers, if they heard a mimicked alarm call they would take longer to carry on foraging than with a drongo-specific call. The results show that false alarm calls by drongos work to distract their target but the call should also be frequently changed and not overused for best results. Written by Areebah Khan Related article: Conserving the Californian condor SUMMARISED FROM Flower, T.P., Gribble, M. and Ridley, A.R. (2014) “Deception by flexible alarm mimicry in an African bird,” Science, 344(6183), pp. 513–516.

The researchers counted over 100,000 neurons and over a billion connections between them within this small cube of brain tissue. To find all the neurons and reconstruct the neural network, researchers had to slice the mouse brain 25,000 times. The issue is Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can a human brain be linked to a computer? Last updated: 08/03/26 Published: 28/12/22 Scientists in the US have succeeded in mapping the three-dimensional structure of the network of neurons in one cubic millimetre of mouse brain- a feat that would require two petabytes of storage. The human brain contains approximately 100 billion neurons, which is one million times the number of neurons found in a cubic millimetre of mouse brain. The researchers counted over 100,000 neurons and over a billion connections between them within this small cube of brain tissue. To find all the neurons and reconstruct the neural network, researchers had to slice the mouse brain 25,000 times. The issue is that the amount of data to store would kill any single computer. Memory and experiences that would have defined people later would be lost if they tried to store their minds too early. Using a computer too late may result in the accumulation of a mind with dementia, which would not work so well. Human tissue would have to be cut into zillions of thin slices using techniques compatible with dying and cutting. Local electrical changes that travel down dendrites and axons allow neurons to communicate with one another. However, when reconstructing the 3D structure, this may not be possible. After we die, our brains undergo significant chemical and anatomical changes. At the age of 20, they begin to lose 85,000 neurons per day due to apoptosis, or programmed cell death. Many memories that would have shaped a person later would be lost if he or she tried to store their mind too early. There are numerous steps involved in developing a computer capable of storing and processing human-level intelligence. The Neuralink trial is a pioneering study that aims to enable interactions with computers via thought. As of January 2026, there are seven patients in the GB-PRIME study, which uses Neuralink's brain-computer interface (BCI) technology. The goal of the study is to restore independence in paralysed individuals. It may be imposs ible for an artificial intelligence to produce sensations and actions identical to those provided and produced by your biological body. Bots are susceptible to hacking and hardware failure. Connecting sensors to the AI's digital mind would also be difficult. Written by Jeevana Thavarajah Related articles: The evolution of AI / Brain metastasis / AI in genetic diagnoses

An overview Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Crab Nebula 14/02/25, 13:44 Last updated: Published: 23/03/24, 17:45 An overview Of the 270 known supernova remnants, the Crab Nebula is one of the more well known in popular science, originating from a violent supernova explosion first discovered by Chinese astronomer Wang Yei-te in July of 1054 AD. Yei-te reported the appearance of a “guest star” so bright that it was visible during the day for three weeks, and at night for 22 months. In 1731, English astronomer John Bevis rediscovered the object, which was then observed by Charles Messier in 1758 prompting the nebula’s lesser-known name, Messier 1. Located approximately 6,500 light years from Earth, the nebula cannot be seen with the naked eye but observations in different wavelengths gives rise to the beautiful colored images often published. The Crab Nebula is the result of a violent explosion process that signals what astronomers call “star death.” This occurs when the star runs out of fuel for the fusion process in its core that produces an outward pressure counteracting the constant inward pressure of the star’s outer shells. With the loss of outward pressure, these layers suddenly collapse inwards and produce an explosion astrophysicists call a supernova. Following the explosion, the original star, named SN1054 in this case, collapsed into a rapidly spinning neutron star, also known as a pulsar, which is generally roughly the size of Manhattan, New York. The pulsar is situated at the center of the nebula and ejects two beams of radiation that, while the pulsar rotates, makes it appear as if the object is pulsing 30 times per second. Studies of the Crab Nebula were primarily conducted by the Hubble Space Telescope. Hubble spent three months capturing 24 images that were assembled into a colorful mosaic resembling not what is visible with human eyes, but rather a kind of paint-by-number image where each color mapped to a particular element. Traces of hydrogen, neutral oxygen, doubly ionized oxygen, and sulfur have been detected across multiple wavelengths as the remains span an expanding six to eleven light-year-wide remnant of the supernova event. It was not until 1942 that the Crab Nebula was officially found to be related to the recorded supernova explosion of 1054. This establishment was jointly provided by Professor J. J. L. Duyvendak of Leiden University as well as astronomers N. U. Mayall and J. Oort. Due to its long history of rediscovery and inherent beauty, the Crab Nebula remains as one of the most studied celestial objects today and continues to provide valuable insight into astrophysical processes. Written by Amber Elinsky REFERENCES Hester, J. Jeff. “The Crab Nebula: An Astrophysical Chimera,” Annual Review of Astronomy and Astrophysics 46 (2008): 127-155. https://doi.org/10.1146/annurev.astro.45.051806.110608 . Hester, J. and A. Loll. “Messier 1 (The Crab Nebula),” NASA. https://science.nasa.gov/mission/hubble/science/explore-the-night-sky/hubble-messier-catalog/messier-1/ . Image ref.: European Space Agency; Space Australia; dreamstime. Mayall, N. U., and J. H. Oort. “FURTHER DATA BEARING ON THE IDENTIFICATION OF THE CRAB NEBULA WITH THE SUPERNOVA OF 1054 A. D. PART II. THE ASTRONOMICAL ASPECTS.” Publications of the Astronomical Society of the Pacific 54, no. 318 (1942): 95–104. http://www.jstor.org/stable/40670293 Project Gallery

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