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  • The environmental impact of EVs | Scientia News

    A chemical perspective Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The environmental impact of EVs 16/01/25, 11:21 Last updated: Published: 07/08/23, 15:58 A chemical perspective Electric vehicles (EVs) are gaining momentum worldwide as a greener alternative to conventional internal combustion engine vehicles (ICEVs). The environmental benefits of EVs extend beyond their efficient use of electricity. In this article, we explore the chemical aspects of EVs and their environmental impact, shedding light on their potential to mitigate climate change and reduce pollution. Greenhouse Gas Emissions Reduction: EVs play a crucial role in addressing climate change by significantly reducing greenhouse gas (GHG) emissions. Unlike ICEVs that rely on fossil fuels, EVs generate zero tailpipe emissions. By utilising electricity as their energy source, EVs minimise the release of carbon dioxide (CO2) and other GHGs responsible for global warming. However, it's essential to consider the environmental implications of electricity generation, emphasising the need for renewable energy sources to maximise the positive impact of EVs. Battery Chemistry and Resource Management: The heart of an EV lies in its rechargeable battery, typically composed of lithium-ion technology. The production and disposal of these batteries present both opportunities and challenges. Raw materials, such as lithium, cobalt, and nickel, are essential components of EV batteries. Responsible mining practices and efficient recycling techniques are vital to minimising the environmental impact of resource extraction and ensuring proper disposal or repurposing of used batteries. Electrochemical Reactions and Energy Storage: Electric vehicles rely on electrochemical reactions within their batteries to store and release energy. These reactions involve the flow of ions, typically lithium ions, between the positive and negative electrodes. Understanding the chemistry behind these processes enables the development of more efficient and durable battery systems. Continued research and innovation in battery chemistry hold the potential to enhance energy storage capabilities, extend EV range, and improve overall performance. Air Quality and Emission Reduction: EVs contribute to improved air quality due to their zero tailpipe emissions. By eliminating the release of pollutants such as nitrogen oxides (NOx), particulate matter (PM), and volatile organic compounds (VOCs), EVs reduce smog formation and respiratory health risks. This is particularly significant in urban areas, where high concentrations of vehicular emissions contribute to air pollution. The adoption of EVs can help combat these issues and create cleaner and healthier environments. Battery Recycling and the Circular Economy: Given the increasing demand for EVs, battery recycling plays a vital role in ensuring a sustainable future. Recycling allows for the recovery of valuable materials and reduces the need for resource extraction. Effective recycling processes can mitigate the environmental impact of battery production, minimise waste generation, and promote a circular economy approach, where materials are reused and recycled to their fullest extent. Future Prospects and Chemical Innovations : Advancements in battery technology and chemical engineering are key to unlocking the full potential of EVs. Research efforts are focused on developing alternative battery chemistries, such as solid-state batteries, which offer improved energy density, safety, and recyclability. Additionally, exploring sustainable materials and manufacturing processes for batteries can further reduce the environmental footprint of EVs. In conclusion, electric vehicles represent a promising solution to combat climate change, reduce pollution, and promote sustainable transportation. From the chemistry behind battery systems to their impact on air quality and resource management, EVs offer a greener alternative to traditional vehicles. Continued research, innovation, and collaboration between the automotive industry, chemical scientists, and policymakers are essential for realising the full potential of EVs and creating a cleaner, more sustainable future. Written by Navnidhi Sharma Related articles: Hydrogen cars / The brain-climate connection / Plastics and their environmental impact Project Gallery

  • From Playboy Model to Danger Model: The (brief) Story of Polly Matzinger | Scientia News

    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

  • Biology Articles | Scientia News

    ​Dive into the latest biological research! Read about animal testing and ethics, and learn about the regulation and policy of stem cell research. Biology Articles Dive into the latest biological research! Read about animal testing and ethics, and learn about the regulation and policy of stem cell research. You may also like: Cancer , Ecology , Genetics , Immunology , Neuroscience , Zoology , and Medicine Regulation and policy of stem cell research The 14-day rule and stem cell-based embryo models Maveerar Naal Health, trauma, and resilience amid decades of war in Sri Lanka COMING SOON COMING SOON Previous

  • What you should know about rAAV gene therapy | Scientia News

    Recombinant adeno-associated viruses (rAAVs) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What you should know about rAAV gene therapy 14/07/25, 15:13 Last updated: Published: 01/10/23, 19:45 Recombinant adeno-associated viruses (rAAVs) Curing a disease with one injection: the dream, the hope, the goal of medicine. Gene therapy brings this vision to reality by harnessing viruses into therapeutic tools. Among them, adeno-associated viruses (AAVs) are the most used: genetically modified AAVs, named recombinant AAVs (rAAVs), are already used in six gene therapies approved for medical use. Over 200 clinical trials are ongoing. AAV, a virus reprogrammed to cure diseases Gene therapy inserts genetic instructions into a patient to correct a mutation responsible for a genetic disorder. Thanks to genetic engineering, researchers have co-opted AAVs (along with adenoviruses, herpes simplex viruses and lentiviruses) into delivering these instructions. Researchers have swapped the genes that allow AAVs to jump from person to person with genes to treat diseases. In other words, the virus has been genetically reprogrammed into a vector for gene transfer. The gene supplemented is referred to as transgene. Biology of AAVs AAVs were discovered in the 1960s as contaminants in cell cultures infected by adenoviruses, a coexistence to which they owe their name. AAVs consist of a protein shell (capsid) wrapped around the viral genome, a single strand of DNA long approximately 4,700 bases (4.7 kb). The genome is capped at both ends by palindromic repetitive sequences folded into T-shaped structures, the Inverted Tandem Repeats (ITRs). Sandwiched between the ITRs, four genes are found. They determine capsid components ( cap ) and capsid assembly ( aap ), genome replication ( rep ) and viral escape from infected cells ( maap ) ( Figure 1, top panel ). The replacement of these four genes with a transgene of therapeutic use and its expression by infected cells (transduction) lie at the heart of gene therapy mediated by rAAVs. Transgene transfer by rAAVs Researchers favour rAAVs as vectors because AAVs are safe (they are not linked to any disease and do not integrate into the genome), they can maintain the production of a therapeutic gene for over ten years and infect a wide range of tissues. In an rAAV, the ITRs are the only viral element preserved. The four viral genes are replaced by a therapeutic transgene, and regulatory sequences to maximise its expression. Therefore, an rAAV contains the coding sequence of the transgene, an upstream promoter to induce transcription and a downstream regulatory sequence (poly-A tail) to confer stability to the mRNA molecules produced ( Figure 1, bottom panel ). Steps of rAAV production Based on the disease, rAAVs can be administered into the blood, an organ, a muscle or the fluid bathing the central nervous system (cerebrospinal fluid). rAAVs dock on target cells via a specific interaction between the capsid and proteins on the cell surface that serve as viral receptors and co-receptors. The capsid mainly dictates which cell types will be infected (cell tropism). Upon binding, the cell engulfs the virus into membrane vesicles (endosomes) typically used to digest and recycle material. The rAAVs escape the endosomes, avoiding digestion, and enter the nucleus, where the capsid releases the single-strand DNA (ssDNA) genome, a process known as uncoating. The ITRs direct the synthesis of the second strand to reconstitute a double-strand DNA (dsDNA), the replication of the viral genome and the concatenation of individual genomes into larger, circular DNA molecules (episomes) that can persist in the host cell for years. Nuclear proteins transcribe the transgene into mRNAs; mRNAs are exported in the cytoplasm where they are translated into proteins. The rAAV has achieved successful transduction : the transgene can start exerting its therapeutic effects. A simplified overview of rAAV transduction is presented in Figure 2 . The triumphs of rAAV gene therapies rAAV gene therapies are improving lives and saving patients. Unsurprisingly, the most remarkable examples of this come from the drugs already approved. Roctavian is an rAAV gene therapy for haemophilia A, a life-threatening bleeding disorder in which the blood does not clot properly because the body cannot produce the coagulation Factor VIII. In a phase III clinical trial, Roctavian reduced bleeding rates by 85% and most treated patients (128 out of 134) no longer needed regular administration of Factor VIII, the standard therapy for the disease, for up to two years after treatment. Similar impressive results were noted for the rAAV Hemgenix, a gene therapy for haemophilia B (a bleeding disorder caused by the absence of the coagulation Factor IX). Hemgenix reduced bleeding rates by 65% and most treated patients (52 out of 54) no longer needed regular administration of Factor IX, for up to two years. The benefits of Zolgensma are even more awe-inspiring. Zolgensma is an rAAV gene therapy for spinal muscular atrophy (SMA), a genetic disorder in which neurons in the spinal cord die causing muscles to waste away irreversibly. The life expectancy of SMA patients can be as short as two years, therefore timing is critical. As a consequence, Zolgensma had to be tested in neonates: babies with the most severe form of SMA were dosed with the drug before six weeks of age and symptoms onset (SPRINT study). After 14 months, all 14 treated babies were alive and breathing without a ventilator, whilst only a quarter of untreated babies did. After 18 months, all 14 could sit without help, an impossible feat without Zolgensma. These and other resounding achievements are fuelling research on rAAVs gene therapies. Current limitations Scientists still have some significant hurdles to overcome : ● Packaging capacity: AAVs can fit in their capsids relatively short DNA sequences, which do not allow the replacement of many long genes associated with genetic disorders, ● Immunogenicity: 30-60% of individuals have antibodies against AAVs, which block rAAVs and prevent transduction, ● Tissue specificity: rAAVs often infect tissues which are not the intended target (e.g., inducing the expression for a transgene to treat a neurological disease in the liver rather than in neurons). Gene therapies, not only those delivered by rAAVs, face an additional challenge, this one only partially of a technological nature: their price tags. Their prices – rAAVs range from $850,000 (£690,000) to $3,500,000 (£2,850,000) – make them inaccessible for most patients. A cautionary tale is already out there: Glybera, the first rAAV gene therapy approved for medical use, albeit only in Europe (2012), was discontinued in 2017 because it was too expensive. Research is likely to reduce the exorbitant manufacturing costs , but the time may have come to reconsider our healthcare systems. Notes One non-viral vector exists , but its development lags behind the viral vector . Glybera for treating lipoprotein lipase deficiency, Luxturna for Leber congenital amaurosis, Zolgensma for spinal muscular atrophy, Roctavian for haemophilia A, Hemgenix for haemophilia B, and Elevidys for Duchenne muscular dystrophy. Written by Matteo Cortese, PhD Related articles: Germline gene therapy (GGT) / A potential treatment for HIV / Rabies / Antiretroviral therapy Project Gallery

  • Can carbon monoxide unlock new pathways in inflammation therapy? | Scientia News

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

  • The power of probiotics | Scientia News

    Unlocking the secrets to gut health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The power of probiotics 14/07/25, 14:59 Last updated: Published: 18/08/23, 19:58 Unlocking the secrets to gut health What are probiotics? Probiotics are dietary supplements that consist of live cultures of bacteria or yeast. In the human body, more precisely in the microbiome, there are about 4 trillion bacteria, which include almost 450 species. These bacteria are necessary for the proper functioning of the entire body, especially the intestines and digestive system. In probiotics, bacteria from the Lactobacillus and Bifidobacterium families are most often used, as well as yeasts such as Saccharomyces cerevisiae. How probiotics work? Probiotics have a wide range of effects on our body. Their main task is to strengthen immunity and improve the condition of the digestive tract. This is because microorganisms produce natural antibodies, and also constitute a kind of protective barrier that does not allow factors conducive to infection to our intestine. Types of probiotics Most often, lactic acid bacteria of the genera Lactobacillus and Bifidobacterium are used as probiotics, but some species of Escherichia and Bacillus bacteria and the yeast Saccharomyces cerevisiae boulardi also have pro-health properties. Probiotics for your gut health The composition of our bacterial flora in the intestines determines the proper functioning of the digestive and immune systems. Probiotics have a positive effect primarily on the intestinal flora. They speed up metabolism and lower bad cholesterol (LDL). Live cultures of bacteria protect our digestive system. They improve digestion, regulate intestinal peristalsis, and prevent diarrhoea. They also increase the nutritional value of products - they facilitate the absorption of minerals such as magnesium and iron as well as vitamins from group B and K. In addition, probiotics strengthen immunity and protect us from infections caused by pathogenic bacteria. Therefore, it is very important to take as many probiotics as possible during and after antibiotic treatment. They will then regenerate the intestinal flora damaged by antibiotic therapy and reduce inflammation. Main benefits · facilitate the digestive process · increase the absorption of vitamins and minerals · during antibiotic treatments, they protect our intestinal microflora · affect the immune system by increasing resistance to infections · some strains have anti-allergic and anti-cancer properties · lower cholesterol · relieve the symptoms of lactose intolerance · ability to synthesize some B vitamins, vitamin K, folic acid Written by Aleksandra Zurowska Related articles: The gut microbiome / Vitamins / Interplay of hormones and microbiome Project Gallery

  • The new age of forensic neurology | Scientia News

    Explaining and predicting the behaviour of serial killers Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The new age of forensic neurology 14/07/25, 14:58 Last updated: Published: 23/08/23, 16:16 Explaining and predicting the behaviour of serial killers Background Nobody can argue that true crime has taken the media by storm in recent years. In 2021, the search to find Gabby Petito inflamed social media, with the r/gabbypetito subreddit having 120,000 members at its peak. Tiktok ‘psychics’ would amass millions of views by attempting to predict how the case would progress, with predictably terrible results. A small solace remains, however; the fact that increased media presence of murder cases increases the rate at which research into murderers is published. The increase in both research and media attention toward true crime continued through 2022, invigorated by the release of Monster: the Dahmer Story on Netflix, which was viewed on Netflix for over 1 billion hours by its user base. It could be argued that the popularity of this show and others depicting serial killers also increased the publication of research on the neurology of serial killers. The neurological basis of the serial killer refractory period Dilly (2021) encompasses some very interesting correlational research into the neurological factors at play in the evocation of the serial killer refractory period. Following analysis of the refractory periods of ten American serial killers, a metaanalysis of prior research was performed to establish which prior theory most thoroughly explained the patterns derived. The American serial killers utilised in this investigation were: The Golden State Killer, Joseph James DeAngelo. Jeffrey Dahmer. Ted Bundy. John Wayne Gacy. The Night Stalker, Richard Ramirez. The BTK Killer, Dennis Rader. The I-5 Killer, Randall Woodfield. Son of Sam, David Berkowitz. The Green River Killer, Gary Ridgway. The Co-Ed Killer, Edmund Kemper III. Theory no. 1 While this research is purely speculative due to the lack of real-time neurological imaging of the killers both during refractory periods and their murderous rampages, this research was demonstrated to lend credence to a prior theory proposed by Simkin and Roychowdhury (2014). This research, titled Stochastic Modelling of a Serial Killer , theorised based on their own collated data that the refractory period of serial killers functions identically to that of the refractory period of neurons. This theory is based upon the idea that murder precipitates the release of a powerful barrage of neurotransmitters, culminating in widespread neurological activation. In line with neurological refractory periods, it is believed that this extreme change in state of activation is followed by a period of time wherein another global activation event cannot occur. Theory no. 2 Hamdi et al. (2022) delineates the extent to which the subject’s murderous impulses were derived from Fregoli syndrome, rather than his comorbid schizophrenia. This research elucidated how schizophrenic symptoms can synergise with symptoms of delusional identification syndromes (DIS) to create distinct behaviours and thought patterns that catalyse sufferers to engage in homicidal impulses. DIS include a range of disorders wherein sufferers experience issues identifying objects, people, places or events; Fregoli Syndrome is a DIS characterised by the delusional belief that people around the sufferer are familiar figures in disguise. The subject’s Fregoli Syndrome caused the degeneration of his trust of those around him, which quickly led to an increase in aggressive behaviours. The killer attacked each member of his family multiple times before undertaking his first homicide- excluding his father, whom reportedly ‘scared him very much’. Unsurprisingly then, his victim cohort of choice for murder were older men. The neurobiological explanation of Fregoli Syndrome asserts that the impairment of facial identification, wherein cerebrocortical hyperactivity catalyses delusional identification of unfamiliar faces as familiar ones. Conclusion Forensic neurology has been a key element in expanding the understanding of serial killers, with the research of Raine et al. (1997) popularising the use of neurology to answer the many questions posed by the existence of serial killers. Since Raine, Buchsbaum and LaCasse of the 1997 study first used brain scanning techniques to study and understand serial killers, the use of brain scanning techniques to study this population has become a near-perfect art, becoming ever more of a valid option for use both in understanding and predicting serial killer behaviour. In all likelihood, future innovations in forensic neurology research will continue to bring about positive change, reducing homicidal crime with the invention and use of different methods and systems to predict and stop the crimes before they happen. Summarised from a full investigation. Written by Aimee Wilson Related articles: Serial killers in healthcare / Brain of a bully Project Gallery

  • Beyond the bump: unravelling traumatic brain injuries | Scientia News

    The yearly incidence of TBI is around 27 and 69 million people worldwide Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Beyond the bump: unravelling traumatic brain injuries 13/11/25, 12:27 Last updated: Published: 15/10/24, 11:32 The yearly incidence of TBI is around 27 and 69 million people worldwide A traumatic brain injury (TBI) is one of the most serious and complex injuries sustained by the human body, often with profound and long-term effects on an individual’s physical, emotional, behavioural and cognitive abilities. What is a traumatic brain injury? A TBI results from an external force which causes structural and physical damage to the brain. The primary injury refers to the immediate damage to the brain tissue which is caused directly by the event. Whereas secondary injuries result from the cascade of cellular and molecular processes triggered by the initial injury and develop from hours to weeks following the initial TBI. Typically, the injury can be penetrating, where an object pierces the skull and damages the brain, or non-penetrating which occurs when the external force is large enough to shake the brain within the skull causing coup- contrecoup damage. Diagnosis and severity The severity of a TBI is classified as either mild (aka concussion), moderate, or severe, using a variety of indices. Whilst more than 75% of TBIs are mild, even these individuals can suffer long-term consequences from post-concussion syndrome. Here are two commonly used measures to initially classify severity: The Glasgow Coma Scale (GCS) is an initial neurological examination which assesses severity based on the patient’s ability to open their eyes, move, and respond verbally. It is a strong indicator of whether an injury is mild (GCS 13-15), moderate (GCS 9-12) or severe (≤8). Following the injury and any period of unconsciousness, when a patient has trouble with their memory and is confused, they are said to have post-traumatic amnesia (PTA). This is another measure of injury severity and lasts up to 30 30 minutes in mild TBI, between 30 minutes and 24 hours in moderate TBI, and over 24 hours in severe TBI. Imaging tests including CT scans and MRIs are used to detect brain bleeds, swelling or any other damage. These tests are essential upon arrival to the hospital, especially in moderate and severe cases to understand the full extent of the injury. Leading causes of TBI Common causes of TBI are a result of: Falls (most common in young children and older adults) Vehicle collisions (road traffic accidents- RTAs) Inter-personal violence Sports injuries Explosive blasts Interestingly, the rate of TBI is 1.5 times more common in men than women. General symptoms The symptoms and outcome of a TBI depend on the severity and location of the injury. They differ from person to person based on a range of factors which include pre-injury sociodemographic vulnerabilities including age, sex and level of education, as well as premorbid mental illnesses. There are also post-injury factors such as access to rehabilitation and psychosocial support which influence recovery. Due to this, nobody will have the same experience of a TBI, however there are some effects which are more common than others which are described: Mild TBI: Physical symptoms: headaches, dizziness, nausea, and blurred vision. Cognitive symptoms: confusion, trouble concentrating, difficulty with memory or disorientation. Emotional symptoms: mood swings, irritability, depression or anxiety. Moderate-to-severe TBI: Behavioural symptoms: aggression, personality change, disinhibition, impulsiveness. Cognitive symptoms: difficulties with attention and concentration, decision making, memory, executive dysfunction, information processing, motivation, language, reasoning, self-awareness. Physical symptoms: headaches, seizures, speech problems, fatigue, weakness or paralysis. Many of these symptoms are ‘hidden’ and can often impact functional outcomes for an individual, such as their capacity for employment and daily living (i.e., washing, cooking, cleaning etc.). The long-term effects of TBI can vary, with some returning to normal functioning. However, others might experience lifelong disabilities and require adjustments in their daily lives. For more information and support, there are some great resources on the Headway website, a leading charity which supports individuals after brain injury. Written by Alice Jayne Greenan Related articles: Why brain injuries affect adults and children differently / Neuroimaging / Different types of seizures Project Gallery

  • Bioorthogonal Chemistry | Scientia News

    The future of targeted cancer therapeutics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Bioorthogonal Chemistry 04/02/25, 15:42 Last updated: Published: 01/09/24, 10:47 The future of targeted cancer therapeutics ‘Bioorthogonal chemistry’ is a term coined in 2003 by American Chemist & 2022 Nobel Prize Laureate Carolyn Bertozzi. It encompasses a set of chemical reactions which can occur within biological environments, whilst exerting minimal effect on native biomolecules or interference with native biochemical processes of the host organism - these reactions exist ‘orthogonal’ (perpendicular) to biology. Key functional groups in Bioorthogonal Chemistry include the alkynes (carbon-carbon triple bonds) and the azides (⁻N=N⁺=N⁻) . The azides are particularly bioorthogonal due to their minute size (which is favourable for cell permeability and avoiding ‘perturbations’ - the alteration of a function of a biological system), metabolic stability, and how, as they don’t naturally exist in cells, they have no competing biological side reactions. Past & present uses of bioorthogonal chemistry include: ● Vehicle airbags: Modern vehicle airbags contain sodium azide (NaN₃), a shock sensitive, explosive compound. When a vehicle’s crash sensor is triggered, an electrical charge is administered which starts the chemical reaction, inflating the air bag with harmless nitrogen gas (2NaN₃ → 2Na + 3N₂). This reaction can occur in as quickly as 0.03 seconds! ● Early HIV treatment: Azidothymidine - AZT - (Fig. 1) was the first drug used to treat HIV infection. For viruses to replicate, they use an enzyme called reverse transcriptase to convert their single-stranded RNA genome to double-stranded DNA in a process termed reverse transcription. When this antiretroviral medicine is used, instead of the virus transcribing thymidine, it instead transcribes the AZT, which contains an azide Group, thus stalling DNA synthesis of HIV and producing less viruses. Another key feature to consider when discussing uses of Bioorthogonal Chemistry are Click Reactions. Click Reactions occur exclusively between the azides (⁻N=N⁺=N⁻) and alkynes (carbon-carbon triple bond), produce no by-products and therefore have a 100% atom economy. Bioorthogonal ‘Click’ Chemistry has enabled complex chemical reactions to be carried out within living organisms: the reactions do not bring harm to, interfere with or disrupt the biological processes occurring within these systems as they cannot be recognised & used by these systems. ‘Click’ Chemistry is therefore vital in understanding how we may be able to develop Targeted Cancer Therapeutics using Bioorthogonal Chemistry. Modern day cancer treatments tend to be delivered intravenously using anthracyclines (notably doxorubicin), a class of antitumour antibiotics used for cancer chemotherapy: they stop the growth of cancerous cells by preventing their enzymatic machinery from engaging in DNA duplication & cell division, causing the cells to die. The long-standing side effect of using such effective drugs is the high likelihood of ‘off-target toxicity’, where non-cancerous cells can also be harmed by the intercalating effects of the anthracyclines. Frequent targets for this ‘off-target toxicity’ tend to be fast growing body cells, like hair & nails, hence why most cancer patients experience some form of hair loss over the course of their chemotherapy treatment. So, scientists began to consider: what if there was a way to develop targeted cancer treatments? Treatments that enabled the activation of these powerful cancer drugs - anthracyclines - at the tumour sites, mitigating the harm of ‘off-target toxicity’? This is where Bioorthogonal ‘Click’ Chemistry comes in. ‘ C lick- A ctivated P rotodrugs A gainst C ancer’ (or ‘ CAPAC ’) is a platform developed by American Biotechnology Company Shasqi. Through ‘CAPAC’, Shasqi are pioneering the use of Bioorthogonal ‘Click’ Chemistry to target cancer drugs directly to the tumour site, minimising side effects and potentially improving the therapeutic index. They’ve achieved this through exploiting one of the fastest click reactions: a Diels-Alder cycloaddition between a tetrazine (C2H2N4) and a trans-cyclooctene (TCO) - 2 bioorthogonal molecules. The treatment involves two key components: a tetrazine-modified sodium hyaluronate biopolymer & doxorubicin that is connected to a TCO (trans-cyclooctene) unit. Over the course of the treatment (Fig. 2) , the patient will undergo multiple stages: ● Local hydrogel injection: The tetrazine-modified sodium hyaluron ate biopolymer is injected into a patient’s tumour ● Protodrug dose: The patient then receives five daily infusions of doxorubicin-TCO ● Concentration: The drug circulates through the body until it meets the tetrazine-modified biopolymer at the tumour site ● Activation: At the point of meeting, the click reaction brings the tetrazine and TCO together, triggering a rearrangement that frees the doxorubicin right next to the tumour cells Compared to prior cancer treatments, this process would not only mitigate the harm of the drug’s ‘off-target toxicity’, limiting the side-effects of the chemotherapy drug, it would also increase the local concentration of doxorubicin far beyond what would normally be possible in a patient, having a greater effect in preventing the growth of cancer cells. In the treatment of this life-threatening disease, Shasqi’s research into the ‘CAPAC’ platform, though still ongoing, looks excitingly promising: as recently as March 2023, they’ve proven their platform’s efficacy in humans. During a Phase 1 dose-escalation clinical trial in adult patients with advanced solid tumours, Shasqi were able to demonstrate the activation of their tetrazine-modified sodium hyaluronate biopolymer & doxorubicin-TCO at tumour sites, evidencing it’s safety, systemic pharmacokinetics, and immunological activity. With the continuation of their innovative research, the future treatment of cancer can be significantly aided with the use of Bioorthogonal ‘Click’ Chemistry. Written by Emmanuella Fernandez REFERENCES Acs.org . (2021). Click chemistry sees first use in humans . [online] Available at: https://cen.acs.org/pharmaceuticals/Click-chemistry-sees-first-use/98/web/2020/10 . Cancer Research UK (2023). Doxorubicin (Adriamycin) | Cancer drugs | Cancer Research UK . [online] www.cancerresearchuk.org . Available at: https://www.cancerresearchuk.org/about-cancer/treatment/drugs/doxorubicin . Wang, Y., Zhang, C., Wu, H. and Feng, P. (2020). Activation and Delivery of Tetrazine-Responsive Bioorthogonal Prodrugs. Molecules , 25(23), p.5640. doi: https://doi.org/10.3390/molecules25235640 . Wikipedia Contributors (2019). Reverse transcriptase . [online] Wikipedia. Available at: https://en.wikipedia.org/wiki/Reverse_transcriptase . Wikipedia. (2020). Zidovudine . [online] Available at: https://en.wikipedia.org/wiki/Zidovudine . Wikipedia. (2022). Bioorthogonal chemistry . [online] Available at: https://en.wikipedia.org/wiki/Bioorthogonal_chemistry . Project Gallery

  • Unleashing the power of the stars: how nuclear fusion holds the key to tackling climate change | Scientia News

    Looking at the option of nuclear fusion to generate renewable energy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unleashing the power of the stars: how nuclear fusion holds the key to tackling climate change 14/07/25, 15:08 Last updated: Published: 30/04/23, 10:55 Looking at the option of nuclear fusion to generate renewable energy Imagine a world where we have access to a virtually limitless and clean source of energy, one that doesn't emit harmful greenhouse gases or produce dangerous radioactive waste. A world where our energy needs are met without contributing to climate change. This may sound like science fiction, but it could become a reality through the power of nuclear fusion. Nuclear fusion, often referred to as the "holy grail" of energy production, is the process of merging light atomic nuclei to form a heavier nucleus, releasing an incredible amount of energy in the process. It's the same process that powers the stars, including our very own sun, and holds the potential to revolutionize the way we produce and use energy here on Earth. Nuclear fusion occurs at high temperature and pressure when two atoms (e.g. Tritium and Deuterium atoms) merge together to form Helium. This merge releases excess energy and a neutron. This energy an then be harvested inform of heat to produce electricity. Progress in the field of creating a nuclear fusion reactor has been slow, despites the challenges there are some promising technologies and approaches have been developed. Some of the notable approaches to nuclear fusion research include: 1. Magnetic Confinement Fusion (MCF) : In MCF, high temperatures and pressures are used to confine and heat the plasma, which is the hot, ionized gas where nuclear fusion occurs. One of the most promising MCF devices is the tokamak, a donut-shaped device that uses strong magnetic fields to confine the plasma. The International Thermonuclear Experimental Reactor (ITER), currently under construction in France, is a large-scale tokamak project that aims to demonstrate the scientific and technical feasibility of nuclear fusion as a viable energy source. 2. Inertial Confinement Fusion (ICF) : In ICF, high-energy lasers or particle beams are used to compress and heat a small pellet of fuel, causing it to undergo nuclear fusion. This approach is being pursued in facilities such as the National Ignition Facility (NIF) in the United States, which has made significant progress in achieving fusion ignition, although it is still facing challenges in achieving net energy gain. In December of 2022, the US lab reported that for the first time, more energy was released compared to the input energy. 3. Compact Fusion Reactors: There are also efforts to develop compact fusion reactors, which are smaller and potentially more practical for commercial energy production. These include technologies such as the spherical tokamak and the compact fusion neutron source, which aim to achieve high energy gain in a smaller and more manageable device. While nuclear fusion holds immense promise as a clean and sustainable energy source, there are still significant challenges that need to be overcome before it becomes a practical reality. In nature nuclear fusion is observed in stars, to be able to achieve fusion on Earth such conditions have to be met which can be an immense challenge. High level of temperature and pressure is required to overcome the fundamental forces in atoms to fuse them together. Not only that, but to be able to actually use the energy it has to be sustained and currently more energy is required then the output energy. Lastly, the material and technology also pose challenges in development of nuclear fusion. With high temperature and high energy particles, the inside of a nuclear fusion reactor is a harsh environment and along with the development of sustained nuclear fusion, development of materials and technology that can withstand such harsh conditions is also needed. Despite many challenges, nuclear fusion has the potential to be a game changer in fight against not only climate change but also access of cheap and clean energy globally. Unlike many forms of energy used today, fusion energy does not emit any greenhouse gasses and compared to nuclear fission is stable and does not produce radioactive waste. Furthermore, the fuel for fusion, which is deuterium is present in abundance in the ocean, where as tritium may require to synthesised at the beginning, but once the fusion starts it produce tritium by itself making it self-sustained. When the challenges are weighted against the benefits of nuclear fusion along with the new opportunities it would unlock economically and in scientific research, it is clear that the path to a more successful and clean future lies within the development of nuclear fusion. While there are many obstacles to overcome, the progress made in recent years in fusion research and development is promising. The construction of ITER project, along with first recordings of a higher energy outputs from US NIF programs, nuclear fusion can become a possibility in a not too distant future. In conclusion, nuclear fusion holds the key to address the global challenge of climate change. It offers a clean, safe, and sustainable energy source that has the potential to revolutionize our energy systems and reduce our dependence on fossil fuels. With continued research, development, and investment, nuclear fusion could become a reality and help us build a more sustainable and resilient future for our planet. It's time to unlock the power of the stars and harness the incredible potential of nuclear fusion in the fight against climate change. Written by Zari Syed Related articles: Nuclear medicine / Geoengineering / The silent protectors / Hydrogen cars Project Gallery

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