The utilisation of Stonehenge as an astronomical calculator Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The celestial blueprint of time: Stonehenge, United Kingdom Last updated: 08/10/25, 17:22 Published: 09/10/25, 08:00 The utilisation of Stonehenge as an astronomical calculator This is Article 3 in a series about astro-archaeology. Next article coming soon. Previous article: The astronomical symbolism of the Giza Pyramids . Stonehenge, located within the south-west of England, is one of the UK’s most notable man-made structures, built during the neolithic period around 3100BC. Not only is this famous UNESCO heritage site a breakthrough in engineering, but the sandstone architecture also holds an enigmatic connection between the land and the sky. Its location and stone arrangement mirrors a blueprint that can be analysed to predict the timings of astronomical phenomena. The utilisation of Stonehenge as an astronomical calculator was established by astronomer Gerald Hawkins in 1965. Using computer software, Hawkins discovered that the location of Stonehenge aligned with several solar and lunar positions. He theorised that Stonehenge was built to predict astronomical events, such as eclipses, and to determine the position of summer and winter solstices. From the shape and positions of the 19 stones that comprise Stonehenge, its ‘horseshoe’ shape could predict the lunar eclipses. A booklet titled Stonehenge: Sun, Moon, Wandering Stars , written by M.W. Postins further detailed the significance of Stonehenge in archaeoastronomy. Postins suggested two scale models, the ‘Temple model’ and the ‘Enclosure model’, which detailed the significance of each stone and its relation to different events. For example, the booklet notes that the Altar Stone, a large sandstone located in the centre of Stonehenge, was placed across the solstice axis and represents the ‘Summer solstice sunrise’. Additionally, Postins hypothesised that the five trilithons, which are the vertical stones that form the structure of Stonehenge, represented planets that can be viewed with the naked eye. These include the two lowest trilithons on the East and Northern sides of the structure, representing Mercury and Venus. There has been new research, currently underway by the universities of Oxford, Leicester and Bournemouth in collaboration with the Royal Astronomical Society, linking the Stonehenge monument to a unique lunar phenomenon, called the ‘Major Lunar Standstill’. Right from the early construction of Stonehenge, researchers note that the major lunar standstill may have influenced the design of the monument. Four of the stones at Stonehenge align with two of the Moon’s positions, which aid to indicate moonrise and moonset. This would have allowed individuals to use the moonlight for longer periods of activity, such as night time hunting, as well as visualise the cycle of the lunar phases as a method of time watching for farming and celebratory purposes. Potentially, there is speculation that this made the positioning and construction of Stonehenge intentional. The timeless effect of the Stonehenge landmark, which shaped life in the past and continues to be of astronomical interest to determine the future, is a remarkable example of the functions of built structures for the analysis of astronomical events. It truly is a celestial blueprint for the relationship between the earth and cosmology. Written by Shiksha Teeluck Related article: Astro-geography of Lonar Lake REFERENCES English Heritage. (2024). Stonehenge: Major Lunar Standstill . https://www.english-heritage.org.uk/visit/places/stonehenge/things-to-do/major-lunar-standstill/ OSR. (2009). Stonehenge: An Astronomical Calculator . https://osr.org/blog/astronomy/stonehenge-an-astronomical-calculator/?srsltid=AfmBOopNQnJ-XUZSyLY_Aqu3L2nOJgSoAceRzQJIVZbsIsFhW6s3U_NT Tiverton & Mid Devon Astronomy Society. (n.d.). Astro-Archaeology at Stonehenge . http://www.tivas.org.uk/stonehenge/stone_ast.html Project Gallery

Unveiling the paradigm shift in cognitive impairment through machine learning Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Brain metastasis hacks brain activity and jams neuronal communication Last updated: 29/05/25, 11:46 Published: 29/05/25, 08:00 Unveiling the paradigm shift in cognitive impairment through machine learning Understanding the impact of brain metastasis on neuronal communication Introduction Researchers from the Spanish National Research Council (CSIC) and the Spanish National Cancer Research Centre (CNIO) have made a ground-breaking discovery related to brain metastasis and its impact on brain activity and neuronal communication. This finding could potentially explain why half of all patients with brain metastasis experience cognitive impairment. Understanding the influence on neural circuits The research , published in Cancer Cell, aimed to comprehend how brain metastasis affects the functionality of neuronal circuits beyond the physical mass of the tumour. The researchers conducted multidimensional modelling of brain functional analyses in the context of brain metastasis and tested various preclinical models from different primary sources and oncogenic profiles. The study was able to separate the effect on local field potential oscillatory activity from cortical and hippocampal areas. This helped researchers learn more about the different ways that brain metastasis can affect people. The authors highlighted the importance of this comprehensive approach in unravelling the complex dynamics of brain metastasis. Detecting metastases through electrical activity Through the measurement of electrical activity in the brains of mice with and without metastases, the researchers discovered distinct electrophysiological differences between the two groups. The researchers used artificial intelligence to confirm that metastases were indeed to blame for these differences. Using an automatic algorithm trained with numerous electrophysiological recordings, the researchers developed a model that could accurately identify the presence of metastases. Furthermore, the algorithm demonstrated the ability to distinguish metastases originating from different primary tumours, such as skin, lung, and breast cancer. These findings provide clear evidence of the specific impact that metastasis has on the brain's electrical activity. Paradigm shift in understanding brain metastases The study represents a significant paradigm shift in the understanding of brain metastases. Traditionally, neurological dysfunction in patients with brain metastasis was attributed solely to the physical mass effect of the tumour. However, this research indicates that changes in brain activity resulting from tumour-induced biochemical and molecular alterations also contribute to these symptoms. The implications of this paradigm shift are far-reaching and have potential implications for the prevention, early diagnosis, and treatment of brain metastasis. By recognising that neurological symptoms are not solely due to the physical presence of the tumour, medical professionals can explore novel diagnostic and therapeutic strategies. Potential therapeutic targets Looking ahead, the researchers are eager to explore potential therapeutic targets that can protect the brain from cancer-induced disruptions in neuronal circuits. They aim to identify molecules involved in metastasis-induced changes in neuronal communication, intending to evaluate them as possible therapeutic targets. The researchers want to create strategies that might stop or lessen the neurological dysfunction that patients frequently experience by understanding the biochemical and molecular changes brought on by brain metastasis. This could lead to advancements in the prevention, early diagnosis, and treatment of brain metastasis, ultimately improving patient outcomes. Conclusion The groundbreaking studies carried out by the Spanish National Research Council and the Spanish National Cancer Research Centre have shed light on how brain metastasis affects brain activity and neuronal communication. By dissociating the effects of tumour mass from changes in brain activity, the study has revealed the complex dynamics of brain metastasis and its contribution to cognitive impairment in patients. The discovery of distinct electrophysiological differences and the development of an algorithm to detect metastases offer promising opportunities for early diagnosis and personalised treatment. This paradigm shift in understanding brain metastases opens the door for novel diagnostic and therapeutic strategies, as well as the exploration of potential therapeutic targets to protect the brain from cancer-induced disruptions. With further research, it is hopeful that advancements in the prevention, early diagnosis, and treatment of brain metastasis will improve patient outcomes and lead to a better understanding of neurological dysfunction in these patients. Written by Sara Maria Majernikova Related articles: Cancer on the move / Cancer magnets / Latent space transformations / Uploading brain to a computer REFERENCE Sanchez-Aguilera A, Masmudi-Martín M, Navas-Olive A, Baena P, Hernández-Oliver C, Priego N, Cordón-Barris L, Alvaro-Espinosa L, García S, Martínez S et al : Machine learning identifies experimental brain metastasis subtypes based on their influence on neural circuits . Cancer Cell 2023, 41 (9):1637-1649.e1611. Project Gallery

Discussing why people with PTSD have intrusive memories Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Boom, and You're Back! 01/04/26, 12:23 Last updated: Published: 19/01/24, 12:14 Discussing why people with PTSD have intrusive memories This is Part I in a two-part series on PTSD and intrusive memories. Next article: PTSD and Tetris Post-traumatic stress disorder (PTSD) is an anxiety disorder which may develop if a person has been involved in or witnessed a stressful event. Whilst most people associate PTSD with soldiers, it also develops in people like you and me. In fact, many events that lead to PTSD development occur in everyday life, such as car crashes, traumatic childbirth, assaults, robberies etc. One of the main symptoms of PTSD is intrusive memories. This is when people involuntarily develop recollections of the event within their consciousness. Dual modality theory The main model which explains the development of intrusive memories in PTSD is the Dual Representation Theory (DRT). DRT was proposed by Brewin, Dalgleish, and Joseph, and this idea suggests that there are two separate memory systems which encode information during an event. The verbally accessible memory system (VAM) holds information about the conscious experience of the event meaning it can be voluntarily recalled afterwards. This is compared to the situationally accessible memory system (SAM) which processes unconscious sensory information, like smells and sounds, which cannot be voluntarily recalled. The theory suggests VAM is impaired and focuses on the frightening information and the fear that we experience during an event, and this affects how we process the information. Coupled with the vivid sensory information captured by SAM, when individuals are in a context where physical or sensory features are like the traumatic event, they unconsciously trigger intrusive memories which are highly distressing and emotionally valanced. Think of the last movie you watched about someone returning from war who was scared of fireworks. Now you understand that the banging sound triggers the highly emotional memories from the SAM and VAM system, forcing them to re-witness situations where a bomb has gone off. One loud boom and they are back in a war zone. Where in the brain is this going on? There are many brain areas involved in PTSD memory processing, but some common areas are associated with the formation and retrieval of traumatic memories. Hippocampus: combines lots of information in the environment into one memory that can be consciously retrieved. It seems likely that this area is essential for creating verbally accessible memories in trauma, so is part of the VAM system. Ventromedial prefrontal cortex: involved in regulating how much emotion is encoded into a memory. It has been said that dysfunction in this area is why people with PTSD have difficulties processing the emotion attached to the traumatic event. Amygdala: Important in how we learn to associate stimuli with the correct emotional response. It has been said in highly stressful events the amygdala becomes hyperactive which is why there is such a strong emotional reaction to certain cues, therefore is likely to be crucial in the SAM system. Hormones: elevated levels of glucocorticoids, cortisol, and norepinephrine can influence the consolidation of memories which creates stronger and more persistent traumatic memories. Written by Alice Jayne Greenan Related articles: Synaptic plasticity / Can you erase your memory? Project Gallery

An analysis of risk and protective factors Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Postpartum depression in adolescent mothers Last updated: 24/06/25, 17:39 Published: 10/07/25, 08:00 An analysis of risk and protective factors Impact and prevalence According to the DSM-5, postpartum depression (PPD), also known as postnatal depression, is characterised by psychological and physical symptoms – including anhedonia, depressed mood and abnormal differences in sleep patterns – with a postpartum onset within one month after childbirth. Long-term effects of PPD, which are the same for adult and adolescent mothers, include weaker attachment between the mother and the child and developmental delays in children. Whilst treatment methods for postnatal depression have been more thoroughly investigated in adult mothers than in teenage mothers, prevalence rates of postpartum depression are found to be higher in adolescent mothers, with teenage mothers being twice as likely to be depressed as adult mothers. Postpartum depression in adolescent mothers is a prominent concern, as studies have found that up to 57% of teenage mothers report moderate to severe symptoms of PPD. Risk and protective factors A definite risk factor for postpartum depression in teenage mothers is a lack of social support. Research shows that adolescent mothers face more challenges but have fewer resources and less social support than adult mothers. This is prominent in Barnet et al.’s (1996) research, which found that adolescent mothers who received emotional support from either their mother or the baby’s father were less likely to exhibit depressive symptoms postpartum. Others support this research and suggest that social support has a direct effect on PPD in teenage mothers. Additionally, a lack of wider social support results in stigma, with a common assumption being that young mothers are incompetent parents and that children should not raise other children. Thus, another aspect of the lack of social support that might lead to PPD is stigma. However, an abundance of social support can also be detrimental, as it might make the young mothers feel incapable or inadequate, also leading to postnatal depression. Therefore, it is vital to determine the appropriate amount of support required for adolescent mothers. Another important risk factor affecting adolescent mothers that leads to postpartum depression is stress, which can be, but does not have to be, caused by a lack of social support. Research shows that higher stress levels are positively associated with depressive symptoms, and teenage mothers who reported higher stress levels displayed higher levels of PPD than adolescent mothers with lower stress levels. Therefore, in order to reduce the rate of postpartum depression in adolescent mothers, interventions should focus on decreasing the mothers’ stress levels. A crucial protective factor for PPD in adolescent mothers is self-esteem. Logsdon et al. (2005) found that lower self-esteem was predictive of postnatal depression in teenage mothers, and Caldwell & Antonucci (1997) found that self-esteem has a strong negative correlation with PPD symptoms in adolescent mothers. Therefore, higher self-esteem can shield young mothers from postpartum depression. Conclusions Overall, adolescent mothers are a particularly vulnerable population due to the additional challenges they face and the common lack of preparation for motherhood amongst teenage mothers. Social support, both a lack thereof or an excess amount, is commonly identified in the literature as a key risk factor for PPD in young mothers, as well as stigma and stress. High self-esteem and confidence in one’s own parenting skills are prominent and promising protective factors. The few interventions that are present demonstrate a promising start towards developing ways to tackle PPD in adolescent mothers. However, there has not been an extensive meta-analysis evaluating existing interventions, a clear limitation and a gap in the literature that should be addressed in future research. Written by Aleksandra Lib Related articles: Depression / Depression in children / Childhood stunting / Gynaecology REFERENCES American Psychiatric Association (APA). (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Barnet, B., Joffe, A., Duggan, A. K., Wilson, M. D., & Repke, J. T. (1996). Depressive symptoms, stress, and social support in pregnant and postpartum adolescents. Archives of pediatrics & adolescent medicine , 150 (1), 64-69. Caldwell, C. H., Antonucci, T. C., Jackson, J. S., Wolford, M. L., & Osofsky, J. D. (1997). Perceptions of parental support and depressive symptomatology among black and white adolescent mothers. Journal of Emotional and Behavioral Disorders , 5 (3), 173-183. Deal, L. W., & Holt, V. L. (1998). Young maternal age and depressive symptoms: Results from the 1988 National Maternal and Infant Health Survey. American Journal of Public Health, 88 , 266–270 Dinwiddie, K. J., Schillerstrom, T. L., & Schillerstrom, J. E. (2017). Postpartum depression in adolescent mothers. Journal of Psychosomatic Obstetrics & Gynecology , 39 (3), 168–175. Field T. (1992). Infants of depressed mothers. Development and Psychopathology, 4 , 49-66. Logsdon, M. C., Birkimer, J. C., Simpson, T., & Looney, S. (2005). Postpartum depression and social support in adolescents. Journal of Obstetric, Gynecologic & Neonatal Nursing , 34 (1), 46-54. Radke-Yarrow, M., Cummings, E. M., Kuczynski, L., & Chapman, M. (1985). Patterns of attachment in two- and three-year-olds in normal families and families with parental depression. Child Development, 56 , 886-893. Schmidt, R. M., Wiemann, C. M., Rickert, V. I., & Smith, E. O. B. (2006). Moderate to severe depressive symptoms among adolescent mothers followed four years postpartum. Journal of Adolescent Health , 38 , 712–718. Project Gallery

The Design Argument vs science Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Anthropic Principle: Science or God? 20/11/25, 15:34 Last updated: Published: 08/11/24, 11:25 The Design Argument vs science One of the most common points of tension between science and religion is the Design Argument – an argument for the existence of an intelligent designer/creator of the universe or God. Individuals who tend to identify with one of the Abrahamic religions (Christianity, Judaism, and Islam) often also believe in a God who created the universe, although it is important to note that not every person agrees here. On the other hand, public opinion often says that scientists do not support the Design Argument because they are studying how the universe was ‘actually’ created, which leads to some tension between the two groups. However, there is some logical support for the Design Argument originating from scientific data: the Anthropic Principle, also known as the Observation-Selection Hypothesis. While there are different takes on the hypothesis, this article will briefly cover how it relates to physics and the Design Argument. In general, the Anthropic Principle states that the parameters of the universe are exactly what they are so that life (intelligent, conscious life) would ultimately be produced. The following are examples of factors that happen to be just right for life to be possible: The electromagnetic force is 39 times stronger than gravity, but if they were more evenly matched, stars would not survive long enough for life to develop on an orbiting planet. If gravity were 1 part in 1040 stronger, the universe would have utterly collapsed long ago. If the combined mass of a proton and electron were slightly more than the mass of a neutron (rather than slightly less as it currently is), then the hydrogen atom would become unstable, which would collapse stars like the Sun. If the mass of neutrinos (the most abundant particles with mass in the universe) was 5 x 10-34 kg instead of 5 x 10-35 kg, the universe would be contracting rather than expanding. There are many more examples, but isn’t it strange how absolutely exact the strengths of these kinds of fundamental forces are? This is the line of reasoning that leads to the Design Argument. How could the universe be so incredibly exact to produce life, unless it was specifically created that way? Such questions are asked by Science and Religion scholars, and while there are no answers yet, it opens the conversation up to explore what information different fields have to offer. Written by Amber Elinsky Related article: Creatio ex Nihilo REFERENCES Davis, John Jefferson. “The Design Argument, Cosmic ‘Fine Tuning,’ and the Anthropic Principle.” International Journal for Philosophy of Religion 22, no. 3 (1987): 139–50. http://www.jstor.org/stable/40018832 . Gale, George. “The Anthropic Principle.” Scientific American 245, no. 6 (1981): 154–71. http://www.jstor.org/stable/24964627 . Project Gallery

DFNB9 affects 1 to 16 newborns every 50,000 Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link DFNB9: The first deafness ever treated by gene therapy 03/04/26, 17:00 Last updated: Published: 05/09/24, 11:03 DFNB9 affects 1 to 16 newborns every 50,000 Two (TWO!) AAV gene therapies have restored hearing in deaf patients! Scientists have corrected DFNB9 deafness! These are headlines you have likely read last January. The technology making this achievement possible rightfully took the spotlight (e ven I chimed in! ). But what is DFNB9 deafness in the first place? Why do DFNB9 patients lose their hearing? In a nutshell, DFNB9 deafness is the failure of the ear to share what it has heard with the brain because of mutations in the OTOF gene. Do you want to learn more? Let me explain. Medical and genetic definitions of DFNB9 deafness DFNB9 is a type of genetic deafness. It affects 1 to 16 newborns every 50,000, and it accounts for 2 to 8% of all cases of genetic deafness. DFNB9 is (take a deep breath!) an autosomal recessive prelingual severe-to-profound non-syndromic sensorineural hearing loss. That’s a mouthful of a definition, I agree. Let’s break it down. In medical terms, DFNB9 deafness is: severe — sounds must be louder than 70 dB (think of a vacuum cleaner) to be heard — to profound — sounds must be even louder, over 90 dB (picture a lawn mower), prelingual, that is hearing is lost before developing language skills (2–3 years of age) not associated with other pathologies (non-syndromic). Geneticists describe DFNB9 as an autosomal recessive disease: the gene mutated is not on the sex chromosomes (but on the autosomes) and both alleles must be mutated for the disease to appear (recessive). This gene is OTOF . OTOF encodes otoferlin, a protein that enables the cells detecting sounds to communicate with neurons. As mutations in OTOF disrupt this dialogue, DFNB9 is classified as a sensorineural type of deafness. Otoferlin enables inner hair cells to speak to neurons How does otoferlin enable us to hear? This question needs a few notions on the two main cell types involved in hearing: auditory hair cells and primary auditory neurons. Auditory hair cells are the sound detector. These cells are surmounted by a structure resembling a tuft of hair, the hair bundle. Sounds bend the hair bundle, opening its ion channels; positive ions rush into the cells generating electrical signals that travel across the cell. Inner hair cells — one of the two types of auditory cells — transmit these signals to the primary auditory neurons ( Figure 1 ) The primary auditory neurons are the first station of the nervous pathway between the ear and the brain. Some primary auditory neurons (type I) extend their dendrites to the inner hair cells and listen. The information received is analysed and sent to the brain along the auditory nerve ( Figure 2 ). The synapse is where inner hair cells speak to primary auditory neurons. Otoferlin is essential for this dialogue: without it, inner hair cells cannot share what they have heard. Otoferlin, the calcium sensor At the synapse, synaptic vesicles are placed just beneath the membrane, like Formula 1 cars lined up the grid waiting for the race to start. In response to a sound, electrical signals trigger the opening of calcium channels and calcium ions (Ca2+) rush in. The sudden increase in Ca2+ is the biological equivalent of the “lights out” signal in Formula 1: as soon as Ca2+ enters, the synaptic vesicles rapidly fuse with the membrane. This event releases glutamate onto the primary auditory neurons ( Figure 3 ). The information in the sound is on its way to the brain. In the inner hair cells, otoferlin enables synaptic vesicles to sense changes in Ca2+. Anchored to the vesicles by its tail, otoferlin extends into the cell multiple regions with high affinity to Ca2+ (C2 domains) ( Figure 4 ). The many roles of otoferlin at the synapse Otoferlin is essential throughout the lifecycle of synaptic vesicles (Figure 5). This is a brief overview of its main roles at the synapse: 1 — Docking : Otoferlin helps position vesicles filled with glutamate at the synapse 2 — Priming : Otoferlin interacts with SNARE proteins, which are essential for the fusion with the membrane, and the vesicles become ready to rapidly fuse 3 — Fusion : electrical signals, triggered by sounds, open Ca2+ channels; Otoferlin senses the increase in Ca2+ and prompts the vesicles to fuse with the cell membrane, releasing glutamate 4 — Recycling : Otoferlin helps clear fused vesicles and recycle their components Imperfect knowledge can be enough knowlege (sometimes) Despite years of studies, the functions of otoferlin at the inner hair cell synapse are still elusive. Even more puzzling is the synapse of inner hair cells as a whole. Researchers are captivated and baffled by its mysterious architecture and properties (we would need a new article just to scratch the surface of this topic!). But let’s not forget that we now have two gene therapies to improve the deafness caused by mutations in the OTOF gene. These breakthroughs should encourage us: even with imperfect knowledge, we can (at least in some cases) still develop impactful treatments for diseases. Indeed, as of mid-2025, follow-up studies indicated that hearing improvements, including the ability to understand speech, are sustained. Written by Matteo Cortese, PhD REFERENCES Manchanda A, Bonventre JA, Bugel SM, Chatterjee P, Tanguay R, Johnson CP. Truncation of the otoferlin transmembrane domain alters the development of hair cells and reduces membrane docking. Mol Biol Cell. 2021 Jul 1;32(14):1293–1305. Morton CC, Nance WE. Newborn hearing screening — a silent revolution. N Engl J Med. 2006 May 18;354(20):2151–64. Johnson CP, Chapman ER. Otoferlin is a calcium sensor that directly regulates SNARE-mediated membrane fusion. J Cell Biol. 2010 Oct 4;191(1):187–97. Pangrsic T, Lasarow L, Reuter K, Takago H, Schwander M, Riedel D, Frank T, Tarantino LM, Bailey JS, Strenzke N, Brose N, Müller U, Reisinger E, Moser T. Hearing requires otoferlin-dependent efficient replenishment of synaptic vesicles in hair cells. Nat Neurosci. 2010 Jul;13(7):869–76. Qi J, Tan F, Zhang L, Lu L, Zhang S, Zhai Y, Lu Y, Qian X, Dong W, Zhou Y, Zhang Z, Yang X, Jiang L, Yu C, Liu J, Chen T, Wu L, Tan C, Sun S, Song H, Shu Y, Xu L, Gao X, Li H, Chai R. AAV-Mediated Gene Therapy Restores Hearing in Patients with DFNB9 Deafness. Adv Sci (Weinh). 2024 Jan 8:e2306788. Roux I, Safieddine S, Nouvian R, Grati M, Simmler MC, Bahloul A, Perfettini I, Le Gall M, Rostaing P, Hamard G, Triller A, Avan P, Moser T, Petit C. Otoferlin, defective in a human deafness form, is essential for exocytosis at the auditory ribbon synapse. Cell. 2006 Oct 20;127(2):277–89 Vona B, Rad A, Reisinger E. The Many Faces of DFNB9: Relating OTOF Variants to Hearing Impairment. Genes (Basel). 2020 Nov 26;11(12):1411. Project Gallery

Simplifying light: photons, wave-particle duality and the Observer Effect Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Light: one of the biggest mysteries in physics Last updated: 20/10/25, 15:28 Published: 23/10/25, 08:00 Simplifying light: photons, wave-particle duality and the Observer Effect Light is one of those few topics where physicists have to say, ‘We don’t yet know why it is the way it is, we just know that it is that way.’ Let’s start simple. Question 1: What is light? When we think of light, we automatically think of visible light- what we can see with our eyes. But that is only 0.0035% of the total light, or electromagnetic, spectrum. The rest of the spectrum includes non-visible light, such as infrared radiation (what we feel as heat), x-rays (what the medical field’s X-ray machine uses to capture images of bones) or ultraviolet radiation (what causes sunburn). Every kind of light is made up of photons. They are tiny little pockets of energy that travel across space at 3 x 10 8 meters/second at different wavelengths and frequencies. Imagine someone tosses you a tennis ball, but instead of it travelling straight towards you, it oscillates up and down in a wave pattern as it travels. If you take a measurement from peak to peak, this distance is called a wavelength. The tennis ball can move up and down in the wave pattern at different speeds. This speed is called the frequency. Photons can travel at different wavelengths and different frequencies depending on where it originated. The unique wavelength and frequency pair of each photon determines what kind of light it is- where it falls on the electromagnetic spectrum. For example, photons with much shorter wavelengths and therefore much higher frequencies fall towards the right-hand side of the spectrum and are likely gamma-rays or x-rays. On the other hand, photons with much longer wavelengths and much lower frequencies are on the left-hand side, meaning the photons are probably radio waves or microwaves. So far, so good. All of this makes sense, and physicists are fairly confident in this information. So, what’s the problem? Question 2: Why is light so problematic? The trouble with light is its behaviour. Remember those little pockets of energy that move up and down in a wave pattern? Well, that’s not exactly what happens. Light has a property that physicists call ‘wave-particle duality’, which is a fancy term for meaning that sometimes light behaves like a particle (photons) and other times it behaves like a wave. When it behaves as a wave, we get the electromagnetic spectrum. As mentioned above, the wave can have different peak-to-peak lengths and travelling speeds that we read as different types of light across the spectrum. But when the photon behaves as a particle, we get this tiny pocket of energy rocketing across the cosmos. It is the fastest thing in the known universe. To understand the difference a little bit better, imagine you put the tennis ball in one of those pitching machines used for baseball players to practice their swing. It shoots the ball straight out of the front in a direct line and incredibly fast. This is light acting like a photon particle. Now, imagine you and a friend have a rope and each of you are holding on to either end. Your friend starts swinging their end up and down creating waves that travel down the rope towards you. The faster your friend swings their end, the faster the waves travel and the smaller the peak-to-peak distances (wavelengths) of the waves get, and vice versa if your friend slowly swings their end. This is light acting like a wave. The tricky bit is that physicists don’t know why the same pocket of energy can act like a photon particle in one instance, yet like a wave in another! The famous Double-Slit Experiment performed by Thomas Young in 1801 demonstrated this behaviour. Since then, the physics sub-field of quantum mechanics has developed and physicists now think that this behaviour is because of what they call the ‘Observer Effect’, which means that particles behave differently depending on whether or not they are observed. How does the particle know when it is being observed? Well, that is still a mystery to all. Written by Amber Elinsky Related articles: Laser Interferometric Gravitational-wave Observatory (LIGO) / Dark Energy Spectroscopic Instrument (DESI) REFERENCES Wavelength/Frequency Image ref: BYJU’s educational tech company Electromagnetic Image ref: Space.com Baclawski, Kenneth. (2018). The Observer Effect. 83-89. 10.1109/COGSIMA.2018.8423983. Project Gallery

A well-studied longevity gene is SIRT1 Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Genetics of Ageing and Longevity 11/07/25, 10:57 Last updated: Published: 13/05/24, 16:20 A well-studied longevity gene is SIRT1 Ageing is a natural process inherent to all living organisms. Yet, its mechanisms remain somewhat enigmatic. While lifestyle factors undoubtedly influence longevity, recent advancements in genetic research have revealed the influence of our genomes on ageing. Through understanding these influences, we can unlock further knowledge on longevity, which can aid us in developing interventions to promote healthy ageing. This article delves into the world of ageing and longevity genetics and how we can use this understanding to our benefit. Longevity genes A number of longevity genes, such as APOE , FOXO3 , and CETP, have been identified. These genes influence various biological processes, including cellular repair, metabolism, and stress response mechanisms. A well-studied longevity gene is SIRT1 . Located on chromosome 10, SIRT1 encodes sirtuin 1, a histone deacetylase, transcription factor, and cofactor. Its roles include protecting cells against oxidative stress, regulating glucose and lipid metabolism, and promoting DNA repair and stability via deacetylation. Sirtuins are an evolutionarily conserved mediator of longevity in many organisms. One study looked at mice with knocked-out SIRT1 ; these mice had significantly lower lifespans when compared with WT mice1. The protective effects of SIRT1 are thought to be due to deacetylating p53, which promotes cell death2. SIRT1 also stimulates the cytoprotective and stress-resistance gene activator FoxO1A (see Figure 1 ), which upregulates catalase activity to prevent oxidative stress3. Genome-wide association studies (GWAS) have identified several genetic variants associated with ageing and age-related diseases. Such variants influence diverse aspects of ageing, such as cellular senescence, inflammation, and mitochondrial function. For example, certain polymorphisms in APOE are associated with an increased risk of age-related conditions like Alzheimer's and Parkinson’s disease4. These genes have a cumulative effect on the longevity of an organism. Epigenetics of ageing Epigenetic modifications, such as histone modifications and chromatin remodelling, regulate gene expression patterns without altering the DNA sequence. Studies have shown that epigenetic alterations accumulate with age and contribute to age-related changes in gene expression and cellular function. For example, DNA methylation is downregulated in human fibroblasts during ageing. Furthermore, ageing correlates with decreased nucleosome occupancy in human fibroblasts, thereby increasing the expression of genes unoccupied by nucleosomes. One specific marker of ageing in metazoans is H3K4me3, indicating the trimethylation of lysine 4 on histone 3; in fact, H3K4me3 demethylation extends lifespan. Similarly, H3K27me3 is also a marker of biological age. By using these markers as an epigenetic clock, we can predict biological age using molecular genetic techniques. As a rule of thumb, genome-wide hypomethylation and CpG island hypermethylation correlate with ageing, although this effect is tissue-specific5. Telomeres are regions of repetitive DNA at the terminal ends of linear chromosomes. Telomeres become shorter every time a cell divides (see Figure 2 ), and eventually, this can hinder their function of protecting the ends of chromosomes. As a result, cells have complex mechanisms in place to prevent telomere degradation. One of these is the enzyme telomerase, which maintains telomere length by adding G-rich DNA sequences. Another mechanism is the shelterin complex, which binds to ‘TTAGGG’ telomeric repeats to prevent degradation. Two major components of the shelterin complex are TRF1 and TRF2, which bind telomeric DNA. They are regulated by the chromatin remodelling enzyme BRM-SWI/SNF, which has been shown to be crucial in promoting genomic stability, preventing cell apoptosis, and maintaining telomeric integrity. BRM-SWI/SNF regulates TRF1/2, thereby, regulating the shelterin complex, by remodelling the TRF1/2 promoter region to convert it to euchromatin and increase transcription. BRM-SWI/SNF inactivating mutations have been shown to contribute to cancer and cellular ageing through telomere degradation6. Together, the mechanisms cells have in place to protect telomeres provide protection against cancer as well as cellular ageing. Future of anti-ageing drugs Anti-ageing drugs are big business in the biotechnology and cosmetics sector. For example, senolytics are compounds that decrease the number of senescent cells in an individual. Senescent cells are those that have permanently exited the cell cycle and now secrete pro-inflammatory molecules (see Figure 3); they are a major cause of cellular and organismal ageing. Senolytic drugs aim to provide anti-ageing benefits to an individual, whereby senescent cells are removed, therefore, decreasing inflammation. Currently, researchers are certain that removing senescent cells would have an anti-ageing effect, although senolytic drugs currently on the market are understudied, and so their side effects are unknown. Speculative drugs could include those that enhance telomerase or SIRT1 activity. Evidently, ageing is not purely determined by lifestyle and environmental factors alone but also by genetics. While longevity genes are hereditary, epigenetic modifications may be influenced by external factors. Therefore, we can attribute the complex interplay between various external factors and an individual’s genome to understanding the role of genetics in ageing. Perhaps we will see a new wave of anti-ageing treatments in the coming years, developed on the genetics of ageing. Written by Malintha Hewa Batage Related articles: An introduction to epigenetics / Schizophrenia, inflammation and ageing / Ageing and immunity REFERENCES Cilic, U et al., (2015) ‘A Remarkable Age-Related Increase in SIRT1 Protein Expression against Oxidative Stress in Elderly: SIRT1 Gene Variants and Longevity in Human’, PLoS One , 10(3). Alcendor, R et al., (2004) ‘Silent information regulator 2alpha, a longevity factor and class III histone deacetylase, is an essential endogenous apoptosis inhibitor in cardiac myocytes’, Circulation Research , 95(10):971-80. Alcendor, R et al., (2007) ‘Sirt1 regulates aging and resistance to oxidative stress in the heart’, Circulation Research , 100(10):1512-21. Yin, Y & Wang, Z, (2018) ‘ApoE and Neurodegenerative Diseases in Aging’, Advances in Experimental Medicine and Biology , 1086:77-92. Wang, K et al., (2022) ‘Epigenetic regulation of aging: implications for interventions of aging and diseases’, Signal Transduction and Targeted Therapy , 7(1):374. Images made using BioRender. Project Gallery

What they are, which groups are affected, and pandemic and economic impacts Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What are health inequalities? Last updated: 05/02/26, 10:08 Published: 08/01/26, 08:00 What they are, which groups are affected, and pandemic and economic impacts This is Article 1 in a series on health inequalities. Next article: Socioeconomic health equalities . Welcome to the first article in a series of articles about health inequalities. This first article will look more in detail at exactly what health inequalities are. Introduction Imagine that you lived in Blackpool, and that your friends or family lived in Kensington. Your life expectancy would be 76 years, while theirs would be 86 years, a full decade of difference! Or consider the fact that even though men have shorter life-spans compared to women, women spend longer living with ill health or major illnesses. These are some examples of health inequalities, which are health differences between different groups of people. They aren’t just random variations in health outcomes between different groups or people: instead, they’re systematic and avoidable. What groups are affected by health inequalities? Health inequalities can be seen across various populations. A person’s health can be impacted by socioeconomic factors, like income or wealth, and geographic factors, like where they live. Other characteristics affecting health include ethnicity or gender. These factors don’t act in isolation. For individuals who experience multiple levels of disadvantage, the effects of inequalities are worsened. For example, ethnic minority groups who live in deprived areas, or socioeconomically disadvantaged women, experience even worse health outcomes. This interconnectedness means that understanding health inequalities and addressing them requires a holistic approach. Health status and health inequalities Differences in health outcomes can manifest in different ways. One indicator is health status, which includes overall life expectancy and healthy life expectancy, which is the time people live in good health. In England, there’s an almost 10-year gap in life expectancy between the most and least deprived areas, shown by the example above, where the life expectancy is 76 years in Blackpool and 86 years in Kensington. Differences in healthy life expectancy between the most and least deprived areas are even more pronounced. Healthy life expectancy is more than 18 years lower for the most deprived areas compared to the least deprived areas, as shown in Figure 1 . Males living in the most deprived areas can expect to live 52.3 years in good health, while for males living in the least deprived areas, this number increases to 70.5 years. For females, it’s 51.9 years in the most deprived areas, compared to 70.7 years in the least deprived. The impact of the COVID-19 pandemic on health inequalities The COVID-19 pandemic has exacerbated health inequalities, with those living in the most deprived areas and people from ethnic minority backgrounds being the worst impacted. For example, as the pandemic strained healthcare services, more deprived areas had longer waiting lists, highlighting issues of unequal access and quality of care. In addition, death rates in the most deprived areas were higher compared to the least deprived areas: at a deprivation level of 1 (most deprived), deaths from COVID-19 were 566.2 per 100,000, with this number decreasing to 228.7 deaths per 100,000 at a deprivation level of 10 (least deprived), as seen in Figure 2 . The economic impact of health inequalities Health inequalities can have economic impacts as a result of the added costs needed to address them. The persistence of health inequalities, particularly among the working-age population, is a challenge to economic growth, as increasing levels of ill health can lead to economic inactivity. For example, data from before COVID-19 suggests that health inequalities cost the UK £31bn to £33bn per year in lost productivity, £20bn to £32bn per year in lost tax revenue and higher benefits payments and £4.8bn of the NHS budget. This is equivalent to almost a fifth of the NHS budget. As the pandemic exacerbated inequalities, these numbers have only increased: for example, the long-term impacts of COVID-19 have varied between demographics. Given that at least 2.5 million working-age adults are unable to work due to long-term sickness, as per the Office for National Statistics estimates, this is a significant economic challenge for the country, as well as a health issue. Conclusion Health inequalities have been shown to affect different groups disproportionately, with deprivation, ethnicity, socioeconomic status and other social factors having compounding effects, resulting in poorer health and shorter healthy lives. The COVID-19 pandemic further exacerbated these inequalities, with the most marginalised communities being the most affected. Failure to address these differences has resulted in not only human costs but also billions in lost productivity and increased burdens on health services. Socioeconomic status is one specific factor that influences health outcomes: as mentioned above, people in the most deprived areas face a gap of approximately ten years in life expectancy compared to the least deprived, seen when comparing life expectancy in Blackpool and Kensington. The next article in this series will look more in detail at socioeconomic inequalities, so watch out for that! Written by Naoshin Haque Related article: Global Health Injustices (series) Project Gallery

They are on the IUCN red list as 'vulnerable' Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Conservation of marine iguanas 29/03/26, 17:01 Last updated: Published: 06/01/24, 10:40 They are on the IUCN red list as 'vulnerable' The marine iguana ( Amblyrhynchus cristatus ), also known as the sea iguana, is a unique species. It is the world’s only ocean- going lizard. Their main food source is algae; large males can dive to forage for this source, while females feed during low tide. They can be found on rocky shorelines, but also on marshes, mangrove swamps and beaches of the Galapagos. Their range is limited to the Galapagos islands, so they are an isolated species. Currently, they are on the IUCN red list as ‘vulnerable’ with a current population estimated at 200,000, and conservation efforts are needed to stabilise populations. Key threats There are three key threats to iguana populations. The first is invasive species; animals such as pigs, dogs and cats feed on young hatchlings and iguana eggs, which reduces the long-term survival rate of the species. Marine iguanas have not yet developed defence strategies against these predators. Even humans introduce pathogens to the islands that pose a threat to the species, because of their isolated habitat, the marine iguana lacks immunity to many pathogens and so has a higher risk of contracting diseases. Climate change is another key threat. El Niño is a weather event that prevents cold, nutrient-rich waters, that the marine wildlife depends on, from reaching the Eastern Tropical Pacific. This depletes algae populations, and this food drop drastically reduces iguana populations ( Figure 1 ). With global warming, El Niño events are expected to be more prominent and more frequent. It has been found that during El Niño events, marine iguanas experience metabolic stress, resulting in reduced metabolic rates. In addition, pollution from humans like oil spills and microplastics are damaging their habitat. Current and future conservation methods Under the laws of Ecuador, marine iguanas are completely protected. Their land range is in the Galapagos National Park, and their sea range is within the Galapagos Marine Reserve. They are also listed on the CITES, which ensures monitoring the trade of endangered animals to inhibit damage to their numbers. Sanctuaries are also in place to mitigate against extinction, but their specialised diet is challenging. So, what does the future hold for marine iguanas? The biggest challenge is the distribution of the species. The population is scattered across the different islands of the Galapagos as such, there are at least 11 subspecies. This brings more complications to marine iguana conservation. As these subspecies specialise, it becomes less likely they will breed, thus more difficult to maintain the species population. Introducing education and awareness programmes will better equip us to the dangers faced by marine iguanas and could be a tourism idea for the Galapagos. This species is one of a kind, which is why it is so important for them to be protected.There should be a monitoring scheme, as suggested by MacLeod and Steinfartz, 2016 ( Figure 2 ), but the location of these subspecies makes it difficult to monitor them. However, there was a recent study using drone-based methods which showed promising results ( Figure 3 ). The overarching question remains: do we continue to conserve the current population in the Galapagos, or should we relocate the species to a less endangered habitat? Written by Antonio Rodrigues Related articles: Conservation of Galapagos Tortoises / 55 years of vicuna conservation Project Gallery