Rising temperatures can affect brain health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Brain-Climate Connection: The Hidden Impact of Rising Temperatures 08/03/26, 20:01 Last updated: Published: 24/05/23, 10:55 Rising temperatures can affect brain health Global warming is not only disrupting ecosystems, affecting the food we eat and the air we breathe, but it’s also impacting our neurological health. According to the Met Office and ECMWF, 2025 was confirmed as one of the top three warmest years on record globally - following 2024 and 2023- with temperatures ~1.41°C to 1.44°C above the 1850-1900 average. To understand this better, let’s start with the basics. The brain is made up of billions of tiny cells called neurons that communicate with each other by generating electrochemical signals. Think of neurons as small batteries capable of producing electricity when triggered by electrically charged chemicals, called ions. When a neuron is at rest, so when it’s not transmitting an electrical signal, it maintains a negative charge inside compared to the outside. This difference in charge is created by the selective movement of ions across the neuron’s membrane through ion channels and pumps. The resting membrane potential of a neuron is typically around -70 millivolts (mV). When a neuron needs to send information, it generates electrical activity called action potential , which causes the electrical charge to become less negative and closer to zero. To trigger a full-sized action potential, the electrical charge needs to reach a threshold of approximately -55 mV. If the charge reaches this threshold, a full-sized action potential is triggered and the neuron will send a signal down to other neurons. However, if the electrical charge does not reach this threshold, the neuron will not send a signal at all. This is known as the “ALL OR NONE” principle. The action potential is a crucial part of the neuron’s communication process, as it allows the neuron to send signals quickly and efficiently to other neurons. But here’s the catch: temperature fluctuations can affect the ion channels that generate and propagate action potentials, which are critical for the neuron’s communication process. It turns out that an increase in temperature can influence the generation , speed , and duration of action potentials. But that’s not all! Hotter temperatures can trigger seizures in individuals with epilepsy or a history of seizures. One of the most concerning findings from scientific research is that climate change, among other factors, may contribute to an increase in seizure severity and frequency, as well as the development of cerebrovascular and neurodegenerative diseases, such as strokes or dementia . Triggering stress and sleep deprivation, heat waves can also exacerbate the symptoms of such pre-existing disorders. The good news is that we can take action to address the direct impact of climate change on our planet and health. Joining initiatives like Climatematch Academy (CMA) , a 2-week interactive online summer school, can help you learn more about climate science and become part of a global community that is working towards a more sustainable future. CMA is an all-volunteer organization run by dozens of science enthusiasts. It aims at introducing computational methods for climate science taking advantage of available open-source tools and datasets to make science accessible to students worldwide. This is your chance to learn cutting-edge techniques from climate science experts and make a difference in the world, ensuring a brighter future for ourselves and future generations. Written by Viviana Greco Related articles: The environmental impact of EVs / Emperor penguins / Impacts of global warming on NTDs Project Gallery

Stockholm syndrome is a psychological phenomenon where a victim forms a connection with their captor, developing feelings of sympathy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Stockholm Syndrome - psychology’s ongoing debate Last updated: 07/07/26, 12:23 Published: 09/07/26, 08:00 Stockholm syndrome is a psychological phenomenon where a victim forms a connection with their captor, developing feelings of sympathy From bank robberies to Disney princesses, Stockholm syndrome has captured the public’s eye for decades. But how much of what we see online reflects psychological reality? Stockholm syndrome is a psychological phenomenon where a victim forms a connection with their captor, developing feelings of sympathy. This connection can lead to adopting the same beliefs of the captor or abuser, resulting in positive attitudes toward them. This phenomenon originated in 1973 after a bank robbery in Stockholm, Sweden. During a six-day standoff against the police, hostage bank employees became sympathetic towards the bank robbers. Once free, some employees declined to testify against the bank robbers and even raised money for their defence. This psychological response allows captors to manipulate their victims into complying with their demands, while victims use it as a survival mechanism. But why do some victims develop Stockholm syndrome and others don’t? Although there is no definitive answer, De Fabrique et al. (2007) and Namnyak et al. (2007) suggest that prolonged captivity may allow emotional bonds to develop and that the phenomenon is more likely when there is no prior relationship between the captor and victim. The most popular view among psychologists is that social and cognitive factors influence the development of Stockholm syndrome, including the “us vs. them” mentality and in-group and out-group perceptions. These perceptions, combined with a distorted cognitive schema, can lead to Stockholm syndrome. De Fabrique et al. (2007) examined existing case studies to investigate the “us vs. them” dynamic. Findings revealed that hostages and captors were in close physical proximity and maintained a high level of interpersonal contact. The researchers inferred that the concept of “us vs. them” may arise when victims and the captor are physically close during an emotionally salient situation. Considering the in-group and out-group dynamic, both the victim and the captor share a common interest in survival, forming the in-group. The captor perceives the authorities as a threat to their own survival, and because intervention by the authorities also endangers the victim's life, the victim comes to share this perception. As a result, the authorities are viewed as the out-group. Overall, this research suggests that social and cognitive processes, particularly in-group and out-group perceptions, play a significant role in the development of Stockholm syndrome. However, psychologists question whether Stockholm syndrome should be accepted as a legitimate psychological syndrome. Stockholm syndrome is not included in diagnostic manuals such as the DSM-5 or the ICD. A systematic review by Namnyak et al. (2008) discussed that scientific evidence supporting the syndrome is limited, with literature relying heavily on case studies and media reports rather than reputable empirical research. Despite this, Stockholm syndrome is quite influential in today’s world. Movies, television shows, and books portray captives forming romantic or emotional attachments to their captors. Disney’s Beauty and the Beast is a prime example of this debate, as some viewers argue that Belle’s building affection for the Beast reflects Stockholm syndrome. On the other hand, others – including the actress Emma Watson, who plays Belle – express that Belle maintains her autonomy and chooses to stay only after the Beast changes his behaviour. However, the influence of Stockholm syndrome extends beyond fictional narratives. Some psychologists argue that identifying a victim’s behaviour as “Stockholm syndrome” can oversimplify complex trauma responses and shift attention from the perpetrator’s abuse. Alternatively, researchers prefer concepts such as trauma bonding or coercive control, which are supported by psychological research and better capture the dynamics of abusive relationships. All in all, the debate surrounding Stockholm syndrome highlights the importance of distinguishing between psychological concepts supported by scientific evidence and those shaped by popular culture. The debate around Stockholm syndrome illustrates that psychological concepts are not always supported by empirical scientific evidence. Regardless of whether it’s considered a trauma response or an oversimplified media label, Stockholm syndrome demonstrates how human behaviour under severe stress can be complex. Ultimately, the concept highlights the complexity and unpredictability of human behaviour in extreme circumstances. Written by Shreya Dhaliwal REFERENCES Arsiwela, A. (2024). Stockholm syndrome as reflected on Belle in beauty and the beast movie (2017). Dinamika Pembelajaran : Jurnal Pendidikan Dan Bahasa, 1 (3), 329–337. https://doi.org/10.62383/dilan.v1i3.822 . Cleveland Clinic. (2022, February 14). S tockholm syndrome: What it is, symptoms & how to treat . https://my.clevelandclinic.org/health/diseases/22387-stockholm-syndrome . De Fabrique, N., Romano, S. J., Vecchi, G. M., & Van Hasselt, V. B. (2007b, July). Understanding Stockholm Syndrome . U.S. Department of Justice. https://www.ojp.gov/ncjrs/virtual-library/abstracts/understanding-stockholm-syndrome . Disney. (n.d.). Beauty and the Beast . https://movies.disney.com/beauty-and-the-beast . EBSCO. (2022). Stockholm Syndrome . https://www.ebsco.com/research-starters/social-sciences-and-humanities/stockholm-syndrome . Goldberg, H. (2017, February 17). Emma Watson Talks Stockholm Syndrome and Beauty and the Beast . SELF. https://www.self.com/story/emma-watson-stockholm-syndrome-beauty-and-the-beast . Henry. (2025, June 20). Stockholm syndrome . All the tropes. https://allthetropes.org/wiki/Stockholm_Syndrome . Johnson, H. N. (2021, April 25). Understanding Individuals with Stockholm Syndrome . Society for the Advancement of Psychotherapy. https://www.societyforpsychotherapy.org/understanding-individuals-with-stockholm-syndrome/ . Mind help. (n.d.). Stockholm syndrome . https://mind.help/topic/what-is-stockholm-syndrome/ . Namnyak, M., Tufton, N., Szekely, R., Toal, M., Worboys, S., & Sampson, E. L. (2007). ‘Stockholm syndrome’: Psychiatric diagnosis or urban myth? Acta Psychiatrica Scandinavica, 117 (1), 4–11. https://doi.org/10.1111/j.1600-0447.2007.01112.x . Project Gallery

Food deserts Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How rising food prices contribute to malnutrition 05/06/26, 21:28 Last updated: Published: 18/08/23, 21:13 Food deserts Introduction Over the past year, there have been news articles explaining how food has become more expensive along with people choosing between heating their homes and paying for groceries. (According to the Office for National Statistics (ONS), the annual inflation rate for food and non-alcoholic beverages fell to 3.6% in the 12 months to January 2026, down from 4.5% in December 2025). There are various reasons for the food price increase; some of them include Brexit, lack of agricultural productivity and weakening of the British pound. Therefore, the spending habits of the general population have shifted towards ultra-processed foods (UPFs) as they tend to be cheaper compared to minimally processed food (MPFs). Yet, UPFs are really unhealthy with a cohort study discovering that there was an increase in mortality by 18% with each additional serving. For people living in food swamps and deserts, this is a harsh reality for them and there have to be policies to properly address this. The difference between food deserts and swamps Food deserts are places where populations have limited access to healthy and affordable food (i.e. MPFs); there are factors that contribute to this phenomenon such as having lower income or geographic location whereby there is a long distance to the nearest market. However, the increase in food prices as illustrated above can even be a part of the problem. In contrast, there are food swamps, which are areas containing more businesses that sell foods lacking nutritional value, so UPFs as opposed to MPFs. This also relates to the cost of groceries because certain populations living in food swamps are likely to purchase UPFs because they are in closer proximity than MPFs, besides being cheaper. Both situations can contribute not only to obesity, but other forms of malnutrition which will be explored below. Malnutrition To suffer from malnutrition means that there is an imbalance of nutrients and can be categorised based on undernutrition or overnutrition along with disparity in macronutrients (carbohydrates, fats and proteins) and micronutrients (vitamins and minerals). Additionally, there are countries experiencing specific forms of malnutrition such as undernutrition in comparison to others due to ongoing warfare, lack of nutritional education and/or living in poverty. The impact of malnutrition on organs in Figure 1 happens because there is deficiency in certain macronutrients and/or micronutrients, which are essential in the structure and functioning of the body. Another consequence of malnutrition is weight loss because there is depletion of fat and muscle mass in the body, leading to impaired muscle function. Food deserts/ swamps and malnutrition Going back to food deserts/swamps, their impact on malnutrition can be drastic. For example, a review focusing on food insecurity (disrupted food intake/eating patterns due to low income or supplementary resources), suggested a link between malnutrition and food insecurity along with a possible association between malnutrition and gut microbiome being negatively altered, though more research is needed. Another review looking at food insecurity in both US adults and children discovered that in a food-insecure adult’s diet, they had less vegetables, fruits and dairy leading to reduced vitamins A and B6, calcium, magnesium and zinc. How do both reviews relate to food swamps/deserts? Well, populations who are food-insecure may be likely to live in areas where there is a lack of access to healthy foods (i.e. food swamps/ deserts). Conclusion Taking into account everything discussed in this article, it seems that governments in countries where food swamps/deserts are prevalent need to address this issue through effective policies. Otherwise, there could be a future where there is an increase in chronic diseases like malnutrition. There is even potential susceptibility to infectious diseases due to malfunctioning organs stemming from malnutrition. Written by Sam Jarada Related articles: Food at the molecular level / Famine-induced epigenetic changes / Junk food advertising Project Gallery

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