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Also known as Major Depressive Disorder (MDD) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What does depression do to your brain? 14/07/25, 15:12 Last updated: Published: 10/10/24, 11:19 Also known as Major Depressive Disorder (MDD) This is Article 1 in a series on psychiatric disorders and the brain. Next article: Inside out: the chemistry of depression. -- I affect 3.8% of the population wide, With 280 million voices struggling inside. In women, my reach is 6%, And 5.7% of those over 60 feel me. Among new mothers, I reach 10%, With over 700,000 lost to my torment each year. What am I? Depression. The most prevalent psychiatric disorder that costs both money and lives. -- Also known as Major Depressive Disorder (MDD), depression is a heterogenous disease, which means the manifestation of the disorder is influenced by multiple genes. It is commonly known that consistent low mood, loss of interest in hobbies you used to enjoy, lethargy, feeling of hopelessness etc. are physical symptoms of depression. However, have you ever wondered what happens in the brain in a depression sufferer, from the neuroscience aspect? Structurally, research into the neuroscience of depression reveals significant structural abnormalities in the brains of affected individuals. Studies using structural magnetic resonance imaging (MRI) have shown that those with MDD show reductions in gray matter volume in regions responsible for emotion regulation. The limbic system of the brain is responsible for producing and regulating emotions. In depressed individuals, the hippocampus—a key component of the limbic system—shows reduced gray matter volume, which is linked to abnormalities in the associated white matter tracts. White matter consists of myelinated axons that facilitate communication between different brain regions, while grey matter contains the neuronal cell bodies responsible for processing information. The presence of abnormalities in white matter suggests a disconnection between regions within the limbic system, potentially impairing their ability to communicate effectively. This disconnection may contribute to the emotional dysregulation observed in depression, highlighting the intricate relationship between grey and white matter in the pathology of this disorder. Depression is a complex disorder that not only affects mood but changes the structure and function of the brain. By understanding the neurobiological changes—including reductions in grey matter and white matter disconnections—we can better grasp the pathogenesis of this condition. Continued research in the neuroscience behind depression is essential for developing more effective treatments. There is still much more to explore and understand in depression research; with each new discovery, we realise how much more there is to learn. Written by Chloe Kam Related article: Depression in children Project Gallery

Tiny solutions for big health problems Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nanomedicine 17/07/25, 10:52 Last updated: Published: 17/01/24, 00:07 Tiny solutions for big health problems As the landscape of the healthcare field expands, new advances are coming forth, and one such area of interest is nanomedicine. Existing on a miniature scale called nanometres, nanomedicine and technology provide a revolutionary solution to many modern-day problems faced by the scientific community. Through this article, we’ll aim to explore what exactly nanomedicine is, its importance, its use in medicine, as well as its limitations and future prospects. The nanoscale When mentioning nanomedicine or nanotechnology, we refer to materials and particles existing on the nanoscale. This lies between 1-100 nanometres. For reference, human hair is 80,000-100,000 nanometres wide, so comparatively, the technology is much smaller. Although the technology may seem small, its impact is far too significant to be discredited. Due to their smaller size, the nanoparticles hold several advantages, making them useful in biomedicine, these include providing greater surface area for molecular interactions in the body, and they are much easier to manipulate, allowing for greater control and precision in terms of diagnostics and medicine delivery (Figure 1). Cancer drug delivery systems Nanotechnology in the field of medicine is being widely used and tested with regards to its application as a drug delivery system. More recently, it’s being investigated for its increased precision in delivering anti-cancer drugs to patients. Nanotechnology enables precise drug delivery through the construction of nanoscale infrastructures called nanoparticles. These can be filled with anti-cancer drug treatments, and their outer structure can be further designed to include elements which target folate receptors, such as folic acid (B9 vitamin), thus increasing their affinity for specific receptors in the body. Folate receptors tend to be overexpressed on the surface of many cancers, including pancreas, breast, and lung. So, by increasing selectivity and targeting only the cells which overexpress these receptors, the nanoparticles can deliver chemotherapy drugs with increased precision. This increased accuracy results in decreased cellular toxicity to surrounding non-cancerous tissues whilst also reducing side effects. In current experiments, lipid nanoparticles loaded with the anti-cancer drug edelfosine were tested on mice with mantle cell cancer. Lipid nanoparticles offer several advantages as a drug delivery system, including biocompatibility, greater physical stability, increased tolerability, and controlled release of the encapsulated drug. Lipid nanoparticles are also advantageous for their ability to be size specific to a tumour. In the study, in vivo experimentation using mice that contained mantle cell lymphoma was used, and they were administered 30mg/kg of the encapsulated drug. After administering the edelfosine loaded nanoparticles every 4 days, it was found that the process of metastasis had been removed; this means that cancer cells could not spread to other parts of the body. Additionally, it was also found that because of the way the nanoparticles were absorbed into the lymphatic system, they could accumulate in the thoracic duct providing precise and slow release of the drug over time, thus preventing metastasis (Figure 2). Imaging and diagnostics Another area of use for nanotechnology includes imaging and diagnostics. This area of expertise is regarded as theranostics, which involves using nanoparticles as detectors to help locate the area of the body affected by a disease, such as the location of a tumour, and aid in diagnosing illnesses. With regards to diagnostics, nanoparticles can also help identify what stage of the disease is being observed as well as enable us to garner more information to form a concrete treatment programme for the patient, thus providing a personalised touch to their care. Nanomaterials can be used to engineer different types of nanoparticles, which can enhance contrast on CT and MRI scans so that diseases can be detected more easily by being more visible when compared to traditional scans. In collaboration with Belcher et al., Bardhan worked to collectively develop different formulations of polymers that would be most effective in imagining and detecting cancers earlier. In the figure below, a nanoparticle made of a core shell was used for imaging. It comprises a yellow polymer with a red fluorescent dye to increase imagining contrast of the area and a blue lanthanide nanoparticle. When the lanthanide particles are excited by a light source, fluorescence in the near infrared range (NIR-II) is emitted, allowing for clear contrast and imaging. This can be seen in the figure below. From the colours involved, the tumour being imaged could be investigated more thoroughly in how it was distributed and learn more about its microenvironment in a mouse affected by ovarian cancer (Figure 3). Nanobots In recent times, new investment in the form of nanorobots has been made apparent. Nanorobots are nanoelectromechanical systems whose size is very similar to human organelles and cells, so there are a variety of ways they could be helpful in healthcare, such as in the field of surgery. Traditionally, surgical tools can be limited to work on a small scale. However, with nanorobots, it can be possible to access areas unreachable to surgical tools and catheters whilst also reducing recovery time and infection risk, as well as granting greater control and accuracy over the surgery. In a study conducted by Chen et al. (2020), the researchers manipulated magnetotactic bacterial microrobots to kill a bacteria known as Staphylococcus aureus enabled by magnetic fields to target them. Using a microfluidic chip, the microrobots were guided to the target site and then were programmed to attach themselves to the bacteria. Once connected, the viability of the bacteria was reduced due to the swinging magnetic fields generated by the device. Although this research is promising, further research must be conducted to understand the compatibility of these nanotechnologies with the human body and any implications they may have in side effects (Figure 4). Challenges and safety concerns From the evidence explored above, it is evident that nanotechnology holds much promise in the field of healthcare. However, they are not without their challenges and resignations when introducing their use to human bodies. The human body is incredibly complex, and therefore the complete biocompatibility of nanoparticles, particularly nanobots, is currently under-researched and under reviewed. To extensively use them, it is vital first to understand how safe they are and their efficacy in treatment and diagnosis. Below is a summary of some of the advantages and disadvantages of these nanotechnologies (Figure 5). The future of nanotechnology in biomedicine In conclusion, nanotechnology indicates an extensive and optimistic field at the forefront of changing medical care from diagnosis to treatment. It has the potential to answer many pressing questions in healthcare including decreasing cytotoxicity via a precise drug delivery system, increased accuracy in diagnosis, and possibly becoming a novel tool in surgery. Although it is imperative for there to be new and evolved techniques to increase the quality of care for patients, it is vital not to rush and to be thorough in our approach. This involves undergoing further research, including conducting clinical trials when investigating the use of nanotechnology inside the human body; this will test for tissue compatibility, side effects, efficacy, and even dosage when using nanoparticles for drug delivery. In summary, the transformative role of nanomedicine is undeniable. It offers a path to a more personalised and precise healthcare system, allowing researchers to reshape treatment, diagnosis, and patient well-being, though its limitations are yet to be overcome. Written by Irha Khalid Related articles: Nanoparticles: the future of diabetes treatment? / Semi-conductor manufacturing / Room-temperature superconductor / Silicon hydrogel lenses / Nanoparticles and plant disease / Nanogels / Nanocarriers Project Gallery

Immunosenescence and related therapies Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Ageing and its association with immune decline Last updated: 24/02/25, 11:28 Published: 20/02/25, 08:00 Immunosenescence and related therapies Introduction Ageing is a profoundly complex and integral part of human life. As pharmaceutical developments have occurred, introducing new medicines and therapies such as biologics and antibiotics within the last 100 years, research has begun to look at malignancy at a more macro scale. To be clear, while it has become easier to combat infectious diseases in recent times, the combating of diseases tied to our genetic composition is far more complicated, whether it be autoimmune diseases or onset conditions such as cases of dementia. Ageing is one such case of a process that is hard to combat because the mechanisms that cause it are diverse and currently not fully understood. Strides have been made under a concept known as senescence, which continues to enlighten researchers and the anti-ageing pharmaceutical industry. This article provides a short summary of what immunosenescence is and how we can utilise our understanding to develop therapies for human immunity. What is immunosenescence? Immunosenescence is the change from a healthy, active immune cell phenotype to one that is no longer conventionally active and begins to secrete inflammatory chemical messengers known as the senescence-associated secretory phenotype (SASP) ( Figure 1 ). A most important aspect of senescence is that a cell undergoes cell cycle arrest, meaning it cannot proliferate. You may now question why cells are programmed to senesce if the outcomes are detrimental to the host? It prevents the continued proliferation of old or damaged cells, including cells with uncontrolled proliferation (such as cancer cells). If we stop senescence altogether, we run the risk of accumulating damaged and/or mutated cells, increasing the chances of disease progression, such as through fibrosis and tumorigenesis, so specific targeting and dosage of drug interventions have to be considered. The immune system in particular, displays biological changes that are indicative of senescent progression. These include thymic involution (shrinking of the thymus associated with a decrease in T cell production), inflammaging (chronic inflammation associated with SASP), an increase in mitochondrial stress through metabolic changes, and an increase in differentiated memory T cells (EMRA T cells). Knowledge of these changes can give insight into potential mechanisms to target for therapeutics. Current and developing therapies for immunosenescence Given our expanding understanding of senescence, as of the time of writing, there are no clinically approved drugs for senescence specifically. The development of therapies for diseases such as cancer, heart disease and diabetes (diabetic patients tend to exhibit increased levels of cellular senescence owing to “accelerated ageing”) have been implicated with suppressing senescence. These drugs would be mTOR inhibitors such as Rapamycin, statins, P13K inhibitors, as well as immune checkpoint inhibitors for T cells, such as anti CTLA-4 PD-L1 and PD-L2, and the anti-diabetic metformin, which have all shown in vitro to be effective against high levels of senescent cells. There was also the development of the recent first senolytic drugs dasatinib and quercetin in 2015 that kill senescent cells selectively against non-senescent cells and stand to provide a proof of concept for targeting disease through senescent mechanisms. Conclusion The field of senescence is certainly one to keep an eye on, with a bibliometric analysis in 2023 showing an increase every year in the number of published papers ( Figure 2 ). It may be sooner rather than later that we see this become a trending topic of discussion for treating an array of disease states. Continuous research into specific immune cell subtypes (B, T and NK cells) and their relation to a decline in immunity in response to age can tell us more about potential therapeutic pathways or lifestyle choices that can improve the health of the immunocompromised elderly. One such example of this is Treg-mediated increased glucose consumption in the tumour microenvironment leading to an increase in cell senescence in effector T cells, suggesting that high sugar diets can accelerate tumorigenesis. Our understanding of ageing through senescence will help reduce the mortality rates of elderly groups in decades to come through knowing that mechanisms such as the SASP and altered immune cell function, which can promote disease states. Written by Yaseen Ahmad Related articles: Genetics of ageing and longevity / Accelerated ageing REFERENCES Henson, S.M. and Aksentijevic, D. (2021) ‘Senescence and type 2 diabetic cardiomyopathy: How young can you die of old age?’, Frontiers in Pharmacology , 12. doi:10.3389/fphar.2021.716517. Wang, R. et al. (2017) ‘Rapamycin inhibits the secretory phenotype of senescent cells by a NRF2-independent mechanism’, Aging Cell , 16(3), pp. 564–574. doi:10.1111/acel.12587. Henson, S.M. et al. (2012) ‘Reversal of functional defects in highly differentiated young and old CD8 T cells by PDL blockade’, Immunology , 135(4), pp. 355–363. doi:10.1111/j.1365-2567.2011.03550.x. Islam, M.T. et al. (2023) ‘Senolytic drugs, dasatinib and quercetin, attenuate adipose tissue inflammation, and ameliorate metabolic function in old age’, Aging Cell , 22(2). doi:10.1111/acel.13767. Li, C., Liu, Z. and Shi, R. (2023) ‘A comprehensive overview of cellular senescence from 1990 to 2021: A machine learning-based bibliometric analysis’, Frontiers in Medicine , 10. doi:10.3389/fmed.2023.1072359. Herranz, N. and Gil, J. (2018) ‘Mechanisms and functions of cellular senescence’, Journal of Clinical Investigation , 128(4), pp. 1238–1246. doi:10.1172/jci95148. Li, L. et al. (2019) ‘TLR8-mediated metabolic control of human Treg function: A mechanistic target for cancer immunotherapy’, Cell Metabolism , 29(1). doi:10.1016/j.cmet.2018.09.020. Project Gallery

The role of CRISPR-Cas9 technology Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Reaching new horizons in Alzheimer's research 10/07/25, 10:34 Last updated: Published: 12/10/23, 10:50 The role of CRISPR-Cas9 technology The complexity of Alzheimer’s Alzheimer's disease (AD) is a formidable foe, marked by its relentless progression and the absence of a definitive cure. As the leading cause of dementia, its prevalence is expected to triple by 2050. Traditional therapies mainly focus on managing symptoms; however, advances in genetics research, specifically CRISPR-Cas9 gene-editing technology, offer newfound hope for understanding and treating this debilitating condition. The disease is characterized by progressive deterioration of cognitive function, with memory loss being its hallmark symptom. Primarily affecting individuals aged 65 and over, age is the most significant risk factor. Although this precise cause remains elusive, scientists believe that a combination of genetic, lifestyle and environmental factors contributes to its development. CRISPR’s role in Alzheimer’s research After the discovery of using CRISPR-Cas9 for gene editing, this technology is receiving interest for its potential ability to manipulate genes contributing to Alzheimer’s. Researchers from the University of Tokyo used a screening technique involving CRISPR-Cas9 to identify calcium, proteins, and integrin-binding protein 1, which is involved in the formation of AD. Furthermore, Canadian researchers have edited genes in brain cells to prevent Alzheimer’s using CRISPR. The team identified a genetic variant called A673T, found to decrease Alzheimer’s likelihood by a factor of four and reduce Alzheimer’s biomarker beta-amyloid (Aβ). Using CRISPR in petri dish studies, they managed to activate this A673T variant in lab-grown brain cells. However, the reliability and validity of this finding are yet to be confirmed by replication in animal studies. One final example of CRISPR application is targeting the amyloid precursor protein (APP) gene. The Swedish mutation in the APP gene is associated with dominantly inherited AD. Scientists were able to specifically target and disrupt the mutant allele of this gene using CRISPR, which decreased pathogenic Aβ peptide. Degenerating neurons are surrounded by Aβ fibrils, the production of Αβ in the brain initiates a series of events which cause the clinical syndrome of dementia. The results of this study were replicated both ex vivo and in vivo and demonstrated this could be a potential treatment strategy in the future. The road ahead While CRISPR technology’s potential in Alzheimer’s research is promising, its therapeutic application is still in its Infancy. Nevertheless, with the aid of cutting-edge tools like CRISPR, deepening our understanding of AD, we are on the cusp of breakthroughs that could transform the landscape of Alzheimer’s disease treatment. Written by Maya El Toukhy Related articles: Alzheimer's disease (an overview) / Hallmarks of Alzheimer's / Sleep and memory loss Project Gallery

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

Aggression has the confluence of individual predisposition and maintenance via social context Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unmasking aggression: a result of personal or social triggers? 14/07/25, 15:10 Last updated: Published: 01/01/25, 14:02 Aggression has the confluence of individual predisposition and maintenance via social context Introduction Anderson & Bushman (2002) define aggression as behaviour aimed at causing harm to another individual. Aggression can be measured by observing a signal of intention or aggression rating by self or others. The social theories of aggression include Dollard's frustration-aggression theory and Bandura's Social Learning Theory, while the individual factors theories account for personality traits and the influence of alcohol. However, there is no definite answer to whether social or individual factors are most important in explaining human behaviour. The interaction between social and individual factors will be explored to gain a deeper understanding of aggression. Social theories The frustration-aggression hypothesis proposed by Dollard et al. (1939) defines frustration as the emotion that follows when the occurrence of an instigated goal-response is interfered with, in turn leading to anger and aggression. According to this hypothesis, a person’s aggressive tendencies will be more intense the closer the individual is to achieving a goal before an obstacle appears. Many support this hypothesis, including Dill and Anderson (1995), who found that levels of aggression resulting from unjustified frustration were higher than justified frustration because they were caused by situational constraints rather than dispositional qualities. However, Berkowitz (1989) criticises Dollard et al.'s hypothesis, saying that frustration can only produce aggressive behaviour if it causes adverse effects. Due to the wide variety of negative and positive effects of frustration, it is important to revisit and clarify the frustration-aggression hypothesis. Additionally, aggression is often explained by the Social Learning Theory (SLT), proposed by Bandura et al. (1963), which states that aggressive behaviour is a learned behaviour reinforced by imitation and rewards or punishment. Bandura conducted the renowned Bobo Doll Study in 1961, in which children mimicked adult behaviour and attacked the doll after watching the researchers physically and verbally abuse a clown-faced inflatable toy in front of them, making this study extremely influential in understanding the role that families and household dynamics play in human behaviour. Based on this theory, exposure to TV violence can teach aggressive conduct and provide a model of behaviour to base actions upon. In SLT, rather than frustration generating an aggressive drive that can only be reduced by injurious behaviour, aversive stimulation creates general emotional arousal that can result in aggressive behaviour. Therefore, social theories encompass a broad range of disinhibitory factors and provide a broad theory explaining both impulsive and principled aggressive conduct. Individual factors theories Individual differences and variables, like personality traits, have also contributed to the study of aggressive behaviour. Hyatt et al. (2019) stated that certain personality traits such as narcissism and sadism have been meta-analytically linked to aggression shown in a lab setting. The lab paradigm captures aggression as it manifests whilst controlling for confounding variables, such as different types of aggression. However, the lab paradigm lacks construct validity because researchers don’t interpret the subjects’ intentions and motives when operationalising aggression. Further evaluation comes from Bettencourt et al. (2006), who meta-analysed personality dimensions and stated that provocation can cause aggression. They note that individuals with Type A personalities often exhibit impulsivity and emotional reactivity, which are positively associated with aggression. Thus, situational circumstances such as provocation and aggressive cues interact with these personality factors, together shaping the likelihood and intensity of aggressive behaviour. Additionally, the interplay between personality and alcohol can explain aggression. Alcohol reduces inhibitions that regulate 'normal' behaviour and increases aggression. Miller et al. (2009) concluded that alcohol may facilitate aggression in high-trait individuals specifically, those who score high on traits associated with aggression, such as impulsivity, hostility, or a predisposition toward anger—by impairing the drinker’s inhibition. Moreover, further research indicates a strong relationship between alcohol consumption and antisocial personality. Therefore, any discussion of personal factors and personality in aggression would be incomplete without considering the influence of alcohol. The interplay between social and individual trait theories Allen et al. (2018) created a model that encompasses both the social and the individual trait theories. The General Aggression Model (GAM) considers social, biological, and individual factors in aggression. This model consists of three stages: input, appraisal, and action. The input stage determines the likelihood of personal and situational factors causing aggression. For instance, individual differences, such as personality, social rejection, and provocation, are identified as risk factors for aggression. During the appraisal stage, the individual decides how to respond. Their response can be aggressive or non-aggressive, depending on the resources, time, and event. The action then influences the social encounter, which can alter personal and situational factors, leading to those factors restarting the cycle. Hence, this model proposes that individuals learn situations that lead to aggressive outcomes. To reduce aggression and offer treatment, the GAM has been applied to intergroup violence and therefore can be applied to a wide range of situations in real life. Conclusion In conclusion, aggression has the confluence of individual predisposition and maintenance via social context. For instance, as discussed previously, socialisation experiences may contribute to aggressive behaviour in individuals with certain personality traits. Thus, it is difficult to distinguish social and individual factors when explaining aggression, as most human behaviour is a multifaceted phenomenon with multiple determinants. Therefore, future research should be more holistic in the explanations of aggression, encompassing both social and individual factors. Written by Pranavi Rastogi Related articles: Emotional chemistry / Psychology of embarrassment / Brain of a bully REFERENCES Allen, J. J., Anderson, C. A., & Bushman, B. J. (2018). The general aggression model. Current Opinion in Psychology,19 , 75-80. doi:10.1016/j.copsyc.2017.03.034 Anderson, C. A., & Bushman, B. J. (2002). Human aggression. Annual Review of Psychology, 53 (1), 27-51. doi:10.1146/annurev.psych.53.100901.135231 Bandura, A., Ross, D., & Ross, S. A. (1963). Imitation of film-mediated aggressive models. Journal of Abnormal and Social Psychology, 66, 3-11 Berkowitz, L. (1989). Frustration-aggression hypothesis: Examination and reformulation. Psychological Bulletin, 106 (1), 59-73. doi:10.1037/0033-2909.106.1.59 Bettencourt, B.A. et al. (2006) ‘Personality and aggressive behavior under provoking and neutral conditions: A meta-analytic review.’, Psychological Bulletin , 132(5), pp. 751–777. doi:10.1037/0033-2909.132.5.751. Dill, J. C., & Anderson, C. A. (1995). Effects of frustration justification on hostile aggression. Aggressive Behavior, 21 (5), 359-369. doi:10.1002/1098-2337(1995)21:5<359::aid-ab2480210505> 3.0.co ;2-6 Dollard, J., Miller, N. E., Doob, L. W., Mowrer, O. H., & Sears, R. R. (1939). Frustration and aggression. doi:10.1037/10022-000 Hyatt, C. S., Chester, D. S., Zeichner, A., & Miller, J. D. (2019). Analytic flexibility in laboratory aggression paradigms: Relations with personality traits vary (slightly) by operationalization of Aggression. Aggressive Behavior, 45 (4), 377-388. doi:10.1002/ab.21830 Miller, C.A., Parrott, D.J. and Giancola, P.R. (2009) ‘Agreeableness and -related aggression: The mediating effect of trait aggressivity.’, Experimental and Clinical Psychopharmacology , 17(6), pp. 445–455. doi:10.1037/a0017727. Project Gallery

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

Establishing causation through Randomised Controlled Trials and Instrumental Variables Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Proving causation: causality vs correlation Last updated: 03/06/25, 13:43 Published: 12/06/25, 07:00 Establishing causation through Randomised Controlled Trials and Instrumental Variables Does going to the hospital lead to an improvement in health? At first glance, one might assume that visiting a hospital should improve health outcomes. However, if we compare the average health status of those who go to the hospital with those who do not, we might find that hospital visitors tend to have worse health overall. This apparent contradiction arises due to confounding – people typically visit hospitals due to existing health issues. Simply comparing these two groups does not tell us whether hospitals improve health or if the underlying health conditions of patients drive the observed differences. A similar challenge arises when examining the relationship between police presence and crime rates. Suppose we compare two cities—one with a large police force and another with a smaller police force. If the city with more police also has higher crime rates, does this mean that police cause crime? Clearly not. Instead, it is more likely that higher crime rates lead to an increased police presence. This example illustrates why distinguishing causation from correlation is crucial in data analysis, and that stating that two variables are correlated does not imply causation. First, let’s clarify the distinction between causation and correlation. Correlation refers to a relationship between two variables, but it does not imply that one causes the other. Just because two events occur together does not mean that one directly influences the other. To establish causation, we need methods that separate the true effect of an intervention from other influencing factors. Statisticians, medical researchers and economists have ingeniously come up with several techniques that allow us to separate correlation and causation. In medicine, the gold standard for researchers is the use of Randomised Controlled Trials (RCTs). Imagine a group of 100 people, each with a set of characteristics, such as gender, age, political views, health status, university degree, etc. RCTs randomly assign each individual to one of two groups. Consequently, each group of 50 individuals should, on average, have similar ages, gender distribution, and baseline health. Researchers then examine both groups simultaneously while changing only one factor. This could involve instructing one group to take a specific medicine or asking individuals to drink an additional cup of coffee each morning. This results in two statistically similar groups differing in only one key aspect. Therefore, if the characteristics of one group change while those of the other do not, we can reasonably conclude that the change caused the difference between the groups. This is great for examining the effectiveness of medicine, especially when you give one group a placebo, but how would we research the causation behind the police rate and crime example? Surely it would be unwise and perhaps unethical to randomise how many police officers are present in each city? And because not all cities are the same, the conditions for RCTs would not hold. Instead, we use more complex techniques like Instrumental Variables (IV) to overcome those limitations. A famous experiment using IV to explain police levels and crime was published by Steven Levitt (1997). Levitt used the timings of mayoral and gubernatorial elections (the election of a governor) as an instrument for changes in police hiring. Around election time, mayors and governors have incentives to look “tough on crime.” This can lead to politically motivated increases in police hiring before an election. Crucially, hiring is not caused by current crime rates but by the electoral calendar. So, by using the timing of elections to predict an increase in police, we can use those values to estimate the effect on crime. What he found was that more police officers reduce violent and property crime, with a 10% increase in police officers reducing violent crime by roughly 5%. Levitt’s paper is a clever application of IV to get around the endogeneity problem and takes correlation one step further into causation, through the use of exogenous election timing. However, these methods are not without limitations. IV analysis, for instance, hinges on finding a valid instrument—something that affects the independent variable (e.g., police numbers) but has no direct effect on the outcome (e.g., crime) other than through that variable. Finding such instruments can be extremely challenging, and weak or invalid instruments can lead to biased or misleading results. Despite these challenges, careful causal inference allows researchers to better understand the true drivers behind complicated relationships. In a world where influencers, media outlets, and even professionals often mistake correlation for causation, developing a critical understanding of these concepts is an essential skill required to navigate through the data, as well as help drive impactful change in society through exploring the true relationships behind different phenomena. Written by George Chant Related article: Correlation between HDI and mortality rate REFERENCE Steven D. Levitt (1997). “Using Electoral Cycles in Police Hiring to Estimate the Effect of Police on Crime”. American Economic Review 87.3, pp. 270–290 Project Gallery

The web of geopolitics surrounding the Rohingyas, and how this impacts their health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Addressing the health landscape of Bangladesh’s Rohingya community Last updated: 16/10/25, 10:19 Published: 18/09/25, 07:00 The web of geopolitics surrounding the Rohingyas, and how this impacts their health This is article no. 6 in a series about global health injustices. Previous article: Health gaps in conflict-affected Kashmir. Next article: A deep, critical reflection . Introduction Welcome to the sixth article of the Global Health Injustices Series, a collaboration with Nasif Mahmood . This article focuses on the ongoing injustices and health issues affecting the Rohingya refugees in Bangladesh. This community leads a vulnerable life and suffering that it is becoming one of the most significant South Asian crises in the 21st century. Due to Bangladesh's inadequate resources and geopolitical situation, the overall health and well-being of the country and the migratory population are severely hampered. A brief history of Bangladesh and the Rohingya population Bangladesh's history is intricate and has been influenced by many cultures. After India was divided in 1947, the area, previously part of ancient Bengal, was ruled by the British and became East Pakistan. Demands for autonomy resulted from tensions between West and East Pakistan. The Bangladesh Liberation War in 1971, culminating in these tensions, led to the country's independence. Bangladesh has made great strides in education, health, and economic growth since gaining its autonomy, despite facing economic hardship, political turmoil, and natural disasters. Rohingya, the Muslim ethnic minority from the state of Rakhine, were denied citizenship by the Myanmar Government, leaving them homeless. They endured years of persecution, discrimination, and violence. In 2017, an inhuman, violent crackdown by the military of the Myanmar government forced over 70,000 Rohingya to flee to Bangladesh. Over 1 million refugees live in Bangladesh, primarily in the Cox Bazar area. A lot of refugees cause overcrowding situations, and limited resources lead to a high rate of nutritional problems and spread of disease, specifically infectious diseases and mental health disorders in the refugee camp. Connecting geopolitics and health: impacts on the Rohingya population The Rohingya crisis is more than just a humanitarian issue; it is a tangled web of geopolitical challenges. The Myanmar government’s ongoing refusal to grant citizenship and fundamental rights to the Rohingya people not only deepens their suffering but also fuels instability in the region. They have not taken the necessary steps to ensure their safety, leaving the crisis unresolved. As refugees continue to pour into neighbouring countries, tensions have escalated, placing a heavy burden on host nations like Bangladesh. This crisis worsens existing socio-economic problems and stretches resources thin in areas struggling to care for their citizens. The international community has responded in various ways; some countries are pushing for tougher sanctions against Myanmar, while others are focused on delivering aid to those affected. However, the underlying issues driving this crisis will unlikely be resolved without a coordinated and sustained political effort ( Table 1, Figure 1 ). Addressing them can lead to improved outcomes for the Rohinyga population. On top of that, the health challenges faced by the Rohingya people go beyond just infectious diseases. The lack of access to essential health services has not only worsened physical health problems but has also led to a growing mental health crisis. Many Rohingya individuals are grappling with post-traumatic stress disorder (PTSD), anxiety, and depression stemming from their traumatic experiences of violence, loss, trauma, isolation, and forced displacement. Yet, mental health services in the refugee camps are severely lacking. A study showed that the prevalence of emotional and behavioural disorders is high among forcefully migrated refugee children, because of traumatic exposure like the unexpected death of parents, forceful displacement, and the witnessing of family violence and abuse. The stigma surrounding mental health in many cultures, including in the Rohingya community, creates additional hurdles for those seeking help. Enhancing access to mental health support is crucial, not just for the immediate well-being of the refugees, but also for their long-term healing and successful integration into the societies that host them. Moreover, providing humanitarian aid and hosting such a large population in Bangladesh is becoming difficult. The national and international NGOs maintain healthcare for the Rohingya population. However, the funding shortage and inadequate infrastructure hinder the provision of adequate medical services. For this reason, the refugee camps have reported significant outbreaks of diphtheria, cholera, and COVID-19. Given the challenges, developing innovative solutions and working collaboratively on a global or regional scale is needed. By empowering local health workers and training them to offer basic healthcare and mental health support, to close the service delivery gaps. Additionally, building partnerships among NGOs, governments, and international organisations can help ensure that resources are allocated more effectively and that comprehensive health programs are created to meet the unique needs of the Rohingya population. It's crucial to engage the community; by listening to the voices and experiences of the Rohingya, we can develop interventions that truly respect their dignity and cultural context. Additionally, raising global awareness about the struggles faced by the Rohingya can lead to stronger advocacy efforts. Involving the media, educational institutions, and civil society can foster a deeper understanding of the interconnected issues of geopolitics and health. Initiatives that share personal stories and experiences can rally public support and drive meaningful change. Ultimately, tackling the Rohingya crisis calls for a multifaceted approach that blends immediate humanitarian aid with long-term strategies aimed at ending their statelessness and ensuring their rights as human beings are upheld and protected. Recommendations from NGOs National NGOs: Several national NGOs play an essential role in supporting the healthcare needs of the Rohingya population: Bangladesh Rural Advancement Committee (BRAC), one of the world's largest NGOs, provides comprehensive health care services, including maternal and child health, immunisation programmes, disease prevention initiatives, and arranges many health campaigns for refugees. Gonoshasthaya Kendra established a field hospital and free clinic in the Cox Bazar area near the refugee camp, focusing on primary health care and emergency medical support. International NGOs MedGlobal, an international NGO, responds to this global crisis by delivering medical assistance within the refugee camp. Support hospitals and clinics for affected refugees between 2017 and 2019. This organisation's volunteers contributed over 17,000 hours of aid, assisting more than 80,000 individuals. Medair is another international NGO offering health and nutritional support to the Rohingya refugees. Migrant Offshore Aid focuses on sea rescue operations and delivering medical aid and assistance to surfers. Together, these national and international organisations make meaningful contributions to the healthcare needs of the Rohingya population, handling both immediate medical concerns and long-term health support in a challenging environment. Their collaborative efforts help ensure that essential services reach those in critical need, facilitating better health outcomes for refugees. Although they address the healthcare needs of the Rohingya, several challenges can limit their effectiveness. For example, coordination issues may lead to overlapping efforts or service gaps, resulting in inequitable and unequal healthcare access. Also, limited resources and funding can slow extensive long-term support, leaving specific medical needs unaddressed. Additionally, the intricate political and social conditions restrict these organisations' capacity to operate effectively, impacting immediate care and sustainable health initiatives for the Rohingya population. Moving forward, it is crucial for host countries to: finance extra healthcare facilities in refugee camps to enhance access and reduce diseases, launch culturally appropriate mental health initiatives with locally trained workers to decrease stigma and provide community-based support, integrate nutrition programmes to address different forms of malnutrition in vulnerable communities and encourage further international support to maintain health initiatives among the Rohingya population. Conclusion The Rohingya crisis is an example of global health injustice exacerbated by geopolitical and humanitarian challenges. At the same time, Bangladesh is trying to provide temporary shelter for the refugees to minimise the crisis. However, this crisis also requires international cooperation, policy support, and increased funding. Solving this issue is essential for global public health and human rights. Notably, finding sustainable solutions will help the Rohingya people recover and thrive, and enhance stability and security in the region. Their future goes beyond humanitarian aid; it is about upholding inclusion, justice, and respect for human dignity, which should guide all efforts to link geopolitics with health outcomes. To truly tackle the health issues faced by the Rohingya community, we need to take a comprehensive approach that looks at the political, social, and economic factors at play. By adopting such all-encompassing systems, we can work towards a brighter and fairer future for the Rohingya community and other vulnerable groups around the globe who are facing similar challenges. The next article will be the final one reflecting on everything discussed in this series. Written by Nasif Mahmood and Sam Jarada Related articles: Health and well-being in- Palestine , Kashmir / South Asian famine / South Asian mental health REFERENCES Tinker HR. History of Bangladesh | Events, People, Dates, & Facts [Internet]. Encyclopedia Britannica. 2023 [cited 2025 Jul 15]. Available from: https://www.britannica.com/topic/history-of-Bangladesh Rahman MM, Bhuiyan MR, Ali MZ, Rahman MS, Hossain MA. Insecurity feelings and mental health status of Rohingya orphan children in BangladeshResearchGate; 2021 https://www.researchgate.net/publication/348521935_Insecurity_Feelings_and_Mental_Health_Status_of_Rohingya_Orphan_Children_in_Bangladesh UNHCR. Rohingya refugee crisis – Bangladesh. 2023. https://www.unhcr.org International Crisis Group (ICG). The health crisis in Rohingya refugee camps. 2022. https://www.crisisgroup.org Tay AK, Riley A, Islam R, Welton-Mitchell C, Duchesne B, Waters V, et al. The culture, mental health and psychosocial wellbeing of Rohingya refugees: a systematic review. Epidemiology and Psychiatric Sciences [Internet]. 2019 Apr 22 [cited 2025 Sep 10];28(5):489–94. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC6998923/ Human Rights Watch. The plight of Rohingya refugees in Bangladesh. 2023. https://www.hrw.org . Nivedita Sudheer, Banerjee D. The Rohingya refugees: a conceptual framework of their psychosocial adversities, cultural idioms of distress and social suffering. Cambridge Prisms Global Mental Health [Internet]. 2021 Jan 1 [cited 2025 Sep 10];8. Available from: https://www.cambridge.org/core/journals/global-mental-health/article/rohingya-refugees-a-conceptual-framework-of-their-psychosocial-adversities-cultural-idioms-of-distress-and-social-suffering/F4D229807D4ED7667EA16195FDF5C787 World Health Organization (WHO). Health challenges in Rohingya refugee camps. 2022. https://www.who.int Médecins Sans Frontières (MSF). Medical response in Rohingya refugee settlements. 2022. https://www.msf.org Project Gallery

A leap forward in primate research Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Monkey see, monkey clone 10/07/25, 10:22 Last updated: Published: 07/09/24, 19:20 A leap forward in primate research Chinese scientists have recently unlocked the secrets of cloning Rhesus monkeys offering new hope for medical breakthroughs. Introduction When we think of cloning, perhaps the first thing that comes to mind is Dolly the sheep, the first mammal ever cloned from an adult cell back in 1996. This groundbreaking achievement inspired a revolution leading to the successful cloning of other mammals such as cattles and pigs. However, cloning primates, especially Rhesus monkeys, has proven to be a significant challenge due to the low success rates and high embryonic losses during development. What is cloning? Cloning is the process of creating an identical genetic copy of an organism. In mammals, this is typically done through a technique called somatic cell nuclear transfer (SCNT). In SCNT, the nucleus (the compartment storing genetic material) from a cell of the animal to be cloned is transferred into an egg cell that has had its own nucleus removed. This hybrid egg cell then develops into an embryo which is implanted into a surrogate mother to grow into a new individual. Despite the success in cloning other mammals, cloning primates has proven to be a significant challenge. However, the potential benefits of cloning primates for medical research make it a worthwhile endeavour. The importance of cloning primates You might be wondering why being able to clone primates is so important. Well, primates like the Rhesus monkey are invaluable models for studying human diseases and create new therapies! The reason we can use them as disease models is because they share about 93% genetic identity and have very similar physiological characteristics with humans. For instance, Rhesus monkeys also experience a decline in their cognitive abilities as they age, and they lose important connections between brain cells in the part of the brain responsible for complex thinking, even when there's no severe brain damage. Moreover, Rhesus monkeys also develop the same kinds of brain changes that we see in people with Alzheimer's disease, such as the buildup of sticky proteins called amyloid-beta and tangled fibres of another protein called tau.These similarities make them excellent models for understanding how human diseases progress and for developing new treatments. So, by cloning these animals, researchers might be able to create monkeys with specific genetic changes that mimic human diseases even more closely. This could allow scientists to study these diseases in greater detail and develop more effective therapies. Cloning primates could give us a powerful tool to fight against some of the most challenging disorders that affect the human brain! A breakthrough in primate cloning Now, a group of scientists in China have made a breakthrough in primate cloning. They successfully cloned a Rhesus monkey using a novel technique called trophoblast replacement (TR).This innovative approach not only helps us better understand the complex process of cloning but also offers a promising way to improve the efficiency of primate cloning, bringing us one step closer to unlocking the full potential of this technology for medical research and beyond. The awry DNA methylation of cloned conkey embryos To understand why cloning monkeys is so challenging, Liao and colleagues (2024) took a closer look at the genetic material of embryos created in two different ways. They compared embryos made through a standard fertility treatment called intracytoplasmic sperm injection (ICSI) with those created via the cloning technique, SCNT. What they found was quite surprising! To make matters worse, the scientists also noticed that certain genes, known as imprinted genes, were not functioning properly in the SCNT embryos. Imprinted genes are a special group of genes that play a crucial role in embryo development. In a healthy embryo, only one copy of an imprinted gene (either from the mother or the father) is active, while the other copy is silenced. But in the cloned embryos, both copies were often incorrectly switched on or off. Here's the really concerning part: these genetic abnormalities were not just present in the early embryos but also in the placentas of the surrogate monkey mothers carrying the cloned offspring. This suggests that the issues arising from the cloning process start very early in development and continue to affect the pregnancy. Liao and colleagues suspect that the abnormal DNA methylation patterns might be responsible for the imprinted gene malfunction. It's like a game of genetic dominos – when one piece falls out of place, it can cause a whole cascade of problems down the line. Piecing together this complex genetic puzzle is crucial for understanding why primate cloning is so difficult and how we can improve its success in the future. By shedding light on the mysterious world of DNA methylation and imprinted genes, Liao and colleagues have brought us one step closer to unravelling the secrets behind monkey cloning. Digging deeper: what does the data reveal? Liao et al. (2024) discovered that nearly half of the cloned monkey foetuses died before day 60 of the gestation period, indicating developmental defects in the SCNT embryos during implantation. They also found that the DNA methylation level in SCNT blastocysts was 25% lower compared to those created through ICSI (30.0% vs. 39.6%). Furthermore, out of the 115 human imprinting genes they examined in both the embryos and placentas, four genes - THAP3, DNMT1, SIAH1, and RHOBTB3 - showed abnormal expression and loss of DNA methylation in SCNT embryos. These findings highlight the complex nature of the reprogramming process in SCNT and the importance of imprinted genes in embryonic development. By understanding these intricacies, scientists can develop targeted strategies to improve the efficiency of primate cloning. The power of trophoblast replacement To avoid the anomalies in SCNT placentas, the researchers developed a new method called TR. In this method, they transferred the inner cell mass (the part of the early embryo that develops into the baby) from an SCNT embryo into the hollow cavity of a normal embryo created through fertilisation, after removing its own inner cell mass. The idea behind this technique is to replace the abnormal placental cells in the SCNT embryo with healthy ones from the normal embryo. And it worked! Using this method, along with some additional treatments, Liao et al. (2024) successfully cloned a healthy male Rhesus monkey that has survived for over two years (FYI his name is Retro!). The ethics of cloning While the scientific advances in primate cloning are exciting, they also raise important ethical questions. Some people worry about the potential misuse of this technology, for instance to clone humans, which is widely considered unethical. Others are concerned about the well-being of cloned animals, as the cloning process can sometimes lead to health problems. As scientists continue to make progress in cloning technology, it is essential to have open discussions about the ethical implications of their work. Rules and guidelines must be put in place to ensure that this technology is developed and used responsibly, with the utmost care for animal welfare and the concerns of society. Looking to the future The successful cloning of a rhesus monkey using TR opens up new avenues for primate research. This technology can help scientists create genetically identical monkeys to study a wide range of human diseases, from neurodegenerative disorders like Alzheimer's and Parkinson's to infectious diseases like HIV and COVID-19. The trophoblast replacement technique developed by Liao et al. (2024) increases the likelihood of successful cloning by replacing the abnormal placental cells in the SCNT embryo with healthy ones from a normal embryo. However, it is important to note that this technique does not affect the genetic similarity between the clone and the original monkey, as the inner cell mass, which gives rise to the foetus, is still derived from the SCNT embryo. Moreover, this research provides valuable insights into the mechanisms of embryonic development and the role of imprinted genes in this process. By understanding these fundamental biological processes, scientists can not only improve the efficiency of cloning but also develop new strategies for regenerative medicine and tissue engineering. As we look to the future, cloning monkeys could help us make groundbreaking discoveries in medical research and develop new treatments for human diseases. However, we must also carefully consider the ethical implications of cloning primates and ensure that this powerful tool is used responsibly and for the benefit of society. Written by Irha Khalid Related articles: Do other animals get periods? / Germline gene therapy (GGT) REFERENCES Beckman, D. and Morrison, J.H. (2021). Towards developing a rhesus monkey model of early Alzheimer’s disease focusing on women’s health. American Journal of Primatology , [online] 83(11). doi: https://doi.org/10.1002/ajp.23289 . Liao, Z., Zhang, J., Sun, S., Li, Y., Xu, Y., Li, C., Cao, J., Nie, Y., Niu, Z., Liu, J., Lu, F., Liu, Z. and Sun, Q. (2024). Reprogramming mechanism dissection and trophoblast replacement application in monkey somatic cell nuclear transfer. Nature Communications , [online] 15(1), p.5. doi: https://doi.org/10.1038/s41467-023-43985-7 . Morrison, J.H. and Baxter, M.G. (2012). The ageing cortical synapse: hallmarks and implications for cognitive decline. Nature Reviews Neuroscience , [online] 13(4), pp.240–250. doi: https://doi.org/10.1038/nrn3200 . Paspalas, C.D., Carlyle, B.C., Leslie, S., Preuss, T.M., Crimins, J.L., Huttner, A.J., Dyck, C.H., Rosene, D.L., Nairn, A.C. and Arnsten, A.F.T. (2017). The aged rhesus macaque manifests Braak stage III/IV Alzheimer’s‐like pathology. Alzheimer’s & Dementia , [online] 14(5), pp.680–691. doi: https://doi.org/10.1016/j.jalz.2017.11.005 . Shi, L., Luo, X., Jiang, J., Chen, Y., Liu, C., Hu, T., Li, M., Lin, Q., Li, Y., Huang, J., Wang, H., Niu, Y., Shi, Y., Styner, M., Wang, J., Lu, Y., Sun, X., Yu, H., Ji, W. and Su, B. (2019). Transgenic rhesus monkeys carrying the human MCPH1 gene copies show human-like neoteny of brain development. National Science Review , [online] 6(3), pp.480–493. doi: https://doi.org/10.1093/nsr/nwz043 . Project Gallery