An explanation of how cumulus clouds form and grow in the atmosphere Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The physics behind cumulus clouds 14/07/25, 15:58 Last updated: Published: 07/10/23, 13:51 An explanation of how cumulus clouds form and grow in the atmosphere When you think of a cloud, it is most likely a cumulus cloud that pops into your head, with its distinct fluffy, cauliflower-like shape. The word ‘cumulus’ means ‘heaped’ in Latin, and aptly describes the clumpy shape of these detached clouds. They are one of the lowest clouds in the sky at altitudes of approximately 600 to 1000 metres, while the highest clouds form nearly 14 km up in the atmosphere. Depending on the position of the clouds in relation to the sun, they can appear in a brilliant white colour, or in a more foreboding grey colour. Cumulus clouds are classified into four different species: cumulus humilis clouds which are wider than they are tall, cumulus mediocris which have similar widths and heights, cumulus congestus which are taller than they are wide, and finally, cumulus fractus which have blurred edges as this is the cloud in its decaying form. Cumulus clouds are often associated with fair weather, with cumulus congestus being the only species that produces rain. So, how do cumulus clouds form, and why are they associated with fair weather? To understand the formation of these clouds, think of a sunny day. The sun shines on the land and causes surface heating. The warm surface heats the air above it which causes this air to rise in thermals, or convection currents. The air in the thermal expands and becomes less dense as it rises through surrounding cool air. The water vapour that is carried upwards in the convection current condenses when it gets cool enough and forms a cumulus cloud. Due to the varying properties of different surface types, some types are better at causing thermals than others. For example, the sun’s radiation will warm the surface of land more efficiently than the sea, leading to the formation of cumulus clouds over land rather than the sea. This is because water has a higher heat capacity than land, meaning it will take more heat to warm the water than the land. As cumulus clouds form on the top of independent thermals, they appear as individual floating puffs. But, what happens when cumulus clouds are knocked off the perch of their thermal by a breeze? How do they keep growing from an innocent, lazy cumulus humilis to a dark cumulus congestus, threatening rain showers? Latent heat gives us the answer. This is the energy that is absorbed, or released, by a body when it changes state. A cumulus cloud forms at the top of a thermal as the water molecules condense (changing state from a gas to a liquid) to form water droplets. When this happens, the warmth given off by the latent heat of condensation heats up the surrounding air causing it to expand and rise further, repeating the cycle and forming the characteristic cauliflower mounds of the cloud. The development of a cumulus humilis to cumulus congestus depends on the available moisture in the atmosphere, the strength of the sun’s radiation to form significant thermals, and whether there is a layer of warmer air higher up in the atmosphere that can halt the rising thermals. If the conditions are right, a cumulus congestus can keep growing and form a cumulonimbus cloud, which is an entirely different beast, more than deserving of its own article. So, the next time you see a cumulus cloud wandering through the sky, you will know how it came to be there. Written by Ailis Hankinson Related article: The physics of LIGO Project Gallery

Famous sites in the Chaco Canyon region include Pueblo Alto and Pueblo Bonito Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Cities designed to track the heavens: Chaco Canyon, New Mexico 06/03/25, 12:25 Last updated: Published: 02/07/24, 11:22 Famous sites in the Chaco Canyon region include Pueblo Alto and Pueblo Bonito This is Article 1 in a series about astro-archaeology. Next article: The astronomical symbolism of the Giza Pyramids . In the desert of New Mexico are the remains of a major center of ancestral Puebloan culture. Within the Chaco Canyon region, several places of incredible architecture and complex cultural life have been identified, called Great Houses. It is suggested that over 150 Great Houses were constructed between the 9th and 12th centuries and connected by intricate road systems. Famous sites in the Chaco Canyon region include Pueblo Alto and Pueblo Bonito, which showcase the incredible architectural feats of the culture. Interestingly, scholars have deduced that the Great Houses were not only built to support the forming society, but the details of construction were specific for another reason: astronomy. Often, the structures were oriented according to at least one of three following ways: The south-southeast direction : Researchers suggest that the south-southeast orientation originates from a Snake Myth, which describes the use of a staff and the stars to facilitate migration in the southeast direction. Aligned with the cardinal directions : A great example of this is Pueblo Alto. Built in the 11th century, its main wall aligned within 5° of the EW latitude. Hungo Pavi is less than 5° offset from true NS. Built at horizon calendrical stations: Calendrical stations are often natural structures that, when viewed at a particular location, the sun can be seen in a memorable relation to it. For example, Figure 1 shows the sun between two prominent rock formations. Imagine this occurred only once per year. The event would mark the same day and thus would denote the annual occasion. Many of the ancestral Puebloan Great Houses are understood to have been built near such calendrical stations that operate for different events like the solstices. Although the ancestral Puebloan culture may not have used physics and astronomy as we do now, it was built into the fundamentals of their society, and central to their community. Written by Amber Elinsky REFERENCES & RESOURCES “History and Culture: The Center of Chalcoan Culture.” Chaco Culture, National Park Service . Accessed May 2024. https://www.nps.gov/chcu/learn/historyculture/index.htm . Munro, Andrew M., and J. McKim Malville. “Ancestors and the Sun: Astronomy, Architecture and Culture at Chaco Canyon.” Proceedings of the International Astronomical Union 7, no. S278 (2011): 255–64. https://doi.org/10.1017/S1743921311012683 . Images from nps.gov Project Gallery

Exploring the genetic roots of a neurological tragedy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Breaking down Tay-Sachs 15/05/25, 11:43 Last updated: Published: 20/04/24, 12:29 Exploring the genetic roots of a neurological tragedy This is article no. 9 in a series on rare diseases. Next article: Ehlers-Danlos Syndrome . Previous article: Pseudo-Angelman Syndrome . Tay-Sachs disease is a heritable metabolic condition that affects the neurons in the brain. The disease is more common in infants and young children as well as people of Ashkenazi Jewish descent, although it can occur in any ethnicity. Symptoms of the disease most commonly manifest themselves in children around six months of age. However, it is possible to develop symptoms from five years old to the teenage years. There are three different forms of the disease, each appearing at different stages of life: infantile, juvenile, and adult. The adult form is much rarer and non-fatal but can still cause neuron dysfunction and psychosis. Early symptoms of the disease include mobility issues such as difficulty crawling, and as the disease progresses, the child may suffer from seizures, vision, and hearing loss. In the classic infantile form, the disease is fatal within the first few years of life or by three to five years old. In infants, infection and respiratory complications, such as pneumonia, are the most common cause of death. Being categorised as an autosomal recessive disease means that in order to display the phenotype, two copies of the mutated HEXA gene must be present in an individual. This HEXA gene is located on chromosome 15 and is responsible for producing enzymes that affect the nerve cells. The carrier frequency of Tay-Sachs is highly dependent on ethnic backgrounds, with carrier frequency being 1 in 30 for those of Ashkenazi Jewish descent and 1 in 300 for others. The chance of developing the disease early or late is predicated on the specific type of HEXA mutation that is inherited within the family. Meaning, if one child in a family possesses the infantile form, all other members of the family will also possess the infantile form (if they express the phenotype). When both parents are carriers of the Tay-Sachs gene mutation, there is a 25% chance with each pregnancy that the child will inherit two mutated copies of the HEXA gene and thus be affected by the disease. Also, there is a 50% chance the child will be a carrier like the parents and a 25% chance the child will inherit two normal copies of the gene and be unaffected. Furthermore, this particular type of gene mutation results in the disease being commonly labelled as a hexosaminidase A deficiency. The HEXA gene’s significance in the disease is further highlighted due to its ability to code for specific alpha subunits in the enzyme β-hexosaminidase A. This enzyme is involved in breaking down molecules that can be recycled in a cell through the use of lysosomes. This key cellular function helps a cell undergo apoptosis (programmed cell death) or help evade bacteria that can damage a cell. However, in individuals with this HEXA gene mutation, less of the enzyme β-hexosaminidase A is produced, which results in less degradation of GM2 ganglioside. GM2 ganglioside is a lipid involved in a host of processes such as membrane organisation, neuronal differentiation, and signal transduction. In addition, due to its lack of degradation, it accumulates inside the body. The rate at which the lipid accumulates inside the cell ultimately determines the form of Tay-Sachs an individual will possess. It is worth noting that this GM2 ganglioside pathology also includes other diseases, such as Sandhoff disease and the AB variant, which have similar disease prognoses. Furthermore, the disease specifically targets the brain as gangliosides are the main lipids that compose neuronal plasma membranes. Their expression is specific to brain regions, impacting key neurodevelopmental processes like neural tube formation and synaptogenesis. Furthermore, ganglioside synthesis is a highly regulated process facilitated by glycosyltransferases during transcription and post-transcription. They also modulate ion channels and receptor signalling, which are crucial for neurotransmission, memory, and learning. The exact mechanism of how this ganglioside accumulation due to HEXA malfunction leads to neuronal death remains unclear. Figure 1 illustrates the dysfunction of the alpha subunit in HEXA as it cannot break down GM2 gangliosides. This results in an accumulation of GM2 within the liposome, contrasting with its concentration in the external environment. This accumulation of GM2 causes lysosomal dysfunction and eventually cell damage, which leads to the symptoms commonly associated with Tay-Sachs. Mouse models have been created to understand this GM2 pathway in greater detail to develop treatments. However, this is quite limited as mice do not have the same pathway of breaking down GM2 as humans. Also, since the disease may be prevalent before birth, it is hard to establish the damage done to a baby inside the womb, making reversing this disease in infants very challenging. However, the later onset types of Tay-Sachs disease might respond to treatment. Implementing ganglioside synthesis inhibitors in combination with existing DNA and enzymatic screening programs holds promise for eventually managing and controlling this condition. Parents can undergo genetic screening to assess their risk of carrying the Tay-Sachs gene, which is done by doing a simple blood test that examines the DNA for mutations in the HEXA gene. Genetic screening is particularly important for couples who have a family history of Tay-Sachs disease or who belong to ethnic groups with a higher prevalence of the condition. Early detection through genetic screening allows couples to make informed reproductive decisions, such as pursuing in vitro fertilisation with preimplantation genetic testing or opting for prenatal testing during pregnancy to determine if the foetus has inherited the mutated gene. Utilising the acronym SHADES as a mnemonic to recognise potential signs of Tay-Sachs disease in their child can help parents get a prompt medical evaluation if any symptoms arise. SHADES: S tartle response H earing loss A ffecting vision D evelopmental delay E pileptic seizures S wallowing difficulties Written by Imron Shah REFERENCES Center, N. (2015). Tay-Sachs disease. Nih.gov . Available at: https://www.ncbi.nlm.nih.gov/books/NBK22250/ . Leal, A.F., Benincore-Flórez, E., Solano-Galarza, D., Garzón Jaramillo, R.G., Echeverri-Peña, O.Y., Suarez, D.A., Alméciga-Díaz, C.J. and Espejo-Mojica, A.J. (2020). GM2 Gangliosidoses: Clinical Features, Pathophysiological Aspects, and Current Therapies. International Journal of Molecular Sciences, 21(17), p.6213. doi: https://doi.org/10.3390/ijms21176213 . Ramani, P.K. and Parayil Sankaran, B. (2022). Tay-Sachs Disease. PubMed. Available at: https://www.ncbi.nlm.nih.gov/books/NBK564432/ . Project Gallery

Preserving trust and exposing betrayal Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Uncovering the Disturbing World of Healthcare Serial Killers 14/07/25, 16:06 Last updated: Published: 25/02/24, 15:08 Preserving trust and exposing betrayal Background We depend heavily on medical professionals during our most defenceless and vulnerable moments, trusting them with our well-being. However, what would happen if this trust was broken? What if the medical professionals were to pose harm rather than fulfil their intended function as protectors? Healthcare serial killers are one of the most disturbing subsets of serial killers - the name itself suggests that individuals within the healthcare industry exploit their position to murder patients. True crime and media often go hand in hand in the modern era. There are many web series, TV dramas, and movies that delve into real-life narratives. Accumulating over 68.31 million hours watched, Netflix's film "The Good Nurse" in 2022, depicts the story of Charles Cullen, a figure recognised as one of the most prolific serial killers in American history. The film quickly rose to prominence and became the best-performing English-language film production on the platform. This phenomenon in media underscores a broader pattern wherein the portrayal of serial killers becomes increasingly prevalent within popular culture. Motives Criminologists and true crime filmmakers engaged in extensive efforts to figure out what motivates serial killers to carry out such horrific crimes for decades. The motives behind killings are diverse, complex and sometimes unknown. Some perpetrators may attempt to justify their actions by claiming to ease the patient's suffering under the guise of “mercy killing”. Others can be driven by the desire to be praised, to exert power or control over the patient, or to gain financial benefits. For example, Dr. Harold Shipman, a British doctor killed over 200 patients, primarily driven by sadistic motives. His misdeeds were ultimately exposed when he attempted to forge the will of one of his victims. Key traits and methods Although it might be tempting to create a list of characteristics typical of healthcare serial killers, no universally applicable formula defines their personalities. However, according to research by Yardley, E., and Wilson, D. (2016), attention-seeking, strange behaviour when a patient dies, and frequent changes in hospital working locations are characteristics that healthcare serial killers frequently exhibit. Furthermore, the study conducted by Birmingham City University criminologists shows that the most popular technique employed by healthcare serial killers is poisoning, specifically through insulin overdose. Notably, insulin overdose was the principal method employed by 25% of healthcare serial killers. For instance, in the case of British nurse Lucy Letby, who was given a life sentence for killing seven infants and attempting to murder six others, the use of an insulin overdose was a notable method employed. Ethics Examining the ethical implications of healthcare serial killing is essential, as it involves the breach of trust and violation of core principles of the healthcare profession. The relationship between a medical professional and a patient is based solely on trust, which healthcare serial killers have exploited. What's worse is that medical professionals frequently target elderly, chronically ill, or vulnerable patients, highlighting significant ethical issues. Challenges Detecting healthcare serial killers is difficult, primarily because their victims are frequently elderly or suffering from chronic illnesses. Investigations typically stem from an unusually high number of deaths rather than patient or family complaints. Even if the police initiate an investigation, it may be too late to collect physical evidence, as bodies may have been cremated or significantly decomposed, leaving no trace of substances in the patients' systems. Furthermore, in rare cases where a medical professional faces charges, they may use defences such as assisted suicides or attribute deaths to unintentional medical errors, potentially resulting in reduced sentences or lesser degrees of homicide . Conclusion Healthcare serial killers are a deeply disturbing phenomenon within the medical profession. The idea that people upon whom we rely on to take care of us can occasionally exhibit malevolence is extremely unsettling. By employing research to understand the existence of serial killers in the healthcare industry, we can address the many questions that surround their behaviour. Studying the motive behind such crimes, looking at the key traits and methods, and addressing the challenges associated with identifying such perpetrators provide insights crucial for safeguarding the community of patients who are at risk and preserving the core moral principles of the medical field. Let’s conclude by saying that the way that healthcare serial killings are portrayed in popular media is a clear reminder of the moral and professional obligations inherent in the provision of healthcare. Written by Prabha Rana Related articles: Neurology of serial killers / Intern Blues References ‘The True Story Behind Netflix’s The Good Nurse’. TIME, 27 Oct. 2022, https://time.com/6225730/the-good-nurse-true-story-netflix/ . Menshawey, Rahma, and Esraa Menshawey. ‘Brave Clarice-Healthcare Serial Killers, Patterns, Motives, and Solutions’. Forensic Science, Medicine, and Pathology, vol. 19, no. 3, Sept. 2023, pp. 452–63. PubMed, https://doi.org/10.1007/s12024-022-00556-4 . Tinning, Danielle. ‘Meet The British Physician Who Killed Hundreds Of His Patients — On Purpose’. All That’s Interesting, 21 Apr. 2023, https://allthatsinteresting.com/haroldshipman . Guy, Fiona. ‘Medical Serial Killers: The So-Called Angels of Mercy’. Crime Traveller, 27 June 2018, https://www.crimetraveller.org/2018/06/healthcare-medical-serial-killers/ . Townsend, Mark. ‘Study Identifies Key Traits and Methods of Serial Killer Nurses’. The Guardian, 22 Nov. 2014. The Guardian, https://www.theguardian.com/uknews/2014/nov/22/study-identified-key-traits-serial-killer-nurses . Project Gallery

New research suggests that the cause extends far beyond the nervous system Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can what we eat, breathe, and do for a living affect our Parkinson’s risk? Last updated: 21/03/25, 11:59 Published: 10/04/25, 08:00 New research suggests that the cause extends far beyond the nervous system Introduction Parkinson’s disease (PD) is the most prevalent movement disorder and the second most common neurodegenerative disorder worldwide. PD is best known for causing tremors and stiffness, but it’s much more than a movement disorder. It also affects mood and speech. While PD is caused by the loss of dopamine-producing neurons in the brain’s substantia nigra, new research suggests that its roots may extend far beyond the nervous system. Surprisingly, the gut microbiome – trillions of bacteria living in our digestive tract – may play a key role in both the development and prevention of PD. These microbes help regulate inflammation and support brain health by influencing microglia, the brain’s immune cells. Diet also seems to matter: a Mediterranean-style diet rich in fruits, vegetables, and healthy fats appears to lower PD risk, while smoking – despite its well-known dangers – has been linked to a puzzling protective effect, possibly due to nicotine’s impact on the brain. Meanwhile, specific jobs, like farming, may increase PD risk due to pesticide exposure, which has been associated with neurodegeneration. The idea that what we eat, breathe, and do for a living could shape our brain health is intriguing. As research continues to uncover these surprising links, it raises an important question: could simple lifestyle changes help protect against neurodegenerative diseases? Gut-Brain Axis The gut-brain axis (GBA) is a two-way communication network between the enteric nervous system of the gastrointestinal (GI) tract and the central nervous system, connecting emotions and cognition with the intestines’ functions. This involves the brain sending signals to the gut and vice versa, which happens through the vagus nerve, gut hormones and the gut microbiome, which can produce chemicals to impact brain activity. This usually explains why stress signals from the brain can influence the digestion of food, causing symptoms such as stomach pain, bloating or changes in bowel movements. Alternatively, signals travelling from the gut to the brain can be seen when we eat something that makes us feel sick – we naturally avoid that food and the place where we ate it. Gut dysbiosis can be triggered by multiple factors, including diet, antibiotic use, infection, inflammation, and chronic stress. Dysbiosis is the imbalance in the composition and activity of the microbiota (microorganisms present in the gut). It is considered a risk factor for PD, but is not a direct cause of it. Changes in the microbiota can induce metabolic changes, which can result in increased local and systemic inflammation in addition to increased permeability of the intestines, making the gut ‘leaky’. Additionally, this can cause increased harmful gut bacteria (such as E. coli or Salmonella ) as they leak through the intestinal lining, producing amyloid proteins which can travel to the brain and cause the accumulation of α-synuclein – a protein linked to neurodegenerative diseases such as PD. There is also a reduction in healthy gut bacteria – which usually produce short-chain fatty acids (SCFAs) such as butyrate – which reduce inflammation and protect the brain cells. Less SCFAs cause an increase in inflammation and loss of the neuroprotective effects of SCFAs. Increased inflammation can eventually cause the weakening of the gut lining and a cycle of worsening dysbiosis, increased inflammation and increased α-synuclein accumulation, which spreads to the brain. Furthermore, gut dysbiosis can decrease the efficacy of dopaminergic treatments, which may be used to treat PD. In gut dysbiosis, harmful bacteria can produce an enzyme called dopa-decarboxylase – which converts Levodopa (a drug used to treat PD) into dopamine within the intestines. Hence, less Levodopa reaches the bloodstream and the brain, where it primarily acts and is converted to dopamine. This results in less Levodopa being converted to dopamine within the brain, reducing the effectiveness of the treatment. Consequently, this leads to motor symptoms and impairments such as tremors, which is a characteristic symptom of PD. Can food protect the brain? Could your diet be influencing your brain health in ways you never imagined? Research suggests that what you eat might play a critical role in either protecting your brain from PD or increasing your risk. People who follow a Mediterranean diet (MD) – rich in olive oil, fish, fruits, vegetables, whole grains, and nuts – may have up to a 25% lower risk of developing PD. Interestingly, this protective effect appears stronger in younger individuals and those in the early stages of PD. So.. what makes the MD so powerful? Gut microbiome boost: the MD promotes beneficial gut bacteria while reducing harmful microbes, supporting overall brain health. Anti-inflammatory effects: fibre from plant-based foods fuels the gut microbiome, leading to the production of SCFAs, which reduce inflammation and may slow PD progression. Mitochondrial protection: compounds in the MD, such as polyphenols in olive oil and omega-3 fatty acids in fish, help repair and protect mitochondria – the powerhouses of our cells. This helps prevent brain cell damage and maintain dopamine function. Neural growth & repair: walnuts and omega-3s may support neuronal growth and reduce protein clumping, a hallmark of PD. On the other hand, a Western diet – high in processed foods, saturated fats, refined sugars, and excess salt – may increase the risk of developing and worsening PD symptoms. Foods commonly associated with faster PD progression include canned fruits and vegetables, soda, fried foods, beef, ice cream, and cheese. Why does this happen? Microbiome disruption: the Western diet fosters an imbalance in gut bacteria, leading to inflammation and potential brain damage. Gut leakiness and neuroinflammation: a diet high in unhealthy fats and low in fibre can damage the gut lining, allowing harmful substances to enter the bloodstream and trigger brain inflammation. Hormonal imbalance: key gut-derived hormones (GLP-1, GIP, and IGN) that help protect neurons are disrupted by poor diet but can be restored through healthier food choices. While diet alone cannot cure PD, growing evidence suggests it can modify the disease course. A diet rich in fibre, healthy fats, and plant-based foods supports gut health, reduces inflammation, and may protect neurons from degeneration. Understanding these diet-microbiome-brain interactions could open new doors to PD prevention and treatment – proving once again that food truly is medicine. The smoking paradox One of the most intriguing findings in PD research is that smokers appear to have a lower risk of developing the disease. Epidemiological studies consistently show that people who smoke are less likely to be diagnosed with PD compared to non-smokers. But why? Scientists believe that nicotine, a key compound in tobacco, may play a neuroprotective role by affecting dopamine-producing neurons – the same cells that are progressively lost in PD disease. Nicotine interacts with receptors in the brain that influence dopamine release, which could help protect these neurons from degeneration. However, clinical trials testing nicotine as a treatment for PD have not shown significant benefits, suggesting that other compounds in tobacco or alternative mechanisms might be involved. Some researchers propose that additional chemicals in cigarette smoke, such as monoamine oxidase inhibitors, antioxidants, or even carbon monoxide at low levels, might contribute to this protective effect. Others suggest that genetic factors or lifestyle differences between smokers and non-smokers could also explain the association. Despite this fascinating link, smoking is not a recommended strategy for preventing PD. The well-documented risks – including cancer, cardiovascular disease, and lung damage – far outweigh any potential benefit. Instead, scientists are investigating whether specific compounds found in tobacco could be harnessed for new treatments without the harmful effects of smoking itself. What about my job? Can your job affect your risk of developing PD? Some studies suggest that certain occupations – like farming – might increase the risk, while others find no clear connection. So, what’s the truth? Let’s break it down. Some research suggests that farmers are more likely to develop PD, possibly due to exposure to pesticides like paraquat and rotenone, which have been linked to brain cell damage. Additionally, heavy metals found in agricultural environments – such as lead and manganese – may contribute to brain inflammation and oxidative stress, both of which play a role in PD. Furthermore, certain metals, including iron, mercury, copper, and manganese, can build up in the brain over time. Scientists believe that long-term exposure could damage the neurons that produce dopamine. However, the exact link isn’t fully understood, and not everyone exposed to these metals develops PD. That said, not all studies agree. Some large-scale research has found no significant link between farming, pesticide exposure, heavy metals and PD risk. This means that while environmental factors might play a role, other things – like genetics, lifestyle, or how long and intensely someone is exposed – could be just as important. So.. should you worry? If you work in farming or are regularly exposed to pesticides and heavy metals, it might be a good idea to take precautions, like using protective equipment and following safety guidelines. However, more research is needed to fully understand how these exposures contribute to PD. For now, staying informed and taking steps to reduce unnecessary exposure to harmful chemicals is a smart approach. What can you do? While there’s no guaranteed way to prevent PD, research suggests that certain lifestyle choices may help reduce the risk. Here are some science-backed steps you can take: 1. Adopt a Mediterranean-style diet: eating a diet rich in whole, plant-based foods, healthy fats (like olive oil and nuts), and lean proteins has been linked to a lower risk of PD. The Mediterranean diet is packed with antioxidants and anti-inflammatory compounds that may help protect brain cells. 2. Stay active: regular exercise isn’t just good for your muscles and heart – it may also help maintain gut health and protect neurons. Activities like walking, swimming, or strength training have been associated with a reduced risk of PD and other neurodegenerative diseases. 3. Limit pesticide exposure: for those in agricultural or industrial settings, protective measures, such as wearing gloves and masks and following safety guidelines, can help reduce exposure to potentially harmful chemicals linked to PD. 4. Monitor gut health: emerging research suggests that the gut microbiome may play a key role in PD. While scientists are still exploring microbiome-targeted therapies, maintaining good gut health by eating fibre-rich foods, fermented foods (like yogurt and kimchi), and staying hydrated may support overall well-being. Conclusion The connection between diet, gut health, lifestyle, and PD is an exciting area of research. While we don’t yet have all the answers, it’s clear that healthy habits – such as eating well, staying active, and minimising harmful exposures – can support both brain and overall health. As science continues to uncover new insights, making informed choices today can help protect your well-being in the long run! Written by Joecelyn Kirani Tan, Hanin Salem, Devikka Sivashanmuganathan & Barayturk Aydin Related articles: TDP43 and Parkinsonism / Diabetes drug to treat Parkinson's REFERENCES Berthouzoz E, Lazarevic V, Zekeridou A, Castro M, Debove I, Aybek S, Schrenzel J, Burkhard PR, Fleury V. Oral and intestinal dysbiosis in Parkinson's disease. Rev Neurol (Paris). 2023 Nov;179(9):937-946. doi: 10.1016/j.neurol.2022.12.010. Epub 2023 Mar 16. PMID: 36934020. Bisaglia M. Mediterranean Diet and Parkinson's Disease. Int J Mol Sci. 2022 Dec 20;24(1):42. doi: 10.3390/ijms24010042. PMID: 36613486; PMCID: PMC9820428. Firestone JA, Lundin JI, Powers KM, Smith-Weller T, Franklin GM, Swanson PD, Longstreth WT Jr, Checkoway H. Occupational factors and risk of Parkinson's disease: A population-based case-control study. Am J Ind Med. 2010 Mar;53(3):217-23. doi: 10.1002/ajim.20788. PMID: 20025075; PMCID: PMC3299410. Gorell JM, Johnson CC, Rybicki BA, Peterson EL, Richardson RJ. The risk of Parkinson's disease with exposure to pesticides, farming, well water, and rural living. Neurology. 1998 May;50(5):1346-50. doi: 10.1212/wnl.50.5.1346. PMID: 9595985. hms.harvard.edu . (2017). The Gut and the Brain. [online] Available at: https://hms.harvard.edu/news-events/publications-archive/brain/gut-brain . Hrncir, T. (2022). Gut Microbiota Dysbiosis: Triggers, Consequences, Diagnostic and Therapeutic Options. Microorganisms, [online] 10(3), p.578. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC8954387/#:~:text=Dysbiosis%20can%20be%20caused%20by,food%20additives)%2C%20and%20hygiene .. Jackson A, Forsyth CB, Shaikh M, Voigt RM, Engen PA, Ramirez V, Keshavarzian A. Diet in Parkinson's Disease: Critical Role for the Microbiome. Front Neurol. 2019 Dec 10;10:1245. doi: 10.3389/fneur.2019.01245. PMID: 31920905; PMCID: PMC6915094. Johns Hopkins Medicine (2025). Can Environmental Toxins Cause Parkinson’s Disease? https://www.hopkinsmedicine.org/health/conditions-and-diseases/parkinsons-disease/can-environmental-toxins-cause-parkinson-disease Kwon, D. et al. (2024) ‘Diet and the gut microbiome in patients with parkinson’s disease’, npj Parkinson’s Disease , 10(1). doi:10.1038/s41531-024-00681-7. Physiopedia. (n.d.). Gut Brain Axis (GBA). [online] Available at: https://www.physio-pedia.com/Gut_Brain_Axis_(GBA) . Project Gallery

Treatment that effectively controls tumours and prolongs survival without side effects Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A breakthrough in prostate cancer treatment 08/07/25, 15:35 Last updated: Published: 04/04/24, 17:00 Treatment that effectively controls tumours and prolongs survival without side effects Introduction Prostate cancer is a devastating disease that affects millions of men worldwide. Despite advancements in treatment options, aggressive forms of the disease, such as metastatic castrate-resistant prostate cancer (mCRPC), remain a major challenge. However, a recent study conducted by researchers at the University of Chicago Medicine Comprehensive Cancer Centre has established a promising "proof-of-concept" for a new treatment approach that could revolutionize the field. The study, published in Clinical Cancer Research, demonstrated the remarkable effectiveness of this novel treatment in a mouse model of advanced prostate cancer. The researchers achieved complete tumour control and long-lasting survival without any side effects. These ground-breaking findings have paved the way for further investigation in human clinical trials. Finding the exact cancer cell and then destroying it but leaving the healthy tissue untouched. In theory, it could be like aiming and shooting at someone in the video game but real world is a bit different, isn’t it? Overcoming Resistance to Hormonal Therapy Hormonal therapy, specifically androgen deprivation therapy (ADT), is the standard treatment for metastatic prostate cancer. However, the majority of patients eventually develop resistance to this therapy, leading to castrate-resistant prostate cancer. This resistance poses a significant challenge for clinicians and leaves patients with limited treatment options. Dr. Akash Patnaik, an accomplished physician-scientist and renowned expert in prostate cancer research and treatment, and his team at the University of Chicago Medical Centre have been exploring new strategies to overcome this resistance. Their research focuses on harnessing the immune system's ability to combat cancer cells. Targeting Macrophages to Control Cancer Growth Dr. Patnaik's team discovered that macrophages, a type of immune cell, play a crucial role in promoting the growth of prostate cancer. These macrophages express a molecule called PD-1, which suppresses the anti-cancer immune response. By targeting these macrophages, the researchers aimed to control the growth of the cancer. In a previous study, the team found that co-targeting the PI3K and PD-1 pathways enhanced the effects of hormonal therapy in PTEN-deficient prostate cancer, a particularly aggressive form of the disease. However, a significant portion of the mice remained resistant to this therapy. Further investigations revealed that the activation of the Wnt/β-catenin pathway restored lactate production in these treatment-resistant cancers, leading to macrophages promoting tumour growth. A Novel Therapeutic Approach Building on their previous findings, Dr. Patnaik and his team developed a novel therapeutic approach. By co-targeting the PI3K, MEK, and Wnt/β-catenin signalling pathways, they achieved an impressive 80% response rate in mouse models. However, a small percentage of the mice still showed resistance due to the restoration of lactate production in the treatment-resistant cancers. This led the researchers to investigate further and uncover the mechanism behind this resistance. They discovered that lactate can interact with macrophages and modify them through a process called histone lactylation, making the macrophages immunosuppressive and promoting cancer growth. In their latest study, the researchers found that targeting lactate as a macrophage phagocytic checkpoint can effectively control the growth of PTEN/p53-deficient prostate cancer. Through intermittent dosing of the three drugs, they achieved complete tumor control and significantly prolonged survival without the long-term toxicity associated with continuous drug administration. These groundbreaking findings provide "proof-of-concept" for a new treatment approach that holds great promise for the most aggressive forms of prostate cancer. The researchers believe that their strategy of harnessing the ability of macrophages to eliminate cancer cells could revolutionize cancer therapy. By flipping the switch in macrophages, the cancer cells can be effectively controlled and eliminated. The next step for Dr. Patnaik and his team is to translate these findings into clinical trials. They plan to develop a phase 1 clinical trial to test the efficacy of the intermittent dosing approach in human patients. If successful, this approach could potentially offer a new therapeutic option for patients with metastatic castrate-resistant prostate cancer, who currently have limited treatment options. The potential of this novel therapeutic approach extends beyond prostate cancer. The researchers have also uncovered new therapeutic opportunities by perturbing signaling pathways in cancer cells that affect the metabolic output of the cancer cell and its interaction with tumor-promoting macrophages. This opens up new avenues for research and the development of targeted therapies for various types of cancer. Conclusion The research conducted by Dr. Patnaik and his team has demonstrated the effectiveness of co-targeting multiple signaling pathways in treating aggressive forms of prostate cancer. Their findings provide a solid foundation for further investigation in human clinical trials and offer hope for patients with limited treatment options. This novel therapeutic approach has the potential to revolutionize cancer therapy and pave the way for more targeted and effective treatments in the future. Written by Sara Maria Majernikova Related article: A breakthrough drug discovery in cancer treatment References: Chaudagar, K., et al . (2023) Suppression of tumor cell lactate-generating signaling pathways eradicates murine PTEN/p53-deficient aggressive-variant prostate cancer via macrophage phagocytosis. Clinical Cancer Research . doi.org/10.1158/1078-0432.CCR-23-1441 Chetta, P., Sriram, R. and Zadra, G. (2023) ‘Lactate as key metabolite in prostate cancer progression: What are the clinical implications?’, Cancers , 15(13), p. 3473. doi: https://doi.org/10.3390/cancers15133473 . Mathieu (2023) Revolutionary breakthrough in prostate cancer treatment at the University of Bern , Greater Geneva Bern area . Available at: https://ggba.swiss/en/revolutionary-breakthrough-in-prostate-cancer-treatment-at-the-university-of-bern/(Accessed: 29 September 2023). Project Gallery

iPSCs are one of the most powerful tools of biosciences Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The endless possibilities of iPSCs and organoids 11/07/25, 11:02 Last updated: Published: 20/01/24, 11:50 iPSCs are one of the most powerful tools of biosciences On the 8th of October 2012, the Nobel Prize in Physiology was given to Shinya Yamanaka and John B. Gurdon for a groundbreaking discovery; induced Pluripotent Stem Cells (iPSCs). The two scientists discovered that mature, specialised cells can be reprogrammed to their initial state and consequently transformed into any cell type. These cells can be used to study disease, examine genetic variations and test new treatments. The science behind iPSCs The creation of iPSCs is based on the procedure of cell potency during mammalian development. While the organism is still in the embryonic stage, the first cell developed is a totipotent stem cell, which has the unique ability to differentiate into any cell type in the human body. “Totipotent” refers to the cell’s potential to give rise to all cell types and tissues needed to develop an entire organism. As the totipotent cell grows, it develops into the pluripotent cell, which can differentiate into the three types of germ layers; the endoderm line, the mesoderm line and the ectoderm line. The cells of each line then develop into multipotent cells, which are derived into all types of human somatic cells, such as neuronal cells, blood cells, muscle cells, skin cells, etc. Creation of iPSCs and organoids iPSCs are produced through a process called cellular reprogramming, which involves the reprogramming of differentiated cells to revert to a pluripotent state, similar to that of embryonic stem cells. The process begins with selecting any type of somatic cell from the individual (in most cases, the individual is a patient). Four transcription factors, Oct4, Sox2, Klf4 and c-Myc, are introduced into the selected cells. These transcription factors are important for the maintenance of pluripotency. They are able to activate the silenced pluripotency genes of the adult somatic cells and turn off the genes associated with differentiation. The somatic cells are now transformed into iPSCs, which can differentiate into any somatic cell type if provided with the right transcription factor. Although iPSCs themselves have endless applications in biosciences, they can also be transformed into organoids, miniature three-dimensional organ models. To create organoids, iPSCs are exposed to a specific combination of signalling molecules and growth factors that mimic the development of the desired organ. Current applications of iPSCs As mentioned earlier, iPSCs can be used to study disease mechanisms, develop personalised therapies and test the action of drugs in human-derived tissues. iPSCs have already been used to model cardiomyocytes, neuronal cells, keratinocytes, melanocytes and many other types of cells. Moreover, kidney, liver, lung, stomach, intestine, and brain organoids have already been produced. In the meantime, diseases such as cardiomyopathy, Alzheimer’s disease, cystic fibrosis and blood disorders have been successfully modelled and studied with the use of iPSCs. Most importantly, the use of iPSCs in all parts of scientific research reduces or replaces the use of animal models, promising a more ethical future in biosciences. Conclusion iPSCs are one of the most powerful tools of biosciences at the moment. In combination with gene editing techniques, iPSCs give accessibility to a wide range of tissues and human disorders and open the doors for precise, personalised and innovative therapies. iPSCs not only promise accurate scientific research but also ethical studies that minimise the use of animal models and embryonic cells. Written by Matina Laskou Related articles: Organoids in drug discovery / Introduction to stem cells Project Gallery

Linking a country's HDI with its COVID-19 mortality rate Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Correlation between wealthy countries and COVID-19 mortality rate 09/03/26, 08:30 Last updated: Published: 24/08/23, 17:20 Linking a country's HDI with its COVID-19 mortality rate Investigation title: Could there have been a correlation between very rich countries and COVID-19 mortality rate? Investigation period: December 2019- November 2020 (Approx. 1 year) Background The World Health Organisation (WHO) were first alerted about coronavirus on the 31st December 2019, by a lot of pneumonia cases in Wuhan, China that has a population of 11 million. Furthermore, by 15th January 2020 there were precisely 289 cases recorded in countries such as: Thailand, Japan, S.Korea, and other places in China. And of the original cases there were 6 deaths, 51 severe cases - 12 of which were in critical condition. Meanwhile, the virus responsible for the cases was isolated and had its genome mapped, and was shared on 12th January. HDI represents the measurement of development. This is a composite of Gross National Income (GNI) per capita, mean years of education and life expectancy at birth, to measure the development of a country. It is calculated between a scale of 0 (least developed) to 1 (most developed) and all its values are to 3 significant figures. HDI values of 2019 and countries of HDI greater than 0.800 were used, as these are all regarded as very high HDI-countries so were in the scope of this investigation. Therefore, this research aimed to determine the impact of human development on the number of mortalities caused by SARS-CoV-2; where human development is measured by HDI, and the number of mortalities per hundred thousand from December 2019 to November 2020. Method Stratified sampling produced 12 countries, in descending order of HDI value: - Australia, Netherlands, UK, Austria, Spain, Estonia, UAE, Portugal, Bahrain, Kazakhstan, Romania, Malaysia See Table 4 . Results See Chart 2 . r= 0.321 (3 s.f.) – Pearson’s test ∴ There is a moderate positive linear correlation between HDI and mortality rate due to SARS-CoV-2 per 100,000. Further stats testing- Spearman’s Rank ∑D^2 = 216 n = 12 Rs = 1 - (6 ∑D^2 )/ n(n^2 – n) = 1 - (6 x 216) 1584 = 0.182 (3 d.p.) Rs = 0.245 ＜ Critical Value (0.0.587591) ∴ There is no correlation between HDI and mortality rate due to coronavirus per 100,000. Conclusion The null hypothesis was accepted: there is no correlation between a country’s HDI and its mortality rate due to SARS-CoV-2. A biogeographical reason for this is that the more developed countries (such as those in my investigation- for example, the UK) have a higher level of immigration from latitudes closer to the equator, therefore there is a section of their society with increased susceptibility to SARS-CoV-2 due to vitamin D deficiency. It is known that low vitamin D levels have a negative impact on immune function and that low vitamin D levels are common in the immigrant population. Therefore, it is likely that there is a link between vitamin D deficiency and mortality rate per 100,000, however this could be overstated due to confounding factors such as socioeconomic status, residence and employment. This would explain why countries at higher latitudes like the Netherlands have higher mortality rates per 100,000 (41.80) which is the third highest HDI-country in this investigation. Another explanation for this non-correlation could be that the less developed countries could be more used to dealing with a pandemic, or stress on a healthcare system, due to previous experience. For example, after the SARS outbreak, many countries decided to prepare in case of a pandemic, however some large HDI-countries such as the UK chose not to and even ignored other warnings on the effects of a pandemic (like the exercise signs simulation). Moreover, studies have shown that as a very high HDI-country becomes more developed, its healthcare system continues to develop until it reaches a peak where its effectiveness is undermined by economic benefit or interest. This would explain why the UK had a death rate of 342 per 100,000 and a total death count of around 232,422 (as of early 2026), and as of 2024/25, the UK recorded higher-than-expected death rates compared to other countries. Implications Since there is no correlation between a country’s HDI index and its mortality rate of COVID-19, this may apply to other diseases that became pandemics such as 1918’s Spanish Flu, or more recent ones like the SARS outbreak in the early 21st century. As for tropical diseases (malaria, dengue, chikungunya and others) and other illnesses such as the common cold and the flu, these diseases present in only certain geographies. This means that the countries with these ailments will be of a similar HDI and economical status; therefore there would be a correlation between a country’s HDI index and its mortality rate of these diseases, to a certain extent. Investigation conducted and written by Roshan Gill Tables, charts, stats and calculations by Roshan Gill Summary by Manisha Halkhoree ‘Implications’ section by Manisha Halkhoree Related articles: Causality vs correlation / Impacts of global warming on dengue fever / Global Health Injustices (series) Project Gallery

What they are, uses, and future outlook Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Advancements in Semiconductor Laser Technology 11/04/26, 15:51 Last updated: Published: 23/06/24, 10:39 What they are, uses, and future outlook Lasers have revolutionised many fields starting from the telecommunications, data storage to medical diagnostics and consumer electronics. And among the semiconductor laser technologies, Edge Emitting Lasers (EEL) and Vertical Cavity Surface Emitting Lasers (VCSEL) emerged as critical components due to their unique properties and performance. These lasers generate light through the recombination of electrons and holes in a semiconductor material. EELs are known for their high power and efficiency and they are extensively used in fiber optic communications and laser printing. VCSELs on the other hand are compact and are used for applications like 3D sensing. Traditionally VCSELs have struggled to match the efficiency levels of EELs however a recent breakthrough particularly in multi junction VCSEL, has demonstrated remarkable efficiency improvements which place the VCSELs to surpass EELs in various applications. This article focuses on the basics of these laser technologies and their recent advancements. EELs are a type of laser where light is emitted from the edge of the semiconductor wafer. This design contrasts with the VCSELs which emit light perpendicular to the wafer surface. EELs are known for their high power output and efficiency which makes them particularly suitable for applications that require long-distance light transmission such as fiber optic communications, laser printing and industrial machining. EELs consist of an active region where electron hole recombination occurs to produce light. This region is sandwiched between two mirrors forming a resonant optical cavity. The emitted light travels parallel to the plane of the semiconductor layers and exits from the edge of the device. This design allows EELs to achieve high gain and power output which makes them effective for transmitting light over long distances with minimal loss. VCSELs are a type of semiconductor laser that emits light perpendicular to the surface of the semiconductor wafer unlike the EELs which emit light from the edge. VCSELs have gained popularity due to their lower threshold currents and ability to form high density arrays. VCSELs consist of an active region where electron-hole recombination occurs to produce light. This region is situated between two highly reflective mirrors which forms a vertical resonant optical cavity. The light is emitted perpendicular to the wafer surface which allows for efficient vertical emission and easy integration into arrays. Recent advancements in VCSEL technology marked a significant milestone in the field of semiconductor lasers. And in particular the development of multi junction VCSEL which led to the improvements in power conversion efficiency (PCE) of the laser. Research conducted by Yao Xiao et al. and team has demonstrated the potential of a multi junction VCSELs to achieve efficiency levels which were previously thought unattainable. This research focuses on cascading multiple active regions within a single VCSEL to enhance gain and reduce threshold current which leads to higher overall efficiency. The study employed a multi-junction design where several active regions are stacked vertically within the VCSEL. This design increases the volume of the gain region and lowers the threshold current density resulting in higher efficiency. Experimental results from the study revealed that a 15-junction VCSEL achieved a PCE of 74% at room temperature when driven by nanosecond pulses. This efficiency is the highest ever reported for VCSELs and represents a significant leap forward from previous records. Simulations conducted as part of the study indicated that a 20-junction VCSEL could potentially reach a PCE exceeding 88% at room temperature. This suggests that further optimization and refinement of the multi-junction approach could yield even greater efficiencies. The implications of this research are profound for the future of VCSEL technology. Achieving such high efficiencies places VCSELs as strong competitors to EELs, particularly in applications where energy efficiency and power density are critical. The multi junction VCSELs demonstrated in the study shows promise for a wide range of applications and future works may focus on optimising the fabrication process, reducing thermal management issues and exploring new materials to further enhance performance. Integrating these high-efficiency VCSELs into commercial products could revolutionise industries reliant on laser technology. Note: latest research shows development of photonic crystal surface-emitting lasers (PCSELs) for free-space optics, offering superior power and beam quality compared to traditional VCSELs. Written by Arun Sreeraj Related articles: The future of semi-conductor manufacturing / The search for a room-temperature superconductor / Advances in mass spectrometry Project Gallery

Completing the human genome puzzle with the missing piece Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Y chromosome unveiled 04/07/25, 14:00 Last updated: Published: 07/10/23, 14:23 Completing the human genome puzzle with the missing piece A brief history of the Human Genome Project The Human Genome Project is one of the most important biomedical research projects of the 20th Century. It aimed to sequence all the human genome and DNA, and by 2003, the Human Genome Project had generated the first sequence of the human genome, accounting for over 90% of the information. By 2022, the sequence was finalised, but it only contained information about the female genome, with two X chromosomes. The Y chromosome was missing as it contains many repetitive sequences that are not transcribed to messenger RNA, making it difficult to assemble it fully. However, due to advancements in sequencing technology, a new study in 2023 published in Nature aimed to, for the first time, assemble complete sequences of multiple human Y chromosomes from 43 unrelated males around the world. Sanger DNA sequencing method DNA sequencing is a method used to determine the exact order of DNA bases (adenine, thymine, cytosine, and guanine) within a DNA molecule. Due to the aim of the Human Genome Project (to sequence all of the DNA), many methods were experimented with, leading to scientists ultimately refining, improving and using the Sanger DNA sequencing method. This method is the most accurate method for sequencing small fragments of DNA. It involves using patient DNA in a polymerase chain reaction (PCR). A mix of normal bases and chain-terminating bases is added. Chain-terminating bases stop DNA growth, creating fragments of different lengths, each ending in a terminator. The DNA fragments are separated by size through capillary gel electrophoresis. Each terminator base (adenine, thymine, cytosine, and guanine) has a different fluorescent tag. The fragments appear in order of length, and their fluorescent tags are recorded. This information is used to create a chromatograph, which is compared to a reference to identify variants, allowing DNA analysis. Analysis of the Y chromosome In 2023, a study published in Nature assembled complete sequences of multiple human Y chromosomes from 43 unrelated males around the world. The study discovered a high level of structural variation across the Y chromosomes, which was unexpected. The analysis showed a high level of diversity of the Y chromosome, and it is the beginning of the exploration of male genetic diversity. The study highlights that the information gained can be used in various fields of biomedicine, such as to gain more insight into the function and evolution of the human genome and to understand more about Y chromosome variants. This discovery can also lead to improved genetic testing accuracy and targeted treatments for personalised medicine. Written by Naoshin Haque Project Gallery