The intersection of physics and religion: the redshift and expanding galaxies Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Creatio ex Nihilo: a Christian creation doctrine including physics Last updated: 09/11/25, 20:52 Published: 20/11/25, 08:00 The intersection of physics and religion: the redshift and expanding galaxies At first glance, physics seems like a fairly straightforward field. Maths is the language that explains how everything in the universe behaves in a particular way. But the more you delve into the field, the more you realise that it actually intersects with all other fields - biology, neuroscience, philosophy, religion, etc. The example covered in this article is the creation of the universe. One of the subfields of physics is cosmology - the study of the universe, or cosmos, including its origin, development and fate. The most famous piece of modern work to come out of this field is the Big Bang theory. This is the suggestion that 13.8 billion years ago, the universe started out as a very hot, very dense point smaller than the size of an atom before it suddenly and rapidly expanded - bang! Out of this came everything. Every atom for all known and unknown things in the universe, all of the laws of time and space, literally everything came into existence in a big explosion of energy. How do we know this? Well, there is evidence of the Big Bang theory all over the universe, as far as physicists can tell. Particles flying about the universe can provide information about where they came from. For example, if we study the light from other galaxies we can see that the light is ‘red-shifted’ - meaning that as the galaxies move away from us, it shows up differently on the light spectrum then it would if it was very close. Think of it like when you drop a stone in the middle of a pond. The ripples start out very close together, but as they move away from the center they stretch out. Light does the same thing and physicists can use this to determine how celestial objects are moving, which is how we know the universe continues to expand. Such evidence not only tells us a lot about the universe as it is now, but it also allows us to theorise about the universe’s beginning. Unfortunately, this then begs the question…what caused the Big Bang? Better yet, what was there before the Big Bang? Nothing? Perhaps, but then how did everything in the universe come into being from nothing? It is questions like these that create an opportunity for other fields to join the conversation. One suggested answer to this particular question comes from the long-held Christian doctrine ‘creatio ex nihilo’, which is Latin for creation from, or out of, nothing. This concept is found in Genesis 1:1, ‘In the beginning God created the heavens and the earth.’ The suggestion is that first, there was nothing (which physics cannot prove or disprove). Then, God the Creator began the act of creation, which physics describes as the Big Bang. Physics cannot prove or disprove God as Creator either. Therefore, the argument is that the creatio ex nihilo doctrine is technically a valid possibility. Regardless of whether these theories are true or not, the topic of creation is an example of how physics works with other fields like religion or philosophy. Physics cannot necessarily answer all of the big questions, but it can certainly help provide information about the universe we live in. Written by Amber Elinsky Related article: The Anthropic Principle- Science or God? Project Gallery

Ibuprofen requires a multistep synthesis to build up to its increased complexity Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Molecular blueprints: the synthesis of ibuprofen Last updated: 26/02/26, 18:28 Published: 05/03/26, 08:00 Ibuprofen requires a multistep synthesis to build up to its increased complexity This is the second and last article in a two-part series on retrosynthesis. First article: Molecular Blueprints: The Art of Synthetic Planning . Introduction In the second article in this series on synthetic planning, the retrosynthetic techniques discussed previously are applied to the synthesis of ibuprofen. Developed by the Boots company in the 1950s and 1960s as an analogue of aspirin, ibuprofen had been taken by more than 100 million people in over 120 countries by 1985. Widely used for pain relief and as an anti-inflammatory, the chemical importance of ibuprofen cannot be overstated. Retrosynthetic analysis of ibuprofen In the previous article, all the syntheses of aspirin shown were achievable in two steps due to its relatively simple molecular structure. However, ibuprofen requires a multistep synthesis to build up to its increased complexity. A useful FGI at the outset would be to convert the carboxylic acid into a nitrile, as this group can later be readily converted back using acid and water. To build the isobutyl fragment, a Friedel–Crafts acylation could be employed, avoiding unwanted side reactions which come from Friedel–Crafts alkylation. Lastly, the resulting ketone product can be easily reduced using a Clemmensen reduction (Zn/Hg) to remove the carbonyl group altogether. Once a retrosynthetic pathway has been proposed, the next step is to identify a suitable starting material — typically something cheap and readily available. For this synthesis, a sensible starting material would be benzene. As shown in Figure 1 , the disconnection strategy targets the isobutyl portion of the side chain. To install the remaining carbon framework, a second Friedel–Crafts acylation will work nicely ( Figure 2 ). At this stage, two challenges remain. Firstly, the molecule is missing a carbon atom — this is not an issue, as the earlier retrosynthetic analysis shows the addition of a nitrile group which will extend the chain. The next question is how to convert a ketone to a nitrile group. This sequence begins with a reduction of the ketone to form a secondary alcohol using sodium borohydride (NaBH₄). Since alcohols are poor leaving groups, direct nucleophilic substitution (SN2) is not possible. Instead, an Appel reaction can be used to convert the alcohol into a halide, creating a stable leaving group. An Appel reaction proceeds via an SN2-like mechanism using triphenylphosphine (PPh₃). The reason the alcohol is now a good leaving group is due to the formation of a phosphorus–oxygen double bond, which drives the reaction forward. This now allows substitution using NaCN, after which acid and water can be added to form the final product ( Figure 3 ). Conclusion Together, the two articles in the Molecular Blueprints series highlight the power of retrosynthetic analysis in guiding organic synthesis. This technique forms the foundation for one of the most active areas of modern chemistry: total natural product synthesis. Written by Antony Lee Related article: Exploring ibuprofen Project Gallery

(LINNAEUS, 1758) Killer Whale Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Orcinus orca 25/03/26, 16:41 Last updated: Published: 06/06/23, 16:19 (LINNAEUS, 1758) Killer Whale DEFINITION & DIAGNOSIS Orcinus orca comes from the Delphinadae family (oceanic dolphins) and are the largest members of the dolphin family. The largest male orcas can grow up to 10 metres while for females, upto 8.5 metres. They have proportionately bigger dorsal fins that other big delphinids ranging between 1/10 th to 1/5 th of their body length. Orcinus orca can be easily identified by their colouration- black and white. It has also been seen that their skull is larger and holds the largest brain compared to all the other dolphins except Pseudorca crassidens (false killer whale). TAXONOMIC HISTORY Species: Orcinus orca Genus Orcinus, Family Delphinidae, Class Mammalia, Phylum Chordata, Kingdom Animalia . Synonyms : Orca ater, Orca capensis, Orcinus glacialis, Delphius gladiator, Orcinus Nannus, Orca recipinna, Delphinus orca FEATURES Killer whales are predominantly black with a white midsection mammals with a blunt head that has no distinct beak. Females usually grow to be 7m and males 8.2m. They also have large flippers which, in adult males, can measure up to 20% of their body length but in females and young males they will only achieve up to 11-13% of their body length. They also have a dorsal fin which in males can reach up to 1.8 m in length but in females it only reaches 0.9m. This difference in dorsal fin length can be useful in determining the sex of O.orca . The white midsection runs across the whole lower jaw but tightens between the flippers. This white area can be seen as more yellowish incertain oceans, mainly in the Antarctic, and more predominantly in adolescents. ANATOMY AND PHYSIOLOGY A killer whale’s skin is very smooth and the outer layer continuously sheds and behind the dorsal fin and back, there is a grey- white patch known as a ‘saddle patch’ (Figure.1). O.Orca have dorsal fins and have paddle shaped pectoral fins which help control directional movement. The skeleton of a killer whale is robust and long and has a skull, backbone and a bone structure of the pectoral flippers. In general it was seen that O.Orca’s facial anatomy was slightly different to a typical delphinid structure of an asymmetrical nasal sac but some structures were smaller compared to several other species. Their teeth are conical shaped and curved inward and backward (Figure 2). The temporal fossa is very large, showing that there is a strong temporal muscle helping with closure of the jaw. Meuth examined that the amino acid sequence of myoglobin of O.Orca had similarities to Globicephala than to other delphinids and phocoenids with myoglobin. The reniculi of the kidney of the killer whale was found to be in groups of four which are connected. Differences have been seen with Hyperoodon based on the venous return in the kidney and the O.Orca have no peripheral venous complex whilst Hyperoodon does. REPRODUCTIVE BEHAVIOUR The breeding cycles range over many months and vary depending on where the species are found. For example, in the northeast Atlantic, mating takes place between late autumn to midwinter. The approximate annual birth is between 4 to 5% and the annual pregnancy rates are roughly around 13.7 to 39.2%, and the growth spurt of an adolescent male killer whale varies within a range of 5.5 to 6.1 m, this is also the the time in which they reach sexual maturity. This was confirmed after comparing and examining two different male adolescents. The individual with 656-cm and testes masses of 3,632 g (R) and 2,270 g (L) was not sexually mature, but the individual that was 724-cm with 11,400 g (R) and 12,200 g (L) testes was sexually mature. A further examination of 57 mature males found in the Antarctic showed us that the average testis width is 22 cm and length is 55 cm. The average testis mass was calculated at 10,000 g with a maximum mass of 23,100 g. Prior to this peak, the growth curves of males are similar to that of females. The length for a female killer whale to become sexually mature ranges between 4.6 to 5.4 m. This length varies depending on whether the individual is found in the northeastern Atlantic or the Antarctic. If they are found in the Atlantic they become sexually mature around 4.6m and if they are found in the Antarctic they become sexually mature around 5.4m. The ovaries size range from 10 to 12 cm by 5 to 7 cm. The maximum size of foetuses varies geographically. The largest found in the North Pacific was 274cm, the one in North Atlantic is 255cm and 250 cm for the Antarctic. The smallest foetuses recorded are 228 cm for the North Pacific, 183cm for the North Atlantic, and 227 cm for the Southern Hemisphere . Calves are usually dependent for at least 2 years and weaning takes place when a calf grows to 4.3 m in length with lactation lasting for around 12 months . The sex ratios at birth on average looks like it is 1:1, however the ratio of males to females has been reported as 1.34:1 for the Marion Islands and 0.83:1 for the northeast Pacific. ECOLOGY O.orca are carnivores and also opportunistic feeders so their diets change seasonally and based on the region they’re in. They mainly consume fish but it has been found that they can also prey on seabirds and other marine mammals such as minke whale, squid and pinnipeds. The estimated daily food intake is thought to be around 4% of their body weight. Predation for killer whales can also determine their migration such as in the Atlantic it is dependent on the migration of herring. Although O.Orca predate on many different species’, the only predator for orcinus orca is humans. They are mainly hunted for oil and meat or killed as they are competition for fishermen. In Japan and Norway the fresh meat of killer whales is eaten and the old meat is usually used for fertilisers or for bait. To figure out the age of O.orca the teeth can be sectioned and the dentine or cementum layers can be counted but this can be hard to determine due to the presence of accessory layers as well. The estimated lifespan of killer whales is thought to be 25 years but could be as long as 35 to 40 years. Killer whales aren’t subject to many diseases but the main one they face is infection in the pulp cavity due to the wearing down of teeth. If the infection penetrates through the pulp cavity it can cause a jaw abscess. In captive killer whales the main killers are pneumonia, bacterial infections, systemic mycosis and mediastinal abscess. Written by Jeevana Thavarajah Related article: Why blue whales don't get cancer Project Gallery

The potential of MSCs to treat diseases like rheumatoid arthritis Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The role of mesenchymal stem cells (MSCs) in regenerative medicine 23/10/25, 11:18 Last updated: Published: 28/11/24, 15:16 The potential of MSCs to treat diseases like rheumatoid arthritis This is article no. 2 in a three-part series on stem cells. Next article: Regulation and policy of stem cell research . Previous article: An introduction to stem cells . Welcome to the second article in a series of three articles about stem cells. I will explore mesenchymal stem cells and their role in regenerative medicine in this article. Additionally, I will consider the potential of mesenchymal stem cells in treating three different diseases: multiple sclerosis (MS), rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). Consider reading Article 1 for more information on mesenchymal stem cells! Multiple sclerosis (MS) Multiple sclerosis (MS) is an autoimmune disease affecting the brain and spinal cord. It can cause symptoms such as muscle stiffness and spasms, problems with balance and coordination, vision problems and more. According to the Multiple Sclerosis Society UK (MS Society UK), it is estimated that there are around 150,000 people with MS in the UK, with nearly 7,100 people being newly diagnosed every year. Scientists have found that MSCs can be used to treat some of the symptoms of MS as MSCs protect the nerves in the CNS by secreting substances called neurotrophic growth factors, which increase nerve growth and the survival of nerve cells. These neurotrophic growth factors can also repair damaged nerves, improving nerve function. However, the exact mechanisms of this are still being studied. Furthermore, MSCs can activate the brain's natural healing mechanisms by stimulating the brain's stem cells to become active and repair the damaged tissue. This results in patients having a reduction in symptoms and the severity of the symptoms, improving the quality of life for those with MS. Rheumatoid arthritis (RA) Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease affecting the joints. The charity Versus Arthritis has said there are around 400,000 adults aged 16 and over affected by RA in the UK. Scientists have found that MSCs can reduce inflammation in the joints as they have immunomodulatory properties, so they can regulate the immune system's abnormal responses that cause RA. MSCs suppress immune cell activity, resulting in a decrease in inflammation and joint damage. In addition, MSCs can migrate (travel) to the inflamed joints and release anti-inflammatory molecules, reducing joint swelling and pain. This results in patients having a reduction in pain and joint swelling, improving the quality of life for those with RA. Inflammatory bowel disease (IBD) Inflammatory bowel disease (IBD) is an umbrella term for chronic inflammatory digestive diseases, including ulcerative colitis and Crohn’s disease (CD), affecting the gastrointestinal tract. A study by the University of Nottingham estimates that 500,000 people in the UK are living with IBD. Scientists have found that MSCs can reduce inflammation and increase tissue repair in the gastrointestinal tract. This is because MSCs can migrate to sites of inflammation in the gut, where they can replace damaged tissue cells. MSCs release signalling molecules that regulate the immune response and reduce inflammation. They can even directly interact with immune cells in the gut, influencing their behaviour and decreasing the inflammatory response. Also, MSCs can transfer mitochondria to damaged cells through cell fusion, helping the damaged cells function better and reduce inflammation. This results in reduced inflammation in patients, improving the quality of life for those with IBD. Looking to the future MS, RA and IBD are just three of the multiple diseases MSCs can target, and while there are many refinements to be made for MSCs to become more viable as treatment options, current findings show promising results. With further development, including more research to understand the exact biology of MSCs, there is massive potential for this method to revolutionise the treatment of various diseases, including cardiovascular diseases, liver diseases and cancer. As stem cell research continues to advance, policies must also adapt to this changing landscape; watch out for the last article in the series, where I will discuss the regulation and policy of stem cell research! Written by Naoshin Haque Related articles: The biggest innovations in the biosciences / Neuromyelitis optica and MS / Crohn's disease Project Gallery

Treatment based on the individual's genetics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Personalised medicine 10/07/25, 11:28 Last updated: Published: 29/04/24, 11:44 Treatment based on the individual's genetics In modern medicine, the concept of genetic risk factors is well understood. Certain individuals will be predisposed to disease based on their family history and DNA. Similar to how we inherit traits like eye colour from our parents, susceptibility to conditions such as diabetes or cancer can also be inherited. However, it is only recently that we have begun to understand that an individual's genetic makeup will affect not only their risk for disease but also their reaction to treatment. Understanding risk factors is crucial for diagnosing disease and implementing preventative measures to maintain a patient's health. Utilising a person’s unique DNA could provide insights into their genetic predisposition towards different health conditions, thus accelerating the diagnostic process. Giving patients the ability to make informed decisions about their health based on their genetic risk could help them prevent disease. For example, women carrying the BRCA1 gene may opt for mastectomies to reduce the risk of breast cancer later in life. Personalised medicine doesn’t only focus on risk; it can also directly influence how treatments are administered. Genomic data can indicate which medicines are most likely to be effective and whether there may be associated side effects. The Human Genome Project has made tremendous advancements in the last decade. Combining this data with medical records could provide doctors with insights into the molecular-level interactions of different drugs with individual patients. Personalised medicine in practice Cancer serves as the best example of the importance of personalised medicine. Patients have a unique combination of risk factors from their DNA and lifestyle. However, the same treatments are often offered to everyone with the same type of cancer. The specific mutations that cause a cell to become cancerous are unique to each patient. The genetic makeup of cancer cells may determine which treatment should be focused on, and this is where personalised medicine plays a critical role. An example of personalised medicine already in use is for lung cancer, particularly for cancers with mutated Epidermal Growth Factor Receptors (EGFRs). EGFRs are surface proteins involved in cell growth and division. If there is a mutation, it can result in unpredictable and uncontrollable cell proliferation. There are drugs specifically designed to treat lung cancer cells carrying this EGFR mutation, with their mechanism of action based on this. These drugs would likely be ineffective for lung cancers with different mutations, as they have different mechanisms of action. Personalised medicine tailors treatment to the genetic makeup of a person to achieve a bespoke and hopefully improved outcome. Transcriptomics, the study of RNA and its alterations instead of DNA, may be a future avenue of investigation in understanding cancer biology. Tumours can arise due to mutated RNA or abnormal transcription events, indicating that DNA is not the only genetic material relevant to oncology. There have been promising innovations in personalised vaccines tailored to each patient. Tissue from an individual is biopsied and studied, and using identified biomarkers, a custom mRNA vaccine can prime the immune system to attack cancer cells. Future potential Genetic variation in a patient’s response to drugs can significantly affect their reactions to treatment. By combining genomic data and AI technology, scientists are developing predictive algorithms to create individualised medication plans for patients, potentially eliminating the guesswork in prescriptions. Personalised precision medication holds great potential. However, the primary limitation currently lies in the cost of treatment. Medical services are stretched thin across the population, making bespoke treatments currently unfeasible. Personalised medicine is expected to improve as new genetic biomarkers are discovered and catalogued, leading to more sophisticated genomic databases over time. As sequencing technology becomes more mainstream, associated costs are likely to decrease, possibly making personalised medicine standard practice in the future. Written by Charlotte Jones Related article: mRNA vaccines Project Gallery

A life of neurology and literature Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Oliver Sacks 10/07/25, 11:26 Last updated: Published: 21/01/24, 11:54 A life of neurology and literature If I had to credit one person for introducing me to the subject that would become my career choice, it would be Oliver Sacks. Trying to develop my interests and finding myself in a world of science textbooks that sounded too complicated – and often simply pedantic – made me desperate to find something that could somehow combine my love for science and my fondness for literature. Luckily, I managed to stumble upon “the poet laureate of literature”, a physician who presented real characters with true medical cases without putting a teenage girl to sleep. Oliver Wolf Sacks was born in London in 1933. He grew up in a family of doctors; his mother was one of the first female surgeons in England and his father, a general practitioner. His interest in science started at a young age, experimenting with his home chemistry set. Following in his parents’ footsteps, he went on to study medicine at The University of Oxford before moving to the US for residency opportunities in San Francisco and Los Angeles. Although he enjoyed the sweeter life on the West Coast, by 1965 he decided to take a more permanent residence in New York, where he continued to work as a neurologist as well as eventually teaching at Columbia and NYU. It was in the city of dreams where he started his literary journey. One of his main creative inspirations was born from his time as a consultant neurologist at Beth Abraham Hospital in the Bronx. There, he found a group of patients who had been in a catatonic state due to encephalitis lethargica. They appeared frozen, trapped in their own bodies, unable to come out. Sacks decided to start a series of trials with L-Dopa, a dopamine precursor drug which was then still in the experimental stage as a treatment for Parkinson’s. Almost miraculously, some of the patients started “waking up” and regaining some movement ability. Although the treatment was not without flaws, the satisfaction of helping his patients and the close relationships he came to develop with them after caring for them for months really touched Sacks. In 1973, he published his narration of the events in Awakenings , a bestseller that was later adapted into a film of the same name starring Robin Williams and Robert de Niro. Oliver Sacks went on to write about music therapy, a rare community of colourblind individuals and his own experience both as a doctor and as a patient, among others. His most notable works are probably “The Man Who Mistook His Wife for a Hat” and “An Anthropologist on Mars”. Both describe in detail fascinating case studies, ranging from more known conditions such as Parkinson’s, epilepsy and schizophrenia, to other relatively more obscure diagnoses at the time including Tourette’s, musical hallucinations and autism. The condition that took my attention the most when reading “The Man Who Mistook His Wife for a Hat” was that which gives the book its title. The man who could not tell apart his hat from his spouse was diagnosed with agnosia: the inability to recognise objects, people or animals as a result of neurological damage along pathways connecting primary sensory areas. Agnosia can affect visual, auditory, tactile or facial recognition (prosopagnosia), or a combination of these. Crucially, Sacks’s works showcase not only a recount of symptoms and abnormalities, but a tale of people who retained their humanity and individuality beyond their medical diagnoses. As he told People magazine in 1986, he loved to discover potential in people who weren’t thought to have any. Instead of merely fitting patients into disease, he liked. To observe how they experienced the world in their unique ways, recognising difference as a path to resilience rather than just a handicap. Written by Julia Ruiz Rua Project Gallery

Setting Neuropsychiatry In a Wider Medical Context Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Schizophrenia, Inflammation and Accelerated Aging: a Complex Medical Phenotype 20/02/25, 11:54 Last updated: Published: 24/05/23, 10:45 Setting Neuropsychiatry In a Wider Medical Context In novel research by Campeau et al. (2022), the proteomic analysis of 742 proteins from the blood plasma of 54 schizophrenic participants and 51 age-matched healthy volunteers. This investigation resulted in the validation of the previously-contentious link between premature aging and schizophrenia by testing for a wide variation of proteins involved in cognitive decline, aging-related comorbidities, and biomarkers of earlier-than-average mortality. The results from this research demonstrated that age-linked changes in protein abundance occur earlier on in life in people with schizophrenia. This data also helps to explain the heightened incidence rate of age-related disorders and early all-cause death in schizophrenic people too, with protein imbalances associated with both phenomena being present in all schizophrenic age strata over age 20. This research is the result of years of medical intrigue regarding the biomedical underpinnings of schizophrenia. The comorbidities and earlier death associated with schizophrenia were focal points of research for many years, but only now have valid explanations been posed to answer the question of the presence of such phenomena. The explanation for the greater incidence rate of early death in schizophrenia was described in this study as the increased volume of certain proteins. Specifically, these included biomarkers of heart disease (Cystatin-3, Vitronectin), blood clotting abnormalities (Fibrinogen-B) and an inflammatory marker (L-Plastin). These proteins were tested for due to their inclusion in a dataset of protein biomarkers of early all-cause mortality in healthy and mentally-ill people published by Ho et al. (2018) for the Journal of the American Heart Association. Furthermore, a protein linked to degenerative cognitive deficit with age, Cystatin C, was present in increased volume in schizophrenic participants both under and over the age of 40. This explains why antipsychotics have limited effectiveness in reducing the cognitive effects of schizophrenia. In this study, schizophrenics under 40 had similar plasma protein content as the healthy over-60 strata set, including both biomarkers of cognitive decline, age-related diseases and death. Schizophrenics under-40 showed the same likelihood for incidence of the latter phenomena compared to the healthy over-60 set. These results could demonstrate the necessity for use of medications often used to treat age-related cognitive decline and mortality-linked protein abundances to treat schizophrenia. One of these options include polyethylene glycol-Cp40, a C3 inhibitor used to treat nocturnal haemoglobinuria, which could be used to ameliorate the risk of developing age-related comorbidities in schizophrenic patients. This treatment may be effective in the reduction of C3 activation, which would reduce the opsonisation (tagging of detected foreign products in blood). When overexpressed, C3 can cause the opsonisation of healthy blood cells in a process called haemolysis, which can catalyse the reduction of blood volume implicated in cardiac events and other comorbidities. However, whether or not this treatment would benefit those with schizophrenia is yet to be proven. The potential of this research to catalyse new treatment options for schizophrenia cannot be understated. Since the publication of Kilbourne et al. in 2009, the impact of cardiac comorbidities in catalysing early death in schizophrenic patients has been accepted medical dogma. The discovery of exact protein targets to reduce the incidence rate of age-linked conditions and early death in schizophrenia will allow the condition to be treated more holistically, with greater observance to the fact that schizophrenia is not only a psychiatric illness, but also a neurocognitive disorder with affiliated comorbidities that have to be prevented adequately. Written by Aimee Wilson Related articles: Genetics of ageing and longevity / Ageing and immunity / Inflammation therapy 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

The advent of recent technology has driven a surge in the use of the REEs Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Looking at the rare earth elements Last updated: 23/02/26, 21:36 Published: 26/02/26, 08:00 The advent of recent technology has driven a surge in the use of the REEs Introduction President Trump said in reference to a proposed minerals deal with Ukraine: We're telling Ukraine they have very valuable rare earths. Over the past few decades, the technological revolution has expanded the applications of the rare earth elements (REEs) from modern electronics to renewable energy sources. Despite the name, the REEs are relatively abundant in the Earth's crust, but their perceived scarcity is centred around difficulties in extracting and processing. As REE refining is currently monopolised by China, access to these materials is a constant source of geopolitical tension. The REEs comprise the lanthanide series as well as scandium (Sc) and yttrium (Y), and are characterised by the similarity of their chemical properties. Therefore, this article aims to introduce some of the fundamental chemistry of the rare earth elements to contextualise their role in modern technologies. Chemical properties of the REEs Scandium and yttrium are considered “honorary lanthanides,” as they form highly ionic, charge‑dense +3 cations when ionised. However, as they are transition metals, their properties cannot be explained by considering the f‑orbitals. The f‑orbitals are a set of seven orbitals which can hold a maximum of 14 electrons. For the lanthanides, each element has a set of 4f and 6s valence orbitals, with cerium (Ce),lanthanum (La), gadolinium (Gd), and lutetium (Lu) also having an occupied 5d¹ orbital. The 4f orbitals are generally contracted because of the nuclear charge felt by the electrons in these orbitals. As the atomic radius across the period decreases, this contraction is felt more strongly, meaning the resulting ions become more charge‑dense. This phenomenon is known as the lanthanide contraction. The contracted nature of the 4f orbitals explains why the lanthanides preferentially adopt a +3 oxidation state (O.S). The 4f electrons are strongly attracted to the nucleus, making them energetically unfavourable to remove. Therefore, once the two 6s electrons and one 4f (or sometimes 5d) electron are removed, further ionisation becomes much more difficult. This is reflected by the ionisation potentials of the lanthanides ( Figure 1 ). However, some lanthanides can form stable +2 O.S (samarium (Sm), europium (Eu), and ytterbium (Yb)), while Ce can form a +4 O.S ( Figure 2 ). This is because of the electronic configurations of these elements. For example, Eu has an electronic configuration of [Xe] 4f⁷ 6s²; therefore, by removing two electrons, the ion becomes exchange‑energy stabilised (Eu²⁺ [Xe] 4f⁷). Another notable property of the lanthanides is their large magnetic moments. This again is a consequence of the 4f orbitals. Magnetism is determined by the number of unpaired electrons an element has and its orbital angular momentum. Orbital angular momentum is an intrinsic property and becomes more prevalent with larger elements. Therefore, as the 4f orbitals can hold up to seven unpaired electrons, coupled with the intrinsic heaviness of the lanthanides, they often exhibit strong magnetic behaviour. Applications Catalytic Converters As previously mentioned, most lanthanides preferentially adopt a +3 O.S, Ce being a key exception due to its ability to cycle between +3 and +4. This property makes Ce particularly valuable in catalytic converters — vehicle exhaust devices which help reduce emissions of toxic pollutants such as carbon monoxide (CO) and nitric oxide (NO). Using CeO₂ as a catalyst, CO₂ and N₂ are generated as less harmful by‑products ( Figure 2 ). Chemical Reagents The redox flexibility of certain lanthanides is also exploited in organic chemistry. Ce(IV) and Sm(II) compounds serve as effective oxidising and reducing agents respectively. Reagents such as ceric ammonium nitrate (CAN) and cerium ammonium sulphate (CAS) are frequently used as selective oxidants, while samarium bromide (SmBr₂) is an effective reductant. MRI & Chiral Shift Reagents The magnetic properties of the lanthanides can be exploited in medical imaging, particularly in magnetic resonance imaging (MRI). Prior to an MRI scan, patients may be injected with a gadolinium (Gd³⁺) complex, such as [Gd(DTPA)]²⁻ ( Figure 4 ), to enhance image contrast. By coordinating water molecules and increasing the proton relaxation rate, these complexes cause certain regions of tissue to appear brighter and more easily distinguishable. Chemically, this principle is utilised when NMR spectroscopy is conducted in the laboratory. Fundamentally, MRI and NMR machines work in the same way, so by adding small quantities of paramagnetic lanthanide reagents to a proton NMR sample, changes in the chemical shift can be induced. These “lanthanide shift reagents” increase the proton relaxation rate, which reduces signal overlap and allows specific proton environments to be more easily identified. Commonly used lanthanide reagents include Eu³⁺ and Pr³⁺ complexes. Conclusion In conclusion, the advent of recent technology has driven a surge in the use of the REEs. While chemically similar, each element has a broad range of diverse applications, whether as magnets, reagents, or even phosphors in TV sets. Certain to dominate geopolitics for the foreseeable future, understanding the chemistry and applications of the REEs has never been more important. Written by Antony Lee Project Gallery

Symmetry in spectroscopy, reaction mechanisms and bonding Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The importance of symmetry in chemistry Last updated: 02/04/26, 18:25 Published: 08/01/26, 08:00 Symmetry in spectroscopy, reaction mechanisms and bonding Introduction Symmetry is everywhere- in snowflakes, flowers and even art. Chemistry is no different and the symmetrical properties of a molecule often dictate its behaviour. From interpreting spectra, to predicting reaction pathways and understanding bonding, symmetry shapes all chemical disciplines. 1. Symmetry in spectroscopy Firstly, understanding the symmetry of molecules is essential in a range of characterisation techniques. In 1 H NMR spectroscopy, the number of peaks seen in a spectrum correspond to the number of unique chemical environments. For example, dibenzylidene acetone has a plane of symmetry and a rotational axis (C 2 ) through the centre of the carbonyl. This explains why the spectrum only has 5 different proton environments. In IR spectroscopy, infrared radiation is absorbed by a molecule causing stretching and bending of bonds when they vibrate. The total number of vibrational modes can be predicted using: • 3N – 5 rule for linear molecules • 3N – 6 rule for non-linear molecules (where N = no. of atoms) However, only vibrations which cause a change in dipole moment are seen in IR spectra. This explains why CO 2 only shows 3 main absorption peaks, despite having 4 vibrational modes. 2. Symmetry in reaction mechanisms Considering the symmetry of molecules also helps chemists predict the stereochemical outcome of organic reactions. A common example is the E2 elimination of a halogenoalkane, where an alkene is formed via elimination of a halogen. For an E2 elimination to occur, the H and the leaving group must be 180 ° from each other, in an ‘anti-periplanar’ conformation. To predict which groups, have this relationship, Newman projections are used to easily assign and rotate bonds. A Newman projection is a perspective of a molecule, typically by imagining you are looking down a specific C-C bond. See Figure 3 . 3. Symmetry in bonding Lastly, considering the symmetry of a molecule is vital for understanding Molecular Orbital (MO) Theory. MO theory explains how covalent bonding occurs by considering the symmetry elements of the valence orbitals. For example, in H 2 , the two valence 1s orbitals are completely symmetric and therefore can overlap effectively to form a σ molecular orbital. However, in HF, the introduction of 2p orbitals means the shape and symmetry has changed. The 2p x and 2p y orbitals can no longer overlap with the 1s H orbital as their symmetries are incompatible. Using this information, a MO diagram can be constructed to show how the orbitals combine, explaining why H 2 has a single bond. In essence, symmetry determines which orbitals can ‘match up’ to form bonds. See Figure 4 . Conclusion Symmetry influences every aspect of chemistry and is frequently employed to rationalise observed molecular characteristics. While sometimes overlooked, considering the symmetry of a molecule underpins any chemistry undertaken across industry and academia. If you enjoyed this article, future articles could build on this topic by introducing Group Theory and showing how you can predict an entire vibrational spectrum, or the molecular geometry of a compound based entirely on its symmetry. Written by Antony Lee Related article: Diels-Alder reaction REFERENCES S. Civis, M. Ferus, A. Knizek, in The Chemistry of CO 2 and TiO 2 : From Breathing Minerals to Life on Mars, ed. S. Civis, M. Ferus, A. Knizek, Springer Nature, Switzerland, 1 st edn., 2019, vol. 1, ch. 1, pp. 1-7 A. Burrows, J. Holman, S. Lancatser, T. Overton, A. Parsons, G. Pilling, G. Price, in Chemistry 3 , Oxford University Press, Oxford, 3 rd edn., 2017, ch.4, pp. 172-219 Project Gallery