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  • STEM book reviews | Scientia News

    An extensive collection of insightful reviews on the best STEM books available. Whether you're a student looking to deepen your knowledge or something to aid your revision and research, an educator seeking great resources for your classroom, or simply a curious mind passionate about science, technology, engineering, mathematics, medicine and more, you'll find something here to inspire and inform you.  Discover Your Next Great Read Deep Dive into STEM Books Here you can explore an extensive collection of insightful reviews on the best STEM books available. Whether you're a student looking to deepen your knowledge or something to aid your revision and research, an educator seeking great resources for your classroom, or simply a curious mind passionate about science, technology, engineering, mathematics, medicine and more, you'll find something here to inspire and inform you. Our Curated Selections: Intern Blues by Robert Marion, M.D. The Emperor of All Maladies by Siddhartha Mukherjee

  • Investigating the interplay of hormones and the microbiome | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Investigating the interplay of hormones and the microbiome 07/02/25, 16:23 Last updated: 08/11/24, 12:00 Published: Known as microbial endocrinology, it is a complex field The microbiome The human body hosts a vast ecosystem of bacteria, with trillions crawling on our skin, colonising our gut, and living throughout our bodies. Most of these microbes serve to protect us against infections influencing our metabolism and even our behaviour. However, scientists have started to question the mechanisms by which these bacteria affect our bodily functions and characteristics. Scientists have studied these communities of microorganisms residing within our bodies and the genes they contain, yielding new and exciting perspectives… …Welcome to the human microbiome. The microbiome is the dynamic community of microorganisms (like fungi, bacteria and viruses) that exist in a particular environment. In humans, the term is most often used to describe the collection of microorganisms that inhabit a particular body area, such as the gastrointestinal tract, mouth or skin. While a person’s core microbiome is established within the first few years of life, its composition can shift over time in response to factors like medication, such as potent antibiotics and environmental factors. Researchers have uncovered that the gastrointestinal microbiota can influence some physiological processes, including a direct line of communication between the gut and the brain. But what facilitates this dialogue? What mechanisms enable the gut to relay signals to the brain? The answer is hormones. Hormones and the endocrine system The endocrine system is a network of glands that produce and release chemical messengers known as hormones. They travel via the bloodstream and bind to specific receptors on their target tissues. This binding of hormones to their receptors triggers a response in the target tissue. For instance, during stressful situations, epinephrine (also known as adrenaline) is produced by the adrenal medulla, the inner region of the adrenal glands. This hormone, released into the bloodstream, acts on target tissues such as the heart, where it increases heart rate. Hormones regulate most of the body’s vital functions through their release. Some of these crucial processes include growth, metabolism, and reproduction. In the following sections, however, we specifically focus on how hormones influence the microbiome. The interactions between hormones and the microbiome Exploring the relationship between hormones and the microbiome is known as microbial endocrinology; it is a complex field because there are numerous interactions to account for, and the effects of each one can have lasting impacts on human physiology. For example, epinephrine and norepinephrine can lead to more bacteria, notably E. coli and Pseudomonas aeruginosa , signifying that imbalance could harm humans. Also, parts of the host, ranging from mood to gender, impact hormones, bacterial presence and activity ( Figure 3 ). An emerging area of microbial endocrinology is how the microbiome and sex hormones engage with each other in disease and female health. One paper noted that disorders from metabolic syndrome (MetS) to type 2 diabetes (T2D) have distinctions in the levels of sex hormones and gut microbiota, indicating that they are essential to understanding in developing those conditions. The influence of gut microbiota on sex hormones can occur through various mechanisms, such as bacteria controlling the activity and expression of endocrine receptors and even bacteria metabolising sex hormones; this knowledge can help create treatments against polycystic ovarian syndrome and ovarian cancer, among other diseases that usually impact females due to gut microbiome imbalances ( Figure 4 ). Another part of microbial endocrinology being researched is how the microbiome impacts human growth. In one study involving adult male mice, decreased growth hormone (GH) led to undeveloped microbiomes, while surplus GH was linked to an expanded microbiome; this depicts that bacteria influences development via the growth hormone-insulin-like growth factor 1 (GH-IGF-1) axis; maintaining a steady dynamic between the microbiome and this axis is vital for development ( Figure 5 ), particularly in children. In puberty, hormones and the gut microbiome interact, as observed in obesity and precocious puberty. Hence, a deeper awareness of the bacteria and sex hormones during puberty is crucial to designing targeted medicines for growth disorders. Moreover, patients with GH-secreting pituitary adenoma (GHPA) have modified gut microbiota, like increased Alistipes shahii and Odoribacter splanchnicus . Still, more research is needed to investigate this. Conclusion The microbiome refers to the millions of microorganisms on and within the human body that influence various physiological functions ranging from digesting food to outcompeting pathogens for resources. Also, the microbiome can affect the endocrine system, which consists of hormones that control glucose and reproduction, among other processes. This bridge, known as microbial endocrinology, has critical applications for understanding women’s health and growth disorders; this emerging area is growing, so it can address knowledge gaps in diseases like cancer and even improve other medical treatments. Written by Sam Jarada and Fozia Hassan The interactions between hormones and the microbiome, and Conclusion sections by Sam The microbiome, and Hormones and the endocrine system sections by Fozia Related articles: The gut microbiome / Dopamine and the gut / The power of probiotics / Vitamins REFERENCES “The Human Microbiome and Its Impacts on Health - PWOnlyIAS.” PWOnlyIAS , 18 Jan. 2024, pwonlyias.com/current-affairs/gut-microbiome-and-health/ . Accessed 17 Oct. 2024. Mittal, Rahul, et al. “Neurotransmitters: The Critical Modulators Regulating Gut-Brain Axis.” Journal of Cellular Physiology , vol. 232, no. 9, 10 Apr. 2017, pp. 2359–2372, www.ncbi.nlm.nih.gov/pmc/articles/PMC5772764/ , https://doi.org/10.1002/jcp.25518 . Accessed 17 Oct. 2024. Neuman, Hadar, et al. “Microbial Endocrinology: The Interplay between the Microbiota and the Endocrine System.” FEMS Microbiology Reviews , vol. 39, no. 4, 1 July 2015, pp. 509–521, academic.oup.com/femsre/article/39/4/509/2467625 , https://doi.org/10.1093/femsre/fuu010 . Hiller-Sturmhöfel S, Bartke A. The Endocrine System: An Overview. Alcohol Health and Research World. 2024;22(3):153. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC6761896/ Neuman H, Debelius JW, Knight R, Koren O. Microbial endocrinology: the interplay between the microbiota and the endocrine system. FEMS Microbiology Reviews [Internet]. 2015 Feb 19 [cited 2024 Sep 18];39(4):509–21. Available from: https://academic.oup.com/femsre/article/39/4/509/2467625?login=false Jose Antonio Santos-Marcos, Mora-Ortiz M, Tena-Sempere M, José López-Miranda, Camargo A. Interaction between gut microbiota and sex hormones and their relation to sexual dimorphism in metabolic diseases. Biology of Sex Differences. 2023 Feb 7;14(1). He S, Li H, Yu Z, Zhang F, Liang S, Liu H, et al. The Gut Microbiome and Sex Hormone-Related Diseases. Frontiers in Microbiology. 2021 Sep 28;12. Siddiqui R, Makhlouf Z, Alharbi AM, Alfahemi H, Khan NA. The Gut Microbiome and Female Health. Biology [Internet]. 2022 Nov 1;11(11):1683. Available from: https://www.mdpi.com/2079-7737/11/11/1683 Jensen E, Young JA, Jackson Z, Busken J, List EO, Ronan O’Carroll, et al. Growth Hormone Deficiency and Excess Alter the Gut Microbiome in Adult Male Mice. Endocrinology [Internet]. 2020 Feb 26 [cited 2023 Nov 9];161(4). Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7341558/ Jensen EA, Young JA, Mathes SC, List EO, Carroll RK, Kuhn J, et al. Crosstalk between the growth hormone/insulin-like growth factor-1 axis and the gut microbiome: A new frontier for microbial endocrinology. Growth Hormone & IGF Research. 2020 Aug;53-54:101333. Huang C, Meng D, Li Y, Lu S, Yang W, Wu B, et al. Gut microbiota composition alteration analysis and functional categorization in children with growth hormone deficiency. Frontiers in Pediatrics. 2023 Feb 24;11. Calcaterra V, Rossi V, Massini G, Regalbuto C, Hruby C, Panelli S, et al. Precocious puberty and microbiota: The role of the sex hormone–gut microbiome axis. Frontiers in Endocrinology. 2022 Oct 21;13. Lin B, Wang M, Gao R, Ye Z, Yu Y, He W, et al. Characteristics of Gut Microbiota in Patients with GH-Secreting Pituitary Adenoma. Microbiology Spectrum [Internet]. 2022 Feb 23 [cited 2023 Aug 7];10(1):e0042521. Available from: https://pubmed.ncbi.nlm.nih.gov/35019688/ Project Gallery

  • Iron deficiency anaemia | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Iron deficiency anaemia 07/02/25, 16:23 Last updated: 27/06/23, 17:10 Published: A type of anaemia This article is no. 2 of the anaemia series. Next article: anaemia of chronic disease . Previous article: Anaemia . Aetiology Iron deficiency anaemia (IDA) is the most frequent in children due to rapid growth (adolescence) and poor diets (infants), and in peri and post -menopausal women due to rapid growth (pregnancy) and underlying conditions. Anaemia typically presents, in around 50% of cases as headache, lethargy and pallor depending on the severity. Less common side effects include organomegaly and Pica which occurs in patients with zinc and iron deficiency and is defined by the eating of things with little to no nutritional value. Pathophysiology Iron is primarily sourced through diet, as haem (Fe2+) and non-haem iron (Fe3+). Fe2+ is sourced through meat, fish, and other animal-based products, Fe2+ can be absorbed directly through the enterocyte via the haem carrier protein1 (HCP1). Fe3+ is less easily absorbed and is mostly found in plant-based products. Fe3+ must be reduced and transported through the duodenum by the enzyme duodenal cytochrome B (DcytB) and the divalent metal transporter 1 (DMT1), respectively. Diagnosis As with any diagnosis, the first test to run would be a full blood count and this will occur with all the anaemias. In suspected cases of anaemia, the Haemoglobin (Hb) levels would be lower than 130 in males and 120 in females. The mean cell volume (MCV) is a starting point for pinpointing the type of anaemia, for microcytic anaemias you would expect to see an MCV < 80. Iron studies are best for diagnosing anaemias, for IDA you would expect most of the results to be low. A patient with IDA has little to no available iron so the body would halt the mechanism’s for storing iron. As ferratin is directly related to storage, low ferratin can be a lone diagnostic of IDA. Total iron-binding capacity (TIBC) would be expected to be raised, as transferrin transports iron throughout the body, the higher it is the more iron it would be capable of binding to. Elliptocytes (tear drop) are elongated RBC, often described as pencil like in structure and are regularly seen in IDA and other anaemias. Typically, one would see hypochromic RBC as they contain less Hb than normal cells, the Hb is what gives red cells their pigment. It’s not uncommon to see other changes in RBC such as target cells, given their name due to the bullseye appearance. Target cells are frequently seen in cases with blood loss. Summary IDA is the most frequent anaemia affecting patients of all age ranges and usually presents with lethargy and headaches. Dietary iron from animal derivatives are the most efficient source of iron uptake. Diagnosis of IDA is through iron studies, red cell morphological investigations alongside clinical presentation, to rule out other causes. Written by Lauren Kelly Project Gallery

  • Immune signals initiated by chromosomal instability lead to metastasis | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Immune signals initiated by chromosomal instability lead to metastasis 07/02/25, 16:21 Last updated: 14/09/24, 21:17 Published: Non-cell-autonomous cancer progression from chromosomal instability Unravelling the intricate relationship between immune cells and cancer cells through STING pathway rewiring. Introduction Chromosomal instability ( CIN ) has long been recognised as a prominent feature of advanced cancers. However, recent research has shed light on the intricate connection between CIN and the STING (Stimulator of Interferon Genes) pathway. Researchers at Memorial Sloan Kettering Cancer Center (MSK) and Weill Cornell Medicine conducted this ground-breaking study, which has provided fascinating insights into the function of the immune system and its interactions with cancer cells. In this article, we will delve into the findings of this study and explore the implications for future cancer treatments. STING pathway The STING pathway plays a crucial role in the response to cellular stress and the innate immunity response to DNA damage and chromosomal instability. Chromosomal instability refers to the increased rate of chromosomal aberrations, such as mutations, rearrangements, and aneuploidy, within a cell population. This instability can lead to genomic alterations that contribute to the initiation and evolution of cancer. This pathway is activated when the presence of cytosolic DNA is detected, which can be indicative of cellular damage or infection, triggering a cascade of signalling events leading to the production of type I interferons and other inflammatory cytokines. Many recent studies have revealed an intriguing relationship between chromosomal instability and the STING pathway, including the STING pathway’s ability to be activated by the accumulation of micronuclei resulting from chromosomal instability in cancer cells. This activation can lead to the promotion of anti-tumour immunity and the suppression of tumourigenesis. The Promise and Limitations of STING Agonist Drugs STING-agonist drugs have shown great potential in preclinical studies, arousing optimism for their use in cancer therapy. However, clinical trials have yielded disappointing results, with low response rates observed in patients. Dr. Samuel Bakhoum, an assistant member at MSK, highlights the discrepancy between lab findings and clinical outcomes. Only a small fraction of patients demonstrated a partial response, leading researchers to question the underlying reasons for this disparity. The Sinister Cooperation: CIN and Immune Cells Chromosomal instability acts as a driver for cancer metastasis, enabling cancer cells to spread throughout the body. The STING pathway, specifically, is where Dr. Bakhoum's team discovered that the immune system has a significant impact on this process. The cooperation between cancer cells with CIN and immune cells is orchestrated by STING, resulting in a pro-metastatic tumour microenvironment. This finding provides a crucial understanding of why STING-agonist drugs have not been effective in clinical trials. Introducing Contact Tracing: Unravelling Cell-to-Cell Interactions Researchers utilised a newly developed tool called ContactTracing to examine cell-to-cell interactions and cellular responses within growing tumours. By analysing single-cell transcriptomic data, they gained valuable insights into the effects of CIN and STING activation. The tool's capabilities allowed them to identify patients who could still mount a robust response to STING activation, enabling the selection of better candidates for STING agonist therapy. STING Inhibition: A Potential Solution Interestingly, the study suggests that patients with high levels of CIN may actually benefit from STING inhibition rather than activation. Treatment of study mice with STING inhibitors successfully reduced metastasis in models of melanoma, breast, and colorectal cancer. These findings open up new possibilities for personalised medicine, where patients can be stratified based on their tumour's response. By identifying the subset of patients whose tumours can still mount a strong response to STING activation, doctors could select better candidates for STING agonists. This biomarker-based approach could help figure out which patients would benefit from turning on STING and which would benefit from turning it off. This could lead to more targeted and effective treatments for people with advanced cancer that is caused by chromosomal instability. Conclusion Based on the research findings, it can be concluded that chronic activation of the STING pathway, induced by CIN, promotes changes in cellular signalling that hinder anti-tumour immunity and facilitate cancer metastasis. This rewiring of downstream signalling ultimately renders STING-agonist drugs ineffective in advanced cancer patients. However, the study also suggests that STING inhibitors may benefit these patients by reducing chromosomal instability-driven metastasis. The research highlights the importance of identifying biomarkers to determine which patients would benefit from STING activation or inhibition. Overall, these findings provide valuable insights into the underlying mechanisms of cancer progression and offer potential opportunities for improved treatment strategies for patients with advanced cancer. The study shown in figure 1, analysed 39,234 single cells within the tumour microenvironment (TME), categorised by cell subtype assignment. It showed that tumour cell rates of CIN were genetically dialled-up or dialled-down. The study also showed CIN-dependent effects on differential abundance at the neighbourhood level, grouped by cell subtype and ranked by mean log2 (FC) within each cell subtype. Node opacity was scaled by the p-value. Written by Sara Maria Majernikova Related articles: Cancer immunologist Polly Matzinger / The Hippo signalling pathway Reference: Li, J., Hubisz, M.J., Earlie, E.M. et al. Non-cell-autonomous cancer progression from chromosomal instability. Nature 620 , 1080–1088 (2023). https://doi.org/10.1038/s41586-023-06464-z Project Gallery

  • STEM research and resources for students | Scientia News

    Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and the other sciences. Log In Welcome to Scientia News DELIVERING INFORMATIVE CONTENT Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and other sciences. We hope this platform helps you discover something that inspires your curiosity, and encourages you to learn more about important topics in STEM. Meet the Official Team NAVIGATE AND CLICK THE PHOTOS BELOW TO LEARN MORE ABOUT US! To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. Latest Articles The role of mesenchymal stem cells (MSCs) in regenerative medicine View More Beavers are back in Britain, ‘wood’ you like to know why? View More The exciting potential of mRNA vaccines View More Investigating the interplay of hormones and the microbiome View More CONTACT CONTACT US Scientia News welcomes anyone who wants to share their ideas and write for our platform. If you are interested in writing for us AND live in the UK; and/ or would like to share any ideas or feedback: Email us at scientianewsorg@gmail.com or fill in our form below and we'll get in touch ... Follow us on our socials for the latest updates. Comment, like and share! Join our mailing list below for latest site content. You can also sign up to become a site member . SUBSCRIPTION Join our mailing list to receive alerts for new articles and other site content. Be sure to check your spam/ junk folders in case emails are sent there. Email Subscribe GET IN TOUCH First Name Last Name Email Message Send Thanks for submitting!

  • Mechanisms of pathogen evasion | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Mechanisms of pathogen evasion 07/02/25, 16:25 Last updated: 05/09/24, 10:54 Published: Ways in which pathogens avoid being detected by the immune system Introduction Pathogens such as bacteria and viruses have evolved strategies to deceive and outsmart the immune system's defences. From hiding within cells to avoiding immune detection to blocking signals crucial for immune function, pathogens have developed an array of tactics to stay one step ahead of the immune system. This article introduces some key strategies pathogens employ to evade the immune system. Antigenic variation The influenza virus is a persistent and challenging pathogen to treat because it employs a clever strategy known as antigenic variation to evade the immune system. Antigenic variation is the pathogen’s ability to alter the proteins on its surface (antigens), particularly hemagglutinin (HA) and neuraminidase (NA), which are the primary targets of the immune system. As the virus conceals itself, it is no longer recognised and attacked by the host's defences. But how do the surface antigens change? This occurs through two primary mechanisms: antigenic drift and antigenic shift. The former process involves gradual changes in the virus's surface proteins by progressive accumulation of genetic mutations. Meanwhile, the latter requires a slightly different explanation. Antigenic shift is an abrupt process. It occurs when two influenza virus strains infect the same host cell and exchange genetic material. The exchange can lead to a new hybrid strain. This hybrid strain usually presents a new combination of surface proteins. It is a more abrupt process, and because the immune system lacks prior exposure to these new proteins, it fails to clear the viral pathogen. Antigenic shifts can lead to the emergence of strains to which the population has little to no pre-existing immunity. Some examples are the 1968 Hong Kong flu and the 2009 swine flu pandemic. Variable serotypes- Streptococcus pneumoniae When the host encounters a pathogen, the body creates antibodies against specific proteins on the pathogen's surface, ensuring long-term immunity. However, some species of pathogens evade this protection by evolving different strains. These strains involve multiple serotypes, each defined by distinct variations in the structure of their capsular polysaccharides. This variability allows them to infect the same host repeatedly, as immunity to one serotype does not confer protection against other serotypes. A perfect example of such a pathogen is the pneumonia-causing bacterium, Streptococcus pneumoniae , which has more than 90 strains. After successful infection with a particular S. pneumoniae serotype, a person will have devised antibodies that prevent reinfection with that specific serotype. However, these antibodies do not prevent an initial infection with another serotype, as illustrated in Figure 1 . Therefore, by evading the immune response, a new primary immune response is required to clear the infection. Latency- chicken pox & Human Immunodeficiency Virus (HIV) Pathogens can cleverly persist in the host by entering a dormant state where they are metabolically inactive. In this state, they are invisible to the immune system. Human Immunodeficiency Virus is well known for its use of HIV latent reservoirs. These reservoirs, consisting of metabolically inactive T-cells infected with HIV, can exist for years on end. When the host becomes immunocompromised at any stage in life, the T-cells in these reservoirs are suddenly activated to renew HIV production. The Varicella-Zoster Virus (VZV) is responsible for causing varicella (chickenpox) and zoster (shingles). Similarly, this virus can remain latent in the host to evade immune detection. VZV establishes latency in sensory ganglia, particularly in neurons. Since neurons are relatively immune-privileged sites, they are less accessible to immune surveillance mechanisms. This provides a safe haven from immune detection. When the host is immunocompromised, the virus reactivates. This renewed viral activity results in the production of viral particles which travel along the sensory nerve fibres towards mucous membranes. When the virus reaches the skin, it causes an inflammatory response. This results in painful vesicular skin lesions, commonly known as shingles (herpes zoster). Conclusion Pathogens employ diverse mechanisms to evade the host immune system, ensuring their survival and propagation through host cells. These evasion mechanisms can hinder the development of treatments for certain infectious diseases. For instance, the diversity in Strep A serotypes challenges vaccine development because immunity to one serotype may not confer protection against another. Additionally, the influenza virus constantly evolves via antigenic variation, always one step ahead of the immune system. The strategies employed by pathogens to evade the immune system are as diverse as they are sophisticated. Scientists continue to study these mechanisms, paving the way for developing more effective vaccines, treatments, and public health strategies to out-manoeuvre these organisms. We can better protect human health by staying one step ahead of pathogen evolution. Written by Fozia Hassan Related article: Allergies REFERENCES Abendroth, Allison, et al. “Varicella Zoster Virus Immune Evasion Strategies.” Current Topics in Microbiology and Immunology , 2010, pp. 155–171, www.ncbi.nlm.nih.gov/pmc/articles/PMC3936337/ , https://doi.org/10.1007/82_2010_41 . Accessed 24 July 2024. Gougeon, M-L. “To Kill or Be Killed: How HIV Exhausts the Immune System.” Cell Death & Differentiation , vol. 12, no. S1, 15 Apr. 2005, pp. 845–854, www.nature.com/articles/4401616 , https://doi.org/10.1038/sj.cdd.4401616 . Accessed 24 July 2024. Parham, Peter. The Immune System . 5th ed., New York, Garland Science, 2015, read.kortext.com/reader/epub/1743564 . Accessed 24 July 2024. Shaffer, Catherine. “How HIV Evades the Immune System.” News-Medical.net , 21 Feb. 2018, www.news-medical.net/life-sciences/How-HIV-Evades-the-Immune-System.aspx . Accessed 24 July 2024. Project Gallery

  • Why South Asian genes remember famine | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why South Asian genes remember famine Last updated: 27/01/25, 17:06 Published: 23/01/25, 08:00 Famine-induced epigenetic changes and public health strategies in affected populations Our genes are often thought of as a fixed blueprint, but what if our environment could change how they work? This is the intriguing idea behind epigenetics—a field that shows how our environment, combined with the body’s adaptive responses for survival, can influence gene expression without altering our DNA. In South Asia, famines such as the infamous Bengal Famine of 1943 caused immense suffering, and these hardships may have triggered genetic changes that continue to affect generations. Today, South Asians face an increased risk of developing Type 2 diabetes by age 25, whereas White Europeans generally encounter this risk around age 40. What is driving this difference in risk? This article will explore the science behind these epigenetic changes, their impact on the descendants of famine survivors and how these insights can shape public health, policy, and research. The legacy of historical famines In 1943, the Bengal Famine claimed around 3 million lives. Nobel laureate Amartya Sen argues that the severity of the famine was not merely a result of prior natural disasters and disease outbreaks in crops. Instead, it was primarily driven by wartime inflation, speculative buying, and panic hoarding, which disrupted food distribution across the Bengal region. Consequently, for the average Bengali citizen, death from starvation, disease, and malnutrition became widespread and inevitable. The impact of the famine extended well beyond the immediate loss of life. Dr Mubin Syed, a radiologist specialising in vascular and obesity medicine, emphasises that these famines have left a lasting mark on the health of future generations. Dr Syed explains that South Asians, having endured numerous famines, have inherited "starvation-adapted" traits. These traits are characterised by increased fat storage. As a result, the risk of cardiovascular diseases, diabetes, and obesity is heightened in their descendants. This tendency towards fat storage is believed to be closely tied to epigenetic factors, which play a crucial role in how these traits are passed down through generations. Epigenetic mechanisms and their impact These inherited traits are shaped by complex epigenetic mechanisms, which regulate gene expression in response to environmental stressors like famines without altering the underlying DNA sequence. DNA methylation, a process involving the addition of small chemical groups to DNA, plays a crucial role in regulating gene expression. When a gene is 'on,' it is actively transcribed into messenger RNA (mRNA), resulting in the synthesis of proteins such as enzymes that regulate energy metabolism or hormones like insulin that manage blood sugar levels. Conversely, when a gene is 'off,' it is not transcribed, leading to a deficiency of these essential proteins. During periods of famine, increased DNA methylation can enhance the body's ability to conserve and store energy by altering the activity of metabolism-related genes. Epigenetic inheritance, a phenomenon where some epigenetic tags escape the usual reprogramming process and persist across generations, plays a crucial role in how famine-induced traits are passed down. Typically, reproductive cells undergo a reprogramming phase where most epigenetic tags are erased to reset the genetic blueprint. However, certain DNA methylation patterns can evade this erasure and remain attached to specific genes in the germ cells, the cells that develop into sperm and egg cells. These persistent modifications can influence gene expression in the next generation, affecting metabolic traits and responses to environmental stressors. This means the metabolic adaptations seen in famine survivors, such as increased fat storage and altered hormone levels, can be transmitted to their descendants, predisposing them to similar health risks. Research has highlighted how these inherited traits manifest in distinct hormone profiles across different ethnic groups. A study published in Diabetes Care found that South Asians had higher leptin levels (11.82 ng/mL) and lower adiponectin levels (9.35 µg/mL) compared to Europeans, whose leptin levels were 9.21 ng/mL and adiponectin levels were 12.96 µg/mL. Leptin, encoded by the LEP gene, is a hormone that reduces appetite and encourages fat storage. Adiponectin, encoded by the ADIPOQ gene, improves insulin sensitivity and supports fat metabolism. Epigenetic changes, such as DNA methylation, in the LEP and ADIPOQ genes have led to these imbalances, which were advantageous for South Asian populations during times of famine. Elevated leptin levels helped ensure the body could maintain energy reserves for survival, while lower adiponectin levels slowed fat breakdown, preserving stored fat for future use. This energy-conservation mechanism allowed individuals to endure long periods of food scarcity. Remarkably, these epigenetic changes can be passed down to subsequent generations. As a result, descendants continue to exhibit these metabolic traits, even in the absence of famine conditions. This inherited imbalance—higher leptin levels and lower adiponectin—leads to a higher predisposition to metabolic disorders. Increased leptin levels can cause leptin resistance, where the body no longer responds properly to leptin’s signals, driving overeating and fat accumulation. Simultaneously, reduced adiponectin weakens the body’s ability to regulate insulin and break down fats efficiently, resulting in higher blood sugar levels and greater fat storage. These combined effects heighten the risk of obesity and Type 2 diabetes in South Asian populations today. Integrating cultural awareness in health strategies Understanding famine-induced epigenetic changes provides a compelling case for rethinking public health strategies in affected populations. While current medicine cannot reverse famine-induced epigenetic changes in South Asians, culturally tailored interventions and preventive measures are crucial to reducing metabolic risks. These should include personalised dietary plans, preventive screenings, and targeted healthcare programmes. For example, the Indian Diabetes Prevention Programme showed that lifestyle changes reduced diabetes risk by 28.5% among high-risk individuals. Equally, policymakers must consider the broader societal factors that contribute to these health risks, and qualitative studies highlight challenges in shifting cultural attitudes. Expectations that women prepare meals in line with traditional norms often limit healthier dietary options.Differing perceptions of physical activity can complicate efforts to promote healthier lifestyles. For example, a study in East London found that some communities consider prayer sufficient exercise, which adds complexity to changing attitudes. Facing our past to secure a healthier future As we uncover the long-term effects of environmental stressors like historical famines, it becomes clear that our past is not just a distant memory but an active force shaping our present and future health. Epigenetic changes inherited from South Asian ancestors who endured famine have heightened the risk of metabolic disorders in their descendants. For instance, UK South Asian men have been found to have nearly double the risk of coronary heart disease (CHD) compared to White Europeans. Consultant cardiologist Dr Sonya Babu-Narayan has stated, “Coronary heart disease is the world’s biggest killer and the most common cause of premature death in the UK.” With over 5 million South Asians in the UK alone, this stark reality requires immediate action. We must not only address the glaring gaps in scientific research but also develop targeted public health policies to tackle these inherited health risks. These traits are not relics of the past; they are living legacies that, without swift intervention, will continue to affect generations to come. To truly address the inherited health risks South Asians face, we must go beyond surface-level awareness and commit to long-term, systemic change. Increasing funding for research that directly focuses on the unique health challenges within this population is non-negotiable. Equally crucial are culturally tailored public health initiatives that resonate with the affected communities, alongside comprehensive education programmes that empower individuals to take control of their health. These steps are not just about improving outcomes—they’re about breaking a cycle. The question, therefore, is not simply whether we understand these epigenetic changes, but whether we have the resolve to confront their full implications. Can we muster the political will needed to confront these inherited risks? Can we unite our efforts to stop these risks from affecting the health of entire communities? The cost of inaction is not just measured in statistics—it will be felt in the lives lost and the potential unrealised. The time to act is now. Written by Naziba Sheikh Related articles: Epigenetics / Food deserts and malnutrition REFERENCES Safi, M. (2019). Churchill’s policies contributed to 1943 Bengal famine – study. [online] the Guardian. Available at: https://www.theguardian.com/world/2019/mar/29/winston-churchill-policies-contributed-to-1943-bengal-famine-study . Bakar, F. (2022). How History Still Weighs Heavy on South Asian Bodies Today. [online] HuffPost UK. Available at: https://www.huffingtonpost.co.uk/entry/south-asian-health-colonial-history_uk_620e74fee4b055057aac0e9f . Sayed, M., Deek, F. and Shaikh, A. (2022). The Susceptibility of South Asians to Cardiometabolic Disease as a Result of Starvation Adaptation Exacerbated During the Colonial Famines. [online] Research Gate. Available at: https://www.researchgate.net/publication/366596806_The_Susceptibility_of_South_Asians_to_Cardiometabolic_Disease_as_a_Result_of_Starvation_Adaptation_Exacerbated_During_the_Colonial_Famines#:~:text=This%20crisis%20could%20be%20the,adapted%20physiology%20can%20become%20harmful . Utah.edu . (2009). Epigenetics & Inheritance. [online] Available at: https://learn.genetics.utah.edu/content/epigenetics/inheritance/ . Palaniappan, L., Garg, A., Enas, E., Lewis, H., Bari, S., Gulati, M., Flores, C., Mathur, A., Molina, C., Narula, J., Rahman, S., Leng, J. and Gany, F. (2018). South Asian Cardiovascular Disease & Cancer Risk: Genetics & Pathophysiology. Journal of Community Health, 43(6), pp.1100–1114. doi: https://doi.org/10.1007/s10900-018-0527-8 . Diabetes UK (2022). Risk of Type 2 Diabetes in the South Asian Community. [online] Diabetes UK. Available at: https://www.diabetes.org.uk/node/12895 . King, M. (2024). South Asian Heritage Month: A Journey Through History and Culture . [online] Wearehomesforstudents.com . Available at: https://wearehomesforstudents.com/blog/south-asian-heritage-month-a-journey-through-history-and-culture . Project Gallery

  • Biochemistry of cancer: integrins, the desirable targets | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Biochemistry of cancer: integrins, the desirable targets 31/01/25, 15:24 Last updated: 24/05/23, 08:39 Published: Integrins are desirable to target cancer Every year, eight million people worldwide pass away from cancer, and this number is expected to rise. Cancer can damage a wide range of organs in people of various ages. It is quite honest to say that Cancer is the most common and severe problem in clinical medicine. Cancer's fundamental problems shed light on the biochemical and genetic processes underlying the unchecked expansion of cancer cells. The extracellular matrix (ECM)'s biochemical and biomechanical properties affect how sensitive cells are. Cell health depends on different reactions, such as proliferation, apoptosis, migration, and differentiation. The tumour microenvironment also largely influences cancer metastasis, medication resistance, and recurrence. Transmembrane glycoproteins called integrins mediate connections between cells and the ECM and connect it to the cytoskeleton. They relay the information from the ECM through downstream signalling pathways and can hence control the properties of the cell. Mammals have so far been found to contain 24 different integrin heterodimers, formed by combining 18 α- and 8 β-subunits. A cell's ability to bind to specific ECM elements depends on the pattern of integrin expression, which also affects how a cell recognises and reacts to its surroundings. These same integrin-mediated pathways are used by tumour cells in the context of cancer to boost invasiveness and oncogenic survival as well as to create a host milieu that supports tumour development and metastatic dissemination (Figure 1). Hence, Integrins are interesting targets for cancer therapy due to their role in tumour progression, and several integrin antagonists, including antibodies and synthetic peptides, have been successfully used in clinics for cancer therapy. Unligated integrins may have a detrimental effect on tumour survival. They are generally unligated in adherent cells, which leads to the cleavage of caspase 8, which in turn causes tumour cells to undergo apoptosis through a process known as integrin-mediated death (IMD) (Figure 2). Integrins' precise chemical signals and the mechanical environment of the ECM control how cancer cells behave. A key role is also played by the ECM's physicochemical environment. Chemically altered substrate surfaces have been used to study this interaction, but topology and functionality control are still difficult to achieve. Modifying a cell's local chemical environment does offer a viable method for selectively controlling the behaviour of cancer cells. Together, targeted external cue presentation has the potential to enhance existing intracellular cancer therapy approaches. When combined with other targeted therapies (tyrosine kinase inhibitors, anti-growth factor antibodies) for anticancer treatment, integrin inhibition may be used as a potential target for drug development. However, it needs to be thoroughly evaluated in the pre-clinical phase, possibly taking into account all of the plausible escape mechanisms by which tumour cells can develop. Written by Navnidhi Sharma Related articles: Why whales don't get cancer / Breast cancer and asbestos / MOFs in cancer drug delivery / Anti-cancer metal compounds REFERENCES Hamidi, H., Pietilä, M., & Ivaska, J. (2016). The complexity of integrins in cancer and new scopes for therapeutic targeting. British Journal of Cancer, 115(9), 1017–1023. https://doi.org/10.1038/bjc.2016.312 Jacob, M., Varghese, J., Murray, R. K., & Weil, P. A. (2016). Cancer: An Overview (V. W. Rodwell, D. A. Bender, K. M. Botham, P. J. Kennelly, & P. A. Weil, Eds.). Access Medicine; McGraw-Hill Education. https://accessmedicine.mhmedical.com/content.aspx?bookid=1366§ionid=73247495 Li, M., Wang, Y., Li, M., Wu, X., Setrerrahmane, S., & Xu, H. (2021). Integrins as attractive targets for cancer therapeutics. Acta Pharmaceutica Sinica B. https://doi.org/10.1016/j.apsb.2021.01.004 Yoshii, T., Geng, Y., Peyton, S., Mercurio, A. M., & Rotello, V. M. (2016). Biochemical and biomechanical drivers of cancer cell metastasis, drug response and nanomedicine. Drug Discovery Today, 21(9), 1489–1494. https://doi.org/10.1016/j.drudis.2016.05.011 Zhao, H., F. Patrick Ross, & Teitelbaum, S. L. (2005). Unoccupied αvβ3Integrin Regulates Osteoclast Apoptosis by Transmitting a Positive Death Signal. Molecular Endocrinology, 19(3), 771–780. https://doi.org/10.1210/me.2004-0161 Project Gallery

  • Apocrine carcinoma: a rare form of breast cancer | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Apocrine carcinoma: a rare form of breast cancer 02/11/24, 11:57 Last updated: 05/09/24, 10:20 Published: Key facts This is article no. 1 in a series on Rare Diseases. Next article: Pseudo-Angelman Syndrome . Apocrine carcinoma (AC) is a rare form of breast cancer, accounting for approximately 1-4% of all breast cancer cases worldwide. It affects a wide range of patients from 19 to 92 years of age, with the reported mean age varying from 53 to 62 years. AC of the skin - primary cutaneous apocrine carcinoma - is the only other known cancer that arises from apocrine cells. This is a very rare cancer with limited research. AC is commonly classified into two subtypes: triple-negative AC (TNAC) and HER2+ AC. Another receptor not included in the ‘triple negative’ name is the androgen receptor (AR). A ‘pure’ apocrine carcinoma is ER-negative, PR-negative, but AR-positive. Among triple negative ACs, ones that are AR-positive have a better prognosis. AC is often associated with triple-negative breast cancers (TNBC), meaning that it does not express oestrogen receptors (ER) and progesterone receptors (PR), and produces very little to no HER2– all of which play key roles in the reproductive system. AC arises from apocrine metaplastic cells that are commonly located in the lobules of the breast. This disease can be aggressive and can metastasise to the lymph nodes and distant organs (eg. lungs, liver, and bone). What makes AC different is the appearance of cells which have abundant granular eosinophilic or cytoplasm with fine empty vacuoles. Despite its rarity, focal apocrine differentiation is relatively common (reported in approximately 60% of not otherwise specified [NOS] invasive ductal carcinoma) and shows clinical presentation and radiographic findings similar to that of invasive ductal carcinoma NOS. TNBCs are generally aggressive and present a poor prognosis. However, studies show apocrine breast cancer to have a better prognosis and low proliferative nature, despite its poor response to neoadjuvant chemotherapy. Treatment of AC may include surgery, radiation therapy, chemotherapy, hormone therapy, or targeted therapy. The problem with TNACs is that therapies targeting the hormone receptors are ineffective. Conversely, targeted therapy is seen to work relatively well with HER2-positive ACs despite them being more aggressive than TNACs. ACs can be diagnosed through a series of tests—usually a mammogram, ultrasound, biopsy, and finally immunohistochemistry. The latter makes it possible to know the status of the ERs and PRs. As with most breast cancers the earlier the detection and treatment implementation, the better the prognosis for the patient. ACs can be hard to diagnose due to its rarity and non-specific presentation. AC has a low proliferative nature, which is shown in its low Ki-67 index. Ki-67 has a higher presentation in cells that have a high division rate. Slower division rates result in slower growth rates of the tumour, and may imply that there is a better prognosis. This could be one of the reasons why apocrine triple-negative breast cancers have a better prognosis than other types of TNBCs. There is promise in the future for AC, however this is not without its challenges. Due to its rarity there are limited patients to participate in clinical trials which are essential in new treatment development. Written by Henrietta Owen & Sherine A Latheef Related article: Epitheliod hemangioendothelioma REFERENCES Apple, S.K., Bassett, L.W. and Poon, C.M. (2011) ‘Invasive ductal carcinomas’, Breast Imaging, pp. 423–482. doi:10.1016/b978-1-4160-5199-2.00022-9. Bcrf (2024) Types of breast cancer: BCRF, Breast Cancer Research Foundation. Available at: https://www.bcrf.org/blog/types-of-breast-cancer/ (Accessed: 05 June 2024). Hu, T. et al. (2022) ‘Triple-negative apocrine breast carcinoma has better prognosis despite poor response to neoadjuvant chemotherapy’, Journal of Clinical Medicine, 11(6), p. 1607. doi:10.3390/jcm11061607. Suzuki, C., Yamada, A., Kawashima, K., Sasamoto, M., Fujiwara, Y., Adachi, S., Oshi, M., Wada, T., Yamamoto, S., Shimada, K., Ota, I., Narui, K., Sugae, S., Shimizu, D., Tanabe, M., Chishima, T., Ichikawa, Y., Ishikawa, T., & Endo, I. (2023). Clinicopathological Characteristics and Prognosis of Triple-Negative Apocrine Carcinoma: A Case-Control Study. World Journal of Oncology, 14(6), 551-557. Vranic, S., Feldman, R. and Gatalica, Z. (2017) ‘Apocrine carcinoma of the breast: A brief update on the molecular features and targetable biomarkers’, Bosnian Journal of Basic Medical Sciences, 17(1), pp. 9–11. doi:10.17305/bjbms.2016.1811 Xiao, X., Jin, S., Zhangyang, G., Xiao, S., Na, F. and Yue, J. (2022). Tumor-infiltrating lymphocytes status, programmed death-ligand 1 expression, and clinicopathological features of 41 cases of pure apocrine carcinoma of the breast: a retrospective study based on clinical pathological analysis and different immune statuses. Gland Surgery, 11(6), pp.1037–1046. doi:https://doi.org/10.21037/gs-22-248. Project Gallery

  • Are hydrogen cars the future of the UK? | Scientia News

    Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Are hydrogen cars the future of the UK? 16/01/25, 11:28 Last updated: 01/01/25, 13:50 Published: Hydrogen fuel cells generate electricity through an electrochemical reaction between hydrogen and oxygen Introduction With the London debut of the first ever hydrogen powered racing car in June 2024, the new off-road racing series, Extreme H, is set to make waves in the motorsport and sustainability industries with its first season in 2025. The first ever hydrogen powered motorsport series was announced in 2022 to replace the carbon-neutral electric racing series Extreme E, with the intention of pioneering the potential of hydrogen fuel cells and diversifying the paths of sustainable mobility. Like its predecessor, Extreme H will continue to race off-road in a spec SUV car, where engineers and machinists from competing teams optimise the SUV for the different range of terrains and topographies. The hydrogen spec SUV, fittingly called the Pioneer 25 ( Figure 1 ), is promising for the rapid advancement of hydrogen fuel research, leading to the integration of hydrogen fuel cells vehicles on local roads. In line with the upcoming ban on the sale of new petrol, diesel, and hybrid cars across the UK in 2035, as well as the UK target of reaching carbon neutral by 2050, the need for sustainable and practical transport options is growing. So far however, electric cars have proved to not be a one-size-fits-all solution. Hydrogen fuel could potentially be the key to filling this gap. EVs vs. HFCVs Working mechanisms Hydrogen Fuel Cell Vehicles (HFCVs): Hydrogen fuel cells generate electricity through an electrochemical reaction between hydrogen and oxygen. The electricity produced is used to power an electric motor, which drives the car. The only byproduct of this process is water vapour. Electric Vehicles (EVs): A motor is powered directly from a charged battery, and equally produces no harmful emissions. As a result of large investments, electric vehicles have already established a strong footing in the UK market, prompting the declining cost of batteries as well as increasing availability of EV charging points in the UK. However, for many households and commercial uses, electric vehicles are not accessible forms of transport due to key barriers including the extensive charging time (around 8 hours), the weight of batteries for large vehicles, and performance decline in cold weather due to lithium-ion batteries being highly sensitive to temperature. HFCVs directly address these problems and present a sustainable and competitive alternative. As the refuelling process is the same as petrol and diesel cars, fuel tanks can be filled in the space of a few minutes and are notably weight efficient. A heavy-duty electric vehicle on the other hand can require a battery of around 7000 kg. Advantages of HFCVs: Significantly shorter refuelling times Can achieve 300-400 miles on a full tank Maintain performance in cold weather and under heavy loads Lighter and more energy-dense than electric vehicles Disadvantages: Expensive as they’re not yet widely available Lack of refuelling infrastructure The current primary method of hydrogen production produces CO2 as a byproduct Despite the key advantages hydrogen cars offer, there are currently only 2 available models of HFC cars in the UK, including the Toyota Mirai ( Figure 2 ) and the Hyundai Nexo SUV. As a result, there are currently fewer than 20 refuelling stations available nationwide, compared to the many thousands of charging points available across the country for electric vehicles. One of the main reasons why progress in hydrogen fuel production has been so delayed is because hydrogen, despite being the most abundant element in the universe, is only available on earth in compound form and needs to be extracted using chemical processes. The true sustainability of hydrogen production There are currently two main methods to extract hydrogen from nature, including steam-methane reforming and electrolysis. Hydrogen is colour-graded by production method to indicate whether it is renewable. Green/ yellow hydrogen The cleanest process for hydrogen production is electrolysis, where a current separates hydrogen from pure water. If the current is sourced from renewable energy, it’s known as green hydrogen. If it’s connected via the grid, then it’s called yellow hydrogen. The source of electricity is particularly important because the electrolysis process is about 75% efficient, which translates to higher costs yet cleaner air. Grey/ blue hydrogen Hydrogen can also be produced by treating natural gas or methane with hot steam. During this process, the methane splits into its four hydrogen atoms while one carbon atom bonds to oxygen and enters the atmosphere as carbon dioxide. This is known as grey hydrogen. If the carbon dioxide can be captured and stored via direct air capture, it’s called blue hydrogen. About 95% of all hydrogen in Europe is produced by methane steam reforming (grey and blue hydrogen), as it is very energy efficient and uses up lots of natural gas in the process, a resource that is quickly diminishing in importance and value as more and more households switch from gas boilers to heat pumps. Two percent of the world’s carbon emissions comes from the grey hydrogen process to produce ammonia for fertiliser and for steel production. For context, this is almost the same as the entire aviation industry. For HFCVs to be a truly sustainable alternative to combustion engines, green hydrogen via electrolysis (or another clean process) needs to be more widely available and economically viable. The UK’s plans for hydrogen As part of the UK hydrogen strategy ( Figure 3 ), the UK aims to reach up to 10GW or low carbon hydrogen production by 2030 (or equivalent to the amount of gas consumed by 3 million households in the UK annually). The government has allocated £240 million to develop hydrogen production and infrastructure. This is particularly for industry uses in the production of steel and cement, and for heavy goods vehicles (HGVs). Plans were also made to extend the use of hydrogen to heat homes, starting with ‘hydrogen village trials’ in 2025, to inform how 100% hydrogen communities would work, although this has understandably been met with local opposition. With greater research, information, and development into hydrogen for domestic uses, the applications of hydrogen energy may extend from industry and transport to households. As car companies (particularly Toyota, Hyundai, and BMW) continue to develop hydrogen car makes, and further investment is made into increased refuelling infrastructure and hydrogen fuel cell research, as well as with the ban on the sale of new combustion engine cars by 2035, commercial hydrogen cars have the potential to be commonly found on UK roads by 2040. Conclusion For now, HFCVs remain in the early stages of development, however they present a promising opportunity for the UK to diversify its clean transport options, particularly in areas where EV technology faces limitations such as for heavy goods vehicles. Rather than being competitors, it is likely that EVs and HFCVs will soon coexist, with each technology serving different needs. The biggest barrier to the progress of HFCVs currently is developing a full hydrogen refuelling infrastructure, where the gas is produced and then transported to stations across the nation, will take billions of pounds and a number of years to develop. If these initial hurdles could be overcome, HFCV technology can quickly become more practically and financially accessible. Written by Varuna Ganeshamoorthy Related articles: Electric vehicles / Nuclear fusion Project Gallery

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