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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 chemistry Chemistry beyond carbon: the heteroelements View More psychology Can we really ‘rewire’ our brain? View More neuroscience What a new study says about smoking and trigeminal neuralgia View More ecology Rock, paper, survival? 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 realising your writing potential with us AND live in the UK; and/ or would like to give feedback: Email us at scientianewsorg@gmail.com or fill in our GET IN TOUCH form below and we'll be in contact... 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!

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 or complement 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 The Molecule by Dr Rick Sax and Marta New

A problem synthesising haem Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Sideroblastic anaemia 09/05/26, 13:50 Last updated: Published: 22/12/23, 15:20 A problem synthesising haem This is the fourth and final article in a series about anaemia. First article: anaemia . Previous article: Anaemia of chronic disease . Sideroblastic anaemia (SA) is like haemochromatosis as there is too much iron. Due to an absence of protoporphyrin, iron transport is inhibited. SA’s include hereditary and acquired conditions; these can be due to alcohol, toxins, congenital defects, malignancies, or mutations. This haem-synthesising defect can be caused by the X-linked chromosome, or the lead poisoning induced mutations- these are main mutations that interrupt the 8 enzymatic cascades in the biosynthesis of protoporphyrin, thus leading to defective haemoglobin (Hg)- moreover, iron accumulation in the mitochondria. X-linked protoporphyria is due to a germline mutation in the gene that produces δ-aminolaevulinic acid (δ-ala) synthase; this interrupts the first step of haem synthesis, Figure 1 . Lead poisoning can interrupt two stages of haem synthesis: δ-ala dehydratase (-δ-ala dehydratase porphyria) and ferrochelatase (erythropoietic protoporphyria). The first step devastates the production of haem, due to the chromosomal abnormality that stops the production of δ-ala dehydratase being X-linked porphyria. The second step and the final step are associated with lead poisoning, and this is more common in children. Ferrochelatase is a catalyst for the incorporation of iron to haem in the final stage of haemoglobin synthesis. This causes ferrochelatase erythrocytic protoporphyrin (FECH EPP). SA clinical presentation Common features of SA are general to microcytic anaemias such as teardrop and hypochromic cells. Dimorphism is common. Pappenheimer bodies and mitochondrial iron clusters which are found in bone marrow smears, where iron accumulates around 2/3 of the nucleus of erythroblasts. Without knowing the etiology of anaemia, standard FBCs and iron studies would be run to initially diagnosis the anaemia. With SA, the iron cannot be transported so transferrin will be reduced, alongside mean cell volume (MCV), haemoglobin and haematocrit (HCT). There will also be an increase in ferratin, % saturation and serum Fe. Microcytic anaemia presents in 20-60% of patients with FECH-EPP. Morphology will present as microcytic and hypochromic with the possible presentation of Pappenheimer bodies, ringed sideroblasts, dimorphism and basophilic stippling may be present in bloods of children suspected in lead >5 µg/dL. Lead poisoning can be misdiagnosed as porphyrin as lead is shed from the body slowly; this allows approximately 80% of the lead to be absorbed. Although lead exits the blood rather quickly, once it’s in the bone, it can have a half-life of 30 years. Written by Lauren Kelly Related articles: Blood / Kawasaki disease Project Gallery

Can CRISPR/Cas9 overcome the challenges posed by current HIV treatments? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A potential treatment for HIV 09/05/26, 13:38 Last updated: Published: 21/07/23, 09:50 Can CRISPR/Cas9 overcome the challenges posed by current HIV treatments? The human immunodeficiency virus (HIV) was recorded to affect 40.8 million people globally at the end of 2024. This virus attacks the immune system, incapacitating CD4 cells: white blood cells (WBCs) which play a vital role in activating the innate immune system and fighting infection. The normal range of CD4 cells in our body is from 500 to 1500 cells/mm3 of blood; HIV can rapidly deplete the CD4 count to dangerous levels, damaging the immune system and leaving the body highly susceptible to infections. Whilst antiretroviral therapy (ART) can help manage the virus by interfering with viral replication and helping the body manage the viral load, it fails to eliminate the virus altogether. The reason for this is due to the presence of latent viral reservoirs where HIV can lay dormant and reignite infection if ART is stopped. Whilst a cure has not yet been discovered, a promising avenue being explored in the hopes of eradicating HIV has been CRISPR/Cas9 technology. This highly precise gene-editing tool has been shown to have the ability to induce mutations at specific points in the HIV proviral DNA. Guide RNAs pinpoint the desired genome location and Cas9 nuclease enzymes act as molecular scissors that remove selected segments of DNA.  Therefore, CRISPR/Cas9 technology provides access to the viral genetic material integrated into the genome of infected cells, allowing researchers to cleave HIV genes from infected cells, clearing latent viral reservoirs. Furthermore, the CRISPR/Cas9 gene-editing tool can also prevent HIV from attacking the CD4 cells in the first place. HIV binds to the chemokine receptor, CCR5, expressed on CD4 cells, in order to enter the WBC. CRISPR/Cas9 can cleave the genes for the CCR5 receptor and therefore preventing the virus from entering and replicating inside CD4 cells. CRISPR/Cas9 technology provides a solution that current antiretroviral therapies cannot solve. Through gene-editing, researchers can dispel the lasting reservoirs unreachable by ART that HIV is able to establish in our bodies. Recent phase 1 and 2 trials for treatment involving CRISPR/ Cas9 (e.g. EBT-101-001) showed promising safety and efficacy, as CRISPR successfully targeted latent HIV in vivo. However, further research and clinical trials are still required to fully understand the safety and efficacy of this approach to treating HIV, before it can be implemented as a standard treatment. Written by Bisma Butt Related articles: Antiretroviral therapy / mRNA vaccines Project Gallery

Understanding what goes wrong in the brain Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Epilepsy 101 09/05/26, 14:01 Last updated: Published: 09/10/24, 11:32 Understanding what goes wrong in the brain Epilepsy is a condition that affects millions of people worldwide, often causing unprovoked seizures due to irregular brain activity. But what exactly happens in the brain when someone has epilepsy? It is important to establish that not everyone with seizures has epilepsy. While epilepsy can start at any age, it often begins in childhood, or in people over the age of 60. Epilepsy can be due to genetic factors - 1 in 3 people with epilepsy have family history- or brain damage from causes like stroke, infection, severe head injury or a brain tumour. However, around half of epilepsy cases have an unknown cause. Now, imagine your brain as a big city with lots of lights. Each light represents a part of your brain that controls things like movement, feelings, and thoughts. Epilepsy is like when the lights in the city start flickering or shut completely. There are three main types of epilepsy, and each affects the lights in different ways: 1) Generalised epilepsy: when all the lights in the city flicker or go out at once, affecting the whole brain. There are two main kinds: Generalised Motor (Grand Mal) Seizures: Imagine the lights in the city going wild, making everything shake. This is like the shaking or jerking movements during myoclonic or tonic-clonic seizures. Generalised Non-Motor (Absence) Seizures: Picture the lights suddenly pausing, making everything freeze. During these seizures, a person might stare into space or make small, repeated movements, like lip-smacking. 2) Focal epilepsy: when only the lights in one part of the city flicker or go out. This means only one part of the brain is affected: Focal Aware Seizures: The lights flicker, but people in that part of the city know what’s happening. The person stays aware during the seizure. Focal Impaired Awareness Seizures: The lights flicker, and people lose track of what’s going on. The person might not remember the seizure. Focal Motor Seizures: Some lights flicker, causing strange movements, like twitching, rubbing hands, or walking around. Focal Non-Motor Seizures: The lights stay on, but everything feels strange, like sudden change in mood or temperature. The person might feel odd sensations without moving in unusual ways. 3) ‘Unknown’ epilepsy: ‘Unknown’ epilepsy is like a power outage where no one knows where it happened because the person was alone or asleep during the seizure. Doctors might later figure out if it's more like generalised or focal epilepsy. Some people can even have both types. But how do doctors find out if someone has epilepsy? A range of tests could be used to look at the brain’s activity and structure, including: Electroencephalogram (EEG): detects abnormal electrical activities in the brain using electrodes. This procedure can be utilised in Stereoelectroencephalography (SEEG), a more invasive method where the electrodes are placed directly on or within the brain to locate the abnormal electrical activities more precisely. Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI): form images of the brain to detect abnormal brain structures such as brain scarring, tumours or damage that may cause seizures. Blood tests: test for genetic or metabolic disorders, or health conditions such as anaemia, infections or diabetes that can trigger seizures. Magnetoencephalogram (MEG): measures magnetic signals generated by nerve cells to identify the specific area where seizures are starting, to diagnose focal epilepsy. Positron emission tomography (PET): detects biochemical changes in the brain, detecting regions of the brain with lower-than-normal metabolism linked to seizures. Single-photon emission computed tomography (SPECT): identifies seizure focus by measuring changes in blood flow in the brain during or between seizures, using a tracer injected into the patient. The seizure focus in this scan is seen by an increase in blood flow to that region. So, how does epilepsy affect the brain? For most people, especially those with infrequent or primarily generalised seizures, cognitive issues are less likely compared to those with focal seizures, particularly in the temporal lobe. The following cognitive functions can be affected: Memory : seizures can disrupt the hippocampus in the temporal lobe, responsible for storing and receiving new information. This can lead to difficulties in remembering words, concepts, names and other information. Language : seizures can affect areas of the brain responsible for speaking, understanding and storing words, which can lead to difficulties in finding familiar words. Executive function: seizures can impact the frontal lobe of the brain which is responsible for planning, decision making and social behaviour, leading to challenges in interacting, organising thoughts and controlling unwanted behaviour. While epilepsy itself cannot be cured, treatments exist to control seizures including: Anti-Epileptic Drugs (AEDs; now also called Anti-Seizure Medications (ASMs)) : suppress the brain’s ability of sending abnormal electrical signals - effective in 70% of patients. Diet: ketogenic diets can reduce seizures in some medication- resistant epilepsies and in children as they alter the chemical activity in the brain. Surgery: 1) Resective Surgery: removal of the part of the brain causing the seizures, such as temporal lobe resection, mainly for focal epilepsy. 2) Disconnective Surgery: cutting the connections between the nerves through which the seizure signals travel in the brain, such as in corpus callosotomy, mainly for generalised epilepsy. 3) Neurostimulation device implantation (NDI): insertion of devices in the body to control seizures by stimulating brain regions to control the electrical impulses causing the seizures. This includes vagus nerve stimulation and Deep Brain Stimulation (DBS). Even though epilepsy can be challenging, many people manage it successfully with the right treatment. Continued research offers hope for even better, long lasting treatments in the future. Written by Hanin Salem Related articles: Different types of epilepsy seizures / Alzheimer's disease / Parkinson's disease / Autism REFERENCES D’Arrigo, T. (n.d.). What Are the Types of Epilepsy? [online] WebMD. Available at: https://www.webmd.com/epilepsy/types-epilepsy [Accessed 5 Aug. 2024]. Epilepsy Foundation. (n.d.). Thinking and Memory. [online] Available at: https://www.epilepsy.com/complications-risks/thinking-and-memory [Accessed 10 Aug. 2024]. GOSH Hospital site. (n.d.). Invasive EEG monitoring. [online] Available at: https://www.gosh.nhs.uk/conditions-and-treatments/procedures-and- treatments/invasive-monitoring/ [Accessed 9 Aug. 2024]. My Epilepsy Team.com. (2016). Epilepsy: What People Don’t See (Infographic) | MyEpilepsyTeam. [online] Available at: https://www.myepilepsyteam.com/resources/epilepsy-what-people-dont-see- infographic [Accessed 29 Aug. 2024]. National institute of Neurological Disorders and stroke (2023). Epilepsy and Seizures | National Institute of Neurological Disorders and Stroke. [online] www.ninds.nih.gov . Available at: https://www.ninds.nih.gov/health- information/disorders/epilepsy-and-seizures [Accessed 10 Aug. 2024]. NHS (2020). Epilepsy. [online] NHS. Available at: https://www.nhs.uk/conditions/epilepsy/ [Accessed 10 Aug. 2024]. Project Gallery

Discussing Peto's Paradox in cancer Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why blue whales don't get cancer 09/05/26, 13:57 Last updated: Published: 16/10/23, 21:22 Discussing Peto's Paradox in cancer Introduction: What is Peto’s Paradox? Cancer is a disease that occurs when cells divide uncontrollably, owing to genetic and epigenetic factors . Theoretically, the more cells an organism possesses, the higher the probability should be for it to develop cancer. Imagine that you have one tiny organism – a mouse, and a huge organism – an elephant. Since an elephant has more cells than a mouse, it should have a higher chance of developing cancer, right? This is where things get mysterious. In reality, animals with 1,000 times more cells than humans are not more likely to develop cancer. Notably, blue whales, the largest mammals, hardly develop cancer. Why? In order to understand this phenomenon, we must dive deep into Peto’s Paradox. Peto’s paradox is the lack of correlation between body size and cancer risk. In other words, the number of cells you possess does not dictate how likely you are to develop cancer. Furthermore, research has shown body mass and life expectancy are unlikely to impact the risk of death from cancer . (see figure 1) Peto’s Paradox: Protective Mechanisms Mutations, otherwise known as changes or alterations in the deoxyribonucleic acid (DNA) sequence, play a role in cancer and ageing. Research scientists have analysed mutations in the intestines of several mammalian species , ranging from mice, monkeys, cats, dogs, humans, and giraffes, to tigers and lions. Their results reveal that these mutations mostly come from processes that occur inside the body, such as chemicals causing changes in DNA. These processes were similar in all the animals they studied, with slight differences. Interestingly, annually, animals with longer lifespans were found to have fewer mutations in their cells ( figure 2 ). These findings suggest that the rate of mutations is associated with how long an animal lives and might have something to do with why animals age. Furthermore, even though these animals have very different lifespans and sizes, the amount of mutations in their cells at the end of their lives was not significantly different – this is known as cancer burden. Since animals with a larger size or longer lifespan have a larger number of cells (and hence DNA) that could undergo mutation, and a longer time of exposure to mutations, how is it possible that they do not have a higher cancer burden? Evolution has led to the formation of mechanisms in organisms that suppress the development of cancerous cells . Animals possessing 1,000 times as many cells as humans do not display a higher susceptibility to cancer, indicating that natural mechanisms can suppress cancer roughly 1,000 times more efficiently than they operate in human cells . Does this mean larger animals have a more efficient protective mechanism against cancer? A tumour is an abnormal lump formed by cells that grow and multiply uncontrollably. A tumour suppressor gene acts like a bodyguard in your cells. They help prevent the uncontrollable division of cells that could form tumours. Previous analyses have shown that the addition of one or two tumour suppressor gene mutations would be sufficient to reduce the cancer risk of a whale to that of a human. However, evidence does not suggest that an increased number of tumour suppressor genes correlated with increasing body mass and longevity. Although a study by Caulin et al . identified biomarkers in large animals that may explain Peto’s paradox, more experiments need to be conducted to confirm the biological mechanisms involved. Perillo et. al (2023) was an investigation of existing evidence on such mechanisms, and revealed a list of factors that may contribute to Peto’s paradox. This includes replicative immortality, cell senescence, genome instability and mutations, proliferative signalling, growth suppression evasion and cell resistance to death. As far as we know, different strategies have been followed to prevent cancer in species with larger sizes or longer lifespans . However, more studies must be conducted in the future in order to truly explain Peto’s paradox. Peto’s Paradox: Other Theories There are several theories that attempt to explain Peto’s paradox. One of which explains that large organisms have a lower basal metabolic rate, leading to less reactive oxygen species. This means that cells in larger organisms incur less oxidative damage, causing a lower mutation rate and lower risk of developing cancer. Another popular theory is the formation of hypertumours . As cells divide uncontrollably in a tumour, “cheaters” could emerge. These “cheaters”, known as hypertumours, are cells which grow and feed on their original tumour, ultimately damaging or destroying the original tumour. In large organisms, tumours have more time to reach lethal size. Therefore, hypertumours have more time to evolve, thereby destroying the original tumours. Hence, in large organisms, cancer may be more common but is less lethal. Clinical Implications Curing cancer has posed significant challenges. Consequently, the focus on cancer treatment has shifted towards cancer prevention . Extensive research is currently underway to investigate the behaviour and response of cancer cells to the treatment process. This is done through a multifaceted approach; investigating the tumour microenvironment and diagnostic or prognostic biomarkers. Going forward, a deeper understanding of these fields enables the development of prognostic models as well as targeted treatment methods. One example of an exciting discovery is the revelation of TP53 . The discovery of this tumour suppressor gene indicates that it plays a role in making elephant cells more responsive to DNA damage and in triggering apoptosis by regulating the TP53 signaling pathway. These findings imply that having more copies of TP53 may have directly contributed to the evolution of extremely large body sizes in elephants, helping resolve Peto’s paradox . Particularly, there are 20 copies of the TP53 gene in elephants, but only one copy of the TP53 gene in humans (see figure 3 ). Through more robust studies and translational medicine, it would be fascinating to see how such discoveries could be applied into human medicine ( figure 4 ). Conclusion The complete mechanism of how evolution has enabled organisms that are larger in size and have longer lifespans than humans is still a mystery. There is a multitude of hypotheses that need to be extensively investigated with large-scale experiments. By unravelling the mysteries of Peto’s paradox, these studies could provide invaluable insights into cancer resistance and potentially transform cancer prevention strategies for humans. Written by Joecelyn Kirani Tan Related articles: Biochemistry of cancer / Orcinus orca (killer whale) / Canine friends and cancer Project Gallery

Second most common anaemia Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Anaemia of chronic disease 09/05/26, 13:55 Last updated: Published: 24/08/23, 16:06 Second most common anaemia This article is no. 3 of the anaemia series. Next article: sideroblastic anaemia . Previous article: Iron-deficiency anaemia. Pathogenesis The second most prevalent anaemia is anaemia of chronic disease (ACD); it is more often seen alongside chronic infections or malignancies. Other causes include infections, autoimmune diseases, and transplant rejection. The pathogenesis of the condition is greatly lead by the effectiveness of the immune system. The immune response to tumour cells and pathogens is to remove and deny access to iron, which is needed to thrive. The processes are mainly thought to be mediated through cytokines such as TNF, IL-6s and IFN as well as the acute phase protein hepcidin. IL-6 is a very powerful cytokine in that it can inhibit erythropoiesis through the downregulation of gene expression; SLC4a1 reducing haemoglobin production, it increases ferratin production whilst inhibiting TNF-α; this upregulates DMT-1, which is a protein (transmembrane) involved in iron uptake in macrophages, and it upregulates the production of hepcidin. Hepicidin Hepcidin is a peptide hormone, 25 amino-acid-chain protein, derived mainly from hepatic cells. Its synthesis is induced as a response to iron overload or inflammation. Its presence crucial in the diagnosis of ACD. IL-6 induces hepcidin release from hepatocytes. Upregulation causes the transport protein (ferroportin) degradation, inhibiting iron absorption in duodenum, enterocytes and macrophage recycling via upregulation of dMT-1, and mobilisation of stored iron, resulting in low iron plasma. Clinical presentation A patient with ACD may have low haemoglobin (Hb), and the reticulocyte index (new RBC) count may be reduced. Also, this is a common feature of an iron deficient anaemia (IDA). A blood film may help diagnose the underlying condition, but the red cell morphology varies greatly, as less than half can be microcytic or hypochromic. Iron studies are what helps ACD stand out from the other anaemias: raised IL-6, hepcidin and ferratin are the key markers; the presence of iron results with raised ferratin and iron will be seen if a blood film is stained correctly. There may also be reduced serum iron, % saturation and TIBC. Should erythrocyte sedimentation rates be high, rouleaux may be seen, which are aggregations of RBC. Conclusion The most efficient way to diagnose an anaemia is through serum biomarkers in a FBC, and iron studies. Hepcidin and other chemical markers play a key role in the diagnosis of ACD. Iron studies help to paint a clearer picture when diagnosing anaemias, but should be supported with a medical history alongside a clinical examination, as comorbidities may influence chronic inflammatory markers. Written by Lauren Kelly Project Gallery

A type of anaemia Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Iron deficiency anaemia 09/05/26, 13:47 Last updated: Published: 27/06/23, 17:10 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 occur 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 TIBC 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 bulls-eye 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

A disease of the blood Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Anaemia 09/05/26, 13:44 Last updated: Published: 17/06/23, 12:40 A disease of the blood This is article no. 1 in a series about anaemia. Next article: iron-deficiency anaemia Introduction Erythrocytes in their typical state are a biconcave and nucleus free cell, responsible for carrying oxygen and carbon dioxide. The production is controlled by erythropoietin and as they mature in the bone marrow, they lose their nuclei. These red blood cells (RBC) contain haemoglobin, which aids in the transport of oxygen and iron. Iron is a key component of haem; insufficient levels of iron leads to anaemic disorders. Low oxygen-carrying capacity may be defined by too few RBC in circulation, or RBC dysfunction. Haem iron is acquired through the digestion of meat, and transported through enterocytes of the duodenum, in its soluble form. Erythrocytic iron accounts for approximately 50% of the iron in blood. Metals cannot move freely throughout the body so they must be transported; the molecule involved in transporting iron is known as transferrin. Plasma transferrin saturation refers to the iron that is attached to transferrin. In iron deficient anaemia (IDA), this will always be low. Anaemia is physiological or pathological. These changes can be due to a plethora of causes; malabsorption due to diet or gastrointestinal (GI) conditions, genetic dispositions such as sideroblastic anaemias (SA), thalassaemia, or deficiency in erythropoietin due to comorbidities and chronic disease; where haemolysis is caused by autoimmune disorders, infections and drugs, or blood loss. Haem The iron is in a protoporphyrin ring at the centre of a haem molecule. The structure of haem consists of two alpha and two beta polypeptide chains, to form a single haemoglobin macromolecule. Microcytic anaemias arise from problems in the creation of haemoglobin; sourcing through diet (IDA), synthesising protoporphyrin (SA) or from globin chain defects caused by thalassaemia. Summary Anaemia is a multifactorial condition with many different mechanisms involved. Microcytic anaemias have an issue at the haemoglobin level. these can be acquired or inherited. A microcytic anaemia is caused by a failure to efficiently synthesise haemoglobin, whether from iron, protoporphyrin rings or globin chains. The diagnosis of anaemias is reliant on a patient’s background and medical history, as there are many factors involved in an anaemic disorder. A diagnosis should be patient led, as the age and sex of the patient can significantly highlight the origin and pathogenesis, as well as the prognosis and follow up care. Written by Lauren Kelly Related article: Blood Project Gallery

Sharpen your knowledge on this subject with articles dissecting the branch of behavioural economics (the role of honesty, endowment effect, loss of aversion, libertarian paternalism, effect of time), among others. Economics Articles Sharpen your knowledge on this subject with articles dissecting the branch of behavioural economics (the role of honesty, endowment effect, loss of aversion, libertarian paternalism, effect of time), among others. You may also like: Maths The role of honesty Article #1 in a series on behavioural economics The endowment effect Article #2 in a series on behavioural economics Loss aversion Article #3 in a series on behavioural economics Libertarian paternalism and the 'Nudge' approach Article #4 in a series on behavioural economics