A Scientia News Biology and Genetics collaboration Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Germline gene therapy (GGT): its potential and problems 09/07/25, 15:14 Last updated: Published: 21/01/24, 11:47 A Scientia News Biology and Genetics collaboration Introduction Genetic diseases arise when there are alterations or mutations to genes or genomes. In most acquired cases, mutations occur in somatic cells. However, when these mutations happen in germline cells (i.e. sperm and egg cells), they are incorporated into the genome of every cell. In other words, should this mutation be deleterious, all cells will have this issue. Furthermore, this mutation becomes inheritable. This is partly why most genetic diseases are complicated to treat and cure. Gene therapy is a concept that has been circulating among geneticists for some time. Indeed, addressing a disease directly from the genes that caused or promoted it has been an attractive and appealing avenue of therapies. The first successful attempt at gene therapy dates back to 1990, using retrovirus-derived vectors to transduce the T-lymphocytes of a 4-year-old girl with X-linked severe combined immunodeficiency disease (SCID-X1) with enzyme adenosine deaminase (ADA) deficiency. The trial was a great success, eliminating the girl's disease and marking a great milestone in the history of genetics. Furthermore, the success of viral vectors also opened new avenues to gene editing, such as zinc finger nucleases and the very prominent CRISPR-Cas9. For example, in mid-November 2023, the UK Medicines and Healthcare products Regulatory Agency or MHRA approved the CRISPR-based gene therapy, Casgevy, for sickle cell disease and β-thalassemia. It is clear that the advent of gene therapies significantly shaped the treatment landscape and our approach to genetic disorders. However, for most of gene therapy history, it is done almost exclusively on somatic cells or some stem cells, not germline cells. How it works As mentioned, inherited genetic disease-associated mutations are also present in germline cells or gametes. The current approach to gene therapy targets genes of some or very specific somatic or multipotent stem cells. For example, in the 1990 trial, the ADA-deficient SCID-X1 T-lymphocytes were targeted, and in recently approved Casgevy, the BCL11A erythroid-specific enhancer in hematopoietic stem cells. The methods involved in gene therapies also vary, each with advantages and limitations and carrying some therapeutic risks. Nevertheless, when aiming to treat genetic diseases, gene therapy should answer two things: how to do it and where. There are a few elucidated strategies of gene therapies. Unlike some popular beliefs, gene therapies do not always directly change or edit mutated genes. Instead, some gene therapies target enhancers or regulatory regions that control the expression of mutated genes. In other cases, such as in Casgevy, enhancers of a different subtype are targeted. By targeting or reducing BCL11A expression, Casgevy aims to induce the production of foetal haemoglobin (HbF), which contains the γ-globin chain as opposed to the defective β-chain in the adult haemoglobin (HbA) of sickle cell disease or β-thalassemia. Some gene therapies can also be done ex vivo or in vivo . Ex vivo strategies involve extracting cells from the body and modifying them in the lab, whilst in vivo strategies directly modify the cell without extraction (e.g. using viral/ non-viral vectors to insert genes). In essence, the list of strategies for gene therapies is growing, each with limitations and a promising prospect of tackling genetic diseases. These methods aim to “cure” genetic diseases in patients. However, the strategies mentioned above have all been researched using and, perhaps, made therapeutically for somatic or multipotent stem cells. Germline gene therapy (GGT), involves directly editing the genetic materials of germline cells or the egg and sperm cells before fertilisation. This means if it is done successfully, fertilisation of these cells will eliminate the disease phenotype from all cells of the offspring instead of only effector cells. Potentially, GGT may eradicate a genetic disease for all future generations. Therefore, it is an appealing alternative to human embryo editing, as it achieves similar or the same result without the need to modify an embryo. However, due to its nature, its advantage may also be its limitation. Ethical issues GGT has the potential to cure genetic disorders within families. However, because it involves editing either the egg or sperm cells before fertilisation, there are prominent ethical issues associated with this method, like the use of embryos for research and many more. Firstly, GGT gives no room for error. Mistakes during the gene modification process could cause systemic side effects or a harsher disease than the one initially targeted, leading to a multigenerational effect. For example, if parents went to a clinic to check if one/both their germ cells have a gene coding for proteins implicated in cystic fibrosis, an off-target mistake during GGT may lead to their child developing Prader-Willi Syndrome or other hereditary disorders caused by editing out significant genes for development. Secondly, an ecological perspective asserts that the current human gene pool, an outcome of many generations of natural selection, could be weakened by germline gene editing. Also, there is the religious perspective, where editing embryos goes against the natural order of how god created living creatures as they should be, where their natural phenotypes are “assigned” for when they are alive. Another reason GGT may be unethical is it leads to eugenics or creating “designer babies”. These are controversial ideas dating back to the late 19th century, where certain traits are “better” than others. This implies they should appear in human populations while individuals without them should be sterilised/killed off. For instance, it is inconceivable to forget the Nazi Aktion T4 program, which sought to murder disabled people because they were seen as “less suitable” for society. Legal and social issues Eugenics is notorious today because of its history. Genetic counselling may be seen like this as one possible outcome may be parents who end pregnancies if their child inherits a genetic disease. Moreover, understanding GGT’s societal influences is crucial, so clinical trial designs must consider privacy, self-ownership, informed consent and social justice. In China, the public’s emotional response to GGT in 2018 was mainly neutral, as shown in Figure 1, but some of the common “hot words” when discussed were ‘mankind’, ‘ethics’, and ‘law’. With this said, regulations are required with other nations for a wider social consensus on GGT research. In other countries, there are stricter rules for GGT. it is harder to conduct experiments using purposely formed/altered human embryos with inheritable mutations in the United States because the legal outcomes can include prison time and $100,000 fines. Furthermore, when donors are required, they must be fairly compensated, and discussing methodologies is crucial because there are issues on how they can impact men and women. South Africa has two opposing thoughts on GGT or gene editing. Bioconservatism has worries about genetic modification and asserts its restrictions, while bioliberalism is receptive to this technology because of the possible benefits. Likewise, revisions to the current regulations are suggested, such as rethinking GGT research or a benefit-risk analysis for the forthcoming human. Conclusion Overall, gene therapies have transformed the therapeutic landscape for genetic diseases. GGT is nevertheless a unique approach that promises to completely cure a genetic disease for families without the need to edit human embryos. However, GGT’s prospects may do more harm than good because its therapeutic effects are translated systemically and multigenerationally. On top of that, controversial ideas such as designer babies can arise if GGT is pushed too far. Additionally, certain countries have varying regulations due to cultural attitudes towards particular scientific innovations and the beginning of life. Reflecting on the ethical, legal and social issues, GGT is still contentious and probably would not be a prominent treatment option anytime soon for genetic diseases. Written by Sam Jarada and Stephanus Steven Introduction, and How it works by Stephanus Ethical issues, and Legal and social issues by Sam Conclusion by Sam and Stephanus Related article: Monkey see, monkey clone References: Cavazzana-Calvo, M. et al. (2000) ‘Gene therapy of human severe combined immunodeficiency (SCID)-X1 disease’, Science , 288(5466), pp. 669–672. doi:10.1126/science.288.5466.669. Demarest, T.G. and Biferi, M.G. (2022) ‘Translation of gene therapy strategies for amyotrophic lateral sclerosis’, Trends in Molecular Medicine , 28(9), pp. 795–796. doi:10.1016/j.molmed.2022.07.001. Frangoul, H. et al. (2021) ‘CRISPR-Cas9 gene editing for sickle cell disease and β-thalassemia’, New England Journal of Medicine , 384(3), pp. 252–260. doi:10.1056/nejmoa2031054. AGAR, N. (2018). Why We Should Defend Gene Editing as Eugenics. Cambridge Quarterly of Healthcare Ethics, 28(1), pp.9–19. doi: https://doi.org/10.1017/s0963180118000336 . de Miguel Beriain, I., Payán Ellacuria, E. and Sanz, B. (2023). Germline Gene Editing: The Gender Issues. Cambridge Quarterly of Healthcare Ethics, 32(2), pp.1–7. doi: https://doi.org/10.1017/s0963180122000639 . Genome.gov . (2021). Eugenics: Its Origin and Development (1883 - Present). [online] Available at: https://www.genome.gov/about-genomics/educational-resources/timelines/eugenics#:~:text=Discussions%20of%20eugenics%20began%20in . Johnston, J. (2020). Budgets versus Bans: How U.S. Law Restricts Germline Gene Editing. Hastings Center Report, 50(2), pp.4–5. doi: https://doi.org/10.1002/hast.1094 . Kozaric, A., Mehinovic, L., Stomornjak-Vukadin, M., Kurtovic-Basic, I., Catibusic, F., Kozaric, M., Mesihovic-Dinarevic, S., Hasanhodzic, M. and Glamuzina, D. (2016). Diagnostics of common microdeletion syndromes using fluorescence in situ hybridization: single center experience in a developing country. Bosnian Journal of Basic Medical Sciences, [online] 16(2). doi: https://doi.org/10.17305/bjbms.2016.994 . Luque Bernal, R.M. and Buitrago BejaranoR.J. (2018). Assessoria genética: uma prática que estimula a eugenia? Revista Ciencias de la Salud, 16(1), p.10. doi: https://doi.org/10.12804/revistas.urosario.edu.co/revsalud/a.6475 . Nielsen, T.O. (1997). Human Germline Gene Therapy. McGill Journal of Medicine, 3(2). doi: https://doi.org/10.26443/mjm.v3i2.546 . Niemiec, E. and Howard, H.C. (2020). Germline Genome Editing Research: What Are Gamete Donors (Not) Informed About in Consent Forms? The CRISPR Journal, 3(1), pp.52–63. doi: https://doi.org/10.1089/crispr.2019.0043 . Peng, Y., Lv, J., Ding, L., Gong, X. and Zhou, Q. (2022). Responsible governance of human germline genome editing in China. Biology of Reproduction, 107(1). doi: https://doi.org/10.1093/biolre/ioac114 . Shozi, B. (2020). A critical review of the ethical and legal issues in human germline gene editing: Considering human rights and a call for an African perspective. South African Journal of Bioethics and Law, 13(1), p.62. doi: https://doi.org/10.7196/sajbl.2020.v13i1.00709 . Thaldar, D., Botes, M., Shozi, B., Townsend, B. and Kinderlerer, J. (2020). Human germline editing: Legal-ethical guidelines for South Africa. South African Journal of Science, 116(9/10). doi: https://doi.org/10.17159/sajs.2020/6760 . Zhang, D. and Lie, R.K. (2018). Ethical issues in human germline gene editing: a perspective from China. Monash Bioethics Review, 36(1-4), pp.23–35. doi: https://doi.org/10.1007/s40592-018-0091-0 . Project Gallery

From the hull to the glass viewpoint- shortcuts in design Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The fundamental engineering flaws of the Titan Submersible Last updated: 14/03/26, 20:23 Published: 03/04/25, 08:00 From the hull to the glass viewpoint- shortcuts in design On June 18, 2023, the Titan submersible made headlines when the expedition to visit the wreck of the Titanic ended in tragedy. In the North Atlantic Ocean, 3,346 metres below sea-level, the underwater vessel catastrophically imploded along with its five passengers. Two years on, this article deep dives into the key points of failure in engineering and reflects on what we can learn from the fatal incident. The Titanic and OceanGate’s mission The Titanic wreck lies around 3800 metres below sea level in the North Atlantic Ocean, approximately 370 miles off the coast of Newfoundland, Canada. Since the wreckage was finally discovered in September 1985, over seven decades after the boat sank from an iceberg collision on the 15th of April 1912, less than 250 people have personally viewed the wreckage. Despite many discussions to raise the wreckage back to the surface, the complete Titanic structure has become too fragile after over a century underwater and will likely disintegrate completely over the next few decades. Hence, viewing the Titanic in person is only possible with an underwater vessel, a feat which has been achieved successfully since 1998 by a range of companies seating historians, oceanographers, and paying tourists. The Titan submersible is one such vessel developed by OceanGate Expeditions. Titan has been attempting dives to the Titanic wreck since 2017 and was first successful in 2021, when it went on to complete 13 successful dives. According to the passenger liability waiver however, this was only 13 out of 90 attempted dives (a 14% success rate), as a result of communication signal failures, structural concerns, strong currents, poor visibility, or logistical issues. On the many failed attempts, the mission was either cancelled or aborted before the Titan reached the depth of the Titanic wreck. Despite concerns raised by engineers, poor success rates in testing and simulation, as well as previous instances of the Titan spiralling out of control, OceanGate continued with their first planned dive of 2023, leading to its catastrophic implosion that claimed five lives. The Titan is the first fatality of a submersible dive to the Titanic. What went wrong: structural design When designing an underwater vessel to reach a certain depth, the body of the vessel called the hull, would need to be capable of withstanding an immense amount of pressure. For 10 metres of depth, the pressure on the submersible’s hull increases by one atmosphere (1 bar or 101kPa). To reach the wreck of the Titanic 3800 metres underwater, the hull would be required to withstand the pressure of over 38 MPa (see Figure 1 ). For perspective, this is around 380 times the pressure we feel on the surface and about 200 times the pressure of a standard car tyre. Over one square inch, this equates to nearly 2500kg. To withstand such high hydrostatic pressure, a submersible hull is normally constructed with high-strength steel and titanium alloys in a simple spherical, elliptical, or cylindrical shell. At this point we discover some of the key points of failure in the Titan. The Titan’s hull was made from Carbon Fibre Reinforced Plastic (CFRP), i.e., multiple layers of carbon fibre mixed with polymers. Carbon fibre is a high-tech and extremely desirable material for its tensile strength, strength-to-weight ratio, high chemical resistance, and temperature tolerance. The material has proven itself since the 1960’s in the aerospace, military, and motorsport industries, however the Titan was the first case of using carbon fibre for a crewed submersible. At first glance, the use of a carbon fibre hull suggests the advantage of significantly reducing the vessel's weight (50-75% lighter than titanium) while maintaining tensile strength, which will allow for a greater natural buoyancy. Without the need for added buoyancy systems, the hull would be able to hold space for more passengers at one time. As carbon fibre is cheaper than titanium and passengers pay $250,000 a seat, carbon fibre may appear to be a better business plan. However, although carbon fibre performs extremely well under tension loads, it has no resistance to compression loads (as with any fibre) unless it is infused with a polymer to hold the fibres together (see Figure 2 ). The polymer in the CFRP holding the fibres in alignment is what allows the material to resist compressive loads without bending by distributing the forces to all the fibres in the structure. This means the material is an isotropic: it is much stronger in the direction of the fibres than against (the same way wood is stronger along the grain). Therefore, individual layers of the CFRP must be oriented strategically to ensure the structure can withstand an expected load in all directions. A submersible hull intending to reach the ocean floor must withstand a tremendous compressive load, much higher than carbon fibre is typically optimised for in the aviation and automotive racing industries, and carbon fibre under such high compressive load is currently an under-researched field. Although it is likely possible for carbon fibre to be used in deep-sea vessels in the future, it would require rigorous testing and intensive research which was not done by OceanGate. Despite this, the Titan had apparently attempted 90 dives since 2017 and the repeated cycling of the carbon fibre composite at a high percentage of its yield strength would have made the vessel especially vulnerable to any defects reaching a critical level. Upon simple inspection, the Titan also raises other immediate structural concerns. Submersible hulls are usually spherical or slightly elliptical, which would allow the vessel to receive an equal amount of pressure at every point. The unique tube-shape of the Titan’s hull (see cover image) would not equally distribute pressure, and this issue was ‘addressed’ with the use of separate end-caps. The joints that attach the end-caps to the rest of the hull only introduced further structural weaknesses, which made the vessel especially vulnerable to collapsing from micro-cracks. The Titan’s glass viewpoint was another structurally unsound feature [Figure 3]. David Lochridge, the former director of OceanGate’s marine operations between 2015 and 2018 who was fired for raising concerns about the submersible’s safety features, claimed the company that made the material only certified its use down to 1300m (falling over 2000 metres short of the Titanic’s depth). The immense forces on materials without the properties to withstand the compressive pressure made the Titan’s failure inevitable. Cutting corners in the interest of business The foundation of the implosion’s cause was OceanGate’s insistence on cutting corners in Titan’s design to save time and money. The Titan was not certified for deep-sea diving by any regulatory boards and instead asked passengers to sign a waiver stating the Titan was ‘experimental’. As underwater vessels operate in international waters, there is no single official organisation to ensure ship safety standards, and it is not essential to have a vessel certified. However, many companies choose to have their ships assessed and certified by one of several organisations. According to The Marine Technology Society submarine committee, there are only 10 marine vessels capable of reaching Titanic level depths, all of which are certified except for the Titan. According to a blog post on the company website, OceanGate claimed the way that the Titan had been designed fell outside the accepted system - but it “does not mean that OceanGate does not meet standards where they apply”. The post continued that classification agencies “slowed down innovation… bringing an outside entity up to speed on every innovation before it is put into real-world testing is anathema to rapid innovation”. According to former engineers and consultants at OceanGate, the Titan’s pressure hull also did not undergo extensive full-depth pressure testing, as is standard for an underwater vessel. Carbon fibre - the primary material of the Titan’s hull - is extremely unpredictable under high compressive loads, and currently has no real way to measure fatigue. This makes it an unreliable and dangerous material to be used for deep-sea dives. OceanGate CEO Stockton Rush, who was a passenger on the Titan during its last fatal dive in 2023, described the glue holding the submersible’s structure together as “pretty simple” in a 2018 video, admitting “if we mess it up, there’s not a lot of room for recovery”. Having attempted 90 dives with a 14% success rate since 2017, it was inevitable that micro-cracks in the Titan from repeated dives, if not for the extremely sudden failure modes of carbon fibre composites, would result in the vessel's instantaneous implosion. On the 15th of July 2022 (dive 80), Titan experienced a "loud acoustic event" likely form the hull’s carbon fibre delaminating, which was heard by the passengers onboard and picked up by Titan's real-time monitoring system (RTM). Data from the RTM later revealed that the hull had permanently shifted following this event. Continued use of the Titan beyond this event without further testing of the carbon fibre - because the hull was ‘too thick’ - prevented micro-cracks and air bubbles in the epoxy resin from being discovered until it was too late. Another fundamental flaw lies in the Titan’s sole means of control being a Bluetooth gaming controller. While this is not an uncommon practice, especially in the case of allowing tourists to try controlling the vessel once it has reached its location, it is essential that there are robust secondary and even tertiary controls that are of a much higher standard. The over-reliance on wireless and touch-screen control, particularly one operating on Bluetooth which is highly sensitive to interference, was a dangerous and risky design choice. Although it was unlikely to have caused the implosion on its own, cutting corners in the electronics and controls of a vessel that needs to be operated in dangerous locations is irresponsible and unsafe. Submersibles operating at extreme depths require robust fail-safes, including emergency flotation systems and locator beacons. Again, OceanGate cut corners in developing Titan’s emergency recovery systems, using very basic methods and off-the-shelf equipment. In the event of catastrophic failure, the absence of autonomous emergency measures is fatal. With the extent of damage and poor design to the vessel’s carbon fibre hull, it was unlikely that even the most advanced emergency systems could prevent the magnitude of the implosion. Still, the carelessness displayed in almost every aspect of the submersible’s design was ultimately the cause of the fatal Titan tragedy. Conclusion In a 2019 interview, OceanGate’s former CEO Stockton Rush said: There hasn’t been an injury in the commercial sub industry in over 35 years. It’s obscenely safe because they have all these regulations. But it also hasn’t innovated or grown — because they have all these regulations. In the world of engineering, shortcuts can be catastrophic. Whilst risk-taking is undeniably essential to support innovation, Titan’s fatal tragedy was entirely preventable and unnecessary if the proper risk management techniques were employed. OceanGate had the potential to revolutionise the use of carbon fibre in deep-sea industries but consistently cutting corners and not investing in the required real-world testing, as well as the arrogance to ignore expert warnings, is what ultimately led to Titan’s story fatefully echoing the overconfidence of Titanic’s “she is unsinkable!”. Whilst regulations on submersibles tighten and research into carbon fibre is increased, it is important to take the fundamental cause of the tragic implosion as a wake-up call. Assumptions are deadly: trust the science, invest in the proper research, test every bolt, and never underestimate the ocean’s relentless power. Written by Varuna Ganeshamoorthy Related articles: Engineering case study- silicon hydrogel / Superconductors / Building Physics Project Gallery

Explaining The Pain Gate Theory Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Gatekeepers of pain: how your body decides what hurts Last updated: 18/09/25, 09:40 Published: 18/09/25, 08:00 Explaining The Pain Gate Theory Pain is an unpleasant bodily sensation that’s usually linked to actual or potential tissue damage. It often acts as the body’s warning system, protecting us from further harm. Now picture this: you hit your leg, and it hurts—but then you instinctively start rubbing it, and the pain begins to ease. Why does that happen? That’s where the Pain Gate Theory (also known as The Gate Theory of Pain, or The Gate Control Theory of Pain) comes in. It’s one of the most fascinating ideas in pain science because it explains how pain isn’t just about injury— it’s also about how our nervous system processes it. Pain can vary greatly between individuals and even in the same person under different circumstances. This variation is due to the fact that pain is not just a physical experience, but also influenced by emotions, attention, and context. The Pain Gate Theory was first coined in 1965 by Ronald Melzack and Patrick Wall to explain this phenomenon. It states that a stimulus must travel through the substantia gelatinosa in the dorsal horn of the spinal cord, the transmission cells and the fibres in the dorsal column in order to have an effect. The substantia gelatinosa acts as a ‘gate’, mediating which signals are able to pass through the nervous system to the brain. As to whether the gate closes is influenced by an array of factors. How does it work? The below figure depicts the relationships in The Pain Gate Theory. The gate mechanism is influenced by the activity of the larger diameter fibres (A-beta) which usually inhibit transmission and the small diameter fibres (A-delta and C) which increase transmission. Take our analogy from earlier about rubbing your leg: when you do this, the large fibres carrying non painful stimuli like touch and pressure are activated. This causes the gate to be ‘closed’ which blocks the pain signals being transmitted by the small fibres. This concept is so interesting as it opens doors to viewing pain holistically; pain is influenced by touch, thoughts and emotions, which explains why you may not notice pain as much when your super excited about something or why placebos have been proven to work in some cases. In a clinical sphere, this theory has opened the door to many pain management techniques, for example Transcutaneous Electrical Nerve Stimulation (TENS), which selectively stimulates A-beta fibres leading to a consequential inhibition in A-delta and C fibres, preventing pain-related signals reaching the brain. It also has been utilised in physiotherapy, labour and chronic pain treatments. One main limitation of this model is its inability to explain certain types of pain like phantom limb since it relies on the assumption that pain requires an input from a limb to the spinal cord . This has led to the development of more advanced models like the neuromatrix model which acknowledges the fact that the brain can create pain on its own. In conclusion, the bottom line is that The Pain Gate Theory was groundbreaking in our understanding of how pain works. Understanding pain as a brain-and-body experience opens the door to innovative treatments that may one day make pain more manageable, or even preventable. Written by Blessing Amo-Konadu Related articles: Ibuprofen / Anthrax toxin to treat pain REFERENCES Cho, In-Chang, and Seung Ki Min. “Proposed New Pathophysiology of Chronic Prostatitis/Chronic Pelvic Pain Syndrome.” Urogenital Tract Infection , vol. 10, no. 2, 2015, p. 92, https://doi.org/10.14777/uti.2015.10.2.92 . Accessed 29 June 2020. Merrick, Mark. “Gate Control Theory - an Overview | ScienceDirect Topics.” Sciencedirect.com , 2012, www.sciencedirect.com/topics/medicine-and-dentistry/gate-control-theory . Tashani, O, and M Johnson. “Transcutaneous Electrical Nerve Stimulation (TENS). A Possible Aid for Pain Relief in Developing Countries?” Libyan Journal of Medicine , vol. 4, no. 2, 10 Dec. 2008, pp. 77–83, www.ncbi.nlm.nih.gov/pmc/articles/PMC3066716/pdf/LJM-4-062.pdf , https://doi.org/10.4176/090119 . The British Pain Society. “What Is Pain?” Britishpainsociety.org , July 2020, www.britishpainsociety.org/about/what-is-pain/ . Trachsel, Lindsay A., et al. “Pain Theory.” PubMed , StatPearls Publishing, 17 Apr. 2023, www.ncbi.nlm.nih.gov/books/NBK545194/ Project Gallery

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

Non-cell-autonomous cancer progression from chromosomal instability Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Immune signals initiated by chromosomal instability lead to metastasis 09/07/25, 15:23 Last updated: Published: 14/09/24, 22:17 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 / Cancer metastasis / Arginine and tumour growth 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

The 14-day rule and stem cell-based embryo models Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Regulation and policy of stem cell research Last updated: 20/10/25, 15:40 Published: 23/10/25, 08:00 The 14-day rule and stem cell-based embryo models This is the last article (article no. 3) in a three-part series on stem cells. Previous article: The role of mesenchymal stem cells in regenerative medicine. Welcome to the final article in this series of three articles about stem cells. Article 1 was an overview of stem cells, and Article 2 focused on mesenchymal stem cells. In Article 3, I will look at the regulation and policy of stem cell research, which is important given the rapidly changing landscape of stem cell research. Introduction If used effectively, stem cells can be used in treating diseases, understanding human development, and more. For example, a recent paper published in September 2025 explains how scientists created embryos from human skin DNA, in an experimental process they named “mitomeiosis”. Here, the scientists attempted to force the egg cell to divide to remove half of its chromosomes so it could be fertilised like a normal egg cell. While mitomeiosis was unsuccessful in creating viable egg cells, new advancements like this raise ethical questions about the use of stem cells, especially those derived from embryos. As a result, policies and regulations must be created and followed to ensure stem cells are used ethically and appropriately. Two major topics in this policy landscape are the 14-day rule for using human embryos and the creation of Stem Cell-Based Embryo Model (SCBEM) frameworks. The 14-day rule One of the most widely known restrictions in the field of stem cells is the 14-day rule. The 14-day rule prohibits scientists from culturing human embryos in vitro (in the laboratory) beyond 14 days or the appearance of the primitive streak. The primitive streak is a developmental marker signalling the point at which an embryo is biologically individualised. The appearance of this streak also marks the beginning of gastrulation, which is when embryonic cells start differentiating into the three primary germ layers: endoderm, mesoderm, and ectoderm. A timeline of human embryo development from day 0 to day 14 is shown in Figure 1 to help visualise the different stages. In the UK, the 14-day rule is a law under the Human Fertilisation and Embryology (HFE) Act 1990 (as amended 2008) . These human embryos are either donated with consent for research purposes due to no longer being needed, are unsuitable for fertility treatments, or are embryos created explicitly from donated sperm and eggs for research purposes. However, scientific advances have meant that human embryo cultures have now become advanced, resulting in embryos being destroyed at the 14-day deadline due to the law. For example, in 2016, researchers developed new in vitro culture systems that allowed human embryos to be maintained in the lab up to the 12th and 13th day of development. This had previously not been possible. Unfortunately, the experiments had to be stopped because they were approaching the 14-day legal limit. Therefore, scientists have questioned whether the 14-day rule is still fit-for-purpose, and if not, how it could be amended in a way that still ensures ethical and appropriate use of these cells. A specific area of development that scientists do not have a lot of information on is the “black box” period, which includes the moment of gastrulation, happening around day 14-15. Having further knowledge of gastrulation could be used to improve the success rate of In Vitro Fertilisation (IVF), by helping scientists to understand possible causes of early miscarriage and implantation failure, and working to mitigate those. Because of this debate, the Nuffield Council on Bioethics has launched a project to better understand the arguments for and against extensions to the 14-day limit on human embryo research. The Council aims to use this project to provide decision-makers, such as policymakers, with the evidence they need to decide whether to extend the time limit. Regulating Stem Cell-Based Embryo Models (SCBEMs) There is also the development of SCBEMs to consider, as seen in Figure 2 . SCBEMs are also called embryoids or embryo models. They are complex, organised three-dimensional structures derived from pluripotent stem cells, which are cells that can differentiate into all cells in the human body. SCBEMs replicate certain features and processes of embryonic development, meaning they can provide new insights into stages of early human development that have been normally inaccessible to scientists. However, SCBEMs are not defined as embryos under existing laws, like the HFE Act 1990, meaning there is a policy and regulation gap covering these structures. To fill this gap, researchers recently created the first-ever UK guidelines for generating and using SCBEMs in research. The new SCBEM Code of Practice was published in July 2024 and has clear guidance and standards, increasing the transparency of research that will be conducted using SCBEMs. The Code requires that research have well-justified scientific objectives and adhere to an approved culture period, the minimum duration needed to achieve the scientific objective. For example, the Code prohibits the transfer of human SCBEMs into a human or animal womb. Furthermore, adherence to the Code requires that a dedicated SCBEM Oversight Committee be created to review and approve proposed work. An SCBEM Register is also needed to record information about successful applications. Both of these increase the transparency and openness of research using SCBEMs. Future of regulation and policy of stem cell research Given the rapid pace of development in stem cell research, policies and regulations must be created and followed to ensure ethical and appropriate use of these cells. The review by the Nuffield Council on Bioethics regarding the 14-day rule will be important in determining if the rule should be extended. The extension could allow scientists to study developmental stages such as gastrulation, currently part of the “black box” period of development occurring after 14 days. The creation of the UK's first-ever SCBEM Code of Practice in July 2024 has introduced guidelines to fill the existing policy gap, requiring research using these models to have well-justified scientific objectives, follow approved culture periods, and be reviewed by an Oversight Committee to ensure transparency and ethical use. However, there is a need for stronger regulations, as opposed to guidelines, for using SCBEMs, and it is an important example of where policy needs to continue to be developed. Written by Naoshin Haque Related articles: Animal testing ethics / How colonialism, geopolitics and health are interwoven Project Gallery

How it's used Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link AI in medicinal chemistry 08/07/25, 17:18 Last updated: Published: 07/07/23, 21:47 How it's used We are always surrounded by medicine, whether this be through, for example, the cabinet in your house containing prescription drugs or walking by a pharmacy during the day. It is no secret that medical drugs are essential - they both mitigate the symptoms of disease and even prevent further future illness. However, whilst ingesting a tablet is easy for most, it seems to be that we can sometimes forget the vigorous amount of scientific research that goes into successfully synthesising a new drug, i.e. the core of medicinal chemistry. This process typically takes up to an astounding 10 years or more, but with new artificial intelligence (AI) emerging it is thought to be that this number will lower. What exactly is artificial intelligence? It can broadly be defined as the ability to produce human intelligence through the use of machinery such as computers or software. Based on this, one may question why AI is needed if we can just simply communicate ideas through writing, speaking and so on. The answer is increased efficiency – one example of man made neurones is discussed on the website Interesting Engineering, which are able to produce impulses up to one billion times per second. Fascinatingly, this is quicker than humans, so it could also be argued that AI is actually better than us! There are many phases of the drug development process, from early pre-clinical research to post-market surveillance. When a drug is administered, the body uses enzymes such as mainly those from the CYP family to break the compound down into smaller structures, through a process known as metabolism. Drug metabolism can create toxic molecules that are able to covalently bind to proteins in the body causing serious illness, but also molecules that can be harmlessly excreted through faeces or urine. Of course, chemists can look for sites of metabolism by studying the angles and positions of atoms, however AI is able to do this much quicker and with higher accuracy. SuperCYPsPred is an example of a free online web application that can predict if a drug may be a CYP enzyme inhibitor in pre-clinical drug discovery, as the software is able to identify five of such inhibitors. Through this, we can understand how a drug’s metabolic pathway may differ and investigate further early on, allowing scientists to make structural changes before proceeding onto the next phase of development. Through this, millions of pounds can be saved from marketing an unsuccessful drug as well as decrease the chances of causing injury to the public. AI is also able to use machine learning (ML) to carry out tasks. ML is when machinery processes a large data set and identifies complex patterns to problem solve. From this then comes deep learning (DL), which allows this ML to be applied in different fields. For example, DeepCE is a “novel deep learning computer model” that helps predict changes in gene expression with certain drugs. It is able to do this by using the following two sources: DrugBank which contains data for 11,000 safely approved drugs and the L1000 dataset that has information on over 1 million perturbed organ tissue gene expressions. From this, researchers were able to obtain 10 drug candidates for the treatment of COVID-19 infection, in which 2 have been successfully marketed. Based on the above, it is clear that AI holds a lot of power in speeding up the drug discovery and development process. With the technology sector advancing in general as well, we are looking at a future where AI will become even more dominant in the pharmaceutical research industry. Whilst AI can predict several drug properties, it is also important to remember that we physically cannot predict every single thing out there – we can only try our best, which AI is aiding. Written by Harsimran Kaur Related articles: AI in drug discovery / A breakthrough procedure in efficient drug discovery / Role of chemistry in medicine Project Gallery

Getting treatment can prevent things from getting worse Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Depression in Children 10/07/25, 11:17 Last updated: Published: 17/06/23, 13:46 Getting treatment can prevent things from getting worse It's normal for kids to feel sad, act grouchy, or be in a bad mood at times. But when a sad or bad mood lasts for weeks or longer, and when there are other changes in a child's behavior, it might be depression. Therapy can help children who are going through sadness or depression. And there are things parents can do, too. Getting the right care can prevent things from getting worse and help a child feel better. Symptoms of depression Sad or bad mood. A child may seem sad, lonely, unhappy, or grouchy. It can last weeks or months. A child may cry more easily. They may have more tantrums than before. Being self-critical. Kids going through depression may complain a lot. They may say self-critical things like, "I can't do anything right." "I don't have any friends." "I can't do this." "It's too hard for me." Lack of energy and effort. Depression can drain a child's energy. They might put less effort into school than before. Even doing little tasks can feel like too much effort. Kids may seem tired, give up easily, or not try. Not enjoying things. Kids don't have as much fun with friends or enjoy playing like before. They may not feel like doing things they used to enjoy. Sleep and eating changes. Kids may not sleep well or seem tired even if they get enough sleep. Some may not feel like eating. Others may overeat. Aches and pains. Some children may have stomach aches or other pains. Some miss school days because of not feeling well, even though they aren't sick. Causes of depression Some common reasons include: - life events like someone dying - moving schools or other big changes - physical health problems - experiencing physical, sexual or psychological abuse or neglect - witnessing violence or a traumatic event - if you have an unstable family environment Intervention Three of the more common methods used in depression treatment include: - cognitive behavioral therapy - interpersonal therapy - psychodynamic therapy Written by Chhaya Dhedi Related articles: Childhood stunting in developing nations / What does depression do to your brain? / Brain of a bully / Anxiety / Postpartum depression in adolescent mothers Project Gallery

The tireless challenge Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Childhood stunting in developing countries 09/03/26, 15:17 Last updated: Published: 09/03/24, 17:53 The tireless challenge Introduction Certain countries worldwide face numerous challenges that decrease their populations' quality of life; some include hunger, poverty and rising harmful emissions, which are complicated to resolve. This is because international cooperation is needed to tackle them effectively. Another significant challenge faced is stunting, defined as diminished growth and development that children experience, because of undernutrition or lack of sufficient nutrients, frequent infections and deficient psychosocial interventions, according to the World Health Organisation (WHO). As of 2025, the latest findings reveal that an estimated 127 million children in the globe are affected by stunting. WHO's target of stunting reduction by 2030 has not yet been met (the target was originally for 2025, but was forced to be pushed back due to slow progress). With this definition in mind, this article will delve into stunting and malnutrition before discussing how stunting is linked to infectious diseases and harmful emissions, and steps forward to reduce this condition in developing countries, as shown in Figure 2 . Undernutrition and stunting Stunting is one of the consequences of undernutrition, possibly due to reduced synthesis of insulin-like growth factor 1 (IGF-1) in the body, leading to amplified growth hormone (6). As for the determinants of undernutrition, a paper from Brazil found socioeconomic characteristics like family income and biological ones such as age notably linked to undernutrition. Another result of undernutrition is being underweight. A systematic review from Ethiopia focusing on nutrition in 5-year-old children amalgamated 18 studies. It estimated that stunting and being underweight had 42% and 33% prevalence, respectively; it could be inferred that undernutrition is linked to stunting. Additionally, a paper that used data from 32 Sub-Saharan African countries discovered that providing maternal health insurance (MHI) reduces stunting and being underweight, which explains that boys are more likely to be affected by stunting than girls in all UN regions and sub-regions. In turn, MHI is necessary for supporting children’s health. Non-nutritional factors and stunting As for infections and stunting, an article highlighted that children with stunted growth are vulnerable to diarrhoeal and respiratory diseases besides malaria. Moreover, conditions worsen undernutrition, causing a vicious cycle between them, manifesting into growth defects. Furthermore, a systematic review of 80 studies found a connection between helminth infections and stunting, but insufficient evidence supported this hypothesis. With this said, there may need to be additional studies to investigate this further. With undernutrition’s impact on the immune system, newborns and small children with extreme protein deficiency have smaller thymuses and underdeveloped peripheral lymphoid organs, leading to immunological cell defects such as reduced T-cell count. Before concluding this article, exposure to harmful emissions is a recurring problem that affects everyone, including children. Different observational studies proposed that inhaling nitrogen oxide and particulate matter in utero could modify DNA methylation, possibly influencing foetal growth. Conclusion Reflecting on all the evidence in this article, stunting in developing countries is heading in a direction where it could become problematic. However, according to findings from UNICEF, stunting has gradually reduced between 2000 and 2020 in children under 5 years old. Nevertheless, awareness of stunting in developing countries is critical because it is the first step to tackling this health issue, and ultimately meet the WHO target by 2030. Written by Sam Jarada Related articles: Childhood obesity / Depression in children / Postpartum depression in adolescent mothers REFERENCES Jamali D, Leigh J, Samara G, Barkemeyer R. Grand challenges in developing countries: Context, relationships, and logics. Business Ethics, the Environment & Responsibility. 2021 Sep;30(S1):1–4. Maleta K. Undernutrition. Malawi medical journal: the journal of Medical Association of Malawi. 2006 Dec;18(4):189–205. World Health Organization. Stunting in a nutshell. www.who.int . 2015 Nov;19. Beal T, Tumilowicz A, Sutrisna A, Izwardy D, Neufeld LM. A review of child stunting determinants in Indonesia. Maternal & Child Nutrition. 2018 May 17;14(4):e12617. Vaivada T, Akseer N, Akseer S, Somaskandan A, Stefopulos M, Bhutta ZA. Stunting in childhood: an overview of global burden, trends, determinants, and drivers of decline. The American Journal of Clinical Nutrition. 2020 Aug 29;112. Soliman A, De Sanctis V, Alaaraj N, Ahmed S, Alyafei F, Hamed N, et al. Early and Long-term Consequences of Nutritional Stunting: From Childhood to Adulthood. Acta Bio Medica : Atenei Parmensis. 2021;92(1) Correia LL, Silva AC e, Campos JS, Andrade FM de O, Machado MMT, Lindsay AC, et al. Prevalence and determinants of child undernutrition and stunting in semiarid region of Brazil. Revista de Saúde Pública. 2014 Feb 1;48:19–28. Abdulahi A, Shab-Bidar S, Rezaei S, Djafarian K. Nutritional status of under five children in Ethiopia: a systematic review and meta-analysis. Ethiopian Journal of Health Sciences. 2017 Mar 15;27(2):175. Kofinti RE, Koomson I, Paintsil JA, Ameyaw EK. Reducing children’s malnutrition by increasing mothers’ health insurance coverage: A focus on stunting and underweight across 32 sub-Saharan African countries. Economic Modelling. 2022 Dec 1;117:106049. Vonaesch P, Tondeur L, Breurec S, Bata P, Nguyen LBL, Frank T, et al. Factors associated with stunting in healthy children aged 5 years and less living in Bangui (RCA). Wieringa F, editor. PLOS ONE. 2017 Aug 10;12(8):e0182363. Raj E, Calvo-Urbano B, Heffernan C, Halder J, Webster JP. Systematic review to evaluate a potential association between helminth infection and physical stunting in children. Parasites & Vectors. 2022 Apr 20;15(1). Schaible UE, Kaufmann SHE. Malnutrition and Infection: Complex Mechanisms and Global Impacts. PLoS Medicine. 2007 May 1;4(5):e115. Sinharoy SS, Clasen T, Martorell R. Air pollution and stunting: a missing link? The Lancet Global Health. 2020 Apr;8(4):e472–5. UNICEF. Malnutrition in Children. UNICEF DATA. 2023. Project Gallery

Using Surface Guided Radiation Therapy (SGRT) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Revolutionising patient setup in cancer treatment 11/07/25, 10:50 Last updated: Published: 18/10/23, 11:50 Using Surface Guided Radiation Therapy (SGRT) Cancer treatment can be a painstaking and difficult procedure to undergo given the complexity in the treatment process. The weight of a cancer diagnosis carries a huge mental and physical burden on the patient. It is therefore important to place emphasis on delivering an efficient and streamlined process whilst at the same time not cutting any corners. Manual methods of delivering care can and should be automated by AI and technology where possible. This is especially applicable in the preparation of delivering a dose of radiotherapy treatment where traditionally, breast cancer patients will undergo a tattoo setup which provides physical guidance on area at which the dose should be delivered. Patients suffer not only by the knowledge of the disease, but they are also marked with reminders of the experience by an increasingly outdated positioning technique. Innovation in radiotherapy treatment allows for a more ethical and streamlined solution. Surface Guided Radiation Therapy (SGRT) treatments provide a means for tracking a patient's position before and during radiation therapy, to help ensure a streamlined workflow for accurate treatment delivery. This type of treatment not only eliminates the need for an invasive tattoo setup but also provides a faster and more accurate way to deliver radiation doses to the patient. For example, precise measurements made by the software will ensure that radiation is delivered specifically to the targeted area and not the surrounding tissue. With a regular tattoo setup, this can be a common issue as patient movement, often triggered by respiration, can alter the accuracy of the tattoo markup, thereby reducing the effectiveness of the radiation treatment. The way in which many SGRTs work is through a system of cameras, mounted to the ceiling, which feed data into a software program. Each camera unit uses a projector and image sensors to create a 3D surface model of the area by projecting a red light onto the patient’s skin. (See Figure 2) This 3D surface model serves as a real-time map of the patient's position and surface contours. By constantly comparing the captured data with the pre-defined treatment plan, any deviations or movements can be detected instantly. If the patient moves beyond a predetermined threshold, the treatment can be paused to ensure accuracy and safety. The use of this cutting-edge technology is an important step in being able to provide some level of comfort for patients in a challenging environment. The integration of such systems represents a significant advancement in patient-centric care in the field of radiation therapy. Written by Jaspreet Mann Related article: Nuclear medicine Project Gallery