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From foe to ally Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Herpes vs devastating skin disease 09/07/25, 14:16 Last updated: Published: 06/01/24, 11:14 From foe to ally This is article no. 3 in a series on rare diseases. Next article: Epitheliod hemangioendothelioma . Previous article: Breast cancer in males . Have you ever plucked loose skin near your nail, ripping off a tiny strip of good skin too? Albeit very small, that wound can be painful. Now imagine that it is not just a little strip that peels off, but an entire sheet. And it does not detach only when pulled, but at the slightest touch. Even a hug opens wounds, even a caress brings you pain. This is life with recessive dystrophic epidermolysis bullosa (RDEB), the most severe form of dystrophic pidermolysis bullosa (DEB). Herpes becomes a therapy DEB is a rare genetic disease of the skin that affects 3 to 10 individuals per million people (prevalence is hard to nail down for rare diseases). A cure is still far off, but there is good news for patients. Last May, the US Food and Drug Administration (FDA) approved Vyjuvek (beremagen geperparvec) to treat skin wounds in DEB. Clinical studies showed that it speeds up healing and reduces pain. Vyjuvek is the first gene therapy for DEB. It is manufactured by Krystal Biotech and - get this- it is a tweaked version of the herpes virus. Yes, you got that right, the virus causing blisters and scabs has become the primary ally against a devastating skin disease. This approval is a milestone for gene therapies, as Vyjuvek is the first gene therapy - based on the herpes virus, - to apply on the skin as a gel, - approved for repeated use. This article describes how DEB, and especially RDEB, affects the skin and wreaks havoc on the body; the following article will explain how Vyjuvek works. DEB disrupts skin integrity We carry around six to nine pounds of skin. Yet we often forget its importance: it stops germs and UVs, softens blows, regulates body temperature and makes us sensitive to touch. Diseases that compromise the skin are therefore devastating. These essential functions rely on the organisation of the skin in three layers: epidermis, dermis and hypodermis ( Figure 1 ). Typically, a Velcro strap of the protein collagen VII firmly anchors the epidermis to the dermis. The gene COL7A1 contains the instructions on how to produce collagen VII. In DEB, mutations in COL7A1 result in the production of a faulty collagen VII. As the Velcro strap is weakened, the epidermis becomes loosely attached to the dermis. Mutations in one copy of COL7A1 cause the dominant form of the disease (DDEB), mutations in both copies cause RDEB. With one copy of the gene still functional, the skin still produces some collagen VII, when both copies are mutated, little to no collagen VII is left. Therefore, RDEB is more severe than DDEB. In people with RDEB, the skin can slide off at the slightest touch and even gentle rubs can cause blisters and tears ( Figure 2 ). Living with RDEB Life with RDEB is gruelling and life expectancy doesn't exceed 30 years old. Wounds are very painful, slow to heal and get infected easily. The risk of developing an aggressive skin cancer is higher. The constant scarring can cause limb deformities. In addition, blisters can appear in the mouth, oesophagus, eyes and other organs. There is no cure for DEB for now; treatments can only improve the quality of life. Careful dressing of wounds promotes healing and prevents infections. Painkillers are used to ease pain. Special diets are required. And, to no one's surprise, physical activities must be avoided. Treating RDEB Over the past decade, cell and genetic engineering advances have sparked the search for a cure. Scientists have explored two main alternatives to restore the production of collagen VII in the skin. The first approach is based on transferring skin cells able to produce collagen VII. Despite promising results, this approach treats only tinyl patches of skin, requires treatments in highly specialised centres and it may cause cancer. The second approach is the one Vyjuvek followed. Scientists place the genetic information to make collagen VII in a modified virus and apply it to a wound. There, the virus infects skin cells, providing them with a new COL7A1 gene to use. These cells now produce a functional collagen VII and can patch the damage up. We already know which approach came up on top. Vyjuvek speeds up the healing of wounds as big as a smartphone. Professionals can apply it in hospitals, clinics or even at the patient’s home. And it uses a technology that does not cause cancer. But how does Vyjuvek work? And why did scientists choose the herpes virus to build Vyjuvek? We will find the answer in the following article. And since perfection does not belong to biology, we will also discuss the limitations of this remarkable gene therapy. NOTES: 1. DEB is part of a group of four inherited conditions, collectively named epidermolysis bullosa (EB), where the skin loses integrity. EB is also known as “Butterfly syndrome” because the skin becomes as fragile as a butterfly’s wing. These conditions are EB simplex, junction EB, dystrophic EB and Kindler EB. 2. Most gene therapies are based on modified, or recombinant in science jargon, adenoassociated viruses, which I reviewed for Scientia News. 3. Over 700 mutations have been reported. They disrupt collagen VII and its function with various degrees of severity. Consequently, RDEB and DDEB display several clinical phenotypes. 4. Two studies have adopted this approach: in the first study, Siprashvili and colleagues (2016) grafted ex vivo retrovirally-modified keratinocytes, the main cell type in the epidermis, over the skin of people with RDEB; in the second study, Lwin and colleagues (2019) injected ex vivo lentivirally-modified fibroblasts in the dermis of people with RDEB. Written by Matteo Cortese, PhD Related article: Ehlers-Danlos syndrome Project Gallery

Looking at the option of nuclear fusion to generate renewable energy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unleashing the power of the stars: how nuclear fusion holds the key to tackling climate change 14/07/25, 15:08 Last updated: Published: 30/04/23, 10:55 Looking at the option of nuclear fusion to generate renewable energy Imagine a world where we have access to a virtually limitless and clean source of energy, one that doesn't emit harmful greenhouse gases or produce dangerous radioactive waste. A world where our energy needs are met without contributing to climate change. This may sound like science fiction, but it could become a reality through the power of nuclear fusion. Nuclear fusion, often referred to as the "holy grail" of energy production, is the process of merging light atomic nuclei to form a heavier nucleus, releasing an incredible amount of energy in the process. It's the same process that powers the stars, including our very own sun, and holds the potential to revolutionize the way we produce and use energy here on Earth. Nuclear fusion occurs at high temperature and pressure when two atoms (e.g. Tritium and Deuterium atoms) merge together to form Helium. This merge releases excess energy and a neutron. This energy an then be harvested inform of heat to produce electricity. Progress in the field of creating a nuclear fusion reactor has been slow, despites the challenges there are some promising technologies and approaches have been developed. Some of the notable approaches to nuclear fusion research include: 1. Magnetic Confinement Fusion (MCF) : In MCF, high temperatures and pressures are used to confine and heat the plasma, which is the hot, ionized gas where nuclear fusion occurs. One of the most promising MCF devices is the tokamak, a donut-shaped device that uses strong magnetic fields to confine the plasma. The International Thermonuclear Experimental Reactor (ITER), currently under construction in France, is a large-scale tokamak project that aims to demonstrate the scientific and technical feasibility of nuclear fusion as a viable energy source. 2. Inertial Confinement Fusion (ICF) : In ICF, high-energy lasers or particle beams are used to compress and heat a small pellet of fuel, causing it to undergo nuclear fusion. This approach is being pursued in facilities such as the National Ignition Facility (NIF) in the United States, which has made significant progress in achieving fusion ignition, although it is still facing challenges in achieving net energy gain. In December of 2022, the US lab reported that for the first time, more energy was released compared to the input energy. 3. Compact Fusion Reactors: There are also efforts to develop compact fusion reactors, which are smaller and potentially more practical for commercial energy production. These include technologies such as the spherical tokamak and the compact fusion neutron source, which aim to achieve high energy gain in a smaller and more manageable device. While nuclear fusion holds immense promise as a clean and sustainable energy source, there are still significant challenges that need to be overcome before it becomes a practical reality. In nature nuclear fusion is observed in stars, to be able to achieve fusion on Earth such conditions have to be met which can be an immense challenge. High level of temperature and pressure is required to overcome the fundamental forces in atoms to fuse them together. Not only that, but to be able to actually use the energy it has to be sustained and currently more energy is required then the output energy. Lastly, the material and technology also pose challenges in development of nuclear fusion. With high temperature and high energy particles, the inside of a nuclear fusion reactor is a harsh environment and along with the development of sustained nuclear fusion, development of materials and technology that can withstand such harsh conditions is also needed. Despite many challenges, nuclear fusion has the potential to be a game changer in fight against not only climate change but also access of cheap and clean energy globally. Unlike many forms of energy used today, fusion energy does not emit any greenhouse gasses and compared to nuclear fission is stable and does not produce radioactive waste. Furthermore, the fuel for fusion, which is deuterium is present in abundance in the ocean, where as tritium may require to synthesised at the beginning, but once the fusion starts it produce tritium by itself making it self-sustained. When the challenges are weighted against the benefits of nuclear fusion along with the new opportunities it would unlock economically and in scientific research, it is clear that the path to a more successful and clean future lies within the development of nuclear fusion. While there are many obstacles to overcome, the progress made in recent years in fusion research and development is promising. The construction of ITER project, along with first recordings of a higher energy outputs from US NIF programs, nuclear fusion can become a possibility in a not too distant future. In conclusion, nuclear fusion holds the key to address the global challenge of climate change. It offers a clean, safe, and sustainable energy source that has the potential to revolutionize our energy systems and reduce our dependence on fossil fuels. With continued research, development, and investment, nuclear fusion could become a reality and help us build a more sustainable and resilient future for our planet. It's time to unlock the power of the stars and harness the incredible potential of nuclear fusion in the fight against climate change. Written by Zari Syed Related articles: Nuclear medicine / Geoengineering / The silent protectors / Hydrogen cars Project Gallery

Through AI Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Revolutionising sustainable agriculture 11/07/25, 09:51 Last updated: Published: 27/06/23, 15:34 Through AI Artificial Intelligence (AI) is taking the world by storm. Recent developments now allow scientists to integrate AI into sustainable farming. Through transforming the way we grow crops, manage resources and pests, and most importantly- protect the environment. There are many applications for AI in agriculture. Outlined below are some of the areas in which the incorporation of AI systems improves sustainability: Precision farming Artificial intelligence systems help improve the overall quality and accuracy of harvesting – known as precision farming. Artificial intelligence technology helps detect plant diseases, pests, and malnutrition on farms. AI sensors can detect and target weeds, then decide what herbicide to use in an area. This helps reduce the use of herbicides and lower costs. Many tech companies have developed robots that use computer vision and AI to monitor and precisely spray weeds. These robots can eliminate 80% of the chemicals normally sprayed on crops and reduce herbicide costs by 90%. These intelligent AI sprayers can drastically reduce the amount of chemicals used in the field, improving product quality, and lowering costs. Vertical farming Vertical farming is a technique in which plants are grown vertically by being stacked on top of each other (usually indoors) as opposed to the ‘traditional way’ of growing plants and crops on big strips of land. This approach offers several benefits for sustainable agriculture and waste reduction. The use of AI brings even more significant advancements making vertical farming more sustainable and efficient- Intelligent Climate Control: AI can use algorithms to measure and monitor temperature, humidity, and lighting conditions to optimise climate control in vertical farms. Thus, reducing energy consumption and improving resource efficiency. Creating an enhanced climate-controlled environment also allows for repeatable and programmable crop production. Predictive Plant Modelling: the difference between a profitable year and a failed harvest can just be the specific time the seeds were sowed. By using AI, farmers can use predictive analysis tools to determine the exact date suitable for sowing seeds for maximum yield and reduce waste from overproduction. Automated Nutrient Monitoring: to optimise plant nutrition, AI systems monitor and adjust nutrient levels in hydroponic (plants immersed in nutrient containing water) and aeroponic setups (plants growing outside the soil, with nutrients being provided by spraying the roots). Genetic engineering AI plays a pivotal role in genetic engineering, enhancing the sustainability and precision of crop modification through- Targeted Gene Editing: AI algorithms help in gene editing to produce desirable traits in crops, such as resistance to disease or improved nutritional content. This allows genetic modification without the need to conduct extensive field trials. Thus, saving time and resources. Computational Modelling: by combining AI modelling with gene prediction, farmers will be able to predict which combinations of genes have the potential to increase crop yield. Pest management and disease detection Artificial intelligence solutions such as smart pest detection systems are being used to monitor crops for signs of pests and diseases. These systems detect changes in the environment such as temperature, humidity, and soil nutrients, then alert farmers when something is wrong. This allows farmers to act quickly and effectively, taking preventive measures before pests cause significant damage. Another way to achieve this is by using computer vision and image processing techniques. AI can detect signs of pest infestation, nutrient deficiencies and other issues that can affect yields. This data can help farmers make informed decisions about how to protect their crops. By incorporating AI into these aspects of sustainable agriculture, farmers can achieve high yields, reduce waste and enable more sustainable farming practices, reducing environmental impacts while ensuring efficient food production. Written by Aleksandra Zurowska Related articles: Digital innovation in rural farming / Plant diseases and nanoparticles 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: 03/04/25, 10:27 Published: 03/04/25, 07:00 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 would require the hull 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

A collaboration with the Mesothelioma Center (Asbestos.com), USA Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Breast Cancer and Asbestos 04/02/25, 15:44 Last updated: Published: 06/06/23, 10:03 A collaboration with the Mesothelioma Center (Asbestos.com), USA Breast cancer is a prevalent disease characterized by abnormal cell growth in the breast. There are various types of breast cancer, including invasive ductal carcinoma, invasive lobular carcinoma, Paget's disease, medullary mucinous carcinoma, and inflammatory breast cancer. In 2022, approximately 287,850 new cases of invasive breast cancer were diagnosed, making it the most commonly diagnosed cancer in women. Natural risk factors for breast cancer include gender, age, race, early onset of menstruation, family history, and genetics. Environmental factors, such as exposure to radiation, pesticides, polycyclic aromatic hydrocarbons, and metals, may also contribute to the risk of developing breast cancer. Some studies have suggested a possible connection between asbestos exposure and breast cancer. While the link between asbestos and other health conditions like mesothelioma cancer is well-established, the exact relationship between asbestos and breast cancer remains unclear. Statistical significance refers to the level of confidence in the results of a study or experiment. In the context of studies investigating the correlation between asbestos exposure and breast cancer, Dr. Debra David points out that many studies fail to establish a conclusive link due to a lack of statistical significance. Certain factors can increase the risk of developing breast cancer, known as "partial risk factors." Some of these factors can be controlled by individuals, such as alcohol consumption. However, many other partial risk factors are not within an individual's control without compromising their overall health. For example, receiving radiation therapy to the chest or making decisions regarding childbirth can be deeply personal choices that impact breast cancer risk. Examples of partial risk factors include consuming more than two alcoholic drinks per day, having children after the age of 30, not having children, not breastfeeding, using the drug diethylstilbestrol (DES) to prevent miscarriage, recent use of birth control pills, receiving hormone replacement therapy (HRT), undergoing radiation therapy to the chest area, and exposure to toxic substances or carcinogens. According to the American Cancer Society, approximately 5 to 10% of breast cancer cases can be directly attributed to inherited gene mutations. However, many other factors, such as exposure to carcinogens, may be beyond a cancer patient's control. Summary written by the Mesothelioma Center ( Asbestos.com ) For more information, visit their website , and also read important facts breast cancer and mesothelioma survival rate . For further information, particularly the legal consequences, check out the Lanier Law Firm, which has more specific information Project Gallery

Celebrating trailblazers in skin cancer, chemotherapy and cervical cancer cells Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link African-American women in cancer research 08/07/25, 16:23 Last updated: Published: 20/04/24, 11:05 Celebrating trailblazers in skin cancer, chemotherapy and cervical cancer cells We are going to be spotlighting the incredible contributions of three African-American women who have carved paths for future scientists while significantly advancing our knowledge in the relentless global battle against cancer. Jewel Plummer Cobb (1924-2017) As a distinguished cancer researcher, Jewel is known for her extensive work on melanoma, a serious form of skin cancer. Alongside her frequent collaborator, Jane Cooke Wright, Jewel evidenced the anticancer effects of the drug methotrexate in addressing skin and lung cancer, as well as childhood leukaemia. She is also recognised for her distinctive research examining the varying responses to chemotherapy drugs among cells from different racial and ethnic groups. This research led to the pivotal finding that melanin, a skin pigment, could serve as a protective shield against the damaging effects of sunlight associated with skin cancer. Her 1979 article titled Filters for Women in Science recognised the low percentage of women working in scientific research and engineering, including the barriers that female scientists face in their professional journey. As a result, throughout her career, she often wrote about the experiences of black women in higher education. She also passionately championed for the advancement of black people and women working in the fields of science and medicine. In an interview, she stated that she would like to be remembered as “a black woman scientist who cared very much about what happens to young folks, particularly women, going into science”. Jane Cooke Wright (1919-2013) As the daughter of Harvard Medical School graduate, Louis Tompkins Wright, one of the first African American surgeons in the United States, Jane followed in her father’s footsteps and became a physician. Working together, they explored and compared the activity of possible anticancer compounds in both tissue cultures and in patients. This was revolutionary at the time, considering that chemotherapy guidelines were barely established. In collaboration with her father and six male doctors, the team established the American Society of Clinical Oncology (ASCO) to address the clinical needs of cancer patients. Later on, Jane led ASCO at just 33 years old, following her father’s death. Throughout her career, she conducted research in chemotherapy, publishing over 100 articles on the topic, aiming to fine-tune and tailor chemotherapeutic treatments for patients to ensure better survival outcomes. Like Jewel, she also played a key role in investigating and demonstrating how different racial and ethnic backgrounds respond to drugs used in chemotherapy. This has now become a field of its own, pharmacoethnicity, which studies the anticancer drug responses across people of different ethnicities and is advancing our knowledge on personalised chemotherapy treatment for patients. During an interview, her daughter, Alison Jones, described Jane as: A very ambitious person... she never let anything stand in the way of doing what she wanted to do. Henrietta Lacks (1920-1951) Although not a scientist herself, Henrietta has made a significant contribution to cancer research and medicine through her cervical cancer cells. Although, tragically, she did not know it. Henrietta was diagnosed with cervical cancer in 1951 and sadly passed away the same year. The cervical cancer cells obtained from her biopsy were found to have a unique ability to continuously grow and divide in vitro. Therefore, they could be grown into cell cultures and used in further research. As a result of this trait, researchers have investigated their behaviour, including mutation, division, and carcinogenesis, allowing them to study the effects of drugs and other treatments on these cells. The “immortal” cell line, termed HeLa, has played a pivotal role in the creation of the polio vaccine in the 1950s and medicines for conditions such as leukaemia, influenza, and Parkinson's disease. The HeLa cells also identified the Human papillomavirus (HPV), which later led to the finding that the virus can cause different types of cervical cancer, leading to the significant development of the HPV vaccine used today. It is estimated that over 110,000 research publications have used HeLa cells, emphasising their demand in research. Were it not for Henrietta Lacks, the HeLa cell line would not have been discovered, which has revolutionised our understanding of cancer and medical advancements. In conclusion, the remarkable journey of these pioneering African American women in cancer research serves not only as an inspiration but also a testament to their perseverance, courage, and dedication. They have championed diversity within science, pushed boundaries, and shaped the field of cancer research, allowing for the progress of scientific research in curing cancer and beyond. Written by Meera Solanki Related articles: Women leading the charge in biomedical engineering / The foremothers of gynaecology / Sisterhood in STEM REFERENCES American Society of Clinical Oncology (2016). Society History. [online] ASCO. Available at: https://old-prod.asco.org/about-asco/overview/society-history . Blood Cancer UK (2023). Blood Cancer UK | The story of Dr Jane C Wright, pioneer of blood cancer research. [online] Blood Cancer UK. Available at: https://bloodcancer.org.uk/news/the-story-of-jane-c-wright-pioneer-of-blood-cancer- research/. Boshart, M., Gissmann, L., Ikenberg, H., Kleinheinz, A., Scheurlen, W. and zur Hausen, H. (1984). A new type of papillomavirus DNA, its presence in genital cancer biopsies and in cell lines derived from cervical cancer. The EMBO Journal, 3(5), pp.1151–1157. doi: https://doi.org/10.1002/j.1460-2075.1984.tb01944.x . Cobb, J.P. (1956). Effect of in Vitro X Irradiation on Pigmented and Pale Slices of Cloudman S91 Mouse Melanoma as Measured by Subsequent Proliferation in Vivo234. JNCI: Journal of the National Cancer Institute, [online] 17(5). doi: https://doi.org/10.1093/jnci/17.5.657 . Cobb, J.P. (1979). Filters for Women in Science. Annals of the New York Academy of Sciences, 323(1 Expanding the), pp.236–248. doi: https://doi.org/10.1111/j.1749- 6632.1979.tb16857.x. Ferry, G. (2022). Jane Cooke Wright: innovative oncologist and leader in medicine. The Lancet, [online] 400(10360). doi: https://doi.org/10.1016/S0140-6736(22)01940-7 . Hyeraci, M., Papanikolau, E.S., Grimaldi, M., Ricci, F., Pallotta, S., Monetta, R., Minafò, Y.A., Di Lella, G., Galdo, G., Abeni, D., Fania, L. and Dellambra, E. (2023). Systemic Photoprotection in Melanoma and Non-Melanoma Skin Cancer. Biomolecules, [online] 13(7), p.1067. doi: https://doi.org/10.3390/biom13071067 . King, T., Fukishima, L., Donlon, T., Hieber, D. and Shimabukuro, K. (2000). Correlation between growth control, neoplastic potential and endogenous connexin43 expression in HeLa cell lines: implications for tumor progression. Carcinogenesis, [online] 21(2), pp.311–315. doi: https://doi.org/10.1093/carcin/21.2.311 . National Institutes of Health (2022). Significant Research Advances Enabled by HeLa Cells - Office of Science Policy. [online] Office of Science Policy. Available at: https://osp.od.nih.gov/hela-cells/significant-research-advances-enabled-by-hela- cells/. Pathak, S., Zajac, K.K., Manjusha Annaji, Manoj Govindarajulu, Nadar, R.M., Bowen, D., R. Jayachandra Babu and Muralikrishnan Dhanasekaran (2023). Clinical outcomes of chemotherapy in cancer patients with different ethnicities. Cancer Reports, 6(1). doi: https://doi.org/10.1002/cnr2.1830 . Project Gallery

Exploring the genetic roots of a neurological tragedy Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Breaking down Tay-Sachs 15/05/25, 10:43 Last updated: Published: 20/04/24, 11:29 Exploring the genetic roots of a neurological tragedy This is article no. 9 in a series on rare diseases. Next article: Ehlers-Danlos Syndrome . Previous article: Pseudo-Angelman Syndrome . Tay-Sachs disease is a heritable metabolic condition that affects the neurons in the brain. The disease is more common in infants and young children as well as people of Ashkenazi Jewish descent, although it can occur in any ethnicity. Symptoms of the disease most commonly manifest themselves in children around six months of age. However, it is possible to develop symptoms from five years old to the teenage years. There are three different forms of the disease, each appearing at different stages of life: infantile, juvenile, and adult. The adult form is much rarer and non-fatal but can still cause neuron dysfunction and psychosis. Early symptoms of the disease include mobility issues such as difficulty crawling, and as the disease progresses, the child may suffer from seizures, vision, and hearing loss. In the classic infantile form, the disease is fatal within the first few years of life or by three to five years old. In infants, infection and respiratory complications, such as pneumonia, are the most common cause of death. Being categorised as an autosomal recessive disease means that in order to display the phenotype, two copies of the mutated HEXA gene must be present in an individual. This HEXA gene is located on chromosome 15 and is responsible for producing enzymes that affect the nerve cells. The carrier frequency of Tay-Sachs is highly dependent on ethnic backgrounds, with carrier frequency being 1 in 30 for those of Ashkenazi Jewish descent and 1 in 300 for others. The chance of developing the disease early or late is predicated on the specific type of HEXA mutation that is inherited within the family. Meaning, if one child in a family possesses the infantile form, all other members of the family will also possess the infantile form (if they express the phenotype). When both parents are carriers of the Tay-Sachs gene mutation, there is a 25% chance with each pregnancy that the child will inherit two mutated copies of the HEXA gene and thus be affected by the disease. Also, there is a 50% chance the child will be a carrier like the parents and a 25% chance the child will inherit two normal copies of the gene and be unaffected. Furthermore, this particular type of gene mutation results in the disease being commonly labelled as a hexosaminidase A deficiency. The HEXA gene’s significance in the disease is further highlighted due to its ability to code for specific alpha subunits in the enzyme β-hexosaminidase A. This enzyme is involved in breaking down molecules that can be recycled in a cell through the use of lysosomes. This key cellular function helps a cell undergo apoptosis (programmed cell death) or help evade bacteria that can damage a cell. However, in individuals with this HEXA gene mutation, less of the enzyme β-hexosaminidase A is produced, which results in less degradation of GM2 ganglioside. GM2 ganglioside is a lipid involved in a host of processes such as membrane organisation, neuronal differentiation, and signal transduction. In addition, due to its lack of degradation, it accumulates inside the body. The rate at which the lipid accumulates inside the cell ultimately determines the form of Tay-Sachs an individual will possess. It is worth noting that this GM2 ganglioside pathology also includes other diseases, such as Sandhoff disease and the AB variant, which have similar disease prognoses. Furthermore, the disease specifically targets the brain as gangliosides are the main lipids that compose neuronal plasma membranes. Their expression is specific to brain regions, impacting key neurodevelopmental processes like neural tube formation and synaptogenesis. Furthermore, ganglioside synthesis is a highly regulated process facilitated by glycosyltransferases during transcription and post-transcription. They also modulate ion channels and receptor signalling, which are crucial for neurotransmission, memory, and learning. The exact mechanism of how this ganglioside accumulation due to HEXA malfunction leads to neuronal death remains unclear. Figure 1 illustrates the dysfunction of the alpha subunit in HEXA as it cannot break down GM2 gangliosides. This results in an accumulation of GM2 within the liposome, contrasting with its concentration in the external environment. This accumulation of GM2 causes lysosomal dysfunction and eventually cell damage, which leads to the symptoms commonly associated with Tay-Sachs. Mouse models have been created to understand this GM2 pathway in greater detail to develop treatments. However, this is quite limited as mice do not have the same pathway of breaking down GM2 as humans. Also, since the disease may be prevalent before birth, it is hard to establish the damage done to a baby inside the womb, making reversing this disease in infants very challenging. However, the later onset types of Tay-Sachs disease might respond to treatment. Implementing ganglioside synthesis inhibitors in combination with existing DNA and enzymatic screening programs holds promise for eventually managing and controlling this condition. Parents can undergo genetic screening to assess their risk of carrying the Tay-Sachs gene, which is done by doing a simple blood test that examines the DNA for mutations in the HEXA gene. Genetic screening is particularly important for couples who have a family history of Tay-Sachs disease or who belong to ethnic groups with a higher prevalence of the condition. Early detection through genetic screening allows couples to make informed reproductive decisions, such as pursuing in vitro fertilisation with preimplantation genetic testing or opting for prenatal testing during pregnancy to determine if the foetus has inherited the mutated gene. Utilising the acronym SHADES as a mnemonic to recognise potential signs of Tay-Sachs disease in their child can help parents get a prompt medical evaluation if any symptoms arise. SHADES: S tartle response H earing loss A ffecting vision D evelopmental delay E pileptic seizures S wallowing difficulties Written by Imron Shah REFERENCES Center, N. (2015). Tay-Sachs disease. Nih.gov . Available at: https://www.ncbi.nlm.nih.gov/books/NBK22250/ . Leal, A.F., Benincore-Flórez, E., Solano-Galarza, D., Garzón Jaramillo, R.G., Echeverri-Peña, O.Y., Suarez, D.A., Alméciga-Díaz, C.J. and Espejo-Mojica, A.J. (2020). GM2 Gangliosidoses: Clinical Features, Pathophysiological Aspects, and Current Therapies. International Journal of Molecular Sciences, 21(17), p.6213. doi: https://doi.org/10.3390/ijms21176213 . Ramani, P.K. and Parayil Sankaran, B. (2022). Tay-Sachs Disease. PubMed. Available at: https://www.ncbi.nlm.nih.gov/books/NBK564432/ . Project Gallery

In bones, neural communications, fertilisation and more Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The importance of calcium in life Last updated: 12/03/25, 16:45 Published: 10/04/25, 07:00 In bones, neural communications, fertilisation and more Did you know that the same mineral that gives your bones strength also helps to maintain your heartbeat and even plays a role in the very start of life? Calcium, the most abundant mineral in the human body, is primarily found in bones and teeth as calcium phosphate (Ca₃(PO₄)₂). But beyond its structural role, calcium ions are essential for nearly every biological function, from muscle contractions to nerve signalling. What makes calcium so versatile, while other minerals like iron, have far more limited roles? To truly understand its significance, we must explore its underlying chemical properties. Calcium and bones The calcium ion carries a 2+ charge allowing it to form stronger ionic bonds and interact strongly with negatively charged molecules like nucleotides and ATP. This makes it essential for energy transfer in cells. In comparison to monovalent ions like Na+ and K+, calcium, therefore, has a more significant charge density, increasing affinity for anions. However, the ion also has more shells than beryllium and magnesium in the same group (Group 2), contributing to reduced charge density. These properties are very crucial in determining the strength of Calcium compounds, as a high charge density may result in problems with toxicity and difficulty in the breakdown of the product. Calcium phosphate exists as hydroxyapatite in bones and teeth, giving them hardness and rigidity. Hydroxyapatite forms hexagonal crystals that are tightly packed, contributing to the dense, durable structure of bones. These crystals are organised into a matrix along collagen fibres, creating a composite material that combines rigidity (from hydroxyapatite) and flexibility (from collagen). The properties of hydroxyapatite make it uniquely suited for its roles in the body. Its hardness provides bones with the ability to resist deformation and compression, while its porous structure allows space for blood vessels, bone marrow, and the exchange of nutrients and waste. Osteoclasts break down the bone releasing calcium and phosphate ions while osteoblasts can reabsorb this calcium to reform bones in another area of the body, maintaining skeletal health and strength. Neural communication Imagine a relay race where one runner must pass the baton to the next for the race to continue. In a similar way, calcium ions act as messengers in the nervous system, triggering the release of neurotransmitters which allow nerve cells to communicate with each other. Upon experiencing a stimulus, sodium ions begin to enter neurones through voltage-gated sodium channels, causing depolarisation, which sends an electrical signal throughout the neurone that results in the opening of other sodium channels, carrying the electrical signal throughout the neurone until the signal reaches the axon terminal. When the action potential reaches the axon terminal, it triggers the opening of voltage-gated calcium channels in the membrane of the presynaptic neurone. Calcium ions from the extracellular fluid flow into the neurone due to the concentration gradient. This influx of calcium ions is a critical step in neural communication, as it directly facilitates the release of neurotransmitters stored in synaptic vesicles. This action helps to coordinate the strength and the timing of each heartbeat. Calcium ions bind to proteins on the surface of these vesicles, which enables the vesicles to fuse with the presynaptic membrane. This fusion releases neurotransmitters, such as acetylcholine, into the synaptic cleft—a tiny gap between the presynaptic and postsynaptic neurones. These neurotransmitters then bind to specific receptors on the postsynaptic neurone, leading to either an excitatory or inhibitory response. For example, acetylcholine often causes an excitatory response, such as muscle contraction or memory formation. Fertilisation Calcium ions are crucial for fertilisation, facilitating key events from sperm-egg interaction to the activation of embryonic development. When a sperm binds to the egg’s outer layer, calcium ions trigger the release of enzymes from the sperm, enabling it to penetrate the egg. Following the sperm-egg fusion, calcium ions are released within the egg, creating a wave-like signal. The rise in intracellular calcium levels in the egg has several critical effects triggers the cortical reaction, in which cortical granules – small vesicles located beneath the egg’s plasma membrane- release their contents into the space between the plasma membrane and the zona pellucida. The enzymes released during this reaction modify the zona pellucida, making it impermeable to other sperm. This process prevents polyspermy, ensuring that only one sperm fertilises the egg. This precise calcium signalling achieves successful fertilisation and the initiation of new life. Role of calcium in other organisms Calcium is a vital element essential for initiating and sustaining human life, but its importance extends far beyond the human body. Its role is not confined to animals as calcium is equally critical in the physiology of plants and fungi, where it contributes to a wide range of biological processes. In plants, calcium ions are used to form calcium pectate, a chemical used to strengthen the cell walls of the cell and make plant cells stick together. Additionally, calcium is vital for root development and nutrient uptake. It helps in the formation of root nodules in legumes, where nitrogen-fixing bacteria establish symbiotic relationships, and it influences the movement of ions across cell membranes to regulate nutrient transport. Furthermore, calcium oscillations play a crucial role in regulating the polarised growth of fungal hyphae, which are essential for environmental exploration and host infection. Hyphal growth is characterised by a highly localised expansion at the tip, requiring cytoplasmic movement and continuous synthesis of the cell wall. Calcium ions are central to these processes, functioning as dynamic signalling molecules. Calcium concentration is highest at the growing hyphal tip, forming a steep gradient essential for maintaining growth direction. This gradient is not static but oscillatory, with periodic fluctuations in cytosolic calcium levels. These oscillations arise from the interplay of calcium influx through plasma membrane channels like voltage-gated channels. These are critical for coordinating key processes at the hyphal tip. Calcium regulates vesicle trafficking by triggering the fusion of vesicles carrying enzymes with the plasma membrane. Additionally, calcium modulates the actin cytoskeleton, which provides tracks for vesicle transport and maintains the structural polarity of the hypha. Periodic calcium signals promote the dynamic assembly and disassembly of actin filaments, ensuring flexibility and responsiveness to physical barriers to mobility during growth. Through its oscillatory signalling, calcium enables the precise regulation required for hyphal growth and network formation. Conclusion In conclusion, calcium is a remarkably versatile element, playing vital roles across a diverse range of organisms. In humans and animals, it not only provides structural integrity through bones and teeth but also regulates critical physiological processes such as nerve signalling. Beyond animal systems, calcium is also essential in plants, where it strengthens cell walls and improves structure. In fungi, calcium oscillations are fundamental to hyphal growth, coordinating vesicle trafficking. From building bones to driving vital biological processes, calcium is a silent powerhouse in life. Its influence stretches across humans, plants, and even fungi. Its role is truly indispensable. Written by Barayturk Aydin Related articles: Bone cancer / Tooth decay REFERENCES Haider, A. et al. (2017) Recent advances in the synthesis, functionalization and biomedical applications of Hydroxyapatite: A Review, RSC Advances. Available at: https://pubs.rsc.org/en/content/articlehtml/2017/ra/c6ra26124h (Accessed: 24 November 2024). Splettstoesser, T. (2024) Action potentials and synapses, Queensland Brain Institute - University of Queensland. Available at: https://qbi.uq.edu.au/brain-basics/brain/brain-physiology/action-potentials-and-synapses (Accessed: 01 December 2024). Abbott, A., L. (2001) ‘Calcium and the control of mammalian cortical granule exocytosis’, Frontiers in Bioscience, 6(1), p. d792. doi:10.2741/abbott. Vaz Martins, T. and Livina, V.N. (2019) What drives symbiotic calcium signalling in legumes? insights and challenges of imaging, International journal of molecular sciences. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC6539980/#:~:text=Currently%2C%20two%20different%20calcium%20signals,formation%20of%20the%20root%20nodule%2C (Accessed: 01 December 2024). Lew, R.R. (2011) ‘How does a hypha grow? the biophysics of pressurized growth in fungi’, Nature Reviews Microbiology, 9(7), pp. 509–518. doi:10.1038/nrmicro2591. Project Gallery

An influential immunologist Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link From Playboy Model to Danger Model: The (brief) Story of Polly Matzinger 13/02/25, 12:47 Last updated: Published: 11/05/24, 11:06 An influential immunologist Polly Matzinger may be one of the most influential and important immunologists, even if her research is still a little controversial. She took the already known ‘Self/Non-self’ model by Frank Macfarlane Burnet and Frank Fenner from 1949 and expanded it to incorporate ‘danger signals’. However, her life prior to becoming a world-leading immunologist might be the most unexpected thing about her. Born into an artistic French-Dutch family in La Seyne she grew up playing instruments and composing music alongside her brother and sister, who would themselves go on to become a rock musician and artist, respectively. By the early 70s, she had already done stints as a dog trainer, jazz musician, and a Playboy Bunny, before settling as a cocktail waitress in California. At this point, she had been in and out of studying biology at the University of California. After eleven years, she completed her Bachelor of Science. While working at the bar, her professor, Robert Schwab brought in scientific articles for her to read after she asked him about animal mimicry. Matzinger would later credit Professor Robert Schwab for her foray into science and her life. While at graduate school, Matzinger began to question the generally accepted idea that the body rejects anything that is ‘non-self’. At first glance, the idea makes sense; the immune system should attack things it does not recognise to keep us healthy. But upon further analysis, it might seem to be counterintuitive. We do not reject food, water, or even foetuses. For example, in organ transplants, it is thought that the body needs immunosuppression so that the immune system does not reject the new organ. But why would the body have evolved for this when not until the mid-20th century, an organ had never been transplanted? Equally, why did the body sometimes attack itself in the case of autoimmune diseases? Matzinger did not pursue this line of thought until ten years later. Thus, the ‘Danger Model’ was derived. Matzinger proposed that in order for the immune response to be activated, there must first be a ‘danger signal’. This danger signal is emitted by unhealthy cells, which might be stressed or infected or have been mutated or damaged. Examples of danger signals include heat-shock proteins, extracellular matrix breakdown products, and cytokines, as well as other proteins and substances released by these stressed cells. Danger signals, or ‘alarmins’, are detected by dendritic cells, which activate T cells and start the immune response. While this model was originally met with scepticism, it has gained more and more support over the years, as the research into it expands and deepens. With the ‘Danger Model’, many routes for potential therapies have opened, including cancer vaccines. Matzinger believes that vaccinations can cure up to 80% of all cancers. If danger signals are induced within tumour cells, the tumour will be visible to the immune system. This is different to the current way that cancer vaccines target the tumour. In current therapeutic cancer vaccines (as opposed to preventative vaccines), the vaccines induce the immune system by showing them what the cancer cell ‘looks like’. It does this by introducing cancer antigens (or tumour-specific antigens, i.e. a protein that is only on the cancer and not on other healthy cells in the body) to the body and, thus, the immune system. Now that the immune cells have seen and identified the cancer antigens, they can search the body for the antigen, induce an immune response against them, and hopefully kill the cancer cells. This means that if the cancer mutates and the antigen changes, which is not unlikely, the vaccine may cease to have any effect because what the immune system is searching for no longer exists. In contrast, with this new method, the actual antigen does not matter. The vaccine works by inducing the danger signals, making the tumours visible to the immune system without the need for the tumour-specific antigen to be identified. This means that even if the cancer undergoes mutation, the vaccine will still be active and working, as its effectiveness does not depend on the cancer molecule itself. In addition to describing the ‘Danger Model’, Matzinger also made a name for herself when she cited ‘Galadriel Mirkwood’ as her co-author on a paper published in the Journal of Experimental Medicine. What is surprising about this, is that Galadriel Mirkwood is not another scientist, but her pet Afghan Hound. It is unknown why she did this, potentially to challenge the strict and rigid rules in the scientific community, to garner more interest in the paper, or just to be funny. Either way, it got her banned from publishing in the journal for more than ten years, but it certainly made her a scientist with a sense of humour and a memorable story. Written by Henrietta Owen Related article: Immune signals and metastasis Project Gallery

An exploration of this genetic concept Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Delving into the world of chimeras 09/07/25, 14:03 Last updated: Published: 03/02/24, 11:13 An exploration of this genetic concept The term chimera has been borrowed from Greek mythology, transcending ancient tales to become a captivating concept within the fields of biology and genetics. In mythology, the chimera was a monstrous hybrid creature. However, in the biological context, a chimera refers to an organism with cells derived from two or more zygotes. While instances of natural chimerism exist within humans, researchers are pushing the boundaries of genetics via the intentional creation of chimeras, consequentially sparking debates and breakthroughs in various fields, spanning from medicine to agriculture. Despite the theory that every cell in the body should share identical genomes, chimeras challenge this notion. For example, the fusion of non-identical twin embryos in the womb is a way chimeras can emerge. While visible cues, such as heterochromia or varied skin tone patches, may provide subtle hints of its existence, often individuals with chimerism show no overt signs, making its prevalence uncertain. In cases where male and female cells coexist, abnormalities in reproductive organs may exist. Furthermore, advancements in genetic engineering and CRISPR genome editing have also allowed the artificial creation of chimeras, which may aid medical research and treatments. In 2021, the first human-monkey chimera embryo was created in China to investigate ways of using animals to grow human organs for transplants. The organs could be genetically matched by taking the recipient’s cells and reprogramming them into stem cells. However, the process of creating a chimera can be challenging and inefficient. This was shown when researchers from the Salk Institute in California tried to grow the first embryos containing cells from humans and pigs. From 2,075 implanted embryos, only 186 developed up to the 28-day time limit for the project. Chimeras are not exclusive to the animal kingdom; plants exhibit this genetic complexity as well. The first non-fictional chimera, the “Bizzaria” discovered by a Florentine gardener in the seventeenth century, arose from the graft junction between sour orange and citron. Initially thought to be an asexual hybrid formed from cellular fusion, later analyses revealed it to be a chimera, a mix of cells from both donors. This pivotal discovery in the early twentieth century marked a turning point, shaping our understanding of chimeras as unique biological phenomena. Chimera is a common form of variegation, with parts of the leaf appearing to be green and other parts white. This is because the white or yellow portions of the leaf lack the green pigment chlorophyll, which can be traced to layers in the meristem (areas found at the root and shoot tip that have active cell division) that are either genetically capable or incapable of making chlorophyll. As we conclude this exploration into the world of chimeras, from the mythological realm to the scientific frontier, it’s evident that these entities continue to mystify and inspire, broadening our understanding of genetics, development, and the interconnectedness of organisms. Whether natural wonders or products of intentional creation, chimeras beckon further exploration, promising a deeper comprehension of the fundamental principles that govern the tapestry of life. Written by Maya El Toukhy Related article: Micro-chimerism and George Floyd's death Project Gallery