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Through photonic integration Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The future of semiconductor manufacturing 11/07/25, 10:03 Last updated: Published: 22/12/23, 15:11 Through photonic integration Recently the researchers from the University of Sydney developed a compact photonic semiconductor chip by heterogeneous material integration methods which integrates an active electro-optic (E-O) modulator and photodetectors in a single chip. The chip functions as a photonic circuit (PIC) offering a 15 gigahertz of tunable frequencies with a spectral resolution of only 37 MHz and is able to expand the radio frequency bandwidth (RF) to precisely control the information flowing within the chip with the help of advanced photonic filter controls. The application of this technology extends to various fields: • Advanced Radar: The chip's expanded radio-frequency bandwidth could significantly enhance the precision and capabilities of radar systems. • Satellite Systems: Improved radio-frequency performance would contribute to more efficient communication and data transmission in satellite systems. • Wireless Networks: The chip has the potential to advance the speed and efficiency of wireless communication networks. • 6G and 7G Telecommunications: This technology may play a crucial role in the development of future generations of telecommunications networks. Microwave Photonics (MWP) is a field that combines microwave and optical technologies to provide enhanced functionalities and capabilities. It involves the generation, processing, and distribution of microwave signals using photonic techniques. An MWP filter is a component used in microwave photonics systems to selectively filter or manipulate certain microwave frequencies using photonic methods (see Figure 1 ). These filters leverage the unique properties of light and its interaction with different materials to achieve filtering effects in the microwave domain. They can be crucial in applications where precise control and manipulation of microwave signals are required. MWP filters can take various forms, including fiber-based filters, photonic crystal filters and integrated optical filters. These filters are designed to perform functions such as wavelength filtering, frequency selection and signal conditioning in the microwave frequency range. They play a key role in improving the performance and efficiency of microwave photonics systems. The MWP filter operates through a sophisticated integration of optical and microwave technologies as depicted in the diagram. Beginning with a laser as the optical carrier, the photonic signal is then directed to a modulator where it interacts with an input Radio-Frequency (RF) signal. The modulator dynamically influences the optical carrier's intensity, phase or frequency based on the RF input. Subsequently, the modulated signal undergoes processing to shape its spectral characteristics in a manner dictated by a dedicated processor. This shaping is pivotal for achieving the desired filtering effect. The processed optical signal is then fed into a photodiode for conversion back into an electrical signal. This conversion is based on the variations induced by the modulator on the optical carrier. The final output which is represented by the electrical signal reflects the filtered and manipulated RF signal which demonstrates the MWP's ability in leveraging both optical and microwave domains for precise and high-performance signal processing applications. Extensive research has been conducted in the field of MWP chips, as evidenced by a thorough examination in Table 1 . This table compares recent studies based on chip material type, filter type, on-chip component integration, and working bandwidth. Notably, previous studies demonstrated noteworthy advancements in chip research despite the dependence on external components. What distinguishes the new chip is its revolutionary integration of all components into a singular chip which is a significant breakthrough that sets it apart from previous attempts in the field. Here the term "On-chip E-O" involve the integration of electro-optical components directly onto a semiconductor chip or substrate. This integration facilitates the interaction between electrical signals (electronic) and optical signals (light) within the same chip. The purpose is to enable the manipulation, modulation or processing of optical signals using electrical signals typically in the form of voltage or current control. Key components of on-chip electro-optical capabilities include: 1. Modulators which alter the characteristics of an optical signal in response to electrical input which is crucial for encoding information onto optical signals. 2. Photonic detectors convert optical signals back into electrical signals extracting information for electronic processing. 3. Waveguides guide and manipulate the propagation of light waves within the chip, routing optical signals to various components. 4. Switches routes or redirects the optical signals based on electrical control signals. This integration enhances compactness, energy efficiency, and performance in applications such as communication systems and optical signal processing. "FSR-free operation" refers to Free Spectral Range (FSR) which is a characteristic of optical filters and resonators. FSR is the separation in frequency between two consecutive resonant frequencies or transmission peaks. The column "FSR-free operation" indicates whether the optical processing platform operates without relying on a specific or fixed Free Spectral Range. It means that its operation is not bound or dependent on a particular FSR. This could be advantageous in scenarios where flexibility in the spectral range or the ability to operate over a range of frequencies without being constrained by a specific FSR is desired. "On-chip MWP link improvement" refers to enhancements made directly on a semiconductor chip to optimize the performance of MWP links. These improvements aim to enhance the integration and efficiency of communication or signal processing links that involve both microwave and optical signals. The term implies advancements in key aspects such as data transfer rates, signal fidelity and overall link performance. On-chip integration brings advantages such as compactness and reduced power consumption. The manufacturing of the photonic integrated circuit (PIC) involves partnering with semiconductor foundries overseas to produce the foundational chip wafer. This new chip technology will play a crucial role in advancing independent manufacturing capabilities. Embracing this type of chip architecture enables a nation to nurture the growth of its autonomous chip manufacturing sector by mitigating reliance on international foundries. The extensive chip delays witnessed during the 2020 COVID pandemic underscored the global realization of the chip market's significance and its potential impact on electronic manufacturing. Written by Arun Sreeraj Related articles: Advancements in semi-conductor technology / The search for a room-temperature superconductor / Silicon hydrogel lenses / Mobile networks 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, 16:20 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

Antifreeze proteins and frozen foods Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Survival Secrets of the Arctic Springtail 04/07/25, 12:59 Last updated: Published: 21/09/24, 16:09 Antifreeze proteins and frozen foods Introduction Approximately 450 million years ago, during the Ordovician period, the Earth was characterised by a hot and humid globe. The sea was teeming with life, with early squids, eel-like fish, and sea worms hunting smaller animals. However, there was no sign of movement above ground as the animals had not yet crawled ashore. This period of warmth created ideal living conditions for wildlife, but it was about to change dramatically. Shortly after, the land masses began to freeze, and an ice cap started to spread. The once warm and accommodating waters turned cold and inhospitable, leading to the second-worst mass extinction in the history of the planet. Many species succumbed to the harsh conditions, but one animal survived - the springtail. The springtail, a small insect-like animal, had developed a special strategy to combat the cold. Its cells started producing proteins that could protect them from freezing. This discovery challenges the previous belief that animals did not develop antifreeze proteins until much later. Research from Aarhus University has shown that the springtail might have been the first animal to develop such proteins. Applications in the Food Industry Since then, scientists have found antifreeze proteins in various animals, plants, and microorganisms. These proteins have also found applications in different industries. One of the industries utilising antifreeze proteins is the food industry, especially in producing frozen foods. Frozen foods often suffer from changes in taste and texture due to the formation of ice crystals. However, by incorporating antifreeze proteins, these undesirable effects can be prevented. Industrial yeast cell cultures have been engineered to produce antifreeze proteins derived from fish genes. These proteins can then be added to different foods, including ice cream, to improve texture and prevent the formation of ice crystals. Exploring Arctic Fish Aside from their contribution to the food industry, springtails have also fascinated scientists due to their ability to survive in extremely cold regions. The discovery of antifreeze proteins explained how arctic fish could swim in icy seawater. The proteins prevent ice from forming in the cells and blood of the fish, allowing them to survive in freezing conditions. Martin Holmstrup, a researcher at Aarhus University, oversees colonies of springtails in his laboratory. These small animals require minimal space and can be easily maintained in Petri dishes with a base of moist plaster and a feed of dry yeast. Researchers have determined that springtails developed these proteins long before other animals by studying the DNA sequences responsible for building antifreeze proteins. The discovery of antifreeze proteins in springtails opens up possibilities for various applications, including in the food industry. These proteins have been found to prevent ice crystal formation, which can affect the taste and texture of frozen foods. The genes responsible for their production have been copied into industrial yeast cell cultures to utilise these proteins. This allows the yeast to produce the antifreeze proteins, which can then be added to different foods. One example is the use of these proteins in ice cream, where they help create a delightful texture and allow the ice cream to be thawed and refrozen without compromising its quality. Conclusion The discovery of antifreeze proteins in springtails has revolutionised various industries, particularly the food industry. These proteins have been found to prevent ice crystal formation, improving the taste and texture of frozen foods. Incorporating antifreeze proteins derived from fish genes into yeast cell cultures can produce and add these proteins to different foods, such as ice cream, ensuring a delightful texture and the ability to thaw and refreeze without compromising quality. This remarkable adaptation of springtails has provided insight into their survival in extremely cold regions and opened up possibilities for further applications of antifreeze proteins in various fields. Written by Sara Maria Majernikova Related articles: p53 protein / Zinc finger proteins / Emperor penguins, kings of ice Project Gallery

An overview Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Crab Nebula 14/02/25, 13:44 Last updated: Published: 23/03/24, 17:45 An overview Of the 270 known supernova remnants, the Crab Nebula is one of the more well known in popular science, originating from a violent supernova explosion first discovered by Chinese astronomer Wang Yei-te in July of 1054 AD. Yei-te reported the appearance of a “guest star” so bright that it was visible during the day for three weeks, and at night for 22 months. In 1731, English astronomer John Bevis rediscovered the object, which was then observed by Charles Messier in 1758 prompting the nebula’s lesser-known name, Messier 1. Located approximately 6,500 light years from Earth, the nebula cannot be seen with the naked eye but observations in different wavelengths gives rise to the beautiful colored images often published. The Crab Nebula is the result of a violent explosion process that signals what astronomers call “star death.” This occurs when the star runs out of fuel for the fusion process in its core that produces an outward pressure counteracting the constant inward pressure of the star’s outer shells. With the loss of outward pressure, these layers suddenly collapse inwards and produce an explosion astrophysicists call a supernova. Following the explosion, the original star, named SN1054 in this case, collapsed into a rapidly spinning neutron star, also known as a pulsar, which is generally roughly the size of Manhattan, New York. The pulsar is situated at the center of the nebula and ejects two beams of radiation that, while the pulsar rotates, makes it appear as if the object is pulsing 30 times per second. Studies of the Crab Nebula were primarily conducted by the Hubble Space Telescope. Hubble spent three months capturing 24 images that were assembled into a colorful mosaic resembling not what is visible with human eyes, but rather a kind of paint-by-number image where each color mapped to a particular element. Traces of hydrogen, neutral oxygen, doubly ionized oxygen, and sulfur have been detected across multiple wavelengths as the remains span an expanding six to eleven light-year-wide remnant of the supernova event. It was not until 1942 that the Crab Nebula was officially found to be related to the recorded supernova explosion of 1054. This establishment was jointly provided by Professor J. J. L. Duyvendak of Leiden University as well as astronomers N. U. Mayall and J. Oort. Due to its long history of rediscovery and inherent beauty, the Crab Nebula remains as one of the most studied celestial objects today and continues to provide valuable insight into astrophysical processes. Written by Amber Elinsky REFERENCES Hester, J. Jeff. “The Crab Nebula: An Astrophysical Chimera,” Annual Review of Astronomy and Astrophysics 46 (2008): 127-155. https://doi.org/10.1146/annurev.astro.45.051806.110608 . Hester, J. and A. Loll. “Messier 1 (The Crab Nebula),” NASA. https://science.nasa.gov/mission/hubble/science/explore-the-night-sky/hubble-messier-catalog/messier-1/ . Image ref.: European Space Agency; Space Australia; dreamstime. Mayall, N. U., and J. H. Oort. “FURTHER DATA BEARING ON THE IDENTIFICATION OF THE CRAB NEBULA WITH THE SUPERNOVA OF 1054 A. D. PART II. THE ASTRONOMICAL ASPECTS.” Publications of the Astronomical Society of the Pacific 54, no. 318 (1942): 95–104. http://www.jstor.org/stable/40670293 Project Gallery

Understanding the cause of bullying can provide effective prevention and intervention Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The brain of a bully Last updated: 13/05/25, 14:22 Published: 29/05/25, 07:00 Understanding the cause of bullying can provide effective prevention and intervention Introduction Bullying is a global social issue affecting any individual regardless of sex, age, or gender, particularly in childhood and adolescence. Approximately one-third of the youth is bullied worldwide; the range could be as low as 7% in Tajikistan to 74% in Samoa. While much neuroscientific research focuses on bullying victimisation and social exclusion, there is a growing field to understand the brain mechanisms behind bullying behaviour. Why does bullying occur? Is there a neurological basis for such behaviour? This article will answer these questions with insights into prevention and intervention strategies. The neural basis of bullying As per Johnna R. Swartz, an assistant professor at the University of California, Davis : Bullying is fairly common during adolescence, with about 25-50% of teenagers in the U.S. reporting that they have bullied or been a victim of bullying. The Swartz team focused on the amygdala, a small almond-shaped structure deep within the brain. The amygdala is critical for processing emotions, particularly fear and aggression. Swartz and her colleagues conducted a functional resonance imaging (fMRI) study on 49 adolescents, examining how their amygdala responded to different emotional expressions during a face-matching task. The findings indicated that the adolescents who engaged in bullying behaviour exhibited a heightened amygdala response to angry faces and a diminished amygdala response to fearful faces. This pattern suggests that bullies may struggle to recognise fear in others, potentially making them less likely to empathise with their victims. Moreover, a study revealed that adolescents who reported higher rates of bullying showed increased activation of the ventral striatum (the area that responds to rewarded feelings), amygdala (emotion processing), medial prefrontal cortex (involved with social cognition, decision-making), and insula (salience detection) while observing social exclusion scenarios. The findings suggest that bullying is not just about aggression but also about maintaining social dominance and hierarchy. Another study by the University of Chicago conceded that bullies might enjoy others in pain by observing a robust activation of the amygdala and ventral striatum when watching pain inflicted on others. Why is knowing the neural basis of bullying useful? Understanding the root cause of bullying can provide effective prevention and intervention strategies: Social-emotional training (SET) to improve emotional regulation and empathy, which can help reshape neural pathways. For example, programmes like the ‘Roots of Empathy’ initiative have shown that training children to recognise emotions can reduce bullying behaviours in schools. Cognitive-behavioural therapy (CBT) allows bullies to reframe negative thoughts and develop a healthier response to social interactions. For instance, the CBT techniques, like role-playing social situations, have been successfully used in school-based interventions. Mindfulness and cognitive training strengthen the prefrontal cortex by meditation and improve decision-making skills and impulse control. School-based interventions (like anti-bullying programs) create supportive environments that reward prosocial behaviour rather than only punishing aggressive behaviour. Conclusion The neuroscience of bullying helps us understand the root cause of bullying scientifically. Bullying is not simply a matter of choice; there is a deeper scientific basis to consider. This knowledge can help to develop comprehensive solutions to prevent bullying and create a healthier social environment. Future studies should focus on longitudinal studies that track brain development in children and adolescents involved in bullying, thereby informing how early interventions can reshape them for positive change. Written by Prabha Rana Related articles: Aggression / Depression in childhood / Forensic neurology REFERENCES Assistant Secretary for Public Affairs (ASPA). “Facts about Bullying.” StopBullying.Gov , 9 Oct. 2024, www.stopbullying.gov/resources/facts . “Bullies May Enjoy Seeing Others in Pain: Brain Scans Show Disruption in Natural Empathetic Response.” University of Chicago News , news.uchicago.edu/story/bullies-may-enjoy-seeing-others-pain-brain-scans-show-disruption-natural-empathetic-response . Accessed 15 Feb. 2025. Dolan, Eric W. “Neuroscience Study Finds Amygdala Activity Is Related to Bullying Behaviors in Adolescents.” PsyPost , 7 Dec. 2019, www.psypost.org/neuroscience-study-finds-amygdala-activity-is-related-to-bullying-behaviors-in-adolescents/ . Perino, Michael T., et al. “Links between adolescent bullying and neural activation to viewing social exclusion.” Cognitive, Affective, & Behavioral Neuroscience , vol. 19, no. 6, 10 July 2019, pp. 1467–1478, https://doi.org/10.3758/s13415-019-00739-7 . 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, 08:40 Published: 18/09/25, 07:00 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

Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and the other sciences. Log In Welcome to Scientia News DELIVERING INFORMATIVE CONTENT Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and other sciences. We hope this platform helps you discover something that inspires your curiosity, and encourages you to learn more about important topics in STEM. Meet the Official Team NAVIGATE AND CLICK THE PHOTOS BELOW TO LEARN MORE ABOUT US! To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. Latest Articles chemistry Molecular blueprints: the synthesis of ibuprofen View More chemistry Looking at the rare earth elements View More biology Ethnic Health Inequalities View More pharmacology The promising effects of magic mushrooms for depression View More CONTACT CONTACT US Scientia News welcomes anyone who wants to share their ideas and write for our platform. If you are interested in realising your writing potential with us AND live in the UK; and/ or would like to give feedback: Email us at scientianewsorg@gmail.com or fill in our GET IN TOUCH form below and we'll be in contact... Follow us on our socials for the latest updates. Comment, like and share! Join our mailing list below for latest site content. You can also sign up to become a site member . SUBSCRIPTION Join our mailing list to receive alerts for new articles and other site content. Be sure to check your spam/ junk folders in case emails are sent there. Email Subscribe GET IN TOUCH First Name Last Name Email Message Send Thanks for submitting!

Pathology and emerging therapeutics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Bone cancer 25/03/26, 16:48 Last updated: Published: 12/10/23, 10:38 Pathology and emerging therapeutics Introduction: what is bone cancer? Primary bone cancer can originate in any b one. However, most cases develop in the long bones of the legs or upper arms. Each year, more than 500 new cases are diagnosed in the United Kingdom (with a projected downward trend). Primary bone cancer is distinct from secondary bone cancer, which occurs when cancer spreads to the bones from another region of the body. The focus of this article is on primary bone cancer. There are several types of bone cancer: osteosarcoma, Ewing sarcoma, and chondrosarcoma. Osteosarcoma originates in the osteoblasts that form bone. It is most common in children and teens, with the majority of cases occurring between the ages of 10 and 30. Ewing (pronounced as YOO-ing) sarcoma develops in bones or the soft tissues around the bones. Like osteosarcoma, this cancer type is more common in children and teenagers. Chondrosarcoma occurs in the chondrocytes that form the cartilage. Chondrosarcoma is most common in adults between the ages of 30 and 70 and is rare in the under-21 age group. Causes of bone cancer include genetic factors such as inherited mutations and syndromes, and environmental factors such as previous radiation exposure. Treatment will often depend on the type of bone cancer, as the specific pathogenesis of each case is unknown. What is the standard treatment for bone cancer? Most patients are treated with a combination of surgical excision, chemotherapy, and radiation therapy. Surgical excision is employed to remove the cancerous bone. Typically, it is possible to repair or replace the bone, although amputation is sometimes required. Chemotherapy involves using powerful chemicals to kill rapidly growing cells in the body. It is widely used for osteosarcoma and Ewing sarcoma but less commonly used for chondrosarcomas. Radiation therapy (also termed radiotherapy) uses high doses of radiation to damage the DNA of cancer cells, leading to the killing of cancer cells or slowed growth. Six out of every ten individuals with bone cancer will survive for at least five years after their diagnosis, and many of these will be completely cured. However, these treatments have limitations in terms of effectiveness and side effects. The limitation of surgical excision is the inability to eradicate microscopic cancer cells around the edges of the tumour. Additionally, the patient must be able to withstand the surgery and anaesthesia. Chemotherapy can harm the bone marrow, which produces new blood cells, leading to low blood cell counts and an increased risk of infection due to a shortage of white blood cells. Moreover, radiation therapy uses high doses of radiation, resulting in the damage of nearby healthy tissues such as nerves and blood vessels. Taken together, this underscores the need for a therapeutic approach that is non-invasive, bone cancer-specific, and with limited side effects. miR-140 and tRF-GlyTCC Dr Darrell Green and colleagues investigated the role of small RNAs (sRNAs) in bone cancer and its progression. Through the analysis of patient chondrosarcoma samples, the researchers identified two sRNA candidates associated with overall patient survival: miR-140 and tRF-GlyTCC. MiR-140 was suggested to inhibit RUNX2, a gene upregulated in high-grade tumours. Simultaneously, tRF-GlyTCC was demonstrated to inhibit RUNX2 expression by displacing YBX1, a multifunctional protein with various roles in cellular processes. Interestingly, the researchers found that tRF-GlyTCC was attenuated during chondrosarcoma progression, indicating its potential involvement in disease advancement. Furthermore, since RUNX2 has been shown to drive bone cancer progression, the identified miR-140 and tRF-GlyTCC present themselves as promising therapeutic targets. CADD522 Dr Darrell Green and colleagues subsequently investigated the impact of a novel therapeutic agent, CADD522, designed to target RUNX2. In vitro experiments have revealed that CADD522 reduced proliferation in chondrosarcoma and osteosarcoma. However, a bimodal effect was observed in Ewing sarcoma, indicating that lower levels of CADD522 promoted sarcoma proliferation, whereas higher levels of the same drug suppressed proliferation. In mouse models treated with CADD522, there was a significant reduction in cancer volumes observed in both osteosarcoma and Ewing sarcoma. Take-home message The results described here contribute to understanding the molecular mechanisms involved in bone cancer. They highlight the anti-proliferative and anti-tumoral effects of CADD522 in treating osteosarcoma and Ewing sarcoma. Further research is necessary to fully elucidate the specific molecular mechanism of CADD522 in bone cancer and to identify potential side effects. Written by Favour Felix-Ilemhenbhio Related articles: Secondary bone cancer / Importance of calcium / Novel neuroblastoma driver for therapeutics Project Gallery

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

A hereditary neurodegenerative disorder Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Huntington's disease 25/03/26, 16:52 Last updated: Published: 18/10/23, 16:12 A hereditary neurodegenerative disorder Huntington’s disease (HD) is a neurodegenerative disorder causing cognitive decline, behavioural difficulties, and uncontrollable movements. It is a hereditary disease that has a devastating effect on the individual’s life and unfortunately is incurable. Genetic component What may come as a surprise, is that in everyone’s genetics there are two copies (one from each parent) of the Huntingtin’s gene coding for the Huntingtin protein. This gene is coded by CAG repeats. In healthy genes, the CAG sequence is repeated between 10 and 26 times. However, if the gene is faulty, CAG repeats over 40 times resulting in a dysfunctional Huntingtin protein. The disease is autosomal dominant meaning regardless of gender, if either parent is a carrier, their child has a 50% chance of inheriting the faulty gene. REMINDER: because the gene is dominant, it means those who inherit even one copy will develop the disease Effect on the brain The faulty Huntingtin protein accumulates in cells, leading to cell death and damage to the brain. If you were to look at the brains of individuals with Huntington’s Disease, you would see a reduction in volume of the caudate and putamen. These areas are part of the striatum, which is a subdivision of the basal ganglia, involved in fine tuning our voluntary movements, i.e., reaching out to grab a cup. As the disease progresses, this atrophy can extend to other areas of the brain including the thalamus, frontal lobe, and cerebellum. Symptoms The symptoms normally manifest in three categories: motor, cognitive and psychiatric. We know that the basal ganglia is involved in our voluntary movement, so the damage causes one of the most visible symptoms in HD- uncontrollable and jerky movements. Cognitive symptoms include personality changes, difficulties with planning and attention. There can also be impairments to how those with HD recognise emotions- all these symptoms can interact to make social interaction more difficult. Finally, the psychiatric symptoms often seen include irritability and aggression, depression, anxiety, and apathy. Impact on life and family At the age when diagnosis usually occurs (around 30 years old), patients are often buying houses, getting married and either having children or deciding to start a family. The diagnosis may change people's outlook on having children and can put a great psychological burden on them if they have unknowingly passed it along to those already born. Diagnosis also brings consequences to seemingly mundane, but incredibly important, issues such as gaining life insurance, with some companies not covering individuals with an official diagnosis. Subsequently this makes life harder for their families, as the patient will eventually be unable to work and there could be associated costs with the need for care facilities as the disease progresses. Unfortunately, this is a progressive neurodegenerative condition with no cure. The only treatment options available at present, are interventions which aim to alleviate the patients’ symptoms. Whilst these treatments will reduce the motor and psychiatric symptoms, they cannot stop the progression of Huntington’s disease. We have only scratched the surface on the impact Huntington’s disease has on a patient and their families. It is so important to understand ways in which everyone that is affected can be best supported during the disease progression, to give all those involved a better quality of life. Written by Alice Jayne Greenan Related articles: A potential gene therapy for HD / Epilepsy Project Gallery