Why the fuss over a couple of km/s/Mpc? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hubble Tension 09/07/25, 15:20 Last updated: Published: 25/11/23, 11:10 Why the fuss over a couple of km/s/Mpc? You have probably heard that the universe is expanding, and perhaps even that this expansion is accelerating. A consequent observation of this is that distant objects such as galaxies appear to recede from Earth faster if they are further away. Here is a helpful analogy: imagine a loaf of raisin bread that is rising as it is baked. A pair of raisins on opposite sides of the loaf will move away from one another at a greater rate than a pair of raisins near the center. The more dough (universe) there is between a pair of raisins (galaxies), the faster they recede from one another. See Figure 1 . This phenomenon is encapsulated in Hubble’s Law, which relates specifically to the recessional velocity due to the expansion of space. Hubble’s Law is given by the equation v = H0 D . Where: v is the recessional velocity D is the distance to the receding object H0 is the Hubble constant It is worth noting that distant objects will often have velocities of their own due to gravitational forces - so-called ‘peculiar velocities’. In order to clarify the meaning of the title of this article, we must explore the unit in which the Hubble constant H0 is most often quoted: km/s/Mpc. This describes the speed (in kilometers per second) at which a distant object, such as a galaxy, is receding for every megaparsec of distance that galaxy is from Earth. Edwin Hubble is the name most often associated with this cosmological paradigm shift; however, physicists Alexander Friedmann and Georges Lemaître worked independently on the notion of an expanding universe, deriving similar results before Hubble verified them experimentally in 1929 at the Mount Wilson Observatory, California. What is the Hubble Tension? Hopefully the above discussion of units and raisin bread convinced you that the Hubble constant H0 is linked to the expansion rate of the universe. The larger H0 is, the faster galaxies are receding at a given distance, thus indicating a more quickly expanding universe. Therefore, cosmologists wish to accurately measure H0 in order to draw conclusions about the age and size of the universe. The Hubble Tension arises from the contradicting measurements of H0 obtained from different experiments. See Figure 2 of Edwin Hubble. CMB measurement One of these experiments uses the Cosmic Microwave Background (CMB), which can be thought of as an afterglow of light from near the time of the Big Bang. The wavelength of this light has expanded with the universe ever since the period of recombination - which I mentioned in my previous article on the DESI instrument. Our current best model of the universe, called ΛCDM, can describe how the universe evolved from a hot, dense state to the universe we see today, subject to a specifically balanced energy budget between ordinary matter, dark matter, and dark energy. From fitting this ΛCDM model to CMB data from missions such as ESA’s Planck Mission, one can derive a value for the expansion rate of the universe, i.e., a value for H0 . The Planck Mission measured temperature variations (anisotropies) across the CMB with unprecedented angular resolution and sensitivity. The most recent estimate for the Hubble constant using this method gave H0 = 67.4 ± 0.5 km/s/Mpc . Local Distance Ladder measurement Another technique to determine the value of H0 uses the distance-redshift relation. This is a wholly observational approach. It relies on the fact that the faster an object recedes from Earth, the more the light from that object is shifted towards longer wavelengths (redshifted). Hubble’s Law relates this recessional velocity to a distance; therefore, one can expect a similar relation between distance and redshift. A ‘ladder’ is invoked since astronomers wish to use objects that are visible from a vast range of distances; the rungs of the ladder represent greater and greater distances to the astronomical light source. Each rung of the ladder contains a different kind of ‘standard candle’, which are sources with reliable, well-constrained luminosities that translate to an accurate distance from Earth. I encourage you to look into these different types; some examples are Cepheid variables, Type Ia Supernovae, and RR Lyrae variables. When this method was employed using the Hubble Space Telescope and SH0ES (Supernova H0 for the Equation of State), a value of H0 = 73.04 ± 1.04 km/s/Mpc was obtained. The disagreement Clearly, these two values for the Hubble constant do not agree, nor do their uncertainty ranges overlap. Figure 3 shows some of the 21st-century measurements of H0 ; an excellent illustration of how the uncertainty has decreased for both methods, therefore making their disagreement more statistically significant. Many sources of scientific engagement with the public cite this disagreement as the ‘Crisis in Cosmology!’. In the author’s opinion, this is unnecessarily hyperbolic and plays on the human instinct to pick a side between two opposing viewpoints. In fact, new methods to measure H0 have been implemented using the tip of the Red-Giant branch (TRGB) as a standard candle, which demonstrate closer agreement with the value derived from the CMB. Some cosmologists believe that eventually this Hubble Tension will dissipate as our calibration of astronomical distances improves with the next generation of telescopes. Constraining the value of the Hubble constant is by no means low-hanging fruit for cosmologists, nor is the field in crisis. To see the progress we have made, one has to look back in time to 1929 when Edwin Hubble’s first estimate using a trend line and 46 galaxies gave H0 = 500 km/s/Mpc ! We must remain hopeful that the future holds a consistent approximation for the expansion rate and, with it, the age of our universe. Written by Joseph Brennan Project Gallery

A rare disease that causes inflammation in the blood vessels Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Understanding and detecting Kawasaki disease on time Last updated: 24/02/25, 11:31 Published: 06/02/25, 08:00 A rare disease that causes inflammation in the blood vessels What is Kawasaki disease? Kawasaki disease is a rare type of vasculitis that damages blood vessels through inflammation and is prevalent in children under the age of five. Kawasaki disease is predominantly found in children of Asian races–mainly in Japan, Korea, Taiwan, and Asian races in the US–and is the leading cause of acquired heart disease in children in most developed countries. What causes Kawasaki disease? There is no known cause of Kawasaki disease, however, studies suggest a link between genetics and the disease, noting a high incidence between siblings and in children with a parental history of Kawasaki disease. Another study provided further evidence of genetic susceptibility, stating that variation in the expression of CASP3 and ITPKC—genes heavily involved in T cell function—leads to an overexpression of T cells.This can be attributed to the inflammatory symptoms of the disease. There are speculations that it may be caused by an airborne agent originating in Central Asia which moves across different geographical regions. This study suggests that through winds, the airborne agent is able to cause Kawasaki disease via infection of the respiratory tract–further investigation is needed regarding this hypothesis. Diagnosing Kawasaki disease Symptoms of Kawasaki disease, which are often accompanied by a fever, are classified into three phases: acute, subacute, and convalescent. The acute phase usually lasts between two to three weeks and symptoms include: Carditis Mucosal inflammation (cracked and dry lips, strawberry tongue, swollen lymph nodes) Polymorphous rash Coronary artery aneurysms The subacute phase also lasts up to three weeks and includes symptoms such as: - Perineal and periungual desquamation - Arthralgia - Myocardial disease The convalescent phase is when most clinical signs dissolve and usually lasts up to three months. It is important to note that while most symptoms clear up during this phase, cardiac issues may still persist in some patients. Misdiagnosing Kawasaki disease is very common as its symptoms are similar to that of many diseases like scarlet fever or toxic shock syndrome. With that being said, confirming its diagnosis is often a case of ruling out these diseases. In addition to identifying symptoms linked to other diseases, conducting laboratory tests such as CRP, CBC, and ESR can help confirm a diagnosis of Kawasaki disease. Additionally, echocardiograms and electrocardiograms can help assess coronary abnormalities as well as overall heart function. Treating Kawasaki disease Following diagnoses, patients are first administered an IVIG and a high dose of aspirin to reduce inflammation as well as eliminate pain, swelling and fever. Patients are then administered lower doses of aspirin which helps prevent blood clotting. Roughly 25% of untreated patients are at a higher risk of developing coronary artery aneurysms and lasting cardiovascular issues in general. This risk drops down to 5% when treated appropriately. IVIG is proven to be effective in treating approximately 85-90% of cases when administered within the first ten days of the illness which is why it is imperative that patients are treated early. X-rays are regularly conducted on patients as they can help visualise blood vessels and potential heart abnormalities that may suggest further complications. It can also observe the effectiveness of treatment over time. Post-recovery, an echocardiogram is recommended periodically to detect any coronary abnormalities that may have developed much later on. Summary Kawasaki disease is a rare disease that causes inflammation in the blood vessels. It normally develops in children under the age of five and is yet to have a known cause. It is often hard to diagnose as its symptoms are similar to that of other diseases, which is why it is important to identify its symptoms (polymorphous rash, mucosal inflammation, desquamation, etc) as well as conduct tests such as CBC, CRP, ESR, an electrocardiogram, etc to help rule out other diseases. It is essential that children with Kawasaki disease are diagnosed and treated early as this can help treat coronary artery aneurysm and prevent lasting coronary and cardiovascular abnormalities. Written by Sherine Latheef Related articles: Sideroblastic anaemia / Blood / Inflammation therapy REFERENCES Onouchi, Y., Ozaki, K., Buns, J.C., Shimizu, C., Hamada, H., Honda, T., Terai, M., Honda, A., Takeuchi, T., Shibuta, S., Suenaga, T., Suzuki, H., Higashi, K., Yasukawa, K., Suzuki, Y., Sasago, K., Kemmotsu, Y., Takatsuki, S., Saji, T. and Yoshikawa, T. (2010). Common variants in CASP3 confer susceptibility to Kawasaki disease. Human Molecular Genetics , 19(14), pp.2898–2906. doi: https://doi.org/10.1093/hmg/ddq176 . Agarwal, S. and Agrawal, D.K. (2017). Kawasaki Disease: Etiopathogenesis and Novel Treatment Strategies. Expert review of clinical immunology , [online] 13(3), pp.247–258. doi: https://doi.org/10.1080/1744666X.2017.1232165 . Wolff, A.E., Hansen, K.E. and Zakowski, L. (2007). Acute Kawasaki Disease: Not Just for Kids. Journal of General Internal Medicine , [online] 22(5), pp.681–684. doi: https://doi.org/10.1007/s11606-006-0100-5 . Oh, J.-H., Cho, S. and Choi, J.A. (2023). Clinical Signs of Kawasaki Disease from the Perspective of Epithelial-to-Mesenchymal Transition Recruiting Erythrocytes: A Literature Review. Reviews in Cardiovascular Medicine , 24(4), pp.109–109. doi: https://doi.org/10.31083/j.rcm2404109 . Team, H.J. (2018). Kawasaki Disease - Causes, Signs, Symptoms,Treatment . [online] Health Jade. Available at: https://healthjade.com/kawasaki-disease/ . Project Gallery

Dysregulation of this pathway occurs in many different types of cancers Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The MAPK/ERK signalling pathway in cancer Last updated: 24/02/25, 11:29 Published: 20/02/25, 08:00 Dysregulation of this pathway occurs in many different types of cancers Introduction The mitogen-activated protein kinase (MAPK) signalling pathway is an important pathway in apoptosis, proliferation, differentiation, angiogenesis and metastasis. It is a protein kinase pathway (causes phosphorylation) with between 3-5 sets of kinases and is known to be activated via Ras, KC-mediated (Kupffer cells/liver macrophages), Ca2+, or G protein-coupled receptors. The MAPK/ERK pathway, also known as the Ras-Raf-MEK-ERK pathway, is conserved in mammals, and dysregulation of this pathway occurs in many different types of cancers. MAPK/ERK function Ras (GTPase) activates Raf (serine/threonine kinase), which activates MEK1/2 (tyrosine & serine/threonine kinases) and ERK1/2 (serine/threonine kinases), which controls certain transcription factors. ERK1/2 also phosphorylates various substrates in the cytoplasm (not shown). This results in gene expression, which can cause apoptosis, cell cycle regulation, differentiation, proliferation, etc. (Fig. 1). It is estimated that there are more than 150 target substrates of ERK1/2, either directly or indirectly. Furthermore, Ras and RAF have several different subtypes which have different functions. Ras has four different subtypes, which are the GTPases: HRAS, KRAS4A/4B, and NRAS, with KRAS being the common form found in human cancers. RAF has subtypes, which are the kinases: ARAF, BRAF, and CRAF (in humans). Ras is activated when GRB2 (growth-factor-receptor bound protein 2) binds to SOS (son of sevenless). This occurs via the complex moving to the cell membrane upon activation of a transmembrane receptor, such as EGFR (epidermal growth factor receptor). SOS transports the signal from the receptor to RAS and aids in the conversion of RAS-GDP to RAS-GTP. This switches ‘on’ RAF, which leads to the phosphorylation of MEK and ERK (Fig. 1). ERK is then able to move into the nucleus and alter gene expression, of genes such as CREB, MYC, FOS, MSK, ELK, JUN, etc., which are involved in processes such as metabolism, proliferation, angiogenesis (formation of blood vessels), haematopoiesis (formation of blood cells), wound healing, differentiation, inflammation, and cancer. However, ERK is also able to activate other substrates in the cytoplasm, such as BIM, RSK, MNK, and MCL, which are involved in processes such as apoptosis and blood pressure regulation. A regular level of ERK expression is needed for activation of genes involved in the cell cycle and to inhibit negative cell cycle control. ERK phosphorylates Cyclin D and Cdk4/6, which are bound together and aid the cell in the movement from G1 (gap) to the S phase (DNA synthesis/repair) of the cell cycle. MAPK/ERK pathway in cancer The MAPK/ERK pathway has been linked with many cancers, such as colon, thyroid, melanoma, pancreatic, lung, and glioblastoma. Mutations in epidermal growth factor receptor (EGFR), Ras, and Raf are well-known to cause cancer, with an estimated 33% of cancers containing Ras mutations, and an estimated 8% being caused by Raf mutations. It is also estimated that 85% of cancers have elevated activity of MEK. The MAPK/ERK pathway has also been shown to interact with the PI3K/Akt pathway, which controls the cell cycle and causes increased cell proliferation, which is obviously an important factor in tumourigenesis (tumour initiation). Regulation of the MAPK/ERK pathway There is a negative feedback mechanism of ERK1/2 on RAS/RAF/MEK, by ERK1/2 phosphorylating SOS, which causes the RAF-RAS link to be disrupted. ERK also inhibits MEK via the phosphorylation of BRAF and CRAF. There are inhibitors for Ras/Raf/MEK/ERK, but not all of these inhibitors work well/are without issues. ERK is problematic, in that their ATP-binding sites are very like cell cycle proteins, so are more difficult to inhibit. Also, it is difficult to target Ras due to its high GTP binding affinity, profuse cellular GTP, and lack of appropriate binding pockets. Therefore, the main focus currently appears to be on Raf/MEK inhibition. Raf inhibitors include drugs such as sorafenib, vemurafenib, encorafenib, and dabrafenib (these drugs are used on specific BRAF mutations). On the other hand, MEK inhibitors include drugs such as trametinib, cobimetinib, binimetinib, and selumetinib (these drugs can be used on specific mutations in Ras and Ras/Raf). Negative feedback mechanisms tightly control the MEK/ERK pathway and therefore great care is taken with inhibitor drug doses. To illustrate, if the doses are too low, the negative feedback loops are activated, which can lead to drug resistance/ poor therapeutic outcome. Conclusion The MAPK/ERK pathway is essential for several cellular processes, such as apoptosis, cell cycle regulation, differentiation, and proliferation. Therefore, it has a critical role in tumourigenesis. Raf and MEK in particular are susceptible to inhibition, which has led to the production of several different drugs for use in various types of cancer. There are currently other clinical trials in progress, and these will hopefully lead to further therapies for other cancers involved in this pathway. Written by Eleanor R Markham Related articles: HIPPO signalling pathway / Thyroid cancer REFERENCES Lake, D., Corrêa, S.A.L. & Müller, J. Negative feedback regulation of the ERK1/2 MAPK pathway. Cell. Mol. Life Sci. 73 , 4397–4413 (2016). https://doi.org/10.1007/s00018-016-2297-8 Song Y, Bi Z, Liu Y, Qin F, Wei Y, Wei X. Targeting RAS-RAF-MEK-ERK signaling pathway in human cancer: Current status in clinical trials. Genes Dis. 2022 May 20;10(1):76-88. doi: 10.1016/j.gendis.2022.05.006. PMID: 37013062; PMCID: PMC10066287 Ullah R, Yin Q, Snell AH, Wan L. RAF-MEK-ERK pathway in cancer evolution and treatment. Semin Cancer Biol. 2022 Oct;85:123-154. doi: 10.1016/j.semcancer.2021.05.010. Epub 2021 May 13. PMID: 33992782. Project Gallery

Explore artificial intelligence, a technology that has taken the world by storm. Learn how it is used in fields like agriculture, drug discovery, and outer space. Elsewhere, get to grips with semi-conductor manufacturing, quantum computing, and biotechnology. Technology Articles Explore artificial intelligence, a technology that has taken the world by storm. Learn how it is used in fields like agriculture, drug discovery, and outer space. Elsewhere, get to grips with semi-conductor manufacturing, quantum computing, and biotechnology. You may also like: Maths , Physics , Engineering Fake science websites Ways fake science websites misinform and misguide readers The evolution of artificial intelligence And its greater role in natural language processor technologies Medical biotechnology Technology in the medical sciences Quantum computing What are its applications? Improving agriculture Revolutionising sustainable agriculture through AI AI in drug discovery Using this technology in drug research Digital disinformation With the use of IT cells Digital innovation in rural farming What are the benefits? AI in space What is artificial intelligence used for in outer space? Radiation therapy to treat cancer Revolutionising patient setup in cancer treatment AI: the good, the bad, and the future A Scientia News Biology group collaboration Photonic integration In semiconductor manufacturing Nanomedicine Tiny solutions for big health problems NHS clinical computer scientist Exploring the day-to-day routine in this new field in healthcare Semi-conductor laser technology The recent advancements Code to cure How bioinformatics and technology helped to develop a vaccine for COVID-19 Virtual reality in healthcare Its potential Mauritius's rise as African leader of mobile networks An in-depth look at the rollout of 5G on the island, and the factors enabling this

Elements, compounds, and mixtures make up the building blocks of materials that shape our world. Read on to uncover how atoms, molecules, and reactions are fundamental to life on Earth. Chemistry Articles Elements, compounds, and mixtures make up the building blocks of materials that shape our world. Read on to uncover how atoms, molecules, and reactions are fundamental to life on Earth. You may also like: Medicine , Pharmacology The role of chemistry in medicine Medicinal chemistry and its uses Metal organic frameworks And their potential use in cancer drug delivery The biochemistry of cancer And how integrins can be desirable targets Metal compounds In anti-cancer drugs Female Nobel prize winners What were their contributions? Drug chirality Why is it important? Green chemistry And sustainability for the future Chemistry in space exploration What is its role? Environmental impact of electrical vehicles A chemical perspective From botulism to beauty Botulinum toxins Chemistry of an atomic bomb What is the key process behind these explosions? Vitamins Discussing their importance in the body The story of pigments and dyes The chemistry in an artist's palette Zinc fingers Transcription factors regulating gene expression Emotional chemistry On a molecular basis Nuclear safety The silent protectors Modern-day chemistry And its related challenges The story of the atom The history of the atomic model Nanoparticles A probable treatment for diabetes Exploring food at the molecular level Gastronomy Next

The future of targeted cancer therapeutics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Bioorthogonal Chemistry 04/02/25, 15:42 Last updated: Published: 01/09/24, 11:47 The future of targeted cancer therapeutics ‘Bioorthogonal chemistry’ is a term coined in 2003 by American Chemist & 2022 Nobel Prize Laureate Carolyn Bertozzi. It encompasses a set of chemical reactions which can occur within biological environments, whilst exerting minimal effect on native biomolecules or interference with native biochemical processes of the host organism - these reactions exist ‘orthogonal’ (perpendicular) to biology. Key functional groups in Bioorthogonal Chemistry include the alkynes (carbon-carbon triple bonds) and the azides (⁻N=N⁺=N⁻) . The azides are particularly bioorthogonal due to their minute size (which is favourable for cell permeability and avoiding ‘perturbations’ - the alteration of a function of a biological system), metabolic stability, and how, as they don’t naturally exist in cells, they have no competing biological side reactions. Past & present uses of bioorthogonal chemistry include: ● Vehicle airbags: Modern vehicle airbags contain sodium azide (NaN₃), a shock sensitive, explosive compound. When a vehicle’s crash sensor is triggered, an electrical charge is administered which starts the chemical reaction, inflating the air bag with harmless nitrogen gas (2NaN₃ → 2Na + 3N₂). This reaction can occur in as quickly as 0.03 seconds! ● Early HIV treatment: Azidothymidine - AZT - (Fig. 1) was the first drug used to treat HIV infection. For viruses to replicate, they use an enzyme called reverse transcriptase to convert their single-stranded RNA genome to double-stranded DNA in a process termed reverse transcription. When this antiretroviral medicine is used, instead of the virus transcribing thymidine, it instead transcribes the AZT, which contains an azide Group, thus stalling DNA synthesis of HIV and producing less viruses. Another key feature to consider when discussing uses of Bioorthogonal Chemistry are Click Reactions. Click Reactions occur exclusively between the azides (⁻N=N⁺=N⁻) and alkynes (carbon-carbon triple bond), produce no by-products and therefore have a 100% atom economy. Bioorthogonal ‘Click’ Chemistry has enabled complex chemical reactions to be carried out within living organisms: the reactions do not bring harm to, interfere with or disrupt the biological processes occurring within these systems as they cannot be recognised & used by these systems. ‘Click’ Chemistry is therefore vital in understanding how we may be able to develop Targeted Cancer Therapeutics using Bioorthogonal Chemistry. Modern day cancer treatments tend to be delivered intravenously using anthracyclines (notably doxorubicin), a class of antitumour antibiotics used for cancer chemotherapy: they stop the growth of cancerous cells by preventing their enzymatic machinery from engaging in DNA duplication & cell division, causing the cells to die. The long-standing side effect of using such effective drugs is the high likelihood of ‘off-target toxicity’, where non-cancerous cells can also be harmed by the intercalating effects of the anthracyclines. Frequent targets for this ‘off-target toxicity’ tend to be fast growing body cells, like hair & nails, hence why most cancer patients experience some form of hair loss over the course of their chemotherapy treatment. So, scientists began to consider: what if there was a way to develop targeted cancer treatments? Treatments that enabled the activation of these powerful cancer drugs - anthracyclines - at the tumour sites, mitigating the harm of ‘off-target toxicity’? This is where Bioorthogonal ‘Click’ Chemistry comes in. ‘ C lick- A ctivated P rotodrugs A gainst C ancer’ (or ‘ CAPAC ’) is a platform developed by American Biotechnology Company Shasqi. Through ‘CAPAC’, Shasqi are pioneering the use of Bioorthogonal ‘Click’ Chemistry to target cancer drugs directly to the tumour site, minimising side effects and potentially improving the therapeutic index. They’ve achieved this through exploiting one of the fastest click reactions: a Diels-Alder cycloaddition between a tetrazine (C2H2N4) and a trans-cyclooctene (TCO) - 2 bioorthogonal molecules. The treatment involves two key components: a tetrazine-modified sodium hyaluronate biopolymer & doxorubicin that is connected to a TCO (trans-cyclooctene) unit. Over the course of the treatment (Fig. 2) , the patient will undergo multiple stages: ● Local hydrogel injection: The tetrazine-modified sodium hyaluron ate biopolymer is injected into a patient’s tumour ● Protodrug dose: The patient then receives five daily infusions of doxorubicin-TCO ● Concentration: The drug circulates through the body until it meets the tetrazine-modified biopolymer at the tumour site ● Activation: At the point of meeting, the click reaction brings the tetrazine and TCO together, triggering a rearrangement that frees the doxorubicin right next to the tumour cells Compared to prior cancer treatments, this process would not only mitigate the harm of the drug’s ‘off-target toxicity’, limiting the side-effects of the chemotherapy drug, it would also increase the local concentration of doxorubicin far beyond what would normally be possible in a patient, having a greater effect in preventing the growth of cancer cells. In the treatment of this life-threatening disease, Shasqi’s research into the ‘CAPAC’ platform, though still ongoing, looks excitingly promising: as recently as March 2023, they’ve proven their platform’s efficacy in humans. During a Phase 1 dose-escalation clinical trial in adult patients with advanced solid tumours, Shasqi were able to demonstrate the activation of their tetrazine-modified sodium hyaluronate biopolymer & doxorubicin-TCO at tumour sites, evidencing it’s safety, systemic pharmacokinetics, and immunological activity. With the continuation of their innovative research, the future treatment of cancer can be significantly aided with the use of Bioorthogonal ‘Click’ Chemistry. Written by Emmanuella Fernandez REFERENCES Acs.org . (2021). Click chemistry sees first use in humans . [online] Available at: https://cen.acs.org/pharmaceuticals/Click-chemistry-sees-first-use/98/web/2020/10 . Cancer Research UK (2023). Doxorubicin (Adriamycin) | Cancer drugs | Cancer Research UK . [online] www.cancerresearchuk.org . Available at: https://www.cancerresearchuk.org/about-cancer/treatment/drugs/doxorubicin . Wang, Y., Zhang, C., Wu, H. and Feng, P. (2020). Activation and Delivery of Tetrazine-Responsive Bioorthogonal Prodrugs. Molecules , 25(23), p.5640. doi: https://doi.org/10.3390/molecules25235640 . Wikipedia Contributors (2019). Reverse transcriptase . [online] Wikipedia. Available at: https://en.wikipedia.org/wiki/Reverse_transcriptase . Wikipedia. (2020). Zidovudine . [online] Available at: https://en.wikipedia.org/wiki/Zidovudine . Wikipedia. (2022). Bioorthogonal chemistry . [online] Available at: https://en.wikipedia.org/wiki/Bioorthogonal_chemistry . Project Gallery

Exploring the microscopic world of molecules Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Quantum Chemistry Last updated: 05/02/26, 10:12 Published: 06/02/25, 08:00 Exploring the microscopic world of molecules Quantum chemistry provides a glimpse into the strange and fascinating world of molecules and atoms, where the principles of traditional chemistry and physics no longer apply. While classical chemistry can explain molecular interactions and bonding, it cannot fully account for particles' unusual, frequently contradictory behaviour at the atomic and subatomic levels. Quantum mechanics provides scientists with a powerful framework for understanding the complicated behaviour of electrons and nuclei in molecules. The basics of quantum chemistry The notion of wave-particle duality, which states that particles, such as electrons, act not just like objects with mass but also like waves, is central to quantum chemistry. Because the exact position and momentum of an electron cannot be known at the same time (according to the Heisenberg Uncertainty Principle), probability distributions are used to describe electrons rather than accurate orbits. These distributions are represented by mathematical functions known as wave functions, which describe the probability of finding an electron in a specific location surrounding the nucleus. This fundamentally affects our understanding of chemical bonding. Instead of conceiving a bond as a solid connection between two atoms, quantum chemistry defines it as the overlap of electron wave functions, which can result in a variety of molecular topologies depending on their energy levels. Quantum mechanics and bonding theories Quantum mechanics has fundamentally altered our knowledge of chemical bonding. The classic Lewis structure model, which explains bonding as the sharing or transfer of electrons, is effective for simple molecules but fails to convey the complexities of real-world interactions. In contrast, quantum chemistry introduces the concept of molecular orbitals. In molecular orbital theory, electrons are not limited to individual atoms but can spread across a molecule in molecular orbitals, which are combinations of atomic orbitals from the participating atoms. These molecular orbitals provide a more detailed explanation for bonding, especially in compounds that do not match simple bonding models, such as delocalised systems like benzene or metals. For example, quantum chemistry explains why oxygen is paramagnetic (it possesses unpaired electrons), a characteristic that classical bonding theories cannot explain. Quantum chemistry and quantum computing One of the most interesting frontiers in quantum chemistry is its application to the development of quantum computers. Traditional computers, despite their enormous processing power, struggle to model the complicated behaviour of molecules, particularly large ones. This is because simulating molecules at the quantum level necessitates tracking all conceivable interactions between electrons and nuclei, which can quickly become computationally challenging. Quantum computers use fundamentally different ideas. They employ qubits, which, unlike classical bits, can exist in a state of both 0 and 1. This enables quantum computers to execute several calculations concurrently and manage the complexity of molecular systems considerably more effectively. This could lead to advancements in quantum chemistry, such as drug discovery, where precisely modelling molecular interactions is critical. Instead of depending on trial and error, scientists may utilise quantum computers to model how possible pharmaceuticals interact with biological molecules at the atomic level, thereby speeding up the creation of novel therapies. Similarly, quantum chemistry could help in the development of novel materials with desirable qualities, such as stronger alloys and more efficient energy storage devices. Why quantum chemistry matters The consequences of quantum chemistry go well beyond the lab. Understanding molecular behaviour at its most fundamental level allows us to create new technologies and materials that have an impact on everyday life. Nanotechnology, for example, relies largely on quantum principles to generate innovative materials with applications in medicine, electronics, and clean energy. Catalysis, the technique of speeding up reactions, also benefits from quantum chemistry insights, making industrial operations more efficient, such as cleaner fuel generation and more effective environmental remediation. Furthermore, quantum chemistry provides insights into biological processes. Enzymes, the proteins that catalyse processes in living organisms, work with a precision that frequently defies standard chemistry. Tunnelling, quantum phenomena in which particles slip past energy barriers, helps to explain these extraordinarily efficient biological processes. In brief, quantum chemistry provides the fundamental understanding required to push the limits of chemistry and physics by exposing how molecules interact and react in ways that traditional theories cannot fully explain. Quantum chemistry has the potential to radically alter our understanding of the microscopic world, whether through theoretical models, practical applications, or future technology advancements. Written by Laura K Related articles: Quantum computing / Topology / Computational organic chemistry Project Gallery

How diseases start and spread, the body’s defence system, vaccines, policies, and public opinion: unravel the maze of infection and immunity with these articles. Immunology Articles How diseases start and spread, the body’s defence system, vaccines, policies, and public opinion: unravel the maze of infection and immunity with these articles. You may also like: Biology , Medicine , Neuroscience , Chemistry COVID-19 misconceptions Common misconceptions during the COVID-19 pandemic Glossary of COVID-19 terms Key terms used during the COVID-19 pandemic A vaccine for malaria? A new hope for a vaccine for malaria The world vs. the next pandemic Can we see it coming? What steps do we need to take? Are pandemics becoming more severe? Arguments for and against Natural substances And how they can tackle infectious diseases A treatment for HIV? Can the CRISPR-Cas9 system be used as a potential treatment? The mast cell Key cells in the immune system Origins of COVID -19 How COVID-19 caused a pandemic Mechanisms of pathogen invasion How pathogens avoid detection by the immune system Astronauts in space How does little gravity affect the immune system? Ageing and immunity Ageing and its association with immune decline The impacts of global warming on dengue fever Dengue fever is a mosquito-borne Neglected Tropical Disease (NTD) Is the immune system 'selfish'? 'Selfish' genes from a Dawkins perspective, and the Modern Evolutionary Synthesis

Wildlife corridors are connecting habitats previously divided by roads Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Wildlife corridors: why did the sloth cross the road? Last updated: 16/09/25, 17:49 Published: 06/11/25, 08:00 Wildlife corridors are connecting habitats previously divided by roads Have you ever run over an animal while driving, or had to suddenly hit the brakes so an animal could cross the road? Engineers and ecologists have come up with genius solutions, collectively called wildlife corridors, so that this happens less often. This article is about two such solutions - green bridges, which are big vegetated overpasses, and rope bridges between trees. More than just roadkill Roads threaten animals because of a concept called habitat fragmentation. This is when big animal populations are split into two smaller populations with less resources and less genetic diversity than the original populations. Animals may try to move between habitat fragments in search of new food or mates, but die trying to cross the road. Either they walk directly onto the road and collide with cars, or they cross by walking over power lines and get electrocuted. Wildlife corridors allow animals to safely walk over roads, un-doing the habitat fragmentation and reducing their chance of extinction. Wolves in Germany A 2021 study analysed the activity of animals crossing a green bridge in Germany. This bridge, one of seven in the state of Brandenburg, was built in 2012 over the important A12 highway ( Figure 1 ). Using camera footage over a year, researchers found that grey wolves were more likely to use the bridge at dusk, at night, and in the winter. The deer and wild boars eaten by wolves were also more likely to use the bridge at dusk and at night, so the presence of wolves on the bridge did not deter their prey. Since 76% of wolves in Germany die in road-related incidents, bridges like this one are crucial for effective wolf conservation. Rope bridges in Costa Rica While Germany’s wolves and deer walk straight onto roads, Costa Rica’s tree-dwelling animals cross the road using power lines. This means the tree dwellers, including monkeys and sloths, are at risk of electrocution - in fact, nearly 1000 animals died of electrocution in Costa Rica in 2018-19. To reduce this risk, Costa Ricans have built rope bridges across the country as a safer alternative for wildlife to cross roads. Most bridges consist of a single blue nylon rope ( Figure 2a ), while researchers at the University of Costa Rica built rope bridges specially designed for howler monkeys ( Figure 2b ). Howler monkeys were targeted because of their endangered status and ecological role as seed and pollen dispersers. While the specialised bridges doubled howler monkey populations between 2015 and 2021, both them and classic rope bridges were used by squirrels, opossums, and kinkajous. However, a 2021 study found that animals use telephone lines to cross roads as frequently as they use rope bridges, and telephone lines are dangerously close to power lines. Some species still are not crossing using rope bridges, many years after their construction. Although the rope bridges are helping to reduce electrocution, they are not perfect. Heathland in the UK Closer to home, a brand-new green bridge called Cockrow Bridge will soon open in Surrey ( Figure 3 ). Surrey has lost 85% of its lowland heath in the last two centuries, but Ockham and Wisley Commons continue to support rare heathland species like the nightjar and sand lizard. These two commons, on either side of the A3/M25 junction, will be connected by the Cockrow Bridge into a 3 km-long stretch. Although existing heathland needs to be destroyed for construction, tree stumps and soil from the destroyed habitat will be repurposed on the bridge. Tree stumps will provide shelter to small animals, while the soil contains native roots and seeds to kickstart the bridge ecosystem. Since the public will be allowed on this bridge, it will improve our access to green spaces and bring revenue to local organisations. Therefore, Cockrow Bridge is expected to benefit wildlife and the public. Conclusion Wildlife corridors could be an important conservation tool by undoing habitat fragmentation, reducing roadkill, and preventing electrocution on power lines. Examples in Germany and Costa Rica look promising, and a unique heathland bridge is under construction here in the UK. Green bridges and rope bridges prove that modern infrastructure does not need to harm biodiversity, and humans can coexist with nature. Written by Simran Patel Related articles: Gorongosa National Park / Protecting rock-wallabies in Australia REFERENCES The Sloth Conservation Foundation. Connected Gardens: facilitating the peaceful co-existence of sloths and people. [Internet]. [cited 2025 Apr 13]. Available from: https://slothconservation.org/what-we-do/habitat-connectivity/ Tobias N. Swinging to safety: How canopy bridges may save Costa Rica’s howlers. Mongabay Environmental News [Internet]. 2023 Feb 15 [cited 2025 Apr 13]; Available from: https://news.mongabay.com/2023/02/swinging-to-safety-how-canopy-bridges-may-save-costa-ricas-howlers/ Gilbey V, Petty R. UK’s first heathland green bridge. Proceedings of the Institution of Civil Engineers - Civil Engineering. 2024 Nov 1;177(6):99–110. Laidlaw K, Broadbent E, Eby S. Effectiveness of aerial wildlife crossings: Do wildlife use rope bridges more than hazardous structures to cross roads? Rev Biol Trop. 2021 Oct 1;69(3):1138–48. Plaschke M, Bhardwaj M, König HJ, Wenz E, Dobiáš K, Ford AT. Green bridges in a re‐colonizing landscape: Wolves ( Canis lupus ) in Brandenburg, Germany. Conservat Sci and Prac. 2021 Mar;3(3):e364. Project Gallery

Not getting enough sleep can increase the risk of developing Alzheimer’s Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Sleep less…remember less: the hidden link between sleep and memory loss Last updated: 10/07/25, 19:27 Published: 17/04/25, 08:00 Not getting enough sleep can increase the risk of developing Alzheimer’s People often don’t get enough sleep for a variety of reasons, ranging from intentional choices like work or study demands (because who needs sleep when you’ve got deadlines, right?), to the growing concern with screen time (a.k.a. the “I’ll just watch one more episode” syndrome), and of course, procrastination (where your brain convinces you that 3 a.m. is a great time to suddenly get productive). But it’s not all fun and games—serious issues like insomnia, sleep apnoea, family responsibilities, or even shift work can also interfere with rest. Sleep disorders are increasingly common, with around one in three people in the UK affected, and they’re particularly prevalent among the elderly. However, not getting enough sleep can increase the risk of developing Alzheimer’s disease (AD). How do sleep disorders impact Alzheimer’s disease? Insomnia is characterised by difficulty falling asleep or staying asleep, which can lead to prolonged fatigue and memory issues. As shown in Figure 1 , people with insomnia tend to have some similarity in markers as those with Alzheimer’s disease, such as an increased level of Aβ and tau proteins in the brain. This is primarily because a lack of sleep prevents the effective removal of harmful products from the brain – this accumulation increases a person’s risk of AD. A plethora of experimental studies on humans and animals have shown that lack of sleep can lead to increased circulating levels of TNF-α and the gene resulting in more TNF-α secretion. This pro-inflammatory cytokine exacerbates AD pathology because neuroinflammation can lead to dysfunction and cell death, which are key markers of AD. Other pro-inflammatory cytokines, like IL-1, have been found to be relevant in the link between sleep deprivation and AD. Overexpression of IL-1 in the brain leads to abnormal changes in nerve cell structures especially relating to Aβ plaques. This highlights IL-1’s key role in plaque evolution and the synthesis of Amyloid Precursor Protein, which promotes amyloid production that eventually results in AD pathology. What type of sleep can impact one’s risk of Alzheimer’s disease? Studies using more objective measures, like actigraphy (which tracks sleep-wake activity), found that sleep quality (sleep efficiency) is more important than total sleep time. For example, women with less than 70% sleep efficiency were more likely to experience cognitive impairment. Increased wakefulness during the night also moderated the relationship between amyloid deposition (a hallmark of AD) and memory decline. Uncertainties… However, it remains unclear whether poor sleep directly causes AD or if the disease itself leads to sleep disturbances. Some studies suggest a bidirectional relationship. Aging itself leads to poorer sleep quality, including reduced sleep efficiency, less slow-wave sleep (SWS), and more frequent awakenings. Sleep disorders like obstructive sleep apnoea, insomnia, and restless legs syndrome also become more common with age. What are the next steps? The good news is that many sleep disorders, including insomnia, are manageable, and improving sleep quality could be a simple yet powerful way to reduce Alzheimer’s risk. Additionally, early diagnosis and treatment of conditions like sleep apnoea and insomnia may help slow or even prevent neurodegenerative changes. s researchers continue to explore the intricate relationship between sleep and Alzheimer’s, one thing is clear: getting a good night’s sleep isn’t just about feeling refreshed. It is a crucial investment in long-term brain health. Written by Blessing Amo-Konadu Related articles: Overview of Alzheimer's / Hallmarks of Alzheimer's / CRISPR-Cas9 in AD treatment / Memory erasure / Does insomnia run in families? REFERENCES Lucey, B. (2020). It’s complicated: The relationship between sleep and Alzheimer’s disease in humans. Neurobiology of Disease , [online] 144, p.105031. doi: https://doi.org/10.1016/j.nbd.2020.105031 . NHS (2023). Insomnia . [online] www.nhsinform.scot . Available at: https://www.nhsinform.scot/illnesses-and-conditions/mental-health/insomnia/ . Pelc, C. (2023). Not getting enough deep sleep may increase the risk of developing dementia . [online] Medicalnewstoday.com . Available at: https://www.medicalnewstoday.com/articles/not-getting-enough-deep-sleep-may-increase-dementia-risk#Clarifying-the-link-between-sleep-aging-and-dementia-risk [Accessed 22 Dec. 2024]. Sadeghmousavi, S., Eskian, M., Rahmani, F. and Rezaei, N. (2020). The effect of insomnia on development of Alzheimer’s disease. Journal of Neuroinflammation , 17(1). doi: https://doi.org/10.1186/s12974-020-01960-9 . Project Gallery