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The utilisation of Stonehenge as an astronomical calculator Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The celestial blueprint of time: Stonehenge, United Kingdom Last updated: 08/10/25, 16:22 Published: 09/10/25, 07:00 The utilisation of Stonehenge as an astronomical calculator This is Article 3 in a series about astro-archaeology. Next article coming soon. Previous article: The astronomical symbolism of the Giza Pyramids . Stonehenge, located within the south-west of England, is one of the UK’s most notable man-made structures, built during the neolithic period around 3100BC. Not only is this famous UNESCO heritage site a breakthrough in engineering, but the sandstone architecture also holds an enigmatic connection between the land and the sky. Its location and stone arrangement mirrors a blueprint that can be analysed to predict the timings of astronomical phenomena. The utilisation of Stonehenge as an astronomical calculator was established by astronomer Gerald Hawkins in 1965. Using computer software, Hawkins discovered that the location of Stonehenge aligned with several solar and lunar positions. He theorised that Stonehenge was built to predict astronomical events, such as eclipses, and to determine the position of summer and winter solstices. From the shape and positions of the 19 stones that comprise Stonehenge, its ‘horseshoe’ shape could predict the lunar eclipses. A booklet titled Stonehenge: Sun, Moon, Wandering Stars , written by M.W. Postins further detailed the significance of Stonehenge in archaeoastronomy. Postins suggested two scale models, the ‘Temple model’ and the ‘Enclosure model’, which detailed the significance of each stone and its relation to different events. For example, the booklet notes that the Altar Stone, a large sandstone located in the centre of Stonehenge, was placed across the solstice axis and represents the ‘Summer solstice sunrise’. Additionally, Postins hypothesised that the five trilithons, which are the vertical stones that form the structure of Stonehenge, represented planets that can be viewed with the naked eye. These include the two lowest trilithons on the East and Northern sides of the structure, representing Mercury and Venus. There has been new research, currently underway by the universities of Oxford, Leicester and Bournemouth in collaboration with the Royal Astronomical Society, linking the Stonehenge monument to a unique lunar phenomenon, called the ‘Major Lunar Standstill’. Right from the early construction of Stonehenge, researchers note that the major lunar standstill may have influenced the design of the monument. Four of the stones at Stonehenge align with two of the Moon’s positions, which aid to indicate moonrise and moonset. This would have allowed individuals to use the moonlight for longer periods of activity, such as night time hunting, as well as visualise the cycle of the lunar phases as a method of time watching for farming and celebratory purposes. Potentially, there is speculation that this made the positioning and construction of Stonehenge intentional. The timeless effect of the Stonehenge landmark, which shaped life in the past and continues to be of astronomical interest to determine the future, is a remarkable example of the functions of built structures for the analysis of astronomical events. It truly is a celestial blueprint for the relationship between the earth and cosmology. Written by Shiksha Teeluck Related article: Astro-geography of Lonar Lake REFERENCES English Heritage. (2024). Stonehenge: Major Lunar Standstill . https://www.english-heritage.org.uk/visit/places/stonehenge/things-to-do/major-lunar-standstill/ OSR. (2009). Stonehenge: An Astronomical Calculator . https://osr.org/blog/astronomy/stonehenge-an-astronomical-calculator/?srsltid=AfmBOopNQnJ-XUZSyLY_Aqu3L2nOJgSoAceRzQJIVZbsIsFhW6s3U_NT Tiverton & Mid Devon Astronomy Society. (n.d.). Astro-Archaeology at Stonehenge . http://www.tivas.org.uk/stonehenge/stone_ast.html 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

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 biology Regulation and policy of stem cell research View More biology How colonialism and geopolitics shape health injustices: a deep, critical reflection View More physics Light: one of the biggest mysteries in physics View More zoology Why some fish change sex during their lifetimes View More CONTACT CONTACT US Scientia News welcomes anyone who wants to share their ideas and write for our platform. If you are interested in realising your writing potential with us AND live in the UK; and/ or would like to give feedback: Email us at scientianewsorg@gmail.com or fill in our GET IN TOUCH form below and we'll be in contact... Follow us on our socials for the latest updates. Comment, like and share! Join our mailing list below for latest site content. You can also sign up to become a site member . SUBSCRIPTION Join our mailing list to receive alerts for new articles and other site content. Be sure to check your spam/ junk folders in case emails are sent there. Email Subscribe GET IN TOUCH First Name Last Name Email Message Send Thanks for submitting!

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

Have you perform the wrong exercises – You must keep revising your exercises and keep upgrading your knowledge about the proper use of equipment, and everything else related to fitness so that you don’t make any mistake in giving your clients the wrong exercises Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Examples of negligence in personal training on the impact of physiology Last updated: 14/11/24 Published: 26/01/23 Negligence in personal training is a failure to look after clients to avoid them getting injured while training. There are many ways this can happen, below are some examples of negligence in personal training. Making use of equipment that is defective – Using a defective equipment can easily lead to injury or at least poor exercising form. Trainers should be able to differentiate between effective and defective equipment if they want to avoid negligence in training their clients. In that scenario, the best thing a personal trainer can do is to repair the equipment or replace it with new ones instead of putting a ‘defect’ or ‘out of order’ sign on it. Telling you to lift too much weight – You can’t just tell your clients to lift too much weight without even knowing their capacity, their way of eating and experience from past training. This is irrational and unprofessional, thus neglecting your clients directly which can lead to causing them injuries like muscle tears, muscle strains and even worse, a wrong death. Have you perform the wrong exercises – You must keep revising your exercises and keep upgrading your knowledge about the proper use of equipment, and everything else related to fitness so that you don’t make any mistake in giving your clients the wrong exercises to do that can lead to stopping them from achieving their desired physiques, and fitness goals. Muscle imbalances will occur as well if not done properly. Make you exercise for too long – Exercising for too long can cause excess fatigue and can lead to muscle strains and sprains. Coaches must not let their clients push themselves too far. It may sound cool but it is not really healthy. Everything we do must be done in an appropriate manner to avoid consequences that will harm us. Written by Kushwant Nathoo Related articles: A perspective on well-being / Gentrification in the context of health

When deciding on the treatment of diseases, experts must gain as much relevant information as they can about that disease, before acting on an informed decision. When cancer is suspected, it might be that the decision for future treatment and prognosis be heavily weighted on the results of biopsies Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Cancer biomarker and evolution Last updated: 27/02/25 Published: 30/01/23 Development of Novel Biomarkers by Studying Cancer Evolution What does cancer evolution mean to cancer diagnosis and prognosis? How does studying it provide a better outlook on cancer precision medicine? =================== When deciding on the treatment of diseases, experts must gain as much relevant information as they can about that disease, before acting on an informed decision. When cancer is suspected, it might be that the decision for future treatment and prognosis be heavily weighted on the results of biopsies. After all, this is the standard for diagnosing many cancers. It takes one needle to take “information” that is used to predict patients’ outcomes and their respective treatment options, in other words, a test that might just predict their future. Cancer is an evolving disease. There have been many studies over the decades that demonstrate solid cancers’ singular-cell origins. Other studies show how cancer may evolve from a single cell to a mass of cells through Darwinian or branched evolution. This also implies that many things that apply to other evolutionary phenomena also apply to evolving cancer lines: mutation, genetic drift, selection and their selection pressures. In the end, what originated from one cell turns out to be a tumour with a unique genetic landscape, made up of numerous cancer subpopulations, each with its own unique genotypic and phenotypic profile and each of these subpopulations of cancerous cells evolving on its own. This phenomenon is more commonly referred to as intratumor heterogeneity (ITH). What all of this means to biopsies, is that when a single-site needle biopsy is done, it might not give an accurate representation of the whole tumour. The tumour itself, depending on its stage of development may be quite uniform with minimal ITH, however, it may also, in the eyes of a geneticist, look like a mosaic with multiple different “populations” of cancerous cells. Say, for example, the biopsy is aimed to target certain biomarkers (e.g. single nucleotide polymorphisms (SNPs)) or other “landmarks” such as satellites, the biopsy will only view whatever the needle so happened to have sampled. In other words, sampling could have made it look like a mosaic is red, even though the majority of the mosaic at the time is blue, but it seemed red for we only found red during the biopsy. Additionally, this mosaic is changing, new colours may emerge just like new lines arise within the same tumour. ITH introduces what is known as sampling bias, where samples taken from biopsies only provide an overview or snapshot of the tumour at its state and only pick up on one piece of the actively evolving puzzle, potentially missing many details, in this case, biomarkers from other tumour subpopulations. To solve the issues of ITH, scientists participating in the TRACERx research consortium are employing unique methods to sample tumours in an approach to cancer evolution. The research involved using multiregional sampling and RNA sequencing to sample tumours from patients with non-small cell lung cancers (NSCLC) at different timestamps, i.e. during the various stages of cancer development, metastasis and relapse. By using this approach, the team managed to document better how cancer evolves and how the genomic landscape and tumour architecture changes over time. Furthermore, they succeeded in honing genes that are uniformly conserved and expressed throughout the tumour, even after the effects of ITH. The research looked over 20,000 expressed genes and found 1,080 genes that despite cancer evolution and ITH, are relatively conserved and clonally expressed, relatively unaffected by sampling bias. Furthermore, using machine learning, 23 genes (from the 1,080) were found to be predictive of patient outcomes. Meaning, this novel set of genes or “biomarkers” may be used as a basis for prognosis and to predict mortality in NSCLC. This novel biomarker is named ORACLE or Outcome Risk Associated Clonal Lung Expression signature and scientists are hopeful that it may be used to determine the relative aggressiveness of lung cancers, whilst maintaining a robust function unaffected by ITH. By targeting ORACLE, it mattered less where the biopsy needle is placed on the tumour, as these genes are found clonally. In terms of its effectiveness, a trial shows that having high scores of ORACLE signatures is associated with an increased risk of death within five years of diagnosis. In addition, other trials show that by targeting ORACLE, scientists were able to identify patients with a substantial risk of poor clinical outcomes. Overall, research on the application of ORACLE has shown satisfactory results in predicting patient outcomes and is found to be relatively resistant to the confounding effects of ITH. In summary, we have seen what cancer evolution may cause, and how it shadows the effectiveness of conventional biopsies and biomarkers due to sampling bias in ITH. We also find the research by the TRACERx Consortium and how they aim to study the effects of cancer evolution and ITH, finding a set of genes that are found and expressed throughout the tumour, yet still provide a favourable measure to patient outcomes. Whilst these topics are still under active research, it is clear, how studying cancer evolution and changing the approach to biopsies and biomarker designs can improve the overall quality of diagnosis and cancer prognosis. After all, finding what is wrong is as important as fixing the problem. We hope that similar biomarkers may be developed in the future, applicable to many other types of cancers. Written by Stephanus Steven Related articles: Thyroid cancer / Arginine and tumour growth / NGAL- a marker for kidney damage REFERENCES Biswas, D. et al. (2019) “A clonal expression biomarker associates with lung cancer mortality,” Nature Medicine, 25(10), pp. 1540–1548. Available at: https://doi.org/10.1038/s41591-019-0595-z. Header image: Lung cancer cells. Anne Weston, Francis Crick Institute. Attribution-Non-Commercial 4.0 International (CC BY-NC 4.0)

Looking at modern society in terms of the food being consumed and the amount of exercise undertaken collectively, it is entirely inevitable that diabetes will become an epidemic. Now before delving into the above statement further, diabetes mellitus (from Greek ‘siphon’ and Latin ‘sweet’) is a non-communicable disease that occurs when blood sugar levels in the body are so high, that the pancreas is unable to produce adequate insulin in order to manage this problem. Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Will diabetes mellitus become an epidemic? Last updated: 07/11/24 Published: 18/05/23 Defining diabetes and its causes Looking at modern society in terms of the food being consumed and the amount of exercise undertaken collectively, it is entirely inevitable that diabetes will become an epidemic. Now before delving into the above statement further, diabetes mellitus (from Greek ‘siphon’ and Latin ‘sweet’) is a non-communicable disease that occurs when blood sugar levels in the body are so high, that the pancreas is unable to produce adequate insulin in order to manage this problem. Also, diabetes can be categorised into various types, but the most common are types 1 and 2 as well as gestational (which happens during pregnancy). There is also diabetes insipidus (from Latin ‘lacking taste’), and this is where the kidneys are unable to conserve water. The causes of diabetes mellitus can be divided based on the type. Since type 1 can be caused by the body’s immune system attacking the pancreas, this means that the beta cells are unable to make enough insulin because they are damaged. Not only can type 1 diabetes arise this way, it is possible that environmental factors such as diet and viral infections lead to the disease. As for type 2, it primarily comes from insulin resistance, meaning that the body does not respond to the hormone effectively compared to a person without diabetes. This in turn impacts insulin mediated glycogen synthesis and glycolysis leading to hyperglycemia as seen in figure 1. There are many reasons why diabetes is likely to become an epidemic. Firstly, there is a clear connection between obesity and type 2 diabetes which cannot be ignored; this is because an article found that people with both conditions are exacerbated perhaps due to increased non esterified fatty acids (NEFAs) and glycerol among other linked biochemicals. On the other hand, this same article stated that people with type 1 diabetes are not usually obese. Nevertheless, it is vital that in order to prevent the incidence of type 2 diabetes in later life, it is important to implement strategies such as regular exercise and lowering carbohydrate intake in the diet. Alluding to the previous paragraph, one of the major factors to the increase in obesity and type 2 diabetes diagnoses is the sedentary lifestyle or decreased mobility through sitting. A meta-analysis evaluated 10 studies with over 500,000 volunteers and concluded that there was a 112% cumulative increase in type 2 diabetes risk linked to watching TV. Additionally, a study showed that more sedentary time had raised body and trunk fat percentage while there was reduced appendicular skeletal muscle mass. Taking into account these findings among others, it is evident that exercise does play a role in reducing the risk of type 2 diabetes. Counteracting the previous paragraphs, it is equally plausible that diabetes will not be epidemic because there are current pharmaceutical drugs taken orally like sulfonylureas and meglitinides that cause the pancreas to release insulin aside from injection based ones such as amylin mimetics, which maintains blood glucose concentration, which are used for type 2 diabetes. As for those afflicted with type 1 diabetes, they mainly take insulin because they are in deficit of the hormone or they can have a pancreatic transplant, which has more than 96% and 83% survival rates after 1 and 5 years of the operations respectively, although it does have a major complication of rejection like any other type of operation. With regards to future treatments, a review discussed how newer drugs for decreasing blood glucose such as dipeptidyl peptidase-4 (DPP-4) inhibitors have been re-evaluated for cardiovascular outcome trials by showing patients experiencing a decrease in other non-communicable diseases like myocardial infarction and albuminuria, indicating that they can be useful for heart and kidney diseases associated with type 2 diabetes. Furthermore, there are other potential therapies such as probiotics and prebiotics that can be used along with faecal transplants to change the gut microbiome for type 2 diabetes patients. It is uncertain that diabetes will/won’t become an epidemic From a more neutral perspective, there is not enough certainty that diabetes will or will not become an epidemic simply because accurately predicting the future 100% of the time is impossible. As such, the future interventions for treating diabetes may not actually get to exist, perhaps due to prospective factors like politics and societal values with respect to science as well as taking into account the difficulty for a therapeutic method to be put onto the market for the patients to consider. Another point to address is the fact that the human body is so incredibly complex that it took humans thousands of years to truly discover all of the current facts known in relation to its anatomy and physiology along with having some level of understanding of them. Not only that, there are still observations about the human body that are still unclear to scientists today and so the drugs for treating diabetes may or may not be effective depending on who is receiving the therapy because each person is genetically unique. Conclusion Referring to all of the arguments made, it is evident that diabetes is a huge burden for modern and future societies because of its links to obesity or sedentary lifestyle and consuming foods high in carbohydrates. Yet, this issue may be prevented by exploring future therapies, exploiting current ones and implementing non-clinical interventions such as increased regular exercise and reducing carbohydrate intake. Therefore, it is the responsibility of each patient and health organisation to manage diabetes before it becomes even worse. Written by Sam Jarada Related articles: Pre-diabetes / Diabetes drug to treat Parkinson's / The world vs the next pandemic REFERENCES Diabetes UK. Types of diabetes. Diabetes UK. 2022. Paschou SA, Papadopoulou-Marketou N, Chrousos GP, Kanaka-Gantenbein C. On type 1 diabetes mellitus pathogenesis. Endocrine Connections. 2018 Jan;7(1):R38–46. Cersosimo E, Triplitt C, Solis-Herrera C, Mandarino LJ, DeFronzo RA. Pathogenesis of Type 2 Diabetes Mellitus. Nih.gov. MDText.com, Inc.; 2018. Algoblan A, Alalfi M, Khan M. Mechanism linking diabetes mellitus and obesity. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 2014 Dec;7(587–591):587. Barnes AS. The epidemic of obesity and diabetes: trends and treatments. Texas Heart Institute journal. 2011;38(2):142–4. Hamilton MT, Hamilton DG, Zderic TW. Sedentary Behavior as a Mediator of Type 2 Diabetes. Medicine and Sport Science. 2014;60:11–26. Li D, Yang Y, Gao Z, Zhao L, Yang X, Xu F, et al. Sedentary lifestyle and body composition in type 2 diabetes. Diabetology & Metabolic Syndrome. 2022 Jan 15;14(1). Mayo Clinic. Diabetes treatment: Medications for type 2 diabetes. Mayo Clinic. 2018. Bahar SG, Devulapally P. Pancreas Transplantation. PubMed. Treasure Island (FL): StatPearls Publishing; 2022. Bailey CJ, Day C. The future of new drugs for diabetes management. Diabetes Research and Clinical Practice. 2019 Sep;155:107785. Bailey CJ, Day C. Treatment of type 2 diabetes: future approaches. British Medical Bulletin. 2018 Jun 1;126(1):123–37.

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