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The science behind tooth decay Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How to prevent tooth decay 10/04/25, 10:52 Last updated: Published: 03/02/24, 11:24 The science behind tooth decay Dental caries, commonly referred to as tooth decay, manifests as a gradual process and progressive disease affecting the dental hard tissues, resulting in the breakdown of tooth structure and the potential for pain and infection within the oral cavity. Understanding the mechanisms behind tooth decay is crucial for adopting effective preventative measures, to stop or reverse the carious process and prevent cavity formation. Several factors contribute to dental caries, including bacteria, time, fermentable carbohydrates, and a susceptible tooth surface. In the absence of regular toothbrushing, a plaque biofilm is allowed to form on the tooth surface—a sticky, colourless film that serves as a breeding ground for bacteria such as Streptococcus mutans and Lactobacillus species. Once these bacterial species encounter fermentable carbohydrates and sugars from our diet, they begin to metabolise them, producing acids as a by-product. These acids contribute to an acidic environment in the mouth. When enamel, the outermost layer of tooth structure, is exposed to an acidic pH below 5.5, its mineral structure weakens, initiating the dissociation of hydroxyapatite crystals. Frequent acid attacks from dietary sugars result in a net mineral loss in teeth, leading to cavity formation, dental pain, and potential infections. The initial stage of decay involves the demineralisation of enamel. At this point, the damage can be reversible with good oral hygiene practices and through remineralising agents. Saliva has the capacity to remineralise initial carious lesions, and fluoride application through fluoridated toothpaste can also aid in reversing the initial stages of dental caries. However, if left untreated and allowed to progress, the decay can develop further into the tooth structure reaching the softer dentine beneath enamel. Dentin decay occurs more rapidly than enamel and can contribute to increased sensitivity and discomfort. As the decay advances, it may reach the dental pulp, which is the nerve of the tooth. Infection of the pulp can trigger severe pain and may necessitate root canal treatment in attempt to save the tooth. Persistent infections can lead to abscess formation—a pocket of pus causing swelling, pain, and systemic health issues, should the infection spread throughout the body. Tooth decay can be preventing through regular brushing with a fluoride toothpaste. The consistent disturbance to the plaque biofilm formation through brushing it away will not allow the caries process to continue, and hence prevent cavity formation. The fluoride aspect will help to strengthen the enamel and remineralise any mineral loss found in early lesions; this can stop and even reverse the carious process, thus preventing dental decay A healthy diet with limited consumption of sugary foods and drinks can significantly reduce the risk of tooth decay; with less sugars in the oral environment there is a lower rate of bacterial metabolisation to create the acids which contribute to the decay process. Regular dental check up appointments enable early detection and intervention of any initial lesions, preventing the progression of decay before reaching an irreversible status. Tooth decay is a preventable yet prevalent oral health issue. Instigated by the action of oral bacteria metabolising sugars in the mouth, our natural tooth structure can be destructed and decayed if the plaque biofilm is not controlled. By understanding the causes and progression of tooth decay, individuals can adopt proactive measures to maintain good oral hygiene, preserve enamel, and safeguard their smiles for a lifetime. Regular dental check-ups and a commitment to a healthy lifestyle play pivotal roles in preventing the onset and progression of tooth decay. Written by Isha Parmar Related article: Importance of calcium REFERENCE (Banerjee & Watson, 2015): Banerjee, A. and Watson, T.F. (2015) Pickard’s Guide to Minimally Invasive Operative Dentistry, King’s College London. Project Gallery

A rare neurological disease that is caused by a flaw in genetics Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Pseudo-Angelman Syndrome 12/09/25, 11:10 Last updated: Published: 07/09/24, 20:20 A rare neurological disease that is caused by a flaw in genetics This is article no. 8 in a series on Rare Diseases. Next article: Breaking down Tay-Sachs . Previous article: Apocrine carcinoma . An overview Name of the disease: Pseudo-Angelman Syndrome Other names the disease is known by: - 2q23.1 microdeletion syndrome - Del(2)(q23.1) - monosomy 2q23.1 Prevalence rate in the US: <1000 Average life expectancy: mid-50s – early 70s for severe to moderate intellectual disabilities Mortality rate: <10% in individuals with severe to moderate intellectual disabilities (this rate is more than double the general population) Pseudo-Angelman syndrome is a neurological disease, which is classified as Rare since it affects fewer than 1000 people in the US (as reported by the National Institute of Health). However, the information on this disease, like other rare diseases, is incomplete. This article aims to raise awareness of rare neurological diseases such as Pseudo-Angelman syndrome. Onset of symptoms: the symptoms of the disorder can appear early as a newborn and an infant Its symptoms include: - Seizures - Moderate-severe learning difficulties- mental retardation (MR)- and behaviour issues (the roles of the frontal and parietal lobes in the brain are planning and executing actions, as well as proprioception) - Speech and developmental delays (one of the functions the temporal lobe in the brain is responsible for is audio processing and speech) - Trouble sleeping - Repetitive movements of the fingers, wrists, etc. or motor stereotypy Hypotonia, slow weight gain, and shorter height may also be present in children affected by the disease. Symptoms help diagnose the diagnosis, but only genetic testing confirms it. The genetic mechanism of the disease Genetic cause of the disease: a microdeletion on 2q23.1 A chromosomal deletion occurs when a region of a chromosome is removed, resulting in the loss of genetic material within that specific segment. A microdeletion affects an even smaller part on the chromosome. Hence, in Pseudo-Angelman syndrome, the 2q23.1 microdeletion involves the loss of a small section of DNA on chromosome no. 2. More specifically, the DNA is lost from position 23.1 on chromosome 2. The exact role of chromosome 2 is not yet known (there is active research in this field), but chromosome 2 likely contains protein-coding genes. The chances are that key proteins that genes in chromosome 2 code for, are not made when there is a 2q23.1 microdeletion i.e. the microdeletion removes these crucial genes, and so cells cannot produce the proteins. Thus, giving rise to Pseudo-Angelman syndrome in the individual. Indeed, research has shown that usually the MBD5 gene is deleted in patients with the syndrome (in one study, all 15 patients had lost this gene from the removed region). The next prominent gene that is deleted is EPC2 , which is a gene that is thought to be involved in causing MR. Inheritance of the disease: mostly de novo A study by van Bon et. al (2009) depicted that 10 out of 11 patients were shown to have de novo inheritance of 2q23.1 microdeletion. Comparison to Angelman syndrome See Table 1 The syndrome is called Pseudo-Angelman, so where does the Angelman part of the name come from? (The disease is named after Dr. Harry Angelman, who had first described and reported the syndrome in 1965). Angelman syndrome (AS) is also a rare disease, however, it has a higher prevalence rate than Pseudo-Angelman. One possibility could be in the way these different conditions come about in the first place. Loss of function (rather than a deletion) of the UBE3A gene in chromosome 15 from the mother, gives rise to AS. It is an example of an imprinting disorder. (Two copies of each chromosome are normally inherited, but in genomic imprinting, only one copy of a particular chromosome is passed on i.e. either the copy from the mother is inherited, or from the father- not both. Deletion, loss of function etc. may cause the other copy to not be inherited. Imprinting disorders lead to developmental and growth problems in the affected individual). In contrast, Pseudo-Angelman syndrome is often de novo, and not inherited. It is not an imprinting disorder like Angelman’s, because Pseudo-Angelman is caused by a microdeletion in 2q23.1. However, AS presents severe physical, learning, and intellectual problems. The syndrome causes seizures and developmental delays. The similarity in patients with Pseudo-Angelman can be seen here; therefore, it may be why Pseudo-Angelman is named so. Table 1: a comparison of AS and Pseudo-Angelman syndrome Angelman syndrome (AS) Pseudo-Angelman Syndrome Prevalence rate 1 in 20,000- 12,000 <1000 in the US Symptoms in common severe physical, learning, and intellectual problems seizures and developmental delays severe physical, learning, and intellectual problems seizures and developmental delays Cause Loss of function of UBE3A gene Microdeletion (of MBD5 and ECP2 genes among others) Chromosome affected Chromosome 15 Chromosome 2 (2q23.1) Mode of inheritance Genomic imprinting; inherited in an autosomal dominant way in rare cases De novo Are there any treatments for Pseudo-Angelman syndrome? Cure available: none There is no one cure to help patients with the disease, but depending on symptoms, treatment may be offered accordingly. Current treatments based on symptoms: - Seizures--> anti-seizure medicines - Behaviour issues--> behaviour therapy - Speech and developmental delays--> speech therapy - Difficulty sleeping--> medicine, sleep training Potential future treatments or cures: targeted therapy in chromosome 2 Research is ongoing for a cure, and it is considering targeting particular genes of chromosome 2 in therapy- perhaps the MBD5 and ECP2 genes. The outlook for research into this disease Aside from discerning the exact roles and functions of the genes on chromosome 2, there is active research in targeted therapy for Pseudo-Angelman syndrome. Likely, once the rest of the roles of the genes on chromosome 2 are elucidated, efforts can be invested towards modifying or even inserting these genes (e.g. MBD5 and ECP2 ) back into the chromosome, which would lead to better protein expression. This could be a possible treatment for the rare neurological disease. Outside the molecular and genetic front, there should be increased awareness about this disease: this helps in reporting and diagnosing the syndrome, in addition to providing care and treatment to patients and their families. Summary In conclusion, Pseudo-Angelman Syndrome is a rare 2q23.1 microdeletion syndrome, which gets its name from the imprinting disorder AS. Pseudo-Angelman is characterised by seizures, moderate to severe learning difficulties, and developmental delays. Hence, making it a neurological disease as well. Treatments are available according to symptoms; but efforts are ongoing to ascertain the roles of other chromosome 2 genes, leading to potential targeted therapy. -- Patient organisations specifically for this disease: - Chromsome Disorder Outreach - Unique The information in this article does not substitute professional medical advice. For any concerns, please refer to your doctor or local genetic centre. -- Written by Manisha Halkhoree Related article: Childhood intelligence REFERENCES van Bon, B., Koolen, D., Brueton, L. et al. The 2q23.1 microdeletion syndrome: clinical and behavioural phenotype. Eur J Hum Genet 18, 163–170 (2010). https://doi.org/10.1038/ejhg.2009.152 Mayo Clinic, 2024. Angelman syndrome . Retrieved from Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/angelman syndrome/diagnosis-treatment/drc-20355627#:~:text=Depending%20on%20your%20child's%20symptoms,sign%20language%20and%20picture%20communication. Medline Plus, 2024. Angelman syndrome . Retrieved from Medline Plus Gov: https://medlineplus.gov/genetics/condition/angelman-syndrome/#:~:text=Angelman%20syndrome%20affects%20an%20estimated%201%20in%2012%2C000%20to%2020%2C000%20people . National Institute of Health, 2024. 2q23.1 microdeletion syndrome . Retrieved from National Institute of Health: https://rarediseases.info.nih.gov/diseases/10998/2q231-microdeletion-syndrome Project Gallery

From the Big Bang to the current model Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Story of the atom 11/02/25, 12:23 Last updated: Published: 20/04/24, 11:16 From the Big Bang to the current model The Greek philosopher and physicist Democritus proposed the idea of an atom at around 440 B.C. The atom is first explained by him using a stone. When a stone is split in half, it becomes two separate stones. There would eventually come to be a portion of the stone that would be too small to be cut if it were to be cut continuously i.e., indivisible. Since then, many scientists have adopted, discarded, or published their own theories about the nature, structure, and size of atoms. However, the most widely accepted, and still the basic model used to study atoms is Rutherford’s model. Rutherford published his theory of the atom suggesting that it had an electron orbiting a positively charged nucleus. This model was created after a series of experiments which included shooting alpha particles at thin gold sheets. Most of the alpha particles flowed through with little disturbance, but a tiny fraction was scattered at extreme angles to their initial direction of motion. Rutherford calculated the estimated size of the gold atom's nucleus and discovered that it was at least 10,000 times smaller than the atom's total size, with a large portion of the atom made up of empty space. This theory paved the way to further the atomic models by various other scientists. (Figure 1) Researchers have discovered unidentified molecules in space which are believed to be the precursor of all chemistry in the universe. The earliest "atoms" in the cosmos were actually nuclei without any electrons. The universe was incredibly hot and dense in the earliest seconds following the Big Bang. The quarks and electrons that make up matter first appeared when the cosmos cooled, and the ideal conditions were met for them to do so. Protons and neutrons were created by quarks aggregating a few millionths of a second later. These protons and neutrons joined to form nuclei in a matter of minutes. (Figure 2) Things started to happen more slowly as the cosmos cooled and expanded. The first atoms were formed 380,000 years ago when electrons were locked into orbits around nuclei. These were mostly hydrogen and helium, which are still the elements that are found in the universe in the greatest quantities. Even now, the most basic nucleus, found in ordinary hydrogen, is only a single, unadorned proton. There were other configurations of protons and neutrons that also developed, but since the number of protons in an atom determines its identity, all these other conglomerations were essentially just variations of hydrogen, helium, and lithium traces. To say that this is an exciting time for astrochemistry is an understatement. Furthermore, the formation mechanism of amino acids and nucleobases is being demonstrated by laboratory simulations of interstellar environments. Now that we are finding answers to these known problems, even more are arising. Hopefully, a more thorough understanding of these chemical processes will enable us to make more precise deductions about the general history of the universe and astrophysics. Written by Navnidhi Sharma REFERENCES CERN (n.d.). The early universe. [online] CERN. Available at: https://home.cern/science/physics/earlyuniverse#:~:text=As%20the%20universe%20continued%20to . Compound Interest (2016). The History of the Atom – Theories and Models | Compound Interest. [online] Compound Interest. Available at: https://www.compoundchem.com/2016/10/13/atomicmodels/ . Fortenberry, R.C. (2020). The First Molecule in the Universe. Scientific American. [online] doi: https://doi.org/10.1038/scientificamerican0220-58 . Sharp, T. (2017). What is an Atom? [online] Live Science. Available at: https://www.livescience.com/37206-atom-definition.html . Project Gallery

Unraveling the mysteries of protein-DNA interactions Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Zinc fingers in action 14/07/25, 15:21 Last updated: Published: 07/01/24, 14:22 Unraveling the mysteries of protein-DNA interactions Zinc-finger proteins are one of the most prevalent proteins used in DNA-binding motifs in biological processes. They are common as eukaryotic transcriptional factors. As they are structurally diverse, they interact in cellular processes like RNA packaging, DNA recognition, and transcriptional activation. Cys2His2 zinc- finger proteins are significant in cellular processes because of their short helical structure. The motif forms from a few amino acid sequences that contain cysteine and histidine residues that coordinate to a zinc ion. The zinc ions are crucial in stabilising the protein during folding. They also hold the α-helix and β-sheetstructures in place. The protein’s stability comes from the weak hydrophobic core and zinc coordination created by chelating. The zinc-finger/DNA complex is formed from the fingers interacting with up to four bases. The zinc finger DNA complex was first discovered from the transcription factor TFIIIA. The transcription factor had a ninefold pattern containing hydrophobic residues, histidine, and cysteine. The zinc finger motif was then concluded to consist of thirty amino acids and have a DNA binding domain with a zinc ion. This was confirmed by an extended x-ray absorption fine structure analysis. It was concluded that the contacts between the DNA strand and α helix occur due to hydrogen bonding and Van der Waals interactions. From these studies, the structures of zinc finger domains play vital roles in many processes other than DNA binding. Their tertiary structure allows the proteins to act as DNA-binding motifs. The alpha helix functions as the protein recognition component by inserting the protein into the main groove of DNA. Immobilizing zinc-finger proteins on a polymer chip can be used as an example to identify infections in the human body. This section provides a summary of the many kinds of DNA recognition and the generic protein-folding principles. Firstly, a specific binding site probe is needed to identify the DNA sequence region. This allows the identification of specific base pairs in the sequence. The hydrogen bonds between the amino acids in the zinc-finger proteins and DNA bases allow the zinc- finger proteins to bind to non-specific backbone phosphates. The non-specific backbone phosphates are formed from the interactions in the major and minor grooves of the DNA. The zinc-finger DNA interactions contribute substantially to hydrogen bonding and overall binding energy. To conclude, zinc fingers are very common structural motifs that are used as model systems to investigate how these proteins can recognise DNA sequences. This research has been involved in developing important therapeutic tools. Their unique structure allows them to be heavily involved in DNA binding, most commonly the Cys2His2 fingers. These binding interactions can be further explored to understand how certain target genes are bound to or how inhibitors can show the pharmacological properties of the zinc finger proteins. Written by Anam Ahmed Related articles: p53 protein / Anti-freeze proteins Project Gallery

Aggression has the confluence of individual predisposition and maintenance via social context Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unmasking aggression: a result of personal or social triggers? 14/07/25, 15:10 Last updated: Published: 01/01/25, 14:02 Aggression has the confluence of individual predisposition and maintenance via social context Introduction Anderson & Bushman (2002) define aggression as behaviour aimed at causing harm to another individual. Aggression can be measured by observing a signal of intention or aggression rating by self or others. The social theories of aggression include Dollard's frustration-aggression theory and Bandura's Social Learning Theory, while the individual factors theories account for personality traits and the influence of alcohol. However, there is no definite answer to whether social or individual factors are most important in explaining human behaviour. The interaction between social and individual factors will be explored to gain a deeper understanding of aggression. Social theories The frustration-aggression hypothesis proposed by Dollard et al. (1939) defines frustration as the emotion that follows when the occurrence of an instigated goal-response is interfered with, in turn leading to anger and aggression. According to this hypothesis, a person’s aggressive tendencies will be more intense the closer the individual is to achieving a goal before an obstacle appears. Many support this hypothesis, including Dill and Anderson (1995), who found that levels of aggression resulting from unjustified frustration were higher than justified frustration because they were caused by situational constraints rather than dispositional qualities. However, Berkowitz (1989) criticises Dollard et al.'s hypothesis, saying that frustration can only produce aggressive behaviour if it causes adverse effects. Due to the wide variety of negative and positive effects of frustration, it is important to revisit and clarify the frustration-aggression hypothesis. Additionally, aggression is often explained by the Social Learning Theory (SLT), proposed by Bandura et al. (1963), which states that aggressive behaviour is a learned behaviour reinforced by imitation and rewards or punishment. Bandura conducted the renowned Bobo Doll Study in 1961, in which children mimicked adult behaviour and attacked the doll after watching the researchers physically and verbally abuse a clown-faced inflatable toy in front of them, making this study extremely influential in understanding the role that families and household dynamics play in human behaviour. Based on this theory, exposure to TV violence can teach aggressive conduct and provide a model of behaviour to base actions upon. In SLT, rather than frustration generating an aggressive drive that can only be reduced by injurious behaviour, aversive stimulation creates general emotional arousal that can result in aggressive behaviour. Therefore, social theories encompass a broad range of disinhibitory factors and provide a broad theory explaining both impulsive and principled aggressive conduct. Individual factors theories Individual differences and variables, like personality traits, have also contributed to the study of aggressive behaviour. Hyatt et al. (2019) stated that certain personality traits such as narcissism and sadism have been meta-analytically linked to aggression shown in a lab setting. The lab paradigm captures aggression as it manifests whilst controlling for confounding variables, such as different types of aggression. However, the lab paradigm lacks construct validity because researchers don’t interpret the subjects’ intentions and motives when operationalising aggression. Further evaluation comes from Bettencourt et al. (2006), who meta-analysed personality dimensions and stated that provocation can cause aggression. They note that individuals with Type A personalities often exhibit impulsivity and emotional reactivity, which are positively associated with aggression. Thus, situational circumstances such as provocation and aggressive cues interact with these personality factors, together shaping the likelihood and intensity of aggressive behaviour. Additionally, the interplay between personality and alcohol can explain aggression. Alcohol reduces inhibitions that regulate 'normal' behaviour and increases aggression. Miller et al. (2009) concluded that alcohol may facilitate aggression in high-trait individuals specifically, those who score high on traits associated with aggression, such as impulsivity, hostility, or a predisposition toward anger—by impairing the drinker’s inhibition. Moreover, further research indicates a strong relationship between alcohol consumption and antisocial personality. Therefore, any discussion of personal factors and personality in aggression would be incomplete without considering the influence of alcohol. The interplay between social and individual trait theories Allen et al. (2018) created a model that encompasses both the social and the individual trait theories. The General Aggression Model (GAM) considers social, biological, and individual factors in aggression. This model consists of three stages: input, appraisal, and action. The input stage determines the likelihood of personal and situational factors causing aggression. For instance, individual differences, such as personality, social rejection, and provocation, are identified as risk factors for aggression. During the appraisal stage, the individual decides how to respond. Their response can be aggressive or non-aggressive, depending on the resources, time, and event. The action then influences the social encounter, which can alter personal and situational factors, leading to those factors restarting the cycle. Hence, this model proposes that individuals learn situations that lead to aggressive outcomes. To reduce aggression and offer treatment, the GAM has been applied to intergroup violence and therefore can be applied to a wide range of situations in real life. Conclusion In conclusion, aggression has the confluence of individual predisposition and maintenance via social context. For instance, as discussed previously, socialisation experiences may contribute to aggressive behaviour in individuals with certain personality traits. Thus, it is difficult to distinguish social and individual factors when explaining aggression, as most human behaviour is a multifaceted phenomenon with multiple determinants. Therefore, future research should be more holistic in the explanations of aggression, encompassing both social and individual factors. Written by Pranavi Rastogi Related articles: Emotional chemistry / Psychology of embarrassment / Brain of a bully REFERENCES Allen, J. J., Anderson, C. A., & Bushman, B. J. (2018). The general aggression model. Current Opinion in Psychology,19 , 75-80. doi:10.1016/j.copsyc.2017.03.034 Anderson, C. A., & Bushman, B. J. (2002). Human aggression. Annual Review of Psychology, 53 (1), 27-51. doi:10.1146/annurev.psych.53.100901.135231 Bandura, A., Ross, D., & Ross, S. A. (1963). Imitation of film-mediated aggressive models. Journal of Abnormal and Social Psychology, 66, 3-11 Berkowitz, L. (1989). Frustration-aggression hypothesis: Examination and reformulation. Psychological Bulletin, 106 (1), 59-73. doi:10.1037/0033-2909.106.1.59 Bettencourt, B.A. et al. (2006) ‘Personality and aggressive behavior under provoking and neutral conditions: A meta-analytic review.’, Psychological Bulletin , 132(5), pp. 751–777. doi:10.1037/0033-2909.132.5.751. Dill, J. C., & Anderson, C. A. (1995). Effects of frustration justification on hostile aggression. Aggressive Behavior, 21 (5), 359-369. doi:10.1002/1098-2337(1995)21:5<359::aid-ab2480210505> 3.0.co ;2-6 Dollard, J., Miller, N. E., Doob, L. W., Mowrer, O. H., & Sears, R. R. (1939). Frustration and aggression. doi:10.1037/10022-000 Hyatt, C. S., Chester, D. S., Zeichner, A., & Miller, J. D. (2019). Analytic flexibility in laboratory aggression paradigms: Relations with personality traits vary (slightly) by operationalization of Aggression. Aggressive Behavior, 45 (4), 377-388. doi:10.1002/ab.21830 Miller, C.A., Parrott, D.J. and Giancola, P.R. (2009) ‘Agreeableness and -related aggression: The mediating effect of trait aggressivity.’, Experimental and Clinical Psychopharmacology , 17(6), pp. 445–455. doi:10.1037/a0017727. Project Gallery

Exenatide as a potential drug Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A common diabetes drug treating Parkinson’s disease 08/07/25, 14:37 Last updated: Published: 24/01/24, 21:15 Exenatide as a potential drug A new investigational drug, originally developed for type 2 diabetes, is being readied for human clinical trials in search of the world's first treatment to impede Parkinson's disease progression. Parkinson's (PD) is the second most common neurodegenerative disorder. The connection between type 2 diabetes (T2DM) and PD was discovered in 1993, when PD patients with co-existing T2DM had worse motor symptoms and response to therapy. Dopaminergic neurons promote eating behaviour in hypoglycaemic states, mediated via insulin receptors in the substantia nigra, because dopaminergic neuronal loss affects glycaemic control. Thus, T2DM patients are more likely to acquire PD than people without diabetes. Excess glucose in the brain, as found in uncontrolled T2DM, may interact randomly with surrounding proteins and interfere with their function. These interactions also result in toxic end products promoting inflammation and α-synuclein clustering, both of which are PD characteristics. Over a 12-year period, retrospective data (N=8,190,323) showed that T2DM responders had considerably greater PD rates when compared to those without diabetes. The rise was significantly more pronounced among individuals with complex T2DM and those aged 25-44. Exenatide: Overview and Mechanism of Action Exenatide is a synthetic form of exendin-4, a naturally occurring protein identified in the saliva of the Gila monster (poisonous lizard endemic to the Southwest US) by Dr. Eng in the early 1990s. In humans, the chemical is produced after a meal to increase insulin production, decreasing blood sugar. GLP-1 degrades fast in humans, and its benefits are short-lived. However, investigations have shown effects of exendin-4 continue longer in people. This finally led to FDA clearance in 2005, when the product was sold as Byetta TM . Its current indications are for the treatment of balancing glucose levels in T2DM with or without additional oral hypoglycemic medications. This glycaemic control is an analogue of human GLP-1, used in T2DM treatment, either alone or in conjunction with other antidiabetic medications. Exendin-4's neuroprotective characteristics may aid in rescuing degenerating cells and neuron protection. Because T2DM and PD are linked, researchers want to explore its effectiveness as a PD therapy. Patients treated with exenatide for one year (in addition to standard medication) experienced less deterioration in motor symptoms when tested without medication compared to the control group. Research on Exenatide as a Potential Parkinson's Disease Therapy 21 patients with intermediate PD were assessed over a 14-month period, and their progress was compared to 24 other people with Parkinson's who served as controls. Exenatide was well accepted by participants, albeit some individuals complained about weight loss. Significantly, exenatide-treated participants improved their PD movement symptoms, while the control patients continued to deteriorate. The researchers investigate exenatide, a possible PD therapy, in an upcoming clinical study, lending support to the repurposing of diabetes drugs for Parkinson's patients. This research adds to the evidence for a phase 3 clinical trial of exenatide for PD patients. Data on 100,288 T2DM revealed that people using two types of diabetic medications, GLP-1 agonists and DPP4-inhibitors, were less likely to be diagnosed with Parkinson's up to 3.3 years follow-up. Those who used GLP-1 agonists were 60% less likely to acquire PD than those who did not. The results revealed that T2DM had a higher risk of Parkinson's than those without diabetes, although routinely given medicines, GLP-1 agonists, and DPP4-inhibitors seemed to reverse the association. Furthermore, a 2-year follow-up research indicated individuals previously exposed to exenatide displayed a substantial improvement in their motor characteristics 12 months after they ceased taking the medication. However, this experiment was an open-label research so the gains may be explained by a placebo effect. The research adds to the evidence that exenatide may assist to prevent or treat PD, perhaps by altering the course of the illness rather than just lowering symptoms. Other risk factors for PD should be considered by clinicians when prescribing T2DM drugs, although further study is required to clarify clinical significance. Findings from Clinical Trials and Studies Based on these findings, the UCL team broadened their investigation and conducted a more extensive, double-blind, placebo-controlled experiment. The findings establish the groundwork for a new generation of PD medicines, but they also confirm the repurposing of a commercially existing therapy for this illness. Patients were randomly randomised (1:1) to receive exenatide 2 mg or placebo subcutaneous injections once weekly in addition to their current medication for 48 weeks, followed by a 12-week washout period. Web-based randomisation was used, with a two-stratum block design depending on illness severity. Treatment allocation was concealed from both patients and investigators. The main outcome was the adjusted difference in the motor subscale of the Movement Disorders Society Unified Parkinson's Disease Rating Scale after 60 weeks in the realistically defined off-medication condition. Six major adverse events occurred in the exenatide group and two in the placebo group, but none were deemed to be connected to the research treatments in either group. It is unclear if exenatide alters the underlying illness mechanism or causes long-term clinical consequences. Implications and Future Directions Indeed, the UCL study showed that exenatide decreases deterioration compared to a placebo. However, participants reported no change in their quality of life. The study team would broaden their study to include a broader sample of people from several locations. Because PD proceeds slowly, longer-term trials might provide a better understanding of how exenatide works in these responders. Overall, findings suggest that gathering data on this class of medications should be the topic of additional inquiry to evaluate their potential. Exenatide is also being studied to see whether it might postpone the onset of levodopa-induced problems (e.g., dyskinesias). Furthermore, if exenatide works for Parkinson's, why not for other neurodegenerative illnesses (Alzheimer's, amyotrophic lateral sclerosis, Huntington's disease, multiple sclerosis) or neurological diseases (including cerebrovascular disorders, traumatic brain injury...)? Exenatide has been FDA-approved for diabetes for many years and has a good track record, but it does have some adverse side effects in Parkinson's patients, namely gastrointestinal difficulties (nausea, constipation). Exenatide as a prospective PD therapy is an example of medication repurposing or repositioning, an essential method for bringing novel therapies to patients in a timely and cost-effectively. However, further research is required, so it will be many years before a new therapy is licenced and available. Drug repurposing, or using authorised medicines for one ailment to treat another, opens up new paths for Parkinson's therapeutic development. Conclusion Exenatide shows potential as a therapy for Parkinson's disease (PD). Studies have shown that exenatide may help improve motor symptoms and slow down the progression of PD. However, further research and clinical trials are needed to fully understand its effectiveness and long-term effects. The findings also suggest that repurposing existing medications, like exenatide, could provide new avenues for developing PD therapies. While exenatide shows promise, it will likely be many years before it is licensed and widely available as a PD treatment. PROJECT GALLERY IMAGES DESCRIPTION Figure 1- The use of GLP-1 is beyond diabetes treatment. Nineteen clinical studies found that GLP-1 agonists can improve motor scores in Parkinson's Disease, improve glucose metabolism in Alzheimer's, and improve quality of. They can also treat chemical dependency, improve lipotoxicity, and reduce insulin resistance. However, adverse effects are primarily gastrointestinal. Thus, GLP-1 analogues may be beneficial for other conditions beyond diabetes and obesity. Figure 2- Potent GLP-1 agonists suppress appetite through a variety of mechanisms, including delayed gastric emptying, increased glucose-dependent insulin secretion, decreased glucagon levels, and decreased food ingestion via central nervous system effects. Short-acting agents, including exenatide, primarily function by impeding gastric evacuation, thereby leading to a decrease in postprandial glucose levels. On the contrary, extended-release exenatide and other long-acting agonists (e.g., albiglutide, dulaglutide) exert a more pronounced impact on fasting glucose levels reduction via their mechanism of action involving the release of insulin and glucagon. The ineffectiveness of long-acting GLP-1 receptor agonists on gastric evacuation can be attributed to the development of tolerance to GLP-1 effects, which is regulated by parasympathetic tone alterations. Figure 3- Illustrated is the cross-communication with insulin receptor signalling pathways and downstream effectors . Biomarkers can be derived from the formation and origin of extracellular vesicles, which indicate the initial inward budding of the plasma membrane. An early endosome is formed when this membrane fuses; it subsequently accumulates cytoplasmic molecules. As a consequence, multivesicular bodies are generated, which subsequently fuse with the plasma membrane and discharge their constituents into the extracellular milieu. Akt denotes protein kinase B; Bcl-2 signifies extracellular signal-related kinase; Bcl-2 antagonist of death; Bcl-2 extra large; Bcl-XL signifies Bcl-2; Bim signifies Bcl-2-like protein 11; cAMP signifies cyclic adenosine monophosphate; CREB signifies cAMP response element-binding protein; Erk1/2 signifies extracellular signal-related kinase IDE, insulin-degrading enzyme; IL-1α, interleukin 1α; IRS-1, insulin receptor signalling substrate 1; MAPK, mitogen-associated protein kinase; mTOR, mechanistic target of rapamycin; mTORC1, mTOR complex 1; mTORC2, mTOR complex 2; NF-kB, nuclear factor–κB; PI3-K, phosphoinositide 3-kinase; PKA, protein kinase; FoxO1/O3, forkhead box O1/O3, forkhead box O1/O3; GRB2, growth factor receptor-bound protein 2; GSK-3β, Written by Sara Maria Majernikova Related articles: Pre-diabetes / Will diabetes mellitus become an epidemic? / Parkinson's risk / Markers for Parkinsonism Project Gallery

The potential of MSCs to treat diseases like rheumatoid arthritis Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The role of mesenchymal stem cells (MSCs) in regenerative medicine 23/10/25, 10:18 Last updated: Published: 28/11/24, 15:16 The potential of MSCs to treat diseases like rheumatoid arthritis This is article no. 2 in a three-part series on stem cells. Next article: Regulation and policy of stem cell research . Previous article: An introduction to stem cells . Welcome to the second article in a series of three articles about stem cells. I will explore mesenchymal stem cells and their role in regenerative medicine in this article. Additionally, I will consider the potential of mesenchymal stem cells in treating three different diseases: multiple sclerosis (MS), rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). Consider reading Article 1 for more information on mesenchymal stem cells! Multiple sclerosis (MS) Multiple sclerosis (MS) is an autoimmune disease affecting the brain and spinal cord. It can cause symptoms such as muscle stiffness and spasms, problems with balance and coordination, vision problems and more. According to the Multiple Sclerosis Society UK (MS Society UK), it is estimated that there are around 150,000 people with MS in the UK, with nearly 7,100 people being newly diagnosed every year. Scientists have found that MSCs can be used to treat some of the symptoms of MS as MSCs protect the nerves in the CNS by secreting substances called neurotrophic growth factors, which increase nerve growth and the survival of nerve cells. These neurotrophic growth factors can also repair damaged nerves, improving nerve function. However, the exact mechanisms of this are still being studied. Furthermore, MSCs can activate the brain's natural healing mechanisms by stimulating the brain's stem cells to become active and repair the damaged tissue. This results in patients having a reduction in symptoms and the severity of the symptoms, improving the quality of life for those with MS. Rheumatoid arthritis (RA) Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease affecting the joints. The charity Versus Arthritis has said there are around 400,000 adults aged 16 and over affected by RA in the UK. Scientists have found that MSCs can reduce inflammation in the joints as they have immunomodulatory properties, so they can regulate the immune system's abnormal responses that cause RA. MSCs suppress immune cell activity, resulting in a decrease in inflammation and joint damage. In addition, MSCs can migrate (travel) to the inflamed joints and release anti-inflammatory molecules, reducing joint swelling and pain. This results in patients having a reduction in pain and joint swelling, improving the quality of life for those with RA. Inflammatory bowel disease (IBD) Inflammatory bowel disease (IBD) is an umbrella term for chronic inflammatory digestive diseases, including ulcerative colitis and Crohn’s disease (CD), affecting the gastrointestinal tract. A study by the University of Nottingham estimates that 500,000 people in the UK are living with IBD. Scientists have found that MSCs can reduce inflammation and increase tissue repair in the gastrointestinal tract. This is because MSCs can migrate to sites of inflammation in the gut, where they can replace damaged tissue cells. MSCs release signalling molecules that regulate the immune response and reduce inflammation. They can even directly interact with immune cells in the gut, influencing their behaviour and decreasing the inflammatory response. Also, MSCs can transfer mitochondria to damaged cells through cell fusion, helping the damaged cells function better and reduce inflammation. This results in reduced inflammation in patients, improving the quality of life for those with IBD. Looking to the future MS, RA and IBD are just three of the multiple diseases MSCs can target, and while there are many refinements to be made for MSCs to become more viable as treatment options, current findings show promising results. With further development, including more research to understand the exact biology of MSCs, there is massive potential for this method to revolutionise the treatment of various diseases, including cardiovascular diseases, liver diseases and cancer. As stem cell research continues to advance, policies must also adapt to this changing landscape; watch out for the last article in the series, where I will discuss the regulation and policy of stem cell research! Written by Naoshin Haque Related articles: The biggest innovations in the biosciences / Neuromyelitis optica and MS / Crohn's disease Project Gallery

The prevalence of diverticulosis is increasing in developed countries Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Understanding diverticular disease 14/07/25, 15:08 Last updated: Published: 27/11/24, 11:31 The prevalence of diverticulosis is increasing in developed countries Diverticulosis, diverticula, diverticulum, and diverticulitis - they may sound similar, but each term describes a specific aspect of diverticular disease. Before diving into diverticular disease, let’s clarify these key terms: Diverticulum: a small, bulging pouch that forms in a weak spot in the lining of the large intestine. Diverticula: the plural form of a diverticulum, indicating multiple bulging pouches in the large intestine's lining. Diverticulosis: a condition where multiple diverticula are present in the large intestine. Diverticulitis: this occurs when one or more diverticula become inflamed or infected. What is diverticular disease? Diverticular disease can be broadly categorised into two main conditions: diverticulosis and diverticulitis. Both involve the presence of diverticula in the colon, but the key difference lies in inflammation. In diverticulitis, the diverticula become inflamed or infected, leading to symptoms. On the other hand, diverticulosis is typically asymptomatic. However, there is a third condition, referred to as symptomatic uncomplicated diverticular disease (SUDD), where diverticula are present without inflammation, but the patient still experiences symptoms. The prevalence of diverticulosis is increasing in developed countries, largely due to the typical 'Western diet', which is high in red meat and low in fibre. Additionally, lifestyle factors such as obesity, smoking, and physical inactivity contribute to this rise. Age is also a significant factor, with 85% of diverticulosis cases occurring in individuals over the age of 50. Pathophysiology The formation of diverticula in the colon is primarily due to three factors: structural abnormalities in the colonic wall, disordered intestinal motility, and a deficiency of dietary fibre. The large intestine has two layers of muscle that work together to move its contents: an inner circular layer and an outer longitudinal layer. The outer layer consists of three bands called the taeniae coli, which run longitudinally along the colon. The gaps between these muscle bands are areas of weakness, making them vulnerable to the development of diverticula. Age-related weakening of the connective tissue further increases the risk of developing diverticula in these vulnerable areas. In some patients, abnormal gut motility can lead to areas of high pressure in the bowel, causing the mucosa to bulge outward, forming diverticula. Similarly, a lack of fibre in the diet can increase bowel pressure and lead to irregular movement, which also promotes outpouching. As we've discussed, some patients with diverticula may remain asymptomatic, while others experience varying levels of discomfort. The transition from diverticulosis to diverticulitis occurs when undigested food or a fecalith becomes trapped in these pouches, causing a blockage. This leads to bacterial growth and multiplication, resulting in infection and inflammation of the pouch. Symptoms Diverticular disease comes with a range of symptoms, some of which are quite common and could be easily mistaken for other conditions. General symptoms like nausea, vomiting, diarrhoea, and fever often overlap with other digestive problems, making diagnosis tricky. However, certain symptoms can hint more strongly at diverticular disease. For instance, experiencing pain in the lower left side of the abdomen (known as the left iliac fossa) or noticing rectal bleeding are more specific indicators that may point towards this condition. Recognising these symptoms can help in getting a more accurate diagnosis and appropriate treatment. Management Managing diverticular disease depends on the individual patient and the severity of their symptoms. For some, simple, conservative treatments are enough—this might include staying hydrated, eating a high-fibre diet, and giving the bowel a short rest by temporarily avoiding food. However, if a patient is experiencing significant pain or signs of infection, medical treatment is necessary. This may involve pain relief based on the WHO pain ladder or antibiotics to tackle the infection. In more serious cases, where other treatments haven’t worked or the patient is in a life-threatening situation, surgery might be required. A common procedure for these severe cases is the Hartmann’s procedure. This surgery removes the damaged section of the large intestine, usually due to infection or blockage. The healthy end of the intestine is brought out through an opening in the abdomen, creating a temporary colostomy that allows waste to leave the body through a bag. This setup gives the intestine time to heal, and in some cases, a follow-up surgery can reconnect it for normal function. Complications There are both short-term and long-term complications associated with diverticulitis, particularly in more severe cases that require more aggressive treatment such as surgery (see Figure 4 ). Future directions Recent changes in the management of diverticulitis have shifted how clinicians approach treatment. One significant update involves the use of antibiotics. Traditionally, diverticulitis was treated with routine antibiotic prescriptions. However, newer guidelines suggest that antibiotics may not be necessary for uncomplicated cases, helping to reduce both antibiotic resistance and the potential medication side effects for patients. Another emerging trend is treating uncomplicated diverticulitis on an outpatient basis. This allows patients to be managed at home with pain relief and dietary adjustments, which in turn frees up hospital resources for those with more severe conditions. Additionally, the management of complicated diverticulitis has evolved. For instance, abscesses may now be treated with percutaneous drainage rather than resorting to emergency surgery. Conclusion In summary, diverticular disease can vary widely in its symptoms and required treatments, ranging from dietary changes to surgical interventions for severe cases. Identifying specific signs and understanding the treatment options can empower patients and help them make informed choices. Advances in treatment approaches are also helping to improve outcomes and quality of life for those affected. Written by Abbasali Gulamhussein Related articles: Crohn's disease / The gut microbiome / Interplay of hormones and microbiome REFERENCES Cater, M. (2023). Foods for Diverticulosis and Diverticulitis . [online] www.hopkinsmedicine.org . Available at: https://www.hopkinsmedicine.org/health/wellness-and-prevention/foods-for-diverticulosis-and-diverticulitis . Matrana, M.R. and Margolin, D.A. (2009a) Epidemiology and pathophysiology of diverticular disease , Clinics in colon and rectal surgery . Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC2780269/ (Accessed: 12 October 2024). Miller, A.S. et al. (2021) The Association of Coloproctology of Great Britain and Ireland consensus guidelines in emergency colorectal surgery , Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland . Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC9291558/ (Accessed: 12 October 2024). NHS (2019). Diverticular disease and diverticulitis . [online] NHS. Available at: https://www.nhs.uk/conditions/diverticular-disease-and-diverticulitis/ . Sciencedirect.com . (2019). Hartmann Procedure - an overview | ScienceDirect Topics . [online] Available at: https://www.sciencedirect.com/topics/medicine-and-dentistry/hartmann-procedure . Singh, B., May, K., Coltart, I., Moore, N. and Cunningham, C. (2008). The Long-Term Results of Percutaneous Drainage of Diverticular Abscess. The Annals of The Royal College of Surgeons of England , [online] 90(4), pp.297–301. doi: https://doi.org/10.1308/003588408x285928 . Ubhi, L. (2023). Prescribing Analgesia and the WHO Analgesic Ladder | Geeky Medics . [online] geekymedics.com . Available at: https://geekymedics.com/prescribing-analgesia-and-the-who-analgesic-ladder/ . Project Gallery

By no means is this an exhaustive list on all the terminology relating to the COVID-19 pandemic. For more information, please refer to the World Health Organisation (WHO) and the Centers for Disease Control and Prevention (CDC). AAdenovirus- a group of related viruses. They were first removed from human adenoid glands (found at the back of the throat), hence the name. Asymptomatic- where a person is infected by the virus but does not present any symptoms. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Glossary for COVID-19 terms Last updated: 23/01/25 Published: 28/12/22 Key terms By no means is this an exhaustive list on all the terminology relating to the COVID-19 pandemic. For more information, please refer to the World Health Organisation (WHO) and the Centers for Disease Control and Prevention (CDC). – A Adenovirus- a group of related viruses. They were first removed from human adenoid glands (found at the back of the throat), hence the name. Asymptomatic- where a person is infected by the virus but does not present any symptoms. Can still pass the virus and infection onto others. C Coronavirus- a group of related viruses that cause diseases in mammals and birds. Named after the crown-like spike protein on the virus’s surface- ‘corona’ in Latin for crown. COVID-19/ COVID – the disease that coronavirus causes D DNA- deoxyribonucleic acid, the cell’s code to life. DNA instructs how to make proteins, which are essential for function in the body. Double helix. E Epicentre- the central point of the virus outbreak. This changed during the COVID-19 pandemic depending on the variant of virus. Epidemic- an outbreak in a localised area at a particular time H Herd immunity- when enough people are protected against the disease, that it lends immunity to those who are not protected. Can achieve protection against the disease through either previous infection, and/ or vaccination. I Immunity- achieving immunity means to be protected from future infections by viruses, and bacteria for example. You can achieve immunity through either previous infection, and/ or vaccination. Immunosuppressed- the immune system is suppressed. In other words, people who are immunosuppressed have a reduced ability to fight diseases. Thus preventing them from being infected in the first place is of great importance. Infection- the unnormal invasion of microorganisms into the body. Some infections present symptoms- at least straight away- while others do not show any symptoms. L Lockdown- preventing people from leaving where they are, to stop the transmission and contain the virus in the COVID-19 pandemic. M Mass vaccination- vaccinating many people in a certain area at a particular time mRNA- messenger RNA (ribonucleic acid). Single helix. Acts as a go-between for DNA and the proteins that are being made. P Pandemic- a global, or national outbreak Protein- an important molecule. Used as a fuel source, a building block, a carrier among other things, in the human body. R Restrictions- impeding or hindering movement and travel during the COVID-19 pandemic, in order to contain the spread of the virus and curb transmission. S Shedding- (in biology) refers to viruses casting off viral particles which can then infect others Side effects- effects that are different and potentially harmful from the main, intended effects of a medication, treatment, or vaccine. Examples of some side effects: headaches, aches, pains, fever. Symptomatic- where a person is infected with the virus and does present symptoms. Can still pass the virus and infection onto others. Symptoms- the signs a person has been infected; this can be physical or mental. With COVID-19, you can show symptoms as symptomatic, or not present symptoms as asymptomatic, if infected. Examples of symptoms for COVID-19 include loss of taste and smell, a persistent cough, fever. T Transmission- how a particular disease, in this case coronavirus, is passed from one person to another. V Vaccination- the administration of vaccine into the body. Vaccine- a form of active immunity, where a weakened, live version of the infection agent is administered into the body. The immune system kicks in and destroys the infection agent, but not before taking note of the genetic material (e.g. mRNA or DNA from the protein) from the agent. The immune system will use this genetic material to ‘remember’ the infection next time it appears, so it can prepare a speedier, more efficient response. Vaccine hesitancy- uncertainty as to whether people should take the vaccine. This could be due to a variety of reasons: being unfamiliar with the vaccine and its contents, and/ or being distrusting of the government and those in the health organisation. Viral load- the amount of virus (or viral genetic material) a person has in their body at a particular time. A person not infected with the virus will have no viral load, whereas a person infected with the virus will have a much higher viral load. Virus- a microorganism. Some spread diseases as vectors, while some are ‘better’. To date, it is being argued whether viruses are alive or not. W Wuhan- Capital of Hubei Province in China. First epicentre of coronavirus. Written by Manisha Halkhoree Related article: The origins of COVID-19

Common questions and answers- along with helpful resources- regarding the International Baccalaureate programme. International Baccalaureate (IB) Are you a student currently studying the IB Diploma Programme (IBDP), or about to commence it? You're in the right place! You may also like: Personal statements , A-level resources , University prep and Extra resources What is the IB? Jump to resources The IB is an International Academic Program which is another alternative to A levels. This is a highly academic program with final exams that prepare students for university and careers. You select one subject from each of the five categories, which include two languages, social sciences, experimental sciences, and mathematics. You must also choose either an arts subject from the sixth group or another from the first to fifth groups. How is the IB graded? Subjects might differ from schools and countries but these are the ideal subjects given in the IB. IB is graded through a point system (7 being the highest and 1 being the lowest) and the highest mark you can achieve in total is 45. For the 6 subjects you study you can achieve a maximum of 42 points. Theory of Knowledge and Extended Essay are combined to gain 3 extra bonus points. These 2 subjects will be marked from A (highest) to E (lowest) and then will be converted to points. What are the benefits of studying the IB? Even though there are a lot of subjects, this programme is great for students to gain new skills and be an all- rounder. IB also helps students to have a better idea of how work will be in university especially with coursework and that is one of the main things you will work on when studying IB- it is known as Internal Asssessment (IA). Doing CAS is also a great opportunity for students to be independent and find activities/ services to do outside of school to build up their portfolio on CAS as well as their CV/ personal statement when applying for university. The marking matrix used in the IB. How do universities use the IB to select students? All universities around the world accept the IB as a qualification gained in secondary school. Depending on the degree you are applying to, universities mainly focus on your Higher Level (HL) subjects. Each university has their own requirements for students applying to study a course at their institution. The most common way is considering your total point score out of 45, and your total point score of your HL subjects. Another way is asking applicants to achieve a certain grade in a particular grade at HL or at standard level (SL). If you complete the IB programme well enough, universities may prefer you over the other qualifications e.g. A-levels. Benefits of completing the IB programme. Resources for revision Websites to help Official IB website and the IB Bookshop Maths IA ideas Maths Analysis and Approaches SL and HL practice questions Maths resources in general / Worksheets and more Biology- BioNinja Biology, Chemistry, Physics, Maths- Revision Village / Save My Exams Biology, Chemistry, Maths- IB Dead IB Psychology IB Computer Science resources YouTube channels to help Chemistry- Richard Thornley Physics- Chris Doner Textbooks for both HL and SL Bio: Oxford IB Diploma Programme: Biology Course Biology for the IB Diploma by Brenda Walpole Chem: Chemistry Oxford IB Diploma Programme: Chemistry Course Chemistry for the IB Diploma Coursebook with Cambridge Elevate Enhanced Edition b y Steve Owen Physics: Physics Oxford IB Diploma Programme: Physics Course Physics for the IB Diploma with Cambridge by T. A. Tsokos Maths: Maths Oxford IB Diploma Programme- IB Mathematics: analysis and approaches / applications and interpretations