[LAW] Is It Ever Okay to Run a Red Light? Navigating the Legal and Ethical Crossroads 🚦

Crossroads. Get it hehe. Okay, enough chuckling at my own jokes. Today, we’re going to look into whether individuals should legally be allowed to run a red light.

Every single driver understands the disappointment of getting so close to the traffic lights only for them to change to amber and then red. Whilst it can be tempting to floor it and just run the red light, there are good reasons not to. Firstly, it’s illegal. But why is it illegal in the first place? Well, it’s because it’s very dangerous and can cause harm to other motorists around you. But… are there any scenarios where we could/should run a red light?

💡 Things to consider

• Balancing Necessity and Regulation: There might be instances where the imperative of the moment clashes with the rigidity of traffic rules. Is a driver ever justified in breaching a red light to swiftly respond to an emergency? If so, when? Is someone ‘allowed’ to run a red light to rush their child to hospital? Is a doctor ‘allowed’ to run a red light because they overslept but need to get to the hospital in time?

• The Greater Good Dilemma: We can agree that traffic laws are generally good for society as a whole. They ensure that people are kept as safe as possible on the roads. However, it might be necessary to reflect on the ethical calculus involved when considering the welfare of society as a whole. Could bypassing a red light be justified if it prevents a more serious harm or aids a person in dire need? It might be helpful to look into the philosophical dimensions of utilitarianism and ethical decision-making.

• Wider Consequences and Civic Responsibility: Consider the wider implications of running a red light. What happens when people start to think that others are not following the rules? How does this relate to the countries in which it is considered considerably harder/more dangerous to drive?

🔎 Find out more

• Act and Rule Utilitarianism - Internet Encyclopaedia of Philosophy

• Road Traffic Act 1988 (specifically Sections 35-37)

[MEDICINE] Are cancer cells smarter than healthy body cells? 🤓

Cancer is a common disease in which an organism’s body cells reproduce uncontrollably and spread to different parts of the body. This can happen to any organ or tissue in the body and may be spontaneous, or initiated by viral infection, radiation, or carcinogenic exposure, to name a few. Cancer cells are not foreign: they are our own body cells that acquire advantageous mutations (changes in their DNA) that accelerate the cell cycle. The adaptive mutations are famously outlined by Hanahan and Weinburg’s “Hallmarks of Cancer”. Key changes to the reproductive cycle include generational immortality (healthy cells are programmed to die as they age through apoptosis, while cancer cells can bypass this) and evasion of cell cycle checkpoints (normally, stages of the cell cycle go through a form of quality-check to ensure there are no catastrophic mutations or disformed cells, all of which can be essentially ignored by cancer cells). Overall, this means that cancer cells are adapted to reproduce extremely rapidly in a selfish manner. That is, the tumours that they make up can grow and grow and grow whether the organism as a whole can support it or not…

💡 Things to Consider

• Why is curing cancer so difficult?: In the media, curing cancer is often suggested as one of medicine’s most challenging tasks. To start, cancer is extremely diverse and can come in many forms, affecting many different body parts, with a range of pathophysiology and symptoms. However, one of the main difficulties is the fact that the cancer cells are still our body cells, making it difficult to distinguish them and fight them pharmaceutically. For example, curing a bacterial infection with antibiotics is relatively straightforward: we can use drugs that target these foreign organisms and kill them without harming our own body, but for cancer, we don’t have the same luxury. Killing cancer cells often comes at the expense of our healthy tissue, leading to common side effects such as hair falling out (hair growth involves rapidly-producing cells, so its production is therefore often caught in the crossfire of cancer treatment).

• How do current treatments for cancer work?: Having just explored how difficult treating cancer is, it opens the door to future drug development to take a new approach and there is a plethora under review. The mutations that allow cancer cells to reproduce in such a rapid and uncontrolled manner can be targeted by treatment methods. For example, if cell-cycle checkpoints are being evaded by cancer cells, irradiation treatment can be used to introduce mutations into cells to paradoxically treat cancer. This way, our healthy body cells that still undergo these checkpoints can be detected and repaired to then continue the cycle, while those cancer cells that are not surveyed by this “quality-check” go on to undergo mitotic catastrophe and die. This is an example of a huge range of treatment options that each build on the mutations that dictate cancer hallmarks.

• What’s the difference between a malignant and benign tumour?: A tumour is a swelling caused by abnormal tissue growth (different to the swelling you get in inflammation), however, this can be either “benign” or “malignant”. A benign tumour stays in its primary location and does not invade to other sites and is therefore relatively safe, and able to be surgically removed, if necessary. However, malignant, or cancerous, tumours can spread (or metastasise) to other sites in the body via the bloodstream or lymphatic system. This is common to the liver, brain, lungs, or bone, where they cause catastrophic damage and often need more intense treatment, such as radiotherapy, to control this spread.

🔎 Find out more

Hallmarks of Cancer: *Hanahan and Weinburg - Hallmarks of cancer: the next generation https://pubmed.ncbi.nlm.nih.gov/21376230/*

Mutation-based treatment: *Waarts et al. – Targeting Mutations in Cancer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9012285/*

[BIOLOGY] Apoptosis 🧬

Cells are very complex, with many biochemical processes that make up their metabolism proceeding constantly and with remarkable accuracy, yet sometimes things can go wrong. When this happens, the consequences can be lethal. Thankfully, cells have evolved a process to stop their division before things get out of hand; apoptosis. There are two types of apoptosis: extrinsic (where proteins bind to receptors on the cell surface membrane to activate the cell death pathway), or intrinsic (where apoptosis is initiated within the cell due to DNA damage, faulty replication or through a developmental pathway). After apoptosis is triggered, the inner membrane of the mitochondrion is damaged and pores form, through which cytochrome c (part of the electron transport chain) is released. At this point, the cell is committed to apoptosis. In the cytoplasm, cytochrome c binds to other proteins to form the apoptosome, causing the activation of the apoptosis cascade. The nucleus and cytoplasm can be broken down into small vesicles and packaged off to be phagocytosed by nearby cells. The protein p53 can trigger apoptosis and act as a tumour suppressor gene.

💡 Things to consider

• Dire consequences: As you have read, one of the purposes of apoptosis is to prevent the continued replication of cells with dangerously mutated DNA, which the cellular proofreading mechanisms in place cannot fix. Why is this important? What might be the consequences of not having this mechanism for a unicellular and multicellular organism respectively?

• Extrinsic apoptosis: Extrinsic apoptosis is usually triggered by the immune system in multicellular organisms. During this process, T cells analyse proteins (or parts of proteins) being displayed in MHC Class 1 proteins located on the cell surface, so that cells can be monitored to ensure correct proteins are being synthesised. In what context(s) might it be beneficial to induce extrinsic apoptosis?

• Necrosis: There is another way cells can die, known as necrosis. This can happen as a result of direct trauma including mechanical damage, heat or cold, pH changes etc. When cells die this way, their contents are not packaged up into easily phagocytosed packages, but sometimes spill out of the cell as it ruptures, which can activate an immune response. Knowing this, why do you think it’s important that cell contents are phagocytosed rather than simply released? What might be the consequences of an immune response being triggered?

🗳️ Poll

👀 Keep your eyes peeled for…

• 10th, 11th, 12th, 14th October - History Skills Workshop - Admissions: the HAT

• 10th October - UEA Webinar: What’s it really like to be a student?

• 10th October - Christ’s College “An Introduction to Oxford & Cambridge” Webinar for students from the West Midlands

• 11th October - deadline for Cambridge SU Shadowing Scheme applications

• 11th October - York Open Lecture: The heart of the state: Emotional and moral economies of migration policing

• 11th October - English Literature Admissions Test (ELAT) Livestreams: Session 4

• 12th October - MAT Past Papers: 2022

• 13th October - St John’s Admissions Clinic