📚 Year 12 CIE Biology: Case Study Practice with Worked Examples | CIE 12年级生物：案例分析实战演练
Case studies in CIE AS Biology require you to apply theoretical knowledge to real-world scenarios. This article walks you through eight detailed case studies spanning enzymes, cell membranes, mitosis, DNA, protein synthesis, plant transport, cardiovascular disease, and immunity. Each example analyses data and explains the reasoning step by step to sharpen your exam technique.
CIE AS 生物中的案例分析要求你将理论知识应用于现实情境。本文通过八个详实案例，涵盖酶、细胞膜、有丝分裂、DNA、蛋白质合成、植物运输、心血管疾病和免疫，每个案例都逐步分析数据并阐述推理过程，旨在提升你的应试技巧。
1. Enzyme Kinetics Case Study: Organophosphate Poisoning | 酶动力学案例：有机磷中毒
Parathion is an organophosphate insecticide that irreversibly inhibits acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in synaptic clefts. It binds covalently to a serine residue in the active site, forming a stable phosphoryl-enzyme complex that cannot be hydrolysed.
对硫磷是一种有机磷杀虫剂，能不可逆地抑制乙酰胆碱酯酶——该酶负责在突触间隙分解神经递质乙酰胆碱。它与活性位点的丝氨酸残基共价结合，形成稳定的磷酸化酶复合物，无法被水解。
A laboratory experiment measured the acetylcholinesterase activity in the presence of different parathion concentrations. The results are shown below.
一项实验测定了不同对硫磷浓度下的乙酰胆碱酯酶活性，结果如下。
| Parathion concentration (nM) | Enzyme activity (%) |
|---|---|
| 0 | 100 |
| 10 | 45 |
| 50 | 12 |
| 100 | 3 |
The enzyme activity drops sharply with increasing inhibitor concentration, and even at low doses the recovery is minimal without the synthesis of new enzyme molecules. This confirms an irreversible mode of inhibition.
酶活性随抑制剂浓度升高急剧下降，即使低剂量下若不合成新酶，恢复也微乎其微，证实了不可逆抑制模式。
Patients exposed to parathion accumulate excessive acetylcholine at cholinergic synapses, leading to continuous muscle contraction, paralysis and eventually respiratory failure. One treatment is intravenous atropine, which blocks muscarinic acetylcholine receptors and alleviates symptoms, while pralidoxime can reactivate the inhibited enzyme if administered early.
接触对硫磷的患者在胆碱能突触积累过量乙酰胆碱，导致持续肌肉收缩、瘫痪甚至呼吸衰竭。治疗包括静脉注射阿托品，阻断毒蕈碱型乙酰胆碱受体以缓解症状；若早期给予解磷定，可重新激活被抑制的酶。
2. Membrane Transport Case Study: Cystic Fibrosis | 膜运输案例：囊性纤维化
Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride ion channel. The most common mutation, ΔF508, leads to misfolded CFTR that is degraded before reaching the cell membrane. As a result, epithelial cells cannot export Cl⁻ effectively.
囊性纤维化由编码CFTR氯离子通道的基因突变引起。最常见的突变 ΔF508 导致CFTR错误折叠，在到达细胞膜前被降解。因此，上皮细胞无法有效排出Cl⁻。
Without chloride secretion, the usual osmotic movement of water out of cells is reduced, dehydrating the mucus layer on airway surfaces. The thick, sticky mucus traps bacteria such as Pseudomonas aeruginosa, which forms biofilms and causes persistent lung infections.
缺少氯离子分泌后，水分子随之渗透出细胞的正常过程减弱，气道表面的粘液层脱水。稠厚粘液捕获铜绿假单胞菌等细菌，后者形成生物膜并引发持续肺部感染。
In a diagnostic sweat test, the sweat chloride concentration of a CF patient often exceeds 60 mmol L⁻¹, compared with <40 mmol L⁻¹ in healthy individuals. This is because the faulty CFTR in sweat glands fails to reabsorb chloride ions. Treatments include inhaled hypertonic saline, which osmotically draws water into the airway mucus, and mechanical chest physiotherapy to clear secretions.
诊断汗液测试中，CF患者的汗氯浓度常超过60 mmol L⁻¹，而健康人低于40 mmol L⁻¹。这是因为汗腺中缺陷CFTR无法重吸收氯离子。治疗包括吸入高渗盐水，通过渗透作用将水带入气道粘液，以及胸部物理疗法帮助清除分泌物。
3. Mitosis and Cancer Case Study: Action of Taxol | 有丝分裂与癌症案例：紫杉醇的作用
Taxol (paclitaxel) is a chemotherapy drug that stabilises microtubules by binding to β-tubulin, preventing their depolymerisation. In a dividing cell, microtubules must shorten to pull sister chromatids apart during anaphase. Taxol thus arrests cells at the metaphase–anaphase checkpoint of mitosis.
紫杉醇是一种化疗药物，通过与β-微管蛋白结合稳定微管，阻止其解聚。在分裂细胞中，微管必须缩短才能在后期拉开姐妹染色单体。紫杉醇因此将细胞阻滞在分裂中期的检查点。
A study treated cultured breast cancer cells with Taxol and determined the mitotic index (percentage of cells in mitosis) over time. Before treatment, the mitotic index was 3.5%. After 12 hours of exposure, it rose to 15%, and after 24 hours it fell to 2% as many cells underwent apoptosis.
一项研究用紫杉醇处理乳腺癌细胞，测定有丝分裂指数随时间的变化。处理前指数为3.5%；暴露12小时后升至15%，24小时后因大量细胞凋亡而降至2%。
The initial rise in mitotic index occurs because cells accumulate in mitosis, unable to progress further. The subsequent decline reflects programmed cell death triggered by prolonged mitotic arrest. However, Taxol also affects rapidly dividing healthy cells, particularly in bone marrow and hair follicles, causing common side effects such as neutropenia and alopecia.
有丝分裂指数最初上升是因为细胞停滞在分裂期无法继续。随后的下降反映了延滞引发的程序性细胞死亡。但紫杉醇也影响骨髓和毛囊等快速分裂的健康细胞，引起中性粒细胞减少和脱发等副作用。
4. DNA Replication and Mutation Case Study: Sickle Cell Anaemia | DNA复制与突变案例：镰刀型细胞贫血
Sickle cell anaemia results from a single nucleotide polymorphism (SNP) in the β-globin gene (HBB). On the coding strand, the normal codon GAG is replaced by GTG. This point mutation substitutes valine for glutamic acid at position 6 of the β-globin polypeptide, producing haemoglobin S (HbS).
镰刀型细胞贫血源于β-珠蛋白基因 (HBB) 中的单核苷酸多态性。编码链上正常密码子GAG被GTG取代，这一突变使β-珠蛋白多肽第6位的谷氨酸变成缬氨酸，产生血红蛋白S (HbS)。
Under low oxygen tension, HbS molecules polymerise into rigid fibres, distorting red blood cells into a characteristic sickle shape. Sickled cells block capillaries, causing painful vaso-occlusive crises, and are prematurely destroyed, leading to anaemia.
在低氧压下，HbS分子聚合成刚性纤维，使红细胞扭曲成镰刀状。镰状细胞堵塞毛细血管，引起疼痛性血管闭塞危象，并过早被破坏，导致贫血。
Interestingly, heterozygous individuals (HbA/HbS) have a degree of protection against malaria, because the intraerythrocytic Plasmodium falciparum parasites find it harder to survive in affected cells. This balanced polymorphism explains the high frequency of the sickle cell allele in malaria-endemic regions, despite the severe disease in homozygotes.
有趣的是，杂合子 (HbA/HbS) 个体对疟疾有一定抵抗力，因为红细胞内的恶性疟原虫在异常细胞中更难存活。这种平衡多态性解释了为什么尽管纯合子患病严重，镰刀型细胞等位基因在疟疾流行区频率仍较高。
5. Protein Synthesis Case Study: Antibiotic Selectivity | 蛋白质合成案例：抗生素的选择性
Tetracycline and erythromycin are antibiotics that target bacterial ribosomes without harming eukaryotic cells. Tetracycline binds reversibly to the 30S subunit and blocks the attachment of aminoacyl-tRNA to the A site. Erythromycin binds to the 50S subunit and inhibits the translocation of peptidyl-tRNA from the A site to the P site.
四环素和红霉素是靶向细菌核糖体而不伤害真核细胞的抗生素。四环素可逆地与30S亚基结合，阻止氨酰-tRNA进入A位点。红霉素结合50S亚基，抑制肽酰-tRNA从A位点向P位点的移位。
An in vitro translation experiment using E. coli extracts showed that adding tetracycline caused an immediate stop in polypeptide elongation, whereas adding erythromycin produced truncated peptides. When the same experiment was repeated with rabbit reticulocyte lysate (a eukaryotic system), neither antibiotic inhibited translation significantly, confirming their selective toxicity.
使用大肠杆菌提取物的体外翻译实验显示，加入四环素后多肽延伸立即停止，加入红霉素则产生截短的肽段。当用兔网织红细胞裂解液（真核系统）重复实验时，两种抗生素均未显著抑制翻译，证实了其选择毒性。
Bacteria can acquire resistance through genes encoding efflux pumps, which actively export tetracycline, or erythromycin resistance methylases (erm) that modify the 23S rRNA of the 50S subunit, reducing drug binding.
细菌可通过获得编码外排泵的基因（主动排出四环素）或红霉素耐药甲基化酶 (erm) 基因（修饰50S亚基的23S rRNA，降低药物结合）而产生耐药性。
6. Plant Transport Case Study: Stomatal Closure and ABA | 植物运输案例：气孔关闭与脱落酸
When soil water is limited, roots synthesise the plant hormone abscisic acid (ABA) and transport it to the leaves via the xylem. In the guard cells, ABA binds to cytosolic receptors, triggering a rise in cytosolic Ca²⁺ concentration. This opens calcium channels and simultaneously inhibits proton pumps, causing membrane depolarisation.
当土壤水分不足时，根部合成植物激素脱落酸 (ABA)，通过木质部运至叶片。在保卫细胞中，ABA与胞质受体结合，引发胞质Ca²⁺浓度升高。这打开了钙通道，同时抑制质子泵，导致质膜去极化。
Depolarisation activates outward-rectifying K⁺ channels, so K⁺ and accompanying anions (Cl⁻, malate²⁻) leave the guard cells. Water follows by osmosis, guard cells become flaccid, and the stomatal pore closes. A classic experiment measured transpiration rate of a leaf before and after ABA application. Before ABA, transpiration was 2.5 g H₂O m⁻² s⁻¹; 30 minutes
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