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MRCP PART 1 · CLINICAL SCIENCES

Clinical sciences questions
for MRCP Part 1.

Clinora has 523 clinical sciences single best answer questions covering 493 topics. Every question explains all five options, separates the key clue from what it means and what to do next, and links to its source. Try the 5 sample questions below, then practise more for free.

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Question 1Cell signallingMedium

A new drug binds a cell-surface G-protein-coupled receptor and activates adenylate cyclase, raising intracellular cyclic AMP. Which class of downstream effector is most directly activated by this second messenger?

  1. APhospholipase C
  2. BProtein kinase A
  3. CReceptor tyrosine kinase autophosphorylation
  4. DGuanylate cyclase
  5. ENuclear steroid hormone receptor translocation
Show answer and explanation

Answer: B Protein kinase A

The receptor described is coupled to Gs. Activated Gαs stimulates adenylate cyclase, which converts ATP to cyclic AMP. Cyclic AMP binds the regulatory subunits of protein kinase A, which release its catalytic subunits. These then phosphorylate target proteins such as enzymes, ion channels and the transcription factor CREB. Examples include β-adrenergic receptors (increased heart rate and contractility, glycogenolysis), glucagon receptors and TSH receptors. It helps to keep the three main GPCR pathways separate: Gs raises cAMP and activates PKA; Gi inhibits adenylate cyclase and lowers cAMP; Gq activates phospholipase C, producing IP3 (calcium release) and DAG (protein kinase C). Cholera toxin locks Gs on and pertussis toxin blocks Gi, and both are common exam links.

Key clue
Gs-coupled receptor raising cyclic AMP
What it means
Classic Gs-adenylate cyclase-cyclic AMP-protein kinase A pathway
What to do
Protein kinase A is the direct downstream effector of cyclic AMP

Why the other options are less appropriate

  • A Phospholipase C sits in the Gq pathway, producing IP3 and DAG. It is not activated by cyclic AMP.
  • C Receptor tyrosine kinases (such as insulin and growth-factor receptors) dimerise and autophosphorylate when their ligand binds. They do not use cyclic AMP.
  • D Guanylate cyclase makes cyclic GMP, which activates protein kinase G. It is driven by nitric oxide or natriuretic peptides, not by cyclic AMP.
  • E Steroid hormone receptors are intracellular and act directly on gene transcription. They are unrelated to the GPCR–cAMP pathway.

Source: StatPearls: Physiology, G Protein Coupled Receptor

Question 2Enzymes and metabolismMedium

A new inhibitor increases the apparent Michaelis constant (Km) of an enzyme for its substrate while the maximum reaction velocity (Vmax) remains unchanged when substrate concentration is raised sufficiently. Which type of enzyme inhibition does this describe?

  1. AAllosteric activation
  2. BNon-competitive inhibition
  3. CUncompetitive inhibition
  4. DIrreversible inhibition
  5. ECompetitive inhibition
Show answer and explanation

Answer: E Competitive inhibition

The key clue is that Vmax is unchanged once enough substrate is added, while the apparent Km rises. That means the inhibitor competes with the substrate for the same active site. It binds only to free enzyme, and a high substrate concentration simply outcompetes it, so the maximum rate can still be reached. More substrate is needed to reach half of Vmax, which is why Km appears higher. On a Lineweaver-Burk (double reciprocal) plot, the lines cross on the y-axis (same 1/Vmax) but meet the x-axis at different points. Non-competitive inhibitors bind a separate site on both free enzyme and enzyme-substrate complex, so they lower Vmax and leave Km unchanged. Uncompetitive inhibitors bind only the enzyme-substrate complex and lower both Km and Vmax, giving parallel lines. Clinical examples of competitive inhibition include methotrexate on dihydrofolate reductase and statins on HMG-CoA reductase. Fomepizole and ethanol act the same way on alcohol dehydrogenase in methanol or ethylene glycol poisoning.

Key clue
Raised Km, unchanged Vmax with excess substrate
What it means
Competitive inhibition
What to do
Overcome by increasing substrate concentration; unchanged Vmax at saturating substrate

Why the other options are less appropriate

  • A Allosteric activation increases enzyme activity. The question describes an inhibitor, and an activator would not raise the apparent Km in this way.
  • B Non-competitive inhibition lowers Vmax and leaves Km unchanged. Here Vmax is preserved, so this does not fit.
  • C Uncompetitive inhibition lowers both Km and Vmax. Here Km rises and Vmax is unchanged.
  • D Irreversible inhibition removes active enzyme, so Vmax falls and cannot be restored by adding more substrate.

Source: StatPearls: Physiology, Noncompetitive Inhibitor

Question 3Innate/adaptive immunityMedium

A patient develops a severe infection with encapsulated bacteria after splenectomy. Which immune mechanism, normally dependent on the spleen, best explains this increased susceptibility?

  1. ALoss of mast cell degranulation
  2. BLoss of T-cell-mediated cytotoxicity
  3. CLoss of the main site of complement protein synthesis
  4. DLoss of neutrophil oxidative burst
  5. ELoss of splenic clearance of opsonised bacteria and of antibody to polysaccharide antigens
Show answer and explanation

Answer: E Loss of splenic clearance of opsonised bacteria and of antibody to polysaccharide antigens

Encapsulated bacteria, such as Streptococcus pneumoniae, Haemophilus influenzae type b and Neisseria meningitidis, resist phagocytosis because their polysaccharide capsule masks the bacterial surface. They are cleared mainly after opsonisation by antibody and complement, and the spleen plays two key roles. First, its macrophages in the red pulp filter blood-borne bacteria that are poorly opsonised. Second, its marginal zone B cells make rapid IgM responses to polysaccharide antigens without T-cell help. After splenectomy, both roles are lost. Risk is highest in the first two years but is lifelong. The blood film shows Howell–Jolly bodies. The UKHSA Green Book advises immunisation against pneumococcus, Hib, meningococcal ACWY and B, and influenza each year. Vaccines should ideally be given at least 2 weeks before elective surgery, or at least 2 weeks after emergency surgery. Prophylactic antibiotics (usually phenoxymethylpenicillin) are offered, along with a standby supply for fever, a patient alert card, and advice about malaria and dog bites (Capnocytophaga).

Key clue
Post-splenectomy susceptibility to encapsulated organisms
What it means
Loss of splenic opsonic clearance and polysaccharide antibody responses
What to do
Vaccinate against encapsulated organisms, give prophylactic antibiotics as indicated, and educate on urgent treatment of fever

Why the other options are less appropriate

  • A Mast cell degranulation drives allergic and early inflammatory responses. It is not spleen-dependent and does not explain this risk.
  • B Cytotoxic T cells kill virus-infected and tumour cells. They are not the main defence against encapsulated bacteria and do not depend on the spleen.
  • C Complement is made mainly in the liver, so splenectomy does not stop its synthesis. What is lost is splenic clearance of opsonised bacteria.
  • D Neutrophil oxidative burst is intact after splenectomy. Its loss, as in chronic granulomatous disease, causes catalase-positive infections.

Source: UKHSA Green Book chapter 7: Immunisation of individuals with underlying medical conditions

Question 4Cell deathEasy

A lymphocyte with irreparable DNA damage releases cytochrome c from mitochondria into the cytosol. Which event most directly follows in the intrinsic apoptotic pathway?

  1. AApaf-1 apoptosome formation with initiator caspase-9 activation
  2. BFas receptor trimerisation with caspase-8 activation
  3. CComplement C5b-9 assembly in the plasma membrane
  4. DLysosomal rupture causing uncontrolled inflammatory necrosis
  5. ECyclin D activation driving the cell into S phase
Show answer and explanation

Answer: A Apaf-1 apoptosome formation with initiator caspase-9 activation

Apoptosis can be started from inside the cell (the intrinsic, or mitochondrial, pathway) or from outside it (the extrinsic, or death-receptor, pathway). In the intrinsic pathway, DNA damage activates p53, which switches on pro-apoptotic Bcl-2 family proteins such as PUMA, NOXA and BAX. BAX and BAK open pores in the outer mitochondrial membrane, and cytochrome c leaks out. In the cytosol, cytochrome c binds Apaf-1, which assembles into the apoptosome. The apoptosome activates the initiator caspase-9, which then activates executioner caspases 3 and 7. These break down the cell in an orderly way: it shrinks, its chromatin condenses, it breaks into apoptotic bodies, and it exposes phosphatidylserine so that it is cleared without inflammation. Anti-apoptotic Bcl-2 opposes this pathway, which is why it is overexpressed in follicular lymphoma, t(14;18). The extrinsic pathway (Fas or TNF receptors, FADD, caspase-8) converges on the same executioner caspases.

Key clue
Mitochondrial cytochrome c release
What it means
This is the defining upstream event of the intrinsic mitochondrial pathway.
What to do
Activate the Apaf-1 apoptosome and initiator caspase-9.

Why the other options are less appropriate

  • B Fas trimerisation and caspase-8 activation belong to the extrinsic, death-receptor pathway.
  • C C5b-9 is the complement membrane attack complex. It lyses cells; it is not part of apoptosis.
  • D Lysosomal rupture with inflammation describes necrosis, which is uncontrolled. Apoptosis is orderly and does not cause inflammation.
  • E Cyclin D drives the cell cycle forward through G1. It promotes proliferation rather than cell death.

Source: Programmed Cell Death (Apoptosis) — Molecular Biology of the Cell

Question 5Upper limbHard

A mid-shaft humeral fracture injures the radial nerve in the spiral groove. Which function is most likely to remain substantially intact despite wrist drop?

  1. AExtension at the metacarpophalangeal joints
  2. BSensation in the dorsal first web space
  3. CWrist extension
  4. DForearm supination by supinator
  5. EElbow extension by most of triceps
Show answer and explanation

Answer: E Elbow extension by most of triceps

The radial nerve winds round the back of the humerus in the spiral groove, so a fracture of the humeral shaft can damage it. That makes it the nerve most often injured in these fractures. What is lost depends on which branches leave the nerve below the lesion. The branches to the long and lateral heads of triceps, and usually most of the medial head, leave in the axilla or upper arm, above the groove. Elbow extension is therefore largely spared. Everything supplied lower down is affected. Brachioradialis and the wrist extensors (extensor carpi radialis longus and brevis) are weak, causing wrist drop. Finger and thumb extension at the metacarpophalangeal joints is lost through the posterior interosseous nerve. Supinator is weak, but biceps can still supinate the forearm, especially with the elbow bent. The superficial radial nerve is affected, so sensation is lost over the dorsal first web space. Most of these palsies are neurapraxias and recover without surgery. Management is a splint, physiotherapy and nerve conduction studies if there is no recovery after several months.

Key clue
Radial nerve injury in the humeral spiral groove
What it means
Branches to most triceps heads have already left the nerve proximally.
What to do
Preserve most elbow extension despite distal radial deficits.

Why the other options are less appropriate

  • A Extension at the finger MCP joints is supplied by the posterior interosseous nerve, distal to the groove, so it is lost.
  • B The superficial radial nerve branches off below the spiral groove. Sensation over the dorsal first web space is usually affected.
  • C The nerve to the radial wrist extensors leaves below the spiral groove. Their weakness is what causes the wrist drop.
  • D Supinator is supplied by the deep radial branch distal to the groove, so it is weakened. Supination is kept mainly by biceps.

Source: Radial Nerve — StatPearls

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Topics covered

Show all 493 clinical sciences topics
  • A G-alpha subunit unable to hydrolyse GTP
  • A negative sequencing panel may not assess repeat expansions
  • A non-degradable mitotic cyclin
  • A non-significant heterogeneity test with few studies
  • A pooled mean confidence interval is not a prediction interval
  • A shared helicase function in transcription and DNA repair
  • Absolute benefit changes with baseline risk
  • Acid-base biochemistry
  • Acid-base compensation
  • Acid-base physiology
  • Acute limb ischaemia
  • Adenosine-deaminase deficiency
  • Adult epiglottitis
  • Affinity maturation
  • Agreement beyond chance
  • AIRE and central tolerance
  • Akt-mediated sequestration of a pro-apoptotic protein
  • Alkaline phosphatase interpretation
  • Allelic heterogeneity
  • Allocation concealment
  • Allosteric enzyme kinetics
  • Alternative complement pathway
  • Altitude acclimatisation
  • Alveolar gas equation at altitude
  • Alveolar ventilation
  • Amyloidosis
  • An antiproliferative signal acting through p15
  • An irreversible outcome makes crossover unsuitable
  • Analytical interference
  • Aneuploidy mechanism
  • Angioedema
  • Antibiotic stewardship
  • Antibody avidity
  • Antibody-dependent cellular cytotoxicity
  • Anticipation
  • Antigen presentation
  • Apoptosis
  • Apoptosis morphology
  • Arterial compliance
  • Artery of Adamkiewicz
  • Arthus reaction
  • Atrioventricular conduction physiology
  • Auditory pathway lesion
  • Autonomic anatomy
  • Autonomic physiology
  • Autosomal dominant inheritance
  • Autosomal recessive disease
  • Autosomal recessive inheritance
  • Avoiding double-counting a shared control group
  • B-cell function
  • B-cell maturation
  • Backbone processing after spontaneous base loss
  • Balanced translocation and recurrent miscarriage
  • Balancing membrane uptake with return
  • Barr bodies
  • Base-excision repair
  • Bayesian credible intervals
  • Bcl-2 prolongs survival rather than increasing mitosis directly
  • Bid links receptor signalling to mitochondria
  • Bland–Altman analysis
  • Blinding
  • Bohr effect
  • Bonferroni correction
  • Branched-chain amino-acid metabolism
  • Brier score
  • C5a function
  • Calculating a weighted pooled mean difference
  • Calibration slope
  • Calibration-in-the-large
  • Cancer genetics
  • Cancer genomics
  • Capacity assessment
  • Carbon-dioxide transport
  • Cardiac pressure-volume relations
  • Cardiovascular physiology
  • Cardiovascular reflexes
  • Case-cohort study design
  • Caseating granulomas
  • Caspase catalytic chemistry
  • Categorical data
  • Cauda equina
  • Causal inference
  • Causal inference and collider bias
  • Caveolae versus clathrin-coated pits
  • Cavernous sinus
  • Cdc25 inhibition at a damage checkpoint
  • Cell cycle
  • Cell death
  • Cell signalling
  • Central B-cell tolerance
  • Central immune tolerance
  • Cerebral blood-flow regulation
  • Change-score variability cannot be inferred from baseline SD alone
  • Chemotaxis towards bacterial formyl peptides
  • Chimerism
  • Cholesterol synthesis regulation
  • Choosing Peto odds-ratio meta-analysis cautiously
  • Chromosomal/mitochondrial disease
  • Citric-acid-cycle energetics
  • Classical homocystinuria
  • Clinical diversity cannot be repaired by a model switch
  • Clinical trials
  • Cluster trials
  • Cobalamin
  • Cochlear hair-cell function
  • Cochlear mechanoelectrical transduction
  • Coefficient of relationship
  • Cohort studies
  • Collagen hydroxylation
  • Combining reciprocal relative effects on a log scale
  • Common fibular nerve at the fibular neck
  • Common gamma-chain immunodeficiency
  • Common variable immunodeficiency
  • Comparing event rates with different follow-up
  • Comparing populations
  • Competing risks
  • Competing-risks analysis
  • Complement
  • Complement C3b opsonisation
  • Complement opsonisation
  • Complement pathway screening
  • Compound heterozygosity
  • Conductive versus sensorineural hearing loss
  • Confidence intervals
  • Confidentiality
  • Consanguinity
  • Contamination bias
  • Contiguous-gene deletion syndrome
  • Copper-dependent lysyl oxidase
  • Cori cycle
  • Coronary perfusion
  • Correlation and causation
  • Cranial anatomy
  • Creatinine assay interference
  • Cricothyroid muscle innervation
  • Cytogenetics
  • Cytosolic DNA sensing
  • Diagnostic accuracy
  • Diagnostic discrimination
  • Diagnostic test studies
  • Diagnostic testing
  • Diagnostic tests
  • Diagnostic tests and screening
  • Diffusing capacity
  • Direct reversal of an alkylated DNA base
  • Disease frequency
  • Distinguishing the G1/S and G2/M cyclin complexes
  • DNA fragmentation during lymphocyte apoptosis
  • DNA repair
  • Dominant-negative effect
  • Dominant-negative variants
  • Dorsal-column pathway
  • Duodenal control of gastric emptying
  • Duty of candour
  • Dynamic mutations
  • Ecological studies
  • Effect modification
  • Encapsulated organisms
  • Endocrine physiology
  • Endocytosis
  • Endoplasmic-reticulum stress
  • Enzyme kinetics
  • Enzymes and metabolism
  • Eosinophil biology
  • Epidemiological impact
  • Epigenetics
  • Epithelial junctions
  • Equivalence-trial confidence intervals
  • ER-to-Golgi vesicle traffic
  • Eustachian-tube function
  • Facial nerve lesions
  • Falciform ligament anatomy
  • Family testing of a VUS can be investigational rather than predictive
  • Fatty-acid oxidation control
  • Femoral triangle
  • Fick principle
  • Filtration fraction
  • Floor of mouth anatomy
  • Foramen spinosum
  • Founder effect
  • Frank-Starling mechanism
  • Frank-Starling preload response
  • Free hormone measurement
  • Fuel metabolism
  • Galactose metabolism
  • Gastric acid secretion
  • Gastrointestinal feedback physiology
  • GATA2 deficiency
  • Gene conversion
  • Genetic anticipation
  • Genetic linkage
  • Genome sequencing does not mean every gene was interpreted
  • Genomic imprinting
  • Genomic technologies
  • Genomic test interpretation
  • Germline mosaicism after an apparently de novo disorder
  • Glossopharyngeal sensory role
  • Gluconeogenesis
  • Glycogen metabolism
  • GPCR desensitisation
  • GPI anchors
  • Gram-positive cocci
  • Granuloma immunology
  • Haem synthesis
  • Haemoglobin chemistry
  • Haploinsufficiency
  • Hardy–Weinberg equilibrium
  • Hawthorne effect
  • Healthy-worker survivor effect
  • Hepatic anatomy
  • Hepatic glycolysis regulation
  • Herd immunity
  • Hereditary fructose intolerance
  • Heteroplasmy and variable mitochondrial phenotype
  • Homologous recombination
  • Horizontal pleiotropy in Mendelian randomisation
  • Hypersensitivity
  • Hypothalamic-pituitary physiology
  • Hypoxic pulmonary vasoconstriction
  • IL-12–interferon-gamma axis
  • Immortal-time bias
  • Immune checkpoint physiology
  • Immune-complex disease
  • Immunoassay interference
  • Immunoglobulin class switching
  • Immunoglobulins
  • Incidence and prevalence
  • Incidence-density sampling
  • Incorporation bias
  • Index event bias
  • Indirect standardisation
  • Inflammasome activation
  • Inguinal canal
  • Initial test for an imprinting disorder
  • Innate/adaptive immunity
  • Intention-to-treat analysis
  • Intention-to-treat dilution
  • Interaction
  • Intercellular communication
  • Interim analyses
  • Intrinsic apoptosis
  • Inverse-variance weighting from standard errors
  • Jugular foramen
  • Jugular venous pulse
  • Ketone-body metabolism
  • Laboratory interpretation
  • Laboratory sodium measurement
  • Laryngeal sensory innervation
  • Law of Laplace
  • LDL binding without internalisation
  • Lead-time bias
  • Lectin complement pathway
  • Length-time bias
  • Leukocyte adhesion deficiency
  • Ligand-induced growth-factor receptor down-regulation
  • Linkage analysis
  • Locus heterogeneity
  • Loss of the p16 cell-cycle brake
  • Lower limb
  • Lumbosacral plexus
  • Lung time constant
  • Lysosomal glycogen metabolism
  • Lysosomal targeting
  • Macroautophagy
  • Macroenzyme interference
  • Major haemorrhage
  • Malate–aspartate shuttle
  • Maple syrup urine disease
  • Maternal inheritance of mitochondrial DNA
  • Median and skew
  • Membrane energetics
  • Membrane lipid composition
  • Membrane transport
  • Mendelian inheritance
  • Meta-analysis
  • Methylation abnormalities are not ordinary sequence variants
  • MHC class I
  • MHC class I antigen processing
  • MHC class II
  • MHC class II invariant chain
  • MHC restriction
  • Microtubules and mitosis
  • Microvascular physiology
  • Middle cerebral artery
  • Missing not at random
  • Missing outcome data
  • Mitochondrial genetics
  • Mitochondrial protein import
  • Mitochondrial uncoupling
  • Mitotic checkpoint
  • Molecular genetics
  • Mucosal antibody
  • Multicollinearity
  • Multifactorial threshold inheritance
  • Multiplicity
  • N-acetylglutamate synthase deficiency
  • Natural-killer-cell recognition
  • Neck
  • Neck and thorax
  • Negative blood mtDNA testing does not exclude tissue-limited disease
  • Negative control outcome
  • Negative likelihood ratio
  • Neonatal Fc receptor
  • Nernst equilibrium potential
  • Neuroanatomy
  • Nitrogen metabolism
  • No events in either arm and relative effects
  • Non-inferiority trials
  • Nonsense-mediated mRNA decay
  • Normal distributions
  • Normal targeted FISH is not a genome-wide exclusion test
  • Nuclear dismantling downstream of caspase activation
  • Nuclear transport
  • Nucleotide-excision repair
  • Number needed to harm
  • Observational studies
  • Obturator nerve
  • Oncogenes
  • One-carbon metabolism
  • Osmolal gap interpretation
  • Otoscope cone of light
  • Oxidative phosphorylation
  • Oxygen delivery
  • Oxygen extraction ratio
  • Oxygen transport
  • Oxyhaemoglobin dissociation
  • Paired categorical data
  • Paired data
  • Paired non-parametric comparison
  • Parathyroid hormone physiology
  • Parotid secretomotor pathway
  • Partial verification bias
  • Pedigree interpretation
  • Pelvic anatomy
  • Penetrance
  • Pentose-phosphate pathway
  • Pericardial referred pain
  • Peripheral B-cell homeostasis
  • Peroxisomal metabolism
  • Peroxisomal protein targeting
  • Persistent lymphocytes after failed death-receptor signalling
  • Phagocyte respiratory burst
  • Phagocytosis of an antibody-coated particle
  • Pharmacogenomics
  • Placental mosaicism and discordant prenatal screening
  • Plasma-membrane phospholipid asymmetry
  • Pooling the same construct measured on different scales
  • Popliteal fossa
  • Population attributable fraction
  • Population genetics
  • Portal-systemic anastomoses
  • Postzygotic mosaicism
  • Pre-analytical variation
  • Pre-mRNA splicing
  • Precision
  • Precision is not freedom from bias
  • Predictive values
  • Preferential repair of an actively transcribed strand
  • Preserving sequence information during mismatch correction
  • Prevalence and disease duration
  • Prevalence–incidence bias
  • Primary carnitine deficiency
  • Propionyl-CoA metabolism
  • Proprioceptive reflexes
  • Protein glycosylation
  • Protein synthesis
  • Pseudo-hyperkalaemia in extreme thrombocytosis
  • Pseudoautosomal inheritance
  • Pudendal nerve
  • Pulmonary closing capacity
  • Purine salvage
  • Pyruvate dehydrogenase complex deficiency
  • Quasi-experimental study design
  • Radial nerve lesion localisation
  • Raising concerns
  • Random exposure measurement error
  • Randomisation
  • Randomised trials
  • Receptor-mediated concentration of a scarce ligand
  • Recurrence risk
  • Recurrent laryngeal nerve
  • Recurrent laryngeal nerve anatomy
  • Red-cell metabolism
  • Reduced penetrance
  • Refractory hypoxaemia from shunt
  • Regression to the mean
  • Regulatory T cells
  • Releasing NF-kappa-B from its cytoplasmic inhibitor
  • Renal ammoniagenesis
  • Renal autoregulation
  • Renal countercurrent exchange
  • Renal glucose handling
  • Renal myogenic autoregulation
  • Renal physiology
  • Renal plasma flow
  • Renal water handling
  • Repeated admissions are counts, not affected individuals
  • Replicative senescence
  • Respiratory dead space
  • Respiratory physiology
  • Restrictive ventilatory physiology
  • Retaining E2F repression after a mitogenic signal
  • Rinne test interpretation
  • Robertsonian translocation
  • Rod phototransduction
  • Rubin rules
  • Screening
  • Screening bias
  • Screening overdiagnosis
  • Secondary immune response
  • Secretin
  • Secretory immunoglobulin A
  • Sensitivity
  • Sensitivity analysis of an uncertain inclusion decision
  • Short reads and highly similar pseudogenes
  • Shoulder girdle
  • Signal transduction
  • Simpson paradox
  • Skeletal-muscle excitation–contraction coupling
  • Skull base
  • Sodium–calcium exchange
  • Somatic mosaicism
  • Specificity
  • Standard errors entered as standard deviations
  • Standardised incidence ratio
  • STAT activation after cytokine binding
  • Statistical inference
  • Statistical power
  • Stepped-wedge cluster randomisation
  • Subgroup analyses
  • Superantigen-mediated T-cell activation
  • Superior laryngeal nerve injury
  • Survival analysis
  • Swallowing phases
  • Systematic reviews
  • T follicular helper cells
  • T-cell co-stimulation
  • T-independent antigens
  • Terminal complement deficiency
  • Testicular lymphatic drainage
  • Th17 effector immunity
  • The adaptor linking IL-1 receptors to downstream kinases
  • The Fas death-receptor adaptor
  • The initiating caspase at a death receptor
  • The proton pump that acidifies endosomes
  • The sorting role of early endosomes
  • Thoracic duct
  • Thoracic wall
  • Thymic T-cell development
  • Thyroid hormone binding physiology
  • Toll-like receptor 4
  • Tonic self-MHC signals and naive T-cell survival
  • Transferrin returns after unloading iron
  • Transplant allorecognition
  • Treatment effects
  • Trials and statistical inference
  • Trio sequencing
  • Tubuloglomerular feedback
  • Tumour suppressors
  • Two eyes from one participant are not independent people
  • Type I error
  • Type I hypersensitivity
  • Type I interferon immunity
  • Type II error
  • Type II hypersensitivity
  • Type IV hypersensitivity
  • Ubiquitin-proteasome system
  • Uncertain non-coding variants after whole-genome sequencing
  • Uncompetitive inhibition
  • Uniparental disomy
  • Upper limb
  • Urea-cycle regulation
  • V(D)J recombination
  • Vagal trunks at the oesophageal hiatus
  • Valid consent
  • Venous stasis and haemoconcentration
  • Ventilation-perfusion mismatch
  • Ventilation-perfusion physiology
  • Ventricular action-potential plateau
  • Vestibulo-ocular reflex
  • Visual pathways
  • Water balance
  • Weak-instrument bias
  • West zone 1
  • What a random-effects pooled estimate represents
  • What is removed by nucleotide-excision repair?
  • Where LDL separates from its receptor
  • Why a bacterial light-dependent repair result cannot be assumed in humans
  • Why a balanced rearrangement can escape a copy-number array
  • Why cyclin binding alone may not activate a CDK
  • Withdrawal of mitogenic support before the restriction point
  • X-chromosome inactivation
  • X-linked recessive inheritance

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