Carbohydrate: monosaccharide; energy and structure (cellulose, glycogen). Lipid: glycerol + fatty acids; energy storage, membranes, hormones. Protein: amino acid; enzymes, structure, transport. Nucleic acid: nucleotide; information storage and expression.
Glycolysis: cytoplasm; net 2 ATP, 2 NADH, 2 pyruvate. Krebs (×2 turns/glucose): mitochondrial matrix; 2 ATP, 6 NADH, 2 FADH₂, 4 CO₂. ETC + chemiosmosis: inner mitochondrial membrane; ~26–28 ATP from oxphos, H₂O as final product.
A, T, G, C. A=T (2 H-bonds); G≡C (3 H-bonds). Antiparallel strands; sugar = deoxyribose.
Resting (~−70 mV; Na/K pump). Depolarization (Na+ in via voltage-gated Na+ channels). Repolarization (K+ out via voltage-gated K+ channels; Na+ channels inactivate). Hyperpolarization & refractory period (overshoot of K+ efflux; pump restores).
K = max sustainable population given resources. r = per-capita growth rate when N << K. Density-dependent (disease, predation, competition) intensify with crowding; density-independent (weather, fire) act regardless of density.
B. Binds an allosteric site, inactivating some enzyme molecules → V_max ↓; remaining active enzymes still bind substrate the same way → K_m unchanged.
B. O₂ accepts electrons at Complex IV → forms H₂O.
Silent: same amino acid (degeneracy of code) — no protein change. Missense: different amino acid (e.g., Glu→Val in sickle-cell). Nonsense: introduces stop codon → truncated protein.
Insulin (β-cells): lowers blood glucose by promoting uptake/storage. Glucagon (α-cells): raises blood glucose via glycogenolysis. ADH (post. pituitary): increases water reabsorption in collecting duct. Aldosterone (adrenal cortex): increases Na+ (and water) reabsorption in distal tubule, raising BP.
(a) Protein: Biuret detects peptide bonds (purple); ninhydrin detects free amine groups. (b) Polymer (Biuret detects peptide bonds, plural). (c) Confirmation: gel electrophoresis (SDS-PAGE) to estimate molecular weight, or denaturation test (heat, acid → coagulation), or specific enzymatic digest (trypsin) followed by mass-spec.
Glycolysis: 2 ATP + 2 NADH (cytosolic) × 1.5 = 2 + 3 = 5. Pyruvate oxidation: 2 NADH × 2.5 = 5. Krebs: 2 ATP + 6 NADH × 2.5 + 2 FADH₂ × 1.5 = 2 + 15 + 3 = 20. Total = 30 ATP per glucose. (32 if malate-aspartate shuttle is used: cytosolic NADH yields 2.5 each.)
(a) Reverse-transcribe Factor IX mRNA from human liver cells using reverse transcriptase to produce cDNA (no introns — bacteria cannot splice). (b) Cut cDNA and plasmid with the same restriction enzyme (matching sticky ends); ligate using DNA ligase. (c) Transform competent E. coli (heat-shock or electroporation); plate on antibiotic agar — only those carrying the plasmid (with antibiotic-resistance marker) grow; screen for insert (blue/white α-complementation or PCR). (d) Induce expression (IPTG); lyse cells; purify by affinity chromatography (e.g., His-tag); refold and verify purity by SDS-PAGE. (e) Concern: endotoxin (LPS) contamination from bacterial membranes — must be rigorously removed before clinical use; also post-translational modifications differ from human cells (Factor IX needs γ-carboxylation), so production sometimes uses CHO mammalian cells instead.
(a) dN/dt = 0.10 × 100 × (5000−100)/5000 = 0.10 × 100 × 0.98 = 9.8 otters/year. (b) dN/dt = 0.10 × 2500 × (5000−2500)/5000 = 0.10 × 2500 × 0.5 = 125 otters/year. (c) Maximum dN/dt occurs at N = K/2 = 2500 — the inflection point of the logistic S-curve, where the product N(K−N) is maximized.
Bilayer of phospholipids (polar heads outward, non-polar tails inward) — selective barrier. Cholesterol — fluidity buffer. Transmembrane proteins — channels/carriers/receptors. Peripheral proteins — anchored to one face; signaling, structure. Glycoproteins/glycolipids — sugar chains on extracellular surface; recognition, immunity (e.g., ABO blood types).
Photosynthesis: chloroplast (thylakoid + stroma); inputs CO₂ + H₂O + light; outputs C₆H₁₂O₆ + O₂; light energy → chemical energy; anabolic. Respiration: cytoplasm + mitochondria; inputs C₆H₁₂O₆ + O₂; outputs CO₂ + H₂O + ATP; chemical energy of glucose → chemical energy of ATP (with heat); catabolic. The two are reciprocal — the basis of energy flow in ecosystems.
DNA → RNA: transcription. RNA polymerase II reads template 3'→5', synthesizes pre-mRNA 5'→3'. Nucleus. Then 5' cap, poly-A, splicing → mature mRNA. mRNA → protein: translation. Ribosome (rRNA + proteins; large + small subunits) reads codons 5'→3'; tRNAs deliver amino acids matching anticodons; peptidyl transferase forms peptide bonds. Cytoplasm or rough ER. Termination at stop codons by release factors. (Reverse transcriptase exists in retroviruses: RNA → DNA.)
Receptors: thermoreceptors in skin and hypothalamus. Control center: hypothalamus (set point ~37 °C). Cold deviation: vasoconstriction of skin arterioles (less heat loss); shivering (skeletal muscle contractions generate heat); piloerection; thyroid hormone release (longer term). Hot deviation: vasodilation; sweating (evaporative cooling); reduced muscle activity. All effects oppose the original change (negative feedback).
(a) ΔF508 is a 3-nucleotide deletion removing phenylalanine at position 508. The CFTR chloride channel misfolds and is degraded in the ER, so the apical membrane has too few channels. (b) Lungs: thick mucus traps bacteria → recurrent infections (Pseudomonas), inflammation, bronchiectasis. Pancreas: pancreatic ducts blocked → digestive enzymes don't reach intestine → malabsorption of fats and proteins → failure to thrive. (c) Without enzymes, fats and proteins are poorly digested; calories lost. High-calorie, high-fat diet plus oral pancreatic-enzyme capsules (lipase, protease, amylase) at meals and fat-soluble vitamins (A, D, E, K) supplementation maintain growth and nutrition.
(a) Casgevy edits the BCL11A enhancer in patient HSCs (hematopoietic stem cells). Disrupting BCL11A re-activates fetal hemoglobin (HbF), which doesn't sickle, compensating for defective adult HbS. (b) Patient HSCs collected by apheresis → ex vivo CRISPR-Cas9 editing → patient receives myeloablative chemotherapy → edited cells re-infused → engraft in marrow → produce HbF-rich red cells. (c) Benefit: potentially curative — reduces vaso-occlusive crises dramatically; one-time therapy. Concerns: cost (~$2 million USD per patient) — equity/access; long-term safety unknown (off-target effects, secondary malignancies); chemotherapy carries significant short-term risk and infertility issues; somatic-cell editing only — does not affect germline (this is generally accepted, in contrast to germline editing).
(a) No insulin → cells cannot import glucose → hyperglycemia; liver also continues gluconeogenesis. Glucose exceeds renal threshold → glucosuria → osmotic diuresis → dehydration. (b) Cells switch to fatty-acid oxidation → liver produces ketone bodies (acetoacetate, β-hydroxybutyrate, acetone) → ketonemia → metabolic acidosis. Acetone exhaled gives the fruity breath. (c) Kussmaul respirations: deep, rapid breathing — respiratory compensation that blows off CO₂ to raise blood pH. (d) Treatment: IV isotonic saline (rehydrate), IV regular insulin infusion, careful K+ replacement (insulin shifts K+ into cells; total-body K+ may be depleted), monitor pH and electrolytes, treat precipitating cause (often infection), then transition to subcutaneous insulin and patient education.
(a) r = (births − deaths)/N₀ = (8 − 4)/30 = 4/30 ≈ 0.133/year. (b) N(5) = 30 × e^(0.133 × 5) = 30 × e^0.67 ≈ 30 × 1.95 ≈ 58 marmots. (c) With K = 200 and r = 0.133, the logistic S-curve approaches but rarely "reaches" K asymptotically. Time to ~95% of K (N ≈ 190) ≈ ln(K/N₀ × 19) / r ≈ ln(126.7)/0.133 ≈ 4.84/0.133 ≈ 36 years. So within 30 years the population would approach but not quite reach K — perhaps ~150–180. Real conservation also faces stochastic events that may slow recovery further.