Stimulus: rise in blood glucose. Sensor: pancreatic beta-cells. Control centre: islets of Langerhans. Effector: liver and muscle cells, which take up glucose under insulin and store it as glycogen. Result: blood glucose returns to ~5 mM (negative feedback).
B. -70 mV; maintained by Na+/K+ pump and selective K+ leak channels.
(1) Resting (~−70 mV; Na/K pump active). (2) Depolarization to threshold (−55 mV) → voltage-gated Na+ channels open → Na+ in → rises to +30 mV. (3) Repolarization: Na+ channels inactivate; voltage-gated K+ channels open → K+ out → potential falls. (4) Hyperpolarization (~−80 mV) and refractory period; pump and K+ leak restore resting state.
B. Lipid-soluble steroids diffuse through the plasma membrane, bind nuclear receptors, and modulate gene expression — slow but durable effects.
Glomerulus/Bowman's: filtration (water, ions, glucose, urea pushed out by BP). Proximal tubule: reabsorption of glucose, amino acids, ~65% Na+ and water. Loop of Henle: countercurrent multiplier creating medullary osmotic gradient (descending: water out; ascending: salt out). Distal tubule + collecting duct: tuned reabsorption under aldosterone (Na+) and ADH (water).
B. Stretch → oxytocin → stronger contractions → more stretch (amplifying loop, ends with delivery).
(a) No depolarization possible — neurons cannot fire action potentials. (b) Motor neurons cannot deliver signals → muscles cannot contract → flaccid paralysis. (c) Diaphragm and intercostal muscles fail → respiratory arrest is the cause of death; victims must be ventilated until toxin clears.
IV: caffeine dose (0, 100, 200 mg). DV: resting heart rate (bpm). Controlled: time of day, recent activity, food intake, age range, no other stimulants. Ethics: informed consent, screen for cardiac conditions, use moderate doses, ensure participants can withdraw. Hypothesis: caffeine (a CNS stimulant blocking adenosine) raises HR; expect dose-dependent increase. Replicate ≥10 participants/condition; analyze with paired t-test.
Dehydration → blood osmolarity ↑ → osmoreceptors in hypothalamus → posterior pituitary releases ADH → ADH binds collecting-duct cells → aquaporin-2 inserts in apical membrane → more water reabsorbed → urine concentrated, blood osmolarity ↓. Low BP path: juxtaglomerular cells release renin → angiotensinogen → angiotensin I → angiotensin II (ACE) → vasoconstriction + adrenal cortex releases aldosterone → distal/collecting tubules reabsorb Na+ and water → BP rises.
X-axis: time (ms). Y-axis: membrane potential (mV). Key points: resting (~−70 mV), threshold (−55 mV; if reached, action potential fires "all-or-none"), peak (~+30 mV), repolarization (rapid fall as K+ exits), hyperpolarization (~−80 mV), return to resting. Refractory period: absolute (cannot fire again until Na+ channels reset) and relative (stronger stimulus required).
Nervous: very fast (ms), short-lived, electrochemical (action potentials, neurotransmitters), highly specific (synaptic). Endocrine: slow (s to min), long-lasting (min to days), chemical hormones via blood, broad — only cells with matching receptors respond. Both systems integrate at the hypothalamus-pituitary axis.
Tropic hormones target endocrine glands. Stress → hypothalamus releases CRH → anterior pituitary releases ACTH (tropic) → adrenal cortex releases cortisol → metabolic effects (gluconeogenesis, immune suppression). Cortisol exerts negative feedback on hypothalamus and pituitary. Chronic stress dysregulates this axis.
Autoimmune destruction of pancreatic beta-cells → no insulin → cells cannot import glucose; blood glucose remains high. Glucosuria: glucose exceeds renal threshold → glucose in urine. Polyuria: glucose in tubule increases osmolarity, drawing water → frequent urination. Polydipsia: water loss triggers thirst. Weight loss / fatigue: cells starve despite high blood sugar; body burns fat (ketogenesis → ketoacidosis if untreated) and protein. Treatment: lifelong insulin replacement.
(a) Demyelination disrupts saltatory conduction; action potentials slow or fail. (b) Symptoms depend on which tracts are affected: vision loss (optic neuritis), weakness, numbness/tingling, gait/coordination problems, fatigue; relapsing-remitting course is common. (c) MRI shows hyperintense plaques in white matter (periventricular, brainstem, spinal cord). Therapies modulate immune attack on myelin.
BPA binds estrogen receptors and can perturb development, reproduction, and metabolism. Concerns: developmental effects in fetuses/infants (links suggested with neurodevelopment, reproductive abnormalities); metabolic effects (insulin resistance, obesity); altered thyroid function. Regulatory response: Health Canada banned BPA in baby bottles (2008/2010) and added it to the Toxic Substances list under CEPA. Current advice: use BPA-free containers, avoid heating food in plastic.