Which bones form the nasal septum?

Correct Answer: B

Rationale: The nasal septum is formed by nasal bones (upper) and vomer (lower), dividing nostrils midline. Maxilla/mandible frame the mouth. Frontal/parietal are cranial. Temporal/sphenoid are lateral/base. Nasal/vomer's septal role, per facial anatomy, makes 'b' correct.

Correct Answer: A

Rationale: The cell is the smallest independently functioning unit of life, capable of metabolism, reproduction, and homeostasis (e.g., a neuron firing), per cell theory. Molecules like DNA or proteins are components, not independently functional. Organs like the heart are multi-tissue structures, far larger. Tissues like muscle are cell groups, not individual units. The cell's standalone vitality, foundational in biology, makes 'a' the correct answer.

Correct Answer: C

Rationale: The heat-loss center (hypothalamus) activates sweat glands to increase output, cooling via evaporation when overheated. Blood vessels dilate (not constrict, a) to release heat. Breathing may adjust but isn't slow/shallow primarily. Not all only 'c' fits. Sweating's cooling role, per thermoregulation, makes 'c' correct.

Correct Answer: B

Rationale: In a sarcomere, the functional unit of skeletal muscle, contraction occurs via the sliding filament theory, where actin (thin) and myosin (thick) filaments slide past each other. During this process, the H zone the central region of the A band with only thick filaments shortens or vanishes as thin filaments overlap it. Similarly, the I band, containing only thin filaments on either side of the Z line, narrows as actin slides toward the sarcomere's center. The A band, spanning the thick filaments' full length, remains constant because myosin doesn't shorten, while Z lines, anchoring actin, move closer together but don't disappear. This dynamic reflects muscle shortening without altering filament lengths, driven by ATP-powered cross-bridge cycling. Electron microscopy and physiological studies confirm that contraction compresses these zones, distinguishing them from static structures like the A band. Misinterpreting these changes could confuse the sarcomere's architecture, but the consistent reduction of H zones and I bands aligns with observed muscle mechanics, critical for understanding force generation.

Correct Answer: A

Rationale: Muscle contraction begins when a nerve impulse triggers the sarcolemma, the muscle fiber's membrane, to depolarize, generating an action potential. This electrical event, initiated by acetylcholine at the neuromuscular junction, spreads across the fiber's surface, reaching T-tubules invaginations that relay the signal inward. Only then does calcium release from the sarcoplasmic reticulum occur, binding to troponin, which shifts tropomyosin to expose actin's myosin-binding sites. Filament sliding follows as myosin heads engage actin, powered by ATP. The sarcolemma's depolarization, measurable via electromyography, precedes all intracellular steps, occurring within milliseconds. Calcium release and T-tubule transmission follow sequentially, not simultaneously, as the signal propagates. Binding site exposure and sliding depend on calcium's presence, placing them later. Physiology texts sequence this: action potential (1-2 ms), T-tubule spread, calcium surge (10-20 ms), then contraction. This initial electrical trigger is foundational, distinguishing it from subsequent chemical and mechanical events in the excitation-contraction coupling cascade.