Which of the following glands produces an oily substance that lubricates the hair and skin?

Achondroplasia is caused by a mutation in a single autosomal gene (not on sex chromosomes), and it is inherited in a dominant pattern. This means:

• A person needs only one copy of the mutant gene to show the disorder.
• Individuals with two copies of the mutant gene (AA) typically do not survive infancy (lethal homozygosity).
• Therefore, an adult living with achondroplasia must have one normal allele (a) and one mutant allele (A) — this is the heterozygous genotype Aa.

Explanation:

Genotypes Explained:

• aa – Normal height individual (no mutation).
• AA – Homozygous dominant; results in severe skeletal malformations and is typically fatal shortly after birth.
• Aa – Heterozygous; the individual has achondroplasia and can live into adulthood.
• XAY – A sex-linked genotype indicating a male with a mutation on the X chromosome; not applicable here since achondroplasia is autosomal, not sex-linked.

Autosomal Dominant Inheritance in Achondroplasia:

• Each child of an Aa parent has:
  • A 50% chance of being Aa (having achondroplasia),
  • A 50% chance of being aa (not having the condition),
  • If both parents are Aa, there's a 25% chance of AA (lethal).

Clinical Note:

• People with achondroplasia typically have shortened limbs, normal-sized torsos, and characteristic facial features.
• Intelligence and life expectancy are typically normal, provided there are no severe complications.

Carrying oxygen to other body cells.

Reasoning

Red blood cells (RBCs), also known as erythrocytes, are specialized cells in the blood with the primary role of transporting oxygen from the lungs to the tissues throughout the body. This function is critical for cellular respiration and energy production in all body cells.

1. Structure and Function:
   • RBCs are biconcave in shape, increasing their surface area for gas exchange.
   • They are filled with hemoglobin, a protein that binds oxygen in the lungs and releases it in tissues.
2. Oxygen Transport:
   • In the lungs, oxygen molecules bind to hemoglobin in the red blood cells.
   • RBCs then circulate through the bloodstream, delivering oxygen to cells for metabolism.
   • They also help transport carbon dioxide (a waste product) from tissues back to the lungs.
3. Why the Other Options Are Incorrect:
   • 1 (Fighting infection): This is the function of white blood cells (leukocytes).
   • 2 (Creating blood clots): This is primarily the role of platelets (thrombocytes) and clotting proteins.
   • 4 (Responding to antigens): This is part of the immune response, mainly involving white blood cells, particularly lymphocytes.

Sarcoplasmic reticulum

Reasoning:

The sarcoplasmic reticulum (SR) is a specialized type of smooth endoplasmic reticulum found in muscle cells. Its main function is to store and release calcium ions (Ca²⁺), which are crucial for muscle contraction and relaxation.

Here’s how the process works:

1. Calcium Storage:
   • In a relaxed muscle, the SR stores large amounts of calcium ions.
2. Calcium Release During Contraction:
   • When a nerve impulse (action potential) reaches the muscle fiber, it triggers the SR to release calcium into the sarcoplasm (cytoplasm of the muscle cell).
   • Calcium binds to troponin, causing a conformational change that moves tropomyosin away from the actin binding sites, allowing myosin heads to attach to actin and begin contraction.
3. Calcium Reuptake During Relaxation:
   • Once the contraction ends, calcium is actively pumped back into the SR.
   • This removal of calcium from the sarcoplasm leads to muscle relaxation.

How It Controls Muscle Contraction-Relaxation:

1.Excitation-Contraction Coupling:

• • A nerve signal triggers an action potential in the muscle fiber, which travels into theT-tubules.
  • This activatesdihydropyridine receptors (DHPR), which openryanodine receptors (RyR)on the SR, releasingCa²⁺.

2. Contraction:

• • Released Ca²⁺ binds totroponinon the thin (actin) filaments, shiftingtropomyosinto expose myosin-binding sites.
  • Myosin headsbind to actin, forming cross-bridges and generating force (sliding filament mechanism).

3. Relaxation:

• • The SR actively pumps Ca²⁺ back into its lumen usingATP-dependent Ca²⁺-ATPase (SERCA).
  • As Ca²⁺ levels drop, tropomyosin re-blocks actin, and the muscle relaxes.

Other Options Explained:

• Myosin filaments: These are motor proteins involved in contraction, not in calcium storage or release.
• Cellular cytoskeleton: Maintains cell shape and structure but plays no role in calcium ion regulation for contraction.
• Troponin complex: Binds calcium during contraction but does not store or release it.

Summary:

The sarcoplasmic reticulum acts as a calcium reservoir and regulator during the skeletal muscle contraction-relaxation cycle, making it essential for proper muscle function.

Clinical Relevance:

• Malignant hyperthermia:A life-threatening condition caused bymutant RyR receptorsthat leak excessive Ca²⁺, leading to uncontrolled muscle contractions and heat production.
• Muscle fatigue:Prolonged activity can deplete SR Ca²⁺ stores.

Gaps between Schwann cells wrapping the axon of a neuron.

Reasoning:

The nodes of Ranvier are critical structures in the nervous system that contribute to the rapid transmission of electrical impulses along myelinated neurons. These gaps are strategically located between Schwann cells in the peripheral nervous system or oligodendrocytes in the central nervous system, where the axon is not covered by myelin.

1. Structure of the Node:

• Each node of Ranvier is a small, unmyelinated segment between two adjacent myelinating cells (e.g., Schwann cells).
• These nodes contain a high density of voltage-gated sodium (Na⁺) channels, which are essential for regenerating the action potential.

2. Function:

• The myelin sheath insulates segments of the axon, but the nodes allow for saltatory conduction—a process where the electrical impulse jumps from one node to the next.
• This jumping dramatically increases the speed and efficiency of nerve signal transmission compared to unmyelinated fibers.

Clinical Relevance:

Damage to the myelin sheath or the nodes of Ranvier can impair nerve signal transmission, leading to neurological disorders such as:

• Multiple Sclerosis (MS): Immune-mediated damage to myelin and nodes disrupts nerve communication.
• Peripheral Neuropathies: Can involve demyelination affecting saltatory conduction and causing weakness or numbness.

Why the Other Options Are Incorrect:

• 1 (Degraded myelin): This describes pathological demyelination, such as in multiple sclerosis, not the normal function of nodes of Ranvier.
• 2 (Spaces between neurons): This refers to the synaptic cleft, not the axon structure.
• 3 (Sodium gates at axon terminals): Sodium channels are at the nodes, not specifically at the axon terminals, which are involved in neurotransmitter release.

Generate a hypothesis.

Reasoning:

Before beginning any experiment, a researcher must first formulate a hypothesis—a testable prediction or explanation based on prior knowledge or observations. This hypothesis guides the entire experimental design and helps determine what data will be collected.

1. Generating a Hypothesis:
   • Provides a clear focus and purpose for the research.
   • Helps define variables and expected outcomes.
2. Why Other Steps Come Later:
   • 1. Designing experimental procedures depends on the hypothesis to determine what methods are appropriate.
   • 2. Applying SI units is part of measurement but comes after the experiment is planned.
   • 4. Selecting laboratory equipment occurs once the procedures and measurements are decided.
3. Examples of Hypotheses:
   • Biology: "An increase in CO₂ concentration will enhance the growth rate of plants."
   • Chemistry: "Raising the temperature will speed up reaction X."

Steps in the Scientific Method

1. Observation
   Notice a phenomenon or pose a question based on curiosity or prior knowledge.
   Example: "Plants grow taller in sunlight than in shade."
2. Research Background Information
   Review existing studies and information to understand what is already known.
3. Formulate a Hypothesis
   Create a testable and falsifiable prediction about the relationship between variables.
   Format: "If [independent variable], then [dependent variable]."
   Example: "If plants receive more sunlight, then their growth rate will increase."
4. Design the Experiment
   • Identify variables:
     • Independent variable (what you change, e.g., sunlight exposure)
     • Dependent variable (what you measure, e.g., plant height)
     • Control variables (constants like water and soil type)
   • Plan methods to reduce bias, such as randomization or blinding.
5. Select Equipment and Materials
   Choose appropriate tools and ensure measurements follow SI units (e.g., meters, grams).
6. Conduct the Experiment
   Collect data carefully and consistently.
   Repeat trials to improve reliability.
7. Analyze Data
   Use statistical methods to evaluate whether the data supports the hypothesis.
   Visualize findings with graphs or tables.
8. Draw Conclusions
   Interpret the results relative to the hypothesis.
   Consider any limitations or errors.
9. Communicate Findings
   Share results through publications or presentations for peer review.
10. Iterate
    Refine the hypothesis or experimental design based on new insights or feedback.

A stem cell maturing to become a muscle cell that can contract.

Reasoning:

Cell differentiation is the biological process by which a less specialized cell (like a stem cell) becomes a more specialized cell type with a specific structure and function, such as a muscle cell, nerve cell, or blood cell.

1. What Is Cell Differentiation?
   • In multicellular organisms, stem cells give rise to different cell types during development or tissue repair.
   • Differentiation involves gene expression changes that lead to specialized structures and functions.
2. Why Option C Is Correct:
   • A stem cell becoming a muscle cell is a classic example of differentiation.
   • This transformation enables the cell to contract, a function unique to muscle cells.
3. Why Other Options Are Incorrect:
   • 1. Muscle cell producing more ATP is an example of cellular metabolism, not differentiation.
   • 2. A pancreatic cell releasing hormones reflects normal cell function, not a change in cell type.
   • 3. A mutation in a stomach cell is a genetic change, possibly harmful, but it is not differentiation.

Key Examples of Differentiation:

1. Embryonic Development:
   During early development, pluripotent stem cells (from the embryo) have the ability to become any cell type in the body. As development progresses, these stem cells differentiate into specialized cells such as:
   • Neurons: Specialized for transmitting electrical signals in the brain and nervous system.
   • Blood cells: Including red blood cells (which carry oxygen) and white blood cells (which fight infection).
   • Cardiomyocytes: Heart muscle cells that contract to pump blood.
2. Adult Tissues (Somatic Differentiation):
   In fully developed organisms, certain tissues still contain multipotent stem cells that can replenish specific cell types. A key example:
   • Hematopoietic Stem Cells (HSCs): Found in bone marrow, these stem cells differentiate into various blood cells, including:
     • Red blood cells (erythrocytes): Carry oxygen.
     • White blood cells (leukocytes): Defend against pathogens.
     • Platelets (thrombocytes): Help in blood clotting.

Skeletal muscle cells are highly active and require a large amount of energy to support continuous and powerful contractions. Mitochondria are the "powerhouses" of the cell, producing ATP (adenosine triphosphate) through cellular respiration, which fuels muscle activity.

Explanation:

• Mitochondria(4): Abundant in skeletal muscle cells to meet high energy demands, especially during exercise or repetitive movements. The more active the muscle, the more mitochondria it contains.
• Lysosomes (1): Help break down waste but are not especially concentrated in muscle tissue.
• Centrioles (2): Involved in cell division, which is not a primary function of mature skeletal muscle cells (they are typically multinucleated and non-dividing).
• Golgi Bodies (3): Package and modify proteins, important in general cell function but not uniquely enriched in muscle cells compared to mitochondria.

Clinical Insight:

Conditions like mitochondrial myopathies involve defective mitochondria and can lead to muscle weakness and fatigue, highlighting the importance of mitochondrial health in skeletal muscle function.

Exercise & Mitochondria

• Endurance training increases mitochondrial density, enhancing muscle efficiency.

Mitochondrial Diseases

• Mitochondrial defects can lead to muscle weakness, fatigue, and exercise intolerance (e.g., mitochondrial myopathy).

Implications for Patient Care

• Monitor fatigue levels in patients with mitochondrial disorders.
• Educate patients on the benefits of aerobic exercise to support mitochondrial health.

Fun Fact:

• Cardiac muscle contains even more mitochondria than skeletal muscle—because the heart never rests!

The Achilles tendon is a type of connective tissue. Tendons are strong, fibrous bands that connect skeletal muscles to bones. In this case, the Achilles tendon connects the gastrocnemius and soleus muscles in the calf to the calcaneus (heel bone). This tendon is essential for walking, running, jumping, and standing on your toes.

Explanation:

1. What is Connective Tissue?

• Connective tissue is one of the four main tissue types in the human body. It serves to bind, support, and protect other tissues and organs.
• Types of connective tissue include:
  • Tendons (connect muscle to bone)
  • Ligaments (connect bone to bone)
  • Cartilage
  • Bone
  • Adipose (fat) tissue
  • Blood (a fluid connective tissue)

2. The Achilles Tendon

• The Achilles tendon is the largest and strongest tendon in the human body.
• It transmits the force from the calf muscles to the heel, allowing the foot to push off the ground.
• Injuries to the Achilles tendon often occur during sports or intense physical activity and may range from inflammation (tendinitis) to complete rupture.

Why the Other Options Are Incorrect:

2. Muscle

• Muscle tissue contracts to produce movement, but the Achilles tendon is not muscle—it connects muscle to bone. Though the injury may affect how the muscle functions, the tendon itself is made of connective tissue, not muscle fibers.

3. Epithelial

• Epithelial tissue forms the outer layers of the body (like skin) and lines internal organs, cavities, and blood vessels. It does not form tendons or support structures like the Achilles tendon.

4. Nervous

• Nervous tissue includes the brain, spinal cord, and nerves. It is responsible for transmitting electrical signals and does not contribute to the structure of tendons. While nerves may be involved in the sensation of injury, they are not the primary tissue affected.

Clinical Note:

• Achilles tendon injuries are common in athletes and can severely limit mobility.
• Treatment may include rest, physical therapy, or surgery depending on severity.

Sebaceous

Reasoning: The sebaceous glands are specialized exocrine glands in the skin that secrete an oily substance called sebum. This sebum plays a vital role in lubricating and waterproofing both the hair and the skin, keeping them soft, flexible, and protected from drying out or cracking.

Location: Found all over the body, except the palms and soles, but aremost concentratedon the face and scalp.

Function: Producesebum, an oily substance that:

• Lubricates hair and skin to prevent dryness.
• Forms a protective barrier against microbes.
• Helps waterproof the skin.

Associated with hair follicles: Sebum is secreted into hair follicles, coating both the hair and skin surface.

Why the other options are wrong.

1. Sudoriferous glands→ Producesweat, not oil. Their primary function is thermoregulation, not lubrication. Includes:

• Eccrine glands(4): Widespread; secrete watery sweat for thermoregulation.
• Apocrine glands(3): Found in armpits/groin; secrete thicker sweat (odor-producing when broken down by bacteria). They release a thicker secretion during stress or hormonal changes but do not produce sebum.

3. Apocrine glands→ A type of sweat gland (not oil-producing).

4. Eccrine glands→ Produce sweat for cooling (no role in lubrication).

Clinical Relevance

• Acne: Caused by overactive sebaceous glands clogged with excess sebum and dead skin cells.
• Seborrheic dermatitis: Flaky skin (dandruff) due to inflammation of sebum-rich areas.

Yersinia pestis

Reasoning:

Yersinia pestis is the bacterium responsible for plague, including the bubonic plague. Its primary mode of transmission is through bites from fleas, particularly rat fleas (Xenopsylla cheopis) that have fed on infected rodents.

1. Pathogen Overview – Yersinia pestis:
   • Gram-negative bacterium.
   • Causes bubonic, septicemic, and pneumonic plague.
   • Historically associated with pandemics such as the Black Death.
2. Transmission Mechanism:
   • Fleas ingest the bacteria by biting infected rodents.
   • The bacteria multiply in the flea's gut, eventually blocking it.
   • When the flea bites a human, it regurgitates infected material into the bite wound.
   • Human infection then spreads from the bite site, typically to lymph nodes.

Why the Other Options Are Incorrect:

• 1. Corynebacterium diphtheriae
  • Causes diphtheria.
  • Transmitted via respiratory droplets, not fleas.
• 2. Neisseria meningitidis
  • Causes bacterial meningitis.
  • Spread by saliva and respiratory secretions.
• 3. Plasmodium falciparum
  • Causes the most severe form of malaria.
  • Transmitted by female Anopheles mosquitoes, not fleas or rats.