Goals for class: Explain structure of organelles in the endomembrane system.
Detail functions of Golgi complex, endoplasmic reticulum, and nuclear membrane.
Discuss evolutionary endosymbiosis and its impact on mitochondria and chloroplasts.
Activity: List organelles in an animal eukaryotic cell within 2 minutes.
Still no responses received; monitoring conducted for live input presentation.
Highlight of intracellular membranes:
Rough endoplasmic reticulum (with ribosomes).
Smooth endoplasmic reticulum.
Role of lysosomes, nucleus, peroxisome, Golgi apparatus, and mitochondria.
Main components:
Outer nuclear membrane, rough/smooth ER, Golgi apparatus, lysosomes, and peroxisomes.
Outer nuclear membrane discussed next.
Rough ER: protein synthesis direction.
Smooth ER: synthesis of lipids.
Golgi apparatus: protein distribution.
Lysosomes (with enzymes) and peroxisomes.
Nucleus holds DNA and proteins.
Nucleolus involved in ribosome assembly.
Nuclear membrane controls transport through nuclear pores.
Distinct features:
Possess bacterial genomes and ribosomes.
Originated through endosymbiosis.
Mitochondria: convert food energy to ATP.
Chloroplasts: convert sunlight and CO2 into ATP, organic molecules.
Similarities: both have their own DNA and ribosomes.
Mitochondria: ATP production focus.
Chloroplasts: photosynthesis role.
Correct sequence identified:
Rough ER ➜ Golgi complex ➜ vesicle ➜ cell membrane.
Reconfirmation of the correct path for secreted proteins.
Composition: Many microtubules enveloped by membranes.
Differ from bacterial structures.
Endomembrane system includes key structures interconnected through membranes.
Responsible for protein synthesis and distribution.
Endosymbiosis led to the formation of mitochondria and chloroplasts.
Focus on transport processes in eukaryotic cells.
Understand endocytosis and phagocytosis mechanisms.
Explain how pathogens exploit these processes.
Two primary modes:
Endocytosis: for particles binding to cell receptors.
Phagocytosis: engulfment of large particles/organisms.
Pinocytosis: uptake of liquids.
Receptor-mediated endocytosis: cells bind specific materials.
Phagocytosis: engulfment of pathogens.
Macrophages can become infected by phagocytosis (e.g., Salmonella).
Definition process where vesicles fuse with the cell membrane, releasing contents.
Identify process where vesicles release contents outside the cell: Exocytosis.
Time allocated for a quick break.
Summary of today's topics for clarity and review.
Understand causative agents, symptoms, treatment, and prevention strategies for malaria.
Malaria as a systemic infection spreading from a localized area throughout the body.
Involves lymphatic and cardiovascular systems.
2023 statistics: ~74% of malaria deaths were in African children under 5.
Global overview of malaria cases and mortality.
Resulting from four species of Plasmodium.
P. falciparum: deadliest variant.
Other species: P. vivax, P. ovale, and P. malariae.
Complexity of life cycle stated.
Classical symptoms: shaking chills, high fever, and sweating; cyclic patterns.
Flu-like symptoms commonly observed.
Stages of Plasmodium development: mosquito bite ➜ liver infiltration ➜ red blood cell lysis.
Awareness and prevention measures highlighted: bite prevention, diagnosis, and controlling mosquitoes.
Methods include mosquito avoidance, chemoprophylaxis, and limiting transmission.
Two vaccines approved since 2021:
RTS,S/AS01: low efficacy but reduces severity.
R21/Matrix-M: higher efficacy noted.
Treatment options: chloroquine, artemisinins, doxycycline.
Importance of failure in treatment to severe malaria.
Malaria is caused by the Plasmodium species, spread via Anopheles mosquito (vector).
Clarification about the causative agents of malaria regarding vector roles.
Sickle cell trait confers protection against Plasmodium infection severity.
Emphasis on preventability and treatability if diagnosed and treated promptly.
Consolidation of lecture content.
Focus on fungal infections: causes, signs, treatment, and prevention.
Includes molds and yeasts, with specific adaptations to human skin.
Clinical manifestations outlined.
Candida species’ role in human flora and potential for infection in various regions.
Risk in immunocompromised patients with severe outcomes possible.
Antifungal medications, hygiene tips, and hospital environment considerations.
Emerging threat from C. auris, details on its drug resistance and importance in healthcare settings.
Case study demonstrating symptoms indicative of Candida albicans.
Examination and identification of likely causative agent for specified symptoms.
General benign nature in healthy individuals but severe in immunocompromised.
Emergence of drug-resistant fungal diseases.
Reminder for quiz and teammate survey deadlines for upcoming dates.