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Genetics

Neuroscience

Cellular & Molecular Biology

Anatomy & Physiology

Evolution & Ecology

Biotechnology

Biochemistry & Biophysics

Molecular Biology

Level: Introductory

Autophagy

Eileen Li


What is Autophagy?


Autophagy is the process of recycling and degrading cells, in which cells dispose of misfolded, aggregated proteins and old or dysfunctional organelles. Often likened to a cell’s recycling “trash chute”, autophagy plays a crucial role in maintaining homeostasis by keeping the cell healthy and clean.


There are three types of autophagy: microautophagy, chaperone-mediated autophagy, and macroautophagy. Of these, macroautophagy is the most extensively studied. It’s been found that macroautophagy is maintained at a low level during normal cellular activity, but can be activated by stressful conditions. 


A Brief History of Autophagy


The concept of autophagy first emerged in the 1960’s, but its detailed mechanisms were not known until Yoshinori Ohsumi, a Japanese researcher, demonstrated the mechanism of autophagy in yeasts, and then later again in humans.


Yoshinori Ohsumi also identified specific genes related to autophagy, which are classified as ATGs (autophagy-related genes). These genes contain code for ATG proteins– specific proteins that are necessary for the formation of the autophagosome; these proteins play a crucial role in the molecular mechanisms of autophagy.

The basic molecular mechanism of autophagy can be described in five steps: 



During initiation, a phagophore is formed at an omegasome, a structure associated with the endoplasmic reticulum. The process of initiation starts with a set of proteins, called the ULK1 Complex (Figure 1), which form a preautophagosome (PAS for short). 


The ULK1 complex then activates the PI3K Complex, which results in nucleation (step 2) and the formation of the phagophore. The phagophore is a cup shaped membrane structure. Although it is currently unclear where this double-membrane of the phagophore originates from, research has suggested that the plasma membrane, endoplasmic reticulum, golgi complex, or mitochondria may be the original source. 


During the process of elongation and maturation, another set of proteins that are classified as ubiquitin-like conjugation systems are activated. The reaction of the lipid in phosphatidylethanolamine (PE) and microtubule-associated protein light chain 3 (LC3) causes the elongation of the phagophore and fusion to a lysosome. An autophagolysosome is formed.


During this stage, some intracellular contents become trapped in this vesicle. Through selective autophagy, these intracellular contents can be selectively trapped. Once the autophagosome is formed, a nearby lysosome and the autophagosome fuse. Thus, the intracellular contents of the autophagosome become engulfed by the lysosome. Finally, cellular degradation occurs. 

Genetics

Level: Introductory

Chromosomal Abnormalities

Rithika Vutukuri


Chromosomal abnormalities are irregularities within an individual’s chromosomes that can lead to various genetic conditions. These abnormalities can be categorized into two groups: numerical abnormalities and structural abnormalities. Numerical abnormalities occur when an individual is missing a chromosome from a pair or has a pair with more than two chromosomes. Normally, chromosomes come in 23 pairs within an individual’s cells. However, if someone has a chromosomal abnormality, they may not have the standard number of chromosomes. If the chromosome count is normal but there is still an abnormality, it is likely due to a structural abnormality. Structural abnormalities occur when there is an alteration in the chromosome's structure, with common types including deletions, duplications, inversions, and translocations. Deletions involve the removal or absence of a portion of a chromosome. Duplications occur when a segment of a chromosome is repeated. An inversion happens when a part of a chromosome breaks off and reattaches upside down. Translocations occur when a segment of a chromosome breaks off and attaches to another chromosome.


The effects of chromosomal abnormalities vary depending on the type of abnormality and its location on the chromosome. These effects can include diseases, growth issues, developmental problems, birth complications, and syndromes such as Down Syndrome and Turner Syndrome.


Chromosomal abnormalities often result from errors in cell division, which can occur during mitosis or meiosis. During these processes, cells divide to form two new cells, necessitating DNA replication. Errors during this replication can lead to chromosomal abnormalities, which may be detected or remain unnoticed, ultimately determining their presence in an individual and in newborns.

Neuroscience

Level: Introductory

Glial Cells

Jaycee Yang

While neurons, the primary message transmitters of the nervous system, often get the spotlight when thinking about brain cells, up to 90% of brain cells are actually glial cells, which play essential but underappreciated roles in supporting brain function. The role of glial cells is to help regulate the environment of the brain for neural activities in various different ways. Many different kinds of glial cells, including astrocytes, Schwann cells, ependymal cells, oligodendrocytes, satellite cells, and microglial cells, contribute to maintaining the brain’s environment in various ways, which we will explore now.

Astrocytes: 

Astrocytes have several functions, such as delivering nutrients to neurons and removing waste products, as well as helping to repair damaged or scarred nerve cells in the central nervous system. Beyond these, astrocytes regulate and control the extracellular environments. Recent research has also suggested that astrocytes play a role in memory within the hippocampus, indicating that their effects on brain function extend beyond just maintaining the environment. 

Ependymal cells:

Ependymal cells line the brain's fluid spaces (ventricles) and help produce cerebrospinal fluid while forming a barrier between these fluid spaces and the cells. Their cilia, hair-like organelles facing the cavity of the ventricles, time their movement to direct cerebrospinal fluid and are also able to influence the distribution of neurotransmitters to neurons. 

Some ependymal cells can divide and form neurons throughout the lifespan of a cell, allowing neuro-regeneration to occur. These cells also provide an environment that protects axon stumps from degeneration after damage, fostering the growth of alternate neuronal connections and restored function. Essentially, this allows the brain to replenish a portion of dead neurons with them.

Microglial cells:

Microglia make up the main active immune defense in the central nervous system. As a type of macrophage (which is a kind of white blood cell) exclusive to this system, their primary role is to respond to injuries and infectious agents, protecting neurons by preventing build-up of toxic waste substances. Microglia cells have also been found to play a role in multiple sclerosis, a neurodegenerative disease where the immune system malfunctions and attacks its own tissues.

Oligodendrocytes:

Oligodendrocytes are a type of glial cell in the central nervous system that produce an insulation layer called myelin sheath on the neuron's axons. Myelin helps increase the speed of electrical signaling in neurons.

Schwann cells (PNS):

Schwann cells perform the same function of Oligodendrocytes, also producing myelin sheath. However, Schwann cells are found in the peripheral nervous system. 

Satellite cells (PNS):

Satellite cells reside on neuron cell bodies in the peripheral nervous system to protect them and maintain their chemical environment.

Neuroscience

Level: Intermediate

Neurodegenerative Disorders: Parkinson's: 

Jaycee Yang - Edited by Tess Chan

Parkinson's disease is a progressive neurological disorder. In the beginning, symptoms are mild and quite unnoticeable, but later, people can develop symptoms that include stiffness, slowness, tremors, and overall impaired balance and coordination. However, keep in mind that everyone has a different biological makeup, so some people may have symptoms that others don’t. There is currently no cure for this neurodegenerative disorder, although there are some medical treatments for it. 

This disorder affects the basal ganglia, a structure in the brain critical for fine movement control. It specifically affects the substantia nigra, one of the 4 nuclei (collections of neurons) in the basal ganglia. They mainly communicate through the neurotransmitter, dopamine. Due to 70% -80% loss of dopaminergic neurons in the substantia nigra, other areas in the basal ganglia become overactive. This is due to the loss of these neurotransmitters, which results in dysfunction in the basal ganglia circuitry; this in turn disrupts the communication and coordination between the basal ganglia and the motor cortex, leading to impaired motor control. 

The neurons in the Locus coeruleus nucleus located in the pons are also affected. The Locus coeruleus is where the neurotransmitter/hormone: norepinephrine is made. Norepinephrine is involved with stress and panic responses; it is a part of the sympathetic nervous system responsible for reactive involuntary responses (these cause the body to involuntarily react instead of relaxing). The loss of norepinephrine explains some of Parkinson's symptoms such as fatigue, irregular blood pressure, and decreased movement of food through the digestive system.

Parkinson's can also cause cellular death. It can be caused by external factors and is hard to predetermine and treat. Parkinson’s can be genetic or caused by external factors. In Parkinson’s, many neurons in the substantia nigra contain Lewy bodies. They are unusual clumps of protein alpha-synuclein, and they transmit between neurons and spread throughout the brain. 

Neuroscience

Level: Intermediate

Neurodegenerative Disorders: Alzheimer's: 

Jaycee Yang - Edited by Tess Chan

Alzheimer's disease (AD) is a common type of dementia involving the loss of cognitive function. It is a fatal progressive neurodegenerative disorder because there is currently no cure. Contrary to popular belief, AD is not a disease of old age, and no one is immune. There are different stages of AD that can develop over the course of 8-10 years.  At first, patients may only experience short-term memory impairment; however, this can later impair long-term memory, and eventually the part of the brain that regulates heartbeat is destroyed. At the most severe stages, Alzheimer's patients completely depend on others to perform basic everyday tasks. 

Brain atrophy (shrinkage of the brain tissue) occurs in Alzheimer's due to 2 abnormal protein fragments, namely amyloid plaques and Neurofibrillary tangles, spreading around the brain and causing cell death. These begin to accumulate in the hippocampus and the entorhinal cortex, which are areas essential for memory formation.

The Amyloid precursor protein (APP) is a large membrane essential for neural growth and repair. However, APP can be mutated. As it is changed through enzymatic processes, it can become beta-amyloid 42, which is toxic to the brain because it can't be broken down naturally. Beta-amyloid 42 accumulates between neurons and disrupts cell function. This causes abnormal glucose regulation which leads to cortical shrinkage. Some recent research done about Alzheimer’s shows that a non-invasive eye exam can detect excess amounts of this amyloid protein in the retina.  

Neurofibrillary Tangles are abnormal accumulations of Tau protein as it collects inside neurons. Tau proteins help stabilize neurons, but in AD, abnormal chemical changes cause Tau proteins to detach from microtubules and stick to each other, forming threads that tangle inside neurons. These blockages harm synaptic communication by preventing the delivery of nutrients.

Chronic inflammation in AD is caused by a build-up of glial cells. The normal TREM2 gene usually triggers microglia (a type of supporting brain cell) to clear up the beta-amyloid plaques. Due to a mutation, this function is impaired and causes the build-up of plaques. The function of astrocytes is also compromised by plagues. The function of glial cells is also impaired, but they still release chemicals due to the innate immune response, which causes inflammation. Chronic inflammation can lead to neural decay.

The build-up of beta-amyloid deposits in brain arteries (atherosclerosis) and mini-strokes can lead to the reduction of blood flow and oxygen to the brain. This causes the breakdown of the blood-brain barrier. 

Microbiology

Level: Introductory

A Simple Introduction to the Life Cycle of a Virus

Rithika Vutukuri - Edited by Dominic Gulaya

Although viruses are not classified as living, it is important to understand the life cycle of a virus in order to create techniques for the prevention of infections. The first part of the cycle is the virus’s entry, in which the virus enters a host cell. In order to gain entry, the virus utilizes various mechanisms to attach to specific receptors on the host cell’s surface. This is often done through endocytosis, the fusion of the virus with the cell membrane. Once inside the host cell, the virus releases its genetic material and becomes available for replication. This step is called uncoating. Then, the genetic material enters the nucleus and takes control of the host cell’s mechanisms. With this new power, it can now use the mechanisms of various organelles to direct the cell to replicate its genetic material and form new virus particles. These virus particles are assembled within the host cell and then released to infect other cells, continuing the cycle of infection and replication. In order to combat the virus, the host organism mounts a defense response against the infection. This often involves the activation of the immune system, which attempts to eliminate the virus and infected cells.


Immunology

Level: Intermediate

Killer T cells and Regulatory T cells

Taili Gao

Killer T cells induce apoptosis of infected host cells by releasing granzymes and perforin. Granzymes activate caspases, which leads to DNA destruction. Because of the destructive abilities of killer T cells, they also produce FAS, a surface receptor. A few days after their activation, killer T cells will also produce FAS ligand, which binds to FAS and promotes the apoptosis of killer T cells. Killer T cells are also inhibited through other means, such as by regulatory T cells. Deficiency in regulatory T cells causes autoimmune diseases and allergies. The activation of the FOXP3 gene is important for the development and maintenance of regulatory T cells. Perforin functions similarly to the membrane attack complex induced by the complement system. 

Immunology

Level: Introductory

Introduction to Leukocytes

Taili Gao

Leukocytes, or white blood cells, include neutrophils, eosinophils, basophils, lymphocytes, and monocytes. The first three cell types are known as granulocytes, characterized by having granules when observed under the microscope. Lymphocytes include B cells and T cells. At a site of infection, neutrophils are the first to arrive, followed by monocytes and T cells. Monocytes can differentiate into macrophages and dendritic cells. Dendritic cells are the main antigen-presenting cells in the body. The other antigen-presenting cells are macrophages and B cells. Antigen-presenting cells have class II MHC showcasing bits of the infectious agent to activate helper T cells. Helper T cells can then activate cytotoxic or killer T cells and stimulate B cells to turn into antibody-releasing plasma cells. Plasma cells have extensive rough endoplasmic reticulum for the production of antibodies. There are five classes of antibodies or immunoglobulins: IgG, IgA, IgE, IgM, and IgD (listed in decreasing abundance). Helper T cells are central players in the immune system. In HIV, the virus uses reverse transcriptase to integrate its genome into those of helper T cells. By infecting helper T cells, HIV increases the risk for developing AIDS. Antiretroviral therapy (ART) can treat HIV, especially early on in the infection. ART uses two reverse transcriptase inhibitors and a protease (needed to assemble the viral coat) inhibitor. 

Cell Biology

Level: Introductory

Cells: The Building Blocks of Life

Rithika Vutukuri - Edited by Tess Chan

Types of cells

There are three domains of life: Archaea, Bacteria, and Eukarya. The first two domains consist of prokaryotic cells, and the last domain consists of eukaryotic cells. The main difference between prokaryotic and eukaryotic cells is that prokaryotic cells lack membrane-bound organelles. For instance, prokaryotic cells do not have a nuclear envelope (the membrane that separates the nucleus from the cytoplasm), endoplasmic reticulum, or Golgi apparatus; some other examples of membrane-bound organelles are the mitochondria and chloroplast. On the other hand, eukaryotic cells, which are found in plants and animals, contain membrane-bound organelles and are more complex than prokaryotic cells. Despite their differences, all cells consist of a cell membrane, cytoplasm, and ribosomes.

What Cells Do

Cells play a vital role in the functioning of organisms. Cells can perform a wide range of functions from simply dividing to regulating metabolism. Many cells work together in humans to carry out metabolism, growth, and reproduction. Additionally, cells can also communicate with each other through chemical signals, allowing them to coordinate and respond to changes in their environment. Without cells, organisms wouldn’t be able to adapt to changes or survive.

Cells are the foundation of life. Although they are small, cells are a key component of our daily activities and support the functions of all life. 

Neuroscience

Level: Introductory

Action Potential

Taili Gao

Electrical signals are transported in neurons through action potentials. On the cell membrane, potassium (K+) and sodium (Na+) channels grant these ions entry into the cell. A higher concentration of K+ is found inside the cell than outside, whereas a higher concentration of Na+ exists outside the cell. K+ channels can be gated or leakage channels. Leakage channels are always open, allowing the passive transport of K+ out of the cell. On the other hand, Na+ channels are all gated. Gated channels usually open in response to a stimulus when the membrane potential reaches its threshold or a certain voltage. When the threshold is reached, gated Na+ channels open, allowing Na+ into the cell, rapidly depolarizing or increasing the membrane potential. Depolarization is followed by repolarization, where gated K+ channels open. The flow of K+ channels out of the cell decreases the membrane potential and causes repolarization, where the membrane potential is brought back to normal. The gated Na+ channels are inactivated, and the gated K+ channels cause an overshoot or hyperpolarization, where the membrane potential is lower than the resting state (-70mV in a neuron). 

Local anesthetics such as cocaine, procaine, and lidocaine function by reversibly binding to Na+ channels in the axon membrane, preventing the opening of these channels to create depolarization and thus inhibiting sensory neurons to propagate action potentials. Local anesthetics also often contain epinephrine or other vasopressors to counter the effects of vasodilation (the dilation of blood vessels) these drugs (except for cocaine) bring. Vasodilation limits the duration of the anesthetics. 

Biochemistry

Level: Introductory

Amino Acids

Taili Gao

Amino acids make up proteins. All amino acids have an amine and a carboxyl functional group. There are twenty amino acids, nine of which are essential. Essential amino acids cannot be produced within the body and must be obtained through our diet. These amino acids are tryptophan, isoleucine, leucine, threonine, phenylalanine, methionine, valine, lysine, and histidine (in children). 

Practice Problem:

The answer is B. Essential amino acids cannot be synthesized in the body!