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146 Cards in this Set
- Front
- Back
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One mole of glucose produces how many moles of ATP?
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38
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Plants get their energy from sunlight and animals get energy from?
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Food (directly and indirectly from plants) in form of carbs, fat and protein
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Proton and voltage gradients established across the inner mitochondria space are established by what initially?
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From glucose, well at least indirectly. Glycolysis will happen in the cytoplasm and make 2 ATP, 2 NADH and 2 pyruvate. Pyruvate will then go into the CAC and make FADH2 and NADH which will then make the voltage and proton gradient in the inner membrane space via ETC.
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Why is glucose not considered a essential nutrient?
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This is because glucose can be made from amino acids and lactate acid (gluconeogenesis) in the liver
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Where is the respiratory electron chain and ATP synthase located?
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The inner membrane space of the mitochondria
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Where is the proton gradient established in the mitochondria?
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In the intermembrane space
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Where is the F1 and Fo subunits located within the mitochondria?
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The F1 is in the mito matrix
The Fo is in the mito membrane |
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In the respiratory chain complex, which complexes create the pH gradint and using what substrates that where generated during the CAC?
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I,III, IV
Succinate, FADH2 and NADH in the CAC |
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blank
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bllank
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Glucose isn't an essential nutrient but it is tightly regulated, what part of the body truly needs glucose?
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Brain
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Is ATP synthase reversible?
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Yes
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In mitochondria and chloroplasts, the synthesis of ATP is done using proton gradients. What is used in bacteria?
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Sodium
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Where does Glycolysis take place?
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Glycolysis takes place in the cytoplasm
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Where does the CAC occur?
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It occurs in the mitochondria
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The CAC indirectly makes 38 moles of ATP, what substances created from the CAC allow for this happen?
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6 moles of NADH and 2 moles of FADH2
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How many protons are needed to make one ATP in the ATP synthase?
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4
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Describe the mechanism needed to get the ATP synthase to rotate?
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The Fo subunit in the membrae has 12 c subunits
Protons will escape through the channels in the Fo subunit This will cause the F1 subunit to rotate The F1 subunit will rotate 120 degress and cause the rotor to rotate 120 degrees The rotor will then cause the ATP synthase to rotate 120 degrees *Remember it takes 4 protons to pass through the Fo subunit in order to get a rotation |
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Where are the VoVi-ATPase's found?
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They are found in vacuoles where ATP is hydrolyzed to generate H+ gradiens.
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Briefly describe the ATP synthase and how it changes conformations when making ATP?
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ATP is first attached to the ATP synthase in order to prime the protein.
-Without ATP here, ADP can't bind ADP will then bind to protein and ATP is relased -Open ADP will then join with Pi and form ATP -Loose ATP is now closely bound to protein -Tight state |
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What are the products of glycolysis?
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2 moles of ATP, PYRUVATE AND NADH
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Pyruvate is converted to CO2 and water in the CAC, what are the products of CAC?
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6 NADH and 2 FADH2
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How many moles of ATP are produced from the CAC?
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38
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The ETC uses 8 NADH and 2 FADH2, 6 NADH come from the CAC, where do the other two come from?
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2 from glycolysis.
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Briefly describes what happens in complex I,III, IV of the ETC?
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I
-NADH is reduced to NAD --Makes two protons III -Electrons from I allow for a proton escape IV -Use protons and 1/2 OXYGEN to make water |
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Molecules from the cytoplasm can pass the outer membrane and go into the intermembrane space via the _________. This aqueous channel is beta barrel in structure, as opposed to alpha helix.
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Porins
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After an ADP has passed through the porin, how can the ADP pass the inner membrane?
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It passes through the inner membrane via the ADP/ATP antiporter.
ATP will come out and ADP will come in. |
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The ADP/ATP transporters proteins arrise from the _____ not the _______ genome
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Nuclear
Mitochondrial |
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What makes cyanide so deadily?
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It inhibits the ETC so it will eliminate the proton gradient from being formed
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What can an uncoupler do?
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This will allow for protons to escape and not have to go through ATP Synthase
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If you are making ATP in mitochondira but ADP/ATP exchanger is not functional what is the problem?
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Can't make any more ATP
AND ATP is not leaving the mitochondria |
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Why is it advised to take antioxidants (Vitamin E and D)?
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Because they want the antioxidant to bind with SOD.
SOD is a superoxide anion created as a side product from the ETC making a proton gradient. Too much leakage from ETC will damage the mitochondria membrane. Damage membrane, will let proton gradient run down, and without making ATP will cause the cell to ultimately die. |
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What is ataxia?
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lose ability to coordinate muscular movement
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UCP1 in brown fat mitochondria allows for ATP to uncouple and release heat. What triggers this?
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This is activated by cold induced release of fatty acids from triglycerides.
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What is homeostasis?
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The coordinated physiological process which maintains most steady states of the organism.
Simply keeping things in balance. |
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Infectious agents such as bacteria lead to cell injury, but what is usually the cause of this injury?
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The hosts response to the bacteria.
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What determines the cell response to cell injury?
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Dose
Duration Cell type -Some cells are more susceptible to oxygen deprivation Nature of injurious agent Cell defense status |
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What kind of cell death requires ATP, is involved in single cells, there is little release of cell contents, no loss of membrane integrity and little inflammation?
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Apoptosis
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What kind of cell death is passive, requires no ATP, results in large inflammation, release of cell contents, often occurs in many adjacent cells and there is disruption of organelles?
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Necrosis
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What are the three initiators of necrosis?
All deal with the loss of ATP |
Ischemia
Membrane damaging agents Mitochondiral poisons |
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Why is the loss of ATP bad for the cell (the steps in necrosis that lead to cell death)?
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Loss of ATP
No Na-K ATPase Lead to intracellular ion accumulation Uptake of water Cell swelling and then death. |
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What are the three cell states that exist in the body?..relating to dividing
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The cells are either always dividing
Cells that divided and will never divide again-such as platelets "Resting" cells that aren't dividing but can be stimulated to begin dividing again in response to a proper stimulus. -Cut a piece of liver, causes liver to go through several cell cycles and replace the piece of the liver |
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What two things must occur in cell division?
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They must accurately replicate all of its DNA, ONCE AND ONLY ONCE
Cell must divide DNA equally between two sibling cells. |
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What are some examples of cells that won't divide again?
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Muscle cells
Platelets Neurons in brain |
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Most cells are growing on a solid support surface because of what?
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Microtubles of the cell form a lattice with the basal portion to adhere to the surface bellow it
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Why is it easy to pick out mitotic cells?
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When the microtubules depolymerize and forms this spindle the cells rounds up and is able to be seen. You can pick out the mitotic cells.
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When cell wants to divide (mitosis), the network of _________depolymerize and form individual _______molecules and then reassemble to form the ______ that separates the chromosomes to the two poles of the cell that is going to divide
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microtubules
tubulin spindle |
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What new discovery allowed people to start evaluating interphase?
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The use of radioactive DNA
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What does this experiment show?
A bunch of tissue culture cells From same original cell Growing on a dish Have a few mitotic cells (rounded up) Other cells are in interphase(flat) We will use radioactivated tritiated thymidine (specific label for DNA) Give cells the radioactivated tritiated thymidine Wash out the radioactivated tritiated thymidine Do with Autoradiograph immediately The Results: Some interphase cells have radioactivated thymidine and some do not Mitotic cells do not have the tymidine incorporated. |
Mitotic cells don't replicate DNA
Of course there is no synthesis in mitosis Some interphase cells are replicating DNA |
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What is shown in this expereiment:
Do again with same setup of cells as experiment #1 Pulse with radioactivated tritiated thymidine for 30 minutes Wash out Then add colchicine, (prevent microtubule polymerization) Prevents the microtubules resembling and forming the spindle Cells will then be arrested in the mitotic phase (can't finish mitosis) But they can go through interphase At intervals, to autoradiograph and count The increasing number of mitotic cells The number of radiolabeled mitotic cells Cells that are treated with colchicine for longer than one cell cycle, most of them will have the colchine Results (1)In beg. no mitotic cells with radioactivated tymidine (2)Then will see some mitotic cells with radioactivate tymidine (3)Then will see no increase in mitotic cells with radioactivated tymidine. |
1st-G2
2nd-S 3rd-G1 |
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How much chromosome is in G1,S,G2 and M?
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G1-2n
S-4n G2-4n M- two cells and 2n |
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What is the mechanism for the flow microflourimter?
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Reservoir in which suspension of cells
Pumped through nozzle that vibrates Number of cells in suspension is setup, so when nozzel vibrates, in each drop will be one cell or no cells Take cells and give dye that intercalates DNA in a stoichmetry way Light on it Light that is emitted, is proportional to dye and the dye is proportional to the amount of DNA. |
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What is the flow microflourimeter used for?
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To check the amount of DNA in an individual cell
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Is more light emitted in the flow microflourimeter in cells that are in G1 or cells that are in G2?
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More light is emitted in cells that are in G2 since there is more DNA
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What is a mitogen?
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Mitogens are agents that stimulate Go cells to enter G1 and progress around the cycle.
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How can we determine when histone synthesis occurs?
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Take a cDNA probe for histone and then tag with p32
Then see where histone message present Only place you will see is where cells synthesize DNA |
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Where are histones synthesized?
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In the S phase
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Histones are phosphrylated more in what part of the cell cycle?
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More at the end of G2 and histone phosphorylation is then removed by a histone phosphatase
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Histone kinase happens in what?
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G2
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Where does the cell make the decision whether it will divide or not?
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At the restriction boundary protein
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What is double thymidine block used for in clinical settings?
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Utilized tool in cellular biology that allows you to synchronize your cells, remember the tick experiments.
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Describe what happens between RBP, ECF and G1/S transition?
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Restriction boundary protein
---At this point certain genes are necessary in preparing cell to go through the G1/S transition. Their transcription factors (such as ECF) which when bound to the repressor (restriction boundary protein) prevent this from happening. Once RB is phosphorylated, transcription can now occur After cell cycle and returning back to G1(AFTER A CELL CYCLE), the RB must then be dephosphorylated to allow for this decision to be made again. |
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What are two ways to synchronize cells?
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Shaking cells in bottle and the mitotic cells will pop off (these cells haven't got the lattice of microtubules) or just blowing off(with tools) from a plate
Since mitotic cells only occupy 2-3% of cell cycle you have cells that are tightly synchronized at a specific point Can then replate these cells -Disadvantae only have a small number of cells or Using DNA synthesis inhibitors (use elevated levels of thymidine which gives negative feedback in synthesis of cytosine--the double thymidine block) |
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Describe what was learned from the chicken s phase cells and human G1 phase cells?
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S/G1 fusions suggest that S phase cells contain an activator that can initiate DNA synthesis in G1 cells.
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Describe what was learned from the human g1 phase cells and human G2 phase cells?
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G2/G1 fusions suggest no S-phase activator is present in G2 phase cells.
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Describe what was learned from the chicken s phase cells and human G2 phase cells?
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G2/S fusions suggest that G2 DNA (replicated DNA) does not respond to the S-phase activator.
G2 phase won't go into mitosis until the S phase is going into mitosis too |
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Describe what was learned from the mitotic cells and any cell that its in interphase cells?
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No matter where you are in interphase, the interphase cells will stop what they are doing and try to compact their chromosome. Premature chromosome condensation
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What causes Premature chromosome condensation?
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The M-Phase promoting factor
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What is asked at the G1/Go checkpoint?
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Is environment favorable for initiation of DNA replication
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What is asked at the S phase checkpoint?
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Is the DNA damaged and can the damage be repaired
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What is asked at the G2/M checkpoint?
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Is all DNA replicated and is environment favorable for mitosis
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What is the factor called that prevents G2 phase cells from re-replicating despite being close to a S phase cell?
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The "licensing" factor
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What does the size of the buds in budding yeast tell you about the cell?
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It tells you where the cells are in progress through the cell cycle
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What is a cdc?
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This means cell cyclic dependent function, A gene that for example lets cell move past the G1/S transition point.
Genes that are necessary for cell cycle specific points |
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What is a temperature sensitive mutation?
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a mutation in a gene that causes a change in the amino acid sequence that results in the mutant protein remaining stable at the “permissive” temperature, but which is unstable, inactive and degraded at the “non-permissive” temperature.
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What was found from the experiments involving yeast cells and human cells with CDC2 genes?
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A cdc-2 gene from humans was cloned, in one step, by correcting the temp sensitive defect in the yeast Cdc-2 gene. The human gene works from yeast to mankind.
Shows how conserved genes are. |
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What is the product of the cdc-2 gene?
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Protein kinase (p34 cdc2)
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What activates the CDC2 kinase?
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The joining of cyclin;
The protein cyclin is increased as we go through G2/M |
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What phosphorylates histones as we go from G2 to M?
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CDC(P34)
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What is the M-Phase factor?
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(cdc) and cyclin
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When is histone activity the greatest?
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At the end of G2
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What three ways to regulate cdc2 gene?
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The phosphorylation of cdc-2's active site (reversible)
The amount of cyclin (irreversible) CK1 inhibitor binding to the cyclin-cdc complex |
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What is used for degredation of cyclins?
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Ubiquitation
There are cyclin specific ubiquitin ligases -Transfer cyclins to the ubiquitones -Ubiquitons take cyclin to proteosome for degreadtion |
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Doe humans have one catalytic subunit and multiple cyclins?
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No we have different catalytic subunits and multiple cyclins
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What phosphorylates the RB protein, so the cell can enter the s phase?
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CDK-G1 cyclin complex
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What can ischemia cause to the cell?
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The cell may undergo cell death(Necrosis), because in ischemia, there will be a reduction in Oxygen, then a reduction in ATP. This will also cause an increase in calcium within the cell, causing several problems to occur.
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What two points in necrosis is when cell death is irreversible?
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This is when the mitochondria is permeable because there is a transition pore formed.
When the lysosomes start degrading cell constituents. |
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The cell stressor hypoxia can lead to what in the cell?
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Cell swelling
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In what clinical setting is necrosis used?
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Can assess the extent of cell injury by measuring the amount of released ITC proteins in the blood
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What is the general pathway for apoptosis?
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Capcases are activated by the intrinsic(mito) and extrinisic(death receptor) pathway
The cell is broken up by executioner capcases The broken up cell is then phagocytosed by a phagocyte |
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What happens in the apoptotic extrinsic pathway?
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Killer lymphocyes with Fas ligand will bind to the Fas death receptor on the cell.
This binding will act as a site for the initiation complex of caspase. |
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What is the general format in the intrinsic pathway of apoptosis?
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There are three families of the BCL2 protein (regulator, effector and sensor).
The sensor will bind to the effector and cause the pore to be formed on the mitochondria outer membrane. This leads to the cytochrome c leaking out of the mitochondria and then form the apoptosome complex. This will then start the cleavage cascade for caspase. However, the regulators inhibit this from happening. So the sensors must displace the regulators. |
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In the terminal stages of apoptosis the caspases are performing several functions, such as:
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Breaking up cytosolic proteins-without these proteins the cell can be broken up into little pieces
Cleavage of nuclear lamin Activated endonucleases(DNA fragmentation) Transglutaminase- protein cross-linking (things that don't usually stick together start sticking together) |
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What are some morphological features of an apoptotic cell?
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The cell shrinks
The cytoplasmic has blebs The chromatin condeses |
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What is one way a phagocyte recognizes an apoptotic cell?
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The apoptotic cell has increased Phosphatidylserine exposure and the phagocyte will recognize this apoptotic cell via beta integrins.
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Why is there no inflammation seen in apoptosis?
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Apoptotic cells keep an intact membrane
Apoptotic cells don't release cytokines Apoptotic cells are rapidly cleared Engagement of receptors by apoptic cells cause them to secrete inhibitors of inflammation |
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Can ischemic cause apoptosis?
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Yes; it can increase both necrosis and apoptosis
Necrosis-complete absence of any blood flow Apoptosis-where there is some collateral but insufficient blood flow (blood flow is dropped but there is some blood) |
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What are three diseases related to a decrease in apoptosis?
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Cancer
Autoimmune disease VIral infections |
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What are some diseases releated to a increase in apoptosis?
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Organ atrophy
Radiation damage to DNA Alzheimer's, Type 1 diabetes Ischemic injury |
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What are some physiological responses for apoptosis which are benefical?
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Post-lactation breast
Post-delivery uterus Post menopause uterine atrophy Development - e.g. hands; neuron selection in brain Thymic atrophy - deletion of thymocytes with potential self-reactivity |
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In a normal cell ROS generation usually comes from the ________ ______ _____.
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Electron transport chain
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What is an example of a reactive oxygen species (ROS)?
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H2O2-Hydrogen Peroxide
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What is an example of a mediator in cell injury?
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ROS/Free radicals
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What can dramatically increase the ROS generation in a normal cell by a factor of 10?
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Phagocytic activation
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What is the worst effect from the SOD generation?
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During this reaction two oxygens will form (using the enzyme superoxide dismutase) and form H2O2.
H2O2 can diffuse out and reactants can't. H2O2 is not that harmful but it can react with Fe(Fenton reaction) or Oxygen (Haber-Weiss) and form hydroxyl free radicals. Hydroxyl free radicals are the most damaging |
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Besides superoxide dismutase, where else can H2O2 be produced?
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In fatty acid oxidation by peroxisomes
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What effects can ROS have on Proteins?
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Cystine residues in proteins are susceptible, leading to protein loss of function via unfolding or scission
Modification of SH groups (form S-S cross linking) Adduct formation (covalently attach some molecule) with lysine, cystenine and tyrosine |
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What effects can ROS have on lipids?
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Polyunsaturated double bonds of fatty acids allow propagation of ROS in membranes.
The products Malondialdeyde and Hydroxynonenal come from the ROS propagation and indicate oxidative damage. Fatty acid oxidation Lipid cross linking Scission of lipids and malondialdyde formation Changes in membrane fluidity |
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What effects do ROS have on DNA?
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Base mutations
Chromosome breaks Base changes that will induce apoptosis |
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Superdioxide mutase is used in antioxidant defense but what else is needed?
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Since there is a converted H2O2, there must be an enzyme to remove the H2O2, such as catalase (H2O2 to H2O) and Gluthione peroxidase (Removes various perioxides)
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What is a major cellular anti-oxidant?
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Glutathione
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What is a major indicator of oxidative stress?
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The ratio of GSSG to GSH
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Besides GSH and Superoxide dimutase, what else is used in antioxidant defense?
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Heme oxygenase (remove iron availabilty from heme)
§ Vitamin E Reduce lipid peroxide radicals Vitamin C replenishes Vitamin E |
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What are two ways to repair ROS damage to proteins?
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Chaperones will try and take proteins back to proper shape. If doens't work, the ubiquitn covalently binding to proteins and taking to a proteosome.
Also the UPR Response Sensor proteins in the ER membrane that recognize proteins that aren't folded or excessive misfolded. -Will shut down making non-essentiel proteins -Will make tranx factors that will interact with response elements (motifs) and increase tranx of proteins you want (ubiquitin ligase, proteosome and glutathione synthase) |
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Describe what gives direct detection for ROS?
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Nrf2 is an effector molecule that binds to antioxidant response element and will trigger tranx of multiple protective genes.
Normally, Nrf2 is kept in the cytoplasm by keap1 and Nrf2 gets ubiquinated and destroyed Under oxidative stress, keap1 is oxidized and will release Nrf2 to go to nucleus and do its thing. Keap1 will be ubiquinated and destroyed. |
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Describe what gives direct detection of Hypoxia
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HIF usually in cytoplasm (enzyme PHID will add OH to HIF and this promotes ubiquitination)
Under hypoxia, PHID is inactive and this will not promote ubiquitation |
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What does PMPM stand for?
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PMPM stands for Per Member Per Month.
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What is in the purchaser tier, the provider tier and the payer tier?
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Provider-doctors
Purchaser-Government, Employer Payer-Inusruance |
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What is risk (healthcare risk)?
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Risk is the legal or contractual obligation to pay for health services.
Risk that one or more students in the class will need health services |
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Who bears the risk for our female patient that was shot?
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Individual
Employer Government County Insurance company via the employer bargining for this -Doctors don't usually own any of that risk |
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What are the three dragons?
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Quality, Cost and Access
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What is an HMO?
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HMO's take a single payment each month and provide preventative treatments
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Who is john Weenberg?
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Found out the rate of certain procedures in counties, varied by about tenfold
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Who is Bob Brook?
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Developed the RAND UCLA appropiateness method (detailed evidence summary + expert opion and found out if a certain medical treatment was a worthwhile medical benifit)
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Why is C-section done so frequently in the United States?
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You can do more C-Sections than vaginal births and this can give you more money, despite the fact that C-sections and vaginal births cost the same.
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What established how access to care came through employers?
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Kaiser owned a boat company and put a clinic on site to attract employees.
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Are most Americans against or fot individual mandate/penalty?
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Against
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What is subsidy?
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Flow of dollars to an individual, where government funds are being used to help out
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What are the reasons for high cost?
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Pricing of individuals
Success at bringing new technology Medical inflation -Malpractice and pharmaceuticals not the biggest facotrs |
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What are services?
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All tests, treatments and other stuff we provide to patients
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What is replicative senescence and the qualities of this process?
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Replicative senescence is when cells that were replicating, will stop replicating, not due to chronology but due to the amount of divisions.
These cells are resistant to apoptosis, are in all human somatic cells, may function as a tumor suppresor mechanism and there is alteration in fuction and gene expression of the cell. |
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As you get older your body has accumulated more senescent cells and they create favorable enivronments for other cesll to become cancers, such as?
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Fibroblasts and T cells
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How do senescent T cells promote cancer?
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They have an increase in inflammation (which contributes to cancer) also they decrease immune surveillance
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How do senescent fibroblasts promote cancer?
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They produce matrix-degrading enzymes and enhance growth of epithelial cell tumors.
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T cells have a decrease immune surveillance which leads to?
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Increased incidence and severity of virus
Re-emergence of latent infections Reduced response to vaccines |
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Where is the TCR variability from?
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The joining of VDJ
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Alot of cell divisions are required of T cells to fight an antigen, with repeatedly encountered antigens, such as ______ , ______, and _________ there will be more cell divisons
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Latent
Tumor Influenza |
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Since extensive proliferation is essential for proper T cell function, the T cells will eventually reach __________.
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Senescence
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What on the chromosome and why, signals for replicate senescence?
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The telomeres, since the telomeres are shortened during each cell division, once it reaches a certain significant short length, will then signal.
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Where is telomerase active?
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Cancer, Germ Cells, stem cells, and activated immune cells.
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Why do T cells senesce if there are Telomerases
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T cells lose there ability to up-regulate telomerase after further stimulation of the T cells.
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At senescenes we lose CD28 expression which is important in ______ stabilizion, ________, glucose _______ and co-stimulation for ______ to recognize antigens.
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mRNA
Trafficking metabolism T cells |
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Can T cells suppress tumor cells?
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Yes
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What cells are used in bone formation?
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Osteoblasts(building)
Osteoclasts (chewing away) |
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What cytokine produced by T cells, in particular senescent T cells, leads to osteoclast activity?
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RANKL
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Do you have shorter or longer telomeres in areas of pressure from blood flow?
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Shorter
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Telomere shortening are not the _______ for sickness just biomarkers for inflammation, oxidative stress, chronic infections and so fourth
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CAUSE
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