Apoptosis lecture:

1. You mentioned in lecture that metamorphosis is unrelated to

programmed cell death, although it’s a process of regulated cell
death. What’s the difference between programmed and regulated cell
death?
It’s PCD but not apoptosis.

2. Do bax/bak/bid/bad all live in the mitochondria? if so, what

compartment are they localized to?
bax/bak/bcl2 are pretty much found everywhere.. bax/bak are always
there. bax/bak are pbb already active.. but regulated by bcl2 somehow.
lots of bcl2 binds up puma. BCL2 IS NOT A TRANSCRIPTION FACTOR.

3. In class, we talked about how some kidney tumor cells produce a

ubiqutinating enzyme that acts on bcl2. Does mean that bcl2 would get
tagged for degradation, which would lead to more apoptosis, and the
tumor would essentially be killing itself?
didn’t say that. kidney cells if damaged will die on their own by inducing
apoptosis. targets bcl2 for deg. TUMOR  knocks out enzyme for
ubiquitination.

caspases just cut once. it results in two chunks of protein that can get
degraded or go on to do other things.

ubiquitin system – once you tag it, the whole protein is degraded.

Blood cell formation lecture:

1. What exactly does the term “formed blood element” encompass? Are
erythrocytes considered to be cellular components of the blood since
they have no organelles?
formed blood element – acellular: platelets & RBCs. no nuclei. they don’t
undergo apoptosis when they’re getting cleared cuz they’re not cells.

2. Under what conditions would reticulocytes enter circulation, and

what consequences would this have on the body?
massive hemorrhage, hematocrit drops super low (lotta serum but not
enough RBCs), nucleated cells won’t leave the sinus, but enucleated cells
will. reticulocytes don’t do as good of a job of carrying oxygen but it’s better
than nothing – it also still has a couple of organelles -- also can’t deform
properly.

3. In class, we talked about RBC population expansion, which involved

BFC-E cells and CFC-E cells, and ultimately mature erythrocytes. Do
BFC-E cells correspond with pluripotent hematopoietic stem cells,
where as CFC-E cells correspond with multipotent myeloid stem cells
and committed progenitor cells?

need epo for division & keep 4m dying. start out w/committed progenitor
cell, expressing IL3-R. at some point, they’re gonna start expressing epo
receptor. need epo-r & epo to divide & keep from living. EPO-R = RTK.

bad is inactivated by plation.

bcelllymphoma – bcl2 levels fall cuz cell doesn’t have right stimulation.
constitutively expressed bcl2 that can’t keep up (cuz it’s getting tagged on
IgG)

4. You mentioned in class that pluripotent stem cells with c-kit

receptors are found in circulation. Are these pluripotent stem cells
the same as the hematopoietic stem cells (HSC) found in marrow, the
only difference being their location?
HSCs are in circulation and in marrow. all stem cells are pbb doing that. all
stem cells probably have a niche where they can develop.

5. Why does the binding of pluripotent stem cells to steel factor

result in receptor downregulation?
insulin binds insulin receptor. u don’t want it to just keep reacting to insulin.
downregulation cuz u want to regulate the signaling via internalization of
receptor.

unbinding ckit and steel – protease to clip boundsteel, phosphatases to

deactivate RTK..

Etc.
Terminal bronchioles have no seromucous glands, but what about
bronchioles closer to the mainstem bronchi?
early bronchioles have goblets but they go away. bronchioles have no
submucosa.?? NO BRONCHIOLES have seromucous. if anything, goblet
cells @ the very beginning.
Are the reticular cells that make the stroma of spleen and lymph nodes?
part of reticular cells are adventitial cells. thinks that in marrow it’s the
same reticular cells (type III).

adventitial cells have nothing to do with adventitia.

steel is tm protein.

endosteum would be the “tunica advneitita” of a capillary in the

marrow. only @ the border.