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30 Cards in this Set

  • Front
  • Back
Essay: Conditional Knockout
in nervous system ^G in blood
neg feedback of HPA axis req. G
-less anxious-->role of G in learning, anxiety, memory in neurons
Essay: Knock-in
-mutation causing failure of receptor dimerization and DNA binding.
-mice survived
-suggests G ^imp't Prot/Prot int.
-reg. of xscrip factors
Essay: Mutation in Human: disease and treatment
-Adrenal Hyperplasia & ^ ACTH (-->^GR)
-from a pituitary tumor (Cushing's)
-Adrenal Neoplasia
-^ use of glucocorticoid
Essay: What happens in nucleus
GR bound by cortisol (g-coritcoid):
1. binds GRE: represses or activates xscription
2. protein:protein interaction - regulates xscrip. factors (AP1&NF-kB)
Essay: Mechanism of action
stress (physical: infection/injury or emotional)
-->hippocampus, amygdala-->hypothalamus -(CRF&AVP)-> Pituitary -(ACTH)-> Adrenal Glands --> secrete glucocorticoid (inhib. ACTH&CRF) --> cyto. G receptor --> nucleus
Essay: Syndrome, causes, symptoms
Cushing Syndrome
causes ^glucocorticoid (hypercortisolism)
symptoms: obesity, hypertension, osteoporosis, diabetes
Physiological Jaundice
^ unconjugated bilirubin in newborns due to low UDP-glucuronyltransferase (b/c liver not fully developed)
--mild form doesn’t req’ treatment & improves
--severe form needs treatment: fluorescent light
However, if there’s ^ levels of conjugated bilirubin, means impaired removal (ie liver damage, bile duct obstruction)
Reason #2 for Decreased Excretion
1.bile duct obstruction(obstructive or posthepatic jaundice) 2. decreased bilirubin excretion (note:rate of bilirubin excretion correlates w/ rate of bile flow) 3.^conjugated bilirubin
Decreased Excretion b/c of:
1. liver damage(hepatocellular or intrahepatic jaundice) 2.decreased bilirubin uptake and conjugation 3.^levels of unconjugated bilirubin (dangerous! Unconjugated bilirubin in excess of albumincapacity„³binds lipids; impairs membrane funct. esp. in nervous system)
bilirubin turnover
By labeling glycine*
Heme turnover in liver (15%)

early-late \
in liver and bone marrow
(poorly incorporated or
easily released from RBC)
^ w/ diseases ie. pernicious anemia
, thalassemia

in RBC’s (85%)
RBC’s>Heme>biliverdein>bilirubin>complexedw/albumin>conjugated w/glucuronic acid>bile>unconjugated bilir.>urobilinogen>urobilin(stercobilin in feces) or urobilin in kidney.
HEME: what makes it up and location of steps
-4 pyrrole rings, 4methylene bridges, synthesized mostly in Liver & bone
-marrow, of the 8 steps, the 1st & last 3 steps are in the mitochondria, 2nd –
5th steps are in cytosol, only Uroporphyrin III is acceptable to body (it’s
assymetrical w/A’s(acetate) & P’s (propionate).
HEME : Found in
: 1.hemoglogin (binds O2) 2.myoglobin 3. cytochromes (e- carrier
(p450) 4. catalase(part of active site)
Phy Active Amines: characteristics
1.All are neurotransmitters 2. All are excitatory except GABA,Gly, Taurine(inhibitory).
1.Decarboxylation w/PLP cofactor (and/or)
2. Hydroxylation w/ BH4
NO synthase

NO char
1.diffuses freely through membranes 2.short ½
life 3.reactive 4. cell signal molec. 5. smooth muscle relaxer 6.prevents platelet aggre. 7.nuerotransmitter 8.made in macrophages as a bacterial/cancer killer
“Small Wimpy Trashy Person is Depressed” so he “Pax” his “Prosac”
GABA (γ-aminobutyric acid): MNEM
someone who “GAB”s a lot can be “inhibited” by “GluEing” their mouth shut.
Glutamate(E) characteristics
is excitatory and found in all neurons GABA is inhibitory and found in only inhibitory neurons. They’re opposites! Some epileptics have decreased GABA levels—treated w/ Valproic Acid = ^GABA
Heme synthesis: overall rxn
8 glycine + 8 succinyl CoA + Fe 2+ ---„³ ---„³ Heme
ALA locations
ALA 1 in liver & ubiquitous, ALA 2 in bone marrow
PORPHYRIAS: Enzymatic abnormalities:
Hepatic & neuropsychiatric effects

Causes ^ALA & PBG and/or with decreased heme in cell body fluids.
you want to “Create” (Creatine) or “GROw” muscle ever since you “Met” “SAM” the trainer
lowers ROS’s, analogs increase tumor sensitivity to ROS from irradiation
Bilirubin in blood =
unconjugated / indirect bilirubin (w/ colorimetric RXN in methanol.
Bilirubin in bile =
conjugated/ direct bilirubin (w/ colorimetric RXN in aqueous solution)
Heme Sources:
85% RBC’s, 15% immature RBC turnover; liver and other extraerythroid tissue.
Yellowing of skin and white of eye from bilirubin deposition… caused by 1.^production or 2. decreased excretion
Increased Production b/c of:
1.excess hemolysis(hemolytic/prehepatic jaundice) 2. insufficient conjugation or complexing 3. ^levels of unconjugated bilirubin (dangerous!)
Essay: Knockout
die shortly after birth due to low production of surfactants--> respiratory failure