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15 Cards in this Set

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Equation for Basal Metabolic Rate
~24 kcal per day per kg body weight

[1 kg = 2.2 lbs]
Respiratory Quotient - Equation and Explanation
Moles of CO2 released/Moles of O2 consumed in oxidation

basically, how efficient the extraction of energy is in terms of oxygen use
Respiratory Control - Equation and Explanation
O2 consumption when ADP low / O2 consumption when ADP is high

WANT LOW NUMBER (0.06-0.2), b/c you should be reducing small amounts of oxygen when there's already a lot of ATP (numerator), and a lot when there is little ATP (denominator). This measures the proper function of the mitochondria, in terms of sensing and responding to ATP levels.
Rank Caloric Content (kcal/gram):

Carbs
Fat
Protein
Ethanol
Carbs (4) *but very high Respiratory Quotient
Protein (4)
Ethanol (7) *but NO nutrients
Fat (9) * but low respiratory quotient
Equation for Body Mass Index with Cutoffs
Weight (kg) / height (m) squared

Weight (lbs) x 704 / Height (in) squared

18.5-24.9 desirable

over 30 - obese
Keq equation and implication spontaneous rxn
Keq = [product]/[reactants] @ equilibrium

greater than 1 indicates a spontaneous rxn
Gibbs free energy - relation to Keq and value needed for spontaneous rxn
∆G must be negative for spontaneous rxn

if Keq > 1, ∆G is negative and rxn is exergonic and spontaneous
Equation for ∆G in terms of ∆H and ∆S
∆G = ∆H - T∆S

to produce -∆G you want small (even better if negative) ∆H and large ∆S
Equation for ∆G in terms of electron transfer and voltage
∆G = - (nF∆E)

n = # electrons transferred

∆E = change in voltage - you want it to be POSITIVE

*this is where you combine half redox reactions*
How does GST work, why does this suck, and how can it be inhibited
GST is a homodimeric enzyme upregulated in tumors that binds xenobiotics (like cancer therapeutics) in the cleft btwn its 2 homodimers and inactivates them. Bivalent synthetic inhibitors of GST bind to both active sites in the cleft of the homodimer and prevent GST from interfering with chemotherapy.
What is Allopurinol?
Allopurinol is a synthetic drug that binds to the active site of xanthine oxidase and prevents it from oxidizing xanthine to urate, and thereby preventing GOUT. This is just an example of an enzyme inhibitor.
Michaelis Menton Graph

(When to use it, Equation for Km and what that means)
Use it for allosteric inhibitors and activators (or any other noncompetitive modes of activation inhibition).

Km = [S] at 1/2 Vmax

Km is inversely proportional to the affinity of an enzyme for its substrate. As the affinity increases (via allosteric activation) the velocity will increase and the MM curve will shift left. This will reduce the value of Km at 1/2 Vmax. This reflects an effective increase in affinity of the enzyme for its substrate.
Lineweaver Burke plot

(when to use it, Equation for slope, Y intercept, and X intercept, and what these mean)
This is used to look at competitive inhibition

Slope = Km/Vmax
Y intercept = 1/Vmax (doesn't change - acts as a pivot for the line)
X intercept = -1/Km

*following competitive inhibition, the Km increases b/c the affinity of enzyme for substrate effectively decreases. Vmax remains the same, and therefore Km/Vmax (slope) increases (has to mathematically).
*The slope increased, but Y intercept stayed the same, and so X intercept (-1/Km) moved closer to zero (increased).
What is erythropoeitin (EPO)? Who uses it?
EPO is a hormone that promotes RBC production by calling the precursors out of the marrow and talking them into differentiating. People with kidney failure induced anemia, as well as people looking to "win, and win" take it. There are 3 different forms - the endogenous one, a recombinant human one, and a hyperglycosylated analog (NESP/Darbepoetin).
What are the major differences btwn the three types of EPO?
1. Endogenous EPO has 3-9 sialic acids (sialic acids increase the half life and RBC stimulation potency)
2. RHumEPO has 9-14 sialic acids, with increased half life and RBC stimulation, BUT has poorer binding to the EPO receptor
3. NESP/Darbepoetin (Amgen) was generated via site directed mutagenesis and has up to 22 sialic acid residues. Has really long half-life and increased RBC stimulation, nad higher in vivo bioactivity that either of the other 2.