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Crush Step 1: The Ultimate USMLE Step 1 Review, 1e by Theodore X. O'Connell

By Theodore X. O'Connell

When you know the entire innovations in Crush Step 1: the final word USMLE Step 1 Review, you need to do far better than pass USMLE Step 1: you want to Crush it! Led through Theodore X. O'Connell, MD, the writer of the best-selling USMLE Step 2 Secrets and Brochert's weigh down Step 2, this targeted, high-yield evaluate of center content material and try out prep options is the simplest USMLE Step 1 training available for this high-stakes examination. Written and reviewed via scholars, citizens, and specialists, Crush Step 1 is the source you must ranking high!

  • Focus on crucial ideas and grasp them efficiently with updated, easy-to-read, high-yield insurance of the entire fabric proven at the exam.
  • Ensure your comprehension with USMLE Step 1 perform questions following key sections in addition to rapid-review high-yield boxes.
  • Learn the way to examine for USMLE Step 1 with a extra strategic approach via a special concentrate on opting for and knowing query stems rather than memorizing buzz words.
  • Spend extra time learning and not more time searching because of a well-written, simply available process, with lots of precious lists and tables to spotlight high-yield data.
  • Depend at the relevance and accuracy of the content because of oversight via authors who scored in the 99th percentile at the USMLE Step 1 examination and evaluation forums constituted of scholars, citizens, and faculty.

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Normal hemoglobin is α2 β2. Fetal hemoglobin is α2γ2. Sickle cell disease (SSD) is α 2 βS2 . The O2-binding curve shifts right with increase in CO2, acidosis (low pH), increase in 2,3-BPG, exercise, and temperature. CO poisoning causes stabilization of the R state, a leftward shift in O2 saturation curve, and a saturation curve for hemoglobin that resembles the curve for myoglobin. 5 P50 for hemoglobin Myoglobin Hemoglobin Figure 2-4 Comparison of oxygen-binding curves for hemoglobin and myoglobin.

DNA polymerase has an exonuclease activity, which excises the damaged strand from 5′ to 3′. Finally, DNA ligase joins the ends together. Xeroderma pigmentosum is an autosomal recessive disorder that results from defective nucleotide excision repair due to a mutant UV-specific endonuclease. This leads to high rates of skin cancer after exposure to UV light, including melanoma, squamous cell carcinoma, and basal cell carcinoma. ❍ In base excision repair (BER), altered bases are recognized by DNA glycosylases and cleaved from the DNA backbone, and several other enzymes assist in repair of the site.

Stabilization of the transition state leads to decreased activation energy, leading to increased rates of substrate to ­product, but no change in reaction equilibrium. Enzymes are described mathematically using MichaelisMenton kinetics (Fig. 2-7): u= Vmax [S] , Km +[S] where Km is the substrate concentration at which the reaction rate is 12 Vmax , v is the velocity of the reaction, and [S] is the substrate concentration. A higher Km means a lower affinity of the substrate for the enzyme. Vmax 1/v Initial velocity (v) 4 1 3 2 Vmax 2 4 3 2 1/Vmax = Y intercept 1 A Km [S] B –1/Km = X intercept 1/[S] Figure 2-7 Michaelis-Menton enzyme kinetics.

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