Essay Instructions: For my Mammalian/Human Physiology lab, I have to do a drug review on the drug: Evista.
Here are the SPECIFIC guidelines provided from my instructor:
Advanced Writing Skills: A Drug Review
Today’s dry lab will give you an opportunity to learn advanced research skills including:
scientific web searches (pubmed), proper citation use and an occasion to hone your
advanced scientific writing skills.
Assignment: Write a 4-6 page review paper on a drug advertisement YOU found (and
brought to class) from a magazine. The review MUST include:
• Generic and Trade Name
• A brief introduction including an indication of use
• An explanation/background of the drug’s mechanism of action
• A summary of its clinical use supported by clinical trail data (should include
information like advantages, disadvantages, contraindications, safety)
• A brief discussion on YOUR perspective of the drug and its use based on the
information presented
• At least 5 References used and included in your reference section of the paper
Format will include a short introduction, summary of drug’s mechanism, summary of
clinical trials regarding clinical use, a brief discussion and references.
This assignment will be graded on the ability to communicate concisely and understand
the scientific information presented as well as will be graded for grammar and proper
citation use.
Please attach the drug advertisement you choose to your assignment!
Successful Writing Assignment Helpful Hints:
Present the information critically and concisely
Synthesize, compare, contrast and evaluate what you read
Don’t just assume the article is right- examine the results section of the papers
Attempt to write down what you remember from each article you read and what the final
conclusions of this paper were
Properly cite articles that you have read (Plagiarism will result in a zero at the very least
if not a visit to HONOR COUNCIL)
Sites to help search and find appropriate information:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi (or www.pubmed.com)
http://www.fda.gov/
http://www.nlm.nih.gov/medlineplus/tutorial.html
In addition:
Here are the paragraphs should be broken down into subtopics These are to be bolded and in caps before each paragraph:
Indication of Usage
Mechanism of Action
Pharmacokinetics
Metabolism
Dosage and Administration
Contradictions, Precautions, and Warnings
Adverse Rxns
Drug Interactions
Comparative Efficacy
Cost Analysis
References
In this drug review, actual trials of experiments in different phases of drug approval by the FDA are needed as support of the author's idea. Here is an example provided by my instructor:
The Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on February 20, 2004; 10.1124
Effects of Alcohols and Anesthetics on Recombinant Voltage-Gated Na+ Channels
Munehiro Shiraishi, and R. Adron Harris
“It has been thought that axonal conduction, and by inference voltage-gated Na+ channels, are not affected by reasonable concentrations of anesthetics (Franks and Lieb, 1994). However, more recent studies show that anesthetics at clinically relevant concentrations can suppress Na+ channel function in synaptosomes (Ratnakumari and Hemmings, 1998), neurohypophysial nerve terminals (Ouyang et al., 2003), and in cells transfected with a rat neuronal sodium channel, Nav1.2 channel (Rehberg et al., 1996)”
“The inhibition of the Na+ channels by isoflurane varied with holding potential; at the more depolarized holding potential, the effect of isoflurane was greater. In other words, the isoflurane effect was much greater when the fraction of the channels in the inactivated state was increased. Most of the channels were in the resting state that are ready for activation at the holding potential of -90 mV, whereas one-half of the channels were in the inactivated state at around -60-mV holding potential. These results are mostly consistent with other publications. For example, Stadnicka et al. (1999) showed that isoflurane, as well as halothane, suppressed heart sodium channels expressed in HEK293 cells by acceleration of the transition from the open to the inactivated state and stabilization of the inactivated states (Stadnicka et al., 1999). Moreover, isoflurane inhibited voltage-gated Na+ currents in a concentration- and voltage-dependent manner in isolated rat neurohypophysial nerve terminals, and the inhibition by isoflurane had no significant effects on V1/2 of the activation curve, but the V1/2 of the inactivation curve was consistently shifted in a negative direction (Ouyang et al., 2003).”
“The local anesthetic lidocaine is known to inhibit Na+ channels in DRG neurons in a voltage- and use-dependent manner. The IC50 of lidocaine on TTX-resistant Na+ currents is almost 200 µM (Roy and Narahashi, 1992; Scholz et al., 1998b). These results are consistent with our finding of 25% inhibition at 100 µM. One possible explanation for the insensitivity of Nav1.8 channels to anesthetics is that they do not bind to the Nav1.8 channel (but bind to other Na+ channels).”
