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  • Book
    Clifford D. Packer.
    Summary: Medical students often struggle when presenting new patients to the attending physicians on the ward. Case presentation is either poorly taught or not taught at all in the first two years of medical school. As a result, students are thrust into the spotlight with only sketchy ideas about how to present, prioritize, edit, and focus their case presentations. They also struggle with producing a broad differential diagnosis and defending their leading diagnosis. This text provides a comprehensive guide to give well-prepared, focused and concise presentations. It also allows students to discuss differential diagnosis, incorporate high-value care, educate their colleagues, and participate actively in the care of their patients. Linking in-depth discussion of the oral presentation with differential diagnosis and high value care, Presenting Your Case is a valuable resource for medical students, clerkship directors and others who educate students on the wards and in the clinic.

    Contents:
    The Importance of a Good Case Presentation, and Why Students Struggle with It
    Organization of the Oral Case Presentation
    Variations on the Oral Case Presentation
    The HPI: A Timeline, Not a Time Machine
    Pertinent Positives and Negatives
    The Diagnostic Power of Description
    The Assessment and Plan
    Approaches to Differential Diagnosi
    Searching and Citing the Literature
    Adding Value to the Oral Presentation
    Teaching Rounds: Speaking Up, Getting Involved, and Learning to Accept Uncertainty
    On Pimping
    The Art of the Five-Minute Talk
    Future Directions of the Oral Case Presentation.
    Digital Access Springer 2019
  • Article
    Venturini S, Monti-Bragadin C.
    Mutat Res. 1978 Apr;50(1):1-8.
    The response to four mutagens (UV radiation, methyl methanesulfonate (MMS), cis-platinum dichlorodiamine (cis-PDD), and a 2-aminopurine (AP)) known to cause different types of DNA damage was investigated in the WP2 strain wild-type for DNA repair and in uvrA-, lexA-, polA-, uvrD- and recL- strains. Each strain was also tested after introduction of either the pKM101 or R648 plasmid. The number of revertants produced by a given mutagen in a given bacterial strain depended in a complex way on: (1) the nature of the mutagen and the type of lesion it created in DNA; (2) the prensence and the nature of defects in the chromosomally determined DNA-repair system; and (3) the presence and the nature of plasmids with mutator effect. The results confirm that plasmids enhance mutagenesis through an error-prone DNA-repair system, which is expressed at different levels for different plasmids. Or, alternatively, different repair mechanisms for different plasmids may exist.
    Digital Access Access Options