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  Brant and Helms Fundamentals of diagnostic radiology. Fifth edition.

  editors, Jeffrey S. Klein, William E. Brant, Clyde Helms, Emily N. Vinson.

  Summary: "Those familiar with previous editions will recognize editors and authors Drs. William Brant and Clyde Helms, who developed the concept of Fundamentals of Diagnostic Radiology 30 years ago. For this fifth edition, Bill has updated his introductory chapter on diagnostic imaging methods and contributed updated material on gastrointestinal and genitourinary radiology and ultrasound. Clyde has updated his section on Musculoskeletal Imaging along with Dr. Emily Vinson, Division Chief of Musculoskeletal Imaging at Duke University Medical Center, who now joins as an editor of Fundamentals. Drs. Erik Gaensler and Jerome Barakos have returned to edit the revised Neuroradiology section. Dr. Jeffrey Klein, along with colleagues from the University of Vermont Medical Center, provides an updated section on Chest Radiology and is now a senior editor of Fundamentals of Diagnostic Radiology"--Provided by publisher.
  
  Contents:
  Sect. I: Basic principles
  Sect. II: Neuroradiology
  Sect. III: Chest
  Sect. IV: Breast radiology
  Sect. V: Cardiac radiology
  Sect. Vi: Vascular and interventional radiology
  Sect. VII: Gastrointestinal tract
  Sect. VIII: Genitourinary tract
  Sect. IX: Ultrasonograpy
  Sect. X: Musculoskeletal radiology
  Sect. XI: Pediatric radiology
  Sec.t XII: Nuclear radiology.

  Digital Access Ovid 2019
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• Article

  The biochemical and genetic basis for high frequency thiomethyl galactoside resistance in lambda,lambdadg lysogens of Escherichia coli.

  Raney ME, Elliott RW.

  J Gen Microbiol. 1978 Feb;104(2):287-97.

  In a culture of Escherichia coli K12 gal (lambdadg), cells which form large colonies on agar plates containing galactose and thiomethyl beta-D-galactoside (TMG) appear at high frequency. These clones are resistant to growth inhibition by TMG on galactose minimal medium. Biochemical studies of the steady-state levels of galactokinase and UDPgalactose 4-epimerase suggest that the resistant clones have extra copies of the genes for the galactose-metabolizing enzymes. The mutation for TMG resistance is not located in either the bacterial or the bacteriophage genome, but is probably due to an aberrant association between cell and prophage DNA. Mapping the TMG-resistant characteristic by phage P1 indicates that TMG-resistant bacteria posses at least two GAL+ OPERONS, ONE OF WHICH IS COTRANSDUCIBLe with bio+. In addition, TMG-resistant bacteria behave like lambdadg polylysogens when challenged with the phage lambdaI90c17. From these genetic experiments we conclude that TMG-resistant bacteria arise by duplication of the lambdadg prophage. Finally, gal+ bacteria which carry a single, additional, lambdadg prophage are TMG-resistant. TMG resistance is probably a gal+ gene dosage effect.

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