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  • Book
    Christopher R. Chapple, Alan J. Wein, Nadir I. Osman, editors.
    Summary: In this book, the authors look at the field of underactive bladder and its presentation, clinical diagnosis, potential etiopathogenesis and treatment. While the editors address a great deal of background information, they clearly identify that many limitations still exist to clinical diagnosis and urodynamic evaluation, and in particular a dearth of appropriate treatment options. This complex condition needs to be recognized and identified in the routine evaluation and clinical management of patients.

    Contents:
    1. Pathophysiology and Associations
    2. Non-invasive diagnostics for Detrusor underactivity/Underactive bladder
    3. Invasive Diagnostic Tests
    4. Epidemiology of Underactive Bladder
    5. Indications For Treatment
    6. Pharmacologic Treatment of Underactive Bladder
    7. Surgical Treatment : Outlet Reduction, Men and Women
    8. Neurostimulation and Neuromodulation for the Treatment for the Underactive Bladder
    9. Reduction Cystoplasty
    10. Bladder Wrap Procedures
    11. Tissue Engineering and cell therapy for underactive bladder: current and future approaches
    12. Reflections and the Way Forward.
    Digital Access Springer 2017
  • Article
    Eckardt F, Haynes RH.
    Genetics. 1977 Feb;85(2):225-47.
    We have measured the frequency of UV-induced reversions (locus plus suppressor) for the ochre alleles ade2-1 and lys2-1 and forward mutations (ade2 adex double auxotrophs) in an excision-deficient strain of Saccharomyces cerevisiae (rad2-20). For very low UV doses, both mutational systems exhibit linear induction kinetics. However, as the dose increases, a strikingly different response is observed: in the selective reversion system a transition to higher order induction kinetics occurs near 9 ergs/mm2 (25% survival), whereas in the nonselective forward system the mutation frequency passes through a maximum near 14 ergs/mm2 (4.4% survival) and then declines. This contrast in kinetics cannot be explained in any straightforward way by current models of induced mutagenesis, which have been developed primarily on the basis of bacterial data. The bacterial models are designed to accommodate the quadratic induction kinetics that are frequently observed in these systems. We have derived a mathematical expression for mutation frequency that enables us to fit both the forward and reversion data on the assumptions that mutagenesis is basically a "single event" Poisson process, and that mutation and killing are not necessarily independent of one another. In particular, the dose-response relations are consistent with the idea that the sensitivity of the revertants is about 25% less than that of the original cell population, whereas the sensitivity of the forward mutants is about 29% greater than the population average. We argue that this relatively small differential sensitivity of mutant and nonmutant cells is associated with events that take place during mutation expression and clonal growth.
    Digital Access Access Options