Browse Health
Urologist
3 years of experience

Education ?

Medical School Score Rankings
University of Maryland (2007)
  • Currently 3 of 4 apples
Top 50%

Awards & Distinctions ?

Associations
American Urological Association

Affiliations ?

Dr. Sofinowski is affiliated with 3 hospitals.

Hospital Affilations

Score

Rankings

  • Hickman Community Health Services
    135 E Swan St, Centerville, TN 37033
    • Currently 2 of 4 crosses
  • Middle Tennessee Medical Center Inc
    400 N Highland Ave, Murfreesboro, TN 37130
    • Currently 2 of 4 crosses
  • Baptist Hospital
    Urology
    2000 Church St, Nashville, TN 37236
    • Currently 1 of 4 crosses
  • Publications & Research

    Dr. Sofinowski has contributed to 2 publications.
    Title Restoring Barrier Function to Acid Damaged Bladder by Intravesical Chondroitin Sulfate.
    Date October 2009
    Journal The Journal of Urology
    Excerpt

    Chondroitin sulfate (Stellar Pharmaceuticals, London, Ontario, Canada), which is less expensive and more inert than heparinoids, hyaluronan or pentosan polysulfate, has been introduced to restore the barrier function lost due to epithelial dysfunction in interstitial cystitis cases. To our knowledge chondroitin sulfate binding to damaged bladder as a function of the urinary pH range, its efficacy in restoring the bladder permeability barrier and the capacity of the damaged bladder to bind chondroitin sulfate have not been determined previously.

    Title Repair Mechanisms for Oxidative Dna Damage.
    Date February 2004
    Journal Frontiers in Bioscience : a Journal and Virtual Library
    Excerpt

    Reactive oxygen species are formed as by-products of mitochondrial aerobic respiration, as induced products upon exposure to certain environmental/exogenous agents (e.g. ionizing radiation), or as intended products during the immune response against invading foreign microbes. Although serving as essential signaling molecules in certain biological processes (e.g. during gene activation responses), these chemicals, particularly during oxidative stress when at excessive concentrations, can react with cellular components, most notably DNA, and in this capacity, promote mutagenesis or cell death, and in turn, human disease. We review here several of the common oxidative DNA damages as well as the DNA repair mechanisms related to maintaining genome integrity, and thus, preventing cancer formation and age-related disease. We focus mainly on participants of the base excision repair (BER) pathway. In brief, the steps of BER include: (a) excision of the damaged base, (b) incision of the DNA backbone at the apurinic/apyrimidinic (AP) site product, (c) removal of the AP terminal fragment, (d) gap-filling synthesis, and (e) ligation of the final nick.

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