Bradley D Figler, MD
Urologist (Male Reconstruction)
4 years of experience

Accepting new patients
Thomas Jefferson University (Navy Yard)
3 Crescent Drive
Philadelphia, PA 19112
(215) 503-3300
Locations and availability (2)

Education ?

Medical School Score Rankings
Case Western Reserve University (2006) *
  • Currently 4 of 4 apples
Top 25%
Residency
Emory University Hospital (2011) *
Urology
Fellowship
University of Washington/Harborview Medical Center (2013) *
Urology
* This information was reported to Vitals by the doctor or doctor's office.

Affiliations ?

Dr. Figler is affiliated with 2 hospitals.

Hospital Affilations

Score

Rankings

  • Thomas Jefferson University Hospital *
    Urology
    111 S 11th St, Philadelphia, PA 19107
    • Currently 4 of 4 crosses
    Top 25%
  • University Of Washington Medical Ctr
    Urology
    1959 Ne Pacific St, Seattle, WA 98195
    • Currently 2 of 4 crosses
  • Publications & Research

    Dr. Figler has contributed to 3 publications.
    Title Preoperative Psa is Still Predictive of Cancer Volume and Grade in Late Psa Era.
    Date December 2007
    Journal Urology
    Excerpt

    OBJECTIVES: To examine the relationship between preoperative prostate-specific antigen (PSA) and pathologic characteristics of the prostate gland and prostate cancer at radical prostatectomy in patients with clinically localized disease in the early (1993 to 1998) and late (1999 to 2004) PSA eras. METHODS: From January 1, 1993 to December 31, 2004, 2067 patients aged 40 to 80 years with clinically localized prostate cancer underwent radical prostatectomy without neoadjuvant therapy at the Cleveland Clinic. The correlation among the preoperative PSA level, prostate volume, percentage of Gleason pattern 4/5, surgical Gleason score, and cancer volume was calculated using Pearson's and Spearman's tests for the early (1993 to 1998) and late (1999 to 2004) PSA eras. Logistic regression analyses were performed to identify independent predictors of the percentage of Gleason pattern 4/5 and cancer volume during each era. RESULTS: In both eras, the PSA level correlated positively with the percentage of Gleason pattern 4/5, surgical Gleason score, and prostate volume, with nearly identical r values. The PSA level also correlated with the cancer volume in the late PSA era (the only era for which cancer volume data were available). In the multivariate model, biopsy Gleason score, clinical T stage, and PSA level were independent predictors of percentage of Gleason pattern 4/5 in both eras and of cancer volume in the late PSA era. CONCLUSIONS: Even in the late PSA era, the preoperative PSA level has retained its predictive value for the percentage of Gleason pattern 4/5 and cancer volume. The PSA level continues to have prognostic value for men with clinically localized prostate cancer treated by radical prostatectomy.

    Title Intestinal Metaplasia of the Bladder.
    Date March 2006
    Journal The Journal of Urology
    Title Bold-fmri of Ptz-induced Seizures in Rats.
    Date January 2006
    Journal Epilepsy Research
    Excerpt

    PURPOSE: To develop a non-invasive method for exploring seizure initiation and propagation in the brain of intact experimental animals. METHODS: We have developed and applied a model-independent statistical method--Hierarchical Cluster Analysis (HCA)--for analyzing BOLD-fMRI data following administration of pentylenetetrazol (PTZ) to intact rats. HCA clusters voxels into groups that share similar time courses and magnitudes of signal change, without any assumptions about when and/or where the seizure begins. RESULTS: Epileptiform spiking activity was monitored by EEG (outside the magnet) following intravenous PTZ (IV-PTZ; n=4) or intraperitoneal PTZ administration (IP-PTZ; n=5). Onset of cortical spiking first occurred at 29+/-16 s (IV-PTZ) and 147+/-29 s (IP-PTZ) following drug delivery. HCA of fMRI data following IV-PTZ (n=4) demonstrated a single dominant cluster, involving the majority of the brain and first activating at 27+/-23s. In contrast, IP-PTZ produced multiple, relatively small, clusters with heterogeneous time courses that varied markedly across animals (n=5); activation of the first cluster (involving cortex) occurred at 130+/-59 s. With both routes of PTZ administration, the timing of the fMRI signal increase correlated with onset of EEG spiking. CONCLUSIONS: These experiments demonstrate that fMRI activity associated with seizure activity can be analyzed with a model-independent statistical method. HCA indicated that seizure initiation in the IV- and IP-PTZ models involves multiple regions of sensitivity that vary with route of drug administration and that show significant variability across animal subjects. Even given this heterogeneity, fMRI shows clear differences that are not apparent with typical EEG monitoring procedures, in the activation patterns between IV and IP-PTZ models. These results suggest that fMRI can be used to assess different models and patterns of seizure activation.


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